Crack The Core Exam 7th Edition
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Chen CohenCrack The Core Exam 7th Edition
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Chen CohenADH_2020
CRACK
THE CORE EXAM
7th (2020) EDITION
VOLUME 1
WRITTEN & ILLUSTRATED BY:
PROMETHEUS LIONHART, M.D.
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CRACK THE COKE EXAM -VOL 1
SEVENTH ED. - VERSION 1.0
DISCLAIMER:
READERS ARE ADVISED - THIS BOOK IS NOT TO BE USED FOR CLINICAL DECISION
MAKING. HUMAN ERROR DOES OCCUR AND IT IS YOUR RESPONSIBlLITY TO
DOUBLE CHECK ALL FACTS PROVIDED. TO THE FULLEST EXTENT OF THE LAW, THE
AUTHOR ASSUMES NO RESPONSIBILITY FOR ANY INJURY AND/OR DAMAGE TO
PERSONS OR PROPERTY ARISING OUT OF OR RELATED TO ANY USE OF THE
MATERIAL CONTAINED IN THIS BOOK.
ISBN: 9781673734270
INDEPENDENTLY PUBLISHED — PROMETHEUS LIONHART (EARTH DIMENSION C-137)
COPYRIGHT © 2019 BY PROMETHEUS LIONHART
ALL RIGHTS RESERVED - UNDER INTERNATIONAL AND PAN-AMERICAN COPYRIGHT CONVENTIONS.
THIS BOOK, OR PARTS THEREOF, MAY NOT BE REPRODUCED IN ANY FORM WITHOUT PERMISSION
FROM THE AUTHOR.
COVER DESIGN, TEXTS, AND ILLUSTRATIONS: COPYRIGHT © 2019 BY PROMETHEUS LIONHART
ADDITIONAL ART PROVIDED BY: HAAJAR DESIGN/SHUTTERSTOCK.COM
NO SLAVE LABOR (RESIDENT OR FELLOW) WAS USED IN THE CREATION OF THIS TEXT
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VOLUME 1
WRITTEN & ILLUSTRATED BY
PROMETHEUS LIONHART, M.D.
01 - ART OF WAR
------9-33
06 - ENDOCRINE
------343-361
02 - PEDIATRICS
------35-139
07 -THORACIC
------363-430
0 3 - GASTROINTESTINAL
------141-222
08 - CARDIAC
------433-466
04 - URINARY
------225-269
09 - NUKES
------469-544
0 5 - REPRODUCTIVE
------271-341
VOLUME 2:
TOPICS: NEURO, MSK, VASCULAR, IR, MAMMO, STRATEGY
WAR MACHINE:
TOPICS: PHYSICS, NON INTERPRETIVE SKILLS, BIOSTATS
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LEGAL STUFF
READERS ARE ADVISED - THIS BOOK IS NOT TO BE USED FOR CLINICAL DECISION MAKING.
HUMAN ERROR DOES OCCUR, AND IT IS YOUR RESPONSIBILITY TO DOUBLE CHECK ALL
FACTS PROVIDED. TO THE FULLEST EXTENT OF THE LAW, THE AUTHOR ASSUMES NO
RESPONSIBILITY FOR ANY INJURY AND/OR DAMAGE TO PERSONS OR PROPERTY ARISING
OUT OF OR RELATED TO ANY USE OF THE MATERIAL CONTAINED IN THIS BOOK.
ARE RECALLS IN THIS BOOK? ABSo LUTELY NOT
THE AUTHOR HAS MADE A CONSIDERABLE EFFORT (IT'S THE OUTRIGHT PURPOSE OF THE
TEXT), TO SPECULATE HOW QUESTIONS MIGHT BE ASKED. A PHD IN BIOCHEMISTRY CAN FAIL
A MED SCHOOL BIOCHEMISTRY TEST OR BIOCHEM SECTION ON THE USMLE, IN SPITE OF
CLEARLY KNOWING MORE BIOCHEM THAN A MEDICAL STUDENT. THIS IS BECAUSE THEY
ARE NOT USED TO MEDICINE STYLE QUESTIONS. THE AIM OF THIS TEXT IS TO EXPLORE THE
LIKELY STYLE OF BOARD QUESTIONS AND INCLUDE MATERIAL LIKELY TO BE COVERED,
INFORMED BY THE ABR'S STUDY GUIDE.
THROUGHOUT THE TEXT THE AUTHOR WILL ATTEMPT TO FATHOM THE MANNER OF
QUESTIONING AND INCLUDE THE CORRESPONDING HIGH YIELD MATERIAL. A CORRECT
ESTIMATION WILL BE WHOLLY COINCIDENTAL.
HUMOR/ PROFANITY WARNING
I USE PROFANITY IN THIS BOOK. I MAKE "GROWN UP" JOKES. PROBABLY NOT A
GOOD IDEA TO READ THE BOOK OUT LOUD TO SMALL CHILDREN OR ELDERLY
MEMBERS OF YOUR CHURCH / TEMPLE / MOSQUE. NOW IS NOT THE OPTIMAL
TIME TO BE RECREATIONALLY OUTRAGED - I'M JUST TRYING TO MAKE THE BOOK
READABLE AND FUN.
I ALSO TALK A MESS OF SHIT ABOUT DIFFERENT MEDICAL SPECIALTIES. I DO THIS BECAUSE
RADIOLOGISTS ARE TRIBAL, AND STROKING THAT URGE TENDS TO CALM PEOPLE. PROBABLY
NOT A GOOD IDEA TO READ THE BOOK OUT LOUD TO MEMBERS OF YOUR FAMILY THAT ARE
IN SPECIALTIES OTHER THAN RADIOLOGY. THE TRUTH IS I RESPECT ALL THE OTHER SUB
SPECIALTIES OF MEDICINE (EVEN FAMILY MEDICINE) - THOSE ARE DIRTY JOBS (POOP, PUS, &.
NOTE WRITING) BUT SOMEONE NEEDS TO DO THEM.
IF YOU STILL FEEL THE DESIRE TO EMAIL ME ABOUT HOW I HURT YOUR FEELINGS AND
RUINED YOUR LIFE, CONSIDER THAT "MAYBE PEOPLE THAT CREATE THINGS AREN'T
CONCERNED WITH YOUR DELICATE SENSIBILITIES."
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WHAT MAKES THIS BOOK VNIQUE?
SHORT ANSWER — FUCKING EVERYTHING
HOW? — WELL FOR STARTERS, THESE BOOKS WEREN'T WRITTEN BY 30 RESIDENTS,
20 FELLOWS, AND 10 TURBO NERD ATTENDINGS.
INSTEAD THE BOOKS WERE WRITTEN BY A RELENTLESSLY SELF IMPROVING MANIAC,
DRIVEN TO PURGE THE HERETICS (ORC SCUM), LAUNCH VENGEANCE UPON THIS
PLANET, AND DELIVER MERCILESS JUSTICE UPON THE ENEMIES OF FREEDOM AND
LIBERTY
THE IMPETUS FOR THIS BOOK WAS NOT TO WRITE A REFERENCE TEXT OK
STANDARD REVIEW BOOK, BUT INSTEAD, A STRATEGY MANUAL FOR SOLVING
MULTIPLE CHOICE QUESTIONS FOR RADIOLOGY THE AUTHOR WISHES TO CONVEY
THAT THE MULTIPLE CHOICE TEST IS DIFFERENT THAN ORAL BOARDS IN THAT YOU
CAN'T ASK THE SAME KINDS OF OPEN-ENDED ESSAY-TYPE QUESTIONS. "WHAT'S YOUR
DIFFERENTIAL?"
QUESTIONING THE CONTENTS OF ONE'S DIFFERENTIAL WAS THE ONLY REAL
QUESTION ON ORAL BOARDS. NOW THAT SIMPLE QUESTION BECOMES NEARLY
IMPOSSIBLE TO FORMAT INTO A MULTIPLE CHOICE TEST. INSTEAD, THE FOCUS FOR
TRAINING FOR SUCH A TEST SHOULD BE ON THINGS THAT CAN BE ASKED. FOR
EXAMPLE, ANATOMY FACTS - WHAT IS IT? ... OR... TRIVIA FACTS - WHAT IS THE
MOST COMMON LOCATION, OR AGE, OR ASSOCIATION, OR SYNDROME? ... OR...
WHAT'S THE NEXT STEP IN MANAGEMENT? THINK BACK TO MEDICAL SCHOOL
USMLE STYLE, THAT IS WHAT YOU ARE DEALING WITH ONCE AGAIN. IN THIS BOOK,
THE AUTHOR TRIED TO COVER ALL THE MATERIAL THAT COULD BE ASKED
(REASONABLY), AND THEN APPROXIMATE HOW QUESTIONS MIGHT BE ASKED
ABOUT THE VARIOUS TOPICS. THROUGHOUT THE BOOK, THE AUTHOR WILL
INTIMATE, "THIS COULD BE ASKED LIKE THIS," AND "THIS FACT LENDS ITSELF WELL
TO A QUESTION." INCLUDED IN THE SECOND VOLUME OF THE SET IS A STRATEGY
CHAPTER FOCUSING ON HIGH YIELD "BUZZWOKDS" THAT LEND WELL TO CERTAIN
QUESTIONS.
THIS IS NOT A REFERENCE BOOK.
THIS BOOK IS NOT DESIGNED FOR PATIENT CARE.
THIS BOOK IS DESIGNED FOR STUDYING SPECIFICALLY FOR MULTIPLE CHOICE TESTS,
CASE CONFERENCE, AND VIEW-BOX PIMPING/QUIZING.
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Radiology Master of Sport - National Champion
Americans love to fight. Americans love the champion.
This right here is about recognizing a commitment to being the best. Being the best, standing on
the top stand - and more importantly the quest to stand on the top stand and wear the yellow
medal is what I want to recognize.
The quest is very lonely. They say it is lonely at the top - that is not true. When I started to
become recognized internationally as the top educator in the field I suddenly had alot of people
who wanted to be my friend. I didn’t have any friends on the way there - nobody was getting up
at 4 am with me to write... nobody, not one person. It was just me - alone. It is lonely getting to
the top and that is where most people fall off. It's Friday and everyone else is going out, or there
is a party or whatever - I’m tired and I want to sleep in. I was on call last night - it is just not
worth it. What I’m hoping to share is that for me that is not what life is. Life is about being the
best person you can be in whatever it is you arc doing. That does not have to be Radiology, but
because you arc reading this book well that is what it means for you now.
You make the quest. If you get the top score on the exam - I'll be putting your name in this book
next year and you can motivate the next legend of tomorrow. Plus, I’ll give you some money and
have an enormous lion trophy made for you.
The most important thing is not actually winning. People think I only care about winning
because I rant and rave about how only the gold medals count - but the quest is what I really
value. I'm not training for silver. I'm training for gold. The quest for gold is more important than
someone handing you a gold medal. The katana sword of the black dragon society cannot be
stolen - it can only be earned. Outcomes really don’t matter, because the truth is in this life you
can do everything 100% perfect and still fail and you can do almost everything wrong and still
win. If you don’t focus on outcomes and instead the quest itself you will get something much
greater besides a high probability of passing the test - what you can gain from the quest, the
ability to really dedicate yourself to something 100% - it is a skill you can use for the rest of your
life. This is the way to always achieve victory. Once you know the way, you can see it in all
things - as the samurai say.
HALL OF CHAMPIONS
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I FIGHT FOR THE USERS
-TRON 1982
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1
THE ART OF WAR
PROMETHEUS EIONHART, M.D.
The art of war is of vital importance... It is a matter of life and death, a road either to safety or to ruin.
Hence it is a subject of inquiry which can on no account be neglected. - Sun Tzu
My idea for this first chapter is to provide some guidance on how to “wage war.” I’m going
to share with you my philosophy on training and performing optimally under pressure.
Specifically, I want to give you some ideas on how to deal with test anxiety, fear of failure,
motivation, and self mastery.
June / November is Coming
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SECTION 1:
Det a i l As s es s men t
a n d Pl a n n i n g
Before we get started with the “when” and “how” of the exam you need to have a clear
understanding of the “what. ” Let us begin with the most important topic - “passing. ”
The official stance is that everyone can theoretically pass the examination - which sounds
good if you are simply testing for safety and competence. The problem occurs when you
bring in professional statisticians and test metric experts (which all professional exams do).
These people insist on creating a normalized curve to validate the exam. An examination with
100% pass rate is statistically invalid (it wasn’t sensitive enough to detect the “dangerous
radiology trainees”).
If they passed everyone they would totally invalidate their own exam. They would risk public
perception perceiving the exam as a cash grab disguised as a formality. If they failed more
than 20 or 25% they would have a full revolt to deal with (lead by Program Directors who
want you reading nodule followups not studying for a repeat exam) - let us not forget the
entire reason the US boards were restructured was to eliminate off service study time for the
more senior residents (oh sorry, I meant “trainee” or maybe “learner”). They can’t set a hard
number or they risk one of these two scenarios. So, like every other standardized exam
you’ve ever taken, it’s curved. They may not “curve” the exam in the traditional sense, but
questions will be removed until the statistics provide an acceptable yield of passing and
failing scores. This is standard operating procedure on any exam of this magnitude.
Which leads me to my second point. Frequently I am asked “what do I need to score to
pass? ” Or “how many can I miss ? ” You can’t think about this exam as requiring a certain
raw score (even though they will give you one - constructed via space magic). You can’t say I
got 9/10 correct so I passed. What if everyone else got 10/10 right? You just got the lowest
score in the country. If anyone is gonna fail it is you - despite getting 90% of the questions
right. You need to think about it as your score relative to the rest of the room. Historically
around 10% of people fail, and 1-2% of people condition physics. So, if you score in the
15th percentile or higher you are probably safe.... probably.
Another common question is, “how many subjects can I condition?” On the old oral boards
there was a certain number of subjects that you could condition (fail) without having to retake
the entire exam. You would just have to come back in a few weeks and be tested on that
subject (or subjects) to meet criteria for a pass. The original official statement on the CORE
exam was something similar, that you could fail up to five categories. However, when no one
ever conditioned anything other than physics after 5-6 years people started to notice that was
probably bullshit. Now there has been an official statement that only physics can be
conditioned. Your clinical totals are lumped into a raw score and then compared to a
“predetermined” minimal score (that is later adjusted to fail around 10% of people).
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You may be thinking to yourself “That doesn't sound hard. I’ve never scored that low on
anything.” There is no greater danger than underestimating your opponent. You have never
competed at this level before. Your shelf exam scores , USMLE, etc... don’t mean shit
because you were competing against Family Medicine , Peds, Psych, etc.... This time you are
competing against Radiology Residents only. Yes, it is less competitive compared to the
“glory days” but Radiology still has a lot of smart people in it. Smart enough to realize how
to avoid the worst parts of medicine anyway. Plus, you are dealing with an extremely
motivated group. Most reasonable people are terrified to fail this exam and will therefore be
putting considerable effort into passing.
But Prometheus!? I heard someone say “all you need to do is take call to pass. ”
Yes... someone did famously say that. Everyone has an agenda in this life. My agenda is to
help you pass this exam. Other people... perhaps they want you to take call for them. Or
perhaps they just want to make sure you are “safe” and “protect the public.” Those people (if
they are reading) can prove their virtuous motives by writing questions that are fair, clinically
relevant, and follow topics on the official provided study guide. If your motivations are truly
genuine consider writing a fair test, free of trickery, on bread and butter topics - as this would
make board review books unnecessary.
I prefer teaching clinical radiology anyway (RadiologyRonin.com)
Let us switch gears and discuss the structure of the exam. The exam is a multiple choice test
consisting of around 600 questions. The punishment is administered over two days, the first is
typically longer than the second (7.5 hours and 6 hours respectively). They give you 30 mins
“break time” but that is built into the exam. You can take this 30 mins in any interval or ratio
you want - (example — you could take thirty 1 min breaks, six 5 min breaks, etc...).
The CORE Exam covers 18 categories (sometimes 17 - in Chicago). The categories include:
breast, cardiac, gastrointestinal, interventional, musculoskeletal, neuro, nuclear, pediatric,
reproductive/endocrinology, thoracic, genitourinary, vascular, computed tomography, magnetic
resonance, radiography/fluoroscopy, ultrasound, physics, and safety. This book is outlined to
cover the above sections, with the modalities of CT, MRI, Radiography, Fluoroscopy, and
Ultrasound integrated into the system based chapters as one would reasonably expect.
On the exam, Physics questions are integrated into each category with no distinct physics
examination administered. However, the physics section is still considered a virtual section, and
you can fail / condition it. In fact, the physics portion is actually the overall largest section. My
book “The War Machine” is dedicated to review of physics and the various non-interpretive
skills.
Useless trivia from a portion of the Radioisotope Safety Exam (RISE), one of the requirements
for Authorized User Eligibility Status, is also included within the Exam - and this material is
also distributed appropriately in my various texts.
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SECTION 2:
Wa g i n g Wa r
In the previous section, I tried to introduce the idea that the exam should not be viewed as a
test on which a certain “minimum score” is required to pass. Instead, I want you to look at
the exam as a contest in which you must finish in the top 85% to achieve victory.
I’m not trying to scare you. I’m just trying to help you understand that you must take this
exam serious. It’s tough and smart people fail it every year.
Over the next 6-12 months, when you are out partying and horsing around - remember that
someone else out there at the same time is working hard. Someone is learning, getting
smarter, and preparing to win.
Life is a struggle. Everybody fights - and that doesn’t mean getting punched in the face.
That means not hitting the snooze button, managing your personal relationships, dealing with
disability, trying to do the right thing for your children - etc... etc... and everyone gets asked
the same question - “Can I move on, or am I going to give up on my dreams?”
Transform a threat into a challenge. A life free of struggle is a life void of meaning. We
are bom for battle. Battle against the beasts of the jungle. Battle against the rival tribes.
And... yes... battle against each other on the glorious field of multiple choice questions.
I encourage you to embrace this as a great opportunity to weaponize your will.
The time has come my brothers (and sisters) to show no mercy.
Retribution is at hand.
Let fury guide you and let vengeance be your song.
Thank all the Gods of War for providing you with this opportunity to prove your greatness.
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SECTION 3:
At t a c k By St r a t a g em
“Victorious warriors win first and then go to war ”
As we begin our discussion of specifics, I will now share with you my 3 Promethean Laws for success
on this exam and in life. These laws are the beginning of understanding “the way,” and once you
know “the way” you will begin in see it in all things.
LAW 1 - You must do anything your opponents are willing to do.
Example: If everyone is reading a certain book, then you must also. If everyone is using a particular
q-bank (or banks) then you must also. If everyone is studying a certain amount per day then you must
also.
LAW 2 - You must do things your opponent is NOT willing to do.
Terry Brands once told me the secret to being a world champion is actually very simple - all it takes is
doing something no one else is doing - and then do it every day. It doesn’t even matter what it is, as long
as no one else is doing it. This principal has more to do with developing a mental edge than cultivating a
specific skill set.
Example - Setting your alarm at 2 am to study while everyone else is asleep. Listening to lectures
while driving to work, while in the shower, while pooping.
Example - Finding ways to maximize your study time. Specific ideas (things that I do) include the
application of “conscious labor’’ to improve efficacy in specific tasks.
Example -1 never take a shower for longer than 3 mins. I turn the water on and get in (while it’s
freezing cold) - I play the game of enduring the cold shower as it heats up. This may sound crazy but
it is a method for callusing the mind. It helps me remember my priorities. I want to win more than I
want to enjoy a warm shower. Warm showers don’t help me win. Less extreme examples would be
never touching the snooze button. Not watching any tv, movies, news, comics, etc... until victory is
achieved.
This is not punishment - and should not looked at as such. These are habits of the ultra-successful.
People who are competing for Olympic gold medals tend to know dick about anything other than their
sport. I remember seeing an interview with a female gold medalist (1 don’t recall the sport) but the
reporter ask her who she was supporting in the presidential election and she didn’t even know who was
running. She acted embarrassed and people watching that probably thought to themselves “Dumb
jock! Doesn’t even know who is running for President!” The people thinking that will never
understand what it’s like to achieve an elite level of success at anything. Knowing political trivia
doesn’t help her win at gymnastics (or whatever) and time spent on anything other than her craft is
wasted. Consider treating your preparation for this exam as if you were in training camp for an
Olympic title (or world championship boxing / MMA fight). This mentality is very useful for
maintaining your priorities. So remember - while you are wasting time the enemy is training and you
can’t allow them to work when you are not (see Law 1). Minimize distractions - Maximize
productivity.
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LAW 2 - continued...
Example - Doing things to improve your mental conditioning. Like a runner might swim to
help cross train muscles that are also useful to running. This is where the habits of the “Sly
Man” are useful (I’ll tell you more about the “Sly Man” later in the chapter). Improving your
focus through forcing yourself to be present in the moment. Not allowing yourself to be
distracted by anxiety, fear, or regret. Present in the moment. Looking for ways to improve.
Etc...
LAW 3 - Performance on “Game Day” must equal performance in practice
Let us take a few minutes and discuss
“test anxiety. ”
“Anxiety” is a dishonest word though isn’t it?
Let’s use a more accurate word. FEAR
No... I’m not afraid. I’m way too macho to be
afraid of things. There is a difference between
being afraid, and being a coward. Only crazy
people don’t experience fear. It’s ok to be
afraid. If you let that fear dominate your
decision making... that is when you run into
In brightest day, in blackest night,
problems. No evil shall escape my sight
Let those who worship evil's might,
The inability to control fear is the root cause of the Beware my power, Green Lantern's light
“test anxiety ” problem. Fear more than anything else Members of the elite Green Lantern Corp
keeps people from achieving their full potential in harness the power of "will" to combat
the evil forces of "fear”
sports, life, business - in everything.
Fear of what?? Fear of failure right? Nope... That is Notice that all these feeling of
not it. That is not what you are afraid of. It’s not dread of anxiety are focused on
failing. It is the fear of a perceived threat to your ego, the future - the consequences
your self esteem. The fear of looking bad and getting which occur after you have
embarrassed in front of your peers. The fear of being failed. This problematic focus
exposed as a fraud. Not really smart enough to be a on the future will become
Radiologist. “Imposter Syndrome” important as we proceed with
this discussion.
Agree?
Now... let us talk about how to conquer fear and channel all that psychogenic energy into a
powerful motivated force.
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SECTION 4:
Wea kn es s es a n d
St r en g t h s
"Confronting fear is the destiny of the Jedi.”
I want to take a few minutes taking some trouble with words, to help explain the various
strategies for controlling fear, and obliterating the negative causatum of anxiety on your game
day performance.
Controlling fear involves two things: (1) choice, and (2) strategy.
The “choice” is the conscious decision to confront your fear. Once you have made the decision
to confront it, you can then begin to implement a “strategy”. The strategy that I am going to
suggest is to not consider this as an effort to eliminate fear. Fear is normal. Only crazy people
don’t have fear. The goal is to increase courage.
Mechanism 1: Generating Courage Through Purpose
One powerful mechanism to increase courage is to have a goal or purpose that is worthy. For
example, a mother may run into a burning building to save her child. Does she do this because
she is no longer afraid of fire? Or does she do it because her purpose as a mother out weighs the
fear and allows her to generate extreme courage?
Purpose → Courage
Mechanism 2: The Perspective of the Joker
Another mechanism for overcoming fear is to begin to view the world from a certain point of
view. A point of view similar to that of the Court Jester.
The point of view of the Jester (or Joker) is to view not just the various social institutions, but all
formations of the natural world as games. You must be careful of the word “game.” When
people use the word “game” they often mean “frivolous.” There can be important games.
Imagine that you were playing a game of Super Mario Brothers. What if you believed that if you
fell into a cavern or were bit by one of those plant things (or a turtle) that you would actually
die ? Do you think this would make you better at the game ? You’d be terrible at it. You
wouldn’t be able to relax, you would second guess every movement, and ultimately your
performance would be awful. All because you believed this game was real and the dangers
within it were real.
Games are best played as games.
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Mechanism 2: The Perspective of the Joker - continued...
Hopefully you can begin to understand the benefits of this strategy. In viewing stressful
challenges as games you can remove the effects of fear. This is not the only benefit though. The
sincerity that exists in the nature of play - the act of doing things simply for themselves actually
improves your performance.
Games are best played as games.
Mechanism 3: “The Art of Not Giving a Fuck”.
In discussing the perspective of the Joker, people will often become upset and insist the
consequences of failure are very real. That the fear of failure is justified. Remember that your
fear lives in just one place - your head.
Confront the fear rationally. Are you afraid of being embarrassed? I can only be embarrassed if
the people I think I’ve embarrassed myself in front of have my respect. If I don’t respect you -
your opinion means very little to me. As the Lebowski says “that’s just like your opinion man.”
Someone worth respecting would understand the difficulty of the task and not judge you poorly
for failure. The only people who never fail are the people who don’t try.
Remember, the Joker sees the whole world as game playing. That's why, when people take their
games seriously - the people who make stern and pious expressions - the Joker can’t help but
laugh. It’s hard to not laugh when you see people pretending that what they do is so very
serious. As Bill Hicks would say “It’s Just a Ride”
I also hear this a lot: “if I fail the test I’ll lose my fellowship.” First of all you don’t need one -
the necessity of a fellowship is a lie propagated by the institution that wants you as a slave for an
extra year. Even if you really want to do one - you won't lose it. They won’t even know you
failed, and passing is not required even to be accredited at hospitals or work as an Attending.
Probably some of your Attendings are international grads who haven’t even sat for the CORE
exam yet - I know some of mine were. Plus, they don’t give a shit - they just want you as a
slave. If they “take” your fellowship away they might have to do your work - and that would
defeat the entire purpose of having fellows. There is nothing really on the line other than your
ego. Our minds project a backdrop of fear onto our reality. That is the default setting.
This idea couples well with John Danaher’s idea of “the parable of the plank.” Where you can
walk on a plank that is strung between two tall laters and be crippled by the fear of falling. But
you can walk on the same plank laid on the ground and feel no instability at all.
It is the same plank. The only thing that changed was your perception of danger.
There is no danger. It is just a game. Games are best played as games.
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SECTION 5:
Va r i a t i o n s a n d
Ad a pt a bi l i t y
I have many hobbies. Disco Dance, Ping Pong, Sunbathe.
But my primary hobby is trying to be the best version of myself. I am obsessed with
maximizing my potential as a human being. Since this is a competition, I thought it might be
helpful to share with you some of my ideas on this topic.
I’ll start off by saying that I can’t necessarily help you be “the best.” What we are talking
about here is being “the best you.” What we are talking about here is “the quest” - the struggle
to be the best version of ourselves. I like to imagine that people are bom as various shaped
and sized canisters. Not all of these canisters will hold the same amount of liquid. My Dad
used to say “all men were NOT created equal.” It’s just a fact that some people are better at
certain things than others. Some people have greater potential than others. We can’t all be
Tony Stark. The point is to try and be the best version of yourself. The best you. You want to
fill that canister all the way up to the brim. Don’t be the half full bottle, that is only half a life.
Method 1: Mental Optimization - The Sly Man
I’m sure you are wondering... why is he so “sly” ?
The Sly Man is the second aspect of the Joker - the deeper aspect. This concept is based on
Gurdjieff’s idea of “the Sly Man” - sometimes referred to as “The Forth Way.”
The idea is that when you play you are doing things only for the purpose of doing them. For
example, when you listen to music you aren’t trying to get to the end of the song, or count the
notes, or derive meaning in the lyrics. You are listening to the music only for the purpose of
listening. The other thing that happens as you play, or dance, or listen to music is that you
become present (mentally) for the process. This in itself is a method to increase focus, and
energy in daily life. This is a method for minimizing day-dreaming and absent mindedness. This
is the way of the Sly Man.
Study only for the purpose of studying. Avoid the mentality of “getting through the material.”
Try and read the material the same way you would if you were reading a novel for pleasure. If
done correctly you will find your studying endurance and recall ability improve.
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Method 2: Mental Optimization - The Self Remembering Exercise:
Most people exist in a state of semi-hypnotic "waking sleep.” Studying or performing like this is
not ideal. The “Self Remembering Exercise” is a tool to increase your ability to harness this
power and increase your focus. People who really dive deep into this stuff will make a big deal
about how “self remembering” and “being present” are not the same thing. For the focused goal
of maximizing performance on the exam, I will just say that either will serve the same purpose.
How this works is that in the morning (or prior to entering the study hall, or exam room) you
must spend 5-10 mins being present in the moment. Close you eyes and repeat to yourself “I am
here in this place.” Generate the sense of being present in the current moment. Concentrate only
on your breathing once you achieve the state of being present.
Mediate until nothing can disrupt you, so that you see and feel nothing - except your own energy.
—Shidoshi Senzo Tanaka
Why waste time doing this? Meditation makes my penis soft!
I agree, it’s not alpha and typically I only endorse alpha male (or female) behavior.. .but this
thing really works. Remember how I said that all your feeling of dread of anxiety are focused on
the future - the consequences which result after you have failed? If you center your mind on the
present, all that shit melts away. It is really just that simple. Anytime you feel anxiety and dread
building inside yourself perform the self remembering exercise. Eyes closed - say “I am here in
this place,” build a sense of presence in the current moment, focus on your breathing, and then
return to the exam / practice room and proceed to kick ass. Repeat as needed. If necessary add
the phrase “retribution is at hand” or “only in death does duty end” or my personal favorite
“happiness is a delusion of the weak,” after centering yourself in the present moment.
Method 3: Mental Optimization - The Accountability Mirror
This is a mechanism I learned from David Goggins. Goggins is the fucking man - if you don’t
know about him, he’s worth a google. He is a man that understands the power of true fucking
will power.
The accountability mirror works like this. In the morning you put sticky notes of the things
you want to accomplish in that day on the mirror. Not just individual tasks but how you
handle yourself and behave. At the end of the day when you are getting ready for bed,
brushing your teeth (or tooth - if you are from West Virginia), you have to look in that mirror
and answer for your progress. You either accomplished your goals or you didn’t. You have to
look at it and face it down. The only way you can improve outcomes is to be 100% honest
about the effort that you put in and the outcomes that resulted. Hearing “you did great!” even
when you didn’t isn’t helping. Be honest with yourself. Make the changes you need to make
and get better.
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Method 4: Physical Optimization - Sunlight
I know that nerds burn easily when exposed to the sun. Plus, the Radiologist walks in shadow
and moves in silence (to guard against extraterrestrial violence).
Seriously - you only need like 5 mins a day. Your pineal gland demands it. I don’t care if it’s
freezing cold outside - get your ass out there and look at the sun for 5 mins. Be mindful in the
moment and play the standing outside in the sun game.
Method 5: Physical Optimization - Sleep
1 have trained myself to sleep 4.5 hours a night by mapping and understanding my REM cycles.
People will say they "can't do that. ” People use the phrase “can’t do that” when they really mean
"I don't want to do that because it will hurt too much.” Callous your mind.
This takes some effort and practice. If I get 3.5 hours sleep I feel terrible. I don’t really care about
“feeling terrible.” A warrior does not complain of physical discomfort. The problem is I can’t
concentrate. I also feel this way with 5.5 hours sleep. At 4.5 hours though... the Lion roars.
The trick is to map your sleep patterns. There are apps that can do this. Alternatively, you can go
full retard and buy a “sleep shepherd,” which is my endorsement if you really want an accurate
map plus the added benefits of binaural beats.
Take two weeks and create a sleep journal. What you are looking for is how long it takes you to go
through two REM cycles. Then you can plot your bed time and wake up time to maximize
productivity. If you do this right you can potentially get 4 extra hours a day to study.
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Method 5: Physical Optimization - Sleep - Continued
Sleep Induction: Another component to getting the most out of your sleep is the ability to
fall asleep rapidly. All that time you might be spending staring at the ceiling is time wasted. I
recommend the use of a “sleep induction mat.” It’s basically a porcupine. This is most
helpful if you have a “busy mind” - full of distracting thoughts.
How this works: It’s a bunch of sharp (dull) plastic points. You take your shirt off and lay on
them. It hurts. The pain distracts you from all the random shit you might be thinking about.
Practice the self remembering exercise. In about 5 mins you will notice that it doesn’t hurt
anymore. That is because your body is releasing a low level of endorphins. Sit up - roll the
thing up - and go to sleep. Some people will tell you that it takes 30 mins to work. That's a
bunch of baloney ~ 5 mins tops.
But Prometheus?! The Codex Astartes Does NOT support this action!
Every year I get at least one belligerent turbo nerd email quoting me sleep research and telling
me that I must have the p.Tyr362 His mutation - a variant of the BHLHE41 gene - and that my
advise to sleep deprive violates both the teachings of the Emperor Leto II Atreides and described
will of the Emperor of Man as transcribed by the Imperial Ecclesiarchy / Adeptus Ministorum.
Before the writing of the annual “I need my teddy bear and 10 hours of sleep email”- allow me to
clarify my points:
• This is about getting a mental edge
• This is about getting a tactical advantage from weaponized will power
• It is possible to maximize your sleep efficiency through REM mapping
• I can do it - and so can other people (you may be one of them)
• Reduced sleep can be augmented with optimized nutrition, hydration, exercise etc...
If my provided methodology (sleep mapping, diet, hydration, exercise, etc..), doesn’t work for
you - consider the following:
Alternative approach to overcoming fatigue:
(Step 1) Make a fist with your brain
(Step 2) Punch sleepy time in the face
Uninitiated: How did you get all those cases right in conference this morning ?
Lionhart Trained: 1 studied 3 hours before conference. I’ve been getting up early.
Uninitiated: Oh... I “need” to get my 8 hours of sleep in. So, I’m gonna study 3 hours this evening.
Lionhart Trained: 1 'll also be studying 3 hours... 3 additional hours this evening.
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Method 6: Physical Optimization - Diet
The human body is designed to operate perfectly... in a world that existed 10,000 years ago.
Despite what the primitive “rat brain” may tell you, sugar is the devil. Foosball, school, girls,
and Ben Franklin are also the devil - but that is unrelated to this discussion.
Avoiding highs and lows is key to optimal function. Avoiding IBS cramps and constant
shitting is also ideal. I’m not going to endorse a particular diet by brand name. I’ll just say
there is a lot of data showing that a Ketogenic diet (or something similar) helps to maximize
mental function.
Method 7: Physical Optimization - Movement
You need 15 mins a day of movement. This can be actual alpha male gym stuff, or beta male
yoga - but any form of movement works and is necessary to maximize your mental health.
I will say this - the more vigorous your training the more sleep your body will require. It is super
important that you move (especially during this stressful time in your life) - and I’m not
suggesting that you avoid working out to sleep less — so don’t get it twisted. I’m instead
advising you to adjust your study schedule to allow more sleep on nights after you have worked
out super hard. Optimizing physical training and sleep management requires flexibility,
patience, and balance. Having said that — don’t use exercise as an excuse to be weak. If you
plan on hitting an hour long spin class, rolling 2 hours straight at an open mat, or doing 15 sets of
squats — plan the night before to sleep 2 extra hours.
No snooze buttons. Snooze buttons are the path to the dark side.
Snooze buttons lead to fear. Fear leads to anger. Anger leads to hate. Hate leads to suffering.
Discipline equals freedom —Jocko. Don’t touch that fucking snooze button.
Also— don’t forget you can also use working out as a weapon against fatigue. The times of the
day when you are the most tired... work out. Oh, and don’t listen to music when you work out
(that shit is cheating). It is supposed to hurt - that’s the point.
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SECTION 6:
Us e o f En er g y
Let’s switch gears and talk about specifics on how to plan a strategy and use resources.
When to Begin Studying:
Frat Answer: Most people put in a 6 month training camp. They will typically being aggressive
studying starting in late December or early January in preparation for the June exam.
I think the amount of time necessary to pass depends on how strong you are as a multiple choice
test taker, how much studying you did in the first 2 years of training, the amount/quality of
teaching at your training institution, and your own ability to retain trivia.
My recommendation would be between 9 and 6 months. Any longer than 9 months and you risk
forgetting the trivia you learned at the beginning of your training camp. I like the analogy of a
bucket with a hole in the bottom. You pour water (knowledge) in the bucket and it slowly drips
out the bottom. You want the bucket to be filled to the brim the morning of the exam.
• 9 Months = The upper limit of trivia retention
• 6 Months = Average
• 3 Month = You better be a trivia machine
• Less than 3 Months = Go ahead and register for the repeat exam.
Now... having said that - this is a critical point:
“Don’t just work longer hours” — ‘Work smart’
—i.e. Stay productive and don’t get distracted.” - Dan Pena
This leads us to my next critical point:
What to do Prior to Starting to Study:
You need to come up with a game plan. The specifics of this plan is not something I can help you
create because each one of you has unique social circumstances and backgrounds. Some of you
have kids. Some of you have jealous wives / husbands. Some of you have program directors who
will not give you one minute off service to study but will still throw you in the pillory if you fail.
Whatever your social situation you need 3 things:
(1) Somewhere quiet to study that is free of distractions.
(2) Time in this ideal study environment
(3) Resources to study (books, questions, videos, and Google).
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The Ideal Study Environment:
There is a person inside you that does not want to study. This person doesn’t care that you
will be humiliated if you fail. This person believes in nothing Lebowski. He/She only wants
to eat, read celebrity gossip, watch internet pom, and sleep.
When it comes to successful preparation this person is your greatest enemy. For me at least, it
seems that dealing with this person (your inner hungry, sleepy, pom crazed, Justin Bieber fan)
is like dealing with a meth addict. Don’t leave the meth lying around where he/she can see it.
If he/she gets ahold of it... the study session is over.
What is “the meth ”? It varies from person to person. It most cases it’s your fucking phone.
Do NOT bring your phone into the study environment. If you must bring your phone (for
child care reasons, etc...) then put it on a shelf on the other side of the room.
Other Tips:
• Don’t show up hungry. Eat prior to going into the study environment. Avoid sugar as it will
make you crash.
• Caffeine is your friend. If your religion forbids the use of caffeine - dig around in your
sacred text for loop holes. Most major religions allow you to ask for forgiveness later. The
best time to ask for forgiveness is after you pass the exam.
• How much caffeine? There is at least one paper that showed that small hourly doses of
caffeine (0.3 mg per kg of body weight [approx 20 mg per hour] is optimal). Caffeine tablets
- cut can help you keep this accurate. Stay away from energy drinks and all that bullshit -
you want to keep the dose steady. Consider keto coffee (bullet proof coffee) or other coffee
brands with high fat content to help improve bioavailability.
• No music in the environment. This feeds the lazy person inside you and is a distraction. I
will listen to music prior to studying. Like a pro wrestler walk out song .
“Replacement Killers” by the Crystal Method is my current suggestion.
And I say this to the night. Let us not forget. There is hope.
• No “Study Buddies.” You need to be alone in this room. Your inner lazy person will try
and small talk with your study partner’s inner lazy person. It will start out innocent with
you asking them a legit questions about radiology / physics. 30 seconds later you will be
chatting about Kardashians (or that reality tv show with the pro wrestlers girlfriends).
• If you must study in a public location, you should make it clear to your classmates that you
don’t want to be interrupted - snarl at them. You should also bring ear plugs for when they
start talking to each other.
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How Many Hours Per Day Should You Study:
You need about 2-3 hours on weekdays, and 8-12 hours a Mad Man (Woman)
day on the weekends. This is the minimum. The real Tactics
answer would be “however much would kill you, minus
Set your alarm for 2 am and
one second.”
study for 30 mins once a
week.
For me, studying early in the morning is superior to the
evening. After work you are tired, your family is the most Why? Because everyone
needy, and you are the most distractible. Most days when I else is asleep while you arc
working hard. This kind of
left work as a Resident I was angry about something.
thinking is how you get an
Usually one or more of my asshole Attendings having no edge - see Law 2.
regard for my need to study. All that hate (although
motivating) was also distracting. It’s hard to study when
you are trying to plot revenge.
I understand some people are just not wired for early morning studying, but it is ideal if you
can make yourself do it.
Along those lines.. .Sleep is for pussies. See prior discussion on optimizing your sleep.
Stealing an hour during the day.
Most programs have a noon and / or morning lecture. At this point in your training you know
when these are useful and when they are a waste of time. I would have zero remorse about
ditching a low yield lecture to study. If you feel bad for even one second just think about what
will happen to you if you fail. If you do decide to ditch a lecture make it count. Have your
hiding place / study environment picked out. Have your goals for what you want to get
through clear. The more productive that hour is the less bad you will feel about doing it.
“Morgen, morgen, nur nicht heute, sagen alle faulen leute. "
— Roughly translated as “tomorrow, tomorrow, not today.... say all lazy people.”
Never — Never — Never put off or delay an opportunity to study. Thinking “I’ll have time to
study later” is a huge mistake. I want to encourage you to adopt the idea of Premeditatio
Malorum - where you consider all the things that can go wrong in your day and fuck up your
plans. Maybe your kid will get sick tonight, or you will have a pipe break in your apartment or
who knows what the fuck can happen. Maybe your little sister will break up with her high
school boyfriend and suck you into an unescapable whirlwind of teenage drama. Recognize that
the world can fuck up your plans pretty easily. Never procrastinate. If you have a chance to do it
now - then fucking do it.
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Resources:
Essentials: Crack the Core Vol 1, Crack the Core Vol 2, Physics War Machine, Crack the
Core Case Companion. Combat Ready - my new Q and A book.
Highly Recommended: TitanRadiology.com / RadiologyRonin.com - Board Review Course
and Clinical Mastery.
Supplemental: Google Images - No single book can match the power of the internet.
Q Banks: Last year I released a Q Bank via TitanRadiology. I’m hoping to improve and
expand the question bank this year. Obviously that is going to be the one I’ll endorse.
Regardless, my opinion is that more questions are better. I would do as many practice
questions as possible which will likely mean using multiple commercial q banks.
How To Use the Resources:
Everyone is starting from a different place depending on your individual background and
interests. Having said that nearly everyone has 5 tasks to accomplish:
(1) Fill in the large holes. Everyone sucks at something. There are probably 3-4 sections
(maybe more) that you feel particularly weak in.
(2) Accumulation of Random Trivia. Even if you think you are strong in a certain subject
there is almost certainly a laundry list of trivia that you don’t have available for recall.
(3) Physics. Nearly everyone starts out knowing almost zero physics.
(4) Non-Interpretive Skills. This is another topic that pretty much no one has any exposure to.
(5) Biostats. You will have to review the basics on this as well.
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Suggested Strategy for the Clinical Portions:
(1) Make a list of the subjects you suck the most at.
(2) Read the corresponding sections / chapters in Crack. Read them slowly. Google image
anything you’ve never seen before.
(3) Watch the corresponding videos to these chapters on TitanRadiology.
(4) Start at the beginning of Crack Vol 1 and work your way to the end of Vol 2. Don’t skip
the Chapters you read already - this is your second time through those. Annotate and mark
up the books. I’ve purposefully provided lots of room for extra notes. Also, the paper is
not glossy for a reason - I did this so you can write in the books without smearing shit
everywhere.
(5) Start back at the beginning of Crack Vol 1. This time we are going to add practice
questions. Pick a QBank, they are all pretty similar (mine is best obviously). Read a
chapter in Crack (example Peds) then do the corresponding Peds questions. Make notes
in the book as needed. Work your way all the way through the book. This process can be
supplemented with the corresponding Titan Videos.
(6) Start to switch over to 90% questions - 10% reading. Now is the time to read the Case
Companion. You should be doing 150 + questions a day. Go ahead and make them
random, that will simulate the exam.
Practice Questions:
Practice questions do two things for you. (1) They help expose holes in your knowledge.
(2) They help you practice your timing and discipline.
I think it’s important to backload questions until you have a foundation. There is no point in
doing practice physics questions if you have never read a page of physics. It’s a total waste.
Clinical radiology is the same way. Don’t mess with questions until you have read the chapter
in Crack at least once.
Once you have entered “phase 2” - which would correspond with step 6 above. It’s time to
start doing questions with a timer. Average one minute per question. Practice your
disciplined approach (reading the entire question, reading all the choices, never change your
answer). You should be doing more and more questions every week leading up to the exam -
revising the material as needed.
In the volume 2 strategy chapter I discuss the “Genius Neuron. ” He (She) is your closest
friend and you must learn to trust his/her advice.
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Learning Physics / Non-Interpretive Skills:
There are two strategies. Both are equally valid depending on your personality.
Strategy 1: Learn it all at once. Blocking out 6-8 weeks of your study schedule and just hit
physics every day.
Strategy 2: Ration it in with the clinical reading. For example if you study for two hours,
1 hour in physics, 1 hour in clinical.
Regardless of which strategy you pick you should follow the same steps:
(1) Read the War Machine cover to cover once. Titan videos may help solidify topics. If
necessary google topics that remain confusing.
(2) Start over and read each chapter - then do corresponding questions.
(3) Continue to do practice questions to keep the material fresh.
(4) Reviewing the ABR’s NIS source document will still be necessary (make sure you are
using the most up to date version). Read the War Machine’s discussion first - it will likely
make the document more digestible.
The Last Month:
(1) Most (90%) of your time should be spent on timed practice questions.
(2) The other 10% you should spend preparing your high yield review. You should start by
putting together a list of all the random trivia that you will forget immediately after the
exam. This is a list of all the numbers, half-lives, photon energies, etc.. The back of the War
Machine has a good start on this but you will likely want to add to it.
The Last Week:
(1) Continue doing practice questions.
(2) Study your high yield numbers / trivia every day. Try and concentrate it to 1-2 pages of
stuff you are having trouble remembering.
(3) Review Biostats, and skim the ABR’s Non-Interpretive Skills study guide.
The Morning of the Exam:
Look at your highest yield notes (the 1 - 2 pages of trivia you have boiled down). Read it over
and over and over again until they make you get rid of all your notes.
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When You Sit Down To Take The Exam:
(1) Check to make sure your markers work. If you got a dud fix it now. You don’t want “dead
marker rage” to make you drop a question mid exam.
(2) Scribble down all the formulas and numbers you can remember on one of the dry erase
boards. Six hours into the exam that information won’t be in your short-term memory any
more.
(3) Give yourself a vigorous scalp massage - like 30 seconds. This increases blood flow to the
brain and reduces stress. Seriously, it really works. I learned this from Ivan Vasylchuk
(Ukrainian Sambist, Merited Master of Sport, World Champion, and Winner of the
SportAccord World Combat Games).
**Don’t forget to do this on the second day of the exam also.
The Night Between Exam Days:
Anticipate the subjects that haven’t been tested yet and review your notes on those. Avoid
drinking or socializing. This is war. The people in the hotel lobby aren’t your friends, those are
the people trying to push you into the bottom 15%. You can be friends with them after you pass
Plus, arguing over who missed what will only increase your anxiety.
• Avoid alcohol - even if you are “sure you failed.” A strong performance day 2 can resurrect
you. In general, most people feel like they did terrible after day 1. Remember, it is all about
how you did relative to you cohort.
• Study 2-3 hours.
• Don’t eat anything that will give you diarrhea.
• 15 minutes on the treadmill can be tremendously helpful to reduce stress.
• Get 6-8 hours sleep.
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SECTION 7:
Wea po n i ze yo u r Wi l l
This last section is a discussion on how to weaponize your will power and stay motivated for
the duration of the training camp.
Attack by Fire
10-15% of people will fail this exam. You must beat those people to pass.
No one has the right to beat you. 1 don’t care where you trained. I don’t care where you came
from. No one has the right to beat you. When doubt seeks in you can go two roads. You can
go to the left or you can go to the right. You may hear people say “failure is not an option.”
This is silly, failure is always an option. Failure is the most readily available option - but it’s
not the only option - it is a choice. You can choose to fail or you can choose to succeed.
Self doubt and negative thoughts are the road to failure. I want to tell you this - as someone
who prides himself on both physical and mental toughness - it is normal to feel that way
sometimes. The vast majority of people reading this book are perpetual winners in life, and
those kinds of people hate to admit weakness to others and to themselves.
You are not your accomplishments. You are not your failures. You are you.
Recognizing that about yourself gives you the power to overcome negative thought through
the awesome power of hard work. Earn your victory. Deserve to win - the Gods of War will
look favorably upon you. Don’t hold back. Go 100% the entire time. You may hear people
say - “you look tired, you look exhausted.” The worst feeling in the world is losing and
knowing that it was because you were lazy and didn’t put in the work. I’d much rather get
beat knowing I did everything I could to be prepared. “You look tired, you look exhausted,”
- yeah... you bet your ass I’m tired, that is the whole fucking point. My goal is always to be
exhausted at the end of each day. You want to feel like you got hit by a fucking freight train.
That’s the feeling I like. That’s how I know I’m giving my best effort.
I train hard, I work hard, I fight hard, and I fight for victory.
In any competition, I want only one thing and that is to leave with my hand raised, at the top
of the podium, with the gold medal - and I make no apologies for that. You shouldn’t either.
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Tactical Dispositions - “Snarl More
Prior to entering the study environment - find a
mirror and make the ugliest face you can.
Not a silly face. Not a sad face. A snarl.
A good snarl can give you what the Bible calls a
psychological edge.
Vacuity and Substance
Most people go through their lives trying to avoid pain. This is a mistake. You are competing
in a high stakes contest. Pain is your friend. If you can endure more time in the study room
relative to your opponents then you have an edge (Law 2). Once you understand this you
won’t avoid pain anymore. Look for pain. Invite him in and have dinner with him.
You don’t look for me pain.... I look for you.
This is a fundamental concept for developing the Lion’s heart. If you want to get somewhere
in life - start by taking stuff away. There is nothing you can add to your life that will make
you stronger. Understanding this is something you can take with you the rest of your life. At
an early age, I was fortunate to learn the truth about despair - that nothing tastes better than a
bologna sandwich when you haven’t eaten for 3 days. There is a reason why a guy like Julio
Cesar Chavez can win 87 boxing matches in a row, because the mother fucker grew up in an
abandoned railroad car with his five sisters and four brothers. You think someone like that is
gonna break when they get tired? Any luxuries that you are enjoying in your life - those aren’t
making you stronger. Take stuff away.
Maneuvering the Army
Many of you have probably had fairly normal lives with loving families and friends.
I imagine that could be a source of motivation. When you feel that you are too tired to study,
or can’t motivate yourself to enter the study environment, think about them. Think about how
much better things will be for them once you are making a real salary.
Rise and Grind.
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Illusion and Reality
For others, perhaps you have traveled a different path. Not everyone has enjoyed a life filled
with good times and noodle salad. Some of us were born in the dark, molded by it.
Now, you are after something. It could be revenge. It could be money.
Or.... it could be something else.
Vengeance is a powerful motivator. Think of all the people who have tried to stop you. Think
of all the people who have mistreated you. Visualize their stupid ugly faces smirking and
smiling when they hear you failed the exam. Let it boil you blood. Now picture those same
people making a face like they smelled a fart when they hear you passed the exam. You will
find that you aren’t tired anymore. You are ready to train.
As a resident I went as far as putting a picture of one of my tormentors in my shoe. That way
every step I took I was walking on this persons face. Feel free to try that
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SELF AFFIRMATION
-A TOOL TO WEAPONIZE YOUR WILL-
I have an oath that I read to myself -especially when I’m tired, as a tool to harness my will. I
encourage you to modify the oath to make it yours. Hang it somewhere you can see it daily.
Perhaps beside a picture of the person you hate the most in this world. Or... if you are less of a
Sith and more of a Jedi - hang it beside a photo of the people you love.
MY NAME IS (youR NAME HERE) AND THIS IS MY OATH
IN SOUND MIND I MAKE THIS OATH.
I DECLARE THAT I AM NOT PERFECT.
I KNOW THAT THERE WILL BE CHALLENGES TO OVERCOME, BUT I SWEAR
ON THE POWERS OF THIS UNIVERSE THAT I WILL FIGHT WITH ALL MY
HEART, ALL MY STRENGTH, AND ALL MY SOUL TO OVERCOME.
I WILL OUTWORK ALL HUMAN BEINGS THAT STAND IN FRONT OF ME.
NO ONE WILL TRY AS HARD AS ME. THEY DO NOT HAVE MY HEART OR
UNRELENTING DESIRE.
I DECLARE THAT I WILL PERSIST WHEN OTHERS GIVE UP.
I WILL ALWAYS BE HUNGRY FOR MORE. EVEN WHEN THINGS SEEM
IMPOSSIBLE, I WILL NOT GIVE UP.
TODAY I AM GOING TO WAR.
NO ONE HAS THE RIGHT TO TAKE MY DREAMS FROM ME.
I WILL SACRIFICE UNTIL I REACH THE TOP. NO TEMPTATION WITH SWAY
ME. I CRAVE ONLY THE BLOOD OF THE ENEMY.
MY HEART IS ON FIRE. NO MATTER HOW LOUD MY BODY SCREAMS, I
WILL SCREAM LOUDER.
I AM FOCUSED. I AM PREPARED FOR BATTLE.
COME AT ME, I DARE YOU. I AM PREPARED FOR WAR.
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Despite these words, this page is intentionally blank.
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PEDIATRICS
PROMETHEUS LIONHART, M.D.
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SECTION 1:
Skul l & Sc a l p
Craniosynostosis
“Craniosynostosis” is a fancy word for premature fusion of one or several of the cranial
sutures. The consequence of this premature fusion is a weird looking head and face (with
resulting difficulty getting a date to the prom). Besides looking like a gremlin (or a cone-
headed extraterrestrial forced to live as a typical suburban human), these kids can also have
increased intracranial pressure, visual impairment, and deafness.
There are different named types depending on the suture involved - thus it’s worth spending
a moment reviewing the names and locations of the normal sutures.
Bones Fusion Fusion
Involved Direction Order
Metopic Front to First
Frontal
(frontal) Back (2-3 months)
Frontal & Lateral to
Coronal Second
Parietal Medial
Parietal & Lateral to
Lambdoid Third
Occipital Medial
Back to
Sagittal Parietal Fourth
Front
• Sutures normally have a serrated (saw tooth) contour
• With early closure the suture will lose the serrated appearance - becoming more dense
and sharp. Eventually the suture will disappear completely.
• For the purpose of multiple choice, you should think about synostosis (early closure) as
likely syndromic - and focus your memorizing on this point.
• Having said that, sagittal and unilateral coronal synostosis are typically idiopathic
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Craniosynostosis Continued... “Plagiocephaly”
Potential Source of Fuckery
Pathology / Sub-type Trivia:
This word basically means “flat.”
You will see it used to describe
unilateral coronal synostosis as
“anterior plagiocephaly.”
You will see it used to describe
unilateral lambdoid synostosis as
“posterior plagiocephaly. ”
The problem is that many people
use the word “plagiocephaly” to
describe the specific entity of
“deformational plagiocephaly” -
which is just benign positional
molding, not a pathologic early
closure. On the following page, I’ll
go into more detail on this. Just
know you may be required to read
the question writer’s mind when the
word is used to differentiate
between the benign and pathologic
entities.
• Eyes are close together (hypotelorism)
• Ethmoid sinuses underdeveloped “Quizzical
Metopic • Medial part of the orbit slants up
Trigonocephaly Eye”
(frontal) • Single suture synostosis most frequently appearance
associated with cognitive disorders (growth
restriction of the frontal lobes)
• Unilateral subtype is more common.
• Unilateral type causes the ipsilateral orbit to “Harlequin
elevate, and contralateral frontal bone to
Coronal Brachycephaly Eye”
protrude “frontal bossing”
* if unilateral.
• Bilateral form is Rare - should make you think
syndromes (Borat's brother Bilo*).
Least
Turricephaly • Tall Cranium (oxycephaly, acrocephaly)
Lambdoid Common
(if bilateral) • See Next Page for Unilateral Discussion
Form
• Long, Narrow Head.
• Looks like an upside-down boat.
Scaphocephaly Most
• Usually the kids have a normal IQ
Sagittal or Common
• Usually the kids do NOT have hydrocephalus
Dolichocephalic Form
• Associated with Marfans
(both are tall and skinny).
*For the purpose of this text, Borat's brother Bilo is presumed to have syndromic mental retardation /
developmental delay. Not iatrogenic encephalopathy related to the intracranial placement of a red haired
woman's tooth - as therapy for demon induced epilepsy - which is suggested in some reports.
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THIS vs THAT: Positional Plagiocephaly vs True Unilateral Lambdoid Synostosis
Infants that sleep on the same side every night
If this is bilateral think underlying
develop a flat spot on the preferred dependent
Rhombencephalosynapsis
area of the head (occipital flattening).
Onset: Weeks After Birth Onset: Birth
Ipsilateral Ear: Anterior Ipsilateral Ear: Posterior / Inferior
Frontal Bossing: Ipsilateral Frontal Bossing: Contralateral
Most common cause of an abnormal Rare as Fuck
skull shape in infant
Management is conservative
Management is Surgery
(sleep on the other side for a bit)
NEXT STEP; Trivia For the purpose of multiple
choice, there are numerous
Outside of the jungle (or the year 1987), the random bone buzzwords
diagnosis of synostosis is going to be made with that are supposed to elicit
CT + 3D. If asked what test to order I would say the reflexive diagnosis
CT with 3D recons. Having said that, they could NF-1 in your brain when
show you a skull plain film (from 1987) and ask you hear / read them.
you to make the diagnosis on that.
The more common ones include:
If the test writer was feeling particularly cruel • Absence / Dysplasia of the Greater
and bitter he/she could show the diagnosis Sphenoid Wing,
with ultrasound. In that case, remember that • Tibial Pseudoarthrosis,
a normal open suture will appear as an • Scoliosis, and
uninterrupted hypoechoic fibrous gap • Lateral Thoracic Meningocele.
between hyperechoic cranial bones (Bright -
Dark - Bright, Bone - Suture - Bone). I’d like to add “bone defect in the region
of the lambdoid suture ” or the “asterion
Although certain MR gradient sequences can
defect" to that list of reflex generators.
be used, MRI has traditionally been
considered unreliable in identifying sutures
individually. It’s rare and poorly described - therefore
potentially high yield.
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Clover Leaf Skull Syndrome
• Also referred to as Kleeblattschädel for the purpose of
fucking with you
• Contrary to what the name might imply - this complex
deformity is not associated with an increased ability to hit
green lights, reliably find good parking spots, or win the
lottery. I think that’s because the shape is more 3 leaf clover,
and not 4 leaf. One might assume, a head shaped like a 4 leaf clover
would probably be luckier.
• Instead, this deformity is characterized by enlargement of the head
with a trilobed configuration, resembling a three-leaved clover.
• Results from premature synostosis of coronal and lambdoid sutures
(most commonly), but often the sagittal closes as well.
• Hydrocephalus is a common finding.
• Syndromic Associations: Thanatophoric dysplasia, Apert syndrome
All the sutures arc
(severe), Crouzon syndrome (severe) closed
except the metric
and squamosal
Trivia Additional Craniosynostosis Syndromes;
Most of the time (85%) premature closure is a primary (isolated) event, although
it can occur as the result of a syndrome (15%). The two syndromes worth having
vague familiarity with are Apert’s and Crouzon’s.
• Brachycephaly (usually)
Apert’s
• Fused Fingers (syndactyly) - “sock hand”
• Brachycephaly (usually)
• 1 st Arch structures (maxilla and mandible hypoplasia).
Crouzon’s • Associated with patent ductus arteriosus and aortic coarctation.
• Short central long bones (humerus, femur) - “rhizomelia”
• Chiari I malformations 3: ~70% of cases
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THIS vs THAT: Skull Markings
Convolutional Markings Copper Beaten Luckenschadel - ''Lacunar''
Normal gyral impressions on The same thing as convolutional Oval, round, and finger shaped
the inner table of the skull. markings (the normal gyral defects (craters) within the
impressions), just a shit ton inner surface of the skull
more of them.
Different than Copper Beaten
You also see them along the in that:
You see them primarily during anterior portions of the skull not
(A) They aren’t gyriform.
normal rapid brain growth (age just the posterior.
(B) They aren’t related to
3-7).
increased ICP.
(C) They are usually present at
Usually mild and favors the
Think about things that cause birth.
posterior skull.
increased intracranial
Instead they are the result of
If you see them along the more pressure.
defective bone matrix.
anterior skull then you should
think about a “copper beaten” Classic examples:
• Craniosynostosis Classic Association:
skull from the increased
• Obstructive Hydrocephalus • Chiari II malformation /
intracranial pressure. Neural Tube Defects.
Lytic Skull Lesions:
Lytic skull lesions in kids can come from a couple of different things (LCH, Infection, Mets,
Epidermoid Cysts, Leptomeningeal Cysts, etc...). The two I want you to focus on are LCH and
the Leptomeningeal Cyst (which I will discuss later in the chapter).
LCH (Langerhans Cell Histiocytosis) - Too many fucking dendritic cells - with local invasion. It
is a sorta pseudo malignancy thing. Nobody really understands it.... For the purpose of the exam
think about this as a beveled hole in the skull. The skull is the most common bone involved with
LCH. It is a pure lytic lesion (no sclerotic border). The beveled look is because it favors the
inner table. It can also produce a sequestrum of intact bone (“button sequestrum).
Gamesmanship: If they tell you (or infer) the kid has neuroblastoma
- think about a met.
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Parietal Foramina
These paired, mostly round, defects in the
parietal bones represent benign congenital
defects. The underlying cause is a delayed or
incomplete ossification in the underlying
parietal bones.
They can get big and confluent across the
midline. Supposedly, (at least for the big ones -
> 5 mm) they are associations with cortical and
venous anomalies.
Wormian Bones
In technical terms, there are a bunch of extra squiggles around the lambdoid sutures.
“Intrasutural Bones” they call them.
These things are usually idiopathic - however, if
you see more than 10 you should start thinking
syndromes.
Gamesmanship:
< 10 = Idiopathic
> 10 = First think Osteogenesis Imperfecta
> 10 + Absent Clavicle = Cleidocranial Dysostosis
There is a massive differential, but I would just
remember these “PORK-CHOP”
Pyknodysostosis
Osteogenesis Imperfecta
Rickets
Kinky Hair Syndrome
(Menke's / Fucked Copper Metabolism)
Cleidocranial Dysostosis
Hypothyroidism I Hypophosphatasia
One too many 21st chromosomes (Downs')
Primary Acro-osteolysis (Hajdu-Cheney)
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Dermoid / Epidermoid of the Skull
In the context of the skull, you can
Epidermoid Dermoid
think about these things as occurring
from the congenital misplacement of Only Skin Skin + Other Stuff
cells from the scalp into the bony Histology (Squamous Like Hair Follicles,
Epithelium) Sweat Glands Etc..
calvarium.
Age of Present between Typically have an
The result is a growing lump of tissue Onset age 20-40 earlier presentation
(keratin debris, skin glands, etc...)
Parietal Region is Tend to be midiinc.
creating a bone defect with benign Location Most Common The skin ones tend to
appearing sclerotic borders. (“behind the ears ”) be around the orbits.
There are a few differences between Associated with
Encephaloceles -
the two subtypes that could be especially when
potentially testable (contrasted midline
masterfully in the chart). - More Heterogeneous,
- Calcifications
Although, I suspect a “what is it?’’ CT CSF Density (internal or peripheral)
type question is more likely. As such, may be present
look through some google image T1 Variable, T1 Bright,
examples to prepare yourself for that MRI T2 Bright, T2 Bright,
NO Enhancement +/- Wall Enhancement
contingency.
Congenital Dermal Sinus
Usually when people talk about these things they are referring to the spina bifida style
midline lumbosacral region defects. However, we arc going to stay focused on the skull /
face. The two classic locations for dermal communications with the dura are the occiput and
the nose. Both of which are classically midline, and can be associated with a dermoid cyst.
For gamesmanship, consider a sinus tract anytime you see a cyst in these locations.
Sinus tracts may or
may not have
associated dermal
or intraosseous
cysts.
Cysts may or may
not have sinus
tracts.
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THIS vs THAT: Scalp Trauma
There are 3 scalp hematoma subtypes. Because the subtypes are fairly similar, there is a high
likelihood a sadistic multiple choice writer will attempt to confuse you on the subtle
differences - so let’s do a quick review.
Caput
Subgaleal Hemorrhage Cephalohematoma
Succedaneum
Subcutaneous
Deep to the Aponeurosis
Under the Periosteum Hemorrhage
Location (between aponeurosis and
(skin of the bone) (superficial to
periosteum) the aponeurosis)
Suture NOT limited by Limited by suture lines NOT limited by
Relationship suture lines (won't cross sutures) suture lines
Outer border may calcify as a rim
Covers a much larger area and leave a deformity - sorta like
Trivia
than a cephalohematoma a myositis ossificans.
Usually requires no intervention
Potentially life-threatening (resolves within a few weeks) Requires no
- rapid blood loss. intervention
Can get super infected (E. Coli).
Complications Often not seen until 12-72 Abscess would require drainage. (resolves within
a few days)
hours post delivery. Can cause skull osteomyelitis.
Prolonged
Cause Vacuum Extraction Instrument or Vacuum Extraction
Delivery
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Skull Fractures
Accidental (and non-accidental) head trauma is supposedly (allegedly, allegedly) the most common
cause of morbidity and mortality in children. As you might imagine, the pediatric skull can fracture
just like the adult skull - with linear and comminuted patterns. For the purpose of multiple choice, I
think we should focus on the fracture patterns that are more unique to the pediatric population:
Diastatic, Depressed, and “Ping-Pong”
• Diastatic Fracture: This is a fracture along / involving the suture. When they intersect it is usually
fairly obvious. It can get tricky when the fracture is confined to the suture itself. The most common
victim of this sneaky fracture is usually the Lambdoid, followed by the Resident reading the case on
night float.. .with Attending backup (asleep in bed). How does one know there is traumatic injury to
a suture? Classically, it will widen. This is most likely to be shown in the axial or coronal plane so
you can appreciate the asymmetry (> 1 mm asymmetry relative to the other side).
• Depressed Fracture: This is a fracture with inward displacement of the bone. How much inward
displacement do you need to call it “depressed”? Most people will say “equal or greater to the
thickness of the skull.” Some people will use the word “compound” to describe a depressed
fracture that also has an associated scalp laceration. Those same people may (or may not) add the
word “penetrating” to describe a compound fracture with an associated dural tear.
Will any of those people be writing the questions? The dark side clouds everything. Impossible to
see the future is.
• Ping Pong Fracture: This is actually another subtype of depressed fracture but is unique in that it is
a greenstick or “buckle” type of fracture. Other potentially testable differences include:
• Outcomes: Ping Pong fractures typically have a favorable / benign clinical outcome
(depressed fractures have high morbidity).
• Etiology: Diastatic and depressed fracture types usually require a significant wack on
the head. Where as “ping pong” fractures often occur in the setting of birth trauma
(Mom’s pelvic bones +/- forceps).
• Imaging Appearance: Ping Pong fractures are hard as fuck to sec. To show this on a
test you’d have to have CT 3D recons demonstrating a smooth inward deformity. You
could never see that shit on a plain film. I can’t imagine anyone being a big enough
asshole to ask you to do that. Hmmm.... probably.
Unlike linear fractures (which usually heal without complication), Normal
depressed fractures often require surgery. Some general indications Fracture
Suture
for surgery would include:
> 3 mm < 2 mm
• Depression of the fragments > 5mm (supposedly fragments more
than 5mm below the inner table are associated with dural tears),
Wide Center Equal Width
• Epidural bleed
“Darker” “Lighter”
• Superinfection (abscess, osteomyelitis)
Straight
• “Form” (cosmetic correction to avoid looking like a gargoyle), Line, with Squiggly
Line, with
• “Function” (if the frontal sinus is involved, sometimes they need Angular
Curves
to obliterate the thing to avoid mucocele formation). Turns
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Leptomeningeal Cyst -“Growing Skull Fracture”
A favorite of board examiners since the Cretaceous Period.
Typical Pathogenesis:
- Step 1: You fracture your noggin,
AND tear the underlying dura.
- Step 2: Leptomeninges herniate through the tom dura
into the fracture site.
- Step 3: Over time (a few months) CSF
pulsations progressively widen the
fracture site and prohibit normal
healing.
- Step 4: You know you shouldn’t, but
you just can’t resist the urge to poke
your own brain through the now
cavernous cranial defect.
- Step 5: The poking triggers a powerful hallucinogenic
experience. You have a telepathic conversation with a room
filled with self transforming elf machines. You
are overwhelmed with tremendous curiosity about exactly what/
who they are and what they might be trying to show you.
- Step 6: You develop epilepsy from poking your brain too much.
Or was it not enough? - you can’t remember
Sinus Pericranii
A rare disorder that can be shown as a focal skull defect with an associated vascular malformation.
The underlying pathology is a low flow vascular malformation - which is a communication
between a dural venous sinus (usually the superior sagittal) and an extra cranial venous structure
via the emissary veins.
Most likely way to show this:
(1) MRI - with some type of vascular sequence
- post contrast or MRA/TOF.
(2) CT showing the skull defect - wanting a next
step (ultrasound or MRI to demonstrate the
vascular component).
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Non-Accidental Trauma (Abusive Head Trauma)
Although car wrecks and falls account for the majority of skull fractures in children, there
still remains the timeless truth — some people just can’t take screaming kids.
For the purpose of multiple choice, the follow clues should make your spider-sense tingle.
• Inconsistent History:
GAMESMANSHIP:
“My 7 month old wrecked his bike ”
Subdurals have a stronger association with NAT
• Subdural Hematoma relative to epidurals. Think about vigorous
shaking (trying to get that last drop of ketchup
• Retinal hemorrhage
out of the bottle) tearing bridging cortical veins.
• DAI / Parenchymal Contusion
“Look High, Look Low”
• Cerebral Edema, Stroke - Sneaky Ways to Suggest NAT -
(less specific but still worrisome) - Look High: Thrombosed (hyperdense)
cortical vein at the vertex
• Depressed Skull Fx, or Fracture
Crossing Suture Line - Look Low: Retroclival hematoma (thin
(less specific but still worrisome) hyperdense sliver in the pre-pontine region)
- Look Lower: Edema within the cervical soft
tissues
Retroclival Hematoma Extra Axial Fluid
Chronic Subdural
Epidural Prominent CSF Spaces
(CSF Density)
Medial Displacement Cortical veins are
Below the Above the
Tectorial Tectorial of Bridging Vein
Membrane Membrane (sometimes smashed and adjacent to the inner table
not well seen)
Usually Unilateral.
If Bilateral Usually Usually symmetric
Asymmetric in Size.
*More on NAT later in the chapter.
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SECTION 2:
Br a i n - Sel ec t To pi c s
Disclaimer: Brain tumors , cord tumors, and a bunch of other random Peds Neuro pathologies arc
discussed in detail within the Neuro chapter found in volume 2. The same is true for congenital
heart, certain GU, GYN, and MSK topics - found within their dedicated chapters. If you find
yourself saying “Hey! What about that thing? This asshole is seriously not going to talk about
that?” Relax, I split things up to reduce redundancy and cluster things for improved retention.
Enlarged extra-axial fluid spaces:
THIS vs THAT:
Extra-axial fluid spaces arc considered enlarged if they are BESSI vs Subdural Hygroma
greater than 5 mm. BESSI is the name people throw around
for “benign enlargement of the subarachnoid space in infancy. BESSI - Cortical veins are
adjacent to the inner table - they
The etiology is supposed to be immature villa (that’s why you are usually seen secondary to
grow out of it). enlargement of the subarachnoid
spaces (positive cortical vein
BESSI Trivia: sign)
Subdural - Cortical veins are
• It’s the most common cause of macrocephaly, displaced away from the inner
• Typically presents around month 2 or 3, and has a strong table - they are often not seen
male predominance. secondary to compression.
• Typically resolves after 2 years with no
treatment,
Enlarged
• There is an increased risk of subdural bleed - symmetric
either spontaneous or with a minor trauma. This subarachnoid
subdural is usually isolated (all the same blood spaces
age), which helps differentiate it from non- favoring the
accidental trauma, where the bleeds are often of anterior aspect
different ages. of the brain
(spaces along
Trivia - Pre-mature kids getting tortured the posterior
on ECMO often get enlarged extra-axial aspect of the
brain are
spaces. This isn’t really the same thing
typically
as BESSI but rather more related to fluid
normal).
changes / stress.
Brain parenchyma is normal and there is either
normal ventricle size or very mild
communicating hydrocephalus. Communicating
meaning that all 4 ventricles are big.
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Periventricular leukomalacia (Hypoxic-Ischemic Encephalopathy of the Newborn)
This is the result of an ischemic / hemorrhagic injury, typically from a hypoxic insult during
birthing. The kids who arc at the greatest risk are premature and little (less than 1500 g). The
testable stigmata is cerebral palsy - which supposedly develops in 50%. The pathology favors
the watershed areas (characteristically the white matter dorsal and lateral to the lateral
ventricles).
The milder finding can be very subtle. Here are some tricks:
(1) Use PreTest Probability: The kid is described as premature or low birth weight.
(2) Brighter than the Choroid: The choroid plexus is an excellent internal control. The
normal white matter should always be less bright (less hyperechoic) when compared to the
choroid.
(3) “Blush ” and “Flaring” : These are two potential distractors that need to be differentiated
from legit grade 1 PVL. “Blush” describes the physiologic brightness of the
posterosuperior periventricular white matter - this should be less bright than choroid, and
have a more symmetric look. “Flaring” is similar to blush, but a more hedgy term. It’s the
word you use if you aren’t sure if it’s real PVL or just the normal brightness often seen in
premature infants white matter. The distinction is that “flaring” should go away in a
week. Grade I PVL persists > 7 days.
The later findings are more obvious with the development of cavitary periventricular cysts.
The degree of severity is described by the size and distribution of these cysts. These things take
a while to develop - some people say up to 4 weeks. So, if they show you a day 1 newborn
with cystic PVL they are leading you to conclude that the vascular insult occurred at least 2
weeks prior to birth (not during birth - which is often the case).
Early: Periventricular White Matter Necrosis Subacute: Cyst Formation
(hyperechoic relative to choroid)
Trivia
The most severe grade (4), which has subcortical cysts, is actually more common in
full term infants rather than preterms.
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Germinal Matrix Hemorrhage (GMH)
I like to think about the germinal matrix as an embryologic seed that sprouts out various
development cells during brain development. Just like a seed needs water to grow, the
germinal matrix is highly vascular. It’s also very friably and susceptible to stress.
Additionally, premature brains suck at cerebral blood flow auto-regulation. Mechanism:
Fragile vessels + too much pressure/flow = bleeds
An important thing to understand is that the germinal matrix is an embryological entity. So it
only exists in premature infants. As the fetus matures the thing regresses and disappears.
By 32 weeks, germinal matrix is only present at the caudothalamic groove.
By 36 weeks, you basically can’t have it (if no GM, then no GM hemorrhage).
Take home point - No GM Hemorrhage in a full term infant.
Gamesmanship: Similar looking bleed in a full term infant say “choroid plexus
hemorrhage” (not GMH).
The scenario will always call the kid a premature infant (probably earlier than 30 weeks). The
earlier they are bom the more common it is. Up to 40% occur in the first 5 hours, and most
have occurred by day 4 (90%). A good thing to remember is that 90% occur in the first week.
Screening: Head US is used to screen for this pathology. Testable trivia includes:
• Who should be screened? Premature Infants (<32 weeks, < 1500 grams), Premature Infants
with Lethargy, Seizures, Decreased Hematocrit or a history of “he don’t look so good.”
• When do you do the head US? First week of life (remember this is when 90% of them occur).
Some people will tell you - “first week and first month” (but that varies from institution).
Some people will also say - “every kid gets a head US prior to discharge from the NICU” - but
that is mainly done to detect PVL (not necessarily GMH).
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Germinal Matrix Hemorrhage (GMH) - Continued
Choroid Plexus is bright (hyperechoic)
on ultrasound. Blood is also bright
(hyperechoic).
You tell them apart based on their
location. Choroid should not extend
anterior to the junction of the caudate
and the thalamus (the so called
caudothalamic groove).
This is the location of the germinal
matrix.
If you see bright stuff there - that is
your grade 1 bleed.
This could also be shown with MRI
(T1 bright = bleed), same location.
Grading System (1-4) - quick and dirty Secondary Consequences GMH
1 - Blood at the caudothalamic groove
2 - Blood in the ventricles
but no dilation.
3 - Blood in the ventricles with dilation
4 - Blood in the brain parenchyma
(from venous infarct)
Few additional things you should see at least once
prior to the exam. Do yourself a favor and
google images of the following:
• Caudothalamic groove in the coronal plane
• Grade 2,3,4 Bleeds
• Subependymal Cysts on US
• Porencephalic Cysts on US
• Choroid Plexus Cysts on US
• Ventricular coarctation on US - this is a mimic
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SECTION 3:
Hea d a n d Nec k
- Sel ec t To pi c s -
Disclaimer: All of the temporal bone pathology you would commonly associate with Peds is also
discussed in detail in the Neuro chapter - found in Volume 2. This is also true for the classic orbital
pathologies of childhood (Retinoblastoma etc...)
Choanal Atresia - Results from a membrane that separates the
nasal cavity from its normal communication with the oral cavity. It is
usually unilateral but can be bilateral. The bilateral ones have a history
of “cyclical cyanosis that improves with crying" (they mouth breath
when they cry). The unilateral classic stories are “can't pass NG
tube," and “respiratory distress while feeding" (neonates have to
breath through their noses). You will also sometimes hear a history of
“a continuous stream of snot draining from one or both nostrils," or
the word “rhinorrhea. ”
There are two different types: bony (90%), and
CHARGE membranous (10%). The appearance is a
Coloboma, unilateral or bilateral posterior nasal narrowing,
Heart defect, with thickening of the vomer.
Atresia (Choanal)
Retarded growth, Trivia: There are many syndromic associations
Genitourinary including CHARGE, Crouzons, DiGeorge,
abnormalities
Ear anomalies Treacher Collins, and Fetal Alcohol Syndrome.
CHARGE is the one people mention the most.
Congenital Piriform Aperture Stenosis
This results from abnormal development of the medial nasal eminences,
and subsequent failure of formation of the primary palate. You can
see this in isolation or with choanal atresia. The piriform aperture of
the nasal cavity (bony inlet of the nose) is stenotic (as the name
suggests), and the palate is narrow. The classic picture is the
associated central maxillary “MEGA-incisor.” Midline defects
of the brain (corpus callosum agenesis, and holoprosenccphaly) are
associated
— as my Grandma always said “face predicts brain".
The big thing to know is the high association with hypothalamic
pituitary-adrenal axis dysfunction.
Next Step - You have to image the brain
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Ectopic Thyroid:
Thyroid topics will be covered again in the endocrine chapter. I do want to mention one or two now for
completeness. To understand ectopic thyroid trivia you need to remember that the thyroid starts
(embryology wise) at the back of the tongue. It then descends downward to a location that would be
considered normal. The “pyramidal lobe” actually represents a persistence of the inferior portion of the
thyroglossal duct - that is why this thing is so variable in appearance. Sometimes this process gets all
fucked up and the thyroid either stays at the back of the tongue (lingual thyroid) or ends up half way
down the neck or even in the chest (ectopic thyroid).
Trivia to know:
• Most “developed” countries test for low thyroid at birth (Guthrie Test). That will trigger a workup for
either ectopic tissue or enzyme deficiencies.
• Nukes (I-123 or Tc-MIBI) is superior to ultrasound for diagnosing ectopic tissue. This is by far the
most likely way to show this on a multiple choice exam. I guess CT would be #2 - remember thyroid
tissue is dense because of the iodine.
• Ultrasound does have a preoperative role in any MIDLINE neck mass - with the point of ultrasound
being to confirm that you have a normal thyroid in a normal place. If you resect a midline mass
(which turns out to be the kids only thyroid tissue) you can expect an expensive well rehearsed didactic
lecture on pediatric neck pathology from an “Expert Witness” sporting a $500 haircut.
• Lingual thyroid (back of the tongue) is the most common location of ectopic thyroid tissue
Thyroglossal Duct Cyst:
As we discussed previously, thyroid related pathology can occur
anywhere between the foramen cecum (the base of the tongue)
and the thyroid gland. In this situation we are talking about the
duct (which is the embryological thyroid interstate highway to the
neck) failing to involute fully. What you get is a left over cyst -
hence the name. The classic locations are (1) at the base of the
tongue, and (2) midline anterior to the hyoid. Now textbooks will
make a big deal about these things becoming slightly lateral below
the hyoid. Do NOT get hung up on that. For the purpose of multiple
choice remember these guys are midline. Midline is the buzzword.
Things to know:
• Classic Buzzword / Scenario = Midline Cyst in the Neck of a Kid.
• Next step once you find one = confirm normal thyroid location and/or
look for ectopic tissue (Ultrasound +/-Tc-MIBI, or I-123).
• They are cystic (it’s not called a “Duct Solid”)
• Enhancing nodule within the cyst = CANCER (usually papillary)
• They can get infected.
Dermoid Cyst
It is true that dermoids almost always occur below the clavicles, but
when they do happen in the neck they have a pretty classic look:
midline sublingual I submandibular space with a “sac of marbles”
appearance. The marbles are lobules of fat within fluid.
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Branchial Cleft Cyst (BCC)
Another cystic embryologic remnant. There are a bunch of types (and subtypes... and sub-
subtypes) and you can lose your fucking mind trying to remember all of them - don’t do that.
Just remember that by far the most common is a 2nd Branchial Cleft Cyst (95%). The angle
of the mandible is a classic location. They can get infected, but are often asymptomatic.
Extension of the cyst between the ICA and ECA (notch sign) just above the carotid
bifurcation is pathognomonic.
How can this be asked on multiple choice:
• What is it? - Most likely on CT or MRI. Ultrasound would be tough, unless they clearly
labeled the area “lateral neck” or oriented you in some other way.
• Location Fuckery. They could (and this would be super mean) ask you the relationship of a
type 2 based on other neck anatomy. So - posterior and lateral to the submandibular gland
or lateral to the carotid space, or anterior to the sternocleidomastoid. How I would handle
that? Just remember it’s going to be lateral to everything. Lateral is the buzzword.
• Mimic - They could try and trick you into calling a necrotic level 2 lymph node a BCC.
Thyroid cancer (history of radiation exposure) and nasopharyngeal cancer (history of HPV)
can occur in “early adulthood.” If you have a “new” BCC in an 18 year old - it’s probably a
necrotic node. Next Step = Find the cancer +/- biopsy the mother fucker.
• I say LATERAL
cyst in the neck,
you say branchial
cleft cyst
• I say MIDLINE
cyst in the neck,
you say
thyroglossal duct
cyst
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Jugular Vein Pathology
There are two jugular vein issues that occur in kids that I should probably mention.
Septic Thrombophlebitis - i.e. clotted jugular vein. You see this classically in the setting of a
recent pharyngeal infection (or recent ENT surgery).
How can this be asked on multiple choice:
• What is it? - Showing the clotted vein with the appropriate clinical history.
• “Lemierre’s Syndrome" - Seeing if you know that it has a fancy syndrome name.
• Next Step? Looking in the lungs for septic emboli. This could also be done in the reverse. Show
you the septic emboli, give you a history of ENT procedure (or recent infection), and have you ask
for the US of the neck veins.
• USMLE Step 1 Association Trivia - Fusobacterium necrophorum is the bacteria that causes the
septic emboli. As this bacteria sounds like a Marvel Comic villain the likelihood of it being asked
increases by at least 5x.
Phlebectasia - Idiopathic dilated jugular vein.
How can this be asked on multiple choice:
• What is it? - Showing the dilated vein.
• Trivia - It is NOT related to a stenosis. There are no other
signs of venous congestion.
• Trivia - It gets worse with the Valsalva maneuver - “neck
mass that enlarges with valsalva, ” Phlebectasia - Dilated Jugular Vein
Misc Venn /Lymphatics
Venous, Arterial and Lymphatic Malformations are complex with overlapping features and
numerous classification schemes. I’ll cover them again in the vascular chapter - this is just a brief
peds neck tangent. Both lymphatic and venous malformations can both look like a large trans-
spatial multicystic mass in the neck. They can both have fluid levels.
If you must try and tell them apart - you could try this:
• Venous Malformations will have enhancement of the cystic spaces.
• Lymphatic Malformations will have enhancement of the septa.
• Phleboliths — suggests venous.
In many cases they coexists together .... so... yeah... hopefully the person writing the question
understands that.
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Hemangioma of Infancy
These things are actually the most common congenital lesions in the head and neck. Just like
any hemangioma they contain vascular spaces with varying sizes and shapes. Most people
consider them a “tumor” more than a vascular malformation.
Things to know:
• How they look = Super T2 bright, with a bunch of
flow voids. Diffusely vascular on doppler. Vocabulary Trivia -
• Phases = Typically they show up around 6 months of THIS vs THAT:
age, grow for a bit, then plateau, then involute (6-10 Infantile Hemangiomas = NOT
years). Usually they require no treatment. present at birth. Show up around
• Indications for Treatment = Large size / Rapid growth 6 months of age. Nearly always
with mass effect on the airway or adjacent vascular involute.
structures. Fucking with the kids eye movement or Congenital Hemangiomas =
eyelid opening. Present at birth. May (RICH) or
• Treatment = Typically medical = Beta blocker may not (NICH) involute.
(propranolol)
• Associations = PHACES Syndrome (discussed later
in the chapter)
Cystic Hygroma (Lymphangioma)
This is another cystic lesion of the neck, which is most likely to be shown as an OB
ultrasound (but can occur in the Peds setting as well). The classic look / location is a cystic
mass hanging off the back of the neck on OB US (or in the posterior triangle if CT/MR1).
Trivia:
• Associations: Turners (most
common association). Downs
(second most common association).
Aortic Coarctation (most common
CV abnormality), Fetal Hydrops (bad
bad bad outcomes).
• Septations = Worse Outcome
• T2 Bright (like a hemangioma).
Does NOT enhance (hemangiomas
typically do). Cystic Hygroma (Lymphangioma)
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Fibromatosis Coli (“Congenital Torticollis”)
This is a benign “mass” of the sternocleidomastoid
in neonates who present with torticollis (chin points
towards the opposite side - or you could say they
look away from the lesion). It’s really just a benign
inflammation that makes the muscle look crazy big.
Ultrasound can look scary, until you realize it’s just
the enlarged SCM. Ultrasound is still the best
imaging test. Sometimes it looks like there are two
of them, but that’s because the SCM has two heads.
It goes away on its own, sometimes they do passive
physical therapy or try and botox them. - This Dragon has Two Heads -
• Most common cause of a neck “mass” in infancy
• Classic scenario is a 4 week old with a palpable neck mass and torticollis toward the affected side
• Best imaging test = US.
• Things that make you think it’s not FC: mass is outside the SCM, or internal calcifications - in
which case you should think to yourself... nice try Mother fuckers- that’s a neuroblastoma.
So... there can be significant fuckery with the “direction” things curve or people look depending
on how the question is ask. What do I mean ?
If you made the mistake of just memorizing the word “towards” in association with fibromatosis
coli you might get tricked if the options were: A - Patient looks towards the involved side.
B - Patient looks toward the uninvolved side. You’d run into the same problem with the word
“away.”
Now, that might seem obvious once I spell it out like that but I’m pretty sure at least a few of you
were making a flashcard that had only the word “towards” on it. You have to assume the test
writer has the worst intentions for you. Don’t provide them with any opportunity to trick you.
Rhabdomyosarcoma
Although technically rare as fuck, this is the most common mass in the masticator space of a kid.
Having said that if you see it in the head/neck region is almost always in the orbit. In fact, its the most
common extra-occular orbital malignancy in children (dermoid is most common benign orbital mass
in child). The most classic scenario would be an 8 year old with painless proptosis and no signs of
infection.
What do sarcomas look like?
I’ll talk about this more in the MSK chapter, but in general I’ll just say they look mean as cat shit
(enhancing, solid, areas of necrosis, etc..).
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SECTION 4:
Ai r w a y
Croup
This is the most common cause of acute upper airway obstruction in young children. The
peak incidence is between 6 months and 3 years (average 1 year). They have a barky
“croupy” cough. It’s viral. The thing to realize is that the lateral and frontal neck x-ray is
done not to diagnosis croup, but to exclude something else. Having said that, the so-called
“steeple sign” - with loss of the normal lateral convexities of the subglottic trachea is your
buzzword, and if it’s shown, that will be the finding. Questions are still more likely to center
around facts (age and etiology). The culprit is often parainfluenza virus.
Epiglottitis
In contrast to the self-limited croup, this one can kill you. It’s mediated by H. Influenza and
the classic age is 3.5 years old (there is a recent increase in teenagers - so don’t be fooled by
that age). The lateral x-ray will show marked swelling of the epiglottis (thumb sign). A fake
out is the “omega epiglottis” which is caused by oblique imaging. You can look for thickening
of the aryepiglottic folds to distinguish.
Trivia: Death by asphyxiation is from the aryepiglottic folds (not the epiglottis)
Exudative Tracheitis (Bacterial Tracheitis)
This is an uncommon but serious (possibly deadly) situation that is found in slightly older
kids. It’s caused by an exudative infection of the trachea (sorta like diphtheria). It’s usually
from Staph A. and affects kids between 6-10. The buzzword is linear soft tissue filling defect
within the airway.
Croup Epiglottitis Exudative Tracheitis
6 months - 3 years Classic = 3.5 years, but now
6-10 years
(peak 1 year) seen with teenagers too
Steeple Sign: loss of the normal Linear soft tissue filling
Thumb Sign: marked
shoulders (lateral convexities) of defect (a membrane) seen
enlargement of epiglottis
the subglottic trachea within the airway
Viral
H-Flu Staph. A
(Most Common - parainfluenza)
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Retropharyngeal Cellulitis and Abscess
Discussed in detail in the Neuro chapter of Volume 2. I’ll just say quickly that you do see this
most commonly in young kids (age 6 months -12 months). If they don’t show it on CT, they
could show it with a lateral x-ray demonstrating massive retropharyngeal soft tissue
thickening. For the real world, you can get pseudothickening when the neck is not truly lateral.
To tell the difference between positioning and the real thing, a repeat with an extended neck is
the next step.
Subglottic Hemangioma
PHACES
Hemangiomas are the most common soft tissue mass in the
P- Posterior fossa
trachea, and they are most commonly located in the subglottic
(Dandy Walker)
region. In croup there is symmetric narrowing with loss of
H- Hemangiomas
shoulders on both sides (Steeple Sign). In contradistinction,
A- Arterial anomalies
subglottic hemangiomas have loss of just one of the sides.
C- Coarctation of aorta,
cardiac defects
Trivia
E- Eye abnormalities
• Tends to favor the left side
S- Subglottic
• 50% are associated with cutaneous hemangiomas
hemangiomas
• 7% have the PHACES syndrome
More on hemangiomas later in the chapter.
Laryngeal Cleft
This is a zebra. The classic scenario is contrast appearing in the tracheal without laryngeal penetration
(aspiration). They could also show you a “thin tract of contrast extending to the larynx or trachea.” This
entity is a communicating defect in the posterior wall of the larynx and the esophagus or anterior hypo
pharynx. There arc a bunch of different cleft classifications - I can’t imagine that shit is appropriate for
the exam. I would just know:
• This is a thing - maybe google a Fluoro swallow picture of it
• These things have other complex malformations associated with them (usually GI)
• It is very tricky to call it with certainty on a swallow exam - definite diagnosis is always made with
direct visualization / scope (so a next step type question would recommend endoscopy to confirm).
Tracheoesophageal Fistula - This is discussed later in the chapter (GI section)
Papilloma - If you see a tabulated grape looking thing in the airway - think Papilloma, especially if
the lungs arc full of nodules (solid and cavitated). When I say Papilloma, You say HPV - typically from
perinatal (birth canal) transmission. These things are usually multiple (papillomatosis) and therefore have
multiple areas of airspace disease (atelectasis etc.). Some potential gamesmanship — because these thing
are typically multiple you will have more areas of air trapping then you would compared with an
aspirated crayon (or green bean), or even a solitary endobronchial lesion like a carcinoid. Multiple areas
of air trapping - think Papillomatosis over carcinoid or a foreign body. Having said that the nodules are a
more common finding... tats of them.
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- Gamesmanship -
Frontal and Lateral Neck Radiographs
For the frontal, there are
two main things to think
about.
(1) Croup and
(2) Subglottic
Hemangioma
You can tell them apart
by the shouldering.
If you can’t tell.... try
and let the history bias
you. Cough? Fever?
Think Croup.
For the lateral, there are 4 main things to think about:
Epiglottitis Retropharyngeal Tonsils (adenoids) Exudative
Abscess Tracheitis
Looks like a Not seen till about
thumb Too wide 3-6 months, and not Linear Filling
( > 6 mm at C2, big till around 1-2 Defect
If the ordering or > 22 mm at C6) years.
suspects the It’s usually staph
diagnosis, do Next Step = CT Too big when they
NOT bring this don’t forget to look encroach the airway
kid to x-ray. Have in the mediastinum
them do a for “Danger Zone”
portable. extension.
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SECTION 5:
CHEST
Before we proceed with the trivia I need to make sure you know / can do two things for me.
1) Know how to tell if a neonatal chest is hyper-inflated or not. Don’t get hung up on this
low vs normal - that’s a bunch of bologna. Just think (a) Hyper-inflated, or (b) NOT
Hyper-inflated.
The easiest way to do this is to just count ribs.
More than 6 Anterior, or 8 Posterior as they
intersect the diaphragm is too much. As a
quick review, remember that the anterior
ribs (grey) are the ones with a more
sloping course as they move medially,
where as the posterior ribs (black) have a
horizontal course.
Other helpful signs suggesting
hyperinflation:
• Flattening of the diaphragms
• Ribs take on a more horizontal appearance
2) Know what “Granular” looks like. Know what “Streaky” or “Ropy” looks like. My
good friends at Amazon are not capable of printing a clear picture of these so I want you
to stop reading and
A. Go to google images
B. Search “Granular neonatal chest x-ray." Look at a bunch of examples. Maybe even
download a few of them for review.
C. Search “Streaky Perihilar neonatal chest x-ray." Look at a bunch of examples.
Maybe even download a few of them for review.
D. Search “Ropy neonatal chest x-ray." Look at a bunch of examples. Maybe even
download a few of them for review.
Random Pearl: We are going to talk about the presence of a pleural effusion as a
discriminator. One pearl is to look for an accentuated (thick) minor fissure on the right. If
you see that shit, kid probably has an effusion. Confirm by staring with fierce intensity at the
lung bases to look for obliteration of the costophrenic sulcus.
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Alphabet - MNoP
As we proceed forward with the
trivia, pay close attention to lung High Volumes Meconium Aspiration
volumes, and the words “granular”, + Perihilar Streaky Non GB Neonatal
“streaky”, and “ropy.” Pneumonia
You will find that you can divide Not High (low or
the big 5 in half by doing something normal) Volumes SSD
like this: + Granular Group B Pneumonia
Meconium Aspiration
This typically occurs secondary to stress (hypoxia), and is more common in term or post-
mature babies (the question stem could say “post term ” delivery). The pathophysiology is all
secondary to chemical aspiration.
Trivia:
•The buzzword “ropy appearance” of asymmetric lung densities
•Hyperinflation with alternative areas of atelectasis
•Pneumothorax in 20-40% of cases
How can it have hyperinflation?? Aren't the lungs full of sticky shit
BUT (literally)??? The poop in the lungs act like miniature ball-valves
Prometheus? (“floaters” I call them), causing air trapping - hence the increased lung
volumes.
Reality vs Multiple Choice: “Meconium Staining” on the amniotic fluid is common (like 15% of all
births), but development of “aspiration syndrome” is rare with only 5% of those 15% actually have
aspiration symptoms. Having said that, if the question header bothers to include “Green colored
amniotic fluid” or “Meconium staining” in the question header they are giving you a major hint.
Don’t overthink a hint like this. If they ask “What color was George Washington's white horse?" the
answer is NOT brown.
Transient Tachypnea of the Newborn (TTN)
The classic clinical scenario is a history of c-section (vagina squeezes the fluid out of lungs
normally). Other classic scenario histories include “diabetic mother” and/or “maternal
sedation.” Findings are going to start at 6 hours, peak at one day, and be done by 3 days. You
are going to see coarse interstitial marking and fluid in the fissures.
Trivia:
•Classic histories: C-Section, Maternal Sedation, Maternal Diabetes
•Onset: Peaks at day 1, Resolved by Day 3
•Lung Volumes - Normal to Increased
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Surffactant-Deficient Disease (SDD)
This is also called hyaline membrane disease, or RDS. It’s a disease of pre-mature kids. The idea
is that they are bom without surfactant (the stuff that makes your lungs stretchy and keeps alveolar
surfaces open). It’s serious business and is the most common cause of death in premature
newborns. You get low lung volumes and bilateral granular opacities (just like B-hemolytic
pneumonia). But, unlike B-hemolytic pneumonia you do NOT get pleural effusions. As a piece
of useful clinical knowledge, a normal plain film at 6 hours excludes SDD.
Surfactant Replacement Therapy
They can spray this crap in the kid’s lungs, and it makes a huge difference (decreased death rate
etc...). Lung volumes get better, and granular opacities will clear centrally after treatment. The
post treatment look of bleb-like lucencies can mimic PIE.
Trivia:
•Increased Risk of Pulmonary Hemorrhage
•Increased Risk of PDA
Neonatal Pneumonia (Beta-Hemolytic Strep - or “GBS”)
This is the most common type of pneumonia in newborns. It’s acquired during exit of the dirty
birth canal. Premature infants are at greater risk relative to term infants. It has some different
looks when compared to other pneumonias (why I discuss it separately).
Trivia:
•It often has low lung volumes (other pneumonias have high)
•Granular Opacities is a buzzword (for this and SDD)
•Often (25%) has pleural effusion (SDD will not)
•LESS likely to have pleural effusion compared to the non Beta hemolytic version (25% vs 75%)
Neonatal Pneumonia (not Beta-Hemolytic Strep - “Non GB” or “Non GBS”)
Lots of causes. Typical look is patchy, asymmetric perihilar densities, effusions, and
hyperinflation. Will look similar to surfactant deficient disease but will be full term. Effusions are
also much more likely (they are rare in SDD).
Persistent Pulmonary HTN
Also called “persistent fetal circulation”. Normally, the high pulmonary pressures seen in utero
(that cause blood to shunt around the lungs) decrease as soon as the baby takes his/her first breath.
Dr. Goljan (Step 1 wizard) calls this a “miracle,” and used this basic physiology to deny
evolution. When high pressures persist in the lungs it can be primary (the work of Satan), or
secondary from hypoxia (meconium aspiration, pneumonia, etc...). The CXR is going to show
the cause of the pulmonary HTN (pneumonia), rather than the HTN itself.
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Solving Cases Using Buzzwords
When I say “Post Term Baby, ” How this could work:
You Say Meconium Aspiration
Blah Blah Blah, Post Term Delivery o f a
When 1 say “C-Section, ” beautiful baby girl. What is the diagnosis?
You say Transient Tachypnea
(A) RDS
(B) Transient Tachypnea
When I say “Maternal Sedation ” (C) Meconium Aspiration
You say Transient Tachypnea
When I say “Premature ”
You say RDS
Solving Cases Using Lung Volumes:
High (flat diaphragms):
Low:
• Meconium Aspiration
•Surfactant Deficiency (no pleural effusion)
• Transient Tachypnea
•Beta-Hemolytic Pneumonia (gets pleural effusions)
• Non BH Neonatal Pneumonia
How this could work:
Blah Blah Blah, This Picture of a beautiful baby
girl. What is the diagnosis?
(A) RDS
(B) Transient Tachypnea
(C) Meconium Aspiration
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- Life in the NICU (Just as glamorous as it sounds) -
Pulmonary Interstitial Emphysema (PIE)
When you have surfactant deficiency and they put you on a ventilator (which pulverizes your
lungs with PEEP), you can end up with air escaping the alveoli and ending up in the
interstitium and lymphatics. On CXR it looks like linear lucencies (buzzword). It’s a
warning sign for impending Pneumothorax. Most cases of PIE occur in the first week of time
(bronchopulmonary dysplasia - which looks similar - occurs in patients older than 2-3
weeks). Surfactant therapy can also mimic PIE. The treatment is to switch ventilation
methods and/or place them PIE side down.
A total zebra is the progression of PIE to a large cystic mass. The thing can even cause
mediastinal mass effect.
Trivia:
•Consequence of ventilation
•Usually occurs in the first week of life
•Buzzword = Linear Lucencies
•Warning Sign for Impending Pneumothorax
•Treatment is to put the affected side down
Chronic Lung Disease - CLD / (Bronchopulmonary Dysplasia - BPD)
This is the kid born premature (with resulting surfactant deficiency), who ends up being
tortured in ventilator purgatory. His/her tiny little lungs take a ferocious ass whipping from
positive pressure ventilation and oxygen toxicity — “barotrauma” they call it. This beating
essentially turns the lungs into scar, inhibiting their ability to grow correctly. That is why
people call this “a disease of lung growth impairment.”
• Classic Vignette: Prolonged ventilation in a tiny (< 1000 grams), premature kid (< 32 weeks)
• Classic Look: Alternating regions of fibrosis (coarse reticular opacities), and hyper-aeration
(cystic lucencies).
• Buzzword: “Band like opacities”
PIE = First week of life,
• Classic This vs That: CLD vs PIE. They both have cystic CLD = After 3 to 4
lucencies. The difference (as is often the case in peds) is weeks' postnatal age
TIME.
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-Congenital Chest-
Pulmonary Hypoplasia
This can be primary or secondary. Secondary causes seem to lend themselves more readily to multiple
choice questions. Secondary causes can be from decreased hemi-thoracic volume, decreased vascular
supply, or decreased fluid. The most common is the decreased thoracic volume, typically from a space
occupying mass such as a congenital diaphragmatic hernia (with bowel in the chest), but sometimes
from a neuroblastoma or sequestration. Decreased fluid, refers to the Potter Sequence (no kidneys →
no pee → no fluid → hypoplastic lungs).
Bronchopulmonary Sequestration (no communication with airway)
These are grouped into intralobar and extralobar with the distinction being which has a pleural
covering. The venous drainage is different (intra to pulmonary veins, extra to systemic veins). You
can NOT tell the difference radiographically. The practical difference is age of presentation;
intralobar presents in adolescence or adulthood with recurrent pneumonias, extralobar presents in
infancy with respiratory compromise.
• Intralobar: Much more common (75%). Presents Intralobar Extralobar
in adolescence or adulthood as recurrent pneumonias
(bacteria migrates in from pores of Kohn). Most
commonly in the left lower lobe posterior segment More Common Less Common
(2/3s). Uncommon in the upper lobes. In
contradistinction from extralobar sequestration, it is
rarely associated with other developmental Presents in Presents in
abnormalities. Pathology books love to say “NO Adolescence Infancy
pleural cover” - but you can ’t see that shit on CT or
MR.
Associated
• Extralobar: Less common of the two (25%). Recurrent
Congenital
Presents in infancy with respiratory compromise Infections
Anomalies
(primarily because of the associated anomalies -
Congenital cystic adenomatoid malformation
(CCAM), congenital diaphragmatic hernia, vertebral
anomalies, congenital heart disease, pulmonary Has its own
No Pleural Cover
hypoplasia). It rarely gets infected since it has its own pleural cover
pleural covering. These arc sometimes described as
part of a bronchopulmonary foregut malformation, and
may actually have (rarely) a patent channel to the Pulmonary Systemic Venous
stomach, or distal esophagus. Pathology books love to Venous Drainage Drainage
say “has a pleural cover” - but you can't see that shit
on CT or MR.
Gamesmanship: I say recurrent pneumonia in same area, you say intralobar sequestration.
Bronchogenic Cysts
Typically an incidental finding. They are generally solitary and unilocular. They typically do NOT
communicate with the airway, so if they have gas in them you should worry about infection.
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Congenital Cystic Adenomatoid Malformation (CCAM)
- (Other Aliases Include - CPAM)
As the name suggests it’s a malformation of adenomatoid stuff that replaces normal lung. Most
of the time it only affects one lobe. There is no lobar preference (unlike CLE which favors the
left upper lobe). There are cystic and solid types (type 1 cystic, type 3 solid, type 2 in the
middle). There is a crop of knuckle heads who want to call these things CPAMs and have 5
types, which I’m sure is evidence based and will really make an impact in the way these things
are treated. CCAMs communicate with the airway, and therefore at least components of them
can fill with air. Most of these things (like 90%) will spontaneously decrease in size in the third
trimester. The treatment (at least in the USA) is to cut these things out, because of the iddy bitty
theoretical risk of malignant transformation (pleuropulmonary blastoma, rhabdomyosarcoma).
Q: What if you see a systemic arterial feeder (one coming off the aorta) going to the CCAM ?
A: Then it’s not a CCAM, it’s a Sequestration. — mumble to yourself “nice try assholes”
Congenital Lobar Emphysema (CLE)
The idea behind this one is that you have bronchial pathology (maybe atresia depending on what
you read), that leads to a ball-valve anomaly and progressive air trapping. On CXR, it looks
like a lucent, hyper-expanded lobe.
Trivia:
•It’s not actually emphysema just air trapping secondary to bronchial anomaly
•It prefers the left upper lobe (40%)
•Treatment is lobectomy
Gamesmanship:
•The classic way this is shown in case conference or case books is with a series of CXRs.
The first one has an opacity in the lung (the affected lung clears fluid slower than normal
lung). The next x-ray will show the opacity resolved. The following x-ray will show it
getting more and more lucent. Until it’s actually pushing the heart over.
Congenital Diaphragmatic Hernia (CDHs)
Most commonly they are Bochdalek type. B is in the Back - they are typically posterior and to
the left. The appearance on CXR is usually pretty obvious.
Trivia:
•Usually in the Back , and on the left (Bochdalek)
•If it’s on the right - there is an association with GBS Pneumonia
•Mortality Rate is related to the degree of pulmonary Hypoplasia
•Most have Congenital Heart Disease
•Essentially all are malrotated
Gamesmanship
•One trick is to show the NG tube curving into the chest.
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Locational Strategy
Left Upper Lobe:
Think Congenital Lobar
Emphysema (CLE) first
But, remember CCAM has no
lobar prevalence, so it can be
anywhere
Left Lower Lobe:
Think Sequestration First
Congenital Diaphragmatic
Hernia (CDHs) favors this
side too
Case 1. Newborn with congenital heart disease
A. Intralobar Sequestration
B. Extralobar Sequestration
C. Congenital Lobar Emphysema
Case 2. 10 year old with recurrent pneumonia
A. Intralobar Sequestration
B. Extralobar Sequestration
C. Congenital Lobar Emphysema
**Intralobar is seen older kids,
**Extralobar is seen in infants with co-morbids
** CLE is in the upper lobe
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-Special Situations in Peds Chests-
Viral — In all ages this is way more common than bacterial infection. Peribronchial edema is the
buzzword for the CXR finding. “Dirty” or “Busy” Hilum. You also end up with debris and mucus in
the airway which causes two things (1) hyperinflation and (2) subscgmental atelectasis. Respiratory
Syncytial Virus (RSV) - This will cause the typical non-specific viral pattern as well. However,
there is the classic testable predilection to cause a segmental or lobar atelectasis - particularly in the
right upper lobe.
Round Pneumonia - Kids get round pneumonia. They love to show
this, and try to trick you into thinking it’s a mass. Younger than 8 you arc
thinking round pneumonia, round pneumonia, round pneumonia - with S.
Pneumonia being the culprit. The PhD trivia is that these occur because you
don’t have good collateral ventilation pathways. Round pneumonia is
usually solitary, and likes the posterior lower lobes. Take home message: No
CT to exclude cancer, just get a follow up x-ray.
Neonatal atypical peripheral atelectasis (NAPA) - It is best
to think about this as a cousin or uncle of Round Pneumonia (they are in the
same family). It is essentially the same thing except it is peripheral. The
classic look is a round, pleural based “mass” in the apex of the lung.
Similarly to the “round pneumonia” this is a transient finding and will
resolve as the primary process improves.
Lipoid Pneumonia - Classic history is a parent giving their newborn a teaspoonful of olive oil
daily to cultivate “a spirit of bravado and manliness.” Although this seems like a pretty solid plan, and
I can’t fault their intentions - it’s more likely to result in chronic fat aspiration. Hot Sauce is probably a
better option. Most people will tell you that bronchoalveolar lavage is considered the diagnostic
method of choice. CXR nonspecific - it is just airspace opacities. CT is much more likely to be the
modality used on the exam. The classic finding is low attenuation ( -30 to -100 HU) within the
consolidated areas reflecting fat content.
Bronchial Foreign Body:
The key concept is that it causes air trapping.
The lung may look more lucent (from air
trapping) on the affected side. You put the
affected side down and it will remain lucent
(from air trapping). Another random piece of
trivia is that under fluoro the mediastinum will
shift AWAY from the affected side on
expiration. Bottom Lung is
Black = Air Trapping
Key Point: A normal inspiratory CXR is meaningless. Don’t forget that the crayon / green bean is going
to be radiolucent. You need expiratory films to elicit air trapping. Normally, the bottom lung is gonna
turn white (move less air). If there is air trapping the bottom lung will stay black.
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Swyer James - This is the classic unilateral lucent lung. It typically occurs after a viral lung
infection in childhood resulting in post infectious obliterative bronchiolitis. The size of the affected
lobe is smaller than a normal lobe (it’s not hyper-expanded).
Papillomatosis - Perinatal HPV can cause these soft tissue masses within the airway and lungs.
It’s also seen in adults who smoke. “Multiple lung nodules which demonstrate cavitation” is the
classic scenario. Some testable trivia includes the 2% risk of squamous cell cancer, and that
manipulation can lead to dissemination. The appearance of cysts and nodules can look like LCH
(discussed more in the thoracic chapter), although the trachea is also involved.
Sickle Cell / Acute Chest - Kids with sickle cell can get “Acute chest.” Acute chest actually
occurs more in kids than adults (usually between age 2-4). This is the leading cause of death in sickle
cell patients. Some people think the pathology is as such: you infarct a rib → that hurts a lot, so you
don’t breath deep → atelectasis and infection. Others think you get pulmonary microvascular
occlusion and infarction. Regardless, if you see opacities in the CXR of a kid with sickle cell, you
should think of this.
Gamesmanship (how do you know it's sickle cell?)
•Kid with Big Heart
•Kid with bone infarcts (look at the humeral heads)
•Kid with H shaped vertebra (look on lateral)
Cystic Fibrosis- So the sodium pump doesn’t work and
they end up with thick secretions and poor pulmonary CF Related Trickery
clearance. The real damage is done by recurrent infections.
• Fatty Replaced Pancreas on CT
Things to know:
•Bronchiectasis (begins cylindrical and progresses to • Abdominal Films with
varicoid) Constipation
•It has an apical predominance (lower lobes are less
affected) • Biliary Cirrhosis (from blockage
•Hyperinflation of intrahepatic bile ducts), and
•They get Pulmonary Arterial Hypertension resulting portal HTN
•Mucus plugging (finger in glove sign)
•Men are infertile (vas deferens is missing)
Primary Ciliary Dyskinesia - The motile part of
the cilia doesn’t work. They can’t clear their lungs and get THIS vs THAT:
recurrent infections. These guys have lots of bronchiectasis
just like CF. BUT, this time it’s lower lobe predominant Primary
(CF was upper lobe). Cystic
Ciliary
Fibrosis
Dyskinesia
Things to know:
•Bronchiectasis (lower lobes) Upper Lobe Lower Lobe
•50% will have Kartagener's (situs inversus). So, 50% Predominant - Predominant -
will not Bronchiectasis Bronchiectasis
•Men are infertile (sperm tails don’t work)
•Women are sub-fertile (cilia needed to push eggs Infertile - Men are Infertile - Men’s
around) Missing the Vas Sperm Don’t Swim
Deferens For Shit
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-Primary Lung Tumors-
Pleuropulmonary Blastoma (PPB) - This is a primary intrathroacic malignancy.
They can look a lot like CCAMs and even have different types (cystic, mixed, solid). These
things are usually right sided, pleural based, and without chest wall invasion or calcifications.
No rib invasion (helps distinguish it from the Askin / Ewing Sarcoma of the Chest Wall - if
they won't tell you the age), No calcification. The more solid types can have mets to the brain
and bones. The cystic type seem to occur more in kids less than a year old, and be more
benign.
Things to know about PPBs:
•Big Fucking Mass (B.F.M.) in the chest of a 1-2 year old
•Shouldn’t have an eaten-up rib (Askin tumors often do)
•10% of the time they have a multilocular cystic nephroma.
-Catheters/Lines-
Umbilical Venous Catheter (UVC) -
A UVC passes from the umbilical vein to the left
portal vein to the ductus venosus to a hepatic vein to
the IVC. You don’t want the thing to lodge in the
portal vein because you can infarct the liver. The
ideal spot is at the IVC - Right Atrium junction.
Development of a “Cystic Liver Mass" (Hematoma)
can suggest UVC erosion into the liver.
Umbilical Artery Catheter (UAC) -
A UAC passes from the umbilicus, down to the
umbilical artery, into an iliac artery then to the aorta.
Positioning counts, as the major risk factor is renal
arterial thrombosis. You want to avoid the renal
arteries by going high (T8-T10), or low (L3-L5)
Things to know about UACs:
•It goes down first
•It should be placed either high (T8-T10)
or low (L3-L5)
•Omphalocele is a contraindication
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ECMO - Extracorporeal Membrane Oxygenation
Neonatologists primarily use this device to torture sick babies - hopefully into revealing the
various government secrets they have stolen, or the location of their organization’s
underground lair. “Enhanced interrogation” or “temporizing measure of last resort,” they call
it - to get around the Geneva Conventions.
Oh you want to pretend you can’t talk? Get the ECMO catheters!
Alternatively, it can be used as a last resort in neonatal sepsis, severe SSD, and meconium
aspiration. Actually, in cases of meconium aspiration ECMO actually does work
(sometimes).
Types:
There are two main types:
(1) Veno-Arterial “V-A”, and (2) Veno-Venous “V-V”
VenoArterial VenoVenous
“V-A” “V-V”
In both cases deoxygenated blood is removed from the
right atrium and pumped into a box (artificial lung) to
Catheter
get infused with oxygen. The difference is in how it is Position: Catheter
returned. RA + Aorta (near Position:
the origin of RA + RA
the innominate “Dual Lumen”
In V-A, blood goes hack to the Aorta (you can see why
artery)
this would help rest the left ventricle). The catheter is
usually placed at the origin of the innominate or Heart + Lung
Lung Support
Support
“overlying the arch.”
Carotid artery
In V-V blood goes right back into the right atrium. In and Right
this situation even if the lungs were totally clogged Jugular Vein are
“Sacrificed” to
with shit (meconium aspiration) and no oxygen the Volcano God
exchange was happening it wouldn’t matter because in the hopes of a
the blood that is being pumped (RA → RV → plentiful harvest.
Pulmonary Artery) already has oxygen in it.
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ECHO - Extracorporeal Membrane Oxygenation - Continued
Things to Know:
• Lung White Out = Normal. Mechanism is variable depending on who you asked. The way
I understand it is that the airway pressure suddenly drops off causing atelectasis, plus you
have a change in the circulation pattern that now mimics the fetal physiology (mom =
artificial lung). Resulting oxygen tension changes lead to an edema like pattern. A multiple
choice trick could be to try and make you say it is worsening airspace disease, or reflects the
severity of the lung injury. Don’t fall for that. It’s an expected finding.
• Consequences of V-A. I mentioned on the prior page that they typically ligate the carotid
when they place the Arterial catheter. No surprise that they will be at increased risk for
neurologic ischemic complications as a result.
• Crucial Complication = Hemorrhage. The combination of anti-coagulation (necessary in
ECMO) and being sick as stink puts these kids at super high risk for head bleeds. This is
why they will get screened for germinal matrix hemorrhage prior to being placed on ECMO
and then routinely screened with head ultrasounds (expertly read by the second year resident
on call).
Catheter Position Gamesmanship:
I think there are two likely ways a multiple choice question could be structured related to
ECMO catheter position. The first would be to show you a series of daily radiographs with the
latest one demonstrating migration of one or both catheters. That's the easy way to do it.
The sneaky way would be to show you the
catheter with the lucent distal end and the dot
marker on the tip. This would be particularly
evil as there are tons of different catheter
brands and looks, but if I was going to try and
trick you, this would be the way that I would do
it.
In this case, the venous catheter looks falsely
high if judged by the lucent tip, but that round
metallic marker (near the black arrow) shows
the tip in the RA.
The arterial catheter “overlies the region of the
aortic arch,” which is normal.
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SECTION 6:
MEDIASTINAL MASSES
Anterior: That Asshole is Guilty!
Things that make you think the
Normal Thymus: This is the most common mediastinal thymus is a cancer!
“mass.” It’s terribly embarrassing to call a normal thymus a
mass, but it can actually be tricky sometimes. It can be • Abnormal Size for patients Age
pretty big in kids less than 5 (especially in infants). (really big in a 15 year old)
Triangular shape of the thymus is sometimes called the “sail • Heterogenous appearance
sign.” Not to be confused with the other 20 sail signs in • Calcification
various parts of the body, or the spinnaker sail sign, which is • Compression of airway or
when pneumomediastinum lifts up the thymus. vascular structure
Thymic Rebound: In times of acute stress (pneumonia, radiation, chemotherapy, bums), the
thymus will shrink. In the recovery phase it will rebound back to normal, and sometimes larger
than before. During this rebound it can be PET avid.
Lymphoma: This is the most common abnormal mediastinal mass in children (older
children and teenagers). Lymphoma vs Thymus can be tricky. Thymus is more in kids under 10,
Lymphoma is seen more in kids over 10. When you get around age 10, you need to look for
cervical lymph nodes to make you think lymphoma. If you sec calcification, and the lesion has
NOT been treated you may be dealing with a teratoma. Calcification is uncommon in an untreated
lymphoma.
Complications: Compression of SVC, Compression of Pulmonary Veins, Pericardial Effusion,
Airway Compression.
ALL/Leukemia - can appear very similar to Lymphoma (soft tissue mass in the anterior
mediastinum). In this scenario, most people will tell you that Lymphoma can NOT be
differentiated from Leukemia on imaging alone.
Germ Cell Tumor (GCT): On I say, Extra Gonadal Germ Cell Tumor,
imaging, this is a large anterior mediastinal
mass arising from or at least next to the You Say Klinefelter’s Syndrome (47 XXY)
thymus. It comes in three main flavors, each Klinefelter patients have the worst syndrome
of which has a few pieces of trivia worth
ever. They have small penises, they get male
knowing:
breast cancer, and as if things couldn’t possibly
1- Teratoma - Mostly Cystic, with fat and get worse... they get germ cell tumors in their
calcium chest. In fact, they are at 300x the risk of
getting a GCT. Pineal gland Germ Cells have
2 - Seminoma - Bulky and Lobulated. also been reported in Klinefelter patients, giving
“Straddles the midline” them vertical gaze palsy. In that case, they can’t
3 - NSGCT - Big and Ugly - Hemorrhage even look up to the sky and say “Why God*?!
and Necrosis. Can get crazy and invade the Why Me!? Why Klinefelter’s!?”
lung. **God, Allah, Mother Earth, Celestial Deity NOS
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Middle
Lymphadenopathy - Middle mediastinal lymphadenopathy is most often from
granulomatous disease (TB or Fungal), or from lymphoma.
Mediastinal Adenopathy Trivia:
Cause: EBV (~90%), CMV (~10%)
Classic Scenario: Adolescent with hilar adenopathy, splenomegaly,
Mononucleosis and fatigue.
Trivia: Rash after Antibiotics (Amoxicillin)
Trivia: “No sports for 3 weeks” - to avoid splenic injury
Distribution of nodes in usually unilateral, right hilar, right paratracheal
Primary TB
Lower and Middle lobe consolidation is common
Midwest and Southeast United States
Histoplasmosis Most have normal CXRs
Can have hilar adenopathy
Southwest United States
Coccidioidomycosis Usually looks like consolidation and nodules
Can have hilar adenopathy
Often cited as the “most common” anterior mediastinal mass in a kid.
Lymphoma
Hilar involvement (usually bilateral) is more common with Hodgkin
Uncommon in children — it usually presents in the early-mid 20s.
Sarcoid
Case reports of early onset Sarcoid exist.
Duplication Cysts - These fall into three categories (a) bronchogenic, (b) enteric,
(c) neuroenteric. The neuroenterics are traditionally posterior mediastinal.
• Bronchogenic - water attenuation - close to the trachea or bronchus. Trivia:
• Tend to be middle mediastinal (70%), the rest arc in the hilum
• Typically filled with mucus or fluid
• Enteric / Esophageal - water attenuation close to the esophagus (lower in the
mediastinum). Trivia:
• Abutment of the esophagus is the key finding.
• Can communicate with the lumen of the esophagus - and have air/fluid levels.
• Usually on the right, involving the distal esophagus
• Can be middle or posterior mediastinal in location
• Second most common GI lumen duplication cyst (distal ileum #1)
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Posterior
Neuroblastoma - This is the most common posterior mediastinal mass in a child under 2. This
is discussed in complete detail in the GU PEDs section. I’ll just mention that compared to abdominal
neuroblastoma, thoracic neuroblastoma has a better outcome. It may involve the ribs and vertebral
bodies. Also, remember that Wilms usually mots (more than neuroblastoma) to the lungs, so if it’s in
the lungs don’t forget about Wilms. More on this later in the chapter.
You can have other Neuroblastic tumors in this region as well. If Neuroblastoma is the most
undifferentiated and aggressive the spectrum looks something like this:
Most Mature Intermediate Undifferentiated
Ganglioneuroma Ganglioneuroblastoma Neuroblastoma
When Compared with Neuroblastoma, Ganglioneuromas are:
• Less Aggressive
• More Circumscribed (less invasive)
• Less Likely to have Calcifications (although they still can)
• Found in Older Children
These tumors can NOT be differentiated with imaging alone
(but that doesn’t mean someone can’t write a multiple choice
question asking you to try).
Ewing Sarcoma - This is discussed in complete detail in the MSK PEDs section.
Askin Tumor (Primitive Neuroectodermal tumor of the chest wall):
This is now considered part of the Ewing Sarcoma spectrum, and is sometimes called an Ewing
sarcoma of the chest wall. They tend to displace adjacent structures rather than invade early on (when
they get big they can invade). They look heterogenous, and the solid parts will enhance.
Neuroenteric Cyst — By convention these are associated with vertebral anomalies (think
scoliosis, hemivertebrae, butterfly vertebrae, split cord, etc..) - think cyst protruding out of an unsealed
canal / defect. The cyst does NOT communicate with CSF, is well demarcated, and is water density.
Favor the lower cervical and thoracic regions.
Extramedullary Hematopoiesis - This occurs in patients with myeloproliferative
disorders or bone marrow infiltration (including sickle cell). Usually, this manifests as a big liver and
big spleen. However, in a minority of cases you can get soft tissue density around the spine
(paraspinal masses), which are bilateral, smooth, and sharply delineated.
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Strategy - The Anterior Mediastinal Mass
Lymphoma - In a kid just assume it’s Hodgkins (which means it’s gonna involve the
thymus). Why assume Hodgkins ? Hodgkins is 4x more common than NHL. Hodgkins
involves the thymus 90% of the time.
Q: How the hell do you tell a big ass normal thymus in a little baby vs a lymphoma?
A: My main move is to go age. Under 10 = Thymus, Over 10 = Lymphoma.
Thymic Rebound - If the test writer is headed in this direction they MUST either (a)
bias you with a history saying stuff like “got off chemo” or “got off corticosteroids” or
(b) show you a series of axial CTs with the thing growing and maintaining normal
morphology. I think “a” is much more likely.
The Funk: In general just think morphology / density:
• Soft Tissue - Kinda Homogenous = Think Lymphoma or Hyperplasia
• Fat = Germ Cell Tumor (Why God!? Why Klinefelter's!?)
• Water = Congenital Stuff - Think Lymphangiomas
Strategy - The Posterior Strategy - The B.F.M.
Mediastinal Mass “Big Fucking Mass”
First Rule of Peds Multiple Choice Test
Taking - TIMING! AGE!
Under 10 - Think malignant,
Think neuroblastoma.
2nd Decade - Think benign.
If it’s a round mass- Think about
Ganglioneuromas & Neurofibromas
If you see a B.F.M. in the chest of a kid,
If it’s cystic (and there is scoliosis) think
you basically have two choices:
Neuroenteric Cyst
If they show you coarse bone (1) Askin Tumor (PNET I Ewings) -
trabeculation - with an adjacent mass (or *AGE 10+, look for an eaten up rib.
a history of anemia) - Think (2) Pleuropulmonary Blastoma
Extramedullary Hematopoiesis *AGE is typically less than 2.
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SECTION 7:
Lu mi n a l Gl
Esophageal Atresia /
TE fistula: This can occur
in multiple subtypes, with the
classic ways of showing it
being a frontal CXR with an
NG tube stopped in the
upper neck, or a fluoro study
(shown lateral) with a blind
ending sac or communication
with the tracheal tree.
There are 5 main subtypes, only 3 (shown above) are worth knowing (being familiar with) for the
purpose of the exam.
Things to Know About Esophageal Atresia / TE Fistula:
•Diagnosis is made with a Fluoro swallow exam
•Most Important Thing To Know arc the VACTERL associations (more on this later)
•The most common subtype is the N-Type (blind ended esophagus, with distal esophagus hooked up
to trachea
• Excessive Air in the Stomach = H type (can also be with N type)
• No Air in the Stomach = Esophageal Atresia
• The presence of a right arch (4%) must be described prior to surgery (changes the approach).
Gamesmanship: Fake out for TE fistula is simple aspiration. Look for the presence or absence of
laryngeal penetration to tell them apart (if shown a dynamic Fluoro swallow exam).
VACTERL: This is extremely high yield. VACTERL is a way of remembering that certain
associations are seen more commonly when together (when you see one, look for the others).
They occur with different frequency: VACTERL association is diagnosed when 3
or more of the defined anomalies affect a
V - Vertebral Anomalies (37%) patient.
A - Anal (imperforate anus) (63%)
C - Cardiac (77%) Therefore, keep investigating when 1-2 of
TE - Tracheoesophageal Fistula these anomalies are found.
or Esophageal Atresia (40%)
R - Renal (72%) The heart and kidneys are the most
L - Limb (radial ray) - 58% commonly affected organs in this
Trivia: If both limbs are involved, then both kidneys tend to be involved. If one limb is involved, then
one kidney tends to be involved.
Stricture: Around 30% of kids with a repaired esophageal atresia will end up with a focal
anastomotic stricture. Strictures can also be seen with caustic ingestion (dishwashing soap) - but those
tend to be long segment. Reflux (if chronic and severe) is another possible cause.
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Esophageal Foreign Bodies: Kids love to stick things in their mouths (noses and ears).
This can cause a lot of problems including direct compression of the airway, perforation, or even
fistula to the trachea. Stuff stuck in the esophagus needs to be removed.
THIS vs THAT: Trachea vs Esophagus:
The esophagus is a dirty sock, it flexes to accommodate that big piece of steak you didn’t even
bother to chew. The trachea is rigid, like that math teacher I had in high school (who hated
music... and colors), but unlike the math teacher it has a flexible membrane in the back.
The point of me
mentioning this is to
help you problem solve
a “where is the coin ”
type question. The
esophagus will
accommodate the coin
so it can be turned in
any direction. The
trachea is rigid and will
force the coin to rotate
into the posterior
membrane — so it will
be skinny in the AP
direction.
Additional trivia relates to swallowed batteries, magnets, and pennies - chart on the following
page.
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Ingested Metallic Foreign Bodies
One magnet is ok. Two or more magnets is a
problem. The reason is that they can attract
Surgical Consult
Magnets each other across intestinal walls leading to
NOT an MRI (dumbass)
obstruction, necrosis, perforation, and a law suit.
Less of a problem relative to other types of Serial plain film exams.
batteries, but can cause serious problems if you Remove if they stay in
AA or AAA Batteries need them for the DVR control because Game of the stomach for more
Thrones season 7 is on (spoiler it sucked). than 2 days.
Stuck in the esophagus
= big problem, gotta
They look like coins, except they
get them out within 2
have two rings. The literature is
hours.
not clear, but it appears that
Disc Batteries
modern batteries rarely leak
Stuck in the stomach =
(leaking is bad - caustic
problem, gotta get
chemicals, heavy metals etc..).
them out within 4 days.
Remove if:
Copper Pennies are relatively
safe.
Coins Retention in the
(Including Pennies esophagus for more
Make sure it is not a disc battery
minted prior to 1982) than 24 hours or
(coins have one order ring, disc
Stomach for more than
battery has two).
28 days.
Those minted after 1982 contain mostly Zinc
which when combined with stomach acid can
cause gastric ulcerations, and if absorbed in
great enough quantity can cause zinc toxicosis
(which is mainly pancreatic dysfunction /
pancreatitis). The ulcers are the more likely thing
Pennies to happen, so just remember that.
Remove from Stomach
-minted after 1982
So how the hell can you tell the date of a penny
that is swallowed? Either (a) the question stem
will have to say something like - “2 year old child
playing with father’s collection of 1984 pennies”,
or the more likely (b) showing you the penny with
characteristic radiolucent holes - from erosion.
Usually Lead Paint Dust - or Any object with lead
Remove immediately
paint.
from stomach. Distal
Lead
passable must be
Bad because the gastric acid leads to immediate
confirmed.
absorption.
Esophagus = Remove Immediately
Stomach = Remove Immediately
Sharp Object NOS
Post Pylorus = Follow vs Surgery — if it does perforate the small bowel it
will be at the IC valve.
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Vascular Impressions
This is a very high yield topic for the purpose of multiple choice exams. Like my Grandma
always said, you never get a second chance to make a first vascular impression.
Right Arch with Aberrant
Innominate ArteryLeft, or Left Arch with
Pulmonary Sling Double Aortic Arch Compression Aberrant Right
Pulmonary Sling:
• The only variant that goes between the esophagus and the trachea.
• Classic question is that this is associated with tracheal stenosis (which is actually primary
and not secondary to compression).
• High association with other cardiopulmonary and systemic anomalies: hypoplastic right lung,
horseshoe lung, TE-fistula, imperforate anus, and complete tracheal rings.
• Treatment is controversial but typically involves surgical repositioning of the artery
Double Aortic Arch:
• Most Common SYMPTOMATIC vascular ring anomaly
Left Arch with Aberrant Right Subclavian
Artery
• Most Common Aortic Arch Anomaly — not
necessarily symptomatic.
• “Dysphagia Lusoria” - fancy Latin speak (therefore
high yield) for trouble swallowing in the setting of
this variant anatomy
• “Diverticulum of Kommerell” pouch like
aneurysmal dilatation of the proximal portion of an
aberrant right subclavian artery
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-Bowel Obstruction (in the neonate)-
Bowel obstruction in the neonate can be thought of as either High Low
high or low. Here arc causes you should keep in your mind
when you think the question stem is leading towards Midgut Volvulus / Hirschsprung
obstruction. Ma (rotation Disease
Why might you think the question is leading you toward Meconium Plug
Duodenal Atresia
obstruction? Anytime you arc dealing with a neonate, and Syndrome
the history mentions “vomiting,” “belly pain,” or “hasn’t Duodenal Web Ileal Atresia
passed a stool yet.”
Annular Pancreas Meconium Ileus
The following sections will walk through an algorithm,
starting with plain films for diagnosis (and sometimes Anal Atresia /
Jejunal Atresia
management). Colonic Atresia
Sub Section 1: “Bubbles”
People who do peds radiology are obsessed with “bubbles” on baby grams. The idea is to develop a
pattern-based approach to bowel obstruction in the newborn.
My preferred “bubble method” favors 8 possible patterns. This is a method originally developed by
the brilliant (and devilishly handsome) Charles Maxfield at Duke.
Single Bubble Double Bubble Diffusely Dilated Diffusely Mildly
-plus distal gas -plus distal gas Dilated
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Sub Section 1: “Bubbles” - Continued
Single Bubble
= Gastric (antral or pyloric) atresia. Duodenal Atresia Trivia:
Double Bubble = Duodenal Atresia • 30% have Downs
• 40% have polyhydramnios and
(highly specific). Some authors will say
arc premature
that UGI is not necessary because of how
• The “single atresia” - cannulation
highly specific this is. The degree of
error
distention will be more pronounced than
• On multiple choice test the
with midgut volvulus (which is a more
“double bubble” can be shown on
acute process). Thought to be secondary
3rd trimester OB ultrasound, plain
to failure to canalize during development
film, or on MRI.
(often an isolated atresia)
Triple Bubble = Jejunal Atresia. When you call jejunal atresia,
you often prompt search for additional atresias (colonic). Just remember
that jejunal atresia is secondary to a vascular insult during development.
• "Multiple Atresia ” - vascular error.
Single Bubble with Distal Gas = Can
mean nothing (lotta air swallowing). If the clinical
history is bilious vomiting , this is ominous and can
be midgut volvulus (surgical emergency). Next test
would be emergent Upper GI.
Double Bubble with Distal Gas = Seeing
distal gas excludes duodenal atresia. The DDx is a
duodenal web, duodenal stenosis, or midgut
volvulus. Next step would be upper GI.
Multiple Diffusely Dilated Loops =
Suggestive of a low obstruction (ileum or colon).
Next step is contrast enema. If the contrast enema is
normal you need to follow with upper GI (to
exclude an atypical look for midgut volvulus).
Mildly Dilated, Scattered Loops =
“Sick Belly” - Can be seen with proximal or
distal obstruction. Will need Upper GI and contrast
enema.
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Sub Section 2: Upper GI Patterns
Upper GI on kids is fair game in multiple choice tests, and real life. Often the answer of this
test can equal a trip to the OR for kids, so it’s no trivial endeavor.
Malrotation - Normally, the developmental rotation of the gut places the ligament of
Trietz to the left of the spine (at the level of the duodenal bulb). If mother nature fucks up and
this doesn’t happen, you end up with the duodenum to the right of the midline (spine). These
patients are at increased risk for midgut volvulus and internal hernias. If you sec the
appearance of malrotation and the clinical history is bilious vomiting, then you must suspect
midgut volvulus.
Trivia regarding Malrotation
•Associated with Heterotaxy Syndromes. Associated with Omphaloceles.
•Classically shown as the SMA to the right of the SMV (on US or CT).
•False Positive on UGI - Distal Bowel Obstruction displacing the duodenum (because of
ligamentous laxity).
Gamesmanship: in an infant-
I say “Non-Bilious Vomiting” — You Say Hypertrophic Pyloric Stenosis
Next Step ? Ultrasound
I say “Bilious Vomiting” — You Say Mid Gut Volvulus (tzZ/proven otherwise)
Next Step ? Upper GI
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Corkscrew Duodenum - This is diagnostic of
midgut volvulus (surgical emergency). The appearance
is an Aunt Minnie.
Ladd’s Bands - In older children (or even adults)
obstruction in the setting of malrotation will present as
intermittent episodes of spontaneous duodenal
obstruction. The cause is not midgut volvulus (a
surgical emergency) but rather kinking from Ladd’s
Bands.
So what the hell is a “Ladd’s Band” ? We are talking
about a fibrous stalk of peritoneal tissues that fixes the
cecum to the abdominal wall, and can obstruct the
duodenum.
Complete Duodenal Obstruction - Strongly associated with midgut volvulus. If
you were thinking duodenal atresia, look for distal air (any will do) to exclude that thought.
Ladd’s Procedure -
Procedure to prevent midgut
volvulus. Traditionally, the
Ladd’s Bands are divided, and
the appendix is taken out. The
small bowel ends up on the
right, and the large bowel ends
up on the left. They are fixed
in place by adhesions (just by
opening the abdomen).
It is still possible to develop
volvulus post Ladd’s (but it’s Ladds Procedure:
• Divide the Adhesive Ladds Bands
rare - 2-5%). • Widen the Mesentery to a safe distance
• Take out the appendix (bill extra for that)
Plus, as discussed above, you want to see a dilated duodenum (double bubble) for duodenal
atresia.
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Partial Duodenal Obstruction - If the
kid is vomiting this might be from extrinsic
narrowing (Ladd band, annular pancreas), or
intrinsic (duodenal web, duodenal stenosis).
You can’t tell.
Hypertrophic Pyloric Stenosis -
Thickening of the gastric pyloric musculature,
which results in progressive obstruction. Step
1 buzzword is “non-bilious vomiting.” Here is
the most likely multiple choice trick; this does
NOT occur at birth or after 3 months.
There is a specific age range of 2-12 weeks (peak at 3-6 weeks).
Criteria is 4 mm and 14 mm (4 mm single wall, 14 mm length).
The primary differential is pylorospasm (which will relax during exam). The most common
pitfall during the exam is gastric over distention, which can lead to displacement of the
antrum and pylorus - leading to false negative.
False positive can result from off axis measurement.
The phenomenon of “paradoxical aciduria” has been described, and is a common buzzword.
Gastric Volvulus- This comes in
two flavors; organoaxial and
mesenteroaxial.
•Organoaxial - The greater
curvature flips over the lesser
curvature (rotation along the long
axis). This is seen in old ladies
with paraesophageal hernias.
•Mesenteroaxial - Twisting over
the mesentery (rotation along short
axis). The antrum flips near the
GE junction. Can cause ischemia
and needs to be fixed.
Additionally this type causes
obstruction. This type is more
common in kids.
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Duodenal Web: This is best thought
of as "almost duodenal atresia.” The
reason I say that is, just like duodenal
atresia, this occurs from a failure to
canalize, but instead of a total failure of
canalization (like duodenal atresia) this
bowel is only partially canalized, leaving
behind a potentially obstructive web.
Trivia to know:
- Because the web is distal to ampulla of
Vater - you get bile-stained emesis
- Associated with malrotation and
Downs syndrome
- The “wind sock” deformity is seen
more in older kids - where the web-like
diaphragm has gotten stretched.
Annular Pancreas: Essentially an embryologic screw up (failure of ventral bud to rotate
with the duodenum), that results in encasement of the duodenum.
In Kids = Think Duodenal Obstruction
In Adults = Think Pancreatitis
How it could be shown:
• On CT: Look for pancreatic tissue
(same enhancement as the nearby
normal pancreas) encircling the
descending duodenum.
• On Fluoro: Look for an extrinsic
narrowing of the duodenum. Obviously
this is non-specific (typical barium -
voodoo), use the location and clinical
history to bias yourself.
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Sub Section 3: “Low Obstruction” in a Neonate
Just like the upper GI and “bubble” plain film in sections 1 & 2, the lower obstruction can
be approached with a pattern-based method. You basically have 4 choices: Normal,
Short Microcolon, Long Microcolon, and a Caliber Change from micro to normal.
Normal:
• This is what normal looks like:
Short Microcolon -
• Think about Colonic Atresia
Long Microcolon - This can be seen with meconium ileus or distal ileal atresia.
•Meconium Ileus - ONLY in patients with CF.
The pathology is the result of thick sticky meconium
causing obstruction of the distal ileum. Contrast will
reach ileal loops, and demonstrate multiple filling
defects (meconium). This can be addressed with an
enema.
•Distal Ileal Atresia - This is the result of
intrauterine vascular insult. Contrast will NOT reach
ileal loops. This needs surgery.
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Caliber Change - This can be seen with small left colon syndrome or Hirschsprung's
•Small Left Colon (Meconium Plug)
Syndrome - This is a transient functional colonic
obstruction, that is self limited and relieved by
contrast enema.
*Most Testable Fact:
It is NOT associated with CF.
*2nd Most Testable Fact:
It is seen in infants of diabetic mothers or
if mom received magnesium sulfate for eclampsia.
•Hirschsprung Disease - Failure of the
ganglion cells to migrate and innervate the distal
colon. Affected portions of the colon are small
in caliber, whereas the normally innervated
colon appears dilated.
Trivia:
•It’s 4:1 more common in boys.
•10% association with Downs.
•Diagnosis is made by rectal biopsy.
How it can be Shown:
-Enema - Rectum smaller than the Sigmoid
“Recto-sigmoid ratio < 1”
-Enema - Rectum with “sawtooth pattern”
Represents bowel spasm
Presentation:
(1) Newborn who fails to have BM > 48
hours (or classically > 72 hours)
(2) “Forceful passage of meconium after
rectal exam”
(3) One month old who shows up “sick as
stink” with NEC bowel
•Total Colonic Aganglionosis - This is a super rare variant of Hirschsprung's, and
can mimic microcolon. The piece of commonly asked trivia is that it can also involve the
terminal ileum.
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Meconium Peritonitis:
This is a potential complication of bowel atresia
or meconium ileus. It has a very characteristic
look. It’s a calcified mass in the mid
abdomen , traditionally shown on plain film. It
is the result of a sterile peritoneal reaction to an
in-utero bowel perforation.
Usually, the perforation seals off prior to birth
and there is no leak.
Imperforate or Ectopic Anus:
This can range from simple membranous anal atresia to an arrest of the colon as it descends
through the puborectalis sling. The thing to know is fistula to genitourinary tract. Imperforate
anus is also associated with a tethered cord (probably need a screening ultrasound).
• I say “Baby with no asshole ”, you say “VACTERL ”
• I say “Baby with no asshole”, you say “Screening US for tethered cord”
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-Obstruction in an Older Child-
“My belly hurts ” questions in an older child.
This scenario should make you think of 6 main things - Classic DDx “AIM” -
- the classic AA-II-MM or “AIM” differential - with Appendicitis, Adhesions
appropriate credit given to the brilliant and under Inguinal Hernia, Intussusception
appreciated Aldrich Killian (A.I.M.s founder).
Midgut Volvulus, Meckel's
Appendicitis - In children older than 4 this is the most common cause for bowel obstruction. If they
show this in the PEDs section it’s most likely to be on ultrasound. In that case you can expect a blind-
ending tube, non-compressible, and bigger than 6 mm.
Inguinal Hernia: This is covered in more depth in the GI chapter. Big points are that indirect hernias
are more common in kids, they are lateral to the inferior epigastric, and incarceration is the most common
complication. Umbilical hernias are common in kids, but rarely incarcerate.
Trivia to know: This is the most common cause of obstruction in boy 1 month - 1 year.
Intussusception - The age range is 3 months - 3 years, before or after that you should think of lead
points (90% between 3 months and 3 years don’t have lead points). The normal mechanism is forward
peristalsis resulting in invagination of proximal bowel (the intussusceptum) into lumen of the distal bowel
(the intussuscipiens). They have to be bigger than 2.5 cm to matter (in most cases- these are enterocolic),
those that are less than 2.0 cm are usually small bowel-small bowel and may reduce spontaneously within
minutes. Just like an appendix, in the peds section, I would anticipate this shown on ultrasound as either
the target sign or pseudo-kidney.
There are 3 main ways to ask questions about this: (1) what is it ?-
these should be straight forward as targets or pseudo kidneys, (2) lead
points - stuff like HSP (vasculitis), Meckle diverticulum, enteric
duplication cysts, and (3) reduction trivia.
Reducing Intussusception Trivia:
• Contraindications: Free Air (check plain film). Peritonitis (based on
exam)
• Recurrence: Usually within 72 hours
• Success Rates - 80-90% with air (Henoch-Schonlein purpura has a
reduced success rate) Not Every Target is an Ileocolic.
• Risk of Perforation - 0.5% You want this this to be > 2.5 cm
• Air causes less peritonitis (spillage of fecal material) than barium
• Pressure should NOT exceed 120 mmHg
• Needle decompression would be the next step if they perforate and get tension pneumoperitoneum
Meckels Diverticulum: This is a congenital diverticulum of the distal ileum. A piece of total trivia is
that it is a persistent piece of the omphalomesenteric duct. Step 1 style, “rule of 2s” occurs in 2% of the
population, has 2 types of heterotopic mucosa (gastric and pancreatic), located 2 feet from the IC valve, it’s
usually 2 inches long (and 2 cm in diameter), and usually has symptoms before the child is 2. If it has
gastric mucosa (the ones that bleed typically do) it will take up Tc-Pertechnetate just like the stomach
(hence the Meckel’s scan).
High Yield Trivia (Regarding Complications)
• Can get diverticulitis in the Meckel's (mimic appendicitis)
• GI Bleed from Gastric Mucosa (causes 30% of symptomatic cases)
• Can be a lead point for intussusception (seen with inverted diverticulum)
• Can Cause Obstruction
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-Luminal 61 - Special Topics-
Gastroschisis - Extra-abominal evisceration of neonatal bowel (sometimes stomach and liver)
through a paraumbilical wall defect.
Trivia to know:
•It does NOT have a surrounding membrane (omphalocele does)
•It’s always on the RIGHT side.
•Associated anomalies are rare (unlike omphalocele).
•Maternal Serum AFP will be elevated (higher than that of omphalocele)
•Outcome is usually good
•For some reason they get bad reflux after repair.
•Associated with intestinal atresias.
Omphalocele - Congenital midline defect, with herniation of gut at the base of the umbilical cord.
Trivia to know:
•It DOES have a surrounding membrane (gastroschisis does
not) Pentalogy of Cantrell
•Associated anomalies are common (unlike gastroschisis)
1. Omphalocoele
•Trisomy 18 is the most common associated chromosomal
2. Ectopia Cordis
anomaly (abnormal location of heart)
•Other associations: Cardiac (50%), Other GI, CNS, GU,
Turners, Klinefelter's, Beckwith-Wiedemann, Pentalogy of 3. Diaphragmatic Defect
Cantrell 4. Pericardial Defect
or Sternal Cleft
•Outcomes are not that good, because of associated
syndromes. 5. Cardiovascular malformations
•Umbilical Cord Cysts (Allantoic Cysts) are associated.
This vs That— Gastroschisis vs Omphalocele
Gastroschisis Omphalocele
Herniated bowel loop through the Herniated bowel loop through the
ventral body wall ventral body wall
NOT surrounded by a membrane Surrounded by a membrane (peritoneum)
Umbilicus is Normal - positioned to the left of the Umbilicus contains herniated bowel, and therefore is
defect (defect is on the right) NOT normal
Defect is on the right Defect is midline
High Association with Cardiac (50%) defects and
Associated anomalies are rare Chromosomal Abnormalities
Multiple Syndromic Associations including Turners,
Associated with intestinal atresias Klinefelter's, Beckwith-Wiedemann, and the
Legendary Pentalogy of Cantrell
Cause: Probably environment - which explains an Cause: Probably Genetic - which explains the
association with bowel atresia associations with the various syndromes
Duodenal Hematoma - Classic injury from bicycle handlebars (or child abuse). You can also
see this as a complication from endoscopy. You could be shown retroperitoneal gas as a way to
suggest perforation.
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Enteric Duplication Cysts - These are developmental anomalies (failure to canalize). They
don’t have to communicate with the GI lumen but can. They are most commonly in the ileal region
(40%). They have been known to cause in utero bowel obstruction / perforation.
Strategy: A common way to show this is a cyst in the abdomen (on ultrasound). If you have a random
cyst in the abdomen you need to ask yourself - “does this have gut signature?”
• Cyst with Gut Signature = Enteric Duplication Cyst
• Cyst without Gut Signature = Omental Cyst
• WTF is “Gut Signature ?” - It’s alternating bands of hyper and hypo echoic signal - supposedly
representing different layers of bowel.
Trivia to know: 30% of the time they are associated with vertebral anomalies.
Distal Intestinal Obstruction Syndrome - This is a cause of bowel obstruction in an older
kid (20 year old) with cystic fibrosis. This is sometimes called the “meconium ileus equivalent,”
because you end up with a distal obstruction (as the name implies) secondary to dried up thick stool. It
more commonly involves the ileum / right colon. Kids who get this, are the ones who aren’t compliant
with their pancreatic enzymes.
Mesenteric Adenitis - Self-limiting, usually viral inflammatory condition of mesenteric lymph
nodes. It is a classic clinical mimic of appendicitis. The finding is a cluster of large right lower
quadrant lymph nodes,
Necrotising Enterocolitis (NEC)
This is bad news. The general thinking is that you have an immature bowel mucosa (from being
premature or having a heart problem), and you get translocated bugs through this immature bowel. It’s
best thought of as a combination of ischemic and infective pathology.
Who gets it?
• Premature Kids (90% within the first 10 days of life)
• Low Birth Weight Kids ( < 1500 grams)
• Cardiac Patients (sometimes occult) - they can be full te
• Kids who had perinatal asphyxia
• Hirschsprung Kids that go home and come back - they present around month 1
What does it look like?
• Pneumatosis - most definitive finding; Look for Portal Venous Gas Next
• Focal Dilated Bowel (especially in the right lower quadrant) - the terminal ileum/right colon is the
region most affected by NEC
• Featureless small bowel, with separation (suggesting edema)
• Unchanging bowel gas pattern - this would be a dirty trick - showing several plain films from
progressing days, with the bowel gas pattern remaining the same
Pneumatosis vs Poop - The age old question.
• First question - has the kid been feed? No food = No poop
• Second question - is it staying still? Poop will move, Pneumatosis win stay still.
Useless Trivia:
• Use of maternal breast milk is the only parameter associated with decreased incidence of NEC.
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SECTION 8:
So l i d Or g a n GI
Pirates of the Pancreas-
CF - The pancreas is nearly always (90%) with CF patients.
Inspissated secretions cause proximal duct obstruction leading to the
two main changes in CF: (1) Fibrosis (decreased T1 and T2 signal) and
the more common one (2) fatty replacement (increased Tl).
Patients with CF diagnosed as adults tend to have more pancreas
problems than those diagnosed as children. Those with residual
pancreatic exocrine function can have bouts of recurrent acute
pancreatitis. Small (1-3 mm) pancreatic cysts are common.
High Yield Trivia:
• Complete fatty replacement is the most common imaging finding Complete Fatty Replacement
in adult CF
• Enlarged with fatty replacement = lipomatous pseudohypertrophy of the pancreas.
• Fibrosing Colonopathy: Thick walled right colon as a complication of enzyme replacement therapy.
Shwachman-Diamond Syndrome - The 2nd most common cause of pancreatic
insufficiency in kids (CF #1). Basically, it’s a kid with diarrhea, short stature, and
eczema. Will also cause lipomatous pseudohypertrophy of the pancreas.
Dorsal Pancreatic Agenesis - You only have a ventral bud (the dorsal bud forgets
to form). Since the dorsal buds makes the tail, the appearance is that of a pancreas without a
tail. All you need to know is that (1) this sets you up for diabetes (most of your beta cells are
in the tail), and (2) it’s associated with polysplenia.
Pancreatitis - The most common cause of pancreatitis in peds is trauma (scat belt).
NAT: Another critical point to make is that non-accidental trauma can present as pancreatitis.
If the kid isn’t old enough to ride a bike (handle bar injury) or didn’t have a car wreck (seat
belt injury) you need to think NAT.
Tumors of the Pediatric Pancreas: Even at a large pediatric hospital its uncommon to see more
than 1-2 of these a year. Obviously, they are still fair game for multiple choice. This is what I would
know:
Solid and Papillary Epithelial Neoplasm (SPEN) - The most common pediatric solid
tumor. It’s found in female adolescents (usually asian, or black). The outcomes are pretty good after
surgical resection. If you get shown a case in the peds setting this is probably it. I’ll mention this
thing again in the Adult GI chapter.
Peds Pancreatic Mass
Otherwise, 1 would try and use age as a discriminator Age 1 = Pancreatoblastoma
(if they are nice enough to give it to you). Age 6 = Adenocarcinoma
Age 15 = SPEN
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-Liver Masses-
Tumors: For Peds liver tumors I like to use an age-based system to figure it out. Mass in the
liver, first think what is the age? Then use the narrow DDx to figure it out.
Age 0-3: With kids that are newborns you should think about 3 tumors:
Infantile Hepatic Hemangioma:
Often < 1. Associated with high output CHF, this is
classically shown as a large heart on CXR plus a mass in
the liver. The aorta above the hepatic branches of the
celiac is often enlarged relative to the aorta below the
celiac because of differential flow. Skin hemangiomas
are present in 50%. Endothelial growth factor is
elevated. These can be associated with Kasabach-Merritt
Syndrome (the platelet eater).
How do they do? - Actually well. They tend to spontaneously involute without therapy over
months-years - as they progressively calcify.
Hepatoblastoma:
Most common primary liver tumor of childhood (< 5).
The big thing to know is that it’s associated with a bunch
of syndromes - mainly hemi-hypertrophy, Wilms,
Beckwith-Weidcmann crowd. Prematurity is a risk factor.
This is usually a well circumscribed solitary right sided
mass, that may extend into the portal veins, hepatic veins,
and IVC. Calcifications arc present 50% of the time. AFP
is elevated. Another piece of trivia is the hepatoblastoma
may cause a precocious puberty from making bHCG.
I would know 3 things: (1) Associated with Wilms, (2) AFP, (3) Precocious Puberty
Mesenchymal Hamartoma:
This is the predominately cystic mass (or multiple cysts), sometimes
called a “developmental anomaly.” Because it’s a “developmental
anomaly” it shouldn’t surprise you that the AFP is negative.
Calcifications are UNCOMMON. What is common is a large portal
vein branch feeding the tumor.
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Age > 5:
HCC: This is actually the second most common liver cancer in kids. You’ll see them in kids
with cirrhosis (biliary atresia, Fanconi syndrome, glycogen storage disease). AFP will be
elevated.
Fibrolamellar Subtype: This is typically seen in younger patients (<35) without cirrhosis
and a normal AFP. The buzzword is central scar. The scar is similar to the one seen
in FNH with a few differences. This scar does NOT enhance, and is T2 dark (the FNH scar is
T2 bright). As a point of trivia, this tumor is Gallium avid. This tumor calcifies more often
than conventional HCC.
Undifferentiated Embryonal Sarcoma: This is the pissed off cousin of the
mesenchymal hamartoma. It’s also cystic, but the mass is much more aggressive. It will be a
hypodense mass with septations and fibrous pseudocapsule. This mass has been known to
rupture.
Any Age:
Mets: Think about Wilms tumor or Neuroblastoma
Now, there are several other entities that can occur in the liver of young children / teenagers
including; Hepatic Adenoma, Hemangiomas, Focal Nodular Hyperplasia, and Angio
Sarcoma. The bulk of these are discussed in greater detail in the adult GI chapter.
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-Congenital Biliary / Liver
Choledochal cysts are congenital dilations of the bile ducts -classified into 5 types by
some dude named Todani. The high yield trivia is type I is focal dilation of the CBD and is by
far the most common. Type 2 and 3 are super rare. Type 2 is basically a diverticulum of the
bile duct. Type 3 is a “choledochocele.” Type 4 is both intra and extra hepatic. Type 5 is
Caroli’s, and is intrahepatic only. I’ll hit this again in the GI chapter.
Caroli’s is an AR disease associated with polycystic kidney disease and medullary sponge
kidney. The hallmark is intrahepatic duct dilation, that is large and secular. Buzzword is
“central dot sign” which corresponds to the portal vein surrounded by dilated bile ducts.
AR Polycystic Kidney Disease: This will be discussed in greater detail in the renal
section, but kids with AR polycystic kidney disease will have cysts in the kidneys, and
variable degrees of fibrosis in the liver. The degree of fibrosis is actually the opposite of
cystic formation in the kidneys (bad kidneys ok liver, ok kidneys bad liver).
Hereditary Hemorrhagic Telangiectasia (Osler-Weber-Rendu):
Autosomal dominant disorder characterized by multiple AVMs in the liver and lungs. It leads
to cirrhosis, and a massively dilated hepatic artery. The lung AVMs set you up for brain
abscess.
Biliary Atresia: If you have prolonged newborn jaundice (> 2 weeks) you should think
about two things (1) neonatal hepatitis, and (2) Biliary Atresia. It’s critical to get this
diagnosis right because they need corrective surgery (Kasai Procedure) prior to 3 months.
Patients with biliary atresia really only have atresia of the ducts outside the liver (absence of
extrahepatic ducts), in fact they have proliferation of the intrahepatic ducts. They will
develop cirrhosis without treatment and not do well.
Trivia to Know about Biliary Atresia:
• Associations with Polysplenia, and Trisomy 18
• Gallbladder may be absent (normal gallbladder - supports neonatal hepatitis)
• Triangle Cord Sign - triangular echogenic structure by the portal vein - possibly remnant of
the CBD.
• Hepatobiliary Scintigraphy with 99m Tc-IDA is the test of choice to distinguish (discussed
in the Nukes Chapter).
• Alagille Syndrome: This is a total zebra. All you need to know is hereditary cholestasis,
from paucity of intrahepatic bile ducts, and peripheral pulmonary stenosis. The purpose of a
liver biopsy in biliary atresia is to exclude this diagnosis.
Gallstones: If you see a peds patient with gallstones think sickle cell.
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- Spleen -
Sickle Cell - These kids bodies have spleen better days - as the spleen will typically
enlarge progressively and then eventually auto-infarct and shrink (during the first decade). If
the spleen remains enlarged it can run into problems - mainly acute splenic sequestration
crisis.
I want you to think about sickle cell spleen as either too big or too small (for the purpose of
multiple choice). First I’ll ex-spleen the too big problems:
Splenic Sequestration - This is the second most common cause of death in SC patients
younger than 10. We are talking about the situation in which the spleen becomes a greedy
little pig and tries to hog all the blood for itself.
Gamesmanship: History of abdominal pain or vital signs suggesting low volume (high HR,
low BP) with a big spleen. Remember most kids with sickle cell will have smaller spleens
(auto infarct) so a big spleen should be your clue.
Other problems you can run into if your spleen stays big are abscess formation and large
infarcts. These large infarcts are not the same pathophysiology as the “auto-infarct” you
typically think of with sickle cell. These are the big wedge shaped infarcts (hypo-perfusion on
CT). As a point of trivia, infarcted splenic tissue should look hypoechoic on US, with linear
"bright bands ” — google that if you haven’t seen it before.
Now the too small problem:
Auto Infarcted Spleen - This is different than the massive infarct in that it is typically the
combined effort of numerous tiny, unnoticeable, and repetitive micro occlusions leading to
progressive atrophy. Supposedly this doesn’t hurt (large infarcts do). This tends to occur
early and is usually “complete" by age 8. The typically look is going to be a tiny (possibly
calcified) spleen. When I say tiny - we are talking like 1 cm. In the imaginary world of
multiple choice you might not even see the fucking thing.
“Where is the fucking spleen?” = Auto Infarct = Sickle Cell
Gamesmanship: If you don't see the spleen but you do see a gallbladder full of stones in a kid
less than 15 - you should think Sickle Cell.
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Polysplenia and Asplenia - Heterotaxia syndromes are clutch for multiple choice
tests. The major game played on written tests is “left side vs right side. ”
So what the hell does that mean? Let me break this down like a cardboard box that you intend
to put in your recycling ... because this gets pretty fucking complicated. I like to start in the
lungs. The right side has two fissures (major and minor). The left side has just one fissure.
So if I show you a CXR with two fissures on each side, (a left sided minor fissure), then the
patient has two right sides. Thus the term “bilateral right sidedness.”
What else is a right sided Heterotaxia Syndromes
structure? The liver. So,
these patients won’t have a Right Sided Left Sided
spleen (the spleen is a left One Fissure in Right Lung
Two Fissures in Left Lung
sided structure).
Asplenia Polysplenia
The opposite is true. Since the Increased Cardiac
spleen is on the left, a Less Cardiac Malformations
Malformations
“bilateral left sided” patient Azygos Continuation
will have polysplenia. Reversed Aorta/IVC
of the IVC
Aorta/IVC: This relationship is a little more confusing when you try to reason it out. The
way I keep it straight is by remembering that the IVC is usually on the right. If you are
“bilateral left” then you don’t have a regular IVC — hence the azygos continuation. Then I
just remember that the other one (flipped IVC/Aorta) is the other one.
Normal Reversed (Aorta/ ICV) Azygos Continuation
IVC (on the right) -Asplenia -Polysplenia
Aorta (on the left)
Right Isomerism Left Isomerism
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Heterotaxia Syndromes / Situs - Cont...
So on the prior page I used terms like “bilateral right sided” and “bilateral left sided” to help
make the concept more digestible. I didn’t make those words up. You will read that some
places but I think to be ready for the full gauntlet of heterotaxia related fuckery you should
also be ready for words that start with "situs” and end with "isomerism. ”
Situs Vocab: There are 3 vocab words that start with the word “Situs.”
• Situs Solitus - Instead of just saying normal, you can be an asshole and say "Situs Solitus. ”
• Situs Inversus Totalis - Total mirror image transposition of the abdominal and thoracic
stuff.
• Situs Ambiguus (Ambiguous) - This is a tricky way of saying Heterotaxy, of which you can
have left or right “isomerism.”
“Isomerism” - I guess some asshole really liked organic chemistry.... This is a fancy
way of saying bilateral right or bilateral left - as explained on the prior page.
Situs
Situs Solitus
Inversus
(Normal)
• Gastric
• Gastric Bubble
Bubble on
on Left
Right
• Larger part of
• Larger part of
Liver on Right
Liver on Left
• Minor fissure on
• Minor fissure
Right
on Left
• Inverted
Bronchial
Pattern
Situs Solitus • Associated
“How Pretentious Assholes with Primary
Ciliary
Say Normal”
Dyskinesia
V.H. with T
Left
Isomerism
• Absent Minor
Fissures
• Interrupted
IVC
• Polysplenia
• Biliary
Atresia
(10%)
Visceral Heterotaxy with Visceral Heterotaxy with
Thoracic Right Isomerism Thoracic Left Isomerism
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- Top 4 Things for Peds Gl -
Biliary Atresia:
• Congenital liver fibrosis → cholangiopathy
→ neonatal jaundice (after 1 week of life)
• US: Bright band of tissue (triangular cord
sign) near branching of common bile duct;
small or absent gallbladder (fasting ~ 3
hours)
• Scintigraphic: No tracer excretion into bowel
by 24 hours
• Biopsy to exclude = Zebra Alagille syndrome
• Treated with Kasai procedure
Malrotation:
• Duodenum to the right of the midline
• Increased risk for mid gut volvulus, and
internal hernia
• “Bilious vomiting”
• SMA to the right of the SMV
SMV - 2 o’clock position relative to SMA
Heterotaxia Syndromes
Right Sided Left Sided
Two Fissures in Left One Fissure in Right
Lung Lung
Asplenia Polysplenia
Increased Cardiac Less Cardiac
Malformations Malformations
Azygos Continuation
Reversed Aorta/IVC
of the I VC
V - Vertebral Anomalies (37%)
A - Anal (imperforate anus) (63%)
C - Cardiac (77%)
VACTERL TE - Tracheoesophageal Fistula
or Esophageal Atresia ( 40%)
R - Renal (72%)
L - Limb (radial ray) - 58%
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SECTION 9:
CONGENITAL GU
Renal Agenesis - This comes in one of two flavors; (1) Both Kidneys Absent - this one is gonna
be Potter sequence related, (2) One Kidney Absent - this one is gonna have reproductive associations.
Most likely way to test this: Show unilateral agenesis on prenatal US - as an absent renal artery (in
view of the aorta) or oligohydramnios - with followup questions on associations. Or make it super
obvious with a CT / MRI and ask association questions.
Unilateral Absence Association
• 70% of women with unilateral renal agenesis have associated genital anomalies (usually
unicornuate uterus, or a rudimentary horn).
• 20% of men are missing the epididymis, and vas deferens on the same side they are missing the
kidney. PLUS they have a seminal vesicle cyst on that side.
Potter Sequence: Insult (maybe ACE inhibitors) = kidneys don’t form, if kidneys don’t form you can’t
make piss, if you can’t make piss you can’t develop lungs (pulmonary hypoplasia).
Lying Down Adrenal or “Pancake Adrenal" Sign - describes the elongated appearance of the adrenal
not normally molded by the adjacent kidney. It can be used to differentiate surgical absent vs
congenitally absent.
Horseshoe Kidney - This is the most common fusion anomaly. The kidney gets hung up on the
IMA. Questions are most likely to revolve around the complications / risks:
• Complications from Position - Easy to get smashed against vertebral body - kid shouldn’t play
football or wrestle.
• Complications from Drainage Problems: Stones, Infection, and Increased risk of Cancer (from
chronic inflammation) - big ones are Wilms, TCC, and the Zebra Renal Carcinoid.
• Association Syndrome Trivia - Turner’s Syndrome is the classic testable association.
Crossed Fused Renal Ectopia - One
kidney comes across the midline and fuses with the
other. Each kidney has its own orthotopic ureteral
orifice to drain through. It’s critically important to the
patient to know that “the Ectopic Kidney is
Inferior.” The left kidney more commonly crosses
over to the right fusing to the normal right kidney
lower pole. Complications include stones, infection,
and hyponephrosis (50%).
The classic way to show this is two axial CTs. The
first at the level of the kidneys hinting that one
kidney may be absent. The second through the
bladder (on a delayed phase) showing two opacified
ureters.
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Congenital UPJ Obstruction
This is the most common congenital anomaly of the GU tract in neonates. About 20% of the time,
these are bilateral. Most (80%) of these arc thought to be caused by intrinsic defects in the circular
muscle bundle of the renal pelvis. Treatment is a pyeloplasty. A Radiologist can actually add value by
looking for vessels crossing the UPJ prior to pyeloplasty, as this changes the management.
Q: 1970 called and they want to know how to tell the difference between a prominent extrarenal pelvis
vs a congenital UPJ obstruction.
A:“Whitaker Test”, which is a urodynamics study combined with an antegrade pyelogram.
Classic History: Teenager with flank pain after drinking “lots of fluids.”
Classic Trivia: These do NOT have dilated ureters (NO HYDROURETER).
Autosomal Recessive Polycystic Kidney
Disease (ARPKD) - These guys get HTN and renal
failure. The liver involvement is different than the adult
form (ADPKD). Instead of cysts they have abnormal
bile ducts and fibrosis. This congenital hepatic fibrosis is
ALWAYS present in ARPKD. The ratio of liver and
kidney disease is inverse. The worse the liver is the
better the kidneys do. The better the liver is the worse
the kidneys arc. Death is often from portal hypertension.
On ultrasound the kidneys are smoothly enlarged and
ARPKD: Big Bright, with Lost
diffusely echogenic, with a loss of corticomedullary Corticomedullary Differentiation.
differentiation. In utero you sometimes will not sec
urine in the bladder. Cysts tend to be tubular and spare
the cortex.
Neonatal Renal Vein Thrombosis - This is an associated condition of maternal diabetes,
sepsis, and dehydration. It is typically unilateral (usually left). The theory is that it starts peripherally
and progresses toward the hilum. When acute, will cause renal enlargement. When chronic, will
result in renal atrophy.
Neonatal Renal Artery Thrombosis - This occurs secondary to umbilical artery
catheters. Unlike renal vein thrombosis it does NOT present with renal enlargement but instead severe
hypertension.
Prune Belly (Eagle Barrett Syndrome)
This is a malformation triad which occurs in males. Classically
shown on a babygram with a kid shaped like a pear (big wide
belly).
Triad:
• Deficiency of abdominal musculature
• Hydroureteronephrosis
• Cryptorchidism
(bladder distention interferes with descent of testes)
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-Congenital Ureter and Urethra-
Congenital (primary) MEGAureter - This is a “wastebasket” term for an enlarged
ureter which is intrinsic to the ureter (NOT the result of a distal obstruction). Causes include
(1) distal adynamic segment (analogous to achalasia, or colonic Hirschsprungs), (2) reflux at
the UVJ, (3) it just wants to be big (totally idiopathic). The distal adynamic type “obstructing
primary megaureter,” can have some hydro, but generally speaking an absence of dilation of
the collecting system helps distinguish this from an actual obstruction.
Retrocaval Ureter (circumcaval)- This is actually a
problem with the development of the IVC, which grows in a
manner that pins the ureter. Most of the time it’s asymptomatic,
but can cause partial obstruction and recurrent UTI. IVP will
show a “reverse J” or “fishhook” appearance of the ureter.
Retrocaval Ureter
Duplicated System - The main thing to know
Upper Pole
about duplicated systems is the so-called “Weigert-
(obstructed I
Meyer Rule” where the upper pole inserts inferior and dilated) inserts
medially. The upper pole is prone to ureterocele Inferior and
Medial
formation and obstruction. The lower pole is prone to
reflux. Kidneys with duplicated systems tend to be
larger than normal kidneys. In girls, a duplicated
Lower Pole
system can lead to incontinence (ureter may insert inserts Superior
below the sphincter - sometimes into the vagina). and Lateral
• Upper Pole Obstructs
• Lower Pole Refluxes
Ureterocele - A cystic dilation of the intravesicular
ureter, secondary to obstruction at the ureteral orifice. IVP
(or US) will show the “cobra head" sign, with contrast
surrounded by a lucent rim, protruding from the contrast
filled bladder. This is associated with a duplicated system
(specifically the upper pole).
Cobra Head
Ectopic Ureter - The ureter inserts distal to the external sphincter in the vestibule. More
common in females and associated with incontinence (not associated with incontinence in
men). Ureteroceles are best demonstrated during the early filling phase of the VCUG.
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Posterior Urethral Valves:
This is a fold in the posterior urethra that leads to
outflow obstruction and eventual renal failure (if it’s
not fixed). It is the most common cause of urethral
obstruction in male infants.
Trivia: The fold is a Wolffian Duct tissue remnant
Now, this can be shown a variety of ways;
Classic VCUG: The key finding on VCUG is an
abrupt caliber change between the dilated posterior
urethra and normal caliber anterior urethra. PUV on VCUG
Fetal MRI: The MRI would have to show hydro in
the kidney and a “key-hole” bladder appearance.
Pre-Natal Ultrasound Classic Triad:
• Hydronephrosis
• Bladder Dilation
• Oligohydramnios
“Peri-renal fluid collection” is a buzzword, and it’s
the result of forniceal rupture. Obviously that is
non-specific and can be seen with any obstructive pathology.
Strategy for 'Next Step' types of Questions : VCUG to evaluate
anatomy. This is the gold
standard.
Adjunctive MAG 3 to
evaluate function and
drainage (obstructive vs
not obstructive)
MR Urography offers
function and structure - but
requires sedation in little
kids
Non-Obstructive Causes of Obstructive Causes of
Hydro in Baby Boys Hydro in Baby Boys
-Vesicoureteral Reflux (VUR) -PUV
-Primary Megaureter -UPJ Obstruction
-Prune Belly = Zebra -Ureteral Ectopia
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This is sometimes described as a
“short submucosal distal ureteral segment"
Vesicoureteral Reflux (VUR) -
Normally, the ureter enters the bladder at an
oblique angle so that a “valve” is developed.
If the angle of insertion is abnormal
(horizontal) reflux can develop. This can
occur in the asymptomatic child, but is seen
in 50% of children with UTIs. The
recommendations for when the boy/girl with
a UTI should get a VCUG to evaluate for
VUR is in flux (not likely to be tested). Most
of the time VUR resolves by age 5-6. Normal Reflux
-Intravesicular -Intravesicular
ureter is oblique ureter is horizontal
Trivia: Hydronephrosis is the most common
cause of a palpable renal “mass" in childhood.
There is a grading system for VUR which goes 1-5.
• One is reflux halfway up the ureter,
• Two is reflux into a non-dilated collecting system, (calyces still pointy),
• Three you have dilation of the collecting system, and calyces get blunted
• Four the system gets mildly tortuous,
• Five the system is very tortuous.
A sneaky trick would be to show the echogenic mound near the UVJ, that results from
injection of “deflux”, which is a treatment urologist try. Essentially, they make a bubble with
this proprietary compound in the soft tissues near the UVJ and it creates a valve (sorta).
Anyway, they show it in a lot of case books and textbooks so just like a midget using a urinal -
remember to stay on your toes.
Additional Pearl: Chronic reflux can lead to scarring. This scarring can result in
hypertension and/or chronic renal failure.
Additional Pearl: If the reflux appears to be associated with a “hutch” diverticulum - people
will use the vocabulary “Secondary” VUR rather than Primary VUR. The treatment in this
case will be surgical. Ureteroceles, Posterior Valves, Neurogenic Bladder - are all causes of
Secondary VUR.
“Hutch” Diverticula
• Occur at or adjacent (usually just above) the UVJ.
• Caused by congenital muscular defect
• Difficult to see on US — better seen with VCUG.
• They are “dynamic” and best seen on the voiding (micturition) phase
• If associated with VUR will often be surgically resected
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- Congenital Bladder -
The Urachus: The umbilical attachment to the bladder (started out being called the allantois, then
called the Urachus). This usually atrophies into the umbilical ligament. Persistent canalization can
occur along a spectrum (patent, sinus, diverticulum, cyst).
• Trivia: Most common complication of
urachal remnant = infection
• Trivia: Urachal anomalies are twice as common in boys
(relative to girls)
• Trivia: The most important piece of trivia is that when
these guys get cancer, it’s adenocarcinoma (90% of
cases). To hint at this multiple choice test writers will
often use the phrase “midline bladder structure”
Urachal Cancer
Urachal Spectrum:
Normal Obliterated Patent Urachus Vesicourachal Urachal Cyst Umbilical
Urachus (only the Diverticulum Urachal Sinus
ligament remains)
Bladder Exstrophy - This is a herniation of the urinary
bladder through a hole in the anterior infra-umbilical
abdominal wall.
What do you need to know?
• Increased incidence of Malignancy in the extruded bladder
• It’s Adenocarcinoma - just like a Urachal Remnant would
get
• Aunt Minnie “Manta Ray Sign” - with unfused pubic
bones. This looks like a monster wide pubic symphysis on
an AP pelvic radiograph.
Cloacal Malformation - GU and GI both drain into a common opening (like a bird).
This only happens in females.
Neurogenic Bladder - I will discuss this more in the adult Urinary chapter, but for kids I want you
to think about spinal dysraphism (tethered cord, sacral agenesis, and all the other fucked up spine stuff).
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SECTION 10:
So l i d Or g a n GU
When it comes to solid renal masses - an age-based strategy is the ticket.
Why an age-based strategy? If they give you the age of the patient, you can use this chart to
eliminate distractors which don’t fit. If you are lucky, you won’t even have to look at the
picture.
Neonate Around Age 4 Teenager
Nephroblastomatosis Wilms RCC
Mesoblastic Nephroma Wilms Variants Lymphoma
Lymphoma
Multilocular Cystic Nephroma
Tumor / Mass Rapid Review Trivia
Mesoblastic
“Solid Tumor of Infancy” (you can be bom with it)
Nephroma
“Nephrogenic Rests” - left over embryologic crap that didn’t go away
Might turn into wilms (bilateral wilms especially)
Nephroblastomatosis
“Next Step” - f/u ultrasound till 7-8 years old
Variable appearance
90% + Renal Tumors
“Solid Tumor of Childhood" - Never born with it
Wilms
Grows like a solid ball (will invade rather than incase)
Met to the lung (most common)
Clear Cell - Wilms Met to Bone
Brain Tumors
Rhabdoid - Wilms It fucks you up, it takes the money (it believes in nothing Lebowski)
Micheal Jackson Tumor (Young Boys, Middle Age Women)
Multi-Cystic Big cysts that don’t communicate
Nephroma Septal Enhancement
Can’t Tell it is not Cystic Wilms (next step = resection)
“Solid Tumor of Adolescent ”
RCC Syndromes - VHL, TS
Non-Hodgkin
Renal Lymphoma
Multifocal
**RCC is rare in childhood. If you see it in the pediatric setting think Von Hippel-Lindau (VHL)
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- Solid Age 0-3
Nephroblastomatosis - These are
persistent nephrogenic rests beyond 36
weeks. It’s sorta normal (found in 1% of
infants). But, it can be a precursor to Wilms
so you follow it. When Wilms is bilateral,
99% of the time it had nephroblastomatosis
first. It goes away on its own (normally).
It should NOT have necrosis — this makes
you think Wilms. It has a variable
appearance, and is often described as
“homogeneous.” Although more commonly Nephroblastomatosis
a focal homogeneous ball, the way it’s -Hypodense Rind -
always shown in case conferences and case
books is as a hypodense rind.
Ultrasound screening q 3 months till age 7-8 is the usual routine - to make sure it doesn’t go
Wilms on you.
Mesoblastic Nephroma - ''Solid renal tumor of infancy." This is a fetal hamartoma,
and generally benign. It is the most common neonatal renal tumor (80% diagnosed in the first
month on life). Often involves the renal sinus. Antenatal ultrasound may have shown
polyhydramnios.
Pearl: If it really looks like a Wilms, but they are just too young (< 1 year) then call it
mesoblastic nephroma.
- Cystic Age 0-3
Multicystic Dysplastic Kidney - You have multiple tiny cysts forming in utero.
What you need to know is (1) that there is “no functioning renal tissue,” (2) contralateral renal
tract abnormalities occur like 50% of the time (most commonly UPJ obstruction).
MCDK vs Bad Hydro?
• In hydronephrosis, the cystic spaces are seen to communicate.
• In difficult cases renal scintigraphy can be useful. MCDK will show no excretory function.
Pearl: MCDK has MACROscopic cysts that do NOT communicate
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- Solid Around Age 4
Wilms
“Solid renal tumor of childhood.” This is the most common solid renal tumor of childhood.
This is NOT seen in a newborn. Repeat, you can NOT be bom with this tumor. The average
age is around 3. It typically spreads via direct invasion.
Associated Syndromes:
Overgrowth
• Beckwith-Wiedemann - Macroglossia (most common
finding), Omphalocele, Hemihypertrophy, Cardiac, Big Organs. I Say Beckwith-
• Sotos - Macrocephaly, Retarded (CNS stuff), Ugly Face Wiedemann
You Say,
Non-Overgrowth •Wilms,
•Omphalocele,
• WAGR - Wilms, Aniridia, Genital, Growth Retardation
•Hepatoblastoma
• Drash - Wilms, Pseudohermaphroditism, Progressive
Glomerulonephritis
Wilms Nevers Wilms in a 1 year old ?
Think about associated
• NEVER Biopsy suspected Wilms syndromes. Wilms loves to
(you can seed the tract and up the stage) pal around with:
• Wilms NEVER occurs before 2 months of age • Hemihypertrophy,
(Neuroblastoma can) • Hypospadias,
• Cryptorchidism
Bilateral Wilms
• About 5-10% will have bilateral disease (“Synchronous Bilateral Wilms”)
Wilms Variants (look just like Wilms)
• Clear Cell - likes to go to bones (lytic)
• Rhabdoid - “Terrible Prognosis” - Associated with aggressive Rhabdoid brain tumors
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-Cystic Around Age 4
Multilocular Cystic Nephroma
“Non-communicating, fluid-filled locules,
surrounded by thick fibrous capsule.” By
definition these things are characterized by
the absence of a solid component or necrosis.
Buzzword is
‘‘protrude into the renal pelvis.’’
There is a classic bimodal occurrence
(4 year old boys, and 40 year old women).
I like to think of this as the Michael Jackson
lesion - it loves young boys and middle-aged
women Multilocular Cystic Nephroma
“Protruding into the renal pelvis ”
Turbo Nerds Are Spoiling My Fun
One of my favorite jokes has been this “Michael Jackson lesion” to help remember
the age distribution. Unfortunately - a bunch of Academic Nerds got together and
decided that the pediatric cystic nephromas are their own thing now, and the adult
ones are their own thing - with the words "adult cystic nephromas” and "pediatric
cystic nephroma” as the preferred nomenclature. Assholes.... ruined a great joke.
Gamesmanship: Board exams usually lag a few years behind these kinds of changes. So if you get
a question asking about the age distribution, you may want to still go with the bimodal occurrence -
especially if they don’t say “adult" or “peds” — just make sure there isn’t another more correct
answer. This is where reading all the choices is critically important. Mind reading is also helpful.
Don’t forget to read the mind of the person who wrote the question - so you can understand his or
her bias.
- Solids in Teenager
Renal Lymphoma and RCC can occur in teenagers. Renal lymphoma can occur in 5 year olds
as well. Both of these cancers are discussed in detail in the adult GU chapter.
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- Other GU Masses / Cancers -
Rhabdomyosarcoma - This is the most common bladder cancer in humans less than 10
years of age. They are often infiltrative, and it’s hard to tell where they originate from.
“Paratesticular Mass” is often a buzzword. They can met to the lungs, bones, and nodes.
The Botryoid variant produces a polypoid mass, which looks like a bunch of grapes. I’ll discuss
this again in the testicle section.
Neuroblastoma - Isn’t a Renal Mass, but is frequently contrasted with Wilms so I want to
discuss it in the renal section. It is the most common extra-cranial solid childhood malignancy.
They typically occur in very young kids (you can be born with this). 95% of cases occur
before age 10. They occur in the abdomen more than the thorax (adrenal 35%,
retroperitoneum 30%, posterior mediastinum 20%, neck 5%).
Staging: Things that up the stage include
STAGE 4 S - HIGH YIELD
crossing the midline, and contralateral positive
nodes. These things make it Stage 3. • Less than 1 year old
• Distal Mets are Confined to Skin, Liver, and
Better Prognosis Seen with - Diagnosis in Age < 1, Bone Marrow
Thoracic Primary, Stage 4S. • Excellent Prognosis.
Associations: **A common distractor is to say 4S goes to
• NF-1, Hirschsprung's, DiGeorge, Beckwith cortical bone. This is false! It’s the marrow.
Wiedemann
• Most are sporadic
Random Trivia:
• Opsomyoclonus (dancing eyes, dancing feet) - paraneoplastic syndrome associated with
neuroblastoma.
• “Raccoon Eyes” is a common way for orbital neuroblastoma mets to present
• MIBG is superior to Conventional Bone Scan for Neuroblastoma Bone Mets
• Neuroblastoma bone mets are on the “lucent metaphyseal band DDx”
• Sclerotic Bone mets are UNCOMMON
• Urine Catecholamines are always (95%) elevated
Neuroblastoma Wilms
Age: Usually around age 4
Age: usually less than 2 (can occur in utero)
(never before 2 months)
Calcifies 90% Calcifies Rarely (< 10%)
Encases Vessels (doesn’t invade) Invades Vessels (doesn’t encase)
Poorly Marginated Well Circumscribed
Doesn’t usually met to bones (unless clear cell
Mets to Bones
Wilms variant). Prefers lung.
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SECTION 11:
Ad r en a l
Neuroblastoma - Discussed previously in the renal section
Neonatal Adrenal Hemorrhage-This can occur in the setting of birth
trauma or stress.
Trivia - Neonatal adrenal hemorrhage is associated with scrotal hemorrhage
THIS vs- THAT: Hemorrhage VS Neuroblastoma:
• Ultrasound can usually tell the difference (adrenal hemorrhage is anechoic and
avascular, neuroblastoma is echogenic and hyper-vascular).
• MRI could also be done to problem solve if necessary (Adrenal Hemorrhage low T2 ,
Neuroblastoma high T2).
Gamesmanship - “Next Step” Adrenal mass of a neonate.
Neonates that are sick enough to be in the hospital hemorrhage their fucking adrenals all the
time. An adrenal hemorrhage can look just like a mass on ultrasound. Yes, technically it
should be anechoic and avascular - but maybe your tech sucks, or maybe you don’t get shown
a picture they just tell you it’s a mass. The question writer is most likely going to try and
trick you into worrying about a neuroblastoma (which is also going to be a mass in the
adrenal).
Next Step? Sticking a needle in it, sedating the kid for MRI, or exposing him/her to the
radiation of CT, PET, or MIBG are all going to go against the “image gently” propaganda
being pushed at academic institutions. Plus it’s unnecessary. As is true with most things in
radiology, they either get better or they don’t. Hemorrhage is going to resolve. The cancer is
not. So the first step is going to be followup ultrasound imaging.
Gamesmanship - History of “adrenal insufficiency” ?
Does that help you in the setting of a newborn adrenal mass?
Nope. Most cases are actually caused by a 21 alpha hydroxylase deficiency (congenital
adrenal hyperplasia). Those tend to look different than hemorrhage or a mass- they are more
“cerebriform.” The problem is you can acquire adrenal insufficiency from neoplastic
destruction (neuroblastoma) or regular good old fashioned hemorrhage.
More on Adrenals in the Endocrine Chapter.
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SECTION 12:
Repr o d u c t i v e
Hydrometrocolpos -
Essentially the vagina won’t drain the uterus. This
condition is characterized on imaging by an expanded
fluid-filled vaginal cavity with associated distention of
the uterus.
You can see it presenting in infancy as a mass, or as a
teenager with delayed menarche.
Causes include imperforate hymen (most common),
vaginal stenosis, lower vaginal atresia, and cervical
stenosis.
For multiple choice trivia think about this as a “midline
pelvic mass” , which can cause hydronephrosis (mass
effect from distended uterus).
Trivia: Associated with Uterus Didelphys (which often
~75% has a transverse vaginal septum)
Ovary - A complete discussion of ovarian masses is found in the GYN chapter. I’ll briefly
cover some PEDs specific ovarian issues.
Torsion: In an adult, ovarian torsion is almost always due to a mass. In a child, torsion can
occur with a normal ovary, secondary to excessive mobility of the ovary. As described in the
GYN chapter you are going to see an enlarged (swollen) ovary, with peripheral follicles, with or
without arterial flow. What is “enlarged”? Unlike an adult you can’t really use a fixed number
to call the ovary enlarged (ovarian volumes in the peds setting are notoriously variable). The
solution is to compare the ovary in question to the contralateral size. Suspect torsion if the ovary
is at least 3 times the size of the opposite “normal” ovary. Fluid-Debris Levels within the
displaced follicles is another described adolescent ovarian torsion finding.
Masses: About two-thirds of ovarian neoplasms are benign dermoids/teratomas (discussed in
detail in the GYN chapter). The other one third are cancer. The cancers are usually germ cells
(75%). Again, mural nodules and thick Septations should clue you in that these might be cancer.
Peritoneal implants, ascites, and lymphadenopathy, are all bad signs and would over-ride
characteristics of the mass.
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Random Scrotum Trivia
Hydrocele: Collection of serous fluid and is the most common cause of painless scrotal
swelling. Congenital hydroceles result from a patent processus vaginalis that permits entry of
peritoneal fluid into the scrotal sac.
Complicated Hydrocele (one with Septations): This is either a hematocele vs pyocele. The
distinction is clinical.
Varicocele: Most of these are idiopathic and found in adolescents and young adults. They are
more frequent on the left. They arc uncommon on the right, and if isolated (not bilateral) should
stir suspicion for abdominal pathology (nutcracker syndrome, RCC, retroperitoneal fibrosis).
“Next Step” - Isolated right-sided varicocele = Abdomen CT
Exclude the extrinsic mass, renal vein thrombus, or
portal hypertension causing a splenorenal shunt
HSP: This vasculitis is the most common cause of idiopathic scrotal edema (more on this in the
vascular chapter).
Acute Pain in or around the Scrotum
The top three considerations in a child with acute scrotal pain are (1) torsion of the testicular
appendage, (2) testicular torsion, and (3) epididymo-orchitis.
Epididymitis - The epididymal head is the most common part involved. Increased size and
hyperemia are your ultrasound findings. This occurs in two peaks: under 2 and over 6. You can
have infection of the epididymis alone or infection of the epididymis and testicle (isolated orchitis
is rare).
Orchitis - Nearly always occurs as a progressed epididymitis. When isolated the answer is
mumps.
Torsion of the Testicular Appendages - This is the most common cause of acute
scrotal pain in age 7-14. The testicular appendage is some vestigial remnant of a mesonephric
duct. Typical history is a sudden onset of pain, with a Blue Dot Sign on physical exam (looks like
a blue dot). Enlargement of the testicular appendage to greater than 5 mm is considered by some
as the best indicator of torsion
Torsion of the Testicle - Results from the testis and spermatic cord twisting within the
serosal space leading to ischemia. The testable trivia is that it is caused by a failure of the tunica
vaginalis and testis to connect or a “Bell Clapper Deformity”. This deformity is usually bilateral,
so if you twist one they will often orchiopexy the other one. If it was 1950 you’d call in your
nuclear medicine tech for scintigraphy. Now you just get a Doppler ultrasound. Findings will be
absent or asymmetrically decreased flow, asymmetric enlargement, and slightly decreased
echogenicity of the involved ball.
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Extra-Testicular Mass:
Paratesticular Rhabdomyosarcoma: By far the most common extra-testicular
mass in young men and the only one really worth mentioning. If you see a mass in the
scrotum that is not for sure in the testicle this is it (unless the history is kick to the balls from a
spiteful young lady - and you are dealing with a big fucking hematoma). If it’s truly a mass -
this is the answer.
Trivia:
• The most common location is actually the head/neck - specifically the orbit and
nasopharynx.
• There is a bimodal peak (2-4, then 15-17).
Testicular Masses
Testicular Masses can be thought of as intratesticular or extratesticular. With regard to
intratesticular masses, ultrasound can show you that there is indeed a mass but there are no
imaging features that really help you tell which one is which. If the mass is extratesticular , the
most likely diagnosis is an embryonal rhabdomyosarcoma from the spermatic cord or
epididymis
Testicular Mircolithiasis - This appears as
multiple small echogenic foci within the testes.
Testicular microlithiasis is usually an incidental
finding in scrotal US examinations performed for
unrelated reasons. It might have a relationship with
Germ Cell Tumors (controversial). Follow-up in 6
months, then yearly is probably the recommendation
(maybe - it’s very controversial, and therefore unlikely
to be asked).
Testicular Cancer:
The histologic breakdown is as follows: THIS vs THAT:
Testicular
• Germ Cell (90%)
Calcifications
• Seminoma (40%) - seen more in the 4th decade
• Non Seminoma (60%)
• Teratoma, Yolk Sacs, Mixed Germ Cells, Etc... Tiny (micro) = Seminoma
• Non Germ Cell (10%) BIG = Germ Cell Tumor
•Sertoli
•Leydig
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Testicular Masses Cont.
The two Germ Cell Tumors seen in the first decade of life are the yolk sac tumor, and the
teratoma.
Yolk Sac Tumor: Heterogeneous Testicular Mass in < 2 year old = Yolk Sac Tumor. AFP is
usually super elevated.
Teratoma - Pure testicular teratomas are only seen in young kids < 2. Mixed teratomas are
seen in 25 year olds. Unlike ovarian teratoma, these guys often have aggressive biological
behavior.
Choriocarcinoma: An aggressive, highly vascular tumor, seen more in the 2nd decade.
Sertoli Cell Tumors - These testicular tumors are usually bilateral and are visualized on US
as “bumed-out” tumors (dense echogenic foci that represent calcified scars). A subtype of Sertoli
cell tumor associated with Peutz-Jeghers syndrome typically occurs in children. If they show you
the Peurtz-Jegher lips and bilateral scrotal masses, this is the answer.
Testicular Lymphoma - Just be aware that lymphoma can “hide” in the testes because of
the blood testes barrier. Immunosuppressed patients are at increased risk for developing
extranodal/ testicular lymphoma. On US, the normal homogeneous echogenic testicular tissue is
replaced focally or diffusely with hypoechoic vascular lymphomatous tissue. Buzzword =
multiple hypoechoic masses of the testicle.
Not Really Reproductive Rut It Is Pelvic
Sacrococcygeal Teratoma - This is the most common
tumor of the fetus or infant. These solid and/or cystic masses are
typically large and found either on prenatal imaging or birth.
Their largeness is a problem and can cause mass effect on the GI
system, hip dislocation, and even nerve compression leading to
incontinence. They are usually benign (80%), although those
presenting in older infants tend to have a higher malignant
potential. The location of the mass is either external to the pelvis
(47%), internal to the pelvis (9%), or dumbelled both inside and
outside (34%).
There is another classification that discusses involvement of the
abdomen.
The easiest way to remember it is like this:
-Type 1 - Totally extra pelvic
-Type 2 - Barely pelvic, but not abdominal
-Type 3 - Some abdominal
-Type 4 - Totally inside abdomen ** this one has the highest rate of malignancy.
Trivia: They have to cut the coccyx off during resection. Incomplete resection of the coccyx is
associated with a high recurrence rate.
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SECTION 13:
MSK
Fracture: In general, little kids bend they don’t break.
You end up with lots of buckles and greensticks. For
problem solving you can get a repeat in 7-10 days as
periosteal reaction is expected in 7-10 days. Kids tend to
heal completely, often with no sign of prior fracture.
Involvement of the Physis: The major concern is growth
arrest, probably best asked by showing a physeal bar
(“early” bony bridge crossing the growth plate). You can
get bars from prior infection, but a history of trauma is Physeal Bar
gonna be the more classic way to ask it.
Salter-Harris Classification lends itself well to multiple choice:
Type 1: S - Slipped
Complete physeal fracture, with or without
displacement.
Type 2: A -Above (or “Away from the Joint”)
Fracture involves the metaphysis. This is the
most common type (75%).
Type 3: L - Lower
(3 is the backwards “E” for Epiphysis)
Fracture involves the epiphysis. These guys have
a chance of growth arrest, and will often require
surgery to maintain alignment
Type 4: T — Through
Fracture involves the metaphysis and epiphysis.
These guys don’t do as well, often end up with
growth arrest, or focal fusion. They require
anatomic reduction and often surgery.
Type 5: R - Ruined
Compression of the growth plate. It occurs from axial loading injuries, and has a very poor
prognosis. These are easy to miss, and often found when looking back at comparisons (hopefully
ones your partner read). The buzzword is “bony bridge across physis”.
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Toddler’s Fracture: Oblique fracture of the midshaft of the tibia seen in a child just
starting to walk (new stress on bone). If it’s a spiral type you probably should query non-accidental
trauma. The typical age is 9 months - 3 years.
Stress Fracture in Children: This is an injury which occurs after repetitive trauma,
usually after new activity (walking). The most common site of fracture is the tibia - proximal
posterior cortex. The tibial fracture is the so-called “toddler fracture” described above. Other
classic stress fractures include the calcaneal fracture - seen after the child has had a cast
removed and returns to normal activity.
- The Elbow -
My God... these peds elbows.
Every first year resident knows that elevation of the fat pad (sail sign) should make you think
joint effusion and possible occult fracture. Don’t forget that sometimes you can see a thin
anterior pad, but you should never see the posterior pad (posterior is positive). I like to bias
myself with statistics when I’m hunting for the peds elbow fracture. The most common
fracture is going to be a supracondylar fracture (> 60%), followed by lateral condyle (20%),
and medial epicondyle (10%).
Radiocapitellar Line: This is a line
through the center of the radius, which
should intersect the middle of the
capitellum on every view (regardless of
position). If the radius is dislocated it
will NOT pass through the center of the
capitellum
Anterior Humeral Line: This time you
need a true lateral. A line along the
anterior surface of humerus, should pass
through the middle third of the
capitellum. With a supracondylar
fracture (the most common peds elbow
fracture) you’ll see this line pass
through the anterior third.
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Ossification Centers are a
source of trickery.
Remember they occur in a set order
(CRITOE),
• Capitellum (Age 1),
• Radius (Age 3),
• Internal (medial epicondyle Age 5),
• Trochlea (Age 7),
• Olecranon(Age 9), and
• External (lateral epicondyle Age 11).
Zig Zag Search Pattern Hunting For the Next Center
-Elbow Tricks:
Lateral Condyle Fx: This is the second most common distal humerus fracture in kids.
Some dude named Milch classified them. The thing to know is a fracture that passes through
the capitello-trochlear groove is unstable (Milch II). Since it’s really hard to tell this,
treatment is based on the displacement of the fracture fragment (> or < 2 mm).
Trochlea - can have multiple ossification centers, so it can have a fragmented appearance.
Medial Epicondyle Avulsion (Little League Elbow) - There are two major tricks
with this one. (1) Because it’s an extra-articular structure, its avulsions will not necessarily
result in a joint effusion. (2) It can get interposed between the articular surface of the
humerus and olecranon. Avulsed fragments can get stuck in the joint, even when there is no
dislocation.
Anytime you see a dislocation - ask yourself THIS vs THAT:
• Is the patient 5 years old ? And if so Common Uncommon
• Where is the medial epicondyle ?
Elbow Elbow
Fractures Fractures
The importance of IT (crIToe) -
• You should never see the trochlea and not see the Lateral
internal (medial epicondyle), if you do it’s probably a Lateral Condylar Epicondyle
displaced fragment
Medial
Medial Condyle
Epicondyle
Nursemaids Elbow: When a child’s arm is pulled on, the radial head may sublux into
the annular ligament. X-rays typically don’t help, unless you supinate the arm during lateral
position (which often relocates the arm).
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- Avulsion Injuries:
Kids tendons tend to be stronger than their bones, so avulsion injuries are more common
(when compared to adults). The pelvis is the classic location to test this.
- Chronic Fatigue Injuries:
Sinding-Larsen-Johansson - This is a
chronic traction injury at the insertion of the patellar
tendon on the patella. It’s seen in active adolescents
between age 10-14. Kids with cerebral palsy are
prone to it.
Osgood-Schlatter - This is due to repeated
micro trauma to the patellar tendon on its insertion at
the tibial tuberosity. It’s bilateral 25% of the time, and
more common in boys.
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- Periosteal Reaction in the Newborn -
Congenital Rubella: Bony changes are seen in 50% of cases, with the classic buzzword
being “celery stalk” appearance, from generalized lucency of the metaphysis. This is usually
seen in the first few weeks of life.
Syphilis: Bony changes are seen in 95% of cases.
Bony changes do NOT occur until 6-8 weeks of life
(Rubella changes are earlier). Metaphyseal lucent
bands and periosteal reaction along long bones can be
seen. The classic buzzword is “Wimberger Sign” or
destruction of the medial portion of the proximal
metaphysis of the tibia.
Wimberger Sign
Caffey Disease - Have you ever seen that giant multiple volume set of peds radiology
books? Yeah, same guy. This thing is a self limiting disorder of soft tissue swelling, periosteal
reaction, and irritability seen within the first 6 months of life. The classic picture is the
really hot mandible on bone scan. The mandible is the most common location (clavicle, and
ulna are the other classic sites). It’s rare as hell, and probably not even real. There have been
more sightings of Chupacabra in the last 50 years.
Prostaglandin Therapy - Prostaglandin El and E2 (often used to keep a PDA open) can
cause a periosteal reaction. The classic trick is to show a chest x-ray with sternotomy wires (or
other hints of congenital heart), and then periosteal reaction in the arm bones.
Neuroblastoma Mets - This is really the only childhood malignancy that occurs in
newborns and mets to bones.
Physiologic Growth: So this is often called “Physiologic Periostitis of the Newborn” ,
which is totally false and wrong. It does NOT happen in newborns. You see this around 3
months of age, and it should resolve by six months. Proximal involvement (femur) comes
before distal involvement (tibia). It always involves the diaphysis.
It is NOT physiologic periostitis if:
• You see it before 1 month
• You see it in the tibia before the femur
• It does not involve the diaphysis.
Abuse — Some people abuse drugs, some just can't stand screaming kids, some suffer both
shortcomings. More on this later.
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- Other “Aggressive Processes” in Kids -
Langerhans Cell Histiocytosis (LCH) - Also known as EG (eosinophilic
granuloma). It’s twice as common in boys. Skeletal manifestations are highly variable, but
lets just talk about the classic ones:
• Skull - Most common site. Has “beveled edge” from uneven destruction of the inner
and outer tables. If you see a round lucent lesion in the skull of a child think this (and
neuroblastoma mets).
• Ribs - Multiple lucent lesions, with an expanded appearance
• Spine - Vertebra plana
LCH - Beveled Edge Skull Lesion LCH - Vertebra Plana
*I’11 touch on this more in the MSK chapter.
Ewing Sarcoma and Osteosarcoma are also covered in depth in the MSK chapter
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Osteomyelitis
It usually occurs in babies (30% of cases less than 2 years old). It’s usually hematogenous
(adults it directly spreads - typically from a diabetic ulcer).
There are some changes that occur over time, which are potentially testable.
Newborns - They have open growth plates and perforating vessels which travel from the
metaphysis to the epiphysis. Infection typically starts in the metaphysis (it has the most blood
supply because it is growing the fastest), and then can spread via these perforators to the
epiphysis.
Kids - Later in childhood, the perforators regress and the avascular epiphyseal plate stops
infection from crossing over. This creates a “septic tank” scenario, where infection tends to
smolder. In fact, 75% of cases involve the metaphyses of long bones (femur most common).
Adults - When the growth plates fuse, the barrier of an avascular plate is no longer present,
and infection can again cross over to the epiphysis to cause mayhem.
Trivia:
- Hematogenous spread more common in kids (direct spread in adult)
- Metaphysis most common location, with target changes as explained above
- Bony changes don’t occur on x-ray for around 10 days.
- It’s serious business and can rapidly destroy the cartilage if it spreads into the joint
**Discussed again in the MSK Chapter
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- Skeletal Dysplasia -
There is a bunch of vocabulary to learn regarding dysplasias:
English Fancy Doctor Speak
Short Fingers Brachydactyly
Too Many Fingers Polydactyly
Two or More Fused Fingers
Syndactyly
(“Sock Hand” — I call it)
Contractures of Fingers Camptodactyly
Radially Angulated Fingers (Usually 5th) Clinodactyly
Long, Spider-Like Fingers Arachnodactyly
Limb is Absent Amelia
Limb is mostly Absent Meromelia
Hands / Feet (distal limbs) are Short Acromelic
Forearm or Lower Leg are short (middle limbs) Mesomelic
Femur or Humerus (proximal limbs) are short Rhizomelic
Short All Over Micromelic
How I remember the lengths:
• Meso is in the Middle,
• Aero sounds like Acromegaly (they get big hands), and
•The other one is the other one (Rhizo).
There are tons of skeletal dysplasias and extensive knowledge of them is way way way way
beyond the scope of the exam. Instead I’m going to mention 3 dwarfs, and a few other
miscellaneous conditions.
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- Dwarfs-
(or “Dwarves” If you are practicing radiology in middle earth):
Achondroplasia - This is the most common skeletal dysplasia, and is the mostly likely
to be seen at the mall (or on television). It results from a fibroblast growth factor receptor
problem (most dwarfisms do). It is a rhizomelic (short femur, short humerus) dwarf. They
often have weird big heads, trident hands (3rd and 4th fingers are long), narrowing of the
interpedicular distance, and the tombstone pelvis. Advanced paternal age is a risk factor.
They make good actors, excellent rodeo clowns, and various parts of their bodies (if cooked
properly) have magical powers.
Thanatophoric - This is the most common lethal dwarfism. They have rhizomelic
shortening (humerus, femur). The femurs are sometimes called telephone receivers. They
have short ribs and a long thorax, and small iliac bones. The vertebral bones are flat
(platyspondyly), and the skull can be cloverleaf shaped.
Asphyxiating Thoracic Dystrophy (Jeune) - This is usually fatal as well. The
big finding is the “Bell shaped thorax” with short ribs. 15% will have too many fingers
(polydactyly). If they live, they have kidney problems (chronic nephritis). You can
differentiate a dead Thanatophoric dwarf, from a dead Jeune dwarf by looking at their
vertebral bodies. The Jeune bodies are normal (the thanatophorics are flat).
Additional Random Dwarf Trivia:
• Ellis-Van Crevald is the dwarf with multiple fingers.
• Pseudoachondroplasia is this weird thing not present at birth, and spares the skull.
• Pyknodysostosis osteopetrosis, in a dwarf, with a wide angled jaw, & Acro-osteolysis.
The Dwarf Blitz - 5 Things I Would Remember About Dwarfs
1. The Vocab: Rhizo (humerus, femur) vs Acro (hands, feet) vs Meso (forearm, tib/fib)
2. Most dwarfs are Rhizomelic - if forced to choose, always guess this
3. The pedicles are supposed to widen slightly as you descend the spinal column,
Achondroplasia has the opposite - they narrow. If you see a live dwarf, with short
femurs / humerus, and narrowing of the pedicles then this is the answer.
(technically thantophorics can get this too - but it’s more classic for achondroplasia)
4. Thanatophoric is your main dead dwarf. Usually the standout feature is the
telephone receiver femur (and a crazy cloverleaf head)
5. Jeune is another dead dwarf - but the short ribs really stand out.
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- Misc Conditions -
Bifid Rib - This is the most common cause of an anterior wall “mass.” If there is just one (usually
the 4th rib) - then it is just a variant. If there arc bunches think Gorlin Syndrome.
Gorlin Syndrome - Bifid Ribs, Calcifications of the Falx, basal cell cancers, odontogenic
keratocysts (lytic jaw lesions).
Osteogenesis Imperfecta - They have a collagen defect and make brittle bones. Depending
on the severity it can be totally lethal or more mild. It’s classically shown with a totally lucent skull,
or multiple fractures with hyperplastic callus. Another classic trick is to show the legs with the
fibula longer than the tibia. They have wormian bones, and often flat or beaked vertebral bodies.
Other trivia is the blue sclera, hearing impairment (otosclerosis), and that they tend to suck at
football.
Osteopetrosis - They have a defect in the way osteoclasts work, so you end up with
disorganized bone that is sclerotic and weak (prone to fracture). There are a bunch of different types,
with variable severity. The infantile type is lethal because it takes out your bone marrow. With less
severe forms, you can have abnormal diminished osteoclastic activity that varies during skeletal
growth, and results in alternating bands of sclerosis parallel to the growth plate. Most likely the way
this will be shown is the “bone-in-bone” appearance in the vertebral body or carpals. Picture frame
vertebrae is another buzzword. Alternatively, they can show you a diffusely sclerotic skeleton, with
diffuse loss of the corticomedullary junction in the long tubular bones.
Pyknodysostosis - Osteopetrosis + Wormian Bones + Acro-Osteolysis. They also
have “wide (or obtuse) angled mandible”, which apparently is a buzzword.
Klippel Feil - You get congenital fusion of the cervical spine (sorta like JRA).
The cervical vertebral bodies will be tall and skinny. There is often a sprengel deformity
(high riding scapula). Another common piece of trivia is to show the omovertebral bone
- which is just some big stupid looking vertebral body.
Hunters / Hurlers / Morquio - All three of these are mucopolysaccharidoses. Findings
include oval shaped vertebral bodies with anterior beak. The beak is actually mid in Morquio, and
inferior in Hurlers. Clavicles and ribs are often thick (narrow more medially) - like a canoe-
paddle. The pelvis shape is described as the opposite of achondroplasia - the iliac wings are tall and
flaired. The hand x-ray is the most commonly shown in case books and gives you wide metacarpal
bones with proximal tapering.
Few More Trivia Points on Morquio:
•They are dwarfs
•The most common cause of death is cervical myelopathy at C2
•The bony changes actually progress during the first few years of life
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Neurofibromatosis - Just briefly remember that type 1
can cause anterior tibial bowing, and pseudarthrosis at the
distal fibula.
This is an Aunt Minnie.
They often have scoliosis. Just think of the elephant man.
Gauchers - This is the most common lysosomal storage
disease. It gives you a big spleen, and big liver among a few
bone signs.
• AVN of the Femoral Heads
• H-Shaped Vertebra
• Bone Infarcts (lots of them)
• Erlenmeyer Flask Shaped Femurs
Caudal Regression Syndrome - This is a spectrum
that includes sacral and/or coccyx agenesis. You see it with NF1
VACTERL and Currarino Triads Syndromes.
Scoliosis - Lateral curvature of the spine, which is usually idiopathic in girls. It can also be from
vertebral segmentation problems. NF can cause it as well (that’s a piece of trivia).
Radial Dysplasia- Absence or hypoplasia of the radius (usually with a missing thumb) is a
differential case (VACTERL, Holt-Oram, Fanconi Anemia, Thrombocytopenia, Absent Radius). As a
point of trivia TAR kids will have a thumb.
Hand Foot Syndrome - The classic history is hand or
foot pain / swelling in an infant with sickle cell. This is a
dactylitis, and felt to be related to ischemia. It will resolve on
its own, after a few weeks. Radiographs can show a
periostitis two weeks after the pain goes away.
Blounts (tibia vara). Varus angulation occurring at the
medial aspect of the proximal tibia (varus bowing occurs at
the metaphysis not the knee). This is often bilateral, and
NOT often seen before age 2 (two sides, not before two).
Later in the disease progression the medial metaphysis will
be depressed and an osseous outgrowth classically develops.
You can see it in two different age groups; (a) early - which
is around age 2 and (b) late - which is around age 12.
• Two Sides - Not Before Two
• Two Different Ages (2-3, 12)
Blount’s -Tibia VARA
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-Feet-
Congenital foot is a complicated and confusing topic, about which I will avoid great detail
because it is well beyond the scope of the exam. I am going to at least try and drop some
knowledge which could be called upon in the darkest of hours to work these problems out.
Step 1: Vocabulary. Just knowing the lingo is very helpful for getting the diagnosis on
multiple choice foot questions.
• Talipes = Congenital,
• Pes = Foot or Acquired
• Equines = "Plantar Flexed Ankle ”, Heel Cord is often tight, and the heel won’t touch the floor
• Calcaneus = Opposite of Equines. The Calcaneus is actually angled up
• Varus = Forefoot in
• Valgus = Forefoot out
• Cavus = High Arch
• Planus = Opposite of Cavus - "bizarro cavus” - FLAT FOOT
• Supination - Inward rotation - "Sole of foot in” - holding soup with the bottom of your foot
• Pronation - Outward rotation - "Sole of foot out"
Step 2: Hindfoot Valgus vs Varus
Normal Hindfoot Valgus Hindfoot Varus
First look at the normal Think about this as the talus This is the opposite
acute angle the talus sliding nose down off the situation, in which you
and calcaneus make on calcaneus. This make the have a narrowing of the
a lateral view. angle wider. angle between the talus
and calcaneus.
If the talus slides off you lose
your longitudinal arch - which Notice the two bones lay
essentially characterizes nearly parallel - like two
hindfoot valgus. “clubs” laying on top of
each other.
Also, note that the nose
down (nearly vertical)
appearance of the talus .
'Too Many Toes”
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Step 3 - Knowing the two main disorders. The flat foot (valgus), and the club foot (varus).
Flat Foot (Pes Planus)- This can be congenital or acquired. The peds section will cover
congenital and the adult MSK section will cover acquired. The congenital types can be grouped into
flexible or rigid (the flexible types arc more common in kids). The distinction can be made with
plantar flexion views (flexible improves with stress). The ridged subtypes can be further subdivided
into tarsal coalition and vertical talus. In any case you have a hindfoot valgus.
Tarsal Coalition - There are two main types (talus to the calcaneus, and calcaneus to the
navicular). They are pretty equal in incidence, and about 50% of the time are bilateral. You
can have bony or fibrous/cartilaginous subtypes. The fibrous/cartilaginous types are more
common than the bony types.
• Talocalcaneal - Occurs at the middle facet.
Has the “continuous C-sign” produced from an “absent middle facet” on
the lateral view. Talar beak (spur on the anterior talus - white arrow) is also
seen in about 25% of cases.
• Calcaneonavicular- Occurs at the anterior facet.
Has the “anteater sign ” Where the elongated anterior process of the
calcaneus resembles the blood thirsty nose of a ravenous ant eater. This
is best seen on an oblique view.
• Vertical Talus (equinus hindfoot valgus) - This is
sometimes called the “rocker-bottom foot” because the talus is
in extreme plantar flexion with dorsal dislocation of the
Navicular - resulting in a locked talus in plantar flexion. As a
point of trivia this is often associated with myelomeningocele.
Club Foot (Talipes Equino Varus) - Translation - Congenital Plantar Flexed Ankle
Forefoot. This is sorta why I lead with the vocab, all the congenital feet can be figured out based on
the translated language. This thing is more common in boys, and bilateral about half the time. The
toes are pointed down (equines), and the talocalcaneal angle is acute (varus).
Key features:
• Hindfoot varus (decreased talocalcaneal
angle)
• Medial deviation and inversion of the
forefoot
• Elevated Plantar Arch
Trivia: The most common surgical complication is
over correction resulting in a “rocker bottom” flat
foot deformity.
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- Hip Dysplasia -
Developmental Dysplasia of the Hip - This is seen more commonly in females,
children born breech, and oligohydramnios. The physical exam buzzwords are asymmetric
skin or gluteal folds, leg length discrepancy, palpable clunk, or delayed ambulation. It’s
bilateral about 1/3 of the time. Ultrasound is done to evaluate (after physical exam), and is
excellent until the bones ossify (then you need x-rays). A common trick is to be careful
making a measurement in the first week of life - the laxity immediately after birth (related to
maternal estrogen) can screw up the measurements.
Angles:
On ultrasound the alpha angle, should be
more than 60 degrees. Anything less
than that and your cup is not deep enough
to hold your ball. The plain film
equivalent in the acetabular angle, which
is the complimentary angle (and
therefore should be less than 30).
Getting them confused? Remember that
the “Alpha Angle is the Alpha Male” -
and therefore the bigger of the two angles.
**But don’t forget that DDH is more
common in women (not alpha males).
The acetabular angle should decrease
from 30 degrees at birth to 22 degrees at
age 1. DDH is the classic cause of an
increased angle, but neuromuscular
disorder can also increase it.
The position of the femoral epiphysis
(or where it will be) should be below
Hilgenreiner’s line “H”, and medial to
Perkin’s Line “P”. Shenton’s Line “S”
should be continuous.
Femoral
Epiphysis
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Proximal Focal Femoral Deficiency - This is a congenital zebra,
which ranges from absent proximal femur to hypoplastic proximal femur. You
get a varus deformity. This is a mimic of DDH, but DDH will have normal
femur leg length.
Slipped Capital Femoral Epiphysis (SCFE) - This is a type 1 Salter Harris,
through the proximal femoral physis. What makes this unique is that unlike most SH Is, this
guy has a bad prognosis if not fixed. The classic history is a fat African American
adolescent (age 12-15) with hip pain. It’s bilateral in 1/3 of cases (both hips don’t usually
present at same time). The frog leg view is the money - this is always the answer on next
step questions.
Legg-Calve-Perthes - This is AVN of the proximal femoral epiphysis. It’s seen more in
boys than girls (4:1), and favors white people around age 5-8. These kids tend to be smaller
than average for their age. This is bilateral about 10% of the time (less than SCFE). The
subchondral lucency (crescent sign) is best seen on a frog leg. Other early signs include an
asymmetric small ossified femoral epiphysis. MRI has more sensitivity. The flat collapsed
femoral head makes it obvious. Sterile joint effusions (transient synovitis) can be associated.
NORMAL
THIS vs THAT:
Perthes SCFE
Often Small Overweight
White Kids Black Kids
“Klein’s Line” - Drawn along the edge of the Age 5-8 Age 12-15
femur and should normally intersect with lateral
superior femoral epiphysis. This line is used to
evaluate for SCFE. When the line doesn’t cross Bilateral 10% Bilateral 30%
the lateral epiphysis think SCFE.
***Testable Trivia - Frog Leg View is more
sensitive for this measurement
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Septic Arthritis- This is serious
business , and considered the most urgent
cause of painful hip in a child. Wide joint
space (lateral displacement of femoral head),
should prompt an ultrasound, and that should
prompt a joint tap. If you have low suspicion
and don’t want to tap the hip, You could pull
on the leg under fluoro and try and get gas in Fluid Distending the Joint Capsule
over the Femoral Neck (arrow)
the joint. This air arthrogram sign supposedly
excludes a joint effusion (and therefore a
septic joint) - depending on who you ask.
Transient Synovitis - This is a sterile
(reactive) hip effusion that occurs in the
setting of a systemic illness (usually viral
URI or GI). As the name suggests this is
“transient” and goes away in a few days.
This is actually very common. Some
sources will say its the most common hip
disorder in growing children (peak age is Hip Joint Effusions Are Seen Here at the Neck
around 5). The ED will be in a full panic and
want you to tap it at 3 am.
THIS vs THAT: Transient Synovitis vs Septic Arthritis
Telling these apart is actually important for real life (not getting sued) since a septic hip will
fucking destroy the kid’s cartilage (usually if it’s missed for more than 4 days).
Ortho (and in very rare situations a “smart” ED doc)
will use a clinical parameter “the Kocher Criteria” to • If 3/4 are positive = Septic
tell them apart. Criteria is 4 parts: • If CRP is negative and the
kid can bear weight it’s
• Fever NOT Septic
• Inability to walk • CRP is the strongest
• Elevated ESR (or CRP) independent risk factor for
• WBC > 12 K septic arthritis
Typical workup is going to be:
1. X-Ray Hip series (AP, Lateral, and Frog Leg) which is usually negative in real life but
will probably show medial joint widening on the exam.
2. Ultrasound which will show an effusion.
3. Then a clinical decision based on Kocher Criteria (> 2) and “Gut Instinct” to Aspirate
4. MRI would only be used if/when hip aspiration can’t/hasn’t been performed.
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- Metabolic -
Rickets - Not enough vitamin D. Affects the most
rapidly growing bones (mostly knees and wrists).
Buzzwords “fraying, cupping, and irregularity along
the physeal margin. ” They are at increased risk for
SCFE. “Rachitic rosary” appearance from expansion of
the anterior rib ends at the costochondral junctions. As a
pearl, rickets is never seen in a newborn (Mom’s
vitamin D is still doing its thing).
Hypophosphatasia - This looks like Rickets in a
newborn. They will have frayed metaphyses and bowed
long bones. The underlying pathology is deficient
serum alkaline phosphatase. There is variability in
severity with lethal perinatal / natal forms, and more mild "Cupping" & Fraying
adult forms.
Scurvy - Not enough vitamin C. This is rare as hell outside of a pirate ship in the 1400s.
For the purpose of trivia (which multiple choice tests love) the following stuff is high yield:
• Does NOT occur before 6 months of age (maternal stores buffer)
o Bleeding Disorders Common
o Subperiosteal hemorrhage (lifts up the periosteum)
• Hemarthrosis
• “Scorbutic rosary” appearance from expansion of the costochondral junctions (very
similar to rickets).
Lead Poisoning - This is most commonly seen in kids less than two who eat paint chips.
The classic finding is a wide sclerotic metaphyseal line (lead line), in an area of rapid
growth (knee). It will not spare the fibula (as a normal variant line might).
Lucent Metaphyseal Bands
- This is a classic peds DDx. - LINE.
• Leukemia
• Infection (TORCH)
• Neuroblastoma Mets
• Endocrine (rickets, Scurvy)
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- Non-Accidental Trauma (HAT)-
“Some People Just Can’t Take Screaming Kids. ”
Any suspicious fracture should prompt a skeletal survey (“baby gram” does NOT count).
Suspicious fractures would include highly specific fractures (metaphyseal comer fracture,
posterior rib fractures) or fractures that don’t make sense - toddler fracture in a non- ambulatory
child.
• Posterior Medial Rib Fracture: In a child under the age of 3,
this is pretty reliable. Supposedly this type of fracture can
only be made from squeezing a child.
• Metaphyseal Corner Fractures: When this is present in a
non-ambulatory patient (infant) it is HIGHLY specific. The
only exception is obstetric trauma. After age 1, this becomes
less specific.
• Skull Fracture: The general idea is anything other than a parietal bone fracture (which is
supposedly seen more with an actual accident) is concerning.
• Solid Organ and Lumen Injury - Don’t forget about this as a presentation for NAT.
Duodenal hematoma and pancreatitis (from trauma) in an infant - should get you to say
NAT. Just think “belly trauma in a kid that is too young to fall on the handle bars of their
bike”.
Dating the Fracture:
• Periosteal Reaction: This means the fracture is less than a week old.
• Complete healing: This occurs in around 12 weeks.
• Exceptions: Metaphyseal, skull, and costochondral junction fractures will often heal
without any periosteal reaction.
Child Abuse Mimics
Rickets and OI, can have multiple fractures at different sites and are the two most
commonly described mimics.
Wormian bones and bone mineral density issues are clues that you are dealing with a
mimic. They will have to show you one or the other (or both) if they are gonna get
sneaky.
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SECTION 14:
Ped i a t r i c Spi n e
- Spinal Cord on Ultrasound -
Normal Ultrasound Appearance / Anatomy Review:
Central Canal - Easily identified as an
echogenic line. Although that is sort of counter
intuitive.
Why would a structure with fluid in it be
echogenic? The reason is that you are actually
seeing a “central echo complex” - which is the
interface between the anterior median fissure and
the myelinated ventral white matter commissure.
Remember that interfaces between things with
large differences in impedance cause a lot of
reflections (thus an echogenic line).
Trivia: Technically in a newborn the central canal is not even fluid filled (it’s packed with
glial fibrils), but that level of trivia is beyond the scope of the exam (probably).
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Low lying cord / Tethered cord: Because the canal grows faster than the cord, a
fixed attachment (“tethering”) results in cord stretching and subsequent ischemia. This can be
primary (isolated), or secondary (associated with myelomeningocele, filum terminale lipoma,
or trauma). The secondary types are more likely shown on MR (to showcase the associated
mass - fluid collection), the primary types are more likely shown on US - as a straight
counting game.
Imaging Features: Low conus (below L2), and thickened filum terminale (> 2 mm).
A common piece of trivia used as a distractor is that meningomyelocele is associated with
Chiari malformations, lipomyelomeningocele is NOT.
High Yield Trivia
• Anal Atresia = High Risk For Occult Cord Problems (including tethering) - should get
screened
• Low lying / tethered cords are closely linked with Spina Bifida (tufts of hair)
• Low Dimples (below the gluteal crease) Do NOT need screening,
o These never extend intra-spinally. They might later become a pilonidal sinuses
- but aren’t ever gonna have shit to do with the cord.
• High Dimples (above the gluteal crease) DO need screening.
Tethered Cord - With a Lipoma (Fat Signal Mass) - This is super classic
For Screening Purposes:
Low dimples (below the butt crease) don’t get screened, basically everything else does.
Most Likely Question Style: “Which of the following does NOT get screened ?”
(Answer = low dimple).
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- Misc Variant Topics -
Terminal Ventricle (ventriculus
terminalis): This is a developmental variant.
Normally, a large portion of the distal cord involutes in a
late stage of spinal cord embryology. Sometimes this
process is not uniform and you get stuck with a stupid
looking cyst at the end of your cord. These things are
usually small (around 4 mm), and cause no symptoms.
Sometimes they can get very big (like this example) and
cause some neurologic symptoms.
Terminal Ventricle
Pars Interarticularis Defects (Spondylolysis):
This is considered a fatigue or stress fracture, probably developing in
childhood. It is a classic cause of back pain in an adolescent athlete.
Although they are usually not symptomatic (only 25% are). The
process represents a hole / break in the connecting bone between the
superior and inferior articular facets. If there is forward “slippage”
you can deploy the word spondylolisthesis.
Almost always (90% +) you see this at L5 (2nd most common at L4). spondylolisthesis
They tend to have more spondylolisthesis and associated degenerative
change at L4-L5 than L5-S1. They can be seen on the oblique plain
film as a “collar on the scottie dog.” The collar on the “scotty dog”
appearance on an oblique plain film is probably the most common
way they show this in case books and conferences. On the AP view
this can be a cause of a sclerotic pedicle (the contralateral pedicle -
from wiggle stress). On CT it is usually more obvious with the break
clearly demonstrated.
**Pars Defects with anterolisthesis will have neuroforaminal stenosis,
Scotty Dog = Collar
with spinal canal widening (when severe will have spinal canal (represent the pars
stenosis as well). If the process is purely a degenerative defect).
spondylolisthesis (not much slippage), the resulting facet arthropathy
will favor the canal with less severe effects on the neuro foramina. Anatomy trivia: the
eye is the pedicle.
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Spinal Dysraphism:
You can group these as open or closed (closed with and without a mass). Open means neural
tissue exposed through a defect in bone and skin (spina bifida aperta). Closed means the
defect is covered by skin (spina bifida occulta).
Open Spinal Dysraphisms: This is the result of a failure of the closure of the primary
neural tube, with obvious exposure of the neural placode through a midline defect of the skin.
You have a dorsal defect in the posterior elements. The cord is going to be tethered. There
is an association with diastematomyelia and Chiari II malformations. Early surgery is the
treatment / standard of care.
• Myelocele: This is the more rare type where the neural
placode is flush with the skin.
• Myelomeningocele: This is the more common type
(98%) where the neural placode protrudes above the
skin. These are more common with Chiari II
malformations.
Closed Spinal Dysraphisms with Subcutaneous Mass
• Meningocele: This is herniation of a CSF filled sac through a
defect in the posterior elements (spina bifida). It is most typical
in the lumbar or sacral regions. Although they can occur in the
cervical spine. They may be anterior (usually pre-sacral). An
important point is that neural tissue is NOT present in the
sac.
• Lipomyelocele / Lipomyelomeningocele: These are lipomas with a dural defect. On
exam you are going to have a subcutaneous fatty mass above the gluteal
crease. These are 100% associated with tethered cord
(myelomeningocele may or may not).
• Terminal Myelocystocele - This is a herniation of a terminal
syrinx into a posterior meningocele via a posterior spinal defect.
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Closed Spinal Dysraphisms without Subcutaneous Mass
• Intradural lipomas - Most common in the thoracic spine along the dorsal aspect.
They don’t need to be (but can be) associated with posterior element defects.
• Fibrolipoma of the filum terminale - This is often an incidental finding “fatty filum".
There will be a linear T1 bright structure in the filum terminate. The filum is not
going to be unusually thickened and the conus will be normally located.
• Tight filum terminale - This is a thickened filum terminale (> 2 mm), with a low lying
conus (below the inferior endplate of L2). You may have an associated terminal lipoma.
The “tethered cord syndrome” is based on the clinical findings of low back pain and leg
pain plus urinary bladder dysfunction. This is the result of stretching the cord with
growth of the canal.
• Dermal Sinus - This is an epithelial lined tract that extends from the skin to deep soft
tissues (sometimes the spinal canal, sometimes a dermoid or lipoma). These are T1 low
signal (relative to the background high signal from fat).
Diastematomyelia - This describes a sagittal split in the spinal cord. They almost always
occur between T9-S1, with normal cord both above and below the split. You can have two thecal
sacs (or just one), and each hemi-cord has its own central canal and dorsal/ventral horns.
Classification systems are based on the presence / absence of an osseous or fibrous spur and
duplication or non-duplication of the thecal sac.
Caudal Regression: This is a spectrum of defects in the caudal region that ranges from
partial agenesis of the coccyx to lumbosacral agenesis. The associations to know are VACTERL
and Currarino triad. Think about this with maternal diabetes. “Blunted sharp” high terminating
cord is classic, with a “shield sign” from the opposed iliac bones (no sacrum).
Fuckery - Note than the Meningocele of Currarino Triad:
Currarino is Anterior. It’s not posterior. A
potential deployment of fuckery is to put Anterior Sacral Meningocele,
“Posterior” Sacral Meningocele as a
distractor for Currarino Triad. Anorectal malformation,
Anyone who would do that is an Asshole
Sacrococcygeal osseous defect
(a structure which also happens to be
(scimitar sacrum).
posterior).
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GASTROINTESTINAL
PROMETHEUS LIONHART, M.D.
Between the time when the oceans drank Atlantis, and the rise of the sons of
Aryas, there was an age undreamed of. And unto this, barium, was used to
differentiate various luminal GI pathologies.
Let me tell you of the days of high adventure!
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SECTION 1:
Lu mi n a l
- Esophagus -
Anatomy:
A Ring: The muscular ring above the
vestibule.
B Ring: The mucosal ring Below the
vestibule. This is a thin constriction at the GE
junction. Symptomatic dysphagia can occur if
it narrows (historically defined at < 13 mm in
diameter). If it’s narrowed (and
symptomatic) you call it a Schatzki. Just
Say “Shatz-‘B’-Rmg”
Z Line: Represents the squamocolumnar junction (boundary between esophageal and gastric
epithelium). This doesn’t necessarily correspond with the B-ring. This is an endoscopy
finding, and is only rarely seen as a thin serrated line.
Mucosa should have thin, parallel uniform folds.
Anatomic Trivia
Hypo Cricopharyngeus
Pharynx • The “true upper esophageal sphincter.”
*Location of • This muscle represents the border
Zenker Div. between the pharynx and cervical
esophagus.
• The typical level is around C5-C6
Cricopharyngeus
Swallowing
Cervical • When you swallow the larynx does two
Esophagus things: (1) it elevates and (2) it moves
*Location of anteriorly
Killian-Jamieson Div.
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Special Topic - Which Hand Does the Barium Go In ?
According to historical records. Left and Right Posterior Oblique positions were commonly
used when performing a thoracic barium swallow exam. So which hand should the barium
cup go in??? The trick is to consider the potential for the barium filled cup to obscure the
field of view as the patient is drinking. If the cup is placed in the more anterior hand this
could happen... so don’t do that.
Pathology:
Mild Fold Thickening
Reflux Esophagitis Severe Fold Thickening
Strictures
and/or Fundiplication
A common cause of fold Barretts (after failed H2 blockers
and PPIs)
thickening, which if left
Cancer
uncheck can cause some Esophagectomy
Death
serious problems.
That Guy You Hate Marries
In anguish your soul cannot enter
Your Now Widowed Wife
Behold the potential “the light” - you decide the best (She is way happier with
option is to haunt your widowed
spectrum of unchecked him. She constantly talks
wife and her new asshole husband
shit about you and how you
aggression → Beetlejuice style. never picked up your dirty
You are featured on the Sci-Fi channel’s towels or helped out with
hit paranormal realty TV show “Ghost the dishes.)
Hunters” after manifesting briefly as a
focused ectoplasmic phantasm or a class 3
full roaming vapor.
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Barretts: This is a precursor to Feline Esophagus:
adenocarcinoma - that develops secondary to
Often described
chronic reflux. The way this will be shown is
as an Aunt
a high stricture with an associated hiatal Minnie
hernia.
You have
transient, fine
transverse folds
which course
mid and lower
esophagus.
It can be
normal, but has
a high
association
with reflux
esophagitis......
correlate
clinically.
*Folds are Transient
(they go away with swallowing)
Barrett’s - High Stricture + Hiatal Hernia *Fords are ONLY in lower 2/3
Cancer: On barium you want to see the words “irregular
contour”, and "abrupt (shouldered) edges.” I like to use
stereotypes to remember the subtypes and associations:
Squamous: This is a black guy who drinks and smokes, and
once tried to kill himself with an alkaloid ingestion (drank
lye). The stricture/ulcer/mass is in the mid esophagus.
Adeno: This is a white guy, who is stressed out all the time.
He has chronic reflux (history of PPI use). He had a scope
years ago that showed Barretts, and he did nothing because
he was too busy stressing out about stuff. The stricture/ulcer/
mass is in the lower esophagus.
Critical Stage: T3 (Adventitia) vs T4 (invasion into adjacent structures) - obviously you need
CT to do this. The earlier stages are distinguished by endoscopy - so not your problem and
unlikely to be tested. T3 vs T4 is in the radiologists world - and therefore the most likely to be
tested.
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Herniation of the stomach comes in several
flavors with the most common being the sliding
type 1 (95%), and the rolling para-esophageal
type 2. The distinction between the two is
based on the position of the GE junction.
Small type 1s are often asymptomatic but do
have an association with reflux if the function of
the GE sphincter is impaired. The Para-E type 2
has a reportedly higher rate of incarceration.
Fundoplication Blitz
What is this Fundoplication ? The gastric fundus is
wrapped around the lower end of the esophagus and
stitched in place, reinforcing the lower esophageal
sphincter. The term “Nissen" - refers to a 360 degree
wrap. Loose ( < 360) wraps can also be done, and
have French sounding names like “toupet,” - these are
less high yield.
Early Complication: The early problem with these is
esophageal obstruction (or narrowing). This occurs
from either post op edema, or a wrap made too tight.
You see this peak around week 2. Barium will show
total or near total obstruction of the esophagus.
Failure: There are two main indications for the procedure (1) hiatal hernia, and (2) reflux. So
failure is defined by recurrence of either of these. The most common reason for recurrent reflux is
telescoping of the GE junction through the wrap - or a “slipped Nissen.”
• Most common reason for recurrent reflux? = slipped Nissen
• Most common reason for slipped Nissen? = short esophagus
• WTF is a “short esophagus"? The exact
definition is elusive (and depends on the
phase of the moon). For the purpose of
multiple choice test I’d go with “Hiatal
Hernia that is fixed/non-reducible, and
greater than 5 cm ”
• How can you tell if the wrap has slipped ?
Fundoplication wrap should have length
of narrowed esophagus < 2 cm (anything
greater suggests a slipped wrap)
• Remember recurrent hernia (GE junction
above the diaphragm) is not normal.
What is the treatment for a “short esophagus" ?
Collis gastroplasty (lengthening + fundoplication).
Trivia: You cannot vomit after a fundoplication (no matter how bad your wife’s cooking is)
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Candidiasis: A hint in the question stem might be “HIV Patient” or “Transplant
Patient” (someone who is immunocompromised). They could also tell you the patient has
“achalasia” or “scleroderma” - because motility disorders are also at increased risk. The most
common finding is discrete plaque-like lesions. Additional findings include: nodularity, granularity,
and fold thickening as a result of mucosal inflammation and edema. When it is most severe, it looks
more shaggy with an irregular luminal surface.
Glycogenic Acanthosis: This is a mimic of candidiasis, which has multiple elevated
benign nodules in an asymptomatic elderly patient. It is essentially an epithelial collection of
glycogen.
Ulcers:
• Herpes Ulcer: Small and multiple with a halo of edema (Herpes has a Halo)
• CMV and HIV: Large Flat Ulcer (they look the same)
Varices:
Linear often serpentine, filling defects causing a scalloped contour.
The differential diagnosis for varices includes varicoid carcinoma
(this is why you need them distended on the study).
THIS vs THAT:
Uphill Varices Downhill Varices
Caused by Portal Caused by SVC obstruction (catheter
Hypertension related, or tumor related) Varicoid appearance that flattens
out with a large barium bolus -
Confined to Bottom Half this dynamic appearance proves
Confined to Top Half of Esophagus
of Esophagus it’s not a fixed varicoid looking
cancer.
Esophageal (enteric) Duplication Cysts: If they show one of these it will be on CT
(what? GI path not on barium?). Seriously, they would have to show this on CT. It is gonna be in the
posterior mediastinum, and have an ROI showing water density. This is the only way you can show this.
Possible Ways This Could Be Tested:
• What is it / What does it look like? - Water density cyst in the posterior mediastinum
• Most common location? - The ileum (esophagus is #2).
• How can they present? Either as an incidental in an adult, or if they are big enough - as an infant with
dysphagia / breathing problems.
Malignant Risk ? Nope - they are benign
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Esophageal Diverticulum
Zenker Diverticulum: Killian-Jamieson Pulsion Traction Diverticulum:
Pulsion Diverticulum in the Diverticulum:
back (Z is in the hack of the Mid esophageal, and
alphabet). This one is anterior and lateral. often triangular in shape.
The question they always ask It protrudes through an area of These occur from
is: site of weakness = Killian weakness below the attachment of the scarring (think
Dehiscence or triangle. cricopharyngeus muscle and lateral to granulomatous disease or
the ligaments that help suspend the
TB).
Another sneaky point of trivia esophagus on the cricoid cartilage.
is that the diverticulum arise
from the hypopharynx (not This one is in the cervical
the cervical esophagus). esophagus.
Epiphrenic Diverticula:
THIS vs THAT:
Located just above the diaphragm Traction Pulsion
(usually on the RIGHT).
Triangular Round
** The para-esophageal hernia is
usually on the LEFT. Will Will NOT
Empty Empty
They are considered pulsion types
(associated with motor (contains no
muscle the
abnormality).
walls)
Esophageal Pseudodiverticulosis:
This is an Aunt Minnie. What you have arc dilated submucosal
glands that cause multiple small out pouchings. Usually due to
chronic reflux esophagitis.
There is controversy about the whole Candida situation. Per the
Mayo GI book, Candida is often cultured but is not the causative
factor.
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Papilloma: Eosinophilic Esophagitis:
Classically a young man with a long history of
The most common benign mucosal lesion of
dysphagia (also atopia and peripheral
the esophagus. It’s basically just hyperplastic
squamous epithelium. eosinophilia). Barium shows concentric rings
(distinct look). They fail treatment on PPIs, but
get better with steroids.
Esophageal Web:
Buzzword = “Ringed Esophagus”
Most commonly located at the cervical
esophagus (near the cricopharyngeus). This
thing is basically a ring (you never see
posterior only web) caused by a thin mucosal
membrane.
It’s a risk factor for esophageal and
hypopharyngeal carcinoma
Plummer -Vinson Syndrome: iron def
anemia, dysphagia, thyroid issues, “spoon-
shaped nails”
Eosinophilic Esophagitis - Rings
Esophageal Spasm:
Most of the time the exam is
normal, but for the purpose
of multiple choice I’d expect
“corkscrew” tertiary
Normal Submucosal contractions favoring the
venous plexus (higher Web - circumferential distal esophagus.
up and shallow) (anterior and posterior)
in lower cervical region The term nutcracker
esophagus requires
Esophageal Pseudodiverticulosis: manometric findings
(> 180 mmHg).
Tons of little tiny out-
pouchings which aren’t
really diverticula but
Dysphagia Lusoria - THIS IS HIGH
instead dilated excretory YIELD. Syndrome refers to problems
mucosal ducts. There is swallowing secondary to compression from
a described association
with esophageal an aberrant right subclavian artery (most
strictures (90%), reflux, patients with aberrant rights don’t have
and candidiasis.
symptoms).
The appearance is fairly
classic and is better ** Refer to page 80 for the chart on
demonstrated with a
single phase of contrast esophageal vascular impressions.
(instead of the fancy double Seriously, you need to know that crap.
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The Dilated Esophagus
If you get shown a big dilated esophagus (full cheerios, mashed potatoes, and McDonald’s
french fries... or “freedom fries” as I call them), you will need to think about 3 things.
(1) Achalasia: A motor disorder where the distal 2/3 of the esophagus (smooth muscle part)
doesn’t have normal peristalsis (“absent primary peristalsis"), and the lower esophageal
sphincter won’t relax.
The esophagus will be dilated above a smooth stricture at
the GE junction (Bird’s Beak).
“Vigorous Achalasia" - An early / less severe form which
classically has repetitive simultaneous non-propulsive
contractions. It’s more common in women, but the
secondary cancer occurs more in men.
Things to know:
• Failure of the lower esophageal sphincter to relax
• Increased risk of Candida
“Chagas Disease " - More common in the jungle. The
esophagus get paralyzed by some parasite transmitted by
a fly. The appearance is identical to Achalasia - and some
people even lump them together (others reserve the term
“achalasia” for idiopathic types only). You’ll simply need
to read the mind of the test question writer to know what
camp he/she falls into.
(2) “Pseudoachalasia” (secondary achalasia) has the appearance of achalasia, but is secondary
to a cancer at the GE junction. The difference is that real Achalasia will eventually relax, the
pseudo won’t. They have to show you the mass - or hint at it, or straight up tell you that the GE
junction didn’t relax. Alternatively they could be sneaky and just list a bunch of cancer risk
factors (smoking, drinking, chronic reflux) in the question stem. Next step would probably be
CT (or full on upper GI).
(3) Scleroderma: Involves the esophagus 80%
of the time. Again the lower 2/3 of the
esophagus stops working normally. The LES
is incompetent and you end up with chronic
reflux, which can cause scarring, Barretts, and
even cancer (Adeno). They will show you
lung changes (most commonly NSIP), and the
barium esophagus (or a small bowel series
showing closely spaced valvulae conniventes -
hide bound).
NSIP - Ground Glass with sub-pleural sparring
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- Esophagus - High Yield Trivia -
Path Trivia
Esophagitis Fold Thickening. May have smooth stricture at GE junction if severe
Buzzword: Reticulated Mucosal Pattern
Barretts
Classically shown as Hiatal Hernia + High Stricture
Medication Induced
Ulcers; Usually at the level of the arch or distal esophagus
Esophagitis
Crohn's Esophagitis Ulcers ; can be confluent in severe disease
Discrete plaque like lesions that arc seen as linear or irregular filling
defects that tend to be longitudinally oriented, separated by normal
mucosa
Candidia
Buzzword: Shaggy - when severe
Not always from AIDS, can also be from motility disorders such as
achalasia and scleroderma
Glycogenic Acanthosis Looks like Candidia, but in an asymptomatic old person
Herpes Ulcers Multiple small, with Edema Halo (herpes has halo)
CMV / AIDS Large Flat ulcers
Buzzword: Bird Beak, - smooth stricture at GE junction
Achalasia Path is failure of LES to relax (but it will slowly relax)
Increased risk of Squamous Cell CA, and Candida
Pseudoachalasia Cancer at the GE junction. Fixed Obstruction, will not relax
Involves the Esophagus 80% of the time
Scleroderma Looks a little like Achalasia (they will show you lung changes - NSIP)
Sequelae of reflux: stricture, Barrets, cancer
Long Stricture DDx: NG tube in too long, Radiation, Caustic Ingestion
Dilated submucosal glands, usually due to chronic reflux esophagitis.
Pseudodiverticulosis
Esophageal stricture is seen in 90% of cases
Zenker in the back (above cricopharyngeus)
Zenker Diverticula
From the hypopharynx
Lateral (below cricopharyngeus)
Killian-Jamieson
From the cervical esophagus.
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- Stomach -
Location Based Trivia
• H. Pylori Gastritis - Usually in Antrum
• Zollinger-Ellison - Ulcerations in the stomach (jejunal ulcer is the buzzword).
Duodenal bulb is actually the most common location for ulcers in ZE. Remember ZE is
from gastrinoma - and might be a way to test MEN syndromes.
• Crohn's - Uncommon in the stomach, but when it is, it likes the antrum
• Menetrier’s - Usually in the Fundus (classically spares the antrum)
• Lymphoma - “Crosses the Pylorus” - classically described as doing so, although in
reality adenocarcinoma does it more.
- Selective Polyposis Syndromes -
100s of polyps - 100% risk of Colon CA (usually before 40)
FAP (Familial Hyperplastic Stomach Polyps, Adenomatous Bowel Polyps
Adenomatous Polyposis)
Locally invasive desmoid tumors are common at surgical sites post
colectomy (these actually kill 10% of FAPers)
As the name implies, this is not a disease of 100s of polyps. Instead
it is DNA Mismatch Repair problem associated with lots of cancers.
Hereditary nonpolyposis
Syndrome (Lynch) -
Another difference between this and FAP is that the cancers of the
colon are usually solitary (and right sided).
HNPCC
They also get lots of other cancers (endometrial being the second
most common)
Gardner Syndrome FAP + Desmoid Tumors, Osteomas, Papillary Thyroid Cancer
Turcots FAP + Gliomas and Medulloblastomas
Hamartoma Style!
Peutz-Jeghers Mucocutaneous Pigmentation (gross Dalmatian dog lips)
Small and Large Bowel CA, Pancreatic CA, and GYN CA
Hamartoma Style!
Cowden BREAST CA, Thyroid CA,
Lhermitte-Duclos (posterior fossa noncancerous brain tumor)
Hamartoma Style!
Cronkhite-Canada Stomach, Small Bowel, Colon,
Ectodermal Stuff (skin, hair, nails, yuck)
Hamartoma Style!
Juvenile Polyps Increased risk for colorectal and gastric cancer (different than
sporadic juvenile polyps -which are typically solitary and benign)
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Stomach Ulcers - Benign vs Malignant
— 1960s style medicine - for the “exam of the future” -
Malignant Benign
Width > Depth Depth > Width
Located within Lumen Project beyond the expected lumen
Nodular, Irregular Edges Sharp Contour
Folds adjacent to ulcer Folds radiate to ulcer
Aunt Minnie: Carmen Meniscus Sign Aunt Minnie: Hampton’s Line
Can be anywhere Mostly on Lesser Curvature
-Gastric Tumors-
GIST (Gastrointestinal Stromal Tumor)
This is the most common mesenchymal tumor of the GI tract (70% in stomach, duodenum is second
most common — colon is actually the least common). Think about this in an old person (it’s rare
before age 40).
Some tricks to know:
• Lymph node enlargement is NOT a classic feature
• Malignant ones tend to be big angry mother fuckers
(>10 cm with ulceration - and possible perforation).
• If they do met - it is typically to the liver.
Carneys Triad
• Having said that, malignancy is rare with these. “Carney’s Eat Garbage”
They typically don’t met anywhere,
which is why lymph node enlargement is uncommon.
Chondroma (pulmonary)
• The association with Carney’s triad Extra Adrenal Pheo
• The association with NF-1 GIST
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- Gastric Tumors 2 - The Final Chapter
Gastric “Cancer" is either Lymphoma (< 5%) or Adenocarcinoma (95%).... Rarely a malignant GIST.
Gastric Adenocarcinoma is usually a disease of an old person (median age 70).
H. Pylori is the most tested risk factor.
Trivia to know: Ulcer Trivia:
• Ulcerated carcinoma (or the “penetrating cancer”) has the Duodenal Ulcers are 2-3x more
look of an advanced cancer common than Gastric Ulcers.
Gastric Ulcers - They have 5%
• Metastatic spread to the ovary is referred to as a chance of being cancer.
Krukenberg Tumor.
Duodenal Ulcers - Are never cancer
(on multiple choice)
• Gastroenterostomy performed for gastric ulcer disease
(old school - prior to PPIs) have a 2x - 6x - increased risk Gastric Ulcers occurs from “altered
for development of carcinoma within the gastric remnant. mucosal resistance”, and favor the
bulb
• Step 1 trivia question: swollen left supraclavicular node = Duodenal Ulcers occur from
Virchow Node.
The Look: Gastric Adenocarcinoma looks very different (usually) than a GIST.
Gastric
Adenocarcinoma
(arrow) is usually a
large, ulcerated,
heterogenous mass
GIST (arrow) is usually
smoothly marginated and
exophytic
Gastric Lymphoma, can be primary (MALT), or
secondary (systemic lymphoma). The stomach is the
most common extranodal site for non-Hodgkin
lymphoma.
Even when extensive, it rarely causes gastric outlet
obstruction. It was classically described as “crossing
the pylorus ”, although since gastric carcinoma is like
10x more common, it is actually more likely to do that.
Has multiple looks and can be big, little, ulcerative,
polypoid, or look like target lesions. It can also look like Lymphoma - Crossing the Pylorus
Linitis Plastica (discussed on the following page).
Trivia: It can rupture with treatment (chemo).
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- Gastric Tumors 3 - A New Beginning
Gastric Cancer is “More Likely” Than Lymphoma to...
•More Likely to Cause Gastric Outlet Obstruction
•More Likely to be in the distal stomach
•More Likely to extend beyond the serosa and obliterate adjacent fat plains
•More Likely to be a focal mass (95% of primary gastric tumors arc adenocarcinoma)
Mets to the Stomach: This is actually very rare.
Melanoma is probably the most common culprit, when it does occur.
This obviously has a variable appearance but multiple button type
soft tissue nodules is probably the most classic look.
Breast (most classic) and Lung are other possibilities -and these are
known for producing a particular look of diffuse infiltration and a
contracted desmoplastic deformity resembling a stiff leather bottle.
This is the so called Linitis Plastica appearance - which can also be
a look for lymphoma as above.
- Misc. Gastric Conditions -
Chronic Aspirin Therapy: “Multiple gastric ulcers” is the buzzword. Obviously this is non-
specific, but some sources say it occurs in 80% of patient’s with chronic aspirin use. As a point of
trivia, aspirin does NOT cause duodenal ulcers.
If you see multiple duodenal ulcers (most duodenal ulcers are solitary) you should think Zollinger-
Ellison.
Areae Gastricae: This is a normal fine reticular pattern seen on double contrast. A favorite
piece of trivia to ask is when does this “enlarge”? The answer is that it enlarges in elderly and
patient’s with H. Pylori. Also it can focally enlarge next to an ulcer. It becomes obliterated by cancer
or atrophic gastritis.
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- Misc. Gastric Conditions - Continued
Menetrier’s Disease: Rare and has a French sounding name, so it’s almost guaranteed to be on
the test. It’s an idiopathic gastropathy, with rugal thickening that classically involves the fundus and
spares the antrum. Bimodal age distribution (childhood form thought to be CMV related). They end
up with low albumin, from loss into gastric lumen.
Essential Trivia: Involves the Hindus, and spares the antrum.
Ram’s Horn Deformity (Pseudo Billroth 1)
Tapering of the antrum causes the stomach to look
like a Ram’s Horn. This is a differential case, and
can be seen with Scarring via peptic ulcers,
Granulomatous Disease (Crohn's, Sarcoid, TB,
Syphilis), or Scirrhous Carcinoma.
Normal
Essential Trivia: The stomach is the
most common GI tract location for sarcoid. Rams Horn - tubular, conical
shape of the distal stomach
Gastric Volvulus
Two Flavors:
• Organoaxial - the greater curvature flips over the lesser
curvature. This is seen in old ladies with paraesophageal
hernias. It’s way more common.
• Mesenteroaxial - twisting over the mesentery. Can cause
ischemia and needs to be fixed. Additionally this type causes
obstruction. This type is more common in kids.
Gastric Diverticulum:
The way they always ask this is by trying to get you to call it an adrenal
mass (it’s most commonly in the posterior fundus).
Gamesmanship: Find the normal adrenal.
Gastric Varices: This gets mentioned in the pancreas section, but I just want to hammer home
that test writers love to ask splenic vein thrombus causing isolated gastric varices. Some sneaky
ways they can ask this is by saying “pancreatic cancer” or “Pancreatitis” causes gastric varices.
Which is true.... because they are associated with splenic vein thrombus. So, just watch out for that,
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- Upper GI Surgical Complications -
Billroth 1 Billroth 2 Roux-en-Y
Pylorus is removed and Partial gastrectomy, Stomach is divided to make a
the proximal stomach is but this time the “pouch.” This gastric pouch is
sewed directly to the stomach is attached attached to the jejunum. The
duodenum. to the jejunum. excluded stomach attaches to
the duodenum as per normal.
Done for Gastric CA, The jejunum is attached to the
Pyloric Dysfunction, or Done for Gastric CA, other jejunum to form the bottom
Ulcers. or Ulcers. of the Y.
Done for patients who have
Less Post Op Gastritis Risks:
spent years steadily gorging on
(relative to Billroth 2)
the "neglected food groups”
• Dumping syndrome
such as the whipped cream
• Afferent loop
group, the congealed group, and
syndrome
the chocolate group. This diet,
• Increased risk of
with combined maintenance of
gastric CA 10-20
the ass in a horizontal position,
year after surgery
has left them with no alternative
but to undergo a dangerous
complex bowel surgery. The
Dumping syndrome is a group of
procedure can also be
symptoms; diarrhea, nausea, and light-
headed / tired after a meal, - caused by performed for gastric cancer as
rapid gastric emptying (seen an alternative to Billroth if the
classically with Billroth 2 and early in primary lesion has directly
the post op period after Roux-en Y). invaded the duodenum or head
of the pancreas.
Insert Taco Bell Joke or a joke about
your wife (or mother in laws cooking). Supposedly these have less
reflux, and less risk of recurrent
My wife's mother is such a prude -
gastric CA.
hates when I use profanity at the
dinner table. Really upsets her. She They are at increased risk for
gets all dramatic. Like if I said the gallstones, and they have all that
word “shit" she hates that.
internal hernia shit.
Well... I'm sorry, that’s what her
cooking tastes like.
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Afferent Loop Syndrome: An uncommon complication post Billroth 2. The most
common cause is obstruction (adhesions, tumor, intestinal hernia) of the afferent. The acute
form may have a closed loop obstruction. The result of this afferent obstruction is the build
up of biliary, pancreatic, and intestinal secretions resulting in afferent limb dilation. The
back pressure from all this back up dilates the gallbladder, and causes pancreatitis. A much
less common cause is if the stomach preferentially drains into the afferent loop.
Jejunogastric Intussusception: This is a rare complication of gastroenterostomy.
The Jejunum herniates back into the stomach (usually the efferent limb) and can cause gastric
obstruction. High mortality is present with the acute form.
Bile Reflex Gastritis: Fold thickening and filling defects seen in the stomach after
Billroth I or II are likely the result of bile acid reflux.
Gastro-Gastric Fistula: This is seen in Roux-en-Y patients who gain weight years
later. The anastomotic breakdown is a chronic process, and often is not painful.
Cancer: With regard to these old peptic ulcer surgeries (Billroths), there is a 3-6 times
increased risk of getting adenocarcinoma in the gastric remnant (like 15 years after the
surgery).
Dumping Syndrome: Different than the “dumping syndrome” associated with late
night Taco Bell. This type of dumping is related to rapid transit of undigested food from the
stomach. Tc-99m Gastric Emptying study is an option to diagnose this. The therapy is typically
conversion of Billroth to Roux-en-Y (and avoiding delicious carbs).
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Small Bowel -
Introduction, the Lost Art, and Historical Perspective:
In the modem age a legitimate working knowledge of the barium fluoroscopic examination is
exceedingly rare. Ever since the late Cretaceous period, when the Oort cloud of comets rained
down upon the dinosaurs of the Yucatan Peninsula legitimate expertise in the field has been
essentially extinct. Now all that remains of this ancient practice is a collection of pretenders
who spend their days in the swamps of fuckery deploying the phrase "Of course I know what
I’m looking at” as subterfuge.
Understanding that this barbaric ancient practice still represents “fair game” on the modem
boards, I set out on a journey to re-discover the lost knowledge. This journey took me across
the globe, into the most primitive comers of the world - as these were the only locations the
modality is still commonly practiced. I was searching for any ancient relic that I could use to
construct a high yield summary. My journey was a treacherous one, necessitating significant
risk to gain favor with the natives. I barely survived several bouts of malaria and one (five)
bouts of gonorrhea in my quest to discover the ancient methods of fluoroscopic interpretation.
Eventually, as is often the case in life - my persistence was rewarded. I was confident I had
finally unearthed a legitimate method of interpretation that I could use to complete the section
on bowel fold patterns.
The method I discovered is as ancient as the practice of barium driven fluoroscopic imaging.
Originally described in the scrolls of Xuthal (a city-state of ancient Valusia) during the
Hyborian Age. The knowledge contained in the scrolls details the chronicle of a low bom son
of a village blacksmith whom after the destruction of the Aquilonian fortress of Venarium,
was struck by wanderlust and began a journey. According to his chronicle - this 20 year
journey saw him encounter skulking monsters, evil wizards, tavern wenches, and beautiful
princesses.
It was during his travels he learned many things, including the ancient 3 step method of the
small bowel follow through - the details of which I will now discuss.
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STEP 1 - Evaluate the Folds
Thin (< 3 mm) • Mechanical Obstruction
• Paralytic Ileus
Straight Folds • Scleroderma
with Dilation • Sprue
• Ischemia
Thick Straight Segmental • Radiation
Folds > 3 mm Distribution • Hemorrhage
• Adjacent Inflammation
• Low Protein
Thick Straight Diffuse
• Venous Congestion
Folds > 3 mm Distribution • Cirrhosis
• Crohn's
Thick Folds Segmental • Infection
with Nodularity Distribution • Lymphoma
• Mets
• Whipples
• Lymphoid Hyperplasia
Thick Folds Diffuse
• Lymphoma
with Nodularity Distribution • Mets
• Intestinal Lymphangiectasia
STEP 2a - Evaluate for Loop Separation with or without Tethering
• Ascites,
• Wall Thickening
Loop Without
(Crohn's, Lymphoma),
Seperation Tethering
• Adenopathy
• Mesenteric Tumors
Tethering looks like
someone is pinching and
Loop With pulling the loops towards
Seperation Tethering the displacing mass.
• Carcinoid
A pearl is that an extrinsic processes will spare the mucosa, intrinsic process will alter the mucosa.
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STEP 2b - If Nodules are Present Evaluate the Distribution and Secondary
Findings To Help Narrow the Differential.
Diffuse micronodules in • Whipples (Tropheryma whipplei)
“Sand Like Nodules”
the jejunum.
• Pseudo-Whipples (MAC Infection)
Uniform
• Lymphoid Hyperplasia
2-4 mm Nodules
Nodules of Larger or • Cancer - think Mets (Melanoma)
Varying Sizes
• Raised islands of mucosa separated by linear
streaks running perpendicular to the lumen of
the bowel.
• These streaks represent ulceration.
“Cobblestoning”
• This findings (especially when combined with
areas of stricture, and loop separation from fat
proliferation) should make you think
Crohn's
STEP 3: Trademark Features:
After comparing this 3 main features - many multiple choice distractors can be eliminated. If necessary
specific features of each disease can be compared - with that discussion to follow.
Bowel is featureless,
atrophic, and has fold
Ribbon Bowel thickening (ribbon-like).
Graft vs Host
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STEP 3: Trademark Features - Continued:
Narrow separation
of normal folds
with mild bowel
dilation.
Hidebound Bowel
Scleroderma
Dilated jejunal
loop with
complete loss of
Moulage sign
jejunal folds -
(tube of wax)
opacified like a
“tube of wax”
Celiac
Jejunum loses folds
to look more like the
normal Ileum, Ileum
gains folds (in the
Fold Reversal right lower
quadrant) to look
more like normal
Jejunum
Celiac
Thread Like Defect in
the Barium Column
A Fucking Worm
Ascaris Suum
(asshole demon worm)
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- Selected Small Bowel Path -
The Target Sign: Clover Leaf Sign:
•Single Target: GIST, Primary This is an Aunt Minnie for Healed Peptic Ulcer of the
Adenocarcinoma, Lymphoma, Duodenal Bulb.
Ectopic Pancreatic Rest, Met
(Melanoma).
•Multiple Target: Lymphoma,
Met (Melanoma)
Whipples: Rare infection (Tropheryma Whippelii)
Just like a stripper - it prefers white men in their 50s. The bug infiltrates the lamina propria with large
macrophages infected by intracellular whippelii bacilli leading to marked swelling of intestinal villi and
thickened irregular mucosal folds primarily in duodenum and proximal jejunum. The buzzword is
“sand like nodules” referring to diffuse micronodules in the jejunum. Jejunal mucosal folds are
thickened. This is another cause of low density (near fat) enlarged lymph nodes.
Pseudo-Whipples: Also an infection - but this time MAI (instead of T. Whippelii). This is seen in
AIDS patients with CD4 < 100. The imaging findings of nodules in the jejunum and retroperitoneal
nodes are similar to Whipples (hence the name). The distinction between the two is not done with
imaging but instead via an acid fast stain (MAC is positive).
Intestinal Lymphangiectasia: Lymphangiectasia results from obstruction to the flow of
lymph from the small intestine into the mesentery. This results in dilation of the intestinal and serosal
lymphatic channels. This can be primary from lymphatic hypoplasia, or secondary from obstruction of
the thoracic duct (or any place in between).
Graft VS Host: Buzzword = Ribbon bowel. It occurs in patients after bone marrow transplant.
It’s less common with modem anti-rejection drugs. Skin, Liver, and GI tract get hit. Small bowel is
usually the most severely affected. Bowel is featureless, atrophic, and has fold thickening (ribbon-
like).
SMA Syndrome: This is an obstruction of the 3rd portion of the duodenum by the SMA (it
pinches the duodenum in the midline). It is seen in patients who have recently lost a lot of weight.
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Celiac Sprue: Small bowel malabsorption of gluten.
High yield points:
• Can cause malabsorption of iron, and lead to iron deficiency anemia.
• Associated with Idiopathic Pulmonary Hemosiderosis (Lane Hamilton Syndrome)
• Increased Risk of bowel wall lymphoma
• Gold standard is biopsy (surprisingly not barium)
• Dermatitis Herpetiformis - some skin thing (remember that from step 1)
Findings (CT / Barium)
• Fold Reversal is the Buzzword (Jejunum like Ileum, Ileum like Jejunum)
• Moulage Sign - dilated bowel with effaced folds (tube with wax poured in it)
• Cavitary Lymph Nodes (low density)
• Splenic Atrophy
Meckel’s Diverticulum / Diverticulitis: This is a congenital true diverticulum of the distal
ileum. A piece of total trivia is that it is a persistent piece of the omphalomesenteric duct. Step 1 style,
“rule of 2s” occurs in 2% of the population, has 2 types of heterotopic mucosa (gastric and pancreatic),
located 2 feet from the IC valve, it’s usually 2 inches long (and 2 cm in diameter), and usually has
symptoms before the child is 2. If it has gastric mucosa (the ones that bleed typically do) it will take up
Tc-99m-Pertechnetate just like the stomach (hence the Meckel’s scan).
High Yield Meckel's Trivia (Regarding Complications)
• Can get diverticulitis in the Meckel's (mimic appendix)
• GI Bleed from Gastric Mucosa (causes 30% of symptomatic cases)
• Can be a lead point for intussusception (seen with inverted diverticulum)
• Can cause Obstruction
Duodenal Inflammatory Disease: You can have fold thickening of the duodenum from
adjacent inflammatory processes of the pancreas or gallbladder. You can also have thickening and fistula
formation with Crohn’s (usually when the colon is the primary site). Primary duodenal Crohn's can
happen, but is super rare. Chronic dialysis patients may get severely thickened duodenal folds which
can mimic the appearance of pancreatitis on barium.
Jejunal Diverticulosis: Less common than colonic diverticulosis, but does occur. They occur
along the mesenteric border. Important association is bacterial overgrowth and malabsorption. They
could show this with CT, but more likely will show it with barium (if they show it at all).
Gallstone Ileus: Not a true ileus, instead a mechanical obstruction secondary to the passage of a
gallstone in the lumen of the bowel. Gallstones access the bowel by eroding through the duodenum
(usually). As you can imagine, only elderly or weak patients (those unworthy of serving in the spartan
infantry) arc susceptible to this erosion.
Classic multiple choice trivia includes the “Rigler's Triad" of pneumobilia, obstruction, and an
ectopic location of a gallstone. The classic trick is to try and get you to say that free air - the
“Rigler's Sign" - is part of the Rigler's Triad (it isn’t) — mumble to yourself “nice try assholes.”
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- Trauma to the Bowel and the Bowel in Trauma -
Bowel Trauma:
Direct Signs
Penetrating Trauma (bullets, knives, light saber, the claws of a • Spilled Oral Contrast
frantic gerbil desperately attempting to escape the rectum, etc...)
• Active Mesenteric Bleed
can yield both direct and indirect signs of injury. It is important
to remember that the absence of direct signs does not exclude
Indirect Signs
injury to the bowel, and the presence of indirect signs docs not
confirm it (although it does raise suspicion in the correct clinical • Fat Stranding
context). This can be tested by asking you what is a direct or • Fluid Layering Along the Bowel
indirect sign, or by showing you a picture containing the findings.
Gamesmanship: Watch the wording on the oral contrast. Yes... oral contrast is helpful when evaluating
possible bowel injury or post surgical leak. However, the type of contrast is important. Barium is always
Bad for any situation where it could possibly end up outside the lumen of the bowel ( “barium gone bad” -
is discussed later in the chapter). So, water soluble contrast is what you want to see. Use your
imagination in how this wording could be used to try and trick you.
Bowel in Trauma — “Shock Bowel” Shock Complex Features Include:
“Hypovolemic Shock Complex”
• Thickened Enhancing Bowel
This is typically seen with severe hypotension , although Loops (small bowel involved
anything that gives you low volume - (cardiac arrest, septic more than larger bowel)
shock, bacterial endocarditis, diabetic ketoacidosis, etc., so on
• On Non-Contrast, bowel loops
and so forth) can also cause it.
may appear denser than the psoas
• Collapsed IVC
Diffuse Intense
• HYPO-enhancement of solid
Bowel Mucosal
organs (liver and spleen)
Enhancement
• Bilateral delayed nephrograms
Flat IVC (arrow)
(persistence nephrograms)
• HYPER-enhancement of the
adrenals
This vs That: Bowel Trauma vs Shock Bowel
Bowel Trauma Shock Bowel
Focal Diffuse
Wall Thickening with Wall Thickening with
High Attenuation Blood in the Submucosa Near Water Attenuation Edema
Mucosa enhances normally (or less than normal) Mucosa demonstrates intense enhancement
Secondary signs of injury (free air, leaked contrast, Other signs of shock
mesenteric hematoma, etc... etc... so on and so forth). (bright adrenals, flat IVC, etc...)
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- Small Bowel Cancer -
Adenocarcinoma: Most common in the proximal small bowel (usually duodenum). Increased
incidence with celiac disease and regional enteritis. Focal circumferential bowel wall thickening in
proximal small bowel is characteristic on CT. The duodenal web docs NOT increase the risk.
Gamesmanship: Adenocarcinoma is more likely to obstruct relative to lymphoma.
Lymphoma: It’s usually the non-Hodgkin
flavor. Patients with celiac, Crohn's, AIDS, and
SLE are higher risk. It can look like anything
(infiltrative, polypoid, multiple nodules etc....).
Key piece of trivia is they usually do NOT
obstruct, even with massive circumferential
involvement. The Hodgkin subtype is more likely
to cause a desmoplastic reaction.
Trivia: Small bowel lymphoma favors the ileum.
Gamesmanship: Obstruction is rare (lymphoma is
a "soft" tumor).
Lymphoma - Circumferential Involvement
Carcinoid: This has an Aunt Minnie look with
a mass + desmoplastic stranding. “Starburst”
appearance of the mesenteric mass with
calcifications. This tumor most commonly occurs
in young adults. The primary tumor is often not
seen. That calcified crap you are seeing is the
desmoplastic reaction. Liver mets are often hyper
vascular. Step 1 style, you don’t get carcinoid
syndrome (flushing, diarrhea) until you met to the
liver. The most common primary location is the
distal ileum (older literature says appendix). The
appendix, has the best prognosis of all GI primary
sites. Systemic serotonin degrades the heart valves
(right sided), and classically causes tricuspid
regurgitation - more on this in the cardiac chapter.
MIBG or Octreotide scans can assist with diagnosis Carcinoid - Sunburst Desmoplastic Rx
and staging - more on this in the nuclear medicine
chapter.
Mets: This is usually melanoma (which hits the small bowel in 50% of fatal cases). You can also
get hematogenous seeding of the small bowel with breast, lung, and Kaposi sarcoma. Melanoma will
classically have multiple targets.
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- Hernias -
Inguinal Hernias: - the most common type of abdominal wall hernia. M > F (7:1)
Direct Indirect
Less common More Common
Medial to inferior epigastric artery Lateral to inferior epigastric artery
Defect in Hesselbach’s Triangle Failure of processus vaginalis to close
NOT covered by internal spermatic fascia Covered by internal spermatic fascia
Femoral: Likely to obstruct. Seen in old ladies. They are medial to the femoral vein,
and posterior to the inguinal ligament (usually on the right).
Obturator Hernia: Another old lady hernia. Often seen in patients with increased
intra-abdominal pressure (Ascites, COPD - chronic cougher). Usually asymptomatic - but
can strangulate.
Lumbar Hernia: Can be superior (Grynfeltt-Lesshaft) through the superior lumbar
triangle, or inferior (Petit) through the inferior lumbar triangle. Superior is more common
than inferior. Otherwise, they are very similar and usually discussed together. Causes are
congenital or acquired (post-surgery).
Spigelian Hernia: The question is
probably the location along the Semilunar
line (“S” for “S”) through the transversus
abdominis aponeurosis close to the level
of the arcuate line.
Littre Hernia: Hernia with a Meckel
Diverticulum in it.
Spigelian Hernia - Causing SBO
Amyand Hernia: Hernia with the
appendix in it.
Richter Hernia: Contains only one wall
of bowel and therefore does not obstruct.
This are actually at higher risk for
strangulation.
Richter - Only one wall herniates
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- Hernias Post Laparoscopic Roux-en-Y Gastric Bypass -
Factors that promote internal hernia after gastric bypass: (1) Laparoscopic over Open - supposedly
creates fewer adhesion, so you have more mobility (2) Degree of weight loss; more weight loss
= less protective, space occupying mesenteric fat.
There are 3 potential sites.
(1) At the defect in the transverse mesocolon, through which the Roux-Loop Passes (if it’s
done in the retrocolic position).
(2) At the mesenteric defect at the enteroenterostomy
(3) Behind the Roux limb mesentery placed in a retrocolic or antecolic position (retrocolic
Petersen and antecolic Petersen type). ** This is the one they will likely ask because it
has an eponym with it.
Internal Hernia: These can be sneaky. The most common manifestation is closed loop
obstruction (often with strangulation). There are 9 different subtypes, of which I refuse to cover.
I will touch on the most common, and the general concept.
General Concept: This is a herniation of viscera through the peritoneum or mesentery. The
herniation takes place through a known anatomic foramina or recess, or one that has been created
post operatively.
Paraduodenal (right or left): This is by far the most common type of internal hernia. They can
occur in 5 different areas, but it’s much simpler to think of them as left or right. Actually, 75%
of the time they are on the left. The exact location is the duodenojejunal junction (“fossa of
Landzert”). Here is the trick; the herniated small bowel can become trapped in a “sac of bowel”
between the pancreas and stomach to the left of the ligament of Treitz. The sac characteristically
contains the IMV and the left colic artery.
The right-sided PDHs are located just behind the SMA and just below the transverse segment of
the duodenum, at the “Fossa of Waldeyer.” The classic setting for right-sided PDHs is non-rotated
small bowel, with normally rotated large bowel.
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- Large Bowel / Rectum -
THIS vs THAT: Crohn's Disease VS Ulcerative Colitis:
Crohn's Disease: Typically seen in a young adult (15-30), but has a second smaller
peak later 60-70. Discontinuous involvement of the entire GI tract (mouth → asshole).
Stomach, usually involves antrum (Ram’s Hom Deformity). Duodenal involvement is rare,
and NEVER occurs without antral involvement. Small bowel is involved 80% of the time,
with the terminal ileum almost always involved (Marked Narrowing = String Sign). After
surgery the “neo-terminal ileum” will frequently be involved. The colon involvement is
usually right sided, and often spares the rectum / sigmoid. Complications include fistulae,
abscess, gallstones, fatty liver, and sacroiliitis.
Crohn's Buzzwords
Squaring of the folds An early manifestation from obstructive lymphedema
Skip lesions Discontinuous involvement of the bowel
Separation of the loops caused by infiltration of the mesentery,
Proud loops
increase in mesenteric fat and enlarged lymph nodes
Irregular appearance to bowel wall caused by longitudinal and
Cobblestoning
transverse ulcers separated by areas of edema
Pseudopolyps Islands of hyperplastic mucosa
Filiform Post-inflammatory polyps - long and worm-like
Found on anti-mesenteric side. From bulging area of normal
Pseudodiverticula
wall opposite side of scarring from disease
Marked narrowing of terminal ileum from a combination of
String-sign
edema, spasm, and fibrosis
Trivia: Inflammatory Bowel Diseases are Associated with an Increased Risk of Melanoma
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Ulcerative Colitis:
Just like Crohn's, it typically occurs in a “young adult” (age 15-40), with a second peak at 60-70.
Favors the male gender. It involves the rectum 95% of the time, and has retrograde progression.
Terminal ileum is involved 5-10% of the time via backwash ileitis (wide open appearance). It is
continuous and does not “skip” like Crohn's. It is associated with Colon Cancer, Primary Sclerosing
Cholangitis, and Arthritis (similar to Ankylosing Spondylitis).
On Barium, it is said that the colon is ahaustral, with a diffuse granular appearing mucosa.
“Lead Pipe” is the buzzword (shortened from fibrosis).
Here is a key clinical point: UC has an increased risk of cancer (probably higher than Crohn's), and it
doesn’t classically have enlarged lymph nodes (like Crohn's does), so if you see a big lymph node in
an UC patient (especially one with long standing disease), you have to think that it might be cancer.
More Common In : Crohn's
Crohn's vs UC -String Sign at IC Valve
More
Path
Common IN
Gallstones Crohn's
Primary
Ulcerative
Sclerosing
Colitis
Cholangitis
Hepatic
Crohn's
Abscess Ulcerative Coliits
Pancreatitis Crohn's -Haustral Loss, Lead Pipe Appearance
THIS vs THftT:
Crohn's UC
Slightly less common in the USA Slightly more common in the USA
Discontinuous “Skips” Continuous
Terminal Ileum - String Sign Rectum
Ileocecal Valve “Stenosed” Ileocecal Valve “Open”
Mesenteric Fat Increased “creeping fat’’ Perirectal fat Increased
Lymph nodes are usually enlarged Lymph nodes are NOT usually enlarged
Makes Fistulae Doesn’t Usually Make Fistulae
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Misc Large Bowel Pathology
Toxic Megacolon: Ulcerative colitis, and to a lesser degree Crohn's, is the primary cause.
C-Diff can also cause it. Gaseous dilation distends the transverse colon (on upright films), and
the right and left colon on supine films. Lack of haustra and pseudopolyps are also seen.
Some people say the presence of normal haustra excludes the diagnosis. Don’t do a barium
enema because of the risk of perforation. Another piece of trivia is that peritonitis can occur
without perforation.
Behcets: Ulcers of the penis and mouth. Can also affect GI tract (and looks like Crohn's) -
most commonly affects the ileocecal region. It is also a cause of pulmonary artery
aneurysms (test writers like to ask that).
Diverticulosis / Diverticulitis: Some trivia worth knowing is that diverticulosis
actually bleeds more than diverticulitis. Right-sided is less common (but is seen in young
Asians). Fistula formation is actually most common with diverticulitis, and can occur to
anything around it (another piece of bowel, the bladder, etc..).
Epiploic Appendagitis / Omental Infarct:
Epiploic appendages along the serosal surface of the colon can torse, most commonly on the
left. There is not typically concentric bowel wall thickening (unlike diverticulitis).
Omental infarction is typically a larger mass with a more oval shape and central low density. It
is more common on the right (ROI - right omental infarct). Both entities are self-limiting.
Appendicitis: The classic pathways are: obstruction (fecalith or reactive lymphoid tissue)
→
mucinous fluid builds up increasing pressure → venous supply is compressed → necrosis
starts → wall breaks down → bacteria get into wall → inflammation causes vague pain
(umbilicus) → inflamed appendix gets larger and touches parietal peritoneum (pain shifts to
RLQ).
It occurs in an adolescent or young adult (or any age). The measurement of 6 mm was
originally described with data from ultrasound compression, but people still generally use it for
CT as well. Secondary signs of inflammation are probably more reliable for CT.
Gamesmanship: In pregnancy MRI without contrast is the test of choice
Appendix Mucocele - Mucinous cystadenomas are the most common mucinous tumor
of the appendix. They produce mucin and can really dilate up and get big. They look similar
to cystadenocarcinomas and can perforate leading to pseudomyxoma peritonei. On ultrasound
the presence of an “onion sign” - layering within a cystic mass - is a suggestive feature of a
mucocele.
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Colonic Volvulus: Comes in several flavors: THIS vs THAT:
Volvulus
• Sigmoid: Most common adult form. Seen in the nursing
home patient (chronic constipation is a predisposing Sigmoid Cecal
factor). This is the “Grandma” volvulus. Buzzword is
Younger
coffee bean sign (or inverted 3 sign). Another less Old Person
Person
common buzzword is Frimann Dahl’s sign - which refers
Points to the Points to the
to 3 dense lines converging towards the site of obstruction.
RUQ LUQ
Points to the RUQ. Recurrence rate after decompression =
50%.
• Cecal: Seen in a younger person (20-40). Associated with people with a “long mesentery.”
More often points to the LUQ. Much less common than sigmoid.
• Cecal Bascule: Anterior folding of the cecum, without twisting. A lot of surgical text
books dispute this thing even being real (they think it’s a focal ileus). The finding is
supposedly dilation of the cecum in an ectopic position in the middle abdomen, without a
mesenteric twist.
Colonic Pseudo-Obstruction (Colonic Ileus, Ogilvie Syndrome): Usually seen after
serious medical conditions and in nursing home patients. It can persist for years, or progress to
bowel necrosis and perforation. The classic look is marked diffuse dilation of the large bowel,
without a discrete transition point.
Diversion Colitis: Bacterial overgrowth in a blind loop through which stool does not pass
(any surgery that does this).
Colitis Cystica: This cystic dilation of the mucous glands comes in two flavors: Superficial or
Profunda (Deep).
Superficial: The superficial kind consists of cysts that are small in the entire colon. It’s associated
with vitamin deficiencies and tropical sprue. Can also be seen in terminal leukemia, uremia, thyroid
toxicosis, and mercury poisoning.
Profunda: These cysts may be large and are seen in the pelvic colon and rectum.
Rectal Cavernous Hemangioma: Obviously very rare. Just know it’s associated
with a few syndromes; Klippel-Trenaunay-Weber, and Blue Rubber Bleb. They might show
you a ton of Phleboliths down there.
Gossypiboma: This isn’t really a GI pathology but it’s an abscess mimic. It’s a retained cotton
product or surgical sponge and it can elicit an inflammatory response.
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- Infections -
Entamoeba Histolytica:
Parasite that causes bloody diarrhea. Can cause liver abscess, spleen
abscess, or even brain abscess. Within the colon it is one of the causes
of toxic megacolon. They arc typically “flask-shaped ulcers” on
endoscopy. With regard to barium, the buzzword is “coned cecum ”
referring to a change in the normal bulbous appearance of the cecum,
to that of a cone. It affects the cecum and ascending colon most
commonly and unlike many other GI infections, spares the terminal
ileum.
Colonic TB:
Typically involves the terminal ileum, and is
another cause of the “coned cecum” Infections
appearance. Causes both ulcers and areas of
that like the Infections that
narrowing. Two other signs: (1) Fleischner
sign - enlarged gaping IC valve, and (2) Duodenum like the
Stierlin sign - narrowing of the TI. (and proximal Terminal Ileum
small bowel)
Colonic CMV:
Seen in patients who are immunosuppressed. Giardia TB
Causes deep ulcerations - which can lead to
perforation. Step 1 question = Cowdry Type A Strongyloides Yersinia
intranuclear inclusion bodies
C-DIff:
Classically seen after antibiotic therapy, the toxin leads to a super high WBC count. CT findings of
the “accordion sign” with contrast trapped inside mucosal folds is always described in review books
and is fair game for multiple choice. The barium findings include thumb printing, ulceration, and
irregularity. Of course it can cause toxic megacolon as mentioned on the prior page.
Neutropenic Colitis (Typhlitis):
Infection limited to the cecum occurring in severe neutropenia.
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-Colon Cancer-
Adenocarcinoma: Common cause of cancer
death (#2 overall). Cancers on the right tend to
bleed (present with bloody stools, anemia). Cancers
on the left tend to obstruct. Apple core is a
buzzword.
Gamesmanship: Large bowel intussusception in
adult = Malignancy
Gamesmanship: Colon likes to Met to the Liver.
Liver Mets will classically be T1 Dark, T2 Mildly
Bright (“evil grey”), heterogenous non-progressive
in enhancement, sometimes target.
Squamous Cell Carcinoma - Apple Core Lesion - Cancer
Occasionally arises in the anus (think HPV).
- Rectal Cancer -
Trivia:
- Nearly always (98%) adenocarcinoma
- If the path says Squamous - the cause was HPV (use your
imagination on how it got there).
- Lower rectal cancer (0-5 cm from the anorectal angle),
have the highest recurrence rate.
- MRI is used to stage - and you really only need T2W
imaging - contrast doesn’t matter
- Stage T3 - called when tumor breaks out of the rectum
and into the perirectal fat. This is the critical stage that
changes management (they will get chemo/rads prior to
surgery).
High Rectal Cancer
- Treated with Low
Anterior Resection (LAR)
- These patients will
maintenance fecal Surgical Treatment is
continence post op classically determined by the
position of the tumor relative
Low Rectal Cancer to the butthole.
- Treated with Abdomino-
Perineal Resection (APR) Most people will use the
- These poor bastards will number “5 cm” above the
end up with colostomies anorectal angle to delineate
“high” vs “low.”
Both surgical approaches are
performed with a total
mesorectal excision (tumor,
nodes, and blood supply).
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- Colon Misc Masses -
Lipomas: The second most common tumor in the colon.
Adenoma - The most common benign tumor of the colon and rectum. The villous adenoma
has the largest risk for malignancy.
McKittrick-Wheelock Syndrome:
This is a villous adenoma that causes a mucous diarrhea leading to severe fluid and electrolyte
depletion.
The clinical scenario would be something like “80 year old lady with diarrhea, hyponatremia,
hypokalemia, hypochloremia... and this” and they show you a mass in the rectum / bowel.
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SECTION 2:
PERITONEAL CAVITY
Pseudomyxoma Peritonei: This is a gelatinous ascites that results from either
(a) raptured mucocele (usually appendix), or intraperitoneal spread of a mucinous neoplasm
(ovary, colon, appendix, and pancreas). It’s usually the appendix (least common is the pancreas).
The buzzword is “scalloped appearance of the liver.” Recurrent bowel obstructions are
common.
Peritoneal Carcinomatosis: The main thing to know regarding peritoneal implants is
that the natural flow of ascites dictates the location of implants. This is why the retrovesical
space is the most common spot, since it’s the most dependent part of the peritoneal cavity.
Omental Seeding/Caking: The omental surface can get implanted by cancer and become
thick (like a mass). The catch-phrase is “posterior displacement of the bowel from the anterior
abdominal wall.”
Primary Peritoneal Mesothelioma: This is super rare. People think
about mesothelioma involving the pleura (and it does 75% of the time), but the
other 25% of the time it involves the peritoneal surface. The thing to know is that
it occurs 30-40 years after the initial asbestosis exposure.
Cystic Peritoneal Mesothelioma: This is the even more rare benign mesothelioma,
that is NOT associated with prior asbestos exposure. It usually involves a women of child-
bearing age (30s).
Mesenteric Lymphoma: This is usually non-Hodgkin lymphoma, which supposedly
involves the mesentery 50% of the time. The buzzword is “sandwich sign.” The typical
appearance is a lobulated confluent soft tissue mass encasing the mesenteric vessels
“sandwiching them.”
Barium Gone Bad
Complications of barium use are rare, but can be very serious. They come in two main flavors:
(1) Peritonitis, and (2) Intravasation.
Barium Peritonitis: This is why you use water soluble contrast anytime you are worried about leak.
The pathology is an attack of the peritoneal barium by the leukocytes which creates a monster
inflammatory reaction (often with massive ascites and sometimes hypovolemia and resulting shock).
If no “real doctor” is available, you should give IV fluids to reduce the risk of hypovolemic shock. The
long term sequela of barium peritonitis is the development of granulomas and adhesions (causing
obstructions and an eventual lawsuit).
Barium Intravasation: This is super rare, but can happen. If barium ends up in the systemic
circulation it kills via pulmonary embolism about 50% of the time. Risk is increased in patients with
inflammatory bowel or diverticulitis (altered mucosa).
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SECTION 3:
Li v er / Bi l i a r y
Bare Area: The liver is covered by visceral peritoneum except at the porta hepatis, bare area, and
the gallbladder fossa. An injury to the “bare area” can result in a retroperitoneal bleed.
Couinaud System: Functional division of the liver into multiple segments. “Functional” is the
key word. Each segment will have its own biliary drainage, inflow, and outflow.
Couinaud System Testable Trivia:
• Right Hepatic Vein Divides 7/8, and 6/5
• Middle Hepatic Vein Divides 4a/8, 4b/5
• Left Hepatic Vein / Fissure for the Ligamentum Teres (falciform) divides 4a/2, 4b/3
• The Portal Vein Divides the Liver into Upper and Lower Segments
• The Caudate Lobe (Segment 1) is unique in that it drains directly to the IVC.
“Cantlie’s Line” divides the liver into a
functional left and right hepatic lobes.
This line runs from the IVC to the middle of the
gallbladder fossa.
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Caudate Lobe: The caudate lobe (segment 1) has a direct connection to the IVC through
it’s own hepatic veins, which do not communicate with the primary hepatic veins.
Additionally, the caudate is supplied by branches of both the right and left portal veins - which
matters because the caudate may be spared or hypertrophied as the result of various
pathologies such as Budd Chiari, etc... (as discussed later in the chapter).
Additional Anatomic Trivia:
Trivia: Along the same lines of anatomy explaining pathology, the intra-hepatic course of the
right portal vein is longer than the left, which is why it is more susceptible to fibrosis (this is
why the right liver shrinks, and the left liver grows in cirrhotic morphology).
Trivia: Most common vascular variant = Replaced right hepatic (origin from the SMA)
Trivia: Most common biliary variant - Right posterior segmental into the left hepatic duct.
Normal MRI Signal Characteristics: I like to think of the spleen as a bag of water/
blood (T2 bright, T1 dark). The pancreas is the “brightest T1 structure in the body” because it
has enzymes. The liver also has enzymes and is similar to the pancreas (T1 Brighter, T2
darker), just not as bright as the pancreas
Fetal Circulation: The fetal circulation anatomy is high yield anatomic trivia.
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Classic Ultrasound Anatomy:
There are 4 high yield looks, that are classically tested with regard to ultrasound anatomy. In years
past, these were said to have been shown by oral boards examiners (likely the same dinosaurs
writing the exam).
Trivia:
Pancreas
should be
more
echogenic
than liver
S = Splenic Vein, SMA = SMA, LRV = Left Renal Vein,
A- Aorta, VB = Vertebral Body, IVC = IVC
RHA - Right Hepatic Artery, CBD = Common Bile Duct, PV = Portal Vein
Mickey Mouse Sign: (1) Bile Duct, (2)
Hepatic Artery, (3) Portal Vein
Fat in the Falciform Ligament /
Ligamentum Teres
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Promethean Dialogue on the Liver -
A discourse on the liver, cirrhosis, portal HTN, and the development of HCC
My idea is that by leading with a discussion of normal physiology, and the changes that
occur with diffuse liver injury, that a lot of the processes and changes that occur with
cirrhosis will make more sense (and be easier to remember). If you are in a rush to cram for
the test just skip this discussion and move on to the charts. If you have more time, I think
understanding the physiology is worthwhile.
Hepatocyte injury can occur from a variety of causes including viruses, alcohol, toxins
(alfatoxins i.e. peanut fungus), and nonalcoholic fatty liver disease. These injuries result in
increased liver cell turnover, to which the body reacts by forming regenerative nodules. The
formation of regenerative nodules is an attempt by the liver not just to replace the damaged
hepatocytes but also to compensate for lost liver function. In addition to activation of
hepatocytes, stellate cells living in the space of Disse become active and proliferate
changing into a myofibroblast -like cell that produces collagen. This collagen deposition
causes fibrosis.
The development of fibrosis first puts the squeeze on the
right portal vein (which usually has a longer intrahepatic Another consequences of the
course). This causes atrophy of segments 6 and 7, and Longer Right Portal Vein Course
is that Hepatic Abscess (often
compensatory hypertrophy of the caudate, segments 2 from ascending hematogenous
and 3. Because of these changes, some people will try sources) nearly always (75%+)
and use a caudate / right lobe ratio (C/RL > 0.75 is 99% involves the right hepatic lobe.
specific) to call cirrhosis.
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All this squeezing can lead to portal hypertension. Portal hypertension is usually the result of
increased hepatic resistance from pre-hepatic (portal vein thrombosis, tumor compression),
hepatic (cirrhosis, schistosomiasis) and post hepatic (Budd-Chiari) causes. Obviously, most
cases are hepatic with schistosomiasis being the most common cause world-wide, and EtOH
cirrhosis being the most common cause in the US. Once portal venous pressure exceeds
hepatic venous pressure by 6-8 mmHg - portal hypertension has occurred (variceal bleeding
+ ascites around > 12). In reaction to this increased resistance offered by the liver, collaterals
will form to decompress the liver by carrying blood away from it. These tend to be
esophageal and gastric varices. As a point of trivia, in pre-hepatic portal hypertension,
collaterals will form above the diaphragm and in the hepatogastric ligaments to bypass the
obstruction.
The liver has a dual blood supply (70% portal, 30% hepatic artery) with compensatory
relationships between the two inflows; arterial flow increases as portal flow decreases. This
helps explain the relationship between these two vessels with regard to Doppler US. As
fibrosis leads to portal hypertension, velocity in the hepatic artery increases.
Another phenomenon related to this “hepatic arterial buffer response” is the THAD. These
Transient Hepatic Attenuation Differences are typically seen in the arterial / early portal phase
- NOT on the equilibrium / delayed phases (hence the word “transient”). The easiest way to
think about them is that they are focal “arterial buffer responses.” In other words, in that tiny
little spot right there the liver feels like there isn’t enough portal flow, so it responses by
increasing the arterial flow. This can happen for several reasons:
• Cirrhosis: A bunch of scar / fibrosis deforms the hepatic sinusoids compressing the tiny
little portal veins (think about arteries and veins in the neck or groin - pressure will
compress the vein first) - people call this “shunting.” This is most typical in the subcapsular
region.
• Clot: Venous blood flow could be compromised from a clot in a portal vein branch (these
enhancement patterns are typically larger, wedge shaped, and extend towards the periphery).
• Mass (B9 or Malignant): This can occur from two primary mechanisms. 1 - You could have
the direct mass effect from the mass smashing the veins. 2 - The tumor could be recruiting /
up-regulating arterial flow (VEGF etc...).
• Abscess / Infection: Also probably a mixed mechanism. Some direct mass effect, but also
some element of “hyperemia” - causing a “siphon effect.” For clarity we aren’t just talking
liver abscess here, cholecystitis can also have this region effect.
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The perfusion related changes you see with cirrhosis aren’t just local, you can also have global
patterns. Since the fibrosis blockade takes place at the level of the central lobular vein (into
sinusoids), flow remains adequate for the central zones of the liver, but not for the peripheral
zones. The arterial response produces enhancement of the peripheral subcapsular hepatic
parenchyma with relative hypodensity of the central perihilar area. The consequent CT pattern
is referred to as the “central-peripheral” phenomenon.
Sometimes you will see reversal of flow (hepatofugal - directed away from the liver). As an
aside, apparently “fugal” is latin for “flee.” So the blood is fleeing the liver, or running away
from it. Reversed flow in the portal system is seen in cirrhosis between 5-25% of the time.
BUT Why does the portal vein reverse flow instead of just clotting off in the
Prometheus!? setting of high resistance to inflow?
The answer has to do with the unique dual hepatic blood supply (70% P / 30% A). As
mentioned above, in cirrhosis, the principal area of obstruction to blood flow is believed to be
in the outflow vessels (the hepatic venules and distal sinusoids). The outflow obstruction also
partially shits on the hepatic artery, causing increased resistance as well. So why doesn’t the
artery clot or reverse ? The difference is that the portal system can decompress through the
creation of collaterals, and the artery cannot. So the artery does something else, it opens up
tiny little connections to the portal system. The enlargement of these tiny communications has
been referred to as “parasitizing the portosystemic decompressive apparatus.” If the
resistance is high enough, hepatic artery inflow will be shunted into - and can precipitate
hepatofugal flow in the portal vein. So, in patients with hepatofugal flow in the main portal
vein or intrahepatic portal vein branches, the shunted blood comes from the hepatic artery.
This is the long answer for why cirrhotic changes can lead to THADs, and why these cirrhosis
related THADs tend to be subcapsular.
With increased resistance in the liver to the portal circulation, you also start to have colonic
venous stasis (worse on the right). This can lead to “Portal Hypertensive Colopathy, ” which
is basically an edematous bowel that mimics colitis. Why is it worse on the right? The short
answer is that collateral pathways develop more on the left (splenorenal shunt, short gastrics,
esophageal varices), and decompress that side. The trivia question is that it does resolve after
transplant. The same process can affect the stomach “Portal Hypertensive Gastropathy”
causing a thickened gastric wall on CT, as well as cause upper GI bleeding in the absence of
varices.
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Earlier I mentioned that hepatocytes react to injury by turning into regenerative nodules. This is
how multi-focal HCC starts. Regenerative nodules → Dysplastic nodules (increased size and
cellularity) → HCC. As this process takes place, the nodule changes from preferring to drink
portal blood to only wanting to drink arterial blood. This helps explain why HCC has arterial
enhancement and rapid washout. The transformation also follows a progression from T2 dark
(regenerative) → T2 bright (HCC). A buzzword is “nodule within nodule” where a central bright
T2 nodule has a T2 dark border. This is concerning for transformation to HCC.
Regenerative Dysplastic HCC
Contains Iron Contains Fat, Glycoprotein
T1 Dark, T2 Dark T1 Bright, T2 Dark T2 Bright
Does NOT Enhance Usually Does NOT Enhance Does Enhance
Another thing that happens with hepatocarcinogenesis is the decrease in a thing called the OATP
bile uptake transporter. This is the transporter that moves biliary contrast agents (example =
Eovist) into the cells. It’s the reason normal liver cells look bright on the delayed phase when
using a hepatocyte specific agent. It’s also the reason FNHs look super bright on delayed images
as they are basically hypertrophied hepatocytes. As hepatocytes become cancer they lose
function in this transporter and become dark on the delayed phase. The exception (highly
testable) is the well differentiated HCC which retains OATP function and is therefore bright on
the 20 min delayed Eovist sequence.
There is one last concept that I wanted to “squeeze” in. The squeezing that causes portal
hypertension also squeezes out most benign liver lesions (cysts, hemangiomas). So, lesions in a
cirrhotic liver should be treated with more suspicion.
Hepatic Contrast Phase Timing & Window
Arterial Phase Portal Venous Phase “Liver Window”
- 25-30 seconds after injection - 70 seconds Center: 100 Width: 200
This ("Late Arterial”) is the most
critical phase for HCC evaluation.
You can recognize this timing as
contrast in the hepatic artery and
portal vein (but none in the
hepatic veins).
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- MR Contrast - Hepatobiliary Considerations -
I want to clarify a few issues that can be confusing (and may also be testable).
How they work: Gadolinium (which is super toxic) is bound to some type of chelation
agent to keep it from killing the patient. The shape and function of the chelation agent
determine the class and brand name. The paramagnetic qualities of gadolinium cause a local
shortening of the T1 relaxation time on neighboring molecules (remember short T1 time =
bright image).
Types of Agents: I want you to think about MRI contrast in two main flavors:
(1) Extracellular and (2) Hepatocyte Specific.
Extracellular: These are nonspecific agents that are best thought of as Iodine contrast for
CT. They stay outside the cell and are blood flow dependent (just like CT contrast). The
imaging features in lesions will be the same as CT - although the reason they look bright is
obviously different - CT contrast increases the density (attenuation), MR contrast shortens the
T1 time locally - which makes T1 brighter. The classic imaging set up is a late hepatic arterial
phase (15-30 seconds), portal venous phase (70 seconds), and a hepatic venous or interstitial
phase (90 seconds - 5 mins) - just like CT.
Classic Example of a Non-Specific Extracellular Agent = Gd-DTPA (Magnevist)
Hepatocyte Specific: Certain chelates are excreted via the bile salt pathway. In other
words, they arc taken up by normal hepatocytes and excreted into the bile. This gives you great
contrast between normal hepatocytes and things that aren’t normal hepatocytes (cancer). The
20 min delay is the imaging sequence that should give you a homogenous bright liver (dark holes
are things that don’t contain normal liver cells / couldn’t drink the contrast). The problem is that
it’s pretty non-specific with a handful of benign things still taking it up (classical example is
FNH), and at least one bad thing taking it up (well-differentiated HCC). Plus, a handful of
benign things won’t take it up (cysts, etc..). There are at least three good reasons to use this
kind of agent: (1) it’s great for proving an FNH is an FNH - as most lesions won’t hold onto the
Gd at 20 mins, (2) it’s great for looking for bile leaks, and (3) once you’ve established a
baseline MRI (characterized all those benign lesions) it’s excellent for picking up new mets
(findings black holes on a white background is easy).
Classic Example of a Hepatocyte Specific Agent = Gd-EOB-DTPA (Eovist).
Is Eovist a pure Hepatocyte Specific Agent ? Nope - It also acts like a non-specific extracellular
agent early on (although less intense). About 55% is excreted into the bile - and gives a nice
intense look at 20 mins.
What about Gd-BOPTA (Multihance)? This is mostly an extra-cellular agent, but has a small
amount (5%) of biliary excretion. The implication is that you can use Multihance to look for a
bile leak you just have to wait longer (45 mins - 3 hours) for the Gd to accumulate.
What about Manganese instead of Gd? This is the old school way to do biliary imaging. It
works the same as Gd - by causing T1 shortening.
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- Liver Masses -
Hemangioma: This is the most common benign liver neoplasm. Favors women 5:1.
They may enlarge with pregnancy. On US will be bright (unless it’s in a fatty liver, than can
be relatively dark). On US, flow can be seen in vessels adjacent to the lesion but NOT in the
lesion. On CT and MRI tends to match the aorta in signal and have “peripheral nodular
discontinuous enhancement”. Should totally fill in by 15 mins. Atypical hemangioma can
have the “reverse target sign.”
Trivia: A hemangioma can change its sonographic appearance during the course of a single
examination. No other hepatic lesion is known to do this.
Hemangioma US Pearls:
• Need to core for biopsy, FNA does not get enough tissue (only blood)
• Hyperechoic (65%)
• Enhanced thru transmission is common
• NO Doppler flow inside the lesion itself
• Atypical appearance - hyperechoic periphery, with hypoechoic center (reverse target)
• Calcifications are extremely rare
Focal Nodular Hyperplasia (FNH): This is the second most common benign liver
neoplasm. Believed to start in utero as an AVM. It is NOT related to OCP use. It is
composed of normal hepatocytes, abnormally arranged ducts, and Kupffer cells
(reticuloendothelial cells). May show spoke wheel on US Doppler. On CT, should be
“homogenous” on arterial phase. Can be a “Stealth” lesion on MRI - T1 and T2 isointense.
Can have a central scar. Scar will demonstrate delayed enhancement (like scars do). Biopsy
Trivia: You have to hit the scar, otherwise path results will say normal hepatocytes. Sulfur
Colloid is always the multiple choice test question (reality is that it’s only hot 30-40%).
Unlike hepatic adenomas, they are not related to the use of birth control pills, although as a
point of confusing trivia and possibly poor multiple choice test question writing, birth control
pills may promote their growth.
T1 - Stealth T2 - Stealth Arterial Homogenous Enhancement
-Also has a Central Scar
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Hepatic Adenoma: Usually a solitary lesion seen in a female on OCPs. Alternatively could be
seen in a man on anabolic steroids. When it’s multiple you should think about glycogen storage
disease (von Gierke) or liver adenomatosis. No imaging methods can reliably differentiate hepatic
adenoma from hepatocellular carcinoma. Rarely, they may degenerate into HCC after a long period
of stability. They often regress after OCPs are stopped. Their propensity to bleed sometimes makes
them a surgical lesion if they won’t regress.
Gamesmanship: Signal Drop Out with in and out of phase can be used to show fat
Trivia:
Q: Most common location for hepatic adenoma (75%)
A: Right Lobe liver
Management: You stop the OCPs and re-image, they should get smaller. Smaller than 5 cm,
watch them. Larger than 5 cm they often resect because (1) they can bleed and (2) they can rarely
turn into cancer.
HCC: Occurs typically in the setting of cirrhosis and chronic liver disease; Hep B, Hep C,
hemochromatosis, glycogen storage disease, Alpha 1 antitrypsin. AFP elevated in 80-95%. Will
often invade the portal vein, although invasion of the hepatic vein is considered a more “specific
finding.”
“Doubling Time ” - the classic Multiple Choice Question. This is actually incredibly stupid to
ask because there are 3 described patterns of growth (slow, fast, and medium). To make it an
even worse question, different papers say different stuff. Some say: Short is 150 days, Medium
to 150-300, and Long is >300. I guess the answer is 300 - because it’s in the middle. Others
define medium at around 100 days. A paper in Radiology (May 2008 Radiology, 247, 311-330)
says 18-605 days. The real answer would be to say follow up in 3-4.5 months.
Other Random Trivia: HCCs like to explode and cause spontaneous hepatic bleeds.
Fibrolamellar Subtype of HCC: This is typically seen in a younger patients (< 35)
without cirrhosis and a normal AFP. The buzzword is central scar. The scar is similar to the one
seen in FNH with a few differences. This scar does NOT enhance, and is T2 dark (usually). As a
point of trivia, this tumor is Gallium avid. This tumor calcifies more often than conventional
HCC.
THIS vs THAT: THIS vs THAT:
Classic HCC vs Fibrolamellar HCC Central Scars of FNH and Fibrolamellar HCC
HCC FL HCC FNH FL HCC
Cirrhosis No Cirrhosis T2 Bright T2 Dark (usually)
Older (50s-60s) Young (30s)
Enhances on Delays Does NOT enhance
Calcifies
Rarely Calcifies Sometimes Mass is Sulfur Colloid Mass is Gallium Avid
Avid (sometimes)
Elevated AFP Normal AFP
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Cholangiocarcinoma: Where HCC is a cancer of Gamesmanship - They could
the hepatocyte, cholangiocarcinoma is a cancer of the bile tell you the dude has ulcerative
duct. Cholangiocarcinoma believes in nothing Lebowski. colitis, as a way to infer that he
also has PSC.
It flicks you up, it takes the money (prognosis is poor).
Who gets it? The most classic multiple choice scenario
would be an 80 year old man, with primary sclerosing Buzzword = “Painless
cholangitis - PSC (main risk factor in the West), recurrent Jaundice.” (just like
pancreatic head CA)
pyogenic "oriental’ cholangitis (main risk factor in the
East), Caroli Disease, Hepatitis, HIV, history of
cholangitis, and fucking Liver Worms (Clonorchis).
Oh who also had a semi-voluntary cerebral angiogram
THIS vs THAT:
performed by a Nazi with a cleft asshole (in 1930s
Germany, Thorotrast was the preferred angiographic • HCC = Invades the Portal Vein
contrast agent). • Cholangiocarcinoma = Encases the
Portal Vein
What does it look like? It is variable and the
described subtypes overlap. The easiest way to
conceptualize this thing is as a scar generating cancer.
Fibrosis (scar) is the main thing you are seeing - Classic Features:
either primarily as a mass that enhances on delayed
imaging (just like scar in the heart), or secondarily • Delayed Enhancement
through the desmoplastic pulling of the scar (example • Peripheral Biliary Dilation
• Liver Capsular Retraction
capsular retraction and ductal dilation). The dilation
• NO tumor capsule
of ducts is most likely to be shown as unilateral and
peripheral, although if the lesion is central the entire
system can obstruct.
Klatskin Tumor: Cholangiocarcinoma that occurs at the bifurcation of the right and left
hepatic ducts. It’s usually small but still causes biliary obstruction (“shouldering / abrupt
tapering” on MRCP). These things are mean as cat shit. It is a “named” subtype, so that
increases the likelihood of it showing up on a multiple choice exam.
Staging Pearls: There are like 3-4 major systems, each one has rules on the subtype
(intrahepatic, extrahepatic, hilar/Klastskin), and honestly resectability is incredibly variable
depending on how much of a gun slinger the surgeons at your institution are. This
combination of factors makes specifics nearly untestable (under “fair” conditions). Having
said that, here are some potentially testable pearls:
• Proximal extent of involvement is a key factor for surgical candidacy (more = bad).
• Atrophy of a lobe implies biliary +/- vascular involvement of that lobe (imaging often
underestimates disease burden).
• Typically combinations of bilateral involvement (veins on the right, ducts on the left - vice
versa, etc., etc... etc... ) is bad news.
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Hepatic Angiosarcoma: This used to be the go to for thorotrast questions. Even
though everyone who got thorotrast died 30 years ago, a few dinosaurs writing multiple
choice test questions still might ask it. Hepatic Angiosarcoma is very rare, although
technically the most common primary sarcoma of the liver. It is associated with toxic
exposure - arsenic use (latent period is about 25 years), Polyvinyl chloride exposure,
Radiation, and yes... thorotrast. Additional trivia, is that you can see it in Hemochromatosis
and NF patients.
It’s usually multifocal, and has a propensity to bleed.
Biliary Cystadenoma Uncommon benign cystic neoplasm of the liver. Usually seen in
middle aged women. Can sometimes present with pain, or even jaundice. They can be
unilocular or multilocular and there are no reliable methods for distinguishing from biliary
cystadenocarcinoma (which is unfortunate).
Mets to the Liver: If you see mets in the liver, first think colon. Calcified mets are
usually the result of a mucinous neoplasm (colon, ovary, pancreas).
With regard to ultrasound: Hyperechoic mets are often hypervascular (renal, melanoma,
carcinoid, choriocarcinoma, thyroid, islet cell). Hypoechoic mets are often hypovascular
(colon, lung, pancreas).
“Too Small To Characterize” - even in the setting of breast cancer (with no definite hepatic
mets) tiny hypodensities have famously been shown to be benign 90-95% of the time.
Lymphoma: Hodgkins lymphoma involves the liver 60% of the time (Non Hodgkins is
around 50%), and may be hypoechoic.
Kaposi Sarcoma: Seen in patients with AIDS. Causes diffuse periportal hypoechoic
infiltration. Looks similar to biliary duct dilation.
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Benign Liver Masses
Ultrasound CT MR Trivia
Kasabach-
Hyperechoic Merritt; the
Peripheral
with Rare in sequestration
Nodular
Hemangioma increased T2 Bright of platelets
Discontinuous Cirrhotics
through from giant
Enhancement
transmission cavernous
hemangioma
Bright on
“Stealth
Homogenous Delayed
Spoke Lesion - Central
FNH Arterial Eovist
Wheel Enhancement Iso on T1 Scar
(Gd-EOB-
and T2”
DTPA)
Fat OCP use,
Can
Hepatic Containing Glycogen
Variable Variable explode
Adenoma on In/Out Storage
and bleed
Phase Disease
Unlike
renal
Hepatic T1/T2 Tuberous
Hyperechoic Gross Fat AML, 50%
Angiomyolipoma Bright Sclerosis
don’t have
fat
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- Congenital Liver -
Cystic Kidney Disease (both AD and AR): Patient’s with AD polycystic kidney disease
will also have cysts in the liver. This is in contrast to the AR form in which the liver tends to have
fibrosis.
Hereditary Hemorrhagic Telangiectasia (Osler-Weber-Rendu)
Autosomal dominant disorder characterized by multiple AVMs in the liver and lungs. It
leads to cirrhosis and a massively
Trivia: The lung AVMs set you up for brain abscess.
- Liver Infections -
Infection of the liver can be thought of as either viral, abscess (pyogenic or amoebic), fungal,
parasitic, or granulomatous. As previously mentioned, the long intra-hepatic course of the right
portal vein results in most hematogenous infection favoring the right hepatic lobe.
Viral: Hepatitis which is chronic in B and C, and
acute with the rest. A point of trivia is that HCC in the Infection Buzzwords
setting of hepatitis can occur in the acute form of
Hep B (as well as chronic). Obviously, chronic hep C Viral Hepatitis Starry Sky (US)
increases risk for HCC. On ultrasound the “starry sky”
appearance can be seen. Although, this is non-specific Pyogenic Abscess Double Target (CT)
and basically just the result of liver edema making the
fat surrounding the portal triads look brighter than Candida Bull’s Eye (US)
normal.
“Extra Hepatic
Amoebic Abscess
Pyogenic: These can mimic cysts. For the purpose Extension”
of multiple choice, a single abscess is Klebsiella, and Water Lily, Sand Storm
multiple are E. Coli. The presence of gas is highly Hydatid Disease
suggestive of pyogenic abscess.
“Double Target” sign with central low density, rim Schistosomiasis Tortoise Shell
enhancement, surrounded by more low density is the
classic sign of a liver abscess on CT.
Next Step Amebic Abscess: A special situation (potentially testable) is the amebic abscess in the left
lobe. Those needs to be emergently drained (they can rupture into the pericardium).
Fitz-Hugh-Curtis Syndrome - This syndrome is seen exclusively
in women of questionable moral standard (“free spirits”). It manifests on
multiple choice exams in the setting of known pelvic inflammatory
disease (Gonococcal salpingitis and/or Chlamydia infection), with right
upper quadrant pain.
The classic imaging features are enhancement of the anterior liver
capsule, perihepatic ascites, and peritoneal Septations. They could show
you a tubo-ovarian abscess in the pelvis to cue you in on the
excessively promiscuous behaviors this young lady has been engaging in.
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- Diffuse liver Processes -
Fatty Liver: Very common in America. Can be focal (next to gallbladder or ligamentum teres),
can be diffuse, or can be diffuse with sparing. You can call it a few different ways.
For CT: If it’s a non-contrast study, 40 HU is a slam dunk. If it’s contrasted, some people say you can
NEVER call it. Others say it’s ok if (a) it’s a good portal venous phase (b) the HU is less than 100,
and (c) it’s 25 HU. less than the spleen.
On US: If the liver is brighter than the right kidney you can call it. Hepatosteatosis is a fat liver.
NASH (hepatitis from a fat liver) has abnormal LFTs.
On MRI: Two standard deviation difference between in and out of phase imaging. Remember the drop
out is on the out of phase images (india ink ones - done at T.E 2.2 ms - assuming 1.5T).
Fuckery: This signal drop out assumes there is more water than fat in the liver. As such, the degree
of signal loss is maximum when the fat infiltration is 50% (exactly 1:1 signal loss). When the
percentage of fat grows larger than 50% you will actually see a less significant signal loss on out of
phase imaging, relative to that maximum 50%.
What causes it? McDonalds, Burger King, and Taco Bell. Additional causes include chemotherapy
(breast cancer), steroids, cystic fibrosis.
Hemochromatosis: Iron overload. They can show this two main ways:
(1) The first is just liver and spleen being T1 and T2 dark.
(2) The second (and more likely) way this will be shown is in and out of phase changes the opposite
of those seen in hepatic steatosis. Low signal on in phase, and high signal on out of phase.
(“Iron on In-phase”)
Watch out now — this is the opposite of the fat drop out
**FAT - Drop out on OUT of phase (india ink one - T.E. 2.2 ms) -1.5 T
**IRON - Drop out on IN phase (non india ink one - T.E. 4.4 ms) - 1.5 T
The second main piece of trivia is to tell primary vs
secondary. Hemochromatosis
Primary is the inherited type, caused by more GI uptake, Primary Secondary
with resulting iron overload. The key point is the pancreas
is involved and the spleen is spared. Genetic - Acquired -
increased chronic illness,
Secondary is the result of cither chronic inflammation or absorption and multiple
multiple transfusions. The body reacts by trying the “Eat transfusions
the Iron,” with the reticuloendothelial system. The key
point is the pancreas is spared and the spleen is not. Liver, Pancreas Liver, Spleen
“Primary = Pancreas” , “Secondary = Spleen” Heart, Thyroid,
Pituitary
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Budd Chiari Syndrome: Classic multiple choice scenario is a pregnant woman, but can
occur in any situation where you are hypercoagulable (most common cause is idiopathic). The
result of hepatic vein thrombosis.
The characteristic findings of Budd-Chiari syndrome include hepatic venous outflow
obstruction, intrahepatic and systemic collateral veins, and large regenerative (hyperplastic)
nodules in a dysmorphic liver. The caudate lobe is often massively enlarged (spared from
separate drainage into the IVC). In the acute phase, the liver will show the classic “flip-flop
pattern ” on portal phase with low attenuation centrally, and high peripherally. The liver has
been described as “nutmeg” with an inhomogeneous mottled appearance, and delayed
enhancement of the periphery of the liver.
Who gets a “Nutmeg Liver” ??? Arterial: Central Enhancement
• Budd Chiari Peripheral Minimal
• Hepatic Veno-occlusive disease
• Right Heart Failure (Hepatic Congestion) Portal V: Central Washout
• Constrictive Pericarditis Peripheral Enhancement
Regenerative (hyperplastic) nodules can be difficult to distinguish from multifocal
hepatocellular carcinoma. They are bright on T1 and typically dark or iso on T2. Multiple big
(> 10 cm) and small (< 4 cm) nodules in the setting of Budd-Chiari suggest a benign process. T2
dark also helps (HCC is usually T2 bright).
Presentation can be acute or chronic. Acute from thrombus into the hepatic vein or IVC. These
guys will present with rapid onset ascites. Chronic from fibrosis of the intrahepatic veins,
presumably from inflammation.
Who gets massive caudate lobe hypertrophy???
• Budd Chiari
• Primary Sclerosing Cholangitis
• Primary Biliary Cirrhosis
Hepatic Veno-occlusive Disease: This is a form of Budd Chiari that occurs from
occlusion of the small hepatic venules. It is endemic in Jamaica (from Alkaloid bush tea). In
the US it’s typically the result of XRT and chemotherapy. The main hepatic veins and IVC will
be patent, but portal waveforms will be abnormal (slow, reversed, or to-and-fro).
Passive Congestion: Passive hepatic congestion is caused by stasis of blood within the
liver due to compromise of hepatic drainage. It is a common complication of congestive heart
failure and constrictive pericarditis. It is essentially the result of elevated CVP transmitted from
the right atrium to the hepatic veins.
Findings include:
• Refluxed contrast into the hepatic veins
• Increased portal venous pulsatility
• Nutmeg liver
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- Misc Liver Conditions -
Portal Vein Thrombosis: Occurs in hypercoagulable states (cancer, dehydration,
etc...). Can lead to cavernous transformation, with the development of a bunch of
serpiginous vessels in the porta hepatis which may reconstitute the right and left portal
veins. This takes like 12 months to happen (it proves portal vein is chronically occluded).
Pseudo Cirrhosis: Treated breast cancer mets to the liver can cause contour changes
that mimic cirrhosis. Specifically, multifocal liver retraction and enlargement of the caudate
has been described. Why this is specific for breast cancer is not currently known, as other
mets to the liver don’t produce this reaction.
Cryptogenic Cirrhosis: Essentially cirrhosis of unknown cause. Most of these cases
are probably the result of nonalcoholic fatty liver disease.
Liver Transplant: The liver has great ability to regenerate and may double in size in as
little as 3 weeks, making it ideal for partial donation. Hepatitis C is the most common
disease requiring transplantation (followed by EtOH liver disease and cryptogenic
cirrhosis). In adults, right lobes (segments 5-8) are most commonly implants. This is the
opposite of pediatric transplants, which usually donates segments 2-3. The modem surgery
has four connections (IVC, artery, portal vein, CBD).
Contraindications include, extrahepatic malignancy, advanced cardiac disease, advanced
pulmonary disease, or active substance abuse. Portal HTN is NOT a true contraindication
although it does increase the difficulty of the surgery and increase mortality.
Normal Transplant US Syndrome of Impending Thrombosis
• Normal Doppler should have a 3-10 days post transplant
RAPID systolic upstroke (1st) Initial Normal Waveform
• Diastolic → Systolic in less (2nd) No diastolic flow
than 80 msec (0.08 seconds) (3rd) Dampening Systolic flow
• Resistive Index is Normally Tardus Parvus
between 0.5 - 0.7 RI < 0.5
• Hepatic Artery Peak Velocity (4 ) Loss of Hepatic Waveform
th
should be < 200 cm/sec
As mentioned before, the normal liver gets 70% blood flow from the portal vein, making it
the key player. In the transplanted liver, the hepatic artery is the king and is the primary
source of blood flow for the bile ducts (which undergo necrosis with hepatic artery failure).
Hepatic artery thrombosis comes in two flavors: early (< 15 days), and later (years). The
late form is associated with chronic rejection and sepsis.
Trivia: Tardus Parvus is more likely secondary to stenosis than thrombosis
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-Biliary-
THIS vs THAT: Portal Venous Gas vs Pneumobilia —These are the two patterns of
branching air in the liver. The classic way to distinguish between the two is Central (Pneumobilia) vs
Peripheral (PVG). The way to remember this is that bile is draining out of the liver into the bowel - so
it is flowing towards the porta-hepatis and should be central. Portal blood, on the other hand, is being
pumped into the liver - so it will be traveling towards the periphery. The potential trivia question is
how peripheral is peripheral — and that is 2 cm. Within 2 cm of the liver capsule = portal venous gas.
Other things to remember - gas in the bile is usually related to a prior procedure (anything that fucks
with the sphincter of Oddi). Gas in the portal system can be from lots of stuff (benign things like
COPD or bad things - the most classic being bowel necrosis ~look for pneumatosis*).
Jaundice: You always think about common duct stone, but the most common etiology is actually
from a benign stricture (post traumatic from surgery or biliary intervention).
Bacterial Cholangitis: Hepatic abscess can develop secondary to cholangitis, usually as the
result of stasis (so think stones). The triad of jaundice, fever, and right upper quadrant pain is the step
1 question.
Primary Sclerosing Cholangitis (PSC): Chronic cholestatic Dilated intrahepatic
liver disease of unknown etiology characterized by progressive bile ducts is very
inflammation which leads to multifocal strictures of the intra and /or rare in all forms of
extrahepatic bile ducts. The disease often results in cirrhosis, and is cirrhosis
strongly associated with cholangiocarcinoma. The buzzword for the
EXCEPT
cirrhotic pattern is “central regenerative hypertrophy”. It is
associated with inflammatory bowel disease (Ulcerative Colitis 80%, Primary Sclerosing
Crohn’s 20%). It is an indication for transplant, with a post transplant Cholangitis
recurrence of about 20%.
PSC Buzzwords:
•“Withered Tree” - The appearance on MRCP, from abrupt narrowing of the branches
•“Beaded Appearance” - Strictures + Focal Dilations
AIDS Cholangiopathy: Infection of the biliary epithelium (classically Cryptosporidium) can
cause ductal disease in patients with AIDS. The appearance mimics PSC with intrahepatic and/or
extrahepatic multifocal strictures.
The classic association/finding is papillary stenosis (which occurs 60% of the time).
THIS vs THAT: AIDS Cholangiopathy vs Primary Sclerosing Cholangitis
AIDS PSC
Focal Strictures of the extrahepatic duct > 2 cm Extrahepatic strictures rarely > 5 mm
Absent saccular deformities of the ducts Has saccular deformities of the ducts
Associated Papillary Stenosis
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Oriental Cholangitis (Recurrent pyogenic cholangitis): Common in Southeast Asia (hence
the culturally insensitive name). They always show it as dilated ducts that are full of
pigmented stones.
Buzzword: “straight rigid intrahepatic ducts.” The anatomically longer,
flatter left biliary system
The cause of the disease is not known, but it may be tends to make the disease
associated with clonorchiasis, ascariasis, and nutritional burden left dominant
deficiency. These guys don’t do as well with endoscopic (the opposite of
decompression and often need surgical decompression. hematogenous processes
which favor the right
Remember this is a major risk factor for lobe).
cholangiocarcinoma in the East.
Primary Biliary Cirrhosis: An autoimmune disease that results in the destruction of
small & medium bile ducts (intra not extra). It primarily affects middle-aged women, who
are often asymptomatic. In the early disease, normal bile ducts help distinguish it from PSC.
In later stages, there is irregular dilation of the intrahepatic ducts, with normal extrahepatic
ducts. There is increased risk of HCC. If caught early it has an excellent prognosis and
responds to medical therapy with ursodeoxycholic acid. The step 1 trivia is
“antimitochondrial antibodies (AMA)” which are present 95% of the time.
Long Common Channel:
An anatomic variant in which the
common bile and pancreatic duct
fuse prematurely at the level of the
pancreatic head (prior to the
sphincter of Oddi complex).
The testable consequence is the
increased incidence of pancreatitis -
as reflux of enzymes is more
common.
There is also an association with Normal Long
Type 1 choledochocysts. Common
Channel
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Choledochal Cysts / Caroli’s: Choledochal cysts are congenital dilations of the bile
ducts - classified into 5 types by some dude named Todani.
The high yield trivia is type 1 is focal
dilation of the CBD and is by far the most
common.
Type 2 and 3 are super rare. Type 2 is
basically a diverticulum of the bile duct.
Type 3 is a “choledochocele.”
Type 4 is both intra and extra.
Type 5 is Caroli’s, and is intrahepatic only.
Caroli’s is an AR disease associated with
polycystic kidney disease and medullary
sponge kidney. The hallmark is intrahepatic
duct dilation, that is large and saccular.
Buzzword is “central dot sign” which
corresponds to the portal vein surrounded by
dilated bile ducts.
Complications
• Cholangiocarcinoma
• Cirrhosis
• Cholangitis
• Intraductal Stones
Gamesmanship: If they give you imaging of dilated biliary ducts and a history of
repeated cholangitis, think choledocal cyst. These things get stones in them and can be
recurrently infected.
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- Ductal High Yield Summary -
Caroli’s Primary Sclerosing Cholangitis
-Communicates with the ducts -40 year old Male with U.C.
-Type 5 Cyst -Withering Tree
-Central Dot Sign (on CT, MR, US) -Beading
-Associated with Polycystic Kidney, -Mild Dilation
Medullary Sponge Kidney, -Strongly Associated with Ulcerative
Cholangiocarcinoma Colitis & Cholangiocarcinoma
Oriental Cholangiohepatitis AIDS Cholangiopathy
(Recurrent Pyogenic) -Related to Cryptosporidium or
-Associations with clonorchiasis, cytomegalovirus.
ascariasis -Segmental Strictures (looks like PSC)
-Lots of Stones -Ducts look like PSC + Papillary
-Favors the left ductal system Stenosis
- Strongly Associated with - Associated with Cholangiocarcinoma
Cholangiocarcinoma
Association:
Cholangiocarcinoma VS B9 Strictures:
If you can’t remember what
the association is, and it’s • CA Strictures tends to be long, with “shouldering.”
ductal pathology, always • B9 strictures tend to be abrupt and short.
guess Cholangiocarcinoma.
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SECTION 4:
Ga l l bl a d d er
Normal Gallbladder
The normal gallbladder is found inferior to the interlobar fissure between the right and left
lobe. The size varies depending on the last meal, but is supposed to be < 4 x < 10 cm. The
wall thickness should be < 3 mm. The lumen should be anechoic.
Variants/Congenital
Phrygian cap: A phrygian cap is seen when the GB folds on itself. It means nothing.
Intrahepatic Gallbladder: Variations in gallbladder location are rare, but the
intrahepatic gallbladder is probably the most frequently recognized variant. Most are found
right above the interlobar fissure.
Duplicated Gallbladder: It can happen.
Duct of Luschka: An accessory cystic
duct. This can cause a big problem (persistent
Accessory Hepaticocystic
bile leak) after cholecystectomy. There are Subvesicular
several subtypes which is not likely to be tested. (most common)
Pathology
GB Wall Thickening (> 3 mm): Very non-specific. Can occur from biliary
(Cholecystitis, AIDS, PSC.,.) or non-biliary causes (hepatitis, heart failure, cirrhosis, etc....).
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Gallstones: Gallstones are found in 10% of asymptomatic patients / Most (75%) are
cholesterol, the other 25% are pigmented. They cast shadows.
Reasons a stone might not cast a shadow
• It’s not a stone
• It’s a stone, but < 3 mm in size
• The sonographer is an amateur (Bush league psyche-out stuff. Laughable, man)
Gallbladder Shadowing
(1) Gallbladder full of stones
*Clean shadowing.
(2) Porcelain Gallbladder
* Variable shadowing
(3) Emphysematous Cholecystitis
*Dirty shadowing.
Mirizzi Syndrome: This occurs when the common
hepatic duct is obstructed secondary to an impacted
cystic duct stone. The stone can eventually erode into
the CHD or GI tract.
Key point is the increased co-incidence of gallbladder
CA (5x more risk) with Mirizzi.
Another key piece of trivia is that Mirizzi occurs more
in people with a low cystic duct insertion (normal
variant), allowing for a more parallel course and closer Mirizzi
proximity to the CHD. -Cystic Duct Stone
Obstructing CBD
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Clinically Meaningless THIS vs THAT:
Gallbladder Adenomyomatosis vs Cholesterolosis
Nothing makes an Academic Radiologist happier than spending time deploying intense
focused concentration targeted at distinguishing between two very similar appearing
completely benign (often incidental) processes. They believe this “adds value” and will
save them from the eventual avalanche of reimbursement cuts with subsequent AI
takeover.
Classic Example: Adenomyomatosis vs Gallbladder Cholesterolosis. These things are
actually different - and even though it makes zero difference clinically, this is just the
kind of thing people who write questions love to write questions about.
Gallbladder Adenomyomatosis: You have hypertrophied mucosa and muscularis
propria, with the cholesterol crystals deposited in an intraluminal location (within
Rokitansky-Aschoff sinuses).
Cholesterolosis: Cholesterol and triglyceride deposition is within the substance of the
lamina propria, and associated with formation of cholesterol polyps.
Adenomyomatosis: Results from hyperplasia of the wall with formation of intramural
mucosal diverticula (Rokitansky-Aschoff sinuses) which penetrate into the wall of the
gallbladder. These diverticula become filled with cholesterol crystals - which manifest from the
unique acoustic signature as comet-tail artifact (highly specific for adenomyomatosis).
Comes in 3 flavors: Generalized (diffuse), Segmental (annular), and Fundal (localized or
adenomyoma). The Localized form can’t be differentiated from GB cancer.
Gamesmanship: Don’t be tricked into selecting “Adenomyosis ” as a distractor. That
shit is in the uterus. Remember the larger word is in the smaller organ. Or, you can
think about the two Ms in MyoMat - turned inward sorta looks like a gallbladder.
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Porcelain Gallbladder:
• Extensive wall calcification.
• The key point is increased risk of GB Cancer.
• These are surgically removed.
Gallbladder Polyps:
These can be cholesterol (by far the most
THIS vs THAT: Gallbladder Polyps
common), or non cholesterol (adenomas,
papillomas). Cholesterol polpys aren’t real Benign Malignant
polyps, but instead are essentially enlarged > 1 cm
< 5 mm
papillary fronds full of lipid filled *between 5 mm - 10 mm
* these are nearly always usually get followed for
macrophages, that are attached to the wall by a cholesterol polyps growth
stalk.
Pedunculated Sessile
The non-cholesterol subtypes are almost Multiple Solitary
always solitary and are typically larger. The
Enhancement on CT/
larger polyps may have Doppler flow. They are Comet Tail Artifact on MRI greater than the
NOT mobile and do NOT shadow. Once they Ultrasound (seen in adjacent gallbladder
cholesterol polyps) wall. Flow on Doppler.
get to be 1 cm, people start taking them out.
Gallbladder Cancer:
• Classic vignette would be an elderly women with nonspecific RUQ pain, weight loss,
anorexia and a long standing history of gallstones, PSC, or large gallbladder polyps.
• Most GB cancers are associated with gallstones (found in 85% of cases)
• Mirizzi syndrome has a well described increased risk of GB cancer
• Other risk factors include smoldering inflammatory processes (PSC, Chronic
Cholecystitis, Porcelain Gallbladder), and large polyps (“large” = bigger than 1cm)
• Unless the cancer is in the fundus (which can cause biliary obstruction) they often present
late and have horrible outcomes with 80% found with direct tumor invasion of the liver or
portal nodes at the time of diagnosis.
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SECTION 5:
Hepa t i c Do ppl er
Brief introduction to terminology.
• “Duplex" means color.
• “Spectral" means color with a waveform.
- Concept of Arterial Resistance -
Some organs require continuous flow (brain), whereas others do not (muscles). The body is
smart enough to understand this, and will make alterations in resistance / flow to preserve energy.
When an organ needs to be “on,” its arteriolar bed dilates, and the waveform becomes low
resistance. This allows the organ to be appropriately perfused. When an organ goes to “power
save” mode, its arterioles constrict, the waveform switches to high resistance, and blood flow is
diverted to other more vital organs.
To help quantify this low resistance high
resistance thing, we use this “Resistive
Index (RI)” - which is defined as V1-V2/VI.
Just remember that things that need blood all
the time, will have continuous diastolic
flow - and thus a low resistance wave
form. Rl = PSV - EDV / PSV
What is this “Tardus Parvus” ?
Tardus: Refers to a slowed systolic
upstroke. This can be measured by
acceleration time, the time from end
diastole to the first systolic peak. An
acceleration time > 0.07 sec correlates with
>50% stenosis of the renal artery
Parvus: Refers to decreased systolic
velocity. This can be measured by
calculating the acceleration index, the
change in velocity from end diastole to the
first systolic peak.
An acceleration index < 3.0 m/sec -
correlates with > 50% stenosis of the renal
artery
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- Understanding Stenosis -
The vocabulary of “Upstream vs Downstream” is somewhat confusing. Try and remember,
that the (low of blood defines the direction.
• Upstream = Blood that has NOT yet passed through the stenosis
• Downstream = Blood that has passed through the area of stenosis
So there are direct and indirect signs of stenosis.
Direct Signs: The direct signs are those found at the stenosis itself and they include elevated
peak systolic velocity and spectral broadening (immediate post stenotic).
Indirect Signs: The indirect signs are going to be tardus parvus (downstream) - with time to
peak (systolic acceleration) > 70 msec. The RI downstream will be low (< 0.5) because the
liver is starved for blood. The RI upstream will be elevated (> 0.7) because that blood needs
to overcome the area of stenosis.
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- Hepatic Veins
Flow in the hepatic veins is complex, with alternating forward and backward flow. The bulk
of the flow should be forward “antegrade” (liver → heart). Things that mess with the
waveform are going to be pressure changes in the right heart which are transmitted to the
hepatic veins (CHF, Tricuspid Regurg) or compression of the veins directly (cirrhosis).
Anything that increases right atrial
pressure (atrial contraction) will
cause the wave to slope upward.
“A” represents atrial contraction.
Anything that decreases right atrial
pressure will cause the wave to
slope downward.
Abnormal Hepatic Vein
Waveforms can manifest in one of three main Increased HV Decreased HV
categories: Pulsatility Pulsatility
(1) More Pulsatile Tricuspid Regurg Cirrhosis
(2) Less Pulsatile Hepatic Venous
Right Sided CHF Outflow Obstruction
(3) Absent = Budd Chiari (any cause)
LOW YIELD - TRIVIA - Study only on second time through
THIS vs THAT: Tricuspid Regurg VS Right Sided CHF
Although certain dinosaur radiologists still
love this stuff, it’s unlikely to show up on
the test, and if it does it probably won’t be
more than one question. If they ask it at all
- I would bet the question is something
regarding the “D Wave to S Wave”
relationship.
• Tricuspid Regurg - D deeper than S
• Right Heart Failure - S deeper than D
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- Portal Vein
Flow in the portal vein should always be towards the liver (antegrade). You can see some
normal cardiac variability from hepatic venous pulsatility transmitted through the hepatic
sinusoids. Velocity in the normal portal vein is between 20-40 cm/s. The waveform should be a
gentle undulation , always remaining above the baseline.
You have three main patterns:
(1) Normal
(2) Pulsatile
(3) Reversed
Causes of Portal Vein Pulsatility: Right-sided CHF, Tricuspid Regurg, Cirrhosis with Vascular
AP shunting.
Causes of Portal Vein Reversed Flow: The big one is Portal HTN (any cause).
Absent Flow: This could be considered a fourth pattern. It’s seen in thrombosis, tumor invasion,
and stagnant flow from terrible portal HTN.
Slow Flow: Velocities less than 15 cm/s. Portal HTN is the most common cause. Additional
causes are grouped by location:
• Pre - Portal Vein Thrombosis
• Intra - Cirrhosis (any cause)
• Post - Right-sided Heart Failure, Tricuspid Regurg, Budd-Chiari
Final Doppler Trivia:
An ultra-common quiz question is to ask “what should the
Doppler angle be?” Now even though ultrasound physics
is covered in more detail in the dedicated section of the War
Machine this is a high yield enough point to warrant
repetition. The answer is “less than 60. ”
Why? Doppler strength follows the cosine of the angle. For
example, Cos 90 = 0, Cos 60 = 0.5, Cos 0 = 1.0 - the
doppler strength follows the Cos.
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SECTION 6:
Pa n c r ea s
Trivia regarding the pancreas can be broadly Classic US Trivia: The
clustered into: Solid Lesions, Cystic Lesions, Pancreatic Echogenicity should be
Pancreatitis, and Misc Trivia (mostly GREATER than the normal liver.
developmental stuff).
- Misc Pancreas Trivia -
Anatomy: The pancreas is a retroperitoneal structure (the tail may be intraperitoneal).
Cystic Fibrosis: The pancreas is involved in 85-90% of CF patients. Inspissated
secretions cause proximal duct obstruction leading to the two main changes in CF:
(1) Fibrosis (decreased T1 and T2 signal)
(2) Fatty replacement (increased T1) - the more common of the two
Patients with CF, who are diagnosed as adults, tend to have more pancreas problems than
those diagnosed as children. Just remember that those with residual pancreatic exocrine
function tend to have bouts of recurrent acute pancreatitis (they keep getting clogged up with
thick secretions). Small (1 - 3 mm) pancreatic cysts are common.
High Yield Trivia:
• Complete fatty replacement is the most
common imaging finding in adult CF
• Markedly enlarged with fatty replacement
has been termed lipomatous
pseudohypertrophy of the pancreas.
*This is a buzzword.
• Fibrosing Colonopathy: Wall thickening
of the proximal colon as a complication of
enzyme replacement therapy.
CF - Fatty Replacement of the Pancreas
Shwachman-Diamond Syndrome: The 2nd most common cause of
pancreatic insufficiency in kids (CF #1). Basically, it’s a kid with diarrhea,
short stature (metaphyseal chondroplasia), and eczema. Will also cause
lipomatous pseudohypertrophy of the pancreas.
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Pancreatic Lipomatosis:
THIS vs THAT:
Pancreatic Agenesis vs
Most common pathologic condition involving the
Pancreatic-Lipomatosis
pancreas. The most common cause in childhood is
CF (in adults it’s Burger King).
Agenesis Lipomatosis
Additional causes worth knowing are Cushing
Does NOT have Does have a
Syndrome, Chronic Steroid Use, Hyperlipidemia,
a duct duct
and Shwachman-Diamond Syndrome.
Dorsal Pancreatic Agenesis: - All you need to know is that (1) this sets you up for
diabetes (most of your beta cells are in the tail), and (2) it’s associated with polysplenia.
Annular Pancreas: Essentially an embryologic screw up (failure of ventral bud to
rotate with the duodenum), that results in encasement of the duodenum. Results in a rare
cause of duodenal obstruction (10%), that typically presents as duodenal obstruction in
children and pancreatitis in adults. Can also be associated with other vague symptoms (post-
prandial fullness, “symptoms of peptic ulcer disease”, etc...).
• Remember in adults this can present with pancreatitis (the ones that present earlier - in
kids - are the ones that obstruct).
• On imaging, look for an annular duct encircling the descending duodenum.
Pancreatic Trauma: The pancreas sits in front of the vertebral body, so it’s susceptible
to getting smashed in blunt trauma. Basically, the only thing that matters is integrity of
the duct. If the duct is damaged, they need to go to the OR. The most common delayed
complication is pancreatic fistula (10-20%), followed by abscess formation. Signs of injury
can be subtle, and may include focal pancreatic enlargement or adjacent stranding/fluid.
Imaging Pearls:
• Remember it can be subtle with just focal enlargement of the pancreas
• If you see low attenuation fluid separating two portions of the enhancing pancreatic
parenchyma this is a laceration, NOT contusion.
• The presence of fluid surrounding the pancreas is not specific, it could be from injury or
just aggressive hydration — on the test they will have to show you the liver and IVC to
prove it’s aggressive fluid resuscitation.
High Yield: Traumatic Pancreatitis in a kid too young to ride a bike = NAT.
Suspected Pancreatic Duct Injury? - Next Step - MRCP or ERCP
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- Pancreatitis -
Acute Pancreatitis:
Etiology: By far the most common causes are gallstones and EtOH which combined make
up 80% of the cases in the real world. However, for the purpose of multiple choice tests, a
bite from the native scorpion of the island of Trinidad and Tobago is more likely to be the
etiology. Additional causes include ERCP (which usually results in a mild course),
medications (classically valproic acid), trauma (the most common cause in a child),
pancreatic cancer, infectious (post viral in children), hypercalcemia, hyperlipidemia,
autoimmune pancreatitis, pancreatic divisum, groove (para-duodenal) pancreatitis, tropic
pancreatitis, and parasite induced.
Clinical Outcomes: Prognosis can be estimated with the “Balthazar Score.” Essentially, you
can think about pancreatitis as “mild” (no necrosis) or “severe” (having necrosis). Patients
with necrosis don’t start doing terrible until they get infected, then the mortality is like
50-70%.
Key Point: Outcomes are directly correlated with the degree of pancreatic necrosis.
Severe Pancreatitis: Severe acute
pancreatitis has a biphasic course. With
the first two weeks being a pro-
inflammatory phase. This is a sterile
response in which infection rarely occurs.
The third and fourth weeks transition to
an anti-inflammatory period in which the
risk of translocated intestinal flora and the
subsequent development of infection
increases.
Let’s Practice
Which of the follow is the most "salient” (important) ?
Sounds scary, but necrosis is
A: Hemorrhage in the Pancreas more important
B: Necrosis in the Pancreas
C: Fluid Collection 2nd Best Option - I’d pick
D: Infection in Necrosis this if D wasn’t a Choice
Best Option - Remember to
Read All the Answer Choices!
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VOCAB - Radiologist LOVE to Argue over Words — therefore high yield
< 4weeks Acute Peripancreatic
Fluid Collection
NO Necrosis > 4weeks Pseudocyst
< 4weeks Acute Necrotic Collection
Necrosis
> 4weeks Walled-Off Necrosis
Vascular Complications:
• Splenic Vein and Portal Vein Thrombosis
O Isolated gastric varices can be seen secondary to splenic vein occlusion
• Pseudo-aneurysm of the GDA and Splenic Artery
Non-Vascular Complications:
• Abscess, Infection, etc... as discussed
• Gas, as a characteristic sign of an infected fluid collection, is detected in only 20% of
cases of pancreatic abscesses.
Random Imaging Pearl:
• On Ultrasound, an inflamed pancreas will be hypoechoic (edematous) when
compared to the liver (opposite of normal).
- Pancreatic Divisum -
Anatomy Refresher: There are two ducts, a major (Wirsung), and a minor (Santorini). Under
“normal” conditions the major duct will drain in the inferior of the two duodenal papilla
(major papilla). The minor duct will drain into the superior of the two duodenal papilla
(minor papilla). The way I remember this is that “Santorini drains Superior”, and “Santorini is
Small,” i.e. the minor duct.
Pancreatic Divisum is the most common
anatomic variant of the human pancreas,
and occurs when the main portion of the
pancreas is drained by the minor or
accessory papilla. The clinical
relevance is an increased risk of Normal (85%) Divisum (~15%)
pancreatitis. -Bifid System with
Rudimentary Dorsal Duct-
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-Chronic Pancreatitis-
CP represents the end result of prolonged inflammatory change leading to irreversible
fibrosis of the gland. Acute pancreatitis and chronic pancreatitis are thought of as different
disease processes, and most cases of acute pancreatitis do not result in chronic disease. So,
acute doesn’t have to lead to chronic (and usually doesn’t), but chronic can still have
recurrent acute.
Etiology: Same as acute pancreatitis, the most common causes are chronic alcohol abuse
and cholelithiasis which together result in about 90% of the cases. (EtOH is #1)
Imaging Findings: Findings can be thought of as early or late:
Early:
• Loss of T1 signal (pancreas is normally the brightest T1 structure in the body)
• Delayed Enhancement
• Dilated Side Branches
Late:
• Commonly small, uniformly atrophic - but can have focal enlargement
• Pseudocyst formation (30%)
• Dilation and beading of the pancreatic duct with calcifications
** most characteristic finding of CP.
THIS vs THAT: Chronic Pancreatitis Duct Dilation
vs Pancreatic Malignancy Duct Dilation
CP Cancer
Dilation is Irregular Dilation is uniform (usually)
Duct is < 50% of the AP gland diameter Duct is > 50% of the AP gland diameter
(obstructive atrophy)
Complications: Pancreatic cancer (20 years of CP = 6% risk of Cancer) is the most crucial
complication in CP and is the biggest diagnostic challenge because focal enlargement of the
gland induced by a fibrotic inflammatory pseudotumor may be indistinguishable from
pancreatic carcinoma.
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Uncommon Types and Causes of Pancreatitis
Autoimmune Associated with Absence of Attack Responds to Sausage Shaped
Pancreatitis elevated IgG4 Symptoms steroids Pancreas, capsule
like delayed rim
enhancement around
gland (like a scar).
No duct dilation.
No calcifications.
Groove Looks like a Less likely to cause Duodenal stenosis Soft tissue within the
Pancreatitis pancreatic head obstructive and /or strictures of pancreaticoduodenal
Cancer - but with jaundice (relative the CBD in 50% of groove, with or
little or no biliary to pancreatic CA) the cases without delayed
obstruction. enhancement
Tropic Young Age at onset, Increased risk of Multiple large calculi
Pancreatitis associated with adenocarcinoma within a dilated
malnutrition pancreatic duct
Hereditary Young Age at Onset Increased risk of SPINK-1 gene Similar to Tropic
Pancreatitis adenocarcinoma Pancreatitis
Ascaris Most commonly Worm may be seen
Induced implicated parasite within the bile ducts
in pancreatitis
When I Say - Autoimmune Pancreatitis
I Say Autoimmune Pancreatitis You Say IgG4
Autoimmune Pancreatitis
Retroperitoneal Fibrosis
I Say IgG4 Sclerosing Cholangitis
Inflammatory Pseudotumor
Riedel’s Thyroiditis
THIS vs THAT:
Autoimmune Pancreatitis vs Chronic Pancreatitis
Autoimmune Pancreatitis Chronic Pancreatitis
No ductal dilation Ductal Dilation
No calcifications Ductal Calcifications
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- Cystic Pancreatic Lesions -
Pseudocyst: When you see a cystic lesion in the pancreas, by far the most common cause
is going to be an inflammatory pseudocyst, either from acute pancreatitis or chronic
pancreatitis.
Simple Cysts: True epithelial lined cysts are rare, and tend to occur with syndromes such
as VHL, Polycystic Kidney Disease, and Cystic Fibrosis.
Serous Cystadenoma (Grandma): The former term “microcystic adenoma” helps
me think of a little old lady, which is appropriate for a lesion primarily found in elderly
ladies. The lesion is benign, and classically described as a heterogeneous, mixed-density
lesion made up of multiple small cysts, which resembles a sponge. They are more commonly
(70%) located in the pancreatic head (mucinous is almost always in the body or tail). An
additional key distinction is that it does NOT communicate with the pancreatic duct (IPMNs
do). About 20% of the time they will have the classic central scar, with or without central
calcifications (mucinous calcifications are peripheral).
Rarely, they can be unilocular. When you see a unilocular cyst with a lobulated contour
located in the head of the pancreas, you should think about this more rare unilocular
macrocystic serous cystadenoma subtype.
Trivia: Serous Cystadenoma is associated with Von Hippel Lindau
Memory Aid: “GRANDMA Serous is the HEAD of the household”
Mucinous Cystic Neoplasm (Mother): This pre-malignant lesion is “always” found
in women, usually in their 50s. All are considered pre-malignant and need to come out. They
are found in the body and tail (serous was more common in the head). There is generally no
communication with the pancreatic duct (IPMNs will communicate). Peripheral calcifications
are seen in about 25% of cases (serous was more central). They are typically unilocular.
When mutlilocular, individual cystic spaces tend to be larger than 2 cm in diameter (serous
spaces are typically smaller than 2 cm).
Memory Aid: “MUCINOUS in the MOTHER”
Solid Pseudopapillary Tumor of the Pancreas - (Daughter): Very rare, low
grade malignant tumor that occurs almost exclusively in young (30s) females (usually Asian
or Black). It is typically large at presentation, has a predilection for the tail, and has a “thick
capsule.” Similar to a hemangioma it may demonstrate progressive fill-in of the solid
portions.
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IPMN - Intraductal Papillary Mucinous Neoplasm: These guys are mucin-
producing tumors that arise from the duct epithelium. They can be either side branch, main
branch, or both.
Side Branch Features
“The pulmonary nodule Main Branch Concerning For
of the pancreas ” Malignancy
•Common and usually meaningless •Produces diffuse dilation of the •Main duct >10 mm
•Typically appear as a small cystic main duct (some sources say 1.5 cm)
mass, often in the head or uncinate •Atrophy of the gland and •Diffuse or multifocal
process dystrophic calcifications may be involvement
•If large amounts of mucin are seen - •Enhancing nodules
produced it may result in main mimicking Chronic Pancreatitis •Solid hypovascular
duct enlargement •Have a much higher % of mass
•Lesions less than 3 cm, are usually malignancy compared to side
benign branch
•All Main Ducts are considered
malignant, and resection should be
considered
- Cystic Pancreatic Lesion Summary -
Solid Pseudopapillary
- Daughter Lesion
- Solid with Cystic
parts, enhances like a
Main Branch IPMN hemangioma
- “The Bad One” - Capsule
- Has malignant potential
Mucinous Cystic
- Mother Lesion
Side Branch IPMN
- Pre-malignant
- “Common One”
- Body / Tail - 95%
- Has much less
malignant - Unilocular with thick
potential wall Septations
- Often in head /
Serous Cystic
uncinate
- Grandma Lesion
- Communicates
- Benign
with duct
- Microcystic, with
central calcifications
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- Solid Pancreatic Lesions -
Pancreatic Cancer basically comes in two flavors. (1) Ductal Adenocarcinoma - which is
hypovascular and (2) Islet Cell / Neuroendocrine which is hypervascular.
Ductal Adenocarcinoma: In the setting of a multiple choice test, the finding of an
enlarged gallbladder with painless jaundice is highly suspicious for pancreatic
adenocarcinoma, especially when combined with migratory thrombophlebitis (Trousseau's
syndrome). The peak incidence is in the 7th or 8th decade. The strongest risk factor is
smoking.
Approximately two-thirds of these cancers arise from the
Peak Parenchyma
pancreatic head. On ultrasound, obstruction of both the Enhancement
common bile duct and the pancreatic duct is referred to as
the “double duct sign”. On CT, the findings are typically a Pancreas = 40 Seconds
hypo-enhancing mass which is poorly demarcated and low
Liver = 60 Seconds
attenuation compared to the more brightly enhancing
background parenchyma. The optimal timing is on a
pancreatic phase (40 seconds).
The key to staging is assessment of the SMA and celiac axis, which if involved make the
patient’s cancer unresectable. Involvement of the GDA is ok, because it comes out with the
Whipple.
Additional Trivia Points about Pancreatic Adenocarcinoma:
• Tumor Marker = CA 19-9
• Hereditary Syndromes with Pancreatic CA:
o HNPCC, BRCA Mutation, Ataxia-Telangiectasia, Peutz-Jeghers
• Small Bowel Follow Through: Reverse impression on the duodenum “Frostburg’s
Inverted 3 Sign” or a “Wide Duodenal Sweep.” They would have to actually find a
case of the inverted 3 to show it, hut could ask it in words. The "Wide Duodenal
Sweep” could actually be shown.
Periampullary Tumor: Defined as originating within 2 cm of the major papilla. It can
be difficult to differentiate from a conventional pancreatic adenocarcinoma as both obstruct
the bile duct, and present as a mass in the pancreatic head. Basically, all you need to know
about them is they can try and treat them with a Whipple and they have a better prognosis
than pancreatic adenocarcinoma.
Trivia: There is an increased incidence of ampullary carcinoma in Gardner’s Syndrome.
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Islet Cell / Neuroendocrine:
Neuroendocrine tumors are uncommon
tumors of the pancreas. Typically
hypervascular, with brisk enhancement
during arterial or pancreatic phase. They
can be thought of as non-functional or
functional, and then subsequently further
divided based on the hormone they make.
They can be associated with both MEN 1
and Von Hippel Lindau. Hyper-Enhancing Tumor
Insulinoma: The most common type (about 75%). They are almost always benign (90%),
solitary, and small (< 2 cm).
Gastrinoma: The second most common
Gastrinoma Triangle
type overall, but most common type
associated with MEN 1. They are The anatomical region where most (90%) of
malignant like 30-60%. They can cause gastrinomas arise.
increased gastric acid output and ulcer Boundaries
formation - Zollinger — Ellison syndrome.
• Superior:
The Buzzword is Jejunal Ulcer = Junction of
the cystic and
Zollinger-Ellison common bile
ducts
Non-Functional: The 3rd most common • Inferior: Start
type, usually malignant (80%), and are of the third
portion of the
usually large and metastatic at the time of duodenum
diagnosis. • Medial: Start
of the body of
I say “non-functional, ”
the pancreas
you say Large with Calcification
Intrapancreatic Accessory Spleen
It is possible to have a pancreatic mass that is actually just a piece of spleen. The typical
scenario is that of post traumatic splenosis. Look for the question stem to say something like
"history of trauma. ’’ Another hint may be the absence of a normal spleen.
Imaging Findings:
-Follows spleen on all image sequences (dark on Tl, and bright on T2 - relative to the liver).
-It will restrict diffusion (just like the spleen).
-The classic give away, and most likely way it will be shown is as a tiger striped mass on arterial
phase (tiger striped like the spleen on arterial phase).
Trivia: Nuclear medicine tests - (1) Heat Treated RBCs, and (2) Sulfur Colloid can be used to
prove the mass is spleen (they both take up tracer —just like a spleen).
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SECTION 7:
SURGICAL
The Whipple Procedure:
The standard Whipple procedure involves resection of the pancreatic head, duodenum, gastric
antrum, and almost always the gallbladder. A jejunal loop is brought up to the right upper
quadrant for gastrojejunal, choledochojejunal or hepaticojejunal, and pancreatojejunal
anastomosis.
An alternative method used by some surgeons is to perform a pancreatoduodenectomy and
preserve the pylorus when possible. There is debate in the surgery literature with regard to
which method should be the standard. In this pylorus-preserving pancreatoduodenectomy, the
stomach is left intact and the proximal duodenum is used for a duodenojejunal anastomosis.
Complications:
Delayed gastric emptying (need for NG tube longer than 1- day) and pancreatic fistula (amylase
through the surgical drain >50 ml for longer than 7-10 days), arc both clinical diagnoses and
are the most common complications after pancreatoduodenectomy. Wound infection is the third
most common complication, occurring in 5%—20% of patients.
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- Transplant -
Pancreas transplant (usually with a renal transplant) is an established therapy for severe type 1
diabetes - which is often complicated by renal failure. The vascular anatomy regarding this
transplant is quite complicated and beyond the scope of this text. Just know that the pancreas
transplant receives arterial inflow from two sources: the donor SMA, (which supplies the head
via the inferior pancreaticoduodenal artery) and the donor splenic artery, (which supplies the
body and tail). The venous drainage is via both the donor portal vein and the recipient SMV.
Exocrine drainage is via the bowel (in older transplants via the bladder).
The number one cause of graft failure is acute rejection. The number two cause of graft failure is
donor splenic vein thrombosis. Donor splenic vein thrombosis usually occurs within the first 6 weeks
of transplant. Venous thrombosis is much more common than arterial thrombosis in the transplant
pancreas, especially when compared to other transplants because the vessels are smaller and the
clot frequently forms within and propagates from the tied-off stump vessels.
Both venous thrombosis and acute rejection can appear as reversed diastolic flow. Arterial
thrombosis is also less of a problem because of the dual supply to the pancreas (via the Y graft).
A point of trivia is that the resistive indices are not of value in the pancreas, because the organ
lacks a capsule. The graft is also susceptible to pancreatitis, which is common < 4 weeks after
transplant and usually mild. Increased rates of pancreatitis were seen with the older bladder
drained subtype.
“Shrinking Transplant” is a buzzword for chronic rejection, where the graft
progressively gets smaller in size.
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SECTION 8:
Spl een
Normal Trivia
By the age of 15 the spleen reaches its normal adult size. The spleen contains both “red
pulp” and “white pulp” which contribute to its tiger striped appearance during arterial phase
imaging. The red pulp is filled with blood (a lot of blood), and can contain up to one liter of
blood at any time. The spleen is usually about 20 HU less dense than the liver, and slightly
more echogenic than the liver (equal to the left kidney). The splenic artery (which usually
arises from the celiac trunk) is essentially an end vessel, with minimal collaterals.
Occlusion of the splenic artery will therefore result in splenic infarction.
Pathology involving the spleen can be categorized as either congenital, acquired (as the
sequela of trauma or portal hypertension), or related to a “mass.” A general rule is that most
things in the spleen are benign with exception of lymphoma or the rare primary
angiosarcoma.
Normal Spleen on MRI:
The spleen is basically a big watery lymph node. It restricts diffusion (like a lymph node).
It’s Bright on T2 It’s Dark on T1 Just like a lymph node it
-Relative to the liver -Relative to the liver will restrict diffusion
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Heterotaxy Syndromes: Super High Yield - please see discussion on page 98
Accessory Spleens: These are very common; we see them all the time. Some random
trivia that might be testable includes the fact that sulfur colloid could be used to differentiate a
splenule from an enlarged pathologic lymph node. Additionally, in the scenario where a patient
is post splenectomy for something like ITP or autoimmune hemolytic anemia, an accessory
spleen could hypertrophy and present as a mass. Hypertrophy of an accessory spleen can also
result in a recurrence of the original hematologic disease process.
Wandering Spleen: A normal spleen that “wanders” off and is in an unexpected location.
Because of the laxity in the peritoneal ligaments holding the spleen, a wandering spleen is
associated with abnormalities of intestinal rotation. The other key piece of trivia is that unusual
locations set the spleen up for torsion and subsequent infarction. A chronic partial torsion can
actually lead to splenomegaly or gastric varices.
Trauma: The spleen is the most common solid organ injured in trauma. This combined with
the fact that the spleen contains a unit or so of blood means splenic trauma can be life
threatening. Remember the trauma scan is done in portal venous phase (70 second), otherwise
you’d have to tell if that is the normal tiger-striped arterial-phase spleen or it is lacerated.
Splenosis: This occurs post trauma where a smashed spleen implants and then recruits blood
supply. The implants are usually multiple and grow into spherical nodules typically in the
peritoneal cavity of the upper abdomen (but can be anywhere). It’s more common than you think
and has been reported in 40-60% of trauma. Again, Tc Sulfur colloid (or heat-treated RBC) can
confirm that the implants are spleen and not ovarian mets or some other terrible thing.
Sickle Cell: I discuss the various sickle cell related changes in the Peds chapter (page 97).
Gamna Gandy Bodies (Siderotic Nodule):
These are small foci of hemorrhage in the splenic
parenchyma that are usually associated with portal
hypertension. They are T2 dark.
Gradient is the most sensitive sequence.
Gamna Gandy Bodies
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Sarcoidosis: Sarcoid is a disease of unknown etiology that results in noncaseating
granulomas which form in various tissues of the body (complete discussion in the chest
section of this text). The spleen is involved in 50% - 80% of patients. Splenomegaly is
usually the only sign. However, aggregates of granulomatous splenic tissue in some patients
may appear on CT as numerous discrete l-2 cm hypodense nodules. Rarely, it can cause a
massive splenomegaly and possibly rupture. Don’t forget that the gastric antrum is the most
common site in the G1 tract.
Peliosis: This is a rare condition characterized by multiple blood filled cyst-like spaces in
a solid organ (usually the liver - peliosis hepatitis). When you see it in the spleen it is
usually also in the liver (isolated spleen is extremely rare). The etiology is not known, but
for the purpose of multiple choice tests it occurs in women on OCPs, men on anabolic
steroids, people with AIDS, renal transplant patients (up to 20%), and patients with
Hodgkin lymphoma. It’s usually asymptomatic but can explode spontaneously.
-Splenic Vascular Abnormalities-
Splenic artery aneurysm is the most common visceral arterial aneurysm.
Pseudo-aneurysm can occur in the setting of trauma and pancreatitis. The incidence is higher
in women of child bearing age who have had two or more pregnancies (4x more likely to get
them, 3x more likely to rupture). It’s usually saccular and in the mid-to-distal artery. They
usually fix them when they get around 2-3 cm.
Colossal fuck up to avoid: Don’t call them a hypervascular pancreatic islet cell mass and
biopsy them.
Splenic vein thrombosis frequently occurs as the result of pancreatitis. Can also
occur in the setting of diverticulitis or Crohn’s. Can lead to isolated gastric varices.
Infarction can occur from a number of conditions. On a multiple choice test the answer is
sickle cell. The imaging features are classically a wedge-shaped, peripheral, low attenuation
defect.
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- Splenic Infections -
Most common radiologically detected splenic infection is histoplasmosis (with multiple
round calcifications). Splenic TB can have a similar appearance (but much less common in
the US). Another possible cause of calcified granuloma in the spleen in brucellosis, but these
are usually solitary and 2 cm or larger. They may have a low density center, encircled by
calcification giving the lesion a “bull’s eye” appearance.
In the immunocompetent patient, splenic abscess is usually due to an aerobic organism.
Salmonella is the classic bug - which develops in the setting of underlying splenic damage
(trauma or sickle cell). In immunocompromised patients, unusual organisms such as fungi,
TB, MAI, and PCP can occur and usually present as multiple micro-abscesses. Occasionally,
fungal infections may show a “bulls-eye” appearance on ultrasound.
- Splenic Size - Too Big vs Too Small -
It’s good to have a differential for a big spleen and a small spleen.
Small Spleen Big Spleen
Passive Congestion (heart failure, portal
Sickle Cell HTN, splenic vein thrombosis)
Post Radiation Lymphoma
Post Thorotrast Leukemia
Malabsorption Syndromes Gauchers
(ulcerative colitis > crohns)
Felty’s Syndrome - abnormality of granulocytes, with a triad of;
(1) Splenomegaly, (2) Rheumatoid Arthritis, (3) Neutropenia
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- Benign Masses of the Spleen -
Cysts;
Post traumatic cysts (pseudocysts) are the most common cystic lesion in the
spleen. They can occur secondary to infarction, infection, hemorrhage, or extension from
a pancreatic pseudocyst. As a point of trivia they are “pseudo” cysts because they have
no epithelial lining. They may have a thick wall or prominent calcifications peripherally.
Epidermoid cysts are the second most common cystic lesion in the spleen. They
are congenital in origin. As a point of absolutely worthless trivia, they are “true” cysts
and have an epithelial lining. They typically grow slowly and are usually around 10 cm at
the time of discovery. They can cause symptoms if they are large enough. They are
solitary 80% of the time, and have peripheral calcifications 25% of the time.
Hydatid or Echinococcal cysts are the third most common cystic lesion in the
spleen. They are caused by the parasite Echinococcus Granulosus. Hydatid cysts consist
of a spherical “mother cyst” that usually contains smaller “daughter cysts.” Internal
Septations and debris are often referred to as “hydatid sand.” The “water lily sign” is seen
when there is detachment of the endocyst membrane resulting in floating membranes
within the pericysts (looks like a water lily). This was classically described on CXR in
pulmonary echinococcal disease.
Hemangioma is the most common benign neoplasm in the spleen. This dude is usually
smooth and well marginated demonstrating contrast uptake and delayed washout. The
classic peripheral nodular discontinuous enhancement seen in hepatic lesions may not occur,
especially if the tumor is smaller than 2 cm.
Lymphangiomas are rare entities in the spleen but can occur. Most occur in childhood.
They may be solitary or multiple, although most occur in a subcapsular location. Diffuse
lymphangiomas may occur (lymphangiomatosis).
Hamartomas are also rare in the spleen, but can occur. Typically this is an incidental
finding. Most are hypodense or isodense and show moderate heterogeneous enhancement.
They can be hyperdense if there is hemosiderin deposition.
Littoral Cell Angioma is a zebra that shows up occasionally in books
and possibly on multiple choice tests. Clinical hypersplenism is almost
always present. Usually presents as multiple small foci which are
hypoattenuating on late portal phase. MR shows hemosiderin (low T1 & T2).
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- Malignant Masses of the Spleen -
Most things that occur in the spleen are benign. Other than lymphoma (discussed below) it is
highly unlikely that you will encounter a primary malignancy of the spleen (but if you do it’s
likely to be vascular). For the purposes of academic discussion (and possible multiple choice
trivia), angiosarcoma is the most common.
Angiosarcoma: It is aggressive and has a poor prognosis. On CT it can manifest as a
poorly defined area of heterogeneity or low density in an enlarged spleen. They can contain
necrosis and get big enough to rupture (spontaneous rupture occurs like 30% of the time).
Contrast enhancement is usually poor. Yes, these can occur from prior thorotrast exposure.
Lymphoma is the most common malignant tumor of the spleen, and is usually seen as a
manifestation of systemic disease. Splenomegaly is the most common finding (and maybe the
only finding in low-grade disease). Although both Hodgkin and Non-Hodgkin types can
involve the spleen, Hodgkins type and high-grade lymphomas can show discrete nodules of
tumor. With regard to imaging, they are low density on CT, T1 dark, and are PET hot.
Metastatic Disease to the spleen is rare. When it does occur, it occurs via common
things (Breast, Lung, Melanoma).
Trivia: Melanoma is the most common primary neoplasm to met to the spleen.
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This page is for notes and scribbles.
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URINARY
PROMETHEUS LIONHART, M.D.
Warning: Men can expect painful urination while sitting,
especially if the penis is caught between the toilet seat and the bowl.
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SECTION 1:
An a t o my / Co n g en i t a l
Normal Anatomy:
The normal adult kidney is shaped like a bean,
with a smooth (often lobulated) outer border.
The kidney is surrounded by a thick capsule
outlined by echogenic perirenal fat. This
echogenic fat is contiguous with the renal
sinus, filling the middle of the kidney. The
cortex extends centrally into the middle of the
kidney, separated by slightly less echogenic
medullary pyramids. The normal kidney
should be between 9 cm and 15 cm in length.
The echogenicity of the kidney should be equal to or slightly less than the liver and spleen.
If the renal echogenicity is greater than the liver, this indicates some impaired renal function
(medical renal disease). Liver echogenicity significantly greater than the kidney indicates a
fatty liver.
Variant Anatomy
Fetal Lobulation - The fetal kidneys are subdivided into lobes that are separated with
grooves. Sometimes this lobulation persists into adult life. The question is always:
Fetal Lobulation VS Scarring:
• Lobulation = Renal surface
indentations overlie the space
between the pyramids
• Scarring = Renal surface
indentations overlie the
medullary pyramids.
Fetal Lobulation Renal Scarring
-Indentations Between Pyramids -Indentations Over Pyramids
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Dromedary Hump
- Focal bulge on the left kidney, which forms as the
result of adaptation to the adjacent spleen.
Prominent (or hypertrophied)
Column of Bertin
- Normal variant in which hypertrophied cortical tissue
located between the pyramids results in splaying of the
sinus. Other than the hypertrophy it looks totally normal.
It will enhance the same as adjacent parenchyma.
Most likely to be shown on ultrasound, - looks like a big
echogenic cortex. On CT or MR it would be too easy.
Renal Agenesis
- Congenital absence of one or both kidneys. If it’s unilateral this can be asymptomatic. If it s
bilateral think about the “Potter Sequence.” When it’s unilateral (it’s usually sporadic), for the
purpose of multiple choice think about associated GYN anomalies in women (70% of women
with unilateral renal agenesis have associated genital anomalies - unicornuate uterus). With
regard to men, 20% with renal agenesis have absence of the ipsilateral epididymis and vas
deferens or have an ipsilateral seminal vesicle cyst.
Associations: Ipsilateral seminal vesicle cysts, absent ipsilateral ureter, absent ipsilateral
hemitrigone and absent ipsilateral vas deferens.
• Potter Sequence: Insult (maybe ACE inhibitors) = kidneys don’t form, if kidneys don’t
form you can’t make piss, if you can’t make piss you can’t develop lungs (pulmonary
hypoplasia).
• Mayer-Rokitansky-Küster-Hauser: - Mullerian duct anomalies including absence or
atresia of the uterus. Associated with unilateral renal agenesis.
• Lying Down Adrenal or “Pancake Adrenal” Sign: - describes the elongated appearance
of the adrenal not normally molded by the adjacent kidney. It can be used to differentiate
surgically absent vs congenitally absent.
Horseshoe Kidney & Crossed Fused Renal Ectopia
Discussed in the Peds chapter (page 101).
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Renal Contrast Phases and Related Trivia
The kidneys drink contrast in a predictable order and their appearance changes accordingly. This
has implications for pathologic sensitivity (looking for tumor, vs urine leak, or urothelial lesions,
etc.. .etc... so on and so forth). Plus, it could be the source of multiple choice trivia - so I’m
compelled and honor bound to discuss it.
There are 4 possible “normal” looks the kidneys can give you:
Corticomedullary
Non- Phase (CMP) Nephrographic Excretory
“Angionephrographic ” - if you
Contrast wanna sound like a pretentious prick Phase (NP) Phase (EP)
25- 40 Seconds 70-180 Seconds 180 Seconds - 8 Mins
Contrast makes its way
through the loops of Contrast is excreted into
Contrast in the vascular system and the
Henle and the collecting the urinary tract /
extracellular interstitial space
tubules (“gets filtered”) collecting system
Progressive decrease in
Fairly uniform
Cortex is enhanced the medulla is not the nephrogram
enhancement of the
(hence the name). (depending on the timing
cortex and medulla
of the exam)
Utility: Utility: Utility:
• Characterizing renal tumor • Detect renal tumors • Evaluated morphology
enhancement (relative to the cortex • Especially useful for of the papilla (necrosis
— clear cell similar to cortex, etc...)
small / central tumors
— papillary less than cortex)
• Evaluate for urothelial
• Evaluation of renal arteries and cell / TCC lesions
veins
• Optimal phase to detect tumor
invasion of the renal veins
(important for staging / treatment
planning)
If CMP lasts longer the
Phase can be delayed (last longer) if NP will have delayed
the kidneys are shit (failure, renal onset.
artery stenosis), obstructed, or in the The NP can onset earlier
setting of cardiac failure. if the contrast rate of
infusion is increased.
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SECTION 2:
Ren a l Ma s s es
- Renal Cell Carcinoma -
Timing
The most common primary renal malignancy. RCC till proven Nephrogram phase
otherwise: (a) Enhances with contrast (> 15 HU), (b) calcifications in
(80 seconds) =
a fatty mass. Risk factors include tobacco use, syndromes like VHL,
chronic dialysis (> 3 years), family history. These dudes make Most sensitive for
hypervascular mets. They are ALWAYS lytic when they met to the detection of RCC
bones.
• Pseudoenhancement: A less than 10 HU increase in attenuation is considered within the
technical limits of the study and is not considered to represent enhancement. More rare once
a cyst is larger than 1.5 cm.
• Can RCC have fat in it? - Oh yeah, for sure -especially clear cell. This leads to the potential
sneaky situation of a fat containing lesion in the liver (which can be a RCC met). Now to
make this work they’d have to tell you the patient had RCC - or show you one. A helpful
hint is that RCCs with macroscopic fat nearly always have some calcification/ossification - if
they don’t it’s probably an AML.
Subtypes:
• Clear Cell - Most common subtype in the general population. This is also the one
associated with VHL. It is typically more aggressive than papillary, and will enhance equal
to the cortex on Corticomedullary phase. The most classic look is a cystic mass with
enhancing components.
• Papillary - This is the second most common type. It is usually less aggressive than clear
cell (more rare subtypes can be very aggressive). They are less vascular and will not
enhance equal to the cortex on Corticomedullary phase. They also are in the classic T2 dark
differential (along with lipid poor AML and hemorrhagic cyst). Risk of primary renal
malignancy in the transplanted kidney is six times that of the regular Joe. A point of
testable trivia is that these cancers are usually papillary subtypes.
• Medullary - Associated with Sickle Cell Trait. It’s highly aggressive, and usually large
and already metastasized at the time of diagnosis. Patient’s are usually younger.
• Chromophobe - All you need to know is that it’s associated with Birt Hogg Dube.
Subtype Syndrome / Association
Conventional RCC Staging: Overall Most Common in Gen Pop
Clear Cell
Stage 1: Limited to Kidney and < 7 cm Von Hippel-Lindau
Stage 2: Limited to Kidney but > 7 cm Hereditary Papillary Renal
Stage 3: Still inside Gerota’s Fascia
Papillary Carcinoma
A: Renal Vein Invaded
B: IVC below diaphragm Transplant Kidney
C: IVC above diaphragm Birt Hogg Dube
Chromophobe
Stage 4: Beyond Gerota’s Fascia
Ipsilateral Adrenal Medullary Sickle Cell Trait
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Sneaky Move
Does AD Polycystic Kidney Disease increase your risk for RCC???? - Well No, but sorta.
The genetic syndrome does NOT intrinsically increase your risk. However, dialysis does.
Who gets dialysis?? People with ADPKD. It would be such a crap way to ask a question -
but could happen. If you are asked, I’m recommending you say no to the increased risk, -
unless the question writer specifies that the patient is on dialysis.
Renal Lymphoma: This can
literally look like anything. Having said
that the most common appearance is
bilaterally, enlarged kidneys, with small,
low attenuation cortically based solid
nodules or masses (“infiltrative soft
tissue in the renal hilum ”), and
associated lymph nodes. A solitary mass
is seen in about 1/4 of the cases.
Trivia: Out of all the renal masses -
lymphoma is the most likely to preserve
the normal reniform shape.
Trivia: Lymphoma is the most common metastatic tumor to invade / infiltrate the kidneys
Renal Leukemia: The kidney is the most common visceral organ involved. Typically
the kidneys are smooth and enlarged. Hypodense lesions are cortically based only, with little
if any involvement of the medulla.
Angiomyolipoma (AML): This is the most common benign tumor of the kidney.
Almost all (95%) of them have macroscopic fat, and this is the defining feature. They are
usually incidental (in the real world).
The things to know about them are:
(1) They are associated with Tuberous Sclerosis —
Tuberous Sclerosis can be called Bourneville Disease (for the purpose of fucking with you)
(2) They can bleed if they get big enough (> 4 cm). It’s controversial if they grow or bleed
more in pregnancy (if they ask you, I guess you should say yes - because that’s the old
knowledge but some modern papers are saying not for sure).
(3) They should never have calcifications (that’s probably a RCC).
(4) They can be lipid poor (about 5% are), and those are T2 dark.
Gamesmanship: Traditional Spectral Fat Sat or In and Out of Phase (India Ink) can be used
to suggest an AML. Just remember, rarely RCCs can have fat:
Fat with Calcifications - RCC, Fat with No Calcifications = Probably AML
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Oncocytoma - This is the second most common benign
tumor (after AML). It looks a lot like a RCC, but has a
central scar 33% of the time (and 100% of the time on
multiple choice). There will be no malignant features (such
as vessel infiltration). They cannot be distinguished from
RCC on imaging and must be treated as RCC till proven
otherwise.
If they want to ask about an Oncocytoma they can show it 3
ways: (1) Solid Mass with central scar - CT or MRI, (2)
“Spoke wheel” vascular pattern on US, (3) Hotter than the
surrounding renal cortex - on PET CT.
Gamesmanship: I have encountered two types of GU radiologists in my life. The first type is the
practical type - he/she doesn’t EVER even mention oncocytoma, because enhancing renal masses
have to come out. Even if you biopsy it and get oncocytes, it doesn’t matter because RCCs can
have oncocytic features.
The second type is more of your classic academic type. To try
and sound impressive this person will often include this (and
other rare entities) in the differential. Another common The PET Trick:
psychopathology in these types is excessive word nazism
(“don’t say that, say this”). I’m fairly certain you have met RCC is typically COLDER
this person - there is usually one in every section. than surrounding renal
parenchyma on PET,
So if you are shown an enhancing renal mass with a central
scar, how do you decide if it’s a RCC or an oncocytoma? The Oncocytoma is typically
way to figure it out is simple - just read the mind of the person HOTTER than surrounding
who wrote the question. If it’s a practical type then all renal parenchyma on PET,
enhancing renal masses are RCC till proven otherwise. If it’s
the academic type then central scar = oncocytoma. You may
also think... which of these two people is more likely to
volunteer to write board questions?
Trivia: A syndrome associated with bilateral oncocytomas is Birt Hogg Dube
(they also get chromophobe RCC).
Multilocular Cystic Nephroma -
“Non-communicating, fluid-filled locules, surrounded by
thick fibrous capsule.” By definition these things are
characterized by the absence of a solid component or
necrosis.
Buzzword: “protrudes into the renal pelvis.”
The question is likely the bimodal occurrence
(4 year old boys, and 40 year old women).
I like to think of this as the Michael Jackson lesion — it loves
young boys and middle aged women.
**Remember this is the "older" nomenclature. It is not the preferred nomenclature dude.
Nerds ruined my joke. Now these are “Adult MLCNs" and “Pediatric MLCNs.” See page 110.
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Retroperitoneum — Masses and Anatomy Review
The retroperitoneum is
“behind the peritoneum” as the
name implies.
It is bordered anterior by the
anterior pararenal space (black
arrows) and posterior by the
transversalis fascia (white
arrows).
Below the level of the kidneys, there is a blending of
the fascial planes which allows for potential spread of
disease between the retroperitoneum and the pelvis.
Illustrated with the light grey part (with the black
arrows) demonstrating the inferior extension /
communication of the retroperitoneum.
• White = Peritoneum
• Light Grey Around the White =
Compartments Communicating with the
Retroperitoneum
Anatomic Trivia: The RP contains the lower esophagus, most of the duodenum, the ascending
and descending colon, the kidneys, ureters, adrenals, pancreas (minus the tail), aorta, IVC, and
the upper 2/3 of the rectum.
The classic tricks for multiple choice are:
• The pancreatic tail is NOT being part of the RP.
• Lower 1/3 of the rectum is NOT being part of the RP.
Pathology: ~75% of the primary retroperitoneal neoplasms are malignant. Any tumor in this
location is guilty until proven otherwise. Having said that, there is an enormous amount of path
that can occur in this location — I’m gonna try and focus on what I think is probably the highest
yield. The chart on the following page does not include adrenal tumors - I’ll cover those in the
endocrine chapter (and peds). RP Fibrosis is mentioned briefly- it is discussed in detail later in
the chapter. Neurogenic tumors will be covered in the neuro chapter.
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Rhabdo-
Lipomatosis Liposarcoma
Myosarcoma
Seen in big fat people Usually seen in the thigh of an old person - but is also the Most common soft
- with the classic most common primary malignant RP in adults. tissue sarcoma in
history of “incomplete These things are notorious assholes with a high rate children.
bladder emptying” (around 2/3) of local recurrence — hence the endless You see a soft tissue
You can also see this surveillance studies you end up reading post treatment.
mass (in a kid) - you
in homeless people, Don’t call it a comeback (I’ve been here for years -
who go to soup should always be
rocking my peers puttin’ suckers in fear). Also - Don’t call thinking about this.
kitchens... that it a lipoma - no matter how simple and homogenous it
specialize in ice cream looks.
soup.
Overgrowth of benign The deeper a fat containing lesion is - the more likely it is About half of them will
fat in the pelvis to be a bad actor. Fat-containing retroperitoneal lesions be in the neck, and
classically perirectal should be thought of like a male resident on the about 1/4 of them in
and perivesicular mammography service- guilty of all crimes until proven the pelvis around the
spaces. innocent. bladder or testicles.
The bladder is Anything that makes them look more complex -
displaced anterior and calcifications, solid components, not fat sating out - all No surprise - it is
superior - and is “pear that makes them even more likely to be bad (not just more gonna look like a
shaped” or inverted likely to be a cancer, but more likely to metastasize). tumor. Heterogenous,
tear drop shaped. enhancing, possibly
If you see something you think is a giant fucking AML -
but you aren’t totally sure it is coming from the kidney destroying nearby
AND it has calcifications - you should think Liposarcoma. bone.
Extra - Medullary
Lymphoma RP Hemorrhage
Hematopoiesis
Abnormal deposits of The Most Common RP malignancy.
hematopoietic tissue outside Tons of Big Nodes or a Confluent Soft Tissue
the bone marrow. Mass. Classically people talk about NHL vs HL. Most Common Cause =
-NHL nodes are more likely to be larger, non- Over-Anticoagulation
The look is super non-
specific -just a bunch of soft continuous, and involve the mesentery. (high PT/INR)
tissue masses in the para- -HL nodes are more likely to involve the para-
aortic region early, and be more continuous 2nd Most Common
vertebral region. Cause = Rupture /
History is the only fair way to Leaking Aorta
test this — they have to tell PET/CT is excellent for Lymphoma (in 3rd Most Common
you (or somehow show you) particular it is very useful for disease vs Cause = Bleeding RCC
that the patient has a history
treated residual scarring — with disease being or AML
of hemoglobinopathy,
myelofibrosis, leukemia - FDG avid).
etc...
“Mantle Like Soft Tissue Mass Around the Aorta , IVC, and/or Ureters"
- This has a classic DDx of:
Lymphoma RP Fibrosis Erdheim Chester
Can displace the aorta forward, Like lymphoma RPF can be hot on Huge Zebra. Gamesmanship would
and be seen above the renal PET. It does not usually displace be to show you plain films of the
arteries. Tends to push things the aorta anterior, is uncommon legs with bilateral symmetric
rather than tether and obstruct. above the renal arteries, and tends sclerosis of the metaphysis
to tether and obstruct. (sparing the epiphysis).
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SECTION 3:
Cys t i c Di s ea s e
Bosniak Cyst Classification:
•Class 1: Simple - less than 15 HU with no enhancement
•Class 2: Hyperdense (< 3 cm). Thin calcifications, Thin Septations
•Class 2F: Hyperdense (> 3 cm). Minimally thickened calcifications (5% chance cancer)
•Class 3: Thick Septations, Mural Nodule (50% chance cancer)
•Class 4: Any enhancement (> 15 HU)
Class 1: Class 2: Class 2F: Class 3: Class 4:
-Simple Anechoic -Hyperdense (< 3 cm) -Hyperdense (>3 cm) -Thick Calcifications -Any Enhancement
- 0% chance of CA -Thin Calcifications -Thin Calcifications -Mural Nodule -100% chance of CA
-Thin Septations - < 5% chance of CA -50% chance of CA This is your classic look
- 0% chance of CA for a clear cell RCC
Hyperdense cysts: Basically, if the mass is greater than 70 HU and homogenous, it’s
benign (hemorrhagic or proteinaceous cyst) 99.9% of the time.
Autosomal Dominant Polycystic Kidney Disease (ADPKD) - Kidneys get
progressively larger and lose function (you get dialysis by the 5th decade). Hyperdense
contents & calcified wall are frequently seen due to prior hemorrhage. What you need to
know is: (1) it’s Autosomal Dominant “ADult”, (2) They get cysts in the liver 70% of the
time, (3) they get seminal vesicle cysts (some sources say 60%), and (4) they get Berry
Aneurysms. As mentioned before, they don’t have an intrinsic risk of cancer, but do get
cancer once they are on dialysis.
Autosomal Recessive Polycystic Kidney Disease (ARPKD) - These guys
get HTN and renal failure. The liver involvement is different than the adult form. Instead of
cysts they have abnormal bile ducts and fibrosis. This congenital hepatic fibrosis is
ALWAYS present in ARPKD. The ratio of liver and kidney disease is inversely related. The
worse the liver is the better the kidneys do. The better the liver is, the worse the kidneys do.
On ultrasound the kidneys are smoothly enlarged and diffusely echogenic, with a loss of
Corticomedullary differentiation.
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Lithium Nephropathy -Occurs in patients who take lithium long term. Can lead to
diabetes insipidus and renal insufficiency. The kidneys are normal to small in volume
with multiple (innumerable) tiny cysts, usually 2-5 mm in diameters. These "microcysts"
are distinguishable from larger cysts associated with acquired cystic disease of uremia.
They are probably going to show this on MRI with the history of bipolar disorder.
Uremic Cystic Kidney Disease - About 40% of patients with end stage renal
disease develop cysts. This rises with duration of dialysis and is seen in about 90% in
patients after 5 year of dialysis. The thing to know is: Increased risk of malignancy with
dialysis (3-6x).
Trivia: The cysts will regress after renal transplant.
Von Hippel Lindau - Autosomal dominant multi-
Cysts in Kidneys
system disorder. 50-75% have renal cysts. 25-50% ADPKD
Liver are BIG
develop RCC (clear cell).
Cysts in
• Pancreas: Cysts, Serous Microcystic Adenomas, VHL
Pancreas
Neuroendocrine (islet cell) tumor
• Adrenal: Pheochromocytoma (often multiple) Acquired Kidneys
• CNS: Hemangioblastoma of the cerebellum, brain (Uremic) are small
stem, and spinal cord
Tuberous Sclerosis - Autosomal dominant multi-system Tuberous Sclerosis
disorder. You have hamartomas everywhere (brain, lung, heart, can be referred to as
skin, kidneys). The renal findings are multiple bilateral Bourneville Disease
(for the purpose of
angiomyolipomas. They also have renal cysts, and occasionally
fucking with you)
RCC (same rate as general population, but in younger patient
population). With regard to other organ systems:
• Lung - LAM - thin walled cysts and chylothorax
• Cardiac - Rhabdomyosarcoma (typically involve cardiac septum)
• Brain - Giant Cell Astrocytoma, Cortical and subcortical tubers, subependymal
nodules
• Renal - AMLs, RCC (in younger patients)
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T2 Dark Renal Cyst
Cysts are supposed to be T2 bright. If you see the “T2 Dark Cyst” then you are dealing with the
classic differential of:
(1) Lipid Poor AML
• A small percentage of AMLs are lipid poor in the
general population.
• For the purpose of multiple choice - If you see a lipid
poor AML (especially if you see a bunch of them)
you need to think about Tuberous Sclerosis - about
30% of their AMLs are lipid poor.
(2) Hemorrhagic Cyst
• These will likely be T1 bright
(3) Papillary Subtype RCC
• Remember that clear cells (the most common sub-type) are T2 HYPER Intense.
• Both Clear Cell and Papillary will enhance, - but the clear cell enhances more avidly (equal
to cortex on corticomedullary phase).
Multicystic Dysplastic Kidney:
This is a peds thing (and is discussed in that chapter).
Quick refresher - this is the situation where you have multiple tiny
cysts forming in utero from some type of insult.
What you should know:
• “No functioning renal tissue,” - shown with MAG 3 exam.
• Contralateral renal tract abnormalities occur like 50% of the time.
Typically you think of reflux (VUR) and UPJ Obstructions
Obstruction
Contralateral
THIS vs THAT: MCDK vs Bad Hydro Kidney
• In hydronephrosis, the cystic spaces are seen to communicate.
• In difficult cases renal scintigraphy can be useful. MCDK will show no excretory function.
THIS vs THAT: Peripelvic Cyst vs Parapelvic Cyst
Para (beside): Originates from parenchyma, may compress the collecting
system. These look a lot like the cortical cysts that you see all the time, but
instead of bulging out - they bulge in.
Peri (around): Originates from renal sinus, mimics hydro. If you didn’t
have a pyelogram (delayed) phase - might be tricky to tell apart.
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SECTION 4
In f ec t i o n
Pyelonephritis - This is a clinical diagnosis. Striated Nephrogram DDx:
However you do end up diagnosing it. It’s
associated with stones. The most common organism Acute ureteral obstruction
Acute pyelonephritis
is E. Coli. In acute bacterial nephritis, alternating Medullary sponge kidney
bands of hypo and hyperattenuation (striated Acute renal vein thrombosis
nephrogram) are seen. These wedge shaped areas Radiation nephritis
are related to decreased perfusion. Perinephric Acutely following renal contusion
stranding is also commonly seen. Hypotension (bilateral)
Infantile polycystic kidney (bilateral)
Abscess - Pyelo may be complicated by abscess, which can Next Step:
present on CT as round or geographic low attenuation collections that • Bigger Than
do not enhance centrally, but do have an enhancing rim. Bigger than 3 cm = Drainage
3 cm and these guys might visit the IR section for drainage.
Chronic Pyelonephritis - Sort of a controversial entity. It is not clear whether the
condition is an active chronic infection, arises from multiple recurrent infections, or represents
stable changes from a remote single infection. The imaging findings are characterized by renal
scarring, atrophy and cortical thinning, with hypertrophy of residual normal tissue. Basically,
you have a small deformed kidney, with a bunch of wedge defects, and some hypertrophied
areas.
Emphysematous Pyelonephritis - This is a life Next Step:
threatening necrotizing infection characterized by gas formation • Urgent
within or surrounding the kidney. What you need to know: Antibiotics
(1) it’s really bad, (2) diabetics almost exclusively get it, followed by
(3) echogenic foci with dirty shadowing on ultrasound. If there is air Nephrectomy
in the perinephric space , that is associated with a miserable shit
outcome.
Emphysematous Pyelitis - This is less bad relative to emphysematous pyelonephritis.
The gas is localized to the collecting system. It’s more common in women, diabetics, and people
with urinary obstruction. Radiographic finding is gas outlining the ureters and dilated calices.
Emphysematous Pyelonephritis Emphysematous Pyelitis
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Pyonephrosis - An infected or obstructed collecting system (which
is frequently enlarged). Can be from a variety of causes; stones, tumor, Next Step:
• Urgent
sloughed papilla secondary to pyelonephritis. Can totally jack your Decompression
renal function if left untreated. Fluid-Fluid level in the collecting (Nephrostomy)
system can be seen on US. CT has trouble telling the difference
between hydro and pyonephrosis.
Xanthogranulomatous
Pyelonephritis (XGP) - chronic
destructive granulomatous process that is
basically always seen with a staghorn stone
acting as a nidus for recurrent infection. You
can have an associated psoas abscess with
minimal perirenal infection. It’s an Aunt
Minnie, with a very characteristic “Bear Paw”
appearance on CT. The kidney is not
functional, and sometimes nephrectomy is Xanthogranulomatous Pyelonephritis - Bear Paw
done to treat it.
Papillary Necrosis:
This is ischemic necrosis of the renal papillae, most
commonly involving the medullary pyramids.
Diabetes is the most common cause.
Other important causes include: pyelonephritis
(especially in kids), sickle cell, TB, analgesic use, and
cirrhosis.
Filling Defect in Calyx
Filling defects might be seen in the calyx.
The appearance of a necrotic cavity in the
papillae with linear streaks of contrast
inside the calyx has been called a “lobster
claw sign. ”
Trivia: 50% of sickle cell patients develop
papillary necrosis
Linear Streak in Calyx
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TB- The most common extra-pulmonary site of infection is
the urinary tract. TB in the kidneys is similar to TB in the
lungs with prolonged latency (years after exposure) and
“reactivation.” You could be shown imaging findings that
occur along a spectrum of severity. For the purpose of
multiple choice strategy the more severe disease would lend
itself better to imaging, and the less severe findings would
be more likely to be asked as trivia questions.
Calyceal blunting (“moth eaten calices”) is the earliest
finding. Remember the normal calyx should have a “gentle Normal IVP (from 1960)
cup shape” — not all pointy and shit. -Cup Shaped Calyces
-Symmetry of the Renal Pelvis
Distortion of the calyx / papillary necrosis will result in
deep cups, and “w” shaped central necrosis patterns.
This is nonspecific - ischemia, diabetes, lots of things can do this
- but it is the “earliest described sign” which makes it testable.
Normal Calyx Progressed Focal stenosis Ureteral
Distortion Necrosis of an Stenosis can
/ Papillary leading to infundibulum Cause
Necrosis “cavity” can result in Infundibulum Stenosis Generalized
formation. the absence of can also be diffuse and Hydronephrosis
This is the most opacification result in caliectasis
characteristic of the calyx Scarring at the renal
sign of renal (phantom pelvis can cause an
TB. calyx) uplifted appearance and
the classic “Kerr Kink”
at the renal pelvis.
Renal calcifications, which are very common with TB, can be
punctate, curvilinear, or replace the entire kidney. This
extensive calcification is a classic (and very testable) look for
TB - called the “Putty Kidney” - or an autonephrectomized end
stage TB kidney.
Another nonspecific finding - that can help you zero in on the
choice of TB is the presence of multiple calcified mesenteric
lymph nodes — arrows in my cartoon. Calcified adrenal glands
could also be seen.
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HIV Nephropathy- This is the most common cause of renal impairment in AIDS
(CD4 < 200) patients. Although the kidneys can be normal in size, they are classically
enlarged, and bright (echogenic). Some sources will go as far as saying that normal
echotexture excludes the disease (this entity is essentially always is bright). Loss of the renal
sinus fat appearance has also been described (it’s edema in the fat, rather than loss of the
actual fat).
Just think - BIG and BRIGHT kidney in HIV positive patient who is clinically in nephrotic
syndrome (massive proteinuria).
Gamesmanship: To show you the kidney is big (longer than 12 cm) they will have
to put calibers on the kidney. Calibers on anything should be a clue that the size
being displayed is relevant.
Final diagnosis is going to be via biopsy of the big bright kidney.
Disseminated PCP in HIV patients can result in punctate (primarily cortical)
calcifications.
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Contrast Induced Nephropathy (CIN)
An Infectious Propaganda
The more you read about this the more you realize it’s probably complete (or at least
near complete) bullshit. Unfortunately a number of academics (mostly nephrologists)
have made a career on this and can be pretty defensive when the subject is brought into
question. For example, just the other day I had the following interaction with one such
member of the nephrology community.
Nephrologist: Hey! Do you believe in the plague of Contrast Induced Nephropathy?
Prometheus: I don’t know. There seems to be some controversy in the literature...
Nephrologist: Don’t jerk me around ! It’s a simple question! A baby could answer it!
Prometheus: 1 guess so...
Nephrologist: Oh, you made a wise choice, my friend! If you had said no, I would have
bitten your ear off! I would have come at you like a tornado made of arms and teeth.
And - and fingernails.
*Adapted from SNL transcript 1/10/98
In your abundant free time, read this paper and become enlightened. I will warn you,
don’t let the nephrologists catch you reading it.
Davenport, Matthew S., et al. "The challenges in assessing contrast-induced
nephropathy: where are we now?." American Journal of Roentgenology 202.4 (2014):
784-789.
For the Exam — Trivia to know:
• Allergic reactions are a NOT considered a risk factor for CIN.
• “Risk Factors” for CIN include pre-existing renal insufficiency, diabetes mellitus (even
more so with pre-existing renal insufficiency), cardiovascular disease with CHF,
dehydration, and myeloma.
• Hydration via IV with 0.9% normal saline 6-12 hours before and continuing 4-12
hours after contrast administration supposedly decreases the incidence of CIN in
patients with chronic renal insufficiency (true mechanism is diluting Cr levels). Oral
hydration has been shown to not work as well.
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SECTION 5:
CALCIFICATIONS
Nephrolithiasis (kidney stones)
There are several different stone types. The most likely testable trivia for each is:
• Calcium Oxalate - By far the most common type (75%)
• Struvite Stone - More common in women and associated with UTI
• Uric Acid - “Unseen” on x-ray.
• Cystine - Rare and associated with congenital disorders of metabolism
• Indinavir - Stones in HIV patients which are the ONLY stones NOT seen on CT.
Treatment Trivia: There are two pieces of trivia that matter with regard to treatment.
Size Matters:
• Stones measuring 5 mm or smaller have a high likelihood of spontaneously passing.
• Stones measuring 1 cm or larger have a high likelihood of NOT passing spontaneously.
Composition (Uric Acid vs Not Uric Acid):
• Uric acid stones very rarely will require any kind of invasive intervention (lithotripsy,
etc...). The reason is they are very pH dependent. Big Fat People and/or diabetics tend to
have more acidic urine (from all that Mountain Dew) which leads to an increase in uric
acid stones. They can be treated with medical therapy (potassium citrate or sodium
bicarbonate) to increase the pH and melt the stones. You can’t melt a calcium stone by
messing with the pH.
Diagnosis of Uric Acid Stones:
Since identification of a uric acid stone is going to change management that makes it a target
for trivia on multiple choice. There are 2 things that I would know:
(1) Uric Acid Stones tend to have lower attenuation (< 500 HU).
(2) Uric Acid Stones will have little if any change in H.U. with dual energy CT. The reason
is they are composed of “light elements.” The larger atoms (Calcium, Phosphorous,
Magnesium, and Sulfur) tend to have a larger change - which is the basis of dual energy
CT (80 kv, and 140 kv) identification of stone composition.
Trivia: Non Uric Acid Stones will have higher HU at 80 kVp relative to 140 kVp.
Trivia: Uric Acid Stones will be very similar at 80 kVp relative to 140 kVp. *If they do
show a small change it will be the opposite - with a slightly higher HU at 140 kVp.
Trivia: Calcium stones are going to show the biggest HU change between high and low
energies. In general, low/high energy ratios are going to be around 1.1 for uric acid, 1.25 for
cystine, and > 1.25 for calcium.
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Cortical Medullary Nephrocalcinosis
Nephrocalcinosis
Hyperechoic renal papilla / pyramids which may or may not
shadow.
This is typically the sequela of
cortical necrosis, which can be Causes:
seen after an acute drop in blood
• Hyperparathyroidism - Most people will say this is the
pressure (shock, postpartum, most common.
burn patients, etc...).
• Medullary Sponge Kidney - Some people will say this is
It starts out as a hypodense non- the most common.
enhancing rim that later • Lasix - Common cause in children.
develops thin calcifications.
• Renal Tubular Acidosis (distal subtype - type 1)
Mimic is disseminated PCP.
Trivia: RTA and Hyper PTH - tend to cause a more dense
calcification that medullary sponge.
Also remember TB can have a
variable calcification pattern as
discussed earlier in the chapter.
Medullary Sponge Kidney
A congenital cause of medullary nephrocalcinosis (usually
asymmetric). The underlying mechanism is a cystic
dilation of the collecting tubules of the kidney - so the
testable association with Ehlers-Danlos makes sense. The
association with Carolis also sorta makes sense. The
association with Beckwith-Wiedemann doesn’t really make
sense (and therefore is the most likely to be tested).
Think about medullary sponge kidney with unilateral less
dense medullary nephrocalcinosis.
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SECTION 6:
Per f u s i o n / Va s c u l a r
Page Kidney
- This is a subcapsular hematoma which
causes renal compression and complex fuckery
with the renin-angiotensin system. The result
is hypertension.
The capsule is the real issue here. That
capsule is tough and won’t expand so the
hematoma puts the squeeze on the “meat” of
the kidney. You could never get a “page
pancreas” because the pancreas has no
capsule. This is the same reason why
resistive indices are worthless in a pancreas Subcapsular Hematoma + HTN = Page
(no capsule) but sometimes useful in a
kidney (which has a capsule).
Classic Clinical History: Hypertension post biopsy, lithotripsy, or trauma.
THIS vs THAT Delayed vs Persistent Nephrogram
Delayed Nephrogram - One kidney enhances and the other doesn’t (or does to a lesser
degree). Basically this is happening from pressure on the kidney, either extrinsic from a
Page kidney situation, or intrinsic from an obstructing stone.
Persistent Nephrogram - This is seen with hypotension/shock and ATN. They can show
this two ways, the first would be on a plain film of the abdomen (with dense kidneys), the
second would be on CT. The tip offs are going to be that they tell you the time (3 hours
etc...) and it’s gonna be bilateral.
Delayed Nephrogram Persistent Nephrogram
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Renal Infarct
So wedge shaped hypodensities in the kidney can be seen with lots of stuff (infarct, tumor,
infection, etc. Renal infarcts are most easily identified on post contrast imaging in the
cortical phase. If the entire renal artery is out, well then it won’t enhance (duh).
Two tricks that they could pull are the:
(1) “Cortical Rim Sign” - which is absent
immediately after the insult, but is seen 8 hours
to days later. You have a dual blood supply,
which allows the cortex to stay perfused.
(2) “Flip Flop Enhancement” can be seen
where a region of hypodensity / poor
enhancement on early phases becomes
relatively hyperdense on delayed imaging.
Renal Vein Thrombosis
Numerous causes; including dehydration, indwelling umbilical venous catheters (most
common in neonates), and nephrotic syndrome (most common in adults). This can mimic a
renal stone; presenting with flank pain, an enlarged kidney, and a delayed nephrogram.
On Doppler they are going to show you Reversed arterial diastolic flow and absent venous
flow. *This is discussed again in the subsequent transplant section.
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SECTION 7:
Tr a n s pl a n t
Renal transplant is the best treatment for end stage renal disease, and the quality of life is
significantly better than that of a long term dialysis patient (which fucking sucks I!!). The
transplanted kidney is most commonly placed in the extraperitoneal iliac fossa so that the
allograft can be anastomosed with the iliac vasculature and urinary bladder.
The way they do this surgery depends on where the kidney comes from (living vs cadaveric). The
main thing to know is that a kidney “harvested” from a hobo found floating in the river will have
not only the kidney and renal artery removed but also a segment of the aorta - that can be used for
end-to-side anastomosis to the recipient external iliac artery. In a living donation they aren’t gonna
carve on the aorta (cuz you need your aorta to live). In both cases, end to side anastomosis is
preferred for the vein and artery - typically to the external iliac vein and artery (although you can
see the internal iliac used in some situations).
Normal: The superficial location of the transplant in the iliac fossa makes ultrasound the
modality of choice for evaluation. A transplant kidney is just like a native kidney. It should
have low resistance (it’s always “on”). The upstroke should be brisk, and the flow in diastole
forward (remember it’s always “on”).
- Understanding Renal RIs
There are two major points to know first when thinking about RIs. The first is the kidney has
a capsule, and that capsule is unforgiving (it believes in nothing Lebowski). The second is a
sick kidney is a swollen kidney.
Now lets look at this formula:
If the meat (parenchyma) of the kidney
is sick and swollen, but can’t expand
because it is wrapped in a tight
unforgiving capsule you can imagine
the blood vessels going through that
kidney are going to get the squeeze.
You can also probably imagine that the
passive diastolic flow would be more
impaired (compared to the active
systolic flow) by this squeeze.
If the meat of the kidney becomes
“sick” from whatever the cause might
be (rejection, infection, inflammation,
etc...) it swells increasing resistance.
RI's should stay below 0.7. The higher the RI the sicker the kidney. This is why RIs are useful,
and this is why an upward trend in Rl is worrisome. It is important to remember, RIs are not
specific since elevation occurs with basically every pathology. For the purpose of multiple
choice, you should never use elevated RIs to exclude answers (unless the answer is normal).
Elevation in RIs does tell you something is wrong, especially if there is an upward trend.
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The 3 Flavors of Complications - (a) Urologic, (b) Vascular (c) Cancer
- Urologic Complications - (more common than vascular complications)
Obstruction - The ureter must also be surgically implanted (ureteral neocystostomy to the bladder
dome). Just like in a native kidney the ureter can get obstructed. Don’t be fooled by the ultimate asshole trick of
showing you mild hydro on a transplant (especially one with normal labs) and trying to get you to call obstruction.
Transplanted kidneys pretty much all have some mild hydro - this is related to denervation of the transplant, and
floppy tone to the ureter. If there is a true obstruction it is usually at the site of ureteral implantation to the bladder.
The common causes are post operative edema, scarring, or technical errors leading to kinking. Stones, clots, etc., are
less common. Having said that - transplants are more likely to have stones compared to the general population - it is
just that other stuff (edema, scar, kink , etc... is more common).
Hematoma - Common immediately post op. Usually resolves spontaneously. Large hematoma can produce
hydro. Acute hematoma will be echogenic, and this will progressively become less echogenic (with older
hematomas more anechoic and septated).
Urinoma - This is usually found in the first 2 weeks post op. Urine leak or urinoma will appear as an
anechoic fluid collection with no Septations, that is rapidly increasing in size. Most leaks (urine extravasation)
are going to be at the ureterovesical anastomosis. MAG3 nuclear medicine scan can be used to demonstrate
this (or the cheaper ultrasound).
Lymphocele - Lymphoceles typically occur 1-2 months after transplant. They are caused by leakage of
lymph from surgical disruption of lymphatics or leaking lymphatics in the setting of inflammation. The fluid
collection is usually medial to the transplant (between the graft and the bladder). They are actually the most
common fluid collection to cause transplant hydronephrosis.
Buzzword = Ipsilateral lower extremity edema from femoral vein compression.
Hematoma Urinoma Abscess Lymphocele
Immediate Post Op — Around Day 10 Weeks to Months 2 weeks - 6 Months
Till about 1 week
Think Simple Collection Think Simple Collection
Think Complex between the bladder and (may have tiny septa).
Collection the kidney Think Complex
Hyperemic Collection CT: If you do a delayed
Heterogenous, Septa, CT: If you do a delayed phase you will NOT see
Etc... phase you can see leakage CT: Peripheral leakage of contrast
of contrast Enhancement
CT: Appearance will Nukes: Tracers like
depend on how acute it is. Nukes: Tracers like US: Hyperemia (increased MAG3 and DTPA will
Acute = more dense. MAG3 and DTPA will flow at the periphery) NOT accumulate outside
accumulate outside the the expected location of
MRI: T1 Bright (usually) expected location of the the bladder.
bladder.
Fluid Cr > Serum Cr Fluid Cr ~ Serum Cr
Fluid K+ > Serum K+ Fluid K+ ~ Serum K+
Fever and Elevated WBC They will Not usually
would be obvious clues - drain these things (they
These things happen from although I expect the just come back). If they
ischemia to the ureter or assholes would do opt to treat them its
obstruction (usually) deliberately withhold that usually via sclerosing
information agent.
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- Urologic Complications Continued - (more common than vascular complications)
Rejection is complicated business with a bunch of fancy sounding French words (maybe Latin)
associated with numerous overlapping biopsy related classification criteria and which subtype of
the T-Cell mediated pathway blah blah blah. None of that shit matters to Radiologists. Rejection
workup involves, labs, considering the time interval, ultrasound, maybe nukes, and in many
cases a biopsy to actually prove it.
Hyperacute Rejection is an immediate failure of the graft - and you rarely see this
imaged. It is basically a dead on arrival transplant.
Acute Rejection is usually seen around week 1-3 (it is actually rare in the first 3 days).
There is overlap between the antibody mediated types (which occur early) and the T-cell
activated types (which occur later) - but again that shit is irrelevant to Radiologists. Up to 20% of
transplant patients will have some early rejection. The graft may swell and RIs will go up.
Rejection vs ATN is the common question - and MAG3 can help (see chart on the next page).
Regardless of the Nukes Exam, most sources say “biopsy” is the standard for differentiating the
two.
Acute Tubular Necrosis (ATN) is common and occurs to variable degrees on basically
every transplant. The mechanism is ischemia in the kidney after they carve it out of the Hobo
(presuming the transplant is from the usual donor - Hobo found floating in the river). So in the
time it takes to carve it out of the Hobo and sew it into an affluent celebrity (Selena Gomez,
Tracy Morgan, etc..) there is going to be some ischemia - and therefore ATN.
Lingo: “Delayed Graft Function (DGF) ” = transplant requiring dialysis in the first week. The
amount of "cold ischemia” (how long the hobo kidney is on ice) is said to be the best predictor.
Cyclosporin Toxicity (Calcineurin Inhibitor) - Immunosuppressive therapy
necessary to keep the body from rejecting the graft can ironically end up poisoning the graft.
The timing is usually later than ATN (around a month). The MAG3 exam can also look like
ATN (normal perfusion, with retained tracer) but will NOT be seen in the immediate post op
period.
Chronic Rejection is a gradual progress process which occurs months to years after
transplant. The kidney may enlarge, and you can lose Corticomedullary differentiation. The RIs
will elevate (> 0.7), which is nonspecific.
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- Urologic Complications Continued - (more common than vascular complications)
Acute
ATN Cyclosporin Toxicity Chronic Rejection
Rejection
US “RIs” Elevated Elevated Elevated Elevated
Antibody /
Ischemia During Nephrotoxic Reaction Cellular Immune
Mechanism Cell
“Harvesting” to Immunosuppressive (T-Cell) Mediated
Mediated
Timing First Week First Week Month Months
Mag 3 - Normal to Mild
Crap Normal to Mild Delay Crap
Flow Delay
Mag 3 - Crap / Pretty Much
Pretty Much Normal Crap / Delayed
Uptake Delayed Normal
Mag 3 - Crap (slow Crap (slow Crap (slow
Crap (slow progressive
Making progressive progressive progressive
excretion)
Piss excretion) excretion) excretion)
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- Vascular Complications -
Renal Artery Thrombosis -Almost always seen within the first month (usually minutes to
hours post op), resulting from technical factors - kinking or torsion of the vessel . Unless the patient
is undergoing rejection, or has renal artery stenosis (which has progressed to full on thrombosis) it is
pretty fucking rare to see this outside the early post-operative period. As a point of trivia - this is
different than hepatic artery transplant thrombosis — which is described as a later complication
(> than 1 month post op) — so don’t get it twisted and let the bastards trick you.
Renal Artery Stenosis - Typically seen within the first year after transplant (usually weeks
to months). Easily the most common vascular complication of transplant. This usually occurs at
the anastomosis (especially end-to-end types). CMV is a risk factor. The clinical / scenario buzzword
is going to be “refractory hypertension.” Criteria include:
• PSV > 200-300 cm/s. (some people say 340-400 cm/s)
• PSV ratio > 1.8-2.5x (Stenotic Part vs Non Stenotic Part)
• Tardus Parvus: Measured at the Main Renal Artery Hilum (NOT at the arcuates)
• Anastomotic Jetting
Renal Vein Thrombosis - Typically seen within the first week. Typically the kidney is
swollen. Instead of showing you the Doppler of the renal vein (which would show no flow), they will
most likely show you the artery, which classically has reversed diastolic flow.
Renal Vein Thrombosis - with the artery showing reversal of diastolic
flow. Some people call this the “reverse M sign.”
Arteriovenous Fistula (AVF) - These occur secondary to biopsy. They occur about 20% of
the time post biopsy, but are usually small and asymptomatic. They will likely show it with tissue
vibration artifact (perivascular, mosaic color assignment due to tissue vibration), with high arterial
velocity, and pulsatile flow in the vein.
Pseudoaneurysm - These also occur secondary to biopsy, but are less common. They can also
occur in the setting of graft infection, or anastomotic dehiscence. They will most likely show you the
classic “yin-yang” color picture. Alternatively, they could show Doppler with biphasic flow at the
neck of the pseudo-aneurysm.
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Renal Allograft
Compartment Syndrome Renal Vein Thrombosis Renal Artery Stenosis (RAS)
(RACS)
Seen immediately - usually
Usually the first 5 days 3 months - Two Years
< 2 hours post
(peak at 48 hours)
transplantation
This is usually an operative
complication where the
kidney was too big for the Depending on who you
ask - like 30% of kids Depending on who you ask - this is the most
pelvic extraperitoneal space
common vascular complication in a transplant.
they decided to jam it and have graft failure because
when they stitch the fascia of this...
back up it puts the squeeze Classic History is “hypertension refractory to
treatment”
on the kidney. You can The incidence is less that
imagine if there was a fluid RAS - but the morbidity
associated with it is still The lesion is usually at the level of the surgical
collection nearby that would
high. anastomosis.
make it worse
Doppler: PSV > 250 cm/s
Doppler: Absent or almost or 1.8-2.5x increase from the “normal” vessel.
Doppler: Flow in the
totally absent cortical flow There is a trend towards using 340-400 cm/s for a
vein is gone. Reversed
in the kidney (color or diastolic arterial flow. more specific call. Which number will the test
power Doppler) writer want you to use? Simply read his or her
mind to find out and answer accordingly.
Rx: Most places will try and angioplasty the
Transplant Size matters - a stenosis first. Having said that, if it is right over the
large transplanted kidney is Grey Scale: Swollen / anastomosis - you will hear people say surgery
the main risk factor enlarged kidney.
might be safer / better (higher risk of ripping the
associated with RACS. thing in half when you stretch it)
Occurring at Anytime After Trauma or Procedure
Renal Artery Thrombosis
AV Fistula Pseudoaneurysm Traumatic Hematoma
Usually very early (mins to
hours) as a post op Feeding artery with a To-and-Fro pattern of This can occur after
complication (clamp injury high velocity low- blood flow within the biopsy or from blunt
etc...) resistance waveform neck trauma.
It is rare to see this late (in Vein with a turbulent Yin-yang sign of Transplant kidneys don’t
the absence of progressive arterial appearance. swirling blood within have ribs and are fairly
stenosis or raging rejection). the sac superficial - so they can
Tissue Vibration Artifact get banged up in minor
Doppler: Flow is gone trauma.
Grey Scale: Might see Usually - no clinically Often need an Complex Collection
wedge shaped hypoechoic significant intervention - especially
infarcts hemodynamic if large (historically > 2 Heterogenous, Septa,
consequence and no cm) or increasing in size Etc...
intervention needed
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- Cancer-
The prolonged immunosuppression therapy that renal transplant patients are on places them
at significantly (100x) increased risk of developing some type of cancer. In particular, they
get more nonmelanomatous skin cancer, lymphoma, and colon cancer. In fact - annual skin
exams are a recommendation for all renal transplant patients — that is kinda random .... and
possibly testable.
RCC - Increased risk, with most of the cancers (90%) actually occurring in the native
kidney. Etiology is not totally understood; maybe it’s the immunosuppression or the fact that
many transplant patients were on dialysis (a known risk factor) that leads to the cancer risk.
In reality it doesn’t matter, and is probably both.
Risk of primary renal malignancy in the transplanted kidney is six times that of the regular
Joe. A point of testable trivia is that these cancers are usually papillary subtypes.
Post Transplant Lymphoproliferative Disorder (PTLD) - This is an
uncommon complication of organ transplant, associated with B-Cell proliferation. EBV is a
risk factor and that is one of the main reasons they screen for it - and will put people on
Rituximab (if they mention that drug - they could be hinting that patient was EBV positive).
It is most common in the first year post transplant, and often involves multiple organs. The
most typical look is a mass lesion encasing / replacing the hilum - although the appearance is
notoriously variable. The treatment is to back off the immunosuppression.
Renal Transplant + BK Virus = Urothelial Malignancy
WTF is “BK Virus ” ? It is some random virus that pretty much everyone gets and doesn’t even
notice. Nephrologists love to write papers on this critter. Supposedly... (yes I read their stupid
papers) it is usually the donor kidney that has it and then it reactivates something crazy once the
patient is immunosuppressed. Sometimes it even mimics rejection.
Just know BK = Urothelial Cancer.
Cyclophosphamide - As a point of trivia, significant exposure to cyclophosphamide
(less common now with the development of cyclosporin A) is associated with increased risk
of urothelial cancer.
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SECTION 8:
Ren a l Tr a u ma
Obviously the kidney can get injured in trauma (seen in about 10%). Injury can be graded
based on the presence of hematoma → laceration → involvement of the vein, artery, or UPJ
obstruction.
Gamesmanship: A good “Next Step” type question in the setting of renal trauma
(or pelvic fracture) would be to prompt you to get delayed imaging - this is helpful
to demonstrate a urine leak.
Terminology:
• “Fractured Kidney” - A laceration, which extends
the full depth of the renal parenchyma. By definition the
laceration must connect two cortical surfaces - so think
about it going all the way through.
• “Shattered Kidney” - This is a more severe form of
a fractured kidney. A kidney with 3 or more fragments -
this is the most severe form of renal fracture.
Renal Trauma - Rapid Pearls
Wedge Shaped Perfusion Diffuse NonPerfusion— Persistent Nephrogram
Abnormality - Think Think Devascularized — Think Renal Vein
Segmental Artery Injury Kidney Injury / Thrombosis
Trivia: A transplant kidney is at increased risk of injury in most trauma because of its superficial
location (and loss of the normal rib protection).
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SECTION 9:
URETER
Developmental Ureteral Anomalies: Discussed in the Peds chapter.
Ureter Infection / Inflammation:
Stones - Stones tend to lodge in 3 spots: UPJ, UVJ, pelvic brim.
Ureteral Wall Calcifications - Wall calcifications should make you think about
two things: (1) TB, (2) Schistosomiasis (worms).
Ureteritis cystica - Numerous tiny subepithelial fluid-filled cysts within the wall of
the ureter. The condition is the result of chronic inflammation (from stones and/or chronic
infection). Typically this is seen in diabetics with recurrent UTI. There may be an increased
risk of cancer.
Ureteral Pseudodiverticulosis - This is similar to ureteritis cystica in that both
conditions are the result of chronic inflammation (stones, infection). Instead of being cystic
filling defects, these guys are multiple small outpouchings. They are bilateral 75% of the
time, and favor the upper and middle third. There is an association with malignancy.
Malakoplakia ("The Accursed”) — Former Lord of the Dark Elves of Svartalfheim and
rare chronic granulomatous condition, this pathology can create soft tissue nodularity /
plaques in the bladder and ureters (bladder more often). It is seen in the setting of chronic
UTIs (highly associated with E.Coli), often in female immunocompromised patients.
There is also a more remote association with the Casket of Ancient Winters. Since
malakoplakia most frequently manifests as a mucosal mass involving the ureter or bladder,
the most common renal finding is obstruction secondary to a lesion in the lower tract. Step
1 buzzword = Michaelis-Gutmann Bodies.
The most easily tested piece of trivia is
this: Malakoplakia is NOT Leukoplakia = Premalignant
premalignant, and usually gets better Malakoplakia = NOT Premalignant
with antibiotics.
Leukoplakia - This is essentially squamous metaplasia secondary to chronic irritation
(stones or infections). The bladder is more commonly involved than the ureter. Imaging
findings are unlikely to be shown, but would be mural filling defects.
The most easily tested piece of trivia is this: Leukoplakia is considered premalignant and the
cancer is squamous cell.
Trivia: Leukoplakia is associated with squamous cell carcinoma NOT transitional cell
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Retroperitoneal Fibrosis
This condition is characterized by proliferation of aberrant fibro-inflammatory tissue, which
typically surrounds the aorta, IVC, iliac vessels, and frequently traps and obstructs the
ureters. It is idiopathic 75% of the time. Other causes include prior radiation, medications
(methyldopa, ergotamine, methysergide), inflammatory causes (pancreatitis, pyelonephritis,
inflammatory aneurysm), and malignancy (desmoplastic reaction, lymphoma).
Things (trivia) to know:
• Mostly (75 %) idiopathic AKA“Ormond Disease”
• Associated with IgG4 disorders (autoimmune pancreatitis, Riedel's thyroiditis,
inflammatory pseudotumor)
• Classically shown with medial deviation of ureters
• It’s more common in men
• Malignancy associated RP fibrosis occurs about 10% of the time (some people advocate
using PET to find a primary)
• The Fibrosis will be Gallium avid, and PET hot in its early stages and cold in its late
stages (mirroring its inflammatory stages). Metabolically active RP fibrosis will show
increased FDG and Gallium uptake, regardless of a benign or malignant underlying
cause
Subepithelial Renal Pelvis Hematoma:
This tends to occur in patients on long-term anticoagulation or a history of hemophilia. You
arc going to have a thickened upper tract wall - which is a classic mimic for TCC.
Gamesmanship: 1 would expect pre and post contrast images so that you can make
the classic findings of hyperdense clot on the pre-contrast that does NOT
enhance. Although a non-contrast alone (showing blood in the urinary pelvis) with
the history of hemophilia should also be enough to seal the deal.
THIS vs THAT: Deviation of the Ureters
Lateral Deviation of Medial Deviation
the Ureters “Waisting” of the Ureters
Retroperitoneal Fibrosis
Retroperitoneal
Adenopathy Retrocaval Ureter
(right side)
Aortic Aneurysm
Pelvic Lipomatosis
Psoas Hypertrophy Psoas Hypertrophy
(proximal ureter) (distal ureter)
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SECTION 10:
URETERAL MASSES
Transitional Cell Carcinoma (Urothelial Carcinoma)
- This histologic subtype makes up a very large majority (90%) of the RISK FACTORS
collecting system cancers. Imaging buzzword is “goblet” or • Smoking
“champagne glass sign” on CT IVP. • Azo Dye
• Cyclophosphamide
High Yield Statistical Trivia • Aristolochic acid (Balkan
— a way to remember this is where ever the urine sits static the Nephropathy - see below)
longest is more likely to have the cancer. • Horseshoe Kidney
So: Bladder > Renal Pelvis > Ureter. If you are getting cancers in the • Stones
ureter than you probably also have them in the bladder • Ureteral
Pseudodiverticulosis
• Ureter is the least common location for TCC of the urinary tract • Hereditary Non-Polyposis
• TCC of the renal pelvis is 2x -3x times more common than ureter Colon Cancer (type 2)
• TCC of the bladder is 100x times more common than ureter
• In the ureter 75% of the TCCs arc in the bottom 1/3
• If you have upper tract TCC there is a 40% chance of developing a bladder TCC
• If you have bladder TCC there is a 4% chance of developing a Renal Pelvis or Ureteral TCC
• Ureteral TCC is bilateral 5%
Balkan Nephropathy - This is some zebra degenerative nephropathy endemic to
the Balkan States. The only reason I mention it is that it has a super high rate of renal
pelvis and upper ureter TCCs. It’s thought to be secondary to eating aristolochic acid
(AA) in seeds of the Aristolochia clematitis plant (herb).
Squamous Cell - This is much less common than TCC (in the US anyway). The major
predisposing factor is schistosomiasis (they both start with an “S”).
Hematogenous Metastasis - Mets to the ureters arc rare but can occur (GI, Prostate, Renal,
Breast). They typically infiltrate the periureteral soft tissues and demonstrate transmural
involvement.
Fibroepithelial Polyp - This is a benign entity presents as a filling defect in the renal pelvis or
proximal ureter - which mimics a TCC (blood clot or radiolucent stone). The diagnosis is typically
made post nephrectomy - since the assumption is nearly always TCC.
Gamesmanship: For the purpose of multiple choice (and real life), renal THIS vs THAT:
pelvis filling defects should always be assumed to be either clot, calcium
(stone), or cancer. The only way I can think that a polyp question could be Polp TCC
ask would be something like “which features would make a polyp more
likely?” It has to be a trivia question, they couldn’t (in good conscious) Younger Older
expect you to pick polyp over TCC with imaging alone — even if the (30-40) (60-70)
findings and demographics were perfect - that would be teaching a terrible Smooth / Irregular
clinical message. Oblong
Mobile Fixed
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SECTION 11:
BLADDER
Normal Anatomy: Normal bladder is an extraperitoneal structure, with 4 layers. The dome
of the bladder has a peritoneal cover. It’s lined with transitional urothelium.
- Developmental Anomalies -
Prune Belly (Eagle Barrett Syndrome)
This is a malformation triad which occurs in males. Classically
shown on a babygram with a kid shaped like a pear (big wide
belly).
Triad:
• Deficiency of abdominal musculature
• Hydroureteronephrosis
• Cryptorchidism
(bladder distention interferes with descent of testes)
Urachus : This is also discussed in the Peds chapter. I will briefly
mention that the primary concern is the development of a midline
adenocarcinoma. Most of the time the presence of a midline mass makes
it obvious although calcification within any urachal soft tissue should
make you think cancer.
Bladder Diverticula - These arc more common in boys, and can be seen in a few situations.
Most bladder diverticula can also be acquired secondary to chronic outlet obstruction (big
prostate). There are a few syndromes (Ehlers Danlos is the big testable one) that you see them in
as well.
“Hutch Diverticulum:” Also discussed in the Peds chapter.
Quick refresher on some key points.
• NOT associated with posterior urethral valves or neurogenic bladder.
• Hutch Diverticula is associated with ipsilateral reflux - and referred to as “secondary reflux”
• Bladder Diverticula typically arise from the lateral walls or near the ureteral orifices
• Diverticula at the anterior / superior bladder are more likely to be urachal diverticula
• Most Diverticula are acquired (not congenital)
• Ureters more commonly deviate medially adjacent to a diverticula
Bladder Ears - “Transitory extraperitoneal herniation of the bladder” if you want to sound
smart. This is not a diverticulum. Instead, it’s transient lateral protrusion of the bladder into the
inguinal canal. It’s very common to see, and likely doesn’t mean crap. However, some sources
say an inguinal hernia may be present 20% of the time. Smooth walls, and usually wide necks can
help distinguish them from diverticula.
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- Bladder Cancer -
Gamesmanship: GROSS hematuria confers a 4x greater risk than microscopic hematuria. If the
question header specifically indicates “GROSS” hematuria - think bladder cancer first.
Next Step: Along these lines if the history is GROSS hematuria, and the patient is 50 or older
they should get a CT Hematuria Protocol / Urography (pre and post, with delays), and also
cystoscopy.
What Does Marcelus Wallus’ Bladder Cancer Look Like ? Short answer = soft tissue in the bladder.
If you are looking at a well distended bladder (which is pretty much required to say shit about the
bladder) focal wall thickening or nodules should be considered cancer till proven otherwise.
What about diffuse circumferential bladder wall thickening? This isn’t usually cancer, especially in
the world of multiple choice. This is probably more of an inflammation or infection situation - or chronic
partial outlet obstruction (if the prostate is enormous). I’d only call a cancer in this situation if there was
really asymmetric nodular thickening superimposed on circumferential thickening.
What about enhancement ? You will hear people refer to bladder cancers as hypovascular tumors - but
they can and often do enhance, especially on early arterial phases. Any focal enhancement should trigger
you to think cancer - unless you’ve got good reasons to think otherwise. Having said all that - most
people will say the delayed phase is the most important for identifying bladder cancers - and that is the
choice I would recommend if you are forced to choose (white background of contrast - makes soft tissue
masses easier to see).
Types of Cancer / Mimics:
Rhabdomyosarcoma - This is the most common bladder cancer in humans less than 10 years of age.
They arc often infiltrative, and it’s hard to tell where they originate. “Paratesticular Mass” is often a
buzzword. They can met to the lungs, bones, and nodes. The Botryoid variant produces a polypoid
mass, which looks like a bunch of grapes.
Transitional Cell Carcinoma (Urothelial Carcinoma) - As stated above, the bladder is the most
common site, and this is by far the most common subtype. All the risk factors, are the same as above.
If anyone asks “superficial papillary” is the most common TCC bladder subtype.
Squamous Cell Carcinoma - When I say Squamous Cell Bladder, you say Schistosomiasis. This is
convenient because they both start with an “S.” The classic picture is a heavily calcified bladder and
distal ureters (usually shown on plain film, but could also be on CT). Another common association
with squamous cell cancer of the bladder in the presence of a longstanding Suprapubic catheter. This
also starts with an “S.”
Adenocarcinoma of the Bladder - This is a common trick question. When I say Adenocarcinoma of
the Bladder, you say Urachus. 90% of urachal cancers are located midline at the bladder dome.
Bladder Exstrophy is also associated with an increased risk of adenocarcinoma.
Leiomyoma (“bladder fibroid”) - Benign • Most common benign bladder tumor.
tumor (not cancer - even though the section is • Looks like a fibroid (smooth, solid, homogeneous)
bladder cancer). It’s often incidentally • Young/Middle Age People (usually)
discovered (most common at the trigone). • Clinical Buzzword “urinary hesitancy” or “dribbling”
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Types of Bladder Cancer
Transitional Cell - also
known as Urothelial Squamous Cell Adenocarcinoma Rhabdomyosarcoma
Carcinoma
By far the Most Common Second Most Third Most Most common bladder
Type (like 90%) Common Type (like ~ Common Type tumor in Peds.
8%) (like 2%)
Smoking is the classic risk Classic Associations: Classic They are often
factor, but other poisons • Recurrent urinary Associations: infiltrative, and it’s
including arsenic, aniline, tract infections and • Urachal Remnant hard to tell where they
benzidine - etc or as they stone disease • Bladder originate.
call it in Flint Michigan “Tap • Schistosoma Exstrophy
Water” - have a documented Hematobium “Paratesticular
relationship (asshole jungle Mass” is often a
worm) buzzword.
Bladder Diverticulum - • Longstanding
2-10% increased risk (related Suprapubic They can met to the
to stasis). In this setting Catheter lungs, bones, and
early perivesical fat invasion nodes.
is classic (because a This is convenient
diverticulum has limited because they both
muscle in the wall to slow start with an “S.”
the invasion)
Favors the base (inferior 90% of urachal
posterior) cancers are located
midline at the
bladder dome.
Sub-divided into The classic picture is The classic picture The classic look is
Papillary vs Non- a heavily calcified is a large midline Grape-like polypoid
Papillary. bladder and distal mass associated masses — this is the
ureters (usually with a urachal sarcoma botryoides
Papillary ones look like shown on plain film, remnant with variant
shrubs “frond like” and tend but could also be on scattered
to be low grade. CT). calcifications.
Non-Papillary tends to be Tumor favors the 70% of cases have
more aggressive. trigone and lateral calcification (if
walls you see
calcifications in a
The ones NOT urachal remnant it
associated with should make you
Schistosomiasis tend think about an
to be more early cancer).
aggressive.
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- Diversion Surgery -
After radical cystectomy for bladder cancer there are several urinary diversion procedures that
can be done. People generally group these into incontinent and continent procedures. There
are a ton of these (over 50 have been described). 1 just want to touch on the big points, and
focus on complications (the most testable subject matter). The general idea is that a piece of
bowel is made into either a conduit or reservoir, and then the ureters are attached to it.
Early Complications:
•Alteration in bowel function: Adynamic ileus is the most common early complication,
occurring in almost 25% of cases. In about 3% of cases you can get SBO, usually from
adhesions near the enteroenteric anastomosis.
•Urinary Leakage: This occurs in about 5% of cases, and usually at the ureteral-reservoir
anastomosis. A urinoma can develop when the leaked urine is not collected by urinary
drains.
•Fistula: This is uncommon and seen more in patients who have had pelvic radiation.
Late Complications ( > 30 days)
•Urinary infection: This can be early or late.
•Stones: Remember to look on the non-contrast study.
•Parastomal Herniation: This occurs about 15% of the time with ileal conduits. Obesity
is a contributing factor. Most don’t matter, but 10% will need a surgical fix.
•Urinary stricture: The left side is higher risk than the right, secondary to the
angulation (it’s brought through or under the mesentery).
•Tumor Recurrence: The more advanced the original disease, the higher the risk for
recurrence. The incidence is between 3-15%, and can present as a soft tissue mass at the
ureter, bladder, or pelvic lymph node.
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- Psoas Hitch -
The “psoas hitch” procedure results in an Aunt Minnie appearance of the bladder, making it
uniquely testable.
This procedure is done in the situation where you have had an injury or pathology (stricture,
cancer, etc...) involving a long segment of the distal ureter. Normally you would just cut that
shit out and re-implant into the bladder. But what if the left over portion of the ureter is too
short? The solution is to stretch the ipsilateral portion of the bladder towards the short ureter
and sew it (“hitch it”) to the psoas muscle. That way you can get away with a short ureter,
because you stretched the bladder to bridge the gap.
Key Points:
• Why it’s done? Used for people with long segment distal ureter injury / disease
• Aunt Minnie Appearance on CT IVP or Plain Film IVP (with contrast filling the bladder).
Aunt Minnie Appearance of the
Hitched Bladder filled with
Stretched Bladder contrast on a delayed IVP.
- “Hitched” to Psoas
The “hitched” side has an upward
projection towards the psoas
muscle.
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- “Acquired” — Infectious / Inflammation -
Emphysematous Cystitis - Gas forming organism in the wall of the bladder. More
than half the time it’s a diabetic patient. It’s usually from E. Coli. It’s gonna be very obvious
on plain film and CT. Ultrasound would be sneaky, and you’d see dirty shadowing.
TB - The upper GU tract is more commonly effected, with secondary involvement of the
bladder. Can eventually lead to a thick contracted bladder. Calcifications might be present.
Schistosomiasis - Common in the third world. Eggs are deposited in the bladder wall
which leads to chronic inflammation. Things to know: the entire bladder will calcify (often
shown on plain film or CT), and you get squamous cell cancer.
Fistula - This occurs basically in 3 Fistula - Most Common Etiology
conditions; (1) diverticulitis,
(2) Crohn's, (3) Cancer. This is more • Colovesical Fistula = Diverticular Disease
common in men, although women are • Ileovesical Fistula = Crohn's
at significantly increased risk after • Rectovesical Fistula = Neoplasm or Trauma
hysterectomy (the uterus protects the
bladder).
Neurogenic Bladder - This comes in two flavors: (a) small contracted
bladder, (b) atonic large bladder. The buzzword / classic sign is "pine cone”
bladder, because of its appearance. It can lead to urine stasis, and that stasis
can predispose to bladder CA, stones, and infection.
Acquired Bladder Diverticula - As mentioned above, these can be acquired mainly
via outlet obstruction (just think big prostate). They are most common at the UVJ. They can
lead to stasis, and that stasis can predispose to bladder CA, stones, and infection.
Bladder Stones - These guys show up in two scenarios: (1) they are bom as kidney
stones and drop into the bladder (2) they develop in the bladder secondary to stasis (outlet
obstruction, or neurogenic bladder). They can cause chronic irritation and are a known risk
factor for both TCC and SCC.
“Pear Shaped Bladder” - This is more of a sign than a pathology.
Think two things (1) pelvic lipomatosis, and (2) hematoma.
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- Bladder Trauma -
In the setting of bladder trauma - Cystography (scanning the bladder after tilling it with contrast
“retrograde” via foley) is the gold standard — this can be done under fluoro or CT. I’ve head people say
this is “100%” sensitive for bladder rupture. It’s pretty obvious — if it looks intact ... its intact. If it
looks like a deflated balloon — its ruptured. Having said that — here is a testable piece of trivia, you
must distend the bladder — that means 300-400 mL of diluted water soluble (not barium!) contrast.
Inadequate bladder distention = loss of sensitivity.
What they want you to know is; extra versus intra peritoneal rupture. CT Cystography (contrast
distending bladder) is the best test - make sure the bladder is distended (300-400 mL).
Extraperitoneal - This one is more common (80-90%). Almost always associated with pelvic fracture.
This can be managed medically.
• If there is a pelvic fracture, then the chance of a bladder rupture is 10%.
• If there is a bladder rupture, there is almost always a pelvic fracture
• Molar Tooth Sign: Contrast surrounding the bladder, in the prevesical space of Retzius. This indicates
extraperitoneal bladder rupture.
Trauma!
“Normal” EP Rupture Molar Tooth Appearance
Potential Prevesicle Space Contrast from the Bladder filling
Anterior to the Bladder the Prevesicle Space (Rezius)
Intraperitoneal - This one is less common. A direct blow to a full bladder, basically pops the balloon and
blows the top off (bladder dome is the weakest part). The dude will have contrast outlining bowel loops
and in the paracolic gutters. This requires surgery.
Trauma!
Normal IP Rupture Contrast
Outlines Bowel
“Pseudo Azotemia” (Pseudo Renal Failure) - If the bladder is ruptured the creatinine in urine can be
absorbed via the peritoneal lining. This will massively elevate the creatinine making it seem like the
patient is in acute renal failure. The kidneys are normal.
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SECTION 12:
URETHRA
- Male -
Normal Anatomy (most commonly seen on a RUG), is high yield. Here are the basics:
• The length is highly variable with most texts using the following graded scale:
(itty bitty → teeny tiny → tiny → small → medium → large → extra large → Lionhart sized).
• Anatomists divide the thing into two main parts - anterior and posterior. The anterior part is made
up of the penile urethra + the bulbar urethra. The posterior part is made up of the membranous and
prostatic urethra.
• The most anterior portion of the urethra is termed the fossa navicularis which has a Latin / French
sound to it, so it is probably testable.
• The “Verumontanum” (another fancy sounding term) is an ovoid mound that lies in the posterior
wall of the prostatic urethra. An additional testable piece of trivia is that in the center of this thing is
the prostatic utricle (which is an embryologic “mullerian” remnant).
• The anterior part fills with a retrograde study (RUG). The posterior part fills with an antegrade
study (voiding urethrography). “Dynamic Urethrography” is the term used when these studies are
combined. You can fill the whole thing with a RUG - but that requires pressure to overcome the
normal spasms of this cruel and unusual procedure.
• There are two methods for identifying the bulbar-membranous junction (which is important for
delineating pathology - anterior vs posterior). The first is to find the “cone” shaped appearance of
the proximal bulbar urethra. The cone will taper into the membranous portion. The second (used if
you can’t opacify the urethra) is to draw a line connecting the inferior margins of the obturator
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Trauma:
Trauma + Blood in the meatus = “Next Step” RUG.
Anterior Injury - Classic = Crashed your bicycle (or tricycle), i.e. = Straddle Injury. Unicycle
wreck is less often associated with urethral injury (because of the lack of cross bar) but is
often associated with various juggling, fire eating, and sword swallowing injury patterns - as
well as mania, and histrionic personality disorder.
Posterior Injury - Classic = Crashed your Ferrari. Testable trivia = Often associated with a
pelvic fracture and bladder injury. I speculate that crashing one’s Ferrari is also associated
with sudden and severe atrophy of the penis.
1970s Classification System - Fair Game for the “Exam of Future.”
Type 1 Type 2 Type 3 Type 4 Type 5
(most common)
“STRETCHED" Membraneous Membraneous + Bladder Base Bulbous Urethra
Urethra Tear Bulbar Urethra injury extending “Anterior”
Tear into Prostatic
Urethra
Posterior Posterior Anterior + Posterior Anterior
Posterior
Urethra is intact ABOVE an UG Diaphragm is
and normal on INTACT UG ruptured.
RUG Diaphragm
Extraperitoneal Extraperitoneal Straddle Injury
contrast is contrast is
present present
No perineum Perineum
contrast (intact contrast (UG
UG diaphragm diaphragm is
prevents this) torn). Contrast in
the scrotum.
Associated with Associated with Associated with
Incontinence Incontinence Incontinence
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- Urethral Strictures -
THIS VS THAT: The Bicycle Crossbar Injury VS
The Injury From a Woman of Questionable Moral Standard
Straddle Injury: The most
common external cause of
traumatic stricture is this type of
mechanism. The physiology is
compression of the urethra
against the inferior edge of the
pubic symphysis. The bulbous
urethra is the site of injury
(this is the most likely
question).
Gonococcal Urethral Stricture: This tends to be a long irregular stricture
(the straddle stricture was short). It occurs in the distal bulbous urethra.
Straddle Injury Gonococcal
Short Segment - Bulbous Urethra Long Segment & Irregular- Bulbous Urethra
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Other Male Urethral Pathologies:
Pancreatic Transplant: This has been known to cause urethral injury, if the drainage is to the
bladder (the old way of doing it). Extravasation from urethral injury is said to occur in about 5% of
cases and is secondary to pancreatic enzymes jacking the urethra.
Condyloma Acuminatum - Multiple small filling defects seen on a RUG should make you
think this. Although, instrumentation including a retrograde urethrography is actually not
recommended because of the possibility of retrograde seeding.
Urethrorectal Fistula: This may occur post radiation, and is classically described with
brachytherapy (occurs in 1% of patients).
Urethral Diverticulum: In a man, this is almost always the result of long term foley
placement.
Cancer: Malignant tumors of the male urethra are rare. When they do occur, 80% are squamous
cell cancers (the exception is that prostatic urethra actually has transitional cell 90% of the time).
Urethral Diverticulum Cancer: Cancer in a urethral diverticulum is nearly ALWAYS
adenocarcinoma (rather than squamous cell).
Female Urethra:
Female Urethral Diverticulum: Urethral diverticulum is way more common in females.
They are usually the result of repeated infection of the periurethral glands (classic history is
“repeated urinary tract infections”).
In case books and
conferences this is
classically shown as
a Sagittal MRI. The
majority of urethral
diverticula are located
in the middle third of
the urethra and
involve the
posterolateral wall
It often coexists with stress urinary incontinence (60%) and urinary infection.
The buzzword is “saddle-bag” configuration, which supposedly is how you tell it from the urethra.
Stones can also develop in these things. All this infection and irritation leads to increased risk of
cancer, and the very common high yield factoid is this is most commonly adenocarcinoma (60%).
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- GU Cancer Blitz! -
Renal Cancer (Adenocarcinoma)
Subtype Syndrome / Association
Enhances equal to Overall Most Common in Gen Pop
Clear Cell
cortex on CM Phase Von Hippel-Lindau
Enhances less than Hereditary Papillary Renal Carcinoma
Papillary
cortex on CM Phase Transplant Kidney
Chromophobe Birt Hogg Dube
Medullary Sickle Cell Trait
Ureteral Cancer (Transitional Cell - now called Urothelial)
Location - think about where you get the most stasis
• Renal Pelvis - Twice as common as Ureter
• Distal Third of Ureter - Most common site
• Middle is 2nd, and Proximal is Third
Relationship to Bladder CA
• Bladder CA is way more common (like 100x more).
• So if you have bladder CA you don’t need upper tract CA.
Since upper tract CA is not all that common, if you smoked
enough Marlboro Reds to get renal pelvis CA, you probably
smoked enough to get multifocal disease including the
bladder.
• Bottom Line: Bladder can be isolated , Ureteral CA usually
also has bladder CA
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Bladder Cancer
Transitional Cell Squamous Cell Adenocarcinoma
(Urothelial Carcinoma) - Think this when you see - Midline Location is Classic
- “The usual one” - like 90% Calcifications - Association with Urachal
- Favors the base (inferior posterior) - Favors the Trigone and Lateral Remnant
- 40% of them are multiple Walls - Association with Bladder
- “Frond like ” Papillary Tumors are - Association with Exstrophy
the Most Common Subtype Schistosomiasis
- Known to be multicentric with - Association with Chronic
synchronous and metachronous Suprapubic Catheter / Urinary
bladder and upper tract lesions — Status
but remember the bladder is the
most common site.
Urethral Cancer
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5
Re pr o d u c t i v e
Pr o met h eus Li o n h a r t , m.d .
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SECTION 1:
CONGENITAL
The Uterus - Changes During Life
• Neonate - Uterus is larger than you would think for a baby (maternal / placental hormones
are still working). If you look close, the shape is a little weird with the cervix often larger
than the fundus.
• Prepuberty - The shape of the uterus changes - becoming more tube-like, with the cervix
and uterus the same size.
• Puberty - The shape of the uterus changes again, now looking more like an adult (pear-like)
- with the fundus larger than the cervix. In puberty, the uterus starts to have a visible
endometrium - with phases that vary during the cycle.
The Ovaries - Changes During Life
Just like with the uterus, infants tend to have larger ovaries (volume around 1 cc), which then
decrease and remain around or less than 1 cc until about age 6. The ovaries then gradually
increase to normal adult size as puberty approaches and occurs.
Turner Syndrome - The XO kids. Besides often having aortic coarctations, and
horseshoe kidneys they will have a pre-puberty uterus and streaky ovaries.
Embryology:
The quick and dirty of it is that the
mullerian ducts make the uterus and
upper 2/3 of the vagina.
The urogenital sinus grows up to meet
the mullerian ducts and makes the
bottom 1/3 of the vagina.
Wolffian ducts are the boy parts, and
should regress completely in girls.
Mullerian Ducts Wolffian Ducts Urogenital Sinus
Uterus Vas Deferens Prostate
Fallopian Tubes Seminal Vesicles Lower 1/3 of the Vagina
Upper 2/3 of the Vagina Epididymis
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My idea for teaching this somewhat confusing topic is to tap into the thought process of
embryology to help understand why anomalies happen, and why they happen together. The
embryology I’m about to discuss is not strict and doesn’t use all the fancy French / Latin
words. It’s more concept related...
Step 1: Step 2: Step 3: Step 4
Imagine that As development Now the bottom But because they are just
the stuff that occurs, this soup two puddles of mashed together, they don’t
makes the gets poured spilled / poured have a central cavity
kidneys and the down the back of soup begin to necessary to carry a baby.
uterus is all the the belly. “fuse” forming
same soup. one puddle So, there is a clean-up
The upper part (uterus). operation (cleavage), and this
You have two making the occurs from bottom to top -
bowls of this kidney, and the like zipping up a jacket.
stuff - half on bottom part
the left, and making the
half on the uterus.
right.
So there are 3 main ways this whole process can get screwed up.
(1) You can only have soup on one side. This is a “failure to form”. As you can imagine,
if you don’t have the soup on one side you don’t have a kidney on that side. You also
don’t have half of your uterus. This is why a unilateral absent kidney is associated with
Unicornuate Uterus (+/- rudimentary horn).
(2) As the soup gets poured down it can fail to fuse completely. This can be on the
spectrum of mostly not fused - basically separate (Uterus Didelphys) or mostly fused
except the top part - so it looks like a heart (Bicornuate). Because the Bicornuate and
Didelphys are related pathologies - they both get vaginal septa (Didelphys more often
than Bicornuate - easily remembered because it’s a more severe fusion anomaly).
(3) The clean up operation can be done sloppy (“failure to cleave”). The classic example
of this is a “Septate uterus,” where a septum remains between the two uterine cavities.
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“Failure to Form”
Vocab
• Mullerian Agenesis (Mayer-Rokitansky-Küster-Hauser (in case you don’t speak
syndrome): Has three features: (1) vaginal atresia, (2) absent or French or whatever)
rudimentary uterus (unicornuate or bicornuate) and (3) normal Cornus = Uterus
ovaries. The key piece of trivia is that the kidneys have issues Collis = Cervical
(agenesis, ectopia) in about half the cases.
• Unicornuate Uterus - The unicornuate uterus can be subdivided into 4 variants.
If you see a unicornuate uterus the classic teaching is to look for a rudimentary horn. The reason is the
rudimentary horns can have endometrium - and if present can cause lots of phantom female belly pain
problems (dysmenorrhea, hematometra, hematosalpinx, etc..., etc..., so on a so forth). Endometrial tissue
in a rudimentary horn (communicating or not) - increases the risk of miscarriage. An additional problem
could be a pregnancy in the rudimentary horn - in both the communicating and noncommunicating types-
although especially bad in the non-communicating sub-type because it nearly always results in
rudimentary horn rupture (life-threatening bleeding).
Renal agenesis contralateral to the main uterine horn (ipsilateral to the rudimentary horn) is the most
common abnormality.
“Failure to Fuse”
Uterus Didelphys Bicornuate T-Shaped
This is a complete This comes in two flavors (one cervix This is the DES related
uterine duplication “unicollis", or two cervix “bicollis”). There anomaly. It is historical
(two cervices, two will be separation of the uterus by a deep trivia, and therefore
uteri, and two upper myometrial cleft - makes it look “heart extremely high yield for the
1/3 vagina). shaped”. Vaginal septum is seen around 25% “exam of the future.” DES
of the time (less than didclphys). Although was a synthetic estrogen
A vaginal septum is they can have an increased risk of fetal loss, given to prevent miscarriage
present 75% of the it’s much less of an issue compared to Septate. in the 1940s. The daughters
time. If the patient Fertility isn’t as much of a “size thing” as it is of patients who took this
does not have vaginal a blood supply thing. Remember you can have drug ended up with vaginal
obstruction this is 8 babies in your belly at once and have them clear cell carcinoma, and
usually live... live long enough to take part in your uterine anomalies -
asymptomatic. reality show. classically “T-Shaped.”
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"Failure to Cleave"
• Septate - This one has two endometrial canals separated
by a fibrous (or muscular) septum. Fibrous vs Muscular can
be determined with MRI and this distinction changes surgical
management (different approaches). There is an increased risk
of infertility and recurrent spontaneous abortion. The septum
has a shitty blood supply, and if there is implantation on it - it
will fail early. They can resect the septum - which improves
outcomes.
This is the most common Mullerian duct anomaly associated
with miscarriage. This is improved with resection of the
septum.
• Arcuate Uterus - Mild smooth concavity of the uterine
fundus (instead of normal straight or convex) This is not really
a malformation, but more of a normal variant. It is NOT
associated with infertility or obstetric complications.
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THIS vs THAT: Bicornuate vs Septate
Bicornuate
• “Heart Shaped” - Fundal contour is
less than 5 mm above the tubal ostia
• No significant infertility issues
• Resection of the “septum" results in
poor outcomes
Septate
• Fundal contour is Normal; more than
5 mm above the tubal ostia
• Legit infertility issues - implantation
fails on the septum (it’s a blood
supply thing)
• Resection of the septum can help
Hysterosalpingogram (HSG)
If you haven’t seen (or done one) before - this is a procedure that involves cannulation
of the cervix and injecting contrast under fluoro to evaluate the cavity of the uterus.
Testable Trivia:
- HSGs are performed on days 7-10 of menstrual cycle, (after menstrual bleeding
complete - i.e. “off the rag”)
- Contraindications: infection (PID), active bleeding (“rag week”), pregnancy, and
contrast allergy.
- Bicornuate vs Septate is tough on HSG - you need MRI or 3D Ultrasound to
evaluate the outer fundal contour.
0-7 “Rag Week,” 7-14 Proliferative, 14-28 Secretory
*Day 14 Ovulation
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SECTION 2:
Ac q u i r ed
Salpingitis Isthmica Nodosa (SIN):
This is a nodular scarring of the fallopian tubes that
produces an Aunt Minnie Appearance. As trivia, it
usually involves the proximal 2/3 of the tube. This is
of unknown etiology, but likely post inflammatory /
infectious (i.e. being a woman of questionable moral
standard / “free spirit”). It’s strongly associated with
infertility and ectopic pregnancy and that is likely
the question. - Nodular diverticula of the
fallopian tubes
- No dominant channel
Uterine AVM - These can be congenital or acquired, with acquired types being way more
common. They can be serious business and you can totally bleed to death from them. The
typical ways to acquire them include: previous dilation and curettage, therapeutic abortion,
caesarean section, or just multiple pregnancies. Doppler ultrasound is going to show:
serpiginous and/or tubular anechoic structures within the myometrium with high velocity
color Doppler flow.
Intrauterine Adhesions (Ashermans) - This is scarring in the uterus, that occurs
secondary to injury: prior dilation and curettage, surgery, pregnancy, or infection (classic GU
TB). This is typically shown on HSG, with either (a) non filling of the uterus, or (b) multiple
irregular linear filling defects (lacunar pattern), with inability to appropriately distend
the endometrial canal. MRI would show a bunch of T2 dark bands. Clinically, this results in
infertility.
Endometritis - This is in the spectrum of PID. You often see it 2-5 days after delivery,
especially in women with prolonged labor or premature rupture. You are going to have fluid
and a thickened endometrial cavity. You can have gas in the cavity (not specific in a
postpartum women). It can progress to pyometrium, which is when you have expansion with
pus.
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Pelvic Floor
Getting old and having a bunch of kids can sometimes make stuff hang out of your vagina and cause you to
pee your pants (when you don’t actually want to pee your pants). It is important to make that distinction
between “prolapse” (stuff hanging out of your vagina), and “relaxation” (peeing and/or pooping your pants
when you sneeze). Both are bad... although one is worse - I’ll let you decide which one that is.
Anatomy Review: This anatomy is complicated - buncha facial bands “ligaments” muscles etc... created a
“sling” which keeps all this stuff from falling out the bottom. The best way to think about the pelvic sling of a
female is to group it into 3 functional compartments: Anterior compartment (bladder and urethra), Middle
compartment (vagina, cervix, uterus, and adnexa), and Posterior compartment (anus and rectum). This anatomy
is incredibly complex - but a few of these vocab terms could make easy questions:
Endopelvic fascia: Buncha ligaments / fascia (pubocervical fascia, rectovaginal fascia, cardinal ligaments,
etc..) most of which have vaginal or cervix in the name. Main support for the anterior & middle compartments.
Levator ani: This is the main muscular component of the pelvic floor composed of the puborectalis,
pubococcygeus, and iliococcygeus. This muscle groups constant contraction maintains the pelvic floor height.
Urogenital diaphragm: This is the most caudal or superficial musculofascial structure. It does not have a
marketable sex toy name (unlike Levator Ani). This thing usually finds it way into multiple choice exams as
the anatomic landmark used in the classification of urethral injury - as discussed in the GU chapter.
Pelvic floor relaxation has two
components (pelvic floor descent and
widening) that can be graded during
maximal strain on sag MRI:
• Hiatal enlargement (H line) - less
than 6 cm - measurement of widening
• Pelvic floor descent (M line) - less
than 2 cm - measurement of descent
Wider H or longer M = Worse.
PCL (pubococcygeal line) = drawn from As the pelvic floor
Organs hanging out = worse. inferior margin of the symphysis pubis to collapses - you will
the junction between the first and second see widening and
MRI Protocol: coccygeal elements.
Steady State - T2 - 3 planes descent evidenced by
H Line = drawn from the inferior margin these measurements.
Dynamic State - Rapid T2 with Fat of the symphysis pubis to the posterior
Sat, Sag Plane Only This is nonspecific -
aspect of the puborectalis muscle sling. it just means the
—performed during Valsalva, Kegel,
M Line = shortest distance between the thing don’t work
and/or taking a shit (seriously)
posterior aspect of the puborectalis right.
muscle sling and the PCL
Axial image through the Ischioanal space (Triangular of fat lateral and caudally to the
levator ani - could show a loss of the normal “H shaped” vagina or direct defects /
asymmetric thinning in the muscular sling. Having said that - for the purpose of multiple
choice - this anatomy is usually demonstrating an anal fistula in the setting of Crohn's.
Anterior Compartment Middle Compartment Posterior Compartment
Cystocele - Bladder Descent > 1 cm Uterine prolapse - Decent of the Rectocele - Abnormal rectal
below the pubococcygeal line. cervix or posterior vaginal fornix bulging (typically anteriorly).
Urethral hypermobility - what you < 1 cm above the pubococcygeal line. Due to weakening
say if the urethra is rotated A big turd can prop up the uterus - so of the rectovaginal fascia.
horizontally. This changes the it is best to measure them with an
treatment from, retropubic empty rectum (post defecation phase). The describe them by how far
urethropexy (for normal stress Axial images could show the vagina they bulge relative to the anal
incontinence) to a pubovaginal sling. lose its normal "H" shape - hanging canal.
Risk Factors: Squeezing a bunch of low like the sleeve of a wizard (or the Risk Factors: Vaginal surgery,
kids out of your vagina - can rupture tongue of a tired dog). Hysterectomy, Chronic
of the pubocervical fascia Risk Factor: Hysterectomy Constipation, Being Old as
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SECTION 3:
Ma s s es a n d Tu mo r s
OF THE UTERUS AND VAGINA
Fibroids (Uterine Leiomyoma): These benign smooth muscle tumors arc the most common
uterine mass. They are more common in women of African ancestry. They like estrogen and arc most
common in reproductive age (rare in prepubertal females). Because of this estrogen relationship
they tend to grow rapidly during pregnancy, and involute with menopause. Their location is
classically described as submucosal (least common), intramural (most common), or subserosal.
Typical Appearance: The general rule is they can look like anything. Having said that, they are
usually hypoechoic on ultrasound, often with peripheral blood flow and shadowing in the so called
“Venetian Blind” pattern. On CT, they often have peripheral calcifications (“popcorn” as seen on
plain film). On MRI, T1 dark (to intermediate), T2 dark, and variable enhancement. The fibroids
with higher T2 signal are said to respond better to IR treatment. A variant subtype is the
lipoleiomyoma, which is fat containing.
Fibroid Types T1 T2 Tl+C
Hyaline (Classic) Most common type Dark Dark Homogenous
Densely packed smooth muscle (without much
Hypercellular Dark Bright Homogenous
connective tissue). Respond well to embolization
Rare fat containing subtype (maybe the result of
Bright
degeneration). This thing will be hyperechoic on Maybe Rim
Lipoleiomyoma (dark if Bright Enhancement
ultrasound. Will look like a fatty uterine mass on
fat sat)
CT. Will drop signal on fat saturation sequences.
Degeneration: 4 types of degeneration are generally described. What they have in common is a lack
of / paucity of enhancement (fibroids normally enhance avidly). The process of degeneration (basically
a fibroid stroke) can cause severe pain as well as fever and/or leukocytosis.
Fibroid Degeneration T1 T2 Tl+C
Most common type.
The fibroid outgrows
Hyaline Variable
its blood supply, and Heterogeneous
(Classic) (usually None
you end up getting the (usually dark)
Degeneration dark)
accumulation of
proteinaceous tissue.
This one occurs during
pregnancy - caused by
Peripheral
Red venous thrombosis.
Rim of Variable None
(Carneous) The classic imaging
finding is a peripheral Bright T1
rim of T1 high signal.
Myxoid Dark Bright Minimal
Uncommon
Degeneration
Cystic Uncommon Dark Bright None
Degeneration
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Uterine Leiomyosarcoma - The risk of malignant transformation to a
leiomyosarcoma is super low (0.1%). These look like a fibroid, but rapidly enlarge. Areas of
necrosis are often seen.
Adenomyosis - This is endometrial tissue that has migrated into the myometrium. You
see it most commonly in multiparous women of reproductive age, especially if they’ve
had a history of uterine procedures (Caesarian section, dilatation and curettage).
Although there are several types, adenomyosis is usually generalized, favoring large portions
of the uterus (especially the posterior wall), but sparing the cervix. It classically causes
marked enlargement of the uterus, with preservation of the overall contour.
They can show it with Ultrasound or MRI.
Ultrasound is less specific with findings
including a heterogeneous uterus
(hyperechoic adenomyosis, with
hypoechoic muscular hypertrophy), or just
enlargement of the posterior wall. MRI is
the way better test with the most classic
feature being thickening of the junctional
zone of the uterus to more than 12 mm
(normal is < 5 mm). The thickening can be
either focal or diffuse. Additionally, the
findings of small high T2 signal regions
corresponding to regions of cystic change is
a classic finding.
Adenomyosis of the Uterus
- Note the T2 Bright Cystic Foci and thick junctional zone
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-Thick Endometrium-
Remember the stripe is measured without including any fluid in the canal. Focal or
generalized thickening in post menopausal women greater than 5 mm should get sampled.
Premenopausal endometriums can get very thick - up to 20 mm can be normal.
Trivia:
Postmenopausal Bleeding:
• Estrogen secreting tumors - Granulosa Cell Is it from atrophy or cancer?
tumors of the ovary will thicken the
endometrium. •Endometrium less than 5 mm =
• Hereditary Non-Polyposis Colon Cancer Probably Atrophy
(HNPCC) - have a 30-50x increased risk of
endometrial cancer •Endometrium > 4-5 mm = Maybe
cancer and gets a biopsy
Tamoxifen Changes - This is a SERM (acts like estrogen in the pelvis, blocks the
estrogen effects on the breast). It’s used for breast cancer, but increases the risk of
endometrial cancer. It will cause subendometrial cysts, and the development of
endometrial polyps (30%). Normally, post menopausal endometrial tissue shouldn’t be
thicker than 4 mm, but on Tamoxifen the endometrium is often thick (some papers say the
mean is 12 mm at 5 years). When do you biopsy? Clear guidelines on this are illusive (if
forced to guess I’d pick 8 or 10 mm). The only thing that seems consistent is that routine
screening is NOT advised. If you are wondering if a polyp is hiding you can get a
sonohysterogram (ultrasound after instillation of saline).
Tamoxifen Changes
Endometrial Fluid - In premenopausal women this is a common finding. In
postmenopausal women it means either cervical stenosis or an obstructing mass (usually
cervical stenosis).
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- Endometrial Cancer -
Basically all uterine cancers are adenocarcinoma (90%+). The only possible exception
for the purpose of multiple choice would be the rare “leiomyosarcoma” - which looks like
a giant fucking fibroid.
Typical Scenario: A postmenopausal patient (60s) with bleeding.
“Work Up” First step is going to be an ultrasound. If the endometrium is too thick (most
people say 4 - 5mm) then it gets a biopsy. Almost always this will be stage 1 disease, and
no further imaging will be done. If there is concern that it’s more than stage 1 - that is
when you would get MRI (CT is shit for the uterus and would never be the right answer).
• First Step Postmenopausal Bleeder = Ultrasound
• Too Thick ? = Biopsy
• Extent of Disease = MRI
Appearance on MRI:
• THso
• T2 Mildly Hyper
• T1+C Homogenous, but less enhancement compared to adjacent myometrium (it’s
dark).
• DWI Will show restricted diffusion. This sequence is good for "Drop mets” into the
vagina, and for lymph node detection.
T1+C: Tumor Enhances T2 : Tumor is Mildly Bright DWI: Tumor Restricts
Less than Adjacent
Myometrium
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- Endometrial Cancer - Continued
Critical Stage (most testable stage) - Stage 1 to Stage 2
• Stage 2 disease is defined as cervical stroma invasion. This is supposedly high risk for
lymph node mets.
• The diagnostic key is the post contrast imaging (obtained 2-3 mins after injection). If
the cervical mucosa enhances normally, you have excluded stromal invasion.
• Stage 2 is probably going to change management by adding pre-op radiation to the
cervix, plus a change from TAH to radical hysterectomy (obviously this varies from
center to center).
Stage 1: Stage 2:
T1+C: Normal Dark Cervical Stroma (star). T1+C: Tumor Invasion of the Cervix
Enhancement of the Cervical Mucosa
(arrows) Excludes Invasion.
Other Possible Trivia:
• Moving from stage 1A (< 50% myometrium) to stage 1B (> 50% of the myometrium)
also increases the risk of lymph node disease.
• Some sites will do lymph node sample at stage 1A, and radical lymph node dissection
at stage 1B.
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- Cervical Cancer -
It’s usually squamous cell, related to HPV (like 90%). The big thing to know is parametrial
invasion (stage IIb). Stage IIa or below is treated with surgery. Once you have parametrial
invasion (stage IIb), or involvement of the lower 1/3 of the vagina it’s gonna get chemo / radiation
In other words, management changes so that is the most likely test question.
Cervical Cancer Staging Pearls
Stage IIA Spread beyond the cervix, but NO parametrial invasion Surgery
Stage II B Parametrial involvement but NOT extension to pelvic side wall. Chemo / Radiation
How can I tell If there is Parametrial Invasion ?
I don’t even know what the hell the “parametrium” is....
What is this parametrium? The
parametrium is a fibrous band that
separates the supravaginal cervix from
the bladder. It extends between the
layers of the broad ligament.
Why is it so important? The uterine
artery runs inside the parametrium,
hence the need for chemo - once
invaded.
How do you tell if it’s invaded ? Normally the cervix has a T2 dark ring. That
thing should be intact. If the tumor goes through that thing, you gotta call it
invaded.
T2 Dark Ring Intact T2 Dark Ring Disrupted - arrow
(No Parametrial invasion) (Parametrial invasion)
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- Vagina -
Could also be referred to as the "Petal-soft Fold of Womanhood,” "Pearl of Passion,” or
"Door of Femininity” - if the question writer is a fan of Romance Novels.
Solid Vaginal Masses:
An uninvited solid vaginal mass is usually a bad thing. It can be secondary (cervical or
uterine carcinoma protruding into the vagina), or primary such as a clear cell adenocarcinoma
or rhabdomyosarcoma.
Leiomyoma - Rare in the vagina, but can occur (most commonly in the anterior wall).
Squamous Cell Carcinoma - The most common cancer of the vagina (85%). This is
associated with HPV. This is just like the cervix.
Clear Cell Adenocarcinoma - This is the zebra cancer seen in women whose mothers took
DES (a synthetic estrogen thought to prevent miscarriage). That plus “T-Shaped Uterus” is
probably all you need to know.
Vaginal Rhabdomyosarcoma - This is the most common tumor of the vagina in children.
There is a bimodal age distribution in ages (2-6, and 14-18). They usually come off the
anterior wall near the cervix. It can occur in the uterus, but typically invades it secondarily.
Think about this when you see a solid T2 bright enhancing mass in the vagina / lower uterus
in a child.
Mets Trivia:
• A met to the vagina in the anterior wall upper 1/3 is "always” (90%) upper genital tract.
• A met to the vagina in the posterior wall lower 1/3 is "always" (90%) from the GI tract.
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Cystic Vaginal / Cervical Masses
Nabothian Cysts - These are usually on the cervix and you see them all the time. They are
the result of inflammation causing epithelium plugging of mucous glands.
Gartner Ducts Cysts - These are the result of incomplete regression of the Wolffian ducts.
They are classically located along the anterior lateral wall of the upper vagina. If they are
located at the level of the urethra, that can cause mass effect on the urethra (and
symptoms).
Bartholin Cysts - These are the result of obstruction of the Bartholin glands (mucin-
secreting glands from the urogenital sinus). They are found below the pubic symphysis
(helps distinguish them from Gartner duct).
Skene Gland Cysts - Cysts in these periurethral glands, can cause recurrent UTIs and
urethral obstruction.
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SECTION :
Ov a r y / Ad n exa
Before we begin, a few general tips (1) never biopsy or recommend biopsy of an ovary,
(2) on CT if you can’t find the ovary, follow the gonadal vein, and (3) hemorrhage in a
cystic mass usually means it’s benign.
A quick note on ovarian size; ovarian volume can be considered normal up until 15 ml
(some say 20 ml). The post menopausal ovary should NOT be larger than 6 cc.
Let’s talk about ovulation - to help understand the normal variation in the ovary.
Follicular Phase Almost Ovulation Corpus
*Note Dominant Follicle Luteum
Follicles seen during the early menstrual cycle are typically small (< 5 mm in diameter). By
day 10 of the cycle, there is usually one follicle that has emerged as the dominant follicle.
By mid cycle, this dominant follicle has gotten pretty big (around 20 mm).
The size isn’t surprising because it contains a mature
ovum. The LH surge causes the dominant follicle to Meaningless Vocab (High Yield)
Premenopausal Ovarian Cyst
rupture, releasing the egg. The follicle then regresses
< 1 cm = Follicle
in size, forming a Corpus Luteum. A small amount of
1-2 cm = Dominant Follicle
fluid can be seen in the cul-de-sac. Occasionally, a > 3 cm = Cyst
follicle bleeds and re-expands (hemorrhagic cyst) -
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Cumulus Oophorus
This is a piece of anatomy trivia. It is a collection of
cells in a mature dominant follicle that protrudes into the
follicular cavity, and signals imminent ovulation (its
absence means nothing).
Cumulus Oophorus
Fertility Meds
Medications such as a Clomiphene Citrate (Clomid), force the maturation of multiple
bilateral ovarian cysts. It is not uncommon for the ovaries of women taking this drug
to have multiple follicles measuring more than 20 mm in diameter by mid cycle.
Theca Lutein Cysts - this is a type of functional
cyst (more on that below), related to overstimulation
from b-HCG. What you sec are large cysts (~ 2-3 cm)
and the ovary has a typical multilocular cystic “spoke-
wheel” appearance.
Think about 3 things:
•Multifetal pregnancy,
•Gestational trophoblastic disease (moles),
•Ovarian Hyperstimulation syndrome. Theca Lutein Cyst
Ovarian Hyperstimulation Syndrome - This is a complication associated with fertility
therapy (occurs in like 5%). They will show you the ovaries with theca lutein cysts, then ascites,
and pleural effusions. They may also have pericardial effusions. Complications include increased
risk for ovarian torsion (big ovaries) and hypovolemic shock.
Paraovarian (Paratubal) Cyst = Cyst that is in the adnexa but not within the ovary. Instead
these things are located adjacent to the ovary or tube. If the cyst is simple (not septated or nodular) and
clearly not ovarian they will not need followup — is doesn't matter how big it is, as they have incredibly
low rate of malignancy.
TLDR: Simple paraovarian cysts do not require follow up.
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THIS vs THAT: Old vs Young
Premenstrual:
• The ovaries of a pediatric patient stay small until around age 8-9.
• Ovaries may contain small follicles.
Premenopausal:
• A piece of trivia; premenopausal ovaries may be HOT on PET
(depending on the menstrual cycle).
• This is why you do a PET in the first week of the menstrual cycle.
Postmenopausal
( > one year after menses stops): If the cyst is simple, regardless of age it’s almost
certainly benign.
• Considered abnormal if it exceeds the
Gamesmanship: What if they don’t tell you if the
upper limit of normal, or is twice the size patient is pre or post menopausal? You can use 50
of the other ovary (even if no mass is years old as a cut off. Under 50 Pre, 50 & up Post.
present).
Incidental Simple Appearing Ovarian Cyst
-Shown on CT-
• Small cysts (< 3 cm) are seen in around
20% of post menopausal women. PreMenopausal: < 3 cm = Call it Normal Follicle
PreMenopausal: > 3 cm = Get an US
• In general, postmenopausal ovaries are
PostMenopausal: < 1 cm = Call it Normal Cyst
atrophic, lack follicles, and can be PostMenopausal: > 1 cm = Get an US
difficult to find with ultrasound.
Incidental Simple Appearing Ovarian Cyst
• The ovarian volume will decrease from -Shown on US-
around 8 cc at age 40, to around l cc at
PreMenopausal: < 7 cm = No Follow Up
age 70. PreMenopausal: > 7 cm = Follow Up (3 months)
• The maximum ovarian volume in a PostMenopausal: < 5 cm = No Follow Up
post menopausal woman is 6 ml. PostMenopausal: > 5 cm = Follow Up (3 months)
• Unlike premenopausal ovaries, post Cyst is not simple (irregular Septations, papillary
projections, or solid elements) = GYN consult.
menopausal ovaries should NOT be
hot on PET.
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- THE SINISTER SIX -
In most clinical practices, the overwhelming majority of ovarian masses are benign (don’t
worry, I’ll talk about cancer, too).
• Physiologic and functioning follicles
• Corpora lutea
• Hemorrhagic cysts
• Endometriomas
• Benign cystic teratomas (dermoids)
• Polycystic ovaries
Functioning Ovarian Cysts: Functioning cysts (follicles) are affected by the menstrual
cycle (as I detailed eloquently above). These cysts are benign and usually 25 mm or less in
diameter. They will usually change / disappear in 6 weeks. If a cyst persists and either does not
change or increases in size, it is considered a non-functioning cyst (not under hormonal control).
Simple cysts that are > 7 cm in size may need further evaluation with MR (or surgical
evaluation). Just because it’s hard to evaluate them completely on US when they are that big,
and you risk torsion with a cyst that size.
Corpus Luteum: The normal corpus luteum arises from a dominant follicle (as I detailed
eloquently above). These things can be large (up to 5-6 cm) with a variable appearance (solid
hypoechoic, anechoic, thin-walled, thick-walled, cyst with debris). The most common
appearance is solid and hypoechoic with a “ring of fire” (intense peripheral blood flow).
THIS vs THAT: Corpus Luteum VS Ectopic Pregnancy
They both can have that “ring of fire” appearance, but Corpus
please don’t be an idiot about this. Most ectopic Ectopic
Luteum
pregnancies occur in the tube (the corpus luteum is an
RI < 0.4, or > 0.7 RI 0.4-0.7
ovarian structure). If you are really lucky, a “hint” is
that the corpus luteum should move with the ovary, THICK Thin
where an ectopic will move separate from the ovary Echogenic Rim Echogenic Rim
(you can push the ectopic away from it). Also, the “Ring of Fire” “Ring of Fire”
tubal ring of an ectopic pregnancy is usually more
echogenic when compared to the ovarian parenchyma.
Moves Separate Moves
Whereas, the wall of the corpus luteum is usually less from the Ovary with the Ovary
echogenic. A specific (but not sensitive) finding in
ectopic pregnancy is a RI of < 0.4 or > 0.7.
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Endometrioma:
This targets young women during their reproductive years and can cause chronic pelvic pain
associated with menstruation. The traditional clinical history of endometriosis is the triad of
infertility, dysmenorrhea, and dyspareunia.
The classic appearance is rounded mass with homogeneous low level internal echoes and
increased through transmission (seen in 95% of cases). Fluid-fluid levels and internal Septations
can also be seen. It can look a lot like a hemorrhagic cyst (sometimes).
As a general rule, the more unusual or varied the
echogenicity and the more ovoid or irregular the shape, the Q: What is the most sensitive
more likely the mass is an endometrioma. Additionally, imaging feature on MRI for the
and of more practical value, they are not going to change diagnosis of malignancy in an
on follow up (hemorrhagic cysts are). In about 30% of endometrioma?
cases you can get small echogenic foci adhering to the
walls (this helps make the endometrioma diagnosis more A: An enhancing mural nodule
likely). Obviously, you want to differentiate this from a
true wall nodule.
The complications of endometriosis (bowel obstruction, infertility, etc...) are due to a fibrotic
reaction associated with the implant. The most common location for solid endometriosis is the
uterosacral ligaments.
Do Endometriomas Ever Become Cancer? About 1% of endometriomas undergo malignant
transformation (usually endometrioid or clear cell carcinoma). How do you tell which one is
which??? Malignancy is very rare in endometriomas smaller than 6 cm. They usually have to be
bigger than 9 cm. Additionally, the majority of women with carcinoma in an endometrioma arc
older than 45 years. So risk factors for turning into cancer: (a) older than 45, (b) bigger than
6-9 cm.
Pregnancy Trivia: There is a thing called a “decidualized
endometrioma.” This is a vocab word used to describe a
solid nodule with blood flow in an endometrioma of a
pregnant girl. Obviously this is still gonna get followed up
- but is a mimic of malignancy. The thing never to forget
is that if the patient is NOT pregnant and you see a solid
nodule with blood flow - that is malignant degeneration -
period - no hesitation, next question.
Endometrioma on MRI: Will be T1 bright (from the
blood). Fat saturation will not suppress the signal
(showing you it’s not a teratoma). Will be T2 dark! (from
iron in the endometrioma). The shading sign is a buzzword
for endometriomas on MR imaging. On T2 you should
look for “shading.” The shading sign describes T2
shortening (getting dark) of a lesion that is T1 bright.
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Hemorrhagic Cysts:
As mentioned on prior pages, sometimes a ruptured follicle bleeds internally and re-
expands. The result is a homogenous mass with enhanced through transmission (tumor
won't do that) with a very similar look to an endometrioma. A lacy “fishnet appearance”
is sometimes seen and is considered classic. Doppler flow will be absent. The traditional
way to tell the difference between a hemorrhagic cyst vs endometrioma, is that the
hemorrhagic cyst will go away in 1-2 menstrual cycles (so repeat in 6-12 weeks).
Hemorrhagic Cyst on MRI - Will be T1 bright (from the blood). Fat saturation will not
suppress the signal (showing you it’s not a teratoma). The lesion should NOT enhance.
Hemorrhagic cysts in old ladies? Postmenopausal women may occasionally ovulate, so
you don’t necessarily need to freak out (follow up in 6-12 weeks). Now, late
postmenopausal women should NEVER have a hemorrhagic cyst and if you are shown
something that looks like a hemorrhagic cyst in a 70 year old - it’s cancer till proven
otherwise.
THIS vs THAT: Endometrioma vs Hemorrhagic Cyst
Endometrioma Hemorrhagic Cyst
Homogeneous with Low Level Echoes Lacy Fishnet Appearance
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Dermoid:
These things typically occur in young women (20s - 30s), and are the most common ovarian
neoplasm in patients younger than 20. The “Tip of the Iceberg Sign” is a classic buzzword and
refers to absorption of most of the US beam at the top of the mass. The typical ultrasound
appearance is that of a cystic mass, with a hyperechoic solid mural nodule, (Rokitansky nodule or
dermoid plug). Septations are seen in about 10%.
Dermoid on MRI: Will be bright on T1
(from the fat). There will be fat
suppression (not true of hemorrhagic
cysts, and endometriomas).
Do Dermoids Ever Become Cancer? About 1% of dermoids can undergo malignant
transformation (almost always to squamous cell CA). Again, risk factors are size (usually
larger than 10 cm), and age (usually older than 50).
Dermoid Gamesmanship = Gross Fat containing ovarian mass on CT
Dermoid Gamesmanship = The Old Tooth Trick - shown on plain film, CT, or even as
susceptibility (dark stuff) on MR. Remember Dermoids arc basically teratomas, and
teratomas grow all kinds of gross shit including teeth, hair, finger nails etc... The tooth is
obviously the classic one.
Dermoid Gamesmanship = “Dot -dash” pattern has been described for hair within a cyst.
Polycystic Ovarian Syndrome:
—Typically an overweight girl with infertility, acne, and a pencil mustache (not a full Ron Swanson)
The imaging criteria is:
• Ten or more peripheral simple cysts (typically small < 5 mm)
• Usually Characteristic 'string-of-pearls' appearance.
• Ovaries are typically enlarged (> 10 cc),
although in 30% of patients the ovaries have a normal volume
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SECTION 5:
Ov a r i a n Ca n c er
Ovarian cancers often present as complex cystic and solid masses. They are typically intra-ovarian
(most extra-ovarian masses are benign). The role of imaging is not to come down
hard on histology (although the exam may ask this of you), but instead to distinguish benign
from malignant and let the surgeon handle it from there.
Think Cancer if:
Unilateral (or bilateral) complex cystic adnexal masses with thick ( > 3 mm)
Septations, and papillary projections (nodule with blood flow).
Solid adnexal masses with variable necrosis
Knee Jerks:
• Multiple thin or thick Septations = Call the Surgeon
• Nodule with Flow = Call the Surgeon
• Solid Nodules Without Flow =
o Get an MR to make sure it’s not a dermoid plug,
o If it’s not a dermoid, then call the surgeon
Serous Ovarian / Cystadenocarcinoma / Cystadenoma
Serous tumors are the most common type of
ovarian malignancy. About 60% of serous
tumors are benign, and about 15% are
considered borderline (the rest are malignant).
They favor women of childbearing age, with
the malignant ones tending to occur in older
women. They typically are unilocular with
few Septations. They are frequently bilateral
(especially when malignant). Papillary
projections are a common finding, and are
suggestive of malignancy. If you see ascites,
Serous Ovarian Neoplasm
they have mets (70% have peritoneal
-Large, Unilocular, Few Septations
involvement at the time of diagnosis).
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Mucinous Ovarian Cystadenocarcinoma
Often a large mass. They are typically multi-loculated (although septa are often thin).
Papillary projections are less common than with serous tumors. You can see low level
echos (from mucin). These dudes can get Pseudomyxoma peritonei with scalloping
along solid organs. Smoking is a known risk factor (especially for mucinous types).
THIS vs THAT: Serous vs Mucinous
Serous: Mucinous:
Unilocular (fewer Septations) Multi-locular (more Septations)
Papillary Projections Common Papillary Projections Less Common
Endometrioid Ovarian Cancer: Gamesmanship:
Ovarian Mass +
This is the second most common ovarian cancer (serous Endometrial Thickening
number one, mucinous number three). These things are
This is a way to show both
bilateral about 15% of the time.
Endometrioid CA (which
What to know: often has both ovarian and
endometrial CA), and
• 25% of women will have concomitant endometrial cancer,
Granulosa-Theca Cell
with the endometrial cancer as the primary (ovary is met). Tumor (which produce
• Endometriomas can turn into endometrioid cancer estrogen - and cause
• 15% are bilateral endometrial hyperplasia)
B.F.M’s - for Adults
It’s useful to have a differential for a B.F.M.
(Big Fucking Mass) in an adult and a child. 1
discuss the child version of this on page 58.
For adults think about 3 main things:
(1) Ovarian Masses - Mucinous and Serous
(2) Desmoids - Remember Gardner Syndrome
(3) Sarcomas
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Fibroma / Fibrothecoma:
The ovarian fibroma is a benign ovarian tumor, most commonly seen in middle aged women.
The fibrothecoma / thecoma spectrum has similar histology. It’s very similar to a fibroid. On
ultrasound it’s going to be hypoechoic and solid. On MRI it’s going to be T1 and T2 dark, with
a band of T2 dark signal around the tumor on all planes. Calcifications are rare.
Similar or Related Conditions:
• Meigs Syndrome: This is the triad of ascites, pleural effusion, and a benign ovarian tumor
(most commonly fibroma).
•Fibromatosis: This is a zebra. You have tumor-like enlargement of the
ovaries due to ovarian fibrosis. It typically hits girls around the age of 25.
It’s associated with omental fibrosis and sclerosing peritonitis. You are
going to get dark T1 and T2 signal. The buzzword for that T2 signal is
“black garland sign. ” The condition is benign, and sometimes managed
with surgical removal of the ovaries.
• Brenner Tumor: Epithelial tumor of the ovary seen in women in their 50s - 70s. It’s fibrous
and T2 dark. Unlike Fibromas, calcifications are common (80%). They arc also sometimes
referred to as "Ovarian Transitional Cell Carcinoma" for the purpose of fucking with you.
Struma Ovarii:
These things are actually a subtype of ovarian teratoma. On imaging you are looking for a
multilocular, predominantly cystic mass with an INTENSELY enhancing solid component. On
MRI - the give away is very low T2 signal in the “cystic” areas which is actually the thick
colloid. These tumors contain THYROID TISSUE, and even though it’s very rare (like 5%), 1
would expect that the question stem will lead you to this diagnosis by telling you the patient is
hyperthyroid or in a thyroid storm.
Metastatic Disease to the Ovary
Around 10% of malignant ovarian tumors arc mets. The primary is most commonly from
colon, gastric, breast, lung, and contralateral ovary. The most common look is bilateral solid
tumors.
Krukenberg Tumor
- This is a metastatic tumor to the ovaries from the GI tract (usually stomach).
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SECTION 6:
Ra n d o m Ov a r i a n Pa t h
-Ovarian Torsion
Rotation of the ovarian vascular pedicle (partial or complete) can result in obstruction to venous
outflow and arterial inflow. Torsion is typically associated with a cyst or tumor (anything that
makes it heavy, so it flops over on itself).
Critical Point = The most constant finding in ovarian torsion is a large ovary.
Features:
• Unilateral enlarged ovary (greater than 4 cm)
• Mass on the ovary
• Peripheral Cysts
• Free Fluid
• Lack of arterial or venous flow
The Ovary is Not a Testicle: The ovary has a dual blood supply. Just because you have flow, does
NOT mean there isn’t a torsion. You can torse and de-torse. In other words, big ovary + pain =
torsion. Clinical correlation recommended.
-Hydrosalpinx
Thin (or thick in chronic states) elongated tubular structure in the pelvis.
The buzzword is “cogwheel appearance,” referring to the normal longitudinal folds of a
fallopian tube becoming thickened. Another buzzword is “string sign” referring to the
incomplete septae. The “waist sign” describes a tubular mass with indentations of its opposing walls
(this is suppose to help differentiate hydrosalpinx from an ovarian mass).
There are a variety of causes, the most common is being a skank, infidel, or free spirit (PID).
Additional causes include endometriosis, tubal cancer, post hysterectomy (without salpingectomy /
oophorectomy), and tubal ligation. Rare and late complication is tubal torsion.
- Pelvic Inflammatory Disease (PID) A plague upon the “dirty, slovenly, untidy woman”
Infection or inflammation of the upper female genital tract. It’s usually secondary to the cultural
behaviors of trollops and strumpets (collectors of Gonorrhea / Chlamydia). As a hint, the question
writer could describe the patient as “sexually disreputable.” The question could also describe the
patient as recently appearing as a guest on the Maury Show (the "Not the Father!” show — google if
unfamiliar, it could be on the exam).
On ultrasound you are gonna sec a Hydrosalpinx. The margin of the uterus may become ill defined
(“indefinite uterus” - is a buzzword). Later on you can end up with tubo-ovarian abscess or pelvic
abscess. You can even get bowel or urinary tract inflammatory changes.
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- Paraovarian Cyst
This is a congenital remnant that arises from the Wolffian duct. They are more common than you
think with some texts claiming these account for 10-20% of adnexal masses. They are classically
round or oval, simple in appearance, and do NOT distort the adjacent ovary (key finding). They
can indent the ovary and mimic an exophytic cyst, but a good sonographer can use the transducer to
separate the two structures.
- Ovarian Vein Thrombophlebitis
This is seen most commonly in postpartum women, often presenting with acute pelvic pain and
fever. For whatever reason, 80% of the time it’s on the right. It’s most likely to be shown on CT
(could be ultrasound) with a tubular structure with an enhancing wall and low-attenuation thrombus
in the expected location of the ovarian vein. A dreaded sequela is pulmonary embolus.
- Peritoneal Inclusion Cyst
This is an inflammatory cyst of the peritoneal cavity that occurs when adhesions envelop an ovary.
Adhesions can be thought of as diseased peritoneum. Whereas the normal peritoneum can absorb
fluid, adhesions cannot. So, you end up with normal secretions from an active ovary confined by
adhesions and resulting in an expanding pelvic mass. The classic history is patient with prior pelvic
surgery (they have to tell you that, to clue you in on the presence of adhesions), now with pain.
They could get tricky and say history of PID or endometriosis (some kind of inflammatory process to
piss off the peritoneum). In that case, it is likely they would show an ultrasound (or MR) with a
complex fluid collection occupying pelvic recesses and containing the ovary. It’s not uncommon to
have septations, loculations, and particulate matter within the contained fluid.
Key Features:
• Lack of walls. “Passive shape” that conforms
to and is defined by surrounding structures.
• Entrapment of an ovary. Ovary will be cither
in the collection, or at the periphery.
Peritoneal Inclusion Cyst -
Adhesions around an Ovary
Classic Vignette: A woman of reproductive age with a history of endometriosis, pelvic surgery, and
pelvic inflammatory disease. Accompanied by images (most likely ultrasound, less likely CT or MR)
or a fluid-filled mass that conforms to the shape of the pelvis and surrounds an ovary.
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- Gestational Trophoblastic Disease
Think about this with marked elevation of B-hCG. They will actually trend betas for tumor
activity. Apparently, elevated B-hCG makes you vomit - so hyperemesis is often part of the
given history. Other pieces of trivia is that moles arc more common in ages over 40, and prior
moles makes you more likely to get another mole.
Hydatidiform Mole
This is the most common form, and the benign form of the disease. There are two subtypes:
• Complete Mole (classic mole) (70%): This one involves the entire placenta. There will be no
fetus. The worthless trivia is that the karyotype is diploid. A total zebra scenario is that you
have a normal fetus, with a complete mole twin pregnancy (if you see that in the wild, write it
up). The pathogenesis is fertilization of an egg that has lost its chromosomes (46, XX).
First Trimester US: Classically shows the uterus to be filled with an echogenic, solid,
highly vascular mass, often described as “snowstorm” in appearance.
Second Trimester US: Vesicles that make up the mole enlarge into individual cysts
(2-30 mm) and produce your “bunch of grapes” appearance.
• Partial Mole (30%): This one involves only a portion of the placenta. You do have a fetus, but
it’s all jacked up (triploid in karyotype). The pathogenesis is fertilization of an ovum by two
sperm (69, XXY). Mercifully, it’s lethal to the fetus.
US: The placenta will be enlarged, and have areas of multiple, diffuse anechoic lesions.
You may see fetal parts.
Remember I mentioned that Theca Lutein cysts are seen in molar pregnancies.
Theca Lutein Cyst Trivia: Most commonly bilateral and seen in the second trimester
Invasive Mole
This refers to invasion of molar tissue into the myometrium. You typically see it after the
treatment of a hydatidiform mole (about 10% of cases). US may show echogenic tissue in the
myometrium. However, MRI is way better at demonstrating muscle invasive. MRI is going to
demonstrate focal myometrial masses, dilated vessels, and areas of hemorrhage and necrosis.
Choriocarcinoma (the guacamole has gone bad)
This is a very aggressive malignancy that forms only trophoblasts (no villous structure). The
typical attacking pattern of choriocarcinoma is to spread locally (into the myometrium and
parametrium) then to spread hematogenous to any site in the body. It’s very vascular and bleeds
like stink. The classic clinical scenario is serum β-hCG levels that rise in the 8 to 10 weeks
following evacuation of molar pregnancy. On ultrasound, choriocarcinoma (at any site) results in
a highly echogenic solid mass. Treatment = methotrexate.
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SECTION 7:
Do n g Bo n e
Could also be referred to as the “Penis. ”
Anatomy of this thing in cross section:
Fractured Penis: This is one of the most tragic situations that can occur in medicine.
There are several potential mechanisms of injury. Anecdotally, it seems to be most common
in older men participating in extra-marital relations with strippers named “Whisper.” There
is at least one article stating “impotence” is protective - which makes sense if you think
about the pathophysiology.
They can show it on ultrasound (look for hematoma) or MRI.
Key Trivia: Defined by fracture of the corpus
cavernosum and its surrounding sheath, the tunica
albuginea (black line outlining the dong bone).
Cartooned T1 axial through the Dong Bone (Penis):
Interruption of the black line (tunica albuginea) - arrow.
It’s helpful to look for hemorrhage (T1 bright) in the
corpus cavernosum (the primary stabilizing strut of this
battering ram).
Stigmata of this injury can include a sub optimal
angulation (Peyronie disease) from fibrous scar formation.
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SECTION 8:
t he Peo pl e’s pr o s t a t e
Cancer: Biopsy of the prostate is a terrible terrible situation, worse than anything you can
imagine in 1000 years of hell. MRI of the prostate (instead of biopsy) is probably a little better
although many sites use an endorectal coil...my God this endorectal coil! You can use prostate
MRI for high risk screening (high or rising PSA with negative biopsy), or to stage (look for
extracapsular extension).
First, let’s talk about prostate anatomy: Anatomists like to use
“zones” to describe locations, and it actually helps with Adenocarcinoma:
pathology. The anterior fibromuscular gland is dark on T1 and • Peripheral Zone: 70%
T2. The central and transitional zones (together called the • Transition Zone: 20%
"central gland”) are brighter than the anterior muscular zone, • Central Zone: 10%
but less bright than the peripheral zone on T2. In other words
the peripheral zone is the most T2 bright.
Don’t Confuse
Dark Stuff = Central Gland “Zones ”and
(this is where BPH nodules live) “Glands”
Vocab interposition
Bright Stuff = Peripheral Zone
is classic multiple
(this is where cancer lives)
choice fuckery.
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Prostate Cancer Continued:
MRI finding for Prostate CA: Cancer is dark on T2 (background is high), restricts on
diffusion (low on ADC), and enhances early and washes out (type 3 curve - just like a breast
cancer).
Dark on T2 Dark on ADC Enhances
(restricts diffusion)
Bone scan is the money for prostate mets (vertebral body mets).
Trivia: PSA can be useful when considering risk of bone mets. There is at least 1 paper that
says a PSA < 20 has a high predictive value in ruling OUT skeletal mets. In other words,
PSA tends to be high when disease is aggressive enough to go to the bones.
Staging: The main
Stage II Stage III
thing to know is
stage II vs stage III,
as extra capsular Confined by capsule (T2) Extension through capsule (T3a)
extension is the
most important Abutment of the capsule Bulging of the capsule,
factor governing without bulging or frank extension through it
treatment.
Seminal vesicles (T3b) and the nerve bundle are also right behind the prostate and can get
invaded (urologists love to hear about that).
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PSA, Gleason Score, and PI-RADS
Key Concept: Prostate Cancer is a lot like Breast Cancer - in that it is
very common and often a “benign” entity (1 in 6 men will be diagnosed Clinically Significant Cancer:
with prostate cancer , 3% will die of it). There are tons and tons of
Gleason Score > 7
elderly people with low grade prostate CA and breast cancers (DCIS)
that will never even know they have it unless somebody does a biopsy Cancer Volume > 0.5 cc
on them... or worse performs screening on them. Which brings us to
the PSA. When family medicine doctors starting doing PSA checks on Extension through the Capsule
everybody suddenly there was this enormous spike in the incidence of (loss of normal T2 signal in the
prostate cancer. Suddenly everyone has cancer (I blame the liberal seminal vesicle, bulging of the
media). capsule / frank invasion through
it, loss of fat between prostate
Who Dies of Prostate Cancer ? There are 3 factors - Gleason Scores and rectum, neurovascular
8-10, Advanced Clinical Stage (mets), and PSA > 20. People with bundle asymmetry).
Gleason scores less than 6, PSA < 10, and staging < 2a (less than half
the lobe) are unlikely to die of the prostate cancer.
Management? It is gonna depend a lot on who you ask. Most people will add hormone therapy around stage
2B (more than half the lobe) but it is complicated.
PSA: This is an antigen produced by the normal prostate and incorporated into the ejaculate (from the window
to the wall), for the purpose of dissolving cervical mucus etc... It also leaks out into the blood in small amounts
in normal men and in larger amounts when the prostate is abnormal (cancer, infected, riding a bicycle, sticking
stuff up your ass that don’t belong up your ass, and benign hypertrophy). Family Medicine docs will screen
people starting at 50. Some numbers to have a vague familiarity with include: Normal < 4. Low Risk Category
< 10. High Risk Category > 20. After prostatectomy normal is zero, if it rises to 0.2 think recurrence. After
radiation anything over 2.0 is concerning for recurrence (although it’s a little more complicated than that). PSA
< 20 = bone mets unlikely.
Gleason: There is a “grade” a “score” and a ‘group — you better fucking believe the distinction is fair game..
• Gleason Grade: This refers to the histological patterns in the sample “1” is normal, “5” is very very not
normal. 2-4 are in the middle.
• Gleason Score: This is the sum of the two most common grades.” The more common pattern is always first.
So “A” 3+5 = 8, and “B” 5+3 = 8. B has more of 5 than A ’ and is therefore worse off. Total scores less
than 6 aren’t usually reported.
• Gleason Group: This uses pattern scores to reflect the actual risk. This removes the confusion over one 7
being worse than another 7. For example 3+4 is grade 2, and 4+3 is grade 3. Grade is 1-5
PI-RADS: Scores are calculated by using data from DWI, T2, and Enhancement. Tumor in the Transition zone
is determined primarily from T2 (t for t). Peripheral zone is determined primarily from DWI.
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Benign prostatic hyperplasia (BPH): Obviously this is super common, and makes
old men pec a lot. Volume of 30 cc is one definition. Most commonly involves the
transitional zone (cancer is rare in the transitional zone - 10%). The central gland enlarges
with age. The median lobe component is the one that hypertrophies and sticks up into the
bladder. It can cause outlet obstruction, bladder wall thickening (detrusor hypertrophy), and
development of bladder diverticulum.
The IVP buzzword is “J shaped”, “Fishhook”, or “Hockey stick” shaped ureter - as
the distal ureter curves around the enlarged prostate.
With regard to the BPH nodules you
see on MRI, they are usually:
• In the Transitional Zone
(Central Gland)
• T2 Heterogenous
• Can Restrict Diffusion
• May enhance and washout
Post Biopsy Changes: Classically T1 bright stuff in the gland. It’s subacute blood.
The People’s Prostate Pathology Summary Chart
So You Can More Easily Smell What the Prostate is Cooking
T2 ADC Enhancement
Peripheral Zone Early Enhancement,
Dark Dark
Tumor Early Washout
Peripheral Zone
Dark
Hemorrhage Dark (less dark) None
(sometimes
*Typically T1 bright)
Post Biopsy
Central Gland /
Early Enhancement,
Transitional Dark “Charcoal” Dark
Early Washout
Zone Tumor
BPH Dark “Well Defined” Less Dark Can Enhance
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SECTION 9:
Mi s c el l a n eo u s Ma l e
It is best to first think about lower pelvic cysts in a male as either midline or lateral.
Male Pelvic Cysts
Midline Lateral
Prostatic Seminal
Utricle Vesicle Cyst
Diverticulosis
Mullerian of the ampulla
Duct Cyst of vas
deferens
Ejaculatory
Duct Cysts
LATERAL:
Seminal Vesicle Cyst:
The classic look is a unilateral cyst that is lateral to the prostate. If they get large they
can look midline, but if they show you a large one you won’t be able to tell it from a utricle
cyst. They can be congenital or acquired.
Congenital Trivia:
• Associated with renal agenesis
• Associated with vas deferens agenesis
• Associated with ectopic ureter insertion
• Associated with polycystic kidney disease
Acquired Trivia:
• Obstruction often from prostatic hypertrophy, or chronic infection/scarring
• Classic history is prior prostate surgery
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MIDLINE:
Prostatic Utricle Cyst: Mullerian Duct Cyst
Things to Know Things to Know
• This represents a focal dilation in the prostatic urethra • This represents a failed
(remnant of the Mullerian duct) - as such they communicate regression of the caudal ends
with the urethra and can cause “dribbling” (both on and off of the Mullerian ducts (male
the basketball court). equivalent of the vagina /
• Hypospadias is the most common associated condition - cervix).
which makes sense given the relationship with the urethra. • Does not communicate with
• Other Associations'. Prune Belly Syndrome, Downs, the urethra and does not have
Unilateral Renal Agenesis, the same associations as
and my personal favorite - the Imperforate Anus utricle cyst.
• The tendency towards Superinfection is also explained by the
communication with the urethra.
• A sneaky trick would be to show it on a RUG, where a
prostate utricle cyst would look like a focal out-pouching
from the prostatic urethra.
THIS vs THAT:
Utricle Cyst Mullerian Cyst
Pear Shaped and Usually Smaller Tear Drop Shaped
Will NOT extend above the base of the prostate Will extend above the base of the prostate
Communicates with the Urethra (Utricle), therefore Does NOT communicate with the Urethra, should
could opacify on a RUG not opacify on a RUG
Both have a tiny risk (mostly case reports) of malignancy (various types: endometrial, clear cell, squamous).
Prostate Abscess: This can cause a thick walled, septated, heterogenous, cystic lesion
anywhere in the prostate. It is usually bacterial (E. Coli). When chronic it can have a more “swiss
cheese” appearance referred to as “cavitary prostatitis.” Usually this is imaged via transrectal
ultrasound - because it gives you (the urologist) the option to do an image guided drain.
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- The Painful Scrotum -
Torsion of the Testicle:
Results from the testis and spermatic cord twisting within the serosal space leading to ischemia.
If it was 1950 you’d call in your nuclear medicine tech for scintigraphy. Now you just get a Doppler
ultrasound.
The grey scale findings are fairly straight forward. The testicle is going to be darker (hypo-echoic)
and asymmetrically enlarged - at least in the chronic setting. If it’s chronic then it will shrink up.
The doppler findings are somewhat complex. The most obviously / basic look would be to show you
absent arterial flow. This would be the equivalent of an underhand slow pitch. The curve ball would
be to show you preserved arterial flow BUT with increased resistance and a decreased diastolic flow
(or reversed diastolic flow).
That is correct my friends. Arterial flow does NOT need not be absent for torsion to be
present (depending on the duration and severity). This leads the way for some seriously
fuckery if the test writer wants to be an asshole.
The best way to think about it is like this: Testicle = Brain.
Just like the brain requires continuous diastolic flow (the thing is never off), so does the testicle.
So when you look at the waveform for a rule out torsion case you need to remember that torsion has
three possible patterns:
1- Classic Absence of Arterial Flow
2 - High resistance Arterial Flow (with Normal
decreased or reversed diastolic flow)
3 - Monophasic Arterial Waveform (loss of
the normal dicrotic notch) Abnormal:
Loss of Diastolic Flow
Fuckery: We are talking about testicular Abnormal:
artery wave forms here. The normal Reversal of Diastolic Flow
cremasteric artery will not have diastolic flow
(think about that think as the artery to a
muscle) - it’s normally high resistance. Abnormal:
Monophasic
• Cause: The “bell-clapper deformity,” which describes an abnormal high
attachment of the tunical vaginalis, increases mobility and predisposes to torsion. It is usually a
bilateral finding, so the contralateral side also gets an orchiopexy.
• liability: The viability is related to the degree of torsion (how many spins), and how long it has
been spun. As a general rule, the surgeons try and get them in the OR before 6 hours.
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High Flow States / Hyperemia:
If torsion demonstrates decreased flow, it is useful to have an idea about what can
demonstrate increased flow (decreased R.I. or increased diastolic flow)
Two things worth thinking about in this scenario: (1) Epididymo-orchitis (2) Detorsion.
The distinction between these two will be the clinical scenario.
Orchitis is painful. Detorsion is pain free.
Epididymitis: Inflammation of the epididymis, and the most common cause of acute
onset scrotal pain in adults. In high-school / college age men (likely sexually active men) the
typical cause is chlamydia or gonorrhea. In married men (not likely to be sexually active) it
is more likely to be E. coli, due to a urinary tract source. The epididymal head is the most
affected. Increased size and hyperemia are your ultrasound findings. You can have infection
of the epididymis alone or infection of the epididymis and testicle (isolated orchitis is rare).
Typical Spread: Tail → Body → Head
Gamesmanship: Could be asked as “where is the most common location”? = Tail (because
in most cases it starts there).
Orchitis: Typically progresses from epididymitis (isolated basically only occurs from
mumps). It looks like asymmetric hyperemia.
Typical: (1) Epididymitis → (2) Epididymitis + Orchitis
Mumps: Straight to Orchitis
Impending Infarct: The swelling of the testicle can become so severe that it compromises
venous flow. In this case you will see loss of diastolic flow (or reversal) - similar to the
atypical torsion patterns. This is reported as a sign of “impending infarct.”
Testicular Trauma: The big distinction is rupture vs fracture. Surgical intervention is
required if there is testicular rupture. Intratesticular fracture, and hematomas (small) do not
get surgery.
• Rupture: Disrupted tunica albuginea, heterogenous testicle, poorly defined testicular
outline
• Fracture: Intact tunica albuginea, linear hypoechoic band across the parenchyma of the
testicle, well defined testicular outline.
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- Random Path-
Epidermoid Cyst: This is a benign mass of
the testicle (no malignant potential), with an Aunt
Minnie “onion skin” look, - alternating
hypoechoic and hyperechoic rings. It’s relatively
non-vascular relative to the rest of the testicle.
Tubular Ectasia of the Rete Testis:
This is a common benign finding, resulting from
obliteration (complete or partial) of the efferent
ducts. It’s usually bilateral - and in older men.
The location of the cystic dilation is next to the
mediastinum testis. Think about this as a normal
variant. It requires no follow up or further
evaluation.
Calcified Vas Deferens: You see this all
the time in bad diabetics.
This can be shown on plain film or CT.
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SECTION 10:
Tes t i c u l a r Ca n c er
Testicle Cancer in the pediatric setting is discussed in the pediatric chapter. This discussion
will focus on the adult subtypes (with some overlap).
In general, hypoechoic solid intratesticular masses should be thought of as cancer until
proven otherwise. Doppler flow can be helpful only when it is absent (can suggest
hematoma - in the right clinical setting). If it’s extratesticular and cystic, it’s probably
benign. The step 1 trivia is that cryptorchidism increases the risk of cancer (in both
testicles), and is not reduced by orchiopexy. Most testicular tumors met via the lymphatics
(retroperitoneal nodes at the level of the renal hilum). The testable exception is
choriocarcinoma, which mets via the blood. Most testicular cancers are germ cell subtypes
(95%) - with seminomas making up about half of those.
Risk Factors: Cryptorchidism (for both testicles), Gonadal Dysgenesis, Klinefelter's,
Trauma, Orchitis, and testicular microlithiasis (maybe).
Testicular Microlithiasis: This appears
as multiple small echogenic foci within the
testes. Testicular microlithiasis is usually an
incidental finding in scrotal US examinations
performed for unrelated reasons. It might have a
relationship with Germ Cell Tumors
(controversial). Follow-up in 6 months, then
yearly is probably the recommendation -
although this recommendation is controversial.
Seminoma: This is the most common
testicular tumor, and has the best prognosis as
they are very radiosensitive. They are much more
common (9x) in white people. The classic age is
around 25. It usually looks like a homogenous
hypoechoic round mass, which classically
replaces the entire testicle. On MRI they are
usually homogeneously T2 dark (non-
seminomatous GCTs are often higher in signal).
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Non-Seminomatous Germ Cell Tumors: Basically this is not a seminoma. We are
talking about mixed germ cell tumors, teratomas, yolk sac tumors, and choriocarcinoma. They
typically occur at a young age relative to seminomas (think teenager). They are more heterogeneous
and have larger calcifications.
Testicular Lymphoma: Just be aware that lymphoma can “hide” in the testes because of the
blood testes barrier. Immunosuppressed patients are at increased risk for developing extranodal/
testicular lymphoma. Almost all testicular lymphomas are non-hodgkin B-cell subtypes. On US, the
normal homogeneous echogenic testicular tissue is replaced focally or diffusely with hypoechoic
vascular lymphomatous tissue.
Buzzword = multiple hypoechoic masses of the testicle.
Burned-Out Testicular Tumor - If you sec large, dense calcifications with shadowing in the
testicle of an old man this is probably what you should be thinking. The idea is that you’ve had
spontaneous regression of a germ cell testicular neoplasm, that is now calcified. An important pearl
is that there can still be viable tumor in there. Management is somewhat controversial and unlikely
to be asked (most people pull them out).
Staging Pearl
Testicular mets should spread to the para-aortic, aortic, caval region (N1-N3).
It’s an embryology thing.
If you have mets to the pelvic, external iliac, and inguinal nodes - this is considered “non-
regional” i.e. Ml disease. The exception is some kind of inguinal or scrotum surgery was done
before the cancer manifested - but I wouldn’t expect them to get that fancy on the test. Just
remember inguinal / pelvic nodes are non-regional and a higher stage (Ml).
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High Yield Testicle Tumor Trivia
Seminoma is the most common and has the best prognosis (it melts with radiation)
Multiple hypoechoic masses = Lymphoma
Homogenous and Microcalcifications = Seminoma
Cystic Elements and Macrocalcifications = Mixed Germ Cell Tumor / Teratoma
Most testicular tumors met via the lymphatics (choriocarcinoma mets via the blood
- and tends to bleed like stink)
Gynecomastia can be seen with Sertoli Leydig Tumors
Sertoli Cell Tumors are also seen with Peutz-Jeghers
Elevated Beta hCG Elevated AFP
Seminoma Mixed Germ Cell (Non-S)
Choriocarcinoma (Non-S) Yolk Sac (Non-S)
Seminoma Lymphoma Mixed Germ Cell
/ Teratoma
= Macrocalcification
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SECTION 11:
Ma l e In f er t i l i t y
Causes: Can be thought of as Obstructive vs Non-Obstructive
• Obstructive: Congenital bilateral absence of the vas deferens (seen in Cystic
Fibrosis), ejaculatory duct obstruction, prostatic cysts. Think about associated
renal anomalies (Zinner Syndrome).
• Non-Obstructive: Varicocele, Cryptorchidism, Anabolic Steroid Use, Erectile
Dysfunction and “The Liberal Media.”
Varicocele: This is the most common correctable cause of infertility. They can be
unilateral or bilateral. Unilateral is much more common on the left. Isolated right sided
should make you think retroperitoneal process compressing the right gonadal vein.
Cryptorchidism: Undescended testes. The testicle is usually found in the inguinal
canal. The testicle has an increased risk of cancer (actually they both will - which is weird).
It’s most commonly seen in premature kids (20%).
Major complication association for cryptorchidism:
• Malignant degeneration - of both the undescended and contralateral testicle
• Infertility
• Torsion
• Bowel Incarceration - related to the association of indirect inguinal hernia
Gamesmanship: A good distractor would be “orchitis.” It’s a pathology that
involves the balls, so it’s not totally far fetched. Obviously they can get
orchitis... but not at a higher rate. It’s not a reported association - so don’t fall
for that.
Zebras and Syndromes Associated With Male Infertility:
• Pituitary Adenoma making prolactin
• Kallman Syndrome (can’t smell + infertile)
• Klinefelter Syndrome (tall + gynecomastia + infertile)
• Zinner Syndrome (renal agenesis + ipsilateral seminal vesicle cyst)
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SECTION 12:
Tr a n s g en d er Mi s c
This is an in vogue topic and you are starting to see articles on this stuff showing up in the various
academic journals. As such I feel compelled (Jordan Peterson style) to at least touch on some of the
basics related to this topic.
Vocab: Transgender: Gender self identity docs not match their genetic / sex assigned identity at
birth. The alternative is a “Cisgender" - A man who identifies as a man (XY) or a woman who
identifies as a woman (XX). Gender and sexual orientation are different things. Sexual Orientation
is the emotion / sexual attraction to others. Transgender people are not necessarily homosexual.
Gender self identity is different than who you want to fuck.
Transgender Man: A female (XX) who identifies as the masculine (male) gender
Transgender Woman: A male (XY) who identifies as the feminine (female) gender
“Top and Bottom” Surgeries: Slang for breast & genital procedures (gender-affirming surgery)
Vaginoplasty: Procedure to create a functional and cosmetically acceptable neovagina.
• Penoscrotal inversion (PIV): The most common procedure with the lowest complication rate. It
involves orchiectomy and “penile disassembly” in a method similar to the induction ceremony of
the feared Unsullied Army. The skin from the disassembled parts is inverted / folded back to
create a tunnel. The clitoris is constructed using the native penile neurovascular anatomy.
• Intestinal Interposition: Second line strategy which involves using a segment of bowel (usually
rectosigmoid colon) to create a neovagina by colopcrincal anastomosis. They do this because
there uhhh - how best to say this - is “insufficient tissue” from the penis to make the tunnel.
Phalloplasty: Procedure to create a functional and cosmetically acceptable neopenis. Standing
urination is a typical metric of success. Several months prior to constructing the neopenis - these
patients typically undergo hysterectomy (+/- oophorectomy).
• Phalloplasty: Vaginectomy and urethroplasty are performed using vascularized vaginal mucosa to
try and elongate the urethra. Skin flaps often fail - but the “RFFF” or radial flap procedure is
probably the most common. Most of these skin grafts use a “tube in tube” strategy. I can’t believe
the details would be on the exam - but you can imagine they roll the skin and subcutaneous fat up
to make something that looks like a dick. Maybe not the most impressive of dicks - but a dick
none the less. Hey... you know what they say, it’s not the size of the dog in the fight - it’s the
size of the fight in the dog. Not sure if this expression applies to a surgically created neo-phallus
but I’m trying to be positive.
• Metoidioplasty: An alternate technique to phalloplasty - which has a lower complication rate.
The downside is the length of the created neopenis is usually not enough to have sex, but they can
still pee standing up (a major metric to success of the procedure). This technique is performed by
first using hormones to hypertrophy the clitoris (like a female body builder). Then the urethra is
lengthened (by dividing various ligaments) and anastomosed to the clitoris, which serves as the
glans. Labia minora is gonna be the source for skin to construct the shaft.
Testicular prostheses / Scrotoplasty: Generally made of silicone (high density on CT) and placed
around 6 month post phalloplasty. Just like the those dick pumps you sometimes see in diabetics -
a hydraulic pump apparatus can be placed - that thing will have tubing and be more water density.
Complications: Older technique didn’t resect the vagina - these patients were prone to fistula
between the neourethra and native vagina. DVT / PE is a post op risk if the patient is taking hormone
therapy. Bleeding, infection, urinary complication (urethral stenosis etc) all can occur - as one
might expect.
Some other surgeries that could come up on the exam include breast implants, and the various neck
surgeries to make a dude look less like a dude (thyroid chondroplasty / tracheal shave) and sound
less like a dude (glottoplasty, cricothyroid approximation).
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SECTION 13:
OB
Early Pregnancy -
Vocab:
•Menstrual Age: Embryologic Age + 14 days
•Embryo: 0-10 weeks (menstrual age)
•Fetus: > 10 weeks (menstrual age)
•Threatened Abortion - Bleeding with closed cervix
•Inevitable Abortion - Cervical dilation and/or placental and/or fetal tissue hanging out
•Incomplete Abortion - Residual products in the uterus
•Complete Abortion - All products out
•Missed Abortion - Fetus is dead, but still in the uterus.
Intradecidual Sign: This is the early gestational
sac. When seen covered by echogenic decidua is very
characteristic of early pregnancy. You can see it
around 4.5 weeks. You want to see the thin echogenic
line of the uterine cavity pass by (not stop at) the sac
to avoid calling a little bit of fluid in the canal a sac. Intradecidual Sign
Small amount of
fluid between
Double Decidual Sac Sign:
This is another positive sign of early
pregnancy.
It’s produced by visualizing the layers
of decidua.
Decidua Vera
Decidua Capsularis
Double Decidual Sac Sign
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Yolk Sac: This is the first structure visible
within the GS. The classic teaching was you
should always see it when the GS measures
8mm in diameter. The thing should be oval or
round, fluid filled, and smaller than 6 mm.
The yolk sac is located in the chorionic cavity,
and hooked up to the umbilicus of the embryo
by the vitelline duct.
Yolk Sac Gone Bad: The yolk sac shouldn’t be
Yolk Sac - in the chorionic cavity
too big (> 6 mm), shouldn’t be too small
(< 3 mm), and shouldn’t be solid or calcified.
The Amnion: The membranes of the
amniotic sac and chorionic space
typically remain separated by a thin
layer of fluid, until about 14-16 weeks
A= Amniotic Space
at which point fusion is normal. If the
amnion gets disrupted before 10 weeks Arrow = Amnion
the fetus might cross into the chorionic C= Chorionic Space
cavity and get tangled up in the fibrous
bands. This is the etiology of amniotic
band syndrome, which can be terrible
(decapitation, limb amputation, etc...).
Double Bleb Sign: This is the earliest visualization of the embryo. This is two fluid
filled sacs (yolk and amniotic) with the flat embryo in the middle.
Double Bleb Sign
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Crown Rump Length - This is typically used to estimate gestational age, and is more
accurate than menstrual history. * Embryo is normally visible at 6 weeks.
Anembryonic Pregnancy - A gestational sac without an embryo. When you see this,
the choices are (a) very early pregnancy, or (b) non-viable pregnancy. The classic teaching
was you should see the yolk sac at 8 mm (on TV). Just remember that a large sac (> 8-10 mm)
without a yolk sac, and a distorted contour is pretty reliable for a non-viable pregnancy.
Pseudogestational Sac - This is
not the same thing as an anembryonic
pregnancy. This is seen in the presence of
an ectopic pregnancy. What you are
seeing is a little bit of blood in the uterine
cavity with surrounding bright decidual
endometrium (charged up from the
pregnancy hormones).
Subchorionic Hemorrhage: These are very common. The thing to know is that the
percentage of placental detachment is the prognostic factor most strongly associated with
fetal demise; hematoma greater than 2/3 the circumference of the chorion has a 2x increased
risk of abortion. Other trivia: women older than 35 have worse outcomes with these.
Implantation Bleeding: This is a nonspecific term referring to a small subchorionic
hemorrhage that occurs at the attachment of the chorion to the endometrium.
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Criteria for Fetal Demise:
Diagnostic of Pregnancy Failure Suspicious for Pregnancy Failure
Crown-rump length of > 7 mm and no heartbeat No embryo > 6 wk after last menstrual period
Mean sac diameter of 16-24 mm and no
Mean sac diameter of > 25 mm and no embryo embryo
No embryo with heartbeat > 2 wk after a scan No embryo with heartbeat 13 days after a scan
that showed a gestational sac without a yolk sac that showed a gestational sac without a yolk sac
No embryo with heartbeat > 11 days after a scan No embryo with heartbeat 10 days after a scan
that showed a gestational sac with a yolk sac that showed a gestational sac with a yolk sac
Pregnancy of Unknown Location:
This is the vocabulary used when neither a normal IUP or ectopic pregnancy is identified in the
setting of a positive b-hCG. Typically this just means it is a very very early pregnancy, but you
can’t say that with certainty. In these cases you have three possibilities:
1 - Normal Early Pregnancy
2 - Occult Ectopic
3 - Complete Miscarriage
The management is follow up (serial b-hCG) and repeat US — assuming the patient is
hemodynamically stable.
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- Ectopic -
High Risk for Ectopic: Hx of PID, Tubal Surgery, Endometriosis, Ovulation
Induction, Previous Ectopic, Use of an IUD.
The majority of ectopic pregnancies (nearly 95%) occur in the fallopian tube (usually the
ampulla). A small percentage (around 2%) are “interstitial” developing in the portion of the
tube which passes through the uterine wall. These interstitials are high risk, as they can grow
large before rupture and cause a catastrophic hemorrhage. It is also possible (although very
rare) to have implantation sites in the abdominal cavity, ovary, and cervix.
Always start down the ectopic pathway with a positive BhCG. At around 1500-2000 mIU/L
you should see a gestational sac. At around 5000 mIU/L you should see a yolk sac. As a
general rule, a normal doubling time makes ectopic less likely.
Tubal Ring Sign: An echogenic ring,
which surrounds an un-ruptured ectopic
pregnancy. This is an excellent sign of
ectopic pregnancy - and has been
described as 95% specific.
Heterotopic Pregnancy: This is a
baby in the uterus and a baby in the tube
(or other ectopic location). This is pretty
rare, and typically only seen in women
taking ovulation drugs, or with prior bad
PID.
The Big 3 to Remember with Ectopics (positive B-hCG)
(1) Live Pregnancy / Yolk Sac outside the uterus = Slam Dunk
(2) Nothing in the uterus + anything on the adnexa (other than corpus luteum) =
75-85% PPV for ectopic
a. A moderate volume of free fluid increases this to 97% PPV
(3) Nothing in the uterus + moderate free fluid = 70% PPV
a. More risk if the fluid is echogenic
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Fetal Biometry and Fetal Growth:
In the second and third trimesters, four standard measurements of fetal growth are made
(Biparietal, Head Circumference, Abdominal Circumference, and Femur Length). The
testable trivia seems to include what level you make the measurement, and what is and is not
included (see chart).
Fetal Measurement For Growth
Measurement Made NOT including Trivia
Recorded at the level Affected by the shape
of the thalamus from of the fetal skull
Biparietal Diameter the outermost edge of (false large from
“BPD” the near skull to the brachycephaly, false
inner table of the far small from
skull dolichocephaly)
Recorded at the same Docs NOT include Affected less by head
Head Circumference
slice as BPD the skin shape
Recorded at the level Does NOT include
Abdominal of the junction of the the subcutaneous soft
Circumference umbilical vein and tissues
left portal vein
Longest dimension of Femoral epiphysis is
Femur Length
the femoral shaft NOT included
Estimated Fetal Weight: This is calculated by the machine based or either
(1) BPD and AC, or (2) AC and FL.
Gestational Age (GA): Ultrasound estimates of gestation age are the most accurate in
early pregnancy (and become less precise in the later portions). Age in the first trimester is
made from crown rump length. Second and third trimester estimates for age are typically
done using BPD, HC, AC, and FL - and referred to as a “composite GA.”
Gestation Age (Less Good Later in the Pregnancy)
First Trimester - Crown Rump Length Accurate to 0.5 weeks
Accurate to 1.2 weeks (between 12 and 18 weeks)
2nd and 3rd Trimester - “Composite GA”
Accurate to 3.1 weeks (between 36 and 42 weeks)
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Intrauterine Growth Restriction:
*Baby is smaller than expected
Readings Suggestive of IUGR:
• Estimated Fetal Weights Below 10th percentile
• Femur Length / Abdominal Circumference Ratio (F /AC) > 23.5
• Umbilical Artery Systolic / Diastolic Ratio > 4.0
Not All is lost: If the kid is measuring small, he might just be a little guy. If he has normal
Doppler studies - most of the time they are ok.
Maybe All is lost: If the kid is measuring small, suggesting IUGR, and he has
oligohydramnios (AFI < 5) or polyhydramnios, he/she is probably toast.
Trivia: Most common cause for developing oligohydramnios during the 3rd trimester =
Fetal Growth Restriction associated with Placental Insufficiency.
THIS vs THAT: Symmetric VS Asymmetric:
• Asymmetric: Think about this as a restriction of weight followed by length. It is
the more common of the two types. The head will be normal in size, with the body
being small. Some people call this “head sparing,” as the body tries to protect the
brain. You see this mainly in the third trimester, as a result of extrinsic factors.
• The classic scenario would be normal growth for the first two trimesters, with a normal
head / small body (small abdominal circumference) in the third trimester - with a mom
having chronic high BP / pre-eclampsia.
• There are a bunch of causes. I recommend remembering these three: High BP, Severe
Malnutrition, Ehlers-Danlos.
• Symmetric: This is a global growth restriction, that does NOT spare the head. This
is seen throughout the pregnancy (including the first trimester). The head and body
are both small. This has a much worse prognosis, as the brain doesn’t develop
normally.
• There are also a bunch of causes. I recommend remembering these: TORCH
infection, Fetal Alcohol Syndrome / Drug Abuse, Chromosomal Abnormalities,
and Anemia.
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Intrauterine Growth Restriction - Continued
Normal Kid Symmetric IUGR Asymmetric IUGR
-Normal Sized Head -Small Head -Abdomen is small
-Normal Sized Body -Skinny Body -Aching Belly
-Same Throughout (Malnutrition)
Pregnancy -Abnormally High BP
-Syphilis (Among -“Alastic” skin (Ehler
other TORCHs) Danlos)
-Scotch Whiskey -Asymmetric Time
(Fetal EtOH) Interval (primarily
-Some Extra seen in 3rd trimester)
Chromosomes
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Umbilical Artery Systolic / Diastolic Ratio:
The resistance in the umbilical artery should progressively decrease with gestational age. The
general rule is 2-3 at 32 weeks. The ratio should not be more than 3 at 34 weeks. An elevated
S/D ratio means there is high resistance. High resistance patterns are seen in pre-eclampsia and
IUGR. Worse than an elevated ratio, is absent or reversed diastolic flow - this is associated with
a very poor prognosis.
The way I remember this: I think about the kid starting out as a clump of cells/mashed up soup.
Early on he/she is basically just a “muscle.” Then as he/she gets closer and closer to viable age
he/she becomes more like a “brain.” Once you think about it like that - muscle vs brain, it’s
much easier to understand why the diastolic flow goes up (S/D ratio goes down).
Remember the brain is always on, so it needs continuous flow. Muscles are only on when you
need to perform amazing feats of strength. So more brain = more diastolic flow. This also
explains why absent or reversed diastolic flow is so devastatingly bad. In fact, the evil socialist
health care systems in Europe use carotid ultrasound as a cheap brain death test (no diastolic
flow in the ICA = brain dead). Coincidently, the absence of diastolic flow in the ICA is also
used in many American Radiology Departments as hiring criteria for the QA Officer.
Biophysical Profile: This thing was developed to look for acute and chronic hypoxia. Points
are assigned (2 for normal, 0 for abnormal). A score of 8-10 is considered normal. To call something
abnormal, technically you have to be watching for 30 mins.
Components of Biophysical Profile
Amniotic Fluid At least 1 pocket measuring > 2 cm in a vertical plane Assess Chronic Hypoxia
Fetal Movement 3 discrete movements Assess Acute Hypoxia
Fetal Tone 1 episode of fetal extension from flexion Assess Acute Hypoxia
Fetal Breathing 1 episode of “Breathing motion” lasting 30 sec Assess Acute Hypoxia
Non-strcss Test 2 or more fetal heart rate accelerations of at least 15 Assess Acute Hypoxia
beats per minute for 30 seconds or longer
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- Macrosomia -
Babies that arc too big (above the 90th percentile). Maternal diabetes (usually gestational, but
could be type 2 as well), is the most common cause. As a point of trivia, type 1 diabetic mothers
can also have babies that are small secondary to hypoxia from microvascular disease of the
placenta. The big issue with being too big is complications during delivery (shoulder dystocia,
brachial plexus injury) and after delivery (neonatal hypoglycemia, meconium
Erb’s Palsy:
Injury to the upper trunk of the brachial plexus (C5-C6),
most commonly seen in shoulder dystocia (which kids with
macrosomia are at higher risk for aspiration).
If you see an aplastic or hypoplastic humeral head / glenoid
in a kid, you should immediately think about an Erbs Palsy.
Clinical Correlation Recommended.
- Amniotic Fluid -
Early on, the fluid in the amnion and chorionic spaces is the result of filtrate from the
membranes. After 16 weeks, the fluid is made by the fetus (urine). The balance of too much
(polyhydramnios) and too little (oligohydramnios) is maintained by swallowing of the urine
and renal function. In other words, if you have too little fluid you should think kidneys aren’t
working. If you have too much fluid you should think swallow or other GI problems. Having
said that, a common cause of too much fluid is high maternal sugars (gestational diabetes).
Fine particulate in the fluid is normal, especially in the third trimester.
Amniotic Fluid Index: Made by measuring the vertical height of the deepest fluid
pocket in each quadrant of the uterus, then summing the 4 measurements.
Normal is 5-20.
Oligohydramnios is defined as AFI < 5 cm.
Polyhydramnios is defined as AFI > 20 cm , or a single fluid pocket > 8 cm.
Oligohydramnios Not Pee’n Enough
-AFI < 5 -Bad Kidneys
Polyhydramnios Not Drinking
-AFI > 20 or Enough Pee
-Single Pocket > 8 cm -Bad GI
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-Normal Development -
I’m going to briefly touch on what 1 think is testable trivia regarding normal development.
Brain: Choroid plexus is large and echogenic. There should be less than 3 mm of
separation of the choroid plexus from the medial wall of the lateral ventricle (if more it’s
ventriculomegaly). The cisterna magna should be between 2 mm - 11 mm (too small think
Chiari II, too large think Dandy Walker).
Face / Neck: The “fulcrum” of the upper lip is normal, and should not be called a cleft lip.
Lungs: The lungs are normally homogeneously echogenic, and similar in appearance to the
liver.
Heart: The only thing to know is that papillary muscle can calcify “Echogenic Foci in the
ventricle,” and although this is common and can mean nothing - it’s also associated with an
increased risk of Downs (look hard for other things).
Abdominal: If you only see one artery adjacent to the bladder, you have yourself a two
vessel cord. Bowel should be less than 6 mm in diameter. Bowel can be moderately
echogenic in the 2nd and 3rd trimester but should never be more than bone. The adrenals
are huge in newborns, and are said to be 20x their relative adult size.
Two Vessel Cord - Gamesmanship
There are two main ways to show a two vessel cord. The first one is a single vessel
running lateral to the bladder down by the cord insertion. The second is to show the cord
in cross section with two vessels.
Cord in Cross Section
- Only Two Vessels
More on the 2 vessel cord in a few pages.
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Classic Normal Pictures
THAT LOOK SCARY
Cystic Rhombencephalon:
The normal rhombencephalon is present
as a cystic structure in the posterior fossa
around 6-8 weeks.
Don’t call it a Dandy-Walker
malformation, for sure that will be a
distractor.
Normal Cystic Rhombencephalon (6-8 weeks)
Physiologic Midgut Herniation:
The midgut normally herniates into the umbilical cord around 9-11 weeks.
Don't call it an omphalocele, for sure that will be a distractor.
Normal Midgut Herniation (9-11 weeks)
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SECTION 14:
PLACENTA AND CORD
http://www.womenshealthmag.com/mom/p|acenta-recipes
My opinion: Use two cups of strawberries in the smoothie.
Normal: You can first start to see the placenta around 8 weeks (focal thickening along the
periphery of the gestational sac). It should be shaped like a disc around 12 weeks. The
normal sonographic appearance is “granular” with a smooth cover (the chorion). Underneath
the basal surface there is a normal retroplacental complex of decidual and myometrial veins.
Normal Placental Aging: As the placenta ages it gets hypoechoic areas, septations, and
randomly distributed calcifications.
Venous Lakes: These are an incidental finding of no significance. They look like focal
hypoechoic areas under the chorionic membrane (or within the placenta). You can
sometimes see slow flow in them.
Variant Placental Morphology:
Increased risk of type 2 vasa
Two near equal previa (vessel cross the internal
Bilobed sized lobes - os), post partum hemorrhage
Placenta connected by a from retained placental tissue,
thin strip. and velamentous insertion of
the cord
One or more Increased risk of type 2 vasa
Succenturiate
small accessory previa, post partum hemorrhage
Lobe
lobes from retained placental tissue
Rolled
Circumvallate placental edges High risk for placental
Placenta with smaller abruption and IUGR
chorionic plate
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THIS vs THAT: Placental Thickness
Too Thin (< 1 cm) Too Thick (> 4cm)
Placental Insufficiency, Maternal Fetal Hydrops, Maternal DM, Severe
Hypertension, Maternal DM, Trisomy 13, Maternal Anemia, Congenital Fetal Cancer,
Trisomy 18, Toxemia of Pregnancy Congenital Infection, Placental Abruption
Placental Abruption: — PAINFUL
This is a premature separation of the placenta from the myometrium. The step 1 history was
always “mother doing cocaine,” but it also occurs in the setting of hypertension. Technically,
subchorionic hemorrhage (marginal abruption) is in the category - as previously discussed.
Retroplacental Abruption is the really bad one. The hematoma will appear as anechoic or
mixed echogenicity beneath the placenta (often extending beneath the chorion).
Buzzword is “disruption of the retroplacental complex.”
THIS vs THAT: Placental Abruption vs Myometrial Contraction / Fibroid
Placental Abruption will disrupt the Myometrial Contractions I Fibroids will
retroplacental complex of blood vessels displace the retroplacental complex
Placenta Previa: — PAINLESS
This is a low implantation of the placenta that covers part of or all of the internal cervical os. A
practical pearl is that you need to have an empty bladder when you look for this (full bladder
creates a false positive). Several subtypes - as seen in my awesome little chart below.
Buzzword is “painless vaginal bleeding in the third trimester.”
Low-Lying Marginal Complete Central
Margin is within 2 cm Extends to the edge of
of the internal cervical the internal cervical os Covers the internal os Centered over the
os (but doesn’t cover it) internal os
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Placenta Creta:
This is an abnormal insertion of the placenta, which Most common (75%)
invades the myometrium. The severity is graded with and mildest form. The
Placenta villi attach to the
fancy sounding Latin names. The risk factors include Accreta myometrium, without
prior C-section, placenta previa, and advanced maternal invading.
age. The sonographic appearance varies depending on
the severity, but generally speaking you are looking for a Placenta Villi partially invade
Increta the myometrium
“moth-eaten” or “Swiss cheese” appearance of the
placenta, with vascular channels extending from the The really bad one.
placenta into the myometrium (with turbulent flow on Villi penetrate through
the myometrium or
Doppler). Thinning of the myometrium (less than 1 mm) Placenta
beyond the serosa.
is another sign. This can be serious business, with life Percreta
Sometimes there is
threatening bleeding sometimes requiring hysterectomy. invasion of the
bladder or bowel.
Risk factors are prior c-section, and placenta previa.
Placenta Chorioangioma:
This is basically a hamartoma of the placenta, and is the most
common benign tumor of the placenta. These arc usually well-
circumscribed hypoechoic masses near the cord insertion. Flow
within the mass pulsating at the fetal heart rate is diagnostic (they
are perfused by the fetal circulation). They almost always mean
nothing, but if they are large (> 4 cm) and multiple
(“choriangiomatosis”) they can sequester platelets, and cause a
high output failure (hydrops).
THIS vs THAT: Placental Chorioangioma VS Placental Hematoma
Chrorioangioma has pulsating Doppler flow Hematoma does NOT
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- Umbilical Cord -
Normal Cord: Should have 3 vessels (2 arteries, 1 vein).
Two Vessel Cord: This is a normal variant - seen in about 1% of pregnancies. Usually the
left artery is the one missing. This tends to occur more in twin pregnancies and maternal
diabetes. There is an increased association with chromosomal anomalies and various fetal
malformations (so look closely). Having said that, in isolation it doesn’t mean much.
Velamentous Cord Insertion:
This is the term for when the cord
inserts into the fetal membranes
outside the placental margin, and
then has to travel back through
the membranes to the placenta
(between the amnion and the
chorion). It’s more common
with twins, and increases the risk
of intra-uterine growth restriction
and growth discordance among
twins.
Marginal Cord Insertion:
This is basically almost a
velamentous insertion (cord is
within 2 cm of the placental
margin). It’s also seen more in
twin pregnancies.
Vasa Previa: Fetal vessels that cross (or almost cross) the internal cervical os. It’s seen more
in twin pregnancies, and variant placental morphologies. There are two types:
•Type 1: Fetal vessels connect to a velamentous cord insertion within the main placental body
•Type 2: Fetal vessels connect to a bilobed placenta or succenturiate lobe.
Nuchal Cord: This is the term used to describe a cord wrapped around the neck of the fetus.
Obviously this can cause problems during delivery.
Umbilical Cord Cyst: These are common (seen about 3% of the time) and are usually
single (but can be multiple). As a point of completely irrelevant trivia, you can divide these into
false and true cysts. True cysts are less common, but have fancy names so they are more likely to
be tested. Just know that the omphalomesenteric duct cyst is usually peripheral, and the allantoic
cyst is usually central. If the cysts persist into the 2nd or 3rd trimester then they might be
associated with trisomy 18 and 13. You should look close for other problems.
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SECTION 15:
CONGENITAL FETAL
-DOWNS-
Ultrasound Findings Concerning for Down Syndrome
More than half of fetuses (or feti, if you prefer) with Downs
Congenital Heart Disease have congenital heart issues, - most commonly AV canal and
VSD
Most common intra abdominal pathology associated with
Duodenal Atresia
Downs (hard to see before 22 weeks)
Short Femur Length Not Specific
Not Specific (can be seen with obstruction, infection, CF,
Echogenic Bowel
ischemia, and lots of other stuff)
Not Specific, and actually seen more with Trisomy 18. It
Choroid Plexus Cyst should prompt a close survey for other findings (normal if in
isolation)
Nuchal Translucency Translucency > 3 mm in the first trimester,
Thickness > 6 mm in the second trimester- nonspecific and
Nuchal Fold Thickness
can also be seen with Turners
Echogenic Focus in
Not Specific, but increased risk of Downs x 4
Cardiac Ventricle
Nuchal Lucency:
Measured between 9-12 weeks, this anechoic area
between the neck/ occiput and the skin should be
less than 3 mm.
Measurements > 3 mm are associated with Downs
(trisomy 21) or other chromosomal abnormalities.
Positioning of the neck is critical to avoid false
positives. The ideal positioning is a neutral neck,
with the nasal bone visualized, and the head in the
mid-sagittal position. A well delineated skin edge.
Maternal blood sample also analyzed for free
Beta hCG and pregnancy associated plasma
protein-A (PAPP-A).
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- OTHER HORRIBLE SHIT THAT CAN HAPPEN -
Amniotic Band Syndrome:
The fetus needs to stay in the amniotic cavity, and stay the hell out of
the chorionic cavity. If the amnion gets disrupted and the fetus wanders
/ floats into the chorionic cavity he/she can get caught in the sticky
fibrous septa. All kinds of terrible can result ranging from decapitation,
to arm/leg amputation.
Losing fingers like this is terrible - it’s much better to cut them off in a
more manly way. For example, drunken chainsaw lumberjack work or
trying to do that thing with the knife that the cyborg did in the Movies
Aliens (youtube “Aliens: Bishop’s Knife Trick”). Not to mention,
unless you are Jean Jacque Machado (youtube “Heart of the champion
documentary” ) your chances of becoming a world champion in Jiu
Jitsu are going to be significantly deceased.
’Amputated Fingers
This is most likely to be shown in one of two ways:
(1) X-ray of a hand or baby gram showing fingers amputated or a hand/arm amputated - with the
remaining exam normal, or
(2) Fetal ultrasound with the bands entangling the arms or legs of a fetus.
Hydrops:
Fetal hydrops is bad news. This can be from immune or non-immune causes. The most common
cause is probably Rh sensitization from prior pregnancy. Some other causes include; TORCHS,
Turners, Twin Related Stuff, and Alpha Thalassemia. Ultrasound diagnosis is made by the
presence of two of the following: pleural effusion, ascites, pericardial effusion, and
Subcutaneous Edema. A sneaky trick is to instead show you a thickened placenta (> 4-5cm)
“placentomegaly” - they call it, although I think it’s much more likely to show a pleural effusion
and pericardial effusion.
Hydrops - Body Wall Edema, Pleural Effusion, Ascites
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- Chiari II / Open Neural Tube Defect
I think at least some general idea of the mechanism for this pathology is helpful for
understanding the ultrasound findings. There are a bunch of purposed mechanisms, and of
course they all think they are right. I don’t give a shit which one is the “real mechanism,” I
just picked the one that helps me understand the findings.
So this is the one I like: You have a hole in your back from a neural tube defect (Step 1 trivia
= not enough folate). The hole in your back (“myelomeningocele”) lets CSF drip out. So
you end up with a low volume of CSF. The CSF volume needs to be at a certain pressure to
distend the ventricular system. If it’s under distended then the hindbrain structures drop into
a caudal position. This caudal herniation of the cerebellar vermis, brainstem, and 4th
ventricle is the hallmark of Chiari II.
This caudal herniation of the cerebellum into the foramen magnum obliterate the normal
contour of the vermis, creating the contour of a banana.
If you can think about a normal pressure in the developing ventricular system being
necessary for the brain to stretch into a normal shape, then it isn’t a far stretch to think about
this normal pressure being needed to shape the skull correctly, too. The low pressure and
abnormal distention of the developing brain results in incomplete stretching of the postal
(front part) skull. The result is a “lemon shaped” rostral skull. The key point (testable) is
that this lemon shape goes away in the 3rd trimester. So it’s only present in the 2nd trimester.
The way I remember this is that the problem was from a lack of volume. Once the brain
grows big enough (even if there isn’t enough CSF distention) it still gets big enough to put a
normal curve on that rostral skull. So they “grow” out of it.
Testable Trivia:
• Both banana and lemon signs are classic for the Chiari II / Spina Bifida Path
• The banana sign is present in both 2nd and 3rd trimesters
• The lemon sign is only in the 2nd trimester (you grow out of it).
• The banana sign is more sensitive and specific
• The lemon sign is less sensitive and specific; it can also be seen in Dandy Walker, Absent
Corpus Callosum, Encephaloceles, etc... Having said that if you see it on the test it’s
Chiari 2 + Open NTD.
• Hydrocephalus is also seen with Chiari II + Open NTD - but only later in gestation, and
only when it’s severe.
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Open Neural Tube Defect
Low CSF Pressure During Development
Banana Lemon
-Loss of the normal bilobed -Flat / Concave
shaped of the cerebellum Frontal Bones
This is what it’s
supposed to
look like
Normal Bilobed Normal Shape
Cavum Septum
Shaped of the of the Frontal
Pellucidum
Cerebellum Bone
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Ventriculomegaly - There are multiple causes including hydrocephalus (both
communicating and non-communicating), and cerebral atrophy. Obviously this is bad, and
frequently associated with anomalies.
Things to know:
• Aqueductal Stenosis is the most common cause of non-communicating hydrocephalus
in a neonate
• Ventricular atrium diameter > 10 mm = too big
• “Dangling choroid” hanging off the wall more than 3 mm = too big
Ventriculomegaly - Shows dangling choroid
Choroid Plexus Cyst -
This is one of those incidental findings
that in isolation means nothing. Having
said that, the incidence of this finding is
increased in trisomy 18, trisomy 21,
Turner’s Syndrome, and Klinefelter
Syndrome.
Choroid Plexus Cyst
Facial Clefts - This is the most common fetal facial anomaly. About 30% of the time
you are dealing with chromosome anomalies. Around 80% of babies with cleft lips have
cerebral palsy. You can see cleft lips, but cleft palate (in isolation) is very hard to see.
Cystic Hygroma - If they show you a complex cystic mass in the posterior neck, in
the antenatal period, this is the answer. The follow-up is the association with Turners and
Downs.
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Anencephaly - This is the most common neural tube defect. You have total absence of
the cranial vault and brain above the level of the orbits. Obviously this is not compatible
with life.
Anencephaly - No brain / vault above the orbits
Congenital Diaphragmatic Hernia - Abdominal contents push into the chest.
Nearly all are on the left (85%). The things to know is that it (1) causes a high mortality
because of its association with pulmonary hypoplasia, and (2) that all the kids are
malrotated (it messes with normal gut rotation). If they show this it will either be (a) a
newborn chest x-ray, or (b) a 3rd trimester MRI.
Echogenic Intracardiac Focus (EIF) - This is a calcification seen in a papillary
muscle (usually in the left ventricle). You see them all the time, they don’t mean that much
but are seen at a higher rate Trisomy 21 (12%) and Trisomy 13. So you are supposed to look
for more features.
Highest Yield Trivia:
• It occurs in the
normal general
population - around
5%,
• It occurs more in
Downs patients -
around 12%.
Echogenic Intracardiac Focus (EIF)
Abnormal Heart Rate: Tachycardia is defined as a rate > 180 bpm. Bradycardia is
defined as a rate < 100 bpm.
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Double Bubble:
This is described in detail in the Peds Chapter.
Just realize this can be shown with antenatal
ultrasound or MRI. It’s still duodenal atresia.
Double Bubble - Duodenal Atresia
Echogenic Bowel: This can be a normal variant but can also be associated with
significant badness. Normally bowel is isoechoic to the liver. If it’s equal to the iliac crest bone
then it’s too bright. The DDx includes CF, Downs and other Trisomies, Viral Infections, and
Bowel Atresia.
Sacrococcygeal Teratoma: This is the most common tumor of the fetus or infant.
These solid or cystic masses arc typically large and found either on prenatal imaging or birth. They
can cause mass effect on the GI system, hip dislocation, nerve compression causing
incontinence, and high output cardiac failure. Additionally, they may cause issues with
premature delivery, dystocia, and hemorrhage of the tumor. They are usually benign (80%).
Those presenting in older infants tend to have a higher malignant potential. The location of the
mass is either external to the pelvis (47%), internal to the pelvis (9%), or dumbell’d both
inside and outside (34%).
Autosomal Recessive Polycystic Kidney Disease - The classic look is
massively enlarged bilateral kidneys with oligohydramnios. Additional details in the Peds
chapter.
Posterior Urethral Valves: The classic look is bilateral hydro on either fetal US or 3rd
Trimester MRI.
Short Femur: A short femur (below the 5th percentile) can make you think of a skeletal
dysplasia.
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SECTION 16:
Ma t er n a l Di s o r d er s
Incompetent Cervix: When shortened, the cervix is associated with a high risk of
premature delivery. You call it short when the endocervical canal is < 2.5 cm in length.
Hydronephrosis: occurs in 80% of pregnancies (mechanical Tilings That Grow
compression of the ureters is likely the cause). It tends to affect the During Pregnancy:
right more than the left (dextrorotation of the pregnant uterus).
• Babies
Fibroids: Fibroids tend to grow in early pregnancy secondary to • Splenic Artery
elevated estrogen. Progesterone will have the opposite effect, Aneurysms
inhibiting growth, in later pregnancy. Stretching of the uterus may • Renal AMLs
affect the arterial blood supply and promote infarcts and cystic • Fibroids
degeneration.
Uterine Rupture: You see this most commonly in the 3rd trimester at the site of prior c-section.
Other risk factors worth knowing are the unicornuate uterus, prior uterine curettage,
“trapped uterus” (persistent retroflexion from adhesions), and interstitial implantation.
HELLP Syndrome: Hemolysis, Elevated Liver Enzymes, Low Platelets. This is the most
severe form of pre-eclampsia, and favors young primigravid women in their 3rd trimester. It’s bad
news and 20-40% end up with DIC. If they are going to show this, it will be as a subcapsular
hepatic hematoma in pregnant (or recently pregnant) women.
Peripartum Cardiomyopathy: This is a dilated cardiomyopathy that is seen in the last
month of pregnancy to 5 months postpartum. The cardiac MRI findings include a global
depressed function, and non-vascular territory subepicardial late Gd enhancement -
corresponding to cellular lymphocytic infiltration.
Sheehan Syndrome: This is pituitary apoplexy seen in postpartum female who suffer from
large volume hemorrhage (causing acute hypotension). The pituitary grows during pregnancy,
and if you have an acute hypotensive episode you can stroke it out (it bleeds). The look on MR is
variable depending on the time period, acute it will probably be T1 bright (if they show a
picture). Ring enhancement around an empty sella is a late look.
Ovarian Vein Thrombophlebitis: This can be a cause of postpartum fever. Risk factors
include C-section and endometritis. The right side is affected five times more often than the left.
They could show you an enlarged ovary and a thrombosed adjacent ovarian vein.
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Retained Products of Conception: The typical clinical story is continued
bleeding after delivery (or induced abortion). The most common appearance is an
echogenic mass within the uterine cavity. The presence or absence of flow is variable, you
can have lots or you can have none. A sneaky way to show this is irregular thickening of
the endometrium (> 10mm) with some reflective structures and shadowing - representing
the fetal parts. You can also think about RPOC when the endometrial thickness is > 5 mm
following dilation and curettage. Testable associations include: medical termination of
pregnancy (abortion), second trimester miscarriage, and placenta accreta.
Retained Products of Conception
Endometritis - Broadly speaking, it is an inflammation or infection of the
endometrium. The history will be (if you are given one) fever, and uterine tenderness and
recent c-section (or prolonged labor). On ultrasound you will see a thickened, heterogenous
endometrium, with or without fluid / air.
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SECTION 17:
Mu l t i pl e Ges t a t i o n s
Placentation Terminology: So you can have monozygotic twins (identical) or dizygotic
twins (not-identical). The dizygotics arc always dichorionic and diamniotic. The placenta of the
monozygotics is more variable and depends on the timing of fertilized ovum splitting (before 8 days =
diamniotic, after 8 days = monoamniotic). As a point of trivia, a late splitting (after 13 days) can
cause a conjoined twin. As a general rule, the later the split the worse things do (monoamniotics have
more bad outcomes - they get all tangled up, and the conjoined ones have even more problems).
THIS vs THAT: Monochorionic VS Dichorionic
Membrane Thickness: To differentiate the different types, some people use a method classifying
thin and thick membranes. Thick = “easy to see” 1-2 mm, Thin = “hard to see.” Thick is supposed
to be 4 layers (dichorionic). Thin is supposed to be 2 layers (monochorionic). Obviously this
method is very subjective.
Twin-Peak Sign: A beak-like tongue between the two membranes of dichorionic diamniotic
fetuses. This excludes a monochorionic pregnancy.
T Sign: Think about this as basically the absence of the twin peak sign. You don’t see chorion
between membrane layers. T sign = monochorionic pregnancy.
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Twin Growth - You can use normal growth charts in the first and second trimester (but
not the third). The femur length tends to work best for twin age in later pregnancy. More
than 15% difference in fetal weight or abdominal circumference between twins is considered
significant.
Twin- Twin Transfusion - This occurs in monochorionic twins when a vascular
communication exists in the placenta. You end up with one greedy fat twin who takes all the
blood and nutrients, and one skinny wimpy looking kid who gets the scraps. The somewhat
counter intuitive part is that the skinny kid actually does better, and the fat one usually gets
hydrops and dies. You are going to have unequal fluid in the amniotic sacs, with the donor
(skinny) twin having severe oligohydramnios and is sometimes (*buzzword) “stuck to the
wall of the uterus,” or “shrink wrapped.” The fat twin floats freely in his polyhydramniotic
sac. The donor (skinny) twin will also have a high resistance umbilical artery.
Twin Reversed Arterial Perfusion Syndrome - You can get intraplacental
shunting that results in a “pump twin” who will pump blood to the other twin. The other
twin will not develop a heart and is typically referred to as an “acardiac twin.” The acardiac
twin will be wrecked (totally deformed upper body). The “pump twin” is usually normal,
and does ok as long as the strain on his/her heart isn’t too much. If the acardiac twin is really
big (> 70% estimated fetal weight of the co-twin) then the strain will usually kill the pump
twin. They could show this as a Doppler ultrasound demonstrating umbilical artery flow
toward the acardiac twin, or umbilical vein flow away from the acardiac twin (opposite of
normal flow).
One Dead Twin - At any point during the pregnancy one of the twins can die. It’s a
bigger problem (for the surviving twin) if it occurs later in the pregnancy. “Fetus
Papyraceous” is a fancy sounding Latin word for a pressed flat dead fetus.
“Twin-Embolization Syndrome” is when you have cmbolized, necrotic, dead baby
being transferred to the living fetus (soylent green is people!). This can result in DIC, tissue
ischemia, and infarct. By the way, a testable point is that this transfer can only occur in a
monochorionic pregnancy.
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6
En d o c r i n e
Pr o met h eus Li o n h a r t , M.D.
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SECTION 1:
ADRENAL
Anatomy: The adrenal glands arc paired retroperitoneal glands that sit on each kidney.
The right gland is triangular in shape, and the left gland tends to be more crescent shaped. If
the kidney is congenitally absent the glands will be more flat, straight, discoid, or ‘‘pancake’’
in appearance. Each gland gets arterial blood from three arteries (superior from the inferior
phrenic, middle from the aorta, and inferior from the renal artery). The venous drainage is via
just one main vein (on the right into the IVC, on the left into the left renal vein).
Zona Glomerulosa
Cortex Zona Fasciculata
Zona Reticularis
Medulla
Step 1 Trivia: There are 4 zones to the adrenal, each of which makes different stuff.
• Zona Glomerulosa: Makes Aldosterone
- prolonged stimulation here leads to hypertrophy.
• Zona Fasciculata: Makes Cortisol
• Zona Reticularis - Makes Androgens
• Medulla - Makes Catecholamines
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Adrenal Ultrasound Cases - Gamesmanship
If you get shown an adrenal case on ultrasound, then you are almost certainly dealing with a
peds case. What that means is that your choices are narrowed down to: (a) normal,
(b) neuroblastoma, (c) hemorrhage, and (d) hyperplasia.
Normal: In babies, the cortex is hypoechoic, and the medulla is hyperechoic. This gives
the adrenal a triple stripe appearance (dark cortex, bright medulla, dark cortex).
Normal Adrenal - Hypoechoic Cortex, Hyperechoic Medulla, Hypoechoic Cortex
- like an Oreo, with a cream filling.
Neuroblastoma:
I talk about this a ton in the peds chapter. To rehash the
important parts, they form in the adrenal medulla
(usually), and typically look like an enlarged gland with
a hyperechoic component. Having said that they can
have cystic components and look like hemorrhage. For
the purpose of multiple choice I'd go with hyperechoic.
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Hemorrhage:
This occurs most commonly in the setting of
trauma or stress (neonates). What this typically
looks like on ultrasound is an enlarged gland with
an anechoic component. With time, the clot
changes and it can be more and more echogenic.
So basically, it can look like anything but for the
purpose of multiple choice I’d go with anechoic.
Second order path type trivia/knowledge:
* Stress: It’s classically seen after a breech birth, but can also be seen with fetal
distress, and congenital syphilis. Imaging features change based on the timing of
hemorrhage. Calcification is often the end result (that could be shown on CT or
MR). It should be avascular. This can occur bilaterally, but favors the right side
(75%).
o Classic Next Step: Serial ultrasounds (or MRI) can differentiate it from a
cystic neuroblastoma. The hemorrhage will get smaller (cancer will not).
o So which is it? Serial ultrasound or MRI? - If forced to pick you want serial
ultrasounds. It’s cheaper and doesn’t require sedation.
• Trauma: This is going to be an adult (in the setting of trauma). Most likely it will be
shown on CT. It’s more common on the right.
• Waterhouse-Friderichsen Syndrome - Hemorrhage of the adrenal in the
setting of fulminant meningitis (from Neisseria Meningitidis).
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Hyperplasia:
What this typically looks like on ultrasound is a “big
adrenal” that “looks like a brain.” So what does "big”
mean? Most sources will say longer than 20 mm, and a
limb that is thicker than 4 mm (although this is debated -
and will likely not be asked). For the purpose of multiple
choice I would say that if they stick calibers on it, then it is
too big. So what does "looks like a brain ” mean? That
means the surface is wrinkled, like it has gyri and sulci. Cerebri form Pattern
Second order path type trivia/knowledge:
• 21-Hydroxylase Deficiency: Congenital adrenal hypertrophy is caused by
21-hydroxylase deficiency in > 90% of cases. It will manifest clinically as either genital
ambiguity (girls) or some salt losing pathology (boys). The salt losing can actually be
life threatening. The look on imaging is adrenal limb width greater than 4 mm. In some
cases you lose the central hyperechoic stripe (the whole thing looks like cortex).
• I say “Genital ambiguity”, you say 21-Hydroxylase Deficiency
• Too much cortisol from overproduction of ACTH - which results in bilateral
adrenal gland hyperplasia. If someone wanted to be a real asshole they could get into the
weeds with vocabulary. For example, the “Disease” vs “Syndrome” THIS vs THAT:
• Cushing Disease: This is an overproduction of ACTH by a pituitary adenoma,
resulting in too much cortisol. This is actually the most common cause of excess
cortisol (75%).
• Cushing Syndrome: The “syndrome” is basically a variety of causes resulting
in common symptoms. So you can have overproduction of ACTH by an ACTH
secreting tumor (classic step 1 example is the small cell lung tumor), or
overproduction of ACTH via an adrenal adenoma (these cases will not have
hyperplasia), or you can have straight up primary adrenal hyperplasia. You could even
get the “syndrome” by taking chronic high dose steroids. Any way you end up with a
fat moon face and big gross lines all over you belly counts as “syndrome.”
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—Summary / Rapid Review—
Normal:
- Triple Stripe
- Hypoechoic Cortex,
- Hyperechoic Medulla,
- Hypoechoic Cortex
- Smooth Surface
Hyperplasia:
- Big (longer than 20 mm)
- Looks like a brain (wrinkled surface)
- Can sometimes lose the central bright layer
- “Genital ambiguity”, = 21-OH Deficiency
Hemorrhage:
- Big with an anechoic (or echogenic) component
- Gets smaller over time
- Seen with “stress” or trauma
Neuroblastoma:
- Big with an echogenic (or anechoic) component
- Does NOT gets smaller over time
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Adrenal Adenoma:
These things are easily the most common tumor in the adrenal gland. Up to 8% of people
have them. Proving it is an adenoma is an annoying (testable) problem.
• Non-Contrast: Less than 10 HU
• Contrast: Two options:
Absolute Washout
Enhanced CT - Delayed CT
________ x 100 Greater than 60% = Adenoma
Enhanced CT - Unenhanced CT
Relative Washout
Enhanced CT - Delayed CT x 100 Greater than 40% = Adenoma
Enhanced CT
• Hypervascular mets (usually renal, less likely HCC) can mimic adenoma washout.
Portal venous HU values > 120 should make you think about a met.
• Along those lines Pheochromocytomas can also exhibit washout. The trick is the same,
if you are getting HU measurements > 120 on arterial or portal venous phase you can
NOT call the thing an adenoma.
• MRI: Look for drop out on in and out of phase T1.
Adrenal Adenoma -Signal drop out in and Out of Phase
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Adrenal Adenoma Continued
• Real Life = Mass in Adrenal = Adenoma
• Multiple Choice = Mass in the Adrenal = Possible Fuckery
• Although most adenomas are not functional, Cushings (too much cortisol) and Conn’s (too
much aldosterone) can present as functional adenoma.
Tips / Tricks:
• Adenoma are usually homogeneous. If they are showing you hemorrhage (in the absence of
trauma), calcifications, or necrosis you should start thinking about other things.
• Adenomas are usually small (less than 3 cm). The bigger the mass, the more likely it is to
be a cancer. How big? Most people will say more than 4 cm = 70% chance cancer, and
more than 6 cm = 85% chance cancer. The exceptions are bulk fat (myelolipomas) or
biochemical catecholamines in the question stem (pheo) - those can be big.
• Bilateral Small = Probably adenoma
• Bilateral Large = Pheo or Met (Lung cancer)
• Portal Venous Phase HU > 120 = Probably a met (RCC, HCC) or pheo.
“Collision Tumors” - Two different tumors that smash together to look like one mass.
Usually one of them is an adenoma. Remember adenoma should be homogenous and small.
If you see heterogenous morphology consider that you could have two tumors. FDG PET
and MRI can both usually tell if the tumor is actually a collision of two different tumors -
those would be the appropriate next steps.
Conn’s Syndrome - Syndrome of excessive aldosterone production. This is most
commonly caused by a benign adenoma (70%). Cortical-carcinoma can also do it, but that
is much more rare and usually accompanied by hypercortisolism.
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Pheochromocytoma
Uncommon in real life (common on multiple choice tests). They are usually large at presentation
(larger than 3 cm). The look is variable (heterogenous, homogenous, cystic areas, calcifications,
sometimes even fat). Having said that, the most classic look is a heterogeneous mass with AVID
ENHANCEMENT. On MRI they are T2 bright. Both MIBG and Octreotide could be used (but
MIBG is better since Octreotide also uptakes in the kidney).
Gamesmanship: The hyper
enhancement washout trick. They
could show you what looks like an
adenoma study (multiple phases to
calculate washout) - but with
mega enhancement (HU > 120).
Remember, I don't care what the
fuck washout out numbers you get
- if they show you HU
measurements > 120 on arterial or
portal venous phase you can NOT
call the thing an adenoma.
Gamesmanship: This thing isn’t
always in the adrenals. They can Pheo at the Organ of Zuckerkandl - T2 Bright
be extra adrenal (organ of
Zuckerkandl - usually at the IMA).
“Rule of 10s”
10% are extra adrenal (organ of Zuckerkandl - usually at the IMA), 10% are bilateral, 10%
are in children, 10% are hereditary, 10% are NOT active (no HTN).
“Syndromes” MEN 2 (subtypes 2a and 2b)
Both subtypes of MEN 2 are associated with
Associated syndromes: First think Von Hippel
Pheochromocytomas (50% of patients).
Lindau, then think MEN IIa and IIb. Other
In the case of MEN 2 they usually occur
things less likely to be tested include NF-1, multiple and bilateral.
Sturge Weber, and TS.
MEN 2 + Adrenal Mass = Pheo
•“Carney Triad”
•Extra-Adrenal Pheo, GIST, and Pulmonary Chondroma (hamartoma).
•Don't confuse this with the Carney Complex
(Cardiac Myxoma, and Skin Pigmentation).
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Other Misc Adrenal Masses:
Myelolipoma
Benign tumor that contains bulk fat. About 1/4 have
calcifications. If they are big (> 4 cm) they can bleed, and present
with a retroperitoneal hemorrhage. Another piece of trivia is the
association with endocrine disorders (Cushings, Congenital
Adrenal Hyperplasia, Conns).
Don’t get it twisted, these tumors are NOT functional, they just
happen to have associated disorders about 5-10% of the time.
Cyst - You can get cysts in your adrenal. They are often
unilateral, and can be any size. The really big ones can bleed.
They have a thin wall, and do NOT enhance.
Mets: Think breast, lung, and melanoma. They have no
specific imaging findings and look like lipid poor adenomas. Myelolipoma - Bulk Fat
If the dude has a known primary (especially lung, breast, or Hyperechoic on US
melanoma), and it’s not an adenoma then it’s probably a met.
Cortical Carcinoma:
These are large (4 cm -10 cm), may be functional (Cushings),
and calcify in about 20% of cases.
They arc bad news and often met everywhere (direct invasion
often first).
As a pearl, an adrenal carcinoma is not likely to be less than 5
cm and often has central necrosis.
Adrenal Cortical Carcinoma
-Direct invasion of the liver
Calcifications
This is often the result of prior trauma or infection (TB). Certain tumors (cortical carcinoma,
neuroblastoma) can have calcifications. Melanoma mets are known to calcify.
Wolman Disease: - This is a total Aunt Minnie (and massive
zebra / unicorn). Bilateral enlarged calcified adrenals. It’s a fat
metabolism error thing that kills (“booka” - Ali G) before the first year of
life.
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SECTION 2:
Syn d r o mes
MEN: “Multiple Endocrine Neoplasia”
There are three of these stupid things, and people who write multiple choice tests love to
ask questions about them.
* MEN 1: Parathyroid Hyperplasia (90%), Pituitary Adenoma, Pancreatic Tumor
(Gastrinoma most commonly)
* MEN 2: Medullary Thyroid Cancer (100%), Parathyroid hyperplasia,
Pheochromocytoma (33%)
* MEN 2b: Medullary Thyroid Cancer (80%), Pheochromocytoma (50%), Mucosal
Neuroma, Marfanoid Body Habitus
MEN Mnemonics
MEN I (3 Ps)
- Pituitary, Parathyroid, Pancreas
MEN IIa (1M, 2Ps)
Medullary Thyroid Ca,
Pheochromocytoma, Parathyroid
MEN IIb (2Ms, 1P)
- Medullary Thyroid Ca, Marfanoid Habitus /mucosal neuroma,
Pheochromocytoma
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Carcinoid Syndrome:
Flushing, diarrhea, pain, right heart failure from serotonin manufactured by the carcinoid
tumor. The syndrome does not occur until the lesion mets to the liver (normally the liver
metabolizes the serotonin). The typical primary location for the carcinoid tumor is the GI
tract (70%). The most common primary location is the distal ileum (older literature says
appendix). The actual syndrome only occurs in 10% of cases - and is actually very rare (in
real life - not on tests).
Carcinoid -Classic Mesenteric Involvement
Trivia: GI carcinoids are associated with other GI tumors (GI adenocarcinoma).
Trivia: Urine Test for Carcinoid = 5-HIAA (5-hydroxyindoleacetic acid)
Trivia: Nukes Test of Choice: 111In-Octreotide (Octreoscan)
Trivia: MIBG is also positive - but less than 25% of the time (like 15%). Gallium is positive,
but super non-specific.
Trivia: Systemic serotonin degrades the heart valves (right sided), and classically causes
tricuspid regurgitation
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Hereditary Syndromes
Pheochromocytoma
Endolymph Sac Tumor is (risk ~10%). Less
Hemangioblastoma
common (~10%). likely to be
is the most
associated with
common tumor
Bilateral clear cell RCC catecholamine
VHL (seen in the
(~risk ~70%) production.
retina,
cerebellum, spinal
Papillary Cystadeoma of the Pancreatic Cysts
cord)
epididymis (~55%) (~75%) and serous
cystadeomas
Multiple head and
PGL Syndrome
neck Pheochromocytoma risk is variable depending on the
(Paraganglioma &
paragangliomas subtype
Pheochromocytoma)
(risk ~70%)
Cortical Tubers, Subependymal Renal AMLs (risk
Nodules, ~80%)
Clinical Triad
(Facial
Tuberous Sclerosis Subependymal Giant Cell Cardiac
Angiofibroma,
(Bourneville Disease) Astrocytoma (SEGA) - found at Rhabdomyoma
Seizures, Retard
the caudothalamic groove
Brain)
adjacent to the foramen of Pulmonary Cysts
monro LAM
Parathyroid Gastrinoma is the
Pituitary Primary Hyperparathyroidism is most common
Pancreas the most common (risk - pancreas /
100%), related to adenomas duodenal tumor —
MEN 1
Less commonly jejunal ulcers and
carcinoids of the Prolactinoma is the most gastric fold
bronchus, and common pituitary tumor thickening (Zollinger
bowel Ellison)
• Pheochromocytoma (~50%)
Medullary Thyroid
MEN 2 A and often bilateral
Cancer
• Primary Hyperparathyroidism Thyroid cancers
occur at younger
ages and are
• Marfanoid Appearance
Medullary Thyroid multicentric
• Mucosal Neuromas
Cancer
MEN 2 B • Intestinal Ganglioneuromas
Elevated levels
• These patients fart alot
Pheochromocytoma of calcitonin cause
(seriously)
flushing and
Can be diarrhea similar to
Familial Medullary considered a carcinoid syndrome
Thyroid (FMTC) subtype of MEN 2
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SECTION 3:
Th yr o i d
Anatomy: The thyroid gland is a butterfly shaped gland, with two lobes connected by an
isthmus. The thyroid descends from the foramen cecum at the anterior midline base of the
tongue along the thyroglossal duct. The posterior nodular extension of the thyroid (Zuckerkandl
tubercle) helps give a location of the recurrent laryngeal nerve (which is medial to it).
Thyroid Nodules: Usually evaluated with ultrasound. Nodules are super super common and
almost never cancer. This doesn’t stop Radiologists from imaging them, and sticking needles
into them. Ultrasound guided FNA of colloid nodules is a major cash cow for many body
divisions, that on very rare occasions will actually find a cancer. Qualities that make them more
suspicious include: more solid (cystic more benign), calcifications (especially
microcalcifications). Microcalcifications are supposed to be the buzzword for papillary
thyroid cancer. “Comet Tail” artifact is seen in Colloid Nodules. “Cold Nodules” on I-123
scans are still usually benign but have cancer about 15% of the time, so they actually deserve
workup.
Colloid Nodules: These are super super common. Suspicious features include
microcalcifications, increased vascularity, solid size (larger than 1.5 cm), and being cold on a
nuclear uptake exam. As above, Comet tail artifact is the buzzword.
Ultrasound Characteristics of Thyroid Nodules
Margins & Size &
Calcifications Vascularity Echotexture
Shape Multiplicity
Increased Risk Complete Peripheral Solid composition has Nodule size is
• Micro x3 hypoechoic pattern of flow the highest sensitivity NOT predictive of
• Macro x2 halo is highly is suggestive of for malignancy malignancy.
suggestive of benign disease (although not specific
benign disease - many benign nodules Suspicious
Microcalcifications have Central pattern are also solid.) features should be
the highest accuracy, of flow is the primary
Pure cystic, or
specificity, and positive suggestive of consideration
spongiform with more
predictive value for malignancy when targeting for
than 50% specific are
detecting malignancy biopsy (not size)
likely benign.
Microcalcifications = the
“hallmark” of papillary CA
Macrocalcification - most Irregular, Solid Change over time Multiple nodules =
common calcification in spiculated, & hypervascular from solid to cystic decreased cancer
medullary CA microlobulated nodules are suggests benign rate per nodule —
margins more likely to disease but the overall
suggest be malignant rate of having
Macrocalcifications in a malignancy Most hyperechoic or cancer in one
single nodule = higher risk isoechoic nodules are nodule is fairly
benign. constant.
Macrocalcifications in a
multi-nodule goiter = lower Solid Hypoechoic =
risk feature of
malignancy
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Thyroid Adenoma: These look just like solid colloid nodules on ultrasound. They can
be hyper functioning (hot on uptake scan). Usually if you have a hyper-functioning nodule
(toxic adenoma), your background thyroid will be colder than normal (which makes sense).
Goiter - Thyroid that is too big. In North America it’s gonna be a multi-nodular goiter or
Graves. In Africa it’s low iodine. You can get compressive symptoms if it mashes the
esophagus or trachea. These are often asymmetric - with one lobe bigger than the other.
Subacute Thyroiditis / De Quervains Thyroiditis: The classic clinical
scenario is a female with a painful gland after an upper respiratory infection. There is a
similar subtype that happens in pregnant women, although this is typically painless. You get
hyperthyroidism (from spilling the hormone) and then later hypothyroidism. As you get over
your cold, the gland recovers to normal function. Radiotracer uptake will be decreased during
the acute phase.
Acute Suppurative Thyroiditis: This is an actual bacterial infection of the thyroid.
It is possible to develop a thyroid abscess in this situation. A unique scenario (highly
testable) is that in kids this infection may start in a 4th branchial cleft anomaly (usually
on the left), travel via a pyriform fistula and then infect the thyroid. Honestly, that is
probably too much for the exam - but could show up on a certification exam under neuro.
Reidels Thyroiditis: This is one of those IgG4 associated diseases (others include
orbital pseudotumor, retroperitoneal fibrosis, sclerosing cholangitis). You see it in women in
their 40s-70s. The thyroid is replaced by fibrous tissue and diffusely enlarges causing
compression of adjacent structures (dysphagia, stridor, vocal cord palsy). On US there will
be decreased vascularity. On an uptake scan you are going to have decreased values. A
sneak trick would be to show you a MR (it’s gonna be dark on all sequences - like a fibroma).
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Thyroglossal Duct Cyst (TGDC): The
most common congenital neck cyst in Pediatrics.
This can occur anywhere between the foramen
cecum (the base of the tongue) and the thyroid
gland (or below). It looks like a thin walled cyst.
Why Care?
• They can get infected
• They can have ectopic thyroid tissue
• Rarely, that ectopic tissue can get Thyroglossal Duct Cyst - Midline
papillary thyroid cancer (if you see an
enhancing nodule)
TGDC - Location Fuckery
These are the general numbers to think about:
Suprahyoid = 25%
At the Hyoid = 30%
Infrahyoid = 45%
So, where is the most common location?
Well, it depends on how they ask. If all things are equal the answer is Infrahyoid (which seems
counterintuitive based on the embryology but is non the less true).
BUT - if "at or above the hyoid” is a choice - then that is actually the right answer
(25+30 > 45). As always, read every choice carefully.
Ectopic and Lingual Thyroid: Similar to a thyroglossal duct cyst, this can be found
anywhere from the base of the tongue through the central neck. The most common location
(90%) is the tongue base (“Lingual Thyroid”). It will look hyperdense because of its
iodine content (just like a normally located thyroid gland). If you find this, make sure you
check for a normal thyroid (sometimes this is the only thyroid the dude has). As a point of
trivia, the rate of malignant transformation is rare (3%).
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Graves - Autoimmune disease that causes hyperthyroidism (most common cause). It’s
primarily from an antibody directed at the TSH receptor. The actual TSH level will be low.
The gland will be enlarged and “inferno hot” on Doppler.
• Graves Orbitopathy. Spares the tendon insertions, doesn’t hurt (unlike pseudotumor).
Also has increased intra-orbital fat.
• Nuclear Medicine: Increased uptake of I-123 %RAIU usually 50-80%. Visualization of
pyramidal lobe is accentuated.
Hashimotos - The most common cause of goitrous hypothyroidism (in the US). It is
an autoimmune disease that causes hyper then hypothyroidism (as the gland burns out later).
It’s usually hypo - when it’s seen. It has an increased risk of primary thyroid lymphoma.
Step 1 trivia; associated with autoantibodies to thyroid peroxidase (TPO) and anti- thyroglobulin.
On Ultrasound:
There are two classic findings;
(a) Heterogeneous “giraffe skin” appearance,
(b) White Knights - uniform hyperechoic nodules -
which are actually regenerative nodules.
Level 6 Nodes - “Delphian Nodes”
- These arc the nodes around the thyroid in the front of the neck.
- You can commonly see them enlarged with Hashimotos.
- However, for the purpose of multiple choice tests, a sick looking level 6 node - or
“Delphian Node” is a laryngeal cancer met.
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Thyroid Cancer: You can get lots of cancers in your thyroid. There are 4 main subtypes
of primary thyroid cancer. Additionally you can get mets to the thyroid or lymphoma in your
thyroid - this is super rare and I’m not going to talk about it.
Microcalcifications is Mets via the
The Most Common the buzzword and lymphatics. Has an
Papillary Subtype. “Papillary is key finding (seen in overall excellent
Popular” the cancer and prognosis, and
nodes). responds well to I-131.
Mets hematogenously
to bones, lung, liver,
The second most etc.. Survival is still
Follicular common subtype. ok, (less good than
papillary). Does
respond to I-131.
Tendency towards
Association with local invasion, lymph
MEN II syndrome. nodes, and
Medullary Uncommon
Calcitonin production hematogenous spread.
is a buzzword. Does NOT respond to
I-131.
Seen in Elderly. Seen Rapid growth, with
in people who have primary lymphatic
Anaplastic Uncommon
had radiation spread. Does NOT
treatment. respond to I-131.
Does not take up
I-131 as well as
Hurthle Cell (variant Seen more in Elderly.
Uncommon normal follicular.
of Follicular) FDG-PET is the way
to go for surveillance.
Metastasis: The buzzword is going to be microcalcifications in a node (with papillary).
The nodes are typically hyperechoic compared to regular nodes, hyperenhancing on CT, and
T1 bright on MR. Remember that thyroid cancer is hypervascular, and it can bleed like stink
when it mets to the brain. If there are mets to the lungs, the classic pattern is “miliary.” The
additional pearl with regard to lung mets is that they can be occult on cross sectional imaging,
and only seen on whole body scintigraphy. For the purpose of multiple choice tests pulmonary
fibrosis is a risk of treating with I-131 if you have diffuse lung mets.
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SECTION 4:
Pa r a -Th yr o i d
Anatomy: There are normally 4 parathyroid glands located posterior to the thyroid. The
step 1 trivia is that the superior 2 are from the 4th branchial pouch, and the inferior 2 are
from the 3rd branchial pouch. The inferior two are more likely to be in an ectopic location.
Parathyroid Adenoma: This is by far the most common cause of
hyperparathyroidism (90%). On ultrasound these things look like hypoechoic beans
posterior to the thyroid. A 4D-CT can be used to demonstrate early wash-in and delayed
wash-out. Nuclear medicine can use two techniques (1) the single-tracer, dual-phase
Sestamibi, or (2) the dual tracer Sestamibi +I-123 (or Pertechnetate). These arc discussed
in detail in the nukes section.
Parathyroid Adenoma - 4D CT shows early enhancement, and delayed washout
Parathyroid Carcinoma: This is pretty uncommon, and only makes up about 1% of
the causes of hyperparathyroidism. It looks exactly like an adenoma on imaging. The only
way you can tell on imaging is if they show you cervical adenopathy or invasion of adjacent
structures.
High Yield Parathyroid Trivia:
Q: What are the causes of hyperparathyroidism?
A: Hyperfunctioning Adenoma (85-90%),
Multi-Gland Hyperplasia (8-10%), Cancer (1-3%).
Q: What factors does sestamibi parathyroid imaging depend on?
A: Mitochondrial density and blood flow
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Th o r a c i c
Pr o met h eus Li o n h a r t , M.D.
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SECTION 1:
An a t o my a n d a t el ec t a s i s
The Lateral CXR “The Radiologists View”
THIS vs THAT:
Right Ribs vs Left Ribs
By convention, lateral CXRs are taken in
the left lateral position (left side against the
x-ray film/cassette). Therefore, the left ribs
will not be magnified (right ribs will be
magnified). Right ribs also project more
posteriorly. Another strategy is to follow
the diaphragm over the stomach bubble
(usually left sided).
Normal Hilum on Lateral:
If you put your finger in the "Dark
Hole” - which is the left upper lobe
bronchus, in front of it will be the right
PA, and overtop of it will be the left
PA. The posterior wall of the
bronchus intermedius runs through the
black hole, and can be thickened by
edema.
Normal Hilum on Frontal:
This is the right hilar anatomy on the
frontal view. Of course it never looks
that nice in the real world. Ben Felson
used to say the right interlobar artery
reminded him of a woman’s leg... but
then again most things did.
The left hilar point should always be
around 1cm higher than the right
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Retrotracheal Triangle
(Raider Triangle).
This is a triangle which sits on the aortic arch and is
bordered anteriorly by the back wall of the trachea,
and posteriorly by the upper thoracic vertebral bodies.
Many things can obliterate this, but for the purpose of
multiple choice tests an opacity in the Raider Triangle
is an Aberrant right subclavian artery.
Heart Valves on CXR: This is high yield. 1 like to use a two intersecting line method on both
the frontal and lateral chest to answer these kinds of questions.
• Notice the
Pulmonic is the
Most Superior
• Notice the
Tricuspid is the
Most Anterior
• Notice the Aortic
is in front of the
Mitral on the
Lateral
A few other sneaky tricks include knowing that the pointy parts of the mechanical valves (Carpentier-
Edwards aortic valve) point out (towards the direction of blood flow). Know that the mitral valve is
larger than the aortic valve (so if you see two metallic rings, the larger is the mitral). Know that a
pacemaker wire going through a valve makes it the tricuspid valve (lead terminates in the right
ventricle).
Fissures:
Notice the right major fissure is
anterior to the left.
A = Horizontal (Minor) Fissure,
B = Right Major (Oblique),
C = Left Oblique
Azygos Lobe Fissure - This is considered variant anatomy. These things happen when the
azygos vein is displaced laterally during development. The result is a deep fissure in the right upper
lobe. It’s not actually an accessory lobe but rather a variant of the right upper lobe. If they show you
one, I suspect the question will revolve around the pleura. Something like “how many layers of
pleura?” The answer is 4.
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Segmental Anatomy
The tertiary bronchi arc grouped into bronchopulmonary segments.
On the right, there are 10 segments (3 upper, 2 middle, and 5 lower).
On the left, there are only 8 (4 upper lobe / lingula, and 4 lower lobe),
Variant Airway Anatomy:
Pig Bronchus Cardiac Bronchus:
(Tracheal Bronchus): Bronchus that comes off bronchus intermedins,
Bronchus that comes right off the trachea (prior opposite to the origin of the right upper lobe bronchus
to bifurcation into right and left mainstem). In, contrast to the Pig Bronchus this thing is often
blind ending - and supposedly represents the only true
Means nothing clinically, but occasionally people supernumerary bronchus
can get some air trapping or recurrent infections
from impaired ventilation. Similar to the pig bronchus, it means nothing
clinically, but occasionally people can get recurrent
Trigger: Recurrent RUL Pneumonia in kid. infections
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Mediastinal Anatomy
The mediastinum is classically divided into 4 sections, superior, anterior, middle, and
posterior. The borders of these areas make good trivia questions.
• Superior - The inferior border is the oblique plane from the stemal-manubrial
junction.
• Anterior - The posterior border is the pericardium
• Middle - The heart, pericardium, and bifurcation of the trachea are all included. On
lateral CXR, people sometimes say posterior to the trachea, and anterior to the
vertebral bodies (or 1 cm posterior to the vertebral bodies).
• Posterior - From the back of the heart to the spine. Contains the esophagus,
thoracic duct, and descending aorta.
Mediastinal Variant Anatomy
Pulmonary Veins: Pulmonary vein anatomy is highly variable. You typically have 4
total (2 right - upper and lower, 2 left - upper and lower). The most common anatomic
variation is a separate vein draining the right middle lobe (seen 30% of the time). Who
cares??? Two people (1) People who write multiple choice tests, (2) Electrophysiologists
prior to ablations.
Proximal Interruption of the Pulmonary Artery: Basically you have
congenital absence of the right (or left) PA with the more distal pulmonary vasculature
present. It’s also called unilateral absence of the PA, but that is confusing because the distal
pulmonary vasculature is present.
How it could be shown:
• Classically with volume loss of one hemi-thorax (could be on CXR or CT), then a
contrast CT shot through the heart with only one PA. Normally, you might think one PA
is just volume averaging - but once you’ve been shown volume loss on one side your
suspicion for this should be raised.
Trivia:
• It’s seen on the opposite side of the aortic arch (Absent right PA with left-sided aortic
arch, Absent left PA with right-sided aortic arch).
• Associated with PDA
• Interrupted left PA is associated with TOF and Truncus
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Patterns of Atelectasis:
Atelectasis (incomplete lung expansion) exists on a scale of
severity; ranging from the tiny horizontal “plate-like” / “discoid”
subsegmental to complete collapse of the lung (lobar).
The degree of collapse depends on the location of obstruction
(peripheral vs central).
There arc some described vocabulary words for the different
subtypes of atelectasis - and those words, the supposed
mechanisms, and the attributed causes are all potentially testable.
Obstructive Compressive Fibrotic Adhesive
(Absorptive) (Relaxation / Passive) (Cicatrization) • Results from loss of
• Result of complete • Results from direct mass • Results from scarring / surface tension /
obstruction of an airway effect on the lung fibrosis which fails to inadequate pleural
• No new air can enter and • Causes: Most classically allow the lung to adherence of the alveolar
any air that is already seen adjacent to a pleural collapse completely. walls - from a surfactant
there is eventually effusion. Could also be • • Causes: Most classic is deficiency.
absorbed leaving a seen from adjacent TB , but scarring from • Alveoli become unstable
collapsed section of lung compression of lung radiation, other and collapse.
• Causes: Obstructing from a mass, hiatal infections, or really any • Causes: RDS (pre-
neoplasms, mucous hernia, or a large bleb — other cause of fibrosis mature infants), ARDS
plugging in asthmatics or anything directly can do this. (more diffuse pattern),
critically ill patients, and pushing on the lung. and in the setting of
foreign body aspiration. pulmonary embolism
(loss of blood flow I lack
of CO2 disrupts integrity
of surfactant).
Another easily testable topic related to atelectasis are the primary and secondary signs. The
big 3 ones being shadow, silhouette, and shift. Just like any normal person would, when I think
of the word “shadow,” I immediately think of either Lamont Cranston (hypnotist and master
detective), or Carl Jung’s “Phenomenology of the Self.” I’m sure you do too. However, in the
case of atelectasis “shadow” refers to the shadow made by the opacified (collapsed lung). This is
the direct sign, and is the most obvious (more on the next page). The silhouette refers to the loss
of interface between this opacity and the adjacent normal structures. This is useful in localization
(more on the next page). The shift refers to the movement of structures as they are “pulled”
towards the site of volume loss. Remember, space occupying things (tumors, pneumonia, pleural
effusion, cavitary lesions, etc...) push things away. Atelectasis is a volume losing process - so it
pulls (examples - pulling the right hilar point above the left, pulling the left hilar point below the
right, shifting the mediastinum, etc...).
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- Lobar Patterns -
Right Middle Lobe: Right Lower Lobe:
- Classic look is increased density at the - Classic look is increased density at the right heart
right heart border with loss of that border similar to collapse of the RML.
border (shadow and silhouette) - The critical distinction is the right heart border.
- The lateral will show anterior density You should NOT lose the border of the right heart
over the heart (as the RML is anterior) with RLL collapse. In fact it should be easier to
see from compensatory hyper-expansion of the
Right Middle Lobe Syndrome: RML.
Chronic collapse of the RML is classically - In some cases, the
described with MAI infection in an elderly mediastinal vessels are
women who is too proper too cough (Lady pulled to the right creating
Windermere syndrome). On CT you’d see a triangle of opacity to the
additional findings of small nodules and right of the trachea
bronchiectasis - with additional (Superior Triangle
involvement of the Lingula.
Sign)
Right Lower Lobe + Right Middle Lobe:
- Uncommon Combination and a Sneaky Move
- The trick is a loss of visualization of the right hemidiaphragm and right
heart border
Right Upper Lobe:
- Closes like a fan attached at the Hilum
- Horizontal Fissure may bow upward
- Hilum may elevate
- The lateral will again show this hilar attachment
with the lobe collapsing from both the anterior
and posterior directions.
- The top half of the oblique fissure will be pulled
anterior.
S Sign of Golden:
Refers to a reverse ”S" shape that the minor fissure
in cases of RUL collapse resulting from a central
obstructing mass.
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- Lobar Patterns Continued-
Left Upper Lobe: Luftsichel Sign:
- This is different than the right upper lobe (which “Air Sickle” - appearance
collapsed like a fan making a dense wedge shaped from the lucent stripe
opacity. appearance of the hyper
- The LUL tends to be more subtle with a subtle increased inflated superior (apical)
density medially. There won’t be any well defined segment of the lower lobe
borders pinned between the medial
- A hint may be non-visualization of the aortic knob. edge of the collapsed
segment and the aortic arch
- Sometimes (if you are lucky) you can get some non-
specific peaking of the diaphragm from upward traction
Left Lower Lobe:
- Can Be sneaky on a frontal
only (opacity is hidden behind
the heart)
- The lateral makes it more
obvious with a posteriorly
directed triangular opacity
The Flat Waist Sign - has
been used as a description of the
flattened appearance of the
contours of the hilum and heart
border.
Cartoon Level demonstrating the “flat ”
appearance of the left heart / hilum.
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SECTION 2:
Lo c a l i za t i o n - 1970s St yl e
This was a known thing done on the old oral boards, so the idea is not new. They show you a
mass on a frontal radiograph and tell you to localize it (anterior, middle, posterior, or
pulmonary). Here are the common tactics you can use to get this right.
Posterior Junction Line is ABOVE the clavicles
Cervicothoracic Sign - This
takes advantage of the posterior
junction line, which demonstrates that
things above the clavicles are in the
posterior mediastinum.
Hilum Overlay Sign: Mass at
the level of the hilum arising from the hilum will obliterate the silhouette of the pulmonary
vessels. If you can see the edge of the vessels through the mass, then the mass is not in the
hilum (so it is either anterior or posterior).
THIS vs THAT:
Pulmonary vs
Mediastinal Origin:
The easiest trick is if they
show you air bronchograms.
Only a pulmonary mass will
have air bronchograms. The
harder trick is the angle with
the lung. The mass will make
an acute angle with the lung if
it’s within the lung. The mass
will make an obtuse margin
Pulmonary Origin Mediastinal Origin
with the lung if it’s in the -makes an acute angle -makes an obtuse angle
mediastinum. with the lung with the lung
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SECTION 3:
In f ec t i o n
Bacterial Infection
Favors lower lobes. Can be severe in sickle cell
Strep Pneumo Lobar Consolidation patients post splenectomy. The most common
cause of pneumonia in AIDS patient.
Bronchopneumonia - Often bilateral, and can make abscess. Can be
Staph A.
patchy opacities spread via the blood in endocarditis patients
Hemorrhagic lymphadenitis, Classic Look: Mediastinal widening with pleural
Anthrax mediastinitis, and effusion in the setting of bio-terrorism
hemothorax
Buzzword: “Bulging
Fissure” from exuberant
inflammation. More likely to Alcoholic and Nursing Home Patients.
Klebsiella
have pleural effusions, Step 1 Buzzword was “currant jelly sputum”
empyema, and cavity than
conventional pneumonia.
Usually bronchitis,
H. Flu sometimes bilateral lower Seen in COPDers, and people without a spleen
lobe bronchopneumonia
ICUers on a ventilator (also CF and Primary
Patchy opacities, with abscess Ciliary Dyskinesia). Pleural effusions are
Pseudomonas
formation common, but usually small
Seen in COPDers, and around crappy air
Peripheral and sublobar conditioners. Only cavitates in immunosuppressed
Legionella
airspace opacity patients. X-ray tends to lag behind resolution of
symptoms.
Posterior lobes if supine when aspirating, Basal
Anaerobes, with airspace Lower lobes in upright aspiration May favor the
Aspiration opacities. They can cavitate, right side, just like an ET tube. The most common
and abscess is not uncommon complication is empyema (which can get a
bronchopleural fistula).
Airspace in peripheral lower
lobes. Can be aggressive and Classic story is dental procedure gone bad, leading
Actinomycosis
cause rib osteomyelitis / to mandible osteo, leading to aspiration.
invade adjacent chest wall.
Fine reticular pattern on
Mycoplasma CXR, Patchy airspace opacity
with tree-in-bud
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Immunocompromised
Post Bone Marrow Transplant: You see pulmonary infections in nearly 50% of people
after bone marrow transplant, and this is often listed as the most common cause of death in this
population. Findings are segregated into: early neutropenic, early, and late - and often tested as such.
Post Bone Marrow Transplant Graft vs Host
Acute (20-100 Days) Chronic (> 100 days)
Favors extrapulmonary systems Lymphocytic Infiltration of the airways and
(skin, liver, GI tract) obliterative bronchiolitis.
Post Bone Marrow Transplant (Pulmonary Findings)
Early Neutropenic (0-30 days) Early (30-90) Late > 90
Pulmonary Edema, Hemorrhage, Bronchiolitis Obliterans, Cryptogenic
PCP, CMV Organizing Pneumonia
Drug Induced Lung Injury
Fungal Pneumonia (invasive
aspergillosis)
AIDS Related Pulmonary Infection:
Questions related to AIDS and pulmonary infection are typically written in one of two ways (1) with
regard to the CD4 count, and (2) by showing you a very characteristic infection.
PCP: This is the most classic AIDS infection. This is the one they are most likely to show you.
Ground glass opacity is the dominant finding, and is seen bilaterally in the perihilar regions with
sparing of the lung periphery. Cysts, which are usually thin-walled, can occur in the ground glass
opacities about 30% of the time.
Buzzwords:
•Most common airspace opacity = Strep Pneumonia
•If they show you a CT with ground glass = PCP
•“Flame-Shaped” Perihilar opacity = Kaposi Sarcoma
•Persistent Opacities Lymphoma
•Lung Cysts = LIP
•Lungs Cysts + Ground Glass + Pneumothorax = PCP
•Hypervascular Lymph Nodes = Castleman or Kaposi
Infections in CT Pattern - With AIDS
AIDS by CD4 Bacteria) Infection (Strep Pneumonia) is
the most common. DDx should include
Bacterial Infections, Focal Airspace Opacity TB if low CD4. If it’s a chronic opacity
>200
TB think Lymphoma or Kaposi.
PCP, Atypical Bacterial, or Fungal
<200 Multi-Focal Airspace
Mycobacterial Opacity
CMV, Disseminated PCP (if that’s not a choice it could be
< 100 Ground Glass
Fungal, Mycobacterial CMV if CD4 is < 100).
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TB
You can think about TB as either:
(a) Primary, (b) Primary Progressive, (c) Latent or (d) Post Primary / Reactivation.
• Primary: Essentially you inhaled the bug, and it causes necrosis. Your body attacks and forms a
granuloma (Ghon Focus). You can end up with nodal expansion (which is bulky in kids, and less
common in adults), this can calcify and you get a “Ranke Complex. ” The bulky nodes can
actually cause compression leading to atelectasis (which is often lobar). If the node ruptures you
can end up with either (a) endobronchial spread or (b) hematogenous spread - depending on if the
rupture is into the bronchus or a vessel. This hematogenous spread manifests as a miliary pattern.
Cavitation in the primary setting is NOT common. Effusions can be seen but are more
common in adults (uncommon in kids).
• Primary Progressive: This term refers to local progression of parenchymal disease with the
development of cavitation (at the initial site of infection / or hematogenous spread). This primary
progression is uncommon - with the main risk factor being HIV. Other risk factors are all the
things that make you immunosuppressed - transplant patients, people on steroids. The ones you
might not think about is jejunoileal bypass, subtotal gastrectomy, and silicosis. This form is
similar in course to post primary disease.
• Latent: This is a positive PPD, with a negative CXR, and no symptoms. If you got the TB
vaccine, you are considered latent by the US health care system/industry if your PPD converts.
This scenario buys you 9 months of INH and maybe some nice drug induced hepatitis.
• Post Primary (reactivation): This happens about 5% of
the time, and describes an endogenous reactivation of a
latent infection. The classic location is in the apical and Immune Reconstitution
posterior upper lobe and superior lower lobe (more Inflammatory Syndrome:
oxygen, less lymphatics). In primary infection you tend The story will be a patient with
to have healing. In post primary infection you tend to TB and AIDS started on highly
have progression. The development of a cavity is the active anti-retroviral therapy
thing to look for when you want to call this. Arteries near (HAART) and now doing worse
the cavity can get all pseudoaneursym’d up - “Rasmussen The therapy is steroids.
Aneurysm” they call it - in the setting of a TB cavity.
Pleural Involvement with TB: This can occur at any time after initial infection. In primary TB
development of a pleural effusion can be seen around 3-6 months after infection - hypersensitivity
response. This pleural fluid is usually culture negative (usually in this case is like 60%). You have
to actually biopsy the pleura to increase your diagnostic yield. You don’t see pleural effusions as
much with post primary disease, but when you do, the fluid is usually culture positive.
High Yield Factoids Regarding TB:
• Primary = No Cavity, Post Primary / Primary Progressive = Cavity
• Ghon Lesion = Calcified TB Granuloma ; sequela of primary TB
• Ranke Complex = Calcified TB Granuloma + Calcified Hilar Node ; Healed primary TB
• Bulky Hilar and Paratracheal Adenopathy = Kids
• Location for Reactivation TB = Posterior / Apical upper lobes, Superior Lower Lobes
• Miliary Spread when? - Hematogenous dissemination (usually in the setting of reactivation), but
can be in primary progressive TB as well
• Reactive TB Pattern (Cavitation) seen in HIV patient when the CD4 is > 200
• Primary Progressive Pattern (Adenopathy, Consolidation, Miliary Spread) in HIV is CD4 < 200
• TB does NOT usually cause a lobar pattern in HIV
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Non Tuberculous Mycobacteria:
Not all mycobacterium is TB. The two non-TB forms worth knowing are mycobacterium
avium-intracellulare complex (MAC) and Mycobacterium Kansasii. I find that grouping
these things into 4 buckets is most useful for understanding and remembering them.
• Cavitary (“Classic”) - This one is usually caused by MAC. It favors an old white man
with COPD (or other chronic lung disease), and it looks like reactivation TB. So you
have an upper lobe cavitary lesion with adjacent nodules (suggesting endobronchial
spread).
• Bronchiectatic (“Non-Classic”) -
This is the so-called “Lady
Windermere” disease (everyone
knows it’s just not lady-like to
cough). They often do not cough,
and are asymptomatic. This
favors an old white lady. You see
tree-in-bud opacities and
Lady Windermere - MAC
cylindric bronchiectasis in the -Bronchiectasis with tree-in-bud funk
right middle lobe and lingula. in the right middle lobe and lingula
• HIV Patients - You see this with low CD4s (< 100). The idea is that it’s a GI infection
disseminated in the blood. You get a big spleen and liver. It frequently is mixed with
other pulmonary infections (PCP, etc...) given the low CD4 - so the lungs can look like
anything. Mediastinal lymphadenopathy is the most common manifestation.
• Hypersensitivity Pneumonitis - This is the so-called “hot-tub lung.” Where you get
aerosolized bugs (which exist in natural sea water and in fresh water). The lungs look
like ill-defined, ground glass centrilobular nodules.
Non Tuberculous Mycobacteria - Rapid Review
Cavitary Type Old White Male Smoker Looks like reactivation TB
Non-Classic Middle Lobe and Lingula,
Old Lady
(Lady Windermere) bronchiectasis and tree in bud.
HIV Low CD4 (< 100) Mediastinal Lymphadenopathy
Hypersensitivity
History of hot tub use Ground glass centrilobular nodules
(Hot Tub Lung)
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Fungal
Aspergillus: 3 flavors: (1) Normal Immune, (2) Suppressed Immune, or (3) Hyper-Immune.
Normal Immune Suppressed Immune Hyper-Immune
Aspergillus makes a Aspergillus behaves differently in
fungus ball the setting of a hyper-acute immune
“Aspergilloma” in a Aspergillus is NOT getting held in check by a system. Allergic Broncho-
pre-existing cavity. normal immune system. “Invasive Aspergillus” Pulmonary Aspergillosis (ABPA)
The fungus didn’t they call it. they call it.
make the cavity - it
found the cavity. It is You are gonna see this in your AIDS, or Transplant
squatting in an Patients.
abandoned cavity -
like a hobo.
Gamesmanship: Gamesmanship: Gamesmanship:
You could be shown a (1) Halo Sign - consolidative This is “Always” seen in patients
fungus ball, and they nodule/mass with a ground glass with long standing Asthma
want you to call it halo. The halo of ground glass is (sometimes CF). You classically
invasive. Don’t fall actually the invasive component. have upper lobe central saccular
for that. This is not bronchiectasis with mucoid
the same thing as (2) Air Crescent Sign - a thin impaction (finger-in-glove).
invasive. crescent of air within the Central Bronchiectasis + Asthma
consolidative mass. This actually (or CF)=ABPA
Fungus balls can represents healing, as the necrotic
occur normal people Diagnosis of ABPA requires
lung separates from the parenchyma. BOTH:
who have a cavity The timing is usually about 2-3
from trauma, or prior • Elevated Serum Immunoglobulin
weeks after treatment. Lastly, they
infection ect... E levels OR a positive skin
could show you some peripheral hypersensitive test against the
wedge shaped infarcts in the setting asshole fungus
of some halo signs.
• Elevated Total IgE levels > 1000
Aspergilloma - Fungus Ball Invasive Aspergillus ABPA
- Normal immune system - Air Crescent Sign - Finger in Glove; think asthma
**That ball will move - Dude has AIDS
with positional change
Mucormycosis - This aggressive fungal infection almost always occurs in impaired patients
(AIDS, Steroids, Bad Diabetics Etc..). You usually think about mucor eating some fat diabetic’s
face off, but it can also occur in the lungs. Think about this when you have invasion of the
mediastinum, pleura, and chest wall.
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Viral
CMV - This can be seen in two classic scenarios: (1) Reactivation of the latent virus after
prolonged immunosuppression (post bone marrow transplant), and (2) Infusing of CMV
positive marrow or in other blood products. The timing for bone marrow patients is “early”
between 30-90 days. The radiographic appearance is multiple nodules, ground glass or
consolidative.
Random Viral Trivia
Pneumonia can be before or
Multifocal ground glass after the skin lesions.
Measles opacities with small nodular Complications higher in
opacities pregnant and
immunocompromised
Coalescent lower lobe
Influenza opacity. Pleural effusion is
rare.
Lower lobe predominant
SARS
ground glass opacities
Most commonly causes
Multiple peripheral nodular Chickenpox in kids. The
opacities. They form small pneumonia more commonly
Varicella round calcific lung nodules occurs in
in the healed version. immunocompromised adults
(with AIDS or lymphoma).
Uncommonly affects the
Most common radiographic
Ebstein Barr lung. Can cause lymph node
abnormality is a big spleen.
enlargement
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Septic Emboli
There are a variety of ways you can
throw infectious material into the
lungs via the bloodstream
(pulmonary arteries).
Some common sources would
include; infected tricuspid valves,
infection in the body, infected
catheters, infected teeth.. .etc...
Septic Emboli - Multiple round opacities, one with cavitation
Septic Emboli Trivia:
• It’s lower lobe predominant (more blood flow)
• You get peripheral nodular densities and wedge shaped densities (can infarct).
• They can cavitate, and likely will be cavitated if they show you a CT image.
• The feeding vessel sign - nodule with a big vessel going into it can be shown (also seen
with hematogenous mets).
• Empyema and pneumothorax are both known complications.
Lemmiere Syndrome:
This is an eponym referring to jugular vein thrombosis with septic emboli classically seen
after an oropharyngeal infection or recent ENT surgery.
High Yield Trivia
Q: What is the bacterial agent responsible in the majority of cases?
A:“Fusobacterium Necrophorum.”
CAVITY Mnemonic For Lung Cavity:
Cancer (usually squamous cell)
Auto-immune (Wegeners, Rheumatoid / Caplan Syndrome)
Vascular - Septic Emboli / Bland Emboli
Infection - TB
Trauma - Pneumatoceles
Young - “Congenital” - CCAMs, Sequestrations
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SECTION 4:
Lu n g Ca n c er
Lung Cancer Risk Factors: include; being over 30 (under 30 is super rare), exposures
to bad stuff (arsenic, nickel, uranium, asbestos, chromium, beryllium, radon), having lung
fibrosis, COPD (even if you didn’t smoke), and family history. Diffuse fibrosis supposedly
gives you 10x the risk. Having said all of that, smoking is still the big one - supposedly a
factor in 90% of cases.
Screening: Pack Years:
Number of packs of cigarettes
Recently, the US preventive services task force has smoked per day multiplied by
approved lung cancer screening with low dose CT for number of years the person has
asymptomatic adults aged 55-80 who have a 30 pack- smoked = “Pack Years”
year history and currently smoke (or have quit within 30 pack years will qualify you
for screening
the past 15 years).
Some trivia related to the screening program:
• Shockingly, it is backed up by evidence (which is extremely rare in medical screening
programs), and legit improves outcomes (also rare in medicine).
• The follow up recommendations are NOT the same as the Fleischner Society
Recommendations. So nodules found on a CT done for any reason other than official lung
cancer screening will follow Fleischner and not the LUNG RADS recommendations used
with the screening program.
• Dose on the screening CTs is supposed to be low - recommended below CTDIvol 3 mGy
• “Growth” is considered 1.5 mm or more in one year
• LUNG RADS scoring is based off the most suspicious nodule. You don’t give multiple
ratings for multiple nodules.
• Endobronchial “lesions” (mucus) are treated as 4a - and given a 3 month follow up.
• A treated remote (> 5 years) lung cancer patient must still meet the normal screening criteria
to be enrolled in die program.____________________________________________ __________
Lung Rads Overview (Abbreviated Version)
Category 0 Scan is a piece of shit and you can’t read, or you need priors Repeat or get priors
Category 1 Negative, <1% chance of cancer. Either no nodules or granulomas. 1 year follow up
Benign < 1 % chance of cancer. Baseline exam - nodules smaller
Category 2 than 6 mm. Subsequent exam - no new nodules larger than 4 mm. 1 year follow up
Ground glass nodule smaller than 20 mm.
Probably Benign, 1-2% chance of cancer. Baseline nodule 6-8 mm.
Category 3 6 month follow up
Subsequent exam new nodule > 4 mm. Ground glass > 20 mm.
Suspicious, 5-15% chance of cancer, Baseline 8-15 mm. New 3 month follow up
Category 4a
nodule 6-8 mm vs PET
Suspicious, > 15% chance of cancer, > 15 mm at baseline PET vs Tissue
Category 4b
New nodule > 8 mm Sampling
>15% chance of cancer PET vs Tissue
Category 4X
Worsening of category 3 or 4 nodules (growth or new spiculation) Sampling
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Nodules (incidental discover):
As discussed on the prior page, nodules discovered incidentally on non-screening scans are treated
different for followup. These nodules are the captives of the dreaded Fleischner Society
recommendations.
Few Pearls:
• Fleischner guidelines only apply for patients older than 35
• They do NOT apply to patients with known or suspected cancer
• They do NOT apply to patients who are immunocompromised
• Measurements are reported as the average diameter (short + long / 2) obtained in the same plane.
• Risk stratification for followup (low, intermediate, high) is based on multiple risk factors (smoking,
cancer history, family history, age, uranium / random / asbestos exposure and nodules
characteristics / size).
• Follow up is based off the arbitrary guess of a cancer risk > 1%
• Perifissural nodules (discussed later) - do not need a follow up, even if they are > 6 mm in size.
• Nodule characterization should be performed on thin-slice CT images ≤ 1.5 mm. This is done to
look for a small solid component hiding behind partial volume effect in a ground glass nodule.
• Multiple nodules (> 5) makes malignancy statistically less likely.
Behold the recommendations.
Fleischner Society Overview for SOLID nodules
Notice how the nodules are (Abbreviated Version)
stratified based on number and
Low Risk No follow up
risk. Single
High Risk 12 month Repeat
Risk is determined based on the < 6 mm
characteristics of the nodule Low Risk No follow up
Multiple
(spiculated, etc..), and the
High Risk 12 month Repeat
characteristics of the patient
(exposure to uranium, etc...). Low Risk 6-12 month follow up
Single
High Risk 6-12 month follow up
This is different than the LUNG-
6-8 mm
RADS algorithm. Low Risk 3-6 month follow up
Multiple
High Risk 3-6 month follow up
Single Low and High PET or Biopsy
> 8 mm Low Risk 3-6 month follow up
Multiple
High Risk 3-6 month follow up
Ground Glass nodule follow up recommendations are variable. Most people will not follow up
nodules smaller than 6 mm. If they are greater than 6 mm people will either do 6 month or 1 year
(depends on who you ask). Follow up is persistent for 5 years, because of the slow growth of the
potential adenocarcinoma in situ.
Part Solid nodules are slightly different. Smaller than 6 mm still gets ignored. However, the ones
larger than 6 mm get a 3 month follow up - with interval widening but persisting up to 5 years.
Regular solid nodules typically get set free after 2 years of stability.
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Nodules
Types and Trivia
Solitary Pulmonary Nodule: A SPN is defined as a round or oval lesion measuring less than
3cm in diameter (more than 3cm = mass). Technically to be “solitary” it needs to be surrounded by
lung parenchyma, with no associated adenopathy, or pleural effusion. So, you can have numerous
“solitary” nodules in the lungs.
There are 4 classic “benign
calcification” patterns:
Solid, Laminated, Central,
and Popcorn.
Solid/Diffuse Laminated Central Popcorn
Anything else is considered suspicious. Eccentric patterns arc considered the most
suspicious. Some notable (testable) exceptions include when you see popcorn and
central calcifications in the setting of a GI cancer. Solid calcifications can also be
bad in the setting of osteosarcoma.
Eccentric
Makes You Think B9 Make You Think Cancer
Presence of Fat Spiculated Margins “Corona Radiata Sign”
Rapid Doubling Time (less than 1 month) Air Bronchogram through the nodules (usually
Adenocarcinoma in situ)
Slow Doubling Time (longer than 16
months) *Stable at two years = B9 Partially solid lesions with ground glass component
Solid and Ground Glass Components: A part solid lesion with a ground glass component is the
most suspicious morphology you can have. Non-solids (only ground glass) is intermediate.
Totally solid is actually the least likely morphology to be cancer.
PET for SPN: You can use PET for SPNs larger than Solid Nodule ( > 1 cm in size):
1 cm. Lung Cancer is supposed to be HOT (SUV > 2.5). HOT = Cancer, COLD = Not Cancer
Having said that, infectious and granulomatous nodules Ground Glass Nodules:
can also be hot. If you arc dealing with a ground glass HOT = Infection , COLD = Cancer
nodule it’s more likely to be:
SPN / Cancer Trivia:
Lung Cancer is 1.5x more likely in the Right Lung
70% of Lung Cancer is in the Upper Lobes
Exception to the rule is pulmonary fibrosis - where peripheral basilar cancer is more common.
SPN in the setting of head and neck CA is more likely to be a primary bronchogenic carcinoma
rather than a metastasis (they have similar risk factors).
Lung Cancer is very rare under 40 (unless the patient has AIDS)
Air Bronchograms arc 5x more common in malignant SPN
Air Bronchograms are found in 50% of BACs
Just because a nodule gets smaller doesn’t mean it is benign. Especially if the nodule increases
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Nodules
- Types and Trivia Continued -
Nodule Volume / Size Change:
Most people will call nodule “growth” at 1.5 mm per year. Anything smaller than that can easily be
attributed to technical factors. Anyone who describes 0.1 mm differences in stuff sucks at Radiology.
This growth, in particular the concept of “doubling time" makes up the basis of differentiated benign
vs malignant. With out this concept you would be forced into follow nodules forever, The trivia
worth knowing is that lung cancers doubling times range from 20 days to 400 days.
Any nodule that doubles in size in less than 20 days is almost certainly benign (statistically
infectious or inflammatory). The same is true with doubling times greater than 400 days.
The notable difference is the ground glass or part solid nodule vs the solid nodule. Ground glass and
part solid nodules are more characteristic of the adenocarcinoma in situ (formerly BAC) and they
tend to grow slower. This is why the follow up term for GGN and part solid nodules in 5 years, vs 2
years for a pure solid nodule.
Perifissural Nodule (PFNs) I Intrapulmonary Lymph Node:
They technically don’t
have to contact a
pleural surface, as long Spiculated or Round
Typical morphological features would as they are within 15 mm nodules are not typical
include well circumscribed, smoothly (some people say for PFNs. These two
marginated, triangular, oval, or polygonal 20 mm). guys should be treated
nodules which either contact the fissure or like “regular” nodules.
pleural surface directly.
Trivia:
• PFNs are probably lymph nodes
• They are almost certainly benign and treated as such by the Fleischner society
• LUNG-RADS v1.1 says mean diameter less than 10 mm = category 2 (benign), larger than
10 mm means you treat than like any other nodule
• Interval growth does NOT mean they are full of cancer - lymph nodes normally fluctuate in size.
• Size greater than 6 mm still doesn’t justify follow up per Fleischner.
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lung Cancer Subtypes Tracheal and Airway Tumors (Carcinoid, Adenoid Cystic, Etc..)
will be discussed in a separate section later in the chapter.
There are 4 main histological subtypes of bronchogenic carcinoma that are broadly categorized
as cither small cell carcinoma or not small cell carcinoma (usually called “non small cell”).
Type Location Features and Trivia
• Strong Association with
Smoking Paraneoplastic
• Cavitation is Classic Syndromes can be
Non Small Cell
Central • Docs NOT express the tissue associated with
Squamous maker thyroid transcription ectopic Parathyroid
factor 1 “TTF-1” (other Hormone
subtypes can).
• Least common subtype (15%)
Non Small Cell • Usually large (> 4cm)
Peripheral
Large Cell • Prognosis Suck — this is the subtype of Cancer that
killed comedy legend Andy Kaufman in his 30s.
• Most Common subtype (35%)
• Favors the upper lobe
• Most Common subtype to present as a solitary
Non Small Cell Peripheral pulmonary nodule
Adenocarcinoma • Most Common subtype in a non smoker (although also
common in smokers)
• Known association with pulmonary fibrosis
• Strong Association with
Smoking (nearly every case is
a smoker) Associated with the
mythical
• May only present with central Paraneoplastic
lymphadenopathy Syndrome of
Lambert Eaton.
• Most Common primary lung They get proximal
CA to cause SVC obstruction weakness from
Small Cell Central
and paraneoplastic syndromes abnormal release of
acetylcholine at the
• Terrible Horrible Incredibly neuromuscular
Shitty Prognosis (metastasizes junction. The clinical
early) presentation often
comes before the
• Paraneoplastic Syndromes can cancer diagnosis.
be associated with SIADH and
ACTH
*Memory Aid — “LA is on the Coast ” - Large and Adeno favor peripheral locations
Gamesmanship: Location of the tumor can sometimes be predicted based on symptoms.
Central tumors = hemoptysis. Peripheral tumors = pleuritic chest pain.
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The Artist Formerly Known as BAC
(Now Adenocarcinoma In-Situ Spectrum)
Why change the name? Well it’s a simple reason. Academic Radiologists need to be on
committees to get promoted. Committees need an excuse to go on vacation (“International
Meetings” they call them). Name changes happen...
Atypical
Adenomatous The smaller (< 5 mm) and more mild pre-invasive sub-
Hyperplasia of type. Usually a pure ground glass nodule.
Pre-invasive lesions Lung (AAH):
Adenocarcino Typically larger than AAH but < 3 cm. Although features
ma in situ overlap with AAH, they tend to be more part-solid (rather
(ACIS): than pure ground glass)
These are also < 3 cm. The distinction is that there is < 5
Minimally Invasive
mm of stromal invasion ( > 5 mm will be called a lepidic
Adenocarcinoma (MIA)
predominant adenocarcinoma).
This is what most people used to call BAC
Invasive Mucinous Adenocarcinoma
(bronchoalveolar carcinoma).
To make this simple, just think about it on a spectrum with the small pre-invasive lesions on one end
and the invasive adenocarcinoma on the other. That same spectrum follows a relative increase in the
density of the nodule. This is why a growing consolidate component inside a previously existing
ground glass nodule is such a suspicious feature.
Key Concept: The larger the solid component of the “part solid” nodule gets the more likely it is to be
malignant. Partially solid nodules are more likely to be cancer than ground glass nodules.
Notice the
nodule getting
more dense
(white)
relative to the
prior year.
Trivia: These Adenocarcinoma subtypes are classically cold on PET.
Superior Sulcus / Pancoast Tumors: Some people make a big deal about only using the
word “pancoast” when the tumor causes the associated syndrome (shoulder pain, C8-T2
radiculopathy, and Homer Syndrome). In my experience most everyone just calls apical tumors
“pancoast” with no regard to symptoms. Having said that, I would remember “shoulder pain” as a
possible hint in the question header. These things are typically non-small cell cancers.
Staging = MRI is the tool of choice (you need to look at that brachial plexus).
General Contraindication to Surgical Resection (may vary by institution): invasion of the
vertebral body (> 50%), invasion of the spinal canal, involvement in the upper brachial plexus (C8 or
higher), diaphragm paralysis (infers phrenic nerve C3-5 involvement), distal mets.
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Staging:
Lung cancer staging used to be different for small cell vs non-small cell (NSCLC) . In 2013 the 7th
edition of the TNM made them the same. Below is a chart describing the staging based on tumor
size. For a solid lesion, the size is defined as maximum diameter in any of the three orthogonal planes
- measured on lung window. If the lesion is subsolid, then you define the T classification by the
diameter of the solid component only (NOT the ground glass part).
Lung Cancer Staging (8th edition)
Tumor is
T1 < 3 cm
Irregardless of size the tumor
• Invades the visceral pleura
Tumor is
T2 • Invades the main bronchus
3-5 cm
• Causes obstruction (atelectasis or pneumonia) that extends to the
hilum
Irregardless of size the tumor Pancoast (Superior
• Invades the chest wall Sulcus) Tumor that is
Tumor is • Invades the pericardium
T3 limited to
5-7 cm
• Invades the phrenic nerve (diaphragm paralysis) involvement of T1
• Has one or more satellite nodule in the same lung lobe and T2 nerve roots
Irregardless of size the tumor
• Invades the mediastinal fat or great vessels Pancoast (Superior
Tumor • Invades the diaphragm Sulcus) Tumor that
T4
> 7 cm • Involves the carina involves level C8 or
• Has one or more satellite nodule in another lobe in the same higher
long
Multiple Lesions: Vocab:
The handling of multiple lung lesion is complicated. Deciding if Synchronous = Two or more
lesions are going to be treated as synchronous primaries or a primary carcinomas which
single lung cancer with metastatic disease often requires a coexist at the time of
discussion at tumor board (after imaging, and path results). diagnosis.
If (he lesions arc decided to be separate primaries each cancer Metachronous = A cancer
will be staged separately within the TNM system and given an that develops consequently
overall stage. If the lesions arc decided to be metastatic their (some time interval) after the
distribution will alter the stage. first primary.
T3 (two in same lobe) T4 (two in different lobes,
but still the same lung) (two in different lungs)
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Lung Cancer Staging Continued (Nodal Disease)
Nodes
Ipsilateral within the lung N1 is a worse prognosis than N0 (no nodes) but
N1 up to the hilar nodes. the management is not changed.
In many cases NOT Resectable
N2 Ipsilateral mediastinal or subcarinal nodes Only those with microscopic disease (negative
mediastinoscopy) will benefit from resection
Contralateral mediastinal
or contralateral hilum. NOT Resectable
N3 *probably
Or
Scalene or Supraclavicular nodes.
First it is important to point out that CT is unreliable for nodal staging. PET-CT is far
superior, regardless of the size threshold that is chosen. This is why PET is pretty much
always done on lung cancer patients prior to surgical evaluation.
For the purpose of multiple choice (and real life) the most important anatomy boundary to
consider is the distinction between level 1 nodes (which at N3) and level 2 nodes (which are
N2).
In some cases, this
can literally make
the difference
between resectable
disease or not. The
border is the lower
level of the
clavicles / upper
border of the
manubrium (above
this is level 1).
Typical Contraindications to Lobectomy / Resection
The big issues (things that make lobectomy impossible) are going to be:
• Growth of the tumor through a fissure
• Invasion of the Pulmonary Vasculature Stage 3B implies
• Invasion of the main bronchus N3 or T4 disease
• Invasion of both the upper and lower lobe bronchi.
Other findings that will make the tumor NOT resectable:
• N2*(if the tumor is > 5 cm) or N3 Nodal Disease — corresponding to a Stage 3B cancer
• Multi-lobar Disease
• Malignant Pleural Effusion
For the purpose of multiple choice, the distinction between 3a_vs 3b is the critical stage because 3b is
surgically unresectable (technically this varies widely by institution and depends on lots of factors).
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Lung Cancer Treatment
Wedge Resection VS Lobectomy: This is on the fringe of what should be considered
fair game, and I’m certain the decision varies by institution and the size and composition (percentage
of brass) of the surgeon’s testicles. In general, if a stage 1A or IB cancer is peripheral and less than
2 cm they can consider a wedge resection. The advantage to doing this over a lobectomy is preserving
pulmonary reserve. If the tumor is larger than 3 cm then lobectomy seems to (in general) be a better
option.
Bronchopleural Fistula:
This is an uncommon complication of
pneumonectomy, that has a characteristic look and
therefore easy to test.
So normally after a pneumonectomy the space will
fill with fluid. If you see it filling with air than this
Normal - Become More Fluid Filled
is the dead give away.
If you are a weirdo, you could confirm the
diagnosis with a xenon nuclear medicine
ventilation study, which will show xenon in the
pneumonectomy space. The major risk factor is
ischemia to the bronchi (disrupted blood supply
from aggressive lymph node dissection, or using a
Bronchopleural Fistula
long bronchial stump).
- Become More Air Filled
Radiation Changes - The appearance of radiation
Radiation Changes
pneumonitis is variable and based on the volume of
lung involved, how much/long radiation was given, and Early
if chemotherapy was administered as well. (within 1-3 Late
months)
Rib Fractures - Ribs within the treatment field arc Dense
susceptible to degradation and fracture. Homogenous or consolidation,
patchy ground traction
RFA/MWA Pearl - It is normal to see bubbles in the glass opacities. bronchiectasis, and
lesion immediately after treatment. volume loss.
Recurrent Disease - Recurrence rates are relatively high (especially in the first 2 years). From
a practical stand point, I always focus my attention towards the periphery of the radiation bed,
regional nodes, and/or the bronchial stump. A useful concept is to focus on morphology - radiation
scarring is usually not round. If you see something with a round morphology - especially if it is
growing over time, that is highly suspicious.
Other findings concerning for recurrence:
• Enhancing solid tissue along the resection line (or bronchial stump) which is enlarging over time.
• New enlarged mediastinal nodes with a short axis greater than 1 cm
• New pleural effusion (that persists on follow ups)
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- Mimics and Other Cancers -
Pulmonary Hamartoma - This is not a cancer, but to
the uninitiated can look scary. It is usually described as is an
Aunt Minnie because it will have macroscopic fat and
“popcorn” calcifications. It is the most common benign
lung mass. It’s usually incidental, but can cause symptoms if
it’s endobronchial (rare - like 2%).
Technically the fat is only seen in 60%, but for sure if the
exam shows it, it will have fat. These can be hot on PET,
they are still benign. Pulmonary Hamartoma
• Popcorn Calcifications
• Fat Density
Mets - Metastatic disease to the lungs can be thought of in 3 categories; direct invasion,
hematogenous, lymphangitic:
• Direct Invasion: This is seen with cancer of the mediastinum, pleura, or chest wall. The most
common situation is an esophageal carcinoma, lymphoma, or malignant germ cell tumor. More rarely
you are going to have mets to the pleura then invading the lung. Even more rarely you can have
malignant mesothelioma, which can invade the lung. It should be obvious.
• Hematogenous Mets: The most common manifestation of
Feeding Vessel Sign: A
hematogenous mets to the lung is the pulmonary nodule
prominent pulmonary vessel
(usually multiple, in a random distribution, and favoring the
heading into a nodule. This
lower lobes which have greater blood volume). The nodules
tend to be smoother than the primary neoplasm. The main supposedly means it’s from
culprits are breast, kidney, thyroid, colon, and head & neck a hematogenous origin. It’s
squamous cells. Obviously the squamous mets can cavitate. nonspecific - but if you sec
it the answer is (1) mets , or
“Cannon ball Mets” are classically from renal cell or
(2) septic emboli.
choriocarcinoma (testicle).
• Lymphangitic Carcinomatosis (LC): The most common cause of unilateral LC is actually
bronchogenic carcinoma lung cancer invading the lymphatics. The most common extrathoracic
culprits are breast, stomach, pancreas, and prostate. The finding is nodular thickening of the
interlobular septa and subpleural interstitium. Unlike interstitial fibrosis, this thickening classically
does NOT distort the pulmonary lobule.
Kaposi Sarcoma: This is the most common lung tumor is
AIDS patients (Lymphoma is number two). The tracheobronchial
mucosa and perihilar lung are favored. The buzzword is “flame
shaped.” A bloody pleural effusion is common (50%).
Key Points:
•Most common lung tumor in AIDS (requires CD4 < 200)
•Most common hepatic neoplasm in AIDS
•Buzzword = Flame Shaped Opacities
•Slow Growth, with asymptomatic patients (despite lungs
looking terrible) Kaposi Sacroma
•Thallium Positive, Gallium Negative • “Flame Shaped” Hilar Opacities
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Lymphoma - There are basically 4 flavors of pulmonary lymphoma; primary, secondary, AIDS
related, or PTLD. Radiographic patterns are variable and can be lymphangitic spread (uncommon),
parahilar airspace opacities, and/or mediastinal adenopathy.
• Primary: This is rare, and usually non-
Secondary NHL Secondary HL
Hodgkin in subtype. You define it as the
lack of extrathoracic involvement for 3 80-90% of lymphoma 10-20% of lymphoma
months. Almost always (80%) we are cases cases
talking about a low grade MALToma.
45% have intrathoracic 85% have intrathoracic
• Secondary: Here we are talking about disease at presentation disease at presentation
pulmonary involvement of a systemic
25% have pulmonary 40% have pulmonary
lymphoma. This is much much much
parenchymal disease parenchymal disease
more common than primary lung
lymphoma. The thing to see is that NHL Pulmonary involvement Lung involvement
is much more common, but if you have frequently occurs in the almost always associated
HL it is more likely to involve the lungs. absence of mediastinal with intrathoracic lymph
With HL you gets nodes and parenchyma, disease node enlargement
in NHL you might just get parenchyma.
• PTLD: This is seen after solid organ or stem cell transplant. This usually occurs within a year of
transplant (late presentations > 1 year have a more aggressive course). This is a B-Cell lymphoma,
with a relationship with EB Virus. You can have both nodal and extra nodal disease. The typical look
is well-defined pulmonary nodules / mass, patchy airspace consolidation, halo sign, and interlobular
septal thickening.
• AIDS related pulmonary lymphoma (ARL) - This is the second most common lung tumor in
AIDS patients (Kaposi’s is first). Almost exclusively a high grade NHL. There is a relationship with
EBV. It is seen in patients with a CD4 < 100. The presentation is still variable with multiple
peripheral nodules ranging from 1 cm - 5 cm being considered the most common manifestation.
Extranodal locations (CNS, bone marrow, lung, liver, bowel) is common. AIDS patient with lung
nodules, pleural effusion, and lymphadenopathy = Lymphoma.
Nukes Cross Over Blitz
• Thallium is a potassium analog. Things with a functional Na/K/ATP pump tend to be alive.
Hence anything this is “alive” will be thallium positive.
• Gallium is an Iron analog. Iron is an
inflammatory marker (acute phase Kaposi Sarcoma Lymphoma
reactant) hence things that are
“smoldering” tend to be gallium negative, Thallium201 Positive Thallium201 Positive
and things that are inflamed - infection, Gallium67 Negative Gallium67 Positive
active sarcoid, most cancers - tend to be
Gallium hot.
• In general, it is safe to say “Lymphoma is HOT on Gallium.” Where things can get sneaky is
the subtype. Hodgkin is nearly always Gallium Avid. Certain Non-Hodgkin subtypes can be
Gallium cold. As such (and because it’s not 1970) PET is usually used for staging and not
Gallium.
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SECTION 5:
Co n g en i t a l
Sequestration, CCAMs, and a bunch of other congenital
path is discussed in detail in the Peds chapter (starting on
page 65). Here arc some other randos.
Poland Syndrome - Unilateral absence of a pectoral
muscle (white arrow). Can cause a unilateral hyper-lucent
chest. Can have limb issues (small weird arms / hands).
Bronchial Atresia - This is a congenital obliteration of a short segment of a lobar, segmental,
or subsegmental bronchus near its origin (most commonly involves the apical-posterior segment of
the left upper lobe). Like many atresias a vascular insult in utero is the probable etiology.
On CT, you will see a hyper lucent region with decreased
vascularity. It is somewhat counterintuitive that loss of the • Bronchial atresia is usually
bronchus would make the lung trap air (hyper lucent). The asymptomatic, although they can
explanation is collateral flow through the varies pores of presentation is recurrent
pneumonia.
Kohn and canals of Lambert. You will often see a large
“nodule” (sometimes with a branching or “finger in the • Hyperinflated lobe is the most
glove” morphology) nearby in the hilum — which represents common radiographic appearance
mucoid impaction in the blind ended bronchus. (sometimes with a hilar nodule
visible).
The primary differential would be an endobronchial tumor.
If you can measure (or they show you) a low density focus • CT will show a blind ending
(< 25 HU) in the mucus plug then you arc safe to call it bronchus, filled with mucus and
the distal lung Hyper-Inflated
mucoid impaction. If you can’t make the distinction the next
(lucent).
step should be bronchoscopy to be certain.
AVM - They can occur sporadically. For the purpose of multiple choice when you see them think
about HHT (Hereditary Hemorrhagic Telangiectasia / Osler Weber Rendu). Pulmonary AVMs are
most commonly found in the lower lobes (more blood flow), and can be a source of right to left shunt
(worry about stroke and brain abscess). The rule of treating once the afferent vessel is 3 mm is
based on some tiny little abstract and not powered at all. Having said that, it’s quoted all the time,
and a frequent source of trivia that is easily tested.
Persistent Left SVC - This is the most common congenital venous anomaly of the chest. It
usually only matters when the medicine guys drop a line in it on the floor and it causes a confusing
post CXR (line is in a left paramedian location). It usually drains into the coronary sinus. In a
minority of cases (like 5%) it will drain into the left atrium, and cause right to left shunt physiology
(very mild though). This is typically shown on an axial CT at the level of the AP window, or with a
pacemaker (or line) going into the right heart from the left.
Swyer-James - This is the classic unilateral lucent lung. It typically occurs after a viral lung
infection in childhood resulting in post infectious obliterative bronchiolitis (from constrictive
bronchiolitis). The size of the affected lobe is smaller than a normal lobe (it’s not hyper-expanded).
Horseshoe Lung: Rare as fuck.
Defined by fusion of the posterior basilar
segments of the lower lobes behind the heart.
The most likely testable points arc:
(1) What is it? and
(2) What is the association? Scimitar syndrome
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SECTION 6:
Cys t i c Lu n g Di s ea s e
Pulmonary Langerhans Cell Histiocytosis (LCH) -
This cystic lung disease classically effects smokers, who are young What Spares the
(20s-30s). The disease starts out with centrilobular nodules with an Costophrenic
upper lobe predominance. These nodules eventually cavitate into cysts Angles???
which arc thin walled to start, and then some become more thick
walled. Late in the disease you are primarily seeing cysts. The (1) LCH and
buzzword is bizarre shaped, which occurs when 2 or more cysts merge
(2)
Hypersensitivity
together. In about half the cases this spontaneously resolves (especially
if you stop smoking). Another piece of trivia is that LCH spares the Pneumonitis
costophrenic angles.
Lymphangiomyomatosis (LAM) -
Alternative strategy to suggest TS
(without telling you the patient has
This cystic lung disease can occur in child bearing aged TS) could be the step 1 “clinical
women or in association with Tuberous Sclerosis (a trick triad” — even though < 50% of TS
is to show the kidneys with multiple AMLs first). The patients have the complete triad.
cysts arc thin walled with a uniform distribution. There is
an association with chylothorax (which is HIGH YIELD 1 - Seizures, 2- Mental Retardation,
Trivia). The pathophysiology is that it is estrogen 3 - Adenoma Sebaceum
dependent (why it strongly favors women). This is usually
progressive despite attempts at hormonal therapy SSS: Seizures, Sebaceum, & Stupid
(tamoxifen).
Birt Hogg Dube
(BHD)
This is a total zebra. This
cystic lung disease has thin
walled “oval” shaped cysts.
There is an association with
renal findings (bilateral
oncocytomas, and chromophobe
RCCs). They also have a bunch
of gross skin stuff.
Birt-Hogg-Dube LAM
-Oval Cysts -Multiple Thin Walled Round Cysts-
LCH LAM Bizarre Thick
LCH
Cysts and Nodules Cysts (no nodules) Shape Wall
Women, Pts with
Smoker Thin
Tuberous Sclerosis LAM Round
Wall
Upper and Mid Lungs Diffuse
Thicker Cysts Thin
Thin Round Cysts BHD Oval
(Bizarre) Wall
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Lymphocytic Interstitial Pneumonitis (LIP) - This is a benign
lymphoproliferative disorder, with infiltration of the lungs. It has an association with
autoimmune diseases (SLE, RA, Sjogrens). The big one to know is Sjogrens which is
concomitant in 25% of LIP cases. The other one to know is HIV - which is the LIP in a
younger patient (children, - LIP in HIV positive adults is rare). There is also an association
with Castlemans. The appearance of LIP varies depending on the underlying cause. The
cystic lung disease is usually thin walled, “deep within the lung parenchyma,” and seen
predominantly with Sjogrens. The dominant feature described as ground glass or nodules is
seen more in the other causes and is far beyond the scope of the exam.
When I say LIP... You say Sjogren's & HIV
When I say LIP in a kid... You say HIV
Pneumocystis Pneumonia (PCP) - This is the most common opportunistic
infection in AIDS.
The typical buzzword is ground glass appearance, predominantly in the hilar and mid
lung zones.
Pneumatoceles are present in 30% of cases. In patients receiving aerosolized prophylaxis, a
cystic form is more common, which may have bilateral thin walled upper lung
predominant cysts. Gallium67 scan will show diffuse uptake (Thallium will be negative).
When I say AIDS + Ground Glass Lungs.... You say PCP
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Emphysema
The textbook definition is "permanent enlargement of the airspaces distal to the terminal
bronchioles accompanied by destruction of the alveolar wall without clear fibrosis.” What
you need to know are (1) the CXR findings and (2) the different types.
CXR Findings: Until it’s really really bad, CXR doesn’t have direct signs, but instead has
indirect signs. Flattening of the hemidiaphrams is regarded as the most reliable sign. The
AP diameter increases. The retrosternal clear space becomes larger. There is a paucity of, or
pruning of the blood vessels.
Types:
• Centri-lobular. By far the most common type. Common in asymptomatic elderly patients.
It has an apical to basal gradient - favoring the upper zones of each lobe. It appears as
focal lucencies, located centrally within the secondary pulmonary lobule, often with a
central dot representing the central bronchovascular bundle. This central dot sign is a
buzzword. This is the type of emphysema dominant in smokers.
• Pan-lobular: In contradistinction to centrilobular this one favors the lower lobes. It also
has a more uniform distribution across parts of the secondary pulmonary lobule. The
association is with alpha 1 antitrypsin. A piece of trivia is the “Ritalin Lung” from IV
Ritalin use can also cause a pan-lobular appearance (“Ritalin keeps you from ‘trypsn’
out”). If they show this it will be in the coronal view on CT to demonstrate the lower lobe
predominance. Patient’s will present in their 60s and 70s (unless they smoke - then they
present in their 30s). Smoking accelerates the process.
• Para-septal. This one is found adjacent to the pleura and septal lines with a peripheral
distribution within the secondary pulmonary lobule. The affected lung is almost always
sub-pleural, and demonstrates small focal lucencies up to 10 mm in size. This looks like
honeycombing but is less than 3 bubbles thick.
Trivia:
• Saber Sheath Trachea - Diffuse coronal narrowing of the trachea, sparing the extrathoracic
portion. This is said to be pathognomonic for COPD.
• If the Main PA is larger than the Aorta COPD patients have a worse outcome (pulmonary
HTN can be caused by emphysema).
• Surgery to remove bad lung “volume reduction” is sometimes done
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Vanishing Lung Syndrome: This is an Vanishing Lung Risk Factors:
idiopathic cause of giant bullous emphysema,
• Smoking (tobacco)
resulting from avascular necrosis of the lung
parenchyma and hyperinflation. It favors the • Alpha-1 antitrypsin deficiency
bilateral upper lobes, and is defined as bullous
disease occupying at least one-third of a • Male
hemithorax. The most common demographic is a • Smoking Marijuana is also a
young man. About 20% of these guys have alpha-1 described risk factor (although it
antitrypsin deficiency. Tension pneumothorax is a is probably bullshit propaganda
described complication. from the pharmaceutical industry)
Compensatory Emphysema (Postpneumonectomy Syndrome): There
is no obstructive process here. Instead you have hyper-expansion of one lung to compensate
for the absence of the other one.
Honeycomb Lung; When I say honeycombing you should say UIP. However, this is
seen with a variety of causes of end stage fibrotic lung processes. The cysts are tightly
clustered (2-3 rows thick) and subpleural. The walls are often thick.
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SECTION 7:
Pn eumo c o n i o s i s
As a general rule, these are inhaled so they tend to be upper lobe predominant. You can have
centrilobular nodules (which makes sense for inhalation), or often perilymphatic nodules -
which makes a little less sense, but is critical to remember * especially with silicosis and
CWP.
Asbestos Exposure: The term “Asbestosis” refers to the changes of pulmonary
fibrosis - NOT actual exposure to the disease. The look is very similar to UIP, with the
presence of parietal pleural thickening being the “most important feature” to distinguish
between I PF and Asbestosis. Obviously, the history of working in a ship yard or finding
asbestos bodies in a bronchoalveolar lavage is helpful.
Things to know about Asbestos:
• “Asbestosis” = the lung fibrosis associated with exposure, NOT actual exposure
• Interstitial pattern looks like UIP + parietal pleural thickening
• There is a 20 year latency between initial exposure and development of lung cancer or
pleural mesothelioma
• There is an association with extrapulmonary cancer including: Peritoneal mesothelioma,
GI cancer, Renal Cancer, Laryngeal Cancer, and Leukemia
• Benign pleural effusions are the “earliest pleural-based phenomenon” associated with
exposure - still with a lag time of around 5 years
Benign Asbestosis Related Changes:
Pleural effusion is the earliest and most common. Pleural plaques may develop around 20-30
years, with calcifications occurring around 40 years. These plaques tend to spare the apices and
Costophrenic angles. Round atelectasis - which is associated with pleural findings is sometimes
called the “asbestos pseudotumor. ”
Malignant Mesothelioma
The most common cancer of the pleura. About 80% of them have had asbestos exposure, and
development is NOT dose-dependent. The lag time is around 30-40 years from exposure.
Key Features:
Evaluating Direct Invasion & Mets
• Circumferential Pleural Thickening extending to
the medial surface of the pleura (near the heart) Mesothelioma believes in nothing
• Pleural Thickness > 1 cm Lebowski with a known tendency for
direct invasion.
• Extension into the fissure = highly suggestive
MRI with Contrast = For evaluating
Thick Lateral Pleural = Common local chest wall, diaphragm and
** think old rib fx pericardial invasion
Buzzword = PET/CT = Good for mets. Useful for
Thick Medial Pleural = NOT Common evaluating treatment response.
Pleural Rind
**think mesothelioma.
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Silicosis: This is seen in miners, and
quarry workers. You can have simple
silicosis, which is going to be multiple
nodular opacities favoring the upper
lobes, with egg shell calcifications of the
hilar nodes. You also get perilymphatic
nodules. The complicated type is called
progressive massive fibrosis (PMF).
This is the formation of large masses in
the upper lobes with radiating strands.
You can see this with both silicosis and
coal workers pneumoconiosis (something
similar also can happen with Talcosis).
These masses can sometimes cavitate -
but you should always raise the suspicion Progressive Massive Fibrosis
of TB when you see this (especially in the -Large Apical Masses with Radiating Strands
setting of silicosis).
MRI : Cancer vs PMF
Silicotuberculosis: Silicosis actually raises your
risk of TB by about 3 fold. If you see cavitation in the Cancer = T2 PMF = T2
setting of silicosis you have to think about TB. Bright Dark
Coal Workers Pneumoconiosis: This is the result of exposure to “washed coal.”
Just like silicosis there are simple and complicated forms. There is also an increased risk of
TB (just like silicosis). The simple form was multiple nodular opacities, with calcifications
showing a central nodular dot. The small nodule pattern tends to have a perilymphatic
distribution. The complicated form gives you a progressive massive fibrosis that is
similar to that seen in silicosis.
Additional Inhalational Diseases - Not Worthy of a Full Discussion
Generalized granulomatous disease
Metal used in aircraft and
Berylliosis with hilar adenopathy and upper lobe
space industries
predominant reticular opacities.
Pulmonary Edema Pattern. Recovery
Silo Filler’s Disease Nitrogen Dioxide
is typically within 5 weeks.
Filler in tablets, sometimes Hyperdense micronodules, with
Talcosis injected (along with drugs) conglomerate masses (similar to PMF).
in IV drug users. Ground glass opacities
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SECTION 8:
ILDS
Don’t Be Scared Homie
Everyone seems to be afraid of interstitial lung diseases. The concept is actually not that
complicated, it’s just complicated relative to the rest of chest radiology (which overall isn’t
that complicated). The trick is to ask yourself two main questions: (1) Acute or Chronic ? -
as this narrows the differential considerably, and (2) What is the primary finding ? - as this
will narrow the differential further. Now, since we are training for the artificial scenario of a
multiple choice test (and not the view box), I’ll try and keep the focus on superficial trivia,
and associations. Remember when you are reading to continue to ask yourself “how can
this material be written into a question?”
Vocab: Like most of radiology, the bulk of understanding the pathology is knowing the
right words to use (plus, a big vocabulary makes you sound smart).
• Consolidation = Density that obscures underlying vessels
• Ground Glass Opacity = Density that does NOT obscure underlying vessels
• Secondary Pulmonary Lobule = The basic unit of pulmonary structure and function.
It is the smallest part of the lung that is surrounded by connective tissue. In the middle
runs a terminal bronchial with an accompanying artery. Around the periphery runs the
vein and lymphatics.
Anatomy of the Secondary Pulmonary Lobule
Anatomy Questions = Fair Game and Easy to Write for MCQs
Stuff like “what goes around the periphery?” or “what goes through the middle of the lobule ?”
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Nodule Vocabulary (Random, Perilymphatic, Centrilobular)
Random Perilymphatic Centrilobular
Telling them apart can be done by first asking if they abut the pleura?
If the answer is no they are
centrilobular.
If the answer is yes, then
ask do they follow a
peribronchovascular
pattern,
if the answer is no then
they are random, if the
answer if yes then they are
perilymphatic.
Nodule Pattern Key DDx
•Sarcoid (90%),
Perilymphatic •Lymphangitic Spread of CA
•Silicosis
•Miliary TB
Random •Mets
•Fungal
•Infection
Centrilobular •RB-ILD
•Hypersensitivity Pneumonitis (if ground glass)
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Patterns
Interlobular Septal Thickening: Reticular abnormality, that outlines the lobules
characteristic shape and size (about 2 cm). It’s usually from pulmonary edema (usually
symmetric and smooth), or lymphangitic spread of neoplasm (often asymmetric and
nodular). Kerley B Lines are the plain film equivalent.
Honeycombing: Cystic areas of lung
destruction in a subpleural location. This is a
hallmark of UIP. Paraseptal emphysema is a
mimic, but the distinction is made by how
many rows of bubbles.
• One Row of Bubbles =
Paraseptal Emphysema.
• Two-Three Rows of Bubbles =
Honey- combing.
Honeycombing - Two examples
Pathology
Idiopathic Interstitial Pneumonias - These are NOT diseases, but instead lung reactions to
lung injury. They occur in a variety of patterns and variable degrees of inflammation and
fibrosis. The causes include: idiopathic, collage vascular disease, medications, and
inhalation.
For practical purposes the answer is either (a) UIP or (b) Not UIP. Not UIP will get better
with steroids. UIP will not. UIP has a dismal prognosis (similar to lung cancer). Not UIP
often does ok. The exam will likely not make it this simple, and will instead focus on
buzzwords, patterns, and associations (which I will now discuss).
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UIP (Usual Interstitial Pneumonia) - The most common ILD. When the cause is
idiopathic it is called IPF. On CXR the lung volume is reduced (duh, it’s fibrosis). Reticular
pattern in the posterior costophrenic angle is supposedly the first finding on CXR.
O Buzzwords include: Definite UIP Criteria:
• Honeycombing (must be present)
• Apical to basal gradient (it’s worse in the
• +/- traction bronchiectasis
lower lobes) • Reticular abnormalities
• Traction bronchiectasis, and honeycombing • Subpleural basal predominant distribution
• Honeycombing is found 70% of the time, • Absence of inconsistent features: upper lobe
and people expect you to kneejerk UIP when predominance, ground glass > reticulations,
air trapping involving 3 or more lobes
that term is uttered
• Histologic Buzzword = Heterogeneous. Definite DIP Pattern =
Don’t Need to Biopsy to Prove Diagnosis
“Histology was heterogeneous” = UIP
It’s important to know that basically any end This vs That: Chronic Hypersensitivity
stage lung disease (be it from sarcoid, RA, Pneumonitis (HP) vs UIP.
Scleroderma, or other collagen vascular disease) Features that favor Chronic HP over UIP:
has a similar look once the disease has mined the • Air Trapping involving 3 more lobes
lungs. *Technically honeycombing is uncommon
• Mid-Upper lobe predominant fibrosis
in end stage sarcoid - but the rest of the lung
looks jacked up.
The prognosis is terrible (similar to lung cancer).
UIP- Honeycombing, Traction Bronchiectasis, Apical-to-Basal Gradient
Fibrosis and Cancer Go Together Like Tacos and Tuesdays
Pulmonary fibrosis is a risk factor for lung cancer
(especially if these patients are dumb enough to also smoke).
Cancer in the Fibrotic Lung Trivia:
• Favors the lower lobes
• Favors the interface between the fibrotic cysts and normal lung
• Progressive wall thickening or a developing nodule within a cyst is suspicious for cancer
(enlarging pericystic nodules are dodgy as fuck - hide your kids / hide your wife)
• NELSON Lung Cancer Screening Trial showed cancers associated with cystic lesions were
commonly missed (people thought they were just areas of focal thickening within a bulla).
— Then I said “Come on Judge... let him go, he s doing his best. ”
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NSIP (Nonspecific Interstitial Pneumonia)
Less Common than UIP. Even though the name infers that its non-specific, it’s actually is
a specific entity. Histologically it is homogenous inflammation or fibrosis (UIP was
heterogeneous). It is a common pattern in collagen vascular disease, and drug reactions.
It comes in 2 flavors (cellular or fibrotic):
■ Ground Glass Alone = Cellular
■ Ground Glass + Reticulation = Cellular or Fibrotic
■ Reticulation + Traction Bronchiectasis = Fibrotic NSIP
■ Honeycombing - uncommon and usually minimal in extent
Trivia: NSIP is the most common Interstitial Lung Disease in Scleroderma
The disease has a lower lobe, posterior, peripheral predominance with sparing of the
immediate subpleural lung seen in up to 50% of cases. This finding of immediate
subpleural sparing is said to be highly suggestive. Ground glass is the NSIP equivalent
of honeycombing.
NSIP - Peripheral Ground Glass with Subpleural Sparing
UIP NSIP
Gradient is less obvious
Apical to Basal Gradient
(but still more in lower lobes)
Heterogeneous Histology Homogenous Histology
Honeycombing Ground Glass
Traction Bronchiectasis Micronodules
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RB-ILD and DIP:
I’m going to discuss these two together because some people feel they are a spectrum. For
sure they are both smoking related diseases.
• RB-ILD - Apical Centrilobular ground glass nodules
• DIP - More diffuse GGO, with patchy or subpleural distribution
RB-ILD: This tends to be
more upper lobe
predominant (note that DIP
tends to be more lower lobe
predominant). Localized
centrilobular ground glass
nodules. The pathology
tends to involve the entire
cross section of lung.
Respiratory Bronchiolitis + RB-ILD- Apical Centrilobular ground glass nodules +
Symptoms = RB-ILD. Smoking History
DIP: Desquamative interstitial pneumonia is
thought of as the end spectrum of RB-ILD,
and generally seen in 50 year old heavy
smokers. Extras from 1984 comedy classic
“Revenge of the Nerds” seem to enjoy going
to radiology conferences to voice their
disapproval of the term “DIP” because the
pathology is not desquamation of alveolar
epithelium but instead represents a filling of
alveolar spaces with macrophages. Could
these same weirdos be writing the questions?
DIP - Bilateral Fairly Symmetric Basilar
The dark side clouds everything. Impossible to Predominant Ground Glass
see the future is.
Just think peripheral lower lobe predominant ground glass, with small cystic spaces.
You can see consolidations - but they are usually associated with cryptogenic pneumonia.
You can see fibrosis - but it is rare (like 5-10%) - I would not expect that on the exam.
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Sarcoid:
This is a multi-system disease that CXR can be used to “Stage” Sarcoid
creates “non-caseating granulomas.”
The classic age is between 20-40. Stage 0 = Normal
Along those lines, if the header to the Stage 1 = Hilar / Mediastinal Nodes Only
question describes an African American Stage 2 = Nodes + Parenchyma Disease
female in her 20s-30s the answer is Stage 3 = Parenchymal Disease
probably sarcoid. The lungs are by far Stage 4 = End Stage (Fibrosis)
the most common organ affected
(90%).
Misc Trivia to know:
• Elevated angiotensin-converting enzyme (ACE)
• Hypercalcemia
Mediastinal lymph nodes are seen in 60-90% of patients (classically in a 1-2-3 pattern of
bilateral hila and right paratracheal). They have perilymphatic nodules, with an upper
lobe predominance. Late changes include, upper lobe fibrosis, and traction bronchiectasis
(honeycombing is rare). Aspergillomas are common in the cavities of patients with end
stage sarcoid.
• 1-2-3 Sign - bilateral hila and right paratracheal
• Lambda Sign — same as 1-2-3, but on Gallium Scan
• CT Galaxy Sign — upper lobe masses (conglomerate of nodules) with satellite
nodules
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CHF:
CHF is obviously not an ILD. However, it can sorta look like one on Chest X-Ray so I
opted to lump it in here. Congestive heart failure occurs because of cardiac failure, fluid
overload, high resistance in the circulation, or some combination of the three. There are
three phases of CHF, and these lend themselves to testable trivia.
Stages of CHF
Wedge Pressure Cephalization of vessels, Big
Stage 1 “ Redistribution”
13-18 heart, Big Vascular Pedicle
Kerley Lines, Peribronchial
Wedge Pressure
Stage 2 “ Interstitial Edema” Cuffing, Less distinct contour of
18-25
Central Vessels
Wedge Pressure Airspace “fluffy” opacity,
Stage 3 “Alveolar Edema”
>25 Pleural effusion
*Swan Ganz Pulmonary Wedge Pressures are an indirect measurement of left atrial
pressure. They can help prove a cardiogenic etiology to pulmonary edema.
Right Heart Failure:
This is less common than left heart failure, which ironically is the most common cause. Left
heart failure causes pulmonary venous HTN which causes pulmonary arterial HTN, which
causes right heart failure. Some other less common causes of right heart failure include
chronic PE and right-sided valve issues (tricuspid regurg). The imaging features of right
heart failure include dilation of the azygos vein, dilation of the right atrium, dilation of the
SVC, ascites, big liver, and contrast reflux into the hepatic veins on CTPA.
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SECTION 9:
Tr a n s pl a n t
Lung transplants are done for end-stage pulmonary disease (fibrosis, COPD, etc..). The
complications lend themselves easily to multiple choice test questions, and are therefore high
yield. The best way to think about the complications is based on time.
Immediate Complications (< 24 hours)
Mismatch up to 25% is ok. You can have a
compressed lung (by the hyperexpanded
Donor-Recipient Size Mismatch
emphysematous lung). Imaging is usually
atelectasis.
Secondary to HLA and ABO antigens. It’s
Hyperacute Rejection rapid and often fatal. Imaging shows massive
homogenous infiltration
Early Complications (24 hours - 1 week)
Peaks at day 4 as a non-cardiogenic edema
Reperfusion Injury related to ischemia-reperfusion. Typically
improves by day 7.
Defined as a continuous leak for more than 7
Air Leak / Persistent Pneumothorax
days.
Intermediate Complication (8 days - 2 months)
Ground Glass opacities and intralobular septal
Acute Rejection thickening. (No ground glass = no rejection).
Improves with steroids.
Leaks occur in the first month, stenosis can
Bronchial Anastomotic Complications
develop later (2-4 months).
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Late Complications (2-4 months)
The most common opportunistic infection.
CMV Infection
Ground glass, tree-in-bud. Rare before 2 weeks.
Later Complications (> 4 months)
Bronchiolitis Obliterans; Affects 50% at 5 years.
Chronic Rejection Brochiectasis, bronchial wall thickening, air
trapping.
Occurs with chronic rejection (but more
Cryptogenic Organizing Pneumonia commonly with acute rejection). Responds to
steroids.
PTLD Typically seen within the first year. EBV in 90%.
Upper Lobe Fibrosis Associated with chronic rejection
Chronic Rejection / Bronchiolitis Obliterans Syndrome: This is the
major late complication, that affects at least half of the transplants at 5 years (most
commonly at 6 months). The term bronchiolitis obliterans is often used interchangeably
with chronic rejection. The findings on CT include bronchiectasis, bronchial wall
thickening, air trapping, and interlobular septal thickening. Just think air trapping on
expiration seen at or after 6 months = chronic rejection.
Recurrence of Primary Disease after Transplant: For the purpose of
multiple choice tests know that sarcoidosis is the most common recurrent primary
disease (around 35%). Lots of other things can recur.
Lung Cancer after Transplant: Just remember that the native lung is still
diseased, and can get cancer. The highest rate is with pulmonary fibrosis, and the most
common risk factor is heavy tobacco use.
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SECTION 10:
Al v eo l a r
Pulmonary Alveolar Proteinosis (PAP): For the purpose of multiple
choice, this is an Aunt Minnie - always shown as crazy paving lung (interlobular septal
thickening with ground glass). This can be primary (90%), or secondary (10%). The
secondary causes worth knowing are cancer or inhalation (silico-proteinosis).
Trivia Worth Knowing:
• They are at increased risk of Nocardia infections, and can have nocardia brain
abscesses.
• Smoking is strongly associated with the disease.
• When seen in children (presenting before age 1) there is a known association with
alymphoplasia.
• Can progress to pulmonary fibrosis (30%).
• Treatment is bronchoalveolar lavage
Crazy Paving -
Interlobular septal
thickening and ground
glass. This isn’t always
PAP, in fact in real life
that it is usually NOT
PAP. There is a
differential that
includes common
things like edema,
hemorrhage, BAC,
Acute Interstitial
Pneumonia.
Just know that for the
purpose of multiple
choice tests, the
answer is almost
always PAP.
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Lipoid Pneumonia - There are actually two types; endogenous and exogenous.
• Exogenous: A certain percentage of elderly people become absolutely obsessed with
their bowel movements. If you did Family Medicine addressing this psychopathology
would steal a certain amount of hours out of your life per week. Lipoid pneumonia is
seen in old people who like to drink/aspirate mineral oil (as a laxative). It can also be
seen with the aspiration of vegetable oil or other animal oils. The look on plain film is an
area of lung opacification that is chronic or slowly increases with time. The look on CT
is a dead give away and the most likely way this will be shown is with low attenuation /
fat density in the consolidation. Having said that this is also in the crazy paving
differential.
• Acute Exogenous Lipoid Pneumonia — This is seen in children who accidentally poison
themselves with hydrocarbons, or idiots trying to perform fire-eating or flame blowing.
• Endogenous - This is actually more common than the exogenous type, and results from
post obstructive processes (cancer) causing build up of lipid laden macrophages.
Lipoid Pneumonia - Fat Density in the Consolidation
Gamesmanship: “Why are you showing me the lung on that window?”
Obviously pulmonary pathology is best shown on a lung window. So anytime the
test writer is showing you a pulmonary pathology on a non-lung window, that
should cue you to think about some different things.
(1) : Is the finding in the mediastinum or ribs?
(2) : If it’s clearly a lung finding then what window are they using?
• Soft tissue window is classically used to show fat in a lesion - think hamartoma or lipoid
pneumonia.
• Bone window might be used to show a diffuse process such as pulmonary
microlithiasis.
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Organizing Pneumonia (cryptogenic/cause not known “COP”)
This used to be called BOOP,
which was a lot more fun to say.
It’s not an active infection (as the
name would suggest) but instead
granulation tissue deposition
within the alveolar spaces
secondary to fibroblast
proliferation. Because it is not an
active infection antibiotics won’t
help. However, it does respond
well to steroids, and has an
excellent prognosis.
There are lots of different causes;
idiopathic, prior infection, drugs
(amiodarone), collagen vascular
disease, fumes, etc... You will see
the word “cryptogenic” used when Cryptogenic Organizing
there is no specific cause known. Pneumonia- Reverse Halo Sign
Then it is COP instead of OP.
The history of “persistent symptoms following treatment for pneumonia” could be a clue to
think OP. The most common “persistent symptoms” are a cough lasting several months, low
grade fever, SOB, and just generally feeling like shit.
Patchy air space consolidation or GGO (90%), in a peripheral or peri-bronchial distribution.
Opacities tend to be irregular in shape. Both OP and Chronic Eosinophilic Pneumonia can
present as peripheral consolidations. Findings of fibrosis are typically absent.
Reverse Halo (Atoll) Sign is the classic sign - seen in around 30% of cases:
Consolidation around a ground glass center.
Chronic Eosinophilic Pneumonia:
Can be idiopathic or associated with a known antigen. Peripheral eosinophilia (blood test) is
usually present. An asthma history is found in about 50% of cases. It looks exactly look COP
(both can present as peripheral consolidations). When you say COP you should say this one too
(some people think it’s the same disease as COP).
CT Findings: Peripheral GGO or consolidation. Upper lobes tend to be favored.
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THIS vs THAT: Halo Signs
Halo Reverse (Atoll)
-Nodule with ground glass around it
Central ground glass with rim of
-Represents hemorrhage / invasion into
consolidation
surrounding tissues
- Invasive Aspergillosis (Classic) - COP (Classic)
- Other Fungus - TB
- Hemorrhagic Mets - Pulmonary Infarct
- Adenocarcinoma in Situ (BAC) - Invasive Fungal and Wegeners ** these
- Wegeners can also be seen with regular Halo
Hypersensitivity Pneumonitis:
This is actually common. It’s caused by inhaled organic antigens. It has acute, subacute,
and chronic stages. Most of the time it’s imaged in the subacute stage.
•Subacute: Patchy ground glass opacities. Ill-defined Centrilobular ground glass nodules
(80%). Often has mosaic perfusion, and air trapping.
• Chronic: Looks like UIP + Air trapping. This vs That: Chronic Hypersensitivity
You are gonna have traction bronchiectasis Pneumonitis (HP) vs UIP.
and air trapping. Features that favor Chronic HP over UIP:
• Air Trapping involving 3 more lobes
• Mid-Upper lobe predominant fibrosis
Buzzword is “headcheese” because it’s a mix of everything (Ground Glass,
Consolidation, Air-Trapping, and Normal Lung)
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SECTION 11:
Ai r w a ys
Anatomy The basic anatomy of the trachea is a bunch of anterior horseshoes of cartilage,
with a posterior floppy membrane. This membrane can bow inward on expiratory CT (and this
is normal). The transverse diameter should be no more than 2.5 cm (same as the transverse
diameter of an adjacent vertebral body).
Tracheal Disease Game Plan: Three big questions to ask yourself.
(1) Does it involve the posterior membrane? (2) is it focal or diffuse ? and
(3) is there calcification?
Relapsing Polychondritis: Spares the posterior membrane. Diffuse thickening of the
trachea. No calcifications. Characterized by recurrent episodes of cartilage inflammation, and
recurrent pneumonia.
Post Intubation Stenosis: Focal Subglottic circumferential stenosis, with an
hourglass configuration.
Wegener’s: Circumferential thickening, which can be focal or long segment. No
calcifications. Subglottic involvement is common.
Tracheobronchopathia Osteochondroplastica (TBO):
Spares the posterior membrane. You have development of cartilaginous and osseous
nodules within the submucosa of the tracheal and bronchial walls.
Amyloidosis:
Irregular focal or
short segment
thickening, which can
involve the posterior
membrane.
Calcifications are
common.
TBO - Note the sparing of the posterior membrane (arrow)
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Spares the Posterior Membrane Does NOT Spare the Posterior Membrane
Recurrent episodes of
cartilage inflammation
(ears, nose, joints, Often confined to the
Relapsing laryngeal and thyroid trachea and main
Amyloid
Polychondritis cartilage). Recurrent bronchi. Calcifications
pneumonia is the most are common.
common cause of
death.
Post Intubation Focal Subglottic
Development of
Tracheobronchopathia cartilaginous and C-ANCA +, Sub-glottic
Osteochondroplastica osseous nodules. Wegeners trachea is the most
(TBO): Typically occurs in common location.
men older than 50.
Saber-Sheath Trachea: Coronal diameter of less than two thirds the sagittal diameter.
I say “saber-sheath trachea,” you say COPP,
Trivia: The main bronchi will be normal in size.
The tracheal wall will be normal in thickness.
Tracheal / Bronchial Tumors
Pulmonary Neuroendocrine Tumors
Typical Carcinoid Atypical Carcinoid Large Cell (LCNEC)
-Low-Grade Malignant- -Intermediate Malignant- and Small Cell (SCLC)
-High Grade Malignant-
< 3 cm > 3 cm
LCNEC: Peripheral
More Likely to Be More Likely to Be pulmonary mass -
Central (tracheal Peripheral (distal to the around 3.5 cm
bifurcation) segmental bronchi).
SCLC: Large central /
May not show a
More likely to appear to mediastinal mass
bronchial relationship -
be within the lumen of involving the hilum
or be partially
the airway. More likely
endobronchial. Trivia: Bronchial
to be calcified (-30%).
Carcinoid is more likely to
Age ~ 60s
Age ~ 50s Met inside the eyeball
Association with Smoking (uveal tract). Where as a
GI carcinoid is most likely
to met to the extra ocular
Typical & Atypical carcinoids show enhancement post contrast. muscles
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Tracheal / Bronchial Tumors Continued
Tumors of the trachea are not common in the real world.
• Extremely rare in the trachea (< 1%).
• More typically seen Endobronchial
• Carcinoids usually have a central endobronchial location
(although they can rarely be found in the pulmonary parenchyma-
presented as a nodule or mass in an older patient).
• Pulmonary carcinoid tends to be slow growing and locally
invasive (only met to nodes about 10% of the time).
• No surprise they can cause obstructive symptoms. They can also
cause hemoptysis because they are highly vascular.
Carcinoid
• For the purpose of multiple choice = No association with smoking
(**there maybe an association with the atypical sub-type)
• An octreotide scan can be used to localize a carcinoid tumor.
• PET can be falsely negative in ~ 25% of cases (they can be cold
on PET).
• Rarely they can cause a carcinoid syndrome with flushing etc...
The valvular degradation that occurs tends to be on the left side
(mitral and aortic), as opposed to the GI carcinoid syndrome
which targets the right side (tricuspid and pulmonic).
• 2nd Most common tracheal malignancy
• Favors the upper trachea, and prefers the posterior lateral trachea
• 20x more likely to be in the trachea (relative to carcinoid).
Adenoid Cystic
• Has a variable look - can be thickening, a mass, or a nodule.
• It is NOT associated with smoking.
• They are usually in the main or lobar bronchus.
• Most Common tracheal malignancy.
• Associated with smoking,
Squamous Cell
• Often multifocal (10%), favors the lower trachea / proximal
bronchus
Mets • Usually via direct extension (lung, thyroid, esophagus)
• Most common benign tumor of the trachea
Squamous Cell
• When it’s a single papilloma think smoking.
Papilloma
• When it’s multiple papillomas think HPV.
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Cystic Fibrosis - The sodium pump doesn’t work and they end up with thick
secretions and poor pulmonary clearance. The real damage is done by recurrent infections.
Things to know:
• Bronchiectasis (begins as cylindrical and progresses to varicoid)
• It has an apical predominance (lower lobes are less affected)
• Hyperinflation
• Pulmonary Arterial Hypertension-
• Mucus plugging (finger in glove)
Primary Ciliary Dyskinesia: Those little hairs in your lungs that clear
secretions don’t work. You end up with bilateral lower lobe bronchiectasis (remember that
CF is mainly upper lobe). Other things these kids get is chronic sinusitis (prominent from an
early age), and impaired fertility (sperm can’t swim, girls get ectopics). They have chronic
mastoid effusions, and conductive hearing loss is common (those little ear nerve hair things
are fucked up too). An important testable fact is that only 50% of the primary ciliary
dyskinesia patients have Kartagener’s Syndrome.
THIS vs THAT:
CF Primary Ciliary Dyskinesia
Abnormal Mucus, Cilia cannot move it Normal Mucus, Cilia don’t work
Abnormal Sperm (they can’t swim),
Normal Sperm, Absent Vas Deferens
Normal Vas Deferens
Upper lobe bronchiectasis Lower lobe bronchiectasis
Williams Campbell Syndrome - Huge zebra that manifests as
congenital cystic bronchiectasis from a deficiency of cartilage in the 4th-6lh
order bronchi.
Mounier-Kuhn
(Tracheobronchomegaly)
There is a massive dilatation of the trachea
(> 3 cm). It’s not well understood, and really the
only thing that does this.
Mounier-Kuhn- Big Fucking Trachea
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Small Airways Disease
Bronchiolitis - This is an inflammation of the small airways. It can be infectious (like
the viral patterns you see in kids) or inflammatory like RB-ILD in smokers, or asthma in
kids.
Air Trapping - When you see areas of lung that
are more lucent than others - you are likely
dealing with air trapping. Technically, air
trapping can only be called on an expiratory
study as hypoperfusion in the setting of
pulmonary arterial hypertension can look
similar. Having said that, for the purpose of
multiple choice test taking, I want you to think
(1) bronchiolitis obliterans in the setting of a
lung transplant, or (2) small airway disease - Air Trapping
asthma / bronchiolitis. — The poster boy for small airway disease
Tree in Bud - This is a nonspecific finding that can make you think small airway disease. It’s
caused by dilation and impaction of the centrilobular airways. Because the centrilobular
airways are centered 5-10 mm from the pleural surface, that’s where they will be. It’s usually
associated with centrilobular nodules.
Follicular Bronchiolitis - This is an inflammatory process seen in rheumatoid arthritis
or Sjogren's. It’s not well understood and is related to lymphoid hyperplasia. It looks like
centrilobular ground glass nodules with scattered areas of bronchial dilation.
Constrictive Bronchiolitis - This is another inflammatory process that can be seen
in viral illness, transplant patients, drug reactions, or inhalation injury. It is also often
identified in patients with DIPNECH. It occurs secondary to mononuclear cells which form
granulation tissue and plug the airway. You see air trapping on expiratory imaging. This is
supposedly the cause of Swyer-James hyperlucent lung.
Small Airway Disease
Infectious Bronchiolitis Tree-in-bud
Smokers. Centrilobular ground glass nodules
RB-ILD (upper lobe predominant)
Inhaling dust / other misc garbage.
Sub-Acute Hypersensitivity Pneumonitis Centrilobular Ground glass nodules
RA and Sjogren's. Centrilobular ground glass
Follicular Bronchiolitis
nodules
Viral, Drugs, Transplant, Inhalation.
Constrictive Bronchiolitis
Air-Trapping. DIPNECH
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Aspiration Pneumonia
Stroked-out old people and drunks love to aspirate.
The testable trivia is to know the typical location of aspiration; posterior segment of upper
lobes and superior segment of lower lobes if supine when aspirating, bilateral basal lower
lobes in upright aspiration. May favor the right side, just like an ET tube.
The most common complication is infection which can manifest as an empyema
(which can then get a broncho-pleural fistula).
Aspiration Patterns (depends on what you aspirated)
Aspiration of Gastric Acid Gives you an airspace opacity, if massive
“Mendelson’s Syndrome” can look like pulmonary edema
Aspiration of water or neutralized gastric
“Fleeting Opacity” that resolves in hours
contents
Gives you a real pneumonia, can get para-
Aspiration of Bugs (often mouth bugs) pneumonic effusion, empyema, or even
broncho-pleural fistula.
Aspiration of Oil (often mineral oil) Lipoid Pneumonia. Will be low density
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SECTION 12:
Sys t emi c
Collagen vascular disease - Interstitial lung diseases are common in patients with
collagen vascular diseases. The association are easily tested, so I made you this chart. I tried
to hit the high points of testable trivia.
Collagen Vascular Disease Pulmonary Manifestations
More pleural effusions and
Lupus Fibrosis is uncommon. Can
pericardial effusions than with
*its never Lupus get a “shrinking lung.”
other connective tissue disease
Reticulations with or without
Looks like UIP and COP. Lower honeycombing, and
Rheumatoid Arthritis
lobes are favored. consolidative opacities which
are organizing pneumonia
NSIP > UIP; lower lobe Look for the dilated fluid
Scleroderma
predominant findings. filled esophagus.
Extensive ground glass
Sjogren's LIP attenuation with scattered thin
walled cysts.
Usually unilateral first, then
Ankylosing Spondylitis Upper lobe fibrobullous disease
progresses to bilateral.
Caplan Syndrome = Rheumatoid Arthritis + Upper Lobe Predominant Lung Nodules.
These nodules can cavitate, and there may also be a pleural effusion.
“Shrinking Lung” - This is a progressive loss of lung volume in both lungs seen in
patients with Lupus ( “S”hrinking “L”ung for “SLe”). The etiology is either diaphragm
dysfunction or pleuritic chest pain.
Trivia: Most common manifestation of SLE in Chest = Pleuritis with/without pleural effusion.
Hepatopulmonary syndrome - This is seen in liver patients with the classic history of
“shortness of breath when sitting up." The opposite of what you think about with a CHF
patient. The reason it happens is that they develop distal vascular dilation in the lung bases
(subpleural telangiectasia), with dilated subpleural vessels that don’t taper and instead extend
to the pleural surface. When the dude sits up, these things engorge and shunt blood - making
him/her short of breath. A Tc-99m MAA scan will show shunting with tracer in the brain (outside the
lungs). They have to either tell you the patient is cirrhotic, show you a cirrhotic liver, or give
you that classic history if they want you to get this.
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Wegener Granulomatosis -
This is now called
“Granulomatosis with
The classic triad is upper tract, lung, and kidneys
Polyangiitis” because Wegener was
(although this triad is actually rare). The lungs are a member of the Nazi party.
actually the most common organ involved (95%).
It is also possible that he worked
There is a highly variable look. with the deep science unit Hydra
which plagued the world with
The most common presentation is also probably the schemes of global domination and
genocide.
most likely to be tested; nodules with cavitation.
The nodules tend to be random in distribution with Seriously, I’ve heard the guy was a
real asshole. Not just a Nazi, but a
about half of them cavitating. They can also show you bad tipper, and a habitual line
ground glass changes which may represent stepper (deliberately didn’t wash
hemorrhage. his hands after he took a shit).
Goodpasture Syndrome -
Another autoimmune pulmonary renal syndrome. It favors young men. It’s a super
nonspecific look with bilateral coalescent airspace opacities that look a lot like edema (but
are hemorrhage). They resolve quickly (within 2 weeks). If they are having recurrent
bleeding episodes then they can get fibrosis. Pulmonary hemosiderosis can occur from
recurrent episodes of bleeding as well, with iron deposition manifesting as small, ill-defined
nodules.
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SECTION 13:
Pl eur a , Ch es t Wa l l
Plaque: Pleural Calcifications
(other than asbestos)
If they show you a pleural plaque they probably want you to say Old Hemothorax
asbestos-related disease. Remember the plaque doesn’t show up for
like 20-30 years after exposure. Old Infection
TB
Remember that the pleural plaque of asbestosis typically spares the Extraskeletal
Costophrenic angles. Osteosarcoma
Mesothelioma - This is discussed earlier in the chapter
(page 395). As a rapid review:
• Most common cancer of the pleura.
• About 80% of them have had asbestos exposure
(NOT dose-dependent).
• Lag time is around 30-40 years from exposure.
• “Pleural rind” - thickening that wraps all the way around
the lung - including the medial surface of the pleura (near
the heart)
• Extension into the fissure is highly suggestive.
Pleural Rind = Grey Arrows
Fissure Extension = White Arrow
Solitary Fibrous Tumor of the Pleura (SFTP) - This is a solitary (usually) tumor
arising from the visceral pleura. The key is to know that they are NOT associated with asbestos,
smoking, or other environmental pollutants. They can get very large, and be a source of chest pain
(although 50% are incidentally found).
Trivia:
- Not associated with asbestos, smoking, or other environmental pollutants
- Even when they are big, they arc usually benign
- Doege-Potter syndrome occurs in like 5% of cases. This is an episodic hypoglycemia (tumor
can secrete an insulin like growth factor)
- Hypertrophic osteoarthropathy occurs in like 30% of the cases.
Metastases - Here is the high yield trivia on this. As a general rule the subtype of
adenocarcinoma is the most likely to met to the pleura. Lung cancer is the most common primary,
with breast and lymphoma at 2nd and 3rd. Remember that a pleural effusion is the most common
manifestation of mets to the pleura.
Lipoma - This is the most common benign soft tissue tumor of the pleura. The patients
sometimes feel the “urge to cough.” They will not cause rib erosion. They “never” turn into a
sarcoma. The differential consideration is extra-pleural fat, but it is usually bilateral and
symmetric.
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Pleural Effusion: Some random factoids on pleural effusions that could be potentially testable.
There has to be around 175 cc of fluid to be seen on the frontal view (around 75 cc can be seen on the
lateral). Remember that medicine docs group these into transudative and exudative based on protein
concentrations (Lights criteria). You are going to get compressive atelectasis of the adjacent lung.
Subpulmonic Effusion - A pleural effusion can accumulate between the lung base and the diaphragm.
These are more common on the right, with “ski-slopping” or lateralization of the diaphragmatic
peak. A lateral decubitus will sort it out in the real world.
Normal
Comparison
Encysted Pleural Effusion
- It is possible to have pleural fluid
Right Sided: Notice Left Sided: The key collect between the layers of the
the high point of the here is the increased pleura creating an oval / round
diaphragm is shifted space between the appearance mimicking a Cancer.
laterally stomach bubble and
lung base.
Empyema - Basically this is an infected pleural
THIS vs THAT:
effusion. It can occur with a simple pneumonia but
is seen more in people with AIDS. Usually these Pulmonary
are more asymmetric than a normal pleural Empyema
Abscess
effusion. Other features include enhancement of the
pleura, obvious Septations, or gas. Lentiform Round
Split Pleural Sign Claw Sign
Empyema Necessitans - This is the fancy (thickening and (acute angle with pleura)
Latin word for when the empyema eats through the separation of the
chest wall and into the soft tissues. It’s classically visceral and parietal
seen with TB (70%), with the second most common pleura)
cause being actinomyces. Treated with chest NOT treated with chest
tube tube (risk of
bronchopleural fistula).
Diaphragmatic Hernia - These can be acquired via trauma, or congenital. The congenital
ones are most common in the back left (Bochdalek), with anterior small and right being less
common (Morgagni). The traumatic ones are also more common on the left (liver is a buffer).
Paralysis - This is a high yield topic because you can use fluoro to help make the diagnosis.
Obviously the dinosaurs that write these tests love to ask about fluoro (since that was the only thing
they did in residency). Diaphragmatic paralysis is actually idiopathic 70% of the time, although
when you see it on multiple choice tests they want you to think about phrenic nerve compression
from a lung cancer. Normally the right diaphragm is higher, so if you sec an elevated left
diaphragm this should be a consideration.
On a fluoroscopic sniff test you are looking for paradoxical movement (going up on inspiration -
instead of down).
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SECTION 14:
Med i a s t i n a l Ma s s es
-Anterior-
Thymus: The thymus can do a bunch of sneaky things.
It can rebound from stress or chemotherapy and look huge. THIS vs THAT:
It can get cysts, cancer, carcinoid, etc... Rebound vs
Residual Lymphoma
Rebound - Discussed in detail in the Peds chapter.
After stress or chemotherapy the thing can blow up 1.5 • PET might help - both are
times the normal size and simulate a mass. Can be hot hot, but lymphoma is hotter.
on PET. • MRI - Thymic Rebound
should drop out on in-out of
Thymic Cyst - Can be congenital or acquired. phase imaging (it has fat in
Acquired is classic after thoracotomy, chemotherapy, it). Lymphoma will not
or HIV. They can be unilocular or multilocular. T2 drop out.
bright is gonna seal the deal for you.
Thymoma - So this is kind of a spectrum ranging from non-invasive thymoma, to invasive
thymoma, to thymic carcinoma. Calcification makes you think it’s more aggressive. The
thymic carcinomas tend to eat up the mediastinal fat and adjacent structures. The average
age is around 50, and they are rare under 20. These guys can “drop met” into the pleural and
retroperitoneum, so you have to image the abdomen.
Associations: Myasthenia Gravis, Pure Red Cell Aplasia, Hypogammaglobulinemia.
Thymolipoma -I only mention this zebra because it has a characteristic look. It’s got a
bunch of fat in it. Think “fatty mass with interspersed soft tissue.”
Germ Cell Tumor: Almost always Teratoma (75%). Mediastinal Teratoma - This is
the most common extragonadal germ cell tumor. They occur in kids (below age 1) and adults
(20s-30s). They are benign, but carry a small malignant transformation risk. Mature subtypes
are equal in Men and Women, but immature subtypes are exclusively seen in men (which should
be easy to remember). There is an association with mature teratomas and Klinefelter
Syndrome. The imaging features include a cystic appearance (90%), and fat. They can have
calcifications including teeth - which is a dead give away.
Pericardial Cyst -
This is uncommon and benign. The classic location
is the right anterior cardiophrenic angle. This
classic location is the most likely question.
Thyroid: described in the endocrine chapter
Lymphoma: described in the cancer section of this chapter
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Fibrosing Mediastinitis (Sclerosing Mediastinitis) -
This is a proliferation of fibrous tissue that occurs
within the mediastinum.
There are two described subtypes:
(1) Granulomatous (the one everyone thinks
about) classically caused by histoplasmosis).
Other causes include TB, and Sarcoid.
This will look like a soft tissue mass with
calcifications that infiltrates the normal fat planes
of the mediastinum.
(2) Non-Granulomatous, is the more rare subtype that people read about once and then
forget. Some people will call this form “idiopathic” although the subtype is better thought
of as a response to an autoimmune disease (SLE, RA, Behcet, etc...) or a complication to
radiation therapy. There is also a testable association with the headache medication
methysergide. It’s associated with retroperitoneal fibrosis when idiopathic.
This subtype also looks like a soft tissue mass but tends to be more infiltrative, lack
calcifications, and can enhance post contrast.
Both subtypes have been known to cause superior vena cava syndrome.
Bronchogenic Cyst - These congenital lesions are usually within the mediastinum
(most commonly found in the subcarinal space) or less commonly intraparenchymal. For the
purpose of the exam, they are going to be in the subcarinal region, causing obliteration of the
azygoesophageal line on a CXR, and being waterish density on CT.
Lymphadenopathy - Could be mets, could be infection, could be reactive. It is
generally abnormal to be larger than 2 cm in short axis (makes you suspect cancer).
Mediastinal Lipomatosis - Excess unencapsulated fat seen in patients with iatrogenic
steroid use, Cushings, and just plain old obesity.
Posterior Mediastinal Masses:
Neurogenic - The most common posterior mediastinal mass is one of neurogenic origin.
This includes schwannomas, neurofibromas, and malignant peripheral nerve sheath tumors.
Bone Marrow - Extramedullary hematopoiesis (EMH) is a response to failure of the bone
marrow to respond to EPO. Classic conditions include CML, Polycythemia vera, myelofibrosis,
sickle cell, and thalassemia.
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SECTION 15:
Pu l mo n a r y Ar t er i es
Pulmonary Embolism:
Historical
This is a significant cause of mortality in
hospitalized patients. The gold standard is Signs of PE on a CXR
catheter angiography, although this is invasive and Westermark
carries risks. As a result tests like the D-Dimer Regional Oligemia
(which has an almost 100% negative predictive
Fleischner
value), and the DVT lower extremity ultrasound Enlarged Pulmonary Artery
Sign
were developed. Now, the CTPA is the primary
tool. Hampton’s Peripheral Wedge Shaped
Hump opacity
Differentiating acute vs chronic PE is useful. Pleural Obviously not specific, but
Effusion seen in 30% of PEs.
THIS vs THAT: Acute vs Chronic PE
Acute Chronic
Clot is Central Clot (if seen) is more Peripheral. May be “web like”
Venous Dilation Shrunken Veins with collateral vessels
Perivenous soft tissue edema Calcifications within the thrombi and within the venous walls
Pleural Effusion is common Lungs may show a mosaic attenuation pattern
Acute PE can cause sudden Chronic PE is a well described cause of pulmonary
death from arrhythmia or acute hypertension (obstruction in the vascular bed causes an increase
right heart failure. in vascular resistance)
CTPA is the exam of choice. VQ Scan (believe it or not) is probably superior to CT.
THIS vs THAT: Massive vs Sub-Massive PE: clinical risk stratification
• Massive = Hypotension (SBP < 90)
• Sub-Massive = Stable BP, but RV dysfunction or positive cardiac enzymes (myocardial
necrosis).
Right Heart Strain - findings on CT (ECHO is still the gold standard).
RV Dilated Larger Contrast
Than LV Reflux into the
-Probably the best sign Hepatic Veins
-Leftward bowing of -Less Reliable.
the ventricular septum
is also helpful.
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Pulmonary Infarct Mimics: A pulmonary infarct is a wedge-shaped opacity that is going to
“melt” (resolve slowly), and sometimes can cavitate. Obviously a cavitary lesion throws up lots of
flags and makes people say TB, or cancer. When it’s an opacity in the lung and the patient doesn’t
have a fever, sometimes people think cancer - plenty of pulmonary infarcts have been biopsied.
Pulmonary Veno-Occlusive Disease: Uncommon variant of primary pulmonary
hypertension, that affects the post capillary pulmonary vasculature. For gamesmanship: PAH +
Normal Wedge, you should think this. The normal wedge pressure differentiates it from other post
capillary causes; such as left atrial myxoma, mitral stenosis, and pulmonary vein stenosis.
Pulmonary Artery Aneurysm/Pseudoaneurysm. - Think about three things for
multiple choice; (1) Iatrogenic from swan ganz catheter *most common (2) Behcets, (3) Chronic
PE. When they want to lead towards swan ganz they may say something like “patient in the ICU.”
The buzzwords for Behcets are: “Turkish descent” and “mouth and genital ulcers.”
• Hughes-Stovin Syndrome: This is a zebra cause of pulmonary artery aneurysm that is similar
(and maybe the same thing) as Behcets. It is characterized by recurrent thrombophlebitis and
pulmonary artery aneurysm formation and rupture.
• Rasmussen Aneurysm: This has a cool name, which instantly makes it high yield for testing.
This is a pulmonary artery pseudoaneurysm secondary to pulmonary TB. It usually involves
the upper lobes in the setting of reactivation TB.
• Tetralogy of Fallot Repair Gone South: So another possible testable scenario is the patch
aneurysm, from the RVOT repair.
Pulmonary Hypertension - Pulmonary arterial pressures over 25 are going to make the
diagnosis. I prefer to use the “outdated” primary and secondary way of thinking about this.
Primary: Idiopathic type is very uncommon, seen in a small group of young women in their 20s.
Secondary: This is by far the majority, and there are a few causes you need to know: Chronic PE ,
Right Heart Failure/ Strain, Lung Parenchymal Problems- (This would include emphysema, and
various causes of fibrosis). COPDers with a pulmonary artery bigger than the aorta (A/PA ratio) have
increased mortality (says the NEJM).
Imaging Signs of Pulmonary HTN: The numbers people use for what is abnormal are all over the
place - if forced I’d pick 29 mm. A superior strategy is to compare the size of the aorta and
pulmonary artery (a normal PA should not be bigger than the aorta). You can also compare the
segmental artery-to adjacent bronchus ( > 1:1 is abnormal). Mural calcifications of central
pulmonary arteries (seen in Eisenmenger phenomenon) have been described. Additional nonspecific
signs include right ventricular dilation / hypertrophy, and centrilobular ground-glass nodules.
Two other modern strategies are based purely on morphology.
Banana and Egg: Carina Crossover:
Visualization of the Right PA crosses the
main pulmonary carina midline
artery (egg) at the anteriorly It normally
level of the aortic crosses in a more caudal
arch (banana) location.
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SECTION 16:
Tr a u ma
Diaphragmatic Injury: There is a lot of testable trivia regarding diaphragmatic injury
and therefore it is probably the most high yield subject with regard to trauma:
Things to know:
• Left side is involved 3 times more than the right (liver is a buffer)
• Most ruptures are “radial”, longer than 10 cm, and occur in the posterior lateral
portion
• Collar Sign - This is sometimes called the hour glass sign, is a waist-like appearance
of the herniated organ through the injured diaphragm
• Dependent Viscera Sign - This is an absence of interposition of the lungs between
the chest wall and upper abdominal organs (liver on right, stomach on left).
Tracheo-Bronchial Injury: Airway injury is actually pretty uncommon. When it
does occur it’s usually within 2 cm of the carina. Injury close to the carina is going to
cause a pneumomediastinum rather than a pneumothorax - that is a testable fact. When
you get a tracheal laceration, it most commonly occurs at the junction of the cartilaginous
and membranous portions of the trachea.
Macklin Effect: This is probably the most common cause of pneumomediastinum in
trauma patients (and most people haven’t heard of it). The idea is that you get alveolar
rupture from blunt trauma, and the air dissects along bronchovascular sheaths into the
mediastinum.
Boerhaave Syndrome: You probably remember this from step 1. The physical exam
buzzword was “Hammonds Crunch.” Basically you have a ruptured esophageal wall from
vomiting, resulting in pneumomediastinum / mediastinitis.
Flail Chest: This is 3 or more segmental (more than one fracture in a rib) fractures, or
more than 5 adjacent rib fractures. The physical exam buzzword is “paradoxical motion with
breathing.”
Pneumothorax: Obviously you don’t want to miss the tension pneumothorax. The thing
they could ask is “inversion or flattening of the ipsilateral diaphragm.”
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Malpositioned Chest Tubes: Sometimes the ED will ram them into the
parenchyma. This is more likely to occur in the setting of background lung disease or
pleural adhesions. You’ll see blood around the tube. Bronchopleural fistula may occur as
a sequela. The placement of a tube in a fissure is sorta controversially bad (might be ok).
Hemothorax: If you see pleural fluid in the setting of trauma, it’s probably blood.
The only way I can see them asking this is a density question; a good density would be
35-70 HU.
Extrapleural Hematoma: This is a little tricky, and they could show you a picture
of it. If you have an injury to the chest wall that damages the parietal pleura then you get
a hemothorax. If you have an injury to the chest wall, but your parietal pleural is still
intact, you get an extrapleural hematoma. The classic history is “persistent fluid
collection after pleural drain/tube placement.” The buzzword / sign is displaced
extrapleural fat. There is a paper out there that suggests a biconvex appearance is more
likely arterial and should be watched for rapid expansion. This may be practically useful,
but is unlikely to be asked. Just know the classic history, and displaced extrapleural fat
sign.
Pulmonary Contusion: This is the most common lung injury from blunt trauma.
Basically you are dealing with alveolar hemorrhage without alveolar disruption. The
typical look is non-segmental ill-defined areas of consolidation with sub pleural sparing.
Contusion should appear within 6 hours, and disappear within 72 hours (if it lasts longer
it’s probably aspiration, pneumonia, or a laceration).
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Pulmonary Laceration: So a tear in the lung will end up looking like a
pneumatocele. If they show you one it will probably have a gas -fluid (blood) level in it.
These things can be masked by surrounding hemorrhage early on. The major difference
between contusion and laceration is that a laceration resolves much more slowly and can
even produce a nodule or a mass that persists for months.
Aorta: The aorta is injured most commonly at the aortic isthmus (some sources say
90%). The second and third most common locations are the root and at the diaphragm.
Some people say the root is actually the most common, but most of these people die prior
to making it to the hospital. This is a minority opinion. If asked what is the most common
site of traumatic aortic injury, the answer is isthmus. It’s usually obvious on a candy cane
CTA. The main mimic would be a “ductus bump,” which is a normal variant. The way to
tell (if it isn’t obvious) is the presence of secondary signs of trauma (mediastinal
hematoma).
Blunt Cardiac Injury: If you have hemopericardium in the setting of trauma, you
can suggest this and have the ED correlate with cardiac enzymes and EKG findings.
Fat Embolization Syndrome: This is seen in the setting of a long bone fracture or
Intramedullary rod placement. You get fat embolized to the lungs, brain, and skin (clinical
triad of rash, altered mental status, and shortness of breath). The timing is 1-2 days after
the femur fracture. The lungs will have a ground glass appearance that makes you think
pulmonary edema. You will not see a filling defect - like a conventional PE. If they don’t
die, it gets better in 1 -3 weeks.
Barotrauma: Positive pressure ventilation can cause alveolar injury, with air dissecting
into the mediastinum (causing pneumomediastinum and pneumothorax). Patients with
acute lung injury or COPD have a high risk of barotrauma from positive pressure
ventilation. Lungs with pulmonary fibrosis are actually protected because they don’t
stretch.
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SECTION 17:
Li n es a n d Dev i c es
Central Lines: The main way to ask questions about central lines is to show them
being malpositioned and asking you where they are. An abrupt bend at the tip of the
catheter near the cavo-atrial junction should make you think azygos. If it’s on the left side
of the heart, it’s either (1) arterial or (b) in a duplicated SVC.
This is a sneaky trick, related to Central Lines. They can show you the pseudo lesion /
hot quadrate sign (seen with SVC syndrome), and then show you a CXR with a central
venous catheter. The idea is that central lines are a risk factor for SVC occlusion.
Hot Quadrate Sign from - SVC Obstruction
Endotracheal Tube (ETT) Positioning - The tip of the ETT should be about 5
cm from the carina (halfway between the clavicles and the carina). The tip will go down
with the chin tucked, and up with the chin up (“the hose goes, where the nose goes”).
Intubation of the right main stem is the most common goof (because of the more shallow
angle) - this can lead to left lung collapse. You can sometimes purposefully intubate one
lung if you have massive pulmonary hemorrhage (lung biopsy gone bad), to protect the
good lung.
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Intra-Aortic Balloon Pump (IABP) - This is used in cardiogenic shock to help
with “diastolic augmentation,” - essentially providing some back pressure so the vessels of
the great arch (including the coronaries) enjoy improved perfusion.
For the purpose of multiple choice tests you can ask three things:
(1) What is the function? - decrease LV afterload and increase myocardial perfusion,
(2) What is the correct
location? the balloon
should be located in the
proximal descending
aorta, just below the
origin of the left
subclavian artery
(balloon terminates just
above the splanchnic
vessels)
(3) Complications ? -
dissection during
insertion, obstruction of
the left subclavian from
malpositioning
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- Cardiac Conduction Device -
Types:
• Pacemakers
• Implantable Cardiac Defibrillators (ICDs) - the one with “shock coils” - i.e. the thick
bands.
• Mixed (Pacemaker + ICD)
Locations:
• Leads arc placed in the RV, RA, and LV. The LV leads get there via the coronary sinus to
the posterior / lateral cardiac vein.
• "Cardiac resynchronization therapy device” is the vocab word the bi-ventricular
pacemaker (RV + LV and usually RA). Remember vocab words are easily testable.
• Pearls on locations: (1) The RV lead should cross the midline on a frontal view,
(2) The RA and RV leads are anterior on the lateral view, (3) The LV lead should be
posterior on the lateral, (4) the idea location for the RA lead is actually the RA appendage
- so it should course down then back up/anterior.
Complications:
• Acute - All the stuff you get with centra] line placement: pneumothorax, hemothorax,
etc...
• Generator Related - Terminal
connector pin displacement. This is
actually common.
• Myocardial Perforation - The number is 3 mm. If the lead is 3 mm within the epidcardial
fat you should suspect penetration.
• Rib Clavicle Crush - The leads are mostly commonly fractured in the region of the
clavicle, and first rib.
• Twiddler Syndrome - The generator pack gets flipped and twisted in the pocket, leading to
lead displacement. This happens because Grandpa just can’t leave the thing alone (gotta
put those dementia mittens on him). Can’t have him dying on us... we need those social
security checks.
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Blank for Scribbles and Notes:
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8
Ca r d i a c
Pr o met h eus Li o n h a r t , M.D.
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SECTION 1:
CHAMBERS
Right Atrium: Defined by the IVC. The Crista Terminalis is a frequently tested normal
structure (it’s not a clot or a tumor). It is a muscular ridge that runs from the entrance of the
SVC to that of the inferior vena cava. Another normal anatomic structure that is frequently
shown (usually on IVC gram) is the IVC valve or Eustachian valve. It looks like a little flap
in the IVC as it hooks up to the atrium. When the tissue of this valve has a more
trabeculated appearance it is called a Chiari Network.
Coronary Sinus: The main draining vein of the myocardium. It runs in the AV groove
on the posterior surface of the heart and enters the right atrium near the tricuspid valve.
Right Ventricle: Defined by the Moderator Band. Has several characteristics that are
useful for distinguishing it (and make good test questions).
Crista Terminalis Coronary Sinus Moderator Band
-Not a clot -Also not a clot
The tricuspid papillary muscles insert on the septum (not the case with the mitral valve).
There is no fibrous connection between the AV valve / outflow tract.
The pulmonary valve has three cusps, and is separated from the tricuspid valve by a thick
muscle known as the crista supraventricularis . This differs from the left ventricular outflow
tract, where the mitral and aortic valves lie side by side.
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Left Atrium: The most posterior chamber. When you think about multiple choice
questions regarding the left atrium, think about the various signs of enlargement.
• Double Density (direct sign): Superimposed second contour on the right heart, from
enlargement of the right side of the left atrium
• Splaying of the Carina (indirect sign): Angle over 90 degrees suggests enlargement
• Walking Man Sign (indirect sign): Posterior displacement of the left main stem
bronchus on lateral radiograph. This creates an upside down “V” shape with the
intersection of the right bronchus (looks like a man walking).
Left Atrial Enlargement
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Left Ventricle: The leaflets of the mitral valve are connected to the papillary muscles
via cord-like tendons called chordae tendinae. The papillary muscles insert into the lateral
and posterior walls as well as the apex of the left ventricle (not the septum, as is the case on
the right).
Echogenic Focus in Left Ventricle:
Relatively common
sonographic observation seen
on pre-natal ultrasound. It is a
calcified papillary muscle that
usually goes away by the third
trimester. So who gives a shit?
Well they are associated with
an increased incidence of
Downs (13%). Don’t get it
twisted, having one means
nothing other than you should
look for other signs of downs Echogenic Focus in Left Ventricle
(most of the time it’s normal).
Lipomatous Hypertrophy
of the Interatrial Septum:
This has a very classic look of a
dumbbell (bilobed) appearance of
fat density in the atrial septum,
Lipomatous
sparing the fossa ovalis. This Normal Hypertrophy of the Lipoma
sparing of the fossa ovalis, Interatrial Septum
creates a dumbbell appearance Common Rare as Fuck
(when it doesn‘t spare it think
Fat in the atrial septum, Encapsulated.
lipoma). It’s associated with thicker than 2 cm
being fat and old. As a point of
Spares the fossa ovalis Does NOT spare the
trivia it can cause fossa ovalis
supraventricular arrhythmia,
If multiple = tuberous
although usually does nothing. sclerosis
Additional even more high-yield
Can be PET HOT Is usually PET HOT ,
trivia is that it can be hot on T1 bright,
PET because it’s often made of Drops out on Fat-Sat
brown fat. Rarely associated with
Rarely associated with
arrhythmia (usually arrhythmia (usually
asymptomatic) asymptomatic)
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SECTION 2:
CORONARIES
Questions regarding the coronaries will likely come in two flavors: Normal (which will be
mostly vocab), and Abnormal (which will only have one or two pathologies).
Normal: There are three coronary cusps; right, left, and non-coronary (posterior).
The left main comes off the left cusp, the right main comes off the right cusp.
With regard to what perfuses what, the following are high yield factoids:
RCA perfuses SA node 60%
RCA perfuses AV node 90%
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Typical vascular perfusion territories are a high yield topic.
THIS vs THAT: 2 VS 3 Chamber View
These cardiac MR views are based off of the standard
views they use in echo.
The 2 Chamber:
— This displays the LV and LA (2 chambers). This is
good for a few things (1) Wall motion / Global LV
function , and (2) Mitral valve issues - regurg, etc.
The anatomy trick would be to have you ID the
coronary sinus on this view.
The 3 Chamber:
- Some people will call this an "apical long axis
view." The major plus to this view is that it lets you
see the left ventricular outflow tract (LVOT), - and is
ideal for look at flow through this area (i.e. aortic
regurg). A way a question could be asked is "what
view is best for aortic regurg? / stenosis?" or “which
of the following views” - and make you pick out the
picture of the 3 chamber. Or just straight ask you -
what is this view?
Dominance: Coronary Dominance is determined by what vessel gives rise to the
posterior descending artery and posterior left ventricular branches (most are right -
85%). You can be “co-dominant” if the posterior descending artery arises from the right
coronary artery and the posterior left ventricular branches arise from the left circumflex
coronary artery.
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NOT Normal: Anomalies of the Origin, Course, and Termination:
Malignant Origin: Most Common and Most Serious: LCA from the Right Coronary
Sinus, coursing between the Aorta and Pulmonary Artery. This guy can get compressed and
cause sudden cardiac death.
• Anomalous right off the left cusp — Repair if symptomatic
• Anomalous left off the right cusp -—Always Repair
Malignant coronary
artery with origin from
the opposite sinus and
an interarterial course
is the second most
common cause of
sudden cardiac death
in young patients
(most common is
hypertrophic
cardiomyopathy).
ALCAPA: Anomalous Left Coronary from the Pulmonary Artery. There are two types:
(a) Infantile type (they die early - CHF & dilated cardiomyopathy), and (b) Adult (still at
risk of sudden death). The multiple choice question is going to be “STEAL SYNDROME”
- which describes a reversed (retrograde) flow in the LCA as pressure decreases in the
pulmonary circulation.
Myocardial Bridging: This is an intramyocardial course of a coronary artery (usually
the LAD). The finding may cause symptoms as the diameter decreases with systole, or may
cause an issue for CABG planning. This can be a source of ischemia.
Coronary Artery Aneurysm: By definition this is a vessel with a diameter greater
than 1.5x the normal lumen. Most common cause is atherosclerosis. Most common cause
in children is Kawasaki (spontaneously resolves in 50%). They can occur from lots of other
vasculitides as well. Last important cause is iatrogenic (cardiac cath).
Coronary Fistula: Defined as a connection between a coronary artery and cardiac
chamber or great vessels. It’s usually the RCA, with drainage into the right cardiac
chambers. They are associated / result in coronary aneurysm. If you see big crazy dilation of
the coronaries - think about this.
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Coronary CT
Who is the ideal patient to get a coronary CT? There are two main groups of people
getting these. (1) Low risk or atypical chest pain patients. A negative coronary CT will
help stop a stress test or cath from occurring. Why do a procedure with risks on someone
with GERD? (2) Suspected aberrant coronary anatomy.
What is the ideal heart rate? To reduce motion related artifacts a slow heart rate is
preferred. Most books will tell you under 60 beats per min. Beta blockers are used to
lower the heart rate to achieve this ideal rate.
Are there contraindications to beta blockers? Yup. Patients with severe asthma, heart
block, acute chest pain, or recent snorting of cocaine - should not be given a beta blocker.
Are all heart blocks contraindications to beta blockers ? 2nd and 3rd Degree are
contraindications. A 1st degree block is NOT.
What if I can’t give the beta blocker? Can he still have the scan? Yes, you just can’t use a
prospective gating technique. You’ll have to use retrospective gating.
What is the difference between prospective and retrospective gating?
-Prospective: “Step and Shoot” - R-R interval * data acquisition triggered by R Wave
• Pro: There is reduced radiation b/c the scanner isn’t on the whole time
• Con: No functional imaging
• Trivia: Always axial, not helical
-Retrospective: Scans the whole time, then back calculates
• Pro: Can do functional imaging
• Con: Higher radiation (use of low pitch - increases dose)
• Trivia: this is helical
Other than beta blockers, are any other drugs given for coronary CT? Yup.
Nitroglycerine is given to dilate the coronaries (so you can see them better).
Are there contraindications to nitroglycerine ? Yup. Hypotension (SBP < 100), severe
aortic stenosis, hypertrophic obstructive cardiomyopathy, and Phosphodiesterase (Viagra-
Sildenafil, “boner pills”) use.
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SECTION 3:
Va l v es
Velocity-encoded cine MR imaging (VENC), also known as velocity mapping or phase-contrast
imaging, is a technique for quantifying the velocity of flowing blood.
Aortic Stenosis: This may be congenital (bicuspid) or Acquired (Degenerative or Rheumatic
Heart). Increased afterload can lead to concentric LV hypertrophy. Peak velocity through the valve
can be used to grade the severity. Velocity-encoded cine MR imaging (VENC), which also answers
to the name “velocity mapping” or “phase-contrast imaging”, is an MRI technique for quantifying the
velocity of flowing blood (if anyone would happen to ask). Dilation of ascending aorta is due to jet
phenomenon related to a stenotic valve. Aortic Stenosis comes in three flavors: (a) valvular, (b)
subvalvular, (c) and supravalvular. Valvular is the most common (90%).
• When I say “Supra-valvular Aortic Stenosis” you say Williams Syndrome
• When I say “Bicuspid Aortic Valve and Coarctation” you say Turners Syndrome
Bicuspid Aortic Valve: This is very common, some
sources will say nearly 2% of the general population. As a
result, it becomes the source of significant fuckery with
regard to one particular multiple choice question - “what is
the most common congenital heart disease?” The answer is
probably bicuspid aortic valve, but because it’s often
asymptomatic and not a problem till later in life when it gets
stenotic and causes syncope - I think it messes with peoples’
math. How do you handle this question? Well... if they list
bicuspid aortic valve then you have to pick it. If they don’t
list it then the answer is VSD.
Trivia to know:
• Aortic Stenosis is the most common complication
• Bicuspid aortic valve (even in absence of stenosis) is an
independent risk factor for aortic aneurysm. Severity of
valve dysfunction does not predict aneurysm formation.
• Association with Cystic Medial Necrosis (CMN)
• Association with Turners Syndrome, and Coarctation
• Association with AD Polycystic kidney disease
Aortic Regurgitation: Seen with bicuspid aortic valves, bacterial endocarditis, Marfan’s, aortic
root dilation from HTN, and aortic dissection. How rapid the regurgitation onsets determines the
hemodynamic impact (acute onset doesn’t allow for adaptation). Step 1 question was “Austin Flint
Murmur.”
Mitral Stenosis: Rheumatic heart disease = most Ortner’s Syndrome
(Cardio Vocal Hoarseness)
common cause. Could be shown as a CXR with left atrial
Hoarseness caused by
enlargement (double density sign, splaying of the carina,
compression of the left recurrent
posterior esophageal displacement). laryngeal nerve by an enlarged
left atrium
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Mitral Regurgitation: The most common acute causes are endocarditis or papillary muscle /
chordal rupture post ML The chronic causes can be primary (myxomatous degeneration) or
secondary (dilated cardiomyopathy leading to mitral annular dilation). Remember the isolated Right
Upper Tobe pulmonary edema is associated with mitral regurgitation.
Pulmonary Stenosis: Just like in
the Aortic Valve, comes in three flavors:
(a) valvular, (b) subvalvular, (c) and
supravalvular. Valvular is the most
common, and can lead to ventricular
hypertrophy. Associated with Noonan
Syndrome (male version of turners).
“Peripheral Pulmonary Stenosis” is
seen with Alagille syndrome (kids with
absent bile ducts). Williams can give Pulmonary Stenosis Syndromes
you supra-valvular aortic stenosis (and
pulmonic).
Pulmonary Regurgitation: The classic scenario is actually TOF patient who has been repaired.
TOF repair involves patch repair of the VSD and relief of the RV outlet obstruction. To fix the RV
obstruction the pulmonary valve integrity must be disrupted. Eventual failure of the valve (regurgitation)
is the primary complication of this procedure.
Cardiac MRI is used to guide the timing of pulmonary regurg repair. If the valve is repaired before the
RV is severely dilated (150 ml end diastolic volume) the outcomes are good. If the RV reaches a certain
degree of dilation- it typically won’t return to normal and the patient is pretty much fucked.
Tricuspid Regurgitation: Most common
Gamesmanship: — Rheumatic heart
form of tricuspid disease, due to the relatively weak disease most commonly involves the mitral
annulus (compared to the mitral). May occur in the and aortic valves. Anytime there is multi valve
setting of endocarditis (IV drug use), or carcinoid disease, think Rheumatic Fever!
syndrome (serotonin degrades the valve). The most
common cause in adults is pulmonary arterial Step 1 Trivia: Rheumatic heart disease is
hypertension. A testable pearl is that TR causes RV an immune modulated response to Group A-
dilation (NOT RV Hypertrophy). Beta hemolytic strep.
Ebstein Anomaly: Seen in children whose moms used Lithium (most cases are actually
sporadic). The tricuspid valve is hypoplastic and the posterior leaf is displaced apically (downward).
The result is enlarged RA, decreased RV (“atrialized”), and tricuspid regurgitation. They have the
massive “box shaped” heart on CXR.
Tricuspid Atresia: Congenital anomaly that occurs with RV hypoplasia. Almost always has an
ASD or PFO. Recognized association with asplenia. Can have a right arch (although you should
think Truncus and TOF first). As a point of confusing trivia; tricuspid atresia usually has pulmonary
stenosis and therefore will have decreased vascularity. If no PS is present, there will be increased
vascularity.
Carcinoid Syndrome: This can result in valvular disease, but only after the tumor has met’d to
the liver. The serotonin actually degrades heart valves, typically both the tricuspid and pulmonic
valves. Left sided valvular disease is super rare since the lungs degrade the vasoactive substances.
When you see left sided disease you should think of two scenarios:
(1) primary bronchial carcinoid, or (2) right-to-left shunts.
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SECTION 4:
GREAT VESSELS
The most common variant in branching is the “bovine arch” in which the brachiocephalic
artery and left common carotid artery arise from a common origin.
The terminology right arch / left arch is
described based on the aortic arch’s
relationship to the trachea.
When I say Right Arch with Mirror
Branching, You say congenital heart.
There are 5 types of right arches, but only
two are worth knowing (Aberrant Left, and
Mirror Branching). The trick to tell these
two apart is to look for the origin of the left
subclavian.
Originating from the Front of the Arch =
Mirror Image
*this is the bad one (lots of congenital heart)
Originating from the Back of the Arch =
Aberrant Left Subclavian
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Right Arch with Mirror Branching: Although these are often asymptomatic they
are strongly associated with congenital heart disease. Most commonly they are associated
with TOF. However, they are most closely associated with Truncus. Obviously, this tricky
wording lends itself nicely to a trick question.
• If there is a mirror image right arch, then 90% will have TOF (6% Truncus).
• If the person has Truncus, then they have a mirror image right arch 33% (TOF 25%).
Right Arch with Aberrant Left Subclavian: The last
branch is the aberrant left subclavian artery. This is a vascular ring
because the ligamentum arteriosum (on the left) completes the “ring”
encircling the trachea.
Left Arch Aberrant Right
Subclavian: The most common arch
anomaly. Although it is usually
asymptomatic it can sometimes be
associated with dysphagia lusoria, as the
RSCA passes posterior to the esophagus. The
last branch is the aberrant right subclavian
artery. The origin of the RSCA may be
dilated = Diverticulum of Kommerell.
Double Aortic Arch: The most
common vascular ring. As a point of
trivia, symptoms may begin at birth and
include tracheal compression and/or
difficulty swallowing. The right arch is
larger and higher, and the left arch is
smaller and lower. Arches are posterior to
the esophagus and anterior to the trachea
(encircling them both).
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Subclavian Steal Syndrome/Phenomenon: So there is a “Syndrome” and
there is a “Phenomenon.” The distinction between the two makes for an excellent distractor.
• SS Phenomenon: Stenosis and/or occlusion of the proximal subclavian with
retrograde flow in the ipsilateral vertebral artery.
• SS Syndrome: Stenosis and/or occlusion of the proximal subclavian artery with
retrograde flow in the ipsilateral vertebral artery AND associated cerebral ischemic
symptoms.
If the level of stenosis and/or occlusion is proximal to the vertebral artery, reversal of flow
in the vertebral artery can occur, resulting in the theft of blood from the posterior
circulation. When the upper limb is exercised, blood is diverted away from the brain to the
arm. Cerebral symptoms (dizziness, syncope, etc...) depend on the integrity of collateral
intracranial flow (PCOMs).
Subclavian Steal is almost always caused by atherosclerosis (98%), but other very testable
causes include Takayasu Arteritis, Radiation, Preductal Aortic Coarctation, and Blalock-
Taussig Shunt. In an adult they will show atherosclerosis. If they show a teenager / 20 year
old it’s gonna be Takayasu. Case books love to show this as an angiogram, and I think
that’s the most likely way the test will show it. They could also show a CTA or MRA
although I’d say that is less likely. More on this in the vascular chapter.
Aortic Aneurysm and Vasculitis: Will be discussed in the Vascular Chapter.
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SECTION 5:
CONGENITAL HEART
An extremely high yield and confusing topic which dinosaur Radiologists love to ask questions about
on CXR. Obviously, this is stupid since you could only add confusion to a bad situation by
suggesting a diagnosis on CXR instead of waiting for ECHO or MRI. Having said that, the next
section will attempt to provide a methodology for single answers on CXR cases.
My thoughts on multiple choice questions regarding congenital heart is that they will come in 3
flavors: (A) Aunt Minnie, (B) Differentials with crappy distractors, and (C) Associations / Trivia.
Aunt Minnies / Differentials:
There are a few congenital heart cases that arc Aunt Minnies, or easily solvable (most are differential
cases). Bottom line is that if they want a single answer they will have to show you either an Aunt
Minnie or a differential case, with crappy distractors.
With regard to straight-up Aunt Minnies, I think the usual characters that most third year medical
students memorize are fair game.
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The easily solvable ones will be shown as a right arch with the associations of Truncus (more
closely associated) and TOF (more common overall). Or, they will show you the big box
heart and want Ebsteins (which is an Aunt Minnie). Another classic trick with regard to the
big box heart is non-cardiac causes of high output failure (Infantile Hemangioendothelioma
and Vein of Galen Malformation). The remaining cyanotic syndromes basically look the
same, so the questions must be either (a) crappy distractors (none of the others arc cyanotic,
etc...), or (b) trivia (which is more likely).
Cyanotic Not Cyanotic
With regard to identifying bad distractors I think the
TOF ASD
easiest way is the cyanotic vs not cyanotic disorders.
TAPVR VSD
They literally must tell you the kid is cyanotic,
otherwise there is no way to know. Transposition PDA
Truncus PAPVR
Tricuspid Aortic Coarctation
Atresia (adult type post ductal)
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There are a few other key differentials that may make it easier to weed out bad distractors, or
get “which of the following do NOT” questions.
Survival dependent on
CHF in Newborn Small Heart DDx
admixture - Cyanotics
Adrenal Insufficiency
TAPVR (Infracardiac type “III”) TAPVR (has PFO) (Addisons)
Congenital Aortic or Mitral Transposition Cachectic State
Stenosis
Left Sided Hypoplastic Heart TOF (has VSD) Constrictive Pericarditis
Cor Triatriatum Tricuspid Atresia (has VSD)
Infantile (pre-ductal) Coarctation Hypoplastic Left
Trivia and Associations:
VSD: The most common congenital heart disease. There are several types with
Membranous (just below the aortic valve) being the most common (70%). Outlet subtypes
(infundibulum) must be repaired as the right coronary cusp prolapses into the defect. On
CXR we are very nonspecific (big heart, increased vasculature, small aortic knob). They
could ask or try and show splaying of the carina (from big left atrium). About 70% of the
small ones close spontaneously.
PDA: The PDA normally closes around 24 hours after birth (functionally), and
anatomically around 1 month. A PDA should make you say three things (1) Prematurity,
(2) Maternal Rubella, (3) Cyanotic Heart Disease. CXR is nonspecific (big heart,
increased pulmonary vasculature, large aortic arch “ductus bump”). You can close it or keep
it open with meds.
ASD: Several types with the Secundum being the most common (50-70%). The larger
subtype is the Primum, (results from an endocardial cushion defect), is more likely to be
symptomatic. Only Secundums may close without treatment (Primum, AV Canal, Sinus
Venosus will not). Primums are not amendable to device closure because of proximity to AV
valve tissue. On CXR, if it's small it will show nothing, if it’s large it will be super
nonspecific (big heart, increased vasculature, and small aortic knob). It’s more common in
female.
• When I say hand/thumb defects + ASD, you say Holt Oram
• When I say ostium primum ASD (or endocardial cushion defect), you say Downs
• When 1 say Sinus Venosus ASD, you say PAPVR
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AV Canal: Also referred to as an endocardial cushion defect. They happen secondary to
deficient development of a portion of the atrial septum, a portion of the inter-ventricular
septum, and the AV valves. Strong association with Downs. You can’t use closure devices
on these dudes either. Surgical approach and management is complex and beyond the scope
of this text.
Trivia: Of all the congenital heart stuff with Downs patients - AV Canal is the most common
Unroofed Coronary Sinus: This is a rare ASD which occurs secondary to a
fenestrated (as in the cartoon) or totally unroofed coronary sinus. The most important
clinical is that you can get paradoxical emboli and chronic right heart volume overload.
Trivia: STRONG association with a persistent left SVC.
PAPVR: Partial anomalous pulmonary venous return,
is defined as one (or more) of the four pulmonary veins
draining into the right atrium. It is often of mild or no
physiologic consequence. It is often associated with
ASDs (secondum and sinus venosus types).
• When I say Right Sided PAPVR,
you say Sinus Venosus ASD
RUL: SVC association with sinus
venosus type ASD
* When I say Right Sided PAPVR + Pulmonary
Sinus Venosus ASD
Hypoplasia, you say Scimitar Syndrome
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ASD Subtypes:
TAPVR: A cyanotic heart disease characterized by all of the pulmonary venous system draining to
the right side of the heart. A large PFO or less commonly ASD is required for survival (this is a high
yield and testable point). There are 3 types, but only two are likely to be tested (cardiac type II just
doesn’t have good testable features). All 3 types will cause increased pulmonary vasculature, but type
3 is famous for a full on pulmonary edema look in the newborn.
• Type 1: Supracardiac:
Most Common Type
Veins drain above the heart, gives a snowman appearance.
• Type 2: Cardiac
Second Most Common Type
• Type 3: Infracardiac
Veins drain below the diaphragm (hepatic veins or IVC)
Obstruction on the way through the diaphragm is common and causes a full on
pulmonary edema look
Key Points on TAPVR:
• Supracardiac Type = Snowman
• Infracardiac Type = Pulmonary Edema in Newborn
• Large PFO (or ASD) needed to survive
• Asplenia - 50% of asplenia patients have congenital heart disease. Of those nearly 100%
have TAPVR, (85% have additional endocardial cushion defects).
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Transposition: This is the most common cause of cyanosis during the first 24 hours. It
is seen most commonly in infants of diabetic mothers. The basic idea is that the aorta arises
from the right ventricle and the pulmonary trunk from the left ventricle (yentricularterial
discordance).
Which one is the Right Ventricle? You have to find the moderator band (that defines the RV)
Just like TAPVR survival depends on an ASD, VSD, or PDA (most commonly VSD). There
are two flavors: D & L. The D type only has a PDA connecting the two systems. Where as
the L type is “Lucky” enough to be compatible with Life.
D-Transposition: Classic
radiographic appearance is the
“egg on a string”. Occurs from
discordance between the
ventricles and the vessels. The
intra-atrial baffle (Mustard or
Senning procedure) is performed
to fix them In D-Transposition, the ductus may be the only connection
between the two systems, which would otherwise be
separate (and not compatible with life)
L-Transposition: The L type is
“Lucky” enough to be
congenitally corrected. This
occurs from a “double
discordance” where the atrium
hooks up with the wrong
ventricle and the ventricle hooks
up with the wrong vessel.
In L-Transposition of the great vessels - there is an
inversion of the ventricles, leading to a "congenital
correction.” No PDA is needed.
A corrected D-transposition has a very
characteristic appearance, lending itself to an
Aunt Minnie-type question.
The PA is draped overtop the Aorta, which occurs
after a surgeon has performed the "LeCompte
Maneuver” — sounds French so must be high
yield.
Corrected D Transposition
via Jatene Arterial Switch
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Tetralogy of Fallot (TOF): The most common cyanotic heart disease. Describes 4
major findings; (1) VSD, (2) RVOT Obstruction - often from valvular obstruction, (3)
Overriding Aorta, (4) RV hypertrophy (develops after birth). The degree of severity in
symptoms is related to how bad the RVOT obstruction is. If it’s mild you might even have a
“pink tet” that presents in early adulthood. This is called a pentalogy of Fallot if there is an
ASD. Very likely to have a right arch.
Surgically it’s usually fixed with primary repair. The various shunt procedures (Blalock-
Taussig being the most famous) are only done if the kid is inoperable or to bridge until
primary repair.
Trivia: The most common complication following surgery is pulmonary regurgitation.
Truncus Arteriosus: Cyanotic anomaly where there is a single trunk supplying both
the pulmonary and systemic circulation, not a separate aorta and pulmonary trunk. It almost
always has a VSD, and is closely associated with a right arch. Associated with CATCH-22
genetics (DiGeorge Syndrome).
Coarctation:
THIS vs THAT: Coarctation of the Aortic
• There are two subtypes
(Narrowing the of the Aortic Lumen)
(as shown in the chart)
• Strong Association with Turners Infantile Adult
Syndrome (15-20%).
Presents with heart Leg Claudication
failure within the first BP differences between
• Bicuspid Aortic valve is the most common
week of life. anus and legs.
associated defect (80%).
Pre-Ductal (Before the Post-Ductal (Distal to
• They have more berry aneurysms. left Subclavian A.) left Subclavian A.)
• Figure 3 sign (appearance of CXR). Aortic Arch = Aortic Arch = Normal
Hypoplastic Diameter
• Rib Notching: most often involves 4th -
8th ribs. It does NOT involve the lsl and Collateral Formation is
2nd because those are fed by the More Likely
costocervical trunk.
Hypoplastic Left Heart: Left ventricle and aorta are hypoplastic. They present with
pulmonary edema. Must have an ASD or large PFO. They also typically have a large PDA
to put blood in their arch. Strongly associated with aortic coarctation and endocardial
fibroelastosis.
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Cor Triatriatum Sinistrum:
This is a very rare situation where you have an abnormal pulmonary vein draining into
the left atrium (sinistrum meaning left) with an unnecessary fibromuscular membrane
that causes a sub division of the left atrium. This creates the appearance of a tri-atrium
heart. This can be a cause of unexplained pulmonary hypertension in the peds setting.
Basically it acts like mitral stenosis, and can cause pulmonary edema. The outcomes are
often bad (fatal within two years), depending on surgical intervention and associated
badness.
Cor Triatriatum Sinistrum
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SECTION 6:
Is c h emi c Hea r t
Imaging regarding ischemic heart disease is going to fall into two modalities; cardiac MR,
and Nuclear. Cardiac MRI currently offers the most complete evaluation of ischemic heart
disease.
Myocardial infarction typically is initiated by rupture of an unstable coronary atherosclerotic
plaque, leading to abrupt arterial occlusion. The wave front of necrosis always starts
subendocardial and progresses to the subepicardium. The ischemic necrosis will affect
not just the myocardium but also blood vessels. The destruction of small capillaries will not
allow contrast to the area of injury. This is termed “microvascular obstruction” and manifests
as islands of dark signal in an ocean of delayed enhancement. The presence of microvascular
obstruction is an independent predictor of death and adverse LV remodeling.
Testable Vocab:
• Stunned Myocardium: After an Acute Injury (ischemia or reperfusion injury), dysfunction
of myocardium persists even after restoration of blood flow (can last days to weeks). A
perfusion study will be normal, but the contractility is crap.
• Hibernating Myocardium: This is a more chronic process, and the result of severe CAD
causing chronic hypoperfusion. You will have areas of decreased perfusion and
decreased contractility even when resting. Don’t get it twisted, this is not an infarct.
On an FDG PET, this tissue will take up tracer more intensely than normal
myocardium, and will also demonstrate redistribution of thallium. This is reversible
with revascularization.
• Scar: This is dead myocardium. It will not squeeze normally, so you’ll have abnormal
wall motion. It’s not a zombie. It will NOT come back to life with revascularization.
Stunned Hibernating Infarct / Scar
Wall Motion Abnormal Wall Motion Abnormal Wall Motion Abnormal
Normal Perfusion
Abnormal Fixed Perfusion Abnormal Fixed Perfusion
(Thallium or Sestamibi)
Will NOT Redistribute with
Will Redistribute with Delayed
Delayed Thallium, will NOT take
Thallium and will take up FDG
up FDG
Associated with chronic high
Associated with acute MI Associated the chronic prior MI
grade CAD
Diastolic Dysfunction = Cardiac MRI Probable Contraindications:
Echocardiography ICDs / Pacemakers
Cochlear Implants
Systolic Dysfunction = Intracranial Shrapnel
Cardiac MRI
**Cardiac Stents are usually safe
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Delayed imaging: It works for two reasons: (1) Increased volume of contrast material
distribution in acute myocardial infarction (and inflammatory conditions) (2) Scarred
myocardium washes out more slowly. It is done using an inversion recovery technique to
null normal myocardium, followed by a gradient echo. T1 shortening from the Gd looks bright
(“Bright is Dead”).
Why stress imaging is done: Because coronary arteries can auto-regulate, a stenosis
of 85% can be asymptomatic in a resting state. So demand is increased (by exercise or drugs)
making a 45% stenosis significant. An inotropic stress agent (dobutamine) is used for wall
motion, and a vasodilator (adenosine) is used for perfusion analysis.
Typical Sequence Pattern / Technique - with approximate times in minutes:
MRI in Acute Ml: Cardiac MRI can be done in the first 24 hours post MI (if the patient is
stable). Late gadolinium enhancement will reflect size and distribution of necrosis.
Characteristic pattern is a zone of enhancement that extends from the subendocardium
toward the epicardium in a vascular distribution. Microvascular obstruction will present as
islands of dark signal in the enhanced tissue (as described above), and this represents an acute
and subacute finding . Microvascular obstruction is NOT seen in chronic disease as these
areas will all turn to scar eventually.
In the acute setting (1 week) injured myocardium will have increased T2 signal, which can be
used to estimate the area at risk (T2 Bright - Enhanced = Salvageable Tissue).
THIS vs THAT: Acute VS Chronic Ml:
How do you diagnose
• Both have delayed enhancement Myocardial Infarction with
Contrast Enhanced MR?
• If the infarct was transmural and chronic you may have
thinned myocardium (1) Delayed Enhancement
follows a vascular
• Acute will have normal thickness (chronic can too but distribution,
shouldn’t for the purposes of MC tests.
(2) The enhancement
• T2 signal from edema may be increased in the acute setting. extends from the
Chronic is T2 Dark (scar) endocardium to the
• You won’t see Microvascular Obstruction in Chronic epicardium
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Microvascular Obstruction: Islands of dark
tissue in an ocean of late Gd enhancement. These
indicate microvascular obliteration in the setting of an
acute infarct. The Gd is unable to get to these regions
even after the restoration of epicardial blood flow.
Microvascular obstruction is a poor prognostic finding,
associated with lack of functional recovery.
Key Point: It’s NOT seen in chronic infarct.
Trivia: Microvascular obstruction is best seen on first pass imaging (25 seconds)
Ventricular Aneurysm: This is rare (5%), but
can occur as the result of MI. The question is always
true vs false:
• True: Mouth is wider than body. Myocardium
is intact. Usually anterior-lateral wall.
• False: Mouth is narrow compared to body.
Myocardium is NOT intact (pericardial
adhesions contain the rupture). Usually
posterior-lateral wall. Higher risk of rupture.
False Aneurysms are Usually Posterior Lateral
True Aneurysms are Usually Anterior Lateral
Viability - You can grade this based on % of transmural Viability Imaging:
thickness involved in the infarct. Segmental imaging (imaging
over multiple heart beats)
• <25%: likely to improve with PCI T1 post contrast (10-15 min
delay) inversion recovery
• 25-50%: may improve gradient echo
• 50-100%: unlikely to recover function
What is the timing on the bad sequelae of an Ml?
Dressier Syndrome (effusion) 4-6 weeks
Papillary Muscle Rupture 2- 7 Days
Ventricular Pseudoaneurysm 3- 7 Days
Ventricular Aneurysm Months - Requires remodeling and thinning.
Myocardial Rupture Within 3 Days (50% of the time)
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SECTION 7:
No n -Is c h emi c Hea r t
Dilated Cardiomyopathy: Defined as dilatation with an end diastolic diameter greater than
55 mm, with a decreased EF. Can be idiopathic, ischemic, or from a whole list of other random
crap (Alcohol, Doxorubicin, Cyclosporine, Chagas, etc...). The ischemic variety may show
subendocardial enhancement. The idiopathic variety will show either no enhancement or linear
mid-myocardial enhancement. There is often an association with mitral regurgitation due to
dilation of the mitral ring.
Restrictive Cardiomyopathy: Basically anything that causes a decrease in diastolic
function. Can be the result of myocardium replaced by fibrotic tissue (endocardial fibroelastosis),
infiltration of the myocardium (Amyloidosis), or damage by iron (hemochromatosis). The most
common cause is actually amyloid.
• Amyloidosis: Deposits in the myocardium causes abnormal
diastolic function with biatrial enlargement, concentric • Restrictive =
thickening of the left ventricle and reduced systolic function of Myocardial Process
usually both ventricles. Seen in 50% of cases of systemic • Constrictive =
amyloid. Has a terrible prognosis. You can sometimes see late Pericardial Process
Gd enhancement over the entire subendocardial circumference.
Amyloid Classic Scenario: A long TI is needed (like 350
milliseconds, normal would be like 200). T1 will be so long that the blood pool may be
darker than the myocardium. Buzzword “difficult to suppress myocardium”.
• Eosinophilic Cardiomyopathy (Loeffler): Bilateral Ventricular thrombus is the classic phrase /
buzzword. You will need a long T1 to show the thrombus.
Constrictive Pericarditis: Historically this used to be TB or Viral. Now the most
common cause is iatrogenic secondary to CABG or radiation. On CT the pericardium is too thick
(> 0.4 cm), and if it’s calcified that is diagnostic. Calcification is usually largest over the AV
groove. “Sigmoidization” is seen on SSFP cine imaging: The ventricular septum moves toward the
left ventricle in a wavy pattern during early diastole (“Diastolic Bounce”). This “bounce” will be
most pronounced during inspiration - indicating ventricular interdependence.
THIS vs THAT: Constrictive vs Restrictive
Cardiomyopathy:
• Pericardium is usually thickened in constrictive
• Diastolic septal bounce is seen in constrictive (Sigmoidization
of the septum).
Myocarditis: Inflammation of the heart can come from lots of
causes (often viral i.e. Coxsackie virus). The late Gd enhancement
follows a non-vascular distribution preferring the lateral free
wall. The pattern will be epicardial or mid wall (NOT Myocarditis
subendocardial). Mid Wall Late Gd Enhancement
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Sarcoidosis: Cardiac involvement is seen in 5% of Sarcoidosis cases, and is associated with an
increased risk of death. Signal in both T2 and early Gd (as well as late Gd) will be increased. Late Gd
pattern may be middle and epicardial in a non-coronary distribution. Focal wall thickening from
edema can mimic hypertrophic cardiomyopathy. It often involves the septum. The RV and
papillaries are RARELY affected.
Takotsubo Cardiomyopathy - A takotsubo is a Japanese Octopus trap, which looks like a pot
with a narrow mouth and large round base. The octopus will go into the pot, but then can’t turn around
and get out (sorta like medical school). A condition with Chest pain and EKG changes seen in post
menopausal women after they either break up with their boyfriend , win the lottery, or some other
stressful event has been described with the shape of the ventricle looking like a takotsubo. There is
transient akinesia or dyskinesia of the left ventricular apex without coronary stenosis.
Ballooning of the left ventricular apex is a buzzword. No delayed enhancement.
Cardiac MRI - Late Gadolinium Enhancement (LGE):
The backbone of multiple choice cardiac MRI related trivia.
Both diseased and normal myocardium will take up gadolinium / enhance - but it depends on when you
image. Early (1-3 mins) you will see normal tissue drink up contrast. Late (5-20 mins) contrast washes out
of the normal tissue and is retained by pathology (lots of different pathologies). The patterns that you see is
helpful for making the diagnosis (picking the answer on multiple choice).
The classic branch-point is ischemic vs non ischemic:
• Ischemic: Enhancement starts subendocardially and spreads transmurally toward the epicardial surface -
in a distribution corresponding to a known coronary artery territory
• Non-Ischemic: Enhancement is often located in the mid-wall of the ventricle - patchy or multifocal in
distribution (not corresponding to a known coronary artery territory)
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SECTION 8:
Gen et i c s
Arrhythmogenic Right Ventricular
Cardiomyopathy (ARVC):
Characterized by fibrofatty degeneration of the RV
leading to arrhythmia and sudden death. Features
include dilated RV with reduced function and fibrofatty
replacement of the myocardium, and normal LV.
People use this major/minor criteria system that includes
a bunch of EKG changes that no radiologist could
possibly understand (if they are stupid enough to ask just
say left bundle branch block). Watch out for the use of
fat sat to demonstrate the fat in the RV wall.
ARVC - Dilated RV, with Fat in the Wall
Hypertrophic Cardiomyopathy: Abnormal hypertrophy (from disarray of myofibrils) of
the myocardium that compromises diastole. There are multiple types but the one they are going to
show is asymmetric hypertrophy of the intraventricular septum. The condition is a cause of sudden
death. There is a subgroup which is associated with LVOT obstruction (“hypertrophic obstructive
cardiomyopathy”). Venturi forces may pull the anterior leaflet of the mitral valve into the LVOT
(SAM - Systolic Anterior Motion of the Mitral Valve). Patchy midwall delayed enhancement of
the hypertrophied muscle may be seen, as is an independent risk factor for sudden death.
Noncompaction:
Left ventricular noncompaction is
an uncommon congenital
cardiomyopathy that is the result
of loosely packed myocardium.
The left ventricle has a spongy
appearance with increased
trabeculations and deep
intertrabecular recesses. Noncompaction - Spongy LV with No Myocardial Thickening
As you might expect, these guys get heart failure at a young age. Diagnosis is based of a ratio of
non compacted end-diastolic myocardium to compacted end-diastolic myocardium of more
than 2.3:1.
Muscular Dystrophy: Becker (mild one) and Duchenne (severe one) are X-linked
neuromuscular conditions. They have biventricular replacement of myocardium with connective
tissue and fat (delayed Gd enhancement in the midwall). They often have dilated cardiomyopathy.
Just think kid with dilated heart and midwall enhancement.
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SECTION 9:
Tu mo r s
Mets: Thirty times more common than a primary malignancy. The pericardium is the
most common site affected (by far). The most common manifestation is a pericardial
effusion (second most common is a pericardial lymph node). Melanoma may involve the
myocardium.
Trivia: Most common met to the heart is lung cancer (pericardium and epicardium)
Angiosarcoma: Most common primary malignant tumor of the heart in adults. They
like the RA and tend to involve the pericardium. They often cause right sided failure and/or
tamponade. They are bulky and heterogenous. Buzzword is “sun-ray” appearance which
describes enhancement appearance of the diffuse subtype as it grows along the perivascular
spaces associated with the epicardial vessels.
Left Atrial Myxoma: Most common primary THIS vs THAT:
cardiac tumor in adults (rare in children). They are Tumor vs Thrombus:
associated with MEN syndromes, and Blue Nevi
Cardiac MRI is the way to tell.
(Carney Complex). They are most often attached to the
interatrial septum. They may be calcified. They may • Tumor will enhance
prolapse through the mitral valve. They will enhance • Thrombus will NOT enhance.
with Gd (important discriminator from a thrombus).
Rhabdomyoma: Most common fetal cardiac tumor. It is a hamartoma. They prefer the
left ventricle. Associated with tuberous sclerosis. Most tumors will regress spontaneously
(those NOT associated with TS are actually less likely to regress).
Fibroma: Second most common cardiac tumor in childhood. They like the IV septum,
and are dark / dark on T1/T2. They enhance very brightly on perfusion and late Gd.
Fibroelastoma: Most common neoplasm to involve the cardiac valves (80% aortic or
mitral). They are highly mobile on SSFP Cine. Systemic emboli are common (especially if
they are on the left side).
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Cardiac Tumors / Mimics
Metastatic
Myxoma Fibroelastoma Rhabdomyoma Angiosarcoma Thrombus
Disease
The most
Most common Much more
2nd most common Most common common Most common
primary common than intra-cardiac
primary cardiac primary cardiac primary
cardiac tumor Primary
tumor (adult) tumor (infants) MALIGNANT “mass”
(adult) tumors
tumor
Lung cancer
is the most
Adult (30-60) common.
with distal Adult (50-60) -
emboli and Melanoma
usually an
fainting spells. incidental finding. Infant with goes to the
tuberous heart with
Younger the greatest
If they are sclerosis
people are percentage
symptomatic its
likely (but
from emboli
syndromic prevalence is
(stroke / T1A)
(Carney less than
Complex) lung)
Favors the left
Involves the atrial
Arise from the
cardiac valves - appendage
intra-atrial Favor the
aortic is most (A-Fib),
septum, ventricular Favors the right Favors the
common myocardium atrium pericardium
usually
usually the aortic Left
growing into
side of the aortic Ventricular
the left atrium
cusp. Apex (post
MI)
Pericardial
About 1/4 have Most are small - They tend to be thickening =
calcification less than 1 cm. multiple invasion
"Ball with
Discriminator:
stalk attached
Fibroma is T2
to the inter- Discriminator:
dark
atrial septum ” Vegetations tend Discriminator:
Rhabdomyoma is Large
Dynamic to involve the Pericardial Thrombus
T2 Bright heterogenous won’t
imaging will valve free edges. nodularity
show Fibroelastoma mass and effusion enhance.
* Fibroma is the Tumors will.
mobility / does NOT do
2nd most common
prolapse of the that.
tumor in this age
“ball”.
group
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SECTION 10:
PERICARDIUM
The pericardium is composed of two layers (visceral and parietal), with about 50 cc of fluid
normally between the layers.
Pericardial Effusion:
Basically more than 50 cc between the pericardial layers. This can be from lots and lots of causes
- renal failure (uremia) is probably the most common. For the purpose of multiple choice tests
you should think about Lupus, and Dressier Syndrome (inflammatory effusion post MI).
On CXR they could show this 3
ways: (1) Normal Heart on
Comparison, Now Really Big Heart
(2) Giant Water Bottle Heart, (3)
Lateral CXR with two lucent lines
(epicardial and pericardial fat) and
a central opaque line (pericardial
fluid) - the so called “oreo cookie
sign.”
Pericardial Effusion: "Oreo Cookie Sign”
Cardiac Tamponade: Pericardial effusion can cause elevated pressure in the pericardium
and result in compromised filling of the cardiac chambers (atria first, then ventricles). This can
occur with as little as 100 cc of fluid, as the rate of accumulation is the key factor (chronic slow
filling gives the pericardium a chance to stretch). The question is likely related to short-axis
imaging during deep inspiration showing flattening or inversion of the intraventricular
septum toward the LV, a consequence of augmented RV filing. Another indirect sign that can be
shown on CT is reflux of contrast into the IVC and azygos system.
Pericardial Cysts: Totally benign incidental finding. Usually seen on the right
cardiophrenic sulcus. They do not communicate with the pericardium. Rarely they can get
infected or hemorrhage. This would be most easily shown as an ROI measuring water density
along the right cardiophrenic sulcus.
Congenital / Acquired Absence: Even though you can have total absence of the
pericardium - the most common situation is partial absence of the pericardium over the left
atrium and adjacent pulmonary artery. When the left pericardium is absent the heart shifts
towards the left. They could show you a CT or MRI with the heart contacting the left chest wall,
and want you to infer partial absence. Another piece of trivia is that cardiac herniation and
volvulus can occur in patients who undergo extrapleural pneumonectomy (herniation can only
occur if the lung has also been removed).
Trivia: The left atrial appendage is the most at risk to become strangulated.
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SECTION 11:
SURGERIES
Palliative Surgery for the Hypoplastic Left Heart: Surgery for Hypoplasts
is not curative, and is instead designed to extend the life (prolong the suffering) of the child.
It is done in a 3 stage process, to protect the lungs and avoid right heart overload:
(1) Norwood or Sano - within days of birth
(2) Glenn - at 3- 6 months
(3) Fontan at 1½ to 5 years
(1a) Norwood: The goal of the surgery is to create an unobstructed outflow tract from
the systemic ventricle. So the tiny native aorta is anastomosed to the pulmonary trunk, and
the arch is augmented with a graft (or by other methods). The ASD is enlarged to create
non restrictive atrial flow. A Blalock-Taussig Shunt (see below) is used between the right
Subclavian and right PA. The ductus is removed as well to prevent over shunting to the lungs
Apparently, when this goes bad it s usually from issues related to damage of the coronary
arteries or over shunting of blood to the lungs (causing pulmonary edema). As a point of
trivia, sometimes the thymus is partially removed to get access.
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(1b) Sano: Same as the Norwood, but instead of using a Blalock-Taussig shunt a conduit is
made connecting the right ventricle to the pulmonary artery. The disadvantage of the BT Shunt
is that it undergoes a steal phenomenon (diverted to low pressure pulmonary system).
(2a) Classic Glenn: Shunt between the SVC and right
pulmonary artery (end-to-end), with the additional step of sewing
the proximal end of the Right PA closed with the goal of reducing
right ventricular work, by diverting all venous return straight to the
lung (right lung).
(2b) Bi-Directional Glenn: Shunt between the SVC and the
right pulmonary artery (end-to-side). The RPA is left open, letting
blood flow to both lungs. This procedure can be used to address
right sided heart problems in general, and is also step two in the
palliative hypoplastic series. If it’s being used as step two the
previously placed Blalock-Taussig Shunt or Sano shunt will come
down as the Glenn will be doing its job of putting blood in the
lungs.
(3) Fontan Operation: Used for Hypoplastic Hearts. The old
school Fontan consisted of a classic Glenn (SVC to RPA), closure of the
ASD, and then placing a shunt between the Right atrium to the Left PA.
The idea is to let blood return from systemic circulation to the lungs by
passive flow (no pump), and turn the right ventricle (the only one the kid
has) into a functional left ventricle. There arc numerous complications
including right atriomegaly with resulting arrhythmias, and plastic
bronchitis (they cough up “casts of the bronchus” that look like plastic).
Other Surgeries:
High Yield Point:
Classic Blalock-Taussig Shunt: Originally
developed for use with TOF. Shunt is created Glenn = Vein to Artery
between the Subclavian artery and the pulmonary (SVC to Pulmonary Artery)
artery. It is constructed on the opposite side of the Blalock-Taussig = Artery to Artery
arch. It’s apparently technically difficult and often (Subclavian Artery to Pulmonary Artery)
distorts the anatomy of the pulmonary artery.
Modified Blalock-Taussig Shunt: This is a gortex
shunt between the Subclavian artery and pulmonary artery,
and is performed on the SAME SIDE as the arch. It’s easier
to do than the original.
BT- Shunt
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Pulmonary Artery Banding: Done to reduce pulmonary
artery pressure (goal is 1/3 of systemic pressure). Most common
indication is CHF in infancy with anticipated delayed repair. The
single ventricle is the most common lesion requiring banding.
Atrial Switch: Mustard and Senning procedures are used to
correct transposition of the great arteries by creating a baffle within
the atria in order to switch back the blood flow at the level of in-
flow. The result is the right ventricle becomes the systemic
ventricle, and the left ventricle pumps to the lungs. This is usually
done in the first year of life.
• Senning: Baffle is created from the right atrial wall and
atrial septal tissue WITHOUT use of extrinsic material
• Mustard: Involves the resection of the atrial septum and
creation of a baffle using pericardium (or synthetic material).
Rastelli Operation: This is the most commonly
used operation for transposition, pulmonary outflow
obstruction, and VSD. The procedure involves the
placement of a baffle within the right ventricle
diverting flow from the VSD to the aorta (essentially
using the VSD as part of the LVOT). The pulmonary
valve is oversewn and the conduit is inserted between
the RV and the PA. The primary advantage of this
procedure is the left ventricle becomes the systemic
ventricle. The primary limitation of this procedure is
that the child will be committed to multiple additional surgeries
because the conduit wears out and must be replaced.
Jatene Procedure: This is another arterial switch method that
involves transection of the aorta and pulmonary arteries about the
valve sinuses , including the removal of the coronaries. The great
arteries are switched and the coronaries are sewn into the new aorta
(formerly the PA). Apparently this (Lecompte Maneuver) is very
technically difficult, but the advantage is there is no conduit to go
bad, and the LV is the systemic ventricle.
Ross Procedure: Performed for Diseased Aortic Valves in Children. Replaces the aortic
valve with the patient’s pulmonary valve and replaces the pulmonary valve with a
cryopreserved pulmonary valve homograft. Follow-up studies have shown interval growth of
the aortic valve graft in children and infants.
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Bentall Procedure:
Operation involving composite graft
replacement of the aortic valve, aortic root and
ascending aorta, with re-implantation of the
coronary arteries into the graft. This operation
is used to treat combined aortic valve and
ascending aorta disease, including lesions
associated with Marfan syndrome.
Summary - Most Common Surgery / Key Points
Glenn Blalock Taussig Fontan
Artery to Artery It’s complicated with multiple
Vein to Artery (Subclavian Artery to Pulmonary versions - steps are unlikely to
(SVC to Pulmonary Artery)
Artery) be tested
Primary Purpose: Take
Primary Purpose: Bypass the
systemic blood directly to the Primary Purpose: Increase
right ventricle / direct systemic
pulmonary circulation (it pulmonary blood flow
circulation into the PAs.
bypasses the right heart).
Most Testable Complications:
Most Testable Complications: Most Testable Complications:
-Enlarged Right Atrium
-SVC Syndrome -Stenosis at the shunt’s
causing arrhythmia
-PA Aneurysms pulmonary insertion site
-Plastic Bronchitis
THIS vs THAT: Heart Transplant Types
Orthotopic Heart Transplant: All of the heart is removed, except the circular
part of the left atrium (the part with the pulmonary veins). The donor heart is trimmed
to fit to the left atrium.
Heterotopic Heart Transplant: The recipient heart remains in place, and the
donor heart is added on top. This basically creates a double heart. The advantages of
this are (1) it gives the native heart a chance to recover , and (2) gives you a backup if
the donor is rejected.
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Blank for Scribbles and Notes
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9
NUCLEAR MEDICINE
PROMETHEUS LIONHART, M.D.
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SECTION 1:
Wh a t scan i s i t ?
Ok, here is the scenario that I want you to be prepared for:
The plane has crashed. All the nuclear techs are dead. Prior to the plane crashing, they
completed several studies, but forgot to label them or give indications. The bean counter (non-
MD) who is running the hospital is breathing down your neck to read these studies now,
because the metrics he set up are gonna look bad at the next QA/QC meeting. So now you have
to interpret nuclear studies, and you don't know why they did them or even what tracer was
given.
Fortunately, you trained for this as part of your preparation for the Exam.
Seriously, this is famously one of the most common ways nuclear medicine is tested. It was
like that on the old oral boards, and probably still like that now (same knuckle heads writing the
questions). It’s such a ridiculous thing to ask.
My primary advice: Don’t Fight It. Games are Best Played As Games.
Octreotide = Higher Count Study = VERY HOT Spleen and Kidneys
* Note the MIBG is under both heart and no heart - this is because it s variable. MIBG with
I-123 is more likely to have heart than I-131.
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This is an alternative pathway that some people prefer. This one focuses more on photon
output (how light or dark stuff is), and liver and spleen. It removes the confusion of heart
“maybe” for MIBG.
Another alternative way to work the bones pathway is to ask Lacrimal Glands? Gallium will
have them, WBC scans and Sulfur Colloid will NOT. The trick on Lacrimal Glands is free
Tc (but bones will be real weak on that one). MIBG can have lacrimal activity , but again no
bones.
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Special Topics
MIBG
I’ll talk about this more later in the chapter, but MIBG can be labeled with either I-123 or I-131.
The energy of the I-123 (159 keV) is better for imaging, you can give a higher dose, and the
results are typically available within 24 hours (I-131 usually requires delated to optimize target to
background noise). Having said that I-131 labeled MIBG is still used all over the place, especially
with adults. I-131 may also be better for estimation of tumor uptake, for planning related to
MIBG therapy. The point of me rambling here is that you have two different MIBGs - so telling
which scan is which requires a little finesse.
It has variable cardiac uptake, so it finds itself on multiple branch points. Cardiac activity is more
often seen on an I-123 MIBG scan (as opposed to I-131 MIBG). Another thing that helps me
remember this stuff: when you do a MIBG you are often looking for neuroblastoma. If the kidney
was also hot it would be hard to tell a mass near the kidney from the kidney - so part of the
reason the study works is that the kidney does NOT take up MIBG.
Adrenal glands: Normal adrenal glands are not seen. However, you can have faint uptake in the
adrenals in about 15% of I-131 patients, and around 75% of I-123 patients. So, if you see
adrenals and you are sure they are normal (faint and symmetric) it’s more likely to be I-123.
DARK SPLEEN + Tc-99m WBC vs In-111 WBC
DARK KIDNEYS Just like MIBG can be labeled with either I-123 or I-131
you can label WBCs with Tc or Indium.
The classic kneejerk for Octreotide.
In WBC vs Tc WBC: Both will
This is a high count study, so the have hot spleens. Additionally,
images should be clearer (relative to Tc is a higher count study and
the normal “un-clear medicine.” will typically look cleaner.
You can go down the “no bones”
pathway, but the trigger should be no Tc WBC: The trick here can be imaging at 4 hours vs
bones + liver + dark spleen + dark imaging at 24 hours. At 4 hours you can see lung
kidneys. uptake. At 24 hours the lungs are clearing up, but you
start to get some bowel uptake. Just like an In-WBC the
spleen is still darker than the Liver.
Hot Kidneys
Hot Spleen
Tc-99m WBC at 4 hours Tc-99m WBC at 24 hours
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SECTION 2:
SKELETON
18F - Sodium Fluoride vs Tc-MDP
You can do bone scans with several different tracers, the main two are 18F Sodium Fluoride and
Tc-MDP. If you were trying to differentiate the two, the primary take home point is F-18 PET is
way way way better than Tc-MDP. By “better” I mean that the image quality and sensitivity of F18
is multiple orders of magnitude better than Tc-MDP. It also has a shorter examination time. So,
why do you never see 18F? Because it costs more, and insurances won’t pay etc... Politics and
Finance are the reasons. Another potentially testable factoid would be which organ gets the
highest dose? The organ receiving the highest dose is Bone with MDP, and Bladder with 18F
(overall 18F > Tc-MDP) — probably... honestly you’ll read different things in different sources.
—Scan on Scan on Scan—
This is a common trick, popular in case books & case conferences - asking you to distinguish F-18
bone scan vs Tc-MDP bone scan vs PET-FDG with marrow stimulation.
This is how you do it:
• Tc-MDP will have bone and kidney uptake. It will be a blurry fuzzy piece of crap.
• 18F will be beautiful, super high resolution, and look like a MIP PET.
• FDG -PET with bone stimulation - will look similar to the F-18, but will have brain
uptake. Also, this can show increased uptake in the spleen.
Of the various soldiers mentioned above, the workhorse of
skeletal imaging is methylene diphosphonate (MDP) tagged with
Tc-99m. This is prepared from a kit which has MDP and stannous
ion. You add free pertechnetate and the stannous ion reduces it so
it will bind to the MDP. If you don’t have enough stannous ion
(or you get air into the vial or syringe — that can cause oxidation)
you might get free Tc (salivary gland, thyroid, stomach uptake).
After you inject the tracer (15-25 mCi) you wait 2-4 hours to let Free Tc:
the tracer clear from the soft tissues (so you can see them bones). Gastric Uptake on Bone Scan
‘incidental note of sternal met
Mechanism: Phosphonate binding to bone (chemisorption). from breast CA
Distribution is based on blood flow and osteoblastic activity.
Gamesmanship - MDP and HDP are both bone agents so don’t get confused if they say HDP to
purposefully confuse you.
What factors will affect Where is tracer uptake NORMAL ?
tracer uptake?
• Bone (duh), but also the Epiphyses in kids
• OsteoBLASTIC activity
• Kidney (not seen *or very faint = Super Scan), Bladder
(why pure lytic lesions can
• Breasts (especially in young women)
be cold)
• Blood Flow • Soft tissues - low levels
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Abnormal Distribution
Increased focal uptake is very nonspecific, and basically is just showing you bone turn over.
So a metastatic deposit can do that (and this is the classic indication). But, you can also see
it with arthritis (classically shoulder) and healing fractures (most commonly shown with
segmental ribs).
Sneaky Situations:
• Skull Sutures: It’s normal to see some persistent visualization of the skull
sutures, BUT when this is marked you may be thinking about renal
osteodystrophy.
• Breast Uptake: Some mild diffuse breast uptake is normal (especially in
younger women), BUT focal uptake can be cancer.
• Renal CORTEX activity: You are supposed to have renal activity (not
seeing kidneys can make you think super scan), BUT when the renal
Asymmetric Breast
cortex is hotter than the adjacent lumber spine you should think
Tissue Uptake
about hemochromatosis. (Primary Breast CA)
• Diffuse Renal Uptake: This often occurs in the setting of chemotherapy
(especially if the study is looking for bone mets). This also can be seen
with urinary obstruction.
• Liver Uptake: This can be several things, but the main ones to think
about are (1) Too Much Al+3 contamination in the Tc, (2) Cancer -
either primary hepatoma or mets, (3) Amyloidosis, (4) Liver Necrosis
• Spleen Uptake: This is a common trick to show an auto-infarcted
spleen - common in sickle cell patients. These same patients are going
to have scattered hot and cold areas from multiple bone infarcts. Diffuse Renal Uptake
(Chemotherapy)
• Lung Uptake: In most cases this is some type of heterotopic calcification (dystrophic or mets).
The classic MDP hot lung met would be an osteosarcoma. Ultimately, it’s not specific and can be
seen in a ton of other random situations (fibrothorax, primarily tung tumors, radiation changes,
sarcoid, berylliosis, alveolar microlithiasis, Wegener’s, etc...).
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Abnormal Distribution Continued
• The Single Lesion: When you see a single hot lesion, the false positive rate for attributing the
finding to a met is high. Only about 15% to 20% of patients with proven mets have a single
lesion (most commonly in the spine). In other words, 80% of the time it’s benign, A classic
exception is a single sternal lesion in a patient with breast cancer. This is due to breast CA
80% of the time.
• Sacral Insufficiency fracture: This is a hot geographic area,
confined to the sacrum, often with a characteristic butterfly or “H”
shaped (Honda sign). Osteoporosis is the most common cause, but
it can also occur in a patient who has had radiation.
• Diffusely Decreased skeletal uptake: This can be seen with
(1) free Tc, or (2) Bisphosphonate therapy.
• Fractures in the Elderly (including elder abuse): In older
populations, bone scans may be negative for several days. A bone
scan obtained at 1 week will exclude a fracture. “Honda Sign”
Sacral Insufficiency Fx
• Vertebra! Body Fracture (Benign vs Malignant): A horizontal linear pattern of tracer uptake is the
classic look for an osteoporotic fracture (especially if they are multiple and of varying intensity).
If the tracer extends from the vertebral body into the posterior elements or just involves the
pedicles then you should think cancer. Lastly, followup of the osteoporotic fracture should show
tracer activity decreasing (cancer isn’t gonna do that).
• Rib Lesions (Benign vs Malignant): Multiple
ribs in a vertical linear pattern should make
you think fractures (think about any trauma
scan you’ve ever seen with rib fractures - they
tend to line up). Now, if the hot spots are
multiple (3 or more) and are jumping around,
bilaterally, etc... you should think mets. The
big thing is that when cancer goes to bones it
rarely just goes to the ribs. So lesions only in
the ribs are more likely to be benign - but
when you have lesions in the ribs and other
spots then you are likely dealing with mets.
Multiple Contiguous Lesions (Rib Fractures)
• Muscle - Yes... MDP is for bones, but it will also localize to injured skeletal muscle. The classic
way to show this is very hot quads, calfs, shoulders in a marathon runner (or military recruit) - as
a way to show rhabdomyolysis.
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Special Topic - Hypertrophic Osteoarthropathy
This is a “Tramline” along the periosteum of long bones,
which is associated with conditions of chronic hypoxia (CF,
Cyanotic Heart Disease, Mesothelioma, Pneumoconiosis).
However, when you see this - you need to think lung cancer.
Apparently it’s actually seen in 10% of patients with lung
cancer.
Next Step? CXR, Chest CT etc...
"Tramline Sign” of
Hypertrophic Osteoarthropathy
Special Topic - “HO”
Normally when we think about the consequences of “HO” we typically think about
nasty things like herpes, crabs, and gonorrhea - but on multiple choice HO can refer to
something totally different - heterotopic ossification. This describes bone (hence the
term “ossification”) growing in soft tissues. Typically use see this acquired after a
muscular trauma. As discussed in the MSK chapter the pattern is typically outside to
in, with the eventual development of mature cortical bone. In some cases this abnormal
bone proliferation can reduce joint motility and cause pain. Therefore, in some cases
surgical resection is performed to preserve the function of the joint.
Enter the MDP Bone Scan.
The main reason you image this is to see if it’s “mature.” Serial exams are used to
evaluate if the process is active or not (not = “mature”). If it’s still active it has a higher
rate of recurrence after it’s resected. The idea is you can follow it with imaging until
it’s mature (cold), then you can hack it out (if someone bothers to do that).
Special Topic - AVN
Avascular Necrosis (AVN) as discussed in the MSK chapter, this can occur from a
variety of causes (EtOH, Steroids, Trauma, Sickle Cell, Gauchers).
The trick on bone scan is the timing.
• Early and late AVN is cold.
• Middle (repairing) will be hot.
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Bone Lesions
Pagets
Seen primarily in older patients (8% at 80),
it’s classically shown five ways:
1. Super Hot Enlarged Femur
2. Super Hot Enlarged Pelvis,
3. Super hot skull,
4. Expanded hot “entire” vertebral body
5. Metabolic Superscan - from widespread
Pagets. Although, as a point of
gamesmanship if they show you a metabolic
superscan the answer is probably hyper PTH.
Pagets Spine - Classically involves BOTH the vertebral body and posterior elements.
Primary Bone Tumors:
Both Osteosarcoma and Ewings will be hot. Primary utility of the bone scan is to see extent
of disease. With regard to benign bone tumors the only ones worth knowing are the HOT
ones and the COLD ones. Osteoid Osteoma is worth knowing a few extra things about
(because they lend themselves easily to multiple choice questions).
Osteoid Osteoma: The lesion will
be focal and three phase hot. A
central hot nidus is often seen
(double density or hotter spot
within hot area). A normal bone
scan excludes this entity.
Fibrous Dysplasia: Be aware that
in case books / case conference this
is sometimes shown as a super hot
mandible. Could also be shown as
a leg that looks similar to Paget.
Osteosarcoma Osteoid Osteoma
-Double Density
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Specific Cancers - Specific Trivia:
• Prostate Cancer Loves Bone Mets (85% of dying patients have it)
• Prostate Cancer bone mets are uncommon with a PSA less than 10 ng/ml
• Lung Cancer bone mets tend to be in the appendicular skeleton
• Lung Cancer can have hypertrophic osteoarthropathy (10%)
• Breast Cancer bone mets are most common to the spine, but the solitary sternal
lesion is more specific
• Neuroblastoma frequently mets to the bones (metaphysis of long bones)
• I-123 and 131 MIBG are superior for detection of neuroblastoma bone mets
BAD BONES!
Any bone uptake on MIBG, I-131, or Octreotide is abnormal, & concerning for mets.
Cold Lesions Bone Island vs
Prostate Met:
• Radiation Therapy (usually segmental)
• Early Osteonecrosis • Both are sclerotic on
plain film / CT
• Infarction (very early or late)
• The Prostate Met
• Anaplastic Tumor (Renal, Thyroid,
should be very HOT on
Neuroblastoma, Myeloma) Bone Scan
• Artifact from prosthesis, pacemaker, spine • The Bone Island should
stimulator, etc.... be cold, or faintly warm
• Hemangioma ** this is variable • Osteopoikilosis should
• Bone Cyst (without fracture) be cold
HOT Lesions
• Fibrous Dysplasia • Osteoblastoma • Aneurysmal Bone Cyst
• Giant Cell Tumor • Osteoid Osteoma *donut sign (centrally cold)
Bone Scan vs Skeletal Survey (Trivia)
• Bone Scan is way better (more sensitive) than skeletal survey for blastic mets
• Skeletal Survey is superior (more sensitive) for lytic mets
• Skeletal survey is the preferred evaluation for osseous involvement in myeloma
Equivocal Lesion Next Step ?
If a bone scan “equivocal lesion” is found the next step is a plain film. If the plain film
shows no corresponding lesion this is MORE suspicious for mets. Next step at that point
would be a MRI.
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Super Scans
This is a common trick, where the scan shows no abnormal focal uptake, but you can’t see
the kidneys. The trick is that everything is hot.
This occurs in two flavors:
• Diffuse Mets: Diffuse skeletal
metastatic activity (breast and
prostate are the common culprits)
• Metabolic: From metabolic bone
pathology; including
hyperparathyroid, renal
osteodystrophy, Paget's, or severe
thyrotoxicosis.
Diffuse Prostate Mets Hyper PTH (hot skull)
How can you tell them apart?
- The Skull will be asymmetrically hot on the metabolic super scan.
Don’t get it twisted- A common sneaky move is to show you a bone scan, with no renals. But it’s
because there is a horseshoe kidney in the pelvis. Could be phrased as a next step question, with
the answer being look at prior CT to confirm normal anatomy.
Flair Phenomenon:
This is a sneaky situation shown on bone scan, where a good response to therapy will mimic
a bad response. What happens is you have increased radiotracer uptake (both in number and
size of lesions) seen 2 weeks to 3 months after treatment.
So how can you tell it is flair and not actually cancer getting worse?
• On plain film lesions should get more sclerotic
• After 3 months they should improve.
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The Three Phase Scan:
Bone scans can be done in a single delayed phase, or in 3 phases (flow, pool, and delayed). A
lot of things can be “3 phase hot”, including osteomyelitis, fracture, tumor, osteoid osteoma,
charcot joint, and even reflex sympathetic dystrophy.
Cellulitis vs Osteomyelitis:
The benefit of using 3 phases is to distinguish between cellulitis (which will be hot on flow
and pool, but not delays), and osteomyelitis (which is 3 phase hot). In children, a whole body
bone scan is often performed to evaluate extent. Additionally, because of subperiosteal pus/
edema you can actually have decreased vascularity to the infected area (cold on initial phases)
but clearly hot on delayed phases.
In the spine, gallium (combined with bone scan) or MRI are the preferred imaging modalities.
Response:
You can also use a bone scan to evaluate response to treatment. Blood flow and blood pool
tend to stay abnormal for about 2 months, with delayed activity persisting for up to 2 years.
This is especially true when dealing with load bearing bones. Gallium-67 and Indium-111 WBC
are superior for monitoring response to therapy.
Reflex Sympathetic Dystrophy (RSD):
Sometimes called “complex regional pain syndrome,” it can be seen after a stroke, trauma, or
acute illness. The classic description is increased uptake on flow and blood pool, with
periarticular uptake on delayed phase. The uptake often involves the entire extremity.
About one third of adult patients with documented RSD do not show increased perfusion and
uptake (which probably means they are faking it. and need a rheumatology consult for
fibromyalgia). In children, sometimes you actually see decreased uptake.
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Sulfur Colloid Bone Scan & WBC Imaging:
Tc can be tagged to sulfur colloid with the idea of getting a normal localization to the bone
marrow. You can actually perform Tc-99m sulfur colloid studies to map the bone marrow in
patients with sickle cell (with the idea to demonstrate marrow expansion and bone infarct).
However, the major utility is to use it in combination with tagged WBC or Gallium.
Both Tc Sulfur Colloid and WBCs will accumulate in normal bone marrow, in a spatially
congruent way (they overlap). The principal is that infected bone marrow will become
photopenic on Tc-Sulfur Colloid. Now, this takes about a week after the onset of infection, so
you have to be careful in the acute setting. WBC, on the other hand, will obviously still
accumulate in an area of infection. Combined Tc-Sulfur Colloid and WBC study is positive
for infection if there is activity on WBC image, without corresponding Tc Sulfur Colloid
activity on the bone marrow image.
Special Situation - The Spine
When imaging the spine, WBC frequently fails to migrate showing a photopenic area
(WBC = False Negative in the Spine). This is why gallium is preferred for osteomyelitis of
the spine.
Tc-Sulfur Colloid In-WBC Gallium
Less Uptake in Less Uptake in More Uptake in
Infected Bone Infected Bone - Infected Bone
*False Negative
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Prosthesis Evaluation:
Differentiating infection from aseptic loosening is challenging and the most common reason a
nuclear medicine doctor would get involved in the situation. Bone scan findings of
periprosthetic activity is very nonspecific, because you can see increased tracer activity in a
hip up to 1 year after placement (even longer in cementless arthroplasty). Typically, there
would be diffusely increased activity on imaging with 99mTc-MDP in the case of infection (more
focal along the stem and lesser trochanter with loosening) - but this isn’t specific either.
Combined Tc-Sulfur Colloid and WBC imaging is needed to tell the difference.
Helpful when negative - A negative bone scan excludes loosening or infection.
Neuropathic Foot:
Most commonly seen in the tarsal and tarsal-metatarsal joints (60%), in diabetics. When the
question is infection (which diabetics also get), it’s difficult to distinguish arthritis changes vs
infection with Tc-MDP. Again, combined marrow + WBC study is the way to go.
An additional pearl that could make a good “next step” question is the need for a fourth phase
in diabetic feet. As these patient’s tend to have reduced peripheral blood flow, the addition of
a 4th phase at 24 hours may help you distinguish between bone and delayed soft tissue
clearance.
Instead of In-111 WBC, What about Tc-99m HMPAO WBC ?
When would you consider Tc-99m HMPAO instead of In-111 WBC for infection? Two main
reasons
(1) Kids - Tc-99m will have a lower absorbed dose & shorter imaging time
(2) Small Parts - Tc-99m does better in hands and feet
Why not use Tc-99m HMPAO all the time ? The downsides to Tc-99m HMPAO are:
(1) It has a shorter half life -6 hrs- which limits delayed imaging, and
(2) It has normal GI and gallbladder activity which obscures activity in those areas.
In-111 WBC Chem and Pharm
• The vast majority (like 90%) of the labeled cells are Neutrophils. This allows you to
“trace” anything that triggers neutrophil migration (inflammation / infection).
• The radiation dose that the Indium deposits on the neutrophil doesn’t mess with its
function (supposedly). Lymphocytes on the other hand, tend to be killed by the radiation
(they don’t turn into cancer).
• In the normal situation the critical organ is the spleen.
• If the cells become fragmented - the Indium binds with transferrin and you see more
uptake in the liver and bone marrow.
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SECTION 3:
Pu l mo n a r y
If 1940 calls and wants to rule out a PE, you’ll want to get the angiography room ready. In 2014,
textbooks and papers still frequently lead with the following statement “Pulmonary angiography is
the definitive diagnostic modality and reference standard in the diagnosis of acute PE.” In reality,
pulmonary angiography is almost never done, and CTPA is the new diagnostic test of choice. V/Q
scan is usually only done if the patient is allergic to contrast or has a very low GFR. The primary
reason V/Q isn’t done is that it’s often intermediate probability, and the running joke is that if you
don’t know how to read one, just say it’s intermediate and you’ll probably be right.
The idea behind the test is that you give two tracers: one for ventilation and one for perfusion. If you
have areas of ventilated lung that are not being perfused, that may be due to PE. Normally
Ventilation and Perfusion are matched, with a normal gradient (less perfusion to the apex - when
standing).
Tracers:
Perfusion: For perfusion, Tc-99m macroaggregated albumin (Tc-99m MAA) is the most common
tracer used. MAA is prepared by heat denaturation of human serum albumin, with the size of the
particles commercially controlled. You give it IV and the tracer should stay in the pulmonary
circulation (vein→ SVC → right heart → pulmonary artery → lung *STOP). The tracer should light up
the entire lung. A normal perfusion study excludes PE. Areas of perfusion abnormality can be from
PE or other things (more on this later). The biologic half life is around 4 hours (they eventually fall
apart, becoming small enough to enter the systemic circulation to eventually be eaten by the
reticuloendothelial system).
Ventilation: There are two ways to do the ventilation; you can use a radioactive gas (Xenon-133) or a
radioactive aerosol (Tc-99m DTPA).
• Xenon-133: The physical half-life is 5.3 days, the biologic half-life is 30 seconds (you breath it
out). Because it has low energy (81 keV) it is essential to do this part of the test first (more on
this in the physics chapter). Additionally, because the biologic half life is so short, you only can
do one view (usually posterior) with a single detector (dual detector can do anterior and
posterior). There are 3 phases to the study: (1) wash in (single max inspiration and breath hold),
(2) equilibrium (breathing room air and xenon mix), and (3) wash out (breathing normal air).
• Tc-99m DTPA: This one requires patient cooperation because they have to breath through a
mouth guard with a nose clamp for several minutes. It is also essential to do this part of the test
first.
Quantitative Perfusion:
You can do quantitative studies typically to evaluate prior to lung resection, or prior to transplant.
You want to make sure that one lung can hold its own if you are going to take the other one out.
Testable Trivia: Quantification is NOT possible if you use Tc-99m DTPA aerosol. You can do it with a
combined Xe + Tc MAA because the Xe will not interfere with the Tc.
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5 Classic Trivia Questions about Tc-99m MAA:
(1) They show tracer in the brain: This is a classic way of showing you a shunt (it
got into the systemic circulation somehow, maybe an ASD, VSD, or Pulmonary
AVM).
(2) How big are the particles? A capillary is about 10 micrometers. You need your
particles to stay in the lung, so they can’t be smaller than that. You don’t want
them to be so big they block arterioles (150 micrometers). So the answer is
10-100 micrometers.
(3) When do you reduce the particle amount? A few situations. You don’t want to
block more than about 0.1 % of the capillaries, so anyone who has fewer
capillaries (children, people with one lung). Also you don’t want to block
capillaries in the brain, so anyone with a right to left shunt. Lastly anyone with
pulmonary hypertension (or who is pregnant).
(4) Is reduced particle the same as reduced dose? Nope. The normal dose of Tc can
be added to fewer particles.
(5) They show you multiple focal scattered hot spots: This is the classic way of
showing “clumped MAA” , which happens if the tech draws blood into the
syringe prior to injection.
Classic Trivia Questions for Xenon-133:
(1) They show you persistent pulmonary activity during washout: This indicates
Air Trapping (COPD)
(2) They show you accumulation of tracer over the RUQ: This is fatty
infiltration of the liver (xenon is fat soluble).
Classic Trivia Questions for Tc-99m DTPA
Xenon TC-99m DTPA
Quick Wash Out only one or two views Slower Wash Out - multiple projections
Activity homogenous in the lungs “Clumping” common in the mouth,
central airways, and stomach (from
swallowing).
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-Gamesmanship-
Q: What if you see tracer in the thyroid or stomach on VQ Scan??
A: You should think 2 things: (1) Free Tc, or (2) Right - to - Left Shunt
Q: What do you need to call a Right - to - Left Shunt ?
A: Tracer in the Brain
Q: If you suspect a shunt (or the shunt is known) how do you alter the scan?
A: You reduce the number of particles. If the normal amount of particles is around 500K,
you would reduce it to around 100K.
Q: What if the patient has pulmonary hypertension?
A: Same deal - reduce the particles
Q: Particle reduction is the same as dose reduction?
A: Nope. You keep the dose the same - otherwise the study is non-diagnostic.
Q: What about a neonate? Do you do anything different?
A: Yes - major particle reduction. Down to 10K - 50K. particles (depending on who you
ask). The reason is that kids have less capillaries than adults. An adult number of
particles (500K) could functionally cause a PE - by blocking the majority of the
capillaries.
Q: What if you see a unilateral perfusion defect (of the whole lung), but no ventilation
defect ?
A: Get a CT or MRI. DDx is gonna be a mass, fibrosing mediastinitis, or Central PE.
Q: Of those which is the MOST COMMON?
A: Most sources will say “central obstructing mass” i.e. “bronchogenic carcinoma”
Q How do you grade this unilateral perfusion defect (of the whole lung), but no
ventilation defect ?
A: It’s technically low probability.
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Gallium-67 Scan
The body handles Ga+3 the same way it would Fe+3 - which as you may remember from
step 1 gets bound (via lactoferrin) and concentrated in areas of inflammation, infection,
and rapid cell division. Therefore it’s a very non-specific way to look for infection or
tumor. Back in the stone ages this was the gold-standard for cancer staging (now we use
FDG-PET). I should point out that Gallium can also bind to neutrophil membranes even
after the cells are dead, which gives it some advantages over Indium WBC - especially in
the setting of chronic infection.
Gallium is produced in a cyclotron via the bombardment
of Zn-68, at which point it’s complexed with citric acid to
make Gallium Citrate. The half life is around 3 days
(78 hours). It decays via electron capture, emitting gamma
rays at 4 photopeaks:
93 keV - 40%
184 keV - 20%
300 keV - 17%
393 keV - 5%
Images are not typically done sooner than 24 hours -
because background is too high. The critical organ is the
colon. Remember “critical organ” = the first organ to be
subjected to radiation in excess of the maximum allowable
amount.
Normal localization: Liver (which is the highest uptake), bone marrow ( “Poor Mans s
bone scan”), spleen, salivary glands, lacrimal glands, breasts (especially if lactating, or
pregnancy). Kidneys and bladder can be seen in the first 24 (faintly up to 72 hours). Faint
uptake in the lungs can be seen in < 24 hours. After 24 hours you will see some bowel. In
children the growth plates and thymus.
“Poor Man's Bone Scan ” - Uptake is in both cortex (like regular bone scan) and marrow.
Degenerative change, fractures, growth plates, all are hot - just like bone scan.
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Gallium uptake is nonspecific and can be seen with a variety of things including infection,
but also CHF, atelectasis, and ARDS.
Sarcoidosis:
The utility of Gallium in Sarcoidosis patients is to help look for active disease. Increased
uptake in the lungs is 90% sensitive for active disease (scans are negative in inactive
disease). Additionally, Gallium can be used to help guide biopsy and lavage - if looking to
prove the diagnosis. The degree of uptake is graded relative to surrounding tissue (greater
than lung is positive, less than soft tissue is negative).
Classic Signs:
• Lambda Sign - The nuke equivalent to the “1-2-3 Sign” on Chest x-ray. You have
increased uptake in the bilateral hila, and right paratracheal lymph node.
• Panda Sign - Prominent uptake in the nasopharyngeal region, parotid salivary gland,
and lacrimal glands. This can also been seen in Sjogren's and Treated Lymphoma.
Other Noninfectious Things
• Gallium can be used to show early drug reaction from chemotherapy (Bleomycin) or
other drugs (Amiodarone).
• Gallium is elevated in IPF (idiopathic pulmonary fibrosis) and can be used to monitor
response to therapy.
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Immunosuppressed Patients
• PCP - Gallium Hot, Characteristic Gallium Pattern is Diffuse Bilateral Pulmonary
Uptake
• Kaposi Sarcoma - Gallium Negative, Thallium Positive
Galium-67 - Pneumonia
- Lung Uptake at 72 Hours
• Bacterial Pneumonia - Intense lobar configuration without parotid or nodal uptake.
Misc Infections That Gallium Can Pick Up:
• Abdominal and Pelvic Infections - In-111 WBC is superior to Gallium
(Gallium has some normal GI uptake).
• Malignant Otitis Media - Will be both Gallium and Bone Scan (Temporal Bone) Hot.
• Spinal Osteomyelitis - Gallium is superior to Indium WBC for spinal infections.
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SECTION 4:
Th yr o i d
The thyroid likes to drink Iodine (it’s sort of its job). Imaging takes advantage of this with
Iodine analogs. The distinction between “trapping” and “organification” is a common
question.
• “Trapping” - Analog is transported into gland. I23I, 1311, and 99mTc all do this.
• “Organification ” - Analog is oxidized by thyroid peroxidase and bound to tyrosyl
moiety. 123I and 131I do this. 99mTc does NOT do this. Instead 99mTc slowly washes
out of the gland.
Tracer options / pros and cons.
I-131: The major advantage here is that it’s cheap as dirt. The disadvantage is that it has a
long half life (8 days), and that it’s a high energy (364 keV) beta emitter. The high energy
makes a crappy image with a 1/2 inch crystal. It’s ideal for therapy, not for routine imaging.
It’s contraindicated in kids and pregnant women.
Trivia: Thyroid formation takes place in fetus at 8-12 weeks.
I-123: This guy has a shorter half life (13 hours) and ideal energy (159 keV). It decays via
electron capture and all around makes a prettier image. The problem is that it costs more.
Tc-99m: Remember that this guy is trapped but not organified. Background levels are higher
because only 1-5% of the tracer is taken up by the thyroid gland. A common scenario to
choose Tc over Iodine is when they’ve had a recent thyroid blocker on board (iodinated
contrast is the sneaky one).
Random Trivia on Breastfeeding
(You know they love this shit):
• Tc-99m: You can resume breast feeding in 12-24 hours
• I-123: You can resume breast feeding in 2-3 days
• I-131: You should not breast feed - pump and dump.
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Iodine Uptake Test:
You give either 5 µCi of 131 or 10-20 µCi of 123. This is conventionally reported
at 4-6 hours, and 24 hours. Normals are 5-15% (4-6 hours), and 10-35% at 24 hours. A
correction for background is done on measurements prior to 24 hours (using the neck counts
- thigh counts).
Factors affecting the test
• Renal Function (increases stable iodine pool, reduces numbers)
• Dietary Iodine - variable and controversial
• Medications - thyroid blockers, Nitrates, IV Contrast, Amiodarone
Increased Uptake Decreased Uptake
Graves Primary or secondary causes of Hypothyroidism
Early Hashimoto Renal Failure
Rebound after Abrupt withdrawal of antithyroid Medications (thyroid blockers, Nitrates, IV
medication Contrast, Amiodarone)
Dietary Iodine Deficiency Dietary Iodine Overload
Graves Disease:
About 75% of the time, if you have hyperthyroidism the
cause is going to be graves. Graves is an autoimmune
disease where an antibody to the thyrotropin receptor
stimulates the thyroid to produce hormone. TSH will be
very low, where T3 and T4 will be high. The classic
clinical scenario is a middle aged women with a protracted
course, pre-tibial edema, and exophthalmos. Scintigraphy
is going to give you a homogeneously increased gland,
with uptakes increased at both 4 hours and 24 hours. Graves
Sometimes the 24 hour uptake is lower than the 4 hours (or -Diffuse Homogenous Uptake
even at a normal range) - this is from rapid thyroid
hormone production.
Visualization of the pyramidal lobe: The pyramidal lobe is seen in about 10%
of normal thyroids. In patients with Graves disease it is seen as much as 45%
of the time. Therefore, it’s suggestive when you see it.
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Multi-nodular Toxic Goiter (Plummer Disease): The classic scenario is an
elderly women with weight loss, anxiety, insomnia, and tachycardia. The gland is typically
heterogeneous, with uptake that is only moderately elevated. The nodules will be hot on the
background of a cold gland.
Toxic Multi-nodular Goiter vs Non-Toxic Multi-nodular goiter:
The toxic goiter will have hot nodules on a background of cold thyroid. The Non-toxic one
will have warm/hot nodules on a normal background of the thyroid.
Graves Toxic Multi-Nodular Goiter
Uptake High : 70s (typically > 50%) Uptake Medium High: 40s (typically <50%)
Homogenous Heterogeneous
Hashimotos:
The most common cause of goitrous hypothyroidism (in the US). It is an autoimmune
disease that causes hyper first then hypothyroidism second (as the gland bums out later). It’s
usually hypo - when it’s seen. It has an increased risk of primary thyroid lymphoma.
Step 1 trivia; associated with autoantibodies to thyroid peroxidase (TPO) and anti-thyroglobulin.
The appearance of the hypothyroid gland is typically an inhomogeneous gland
with focal cold areas. The hyperthyroid (acute) gland looks very much like Graves with
diffusely increased tracer.
Subacute Thyroiditis:
If you have a viral prodrome followed by hyperthyroidism, and then thyroid uptake scan
shows a DECREASED % RAIU you have de Quervains (Granulomatous thyroiditis).
During this acute phase, the disease can mimic Graves with a low TSH, high T3 and high T4.
The difference is the uptake scan. After the gland bums out, it may stay hypothyroid or
recover. If they ask you about this, it’s most likely going to try and fool you into saying
Graves based on the labs, but have a low % RAIU.
Solitary Nodules
20-40% Cold Nodules = Cancer
< 1% Warm Nodules = Cancer
Hot Nodule vs Cold Nodule:
Most thyroid nodules are actually cold, and therefore most are benign (colloid, cysts, etc..).
In fact, cold nodules in a multi-nodular goiter are even less likely to be cancer compared to a
single cold nodule. Having said that, cold nodules are much more likely to be cancer when
compared to a functional (warm) nodule.
Discordant Nodule: This is a nodule that is HOT on Tc-99m but COLD on I-123. Because some
cancers can maintain their ability to trap, but lose the ability to organify a hot nodule on Tc, it
shouldn’t be considered benign until you show that it’s also hot on 123I
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Gamesmanship: Iodine vs Tc
A classic move is to show you a thyroid that will take up Tc, but NOT Iodine on 24 hour
imaging. This can be from a couple of things: (1) congenital enzyme deficiency that
inhibits organification, (2) a drug like propylthiouracil that blocks organification.
Now if they just show you an Iodine Thyroid with low uptake on 24 hours, this is de
Quervains, or a burned out Hashimotos.
Radioiodine Therapy
131I can be used to treat both malignant and non-malignant thyroid disease.
Cancer
Actual subtypes and pathology of thyroid cancer have been discussed at length in the
endocrine chapter. However, just a few points that are relevant to discuss here. Papillary is
the most common subtype (papillary is popular), and it does well with surgery + I-131.
Medullary thyroid CA (the one the MENs get), does NOT drink the I-131 and therefore
doesn’t respond well to radiotherapy. Prior treatment can also make you more resistant to
treatment, and re-treatment dosing is typically 50% more than the original dose.
Things that make you treatment resistant: Medullary Subtype CA
• Medullary Subtype CA (will not drink the Neuroendocrine in origin, so can
tracer) occasionally (around 10%) have uptake on
• History of prior I-131 (“easy gland has been MIBG or Octreotide. They will be cold on
thyroid scan and don’t drink the treatment
killed off’) I-131. If forced to pick - I’d go with
• History of Methimazole treatment (even if Octreoscan for medullary CA.
years ago)
Associated with MEN 2a and 2b
So, normally the patient gets diagnosed and then they go for surgery. After surgery they will
come to nuclear medicine. You expect that they will have some residual thyroid (it’s really
hard to get it all out). Prior to actually treating them you will give them a tiny dose of I-131 to
see how much thyroid they have left. If the uptake is less than 5% this is ideal. Uptake more
than 5% will result in a painful ablation (may need steroids on top of the NSAIDs) and may
need to go back to the OR. Next, you will treat them. You want their TSH really ramped up.
The higher the TSH the thirstier the cancer /residual thyroid tissue. An ideal TSH is like 50
(30 would be a minimum).
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Radioiodine Therapy - Continued
How do you get the TSH up?
• There are two ways;
(1) is to stop the thyroid hormone (post op they are obviously hypothyroid),
(2) is to give recombinant TSH “Thyrogen.”
How do you decide on dosing?
• Dosing is dependent on the stage of the disease; 100 for thyroid only, 150 for thyroid
+ nodes, 200 for distal. They are told about the precautions etc... Then you give them
the dose. Before you let them go home, you test them to see if they need to go to the
hospital.
So when do patients need to be admitted to the hospital?
• NRC limit is 7 mR/h measured at 1 meter from the patient’s chest (some agreement
states use 5 mR/h). The number to remember is 33 mCi of residual activity (or 30 mCi
in some strict agreement states).
Possible Side Effects of Treatment:
• Can cause pulmonary fibrosis if given to patient with lung mets. This is really only
the case of macro-nodular disease (as opposed to micronodular disease). That isn’t
necessarily a contraindication
• Sjogren's have a greater risk of salivary gland damage
• Salivary gland damage is dose related - so cancer treatment patients have a greater risk
What routes does the body use to eliminate I-131?
• Urine is the main way it is eliminated but sweat, tears, saliva, and breast milk are other
routes.
If they don’t need to be admitted to the hospital, what precautions should they take?
• There is a whole bunch of crap they are asked to do. Drink lots of water (increase renal
excretion). Suck on hard candy (keep radiotracer from jacking your salivary glands).
Patients are encouraged to stay away from people (distance principal). Sleep alone for
3 days (no sex, no kissing - keep that dirty dick in your pants!). Good bathroom
hygiene (flush twice, and sit down if you are a guy). Use disposable utensils and
plates. Clothes and linens should be washed separately. Most of these things are done
for 3 days.
Is it ok to breast feed? Is it ok to try and get pregnant?
• No breast feeding. If you take 131I your breast feeding days are over (at least this time
around).
• No getting pregnant for at least 6-12 months after therapy
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Radioiodine Therapy - Continued
Other Trivia:
• If you participated in the therapy, you need your thyroid
checked 24 hours later. Gamesmanship
• If the patient got admitted to the hospital the RSO needs to - Iodine Post Treatment -
inspect the room after discharge before the janitor can
clean it or the next patient can move in. If you see an Iodine Scan,
• Thyroglobulin is a lab test to monitor for recurrence. and you see uptake in the
Anything over zero - after thyroidectomy, is technically liver , this is ALWAYS a post
abnormal, although the trend is more important (going up treatment scan.
is bad)
• Severe uncontrolled thyrotoxicosis and pregnancy are
absolute contraindications.
Classic Scenario - Patient is on dialysis and needs 131I Rx
Give 131I immediately following dialysis to maximize the time the 131I is on board. Decrease
dose as there is limited (essentially no) excretion until next dialysis. Dialysate can go down
sewer. Dialysis tubing needs to stay in storage.
Hyperthyroidism:
Why not just treat if they are
I131 can also be used to treat hyperthyroidism. Dosing depends
experiencing severe thyrotoxicosis ?
on the etiology; 15 mCi for Graves (more vascular), 30 mCi
for multi nodular (harder to treat the capsule). Again the TSH Supposedly you should never treat
must be high for the therapy to be effective. By 3-4 months, severe thyrotoxicosis because you risk a
there should be clinical evidence of resolution of signs and thyroid storm (fever, hypertension,
symptoms of hyperthyroidism, if I-131 therapy was etc). Most people will say to block
them with meds, and cool them off.
successful.
Having said that, the risk of a true
As an aside, there is no such thing as an “emergent storm is probably exaggerated and you
hyperthyroid treatment.” You can always use meds to cool it will hear people say “fuck it dude, treat
down. The standard medication is Methimazole. However, if them” ... but even the wildest gun
there is an allergy to Methimazole, the patient is having WBC slingers will still give beta blockers to
issues (side effect is neutropenia) or the patient is pregnant reduce the risk of cardiac
-use propylthiouracil (PTU). PTU is recommended during complications.
pregnancy.
What about Thyroid Eye Disease? It’s controversial, but some people believe that thyroid eye
disease will worsen after I-131 treatment. If you are prompted, I would just have optho look at
their eyes, bad outcome is likely severity related. *You might not want to treat a bug-eyed dude
(depends on who you ask).
Wolff-Chaikoff Effect: Since we arc talking about hyperthyroid treatment, there is no better time than
to discuss the W.C. effect. Essentially, this is a reduction in thyroid hormone levels caused by ingestion
of a large amount of iodine. The Wolff-Chaikoff effect lasts several days (around 10 days), after which
it is followed by an "escape phenomenon." The W.C. effect can be used as a treatment principle
against hyperthyroidism (especially thyroid storm) by infusion of a large amount of iodine to suppress
the thyroid gland. The physiology of the W.C. effect also explains why hypothyroidism is sometimes
produced in patients taking several iodine-containing drugs, including amiodarone.
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SECTION 5:
PARATHYROID
What Causes Hyperparathyroidism?
• Most common cause is a hyperfunctional adenoma (85%).
• Second most common cause is multiple gland hyperplasia (12%).
• Third most common cause is cancer (3%).
Nuclear medicine can offer two techniques to localize these lesions; dual phase, and dual tracer.
Dual Phase Technique
In dual phase technique, a single tracer (Tc-99m Sestamibi) is administered, and both early (10 min)
and delayed (3 hours) imaging is performed. The idea is that sestamibi likes things with
lots of blood flow, and lots of mitochondria. Parathyroid pathology tends to have both of
these things, so the tracer will be more avid early, and stick around longer (after the tracer
washes out of normal tissue). SPECT can give you more precise localization.
Initial Phase Delayed Phase
-Both Thyroid and -Uptake Remains in
Parathyroid Abnormal Parathyroid
(Hyperplasia in this case)
Trivia: Sestamibi parathyroid imaging depends on mitochondrial density and blood flow
False Positives: Caused by things other than parathyroid pathology that like to drink Sestamibi.
• Thyroid Nodules
• Head and Neck Cancers
• Lymphadenopathy
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Dual Tracer Technique
In dual tracer technique two different agents are used and then subtraction is done. The first
agent is chosen because it goes to both thyroid and parathyroid (options are either Tc-99m-
Sestamibi or 201-Thallium Chloride). The second agent is chosen because it only goes to the
thyroid (options are either I-123 or Pertechnetate). When subtraction is done, anything left hot
could be a parathyroid adenoma.
Problems:
• Mo Tracers, Mo Problems
• Motion: subtraction imaging can’t tolerate much motion
• Stuff Messing with the Thyroid Tracers: recent iodinated contrast, etc...
Tc - Sestamibi I-123 Subtraction Ultrasound Correlation
Parathyroid Adenoma - Shown on Dual Tracer Method
The parathyroid gland can be surgically implanted into the forearm - typically done with hyperplasia
surgery where they carve out 3½ glands.
Successful surgical treatment of hyperparathyroidism is often defined as intra-operative reduction of
PTH by 50%.
False Positives: Thyroid adenoma (most common), thyroid cancer, parathyroid cancer.
False Negative: Small sized adenoma (most common), 4 gland hyperplasia. A negative study in the
setting of abnormal / suspicious labs should raise concern for these things (multiple gland
hyperplasia or a small adenoma).
Gamesmanship - MIBI - Lymph Nodes
On any study, parathyroid or a heart, if the tracer is MIBI than you should NOT sec lymph
nodes. If you see lymph nodes they are suspicious (maybe cancer). Next step would be
ultrasound to further evaluate them.
Oh, and don’t forget about focal breast uptake (also cancer), - Breast Specific Gamma
Imaging (BSGI) uses MIBI for a reason.
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SECTION 6:
CNS Ima g i n g
The goal of brain imaging in nuclear medicine is to evaluate function (more than anatomy).
Typically you are dealing with SPECT brain (seizures, ischemia), FDG Brain (dementia), and
Cisternograms / shunt studies.
This is the general idea:
I want to start out talking about 3 of the agents that are commonly used in CNS Nukes;
HMPAO, ECD, and DTPA. The focus of course is on how questions can be asked about
these tracers. First let’s group them:
Extracted (Can be used for Parenchymal Imaging)
HMPAO
ECD
NOT Extracted (Not used for Parenchymal Imaging - i.e. no SPECT)
DTPA
HMPAO and ECD are very similar, and any time you have similar things, someone will be
scheming about how to ask a question about the one or two ways they are slightly different.
On the next page I’m going to compare and contrast these agents - and their potential uses.
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THIS vs THAT - - HMPAO and ECD
Tc-99m HMPAO (hexamethylpropyleneamine oxime) and Tc-99m ECD (ethyl cysteinate dimer).
HMPAO and ECD can be used in both dementia imaging and for seizure focus localization.
These studies are typically performed with SPECT. The idea behind brain SPECT is that you
can look at brain blood flow, which should mimic metabolism. These two agents are neutral
and lipophilic, which lets them cross the blood brain barrier and accumulate in the brain.
Where and how much they accumulate should follow flow (and metabolism).
As I mentioned previously, the two tracers have similarities and differences, and the contrast
between them lends well to multiple choice tests.
HMPAO ECD
Neutral and Lipophilic Neutral and Lipophilic
Accumulate in the cortex proportional to Accumulate in the cortex proportional to
blood flow (Gray Matter > White Matter) blood flow (Gray Matter > White Matter)
Washout is fast Washout is slow (more rapid clearance
from blood pool)
Uptake favors the frontal lobe, thalamus, and Uptake favors the parietal and occipital lobes
cerebellum * Makes comparison between HMPAO and
ECD difficult
Key points:
• Both agents pass blood brain barrier and stick to gray matter proportional to CBF
• HMPAO washes out faster
• ECD washout is slower, has better background clearance, and does not demonstrate
intracerebral redistribution.
The Other Guy - 99m
Tc-DTPA
Unlike HMPAO or ECD, this agent is lipoPHOBIC - and is best thought of as an
“angiographic tracer” because it stays in the blood (or CSF if you put it there).
Key Points:
• DTPA does NOT cross the blood brain barrier and therefore cannot be used for brain
parenchymal imaging. *You can NOT do SPECT
• Has the advantage over HMPAO and ECD in that it can be repeated without delay
• DTPAs main utility is for shunt studies, NPH, and Brain Death.
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Seizure Focus:
The goal of nuclear imaging regarding
seizures is to attempt to localize a
seizure focus (sometimes they do ok if
they cut it out).
The idea is that a seizure focus will
be hot (hypermetabolic and
hyperperfusion) during the seizure
“ictal.” Then cold between seizures
“interictal.” You need to inject tracer
(HMPAO or ECD) within 30 seconds
of the seizure to get a good study.
PET can be used, but is less practical.
Thallium-201
Thallium is produced in a cyclotron, decays via electron capture, and has a half life of
around 3 days (73 hours). The major emissions are via the characteristic x-rays of its
daughter product Mercury 201 - at 69 keV and 81 keV. The tracer is normally given as a
chloride and will therefore rapidly be removed from the blood
Thallium behaves like potassium, crossing the cell membrane by active transport (Na+/K
pump). Tumors and inflammatory conditions will increase the uptake of this tracer.
The higher the grade tumor, the more uptake you get. As Thallium requires active
transport, it can be thought of as a viability marker - you need a living cell to transport it.
Normal Distribution: Thyroid, salivary glands, lungs, heart, skeletal muscle, liver, spleen,
bowel, kidneys, and bladder. Any muscle twitching will turn hot.
If you are going to use it with Gallium, you must use the Thallium first as the Gallium
will scatter all over the Thallium peaks.
High Yield Generalizations / Uses:
• Toxoplasma Infection is Thallium Negative
• Lymphoma is Thallium Positive
• Kaposi Sarcoma is Thallium Positive (Gallium Negative)
• Tumor is Thallium Positive
• Necrosis is Thallium Negative
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Tumor vs Necrosis:
The tracers used for SPECT tumor studies are different than
those used for dementia or seizures. The tumor tracers are Tumor vs Necrosis
201Tl (more common) and 99mTc Sestamibi (less common).
201Tl is a potassium analog, that enters the cell via the Na/K
Thallium Hot,
pump. Inflammatory conditions will increase the uptake of this Tumor
HMPAO Cold
tracer, but not as much as tumors. The higher the tumor grade,
the more intense the uptake. Thallium can be thought of as a
marker of viability, as it will localize in living tumor cells, and
Thallium Cold,
not necrosis. The control is the scalp (abnormalities will have Necrosis
HMPAO Cold
greater uptake than the scalp). You can use Thallium in
combination with perfusion tracers (HMPAO).
CNS Lymphoma vs Toxoplasmosis:
As discussed in the neuro chapter CNS lymphoma
Typically CNS lymphoma, toxoplasmosis,
vs CNS Toxoplasmosis can be a diagnostic bacterial abscess, cryptococcus infection,
dilemma. Thallium has a role in helping to and tuberculosis are all positive on Ga-67
scintigraphy.
distinguish the two (Toxo Cold, Lymphoma
Hot). Please refer to the neuro chapter for CNS lymphoma will be positive on Tl-201.
additional discussion.
Brain Death
You are looking for the absence of intracerebral perfusion to confirm brain death. So that
you don’t keep Grandma around as a piece of broccoli, you need to have a tourniquet on the
scalp - otherwise you might think scalp perfusion is brain perfusion and say she’s still alive.
You have to identify tracer in the common carotid - otherwise the study must be
repeated. In the setting of brain death, tracer should stop at the skull base. The hot
nose sign, is seen secondary to perfusion through the external carotid to the maxillary
branches. As a point of trivia - the hot nose sign cannot be used to call brain death , it is a
“Secondary Sign.” Some institutions will say you have to image the kidneys (to prove
adequate systemic circulation / perfusion) and the injection site (to prove the tracer didn’t
extravasate).
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Stroke
There is no reason, ever, under any circumstances known to man, women, or beast to ever, ever
use SPECT to diagnose stroke. Having said that, you can look at stroke with SPECT and will
therefore likely be asked questions about it.
The big take home points are this:
• Acute Stroke is Cold
• Subacute Stroke can he warm - from luxury perfusion (blood flow is more than dead
cells need)
• Chronic Stroke is Cold
Ischemia (TIAs)
You can evaluate for cerebrovascular reserve by first giving acetazolamide (Diamox) - which
is a vasodilator , followed by a perfusion tracer. Normally you should get a 3-4x increase in
perfusion. However, in areas which have already maxed out their auto regulatory
vasodilation (those at risk for ischemia) you will see them as relatively hypointense. These
areas of worsening tracer uptake may benefit from some revascularization therapy.
PRE-DIAMOX POST-DIAMOX
Worsening Uptake = Ischemia
This might benefit from
revascularization. Next Step = Angio
Bottom Line = Ischemic Tissue Looks WORSE (relatively) compared to surrounding tissue,
after vasodilation (Diamox / Acetazolamide)
Gamesmanship = Diamox = Acetazolamide... don’t just remember one.
You don’t know which one they will use.
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FDG-PET
PET can assess perfusion (l5O-H2O) but typically it uses 18FDG to assess metabolism (which
is analogous to perfusion). Renal clearance of 18FDG is excellent, giving good target to
background pictures. Resolution of PET is superior to SPECT.
It’s important to remember that external factors can affect the results; bright lights
stimulating the occipital lobes, high glucose (> 200) causes more competition for the tracer
and therefore less uptake, etc...
The most common indication for FDG Brain PET is dementia imaging. Because blood flow
mimics metabolism HMPAO, and ECD can also be used for dementia imaging and the
patterns of pathology are the same.
Dementia is discussed in detail in the neuroradiology chapter. Please refer to the
masterpiece that is the neuro chapter in volume 2 for additional details.
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CSF Imaging
The principle involved in imaging the CSF consists of intrathecal administration that will
safely follow CSF and remains in the CSF compartment until it is absorbed through the
conventional pathways. The most common tracer used is 111 In - labeled DTPA. So, you
have to do an LP on the dude (it’s intrathecal).
Normal Examination
• Time Zero - You do the LP
• 2-4 hours it ascends and reaches the basal cisterns
• 4 hours - 24 hours it flows around the sylvian fissures and interhemispheric cistern
• At 24 hours it should clear from the basilar cisterns and be over the cerebral
convexities
Abnormal Examination (general principles)
• Tracer in the lateral ventricles
• Failure to clear from the cisterns and localize over the convexities by 24 hours
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Communicating Hydrocephalus:
Normal pressure hydrocephalus is wet, wacky, and wobbly (incontinent, confused, and ataxic)
clinically, and demonstrates “ventricular enlargement out of proportion to atrophy” on CT.
On scintigraphy you are looking for:
• Early entry (4-6 hours) of tracer in to the lateral ventricles
• Persistence of tracer in the lateral ventricle > 24 hours
• Delay in Assent to the parasagittal region > 24 hours
NPH -
Persistent
Tracer in the
Ventricles
> 24 Hours
Since radiotracer shouldn’t normally enter the ventricles, a radionuclide cisternogram cannot be used
to distinguish communicating from noncommunicating hydrocephalus. Historically (1930s) you could
tell by injecting the material directly into the lateral ventricles.
THIS vs THAT. NPH vs Non Obstructive (Communicating) Hydrocephalus.
NPH will have a normal opening pressure on LP.
CSF Leak:
You can use CSF tracers to localize a leak. The most common sites of CSF leak (fistulas) arc between
the cribriform plate and ethmoid sinuses, from the sella turcica into the sphenoid sinus and from the
ridge of the sphenoid to the car. The study is like a bleeding scan, in that the leak must be active
during the test for you to pick it up.
How is it done? You image around the time the CSF is at the basilar cisterns (1-3 hours) and also
image pledgets (jammed up the nose prior to the exam). You compare tracer in the pledgets to serum
(ratio greater than 1.5 is positive).
Shunt Patency:
There arc a bunch of ways to do this. Most commonly, Tc labeled DTPA is used (111In - labeled DTPA
could also be used). Usually, the tracer is injected straight into the tubing.
• Normal Test will show tracer in the peritoneum - shows distal end is patent.
• You can manually occlude the distal limb to force tracer into the ventricles - shows proximal end
is patent.
• If the tracer fails to reflux into the ventricles, or it docs but then doesn’t clear, you can think
proximal obstruction
• If there is delayed tracer flow into the peritoneum (> 10 minutes = delayed), this can mean partial
distal obstruction.
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SECTION 7:
GI NUKES
Gastric Emptying : Believe it or not, this study is actually considered the “gold standard”
to evaluate gastric motor function. The primary indication is typically gastroparesis (usually in
a diabetic). The exam should be performed fasting (at least
4 hours). Some texts say that it should be done in the first 10
days of the menstrual cycle to prevent hormones from Standard Meal
interfering (I’m sure this recommendation is evidence based). - 4 oz of Egg Whites
Most commonly Tc labeled sulfur colloid is used on a - 2 Slices of White Bread
standardized liquid meal, solid meal (egg whites), or both. - Strawberry Jam
Solids are more sensitive, but you can have emptying - Water
problems from liquids only and normal emptying from
- Tc Sulfur Colloid
solids.
Gamesmanship: One sneaky way to test this would be related
to the differences between solid food and liquid food curves. The main point is that solids have a
“lag phase” in which the stomach helps grind up the food into smaller parts (liquids don’t have
this). Lag Time can be increased
in diabetic patients.
Gamesmanship: Another possible
question is that “attenuation
correction” plays a role in
calculation of emptying times, as
movement from the back of the
stomach to the front can increase
counts due to attenuation.
Pharmacology Trivia:
• Prokinetic drugs (which enhance gastric emptying) metoclopramide (Reglan), tegaserod
(Zelnorm), erythromycin, and domperidone (Motilium) are stopped at least 2 days prior
to the test. - this can cause a false negative exam.
• Opiates (which delay gastric emptying) are stopped 2 days prior to the test. These can
cause a false positive exam.
• Anticholinergic/Antispasmodic drugs such as Donnatal, Bentyl, Robinul, and Levsin, are
stopped for 2 days prior to the test
• Serotonin receptor antagonists - the classic one being Ondansetron (Zofran) are fine and can
be given prior to the exam.
Esophageal Transit: Used (rarely) in the evaluation of esophageal motility disorders.
The supposed advantage is the ability to give quantitative information. The patient is made to
fast overnight, then fed Tc-99m sulfur colloid. Dynamic imaging is performed and transit time
and /or residual esophageal activity is measured.
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GI Bleeding: GI bleed scan sensitivity
The goal of a GI bleeding scan is to localize the bleed (not to say there = 0.1 ml/min
is one). Bleeding scan is sensitive to GI bleed rates as low as at 0.1
Angiogram sensitivity =
ml/min (Mesenteric angiography requires 1-1.5 ml/min bleeding).
1.0 ml/min
First Some Technical Stuff (Very Boring and High Yield)
Before the Tc-99m can be tagged to a RBC (beta chain of the hemoglobin); it must first be reduced.
This is accomplished with stannous ion (tin). This is referred to as “tinning.” There are 3 methods:
In Vivo
1. Tin (stannous ion) is injected into the patient
2. Then Tc-99m pertechnetate is injected
3. Tin binds to the hemoglobin then reduces the Tc (which then binds)
Although the process is super simple, you only get about 60-80% of it bound. So you have
a lot of free Tc and a dirty image (poor target to background). Sometimes it fails miserably
(via drug interaction - heparinized tubing, or recent IV contrast). The images are too
crappy for cardiac wall motion studies, but can work for GI bleeding.
In Vivo - In Vitro (Modified Method)
1. Tin (stannous ion) is injected into the patient
2. After 15-30 mins, you pull 3-5 cc of blood out of an IV line into a syringe with both
Tc-99m pertechnetate and an anticoagulant
3. It’s then re-injected 10 mins later
This one does a little better, binding close to 85%. Drug interactions (like heparin) are the
most common cause of failure.
In Vitro
Blood is withdrawn and added to a kit with both Tin (stannous ion) and Tc. It’s then re-
injected. This method works the best (98% binding), but is the most expensive.
Image Acquisition: GI bleeding scan is acquired with DYNAMIC imaging (as opposed to 5 min
static, transmission, SPECT, or dual tracer protocol). This allows the detection of
intermittent bleeds and better localization of the origin of the bleed.
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Reading the Study: You are looking for; You can get faked out by a lot of stuff; renal
or bladder excretion (possibly with hydro),
(1) Tracer outside the vascular distribution transplant kidney (classic trick - but again it
won’t move), varices or angiodysplasia (these
(2) Tracer that Moves like bowel shouldn’t move), a penis with blood in it (this
will look like a penis), hemangioma (this will
(can be antegrade or retrograde) be over the liver or spleen - and not move),
and the last trick - Free Tc in the stomach.
(3) Tracer that Increases Intensity over time
It you see gastric uptake* next look at the
salivary glands and thyroid to confirm it’s
The distal colon is an exception to the rule of free Tc, and not an actual bleed.
mobility — tracer here may not move.
Normal Scan - No Abnormal Tracer Abnormal Scan - Abnormal Tracer
Accumulation. Normal Uptake in Blood accumulation at the Hepatic Flexure,
Pool, Liver, & Heart. increases over time. SMA territory.
Rapid Review of Vascular Territories (localization on GI bleed exam helps direct
angiographic therapy to the specific vascular territory — plus it’s an easy way to ask a
multiple choice question).
• Celiac: Distal Esophagus, Stomach, 1st part of the Duodenum
• SMA: 2nd - 4th Parts of the Duodenum, the rest of the small and large bowel to the
transverse colon at the level of the splenic flexure.
• IMA: Distal 1/3 of the Transverse Colon to the Proximal Rectum
Alternative (Stone Age) Way of Doing A Bleeding Scan; Back when dinosaurs roamed the
earth, they used to do bleeding scans with Tc Sulfur Colloid. This had a variety of
disadvantages: fast clearance (had to do scan in 30 mins), multiple blind spots (the stomach,
splenic flexure, and hepatic flexures - as sulfur colloid goes to the liver and spleen normally).
The only possible advantages are that it requires less prep and has good target to background.
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Meckel Scan:
The Meckel Diverticulum is a remnant of the
omphalomesenteric duct located near the
distal ileum. These things can have ectopic
gastric mucosa and present with painless
bleeding in the pediatric population.
Pertechnetate is used because it is taken up
by gastric mucosal cells. So you are looking
for tracer uptake in the pelvis (usually RLQ)
around the same time as the stomach.
Only about 10-30% of Meckel's diverticulum
will have gastric mucosa (these are the ones
most likely to bleed).
Meckel Scan
Here are the Tricks:
• You need to do the study when the patient is NOT bleeding (if they are bleeding -
then do a bleeding scan).
• Pre-Treatmenf. You can use a bunch of different stuff to make the exam better:
Pentagastrin - enhances uptake of pertechnetate by gastric mucosa (also
stimulated GI activity)
H2 Blockers (Cimetidine and Ranitidine) block secretion of the pertechnetate
out of the gastric cells making it stick around longer.
Glucagon - slows gastric motility.
• False Positive: Can occur from bowel irritation (recent scope, laxative use)
• False Negative: Recent In vivo labeling of RBCs , Recent Barium Study
(attenuated)
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HIDA Scan:
Function and integrity of the biliary system can be evaluated by using Tc-99m labeled tracers that mimic
bilirubin’s uptake, transport, and excretion. All the tracers are basically analogs of this iminodiacetic acid
stuff. Trivia: You need higher doses of tracer if the patient has hyperbilirubinemia
Prep for the test is diet control. You need to have not eaten within four hours (so your gallbladder is ready
to fill), and have eaten within 24 hours (so your gallbladder isn’t so full, it can’t let any tracers in). If you
haven’t eaten for over 24 hours, then CCK can be given. CCK makes the GB contract.
Normally, the liver will have prompt tracer uptake (within 5 minutes), then you will have excretion into
the ducts, then the bowel - pretty much the same time you see the gallbladder. If the gallbladder is sick
(obstructed), it will still not have filled within 60 min. This is the basic idea.
Acute Cholecystitis: Almost always (95%) patients with acute cholecystitis have an obstructed cystic
duct. If you can’t get tracer in the gallbladder within 4 hours, this suggests obstruction.
Rim Sign Cystic Duct Sign:
A curved area of increased activity
This sign is seen with acute
along the gallbladder fossa (hot
cholecystitis. The sign describes a
rim, or pericholecystic hepatic
nub of activity in the cystic duct, with
activity sign) suggests a more
the
angry gallbladder - (supposedly
seen in 20% of gangrenous
cholecystitis).
Mechanism of the Rim Sign: The mechanism is the result
of inflammation causing regional hepatic hyperemia, with
more radiopharmaceutical being delivered to this area of
hepatic parenchyma;
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Chronic Cholecystitis: This can be shown two ways; (1) delayed filling of the GB (not
seen at 1 hour, but seen at 4 hours), or (2) with a low EF (< 30%) with CCK stimulation. A
reduced EF can also be seen in acute acalculous cholecystitis.
Testable Trivia
- The Dose of CCK: 0.02 microgram/kg over 60 mins
- The Dose of Morphine 0.02-0.04 mg/kg over 30-60 mins
Biliary Obstruction: The classic way to show this is a lack of visualization of the
biliary tree - sometimes call a “Liver Scan Sign.” It’s caused by back pressure in an
obstructed CBD.
Prompt Uptake - With Delayed Excretion (Medication)
Cholestatic jaundice can be drug induced. The classic offenders:
Chlorpromazine, Erythromycin, Birth Control (Estrogens), Anabolic
Steroids, and sometimes Statins. This can mimic biliary obstruction.
THIS vs THAT: Biliary Atresia VS Neonatal Hepatitis
If you see a hepatobiliary scan (HIDA) in a kid, for sure this is the indication. Apparently,
these two things are hard to tell apart clinically. If you see tracer in the bowel it’s hepatitis,
but just remember that it might be slow so you need super delays (24 hours if necessary). If
you don’t see it in the bowel, you might still need to repeat the study if you didn’t charge up
those hepatocytes with some phenobarb (up regulates the cytochrome system). In other
words, a lot of places pre-medicate with phenobarbital to increase the utility of the test. If
you operate early (Kasai procedure) they do a lot better, so it’s important not to screw this up.
Trivia: Dose of Phenobarb to prime the liver = 5 mg/kg x 5 days Technically it’s 2.5 mg/kg
"5 for 5 keeps the liver alive ” twice a day - but that
doesn’t rhyme
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Bile Leak
You can use HIDA tracer after
trauma or surgery to look for bile
leak. The trick is that you need
delayed images, and look in the right
paracolic gutter / pelvis. You can get
tracer in the gallbladder fossa,
mimicking a gallbladder.
Reappearing Liver Sign - Labeled
bile may track superiorly into the
peri-hepatic space and coat the
surface of the liver. This can give the
appearance of paradoxically
increasing activity in the liver after
an initial decrease in activity from
liver emptying into the bowel.
HIDA Scan - Rapid Path Summary:
No Bowel Activity, Persistent Blood Pool = Hepatocyte Dysfunction (Hepatitis)
No Bowel Activity, Blood Pool Goes Away Normally = Common Duct Obstruction
No Gallbladder Activity x 4 hours (or 1 hour + morphine) = Acute Cholecystitis
Abnormal GB emptying (EF < 30%) = Chronic Cholecystitis
Narcotics
Most people will say something like - “hold the morphine for at least 6 hours — or 3 half lives -
prior to the HIDA scan.” Having said that narcotics alone should not prevent you from seeing the
gallbladder. What narcotics can do is delay bowel visualization by triggering the sphincter of oddi
to contract. This can mimic a biliary obstruction.
Don’t get it twisted - morphine is not the devil - it is a tool. Remember you will give moiphine to
help promote visualization of the gallbladder in the scenario where there is dumping of the tracer
into the small bowel, but no GB activity seen.
Never inject CCK and morphine within 30 minutes of one another. Why Not? It would be bad.
Try to imagine all life as you know it stopping instantaneously and every molecule in your
body exploding at the speed of light— Total protonic reversal.
Elevated Bilirubin
Elevated bilirubin (total > 5 mg/dl) will increase the number of non-diagnostic/inconclusive and
false negative exams.
Gamesmanship: Increased renal activity can suggest elevated bilirubin
Next Step: Alternative agents DISIDA and BROMIDA arc preferred over HIDA in the setting of
high levels of bilirubin
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Sulfur Colloid Liver Scan
Not frequently done because of the modem invention of CT. Sulfur Colloid tagged with Tc is quickly
eaten by the liver’s reticuloendothelial system. It can be used to see “hot” and “cold” areas in the liver.
Classically, the multiple choice question is Focal Nodular Hyperplasia is Hot on sulfur colloid
(although in reality it’s only hot 30-40% of the time).
Sulfur Colloid Liver Scan
Hepatic Adenoma COLD
FNH 40% HOT, 30% COLD, 30% Neutral
Cavernous Hemangioma COLD (RBC Scan HOT)
HCC COLD (Gallium HOT)
Cholangiocarcinoma COLD
Mets COLD
Abscess COLD (Gallium HOT)
Focal Fat COLD (Xe HOT)
Particle size is worth discussing briefly. Particles for this scan need to be 0.1 - 1.0 micrometers. This
is the right size for the liver to eat them. If they are too big the spleen will eat them, and if they are too
small the bone marrow will eat them. Also, realize that if they were too big they would get stuck in the
lungs like a V/Q on the first pass through.
Colloid Shift - In a normal sulfur colloid scan, 85% of the colloid is taken up by the liver (10%
spleen, 5% bone marrow). In the setting of diffuse hepatic dysfunction, portal hypertension,
hypersplenism, or bone marrow activation you can see change in uptake - shift to the spleen and bone
marrow. The most specific causes of colloid shift are cirrhosis, diffuse liver mets, diabetes, and blunt
trauma to the spleen.
Diffuse Pulmonary Activity - This is not normal localization of sulfur colloid. This is non-specific
and can be seen with a ton of things (most commonly diffuse liver disease), but the first thing you
should think (on multiple choice) is excess aluminum in the colloid. It can also be seen in primary
pulmonary issues (reflecting phagocytosis by pulmonary macrophages).
Renal Activity on Sulfur Colloid = The most common cause is CHF (maybe due to decreased renal
blood flow and filtration pressure). Alternatively, in the setting of renal transplant - this can
indicate rejection (due to colloid entrapment within the fibrin thrombi of the microvasculature).
Other more rare causes include coxsackie B viral infection, disseminated intravascular coagulopathy,
and thrombotic thrombocytopenic purpura.
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Hemangioma Scan
You can “prove” a liver lesion is a hemangioma with a Tc Labeled RBC scan.
Why would you do that instead of using MRI or CT ? Well... lots of reasons.
(1) Maybe you got sucked into an interdimensional vortex and landed in an alternate reality
where Taco Bell makes better French Fries than McDonalds, Adolf Hitler cured cancer,
MRI and CT were never invented, and only scintigraphy is available for the
characterization of hemangiomas.
(2) Or... or., uhhh maybe you uhhh had a stroke and lost access to the part of your brain that
remembers how to read MR or CT.
(3) Or., maybe you are trying to win a bet.
So, you can see why it would be reasonable to ask about this on an intermediate level exam.
How is this study done ? Using Tc labeled RBCs with anterior and posterior projection
images . Delayed blood pool is typically done (30 mins - 3 hours).
What if it is small? “Small” is actually the most common reason for a false negative exam.
You need the thing to be at least 1.5 cm, otherwise your sensitivity really drops off. You
could try SPECT but first you seriously need to consider what you are doing with your life.
What is the classic look ? You want to see marked HOT on delays, with no real hot spot
on immediate flow or immediate pool. Angiosarcoma could be HOT on delays but would
also be hot on flow. A partially fibrosed hemangioma may be a false negative.
Spleen Scan
You can use Tc Sulfur Colloid or heat damaged Tc labeled RBCs to localize to the spleen. A
possible indication might be hunting ectopic spleen.
Fatty Changes
A fatty liver can alter the distribution of several tracer. Examples:
• Reduced uptake in the Liver on Tc Sulfur Colloid - including the possible reversal of
normal liver > spleen uptake pattern (Colloid Shift).
• There will be increased uptake in a fatty liver with Xenon-133.
• Trivia - FDG-PET uptake in the liver is not altered by background steatosis.
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SECTION 8:
GU NUKES
Imaging of GU system in nuclear medicine can evaluate function (primary role), or it can
evaluate structure.
Function (Dynamic):
Normal kidney function is 80% secretion and 20% filtration. Tracer choice is based on which
of these parameters you want to look at.
Tc-DTPA: Almost all filtered and therefore a great agent for determining GFR. A piece of
trivia is that since a small (5%) portion of DTPA is protein bound (and not filtered) you are
slightly underestimating GFR. Critical organ is the bladder.
Tc-MAG3: This agent is almost exclusively secreted and therefore estimates effective renal
plasma flow (ERPF). It is cleared by the proximal tubules. Critical organ is the bladder.
Tc-GH (glucoheptonate): This agent can be used for structural imaging (discussed later in this
section), or functional imaging as it is filtered. Critical organ is the bladder.
Tc DTPA Tc MAG 3 Tc GH
Filtered (GFR) Secreted (ERPF) Filtered
Good For Native Kidneys with Concentrated better by kidneys Good for dynamic and cortical
Normal Renal Function with poor renal function imaging.
Critical Organ Bladder Critical Organ Bladder Critical Organ Bladder
There are essentially 5 indications for dynamic (functional) scanning: (1) Differential
Function (2) Suspected Obstruction, (3) Suspected Renal Artery Stenosis, (4) Suspected
Complication from Rental Transplant, (5) Suspected Urine Leak.
Some basics:
Images are obtained posteriorly (anterior if patient has a transplant or horseshoe).
Typically dynamic exams have 3 phases: blood flow phase, cortical phase, and clearance
phase.
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Differential Function
This is a basic exam with the standard flow, cortical, and clearance phases.
Flow: Begins within 20 seconds of injection. Flow will first be seen in the aorta. Then as it
reaches the renal arteries, the kidneys should enhance symmetrically and about equal to the
aorta (at that time).
Flow
Decreased (symmetric) Technical Error - poor bolus
Renal Artery Thrombosis
Renal Vein Thrombosis
Decreased (asymmetric) Chronic High Grade Obstruction
Acute Rejection
Acute Pyelonephritis
Increased (asymmetric) Renal Artery Aneurysm
An important piece of trivia is that ATN, Interstitial Nephritis, and Cyclosporin toxicity
will all have normal perfusion/flow.
Cortical (parenchymal): This is the most important portion of the exam (with regard to
differential function). An area of interest in drawn around the kidneys and a background area
of interest is also drawn (to correct for the background). This can be screwed up by drawing
your background against the liver or spleen (which is not true background since they will take
up some tracer). You want to measure this at a time when the kidney is really drinking that
contrast, but not so late that it is putting it in the collection system. Most places use around 1 min.
A steep slope is good.
Clearance (excretory): Radiotracer will begin to enter the renal pelvis, collecting system, and
bladder. In a normal patient, you will be down to half peak counts at around 7-10 mins. If
you wanted to quantify retention of tracer you could look at a 20/3 or 20/peak ratio.
20/3 or 20/peak ratio: This is a method of quantifying retention of radiotracer by comparing
the peak count at 20 minutes with the peak count at 3 mins (normal < 0.8) or the peak count
(normal 0.3).
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Suspected Obstruction (“The Lasix Renogram”)
The exam is performed the same as a standard dynamic exam (blood flow, cortical, and
clearance), with a 30 minute wait after clearance. If there is still activity in the collecting
system, a challenge is performed with Lasix. The idea is that a true obstruction will NOT
respond to Lasix, whereas a dilated system will empty when overloaded by Lasix. The study
can be done with MAG3 or DTPA. MAG3 does better with patients with poor renal
function, and thus is used more commonly.
The exam is interpreted as follows:
• No obstruction = tracer clears from
collecting system without need for
Lasix
• No obstruction = Washout of 50% of
the tracer within 10 minutes of Lasix
administration
* Indeterminate = Washout of 50% of
the tracer within 10-20 minutes of
Lasix administration
The most common cause for
this indeterminate result is a
very dilated pelvis and
subsequent “reservoir effect.”
• Obstructed = Washout taking longer
than 20 mins after Lasix administration
Source of False Positive for Obstruction:
• Poor response to Lasix - secondary to bad renal function, or dehydration at baseline
• “Reservoir Effect” - very dilated renal pelvis, delaying transit time
• Back Pressure Effects - Full or Neurogenic Bladder can generate back pressure and
not let the kidneys empty (can be resolved with a foley catheter).
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Suspected Renal Artery Stenosis
The study can be performed in one
of two ways (both using MAG3
as the typical tracer). The first is
a standard dynamic study,
followed by ACE inhibitor. The
second is a baseline study with ½
dose, followed by a full dose of
ACE inhibitor. A “normal
study” will occur if there is no
difference between the baseline
Normal Exam - No Difference Between Pre and Post
and the captopril studies.
The appearance of RAS will vary depending on the tracer given:
• DTPA - Remember
this is a GFR tracer. A
sick kidney will have
decreased uptake
and flow, because of
loss of perfusion
pressure.
• MAG3 - Remember
this is a Secreted tracer.
A sick kidney will have
marked tracer
retention, with a curve
similar to obstruction.
If it’s bilateral up or bilateral down, it’s not RAS. If the baseline study has asymmetrically
poor function, that isn’t positive for RAS, you need to see it worsen (> 10%).
Trivia related to ACE inhibitor administration: they need to stop their ACE inhibitor prior to
the renal study (3-5 days if captopril). They should be NPO for 6 hours prior to the test (for
PO ACE inhibitors).
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Suspected Complication from Renal Transplant
ATN vs Rejection: The most common indication for nuclear medicine in the setting of renal
transplant is to differentiate rejection from ATN. ATN is usually in the first week after
transplant, and is more common in cadaveric donors. There will be preserved renal perfusion
with delayed excretion in the renal parenchyma (elevated 20/3 ratio, delayed time to peak).
ATN usually gets better. There is an exception to this rule, but it will confuse the issue with
respect to multiple choice, so I’m not going to mention it. Cyclosporin toxicity can also look
like ATN (normal perfusion, with retained tracer) but will NOT be seen in the immediate post
op period. Rejection will have poor perfusion, and delayed excretion. A chronically rejected
kidney won’t really take up the tracer.
Immediate Post
In a Normal DMSA or ATN ATN Perfusion Excretion
OP (3-4 days
Normal Delayed
(with MAG 3 tracer), the post op)
nephrographic appearance is Cyclosporin Perfusion Excretion
the same. Tracer in the Toxicity Long Standing
Normal Delayed
cortex, and that's it.
Acute
Immediate Post Poor Excretion
Rejection
OP Perfusion Delayed
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Suspected Complication from Renal Transplant Cont...
Fluid Collections: Fluid collections seen after a transplant include urinomas, hematomas,
and lymphoceles. All 3 can cause photopenic areas on blood pool imaging.
• Urinoma: Usually found in the first 2 weeks post op. Delayed imaging will show
tracer between the bladder and transplanted kidney. The primary differential in this
time period is the hematoma. A hematoma is not going to have tracer in it.
Urinoma = Hot with Tracer
Hematoma = No Tracer
• Lymphocele: Usually found 4-8 weeks after surgery. The cause is a disruption of
normal lymphatic channels during perivascular dissection. Most are incidental and
don’t need intervention. If they get huge, they can cause mass effect. This will look
like a photopenic area on the scan.
Hematoma Urinoma Lymphocele
Timing Early (< Month) Early (< Month) Late (> Month)
Blood Pool COLD - No Tracer COLD - No Tracer COLD - No Tracer
Delay COLD - No Tracer HOT with Tracer COLD - No Tracer
Vascular Complications: Both arterial and venous thrombosis will result in no flow or
function. If you suspect renal artery stenosis (most common at the anastomosis), you can do
a captopril study, with results similar to RAS if there is a stricture.
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Structure
If you want to look at the renal cortex, you will want to use an agent that binds to the renal
cortex (via a sulfhydryl group). You have two main options with regard to tracer.
•99mTc-DMSA: This is the more commonly used tracer. It binds to the renal cortex and is
cleared very slowly. Critical organ is the kidney (notice other renal tracers have the
bladder as their critical organ).
•99mTc GH (glucoheptonate): This is less commonly used and although it binds to the
cortex, it is also filtered and therefore can be used to assess renal flow, the collecting
system, and the bladder. Critical organ is the bladder.
DMSA is the preferred cortical imaging agent in pediatrics, because it has a lower dose to the
gonads (even though its renal dose is higher than 99mTc GH).
Indications for the exam:
• Acute Pyelonephritis: Can appear as (a) focal ill-defined area of decreased uptake,
(b) multifocal areas of decreased uptake, (c) diffuse decreased uptake - in an
otherwise normal kidney.
° Scarring and Masses can also appear as focal areas of decreased uptake -
although scarring usually has volume loss.
• Column of Bertin vs Mass: Simply put, the mass will be cold. The Column of Bertin
(normal tissue) will be take up tracer.
The trick on DMSA is just like reading CXR or Chest CT - you need to know if it is acute
or chronic. The clinical history changes your DDx.
• Defects on DMSA with acute renal problems - pyelo.
• Defects on DMSA with chronic renal problems = scar (or mass).
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Testicular
This hasn’t been done in the United States since 1968, therefore it is very likely to be on the
test. The study is basically a blood flow study. The primary clinical question is testicular
torsion vs other causes of pain (epididymitis). The tracer used is sodium pertechnetate
(Na99mTcO4). Oh, don’t forget to tape the penis out of the way - tape it up, not down like is
required for the male residents on mammography rotations.
• Normal - Symmetric low level flow to the testicles.
• Acute (early) Torsion - Focal absence of flow to the affected side (“nubbin sign”).
• Delayed (late) Torsion - Sometimes called a missed torsion. The appearance is a
halo of increased activity, with central photopenia.
• Testicular Abscess - Identical to delayed torsion - halo of increased activity, with
central photopenia.
• Acute Epididymitis- Increased flow and blood pool to the affected side.
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SECTION 9:
PET f o r Ca n c er
As mentioned before, 18-FDG is cyclotron produced and decays via beta positive emission to
18-O. The positron gets emitted, travels a short distance, then collides with an electron
producing two 511 keV photons which go off in opposite directions. The scanner is a ring
and when the two photons land 180 degrees apart at the same time the computer does math
(which computers are good at) to localize the origin.
A CT component is fused over the PET portion. This is done for two reasons:
(1) Anatomy - so you can see what the hell you are looking at.
(2) Attenuation Correction - Dense stuff will slow down the photons, and the CT
allows for correction of that. It also leads to errors, the classic one being a metallic
pacemaker looks bright hot on the corrected image (the computer overcorrected). This
is a classic question. The answer is look at the source images (uncorrected).
Some other technical trivia is that FDG enters the cell via a GLUT 1 transporter and is then
phosphorylated by hexokinase to FDG-6-Phosphate. This locks it in the cell. Normal bio
distribution is brain, heart, liver, spleen, GI, blood pool, salivary glands, and testes. The
collecting system and bladder (critical organ) will also be full of it, because that’s where it’s
getting excreted.
Variable areas of uptake: Muscles (classic forearm muscle uptake in the nervous chair
squeezing patient). Breast and ovaries in females at certain stages of the menstrual cycle.
Thymus in younger patients. Lastly, brown fat around the neck, thorax, and adrenals
(especially in a cold room).
Ways to minimize brown fat uptake: Keep the room warm. Medications like
benzodiazepines or beta blockers.
Insulin and Blood Glucose:
• High Blood Glucose (> 150-200): The more glucose the patient has, the more
competition is created for the FDG and you will have artificially low SUVs.
* Insulin: So why not just give the patient some insulin??? It will drive it all into the
muscles. This is a classic trick. PET with diffuse muscle uptake = Insulin
Administration
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Consequences of being fat:
• Fat people will have HIGHER SUV values, because the fat takes up less glucose
• You leave the house in high heels... and come back home in flip flops
When do you image? Following therapy; an interval of 2-3 weeks for chemotherapy and 8-12 weeks
for radiation is the way to go. This avoids “stunning” - false negatives, and
inflammatory induced false positive.
Who do you image? The main utility is extent of disease, and distal metastatic spread. Local
invasion is tricky with a lot of things. Usually straight up CT or MRI is better for local
invasion and characterization.
What if you see the right ventricle ? The RV is not typically seen on PET unless it’s enlarged.
If you see the RV think about RVH.
FDG Concentration at time “T”
SUV =
(Dose / Body Weight)
Tumors that are PET COLD Not Cancer but PET HOT
BAC (Adeno In Situ) - Lung Cancer Infection
Carcinoid Inflammation
RCC Ovaries in Follicular Phase
Peritoneal Bowel/Liver Implants Muscles
Anything Mucinous Brown Fat
Prostate Thymus
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Special Situations - FDG PET Cancer Trivia
• Focal Thyroid Uptake - Requires Further Workup - might be cancer, might be nothing
• Diffuse Thyroid Uptake - Most often Autoimmune (Hashimoto) Thyroiditis
• RCC are COLD (usually), Oncocytomas are HOT
• COLD Ground Glass Nodule = Cancer, HOT Glass Nodule = Infection
• The Reason HCC is often cold (60%) is that it has variable glucose-6- phosphatase and
can’t trap the FDG
• Testicular cancers skip right to the retroperitoneum. The trivia is the seminomatous CA
is FDG hot, whereas non-seminomatous tends to be FDG COLD (or Luke Warm).
• While it’s OK for ovaries to be hot in functional (ovulating) young people, Grandma
should NOT have FDG up-take in her dried-up raisin ovaries. This is suspicious - next
step Ultrasound.
• Metformin is classic for causing false positive bowel uptake. The uptake is typically
intense and diffuse. It tends to favor the colon (small bowel to a lesser extent).
• Adrenal Glands - mild uptake is normal. In general, an adrenal pathology is typically
considered malignant if the uptake is higher than the liver (used as an internal control).
Although this does not really hold up that well in my experience (especially since liver
uptake is variable). For example, Adrenal Adenomas can have moderate uptake (still
usually not super hot).
• Lymphoma
• Most Lymphoma is Super Hot
• Thymic Rebound vs Recurrent Lymphoma: Thymic Hyperplasia (or Rebound) can be
“Warm” on PET, but recurrent Lymphoma should be HOT. Also, Rebound tends to
maintain the normal thymus look (it sorta drapes over the heart). Lymphoma is round
like a ball. A hot ball of death, or a “great ball of fire”
• Extranodal marginal zone lymphomas, including the mucosa-associated lymphoid
tissue (MALT) marginal zone lymphoma, have been shown to have LOW Avidity for
FDG.
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Special Situations - FDG PET Cancer Trivia
Gynecologic and Genitourinary
GYN PET
False Positives False Negatives
Physiologic FDG in the endometrium.
Two described peaks of FDG
Necrotic, Mucinous, Cystic, or
(1) Rag Week / Menstruation (first 4 days of
Low-grade Cancers — you gotta correlate with
cycle) and (2) Ovulation (~ day 14) and
US and/or MRI to avoid looking stupid.
menstruation may mimic disease.
Physiological uptake in the endometrium is 50% of RCC may not be FDG avid
usually diffuse. Cancer is usually more focal.
You won’t see this in postmenopausal women
Physiologic FDG in the ovaries. Small-volume peritoneal disease and small
Seen during ovulation lymph nodes — can be missed because they
are small, can also be missed because the
Typically appears as ovoid or a rim of activity adjacent bowel (which has physiological uptake)
with a photopenic center. masks them
You won’t see this in postmenopausal women
Endometrial or ovarian FDG activity in the
postmenopausal = suspicious (next step
ultrasound)
Benign lesions:
• Uterine Fibroids
• Benign Endometriotic Cysts
Misregistration: Focal uptake in the ureter or the Perivesical disease - can be missed because of
bladder - if mapped incorrectly can simulate the high uptake in the adjacent bladder — look
disease. at source images (uncorrected)
Main strategy to reduce this artifact is to
minimize the time between the PET and CT
acquisitions
Vesicovaginal fistulas (common in advanced
disease) — can falsely elevated SUV values by
spilling urinary FDG excretion
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Special Situations - FDG PET Cancer Trivia
Osteosarcoma and Bone Misc...
• Remember secondary osteosarcomas (the ones from Paget's, Radiation, Multiple
Chondromas, etc....) are the bad mother fuckers. They have by far the worst outcome.
• Back in the stone ages - if you got diagnosed with an osteosarcoma they assumed that
80% of the time you had distal mets. This was prior to effective chemotherapy for
osteosarcoma... it was basically a death sentence. They do better now (little bit).
• Typically mets go to (a) second bone sites, and (b) the lungs. Remember the classic
vignette of a spontaneous pneumothorax in an osteosarcoma patient = lung met.
• With the modem addition of effective chemo, accurate staging and restaging actually
matters - and this is why I’m rambling on about osteosarcoma. PET may/could
actually play a key role in treatment and is therefore testable.
• Average SUV is used at some institutions for describing tumor metabolism. Most
literature says you should use the SUV Max for describing osteosarcoma - because it’s
a very heterogenous tumor.
• Multiple papers have shown a correlation between tumor grade and FDG uptake (SUV
values). Higher SUV Max = Higher Tumor Grade.
• Baseline SUV Max is an independent and significant predictor of overall survival
(more = bad). Having said that PET is not typically used for baseline staging.
• An important point is that especially with bone stuff, nukes is highly non-specific.
Remember earlier in the chapter I said several B9 bones lesions are hot on 99mTc-MDP?
Same thing with PET. Giant Cell is the classic example. Lots of cases of GCTs have
higher SUV than sarcomas. Fibrous dysplasia is another classic that can be hot on
PET.
• There is no cutoff to tell the difference between a B9 bone lesion and a bone sarcoma.
Same deal with infection. Osteomyelitis can have very high FDG uptake.
• Important point = Because PET is so nonspecific, it is NOT used clinically to avoid
biopsy.... but can sometimes guide biopsy.
• The most important prognostic factor = response to preoperative (neoadjuvant)
chemotherapy.
• There is a proven positive correlation of FDG uptake and viable tumor tissue. In other
words, F18-FDG PET can be used to evaluate the effectiveness of neoadjuvant
chemotherapy.
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SECTION 10:
No n -PET f o r Ca n c er
In-111 Octreoscan
111In Pentetreotide is the most commonly used agent for somatostatin receptor imaging. The
classic use is for carcinoid tumors, gastrinomas, paragangliomas, merkel cell tumors,
lymphoma, small cell lung cancer, medullary thyroid cancer, and meningiomas.
111Indium
Indium is produced in a cyclotron and decays with a 67 hour half life via electron capture.
It produces two photopeaks at 173 keV and 247 keV. Just like Gallium, In-111 in a liquid
will carry a +3 valence and behaves like Fe+3, with the capability of forming strong bonds
with transferrin.
The most common application is to bind it to WBC,
although it can also be hooked to octreotide, or DTPA
for CNS imaging (cisternography). Basically, you can
hook indium to almost anything if you hook it first to
a strong chelator like DTPA. As a point of trivia, you
need to isolate the WBCs prior to labeling because the
transferrin in the blood binds with greater affinity and
will out-compete them.
Trivia: Meningiomas take up Octreotide (and Tc MDP).
As a point of trivia, there are 5 somatostatin receptors but 111In Pentetreotide can only bind to
two of them. The scan works because 80% of neuroendocrine tumors express these two
receptors.
Normal uptake is in the thyroid, liver,
gallbladder, spleen, kidneys, bladder, and GI
tract. Imaging is done in early and delayed
phase. The advantage of the early phase (4 hours)
is that the bowel activity is absent.
The delayed is done to clarify that the
abdominal tracer is of GI origin. Meningioma - Hot on Octreotide and Tc MDP
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MIBG
MIBG is an analog of noradrenalin and is therefore taken up by adrenergic tissue. MIBG is
first line for tumors like pheochromocytoma, paraganglioma, and neuroblastoma. You can
have MIBG with either I-123 or I -131. I-123 is better because it has better imaging quality.
I-131 is cheaper, and the long half life allows for delayed imaging.
Blocking the Thyroid Gland: The thyroid gland should be blocked, to prevent unintended
radiation to the gland from unbound I-123 or I-131. This is accomplished with Lugol’s Iodine
or Perchlorate. Sometimes you’ll see “SSKI" which is Super Saturated Potassium Iodine
Biodistribution: Normal in liver, spleen, colon, salivary glands. The adrenals may be faintly
visible. Note the kidneys are NOT seen.
Trivia: MIBG is superior to MDP bone scan for neuroblastoma bone mets. *If you see a
skeleton on MIBG the answer is diffuse bone mets.
Trivia: MIBG is better for Pheo than In-111 Octreotide. MIBG is better than CT or MRI for the
extra-adrenal Pheos.
Medication Interaction with MIBG - High Yield Trivia
Certain medications interfere with the workings of MIBG and must be held.
Medications include calcium-channel blockers, labetalol (other beta-blockers have no
effect), reserpine, tricyclic antidepressants and sympathomimetics.
THIS vs THAT: MIBG Scans
What’s Different Between
Patient “A” and “B” - who
both recently got MIBG
Scans?
Patient B - Forgot to take
her Lugol’s !
So, she just cooked her
thyroid.
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Gamesmanship - MIBG
Brown Fat - Just like you can see it on FDG PET (around the shoulders / traps) you can also see
it with MIBG. In fact, it’s the MOST COMMON variant in 123I MIBG bio distribution.
Mechanism? Apparently brown fat has sympathetic innervation.
Utility: The classic use for MIBG is Neuroblastoma. But.... if someone wanted to get sneaky
they could also show you a pheochromocytoma, paraganglioma, or carcinoid on MIBG.
Essentially any catecholamine producing tumor. See the chart on the next page for specifics.
Gamesmanship - Octreotide:
Octreotide Mechanism Nitty Gritty: Octreotide works as an analog to somatostatin and will
bind to the same receptors as somatostatin. Well... sorta. Technically, there are 5 subtypes of
somatostatin receptors and Octreotide will only bind to 2 of them. As you can imagine, the
sensitivity of the agent is going to depend on which receptors are expressed by the tumor.
Fortunately, most tumors express those 2 receptors.
Suspected Insulinoma: Some sources will say that Octreotide can trigger hypoglycemia in the
setting of an insulinoma. What to do about this seems to vary a lot on who you ask and what you
read. Some places will say to give them some IV solution with glucose before and during the
administration of Octreotide. Other places will just say have D50 ready just in case.
What should you do if both of those options are choices on the exam? Simply read the mind of
the person who wrote the question and choose the correct answer.
Already on Octreotide Therapy: You will need to stop the treatment for 3 days prior to giving
the labeled agent.
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MIBG Octreotide
Octreotide and MIBG are
Inferior Superior
Carcinoid similar for detection of Liver
(Sensitivity 50-70%) (Sensitivity 80-90%)
Mets
SHIT
Insulinoma Insulinoma is usually B9
(Sensitivity ~ 30%)
Good Gastrinoma is usually
Gastrinoma
(Sensitivity ~ 85%) Malignant
Crap Crap
Non-Functional
(No Function, (No Function, FDG PET is the test of choice.
Islet Cell Tumor
No Receptors) No Receptors)
Superior For Non- Superior For Malignant FDG is also good - but
Malignant (Adrenal) (Extra-Adrenal) Types Octreotide is cheaper - so
Pheo
Types (which is like (which is a minority of people go that route first when
90% of them) them 10%) malignancy is suspected
Less Sensitive and
Less Specific (*only Superior
Paraganglioma
concentrates in the (Sensitivity ~ 95%)
functional subtypes)
Octreotide is still the first line
as a nukes agent. If it’s
Medullary Inferior Superior -
negative (in the setting of
Thyroid CA (Sensitivity 30 %) (Sensitivity 50-80%)
rising calcitonin) the next step
is FDG-PET.
Superior Inferior
Neuroblastoma
(Sensitivity ~ 95%) (Sensitivity ~ 64%)
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Gallium
Gallium can be used for tumors. Remember, it’s very nonspecific with regard to infection,
inflammation, or tumor.
Trivia: During the Cretaceous Period (when many of your attendings trained); Gallium was
used to differentiate residual tumor vs fibrosis, scarring, necrosis etc... in patients with
Hodgkin’s disease and Malignant Lymphoma
Trivia: If you are going to use Gallium for treatment monitoring it’s important to have a pre-
treatment exam (to ensure that the tumor site is actually Gallium - avid).
ProstaScint
111In can be labeled to the antibody Capromab Pendetide (ProstaScint). Capromab is a
monoclonal antibody which recognizes PSA membrane antigen “PSMA” - which is slightly
different that PSA. Pendetide is the chelating agent. In my opinion, the exam is shit and
doesn’t work well.
When do you do the test? If you have a rising PSA and negative bone scan. The purpose of the
study is to look for mets outside the prostate bed (soft tissue mets). If they do not have distal
mets, they can be offered salvage therapy (radiation to the surgical bed). It’s important to not
obsess over the surgical bed, the real question is distal mets. Having said that, the prostate bed
is best seen on the lateral between the bladder and penis.
Testable Trivia: ProstaScint will localize to soft tissue mets, NOT bone mets.
Testable Trivia: ProstaScint’s critical organ is the LIVER.
This confuses some people. Avoid this trap: Indium = WBC. It’s slang to say “Indium Scan”
and people in Nukes just think tagged WBC with Indium. But.... Not all Indium is WBC.
Remember that Octreotide is actually labeled with Indium, and so is a bunch of other stuff.
Bottom LAne: For Critical Organ Trivia
Indium ProstaScint = Liver
Indium WBC = Spleen
Indium Octreotide = Spleen
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Sentinel Node Detection
A sentinel node is the node which receives afferent drainage directly from a primary cancer.
Surgeons want to know where these are at; especially with melanoma and breast cancer. The
agent used for lymphoscintigraphy is 10-50 nm Tc99m sulfur colloid.
Melanoma: Sentinel node mapping is done when you have a lesion between 1 mm - 4 mm deep.
Less than 1 mm you are typically safe. More than 4 mm you are totally screwed and it makes
no difference. The utility of the test is to go after the ones in that middle zone (between
1-4 mm). Intradermal injection in 4 spots around the lesion / excision scar and imaging is done.
Breast Cancer: Cancer drains to the internal mammary chain nodes about 3% of the time.
Knowing this, and which axillary node to go for first, can help avoid aggressive lymph node
dissection. Injections can be done superficial or deep (into the pectoral muscle).
Size Matters
Does particle size matter for sentinel node detection? Yes and No.
The idea is that particles have to be small enough to travel through the lymphatics. A
particle that is 500 nm will not go anywhere. So any answer choice with 500 nm or larger
for a lymph node study is universally incorrect. Now this is where you will read different
stuff (and send me nasty emails). Some sources say < 200 nm. This will probably work,
but you will be waiting all day for the study. The larger the particles the slower the study.
More sources will say <100 nm. This this will work, but again slow study. There is at
least one paper out that advocates for using a 0.22 mm filter (available in most hospital
pharmacies because it is commonly used for sterilization of hyperalimentation solutions).
If you do that you end up with particles that are 10-100 nm. If you use this 0.22 mm filter
method you can routinely visualize lymphatic channels and sentinel nodes within 30 mins
after administration.
Gamesmanship - How do you know what the question writer does at his/her institution?
If it was me - I would pick a choice less than 100 nm. If forced to choose between 100 and
50 - I would pick 50, and there is literature to back you up (not that you’d have a chance to
defend yourself), but practically most places do filter the particles and use small ones.
Test Particle Size
Lymphoscintigraphy < 0.2 microns (< 200 nm)
VQ 10-100 microns (10,000 - 100,000 nm)
Liver Spleen “Unfiltered” - so all sizes big and small
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Breast Specific Gamma Imaging
Tc-99m Sestamibi will concentrate in a breast cancer 6 times more than normal background
breast tissue. It does pretty well, with the sensitivity supposedly near 90%. The technique is
to give 20-30 mCi of Tc-99m Sestamibi in the contralateral arm then image 20 mins later. A
foot injection is often done if you are going to image both breasts. You are supposed to use a
dedicated gamma camera that can mimic a mammogram and provide compression.
Does Breast Density Affect Uptake / Distribution?
Nope. The distribution is homogeneous regardless of density. Having said that, hormonal fluctuation
can increase the background uptake.
When will background activity be lowest?
Around mid-cycle in premenopausal women.
What are some causes of false positive studies?
Fibroadenoma, fibrocystic change, or inflammation can give a false positive
What are some causes of false negative studies?
Lesions that are small (< 1 cm), or deep. Lesions located in the medial breast, and/or those
overlapping with heart activity.
What about lymph nodes?
You see lymph nodes on a “MIBI” scan - this is NOT normal, it is concerning for mets.
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SECTION 11:
Ca r d i a c
Myocardial Perfusion I SPECT:
99mTc Sestamibi and 99mTc Tetrofosmin are the most common tracers. They work by crossing the cell
membrane and localizing in mitochondria (passive diffusion). They don’t redistribute (like
Thallium), giving better flexibility.
Sestamibi vs Tetrofosmin - Tetrofosmin is cleared from the liver more rapidly and decreases the
chance of a hepatic uptake artifact.
Thallium - This is historical with regard to cardiac imaging. It mimics potassium and crosses
the cell membrane first by distribution related to blood flow - second by delayed redistribution
(washout). Washout is delayed in areas with poor perfusion.
Imaging Timing:
99mTc studies (sestamibi and tetrofosmin) are done 30-90 mins after injection - allowing for
clearance from background
Thallium Sestamibi and Tetrofosmin
Old Newer
Crosses cell via Na/K pump Crosses cell via passive diffusion (localizes
in mitochondria)
Redistributes Does NOT redistribute
Imaging must be done immediately after Imaging typically done 30-90 mins after
injection injection to allow for background to clear
Lung/ Heart Ratio: Only done with Thallium. If there is more uptake in the lungs, this
correlates with multi-vessel disease or high grade LAD or LCX lesions.
General Principal: You will sec less perfusion distal to an area of vascular obstruction
(compared to normal myocardium). To improve sensitivity, the heart is stressed. Under stress
you need about 50% stenosis to see a defect (it needs to be like 90% without stress).
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Preparation: Patient shouldn’t eat for 4 hours prior to imaging (decreases GI blood flow). Patients
should (ideally) stop beta-blockers, calcium channel blockers, and long-acting nitrates for 24 hours
prior to the exam - as these meds mess with the sensitivity of the stress portion. There are reasons to
keep people on these meds (they might be getting risk stratification on medical therapy) - but I’d say
for the purpose of multiple choice just know that those medication classes mess with stress imaging
sensitivity.
Protocols: There are multiple ways to skin this particular cat. People will do two day exams; rest then
stress. People will do one day exams stress then rest. The advantage to doing stress first is that you can
stop if it’s normal. Typically the dosing is low for the rest and high for the stress.
Chemical Stress: If you can’t exercise, the modem trend is to give you Regadenoson (coronary
vasodilator) - which is a specific adenosine receptor agonist. It’s specific to a certain receptor having
less bronchospasm than conventional adenosine or dipyridamole. If they get bronchospasm anyway you
need to give them albuterol.
Known Left Bundle Branch Block: A known LBBB will make ECG stress testing non-diagnostic. So
diagnostic imaging (radionuclide myocardial perfusion) is typically the way to go. The important trivia
LBBB Classic Artifact = False Positive Reversible Perfusion Defect at the Septum (anteroseptal
region). Supposedly this has something to do with the septum not relaxing correctly during diastolic
coronary filling (because the rhythm is not totally coordinated with the left sided block).
Pharmaceutic Choice = Adenosine or Dipyridamole is supposedly better for LBBB patients than
Dobutamine. The reason is Dobutamine increases the HR more, and the more rapid the HR, the worse
the septal relaxation stuff is. Dobutamine = More False Positives.
Findings;
Fixed Defect (seen on stress and rest) Scar (prior infarct)
Reversible Defect (seen on stress, better on Ischemia
rest)
Fixed Defect with Reversible Defect around it Infarct with peri-infarct ischemia
Transient Ischemic Dilation From diffuse subendocardial hypoperfusion
(LV cavity is larger on stress) producing an apparent cavity dilation.
Correlated with high risk disease (left main
or 3 vessel).
Fixed Cavity Dilation Dilated cardiomyopathy
Right Ventricular Activity on Rest If has intensity similar to LV then think
right ventricular hypertrophy
Lots of splanchnic (liver and bowel) activity Means you aren’t exercising hard enough -
not shifting enough blood out of the gut.
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THIS vs THAT: Stunned VS Hibernating Myocardium
Stunned: This is the result of ischemia and reperfusion injury. It is an acute situation. The perfusion
will be normal, but contractility will be crap. It will get better after a few weeks.
Hibernating: This is a more chronic process, and the result of severe CAD causing chronic
hypoperfusion. You will have areas of decreased perfusion and decreased contractility even when
resting (just like scar). Don’t get it twisted, this is not an infarct. This tissue will take up FDG more
intensely than normal myocardium, and will also demonstrate redistribution of thallium.
Rapid Review
Ischemia = Will take up less tracer (relative to other areas) on stress, and the same amount of tracer
(relative to other areas) on rest. It’s not normal heart so it won’t contract well.
Scar = Won’t take up tracer on rest or stress (it’s dead Jim). It’s scar not muscle, so it won’t
contract normally either.
Stunned = The perfusion will be normal on both stress and rest, but the contractility is not normal.
Hibernating = Won’t take up tracer on rest or stress (it’s not dead, just asleep - like a bad soap
opera plot). The difference between hibernating muscle and scar is that the hibernating muscle will
take up FDG and redistribute thallium. The defect at rest will resolve / “redistribute” on delayed
thallium imaging. Remember thallium works with the Na/K pump - so cells need to be alive to
pump it in. A truly dead cell won’t have a functioning Na/K pump and therefore won’t be able to
redistribute / resolve the defect.
MUGA (Multigated Acquisition Scan):
This is an equilibrium radionuclide angiogram with cardiac pool images taken after the tracer has
equilibrated to the intravascular space. Drugs like Adriamycin and Doxorubicin can be cardiac toxic.
Oncologists will alter treatment protocols when the LVEF drops (usually by 10%).
Huh? - It’s an angiogram using tagged RBCs. You time (gate) the exam to get pictures that can be used
to estimate the Ejection Fraction (and evaluate motion etc...)
These studies requires gating (the “G” in MUGA). The study is done using Tc-99m labeled RBCs, and
the objective is to calculate an EF (MUGA is more accurate than myocardial perfusion for LVEF).
Photopenic halo around the cardiac blood pool is a classic look for pericardial effusion. Regional wall
motion abnormality on a resting MUGA is usually infarct (could be stunned or hibernating as well).
The easiest way to ask a question about MUGA is also probably the most important practical pearl
(wow... I can’t believe I said that):
• False Low EF: Screwed up LAO view can cause overlap of LV Left Anterior Oblique
with LA or RV or even great vessels - causing a false low EF. (LAO) is the “best septal
Inclusion of the Left Atrium (which happens when it is enlarged) - view” - and the one usually
the result of LA inclusion is inclusion of the LA counts — this used to measure the LVEF.
falsely lowers the EF. A basic internal QA step
when reading these studies
• False High EF: Wrong background ROI (over the spleen), will is to confirm a good
cause over subtraction of background and elevate the EF. photopenic septum.
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Misc Trivia:
Rubidium 82: This is a potassium analog (mechanism is Na/K. pump). This is similar to Tl-201,
and can be used as a similar agent. You can use it for PET myocardial perfusion, although it’s
not used in most places because of cost limitations. Also, because of the very short half life ( 75
seconds) it tends to give a dirtier image compared to PET of NH3.
I say made with a generator, you say Tc-99m and Rubidium. *Rubidium is the only PET agent
made like this, so that instantly makes it a testable fact.
Short Axis Anatomy Review - I always found this confusing:
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Artifacts
Decreased activity in Check for ECG changes and
Breast Tissue anterior wall (may also wall motion. If normal, then
“Soft Tissue Attenuation” affect septal and lateral - call it artifact. If not sure
depending on body habitus) can repeat in prone position.
Check for ECG changes and
Left Hemidiaphragm Decreased activity in
wall motion. If normal, then
“Soft Tissue Attenuation” inferior wall
call it artifact.
Increased activity in inferior
Liver Excretes Tc, so you
wall, can mask true defect.
see it in the liver and bowel.
Subdiaphragmatic Can also mess with
Little bit of exercise can be
Radiotracer Activity “normalization” of the
used to reduce GI blood
ventricle and make the rest
flow.
of the LV look low.
You can repeat because
Patient Motion
Causes all kinds of problems tracer is fixed for around 2
(usually respiration)
hours
Misregistration Causes all kinds of problems
Seen more in exercise or
Reversible or Fixed Septal
Left Bundle Branch Block dobutamine stress compared
Defects , sparing the apex
to vasodilators
Look for matching stress
and rest perfusion patterns
Normal Apical Thinning Normal variant with preserved wall function
to show you this is normal
(and not infarct)
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Medication Trivia:
Mechanism Trivia
Inhibits the breakdown of
adenosine - which builds up.
Dipyridamole No caffeine
Adenosine is a potent
vasodilator.
No caffeine
Side effects are worse than
with dipyridamole. Rare
Adenosine Vasodilator
side effect is AV block -
which will get better when
adenosine short half life
runs out.
Selective A2a - causes fewer
Regadenoson No caffeine
side effects
Patient Can NOT be on a
beta blocker.
Best used in patients who
Beta 1 agonist - acts like
cannot have Adenosine or
exercise by increasing heart
Dobutamine Dipyridamole. Better in
rate and myocardial
patients with COPD or
contraction.
Asthma, or who have taken
caffeine in the last 12 hours.
Avoid with LBBB
Half life is shorter than
Aminophylline Antidote for Adenosine Dipyridamole - so must
continue to monitor.
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SECTION 12:
Th er a py
Treatment for Bone Pain:
There are currently three approved agents for bone pain associated with metastatic disease
from breast and prostate cancer: (1) Sr89-Chloride, (2) Sm153 EDTMP, and (3) Ra223-dichloride.
Why does cancer cause bone pain / bone problems?
Metastatic disease leads to a tumor derived factor that increases osteolytic activity. You end up
with increased fracture risk, osteopenia, and hypercalcemia of malignancy.
Can the patient get external radiation treatment with the therapy?
Yes, External radiation is not a contraindication and can be used with the therapy.
Absolute contraindications (for Sr and Sm) include: Pregnancy, Breastfeeding, and renal
Failure (GFR < 30). Patients with extensive bony mets (superscan) maybe shouldn’t be treated
either * controversial - and therefore not likely tested.
Strontium - Sr89 (Metastron): It works by complexing with the hydroxyapatite in areas where
bone turnover is the highest. It’s the oldest, and worst of the three agents. It is a pure beta
emitter. It has a high myelotoxicitiy, relative to newer agents and therefore isn’t really used.
Samarium - Sm153 (Quadramet): This is probably the second best of the three agents;
“Samarium is a good Samaritan. ” It works by complexing with the hydroxyapatite in areas
where bone turnover is the highest. It is a beta decayer. The primary method of excretion is
renal. Unlike Sr-89, about 28% of the decay is via gamma rays (103 kev) which can be used for
imaging. Does have some transient bone marrow suppression (mainly thrombocytopenia and
leukopenia), but recovers faster than Sr.
Sr89 (Metastron): Sm153 (Quadramet)
15-30% drops in platelet and WBC from pre- 40-50% drops in platelet and WBC from pre-
injection injection
8-12 weeks needed for full recovery 6-8 weeks needed for full recovery
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Radium - Ra223 (Xofigo): This is the most recent of the three agents, and probably the best.
The idea is that Ra223 behaves in a similar way to calcium. It is absorbed into the bone matrix
at the sites of active bone mineralization. Its primary mechanism is the emission of 4 alpha
particles, causing some serious double stranded DNA breaks.
Why is it the best?
(1) It’s an alpha emitter with a range shorter than Sr and Sm. This means less hematologic
toxicity.
(2) At least one trial actually showed a survival benefit in prostate CA.
(3) It has a long half life (11.4 days), allowing for easy shipping.
What are the side effects?
Non-hematologic toxicities are generally more common than hematologic ones; diarrhea,
fatigue, nausea, vomiting, and bone pain make the list.
Trivia: The general population is safe, as the gamma effects are low. Soiled clothing and
bodily fluids should be handled with gloves, and clothes should be laundered separately. A 6 month
period of contraception is recommended although none of this is evidence based (as per
usual).
Sr89 Sm153 Ra 223
Beta Emitter, with some
Pure Beta Emitter Alpha Emitter
imageable gamma rays
Most Bone Marrow Toxicity
Less Bone Marrow Toxicity Least Bone Marrow Toxicity
(longest recovery).
Renal excretion Renal excretion GI excretion
Improves Survival (prostate
mets)
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Yttrium-90
This can be used as a radioembolization method for unresectable liver tumors. This is a pure Beta
emitter that spares most of the adjacent normal liver parenchyma (as the maximum tissue penetration is
about 10 mm).
Prior to treatment with Y-90 the standard is to do a 99mTc MAA hepatic arterial injection. The primary
purpose of this injection is to look for a lung shunt fraction. This fraction needs to be < 10% under
ideal circumstances. You can still use Y-90 for 10-20% shunts but you need to decrease the dose.
Above 20% the risk of radiation pneumonitis is too large.
Particle Size: The optimal particle size is between 20-40 um, as this allows particles to trap in the
tumor nodules, but large enough to get stuck without totally obstructing. If you create a true
embolization the process actually doesn’t work as well because you need blood flow as a free radical
generation source.
Radiation Dose: The dose is typically 100-1000 Gy delivered. The current thinking is that lesions
require at least 70 Gy for monotherapy success.
Imaging: There are 175 Kev and 185 keV emissions you can use to image.
Trivia: The average half life is 2.67 days.
Radioimmune Therapy (RIT):
Monoclonal antibodies can be used with Indium111 , such as ibritumomab tiuxetan (Zevalin) for
refractory non-Hodgkin lymphoma treatment or as a first line treatment.
The idea is that you can give the antibody labeled with Indium111 for diagnostic evaluation of the tumor
burden and then if the biodistribution is ok you can give the antibody labeled with Y-90 for treatment.
Trivia: The antibody binds to the CD-20 receptors on B-cells.
What is considered altered distribution?
(1) Uptake in the lungs is more intense than the heart day one, or more intense than liver on day 2 & 3.
(2) Uptake in the kidneys more than the liver on day 3.
(3) Uptake in the bowel that is fixed, and/or more than the liver
(4) Uptake in the bone marrow > 25%
Trivia: Don’t give to patients with platelets less than 100K
Most Common Side Effect? Thrombocytopenia and neutropenia (about 90% of cases).
Can you send them home post treatment? Dose to caretakers or persons near the patient is low, and they
can be released to the general population after treatment. Although some things like sleeping apart, no
kissing, etc... for about a week are still usually handed out.
Protocol: You need to first give rituximab to block the CD20 receptors on the circulating B cells and
those in the spleen to optimize biodistribution. Then you can give the In111 labeled antibody to assess for
altered biodistribution. If you suspect altered distribution you should get delayed full body imaging at
90-120 hours. If altered you shouldn’t treat. If ok, then blast ’em.
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SECTION 13:
HIGH YIELD
THIS vs THAT:- Critical Organ vs Target Organ:
“Critical Organ” - An organ that limits the dose of the radiopharmaceutical due to the increased
susceptibility of the critical organ for cancer. This may or may not be the “Target Organ.”
“Target Organ” - This is the organ you want the tracer to accumulate in. It’s your organ of interest.
A few generalizations on Critical Organs: If you are trying to
Why all the Controversy ?
figure it out, it’s the organ that the tracer is going to spend the
most time in. For example, Gallium ends up in the bowel. Tc
You will read conflicting
RBC scans are going to end up passing through the heart a lot information for many of these.
unless they are heat treated then the spleen eats them. Tc- Apparently, there is a fair :
MAG3s and DTPA is going to be the bladder, but DMSA (which amount of bickering among :
sticks to the kidney) is going to be the kidney. PhDs on how / when to :
calculate the dose to come up :
with these numbers.
To know which organ to pick :
on the test simply read the :
mind of the person who wrote :
the question.
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Tracer Analog Energy Physical Half Life
Tc-99m “Low” - 140 6 hours
Iodine-123 Iodine “Low”-159 13 hours
125 hours
Xenon-133 “Low”-81
(biologic T½ 30 seconds)
“Low” - 135 (2%), 167
Thallium-201 Potassium (8%), use 71 201Hg 73 hours
daughter x-rays
“Medium” - 173 (89%),
Indium-111 67 hours
247 (94%)
Multiple; 93 (40%),
Gallium - 67 Iron 184 (20%), 300 (20%), 78 hours
393 (5%)
Iodine-131 Iodine “High” - 365 8 days
Fluorine-18 Sugar “High”-511 110 mins
Cardiac Radionuclides
Treatment Radionuclides Half Life
Half Life
50.5 DAYS
Strontium-89 Rubidium-82 75 seconds
(14 days in bone)
Samarium-153 46 Hours Nitrogen-13 10 mins
Radium-223 11 Days
Yttrium-90 64 Hours
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ADH_2020
スキャンした＿ADH_2020
THE CORE EXAM
7th (2020) EDITION
VOLUME 2
WRITTEN & ILLUSTRATED BY:
PROMETHEUS LIONHART, M.D.
スキャンした＿ _2020
SEVENTH ED. -VER.. 5ION 1.0
READER.. 5 AR..E ADVISED - THIS BOOK 15 NOT TO BE USED FOR.. CLINICAL
DEC! 510N MAKIN c;. HUMAN ER..R..OR.. DOES OCCUR.., AND IT 15 yo UR..
R..E5PON5IBILITY TO DOUBLE CHECK ALL FACTS PR..OVIDED. TO THE
FULLEST EXTENT OF THE LAW, THE AUTHOR.. A55UME5 NO
R..E5PON5IBILITY FOR.. ANY INJUR..Y AND/OR.. DAMAGE TO PER.. 50N5 OR..
P R..O PE R..TY AR..I51N G OUT OF OR.. R..ELATED TO ANY U5E OF THE MATER..IAL
CONTAINED IN THIS BOOK.
ISBN: 9781673777888
INDEPENDENTLY PUBLISHED --- PKOMETHEUS LIONHAKT (EAKTH DIMENSION C-137)
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COVEK DESlc;N, TEXTS, AND ILLU5TK ATIONS: COPYKlc;HT © 2019 BY PKOMETHEUS LIONHAKT
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NO SLAVE LABOK (RESIDENT OK FELLOW) WAS USED IN THE CKEATION OF THIS TEXT
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VOLUME 2
WRITTEN&. ILLVSTRAHD BY
PROMETHEV5 LIONHART, M.D.
@10 - NEUKO--9-182
(i) II - MUSCULOSKELED,L --185-302
® 12 -VASCULAIZ-,- 305 - 351
(i) 13 - INTEKVENTIONAL --353-454
® 14 - MAMMO --457-521
® 15 - STKATEc;Y --529-588
VOLUME l:
TOPIC5: PED5, Cl, CV, REPR..ODUCTIVE, ENDOCR..lNE, THOR.. ACIC, CAR..DIAC, NUKES
WAR MACHINE:
TOPl C5: PHY5IC5, NON INTER..PR..ETIVE 5KI LU, BIO5TAT5
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LEGAL STUFF
READER..5 AR..E ADVISED - THIS BOOK 15 NOT TO BE USED FOR.. CLINICAL DECISION MAKINc;.
HUMAN ER..R..OR.. DOES OCCUR.. , AND IT 15 YOUR.. R..E5PON51BILITY TO DOUBLE CHECK ALL
FACTS PR..OVIDED. TO THE FULLEST EXTENT OF THE LAW, THE AUTHOR.. A55UME5 NO
R..E5PON51BILITY FOR.. ANY INJUR..Y AND/OR.. DAMAc;E TO PER..5ON5 OR.. PR..OPER..TY AR..151Nc;
OUT OF OR.. R..ELATED TO ANY USE OF THE MATER..IAL CONTAINED IN THIS BOOK.
AKE RECALLS IN THIS BOOK? AB50LVHL'Y NOT.
THE AUTHOR.. HA5 MADE A CON51DER..ABLE EFFOR..T (IT'S THE OUTR..lc;HT PUR..PO5E OF THE
TEXT), TO SPECULATE HOW Q__UE5TION5 Mlc;HT BE ASKED. A PHD IN BIOCHEMl5TR..Y CAN FAIL
A MED SCHOOL BIOCHEMl5TR..Y TEST OR.. BIOCHEM SECTION ON THE V5MLE, IN SPITE OF
CLEAR..LY KNOWINc; MOR..E BIOCHEM THAN A MEDICAL STUDENT. THIS 15 BECAUSE THEY
AR..E NOT USED TO MEDICINE STYLE Q__UESTION5. THE AIM OF THIS TEXT 15 TO EXPLOR..E THE
LIKELY STYLE OF BOAR..D Q__UE5TION5 AND INCLUDE MATER..IAL LIKELY TO BE COVER..ED,
INFOR..MED BY THE ABR'5 STUDY c;UIDE.
THR..oUc;HOUT THE TEXT THE AUTHOR.. WILL ATTEMPT TO FATHOM THE MANNER.. OF
Q__UE5TIONINc; AND INCLUDE THE COR..R..E5PONDINc; Hlc;H YIELD MATER..IAL. A COR..R..ECT
ESTIMATION WILL BE WHOLLY COINCIDENTAL.
H UM O K / PKOFAN ITY WA KN IN G
I USE PR..OFANITY IN THIS BOOK. I MAKE "c;R..OWN UP" JOKES. PR..OBABLY NOT A
c;ooD IDEA TO R..EAD THE BOOK OUT LOUD TO SMALL CHILDR..EN OR.. ELDER..LY
MEMBER..5 OF YOUR.. CHUR..CH / TEMPLE / MO5Q__UE. NOW 15 NOT THE OPTIMAL
TIME TO BE R..ECR..EATIONALLY OUTR.. Ac;ED - l'M JUST TR..YINc; TO MAKE THE BOOK
R..EADABLE AND FUN.
I ALSO TALK A ME55 OF SHIT ABOUT DIFFER..ENT MEDICAL 5PECIALTIE5. I DO THIS BECAUSE
RADIOLOc;l5T5 AR..E TR..IBAL, AND 5TR..OKINc; THAT UR..c;E TENDS TO CALM PEOPLE. PR..OBABLY
NOT A c;ooD IDEA TO R..EAD THE BOOK OUT LOUD TO MEMBER.. 5 OF YOUR.. FAMILY THAT AR..E
IN 5PECIALTIE5 OTHER.. THAN RADIOLOc;Y. THE TR..UTH 15 I R..E5PECT ALL THE OTHER.. 5UB-
5PECIALTIE5 OF MEDICINE (EVEN FAMILY MEDICINE) -THOSE AR..E DIR..TY JOBS (POOP, PU5, &.
NOTE WR..IT!Nc;) BUT SOMEONE NEEDS TO DO THEM.
IF you STILL FEEL THE DE51R..E TO EMAIL ME ABOUT HOW I HUR..T YOUR.. FEELINc:;5 AND
R..UINED YOUR.. LIFE, CONSIDER.. THAT "MAYBE PEOPLE THAT CR..EATE TH!Nc:;5 AR..EN'T
CONCER..NED WITH YOUR.. DELICATE 5EN51BILITIE5."
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WHAT MAKES THIS BOOK VNIQ_UE?
5HOKT AN5WEK - FUCK!Nc; EVEKYTHIN(;
HOW ? -WELL FOK 5TAKTEK5, THESE BOOK5 WEKEN'T WKITTEN BY 30 KE51DENTS,
20 FELLOWS, AND 10 TUKBO NEKD ATTENDIN(;S.
INSTEAD THE BOOK5 WEKE WKITTEN BY A KELENTLE55LY 5ELF IMPKOV!Nc; MANIAC,
DKIVEN TO PUK(;E THE HEKETIC5 (OKC SCUM), LAUNCH VEN(;EANCE UPON THl5
PLANET, AND DELIVEK MEKCILE55 JUST! CE UPON THE ENEMIES OF FKEEDOM AND
LfBEKTY.
THE IMPETUS FOK THl5 BOOK WA5 NOT TO WKITE A KEFEKENCE TEXT OK
STANDAKD KEVIEW BOOK, BUT INSTEAD, A 5TK ATE(;Y MANUAL FOK SOLVIN(;
MULTIPLE CHOICE Q__UESTION5 FOK RADIOLO(;Y. THE AUTHOK WISHES TO CONVEY
THAT THE MULTIPLE CHOICE TEST 15 DIFFEKENT THAN OK AL BOAKDS IN THAT YOU
CAN'T ASK THE SAME KINDS OF OPEN-ENDED E55AY-TYPE Q__UESTIONS. "WHAT'S YOUK
Df FFEKENTIAL?"
Q__UESTION!Nc; THE CONTENTS OF ONE'S DIFFEKENTIAL WAS THE ONLY KEAL
Q__UESTION ON OKAL BOAKDS. NOW THAT SIMPLE Q__UESTION BECOMES NEAKLY
IMPO551BLE TO FOKMAT INTO A MULTIPLE CHOICE TEST. INSTEAD, THE FOCUS FOK
TK AININ(; FOK 5UCH A TEST SHOULD BE ON THIN(;5 THAT CAN BE A5KED. FOK
EXAMPLE, ANATOMY FACTS - WHAT 15 IT? ... OR... TKIVIA FACTS -WHAT 15 THE
MOST COMMON LOCATION, OK A(;E, OK ASSOCIATION, OK 5YNDKOME? ... OR...
WHAT'S THE NEXT 5TEP IN MANA(;EMENT? THINK BACK TO MEDICAL SCHOOL
V5MLE STYLE, THAT 15 WHAT you AKE DEALIN(; WITH ONCE A(;AIN. IN THl5 BOOK,
THE AUTHOK TKIED TO COVEK ALL THE MATEKIAL THAT COULD BE ASKED
(KEA5ONABLY), AND THEN APPKOXIMATE HOW Q__UESTIONS Mf(;HT BE ASKED
ABOUT THE VAKIOU5 TOPICS. THKOU(;HOUT THE BOOK, THE AUTHOK WILL
INTIMATE, "THl5 COULD BE ASKED LIKE THl5," AND "THIS FACT LENDS ITSELF WELL
TO A Q__UE5TION." INCLUDED IN THE SECOND VOLUME OF THE SET 15 A 5TKATE(;Y
CHAPTEK FOCU51N(; ON Hf (;H YIELD "BUZZWOKD5" THAT LEND WELL TO CEKTAIN
Q__UESTION5.
THI5 15 NOT A KEFEKENCE BOOK.
THl5 BOOK 15 NOT DE5f(;NED FOK PAT! ENT CAKE.
THIS BOOK 15 DE5f (;NED FOK 5TUDYIN(; SPECIFICALLY FOK MULTIPLE CHOICE TE5T5,
CASE CONFEKENCE, AND VIEW-BOX PIMPIN(;/Q__UIZ!Nc;.
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Radiology Master of Sport .. National Champion
Americans love to fight. Americans love the champion.
This right here is about recognizing a commitment to being the best. Being the best, standing on
the top stand - and more importantly the quest to stand on the top stand and wear the yellow
medal is what I want to recognize.
The quest is very lonely. They say it is lonely at the top - that is not true. When I started to
become recognized internationally as the top educator in the field I suddenly had alot of people
who wanted to be my friend. I didn't have any friends on the way there - nobody was getting up
at 4am with me to write... nobody, not one person. It was just me - alone. It is lonely getting to
the top and that is where most people fall off. It's Friday and everyone else is going out, or there
is a party or whatever - I'm tired and I want to sleep in. I was on call last night- it is just not
worth it. What I'm hoping to share is that for me that is not what life is. Life is about being the
best person you can be in whatever it is you arc doing. That docs not have to be Radiology, but
because you are reading this book well that is what it means for you now.
You make the quest. If you get the top score on the exam - I'll be putting your name in this book
next year and you can motivate the next legend of tomorrow. Plus, I'll give you some money and
have an enormous lion trophy made for you.
The most important thing is not actually winning. People think I only care about winning
because I rant and rave about how only the gold medals count - but the quest is what I really
value. J'm not training for silver. I'm training for gold. The quest for gold is more important than
someone handing you a gold medal. The katana sword of the black dragon society cannot be
stolen - it can only be earned. Outcomes really don't matter, because the truth is in this life you
can do everything 100% perfect and still fail and you can do almost everything wrong and still
win. If you don't focus on outcomes and instead the quest itself you will get something much
greater -- besides a high probability of passing the test - what you can gain from the quest, the
ability to really dedicate yourself to something 100% - it is a skill you can use for the rest of your
life. This is the way to always achieve victory. Once you know the way, you can sec it in all
things - as the samurai say.
HALL OF CHAMPIONS
2017 Champion 2018 Champion 2019 Champion 2020 Champion
,,• ,,•
Dr. Gary Dr.Thomas Dr. Nick
Dellacerra, D.O. Pendergrast, M.D. Broadbent, D.O.
y
May the Mightiest
Warrior Prevail
- l Iofatra (formerly -Wake Forrest - Universityoflllinois
North Shore-LU) in Peoria
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I FIGHT FOR THE USERS
-TRON 1982
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,11�1�•
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10
NEURORADIOLOGY
PROMETHEUS LIONHART, M.D.
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SECTION 1:
ANATOMY
There is a ton of anatomy that can be asked on a multiple choice test. My idea is to break it
down into three categories: (1) soft tissue - brain parenchyma (including normal
development), (2) bony anatomy - which is basically foramina, and (3) vascular anatomy.
son Tissue Brain Anatomv:
Central Sulcus - This anatomic landmark separates the frontal lobe from the parietal lobe,
and is useful to find if you haven't learned the lazy Neuroradiolgist's go to descriptor
"fronto-parietal region." Old school grey bearded Radiologists (likely the ones who are
important enough to write test questions) love to ask how you find this important structure.
There are about 10 ways to do this, which brings me to the main reason this is a great
pimping question. Even if you can name 9 ways to do it, they can still correct you by naming
the l 0th way. I noticed during my time as a "trainee" that Attendings tend to be excellent at
knowing the answers to the questions they are asking.
Practically speaking, this is the strategy I use for finding the central sulcus:
Pretty high up on the brain, maybe the 3rd or 4th cut, I find the pars marginalis. This is
called the "pars bracket sign" - because the bi-hemispheric symmetric pars marginalis form
an anteriorly open bracket. The bracket is immediately behind the central sulcus. This is
present about 95% ofthe time - it's actually pretty reliable.
Central Sulcus
Pars Bracket Sign
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Central Sulcus Trivia - Here are the other less practical ways to do it.
• Superior frontal sulcus / Pre-central sulcus sign: The posterior end of the superior frontal
sulcus joins the pre-central sulcus
• Inverted omega (sigmoid hook) corresponds to the motor hand
• Bifid posterior central sulcus: Posterior CS has a bifid appearance about 85%
• Thin post-central gyrus sign - The precentral gyms is thicker than the post-central gyms
(ratio 1.5 : 1).
• Intersection - The intraparietal sulcus intersects the post-central sulcus (works almost
always)
• Midline sulcus sign -The most prominent sulcus that reaches the midline is the central
sulcus (works about 70%).
Superior Frontal Sulcus
, -Often intersects the pre CS
PreCentral (THICK)
PostCentral (thin)
• Inverted Omega ,,. ,,,. "'
• -On the central sulcus
-Represents the motor hand
The Post CS is Bifid about
• lntraparietal sulcus 85% of the time .
i -Intersects the post CS
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Homunculous Trivia:
• The inverted omega
(posteriorly directed knob)
on the central sulcus /
gyrus designates the motor
cortex controlling hand
function.
• ACA territory gets legs,
• MCA territory hits the rest.
Normal Cerebral Cortex: As a point of trivia, the cortex is normally 6 layers thick, and the
hippocampus is normally 3 layers thick. I only mention this because the hippocampus can look
slightly brighter on FLAIR compared to other cortical areas, and this is the reason why (supposedly).
Dilated Perivascular Spaces (Virchow-Robins): These are fluid filled spaces that accompany
perforating vessels. They are a normal variant and very common. They can be enlarged and associated
with multiple pathologies; mucopolysaccharidoses (Hurlers and Hunters) ,"gelatinous pseudocysts" in
cryptococcal meningitis, and atrophy with advancing age. They don't contain CSF, but instead have
interstitial fluid. The common locations for these are: around the lenticulostriate arteries in the lower
third of the basal ganglia, in the centrum semiovale, and in the midbrain.
Cavum Variants:
Normal -100% of preterm infants, -Posterior continuation of -Extension ofthe
-15% of adults. the cavum septum quadrigeminal plate
-Rarely, can cause pellucidum (never exists cistern to foramen of
hydrocephalus without a cavum septum Monro.
-Anterior to the foramen pellucidum) -Seen above the }rd
of Monroe -Posterior to the foramen of ventricle and below
Monroe the fornices.
-Between frontal horns -Between bodies oflateral
ventricles
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Ventricular Anatomv:
I Arachnoid Granulations: These are regions where l
,••••••••••••••••••••••••••••••••••••••••n•••••••••••••••••••••••••••••••••••••••••••••••••n••••••••••••••••••••••••••••••••
Just a quick refresher on this.
1 the arachnoid projects into the venous system l
You have two lateral ventricles l allowing for CSF to be reabsorbed. They are i
that communicate with.the third !1 hypodense on CT (similar to CSF), and usually round !
ventricle via the interventricular or oval. This round shape helps distinguish them
from clot in a venous sinus (which is going to be
l
foramen ( of Monro), which in tum !
communicates with the fourth linear). On MR they are typically T2 bright (iso to !
CSF), but can be bright on FLAIR (although this 1
ventricle via the cerebral varies a lot and therefore probably won't be tested). i
aqueduct. These things can scallop the inner table (probably !
from CSF pulsation) !
· ····· . · · · · · ··
• ·······•• ··•••····•·················•···•••·••··•········· ,····•·········••--•······••···· ...............................:
- ·· ...
v
· ..
•
,,,,,,,. .. . .... .. .
..
,,.,
.,,,,. ; .
.,,,,.
- ·- ·. ,.. Lateral Vents
, ,,
Monro
Cerebral
Aqueduct
oramen
of
Ambient Cistern Magendie
The fluid in the fourth ventricle escapes via the median aperture (foramen ofMagendie), and the
lateral apertures (foramen ofLuschka). A small amount of fluid will pass downward into the
spinal subarachnoid spaces, but most will rise through the tentorial notch and over the surface of
the brain where it is reabsorbed by the arachnoid villi and granulations into the venous sinus
system.
Blockage at any site will cause a noncommunicating hydrocephalus. Blockage ofreabsorption at
the villi/ granulation will also cause a noncommunicating hydrocephalus.
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Basal Cisterns: The basal cisterns arc good for (l) evaluating mass effect, and (2) anatomy questions.
People say the suprasellar cisterns look like a star, with the five corners lending themselves nicely
, tu 11mltipfo dwicc 4ucstiuns. Su let us <lo a quick review; the top of the star is the interhemisphet'ic
fissure, the anterior points are the sylvian cisterns, and the posterior points arc the ambient cisterns.
. The quadrigeminal plate looks like a smile, or ... I guess it looks like a sideways moon,ifyou
· don't like smiles.
No Time for Smiles. Training/or Domination.
; Snarls Not Smiles.
*
Smile later ... once you've passed the test.
Anterior
.,,_ Interhemispheric
issure
+-Sylvian Cistern
Ambient
+-
Cistern
\.... � +- Quadrigeminal
,..,. Plate Cistern
The Ambient Cistern is a bridge between the
Interpeduncular C.
11111 ► Quadrigeminal C.
Midbrain Tectum vs Teumentum
Atrophy patterns of the midbrain will become important when we start talking about some of
the more obscure neurodegenerative disorders. So it's good to review the vocab words.
When I was in medical school my anatomy teacher told me the midbrain looks like a monkey face.
I said "Please don't confuse me. Last week you said the monkey face was a penis cut in cross section."
I always thought the midbrain looked more like a stoner dog that just got higher than a giraffe's vagina.
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Bonv Anatomv: Skull Base Foramina l Rotundum, oval, Spinosum, Hvpoglossal J
First let us review the where - then we will do the what. Remember, they don't have to show you the
hole in the axial plane. They can be sneaky and show it in the coronal or sagittal plane. In fact,
showing Foramen Rotundum (FR) in the coronal and sagittal planes is a very common sneaky trick.
On the coronal view,
FR looks like you are
staring into a gun
barrel.
On the sagittal view,
think about FR as
being totally level or
horizontal.
With regard to the relationship between Spinosum and Ovale, I like to think of this as the footprint a
woman's high heeled shoe might make in the snow, with the oval part being Ovale, and the pointy
heel as Spinosum.
:n:
The Hypoglossal Canal is ve1y posterior
and inferior.
This makes it unique as a skull base foramen.
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Bonv Anatomv: Skull Base Foramina I Jugular Foramen J
The jugular foramen has two parts which are
separated by a bony "jugular spine."
Pars Nervosa -The nervous guy in the
front. This contains the Glossopharyngeal
nerve (CN 9), along with it's tympanic
brach - the "Jacobson's Nerve"
Pars Vascularis - This is the "vascular
part" which actually contains the jugular
bulb, along with the Vagus nerve (CN 10),
Auricular branch "Arnold's Nerve," and
the Spinal Accessory Nerve (CN 11)
Bonv Anatomv: Orbital Fissures and the PPF
The relationship between the Superior Orbital Fissure (SOF), the Inferior Orbital Fissure (IOF), Foramen
Rotundum (FR), and the Pterygopalatine Fossa (PPF) is an important one, that can really lead to some
sneaky multiple choice questions (mainly what goes through what - see chart on page 18).
I've attempted to outline this relationship on both sagittal and coronal views.
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Anatomv: cavernous Sinus
CN III
CN IV
CN V l
CNV2
C arotid �,/
l1:w
CNV I /
The question is most likely, what's in it (or asked as what is NOT in it).
• CN 3, CN 4, CN V 1, CN V 2, CN 6, and the carotid - run through it.
• CN 2 and CN V3 - do NOT run through it.
The only other anatomy trivia I can think of is that CN6 runs next to the carotid, the rest of the nerves are
along the wall. This is why you can get lateral rectus palsy earlier with cavernous sinus pathologies.
Anatomv: Internal Auditorv canal - IAC" 11
Fundus (top) of
Superior the IAC
CN 7 Vestibular
CN8 Inferior
Vestibular
The thing to remember is "7UP, and C OKE Down" If it is shown, it is always shown in
- with the 7th cranial nerve superior to the 8th this orientation.
cranial nerve (the cochlear nerve component).
The ideal sequence to find it is a
As you might guess, the superior vestibular branch heavily T2 weighted sequence with
is superior to the inferior one. super thin cuts through the IAC .
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Anatomv - Whafs in It;,
Considering multiple choice questions regarding the skull base anatomy.
"What goes where?" questions essentially write themselves.
Hole/ Compartment
Foramen Ovale CNV3, and Accessory Meningeal Artery
Foramen Rotundum CNV2 ("R2V2"),
Superior Orbital Fissure CN 3, CN 4, CNVl, CN6
Inferior Orbital Fissure CNV2
Foramen Spinosum Middle Meningeal Artery
Pars Nervosa: CN 9,
Jugular Foramen
Pars Vascularis: CN 10, CN 11
Hypoglossal Canal CN 12
Optic Canal CN 2 , and Opthalmic Artery
Cavernous Sinus CN 3, CN 4, CN V l , CN V2, CN 6, and the carotid
CN 7, CN 8 (Cochlear, Inferior Vestibular and Superior
Internal Auditory Canal Vestibular components). "7 Up - Coke Down"
Meckel Cave Trigeminal Ganglion
Dorello's Canal Abducens Nerve (CN 6), Inferior petrosal sinus
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vascular Anatomv
Arterial vascular anatomy can be thought of in four sections. (1) The branches of the external
carotid (commonly tested as the order in which they arise from the common carotid).
(2) Segments of the internal carotid, with pathology at each level and variants. (3) Posterior
circulation, (4) Venous anatomy
l1J Branches 01 the External carotid
Some Administrative assistants Love Fucking Over Poor Medical Students
Superior Thyroid /
,,.
Ascending Pharyngeal
Lingual I Superficial
I Temporal
Facial
Maxillary
Occipital
Posterior Auricular
Maxillary
Superficial Temporal
Occipital
Lingual
Superior
Thyroid
!p. THIS vs THAT: External vs Internal Carotid via Ultrasound
Internal External
Branches Nope Yup
Orientation Posterior Anterior
Resistance Low (continuous diastolic) High
Temporal Tap (poking the head) No Change in Waveform Waveform Reacts
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l2J Segments of the Internal Carotid
• The bifurcation of the IAC and ECA usually occurs at C3-C4
• C:ervical TCA has no hranches in the neck - if you see branches either
(a) they are anomalous or more likely
(b) you are a dumb ass and actually looking at the external carotid.
Internal Carotid *Remember finding branches is a way you can tell ICA from ECA on
ultrasound.
• Low resistance waveform with continuous forward flow during diastole
• Flow reversal in the carotid bulb is common
• Atherosclerosis: The origin is a very common location
• Dissection: Can be spontaneous (women), and in Marfans or Ehlers
Danlos, and result in a partial Homer's (ptosis and miosis), followed by
C l (Cervical)
MCA territory stroke.
• Can have a retropharyngeal course and get "drained" by ENT accidentally.
• Pharyngeal infection may cause pseudoaneurysm at this level.
Aneurysms here can be
C2 (Petrous) Not much goes on at this level.
surprisingly big (thats what she said).
Not much here as far as vascular pathology. The anatomic location is
C3 (Lacerum) impo1iant to neurosurgeons for exposing Meckel's cave via a transfacial
approach.
This segment is affected by
multiple pathologies including Anemysms here are strongly
C4 (Cavernous)
the development of cavernous - associated with hypertension.
carotid fistula.
Aneurysm here could compress the
CS (Clinoid)
optic nerve and cause blindness.
C6 (Ophthalmic Origin at the "dural ring" is a Common site for aneurysm
- Supraclinoid): buzzword for this artery. formation.
C7 Aneurysm here may compress CN
(Communicating) III and present with a palsy.
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Schematic ICA Anuiouraphic Runs
You don't need to know every branch, but you should be able to recognize the main vessels.
Lateral ICARuns:
C
C3
Petrolingual
Ligament _,,
cF
, -�2)
-'
Carotid C y-
C
-......, Anterior Choroidal
Posterior Communicating C1
APICARun:
This is a pretty good look for an AP
ICA run.
Notice that half the image is relatively
blank. This is because you have 2
ICAs (right and left), only one of
which is getting injected. For the
total neuro angiography novice (most
residents), this is a helpful thing to
notice when deciding AP vs Lateral.
Also notice the MCA is lateral, and
the ACA is medial.
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ACA
Anterior
Q/l Trivia
Communicating/\. Acute CN3 Palsy (unilateral
pupil dilation) a classic
neurology boards question -
grab a relax hammer STAT!
Anterior
Posterior
Choroidal The answer is PCOM aneurysm
Communicating A.
A. until proven otherwise (although
it can also be caused by an
aneurysm at the apex of the
basilar artery or its junction with
the superior cerebellar/
Superior posterior cerebral arteries).
Cerebellar A.
The reason is the relationship
between the CN3 and vessels
(arrows).
Anterior
AICA Inferior
Cerebellar
A.
PICA (70%) Anterior Spinal A.
AP Vertebral Run Lateral
Vertebral
Rnn
Choroid Point
SCA�
PICA�
AIC� /
PICA Caudal Point
22
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vascular variants:
Fetal Origin of the PCA: Most common vascular variant
(probably) - seen in up to 30% of general population.
Definitions vary on what a fetal PCA is. Just think of this as
a situation where the PCA is feed primarily as an anterior
circulation artery (occipital lobe is feed by the ICA).
Therefore, the PCOM is large (some people define this
vessel as PCOM larger than Pl).
Another piece of trivia is that anatomy with a fetal PCA has
the PCOM superior I lateral to CN3 (instead of superior I
medial - in normal anatomy).
Persistent Trigeminal Artery:
Persistent fetal connection between the cavernous ICA to the basilar.
A characteristic "tau sign" on Sagittal MRI has been described.
It increases the risk of aneurysm (anytime you have branch points).
Axial - Connected Bas1 ar and IC
Fetal Connection
Carotid
Sag - Connected Basilar and ICA
-Looks like a "T"au
Aberrant Carotid Artery: Discussed later with T-Bone pathology.
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l4JVenous:
You can ask questions about the venous anatomy in roughly three ways (1) what is it- on a
picture, (2) what is a deep vein vs what is a superficial vein, (3) trivia.
What is it?
Superior
Sagittal Sinus
Inferior
Sagittal Sinus
Internal Cerebral V.
Straight Sinus
Basal Vein of
Rosenthal
Cavernous Sinus
Transverse Sinus Superior Petrosal
Great V. of Galen Inferior Petrosal
Sigmoid Sinus
Jugular V. ..
..
$igmoid Sinus
Cavernous Sinus
Superior Petrosal
Inferior Petrosal
i----- Transverse Sinus
Occipital Sinus
Superior Sagittal Sinus
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Anastomotic Superficial Veins:
Rolandic Vein (Central Sulcus)
Anastomotic Vein ofTrolard
Superior Sagittal Sinus
- Connects the Superficial
Middle Cerebral Vein and
Superior the Superior Sagittal Sinus
Anastomotic Vein
(Trolard) Anastomotic Vein ofLabbe
- Connects the Superficial
Middle Cerebral Vein and
the Transverse Sinus
Inferior
Anastomotic Vein
(Labbe) Superficial Middle
Cerebral Vein
*drains to
Cavernous Sinus
Inferior Petrosal Sinus
Middle -------- Cavernous Sinus /
Cerebral Vein __ :::: = · · - ... __
i0!7r "",
�, ,.
0'
· • • · •• • - •• !clbb0
.........
\
Superior Petrosal Sinus
Internal Jugular Veins
�l
Superior Superior Sigmoid Sinus
-
Cere bral Vein - -►-- Sagittal Sinus
/
� Confluence -+ Transverse Sinus
of Sinuses
Inferior
Sagittal Sinus ------. Straight /
Sinus
Vein of Galen �
!p THIS vs THAT: Superficial vs Deep: Superficial Deep·
Basal Vein of
Superior Cerebral Veins
There is a superficial venous system and a deep Rosenthal
venous system. The easiest way to test material Superior Anastomotic
Vein of Galen
like this is your "which of the following is not?" Vein ofTrolard
or "which of the following is ? " type question. Inferior Anastomotic Inferior Petrosal
Vein of Labbe Sinus
The big ones to remember are in the chart. Superficial Middle
Cerebral Veins
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� Venous Trivia:
Collateral Pathways: The dural sinuses have accessory drainage pathways (other than the jugular
veins) that allow for connection to extracranial veins. These are good because they can help
regulate temperature, and equalize pressure. These are bad because they allow for passage of
sinus infection / inflammation, which can result in venous sinus thrombosis.
Inverse Relationship: There is a relationship between the Vein of Labbe, and the Anastomotic
Vein ofTrolard. Since these dudes share drainage of the same territory, as one gets large the
other get small.
Sounds Latin or French: As a general rule, anything that sounds Latin or French has an increased
chance of being on the test.
• Vein ofLabbe: Large draining vein, connecting the superficial middle vein and the
transverse sinus
• Vein of Trolard: Smaller (usually) vein, connecting the superficial middle vein and
sagittal sinus
• Basal veins ofRosenthal: Deep veins that passes lateral to the midbrain through the
ambient cistern and drains into the vein of Galen. Their course is similar to the PCA.
• Vein of Galen: Big vein ("great") formed by the union of the two internal cerebral veins.
Superior
Ill"
Anastomotic Vein
..� (Trolard)
Inferior
Anastomotic Vein
(Labbe)
Basal veins of
I L,
I
Rosentha: [
Vein of Galen
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� Venous Gamesmanship
An embolus of venous gas is common and often not even noticed. The classic location is the
cavernous sinus (which is venous}, but if the volume is large enough, air can also be seen in
the orbital veins, superficial temporal veins, frontal venous sinus, and petrosal sinus.
Why does this happen?
Peripheral (or central IV) had some air in the tubing. Thats right, you can blame it on the
nurse (which is always satisfying). ''.Nurse Induced Retrograde Venous Air Embolus"
Significance?
Don't mean shit. It pretty much always goes away in 48 hours with no issues.
Cavernous Sinus
-The most common
spot to see this
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Qj't Sinus Trivial Anatomv Bonus - The Concha Bullosa
This is a common variant where the middle concha
is pneumatized. It's pretty much of no consequence
clinically unless it's fucking huge - then (rarely) it
can cause obstructive symptoms.
In my private practice, an ENT told me he wanted
these mentioned in all his CT sinus reports.
That way he can justify doing FESS ...
He drives a nice car.
� Gamesmanship for Neuro Anatomv
• First Order Trivia:
• "What is it?" Style questions are most likely; with possibilities including
CTA, MRA, or Angiograms. Considering when the people writing the
questions trained, angiograms are probably the most likely.
• "What goes through there?" Neuro foramina
• "What doesn't?" Style questions - CN 2 and CN V3 don't go through the
cavernous sinus.
• Second Order Trivia:
• CN 3 Palsy - Think Posterior Communicating Artery Aneurysm
• CN 6 Palsy - Think increased ICP
Increased ICP -+ Brain Stem Herniates Interiorly -+ CN 6 Gets Stretched
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.
•
• •
.
�
SECTION 2:
BRAIN DEVELOPMENT �
••
.
.
Brain Mvelination:
The baby brain has essentially the opposite signal characteristics as the adult brain. The Tl pattern
of a baby is similar to the T2 pattern of an adult. The T2 pattern of a baby is similar to the T l
pattern of an adult. This appearance is the result of myelination changes.
The process of myelination occurs in a predetermined order, and
therefore lends itself easily to multiple choice testing. The basic Immature Mature
Myelin Myelin
concept to understand first is that immature myelin has a higher
water content relative to mature myelin and therefore is brighter High Water, Low Water,
on T2 and darker on T l . During the maturation process, water Low Fat High Fat
will decrease and fat (brain cholesterol and glycolipids) will
Tl dark, Tl bright,
increase. Therefore mature white matter will be brighter on T l T2 bright T2 dark
and darker on T2.
Testable Trivia: the Tl changes precede the T2 changes (adult T l pattern seen around age 1, adult T2
pattern seen around age 2). Should be easy to remember (1 for Tl, 2 for T2).
Take Home Point: T l is most useful for assessing myelination in the first year (especially 0-6
months), T2 is most useful for assessing myelination in the second year (especially 6 months to 18
months).
Order of progression: Just remember,
inferior to superior, posterior to Brain Myelination Pattern
anterior, central to peripheral, and
sensory fibers prior to motor fibers.
The testable trivia is that the
subcortical white matter is the last
part of the brain to myelinate, with
the occipital white matter around 12
months, and the frontal regions
finishing around 18 months. The
"terminal zones" of myelination occur
Inferior to Superior, Posterior to Anterior
in the subcortical
frontotemporoparietal regions -
finishing around 40 months.
Another high yield piece of testable trivia is that the brainstem, and posterior limb of the internal
capsule are normally myelinated at birth.
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Additional Brain / Skull Development Trivia: Birth Adult
Ant Tl Hyper Tl lso,
Pituitary: Both the Anterior and Posterior Pituitary are Tl Pituitary T2 lso
Bright at Birth (anterior only Tl bright until 2 months). Posterior · Tl Hyper,
Pituitary Tl Hyper T2Hypo
Brain Iron: Brain Iron increases with age (globus pallidus darkens up).
Bone Marrow Signal: Calvarial Bone Marrow will be active (Tl hypointense) in young kids
and fatty (Tl hyperintense) in older kids
Sinus Development:
. Visible
The sinuses form in the Order
on CT
following order:
• Present at
1- Maxillary, Maxillary 1 • 5 month
. Birth
2- Ethmoid,
3- Sphenoid, Present at
Ethmoid 2 1 year
4- Frontal · Birth
Most are finished NOT Present
Frontal 4 6 year
forming by around 15 • at Birth
years.
NOT Present
Sphenoid 3 4 year
at Birth
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Congenital Malformations:
This is a very confusing and complicated topic, full oflots oflong Latin and French sounding
words. Ifwe want to keep it simple and somewhat high yield you can look at it in 5 basic
categories: (1) Failure to Form, (2) Failure to Cleave, (3) Failure to Migrate,
(4) Development Failure Mimics, and (5) Herniation Syndromes.
Failure to Form - ovsuenesls / Auenesis of the Corpus Callosum
A classic point oftrivia is that the corpus
callosum forms front to back
(then rostrum last).
Therefore hypoplasia ofthe corpus
callosum is usually absence ofthe
splenium (with the genu intact).
Rostrum
GAMESMANSHIP:
With agenesis ofthe corpus callosum, a common
trick is to show colpocephaly (asymmetric dilation
ofthe occipital horns).
When you see this picture you should think:
(l) Corpus Callosum Agenesis
(2) Pericallosal Lipoma
* Discussed on next page
Colpocephaly
(asymmetric dilation of the occipital horns).
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Failure to Form -ovsuenesls / Agenesis of the Corpus Callosum Continued
Other common ways to show this include:
······················································•·······················
Why are the lateral
ventricles widely spaced
when you have no corpus
callosum?
l There are these things called
I "Probst bundles" which are
! densely packed WM tracts -
destined to cross the CC -
but can't (because it isn't
there).
So instead they run parallel
to the interhemispheric
The "steer horn" "Vertical Ventricles" ; fissure - making the vents
appearance on coronal. widely spaced j look widely spaced.
(racing car) on axial. :••••••.. ••••••••••••.. •••••••••••••••••u•••••••••.. • ..•••••••••••••••••••••••=
Failure to Form -Associations - lntracranial Lipoma
Dysgenesis / Agenesis of the Corpus Callosum is associated with lots of other syndromes/
malformations (Lipoma, Heterotopias, Schizencephaly, Lissencephaly, etc...). Some sources
will even say it is the "most common anomaly seen with other CNS malformations. " -
whatever the fuck that means.
Intracranial Lipoma:
The most classic association with CC Agenesis.
50% are found in the interhemispheric fissure, as
shown here. The 2nd most common location is the
quadrigeminal cistern (25%).
Trivia • CNS Lipomas are congenital malformations, not true neoplasms.
• "Maldffferenitation of the Meninx Primitiva" - is a meaningless French
sounding explanation for the frequent pericollasal location.
• Non Fat Sat Tl is probably the most helpful sequence (most non-bleeding
things in the brain are not T l bright).
• These things don't cause symptoms (usually) are rarely treated.
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Failure to Form - Open Neural Tube Defects
Anencephalv
Neuro Tube Defect Neural Tube Defect
(Defect at the top o_f'head) (Defect at the level of the cervical spine)
The Top of the Head is Absent Deficient Occipital Bone with Defect in the
(Above the Eyes) Cervical Region. Inion = Back of Head/ Neck
Extreme Retroflexion of the Head.
Reduced/Absent cerebrum and cerebellum. Enlarged foramen magnum.
The hindbrain will be present. Jacked up spines.
Often visceral problems.
Usually, not compatible with life.
Mercifully, not compatible with life.
When they do survive, they tend to have a
Potential to be awful at Jeopardy
natural talent for amateur astronomy
Classic Image Appearance:
Classic Image Appearance: "Star Gazing Fetus" - contorted in a way that
makes their face turn upward (hyper-extended
Incredibly creepy "Frog Eye" appearance on cervical spine, short neck, and upturned face).
the coronal plane (due to absent cranial bone I
brain with bulging orbits). It's every bit as horrible as the Frog Eye thing
(both would make incredible Halloween costumes.)
Secondary Signs I Gamesmanship: APP will be elevated
(true with all open neural tube defects)
• Antenatal Ultrasound With Polyhydramnios
(hard to swallow without a brain)
• AFP will be elevated
(true with all open neural tube defects)
Failure to Form - Open Neural Tube Defects - Encephalocele l meninuoencephalocele J
Neural tube defect where brain+ meninges herniate through a defect
in the cranium. There are lots of different types and locations - but
most are midline in the occipital region.
There are numerous associations: - most classic = Cbiari HI
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Failure to Form - Cerebellar Vermis
Rho111Qepcepbalo$Vll8IISiS
-Note the Vertical Lines Across the Cerebellum
Vennis is Absent. Vermis is Absent (or Small)
Classic Image Appearance:
Classic Image Appearance:
"Molar Tooth" appearance of the
Transversely oriented single lobed cerebellum as
superior cerebellar peduncles
shown above (this is an Aunt Minnie).
(elongated like the roots of a tooth).
Absence of the vermis results in an Small Cerebellum
abnormal fusion of the cerebellum.
Absence of pyramidal decussation
(whatever thefuck the means)
Small 4th. Ventricle Large 4th Ventricle "Batwing Shaped"
Rounded Fastigial Point, Absent Fastigial Point,
Absent Primary Fissure Absent Primary Fissure
Associations: Retinal dysplasia (50%),
Associations: Holoprosencephaly Spectrum Multicystic dysplastic kidneys (30%).
Liver Fibrosis ("COACH" Syndrome)
Gamesmanship: This stuff is tricky. Let me suggest the following tactics.
If you arc faced with this level of trivia (on an intermediate level exam), first start by looking for
the two markers of normal vermian development: (1) the primary fissure and (2) fastigial point -
both of which are best seen mid sagittal. The ''fastigial point" is normal angular contour (not
round) along the ventral surface of the cerebellum. The primary cerebellar fissure is a deep
trapezoid shaped cleft along the posterior cerebellum. Absence or abnormal morphology of these
landmarks should trigger a multiple choice brain reflex indicating the vennis is not nonnal.
Absent Fissure
Fissure
· Point should be located Abnormal Ventral Contour
Point just below the mid pons. Absent Vermis
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Failure to Form - Dandv Walker and Friends
Radiologists love to nitpick and obsess over details. The more meaningless the details the more
intense and emotional the debate. Along those lines, Dandy Walker malformations are typically
described along a spectrum. The arbitrary stops along this spectrum often lead to ferocious beta
male nerd confrontations amongst Academics - filled with ferocious exchanges of
gossip, innuendo, finger nail scratching / pinching, biting, hair pulling, and empty threats of
reputation destruction.
Despite the very real threat of being scratched and pinched by an enraged Academic
- I now offer my simplified strategy for dealing with this complex pathology.
"Classic" Dandy Walker:
There are 3 key findings which are consistently present and reliable to make the diagnosis.
1 Hypoplasia of the Vermis 2 Hypoplastic Vermis is 3 Dilated Cystic 4th Ventricle
(usually the inferior part) Elevated and Rotated
On axial, there is the nonspecific appearance of an
enlarged posterior fossa CSF space. It can look like a
retrocerebellar cyst on axial only (although it's not a cyst
- it's the expanded 4th ventricle).
The cerebellar hemispheres will be displaced forward
and laterally but their overall volume and morphologic ·
. Bunch ofPosterior Fossa CSF
characteristics should be preserved. ! Cerebellum Displaced Anterolaterally
· ······················-·····················.. ··········--.
'IJORCULAR·LAMBDOID INVERSION"
This classic buzzword(s) describes the torcula
(confluence of venous sinuses) above the level of the
lambdoid suture, seconda1y to elevation of the tentorium.
It's worth mentioning that this inversion is often NOT - Normal - Dandy Walker -
seen in the "variant" version of Dandy Walker. Lambdoid Torcula Above Lambdoid
Above Torcula
"High-Inserting
Venous Confluence"
Trivia • Often identified on OB screening US.
• Otherwise, presents with symptoms of increased intracranial pressure (prior to month 1)
• Most Common Manifestation == Macrocephaly (nearly all cases with the first month)
• Associations: Hydrocephalus (90%), Additional CNS malformations (~ 40%)
(agenesis of the corpus callosum, encephaloceles, heterotopia, polymicrogyria, etc ... ).
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Failure to Form - oandv Walker and Friends
As I mentioned on the prior page, Dandy Walker malformations are typically described along a
spectrum. We covered the "classic" subtype in depth on the prior page. The stragglers
(presumed to be of lower yield) and classic type are contrasted on the chart below.
Least Severe ,., "" • ....... Most Severe
Name Mega Cisterna Magna Blake Pouch "Variant" DWM "Classic" DWM
Alternative
"Hypoplastic
Term Used
Rotated Vermis"
. To Trick You
Mid Sagittal
· Doodle
Normal Variant: Sac like cystic Hypoplastic,
protrusion through the Hypoplastic vermis elevated, rotated
Overview Focal enlargement of foramen of Magendie with dilation of the vermis with cystic
the retrocerebellar CSF into the infra / retro 4th ventricle. dilation of the 4th
space. cerebellar region. ventricle.
Normally Formed But Hypoplastic Hypoplastic
Vermis Normal
Upwardly Displaced (less severe) & Rotated
4th Ventricle Normal Dilated Dilated Markedly Dilated
- Nonnal In Size
Cerebellar
Normal Normal Hypoplastic - Displaced
. Hemispheres
Anterolaterally
Posterior Fossa Nonna! Normal Nonna! Expanded
Torcula Nonna! Normal Normal High Insertion
Hydrocephalus Nope Yes 25 % of Cases 90% of Cases
• Choroid from the 4th
ventricle swinging
into the pouch is
classic (but not • Diagnosis on antenatal ultrasound must
• No supratentorial
always present). be done after 18 weeks
abnormalities
· Trivia
• The pouch only (prior to 18 weeks the vermis hasn't
communicates with finished.forming).
the 4th ventricle.
NOT the cisternal
CSF.
Now, let us switch gears from fusion to cleaving problems.
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Failure to Cleave - Holoprosencephalv l HPE J
This entity also occurs along a spectrum with the common theme being some element of abnormal
central fusion. Although, it isn't actually a fusion problem. Instead, it is a failure to perform the
normal midline cleaving. In the normal embryology, the fancy latin word "P-lon" sta1is out like a
peanut butter sandwich, then mom cuts the bread into two perfect halves (separate lateral
hemispheres). The sandwich cutting (cleavage) always occurs back to front (opposite of the
formation of the corpus callosum), so in milder forms the posterior cortex is normal and the anterior
cortex is fused.
Least Severe •·•·-·"• '"'""""'...... Most Severe
Lobar Semi-Lobar Alobar
Mild
Fusion
Frontal
Normal
Doodles Comparison
Incomplete Ball
Septum Shaped
Normal
Comparison
Focal areas of Zero midline cleavage.
incomplete fusion The back is cleaved (not the front) Cerebral hemispheres are
Overview anteriorly (usually the > 50% fusion of the frontal lobes fused and there is a single
fornix) midline ventricle
The body of the lateral ventricles
Variable mild fusion of are 1 chamber. Occipital and Single Ventricle
Ventricles the frontal horns of the ( distinct lateral and third
Temporal horns are partially
lateral ventricles. developed. ventricles are absent)
Thalamus Normal Fused (partial or complete) Fused
• Septum Pellucidum • Septum Pellucidurn
Absent • Septum Pellucidum • Corpus Callosurn (partial) • Corpus Callosum
• Corpus Callosum • Anterior Interhernispheric Fissure • Interhernispheric Fissure
Structures (partial vs nonnal) • Anterior Falx Cerebri • Falx Cerebri
Horrible Cleft Lip / Palate Cyclops Monster Face
Things Borat's Brother Bilo (he is retard) (one eye, one nose hole, etc)
Survive into Adulthood,
Outcome Survive into Adulthood but terrible at Jeopardy Mercifully Bad
(average at Wheel ofFortune) (stillborn I dead< 1 year)
Face predicts Brain, BUT Brain doesn't predict Face
� Possible BUZZWORDS for HPE spectrum.
/
Monster Cyclops Eyes
Cleft lips / Palates
Pyriform Aperture Stenosis (from nasal process overgrowth)
Solitary Median Maxillary Incisor (MEGA-Incisor)
' •••• .. •••••• .. •••••--•u•••••••••••••--•--••••••••••••••••••••••••0HOOOOOOOhOh••••••·••••••••••oho•••o••oo••••••••••••oU0••o•o•••o0o•OOOO•OOO•OhOO•--••·••••••••--••••••••••• .. ••••••••noOOOUOOOOO .. UO•noooo,oOOOoooo'
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Arhinencephalv: r't/1 n I: Meckel-Gruber svudrome:
i ;
! <I>
! :: Classic triad:
i • "Minor" HPE expression. !: 1. Occipital Encephalocoele �})� � �
i • Midline olfactory bulbs/ tracts are absent. :: 2. Multiple Renal Cysts l�l)J/1�
i: • "Can't Smell" - is the clinical buzzword. 1:
11
3. Polydactyly S7
- ,..
:�
,, ,..
I:
! • Could be tested as Kallmann Syndrome 1o. '" ,. ""
l (which also has hypogonadism, & mental l1
i 1: Also strongly associated with
r retardation). r: Holoprosencephaly
1-......................................................................................................... J, - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - -
Septo Optic ovsplasia:
i This "Minor" HPE expression could be referred to by its French sounding name, for the sole
The classic
findings are
inferred by
the name.
comparison
Absent Septum Pellucidum "Septa" and
Hypoplastic "Optic" structures such as the Optic Chiasma (circle) and Optic Nerves
!
Normal
[' \'tJJ n<I> Trivia - Associated with Schizencephaly
L
r
Gamesmanship - The other thing they can show is
i. an azygos anterior cerebral artery - which is basically
j '"' a common trunk of the ACAs. This is rare , but
associated with SOD and lobar HPE.
!
i.......................................................................................................................................................Azygos.ACA (1..trunk)······················•·
Now... switching gears to failures in migration/ proliferation.
Failure to Migrate / Proliferate: lissencephalv-Pachvuvria Spectrum and Friends
An understanding of this complex pathology requires a rapid review of embryologic
neuronal cortex formation. Unfortunately, my medical school embryology
professor was Dr. Eleanor Abernathy, M.D. (youtube her if you aren't familiar).
Anytime I read embryology I can't help but think of her and wonder "can anyone
who loves animals so much, really be crazy?" The answer to that... is yes.
Yes they can. They can be a drunken lunatic. So much so, that I was convinced
Dr. Abernathy as
that anyone who understood embryology risked ending up just like her.
I remember her.
Then I accepted the truth. You either die a hero or live long enough to see
yourself become the villain. *Many more Batman references coming up in the next few pages.
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THE FIRE RISES
-A PR..OMETHEAN DIALO(;UE ON COR..Tf CAL FOR..MATION -
Prologue: The brain is said to form "inside-out, " as neurons that will eventually make up the cortex
are originally birthed from a thick shmy surrounding the fetal ventricles. Sleep inducing texts will
refer to this as the "proliferative neuroepithelium." I prefer the term "Lazarus Pit," or just the "Pit."
It is from this Periventricular Pit, where cells will make "the climb" to the cortex.
Act 1 - Proliferation: Before making "the climb" to the cortex the neuronal-glial stem cells are
born into (and molded by) the darkness of the periventricular Lazarus Pit. It is there that they learn
the truth about despair, first by dividing into additional stem cells in a symmetric fashion ( 1 stem cell
splits into 2 stem cells). Later this process will change to asymmetric proliferation (1 stem cell splits
into 1 stem cell and 1 differentiated cell - glial cell or neuron). This process continues for several
cycles until the stem cells receive the signal to undergo apoptosis - they expect one of us in
the wreckage brother.
The number of neurons in the cortex is determined by the frequency and
number of symmetric / asymmetric divisions by these stem cells.
Disturbance in this process will therefore result in either too many, too
few, or improperly differentiated neurons.
�i�
Symmetric Asymmetric
Act 2 - Migration (RISE): From the periventricular proliferative pit of despair, cells will make the
climb. As they climb to freedom, they are guided by structural cells, chemical signals, and the chant
"Deshi, Deshi, Basara, Basara." They make the climb in 6 waves, with the first generation forming
the "pre-plate" and the second generation forming the more permanent "cortical plate."
In other words, the younger cells always moving past the older ones
becoming more superficial in their final position, (hence the idea -
"inside out" or "outside last"). Disturbance in this mechanism
(guidance, timing of detachment etc ...) will result in under
migration, over-migration, or ectopic neurons.
Act 3 - Organization: At this point you may think the cells have given
everything to the cortex, and they don't owe them anymore. But, they haven't
given everything... not yet. There is still the process of cortical folding
(gyrification).
The process actually occurs simultaneously with and depends heavily on the first two steps. The
differential speed of cortex expansion (relative to the deeper white matter) is probably the key
mechanism for brain folding. For this expansion to occur properly there needs to be the right
number of cells (act 1) migrated in the right order (act 2). There is the additional mechanism of
continued differentiation into structural cell types which organize into horizontal / vertical columns
creating an underlying cytoarchitecture need for structure and function. Disturbance in these
mechanisms will result in an absence of or excessive number of folds.
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Failure to Migrate / Proliferate: lissencephalv-Pachvuvria Spectrum and Friends
Now, we are going to discuss the testable pathologies associated with how this process can fuck up.
I'm going to try and group them according to the stage of disturbance (although they don't always fit
nicely into a single stage).
Failure to Proliferate: Hemimeualencephalv:
Rare, but unique (Aunt Minnie), malformation characterized by enlargement (from hamartomatous
overgrowth) of all or part/s of one cerebral hemisphere. The presumed cause is a failure in the
normal neuronal differentiation in the involved hemisphere - resulting in an "abnormal mixture of
normal tissues" - which defines a hamartoma. This process is often mixed with other errors in
migration resulting in associated polymicrogyria, pachygyria, and heterotopia.
The combo of (1) dilated ventricle and (2) mismatched hemisphere size can be confused with
destmctive pathologies. So lets do a quick comparison to negate any potential fuckery.
!p.THIS vs The trick is to look at which side the dilated ventricle is on.
THAT:
"Hamartomatous
Overgrowth " of all
BIG Side or part of a cerebral
with BIG Ventricle = hemisphere,
Hemimegalencephaly secondary to
differentiation /
migration failure.
SMALL Side The shmnken half is
with BIG Ventricle = atrophic, resulting in
ex-vacuo dilation of
Atrophy the ventricle.
.Rasmussen's
Encephalitis Zebra viral ( or maybe Just like an old
autoimmune) disease grandpa brain (only
that fucking this is just half the
annihilates half the brain, and the kid is
brain. usually less than 10).
Dyke-Davidoff-Masson (Cerebral Hemi-Atrophy):
This is another zebra that can look a lot like Rasmussen encephalitis - but also has
weird unilateral skull thickening and expanded sinuses.
The superior sagittal sinus and fissure are moved across the midline.
It is supposedly caused by an in utero or childhood stroke (supposedly).
Since literally anything is fair game on this exam, I'm including it for completeness
(it's probably low yield).
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Failure to Migrate / Proliferate: ussencephalv-Pachvuvria Spectrum and Friends
The pathologies related to abnormal migration are best though of along a spectrum ranging
from agyria (no gyri) to pachygyria (flat gyri) to band heterotopias.
Lissencephaly
"Classic" Type.•1
Smooth Surface
Thick Cortex
Colpocephaly
Figure 8 Shape
Undermigration U ndermigration Overmigration Failed Migration
Considered the Neurons in the
Failure to migrate both in mildest form of periventricular
amount an in order - with a Classic Instead of failing to migrate (subependymal)
reverse outside-in pattern. Large Lissencephaly an adequate number of region were too
numbers of neurons do not even neurons to the cortical lazy to migrate to
reaching the cortical plate, Disorganized surface (as is the case in the the cortex.
depositing diffusely between the migration results in a classic type of
ventricular and pial surfaces. second layer of lissencephaly), this The result is
cortical neurons deep pathology is the result of an nodular grey
over migration.
The distribution is fucked with 4 to the more matter deposition
superficial cortex. along the ventricle
thick layers formed instead of 6. This over migration results borders.
This creates the in an additional layer of
classic "double cortex composed on gray Most common
cortex" appearance. matter nodules. location for grey
matter heterotopia.
These nodules come in a
variety of shapes and sizes Associated with
(unilateral, bilateral, small,
large, symmetric or seizure disorders.
asymmetric).
As a result of this disorganized / Associated with
seizure disorders. Most commonly It is THIS VS THAT:
inadequate migration the process
commonly located adjacent
of cortical folding does not take Gyral pattern is to the Sylvian fissures Heterotopias
place. normal follow grey matter
(or mildly on all sequences
Smooth Surface, Thick Cortex simplified). and NOT enhance.
Cobblestoned Cortex
Colpocephaly is Common. Subcortical band of Subependymal
(variable in size/ location)
heterotopic gray tubers of TS are
"Figure 8" shaped brain on axial
-due to shallow, vertical Sylvan matter Associated with congenital usually brighter on
fissures muscular dystrophy. and T2 relative to grey
X-Linked Inheritance retinal detachment - matter and may
Autosomal Inheritance (M=F) (F>M) "muscle- eye-brain disease" also be calcified.
Associated with CMV (maybe)
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Failure to Organize: Polvmicrouvria .,PMG"
I've heard people blame this on TORCH infections, toxic exposure, chromosomal issues, God's wrath
for "stuff the Democrats do." There are likely many causes. I wouldn't expect someone to ask for
"the cause," other than perhaps the broad category of failed organization.
Having said that, I've read some PhD papers saying that layer 5
gets obliterated (by infection, toxins, wrath, etc ..) after
completion of normal migration. With layer 5 gone the other
more superficial layers overfold and fuse resulting in an excessive
number of small folds - the hallmark finding.
Classic Look: Fine undulating / bumpy cortex.
This anomaly come in a variety of shapes and sizes
(unilateral, bilateral, small, large, symmetric or asymmetric).
Most common location is adjacent to the Sylvian fissure Fine Undulations / Bumps
bilaterally.
Wl Trivia: Zika Virus is the most common cause of PMG in Brazil and South America
Failure to Organize: Schizencephalv- .,Split Brain"
Just like polymicrogyria there are likely many causes and I wouldn't expect someone to ask for "the
cause," other than perhaps the broad category of failed organization.
Having said that, one popular theory is the idea of a vascular insult. What is this vascular insult ?
Well, you could say it's the cortex's reckoning (it damages the radial glial fibers). These radial glial
fibers are in charge (or at least they "feel in charge") of the ropes used by neurons to "make the
climb." Although, I've head it's best to make the climb as the child did - without the rope. I mention
this because about 30% of patient's with schizencephaly also have non-CNS vascular stigmata
(example = gastroschisis - which supposedly occurs from a vascular insult to the abdominal wall).
Classic Look: Schizencephaly literally means "split brain" with the defining feature being a cleft
(lined with grey matter) connecting the CSF spaces with the ventricular system. How wide this cleft is
depends on the flavor; Closed Lip (20%) or (2) Open Lip (80%), although in both cases the cleft
should span the full thickness of the involved hemisphere. The clefts can be unilateral or bilateral.
, ........................................................................................................... r··········..············· ..····........................................................................ .,,
! Closed Lip (20%) - Less Common, Less Severe !
! appear
In this form, the "Lip" will ! This one is more obvious.
! closed without a !
! CSF filled cleft. To make i To make the call you want
i the call you want to look j to see a CSF-filled cleft
! for is the grey matter i (lined with grey matter)
jrunning across the normally ! extending from the
! uniform corona radiata.
! ventricle to the pial
!ipouching !i
surface.
Sometimes you can see a "nipple" of grey mater
at the ependymal (ventricular) surface. jThe gray matter lining is often weird looking
:
:
:
:: !(kinda nodular like a heterotopia).
:
: :
'l,••••••••--•••••••.... •••••••--••• .. •• .. •••• ..•uou••••o•..••••••••••--•--••••••••n.. ,,,,,,,,,,,,,,,,,, • : ........................................................................................................J
Associations: Absent Septum Pellucidum (70%), Focally Thinned Corpus Callosum,
Optic Nerve Hypoplasia (30%), Epilepsy (demonic possession)
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oeve1opmen1a1 Failure Mimics - Hvdranencephalv and the Porencephalic cvst
These can be thought of along a
spectrnm of severity.
Least Severe _..,,,,,.,._► ► More Severe
These things may look like a severe
developmental anomaly but the
underlying mechanism is different.
They are "acquired." Classically by a
vascular insult - but really from
anything that can cause
encephalomalacia (focal necrosis of
both the gray matter and white matter
with eventual cystic degeneration).
This would include a trauma after bitih
(this doesn't have to happen in utero).
Internal
Understanding that the brain develops Brain cleft/ hole from Bilateral ICA Herpes is
normally first - then gets crushed, a prior ischemic event occlusion the most
helps to remember the key findings. resulting in causes classic, but
In particular, the absence of a� encephalomalacia. massive in utero
matter lining along the defect. destruction of infection
Cyst/Cleft can both cerebral with toxo or
It's almost like someone took an ice communicated with hemispheres. CMVare
cream scoop to the brain. In the case the Subarachnoid only the also
of Porenchephaly, they just took one Space ("external") cerebellum, described
scoop. In the case of Hydranencephaly, mimicking an open lip midbrain, and causes.
the glutinous pig took pretty much the Schizencephaly or the falx
entire brain - leaving only the communicated only (usually)
cerebellum, midbrain, and the fal� with the ventricular remain.
system ("internal").
The trick is to lookfor gray matter lining the cleft.
Brain cleft/ hole from a prior CSP-filled
event (maybe ischemic) cleft
Cleft is
resulting in damage to the extending
Lined with
structural cells needed to from the
Gray
properly organize the co1iex. ventricle to
Matter
the pial
Not Normally Formed surface.
Brain cleft/ hole from a prior CSP-filled
ischemic/ traumatic event cleft
CJ
Cleft is
=a
..c::
resulting in encephalomalacia. extending
NOT Lined
from the
=
�
�
Normally formed - but massive
insult make it look
ventricle
and/or the pial
with Gray
Matter
developmental. surface.
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� "That Brain is Fucked" �
His onlv hope for emplovment is Hospital Administration... or mavbe QA Officer.
Unless "Brain is Fucked" is a choice on the exam, you'll need to narrow down your
choices. I suggest the following strategic algorithm, simplified essentially into 2 questions.
(1) Is the Cortical Mantle (outside of brain) present or gone fishing ?
(2) If the Mantle is still there (even if it's very thin), look for the falx cerebri.
+
"That Brain Appears to Be Fucked"
Cortical Mantle ?
Still The �e
"
Faix? Hvdranencephalv
SUH There� \, Nope
Severe Hvdrocephalus Holoprosencephalv-Alobar
-Still Got a Faix -Anterior falx usuallv missing in the semi-lobar form
-lobar [ mild J SUblVPB should still have the flax
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Herniation svndromes - Testable Vocab and Chiari Malformations
Testable Vocab: Cephaloceles
"Cephalocele" is an umbrella term for a herniation of the cranial contents through a defect in the
skull. While retaining the suffix "cele" they are then sub-classified based on (1) location, and (2)
what is in the herniation sac.
Meningocele Meningo-
;;
I I
-CSF & Encephalocele
, � ttf,,1" �3 ;ie:i1N
i
ges
-<;:Jlt�';; ,
7
:
� Fronto-
!
!
Ethmoid�
Thans- t'
IIi l Meningoencephaloceles
*For the purpose of fucking with you,
are sometimes
l Sphenoidal Occipital ! i called Encephaloceles.
*most classic
!.,,., Additional Trivia:
........................................................................................................................ • Cystocele = CSF, Meninges,
Brain, and Ventricle
• Myelocele = Spinal Cord
Herniation svndromes: Chlarl Malformations 'I. .............................................................................................. .
This topic is incredibly complicated. There are literally entire books written on the individual
subtypes. The following is my best effort to distill the potentially testable trivia down to about 1.5
pages.
There are several numbered sub-types of Chiari malformations, with the shared finding of a
downward displacement of the cerebellum. Here is a quick overview of the subtypes.
Type I Type II
Historically used to describe
Relatively less severe cerebellar hypoplasia
Features of Chiari 2
Herniation of cerebellar tonsillar herniation. without herniation. T he term
has fallen out of favor with the
tonsils (more than 5 Relatively more AND powerful men and women
mm) cerebellar vermian Occipital Encephalocele who control the Chiari
displacement nomenclature.
We shall not speak of it again.
Classic Association Classic Features: Type 1.5
(not always present):
-Low lying torcula Hybrid term used to describe conditions that have features of
both type 1 and type 2.
• Syrinx (cervical cord) -Tectal beaking
-Hydrocephalus
-Clival hypoplasia Not associated with neural tube defects, despite the significant
downward movement of the tonsils and brain stem.
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Chiari Type I <Chjari Type II
" ' . -
Thinned Corpus Callosum Tectal Beak
Occipital Encephalocele,
Clival Low Lying (meningoencephalocele)
Classically defined as 1 or Hypoplas1a Torcula containing cerebellum and/
both tonsils > 5mm below Opposite of or the brainstem, occipital
*Also note Dandy Walker lobe, and sometimes even
the level of the the long skinny
Basion - - - Opisthion. 4th ventricle, and the fourth ventricle. PLUS
the "towering features of of Chiari 2
Note the commonly cerebellum."
associated Syrinx.
Classic Mechanism: Normal for
Congenital underdevelopment Comparison
of the posterior fossa, leading
to overcrowding, and Compared to Type 1, there is relatively less
downward displacement. tonsillar herniation, but more cerebellar vennian
displacement
Non-Classic: Post traumatic
deformity - acquired later in
life.
Clinical Symptoms are
produce in two flavors:
(1) Occipital headache from
pressure of the cerebellar
tonsils - worse with sneezing
(2) Weakness, spasticity, and Interdigitated
loss of proprioception from Cerebral Gyri
pressure on the cord (most classically Myelomeningocele
demonstrated on Lumbar Spine
Classic Association axial CT)
(not always present): Classic Associations:
Classic Mechanism: Neural Tube Defect
• Syrinx of the cervical cord "sucks" the cerebellum downward prior to full • Syrinx (cervical)
development of the cerebellar tonsils.
• Tethered cord
Less Classic (but still highly Classic Association:
• Hydrocephalus
testable) association:
-Lumbar myelomeningocele / Spina Bifida
-Klippel-Feil Syndrome • Agenesis of the corpus
(congenital C-spine fusion). callosum
Only seen in patients .with_a
NOT associated with a
Only seen in patients with a neural tube defect neural tube defect (NTD).
neural tube defect
Encephalocele == NTD
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Special Topic - Mesial Temporal Sclerosis
This is a pattern offindings (hippocampal volume loss + gliosis/ scar), which classically result in
intractable seizures. The etiology is not certain, but it is most likely developmental (hence the
inclusion in this section).
� Clinical Trivia: This is the most common cause ofpartial complex epilepsy.
Clinical Trivia: Surgical removal can "cure" the seizures/ demon. Alternatively, perfect
' intracranial positioning ofa tooth (from a red haired woman) has been described as
therapeutic in the Kazakhstani literature.
The hippocampal region represents the medial portion ofthe temporal lobe (black box).
For the purpose of multiple choice, the primary imaging findings are:
• Reduced Hippocampal Volume (best seen when compared to the opposite site).
* I 0% of the time volume loss is bilateral - other.findings are necessary to exclude fuckery
• Increased T2 Signal (from gliosis/ scar)
• Loss of Normal Morphology (loss ofnonnal interdigitations)
Note the
compensatory
enlargement of the
temporal horn of the
lateral ventricle
*white arrow
Reduced Volume,
Increased T2 Signal Normal Side for Comparison
*black arrow
Additional described findings - less likely to be shown (more likely to be asked)
• Atrophy ofthe ipsilateral fornix and maxillary body
• Contralateral amygdala enlargement
MRI Epilepsy Protocol Trivia:
• Tl - Superior for Cortical Thickness, Eval ofGrey / White
• FLAIR - Superior for Cortical/ Subcortical Hight Signal (Gliosis)
• T2* I SWI - Superior for Blood Breakdown Products (for other things that can cause seizures;
calcifications oftuberous sclerosis, Sturge-Weber, Cavernomas, Gangliogliomas etc.. )
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..
•
..
�; ,·i•': .··
�
SECTION 3:
VOLUME & EDEMA �
• • • •
;.
Monro-Kellie Hypothesis:
The Monro-Kellie Hypothesis is the idea that the head is a closed shell, and that the three
major components: (1) brain, (2) blood- both arterial and venous, and (3) CSF, are in a state
of dynamic equilibrium. As the volume of one goes up, the volume of another must go
down.
Normal Situation Leaking CSF lntracranial Hypertension
-Venous Blood Expands -Venous Sinuses Compress
to Compensate
lntracranial HVPOtension: If you are leaking CSF, this will decrease the overall fixed volume,
and the volume of venous blood will increase to maintain the equilibrium. The result is
meningeal engorgement (enhancement), distention of the dural venous sinuses, prominence
of the intracranial vessels, and engorgement of the pituitary ("pituitary pseudo-mass"). The
development of subdural hematoma and hygromas is also a classic look (again, compensating
for lost volume).
Idiopathic lntracranial Hypertension [Pseudotumor CerebriJ: Classic scenario of a fat
middle-aged women with a headache. Etiology is not well understood (making too much
CSF, or not absorbing it correctly). It has a lot of associations (hypothyroid, cushings,
vitamin A toxicity). The findings follow the equilibrium idea. With increased CSF the
ventricles become slit-like, the pituitary shrinks (partially empty sella), and the venous
sinuses appear compressed. You can also have the appearance of vertical tortuosity of the
optic nerves and flattening of the posterior sclera.
Changes in intracranial pressure can create a downward displacement of the brainstem
stretching the 6th cranial nerve - it is said that 1/3 of patients with pseudotumor cerebri have
sixth nerve paresis as their only neurologic deficit
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Hvdrocephalus- Too Much CSF"
11
Questions on this topic are most likely to be centered on the sub-type, location of obstruction, and
cause. So, let us now review
· the vocab. ----·----·--
True Obstruction
"Communicating" Blood, Pus, and Cancer -Anything that
plugs up the villi - the three most common
-All Ventricles are Big causes being SAH, Meningitis (TB or
(25% of the time the fourth Bacterial), and Carcinomatous Meningitis.
ventricle is normal) /
Without Obstruction
-Level of obstruction
between basal cisterns and Brain Atrophy (ex-vacuo)
arachnoid granulations
I
Normal Pressure Hydrocephalus
- CSF can exit all the -see discussion below
ventricles
Choroid Plexus Papilloma
�
-Tumor that secretes CSF.
-Discussed more later in the chapter
Ventricles "NON-Communicating" Level of Obstruction
are Big
(one or all) -Upstream Ventricles are Foramen of Monro =
\
Big • Colloid Cyst
Aqueduct =
-Level of Obstruction is
• Aqueduct Stenosis
within the ventricle System
• Tectal Glioma
- CSF can NOT exit all the 4th Ventricle =
ventricles • Posterior Fossa Tumor
• Cerebellar Edema / Bleed
Normal Pressure Hvdrocephalus: It's not well
understood - and idiopathic. The step 1 trivia is "wet. Quiz: Is
wacky. and wobbly" - describing the clinical triad of transependymal
urinary incontinence, confusion, and ataxia. The key flow seem more
points clinically are the patient is elderly (60s), and with acute
the ataxia comes first and is most pronounced. hydrocephalus
or chronic
The buzz-phrase is "ventricular size out of proportion
hydrocephalus?
to atrophy." The frontal and temporal horns of the
lateral ventricles are the most affected. "Upward Answer: Acute.
bowing of the corpus callosum" is another catch
phrase. On MRI you may see transependymal flow
and/or a flow void in the aqueduct and 3rd ventricle. Communicating Hydrocephalus +
This is treated with surgical shunting. Elderly + Ataxia = NPH.
Syndrome of Hydrocephalus in the Young and Middle-aged Adult (SHYMA): Similar to NPH but in a
middle aged population - and more headaches less peeing of the pants (HA+Wacky+Wobbly).
Communicating Hydrocephalus + Middle Aged + Headache = SHYMA.
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Congenital Hvdrocephalus
There are several causes of hydrocephalus that can be present at bhih or be related to fetal
development. These conditions are typically diagnosed prior to birth via routine ultrasound
(discussed partially in the reproductive chapter in volume 1).
The big 4 are: (1) Aqueductal stenosis, (2) Neural tube defect - usually Chiari II, (3) Arachnoid cysts,
and (4) Dandy-Walker. I've discussed Chiari II and Dandy-Walker already.
So, let us turn our attention to Aqueductal Stenosis and Arachnoid Cysts.
Aqueductal Stenosis:
This is the most common cause of congenital obstructive hydrocephalus. Classically from a web or
diaphragm at the aqueduct (hence the name). Because of the location you get a "non-communicating"
pattern with a dilation of the lateral ventricles and 3rd ventricle with a normal sized 4th ventricle. You
can have a big noggin (macrocephaly) with thinning of the cortical mantle.
12nd Obstruction at the
level of the
aqueduct
Normal for Com
\'-r./1 r'\\J> Treatment is going to be either shunting or
poking a hole in the 3rd ventricle (third ventriculostomy).
Qµ Clinical Trivia: Question header may describe "sunset eyes" or an upward gaze paralysis.
\! r'\ Clinical Trivia: A male with ''flexed thumbs" should make you think about the x-linked variant.
'-r./ \J> (Bickers Adams Edwards syndrome).
Arachnoid cvsts:
As the name implies, these are cysts located in the subarachnoid
space. They are CSF density, without any solid components, or
abnormal restricted diffusion. You wouldn't even notice them
expect that they can exert mass effect on the adjacent brain, or in
the context of this discussion block a CSF pathway (obstructive
type).
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CSF Shunt Malfunction
Normal: The most basic shunt consists of a proximal tube (usually placed in
the frontal hom of the lateral ventricle just anterior to the foramen of Monro), a
valve to control flow, and a distal tip (usually dumped in the peritoneum, but
can be placed in the pleural space or right atrium).
Shunt Evaluation Options: Your first line options for shunt evaluation are going to be (a) non-con CT or
(b) rapid single shot T2 sequence - mainly looking at catheter position and ventricle size. *May need to
verify shunt settings with a plain film post magnet. If the ventricles are big (shunt is not working) you
might follow that up with a radiograph series (neck, chest, abd) to make sure the catheter is intact.
Ultrasound or CT can be used to inspect the distal tip for a fluid collection. Alternatively (if you are a
weirdo) you can inject < 0.4ml pertechnetate into the shunt reservoir and take images to look for leakage
or blockage (remember to not aspirate when you inject).
-Proximal> Distal
Obstruction -Most common cause = ingrowth of choroid
(proximal) plexus and particulate debris/ blood products
-Can also be from catheter migration
-Pseudocyst
Obstruction (loculatedjluid along the distal tip) Loculated fluid
(distal) -Catheter migration around the tip of
(more common in children) the catheter
- "Slit Like Ventricles" - can be meaningless or Slit Ventricles
suggest too much shunting.
Over - The big fear is that not enough CSF will cause Extra-Axial Fluid
Shunting subdural hygroma or hematoma formation via Collections
Monroe Kelly mechanics (less CSF - more (subdural hygroma)
blood).
-Usually within 6 months of placement
-Blood cultures are usually negative (fluid from
the shunt should be cultured instead).
-Mild enhancement after catheter placement can
be normal - be on guard for fuckery.
-The best sign is debris within the ventricles,
ideally shown with 12M - this is the weapon of
Infection choice for diagnosis of ventriculitis. Tl+C: ventricular DWI: Debris/
ependymal Pus Restricts
enhancement Ditfosion
-Late stigmata may include ventricular
loculations - which can cause restricted flow/
obstruction and in some case isolate or "trap" the
4th ventricle - as shown in diagrams.
►
Either deliberately or via migration the catheter can end up in the pleural space. A little
Hydrothorax bit of pleural fluid doesn't mean shit. But, if the volume gets large enough and the
patient becomes symptomatic - then revision might be needed.
Usually the ascites from a VP shunt isn't symptomatic, although there are reports of
Ascites inguinal hernias and hydroceles forming secondaiy to the increased abdominal pressure.
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Edema:
Cytotoxic: This type ofedema can be thought about as intracellular swelling secondary to
malfunction ofthe Na/K pump. It tends to favor the gray matter, and looks like loss of the
gray-white differentiation. This is classically seen with stroke (or trauma), and is why
EARLY signs ofstroke involve loss ofthe GM-WM interface.
Vasogenic: This type ofedema is extracellular, secondary to disruption ofthe blood-brain
barrier. It looks like edema tracking through the white matter (which is less tightly
packed than the gray matter). This is classically seen with tumor and infection. You can
also see this type ofedema as a LATE stage ofcerebral ischemia. A response to steroids is
characteristic ofvasogenic edema.
� THIS vs THAT:
cvtotoxic Edema vasogenic Edema
Failed Na/K Pump Increased Capillary Permeability
(BBB intact) (BBB NOT intact)
Classic = lschemia (EARLY) Classic = Tumor, Infection, lschemia (LATE)
White Matter + Gray Matter - "blurring" White Matter (Spares Gray Matter)
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Brain Herniation:
Subfalcine (Cingulate) Herniation: This is just a fancy way of saying midline shift (deviation of
ipsilateral ventricle and bowing of the falx). The trivia to know is that the ACA may be compressed,
and can result in infarct.
Descending Transtentorial (Uncal) Herniation: The uncus and hippocampus herniate through the
tentorial incisura. Effacement of the ipsilateral suprasellar cistern occurs first.
Things to know:
• Perforating basilar arte1y branches get compressed resulting in "Duret Hemorrhages"-
classically located in the midline at the pontomesencephalic junction (in reality they can also
affect cerebellar peduncles).
• CN 3 gets compressed between the PCA and Superior Cerebellar Artery causing ipsilateral
pupil dilation and ptosis
• "Kernohan's Notch I Phenomenon" -The midbrain on the tentorium forming an indentation
(notch) and the physical exam finding of ipsilateral hemiparesis -which Neurologists call a
''false localizing sign. " Of course, localization on physical exam is stupid in the age of MRI,
but it gives Neurologists a reason to cany a reflex hammer and how can one fault them for
that.
Ascending Transtentorial Herniation: Think about this in the setting of a posterior fossa mass. The
vermis will herniate upward through the tentorial incisura, often resulting in severe obstructive
hydrocephalus.
Things to know
• The "Smile" of the
quadrigeminal cistern will
be flattened or reversed
• "Spinning Top" is a
buzzword, for the
appearance of the midbrain
from bilateral compression
along its posterior aspect
• Severe hydrocephalus (at
the level of the aqueduct). Transcalvarial
*through
l
Fracture
Cerebellar Tonsil Herniation: scending
Ascending Transtentorial
Can be from severe herniation after
Transtentorial
downward transtentorial herniation.
Alternatively, if in isolation you are
thinking more along the lines of Downwa,tJ
Chiari (Chiari I= 1 tonsil - 5 mm). Cerebellar
Tonsillar
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..
.,.
;
. . �
SECTION 4:
METABOLIC & TOXIC
�-
Metabolic Plagues on the Alcoholic Urban Outdoorsman - part 1
Osmotic Demyelination or
Wernicke Encephalopathy
Central Pontine Myelinolysis
High T2/FLAIR
IR
High T2/FLA Signal in Signal in the
T2 Bright Central Pons (spares the periphery) the Medial Thalamus Periaqueductal Gray
Most Classic Scenario: Asshole drunk Hobo shows Most Classic Scenario: Ve1y friendly Hobo - known
up to the ER with a low Na. Like most asshole for singing songs from the 70s (mostly Supertramp's
drunks in the ER, he starts out demanding a goodbye stranger) - starts acting squirrelly. "His
cheeseburger and a Sprite (not a fucking Sierra tempo seems off'' - notes the feminine male nurse.
Mist!), then threatens to leave against medical advice.
. . . after finishing the burger. An above average medical student suggests he is
Family Medicine Resident begs him to stay exhibiting the clinical triad of (1) acute confusion,
(a decision he will soon regret). The Resident (2) ataxia. and (3) ophthalmoplegia, but is dismissed
eventually tires of his bullshit and decides to correct by the Medicine Intern who talks non-stop about
his hyponatremia as rapidly as possible - with the going into Cardiology ("Cards" - he calls it).
goal of expediting discharge.
Only moments later the same Intern will suggest to
2 days later the guy is still in house, acting like a his Attending the same triad of findings before
massive prick - acutely encephalopathic with spastic stating "my medical student" seems disinterested and
quadriparesis. may benefit from more call.
Neurology gets consulted and writes "pseudobulbar
palsy" in the chart. Family Medicine Resident Still desperate to honor the clerkship, the student
doesn't know what the fuck that means, but is humble suggests thiamine (vitamin Bl) deficiency as the
enough to ask. A below average 2nd year medical etiology, and says the symptoms could progress to
student explains to him that it is slurred speech, chronic memory loss and confabulation (Korsakoff
sensitive gag reflex, and being an even bigger cry psychosis) or even death.
baby than nonnal- "labile emotional response".
Coma, the above MRI, death, then a lawsuit follow The cycle repeats - additional call is assigned, and a
(in that order). formal letter of reprimand is issued to the student.
• T2/FLAIR bright classically seen in medial/dorsal
• T2 bright in the central pons (spares periphery) thalamus (around the 3rd ventricle), periaqueductal
• Earliest change: restricted diffusion in lower pons gray, mamillary bodies, and the tectal plate.
• Trivia: Can also have an extra-pontine presentation • Enhancement is classic in the mamillary bodies
involving the basal ganglia, external capsule, • MR Spect = Lactate
amygdala, and cerebellum. • Treatment = Thiamine replacement.
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Metabolic Plagues on the Alcoholic Urban Outdoorsman - part 2
Marchiafava-Bignami Misc
Direct Alcoholic Injury:
Most Common I Classic Finding(s):
Brain Atrophy. Particularly the cerebellum
and especially the cerebellar vermis
Cerebellar Atrophy
-High T2/FLAIR in the Corpus Callosum-
Most Classic Scenario: A middle aged (50s) man is Copper & Manganese Deposition:
stumbles into the ER. On the pre-assessment forms
he has described himself as a "semi-professional red
wine taster." He seems to exhibit variable degrees of
mental confusion, and his gait appears altered.
His chief complaint is seizure and muscle rigidity.
He interrupts the H&P stating that he needs to urinate
("drain his hog" - he says). A nurse hands him a
urinal but his muscle rigidity seems to be impair his Tl Bright
coordination. It looks like the floor is about to get Basal
very wet, when his the nurse (a shy, but aggressively Ganglia
religious, elderly women) tries to assist him. The
patient barks at the nurse "Not now woman! Leave
the dick alone!" Her face blushes with
embarrassment. The ER Attending can't help but
laugh. The medical student shadowing him also
laughs (but only after the Attending does so first). -Non-Specific and related To Liver Disease.
-Can be seen without hepatic encephalopathy
Later the Attending will reprimand the medical -Also seen in TPN, Wilson's Disease,
student for laughing. In a formal letter, the Attending -Also seen in Non-Ketotic Hyperglycemia (HNK) in
says the student's lack of professionalism is shocking which it's often unilateral
- additional call is assigned.
• Swelling/ T2 bright signal at the corpus callosum
Methanol Toxicity:
(represents an acute demyelination)
• Order is progressive - typically beginning in the "Drinking Windshield Wiper Fluid" as an idiotic
body, then genu, and lastly splenium attempt to get drunk. Can also be seen from
consuming "poorly adulterer moonshine" - or "West
• "Sandwich sign" on sagittal imaging - describes Virginia Budweiser."
the pattern of preference for central fibers with
relative sparing of the dorsal and ventrals fibers Classic Findings: Optic nerve atrophy, hemorrhagic
• Chronic Phase: Thinned corpus callosum + cystic putaminal and subcortical white matter necrosis
cavities favoring in the genu and splenium
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£11 THIS vs THAT: Carbon Monoxide vs Methanol:
Carbon CT Hypodensity / T2 Bright: Globus Pallidus
Monoxide ( carbon monoxide causes "globus" warming).
T2 Bright: Putaminal - which may be
Methanol hemorrhagic, and thus CT Hyperdense.
PRES (Posterior Reversible Encephalopathv svndromeJ:
Classic Features:
• Asymmetric cortical and subcortical white matter
edema (usually in parietal and occipital regions
*but doesn't have to be - superior frontal sulcus is
also common).
• Does NOT restrict on diffusion (helps tell you it's not
a stroke).
Etiology: Poorly understood auto regulation fuck up.
Vasogenic Edema Pattern
Classic History: Acute Hypertension or Chemotherapy. Bilateral, Posterior, Mildly Asymmetric
Post Chemotheraov:
It is fairly common. There are lots of named offenders. Methotrexate seems to be the one people
write the most papers about ( especially in kids with ALL)
There are two main looks:
(1) PRES - As above, chemo is a classic cause. BUT! It tends to have a "non-classic" look relative
to the hypertension type. It will often spare the occipital lobes, and instead target the basal
ganglia, brainstem, and cerebellum.
(2) Leukoencephalopathy (treatment induced): The classic look would be centered in the
periventricular white matter - bilateral, symmetric, confluent, T2/FLAIR bright changes (histo1y
is obviously key to the diagnosis).
Other Misc Trivia:
• Can progress to brain atrophy.
• "Mineralizing Microangiopathy" - the vocab word to use if there are calcifications
• "Disseminated necrotizing leukoencephalopathy" - severe white matter changes, which
demonstrate ring enhancement , classically seen with leukemia patients undergoing radiation
and chemotherapy. It is bad news and can be fatal (it believes in nothing Lebowski).
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Post Radiation:
The quick and dirty version is that after radiation therapy to the brain you can see T2 bright areas
and atrophy corresponding to the radiation portal. You can also see hemosiderin deposition and
mineralizing microangiopathy (calcifications involving the basal ganglia and subcortical white
matter). There is a latent period, so imaging findings don't typically show up for about two months
post therapy. Now ... if you want to get crazy, you can discuss changes at different time periods.
Acute
Too rare to give a fuck about (at least for the test)
(Days-Weeks):
Early Delayed The classic look is similar to chemo - high T2/FLAIR This is reversible
(1-6 months): signal in the periventricular white matter. change (usually).
Described as a "mosaic" pattern with high WM signal
Late Delayed changes again favoring the deep white matter. Can Progressive ... but
(6 months): appear "mass-like" and expansile. reversible (mostly)
Classically sparing of the U-Fibers & Corpus Callosum.
Radiation-Induced Vasculopathy: Strokes and Moya-Moya type of look.
Mineralizing Microangiopathy - I mentioned this on the previous page. This is a
delayed finding - like two years following treatment. Think calcifications (basal
ganglia and subcortical white matter) - hence the term "mineralizing."
Radiation-Induced Vascular Malformations: The most classic types are capillary
Long Term telangiectasias / cavernous malformations. The most classic scenario is a kid
Sequela getting whole brain radiation for ALL. Remember the key finding is blooming on
GRE/SWI sequences.
Radiation-induced Brain Cancer:
• XRT is the "most important risk factor" for primary CNS neoplasm.
• Most common type is a meningiomas (70%) - usually seen - 15 years post XRT
• More aggressive types Gliomas, Sarcomas, etc, have a shorter window< 10 years
"Chasing the Dragon" - Heroin lnhalational Leukoencephalopathv
Most toxic leukoencephalopathies (either from chemotherapy, immunosuppressives, antibiotics,
or the aristocratic art of paint thinner huffing) all create a similar non-specific pattern of widespread
high T2/FLAIR signal in the supra and infratentorial white matter. The "Chasing the Dragon"
pattern is also not specific - but it does have a catchy name, so people love collecting cases of it to
show in conference ("catchy name"= high yield for boards).
The most classic look (diagrams are FLAIR sequences):
nucleus
Symmetric "Butterfly" in High Signal in the Posterior High Signal in the Deep (arrows)
the Centrum Semiovalc Limb of the Internal Capsule Cerebellar White Matter
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SECTION 5:
NEURO--DEGENERATIVE
Multiple Sclerosis:
White matter patterns can be confusing as there are tons of
overlapping non-specific features. To help understand this (and
avoid being tricked) let me introduce a few concepts. White matter
lesions come in a few patterns. MS is the poster child of the
"perivascular pattern." This pattern favors involvement of the
juxtacortical and periventricular regions with lesions that have
ovoid and/or fusiform morphology.
Juxtacortical
Ovoid, Fusiform Periventricular
Size can be helpful. A single
lesion > 15 mm in size suggests the underlying etiology is not
vascular.
Certain locations will also make you think "not Vascular Perivascular
vascular." When you think "not vascular Pattern Pattern (MS)
pattern" you should think demyelinating. Corpus Callosum RARE COMMON
When you think demyelinating you should think
MS first (it's by far the most common). Juxtacortical . RARE COMMON
lnfratentorial RARE COMMON
Basal Ganglai COMMON RARE
McDonald Diagnostic Criteria for MS:
This was last revised in 2010, so it's kind of an old McDonald's Diagnostic Criteria.
• And on his criteria he had a section of lesions disseminated in space (periventricular,
juxtacortical, infratentorial, spinal cord) - more than 1 in at least 2 of these locations.
• And on his criteria he had a section on dissemination in time: best shown as a T2 bright lesion
that does enhance (active) and a T2 bright lesion that does not enhance (in-active)- lesions
are in different phases of the disease and therefore separated by time.
Epidemiological trivia:
• Usually targets women 20-40 (in children there is no gender difference).
• There are multiple sub-types with the relapsing-remitting form being the most common (85%).
• Clinical history of "separated by time and space " is critical.
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Additional MS Related Trivia:
• Most Classic Finding: T2/FLAIR oval and periventricular perpendicularly oriented lesions.
• Involvement of the calloso-septal interface is 98% specific for MS (and helps differentiate it
from vascular lesions and ADEM).
• In children the posterior fossa is more commonly involved.
• Brain atrophy is accelerated in MS.
• Solitary spinal cord involvement can occur but it is typically seen in addition to brain lesions.
• The cervical spine is the most common location in the spine (65%).
• Spinal cord lesions tend to be peripherally located.
• FLAIR is more sensitive than T2 in detection of juxtacortical and periventricular plaques.
• T2 is more sensitive than FLAIR for detecting infratentorial lesions
• MR spectroscopy (discussed later in the chapter) will show reduced NAA peaks within the
plaques.
Active vs Not Active : Acute demyelinating plaques should enhance and restrict diffusion (on
multiple choice tests and occasionally in the real world).
Tumor vs MS: You can sometimes get a big MS plaque that looks like a tumor. It will ring
enhance but classically incomplete (like a horseshoe), with a leading demyelinating edge.
Tumor = Complete Ring Demyelination = Incomplete Ring
Multiple Sclerosis Variants:
ADEM (Acute Disseminated Encephalomyelitis): Typically presents in childhood or
adolescents, after a viral illness or vaccination. Classically has multiple LARGE T2 bright
lesions, which enhance in a nodular or ring pattern (open ring). Lesions do NOT involve the
calloso-septal interface.
Acute Hemorrhagic Leukoencephalitis (Hurst Disease): This a fulminant form of ADEM with
massive brain swelling and death. The hemorrhagic part is only seen on autopsy (not imaging).
Devics (neuromyelitis optica): Transverse Myelitis+ Optic Neuritis.
Lesions in the Cord and the Optic Nerve
Marburg Variant: Childhood variant that is fulminant and terrible leading to rapid death. It
usually has a febrile prodrome. "MARBURG!!!" = DEATH
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Subconlcal Arteriosclerotic Encephalopathv lSAEJ
Also referred to as Binswanger Disease - for the purpose of fucking with you.
It's best thought of as a multi-infarct dementia that ONLY involves the white matter.
Trivia:
• It favors the white matter of the centrum
semiovale (white matter superior to the
WTF are "U Fibers" ?
lateral ventricles/ corpus callosum).
They are the
• Classically spares the subcortical U fibers. fibers under the
• Strong association with Hypertension. cortex, that look
like "U"s.
• It's seen in older people - 55 and up
They come up a
• If they show you a case that looks exactly lot, as being
like SAE but that patient is 40 and has spared or not
migraines they are leading you to the
genetically transmitted form of this disease spared.
called CADASIL.
CADASIL (Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts & Leukoencephalopathy)
Basically it is SAE in a slightly younger person (40), with migraines.
Classic Scenario: 40 year old presenting with migraine headaches, strokes, then eventually
dementia. CADASIL is actually the most common hereditary stroke disorder.
Step 1 Trivia: NOTCH3 mutations on chromosome 19
Classic Imaging Findings: Severe white matter disease (high T2/FLAIR signal) involving multiple
vascular territories, in the frontal and temporal lobe. The occipital lobes are often spared. Temporal
lobe involvement is classic.
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Dementia Disorders:
This topic was split up in prior editions on the text, with half in neuro and half in nukes. The
reason I did that was because these disorders are often evaluated with FOG PET. To keep
you from having to hop around I decided to consolidate it this time around.
FDG PET for dementia is a worthless and expensive component of the workup. Like most
imaging exams it is ordered with no regard to the impending collapse of the health care
system under crippling rising costs (with inevitable progression into a Mad Max style
dystopian future or even better Mega-City 1 ). As such, it is standard practice in most
academic centers to obtain the study.
The idea is that "demented brain" will have less perfusion and will have less metabolism
relative to "not demented brain." PET can assess perfusion ( 15 O-H20) but typically it uses
ISFDG to assess metabolism (which is analogous to perfusion). Renal clearance of 18FDG is
excellent, giving good target to background pictures. Resolution of PET is superior to
SPECT.
HMPAO, and ECD (tracers that are discussed in more depth in the nukes chapter) can also be
used for dementia imaging and the patterns of pathology are the same.
It's important to remember that external factors can affect the results; bright lights
stimulating the occipital lobes, high glucose (>200) causes more competition for the tracer
and therefore less uptake, etc ... etc ... so on and so forth.
Before we begin with the subtypes, a quick pearl:
On FDG PET the motor strip is always preserved
in a degenerative type ofdementia.
Preserved Motor Strip
-Seen in degenerative dementias
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Dementia - The Primarv Tribes
Alzheimer Disease Multi-infarct Dementia Dementia with Lewv Bodies
Most common cause 2nd most common 3rd most common
Tauopathy, Amyloid Cascade, Also called "Vascular Alpha synuclein and synucle
and Neurofibrillary Tangles are Dementia" - for the purpose of inopathy are buzzwords people
all buzzwords people use when fucking with you. use when they pretend to
they pretend to understand the understand the
pathophysiology. pathophysiology.
Risk Factor(s): Risk Factor(s): Clinical Scenario: There is a
triad of classic features.
The biggest one is Age. • McDonalds, Burger King, (1) Visual hallucinations
Taco Bell, Pizza Hut (2) Spontaneous parkinsonism,
A more obscure one (but (3) Fluctuating ability to
certainly testable) is Downs • Hypertension, concentrate / stay ale1t
Syndrome. Downs patients
nearly always get AD, and they • Smoking (tobacco), and Clinical picture can be similar
get it earlier than normal - that to Parkinson's dementia - the
extra 21st isn't doing them any • CADASIL major difference in DLB, the
favors. dementia comes before the
Parkinsonism
Most Classic Feature(s): Most Classic Feature(s): Most Classic Feature(s):
hippocampal atrophy (which Cortical infarcts and lacunar Mild generalized atrophy
is first and out of proportion to infarcts are seen on MRI. Brain without lobar predominance
the rest of the brain atrophy). atrophy (generalized) is usually (unlike multi-infarct).
They could ask temporal horn advanced for the patients age. Hippocampi will be normal in
atrophy > 3 mm , which is seen size (unlike AD)
in more than 65% of cases.
FDG Pattern: Low posterior FDG Pattern: Multiple FDG Pattern: decreased FOG
temporoparietal uptake - scattered areas of decreased uptake in the lateral occipital
"headphones" or "ear muffi. " activity. No specific lobar cortex, with sparing of the mid
predominance. posterior cingulate gyrus
(Cingulate Island Sign).
llC PiB (Pittsburgh Unlike the neurodegenerative
compound B) is an even better dementias - this one could
way to waste money making knock out the motor strip (if the
this diagnosis. It works as an strokes happen to involve that
Amyloid Binding Tracer. region). This is different that
AD and DLB.
Picks: Also be referred to a ''frontotemporal dementia" - for the purpose of fucking with you.
Clinical: Onset is earlier than AD (like 40s-50s). Classic presentation is described as "compulsive
or inappropriate behaviors." In other words, acting like an asshole (fucking prostitutes, and buying
miracle weight loss potions from Dr. Oz - when you aren't even going to the gym or trying to eat
right). Just being a real Prick.
Classic Feature(s): Severe symmetric atrophy of the frontal lobes (milder volume loss in the
temporal lobes).
FDG Pattern: Low uptake in the frontal and temporal lobes.
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FIG PET- Brain
-Identical to Parkinson
Low posterior
Dementia
Alzheimers temporopar ietal cortical
-Posterior Cingulatc gyrus is
activity
the first area abnormal
. . -·----- --·-- . --··· '"""" ·····---- ·-· ··-· -··---- ..
Scattered areas of decreased
Multi Infarct
activity.···· ······•··········-·--·····--···-····--·-····· ···-····· ·
Preservation of the mid
Dementia with Lewy Bodies Low in lateral occipital cortex posterior cingulate gyrus
.. ............ . . ..... . ...... _ . ........... (Cingulate}sland.Sign) ...... .
Picks / Frontotemporal Low frontal lobe
Normal Alzheimers Frontotemporal
-Low posterior temporoparietal -Low Frontal Lobe
Lew Body Dementia Multi-Infarct
-Low Lateral Occipital with -Scattered Areas ofLow Uptake
sparing ofthe cingulate gyrus
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The Detias Brotherhood of Neurodeueneration - Part 1
Also called "Bilateral
Striatopallidodentate Calcinosis", and Extensive
sometimes "Primary Familial Brain C<1lcijiclltion in the
Fahr Disease Calcijkation " for the sole purpose of Basal Ganglia and
fucking with you on the exam. Thalami.
(syndrome)
*Globus is typically
Many are asymptomatic. Others go involved.first
insane and start stumbling around
Also called PKAN (pantothenate kinase
associated neuropathy) for the sole
purpose of fucking with you on the exam.
Hallervorden
Etiology: Iron in the Globus Pallidus
Spatz
T2 Dark Giobus with central bright area
of necrosis "Eye of the Tiger". No T2: D<1rk Medi<1l Blls<1l G<111gli<1 (Globus),
enhancement. No Restricted Diffusion. with central high signal dot (necrosis)
Amyotrophic Upper motor neuro loss in the brain and • Does NOT show gross volume loss.
Lateral · spine. Most people die within 5 years • T2/FLAIR tends to be Nonnal (rarely can
Sclerosis (unless you are really good at physics). be bright in the posterior internal capsule).
Tauopathy (whatever the F that means).
Cortico-basal
• Asymmetric frontoparietal atrophy.
Degeneration Awesome clinical manifestations like the
"Alien limb phenomenon" -50% of cases.
One of those AD repeat sequence things. Caudate Atrophy and reduced FDG uptake.
What Sequence ? 38 CAGs Mother The frontal horns will become enlarged and
Fuckers. Yes, I still remember that outwardly convex (from the atrophy pattern)
worthless factoid from Step 1.
Huntington Why? It's a curse. My mind is like a bear
trnp, you gotta chew your leg off to get
Disease out. So, between Step 1 & the CORE
exam, I've got tons of worthless bullshit
· up there.
Remember these poor guys turn into huge
assholes - then start flopping around. Normal Comparison Huntington
Mitochondrial Disorder • T2/FLAIR bright lesions in the Brainstem,
Leigh
Basal Ganglia , and Cerebral Peduncles.
Disease Elevated Lactate peak at 1.3 ppm • They can restrict, but do NOT enhance.
Mitochondrial Disorder • Atypical strokes in the cortical gray matter
with a nonvascular distribution (usually
MELAS Lactic Acidosis, Seizures, and Strokes occipital and parietal).
Syndrome
Elevated Lactate "doublet" at 1.3 ppm • Underlying WM is normal
Lysosomal Storage Disease / h1ferior Anterior Beak
Mucopolysaccharidoses
Hurler
Syndrome ( I) Macrocephaly with Metopic "beak"
(2) Enlarged Perivascular Spaces
(3) Beaked Inferior L 1 Vertebral Body
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The Defias Brotherhood of Neurodeueneration - Part 2
Classic Clinical Hx: Resting tremor, Rigid /
Slow movements (shutl1ing gate, etc .. ).
Impossible to diagnose on CT or MR alone -
Etiology: Reduced dopamincrgic input to but supposedly has mild midbrain volume
striatum {whatever the fuck that means). loss with a "butterfly" pattern (this would
Parkinson have to be stated, it is too subtle to show).
Disease DAT Scan -1ojlupane 123 - This exotic
Nukes study is certainly fair game for an Worth noting in the sparing ofthe midbrain
(PD) and superior cerebellar peduncles. This is a
"intermediate level" exam.
, ABnormal fairly high yield piece of trivia as it helps
•• (Period1� distinction Parkinsons from multi-system
atrophy.
rmal Possible Parkinsonian Syndrome
(Commas) (PD, MSA or PSP)
This is a monstrously complex entity, that is
"Parkinson actually 3 separate renamed entities
Plus" ("P", "C", and "A").
The highest yield pearl is the appearance of
Multi the Cerebellar subtype MSA-C ---•
System -
Trivia: I-123 MIBG can be used to �
Atrophy Cerebellar Hemisphere / Hot Cross Bun
differentiate PD from MSA, by looking at
(MSA) Peduncle Atrophy with a Sign (loss of the
the cardiac/mediastinal ratio (which is
normal in MSA, and abnormal in PD) Shrunken Flat Pons & transverse fibers)
an enlarged 4th vent.
• Also called Steele-Richardson-Olszewski
"Parkinson for the purpose of fucking with you.
Plus" • PSP = Most Common Parkinson Plus
• Unlike PD & MSA, PSP is a Tauopathy
(whatever the fuck that means).
Progressive
Supra
nuclear
Palsy
(PSP)
AR copper metabolism malfunction. Once Tl T2
the liver fills up with copper it starts
spilling over into other organs including the
brain.
Trivia: "Kayser-Fleischer Rings" - seen in
95% of patients. Prepare the Slit Lamp. Tl and T2 Bright Basal Ganglia
Trivia: Cortical Atrophy is the most . T2 Bright Dorsal Medial Thalamus
Wilson common CT finding (although obviously -�
Disease very non-specific).
Trivia: TI Bright BG is the most common
initial MR findings (supposedly).
Trivia: Copper has been suggested to be
Metro Man's only vulnerability (this is
controversial). Since literally anything is
fair game for the exam, I figured I better Panda Sign: T2 Bright Tegmentum with
mention that for completeness. normal dark red nuclei & substantial nigra
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Deep Brain Stirnulators
I want to quickly touch on deep brain stimulators. These things arc used in the treatment of Parkinson
disease, essential tremor, and chronic pain.
It is common to get a CT
immediately after DBS placement to
evaluate for correct positioning of
the electrode or any obvious
complications (bleeding, etc...).
Knowing the "correct" position is the
most useful piece of trivia.
For Parkinson Disease, the
electrodes arc typically positioned in
the sub thalamic nucleus with the
tips of the electrons located 9mm
from the midline Gust inside the
upper most margin of the cerebral ++ ◄ ►
9mm 9mm
peduncle).
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···
'.:
-\ ,• �
Introduction to MRI fpectroscopv
SECTION 6:
INTRO TO MRS,
LEUKODYSTROPHIES, 8c FRIENDS
�
• .
···· _.
The old joke in Neuroradiology is if you need to use MRS to figure something out, then you need to
go back and read the book again - starting at page 1. Someone told me that's Yousem 's joke, hut T
don't see how that is possible - because it's actually a little funny. Regardless of who made the joke
first, there is near universal acceptance that MRS is "of limited clinical utility" (a worthless turd).
Therefore, it is fair game for an intermediate level exam and we should at least talk about it a little.
I'm not going to get into the physics much here (there will be a write up in the new 3rd Edition of the
War Machine covering that). For now, I'm going to give a very basic overview and emphasize the
pathology/ clinical trivia. Then I'll be sprinkling more MRS in sporadically throughout the chapter.
Overview: The general idea is that the various metabolites which exist on the cellular level (choline,
lactate, N-acetylaspartate "NAA," etc ... etc ..., so on and so forth ...) occur in different concentrations
depending on the pathology. For example, "NAA'' is a neuronal marker. Things that destroy neurons
(like tumors) will decrease NAA. So, in general the lower the NAA the higher the grade tumor.
You will see a graph like this one, with "PPM" on the X-Axis, and "Intensity" on the Y-Axis.
.. NAA
l
Intensity is Creatine Normal ;
,, ,,"
going to tell you Hunter's ,, "'
"how much" of a
thing there is. �
Choline
'
Angle
X
,,
,, ,,
/.
It's not a raw ,,
number, and �
better thought of 2S --------""
as a ratio.
4.0 ppm 3.0 ppm 2.0 ppm 1.0 ppm
PPM stands for parts per million. Better understood as a percent of the Larmor Frequency
(1 ppm = 1 millionth of the Larmor frequency). This is important because each metabolite will
have a unique frequency distribution. For example NAA is at 2.0 ppm.
Why are the numbers counting backwards on the scale ? I'm going to answer this with the same
explanation I received as a small child when I asked why I couldn't just eat my dessert first, and my
vegetables last-- "because I'm your mother that's why!"
Hunter's Angle: This is a method to quickly , Reversed Hunter's
decide if the MRS is normal or not. Under ', Angle in a High Grade
', Glioma (GBM)
normal conditions Choline, Creatine, and NAA
should ascending in that order. Using a line to
'''
connect the tips gives you a 45 degree~ish angle. ''
If it slopes the other way (as shown) then it is '
not normal.
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MRI &Pectrosconv High Yield Pearls
Product of brain
destruction - Necrotic Tissue (spilling of membrane lipids).
lipids are present
Lipid 0.9-1.4 in necrotic brain Elevated with high grade tmnors, brain infarcts,
tissue (necrosis and brain abscess.
marker).
Classic Trivia: It's
normal to see lactate
elevated in the first
hours of life
Product of Brain tumor has outgrown
anaerobic its blood supply - is Classic Trivia: Lactate
metabolism. forced into anaerobic and Lipid peaks
Lactate 1.3 pathways for metabolism. superimpose - you
Absent under
nmmal need to use an
conditions. Also elevated with intermediate TE
cerebral abscess. (around 140) to causes
an "inversion" of the
lactate peak (so you
can see it)
Alanine 1.48 Amino Acid Found in Meningiomas
Neuronal Marker
(Neuron Glial tumors have NAA. Classic Trivia: NAA
N-acetylaspartate Viability). The higher the Glial peak is super high
"N AA" 2.0 tumor grade, the lower
Usually the tallest with Canavans.
peak. the NAA
Glutamine-
2.2-2.4 Neurotransmitter Increased with Hepatic Encephalopathy
"GLX"
Energy
Creatine - "Cr" 3.0 Metabolism Decreased in tumor necrosis.
More turnover more Choline
Choline - "Co" 3.2 Cell Membrane (thus elevated in high grade tumor, demyelination,
Turnover inflammation).
- Elevated in low grade
gliomas.
Cell Volume - Elevated in - Reduced in high
Regulator and Alzheimer's (decreased grade gliomas
Myoinositol - in other dementias)
3.5 Byproduct of
"ml" - Elevated in Progressive - Reduced in Hepatic
Glucose multifocal Encephalopathy
Metabolism. leukoencephalopathy
(PML)
� THIS vs THAT: Demyelinating vs D�myelinating
D£myelinating
Example = MS Disease that destroys normal myelin
Disease
D;xsmyelinating Example = Metachromatic Disease that disrupts the normal formation
Disease Leukodystrophy and turnover of myelin
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leukodvstroPhieS&Jriends��� � �
On the prior page, I introduced the vocab work "dysmyelinating" disease. Leukodystrophies are the classic
example of this group of pathologies. Technically speaking Leukodystrophies can occur from deficiencies
in lysosomal storage, peroxisomal function, or mitochondrial dysfunction. I'm gonna hit on mitochondrial
diseases separately as they tend to he more asymmetric and favor the grey matter. Where as the classic
forms target the white matter in a more symmetric and extensive manner.
The distinction between the Leukodystrophy subtypes is totally academic mental masturbation, since they
are all untreatable and fatal. Therefore, distinguishing between them is fair game on an intennediate level
exam (and specifically listed on the official study guide).
Leukodystrophy = Fucked White Matter in a Kid
Parieto-occipital Sex-linked recessive
Adreno (peroxisomal
Leukodystrophy Normal Predominance
enzyme deficiency)
(ALO) Head Male Predominant
Size "Extends across the
"X-Linked" Splenium of the Corpus Can Enhance &
Callosum" Restrict
Frontal Predominance
Periventricular and Most common
Nonna! Leukodystrophy.
Metachromatic Head Deep White Matter -
Size Tigroid Pattern U-fibers are
(stripes of milder relatively spared
disease).
Also hits the
cerebellum and
Weird Frontal middle cerebellar
Alexander Disease Big Head Predominance peduncles
Can Enhance
Diffuse Bilateral
Weird subcortical U fibers. Elevated NAA
Canavan Disease Big Head "Subc01iical (MRS).
Predominance"
High density foci on
Centrum semiovale and CT (in the thalamus,
Small periventricular white caudate, and deep
Krabbe white matter).
Head matter with parieto
occipital predominance Early sparing of the
subcortical U fibers.
Typically diffuse "total lack of normal
myelination" with extension to the subcortical
Normal U fibers.
Pelizaeus Head Patchy variant is also described as "tigroid" -
Merzbacher Size although that term is more classic for
Metachromatic
No enhancement. No restricted diffusion.
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leukodVStrauhles & Friends�����
As discussed on the prior page Leukodystrophies can occur from deficiencies in lysosomal storage,
peroxisomal function, or mitochondrial dysfunction. The classic forms tend to target the white matter in a
more symmetric and extensive manner. This is different than mitochondrial diseases which are more
asymmetric and favor the grey matter. Grey Matter needs more oxygen than White Matter (and White
Matter needs more oxygen than trial lawyers). Inability to process oxygen (mitochondrial dysfunction) -
helps me remember the grey matter> white matter thing.
MELAS - Mitochondrial Encephalomyopathy, Lactic
Lactate
l
Acidosis, and Stroke-like episodes. This is a Cr
mitochondrial disorder with lactic acidosis and stroke Ch
like episodes.
Tends to have a parietooccipital distribution
c;:{?
}Wr') BUZZWORD(s): "Migrating Infarcts"
Typical MRS Pattern for MELAS:
/
Increased Lactate, Decreased NAA.
Leigh Disease - Also called Subacute Necrotizing Encephalo-Myelopathy - for the purpose of fucking
with you.
White Matter Distribution: Focal areas of subcortical white matter.
Gray Matter Distribution: Basal ganglia and Periaquaductal Gray
Trivia: Head size tends to be normal.
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--.:- :
SECTION 7:
BRAIN TUMORS � -_.
I want to introduce my idea for multiple choice brain tumor diagnosis. The strategy is as
follows; (1) decide if it's single or multiple, (2) look at the age of the patient - adults and kid'>
have different differentials, (3) look at the location - different tumors occur in different �pots,
(4) now use the characteristics to separate them. The strategy centers around narrowing the
differential based off age and location till you are only dealing with 3-4 common things, then
using the imaging characteristics to separate them. It's so much easier to do it that way.
Multifocal Primary from Seeding
�
Multiple Masses --+- Mets (*50% at solitary)
------.. Syndromes (example NF-2)
Cortical
�
lntraventricular
Adult ---+ CP Angle
Single Mass / �
lnfratentorial
"".. Kid
�
Supratentorial
\\\
Skull Base / Dura
Sella / Parasella
Pineal Gland
Before we get rolling, the first thing to do is to ask yourself is this a tumor, or is it a mimic?
Mimics would be abscess, infarct, or a big MS plaque. This can be tricky. If you see an
incomplete ring - you should think giant MS plaque. If they show you diffusion, it is either
lymphoma or a stroke (or an abscess) - you'll need to use enhancement to straighten that out
(remember lymphoma enhances homogeneously).
Yes ... GBM can restrict, but for multiple choice it is way more likely to be lymphoma.
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Two more high yield topics before we start crushing the differentials:
..Intra-Axial" vs .. Extra-Axial"
The Brant and Helms discussion on brain tumors will have you asking "intra-axial" vs
"extra-axial" first. This is not always that simple, but it does lend itself very well to
multiple choice test questions (therefore it's high yield).
Basicanv you need to memorize the "signs of extra-axial location"
• CSF Cleft
• Displaced Subarachnoid Vessels
• Cortical Gray matter between the mass and white matter
• Displaced and expanded Subarachnoid spaces
• Broad Dural Base / Tail
• Bony Reaction
Whv Do Things Enhance;»
Understanding the WHY is very helpful for problem solving. Let me first answer the
question "Why DON'T things enhance?" They DON'T enhance because of the blood brain
barrier. So, when things DO enhance it's because either:
(a) They are outside the blood brain barrier (they are extra-axial), or
(b) They have melted the blood brain barrier.
In other words, extra axial things (classic example is meningioma) will enhance. High
grade tumors (and infections) enhance. Low grade tumors just aren't nasty enough to
take the blood brain barrier down.
Are there exceptions? HA! There always are. And Yes... they are ALWAY S testable.
Gangliogliomas and Pilocytic Astrocytomas are the exceptions - they are low-grade
tumors, but they enhance.
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Multiple Masses
In adults or kids, if you see multiple masses you are dealing with mets (or infection). Differentiating
between mets and infection is gonna be done with diffusion (infection will restrict). If they want you
to decide between those two they must show you the diffusion otherwise only one or the other will be
listed as a choice.
Mets-High Yield Trivia:
• Most common CNS met in a kid = neuroblastoma (BONES, DURA, ORBIT - not brain)
• Most common location for mets = Supratentorial at the Grey-White Junction (this area has a lot of
blood flow+ an abrupt vessel caliber change ... so you also see hematogenous infection/ septic
emboli go there first too).
• Most common morphology is "round" or "spherical"
• Remember that mets do NOT have to be multiple. In fact, 50% of mets are solitary. In an adult, a
solitary mass is much more likely to be a met than a primary CNS neoplasm.
• MRCT is the mnemonic for bleeding mets (Melanoma, Renal, Carcinoid/ Choriocarcinoma,
Thyroid).
• Usually Mets have more surrounding edema than primary neoplasms of similar size.
• "Next Step Gamesmanship" - Because the most common intra-axial mass in an adult is a met, if
they show you a solitary mass (or multiple masses) and want a next step it's gonna be go hunting
for the primary (think lung, breast, colon ... the common stuff).
Primary Brain Tumors Can Also Be Multiple:
Tumors that Like to be Multifocal Tumors that are Multifocal
--�--.--------·--�------- ··- ···-- ---------· -··-·---·-··--· ·---------·-· -- ----·
from Seeding
___________ _ ___________ --· .. ·---·--·-- · -- --··-· ---· •-·-.-- --·
_,._., ,.
Mets - you should still think this first when you
Medulloblastoma
see multiple tumors
Lymphoma Ependymoma
Multicentric GBM GBM
Gliomatosis Cerebri Oligodendroglioma
SYNDROMES - Tumors in Syndromes are more likely to be Multifocal
NF 1 NF 2 "MSME" Tuberous Sclerosis VHL
Optic Gliomas Multiple Schwannomas Subependymal Tubers Hemangioblastomas
IV Giant Cell
Astrocytomas Meningiomas
Astrocytomas
Ependymomas
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Corticallv Based (P-noc;.-
Most intra-axial tumors are located in the P-DOG:
white matter. So when a tumor spreads to or
is primarily located in the gray matter, you Pleomorphic Xanthoastrocytoma (PXA)
get a shorter DDx. High yield piece of trivia Dysembryoplastic Neuroepithelial Tumor (DNET)
regarding the cortical tumor / cortical met is Oligu<lemlrugliuma,
that they often have very little edema and so Ganglioglioma
a small cortical met can be occult without IV
contrast.
PXA
PXA (Pleomorphic Xanthroastrocytoma):
PEDS (10-20)
Superficial tumor that is ALWAYS supratentorial and
usually involves the temporal lobe. They are often in Will Enhance
the cyst with a nodule categ01y (50%). There is usually Dural Tail***
no peritumeral T2 signal. The tumor frequently invades
the leptomeninges. Looks just like a Desmoplastic Cyst with Nodule Cyst with Nodule
Infantile Ganglioglioma - but is not in an infant. Temporal Lobe
DNET (Dysembryoplastic Neuroepithelial Tumor): DNET
Kid with drug resistant seizures. The mass will always be in
PEDS (< 20)
the temporal lobe (on the test - real life 60% temporal).
Focal cortical dysplasia is seen in 80% of the cases. It is No enhancement
hypodense on CT, and on MRI there will High T2 Signal
be little if any surrounding edema. with Bright
High T2 signal "bubbly lesion." FLAIR Rim
Bright Rim Sign "Bubbly"
Persistent rim of FLAIR signal Temporal Lobe
* Looks Similar to T2-FLAIR
Mismatch of Astrocytomas Oligodendroglioma
**discussed later FLAIR
"T2 Bright & Bubbly" ADULT- (40s-50s)
Bright Rim
Oligodendroglioma: Can Enhance
Remember this is the guy that calcifies 90% of the time. It's Calcification Common
most common in the frontal lobe and the buzzword is
"Expands the Cortex"
"expands the cortex". This takes after its most specific
feature of cortical infiltration and marked thickening. It's Frontal Lobe
likely you could get asked about this lp/19q deletion which I lp /19q
will discuss later when I go into detail about Gliomas (pg 83).
Ganglioglioma
Ganglioglioma:
Any Age
This guy can occur at any age, anywhere (usually temporal
lobe), and look like anything. However, for the purpose of Can Enhance
multiple choice testing the classic scenario would be a 13 NOT Bubbly
year old with seizures, and a temporal lobe mass that is
cystic and solid with focal calcifications. There may be Mixed Cystic Can look like Anything
& Solid
overlying bony remodeling. Temporal Lobe
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lntraventricular
Tumors can arise from the ventricular wall, septum pellucidum, or choroid plexus.
Ventricular Wall &
Choroid Plexus Misc
Septum Pellucidum
Choroid Plexus Papilloma
Ependymoma (PEDS) (PEDS in Trigone) Mets
(ADULT in 4th Vent)
Choroid Plexus
Medulloblastoma (,PEDS) Meningioma
Carcinoma (PEDS)
SEGA(Subependymal
Xanthogranuloma
Giant Cell Astrocytoma) = Colloid Cyst
("Found" in ADULTS)
PEDS
Subependymoma (ADULT)
Central Neurocytoma
(YOUNG ADULT)
Ventricular Wall / Septum Pellucidum Origin:
Ependymoma: Bimodal distribution on this one(large peak around 6 years of age,
tiny peak around 30 years of age). I would basically think of this as a PEDS tumor.
They come in two flavors:
(a) 4th Ventricle - which is about 70% of the time. There is frequent extension into the
foramen of Luschka and Magendie. They are the so-called "plastic tumor" or
"toothpaste" tumor because they squeeze out of the base of the 4th ventricle.
(b) Parenchymal Supratentorial - which is about 30% of the time.
These are usually big(> 4cm at presentation).
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Medulloblastoma: Let us just assume we are talking about the "Classic Medulloblastoma"
which is a type of PNET. If you want to understand the genetic spectrum of these things, read
Osborn's Brain - seriously don't subject yourself to that.
This is a pediatric tumor - with most occurring before age 10 (technically there is a second
peak at 20-40 but for the purpose of multiple choice tests I'm going to ignore it). These guys
are cerebellar arising from vennis / ROOF of the 4th ventricle -projec.;L inlu 4th ventricle. They
are much more common than their chief differential consideration the Ependymoma (which
originates from the FLOOR of the 4th ventricle).
The classic look is a dense mass on CT, heterogeneous on T 1 and T2, and enhances
homogeneously. They are hypercellular and may restrict. They calcify 20% of the time (less
than Ependymoma).
This is a tumor that loves to met via CSF pathways - they like to "drop met." The buzzword is
"zuckerguss" which apparently is German for sugar icing, as seen on post contrast imaging of
the brain and spinal cord (leptomeningeal carcinomatosis). As a point of absolute trivia, they
are associated with Basal Cell Nevus Syndrome and Turcots Syndrome.
Gorlin Syndrome - If you see a Medulloblastoma next look for dural calcs.
�l),$�
@ \YI/� If you see thick dural calcs you might be dealing with this syndrome.
t\, {t They get basal cell skin cancer after radiation, artd have odontogenic cysts.
NEXT STEP Trivia: Preoperative imaging of the entire spinal axis should be done in
any child with a posterior fossa neoplasm, especially if Medulloblastoma or
Ependymoma is suspected. Evidence of tumor spread is a statistically significant
predictor of outcome.
Medulloblastoma Ependymoma
More common Less Common
Originate from Vermis / Originate from the
ROOF of the 4th Ventricle FLOOR of the 4th ventricle.
Can extend into basal cisterns like tooth
Can project into 41h ventricle, do NOT usually
paste pushing though foramina of
extend into basal cisterns
Luschka and Magendie
Enhance Homogeneously
Enhance Heterogeneously
(more so than Ependymoma anyway)
Calcify Less (20%) Calcify More (50%)
Linear "icing-like" enhancement of the brain
surface is referred to as "Zuckerguss"
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Subependymal Giant Cell Astrocytoma (SEGA): This is going to be shown
in the setting of TS. They will more than likely show you renal AMLs or tell you the kid has
seizures / developmental delay.
Because it's syndromic, you see it in kids (average age 11).
It will arise from the lateral wall of lhe ventricle (near the foramen of Monro), often causing
hydrocephalus. It enhances homogeneously.
THIS vs THAT: SEGAvs Subependymal Nodule (SEN) -The SEN will stay stable in size,
the SEGAwill grow. The SEGAis found in the lateral ventricle near the foramen of
Monroe, the SEN can occur anywhere along the ventricle. SENs are way more common.
Both SEN and SEGAcan calcify.
.L Pearl - Enhancing, partially calcified lesion at the foramen of Monro,
'"' bigger than 5 mm is a SEGAnot a SEN.
- (the next 2 IV tumors are in ADULTS) -
Subependymoma: Found in ADULTS. Well-circumscribed IV mass most commonly
at the foramen of Monro and the 4th ventricle. They can cause hydrocephalus. They
typically don't enhance. They are T2 bright (like most tumors).
Central Neurocytoma:
This is the most common IV
mass in an ADULT aged
20-40. The buzzword is
"swiss cheese," because of
the numerous cystic spaces
on T2. They calcify a lot
(almost like
oligodendrogliomas).
Central Neurocytoma - Two Examples - Cystic IV Mass
Swiss Cheese +
Calcification in the
Ventricle
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Choroid Plexus Origin:
Choroid Plexus Papilloma I Carcinoma: Can occur in peds (85% under the age of 5) or
adults. They make up about 15% of brain tumors in kids under one. Basically you are
dealing with an intraventricular mass, which is often making CSF, so it causes
hydrocephalus
. � Here is the trick: Brain tumors are usually supratentorial in adults and posterior fossa
fl9 in kids. This tumor is an exception. Remember exceptions to rules are testable.
Qp Trivia:
• In Adults it's in the 4th Ventricle, in Kids it's in the lateral ventricle (usually trigone).
• Carcinoma type is ONLY SEEN IN KIDS - and are therefore basically ONLY SEEN IN
LATERAL VEN TRICLE / TRIGONE
• Carcinoma association with Li-Fraumeni syndrome (bad p53)
• Angiography may show enlarged choroidal arteries which shunt blood to the tumor,
• Carcinoma type of this tumor looks very similar (unless it's invading the parenchyma) and
is almost exclusively seen in kids.
• The tumor is typically solitary but in rare instances you can have CSF dissemination
Xanthogranuloma
This is a benign choroid plexus
mass. You see it all the time (7%)
and don't even notice it.
The trick is that they
restrict on diffusion, so
they are trying to trick you
into working them up.
They are benign ... leave
Xanthogranuloma - Note the Restricted Diffusion
them alone.
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Misc:
Mets - The most common location of intraventricular metastasis is the trigone of lateral
ventricles (because of the vascular supply of the choroid). The most common primary is
controversial - and either lung or renal. If forced to pick I'd go Lung because it's more
common overall. I think all things equal renal goes more - but there are less renal cancers.
It all depends on how the question is worded.
Colloid Cyst - These are found almost
exclusively in the anterior part of the 3rd
ventricle behind the foramen of Monro.
They can cause sudden death via acute onset
hydrocephalus.
Their appearance is somewhat variable and
depends on what they are made of If they have
cholesterol they will be T l bright, T2 dark. If
they don't, they can be T2 bright. The trick is a
round well circumscribed mass in the anterior
3rd ventricle. If shown on CT, it will be pretty
dense.
Colloid Cyst -
- Anterior 3rd Ventricle
- Hyperdense on CT
Meningioma - Can occur in an intraventricular location, most commonly (80%) at the
trigone of the lateral ventricles (slightly more on the left). Details on meningiomas are
discussed on the following page.
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Cerebellar Pontine Angle (CPA)
Age is actually less of an issue here because the DDx isn't that big. Most of these are adult
tumors, but in the setting ofNF-2 you could have earlier onset.
Epidemiology: Vestibular Schwannoma is #1 - making up 75% of the CPA masses, #2 is the
meningioma making up 10%, and the Epidermoid is #3 making up about 5%. The rest are
uncommon.
(75 %) Schwannoma (Vestibular)-These guys Schwannoma Meningioma
account for 75% of CPA masses. When they are bilateral
you should immediately think NF-2 (one.for each side).
Enhances strongly but more heterogeneous than Enhance Less Enhance
meningomas. May widen the porns acousticus resulting Homogeneously Homogeneously
in a "trumpet shaped" IAC. "Ice Cream Cone !AC. "
Don't Usually
(10 %) Meningioma -Second more common CPA Invade IAC
Invade IAC
mass. One of the few brain tumors that is more common
in women. They can calcify, and if you are lucky they
will have a dural tail (which is pretty close to
pathognomonic- with a few rare exceptions). Because IAC can have
Calcify more
"trnmpeted" often
they are extradural they will enhance strongly. Radiation
appearance
of the head is known to cause meningiomas.
Trivia:
•Most common location of a meningioma is over the cerebral convexity.
•Meningiomas take up octreotide and Tc-MDP onNuclear Medicine tests (sneaky).
(5 %) Epidermoid-
Can be congenital or acquired (after trauma-- classically after LP
in the spine). Unlike dermoids they are usually off midline.
They will follow CSF density and intensity on CT and MRI
(the exception is this zebra called a "white epidermoid" which is
T l bright- just forget I ever mentioned it).
The key points are
(1) Unlike an arachnoid cyst they are bright on FLAIR
(sometimes warm - they don't completely null), and
(2)They will restrict diffusion.
Epidermoid - Follows CSF
Signal - Restricts Diffusion
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' '
UN• •ww mwN•M g NM•M- � -M•-•* mM M NU U nMMNM •NN• aMM_R ____ WY M �M•n•MnM •K• •M
' "
Dermoid Cyst - This is about 4x
The Ruptured Dermoid
less common than an epidermoid. It's '
'
more common in kids / young adults. It is possible for a dermoid cyst to explode
Usually midline, and usually are -rare in real life, common on multiple choice.
found in the 3rd decade. They contain Sometimes this is after a trauma, but usually
lipoid material and are usually it's spontaneous. The most common clinical
hypodense on CT and very bright on scenario is "headache and seizure" - which is
pretty much every brain tumor, so that is not
Tl. They are associated with NF2.
helpful. What is helpful is this:
Trivia -
• Buzzword: "Chemical Meningitis"
•These are usually midline
• Aunt Minnie Appearance: Fat droplets
• Most common location for a (typically shown as low density on CT, or
dermoid cyst is the suprasellar High Signal on Tl) floating in the ventricles
cistern (posterior fossa is #2) and/or subarachnoid space.
THIS vs THAT: Dermoid vs Epidermoid-The easy way to think of this is that the
Epidermoid behaves like CSF, and the Dermoid behaves like fat.
IAC Lipoma - It can occur, and is basically the only reason you get a T l when you are
working up CPA masses. It will fat sat out - because it's a lipoma. There is an association
with sensorineural hearing loss, as the vestibulocochlear nerve often courses through it.
-----------------------------------------,
Arachnoid Cyst - Common benign lesion that is
How can you tell an epidermoid :
located within the subarachnoid space and contains from an arachnoid cyst? :
CSF. They are increased in frequency in
mucopolysaccharidoses (as are perivascular spaces). The epidermoid restricts,
They are dark on FLAIR (like CSF), and will NOT the arachnoid cyst does NOT.
restrict diffusion. ------------------------------------------
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lnfratentorial - Most are PEDS (Hemangioblastoma is the exception).
-------------------------------
THIS vs THAT:
1
I
Atypical Teratoma / Rhabdoid Tumor I
AT/RT vs Medulloblastoma
I
(''AT/RT") - Highly malignant tumors (WHO IV), and
I
I
I
rarely occur in patients older than 6 years. The average : Both are WHO Grade 4 destroyers
age is actually 2 years, but they certainly occur in the : (AT/RT is worse) that are often seen in the
first year of life. : posterior fossa of a kid.
Technically they are both subtypes of
1
They can occur in supra and infratentorial locations : Medulloblastoma - but that's the kind of
: knowledge that causes you to miss
(most common in the cerebellum). These are usually
: multiple choice questions. For the
large, pissed off looking tumors with necrosis and : purpose of multiple choice:
heterogeneous enhancement. They believe in nothing
: • AT/RT is a 2 year old
Lebowski. They fuck you up. They take the money. , • Medulloblastoma is a 6 year old
I
: • AT/RT has calcifications
c;£) Buzzword=
: • Medulloblastoma does not
)�r:) "Increased Head Circumference" I
Medulloblastoma & Ependymoma : Both are discussed with the IV lesions
Juvenile Pilocytic Astrocytoma
(JPA): Just think cyst with a nodule in a kid.
They are WHO grade 1, but the nodule will still
enhance. This will be located in the posterior
fossa (or optic chiasm).
JPA Hemangioblastoma
Pilocytic Astrocytoma: Cyst + Nodule in Kid
Gamesmanship - if they don't tell you the age, you can look for enhancement of the cystic wall which
JPA can have (�50%) but Hemangioblastomas don't ----------------------------------·-·-···-
I Say Posterior Fossa Cyst
Hemangioblastoma: First things first - immediately think with a Nodule - PEDS,
about this when you see a cyst with a nodule in an ADULT. Then
think Von Hippel Lindau, especially if they are multiple. These you say JPA
things are slow growing, indolent vascular tumors, that can cause
hydrocephalus from mass effect. 70% of the time you will see flow I say Posterior Fossa Cyst
voids along the periphery of the cyst. About 90% of the time they with a Nodule - ADULT,
are found in the cerebellum. There is an association with
, you say Hemangioblastoma
polycythemia. .. ---.. --.... -........ --. -.. -......... -.......................... -.... ..
Ganglioglioma: Occurs at any age, anywhere, can look like anything - see cortical lesions.
Diffuse Pontine Glioma (DPG): Seen in kids age 3-10. Most common location is the pons,
which is usually a high grade fibrillary glioma. It's going to be T2 bright with subtle or no
enhancement. 4th ventricle will be flattened. Imaging features are so classic that no biopsy is needed.
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Supratentorial - Adults Tumors
Astrocytoma: Most common primaiy brain tumor in adults. There is a trend towards "genetically
classifying" tumors - this actually changes the way they are treated and could be the source of trivia.
I'm going to attempt to simply this - because it can get pretty fucking l:Otnplicateu.
In the simplest terms, you have the neurons and you have the glial NeuralProgenitor Neuron
cells. The glial cells arc the "support staff' - there are lots of them
and lots of different kinds. Astrocytes and Oligocytes share a
common origin (both are support staff - "glial cells") and have a lot
of similarities. In other words, they are both "Gliomas" and are Astrocyte
going to get lumped together in this discussion.
Stem Cell ��
The new way to think about these things is a spectrnm of severity
based on genetic classification - and the treatment and prognosis
follows that. GlialProgenitor �
IDH Mutation Oligocyte
(earliest genomic event)
IDH Mutation
(earliest genomic event)
Yes. No
Yes(IOo/1 �(90%)
Oligodendroglioma Astrocytoma Astrocytoma Astrocytoma Astrocytoma
Low Grade Higher Grade Grade 4- Grade 4-
Calcification on -Grade 2 - Diffuse Glioblastoma Glioblastoma
preoperative CT is -Grade 3 - Anaplastic - Younger Patients -Older Patients
associated with -Better prognosis -The Worst
codeletion (Jp/19q) T2 - FLAIR -Probably Prognosis
Mismatch Sign "Secondary GBM" -Probably
from progression of "Primary GBM"
Ribbon pattern of a previous lower
calcification grade tumor
Classic for
Oligodendroglioma
Bad Prognosis
You probably noticed me using this WHO classification (1-4). All brain tumors are bad, but 4 is the
worst - this is your GBM. On the following page, I'll get into a few more details on each type but as a
general rule low grade tumors don't typically enhance (WHO 2) and higher grades do (mild for grade
3, and intense for grade 4 GBM). The exception to this rule is the pilocytic astrocytoma which often
has an enhancing nodule, and the Subependymal Giant Cell Astrocytomas which enhances because of
its location (Intraventricular).
GBM is the beast that cannot be stopped. It believes in nothing Lebowski. It grows rapidly, it can
necrose (creating the ring of enhancement, with a non-enhancing central necrotic core) , it can cross
the midline, and it can restrict diffusion. Remember Turcot Syndrome (that GI polyp thing), and NF
1 are associated with GBMs.
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Supratentorial - Adults Tumors - Continued
Astrocytoma Astrocytoma Astrocytoma Astrocytoma
Grade 1 Grade 2 - Diffuse Grade 3 - Anaplastic Grade 4- GBM
Subependymal Giant White Matter is White Matter is White Matter is
Cell Astrocytomas Preferred Preferred Preferred - can cross
the midline.
-lntraventricular mass
near the foramen of NO ENHANCEMENT Mild ENHANCEMENT
Monro in a young
RING ENHANCEMENT
patient with tuberous T2 Bright - FLAIR lso T2 Bright - FLAIR lso (can also be diffuse
sclerosis. (mismatch sign) (mismatch sign) heterogenous
-Can cause obstructive enhancement)
hydrocephalus
T2 & FLAIR Bright
Pilocytic Astrocytoma
Central locations (like
- Cyst with nodule in the thalamus) are
the posterior fossa of a worse than normal.
kid
Remember these NF type 1,
tumors break the rule - Turcot syndrome
T2 I FLAIR Mismatch: Seen with WHO 2
and enhance despite Li Fraumeni syndrome
(diffuse) and 3 (anaplastic) astrocytoma, not
being low grade.
with WHO 1. T2 tumor has high signal with
surrounding vasogenic edema. On FLAIR the
tumor signal become isointense.
Gliomatosis Cerebri: A diffuse glioma with extensive infiltration. It involves at least 3 lobes
and is often bilateral. The finding is usually mild blurring of the gray-white differentiation on CT, with
extensive T2 hyperintensity and little mass effect on MR. It's low grade, so it doesn't typically
enhance.
Mets: The most common supratentorial mass. Just like mets favor the lower lobes in the lm1gs, the
cerebrum is favored over the cerebellum (it is a blood flow thing). They are usually multiple, but can
be solitary- some sources say 50% of the time, so don't be fooled a solitary lesion can totally be a
met. Some other trivia worth knowing- melanoma can be T l bright even if it doesn't bleed.
CT-MR is a good way to remember the ones that like to bleed (C.horiocarcinoma / Carcinoid, Ihyroid,
Melanoma, Renal).
Metastatic GBM
Inegular
Margin Spherical
-Multifocal -Solitary
(25-50% solitary) (25% multifocal)
-Favors -Favors
Grey-White Junction Deep White Matter
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Supratentorial - Adults Tumors - Continued
Primary CNS Lymphoma: Seen in end stage AIDS patients, and those post-transplant. EB
vims plays a role. Most common type is Non-Hodgkin B cell.
Classic picture would be an intensely enhancing homogeneous solid mass in the periventricular
region, with restricted diffusion. However, it can literally look like and do anything.
Classic Multiple choice test question is that it is Thallium Positive on SPECT
(toxo is not).
I say restricting brain tumor, you say Lymphoma (although GBM can do this also)
THIS vs THAT: Periventricular / Ependymal Enhancement Patterns
=
:...
C'!I
�
.....
-==
C'!I · Ependymitis
0
(Classic Example Lymphoma
0 =CMV) "Rim Phoma"
00
.....
..=
�
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Supratentorial • Peds Tumors
DNET & PXA (Pleomorphic Xanthroastrocytoma):
Discussed under the cortical tumors .
Desmoplastic Infantile Ganglioglioma / Astrocytoma "DIG":
These guys are large cystic tumors that like to involve the superficial
cerebral cortex and leptomeninges. Unlike the Atypical Teratoma /
Rhabdoid, these have an ok prognosis ( WHO 1). They ALWAYS arise in
the supratentorial location, usually involve more than one lobe (frontal
and parietal most commonly), and usually present before the first birthday.
� -Buzzword is "rapidly increasing head circumference."
/
Big Cystic Tumor
with Hydro
Skull Base:
Chordoma - This is a locally aggressive tumor that originates from the notochord.
WTF is the "notochord" ? It's an embryology thing that is related to spine development.
The thing you need to know is that the notochord is a midline structure. Therefore all
Chordomas are midline - either in the clivus, vertebral bodies (especially C2), or Sacrum. You
can NOT get them in the hips, ribs, legs, arms, or any other structure that is not totally midline
along the axis of the axial skeleton.
•It is most common in the sacrum (#2 is the clivus)
• When it involves the spine, it's most common at C2 - but typically extends across a disc
space to involve the adjacent vertebral body.
•It's T2 Bright
•It's ALWAYS Midline. - it is never in a leg, arm, etc ... ONLY MIDLINE structures.
Chondrosarcoma - This is the main differential of the chordoma in the clivus. The thing
to know is that it is nearly always lateral to midline (chordoma is midline). These are also T2
bright, but will have the classic "arcs and rings" matrix of a chondrosarcoma. Obviously you'll
need a CT to describe that matrix.
Dura:
Meningioma - As described above, it is common and enhances homogeneously. The most
common location is over the cerebral convexity and it has been known to cause hyperostosis.
Hemangiopericytoma - This is a soft tissue sarcoma that can mimic an aggressive
meningioma because they both enhance homogeneously. They also can mimic a dural tail, with a
narrow base of dural attachment. They won't calcify or cause hyperostosis , but will invade the
skull.
Mets - The most common met to the dura is from breast cancer. 80% will be at the gray-white
junction. They will have more edema than a primary tumor of similar size.
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Sella / Parasella - Adults
Pituitary Adenoma - The most common tumor of the sella. They are seen 97% of the
time in adults. If they are greater than 1 cm they are "macroadenomas." When functional,
most are prolactin secreting (especially in women). Symptoms are easy to pick up in women
(menstrual irregularity, galactorrhea). Men tend to present later because their symptoms are
more vague ( decreased libido). On MR, 80% are Tl dark and T2 bright. They take up contrast
more slowly than normal brain parenchyma. Next step= Dynamic contrast enhanced MR.
Things to know (about Pituitary adenoma�r
. L •• Microadenoma under 10 mm,
flt • Macroadenoma over 10 mm.
Microadenomas typically form in the adenohypophysis (anterior 2/3).
.L
flt •• Prolactinoma is the most common functional type.
Typically they enhance less than normal pituitary.
Pituitary Apoplexy- Hemorrhage or Infarction of the pituitary, usually into an enlarged
gland (either from pregnancy or a macroadenoma). Here are the multiple choice trivia
association: taking bromocriptine (or other prolactin drugs), "Sheehan Syndrome" in
postpartum woman, Cerebral Angiography. They will be Tl bright (remember adenoma is
usually Tl dark). Supposedly this is an emergent finding because the lack of hormones can
cause hypotension.
Rathke Cleft Cyst- Usually an incidental finding. Rarely symptomatic. The "cleft" is
between the anterior and posterior pituitary. They are variable on T l and T2, but are usually
very bright on T2. They do NOT enhance.
Epidermoid - Discussed on page 80. Remember these guys restrict diffusion.
I say "Midline Suprasellar Mass that Restricts Diffusion", You say Epidermoid.
Craniopharyngioma - They come in two flavors: (a) Papillary - 10% and (b)
Adamantinomatous - 90%. The Papillary type is the adult type (Papi for Pappi). They are solid
and do not have calcifications. They recur less frequently than the Adamantinomatous form
(because they are encapsulated). They strongly enhance. The relationship to the optic chiasm is
key for surgery. These things occur along the infundibulum. Pediatric type is discussed below
(under on the next page with the peds tumors).
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Sella / Parasella - Peds
Craniopharyngioma -As stated above, they
come in two flavors: (a) Papillary and
(b) Adamantinomatous. The kid type is the
Adamantinomatous form. These guys are calcified
(papillary is not). These guys recur more (Papillary
does less - because it has a capsule).
Buzzword is "machinery oil. "
• Tl Bright
• T2 Bright
Craniopharyngioma
• CT I GRE = Calcifications - Shown on bone window
• Enhance Strongly (in the solid parts) - Calcifications in the Sella
Hypothalamic Hamartoma - A classic Aunt
Minnie. This is a hamartoma of the tuber cinereum (part
of the hypothalamus located between the mammillary
bodies and the optic chiasm). The location is the key.
Hamartoma of the
Tuber Cinereum
lnfundibulum
Pituitary
• Tl Iso
• T2 Iso
• Do NOT enhance.
The Classic History is Gelastic Seizures
(although precocious puberty is actually more common).
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Pineal Region -
There are 3 main characters here, all of which can present
with "vertical gaze palsy" (dorsal Parinaud syndrome).
Germinoma: The most common of the 3, and seen
almost exclusively in boys (Germinomas in the suprasellar
region are usually in girls). Precocious puberty may occur
from secretion of hCG. Characteristic findings are a mass
containing fat and calcification with variable contrast
enhancement. It is heterogeneous on T 1 and T2 (because Germinoma:
of its mixed components). "Engulfed" Calcification Pattern
Pineoblastoma: Does occur in childhood. Unlike the
pineocytoma, these guys are highly invasive. Some people
like to think of these as PNETs in the pineal gland. They
are associated with retinoblastoma ("trilateral"). They
are heterogeneous and enhance vividly.
Pineocytoma: Rare in childhood. Well-circumscribed,
and non-invasive. Tend to be more solid, and the solid
components do typically enhance. Pineoblastoma & Pineocytoma:
"Expanded" Calcification Pattern
Pineal Cyst - An incidental findings that is
meaningless ... although frequently obsessed over. They can
have thin enhancement. Calcifications occur in 25%.
Pineal Cyst:
Classically- looks like a cyst
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Special Topics - A Few Extra Tips on Characterization:
"Restriction"
If they show a supratentorial case with restriction it's likely to be one of two things
(1) Abscess or (2) Lymphoma. Technically any hypercellular tumor can restrict
(GBM & Medulloblastoma), but lymphoma is the one they classically show restricting.
If it's a CP angle case, then it's an Epidermoid.
Lastly, a dirty move could be to show Herpes encephalitis restricting in the temporal horns.
"Midline Crossing"
If they show it crossing the midline, it's most likely going to be a GBM or Lymphoma.
Alternative sneaky things they could show doing this would be radiation necrosis, a big
MS plaque in the corpus callosum, or Meningioma of the falx simulating a midline cross.
"Calcification"
If they show it in the brain it is probably an Oligodendroglioma. The trick is that
Oligodendrogliomas calcify 90% of the time by CT (and 100% by histopathology),
whereas astrocytomas only calcify 20% of the time. But astrocytoma is very common and
oligodendroglioma is not. So in other words, in real life it's probably still an astrocytoma.
"T1 Bright"
Most tumors are T l dark (or intermediate).
Exceptions might include a tumor that has bled
(Pituitary apoplexy or hemorrhagic mets). Tl Bright:
Hemorrhagic mets are classically seen on MR and
Fat: Dermoid, Lipoma
CT (Melanoma, Renal, Carcinoid /
Melanin: Melanoma
Choriocarcinoma, Thyroid). Tumors with fat will
also be T l bright (Lipoma, Dermoid). Melanin is Blood: Bleeding Met or Tumor
T l bright (Melanoma). Lastly think about Cholesterol: Colloid Cyst
cholesterol in a colloid cyst.
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Special Topics - svndromes
NF-1 Optic Nerve Gliomas
NF-2 MSME: Multiple .S.chwannomas, Meningiomas, E.pendymomas
VHL Hemangioblastoma (brain and retina)
TS Subependymal Giant Cell Astrocytoma, Cortical Tubers
Nevoid Basal Cell
Medulloblastoma
Syndrome (Gorlin)
Turcot GBM, Medulloblastoma, Intestinal Polyposis
Cowdens- "COLD" Lhermitte-Duclos (Dysplastic Cerebellar Gangliocytoma)
MSME
If you see tumors EVERYWHERE then you are
dealing with NF-2. Ironically there are no
neurofibromas in neurofibromatosis type 2 (obviously
that would make a great distractor).
Just remember MSME
Multiple S,chwannomas,
Meningiomas,
Ependymomas
Lhermitte-Duclos (Dysplastic Cerebellar Gangliocytoma)
This thing is very uncommon, but when you see it you need to have the following thoughts:
- Hey! That is Lhermitte Dulcos....
- I guess she has Cow dens syndrome ....
- I guess she has breast CA
Next Step? - Mammogram
The appearance is classic, with a "tiger stripe" mass, typically
contained in one cerebellar hemisphere (occasionally crosses
the vermis). It's not a "cancer", but actually a hamartoma -
which makes sense since Cowdens is a hamartoma syndrome.
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Brain Tumors - MRS Pearls
As cell walls get broken downNAA (a maker for neuronal viability) will go down,
Creatine (marker for cellular metabolism) will go down, and Choline (a maker for cell
membrane turnover) will go up. This is why the ratios ofNAA/Cho, Cho/Cr andNAA/Cr
get throw around.
Other relevant marker changes:
• Lactate may go up. You see this in the scenario of a high grade tumor outgrowing its
blood supply and changing over to anaerobic pathways.
• Lipids may go up. You see this in the scenario of a necrotic tumor. Lipids are associated
with necrosis.
• Alanine - is associated with meningiomas.
• NAA - This is a glioma maker. Non gliomas tend to have little or noNAA.
Tumor Grade: Recurrent Tumor vs GBM vs Met:
Radiation Necrosis
Higher Grade Tumors will Both can look gnarly on
have more cellular Recurrent Tumor: Rising conventional MR (big
destmction, inflammation, choline infers that cell walls enhancing tumor).
and more ischemia / are being turned over The GBM is classically
necrosis. (something is growing). underestimated on brain MRI
Mo Choline, Mo Problems (if you are just looking at the
Higher Grade Will Have: solid enhancing tumor). The
Radiation Necrosis: When surround T2 edema often
LessNAA you think necrosis you should contains infiltrative mirco
Less Creatine think elevated lipids (found in tumor. By using a multiple
More Lactate necrotic tissue) and elevated voxel analysis (looking at the
More Choline lactate. You could also reason tumor, and also surrounding
More Lipids thatNAA, Creatinine, and tissue) MRS supposedly adds
Choline (makers of cell value (allegedly).
Relative to a lower grade integrity, metabolism, and
tumor. turnover) would also be low For the purpose of multiple
if the tissue in that region was choice, elevated Choline in
fried like chicken (or bananas the T2 signal surrounding the
- if you enjoy denying your tumor = infiltrating glioma
tme nature as the apex (rather than a met)
predator).
Voxel Selection: It is important to choose an area of interest with enhancing tumor (avoid
cystic parts of the tumor, calcifications, blood, or frank necrosis).
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·
.
,·.·.
.. � .
.. '..
�
-
SECTION 8:
INFECTION
Neonatal Infections:
�
• .
We are talking about TORCH infections. The first critical thing is that they only really matter in
the first two trimesters (doesn't cause as much harm in the third trimester). Calcifications and
microcephaly are basically present in all of them.
Trivia Classic Look Highest Yield Trivia
. Most Common It prefers to target the germinal matrix · Most Common
TORCH resulting in periventricular tissue necrosis. TORCH
(3x more The result is the most likely test question =
CMV common than Periventricular calcifications. Periventricular
Toxo - which is Calcifications
• the second Of the TORCHs CMV has the highest
association with polymicrogyria. Polymicrogyria
most common).
. It's seen in the children of women who
clean up cat shit.
The calcification pattern is more random,
. This is the and targets the basal ganglia (like most Hydrocephalus,
second most other TORCH infections).
Toxoplasmosis common • Basal Ganglia
TORCH. . The frequency is increased in the 3rd Calcifications
trimester (but only causes a problem in the
first two).
Associated with Hydrocephalus.
Calcifications are less common than in Vasculopathy /
other TORCHs. Ischemia.
. Less common
Rubella because of Focal high T2 signal might be seen in High T2 signal
vaccines white matter (related to vasculopathy and 'Fewer
. ischemic injury). Calcifications
Unlike adults, the virus does not primarily . Hemorrhagic
. target the limbic system but instead prefers Infarct, with
It's HSV�2 in
HSV 90% of cases.
the endothelial cells resulting in thrombus resulting Bad
and hemorrhagic infarction with Encephalomalacia
resulting encephalomalacia and atrophy. (Hydranencephaly)
Not a TORCH · You may have faint basal ganglia
· but does occur enhancement seen on CT and MRI
preceding the appearance of basal ganglfa Brain Atrophy,
dming
HIV pregnancy, at calcification. predominantly in
. the Frontal Lobes
delivery, or via Brain atrophy pattern favors the Frontal
breast feeding. Lobes
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Infections of the lmmunosuppressed I people with AIDS J
The most common opportunistic infection in patients with AIDS is Gamesmanship:
toxo. The most common fungal infection (in people with AIDS) is • Nipple Rings = AIDS
Cryptococcus. Two other infections worth talking about are JC • From South Africa = AIDS
Virus, and CMV
HIV Encephalitis:
The encephalitis that people
with AIDS get. This is
We are talking about a
actually pretty common and
situation with a CD4 < 200.
affects about 50% of AIDS
patients.
Symmetric increased T2 /
FLAIR signal in the deep
white matter.
These tend to spare the
Tl will be normal. subcortical U-fibers (PML
The lesions will not enhance. will involve them). HIV Encephalitis
-Symmetric, and Spare Cortical U Fibers
There may be associated brain
atrophy.
Progressive Multifocal Leukoencephalopathy (PML):
We are talking about a
Caused by the JC virus.
situation with a CD4 < 50.
CT will show single or
multiple scattered
Hypodensities, with
corresponding Tl
hypointensity (remember Will involve
HIV was T l normal), subcortical U-fibers
T2/FLAIR hyperintensities PML
out of proportion to mass -Asymmetric, and Involves Cortical U Fibers
effect - buzzword
CMV: Think about brain atrophy, periventricular Ependymal cells are the cells that line
hypodensities (that are T2/FLAIR bright), and thin the ventricles and central portion of
ependymal enhancement. the spinal cord.
Cryptococcus: The most common fungal infection in AIDS. The most common
presentation is meningitis that involves the base of the brain (leptomeningeal enhancement).
The most likely way this will be shown on a multiple choice exam is dilated perivascular
spaces filled with mucoid gelatinous crap (these will not enhance). The second most likely
way this will be shown is lesions in the basal ganglia "cryptococcomas" - these are Tl dark,
T2 bright, and may ring enhance.
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Infections of the lmmunosuppressed c people with AIDS J - part 2
Toxo: Most common opportunistic infection in AIDS. Classically we are talking about T l
dark, T2 bright, ring enhancing (when larger than 1 cm) lesions. These guys will NOT show
restricted diffusion. Just think "ring enhancing lesion, with LOTS of edema."
High Yield Trivia = Toxo is Thallium Cold, and Lymphoma is Thallium hot.
,· ······ ·wrr1·i· ··�
I thought abscesses
restrict diffusiot1?
Typical they do.
However, atypical
infections like Toxo or
fungal don't always
follow this rule.
Tl+C Ring Enhancing T2 Lots of Edema DWI: NO Restriction
THIS vs THAT:
Toxo Lymphoma
Ring Enhancing Ring Enhancing
Hemorrhage more common after treatment Hemorrhage less common after treatment
Thallium Cold Thallium HOT
PET Cold (acts like necrosis) PET Hot (acts like a tumor)
- . ·-- �... -· . .
MR Perfusion: Decreased CBV MR Perfusion: Increased (or Decreased) CBV
Infections of the lmmunosuppressed I people with AIDS J - summarv
AIDS
PML CMV Toxo Cryptococcus
Encephalitis
Ring Dilated
Symmetric T2 Asymmetric T2 Periventricular
Enhancement + Perivascular
Bright Bright T2 Bright
Lots of Edema Spaces
No Restricted Basilar
T l Dark
Thin Ependymal Diffusion Meningitis
Enhancement
Spare U Fibers Involve U Fibers Thallium Cold
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Characteristic Infections:
TB Meningitis:
Has a predilection for the basal cisterns
(enhancement of the basilar meninges Complications include vasculitis which may
with minimal nodularity). result in infarct (more common in children).
Obstructive hydrocephalus is common.
May have dystrophic calcifications.
Enhancement of the Basilar Meninges+ Hydrocephalus = TB
*Sarcoid can have a nearly identical appearance.
If it looks like TB - but that isn't a choice, it's probably Sarcoid.
HSV - "Herpes" or "The Dirty Herp"
HSV 1 in adults and HSV 2 in neonates.
I mention that because For the purpose of
a multiple choice
(1) It seems like testable trivia and test think swollen
T2 bright
(2) They actually have different imaging (unilateral or
appearances (as previously bilateral) medial
mentioned, type l prefers the limbic temporal lobe.
system).
Earliest Sign = Restricted D[fjitsion -
related to vasogenic edema.
THIS vs THAT:
This could be tested by asking
"What sequence is more sensitive?", HSV spares the
with the answer being that diffusion is basal ganglia
more sensitive than T2. (distinguishes it
from MCA stroke). Herpes
Blooming on gradient means it's bleeding Edema in the Temporal Lobe
(common in adults, rare in neonate form).
Limbic Encephalitis:
Not an infection, but a commonly tested mimic. This could be asked by showing a classic
It is a paraneoplastic syndrome (usually HSV image, but then saying the HSV titer
small cell lung cancer), that looks very is negative. The second order question
similar to HSV. would be to ask for lung cancer screening.
West Nile:
Several viruses characteristically involve the Classic Look: T2 bright basal ganglia and
basal ganglia (Japanese Encephalitis, Murray
thalamus, with corresponding restricted
Valley Fever, West Nile ... ), the only one
realistically testable is West Nile. diffusion. Hemorrhage is sometimes seen.
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CJD: Creutzfeldt-Jakob Disease
Random Factoids:
The imaging features are variable There are 3 types:
and can be unilateral, bilateral, - Characteristic look on EEG
symmetric, or asymmetric. the "periodic sha,p wave" - Sporadic (80-90%),
. (whatever the fuck that is). - Variant "Mad Cow" (rare)
Three most likely testable
appearances diagramed below. · - "14-3-3" protein assay is a - Familial (10%).
. CSF test neurologists order.
DWI Cortical Gyriform Hockey Stick Sign: Pulvinar Sign:
Restricted Diffusion- - Bilateral FLAIR bright dorsal - Bilateral FLAIR bright
Supposedly diffusion is the most medial thalamus pulvinar thalamic nuclei
sensitive sign, & the cortex is the most - Described in the variant (posterior thalamus).
common early site of manifestation. subtype. - Classic in the variant subtype.
Basal Ganglia may also be involved.
Another way to show this (which would be more work for the test writer - and is therefore less
likely) would be a series of MRs or CTs showing rapidly progressive atrophy.
Neurocysticercosis
Most common locations (in descending order):
Caused by eating pig shit (or undercooked pork). 1- Subarachnoid over the cerebral hemispheres,
The bug is tinea solium (pork tapeworm).
2- Basal cisterns,
Trivia: Involvement of the basal cisterns carries the
worst outcome. 3- Brain parenchyma,
4- Ventricles
Stage 1: Vesicular Stage 2: Colloidal Stage 3: Granular Stage 4: Calcified /
Cyst + Scolex CT: Hyperdense Cyst CT: Early Calcification Involution
No Enhancement MR: Edema + Enhancement MR: Smaller Cysts, CT: Calcification
Less Edema, MR: Blooming on SWI
Less Enhancement (T2* etc..)
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Meningitis and Cerebral Abscess
You can think of meningitis in 4 main categories: Vocab
bacterial (acute pyogenic), viral (lymphocytic), chronic Leptomeningcal: Pial +Arachnoid
(TB or Fungal), and non-infectious (sarcoid). Pachymeningeal: Dural
Complications include:
This pattern
can be seen Venous thrombosis,
Essentially, we with Bacterial Vasospasm (leading to the stroke),
arc talking Meningitis or Empyema,
about thick Carcinomatous Vcntriculitis,
leptomcningeal Meningitis Hydrocephalus,
enhancement, in Abscess
the appropriate
clinical setting. Leptomeningeal (Pia-Arachnoid) Fungal and Carcinomatous
Enhancement: Fills the subarachnoid meningitis tend to be "more lumpy"
spaces & extends into the sulci & cisterns. and "thicker"
Abscess Facts (trivia)
A very testable piece of trivia is that infants will often get - DWI - Restricts
sterile reactive subdurals (much less common in adults). - MRS - Lactate High
- FDG PET - Increased Metabolic
Pachymeningeal (Dural) Enhancement
Key Feature: Enhancement does NOT extend into the sulci
Seen this with lots of stuff: Intracranial Hypotension, Dural attachment of
a Meningioma , Sarcoid, TB, Wegener's , Fugal Infections.
Both Breast and Prostate Cancer can deposit a solitary dural met.
Secondaiy CNS Lymphoma is often extra-axial and can be dural based or
fill the subarachnoid space ( "Rim Phoma ")
Empyema
Can be subdural or epidural (just like blood).
Follows the same rules as far as crossing dural
attachments (epidurals don't) and crossing the
falx (subdurals don't).
Subdurals are more common and have more
complications relative to epidurals.
The vast majority of subdurals are the sequcla of
frontal sinusitis. The same is true of epidurals
with some sources claiming 2/3 of epidurals are
secondary to sinusitis.
Subdural Empyema:
Classic Look: Tl bright and restrict diffusion. Dural Enhancement, Restricts Dfffusion
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lntraaxial Infections: Abscess Continued, with Cerebritis, & Ventriculitis
Abscess: A cerebral abscess is a cavity that contains pus, debris, and necrotic tissue. These can
develop secondary to to bacterial, fungal, or parasitic infection - most c01mnonly via
hematogenous spread. For the purpose of multiple choice, remember to think about right-to-left
shunts and pulmonaiy AVMs. Direct spread (example = sinus) is possible, but just less common
because of the dura.
CT: Focal area of T l+C: Smooth Ring T2: Multiple Lesions DWI: Typical Abscess
low density with Enhancement with with Vasogenic Edema (bacteria) will restrict.
surrounding low Multiple Lesions - - this is nonspecific Remember Atypical
density vasogenic Suggests Abscesses (could be mets) (Toxo etc.. ) doesn't
edema. always restrict
CT: Hypercellular
Tumor (classic
example would be
Lymphoma) will be
hyper dense instead
on low density like
an abscess
�����;�:·;��;;·��;;..�;·�;��::;� Smooth Ring = Abscess Irregular Ring = Tumor
Abscess Rings tend to be
The smooth margin suggests Abscess, but thicker on the "Oxygen "Bumpy" or "Shaggy"
doesn't exclude mets. The difference is that Side" or "Grey Matter inner lip of the ring is
tumor usually starts out as a solid enhancing Side" of the Brain - and supposed to suggest
mass then becomes ring enhancing with thinner towards the necrosis
necrosis. Also, Abscesses tend to be smaller ventricle.
(usually less than 10mm). Both Tumor & Abscess will have Vasogenic Edema
Cerebritis is the early form of intra-axial '. Ventriculitis: Usually the result of a shunt
infection, which can lead to Abscess if not · placement or intrathecal chemo - as discussed
treated. The typical look is the vasogenic • on page 51. The ventricle will enhance and you
can sometimes see ventricular fluid-fluid levels
edema without the well defined central
enhancing lesion. There may be spotty If septa start to develop you can end up with
restricted diffusion. obstructive pattems of hydrocephalus.
· The intraventricular extension of abscess is a
very serious/ ominous "pre-terminal event".
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MRI Gamesmanship - Enhancement Patterns
In general, to solve MR puzzles you will need to be able to work through some MR sequences.
The trick is to have a list of things that are Tl bright, T2 bright, Restrict diffusion, and Enhance.
Plus you should know the basic enhancement patterns (homogenous, heterogenous, ring, and
incomplete ring).
STROKE vs TUMOR vs ABSCESS vs MS Plaque
T2: For the most part, T2 is not super helpful for lesion characterization
- as stroke, tumors, abscess, MS, all have edema.
DWI: This is helpful only if they follow the classic rules. Out of those 4 (stroke, tumors, abscess,
MS) the classical diffusion restrictors are: Abscess, and Stroke. Certain hypercellular tumors
( classically lymphoma) can restrict, and demyelinating lesions with acute features can restrict.
Enhancement: In this situation this is probably the most helpful.
Out of those 4 (Tumor, Abscess, MS, and Stroke) each should have a different pattern.
• Tumor usually heterogeneous or homogenous if high I -----------------------
grade (or none if low grade). Technically ring
1
How Many Rings ?
enhancement can also be seen with Gliomas, and Mets
(though I expect this is less likely to be shown on multiple The number of rings can be a
helpful strategy. A single ring
choice). is more likely to be tumor
(around half of mets and 3/4
• Abscess will classically have RING pattern. of gliomas are solitary).
• MS will classically have an INCOMPLETE RING pattern.
Abscess and MS Lesions are
almost always (like 75-85%)
• Stroke will have co1iical ribbon (GYRIFORM) type I •
multiple.
enhancement in the sub-acute time period (around 1
1
I
I
week).
Heterogeneous Ring Incomplete Ring Gyriform
-Most likely Tumor -Can be lots of -Classic for -Classic for
(higher grade) stuff: Abscess and demyelinating subacute stroke
Tumor are both l.asiQn (can also be seen
prime suspects with PRES or
encephalopathy I
encephalitis)
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• . .' �
SECTION 9:
BRAIN TRAUMA & BLEEDING
�
Parenchymal Contusion: The rough part of the skull base can scrape the brain as it slides
•
• •
'
around in a high speed MVA. Typical locations include the anterior temporal lobes and inferior frontal
lobes. The concept of coup (site of direct injury) and contre-coup (opposite side of brain along vector
of force). Contusion can look like blood with associated edema in the expected regions.
Diffuse Axonal Injury/Shear Injury: There are multiple theories on why this happens
(different density of white and gray matter etc ... ) they don't matter for practical purposes or for
multiple choice.
Things Worth Knowing: I DAI Grading I
• Initial Head CT is often normal Grade 1 = Grey-White Interface
i
• Favorite sites of DAI are the posterior corpus callosum, and Grade 2 = Corpus Callosum
GM-WM junction in the frontal and temporal lobes
• Multiple small T2 bright foci on MRI
� :�:��-� :=��11'_ - - __
r r
J
Subarachnoid Hemorrhage: Trauma is the most common cause. FLAIR is the most
sensitive sequence. This is discussed in more later in the chapter.
THIS vs THAT: Subdural vs Epidural
- Crescent
Subdural
Shape
Epidural Subdural
-No Respect
Classic History: Elderly alcoholic with
For the
a shriveled up atrophic brain spent the
Sutures
evening with a bottle of
Classic History: "Rotgut - Hobo Tranquilizer" brand
Trauma Patient - with a whiskey, then fell over stretching &
skull fracture tearing his cortical bridging veins.
A week later he seems to be acting
progressively more confused.
"Bi-conve�" or
- Lentiform
"Bi-concave" Epidural
Lenticular
Can cross the midline
Does not cross the midline, may extend Shape
into interhemispheric fissure
Can NOT cross a suture Can cross a suture
-Respect for
the Sutures
Usually arterial Usually venous
Can rapidly expand and
kill you More mass effect than expected for size
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How Old is that Blood?
CT: This is an extremely high yield topic. Maybe the most high yield topic in all of neuro,
with regard to multiple choice. The question can be asked with CT or MRI (MRI more
likely). If they do ask the question with CT it's most likely to be the subacute subdural that is
isointense to brain, with loss of sulci along the margins. They could also show the "swirl
sign"- see below.
Blood on CT
Hyperacute Acute (< I hour) Hypodense
Acute (1 hour- 3 days) Hyperdense
Progressively less dense, eventually becoming
Subacute (4 days- 3 weeks) isodense to brain. Peripheral rim enhancement
may occur with contrast.
Chronic (> 3 weeks) Hypodense
Swirl Sign - This is an ominous sign of active
bleeding. The central low attenuation blood
represents hyper-acute non-clotted blood, with
surrounding acute clotted blood.
Blood Age Via MR:
MRI is more difficult to remember. Some people use the mnemonic "IB, ID, BD, BB, DD" or
"It Be Iddy Biddy, BaBy, Doo-Doo" which I find very irritating. I prefer mnemonics that
employ known words (just my opinion). Another one with actual words is "George
Washington Bridge" For Tl (Gray, White, Black), and Oreo Cookie for T2 (Black, White,
Black).
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Blood Age Via MR (continued): Instead of memorizing baby babbling noises, I use
this graph showing a clockwise movement. This thing may seem tricky and too much to bear,
at first, but it does actually work and once you draw it twice, you'll have it memorized.
You'll also notice a few things: (1) you won't feel like a dipshit for making baby noises,
(2) you'll have a renewed sense of self-esteem, and (3) you are likely to notice marked
improvement in your golf-swing.
Intracellular MetHb Ext raceIIular
"Early-Subacute" "Late-Subacute"
T1 Brighto
0
T1 lso
Oxy-Hb
0
DeOxy-Hb "Hyperacute"
"Acute"
Hemosiderin - Chronic
T1 Dark
T2 Dark
T21so
0 T2 Bright
Another strategy (which is somewhat unconventional) is to actually try and understand the
MRI changes (I strongly discourage this). If you insist on trying to understand this I have a 40
min lecture on TitanRadiology.com explaining it (this lecture is a]so free on my YouTube
Channel - google "Prometheus Lionhart Blood Age").
Hyperacute < 24 hours Oxyhemoglobin, Intracellular Tl- Iso, T2 Bright
Acute 1-3 days Deoxyhemoglobin, Intracellular Tl - Iso, T2 Dark
Early Subacute > 3 days Methemoglobin, Intracellular T1 Bright, T2 Dark
Late Subacute >7 days Methemoglobin, Extracellular Tl Bright, T2 Bright
Tl/ T2 Dark Peripherally,
Chronic > 14 days Fetritin and Hemosiderin, Extracellular
Center may be T2 bright
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Hemorrhage l Non-Traumatic J
Subarachnoid Hemorrhage:
Yes, the most common cause is trauma. A common point Sequela of SAH
of trivia is that the most sensitive sequence on MRI for
(1) Hydrocephalus - Early
acute SAH is FLAIR (because it won't suppress out -
(2) Vasospasm - 7-10 days
making it hyperintense). Be aware that supplemental
(3) Superficial Siderosis - Late
oxygen (usually 50-100%) can give you a fake out that
looks like SAH on FLAIR.
When the blood is real, in the absence of trauma, there are a few other things to think about.
Aneurysm - Discussed later in the chapter.
Benign Non-Aneurysm Perimesencephalic hemorrhage:
This is a well described entity (although not well
understood). This is NOT associated with aneurysm
(usually- 95%), and may be associated with a venous
bleed. *You have to prove that - you need a negative CTA.
The location of the blood- around the midbrain and pons
without extension into the lateral Sylvian cisterns or
interhemispheric fissures is classic. Just think anterior to
the brainstem. Re-bleeding and ischemia are rare- and
they do extremely well.
Superficial Siderosis: This
is a side effect of repeated
episodes of SAH. I like to
think about this as "staining
the sur:face of the brain with
hemosiderin. " The classic
look is curvilinear low
signal on gradient coating
the surface of the brain.
The classic history is
Superficial Siderosis - Hemosiderin Staining
sensorineural hearing loss
and ataxia.
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Pseudo-Subarachnoid Hemorrhage
This is a described mimic of SAH that is seen in
the setting of diffuse cerebral edema (most
commonly anoxic brain injury). Near
drowning, or suicide attempt by hanging would
be classic clinical vignettes.
What you are seeing is actually two things at
once. (1) You are seeing diffuse edema which
lowers the attenuation of the brain (makes it
darker). (2) You are seeing compression and
collapse of the sub arachnoid spaces which
gives them a hyper dense appearance. The
combination of these factors gives the
suggestions of hyper density in the cerebral
sulci, fissures, and cisterns which can mimic
SAH (hence the name).
THIS vs THAT:Pseudo SAH vs Real SAH: If they give you history that should help (anoxic brain
injury vs headache/ trauma). The absence of any intraventricular bleeding can suggest pseudo SAH.
Lastly density of the Pseudo SAH will be less than 40. Acute blood tends to be around 60-70 HU.
lntraparenchymal Hemorrhage:
• Hypertensive Hemorrhage: Common locations are the basal ganglia, pons, and cerebellum.
For the purpose of multiple choice tests, the basal ganglia is the most common location
(specifically the putamen). You typically have intraventricular extension of blood.
• Amyloid Angiopathy: History of an old dialysis patient (or some other history to think
Amyloid). The classic look is multiple lobes at different ages with scattered microbleeds on
gradient.
• Septic Emboli: These are seen in ce1iain clinical scenarios (IV drug user, organ transplant,
cyanotic heart disease, AIDS patients, people with lung AVMs). The classic look is
numerous small foci of restricted diffusion. Septic emboli to the brain result in abscess
and mycotic aneurysms (most commonly in the distal MCAs), The location favors the
gray-white interface and the basal ganglia. There will be surrounding edema around the tiny
abscesses. The classic scenario should be parenchymal bleed in a patient with infection.
• Other Random Causes: These would include AVMs, vasculitis, brain tumors (primary and
mets) - these are discussed in greater detail in various sections of the text.
lntraventricular Hemorrhage:
• Not as exciting. Just think about trauma, tumor, hypertension, AVMs, and anemysms - all
the usual players.
Epidural / Subdural Hemorrhage:
• Obviously these are usually post-traumatic.
• Dural AVFs and High Flow AVMs can bleed causing subdurals/ subarachnoid hemorrhage.
These are discussed further later in the chapter.
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·•\. �
SECTION 10:
VASCULAR
Stroke
Stroke is a high yield topic. You can broadly categorize stroke into ischemic (80%) and
hemorrhagic (20%). It's critical to remember that stroke is a clinical diagnosis and that imaging
findings compliment the diagnosis (and help exclude clinical mimic of stroke - tumor etc .. ).
Vascular Territories: Below is a diagram showing the various vascular territories. The junction
between these zones is sometimes referred to as a "watershed'. These areas are prone to ischemic
injury, especially in the setting of hypotension or low oxygen states (near drowning or Roger
Gracie's mounted cross choke or a Marcello Garcia high elbow guillotine).
Lenticulostriate
Watershed Ischemia favors the border
zones of different vascular territories (just Border Zone
BetweenACA
like the bowel). and MCA
The classic clinical scenario for watershed Border Zone Between
infarcts would be severe hypotension Deep White Matter
(shock/ CPR/ Etc .. ), severe carotid Branches of the MCA
stenosis, or a 2009 IBFFJ worlds match and theACA.
up with Roger Gracie.
. � Gamesmanship: Watershed Infarcts
A
'" in a Kid = Moyamoya (Idiopathic
supraclinoid ICA vasculo-occlusive
disease)
Border Zone
Between MCA
andPCA
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Subacute Infarct:
Imaging Signs on CT: Unique that it Enhances but creates NO Mass Effect
Dense MCA Sign Intraluminal thrombus is dense, usually in the M l and/or M2 segments
Insular Ribbon Sign Loss of normal high density insular cortex from cytotoxic edema
Loss of GM-WM
Basal Ganglia / Internal Capsular Region and Subcortical regions
differentiation
Mass Effect Peaks at 3-5 days
Enhancement Rule of 3s: Starts in 3 days, peaks in 3 weeks, gone by 3 months.
Fogging:
"Fogging" is classically
described with non-contrast CT,
but T2 MRI sequences have a
similar effect (typically
occurring around day 10). In the
real world, you could give IV
This is a phase in the evolution of stroke when the infarcted contrast to demarcate the area of
brain looks like normal tissue. This is seen around 2-3 weeks infarct or just understand that
post infarct, as the edema improves. fogging occurs.
T
Artery of Percheron Stroke:
Classic V Shaped bilateral infarct of the paramedian thalami.
This can only occur in the setting of the Artery of Percheron
vascular variant . This variant is characterized by a solitary trunk ...,
originating from one of the two PCAs to feed the rostral midbrain
and both thalami (normally there are several bilateral paramedic
arteries originating from the PCAs).
Recurrent Artery of
Heubner Stroke
Classic Caudate Infarct
The Artery of H is a deep branch off
the proximal ACA
This thing can get "bagged" during the
clipping of ACOM arte1y aneurysm.
Fetal PCOM Stroke Pattern
Cardioembolic Stroke:
This pattern demonstrates infarcts
This has the classic pattern of
in both the anterior and posterior
multiple foci of restricted diffusion
circulation of the same
scattered bilaterally along multiple
hemisphere.
vascular territories.
This pattern is possible as the
The clinical history is usually A-Fib or
variant anatomy with the PCA
endocarditi s.
feeds primarily from the ICA.
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Restricted Diffusion: Not Everything That Restricts
is a Stroke
Acute infarcts usually are bright from about 30 Bacterial Abscess, CJD (cortical), Herpes,
mins after the stroke to about 2 weeks. Epidermoids, Hypercellular Brain Tumors
Restricted diffusion without bright signal on (Classic is lymphoma), Acute MS lesions,
FLAIR should make you think Oxyhemoglobin, and Post Ictal States. Also
hyperacute (< 6 hours). artifacts (susceptibility and T2 shine through).
Enhancement: The rule of 3 's is still useful. Starts day 3, peaks ~ 3 weeks, gone by 3 months.
0-6 hours 6-24 hours 24 hours -1 week
Diffusion Bright Bright Bright
FLAIR NOT BRIGHT Bright Bright
Tl Iso Dark Dark, with Bright Cortical Necrosis
T2 Iso Bright Bright
Hemorrhagic Transformation: Predictors of
Hemorrhagic
This occurs in about 50% of infarcts, with the typical time period Transformation in
between 6 hours and 4 days. If you got TPA it's usually within 24 Patients Getting TPA
hours of treatment.
• Multiple Strokes,
People break these into (1) tiny specs in the gray matter called • Proximal MCA occlusion,
"petechial" which is the majority (90%) and (2) full on hematoma • Greater than 1/3 of the
- about 10%. MCA territory,
• Greater than 6 hours since
Who gets it? People on anticoagulation, people who get TPA, onset "delayed
people with embolic strokes (especially large ones), people with rccanalization",
venous infarcts. • Absent collateral flow
Venous Infarct:
Not all infarcts are arterial, you can also stroke secondary to venous occlusion (usually the sequelae
of dural venous sinus thrombosis or deep cerebral vein thrombosis). In general, venous infarcts are at
higher risk for hemorrhagic transformation. In little babies think dehydration, in older children think
about mastoiditis, in adults think about coagulopathies (protein C & S def) and oral contraceptives.
The most common site of thrombosis is the superior sagittal sinus, with associated infarct occurring
75% of the time.
Venous thrombosis can present as a dense sinus (on non-contrast CT) or "empty delta" (on contrast
enhanced CT). Venous infarcts tend to have heterogeneous restricted diffusion. Venous thrombosis
can result in vasogenic edema that eventually progresses to stroke and cytotoxic edema.
• Arterial stroke = Cytotoxic Edema
• Venous Stroke = Vasogenic Edema+ Cytotoxic Edema
Stigmata of chronic venous thrombosis include the development of a dural AVF, and/or
increased CSF pressure from impaired drainage.
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ASPECTS (Alberta Stroke Program Early CT Score)
This was developed to give "providers" a more specific guideline for giving TPA - as an
alternative to the previous 1/3 vascular territory rule. The idea being that the greater the vascular
territory involved, the worse the clinical outcome (post TPA bleed etc..).
The way this works is that you start out with 10 points, and lose points based on findings of acute
cytotoxic ischemia to various locations (example: minus 1 for caudate, or lentiform nucleus, or
insular ribbon, etc.. etc .. so on and so forth).
Testable P earls:
• This is for MCA ONLY (not other vascular territories)
• This is for ACUTE ischemia (don't subtract points for chronic lacunar infarcts etc .. )
• A score of 8 or greater has a better chance of a good outcome (score of 7 or less may
contraindicate TPA- depending on the institutional policy.
CT Perfusion - Crash Course
After an arterial occlusion perfusion pressure is going to be rapidly reduced. Millions of neurons will
suddenly cry out in terror then suddenly silenced, unless they are lucky to have arteriolar dilation with
capillary recruitment to bring in as much blood to that area of brain as possible. This process is called
physiologic auto-regulation and should result in an increase in capillary blood pool. The key point is
that you need live neurons (penumbra) to cry out for help. If they cry out and are suddenly silenced
(infarct core) you won't see any auto regulation attempts. This physiology makes up the basis of
perfusion for stroke.
Parameters:
• Cerebral Blood Flow (CBF): Represents instantaneous capillary flow in tissue.
• Cerebral Blood Volume (CBV ): Describes the blood volume of the cerebral capillaries and venules
per cerebral tissue volume.
• Mean Transit Time (MTT) = CBV divided by CBF ; it is the average length of time a certain
volume of blood is present in the capillary circulation.
• Time to Peak (TTP): This is the opposite of.CBF. Less flow = Longer Time to reach maximum
concentration of contrast.
iCBF t CBV t MTT For additional
! csv
information on
Regulation please see
UcsF the collective works of
Warren Griffin the 3rd.
Dead Tissue Can't Auto-Regulate
The primary role of perfusion is to distinguish between salvagable brain (penumbra), and dead brain.
The penumbra may benefit from therapy. The dead brain will not- "He :S' Dead Jim" - Dr. McCoy
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Aneurrsm Dolichoectasia of the
Basilar Artery
Who gets them? People who smoke, people with
polycystic kidney disease, connective tissue disorders This refers to a widened elongated
(Marfans, Ehlers-Danlos), aortic coarctation, NF, FMD, twisty appearance of the basilar
and AVMs. artery. This is probably the result
of chronic hypertension (abnormal
Where do they occur? They occur at branch points (why vessel remodeling).
do persistent trigeminals get more aneurysms ? - The height of the bifurcation and
because they have more branch points). They favor the the more lateral the position of the
anterior circulation (90%) - with the anterior vessel (relative to the clivus) the
communicating artery being the most common site. more severe - so says the Smoker
As a piece of random trivia, the basilar is the most criteria.
common posterior circulation location (PICA origin is
the second most common).
When do they rupture? Rupture risk is increased with
size, a posterior location, history of prior SAR, smoking
history, and female gender.
Which one did it? A common dilemma is SAR in the
setting of multiple aneurysms. The things that can help
you are location of the SAR/Clot, location of the Complications include: nothing
vasospasm, size, and which one is the most irregular (most have no symptoms),
Focal out-pouching - "Murphy :s· tit") dissection, compression of cranial
nerves (hemi-facial spasm), stroke
(brainstem), and hydrocephalus.
Aneurysm Types:
Saccular (Berry):
The most common type and the
most common cause of non
traumatic SAH. They are commonly
seen at bifurcations.
Ml/M2 The underlying pathology may be a
Junction congenital deficiency of the internal
~30% elastic lamina and tunica media
(at branch points).
TCA / PComm Junction ~ 30%
Basilar Tip ~ 3% Remember that most are idiopathic
+iPICA~2%
(with the associations listed above).
They are multiple 15-20% of the
time.
*Note that around 90% arise
from the Anterior Circulation
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Aneurysm Types Continued:
Fusiform Aneurysm -Associated with PAN,
Connective Tissue Disorders, or Syphilis. These AVM Associated
more commonly affect the posterior circulation. Pedicle Aneurysm:
May mimic a CPA mass.
Aneurysm associated with an AVM.
Pseudoaneurysm - Think about this with an
irregular (often saccular) arterial out-pouching The trivia to know is that it's found on the
at a strange / atypical location. You may see artery feeding theAVM (15% of the time).
focal hematoma next to the vessel on non
contrast. These may be higher risk to bleed than the
Traumatic - Often distal secondary to AVM itself (because they are high flow).
penetrating trauma or adjacent fracture.
Mycotic - Often distal (most commonly in the
MCA), with the associated history of
endocarditis, meningitis, or thrombophlebitis.
Aneurysm Rupture Trivia:
Blister Aneurysm - This is a sneaky little dude
(the angio is often negative). It's broad-based • Aneurysm > 10mm have a 1% risk of
at a non-branch point (supraclinoid ICA is the rupture per year.
most common site).
• Although controversial, 7 mm is often
Infundibular Widening- Not a true thrown around as a treatment threshold
aneurysm, but instead a funnel-shaped for anterior circulation aneurysms
enlargement at the origin of the Posterior • In general, posterior circulation
Communicating Artery at the junction with the aneurysms have a higher rate of
ICA. Thing to know is "not greater than 3 rupture per mm in size.
mm."
Aneurysm Subtypes Summary Maximum Bleeding
- Aneurysm Location
Saccular Branch Points -in the
(Berry) Anterior Circulation
ACOM Interhemispheric Fissure
Fusiform Posterior Circulation
PCOM Ipsilateral Basal Cistern
Pedicle
Artery feeding the AVM MCA
Aneurysm Sylvian Fissure
Trifurcation
Mycotic Distal MCAs Interpeduncular Cistern,
Basilar Tip
or Intraventricular
Blister Broad Based Non-Branch
Posterior Fossa or
Aneurysm Point (Supraclinoid ICA) PICA
Intraventricular
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vascular Malformations
High Flow
•
•
•
•
•
Most Common Most Common Type of High Flow
Congenital malformation
Supratentorial location (Usually)
Most common complication = bleeding (3% annual)
Ri:-;k incre11sed with: Smaller AVMs (they are under
Nidus €
Arterial Component
Draining veins
AVM higher pressure), Small Draining Veins (can't reduce
pressure), Perinidal Aneurysm, and Basal Ganglia • Adjacent brain may
location be gliotic (T2 bright)
• Symptoms: Headache (#1), Seizure (#2) and atrophic.
• Flow Rate is Variable (can be high or low flow)
• SPINAL AVFs are actually the most common type of
AVFs - a helpful hint is the classic clinical history of • No Nidus
"gradual onset LE weakness"
• Risk of Bleeding - increased with direct cortical venous . • Can be occult on
Dural AVF drainage. MRI/MRA _ need
• These aren't congenital (like AVMs) but instead are catheter angio if
acquired - classically from dural sinus thrombosis suspicion high
• Symptoms: Tinnitus - especially if the sigmoid sinus
is involved.
• "Caput medusa" or
"large tree with
• Variation in normal venous drainage multiple small
• Resection is a bad idea = venous infarct branches"
• Associated with cavernous malformations. collection of vessels
DVA • They almost never bleed in isolation. If you see converging towards
evidence of prior bleeding (blooming on gradient) there an enlarged vein
is probably an associated cavernoma. (seen on venous
phase only).
• Can have a halo of
T2 bright gliosis.
· • Low Flow - WITHOUT intervening normal tissue
• Can be induced from radiotherapy • • "Popcorn-like" with
Cavernous • Can ooze some blood, but typically don't have full-on "Peripheral Rim of
Malformation catastrophic bleeds. Presence of a "fluid-fluid" level Hemosiderin."
(cavernoma, or suggests recent intralesional hemorrhage • Best seen on
cavernous angioma) • Single or multiple (more common in Hispanics). gradient
• Classic gamesmanship is to show you a nearby DVA
· • Brush-like" or
• Low Flow - WITH intervening normal tissue "Stippled pattern"
Capillary • Can also be radiation induced of enhancement
• Usually don't bleed (thought of as an incidental : • Best seen on
Telangiectasia finding) gradient (slow flow
• Classic Look = Single lesion in the Pons and
deoxyhemoglobin)
• Wastebasket term, most often used for DVA with AV
Mixed shunting or DVAs with telangiectasias
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Calcification Rapid Review / Summary
Pineal Gland -Common in adults, Rare in kids. If you see
calcification in a kid under 7, it could suggest underlying neoplasm.
-Germinoma = "Engulfed" Pattern "1"
-Pineoblastoma & Pineocytoma: "Expanded" Pattern "2"
Habenular -Curvilinear structure (solid white arrow) located a few
millimeters anterior to the pineal body (open arrow). About 1 in 5
normal adults will have calcification here. The trivia is an increased
association with schizophrenia.
Choroid plexus -Common in adults. Remember there is no choroid
plexus in the frontal/occipital horn of the lateral ventricles or the
cerebral aqueduct.
Dural Calcifications - Common in adults. If the calcs are bulky and
there are a bunch of tooth cysts (Odontogenic keratocysts) think Gorlin
Syndrome.
Basal Ganglia -Very common with age, favors the globus pallidus. If
extensive & symmetrical think Fahr disease.
Sturge-Weber -Tram
track / double-lined
gyriform pattern parallel to
the cerebral folds.
Tuberous Sclerosis - Calcifications of the subependymal Etiology= subcortical
nodules are pathognomonic typically found at the ischemia secondary to pial
caudothalamic groove and atrium. You can see calcified angiomatosis.
subcortical tubers - more typical in older patients.
Congenital CMV - Periventricular calcifications.
Can also have brain atrophy
Congenital Toxo - Basal Ganglia Calcifications +
Hydrocephalus,
Neurocysticercosis - Etiology: Eating Mexican pork
sandwiches -end-stage will have scattered quiescent Ncurocysticercosis
calcified cyst remnants. CMV Toxo
Cavernoma- scattered Brain Tumors can calcify. The ones most people talk about are
dots or stippled Qld _Elephants Age Qracefully
"popcorn" calcification
0: Oligodendroglioma - variable, but "ribbon" pattern is most commoon
E: Ependymoma (Medulloblastomas can also calcify -just less often)
A: Astrocytoma
G: Glioblastoma - mural calcified nodule
AVM- calcifications in
the tortuous veins or the Even though more Oligodendrogliomas calcify, Astrocytoma is still the
nidus most common calcified tumor (because there are alot more of them).
Craniopharyngioma, Meningioma, Choroid plexus tumors are all known
to calcify as well. Osteosarcoma mets famously calcify.
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Vasospasm
Vessels do not like to be bathed in blood (SAH), it makes them freak out (spasm). The
classic timing for this is 4-14 days after SAH (NOT immediately). It usually looks like
smooth, long segments of stenosis. It typically involves multiple vascular territories. It can
lead to stroke.
Who gets it? It's usually in patients with SAH and the more volume of SAH the greater the
risk. In 1980 some neurosurgeon came up with this thing called the Fisher Score, which
grades vasospasm risk. The gist of it is greater than 1 mm in thickness or intraventricular /
parenchymal extension is at higher risk.
Are there Non-SAH causes ofvasospasm? Yep. Meningitis, PRES, and Migraine Headache.
Critical Take Home Point - Vasospasm is a delayed side effect of SAH. It does NOT occur
immediately after a bleed. You see it 4-14 days after SAH.
Vascular Dissection
Vascular dissection can occur from a variety
of etiologies (usually penetrating trauma, or a
trip to the chiropractor).
Penetrating trauma tends to favor the
carotids, and blunt trauma tends to favor the
vertebrals.
This would be way too easy to show on CT
as a flap, so if it's shown it's much more
likely to be the Tl bright "crescent sign", or "Crescent Sign" of Dissection
intramural hematoma. - it's the T1 bright intramural blood.
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Vasculilis
You can have a variety of causes of CNS vasculitis. One way to think about it is by clumping
it into (a) Primary CNS vasculitis, (b) Secondary CNS vasculitis from infection, or sarcoid,
(c) systemic vasculitis with CNS involvement, and (d) CNS vasculitis from a systemic disease.
Primary CNS Vasculitis Primary Angiitis of the CNS (PA CNS)
Secondary CNS vasculitis Meningitis (bacterial, TB, Fungal),
from infection, or sarcoid Septic, Embolus, Sarcoid,
Systemic vasculitis with
PAN, Temporal Arteritis, Wegeners, Takayasu's,
CNS involvement
CNS vasculitis from a
Cocaine Use, RA, SLE, Lyme's
Systemic Disease
They all pretty much look the same with multiple segmental areas of vessel narrowing, with
alternating dilation ("beaded appearance"). You can have focal areas of vascular occlusion.
Trivia:
Qp PAN is the Most Common systemic vasculitis to involve the CNS
(although it is a late finding).
Qfa SLE is the Most Common Collagen Vascular Disease
Misc Vascular Conditions
Moyamoya -This poorly understood entity (originally described in Japan- hence the name),
is characterized by progressive non-atherosclerotic stenosis of the supraclinoid ICA, eventually
leading to occlusion. The progressive stenosis results in an enlargement of the basal
perforating arteries.
Trivia:
• Buzzword = "Puff ofSmoke" - for angiographic appearance
• Watershed Distribution
• In a child think sickle cell
• Other notable associations include: NF, prior radiation, Downs syndrome
• Bi-Modal Age Distribution (early childhood and middle age)
• Children Stroke, Adults Bleed
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Crossed Cerebellar Diaschisis (CCD):
Depressed blood flow and metabolism affecting the cerebellar hemisphere after a
contralateral supratentorial insult (infarct, tumor resection, radiation).
Creates an Aunt Minnie Appearance:
Mechanism I Gamesmanship: When I was a medical student, I
had to memorize a bunch of tiny little tracks and pathways all over
the brain, cerebellum, and spine. It (like many things in medical
school) made me super angry because it was such a colossal waste
of time. More PhD bullshit, lumped right in with those step 1
"what chromosome is that on ? " questions.
Redemption for the PhDs has arrived. Apparently, one of these
pathways, the "corticopontine-cerebellar pathway," is actually
important. Sorta ....
Allegedly, this pathway connects one cerebral hemisphere to the
opposite cerebellar hemisphere. If the pathway gets disrupted (by
tumor, radiation, etc ...), then metabolism shuts down in the
opposite cerebellum even though there is nothing structurally
wrong with it. That is why you get this criss-crossed hypo
metabolic appearance on FDG-PET.
The trick is to show you the FDG-PET picture, and try and get
you to say there is a pathology in the cerebellum. There isn't! The
cerebellum is normal - the problem is in the opposite cerebrum
where the pathway starts.
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NASCET Criteria: The North American
Symptomatic Carotid Endarterectomy Trial
(NASCET) criteria, are used for carotid
stenosis.
The rule is: measure the degree of stenosis
using the maximum internal carotid artery
stenosis ("A") compared to a parallel (non
curved) segment ofthe distal cervical
internal carotid artery ("B").
ECA
You then use the formula:
[1-A/B] X 100% = % stenosis
Carotid endarterectomy (CEA) is often performed
for symptomatic patients with> 50% stenosis.
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SECTION 11:
.. '
� FACE AND T ... BONE SMASH
: .�'..
..
.. ... ..
'
The Lefort Fracture Pattern svstem: In the dark ages, Rene LeFort beat the shit out of
cadavers with clubs and threw them off buildings ...... it was "science". He then described three
facial fracture patterns that interns in ENT and people who write multiple test questions think are
important. It can be overly complicated but the most common way a test question is written
about these is either by asking the buzzword or the essential component (or showing them).
� Buzzwords:
LeForts
/
LeFort 1: "The Palate
Separated from the Maxilla"
or "Floating Palate"
LeFort 2:"The Maxilla
Separated from the Face" or
"Pyramidal"
LeFort 3: "The Face
Separated from the
Cranium"
Essential Elements: All three fracture types share the pterygoid process fracture. If the
pterygoid process is not involved, you don't have a LeFort. Each has a unique feature (which
lends itself easily to multiple choice).
* LeFort 1 : Lateral Nasal Aperture
* LeFort 2: Inferior Orbital Rim and Orbital Floor
* LeFort 3: Zygomatic Arch and Lateral Orbital Rim/Wall
Mucocele: If you have a fracture that disrupts the frontal sinus outflow tract (usually
nasal-orbital-ethmoid types) you can develop adhesions, which obstruct the sinus and result
in mucocele development. The buzzword is "airless, expanded sinus." They are usually Tl
bright, with a thin rim of enhancement (tumors more often have solid enhancement). The
frontal sinus is the most common location- occurring secondary to trauma (as described
above). More on this later....
CSF Leak: Fractures of the facial bones, sinus walls, and anterior skull base can all lead
to CSF leak. The most common fracture site to result in a CSF leak is the anterior skull base.
"Recurrent bacterial meningitis" is a known association with CSF leak.
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Temporal Bone Fractures:
The traditional way to classify these is longitudinal and transverse, and this is almost
certainly how the questions will be written. In the real world that system is old and
worthless, as most fractures are complex with components of both. The real predictive
finding of value is violation of the otic capsule - as described in more modern papers.
Longitudinal Transverse
Long Axis of T-Bone Short Axis of T-Bone
More Common Less Common
More Ossicular Dislocation More Vascular Injury (Carotid/ Jugular)
Less Facial Nerve Damage (around 20%) More Facial Nerve Damage (>30%)
More Conductive Hearing Loss More Sensorineural Hearing Loss
Transverse
Things to Know About Facial Fractures:
• Nasal Bone is the most common fracture
• Zygomaticomaxillary Complex Fracture (Tripod) is the most common fracture
pattern, and involves the zygoma, inferior orbit, and lateral orbit.
• Le-Fort Fractures are both a stupid and a high yield topic in facial trauma - for
multiple choice. Floating Palate = 1, Pyramidal = 2, Separated Face = 3
• Transverse vs Longitudinal Temporal Bone Fractures - this classification system
is stupid and outdated since most are mixed and otic capsule violation is a way
better predictive factor ... but this is still extremely high yield
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SECTION 12:
TEMPORAL BONE
It would be very easy to get completely carried away with this anatomy and spend the next
�Ml.·-., :· ...
20 pages talking about all the little bumps and variants. I'm gonna resist that urge and instead
try and give you some basic framework. Then as we go through the various pathologies I'll
try and give "normal" anatomy comparisons and point out some landmarks that are relevant
for pathology. Additionally, I'm gonna do a full anatomy T-Bone talk for RadiologyRonin
this year - so if your really want to understand this deeper, that might be helpful.
t' I
,- ... 1
f· .._ .., , /
.....
: .... ... , '\
I
Epitympanum I
I
I
• I
I
"The Attic" \
\
,_, ..........Ill!"':'"'
' ·. ;.' . .·
Mesotympanulll' . • ·••• ·.·•· - ·•··
'.· ·.. :·>·· __·,:_·:•
'__..· .·>,._:>· . ':__ . ·,
Hypotympanum
A closer look at the middle ear gives us 3 more
At the most basic level you can think about 3 general locations
general locations: External, Middle, and Inner.
The Epitympanum, also called "the attic" is
The External ear is everything superficial to the basically everything above the tip of the scutum
ear drum (tympanic membrane). (see below).
The Inner ear is everything deep to the medial The Hypotympanum is everything below the
wall of the tympanic cavity. tympanic membrane. This is where the
Eustachian tube arises.
The Middle ear is everything in-between.
The Mesotympanum is everything in-between
(or everything directly behind the ear drum).
The scutum (arrows) is a "shield" like osseous spur formed
via the lateral wall of the tympanic cavity. This anatomic
land mark is often brought up with discussion of the
erosion pattern of Cholesteatomas.
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Middle & Inner Ear Pathology
Cholesteatoma - The simple way to think about this is "a bunch of exfoliated skin
debris growing in the wrong place."It creates a big inflammation ball which wrecks the
temporal bone and the ossicles.
There are two parts to the ear drum, a flimsy whimpy part "Pars
Flaccida", and a tougher part "Pars Tensa." The flimsy flaccida
is at the top, and the tensa is at the bottom. P. Tensa
If you "acquire"a hole with some
inflammation / infection involving the Pars
Flaccida you can end up with this ball of
epithelial crap growing and causing
inflammation in the wrong place.
- Typical location of this
soft tissue blob with
erosion of scutum
(arrow)
- They restrict diffusion
There are two subtypes based on the location.
Pars Flaccida Type Pars Tensa Type:
• Acquired Types are more common - typically involving •The inner ear structures are
the pars flaccida. They grow into Prussak's Space involved earlier and more
• The Scutum is eroded early (maybe first)- considered often
a very specific sign of acquired cholesteatoma •This is less common than
• The Malleus head is displaced medially the Flaccida Type
• The long process of the incus is the most common
segment of the ossicular chain to be eroded.
• Fistula to the semi-circular canal most commonly
involves the lateral segment
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Prussak's Space and Scutum Erosion:
This is a coronal view of the T-Bone. To orient you I
drew I cartoon finger in the ear. That finger is running
right up to the ear drum (tympanic membrane). The
membrane is usually too thin to see, but it's right around
there. Remember the flimsy Flacida is at the top and the
thicker Tensa is at the bottom.
There are two white arrows here.
The top arrow is pointing to a space between an ossicle
(incus) and the lateral temporal bone. This is called
"Prussak's space" and is the most common location of
a Pars Flacida Cholesteatoma. Remember the incus was
the most common ossicle eroded.
The bottom arrow is pointing to a bony shield shaped
bone - "the scutum" which will be the first bone eroded
by a pars flaccida.
Labyrinthine Fistula (perilymphatic fistula):
This is a potential complication of
cholesteatoma (or other things - iatrogenic,
trauma, etc ... ). What we are talking about here
is a bony defect creating an abnormal
communication between the normally fluid
filled inner ear and normally air filled tympanic
cavity. In the case of cholesteatoma, the
lateral semicircular canal (arrows) is most
Coronal
often involved.
The classic clinical history is "sudden fluctuating sensorineural hearing loss and vertigo."
On CT, you want to see the soft
tissue density of the cholesteatoma
eating through the otic capsule into
the semicircular canal. The
presence of air in the semicircular
canal (pneumolabyrinth) is
definitive evidence of a fistula
(although it's not often seen in the
real world).
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Otitis Media (OM) -This is a common childhood disease with effusion and infection of the
middle ear. It's more common in children and patients with Down Syndrome because of a more
horizontal configuration of the Eustachian tube. It's defined as chronic if you have fluid persisting for
more than six weeks.
It can look a lot like a cholesteatoma (soft tissue dtmsity iu the middle eat).
THIS vs THAT: Complications of OM
: Chronic Otitis Coalescent ; Erosion of the mastoid septae with or
Media • Cholesteatoma Mastoiditis · without intramastoid abscess
Poorly Poorly Secondary to inflammation of the
Mastoids . pneumatized pneumatized Facial Nerve • tympanic segment (more on this later in
Palsy the chapter).
Middle Ear ' Can completely · Can completely
Opacification : opacity 1 opacity • Adjacent inflammation may cause
t thrombophlebitis or thrombosis of the
For the Purpose 'Non sinus. This in itself can lead to
of Multiple · Thickened Dependent • complications:
Choice - this mucosa . Mass
could be a hint Dw-al Sinus · Venous Infarct: Otitic
Thrombosis This can occur . Hydrocephalus:
Erosions · Lateral sinus
(scutum and : Rare ( < 10%) i Common secondary to thrombosis can
ossicular chain) '(75%) dural sinus alter resorption of
thrombosis CSF and lead to
Displacement
of the ossicular NEVER It can happen hydrocephalus.
chain Meningitis,
and , It can happen
Labyrinthitis
Labyrinthitis Ossificans -
• Gamesmanship - "history of childhood meningitis. " WTF is a "membranous labyrinth" ?
• You see it in kids (ages 2-18 months).
• Classic Appearance on CT - Ossification of the The world "Labyrinth" most commonly
refers to the timeless 1986 science
membranous labyrinth. fiction adventure staring
• They present with sensorineural hearing loss. David Bowie as Jareth the Mother
• Calcification in the cochlea is often considered a Fucking Goblin King.
contraindication for cochlear implant.
Another less popular use of the word
"Labyrinth" is the anatomical blanket
term encompassing the Vestibule,
Cochlea, and Semicircular Canals.
Under the umbrella of the "Labyrinth"
you can have the bony portion (the
series of canals tunneled out of the t
bone), and the membraneous portion
(which is basically the soft tissue lining
inside the bony part).
You can then further divide the
"membranous" portion into the
cochlear & vestibular labyrinths.
Normal - For Comparison Labyrinthitis Ossificans
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Labyrinthitis -This is an inflammation of the
membranous labyrinth, probably most commonly the
result of a viral respiratory track infection. Acute
otomastoiditis can also spread directly to the inner ear
(this is usually unilateral). Bacterial meningitis can
cause bilateral labyrinthitis.
Classic Look: The cochlea and semicircular canals
will be shown enhancing on T l post contrast imaging.
The Facial Nerve (CN 7)
Enhancement
Most people will describe 6 segments to the facial nerve.
The facial nerve is unique in that
• Intracranial ("Cisternal") segment portions of it can enhance normally.
The trick is which parts are nonnal
• Meatal ("Canalicular") segment - the part inside the
and which paiis are NOT.
Internal Auditory Canal "IAC").
Normal Enhancement: Tympanic &
• Labyrinthine segment (LS) - from the IAC to Mastoid Segments including the
geniculate ganglion (GG). Geniculate Ganglia. The
• Tympanic segment (TS) - GG to pyramidal eminence Labyrinthine segment can also
• Mastoid segment (MS) - from pyramidal eminence sometimes.
to stylomastoid foramen "SMF" No normal enhancement = Cisternal,
• Extratemporal segment - Distal to the SMF Canalicular, or Extratemporal
Axial MR T2 - Cisternal Segment Axial CT- Level of IAC
-CN8 is posterior also -the bend at the GG = Sagittal CT-
entering the IAC "anterior genu"
What causes abnormal enhancement? Bells Palsy & Ramsey Hunt
Big one is Bell's Palsy. Lymes, Ramsay Bells: Etiology is probably viral. Usually a
Hunt, and Cancer can do it too. clinical diagnosis. Abnormal enhancement in
When do you think Cancer ? the Canalicular Segment (in the IAC) is
probably the most classic finding.
Nodular Enhancement.
When do you damage thefacial nerve? RH: Caused by reactivation varicella zoster
virus. Classic rash around ear. CN 5 is
T-Bone fracture (transverse> longitudinal). usually also involved.
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Otosclerosis (Fenestral and Retrofenestral):
A better term would actually be "otospongiosis," as the bone becomes more lytic (instead of sclerotic).
When I say conductive hearing loss in an adult female, you say this.
Fenestral - This is bony resorption anterior to the oval widow at the fissula ante fenestram.
If not addressed, the footplate will fuse to the oval window.
Retro-fenestral - This is a more severe form, which has progressed to have demineralization around
the cochlea. This form usually has a sensorineural component, and is bilateral and symmetric nearly
100% of the time.
Bony
resorption
anterior to the
oval widow at Comparison
the fissula ante
fenestram
Treatment Options:
Early on (if the focus is small) dietary supplementation with Fluoride
may be useful. Although this is controversial - may or may not work. ..
and may or may not be part of a new world order David Icke Reptilian
conspiracy to lower IQs (Alex Jones has the documents).
Slithery space born
Later on they might try a stapedectomy (partial removal of the stapes
illuminati villains
with implantation of a prosthetic device) or a Cochlear implant. advocate for
Fluoride treatment.
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Superior Semicircular Canal Dehiscence
Pietro Tullio
This is an Aunt Minnie . It's supposedly from long standing elevated
Mad scientist who drilled
ICP. The most likely way this will be asked is either (1) what is it? with holes in the semicircular
a picture or (2) "Noise Induced Vertigo" or "Tullio's Phenomenon." canals of pigeons then
observed that they became
off balance when he
exposed them to loud
sounds.
He also created a "pigeon
rat" like Hugo Simpson did
in the 1996 Simpsons
Halloween Special.
Normal Anatomy
Note the intact Bony Roof (Arrow) Superior Semicircular Canal
Dehiscence Note the Absence
of a Bony Covering
"Look, I've been practicing"
Large Vestibular Aqueduct Syndrome
The vestibular aqueduct is a bony canal that connects the vestibule (inner ear) with the endolymphatic
sac. The enlargement of the aqueduct (> 1.5 mm) has an Aunt Minnie appearance. The classic
history is progressive sensorineural hearing loss. Supposedly the underlying etiology is a failure of
the endolymphatic sac to resorb endolymph, leading to endolymphatic hydrops and dilation.
Trivia:
•This is the most common cause of congenital sensorineural hearing loss
•The finding is often (usually) bilateral.
•There is an association with cochlear deformity - near 100%
(absence of the bony modiolus in more than 90%)
•Progressive Sensorineural Hearing Loss (they are NOT born deaf)
The normal Vestibular Aqueduct (VA) is Enlarged Vestibular Aqueduct
NEVER larger than the adjacent (larger than PSCC- grey arrow)
Posterior Semicircular Canal (PSCC)
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Congenital malformations of the inner ear can be thought about along a spectrum of severity.
As the construction of the hearing machinery is complicated business, you can imagine that
the earlier things go wrong in this multi-stage anatomical development the more severe the
anomaly.
Along those lines, we can discuss two disorders on opposite ends of that severity spectrum
with the Michel's Aplasia being the earliest and most severe, and the Classic Mondini's
Malformation (incomplete partition II) being the latest and least severe.
Mondini Malformation - Type of cochlear hypoplasia where the basal turn is normal, but
the middle and apical turns fuse into a cystic apex. This is usually written as "only 1.5 turns" -
instead of the normal 2.5. There is an association with an enlarged vestibule, and enlarged
vestibular aqueduct. They have sensorineural hearing loss, although high frequency sounds are
typically preserved (as the basal tum is normal).
Michel's Aplasia - This is also referred to as complete labyrinthine aplasia or "CLA." As
above, this represents the most severe of the congenital abnormalities of the inner ear - with
absence of the cochlea, vestibule, and vestibular aqueduct. No surprise these kids are
completely deaf.
Associations: Anencephaly, Thalidomide Exposure
Gamesmanship: Some people think this looks like labyrinthitis ossificans. Look for the
absent vestibular aqueduct to help differentiate.
THIS vs THAT: Mondinivs Michel
Mondini Michel
Timing Late (7th Week) Early (3rd Week)
Severity Some Preserved High Frequency Hearing Total Deafness
Cochlea: Cystic Apex (basilar tum is normal) Absent
Vestibule Sometimes Enlarged (can be normal) Absent
Vestibular
Large Absent
Aqueduct
Common
Frequency Rare As Fuck
(relative to other malformations)
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Endolymphatic Sac Tumor
Rare tumor of the endolymphatic sac and duct. Although most are sporadic, when you see this
tumor you should immediately think Von-Hippel-Lindau.
Classic Look: They almost always have internal amorphous calcifications on CT. There are
T2 bright, with intense enhancement. They are very vascular often with flow voids, and
tumor blush on angiography.
Cochlea
Aperture of
Vestibular Aqueduct - �,.
Tumor'?
Endolymph Sac
Paraganglioma
On occasion, paraganglioma of the jugular fossa (glomus jugulare or jugulotympanic tumors)
can invade the occipital bone and adjacent petrous apex.
Trivia:
•40% of the time it's hereditary, and they are multiple.
•The most common presenting symptom is hoarseness from vagal nerve compression.
• They are very vascular masses and enhance avidly with a "salt and pepper"
appearance on post contrast MRI, with flow voids.
•They are FDG avid.
More on these later in the chapter
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Petrous Apex -Anatomic variations:
Variation can occur in the amount of pneumatization, marrow fat, bony continuity, and
vascular anatomy.
Asymmetric Marrow: - Typically the petrous apex contains significant fat, closely
following the scalp and orbital fat (Tl and T2 bright). When it's asymmetric you can have
two problems (1) falsely thinking you've got an infiltrative process when you don't, and (2)
overlooking a T l bright thing (cholesterol granuloma) thinking it's fat. The key is to use
STIR or some other fat saturating sequence.
Cephaloceles: - A cephalocoele describes a herniation of CNS content through a defect
in the cranium. In the petrous apex they are a slightly different animal. They don't contain any
brain tissue, and simply represent cystic expansion and herniation of the posterolateral portion
ofMeckel's cave into the superomedial aspect of the petrous apex. Describing it as a
herniation of Meckel's Cave would be more accurate. These are usually unilateral and are
classically described as "smoothly marginated lobulated cystic expansion ofthe petrous
apex."
Aberrant internal carotid. The classic history is pulsatile tinnitus (although other
things can cause that). This term is used to describe the situation where the Cl (cervical)
segment of the ICA has involuted/underdeveloped, and middle ear collaterals develop
(enlarged caroticotympanic artery) to pick up the slack. The hypertrophied vessel runs
through the tympanic cavity and joins the horizontal carotid canal. The ENT exam will show a
vascular mass pulsing behind the ear drum (don't expect them to make it that easy for you).
The oldest trick in the book is to try and fool you
into calling it a paraganglioma.
Look for the connection to the horizontal carotid
canal - that is the most classic way to show this.
DO NOT BIOPSY !
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Apical Petrositis
Infection of the petrous apex is a rare complication of infectious otomastoiditis. It can have
some bad complications if it progresses including osteomyelitis of the skull base, vasospasm of
the ICA(if it involves the carotid canal), subdural empyema, venous sinus thrombosis, temporal
lobe stroke, and full on meningitis.
In children, it can present as a primary process. In adults it's usually in the setting of chronic
otomastoiditis or recent mastoid surgery.
Tl+C
r------------------
Gradenigo Syndrome Dorello's Canal I
I
This is a complication of apical petrositis, when Dorello's canal The most medial point :
of the pertrous ridge
(CN 6) is involved. They will show you (or tell you) that the patient between the pontine
has a lateral rectos palsy. cistern and cavernous :
sinus :
I_ - - - - - - - - - - - - - - - - - �
Classic Triad:
• Otomastoiditis,
• Face pain (trigeminal
neuropathy), and
• Lateral Rectus Palsy
Look Straight Look Left Look Right
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Petrous Apex - lnflammatorv lesions
Cholesterol Granuloma
The most common primary petrous apex lesion. Mechanism is likely obstruction of the air
cell, with repeated cycles of hemorrhage and inflammation leading to expansion and bone
remodeling. The most common symptom is hearing loss.
On CT the margins will be
sharply defined. On MRI
it's gonna be Tl and T2
bright, with a T2 dark
hemosiderin rim, and faint
peripheral enhancement.
Key Point:
Cholesterol Granuloma =
Tl and T2 Bright.
The slow growing ones can
be watched. The fast Cholesterol Granuloma = T1 and T2 Bright
growing ones need surgery.
Cholesteatoma
This is basically an epidermoid (ectopic epithelial tissue). Unlike the ones in the middle ear,
these are congenital (not acquired) in the petrous apex. They are typically slow growing, and
produce bony changes similar to cholesterol granuloma.
The difference is their MRI findings; T l dark, T2 bright, and restricted diffusion.
Key Point: Cholesteatoma = Tl Dark, T2 Bright, Restricted Diffusion
THIS vs THAT:
Cholesterol Granuloma Cholesteatoma
Tl Bright T l Dark
T2 Bright T2 Bright
Doesn't Restrict Does Restrict
Smooth Expansile Bony Change Smooth Expansile Bony Change
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External Ear
Regular and Necrotizing Otitis Externa:
Otitis Externa - the so called "swimmers ear" is an infection (usually bacterial) of the
external auditory canal. The more testable version Necrotizing Otitis Externa (also called
"Malignant" Otitis Externa - for the purpose of fucking with you) is a more aggressive
version seen almost exclusively in diabetics.
You are going to see swollen EAC soft tissues, probably with a bunch of small abscesses, and
adjacent bony destruction.
They always (95%) have diabetes and the causative agent is always (98%) Pseudomonas.
External Auditory Canal Exostosis ("Swimmers Ear") - This is an
overgrowth of tissue in the ear canal, classically seen in Surfers who get repeated bouts of ear
infections. It's usually bilateral, and when chronic will look like bone. Unlike Necrotizing
Otitis, these patients are immunocompetent and non-diabetes (although they are dirty hippie
surfers).
External Auditory Canal Osteoma - This is a benign bone tumor, maybe best
thought of as an overgrowth of normal bone. They are usually incidental and unilateral
(remember exostosis was bilateral) occurring near the junction of cartilage and bone in the
ear canal.
External Auditory Canal Atresia:
This is a developmental anomaly where the external
auditory canal (secondary crayon storage
compartment) doesn't form. As you might imagine,
this results in a hearing deficit (conductive subtype).
There may or may not be a mashed up ossicular
chain.
Normally, there is a place to stick a
crayon right around here (arrow).
Trivia: ENT will want to know: (1) if the tissue covering the normally open ear hole (atretic
plate) is soft tissue or bone, and (2) if there is an aberrant course of the facial nerve.
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.
• .
· •
�
SECTION 13:
SKULL BASE & SINUSES �
• .
Pagets - This is discussed in great depth in the MSK chapter. Having said that, I want to
remind you of the Paget skull changes. You can have osteolysis as a well-defined large
radiolucent region favoring the frontal and occipital bones. Both the inner and outer table are
involved. The buzzword is osteolysis circumscripta.
Paget'.,; Skull related complications:
• Deafness is the most common complication
• Cranial Nerve Paresis
• Basilar Invagination ->Hydrocephalus-> Brainstem Compression
• Secondary (high grade) osteosarcoma.
Pagets - Osteolysis Circumscripta (lytic phase) Thickened Expanded Skull (Sclerotic Phase)
Chordoma (midline) & Chondrosarcoma (o.ffmidline) discussed in MSK chapter.
Fibrous Dysplasia - The ground-glass lesion. If you are getting ready to call it Pagets,
stop and look at the age. Pagets is typically an older person (8% at 80), whereas fibrous
dysplasia is usually in someone less than 30.
• Classically, fibrous dysplasia of the skull spares the otic capsule
• McCune Albright Syndrome - Multifocal fibrous dysplasia, cafe-au-lait spots, and
precocious puberty.
• The outer table is favored (Pagets tends to favor in the inner table)
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Sinus Disease Strategy Intro: You will sec CT and MRI used in the evaluation of sinus
disease. It is useful to have some basic ideas as to why one modality might be preferred over the
other (for gamesmanship and distractor elimination). CT is typically used for orbital and sinus
infections. In particular it is useful to sec if the spread of infection involves the anterior 2/3 of the
orbit. If you wanted to know if the patient has cavernous sinus involvement, or involvement of the
posterior l/3 (orbital apex) MRI will be superior.
CT also has the ability to differentiate common benign disease - Hyper Dense Sinus -
(inspissated secretion and allergic fungal sinusitis) from the more
rare sinus tumors. The trick being that a hyperdense opacificd sinus • Blood
• Dense (inspissated)
is nearly always benign (tumor will not be dense). In addition to Secretions
that CT is useful for characterization of anatomical variation • Fungus
(justification of endoscopic nasal surgery for recurrent sinusitis).
MRI is going to be more valuable for tumor progression/ extension (perineural spread, marrow
involvement etc.. ).
Fungal Sinusitis
This comes in two flavors; the good one (allergic) and the bad one (invasive). The chart below will
contrast the testable differences:
Allergic Fungal Sinusitis Acute Invasive Fugal Sinusitis
Opacification of multiple sinuses. Stranding /
Opacification of multiple sinuses, ususually bilateral Extension into the fat around the sinuses in the key
favoring the ethmoid and maxillary sinuses. finding.
lmmunocompromised
Normal Immune System (Asthma is common) - Neutropenic = Aspergillus
- Diabetic in DKA = Zygomycetes / Mucor
CT: Opacified Sinus with is NOT hyperdense. Fat
CT: Hyperdense centrally or with layers. Can stranding in the orbit, masticator fat, pre-antral fat,
erode and remodel sinus walls if chronic. or PPF suggests invasion. This does NOT require
bone destruction.
MRI: Tl-T2 Dark- because of the high protein
content / heavy metals. Can mimic an aerated sinus. MRI: Also can be Tl/T2 Dark. However, the
Inflamed (T2 bright) mucosa which will enhance. mucosa may not enhance (suggesting it is necrotic).
The glob of fungus snot will not enhance (thats how The extension of disease out of the sinus will be
you know it is not a tumor). bright on STIR and enhance.
Chronic Inflammatory SinonasaB Disease
This is typically thought of as an inflammation of the paranasal sinuses
that lasts at least 12 weeks. The causes arc complex and people write
long boring papers about the various cytokincs and T-Cell mediation
pathways are involved but from the Radiologist's point of view the issue
is primarily anatomical patency of sinus Ostia (box with arrow).
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Chronic Inflammatory Sinonasal Disease Continued ...
There arc several described patterns ofrccurring sinonasal disease.
lnfundlibular Ostiomeatal Unit Pattern Sinonasal Polyposis
Pattern. Pattern.
Second most common pattern. I'm
The most common not going to get into depth on the
The pattern is characterized by a
pattern. various subtypes
combination of soft tissue nasal
polyps (found throughout the nasal
In this pattern, just think about
cavity) and variable degrees of sinus
disease is limited to this as more
opacification. About half the time
the maxillary sinus centered at the
fluid levels will also be present.
and occurs from the middle
obstruction at the meatus (star)
A key feature is the bony remodeling
ipsilateral ostium / with disease
and erosion. In particular the
infundibulum (star). involving the
"widening of the infundibula" is the
ipsilateral
classic description. This erosion and
maxillary,
remodeling is important to distinguish
frontal and
between the "expansion" of the sinus
ethmoid·
- which is more classic for a
sinuses.
mucocele.
The contributors to this pattern
Testable associations include CF and
involve all the usually suspects
Aspirin Sensitivity.
(hypertrophied turbinates, anatomic
variants - concha bullosa, middle
turbinates which curl the wrong way
"paradoxical", and septa! deviation).
Mucocele
This is how I think about these things. You have an obstructed sinus.
Maybe you had trauma which fucked the drainage pathway or you've got
CF and the secretions just clog things up. Mucus continues to accumulate
in the sinus, but it can't clear (because it's obstructed). Over lime the sinus
become totally filled and then starts lo expand circumferentially. Hence the
buzzword "m2ancled airless sinus." The frontal sinus is the most common
location. It won't enhance centrally (it is not a tumor), but the periphery
may enhance from the adjacent inflamed mucosa.
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Antrochoanal Polyp
Seen in young adults (30s-40s), classically presenting with nasal congestion/ obstruction symptoms. Arises
within the maxillary sinuses and passes through and enlarges the sinus ostium (or accessory ostium).
� Buzzword is "widening of the maxillary ostium."
/
Classically, there is no associated bony destruction but instead smooth enlargement of the sinus. The polyp
will extend into the nasopharynx. This thing is basically a monster inflammatory polyp with a thin stalk
arising from the maxillary sinus.
Juvenile Nasal Angiofibroma (JNA)
Often you can get this one right just from the history - Male teenager with nose bleeds (obstruction is
actually a more common symptom in real life, but not so much on multiple choice).
•Location = Centered on the sphenopalatine foramen
•Bone Remodeling (not bone destruction)
•Extremely vascular (super enhancing) with intratumoral Flow Voids on MR
•Pre-surgical embolization is common (via internal maxillary & ascending pharyngeal artery)
Inverted Papilloma:
This uncommon tumor has distinctive imaging features (which therefore make it testable). The classic
location is the lateral wall of the nasal cavity - most frequently related to the middle turbinate.
Impaired maxillary drainage is expected.
•A focal hyperostosis tends to occur at the tumor origin.
•Another high yield pearl is that 10% harbor a squamous cell CA.
•MRI "cerebriform pattern" -which sorta looks like brain on T l and T2.
Esthesioneuroblastoma:
This is a neuroblastoma of olfactory cells so it's gonna start at the cribifo1m plate. It classically has a
dumbbell appearance with growth up into the skull and growth down into the sinuses, with a waist at the
plate. There are often cysts in the mass. There is a bi-modal age distribution.
. L •Dumbbell shape with wasting at the cribiform plate is classic
� •lntracranial posterior cyst is a "diagnostic" look
f'9 •Octreotide scan will be positive - since it is of neural crest origin
Squamous Cell/ SNUC:
Squamous cell is the most common head and neck cancer. The maxillary antrum is the most common
location. It's highly cellular, and therefore low on T2. Relative to other sinus masses it enhances less.
SNUC (the undifferentiated squamer), is the monster steroided-up version of a regular squamous cell. They
are massive and seen more in the ethmoids.
Epistaxis (Nose Bleeds)
This is usually idiopathic, although it can be iatrogenic (picking it too much - or not enough). They could
get sneaky and work this into a case of HHT (hereditary hemorrhagic telangiectasia). The most common
location is the anterior septal area (Kiesselbach plexus) - these tend to be easy to compress manually. The
posterior ones are less common (5%) but tend to be the ones that "bleed like stink" (need angio). Most
cases are given a trial of nasal packing. W hen that fails, the N-IR team is activated.
The main supply to the posterior nose is the sphenopalatine artery (terminal internal maxillary
artery) and tends to be the first line target. Watch out for the variant anastomosis between the ECA
and ophthalmic artery (you don't want to embolize the eye).
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Nasal Septal Perforation
Typically involves the
anterior septal cartilaginous
area.
There are a bunch of things
that can do this. These are
the ones I'd think about:
• Surgery - Old school
Septoplasty techniques
essentially resecting the
thing(Killian submucous
resection)
• Cocaine use(> 3 months)
• Too much nose picking(or perhaps not picking it enough)
• Granulomatosis with polyangiitis (Wegener granulomatosis)-Triad of renal masses, sinus
mucosa] thickening and nasal septal erosion, disease, and cavitary lung nodules / fibrosis.
cANCA positive.
• Syphilis - affects the bony septum(most everything else effect the cartilaginous regions).
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····
;·
. i,
'. �
SECTION 14:
MOUTH & JAW � •..:
,·: '
Sialolithiasis - Stones in the salivary ducts. The
testable trivia includes: (1) Most commonly in the Submandibular = Wharton
submandibular gland duct(wharton's), Parotid = Stenson
(2) can lead to an infected gland "sialoadenitis"., and Sublingual = Rivinus
(3) chronic obstruction can lead to gland fatty atrophy.
Odontogenic Infection - These can be dental or periodontal in origin. IfI were writing
a question about this topic I would ask three things. The first would be that infection is more
common from an extracted tooth than an abscess involving an intact tooth.
The second would be that the
attachment of the mylohyoid Sublingual
muscle to the mylohyoid ridge Space
dictates the spread of infection to -Above the Mylohyoid Line
the sublingual and submandibular (Anterior Mandibular Teeth)
spaces. Above the mylohyoid line
(anterior mandibular teeth) goes to
the sublingual space, and below the
mylohyoid line (second and third
molars) goes to the submandibular
space.
The third thing I would ask would be
that an odontogenic abscess is the Submandibular
most common masticator space Space
"mass" in an adult. -Below the Mylohyoid Line
(2nd and 3rd Molars)
Ludwig's Angina:
This is a super aggressive cellulitis in the floor of the
mouth. If they show it, there will be gas everywhere.
Trivia: most cases start with an odontogenic infection.
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Torus Palatinus: Osteonecrosis of Ranula:
the Mandible:
This is a normal variant that
looks sca1y. This is a mucous retention
The trivia is most likely cyst. They are typically
Because it looks scary some lateral. There are two
gonna be etiology.
multiple choice writer may try testable pieces of trivia to
and trick you into calling it know:
Just remember it is related
cancer.
to prior radiation, licking (1) They arise from the
It's just a bony exostosis that a radium paint brush, or sublingual gland / space,
comes off the hard palate in and
bisphosphonate
the midline.
treatment. (2) Use the word
Classic History: "Grandma's "plunging" once it's under
dentures won't stay in." the mylohyoid muscle.
T hyroglossal Duct Cyst-This can occur anywhere between the foramen cecum (the
base of the tongue) and the thyroid gland. They are usually found in the midline. It looks like a
thin-walled cyst. Further discussion in the endocrine & peds chapters.
Floor of Mouth Dermoid / Epidermoid - There isn't a lot of trivia about these other
than the buzzword and what they classically look like. The buzzword is "sack of marbles" -
fluid sack with globules of fat. They are typically midline. Further discussion in the peds
chapter.
Cancer - Squamous cell is going to be the most common cancer of the mouth (and head and
neck). In an older person think drinker and smoker.
In a younger person think HPV. HPV related SCCs tend to be present with large necrotic level
2a nodes (don't call it a branchial cleft cyst!).
Classic Scenario = Young adult with new level II neck mass = HPV related SCC.
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lesions of the Jaw
There are a BUNCH of these and they all look pretty similar. Lesions in the jaw are broadly
grouped into either odontogenic (from a tooth) or non-odontogenic (not from a tooth). The
non-odontogenic stuff you see in the mandible is the same kind of stuff you see in other bones
(ABCs, Simple Bone Cysts, Osteomyelitis, Myeloma / Plasmacytoma etc ...). I think if a test
writer is going to show a jaw lesion - they probably are going to go for odontogenic type.
Obviously your answer choices will help you decide what they are going for. The other tip is
that odontogenic lesions are usually associated with a tooth.
I'm going to pick 5 that I think are most likely to be asked and focus on how I would tell them
apart.
Periapical Cyst (Radicular Cyst) -This is the most
common type of odontogenic cyst. They are typically the result
of inflammation from dental caries (less commonly trauma).
The inflammatory process results in a cystic degeneration
e o i
�
•::::: .::� :;::�: :::::tal toofu
•Round with a Well Corticated Border
•Usually< 2 cm
Dentigerous Cyst (Follicular Cyst) -This is a
cyst that forms around the crown of an un-erupted tooth.
It's _best thought of as a developmental cyst (peri-apicals
are acquired). These things like to displace and resorb
adjacent teeth - usually in an apical direction. This is the
,/tit kind of cyst that will displace a tooth into the condylar
regions offue mandible or into fue floor of the orbit.
,/tit •Located at the crown of an un-erupted tooth
•Tend to displace the tooth
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Keratogenic Odontogenic Tumor
(Odontogenic Keratocyst) - Unlike the prior two
lesions (which were basically fluid collections) this
is an actual tumor. They tend to occur at the
mandibular ramus or body. Although they can be
uni-locular the classic look is multi-locular
( "daughter cysts") and that's how I would expect
them to look on the test.
• Body / Ramus Mandible
• They typically grow along the length of the bone
• Without significant cortical expansion
• May have daughter cysts
• When multiple think Gorlin Syndrome
Ameloblastoma (Adamantinoma of the
jaw) -This is another tumor (locally aggressive).
The appearance is variable but for the purpose of
multiple choice I would expect the most classic
look - multi-cystic with solid components and
expansion of the mandible.
Out of the four I've discussed, this will be the
most aggressive-looking one. If they show you a
really aggressive-looking lesion, especially if it
has multiple "soap bubbles" - you should
consider this.
• Hallmark = ExtensiveTooth Root Absorption
• Mandibular Expansion
• Solid component (shown on MR or CT) favors the Dx of Ameloblastoma
• About 5% arise from Dentigerous C ysts
Odontoma -This is the easy one to pick out because it's
most likely to be shown in it's mature solid form (they start
out lucent). It's actually the most common odontogenic
tumor of the mandible. It's basically a "tooth hamartoma."
• Radiodense with a lucent rim
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SECTION 15:
SUPRAHYOID NECK
• Can be LARGE with "fluffy" calcifications
The suprahyoid neck is usually taught by using a "spaces" method. This is actually the best
way to learn it. What space is it? What is in that space? What pathology can occur as the
result of what normal structures are there? Example: lymph nodes are there- thus you can get
lymphoma or a met.
Parotid Space:
The parotid space is basically
the parotid gland, and portions
of the facial nerve. You can't
see the facial nerve, but you can
see the retromandibular vein
(which runs just medial to the
facial nerve).
Another thing to know is that
the parotid is the only salivary
gland to have lymph nodes, so
pathology involving the gland
itself, and anything lymphatic
related, is fair game.
Parotid Space Contains:
- The Parotid Gland
- Cranial Nerve 7 (Facial)
- Retro-mandibular Vein
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Pathology:
1 ----------------------1
Major Salivary Glands:
Pleomorphic Adenoma (benign mixed tumor) • Parotid
This is the most common major (and minm) salivary gland • Submandibu/ar
tumor. It occurs most commonly in the parotid, but can also • Sublingual
occur in the submandibular or sublingual glands. 90% of
these tumors occur in the superficial lobe. They are Minor Salivary Glands
commonly T2 bright, with a rim of low signal. They have a : • Literally 100s of un-
: named minor glands
small malignant potential and are treated surgically. � ----------------------J
• Superficial vs Deep: Involvement of the superficial (lateral to the facial nerve) or deep
(medial to the facial nerve) lobe is critical to the surgical approach. A line is drawn
connecting the lateral surface of the posterior belly of the digastric muscle and the
lateral surface of the mandibular ascending ramus to separate superficial from deep.
• Apparently, if you resect these like a clown you can spill them, and they will have a
massive, ugly recurrence.
Warthins: This is the second most common benign tumor. This one ONLY occurs in the
parotid gland. This one is usually cystic, in a male, bilateral (15%), and in a smoker. As a
point of total trivia, this tumor takes up pertechnetate (it's basically the only tumor in the
parotid to do it, ignoring the ultra rare parotid oncocytoma).
Mucoepidermoid Carcinoma - This is the most common malignant tumor of minor
salivary glands. The general rule is - the smaller the gland, the more common the malignant
tumors; the bigger the gland, the more common the benign tumors. There is a variable
appearance based on the histologic grade. There is an association with radiation.
Adenoid Cystic Carcinoma - This is another malignant salivary gland tumor, which
favors minor glands but can be seen in the parotid. The number one thing to know is
perineural spread. This tumor likes perineural spread.
. L When I say adenoid cystic, you say perineural spread.
,.,, Pearl: I used to think that perineurial tumor spread would widen a neural foramen
. L (foramen ovale for example). It's still might. .. but it's been my experience that a nerve
sheath tumor (schwannoma) is much more likely to do that. Let's just say for the
,.,, purpose of multiple choice that neural foramina widening is a schwannoma - unless
there is overwhelming evidence to the contrary.
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Lymphoma
Because the parotiJ has lymph nuJes (it's the uuly salivary gland that does), you can get
lymphoma in the parotid (primary or secondary). If you see it and it's bilateral, you should
think Sjogrens. Sjogrens patients have a big risk (like 1 000x) of parotid lymphoma. Like
lymphoma is elsewhere in the body, the appearance is variable. You might see bilateral
homogeneous masses. For the purposes of the exam, just knowing you can get it in the
parotid (primary or secondary) and the relationship with Sjogrens is probably all you
need.
Sjogrens
Autoimmune lymphocyte-induced destruction of the gland. "Dry Eyes and Dry Mouth."
Typically seen in women in their 60s. Increased risk (like lO00x) risk of non-Hodgkins MALT
type lymphoma. There is a honeycombed appearance of the gland.
Benign Lymphoepithelial Disease:
You have bilateral mixed solid and cystic lesions with diffusely enlarged parotid glands. This
is seen in HIV. The condition is painless (unlike parotitis - which can enlarge the glands).
Acute Parotitis:
Obstruction of flow of secretions is the most common cause. They will likely show you a stone
(or stones) in Stensen's duct, which will be dilated. The stones are calcium phosphate. Post
infectious parotitis is usually bacterial. Mumps would be the most common viral cause. As a
point of trivia, sialography is contraindicated in the acute setting.
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ParaoharvnuealSpace
Also referred to as the
"pre-styloid" parapharyngeal
space - for the purpose of
fucking with you.
The parapharyngeal
The primary utility of the space is primarily a
space is when it is ball of fat with a few
displaced (discussed branches of the
below). trigeminal nerves, and
the pterygoid veins.
Mets and infections can
spread directly in a
vertical direction through
this space (squamous cell
cancer from tonsils, Parapharyngeal Fat (PPF) Displacement
tongue, and larynx).
A cystic mass in this
location could be an
atypical 2nd Branchial
Cleft Cyst (but is more Carotid
Parotid
Space=
likely a necrotic lymph Space=
Medial
Anterior
node). Displacement
Displacement
The parapharyngeal space is
bordered on four sides by
different spaces. If you have
a mass dead in the middle, it
can be challenging to tell
where it's coming from.
Using the displacement of Masticator
fat, you can help problem Space= Superficial
Posterior Mucosal
solve. Much more important Medial Space=
than that, this lends itself Displacement Lateral
very well to multiple choice. Displacement
Parotid Mass Pushes
Medially (PMPM)
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Carotid Space:
The carotid space is also sometimes called the
"post styloid" or "retro-styloid" parapharyngeal
space - for the purpose of fucking with you.
There are 3 Classic Carotid Space Tumors:
( 1) Paraganglioma
(2) Schwannoma
(3) Neurofibroma
Although it is w01th noting
that this space is
commonly involved in Carotid Space
secondary spread of Contains:
aggressive multi-spatial
disease - such as - Carotid artery
infectious path - Jugular vein
(necrotizing otitis external) - Portions of CN 9,
or malignant spread CN 10, CN 11
(nasopharyngeal,
squamous cell etc.. ). - Internal jugular
chain lymph nodes
Metastatic squamous cell
is what you should think
for nodal disease in this Lesions Displace the Paraphaiyngeal Fat ANTERIOR
region.
Paragangliomas: There are three different ones worth knowing about - based on location.
The imaging features are the same. They are hypervascular (intense tumor blush), with a
"Salt and Pepper" appearance on MRI from the flow voids. They can be multiple and
bilateral in familial conditions (10% bilateral, 10% malignant, etc.). 111 In-octreotide
accumulates in these tumors (receptors for somatostatin).
Carotid Body Tumor = Carotid
Bifurcation (Splaying !CA and
ECA)
Glomus Jugulare = Skull Base
( often with destruction o,fjugular
foramen)
Middle Ear Floor Destroyed =
Glomus Jugulare.
Glomus Vagale = Above Carotid
Bifurcation, but below the Jugular
Foramen
Glomus Tympanicum =
Confined to the middle ear.
Buzzword is "overlying the
cochlear promontory. "
Middle Ear Floor Intact =
Glomus Tympanum
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Schwannoma ,.,__
Surgical 7S z..
Most commonly in this location we are talking about vagal nerve Planning Trivia:
(CN 10), but if the lesion is pretty high up near the skull base it • Distance of Skull
could also be involving CN 9, 11, or even 12. The typical MR Base ( > 1cm =
appearance is an oval mass, heterogenous (cystic and sold parts) Neck Dissection)
with heterogenous bright signal on T2. • Degree of
These things enhance a ton (at least the solid parts anyway). They Vascularity
(might need pre
enhance so much you might even think they were vascular. embolization)
Ironically, schwannomas are considered hypo vascular lesions and
• Relationship to the
the only reason they enhance is because of extravascular leakage Carotid (Don't Fuck
(and poor venous drainage). with Big Red)
Neurofibroma
These are less common than the schwannoma. About 10% of the time they are related to
NF-1 (in which case you should expect them to be bilateral and multiple). In contrast to
schwannomas they tend to be more homogenous, and demonstrate the classic target sign on
T2 with decreased central signal.
Neurofibroma Schwannoma Paraganglioma
Mildly Heterogenous Although they enhance intensely Hypervascular
Enhancement they are not vascular on Angio (tumor blush on angio)
T2: Target Sign T2: Moderate to High Signal - T2: Light Bulb Bright with
(bright rim, dark middle) Heterogenous Salt and Pepper (flow voids)
NF-1 Association NF-2 Association '''ln-Octreotide avid
Neck Infection Syndromes
Lemierre's Syndrome - This is a thrombophlebitis of the jugular veins with septic emboli in
the lung. It's found in the setting of oropharyngeal infection (pharyngitis, tonsillitis, peritonsillar
abscess) or recent ENT surgery. Buzzword bacteria = "Fusobacterium Necrophorum"
Grisel's Syndrome - Torticollis with atlanto-axial joint inflammation seen in H&N surgery or
retropharyngeal abscess
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Masticator Space:
As the name implies this space contains the
muscles of mastication (masticator,
temporalis, medial and lateral pterygoids).
Additionally, you have the angle and ramus
of the mandible, plus the inferior alveolar
nerve (branch ofV3).
A trick to be aware of is that the space
extends superiorly along the side of the skull
via the temporalis muscle. So, aggressive
neoplasm or infection may ride right up there.
Lesions Displace the Parapharyngeal Fat
POSTERIOR and MEDIAL
Odontogenic Infection-
In an adult, this is the most common cause of a masticator space mass. Ifyou see a mass here, the next
move should be to look at the mandible on bone windows. Just in general, you should be on the look
out for spread via the pterygopalatine fossa to the orbital apex and cavernous sinus. The relationship
with the mylohyoid makes for good trivia - as discussed above.
Sarcomas-
•
In kids, you can run into nasty angry masses like Rhabdomyosarcomas. You can also get sarcomas
from the bone ofthe mandible (chondrosarcoma favors the TMJ).
Cavernous Hemangiomas- Key Point:
Congenital Stuff and
These can also occur, and are given away by the presence of Aggressive Infection/
phleboliths. Venous or lymphatic malformations may involve multiple Cancer tends to be Trans
compartments / spaces. Spatial.
Perineural Spread- You can have perineural spread from a head and neck primary along V3.
When I say "perineural spread" you should think two things:
(1) Adenoid Cystic Carcinoma of the minor salivary gland
(2) Melanoma
Nerve Sheath Tumors- Since you have a nerve, you can have a schwannoma or
neurofibroma ofV3. Remember the schwannoma is more likely to cause the foramina expansion vs
perineural tumor spread.
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Retropharvnueal Space / Danger Space
The retropharyngeal space has some complex anatomy. Simplified, this is a midline space, deep
to the oral & nasal pharynx. The retropharyngeal space has an anterior "true" space which
extends caudal to around C6-C7, and a more posterior "danger space" - which is dangerous
because it listens to rap music and plays first person shooter video games - plus it extends into
the mediastinum - so you could potentially dump pus, or cancer, right into the mediastinum.
True
Retropharyngeal
Retropharyngeal Space
\\pace//
)
,, ' --- Alar Fascia
•
Infectious behind this deep cervical fascia (the Prevertebral Space) are different than the ones
discussed below in that they are not spread from the neck but instead the spine/disc (osteomyelitis).
Infection - Involvement of the retropharyngeal Necrotic Nodes (nodes of
space most often occurs from spread from the tonsillar Rouviere) - These things are located
tissue. You are going to have centrally low density in the lateral retropharyngeal region.
tissue and stranding in the space. You should evaluate In kids you can see suppurative
for spread of infection into the mediastinum. infection in these, but around age 4
they start to regress - so adults are
actually much less to get infection in
this region. Now, you can still get
mets (squamous cell, papillary
thyroid, etc..). Lymphoma can
involve these nodes as well - but
won't be necrotic until treated.
Cartoon Axial
Showing Infection �::�:g':;:!�odes �\�
Spreading from a of Rouviere
Tonsillar Abscess to Peritonsillar Abscess • • •
the Danger Zone
Don't Forget:
Delays are often
critical for
differentiate
phlegmon and
drainable abscess
Retropharyngeal Abscess (midline) Suppurative Node ofRouviere (lateral)
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...
··�
-; . �
SECTION 16:
SQUAMOUS CELL CA &
INFRAHYOID NECK � •' » .·
When you are talking about head and neck cancer, you are talking about squamous cell cancer.
Now, this is a big complex topic and requires a fellowship to truly understand/ get good at.
Obviously, the purpose of this book is to prepare you for multiple choice test questions not
teach you practical radiology. If you want to actually learn about head and neck cancer in a
practical sense you can try and find a copy of Hamsberger's original legendary handbook
(which has been out of print for 20 years), but who has time for that? Now, for the trivia ....
Lvmnh Node Anatomv:
Posterior Border Testable Trivia:
Submandibular Jugular Fossa
Gland Anterior Belly of Digastric
separates 1 A from 1 B
Stylohyoid muscle
(posterior submandibular
gland) separates 1 B from
Lower Border 2A
of Hyoid
Jugular Vein (Spinal
Lower Border
of Cricoid Accessory Nerve) separates
2A from 2B *see below
Vertical borders:
2-3 = Lower Hyoid
3-4 = Lower Cricoid
2A: Anterior, Medial, Lateral or Abutting the Posterior Internal Jugular
28: Posterior to the Internal Jugular, with a clear fat plane between node and IJ
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Cancers
Floor of the Mouth sec:
I touched on this once already. Just remember smoker/drinker in an old person. HPV in a
young person. Necrotic level 2 nodes can be a presentation (not a branchial cleft cyst).
NasopharyngealSCC:
This is more common in Asians
and has a bi-modal distribution:
• group 1 (15-30)
typically Chinese
• group 2 (> 40).
Involvement of the
parapharyngeal space results in
worse prognosis (compared to Eossa Qf Rosenmuller (arrows)
nasal cavity or oropharynx
The FOR is the MOST COMMON location for
invasion).
Nasopharyngeal Cancer
.MindMaps:
'iiiiJ'
See a Unilateral
Mastoid Effusion
Look
OR at the
FOR
See a Pathologic
Retropharyngeal Node
"Earliest Sign" of nasopharyngeal SCC is
the effacement of the fat within the FOR.
Look at the Clivus
About 30% of the patients with nasopha1yngeal tumors
See a Pathologic have skull base erosion.
Retropharyngeal or (MRI > CT for skull base invasion)
Supraclavicular Node
Nodal mets are present in 90% of
nasophaiyngeal tumors, with the
retropharyngeal nodes usually the
first involved.
Normal Comparison Invasion (loss of Normal Tl
(Tl Bright Marrow Signal) Marrow Signal)
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Neck Anatomv Blitz
S11pn1glottic Region:
Arrow on the Tip of
the Epiglottis
Supraglottic Region:
Valleculae (grey
arrows),
Hypoepiglottic
Ligament (white
arrow), Epiglottis
(multiple tiny white
arrows)
Supraglottic Region:
Pre-Epiglottic Fat
(star), Aryepiglottic
folds (grey arrows),
piriform sinuses
(white arrows)
Supraglottic Region:
Para-Epiglottic
Spaces (open arrows),
Aryepiglottic folds The Para-Epiglottic communicates with the
(grey arrows), Pre-Epiglottic Space I Fat superiorly.
piriform sinuses
(white arrows) The Pre-Epig!ottic fat is rich in lymphatics,
makes tumor invasion of these regions
important for tumor staging.
Supraglottic Region: Level of the Glottic Region: Level of the True Sub- Glottic Region: Level
False Cords (white arrows), with Cords (white arrows), with the of the Cricoid Ring
para-glottic spaces (open arrows), cricoaiytenoid joint (black
and arytenoid cartilages (black arrows), and Anterior Commissure
arrows) (open arrow)
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Larvnx
Laryngocele:
When the laryngeal "saccule" dilates with air you call it a
laryngocele. If it is filled with fluid you still might call it a
larygocele (but if saccular cyst is a choice - consider that). If it
is filled with fluid and air you still might call it a larygocele
(but it la,yngopyocele is a choice -and you have any hint of
infection - consider that).
What thefuck is a "saccule" ? The "saccule" is the
appendix of the laryngeal ventricle (a blind ending sac that
extends anterior and upwards). It's usually closed or
minimally filled with fluid (you don't typically see it in
normal adults).
Why does it dilate ? Usually because it's obstructed (ball
valve mechanics at the neck of the saccule), and the testable
point is that 15% of the time that obstruction is a twnor.
You can also see them in forceful blowers (trumpet players,
glass blowers) -well maybe, this depends on what you
read. Simply read the mind of the question writer to know if
There are internal and external
they are on team trumpet player laryngocele.
version of this (based on
containment of violation of
the thyrohyoid membrane).
Vocal Cord Paralysis:
The involved side will have an expanded ventricle (it's the opposite side with a cancer). If you see
it on the left, a good "next step" question would be to look at the chest (for recurrent laryngeal nerve
involvement at the AP window).
s::{) Buzzword= "Hoarseness" - If you see "Hoarseness" in the question header, you need to
� r') think recurrent laryngeal nerve compression in the AP Window - either from a mass/node
/ or aortic path. *Hoarseness is also a classic Laryngeal CA buzzword (so look there too).
Vocal Cord Paralysis - lpsilateral Expanded Ventricle AP Window PET Avid Node
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Larvnueal cancer
( Nearly Always~ 85% Squamous Cell)
Risk Factors: Smoking, Alcohol, Radiation, Laryngeal Keratosis, HPV, GERD, & Blasphemy against the
correct religion (false religions are safe to talk shit about).
The role of the Radiologist is not to make the primary cancer diagnosis here, but to assist in staging.
Laiyngeal cancers are subdivided into (a) supraglottic, (b) glottic, and (c) subglottic types.
"Transglottic" would refer to an aggressive cancer that crosses the laryngeal ventricle.
Epiglottic mass
Supra-Glottic:
Epiglottic Centered spreading anterior
Supra-Glottic across the hypo
-Anterior epiglottic ligament
-More Aggressive -Likes to Invade the Pre- into the preepiglottic
-Early Lymph Epigolttic Space /Fat (which space and into the
Node Mets
is rich in lymphatics paired vallecula.
-They don't get
hoarseness False Cord mass
Supra-Glottic: spreading into the
False Cord / Fold para-glottic space
You always need to.find Centered Paraglottic space
(guess at) the inferior margin
ofa supraglottic mass. involvement makes the
-Posterior Lateral tumor TJ and
Partial lmyngectomy usually -Likes to Invade the Para- "transglottic. "
can only be done ifthe tumor Glottic Space /Fat (which *Best seen in coronals.
is restricted to the communicates superiorly
supraglottis and does not with the Pre-Epiglottic
involve the arytenoids or Aryepiglottic fold
Space mass spreading into
/a,yngeal ventricle.
the paraglottic space
& piriform sinus
Usually involve the Glottic mass spreading
Glottic anterior cord and
forward towards the
spread into the
anterior commissure anterior commissure
-Most Common
(typically defined as Fixation of the cords
-Best Outcome soft tissue thickening indicates at least a T3
-Grow Slowly of> 2mm) tumor - this is best
-Metastatic Disease assessed with a scope
Classic Clinical History: but can be suspected
is Late "Progressive and with disease in the
Continuous Hoarseness. "
cricoarytenoid joint.
Sub-Glottic The only reliable sign of
-Least Common The typical look is cricoid invasion is
soft tissue thickening tumor on both sides of
-Often small between the airway
compared to nodal the cartilage (irregular
and the cricoid ring. sclerotic cartilage can
burden be normal).
-Bilateral nodal
disease & Invasion of the cricoid cartilage is a contraindication to all types of laryngeal
mediastinal conservation surgery (cricoid cartilage is necessary.for postoperative stab;!ity
extension of the vocal cords).
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SECTION 17:
ORBIT �
• '
--- - _
Tumors and Tumor like Conditions:
Retinoblastoma - This is the most common primary malignancy of the globe. If you see
calcification in the globe of a child - this is the answer.
The step I question is RB suppressor gene (chromosome 13 - "unlucky 13"). That's the same
chromosome osteosarcoma patients have issues with and why these guys are at increased risk of
facial osteosarcoma after radiation.
The globe should be normal in size (or bigger), where Coats' is usually smaller. It's usually seen
before age 3 (rare after age 6). The trivia is gonna be where else it occurs. They can be bilateral
(both eyes - 30%), trilateral (both eyes and the pineal gland), and quadrilateral (both eyes,
pineal, and suprasellar).
Coats' Disease - The cause of this is retinal telangiectasia which results
CT-Dense
in leaky blood and subretinal exudate. It can lead to retinal detachment. It's T l -Hyper
seen in young boys and typically unilateral. The key detail is that it is NOT T2 - Hyper
CALCIFIED (retinoblastoma is).
Coats disease has a smaller globe. Retinoblastoma has a normal sized globe.
Persistent Hyperplastic Primary Vitreous (PHPV) -
This is a failure of the embryonic ocular blood supply to regress. It can lead to retinal
detachment. The classic look is a small eye (microphthalmia) with increased density of
the vitreous. No calcification.
Retinal Detachment - This can occur
secondary to PHPV or Coats. It can also be
caused by trauma, sickle cell, or just old age.
The imaging finding is a "V" or "Y" shaped
appearance due to lifted up retinal leaves and
subretinal fluid.
Retinal Detachment in the setting of PHPV
Globe Size Comparison
- A Strategy for Eliminating Distractors
• Retinoblastoma - Normal Size • PHPV - Small Size (Normal Birth Age)
• Toxocariasis - Normal Size • Retinopathy of Prematurity - Bilateral Small
• Coats' - Smaller Size
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Melanoma - This is the most common intra-occular lesion in an adult. If you see an
enhancing soft tissue mass in the back of an adult's eye this is the answer.
Here are 4 ways you could ask a question about this:
(1) show a picture - what is it?,
(2) ask what the most common intra-occular lesion in an adult is?
(3) ask the buzzword "collar button shaped" ? - which is related to
Bruch's membrane,
(4) strong predilection for liver mets - next step Liver MR.
Optic Nerve Glioma: These almost always (90%)
occur under the age of 20. You see expansion/ enlargement
of the entire nerve. If they are bilateral you think about
NF-1. They are most often WHO grade 1 Pilocytic
Astrocytomas. If they are sporadic they can be GBMs and
absolutely destroy you.
Optic Nerve Sheath Meningioma: The buzzword
is "tram-track" calcffications. Another buzzword is
"doughnut" appearance, with circumferential enhancement
around the optic nerve. "Tram-Track"= Meningioma
Dermoid: This is the most common benign
congenital orbital mass.
It's usually superior and lateral, arising from the
frontozygomatic suture, and presenting in the first
10 years of life. It's gonna have fat in it (like any
good dermoid). The location is classic.
Orbital Dermoid - Classic Location
Rhabdomyosarcoma - Most common extra-occular orbital malignancy in children
(dermoid is most common benign orbital mass in child). Favors the superior-medial orbit and
classically has bone destruction. Just think "bulky orbital mass in a 7 year old."
When they do occur - 40% of the time it's in the head and neck - and then most commonly it's in
the orbit. It's still rare as hell.
Lymphoma - There is an association with Chlamydia Psittaci (the bird fever thing) and
MALT lymphoma of the orbit. It usually involves the upper outer orbit - closely associated with
the lacrimal gland. It will enhance homogeneously and restricts diffusion - just like in the brain.
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Metastatic Neuroblastoma - This has a very classic appearance of "Raccoon Eyes" on
physical exam.
The classic location is periorbital tumor infiltration
with associated proptosis. Don't forget a basilar skull
fracture cun uhlo cuuse Raccoon Eyes... so clinical
correlation is advised. Ncuroblastoma mets tend to be
more
Another thing worth mentioning is the bony
involvement of the greater wing of the sphenoid.
Ncuroblastoma is gonna be bilateral. Ewings favors
this location also - but will be unilateral.
Metastatic Scirrhous (fibrosing)
Breast Cancer -
This is classic gamesmanship here. The important point to
know is that unlike primary orbital tumors that are going to
cause proptosis, classically the breast cancer met causes a
desmoplastic reaction and enophthalmos (posterior
displacement of the globe).
Trivia: Mets are actually more common to the eye Infiltrative retrobulbar mass +
relative to the orbit (like Bx more common). enophthalmos = scirrhous carcinoma
of the breast
lgG4-0rbit
Orbital Pseudotumor: Tolosa Hunt Syndrome: Lymphocytic
Hypophysitis:
This is one of those IgG4 This is histologically the same
idiopathic inflammatory thing as orbital pseudotumor This is the same deal as
conditions that involves the but instead involves the orbital pseudotumor and
cxtraoccular muscles. It looks like cavernous sinus. Tolosa Hunt, except it's the
an expanded muscle. The things pituita1y gland. Just think
to remember are that this thing is It is painful Gust like enlarged pituitary stalk in a
painful, unilateral, it most pseudotumor), and presents postpartum / 3rd trimester
commonly involves the lateral with multiple cranial nerve woman. It looks like a
rectus and it does NOT spare palsies. It responds to steroids pituitary adenoma, but it
the myotendinous insertions. Gust like pseudotumor). classically has a T2 dark rim.
Remember that Graves docs not
cause pain, and does spare the
myotendinous insertions. It gets
better with steroids. It's
classically T2 dark.
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Thyroid Orbitopathy: This is seen in
I/4th of the Graves cases and is the most
common cause of exophthalmos. The
antibodies that activate TSH receptors also
activate orbital fibroblasts and adipocytes.
Things to know:
• Risk of compressive optic
neuropathy
• Enlargement of ONLY MUSCLE
BELLY (spares tendon) - different
than pseudo tumor
• NOT Painful - different than pseudo Thyroid Orbit - Spares Tendon Insertion
tumor
• Order oflnvolvement:
IR> MR> SR> LR> SO/IO
Inferior, Middle, Superior, Lateral, Oblique
Orbital Vascular Malformations
Lymphangioma Varix Carotid-Cavernous Fistula
These are actually a mix of These occur These come in two flavors:
venous and lymphatic secondary to (1) Direct - which is secondary to
malformations. They are ill weakness in the trauma, and (2) Indirect - which just
defined and lack a capsule. The post-capillary occurs randomly in post menopausal
usual distribution is infiltrative venous wall (gives women.
(multi-spatial), involving, pre you massive The direct kind is a communication
septal, post-septal, extraconal, dilation of the between the intracavemous ICA and
and intraconal locations. valveless orbital cavemous sinus. The indirect kind is
Fluid-Fluid levels are the most veins). usually a dural shunt between meningeal
classic finding , with regard to branches of the ECA and the Cavernous
multiple choice. Most likely question Sinus.
is going to pertain
Do NOT distend with to the fact that they Buzzword: Pulsatile Exophthalmos
provocative maneuvers distend with *although this can also be a buzzword
(valsalva). provocative for NF-I in the setting of sphenoid wing
maneuvers dysplasia.
(valsalva, hanging
head, etc... ). Prominent left
superior ophthalmic
Another piece of vein with proptosis
trivia is that they are
the most common
cause of
spontaneous orbital
hemorrhage. They
can thrombose and
present with pain.
Prominent left
Fluid-Fluid Levels
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Orbital lntection
Orbital Anatomv Review Lacrimal Sac
Intraconal
Space - is the
Fossa space inside the
rectus muscle
pyramid.
Extraconal
Space - is the
space outside
the rcctus
muscle pyramid.
Differentiation between Orbital (post-septal) and
Periorbital (pre-septal) cellulitis is based on the
relationship to the orbital septum (arrows). Extraconal Space
Pre-Septal/ Post-Septal Cellulitis -
As above, location of orbital infections arc described by their relationship to the orbital septum. The
testable trivia is probably (1) that the orbital septum originates from the periosteum of the orbit and
inserts in the palpebral tissue along the tarsal plate, (2) that pre-septal infections usually start in
adjacent structures (likely teeth and the face) , (3) post-septal infections are usually from paranasal
sinusitis, and (4) pre-septal infections are treated medically, post septal is surgical.
Trivia: Periorbital abscess can cause thrombosis of the ophthalmic veins or cavernous sinus (in
extreme examples infection - usually aspergillosis - can even cause a cavernous-carotid fistula).
Dacryocystitis
This is inflammation and dilation of the
lacrimal sac. It has an Aunt Minnie
look, with a well circumscribed, round
rim enhancing lesion centered in the
lacrimal fossa. The etiology is typically
obstruction followed by bacterial
infection (staph and strep).
Usually this is diagnosed clinically unless there is an associated peri-orbital cellulitis in which can
CT is needed to exclude post septal infection (treated surgically) from simple dacryocystitis
(treated non-surgically).
Orbital Subperiosteal Abscess:
If you get inflammation under the periosteum
it can progress to abscess formation.
This is usually associated with ethmoid
sinusitis. This also has a very classic look.
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Misc Orbital Conditions
Optic Neuritis:
There will be enhancement of the optic
nerve, without enlargement of the nerve/
sheath complex. Usually (70%) unilateral,
and painful.
You will often see intracranial or spinal cord
demyelination - in the setting of Devics
(neuromyelitis optica). 50% of patient's with
acute optic neuritis will develop MS.
c,az..4lfthe optic nerve is enlarged, think glioma... then think NF-1.
Papilledema:
This is really an eye exam thing.
Having said that you can sometimes see dilation/ swelling of the optic nerve sheath.
lntraocular Lens
Ectopia Lentis (lens
Drusen - Mineralization at the Implant�
optic disc. Supposedly there is an dislocation) - Causes include
The standard treatment for
association with age-related Trauma, Marfans, and
cataracts. A replaced lens has
maculopathy Homocystinuria.
a thin linear appearance.
Coloboma:
This is a focal discontinuity of the globe
(failure of the choroid fissure to close).
They are usually posterior. If you see a
unilateral one - think sporadic.
If you see bilateral ones - think CHARGE
(coloboma, heart, GU, ears). Bilateral Coloboma - CHARGE Syndrome
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, -·;
'.\
,, .
', , �
SECTION 18:
SPINE
�
• ,
Anatomv Trivia
Cord Blood Supply: There is an anterior blood supply and a posterior blood supply to the cord.
These guys get taken out with different clinical syndromes.
Anterior spinal artery - arises bilaterally as two small branches at the level of the termination of
the vertebral arteries. These two arteries join around the level of the foramen magnum.
Artery ofAdamkiewicz - This is the most notable Anterior
reinforcer of the anterior spinal artery. In 75%
of people it comes off the left side of the aorta
between T8 and Tll. It supplies the lower 2/3
of the cord. This thing can get covered with the
placement of an endovascular stent graft for
aneurysm or dissection repair leading to spine
infarct.
Posterior Spinal Artery - Paired arteries which
arise either from the vertebral arteries or the
posterior inferior cerebellar artery. Unlike the
anterior spinal artery this one is somewhat
discontinuous and reinforced by multiple
segmental or radiculopial branches.
Conus Medullaris: This is the terminal end of the spinal cord. It usually terminates at around Ll.
Below the inferior endplate of the L2 / L3 body should make you think tethered cord (especially if
shown in a multiple choice setting).
Epidural Fat: The epidural fat is not evenly distributed. The epidural space in the cervical cord is
predominantly :filled with venous plexus (as opposed to fat). In the lumbar spine there is fat both
anterior and posterior to the cord. "Epidural Lipomatosis" = is a hypertrophy of this fat that only
occurs with patients on steroids ("on corticosteroids" would be a huge clue).
Stenosis: Spinal stenosis can be congenital (associated with short
.......
A B
pedicles) or be acquired. The Torg-Pavlov ratio can be used to call it
(cervical canal diameter to vertebral body width< 0.85).
Symptomatic stenosis is more common in the cervical spine (versus
the thoracic spine or lumbar spine). You can get some congenital
stenosis in the lumbar spine from short pedicles, but it's generally not
symptomatic until middle age. Sagittal View
BIA<0.85
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Degenerative Changes
What is this degenerative change you speak of? The best wa y to understand this is through
two mechanisms; Spondylosis Deformans and Intervertebral Osteochondrosis.
Spondylosis Deformans lntervertebral Osteochondrosis
This is
probably part Pathologic (but
of"normal not necessarily
aging" symptomatic)
"Degenerative Change" or spine
"Deteriorated Disc" - This process is more
osteoartlu·itis. This is more rim/ margin
centered in the disc space favoring the nucleus
centered. Process is characterized by
pulposus & vertebral body endplates.
osteophyte formation.
THIS vs THAT: Osteophytes vs Syndesmophytes
Osteophytes: Syndesmophytes:
• More horizontal/ • More vertical
oblique with a symmetric, and
"claw" like thinner
appearance. • Represent
• Formed also the ossification of the
vertebral margin. annulus fibrosis.
• Seen in "DJD"/ • Seen in Ankylosing
Spondylosis Spondylitis.
Endplate Changes: Conunonly referred to as "Modic Changes."
There is a progression in the MRI signal characteristics
that makes sense if you think about it. You start out with Type I Tl Dark,
degenerative changes causing irritation / inflammation "Edema" T2 Bright
so there is edema (T2 bright). This progresses to chronic
inflammation which leads to some fatt y change - just Tl Bright,
Type 2 "Fat"
like in the bowel of an IBD patient - causing Tl bright T2 Bright
signal. Finall y, the whole thing gets burned out and Type 3
fibrotic and it's Tl and T2 dark. As a prominent factoid, TI Dark, T2 Dark
"Scar"
Type I changes look a lot like Osteom yelitis ( clinical
correlation is recommended).
Type 1 Type2 Type3
T2 Tl
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Annular Fissure:
As the disc ages, it tends to dry out making it more friable and easily torn. "Tears" in the annulus
(which are present in pretty much every degenerated disc) aren't called "tears" but instead "fissures".
People who write the papers on this stuff make a big fucking deal about that - with the idea being that
"tear" implies pathology'. Fissuring can be asymptomatic and part of the aging process.
Even though fissures are present
in basically every degenerated
disc you don't always see them
on MRJ. What you do see (some
of the time) is a fluid signal gap
in the annulus - which has been
given the official vocabulary
word "High Intensity
Zone," and anything with
official vocabulary nomenclature
should be respected as possible
multiple choice fodder. "High Intensity Zone" -MR with Fluid Signal in the Annulus
•Annular fissures may be a source of pain
(radial pain fibers - trigger "discogenic pain") but are also seen as incidentals.
•Fissures are found in all degenerative discs but are not all fissures are visualized as HIZs.
•Discography is more sensitive to fissures relative to MRJ, but still not 100% sensitive.
•Also, Dude, "Tear" is not the preferred nomenclature - "Fissure."
Schmorl Node: Scheuermann's Limbus
Intravertehral Herniation Vertebra
This is multiple levels
This is a herniation of disc material (at least 3) of wedged vertebral
through a defect in the vertebral bodies with associated This is a fracture
body endplate into the actual Schmorl's nodes - mimic that is the
marrow.
result of herniated
Common - like 75% of people have disc material
them. between the non
Classic look is to favor the inferior fused apophysis and
endplate of the lower thoracic / adjacent vertebral
upper lumbar spine. When they are body.
acute they can have edema on T2
and be dark on T l - mimicking
osteomyelitis. Chronic versions will
have a sclerotic rim.
Most classically the thoracic
spine of a teenager, resulting in
kyphotic deformity (40 degrees
in thoracic or 30 degrees in
thoracolumbar).
25% of patients have scoliosis.
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Disc Nomenclature:
In order to "improve accuracy" in the description of lumbar spine disc disease, a handful of
elites gathered at an unknown location, ate caviar, drank wine, and then made a sacrifice to
Moloch the Owl God - after which they issued a proclamation on what vocabulary words you
are and are not allowed to use when describing degenerative disc herniation.
Herniation: Bulge:
This is the approved
This is the approved verbiage for the verbiage for the
displacement of LESS THAN 25% of displacement of MORE
disc material beyond the limits of the THAN 25% of disc
disc.space. material beyond the limits
of the disc space.
Protrusion (subtype Sequestration Asymmetric Bulge
of herniation) Free (broken off)
disc fragment.
Term used when the Term used when Symmetric Bulge
distance between the the edges of the
edge of the disc disc are greater
herniation is less than than the distance of
the distance between the base
the edges of the base (neck narrower
(base wider than than herniation).
herniation).
}- Disc Level
}- Suprapedicle Level
Localization
Cranial }Pedicle Level
r----=-1-----1
Caudal Plane } Infrapedicle Level
-11111''--------l
Extra Foraminal
""
Foraminal •••••
Localization *Often symptomatic
Axial Plane because of the relationship
to the Dorsal Root Ganglia
*Most Common Location Central
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Which Nerve is Compressed?
There are 31 pairs of spinal nerves, with each pair corresponding to the adjacent
vertebra - the notable exception being the "C8" nerve. Cervical disc herniations are
less common than lumbar ones.
The question is most likely to take place in the lumbar spine (the same spot most disc
herniations occur). In fact more than 90% of herniations occur at L4-L5, and L5-Sl.
A tale of two herniations. It was the best of times, it was the worst oftimes ...
Scenario 1:
Scenario 2:
A Central or Sub
Articular Disc Will
Smash the
Descending Nerve.
In this case the S1
Nerve
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lP / Mvelouram Technique�------------�
Prior to the LP
• Increased intracranial pressure or obstructed CSF flow
Absolute Contraindications:
(ACR-ASNR recommendations)
• Bleeding diathesis (11'Allicoagulability) - STOP Coumadin 4-5 days
• Myelogram Specffic - Iodinated contrast allergy - STOP Plavix for 7 days
- Hold LMW Heparin for 12 hours
Relative Contraindications (vary per institution): - Hold Heparin for 2-4 hours -
• Overlying infection, hematoma, or scarring document normal PTT
• Myelogram Specffic - Recent myelogram (< I week) - Aspirin and NSAIDs are fine (not
• Myelogram Specific � Histo1y ofseizures contraindicated)
• Advanced degenerative spondylosis,
Legit Indications for Fluoro Guided LP:
• Post-surgical changes,
• Patient is so fat ("a person ofsize"), when Dracula sucked his/her blood, he got diabetes.
• Myelogram Specffic - MRI contraindication
• Myelogram Specific - Geriatric Professor Emeritus ofNeurosurgery wants it, and it is better than
doing the pneumoencephalogram he originally ordered.
• "The patient is crazy"
NOT Legit Indications for Fluoro Guided LP - all of which I've heard:
• "The patient is crazy & violent"
• "The patient is crazy, violent, and has high viral load HIV .... and Hep C"
• "The patient recently escaped a locked mental institution for the extremely violent and criminally
insane, has both HIV and Hep C. He spits like a camel and has really terrible body odor."
L2-L3 or L3-L4 are common
The needle will
Technical Overview
entry points. A potential trick Target the
would be to show you imaging interlaminar naturally steer toward
with a low lying conus (usually space, just off the sharper side and
that thing stops at L l -L2). ofmidline. �I away from the bevel.
So, ifyou are directing
Remember you need to be Always the needle, you'll want
I
below the conus - so you might aspirate the bevel side opposite
I
I
need to adjust down, before you
I
the direction you are
I
I
depending on how low it is. inject attempting to steer.
I
I
anything.
I
'
\
Myelogram Specific - Contrast should flow freely away from the needle tip, gradually filling the thecal
sac. The outlining ofthe cauda equina is another promising sign that you did it right. Ifcontrast pools at
the needle tip or along the posterior or lateral thecal sac without free-flow, a subdural injection or
injection in the fat around the thecal sac should be suspected.
Technical Strategies to Reduce the Incidence of Post Dural Puncture Headache (PDPH):
• Use a small needle (25 G), especially for epidural pain injections or myelography. You might have
to use a 22G for a diagnostic LP or you are going to struggle to get enough fluid for a sample, and
your opening pressures may not be accurate.
• Non-cutting "atraumatic" needle (diamond shaped tip) reduce incidence ofPDPH
• Replace the stylet before you withdraw the needle. This isn't just for the 1 in a million chance that
you suck a nerve root up in the needle. This has also been shown to reduce incidence ofPDPH
• Direction ofthe bevel: This actually matters
You want to run the Perpendicular is wrong. You are
bevel parallel with the going to cut those fibers. Coming in
fibers to push them ___I _11• - -• - at a crazy sideways angle is also not
__ ,
apart...not cut them. 11 ideal (same reason).
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Blood Patch
Even a miniscule defect within the thecal sac post LP • Most PDPHs start 24 hours after the
can allow leakage of spinal fluid resulting in puncture (between 24-48 homs) - larger
intracranial hypotension and the dreaded chronic/ leaks can present earlier.
debilitating p_ost dural pu_ ncture..headache. • Most people will wait 72 hours after the
headache begins ("conservative
Classic PDPHs are bilateral, better laying down, and therapy") prior to attempting the patch.
worse sitting up. They are also worse with coughing, • Most people will try at least twice before
sneezing, or straining to push out a large turd (from calling nemosurgery to sew to hole you
chronic opioid abuse). carved out of the dura (you fucking
psycho)
The procedure involves injecting between 3-20cc of the • Severe atypical symptoms should
patients own blood into the epidural space near the prompt a CT (to exclude a subdural from
original puncture site with the hope of sealing the hole. severe hypotension).
"Failed Back Surgery Syndrome" (FBSS)
Another entity invented by NEJM to take down the surgical subspecialties. Per the NEJM these
greedy surgeons generally go from a non-indicated spine surge1y, to a non-indicated leg amputation,
to a non-indicated tonsillectomy on an innocent child.
Text books will define it as recurrent or residual low back pain in the patient after disk surgery. This
occurs about 40% of the time (probably more), since most back surgery is not indicated and done on
inappropriate candidates. Causes ofFBSS are grouped into early and late for the purpose of multiple
choice test question writing:
Complications of Spine Surgery
Recurrent Residual Disk Will lack enhancement (unlike a scar- which will enhance on delays)
EpiduralFibrosis
- --•--•-· - -·--· -·· -·--···
Scar, that is usually posterior, and enhances homogeneously
. ·• •-' •-···--·-···· ·· · ~ ··-- ... ·······--····--·······----- ... ·· ·--··----- -··········· ···••-'• -'-••-·
Buzzwords are "clumped nerve roots" and "empty thecal sac",
Arachnoiditis Enhancement for 6 weeks post op is considered normal. After 6 weeks
may be infectious or inflammatory.
12,000 SquareFoot As spine surgeons perform more and more unnecessaiy surgeries they
Mansion Syndrome need something to spend all that money on.
� THIS vs THAT: Scar vs Residual Disc:
T l Pre Contrast they will look the same ... like a bunch of mushy crap.
T l Post Contrast the disc will still look like mushy crap, but the scar will enhance.
Conjoined Nerve Roots:
Two adjacent nerve roots sharing an enlarged common sleeve - at a point during their exit from the
thecal sac. This can be a source ofFBSS if it is the source of pain instead of a disc. Alternatively it
could be misidentified as a disc preoperatively. In both cases, the Radiologist will be cast in the roll
of "Scapegoat" during the malpractice suit.
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,.
.. .....
. . .\
� .'
SECTION 19:
SEATBELTS ARE FOR PUSSIES
� •.. ,,
' -.:
Odontoid Fracture Jefferson Fracture:
Classification: This is an axial loading injury (jumping into a
1--------------------4
Type 3
shallow pool) - with the blow typically to the
Type2 top of the head.
Type 1 (best
(most
(rare) prognosis for The anterior and
common)
healing) posterior arches blow
out laterally.
• About 30% will also have a C2 Fracture
• Neurologic (cord) damage is rare, because
all the force is directed into the bones.
Could be shown on a plain
Fracture at film open mouth odontoid
upper part of view.
Odontoid Fracture at Fracture Remember the C 1 lateral
(related to the base through dens masses shouldn't slide off Normal Comparison
avulsion of the (high non into the body laterally.
alar ligament) union rate) ofC2.
May be Increased distance
Unstable Unstable between the lateral
Stable
masses of CJ and
odontoid peg
Os Odontoideum / Os Terminale:
These variants can mimic a type 1 Odontoid fracture. In both cases, you have an ossicle located at the
position of the odontoid tip (the orthotopic position). The primary difference is that with an
Os Odontoideum the base of the dens is usually hypoplastic.
• Prone to subluxation and instability.
• Associated with Morquio's syndrome.
• Orthotopic is the position on top of the dens.
• Dystopic is when it's fused to the clivus.
Normal Os Terminale oS <idontoideum
(hypoplastic dens)
Hangman's Fracture:
Seen most commonly when the chin hits the dashboard in an MVA
("direct blow to the face"). The fracture is through the bilateral pars at
C2 (or the pedicles -which is less likely). You will have anterior
subluxation of C2 on C3 (> 2mm). Cord damage is actually uncommon
with these, as the acquired pars defect allows for canal widening. There is
often an associated fracture of the anterior inferior corner at C2 -from
avulsion of the anterior longitudinal ligament. Traction is
contraindicated.
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Flexion Teardrop: Extension Teardrop:
This represents a teardrop shaped fracture Another anterior inferior teardrop
fragment at the anterior-inferior vertebral body. shaped fragment with avulsion of the
Flexion injury is bad because it is associated anterior longitudinal ligament. This is
with anterior cord syndrome (85% of patients less serious than the flexion type.
have deficits). This is an unstable fracture,
associated with posterior subluxation of the
vertebral body.
1
t
Flexion Teardrop Extension Teardrop
._
Impaction Injmy
·---·� •-··-.,·-. - ·-··------··--·-·---·�"---'"····-------···--·--·-·--·· ..
-. -•.--·•
Distraction Injury
Extremely Unstable Stable in flexion (unstable in extension)
-- -- --
Hyperflexion
--------- ------------ -------------- ------- --------- --------
- ----- - -- ---- -------------------------·r-- -
- - ---
Hyperextension
Classic History: "Ran into wall" Classic History "Hit from behind"
Clay-Shoveler's Fracture: This is an avulsion injury of a
lower cervical/ upper thoracic spinous process (usually C7). It is
the result of a forceful hyperflexion movement (like shoveling).
The "ghost sign" describes a double spinous process at C6-C7 on
AP radiograph.
Chance Fracture:
These are flexion-distraction fractures that are
classically associated with a lap-band seatbelt.
There are 3 column (unstable) fractures.
Most commonly seen at the upper lumbar levels &
thoracolumbar junction.
High association with solid organ trauma.
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Facet Dislocation: This is a spectrum: Subluxed facets -> Perched -> Locked.
Unilateral: If you have unilateral locked facet (usually from hyperflexion and rotation) the
superior facet slides over the inferior facet and gets locked. The unilateral is a stable injury.
You will have the inverted hamburger sign on axial imaging on the dislocated side.
Bilateral: This is the result of severe hyperflexion.
You are going to have disruption of the posterior
ligament complex. When this is full on, you are
going to have the dislocated vertebra displaced
forward one -half the AP diameter of the vertebral
body. This is highly unstable, and strongly
associated with cord injury.
Atlantoaxial Instability:
The articulation between Cl and C2 allows for lateral movement (shaking your head no). The
transverse cruciform ligament straps the dens to the anterior arch of C1. The distance between
the anterior arch and dens shouldn't be more than 5 mm. The thing to know is the association
with Down syndrome and juvenile RA.
Rotary subluxation can occur in children without a
fracture, with the kid stuck in a "cock-robin"
position - which looks like torticollis. Actually
differentiating from torticollis is difficult and may
require dynamic maneuvers on the scanner.
This never, ever, ever happens in the absence of a
fracture in an adult (who doesn't have Downs or
RA). Having said that, people over call this all the
time in adults who have their heads turned in the
scanner.
Pars lnterarticularis Defect (Spondylolysis or Adult lsthmic
Spondylolisthesis) : This is also discussed in the Peds chapter (vol 1, page 137).
I'll make a few comments for the adult version. Defects in the pars interarticuaris are
usually caused by repetitive micro-trauma (related to hyper-extension). It is nearly
always at L5-S1 (90%). Pain is typically a L5 radiculopathy caused by foraminal
stenosis at L5-S1. The term "pseudo-disc" is sometimes used to describe the
deformed annular fibers seen in the setting of a related anterolithesis (forward
slippage).
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lnstabililV
You will read different definitions of "instability" as it relates to spinal trauma. The one I prefer
is something along the lines of "lost capacity to withstand even a normal physiologic load
without: potential damage to the spinal cord, nerve roots, or developing an incapacitating
deformity thatforces one to seek employment in a cathedral bell tower."
For lhe purpose of multiple choice you will see the words "stable" or "unstable·· associated with
specific fracture types. There are also some radiologic "definitions" of instability which seem to
vary depending on who you ask. In general, if you have acute segmental kyphosis greater than 11
degrees, acute anterolisthesis greater than 3-4 mm, or gross motion on flexion / extension imaging
it is probably an unstable fracture. You will also hear people talk about a "power ratio" for
occipitocervical instability, and a spinal column theory for the thoracolumbar injury.
Occipitocervical Instability Denis 3 Spinal Column Concept
This can be traumatic (in which case Most often you will see this idea applied to
the patient rarely lives because they rip thoracolumbar spinal fractures, although
their brainstem in half), or congenital technically it has some validity in the lower
(classically seen with Down cervical segments as well.
Syndrome). Two popular methods for The idea is to divide the vertebral column into 3
evaluating this: vertical parallel columns , with instability
suggested when all 3 or 2 contiguous columns
Powers Ratio (anterior and middle column or middle and
= C-D:A-B posterior column) are disrnpted.
Ratio is greater
than 1.0 =
Ligamentous Anterior:
Instability • Anterior
Longitudinal
Ligament
• Anterior 2/3
Vertebral Body
Harris Lines
Rule of 12 Middle:
• Posterior
Both the Longitudinal
Basion-Dens Ligament
(A) and • Posterior 1 /3
Basion Vertebral Body
Posterior Axial Posterior:
Distance (B) • Posterior
should be less
than 12 mm. p Ligaments
• Pedicles, Facets,
Lamina, Spinous
Process
The management does typically change with unstable fractures typically stabilized (either internal
fusion or external bracing/reduction).
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When Does a "Trauma" Indicate Imaging ii
Canadian C-Spine Rule: Nexus Criteria:
• Age �65 years • Focal neurologic deficit
• Paresthesias in extremities • Midline spinal tenderness
• Dangerous mechanism: • Altered level of consciousness
• Fall �3 ft or 5 stairs • Intoxication (you can't clear a dnmk
• Axial load to the head (empty guys/girls c-spine while they are
swimming pool diving, piano fell on drunk).
head - while chasing a road runner) • Distracting injury
• High Speed MVA,
• Pedestrian vs Car
• Hulk Smash
THIS vs THAT: Stability
Unstable Stable
Vertebral Overriding> 3mm ("Subluxation")
Angulation > 11 Degrees
Flexion Tear Drop Extension Tear Drop (At least in Flexion)
Bilateral Facet Dislocation "Double-Locked" Unilateral Facet Dislocation
Odontoid Fracture Type 2 and 3 Odontoid Fracture Type l
(most sources will say Type 2 & 3 or deploy the word (usually stable -flex/extension films still usually done
"usually", but for sure if there is lateral displacement) to exclude atlantooccipital instability)
Two Contiguous Thoracolumbar Columns
(anterior & middle or middle & posterior)
Isolated Single Thoracolumbar Column Fracture
Three Thoracolumbar Columns
(Chance Fracture, Etc ... )
Jefferson Fracture Clay Shoveler's Fracture
Hangman Fracture Transverse Process Fracture
Atlanto-Occipital and Atlanto-Axial Dislocations
Named Spine Fractures
Jefferson Burst Fracture of C l Axial Loading
Hangman Bilateral Pedicle or Pars Fracture of C2
�.----�----.----•
Hyperextension
---- - ------+ ➔➔---- ·-·------···-----··---------··-···---------··-··--·----
. .. __ ________ _ _ ______ . ___ ______________.._......... _.__ ____" •" •------·----·--·-------·-· ·-·----.-----·-· ---�----'--••··
Teardrop Can be flexion or extension
_.._, ,. , _, ,.
Flexion (more common)
Clay-Shoveler's Avulsion of spinous process at C7 or T l Hyperflexion
Chance Horizontal Fracture through thoracolumbar spine "Seatbelt"
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Trauma to the Cord:
There is a known correlation between spinal cord edema length and outcome. Having said
that, you need to know the most important factor for outcome is the presence of a
hemorrhagic spinal cord injury (these do very very badly).
Spinal Cord Syndromes
Upper Extremity
Old lady with
Deficit is worse than
spondylosis or young
Central Cord lower ( corticospinal
person with bad
tracts are lateral in
extension injury.
lower extremity)
Anterior Cord Flexion Injury Immediate Paralysis
Rotation injury or One side motor, other
Brown Sequard
penetrating trauma side sensory deficits
Uncommon - but
Posterior Cord sometimes seen with Proprioception gone
hyperextension
Anterior Cord Syndrome (The Really Bad One):
The anterior portion of the cord is jacked. Motor function and anterior column sensations (pain and
temperature) are history. The dorsal column sensations (proprioception and vibration) are still intact.
This is the reason FLEXION injuries arc so bad.
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SECTION 20:
VASCULAR
� Yi
AVFs / AVMs:
There are4 types. Type l is by far the most common (85%). It is a Dural AVF; the result
of a fistula between the dorsal radiculomedullary arteries and radiculomedullary vein /
coronal sinus - with the dural nerve sleeve. It is acquired and seen in older patients who
present with progressive radiculomyelopathy. The most common location is the thoracic
spine. If anyone asks, the "gold standard for diagnosis is angiography" , although CTA or
MRA will get the job done. You will have T2 high signal in the central cord (which will be
swollen), with serpentine perimedullary flow voids (which are usually dorsal).
Spinal AVM / AVFs
Type 1 Most Common Type (85%). Dural AVF-with a single coiled vessel
Intramedullary Nidus from anterior spinal artery or posterior spinal artery. Can
Type 2 have aneurysms, and can bleed. Most common presentation is SAH. Associated
with HHT and KTS (other vascular syndromes).
·-· -- ·- --- ··• •.,---·---•--·· . --•-··· .
Type 3 Juvenile, very rare, often complex and with a terrible prognosis
Intradural perimedullary with subtypes depending on single vs multiple arterial
Type4
supply. These tend to occur near the conus.
Foix Alajouanine Syndrome:
This is a congestive myelopathy associated with a Dural AVF. The classic history
is a45 year old male with lower extremity weakness and sensory deficits.
You have increased T2 signal (either at the conus or lower thoracic spine), with
associated prominent vessels (flow voids). The underlying pathophysiology is
venous hypertension - secondary to the vascular malformation.
\.·. .,;.
41111111111111111len Key Finding Swollen High Signal
Blob Like Cord with Serpentine
The vascular malformation flow voids are CSF flow voids along the
- punctate, serpiginous, and serpentine. Pulsation surface of cord
Artffacts
They are NOT blob like
- sorta like what you see with CSF pulsation signal loss.
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••
• '\
, ·,·,
.
', ,
� SECTION 21:
CORD PATHOLOGY
�
• '
,
Syrinx -Also known as "a hole in the cord". People use the word "syrinx" for all those fancy
French/ Latin words (hydromyelia, syringomyelia, hydrosyringomyelia, syringohydromyelia,
syringobulbia etc ... ). They usually do this because they
don't know what those words mean.
This is the simple version:
• Hydromyelia = Lined by ependyma.
• Syringomyelia = NOT lined by ependyma
These is zero difference clinically - which is why "Central Cord "Syrinx with
everyone just says "syrinx." The distinction is strictly Dilation" Myelopathy"
academic (i.e. multiple choice trivia).
Most (90%) cord dilations (healthy and sick ones) are congenital, and associated with Chiari I and II,
as well as Dandy-Walker, Klippel-Feil, and Myelomeningoceles. The other 10% are acquired either
by trauma, tumor, or vascular insufficiency.
In clinical practice, if there is perfectly central mid cord high signal dilation, surrounded by totally
normal cord I call it "central cord dilation" or "benign central cord dilation." If there is the same
thing but the cord around the dilation looks "sick" - grayish/ high signal, or the cord is atrophic, then
I use the word "myelopathy" or "myelopathic changes." Myelopathy is a word for a diseased cord -
usually from disc/osteophyte compression. Although, you can have myelopathy for any number of
neoplastic, post traumatic, or inflammatory processes.
Spinal Cord Infarct: - Cord infarct/ ischemia can have a variety of causes. The most
common cause is "idiopathic," although I'd expect the most common multiple choice scenario
to revolve around treating an aneurysm with a stent graft, or embolizing a bronchial artery.
Impairment involving the anterior spinal artery distribution is most common. With anterior
spinal artery involvement you are going to have central cord/ anterior horn cell high signal on
T2 (because gray matter is more vulnerable to ischemia).
The "owl's eye" sign of anterior spinal cord infarct is a buzzword.
It's usually a long segment, (more than 2 vertebral body segments). Diffusion using single
shot fast spin echo or line scan can be used with high sensitivity (to compensate for artifacts
from spinal fluid movement).
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Oemvelinating (T2 / FLAIR Hyperintense):
Broadly you can think of cord pathology in 5 categories: Demyelinating, Tumor, Vascular, Inflammatory,
and Infectious.
In the real world, the answer is almost always MS - which is by far the most common cause. The other
three things it could be arc Neuromyelitis Optica(NMO), acute disseminating encephalomyelitis
(ADEM) or Transverse Myelitis(TM).
MS in the Cord: "Multiple lesions, over space and time." The lesions in the spine are typically
short segment(< 2 vertebral segments), usually only affect half/ part of the cord. The cervical cord is
the most common location. There are usually lesions in the brain, if you have lesions in the cord
(isolated cord lesions occur about 10% of the time). The lesions can enhance when acute - but this is
less common than in the brain. You can sometimes see cord atrophy if the lesion burden is large.
Transverse Myelitis: This is a focal inflammation of the cord. The causes are
numerous(infectious, post vaccination - classic rabies, SLE, Sjogren's,
Paraneoplastic, AV-malformations). You typically have at least 2/3 of the cross
sectional area of the cord involved, and focal enlargement of the cord. Splitters will
use the terms "Acute partial" for lesions less than two segments, and "acute
complete" for lesions more than two segments. The factoid to know is that the
"Acute partials" are at higher risk for developing MS.
ADEM: As described in the brain section, this is usually seen after a viral illness or infection
typically in a child or young adult. The lesions favor the dorsal white matter(but can involve grey
matter). As a pearl, the presence of cranial nerve enhancement is suggestive of ADEM. The step 1
trivia, is that the "anti-MOG IgG" test is positive in 50% of cases. Just like MS there are usually brain
lesions(although ADEM lesions can occur in the basal ganglia and pons - which is unusual in MS).
NMO (Neuromyelitis Optica): This is also sometimes called Devics. It can
be monophasic or relapsing, and favors the optic nerves and cervical cord. Tends
to be longer segment than MS, and involve the full transverse diameter of the cord
(mild swelling). Brain lesions can occur(more commonly in Asians) and are
usually periventricular. If any PhDs ask, the reason the periventricular location
occurs is that the antibody(NMO IgG) attacks the Aquaporin 4 channels - which
are found in highest concentration around the ventricles.
Subacute Combined Degeneration: This is a fancy way of describing the
effects of a Vitamin B12 deficiency. The classic look is bilateral, symmetrically
increased T2 signal in the dorsal columns, without enhancement. The
appearance has been described as an "inverted V sign." The signal change
typically begins in the upper thoracic region with ascending or descending
progression.
HIV Vacuolar Myelopathy: This is the most common cause of spinal cord
dysfunction in untreated AIDS. Key word there is "untreated" - this is a late
finding. Atrophy is the most common finding(thoracic is most common). The T2
high signal will be ve1y similar to B12 (subacute combined degeneration) -
symmetrically involving the posterior columns. It can only be shown 2 ways -(a)
by telling you the patient has AIDS or risk factors such as unprotected anal sex at
a truck stop with a man "bear" with a thick mustache while sharing IV drug
needles, (b) not including B 12 as an answer choice.
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MS: Lesions favor the white matter of the cervical region.
They tend to be random and asymmetric.
"Owl's Eye" -lschemia -lschemia Vitamin B12 (SCD)
-Classic for lschemia - More extensive -This time a HIV
(Anterior) anterior involvement. posterior circulation
-Also seen in Polio -Also seen in NMO, pattern. These tend Posterior. Can look
TM, or MS to be unilateral.
like an inverted "V"
-MS can also look
like this
Can Enhance /
Usually Short Usually Part of the Not swollen, or
MS Restrict when
Segment Cord Less Swollen
Acute
-------·-------. - ··-···
Usually Long Usually involves both Expanded,
TM Can Enhance
Segment sides of the cord Swollen Cord
--- --···----···-- -- ······~-·-······-�•--·------- -··--·
Usually Long Usually involves both Optic Nerves
NMO sides of the cord Involved
Segment
�----..------- ·---·····-···
Not swollen, or
ADEM Less Swollen
Usually Long Restricted
Infarct
Segment Diffusion
---
Expanded,
Tumor Can Enhance
Swollen Cord
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lnflammatorv / Infectious:
Arachnoiditis: This is a general term for inflammation of the subarachnoid space. It can
be infectious but can also be post-surgical. It actually occurs about 10-15% of the time
after spine surgery, and can be a source of persistent pain / failed back.
It's shown two ways:
(1) Empty Thecal Sac Sign -Nerve roots are
adherent peripherally, giving the appearance of an
empty sac.
(2) Central Nerve Root Clumping. This can range in
severity from a few nerves clumping together, to all
of them fused into a single central scarred band.
Empty Thecal Sac Sign
Guillain Barre Syndrome (GBS) - Also
known as "Acute inflammatory demyelinating polyneuropathy" (AIDP). One of those weird
auto-immune disorders that causes ascending flaccid paralysis. The step 1 trivia was
Campylobacter, but you can also see it after surgery, or in patients with lymphoma or SLE.
The thing to know is enhancement of the nerve roots of the cauda equina.
Other pieces of trivia that are less likely to be asked are that the facial nerve is the most
common cranial nerve affected, and that the anterior spinal roots enhance more than the
posterior ones.
Chronic Inflammatory
Demylinating
Polyneuropathy (CIDP)
The chronic counterpart to GBS.
Clinically this has a gradual and
protracted weakness (GBS
improves in 8 weeks, CIDP does
not). The buzzword is thickened,
enhancing, "onion bulb" nerve
roots.
"Dreadlocks' ""Locs' ""Jata"
.
some people call them.
CIDP - Diffuse Thickening of the Nerve Roots
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Tumor
The classic teaching with spinal cord tumors is to first describe the location of the tumor, as
either (1) Intramedullary, (2) Extramedullary Intradural, or (3) Extradural. This is often easier
said than done. Differentials are based on the location.
lntramedullary Extramedullary Extradural
lntradural
Astrocytoma, Schwannoma, Disc Disease
Ependymoma, Meningioma, (most common)
Hemangioblastoma Neurofibroma, Bone Tumors,
Drop Mets Mets,
Lymphoma
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lntramedullarv:
Astrocytoma - This is the most common Astrocytoma Ependymoma
intramedullary tumor in peds. It favors the
-· ···~- . --·�·-··
Most common in child Most common in Adults
upper thoracic spine. There will be fusiform
Eccentric Central
dilation of the cord over multiple segments.
Heterogenous I-Iomogenous
They are eccentric, dark on T l , bright on T2, Enhancement Enhancement
and they enhance. They may be associated
More Often Hemorrhagic
with rostral or caudal cysts which are usually
benign syrinx(es).
Ependymoma - This is the most common primary
cord tumor of the lower spinal cord and conus / filum
tenninale. You can see them in the cervical cord as well.
This is the most common intramedullary mass in adults.
The "myxopapillary form" is exclusively found in the
conus /filum locations. They can be hemorrhagic, and
have a dark cap on T2. They have tumoral cysts about ¼
of the time. They are a typically long segment (averaging
4 segments). Ependymoma - Cervical Cord
Myxopapillary = Most commonly located in the Lumbar spine (conus/filum location)
VHL Associations:
Hemangioblastoma
These are associated with Von Rippel Lindau (30%). •Pheochromocytoma
•CNS Hemangioblastoma
The thoracic level is favored (second most common is (cerebellum 75%, spine 25%)
cervical). •Endolymphatic Sac Tumor
•Pancreatic Cysts
The classic look is a wide cord with considerable edema.
•Pancreatic Islet Cell Tumors
Adjacent serpinginous draining meningeal varicosities can
•Clear Cell RCC
be seen.
lntramedullary Mets -
This is very very rare, but when it does happen it is usually lung (70%).
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Extramedullarv lntradural:
Schwannoma: This is the most common tumor to occur in the Extramedullary
Intradural location. They are benign, usually solitary, usually arise from the dorsal nerve
roots. They can be multiple in the setting ofNF-2 and the Camey Complex. The appearance
is variable, but the classic look is a dumbbell with the skinny handle being the intraforaminal
component. They are T l dark, T2 bright, and will enhance. They look a lot like
neurofibromas. If they have central necrosis or hemorrhage, that favors a schwannoma.
Neurofibroma: This is another benign nerve tumor (composed of all parts of the nerve:
nerve + sheath), that is also usually solitary. There are two flavors: solitary and plexiform.
The plexiform is a multilevel bulky nerve enlargement that is pathognomonic forNF-1.
Their lifetime risk for malignant degeneration is around 5-10%. Think about malignant
degeneration in the setting of rapid growth. They look a lot like schwannomas. If they have
a hyperintense T2 rim with a central area of low signal - "target sign" that makes you favor
neurofibroma.
Schwannoma Neurofibroma
Does envelop the adjacent nerve root
Does NOT envelop the adjacent nerve root
(usually
·· ---
a dorsal sensory root)
.--·- ·- -----·- - · ·---·- -····-
Solitary Solitary
· ·-- - · · ···---·····
Multiple
- ------ -··---· ··- .
makes you think NF-2 Associated
--···- --- -·- - - .
withNF
--- --
-1 (even when single)
Cystic change / Hemorrhage T2 bright rim, T2 dark center "target sign"
--·-- - ·-· · · ---· ---·--
Plexiform = Pathognomonic for NF-I
Meningioma: These guys adhere to but do not originate from the dura. They are more
common in women (70%). They favor the posterior lateral thoracic spine, and the anterior
cervical spine. They enhance brightly and homogeneously. They are often Tl iso to hypo,
and slightly T2 bright. They can have calcifications.
Drop Mets: Medulloblastoma is the most common primary tumor to drop. Breast cancer
is the most common systemic tumor to drop (followed by lung and melanoma). The cancer
may coat the cord or nerve root, leading to a fine layer of enhancement ("zuckerguss").
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Extradural:
Vertebral Hemangioma: These are very common - seen in about 10% of the
population. They classically have thickened trabeculae appearing as parallel linear densities
"jail bar" or "corduroy" appearance. In the vertebral body they are T l and T2 bright,
although the extraosseuous components typically lack fat and are isointense on T 1.
Osteoid Osteoma: This is also covered in the MSK chapter, but as a brief review
focusing on the spine, they love to involve the posterior elements (75%), and are rare after
age 30. They tend to have a nidus and surrounding sclerosis. The nidus is T2 bright and will
enhance. The classic story is night pain, improved with aspirin. Radiofrequency ablation can
treat them (under certain conditions).
Osteoblastoma: This is similar to an Osteoid osteoma but larger than 1.5 cm. Again,
very often in the posterior elements - usually of the cervical spine.
Aneurysmal Bone Cyst: These guys are also covered in the MSK chapter. They also
like the posterior elements and are usually seen in the first two decades of life. They are
expansile (as the name implies) and can have multiple fluid levels on T2. They can get big
and look aggressive.
Giant Cell Tumor: These guys are also covered in the MSK chapter. These are common
in the sacrum, although rare anywhere else in the spine. You don't see them in young kids.
If they show this, it's going to be a lytic expansile lesion in the sacrum with no rim of
sclerosis.
Chordoma: This is most common in the sacrum (they will want you to say clivus - that
is actually number 2). The thing to know is that a vertebral primary tends to be more
aggressive / malignant than its counter parts in the clivus or sacrum. The classic story in the
vertebral column is "involvement of two or more adjacent vertebral bodies with the
intervening disc. " Most are very T2 bright.
Leukemia: They love to show it in the spine. You have loss of the normal fatty marrow -
so it's going to be homogeneously dark on Tl. More on this in the MSK chapter.
Mets: The classic offenders are prostate, Vertebra Plana:
breast, lung, lymphoma, and myeloma.
Think multiple lesions with low Tl The pancake flat vertebral body.
Just say Eosinophilic Granuloma in a
signal. Cortical breakthrough or adjacent kid (could be neuroblastoma met), and
paravertebral components are also helpful. Mets/ Myeloma in an adult.
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Blank for Scribbles:
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111�1�
�
. .
�11 ·_ - :,'/ :,. 1
� / ·,·
..
.
1
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1 1
MUSCULOSKELETAL
PROMETHEUS LIONHART, M.D.
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'
·:•
-- - \_- --
'.: :
�
SECTION 1:
TRAUMA AND OVERUSE
�
• "'
'
,.
Fracture Vocab
Stress Fracture = Fracture resulting from the Pathologic Open Fracture
mismatch of bone strength and chronic Fracture: (Compound
mechanical force. They come in two flavors Fracture):
(A) Fatigue, and (B) Insufficiency. You will sometimes
hear people use this A fracture associated
Fatigue Fracture term synonymously with an open wound.
(sometime simply Insufficiency with "Insufficiency Typically these will
called a "stress Fracture Fracture". However, go to the OR for
fracture"). for the purpose of reduction and
Abnormal stress on Normal stress on multiple choice this washout - given the
Normal Bone. Abnormal bone. term will most likely obvious risk for
refer to a fracture infection.
Classic Scenario - Classic Scenario - through a l�tic bone
lesion. Tuft Fractures (finger
Insane (but kinda hot) Old lady with horrible tip fracture) with
Type A Female Cross osteoporosis breaks These lytic lesions disruption of the nail
Country Runner her back (compression can be mets or be plate are considered
literally runs until her fracture) by walking benign primary bone "open" fractures - and
legs & feet break in down a few steps. She lesions (like an although the typically
half. blames Obama for the ABC, or Bone Cyst). won't go to the OR
fracture. they do get antibiotics
(whereas an intact
nail bed often won't).
Phases of Fracture Healing:
Physiology PhDs will describe 3 phases of bone healing (Inflammatory, Reparative, and
Remodeling). From a Radiologist's perspective the most important thing to understand
about this process is that around 7-14 days granulation tissue will be forming between the
bone fragments. This results in an increased lucency of the fracture site related to bone
resorption.
In other words, a healing fracture will be MORE LUCENT at 7-14 days.
This explains the disclaimer cowardly Radiologists throw out when they are afraid they
missed a fracture "Consider Repeat in 7-10 days," The idea is that in 7-10 days, you
should be able to see the fracture line , if one is present , because of the increase in bone
lucency that occurs normally in the healing process.
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fracture Healing Continued
In general, bones heal in about 6-8 weeks, but is location
Phalanges = Heal Fast (3 Weeks)
dependent. Healing is the fastest in the phalanges
Tibia = Heal Slow (10 Weeks)
(around 3 weeks), and the slowest is either the tibia or
Everything Else = 6-8 weeks
femoral neck/shaft - depending on what you read
(around 2-3 months).
Abnormal Healing vocab
Delayed Union Non-Union Mal-Union
fracture not healed within the fracture is not going to heal This is union in poor anatomic
expected time period (but still without intervention. Some position (healed crooked as a
might). Some sources will say sources will say "6-9 months." politician).
"twice as long as expected" The classic locations are the
scaphoid, anterior tibia, and
lateral femoral neck.
Risk factors for Abnormal Healing I Delaved and Non-Union J
(these are the ones I think are most testable):
Vitamin D Deficiency Gastric Bypass Drugs/ Meds
Vitamin D plays a vital role in Having your gut rewired results
calcium uptake and metabolism. in altered calcium absorption Tobacco (Smoking or Chewing)
(causes secondary
Vitamin D deficiency is actually hyperparathyroid and stripping NSAIDS
the most common vitamin of calcium from bones) and
deficiency in America therefore higher rates of non- Prednisone (steroids)
(supposedly). muon.
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THIS vs THAT-Compressive Side vs Tensile Side:
This comes up in two main areas - the femoral neck and the tibia.
• Fractures of the Compressive side arc constantly pushed back together - these do well.
• Fractures of the Tensile side arc constantly pulled apart - these arc a pain in the ass to heal.
Tibial Stress Fracture:
This is the most common
site of a stress fracture in
young athletes.
These arc most common
on the compressive side
(posterior medial) in either
the proximal or distal third.
Less common arc the Femoral Stress Fracture:
tensile side (anterior)
Fractures along the compressive (medial)
fractures, and these side are more common, typically seen in
favor the mid shaft. They are a younger person along the inferior
bad news and don't heal - femoral neck.
often called "dreaded
black lines." Fractures along the tensile (lateral) side
are more common in old people.
SONK (Spontaneous Osteonecrosis of the Knee):
This is totally named wrong, as it is another type of
insufficiency fracture. You see this in old ladies with
the classic history of "sudden pain after rising from
a seated position." Young people can get it too
(much less common), usually seen after a meniscal
surgery
. L Key Factoids:
f1' • It's an insufficiency fracture (NOT
.f1'
L osteonecrosis) think SINK not SONK
• Favors the medial femoral condyle
.L (area of maximum weight bearing)
f1' • Usually unilateral in an old lady without
.f1'
L • Associated
history of trauma
with meniscal injury
SONK-LOTS OFEDEMA
- Subchondral Deformity (arrows)
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Navicular Stress Fracture- You see these in runners who run on hard surfaces. The
thing to know is that just like in the wrist (scaphoid), the navicular is high risk for AVN.
March Fracture: This is a metatarsal stress fracture which is fairly common.
Classically seen in military recruits that are marching all day long.
Calcaneal Stress Fracture - The calcaneus is actually the most fractured tarsal
bone. The fractures are usually intra-articular (75%). The stress fracture will be seen with
the fracture line perpendicular to the trabecular lines.
You'll rue the day you crossed me Trebek-ular Lines.
Typical Calcaneal
Trabecular Lines
Orientation/
of Calcaneal
Stress Fx
I'll take the Penis Mightier for $600
THIS vs THAT: High Risk vs Low Risk Stress Fractures:
You can sort these based on the likelihood of
uncomplicated healing when treated conservatively.
High Risk Low Risk
Femoral Neck (tensile side) Femoral Neck (compressive side)
Transverse Patellar Fracture Longitudinal Patellar Fracture
Anterior Tibial Fracture (midshaft) Posterior Medial Tibial Fracture
5th Metatarsal 2nd and 3rd Metatarsal
Talus Calcaneus
Tarsal Navicular
Sesamoid Great Toe
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Site-Specific Entities - Hand and Wrist
Scaphoid Fracture
Most common carpal Blood flow is "retrograde" (distal
bone fracture. "Retrograde"
to proximal). This is because the
scaphoid surface is almost (distal to
Typical age group is an proximal) via
adolescents and young entirely (80%) covered with
f� the Dorsal
adults (Grandma is more cartilage. �; Carpal
likely to get a distal As such, the proximal pole most 1 Branch of
radial fracture with a Radial Artery
similar mechanism - susceptible to AYN and Non
fall). ll.nion,
Distal Pole / The first sign ofAVN = Sclerosis
(the dead bone can't turn over /
?f)·
Scaphoid Tubercle
Waist recycle)
· · .iM•
� Most common (70 %) fracture Proximal
site = waist Pole is at
Risk for AYN
Displacement of> 1mm will / Mal-Union
Proximal likely get a fixation screw to pull
Pole the fragments together.
Trans-Scaphoid Scapholunate Ligament Humpback Deformity
a·.
Perilunate Dislocation Disruption This deformity
results from
Capitate angulation of the
proximal and distal
fragments - in the
setting of a waist
fracture.
Can progress to Normal
.progressive collapse ...._.___.___.
and non-union. Humpback shown
Associated with DISI on lateral view
Seen with 10-30% of distal radius AVN
and/or carpal fractures
As above the proximal pole is at
Perilunate dislocation greatest risk.
(discussed later in the The SL ligament is composed of 3
chapter) have a high parts (volar, dorsal, and middle), The first sign of
association (60%) with with the dorsal band being the AVN = Sclerosis
a scaphoid fracture most important for carpal stability (the adjacent bones
(opposite of luno-triquetral which will demineralize,
is volar). but the avascular
bone will not).
Disruption of the ligament Later the bone will
predisposes for DISI deformity fragment.
(discussed later in the chapter in
MRI=T l Dark
greater depth).
Trivia: "Prieser Disease" is an
atraumatic AVN of the scaphoid
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SlAC and SNAC Wrists
Both are potential complications of trauma, with
similar mechanisms.
SLAC Wrist (Scaphoid-Lunate Advanced Collapse)
occurs with injury (ot degeneration via CPPD) to the
S-L ligament.
SNAC Wrist (Scaphoid Non-Union Advanced
Collapse) occurs with a scaphoid fracture.
SNAC
Just remember that the scaphoid always wants to
rotate in flexion - the scaphoid-lunate ligament is the
only thing holding it back. If this ligament breaks it
will tilt into flexion, messing up the dynamics of the
wrist. The radial scaphoid space will narrow, and the
capitate will migrate proximally. • Radioscaphoidjoint is first to
develop degenerative changes
Treatment depends on the occupation/needs of the
wrist. Wrist fusion will maximize strength, but cause • Capitate will migrate proximally and
a loss of motion. Proximal row carpectomy will there will eventually be a DISI
maximize ROM, but cause a loss of strength. deformity
Scapholunate Ligament Tear:
The Terry Thomas look (gap between the scaphoid and lunate) on plain film.
There are actually 3 parts (volar, dorsal, and middle), with the dorsal band being the most
important for carpal stability. If they tear the carpals will migrate away from each other.
Predisposed for DISI deformity and all that crap I talked about earlier. More on this
complex carpal instability on the next page.
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� THIS vs THAT- DISI vs VISI
This topic can be very confusing. Here is the way I like to think about it.
I imagine two people (Lunate and Scaphoid) standing on
opposite sides of a very steep hill. At the apex of the hill is
a man named "Scapholunate Ligament" - I agree, it's a
strange name. His parents were probably vegetarians.
This hill is very steep, so Scapholunate Ligament has
grabbed each of the people (Lunate and Scaphoid) by the
hand - he was worried they might fall. In fact, the only
thing keeping these two people from tumbling down the
hill is the insane grip strength of Scapholunate Ligament
(rumor has it he can close a #3 Captain of Crush - which
would certify him as an official Captain of Crush).
By using this analogy perhaps you can infer that if you
have carpal ligament disruption, the carpal bones will
rotate the way they naturally want to (down the hill).
The reasons for their rotational desires are complex but
basically have to do with the shape of the fossa they sit
on.
· - ,
Just remember the scaphoid wants to flex (rock volar)
. -._
and the lunate wants to extend (rock dorsal). The only DORSAL /i , VOLAR
thing holding them back is their ligamentous attachment :,:...... · ',_-;':. /·:···;•::'. �----
to each other.
DISI (Dorsal Intercalated Segmental Instability) VISI (Volar Intercalated Segmental Instability) - I
- I like to call this dorsiflexion instability like to call this volar-flexion (palmar-jlexion)
because it helps me remember what's going on. instability because it helps me remember what's
After a "Radial sided injury" (scapholunate going on. After a "Ulnar sided
side), the lunate becomes free of the stabilizing injury" (lunotriquetral side), the lunate no
force of the scaphoid and rocks dorsally. longer has the stabilizing force of the
Remember SL ligament injury is common, so lunotriquetral ligament and gets ripped volar
this is common. with the scaphoid (remember the scaphoid stays
'\ up late every night dreaming of tilting volar).
Remember LT ligament injury is not common,
.··· · Volar
so this is not common. It's so uncommon in fact
-----
·_,.'.> that if you see it - it's probably a normal variant
due to wrist laxity.
VISI: Narrowing of
the SL angle - with
Normal volar-flexion of the
Scaphoid lunate & scaphoid.
\
Lunate Angle Angle < 30 (this acute
DISI: Widening of the SL is 30-60
angle - with dorsiflexion of angle looks like a V to
degrees 1ne - "V" for "V")
the lunate.
()Dorsal
Angle> 60
(some sources say 80) Volar
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Carpal Dislocations - A spectrum ofseverity
Lea�t$0
Scapho-Lunate Peri-Lunate Mid-Carpal Lunate
Dissociation Dislocation Dislocation Dislocation
• SL- Wider Than 3 mm Trivia to Know = Trivia to Know = Trivia to Know =
• Clenched Fist View can
worsen it (would make a Note that the Lunate Both Lunate and Lunate moves,
good next step question) stays put - it's the Capitate lose radial others stay
• Chronic SL dissociation carpal bones around alignment.
can result in a SLAC the lunate ("peri- It happens with a
wrist lunate bones") that Associated with Dorsal radiolunate
move. Triquetro-Lunate ligament injury
interosseous ligament
60% associated with disruption "Most Severe"
Scaphoid Fractures
Associated with a
Triguetral Fracture
Vulnerable Zones Theory
Dislocations around the lunate are described
in two flavors
Lesser Arc: Pure Ligament Injury (No
Fractures)
Greater Arc: Associated with fractures.
Described by saying "trans" the name of the
fracture then the dislocation. Example
"Trans-scaphoid, peri-lunate dislocation"
Lesser Arc-
Space of Poirier - Ligament free ("poor")
area, that is a site of weakness
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Anatomic Trivia Regarding the Spaces of the Wrist:
Which synovial spaces normally communicate ?
The answer is pisiform recess
and radiocarpal joint. I can
think of two ways to ask this
( 1) related to fluid - the bottom
line is that excessive fluid in the
pisiform recess should not be Midcarpal
Pisiform
considered abnormal if there is a
radiocarpal effusion, and
(2) that either space can be used
for wrist arthrography.
Radiocarpal
Distal Radioulnar
Other joint spaces in the body, easily lending to multiple choice testing:
Glenohumeral Joint and Should NOT communicate. Implies the presence of a
Subacromial Bursa full thickness rotator cuff tear.
----
Ankle Joint and Common Should NOT communicate. Implies a tear of the
(lateral) Peroneal Tendon Sheath calcaneofibular Ligament.
-·-------·- -------·-··-
Achilles Tendon and Should NOT communicate. The Achilles tendon
Posterior Subtalar Joint does NOT have a true tendon sheath.
________________
, -------·------·----·-·-------· ·---- -·----------·---·----- ----------•-'---•·-------------·--· _ _________________ _________________ ._,__
_. ,
Pisifrom Recess and
Should normally communicate.
Radiocarpal Joint
Anatomic Trivia -Iriangular fibroiartilage Complex -TFCC
I'll begin by saying that this is arguably the most complex anatomy in the entire body
(maybe second only to the posterior lateral comer). A detailed understanding is well
beyond the scope of the exam (probably ...). Having said that, the TFC is specifically
mentioned on the official study guide, so we need to at least talk about it.
The TFCC functions as the primary stabilizer and shock absorber of the distal radial ulnar
joint (DRUJ). The TFCC is critical for a range of activities (doing a pushups , punching
General Zod, etc ...).
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Anatomic Trivia - Irianuular flbro�artilaue Complex - TFCC - Continued
It looks crazy complicated - but you really only TFCC 5 Components:
need to know at most 5 structures, 1. Triangular Fibrocartilage (Articular Disc)
2. Volar & Dorsal Radioulnar Ligaments
Of the 5, the Hand Surgeon only really gives a 3. Meniscus Homologue
4. UCL
shit about the Articular .Disc and Radioulnar 5. Tendon Sheath of the UCU
Ligaments.
MR Signal:
Ulnar Collateral
Ligament (UCL) "TFC Proper" (Articular
Volar Disc) will be dark on every
Distal Extensor Carpi sequence.
Radial Ulnaris (ECU)
Tendon / Sheath - The ulnar attachment often
Ulnar looks intermediate in signal,
Ligament this is normal related to loose
connective tissue in the
Triangular region.
Articular Triangular Lig
Disc (styloid - The radial attachment will
attachment) also have intermediate signal,
but this is from the normal
Ligamentum articular cartilage.
Subcruentum
Dorsal Triangular Lig.
Distal (foveal
Radial PSR = r_re§.tyloid Recess attachment)
Ulnar
Dorsal Distal Radial Extensor Carpi
TFCC Injuries:
Ulnar Ligament Ulnaris (ECU)
Sheath and Tendon You can group these into:
"Class 1" Acute Injuries: Usually
via fall onto extended wrist.
"Class 2" Chronic Degeneration:
These are more common, and
UCL associated with positive ulnar
variance and ulnar impaction.
Central perforations are common
Meniscus - and might even be "expected"
Homologue on an old person.
Volar Distal
Radial Ulnar
Ligament
Central Tear, with Ulnar Positive
Variance and Abutment (cystic change
in the lunate) - more on next page.
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TFC vasculature & Healing
Similar to how the knee
meniscus has "red" and
"white" zones - the ulnar
side of the TFC is vascular
and more likely to heal. Radius Ulna
Radial sided injuries are Radius
relatively avascular and
less likely to heal.
Ulnar variance / Impaction
Ulnar Variance
This is determined by
comparing the lengths of the
ulna and distal radius.
Neutral
These length differences can
occur congenitally, or be Positive Negative
acquired from impaction / Variance: Variance:
fracture deformity. Association: Association:
- Ulnar Impaction - AVN of the Lunate
Syndrome ("Kienbock")
Ulnar Impaction Syndrome Kienbocks:
(Ulnar Abutment): AVN of the lunate, seen in people in their
Seen with positive ulnar variance. 20s-40s. The most likely testable trivia is
the association with negative ulnar
Essentially the distal ulna smashes into
variance. It's going to show signal drop
the lunate, degenerating it (cystic change
out on Tl.
I geodes etc ...) and tears up the TFCC.
Sclerotic on Plain Film Low Signal on Tl
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Distal Radius / Wrist Fractures:
There are 3 named fractures of the distal radius / wrist worth knowing.
Distal Radius Radial Rim
Colles' Fracture Smith Fracture Barton Fracture
(Outward) (Inward) (Dorsal or Volar)
"Collie Dogs" Like it Outside
• Distal Metaphysis Fx • Distal Metaphysis Fx • Radial Rim Fx
• Dorsal Angulation • Volar Angulation • Volar is More Common
• Old Lady Fracture • Younger Patient • Radial-Carpal Dislocation is the
• Ulnar Styloid Fx is • Ulnar Styloid Fx is "hallmark"
Commonly Associated Commonly Associated • Typically Surgical (they have a
high rate of re dislocation /
mal-union)
Radial Tilt
• There is a normal volar tilt of around 11 degrees
• With distal radial fractures this can get fucked up
• Most Orthopods won't accept anything past neutral
• A TRUE lateral is necessary to measure it
How do you know your lateral is "true"?
The volar cortex of the pisiform overlies the central
1/3 of the interval between the scaphoid and capitate
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Wrist Tendon Anatomv Review:
With regard to the extensor tendons, there are four things to know:
• There are 6 extensor compartments
(5 fingers+ 1 for good luck).
Lister's Tubercle
• First compartment (APL and EPB) are the 11.4n
ones affected in de Quervain's
''6'' i\51,r
, .· 1111:r
• Third compartment has the EPL which
courses beside Lister's Tubercle. •·
imur:na
1
• The sixth compartment (Extensor Carpi
Ulnaris) - can get an early tenosynovitis in
rheumatoid arthritis.
Carpal Tunnel: They could show you the carpal tunnel, but only to ask you about anatomy.
What goes through the carpal tunnel (more easily asked as "what does NOT go through'')?
Knowing what is in (and not in) the carpal
tunnel is high yield for multiple choice testing.
The tunnel lies deep to the palmaris longus, FCR Median
and is defined by 4 bony prominences Not in the Nerve FDP + FDS
(pisiform, scaphoid tubercle, hook of hamate,
trapezium tubercle), with the transverse carpal
ligament wrapping the contents in a fibrous
sheath.
The tunnel contains 10 things
• 4 Flexor D. Profudus (FDP)
• 4 Flexor D. Superficials (FDS)
Does NOT go
• 1 Flexor Pollicis Longus (FPL), and
through the tunnel
• l Median Nerve
-Flexor Carpi Radialis
The Flexor Carpi Radialis (FCR) is NOT truly in the tunnel.
The extensor tendons are on the other side of the hand. Note that -Flexor Carpi Ulnaris
Flexor Pollicis Longus (FPL) goes through the tunnel, but -Palmaris Longus
Flexor Pollicis Brevis does not (it's an intrinsic handle muscle). (if you have one)
Palmaris longus (if you have one) does NOT go through the
tunnel. -Flexor Pollicis BREVIS
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Carpal Tunnel Syndrome (CTS):
• Median Nerve Distribution (thumb-radial aspect of 4th digit), often bilateral, and may have
thenar muscle atrophy.
• On Ultrasound, enlargement of the nerve is the main thing to look for
• It's usually from repetitive trauma,
• Trivia = Association with Dialysis, Pregnancy, DM, and HYPOthyroidism
Classic Findings:
• Increased Signal in the Median Nerve
• The Nerve May Also Be Swollen or
Look Smashed / Flattened
• Bowing of the Flexor Retinaculum
Guyon's Canal Syndrome:
• Entrapment of the ulnar nerve as it passes through Guyon's canal (formed by the pisiform
and the hamate - and the crap that connects them).
• Classically caused by handle bars "handle bar palsy."
• Fracture of the hook of the hamate can also eat on that ulnar nerve.
Sub-Sheath Tear / Dislocation
This refers to a traumatic dislocation to the
extensor carpi ulnaris (ECU - compartment 6) out A• ..>:.::\:)-} c
~)
of its normal groove at the level of the distal ulna.
This dislocation/ subluxation implies rupture of
the overlying sheath.
Trivia - the direction of dislocation is medial.
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Tenosvnovitis:
This is an inflammation of the tendon, with increased fluid seen around the tendon. This will be
shown on MRI (or US).
DIFFUSE FOCAL
Tuberculous or
Rheumatoid Penetrating Infection
Nontuberculous Overuse
Arthritis: (can be focal or diffuse)
Mycobacterial
Hand and wrist are the most Tenosynovitis of any flexor tendon is
common tendons affected Multiple Flexor a surgical emergency as it can spread
Tendons rapidly to the common flexors of the
or wrist.
Isolated Extensor This is going to
Increased pressure in the sheath can be classic
Diffuse exuberant tenosynovitis Cargi Ulnaris if cause necrosis of the tendons. locations like
that spares the muscles. early (ECU =
Compartment 6) Patients with delayed treatment tend 1st extensor
to do terrible compartment for
De Quervains
Usually occurs in patients who Tenosynovitis -discussed
are immunocompromised. can present as an Myocobacterium Marinum is usually more below.
Discrete filling defects in the early RA direct infection in a fishennan or
fluid filled sheaths ("rice findings (before sushi chef.
bodies") is a classic TB finding. bone findings).
De Quervain's Tenosynovitis: Intersection Syndrome:
So called "Washer Woman's Sprain" or "Mommy Thumb."
Occurs from repetitive activity/ overuse. , A repetitive use issue
The classic history is "new mom - holding a baby." (classically seen in rowers),
Ultrasound: Increased fluid Occurs where the first extensor
First Extensor Compartment within the first extensor tendons, "intersects" the second
(Extensor Pollicis Brevis and tendon compartment extensor compartment tendons.
Abductor Pollicis Longus MRI: increased T2 signal in The result is extensor carpi radialis
the tendon sheath brevis and longus tenosynovitis.
Finkelstein Test = Pain on passive ulnar deviation.
The presence or absence of an intratendinous septum (between the EPB
and APB) - tendons on the is a prognostic factor. If its absent, this will
nearly always resolve with conservative treatment alone.
Occurs 5cm Proximal
to Listers Tubercle
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Bennett and Rolando
Fractures:
• They are both fractures at the base of
the first metacarpal
• The Rolando fracture is comminuted
(Bennett is not)
• Trivia: The pull of the Abductor
Pollicis Longus (APL) tendon is
what causes the dorsolateral
BENNETT Fx Rolando Fx
dislocation in the Bennett
Fracture
DONOT
Gamekeeper's Thumb (Skier): perform
• Avulsion fracture at the base of the proximal first phalanx radiographic
associated with ulnar collateral ligament disruption. stress views
for
• The frequently tested association is that of a "Stener Gamekeepers
Lesion." A Stener Lesion is when the Adductor tendon Thumbs
aponeurosis gets caught in the torn edges of the UCL.
The displaced ligament won't heal right, and will need
surgery.
• It makes a "yo-yo" appearance on MRI - supposedly ...
• Next Step - Don't do "stress views" that can cause a
stener. MRI is the more appropriate test.
Cl)
C
0
IXl
Cl)
C
0
IXl
I •
Cl)
C
0
Ulnar collateral
ligament is
retracted and
displaced
superficial to
the adductor
aponeurosis.
Stener
Trigger Finger: The idea is the overuse I
repetitive trauma causes scarring in the flexor tendon
sheath. The fancy word is "stenosing tenosynovitis."
This is most commonly shown with ultrasound. If
they should you a hand ultrasound think about this.
Another common area of "stenosing tenosynovitis" is Thick Sheath Normal for
at the ankle specifically the flexor hallucis longus Comparison
tendon around the ankle in patients with the os
trigonum syndrome.
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Site-Specific Entities - Elbow & Forearm
General Trivia:
• Radial Head Fracture is most common in adults (supracondylar is most common in PEDs)
• Sail sign - elevation of the fat pads from a joint effusion. Supposedly a sign of occult
fracture. The testable trivia is (1) the posterior fat pad is more specific (posterior is
positive), and (2) the posterior fat pad can appear falsely elevated (false positive) if the
lateral isn't a true 90 degree flexed lateral. "Posterior Positive, Posterior Position
Dependent"
• Capitellum fractures are associated with posterior dislocation
Forearm Fractures / Eponyms:
Forearm fractures are "ring" or "pretzel" type fractures, similar to the pelvis or mandible.
Think about breaking a pretzel, it always snaps in two spots (not just one). So forearm
fractures are often two fractures, or a fracture + dislocation.
There are 3 French sounding (therefore high yield) fractures of the forearm which follow this
ring / pretzel principal.
Monteggia Fracture (MUGR):
Fracture of the proximal ulna, with
anterior dislocation of the radial head.
Dislocation of the radial head follows
the angulation of the Ulnar Fx.
Galeazzi Fracture (MUGR)
Radial shaft fracture, with anterior
dislocation of the ulna at the DRUJ.
Essex-Lopresti
Fracture of the radial head + Anterior
dislocation of the distal radial ulnar
joint.
Unstable fracture - With rupture of the
interosseous membrane
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Cubital Tunnel Syndrome
There are several causes - the most common in the real world is probably repetitive valgus
stress. The most common shown on multiple choice is probably an accessory anconeus.
WTF is an "Anconeus" ? It a piece of shit muscle that does nothing but get in the way of an
orthopedic scope. It's normally on the lateral side the elbow. You can have an "Accessory
Anconeus" - also called an "Anconeus Epitrochlearis" - on the medial side which will exert
mass effect on the ulnar nerve.
Anatomic Trivia: The site where the ulnar nerve passes beneath the cubital tunnel
retinaculum also known as the epicondylo-olecranon ligament or Osborne's ligament.
Cubital Tunnel Syndrome
NORMAL
Secondary to an Accessory Anconeus
\
\
Ulnar Nerve
Posterior Band of the UCL
Accessory Anconeus" AKA
"Anconeus Epitrochlearis"
Lateral Epicondylitis (more common than medial) - seen in Tennis Players -
• Extensor Tendon Injury (classically extensor carpi radialis brevis)
• Radial Collateral Ligament Complex - Tears due to varus stress
Medial Epicondylitis (less common than lateral) - seen in go(fers
• Common flexor tendon and ulnar nerve may enlarge from chronic injury
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Partial Ulnar Collateral Ligament Tear:
For the exam all you really need to know is
that throwers (people who valgus overload)
hurt their ulnar collateral ligament (which
attaches on the medial coronoid - sublime
tubercle). The ligament has three bundles,
and the anterior bundle is by far the most
important. If you get any images it is most
likely going to be of the partial UCL tear,
described as the "T sign," with contrast
material extending medial to the tubercle.
Normal T-Sign
"UCL Partial Tear"
Little Leaguer Elbow
The children of insecure men who sucked at sports in high school are most
susceptible to this injury. The mechanism is repetitive micro-trauma from
endless hours of training (necessary to finally rectify the injustice which
beset their family when dad was benched senior year from the junior varsity
baseball squad).
We are talking about a repetitive
chronic injury to the medial
epicondyle. When I say injury I mean
stress fracture, avulsion, or delayed
closure of the medial epicondylar
apophysis. This is usually associated
with UCL injury.
Children aren't the only ones who can
fuck up their elbows pursuing the kind
of immortality that is only offered to
those worthy enough to step foot on
the field at Yankee stadium. There is a
well described "valgus overload
syndrome" seen in throwers,
consisting of a triad of lateral
compression, medial tension, and
posterior sheer. This mechanism
results in UCL injmy (often anterior
band), Arthritis at the Posterior
Humems / Ulna, and the development
of an OCD at the capitellum.
Epitrochlear Lymphadenopathy - This is a classic look for cat-scratch disease.
Dialysis Elbow: This is the result of olecranon bursitis from constant pressure on the area, related to
positioning of the arm during treatment.
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Biceps Tear
Tears can be partial or complete. When complete the tear typically occurs in shoulder with the
tendon avulsing off the labrum (or at the level of the bicipital groove).
Common mechanism is incorrect deadlift form (while doing cross fit like an ape on cocaine). If
you plan on going nuts slinging that shit around consider switching to a double over grip. If you
want to use over under grips - you need strict form (keep your arms locked out dummy). There
are tons of highlight reals on youtube of people tearing biceps while deadlifting - notice every
single one is using an over under grip, and not maintaining straight arm technique.
.L Partial Biceps Tear - Gamesmanship
\J'l9 -Partial tears often are associated with bicipitoradial bursitis
Patients present with a painful mass in the antecubital fossa (rolled up muscle) - with the classic
history of "trying to impress the girl in the pink spandex sports bra with my deadlift." This rolled
up muscle is sometimes referred to as the "Popeye Deformity" - in reference to my childhood
hero - a heavily muscled blue collar worker, who smokes, and solves his all of his problems with
violence.
Sneaky: Injury to the bicep is associated with median nerve symptoms
Tricep Rupture
The tricep tendon has the honorable distinction of being the LEAST
common tendon in the body to rupture. Even tendinopathy is fairly
uncommon relative to other nearby structures. When it does tear you Normal
should be thinking about salter harris II fractures of the olecranon Striations
that is the classic scenario.
I think because this is so uncommon that mimics would be more likely
on the exam. So, I'd be aware of two things: (1) the normal striated
appearance of the inse1iion at the olecranon, and (2) the common entity
of olecranon bursitis - which you should think of first if you see a
bunch of fluid signal in the posterior elbow.
Elbow Dislocation
This is the second most common joint dislocated in the adult. The associated fractures
are usually the radial head and the coronoid process.
Instability in the elbow (so called Posterior Rotary Instability) is described in a
pattern starting in the posterior lateral corner with tearing of the lateral UCL.
+
Partial Dislocation Dislocation
➔
Tearing of the Coronoid Perched on Coronoid Posterior
LUCL Trochlea to Humerus with a
(lateral UCL). UCL Tear
(LUCL + LCL + Capsule)
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Site-Specific Entities - Shoulder
Dislocation:
• Anterior inferior (subcoracoid) are by far the most common (like 90%).
o Hill-Sachs is on the Humerus.
o Hill-Sachs is on the posterior lateral humerus, and best seen on internal
rotation view.
o Bankart- anterior inferior labrum
o Greater tuberosity avulsion fracture occurs in 10-15% of anterior dislocations
in patient's over 40.
• Posterior Dislocation: uncommon - probably from seizure or electrocution
o Rim Sign - no overlap glenoid and humeral head
o Trough Sign - reverse Hill Sachs, impaction on anterior humerus
o "Light Bulb Sign" - Arm may be locked in internal rotation on all views
• Inferior Dislocation (luxatio erecta humeri) - this is an uncommon form, where the
arm is sticking straight over the head. The thing to know is 60% get neurologic
injury (usually the axillary nerve).
Posterolateral humeral head CB111111111�fl.� Memory Tool
Hill-Sachs impaction fracture (anterior
dislocation) I remember that hip dislocations are
posterior - from the straight leg
Anterior Glenoid Rim dashboard mechanism.
Bankart
(anterior dislocation)
Anterior humeral head impaction Then I just remember that shoulders
Trough Sign are the opposite of that (the other
fracture (posterior dislocation)
one, is the other one).
Reverse Posterior Glenoid Rim
Bankart (posterior dislocation) Shoulder == Usually Anterior
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Proximal Humerus fracture:
This is usually in an old lady falling on an out stretched arm. Orthopods use the Neer
classifications (how many parts the humerus is in?). Three or four part fractures tend to do
worse.
The Post Op Shoulder (Prosthesis)
There are 4 Main Types: Humeral Head Resurfacing, Hemi-Arthroplasty, Total Shoulder
Arthroplasty, and the Reverse Total Shoulder Arthroplasty.
What is this "reverse total shoulder" ?
A conventional total shoulder mimics normal
anatomy. A reserve total shoulder is the bizan-o
version; with a plastic cup on the humeral head
and metallic sphere on the glenoid.
Conventional Reverse
Who gets what?
The surgical choice
depends on two main Resurfacing Hemi or
factors: or Hemi Reverse
( 1) Is the Cuff Intact?
(2) Is the Glenoid
Trashed ? TSA Reverse
Complications / Trivia:
-Total Shoulder Most Common Complication = Loosening of the Glenoid Component
-Total Shoulder Complication - "Anterior Escape" - This describes anterior migration of
the humeral head after subscapularis failure.
-Reverse Total Shoulder Does NOT require an intact rotator cuff - patient rely heavily on
the deltoid.
-Reverse Shoulder Complication - Posterior Acromion Fracture - from excessive deltoid
tugging.
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Impingement / Rotator Cuff Tears:
This is a high yield/ confusing subject that is worth talking about in a little more detail. In
general, rotator cuff pathology is the result of overuse activity (sports) or impingement
mechanisms. There are two types of impingement with two major sub-divisions within those
types. Like many things in Radiology, if you get the vocabulary down, the pathology is easy to
understand.
External: This refers to impingement of the rotator cuff overlying the bursal surfaces
(superficial surfaces) that are adjacent to the coracoacromial arch. As a reminder, the arch is
made up of the coracoid process, acromion, and coracoacromial ligament.
Primary External Causes (Abnormal Coracoacromial Arch):
• The hooked acromion (type III Bigliani) is more associated with external impingement
than the curved or flat types.
• Subacromial osteophyte formation or thickening of the coracoacromial ligament
• Subcoracoid impingement: Impingement of the subscapularis between the coracoid
process and lesser tuberosity. This can be secondary to congenital configuration, or a
configuration developed post traumatically after fracture of the coracoid or lesser
tuberosity.
Secondary External Causes (Normal Coracoacromial Arch):
• "Multidirectional Glenohumeral Instability" - resulting in micro-subluxation of the
humeral head in the glenoid, resulting in repeated micro-trauma. The important thing to
know is this is typically seen in patients with generalized joint laxity, often involving both
shoulders.
Internal: This refers to impingement of the rotator cuff on the undersurface (deep surface)
along the glenoid labrum and humeral head.
• Posterior Superior: This is a type of impingement that occurs when the posterior superior
rotator cuff (junction of the supra and infraspinatus tendons) comes into contact with the
posterior superior glenoid. Best seen in the ABER position, where these tendons get
pinched between the labrum and greater tuberosity. This is seen in athletes who make
overhead movements (throwers, tennis, swimming).
• Anterior Superior: This is internal impingement that occurs when the arm is in horizontal
adduction and internal rotation. In this position, the undersurface of the biceps and
subscapularis tendon may impinge against the anterior superior glenoid rim.
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Impingement Continued ...
Primary
*Abnormal Coracoacromial Arch __.. Subacromial
- Hook Shaped (83) *F's With Supra S
- Osteophytes
-Post Traumatic __.. Subcoracoid
-Thickened Ligaments *F's With Sub S
External
Secondary
*Multidirectional Instability
-Labrum Often Normal
-"Increased Glenohumeral
Volume" - with injection
Posterior Superior --------- If the exam writers
*T hrowers just say "Internal
-F's with lnfraspinatus (and posterior Supra) Impingement"
-Posterior Superior Labrum Torn this is the one
-Cystic Change in Greater Tuberosity they are talking
Internal about
� Anterior Superior
-Associated with Sub Scapular damage
(Maybe the cause rather than the result)
-Anterior Superior Labrum Torn
High Yield Trivia Points on Impingement
Subacromial Impingement - most common
form, resulting from attrition of the Damages Supraspinatus Tendon.
coracoacromial arch.
Damages Subscapularis (remember the
Subcoracoid Impingement - Lesser
coracoid is anterior - and so is the
tuberosity and coracoid do the pinching.
subscapularis).
Posterior Superior "Internal" Impingement
- Athletes who make overhead movements. Damages lnfraspinatus (and posterior
Greater tuberosity and posterior inferior fibers of the supraspinatus).
labrum do the pinching.
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Rotator Cuff Tears:
People talk about these tears as
either "Bursa! Sided" (meaning the
top part), or "Articular
Sided" (meaning the undersurface).
A tear of the articular surface is
more common (3x more) than the
bursal surface. The underlying
mechanism is usually degenerative,
although trauma can certainly play a
role.
The most common of the four muscles to tear is the Supraspinatus - with most tears
occun-ing at the "critical zone" - I-2 cm from the tendon footprint. This relatively
avascular "critical zone" is also the most common location for Calcium Hydroxyapatite
(HADD) - or "calcific tendinitis." The Teres Minor is the least common to tear.
A partial tear that is > 50% often results in a surgical intervention.
"Massive rotator cuff tear" - refers to at least 2 out of the 4 rotator cuff muscles.
A final general piece of trivia is that a tear of the fibrous rotator cuff interval (junction
between anterior fibers of the Supraspinatus and superior fibers of the subscapularis), is still
considered a rotator cuff tear.
How do you know it�· a.full thickness tear? You will have high T2 signal in the expected
location of the tendon. On T l you will have Gad in the bursa.
Full
Thickness
Tear
- With Gad
crossing over
the cuff into
the bursa.
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Adhesive Capsulitis "Frozen Shoulder"
An inflammatory condition characterized by a global decrease in motion. You can have
primary types, but a multiple choice key would be a history of trauma or surgery.
It most commonly effects the rotator cuff interval - and that is the most likely spot they
will show it. The classic look is a Tl (or non-fat sat T2) in the sagittal plane showing loss
offat in the rotator cu;,(finterval (the spot with the biceps tendon - between the Supra S,
and the Sub Scap).
Grey Smudgy Shit Instead of Clean Fat in the Rotator Cuff Interval
BUZZWORD: "Decreased Glenohumeral Volume" - with injection
� ** Remember in Multi-Directional Instability the volume was increased.
/
BUIZW�DS: "Thickened Inferior and Posterior Capsule"
�
') "Enhancement ol the Rotator CuffInterval" - Post gad
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Injury to the Labrum:
SLAP: Labral tears favor the superior margin and track anterior to posterior. As this tear
involves the labrum at the insertion of the long head of the biceps, injury to this tendon is
associated and part of the grading system (type 4).
Things to know about SLAP tears:
• When the SLAP extends into the biceps anchor (type 4), the surgical management
changes from a debridement to a debridement + biceps tenodesis.
• The mechanism is usually an over-head movement (classic = swimmer)
• People over 40 usually have associated Rotator Cuff Tears
• NOT associated with Instability (usually)
SLAP Mimic - The Sublabral Recess. This is essentially a normal variant where you have
incomplete attachment of the labrum at 12 o'clock. The 12 o'clock position on the labrum
has the shittiest blood flow - that's why you see injury there and all these development
variants.
Follows Contour of Glenoid Extends Laterally
SMOOTH Margin Ratty Margin
Located at Biceps Anchor Located at Biceps Anchor & Posteriorly
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Labral Tear Mimic - The Sublabral Foramen
- This is an unattached (but present) portion of
the labrum - located at the anterior-superior
labrum (1 o'clock to 3 o'clock).
As a rule it should NOT extend below the
equator (3 o'clock position).
Labral Tear Mimic - The Buford Complex - A commonly tested (and not infrequently
seen) variant is the Buford Complex. It's present in about 1 % of the general population. This
consists of an absent anterior/superior labrum (1 o'clock to 3 o'clock), along with a
thickened middle glenohumeral ligament.
Buford Complex:
- Thick Middle GH Ligament
- Absent Anterior Superior Labrum
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Bankart Lesions:
There is an alphabet soup of Bankart (anterior dislocation) related injuries.
GLAD Perthes ALPSA Bankart Bankart
(Cartilaginous) (Osseous)
GLAD= Glenolabral Articular Disruption. It's the most mild version, and it's basically a
superficial anterior inferior labral tear with associated articular cartilage damage
("impaction injury with cartilage defect"). Not typically seen in patients with underlying
laxity. It's common in sports. No instability (aren't you GLAD there is no instability)
Memory Aid:
-The detached
Perth es = Detachment of the anteroinferior labrum labrum sorta
(3-6 o'clock) with medially stripped looks like a
"P"
but intact periosteum.
ALPSA = Anterior Labral Periosteal Sleeve Avulsion. Medially displaced labroligamentous
complex with absence of the labrum on the glenoid rim. Intact periosteum. It scars down to
glenoid.
True Bankart: Can be cartilaginous or osseous. The periosteum is disrupted. There is
often an associated Hill Sach's fracture.
GLAD 'eerthes ••. iLPSA > ··.•·.
.
Truemmkart
Superficial partial Avulsed anterior Similar to perthes but Torn labrum
labral injury with labrum (only with "bunched up"
cartilage defect minimally displaced). medially displaced
inferior GH complex
Inferior GH complex
still attached to
periosteum
No instability Intact Periosteum Intact Periosteum Periosteum Disrupted
(lifted up)
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Posterior Glenohumeral Instability
As I mentioned previously, anterior shoulder dislocations are way more common than posterior
shoulder dislocations. Therefore the Bankart, ALPSA, Perthes, etc ... are the ones you typically
think of as the stigmata of prior dislocation.
However, all that shit can happen in reverse with a posterior dislocation.
Reverse Osseous Bankart: POLPSA:
This is the bizarro
version of the
ALPSA, where the
A fracture of the
posterior labrum and
posterior inferior
the posterior
rim of the
scapular periosteum
glenoid.
(still intact) are
stripped from the
glenoid resulting in
a recess that
communicates with
"Bennett Lesion" the joint space.
An extra-articular curvilinear
calcification - associated with posterior "Kim's Lesion"
labral tears (maybe the POLPSA).
An incompletely
It's related to injury of the posterior avulsed / flattened /
band of the inferior glenohumeral mashed posterior
ligament. inferior labrum.
A key (testable)
point is the glenoid
cartilage and
posterior labrum
relationship is
preserved.
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HAGL:
A non-Bankart lesion that is frequently tested is the HAGL (Humeral avulsion
glenohumeral ligament). This is an avulsion of the inferior glenohumeral ligament, and
is most often the result of an anterior shoulder dislocation (just like all the above bankarts).
The "J Sign" occurs when the normal U-shaped inferior glenohumeral recess is retracted
away from the humerus, appearing as a J.
Axial MR - Showing the IGHL
Torn at its Humeral Attachment
Subluxation of the Biceps Tendon: The subscapularis attaches to the lesser
tuberosity. It sends a few fibers across the bicipital groove to the greater tuberosity , which
is called the "transverse ligament". A tear of the subscapularis opens these fibers up and
allows the biceps to dislocate (usually medial). Subscapularis Tear = Medial Dislocation
of the Long Head of the Biceps Tendon.
Subluxation of the Biceps Tendon
Sub Scap Tendon - Forming Occurs with a Tear of the Subscapularis
portions of the "Transverse
Ligament" that holds the biceps
tendon in the groove
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Nerve Entrapment: High Yield Trivia:
Suprascapular Notch vs Spinoglenoid Notch: A cyst at the level of the
suprascapular notch will affect the supraspinatus and the infraspinatus. At the level of the
spinoglenoid notch, it will only affect the infraspinatus.
Cyst in the spinoglenoid notch causing
fatty atrophy of the lnfraspinatous
***Dotted Line = Suprascapular
Quadrilateral Space Syndrome: Compression of the Axillary Nerve in the
Quadrilateral Space (usually from fibrotic bands). They will likely show this with atrophy
of the teres minor. Another classic question is to name the borders of the quadrilateral
space: Teres Minor Above, Teres Major Below, Humeral neck lateral, and Triceps medial.
Humerus
Quadrilateral Space Syndrome
-Atrophy of Teres Minor
Parsonage-Turner Syndrome: This is an idiopathic involvement of the brachia]
plexus. Think about this when you see muscles affected by pathology in two or more nerve
distributions (suprascapular and axillary etc.. ).
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Site-Specific Entities - Hip / Femur / Sacrum
Femoral Shaft Fractures:
• On the inside (medial) is the classic
stress fracture location
• On the outside (lateral) is the classic
bisphosphonate related fx location.
As shown in the image, you see cortical
thickening (white arrow) along the lateral
femur, eventually progressing into a
fracture.
Hip Fracture / Dislocation:
You see these with dash board injuries. The
posterior dislocation (almost always associated
with a fracture as it's driven backwards) is much
more common than the anterior dislocation.
BUZZWORD:
"Foot in internal rotation"
Anterior Column vs Posterior Column - the
acetabulum is supported by two columns of bone
that merge together to form an "inverted Y"
lliopectineal Line = Anterior
llioischial Line = Posterior (remember you sit on your ischium)
The both column fracture by definition divides the ilium proximal to the hip joint, so you have no
articular surface of the hip attached to the axial skeleton (that's a problem).
Corona Mortis: The anastomosis of the inferior epigastric and obturator vessels sometimes rides
on the superior pubic ramus. During a lateral dissection - sometimes used to repair a hip fracture
- this can be injured. I talk about this more in the vascular chapter.
Hip Fracture Leading to AVN: The location of the fracture may predispose to AYN. It's
important to remember that, since the femoral head gets vascular flow from the circumflex
femorals, a displaced intracapsular fracture could disrupt this blood supply - leading to
AVN. Testable Point: Degree of fracture displacement corresponds with risk of AVN.
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Avulsion Injury:
This is seen more in kids than adults. Adult bones are stronger than their tendons. In kids it's the
other way around. One pearl is that if you see an isolated "avulsion" of the lesser trochanter
in a seemingly mild trauma/ injury in an adult - query a pathologic fracture. Now, to
discuss what I believe to be one of the highest yield topics in MSK, "where did the avulsion
come.fi·om?"
The easiest way to show this is a plain film pelvis (or MRI) with a tug/avulsion injury to one of
the muscular attachment sites. The question will most likely be "what attaches there?" or
"which muscle got avulsed?"
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Snapping Hip Syndrome:
The clinical sensation of "snapping" or "clicking" with hip flexion and extension.
The key point is that it is clinical. This is the way people work this thing up:
Clinical Eval for the "External Type"
(IT band "snapping" over the Greater Trochanter)
This is to evaluate for the "Intra-Articular Type"
Looking for Hip Degen / Loose Bodies, Etc
IF NO Degen
NEXT STEP = Ultrasound
This is to look for the "Internal Type"
Look for Dynamic "Snapping" of the
Iliopsoas over the Iliopectineal eminence or femoral head
*This has to be shown with a CINE - because the finding is a dynamic moving of a tendon
ff you see a hip ultrasound/or snapping - this is what they are going for
IF US Negative
NEXT STEP = MRI Arthrogram
This is to evaluate for the "Intra-Articular Type" ... Again
This time looking for Labral Tears
Trivia:
• "Snapping Hip" is a "clinical sensation" - they have to tell you that patient feels "snapping"
• The 3 Types, and the Work-Up Algorithm Above:
• Types:
• External (most common) = Iliotibial Band over Greater Trochanter
• Internal = Iliopsoas over Iliopectineal eminence or femoral head
• Intra-Articular = Labral tears I joint bodies
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IT Band Syndrome
This is a repetitive stress syndrome seen most classically in runners.
The key finding is fluid on both sides of the IT band, extending
posterior and lateral.
Fluid in the joint does not exclude the diagnosis, but for the purpose of
multiple choice if you see fluid around the band and none in the joint
you can be fairly certain this is the pathology the question writer is
after.
Hip Labrum
This is complicated and l 'm not going to go into depth talking about all the little bumps
and variants. I would just know a few things:
1 : Anterior-Superior Tears (white
arrows) are by far the most common.
2: Paralabral Cysts (black arrow) are
associated with tears and likely a hint
that a tear is present.
3: Just like a shoulder intra-articular Coronal View Sagittal View
contrast will increase your sensitivity. -Showing the classic anterior superior cleft of a tear
Gamesmanship: A fluid signal "mass" with anterior to
the femur (adjacent to the psoas tendon) at the level of
I liopsoas Bursa the ischial tuberosity is likely Iliopsoas Bursitis
• Largest bursa of the entire body.
• Communicates with the joint in 15% of the population
• Seen Anterior to the hip
• Trivia: The illiospsoas tendon runs anterior to the labrum
on axial and can mimic a tear.
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femoroacetabular Impingement (FAI): This is a syndrome of painful hip movement.
It's based on hip/ femoral deformities, and honestly might be total BS. Supposedly it can lead to early
degenerative changes. There are two described subtypes: (A) Cam and (B) Pincher (technically there is a
mixed type - but I anticipate multiple choice to make it more black and white).
CAM Type: This is an osseous "bump" along the femoral head-neck junction.
Memory Aid
I remember that the femoral one (cam-type)
is more common in men because the femoral
head kinda looks like a penis.
Normal Cam-Type Be honest, you were thinking that too.
Pincer Tvpe: Whereas the CAM type is a deformity of the femur, the pincer type represents a deformity of
the acetabulum. Whereas the CAM type is more common in a young athletic male, the pincer is more
common in a middle aged woman (insert sexist joke here).
The most classic way to show or ask this is the so-called
"cross over sign", where the acetabulum is malfonned -
causing the posterior lip to "Cross over" the anterior lip. A
Key point is that the coccyx needs to be centered at the
symphysis pubis to even evaluate this (rotation fucks things
up).
The other associated finding(s) of the pincer subtype wmih
knowing are the acetabular over coverage buzzwords
(Coxa Profunda and Protrusio), and the Ischial Spine Sign:
Normal Coxa Profunda Acetabular Protrusion Prominent
(Acetabulum projects medial to (Femur projects medial to the Ischial Spine
the ilioischial line) ilioischial line)
Classic FAI Association: Os Acetabuli
This is an unfused secondary
• Os Acetabuli (40%) ossification center. It's actually normal
in kids (should fuse by adult hood).
• Labral Tears It has several testable associations
• Early Arthritis including FAI and Labral Tears
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Total Hip Arthroplastv
Bone Remodeling/ Stress Shielding: Proximal stress shielding -
greater trochanter
The stress is transferred through the bone resorption
metallic stem, so the bone around it is not
loaded. Otihopods call this "Wolff's Law"
- where the unloaded bone just gets
resorbed.
Calcar
Happens more with uncemented Resoption
arthroplasty. To some degree this is a
normal finding - but when advanced can
predispose to fracture.
Potentially Asymptomatic
Complications of Hip
Arthroplasty: Distal stress loading: cortical
thickening & pedestral (around
• Stress Shielding the bottom)
• Aggressive Granulomatosis "Zone 4"
Heterotopic Ossifications: This is very common (15-50%). It's usually asymptomatic. The trivia
regarding multiple choice tests is that "hip stiffness" is the most common complaint.
Also in Ank Spon patients, because they are so prone to heterotopic ossifications, they sometimes
give them low dose prophylactic radiation prior to THA.
Aseptic Loosening: This is the most common indication for revision. The criteria on x-ray is > 2
..
mm at the interface (suggestive). If you see migration of the component, you can call it
(migration includes varus tilting of the femoral stem).
Subsidence: Basically an arthroplasty
----- .- --------1
that is sliding downward. This is a -- ·
---
_""'! ___•
described reason for early failure of
THA. You see this most often in
arthroplasty implants without a
collar. baseline follow up
Greater than 1 cm along the
femoral component , or Distance from the tip of the greater
trochanter to the superolateral
progression after 2 years are shoulder of the stem is increased
indications of loosening. relative to baseline.
Wear Patterns: It is normal to have a little bit of thinning in the area of
weight bearing -- this is called "Creep." It is not normal to see wear
along the superior lateral aspect. Wear
• Wear = Pathologic
• Creep = Normal
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Total Hip Arthroolastv Continued -
Particle Disease (Aggressive Granulomatosis): Any component of the device that sheds will
cause an inflammatory response. The more wear that occurs the more particles - wear is the
primary underlying factor. Macrophages will try and eat the particles and spew enzymes all over
the place. This process can cause progressive lytic focal regions around the replacement and joint
effusions.
Things to know about particle disease (in THA):
• Most commonly seen in non-cemented hips
• Tends to occur 1-5 years after surgery
- "late complication"
• X-ray shows "smooth" endosteal scalloping
(distinguishes from infection)
• Aseptic - ESR & CRP will be normal
• Produces no secondary bone response
- no sclerosis
• Can be seen around screw holes (particles are
transmitted around screws)
I Wear � Particle Disease � Osteolysis
Wear= Arrow
Sacrum:
You can get fractures of the sacrum in the setting of trauma, but if you get shown or asked
anything about the sacrum it's going to be either (a) SI degenerative change - discussed later,
(b) unilateral SI infection, (c) a chordoma - discussed later, (d) sacral agenesis, or (e) an
insufficiency fracture. Out of these 5 things, the insufficiency fracture is probably the most
likely.
Sacral Insufficiency Fracture - The most
common cause is postmenopausal osteoporosis.
You can also see this in patients with renal failure,
patients with RA, pelvic radiation, mechanical
changes after hip arthroplasty, or extended
steroid use. They are often (usually) occult on
plain films.
They will have to show this either with a bone
scan, or MRL The classic "Honda Sign" from the
"H" -shaped appearance is probably the most likely
"Honda Sign"
presentation on a multiple choice test. Sacral Insufficiency Fx
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Site-Specific Entities .. Knee / Tibia / Fibula
Segond Fracture:
This is a fracture of the Lateral Tibial Plateau
(common distractor is medial tibia). The thing to
know is that it is associated with ACL tear (75%),
and occurs with internal rotation.
Reverse Segond Fracture:
This is a fracture of the Medial Tibial Plateau. The
thing to know is that it is associated with a PCL
tear, and occurs with external rotation. There is
also an associated medial meniscus injury.
Arcuate Sign:
This is an avulsion of proximal fibula (insertion of
arcuate ligament complex). The thing to know is
that 90% are associated with cruciate ligament
injury (usually PCL)
Deep lntercondylar Notch Sign:
This is a depression of the lateral femoral condyle
(terminal sulcus) that occurs secondary to an impaction
injury. This is associated with ACL tears.
Anatomy Blitz:
Ligaments: ACL & PCL arc extrasynovial and intra
articular. The synovium folds around the
• ACL: Composed of two bundles (anteromedial & ligaments. This is why a torn ACL won't
posterolateral). The tibial attachment is thicker then heal on its own (usually).
the femoral attachment. Both the ACL and PCL are
intra-articular and extrasynovial. The ligament can be torn even if the
synovium is intact - this is why the
• PCL: The strongest ligament in the knee (you don't "taunt" angle of the ligament is a key
feature of integrity - more on that later
want a posterior dislocation of your knee resulting
in dissection of your popliteal artery).
• MCL: The MCL fibers are laced into the joint capsule
at the level of the joint, with connection to the medial
meniscus. Unlike the ACL and PCL, the MCL is an
extra-articular structure.
• Conjoint Tendon: Formed by the biceps femoris
tendon and the LCL.
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Magic Angle Phenomenon
The PCL and Patellar tendon may have foci of intermediate signal intensity on sagittal
images with short echo time (TE) sequences where the tendon forms an angle of 55 degrees
with the main magnetic field (magic angle phenomenon).
This will NOT be seen on T2 sequences (with long TE). This phenomenon is reduced at
higher field strengths due to greater shortening of T2 relaxation times.
Magic Angle: You see it on short TE sequences (Tl, PD, GRE). It goes away on T2
ACL Tear: ACL tears happen all the time, usually in
people who are stopping and pivoting.
• Associated with Segond Fracture (lateral tibial
plateau) and tibial spine avulsion
• ACL Angle lesser than Blumensaat's Line
• O'donoghue's Unhappy Triad: ACL Tear, MCL
Tear, Medial Meniscal Tear
• Classic Kissing Contusion Pattern: The lateral
femoral condyle (sulcus terminals) bangs into the
posterior lateral tibial plateau. This is 95% specific
in adults.
• Anterior Drawer Sign = Ortho Physical Exam ACL Tear
Finding suggesting ACL Tear. -Kissing Contusion Pattern
ACL Mucoid Degeneration:
This can mimic acute or chronic partial
tear of the ACL. There will be no
secondary signs of injury (contusion
etc..). It predisposes to ACL ganglion
cysts, and they are usually seen
together. The T2/STIR buzzword is
"celery stalk" because of the striated
look. The Tl buzzword is
"drumstick" because it looks like a
drum stick. Mucoid Degeneration of the ACL
- "Drumstick I Celery Stick"
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ACL Repair:
ACL can be repaired with two primaiy methods. Method 1: Using the middle one-third of the
patellar tendon, with the patella bone plug attached to one end and tibial bone plug attached at the
other. Method 2: Using a graft made of the semitendinosus or gracilis tendon, or both. The graft is
then attached with all sorts of screws, bolts, etc ... There is a lower reported morbidity related to
harvest site using this method.
Graft Evaluation:
,
There are two tunnels (tibial and femoral) between which the graft
runs. Here arc the testable pearls:
Tibial Tunnel: Should parallel the roof of the femoral intercondylar
notch. Too Steep = Impinged by femur on extension. Too Flat = Lax
& won't provide stability. Too Far Anterior ("Intersection with
Blumensaat line") = Can lead to pinching at the anterior inferior Normal ABnormal
Tibial Tunnel Steep & Anterior to B
intercondylar roof. Buzzword "Rooflmpingement." Line (both are bad)
Femoral Tunnel: Supposedly the primary factor for maintaining length and tension during range of
motion. This is referred to as "maintained isometry."
Femoral Tunnel = Maintains Isometry. Tibial Tunnel = Roof Impingement.
"Arthrofibrosis" Can be focal or diffuse
(focal is more common). The focal form
is the so called "Cyclops" lesion - so
named because of its arthroscopic
appearance. It's gonna be a low signal
mass-like scar in Hoffa's fat pad. It's bad
because it limits extension.
Buzzword ''palpable audible clunk"
Seen around 16 weeks - it obviously
won't occur immediately post op because
you have to build up your scar. Cyclops Lesion - Scar Associated with Ventral Graft
"Graft Tear" - Usually Ortho can just pull on his fucking leg
Fern,_ Femur
is see if the graft is trashed (anterior drawer sign). For
imaging, the simple way to understand this: "flat angle = tear."
The ACL should parallel the roof of the intercondylar notch.
If the angle becomes flat, a tear is likely.
Tibia,
T,·ivia: The graft is most susceptible to tear in the remodeling
process (4-8 months post op). Normal Angle Flat
Trivia: Other signs of graft tear: grossly high T2 signal (some is ok), fiber discontinuity, uncovering
of the posterior horn of the lateral meniscus (secondary sign), anterior tibial translation (secondaiy
sign).
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Posterior Lateral Corner (PLC): The most complicated anatomy in the entire body.
My God this posterior lateral corner! Just think about the LCL, the IT band, the biceps
femoris, and the popliteus tendon. The most likely way to show this on a single image
(multiple choice style) is edema in the fibular head.
Who cares? Missed PLC injury is a very common cause ofACL reconstruction failure.
PCL Tear: The posterior collateral ligament is the strongest ligament in the knee. A tear
is actually uncommon, it's more likely to stretch and appear thickened ( > 7 mm). PCL tears
should make you think about posterior dislocation as the mechanism ofinjury..
Next Step I Association = lfyou see a PCL Tear - look at the popliteal flow void. Ifthe knee
dislocated posterior, a dreaded consequence is vascular compromise. Depending on the wording
ofthe question they might need a run-off (watch your back).
Meniscal Anatomy:
The meniscus is "C
shaped", thick along the
periphery and thin
centrally.
Medial meniscus is
thicker posteriorly.
Lateral meniscus has
equal thickness between
anterior and posterior
portion.
Meniscal Healing
The Peripheral "Red Zone" is vascular and
might heal.
The Central "white zone" is avascular and will
not heal. The blood supply comes from the
geniculate arteries (which enter peripherally).
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Meniscal Tears:
As stated, the peripheral meniscus (red zone) has better vasculature than the inner 2/3s (white zone) and
might heal on its own. In general, you can group tears based on their general direction (as seen on a
sagittal section MRI - i.e. the triangles and bowties) - as either vertical (top-to-bottom) or horizontal
(front-to-back). You can then sub-group them depending how they look on subsequent sections.
Radial Tear:
- Bad because they
cause "loss of hoop
strength." Radial Tearing
- Can lead to extrusion, Cuts the Circular
Hoop Fibers that
early OA etc .. Hold the Meniscus
Together
Flap Tear {Parrot Beak):
- Radial Tear that Changes
Direction into the
longitudinal direction
Longitudinal Tear:
- Can be vertical or
horizontal (or mixed
oblique patterns)
- Defined by a long
extension in the axial
direction
- Vertical Types can flip
(bucket- handle)
Horizontal Cleavage Tear:
- Pure cleavage tears extend to
the apex
Idealized Horizontal Tear - Associated with Meniscal Cysts
- Most common in posterior horn
of the medial meniscus
Radial Tears: There are 3 classic Signs - two of which are usually present.
.--, ...
I
I
I
L---A
I
I
I
r-------,
I
I
I
:+aa
I
l________
Truncated Triangle Cleft - Most Reliable "Ghost" or Absent Triangle
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Bucket Handle Tear:
Discoid Meniscus:
This is a torn meniscus (usually medial -
This is a normal variant of the lateral meniscus , 80%) vertical longitudinal sub-type, that flips
. that is prone to tear. It's not C-shaped, but • medially to lie anterior to the PCL.
instead shaped like a disc. In other words, it's too
• big (too many bowties!). ! Gamesmanship - Most likely shown as the
· classic Aunt Minnie appearance of a "double
: Gamesmanship - "Pediatric Patient with Mcniscal PCL."
Tear".
Trivia - There are three types, with the most rare
· and most prone to injury being the Wrisberg
Variant.
: Gamesmanship "Bow Ties" If shown on sagittal
' they have to show you 3 or more "bow ties" /
double triangles.
Buckle Hand Tear
-Double PCL Sign
Gamesmanship - Can also be shown as "not
: enough bowties," the opposite of the "too
'. many bowties" look of a discoid meniscus.
Only I
bowtie
Normal Meniscus will have 2 bowtie shapes in the instead of
• sagittal plane - assuming 3mm slices with 1mm the
gap. normal 2.
Discoid Meniscus will have 3 or more bowties The
middle of
the second
bowtie is
flipped
Gamesmanship: If medially.
· shown on coronal they
need to show you a
meniscus stretching
into the notch. · Trivia: The appearance of a double PCL can
. only occur in the setting of an intact ACL,
otherwise it won't flip that way. Just know it
· sorta indirectly proves the ACL is intact (I
· can just see some knucklehead asking that).
Discoid Meniscus
-Extending into Notch
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Meniscal Cysts:
Bakers Cyst:
Most often seen near the lateral meniscus and are often Occurs between the
associated with horizontal cleavage tears. semimembranosus and the
MEDIAL head of the gastroc
Meniscocapsular Separation:
This is a rare (in real life - maybe not on exams) injury. The idea is that the deepest layer of the
MCL complex (capsular ligament) is relatively weak and is the first to tear. This deep tearing
may result in the separation of the meniscus and the MCL. I've never seen it occur in isolation
(theoretically it can). The important things to remember are probably (1) it happens more with
proximal MCL tears, and (2) this is a serious injury - requires immobilization or surgery.
Meniscal Ossicle:
This is a focal ossification of the posterior horn of the medial meniscus, that can be
secondary to trauma or simply developmental. They are often associated with radial root
tears.
Meniscofemoral Ligaments:
There are 2 (Wrisberg, Humphry) which can be mimics of meniscal tears. Wrisberg is in
the back ( "humping Humphry"). You could also remember that "H" comes before "W" in
the alphabet.
Meniscal Flounce:
This an uncommon finding of a "ruffled"
appearance of the meniscus that mimics a tear.
It's NOT associated with an increased incidence of
tear - but can look like one, if you don't have any
idea what one looks like.
"Flounce"
Ruffled= Not a Tear
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Patella Dislocation:
Dislocation of the patella is usually lateral
because of the shape of the patella and femur.
The contusion pattern is classic.
• It's Lateral
•Contusion Pattern - Classic
•Associated tear of the MPFL
(medial patellar femoral ligament)
•Associated with "Trochlear
Dysplasia" - the trochlea is too flat.
Patellar Dislocation
Patella Alta / Baja: Classic Contusion Pattern (arrows)
The patella will move up or down in certain
traumatic situations. If the quadricep tendon
i
tears you will get unopposed pull from the
patellar tendon resulting in a low patella
(Baja). If the patella tendon tears you will get
unopposed quadriceps tendon pull resulting in
a high patella (Alta).
The "classic" association with patellar tendon
tear (Alta) is SLE, (also can see in elderly,
trauma, athletics, or RA). Patella Alta Patella Baja
� "Bilateral patellar rupture" is a buzzword for chronic steroids.
/
Normal
Comparison
Prepatellar Fat Impingement Jumpers Knee
Bursitis Syndrome
High T2 Signal +
Fluid superficial High T2 Signal in Hoffa's Thickening of the
to the Patella Fat Inferior to the Patella Inferior Patella
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Tibial Plateau Fracture: This injury most commonly occurs from axial loading (falling
and landing on a straight leg). The lateral plateau is way more common than the medial. If
you see medial, it's usually with lateral. Some dude named Schatzker managed to get the
classification system named after him, of which type 2 is the most common (split and
depressed lateral plateau).
Pilon Fracture (Tibial plafond fracture): This injury also most
commonly occurs from axial loading, with the talus being driven into the
tibial plafond. The fracture is characterized by comminution and articular
impaction. About 75% of the time you are going to have fracture of the distal
fibula.
Tibial Shaft Fracture: This is the most common long bone fracture. It was also listed
as the most highly tested subject in orthopedic OITE exam (with regard to trauma), over the
last 8 years. Apparently there are a bunch of ways to put a nail or plate in it. It doesn't seem
like it could be that high yield for the CORE compared to other fractures with French or Latin
sounding names. I will point out that the tibia is one of the slowest healing bones in the body
(10 weeh).
Tillaux Fractures: This a Salter-Harris 3,
through the anterolateral aspect of the distal tibial
epiphysis.
Trivia: This pattern requires an open physis along the
lateral distal tibia. This is why you see this fracture
pattern in the window between the start of medial
physis fusion and the complete fusion of the lateral
physis (lateral physis typically closes around 12-15).
Trivia: The distal tibial growth plate closes from
medial to lateral (medial first).
Triplane Fracture: This is a Salter-Harris
4, with a vertical component through the
epiphysis, horizontal component through the
physis, and oblique through the metaphysis.
*The addition of the.fracture plane in the
posterior distal tibial metaphysis (coronal plane)
distinguishes this from the Tillaux.
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Maisonneuve Fracture:
This is an unstable fracture involving the medial tibial malleolus and/or disruption of the
distal tibiofibular syndesmosis.
The most common way to show this is to first show you the ankle with the
�
widened mortis, and "next step?" get you to ask for the proximal fibula - which
..,I will show the fracture of the proximal fibular shaft.
This fracture pattern is unique as the forces begin distally in the tibiotalar joint and then ride
up the syndesmosis to the proximal fibula.
Qp Trivia: The fracture does not extend into the hindfoot.
Wide Medial Malleolus Proximal Fibula Fracture
(+/- Medial Malleolus Fracture) - From upward force extension
- Distal Tibia.fibular syndesmosis ("the rippin and the tearin ") via the syndesmosis
+/- Deltoid Lig Injury
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Site-Specific Entities -Ankle [ the rest of it J / Foot
Casanova Fracture - If you see bilateral calcaneal fractures, you should "next step?" look
at the spine (Tl2-L2) for a compression or burst fracture. These tend to occur in axial loading
patterns (possibly from jumping out a window to avoid an angry husband).
Trivia:
• Peroneal tendons can become entrapped with lateral calcaneal fractures.
• Calcaneal fractures are the most common (60%) Tarsal Bone Fx
• Fractures of the calcaneus are either extra-articular or intra-articular - depends on subtalar joint
involvement. Intra-articular fractures will have a fracture line through the "critical angle of
Gissane"
Bohler s Angle - The line
drawn between the anterior
and posterior borders of the
calcaneus on a lateral view.
An angle less than 20
degrees, is concerning for a
Bohler's Angle (20-40) Critical Angle of Gissane (95-105)
fracture. "More Flat" (Less than 20) "More Flat" (More than 130)
Equals Calcaneal Fracture Equals Depression of the Posterior Facet
Stress Fracture of the 5th Metatarsal:
This is considered a high risk fracture (hard to heal).
Jones Fracture: This is a fracture
at the base of the fifth metatarsal, 1.5cm
distal to the tuberosity. These are placed
in a non-weight bearing cast (may
require internal fixation- because of risk
of non-union. StressFx---1►►
Avulsion Fracture of the 5th H"'
JonesFx---1►► �
Metatarsal:
This is more common than a jones
fracture. The classic history is a dancer. Avulsion Fx /
It may be secondary to tug from the
lateral cord of the plantar Os Peroneum
/
aponeurosis or peroneus brevis (this is (within peroneus longus)
controversial).
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Painful Os Peroneus Syndrome (POPS)
•Os Peroneus (accessory ossicle) is within the Peroneus LONGUS
•This ossicle is seen in about 10% of gen pop
•Stress reaction and pain can progress to tendon disruption = POPS
MR Key Findings: Edema in the os peroneus just before the peroneus
longus tendon enters the cuboid tunnel
Lisfranc Injury: This is the most common dislocation of the
foot. The Lisfranc joint is the articulation of the tarsals and
metatarsal bases. This joint is recessed creating a "keystone"
locking mechanism, and would make a good place to amputate if
you were a surgeon assisting in the Napoleonic invasion of
Russia. The Lisfranc ligament connects the medial cuneiform to
the 2nd metatarsal base on the plantar aspect.
•Can't exclude it on a non-weight bearing film
.�
•Associated fractures are most common at the base of the 2nd MT - "Fleck Sign"
,�
•Fracture non-union and post traumatic arthritis are gonna occur if you miss it
. � (plus a lawsuit).
,,,,
"Fleck Sign " - This is a small bony fragment A "fleck" of bone near
in the Lisfranc Space (between l st MT and 2n the base of the 2nd MT
MT) - that is associated with an avulsion of the
' '
can sometimes be the
only clue.
LF ligament.
<:09
&
Normal Homo-Lateral Divergent
--./ Mechanism =
3 Ligaments make up the
AxialLoad complex between the
medial cuneiform and
2nd MT.
Medial
The plantar band is the
strongest 2nd MT
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Anatomic Trivia Achilles Tendon
This is the largest tendon in the
body. It represents the fused
tendons of the gastrocnemius and
f x.tensor
� b unch O e gives Tibialis Anterior
the soleus muscles.
oone
,,, .
ten dons n t __ -"
�
It does NOT have a tendon
h
aS I · t abo u ,,,.,,,,. sheath, so it cannot have a
tenosynovitis (fluid in the sheath).
Instead inflammatory change
..------ · \
)
around the tendon is refened to
as a "paratendinitis."
I Tibia
Fibula
-� Tibialis Posterior "Tom"
• ,, Flexor Digitorum Longus
Peroneus Tibial Nerve
Longus "' Flexor Hallucis Longus "Harry"
Peroneus "--
Brevis
Achilles
The Mythical Master Knot of Henry - This has a funny sounding name, therefore it's high
yield. This is where Dick (FDL) crosses over Harry (FHL) at the medial ankle.
Harry (white) starts out lateral relative to Dick (black). They cross at the "master knot" and then
Harry (white) ends up medial on it's way to the big toe (Harry= Hallucis).
What is the Master Knot ofHenry? It's a "Harry Dick"
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Ligamentous Injury: The highest yield fact is that the anterior talofibular ligament
is the weakest ligament and the most frequently injured (usually from inversion).
Posterior Tibial Tendon Injury / Dysfunction: This results in a progressive
flat foot deformity, as the PTT is the primary stabilizer of the longitudinal arch. When
chronic, the tear is most common behind the medial malleolus (this is where the most
friction is). When acute, the tear is most common at the insertion into the navicular bone.
Acute Flat Arch should make you think of PTT tear.
You will also have a hindfoot valgus deformity (from unopposed
peroneal brevis action). The other point of trivia to know is that
the spring ligament is � sec_ond �ry supporter of the arc� (it holds
up the ta 1ar head), and 1t w1 1 1th1c 1<en and degenerate without the ·
help of the PTT. Don't get it twis�ed though, the spring ligament is �. � .
). ....·.·· ·.\·.
very thick and strong and almost never ruptures in a foot/ankle
trauma. ·
Hindfoot Valgus
"Too Many Toes"
I Say Acute Flat Foot, You Say Posterior Tibial Tendon Injury
Sinus Tarsi Syndrome: *Never make this diagnosis in the setting o.facute trauma
The space between the lateral talus and calcaneus. The sinus tarsi is not just a joint space.
It is an important source of proprioception and balance. Fucking it up has consequences (if
your goal is to make prima ballerina assoluta).
The "syndrome" is caused by hemorrhage or inflammation of the synovial recess with or
without tears of the associated ligaments (talocalcaneal ligaments, inferior extensor
retinaculum). There are associations with rheumatologic disorders and abnormal loading
(flat foot in the setting of a posterior tibial tendon tear).
MRI finding is obliteration of fat in the sinus tarsi space, and replacement with scar.
Loss of Normal T1 Bright Fat (arrow) Normal For Comparison
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Plantar Fasciitis:
This is an inflammation of the fascia secondary to either repetitive trauma �
(overuse via endless rounding on fat diabetic, smokers as a medicine intern), Buzzword is
abnormal mechanics (pes cavus, etc), or arthritis (Reiters, etc ...). "most severe
The pain is localized to the origin of the plantar fascia, and worsened by in the
dorsiflexion of the toes. This is usually a clinical diagnosis. morning."
Plain film might show heel spurs (which are not
As a rapid anatomy review, the specific), but could be a hint. A bone scan may
plantar fascia consists of 3 bands with show increased tracer in the region of the
the central / lateral part normally calcaneus (from periosteal inflammation).
thicker than the medial part the
thinnest.
MRI may show:
Coronal T l diagram through the heel
a thickened fascia
(> 4mm) , most
often the central
Calcaneus band
with increased T2
signal, most
significant near
its insertion at the
heel.
CLASSIC - FLAT FOOT PROGRESSION
Posterior Tibial
Tendon Goes Out Show up in the
ER at 3am
because your
You start
feet hurt and
Spring Ligament Out walking like
you need an
an idiot, Plantar
excuse to not
heel striking Fasciitis
go to work
over and
Sinus Tarsi getsjacked tomorrow
over again
(including those little (and you want
proprioception nerves a Sprite and a
that are in it) Cheeseburger)
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Split Peroneus Brevis:
You can see longitudinal splits in the peroneus in
people with inversion injuries. The history is
usually "chronic ankle pain".
The tendon will be C shaped or boomerang
shaped with central thinning and partial
envelopment of the peroneus longus.
Alternatively, there may be 3 instead of 2 tendons.
The tear occurs at the lateral malleolus.
There is a strong (80%) association with lateral Split Peroneus Brevis
ligament injury. -Boomerang
Anterolateral Impingement Syndrome:
Injury to the anterior talofibular ligaments and tibiofibular ligaments (usually from an
inversion injury) can cause lateral instability, and chronic synovial inflammation.
You can eventually produce a "mass" of hypertrophic synovial tissue in the lateral gutter.
The MRI finding is a "meniscoid mass" in the lateral gutter of the ankle, which is a
balled up scar (Tl and T2 dark).
Tarsal Tunnel Syndrome:
Pain in the distribution of the posterior tibial
nerve (first 3 toes) from compression as it
passes through the tarsal tunnel (behind the
medial malleolus).
It's usually unilateral (unlike carpal tunnel Tarsal tunnel is a covered by the flexor
retinaculum (arrows) and includes tom, dick,
which is usually bilateral), unusually harry the posterior tibial artery and nerve.
"idiopathic" although pes planus (hindfoot
valgus) can predispose by tightening the You can see atrophy of multiple foot muscles
retinaculum. (not just minimi as seen with "Baxter").
Having said that, any mass lesion (ganglion cysts, neurogenic tumors, varicosities, lipomas,
severe tenosynovitis, and accessory muscles) can cause compression of the nerve in the
tunnel.
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Morton's Neuroma: Soft tissue mass (tear drop shaped) shown between the 3rd and 4th
metatarsal heads (third intermetatarsal space) is most likely a Morton's Neuroma (especially on
multiple choice tests). The proposed pathology results from compression / entrapment of the plantar
digital nerve in this location by the intermetatarsal ligament. Over time this results in thickening and
development of perineural fibrosis.
\1 I"\ "Mulder's Sign" - is a physical exam (a sonographic sign) where you squeeze the patients
foot and reproduce the pain (or see the scar pop out under ultrasound).
"(J 4>
Trivia: Morton's Neuroma is NOT a Neuroma (a tumor).
It's a scar.
Classic Look: It is a scar, so it's gonna be dark on T l and T2
(usually). It is tear drop shaped and projects downward.
Mortons: T l Dark Below the
People make a big deal about this thing staying below the Plantar Ligament
plantar ligament.
The reason is that your primary differential is intermetatarsal bursitis - which will extend above
the transverse ligament, be fluid signal, and have a more cystic look. Small bursa in this location can be
normal as long as the stay smaller than 3mm.
Bursitis:
Bursitis: T2 Bright
Above the
Ligament
(dumbbell
shaped)
Haglund's Syndrome / Deformity
This is also called the "Mulholland deformity" for the
purpose of fucking with you. Depending on what you
read there are either 3 or 4 classic features:
• Retro-Achilles bursitis, /
• Retrocalcaneal bursitis,
• Thickening of the distal Achilles tendon
(insertional portion)
• Calcaneal Bony Prominence "prominent posterior
superior os calcis"
The deformity is the "bump."
The "syndrome" is the bursitis
and Achilles tendon thickening.
They call this thing the "pump Retrocalcaneal Bursitis (black arrow)
bumps," because wearing high Retro-Achilles / Adventitial Bursitis
heeled shoes is supposedly a (white arrow)
predisposing factor
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Os Trigonum Syndrome What is this
"Synchondrosis" ?
The idea is that the Os Trigonum (accessory
ossiclc) puts the smash on the FHL ("Harry") This is a joint that has
during extreme ankle flcxion - toe pointing essentially no
shit ("Pointe technique") that ballet dancers movement and is
do ... or other repetitive micro trauma. lined with cartilage.
Classic findings arc going to be
( 1) "Stenosing" tenosynovitis /
collection of fluid around the FHL, and
(2) edema within the Os Trigonum and
across the synchondrosis between the
Os and the Posterior Talus.
Buzzword is
"Ballet Dancer" Axial T2 - Fluid Around the FHL Sag T2 - Edema in the
Edema in the Os and Posterior Os and Posterior Talus
Achilles Tendon Injury: Achilles Tendon Tear
(partial / small gap) Xanthoma
Acute rnpture is usually obvious with a fluid filled gap.
The gap size will determine treatment (big gaps need Thick Tendon Thick Tendon
surgery). The tear is usually 4 cm above the calcancal ( > 7mm) (> 7mm)
insertion and the classic history is an unconditioned middle
aged fake athlete ("weekend warrior") with acute pain and Unilateral Bilateral (usually)
loss of the ability to plantar flex. Associated with being Associated with
a fake athelete having ve1y high
Without a large gap these things can be very hard to tell cholesterol
apart from a Xanthoma (both can just look like a vc1y
thick tendon). There arc a few differences that can be used Step 1 Trivia:
Fluoroquinolone
to diffcrcntiate - per my chart. antibiotics
Plantaris Rupture
("Tennis Leg"): This is usually presented as the classic trick: "Achilles
tendon ruptured but can still plantar flex." Remember not everyone
has this tendon (it's absent in 10% of the population). The classic look
on MRI is focal fluid collection between the solcus and the medial
head of the gastrocncmius. There is an association with ACL tears.
Avulsions of the Calcaneal Tuberosity:
This is sort of an Aunt Minnie with the back of the bone totally ripped
off via the Achilles. The classic association is diabetes. When you see
this you have to think diabetes. Calcaneal Avulsion
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SECTION 2:
OSTEOPOROSIS, OSTEOPENIA, & AVN
�-
Osteopenia: This just means increased lucency of bones. Although this is most
commonly caused by osteoporosis, that is not always the case.
Osteomalacia: This is a soft bone from excessive uncalcified osteoid. This is
typically related to vitamin D issues (either renal causes, liver causes, or other misc
causes). It generally looks just like diffuse osteopenia. For the purpose of multiple choice
you should think about 4 things: Ill-defined trabeculae, Ill-defined corticomedullary
junction, bowing, and "Loosers Zones."
Looser Zones: These things are wide lucent
bands that transverse bone at right angles to
the cortex. These things can happen in lots
of different locations - but the classic two
are the femoral neck and the pubic rami.
Typically there is sclerosis surrounding the
lucency. You should think two things:
osteomalacia and rickets. Less common is
01. The other piece of trivia is to
understand they are a type of insufficiency
fracture. Looser Zones
- Raise your suspicion for this shit when
you see (1) Symmetric Findings
(2) The "90 Degree" to the cortex line
Osteoporosis: The idea is that you have low bone density. Bone density peaks around
30 and then decreases. It decreases faster in women during menopause. The imaging
findings are a thin sharp cortex, prominent trabecular bars, lucent metaphyseal bands, and
spotty lucencies.
Causes: Age is the big one. Medications (steroids, heparin, dilantin), Endocrine issues
(cushings, hyperthryoidism), Anorexia, and Osteogenesis Imperfecta.
Complications: Fractures - Most commonly of the spine (2nd most common is the hip,
3rc1 most common is the wrist).
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DEIA:
This is a bone mineral density test and an excellent source of multiple choice trivia.
General Things to know about DEXA
• T score = Density relative to young adult
• T score defines osteopenia vs osteoporosis
• T score> -1.0 = Normal, -1.0 to -2.5 = Osteopenia, <-2.5 Osteoporosis
• Z score = Density relative to age-matched control "to Za Zame Age"
• False negative/ positive (see below)
False Positive I Negative on DEXA: DEXA works by measuring the density. Anything
that makes that higher or lower than normal can fool the machine.
False Positive:
• Absent Normal Structures: Status post laminectomy
False Negative:
• Including excessive Osteophytes, dermal calcifications, or metal
• Including too much of the femoral shaft when doing a hip - can elevate the
number as the shaft normally has denser bone.
• Compression Fx in the area measured
FRAI:
The Fracture Risk Assessment Tool is a clinical risk tool used to predict fractures by
using clinical risk factors (age, sex, race, BMI, family history, personal fracture history,
prior steroid use, where the patient lives, etc ...) with or without femoral neck bone
density. The fracture risk is calculated as a ten year fracture probability.
Trivia:
• FRAX calculates fracture risk at a 10 year probability
• FRAX adds "value" by helping to identify the subset of osteopenic patients who are at a
higher risk for fracture - and might benefit from pharmacologic intervention
• FRAX is NOT supposed to be used in patient who have already been placed on meds for
osteoporosis. The entire point of the FRAX is to make big pharma more money ... I
mean help identify those who would benefit most from pharmacologic intervention -
those already on meds don't need identified.
• FRAX is applicable for men and women
• FRAX is recommended to calculate 10 year fracture risk in patients with a T-Score
between -l and -2.5.
• Some guidelines suggest pharmacologic intervention for patients with a FRAX
calculated 10 year hip fracture risk of> 3% or major fracture risk of> 20%
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Reflex Sympathetic Dystrophy (RSD):
Also called "Complex Regional Pain Syndrome" - which makes it sound like some
Rheumatology Psycho-somatic bullshit (i.e. fibromyalgia).
Also called "Sudeck Atrophy" - which makes it sound serious - like some incurable
neurodegenerative death sentence.
The classic clinical vignette is a history of trauma or infection.
On plain film, it can cause severe osteopenia (like disuse osteopenia). Some people say it looks
like unilateral RA, with preserved joint spaces. Hand and shoulder are the most common sites
of involvement.
It's one of the many causes of a 3 phase hot bone scan. In fact, intra-articular uptake of tracer on
bone scan is typically seen (on multiple choice) in patients with RSD (secondary to the increased
vascularity of the synovial membrane), and this is somewhat characteristic.
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Transient Osteoporosis:
There are two types of presentations.:
Transient osteoporosis of the hip: For the purpose of multiple choice tests, by far you
should expect to see the female in the 3,11 trimester of pregnancy with involvement of
the left hip. Having said that, it's actually more common in men in whom it's usually
bilateral. The joint space should remain normal. It's self limiting (hence the word
transient) and resolves in a few months. PlainfUm shows osteopenia, MRI shows Edema,
Bone scan shows increased uptake.focally.
Regional migratory osteoporosis - This is an idiopathic disorder which has a very classic
history of pain in a joint, which gets better and then shows up in another joint. It's
associated with osteoporosis - which is also self-limiting. It's more common in men.
Hip Edema - Strategy Session - This vs That - Transient Osteoporosis vs AVN vs Fx
On radiograph, transient osteoporosis and AVN
look totally different. Transient Osteoporosis is
super lucent - so lucent that sometimes you can
barely see the femoral head. AVN on the other
hand, will have patchy areas of sclerosis.
On MRI, the story is different. These things can look similar. They both have edema on STIR, and
they are both are dark on T 1. The difference is that AVN should be shown with a serpiginous dark
line (double line if you are lucky) - that represents infarct core. Joint effusions can be seen in both -
so this isn't helpful.
Now - if these assholes want to take it to the twilight zone, they can add "insufficiency fracture" to
the list of distractors. This is really a dirty trick as both Transient Osteoporosis and AVN are
susceptible to this. The distinction is that this fracture line should be less serpiginous and instead
parallel the subchondral bone of the femoral head.
T1
STIR
Normal Transient AVN Insufficiency
Osteoporosis Fracture
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Osteoporotic Compression Fracture: Super Common. On MR you want to see
a "band like" fracture line - which is typically T l dark (T2 is more variable). The non
deformed portions ofthe vertebral body should have normal signal.
Neoplastic Compression
What is this "Abnormal Marrow Signal"?
Fracture: Most vertebral mets
don't result in compression fracture Normally (in an adult) the marrow of the spine is
until nearly the entire vertebral fatty - so it should be Tl bright. The internal control
body is replaced with tumor. Ifyou is an adjacent normal disc (not a desiccated disk).
see abnormal marrow signal (not If you see dark stuff - it might just be red marrow.
band like) with involvement ofthe BUT if it is darker than the adjacent (normal) disc,
posterior margin you should think you have to assume that it's a bad thing.
about cancer.
!) Next Step?- Look at the rest ofthe spine - mets are often multiple.
!_11, THIS vs THAT - Osteoporotic Fx vs Neoplastic Fx
lfl was going to show a Neoplastic vs Osteoporotic Fracture case, this is how I would do it.
I would have 2 sequences, a T l and a STIR. The STlR would be positive (bright on both).
The Osteoporotic Fracture would have a T l dark line. The Neoplastic Fracture would be
diffusely low T l signal and blobby - and I would stick a few lesions in other vertebral bodies.
T1 STIR T1 STIR T1 STIR
NORMAL Osteoporotic Fx Neoplastic Fx
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OCDs/OCls
Osteochondritis Dissecans (OCD):
OCD Trivia:
The new terminology is actually to call these "OCLs" (the "L" is for
Most common in
Lesion). This a spectrum of aseptic separation of an osteochondral males under 18
fragment which can lead to gradual fragmentation of the articular surface
Most common in
and secondary OA. Most of the time it is secondary to trauma, although it the lateral aspect
could also be secondary to AVN. of the medial
femoral condyle
Where it happens: Classic locations include the femoral condyle (most
common site in the knee), patella, talus, and capitellum.
Staging: There is a staging system, which you probably need to know exists.
• Stage 1: Stable - Covered by intact cartilage, Intact with Host Bone
• Stage 2: Stable on Probing, Partially not intact with host bone.
• Stage 3: Unstable on Probing, Complete discontinuity of lesion.
• Stage 4: Dislocated fragment
Treatment I Who cares? If the fragment is unstable you can get secondary OA. You want to
look for high T2 signal undercutting the fragment from the bone to call it unstable
(edema can force a false positive). Thus, the absence of high T2 signal at the bone fragment
interface is a good indicator of osseous bridging and stability. Granulation tissue at the
interface (which will enhance with Gd), does not mean it's stable.
THIS vs THAT: Capitellum Lesions
Osteochondritis
Panner's Disease Pseudo-Lesion
Dissecans
Capitellum of the dominant arm Also in the capitellum of
in throwers throwers
Anterior convex margin of the
capitellum. Unstable lesions are
Entire Capitellum
characterized by high signal
is abnormal in signal Posterior Capitellum
fluid that encircles the
(low T1, high T2)
osteochondral
fragment on T2W image
Can lead to intra-articular Loose body formation is A coronal image through the
loose bodies NOT seen (usually) posterior capitellum can mimic
a defect. This occurs because
the most posterior portion of
5 to 10 years old the capitellum has an abrupt
Slightly older patients
"Peter Pan wanted to stay slope.
(12-16 years)
young"
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Osteochondroses:
These are a group of conditions (usually seen in childhood) that are characterized by
involvement of the epiphysis, or apophysis with findings of collapse, sclerosis, and
fragmentation - suggesting osteonecrosis.
Kohlers Tarsal Navicular Boys 4-6. Treatment is not surgical.
Second Metatarsal Adolescent Girls
Freiberg Infraction
Head - can lead to secondary OA
Calcaneal Some say this is a normal
Sever's
Apophysis "growing pain"
Kid 5-10 "Thrower";
Panner's Capitellum
does not have loose bodies.
Perthes (LCP) Femoral Head White kid; 4-8.
Associated with negative ulnar
Kienbock Carpal Lunate
variance. Seen in adults 20-40.
Causes kyphosis. 3 adjacent levels
Scheuermann Thoracic Spine with wedging, plus a thoracic kyphosis
of> 40 degrees (normal 20-40)
Adolescents (10-15) who jump and
Osgood-Schlatter Disease (OSD) Tibial Tubercle kick. Need Fragmentation + Soft
Tissue Swelling.
•••-•-• •---•-.-- ~••••••--•••-•••-- •••,-•••- • ••••-• •••• ••••--• • •- , . • • - • • ••••-•• _.__,__ •-•••-•• • • •-ss•••-
Sinding-Larsen-Johansson (SLJ) Inferior Patella Adolescents (] 0-15) who jump.
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,.
:'.
.
. .
'i
�
SECTION 3:
INFECTION
�
• .
•
With regard to osteomyelitis, radiographs will be normal for 7-10 days. Essentially,
osteomyelitis can have any appearance, occur in any location, and occur at any age. Children
have hematogenous spread usually hitting the long bones (metaphysis). Adults are more
likely to have direct spread (in diabetic).
I Say This, You Say THAT
However, you can
have hematogenous
Osteomyelitis in Spine = IV Drug User
spread in certain
Osteomyelitis in Spine with Kyphosis (Gibbus Deformity) = TB
situations as well (IV
Unilateral SI joint = IV Drug User
Drugs).
Psoas Muscle Abscess = TB
General Rule: Septic joints more common in adults. Osteomyelitis more common in kids.
Classic Look: Hallmarks are destruction of bone and periosteal new bone formation.
Vocab:
Sequestrum = Piece of necrotic bone
Sequestrum
surround by granulation tissue
lnvolucrum = Thick sheath of
periosteal bone around sequestrum
Cloaca = Defect in the periosteum
(bone skin) caused by infection
Cloaca
Sinus Tract: A cham1el from the
bone to the skin (lined with
Abscess granulation tissue).
Chronic Osteomyelitis: This is defined as osteomyelitis lasting longer than 6 weeks.
Some trivia worth knowing:
• Draining sinus tracts are a risk factor for squamous cell CA
• Most specific sign of active chronic osteomyelitis is the presence of a
sequestrum (best shown with computed tomography)
• MRI diagnosis of healed osteomyelitis is based on the return of normal fatty marrow
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Acute Bacterial Osteomyelitis can be thought of in three different categories:
1) hernatogenous seeding (most common in child), 2) contiguous spread, and 3) direct
inoculation of the bone either from surgery or trauma.
Acute hematogenous osteornyelitis has a predilection for the long bones of the body,
specifically the rnetaphysis, which has the best blood flow and allows for spreading of the
infection via small channels in the bone that lead to the subperiosteal space.
• Age < 1 month = Multi-centric involvement, often Infant
with joint involvement. Bone scan often negative
(75%) at this age
• Age < 18 months = Spread to epiphysis through Child
blood
• Age 2-16 years = Trans-physeal vessels are closed
(primary focus is metaphysis). Adult
In the slightly older baby (<18 months) these vessels from the metaphysis to the epiphysis
atrophy and the growth plate stops the spread (although spread can still occur). This creates
a "septic tank" effect. This same thing happens with certain cancers (leukemia); the garbage
gets stuck in the septic tank (metaphysis). Once the growth plates fuse, this obstruction is
no longer present.
MRIfindings of osteomyelitis: Low signal in the bone marrow on T l imaging adjacent to an
ulcer or cellulitis is diagnostic.
STIR - High Signal in
Bone Adjacent to Ulcer
(more sensitive sign)
T1 - Corresponding Low Signal
(more specifi c sign)
The Ghost Sign: Neuropathic Bone vs Osteomyelitis in a Neuropathic Bone
A bone that becomes a ghost (poor definition of margins) on Tl imaging, but then re-appears
(more morphologically distinct) on T2, or after giving IV contrast, is more likely to have
osteornyelitis.
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Discitis / Osteomyelitis:
Mechanism (Adult)
( 1) Seeding of the (2) Eruption and (3) Eventual
Infection of the disc and vertebral endplate crossing into the involvement of the
infection of the ve1iebral (which is vascular) adjacent vertebral body
disc space
body nearly always go
J;J
together.
The reason has to do
D
with the route of seeding;
which typically involves
Typical Look & Trivia
Early: Later Plain Film: Later MR:
• Plain Film: Hard to see • Adjacent • Tl - Dark
• MRI: Paraspinal and irregular Man-ow
Epidural inflammation, endplate • T2 - Bright
T2 bright disc signal, destruction. Man-ow
and disc enhancement. • Disc Space Post Contrast
Nan-owing Enhancement
Trivia: Epidural Abscess
• Adults: the source is usually from a This is an infected
recent surgery, procedure, or systemic collection between the
infection. dura and periosteum.
• Children (younger than 5) it's usually Classic Appearance:
from hematogenous spread. • T l Dark, T2 Bright,
• Step 1 trivia: Staph A is the most • Peripheral
common bug, and always think about Enhancement, &
an IV drug user. • Restricted
• Almost always (80% of the time) the Paraspinal Epidural Diffusion.
ESR and CRP are elevated. Abscess Abscess Classic Scenario:
• Gallium is superior to WBC scan in • HIV patient
the spine. • Bad Diabetic.
Pediatric Discitis / Osteomyelitis
Children have direct blood supply to the intervertebral disc, so they can get isolated discitis.
Isolated Discitis is basically never seen in adults. The classic scenario is: kid (younger than 4)
with a upper respiratory infection, now with back pain - usually lumbar.
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TB
This is a special topic (high yield) with regard to MSK infection. It's not that common,
with< 5% of patients with TB having MSK involvement. Although on multiple choice
tests, I think you'll find it appears with a high frequency.
Pott Disease
(tuberculosis of the spine) "Gibbus Deformity"
The vertebral body is involved with sparing of This is a focal
the disc space until late in the disease (very kyphosis seen in "Pott
different than more common bacterial infections). Disease" , among
many other thing
It tends to spare the disc space
It tends to have multi-level thoracic "skip"
involvement
Buzzword "Large paraspinal abscess
Buzzword "Calcifzed Psoas Abscess"
Buzzword "Gibbus D�formity" - which is
a destructive focal kyphosis
Mimic - Brucellosis (unpasteurized milk
from an Amish Person) , can also have disc
space preservation.
"Tuberculosis Dactylitis" (Spina Ventosa)
"Rice Bodies"
Typically seen in kids with involvement of the
short tubular bones of the hands and feet. These are sloughed, infarcted
synovium seen with end stage
It is often a
RA, and TB infection of joints.
smoldering infection
without periosteal
reaction.
Classic look is a
diaphyseal
expansile lesion
with soft tissue
swelling.
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Septic Arthritis
You see this the most in large joints which have an abundant blood supply to the metaphysis
(shoulder, hip, knee).
JV drug users will get it in the SIjoint, and sternoclavicular joint.
Conventional risk factors include being old, having AIDS, RA, and prosthetic joints.
On plain film you might see a joint effusion, or Pneumoarthrogram Sign
MRI will show synovial enhancement. If
untreated this will jack your joint in less than If you can demonstrate air within a joint -
48 hours. you can exclude a joint effusion.
No joint effusion
No septic joint
Necrotizing Fasciitis:
This is a very bad actor that kills very quickly. The good news is that it's pretty rare,
typically only seen in HIVers, Transplant patients, diabetics, and alcoholics. It's usually
polymicrobial (the second form is Group A Strep).
Gas is only seen in a minority of cases, but if you see gas in soft tissue this is what they
want. Diffuse fascial enhancement is what you'd see if the ER is dumb enough to order
cross sectional imaging (they often are).
Fournier Gangrene is what they call it in the scrotum ( "testes satchel").
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• .
�
SECTION 4:
AGGRESSIVE LESIONS
There are tons of primary osseous malignancies, the most common are myeloma/plasmacytoma (27%),
Osteosarcoma (20%) and Chondrosarcoma (20%). I'll discuss myeloma/plasmacytoma later in the chapter
when I get to lucent lesions. This discussion will focus more on the bone forming aggressive tumors.
I guess before I do that though, I should review what "aggressive" means. In the real world, dealing with
bone lesions is simple - it's either aggressive, not aggressive, or not sure. Even though multiple choice is
ve1y different than actual clinical radiology, that first mental calculus of - aggressive vs not aggressive -
may still be useful in eliminating distractors.
What makes a lesion "aggressive" ?
According to Helms, the wide zone of transition is the
best sign that a lesion is aggressive. This is actually a
useful pearl. The simplest way to conceptualize this is
to ask yourself if you can trace the edges of the lesion
with a pencil. If you can the lesion is probably benign.
If the edges are bluny or there is a gradient to the edge
- this is a more likely an aggressive lesions. Narrow Zone Wide Zone
Benign Aggressive
The reason is that margins reflect the growth the lesion. Bones are dumb. They really only know how to
do two things - make bone and destroy bone. The margins are the reflection of bone formation. If the
margins are sharp and sclerotic, this means the bone has time to adjust to the irritation and lay down a
coat of mature bone. If the margins are not distinct (zone of transition is wide) this indicates a faster
growing lesion and therefore a higher probability of malignancy (or infection).
If the tumor grows rapidly enough it can break through the cortex and destroy the
newly formed bone capsule / lamellated bone. When this happens you end up with
a triangular structure - called the Codman triangle (as shown in diagram).
When we think about bone lesions, we often imagine lytic holes or bone destruction. Bone destruction
occurs from complex methods best understood as either direct obliteration via the tumor or pissed off
osteoclasts enraged by the uninvited tumor / hyperemia. Trabecular bone loss occurs more rapidly
(relative to cortical bone), but is noticed later because cortical bone is more smooth and organized.
Supposedly you need to destroy 70% of the trabecular bone before it is noticed radiographically.
Bone destruction that occurs in a uniform geographic pattern
(especially with a sharp well defined border) is more suggestive
of a benign slow growing lesion. A moth-eaten (cluster of small
lytic holes) or permeative (ill-defined tiny oval or streak like
lucencies) suggests rapid infiltrative tumor growth - as seen in
myeloma, lymphoma, and Ewings sarcoma. It is worth noting
that osteomyelitis and hyperparathyroidism can also demonstrate Moth Permeative
these aggressive patterns - pre-test probably is always important. Geograph.tc Eaten
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Osteosarcoma:
There are a bunch of subtypes, but for the purpose of this discussion there are 4.
Conventional Intramedullary (85%), Parosteal (4%), Periosteal (1%), Telangiectatic (rare).
All the subtypes produce bone or osteoid from neoplastic cells. Most are idiopathic but you
can have secondary causes (usually seen in elderly) XRT, Pagets, Infarcts, etc ...
Conventional lntramedullary: More common, and higher grade than the surface
subtypes (periosteal, and parosteal). Primary subtypes typically occur in young patients
(10-20). The most common location is the femur (40%), and proximal tibia (15%).
Buzzwords include various types of aggressive periosteal reactions:
• "Sunburst"- periosteal reaction that is aggressive and looks like a sunburst
• Cadman triangle - With aggressive lesions, the periosteum does not have time to
ossify completely with new bone (e.g. as seen in single layer and multi-layered
periosteal reaction), so only the edge of the raised periosteum will ossify - creating
the appearance of a triangle.
• Lame/lated (onion skin reaction) - multi layers of parallel periosteum, looks like an
onion's skin.
Trivia:
• Osteosarcoma met to the lung is a "classic" cause of occult pneumothorax.
"Reverse Zoning Phenomenon" - more 0
dense mature matrix in the center, less
peripherally (opposite ofmyositis ossificans).
Progress Over Time
"Reverse Zoning" = Bad
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Parosteal Osteosarcoma: Generally low grade, BULKY parosteal bone formation.
Think Big ... just say Big. This guy loves the posterior distal femur (because ofthis location
it can mimic a cortical desmoid "tug lesion" early on). The lesion is metaphyseal 90% of the
time. The buzzword is "string sign" - which refers to a radiolucent line separating the bulky
tumor from the cortex.
THIS vs THAT
Periosteal Parosteal Periosteal
Osteosarcoma: Early Adult/ Middle Age Age Group (15-25)
Worse prognosis than parosteal
Metaphyseal (90%) Diaphyseal
but better than conventional
Likes Posterior Distal Femur Likes Medial Distal Femur
osteosarcoma. Tends to occur
in the diaphyseal regions, Marrow extension (50%) Usually no marrow extension
classic medial distal femur. Low Grade Intermediate Grade
FLUID-FLUID LEVELS DDx:
Telangiectatic
Osteosarcoma:
About 15% have a narrow zone of
transition. Fluid-Fluid levels on Telangiectatic
MRI is classic. They are High on Osteosarcoma
T l (from methemoglobin). Can be Aneurysmal Bone Cyst
Giant Cell Tumor
differentiated from ABC or GCT
(maybe) by tumor nodularity and
enhancement.
Parosteal Periosteal Telangiectatic Classic (lntramedullary) Secondary OS
4% 1% Rare As Fuck 85% Started off as Pagets
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Other Bad Actors
Chondrosarcoma:
Usually seen in older adults (M>F). Likes flat bones,
limb girdles, proximal tubular bones. Can be central
(intramedullary) or peripheral (at the end of an THIS vs THAT
osteochondroma). Most are low grade. Enchondroma vs Low Grade
Chondrosarcoma
Risk Factors: Pagets, and anything cartilaginous
( osteochondromas, Maffucci etc ...) Factors Favoring
Chondrosarcoma:
Gamesmanship: If you want to say chondroblastoma but
it's an adult think clear cell chondrosarcoma Pain
Cortical Destruction
Gamesmanship: Scalloping of> 2/3 of the cortex
>5cm in Size
If shown with CT - they have to "Changing Matrix"
show you some "chondroid
matrix" - "arcs and rings"
Ewings:
Permeative lesion in the diaphysis of a child = Ewings
(could also be irifection, or EG).
Extremely rare in African-Americans. Likes to met bone to bone (,;;kip lesions are more common
in Ewings, relative to Osteosarcoma). Does NOT form ostcoid from tumor cells, but can mimic
osteosarcoma because of its marked sclerosis (sclerosis occurs in the bone only, not in the soft
tissue - which is NOT the case in osteosarcoma).
Chordoma:
Usually seen in adults (30-60), usually slightly younger in the clivus and slightly older in the
sacrum. Most likely questions regarding the chordoma include location (most common sacrum,
second most common clivus, third most common vertebral body), and the fact that they are very
T2 bright.
Chordoma Most Commons: ··
• Most common primaiy malignancy of the spine.
• Most common primary malignancy of the sacrum.
• When involving the spine, most common at C2.
I Say Chordoma, You Say "Midline, Midline, Midline!"
Why is it always midline? It's made of cells left over from the "notochord" (some embryology
bullshit that was involved in making MIDLINE structures).
Chordomas are NEVER EVER seen off the midlinc (NEVER in the hip, leg, arm, hand, etc ...).
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rw--.r �
-
SECTIONS:
LUCENT LESIONS . : � •. .• �
' :'. .
FEGNOMASHIC is a "useful" mnemonic for lucent bone lesions made popular by Clyde Helms. As
it turns out, you can rearrange the letters ofFEGNOMASHIC to form a wordFOGMACHJNES. I
find it a lot easier to remember a mnemonic if it actually forms a real word. Having said that, the
whole idea of memorizing a list of 11 or 12 barely related things is stupid. You would never give a
differential that included all of those, as they occur in different places, in different ages, and often
look very different.
Differentials (for people who know what they are looking at) are usually never deeper than 3 or 4
things. If you are giving a differential of 12 things, just say you don't know what it is. Seriously in
the real world bone lesions only come in 3 flavors: 1 - Bad (cancer or infection), 2 - Obviously
benign (not sure I'll waste saliva mentioning it in my report) , 3 - Ehh hard to tell - get a follow up.
This is actually pretty much true of lesions everywhere in the body. Realizing this allows for the
following paradigm shift:
Eyeball: Oh Shit! A lesion that has non-aggressive Eyeball: Oh Shit! A lesion that has non-
features. I wonder what it is .... aggressive features. I wonder what it is ....
Neuron 1: We better look it up and give it a name. Lion Neuron 1: Who gives a shit? It's
Neuron 2: Maybe we should give a list of possible benign ... next case.
names. Then people will read our report and think Lion Neuron 2: This is an ortho study.
we are smart. Literally no one will ever read this report.
Bystander Neurons: Initiate Waffle Protocol Bystander Neurons: Bro ... can we finish this
fucking list already? We need to look at that
new Tesla Roadster, 0-60 is sub 2 seconds.
But. .. we arcn 't training for real life. The realm of multiple choice is obviously different.
For multiple choice, when you encounter a lucent bone lesion you can expect one of two questions
(1) what is it ? or (2) what is it associated with ? In either case you are going to need to figure out
what it is. In the real world you would probably have to give a short differential, but in the world of
multiple choice you will have to come up with one answer. Don't fret, they have to give you clues
so you can pick just one. A useful mental exercise when eliminating multiple choice distractors is to
ask yourself "why is it NOT this?" It's an exercise that is often not performed at the workstation -
but vc1y valuable in the test environment - especially for these types of questions.
Here is my suggested method:
Age - Key Facts
(]) Age ofthe patient? - If you are lucky they will tell • < 30 = EG, ABC, NOF,
you. If you arc less lucky you will have to guess. Chondroblastoma, and Solitary
Growth plates open = kid. Growth plates closed with Bone Cysts
no degenerative change = young adult. Growth plates • Any Age = Infection
closed with degenerative changes = older than 40. • > 40 = Mets and Myeloma
(unless it's neuroblastoma mets).
(2) Location of the lesion ? Metaphysis, Epiphysis,
Diaphysis? Is this an epiphyseal equivalent discussion (see the next page for discussion).
(3) Classic Locations and Looks ? See my summary at the end of this section
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location:
Epiphysis:
In general, only a few lesions tend to arise in the epiphysis. The "four horseman of the
(e)apophysis" is the mnemonic I like to use, and I think about the company AIG that was
involved in some scandal a few years ago. AIG "the evil" Company.
ABC, Infection, Giant Cell, and Chondroblastoma.
*The caveat is that ABC is usually metaphyseal but afier the Epiphyseal Equivalents:
growth plate closes it can extend into the epiphysis. (bones that will have the
same lesions as
the epiphysis)
For the purpose of multiple choice tests, it is important to not
forget about the malignant tumor at the end of the bone Carpals,
(epiphysis) - Clear Cell Chondrosarcoma. This guy is slow Patella,
growing, with a variable appearance (lytic, calcified, lobulated, Greater Trochanter,
ill defined, etc ... ). Just remember if they say malignant Calcaneus
epiphyseal you say Clear Cell Chondrosarcorna.
Metaphysis
The metaphysis is the fastest growing area of a bone, with the best blood supply. This
excellent blood supply results in an increased predilection for Mets and Infection. Most of the
cystic bone lesions can occur in the metaphysis.
Diaphysis
Just like the metaphysis, most entities can occur in the diaphysis (they just do it less).
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Patholouv - For Trivia
Fibrous Dysplasia:
Fibrous dysplasia is a skeletal developmental anomaly of osteoblasts - failure
of normal maturation and differentiation which results in replacement of the
normal medullary space.
Famously "can look like anything", with phases like Pagets (lytic, mixed,
blastic) - although the most classic appearance is a "long lesion. in a long
bone. with ground glass matrix. " Sometimes the vocabulary "lytic lesion Shepherd Crook
with a hazy matrix" is used instead of the word "ground glass" - for the -Coxa Varus Angulation
purpose of fucking with you. The discriminator used by Helms is "no -Classic.for FD (but can be
periosteal reaction or pain." seen in Paget and OJ)
Likes the ribs and long bones. If it occurs in the pelvis, it
also hits the ipsilateral femur (Shepherd Crook deformity). THIS vs THAT
If it's multiple it likes the skull and face (Lion-like faces). McCune
Mazabraud
Albright
The disorder can occur at any age - but the multiple lesion Polyostotic Fibrous
Polyostotic Fibrous
Dysplasia Dysplasia
variety "polyostotic" - tends to occur earlier.
Girl Woman (middle a)?ed)
Cafe au lait spots
Soft Tissue Myxomas
You could think monostotic (20's & 30's) or polyostotic (<
Increased Risk Osseous
10 year old). When you see the polyostotic fonn (often with a Precocious Puberty Malignant
mangled horrible horrible face... a face that only a Transformation
mother could love) - you should think syndromes.
Adamantinoma:
A total zebra (probably a unicorn). A tibial lesion that resembles fibrous dysplasia
(mixed lytic and sclerotic). It is potentially malignant.
Nonossifying Fibroma (NOF):
These are very common. They arc seen in children, and will spontaneously regress (becoming more
sclerotic before disappearing). They are rare in children not yet walking. Just like GCTs they like to
occur around the knee. They are classically described as eccentric with a thin sclerotic border
(remember GCTs don't have a sclerotic border). They are called fibrous cortical defects when
smaller than 2 cm.
Vocab: NOFs are the larger version (> 3cm) of a fibrous cortical defect (FCD). A wastebasket term
for the both of them is simply "fibroxanthoma."
Jaffe-Campanacci Syndrome: Syndrome of multiple NOFs, cafe-au-lait
spots, mental retardation, hypogonadism, and cardiac malformations.
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Enchondroma:
This guy is a tumor of the medullary cavity composed of hyaline cartilage. They become progressively
more common with age - peaking around 10-30 years old.
The sneaky thing about this lesion is that it looks different depending on the body part it is in.
• Humerus or Femur = Arcs and Rings
• Fingers or Toes = Lytic
The ARCS AND RINGS is the more classic textbook look with the irregularly
speckled calcification of chondroid matrix. Just don't forget that this classic matrix
is not found in the fingers or toes.
The enchondroma is actually the most common cystic lesion in the hands and feet. Just like fibrous
dysplasia, this lesion does not have periostitis.
Differentiating Enchondroma vs Low Grade Chondrosarcoma ·
Strategies to Deal with the Chondroid Matrix Lesion in a Long Bone ,.,,
L
Primary Tactic: History of pain - Enchondroma vs a Low Grade Chondrosarcoma
Not Pain/it! PA!Nful
Secondary Tactic: Size - Enchondroma vs a Low Grade Chondrosarcoma
1-2 cm > 4-5 cm
Tertiary Tactic: Glitch in the Matrix - Enchondroma vs a Low Grade Chondrosarcoma
Arcs & Rings Arcs & Rings Pattern
Pattern does Changes - moves
NOT Change around grows etc ...
When multiple- especially when in the hands you should think syndromes:
THIS vs THAT
Maffucci Syndrome
OIiier Disease "Mar[fucci Has More"
More Cancer Risk and More Vascular Malformations
Multiple Enchondromas (3 or more) Multiple Enchondromas
Hemangiomas
(bunch lucent centered calcifications)
Increase risk in Chondrosarcoma
Slight increase risk in Chondrosarcoma (probably more than Oilier)
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Eosinophilic Granuloma (EG):
This is typically included in every differential for people less than 30 (peak age is 5-10).
It can be solitary (usually) or multiple.
There are 3 classic appearances - for the purpose of multiple choice:
(1) Vertebra plana in a kid
(2) Skull with lucent "beveled edge" lesions (also in a kid).
(3) "Floating Tooth" with lytic lesion in alveolar ridge --- this would be a differential case
The appearance is highly variable and can be lytic or blastic, with or without a sclerotic border,
and with or without a periosteal response. Can even have an osseous sequestrum.
Classic DDx for Vertebra Plana Classic DDx for Osseous Sequestrum:
(MELT) • Osteomyelitis
• Mets/ Myeloma • Lymphoma
• EG • Fibrosarcoma
• Lymphoma • EG
• Trauma/ TB *Osteoid Osteoma can mimic a sequestrum
Giant Cell Tumor (GCT):
This guy has some key criteria (which lend themselves well to multiple choice tests).
They include:
. L - Physis MUST be closed
� - Non Sclerotic Border
f1' - Abuts the articular surface
Another trick is to show you a pulmonary met, and ask if it could be a GCT? The answer is
yes (although this is rare) GCT is considered "quasi-malignant" because it can be locally
invasive and about 5% will have pulmonary mets (which are still curable by resection). As a
result of this, it should be resected with wide margins.
Things to know about GCTs:
- Most common in the knee - abutting the articular surface
- Most common at age 20-30 * physis must be closed
- There is an association with ABCs (they can tum into them)
- They are "quasi-malignant" - 5% have lung mets
- Fluid levels on MRI
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Associations of
Osteoid Osteoma "Pain at night, relieved by aspirin. " Osteoid Osteoma
Painful Scoliosis
- Most Classic Age: "Adolescent" -- 10-25 ish. .. - - · ······ ., ···--···--·-·-··-···--··-··-·-··--· ---•--.--- -·····- ··---
Growth Deformity:
- Most Classic Look: Oval lytic lesion ("lucent nidus") Increased length and
surrounded by dense sclerotic cortical bone ("periosteal girth of long bones
reaction").
_______ , .,.---- ·· ---·--· ··- - · ··· ·--
Synovitis: Can be seen if
- Most Classic Locations: (l) Meta/diaphysis of long bones intra-articular, joint
(femoral neck= most common) and (2) Posterior elements of effusions
the spine (lumbar > cervical > thoracic). Technically the Arthritis: Can occur from
fingers are more common than the spine, but that's rarely show primary synovitis, or
on multiple choice. secondarily from altered
joint mechanics.
Modality Trivia:
• MRI: "Lots of edema." I' 11 say that again "large amount of edema for the size of the lesion."
Adjacent soft tissue edema is also common - don't let that fool you.
• Nuke Bone Scan: "Double Density Sign" - very intense central activity at nidus, surrounded
by less intensity of reactive bone. A common distractor is a stress fracture. Stress fractures
are linear. 0.0. should be round.
Scoliosis Trivia: When you have them in the spine (most common in Convex
the posterior elements of the lumbar spine), you frequently have an
associated painful scoliosis with the convexity pointed away from
the lesion.
Treatment:
These can be treated with percutaneous radiofrequency ablation (as long as it's not within 1 cm
of a nerve or other vital structure - typically avoided in hands, spine, and pregnant patients).
Osteoblastoma:
Basically it's an osteoid osteoma that is larger than 2 cm. It's seen in patients< 30 years old.
They are most likely to show this in the posterior elements. It also occurs in the long bones
(35%) and when it does it is usually diaphyseal (75%).
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Chondroblastoma:
This is seen in kids (90% age 5-25). They classically show it in two ways
(1) in the epiphysis of the tibia on a 15 year old, or (2) in an epiphyseal equivalent.
So what are the epiphyseal equivalents???
• Patella
• Calcaneus
• Carpal Bones
• And all the Apophyses (greater and less trochanter, tuberosities, etc .. .)
Features of the tumor include; A thin sclerotic rim, extension across the physeal plate
(25-50%), periostitis (30%). Actual location: femur> humerus> tibia . This may show bone
marrow edema, and soft tissue edema on MRI (MRI can mislead you into thinking it's a bad
thing). This is one of the only bone lesions that is often NOT T2 bright. They tend to
reoccur after resection (like 30% of the time).
\j r'\ Gamesmanship Hip: When you have a chondroblastoma in the hip, it tends to.favor
'-r!J � the greater trochanter (more than the.femoral epiphysis).
Chondromyxoid Fibroma:
This is the least common benign lesion of cartilage. It is usually in patients younger than 30.
The typical appearance is an osteolytic, elongated in shape, eccentrically located,
metaphyseal lesion, with cortical expansion and a "bite" like configuration. Sorta looks like
an NOF - with the classic location in the proximal metaphyseal region of the tibia.
The Hip
Greater Trochanter - Remember this is an epiphyseal equivalent and the
chrondroblastomas prefer it to the femoral epiphysis. You can get all the other DDxs
(ABC, Infection, GCT, etc... here as well). Plus, you can have avulsions of the gluteus
medius and minimus.
Lesser Trochanter - An avulsion here without significant clinical history should make you
think pathologic fracture.
The Intertrochanteric Region: Classic DDx here: Lipoma, Solitary Bone Cyst, and
Monostotic Fibrous Dysplasia.
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Aneurysmal Bone Cyst (ABC): I Classic DDx for
i Lucent Lesion in
Aneurysmal bone cysts are aneurysmal lesions of bone with thin Posterior Elements:
walled, blood-filled spaces (fluid-fluid level on MRI). Patients are Osteoblastoma
usually < 30. They may develop following trauma. ABC
I, TB
Location: Tibia> Vert> Femur> Humerus 1 .....................................................................
They can be described as primary ABC, presumably arising denovo or secondary ABC,
associated with another tumor (classic GCT). They are commonly associated with other
benign lesions.
Things to know about ABC:
- Up to 40% of secondary ABC's are associated with giant cell tumor of bone.
- It's on the DDx for Fluid - Fluid Level on MRI
- Patient < 30
- Tibia is the most common site
Solitary (Unicameral) Bone Cyst:
It would be unusual to see one of these in a patient older than 30. Most common in the
tubular bones (90-95 %) usually humerus or femur. Unique feature: "Always located
centrally."
It's going to be shown one of two ways: (1) With a fracture through it in the humerus
(probably with a fallen fragment sign) or (2) As a lucent lesion in the calcaneus (probably
with a fallen fragment sign).
The fallen fragment sign (bone fragment in the dependent portion of a lucent bone lesion) is
pathognomonic of solitary bone cyst.
Brown Tumor (Hyperparathyroidism):
The "brown tumor" represents localized accumulations of giant cells and fibrous tissue (in
case someone asks). They appear as lytic or sclerotic lesions with other findings of
hyperparathyroidism (subperiosteal bone resorption). In other words, they need to tell you he/
she has hyperparathyroidism first. They may just straight up tell you, or they will show you
some bone resorption first (classically on the side of a finger, edge of a clavicle, or under a
rib).
These things have different stages of healing / sclerosis. They resorb and can become totally
sclerotic / healed, when the Hyper PTH is treated.
More on this in the arthritis section - later in the chapter
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Classic (& sneaky non-classic) Lesions Posterior Metaphysis Superior Epiphysis
that can be shown in the calcaneus.
The suggested Promethean method is to first use
location within the bone, and then use characteristic
appearance as a secondary discriminator.
First let us take a closer look at the calcaneus.
Remember this thing is an epiphyseal equivalent, but
only in certain locations. It's probably better to think
about the bone like a hybrid long bone - complete
with a diaphysis, two metaphysis, and three
epiphysis.
Chondroblastoma: Giant Cell Tumor: Can also involve the epiphysis
0
(although it typically starts out metaphyseal and grows into the
epiphysis). Remember these things required a closed physis.
0
The Posterior Metaphysis / Epiphysis is favored.
Osteoid Osteoma:
• Talus > Calcaneus
• Similar to Chondroblastoma in
• Most classic epiphysis lesion - with a favoring the superior epiphysis
preference for the superior epiphysis near near the talocalcaneal
the talocalcaneal articulation (although articulation.
they can be at any ofthe 3 epiphysis) . • Distinction is the sclerotic
• Lucent lesion, that can have some thickening ofthe adjacent bone
internal calcifications. and the radiolucent nidus.
Geode: Older Patient+ Subtalar degenerative change/ Obvious Arthritis
Osteomyelitis & Mets: Osteomyelitis
•
The calcaneal apophysis (equivalent to the metaphyseal region oflong bones) G:J . .
· .· · • .·· · • ..
will have a similar predilection for collection hematogenous spread ofboth • ··. · ·
o·
infection or cancer (GU or Colon).
ets
In both cases the involvement favors the posterior meta-epiphyseal region
(which has the richest blood supply), with lesions potentially growing large �
enough to involve the entire calcaneus.
Solitary Bone Cyst: The typical location for this lesion is the Younger than 20
diaphysis (anterior 1/3 laterally). This will have sharp edges. A Fallen Fragment . . •
thick sclerotic edge with a multiloculated appearance is helpful. The Tl Dark, T2 Bright •· . ..
"fallen fragment" will be more in the bottom ifshown - although
(�J
fractures in the calcaneus are much less common than in the arm.
lntraosseous Lipoma: This is also typically located in the
diaphysis (anterior 1/3 laterally). Ifthey show you this, it will either Older than 20
have (a) fat density on CT or MRI, or (b) a central fragment - Central Fragment
stuck within the middle ofthe fat. This calcification/ fat necrosis Jsointense to Fat
occurs about 50% ofthe time in the real world (nearly 100% on on all sequences
pictures shown on tests), and is secondary to fat necrosis.
Pseudo-cyst: This is a variation on the normal trabecular
pattern, which creates a central triangular radiolucent area. This area
is sometimes called the "pseudo-cyst triangle" and is obnoxiously
located in the same anterior 1/3 as the SBC and Lipoma. Supposedly
the persistence ofthin trabeculae, visible nutrient foramen, and the
classic location are helpful in telling it from the other benign
entities.
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Metastatic Disease: Should be on the differential for any patient over 40 with a lytic
lesion. As a piece of trivia renal cancer is ALWAYS lytic (usually).
• Classic Elastic Lesions: Prostate, Carcinoid, Medulloblastoma
• Classic Lytic Lesions: Renal and Thyroid
Next Step - Prostate Met vs Bone Island??? - Get a Bone Scan
• Bone Island should be mild (or not active)
• Prostate Met should be HOT
Multiple Myeloma (MM): Plasma cell proliferation increases surrounding osteolytic
activity (in case someone asks you the mechanism). Usually in older patient (40's-80's).
Plasmacytomas can precede clinical or hematologic evidence of myeloma by 3 years.
They usually have discrete margins, and can be solitary or multiple. Vertebral body
destruction with sparing of the posterior elements is classic. Bone Scan is often negative,
skeletal survey is better (but horribly painful to read), and MRI is the most sensitive.
Additional classic (testable) scenario: MM manifesting as Diffuse Osteopenia
Myeloma Related Conditions:
Plasmacytoma (usually under 40): This is a discrete, solitary mass of neoplastic monoclonal
plasma cells in either bone or soft tissue (extramedullary subtype). It is associated with latent
systemic disease in the majority of affected patients. It can be considered as a singular
counterpart multiple myeloma. The lesions look like a geographic lytic area, sometimes with
expansile remodeling.
"Mini Brain Appearance" - Plasmacytoma in vertebral body
POEMS: This is basically "Mveloma with Sclerotic Mets." It's a rare medical syndrome with
plasma cell proliferation (typically myeloma) , neuropathy, and organomegaly.
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Lucent Lesion Classic Looks and Locations
Long Lesion in a Long Bone Fibrous Dysplasia
Ground Glass Fibrous Dysplasia
Lytic lesion with a hazy matrix Fibrous Dysplasia
Chondroid Matrix in the Proximal Humerus or
Distal Femur Enchondroma
Lucent Lesion in the Finger or Toe Enchondroma
Epiphyseal Tibial Lesion in a Teenager Chondroblastoma
Chondroblastoma or Giant Cell Tumor
Epiphyseal Equivalent Lesion **technically GCTs grow into the Epiphysis
Chondroblastoma
Lucent Lesion in the Greater Trochanter
Lucent Lesion with a Fracture Solitary Bone Cyst
(Fallen Fragment) in the Humerus
Calcaneal Lesion with Central Calcification Lipoma
Lucent Lesion in the Skull EG
Vertebra Plana in a Kid EG
Vertebra Plana in an Adult Mets
Sequestrurn I Nidus in the Tibia/ Femur Osteoid Osteoma
"Painful Scoliosis" Osteoid Osteoma
Calcified Lesion in the Posterior Element
of the C-Spine Osteoblastoma
Solitary vs Multiple (Generalization for Multiple Choice Trivia)
Multiple Sclerotic Lesions Mets
Multiple Sclerotic Lesions Centered Around a
Joint Osteopoikolosis
Mets, Myeloma, Metastatic Non-Hodgkin
Multiple Lucent Lesions ( older than 40) Lymphoma
Size Matters
Nidus < 2.0 cm Osteoid Osteoma
Nidus> 2.0 cm Osteoblastoma
Well-defined lytic lesion in the cortex of a long
Fibrous cortical defect
bone with a sclerotic rim < 3 cm
Well-defined lytic lesion in the cortex of a long
Nonossifying fibroma
bone with a sclerotic rim> 3 cm
Chondral lesion in a long bone 1-2 cm Probably an Enchondroma
Chondral lesion in a long bone> 4-5 cm Increased risk of low-grade chondrosarcoma
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. ';
. ..
...
. �.
. RANDOM Ass
SECTION 6:
COLLECTION OF TRIVIA
�.
Liposclerosing Myxofibroma:
Very characteristic location- at the intertrochanteric region of the femur.
Looks like a geographic lytic lesion with a sclerotic margin. Despite non
aggressive appearance, I0% undergo malignant degeneration so they need to
be followed.
Osteochondroma:
Some people think of this as more of a developmental anomaly (although
they still always make the tumor chapter). Actually, it's usually listed as the
most common benign tumor ("exostosis"). They can be radiation induced,
making them the only benign skeletal tumor associated with radiation.
They have a very small risk of malignant transformation (which supposedly
can be estimated based on size of cartilage cap).
Supposedly a cap > 1.5 cm is concerning.
Key Points:
• They point away from the joint
• The bone marrow flows freely into the lesion *Away.from Joint
Multiple Hereditary Exostosis:
AD condition with multiple osteochondromas.
They have an increased risk of malignant transformation.
Trevor Disease (Dysplasia Epiphysealis Hemimelica - DEH):
This is a disease characterized by the development of osteochondromas develop at the epiphysis
which result in significant joint deformity (most common in ankle and knee)- making you
terrible at tennis and soccer. Instead of pointing away from the joint (like a normal
osteochondroma) these assholes point into the joint- this is why you have so many joint
issues. You see this is young children. The osteochondroma looks more like an irregular mass.
They tend to be treated with surgical excision.
Supracondylar Spur (Avian Spur):
Avian Spur
This is an Aunt Minnie, and normal variant. This is an
osseous process, that usually does nothing, but can
compress the median nerve if the Ligament of Ligament of
Struthers smashes it. Struthers
Notice this thing points towards the joint, that is how
you know it is not an osteochondroma. Also - it is not Supracondylar
a Trevor Disease thing - because Canal
(I) of the characteristic location and
(2) it is not originated from the epiphysis.
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Periosteal Chondroma (Juxta-Cortical
Chondroma): When you see a lesion in the finger
of a kid think this. It's a rare entity, of cartilaginous
origin. "Saucerization" of the adjacent cortex with
sclerotic periosteal reaction can be seen.
Osteofibrous Dysplasia: This is a benign lesion found exclusively in the tibia or
fibula in children (10 and under - usually). It looks like an NOF , but is centered in the
anterior tibia, and has associated anterior tibial bowing. It can occur with Adamantinoma,
and the two cannot be differentiated with imaging.
When I say looks like NOF in the anterior tibia with anterior bowing, you say Osteo_fzbrous
Dysplasia.
Distal Femoral Metaphyseal Irregularity (Cortical Desmoid):
This is a lucency seen along the back of the
posteriomedial aspect of the distal femoral
metaphysis. If they show you a lateral knee x
ray, and there is an irregularity or lucency on the
back of the femur this is it. It's often bilateral.
Buzzwords include "Scoop like defect" with an
"irregular but intact cortex."
This is a total incidental finding and is a don't
touch lesion. Don't biopsy it, Don't MRI it.
Just leave it alone. If you really want to know,
it's probably a chronic tug lesion from the
adductor magnus.
Cortical Oesmoid - Scoop Like Detect
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Calcium Hydroxyapatite: Most pathologic calcification in the body is calcium
hydroxyapatite, which is also the most abundant form ofcalcium in bone.
Calcium hydroxyapatite deposition disease = calcific tendinitis.
The calcium is deposited in tendons around the joint. The most common location for
hydroxyapatite deposition is the shoulder. Specifically, the supraspinatus tendon is the
most frequent site of calcification, usually at its insertion near the greater tuberosity. The
longus colli muscle (the muscle anterior to atlas-> T3) is also a.favorite location.for multiple
choice test writers. It may be primary (idiopathic) or secondary. Secondary causes worth
knowing are: chronic renal disease, collagen-vascular disease, tumoral calcinosis and
hypervitaminosis D.
Osteopoikilosis: It's just a bunch ofbone islands. Usually in epiphyses (different from
blastic mets or osteosarcoma mets). It can be inherited or sporadic but ifyou are forced to
pick a pattern - I'd go with autosomal dominant.
Mets vs Osteopoikilosis - Osteopoikilosis tends to be joint centered (clustered around
centered). Sclerotic mets will be all over the place. Sclerotic mets believe in nothing
Lebowski.
Trivia - Osteopoikilosis patients tend to be keloid formers.
Osteopathia Striata: Linear, parallel, and longitudinal lines in
metaphysis oflong bones. Doesn't mean shit (usually - but can in some
situations cause pain).
Engelmann's Disease: This is also known as progressive diaphyseal
dysplasia or PDD. What you see is.fusiform bony enlargement with sclerosis of
the long bones. This is a total zebra that begins in childhood.
Things to know:
• Its Bilateral and Symmetric
• It likes the long bones - usually shown in the tibia
• It�, hot on bone scan
• It can involve the skull - and can cause optic nerve compression
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Thalassemia: This is a defect in the hemoglobin chain
Thalassemia Sickle Cell
(can be alpha or beta - major or minor). From the MSK
Radiologist prospective, we are talking about "hair-on-end" Will Not
skulls, expansion of the facial bones, "rodent faces," Will Obliterate
Obliterate
expanded ribs "jail-bars". It is frequently Sinuses
Sinuses
associated with extramedullary Lytic --Usiia y symp oma 1c
hematopoiesis.
Mixed Elevated Alkaline
(reparative) Phosphate. Fractures
Sclerotic Elevated Hydroxyproline.
AVN of the Hip:
(latent More fractures. Sarcomas
inactive) ma develo .
Variety of causes including Perthes in kids,
sickle cell, Gaucher's, steroid use etc .... It can also be traumatic with femoral neck
fractures (degree o[risk is related to degree ofdisplacement I disruption of the retinacular
vessels). AYN of the hip typically involves the superior articular surface,
� beginning more anteriorly.
�')
/ �------------�-----------�
Double Line Rim Sign: Crescent Sign:
Sign: Best seen on T2; high T2 signal line Seen on X-ray (optimally frog
Best seen on T2; inner sandwiched between two low signal leg); Refers to a subchondral
bright line (granulation lines. This represents fluid between lucency seen most frequently in
tissue), with outer dark sclerotic borders of an osteochondral the anterolateral aspect of the
line (sclerotic bone). fragment, and implies instability. proximal femoral head. It
(Stage III). indicates i1mninent collapse.
Plain Film Stages of Osteonecrosis
(there are MR stages also - presumed to be beyond the scope of this exam):
o Zero = Normal
o One = Normal x-ray, edema on MR
o Two = Mixed Lytic / Sclerotic
o Three = Crescent Sign, Articular Collapse, Joint Space Preserved
o Four = Secondary Osteoarthritis
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Paget Disease (Osteitis Deformans):
A relatively common condition that affects 4% of people at 40, and 8% at 80 (actually 10%,
but easier to remember 8%). M > F. Most people are asymptomatic. The pathophysiology of
Paget is not well understood.
The bones go through three phases which progress from lytic to mixed to sclerotic (the
latent inactive phase). The phrase "Wide Bones with Thick Trabecula" make you
immediately say Pagets (nothing else really does that).
Comes in two flavors: (1) Monostotic and (2) Polyostotic - with the poly subtype being
much more common (80-90%).
� Buzzwords I Signs:
• Blade of Grass Sign: Lucent leading edge in a long bone
•Osteoporosis Circumscripta: Blade of Grass in the Skull
•Picture Frame Vertebra: Cortex is thickened on all sides (Rugger Jersey is only superior and inferior
endplates)
•Cotton Wool Bone: Thick disorganized trabeculae
• Banana Fracture: Insufficiency fracture of a bowed soft bone (femur or tibia).
• Tam O 'Shanter Sign: Thick Skull - with the frontal aspect "falling over the facial bones"
• Saber Shin: Bowing of the tibia
• Ivory Vertebra: This is a differential finding, including mets. Pagets tends to be expansile.
Complications: Deafness is the most common
complication. Spinal stenosis from c01iical thickening
is ve1y characteristic. Additional complications include
cortical stress fracture, cranial nerves paresis, CHF Classic Look:
(high output), secondary hyperparathyroidism (10%),
Secondary development of osteosarcoma (1 %) - Expanded
which is often highly resistant to treatment. As a
Bone
piece of ridiculous trivia - giant cell tumor can arise
from Paget.
Coarse or
Trivia: Of all the tumors to which Paget may devolve Thick
to, Osteosarcoma is the Most Common.
Trabecular
Total Trivia: Paget bone is hypervascular and may be 5 Pattern
degrees hotter than other bone (get your thermometer
ready). Alk Phos will be elevated (up to 20x) in the
reparative phase.
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Skull:
Long Bones
Large Areas of Osteolysis
in the Frontal and Occipital Advancing margin of
Bones "Osteoporosis
Circumscripta", in the lytic
lucency from one end to
phase. the other is the so-called
"blade of grass" or
"flame." Will often spare
the fibula, even in diffuse
The skull will look disease.
"cotton wool" in the
mixed phase. Tibia Bowing "saber
shin" is also classic.
Thickened sclerotic
appearance is a good chronic look. Involves Pelvis:
BOTH inner and outer table (Fibrous Dysplasia
favors the outer table)
Most common bone involved. "Always"
involves the iliopectineal line on the
pelvic brim.
Can cause advanced arthritis and
acetabular protrusio.
Has a classic look
on bone scan.
Tam O 'Shanter Sign: Skull sorta looks like one
of those stupid hats with the frontal aspect
"falling over the facial bones"
Spine:
Cortical Thickening can cause a "picture
frame sign" (same as osteopetrosis). Also
can give you an ivory vertebral body.
Discussed more on the next page
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THIS vs THAT Pagets Spine vs Other Spine Changes
Pagets - This is discussed in detail in the MSK chapter, but is such a high yield topic that it's
worth touching on again. The incidence increases with age (around 8% at age 80). It's at
increased risk for fracture, and has a 1% risk of sarcoma degeneration (usually high grade).
It's shown two ways in the spine:
(1) An enlarged "ivory vertebrae", I Picture
(2) Picture frame vertebrae (sclerotic border) I Ivory Frame
-- with central lysis (mixed phase)
Renal Osteodystrophy - Another high yield topic covered in depth in the MSK chapter. The
way it's shown in the spine is the "Rugger Jersey Spine" - with sclerotic bands at the top and
bottom of the vertebral body. You could also have paraspinal soft tissue calcifications
This vs That: Rugger Jersey vs "Paget" Picture Frame:
• Rugger Jersey= Top and Bottom Only
• Paget Picture Frame= All 4 margins of the vertebral body
Osteopetrosis - Another high yield topic covered in depth in the MSK chapter. This is a
genetic disease with impaired osteoclastic resorption. You have thick cortical bone, with
diminished marrow. On plain film or CT it can look like a Rugger Jersey Spine or Sandwich
vertebra. On MR you are going to have loss of the normal Tl bright marrow signal, so it will
be Tl and T2 dark.
"H-Shaped Vertebra" - This is usually a buzzword for sickle cell, although it's
only seen in about 10% of cases. It results from microvascular endplate infarct.
If you see "H-Shaped vertebra," the answer is sickle cell. If sickle cell isn't a
choice the answer is Gauchers. Another tricky way to ask this is to say which of
the following causes "widening of the disc space." Widened disc space is
another way of describing a "H Shape" without saying that.
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Paget on Other Imaging Modalities:
MRI: There are three maffow patterns
Lytic / Early Heterogenous T2; T l is
that closely (but not exactly) follow the
Mixed isointense to muscle, with a
phases on x-ray.
"speckled appearance"
Late Mixed Maintained fatty high T 1 and
T2 sig11aJs
Sclerotic Low sig11al on T l and T2
This vs That: Malignant Transformation vs Active Disease:
• Both are T2 Bright and Will Enhance
• Malignant Transformation will lose the Normal T l signal (just like a cancer would)
• Best Sequence for Distinguishing the two? T l Pre Con
Nuclear Medicine: The primary utility of a bone scan is in
defining the extent of disease and to help assess response R
to treatment. The characteristic look for Paget is "Whole
Bone Involvement."
For example, the entire vertebral body including the
posterior elements, or the entire pelvis. The classic
teaching is that Paget is hot on all three phases (although
often decreased or normal in the sclerotic phase).
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Tibial Bowing
Most likely shown as an Aunt Minnie: NF-1 anterior with a fibular pseudoarthrosis, Rickets
with wide growth plates, or Blounts tibia vara. Pagets can also cause this.
The most likely pure trivia question is that physiologic bowing is smooth, lateral, and occurs
from 18 months - 2 years.
NF-I Anterior Lateral - Unilateral May be unilateral. May
have hypoplastic fibula with
pseudarthrosis.
Lateral Frontal
Foot Deformities Posterior
Physiologic Bowing Lateral - Bilateral Symmetric Self limiting between 18
months and 2 years.
Hypophosphatasia Lateral "Rickets in a newborn"
Rickets Lateral Fraying of the metaphyses
and widening of the growth
plates.
Seen best in "fast growing
bones" - knee, wrist
Blount Tibial Vara - Often Early walking, Fat, black
asymmetric kid.
Proximal tibia posteromedial
physeal growth disturbance
resulting in deformity
Osteogenesis Imperfecta Involves all long bones
Dwarfs Short Limbs
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•. �
SECTION 7:
SOFT TISSUE MASSES
�
• .
Studying / learning MSK soft tissues masses / tumors tends to create tons of anxiety. This is
because Academic Radiology tends to overcomplicate the issue.
Here is the simple part - only about 20-30% of them can be accurately diagnosed on MRI. That's
because they are almost all T2 bright and enhance. This is actually good news for the purpose of
multiple choice, because you only need to learn the ones that don't behave like that - or are
overwhelming likely due to epidemiological stats (which has to be provided for you - either
directly "the patient is 65" or with clues - "arthritis = old" , "no arthritis = not old").
Here is the list I would know:
• MFH -Malignant Fibrous Histiocytoma aka - Pleomorphic Undifferentiated Sarcoma
• Synovial Sarcoma
• Lipoma, Atypical Lipoma, Liposarcoma
• Hemangioma
• Myxoma
Malignant Fibrous Histiocytoma (MFH)
Yes - they changed the name to Pleomorphic Undifferentiated Sarcoma "PUS." However, I want
you to continue to think of this as MFH because it will help you remember some of the imaging
features.
First, the generalizations -This is very common. It's seen in old people. It's seen in a central
location (proximal arms and legs).
Features -About half the time it's dark to intermediate on T2 (remember most soft tissue
tumors are T2 bright). The way I remember this is the word "fibrous" - makes me think scar
(which is dark).
Gamesmanship - These things are often associated with spontaneous hemorrhage - they outgrow
their blood supply. The history is often "old lady, stood up from a chair" - has a big proximal
muscular hematoma -under that hematoma is the MFH.
Trivia: Bone infarcts can turn into MFH - "sarcomatous tran�formation of infarct"
Trivia: Radiation is a risk factor.
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Synovial Sarcoma:
Generalization - Seen most commonly in the peripheral lower extremities of patients aged
20-40.
Baker's Cyst Fuckery
Gamesmanship - They occur close to the joint (but not in the
joint). To confuse the issue they may have secondary Baker's Cyst MUST be
located between the medial
invasion into the joint (10%), however for the purpose of head of the gastrocnemius
multiple choice tests they "never involve the joint." A and the semimembranosus.
common trick is to show an ultrasound of the leg with looks
like a Baker's cyst - but the mother fucker is too complex - or If it's NOT - you should
think Synovial Sarcoma -
has flow in it. *Not everything in the popliteal fossa is a and "next step" MRI.
Baker's cyst - especially on multiple choice.
Besides the "not-a-Baker's cyst" trick - there are 3 other ways to show this. (1) as the "triple
sign", which is high, medium, and low signal all in the same mass (probably in the knee) on
T2, (2) as the "bowl of grapes" which is a bunch of fluid -fluid levels in a mass (probably in
the knee), or (3) as a plain x-ray with a soft tissue component and calcifications - this would
be the least likely way to show it.
Synovial Sarcoma Trivia:
• Most sarcomas don't attack bones; Synovial Sarcoma Can
• Most sarcomas present as painless mass; Synovial Sarcomas Hurt
• Soft tissue calcifications + Bone Erosions are highly suggestive
• They are slow growing and small in size, often leading to people thinking they are B9.
• 90% have a translocation ofX-18.
• Most common malignancy in teens/young adults of the foot, ankle, and lower
extremity
When I say "Ball-like tumor" in the extremity ofa young adult, you say Synovial Sarcoma.
When I say "So.ft Tissue Tumor in the Foot" of a young adult, you say Synovial Sarcoma.
MFH (PUS) Synovial Sarcoma
OLD YOUNG
Central (Upper Thigh, Upper Arm) Peripheral (Foot, Knee)
T2 - Variable (Sometime Dark) T2 - "Triple Sign"
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Lipoma vs Atypical Lipoma vs Liposarcoma
These exist on a spectrum, with Lipoma being totally benign, and Liposarcoma being a bad
bad boy. A pearl is that, histologically, Atypical Lipoma behaves and looks just like a low
grade Liposarcoma. It would be total horse-shit to ask you to tell those apart. It's more likely
the distinction will be either Lipoma vs Liposarcoma.
Think about them like this:
Atypical Lipoma/ Low Grade High Grade Liposarcoma
Lipoma
Liposarcoma "The One That Fucks You Up"
May not even have fat (for the
May have parts that are slightly
Signal Intensity parallels fat on exam it will have some
darker (or brighter) than fat on
all sequences. otherwise you can't even tell for
T1.
sure that it is a Liposarcoma)
May incompletely fat sat (or not
Will Fat Sat Out May incompletely fat sat
fat sat at all)
No Sepations (or thin ones) Thick Chunky Septations Thick Nodular Complex Stuff
Enhancing Components
Pearls:
•Liposarcornas tend to be DEEP (retroperitoneurn)
•Liposarcomas tend to be BIG
• Lipomas tend to be Superficial
Trivia: Myxoid Liposarcoma is the most common liposarcoma in patients < 20. They can be
T2 Bright (expected), but T l dark (confusing) - don't call it a cyst. Also, don't call it a
comeback (I've been here for years). They'll need gad+
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Hemangioma
Mazabraud Syndrome
These are common.
Here are the tricks: It's a totally zebra syndrome - which
• T2 bright (like most tumors) makes it totally appropriate for an
• Flow voids. They have to show you flow voids "intermediate level exam." It has 3 main
(buncha dark holes). findings:
• Hemangiomas don't respect fascial boundaries
- they will infiltrate into stuff (this is a ( 1) Polyostotic Fibrous Dysplasia -
somewhat unique feature). which makes you ugly
• Enhances Intensely - Duh - they are a vascular (2) Multiple Soft Tissue Myxomas
tumor (3) Difficulty finding a date to the prom
• They can contain fat - and likely will on - *see finding "1"
multiple choice.
Next Step: A great next step question would be to ask for a plain film. Why a plain film?
phleboliths my friend- If they show you soft tissue phleboliths then hemangioma is the answer.
Myxoma
If this shows up on the exam, it is almost certainly going to be shown in the setting of
Mazabraud Syndrome.
What do Myxomas Look Like? They are T2 bright (like every tumor), but tend to be lower signal
than muscle on T 1 - which makes them sorta unique.
What does Marsellus Wallace Look Like ? *Hint - Don't say "what?"
CT vs MRI Treatment High Yield Trivia:
for Lesion Characterization:
•Osteosarcoma: Chemo first (to kill micro
mets) , followed by wide excision
CT is Good for:
-Occult Bone Destruction •Ewings: Both Chemo and Radiation,
-Matrix and Mineralization- Example, followed by wide excision.
better look at the lucent nidus of an •Chondrosarcoma: Usually just wide
osteoid osteoma. excision (they are usually low grade, and
MR is Good for: main concern is local recurrence).
-Staging - specifically local extend and • Giant Cell Tumor: Because it extends to
tumor spread. the articular surface usually requires
-Follow up - to assess response to
therapy. arthroplasty.
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Other Soft Tissue Masses land related conditions)
Pigmented Villonodular Synovitis (PVNS) : PVNS is an uncommon benign
neoplastic process that may involve the synovium of the joint diffusely or focally. It can also
affect the tendon sheath.
Intra-Articular Disease : Basically, it's Synovial Proliferation + Hemosiderin Deposition.
The knee is by far the most common joint affected (65-80%). On plain film, features you will
probably see are a joint effusion with or without marginal erosions. Osseous erosions with
preservation of the joint space and normal mineralization is typical. It is not possible to
distinguish PVNS from synovial chondromatosis (see below) on plain film. MRI will be
obvious with blooming on gradient echo, and this is the most likely way they will show this.
Treatment is with complete synovectomy, although recurrence rate is 20-50%.
Trivia: Unusual in kids, but when present is typically polyarticular.
Giant Cell Tumor of the Tendon Sheath (PVNS of the tendon): Typically found in the hand
(palmar tendons). Can cause erosions on the underlying bone. Will be soft tissue density, and be
Tl and T2 dark (contrasted to a glomus tumor which is Tl dark, T2 bright, and will enhance
untformly).
Primary Synovial Chondromatosis: There are both primary and secondary types;
secondary being the result of degenerative changes in the joint. The primary type is an
extremely high yield topic. It is a metaplastic / true neoplastic process (not inflammatory) that
results in the formation of multiple cartilaginous nodules in the synovium of joints, tendon
sheaths, and bursea. These nodules will eventually progress to loose bodies. It usually affects
one joint, and that one joint is usually the knee (70%). It is usually a person in their 40's or 50's.
Joint bodies (which are usually multiple and uniform in size) may demonstrate the ring and arc
calcification characteristic of chondroid calcification. Treatment involves removal of the loose
bodies with or without synovectomy.
PVNS Synovial Chondromatosis
Benign Neoplasia Benign Neoplasia
Associated with Hemarthrosis NOT Associated with Hemarthrosis
Never Calcifies May Calcify
Secondary Synovial Chondromatosis: A lower yield topic than the primary type.
This is secondary to degenerative change, and typically seen in an older patient. There will be
extensive degenerative changes, and the fragments are usually fewer and larger when compared
to the primary subtype.
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Diabetic Myonecrosis:
This is basically infarction of the muscle seen in poorly controlled type l diabetics. It almost
always involves the thigh (80% ), or calf (20% ). MRI will show marked edema with
enhancement and irregular regions of muscle necrosis. You should NOT biopsy this: it
delays recovery time and has a high complication rate.
Lipoma Arborescens:
S\_�l)r'4 This is a zebra that affects the synovial lining of the joints and bursa.
§'Wt,�
t\ {\.
The buzzword is "frond-like" deposition
of fatty tissue.
It's seen in late adulthood (50's-70's), with
the most common location being the
suprapatellar bursa of the knee. Although
it can develop in a normal knee, it's
often associated with OA, Chronic RA,
or prior trauma. It's usually unilateral.
On MRI it's going to behave like fat - Tl
and T2 bright with response to fat
saturation.
A sneaky trick is to show this on gradient
- and have you pick up the chemical shift
Lipoma Arborescens
artifact at the fat-fluid interface.
This could also be shown on ultrasound with a "frond-like hyperechoic mass" and associated
joint effusion.
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Bone Biopsy
The route of biopsy should be discussed with the orthopedic surgeon, to avoid
contaminating compartments not involved by the tumor (or not going to be used in the
resection process).
Special considerations:
• Pelvis: Avoid crossing gluteal muscles (may be needed for reconstruction).
• Knee: Avoid the joint space via crossing suprapatellar bursa or other
communicating bursae. Avoid crossing the quadriceps tendon unless it is
involved.
• Shoulder: Avoid the posterior 213rd (axillary nerve courses post-> anterior,
therefore a posterior resection will denervate the anterior 1/3).
"Don't Touch Lesions"
Characteristically Benign Lesions that look Aggressive but are NOT
- and should NOT be biopsied because of possibly misleading pathology.
Circumferential Can look scary on MRI if
Myositis Ossificans calcifications with a lucent imaged early because of
center edema, and avid enhancement
Typical location near the Can have an aggressive
Avulsion Injury
pelvis periosteal reaction
Can be hot on bone scan.
Characteristic location on
the posterior medial
NOT a desmoid (despite the
epicondyle of the distal
Cortical Desmoid name). It's actually a tug
femur.
lesion from the medial
gastrocnemius and ADDuctor
Bilateral 30% of the time.
magnus.
Characteristic location in the
anterosuperior femoral neck.
Lytic appearing lesion
Synovial Herniation Pit
Associated with femoral
"Pitt's Pit"
acetabular syndrome
(probably).
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SECTION 8:
ARTHRITIS
Arthritis is tricky. Anne Brower wrote a book called Arthritis in Black and White, which is
probably the best book on the subject. The problem is that book is 415 pages. So, I'm going
to try and offer the 10 page version.
Epidemiology
Although there are over 90 different rheumatic diseases recognized by the American College
of Rheumatology, only a few tend to show up on multiple choice tests (and at the view box).
You can broadly categorize arthritis into 3 categories:
• Degenerative (OA, Neuropathic)
• Inflammatory (RA and Variants)
• Metabolic (Gout, CPPD)
Degenerative:
Osteoarthritis is the most common cause. The pathogenesis is that you have mechanical breakdown
(hard work) which leads to cartilage degeneration (fissures, micro-fractures) and fragmentation of
subchondral bone (sclerosis and subchondral cysts). You get all the classic stuff, joint space
narrowing (NOT symmetri.Q), subchondral cysts, endplate changes, vacuum phenomenon, etc ... The
poster boy is the osteophyte.
Neuropathic Joint. The way the case is classically shown is a bad joint followed by the reason for a
bad joint (syringomyelia, spinal cord injury, etc ... ). A way to think about this is "osteoarthritis with a
vengeance." The buzzword is "Surgical Like Margins." Basically nothing else causes this kind of
destruction. I like to describe the joints as a deformity, with debris, and dislocation, having dense
subchondral bone, and destrnction of the articular cortex. The classic scenario is a shoulder that looks
like it's been amputated, and then they show you a syrinx.
Charcot Foot - The classic example of a diabetic neuropathic foot with
the deformity, with debris, and dislocation, having dense subchondral
bone, and destruction of the articular cortex - favoring the midfoot
eventually causing a "rocker-bottom deformity" of the foot resulting
from the collapse of the longitudinal arch.
This vs That - Charot vs Infection: Diabetics get neuropathic feet and infections - so there can be overlap.
To tell them apaii you can look for the presence of an ul.�er or sinus tract (that infers infection).
Location is helpful - charcot prefers the midfoot (osteomyelitis prefers the pressure points of the forefoot -
metatarsal heads, IP joints - and the posterior plantar aspect of the calcaneus).
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Inflammatory:
Erosive Osteoarthritis (Inflammatory
Osteoarthritis). The buzzword is "gull wing",
which describes the central erosions. It is seen in
postmenopausal women and favors the DlP joints.
Rheumatoid Arthritis: There is a ton of trivia
Erosive OA- Gullwing
related to this disease. It's not a disease of bone production. Instead it is characterized by
osteoporosis, soft tissue swelling, marginal erosions and unif01mjoint space narrowing. It's
often bilateral and symmetric. Classically spares the DIP joints (opposite of erosive OA).
Trivia: The 5th Metatarsal head is the first spot in the foot
RA in the Hand Pearls - Expect the PIP joints to be involved AFTER the MCP joints. The
First CMC is classically spared (or is the last carpal to be involved). The first CMC should
NOT be first. Obviously OA loves the first CMC so this is helpful in separating them.
Psoriasis, on the other hand, also tends to make the first CMC go last.
• Felty Syndrome: RA> 10 years+ Splenomegaly+ Neutropenia
• Caplan Syndrome: RA + Pneumoconiosis
The distribution of RA vs OA in the
hip is a classic teaching point:
Axial
OA RA
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Rheumatoid Variants:
• Psoriatic Arthritis
• Reiter's syndrome (Reactive arthritis)
• Ankylosing Spondylitis
• Inflammatory Bowel Disease
Psoriatic Arthritis: This is seen in 30% of patients with psoriasis. In almost all cases
(90%) the skin findings come first, then you get the arthritis. As a point of trivia, there is a
strong correlation between involvement of the nail and involvement of the DIP joint. The
classic description is "erosive change with bone proliferation (IP joints> MCP joints).
The erosions start in the margins of the joint and progress to involve the central portions
(can lead to a "pencil sharpening" effect). The hands are the most commonly affected
(second most common is the feet). Up to 40% of cases will have SI joint involvement
(asymmetric).
Additional Buzzwords
• "Fuzzy Appearance" to the bone
around the joint (bone proliferation)
• Sausage Digit - whole digit has soft
tissue swelling
• Ivory Phalanx - sclerosis and/or
bone proliferation (most commonly
the great toe)
• Pencil in Cup Deformities IP Joints Ray Pattern Pencil Mouse
• Ankylosis in Finger in Cup Ears
• "Mouse Ears"
• Acro-osteolysis
When I say Ankylosis in the Hand, You Say (1) Erosive OA or (2) Psoriasis
RA Psoriasis Mutilans
Symmetric Asymmetric Severe bone resorption leading to
Proximal Distal soft tissue "telescoping" collapse.
(favors MCP, carpals) (favors IP joints) Trivia: If you
Osteoporosis No Osteoporosis pulled on the
patient's fingers
they would
Bone Proliferation
No Bone Proliferation lengthen - but who
- the form of pcriostitis
would want to
Can Cause "Mutilans" Can Cause "Mutilans" touch a patient ?
When Severe When Severe Yuck!
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Reiter's (Reactive Arthritis): Reiter's Triad:
Apparently Reiter was a Nazi (killed a bunch of people with Urethritis
Conjunctivitis
typhus vaccine experiments). So, people try not to give him any Arthritis
t:re<lil for lhings (hent:e lhe name diange lo Readive arlhrilis).
Regardless of what you call it, it's a very similar situation to (Can't See or Climb a
Psoriatic arthritis - both have bone proliferation, erosions, and Tree to Pee on a Nazi
named Reiter).
asymmetric SI joint involvement.
The difference is that Reiter's is rare in the hands (tends to fou Know Who Else
Was A Nazi?
affect the feet more). Just remember Reiter's favors things below
the waist (like the penis = urethritis, and the foot). Henry Ford
- Google It.
Ankylosing Spondylitis: This disease favors the spine and SI joints. The classic
buzzword is "bamboo spine" from the syndesmophytes flowing from adjacent vertebral
bodies. Shiny corners is a buzzword, for early involvement. As you might imagine, these
spines are susceptible to fracture in trauma. SI joint involvement is usually the first site
(symmetric). The joint actually widens a little before it narrows. As a point of trivia, these
guys can have an upper lobe predominant interstitial lung disease, with small cystic spaces.
Next Step - Any significant Ank Spon / DISH + Even Minor Trauma = Whole Spine CT
Random High Yield Topic: Ankylosing Spondylitis in the Hip
. - - ·---·· -· · --·- ··· -·-----•-a, ··--·-··---·- ______,.. - ····---·---- · · · - ·-··- •-····· ··- --· ··-·--- --- -·-·-···· - --•->s - ••-·--···· ·· · ····--· ------·
When the peripheral skeleton is involved in patient's with Ank Spond, think about the
shoulders and hips (hips more common). Hip involvement can be very disabling.
Heterotopic Ossification tends to occur post hip replacement or revision. It occurs so
much that they often get postoperative low dose radiation and NSAIDs to try as
PI"()phylcic;!_ic; t]:i�rcipy: _ _. __ . . _ --·
If they show you nonnal SI joints - then show you anything in the spine it's not AS. It has
to hit the SI joints first (especially on multiple choice).
Inflammatory Bowel Disease (Enteropathic)-Allegedly 20% of patient's
with Crohns & UC have a chronic inflammatory arthritis. The imaging findings occurs in
two distinct flavors.
(A): Axial Arthritis (favors SI joints and spine) - often unrelated to bowel disease
(B): Peripheral Arthritis - this one varies depending on the severity of the bowel disease.
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SI Joint Involvement Patterns (Rheumatoid Variants)
--. P-A-1-R -
Unilateral= Infection Asymmetric=
l> V ,___
Symmetric=
I
,__j
Psoriasis, Reiters Inflammatory Bowel, AS
Psoriatic Arthritis Reiters (Reactive) Ankylosing Spondylitis
M=F M> F M>F
Asymmetric SI Joint Asymmetric SI Joint
--··--·-··-··-- . - --·-·· --····- --•• •--
Symmetric SI Joint
•- so~••--••• •- • • •• • •~•••• -•••-•••-~•.-••
Hands, Feet, Thoracolumbar Spine Feet, Lumbar Spine, SI joint SI joint, Spine (whole thing)
Metabolic:
Gout: This is a crystal arthropathy from the deposition of uric acid crystals in and around the
joints. It's almost always in a man over 40. The big toe is the classic location.
Buzzwords I Things to Know:
• Earliest Sign = Joint Effusion Gout on MR
• Spares the Joint Space (until late in the disease); Juxta
• Juxta-articular soft
articular Erosions - away from the joint. tissue mass (LOW
• "Punched out lytic lesions" ONT2).
• "Overhanging Edges" • The tophus will
typically enhance.
• Soft tissue tophi
Gout Mimickers:
There are 5 entities that can give a similar appearance to a gouty arthritis, although they are much
less common. This is the mnemonic I was taught in training:
"American Roentgen Ray Society Hooray"
• Amyloid
• RA (cystic)
• Reticular Histocytosis (the most rare)
• Sarcoid
• Hyperlipidemia
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CPPD: Calcium Pyrophosphate Dihydrate Disease is super common in old people. lt often
causes chondocalcinosis (although there are other causes). Synovitis + CPPD =
"Pseudogout." CPPD loves the triangular fibrocartilage of the wrist, the peri-odontoid tissue,
and intervertebral disks. Another important phrase is "degenerative change in an
uncommon joint'' - shoulder, elbow, patellofemoral joint, radiocarpal joint. Having said
lhat, pyrophosphate arthropathy is most common at the knee.
• .(fyou see isolated disease in the patellofemoral, radiocarpal, or talonavicular joint,
think CPPD.
• Hooked MCP Osteophytes with chondrocalcinosis in the TFCC is a classic look
(although hemochromatosis can also look that way).
CPPD can (and does commonly) cause SLAC wrist by degenerating the SL Ligament.
THIS vs THAT-DA vs CPPD?
There are many overlapping features including joint space narrowing, subchondral
sclerosis, subchondral cyst, and osteophyte formation. However, CPPD has some unique
features, such as an "atypical joint distribution" - favoring compartments like the
patellofemoral or radiocarpal. Subchondral cyst fonnation can be bigger than expected.
Hemochromatosis:
This iron overload disease also is known for calcium
pyrophosphate deposition and resulting
chondrocalcinosis. It has a similar distribution to
CPPD (MCP joints). Both CPPD and
Hemochromatosis will have "hooked osteophytes"
at the MCP joint.
THIS vs THAT- CPPD and Hemochromatosis:
Hemochromatosis has uniform joint space loss at
ALL the MCP joints. CPPD favors the index and
middle finger MCPs.
Trivia: As a point of trivia, therapy for the
systemic disease does NOT affect the arthritis. Hooked Osteophytes
-CPPD vs Hemochromatosis
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"Milwaukee Shoulder" - This is an apocalyptic
destruction of the shoulder (almost looks neuropathic)
secondary to the demon mineral hydroxyapatite.
The articular surface changes will be very advanced,
and you have a lot of intra-articular loose bodies.
Humeral Head has
The humeral head will look like it needed the United been massacred.
Nations to delivery a binding resolution to keep the -I'm talking scorched
Earth Mother Fuckers
hydroxyapatite from fucking destroying it.
Classic History: Old women with a history of trauma to
that joint.
Hyperparathyroidism - As you may remember from medical school, this can be
primary or secondary, and its effects on calcium metabolism typically manifest in the bones.
Here are your buzzwords: "Subperiosteal bone resorption" of the radial aspect of the 2nd and
3rd fingers, rugger-jersey spine, brown tumors, and terminal tuft erosions.
The classic ways this can be shown:
• Superior and i"nferior rib notching - bone resorption
• Resorption along the radial aspect of the.fingers with brown tumors
• Tiift Resorption
• Rugger Jersey Spine
• Pelvis with Narrowing or "Constricting" of the.femoral necks, and wide SIjoints.
Hyperparathyroidism
Subperiosteal Resorption, Tuft Resorption Rugger Jersey Spine Brown Tumor
and brown tumors
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Problem Solving:
If you are given a picture of a hand or foot and asked what the arthritis is, it wi11 probably be
obvious (they show a gull-wing for erosive OA, or bad carpals for RA, or the pencil in cup for
psoriasis, or the 5th metatarsal for RA). If it's not made obvious with an "Aunt Minnie"
appearance, I like to use this approach to figure it out (I also use this in the real world).
Infection
Has one or more: OneJoint /
-Symmetric Joint
/f
►► Inflammatory
----1
No Bony Proliferation
Proximal Distribution
➔ RA
Space Narrowing
-Erosions
MultipleJoints
AS
� Bony Proliferation
Distal Distribution ➔ Psoriasis
Reactive
Inflammatory
Bowel Related
TypicalJoints (Hands, Knees) --�►� OA
Has one or more:
/f -Post Traumatic
-AsymmetricJoint +Degenerative+ AtypicalJoint
-Gout or CPPD
Space Narrowing Atypical Age -Hemophilia
-Osteophytes
\
AtypicalJoint
Atypical Age ➔ Neuropathic
SEVERE or "Surgical Destruction"
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Spine Degenerative Change:
In the real world it's usually just multilevel degenerative change. But in multiple choice
world you should be thinking about other things. Shiny corners with early AS, or flowing
syndcsmophytcs with later AS. DISII with the bulky ostcophytcs sparing the disc space.
The big bridging lateral osteophyte is classically shown for psoriatic arthritis.
Vertebral Ossifications
·--····· · •--·•--··-·· - . ···--·· · ··· Cervical Spine:
"Flowing Ankylosing Gamesmanship
Bamboo Spine
Syndesmophytes" Spondylitis Fusion: Either
- ·--·- -·· ---·--····-··- -····••s.- - · ··-- ---·-··- · ··------ ----- --- ·---------- ----------·--- .. -- -------·-- --··,. -
congenital (Klippel-
Diffuse Paravertebral Feil) or Juvenile RA.
DISH Ossification of ALL
Ossifications
I-·· - - · -·-· -•--- -· -·-·---- . ----···--·-··---- ... .
Erosions of the
Dens: CPPD and RA
Focal Lateral
Ossification of famously do this.
Paravertebral Psoriatic Arthritis
Annulus Fibrosis
Ossification Bad Kyphosis = NFl
DISH {Diffuse Idiopathic Skeletal Hyperostosis) :
You see ossification of the anterior longitudinal ligament involving more than 4 levels with
sparing of the disc spaces, you say DISH. The thoracic spine is most commonly used.
These guys often have bony proliferation at pelvis, ischial tuberosities, trochanters, and iliac
crests. There is no sacroiliitis {helps you differentiate from AS).
OPLL {Ossification of the Posterior Longitudinal Ligament):
This is an ossification of the posterior longitudinal ligament. It is associated with DISH,
ossification of the ligamentum flavum, and Ankylosing Spondylitis. It favors the cervical
spine of old Asian men. It can cause spinal canal stenosis, and can lead to cord injury after
minor trauma. A key point is that it's bad news in the cervical spine (where it is most
common); in the thoracic spine it is usually asymptomatic.
Destructive Spondyloarthropathy.:
This is associated with patients on renal dialysis (for at least 2 years), and it most commonly
affects the C-spine. It looks like bad degenerative changes or CPPD. Amyloid deposition is
supposedly why it happens.
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Misc Stun That's Sorta in the Arthritis Cateuorv:
Systemic Lupus Erythematosus:
The Aunt Minnie look is reducible deformity
of joints without articular erosions. Joint
space narrowing and erosions are uncommon
findings. They can show you the hands with
ulnar subluxations at the MCPs on Norgaard
view, then they reduce on AP (because the
hands are flat).
This ligamentous laxity also increases risk of
patellar dislocations.
SLE: Shows Reversible Ulnar Deviation
Jaccoud's Arthropathy: This is very similar to SLE in the hand (people often say them together).
You have non erosive arthropathy with ulnar deviation of the 2°d-5th fingers at the MCP joint. The
history is post rheumatic fever.
Mixed Connective Tissue Disease: One unique feature is that it is positive for some antibody -
Ribonucleoprotein (RNP) - and therefore serology is essential to the diagnosis.
Juvenile Idiopathic Arthritis: This occurs before age
16 (by definition). What you see is a washed out hand
that has a proximal distribution (carpals are jacked),
and is ankylosed (premature fusion of growth plates).
Serology is often negative (85%). In the knees, you see
enlargement of the epiphyses and widened intercondylar
notch - similar to findings in hemophilia.
Widened
� Buzzword: "Epiphyseal Overgrowth" lntercondylar
/
Notch
Amyloid Arthropathy: This is seen with patients on dialysis (less commonly in patients with chronic
inflammation such as RA). The pattern of destruction can be severe - similar to septic arthritis or
neuropathic spondyloarthropathy. The distribution is key, with bilateral involvement of the shoulders,
hips, carpals, and knees being typical. Carpal tunnel syndrome is a common clinical manifestation.
The joint space is typically preserved until later in the disease. When associated with dialysis, it's rare
before 5 years of treatment, but very common after 10 years (80%).
Pituitary Gigantism: If they happen to show you x-rays of Andre the Giant, look for "widening of
the joint space in an adult hip" - can be a classic buzzword. Late in the game, the caiiilage will
actually outgrow its blood supply and collapse, leading to early onset osteoarthritis. The formation of
endochondral bone at existing chondro-osseous junctions results in widening of osseous structure.
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•. ·,
·._ ., �
SECTION 9:
MARROW '
.
� •....,.,'
·.·
This is a confusing topic and there are entire books on the su�ject. I'm going to attempt to
hit the main points, and simplify the subject.
Bone marrow consists of three components: (1) Trabecular Bone - the support structure, (2)
Red Marrow - for making blood, and (3) Yellow Marrow -fat for a purpose unknown at this
time.
Marrow Conversion: The basic rules are that
yellow marrow increases with age, in a
predictable and progressive way. This is usually
completed by the mid 20s. You are born with all
red marrow, and the conversion of red to yellow
occurs from the extremities to the axial skeleton
(feet and hands first). Within each long bone the
progression occurs epiphyses / apophyses first ->
diaphysis -> followed by the distal metaphysis ,
and finally the proximal metaphysis. Red Red Marrow Coverts to Yellow Marrow from
Distal to Proximal
marrow can be found in the humeral heads
and femoral heads as a normal variant in
adults.
C----\ As a child, you have
diffuse red marrow
except for ossified
epiphyses and apophyses.
Persistent
Red As adults, you have
Marrow ;
Expands Marrow yellow marrow
out from the / everywhere except in the
Middle axial skeleton, and
proximal metaphyses of
(_�\ (� proximal long bones.
Baby Child Teenager Adult
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Few Pearls on Marrow:
• Yellow marrow increases with age (as trabecular bone decreases with osteoporosis,
yellow marrow replaces it).
• T l is your money sequence: Yellow is bright, Red is darker than yellow (near iso
intense to muscle).
• Red marrow should never be darker than a normal disk or muscle on Tl (think about
muscle as your internal control).
• Red marrow increases if there is a need for more hematopoiesis (reconversion -
occurs in exact reverse order of normal conversion)
• Marrow turns yellow with stress / degenerative change in the spine
Three most classic marrow questions:
(1 Q) What is the normal pattern of conversion ?
(A) The epiphyses convert to fatty marrow almost immediately after ossification. Distal then
proceeds medial / proximal (diaphysis first, then metaphysis).
(2 Q) What is the normal pattern ofREconversion ? Spine
(A) The pattern of reconversion: This occurs in the reverse t
Flat Bones
t
order of normal marrow conversion, beginning in the axial
skeleton and heading peripheral. The last to go are the more
distal long bones. Typically, the epiphyses are spared unless Long Bone Metaphysis
the hematopoietic demand is very high.
t
Long Bone Diaphysis
Long Bone Epiphyses
(3 Q) What areas are spared I normal variants?
(A) Patchy areas of red marrow may be seen in the proximal femoral metaphysis of
teenagers. Distal femoral sparing is seen in teenagers and menstruating women.
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leukemia:
Proliferation of leukemic cells results in replacement of red marrow. Marrow will look
darker than muscle (and normal disks) on Tl. On STIR, marrow may be brighter than
muscle because of the increased water content. T2 is variable, often looking like diffuse red
marrow.
� They can show leukemia in two main ways:
(1) Lucent metaphyseal bands in a kid
(2) Tl-weighted MRI showing marrow darker than
adjacent disks and muscle. Remember that Red
Marrow is still 40% fat and should be brighter than
muscle on T 1.
Most infiltrative conditions affect the marrow diffusely.
The exceptions are multiple myeloma, which has a
predilection for focal "speckled" deposits, and
Waldenstrom's macroglobulinemia, which causes infarcts.
T1 Sag - Marrow is Darker
than Disk -
Chloroma (Granulocytic Sarcoma)
Just say "destructive mass in a bone of a leukemia
patient. " It's some kind of colloid tumor.
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• .
�
SECTION 10:
ULTRASOUND �
• .
It's absolutely iH(;n:.:diblt: tlmt I t:Vt:11 111.::t:d tu gu uvt:r this, but di11usaur rndiulugists luvt: this
stuff. Plus it is popular in Europe, so logically it belongs on an intermediate exam in the US.
Anisotropy: The most common and
most problematic issues with
Normal
ultrasounding tendons is this thing called Appearing
"anisotropy." The tendon is normally Hyperechoic
hyperechoic, but if you look at it when Tendon
it's NOT perpendicular to the sound
beam it can look hypoechoic (injured?).
Exact same
It S' the biggest pain in the ass: tendon - now
appearing
•supraspinatus tendon - as it curves hypoechoic
when
along the contours of the humeral head scanned non
•Long Head of the Biceps - In the perpendicular
bicipital groove
Tears: The tendon is usually hyperechoic. Focal hypoechoic areas are tears. It can be
really tricky to tell if it's partial or complete (that's what MRI is for).
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Tenosynovitis: As discussed above, there are a variety of causes. If they show it on
ultrasound, you are looking for increased fluid within the tendon sheath. You could also see
associated peritendinous subcutaneous hyperemia on Doppler.
Tenosynovitis - Increased fluid in the tendon sheath
Plantar Fasciitis: This is another
pathology that lends itself to a "what is it ? "
type of ultrasound question. Hopefully, they at
least tell you this is the foot (they could label
the calcaneus ). The finding will be thickening
of the plantar fascia (greater than 4 mm), with
loss of the normal fibrillar pattern. If you see
calipers on the plantar fascia - this is going to
be the answer.
Trivia - Most commonly involves the central band (there are 3 bands - people who don't
know anatomy think there are two).
Calcific Tendonitis: As described above, this is very common and related to
hydroxyapatite. The most common site is the supraspinatus tendon, near its insertion. It will
shadow just like a stone in the GB.
Calcific Tendonitis - Shadowing calcification in the classic location (supraspinatus)
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• .
• •
�
SECTION 11:
PROCEDURES
An important point to remember is that the target is not actually the joint. The target is the
capsule. In other words, you just need the needle to touch a bone within the capsule. The trick
is to do this without causing contamination or damaging an adjacent structure (like an artery).
General Tip - Avoid putting air in the joint, as this will cause susceptibility artifact.
Hip: The general steps are as follows: (1) Mark the
femoral artery. (2) Internally rotate the hip (slightly)
to localize the femoral head-neck junction (your
target). (3) Clean and numb the skin. (4) Advance a
20-22 gauge spinal needle into the joint - straight
down on the superior head neck junction. (5) Inject a
small amount of contrast to confirm position. Contrast
should flow away from the tip. If the contrast just
stays there it's not in the capsule. (6) Put the rest of the
contrast in.
Trivia: Capsule is widest at the head-neck junction.
Trivia: The cocktail injected is around 14 cc total
(4 cc Lidocaine, 10 cc Visipaque, and only about O. 1 cc Gd).
Shoulder: The general steps are as follows: (1)
Supinate the hand (externally rotate the shoulder) (2)
Clean and numb the skin. (3) Advance a 20-22 gauge
spinal needle into the joint - straight down on the
junction between the middle and inferior third of the
humeral head - 2 mm inside the cortex. (4) Once you
strike bone, pull back 1 mm and turn the bevel towards
the humeral head - this should drop into the joint (5)
Inject a small amount of contrast to confirm position.
Contrast should flow away from the tip. If the contrast
just stays there it's not in a space. (6) Put the rest of
the contrast in.
Trivia: The cocktail injected is around 12cc total
(4cc Lidocaine, 8cc Visipaque, and only about 0.1 cc Gd).
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Special Situations - Problem Solving
So there are three main reasons that you might get asked to put a needle in a joint
1 .. Needs Arthrogram to Evaluate the Labrum
2 - Needs Steroid I Lidocaine Injection for Pain Management
3 - Possible Joint Infection - Need,; Aspiration
Only one of these is going to end up getting imaged (the arthrogram), the other two just need
the needle in the correct spot - and it doesn't matter what you had to do to get it there.
Scenario 1 - Patient is allergic to (has a phobia of) Gd, but needs an arthrogram?
You could try a CT Arthrogram. So - not Gad, just Visipaque and Lidocaine.
Scenario 2 - Patient is allergic to (has a phobia of) CT Contrast (Visi or Omni), but needs a
steroid joint injection?
You can inject air into the joint (instead of visi) to confirm placement - then put the steroid in.
Scenario 3 - Patient is allergic to (has a phobia of) CT Contrast (Visi or Omni), but needs an
arthrogram ?
This situation is different. You can't inject air because you will end up with a big blooming
mess on MR. CT isn't an option either - because obviously you need the CT Contrast or it's
not an arthrogram. Your only choices would be to either (1) pre-medicate them, or (2) use the
force (trust your feelings...) and hope you can get in the joint without confirming positioning
with fluoro.
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Blank for Scribbles
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PROMETHEUS LIONHART, M.D.
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SECTION 1:
ANATOMY �
• • • •
Aorta: The thoracic aorta is divided anatomically into four regions; the root, the ascending aorta,
the transverse aorta (arch), and the descending aorta. The "root" is defined as the portion of the aorta
extending from the ao1iic valve annulus to the sino-tubular junction. The diameter of the thoracic
aorta is largest at the aortic root and gradually decreases (average size is 3.6 cm at the root, 2.4 cm in
the distal descending).
• Sinuses of Valsalva: There are 3 outpouchings (right,
left, posterior) above the annulus that terminate at the
ST Junction. The right and left coronaries come off the
right and left sinuses. The posterior cusp is sometimes Ductus
Bump
called the "non-corona1y cusp."
• Isthmus: The segment of the aorta between the origin
of the left Subclavian and the ligamentum arteriosum.
• Ductus bump: Just distal to the isthmus is a contour
bulge along the lesser curvature, which is a normal
structure (not a pseudoanemysm).
Aortic Arch Variants: There are 4 common variations:
Normal (75%), Bovine Arch
( 15%) - common origin of
brachiocephalic arte1y and left
common carotid artery, left
common carotid coming off
the brachiocephalic proper
(10%), and in 5% of people
the left vertebral artery
originates separately from the
arch. Branching with regards Left CC off Separate Origins
Normal Bovine
to right arch, left arch and Brachiocephalic
double arch was discussed in
more detail in the cardiac chapter.
Pulmonary Sling: Aberrant Left pulmonary artery coming off the
right pulmonary artery.
-Unique as the only anomaly to create indentations in the posterior
trachea and anterior esophagus.
-Unique as the only anomaly that can cause stridor in a patient with
a normal left sided arch.
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Adamkiewicz:
The thoracic aorta puts off multiple
important feeders including the great
anlerior me<lullary artery (Artery of
Adamkiewicz) which serves as a dominate
feeder of the spinal cord.
This thing usually comes off on the left side
(70%) between T9-T12.
"Hairpin Turn"
"Beware of the Hairpin Turn"
-The classic angiographic appearance of the artery is
the "hairpin turn" as its anastomosis with the anterior
spinal artery.
Mesenteric Branches:
The anatomy of the SMA and IMA is high yield, and can be shown on a MIP coronal CT, or
Angiogram. I think that
Inferior SMA knowing the inferior
Pancreatico Arc of Riolan pancreaticoduodenal
duodenal ·· .. comes off the SMA first,
and that the left colic
Middle (from IMA) to the
Colic Left Colic middle colic (from
SMA) make up the Arc
Right··•· Marginal of Riolan are probably
Colic Artery the highest yield facts.
· · ,,;.. ,:.-,.Sigmoid
lleo- Colic Branches
Appendicular A.
Celiac Branches:
'\\,,,�,,
The classic branches of the celiac axis are the
""11?t0\1et
common hepatic, left gastric, and the splenic f \-\e?a\iC
arteries. �{)
Celiac
The "common" hepatic artery becomes the Trunk
"proper" hepatic artery after the GDA.
GOA
This "traditional anatomy" is actually only seen in
55% of people.
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Celiac Anatomy - Remember this can be shown with an angiogram, CTA, or MRA.
Variant Hepatic Artery Anatomy - The right hepatic artery and ]eft hepatic arteries
may be "replaced" ( originate from a vessel other than the proper hepatic) or duplicated -
which anatomist called "accessory." This distinction of "replaced" vs "accessory" would
make a great multiple choice question.
Trivia to know:
•Replaced = Different Origin, usually off the left gastric or SMA
•Accessory = Duplication of the Vessel, with the spare coming off the left gastric or SMA
•If you see a vessel in the fissure of the
ligamentum venosum (where there is
not normally a vessel), it's probably an
accessory or replaced left hepatic
artery arising from the left gastric
artery.
•The proper right hepatic artery is
anterior to the right portal vein,
whereas the replaced right hepatic
artery is posterior to the main portal
vein. This positioning of the replaced Vessel in the Ligamentum Venous
right increases the risk of injury in (probably replaced left hepatic)
pancreatic surgeries.
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Iliac Anatomy: The branches of the internal iliac are high yield, with the most likely
question being "which branches are from the posterior or anterior divisions?" A useful
mnemonic is "I Love Sex, "Illiolumbar, Lateral Sacral, Superior Gluteal, for the posterior
division.
My trick for remembering that the mnemonic is for posterior and not anterior is to think of
that super religious girl I knew in college - I Like Sex in the butt I posterior.
I don't think they will actually show a picture, it's way more likely to be a written question.
Superior lliolumbar
Vesicular
Lateral
Sacral
Obturator Superior
Gluteal
1'
1'
Middle Rectal
Internal
Pudenda!
Anterior Division Posterior Division
Umbilical lliolumbar
Superior Vesicular (off umbilical) Lateral Sacral
Interior Vesicular Superior Gluteal
Uterine (it you have a uterus) Inferior Gluteal *** sometimes
Middle Rectal
Internal Pudenda!
Interior Gluteal
Obturator
Trivia: The ovarian arteries arise from the anterior-medial aorta 80-90% of time.
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Persistent Sciatic Artery - An anatomic variant, which is a continuation of the
internal iliac. It passes posterior to the femur in the thigh and then will anastomose with the
distal vasculature. Complications worth knowing include aneurysm formation and early
atherosclerosis in the vessel. The classic vascular surgery boards question is "external iliac is
acutely occluded, but there is still a strong pulse in the foot" , the answer is the patient has a
persistent sciatic.
Persistent Sciatic Artery
Mesenteric Arterial Collateral Pathwavs:
Celiac to SMA: The conventional collateral pathway is Celiac -> Common Hepatic ->
GDA -> Superior Pancreatic Duodenal -> Inferior Pancreatic Duodenal-> SMA.
Arc ofBuhler: This is a variant anatomy (seen in like 4% of people), that represents a
collateral pathway from the celiac to the SMA. The arch is independent of the GDA and
inferior pancreatic arteries. This rare collateral can have an even more rare aneurysm, which
occurs in association with stenosis of the celiac axis.
Hepatic Celiac
Hepatic Celiac
GOA
Inferior Inferior
Pancreatic
Pancreatic
Duodenal Duodenal
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SMA to IMA: The conventional collateral pathway is SMA-> Middle Colic-> Left
Branch of the Middle Colic-> Arc of Riolan (as below)-> Left Colic - > IMA.
Arc ofRiolan - Also referred to as the
meandering mesenteric artery. Classically a
connection between the middle colic of the
SMA and the left colic of the IMA.
Marginal Artery ofDrummond - This is
another SMA to IMA connection. The Marginal Artery
anastomosis of the terminal branches of the of Drummond
ileocolic, right colic and middle colic arteries
of the SMA, and of the left colic and sigmoid
branches of the IMA, form a continuous
arterial circle or arcade along the inner
border of the colon.
IMA to lliacs: The conventional collateral pathway is IMA-> Superior Rectal-> Inferior
Rectal-> Internal Pudenda} -> Anterior branch of internal iliac.
Left Colic
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Winslow Pathway-This is a collateral pathway that is seen in the setting of aorto-iliac
occlusive disease. The pathway apparently can be inadvertently cut during transverse
abdominal surgery. The pathway runs from subclavian arteries-> internal thoracic (mammary)
arteries -> superior epigastric arteries -> inferior epigastric arteries -> external iliac arteries.
Corona Mortis - Classically described as a vascular connection between the obturator
and external iliac. Some authors describe additional anastomotic pathways, but you should
basically think of it as any vessel coursing over the superior pubic rim, regardless of the
anastomotic connection. The "crown of death" is significant because it can (a) be injured in
pelvic trauma or (b) be injured during surgery- and is notoriously difficult to ligate.
Some authors report that it causes 6-8% of deaths in pelvic trauma. The last piece of trivia is
that it could hypothetically cause a type 2 endoleak.
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Upper Extremitv Anatomv:
The scalene muscles make a triangle in the neck. If you have ever had the pleasure of reading a
brachia! plexus MRI finding this anatomy in a sagittal plane is the best place to start (in my
opinion). The relationship to notice (because it's testable) is that the subclavian vein runs anterior to
the triangle, and the subclavian artery runs in the triangle (with the brachial plexus).
Trivia to Remember: The subclavian artery runs posterior to the subclavian vein.
' Transverse Process C2-C3
Brachia! Plexus
Middle Scalene Muscle
Anterior Scalene Muscle
First Rib
Subclavian VEIN
Phrenic Nerve --1111.,.
►
Subclavian ARTERY
The subclavian artery has several major branches: the vertebral , the internal thoracic, the
thyrocervical trunk, the costocervical trunk, and the dorsal scapular.
As the subclavian artery progresses down the arm,
anatomists decided to change it's name a few times. This
name changing makes for great multiple choice fodder.
The highest yield thing you can know with regard to
upper extremity vascular anatomy is when stuff becomes
j
stuff:
• Axillary Artery: Begins at the first rib
A,ma,yA
• Brachial Artery: Begins at the lower border of the
teres major (major NOT minor!)
........_J
• Brachial Artery: Bifurcates to the ulnar and radial
Brachia! A.
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How To Tell The Ulnar From The Radial Artery On Angiogram Or CTA:
Around the radial head the brachia} artery splits into the radial and ulnar arteries. I have
three tricks for telling the radial from the ulnar artery apart (in case it's not obvious).
1. The ulnar artery is usually bigger.
2. The ulnar artery usually gives off the common interosseous
3. The ulnar artery supplies the superficial palmar arch (usually), and therefore the
radial supplies the deep arch (usually).
Upper Extremity Normal Variants:
• Anterior Interosseous Branch (Median Artery) persists and supplies the deep palmar arch
of the hand.
• "High Origin of the Radial Artery" - Radial artery comes off either the axillary or
high brachial artery (remember it normally comes off at the level of the radial head).
Deep
Arch High Origin of the Radial Artery
Superficial Uinc1
Arch
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Lower Extremitv Anatomv:
Every medical student knows the aorta bifurcates into the right and left common iliac
arteries, which subsequently bifurcate into the external and internal iliac arteries. The
nomenclature pearl for the external iliac is that it becomes the common femoral once it
gives off the inferior epigastric (at the inguinal ligament).
Inferior Epigastric
Aorta Common Iliac External Iliac I Common
I Femoral
Once the inferior epigastric comes off (level of the inguinal ligament) you are dealing with
the common femoral artery(CFA). The CFA divides into the deep femoral (profunda) and
superficial femoral. The deep femoral courses lateral and posterior. The superficial femoral
passes anterior and medial into the flexor muscle compartment (ADDuctor / Hunter's Canal).
At the point the vessel emerges from the canal it is then the popliteal artery. At the level of
the distal border of the popliteus muscle the popliteal artery divides into the anterior tibialis
(the first branch) and the tibioperoneal trunk. The anterior tibialis courses anterior and
lateral, then it transverses the interosseous membrane, running down the front of the anterior
tibia and terminating as the dorsalis pedis. The tibioperoneal trunk bifurcates into the
posterior tibialis and fibular (peroneal) arteries. A common quiz is "what is the most medial
artery in the leg?", with the answer being the posterior tibial (felt at the medial malleolus).
Notice how lateral the AT is - you can imagine it running across the interosseous membrane,
just like it's suppose to.
lnterosseous
Anterior Tibialis Membrane
Anterior Tibialis
Posterior Tibialis ----
Peroneal
Medial Peroneal
Posterior Tibialis
Malleolus
Dorsalis Pedis
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Mesenteric Venous Collaterals:
Gastric Varices: As described in more detail in the GI chapter, portal hypertension
shunts blood away from the liver and into the systemic venous system. Spontaneous portal
systemic collaterals develop to decompress the system. The thing to know is that most
gastric varices are formed by the left gastric (coronary vein) . That is the one they
always show big and dilated on an angiogram. Isolated gastric varices are secondary to
splenic vein thrombosis. Gastric Varices (80-85%) drain into the inferior phrenic and then
into the left renal vein, forming a gastro-renal shunt.
Short Gastric
Portal • Left Gastric
Vein (Coronary) = Cardia
• Posterior and Short
Gastric = Fundus
Gastroepiploic Vein
Splenorenal Shunt: Another feature of portal hypertension, this is an abnormal
collateral between the splenic vein and renal vein. This is actually a desirable shunt because
it is not associated with GI bleeding. However, enlarged shunts are associated with
hepatic encephalopathy (discussed in greater detail in the BRTO section of the IR chapter).
A common way to show this is an enlarged left renal vein and dilatation of the inferior vena
cava at the level of the left renal vein.
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caval variants
Left Sided SVC The most common
congenital venous anomaly in the chest. In a few
rare cases these can actually result in a right to
left shunt. They are only seen in isolation in 10%
of cases (the other 90% it's "duplicated"). The
location and appearance is a total Aunt Minnie.
Trivia to know:
• Most commonly associated CHD is the ASD
• Associated with an unroofed coronary sinus
Left Sided SVC - When you see that
• Nearly always (92% of the time) it drains into son of a bitch right there, that thing
can only be one of two things - a
the coronary sinus : lymph node or a duplicated SVC.
Duplicated SVC - The above discussed "Left Sided SVC" almost never occurs in
isolation. Instead, there is almost always a "normal" right sided SVC, in addition to the left
sided SVC. It is in this case (which is the majority of cases of left sided SVC) that the
terminology "duplicated SVC" is used. It is so common that people will use the terms
duplicated and left sided interchangeably. But, technically to be duplicated you need a right
sided and left sided SVC (even if the right one is a little small - which is often the case in the
setting of a left SVC).
Duplicated IVC - There are two main points
worth knowing about this: ( 1) that the appearance
is an Aunt Minnie, and (2) it's associated with
Renal stuff. Renal associations include
horseshoe and crossed fused ectopic kidneys.
Also these dudes often have circumaortic renal
collars (see below).
Duplicated IVC (IVCs are the bread,
Aorta is the cheese or peanut butter ...
or bacon)
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Circumaortic Venous Collar - Very common variant with an additional left renal
vein that passes posterior to the aorta. It only matters in two situations (a) renal transplant,
(b) IVC filter placement. The classic question is that the anterior limb is superior, and the
posterior limb is inferior.
Azygos Continuation - This is also known as absence of the hepatic segment of the
IVC. In this case, the hepatic veins drain directly into the right atrium. Often the IVC is
duplicated in these patients, with the left IVC terminating in the left renal vein , which then
crosses over to join the right IVC.
The first thing you should think when I say azygous continuation is polysplenia (reversed
IVC/Aorta is more commonly associated with asplenia).
Azygos Continuation - No IVG in the Liver, Dilated Azygos in the Chest
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.•.
.•
.
'-; ·.'
·.·. �
SECTION 2:
ACUTE AORTIC SYNDROMES
� •.:. "
-. -.
.
:·
There are 3 "acute aortic syndromes" , aortic dissection,
intramural hematoma, and penetrating ulcer. Lets take these one at
a time and talk about the trivia.
Anatomy Review:
Remember vessels have 3 layers: lntima, Media, and that other
one no one gives a shit about.
Penetrating Ulcer:
This is an ulceration of an atheromatous plaque that has eroded the inner elastic layer of the
aortic wall. When it reaches the media it produces a hematoma within the media.
• #1 Risk Factor = Atherosclerosis
(Delicious Burger King and Tasty Cigarettes)
• Classic Scenario: Elderly patient with hypertension and
atherosclerosis usually involving the descending thoracic
aorta
• Genesis: Eating like a pig and smoking results in
atherosclerosis. Nasty atherosclerotic plaque erodes
through the intima. Hematoma forms in the media (intra
mural hematoma). With severe disease can eventually
progress to a pseudo aneurysm (and maybe even rupture)
• Pearl: Look for a gap in the intimal calcifications (that's how you know it's truly
penetrated through the intima, and not just some funky contour abnormality).
• Classification: All 3 AASs can be classified as type A or B Stanford, based on their
locations before (type A) or after the takeoff the of the left subclavian (type B).
• These things often result in a saccular morphology around the arch. In general, sac
like aneurysm above the diaphragm is related to penetrating ulcer. Sac like aneurysm
below the diaphragm is gonna be septic ("mycotic").
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Relationship between Penetrating Ulcer and Dissection:
-Controversial (which usually means it won't be tested) - famous last words
If forced to answer questions on this relationship, I would go with the following:
• Penetrating Ulcers are caused by atherosclerosis (this is a fact)
• Penetrating Ulcer can lead to Dissection (this is probably true in some cases)
• Atherosclerosis does NOT cause Dissection (which is confusing, may or may not be true,
and is unlikely to be tested). What is true is that the presence of dense calcified plaque can
stop extension of a dissection tear.
• Dissections often occur in the aortic root - where you have the highest flow pressures
• Penetrating Ulcers nearly never occur in the root - as these flow pressures prevent
atherosclerosis (wash those cheeseburger crumbs away).
Treatment of Penetrating Ulcer ?
• "Medical"= Similar to Type B Dissections. If they do get treated (grafted etc ... ) they tend
to do WORSE than dissections (on average)
• Q: When are they Surgical ?
• A: Hemodynamic instability, Pain, Rupture, Distal Emboli, Rapid Enlargement
Dissection
• The most common cause of acute aortic syndrome (70%)
• Hypertension is the main factor - leads to an intimal tear resulting in two lumens
• Marfans, Turners, and other Connective Tissue Diseases increase risk
Classic Testable Scenarios:
• Pregnancy - known to increase risk
• Cocaine Use in a young otherwise healthy person
• Patient with "Hypertension" and a sub-sternal "Tearing Sensation."
Chicken vs Egg: Some people say that hypertensive pressures kill the vasa vasorum (the
little vessels inside the vessel walls) leading to development of intramural hematoma which
then ruptures into the intima. This is the "inside out" thinking. Other people think the
hypertensive forces tear the inner layer directly ("outside in" thinking).
Honestly ... who gives a shit? Not even sure why I mentioned that.
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Dissection Continued...
There are two general ways to classify these things:
(1) Time: Acute(< 2 weeks), or Chronic
(2) Lo<..:ation:
• Stanford A: Account for 75% of dissections and involves the ascending aorta and arch proximal
to the take-off of the left subclavian. These guys need to be treated surgically.
• Stanford B: Occur distal to the take-off of the left subclavian and are treated medically unless
there are complications(organ ischemia etc...)
THIS vs THAT: Floating Viscera Sign:
True Lumen False Lumen This is a classic angiographic sign of
Continuity with "CobWeb Sign" - slender abdominal ao1tic dissection.
undissected portion of linear areas of low
aorta attenuation It is shown as opacification of
abdominal aortic branch vessels during
Smaller cross sectional Larger cross section area aortography(catheter placed in the aortic
areas(with higher velocity (slower more turbulent true lumen), with the branch vessels-
blood) flow) ( celiac axis, superior mesenteric artery,
"'
SmTounded by Beak Sign - acute angle at and right renal artery) arising out of
calcifications(if present) edge of lumen - seen on nowhere.
axial plane
They appear
to be
.floating, with
�Tu�e�) little or no
antegrade
Usually contains the origin Usually contains the origin opacification
of celiac trunk, SMA, and of LEFT renal artery of the ao1tic
RIGHT renal artery true lumen.
Surrounds true lumen in
Type A Dissection
**just remember.false is left (like left handed people are
evil, or false) - then everything else is true.
Dissection Flap in the Abdomen - Vocab Trivia:
• Static = dissection flap in the feeding artery (usually treated by stenting)
• Dynamic = dissection flap dangling in front of ostium (usually treated with fenestration).
It can be hard to tell these apart. If asked I'd expect them to just use the vocab word�.
THIS vs THAT:Aneurysm with Mural Thrombus VS Thrombosed Dissection
• The dissection should spiral, the thrombus tends to drop straight down
• Intimal Cales - the dissection will displace them.
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Intramural Hematoma
Hern
IMH Mechanism Flow:
Pseudo
This can occur as:
• Primary Event Secondary to HTN
• Secondary Event usually From Atherosclerosis, but also as a Focal Hematoma on the road to dissection
For the purpose of multiple choice - the cause is HTN
Ways this can be shown:
Hyperdense on Non Con
distinguish from plaque
Treatment:
• Also uses the Stanford A vs B idea
• Some people will say Type A= Surge1y, Type B medical
• This is controversial and unlikely to be tested
Predictors of Shitty Outcome:
• Most of these will spontaneously regress. These are the things that make that less likely:
• Hematoma Thickness Greater than 2 cm
• Association with anemysmal dilation of the aorta - 5 cm or more
• Progression to dissection or penetrating ulcer
• IMH + Penetrating Ulcer has a worse outcome compared to IMH + Dissection
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• '
'
�
SECTION 3:
ANEURYSM, MISC... /
·" ·.-\,·
�
•
THIS vs THAT: Aneurysm vs Pseudo-aneurysm - The distinction between a true
and false aneurysm lends itself well to multiple choice testing. A true aneurysm is an
enlargement of the lumen of the vessel to 1.5 times its normal diameter. True = 3 layers are
intact. In a false (pseudo) aneurysm all 3 layers are NOT intact, and it is essential1y a
contained rupture. The risk of actual rupture is obviously higher with false aneurysm. It
can sometimes be difficult to tell, but as a general rule fusiform aneurysms are true, and
saccular aneurysms might be false. Classic causes of pseudoaneurysm include trauma,
cardiologists (groin sticks), infection (mycotic), pancreatitis, and some vasculitides. On
ultrasound they could show you the classic yin/yang sign, with "to and fro" flow on pulsed
Doppler. The yin/yang sign can be seen in saccular true aneurysms, so you shouldn't call it
on that alone (unless that's all they give you). To and Fro flow within the aneurysm neck +
clinical history is the best way to tell them apart.
SVC Syndrome - Occurs secondary to complete or near complete obstruction of flow
in the SVC from external compression (lymphoma, lung cancer) or intravascular
obstruction (Central venous catheter, or pacemaker wire with thrombus). A less common
but testable cause is fibrosing mediastinitis (just think histoplasmosis). The dude is gonna
have face, neck, and bilateral arm swelling.
Traumatic Pseudoaneurysm -
Again a pseudoaneurysm is basical1y a
contained rupture. The most common place
to see this (in a living patient) is the aortic
isthmus (90%). This is supposedly the
result of tethering from the ligamentum
arteriosum. The second and third most
common sites are the ascending aorta and
diaphragmatic hiatus - respectively.
Ascending aortic injury is actually probably
number one, it just kills them in the field so
you don't see it. They could show you a
CXR with a wide mediastinum, deviation
of the NG Tube to the right, depressed left Classic Isthmus Pseudoaneurysm
main bronchus, or left apical cap and want
you to suspect acute injury.
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Ascending Aortic Calcifications - There are only a few causes of ascending aortic
calcifications,as atherosclerosis typically spares the ascending aorta. Takayasu and
Syphilis should come to mind. The real-life significance is the clamping of the aorta may
be rliftklllt rlmine CA Hn.
Aneurysm - Defined as enlargement of the artery to 1.5 times its expected diameter
(> 4 cm Ascending and Transverse,> 3.5 cm Descending,> 3.0 cm Abdominal).
Atherosclerosis is the most common overall cause. Medial degeneration is the most
common cause in the ascending aorta. Patients with connective tissue (Marfans,Ehlers
Danlos) diseases tend to involve the aortic root. When I say cystic medial necrosis you
should think Ma1:fans. Aneurysms may develop in any segment of the aorta,but most
involve the infra-renal abdominal aorta. This varies based on risk factors,rate of growth,
etc ... but a general rule is surgical repair for aneurysms at 6cm in the chest (5.5 cm with
collagen vascular disease) and 5 cm in the abdomen.
Sinus of Valsalva Aneurysm -Aneurysms of the valsalva sinus (aortic sinus) are
rare in real life,but have been known to show up on multiple choice tests. Factoids worth
knowing are that they are more common in Asian Men,and typically involve the right
sinus. They can be congenital or acquired (infectious). VSD is the most common associated
cardiac anomaly. Rupture can lead to cardiac tamponade. Surgical repair with Bentall
procedure.
Endoleaks - There are 5 types,and type 2 is the most common. These are discussed in
detail in the IR chapter.
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Rupture / Impending Rupture- Peri-aortic stranding, rapid enlargement (IO mm or
more per year), or pain are warning signs of impending rupture. A retroperitoneal hematoma
adjacent to an AAA is the most common imaging finding of actual rupture. The most
common indicc1tor for elective repc1ir is the maximum rliameter of the aneurysm , "Sac Size
Matters," with treatment usually around 6 cm (5.5 cm in patients with collagen vascular
disease). A thick, circumferential mural thrombus is thought to be protective against rupture.
Enlargement of the patent lumen can indicate lysis of thrombus and predispose to rupture.
Findings of Impending Rupture
Posterior wall of the aorta drapes over the vertebral
Draped Aorta Sign column.
Increased Aneurysm Size 10 mm or more increased per year
Focal Discontinuity in Circumferential Wall
Calcifications
Well-defined peripheral crescent of increased
Hyperdense Crescent Sign attenuation. One of the most specific manifestations
of impending rupture.
Mycotic Aneurysm - These are most often saccular and most often
pseudoaneurysms. They are prone to rupture. They most often occur via hematogenous
seeding in the setting of septicemia (endocarditis). They can occur from direct seeding via a
psoas abscess or vertebral osteomyelitis (but this is less common). Most occur in the
thoracic or supra-renal aorta (most atherosclerotic aortic aneurysms are infra-renal).
Typical findings include saccular shape, lobular contours, peri-aortic inflammation, abscess,
and peri-aortic gas. They tend to expand faster than atherosclerotic aneurysms. In general
small, asymptomatic, and unruptured.
. � Gamesmanship - If you see a saccular aneurysm of the aorta (especially the
'" abdominal aorta) you have to lead with infection.
NF 1 - One of the more common neurological genetic disorders, which you usually think
about causing all the skin stuff (Cafe au lait spots and freckling), and bilateral optic gliomas.
Although uncommon, vascular findings also occur in this disorder. Aneurysms and stenoses
are sometimes seen in the aorta and larger arteries, while dysplastic features are found in
smaller vessels. Renal artery stenosis can occur, leading to renovascular hypertension
(found in 5% of children with NF). The classic look is orificial renal artery stenosis
presenting with hypertension in a teenager or child. The mechanism is actually Dysplasia
of the arterial wall itself (less common from peri-arterial neurofibroma).
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Marfan Syndrome - Genetic disorder caused by mutations of the fibrillin gene (step 1
question). There are lots of systemic manifestations including ectopic lens, being tall, pectus
deformity, scoliosis, long fingers etc ... Vascular findings can be grouped into aneurysm,
dissection, and pulmonary arte1y dilation:
• Anewysm: Dilation with Marfans is classically described as "Annuloaortic ectasia",
with dilatation of the aortic root. The dilation usually begins with the aortic sinuses, and
then progresses into the sinotubular junction, ultimately involving the aortic annulus.
Dilatation of the aortic root leads to aortic valve insufficiency. Severe aortic
regurgitation occurs that may progress to aortic root dissection or rupture. The
mechanism for all this nonsense is that disruption of the media elastic fibers causes
aortic stiffening, and predisposes to aneurysm and dissection. The buzzword for the
Marfans ascending aneurysm is "tulip bulb." They are usually repaired earlier than
normal aneurysm (typically around 5.5 cm).
Marfan's - Annuloaortic Ectasia, with dilation of the aortic root
• Dissection: Recurrent dissections are common, and even "triple barreled dissection" can
be seen (dissections on both sides of a true channel).
• Pulmonary Artery Enlargement: Just like dilation of the aorta, pulmonmy artery
enlargement favors the root.
Loeys Dietz Syndrome - Despite the name,
Loeys Dietz Classic Triad:
this is actually not a Puerto Rican DJ. Instead think of
this as the really shitty version of Marfans. They 1. Hypertelorism (frog eyes),
have a terrible prognosis, and rupture their aortas all 2. Bifid uvula or cleft palate
3. Aortic aneurysm with tortuosity
the time. Vessels are very tortuous (twisty). They
also have crazy wide eyes (hypertelorism).
Classic Look: Crazy twisty vertebral arteries
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Ehlers-Danlos - This one is a disorder in collagen, with lots of different subtypes. They
have the stretchy skin, hypermobile joints, blood vessel fragility with bleeding diatheses.
Invasive diagnostic studies such as conventional angiography and other percutaneous
procedures should he avofrlecl heca11se of the excessive risk of m-terial <iissection. Imaging
characteristics of aortic aneurysms in Ehlers-Danlos syndrome resemble those in Marfan
syndrome, often involving the aortic root. Aneurysms of the abdominal visceral arteries
are common as well.
Syphilitic (Luetic) Aneurysm -This is super rare and only seen in patients with
untreated tertiary syphilis. There is classically a saccular appearance and it involves the
ascending aorta as well as the aortic arch. Classic description "saccular asymmetric aortic
aneurysm with involvement of the aortic root branches. " Often heavily calcified "tree
bark" intimal calcifications. Coronary artery narrowing (at the ostium) is seen 30% of the
time. Aortic valve insufficiency is also common.
Aortoenteric Fistula - These come in two flavors: (a) Primary, and (b) Secondary.
• Primary: Very, very, very rare. Refers to an A-E fistula without history of
instrumentation. They are only seen in the setting of aneurysm and atherosclerosis.
• Secondary: Much more common. They are seen after surgery with or without stent
graft placement.
The question is usually what part of the bowel is involved, and the answer is Jrd and 4th
portions of the duodenum. The second most likely question is A-E fistula vs perigraft
infection (without fistula)? The answer to that is unless you see contrast from the aorta into
the bowel lumen (usually duodenum), you can't tell. Both of them have ectopic perigraft gas
> 4 weeks post repair, both have perigraft fluid and edema, both lose the fat place between
the bowel and aorta (tethering of the duodenum to the anterior wall of the aorta), both can
have pseudoaneurysm formation.
Aortoenteric Fistula - Primary Type
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Inflammatory Aneurysms - Most are symptomatic, more common in young men,
and associated with increased risk of rupture regardless of their size. Unlike patients with
atherosclerotic AAA, most with the inflammatory variant have an elevated ESR. Their etiology
is not well understood but may be related to periaortic retroperitoneal fibrosis or other
autoimmune disorders (SLE, Giant Cell, RA). Smoking is appanmtly a strung risk faciuf',
an<l smoking cessation is the first step in medical therapy. In 1/3 of cases hydronephrosis or
renal failure is present at the time of diagnosis because the inflammatory process usually
involves the ureters. Imaging findings include a thickened wall and inflammatory or fibrotic
changes in the periaortic regions. Often there is asymmetrical thickening of the aorta with
sparing of the posterior wall (helps differentiate it from vasculitis).
Leriche Syndrome - Refers
to complete occlusion of the aorta
distal to the renal arteries (most
often at the aortic bifurcation). It
is often secondary to bad
atherosclerosis. There can be
large collaterals.
Clinical Triad:
• Limp Dick (impotence)
• Ass claudication
• Absence femoral pulses
Leriche Syndrome - Complete occlusion of the
aorta/ distal to the renal arteries
Mid Aortic Syndrome (Coarctation of
the Abdominal Aorta) - Refers to progressive
narrowing of the abdominal aorta and its major
branches. Compared to Leriche, this is higher, and
longer in segment. It's also a total freaking zebra. It
tends to affect children / young adults. This thing is
characterized by progressive narrowing of the aorta.
It is NOT secondary to arteritis or atherosclerosis
but instead the result of some intrauterine insult
(maybe) with fragmentation of the elastic media.
This also has a clinical triad:
• HTN (most common presenting symptom) - this Mid Aortic Syndrome - Narrow aorta
is the most common cause ofdeath tfnot treated without arteritis or atherosclerosis
• Weak or Absent Femoral Pulses
• Claudication
• Renal failure
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,I•'\< .. o\' I
�-� c,
( �.l.,Q.._�GI
"IV'\J�'-"'"C..Tl\J ..... I
Aortic Coarctation -
THIS vs THAT: Coarctation of the Aortic
• There are two subtypes (Narrowing the of the Aortic Lumen)
(as shown in the chart)
Infantile Adult
• Strong Association with Turners
Syndrome (15-20%). Presents with heart Leg Claudication
failure within the first BP differences between
• Bicuspid Aortic valve is the most common week oflife. arms and legs.
associated defect (80%).
Pre-Ductal (Before the Post-Ductal (Distal to
• They have more berry aneurysms. left Subclavian A.) left Subclavian A.)
• Figure 3 sign (appearance of CXR). Aortic Arch = Aortic Arch =
Hypoplastic Normal Diameter
• Rib Notching: most often involves 4th -
lateral Fonuation is
8th ribs. It does NOT involve the 1st and p,6 r,01-<l,,,n'J _,. J.I\""""
.·e Likely
0->''°" �,.,..\
\-'"'1·\e,'-o!,,�\
211c1 because those are fed by the /
turpI j J,0,, .D
costocervical trunk.
Pseudocoarctation - This is a favorite of multiple choice writers. You will have
elongation with narrowing and kinking of the aorta. It really looks like a coarctation, BUT
there is NO pressure gradient, collateral formation, or rib notching - that is the most
likely question. The second most likely question is the area of aneurysmal dilation may
occur distal to the areas of narrowing in pseudocoarctation, and they may become
progressively dilated and should therefore be followed.
Thoracic Outlet Syndrome- Congenital or acquired compression of the Subclavian
vessels (artery and vein), and brachial plexus nerves as they pass through the thoracic inlet.
It is a spectrum: Nerve (95%) >>>>>> Subclavian Vein>> SubclavianArtery. With
symptoms varying depending on what is compressed. Compression by the anterior
scalene muscle is the most common cause. However, cervical rib, muscular hypertrophy,
fibrous bands, Pagets, tumor etc ... can all cause symptoms. Treatment is usually surgical
removal of the rib / muscle. The classic way to show this is arms up and arms down
angiography (occlusion occurs with arms up).
Paget Schroetter - This is essentially thoracic outlet syndrome, with development
of a venous thrombus in the Subclavian vein. It's sometimes called "effort thrombosis"
because it's associated with athletes (pitchers, weightlifters) who are raising their arms a lot.
They will use catheter directed lysis on these dudes, and surgical release of the offending
agent as above. Stenting isn't usually done (and can only be done after surgery to avoid
getting the stent crushed).
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Pulmonary Artery Aneurysm/Pseudoaneurysm - Think about three things for
multiple choice; (1) Iatrogenic from Swan Ganz catheter '''most common (2) Behcets, (3)
Chronic PE. When they want to lead Swan Ganz they may say something like "patient in the ICU."
The buzzwords for Behcets are: "Turkish descent", and "mouth and genital ulcers."
• Hughes-Stovin Syndrome: This is a zebra cause of pulmonary artery aneurysm that is similar
(and maybe the same thing) as Behcets. It is characterized by recurrent thrombophlebitis and
pulmonary artery aneurysm formation and rupture.
• Rasmussen Aneurysm: This has a cool name, which instantly makes it high yield for testing.
This is a pulmonary arte1y pseudoaneurysm secondary to pulmonary TB. It usually involves
the upper lobes in the setting of reactivation TB.
• Tetralogy of Fallot Repair Gone South: So another possible testable scenario is the patch
aneurysm, from the RVOT repair.
Splenic Artery Aneurysm: The most common visceral arterial aneurysm (3rd most
common abdominal - behind aorta and iliac).
Etiology of these things depends on who you ask. Some source - High Risk For Rupture -
will say arteriosclerosis is the most important cause. However, it
• Liver Transplantation
seems that most sources will say that arteriosclerosis less • Portal Hypertension
important and things like portal hypertension and a history of • Pregnancy
multiple pregnancy are more important. More common in • Connective Tissue Disorders
pregnancy, and more likely to rupture in pregnancy. • Alpha 1 Antitrypsin Def
Most are located in the distal artery. False aneurysms are
associated with pancreatitis.
An important mimic is the islet cell pancreatic tumor (which is hypervascular). Don't be a dumb
ass and t1y to biopsy the anemysm. If you are forced to choose which ones to treat I guess I'd go
with: anything over 2 cm, any pseudoaneurysm, and any in a women planning on getting pregnant.
SMA Aneurysm: All SMA aneurysms should be treated - as there is a high rate of rupture and
association with mesenteric ischemia.
Hepatic Artery Aneurysm: Treated if the patient is symptomatic or size exceeds 2cm (just
like the spleen). In patients with FMD or polyarteritis nodosa - typically they are treated regardless
of size.
Median Arcuate Ligament Syndrome (Dunbar
Syndrome): This is compression of the celiac miery by the
median arcuate ligament (fibrous band that connects the
diaphragm). Most people actually have some degree of
compression, but it's not a syndrome until there are symptoms
(abdominal pain, weight loss). Typical age is 20-40 years old.
The buzzword is "hooked appearance." It's classically shown
on angiography and they will want you to know that it gets
worse with expiration. It can actually lead to the development
of pancreaticoduodenal collaterals and anemysm formation. It's
treated surgically.
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SECTION 4:
MESENTERIC ISCHEMIA
� ..
y:·
This can be broadly classified as acute or chronic.
Chronic: Significant Stenosis of 2 out of 3 main mesenteric vessels + symptoms ("food
fear") , LUQ pain after eating, pain out of proportion to exam). Some practical pearls are
that you can have bad disease and no symptoms if you have good collaterals. Alternatively
if you have bad one-vessel disease you can have symptoms if you have crappy collaterals.
Remember that the splenic.flexure ("Griffiths Point") is the most common because it's the
watershed of the SMA and IMA.
Acute: This comes from 4 main causes. Arterial, Venous, Non-occlussive, and
Strangulation.
• Arterial: Occlusive emboli (usually more distal, at branch points), or Thrombus
(usually closer to the ostium). Vasculitis can also cause it. The SMA is most
commonly affected. Bowel typically has a thinner wall (no arterial inflow), and is
NOT typically dilated. After reperfusion the bowel wall will become thick, with a
target appearance.
• Venous: Dilation with wall thickening (8-9mm, with< 5mm being normal) is
more common. Fat stranding and ascites are especially common findings in venous
occlusion.
• Non-Occlusive: Seen in patients in shock or on pressors. This is the most difficult
to diagnose on CT. The involved bowel segments are often thickened.
Enhancement is variable. Look for delayed.filling of the portal vein at 70 seconds.
• Strangulation: This is almost always secondary to a closed loop obstruction. This
is basically a mixed arterial and venous picture, with congested dilated bowel.
Hemorrhage may be seen in the bowel wall. The lumen is often fluid-filled.
Trivia: Mesenteric lschemia has a described association with SMAAneurysm.
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Mesenteric lschemia
Arterial Venous Strangulation Non-Occlusive
Thin Bowel Wall
(thick after Thick Bowel Wall Thick Bowel Wall Thick Bowel Wall
reperfusion)
Diminished
Variable Variable Variable
Enhancement
Severe Dilation (and
Bowel Not Dilated Moderate Dilation Bowel Not Dilated
fluid filled)
Hazy with Ascites,
Mesentery Not Hazy Mesentery Not Hazy
Hazy with Ascites and "whirl sign" with
(until it infarcts) (until it infarcts)
closed loop.
Griffith's Point
• SMA-IMA
Watershed
• "Most Common
Location for
lschemia"
Sudeck's Point
• /MA - Iliac Watershed
• Highly Susceptible to
/schemia
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'..-
SECTION 5:
MISC, So ON AND So FORTH,
I&.,. � ),
ETC .. ETC..
This is my general algorithm if I see angry (thick walled) bowel
Infection
-diffuse or Tl
Embolic
Colitis / Enteritis • Inflammatory -Brach points
-Tl Occlusive
Thrombotic
Arterial
-Closer to ostium
.,,,,,,,
lschemic Non-Occlusive
-think hypotension (watershed)
Colonic Angiodysplasia - This is the second most common cause of colonic arterial
bleeding (diverticulosis being number one). This is primarily right sided with angiography
demonstrating a cluster of small arteries during the arterial phase (along the antimesenteric
border of the colon), with early opacijication ofdilated draining veins that persists late into
the venous phase. There is an association with aortic stenosis which carries the eponym
Heyde Syndrome (which instantly makes it high yield for multiple choice).
Colonic Angiodysplasia
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Osler Weber Rendu (Hereditary Hemorrhagic Telangiectasia) -This is an
AD multi-system disorder characterized by multiple AVMs. On step 1 they used to show you
the tongue I mouth with the telangiectasis and a history of recurrent bloody nose. Now, they
will likely show multiple hepatic AVMs or multiple pulmonary AVMs. Extensive shunting in
the liver can actually cause biliary necrosis and bile leak. They can have high output cardiac
failure. **Most die from stroke or brain abscess.
c;
Gamesmanship "Next Step" - If the syndrome is suspected, these guys need CT of the
Lung & Liver (with contrast), plus a Brain MR/ MRA
Renal Artery Stenosis -Narrowing of the renal artery most commonly occurs
secondary to atherosclerosis (75%). This type of naiTowing is usually near the ostium, and can
be stented. FMD is the second most common cause and typically has a beaded appearance
sparing the ostium (should not be stented). Additional more rare causes include PAN,
Takayasu, NF-1, and Radiation.
FMD (Fibromuscular Dysplasia) -A non-atherosclerotic vascular disease, primarily
affecting the renal arteries of young white women.
Things to know:
- Renovascular HTN in Young Women = FMD
- Renal arteries are the most commonly involved (carotid #2, iliac #3)
- There are 3 types, but just remember medial is the most common (95%)
- They are predisposed to spontaneous dissection
.,,,�3 - Buzzword = String of Beads
- Treatment = Angioplasty WITHOUT stenting. Eating walnuts helps (seriously, there is a
paper on it). Eating cashews does not help (same paper), which is too bad because
cashews are delicious... and walnuts taste like shit.
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Nutcracker Syndrome - Usually a healthy female 30s-40s. The left renal vein gets
smashed as it slides under the SMA, with resulting abdominal pain (left flank) and
hematuria. The left renal vein gets smashed a lot, but it's not a syndrome without
symptoms. Since the left gom1dal vein drnins into the left renal vein, it r-m1 <1lso r,m1se left
testicle pain in men, and LLQ pain in women.
Left RV
Nutcracker
Duodenum
SMA
Syndrome
Nutcracker: Renal Vein, Smashed by SMA. Nutcracker Diagnostic Gold Standard:
Retrograde venography with renal/ caval
Note the prominent venous collateral (arrow) pressure measurements
SAM (Segmental Arterial Mediolysis)-Targets WTF is a
the splanchnic arteries in the elderly, and the coronaries in "Splanchnic" Artery?
young adults. Not a true vasculitis, with no significant
Typically the splanchnic
inflammation. It's complicated but essentially the media of circulation of the GI tract
the vessel turns to crap, and you get a bunch of aneurysms. refers to the Celiac,
The aneurysms are often multiple. The way this is shown is SMA, and IMA.
multiple abdominal splanchnic artery saccular
aneurysms, dissections, and occlusion - this is the disease
hallmark. Can also be shown as spontaneous intra-abdominal hemorrhage.
Pelvic Congestion Syndrome - This is a controversial entity, sometimes grouped
in the fibromyalgia spectrum. Patients often have "chronic abdominal pain." They also
often wear a lot of rings and drink orange soda. The classic demographic is a depressed,
multiparous, pre-menopausal women with chronic pelvic pain. Venous obstruction at the left
renal vein (nutcracker compression) or incompetent ovarian vein valves leads to multiple
dilated parauterine veins. This very "real" diagnosis can be treated by your local
Interventional Radiologist via ovarian vein embolization.
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Testicular Varicocele -Abnormal dilation of veins in the pampiniform plexus. Most
cases are idiopathic and most (98%) are found on the left side (left vein is longe1� and
drains into renal vein at right angle). They can also occur on the left, secondary to the
above mentioned "nutcracker syndrome." They can cause infortility. "Non
decompressible" is a buzzword for badness. Some sources state that neoplasm is actually the
most likely cause of non-decompressible varicocele in men over 40 years of age; (left renal
malignancy invading the renal vein). Right-sided varicocele can be a sign of malignancy as
well. When it's new, and on the right side (in an adult), you should raise concern for a pelvic
or abdominal malignancy. New right-sided varicocele in an adult should make you think
renal cell carcinoma, retroperitoneal fibrosis, or adhesions.
Non-Decompressible= Bad
Right= Bad
Left= Ok
Bilateral = Ok (probably)
Gamesmanship - This diagnosis is the classic next step question of all next step
questions because you need to recognize when this common diagnosis is
associated with something bad.
· • Isolated Right Varicocele = Get an ABD CT (or MR, or US)
• Non-decompressible Varicocele = Get an ABD CT (or MR, or US)
• Bilateral Decompressible Varicoceles = Might need treatment if infertile etc.. , but doesn't
need additional cancer hunting imaging.
• Isolated Left Varicocele = Might need treatment if infertile etc.., but doesn't need
additional cancer hunting imaging.
Uterine AVM -This can present with life threatening massive genital bleeding. Rarely
they can present with CHF. They come in two flavors (a) Congenital, and (b) Acquired.
Acquired occurs after D&C, abortion, or multiple pregnancies. They are most likely to
show this on color Doppler with serpiginous structures in the myometrium with low
resistance high velocity patterns. This one needs embolization. Could look similar to
retained products of conception (clinical history will be different, and RPOC is usually
centered in the endometrium rather than the myometrium).
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.....
;
�
SECTION 6:
EXTREMITY .
� •...' '
'
May Thurner -A syndrome resulting in DVT of the left common iliac vein. The pathology
is compression of the left common iliac vein by the right common iliac artery. Treatment
is thrombolysis and stenting. Jfthey show you a swollen left leg, this is probably the answer.
PE and acute limb ischemia from severe venous obstruction (Phlegmasia cerulea dolens) are
two described complications.
Popliteal Aneurysm -This is the most common peripheral arterial aneurysm (2nd most
common overall, to the aorta). The main issue with these things is distal thromboembolism,
which can be limb threatening. There is a strong and frequently tested association with AAA.
• 30-50% of patients with popliteal aneurysms have a AAA
• 10% o_f'patients with AAA have popliteal aneurysms
• 50-70% <�f'popliteal aneurysms are bilateral
The most dreaded complication of a popliteal artery aneurysm is an acute limb from
thrombosis and distal embolization of thrombus pooling in the aneurysm.
Popliteal Entrapment- Symptomatic compression or occlusion of the popliteal artery
due to the developmental relationship with the medial head of the gastrocnemius (less
commonly the popliteus). Medial deviation of the popliteal artery is supposedly diagnostic.
This usually occurs in young men (<30). These patients may have normal pulses that decrease
with plantarflexion or dorsfflexion o_f'the foot. They will show you either a MRA or
conventional angiogram in rest and then stress (dorsi / plantar flexion) to show the artery
occluding.
Hypothenar Hammer -Caused by blunt trauma (history of working with a jack
hammer) to the ulnar artery and superficial palmar arch. The impact occurs against the hook of
the hamate. Arterial wall damage leads to aneurysm formation with or without thrombosis of
the vessel. Emboli may form, causing distal obstruction of digits (this can cause confusion with
the main DDx Buergers). Look for corkscrew configuration of the superficial palmar arch,
occlusion of the ulnar artery, or pseudoaneurysm of the ulnar artery.
Venous Thromboembolism {VTE) - Blanket term used to refer to PE and DVT (PE
and DVT are both forms of VTE).
Trivia: You are more likely to develop VTE if you are paraplegic vs tetraplegic.
Having said that, VTE is more likely in "motor complete" AIS A patients (those that have lost
motor and sensory) vs motor incomplete AIS B,C,D (those with some residual sensory or
motor function) -- which is more intuitive. Quad being worse than tetra for VTE risk makes
zero sense (and therefore makes a good trivia question).
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Peripheral Vascular Malformations - About 40% of vascular malfonnations
involve the extremities (the other 40% are head and neck, and 20% is thorax). Different than
hemangiomas, vascular malformations generally increase proportionally as the child grows.
This dude Jackson classified vascular malformation as either low flow or high flow. Low
flow would include venous, lymphatic, capillary, and mixes of the like. High flow has an
arterial component. Treatment is basically determined by high or low flow.
Klippel-Trenaunay Syndrome (KTS) - This is often combined with Parkes
Weber which is a true high flow AV malformation. KTS has a triad of port wine nevi,
bony or soft tissue hypertrophy (localized gigantism), and a venous malformation. A
persistent sciatic vein is often associated. The marginal vein of Servelle (some superficial
vein in the lateral calf and thigh) is pathognomonic (it's basically a great saphenous on the
wrong side).
Additional trivia: 20% have GI involvement and can bleed, if the system is big enough it can
eat your platelets (Kasabach Merritt). Basically, if you see a MRA/MRV of the leg with a
bunch of superficial vessels (and no deep drainage) you should think about this thing.
• KTS = Low Flow (venous)
• Parkes Weber = High Flow (arterial)
• "Klippel Trenaunay Weber" = Something people say when they (a) don't know what they
are talking about, or (b) don't know what kind of malformation it is and want to use a
blanket term.
ABls - So basic familiarity with the so called "Ankle to Brachia! Index" can occasionally
come in handy, with regard to peripheral arterial disease. This is basically a ratio of systolic
pressure in the leg over systolic blood pressure in the arm. Diabetics can sometimes have
unreliable numbers (usually high), because dense vascular calcifications won't let the vessels
compress.
Opinions vary on what the various cut off numbers mean. Most people will agree that you
can safely deploy the phrase "peripheral arterial disease" if the resting ABI is less than 0.90
You can also deploy the following generalizations: 0.5-0.3 = claudication, < 0.3 = rest pain
**More on this in the IR chapter
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Intimal Hyperplasia - "The bane of endovascular intervention." This is not a true
disease but a response to blood vessel wall damage. Basically this is an exuberant healing
response that leads to intimal thickening which can lead to stenosis. You hear it talked
about the most in IR after they have revascularized a limb. Re-Stenosis that occurs 3-12
months after angioplasty is probably from intimal hyperplasia. It's sneaky to treat and
often resists balloon dilation and/
or reoccurs. If you put a bare
stent in place it may grow through
the cracks and happen anyway. If
you put a covered stent in, it may
still occur at the edges of the
stent. The take home point is that
it's a pain in the ass, and if they
show an angiogram with a stent
in place, that now appears to be Intimal Hyperplasia
-dark stuff growing along the inside of the stent walls
losing flow, this is probably the
answer.
Cystic Adventitial Disease - This uncommon disorder classically affects the
popliteal artery, of young men. Basically you have one or multiple mucoid-filled cysts
developing in the outer media and adventitia. As the cysts grow, they compress the artery.
MJP CTA showing Vascular Narrowing Fluid sensitive MR showing a bunch of
cysts around the vessel, extrinsically
narrowing it
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SECTION 7:
VASCULITIS "
� •.. •.
,1. ,
.·:,,
Basically all vasculitis looks the same, with wall thickening, occlusions, dilations, and
aneurysm formation. The trick to telling them apart is the age of the patient, the gender/
race, and the vessels affected. Classically, they are broken up into large vessel, medium
vessel, small vessel ANCA +, and small vessel ANCA negative.
Larue:
Takayasu - "The pulseless disease." This vasculitis loves young Asian girls (usually
15-30 years old). If they mention the word "Asian," this is likely to be the answer. Also, if
they show you a vasculitis involving the aorta this is likely the answer. In the acute phase
there will be both wall thickening and wall enhancement. There can be occlusion of the
major aortic branches, or dilation of the aorta and its branches. The aortic valve is often
involved (can cause stenosis or AI). In the late phase there is classically diffuse narrowing
distally. The pulmonary arteries are commonly involved, with the typical appearance of
peripheral pruning.
If anyone was a big enough jerk to ask, there are 5 types with variable involvement of the
aorta and its branches. Which type is which is beyond the scope of the exam, just know type
3 is most common - involves arch and abdominal aorta.
Takayasu - Wall Thickening Involving the Aorta
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Giant Cell (GCA) -The most common primary system vasculitis. This vasculitis loves
old men (usually 70-80)** although there are a.few papers that will say this is slightly more
common in women. This vasculitis involves the aorta and its major branches particularly
those of the external caroti<i (temporal artery). This can be shown in two ways: (I) an
ultrasound of the temporal artery, demonstrating wall thickening, or (2) CTA / MRA or even
angiogram of the armpit area (Subclavian/ Axillary/ Brachia!), demonstrating wall
thickening, occlusions, dilations, and aneurysm. Think about it as the part of the body that
would be compressed by crutches (old men need crutches).
Trivia worth knowing:
• ESR and CRP are markedly elevated,
• Disease responds to steroids.
• "Gold Standard" for diagnosis is temporal artery biopsy (although it's often negative).
• Clinical connection between GCA and polymyalgia rheumatica, (they might be different
phases of the same disease). History might be "morning stillness in shoulders and hips."
Giant Cell - "Armpit" Vessel Thickening
Cogan Syndrome - Total Zebra probably not even worth
mentioning. It is a large vessel vasculitis that targets children and young
adults. It likes the eyes and ears causing optic neuritis, uveitis, and
audiovestibular symptoms resembling Menieres. They can also get
aortitis, and those that do have a worse prognosis.
Basically, kid with eye and ear symptoms + or - aortitis.
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Medium
PAN (Polyarteritis Nodosa) -This is one of two vasculitides (the other being
Buergers) that is more common in men. PAN is more common in a MAN. This can effect
a lot of places with the big 3 being Renal (90%), Cardiac (70%), and GI (50-70%). Typically
we are talking about microaneurysm formation, primarily at branch points, followed by
infarction. I would expect this to be shown either as a CTA or angiogram of the kidneys
with microaneurysms, or a kidney with areas of infarct (multiple wedge shaped areas).
Trivia to know is the association with Hep B.
Also, as a point of trivia the micro-aneurysm formation in the kidney can also be seen in
patients who abuse Crystal Meth (sometimes called a "speed kidney").
Kawasaki Disease - Probably the most common . Clinical Trivia:
vasculitis in children (HSP also common). Think about this as
"Fever for 5 Days"
a cause of coronary vessel aneurysm. A calcified coronary
artery aneurysm shown on CXR is a very rare aunt • Strawberry Tongue
Minnie. • Neck Lymph Nodes
• Rash of Palms of
Hands / Soles of Feet
-Coronary Artery Aneurysms > 8mm are "Giant" and prone
• Sore T hroat Diarrhea
to badness including MI
• "Etiology Unknown"
-Coronary Artery Aneurysms < 8mm may regress
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Small Vessel Disease (ANCA +)
Wegeners - I think about upper respiratory tract As I've previously mentioned, you
(sinuses), lower respiratory tract (lungs), and aren't supposed to say "Wegener"
kidneys. cANCA is (+) 90% of the time. Ways this because apparently he ate his boogers,
is shown are the nasal perforation (like a cocaine and was a Nazi. He also could not
addict) and the cavitary lung lesions. (more likely deliberately chose not to)
correctly pronounce the word "Gyro."
Churg Strauss -This is a necrotizing No matter how many times people
corrected him. Dude- it is "YEE-roh."
pulmonary vasculitis which is in the spectrum of
Eosinophilic lung disease. They always have asthma Wegener was truly one of histories
and eosinophilia. Transient peripheral lung greatest assholes.
consolidation or ground glass regions is the most
frequent feature. Cavitation is rare (this should make So we don't say his name. Instead say
"Granulomatosis with polyangiitis."
you think Wegeners instead). They are pANCA (+)
75% if the time. You know who else was a Nazi??
Henry Ford. No one ever talks about
Microscopic Polyangiitis -Affects the that. .. Google it - he wrote a book
kidneys and lungs. Diffuse pulmonary hemorrhage called "The International Jew, the
is seen in about 1/3 of the cases. It is pANCA (+) World's Foremost Problem, "and got
80% of the time. an awardfi'om Hitler.
Small Vessel Disease (ANCA -)
HSP (Henoch-Schonlein Purpura) -The most common vasculitis in children
(usually age 4-11). Although it is a systemic disease, GI symptoms are most common
(painful bloody diarrhea). It is a common lead point for intussusception. They could show
this two classic ways: (1) ultrasound with a doughnut sign for intussusception, or (2) as a
ultrasound of the scrotum showing massive skin edema. A less likely (but also possible)
way to show this case would be multi-focal bowel wall thickening, or a plain film with
thumbprinting.
Behcets -Classic history is mouth ulcers and genital ulcers in someone with Turkish
descent. It can cause thickening of the aorta, but for the purpose of multiple choice test I
expect the question will be pulmonary artery aneurysm.
Buergers -This vasculitis is strongly associated with smokers. It affects both small and
medium vessels in the arms and legs (more common in legs). Although it is more commonly
seen in the legs, it is more commonly tested with a hand angiogram. The characteristic
features are extensive arterial occlusive disease with the development of corkscrew collateral
vessels. It usually affects more than one limb. Buzzword = Auto-amputation.
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Gamesmanship Hand Angiograms:
If they are showing you a hand angiogram, it's going to be either Buergers of Hypothenar
Hammer Syndrome (HHS).
My strategy centers around the ulnar artery.
(1) Ulnar artery involved= HHS. The most helpful finding is a pseudo-aneurysm off the
ulnar artery - this is a slam dunk for HHS.
(2) Ulnar artery looks ok - then look at the fingers - if they are out, go with Buergers. It
sure would be nice to see some "corkscrew collaterals" - to make it a sure thing.
Be careful, because the fingers can be out with HHS as well (distal emboli), but the ulnar
artery should be fucked. Look at that ulnar artery first.
Location - Location
Central=
Think Takayasu
Mid-Clavicle =
Think Thoracic
Syndrome
Armpit=
Think Giant Cell
Takayasu
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Large Vessel
Takayasu Young Asian Ftmiale - lhii..:keneu aneurysmal aorta
Old Person with involvement of the "crutches" / armpit region
Giant Cell
(Subclavian, axillary, brachia!).
Cogan Syndrome Kid with eye and ear symptoms + Aortitis
Medium Vessel
PAN is more common in a MAN (M > F). Renal Microaneurysm
PAN
(similar to speed kidney). Associated with Hep B.
Kawasaki Coronary Artery Aneurysm
Small Vessel (ANCA +)
Wegeners Nasal Septum Erosions, Cavitary Lung Lesions
Churg Strauss Transient peripheral lung consolidations.
Microscopic Polyangiitis Diffuse pulmonaiy hemorrhage
Small Vessel (ANCA-)
HSP Kids. Intussusception. Massive scrotal edema.
Behcets Pulmonary artery aneurysm
Buergers Male smoker. Hand angiogram shows finger occlusions.
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•:
. '
· _ �
SECTION 8:
CAROTID DOPPLER
�-
General Vascular Ultrasound Concepts - Stenosis:
The waveform will go through changes before entering a stenosis, within the stenosis, and after
exiting the stenosis.
Proximal (Upstream) Stenosis Distal (Downstream)
Waveform can be normal, Waveform usually has a Waveform can be Tardus
monophasic decreased high velocity jet -might Parvus (prolonged "slow"
peak systolic velocity, or see aliasing. systolic acceleration /
loss of diastolic flow. upstroke, and small
High velocity = low systolic peak - "rounding
Diastolic flow is reduced in pressure (Bernouli's effect of the peak")
proportion to the severity mother fuckers)
of the stenosis.
Fuckery with words: It would be correct to say that Tardus Parvus is found downstream from a
stenosis. It would also be correct to say that Tardus Parvus is the result of upstream stenosis.
See what I did right there? I'm not the only one who can pull some shit like that. ..
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High Yield Topics of Carotid Doppler
Stenosis: They will show you an elevated velocity(normal is< 125cm/s). They may also show
you the ICA/CCA ratio(normal is< 2), or the ICA end diastolic velocity(< 40 cm/s is normal).
Here arc the rules:
• Less that 50% stcnosis will not alter the peak systolic velocity
• 50-69% Stenosis: ICAPSV 125-230 cm/s , ICA/CCAPSV ratio: 2.0-4.0 , ICAEDV 40-100
• >70 % Stenosis: ICAPSV > 230 cm/s, ICA/CCAPSV ratio: > 4.0 , ICAEDY>100
Proximal Stenosis: OK here is the trick; they will show a tardus parvus waveform. If they show it
unilateral, it is stenosis of the innominate. If it's bilateral then it's aortic stenosis.
Subclavian Steal: This is discussed in greater detail in the cardiac chapter, but this time lets
show it on ultrasound. As a refresher, we arc talking about stenosis and/or occlusion of the
proximal subclavian artery with retrograde flow in the ipsilateral vertebral artery.
How will theyshow it? They are going to show two things: (1) Retrograde flow in the left vertebral,
and(2) a stenosis of the subclavian artery with a high velocity.
How theycangetreallysneaky? Thcy can
===�
show this thing called "early steal." Steal is
apparently a spectrum, which starts with mid- �
systolic deceleration with antegrade late-
systolic velocities. Some people think the �
"early steal" waveform looks like a rabbit. __ _
Early Steal
Systolic Deceleration
"Early Steal"
To-and-fro flow
"Incomplete Steal"
Retrograde Flow
"Complete Steal"
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THIS vs THAT: Gamesmanship Internal Carotid vs External Carotid
This really lends itself well to multiple choice test questions. The big point to
understand is that the brain is always on. You need blood flow to the brain all the time,
which means diastolic flow needs to be present all the time, and thus continuous color
flow throughout the cardiac cycle. The external carotid feeds face muscles... they only
need to be on when you eat and talk.
Internal Carotid External Carotid
Low Resistance High Resistance
Low Systolic Velocity High Systolic Velocity
Diastolic velocity does not return to Diastolic velocity approaches zero
baseline baseline
Continuous color flow is seen throughout Color flow is intennittent during the
the cardiac cycle cardiac cycle
Temporal Tap - It is a technique Sonographers use to tell the external carotid from the
internal carotid. You tap the temporal artery on the forehead and look for ripples in the
spectrum. The tech will usually write "TT" on the strip - when they do this.
*You can also look.for branches to tell the external carotid vs the internal.
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Aortic Regurgitation: - Just like aortic stenosis they are going to show you bilateral
CCAs. In this case you are going to get reversal of diastolic flow.
Brain Death Apparently in the ever-feuding monarchies of Europe, ultrasound can be
used for brain death studies. A loss of diastolic flow suggests cessation of cerebral blood
flow.
Aneurysms - In case someone asks you, distal formation of an aneurysm (such as one in
the skull) cannot be detected by ultrasound, because proximal flow remains nonnal.
Intra-Aortic Balloon Pump - Remember these guys are positioned so that the
superior balloon is 2 cm distal to the take off of the left subclavian artery, and the inferior
aspect of the balloon is just above the renals (you don't want it occluding importing stuff
when it inflates). When the balloon does inflate it will displace the blood in this segment of
the aorta - smashing it superior and inferior to the balloon. The balloon will inflate during
early diastole (right after the aortic valve closes) because this is when the maximum amount
of blood is available for displacement.
What does this do to the internal carotid (ICA) waveform? You are going to see an extra
bump or "augmentation" as the balloon inflates and displaces blood superior.
Pump�
Inflates
Which wave would you measure to evaluate the velocity?
The first one (the one that is not assisted).
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Doppler Evaluation in the LVAD
Bro ... WTF is a "LVAD"?
The Left Ventricular Assist Device is a surgically
implanted device that helps pump blood from the left
ventricle to the aorta. It's done in the setting of severe
heart failure, typically as a bridge to cardiac
transplantation, or in those who are simply too evil to die
of natural causes (Dick Cheney) and require an
intermediate step while the Darth Vader suit is prepped.
Testable Doppler Changes:
LVAD Waveforms will lose the normal high resistance spiked look of the ICA, CCA,
Vertebral Arteries. Instead they are mostly flat, with a tardus parvus look. The flow is
continuous through systole and diastole. The little spikes you see during systole are from
the small amount of residual LV function.
ICA- LVAD Patient
ICA - Normal Patient
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Classic Carotid Doppler Cases
} Normal Peak Velocity 60-1 OOcm/s
} Continuous Diastolic Flow
Lower Peak Velocity
High Velocity Continuous Diastolic Flow
} Higher Peak Velocity
} Less Diastolic Flow
ICA Occlusion
-The CCA looks like the ECA, with a high
resistance waveform, and loss of diastolic
flow
Aortic Regurgitation
-With Classic Reversal of Diastolic Flow
-Most Likely Shown Bilaterally
Aortic Regurgitation
-This time showing the "Pulsus Bisferiens"
or double systolic peak. This is also seen in
hypertrophic obstructive cardiomyopathy.
Aortic Stenosis
-Characteristic Tardus Parvus waveform
-This will be shown BILATERAL - to prove it's
the aortic valve. Unilateral will be amore central
vascular stenosis.
Dissection - with Flap
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13
INTERVENTIONAL
PROMETHEUS LIONHART, M.D.
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SECTION 1:
INSTRUMENTS OF INTERVENTION
Puncture Needles:
• The smaller the "gauge" number, the bigger the needle. It's totally Puncture Needle sizes
counterintuitive. For example, an 8G Needle is much bigger than are designated by the
a 16G Needle. *This is the opposite ofa "French," which is used
to describe the size ofa catheter or dilator. The larger the French,
OUTER diameter
the larger the catheter.
Catheter and Dilator
• The Gauge "G" refers to the OUTER diameter of the needle. sizes are designated by
Wires: the OUTER diameter
Just some general terminology: Sheaths are designated
by their INNER lumen
• 0.039 inch= 1mm
• size, (the maximum
0.035 inch is the usual size for general purposes
• 0.018 and 0.014 are considered microwires capacity of a diameter
• "Glide Wires" are hydrophilic coated wires that allow for they can accommodate)
easier passage of occlusions, stenosis, small or tortuous
vessels.
Catheters - General
• 3 French= 1 mm (6 French= 2 mm, 9 French= 3 mm) Diameter in mm = Fr/ 3
• Important trivia to understand is that the French size is the external diameter of a catheter (not the
caliber of the internal lumen).
• The standard 0.035 wire will.fit through a 4F catheter (or larger)
Sheaths
• Sheaths are used during cases that require exchange of multiple catheters. The sheath allows you to
change your catheters/ wires without losing access.
• They are sized according to the largest catheter they will accommodate.
• The outer diameter of a vascular sheath is usually l .5F to 2F larger than the inner lumen.
Sheath - Size is Given by
INNER Diameter
Add 2 F for the Outer
2F
Diameter (1 F + 1 F = 2F) if
(Total Outer
Diameter) you want to know how big
the hole in the skin will be.
• This would be a 6F Sheath
• The hole in the skin would be BF
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Gamesmanship - Various Forms of'Fuckery That Can Be Performed~
There are a few classic ways this can be asked. You can get all these questions right if you
understand the following trivia:
• 3 French= 1 mm, so 1 French= 0.3 mm
• Puncture Needles, Guide Wires, and Dilators are designated with sizes that describe their
OUTER diameters.
• Sheaths are designated with sizes that describe their INNER diameter
• The rubber part of the sheath is about 2F (0.6 mm) thick, so the hole in the skin is about
0.6mm bigger than the size of the sheath.
• Wire DIAMETERs are given in INCHES (example "0.035 wire" is 0.035 inches thick)
• Wire LENGTHS is typically given in CENTIMETERS (example "180 wire" is 180 cm
long)
Example Quiz 1: What is the size of a puncture hole in mm of a 6 French sheath?
Diameter in mm = Fr I 3 • 6 French Describes the Inner Diameter
2. 7 mm = (6 + 2) I 3 • Add 2 French for the thickness of the rubber
• Total is 8 French
Answer = 2. 7 mm
Example Quiz 2: What is the size of a puncture hole in mm of a 6 French sheath, placed
coaxially into a short access sheath ?
**This is some second level fuckery.
6 French sheath is being placed inside of another sheath
6 French sheath is actually 8 French Big (remember you add 2F for the rubber wall).
So you need a sheath that can accommodate an 8 French Diameter. Remember that
sheaths are named.for what they can accommodate, so you need an 8 French Sheath.
8 French sheath is actually 10 French Big (remember you add 2F for the rubber
'I
wall).
sF· 10F*
Diameter in mm = Fr I 3
• 8 French Describes the Inner Diameter
3.3 mm = (8 + 2) 13 • Add 2 French for the thickness of the rubber
• Total is 10 French
Answer = 3.3 mm
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Puncture Needles .. The Legend Continues:
Some Conversions:
• 16G needle has an outer diameter of 1 .65 mm, = 5 F catheter;
• 20G needle has an outer diameter of 0.97 mm, = 3 F catheter.
Some Needle Wire Rules:
Old School Seldinger Technique:
*Remember 0.035 is probably the
• 18G needle will accept a 0.038 inch guidewire most common wire used. Thus the
19G is the standard needle in
• 19G needle will allow a 0.035 inch guidewire many JR suites.
Micro Puncture Style:
• Initial puncture is performed with a 21G (rather than a typical 18G or 19G) needle.
• 21G needle will allow a 0.018 inch guidewire
• After you have that tiny wire in, you can exchange a few dilators up to a standard
4F-5F system with the popular 0.035 wire.
Micro Puncture is Good when.... Micro Puncture is Bad when ....
• Access is tough (example= a.fucking • Scarred Up Groins
antegrade femoral puncture) • Big Fat People
• You suck ("lack experience") • When you try and upsize, sometimes
• Anatomically sensitive areas ( internal that.flimsy 0.018 won't give enough
jugular, dialysis access) support for antegrade passage of a
dilator.
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Guidewires - The Legend Continues to Continue:
There are two main flavors of guidewires:
(1) Non-Steerable - These are used as supportive rails for catheters. These are NOT for
negotiating stenosis or selecting branches
(2) Steerable - These have different shaped tips that can be turned or flipped into tight spots.
Within this category is the "hydrophilic" coated which are used to fit into the tightest
spots.
Hydrophilic Guidewires - "Slippery when wet". They are sticky when dry, and super slippery
when wet. At most academic institutions dropping one of these slippery strings on the floor
will result in "not meeting the milestone" and "additional training" (weekend PICC workups).
• Next Step Questions: Could revolve around the need to "wipe the wire with a wet sponge
each time it is used."
• Next Step Questions: Pretty much any situation where you can't get into a tight spot. This
could be a stenotic vessel, or even an abscess cavity.
Length - Here is the testable trivia regarding wire length.
• Remember Diameter is in INCHES, Length is in CENTIMETERS
• 180 cm is the standard length
• 260 cm is the long one. These are used if you are working in the upper extremity (from a
groin access), working in the visceral circulation and need to exchange catheters, using a
guide cath that is longer than 90 cm, through-and-through situation ("body flossing").
• Minimal guidewire length = length of catheter + length of the guidewire in the patient.
Floppy Tips - A lot of wires have pointy ends and soft floppy ends. The floppy ends are
usually available in different sizes. The testable point is that the shorter the floppy part the
greater the chance of vessel dissection. For example, a 1 cm floppy tip has a greater risk of
dissection compared to a 6 cm floppy tip. The practical tip is to choose a wire with a long
floppy tip (unless you are trying to squeeze into a really tight spot).
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Guidewires - The Legend Continues to Continue to Continue
Stiffness: I feel like there are two primary ways to ask questions about stiffness:
(1) Your classic "right tool for the right job" questions.
Unfortunately, these are often "read my mind, and understand my prejudices" questions.
The following are probably the clearest scenarios:
• Bentson (floppy tip)= Classic guidewire test for acute thrombus lysability
• Lunderquist (super stiff)= "The coat hanger." This thing is pretty much only for aortic
stent grafting.
• Hydrophilic= Trying to get into a tight spot. Yes a Bentson is also an option, but this is
more likely the "read my mind" choice.
(2) Which is "Stiffer ? " or Which is "Less Stiff?" types of question. Basically just have a
general idea of the progression. A second-order style question would be "Which is more or
less likely to cause dissection?" Remember the rule is "more stiff= more dissection."
Less
"Noodle Like" Normal Supportive Stiff Hulk Smash!!
Bentson Hydrophilic Stiff Hydrophilic Flexfinder Lunderquist
Standard 0.035 J or "Heavy Duty" J or Amplatzer Stiff or Backup Meier
Straight Straight Extra Stiff
0.018 Platinum
Plus
V 18 - shapeable tip
Trivia: Stiff guidewires should NEVER be steered through even the mildest of curves. You
should always introduce them through a catheter (that was originally placed over a
conventional guidewire).
J Tip Terminology: A "J Shaped" Tip supposedly has the advantages of not digging up
plaque and of missing branch vessels. Often you will see a number associated with the J
(example 3 mm, 5 mm, 10 mm, 15 mm etc...). This number refers to the radius of the
curve. Small curves miss small branch vessels, larger curves miss larger branch vessels. The
classic example is the 15mm curve that can be used to avoid the profunda femoris during the
dreaded arterial antegrade stick.
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Catheters .. The Legend Continues
- Fuckery with Numbers
If you look at a "buyers guide" or the packaging of an angiographic catheter you may (if you
look hard enough) find 3 different numbers. I think it would be easy to write a question asking
you to ID the numbers, or asking what size sheath or wire you can use with the catheter.
The three numbers that you are going to see on the package are: the outer diameter size (in
French), the inner diameter size (in INCHES), and the length (in CENTIMETERS).
Example Question 1: What size is this catheter?
VANDELAY INDUSTRIES
FINE ANGIOGRAPHIC CATHETERS
Answer= 4F
4, 110, 0.035
Remember that the outer diameter of a catheter defines it's size (unlike the sheath which is
defined by the inner diameter), and that these sizes are given in French. 4F catheters are very
commonly used. 110 and 0.035 are not catheter sizes available for humans existing outside of
middle earth.
Remember that length of the catheter is given in centimeters. The standard lengths vary from
about 45 cm to 125 centimeters.
Lastly the inner diameter of a catheter is given in inches and will pair up with the size wire.
For example, the largest wire a 0.035 catheter will accommodate is a 0.035.
Example Question 2: What size sheath and guidewire can you use with this catheter?
VANDELAY INDUSTRIES Answer=
FINE ANGIOGRAPHIC CATHETERS • 4F Sheath or Larger
• 0.035 wire or Smaller
4, 110, 0.035 *a 0.038 wire would NOT fit
It's a 4F sheath because sheaths are defined by their INNER diameter. So a 4F snake can crawl
through a 4F tube. Obviously a bigger tube (SF, 6F, etc ...) will also have enough room for a 4F
snake.
It's a 0.035 wire because the inner diameter measurements are given in inches, just like the
guidewires. In this case the tube is the catheter and the wire is the snake. So a bigger snake (any
wire thicker than 0.035) wouldn't fit.
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Catheters - Selective vs Non-Selective
Just like Guidewires can be grouped into "steerable" or "non-steerable" , catheters can be
grouped into "non-selective (flush) catheters" and "selective catheters".
• Non-Selective Catheters: These things are used to inject contrast into medium and large
shaped vessels. This is why you"ll hear them called "flush catheters."
• Selective Catheters: These things come in a bunch of different shapes/angles with the
goal of "selecting" a branch vessel (as the name would imply).
Non-Selective Catheters
Pigtail: For larger vessels this is the main workhorse. It's called a "pigtail" because the
distal end curls up as you retract the wire. This curled morphology keeps it out of small
branch vessels. The catheter has both side and end holes.
Q: What might happen if you consistently inject through the pigtail like a pussy?
A: All the contrast will go out the proximal side holes and not the tip. Eventually, if
you keep flushing like a pansy you will end up with a clot on the tip.
Q: What should you do prior to giving it the full on alpha male injection ?
A: Give a small test injection to make sure you aren't in or up against a small branch
vessel. Pigtails are for use in medium to large vessels.
Q: What if the pigtail fails to form as you retract the wire?
A: Push the catheter forward while twisting.
Straight Catheter: This one doesn't curl up as you retract the wire. Otherwise, it's the
same as a pigtail with side holes and an end hole. The utility of this catheter is for smaller
vessels (with the caveat that they still need decent flow).
The classic location is the iliac.
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Catheters .. Selective vs Non-Selective cont....
Selective Catheters
Selective catheters come in two main flavors: (1) end hole only, or (2) side+ end holes
(that '.S' what she said).
Side + End Holes
End Hole Only "Girl who went to catholic school"
Hand Injection Only
*high flow injection can displace the catheter, or Works fine with Pump Injected runs
cause dissection (can handle a rapid bolus without displacing)
Utility= DiagnosticAngiograms and
Utility= Classic would be a SMAAngiogram
Embolization Procedures
NEVER use with Embolotherapy.
The fucking coils can get trapped in the
sideholes or the particulate matter/mush may go
out a side hole and go crush the wrong vessel.
"Non-targeted" they call it.
I think the above chart is probably good enough to get most reasonable selective catheter
questions correct. Unfortunately, it's also possible that you could be asked a "read my mind,
understand my prejudices" type of question in the form of "which catheter would you use?"
This is how I would guess - [[forced.
Acute Angle ( < 60) Angle of 60-120 Obtuse Angle ( > 120)
Example= Renals,
Example= Aortic Arch Vessels Example= Celiac, SMA, IMA I
Maybe SMA and Celiac
"Angled Tip Catheter" "Curved Catheter" "Recurved"
Sidewinder (also called a
-Berenstein or Headhunter
"ROG" Renal Double Curve,
or a "Cobra" Simmons), or a "Sos Omni"
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WTF is a "Recurve" ?
For whatever reason Academic Angio guys tend to spaz if residents don't
understand why a "recurve" is different than a regular curved catheter.
Basically any curved catheter has a "primary" curve and a "secondary" curve.
On a regular curved cath both are in the same direction. However, on a
recurved cath the primary goes one way, and the secondary goes the other.
These catheters are good for vessels with an obtuse angle. You pull the
catheter back to drop into them.
I trained under a guy who was always very
impressed with himself when he could perform a
basic catheter maneuver like this. After dropping
into the IMA he would sometimes slowly turn to
one of the female techs and say "that's why I'm
the king."
I was really afraid he was going to break his own
arm, jerking himself off that hard.
That guy (or someone like him) is probably Recurve Curve
writing questions for the IR section (guessing/
not confirmed - but makes me smile to think so).
Vocab
"Co-Axial Systems" - Basically one catheter inside another catheter/sheath. The most
basic example would be a catheter inside the lumen of an arterial sheath.
"Guide Catheters" - These are large catheters meant to guide up to the desired vessel.
Then you can swap them for something more conventional for distal catheterization.
"Introducer Guide" - This is another name for a long sheath. The assholes are trying to
trick you.
"Microcatheter" - These are little (2-3 French). They are the weapon of choice for tiny
vessels (example "super-selection" of peripheral or hepatic branches).
"Vascular Sheath" - It's a sheath (plastic tube) + hemostatic valve+ side-arm for
flushing
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Flow Rate
"Give me 20.for 30" - typical angio lingo for a run at 20cc/sec for a total of 30cc.
How do you decide what the correct.flow rate is? For the purpose of multiple choice, I'll
just say memorize the chart below. In real life you have to consider a bunch of factors:
catheter size, catheter pressure tolerance, flow dynamics, vessel size, volume of the distal
arterial bed (hand arteries can tolerate less blood displacement compared to something like
the spleen), and interest in the venous system (a common concern in mesenteric angiography
- hence the relatively increased volumes in the SMA, IMA, and Celiac on the chart).
Bigger Artery= Higher Rate. You want to try and displace 1/3 of the blood per second to get
an adequate picture.
Typical Rates / Volumes
Rate 1-2m1Jsec Rate 4-SmLJsec Rate 5-7m1Jsec Rate 20-30m1Jsec
Volume 4-10 ml Volume 8-15 ml Volume 30-40 ml Volume 30-40 ml
Bronchial Artery Carotid Celiac Aorta,
lntercostal Artery Subclavian SMA Aortic Arch,
_Reng_l IVC,
Femoral Pulmonary Artery
IMA
*/MA are typically *Abdominal Aorta has
given a higher a slightly lower rate
volume (15-30 mL) (15-20 ml/sec) as it is
smaller than the
Thoracic Aorta
Maximum flow Rates:
These are determined by the INTERNAL diameter, length, and number of size
holes. In general, each French size gives you about 8ml!s.
These are the numbers I would guess if forced to on multiple choice. In the real
world its (a) written on the package and (b) a range of numbers
3F = 8 ml/s, 4F = 16 rnl/s, 5F = 24 rnl/s.
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Catheter Flushing
Double Flush Technique - This is used in situations where even the smallest thrombus or air
bubble is going to fuck with someone's golf game (neuro IR/ cerebral angiograms). The
technique is to (1) aspirate the catheter until you get blood in the catheter, then (2) you attach
a new clean saline filled syringe and flush.
Single Flush Technique - This is used everywhere else (below the clavicles). The technique
is to (1) aspirate until you get about 1 drop of blood in a saline filled syringe, and (2) tilt the
syringe 45 degrees and flush with saline only.
What ifyou accidentally mixed the blood in with the saline?
Discard the syringe and double flush
What if you are unable to aspirate any blood ?
Hopefully you are just jammed against a side wall. Try pulling back or manipulating the
catheter. If that doesn't work then you have to assume you have a clot. In that case your
options are to (1) pull out and clear the clot outside the patient, or (2) blow the clot inside the
patient - you would only do this if you are embolizing that location anyway (and a few other
situations that are beyond the scope of this exam).
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• . •
�
Arterial Access
SECTION 2:
VASCULAR ACCESS
General "Next Step" Scenarios:
• You meet resistance as you thread the guidewire. Next Step= STOP! "Resistance" is an
angio buzzword for something bad. Pull the wire out and confirm pulsatile flow.
Reposition the needle if necessary.
• The wire will not advance beyond the top of the needle even after you pull the wire back
and have normal pulsatile flow. Next Step= Flatten the needle against the skin. You are
assuming the need to negotiate by a plaque.
• The wire stops after a short distance. Next Step = Look under fluoro to confirm correct
anatomic pathway. If it is normal then you could put a 4F sheath in and inject some
contrast. After that monkeying around with a hydrophilic wire is the conventional answer.
Femoral Artery Access - This is the most common arterial access route.
Anatomy review = the external iliac becomes the CFA after it gives off the inferior epigastric.
The ideal location is over the femoral head (which gives you something to compress against),
distal to the inguinal ligament / epigastric artery and proximal to the common femoral
bifurcation.
• If you stick too high (above inguinal ligament): You risk retroperitoneal bleed
• If you stick too low, you risk AV Fistula
• If you stick at the bifurcation: You risk occluding branching vessels with your sheath.
Inguinal
Ligament
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Brachia! Access - Possible situations when you might want to do this:
• Femoral Artery is dead/ unaccessible.
• The patient's abdominal pannus, vagina, or ball sack is really stinky.
• Upper limb angioplasty is needed
Special Testable Facts/Trivia:
• Holding pressure is often difficult. Even a small hematoma can lead to medial brachia!
fascia! compartment syndrome (cold fingers, weakness)- and is a surgical emergency
which may require fasciotomy.
• The risk of stroke is higher (relative to femoral access), if the catheter has to pass across
the great vessels/ arch.
• A sheath larger than a 7F may require a surgical cut down.
• The vessel is smaller and thus more prone to spasm. Some people like to give prophylactic
"GTN" - glyceryl trinitrate, to prevent spasm.
Which arm?
• Left Side if headed south (abdominal aorta or lower extremity).
• Right Side if headed north (thoracic aorta or cerebral vessels).
• All things equal = Left side (it's usually non-dominant, and avoids the most cerebral
vessels).
• Blood pressure difference greater than 20 Systolic suggest a stenosis (choose the other
arm).
Radial Access - This is also a thing. There are two pieces of trivia that I think are the most
testable about this access type.
(1) Bedrest is not required after compression.
(2) You need to perform an "Allen Test" prior to puncture. The "Allen Test" confirms
collateral flow via the ulnar artery to the hand (just in case you occlude the radial artery).
The test is done by manually compressing the radial and ulnar arteries. A pulse ox placed
on the middle finger should confirm desaturation. Then you release the ulnar artery and
saturation should improve, proving the ulnar artery is feeding the hand.
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Translumbar Aortic Puncture - This was more commonly performed in the dark ages I
Cretaceous period. You still see them occasionally done during the full-on thrash that is the
typical type 2 endoleak repair.
Trivia:
• The patient has to lay on his/her stomach (for hours!) during these horrible thrashes
• Hematoma ofthe psoas happens pretty much every case, but is rarely symptomatic.
• Known supraceliac aortic aneurysm is a contraindication
• Typically "high" access - around the endplate of T 12 - is done. Although you can
technically go "low" - around L3.
• The patient "Self compresses" after the procedure by rolling over onto his/her back.
• Complaining about a "mild backache" occurs with literally every one of these cases
because they all get a psoas hematoma.
Pre Procedure Trivia: Prior to an arterial stick you have to know some anticoagulation
trivia.
• Stop the heparin 2 hours prior to procedure (PTT l .2x ofcontrol or less; normal
25-35 sec)
• INR of 1.5 is the number I'd pick ifasked (technically this is in flux)
• Stop Coumadin at least 5-7 days prior (vitamin K 25-50 mg IM 4 hours prior, or FFP/
Cryo)
• Platelet count should be> 50K (some texts say 75)
• Stop ASA/Plavix 5 days prior (according to SIR)
• Per the ACR - diagnostic angiography, routine angioplasty, and thrombolysis are
considered "clean procedures." Therefore, antibiotic prophylaxis is unnecessary.
Post Procedure Trivia: By the book, you want 15 minutes of compression. You can
typically pull a sheath with an ACT of<150-180. Heparin can get turned back on 2 hours
post (assuming no complications). Groin check and palpate pulses should be on the post
procedure nursing orders.
Closure Devices: Never used ifthere is a question ofinfection at the access site.
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Venous Access:
PICC lines: Use the non-dominant arm. The preference is basilic>brachia]>cephalic.
You don't place these in patients with CRF, on dialysis, or maybe going to be on dialysis.
Central Lines/Port: The right IJ is preferred. External jugular veins can be used.
Subclavian access is contraindicated in patients with a contraindication to PICC lines.
Don't place any tunneled lines/ports in septic patients (they get temporary lines).
National Kidney Foundation-Dialysis Outcome Quality Initiative (NKF-KDOQI): Order of
preference for access: RIJ>LIJ>REJ>LEJ. "Fistula First Breakthrough Initiative": is
the reason you don't place PICCs in dialysis patients.
What is the preferred access site.for a dialysis catheter? The right IJ is the preferred
access, because it is the shortest route to the preferred location (the cavoatrial junction). It
will thrornbose less than the subclavian (and even if it does, you don't lose drainage from
the am1- like you would with a subclavian). Femoral approach is less desirable because
the groin is a dirty dirty place.
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Bleeding Applying Pressure
- Where dat hole be?
The word "hypotension" in the clinical vignette after an
arterial access should make you think about high sticks / The hole in the skin and
retroperitoneal bleeds. the hole in the artery don't
typically line up.
Things that won 1 help: • Antegrade Puncture =
Below the skin entry point
• Yelling "Mother Fucker!!" - trust me, I've tried this • Antegrade Puncture on a
Fatty= Well Below the
skin entry point
Things that might help: • Retrograde Puncture =
Above the skin entry
• Placing an angioplasty balloon across the site of the
bleeding( or inflow) vessel.
Pseudoaneurysm Treatment: As described in the vascular chapter, you can get a
pseudoaneurysm after a visit to the cardiology cath lab(or other rare causes). A lot of the
time, small ones(< 2 cm) will undergo spontaneous thrombosis. The ones that will typically
respond to interventional therapy are those with long narrow necks, and small defects. There
are 3 main options for repair: (1) open surgery, (2) direct ultrasound compression, or
(3) thrombin injection.
Next Step: Pain disproportionate to that expected after a percutaneous stick= Get an US to
look for a pseudoaneurysm
Direct compression of the Painful for the Patient(and
neck (if possible avoid the Radiologist), can take 20
compression of the sac). mins to an hour.
Direct Compression
Enough pressure should be
applied to stop flow in the Don't compress if it's above
neck. the inguinal ligament.
Needle into apex of cavity Contraindications: Local
(aim towards the infl.ow infection , Rapid
defect) - inject 0.5-1.0 ml Enlargement, Distal Limb
Thrombin Injection (500-1000 units). Ischemia, Large Neck (risk
for propagation),
Do NOT aspirate blood into Pseudoaneurysm cavity size
syringe - will clot. < 1cm.
May be needed if thrombin injection fails, there is
Surgery infection, there is tissue breakdown, or the aneurysm neck
is too wide.
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Pseudoaneurysm Treatment Cont:
Which option do you pick? For the purpose of multiple choice I would suggest the following:
Standard Starting Point: Cardiac Cath Lab
Infected Depends -
Yes
Actively Bleeding No Yes
Combined ---1� Probably a
41---� Skin Necrosis AV Fistula ? covered
Thrombotic Event stent
Got
◄ Better?
Repeat US
1 Week
N eck Size
-
1"' < 1cm?
._ ._
�-,-------x-�
Yes/ No
-
�---�
Got Bigger? ._ ._
J"
Above vs Below
Thrombin Inguinal
Ligament
Above
Got Repeat US
Better? 2 Days Depends
Compression
with US Probably a
*might be worth covered stent
a try, but wide
Try ♦ 1111 Failure neck reduces
success rate
again
Failure
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Pseudoaneurysm Treatment Cont:
This algorithm on the prior page assumes the Test Writer agrees that Thrombin is superior to
Compression (it hurts less, and probably has a higher success rate). Most modernly trained guys
will think like this. However, some conservative strategies favor trying to compress all the ones
below the Inguinal ligament.first - then trying thrombin second line. Simply read the test writers
mind to know his I her bias prior to answering.
Thrombin Injection - Where do you stick the needle ?
The needle should be placed
in the apex of the cavity (tip
directed towards the inflow
defect).
Ultrasound Compression - Where do you compress ?
Orthogonal plane to the neck of the
pseudoaneurysm. Pressure is
directed to obliterate flow in the
neck/ sac.
Trivia - Seriously Watch the Wording Carefit!/y:
• Anticoagulation has no effect on thrombin injection treatment - primary success**
• Anticoagulation docs* increase the risk of recurrence (I 0%?) after thrombin injection treatment
• Anticoagulation is NOT a contraindication to attempting direct compression, although it DOES
reduce success rate and most people will tell you to stop them prior to the procedure (if possible).
• Failure to respond to thrombin = Occult vascular issue (big puncture site laceration, infection)
• Untreated Pseudoaneurysm for greater than 30 days tend to resist compression and thrombin
therapy to variable degrees. They do best if treated within 2 weeks.
• Attempted compression of a Pseudoancurysm above the inguinal ligament can cause a RP bleed.
It is still safe to tty and thrombin inject
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SECTION 3:
PTA AND STENTS
General Tips/Trivia regarding angioplasty: The balloon should be big enough to take out
the stenosis and stretch the artery (slightly). The ideal balloon dilation is about 10-20% over
the normal artery diameter. Most IR guys/gals will claim success if the residual stenosis is
less than 30%. Obviously you want the patient anticoagulated, to avoid thrombosis after
intimal iqjury. The typical rule is 1-3 months of anti-platelets (aspirin, clopidogrel) following
a stent.
"Primary Sten ting": This is angioplasty first, then stent placement. You want to optimize
your result. Stenting after angioplasty usually gives a better result than just angioplasty alone
(with a few exceptions - notably FMD - to which stenting adds very little). An important
idea is that a stent can't do anything a balloon can't. In other words, the stent won't open it
any more than the balloon will, it just prevents recoil.
Balloon Expanding vs Self Expanding: Stents come in two basic flavors, balloon
expandable or self expandable. Location determines the choice.
Se(fExpandable stents are good for areas that might get compressed (superficial locations).
• Classic Examples = Cervical Carotid or SFA.
Balloon Expandable stents are good for more precise deployment
• Classic Example = Renal ostium
Closed vs Open Cell Stents - Vascular stent designs may be categorized as (a) closed-cell -
where every stent segment is connected by a link (less flexible, with better radial force) or
(b) open-cell in which some stent segment connections are deliberately absent (flexible/
conforms to tortuous vessels, less radial force).
Nitinol (magic?): Nitinol is said to have a "thermal memory." It is soft at room
temperature, but can become more rigid at body temperature. This is exploited for self
expanding stents.
Drug Eluting Stents - These things have been used for CAD for a while. The purpose of
the "drug" is to retard neointimal hyperplasia.
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Balloon Selection - Balloons should be 10-20% larger than the adjacent normal (non-stcnotic)
vessel diameter. A sneaky move would be to try and get you to measure a post-stcnotic dilation.
A rough guessing guide (!/forced):
li�c) External Iliac CFA, Prox SFA Distal SFA = 5111111
=7mm =6mm
**Popliteal would be 4 mm
As a general rule, larger balloons allow for more dilating force but the risk of exploding the vessel or
creating a dissection is also increased.
Stent Selection - Stcnts should be 1-2 cm longer than the stcnosis and 1-2 111111 wider than the un
stcnoscd vessel lumen
Special Situations
(l) You have more than 30% residual stenosis (failed you have). The first thing to do (if possible)
is to measure a pressure gradient. If there is no gradient across the lesion, you can still stop and
claim victory. If there is a gradient you might be dealing with elastic recoil (the lesion
disappeared with inflation, but reappeared after deflation). The next step in this case is to place a
stent.
(2) You can't make the waist go away with balloon inflation. Switch balloons to either a higher
pressure rated balloon, or a "cutting balloon."
(3) You caused a distal cmbolization. First do an angiographic rnn. If the limb/ distal vessels look
fine then you don't need to intervene. If you threatened the limb, then obtain ipsilatcral access
and go after the clot ("aspiration").
(4) You exploded the vessel ("Extravasation"). This is why you always leave the balloon on the
wire after angioplasty. If you sec extravasation get that balloon back in there quickly, and
perform a low pressure insufflation proximal to the rupture to create tamponade. You may need
to call vascular surgery ("the real doctors").
(5) What if you are trying to cross a tight stenosis and you see something like this ?
This is the classic "spiral" of a dissecting wire.
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SECTION 4:
STENT GRAFTS
�•-
"EVAR" = EndoVascular THIS vs THAT: Endografts VS Open Repair:
abdominal aortic Aneurysm Repair.
These include the bifurcated iliac • 30 Day Mortality is LESS for Endovascular Repair
systems and unilateral aortic + iliac (like 30% less)
systems. • Long Term Aneurysm Related Mortality (and total
mortality) is the SAME for open vs endovascular
"TEVAR" = Thoracic
EndoVascular aortic Aneurysm repair
Repair. • Graft Related Complications and Re-interventions
are HIGHER with Endovascular Repair
Indications/or EVAR:
(1) AAA larger than 5 cm (or more than 2x the size of the normal aorta)
(2) AAA growing "rapidly" (more than 0.5 cm in 6 months)
Anatomy Criteria/or EVAR:
• Proximal landing zone must be:
• 10 mm long,
• Non- aneurysmal (less than 3.2 cm), 10 mm Long
<3.2 cm Wide
• Angled less than 60 degrees. < 60 Degree of Tortuosity
Device Deployment:
Tortuosity and Vessel Size are issues for device deployment. The general rules are that you have
problems if:
• Iliac vessels have an angulation > 90 degrees (especially if heavily calcified)
• Iliac artery diameters< 7 mm (may need a cut down and the placement of a temporary conduit).
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Absolute Contraindication to Infrarenal EVAR:
• Landing sites that won't allow for aneurysm exclusion
• Covering a critical artery (IMA in the setting of known SMA and Celiac occlusion,
Accessory renals that are feeding a horseshoe kidney, dominant lumbar arteries feeding the
cord).
Dealing with the Renals.
There are several anatomy vocab words that are worth knowing for aneurysms near the renals.
• "Para-Renal" - which is an umbrella term for aneurysms near the renals
• "Juxta-Renal" -Aneurysm that has a "short neck" (proximal landing zone < l cm) or one
that encroaches on the renals.
• "Supra-Renal" -Aneurysm that involves the renals and extends into the mesenterics.
• "Crawford Type 4 Thoracoabdominal Aortic Aneurysm" -Aneurysm that extends from the
12th intercostal space to the iliac bifurcation with involvement of the origins of the renal,
superior mesenteric, and celiac arteries.
Treating these types of aneurysms requires all kinds of fancy stuff; snorkels, chimney
technique, etc ... All is beyond the scope of the exam. Just know that it can be done, but it's
not easy.
Complications:
Adamkiewicz
The most feared/dreaded (testable)
complication of an aortic stent graft is
Celiac
paraplegia secondary to cord
ischemia. You see this most
commonly when there is extensive SMA
coverage of the aorta (specifically T9-
T l2 Adamkiewicz territory), or a Renals
previous AAA repair. "Beware of the
hair pinned turn" - famously refers to
the morphology of Adamkiewicz on IMA••·
ang10gram.
Symptoms of possible / developing paraplegia post
procedure. Next Step= CSP drainage.
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AAA pre/ post Endograft
After an aneurysm has been treated with an endograft, things can still go south. There are 5
described types of endoleaks that lend themselves easily to multiple choice questions.
• Type 1: Leak at the top (A) or the bottom (B) of the graft. They are typically high
pressure and require intervention (or the sac will keep growing).
• Type 2: Filling of the sac via a feeder artery. This is the MOST COMMON type,
and is usually seen after repair of an abdominal aneurysm. The most likely culprits
are the IMA or a Lumbar artery. The majority spontaneously resolve, but some may
require treatment. Typically, you follow the sac size and if it grows you treat it.
• Type 3: This is a defect/fracture in the graft. It is usually the result of pieces not
overlapping.
• Type 4: This is from porosity of the graft. ("4 is.from the Pore"). It's of historic
significance, and doesn't happen with modern grafts.
• Type 5: This is endotension. It's not a true leak and it may be due to pulsation of the
graft wall. Some people don't believe in these, but I've seen them. They are real.
Type 1
Treatment: The endoleaks that must be emergently treated are the high flow ones - Type 1
and Type 3. Most IR guys I vascular surgeons (real doctors) will watch a Type 2 for at least a
year (as long as it's not enlarging). Most Type 4s will resolve within 48 hours of device
implantation.
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SECTION 5:
EMBOLIZATION
There's a bunch of reasons you might want to do this. The big ones are probably stopping a
bleed and killing a tumor.
Which agent do you want? Unfortunately just like picking a catheter these types of
questions tend to fall into the mind reading category.
In general you are going to choose the agent based on the desired outcome, and the need to
minimize risk. The most classic thinking goes something like this:
Size of the Vessel I Wish this Destruction to be Kill the Mother Fucker Examples/
I Wish to Destroy: Temporary or Permanent: (or just give him Sample
nightmares): Indications:
_,
__.._..V' Permanent -----------� ►� Coils (Lung AVM)
Big -
--�� Gelfoam Pledget
♦ llia... Temporary ---------
_,.
..,.,,-""'1111111--.J
JIii (Trauma)
--c Jlllllll!l'Jlllllll!l'Jlllllll!l'�:I""
Kill --llllllllllll► Liquid Agent
Permanent 1111111111111
(RCC Ablation)
_....Jf/T
....,.....��._.a_.._
Small � ,,.
- Particles
Wound
►
'-- ._
-....._. Temporary -= - - --------at.. Fibroid Embo)
(
► Micro Sphere
(Chemo)
Another way to think/ groups the agent is the general class. I think this is the most helpful to
talk about them in an introductory sense. After 1 introduce them, we will revisit what to pick
based on a multiple choose vignette.
Mechanical Particulate Liquid Agents
Coils PVA - Particles (permanent) Sclerosants
Vascular Plugs (Amplatzer) Gelfoam (temporary) Non-Sclerosants
Autologous Blood Clot
(temporary)
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Mechanical Agents:
Coils:
These are typically used to permanently occlude a THIS vs THAT:
large vessel. They come in all kinds of different sizes Coils vs Micro-Coils
and shapes. You can deploy them with a "push" via a
coaxial system, or if you don't need exact precision Coils: Deployed via standard
you can "chase" them with a saline bolus. 4-?F catheter
It gets complicated and beyond the scope of the exam Micro: Deployed via Micro
(probably), but there are a variety of strategies for Catheter. If you try and
deploy them through a
keeping these in place. Just know you can pack these
standard cath they can ball up
things behind an Amplatzer, or you can use
inside the thing and clog it.
scaffolding techniques to hook small coils to a large
one
,,,�3 Buzzword "Accurate Deployment"= Detachable Coil
Trivia: Remember never deploy these with a side-hole+ end-hole catheter. You want end
hole only for accurate deployment.
Trivia: Never pack coils directly into an arterial pseudoaneurysm sac - more on this later in
the chapter.
Amplatzer Vascular Plug (AVP)
This is a self expanding wire mesh that is made of Nitinol (thermal memory James Bond
shit). You mount this bomb on the end of a delivery device/wire. When deployed it
shrinks in length and expands in width.
Best Use = High Flow Situations, when you want to kill a single large vessel. If you are
thinking to yourself - I'm gonna need a bunch of coils to take that beast down the answer is
probably an amplatzer plug.
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Particulate Agents:
THIS vs THAT:
These are grouped into: Gelfoam Powder vs
Gelfoam Pledgets/Sheets
• Temporary: Gelfoam, Autologous Blood Clot
Powder causes occlusion at the
• Permanent: PVA Particles capillary level (tissue necrosis)
Best Use = Situations where you want to block Pledgets/Sheets cause occlusion
multiple vessels. Classic examples would be fibroids at the arteriole or larger level
and malignant tumors. (tissue infarct is uncommon)
You are Doing it Wrong I Avoiding Re,fiux = An easy way to ask this would simply be "When do
you stop deploying the agent?"
The classic teaching is to stop embolization when the flow becomes "to and fro." If you
continue to pile the particulate agent in until you get total occlusion you risk refluxing the agent
into a place you don't want it to go.
THIS vs THAT: Coils vs PVA Particles
In many cases if you can use coils, you can also use appropriately sized particles.
Size is one way to pick. Coils are good for medium to small arteries. PVA is good for
multiple small arteries or capillaries.
Smaller particles(less than 300 microns) are going to risk tissue necrosis in many cases -
so if you want to preserve the tissue, that's probably the wrong answer.
Another tip for picking between the two is the need for repeat Access. The classic example
is the bronchial artery embolization. These things tend to re-bleed. So you should NEVER
ever use coils(this will block you from re-accessing).
Bronchial artery embolization =Particles(> 325 micrometers).
Next Step?
Q: What do you do after placement of an occlusion balloon in the setting of particle
embolization ?
A: Test injection to confirm adequate occlusion.
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Liquid Agents:
These are grouped into:
• Sclerosants: Absolute Alcohol (the one that hurts) and Sodium Dodecyl Sulfate (SDS)
• Non-Sclerosants: Onyx (Ethylene-Vinyl Alcohol Copolymer) , Ethiodol
Sclerosants:
As would be expected, the sclerosant agents work by producing near immediate thrombosis /
irreversible endothelial destruction. As a result, non-targeted embolization can be fairly
devastating. There are three main strategies for not causing a major fuck up (i.e. burning a
hole in the dude's stomach, infarcting his bowel, etc... ).
(1) Knowing the anatomy really well through careful mapping
(2) Frequent intermittent angiograms during the embolization procedure
(3) Use of Balloon Occlusion to protect non-target sites.
Next Step?
Q: What do you do prior to deflating the occlusion balloon?
A: Aggressively aspirate (with a 60 cc syringe) to make sure all the poison is out of there.
Non-Sclerosants:
Onyx: Typically used for neuro procedures, hypervascular spine tumors, shit like that.
It drys slowly (outside in) and allows for a slower, more controlled delivery.
Ethiodol: This is an oil that blocks vessels at the arteriole level (same as the really
small PVA particles). For some reason, hepatomas love this stuff, and it will
preferentially flow to the hepatoma. It is also unique in that it is radio-opaque, which
helps decrease non-targeted embolization and lets you track tumor size on follow up.
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Single Best Answer Classic Scenario
• Autologous Blood Clot= Post-Traumatic High-Flow Priapism(or Priapism induced by the female
Brazilian olympic volleyball team)
• Varicocele(Spennatic Vein)= Coils
• Uterine Fibroid embolization(Bilateral Uterine Artery)= PVA or microspheres 500-1000 µm
• Generic Trauma= Gel Foam in many cases.
• Diffuse Splenic Trauma(Proximal embolization) = Amplatzer plug in the splenic artery proximal
to the short gastric arteries. **Discussed in detail later in the chapter.
• Pulmonary AVM = Coils
• Hemoptysis (Bronchial artery embolization) = PVA Particles(> 325 µm).
• Hyper-vascular Spinal Tumor= Onyx
• Total Renal Embolization = Absolute ethanol
• Partial or Selective Renal Embolization= Glue(bucrylate-ethiodized oil)
• Segmental Renal Artery Aneurysm= Coils
• Main Renal Artery Aneurysm= Covered Stent(or coils after bare metal stent)
• Peripartum hemorrhage = Gel Foam
• Upper GI Bleed= Endoscopy First(if that fail then in most cases coils)
• Lower GI Bleed= Usually Microcoils
LARGE Vessel - small Vessel Post Embolization Syndrome:
Permanent Permanent
Pain, nausea, vomiting, and low grade fever - is
Particles
Coils basically an expected finding. You don't need to
Liquid Sclerosants order blood cultures - without other factors to
Amplatz Occluder make you consider infection. There is a rule of
Thrombin 3 days - it starts within the first 3 days, and goes
away within 3 days of starting.
LARGE Vessel - Ethiodol
Temporary
The vignette is most classic for a large fibroid
small Vessel - embolization, but it's actually common after a
Temporary solid organ (e.g. liver) - the tumor just needs to
Gelfoam Pledget /
Sheet be big. Some texts suggest prophylactic use of
Microspheres anti-pyrexial and antiemetic meds prior to the
Autologous Clot procedure.
Gelfoam Powder
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SECTION 6:
THE ACUTE LIMB
CVR-.5E OF THE SACONATOR-.
"Threatened Limb" - Acute limb ischemia can be secondary to thrombotic or embolic events.
Frequent sites for emboli to lodge are the common femoral bifurcation and the popliteal
trifurcation. You can also get more distal emboli resulting in the so called blue toe syndrome.
As crazy as this may sound to a Radiologist, physical exam is actually used to separate patients
into 3 categories: viable, threatened, or irreversible. This chart (or something similar) is how
most people triage.
Capillary Muscle Sensory Arterial Venous
Category
Return Paralysis Loss Doppler Doppler
Not
1 - Viable Intact None None + +
Threatened
2a -Threatened Salvageable Intact/Slow None Partial +
Salvageable
Slow/
2b - Threatened if immediate Partial Partial +
Absent
intervention
NOT
3 - Irreversible Salvageable Absent Complete Complete
*Amputation
Know who you can and can 't treat
"Critical Limb Ischemia" -This is described as rest
pain for two weeks (or ulceration, or gangrene). ACR Appropriate:
Embolism Above/ Below
General Idea on Treatment: An important point to the Common Femoral
realize is that lysis of a clot only re-establishes the Artery
baseline (which was likely bad to start with). So
after you do lysis, consider additional therapy - Isolated suprainguinal
(angioplasty, surgery, stcnting, etc ... ). lf there is embolism probably should be
combined inflow and outflow disease, you should removed surgically.
treat the inflow first (they just do better). - Fragmented distal emboli
should have endovascular
Surgery vs Thrombolysis: lf it has been occluded
thrombolytic therapy
for less than 14 days, thrombolysis is superior, if
more than 14 days, (surgery is superior).
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Ankle - Brachial Index (ABI)
The idea behind the ABI is that you can compare the blood pressure in the upper arm, to that of
the ankle and infer a degree of stenosis in the peripheral arteries based on that ratio. In a normal
person, ratios are usually slightly greater than 1. In patients with occlusive disease, they will be
less than that - with a lower number correlating roughly with the extent of disease.
ABI
1.0 Normal No Symptoms
0.75-0.95 Mild Mild Claudication
0.5-0.75 Moderate Claudication
0.3-0.5 Moderate - Severe Severe Claudication
< 0.3 Severe or "Critical" Rest Pain
How they do it: You take blood pressures in both arms, and both ankles. You only use one of
the arm measurements (the higher one). For the actual ratios, opinions vary on this - most
people do it by dividing the higher of either the dorsalis pedis or posterior tibial systolic pressure
(at the ankle) by the higher of either the right or left ann systolic pressure.
False Numbers? Arterial calcifications (common in diabetics with calcific medial sclerosis)
make compression difficult and can lead to a false elevation of the ABI. This is when you
will see ratios around 1.3 - those are bullshit, means the exam is non-diagnostic.
Toe Pressures: As above, diabetics will have noncompressible vessels - which makes ABis
worthless. What you can do is look at the toe pressure. The reason this works is because the
digital arteries are not as affected by this disease process. A normal systolic toe pressure is
greater than 50 mm Hg, and the ratio (toe-brachia! index) should be more than 0.6. The testable
trivia is that if the toe pressures are less than 30 mm ulcers are less likely to heal.
Segmental Limb Pressures: A modification to the standard ABI involves pressures at the thigh,
calf, and ankle - if there is a pressure drop of more than 20-30 you can infer that this is the level
of disease. This allows you to sorta sorta sorta guess where the level of disease is.
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Spectral Waveform Analysis:
The normal pulsatile wave is the result of the
pumping action of the left ventricle
transmitted to the aortic root and then to the
foot. As the LV contracts you have a jet of
blood that dynamically expands the aortic
root. As the bolus of blood travels towards
the feet the vessels will continue to expand
along the path - like a cartoon snake that has
eaten a mouse ( or your neighbors cat). The
wave falls as the cardiac cycle enters diastole.
There is a secondary event which is the rebound off Normal
the high resistance tibial vascular tree. This is why Worsening Disease
the normal wave has an up-down-up look to it -
"triphasic" they call it. This bounce back or
rebound effect demonstrates normal arterial
compliance. As the vessel hardens you lose this.
With progressive disease there is less and less
compliance to the point where the primary wave
Tri-Phasic Bi-Phasic Mono-Phasic
barely even stretches the vessel.
Ulcer Location Trivia (dinosaur IR guys love this - it really gets their dicks hard):
• Medial Ankle = Venous Stasis
• Dorsum of Foot = Ischemic or Infected ulcer
• Plantar (Sole) Surface of Foot = Neurotrophic Ulcer
Who are Rutherford and Fontaine? These are "useful" categories and classifications of
signs and symptoms of peripheral arterial disease.
False Numbers? Arterial calcifications (common in diabetics) make compression difficult
and can lead to a false elevation of the ABI.
Post-Operative Bypass Vocabulary:
• Primary Patency - Uninterrupted patency of the graft with no procedure done on the
graft itself (repair of distal vessels, or vessels at either anastomosis does not count as loss
of primary patency).
• Assisted Primary Patency - Patency is never lost, but is maintained by prophylactic
interventions (stricture angioplasty etc.. ).
• Secondary Patency - Graft patency is lost, but then restored with intervention
(thrombectomy, thrombolysis, etc.. ).
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" Where to Access ? "
One simple way to ask a threatened leg treatment question is to ask for the best route of
access per lesion. Again, like many IR questions, this falls into the "depends on who you
ask" , and/or "read my mind" category. If forced to choose, this is how I would guess:
lesion Access
First Choice - Ipsilateral CFA. If that is down also
Iliac (which it often is), J'd pick the contralateral CFA
CFA Contralateral CFA
SFA Ipsilateral CFA
Fem-Pop Graft Ipsilateral CFA
First Choice - Direct Stick.
Fem-Fem Cross-Over Second choice-inflow CFA
If you are presented with other scenarios, the rule most people use is "shortest, most direct
approach."
When would you use the contralateral CFA ? There are two general situations:
1. The Ipsilateral CFA is occluded.
2. The patient is very very fat. Even fatter than your normal acute leg patient. These are
the guys/gals who got the milkshake (instead of the diet coke) with the baconator. As a
point of gamesmanship, if the question header specifically mentions that the patient is
obese they are likely leading you towards contralateral access.
Gamesmanship: Watch out for "retrograde" vs "antegrade" access terminology in
the distractors. The nomenclature for a downward (towards the toe) access is
"antegrade." The terminology is based on the directions of the arterial flow.
•Antegrade access = towards the toes.
• Retrograde access = towards the heart.
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General Procedural Trivia / Possible "Next Steps"
There are a whole bunch of ways to do this. In the most generic terms, you jam the catheter into the
proximal clot and infuse TPA directly into the mother fucker. Every 6-8 hours you check to sec if you
arc making progress. People call that "check angiography."
What ffyou can't cross the clot with a wire? If they spell that out in the vignette, they arc trying to tell
you that this clot is organized and probably won't clear with thrombolysis.
What ffthere is no clearing of the clot during a "check angiogram"? If they specifically state this,
they are describing "lytic stagnation," which for most reasonable people is an indication to stop the
procedure.
The patient develops "confusion"? Neuro symptoms in a patient getting TPA should make you think
head bleed. Next step would be non-con CT head.
The patient develops "tachycardia and hypotension" ? This in the setting of TPA means the patient is
bleeding out. Next step would be (I) go to the bedside and look at the site. Assuming he/she isn't
floating in a lake of their own blood (2) CT abdomen/pelvis and probably stopping the TPA.
End Point ? Most people will continue treating till the clot clears. Although continuing past 48 hours
is typically bad form.
Venous Treatment
Varicose Vein Treatment: Just know that "tumescent anesthesia" (lots of diluted subcutaneous
lidocaine) is provided for ablation of veins. Veins arc ablated using an cndoluminal heat source. A
contraindication to catheter-based vein ablation is DVT (they need those superficial veins).
DVT: The primary complications of DVT are acute PE and chronic post thrombotic syndrome (PTS).
There are several clinical predictive models to keep everyone who comes in the ER from getting a CTPA
"Wells Score" is probably the most famous. Recently described is this "11irombus Density Ratio" as a
superior predictor of PE in patients with known DVT on CTV. The density of thrombus on CTV has been
shown to be higher in patients with both DVT and PE relative to just DVT. Thrombus Density Ratio of
46.5 (thrombus HU / normal vein HU)= probable PE.
Phlegmasia alba (painful white leg) and Phlegmasia cerulea dolens (painful blue leg) - archaic
physical diagnosis terms that are high yield for the exam of the future. Phlegmasia alba= massive DVT,
without ischemia and preserved collateral veins. Phlegmasia cerulea dolens= massive DVT, complete
thrombosis of the deep venous system, including the collateral circulation. These are described as
extreme sequella of May-Thurner - but can occur in any situation where you get a punch of DVT
(pregnancy, malignancy, trauma, clogged IVC filter, etc ..)
Post T hrombotic Syndrome (PTS): This is basically pain and stuff (venous ulcers) after a DVT. Risk
factors include being old (>65), a more proximal DVT, recurrent or persistent DVT, and being fat.
PTS is usually diagnosed between 6 months and 2 years after DVT. VEINES-QOL is the scoring
system used to diagnose and classify severity of PTS. Catheter-directed intrathrombus lysis of
iliofcmoral DVT is done to prevent post thrombotic syndrome. This is not needed as much with
femoropoplitcal DVT as it will rccanalize more frequently and have less severe post thrombotic
syndrome.
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SECTION 7:
� . .
FILTERS
An IVC filter is used in the following situations:
• Proven PE while on adequate anticoagulation
• Contraindication to anticoagulation with clot in the femoral or iliac veins
• Needing to come off anticoagulation - complications. There are a few additional
indications that are less firm (basically, we think he/she might get a DVT and we can't anti
coagulate).
Vocab: Why Not Leave Them In?
• Permanent Filters: Do Not Come Out Depending on who bought
you lunch (gave you a free
• Retrievable Filters: Can Come Out, But Do Not Have To
pen), thrombosis rates vmy.
• Temporary Filter: Come out, and have a component sticking
outside the body to aide in retrieval In general (for the purpose
of multiple choice) about
Position (before submission): 10% of the permanent
filters thrombose within 5
years.
The device is usually placed infrarenal with a few exceptions
(see below chart).
Why isn't it alwaysjust positioned suprarenal? A supra-renal filter has a theoretic increased
risk of renal vein thrombosis. There is zero evidence behind this - like most things in
medicine.
Indication Filter Placement Rationale
Pregnancy Supra-renal To avoid compression
Clot in the Renals or
Supra-renal Get above the clot
Gonadals
Either bilateral iliac, or
Duplicated IVCs supra-renal (above the Gotta block them both
bifurcation)
Risk of clot by passing filter
Circumaortic Left Renal Below the lowest renal
via the renals
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MEGA-Cava: If the IVC is less than 28 mm, then any filter can be placed. If it's bigger
than that, you might need to place a bird's nest type of filter which can be used up to 40 mm.
You can also just place bilateral iliac filters.
Random Trivia:
• A "Gunther Tulip" has a superior end hook for retrieval
• A "Simon-Nitinol" has a low profile (7F) and can be placed in smaller veins (like an arm
vein).
• All filters are MRI compatible
Prior to placing the Filter:
You need to do an angiographic run. Where I trained, the classic pimping question for
residents on service was to "name the 4 reasons you do an angiogram prior to filter
placement!" The only answer that would not result in "additional training" (more weekend
PICC workups) was:
1. Confirm patency of the IVC
2. Measure the size of the IVC
3. Confirm that you are dealing with 1 IVC
4. Document the position of the renal veins
Comp I ications/Risks:
• Ma/position: The tip of the filter should be positioned at the level of the renal vein. If it's
not, honestly it's not a big deal
• Migration: The filter can migrate to another part of the IVC, the heart, or even the
pulmonary outflow tract. If it goes to the heart, you need surgery. If it's just superior, you
need to snare it out.
• Thrombosis: Although the incidence of PE is decreased, the risk of DVT is increased.
Caval thrombosis is also increased, and you should know that clot in the filter is a
contraindication to removal (you need to lyse it, before you remove it).
" IVC Per:foration: A strut going through the caval wall is common and doesn't mean
anything. However, aortic penetration, ureteral perforation, duodenal perforation, or
lumbar vessel laceration can occur (rarely) from a strut hanging out of the cava- this is a
bigger problem.
• Device Infection: A relative contraindication to IVC filter placement is bacteremia.
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Positioning the Filter:
Renals on an IVC Gram: There are two ways
to show the renals on an IVC Gram. There is
the nice way where they opacify normally and
it's obvious, and there is the sneaky way where
you see the "steaming effect" of unopacified
blood allowing you to infer the position.
Obviously the sneaky way is more likely to
show up on the exam.
The Tip: For standard anatomy, the standard answer for a cone shaped filter is to put the apex
at the level of the renals. Some people think the high flow in this location helps any clot that
might get stuck in the filter dissolve.
What if"there is clot in the IVC? The filter should be positioned above the most cranial
extension of the clot. As mentioned in my glorious IVC Filter position chart, if the clot extends
beyond the renals you need a suprarenal filter.
What ifyou fuck up the deployment (severe tilt, legs won't open, etc ...)? If it's retrievable,
you may be able to snare it and restart. If it's permanent you are kind of hosed. Some people
will try and stick a second filter above the retarded one.
Filter Removal:
The longer these things stay in, the more likely they will thrombose.. Prior to removal you
should perform an angiogram of the IVC. The main reason to do this is to evaluate for clot.
• More than 1 cm3 of clot = Filter Stays In
• Less than 1 cm3 of clot = Filter Comes Out
You snare the.filter but when you pull on it you meet resistance ? In the real world, people
will yank that mother fucker out of there. The IVC is the Rodney Dangerfield of vessels - no
respect. For multiple choice? Stop and assume that it can't be retrieved.
Angiogram should also be done after removal of the filter to make sure you didn't rip a hole in
the IVC. !{you did rip a hole in it- Next Step -Angioplasty balloon with low pressure
insufflation to to create tamponade. If that doesn't work, most people would try a covered stent
graft. If you created a wall b�iuryldissection ? Again - answers will vary, but the classic
answer is systemic anticoagulation.
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SECTION 8:
DIALYSIS
- THE FUCKING FISTULOGRAM -
Generally speaking there are two types of "permanent" access options for dialysis;
(1) the arterio-venous fistula and (2) the arterio-venous graft.
AV Fistula - This is a subcutaneous anastomosis between an artery and adjacent native vein
(for example the radial artery to the cephalic vein). All things equal, the prefe1Ted access
(over the graft).
AV Graft- This is also a subcutaneous anastomosis between an artery and adjacent native
vem. Except this time the distance between the vessels is bridged with a synthetic tube graft.
Vein----+,
+- Artery
Vein
Graft�
Arteriovenous Fistula Arteriovenous Graft
What are the pros and cons of each types?
Pros of AV Graft: Cons of AV Graft:
- Ready for use in 2 weeks -Less overall longevity
- Easier to declot (clot is usually confined -Promotes hyperplasia of the venous intima
to the synthetic graft) at or downstream from the graft vein
anastomosis, resulting in stenosis and
eventual obstruction
Pros of AV Fistula:
-More infections (foreign graft material)
- Lasts Longer & More Durable
- Much less prone to development of
Cons of AV Fistula:
venous neointimal hyperplasia at or
downstream from the artery-vein -Needs 3-4 Months to "Mature" (vein to
anastomosis. enlarge enough for dialysis)
- Fewer infections
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Why do grafts(fistulas need treatment (politics and greed) ? The primary reason is "slow
flows." It's important to understand that nephrologists get paid per session of dialysis. If
they can do a session in 1 hour or 4 hours they make the same amount of money. Therefore
they want them running fast. So, really "slow-flow" is referring to slow cash flow in the
direction of the nephrologist's pocket.
For the purpose o.fmultiple choice I'd go with:
< 600 cc/min for graft = diagnostic fistulogram
< 500 cc/min for fistula = diagnostic fistulogram
Having said that, you may find different numbers different places - the whole issue is
controversial based on the real motivation people have for treating these. Some texts say a
fistula can maintain patency with rates as low as 80 cc/min, and grafts can maintain patency
with rates as low as 450 cc/min. Also remember medicare won't pay for two treatments
within 90 days, so make sure you treat on day 91.
Why do grafts(fistulas need treatment (actual pathophysiology)? Its a violation of nature to
have a AF Fistula / Graft pulsating in your arm. Your body won't tolerate it forever.
Neointimal hyperpasia develops causing an ever-worsening stenosis. If they don't get
treated, they will eventually thrombose. All fistulas/grafts must die.
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''Working it Up"
The only thing worse then actually doing a fistulogram is having to talk with and examine the
patient prior to the procedure. Nearly all the IR texts and any program worth its snuff will
"work them up" starting with physical exam.
Patient arrives in the IR department for "slow flows." Next Step = Physical Exam
This is the buzzword orientated algorithm that I would suggest for dealing with physical
exam/ history related fistula/graft questions:
"Arm Swelling"
LOOK "Chest Wall Collaterals" Central Venous Stenosis
"Breast Swelling"
"Discolored Hand"
Dialysis-Associated Steal
LOOK "Pale Colored Hand"
Syndrome (DASS)
"Pallor of the Hand"
"High-Pitched Bruit"
LISTEN "Bruit in Systole Only" Localized Stenosis
"Discontinuous Bruit"
"Water Hammer Pulse" Pre Stenosis
FEEL
"Diminished Pulse" Post Stenosis
What is normal? A no1111al graft has an easily compressible pulse, a low-pitched bruit that is
present in both �ystole + diastole, and a thrill that is palpable with compression only at the
arterial anastomosis.
Localizing a Stenosis - Classic Example - Straight Forearm Graft:
Stenosis is at the Venous Anastomosis
Graft
Forceful/ Pulse
High Pitch Bruit I Strong Thrill
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GRAFTS:
Where is the problem (usually) in grafts? The most common site of obstruction is venous
outflow (usually at or just distal to the graft-to-vein anastomosis). This is usually secondary
to intimal hyperplasia.
What about the normal thrill and bruit in a graft ? There should be a thrill at the arterial
anastomosis, and a low pitched bruit should be audible throughout the graft.
What if the bruit is high pitched? High Pitch= Stenosis, Low Pitch= Normal
What are you thinking ifI tell you the dude has a swollen arm and chest ? This is classic
for central venous stenosis.
FISTULAS:
Where is the problem (usually) in fistulas? It's more variable - you are less likely to be
asked this. If you are forced - I'd say venous outflow stenosis - typically junta-anastomotic
or runoff vein (AV anastomosis stenosis is uncommon).
If you.fix a stenotic area - they are good to go right ? Nope - they reoccur about 75% of the
time within 6 months.
What about the "thrill"in the fistula, is this a helpful finding? Yes - there should be a
continuous thrill at the anastomosis. If it is present only with systole then you are dealing
with a stenosis. Also, if you can localize a thrill somewhere else in the venous outflow - that
is probably a stenosis.
What if the.fistula is very "pulsatile"? This indicates a more central stenosis - the fistula
should be only slightly pulsatile.
Should there be a bruit ? A low pitched bruit in the outflow vein is an expected finding.
"Steal Syndrome"-The classic story is "cold painful fingers" during dialysis, relieved by
manual compression of the fistula. Too much blood going to the fistula leaves the hand
ischemic. The issue is usually a stenosis in the native artery distal to the fistula. Fixing this
is typically surgical (DRIL = Distal Revascularization and Interval Ligation of Extremity, or
Flow Reduction Banding).
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ACCESS and TREATMENT:
Contraindications ? Infection is the only absolute one. If you fuck with an infected fistula or graft
the patient could get cndocarditis. If you don't fuck with it, the patient will probably still get
cndocarditis but infectious disease will have to blame it on someone else at the QA meeting.
What ?fit's "Fresh"? A "relative contraindication" is a new graft or fistula. "New" to most people
means less than 30 days. Significant stenosis prior to 30 days strongly suggests a surgical fuck up
("technical problem" they call it). Not to mention that a new dilating anastomosis is high risk for
rupture. Those grafts arc doomed to never reach long-term patency.
Access less than 30 days old with stenosis. Next Step = Send them back to the surgeon.
What about "long segments"? You will read some places that stenotic segments longer than 7 cm
respond poorly to treatment. Some people even consider this a "relative contraindication." If the
question writer actually spells out the length of the stenosis greater than 7 cm he/she probably wants
you to say send them back to surgery. In reality there are plenty of stubborn IR guys that will try and
treat multiple long lesions because there is no better way than to prove one's manhood.
What about a contrast allergy? You can use CO2 for runs.
What direction do you access the graft ? Access is typically directed towards the venous
anastomosis - unless you arc thinking arterial is the problem (which is much less common).
Remember the lingo "antegrade" and "retrograde" refers to the direction of blood flow. Antegrade is
the typical route for venous problems, and retrograde is the typical route for arterial inflow issues.
How do you typically look at the arterial anastomosis ? The move most places teach is to obstruct
the venous outflow (with a clamp, blood pressure cuff, angioplasty balloon, finger - or whatever)
which allows the contrast to reflux into the artery.
What are the moves for angioplasty of a narrow spot ? Give them heparin (3000-5000 units).
Exchange your catheter for a 5 or 6 F sheath over a standard 0.035-inch guidewire. Dilate the
narrow spot with a 6-8 mm balloon with multiple prolonged inflations. Remember to never take that
balloon off the wire when you are doing diagnostic runs - as you might need to rapidly put it back if
you caused a tear.
When do you place a stent ? There are two main reasons (1) you are getting bad elastic recoil, or
(2) you have recurrent stenosis within 3 months of angioplasty.
Does Nitro have a role? You can use a vasodilator (like nitroglycerin) to distinguish between spasm
and stenosis. The spasm should improve. The stenosis will be fixed.
What is considered a Succes,\ful Treatment? (1) Improved Symptoms (arm swelling better, etc.. ),
or (2) less than 30% residual stenosis.
What about Aneurysms ? Small ones get monitored for size increase, but the classic teaching is that
these are managed surgically.
General Vascular Access Trivia: Remember that PICC lines should not be put in dialysis (or
possible dialysis - CKD 4 or 5) patients because they might need that arm for a fistula.
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-
·•"lllf �
SECTION 9:
TIPS & BRTO
TIPS (Transjugular lntrahepatic Portosystemic Shunt) -
What is this portal hypertension? The portal vein gives you 70-80% of your blood flow to
the liver. The pressure difference between the portal vein and IVC("PSG", portosystemic
gradient) is normally 3-6 mm Hg. Portal HTN is defined as pressure in the portal vein >
10mm Hg or PSG > 5 mm Hg. The most common cause is EtOH (in N01ih America).
What does portal hypertension look like? On ultrasound we are talking about an enlarged
portal vein(> 1.3-1.5 cm), and enlarged splenic vein(> 1.2 cm), big spleen, ascites,
portosystemic collaterals (umbilical vein patency), and reversed flow in the portal vein.
Who gets a TIPS ? Accepted indications include:
• Variceal hemorrhage that is refractory to endoscopic treatment
• Refractory ascites.
• Budd Chiari (thrombosis of the hepatic veins) ** most authors will include this
Preprocedural steps/or TIPS? You need two things. (1) An ECHO to evaluate for heart
failure(right or left). (2) Cross sectional imaging to confirm patency of the portal vein.
How is a TIPS done? The real answer is do an IR fellowship.
First thing you do is measure the right heart pressure. If it is elevated(10-12 mmHg) you stop
(absolute contraindication). A normal right heart pressure is around 5 mmHg.
If it is normal, you proceed with the procedure.
Access the jugular vein on the right, go down the
IVC to the hepatic veins, opacify the veins, do a
wedge pressure(don't blow the capsule off), use
CO2 to opacify the portal system. Then stick
"Crotch to Crotch" from the hepatic veins to the
portal vein(usually right to right). Then put a
covered stent in and balloon it up.
Lastly check pressures and make you sure you
didn't over do it(usually want a gradient around
9-12 --- "less than 12").
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Which direction do you
turn the catheter when
you are movingfrom the
right hepatic vein, to the
right portal vein?
You want to turn
anterior.
Keeping Score
While you are busy pretending you are a surgeon, why not pretend that you are a
medicine doctor also? For the purpose of multiple choice, anything that resembles "Real
Doctor" work is always high yield. "Score Calculation" is the poster child for the kind
of fringe knowledge board examiners have traditionally loved to ask (this was definitely
true for the old oral boards). The two highest yield scores are the MELD and the Childs
Pugh.
What is this "MELD" Score ? This was initially MELD Child Pugh
developed to predict three month mortality in TIPS
patients. Now it's used to help prioritize which
drunk driving, Hep C infected, Alcoholic should Bilirubin Bilirubin
get a transplant first. MELD is based on liver and ------ ---
renal function - calculated from bilirubin, INR, INR PT
creatinine. MELD scores greater than 18 are at
higher risk of early death after an elective TIPS.
creatinine Albumin
What about this "Childs-Pugh" Score? This is
the "old one," which was previously used to Ascities, Hepatic
determine transplant urgency prior to the MELD. ---
Encephalopathy
It works for TIPS outcomes, too, but is "less
accurate" than a MELD. This score assesses the
f-·
severity of liver disease by looking at the bilirubin, Greater than 18 = Class B and C are
albumin, PT, ascites, and hepatic encephalopathy. High Risk Death High Risk
The trivia to know is that class B & C are risk
factors of variceal hemorrhage.
Trivia = "Simplest prognostic measure"= Serum Bilirubin. > 3 mg/dL is associated with
an increase in 30-day mortality after TIPS.
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What are the contraindications for TIPS? Some sources will say there is no "absolute"
contraindication. Others(most) will say severe heart failure(right or left), - but especially
right. That the whole reason you check the right heart pressure at the beginning of the
procedure. If you are forced to pick a contraindication and right heart failure is not an
option, I would choose biliary sepsis, or isolated gastric varices with splenic vein
occlusion. Accepted (by most) "relative" contraindications include cavernous
transformation of the portal vein, and severe hepatic encephalopathy.
The main acute post procedural complications of TIPS include: Cardiac decompensation
(elevated right heart filling pressures), accelerated liver failure, and worsening hepatic
encephalopathy.
Evaluation of a "Normal TIPS"
Because the stent decompresses the portal system, you want to see flow directed into the
stent. Flow should reverse in the right and left portal vein and flow directly into the stent.
Flow in the stent is typically 90-190 cm/s.
Stenosis I Malfunction:
• Elevated maximum velocities(> 200 cm/s) across a narrowed segment.
• Low portal vein velocity(< 30 cm/s is abnormal).
A temporal increase(or decrease) in shunt velocity by more than 50 crn/s is also
considered direct evidence.
• "Flow Conversion" with a change of flow in a portal vein branch from towards the
stent to away from the stent.
• An indirect sign of malfunction is new or increased ascites.
TIPS Follow-Up
These things tend to fail (50% primary patent within 1 year for a bare metal stent), so they
need tight follow up.
Worsening Ascites, Bleeding, Etc(things that make you think the TIPS isn't working)
Next Step = Venogram with pressures
PSG > 12 mrnHg. Next Step= Treat the stenosis (angioplasty+ balloon)
Trivia: The stenosis usually occurs in the hepatic vein, or within the TIPS tract.
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Addressing Hepatic Encephalopathy- Dropping the gradient too low increases the risk of
HE. If the TIPS is too open you may need to tighten it down with another stent.
What is an alternative to TIPS.for treatment of refractory ascites? There is a rarely
indicated thing called a "peritoneovenous shunt." This stupid thing has a high rate of
infection and thrombosis, and can even lead to DIC. It's designed to allow drainage of the
ascites through a tunneled line all the way up to the systemic circulation (jugular).
BRTO (Balloon-Occluded Retrograde Transverse Obliteration).
TIPS and BRTO are brother and sister procedures. Where the TIPS takes blood and steers it
away from the liver (to try and help the side effects of portal hypertension), the BRTO does
the opposite - driving more blood into the liver (to try and help with the side effects of extra
hepatic shunting). The inverted indications and consequences are highly testable:
TIPS BRTO
Treat Esophageal Varices Treat Gastric Varices
Place a shunt to divert blood around liver Embolize collaterals to drive blood into liver
Complication is worsening hepatic Complication is worsening esophageal varices
encephalopathy and worsening ascites
Improves esophageal varices and ascites Improves hepatic encephalopathy
"The Moves": The general idea is that you
access the portosystemic gastrorenal shunt
from the left renal via a transjugular or
transfemoral approach. A balloon is used to
occlude the outlet of either the gastrorenal or
gastro-caval shunt. Following balloon
occlusion, a venogram is performed. A
sclerosing agent is used to take the vessels
out. After 30-50 minutes you aspirate the
remaining sclerosing agent and let down the
balloons.
Trivia: The most common side effect of BRTO
is gross hematuria.
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SECTION 10:
HEPATIC 8c BILIARY INTERVENTION
Biliary Duct Anatomy Trivia:
The ductal anatomy mimics the segmental anatomy. The simple version is at the hilum.
There are two main hepatic ducts (right and left) which join to make the common hepatic
duct. The right hepatic duct is made of the horizontal right posterior (segment 6 & 7) and
vertical right anterior (segment 5 & 8). The left duct has a horizontal course and drains
segment 2 and 4.
For whatever reason, IR guys love to grill residents about ductal variants (of which there are
many). There was a dinosaur GI guy where I trained who also obsessed over this stuff.
Apparently, obscure anatomic trivia tickles a psychopathology common to Academic
Radiologists. As a result, I would know the 2 most common variants. The right posterior
segment branch draining into the left hepatic duct is the most common. The second most
common is trifurcation of the intrahepatic radicles.
Right Right
Anterior Anterior
Duct Duct
Left Left
Duct Duct
Left
Duct
Right
Posterior
Duct
Common Hepatic Duct
"Normal" Duct Anatomy (57%) (16%) (12%)
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Biliary Drainage:
The role of PTC (Percutaneous Transhepatic Cholangiogram) and PTBD (Percutaneous
Transhepatic Biliary Drainage) is centered around situations when ERCP and endoscopy
have failed or are not possible (Roux-en-Y).
Things to do before the procedure:
• Check the coags - correct them if necessary (vitamin K, FFP, etc ...).
• Most institutions give prophylactic antibiotics (ascending cholangitis is bad).
Approaches:
There are two approaches: right lateral mid axillary for the right system, or subxyphoid for
the left system. Realistically, diagnostic cholangiogram and PTBD is usually done from
the right. The left is more technically challenging (although better tolerated by the patient
because the tube isn't in-between ribs) and usually there is a hilar stricture that won't
allow the left and right system to communicate.
"The Moves" - Right-Sided Approach
Line up on the patient's right flank / mid axillary line. When I say "Below the 10th
Find the 10th rib. Don't go higher than the 10th rib - Rib," I mean caudal to the 10th
rib, not actually under the rib.
always below (avoiding the pleura can save you a ton
Always puncture at the TOP
of headaches). Prior to jamming the needle in, most EDGE OF A RIB to avoid the
reasonable people put metal forceps (or other metal intercostal artery (which runs
tool) over the target and fluoro to confirm you are over under the rib).
the liver and below the pleural reflection.
Now the fun begins. The basic idea is to pretend the patient is a voodoo doll of the
Attending (or childhood tormentor) that you hate the most. Proceed to blindly and
randomly jam a chiba needle in and inject slowly under fluoro as you pull back (but not all
the way out). Obviously less sticks is better and it's ideal to do in less than 5 (most places
will still consider less than 15 ok). Once you get into a duct the system will opacify. You
then can pick your target (posterior is best for best drainage). You stick again, wire in, and
place the catheter into the duodenum.
A non-dilated system can be very difficult and In the Duct?
there is an old school trick where you stick the • Ducts = Flow Towards the Hilum
gallbladder (on purpose) and retrograde fill the • Vein= Flow Cranially towards the
system. The problem with that is you have to Heart
keep a drain in the gallbladder as well. • Artery= Flow Towards the Periphery
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The Moves" - Left Sided Approach
This time you use a sub-sternal/ subxyphoid approach with ultrasound. Most people aim
for the anterior inferior peripheral ducts. Otherwise the moves are pretty much the same.
Catheter I Stent Choice - Bare Bones of Trivia:
Most stent placement is preceded by a period of biliary decompression with an internal
external drain. Plastic stents are cheaper but have a short patency period. Metal stents will
stay patent longer but can't be removed. Metal stents are not usually used in benign disease
unless the patient has a long life expectancy.
Internal-External drains are the standard for crossing lesions. They have superior stability
to a straight drain or pigtail. They offer the advantage of possible conversion to an internal
only drain (save those bile-salts).
Some testable
trivia is that many
centers will
manually punch
some additional
-· · --·------------------
· · · --· -----·· -----·:::
-
:: : ·: = = Side
Holes
side holes in the
proximal portion of
the tube to make
7
sure that drainage
adequate.
Cancer
The key is to NOT
position any side
holes outside the Do NOT Put the
liver (proximal to Side Holes Here the
liver parenchyma).
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(;' "Next Step" - Testable Scenarios / Trivia:
• There is extensive ascites. Next Step = Drain it prior to doing the PTC.
• There is a small amount of ascites. Next Step = Opinions are like assholes (everyone has
one), so you'll hear different things for this. I think most people would look to make sure
the liver still abuts the peritoneum at the puncture site. If it does, then they will do a right
sided approach. If it doesn't then they will use ultrasound and go substernal on the left.
• Right Approach with no filling of the left ducts. Next Step = Slowly and carefully roll
the patient on their side (right side up). The right ducts are dependent - so this is actually
fairly common. Now obviously if there is a known obstruction you don't need to roll
them. The rolling is to prove it's not a real obstruction.
• You do your contrast run and the patient instantly goes into a full rigor.
Next Step = Look around the room for the person you are going to blame for injecting too
forcefully. "Rigor" is a multiple choice buzzword for cholangitis. Yes ... full on biliary
sepsis can happen instantly with a forceful injection. This is actually pretty easy to do if
the patient has strictures or an obstructive neoplastic process. In those cases you will want
to have your Scapegoat / "Not Me" (tech, med student, resident, fellow, drug rep, 11011-
english-speaking international observer) do the injection. For the purpose of multiple
choice some good next step options would be: aggressive resuscitation, place a drain, and
inform the primary team / ICU that the Scapegoat gave the patient biliary sepsis.
Forceful Injection = ICU Visit for Cholangitis
� Buzzword = "Rigors after Injection"
,,
• You encounter (or expect stones). Next Step = Dilute contrast to 200-250 mg/ml to
avoid obscuring filling defects.
• You can't cross the obstruction with a wire. Next Step = Place a pigtail drain and let the
system cool down for like 48 hours. Try again when there is less edema.
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Cholecystostomy:
This is done when you have a super sick patient you can't take to the OR, but the patient has
a toxic gallbladder. In cases of acalculous cholecystitis (with no other source of sepsis), 60%
of the time cholecystostomy is very helpful. It's a "temporizing measure." You have to give
pre-procedure antibiotics. There are two approaches:
• Transperitoneal - This is preferred by many because it's a direct approach, and avoids
hitting the liver. The major draw back is the wire / catheter often buckles and you lose
access (and spill bile everywhere). This is typically not the first choice. However in
patients with liver disease or coagulopathy it may be preferred (depending on who you
ask). If the question writer specifically states (or infers) that the patient has an increased
risk of bleeding this is probably the right choice. Otherwise, if forced to choose, pick the
Transhepatic route
• Transhepatic - The major plus here is that when
you cross the liver it stabilizes the wire and
minimizes the chance of a bile leak. This is the
route most people choose.
o Trivia = Typically you go through segments 5
and 6 on your way to the gallbladder
o Trivia = This route transverse the "bare area" /
upper one third of the gallbladder
(hypothetically).
Important Trivia:
• Prior to the procedure, make sure the bowel isn't interposed in front of the liver/
gallbladder. If a multiple choice writer wanted to be sneaky he/she could tell you the
patient has "Chilaiditi Syndrome" - which just means that they have bowel in front of
their liver. Some sources will list this as a contraindication to PC.
" Even if the procedure instantly resolves all symptoms, you need to leave the tube in for
2-6 weeks (until the tract matures), otherwise you are going to get a bile leak.
• After that "at least 2 week" period you should perform a cholangiogram to confirm that
the cystic duct is patent before you pull the tube.
• Most places will clamp the tube for 48 hours prior to removal. This helps confirm
satisfactory internal drainage.
Managing Bile Leak - Bile leak is bad as it can lead to massive biliary ascites and chemical
peritonitis. Most people will try and place a tube within the bile ducts to divert bile from the
location of the leak (this usually works).
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General Biopsy Pearls
There are two primary techniques for sampling tissue:
(I) Fine Needle Aspiration - Cytology
(2) Cutting Needle ("Core") - Biopsy
Fine Needle Aspiration:
This is for situations when you only need a few cells. It is typically performed through a
21 or 220 Chiba needle. Vacuum aspiration with a 20 cc syringe is applied as you pass
the needle back and forth through the target.
Trivia: Apply "gentle" suction as you remove the needle. If you suck too hard a tiny
sample could get lost in the syringe. If you forget to apply suction the sample will stay in
the patient.
The needle is small so the risks are small.
Cutting / Core Needle t
oute r sw ie
This is for situations when you need
a larger sample. There are lots of
devices but the most basic
·'-
mechanism involves a needle with
two parts; an outer shaft for cutting,
and an inner stylet.
Trivia: For the purpose of multiple
choice, the target is "cut" where the
outer shaft is advanced.
Trivia: The general rule is pick the shortest length needle that will reach the target.
Trivia: "Automated Systems" fire both the inner and outer components to take the
sample. The key point is that with these systems the sample is taken from tissue 10-20
mm in front of the needle.
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Conventional Liver Biopsy -
You can do targeted approaches
(for a specific lesion) or you This path might
can do non-targeted approaches be ok - if it's thick
enough
(sampling). General pearls
include: trying to cross the
capsule only once, biopsy the
subcapsular masses through an
area of uninvolved liver, and
avoid the diaphragm.
This path might
If given the choice, you want to This direct path into the be ok - if it's thick
biopsy peripheral lesions lesion will "bleed like enough
stink" >2cm
through 2-3 cm of nonnal liver would be
ideal
prior to hitting the target.
This is done to avoid a blood bath.
Next Step: There is ascites = Drain it prior to doing the biopsy
Trivia: Mild shoulder pain(referred pain) is common after liver biopsy.
Trivia: Prolonged Shoulder Pain(> 5 mins) = Possible Bleed "Kehr Sign".
Next Step: Prolonged Shoulder Pain(> 5 mins) = Re-evaluation with ultrasound. Always
look behind the liver(Morrison's pouch) to see if blood is accumulating. Bleeding after
liver biopsy occurs more from biopsy of malignant lesions(compared to diffuse disease).
Contraindications: Uncorrectable coagulopathy, thrombocytopenia(< 50,000), infections in
the right upper quadrant - are contraindications for a conventional biopsy.
Trivia: Biopsy of carcinoid mets is controversial and death by carcinoid crisis has occurred
after biopsy.
Next Step: Massive ascites or severe coagulopathy = Tran�jugular approach
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Transjugular Liver Biopsy
The rationale is that the liver Specific Indications:
capsule is never punctured, so • Severe Coagulopathy
bleeding is less of a risk.
• Massive ascites
Obviously this is a non
targeted biopsy for the • Failure of prior percutaneous liver biopsy
diagnosis of infectious, • Massive obesity ("Fat Even By West Virginia Standards·")
metabolic, and sometimes
neoplastic processes • Patients on mechanical ventilation
(classic example = grading • Need for additive vascular procedures like TIPS
chronic hep C).
Procedural Trivia:
The general technique is to access the hepatic veins via the IVC (via the right jugular vein).
Most people will tell you to biopsy through the right hepatic vein while angling the sheath
anterior. The reason this is done is to get the biggest bite of tissue, and avoid capsular
perforation (which was the entire point of this pain in the ass procedure).
Trivia: Right Sided Jugular Route
is the superior route (better than left
IJ, or femoral)
Trivia: Biopsy via the Right
Hepatic Vein by angling anterior.
Never perform an anterior biopsy
from the middle hepatic vein.
Trivia: This procedure has the
added benefit of allowing you to
measure hepatic venous pressures
which can guide therapy or assess
varix bleeding risk.
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Hepatic / Splenic Trauma -
Embolization is a potential method for dealing
Indications
with significant trauma to the hepatic or 'agreed upon by most:
1
splenic arteries. Opinions on the exact role of
• Continuous hemorrhage (active extrav)
angiography vary between institutions, so
in a patient who is borderline stable
"read my mind" questions are likely. post resuscitation
l think the most likely type of indication • Early ongoing bleeding after a surgical
question might actually be who does NOT go attempt to gain primary hemostasis
to angio? • Rebleeding after successful initial
embolization
The most accepted contraindication in a
bleeding patient is probably a very busted-up • Post traumatic pseudo-aneurysm and
AVFs ( even if they aren't currently
unstable dude who needs to go straight to the
bleeding).
OR for emergent laparotomy.
Olllllllillllllllll!ll!(f:;r.1.,� Tools and Strategy - Hepatic Considerations:
• Gelfoam, pledgets, particles, and/or microcoils are typically used.
• Massive non-selective hepatic artery embolization is usually avoided to reduce the risk of
large volume tissue necrosis.
• What'.\' the main issue with tissue necrosis? Hepatic abscess development (which is fairly
common in a major liver injury anyway).
• Trivia: Coils should NOT be placed in the
,,,-
c~-)
;;;�rgr--D
pseudoaneurysm sac. This can lead to a
late rupture. The strategy is to occlude
l2�
��-�
(�· r - I O --=Q1__]
Distal End First
the distal and proximal parent vessels.
You'll want to perform "completion
angiography" to prove the thing is "Sandwich Technique"to exclude ""'i""::_·_�ML_
__·· _
arterial pseudo aneurysm
occluded prior to catheter removal. Then Pull Back
• Hepatic surface is bleeding from more
than one spot. Next Step= Gelfoam or particles.
• Hepatic Pseudoaneurysrns can be treated at the site of injury (with the sandwich technique)
because they are not end arteries (no collaterals). Plus the liver has a dual blood supply.
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•e••ll!lllllll.llil Tools and Strategy Continued - Spleen Considerations:
• Splenic laceration (without active extravasation) is NOT considered an indication to angio
(by most people). Remember to use your mind reading powers to confirm the question
writer agrees.
• The spleen does not have a dual blood supply, and is considered an "end organ" unlike the
liver. So if you go nuts embolizing it you can infarct the whole fucking thing.
• Focal Splenic Abnormality. Next Step = Selective Embolization treatment
• Multiple Bleeding Sites. Next Step = Use a proximal embolization strategy, and drop an
Amplatzer plug into the splenic artery proximal to the short gastric arteries. The idea is to
maintain perfusion but reduce the pressure to the spleen (slower blood will clot), with the
benefit of preserved collateral supply and less infarction risk.
• Trivia: Even with this proximal embolization strategy the patient usually does not require
vaccination post embolization, as a lot of functional tissue should remain.
Short
Gastric-- ►
Arteries __,.
Proximal
Embolization Site
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HCC Treatment:
ACR Appropriate: Liver
You will read in some sources that transplant is the only way Transplant
to "cure" an HCC. Others will say transplant, resection, or - Transplantation should be
ablation are "curative" if the tumor is small enough. Arterial considered ONLY in patients
embolization (TACE) is typically used in situations where < 65 years of age with limited
tumor burden ( l tumor :S 5
the tumor burden is advanced and the patient cannot undergo cm or up to 3 tumors < 3 cm).
surgery.
Transarterial Chemoembolization (TACE) - Most people will consider this first line for
palliative therapy in advanced cases. The mechanism relies on HCC's preference for arterial
blood. High concentration of chemotherapy within Lipiodol (iodized oil transport agent) is
directly delivered into the hepatic arterial system. The tumor will preferentially take up the oil
resulting in a prolonged targeted chemotherapy. The Lipiodol is usually followed up with
particle embolization, with the goal of slowing down the washout of the agent.
Absolute Contraindication = Decompensated (acute on chronic) Liver failure.
Trivia: Some sources will list portal vein thrombosis as a contraindication (because of the risk
of liver infarct). Others say portal vein thrombosis is fine as long as an adjustment is made to
limit the degree of embolization and you can document sufficient hepatic collateral flow.
Simply read the mind of the question writer to know which camp they are in.
Trivia= TACE in Patients with a biliary stent, prior sphinctertomy, or post Whipple are all
high risk for biliary abscess.
Trivia = "Sterile cholecystitis" or "chemical cholecystitis" are buzzwords that when used in
the setting of TACE should lead you to believe that the agent was injected into the right
hepatic artery prior to the takeoff of the cystic artery (artery to the gallbladder) .
Trivia = TACE will prolong survival better than systemic chemo
Trivia: Unfortunately, repeat TACEs can result in a ton of angio time and therefore a ton of
radiation. Patient do sometimes get skins burns (usually on their left back because of the
RAO camera angle).
RFA: Tumor is destroyed by heating the tissue to 60 degrees C (140 F). Any focal or nodular
peripheral enhancement in the ablation lesion should be considered residual / recurrent
disease. Sometimes, on the immediate post treatment study you can have some reactive
peripheral hyperemia - but this should decrease on residual studies. Important trivia is that
RF ablation is indicated in patients with HCC and colorectal mets (who can't get surgery).
TACE + RFA: As a point of trivia, it has been shown that TACE + RFA for HCC lesions
larger than 3cm, will improve survival (more so than either treatment alone). This is still not
curative.
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Yttrium-90 Radioembolization - An alternative to
TACE is using radioactive embolic materials
(Y-90). The primary testable trivia regarding Y-90 What is this Yttrium ?
therapy is understanding the pre-therapy work up.
Yttrium-90 is a high-energy beta
There are basically two things to know: emitter with a mean energy of
0.93MeV. It has no primary gamma
(1) Lung Shunt Fraction - You give Tc-99 emission. Yttrium-90 has a half-life of
64 hours. After administration, 94% of
MAA to the hepatic artery to determine how
the radiation is delivered over 11 days
much pulmonary shunting occurs. A shunt (4 half-lives). The maximum range of
fraction that would give 30 Gy in a single irradiation from each bead is 1 .1 cm.
treatment is too much (Y-90 is
contraindicated).
(2) The take off of the right gastric. The fear is that you get non-targeted poisoning of
the stomach, leading to a non-healing gastric ulcer. To help prevent reflux of the
Y-90 (poison) into places you don't want (basically anywhere that's not liver)
prophylactic embolization of the right gastric and the GDA is performed. The right
gastric origin is highly variable, and can come off the proper hepatic or the left
hepatic.
Trivia Review:
• Shunt Fraction > 30 Gy to the Lungs = No Y-90
• Before you give the poison, embo the right gastric (which has a variable take off) and
GDA - so you don't put a hole in the stomach.
If you inject the V-90 here, you can
imagine it refluxing into the right
gastric or GOA
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Generalized Tumor Treatment Trivia (Regardless of the Organ)
RFA
• Tumors need to be less than 4 cm or you can't "cure" them. You can • Cure = < 4 cm
still do RFA on tumors bigger than 4 cm but the buzzword you want • Debulk = > 4 cm
for this is "debulking".
• You always need a burn margin of 0.5-1.0 cm around the tumor. So your target is the tumor
+ another 1 cm of healthy organ.
• A key structure (something you don't want to burn up) that is within 1 cm of the lesion is
considered by most to be a contraindication to RFA. Some people won't cook lesions near
the vascular hilum, or near the gallbladder. Be on the look out for bowel. It is possible to
cook bowel adjacent to a superficial lesion. If they are asking you if a lesion is appropriate
for RFA and it's superficial look for adjacent bowel - that is probably the trick.
• RFA requires the application of a "Grounding pad" on the patient's leg. Blankets should be
jammed between the arms/body and between legs to prevent closed circuit arcs/bums.
• "Hot Withdrawal" supposedly can reduce the risk of tumor seeding. Basically you leave
the cooker on as you remove the probe to burn the tract.
• "Heat Sink" - this is a phenomenon described exclusively with RFA. Lesions that are near
blood vessels 3mm or larger may be difficult to treat (without getting fancy) because the
moving blood removes heat away from the lesion.
• You can overcook the turkey. Temperatures at l 00 C or greater tend to carbonize the tissue
near the probe, reducing electrical conductance (resulting in suboptimal treatment). Around
60 C is the usual target.
• "Post Ablation Syndrome" - Just like a tumor embolization you can get a low grade fever
and body aches. The larger the tumor, the more likely the syndrome (just like
embolization).
• Low Grade Fever and Body Aches Post Ablation. Next Step = Supportive Care
• Persistent Fever x 2-3 weeks post ablation. Next Step = Infection workup.
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Microwave
Similar to RFA is that it cooks tumors. The testable differences are that it can generate more
power, can cook a bigger lesion, requires less ablation time, it's less susceptible to heat sink
effect, and it does NOT require a ground pad.
Cryoablation
Instead of burning the tumors, this technique uses extreme cold in cycles with thawing. The
freeze-thaw cycles fuck the cells up pretty good. The cold gun is generated by the
compressing argon gas. I actually knew a guy who constructed a similar device shortly after
an industrial accident left him unable to survive outside of subzero environments.
Trivia = Thawing is what actually kills the cancer cells
Trivia = If you are planning on treating immediately after biopsy, most sources will advise
you to place the probes first, then biopsy, then treat. If you try and place the probes you
make a bloody mess then you might not get accurate probe placement. Just don't biopsy the
probe. Seriously, if you crack the probe and the high pressure gas leaks out - shit is gonna
explode (better have your medical student ready as a shield).
Trivia: It hurts less than RFA - so patients need less sedation
Trivia: The risk of bleeding is higher than with RFA- because you aren't ablating the small
vessels
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Treatment Response
RFA Treatment Response:
Size:
• Week 1-4: It's ok for the lesion to get bigger. This is a reactive change related to edema,
tissue evolution, etc ...
• Month 3: The lesion should be the same size (or smaller) than the pre-treatment study.
• Month 6: The lesion should be smaller than pre-treatment.
Contrast Enhancement:
• Central or Peripheral Enhancement is NEVER normal in the lesion post treatment.
• You can have "benign peri-ablational enhancement" - around the periphery of the ablation
zone. This should be smooth, uniform, and concentric. 1t should NOT be scattered,
nodular, or eccentric (those are all words that mean residual tumor).
Time Interval
• Multiphase CT ( or MR) at 1 month. If residual disease is present at this time, Next Step =
Repeat treatment (assuming no contraindications)
• Additional follow up is typically at 3-6 months intervals.
TACE Treatment Response
On follow up CT, you need to have pre and post contrast imaging including washout. The
iodized oil is going to be dense on the pre-contrast. The more dense oil is in the tumor the
better outcome is likely to be. The necrotic tissue should not enhance. lf there is enhancement
and/or washout in or around the tumor, then you have viable tumor that needs additional
treatment. Beam hardening from the iodized oil can cause a problem.
"Zone o.fAblation" is the preferred nomenclature for the post-ablation region on imaging.
Also, Dude, "Chinaman" is not the preferred nomenclature. Asian-American
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Cryoablation Treatment Response
Post therapy study is typically performed at 3 months, with additional follow ups at 6 months
and 12 months.
A good result should be lower in density relative to the adjacent kidney. On MR, a good result
is typically T2 dark and Tl iso or hyper.
Size: Just like RFA, ablated lesions can initially appear that they grew in size relative to the
pre-treatment study. With time they should progressively shrink (usually faster than with RFA).
An increase in size (after the baseline post treatment) should be considered recurrent tumor.
Enhancement: Any nodular enhancement ( > I OHU change from pre-contrast rnn) after
treatment should be considered cancer.
Vocab
"Residual tumor" or "Incomplete Treatment" = Vocab words used when you see focal
enhancement in the tumor ablation zone of a patient for their first post therapy study.
"Recurrent tumor" = Word used when you see focal enhancement in the tumor ablation zone
that is new from the first post therapy study.
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• .
G Tubes:
�
SECTION 11:
LUMINAL GI
A "G- Tube" is a gastric tube, placed directly into the stomach. They are primarily used as an
attempt to prolong the suffering of stroked out Alzheimer Patients with stage 4 sacral decubitus
ulcers.
Traditional method (Radiographically Inserted Gastrostomy - RIG): The basic idea is that you
put an NG tube down and pump air into the stomach until it smushes flat against the anterior
abdominal wall. Then you spear it and secure it with 4 "T-Tacks" to tack the stomach to the
abdominal wall in the gastric body. Then spear it again, wire in and dilate up to the size you
want. Typically, the T-Tacks are removed in 3-6 weeks. Other things that you can do is give a
cup of barium the night before to outline the colon.
If the patient has ascites. Next Step = Drain that first.
The Ideal Target:
Left of Midline (lateral to
the rectus muscle to avoid
inferior epigastric)
Mid to Distal Body
Equal distance from the
greater and less curves - to
avoid arteries
Anatomy Trivia: The cardia of the stomach is actually the most posterior portion.
There is another method often called a "PIG" because of the Perioral route. In that version you
stab the stomach and tread a wire up the esophagus. Then you grab the wire, slip the tube over
it, and advance the tube over the wire into the stomach all the way out the stabbed hole.
Then it's back to the nursing home for Grandma.
Honestly, it's probably best to do it with a scope, but since we are Radiologists my official
statement is that only a Radiologist can do this procedure well.
How long does Granny need to wait b�fore she can have her ensure via the G-Tube? Depends
on who you ask. Some people will say 12-24 hours fasting post placement. Other people will
say use it right away. It depends on the brand and practitioners bias. To know the correct
answer for the exam - simply read the mind of the person who wrote the question.
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EsophagealStents
Probably the most common indication for one of these is esophageal cancer palliation. These
are usually placed by GI, but that doesn't mean you won't get asked about them.
In the real world, most people don't even size these things. The overwhelming majority of
lesions can be covered by one stent. Having said that, for the purpose of multiple choice you
need a stent with a length at least 2 cm longer than the lesion on each side. You do the
procedure through the mouth. I imagine it would be great fun to try and place a stent through
the nose - if you really hated the person. You give them some oral contrast to outline the
lesion. An amplatz wire is dropped down into the stomach. The stent (usually self expanding)
is deployed over the wire.
Post Angioplasty? Most people don't angioplasty after deployment of the stent. However, if
the tumor is bulky and near the carina, some sources will suggest doing a pre-stent
angioplasty test up to 20 mm to see if this invokes coughing / stridor. The concern is that a
large tumor may get displaced against the carina and cause a respiratory emergency. If the
patient doesn't cough from the test you are safe to deploy the stent (probably).
Upper 1/3 Cancer: Most esophageal cancers are in the lower 1/3. If the question specifically
tells you it's higher up (or shows you), they may be leading you towards a "don't cover the
larynx dumbass!" question. The way to avoid this is to have endoscopy do the case so they
can identify the cords. If that isn't an option then placing a smaller device might be an
alternative.
Stent Drops into the Stomach: Most people will just leave the motherfucker alone.
However, if the patient is symptomatic, endoscopic removal is the textbook answer.
Stent Occludes. Next Step = Esophagram. The most common cause is food impaction - which
sometimes can be cleared with a soda. If that fails, the next step is endoscopy. If it's not food
but instead tumor overgrowth, sometimes you can place a second stent. It depends on a lot of
factors and asking that would be horse shit.
Gamesmanship:
• Acute obstruction is likely food
• Worsening symptoms over time is likely tumor.
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GI Bleed
You can split GI bleeds into two categories upper (proximal to ligament of Treitz) and lower.
Upper GI:
Some testable trivia is that 85% of upper GI bleeds are from the left gastric, and often if a
source cannot be identified, the left gastric is taken down prophylactically. If the source of
bleeding is from a duodenal ulcer, embolization of the GDA is often performed. About 10% of
the time, an upper GI bleed can have bright red blood per rectum.
"Pseudo-Vein" Sign - This is a sign of active GI bleeding, with the appearance of a vein
created by contrast pooling in a gastric rugae or mucosa} intestinal fold. If you aren't sure if
it's an actual vein, the "pseudo-vein" will persist beyond the venous phase of injection.
Dieulafoy's Lesion - This is a monster artery in the submucosa of the stomach which pulsates
until it causes a teeny tiny tear (not a primary ulcer). These tears can bleed like stink. It's
typically found in the lesser curvature. It's not exactly an AVM, more like angiodysplasia.
Sometimes you can treat it with clips via endoscopy. Sometimes it needs endovascular
embolization.
When I say pancreatic arcade bleeding aneurysm, you say celiac artery stenosis.
There is a known association with celiac artery compression (median arcuate
ligament) and the dilation of pancreatic duodenal arcades with pseudoaneurysm
formation.
Retrograde filling of the
hepatic artery should make
Gamesmanship: It is you think about Celiac
stenosis (or occlusion)
classically shown with
an angiographic run
through the SMA,
showing a dilated
collateral system and
retrograde filling of the Injection in SMA, fills
hepatic artery. ....-- a dilated pancreatic
duodenal collateral
system
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Upper GI Bleed "Next Step" Algorithm
Treat with Fai led or Not
Positive ossible
/ Endoscopy �
/ \.
Endoscopy Angio
Upper GI Bleed -
� Three /2pefully
Phase CTA
Negative Targeted, Non
Target if Needed
Lower GI:
The work-up for lower GI bleeds is different than upper GI bleeds. With the usual caveat that
algorithms vary wildly from center to center, this is a general way to try and answer next step
type questions regarding the workup.
Stable "Conservative
Endoscopy
Lower GI Bleed
Unstable
*Tachycardia +
Hypotension
ACR Appropriateness specifically states that in a STABLE patient with lower GI bleeding that
endoscopy is first line.
ACR Appropriate: High Yield Trivia is that
Intermittent/ Obscure GI Bleeding nuclear scintigraphy
- GI Bleeding that continues (or recurs) despite negative
upper endoscopy and colonoscopy is described as "obscure GI (RBC bleeding scan) is
bleeding. " The actual culprit is often from the small bowel more sensitive than
(arteriovenous malformation). angiography.
- There is no clear consensus on the optimal study to
interrogate the small bowel. Bleed Scan = 0.1 mL/min
CTA = 0.4 ml/min
- ACR Appropriateness Criteria rank CT angiography and
capsule endoscopy as the most appropriate choices in this Angiography = 1.0 mL/min
situation. Tc-99m RBC scan is considered as a "reasonable
alternative" for localization - but only in the setting of active
bleeding. Remember GI bleed scan only works if there is
active bleeding.
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Causes with Angiographic Buzzwords:
�?J •Angiodysplasia - Right Sided Finding.
,,,
"Early Draining Vein." Embolization of
angiodysplasia rarely stops a re-bleed and these often need surgery.
-3 • Diverticulosis - Left Sided Finding (usually).
,,,
More commonly venous. lf arterial,
"filling the diverticulum first" is classic.
99111
�n •Meckles - Usually shown on Meckles scan ( Tc-Na-pertechnetate). The feeding
;..') artery (vitelline) has a classic look with "extension beyond the mesenteric border,"
"no side branches" and "a corkscrew appearance" of the terminal portion.
Technical Aspects/ Trivia:
You will want runs of all 3 vessels (SMA, Celiac, IMA). Some old school guys will say to start
with the IMA because contrast in the bladder will obscure that territo1y as the procedure
continues. That's not really an issue anymore with modem DSA and starting with the SMA
will typically be the highest yield. You have to sub select each vessel. Runs in the aorta are
not good enough and that would never be the right answer.
What ifyou don't see bleeding? You can try "provocative angiography" - which is not nearly
as interesting as it sounds. This basically involves squirting some vasodilator (nitro 100-200
mcg) or thrombolytic drug (tPA 4 mg) into the suspected artery to see if you can make it bleed
for you.
What ifyou do see it bleeding? Administer some street justice. Anyone who trained in the last
30 years is going to prefer microcoils and PVA particles. Old guys might use gel-foam.
Alcohol should not be used for lower GI bleeds (causes bowel necrosis).
Microcoils: Good because you can see them. Good because you can place them precisely.
Bad because they deploy right where you drop them. So you need to go right up next to that
bleed to avoid a large bowel infarct.
Trivia = Inability to advance the micro-catheter peripherally is the most common cause of
microcoil embo failure
I say "non-selective embolization of bowel with microcoils," you say "bowel infarct"
PVA: Good because they are "flow directed." So you don't need to be as peripheral
compared to the microcoils. Bad because you have less control.
Trivia: Particles must be 300-500 microns. Particles that are smaller will/could cause
bowel infarct.
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But Prometheus my Geriatric Attending says to use Vasopressin?
Between me and you this argument was settled in 1986 by a lady
named Gomes. Her study showed coils stopped GI bleeds 86% of the
time, compared to 52% for vasopressin and the shit we have today is
way better making the disparity even greater. Having said that, some
Dinosaurs still do it.
For the purpose of multiple choice, this is what I would know:
• Vasopressin works as a vasoconstrictor
• Vasopressin does not require superselection. You can squirt it right into the main trunk of
the artery.
• Vasopressin sucks because the re-bleed rates are high (once the drug wears off)
• Vasopressin can actually cause non-occlusive mesenteric ischemia (NOMI)
• Vasopressin should NOT be used with large artery bleeding (i.e. splenic pseudoaneurysm),
bleeding at sites with dual blood supply (classic example is pyloroduodenal bleed), severe
coronary artery disease, severe hypertension, dysrhythmias, and after an embolotherapy
treatment (risk of bowel infarct).
Post Embolization: You need to do angiography post
embolization to look for collateral flow (if there is a dual
supply). The classic example is: after performing an
embolization of the GDA (for duodenal ulcer), you need to
do a run of the SMA to look at the inferior
pancreaticoduodenal (collateral to the GDA). You might
have to take that one out too, but obviously that would
increase the risk of bowel infarct.
Trivia - Risk of bowel infarct is way lower for upper GI
bleeds (because of the extensive collateral supply), relative
to bleeds distal to the ligament ofTrietz.
*First branch off
the SMA
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.
,,•
••
•• •
• •
� SECTION 12:
ABSCESS DRAINAGE
�
• • • •
General Tactics:
In general, there are two methods, you can use a trocar or you can use the seldinger technique
(wire guided).
• Trocar: You nail it with a spinal needle first. Then adjacent to the needle (in tandem)
you place a catheter.
• Seldinger: One stick with a needle, then wire in, dilate up and place a catheter.
Drain Size: The grosser and thicker stuff will need a bigger tube. If forced I'd go with:
• 6-8 F for clear fluid
• 8-10 F for thin pus
• 10-12 F for thick pus
• 12F+ for collections with debris or in collections that smell like a Zombie farted.
Drain Type: You pretty much always use a pigtail. I wouldn't guess anything else.
� Trivia / Gamesmanship
• Any "next step" question that offers to turn doppler on prior to sticking it with a needle is
always the right answer. Trying to trick you into core needling a pseudoaneurysm is the
oldest trick in the book.
• Decompressing the urinary bladder prior to a pelvic abscess drainage is often a good idea.
• Collection has pus. Next step = aspirate all of it (as much as possible) prior to leaving the
drain
• You can't advance into the cavity because it's too fibrous/thick walled. Next Step ? I'd try
a hydrophilic coated
• Family medicine want you to put a 3 way on that 12 F drain. Next step= don't do that.
You are reducing the functional lumen to 6F.
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Trivia / Gamesmanship Continued
• Family medicine wants you to hold off on antibiotics till after you drain this unstable septic
shock patient's abscess. Next step = don't do that. Antimicrobial therapy should never be
withheld because some knuckle head is worried about sterilizing cultures. (1) Cultures
almost never change management from the coverage they were on anyway, (2) the trauma
of doing the drainage will seed the bloodstream with bacteria and make the sepsis worse.
• Family medicine wants to know how many cc to flush this complex (but small) abscess
with? Remember that ''flushing" and "irrigation" are different. Flushing is done to keep
the tube from clogging with viscous poop. Irrigation is when you are washing out the
cavity (the solution to pollution is dilution) for complete cavity drainage. Going nuts with
the irrigation can actually cause a bacteremia. The vignette could say something like
"waxing and waning fever corresponding to flush schedule." The next step would be to
train the nurses / family medicine to limit the volume to less than the size of the cavity.
• You irrigate the abscess with 20 cc of fluid but when you aspirate back you only get Secs.
Next Step? Stop irrigating it! You have a big problem. The fluid (which is dirty) is being
washed into a location that is not able to be sucked back out by the tube. So you are
creating a new pocket of infection that isn't being drained.
• Catheter started out draining but now is stopped. Next Step = (1) confirm that it is in the
correct location and not kinked - might need imaging if not obvious at bedside, then (2) try
flushing it or clearing an obstruction with a guidewire. If the catheter is clogged for real
then you'll need to exchange it - probably for a larger size. If the tract is mature (older than
a week) you can probably get a hydrophilic guidewire through the tract into the collection
to do an easy exchange.
• Remove the catheter when: (1) drainage is less than 10cc / day, (2) the collection is
resolved by imaging (CT, Ultrasound, etc...), and (3) there is no fistula.
• Persistent Fever > 48 Hours post drainage. The patient should get better pretty quickly
after you drain the abscess. If they aren't getting better it implies one of two things (1) you
did a shitty job draining it, or (2) they have another abscess somewhere else. Either way
they need more imaging and probably another drain.
• The drainage amount spikes. This is a bad sign. In a normal situation the drainage should
slower taper to nothing and then once you confirm the abscess has resolved you pull the
drain. Spikes in volume (especially on multiple choice exams) suggest the formation of a
fistula. Next step is going to be more imaging, possibly with fluoro to demonstrate the
fistula (urine, bowel, pancreatic duct, bile duct, etc...).
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Pelvic Abscess Drainage - tuba-ovarian abscess, diverticular abscess, or peri-appendiceal
General Ideas for Choosing the Correct Route:
(1) All things equal, pick the shortest route
(2) Avoid bowel, solid organs, blood vessels (inferior epigastrics are classic), nerves
(3) Try not to contaminate sterile areas
(4) Choose the most dependent position possible (usually posterior or lateral) to facilitate
drainage
Routes
Most abscesses in the pelvis are layering in a dependent position so anterior routes are
typically not easy. In general there are 4 routes; transabdominal, transgluteal, transvaginal,
and transrectal. I'm gonna try and cover the pros/cons and testable trivia for each route.
Transabdominal - The pull of gravity tends to cause infection to layer in the more posterior
spaces. As a result transabdominal approaches tend to be long, and therefore violate one of
the 4 general ideas. If you are shown an abscess where this would be the best, shortest route
then remember to watch out for the inferior epigastrics. For sure there will be an option to
stick the trocar right through one of them. Make sure you ID them before you choose your
answer.
Transgluteal - The transgluteal
approach is done for a variety of {
o''«P 0-o� Presacral
posterior targets. The patient is
positioned prone for targeting. ', , a��rl° Collection
Gluteal',, Sciatic
Artery '
Avoid the sciatic nerve and gluteal Sciatic
arteries by: Nerve" /
,,,//
• Access through the sacrospinous
ligament
• Medial as possible
• Inferior to the piriformis
Disadvantages: Legit risk of artery/
nerve injury. Prone to catheter
kinking. Gotta use CT (radiation). Piriformis Femoral
Artery
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Endoluminal Routes: There is a subset of perverts who prefer to biopsy and drain things through
the vagina (tuna purse) and/or the rectum.... Not that there's anything wrong with that. Well
actually the primary disadvantage of both of these "endoluminal routes" is catheter stability.
Many catheters are literally pooped out within 3-4 days. Although advocates for these routes will
argue that (a) they are more fun to do, and (b) most collections resolve within 3 days.
Transvaginal: Biopsy and/or drainage through the vagina (pink taco) has the advantage of
providing a very short safe route that can be guided by transvaginal ultrasound, allowing for no
radiation and very accurate placement. This was the classic in office route for drainage of
infected gynecologic fluid collections (PID related). The procedure is done in the lithotomy
position. Catheter size is traditionally limited to 12F (or smaller). You should never do this to a
patient under the age of 14 - not even Jared from Subway would try that.
Although controversial, it is possible (and well described in the literature) to drain / biopsy
adnexa cysts through the vagina (penis fly trap).
Vaginal prep / cleansing prior to the procedure is controversial and unlikely to be tested.
Transrectal: Of the three routes (gluteal, vaginal, rectal) transrectal is supposedly the least
painful - although in my literature review the psychological pain was not discussed (this kinda
thing would really fuck with my machismo). Essentially this route offers all the advantages of
the transvaginal route (ultrasound guidance, very short / safe route) plus the added advantage of
pre-sacral access. Depending on what you read, people will argue this is first line (over trans
gluteal) for pre-sacral collection but that is highly variable.
Choosing between transgluteal and trans-rectal for a pre-sacral collection would be the worst
"read my mind" question ever. If forced into that scenario I would set aside the psychologic
trauma to the alpha male ego and use (1) the size of the collection - do y ou think that will drain
before he/she poops the catheter out?, and (2) is the transgluteal route safe - are the vessels
nerves obviously in the way?
Prep with a cleansing enema is not controversial and is endorsed pretty much everywhere.
Pre-sacral
Rectouterine collection Pre-sacral
pouch collection L4 \
L4 Rectovesical
collection pouch
Vesicouterine \ LS
\
pouch collection collection
d\
The Baby
80
;:---�
��
Rectum
(prison wallet)
Cannon *not drawn to sca le
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Diverticular Abscess
There are a few pearls/ special considerations that we should discuss regarding the
diverticular abscess.
Size: The typical threshold for a diverticular abscess to be drained is 2 cm. Anything smaller
than that will be more trouble than it is worth.
Tube Choice: Remember the grosser and thicker stuff will need a bigger tube. Diverticular
abscesses form because of a perforated diverticulum. Thus, you can come to the logical
conclusion that you need a tube capable of draining shit. For the purpose of multiple choice,
anything smaller than 1 OF is probable NOT the right answer.
Gas: If the abscess is gas producing (they would have to tell you the bulb suction fills rapidly
with gas), the c01Tect next step is to treat the collection like a pleural drain in a patient with an
air leak (i.e. put on water seal).
Liver Abscess
Lots of etiologies for these, but don't forget to think about the appendix or diverticulitis. The
draining of these things is somewhat controversial with some authors feeling the risk of
peritoneal spread out weighs the benefits and reserving the drainage for patient's with a poor
prognosis. Other authors say that everyone and their brother should get one, and consider it
first line treatment.
A pearl to draining these things is to not cross the pleura (you'll give the dude an empyema).
If there is a biliary fistula, prolonged drainage will usually fix it (biliary drainage or surgery is
rarely needed).
Trivia: Biopsy/ Aspiration of Echinococcal cysts can cause anaphylaxis. Surgical removal of
the presumed echinococcal cysts should be discussed with surge1y before attempting the
procedure inIR (you want to be able to blame it on them, if shit goes bad).
Renal Abscess
Renal abscess is usually secondary to ascending infection or hematogenous spread. The term
''perinephric abscess" is used when they perforate into the retroperitoneal space. When they
are small (< 3-5 cm) they will resolve on their own with the help ofIV antibiotics.
Indications for aspiration or drainage include a large (> 3-5 cm), symptomatic focal fluid
collection that does not respond to antibiotic therapy alone.
The strategy is to use ultrasound and stick a pig tail catheter in the thing. After a few days if
the thing is not completely drained you can address that by upsizing the tube. If you create or
notice a urine leak, you'll need to place a PCN. There are really only relative contraindication
- bleeding risk etc ..., and the procedure is generally well tolerated with a low complication
rate.
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Perirenal Lymphocele
This is seen in the setting of a transplant. When they are small you typically just watch them.
However, on occasion they get big enough to cause local mass effect on the ureter leading to
hydronephrosis. You can totally aspirate them, but they tend to recur and repeated aspiration
runs the risk of infecting the collection. For multiple choice I would say do this: Aspirate the
fluid and check the creatinine. If it's the same as serum it's probably a lymphocele (if it�,
more then it�, a urinoma). Either way you are going to drain them with a catheter. However,
if it's a lymphocele you might sclerose the cavity (alcohol, doxy, povidine-iodine).
*Urinomas (that are persistent) of any size are drained.
Pancreas Drainage
Remember that necrotizing pancreatitis is bad, but infected necrotizing pancreatitis is a
death sentence. So, be careful draining something that is NOT infected already (otherwise
you might make it infected). If you aren't sure if it's infected, consider aspirating some for
culture (but not placing a tube).
Indications: General indications include infected collections or collections causing mass
effect (bowel or biliary obstruction).
Progression to surgery: If you can get 75% reduction in 10 days, the drain is good enough.
If not, the surgeons can use the tract for a video-assisted retroperitoneal debridement (which
still avoids open debridement).
Pancreatic Cutaneous Fistula: Other than pancreatic pseudocysts, most pancreatic
collections are either brown or grayish. When the fluid is clear, you should think about
pancreatic fluid, and send a sample for amylase to confirm. If this lasts more than 30 days
then you have yourself a "persistent pancreatic.fistula." Nice job idiot... you could have just
left it alone. That will teach you to let those medicine docs pressure you into doing stuff
that's not indicated. It may be possible to treat that with octreotide (synthetic somatostatin)
to inhibit pancreatic fluid, although in these cases extended drainage is usually needed.
You've Been Talked into Draining the Pseudocyst - Which Route:
General Rule: If the pseudocyst communicates with the pancreatic duct drainage will be prolonged
(6-8 weeks in most cases). You can t1y and use somatostatin to slow it down.
Most Cases: Transperitoneal with CT guidance - avoid organs, avoid going through the stomach
twice.
Can't Avoid the Stomach or Patient has a known Duct Communication (so they gonna have a tube
for a long time) - Trans gastric Approach - so it drains into the stomach
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-;.- �
SECTION 13:
URI NARY INTERVENTION '·" � ... :
•.··.:
Percutaneous Nephrostomy (PCN) -
There are 3 main reasons you might subject someone to this:
Stones
Relief of Urinary
Obstruction ◄
Cancer
Urine Leak
Urinary
Diversion Urine Fistula (for pelvic CA
or inflammatory process)
Whitaker Test (if it's 1970)
Access for
Diagnostic and Access for Stone Removal
(PCNL)
Therapeutic
Procedures Dilation or Stenting of
Stricture
PCN Contraindications (Absolute):
• INR Should be less than 1.5
Severe Coagulopathy
�
• PLT>50K
Technically Not Possible ► • Approach would cross colon,
spleen, or liver
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Technical Stuff:
• Prior to the procedure, it would be ideal if you normalized the potassium (dialysis). Certainly
anything about 7 should be corrected prior to the procedure.
• Hold anti-platelet drugs for at least 5 days prior to the procedure.
• The lower pole of a posteriorly oriented calyx is ideal.
The reason you use a posterior lateral (30 degrees) 30 Degrees off sagittal
(towards the back)
approach is to attack along Brodel's Avascular Zone
(area between the arterial bifurcation).
• Skin entry site should be 10 cm lateral to the midline (not beyond the posterior axillary line).
You don't want to go too medial unless you want to try and dilate through the paraspinal
muscles. You don't want to go too lateral or you risk nailing the colon.
• Choosing a lower target minimizes the chance of pneumothorax. Additional benefit of the
posterior calyces approach is that the guidewire takes a less angled approach (compared to an
anterior calyces approach).
• Direct stick into the collecting system without passing through renal parenchyma is NOT a
good move (high risk of urine leak).
• Dilated System = Single Stick: Ultrasound and stick your ideal target (low and posterior), then
use fluoro to wire in, dilate up, and then place the tube. Alternatively you can do the whole
thing under CT.
• Non-Dilated System = Get your partner to do it (these blow). If forced to do = Double Stick.
Ultrasound and stick anything you can. Opacify the system. Then stick a second time under
fluoro in an ideal position (low and posterior), then wire in, dilate up, and then place the tube.
Alternatively you can do the whole thing under CT.
• The posterior calyces (your target) will be seen "end on" if you use contrast. The anterior ones
should be more lateral. If you use air, you should just fill the posterior ones (which will be
non-dependent with the patient on their belly. Air is useful to confirm.
• You place the drain and get frank pus back. Next Step= Aspirate the system
d/ine
Lateral to Mi
About 10 cm
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Special Situations:
Nephrostomy on Transplant - The test writer will likely write the question in a way to
make you think it's crazy to try one of these. Transplant is NOT a contraindication. In fact
it's technically easier than a posterior/ native kidney.
Testable Transplant Trivia:
• A nterolateral Calyx Should be Targeted (instead �f posterior)
• Entry site should be LATERAL to the transplant to avoid entering the peritoneum
• Middle to Upper Pole (instead of a lower pole)
Percutaneous Nephrostolithotomy -This is done to remove stones in conjunction with
urology. The idea is very similar with a few differences. The most testable difference is
that the site is often the upper pole (instead of lower pole) to make stone access easier.
The tube/ hole is bigger and there is more risk of bleeding.
"Tube Fell Out" -The trick to handling these scenarios is the "freshness" of the tube. If the
tract is "fresh, " which usually means less than 1 week old, then you have to start all over
with a fresh stick. If the tract is "mature," which usually means older than 1 week, you can
try and re-access it with a non-traumatic wire.
Catheter Maintenance: Exchange is required every 2-3 months because of the
crystallization of urine in the tube. Some hospitals/ departments will do exchanges more
frequently than 2 months and that is because of how well this pays ... uh I mean they do it
for excellent patient care.
"Encrusted Tube" - If this thing gets totally gross it can be very difficult to exchange in the
normal fashion. The most likely "next step" is to use a hydrophilic wire along the side of
the tube (same tract) to maintain access.
Ureteral Occlusion - Sometimes urology will request that you just kill the ureters all
together. This might be done for fistula, urine leak, or intractable hemorrhagic cystitis.
There are a bunch of ways to do it. The most common is probably a sandwich strategy
with coils. The sandwich is made by placing large coils in the proximal and distal ends of
the "nest", and small coils in the middle. Big Coils = Bread, Small Coils = Bacon.
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Nephroureteral Stent (NUS)
This is used when the patient needs long-term drainage. It's way better than having a bag of
piss strapped to your back.
Benign ureter strictures
Malignant ureteral obstruction (by.far
the most common indication) LONGTERM
Relief of Urinary- NUS
Obstruction
Ureteric injury
Ureteric calculus undergoing lithotripsy.
Technically they can be placed in a retrograde (bladder up) or an antegrade (kidney down)
fashion. You are going to use the antegrade strategy if (a) you've got a nephrostomy tube,
or (b) retrograde failed.
Can you go straight from Nephrostomy to NUS? Yes, as long as you didn't fuck them up
too bad getting access. If they are bleeding everywhere or they are uroseptic you should
wait. Let them cool down, then bring them back to covert to the NUS.
Who should NOT get a NUS? Anyone who doesn't have a bladder that works (outlet
obstrnction, neurogenic bladder, bladder tumors, etc..). It makes no sense to divert the urine
into a bladder that can't empty.
Obstruction Obstruction Obstruction
i - ,---:
/ /
: - ,. __:
Bag o Piss
0
PCN NUS - with External and Internal Drainage. Double J
Allows urine to pass from the kidney to bladder The Ultimate Goal
through the obstruction (for those that can get one)
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Internal NUS - Double J: This is the ultimate goal for the patient. The testable
stipulation is that this will require the ability to do retrograde exchanges (via the bladder).
"The Safety" - A safety PCN - is often left in place after the deployment of a double J PCN.
The point is to make sure the stcnt is going to work.
The typical protocol:
1. Place the double J and the safety
2. Cap the safety - so that the internal NUS is draining the patient
3. Bring the patient back in 24-48 hour and "squirt the tube" (antegrade nephrostogram).
The system should be non-obstructed.
4. If it's working you pull the safety.
5. If it's NOT working you uncap the safety and just leave it as a PCN.
Suprapubic Cystostomy -
Done to either (a) acutely decompress the bladder or (b) decompress long-term outflow
obstruction (neurogenic bladder, obstructing prostate cancer, urethral destruction, etc. .)
The best way to do it is with ultrasound in the fluoro suite. The target is midline just above the
pubic symphysis at the junction of the mid and lower thirds of the anterior bladder wall. You
chose this target because:
• The low stick avoids bowel and the peritoneal cavity
• The low 1/3 and mid 1/3 junction avoids the trigone (which will cause spasm).
• The vertical midline is chosen to avoid the inferior epigastric.
Use ultrasound and stick it, confirm position with contrast, wire in and then dilate up. Use a
small tube for temporary stuff and a larger tube for more long-term stuff. You can always
upsize to a foley once the tract is mature. A 16F foley is ideal for long-term drainage.
Contraindications:
• Buncha Pelvic Surgeries - Extensive scar
• Being a Big Fat Pig/Cow
• Coagulopathy
• Inability to distend bladder
• Inability to displace overlying small bowel
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Weapon of Choice
Let's do a rapid review of urinary diversion options.
Obstruction Obstruction
,--
I
I
1___
---,I
I
__ .,!
/ r-- --, /
·---
I
I
--·
I
I
!
Obstruction
,-- ---1
I I
I I
1___ __ .,!
Scenario 1: Scenario 2:
Obstruction
----..
Scenario 3:
:_ _-=<:!_
r- ---:
Dude with a ureteral stricture Dude with a ureteral TCC Dude with an outflow
PLUS a Bladder Mass obstruction (horrible
prostate cancer)
Obstruction Obstruction
/ /
I __I
·--- __ _!
Obstruction
-----------_ -- JI
I
I
I
t___ __ .,!
If you can cross the lesion, This guy has obstruction at This guy has obstruction
and the bladder works then the ureter and the bladder. at the bladder. He
internal Double J NUS is idea The only option is to divert at doesn't need to cross
the level of the kidney He the ureter. He gets a
gets a PCN. Cystostomy
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Renal Biopsy -- This can be done for two primary reasons:
(1) renal failure or (2) cancer biopsy.
Non-Focal: The renal failure workup "non-focal biopsy" is typically done with a 14 - 18
gauge cutting needle , with the patient either prone or on their side (target kidney up). The
most obvious testable fact is that you want tissue from cortex (lower pole if possible) to
maximize the yield of glomeruli on the specimen and minimize complications by avoiding
the renal sinus. The complication rate is relatively low, although small AV fistulas and
pseudo-aneurysms are relatively common (most spontaneously resolve). Some hematmia is
expected. In a high risk for bleeding situation a transjugular approach can be done but that
requires knowing what you are doing.
Focal: It used to be thought that focal biopsy should NEVER be done because of the
dreaded risk of upstaging the lesion and seeding the track. This has been shown to be very
rare (<0.01%). Having said that I think it's still the teaching at least in the setting of
pediatric renal masses. This procedure is probably better done with CT. The patient is
placed in whatever position is best, but the lateral decubitus with the lesion side down is
"preferred" , as it stabilizes the kidney from respiratory motion, and bowel interposition.
Just like with ultrasound, not crossing the renal sinus is the way to go. Just put the needle in
the tumor. If it's cystic and solid make sure you hit the solid part. Some texts recommend
both fine needle and core biopsy. The core biopsy is going to give a higher yield. A testable
pearl is that if lymphoma is thought likely, a dedicated aspirate should be sent for flow
cytometry. A s with any renal procedure hematuria is expected (not gross - just a little).
Renal colic from blood clots is rare.
ACR Appropriate/ SIR Practice Guidelines: Renal Biopsy
- Renal Bx is a procedure with "significant bleeding risk, difficult to detect or control."
- SIR guidelines recommend holding aspirin for 5 days prior to the procedure.
- Why 5 Days ? Aspirin irreversibly inhibits platelet function and since platelet lifespan is
about 8-10 days, patients with normal marrow will replenish 30-50% of their platelets
within 5 days of withholding the willow bark (aspirin).
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Renal RFA: Radiofrequency ablation (RFA) is an alternative to partial nephrectomy and
laparoscopic nephrectomy. It can be used for benign tumors like AMLs, renal AVMs, and even for
RCCs. Angiomyolipomas (AMLs) are treated at 4cm because of the bleeding risk. Sort of a general
rule is that things that arc superficial you can burn with RFA. Things that are closer to the collecting
system it may be better to freeze (cryoablation) to avoid scaring the collecting system and making a
stricture. Pyeloperfusion techniques (cold D5W irrigating the ureter) can be done to protect it if you
really wanted to RFA. If anyone would ask, RFA has no effect on GFR (it won't lower the GFR).
Things that make you think recurrent/residual disease after therapy:
(1) Any increase in the size beyond the acute initial increase,
(2) Areas of "nodular" or "crescentic" enhancement, or
(3) A new or enlarging bright T2 signal.
There is a paper in AJR (2009) that says that lesions that are < 3cm will appear larger in 1-2 months
and lesions >3cm do not grow larger- when successfully treated. So, smaller lesions may initially
get bigger but after that - any increase in size should be considered tumor recurrence.
Renal Arteriography: You should always do a non
selective aortogram first to see how many arteries feed the
kidney, where they are , etc. Sometimes the aortogram will show
you an obvious ostial problem which you can then select down
on and address. Otherwise, you need to do selective angiography
and look at each vessel. LAO is the projection of choice for
LAO Minimizes Angiographic
looking at the renals. Sometimes the stenosis is further out, in
Overlap from the Aorta
fact branch artery stenosis is a cause of hypertension in kids.
Angioplasty ofRenal Arteries: Used to treat hypertension caused by atherosclerosis (usually ostial)
or FMD. Risks include thrombosis, and vessel spasm. Calcium channel blockers can be given to
decrease the risk of spasm. Heparin should be on board to reduce thrombosis risk. Most people take
daily aspirin the day before and every day after for 6 months, to reduce the risk of restenosis.
• Indications for angioplasty = Renal Vascular HTN or Azotemia
• Atherosclerosis at the Ostium =Angioplasty+ Stent
• FMD - usually mid vessel = Angioplasty Alone
But Prometheus!?! - I was reading the New England Journal...
Don't read the NEJM. The NEJM is run by a bunch of family medicine doctors who hate all
procedures. They published a thing called the CORAL trial in 2014, that showed no added
benefit from angio + stenting in the setting of renal vascular stenosis compared to high quality
medical therapy.
This remains controversial and several prominent IR guys still like to stent, especially if they can
measure a pressure gradient in the renal artery. For the purpose of multiple choice, if "high
quality medical therapy" is a choice for treated RAS related hypertension, that is probably the
right answer - otherwise, pick angio + stent.
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Renal Hemorrhage:
Trauma to the kidney (usually iatrogenic from biopsy or diversion procedure) can typically be
embolized. The renal arteries are "end arteries," which means that collaterals are not an
issue. It also means that infarction is a legit issue so if you want to salvage the kidney you
need to try and get super selective. Having said that, don't be an idiot and fuck around trying
to get super selective while the patient is bleeding to death. Remember most people have two
of these things, plus in a worst case scenario there is always dialysis. Bottom line: if you get
into trouble and the patient is crashing, just trash the whole thing.
Next Step: Arterial trauma from the nephrostomy tube placement. Bleeding source is occult
on angio. Next step ? Remover the nephrostomy tube (over a guidewire), then look again.
Often the catheter tamponades the bleed, making it tougher to see.
Gamesmanship: Oral boards guys used to be sticklers for the phrase "over a wire. " In other
words if you just said "I'd remove the PCN" they would ding you. You have to say "I'd
remove the PCN over a wire." The only reason I bring this up is the use of possible
distractors / fuckery.
Maybe something like this:
Q..;_ The highly skilled Interventionalist grants the Fellow the great privilege of performing a
fresh stick nephrostomy. The clumsy, good for nothing Fellow manages to place the tube, but
now there is a large volume of bright red blood in the tube and the Patient's blood pressure is
dropping rapidly. You start fluids and perform an emergent renal arteriography. The source of
bleeding is not seen. What is the best next step?
A: Remove the PCN and repeat another angio run
B: Kick the fellow in the shin for using too much fluoro time Just like a Midget using
C: Call Urology and admit you need help from a "real doctor" a urinal ... you gotta
D: Remove the PCN over a wire and repeat another angio run. ._ __, stay on your toes.
Read all the choices!
Renal Aneurysms
"Look, man. I only need to know one thing: where they are" - Private Vasquez
• Small Segmental Arteries = coils
• Main Renal Artery = Covered Stent to exclude the aneurysm. Alternatively, you could place
a bare metal stent across the aneurysm and then pump detachable coils into the sac.
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SECTION 14:
PULMONARY INTERVENTION
Pleural Drainage - Most everyone has done a
few thoraccntcscs as a resident. I just want to touch on a
few testable points.
• Remember that you go "above the rib" to avoid the
neurovascular bundle.
• If you pull off too much fluid too fast you can possibly
"Above the Rib"
get pulmonary edema from re-expansion (this is avoid the neurovascular bundle.
uncommon).
• If it's malignant you might end up with a trapped lung (lung won't expand fully)- in other
words a thick pleural rind or fibrothorax, can prevent lung reexpansion - makes
percutaneous drainage pointless in many cases. A "vacu-thorax" - in the setting of a
trapped lung, does not mean anything, and does not need immediate treatment even if it's
big. If you really need to fix it, you'll need a surgical pleurectomy / decortication.
Pleurodesis (which can be done to patients with recurrent pleural effusions), does NOT
help in the setting of trapped lung.
• Pneumothorax is rare but is probably the most common complication (obviously it's more
common when done blind).
Additional Trivia related to Chest Tubes:
• Continuous air bubbles in the Pleur-evac chamber represent an air leak, either from the
drainage tubing or from the lung itself. In the setting of multiple choice - think about a
bronchopleural fistula.
• INR should generally be < 1.5 prior to placement of a chest tube.
• In the paravertebral region, the intercostal vessels tend to course off of the ribs and are
therefore more prone to injury if this route is chosen for chest tube placement
Choice of Drainage Catheter
Parapneumonic Effusion / Empyema Malignant Effusion
Inpatient Outpatient Inpatient Outpatient
15.5 Indwelling
12-14 Fr 10 Fr 14 F
(PleurX etc ...)
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Lung Abscess: Just remember that you can drain an empyema (pus in the pleural
space), but you should NOT drain a lung abscess because you can create a bronchopleural
fistula (some people still do it).
Lung RFA- Radiofrequency ablation of lung tumors can be performed on lesions
between 1.5cm and 5.2cm in diameter. The most common complication is pneumothorax
(more rare things like pneumonia, pseudoaneurysm, bronchopleural fistula, and nerve
injury have been reported). The effectiveness of RFA is similar to external beam radiation
with regard to primary lung cancer. The major advantage of lung RFA is that it has a
limited effect on pulmonary function, and can be performed without concern to prior
therapy.
Imaging (CT and PET) should be performed as a follow up of therapy. Things that make
you think residual/recmTent disease: nodular peripheral enhancement measuring more than
10 mm, central enhancement (any is bad) , growth of the RFA zone after 3 months (after 6
months is considered definite), increased metabolic activity after 2 months, residual activity
centrally (at the burned tumor).
Lung Biopsy - The most common Reducing the Risk of Pneumothorax
complication is pneumothorax, which occurs - Post Biopsy
about 2 5% of the time (most either resolve Enter the lung at 90 degrees to pleural
spontaneously or can be aspirated), with surface
about 5% needing a chest tube. The second Avoid interlobar fissures
most common complication (usually self Put the patient puncture side DOWN after
the procedure
limiting) is hemoptysis.
No talking or deep breathing after the
The testable pearls include: procedure (at least 2 hours)
If the patient is a cougher, consider
• The lower lung zones are more affected by postponing the procedure - or giving
respiratory motion, empiric anti-tussive meds
• The lingula is the most affected by cardiac Nonspecific Thoracic Core Biopsy
motion, Results - Next Step:
• Avoid vessels greater than 5 mm, Repeat the biopsy and/ or close follow up.
Nonspecific biopsy results don't mean shit
• Try and avoid crossing a fissure (they - especially in the lung.
almost always get a pneumothorax),
Biopsy is only helpful when you get an
• Areas lateral to and just distal to the tip of a actual result (cancer, hamartorna, etc ...).
biopsy gun will be affected by "shock wave Otherwise - you could have just missed, or
targeted the infection behind the cancer.
injury", so realize vessels can still bleed
from that.
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Chests Tube / Pigtail Placement:
Potential algorithm to deal with Procedural Pearls
pneumothorax post biopsy cases: You can usually get away with a small-caliber,
(6-10 French) catheter. A 10 French Pigtail
Catheters would require an 18G needle/ 0.035
Pneumothorax ! ! ! !
I
+
Amplatz wire. You would need a larger tube if
there is fluid (otherwise it will get clogged). You
should useCT guidance since you obviously
Oxygen via nasal cannula have it available. Most people will tell you to
(speed the resorption of the pneumothorax) use the so called " triangle of safety," located
+
above the 5th intercostal space, mid-axillary line.
This has the thinnest muscle, lets you avoid the
breast in females (and fat sloppy dudes) - plus
Attempt Manual Aspiration keeps you free of the axilla1y vasculature,
through the introducer needle diaphragm, liver, and spleen.
(place a new 16 G needle ffyou already took it out)
Use a 50cc syringe and aspirate as you back
�'P
the needle out and eventually remove it.
+
�
,.,
,
Ede
Did You Aspirate More than 650 cc of Air?
ec , ' Edge of the Lat
...
...
,,
Yes No 5th IC space
u
Probable should Get aCXR Always go along the superior aspect of the rib to
place a tube 1 & 3 hours avoid the neurovascular bundle along the inferior
border of each rib.
Pneumothorax > 2cm Heimlich valves will let the patient remain
Pneumothorax is enlarging Any of these ambulatory, otherwise you can use a
Patient is short of breath conventional water seal device.
u In most cases, the tube can be removed 1-2 days
Probable should place a tube after the procedure.
Obstruction Air Leak Subcutaneous
Emphysema
Detected by noticing (being told) Detected by persistent bubbling
that the water-seal chamber isn't within the water seal chamber. Typically detected by
fluctuating with respiration or Air leak= Air within the pleural crepitus on physical exam, or
coughing while the drainage system space. This is expected after initial shown on chest x-ray.
is set to gravity. insertion of a chest tube, (with an Confirm the tube is in the
This means either (1) the lung is actively resolving pneumothorax). pleural space. Specially,
fully expanded or (2) the tube is It becomes a problem when it is make sure the side holes are
clogged - CXR will tell you the new or persistent. ALL within the pleural space.
difference. Next Step: CXR confirm position Look for those fucking side
It is controversial to "milk" the of the tube. Inspect the bandage - holes. Reposition if needed.
tubing - plenty of people still do it. usually a vaseline bandage covers If the tube is appropriately
Some people put TPA in the tube - the insertion site. If everything positioned, subcutaneous
people do lots of crazy shit beyond looks ok - you might be dealing emphysema is self-limited -
the scope of the exam.... probably. with a bronchopulrnonary fistula. do nothing.
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Thoracic Angio:
This section is going to focus on the two main flavors of pulmonary angio; pulmonary artery
(done for massive PE and pulmonary AVM treatment) and bronchial artery (done for
hemoptysis).
Pulmonary Artery
The primary indications for pulmonary arteriography is diagnosis and treatment of massive PE
or pulmonary AVM.
Technical Trivia:
The "Grollman" catheter, which is a preshaped 7F, is the classic tool. You get it in the right
ventricle (usually from the femoral vein) and then turn it 180 degrees so the pigtail is pointing
up, then advance it into the outflow tract. Some people will say that a known LBBB is high
risk, and these patients should get prophylactic pacing (because the wire can give you a
RBBB, and RBBB + LBBB = asystole). A n important thing to know is that patients with
chronic PE often have pulmonary hypertension. Severe pulmonary hypertension needs to be
evaluated before you inject a bunch of contrast. Pressures should always be measured
before injecting contrast because you may want to reduce your contrast burden. Oh, one last
thing about angio ... never ever let someone talk you into injecting contrast through a swan
ganz catheter. It's a TERRIBLE idea and the stupid catheter will blow apart at the hub. I
would never ever do that. ...
Next Step: Cardiac dysrhythmias (v-tach) during
procedure. Next Step ? Re-position the catheter/ Pulmonary Angiography
wire Relative Contraindications
Pulmonary Embolism -- Patients with PE should Pulmonary HTN with elevated right
be treated with medical therapy (anticoagulation heart pressures (greater than 70
systolic and 20 end diastolic).
with Coumadin, Heparin, or various newer agents),
allowing the emboli to spontaneously undergo If you need to proceed anyway - they
lysis. In patients who can't get anticoagulation (for get low osmolar contrast agents
whatever reason), an IVC filter should be placed. injected in the right or left PA (NOT the
The use of transcatheter therapy is typically main PA).
reserved for unstable patients with massive PE.
Left Bundle Branch Block - The
Massive PE? Just think lotta PE with lzyp_otension. catheter in the right heart can cause a
right block, leading to a total block.
In those situations, catheter directed thrombolysis,
thrornboaspiration, mechanical clot fragmentation, If you need to proceed anyway - they
and stent placement have all been used to address get prophylactic pacing.
large clots.
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Pulmonary AVM-They can occur sporadically. For the purpose of multiple choice when
you see them think about HHT (Hereditary Hemorrhagic Telangiectasia / Osler Weber
Rendu). Pulmonary AVMs are most commonly found in the lower lobes (more blood flow)
and can be a source of right to left shunt (worry about stroke and brain abscess). The rnle
of treating once the afferent (feeding) artery is 3mm is based on some tiny little abstract
and not powered at all. Having said that, it's quoted all the time and a frequent source of
trivia that is easily tested. The primary technical goal is to crnsh the feeding artery (usually
with coils) as close to the sac as possible. You don't want that think reperfusing from
adjacent branches. Pleurisy (self limited) after treatment seems to pretty much always
happen.
Key Trivia:
• HHT Association
• Brain Abscess / Stroke - via paradoxical emboli
• Treat once the afferent (feeding) artery is 3mm
• Coils in the feeding vessel, as close as possible to the sac
Special Situation - Rasmussen Aneurysm
This is an aneurysm associated with chronic pulmonary infection, classically TB. The trick
on this is the history of hemoptysis (which normally makes you think bronchial artery).
"It's a Trap!" -Admiral Gia! Ackbar
Next Step Strategy to avoid the trap:
Patient blah blah blah hemoptysis ..... Next Step? Bronchial Artery Angio
• Bronchial Artery Angio is negative, still bleeding. Oh, and his PPD is positive. Next
Step ? Pulmonary Artery angio to look for Rasmussen Aneurysms
• Rasmussen Aneurysm identified. Next Step ? Coil embolization (yes coils for hemoptysis
- this is the exception to the rnle).
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Bronchial Artery
The primary indication for pulmonary arteriography is diagnosis and treatment of massive
hemoptysis.
Hemoptysis - Massive hemoptysis (> 300 cc) can equal death. Bronchial artery embolization
is first line treatment (bronchial artery is the culprit 90% of the time). Unique to the lung,
active extravasation is NOT typically seen with the active bleed. Instead you see tortuous,
enlarged bronchial arteries. The main thing to worry about is cord infarct. For multiple
choice the most likely bad actor is the "hairpin-shaped" anterior medullary artery
(Adamkiewicz). Embolizing that thing or anywhere that can reflux into that thing is an
obvious contraindication. If present, those bad boys typically arise from the right intercostal
bronchial trunk.
Particles(> 325 micrometers) are used (coils should be avoided - because if it re-bleeds you
just jailed yourself out).
"Hairpin Turn" of
The vast majority (90%) of theAnterior
bronchial arteries are located Medullary
Artery
within the lucency formed by .
the left main bronchus. This is �
'
right around the T5-T6 Level '
There is a ton of vascular
variation but the pattern of an
intercostobronchial trunk on the
right and two bronchial arteries
on the left is most common
(about 40%}
In the lower thoracic / upper lumbar region the primary feeding artery of the anterior spinal
cord is the legendary anterior radiculomedullary artery (artery of Adamkiewicz). This
vessel most commonly originates from a left sided posterior intercostal artery (typically
between T9-T12) , which branches from the aorta. The distal portion of this artery, as it
merges with the anterior spinal artery, creates the classic (and testable) "hailpin" tum.
It is worth noting that Adamkiewicz can originate from the right bronchus (like 5%).
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Occlusion of Central Veins (SVC Syndrome) -
Yes - I know this really isn't a pulmonary thing, but it is in the chest so I'm going to talk
about it here.
Acute vs Chronic SVC Occlusion:
• Acute = No Collaterals
• Acute = Emergency
• Chronic = Has Collaterals
• Chronic = Not an Emergency
There are a variety of ways to address occlusion of the SVC. The goal is to return in line
flow from at least one jugular vein down through the SVC. Most commonly thrombolysis is
the initial step, although this is rarely definitive. The offending agent (often a catheter)
should be removed if possible. If the process is non-malignant, often angioplasty alone is
enough to get the job done (post lysis).
Technical Trivia:
• Malignant causes: you should do lysis, then angioplasty, then stent.
• Non-malignant causes: may still need a stent if the angioplasty doesn't remove the
gradient (if the collateral veins are still present).
• Self-expanding stents should NOT be used, as they tend to migrate.
• The last pearl on this one is not to forget that the pericardium extends to the bottom part of
the SVC and that if you tear that you are going to end up with hemopericardium and
possible tamponade.
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•
'· · '·. . �
SECTION 15:
REPRODUCTIVE INTERVENTION' �- y:. .·
Uterine Artery Embolization (UAE):
Can be used for bleeding or the bulk symptoms of fibroids. Procedure may or may not help with
infertility associated with fibroid. If you are paying cash.... it definitely helps.
Patient Selection (not all fibroids were created equal). To do this you need a pre-op MRI/MRA to
characterize the fibroids and look at the vasculature.
Subtypes:
• Degenerated leiomyoma are more likely to have a poor response
(these are the ones that don't enhance).
• "Cellular" Fibroids - the ones with high T2 signal tend to respond well to embolization.
Most fibroids "Hyaline Subtype" are T2 dark.
• Smaller lesions do better than larger lesions.
Location:
• Submucosal does the best. Intramural does the second best.
• Serosal does the third best (it sucks). It speaks the third most Italian -
• Cervical fibroids do NOT respond well to UAE -- they have a different blood supply.
• Intracavitmy Fibroids - Less than 3 cm.
o Next Step= GYN referral for hysteroscopic resection
• Intracavitary Fibroids - Less than 3 cm , with failed hysteroscopic resection
o Next Step= IR Embo
• Large Serosal Fibroid, patient wants to be pregnant, no hist01y of prior myomectomy
o Next Step= GYN referral for myomectomy
• Pedunculated Serosal Fibroid
o Next Step= GYN referral for resection
• Broad Ligament Fibroid
o Next Step= Refer to voodoo priest (these don't do well with UAE and are
technically challenging to operate on).
Pedunculated Subserosal
Subserosal
Intracavitary
Pedunculated
Submucosal
Intra
Ligamentary
Submucosal
Intramural
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PreTreatment Considerations I Trivia
• Remember fibroids arc hormone responsive. They grow with estrogen (and really grow during
pregnancy). Gonadotropin-rcleasing medications are often prescribed to control fibroids by
blocking all that fancy hormone axis stuff.
• The testable trivia is to delay embolization for 3 months if someone is on the drugs because
they actually shrink the uterine arteries which makes them a pain in the ass to catheterize.
• The EMMY trial showed that hospital stays with UAE are sho1ier than hysterectomy
• The incidence of premature menopause is around 5%
• DVT / PE is a known risk of the procedure (once pelvic vein compression from large fibroid
releases - sometimes the big PE flies up). The risk is about 5%.
Contraindications: Pregnancy, Uterine/Cervical Cancer, Active Pelvic Infection, Prior Pelvic
Radiation, Connective Tissue Disease, Prior Surge1y with Adhesions (relative)
Treatment Trivia
• Occlusion of small feeding arteries cause fibroid infarction (and hopefully shrinkage). Embolic
material is typically PVA or embospheres for fibroids (targeting the pre-capillary level). If ask to
choose an agent - I'd say "particles" - don't pick coils, or glue. For postpartum hemorrhage /
vaginal bleeding, gel foam or glue is typically used.
• Most people will say either 500-700 micro or 700-900 micron particle sizes. As a point of trivia
smaller particle size does not give you a better result for fibroids -- but can help with
Adenomyosis.
• Treatment of adcnomyosis with UAE is done exactly the same way, and is an effective treatment
for symptomatic relief (although symptoms recur in about 50% of the cases around 2 years post
treatment). As above - slightly smaller paiiicles are typically used for this (vs fibroids).
• Fibroids should reduce volume 40-60% after the procedure. If you are treating intracavitary
fibroids they should turn to mush and come out like a super gross chunky vegetable soup period
mix. You actually want that - if they stay ("retained") inside they can get infected.
Anatomy Trivia:
• Remember the uterine arte1y is off the anterior division of the internal iliac
• Regardless of the fibroid location, bilateral uterine arte1y embolization is necessa1y to prevent
recruitment of new vessels
• In most cases, branches of the ovarian artery feed the fibroids via collaterals with the main
uterine artery. Uterine arte1y can be identified by the characteristic "corkscrew" appearance of
its more disc branches -- named the Helicine branches (twisty like a helix)
Ovarian
Twisty "Corkscrew"
Vaginal A. Helicine Branches
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Uterine Artery Embolization Continued:
Post Embo/ization Syndrome: I mentioned this earlier but just wanted to remind you that it's
classically described with fibroid embolization. Remember you don't need to order blood cultures
without other factors to make you consider infection. The low-grade fever should go away after 3
days. Some texts suggest prophylactic use of anti-pyrexial and antiemetic meds prior to the
procedure.
• 3 Days or less with low grade fever = Do nothing
• More than 3 Days with fever = "Work it up" , cultures, antibiotics, etc...
Hysterosalpingogram (HSG):
I'm 100% certain no one went into radiology to do these things. You do it like a GYN exam. Prep
the personal area with betadine, drape the patient, put the speculum in and find the cervix. There
are various methods and tools for cannulating and maintaining cannulation of the cervix (vacuum
cups, tenaculums, balloons). Insertion of any of these devices is made easier with a catheter and
wire. Once the cervix and endometrial cavity have been accessed, the contrast is inserted and
pictures are obtained.
Contraindications: Pregnancy, Active Pelvic Infection, Recent Uterine or Tubal Pregnancy.
Trivia:
• The ideal time for the procedure is the proliferative phase (day 7-14), as this is the time the
endometrium is thinnest (improves visualization, minimizes pregnancy risk).
• It's not uncommon for a previously closed tube to be open on repeat exam (sedative, narcotics,
tubal spasm - can make a false positive).
• Air bubbles can cause a false positive filling defect.
• Intravasation - The backflow of injected contrast into the venous or lymphatic system, used to
be an issue during the Jurassic period (when oil based contrast could cause a fat embolus). Now
it means nothing other than you may be injecting too hard, or the intrauterine pressure is
increased because of obstruction.
• The reported risk ofperitonitis is 1%.
Fallopian Tube Recanalization (FTR):
Tubal factors (usually PID/ Chlamydia) are responsible for about 30% of the cases in female
infertility ~ depending on what part of the country you are from sometimes much more (insert joke
about your hometown here). Tubal obstruction comes in two flavors; proximal/ interstitial, or
distal. The distal ones get treated with surgery. The proximal ones can be treated with an
endoscope or by poking it with a wire under fluoro.
Things to know:
• You should schedule it in the follicular/proliferative phase (just like a HSP) - day 6-12ish.
• You repeat the HSG first to confirm the tube is still clogged. If clogged you tty and unclog it
with a wire ( "selective salpingography ").
• Hydrophilic 0.035 or 0.018 guidewire (plus/ minus microcatheter) is the typical poking tool
• Repeat the HSG when you are done to prove you did something
• Contraindications are the same as HSG (active infection and pregnancy)
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Pelvic Congestion Syndrome
- Women have mystery pelvic pain. This is a real (maybe) cause of it. They blame dilated
ovarian and periuterine veins in this case, and give it a name ending in the word "syndrome" to
make it sound legit. The symptoms of this "syndrome" include pelvic pain, dyspareunia,
menstrual abnormalities, vulvar varices, and lower extremity varicose veins. The symptoms
are most severe at the end of the day, and with standing.
Diagnosis ? Clinical symptoms+ a gonadal vein diameter of 10 mm (normal is 5 mm).
Treatment ? GnRH agonists sometimes help these patients, since estrogen is a vasodilator. But
the best results for treatment of this "syndrome" are sclerosing the parauterine venous plexus,
and coils/plugs in the ovarian and internal iliac veins (performed by your local Interventional
Radiologist). This is often staged, starting with ovarian veins plugged first, and then (if
unsuccessful) iliac veins plugged second.
Trivia: Most optimal results occur when the entire length of both gonadal veins are embolized.
Complications ? Complications are rare but the one you worry about is thrombosis of the
parent vein (iliac or renal), and possible thrombus migration (pulmonary embolism).
Will it get better on its own ? The symptoms will classically improve after menopause.
Varicocele
-They are usually left-sided (90%), or bilateral (10%). Isolated right-sided varicoceles should
prompt an evaluation for cancer (next step = CT Abd).
When do you treat them? There are three indications: (1) infertility, (2) testicular atrophy in a
kid, (3) pain.
Anatomy Trivia (regarding varicoceles): Remember that multiple venous collaterals
"pampiniform plexus" or "spermatic venous plexus" drain the testicles. Those things come
together around the level of the femoral head, forming the internal spermatic vein. The left
internal spermatic vein drains into the left renal vein, and the right internal spermatic vein
drains into the IVC. Common variants include: multiple veins on the right tern1inating into the
IVC or renal vein, or one right-sided vein draining into the renal vein (instead of the IVC).
Why Varicoceles Happen: The "primary factor" is right angle entry of the left spermatic vein
into the high pressure left renal vein. Nut-cracker syndrome (compression of the left renal vein
between the SMA and aorta) on the left is another cause (probably more likely asked).
Basic Idea: You get into the renal vein and look for reflux into the gonadal vein (internal
spermatic) which is abnormal but confirms the problem. You then get deep into the gonadal
vein, and embolize close to the varicocele (often with foam), then drop coils on the way back,
and often an Amplatzer or other occlusion device at the origin.
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SECTION 16:
MISC TOPICS "\, � ., .. ,_.·
,' ',
Vertebroplasty
There is a paper in the NEJM that says this doesn't work. Having said that, NEJM doesn't like
any procedures. They're run by family medicine doctors. They are equally amoral to the
person that will do any non-indicated procedure. Regardless of the actual legitimacy, it's a big
cash cow and several prominent Radiologists have made their names on it. . . so it will be
tested on as if it's totally legit and without controversy.
Trivia to Know:
• Indications = Acute to subacute fracture with pain refractory to medical therapy or an
unstable fracture with associated risk if further collapse occurs.
• Contraindications = Fractures with associated spinal canal compression or improving
pain without augmentation.
• There is a risk of developing a new vertebral fracture in about 25% of cases. The
literature says you should "counsel patients on the need for additional treatments
prior to undergoing vertebroplasty. ".
• The cement can embolize to the lungs.
• Risk of local neurologic complications are about 5%.
Lymphangiogram:
1950 called and they want to stage this cancer. Prior to CT, MRI, and US injecting dye into
the toes was actually a way to help stage malignancy (mets to lymph nodes, lymphoma, etc..).
Another slightly more modem application is to use this process as the first step in the
embolization of the thoracic duct. Why would you take down the thoracic duct? If it's
leaking chylous pleural effusions - status post get hacked to pieces by a good for nothing
Surgery Resident.
Technical Trivia:
This is done by first injecting about 0.5 cc methylene-blue dye in between the toes bilaterally.
You then wait half an hour until the blue lymphatic channels are visualized. You then cut
down over the lymphatic channels and cannulate with a 27 or 30 gauge lymphangiography
needle. An injection with lipiodol is done (maximum 20 ml if no leak). If you inject too
much there is a risk of oil pneumonitis. You take spot films in a serial fashion until the
cisterna chyli (the sac at the bottom of the thoracic duct) is opacified. At that point you could
puncture it directly and superselect the thoracic duct to embolize it, typically with coils.
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Standing Waves:
Standing waves are an angiographic phenomenon (usually) that results in a ringed layering
of contrast that sorta looks like FMD. A common trick is to try and make you pick between
FMD and Standing Waves.
Obviously it's bullshit because in real life standing waves typically resolve prior to a
second run through the same vessel, and even if they stayed around they tend to shift
position between each run (up or down). FMD on the other hand is an actual physical
irregularity of the vessel wall so it's fixed between runs and doesn't go away.
Morphology should be your strategy.for multiple
choice:
Standing waves are very symmetric and evenly
spaced.
FMD is more irregular and asymmetric.
Standing Waves FMD
"The Lingo"
"Give me a 10 x 6 Balloon" - This means a 10 mm diameter x 6 cm length balloon
"Give me 20.for 30" - This means do an angio run at 20 cc/sec for a total of 30 mL.
"Squirted" - An Angiogram - Oh really? A splenic lac with active extrav? Let's call IR
right away and get him squirted.
"Thrash" - A difficult case
"Hot Mess" - I have an admit for you. This lady is a hot mess.
"That poor lady" - A way of feigning sympathy.
"Sick as Stink" - also, "sick AND stinks" be careful not to mess this up.
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Artery of Interest C Arm Angulation Misc
Aortic Arch 70 Degrees LAO "Candy Cane"
Innominate (Right Subclavian RAO In the LAO the right
& Right Common Carotid) subclavian and right
common carotid overlap
Left Subclavian LAO --
Mesenteric Vessels Lateral to Steep RAO --
Left Renal LAO Same side as renal
Right Renal RAO or LAO- This is controversial - a
depending on who you lot of sources will say
ask. you can get away with
LAO.
Left Iliac Bifurcation RAO Opposite side common
Right Iliac Bifurcation LAO Opposite side common
Left Common Femoral Bifurcation LAO Ipsilateral Oblique
Right Common Femoral Bifurcation RAO Ipsilateral Oblique
The Confusing Oblique Views
Normally, views are defined by the direction of the x-ray beam.
However, in Angio it gets a little squirrely. The sidedness refers to the side of the I. I.
RAO: The LAO: The
imaging imaging
intensifier is intensifier is
on the right on the left
side of the side of the
patient. patient.
A reasonable A reasonable
person might person might
call this LPO call this RPO
- but they - but they
would be would be
wrong. wrong.
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Superficial or Deep? - Understanding Geometry
Sometimes it's difficult to tell if you are superficial or deep to the lesion you are trying to
put a needle in under fluoro. You can problem solve by tilting the I.I. towards the patient's
head or towards the patient's feet.
If you tilt towards the head, a superficial needle will be shorter but a deep needle will look
longer.
If you tilt towards the feet, a superficial needle will be longer but a deep needle will look
shorter.
Arrow = Needle
Image Receptor
e
< ~
+----
8
C
I.I. tilted towards
I.I. tilted towards
patients feet:
patients head:
• Superficial Needle
Superficial Needle
looks longer
looks shorter
,<,,...,.......... • Deep Needle looks
• Deep Needle looks
shorter
longer
Air Embolus
Classic Clinical Buzzwords: "Sudden onset shortness of breath" "Whoosh sound" or
"Sucking sound" during central catheter insertion.
Next Step: "Durant's maneuver"= left-lateral decubitus + head-down positioning. Other
verbiage = "right side up" or "left side down", "trendelenburg"
Next Next Step: 100% Oxygen
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Medications:
Anti-Coagulation Issues:
• Remember that Platelets Replace Platelets.
• Cryoprecipitate is used to correct deficiencies of fibrinogen.
• Heparin: The half life is around 1.5 hours. Protamine Sulfate can be used as a more
rapid Heparin Antidote.
• Protamine can cause a sudden fall in BP, Bradycardia, and flushing
• Coumadin: Vitamin K can be given for Coumadin but that takes a while (25-50mg IM
4 hours prior to procedure), more rapid reversal is done with factors
(cryoprecipitate).
• Remember that patients with "HIT" (Heparin Induced Thrombocytopenia) are at
increased risk of clotting - not bleeding. If they need to be anti-coagulated then they
should get a thrombin inhibitor instead (remember those end in "rudin" and "gatran").
• The Life Span of a Platelet is 8-10 days
• IV Desmopressin can increase factor 8 - may be helpful of hemophilia
Medication Mechanism Trivia
Inhibits thromboxane A2 Irreversible - works the life
Aspirin from arachidonic acid by an of the platelet (8-12 days).
irreversible acetylation
Binds antithrombin 3 - and Monitored by PTT. Can be
Heparin increases its activity. reversed with protamine
sulfate
Inhibits the binding of ADP
Plavix (Clopidogrel) to its receptors - leads to --
inhibition of GP Ilb/Illa
Inhibits vitamin K Monitored by INR. Delay
dependent factors (2, 7 ,9, 10) in onset of activity (8-12
hours). Action can be
Coumadin antagonized by vitamin K
but this takes time (4 hours).
For immediate reversal give
factors (cryopercipitate)
Act directly or indirectly to TPA has a ve1y short
Thrombolytic Agents
convert plasminogen to biologic half life - between
(TPA)
plasmin (cleaves fibrin) 2-10 mins.
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ACR Appropriate:/ SIR Practice Guide: Pre-Procedure Hold
-For procedures with a MODERATE risk of bleeding (liver or lung biopsy, abscess
drain placement, vertebral augmentation, tunneled central line placement)
-INR should be corrected to < 1.5 prior to the procedure.
-Aspirin need not be held,
-Clopidogrel (plavix) should be held for 5 days.
-Platelet count should be more than 50,000.
Sedation Related:
• "Conscious Sedation" is considered "moderate sedation", and the patient should be
able to respond briskly to stimuli (verbal commands, or light touch). No airway
intervention should be needed.
• Flumazenil is the antidote for Versed (Midazolam).
• Narcan is the antidote for Opioids (Morphine, Fentanyl).
Local Anesthesia (Lidocaine)
• Maximum Dose is 4-5 mg/kg
• A dirty trick would be to say - "Lido with Epi" - in which case it is 7 mg/kg
• Some basic scrub nurse math:
• 1 % Plain Epi - 10 mg per 1 mL
• So 1 mg per 0.l mL
• And we said Maximum Dose is 5 mg/kg, so it would be equal to 0.5 mL / kg
• Remember that small doses in the right spot can cause a serious reaction.
• 150 mg in the thecal sac can cause total spine anesthesia and the need for a
ventilator.
• Direct arterial injection can cause immediate seizures.
• Tinnitus and dizziness are the earliest signs of toxicity.
• Local anesthesia agents have a low potential for allergy - although it can still occur, it's
usually a bogus allergy once a real history is taken. Most "allergies" to lidocaine are
actually vaso-vagal, or other CV side effects from epinephrine mixed with lidocaine
• There are elaborate mechanisms for testing for a true allergy, or reaction to
methylparaben (a preservative).
• So what if the allergy is real? or you can't prove it's false? - Some texts describe using
an antihistamine such as diphenydramine (which can have anesthetic properties).
Green, Steven M, Steven G. Rothrock, and Julie Gorchynski. "Validation of diphenhydramine as a dermal
local anesthetic." Annals ofemergency medicine 23.6 (1994): 1284-1289.
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Indications Contraindications
Only one absolute which is an
unstable patient with multisystem
dysfunction (unless angio is life
Numerous; usually saving).
Angiography diagnosis of and treatment
of vascular disease There are numerous relatives
including inability to lay flat,
uncooperative patient, and connective
tissue diseases
Diagnosis of DVT,
Ascending Evaluate Venous
Venography malformation or tumor
encasement.
Evaluation of post-
Contrast Reaction
Descending thrombotic syndrome;
Venography valvular incompetence and
Pregnancy
damage following DVT
Thoracic Outlet Severely compromised
Venography Syndrome, Venous cardiopulmonary status
(Non-inclusive) Access, Pacer Placement,
Eval for fistula
Can't get anticoagulation,
Failed anticoagulation Total thrombosis of IVC
(clot progression),
Massive PE requiring IVC too big or too small
IVC Filter
lysis, Chronic PE treated
with *Sepsis is NOT a contraindication,
throm boendarterectomy. including septic thrombophlebitis
Trauma high risk DVT
Absolute: Right to left
cardiopulmonary shunt, Uncorrectable
Making the nephrologist coagulopathy, fistula infection.
Fistulography money ("slow flows" they
call it). Relative is significant
cardiopulmonary disease (a declot
invariably causes PE)
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Indications Contraindications
Absolute: Heart Failure (especially
Variceal bleeding
right heart failure). Severe
TIPS refractory to endoscopy.
encephalopathy. Rapidly progressing
Refractory ascites.
liver failure.
Performed prior to Absolute: Uncorrectable
Percutaneous percutaneous biliary Coagulopathy, Plavix or other anti-
Transhepatic interventions, platelet agent
Choledochojejunostomy
Cholangiography
patients (liver transplant) Relative: Large Volume Ascites
(PTC)
with suspected (consider para and left sided
obstruction approach)
No absolute contraindications
Basically CBD
Percutaneous obstruction (with failed
Relative: Large Volume Ascites
Biliary Drainage ERCP), cholangitis, bile
(consider para and left sided
duct injury/leak.
approach), Coagulopathy
Cholecystitis in patients
who are not surgical
candidates, Unexplained
No absolute contraindications
sepsis when other
Percutaneous sources excluded, Access
Relative: Large Volume Ascites
Cholecystosomy to biliary tree required
(consider para and left sided
and other methods failed
approach), Coagulopathy
Obstructive Uropathy
(Not hydronephrosis),
Percutaneous Urinary diversion (leak, Uncorrectable coagulopathy,
Nephrostomy fistula), Access for Contrast Reactions
percutaneous
intervention
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Blank for Scribbles
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,1. 1�1�
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PROMETHEUS LIONHART, M.D.
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A Brief Overview - For the complete novice:
Many foreign graduates have had little or no experience with mammography. I'll try and give you a
ve1y brief overview before I get into the testable trivia.
In America, women are told they need to have screening mammograms done once a year. Because
breast cancer is common (and scaty), most women will get this done, and will continue to get it
done into their 90s. They will literally take people from the ICU who are in cardiogenic shock
down to x-ray to keep them up to date on their screening manunograms (usually at the patient's
request).
I want you to think about mammograms in two categories: (a) the screener - these are the people
who are coming in once a year, and have no symptoms other than being female, and (b) the
diagnostic - these people have a symptom (palpable lump, nipple discharge, breast pain, etc..).
These two are handled totally different.
Nomenclature is rigidly controlled with regard to reporting. "BI-RADS" is a book of approved
vocabulary words for describing the findings, and a system for reporting results based on a
percentage of risk. The basic idea is that you use scary words like "spiculated" to describe things
you think are cancer, and benign words like "fat density" to describe things you think are not cancer.
Here are some basic scenarios - I'll explain all the stuff in the chapter and we can revisit some more
scenarios at the end of the chapter. This is just for you to get a feel for how this works if you have
never been around it before. Don't spaz if you are lost, it will be clear by the end of the chapter and
then we will do them again with some quizzing.
( l a) A 50 year old women comes in for a normal annual screening mammogram. She has no
symptoms, and is just following the recommendation. She gets two standard views - a cranial caudal
view "CC" and a medial lateral oblique view "MLO." The Radiologist is in a hurry because he has
200 of them to read, so he just calls it normal (Bi-Rads 1 ). The patient returns to the screening pool
- and will get imaged again in 1 year. She is relieved to know she doesn't have cancer.
(1 b) The same 50 year old returns 1 month later after she feels a lump. This is no longer a screening
study but instead a "diagnostic" because she has a symptom. She gets another mammogram - this
time with a palpable marker on the image. She also gets compression spot views (smaller paddle)
over the palpable area. In the area of the palpable finding, there is a cluster of calcifications. They
were present in retrospect on the mammogram performed 1 month prior, but are new from the year
before. Because they are calcifications you need magnification views to fully characterize them. On
the mag views you describe them as "coarse heterogeneous." Because they are new from the prior
year they must be biopsied, but you aren't done yet. Diagnostic mammogram usually includes an
ultrasound - not because of the calcifications but because there was a palpable finding. Just
remember no FEMALE with a palpable gets out the door without an ultrasound. You ultrasound the
area and fmd no mass. The next step is to biopsy the calcs (which are BR-4, for intermediate
suspicion). You recommend stereo to biopsy them (NOT ultrasound) because you couldn't see
them with ultrasound. The results yield fibrocystic change, which you agree is a possibility given
the BR-4. When you agree that the biopsy results make sense with the imaging/ clinical scenario
you use the word "concordant. " "The results were concordant" said the Resident to his Attending.
You inform the patient of the results. She is relieved to know she doesn't have cancer.
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(2) A 60 year old women comes in for a 1101mal annual screening mammogram. She has no
symptoms, and is just following the recommendation. She gets two standard views - a cranial
caudal view "CC" and a medial lateral oblique view "MLO." The Radiologist is in a hurry
because he has 200 ofthem to read, but still manages to see a new mass in the medial breast on
the CC view. The breasts are pretty dense and it's hard to find it in on the MLO. So the
Radiologist calls it an "asymmetry" and BR-0 (BR-0 because more work up is needed). The
patient returns in a week for a diagnostic study - she is convinced that she's gonna die ofbreast
cancer. You can hear her crying in the waiting room. She gets a diagnostic study with spot
compression over the mass on the CC view, as well as ML and MLO views. You do manage to
see the mass on the CC and in the superior breast on the ML view. The mass is well
circumscribed, round, and equal density. Because she is getting a diagnostic work up, she gets an
ultrasound too. Before you go in the ultrasound room you guess about where the mass is going to
be. Since it's medial and superior on the right breast you guess 2 o'clock. You locate it quickly,
and find it to be an anechoic cyst - common in women going into menopause. You tell her it's
consistent with a benign cyst. She cries with joy and thanks you repeatedly for "saving her life."
She sends you cookies and brownies every year at Christmas with very long letters about how you
saved her. She uses a lot ofreligious references that make you uncomfortable. Some years you
throw the food away without eating it, other years you give it to the techs. The simple cyst was
reported as a BR-2 (essentially 0% chance ofcancer).
(3) A 45 year old woman comes in for a normal annual screening mammogram. She has no
symptoms and is just following the recommendation. She gets the two standard views - "CC" and
"MLO." The Radiologist is in a hurry because he has 200 ofthem to read, but still manages to see
a new mass in both the MLO and CC views. Because this is a screener he still has to give it a
BR-0 (you never BR-4 or BR-5 off a screener). She returns for additional imaging as a diagnostic
patient with spot compression views. A spiculated, irregular, high density mass is seen. She is
placed in an ultrasound room for further characterization. The ultrasound shows an irregular,
circumscribed, anti-parallel, hypoechoic mass, with posterior shadowing and an echogenic halo
(all the scary bad words). You are certain the mass is a cancer based on these features so you scan
the rest ofher breast looking for other tumors, and you look in her axilla for abnormal nodes. You
find several enlarged lymph nodes in her axilla. You recommend ultrasound guided biopsy of
both the mass and the most suspicious lymph node. You give her a BR-5 (>95% chance of
cancer). The biopsy results come back as fibrocystic change. This result is not "concordant" with
the findings you made on mammography and ultrasound so you instead use the word
"discordant" and recommend surgical excision. "The results were discordant" said the Resident
to his Attending. Gross path shows a high grade invasive lesion.
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"
....
...
····
�
SECTION 1:
ANATOMY �
• .
Nipple: The nipple is a circular smooth muscle that overlies the 4th intercostal space. There
are typically 5-10 ductal openings. Inversion is when the nipple invaginates into the breast.
Retraction is when the nipple is pulled back slightly. They can both be normal if chronic. If
they are new, it should make you think about underlying cancers causing distortion. The
nipple is supposed to be in profile so you don't call it a mass. The areola will darken
normally with puberty and parity. Nipple enhancement on contrast enhanced breast MRI is
normal , don't call it Pagets!
Fibroglandular Tissue: The breast mound is fibrous
tissue with fat, ducts, and glands laying on top of the
anterior chest wall. The axillary extension is called the
"tail of Spence." The upper outer quadrant is more
densely populated with fibroglandular tissue, which is
why most breast cancers start there. There is usually no
dense tissue in the medial/ inferior breast and
retroglandular regions. These are considered "danger
zones" and are often where the cancer hides.
Danger Zones - where there is
usually no dense fibroglandular
tissue
Cooper's Ligaments: These are thin sheets of fascia
that hold the breasts up. They are the tiny white lines on mammography and the echogenic
lines on US. Straightening and tethering of the ligaments manifests as "architectural
distortion" which occurs in the setting of surgical scars, radial scars, and IDC.
Breast Asymmetry: This is common and normal (usually), as long as there are no other
findings (lumps, bumps, skin thickening, etc.. ). For multiple choice, an asymmetric breast
should make you think about the "shrinking breast" of invasive lobular breast cancer. If the
size difference is new or the parenchyma looks asymmetrically dense, think cancer.
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Lobules: The lobules are the flower shaped milk makers of the breast. The terminal duct
and lobule are referred to as a "tenninal duct lobular unit" or TDLU. This is where most
breast cancers start.
Lactiferous Sinus
Major Duct
Lobules
Ducts: The ductal system branches like the roots or branches of a tree. The branches overlap
wide areas and are not cleanly segmented like slices of pie. The calcifications that appear to
follow ducts ("linear or segmental") are the ones where you should worry about cancer.
Lactiferous Sinus: Milk from the lobules drains into the major duct under the nipple. The
dilated portion of the major duct is sometimes called the lactiferous sinus. This thing is
n01mal (not a mass).
Blood Supply/ Lymphatic Drainage: The majority (60%) of blood flow to the breast is via
the internal mammary. The rest is via the lateral thoracic and intercostal perforators. Nearly
all (97%) of lymph drains to the axilla. The remaining 3% goes to the internal mammary
nodes.
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Axillary Node Levels: The axilla is sub-divided into three separate levels using the
pectoralis minor muscle as a landmark. Supposedly drainage progresses in a step wise
fashion - from level 1 -> level 2 -> level 3 and finally into the thorax.
Rotter Nodes: These are the nodes between the pee minor and major. They have a fancy
name which usually makes them high yield. However, Rotter was German and test writers
tend to prefer French sounding trivia. The only exception to this is Nazis. German sounding
medical vocab words named after Nazis are fair game. To save you the trouble of looking it
up - Rotter died before Hitler took power so he wasn't a Nazi (probably). Since they
probably aren't gonna ask the vocab word, the only other conceivable piece of trivial can
imagine being asked would be that these are at the same level as level 2.
Axillary Lymph Node Levels
Level 1 : Lateral to Pee Minor
Level 2: Deep to the Pee Minor
Level 3: Medial and Above Pee Minor
Rotter Node: Between the Pee Minor and Major
Metastasis to the Internal Mammary Nodes: If you can see them on ultrasound they are
abnormal. Isolated mets to these nodes is not a common situation (maybe 3%). When you
do see it happen, it's from a medial cancer. More commonly, mets in this location occur after
disease has already spread into the axilla (in other words - it's spreading everywhere).
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Sternalis Muscle: This is an Aunt Minnie. It's a non-functional muscle next to the sternum
that can simulate a mass. About 5% of people have one and it's usually unilateral.
Sternalis - Only on CC, Never on MLO
The main testable trivia is:
I. WTF is that?- Recognize the Aunt Minnie, and don't get tricked into doing a biopsy on
it, etc ...
2. How You See It? It is ONLY SEEN ON THE CC VIEW.
Handling this in real life is all about the old gold. Find that thing on the priors (even better is
a CT) , CC only, never on the MLO.
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Breast Development:
The "milk streak" is the embryologic buzzword to explain the location of the normal breast
and location of ectopic breast tissue. Just know that the most common location for ectopic
breast tissue is in the axilla (second most common is the inframammary fold). Extra
nipples are most commonly in the same locations (but can be anywhere along the "milk
streak"). At birth, both males and females can have breast enlargement and produce milk
(maternal hormones). As girls enter puberty, their ducts elongate and branch (estrogen
effects), then their lobules proliferate (progesterone effects). If you biopsy a breast bud
(why would you do that?) you could damage it and potentially fuck up breast
development.... and then get sued.
• Follicular Phase (day 7-14): Estrogen Dominates. Best time to have both
mammogram and MRI.
• Luteal Phase (day 15-30): Progesterone Dominates. This is when you get some
breast tenderness (max at day 28-30). Breast density increases slightly.
• Pregnancy: Tubes and Duct Proliferate. The breast gets a lot denser (more
hypoechoic on US), and ultrasound may be your best bet if you have a mass.
• Perimenopausal: Shortening of the follicular phase means the breast gets more
progesterone exposure. More progesterone exposure means more breast pain, more
fibrocystic change, more breast cyst formation.
• Menopause ("The Floppy Stage''): Lobules go down. Ducts stay but may become
ectatic. Fibroadenomas will degenerate (they like estrogen), and get their "popcorn"
calcifications. Secretory calcifications will develop (*but not for 15-20 years post
menopause).
• Hormone Replacement Therapy: Breasts get more dense (especially estrogen
progesterone combos). Breast pain can occur, typically peaking in the first year.
Fibroadenoma (who like to drink estrogen) can grow.
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High Yield Trivia Regarding Breast Anatomy / Physiology
• The nipple can enhance with contrast on MRI. This is normal (not Pagets).
• Most cancers occur in the upper outer quadrant.
• Most cancers start in the terminal duct lobular unit (TDLU).
• Majority (60%) of blood flow is via the internal mammary.
• Mets to the Internal Mammary Nodes are uncommon (3%)- seen in medial cancers.
• Axillary Node Levels (1, 2, 3 - lateral to medial)
• Sternalis is usually unilateral, and only on the CC, NEVER on MLO.
• Breast Tenderness is max around day 27-30.
• Mammography and MRI are best performed in the follicular phase (days 7-14).
• Don't Biopsy a prepubescent breast- you can affect breast development
• Perimenopause (50's) is the peak time for breast pain, cyst formation
• Fibroadenomas will degenerate (buzzword popcorn calcification) in menopause
• Secretory Calcifications (buzzword "rod-like) will develop 10-20 years post
menopause
Whatcha You Know About Lactation?
Loaded.fa-Jo on the low where the cheese at?
Density: As mentioned above, the breast gets a lot denser in the 3rd trimester.
Mammograms might be worthless, and ultrasound could be your only hope. In other
words, ultrasound has greater sensitivity than mammo in lactating patients.
Density Trick: Pituitary Prolactinoma, or meds (classically antipsychotics) can create a
similar bilateral increased density.
Biop,sy: You can biopsy a breast that is getting ready to lactate/ lactating - you just need
to know there is the risk of creating a milk fistula. If you make one, they will have to
stop breast feeding to stop the fistula. The fistula can get infected, but that's not very
common.
Galactocele: This is one of those "benign fat containing lesions" that you can BR-2.
This is typically seen on cessation of lactation. The location is typically sub-areolar. The
appearance is variable, but can have an Aunt Minnie look with a fat-fluid level. It's
possible to breast abscess these things up.
Lactating Adenoma: These things look like fibroadenomas, and may actually be a
charged up fibroadenoma (they like to drink estrogen). Usually these are multiple. If
you get pressed on follow up recommendation for these I would say 4-6 months
postpartum, post delivery or after cessation of lactation -via ultrasound. They usually
rapidly regress after you stop lactation.
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•
.
•
.
• •
� SECTION 2:
TECHNIQUE & ARTIFACTS �-
Basics: As I mentioned in the introduction, a screening mammogram starts with two standard
views; a cranial caudal view and a medial lateral oblique view.
Technically Adequate?
The first step in reading a mammogram is verifying that the technique is satisfactory. For the
purpose of multiple choice there are a few easy ways to test this.
Cranial Caudal View "CC" Medial Lateral Oblique View "MLO"
The Posterior Nipple Line - this is drawn on the MLO from the nipple to the chest wall.
You need to touch pectoralis muscle to be adequate.
Then on CC, you draw a line from the
nipple back towards the chest wall.
To be adequate you must be within 1
cm of the length of the posterior
nipple line.
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Technically Adequate Cont.
So other points and trivia:
• Ideally, the inframammary fold should be visualized
• "Camel Nose" is the buzzword used to describe a breast on MLO that has not be pulled
"up and out" by the tech
• The nipple should be in profile in one of two views (to avoid missing the subareolar
cancer).
• Relaxed pectoralis muscles are preferred ( convex, instead of concave) - showing more
breast tissue.
Positioning Trivia:
When do you get a LMO view? The MLO is the standard, but sometimes you need a LMO.
The answer is women with kyphosis or pectus excavatum. Or to avoid a medial
pacemaker / central line.
MLO View Trivia: The MLO view contains the most breast tissue of all the possible views
When using Spot Compression Views: A big point is the recommendation to leave the
collimator open, giving you a larger field of view, and helping to ensure that you got what
you wanted to get. Small paddles give you better focal compression. Large paddles allow
for good visualization of land marks.
When using Magnification Views: A CC and ML (true lateral) are obtained. You get a ML
(as opposed to a MLO) to help catch milk of calcium.
When using a True Lateral View ML vs LM: Using a true lateral is useful for localizing things
seen on a single view only (the CC). A trick I use is whatever I said on the screener, is the
last letter I'd use on the call backs. In other words, if it's Lateral on the screener you want an
ML on the diagnostic. If it's Medial on the screener then you want a LM on the diagnostic.
The reason is that you are moving it closer to the receptor. If you see the area of interest on
the MLO only (not the CC), you should pick ML- because most (70%) breast cancers
occur laterally. --- This would make a good multiple choice question.
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• Primary Image • Pectoral Motion Artifacts Predominates at the
View Muscle should Inferior Part of the Breast (especially in
be seen to the wrinkly floppy stinky saggy ones)
• Maximized Level of the secondary to a lack of compression.
Visualization of Nipple
Mediolateral the Axillary and The "sweep
Oblique View Posterior Tissue • Pectoral up and out"
{MLO) Muscle should technique is
be Relaxed used by techs
(convex to reduce
anterior artifact in this
border) location.
• Primary Image • Should have a small amount of If you lack adequate
View skin at the most medial aspect coverage at the
to confirm adequate coverage posterior lateral edge or
• Ideally axillary tail the next
Craniocaudal maximizes the • Chest wall to nipple should be appropriate step is an
View (CC) posterior medial within 1 cm of the chest wall to exaggerated lateral CC
tissue (the spot pectoral muscle on the MLO. view (XCCL).
that can be
missed on the
MLO)
90 degree view 90 degree view
Can be used to
Can be used to triangulate (medial to
triangulate (medial to
the nipple lesions will rise on the true
the nipple lesions will
lateral - "muffins rise")
rise on the true lateral
Mediolateral Lateromedial "muffins rise")
Shows the lateral breast (the one
(ML) (LM)
closest to the detector) in better detail Shows the medial breast
in better detail.
Remember the posterior
medial breast is the
toughest is image.
Q: Conan! What is Best in Lffe ? A: To crush your enemies, and see them driven before you
Q: Conan! What is Best . . . View Given the Following Circumstances ?
"Nodule" seen only in CC View Rolled CC
"Nodule" favored to be in the skin Tangential (TAN)
"Nodule" favored to be milk of calcium True Lateral
"Nodule" in the far posterior medial breast Cleavage View (CV)
"Eklund Views" or
Breast Implants
Implant Displaced (MLOID, CCID)
Calcifications Magnification View
Yes, I'm using the term "nodule" deliberately to annoy academic breast imagers who hate that word.
Never pick the word "nodule" on the exam !
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Basic Artifacts:
Blur: Can be from breathing or inadequate compression (typically along the inferior breast
on the MLO). It can be tricky to pick up. The strategy I like to use is to look at Cooper's
Ligaments - they should be thin white lines in the fat. Ifthey are thick or fuzzy - it is
probably blur (or edema). lfthere is skin thickening, think edema.
You see blur in 3 scenarios
( l) patient moved,
( 2) exposure was too long,
( 3) exposure was too short.
Blur: "Coopers are too thick"for normal skin
Grid Lines: Basically mammograms always use a grid (unless it's a mag view). That
would make a good multiple choice question actually. No grid on mag views. So, the grid
works by moving really fast, and only keeping x-rays that move straight in.
Grid Lines: 3 Examples - "Horizontal Lines"
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•
-
•
. •
� SECTION 3:
LOCALIZATION � • •'. ·
You are trying to find around 3-8 cancers
per 1000 mammograms. Another way to
ask this is to say that you are supposed to
have a Positive Predictive Value (PPV 1)
of around 4% (in other words anything
other than a BRl or BR2 on a screener).
This is demanded by the various
regulating bodies.
',
Be aware that certain areas can sometimes
only be seen on a single view. For
example, the medial breast on a CC may
not be seen on MLO, and the Inferior
t-''
Posterior Breast on MLO may be I
excluded from the CC. That makes these Medial Breast
areas "high risk" for missing a cancer. - Can be excluded on Inferior Posterior
the MLO View Breast
- Can be excluded on
the CC View
It's recommended to look at mammograms from 2 years prior (if available) for comparison.
Makes it a little easier to see early changes.
Localizing a lesion (only seen in the MLO view): This is a very basic skill, but if you had
absolutely no interest in mammography or just terrible training, a refresher might be useful as
this is applicable to multiple choice tests. A lesion that is seen in the MLO only will rise on the
true lateral (ML) if it is medial on the CC film. A lesion that is seen on the MLO only will fall
on the true lateral (ML) if it is lateral on the CC film. The popular mnemonic is "Lead Sinks,
and Muffins Rise" - L for lateral, and M for medial.
"Muffins
ML "Lead MLO cc
Sinks"
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Localizing a lesion (only seen in the CC view): Sometimes you can only see the finding in
the CC view. If you want to further characterize it with ultrasound, figuring out if it's in the
superior or inferior breast could be very helpful. One method for doing this is a "rolled CC
view."
Rolled CC View: This works by positioning the breast for a CC view, but prior to placing the
breast in compression you rotate the breast either medial or lateral along the axis of the
nipple. Your reference point is the top of the breast.
• If you roll the breast medial; a superior tumor will move medial, an inferior tumor will
move lateral.
• If you roll the breast lateral; a superior tumor will move lateral, an inferior tumor will
move medial.
In other words, superior tumors move in the direction you roll and inferior tumors move
in the opposite direction you roll. The "superior" vs "inferior" is inferred based on how it
moves when you (the tech) roll the boob.
------1 �
Cancer in superior breast
only seen in CC view
�_,
Rolled Medially CC view,
moves the cancer medial
1® Rolled Laterally CC view,
moves the cancer laterally
____, I �
Cancer in inferior breast
only seen in CC view
.......,_______, I
Rolled Medially CC view,
moves the cancer lateral
i,,f
Rolled Laterally CC view,
moves the cancer medially
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� SECTION 4:
Bl-RADS
.
'.
..
.• ·.• ····
.
BI-RADS is an acronym for Breast Imaging-Reporting and Data System. It was developed
by the ACR to keep everyone on the same page, in a similar way the DSM was developed for
psych. You can't have people just calling stuff "breast nodules".
• BI-RADS Assessment Categories:
0: Incomplete
1: Negative
2: Benign finding(s)
3: Probably benign - < 2% Chance of CA
4: Suspicious abnormality - 2 - 95% Chance of CA
• Some people use 4a (low suspicion), 4b (intermediate suspicion), and 4c
(moderate suspicion).
5: Highly suggestive of malignancy - > 95% Chance of CA
6: Known biopsy -proven malignancy
Bl-RADS 0: This is your incomplete workup. They come in for a screener, you find
something suspicious. You give it a BI-RADS 0, and bring them back for spots, mags, or
ultrasound. You would also BI-RADS 0 anything that required a technical repeat (blur,
inadequate posterior nipple line, camel nose, etc.... ).
Bl-RADS 1: It's normal.
Bl-RADS 2: Benign findings. Examples would be cysts, secretory calcifications, fat
containing lesions such as oil cysts, lipomas, galactoceles and mixed-density hamartomas.
• Multiple bilateral well circumscribed, similar appearing masses - This is BR-2
unless one is growing or different than the rest. The general rule is to not ultrasound
these things unless one is palpable.
• Multiple Foci -This MRI finding is also a classic BR2.
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Bl-RADS 3: A key point is that BR-3 by definition means it has less than 2% chance of
being cancer. This is often a confusing topic. You can only use BR3 on a baseline. You
can't call anything BR3 that is new. The typical BR3 scenario: 45 year old comes in for
screening and has a focal asymmetry. She gets called back for diagnostic work up with spots
and ultrasound. She is found to have mass with imaging features classic for fibroadenoma.
This can get a BR-3, and be followed (some places follow for 2 years, in 6 month intervals).
Any change over that time ups it to BR-4 and it gets a biopsy.
Things you can BR-3:
• Finding consistent with fibroadenoma
• Focal m,ymmetry that looks like breast tissue (becomes less dense on compression).
• Grouped Round Calc(fzcations
What if it's palpable? This is a controversial topic. Classic teaching is that palpable lesions can
not be BR3. However, recent papers have shown that a palpable lesion consistent with a
fibroadenoma has less than 2% chance of cancer. Some people think the new BI-RADS will
change this rnle. I really doubt they will paint you into a corner on this one - given the
controversy.
Bl-RADS 4: This is defined as having a 2-95% chance of malignancy. Some people will
subdivide this into 4A, 4B, 4C depending on the level of suspicion. Ultimately you are going to
biopsy it, and be prepared to accept a benign result.
Bl-RADS 5: This is defined as> 95% chance of malignancy. When you give a BR-5, you are
saying to the pathologist "if you give me a benign result, I'll have to recommend surgical
biopsy." In other words, you can't accept benign with a BR-5.
Bl-RADS 6: This is path proven cancer.
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Basic Flow - These are essentially your choices in a work up.
BR O - You made a suspicious finding
and they need a diagnostic workup
BR O - Technical Repeat for Blur,
inadequate positioning etc ...
//
� BR 1 - Totally Normal
Screening Mammogram
(no symptoms) � BR 2 - Multiple bilateral, well circumscribed,
similar appearing masses
BR 2 - Redemonstration of an unchanged
previously worked up thing - a cyst etc...
BR 2- You work it up and it's a benign thing -
fat c01�taining lesion, cyst, etc ... This returns to
/ screenmg
Diagnostic Mammogram
(either a call back, BR 3 - Very specific situation where you
or someone with are dealing with a baseline screener, now
a symptom) called back. Findings meet one of the
three things described above;
(fibroadenoma, fat with breast tissue,
group of round calcs). This gets 2 years
of follow up.
BR 4 - Suspicious finding, but you aren't
convinced it's cancer. In other words,
you would accept a benign result. - This
gets a biopsy.
BR 5 - Suspicious finding, that you are
convinced is cancer. In other words, you
would NOT accept a benign result. - This
gets a biopsy.
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Bl-RADS Terminologv
In addition to the "0-6" babysitting, the various regulatory bodies have decided there are only
a few words they will trust you with, depending on what modality you are using.
Plain Mammography:
"Mass" - This is a space occupying lesion seen in two different projections
Describing the mass: You need to cover (1) Shape, (2) Margin, (3) Density
(I) Shape: Round, Oval, Irregular - "ROI"
(2) Margin: Circumscribed, Obscured, Microlobulated, Indistinct, Spiculated - "COMIS"
(3) Density (relative to breast parenchyma: Fat Density (radiolucent), Low Density, Equal
Density, High Density
Trivia: Of all the possible descriptors - margin is the most reliable feature for dete1mining
benign vs malignant.
"Asymmetry" - Unilateral deposition of tissue that doesn't quite look like a mass.
• A�ymmetJy - This is a density (only seen in one view) that may or may not be a mass,
and is often a term used in screeners for BR-0 prior to call back.
• Global Asymmetry- "greater volume of breast tissue than the contralateral side",
around one quadrants worth (or more). It's gonna get a call back, and then BR-2'd on
a baseline.
• Focal Asymmetry - This is seen in two projections, might be a mass - needs a spot
compression.
• Developing A�ymmetry- Wasn't there before, now is ... or bigger than prior.
Ultrasound:
Describing the mass: You need to cover : (1) Shape, (2) Orientation, (3) Margin, (4) Echo
pattern, (5) Posterior acoustic features
(1) Shape: Round, Oval, Irregular (not round or oval)
(2) Orientation: Parallel (wider than tall), Not-Parallel (taller than wide)
(3) Margin: Circumscribed, Indistinct, Angular, Microlobulated, Spiculated
(4) Echo Pattern: Anechoic, Hyperechoic, Hypoechoic, lsoechoic, or Complex (cystic/
solid)
(5) Posterior Features: None, Enhancement, Shadowing
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MRI:
There has recently been a vocabulary change in the Lexicon, and I'm going to briefly cover
the changes.
Background Parenchymal Enhancement:
• This is a newly added BI-RADS "feature." In the literature, they specify that this
description is based off the first post contrast sequence (sounds testable to me). The
• Categories are : none, minimal, mild, moderate, and marked.
Lesion Analysis: There are 3 basic categories for this:
• Foci ( < 5 mm): You don't need to describe shape and margin on these. They are too
small.
• Mass ( > 5 mm): This will have shape, margin, internal enhancement characteristics, &
T2.
• Non-Mass Enhancement: Distribution, Internal Enhancement, T2
Describing Masses:
• Shape: Round, Oval, and Irregular. The word "lobulated" has been removed from the
lexicon, so expect that to be a distractor.
• Margin: Circumscribed, Irregular, and Spiculated. The word "smooth" has been removed
from the lexicon, so expect that to be a distractor.
• Internal Enhancement Patterns: Homogenous, Heterogenous, Rim, and Dark Internal
Septations. "Enhancing Internal Septations" and "Central Enhancement" are NOT terms in
the new vocab - and will likely be distractors.
T2 Signal - This is a new "feature" of the lexicon
• Hyperintense:
• Greater than parenchyma (on T2)
• Greater than or equal to fat ( on T2)
• Greater than or equal to water (on T2 Fat Sat)
NME - "Distribution"
• Focal, Linear, Segmental (triangle shaped pointing towards nipple - suggestive of a duct),
Regional (large area - not a duct), Multiple Regions (two or more regions) and Diffuse.
NME - Internal Enhancement
• Homogenous, Heterogenous, Clumped (looks like cobblestone), Clustered Ring (this is a
buzzword.for DCIS or JDC). "Reticular" and "Dendritic" have been removed and will
likely be distractors.
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MRI BIRADS Cont..
Kinetic Curves are also described. I'll talk about this more in the Breast MRI Section.
Assuc:iated Findings: You are allowed to talk about nipple retraction, skin thickening, edema,
invasion of the pee muscles, pre contrast signal, and artifacts.
Implants: When you talk about implants you have to describe the type (silicone vs saline),
location (retroglandular vs retropectoral), and luminal features like radial folds, keyhole,
linguine, etc ... I'll cover this more in the Breast MRI section.
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SECTIONS:
CALCIFICATIONS
Calcifications can be an early sign of breast cancer. "The earliest sign," actually, according
to some. Calcifications basically come in three flavors: (1) artifact, (2) benign, and (3)
susp1c10us.
Artifacts Simulating Calcifications:
Deodorant: High density material seen in the
axilla is the typical appearance. Another trick
is to show a speck of high density material
that doesn't change position on different
views (inferring that it's on the image
receptor).
Deodorant Artifact
Zinc Oxide: This is in an ointment old ladies like to put on their floppy sweaty breasts. It
can collect on moles and mimic calcifications. If it disappears on the follow up it was
probably this (or another dermal artifact).
Metallic Artifact: It's possible for the electrocautery device to leave small metallic
fragments in the breast. These will be very dense (metal is denser than calcium). It will also
be adjacent to a scar.
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Benion vs suspicious:
The distinction between benign and suspicious is made based on morphology and distribution
(those BI-RADS descriptors). Since most breast cancers start in the ducts (a single duct in most
cases), a linear or segmental distribution is the most concerning. The opposite of this would be
bilateral scattered calcifications.
Segmental Linear Grouped Regional Scattered/ Diffuse
More Evil than Ursula
(vjllainous sea witch) Benign
from the Little Mermaid
Benion:
Dermal Calcifications: These are found anywhere women sweat (folds, cleavage,
axilla). Just think folds. They are often grouped like the paw of a bear, or the foot of a baby.
The trick here is that these stay in the same place on CC, and MLO views. This is the so
called "tattoo sign. " If you are asked to confirm these are dermal calcs, I'd ask for a
"tangential view."
Tangential
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Benion - Continued
Vascular Calcifications: These are parallel linear calcifications. It's usually obvious,
but not always.
Popcorn Calcifications: This is an immediate buzzword for degenerating fibroadenoma.
The typical look is they begin around the periphery and slowly coalesce over subsequent images.
Secretory (Rod-Like) Calcifications: These are
big, easily seen, and point toward the nipple. They are
typically bilateral. The buzzword is "cigar shaped with a
lucent center. " Another buzzword is "dashes but no dots. "
The buzz age is "l 0-20 years after menopause." Don't be
an idiot and call these in a premenopausal patient, they
happen because the duct has involuted.
Secretory Calcifications
Eggshell Calcifications: "Fat necrosis" I call them. It can be from any kind of trauma
(surgical, or accidental - play ground related). If they are really massive you may see the word
"liponecrosis macrocystica." As I've mentioned many times in this book, anything that sound
Latin or French is high yield for multiple choice. "Lucent Centered" is a buzzword.
Dystrophic Calcifications: These are also seen after radiation, trauma, or surgery. These
are usually big. The buzzword is "irregular in shape." They can also have a lucent center.
..
Round: The idea is that these things develop in lobules, are usually scattered,
bilateral, and benign. When benign (which is most of the time) they are going to
be due to.fibrocystic change (most of the time). The best way I've heard to think
about these is the same as a mass.
When masses are bilateral, multiple, and similar they are considered benign (BR-2). When a
mass is by itself or different it's considered suspicious. Round calcifications are the same
way. They are usually bilateral and symmetric (and benign). If they are clustered together,
by themselves, or new, they may need worked up (just like a mass). Remember that if
grouped round calcs are on the first mammogram you can BR-3 them.
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Benion - Continued
Milk of Calcium:
This has a very characteristic look, and because of
that, questions can only be asked in one of two
ways: ( 1) what is it? - shown as CC then ML, w
(2) what is it due to ? lllfjl '&iii'
(1) On the CC view the calcifications look powdery
and spread out, on the MLO view they may '@111
..
'111V
\@I'
w
w
layer. I suspect they will show you a ML view 11!1!1
because they should layer into a more linear
appearance, with a curved bottom "tea-cupped." "tea-cupped"
appearance on
For the purpose of gamesmanship [[they show true lateral view.
you a ML view on a ca/cs question - look hard
for anything that resembles tea-cupping. Fluid-Fluid in
(2) It's fluid-fluid in a lobule - due to fibrocystic a lobule
change.
Milk of Calcium - Tea Cups on ML
No Calcifications on the Biopsy?
This is a common trick. Apparently Milk of Calcium needs to be viewed with polarized
light to assess birefringence. Otherwise, you can't see it. I imagine there are several ways to
get at that via multiple choice.
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Suspicious
Amorphous - These things look like powdered sugar, and you should
not be able to count each individual calcification.
Distribution is key with amorphous calcs (like many other types before). If
the calcs are scattered and bilateral they are probably benign, if they are
segmental they are probably concerning.
Coarse Heterogeneous - These calcifications are countable, but
their tips are dull. If you picked one up it would not be poke you.
They are usually bigger than 0.5 mm. Distribution and comparison to
priors is always important. They can be associated with a mass
(fibroadenoma, or papilloma).
Fine Pleomorphic - These calcifications are countable, and their tips
appear sharp. If you picked one up it would poke you. They are usually
I
smaller than 0.5 mm. This pattern has the second highest likelihood of
malignancy... probably - see discussion on the following page.
I I
I I
Fine Linear / Fine Linear Branching - This is a distribution
\ I I
\ I I
'- \ I I
'-
,
'-
\
\
I
I that makes fine pleomorphic calcifications even more suspicious. The
----'-, \ I
DDx narrows to basically DCIS or an atypical look for secretory calcs or
" " \,,,,
'- I
', "� vascular calcs. This pattern has the highest likelihood of malignancy.
DDx Amorphous Ca+2 DDx Fine
DDx Coarse Heterogeneous Ca+2
Pleomorphic Ca+2
Fibrocystic Change
Fibroadenoma
(most likely) Fibroadenoma (less likely)
Papilloma
Sclerosing Adenosis Papilloma (less likely)
Fibrocystic Change
Columnar Cell Change Fibrocystic Change
DCIS (low - intermediate grade)
DCIS (low grade) DCIS (high grade)
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Suspicious - Continued
Calcifications Associated with Focal Asymmetry/Mass:
When you see increased tissue density around suspicious calcifications, the chance of an
actual cancer goes up. This is sometimes called a "puff of smoke" sign , or a "warning
shot." This is a situation where ultrasound is useful, for extent of disease.
Gamesmanship - Next Step:
Ultrasound is NOT typically used to evaluated pure calcification findings. Exceptions
would be (a) if the patient had a mass associated with the calcifications, or (b) if the patient
had a palpable finding - then they would get additional evaluation with ultrasound.
Q/1 Gamesmanship "Highest Suspicion for Malignancy" Wl
Depending on what you read and who you ask, Fine Linear Branching and Fine Pleomorphic
Calcifications have the Highest Suspicion for Malignancy. So which one is it?
For sure fine linear branching is the worst. Morphologically it mimics the ductal
proliferation of suspicious calcifications (DCIS). The confusion is that some people use
fine pleomorphic as an umbrella term under which linear and branching forms exist.
So how to handle this on multiple choice?
• If the answer choices include fine linear branching then that is the correct answer.
• If the answer choices do NOT include fine linear branching but instead have you pick fine
pleomorphic vs coarse heterogenous or some other obviously benign calcs (egg shell,
etc ...) then for sure pick fine pleomorphic.
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•-�.--. �
SECTION 6:
BENIGN PATH
Mondor Disease: This is a thrombosed vein that presents as a tender palpable cord. It
looks exactly like you'd expect it to with ultrasound. You don't anticoagulate for it (it's not
a DVT). Treatment is just NSAIDS and wann compresses.
Fat Containing Lesions: There are five classic fat containing lesions, all of which
are benign: oil cyst / fat necrosis, hamartoma, galactocele, lymph nodes, and lipoma. Of
these 5, only oil cyst/fat necrosis and lipoma are considered "pure fat containing" masses.
• Hamartoma -The buzzword is "breast within a
breast." They have an Aunt Minnie appearance on
mammography, although they are difficult to see on
ultrasound (they blend into the background).
• Galactocele -Seen in young lactating women.
This is typically seen on cessation of lactation. The
location is typically sub-areolar. The appearance is
variable, but can have an Aunt Minnie look with a
fat-fluid level. It's possible to breast abscess these
�;��ft&�� < .'·•·\.....
·.•;/.·• ••·i/iC
· - "E3re1:1.stwithin a E3reast" · · ·
t
things up.
• Oil Cyst/ Fat Necrosis -These are areas of fat necrosis walled off by fibrous tissue.
You see this (1) randomly, (2) post trauma, (3) post surgery. The peripheral
calcification pattern is typically "egg shell." ffyou see a ton of them you might think
about steatocystoma multiplex (some zebra with hamartomas).
• Lipoma -These are typically radiolucent with no calcifications. Enlargement of a
lipoma is criteria for a biopsy.
• Intramammary Lymph node: These are normal and typically located in the tissue
along the pectoral muscle, often close to blood vessels. They are NOT seen in the
fibroglandular tissue.
Practice Point: Does she need an ultrasound ifit'.,;; palpable? Usually a palpable finding
is going to get an ultrasound. If you are under 30, most people will skip the mammo and
go straight to ultrasound. One of the exceptions is a fat containing lesion definite benign
BR-2er on diagnostic mammography.
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Pseudoangiomatous Stromal Hyperplasia (PASH): This is a benign
myofibroblastic hyperplastic process (hopefully that clears things up). It's usually big (4-6
cm), solid, oval shaped, with well defined borders. Age range is wide they can be seen
between 18-50 years old. Follow up in 12 months (annual) is the typical recommendation.
� Pseudoangiomatous Stromal Hyperplasia = Benign thing with a scary sounding name
Fibroadenoma - This is the most common palpable mass in young women. The typical
appearance is an oval, circumscribed mass with homogeneous hypoechoic echotexture, and a
central hyperechoic band. If it's shown in an older patient, it's more likely to have coarse
"popcorn" calcifications - which is a buzzword. On MRI, it's T2 bright with a type 1
enhancement (progressive enhancement).
Phyllodes: Although I clumped this in benign disease, this thing has a malignant
degeneration risk of about l 0%. They can metastasize - usually hematogenous to the lungs
and bone. This is a fast growing breast mass. They need wide margins on resection, as they
are associated with a higher recurrence rate if the margin is < 2 cm. It occurs in an older age
group than the fibroadenoma (40s-50s). Biopsy of the sentinel node is not needed, because
mets via the lymphatics are so incredibly rare (if it does met - it's hematogenous).
Distinguishing Features ofPhyllodes Tumor
• Rapid Growth
• Hematogenous Mets
• Middle-Age to Older Women
• Mimics a Fibroadenoma
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� SECTION 7:
....
..
.
. . ;,
.. CANCER
IDC - Invasive ouctal Carcinoma
I DC - Invasive Ductal Carcinoma is by far the most common invasive breast cancer, making
up about 80-85% of the cases. This cancer is ductal in origin (duh), but unlike DCIS is not
confined to the duct. Instead it "invades" through the duct and if not found by the heroic
actions of Mammographers it will progress to distal mets and certain death. Clinically, the
most common story is a hard, non-mobile, painless mass. On imaging, the most common
look is an irregular, high density mass, with indistinct or spiculated margins, associated
pleomorphic calcifications, and an anti-parallel shadowing mass with an echogenic halo on
ultrasound.
Invasive Ductal NOS - By far the most common type of breast cancer is the one that is
undifferentiated and has no distinguishing histological features. "Not Otherwise Specified"
or NOS they call it. These guys make up about 65% of invasive breast cancer.
Less Common (but still testable) IDC Subtypes
IDC Types - (Other than NOS)
Small spiculated slow Often conspicuous on ultrasound. Associated
Tubular growing mass with a with a Radial Scar. Contralateral breast will
favorable prognosis. have cancer 10-15% of the time.
Round (or lobulated) and
Mucinous Uncommon. Better outcomes than IDC-NOS
circumscribed mass
Round or Oval Axillary nodes can be large even in the
circumscribed mass, absence of mets. Typically younger patient
Medullary
without calcifications. (40s-50s). Better outcome than IDC-NOS
-25% have BRCA 1 mutation
Axillary nodes are NOT common. Typically
Complex cystic and seen in elderly people, favors people who are
Papillary
solid. not white, and is the 2nd most common (behind
IDC-NOS).
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Multifocal Breast Cancer Multicentric Breast Cancer
Multiple primaries in the same quadrant Multiple primaries in different quadrants
(classically same duct system)
Think of this like "multi-center" clinical
Less than 4-5 cm apart.from one another trial; multiple discrete un-related sites.
Synchronous Bilateral Breast Cancer - This is seen in 2-3% of women on
mammography, with another 3-6% found with MRI. The risk of bilateral disease is increased
in infiltrating lobular types, and multi-centric disease.
DCIS - This is the "earliest form of breast cancer." In this situation the "cancer" is confined
to the duct. Histologists grade it as low, intermediate, or high. Histologists also use the terms
"comedo", and "non-comedo" to subdivide the disease. If anyone would ask, the comedo
type is more aggressive than than the non-comedo types.
Testable Trivia:
• 10% of DCIS on imaging may have an invasive component at the time biopsy is done
• 25% of DCIS on core biopsy may have an invasive component on surgical excision.
• 8% of DCIS will present as a mass without calcifications
• Most common ultrasound appearance = microlobulated mildly hypoechoic mass with
ductal extension, and normal acoustic transmission
If a test writer wants you to come down on this they will show it in 1 of 3 classic ways:
(1) suspicious calcifications (fine linear branching or fine pleomorphic - as discussed above),
(2) non mass enhancement on MRI, or (3) multiple intraductal masses on galactography.
Pa gets - Paget's disease of the breast is a high yield topic. It is basically a carcinoma in
situ of the nipple epidermis. About 50% of the time the patient will have a palpable finding
associated with the skin changes.
Things to know about Breast Pagets:
• Associated with high grade DCIS (96 % )
• Wedge biopsy should be done on any skin lesion that affect the nipple-areolar
complex that doesn't resolve with topical therapy.
• Pagets is NOT considered T4. The skin involvement does not up the stage in this
setting.
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lobular - ILC
Lobular (ILC): This is the second most common type of breast cancer (IDC-NOS being the
most common). It makes up about 5-10% of the breast CA cases.
This pathophysiology lends itself well to multiple choice questions:
Cell decides to be cancer -> Cells lose "e-cadherin"-> Cells no longer stick to one another and
begin to infiltrate the breast "like the web of a spider"-> This infiltrative pattern does not cause
a desmoplastic reaction so it gets missed on multiple mammograms-> Finally someone (you)
notices some architectural distortion without a central mass, on the CC view only. You get
fancy and call it a "dark star."
On Ultrasound: The typical look is an
ill-defined area of shadowing without a
mass.
ILC - Shadowing without discrete mass
"Shrinking Breast" -
This is a buzzword for
ILC. The breast isn't
actually smaller, it just
doesn't compress as much.
So when you compare it to
a normal breast, it appears
to be getting smaller. On
physical exam, this breast
may actually look the
same size as the other one.
"Shrinking Breast"
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lobular - ILC - Continued
q1, THIS vs THAT: ILC VS IDC: ILC is more often multifocal. ILC less often mets to
the axilla. Instead, it likes to go to strange places like peritoneal surfaces. ILC more often has
positive margins, and is more often treated with mastectomy although the prognosis is similar to
IDC.
Things to know about ILC:
• It presents later than IDC
• Tends to occur in an older population
• It often is only seen on one view (the CC - as it compresses better)
• Calcifications are less common than with ductal cancers
• Mammo Buzzword = Dark Star
• Mammo Buzzword = Shrinking Breast
•
Ultrasound Buzzword = Shadowing without mass
• On MRI - washout is less common than with IDC
• Axillary mets are less common
• Prognosis of IDC and ILC is similar (unless its a pleomorphic !LC - which is bad)
• More often multifocal and bilateral (compared to IDC) - up to 1/3 are bilateral
Dark Star
"Dark Star" - Distortion without a central mass
Architectural distortion without a central mass.
The DDx includes: lobular carcinoma, radial scar, surgical scar, and IDC-NOS.
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lnllammatorv Breast Cancer I IBC J
IBC an asshole with a notoriously terrible prognosis (at presentation ~30% will have metastases).
Clinical Scenario: The classic clinical scenario is a hot swollen red breast that developed rapidly
over 1-3 months. They may even deploy the French sounding word "peau d'orange," - which
basically means skin that looks like a delicious ripe grapefruit. Although there may be a mass on the
mammogram, in the most classic scenario there isn't a focal palpable mass.
"Skin Thickening" is a mammography buzzword (non-specific). Skin thickening is not (by itself)
specific and lots of stuff including CHF can also cause skin thickening. In the case of inflammatory
breast cancer the skin thickening is the result of tumor emboli obstmcting the lymphatics.
Probably Fuckery: It is likely the question writer will try to make you think mastitis - even though the
scenario isn't really classic for that. Remember - mastitis is seen in breast feeding women - that is
the most common scenario. If it is just "random woman with a hot swollen breast" - you 100% should
think cancer first. Even if they put them on antibiotics, and she has a history of recurrent infections
or whatever - that is all probably bullshit.
.MindMap: Swollen, Red Breast, Thick Confirming the diagnosis of IBC requires: Both
Skin - looks like the peel (l)Tissue Diagnosis and (2)Clinical Evidence of
of a Grapefruit - rapid inflammato1y disease the diagnosis of IBC
�----.<-"""zyclinical presentation
Evaluate for (< 3 months)+/- fever
a focal lump MRI
or skin • Best method for detecting the primary lesion in IBC
fluctuance to�-...-.___'f" • Most common finding= extensive or segmental
help target NML enhancement + diffuse skin thickening
your US scan
�················· . .........•.••••••. Consider
Hypoechoic : : Solid mass with :
■
Skin thickening _:_.....,_Punch Biopsy MRI for
Multiloculated : : suspicious : but no focal mass : (usually works, biopsy
ollection :• ■: features but not always) targeting
............. � •..............
Drain it under Ultrasound Confirm Incomplete response to
& Give Antibiotics Response/ antibiotic treatment within
(send culture & gram) Resolution 1-2 weeks -Presume IBC-
The inflammation associated with
inflammatory breast cancer can actually
Trivia: improve with antibiotics, but does NOT
resolve. So, don't be.fooled (in the real
• IDC is the most common subtype to result world or on a multiple choice test).
in IBC (although any subtype of primary
breast CA can)
This vs That = IBC vs LABC
• IBC is stage 4
Inflammatory Breast Locally Advanced
Cancer (IBC) Breast Cancer (LABC)
Treatment: They will try and do
chemotherapy prior to surgery because the Rapid onset Prolonged onset
chance of a positive margin is so high. The
standard mastectomy is done for "local Younger (mid 50s) Older (mid 60s)
control" , which just sounds awful. 30% mets at presentation l 0%i mets at presentation
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High Risk lesions:
There are 5 classic high risk lesions that must come out after a biopsy; Radial Scar, Atypical
Ductal Hyperplasia, Atypical Lobular Hyperplasia, LCIS, and Papilloma.
Radial Scar: This is not actually a scar, but does look like one on histology. Instead you
have a bunch of dense fibrosis around the ducts giving the appearance of architectural
distortion (dark scar).
Things to know:
• This is high risk and has to come out
• Its associated with DCIS and/or JDC 10%-30%
• Its associated with Tubular Carcinoma*
Atypical Ductal Hyperplasia (ADH): This is basically DCIS but lacks the
quantitative definition by histology (< 2 ducts involved). It comes out (a) because it's high risk
and (b) because DCIS burden is often underestimated when this is present. In other words,
about 30% of the time the surgical path will get upgraded to DCIS.
Lobular Carcinoma in Situ (LCIS): This is classically occult on mammogram. "An
incidental finding" is sometimes a buzzword. The best way to think about LCIS is that it can
be a precursor to ILC, but isn't obligated to be. The risk of conversion to an invasive cancer is
less when comparing DCIS to IDC. Just like pleomorphic ILC is worse than regular ILC, a
pleomorphic LCIS is mo' badder than regular LCIS.
Atypical Lobular Hyperplasia (ALH): This is very similar to LCIS, but histologists
separate the two based on if the lobule is distended or not (no with ALH, yes with LCIS). It's
considered milder than LCIS (risk of subsequent breast CA is 4-6x higher with ALH, and 1 l x
higher with LCIS). For the CORE, the answer is excision. In the real world, some people do
not cut these out, and it's controversial.
Papilloma: A few most commons come to mind with this one. Most common intraductal
mass lesion. Most common cause of blood discharge. You typically see these in women in
their late reproductive years/ early menopausal years (average around 50). The classic
location is the subareolar region (1cm from the nipple in 90% of cases).
--Mammogram: Often normal - occasionally just showing calcifications.
--US: Well-defined smooth walled hypo-echoic mass. Maybe cystic with solid components.
Also, tends to have associated duct dilation.
-Galactography: Solitary filling defect, with dilated duct.
Mult;ple Papi/lamas: These tend to be more peripheral. On mammography it's gonna be a
mass(es) or a cluster of calcifications without a mass.
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Phyllodes: Yes ... I mentioned this already under benign disease. I just wanted to bring it
up again to make sure you remember that this thing has a malignant degeneration risk of
about 10% (some texts say up to 25%). This is a fast growing breast mass. It occurs in an
older age group than the fibroadenoma (40s-50s).
Multiple Masses: Sounds Bad But Actually BR-2
To call multiple masses you need to have
multiple (at least 3) bilateral well
circumscribed masses without suspicious
features. This gives you a BR-2.
One common trick is to show multiple
unilateral masses, that doesn't fly- they
have to be bilateral.
Lymphoma:
Breast lymphoma
Primary Breast Lymphoma Primary Lymphoma Secondary Lymphoma
Less Common More Common
Always , for the purpose of multiple choice, most common secondary
malignancy or mets to
Non Hodgkin (Diffuse Large B-Cell)
involve the breast
Typical Look:
Usually a hyperdense mass • Usually Solitary Typical Look:
(Architectural distortion is rare) • Usually Larger • Inflammatory
(compared to thickening without a
secondary) and most mass (but can look
"IHC" staining is need to confirm lymphoma often palpable like anything)
• Cystic on US
Do axillary nodes = lymphoma? Bro .... anything can give you axillary nodes
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• '
• •
� SECTION 8:
SYMPTOMATIC DIRTY PILLOWS
' ( '·
Breast Pain: This is super common and typically cyclic (worse during the luteal phase of
� •. ' _I' .
the menstrual cycle). Pain in both breasts that is cyclical does not need evaluation. Instead it
needs a family medicine referral for some "therapeutic communication." Focal non-cyclic
breast pain may warrant an evaluation.
Trivia: The negative predictive value of combined mammogram and US for "focal pain" is
right around 100%. When breast cancer is found it's usually elsewhere in the breast
(asymptomatic).
Symptoms that are actually worrisome for cancer include: skin dimpling, focal skin
thickening, and nipple retraction.
Non-Focal Skin Thickening / Breast Edema: This is usually the result of
benign conditions (congestive heart failure, renal failure). For multiple choice tests it will
always be bilateral (in the real world you can sleep on one side and have asymmetric edema).
As long as the breast isn't red, you can feel confident that it will be benign. On
mammography you will see trabecular thickening (diffuse, and favoring the dependent
portions of the breast).
Breast Inflammation: The swollen red breast. This finding has a differential of two
things: (I) mastitis / abscess, (2) inflammatory breast cancer.
• Mastitis / Abscess: This is a swollen red breast which is painful (Inflammatory breast CA
is often painless). Patients are usually sick as a dog. Obviously it's associated with
breast feeding, and is more common in smokers and diabetics. Abscess can develop
(usually Staph A.).
• Inflammatory Breast Cancer: As previously discussed, this has a terrible prognosis.
The general rule is that a breast that doesn't respond to antibiotics gets a skin biopsy to
exclude this. The typical age is 40s-50s. You are going to have an enlarged, red breast
with a "peau d'orange" appearance. The breast is often NOT painful, despite its
appearance. Mammogram might show a mass (or masses), but the big finding is diffuse
skin and trabecular thickening. The treatment is fair game for multiple choice because it
is different than normal breast cancer. Instead of going to surgery first, inflammatory
breast cancer gets "cooled down" with chemo and/or radiation - then surgery.
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The leakv Tit
Women present with nipple discharge all the time, it's usually benign Multiple Ducts
(90%). The highest yield information on the subject is that: (Benign)
spontaneous, bloody, discharge from a single duct is your most
Single Ducts
suspicious feature combo. Serous discharge is also suspicious. (Maybe Malignant)
The risk of discharge being cancer is directly related to age (very • Papilloma
uncommon under 40, and more common over 60). • DCIS
*Discharge is Bad when it's - Spontaneous, Bloody, and from a Single Duct
Milky Discharge: Milky discharge is NOT suspicious for breast cancer but can be
secondary to thyroid issues or a pituitary adenoma (prolactinoma). Any medication that messes
with dopamine can stimulate prolactin production - (antidepressants, neuroleptics, reglan).
Causes of Discharge (Not Milky)
Benign Causes Worrisome Causes
Intraductal Papilloma (90%) - single intraductal
Pre-Menopausal Woman = Fibrocystic Change
mass near nipple
Post Menopausal Women = Ductal Ectasia DCIS (10%) - multiple intraductal masses
Ductal Ectasia - The most common benign cause of nipple discharge in a post menopausal
woman. On galactography you will see dilated ducts near the subareolar region, with
progressive attenuation more posteriorly.
Papilloma - Discussed previously- this is the most common cause of bloody discharge.
As before they can be single or multiple, and carry a small malignant risk (5%).
Galactography
• Ugh ... you take a 27 or 30 gauge blunt tipped needle and attempt to cannulate the duct
which is leaking. To determine which duct you want - you'll need to have the patient
squeeze the breast to demonstrate where it's coming from.
• If you manage to cannulate the duct - gently inject 0.2 - 0.3 cc contrast (rare to need more
than 1 cc). You then do mammograms (magnification CC and ML). Filling defect(s) get
wire localization.
• Contraindications: Active infection (mastitis), inability to express discharge at the time of
galactogram, contrast allergy, or prior surgery to the nipple areola complex.
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.•
... .
,.
:·:.··.··.
� SECTION 9:
ARCHITECTURAL DISTORTION
�-
AD: We're talking about unchecked aggression here, Dude. We are talking about distortion
of the normal architecture without a visible mass. This manifests in a few ways, including
focal retraction, distortion of the edge of the parenchyma, or radiation of the normal thin
lines into a.focal point.
Architectural Distortion vs Summation Artifact: This is the primary differential
consideration, with summation of normal vessels, ducts, and ligaments being much more
common. The difference is summation should NOT radiate to a central point (AD will).
AD - All lines radiate to a point Summation - Lines continue past each other
Surgical Scar vs Something Bad: Scars should progressively get lighter and harder to see.
Some people say that in 5-10 years a benign surgical scar is often difficult to see.
Lumpectomy scars tend to stick around longer than a benign biopsy. Basically, look at the
priors; if it is a surgical scar, it better be getting less dense. If it's increasing, you gotta stick
a needle in it.
Work Up ofAD: If you see it on a screener you will want to BR-0 it, and bring it back for
spot compression views. If it persists just know you are either going to BR-4 or BR-5 it
(unless you know it's a surgical scar). You should still ultrasound it for further
characterization (may help you decide between a 4 and a 5).
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Ultrasound Trivia: The use of harmonic tissue imaging can make it easier to see some
lesions. Be aware that compound imaging can make you lose your posterior features,
especially when they are soft to start with - like the shadowing of an ILC. Remember, even
if you see nothing, this gets a biopsy. Harmonics can also make not so simple cysts look
simple by reducing superficial reverberation.
Things to Know.for AD:
•Radiating lines to a single point= AD
•AD + Calcifications= IDC + DCIS
•AD without Calcifications= ILC
•Even with no ultrasound or MRI correlate, AD gets a biopsy.
•Never ever ever ever ever BR-3 an area of AD.
•Even if it has been there a while, it still needs to be worked up.
•Remember lLC can grow slowly.
•surgical scars should get less dense with time ... not more dense.
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• '
• •
SECTION 10:
LYMPH NODES
You found a breast cancer - now what? Before you make the patient cry, it's time to stage the
disease. Ultrasound her ann pit. About 1 in 3 times you are going to find abnormal nodes.
Unilateral vs Bilateral: This can help you if you are thinking this could be systemic. Unilateral
adenopathy should make you worry about a cancer ( especially if they have a cancer on that
side).
Biop()y It? Some people will recommend biopsy if you have the following abnormal features.
• Cortical Thickness greater than 2.3 mm (some people say 3 mm)
• Loss of Central Fatty Hilum - "most specific sign"
• Irregular Outer Margins.
Staging Trivia: Level 1 and Level 2 nodes are treated the same. Rotter nodes are treated as
Level 2. Level 3 and supraclavicular nodes are treated the same.
Special "Sneaky" Situations:
Gold Therapy: Long ago, when the pyramids were still young, rheumatoid arthritis was
treated with "chrysotherapy." What they can do is show you an "Aunt Minnie" type picture
with very dense calcifications within the node.
Snow Storm Nodes: Another Aunt Minnie look is the silicone infiltration of a node from either
silicone leaking or rupture.
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-·;'
;.\ �
SECTION 11:
MALE BREAST � • ! ...-....
There is no more humiliating way to die for a man than breast cancer. The good news is male
breast cancer is uncommon. The bad news is that when it occurs it is often advanced and
invasive at the time of diagnosis - Valar Morghulis.
The male breast does NOT have the elongated and branching ducts, or the proliferated lobules
that women have. This is key because men do NOT get lobule associated pathology (lobular
carcinoma, fibroadenoma, or cysts).
Gynecomastia: This is a non-neoplastic enlargement of the epithelial and stromal elements
in a man's breast. It occurs "physiologically" in adolescents, affecting about 50% of adolescent
boys, and men over 65. If you aren't 13 or 65 it's considered embarrassing and you should hit the
gym. If you are between 13-65 it's considered pathology and associated with a variety of
conditions (spironolactone, psych meds, marijuana, alcoholic cirrhosis, testicular cancer). There
are three patterns (nodular is the most common). Just think flame shaped, behind nipple,
bilateral but asymmetric, and can be painful. Things that make you worry that it's not
gynecomastia include not being behind the nipple, eccentric location, and calcification.
Patterns of Gynecomastia
"Flame Shaped" centered behind
the nipple, radiating posterior as it
Nodular
blends into the fat. Breast is often
(moSt common)
tender. Usua11y Iast·s less than 1
year.
Resembles a branching tree. This
Dendritic is a chronic fibrotic pattern.
Usually not tender.
Mamrnographic pattern looks like
a woman's breast (diffuse
Diffuse
increase in density). You see this
Glandular
in men receiving estrogen
treatment.
Gynecomastia
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Pseudogynecomastia "Bitch Tits" - This is an increase in the fat tissue of the breast
(not glandular tissue). There will NOT be a discrete palpable finding, and the mound of
tissue will not be concentric to the nipple.
Lipoma - After gynecomastia, lipoma is the second most common palpable mass in a man.
Male Breast Cancer: It's uncommon in men, and very uncommon in younger men
(average age is around 70). About 1 in 4 males with breast cancer have a BRCA mutation
(BRCA 2 is the more common). Other risk factors include Klinefelter Syndrome, Cirrhosis,
and chronic alcoholism. The classic description is eccentric but near the nipple. It's almost
always an IDC-NOS type. DCIS can occur but is very rare in isolation. On mammography it
looks like a breast cancer, if it was a woman's mammogram you'd BR-5 it. On ultrasound
it's the same thing, it looks like a BR-5. Having said that, nodular gynecomastia can look
suspicious on ultrasound.
Things that make you think it�, breast cancer:
• Eccentric to Nipple
• Unilateral
• Abnormal Lymph nodes
• Calcifications
• Looks like breast cancer
Male Breast CA
Some trivia on calc[fications: Micro-calcifications alone are uncommon in men. When you
see them they are less numerous, coarser, and associated with a mass (25% of male breast
cancers have calcifications).
Should men get screening mammograms? Honestly, women shouldn't even get them
(according to the New England Journal of Medicine). This remains controversial, with the
bottom line being this: only Klinefelter patients approach the screening range with regards to
risk.
As a point of trivia: males with gynecomastia from gender reassignment on hormone
therapy are not high enough risk for screening mammograms. Obviously, if they have a
palpable finding, they can get a diagnostic work up.
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SECTION 12:
IMPLANTS
�
• .
•
Basic Overview: There are two types , saline and silicone. They both can rupture, but no
one really gives a shit if saline ruptures. Saline does not form a capsule, so you can't have
intracapsular rupture with saline. There is no additional imaging past mammo for saline
rupture, and you just follow up with primary care/ plastic surgeon. You can tell it's saline
because you can see through it. For silicone you can have both intra and extra capsular rupture.
You can only see extra on a mammogram (can't see intra). Extra creates a dense "snow storm"
appearance on US. Intra creates a "step ladder" appearance on US and a ''linguine sign" on
MRI. MRI is done with PS T2 to look at implants.
Big Points:
• You CAN have isolated intracapsular rupture.
• You CAN NOT have isolated extra (it's always with intra).
• If you see silicone in a lymph node you need to recommend MRI to evaluate for
intracapsular rupture
Implant Location: There are two subtypes:
• Subglandular (retromammary): Implant behind breast tissue, anterior to pectoral
muscle
• Subpectoral (retropectoral): Implant between pectoralis major and minor muscles
Silicone Implants
The body will form a shell around the foreign body (implant), which allows for both
intracapsular and extracapsular rupture (an important distinction from saline). About 25% of
the time you will see calcifications around the fibrous capsule.
Things to know:
• Implants are NOT a contraindication for a core needle biopsy
• Implants do NOT increase the risk for cancer.
Saline Implants
There are also subglandular and subpectoral subtypes. You can tell the implant is saline
because you can see through it. Implant folds and valves can also be seen. If it ruptures no one
really cares (other than the cosmetic look). The saline is absorbed by the body, and you have a
collapsed implant. A practical point of caution, be careful when performing a biopsy in these
patients - even a 25g FNA needle can burst a saline implant.
Trivia: Some sources say that "physical exam" is the test of choice for diagnosing saline
implant rupture - this is variable depending on what you read/ who you ask.
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Implant Complications:
Generally speaking, MRI is the most accurate modality for evaluating an implant.
Capsular Contracture: This is the most common complication of implants. It
occurs secondary to contraction of the fibrous capsule, and can result in a terrible cosmetic
deformity. You see it in both silicone and saline implants, but is most common in
subglandular silicone implants. On mammo it looks like rounding or distortion of the
implant (comparisons will show progression).
Gel Bleed: Silicone molecules can (and do) pass through the semi-permeable implant
shell coating the exterior of the surface. This does NOT mean the implant is ruptured. The
classic look is to show you silicone in the axillary lymph nodes (remember I showed a case
ofthis under the lymph node section). Even with axillary lymph nodes, this does NOT mean
it has ruptured.
Rupture: As a point of testable trivia, the number one risk factor for rupture is age of the
implant. Rupture does not have to be post traumatic, it can occur spontaneously. Rupture
with compression mammography is actually rare.
• Saline: Saline rupture is usually very obvious (deflated boob). It doesn't matter all
that much (except cosmetically), as the saline is just absorbed. On mammo, you will
see the "wadded up" plastic wrapper. They could easily write a question asking you
what modality you need to see a saline rupture. The answer would be plain mammo
(you don� need ultrasound or MRI).
• Silicone: This is a more complicated matter. You have two subtypes; isolated
intracapsular and intracapsular with extracapsular.
o Isolated Intracapsular: This wil1 be occult on physical exam, mammography
and possibly ultrasound. You might see a stepladder on Ultrasound. MRI is
way more sensitive.
o Intracapsular with Extracapsular Rupture: This is usually obvious on
mammogram with dense silicone seen outside the capsule. The contour of a
normal intact implant is smooth. Silicone outside the implant can go to lymph
nodes. On ultrasound you want to know the buzzword "snow storm" pattern
- which is really echogenic with no posterior shadowing. A sneaky trick is
to show a lymph node with a snow storm appearance on ultrasound. On MRI
extracapsular silicon is T l dark, and T2 bright. Lastly, a very important
concept is that you cannot have isolated extracapsular rupture. If it '.s·
extracapsular, then its also intracapsular.
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Radial Folds - The Mimic of Rupture:
Radial folds are the normal in-foldings of the elastomer shell. They are the primary mimic
for the linguine sign of intracapsular rupture. To tell them apart ask yourself "do the.folds
connect with the periphery of the implant?" Radial folds should always do this (linguine
does not).
Silicone Implant Rupture Summarv
lntracapsular Rupture:
- Remember the "capsule" is not part
of the implant. It's the fibrous coat
your body makes around the implant
(the outer black line in my diagram).
Silicone can rupture through the
shell of the implant, but stays
confined inside the fibrous coat - this
is intra-capsular rupture.
The classic sign is the floating
"linguine" - as in this case.
Extra & lntracapsular:
- This is when the rupture goes
through the "capsule" (the thing your
body made).
You can NOT have isolated extra
capsular silicone. It has to make it
through the implant shell first.
Silicone outside the capsule can
create a "snow storm" look on
ultrasound. It can also infiltrate lymph
nodes and do the same (snow storm
nodes). Remember gel bleed can
also give you a node like this.
Radial Folds
- Guys like squishy boobs. The bigger
and the squishier the better.
Therefore, implants are not bound
tightly - so they can be squishy.
Because they are loosely bound the
shell in-folds creates radial folds
The folds always attach to the
shell*
The folds are thicker than a rupture,
because they represent both layers.
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• ' ,
�,
SECTION 13:
!POST OP / POST THERAPY
Reduction Mammoplasty and Mastopexy
Reduction Marnrnoplasty- Yes, there
is actually a subpopulation of women
who want SMALLER breasts. I know,
it sounds impossible to believe , but
Mammoplasty is actually done to
reduce breast size. I can only pray that
the sadistic bastard who developed this
procedure has received appropriate
punishment (in this life or the next).
Mastopexy-This is a "breast lift,"
Essentially, just a removal of skin.
Women get this done to address floppy,
saggy, pancake, or "ptotic" boobs. Typical Changes from Mammoplasty
Normal Findings Post Mastopexy:
• Swirled Appearance Affecting
Inferior Breast
• Fat Necrosis I Oil Cysts
• Isolated Islands of Breast Tissue
Keyhole Incision - This is done for Mammoplasty Keyhole Incision Mastopexy Keyhole Incision
both mammoplasty and mastopexy,
creating a "swirled" appearance in the
inferior aspect of the MLO.
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Surgical BiOPSV / Radiation
Terminology:
• Lumpectomy - Surgical Removal of Cancer(palpable or not)
• Excisional Biopsy - Surgical Removal of Entire Lesion
• Incisional Biopsy - Surgical Biopsy of a Portion of the Lesion
Post Biopsy Changes:
The first post operative mammogram is usually obtained around 6-12 months after biopsy. The
key is that distortion and scarring are worst on this film, and should progressively
improve. On ultrasound, scars are supposed to be thin and linear. If they show you a focal
mass like thickening in the scar - you've gotta call that suspicious for local recurrence.
Fat necrosis and benign dystrophic calcifications may evolve over the first year or two, and are
the major mimics of recurrence. Fat necrosis can be shown on MR(Tl/ T2 bright, and then fat
sat drops it out).
Recurrence / Residual Disease:
Numerical Trivia: Local recurrence occurs 6-8% of the time when women have breast
conserving therapy. The peak time for recurrence is 4 years(most occur between 1-7).
Without radiation local recurrence is closer to 35%. Tumors that recur early(< 3 years)
typically occur in the original tumor bed. Those that occur later are more likely to be in a
different location than the original primary.
What gets recurrent disease ? Risk of recurrence is highest in the );1.@_menopausal woman
(think about them having an underlying genetic issue). Other risks include: having an
extensive inarticulate component, a tumor with vascular invasion, multi centric tumors,
positive surgical margins, or a tumor that was not adequately treated the first go around.
Residual Cales: Residual calcifications are not good. Supposedly, residual calcifications near
or in the lumpectomy bed correlates with a local recurrence rate of 60%.
New Cales: When it does reoccur, something like 75% ofDCIS will come back as
calcifications(no surprise). The testable pearl is the benign calcifications tend to occur early
(around 2 years), vs the cancer ones which come back around 4 years.
Sentinel Node Failure: Sentinel node biopsy works about 95% of the time(doesn't work 5% of
the time). So about 5 times in l00 you are going to have a negative node biopsy that presents
later with an abnormal armpit node.
Tissue Flap: The cancer is not going to start in the belly fat/ muscle. The cancer is going to
come from either the residual breast tissue or along the skin scar line. Screening of the flaps is
controversial - with some saying it's not necessary. The need for screening of tissue flaps is not
going to be asked. If you get asked anything it's "where the recurrence is coming from / going
to be?"
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Specimen Radiography
If the path report says "close margins" or "positive
margins," there is a very high chance you are
going to have cancer still in the breast. If you are
shown a specimen radiograph, there are two things
you need to look at in real life and on multiple
choice: (1) is the mass/ calcifications on the
sample, and (2) is the mass/ calcifications near
the edge or touching the edge. If the mass is at the
edge, the chance of incomplete excision is going to
be near 80%. The "next step" would be to call the
surgeon in the OR and tell him/her that. Specimen Radiograph - Cancer at the Margin
-High chance of positive margin
Post Radiation Changes:
Practical Point (the before picture): The pre-radiation mammogram is very important. If
you can identify residual disease on it, the patient has many more treatment options. If you
discover the residual disease after the radiation therapy has been given, you've forced the
patient to undergo mastectomy.
Radiation Changes: You are going to see skin thickening and trabecular thickening. This is
normal post radiation, and should peak on the first post-RT mammogram.
This would be a classic testable scenario:
• Film 1 Post RT: You see skin thickening/ trabecular thickening
• Film 2: Skin thickening/ trabecular thickening is better
• Film 3: Skin thickening/ trabecular thickening is worse* - this is recurrent disease
(maybe inflammatory breast CA).
Secondary Angiosarcoma
The primary type is so rare I won't even mention it. The secondary type is seen after
breast conservation therapy/ radiation therapy. It takes around 6 years post radiation
therapy to develop one of these things. Clinically the classic presentation is "red plaques
or skin nodules." The challenge with these is that the skin thickening due to the cancer is
often confused with post therapy skin thickening.
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Staging/ Surgical Planning
Breast Cancer Staging: The staging is based on size from T l-T3, then invasion for T4.
• T l=< 2 cm.
• T2 = 2-5 cm
• T3= > 5 cm
• T4 = "Any size" with chest wall fixation, skin involvement, or inflammatory breast CA.
*Remember that Pagels is NOT T4.
Trivia: Axillary Status is the most important predictor of overall survival in breast cancer
Trivia: Melanoma is the most common tumor to met to the breast.
The contraindications for breast conservation are high yield.
Contraindications for Breast Conservation
Inflammatory Cancer,
Large Cancer Size Relative to Breast
Multi-centric (multiple quadrants)
Prior Radiation Therapy, to the same breast
Contraindication to Radiation Therapy (collagen-vascular disease).
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SECTION 14:
BREAST MRI
Breast MRI can be used for several reasons: High risk screening, extent of disease (known
cancer), axillary mets with unknown primary, diagnostic dilemmas, and possible silicone
implant rupture. The big reason is for high risk screening.
I'll just briefly go over how it's done, and how it's read.
You need a special breast coil and table set up to make it work. The patient lies belly down
with her breasts hanging through holes in the table. You have to position them correctly
otherwise they get artifact from their breasts rubbing on the coil. Basic sequences are going
to include a T2, and pre and post dynamic (post contrast) fat saturated T l. Remember the
breast is a bag of fat - so fat sat is very important. Dynamic imaging is done to generate
wash out curves (similar to prostate MRI).
My basic algorithm for reading them is to:
(1) Look at the background uptake. I use this to set my sensitivity when I compare it to prior
studies. Ideally you used the same kind of contrast, and imaged at the same time of the
month. As I'll mention below, hormone changes with female cycles cause changes in
how much contrast gets taken up (less early, and more later).
(2) I look for masses or little dots (foci). MIPS (maximum intensity projections) are helpful
just like looking for a lung nodule. If I see a mass or dot I try and characterize it - first by
seeing if I can make it T2 bright. Most T2 bright things are benign (lymph nodes, cysts,
fibroadenoma). If it's not T2 bright, I look at the features - is it a mass? is it spiculated,
etc? These features are more important than anything else. Is it new? Nipple
enhancement is ok - don't be a dumb ass and call it Pagets.
(3) Finally I'll look at the wash out curve, but honestly I've made up my mind before I even
look at that. I will never let a benign curve back me off suspicious morphology.
(4) I deal with the findings similar to mammo. New masses get BR-4 or BR-5. NMLE (non
mass enhancement) gets BR-4'd if new. T2 bright stuff for the most part (there is one
exception of mucinous cancer) gets BR-2'd. Anything with a 4 or a 5 gets biopsy - via
MR guided stereo. I never pussy foot out and BR-0 something on MRI - unless it's a
technical problem (example inadequate fat sat).
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Who gets a screening MJU ?
• People with a lifetime risk greater than 20-25%
• Includes people who got 20 Gy of radiation to the chest as a child
How do you estimate this risk, to decide who is 20-25%?
• You use one o.fthe risk models that includes.family history (NOT the Gail model). 1.fthe
question is which of the.following is Not one to use ? The answer is Gail. 1.fthe
question is which of the.following do you pick? I'd chose Tyrer-Cuzick, its probably the
best one out now.
Parenchyma Enhancement:
• Is it normal ? - Yes
• Where is it most common ? - Posterior Breast in the upper outer quadrant, during the later
part of the menstrual cycle(luteal phase - day 14-28)
• How do you reduce it? -Do the MRI during the first part of the menstrual cycle(day 7-14).
• What does Tamoxifen do? - Tamoxifen will decrease background parenchyma uptake.
Then it causes a rebound.
Foci:
• How is it defined? Round or oval, circumscribed, and less than 5mm,
• Are they high risk? Usually not. Usually they are benign(2-3% have a chance of being
a bad boy).
• What would make you biopsy one? Seemed different than the rest, ill-defined borders,
or suspicious enhancement.
• Can you BI-RADs 3 one? If you have a solitary focus(< 5mm) with persistent kinetics
on a baseline exam - you can Bl-RADS 3 it.
NME (Non-Mass Enhancement):
• What is NME ? It's not a mass - but more like a cloud or clump of tissue enhancement.
• What are the distributions ? Segmental(triangular blob pointing at the nipple, indicates a
single branch), Regional(a bigger triangle), and Diffuse (sorta all over the place).
• Which one is more suspicious - homogenous or heterogeneous enhancement ofNME?
Heterogeneous is much more suspicious.
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Masses:
• These are defined as being 5 mm or larger. They have definable vocabulary for their
features (round, oval, indistinct, etc ... )
• When are these bad? They are bad when you call them bad words. Irregular shape,
speculated margins, heterogeneous enhancement, or rim enhancement. Once you say
those words you are going to have to biopsy them, because morphology trumps
kinetics. It doesn't matter what the kinetics shows, you must biopsy suspicious
morphology.
• When is kinetics helpful? When you are on the fence. If you have benign morphology
and you have suspicious kinetics - you probably are going to need to biopsy that also.
Kinetics:
• Breast kinetics are performed in two portions:
o (1) Initial upslope phase that occurs over the first 2 minutes. This is graded as
slow, medium, or rapid (fast).
o (2) The washout portion which is recorded sometime between 2 minutes and 6
minutes (around about). These are graded as either continued rise "type 1",
plateau "type 2", or rapid washout "type 3".
• Risk of Cancer: Washout "3"
*High Risk
o Type 1: Curve: 6%
o Type 2: Curve: 7%-28%
O Type 3: 29% or more.
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Classic Looks:
• F'ibroadenoma: These things are classically T2 bright, round, with "non-enhancing
septa", and a type 1 curve.
• DCIS: Clumped, ductal, linear, or segmental non-mass enhancement. Kinetics are
typically not helpful for DCIS.
• lDC: Spiculated, irregular shaped masses, with heterogeneous enhancement and a
type 3 curve.
• ILC: Doesn't always show enhancement.
Fibroadenoma DCIS IDC
-Non-enhancing Septations -Segmental NME -Spiculated, with Type 3 Curve
T2 Bright Things:
• Usually T2 Bright = Benign.
• Things that are T2 Bright include: Cysts, Lymph nodes, fat necrosis, Fibroadenoma.
• The exceptions (anytime I say the word "except" you need to think high yield!):
Colloid Cancer, and Mucinous Cancer can be T2 bright.
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� Pure Trivia: �
• (fyou have a patient with known breast CA, how often do you.find a contralateral breast
CA? - Answer is 0.1-2% by mammogram, and 3-5% by MRL
• Never BR-0 an MRI case. This is as much workup as you are going to get, so just call it
benign or biopsy it. You can actually BR-0 something if you really want to prevent a
biopsy - possible lymph node - US and mammo to confirm benign sorta situation. This
is still kinda weak. For the purpose of multiple choice, think twice before you BR-0 a
MRI case.
• Spiculated margins = 80% malignancy. This is the single most predictive feature of
malignancy.
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,.
:
.· . _ �
SECTION 15:
RISK �-
Estrogen: The more exposure to estrogen, the higher your risk
Estrogen Related Risks
of breast cancer. Anything that prolongs this exposure is said
to increase risk. For example, an early age to begin Early Menstruation
menstruating or a late age to have menopause. Hormone Late Menopause
replacement therapy with estrogen alone obviously increases Late age of first
exposure. Early maturation of lobules, which can be achieved pregnancy / or no kids.
Being Fat
by getting pregnant young, reduces your risk. Being fat Being a Drunk
increases estrogen exposure (more aromatase = more Hormone Replacement
estrogen). Being a drunk increases estrogen exposure - via (with estrogen)
messing with its normal breakdown in the liver.
High Risk Lesions: Any of the high risk lesions (ADH, ALH, LCIS, Radial Scar, Papilloma)
are associated with an increased risk. These are discussed more in detail later in the chapter.
Density: Density is considered a "medium risk," and is "dose dependent" with the denser you
are the more risk you have.
Chest Wall Radiation: Chest wall radiation (usually seen in lymphoma patients) is a big risk
factor, especially at a young age. The risk is supposed to peak around 15 years post treatment.
If the child had more than 20 Gy to the chest she is going to qualify for an annual
screening MRI- at age 25 or 8 years post exposure (whichever is later).
Relatives with Cancer: A first degree relative with breast cancer increases your lifetime risk
from 8% to 13%. Two first degree relatives increases your risk to 21%.
Actual Mutations:
Chromosome 17. More common than type 2. Increased risk
BRCAl
for breast, ovary, and various GI cancers.
- -- -· ·-- -- --- .
Chromosome 13. Male carriers have a higher risk with 2.
BRCA2
Increased risk for breast, ovary, and various GI cancers.
Their p53 does NOT work, and they are high risk for all
Li Fraumeni
kinds of rare cancers.
Risk for breast cancer, follicular thyroid cancer, endometrial
Cowden Syndrome
cancer, and Lhermitte-Duclos (a brain hamartoma).
-·- · - - ·- - -- .-. .
Bannayan-Riley Ruvalcaba Associated with developmental disorders at a young age.
NF-1 "Moderate Risk" of breast cancer
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Female Cancer Risk Syndromes:
Hereditary Syndromes
Triple Negative (estrogen,
Breast Cancer (risk
Hereditary Breast and progesterone, HER2
72%)
Ovarian Cancer negative) - IDC Medullary
Ovarian Cancer (risk Fallopian Tube,
Syndrome -BRCA 1 Subtype is the most
44%) Pancreas, Colon
common breast CA
Cancers Also at
Breast Cancer (risk increased risk
Hereditary Breast and
69%)
Ovarian Cancer
Ovarian Cancer (risk
Syndrome -BRCA 2
17%)
Thyroid Cancer
(usually papillary).
Also increased risk
Breast CA is the most
of various benign
Hamartomas in common malignancy (risk
thyroid disease.
multiple organs and 77%).
Annual thyroid
gross facial and
Cowden Syndrome screening is
mouth bumps Increased risk of other
typically advised.
plague these breast conditions
unfortunate souls (fibroadenomas, ADH,
Lhermitte-
fibrocystic changes)
Duclos (dysplastic
gangliocytoma of
the cerebellum)
Hereditary Diffuse Prophylactic
Diffuse Gastric Lobular Breast Cancer
Gastric Cancer Gastrectomy is
Cancer Risk~ 70% Risk~40%
Syndrome recommended.
- '" · ~ <+••·-----·•-···-· -�"·---·�-
Breast Cancers are
Li-Fraumeni Syndrome Cancers literally
usually seen in 30s-40s
(bad p53) everywhere.
with high grade.
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Breast Cancer Risk Models:
There are several risk models, which have pros/cons and differences. I apologize in advance
for even suggesting you learn about these .... but it ,iust seems testable to me. I'm sorry ...
Focuses on personal Doesn't use genetics
Oldest and most
risk factors, biopsy of (it's too old school).
Gail Model validated breast cancer
ADH, and family Only validated in
risk model
history African Americans.
Do NOT include
Claus, BODICEA, and
Focus on genetics personal risk or breast
BRCApro related risk factors.
Focus on personal
risk, biopsy with Does NOT include
Tyrer-Cuzick "Most Comprehensive"
ADH or LCIS, family breast density.
history
High Yield Take Home Points Regarding Risk:
• Anything that gets you more estrogen increases your risk
• BRCA 1 is more common than BRCA 2 (in women).
• Men with BRCA 2 get more cancer than men with BRCA 1.
• Breast Density is an independent risk factor (denser the breast, the more the risk)
• 20 Gy of Radiation to your chest as a kid buys you a screening MRI - at 25 or 8
years after exposure (*whichever is later)
• Cowden Syndrome - Bowel Hamartoma, Follicular Thyroid Cancer, Lhermitte
Duclos, and Breast Cancer
• All current risk models underestimate life time risk.
• Tyrer Cuzick is the most comprehensive risk model, but does not include breast
density.
• Exercise (probably more like not being.fat) reduces the risk of breast cancer
• Tamoxifen and Raloxifene (SERMs) reduce incidence of ER/PR positive cancers.
Mortality may not actual be reduced (sound.familiar?).
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Screening Controversy
A red glow burst suddenly across the enchanted sky as the dark lord of statistics Gilbert
Welch published his now infamous and devious work - "Effect of three decades of
screening mammography on breast-cancer incidence, " in the unscrupulous New England
Journal of Medicine.
"I can make things move without touching them. I can make animals do what I want
without training them. I can make bad things happen to people who are mean to me. I can
make them hurt, if I want ... " - Gilbert Welch when asked about his thoughts on screening
mammography.
This loathsome, maleficent, and repugnant study (along with several other large heavily
powered studies) have brought into question the practice of screening mammograms. I
highly recommend you read these "despicable" papers, but please wait till after the exam,
because the people who write multiple choice questions about mammography are
definitely not the same people who wrote these papers.
For the purpose of multiple choice tests, screening mammography saves lots of lives, you
should buy pink ribbons, and low grade DCIS in a 95 year old needs a surgical consult.
Bleyer, Archie, and H. Gilbert Welch. "Effect of three decades of screening
mammography on breast-cancer incidence." New England Journal ofMedicine 367.21
(2012): 1998-2005.
Miller, Anthony B., et al. "Twenty five year follow-up for breast cancer incidence and
mortality of the Canadian National Breast Screening Study: randomised screening trial."
BMJ: British Medical Journal 348 (2014).
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:···
·-· �
, ·:
SECTION 16:
ACR APPROPRIATENESS
�-
These all make great "next step questions."
Remember scoring is 1-9, with 9 being the most appropriate and 1 being the least.
Breast Cancer Screening:
Variant 1: High Risk Women. BRCA (plus untested first degree relatives), History of Chest
Radiation, Risk Model Showing 20% or greater lifetime risk
• Mammo (Highly Appropriate "9"):
• Beginning at age 25-30 or 10 years before age of first-degree relative with breast cancer
• 8 years after radiation therapy, but not before age of 25.
• Mammography+ MRI? They are complementary examinations, both should be performed.
• Tomosynthesis (Highly Appropriate "9"):
• Beginning at age 25-30 or 10 years before age of first-degree relative with breast cancer
• 8 years after radiation therapy, but not before age of 25.
• Mammography + MRI? They are complementary examinations, both should be performed.
• MRI (Highly Appropriate "9"):
• Mammography+ MRI? They are complementary examinations, both should be performed.
Variant 2: Medium Risk Women. Women with person history of Breast CA, lobular
hyperplasia, Atypical Ductal Hyperplasia, or Risk Model Showing 15-20% life time risk
• Mammo and Torno are "9s"
• MRI is a 7. Mammography+ MRI? They are complementary examinations, MRI should NOT replace
mammography.
Variant 3: Average Risk Women. Women with< 15 % Lifetime Risk
• Mammo and Torno are "9s"
• MRI is a "3" which means it is NOT appropriate.
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Screening for Transgender Women
Screening Annual Mammogram IF:
• Past or Current Hormones (Estrogen & Progestin for > 5 years)
• > 50 years old
Trivia: BMI > 35 = increases Risk
Screening for Transgender Men
Screening Annual Mammogram IF:
• They still have breast tissue (even if they had a reduction mammoplasty)
Breast Pain:
Variant 1: Cyclical, Unilateral or Bilateral. Age< 40.
• No imaging is appropriate.
• Ultrasound is the least inappropriate and it's rated at a "2"
Variant 2: Cyclical, Unilateral or Bilateral. Age> 40.
• No imaging is appropriate.
• Ultrasound, Mammo, and Torno are the least inappropriate and all rated at a "2"
Variant 3: NON-Cyclical, Unilateral or Bilateral. Age< 40.
• Ultrasound Might Be Appropriate and is rated as a "5."
Stage 1 Breast CA- Initial Workup and Surveillance (No Symptoms)
Newly Diagnosed - rule out mets to the bones, chest, liver, and/or brain
• No imaging is appropriate. (CT, MRI, PET etc... not indicated with initial stage 1)
Surveillance/ Rule Out Local Recurrence
• Diagnostic Mammo or Torno is Appropriate and is rated as a "9."
• Ultrasound might be appropriate and is rated as a "5."
• MRI might be appropriate and is rated as a "5."
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Symptomatic Male Breast:
Variant 1: Any Age with Physical Exam and History Consistent with
Gynecomastia or Pseudogynecomastia (bitch tits).
• No imaging is appropriate.
Variant 2: Younger than 25 years old with indeterminate palpable.
• Ultrasound is Appropriate and is rated as an "8."
• Mammo is in the "May Be Appropriate" category as a "5." I would only do this if the ultrasound
doesn't answer your question. ** Page 44 I, Scenario 4A - has suggested multiple choice strategy.
Variant 3: Older than 25 years old with indeterminate palpable.
• Mammo is Appropriate and is rated as an "8"
• Ultrasound is in the "May Be Appropriate" category as a "5."
Variant 4: Older than 25 years old with indeterminate palpable. The
mammogram was indeterminate or suspicious.
• Ultrasound is Appropriate and is rated as a "9."
Variant 5: Physical exam is highly concerning for cancer. Dude has an
ulcerative mass, axillary nodes, nipple retraction, etc...
• Mammo is Appropriate and is rated as an "9"
• Ultrasound is Appropriate and is rated as an "8" - to stage the breast and axilla just like a female breast
CA workup.
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Random Situations - First/Next Step:
Women> 40 with Palpable
• Mammo is Appropriate and is rated as a "9."
Women> 40 with Mammo Suspicious for CA
• Ultrasound is Appropriate and is rated as a "9."
Women> 40 with Mammo findings of a Lipoma at the Site of a Palpable.
• No additional imaging is appropriate.
Women> 40 with Palpable Findings and a Negative Mammo
• Ultrasound is Appropriate and is rated as a "9."
Women< 30 Initial Evaluation
• Ultrasound is Appropriate and is rated as a "9."
Women 30-39 Initial Evaluation
• Ultrasound is Appropriate and is rated as a "8."
• Mammo is Appropriate and is rated as a "8."
Women< 30 Ultrasound is Suspicious for CA
• Core Biopsy is Appropriate and is rated as a "9."
• Mammo is Appropriate and is rated as a "8."
Women< 30 Ultrasound is Negative
• No imaging is appropriate.
Women< 30 Ultrasound has a B9 finding (like a cyst)
• No imaging is appropriate.
Women< 30 Ultrasound is BR3 able - example fibroadenoma
• Short interval followup - usually Q6 months x 2 years.
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-�
-'.- SECTION 17:
PROCEDURES � •... '
;, .
· ..
The most common procedures are going to be ultrasound guided and stereotactic biopsy of
masses and calcification. I'll try and touch on the testable points.
Ultrasound:
• Overall ultrasound is faster and easier than stereo. If you can see the mass under US - you
should do the biopsy under US.
• Usually a 14 gauge automatic spring loaded device is used for masses
• You should put the mass on the far side of the US screen - lets you see the length of the
needle better
• Ideally 4 things should line up during the biopsy: the lesion, the transducer, the skin nick,
and the biopsy needle
• The needle angle should be parallel to the chest wall (pneumothorax is an embarrassing
complication of a breast biopsy)
• Anesthetic should be placed right up to but not into the lesion (especially when the lesions
is small).
• You should try and biopsy the deeper part of a lesion first. If you obscure it from bleeding
at least you can still get the superficial part.
• If you have two lesions to biopsy, try and hit the smaller one first. If the bigger one bleeds
it may obscure the smaller one - it's less likely the other way around.
• If you have a solid and cystic lesion - you should biopsy the solid part.
• About 90% of the time you can make a diagnosis off 1 or 2 passes (though most texts still
recommend doing 5).
Next Step Scenario - Like an idiot you injected a bunch of air around the mass, while you were
trying to give lidocaine. Now you can't see the mass. What do you do? You have to reschedule.
Don't try to biopsy it blind.
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Axilla:
• When you biopsy an axillary lymph node you should target the node's cortex.
• Core biopsy is preforreJ over FNA if you have no due what it is. If you have known breast
cancer and you are nearly certain you are dealing with a met - FNA works fine.
Special Scenario - The Cyst Aspiration
• Indications - Anxiety, pain, uncertain diagnosis.
• Size is NOT an indication for aspiration
• Cysts recur about 70% of the time (this drops to around 15% if you inject air after you
aspirate).
The Hypoechoic Mass vs Dirty Cyst Scenario
-Classic "Next Steps" -
Next Step Scenario #I - You suspect a hypoechoic mass is a debris filled cyst rather than
a solid mass ... but you aren't totally sure. What should you do first ? Aspirate it.
Next Step Scenario #2 - Same hypoechoic mass vs cyst - you aspirate it and you get non
bloody fluid. You also notice the lesion disappeared. What do you do ? You should pitch
it, no need for cytology. You are done.
Next Step Scenario #3 - Same hypoechoic mass vs cyst - you aspirate it and you get
bloody fluid. You also notice the lesion disappeared. What do you do ? Send it to
cytology and then place a clip.
Next Step Scenario #4 - Same hypoechoic mass vs cyst - you aspirate it and you get
purulent "poop like" fluid. The fluid smells like a zombie farted. You also notice the
lesion disappeared. What do you do ? Send it to the microbiology lab for culture and
sensitivity.
Next Step Scenario #5 - Same hypoechoic mass vs cyst - you aspirate it and you get fluid.
You also notice the lesion does NOT disappear. What do you do ? Proceed to core biopsy
of the residual solid mass.
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Stereotactic Biopsy (using a mammogram to localize and target the lesion).
• This is the preferred move for calcifications. Typically the specimen
is x-rayed after the sample to confirm there are calcifications within Gauge Size vs
Samples:
the biopsied tissue.
- 10-11 Gauge
• Vacuum assisted devices are typically used for calcifications. Needle= 12
Samples
• The biopsy is performed in compression - with slightly less pressure
than a normal mammogram. Compressibility of the breast tissue can · - 7-9 Gauge
Needle= 4
NOT be less than 2-3cm (some texts say 28 mm). Otherwise you risk
Samples
throwing the needle through the other side of the breast into the ,_ ---------------------------
digital receptor. This is called a "negative stroke margin."
• Next Step Scenario: What if the breast compresses too small(< 20 mm) ? You should do a
wire localization for excisional biopsy.
• A marker (tiny piece of metal) should be placed after each biopsy. Clip migration can occur
(accordion effect). You will need a mammogram in the orthogonal view to evaluate for this
post placement.
• QC "Localization and Accuracy Test" to verify system alignment and performance is
performed Daily before patient exams.
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.
•
.
�
SECTION 18:
MQSA � •.:.";
The U.S. Food and Drug Administration Mammography Quality Standards Act(MQSA) - yes that
is a real thing - demands a medical audit and outcome analysis be performed once a year. You are
forced to follow up patients with positive mammos, and correlate with biopsy pathology results(so
you can see how much benign disease you biopsy and how much fear / anxiety you generate). You
have to grade the biopsy with the risk category(you can't accept benign results with a BR-5).
MQSA and Other Crap they could ask:
• 3 months of mammography is required during residency training
• The recall rate should be less than 10%
• Mammography facilities are required to provide patients with written results of their
mammograms in language that is easy to understand. Also known as a "lay report," and
must be given within 30 days of the study.
• A consumer complaint mechanism is required to be established in mammography
facilities to provide patients with a process for addressing their concerns.
• Patients can obtain their original mammograms, not copies, when they are needed.
• For cases in which a facility's mammograms are determined to be substandard and a
risk to public health, facilities will notify the patients and their doctors and suggest an
appropriate plan of action.
• The "Interpreting Physician" is ultimately responsible for the Quality Control program.
• The required resolution of line pairs is 13 lp/mm in the anode to cathode direction and
11 line pair / mm in the left right direction
• To make it pass image quality; must show 4 fibers, 3 microcalcification clusters, and 3
masses, plus "acceptable artifacts".
• The dose phantom is 50% glandularity, 4.2 cm thick, and is supposed to have a dose
less than 3 mGy per image(+ grid).
• Don't get it twisted; there are no patient dose limits in mammography, only a phantom
dose. A dense breast can result in a higher patient dose, which could easily exceed 3
mGy/view.
• Typical patient and phantom doses are about 2 mGy per view, or 8 mGy for a bilateral
two view(Left CC+ MLO, Right CC+ MLO) screening examination.
• The typical(average) compressed breast is 6 cm, glandularity of 15 to 20%.
• Digital systems generally uses higher beam qualities which results in lower doses;
• Digital mammography does not use fixed dose(screen-film); can use as much(or little)
radiation as deemed appropriate.
• Male Residents must urinate in the sitting position while on the mammography service
(standing urination is not allowed per MQSA).
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Processor QC Daily
Darlaoom Cleanliness Daily
Viewbox Conditions Weekly
Phantom Evaluation Weekly
Repeat Analysis Quarterly
Compression Test Semi-Annually
Darlaoom Fog Semi-Annually
Screen-Film Contrast Semi-Annually
Evil Overlord behind MQSA? FDA
During the last two years of training you have to read 240
Formal Training Requirement 3 months
Documented Hours of Education 60
-
'=::)i\ :'.·_;;'::/':::·-_: .·:\:';::::�/-i_-:·::;--... -;:
·_ - ··_-_=·:::_ -\· ;_:-·-_;<-:-:.; ,-____ ·----- s..____.______
:
- ·: >y · :
Male residents may urinate in the following
Seated only. Standing urination is prohibited.
position(s) while on the mammo service?
The penis of the male resident should be in
Tucked posterior and secured with tape*
what orientation while on the mammo
(Glue - ffperforming a 3 month focus time)
service?
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•
. ·. �
SECTION 19:
SCENARIO/ REVIEW
As l promised in the first pages of the chapter, l want to finish by rolling through some
scenarios. This is mainly to demonstrate the work flow process and how you handle "next
step" type questions.
Scenario l: A 40 year old woman presents for her baseline screening mammogram. You have the
great pleasure of reading it. While conducting your normal reading pattern you notice the posterior
nipple line is 9cm on the MLO, but only 6 cm on the CC.
What do you do ? - The would be a technical call back
What BR ? - This is a BR-0
Scenario 2a: A 50 year old woman presents for her annual screening mammogram. You have the
great pleasure of reading it. You notice a mass on two views in the lateral left breast.
What BR? - This is also BR-0.
Next Step ? Return for diagnostic mammogram, including spot compression views and likely an
ultrasound.
Scenario 2b: Same patient returns for the diagnostic mammogram. You can clearly see the mass in
two views.
Next Step ? Ultrasound to further characterize
Scenario 2c: You put her in ultrasound and see an obvious shadowing angry, pissed off, mass that is
ulcerating through the skin etc.... It I 00% for sure cancer.
Next Step? You need to stage. Scan the rest of the breast for multi-focal masses, AND scan the axilla
for pathologic nodes.
Scenario 3a: A 50 year old woman presents for her annual screening mammogram. You have the
great pleasure of reading it. You notice what looks like a mass in the CC view only (can't find it in
the MLO). You call it an "asymmetry" because you can only see it in one view.
Next Step ? BR-0, and bring it back with spot compression views
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Scenario 3b: Same patient returns for the diagnostic mammogram. After the paddle is applied there
does not appear to be any mass. It just looks like normal breast tissue. You look at prior imaging and
it looks pretty similar to the priors now.
Next Step? BR-1, and return to screening. This is the classic scenario of a "does not persist" callback.
But Prometheus!? ACR Criteria says .•..
A common source of confusion is the distinction is between variant 1 and variant 2 ACR criteria for
male breasts. The overwhelming majority of male breast path is gynecomastia which will look like
a BR-5 mass on ultrasound. The ACR actually says you need no imaging to work it up.
This is how I would handle multiple choice on this:
(Scenario A) If the question specifically says "ACR criteria" and describes a palpable lesion in a
male, less than 25, with no other information in the question header to make you believe its gyno:
You need to pick Ultrasound.
(Scenario B) if the question does NOT say "ACR criteria" and describes a palpable lesion in
someone with risk factors for gyno (anabolic steroid use, pot smoking, etc ....)
Then you should either do no imaging, (if physical exam is a choice pick that), or start with a plain
film (mammogram).
(Scenario C) The third possible scenario, which would be the sneakiest way to do this, would be to
show you a study obtained at another hospital of a breast ultrasound showing a suspicious lesion in
a male around this age and ask you what to do next.
The answer here is always going to be x-ray (mammogram). A work up for cancer on a male
breast is NEVER EVER EVER complete without a mammogram ("man" o gram) - with the
teaching point being that gynecomastia looks like cancer on ultrasound, but is easily identified as
benign on a mammogram
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Scenario 4a: A 24 year old MALE presents as with a palpable mass in his left breast.
Next Step? Mammogram (never ultrasound a male breast before you get a mammogram).
Scenario 4b: A mammogram is obtained, and shows a flame shaped density under the nipple,
correlating with the palpable marker.
Next Step ? Interview the patient to see if you can come up for a reason for his gynecomastia (psych
meds, marijuana use, etc ... ). You don't want to miss a pituitary tumor. He tells you he smokes pot
every day. You tell him that he is a very bad boy - even though there is no evidence that marijuana
causes real harm and it's criminalization was based on false propaganda from the hemp industry.
Scenario 4c: After you tell him he is a bad boy for smoking the sticky icky, he still seems worried.
He tells you that he got an ultrasound at the outside hospital and they told him he had breast cancer.
He pulls a CD out of his pocket and asks you to look at it. You look at the outside images and sure
enough there is a shadowing mass in the area of the palpable finding.
Next Step? BR-2 Gynecomastia. This is the oldest trick in the book - gynecomastia looks like a scary
mass on US - that's why you always start with the mammogram.
Scenario Sa: Screening mammogram is performed on a 70 year old woman, who has a history of
prior lumpectomy 4 years ago. You read in her chart that she refused radiation therapy. She
heard on the news that radiation was bad, so she decided on a more holistic approach (bananas)
- she also gets yearly thermograms. The area of scarring in the resection bed looks more dense.
Next Step? BR-0, and recall for spot compressions.
Scenario Sb: The spot compressions show small calcifications in the area of the lumpectomy
bed, and the scar is definitely more dense.
Next Step ? Mag views to further characterize the calcifications. You decide they look pointy so
you call them fine pleomorphic.
Scenario Sc: You stick her in ultrasound to be complete - it looks like a small mass. You stage
the remainder of the breast and axilla - and it looks pretty clean.
Diagnosis ? BR-5 - local recurrence.
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111�1�
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? C
, ) ::t'
�,
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15
STRATEGY
PROMETHEUS LIONHART, M.D.
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• .
�
SECTION 1:
PLAYER VS ENVIRONMENT
.. � •
The 3 Kinds of Questions
1. The ones you know - you want to get 100% of these right
2. The ones you don't know-you want to get 25% of these right (same as a monkey
guessing)
3. The ones you can figure out with some deep thought - you want to get 60-70% of
these right.
If you can do that you will pass the test, especially if you've read my books.
My recommendations:
- For the ones you know, just get them right.
For the ones you don't know - just say to yourself "this is one I don� know,
Prometheus says just try and narrow it down and guess. "
For the ones you think you can figure out, mark them, and go through the entire exam.
If you follow my suggestion on the first two types of questions you will have ample
time left over for head scratching. Other reasons to go ahead and do the whole exam
before trying to figure them out is (a) you don't want to rush on the questions you can
get right, and (b) sometimes you will see a case that reminds you of what the answer
is. In fact it's not impossible that the stem of another question flat out tells you the
answer to a previous question.
Let your plans be dark, and impenetrable as night, and when you move, fall like a thunderbolt.
-Sun Tzu
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Studying for a C-
For many of you this is the first time you truly do not need an A on the exam. I can
remember in undergrad and medical school feeling like I needed to get every question
right on the exam to maintain my total and complete dominance.
I felt like if I missed a single question that I wouldn't honor the class, I wouldn't match
radiology, and I'd end up in rural West Virginia checking diabetic feet for ulcers in my
family medicine clinic. The very thought of a career in family medicine was so horrible
that I'd begin to panic.
Panic doesn't help!
Truly this exam is not like that. You can miss questions. You will miss questions. You
can miss a lot of questions. You just need to miss less than about 10% of the room. No
matter what they tell you, no matter what you read all standardized exams are curved. If
they passed 100% - the exam would be called a joke. If they failed 50% the program
directors would riot (after first punishing the residents with extra call). The exam will
maintain a failure rate around 10-15%. What that means is that you only need to beat
10-15% of the room. You don't need 99th percentile. There is no reward for that. You
need 16th percentile. 16th percentile is a C-, that is the goal.
The reason I'm perseverating on this is that you need to avoid panic. If you mark
20-30% of the questions as "not sure" - or Promethean category 2 or 3 - you might begin
to freak out. Especially if the inner gunner medical student in you thinks you won't get
honors. Chill Out! It's ok to miss questions. Look around the room and know that you
studied harder and are smarter than 15% of the room.
Do not flee the exam in tears I
Fate rarely calls upon us at a moment of our choosing.
-Optimus Prime
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Exploiting the "Genius Neuron" �
Have you ever heard someone in case conference take a case and lead with"It's NOT this," when
clearly"this" is what the case was? It happens all the time. Often the first thing out of people's
mouths is actually the right answer, but many times you hear people say"it's not" first. Ever
wondered why?
I have this idea of a"Genius Neuron." You have one neuron that is superior to the rest. This guy
fires faster and is more reliable than his peers and because of this he is hated by them. He is the
guy in the front row waving his hand shouting"I know the answer!" You know that guy, that guy
is a notorious asshole. So, in your mind he shouts out the answer first, and then the rest of the
neurons gang up on him and try and talk him out of it. So the end product is"It's NOT this."
For the purpose of taking cases in conference, this is why you should always lead with"this
comes to mind," instead of"it's not." Now, the practical piece of advice I want to give you is to
trust your genius neuron. Seriously, there is a lot of material on this test. But if you read this
book, there will be enough knowledge to pass the test existing somewhere between your cars. You
just have to trust that genius neuron.
How?? - Do it like this:
(l) Read the entire question. Look at all the pictures.
(2) Read ALL the answer choices. Never stop at A thinking that is the answer.
(3) Look again at ALL the pictures - now that you sec the choices.
( 4) Choose the first answer your mind tells you is correct - the one your genius neuron thinks
it correct.
(5) After you have finished the test, and you arc re-reviewing your answers, NEVER change
the genius neuron's answer except for two criteria. (A) You read the question wrong. (B)
You are 100% sure that it is another choice, and you can give a reason why. Never change
based on your gut feelings. Those secondary gut feelings arc the stupid neurons trying to
gang up on the smart one. Just like in the real world, the stupid people significantly
outnumber the smart ones.
I know this sounds silly, but I really believe in this. This is a real thing. I encourage you to try it
with some practice questions.
You either believe in yourself or you don't
-Captain James T Kirk.
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Dealing with the Linked Question
It is a modem trend for multiple choice tests to have "linked" questions. You may remember
that USMLE Step 3 had them, and it is rumored that the CORE Exam has them as well.
These are the questions that prompt you with "this is your final answer, you can't change
your answer." When you see this STOP!
If you are 100% sure you are right, then go on. If you had it narrowed down to two choices,
think about which one would be easier to write a follow up question about. This might seem
obvious, but in the heat of the battle you might get too aggressive. Slow down and think
twice on these.
The second point I want to make about these questions is finding some Zen if you miss it.
There are a lot of questions on this test, it's ok to miss some. You will still pass (probably).
People like you have always studied for the A+, not the C-. So when you miss a question it
makes you freak out because you think you blew it. Calm the fuck down. You don't need an
A+ this time. You don't need a B. You just need to pass so they don't get any more money
from you. Believe me they have taken enough from you already. I just want you to
understand that you will miss questions and it's ok. If the second part reveals that you
dropped one, don't let it phase you. Just do your best. The most important fight is always
your next one.
It isn't the mountains ahead to climb that wears you out; its the pebble in your shoe
-Muhammad Ali
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It's Possible to Know Too Much
If you were to begin studying and begin taking multiple choice practice questions and you plotted
your progress as you gained more knowledge you would notice something funny. At first you
would begin to get more and more questions right. .. and then you would start to miss them.
J
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Knowledge
Well how can that be? I will tell you that once you know enough all choices on the exam become
correct. Which of the following can occur? ... well actually they can all occur - I've read case
reports of blah blah blah. That is what happens.
The trick is to not over think things. Once you've achieved a certain level of knowledge, if they
give you a gift - take it. It's usually not a trick (usually). Don't look for obscure situations
when things are true. Yes ... it's possible for you to know more than the person writing the
questions. Yes ... I said it and it's fucking true. These people don't know everything. You can out
knowledge them if you study enough - and that is when you get yourself into trouble.
Take home point - once you've reached the peak (arrow on chart) - be careful over thinking
questions past that point.
"Always remember: Your.focus determines your reality"
-Jedi Master Qui-Gan Jinn
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Jii:I 8 Promethean Laws For Multiple Choice Jii:I
#1 - If you have a gut feeling - go for it! (trust the genius neuron)
#2 - Don't over think to the extent that you veer from a reflexive answer -
especially if choices seem equally plausible (you can know too much).
#3 - Read ALL the choices carefully
#4 - If it seems too obvious to be true (trickery), re-read it and then go with it
(even if it seems too easy). Let it happen - it's usually not a trick ... usually.
#5 - Add up what you know you know, and compare with what you think you
know. Weight your answers by what you KNOW you KNOW.
#6 - If you are torn between two choices, ask yourself "which of these is
NOT correct?" - Sometimes making your brain work backwards will
elucidate the solution.
#7 - Do NOT change your answers! (trust the genius neuron)
#8 - Most Iinportantly - Don't Panic
Maybe I can't win, maybe the only thing I can do is just take everything hes got. But to beat me,
he�, gonna have to kill me, and to kill me, hes gonna have to have the heart to stand in front of
me, and to do that, he has to be willing to die himself
- Rocky Balboa
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a...
; �
SECTION 2:
KNIT THE SOCKS OF DEATH
AS GIFTS FOR ALL WHO DARE OPPOSE YOU
Problem Solving Through MRI
Different programs have variable volume with MRI. Some of you will be excellent at it.
Some of you will suck at it. An important skill to have is to understand how to problem solve
with different sequences. The best way to do this is to have a list of T l bright things, T2
bright things, dark things, and things that restrict diffusion.
Tl Bright T2 Bright
Fat Fat
Melanin (Melanoma) Water
Blood (Subacute) Blood (Extracellular
Methemoglobin)
Protein Rich Fluid Most Tumors
Calcification
(Hyalinized)
Slow Moving Blood
Laminar Necrosis
Be able to move through sequences and problem solve.
Think about a Lipoma for example. This will be T l bright, T2 bright, and fat sat out.
Another example might be something with layers in it. What can layer? Fat could layer,
water could layer, blood could layer, pus could layer. Fat would be bright/ bright. Water
would be dark on T l . Pus would be dark on T2. Blood could do different things depending
on it's age. Fat would sat out. Pus may restrict diffusion (like a subdural empyema). You get
the idea. Run through some scenarios in your mind. The key point is to know your
differentials for this.
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Battle Tactics: Peds Neck
This is my suggested strategy. I typically start with cyst vs solid. Then I consider location,
morphology, and choice of modality (attempted mind reading of the question writer).
• *MIDLINE
• Ultrasound in Axial Planes
Thyroglossal Duct Cyst • CT I MRI in Sagital Planes
• Posterior to Tongue
• Anterior to Hyoid
• *LATERAL
Brachia! Cleft Cyst • Axial Plane Most Likely
• Anterior to the
Sternocleidomastoid (type 2)
• Looks Just like BC Cyst - but
Necrotic Level 2 Node the kid is too old (late teens /
"young adult")
• Thyroid CA, or Nasopharyngeal
HPV related CA
• CT axial plane - most likely
• T2 Bright
Looks Cystic • Enhances
Hemangioma of Infancy
• Will have flow in it on doppler
• If you saw it you'd think to
yourself "if that doesn't involute
that kid is never getting a date
to prom"
• OB Ultrasound - most likely
modality
Cystic Hygroma • T2 Bright
• DOES NOT Enhance
• Will NOT have flow in it on
doppler
• Turners, Downs.
• Kinda looks like a big dilated
Phlebectasia jugular vein (because it is a big
dilated jugular vein)
• No stenosis or collaterals
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• Jugular Vein with a clot - they
will have to prove that has a
Septic Thrombophlebitis clot in it - probably with
Doppler US
• Lemierre's Syndrome
• Septic Emboli to the lungs
• Recent ENT procedure, or
Infection
• Fusobacterium Necrophorum
• Back of the tongue or in front
Ectopic Thyroid of the hyoid
• Tc-MIBI, or 1-123
• Ultrasound
Looks Solid Fibromatosis Coli • "Two Heads" of the
Sternocleidomastoid
• MRI or CT
Rhabdomyosarcoma • Seriously pissed off looking
mass (probably in the orbit -
maybe in the masticator
mass)
• Enhances heterogenous,
• MRI or CT
• Soft Tissue Mass,
• Calcifications,
Metastatic Neuroblastoma
• Restricted Diffusion
• Classic is the orbit
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Battle Tactics: Congenital Heart on CXR
Right
I ► TOF or Truncus
r \
(1) What side is the arch on?
.
'b' Pulmonary
&<o Vasculature
,<::-
Left
Truncus TOF
Types 1-3
�-----� Massive
Cyanotic (2) Heart Size ► Ebsteins or
Pulmonary Atresia without VSD
*They have to tell you this,
Non-Cardiac (won't be cyanotic)
if they want a single answer -Infantile Hemangioendothelioma
-Vein of Galen Malformation
NOT-Cyanotic (3) Pulmonary Blood Flow
-TAPVR (especially type 3) -TOF
-D-Transposition -Ebsteins
-Truncus (look for R Arch) -Tri cuspid Atresia
-"Tingle Ventricle"
Cyanotic Not Cyanotic
Walking through this outline. First ask -·---······�·---···--•e.•
TOF t
"'. ··---·- ·-·. --··-· -···---·----- ... ·--·-···-·--·-- -·--·-···-·
ASD
yourself is it cyanotic or not? They will TAPvi
- •···-···· -·
have to tell you this in the stem. Look Tr1111�pC>�i!i()11 PDA
for this in the stem every time, then cross Truncus PAPVR
--·--·· ··----·••-'••�·-··---•-·------j
Tricuspid Atresia Aortic Coarctation (adult type -
out answers that are not cyanotic. post ductal)
Example: Patient ''X" is a newborn cyanotic, what is the most likely Dx?
A-VSD
B-ASD
C- Demonic Possession
D-TOF
Without even looking at a picture (which they will probably show), you know the answer is
D, because that is the only cyanotic one listed. If you were wondering about C - I did a
google scholar search for "Demonic Possession causing cyanosis ", and although there were
a few case reports none come down hard on cyanosis.
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Battle Tactics: Neonatal Chest
Lung Volume
Symmetric Pattern
Pleural Effusions
ess Symmetric
✓
(looks like
i;t / \ � erihilar I Streaky Not Usually
pulm ry
\
ede
25Y_�P
°,/
\
Transient Meconium
Tachypnea Aspiration Beta
Surfactant-
Hemolytic
Deficient
or
Non GB Pneumonia
"Pulmonary Edema Disease (SOD)
Neonatal
+ Effusions" "Diffuse Granular"
Pneumonia
"Diffuse Granular"
THIS vs THAT: Meconium Aspiration or Non Group B Strep Pneumonia
This is super tough without any history, and because of that I feel like the test writer has
two options: (1) Stop being an asshole and give you some history, (2) not include both as
answer choices - assuming only one is correct. Now, along those lines if you saw both as
choices and the question header gives you no history you could eliminate them both as
distractors - because they both can't be correct.
Example: What color is this box
A-Blue ✓
B-Looks Red
There can be situations where the picture is not
C - It has a Red Appearance necessary to get the question right. They could
show you a picture of a grilled cheese sandwich
and call it a chest x-ray. It could still be possible
to get the question right by eliminating all but one
possible choice. The question header can help
you disqualify (as we discussed with cyanotic
heart disease) or you can try and find choices that
cannot be distinguished from each other. Both
answers can't be right - so they must both be
wrong.
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Battle Tactics: Peds Chest & Misc
Prematurity - Guessing that the kid is premature can be helpful for eliminating
choices (Meconium Aspiration is more of a post term thing), and raising your pretest
probability (SDD, or NEC in a belly film). There are two main clues:
(l) Humeral Head Ossification - This tends to occur closer to term. If the humeral
head is NOT ossified you can assume (in the world of multiple choice) that the kid
is likely premature.
(2) Lack of Subcutaneous Fat - Premature kids tend to be very skinny, although I think
of this more of a soft sign that is useful when absent more than present. I'll just
say that if the kid appears chubby he is probably NOT premature.
The Thing in the Lung:
Left Upper Lobe:
Think Congenital Lobar Emphysema (CLE) first. But,
remember CCAM has no lobar prevalence, so it can be
anywhere
Left Lower Lobe:
Think Sequestration First. Congenital Diaphragmatic
Hernia (CDHs) favors this side too
Case 1. Newborn with Case 2. 10 year old with *Intralobar is seen
congenital heart disease recurrent pneumonia older kids,
**Extralobar is seen
A. Intralobar Sequestration A. lntralobar in infants with co
B. Extralobar Sequestration morbids
Sequestration B. Extralobar Sequestration ** CLE is in the
C. Congenital Lobar C. Congenital Lobar upper lobe
Emphysema Emphysema
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NG Tube Tricks: The presence of an NG
tube (especially if not placed correctly) should
alert you to some form of trickery.
The NG tube stops in the upper thoracic
esophagus: Think esophageal atresia (probably in
the setting ofVACTERL).
The NG tube curling into the chest- it's either (1)
in the lung, or (2) it's in a congenital
diaphragmatic hernia. If I had to pick between the NG Tube Curls in the upper thoracic
two (and it wasn't obvious), I'd say left side esophagus. First think Esophageal
hernia, right side lung - just because those are the Atresia. Then think VACTERL
more common sides.
The Classic Congenital Lobar Emphysema Trick: They can show you a
series of CXRs. The first one has an opacity in the lung (the affected lung is fluid filled). The
next x-ray will show the opacity resolved. The following x-ray will show it getting more
lucent, and more lucent. Until it's actually pushing the heart over. This is the classic way to
show it in case conference, or case books
The School Aged CXR: Things to look.for:
• Big Heart - Probably showing you a sickle cell case. Look for bone infarcts in shoulders.
• Lucent Lung - Think foreign Body (air trapping). Remember you put the affected side
down (if it remains lucent- that confirms it).
THIS vs THAT: Cystic Fibrosis vs Primary Ciliary Dyskinesia
CF PCD
-
Abnormal Mucus-Cilia can't clear it
- •• •---• •• • • - •-••••o••-••-• •• • -••••�• . , • • • --••-
Normal Mucus-Cilia don't work
. . ·-•·s, ·-·····--·---------- --· ---- •--·------- -· ......,. ..... -··· -·------
I3r()�c,lli�c.tctsi�. (t1pp��)'?9��) I3r<:li.-ic._lli�<.:!ct�j�_{l()',\f�� l�b�s)_
Normal sperm, obliterated vas deferens Normal vas deferens, sperm cannot swim
normall
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Battle Tactics: Peds Misc
The Mandible: There are only a few things that a mandible will be shown for with
regards to Peds. Think Caffeys first - especially if the picture looks blurry and old (there
hasn't been a case of this in 50 years). If it's osteonecrosis think about O.I. on
bisphosphonates. If it's a dwarf case, think wide angled mandible with Pycnodysostosis. A
"floating tooth" could be EG.
The Abdominal Plain Film - on a newborn - Problem Solving Bubbles:
Pattern Path Next Step
Single Bubble: In a newborn this is Gastric
(antral or pyloric atresia).
In an older child think
gastric volvulus
Double Bubble Duodenal Atresia
Triple Bubble Jejuna! Atresia
Single Bubble + Distal Gas Concern for Mid Gut Next Step= Upper GI
+ "Bilious Vomiting Volvulus
Multiple Dilated Loops Concern for lower Next Step= Contrast Enema
obstruction
THIS vs THAT: Duodenal Atresia vs Jejunal Atresia:
.Duodenal Atresia . Jejunal Atresia
Double Bubble Triple Bubble
Failure to Canalize (often isolated atresia) Vascular Insult * More likely associated with
other atresias
Associated with Downs
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THIS vs THAT: Intralobar vs Extralobar Sequestration
No pleural covering Has its own pleural covering
More Common Less Common
Presents later with recurrent infection Presents early with other bad congenital things
(heart, etc ... )
Heterotaxia: This can be infe1Ted or asked several ways.
lljgllt §!ded Left Sided ... -- - ·- - - · - .. .
Two Fissures in Left ______,._,______ - ---- --- ----- - ------ ----- --- --IQ11�__fi��1:lt�
- i11 B}ght[:,1:1J:1g____
Asple11ic1 - -- - ----------- - i:>�ly�pl�l'.lict
Increased Cardiac Malformations Less Cardiac Malformations
Reversed Aorta/IVC Azygous Continuation of the IVC
Orbital Calcifications: Lesstha113 Oldertha113
Retinoblastoma Toxo
CMV Retinal Astrocytoma
Colobomatous Cyst
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Battle Tactics: Abdominal Masses / Diffuse Pathology
·.
J>eds Liver Masses
Atwociatcd:
Infantile Hepatic
Endothelial Progressively High Output CHF
Hemangioma Age 0-3 growth factor Calcify - as they
is elevated involute Skin Hemangiomas
Risk Factor =
Prematurity
may cause
Age 0-3 AFPis Calcifications Many
Hepatoblastoma precocious
elevated are Common Association:
puberty
Wilms,
Beckwith-
Weidemann
Calcification are
RARE
Mesenchymal
Age 0-3 AFPis CYSTIC MASS "Developmental anomaly"
Hamartoma negative
Favors Right
Lobe
AFPis Kids with cirrhosis (biliary
HCC Age> 5 elevated atresia, Fanconi syndrome,
glycogen storage disease)
Calcifies more No Cirrhosis
Fibrolamellar Subtype AFPis often than
HCC Age> 5 negati� conventional Central Scar (scar does NOT
HCC enhance, and is T2 dark)
Undifferentiated AFPis Cystic I
Embryonal Sarcoma Age> 5 negative Heterogeneously Known to rupture
Solid Mass
Fetus - 4
Mets
(Neuroblastoma, Wilms) 6 - Early Multiple Masses in the Setting of Known Primary
Teens
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Adult Benign Liver Masses
Ultrasound CT MR Trivia
Hemangioma Hyperechoic Peripheral T2 Bright Rare in
Nodular Cirrhotics
Discontinuous
Enhancement
FNH Spoke Wheel Homogenous "Stealth Central Scar Bright on
Arterial Lesion - Iso Delayed Eovist
Enhancement on Tl and (Gd-EOB-
T2" DTPA)
Hepatic Adenoma Variable Variable Fat OCP use, Can explode
Containing Glycogen and bleed
on In/Out Storage
Phase Disease
Hepatic Hyperechoic Gross Fat Tl/T2 Bright Unlike renal Tuberous
Angiomyolipoma AML, 50% Sclerosis
don't have fat
Sulfur Colloid HOT or COLD
Hepatic Adenoma COLD
40%HOT,
FNH 30%COLD,
30% Warm
Cavernous Hemangioma COLD RBC Scan HOT
HCC COLD Gallium HOT
Cholangiocarcinoma COLD
Mets COLD
Abscess COLD Gallium HOT
Focal Fat COLD Xenon HOT
Regenerative Nodules Dysplastic Nodules HCC ..
Contains Iron Contains Fat, Glycoprotein
Tl Dark, T2 Dark Tl Bright, T2 Dark T2 Bright
Does NOT Enhance Usually Does NOT Enhance Does Enhance
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HCC FLHCC
FNH FLHCC
Cirrhosis No Cirrhosis
T2 Bright T2 Dark (usually)
Older (50s-60s) Young (30s)
Enhances on Delays Does NOT enhance
Rarely Calcifies Calcifies
Sometimes Mass is Sulfur Colloid Mass is Gallium Avid
Avid (sometimes)
Elevated AFP Normal APP
Think Colon First
Mets - unless they have a known primary
HCC Does the Liver look Cirrhotic?
Regeneratice Nodules Does the Liver look Cirrhotic ?
Low Density Nodes - Think Mycobacterium
Infections
Hyperenhancing Nodes - Think Bartonella
Spleen Should be Involved Also
Sarcoid Gamesmanship - Probably gets some hints in the form of a CXR, or
Labs ( elevated ACE)
Different Size Cysts Viral Hepatitis Starry Sky (US)
AD Polycystic (small and big)
Kidney Renal Cystic Disease
Pyogenic Abscess Double Target (CT)
Von
Small ( < 1.5 cm)
0
Meyenburg
Complex Will NOT connect with Ducts
(Hamatromas) Uniform distribution Candida Bull's Eye (US)
Choledochal WILL communicate with duct Amoebic Abscess "Extra Hepatic
Cysts (Caroli) Central "dot" Sign Extension"
Bacterial and Fungal =
Multiple, R > L Hydatid Disease Water Lily, Sand Storm
Amoebic = Single and Sub-
Abscess diaphragmatic cT@ @us
Peripheral Enhancement
Necrotic center will not Schistosomiasis Tortoise Shell
enhance
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Primary Hemochromatosis Secondary Hemochromatosis
Genetic - increased absorption Acquired - chronic illness, and multiple
transfusions
Liver, Pancreas Liver, Spleen
Heart, Thyroid, Pituitary
AIDS PSC
Focal Strictures of the extrahepatic duct> 2cm Extrahepatic strictures rarely> 5mm
Absent saccular deformities of the ducts Has saccular deformities of the ducts
Associated Papillary Stenosis
lntrahepatic Extrahepatic ONLY
Primary Sclerosing Cholangitis Post Cholecystectomy
Infectious Cholangitis Sphincter of Oddi Dysfunction
Pancreatic Head Mass Type 1 Choledochocyst
CBD Stone - Late CBD Stone - Early
Biliary Stricture
CP Cancer
Dilation is Irregular Dilation is unifonn (usually)
Duct is< 50% of the AP gland diameter Duct is> 50% of the AP gland diameter
(obstructive atrophy)
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Primary Hemochromatosis Secondary Hemochromatos.is
Genetic - increased absorption Acquired - chronic illness, and multiple
transfusions
Liver, Pancreas Liver, Spleen
Heart, Thyroid, Pituitary
AIDS PSC
Focal Strictures of the extrahepatic duct> 2cm Extrahepatic strictures rarely> 5mm
Absent saccular deformities of the ducts Has saccular deformities of the ducts
Associated Papillary Stenosis
Intrahepatic Extrahepatic ONLY
Primary Sclerosing Cholangitis Post Cholecystectomy
Infectious Cholangitis Sphincter of Oddi Dysfunction
Pancreatic Head Mass Type 1 Choledochocyst
CBD Stone - Late CBD Stone - Early
Biliary Stricture
. •· •.· vsTIHITfChronfo
·. . ·. • · · }e�ttf l\tf1iii}J.>�ncr��titis Du
niitc£Y QijcfDil
CP Cancer
Dilation is Irregular Dilation is uniform (usually)
Duct is < 50% of the AP gland diameter Duct is> 50% of the AP gland diameter
(obstructive atrophy)
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Uncomn1on Types and Causes, ofPancreatitis
,,
,
,, ,, ' '', ,' , ,' , ,, ',',
Autoimmune Associated with Absence of Attack Responds to Sausage Shaped
Pancreatitis elevated lgG4 Symptoms steroids Pancreas, capsule
like delayed rim
enhancement around
gland (like a scar).
No duct dilation.
No calcifications.
Groove Looks like a Less likely to cause Duodenal stenosis Soft tissue within the
Pancreatitis pancreatic head obstructive and /or strictures of pancreaticoduodenal
Cancer - but with jaundice (relative the CBD in 50% of groove, with or
little or no biliary to pancreatic CA) the cases without delayed
obstruction. enhancement
Tropic Young Age at onset, Increased risk of Multiple large calculi
Pancreatitis associated with adenocarcinoma within a dilated
malnutrition pancreatic duct
Hereditary Young Age at Onset Increased risk of SPINK-] gene Similar to Tropic
Pancreatitis adenocarcinoma Pancreatitis
Ascaris Most commonly Worm may be seen
Induced implicated parasite within the bile ducts
in pancreatitis
, ,
WhenJ Say .; Autoimmune P�11creatitis
,'
' ,
I Say Autoimmune Pancreatitis You Say IgG4
Autoimmune Pancreatitis
Retroperitoneal Fibrosis
I Say IgG4 Sclerosing Cholangitis
Inflammatory Pseudotumor
Riedel 's Thyroiditis
THIS vs THAT:. .. . .
Autoimmune Pancreatitis vs Chronic Pancreatitis
Autoimmune Pancreatitis Chronic Pancreatitis
No ductal dilation Ductal Dilation
No calcifications Ductal Calcifications
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· •.
' . ·•· . . .. ·
·.
' . ·.. ·' .. •·.·
' ..· ...
.. '
.·..
Cystic' Pancre�t-� t�sio�s
·
. ··• · .
. .. '
' ·. ' .·. .. .
Main Branch
IPMN 40s - 50s Main Duct High Malignant Potential (60%)
Typically Benign
Side Branch 50s - 60s Favor Head, Uncinate (maybe 5% will develop malignancy)
IPMN CQmmunicates with duct
Does NOT Communicate with Main Duct
Central Calcifications
Grandma "Micro-Cystic" - "Honeycomb"
Serous Cystic F>M Favor Head Benign
>60 Glycogen Rich
Associated with von Hippe! Lindau
Does NOT Communicate with Main Duct
Mucinous Mother Peripheral Calcifications
Cystic F>M Favor Body / Tail Larger Cysts (sometimes uni-locular)
40s Premalignant
Large ( 5-10 ems)
Daughter Solid with Cystic Parts
Solid Pseudo- F>M Favor Tail Enhances like a Hemangioma
Papillary 20s Has a Capsule
Asian or Black Female
Malignant Ulcer Benign Ulcer Direct Hernia Indirect Hernia
Width > Depth Depth > Width Less common More Common
Project behind the Medial to inferior Lateral to inferior
Located within Lumen
expected lumen Epigastric epigastric
Nodular, Irregular Edges Sharp Contour Defect in Hesselbach Failure of processus
triangle vaginalis to close
Folds adjacent to ulcer Folds radiate to ulcer
NOT covered by
Covered by internal
Aunt Minnie: Carmen Aunt Minnie: internal spermatic
spennatic fascia
Meniscus Sign . Hampton's Line fascia
Sigmoid Volvulus Cecal Volvulus
Old Person (Constipated) Younger Person (mass, prior surgery, or 3rd
Trimester Pregnancy)
Points to the RUQ Points to the LUQ
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More Common
Slightly less common in Slightly more common in Path
With
the USA the USA
. Discontinuous "Skips" Continuous
Crohns
Terminal Ileum - String
Rectum
Sign
Primary
Ileocecal Valve Sclerosing Ulcerative Coliits
Ileocecal Valve "Open"
"Stenosed" Cholangitis
Mesenteric Fat Increased
Perirectal fat Increased
• "creeping/at"
Crohns
Lymph nodes are usually Lymph nodes are NOT
enlarged usually enlarged
Doesn't Usually Make Crohns
Makes Fistulae
Fistulae
t t
This Could Be Useful
t
Cholangio: CEA CA19-9
t
Pancreatic CA: CEA CA19-9
Colon CA: CEA CA19-9
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Peds Cystic Renal Mass
Multicystic Dysplastic Kidney AR- Polycystic Kidney Disease
- Neonate, No Renal Function (MAG 3) - Enlarged, Hyperechoic
- Associated with congenital UPJ obstruction - Microcystic
- Associated with reflux (VUR) -
Multilocular Cystic Nephroma
- "Micheal Jackson - Young Boy, Older Woman"
Multiple Cysts - Herniates into the Renal Pelvis"
Cystic Wilms
: ,:· '
·" ' . .· . .. '
Peds Tohiorl Mass·
' :· ,:
....
J{apicl l{evi�w'Iriyj� _-·,.-
. ' ..
:. . . : ': ; /
i,:, : / ·-·
,, · . - ," . ' . : ·. ,·-_;,
.. ·:- .. ' ·.. . ,· :
.
Mesoblastic
"Solid Tumor of Irifancy" (you can be born with it)
Nephroma
"Nephrogenic Rests" - left over embryologic crap that didn't go away
Might turn into wilms (bilateral wilms especially)
Nephroblastomatosis
"Next Step" - flu ultrasound till 7-8 years old
Variable appearance
90% + Renal Tumors
"Solid Tumor o.f Childhood" - Never born with it
Wilms
Grows like a solid ball (will invade rather than incase)
Met to the lung (most common)
Clear Cell - Wilms Met to Bone
Brain Tumors
Rhabdoid - Wilms
It fucks you up, it takes the money (it believes in nothing Lebowski)
Micheal Jackson Tumor (Young Boys, Middle Age Women)
Multi-Cystic Big cysts that don't communicate
Nephroma Septal Enhancement
Can't Tell it is not Cystic Wilms (next step= resection)
RCC "Solid Tumor ofAdolescent"
Syndromes - VHL, TS
Non-Hodgkin
Renal Lymphoma
Multifocal
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Neuroblastoma Wilms
Age: Usually around age 4
Age: usually less than 2 (can occur in utero)
(never before 2 months)
Calcifies 90% Calcifies Rarely (<10%)
Encases Vessels ( doesn't invade) Invades Vessels (doesn't encase)
Poorly Marginated Well Circumscribed
Doesn't usually met to bones (unless clear cell
Mets to Bones
Wilms variant). Prefers lung.
Neuroblastoma Adrenal Hemorrhage
Heterogenous and vascular Centrally Hypoechoic and Avascular
High on T2 , Iso-Low on T 1 High on T l (7 days - 7 weeks)
·--
Will grow on followup Should shrink on followup
Adult RCC Associations Bladder Cancer
Subtype Syndrome / Association
Transitional Cell The "normal" kind
Clear Cell Von Hippel-Lindau CA Bladder CA>>> Ureter CA
Papillary Hereditary papillary renal Squamous Cell Calcifications
carcmoma CA Chronic Catheter
Chromophobe Birt Hogg Dube Schistosomiasis (worm)
Adeno- Midline
Carcinoma Urachus Association
Medullary Sickle Cell Trait
Bladder Exstrophy
-·-. �
Renal Cyst Associations Urethra
Cysts in Kidneys are
ADPCKD Prostatic Urethra Transitional Cell
Liver BIG
Cysts in Bulbar / Penile Squamous Cell
VHL
Pancreas Urethra
Acquired Kidneys are Urethral Adenocarcinoma
(uremic) small Diverticulum
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Big Kidney with Lots of Cysts
AD Polycystic Kidney
Liver Cysts
Normal Sized Kidneys with Lots of Cysts
Solid Renal Masses (RCCs)
Pancreatic Cysts (simple and serous cystic) von Rippel - Lindau
Pancreatic Masses
Adrenal Masses (paragangliomas)
Renal Cysts
Multiple Fat Containing Renal Masses
Tuberous Sclerosis
(AMLs) - maybe bleeding
Lungs Cysts (LAM)
Small / Calcified Spleen
Gallstones (or absent GB) Sickle Cell
Bone Infarcts
Severe Pancreatic Fatty Atrophy
Small bowel stool Cystic Fibrosis
Fatty Liver
Big Liver, Big Spleen
Gaucher
Bone Infarcts
Extramedullary Hematopoiesis
Bilateral Adrenal Masses
(Pheochromocytoma - not adenoma) MEN2
Thyroid Cancer
Islet Cell Tumors
Pituitary Adenoma MEN l
Renal Masses (Wilms, AML)
Adrenal Masses (Pheochromocytoma)
NF-1
Skin Nodules
Scoliosis
Vascular Malformation in the Liver
Bowel Angiodysplasia
Osler Weber Rendu
Enlarged Hepatic Artery
(Hereditary Hemorrhagic Telangiectasia)
Pulmonary AV M
Brain Abscess
Cyst Morphology Trivia:
• ADPCKD - Round and Distributed Throughout Kidney
• ARPCKD - Tubular Cysts which Spare Cortex
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Battle Tactics: Schematic Thoracic Pathology
Normal Thymus Lymphoma
- Age< 10 - Age> 10
- Mass Effect - Lymph Nodes
- Homogenous _
- No Mass Effect - SVC Compression- Hodgkin> NHL
Teratoma NS - Germ Cell Tumor
- Fat - Big ·
- Cystic - Aggress1ve
- Hemorrhage - Klinefelter
- Calcifications - Necrosis
Seminoma
- Straddle Midline
- Bulky
- Lobulated
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DIP NSIP
- Apical Emphysema - Basilar Ground Glass - Honeycombing - basilar
(smoking related) (sub-pleural sparing) predominant
- Basilar Ground Glass - Traction Bronchiectasis
- Peripheral Basilar - Scleroderma Association
Reticulation (dilated esophagus)
- Smoker - Severe end of
RB-ILD
- Thin walled cysts - - Nodules with cavitation - Thin walled cysts (less than
distributed evenly (early) LAM)
- Tuberous sclerosis - Apical - "Bizarre" Cysts (late) - Ground Glass - clears with
- Smoker -20s-30s treatment
- Sparing of the costophrenic - Sjogrens, RA, HIV
recesses
Eosinophilic Aspergillosis
Pneumonia - Atoll I Reverse Halo Sign -
Consolidation around - Halo Sign - Ground Glass
- Reverse Pulmonary around consolidation
Edema Pattern Ground Glass
- Patchy, Peripheral - Air Crescent - "invasive"
(peripheral)
- Ground glass and Consolidation
consolidation
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·
·..·.
UpperLol)f Ptedominant Lower Lobe··Pre<Jo111i1lanJ
·•···
·.·. ··.• . ··
• . ·. . ..
Most inhaled stuff (not asbestosis). Coal Asbestosis
Workers, and Silicosis. This includes
progressive massive fibrosis.
CF Primary Ciliary Dsykinesia
RB-ILD Most Interstitial Lung Diseases
(UIP, NSIP, DIP)
Centrilobular Emphysema Panlobular Emphysema (Alpha 1)
Ankylosing Spondylitis Rheumatoid Lung
Sarcoid Scleroderma (associated with NSIP)
More pleural effusions and Fibrosis is uncommon. Can
pericardial effusions than get a "shrinking lung."
Lupus
with other connective tissue
disease
Looks like UIP and COP. Reticulations with or without
Lower lobes are favored. honeycombing, and
Rheumatoid Arthritis
consolidative opacities which
are orgamzmg pneumoma
NSIP > UIP; lower lobe Look for the dilated fluid filled
Scleroderma
predominant findings. esophagus.
LIP Extensive ground glass
Sjogrens attenuation with scattered thin
walled cysts.
Upper lobe fibrobullous Usually unilateral first, then
Ankylosing Spondylitis
disease progresses to bilateral.
Infections in AIDS by CD4 · ACR Appropriateness Criteria:
• First Line for Suspected Metastatic Disease
>200 Bacterial Infections, TB
=CXR
• Recommendation for patients on
<200 PCP, Atypical Mycobacterial mechanical ventilation = Daily CXR
• First Line for Chest Pain and High
CMV, Disseminated Fungal, Suspicion for Aortic Dissection =CXR
< 100
Mycobacterial
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Cardiac Trivia:
Pathology · \Vijl¢liS'1q11��ce(s).m<1st us.efril?
.
.... ,,,...___ "'"':· "" --··-··· .·.__ : �' ·:.• '_• .. _:...., .• '•.._. '.:"·. ·.. '..' •.,.;·.... ··--·- •. --· ,____ ····-••-<•'s ··--··-·····-·--·-·· .-••.•.,..
Cardiac Myxomn Low Tl, High T2 (high myxoid content)
Acute vs Chronic MI Look at T2 - Bright on Acute ; Dark on Chronic
(fibrous scar)
Arrhythmogenic Right Ventricular Tl Bright
Dysplasia (ARVD)
Microvascular Obstruction First Pass Perfusion (25 seconds post Gad)
Infarct Delayed Enhancement (10-12 mins post Gad)
Cardiac MRI Enhancement Patterns:
Subendocardial: Infarct Transmural: Infarct Subendocardial Circumferential:
Amyloidosis *can also be transmural
Midwall: Midwall: Midwall:
HCM Myocarditis, Idiopathic Dilated CM Myocarditis, Sarcoidosis
Epicardial:
Myocarditis, Sarcoidosis
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Cardiac Surgery Types / Indications
Pulmonary Artery Banding CHF in Infancy, Single Ventricle
Arterial Switch (Senning and Mustard) Transposition of the Great Arteries
Rastelli (RV Baffle) Transposition, Pulmonary Outflow Obstruction
Jatene (a type of arterial switch) Transposition
Ross Diseased Aortic Valves in Children
Bentall Aortic Root I Valve Replacement in Marfan
Additional Cardiac Surgery Pearls
Glenn Blalock Taussig Fontan
Vein to Artery Artery to Artery It's complicated with multiple
(Subclavian Artery to Pulmonary versions - steps are unlikely to
(SVC to Pulmonary Artery) Artery) be tested
Primary Purpose: Take
Primary Purpose: Bypass the
systemic blood directly to the Primary Purpose: Increase
right ventricle I direct systemic
pulmonary circulation (it pulmonary blood flow
circulation into the PAs.
bypasses the right heart).
Most Testable Complications:
Most Testable Complications: Most Testable Complications:
-Enlarged Right Artium causing
-SVC Syndrome -Stenosis at the shunt's
arrhythmia
-PA Aneurysms pulmonary insertion site
-Plastic Bronchitis
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Vasculitis:
Large Vessel
Takayasu Young Asian Female - thickened aneurysmal aorta
Old Person with involvement of the "crutches" / armpit region
Giant Cell
(Subclavian, axillary, brachia!).
Cogan Syndrome Kid with eye and ear symptoms + Aortitis
Medium Vessel
PAN is more common in a MAN (M > F). Renal Microaneurysm
PAN
(similar to speed kidney). Associated with Hep B.
Kawasaki Coronary Artery Aneurysm
Small Vessel (ANCA +)
Wegeners Nasal Septum Erosions, Cavitary Lung Lesions
Churg Strauss Transient peripheral lung consolidations.
Microscopic Polyangiitis Diffuse pulmonary hemorrhage
Small Vessel (ANCA-)
HSP Kids. Intussusception. Massive scrotal edema.
Behcets Pulmonary artery aneurysm
Buergers Male smoker. Hand angiogram shows finger occlusions.
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Nukes Trivia:
Tracer Aual()g Physical HalfLife
Tc-99m "Low" - 140 6 hours
Iodine -123 Iodine "Low" - 159 13 hours
----···· · -· · ···..--. . . .... . . .. .
"Low" - 81 125 hours (biologic tl/2
Xenon - 133 30 seconds)
- . . ···-·---· ·-·-····-·-·· -·-··----- ·-• --- · -
Potassium "Low" - 135 (2%), 167 73 hours
(8%), use 71 201Hg
Thallium - 201 daughter x-rays
"Medium" - 173 (89%), 67 hours
Indium -111 247 (94%)
- ... .. . --··-·- . ... -·-·-- .. ---- · - --·-····--- -·
Iron Multiple; 93 (40%), 184 78 hours
(20%), 300 (20%), 393
Gallium - 67 (5%)
Iodine -131 Iodine "High" - 365 8 days
Fluorine -18 Sugar "High" - 511 110 mins
. . . ----�
50.5 DAYS
Strontium 89
....... (14 days i11bone)
Samarium 153 46 Hours
Radium 11 Days
Yttrium 90 64 Hours
Rubidium 82 75 seconds
Nitrogen 13 10 mins
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·.
J>I"obable. Critical Organ (depmdhtf! on w!t� you ask)
•· . ' . . :
Tc-MOP Bladder (some sources say bone)
Tc-Sulfur Colloid (IV) Liver
Tc-Sulfur Colloid (Oral) PmximA 1 rolon
Tc-Pertechnetate Stomach > Thyroid (some sources say colon)
Tc - Sestamibi Proximal Colon
Tc-Heat Treated RBC Spleen> Heart
Tagged RBC -MUGA Heart
Tc-MAA Lung
Tc-DMSA Renal Cortex
Tc-MAG 3 Bladder
DTPA Bladder
I-123MIBG Bladder (some sources say adrenal medulla)
I-131MIBG Liver (some sources say adrenal medulla)
I-131, I-123 Thyroid
In-111W BC Spleen
In-111ProstaScint Liver
In-111Octreoscan Spleen
Thallium 201 Renal Cortex
F 18 FDG Bladder
Gallium Distal Colon
HIDA Gallbladder Wall
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{\op:i;a'
<··. .. , >-·.; •· .•.•: . / ,i >,'. ./·. \ ,,. ..·. •·. /<,. .•. .... ,'( • .·. ...· •·
'1'110,. "'<II II ,oo '",>·
I> >• ./ .. .·,. :' ,, ,; .·, ... ,·. .. · .. :-:-,:, \ >
Cross the cell membrane via lipophilic
Tc-Sestamibi Passive Diffusion diffusion
Cw:m lhc, cell membrane via lipophilic
Tc - Tetrofosmin Passive Diffusion diffusion
··-····'"-··· ...
Delivery is flow related-then diffuse into
Tc-HMPAO Passive Diffusion brain
Delivery is flow related-then diffuse into
Tc-ECD Passive Diffusion brain
DTPA Filtration
Carrier mediated transport across membrane
F l8 -FDG Facilitated Diffusion via GLUT
Use ATP to move AGAINS T concentration
1-123, 1-131 Active Transport gradient
Thallium Active Transport (Na/K Pump)
Rubidium Active Transport (Na/K Pump)
Active Transport (Na facilitated
MIBG nmepinephrine uptake system)
DMSA Active Transport
Secretion
Pertechnatate Active transport OUT of a gland or tissue
Secretion
MAG-3 Secreted by peritubular capillaries
Secretion
Tc-99m IDA Secreted by hepatocytes
Sulfur Colloid Phagocytosis RES eats the colloid particles
Heat Treated RBCs Sequestration
MAA Capillary Blockade Lung Perfusion
MOP Chemisorption Chemical Covalent+ Hydrogen Bonding
SM -153 Chemisorption
Indium WBC Cellular Migration Cells migrate to the response of stimuli
Octreotide Receptor Binding
DAT Scan
(1-123 lsoflupane) Receptor Binding
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Not Cancer but PET HOT
BAC (Adeno In Situ) - Lung Cancer Infection
Carcinoid Inflammation
RCC Ovaries in Follicular Phase
Peritoneal Bowel/Liver Implants Muscles
Anything Mucinous Brown Fat
Prostate Thymus
FDG PET - Brain
Alzheimer Low posterior Identical to Parkinson
temporoparietal cortical Dementia
....... activity ... •···· ·· ····-·· ........ -
Multi Infarct Scattered areas of decreased
activity ..
Dementia with Lewy Bodies Low in lateral occipital Preservation of the mid
cortex posterior cingulate gyrus
(Cingulate Island Sign)
Picks / Frontotemporal Low frontal lobe
Huntingtons Low activity in caudate
nucleus and putamen
TcDTPA TcMAG3
Filtered (GFR) Secreted (ERPF) Filtered
Good For Native Kidneys with Concentrated better by kidneys Good for dynamic and cortical
Normal Renal Function with poor renal function imaging.
Critical Organ Bladder Critical Organ Bladder Critical Organ Bladder
Perfusion Normal Excretion Delayed
Cyclosporin Toxicity Long Standing Perfusion Normal Excretion Delayed
---·-�»·-----·-···�---�
Acute Rejectipn· Immediate Post OP Poor Perfusion Excretion Delayed
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·.·
"
Agent Localization
TcWBC TcWBC
·.
TcWBC InWBC
Indium WBC Spleen 4 Hours 24 Hours
. .. , . .... ..
Indium WBC Liver and Bone
Renal NO Renal Lung Clear
Damaged Marrow
.... . .
RBC Tagged Heart Lung
Bowel
GI NOGI Starting
RBCDamaged Spleen
ln(liurn .is BET.'fERtltan Gallium
for Evaluating
• Suspected abdominal-pelvic abscess due • Spine
to the lack of a normal bowel excretory • Diffuse Pulmonary Processes: Gallium is
pathway probably the agent of choice for the
evaluation of pulmonary inflammatory
abnormalities.
• Lymphocyte mediated infection
TcJIMPAOis J3ETTER tlianJ'.n WBC
for Evaluating
• Children (lowerDose) • Fever of Unknown Origin
• Inflammatory Bowel - *but you have to
image early- like around an hour (or 30
mins - depending on who you ask).
• Osteomyelitis in Extremity
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Neuro Trivia:
Toxo
Ring Rnhancing Ring Enhancing
Hemorrhage more common after treatment Hemorrhaee less common after treatment
Thallium Cold Thallium HOT
PET Cold PET Hot
MR Perfusion: Decreased CBV MR Perfusion: Increased (or Decreased) CBV
Symmetric T2 Asymmetric T2 Periventricular Ring Dilated
Bright Bright T2 Bright Enhancement Perivascular
Spaces
T l dark Ependymal Thallium Cold Basilar
Enhancement Meningitis
NF-1 Optic Nerve Gliomas
NF-2 MSME; Multiple Schwannomas, Meningiomas, Ependymomas
VHL Hemangioblastoma (brain and retina)
TS Subependymal Giant Cell Astrocytoma, Cortical Tubers
Nevoid Basal Cell Medulloblastoma
Syndrome (Gorlin)
Turcot GBM, Medulloblastoma
Cowdeus Lhermitte-Dulcos (Dysplastic cerebellar gangliocytoma)
Maximum Bleeding -Aneurysm Location
ACOM Interhemispheric Fissure
PCOM Ipsilateral Basal Cistern
MCA Trifurcation Sylvian Fissure
Basilar Tip Interpeduncular Cistern, or Intraventricular
PICA Posterior Fossa or lntraventricular
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40% show
Lateral nasal wall "entrapped bone"
centered flt the: middle: .mhr(fnrm
(:/0 C:erehrifonn Pattern
Inverting Papilloma 40-70 meatus, with Pattern May have focal
M>F (4:1) occasional extension 10% Harbor a hyperostosis on CT
into the antrum Squamous Cell
CA
Dumbbell shaped with
Bimodal 20s & AVID homogeneous
Esthesioneuroblastoma G0s waist at the cribiform enhancement
plate
Fungating and
Ethmoid origin more L.w:g£.. typically> Poorly defined
SNUC Broad Range common than 4cm on Heterogeneous
(30s-90s) maxillary presentation enhancement with
necrosis
Aggressive Antral Soft
Tissue M ass, with
destruction of sinus
Most Common walls Low signal
Squamous Cell CA 95% > 40 years Maxillary Antrum is Malignancy of on T2 (highly
old involved in 80% Sino-Nasal track cellular)
Enhances less than
some other sinus
malignancies
- -- --·------~· .. ·•-------·-
Enhancing mass
JNA Nearly arising from the SPF
Exclusively Origin in the Radiation alone in adolescent male
(Juvenile
Nasopharyngea! Male Spenopalantine cures in 80% Dark Flow Voids on
Angiofibroma) Rare< 8 or> Foramen (SPF) Tl
25 Avidly Enhances
··---·--··--····-·.,-----.,--•---- .
Homogeneous mass in
Nasal Cavity> Highly variable nasal cavity with bony
Usually older,
Sinonasal Lymphoma peak is 60s Sinuses appearance destruction
Low Signal on T2
(highly cellular)
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•
•
.
�
SECTION 3:
BECOME SUPREME COMMANDER
OF THE BATHROOM
*HIGH YIELD TRIVIA, FORMATTED FOR OPTIMAL REVIEW WHILE POOPING
When I say "Subglottic Hemangioma," You Say PHACES Syndrome
�a-.,
When I say "PHACES Syndrome," You say Cutaneous Hemangioma
• When I say "Ropy Appearance," You say Meconium Aspiration
When I say "Post Term Delivery," Yuu Say Meconi um Aspiration
• When I say "Fluid in the Fissures," You say Transient Tachypnea
• When I say "History of c-section", You say Transient Tachypnea
When I say "Maternal sedation", You say Transient Tachypnea
When I say "Granular Opacities+ Premature", You say RDS
When I say "Granular Opacities+Term+High Lung Volume," You say Pneumonia
• When I say "Granular Opacities+Term+Low Lung Volume," You say B-Hemolytic Strep
• When I say "Band Like Opacities", You say Chronic Lung Disease (BPD)
• When I say "Linear Lucencies" , You say Pulmonary Interstitial Emphysema
• When I say "Pulmonary Hypoplasia," You say diaphragmatic hernia
• When I say "Lung Cysts and Nodules," You Say LCH or Papillomatosis
• When I say "Lower lobe bronchiectasis," You Say Primary Ciliary Dyskinesia
• When I say "Upper lobe bronchiectasis," You Say CF
• When I say "Posterior mediastinal mass (under 2)," You Say Neuroblastoma
• When I say "No air in the stomach", You say Esophageal Atresia
• When I say "Excessive air in the stomach", You say "H" Type TE fistula
• When I say "Anterior Esophageal Impression," You say pulmonary sling
• When I say "Pulmonary Sling," You say tracheal stenosis.
• When l say "Single Bubble," You say Gastric (antral or pyloric) atresia
• When I say "Double Bubble," You say duodenal atresia
• When I say "Duodenal Atresia", You say Downs
• When I say "Single Bubble with Distal Gas," You say maybe Mid Gut Volvulus
• When I say "Non-bilious vomiting", You say Hypertrophic Pyloric Stenosis
• When I say "Paradoxial aciduria" You say Hypertrophic Pyloric Stenosis
• When I say "Bilious vomiting - in an infant", You say Mid Gut Volvulus
• When I say "Corkscrew Duodenum" You say Mid Gut Volvulus
• When I say "Reversed SMA and SMV" You say Malrotation
• When I say "Absent Gallbladder" You say biliary atresia
• When I say "Triangle Cord Sign" You say biliaiy atresia
• When I say "Asplenia" , You say "cyanotic heart disease"
• When I say "Infarcted Spleen," You say Sickle Cell
• When I say "Gall Stones," You say Sickle Cell
• When l say "Short Microcolon," You say Colonic AtTesia
• When I say "Long Microcolon," You say Meconium ileus or distal ilea] atresia
• When I say "Saw tooth colon," You say Hirschsprung
• When I say "Calcified mass in the mid abdomen of a newborn", you say Meconium Peritonitis
• When I say "Meconium ileus equivalent," you say Distal Intestinal Obstruction Syndrome (CF).
• When I say "Abrupt caliber change of the aorta below the celiac axis" , You say Hepatic
Hemangioendothelioma.
• When I say "Cystic mass in the liver of a newborn," you say Mesenchymal Hamartoma
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• When I say "Elevated AFP, with mass in the liver of a newborn," you say Hepatoblastoma
• When I say "Common Bile Duct measures more than 10 mm", You say Choledochal Cyst
• When I say "Lipomatous pseudohypertrophy of the pancreas," You say CF
• When I say "Unilateral Renal Agenesis" You say unicornuate uterus
• When I say "Neonatal Renal Vein Thrombosis," You say maternal diabetes
• When I say "Neonatal Renal Artery Thrombosis," You say Misplaced Umbilical Artery Catheter
• When I say "Hydro on Fetal MRI," You say Posterior Urethral Valve
• When I say "Urachus," You say bladder Adenocarcinoma
• When I say "Nephroblastomatosis with Necrosis," you say Wilms
• When I say "Solid Renal Tumor oflnfancy," you say Mesoblastic Ncphroma
• When I say "Solid Renal Tumor of Childhood," you say Wilms
• When I say "Midline pelvic mass, in a female," you say Hydrometrocolpos
• When I say "Right sided varicocele," you say abdominal pathology
• When I say "Blue Dot Sign," you say Torsion of the Testicular Appendage
• When I say "Hand or Foot Pain/ Swelling in an Infant", You say - sickle cell with hand foot syndrome.
• When I say Extratesticular scrotal mass, you say embryonal rhabdomyosarcoma
• When I say "Narrowing of the interpedicular distance," you say Achondroplasia
• When I say "Platyspondyly (flat vertebral bodies)," you say Thanatophoric
• When I say "Absent Tonsils after 6 months" You say "Immune Deficiency"
• When I say "Enlarged Tonsils well after childhood (like 12-15)" You say "Cancer" ... probably
lymphatic
• When I say "Myste1y Liver Abscess in Kid, "You say "Chronic Granulomatous Disease"
When I say "narrowed B Ring," You say Schatzki (Schat"B "ki Ring)
When I say "esophageal concentric rings," You say Eosinophilic Esophagitis
When I say "shaggy" or "plaque like" esophagus, You say Candidiasis
When I say "looks like candida, but an asymptomatic old lady," you say Glycogen Acanthosis
When I say "reticular mucosa! pattern," you say Barretts
When l say "high stricture with an associated hiatal hernia," you say Barretts
When I say "abrupt shoulders," you say cancer
When I say "Killian Dehiscence," you say Zenker Diverticulum
When l say "transient, fine transverse folds across the esophagus," you say Feline Esophagus.
When l say "bird's beak," you say Achalasia
When I say "solitary esophageal ulcer," you say CMV or AIDS
When l say "ulcers at the level of the arch or distal esophagus," you say Medication induced
When I say "Breast Cancer+ Bowel Hamartomas," you say Cowdens
When I say "Desmoid Tumors+ Bowel Polyps," you say Gardners
When I say "Brain Tumors+ Bowel Polyps," you say Turcots
When I say "enlarged left supraclavicular node," you say Virchow Node (GI Cancer)
• When I say "crosses the pylorus," you say Gastric Lymphoma
When I say "isolated gastric varices," you say splenic vein thrombus
When I say "multiple gastric ulcers," you say Chronic Aspirin Therapy.
When I say "multiple duodenal (or jejuna!) ulcers," you say Zollinger-Elision
• When I say "pancreatitis after Billroth 2," you say Afferent Loop Syndrome
When l say "Weight gain years after Roux-en-Y," you say Gastro-Gastro Fistula
When I say "Clover Leaf Sign - Duodenum," you say healed peptic ulcer.
When I say "Sand Like Nodules in the Jejunum," you say Whipples
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• When I say "Sand Like Nodules in the Jejunum+ CD4 < I 00," you say MAI
When I say "Ribbon-like bowel," you say Graft vs Host
When I say "Ribbon like Jejunum," you say Long Standing Celiac
• When I say "Moulage Pattern," you say Celiac (moulage = loss ofjejunalfolds)
When I say "Fold Reversal - of jejunum and ileum," you say Celiac
When I say "Cavitary (low density) Lymph nodes," you say Celiac
• When I say "hide bound" or "Stack or coins," you say Scleroderma
When I say "Megaduodenum," you say Sclerodenna
When I say "Duodenal obstruction, with recent weight loss," you say SMA Syndrome
When I say "Coned shaped cecum," you say Amebiasis
When I say "Lead Pipe," you say Ulcerative Colitis
When I say "String Sign," you say Crohns
When I say "Massive circumferential thickening, without obstruction," you say Lymphoma
When I say "Multiple small bowel target signs," you say Melanoma
When I say "Obstructing Old Lady Hernia," you say Femoral Hernia
When I say "sac of bowel," you say Paraduodenal hernia.
When I say "scalloped appearance of the liver," you say Pseudomyxoma Peritonei
• When I say "HCC without cirrhosis," you say Hepatitis B (or Fibrolamellar HCC)
When I say "Capsular retraction," you say Cholangiocarcinoma
When I say "Periportal hypoechoic infiltration+ AIDS," you say Kaposi's
When I say "sparing of the caudate lobe," you say Budd Chiari
When I say "large T2 bright nodes+ Budd Chiari," you say Hyperplastic nodules
• When I say "liver high signal in phase, low signal out phase," you say fatty liver
When I say "liver low signal in phase, and high signal out phase," you say hemochromatosis
When I say "multifocal intrahepatic and extrahepatic biliary stricture," you say PSC
When I say "multifocal intrahepatic and extrahepatic biliaty strictures+ papillary stenosis," you say AIDS
Cholangiopathy.
When I say "bile ducts full of stones," you say Recurrent Pyogenic Cholangitis
When I say "Gallbladder Comet Tail Atiifact," you say Adenomyomatosis
When I say "lipomatous pseudohypertrophy of the pancreas," you say CF
When I say "sausage shaped pancreas," you say autoimmune pancreatitis
• When I say "autoimmune pancreatitis," you say lgG4
When I say "lgG4" you say RP Fibrosis, Sclerosing Cholangitis, Fibrosing Mediastinitis, Inflammatory
Pseudotumor
When I say "Wide duodenal sweep," you say Pancreatic Cancer
When I say "Grandmother Pancreatic Cyst" you say Serous Cystadenoma
When I say "Mother Pancreatic Cyst" you say Mucinous
When I say "Daughter Pancreatic Cyst," you say Solid Pseudopapillaty
When I say "bladder stones," you say neurogenic bladder
When I say "pine cone appearance," you say neurogenic bladder
When I say "urethra cancer," you say squamous cell CA
When I say "urethra cancer - prostatic portion," you say transitional cell CA
When I say "urethra cancer - in a diverticulum," you say adenocarcinoma
When I say "long term supra-pubic catheter," you say squamous Bladder CA
When I say "e-coli infection," you say Malakoplakia
When I say "vas defercns calcifications," you say diabetes
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When I say "calcifications in a fatty renal mass," you say RCC
• When I say "protrude into the renal pelvis," you say Multilocular cystic nephroma
• When I say "no functional renal tissue," you say Multicystic Dysplastic Kidney
When I say "Multicystic Dysplastic Kidney," you say contralateral renal issues (50%)
When I say "Emphysematous Pyelonephritis," you say diabetic
When I say "Xanthogranulomatous Pyelonephritis," you say staghorn stone
When I say "Papillary Necrosis," you say diabetes
When I say "shrunken calcified kidney," you say TB ("putty kidney")
When I say "bilateral medulla nephrocalcinosis," you say Medullary Sponge Kidney
When I say "big bright kidney with decreased renal function," you say HI V
When I say "history oflithotripsy," you say Page Kidney
When I say "cortical rim sign," you say subacute renal infarct
When l say "history ofrenal biopsy," you say AV F
When I say "reversed diastolic flow," you say renal vein thrombosis
When I say "sickle cell trait," you say medullaiy RCC
When I say "Young Adult, Renal Mass,+ Severe HTN," you say Juxtaglomerular Cell Tumor
When I say "squamous cell bladder CA," you say Schistosomiasis
• When I say "entire bladder calcified," you say Schistosomiasis
• When I say "urachus," you say adenocarcinoma ofthe bladder
• When I say "long stricture in urethra," you say Gonococcal
When l say "short stricture in urethra," you say Straddle Injury
When l say "Unicornuate Uterus," you say Look at the kidneys
When I say "T-Shaped Uterus," you say DES related or Vaginal Clear Cell CA
When I say "Marked enlargement ofthe uterus," you say Adenomyosis
When I say "Adenomyosis," you say thickening of the junctional zone(> 12 mm)
When I say "Wolffian duct remnant," you say Gartner Duct Cyst
When I say "Theca Lutein Cysts," you say moles and multiple gestations
When l say "Theca Lutein Cysts+ Pleural Effusions," you say - Hyperstimulation Syndrome(patient on
fertility meds).
When I say "Low level internal echoes," you say Endometrioma
When I say "T2 Shortening," you say - Endometrioma - "Shading Sign"
When I say "Fishnet appearance," you say Hemorrhagic Cyst
When I say "Ovarian Fibroma+ Pleural Effusion," you say Meigs Syndrome
When I say "Snow Storm Uterus, " you say Complete Mole - l st Trimester
• When I say "Serum �-hCG levels that rise in the 8 to 10 weeks following evacuation of molar pregnancy,"
you say Choriocarcinoma
When I say "midline cystic structure near the back of the bladder of a man," you say Prostatic Utricle
When I say "lateral cystic structure near the back ofthe bladder ofa man," you say Seminal Vesicle Cyst
When I say "isolated orchitis," you say mumps
When I say "onion skin appearance," you say epidermoid cyst
• When I say "multiple hypoechoic masses in the testicle," you say lymphoma
When I say "cystic elements and macro-calcifications in the testicle," you say Mixed Germ Cell Tumor
When I say "homogenous and microcalcifications," you say seminoma
When I say "gynecomastia+ testicular tumor," you say Sertoli Leydig
When l say "fetal macrosomia," you say Maternal Diabetes
When I say "one artery adjacent to the bladder," you say two vessel cord
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When I say "painless vaginal bleeding in the third trimester," you say placenta previa
• When I say "mom doing cocaine," you say placenta abruption
• When I say "thinning of the myometrium - with turbulent doppler," you say placenta creta
When I say "mass near the cord inse11ion, with flow pulsating at the fetal heart rate," you say placenta
chorioangioma
When I say "Cystic mass in the posterior neck -antenatal period," you say cystic hygroma.
When I say "Pleural effusions, and Ascites on prenatal US," you say hydrops.
• When I say "Massively enlarged bilateral kidneys," you say ARPKD
• When I say "Twin peak sign," you say dichorionic diamniotic
• When I say "obliteration of Raider's Triangle," you say aberrant right subclavian
When I say "flat waist sign," you say left lower lobe collapse
When I say "terrorist+ mediastinal widening," you say Anthrax
When I say "bulging fissure," you say Klebsiella
When I say "dental procedure gone bad, now with jaw osteo and pneumonia," you say Actinomycosis.
• When I say "culture negative pleural effusion, 3 months later with airspace opacity," you say TB
• When I say "hot-tub," you say Hypersensitivity Pneumonitis
• When I say "halo sign," you say Fungal Pneumonia - Invasive Aspergillus
When I say "reverse halo or atoll sign," you say COP
When I say "finger in glove," you say ABPA
When I say "ABPA," you say Asthma
When I say "septic emboli + jugular vein thrombus," you say Lemierre
When I say "Lemierre," you say Fusobacterium Necrophorum
• When I say "Paraneoplatic syndrome with SIADH," you say Small Cell Lung CA
• When I say "Paraneoplatic syndrome with PTH," you say Squamous Cell CA
• When I say "Small Cell Lung CA+ Proximal Weakness," you say Lambert Eaton
When I say "Cavity fills with air, post pneumonectomy," you say Bronchopleural Fistula
When I say "malignant bronchial tumor," you say carcinoid
When I say "malignant tracheal tumor," you say Adenoid Cystic
When I say "AIDS patient with lung nodules, pleural effusion, and lymphadenopathy," you say
Lymphoma
When I say "Gallium Negative," you say Kaposi
When I say "Thallium Negative," you say PCP
When I say "Macroscopic fat and popcorn calcifications," you say Hamartoma
When I say "Bizarre shaped cysts," you say LCH
• When I say "Lung Cysts in a TS patient," you say LAM
• When I say "Panlobular Emphysema - NOT Alpha l ," you say Ritalin Lung
• When I say "Honeycombing," you say UIP
When I say "The histology was heterogeneous," you say UIP
When I say "Ground Glass with Sub pleural Sparing," you say NSIP
When I say "UIP Lungs + Parietal Pleural Thickening," you say Asbestosis
When l say "Cavitation in the setting of silicosis," you say TB
When I say "Air trapping seen 6 months after lung transplant," you say Chronic Rejection / Bronchiolitis
Obliterans Syndrome
When I say "Crazy Paving," you say PAP
When I say "History of constipation," you say Lipoid Pneumonia - inferring mineral oil use / aspiration.
When I say "UIP+ Air trapping," you say Chronic Hypersensitivity Pneumonitis
• When I say "Dilated Esophagus+ ILD," = Scleroderma (with NSIP)
When I say "Shortness of breath when sitting up," you say Hepatopulmonary syndrome
When I say "Episodic hypoglycemia," you say solitary fibrous tumor of the pleura
When I say "Pulmonary HTN with Normal Wedge Pressure," you say Pulmonary Veno-occlusive disease.
• When I say "Yellow Nails" you say Edema and Chylous Pleural Effusions (Yellow Nail Syndrome).
• When I say "persistent fluid collection after pleural drain/tube placement," you say Extrapleural
Hematoma.
• When I say "Displaced extrapleural fat," you say Extrapleural Hematoma.
When I say "Massive air leak, in the setting of trauma," you say bronchial or tracheal injmy
• When I say "Hot on PET - around the periphery," you say pulmonary infarct
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When I say "Multi-lobar collapse," you say sarcoid
When I say "Classic bronchial infection," you say TB
When I say "Panbronchiolitis," you say tree in bud (not centrilobular or random nodules)
When I say "Bronchorrhea," you say Mucinous BAC
When I say "ALCAPA," you say Steal Syndrome
When I say "Supra-valvular Aortic Stenosis" you say Williams Syndrome
When I say "Bicuspid Aortic Valve and Coarctation" you say Turners Syndrome
When I say "Isolated right upper lobe edema," you say Mitra] Regurgitation
When I say "Peripheral pulmonary stenosis," you say Alagille Syndrome
When I say "Box shaped hemi", you say Ebsteins
When I say "Right Arch with Mirror Branching," you say congenital heart.
When I say "hand/thumb defects+ ASD," you say Holt Oram
When I say "ostium primum ASD (or endocardial cushion defect)," you say Downs
When I say "Right Sided PAPV R," you say Sinus Venosus ASD
When I say "Calcification in the left atrium wall," you say Rheumatic Heart Disease
When I say "difficult to suppress myocardium," you say Amyloid
When I say "blood pool suppression on delayed enhancement," you say Amyloid
When I say "septa] bounce," you say constrictive pericarditis
When I say "ventricular interdependence," you say constrictive pericarditis
When I say "focal thickening of the septum - but not Hypertrophic Cardiomyopathy," you say Sarcoid.
When I say "ballooning of the left ventricular apex," you say Tako-Tsubo
When I say "fat in the wall of a dilated right ventricle," you say Arrhythmogenic Right Ventricular
Cardiomyopathy (ARVC)
When I say "kid with dilated heart and mid wall enhancement," you say Muscular Dystrophy
When I say "Cardiac Rhabdomyoma," you say Tuberous Sclerosis
When I say "Bilateral Ventricular Thrombus," you say Eosinophilic Cardiomyopathy
When I say "Diffuse LV Subendocardial enhancement not restricted to a vascular distribution," you say
Cardiac Amyloid.
When I say "Glenn Procedure," you say acquired pulmonary AVMs
When I say "Pulmonary Vein Stenosis," you say Ablation for A-Fib
When I say "Multiple Cardiac Myxomas," you say Carney's Complex
• When I say "vessel in the fissure of the ligamentum venosum," you say replaced left hepatic arte1y.
• When I say "vessel coursing on the pelvic brim," you say Corona M01iis
• When 1 say "ascending aorta calcifications," you say Syphilis and Takayasu
• When I say "tulip bulb aorta," you say Marfans
• When I say "really shitty Marfan's variant," you say Loeys-Dietz
• When I say "tortuous vessels," you say Loeys-Dietz
• When I say "renal artery stenosis with HTN in a child," you say NF-I
• When I say "nasty looking saccular aneurysm, without intimal calcifications" you say Mycotic .
• When I say "tree bark intimal calcification," you say Syphilitic (Luetic) aneurysm
• When I say "painful aneurysm in smoker, sparing the posterior wall," you say Inflammatory aneurysm .
• When I say "Turkish guy with pulmonary miery aneurysm," you say Behcets
• When I say "GI bleed with early opacification of a dilated draining vein," you say Colonic Angiodysplasia
• When I say "spider web appearance of hepatic veins on angiogram," you say Budd Chiari
• When I say "non-decompressible varicocele," you say look in the belly for badness
• When I say "right sided varicocele," you say look in the belly for badness
0
When I say "swollen left leg," you say May Thurner
• When I say "popliteal aneurysm," you say look for the AAA (and the other leg)
• When I say "most dreaded complication of popliteal aneurysm," you say distal emboli
• When I say "Great saphenous vein on the wrong side of the calf - lateral side," you say Marginal Vein of
Servelle - which is supposedly pathognomonic for Klippel-Trenaunay Syndrome
• When I say "Asian," you say Takayasu
• When I say "Involves the aorta," you say Takayasu
• When I say "Kids with vertigo and aortitis," you say Cogan Syndrome
• When I say "Nasal perforation+ Cavitary Lung Lesions," you say Wegeners
• When I say "diffuse pulmonary hemorrhage," you say Microscopic Polyangitis
• When I say "Smoker+ Hand Angiogram," you say Buergers
• When I say "Construction worker+ Hand Angiogram," you say Hypothenar Hammer
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• When I say "Unilateral tardus parvus in the carotid," you say stenosis of the innominate
• When I say "Bilateral tardus parvus in the carotids," you say aortic stenosis
• When I say "Bilateral reversal of flow in carotids," you say aortic regurg
• When I say "Lack of diastolic flow on carotid US," you say Brain Death
When I say I V C greater than 28 mm, you sat Mega Cava
When I say Mega Cava, you say Birds Nest Filter
When I say "Hairpin turn - during bronchial angiography," you say anterior medullary (spinal cord) arte1y
When I say "Fever, WBC, Nausea, and Vomiting after Uterine Artery Embolization," you say Post
Embolization Syndrome (obviously could also be infection)
When I say "Most medial vessel in the leg," you say posterior tibial artery
When I say "the source of 85% of upper GI bleeds," you say left gastric artery
When I say "the source of bleeding from a duodenal ulcer," you say GDA
When I say "Pulmonary AVM," you say HHT
When I say "most feared complication of bronchial artery embolization," you say spinal cord infarct
When I say "high risk of bleeding for liver transplant," you say transjugular approach
When I say "most feared complication of brachial arterial access," you say compartment syndrome
When I say "cold painful fingers during dialysis," you say "Steal syndrome"
When I say "ulcer on medial ankle," you say venous stasis
When I say "ulcer on dorsum of foot," you say ischemia or infected ulcer
When I say "ulcer on plantar surface of foot," you say neutropenic ulcer\
When I say "pulsatile lower limb venous doppler," you say right heart failure.
When I say "hot clumps of signal in the lungs on Liver Spleen sulfur colloid," you say too much Al in the
Tc.
When I say "HOT spleen," you say WBC scan or Octreotide (sulfur colloid will be a warm spleen.
• When I say "Bone Scan with Hot Skull Sutures," you say renal osteodystrophy
When I say "Bone Scan with Focal Breast Uptake," you say breast CA
When I say "Bone Scan with Renal Cortex Activity," you say hemochromatosis
When I say "Bone Scan with Liver Activity," you say either too much Al, Amyloid, Hepatoma, or Liver
Necrosis
When I say "Bone Scan with Sternal Lesion," you say breast CA.
When I say "Bone Scan with Diffusely Decreased Bone Uptake," you say (1) Free Tc, or (2)
Bisphosphonate Therapy.
• When I say "Tramline along periosteum of long bones," you say lung CA
When I say "Super Hot Mandible in Adult," you say Fibrous Dysplasia
When I say "Super Hot Mandible in Child," you say Caffeys
When I say "Perimiicular uptake on delayed scan," you say RSD
When I say "Focal uptake along the lesser trochanter," you say Prosthesis loosening
When I say "Tracer in the brain on a VQ study," you say Shunt
When I say "Tracer over the liver on Ventilation with Xenon," you say Fatty Liver
When I say "Gallium Negative, Thallium Positive," you say Kaposi
When I say "High T3, High T4, low TSH, - low thyroid uptake," you say Quervains (Granulomatous
thyroiditis).
When I say "persistent tracer in the lateral ventricles > 24 hours," you say NPH
When I say "Renal uptake on sulfur colloid," you say CHF
When I say "Renal transplant uptake on sulfur colloid", you say Rejection
When I say "Filtered Renal Agent," you say DTPA ( or GH)
• When I say "Secreted Renal Agent," you say MAG-3
• When I say "PET with increased muscle uptake," you say insulin
When I say "Diffuse FDG uptake in the thyroid on PET," you say Hashimoto
When I say "I see the skeleton on MIBG," you say diffuse neuroblastoma bone mets
When I say "Cardiac tissue taking up FDG more intense than normal myocaridum," you say hibernating
myocardium
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I say "made with a generator", you say Tc99 and Rubidium
When I say "cervical kyphosis", you say NF-1
When I say "lateral thoracic meningocele,"you say NF-1
When I say "bilateral optic nerve gliomas,"you say NF-1
When I say "bilateral vestibular schwannoma,"you say NF-2
When I say "retinal hamartoma,"you say TS
When I say "retinal angioma," you say V HL
When I say "brain tumor with restricted diffusion,"you say lymphoma
When I say "brain tumor crossing the midline," you say GBM (or lymphoma)
When I say "Cyst and Nodule in Child,"you say Pilocystic Astrocytoma
When I say "Cyst and Nodule in Adult,"you say Hemangioblastoma
When I say "multiple hemangioblastoma,"you say Von Hippel Lindau
When I say "Swiss cheese tumor in ventricle," you say central neurocytoma
When I say "CN3 Palsy,"you say posterior communicating artery aneurysm
When I say "CN6 Palsy,"you say increased ICP
When I say "Ventricles out of size to atrophy,"you say NPH
When I say "Hemorrhagic putamen,"you say Methanol
When l say "Decreased FDG uptake in the lateral occipital cortex," you say Lewy Body Dementia
When I say "TORCH with Periventricular Calcification,"you say CMV
When I say "TORCH with hydrocephalus,"you say Toxoplasmosis
When I say "TORCH with hemorrhagic infarction,"you say HSY
When I say "Neonatal infection with frontal lobe atrophy,"you say HIV
When I say "Rapidly progressing dementia+ Rapidly progressing atrophy,"you say CJD
• When I say "Expanding the c01iex,"Oligodendroglioma
When I say "Tumor acquired after trauma (LP)," you say Epidermoid
When I say "The Palate Separated from the Maxilla/ Floating Palate,"you say Lefort 1
When I say "The Maxilla Separated from the Face"or "Pyramidal"you say Lefort 2
When I say "The Face Separated from the Cranium,"you say Lefort 3
When I say "Airless expanded sinus,"you say mucocelc
• When I say "DVA,"you say cavernous malformation nearby
• When I say "Single vascular lesion in the pons,"you say Capillary Telangiectasia
• When I say "Elevated NAA peak,"you say Canavans
When I say "Tigroid appearance,"you say Metachromatic Leukodystrophy
When I say "Endolymphatic Sac Tumor,"you say VI-IL
When I say "Tl Bright in the petrous apex,"you say Cholesterol Granuloma
When I say "Restricted diffusion in the petrous apex," you say Cholesteatoma
When I say "Lateral rectus palsy+ otomastoiditis,"you say Grandenigo Syndrome
When I say "Cochlear and semicircular canal enhancement,"you say Labyrinthitis
When I say "Conductive hearing loss in an adult,"you say Otosclerosis
When I say "Noise induced vertigo,"you say Superior Semicircular Canal dehiscence
When I say "Widening of the maxillary ostium,"you say Antrochonal Polyp
When I say "Inverting papilloma,"you say squamous cell CA (10%)
When l say "Adenoid cystic," you say perineural spread
When I say "Left sided vocal cord paralysis," you say look in the AP window
When I say "Bilateral coloboma," you say CHARGE syndrome
When I say "Retinal Detaclunent+ Small Eye"you say PHPV
When I say "Bilateral Small Eye,"you say Retinopathy of Prematurity
When I say "Calcification in the globe of a child,"you say Retinoblastoma
When I say "Fluid-Fluid levels in the orbit,"you say Lymphangioma
When I say "Orbital lesion, worse with Valsalva,"you say Varix
When I say "Pulsatile Exophthalmos,"you say NF-1 and CC Fistula
When I say "Sphenoid wing dysplasia,"you say NF-1
When I say "Scimitar Sacrum,"you say Currarino Triad
When I say "bilateral symmetrically increased T2 signal in dorsal columns," you say B12 (or HIV )
When I say "Owl eye appearance of spinal cord,"you say spinal cord infarct
When I say "Enhancement of the nerve roots of the cauda equina,"you say Guillain Barre
When J say "Subligamentous spread of infection," you say TB
When I say, "Posterior elbow dislocation,"you say Capitellum fracture
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• When I say "Chondroblastoma in an adult", you say "Clear Cell Chondrosarcoma"
When I say "Malignant epiphyseal lesion", you say "Clear Cell Chondrosarcoma"
When I say "Permeative lesion in the diaphysis of a child" , you say "Ewings"
When I say "T2 bright lesion in the sacrum" , you say "Chordoma"
When I say "Lytic T2 DARK lesion" , you say "Fibrosarcoma"
When I say "Sarcomatous transformation of an infarct", you say "MFH"
When I say, "Epiphyseal Lesion that is NOT T2 Bright" , You say Chondroblastoma
• When J say, "short 4th metacarpal," You say pseudopseudohypoparathyroidism and Turner Syndrome
When I say, "band like acro-osteolysis," You say Hajdu-Cheney
When I say "fat containing tumor in the retroperitoneum," you say liposarcoma
When I say "sarcoma in the foot" you say synovial sarcoma.
• When I say "avulsion of the lesser trochanter," you say pathologic fracture
• When I say "cross over sign," you say pincher type Femoroacetabular Impingement
• When I say "Segond Fracture," you say ACL tear
When I say "Reverse Segond Fracture," you say PCL
When I say "Arcuate Sign," you say fibular head avulsion or PCL tear
• When I say "Deep Intercondylar Notch," you say ACL tear
• When I say "Bilateral Patellar Tendon Ruptures," you say chronic steroids
When I say "Wide ankle mortise," you say show me the proximal fibula (Maisonneuve).
• When I say "Bilateral calcaneal fractures," you say associated spinal compression fx ("lover's leap")
When I say "Dancer with lateral foot pain," you say avulsion of 5th MT
When I say "Old lady with sudden knee pain with standing," you say SONK
When I say "Looser's Zones," you say osteomalacia or rickets (vitamin D)
• When I say "Unilateral RA with preserved joint spaces," you say RSD
When I say "T2 bright tumor in finger," you say Glomus
When I say "Blooming in tumor in finger," you say Giant Cell Tumor of Tendon Sheath (PVNS)
When I say "Atrophy of teres minor," you say Quadrilateral Space syndrome
When I say "Subluxation of the Biceps Tendon," you say Subscapularis tear
When I say "Too many bow ties," you say Discoid Meniscus
• When I say "Celery Stalk ACL - T2" you say Mucoid Degeneration
• When I say "Drumstick ACL - Tl" you say Mucoid Degeneration
• When I say "Acute Flat foot," you say Posterior Tibial Tendon Tear
• When I say "Boomerang shaped peroneus brevis," you say tear - or split tear
When I say "Meniscoid mass in the lateral ankle," you say Anteriolateral Impingement Syndrome
When I say "Scar between 3rd and 4th metatarsals," you say Morton's neuroma
When I say "Osteomyelitis in the spine," you say IV drug user
When I say "Osteomyelitis in the spine with Kyphosis," you say TB (Gibbus Deformity)
• When I say "Unilateral SI joint lysis," you say IV Drug User
When I say "Psoas muscle abscess," you say TB
When I say "Rice bodies in joint," you say TB - sloughed synovium
When I say "Calcification along the periphery," you say myositis ossificans
• When I say "Calcifications more dense in the center," you say Osteosarcoma - reverse zoning
When I say "Permeative lesion in the diaphysis of a child," you say Ewings
• When I say "Long lesion in a long bone," you say Fibrous Dysplasia
When I say "Large amount of edema for the size of the lesion," you say Osteoid Osteoma
When I say "Cystic bone lesion, that is NOT T2 bright," you say Chondroblastoma
When I say "Lesion in the finger of a kid," you say Periosteal chondroma
When I say "looks like NOF in the anterior tibia with anterior bowing," you say Osteofibrous Dysplasia.
When I say " RA+ Pneumoconiosis," you say Caplan Syndrome
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• When I say" RA+ Big Spleen+ Neutropenia," you say Felty Syndrome
When I say"Epiphyseal Overgrowth," you say JRA (or hemophilia).
When I say"Reducible deformity ofjoints - in hand," you say Lupus.
• When I say"destructive mass in a bone of a leukemia patient," you say Chloroma
• When I say"shrinking breast," you say ILC
• When I say"thick Coopers ligaments," you say edema (CHF)
• When I say"thick fuzzy coopers ligaments - with normal skin," you say blur
When I say"dashes but no dots," you say Secretory Calcifications
When I say"cigar shaped calcifications," you say Secretory Calcifications
When I say"popcorn calcifications," you say degenerated fibroadenoma
When I say"breast within a breast," you say hamartoma
When I say"fat-fluid level," you say galactocele
When I say"rapid growing fibroadenoma," you say Phyllodes
When I say "swollen red breast, not responding to antibiotics," you say Inflammatory breast CA
When I say"lines radiating to a single point," you say Architectural distortion.
When I say"Architectural distortion+ Calcifications," you say IDC+ DCIS
When I say"Architectural distortion without Calcifications," you say ILC
When I say"Stepladder Sign," you say lntracapsular rupture on US
When I say"Linguine Sign," you say lntracapsular rupture on MRI
When I say"Residual Cales in the Lumpectomy Bed," you say local recurrence
When I say"No Cales in the core," you say milk of calcium (requires polarized light to be seen).
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SECTION 4:
� JII
.·. :
THE SLEDGEHAMMER
BRUTE FORCE TACTICS ?:
• Pulmonary Interstitial Emphysema (PIE) - put the bad side down
• Bronchial Foreign Body - put the lucency side down (if it stays that way, it's positive)
• Papillornatosis has a small (2%) risk of squamous cell CA
• Pulmonary sling is the only variant that goes between the esophagus and the trachea. This is associated
with trachea stenosis.
• Thyrnic Rebound- Seen after stress (chemotherapy)- Can be PET-Avid
• Lymphoma - Most common mediastinal mass in child (over 10)
• Anterior Mediastinal Mass with Calcification - Either treated lymphoma, or Thymic Lesion (lymphoma
doesn't calcify unless treated).
• Neuroblastoma is the most common posterior mediastinal mass in child under 2 (primary thoracic does
better than abd).
• Hypertrophic Pyloric Stenosis - NOT at birth, NOT after 3 months (3 weeks to 3 months )
• Criteria for HPS - 4 mm and 14 mm (4mm single wall, 14mm length).
• Annular Pancreas presents as duodenal obstruction in children and pancreatitis in adults.
• Most common cause of bowel obstruction in child over 4 = Appendicitis
• lntussusception - 3 months to 3 years is ok, earlier or younger think lead point
• Gastroschisis is ALWAYS on the right side
• Omphalocele has associated anomalies (gastroschisis does not).
• Physiologic Gut Hernia normal at 6-8 weeks
• AFP is elevated with Hepatoblastoma
• Endothelial growth factor is elevated with Hemangioendothelioma
• Most Common cause of pancreatitis in a kid = Trauma (seatbelt)
• Weigert Meyer Rule - Duplicated ureter on top inserts inferior and medial
• Most common tumor of the fetus or infant - Sacrococcygeal Teratorna
• Most common cause of idiopathic scrotal edema - HSP
• Most common cause of acute scrotal pain age 7-14 - Torsion of Testicular Appendages
• Bell Clapper Deformity is the etiology for testicular torsion.
• SCFE is a Salter Harris Type l
• Physiologic Periostitis of the Newborn doesn't occur in a newborn - seen around 3 months
• Acetabular Angle should be< 30, and Alpha angle should be more than 60.
• Most Common benign mucosal lesion of the esophagus = Papilloma
• Esophageal Webs have increased risk for cancer, and Plummer-Vinson Syndrome (anemia+ web)
• Dysphagia Lusoria is from compression by a right subclavian artery (most patients with aberrant rights
don't have symptoms).
• Achalasia has an increased risk of squamous cell cancer (20 years later)
• Most common mesenchymal tumor of the GI tract = GIST
• Most common location for GIST = Stomach
• Abscesses are almost exclusively seen in Crohns (rather than UC)
• Nodes+ UC = Common in the setting of active disease
• Nodes (larger than 1cm)+ Crohns = Cancer
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• Diverticulosis +Nodes = Cancer (maybe) -> next step endoscopy.
• Krukenberg Tumor = Stomach (GI) met to the ovary
• Menetrier's involves fundus and spares the antrum
• The stomach is the most common location for sarcoid (in the GI tract)
• Gastric Remnants have an increased risk of cancer years after Billroth
• Most common internal hernia = Left sided paraduodenal
• Most common site of peritoneal carcinomatosis = retrovesical space
• An injury to the bare area of the liver can cause a retroperitoneal bleed
• Primary Sclerosing Cholangitis associated with Ulcerative Colitis
• Extrahepatic ducts are normal with Primary Biliary Cirrhosis
• Anti-mitochondrial Antibodies - positive with primary biliary cirrhosis
• Mirizzi Syndrome - the stone in the cystic duct obstructs the CBD
• Mirizzi has a 5x increased risk of GB cancer.
• Dorsal pancreatic agenesis - associated with diabetes and polysplenia
• Hereditary and Tropical Pancreatitis - early age of onset, increased risk of cancer
• Felty's Syndrome - Big Spleen, RA, and Neutropenia
• Splenic Artery Aneurysm - more common in women, and more likely to rupture in pregnant women.
• lnsulinoma is the most common islet cell tumor
• Gastrinoma is the most common islet cell tumor with MEN
• Ulcerative Colitis has an increased risk of colon cancer (if it involves colon past the splenic flexure).
UC involving the rectum only does not increase risk of CA.
• Calcifications in a renal CA - are associated with an improved survival
• RCC bone mets are "always" lytic
• There is an increased risk of malignancy with dialysis
• Horseshoe kidneys are more susceptible to trauma
• Most common location for TCC is the bladder
• Second most common location for TCC is the upper urinary tract
• Upper Tract TCC is more commonly multifocal (12%) - as opposed to bladder (4%)
• The cysts in acquired renal cystic disease improve after renal transplant, although the risk of renal CA in
the native kidney remains elevated. In fact, the cancers tend to be more aggressive because of the
immunosuppressive therapy needed to not reject a transplant.
• Weigert Meyer Rule - Upper Pole inserts medial and inferior
• Ectopic Ureters are associated with incontinence in women (not men)
• Leukoplakia is pre-malignant; Malakoplakia is not pre-malignant
• Extraperitoneal bladder rupture is more common, and managed medically
• lntraperitoneal bladder rupture is less common, and managed surgically
• Indinavir (HIV medication) stones are the only ones not seen on CT.
• Uric Acid stones are not seen on plain film
• Endometrial tissue in a rudimentary horn (even one that does NOT communicate) increases the risk of
miscarriage
• Arcuate Uterus does NOT have an increased risk of infertility (it's a normal variant)
• Fibroids with higher T2 signal respond better to UAE
• Hyaline Fibroid Degeneration is the most common subtype
• Adenomyosis - favors the posterior wall, spares the cervix
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• Hereditary Non-Polyposis Colon Cancer (HNPCC) - have a 30-50x increased risk of endometrial
cancer
• Tamoxifen increases the risk of endometrial cancer, and endometrial polyps
• Cervical Cancer that has parametrial involvement (2B) - is treated with chemo/radiation. Cervical
Cancer without parametrial involvement (2A) - is treated with surgery
• Vaginal cancer in adults is usually squamous cell
• Vaginal Rhabdomyosarcoma occurs in children / teenagers
• Premenopausal ovaries can be hot on PET (depending on the phase of cycle). Post menopausal ovaries
should Never be hot on PET.
• Transformation subtypes: Endometrioma = Clear Cell, Dermoid = Squamous
• Postpartum fever can be from ovarian vein thrombophlebitis
• Fractured penis = rupture of the corpus cavernosum and the surrounding tunica albuginea.
• Prostate Cancer is most commonly in the peripheral zone, - ADC dark
• BPH nodules are in the central zone
• Hypospadias is the most common association with prostatic utricle
• Seminal Vesicle cysts are associated with renal agenesis, and ectopic ureters
• Cryptorchidism increases the risk of cancer (in both testicles), and the risk is not reduced by
orchiopexy
• Immunosuppressed patients can get testicular lymphoma -hiding behind blood testes barrier
• Most common cause of correctable infertility in a man is a varicocele.
• Undescended testicles are more common in premature kids.
• Membranes disrupted before 10 weeks, increased risk for amniotic bands
• The earliest visualization of the embryo is the "double bleb sign"
• Hematoma greater than 2/3 the circumference of the chorion has a 2x increased risk of abortion.
• Biparietal Diameter - Recorded at the level of the thalamus from the oute1most edge of the near skull
to the inner table of the far skull.
• Abdominal Circumference - does not include the subcutaneous soft tissues
• Abdominal Circumference is recorded at the the level of the junction of the umbilical vein and left
portal vein
• Abdominal Circumference is the parameter classically involved with asymmetric IUGR
• Femur Length does NOT include the epiphysis
• Umbilical Artery Systolic / Diastolic Ratio should NOT exceed 3 at 34 weeks - makes you think pre
eclampsia and IUGR
• A full bladder can mimic a placenta previa
• Nuchal lucency is measured between 9-12 weeks, and should be< 3 mm. More than 3mm is associated
with Downs.
• Lemon sign will disappear after 24 weeks
• Aquaductal Stenosis is the most common cause of non-communicating hydrocephalus in a neonate
• The tricuspid valve is the most anterior
• The pulmonic valve is the most superior
• There are 1 0 lung segments on the right, and 8 lung segments on the left
• If it goes above the clavicles, it's in the posterior mediastinum (cervicothoracic sign)
• Azygos Lobe has 4 layers of pleura
• Most common pulmonary vein variant is a separate vein draining the right middle lobe
• Most common cause of pneumonia in AIDS patient is Strep Pneumonia
• Most common opportunistic infection in AIDS = PCP.
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• Aspergilloma is seen in a normal immune patient
• Invasive Aspergillus is seen in an immune compromised patient
• Fleischner Society Recommendations do NOT apply to patient's with known cancers
• Eccentric calcifications in a solitary pulmonary nodule pattern is considered the most suspicious.
• A part solid nodule with a ground glass component is the most suspicious morphology you can have
• Most common early presentation of lung CA is a solitary nodule (right upper lobe)
• Lung Fibrosis patients (UIP, etc ...) more commonly have lower lobe CA
• Stage 3B lung CA is unresectable (contralateral nodal involvement ; ipsilateral or contralateral
scalene or supraclavicular nodal involvement, tumor in different lobes).
• The most common cause of unilateral lymphangitic carcinomatosis is bronchogenic carcinoma lung
cancer invading the lymphatics
• There is a 20 year latency between initial exposure and development of lung cancer or pleural
mesothelioma
• Pleural effusion is the earliest and most common finding with asbestosis exposure.
• Silicosis actually raises your risk of TB by about 3 fold.
• Nitrogen Dioxide exposure is "Silo Filler's Disease," gives you a pulmonary edema pattern.
• Reticular pattern in the posterior costophrenic angle is supposedly the first finding of UIP on CXR
• Sarcoidosis is the most common recurrent primary disease after lung transplant
• Pleural plaque of asbestosis typically spares the costophrenic angles.
• Pleural effusion is the most common manifestation of mets to the pleura.
• There is an association with mature teratomas and Klinefelter Syndrome.
• Injury close to the carina is going to cause a pneumomediastinum rather than a pneumothorax
• Hodgkin Lymphoma spreads in a contiguous fashion from the mediastinum and is most often
unilateral.
• Non-Hodgkin Lymphoma is typically bilateral with associated abdominal lymphadenopathy
• MRI is superior for assessing superior sulcus tumors because you need to look at the brachial plexus.
• Leiomyoma is the most common benign esophageal tumor (most common in the distal third).
• Esophageal Leiomyomatosis may be associated with Alport's Syndrome
• Bronchial / Tracheal injury must be evaluated with bronchoscopy
• If you say COP also say Eosinophilic Pneumonia
• If you say BAC also say lymphoma
• Bronchial Atresia is classically in the LUL
• Pericardia! cysts MUST be simple, Bronchogenic cysts don't have to be simple
• PAP follows a rule of 1/3s post treatment; 1/3 gets better, 1/3 doesn't, 1/3 progresses to fibrosis
• Dysphagia Lusoria presents later in life as atherosclerosis develops
• Carcinoid is COLD on PET
• Wegener's is now called Granulomatosis with Polyangiitis - Wegener was a Nazi. Apparently he was
not just a Nazi, he was a real asshole. I heard the guy used to take up two parking spots at the grocery
store on Sunday afternoons.
• The right atrium is defined by the IVC.
• The right ventricle is defined by the moderator band.
• The tricuspid papillary muscles insert on the septum (mitral ones do not).
• Lipomatous Hypertrophy of the Intra-Atrial Septum - can be PET Avid (it's brown fat)
• LAD gives off diagonals
• RCA gives off acute marginals
• LCX gives off obtuse marginals
• RCA perfuses SA and AV nodes (most of the time)
• Dominance is decided by which vessel gives off the posterior descending - it's the right 85%
• LCA from the Right Coronary Cusp - always gets repaired
• RCA from the Left Coronary Cusp - repaired if symptoms
• Most common location of myocardial bridging is in the mid portion of the LAD.
• Coronary Artery Aneurysm - most common cause in adult = Atherosclerosis
• Coronary Artery Aneurysm - most common cause in child = Kawasaki
• Left Sided SVC empties into the coronary sinus
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• Rheumatic heart disease is the most common cause of mitral stenosis
• Pulmonary Arterial .Hypertension is the most common cause of tricuspid atresia.
• Most common vascular ring is the double aortic arch
• Most common congenital heart disease is a VSD
• Most common ASD is the Secundum
• Infracardiac TAPVR classically shown with pulmonary edema in a newborn
• "L" Transposition type is congenitally corrected(they are "L"ucky).
• "D" Transposition type is doomed.
• Truncus is associated with CATCH-22(DiGeorge)
• Rib Notching from coarctation spares the l st and 2nd Ribs
• Infarct with > 50% involvement is unlikely to recover function
• Microvascular Obstruction is NO T seen in chronic infarct
• Amyloid is the most common cause of restricted cardiomyopathy
• Primary amyloid can be seen in multiple myeloma
• Most common neoplasm to involve the cardiac valves= Fibroelastoma
• Most commonly the congenital absence of the pericardium is partial and involves the pericardium
over the left atrium and adjacent pulmonary artery (the left atrial appendage is the most at risk to
become strangulated).
• Glenn shunt - SVC to pulmonary artery(vein to artery)
• Blalock- Taussig Shunt - Subclavian Artery to Pulmonary Artery(arte1y - aiiery)
• Ross Procedure - Replaces aortic valve with pulmonic, and pulmonic with a graft(done for kids).
• Aliasing is common with Cardiac MRI. You can fix it by: (l) opening your FOY, (2) oversampling
the frequency encoding direction, or(3) switching phase and frequency encoding directions.
• Giant Coronary Artery Aneurysms(> 8mm) don't regress, and are associated with Mis.
• Wet Beriberi(thiamine def) can cause a dilated cardiomyopathy.
• Most common primary cardiac tumor in children = Rhabdomyoma.
• 2nd most common primary cardiac tumor in children= Fibroma
• Most common complication of MI is myocardial remodeling.
• Unroofed coronary sinus is associated with Persistent left SVC.
• Most common source of cardiac mets = Lung Cancer(lymphoma #2).
• A-Fib is most commonly associated with left atrial enlargement
• Most common cause of tricuspid insufficiency is RVH(usually from pulmonary HTN / cor
pulmonale).
• Artery of Adamkiewicz comes off on the left side(70%) between T8-Ll (90%)
• Arch of Riolan - middle colic branch of the SMA with the left colic of the IMA.
• Most common hepatic vascular variant = right hepatic artery replaced off the SMA
• The proper right hepatic artery is anterior the right portal vein, whereas the replaced right hepatic artery is
posterior to the main portal vein.
• Accessory right inferior hepatic vein - most common hepatic venous variant.
• Anterior tibialis is the first branch off the pop Iiteal
• Common Femoral Artery (CFA): Begins at the level of inguinal ligament
• Superficial Femoral Artery(SFA): Begins once the CFA gives off the profunda femoris
• Popliteal Artery: Begins as the SFA exits the adductor canal
• Popliteal Artery terminates as the anterior tibial artery and the tibioperoneal trunk
• Axillary Artery: Begins at the first rib
• Brachia! Artery: Begins as it crosses the teres major
• Brachia! Artery: Bifurcates to the ulnar and radial artery
• Intraosseous Branch: Typically arises from the ulnar artery
• Superficial Arch = From the Ulna, Deep Arch= From the Radius
• The "coronary vein," is the left gastric vein
• Enlarged splenorenal shunts are associated with hepatic encephalopathy.
• Aortic Dissection, and intramural hematoma are caused by HTN (70%)
• Penetrating Ulcer is from atherosclerosis.
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• Strongest predictor of progression of dissection in intramural hematoma = Maximum aortic diameter>
5cm.
• Leriche Syndrome Triad: Claudication, Absent/ Decreased femoral pulses, Impotence.
• Most common associated defect with aortic coarctation = bicuspid aorta (80%)
• Neurogenic compression is the most common subtype of thoracic outlet syndrome
• Splenic artery aneurysm - More common in pregnancy, more likely to rupture in pregnancy.
• Median Arcuate Compression - worse with expiration
• Colonic Angiodysplasia is associated with aortic stenosis
• Popliteal Aneurysm; 30-50% have AAA, I 0% of patient with AAA have popliteal aneurysm, 50-70% of
popliteal anemysms are bilateral.
• Medial deviation of the popliteal artery by the medial head of the gastrocnemius = Popliteal Entrapment
• Type 3 Takayasu is the most common (arch+ abdominal aorta).
• Most common vasculitis in a kid = HSP (Henoch-Schonlein Purpura)
• Tardus Parvus infers stenosis proximal to that vessel
• ICA Peak Systolic Velocity < 125 = "No Significant Stenosis" or< 50%
• lCA Peak Systolic Velocity 125-230 = 50-69% Stenosis or "Moderate"
• ICA Peak Systolic Velocity> 230 =>70% Stenosis or "Severe"
• 18G needle will accept a 0.038 inch guidewire,
• 19G needle will allow a 0.035 inch guidewire.
• Notice that 0.039, 0.035, 0.018 wires are in INCHES
• 3 French = 1 mm
• French size is the OUTSIDE of a catheter and the INSIDE of a sheath
• End Hole Only Catheters = Hand Injection Only
• Side Hole+ End Hole = Power Injection OK, Coils NOT ok
• Double Flush Technique = For Neuro IR- no bubbles ever
• "Significant lesion" = A systolic pressure gradient> IO mm Hg at rest
• Things to NOT stick a drain in: Tumors, Acute Hematoma, and those associated with acute bowel
rupture and peritonitis
• Renal Artery Stenting for renal failure - tends to not work if the Cr is> 3.
• Persistent sciatic artery is prone to aneurysm
• Even if the cholecystostomy tube instantly resolves all symptoms, you need to leave the tube in for 2-6
weeks (until the tract matures), otherwise you are going to get a bile leak.
• MELD scores greater than 24 are at risk of early death with TIPS
• The target gradient post TIPS (for esophageal bleeding) is between 9 and 11.
• Absolute contraindication for TIPS - Heart Failure, Severe Hepatic Failure
• Most common side effect of BRTO is gross hematuria
• Sensitivity = GI Bleed Scan = O. lmL/min , Angiography = 1.0 mL/min
• For GI Bleed - after performing an embolization of the GOA (for duodenal ulcer), you need to do a run
of the SMA to look at the inferior pancreaticoduodenal
• Most common cause of lower GI bleed is diverticulosis
• TACE will prolong survival better than systemic chemo
• TACE: Portal Vein Thrombosis is considered a contraindication (sometimes) because of the risk of
infarcting the liver.
• Go above the rib for Thora
• Left Bundle Branch Block needs a pacer before a Thoracic Angiogram
• Never inject contrast through a Swan Ganz catheter for a thoracic angiogram
• You treat pulmonary AV Ms at 3mm
• Hemoptysis - Active extravasation is NOT typically seen with the active bleed.
• UAE - Gonadotropin-releasing medications (often prescribed for fibroids) should be stopped for 3
months prior to the case
• The general rule for transgluteal is to avoid the sciatic nerves and gluteal arteries by access through the
sacrospinous ligament medially (close to the sacrum, inferior to the piriformis).
• When to pull an abscess catheter; As a general rule - when the patient is better (no fever, WBC
normal), and output is< 20 cc over 24 hours.
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• lf the thyroid biopsy is non-diagnostic, you have to wait 3 months before you re-biopsy.
• Posterior lateral approach is the move for percutaneous nephrostomy
• You can typically pull a sheath with an ACT< 150-180
• Artery calcifications (common in diabetics) make compression difficult, and can lead to a false
elevation of the ABI.
• Type 2 endoleaks are the most common
• Type 1 and Type 3 endoleaks are high pressure and need to be fixed stat
• Venous rupture during a fistula intervention can ofter be treated with prolonged angioplasty (always leave
the balloon on the wire).
• Phlegmasia alba = massive DVT, without ischemia and preserved collateral veins.
• Phlegmasia cerulea dolens = massive DVT, complete thrombosis of the deep venous system, including the
collateral circulation.
• You are more likely to develop Venous Thromboembolism if you are paraplegic vs tetraplegic.
• Circumaortic left renal vein: the anterior one is superior, the posterior one is inferior, and the filter should
be below the lowest one.
• Risk of DVT is increased with IV C filters
• Filter with clot > 1 cm3 of clot = Filter Stays In
• Acute Budd Chiari with fulminant liver failure = Needs a TIPS
• Pseudoaneurysm of the pancreaticoduodenal artery = "Sandwich technique" - distal and proximal
segments of the artery feeding off the artery must be embolized
• Median Arcuate Ligament Syndrome - First line is surgical release of the ligament
• Massive Hemoptysis = Bronchial artery - Particles bigger than 325 micrometers
• Acalculous Cholecystitis = Percutaneous Cholecystostomy
• Hepatic encephalopathy after TIPS= You can either (1) place a new covered stent constricted in the
middle by a loop of suture - deployed in the pre-existing TIPS, (2) place two new stents - parallel to each
other (one covered self expandable, one uncovered balloon expandable).
• Recurrent variceal bleeding after placement of a constricted stent - balloon dilation of the constricted stent
• Appendiceal Abscess - Drain placement * just remember that a drain should be used for a mature (walled
off) abscess and no frank pertioneal symptoms
• Inadvertent catheterization of the colon (after trying to place a drain in an abscess) - wait 4 weeks for the
tract to mature - verify by over the wire tractogram, and then remove tube.
• DVT with severe symptoms and no response to systemic anticoagulation = Catheter Directed
Thrombolysis
• Geiger Mueller - maximum dose it can handle is about 100mR/h
• Activity level greater than 100 mCi of Tc-99m is considered a major spill.
• Activity level greater than 100 mCi of Tl-201 is considered a major spill.
• Activity level greater than 10 mCi of ln-111, is considered to represent a major spill.
• Activity level greater than 10 mCi of Ga-67, is considered to represent a major spill.
• An activity level greater than 1 mCi of 1-131 is considered to constitute a major spill.
• Annual Dose limit of 100 mrem to the public
• Not greater than 2 mrem per hour - in an "unrestricted area"
• Total Body Dose per Year = 5 rem
• Total equivalent organ dose (skin is also an organ) per year = 50 rem
• Total equivalent extremity dose per year = 50 rem (500mSv)
• Total Dose to Embryo/fetus over entire 9 months - 0.5rem
• NRC allows no more than 0.15 micro Ci of Mo per 1 mili Ci of Tc, at the time of administration.
• Chemical purity (Al in Tc) is done with pH paper
• The allowable amount of Al is< l 0 micrograms
• Radiochemical purity (looking for Free Tc) is done with thin layer chromatography
• Free Tc occurs from - lack of stannous ions or accidental air injection (which oxidizes)
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• Prostate Cancer bone mets are uncommon with a PS A less than 10 mg/ml
• Flair Phenomenon occurs 2 weeks - 3 months after therapy
• Skeletal Survey is superior (more sensitive) for lytic mets
• AYN - Early and Late is COLD, Middle (repairing) is Hot.
• Particle size for VQ scan is 10-100 micrometers
• Xenon is done first during the VQ scan
• Amiodarone - classic thyroid uptake blocker
• Hashimotos increases risk for lymphoma
• Hot nodule on Tc, shouldn't be considered benign until you show that it's also hot on I123• This is the
concept of the discordant nodule.
• History of methimazole treatment (even years prior) makes I-131 treatment more difficult
• Methimazole side effect is neutropenia
• In pregnancy PTU is the blocker of choice
• Sestamibi in the parathyroid depends on blood flow and mitochondria
• You want to image with PET - following therapy at interval of 2-3 weeks for chemotherapy, and 8-12
weeks for radiation is the way to go. This avoids "stunning" - false negatives, and inflammatory
induced false positive.
• 111 In Pentetreotide is the most commonly used agent for somatostatin receptor imaging. The classic
use is for carcinoid tumors
• Meningiomas take up octreotide
• In 111 binds to neutrophils, lymphocytes, monocytes and even RBCs and platelets
• Tc99m HMPAO binds to neutrophils
• W BCs may accumulate at post op surgical sites for 2-3 weeks
• Prior to MIBG you should block the thyroid with Lugols Iodine or Perchlorate
• Scrotal Scintigraphy: The typical agent is Tc-99m Pertechnetate. This agent is used as both a flow
agent and a pool agent.
• Left bundle branch block can cause a false positive defect in the ventricular septum (spares the apex)
• Pulmonary uptake of Thallium is an indication of LV dysfunction
• MIBG mechanism is that of an Analog of Norepinephrine - actively transported and stored in the
neurosecretory granules
• MDP mechanism is that of a Phosphate analog - which works via Chemisorption
• Sulfur Colloid mechanism = Particles are Phagocytized by RES
• The order of tumor prevalence in NF2 is the same as the mnemonic MSME (schwannoma >
meningioma > ependymoma).
• Maldeveloped draining veins is the etiology of Sturge Weber
• All phakomatosis (NF 1, NF -2, TS, and VHL) EXCEPT Sturge Weber are autosomal dominant -
family screening is a good idea.
• Most Common Primary Brain Tumor in Adult = Astrocytoma
• "Calcifies 90% of the time"= Oligodendroglioma
• Restricted Diffusion in Ventricle = Watch out for Choroid Plexus Xanthogranuloma (not a brain
tumor, a benign normal variant)
• Pituitary - Tl Big and Bright = Pituitary Apoplexy
• Pituitary - Normal T 1 Bright = Posterior Part (because of storage of Vasopressin , and other storage
proteins)
• Pituitary - T2 Bright = Rathke Cleft Cyst
• Pituitary -Calcified = Craniopharyngioma
• CP Angle -Invades Internal Auditory Canal = Schwannoma
• CP Angle - Invades Both Internal Auditory Canals = Schwannoma with NF2
• CP Angle Restricts on Diffusion = Epidermoid
• Peds -Arising from Vermis = Medulloblastoma
• Peds - "tooth paste" out of 4th ventricle = Ependymoma
• Adult myelination pattern: T l at 1 year, T2 at 2 years
• Brainstem and posterior limb of the internal capsule are myelinated at birth.
• CN2 and CNV 3 are not in the cavernous sinus
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• Persistent trigcminal artery (basilar to carotid) increases the risk of aneurysm
• Subfalcine herniation can lead to ACA infarct
• ADEM lesions will NOT involve the calloso-septal interface.
• Marchiafava-Bignami progresses from body -> genu -> splenium
• Post Radiation changes don't start for 2 months (there is a latent period).
• Hippocampal atrophy is first with Alzheimer Dementia
• Beaked Tecturn = Chiari 2
• Beaker Anterior Inferior L 1 = Hurlers
• Sometimes Beaked Pons = Multi-System Atrophy
• Most common TORCH is CM V
• Toxo abscess does NOT restrict diffusion
• Small cortical tumors can be occult without I V contrast
• JPA and Ganglioglioma can enhance and are low grade
• Nasal Bone is the most common fracture
• Zygomaticomaxillary Complex Fracture (Tripod) is the most common fracture pattern and involves
the zygoma, inferior orbit, and lateral orbit.
• Supplemental oxygen can mimic SAH on FLAIR
• Putamen is the most common location for hypertensive hemorrhage
• Restricted diffusion without bright signal on FLAIR should make you think hyperacute (< 6 hours)
stroke.
• Enhancement of a stroke: Rule of3s - starts at day3, peaks at3 weeks, gone at3 months
• PAN is the Most Common systemic vasculitis to involve the CNS
• Scaphocephaly is the most common type of craniosynostosis
• Piriform aperture stenosis is associated with hypothalamic pituitary adrenal axis issues.
• Cholesterol Granuloma is the most common primary petrous apex lesion
• Large vestibular aqueduct syndrome has absence of the bony modiolus in 90% of cases
• Octreotide scan will be positive for esthesioneuroblastoma
• The main vascular supply to the posterior nose is the sphenopalatine artery (terminal internal
maxillary artery).
• Warthins tumors take up pertechnetate
• Sjogrens gets salivary gland lymphoma
• Most common intra-occular lesion in an adult = Melanoma
• Enhancement of nerve roots for 6 weeks after spine surgery is normal. After that it's arachnoiditis
• Hemorrhage in the cord is the most important factor for outcome in a traumatic cord injury.
• Currarino Triad: Anterior Sacral Meningocele, Anorectal malformation, Sarcococcygeal osseous
defect
• Type 1 Spinal AVF (dural AVF) is by far the more common.
• Herpes spares the basal ganglia (MCA infarcts do not)
• Most common malignant lacrimal gland tumor = adenoid cystic adenocarcinoma
• Arthritis at the radioscaphoid compartment is the first sign of a SNAC or SLAC wrist
• SLAC wrist has a DISI deformity
• Pull of the Abductor pollucis longus tendon is what causes the dorsolateral dislocation in the Bennett Fx
• Carpal tunnel syndrome has an association with dialysis
• Degree of femoral head displacement predicts risk of AVN
• Proximal pole of the scaphoid is at risk for AVN with fracture
• Most common cause of sacral insufficiency fracture is osteoporosis in old lady
• Patella dislocation is nearly always lateral
• Tibial plateau fracture is way more common laterally
• SONK favors the medial knee (area of maximum weight bearing)
• Normal SI joints excludes Ank Spon
• Looser Zones are a type of insufficiency fracture
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• T score of -2.5 marks osteoporosis
• First extensor compartment = de Quervains
• First and Second compartment = intersection syndrome
• Sixth extensor wrnparlmenl - early RA
• Flexor pollicis longus goes through the carpal tunnel, flexor pollicis brevis does not
• The pisiform recess and radiocarpal joint normally communicate
• The periosteurn is intact with both Perthes and ALPSA lesions. In a true bankart it is disrupted.
• Absent anterior/superior labrum, + thickened middle glenohumeral ligament is a Buford complex.
• Medial meniscus is thicker posteriorly.
• Anterior talofibular ligament is the most commonly torn ankle ligament
• TB in the spine - spares the disc space (so can brucellosis).
• Scoliosis curvature points away from the osteoid osteoma
• Osteochondroma is the only benign skeletal tumor associated with radiation.
• Mixed Connective Tissue Disease requires serology (Ribonucleoprotein) for Dx
• Medullary Bone Infarct will have fat in the middle
• Bucket Handle Meniscal tears are longitudinal tears
• Anterior Drawer Sign = ACL
• Posterior Drawer Sign = PCL
• "McMurray" = MCL
• No grid on mag views.
• BR-3 = < 2% chance of cancer
• BR-5 = > 95% chance of cancer
• Nipple enhancement can be normal on post contrast MRI - don't call it Pagets.
• Upper outer quadrant has the highest density of breast tissue, and therefore the most breast cancers.
• Majority of blood (60%) is via the internal mammary
• Majority of lymph (97%) is to the axilla
• The stemalis muscle can only be seen on CC view
• Most common location for ectopic breast tissue is in the axilla
• The follicular phase (day 7-14) is the best time to have a mammogram (and MRI).
• Breast Tenderness is max around day 27-30.
• Tyrer Cuzick is the most comprehensive risk model, but does not include breast density.
• If you had more than 20Gy of chest radiation as a child, you can get a screening MRI
• BRCA 2 (more than 1) is seen with male breast cancer
• BRCA 1 is more in younger patients, BRCA 2 is more in post menopausal
• BRCA 1 is more often a triple negative CA
• Use the LMO for kyphosis, pectus excavatum, and to avoid a pacemaker / line
• Use the ML to help catch milk of calcium layering
• Fine pleomorphic morphology to calcification has the highest suspicion for malignancy
• Intramammary lymph nodes are NOT in the fibroglandular tissue
• Surgical scars should get lighter, if they get denser - think about recurrent cancer.
• You CAN have isolated intracapsular rupture.
• You CAN NOT have isolated extra (it's always with intra).
• If you see silicone in a lymph node, you need to recommend MRI to evaluate for extracapsular rupture
• The number one risk factor for implant rupture is the age of the implant
• Tamoxifen causes a decrease in parenchymal uptake, then a rebound.
• T2 Bright things - these are usually benign. Don't forget colloid cancer is T2 bright.
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