Edmonton Manual 6th Edition
Edmonton Manual 6th Edition
TH
EDITION
Parnian Riaz MD
SENIOR EDITORS
Nazlin Karmali BSc
Cailey Turner BSc
JUNIOR EDITORS
Scott Wong MSc
Trent Schimmel BSc
Printed in Canada.
Edmonton Manual
c /o Medical Students' Association
1-002 Katz Group Centre for Pharmacy and Health Research
University of Alberta
.
Edmonton AB T6G 2E1
Canada
editor @edmontonmanual.com
Additional copies of this publication may be purchased online. Our website also hosts more information on this
publication.
www.edmontonmanual.com
This book is published by the Edmonton Manual team, a not for profit operated by University of Alberta Medical
.
Students. It is a " for students, by students" resource and as such, this publication is a work in progress. Although the
authors, editors, and publisher have made efforts to ensure the accuracy of the information contained herein at the
time of publication, they do not guarantee that this information is accurate, complete, current, or suitable for
any particular purpose.
This book may be used as a guide to assist readers who are preparing for clinical clerkship and for objective structured
clinical examinations. This manual is simply a framework for guided learning. This book should only be used in
combination with other textbooks and resources, and strong clinical mentorship and teaching offered through an
accredited medical educational institution .
Knowledge of medical sciences and practice is constantly changing; therefore, readers should use individual judgment
and reference current sources of information as they become available.
The authors, editors, and publisher make no representations or warranties, explicit or implied, in relation to this book or
the contents herein. The authors, editors, and publisher are not responsible for any errors or omissions in this book. The
authors, editors, and publisher will not be held liable for any loss, damage, or injury arising from the use of this book.
The courts of the Province of Alberta shall have exclusive jurisdiction over any legal disputes relating to this book.
Family Medicine .
Sheny Khera MD CCFP MPHt Assistant Professor University of Alberta
. .
Jennifer Ringrose MD FRCPC Assistant Professor University of Alberta
Internal Medicine Selina Dobing MD CCFP MPH Assistant Professor. University of Alberta
,
Pediatrics . .
Melanie Lewis BN MD MEd FRCPC Associate Professor University of Alberta
Psychiatry .
Melanie Marsh- Joyal MD FRCPC Clinical Lecturer and Associate Program Director .
. .
Jorge Perez - Parada MD FRCPC Associate Professor University of Alberta
Jonathan Hamill MD FRCPC BMus ARCT
Surgery .
Daniel W. Birch MD MSc FRCSC FACS, Professor University of Alberta
. . . .
Caroline Jefferyy MD MPH FRCSC Associate Professor University of Alberta
Physical Exam . .
Laurie Mereu MD FRCPC Professor University of Alberta
PHELO .
Laurie Mereu MD FRCPC, Professor University of Alberta
Previous Editors-in-Chief Aaron Knox MD; Shaheed Merani MD PhD; Ryan Gallagher MD; Jasmine Pawa MD;
David Lesniak PhD MD; Anthony Lott BSc MD; Brent Turner MD
Nikhil Raghuram PhD MD. Marvi Cheema MD; Mark Mckinney MD
2 Physical Exam
Introduction 76
Abdominal Exam 77
Blood Pressure Measurement 78
Cranial Nerve Exam 79
Diabetic Foot Exam 81
Examination for Liver Disease 82
Eye Exam 83
Female Genitourinary Exam 84
Hand Exam 85
HEENTExam 86
Hip Exam 87
JVP Exam 88
Knee Exam 89
Lymphadenopathy & Spleen Exam 90
Male Genitourinary Exam 91
Neurological Exam 92
Precordial Exam 96
Respiratory Exam 98
Edmonton Manual of Common Clinical Seer
Shoulder Exam 99
Thyroid Exam 101
3 Family Medicine
Introduction 108
Adult Periodic Health Exam 109
Constipation 111
Cough 113
Diarrhea 115
Dyspepsia 117
Dysuria 119
Erectile Dysfunction 121
Fatigue 123
Fever 125
Headache 127
Hypertension 129
Insomnia 131
Lower Back Pain 133
Nausea & Vomiting 135
Obesity 137
Respiratory Tract Infection 139
Sexual & High - Risk Infections 141
.
Skin, Hair & Nails 143
Smoking Cessation 145
Sore Throat ( Pharyngitis) 147
Urinary Incontinence 149
Weight Loss 151
4 Internal Medicine
Introduction 159
An Explanation of Likelihood Ratios 160
Ascites 161
Abnormal Heart Sounds 163
Acute Confusion 165
Acute Liver Injury 167
Allergic Reactions 169
Altered Level of Consciousness 171
Anemia 173
Bleeding Disorders 175
Cardiac Chest Pain 177
Congestive Heart Failure 179
Dehydration/ Hypovolemia 181
Dementia 183
Diabetes - Acute Complications 185
Diabetes - Chronic Management 187
Dyspnea 189
Falls 191
Gait Disturbance 193
Hearing Loss & Deafness 195
Hematologic Malignancies 197
Hemiplegia /Hemisensory Loss 199
Hemoptysis 201
7 Psychiatry
Introduction 380
Mental Status Exam 382
Abuse 383
Anxiety Disorders 385
Bipolar Disorders 387
Depressive Disorders 389
Eating Disorders 391
Gender Dysphoria 393
Neuroleptic Malignant Syndrome 395
Personality Disorders 397
Peripartum Depression 399
Schizophrenia Spectrum Disorders 401
Substance Use Disorders 403
Suicidal Behavior 405
8 Surgery
Introduction 410
Abnormal Mass & CRC Screening Guidelines 411
Abdominal Pain 413
>n Manual of Common Clinical Scenarios
jntc
Ankle & Foot ( Pain, Fractures, & Dislocations) 415
Anorectal Pain 417
Approach to Fracture 419
Biliary Disease: Cholelithiasis 421
Bites & Dirty Wounds 423
Bladder Obstruction & Prostate Cancer 425
Breast Lump & Cancer Screening 427
Burns 429
Diplopia 431
Dizziness / Vertigo 433
Dysphagia 435
Epistaxis 437
Gastrointestinal Bleed ( Lower ) 439
Gastrointestinal Bleed ( Upper ) 441
Gynecomastia 443
Hand ( Pain, Fractures. & Dislocations ) 445
Head Trauma 447
Hematuria 449
Hernia 451
Hip ( Pain, Fractures, & Dislocations) 453
Jaundice 455
Knee ( Pain, Fractures, & Dislocations ) 457
Neck Mass /Goiter 459
Pupil Abnormalities 461
Red Eye 463
Scrotal Mass & Scrotal Pain 465
Shoulder ( Pain. Fractures & Dislocations) 467
Tinnitus 469
Trauma 471
9 PHELO
Introduction 480
Approach to End of Life Care & Bereavement 481
Approach to Medical Literature 483
Capacity Assessment 485
Clinical Epidemiology 486
Confidentiality 487
Doctor - Patient Relationship 488
Informed Consent 489
Medical Assistance in Dying ( MAID) 490
Personal & Professional Conduct 491
Research Ethics 492
Resource Allocation 493
Sexual Health History 494
Truth Telling 495
Appendices
Appendix A : Abbreviations 499
Appendix B: Triads. Tetrads, & Pentads 507
-
Edmonton Manual of Common Clinical Scenario
PRIMER ASSESSMENT IN MEDICAL
EDUCATION
Vi jay Daniels MD FRCPC
.
If you are reading this you have been around longenough to know that assessment in medical school is far different than assessment in
high school or undergraduate courses where multiple choice examinations and short - or long- answer essays are used. Why? Because
these methods assess mainly knowledge and not performance. Being a doctor is about doing, not just knowing. This distinction is
best demonstrated by the Miller pyramid, a commonly used paradigm amongst medical educators. The Knows level involves basic
recall of information such as anatomy, physiology, and other basic sciences. The Knows How level is a bit more complex and often
involves the application of knowledge. The Shows How level involves the learner demonstrating clinical skills in a structured, in vitro
environment. Finally, the Does level involves the real life or in vivo performance of the learner.
An Objective Structured Clinical Examination (or OSCE) is a method that assesses the Shows How level. To contrast between
the Shows How level and the Does level, you need not look that far: every teacher has had the medical student who, in an OSCE,
palpates the radial before inflating the blood pressure cuff and then, after finding the systolic
.
blood pressure, reinflates to 20 mmHg above the systolic. Yet this same medical student simply
<
inflates the cuff to 300 mmHg on the real patient ( this is at least better than the student who Does
says the BP has not been taken yet !).
lAttion )
Shows How
( PwfornMiwe)
Why an OSCE?
Having examined what an OSCE assesses — performance, not just knowledge — next is how it Knows How
{Competence)
assesses. In the past (and possibly still today in some specialties/countries), the physician’s
certification exam often involved the candidate being grilled on one topic or being assessed on Knows
the examination of one organ system in one patient. An OSCE involves multiple short samples ( Knowledge)
of your clinical performance. It should come as no surprise that multiple short samples of Fremewcdi to* CV*c*l Aueumcnt
various content areas are a better representation of you as a student than one long sample of
one content area. Hence, the OSCE !
ACKNOWLEDGMENTS
We would like to thank the medical students, residents, and staff physicians who helped move this project forward from an idea
into production; in particular, we thank those students who were involved in the initial conceptual design of the project through
informal feedback during hallway discussions as well as those who contributed to formal focus groups. It was the dedication and
energy of our student authors who ensured that content was produced, and then later reviewed by resident and staff physician co -
authors. Finally, we thank our mentors in medical education: resident and staff physician educators alike, who have encouraged the
development of the project and peer - assisted learning.
Original start -up funds for the first edition were provided by the University of Alberta Medical Students ’ Association and, in part,
by a grant from the Canadian Federation of Medical Students.
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C 1 ESSENTIAL CLINICAL SKILLS
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Introduction 16
Admission & Daily Orders 17
Approach to Acute & Chronic Pain 19
Essential Dermatology 21
Fluid Resuscitation 23
Interpretation of Abdominal Radiograph 25
Interpretation of ABG 27
Interpretation of Chest Radiograph 29
Interpretation of CBC- D 31
Interpretation of Creatinine 33
Interpretation of C- Spine Imaging 35
Interpretation of CT 37
Interpretation of ECG 39
Interpretation of Electrolytes: Calcium 41
Interpretation of Electrolytes: Potassium 43
Interpretation of Electrolytes: Sodium 45
Interpretation of LFTs & Enzymes 47
Interpretation of Lipids 49
Interpretation of PFT 51
Interpretation of Urinalysis 53
Intubation & Lumbar Puncture 55
Family History & Pedigree 57
Pre-Operative Exam 59
Prescriptions & Progress Notes 61
Procedure & Ward Call Notes 63
Understanding Antibiotics 65
Pre - & Post -Operative Orders 69
ECG (Examples) 70
Station Contributors 71
References 72
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INTRODUCTION LO
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In this section, you will find some of the basic skills required to be a clinical clerk or intern. Your
role as a medical student will transition from preclinical to clinical years. As a student, your primary
goal is to gain an understanding of normal human physiology and pathology, while your clerkship
experience will require you to act as an information gatherer ( in the form of a patient history and
physical examination) and then as an interpreter, using your evolving knowledge of disease and
treatment. At this juncture, a refresher on the basic skills will be useful to ensure your performance
and value in the context of your clinical team.
In an OSCE or clinical scenario, you may be asked to interpret basic clinical laboratory tests or
radiographic images to demonstrate your skill as a diagnostician. The following pages discuss those
skills in further detail. Regardless of the test, do not forget the clinical context in which these tests
are being interpreted. Carefully read the clinical vignette provided with the case and use it to
corroborate your interpretation of the test. That is, do not let the pressure of limited time in the
OSCE allow you to forget that there is an individual behind the numbers reported.
This section also contains information on the basic written clinical communication skills:
prescriptions, progress notes, and orders. These written forms of medical communication are
essential to the work that physicians do. On the wards, a clearly written and concise progress note
will give your colleagues, residents, staff, consultants, and interdisciplinary team members the
ability to follow a patient ’s progress during a hospital stay or over the course of multiple clinic visits.
It will also give you the ability to track and quickly recall the details of a patient you are following.
Having a systematic approach to constructing clearly written prescriptions and orders will ensure
that the care of your patients is carried out and medication errors are reduced.
On the ward, in clinic, and in examination settings, medical students often are asked to provide
an oral summary of a patient interaction. When a resident or staff physician asks you to present a
case, organization is key to delivering a useful synopsis. Before beginning the presentation, take a
few seconds to think about what it is that you want to convey. Consider your message. Implicitly
painting a picture of the pertinent positives and negatives will help your audience understand the
patient ’s presentation and help narrow the differential diagnosis. It also will demonstrate that you
have paid careful attention to the possible differential. A clinical presentation does not need to
include every last detail about the patient -it should simply provide sufficient information to make
a decision on the current clinical presentation. As an analogy, think of your clinical presentation
as an iceberg, of which only 30 percent is above the water ’s surface with the vast majority hidden
below. Similarly, you should present only the key findings, while keeping in your own mental reserve
the remaining 70 percent of detail in the event you are asked. Practicing your own oral presentation
style and taking into account the type of feedback and questions that are asked are essential
to building your confidence and skill. At the end of your presentation, be ready to discuss your
differential diagnosis and steps that can be taken in the investigation, management, and disposition
of the patient.
We hope that you find these essential clinical skills useful as you begin your clinical placements and
prepare for OSCEs.
Sincerely,
Edmonton Manual Editorial Team
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c ADMISSION & DAILY ORDERS
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Authors: Shawna Pandya MD. Brian Yong MD Darren Nichols MD CCFP
. . . . .
Ca2 \ Mg2* P04 TSH Vit B12, folate CK CKMB V)
> Blood - Culture: viral serology, culture
.
> Urine: R & M C&S
.
> Imaging: X -ray, MRI CT, bone scan
.
> Other: ABGs ECG, echo
> Consults: Pharmacy, OT/ PT, Dietician, Social Work, Pastoral Care, other specialties
D
• Drugs
> Check allergies (include latex, iodine, and tape allergies)
> Include drug name, dosage, route, frequency and stop date if applicable (i.e., ATBx, narcotics)
• 6 Ps:
> Pain ( analgesia) - always include a Tylenol order unless contraindicated (maximum 4 g from all sources per day; max 2 g if
hepatic dysfunction)
> Puke (antiemetics) - always include an antiemetic order, especially if patient on narcotics
> Poop (bowel care) - especially important if patient is on narcotics
> Pillow ( sedation) - sleeping pills
> PE ( DVT prophylaxis)
> Previous home medications
• Drains
> Foley ( to urometer)
> NG to low wall suction
> G - tube or T- tube to straight drainage
> Reprime JP/hemovac qshift and PRN
• Dressings
> Change dressing QD. PRN: remove staples day x post - op
Signature
.
• Signature, printed name, training (e.g., SI - 3, PGY- 4, etc ), pager number
.
Note: Be sure to flag the patient’s chart once orders are written. Any stat important, or nuanced orders should be communicated to
nursing colleagues.
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APPROACH TO ACUTE & CHRONIC PAIN
Current Editor: Hana Yu MSc MD
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Background
• Pain is the most common reason for emergency department visits
• Pain is both a physical and psychological experience
• Chronic pain is a common and complex disorder often requiring multidisciplinary treatment
• Nociceptive pain: the activation of nociceptive pain pathways via tissue damage. Differentiate between somatic pain ( sharp,
stabbing, well localized, etc.) and visceral pain (dull, achy, poorly localized )
• Neuropathic pain: pain resulting from an abdominal neural activity. Patients may experience burning, tingling, shooting, or
electric pain
History
• OPQRST pain history: Onset. Provoking or Palliating factors. Quality,
. .
Radiation Severity Treatment
• Are there associated symptoms such as fever/chills, cough, decreased / Potent Opioid \
range of motion in joints, paresthesias, etc. / (eg. Morphine, \
• Assess how pain is affecting day to day function ( work, activities of daily - / Dilaudid,
2 Oxyconlin, Fcntanyl ]
living, personal life, sleep) O
<
- -
+/ Non opioid
• Past medical history and medication use (history of cancer,
musculoskeletal injury, psychiatric diagnoses, peptic ulcer disease,
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chronic kidney disease, cardiovascular disease, anticoagulation) * Mild Opioid ( codeine, hydrocodone]
• .
Social history (occupation, recreational drug use social support system) - -
+/ Non opioid +/ Adjuvant
• The Visual Analog Scale ( VAS) is a standardized means of assessing pain
severity. Clinically, patients can also rate pain severity between 1- 10 Non opioid ( Acetaminophen, NSAID] +/- Adjuvant
( Verbal Numeric Rating Scale) or use the Wong- Baker FACES pain scale,
which is suitable for patients of a variety of ages, all cultures, and those Adapted from WHO Pain Ladder
with cognitive impairment. Analgesic Ladder: initially developed by WHO to address
• Address chronic pain and its management in the acute pain setting .
cancer pain It has now been adapted as a stepwise
(e.g., post -operatively). It is recommended that patients continue their approach to the management of pain from any etiology
baseline analgesics even in the setting of new acute pain. Multimodal Analgesia: involves the use of medications
• Continually reassess the etiology of the pain in the setting of failing synergestic analgesic effects while minimizing the side
analgesia as medical comorbidities and surgical complications may be effects of approaching the dose ceiling of individual
confounding variables.
Acute Pain
• Definition: " the normal, predicted, physiological response to an
adverse chemical, thermal, or mechanical stimulus" (Carr and Goudas, 1999
• Generally resolves within one month.
• Treatment - Effective pain control is achieved via multimodal analgesia
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• Definition: a transient exacerbation of pain that occurs in the context of otherwise stable baseline pain
</>
> When treating BTP pharmacologically, one must first ensure that baseline pain is being treated effectively with appropriate
doses of around - the -clock ( ATC) analgesics. This results in smoother pain control and decreased need to "play catch up” with
PRN medications.
> Regular reassessment of baseline pain is recommended. Should persistent BTP be occurring before scheduled doses of ATC
analgesic, consider either increasing the total daily dose of ATC medication by 25 - 50% or shortening the dosing interval if the
patient is already at the maximum tolerable daily dose (i.e., divide the same dose of daily medication such that it is administered
at shorter intervals throughout the day).
> If the patient is utilizing several PRN doses in addition to ATC medication, adjust the total daily ATC dose. This is done by taking
the daily sum of the PRN doses, converting it into the dose equivalency of the ATC medication, and then dividing it equally to be
added to the ATC medication. A new PRN dose can be added, which is usually 5 -10% of the new total daily ATC dose.
Chronic Pain: pain persisting for 3 months or longer
• Treatment:
> Multidisciplinary approach is key
> Treatment options in chronic pain generally include pharmacological, behavioral medicine, physical medicine, neuromodulation,
and surgical approaches
> Generally, the initial pharmacological therapy is targeted depending on whether the pain is nociceptive or neuropathic
Nociceptive Pain
• Medication:
.
> Similar medications as neuropathic pain; however first line therapy includes both non-opioid analgesics (e.g., acetaminophen .
.
NSAIDs) and in some cases, extended release opioids in addition to attempts to relieve source of pain (see pain ladder )
• Non-pharmacological:
> Cognitive Behavioral Therapy (CBT) , relaxation therapy, meditation, aerobic exercise, acupuncture
> .
Physical Therapy Occupational Therapy
> Thermal compresses
Neuropathic Pain
• Initially try to establish etiology of chronic pain and target therapy to the cause
• Medication:
> First line therapy includes: TCA Antidepressants, Gabapentin, and Pregabalin
» SSRIs
. .
> Topical therapy (e.g. topical lidocaine capsaicin cream) may be used in conjunction
> Opioids are not considered first line therapy as they are not as efficacious in neuropathic pain yet carry many side effects. May
sometimes be used for BTP.
> Surgical intervention in the form of spinal cord stimulators or transcutaneous electrical nerve stimulation (TENS) may be an
option for certain patients with refractory, severe neuropathic pain
Many patients will benefit from referral to chronic pain or palliative care clinics to ensure continuity and close monitoring.
‘Always remember to manage the side effects of the medications being used (i.e., oversedation, nausea, and constipation with
opiates and the need for gut protection in the form of Proton Pump Inhibitors when using NSAIDs).
Pain Management
Acute Pain (< 3mo) Chronic Pain ( > 3mo)
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ESSENTIAL DERMATOLOGY
Current Editor: Yan Fci Chen
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Common Conditions
• Acne vulgaris, atopic eczema, psoriasis vulgaris, actinic keratosis, seborrheic keratosis, basal cell carcinoma, androgenic alopecia,
vitiligo, melasma
High Mortality/Morbidity
• .
Melanoma Stevens - Johnson syndrome, toxic epidermal necrolysis, necrotizing fasciitis, pemphigus vulgaris
HISTORY
ID . . gender, ethnicity, occupation (occupational exposures)
• Patient 's name age
HP1 • Seven key questions: when, where ( site ofonset), symptoms (e.g.,pruritic, painful, asymptomatic, systemic
. . .
symptoms) , how has it spread, have the lesions changed, provocative factors ( heat cold sun exercise, travel
history, drug ingestion, pregnancy, season) , which treatment( s) have been tried and which have worked
RED FLAGS • Constitutional symptoms (malaise, unexplained fevers, weight loss, anorexia, night sweats, etc.)
• Signs of Stevens-Johnson syndrome/toxic epidermal necrolysis: positive Nikolsky 's sign (light lateral pressure
causes the skin to form a bullae or slough off), painful rash with mucosal involvement
• Pain out of proportion to physical exam findings ( necrotizing fasciitis)
PMHX • Previous skin cancers, shingles, psoriasis, thyroid disorders . DM. atopy (atopic dermatitis, allergies, allergic rhinitis)
PSHX • Previous operations
PO&GHX • STIs, pregnancy, sexual activity. HIV risk factors
MEDS • Present and past medications (both topical and systemic), supplements
ALLERGIES • Food, medication, environmental
FHX • Psoriasis, atopy, skin cancer, genodermatoses ( e.g. . tuberous sclerosis, neurofibromatosis)
SOCIAL • Sun/chemical exposure, smoking, EtOH, IVDU, pets, travel history, hobbies, sick contacts
ROS • Done as indicated by the clinical situation with particular attention paid to possible connections between
.
signs and disease of other organ systems (e.g. a patient with a lesion suspicious for melanoma would require a
complete ROS looking for any sign of organ dysfunction suggesting metastases)
• Myalgia, arthralgia, fever, oral ulcers, Raynaud’s phenomenon
• Remember to ask about hair and nail changes as many conditions that affect the skin also affect hair and nails (e.g.
psoriasis)
.
PHYSICAL
Define lesions using SCALD
• Size of lesion
• Color: erythematous, violaceous, hyperpigmentation, hypopigmentation
• Arrangement: grouped (clustered lesions), serpiginous ( wavy or serpent - like appearance), reticular (net -like arrangement ), target
( looks like a bull’s eye - central erythema surrounded by pale edema and peripheral erythema), discoid (resembles a disc)
• Lesion morphology: primary morphology ( see Box 2) and. if applicable, the secondary morphology (see Box 3)
. .
• Distribution: diffuse (e.g. viral rashes and drug reactions), extensor (e.g., psoriasis), flexural (e.g. atopic dermatitis), dermatomal
.
(e.g. shingles), symmetric, photodistributed ( areas exposed to the sun)
• In addition
> Assess suspicious lesions for malignancy ( Box 1) BOX 1: Signs of Melanoma
> Examine the hair, scalp, and nails ( Box 3) Asymmetrical skin lesion
> Look for other systemic features common in autoimmune and infectious Border irregularity
disorders: arthralgias ( psoriatic arthritis, Reiter 's syndrome or Lupus), fever Color variation
( viral), oral ulcers, sores on palms and feet ( syphilis) , malar rash (SLE), Gottron’s Diameter (new lesion > 6mm)
papules and heliotrope rash around eyes (dermatomyositis) Evolution (changes in size, color or bleeding)
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BOX 2: Primary Lesions BOX 3: Secondary Lesions
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• Macule: flat, non-palpable lesion, <1cm ..
• Scales: excess keratin (e g , psoriasis) 7T Q)
• Patch .
flat, non- palpable lesion, >1cm (e.g. vitiligo, cafe au lait spot ) • Crusts: dried serum, scab (e.g., impetigo) ts>
TREATMENT
Emergent
..
• Stop offending agent if drug reaction (e g , Stevens - Johnson syndrome/toxic epidermal necrolysis)
.
• Start antimicrobials for infection (e g., cellulitis) or immunosuppressive agent for immune mediated disease
Treatment Options
• Topical: steroids, antibiotics, antifungals, emollients, retinoids, etc.
> steroid strength depends on dosage and vehicle
> steroid examples: weak ( hydrocortisone acetate 0.1% cream) , moderate (mometasone furoate 0.1% cream) , strong
(clobetasol 0.05% ointment )
.
• Systemic medications: immunosuppressives (oral/IV steroids, methotrexate), retinoids ATBx antimalarials .
.
• Light: narrow band ultraviolet B ultraviolet A ( PUVA ), laser therapy
• Surgical: curettage, cryotherapy, electrotherapy, scalpel
Follow- up
• Monitor skin findings over time to evaluate progression, monitor for medication side effects
Referral as indicated
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Authors: Malgorzata Ejsmont MD Adam Dryden MD Timothy Yeh MD FRCPC
FLUID BALANCE
Fluid Distribution
Basics
• Fluid makes up 50- 60% total body weight (TBW) TBW 42 L
• Water movement: mainly osmotic forces ( Na, K)
/ \
IFC 2/3 EFC 1/3
Distribution ( see figure)
• Note: Intravascular volume ECF ( plasma 3- 3.5 L) + ICF ( RBC 2 - 2.5 L) — Interstitial 3/4
in 70kg male J
Intravascular 1 / 4
Fluid Requirements
Maintenance Fluids
• Total: maintenance + replacement (existing and ongoing deficits)
• Maintenance requirements: ~ 2.5 L/day (4 - 2-1Rule) (see table) Wt mL/kg/ hr
CRYSTALLOID • Aqueous solution of salts ± glucose (see table below: Common Crystalloid Solutions)
• Equilibrate in entire ECF: given as 3 - 4 x volume deficit
• Initial resuscitation in hemorrhagic/septic shock, burns - maintain cerebral perfusion
> Isotonic (replacement): if H20 and electrolyte deficit (distribute ECF)
> Hypotonic: if free H20 deficit only (distribute ICF/ECF)
> Hypertonic: in severe, symptomatic hyponatremia (shift ICF - ECF)
.
Crystalloid vs Colloid
• Extensive meta - analysis found no difference in survival between resuscitation with colloid vs crystalloid .
• Cost differential guides recommendations in favor of crystalloids (controversial in some cases)
JD
• Preferred in pediatric patients with mild - moderate dehydration (equivalent to IV therapy) i/>
• Maintenance solutions ( Pedialyte , Ricelyte ): Na 45 - 50 mEq/ L, glucose 2 - 3 %
. f
• Rehydration solutions ( WHO formulation Rehydralite): Na ( 60 - 90 mEq/L) - improve water absorption
• Administer slowly to decrease emesis: mild ( 50 ml/ kg over 4 hrs), moderate ( 100 ml/kg over 4 hrs)
III 1500- 2000 30- 40% > 120 30- 40 5 - 15 confused, anxious
IV > 2000 > 40% > 140 > 35 Anuric confused, lethargic
IV Access
• 2 large bore IVs (16/18) in peripheral veins - investigations, type & cross match (if necessary)
• If severe shock or peripheral IV not achieved - large catheter introducer (8 - 9 Fr) in internal jugular/femoral vein
• If major vascular injury in abdomen/pelvis - establish vascular access above diaphragm (subclavian/jugular)
Hemodynamic Assessment
• . . .
Continuous monitoring of VS (BP HR RR Temp Sa02), ECG .
• Frequent reassessment for signs of decreased perfusion: mental status, capillary refill, temperature of extremities
• Other: urine catheter (end organ perfusion), arterial line ( serial ABGs, normalization of lactate), central venous pressure, central
venous oxygen saturation ( ScV02 - 02 extraction, global perfusion)
IV Therapy (also see Pediatric Emergency [ in Pediatrics ])
• Isotonic crystalloids: ( RL or NS) x 2- 3 L wide open ( adult)
> Hemodynamically unstable: suggests > 15 - 20% blood volume lost or significant ongoing loss - transfusion
> Adequate response -continue crystalloid, monitor hemodilution
• Blood transfusion
.
> If not typed /cross - matched - transfuse 0+ (male) O - ( female)
> Severe hemorrhagic shock - transfuse initially
> Bleed controlled - target Hgb > 70 g/L
• Hemorrhage, large volume resuscitated: dilutional coagulopathy
. .
> Massive transfusion protocol: 6u PRBC 6u FFP 1pool PLTs
Referrals
• .
Surgery (control bleed) ICU if need for vasoactive drugs to support arterial pressure or cardiac output, circulatory instability
unresponsive to volume replacement, decreased LOC, need for invasive monitoring, etc .
HISTORY
Determine the following prior to acquiring/reading the radiograph:
•
•
.
Patient ’s name. age gender, and date of image
HPI: acute/chronic, level of progression of the disease
• Availability of previous imaging
• Determine the type of the image ( supine /prone /decubitus)
. .
• Ensure completeness of the abdominal film series (i.e., " the 3 views ": supine AXR erect AXR and a CXR )
> Note: if patient is unable to stand for an upright abdominal radiograph, acquire a left lateral decubitus AXR
INTERPRETATION
Basic approach: ABCD or GreatBigFART Great - gas pattern
• Air ( free air /gas pattern) Big - bowel wall air
• Bones (fractures, metastatic disease) F - free air
• Calcifications (GU stones, gallstones, A - air fluid levels
lymph nodes, calcified AAA wall ) R - air in rectum
• Density ( soft tissue structures) T - thickened bowel wall
Technical Quality
• Level of penetration
> Normal penetration: vertebral columns (lumbar and thoracic ) can be seen clearly
> Under -penetration: AXR is too white
> Over - penetration: AXR is too dark
• Inclusion: ensure that the entire abdomen (diaphragm to the proximal femoral head) is included in the study
Foreign/Therapeutic Objects
• . .
Comment on any lines, iatrogenic devices, tubes present (e.g., foley NG tube ECG leads), and/or swallowed/ inserted items
Gas Patterns
• Normal: gas present in the stomach and a few loops of transverse colon/sigmoid, colon/rectum
> In a healthy, ambulatory adult the small bowel usually has very little or no air unless the patient has recently eaten
• Abnormal: multiple loops of small bowel and/or large bowel filled with gas (supine): multiple air fluid levels and/or a paucity of
gas in the sigmoid colon/rectum (upright AXR ); bubbles of air in bowel wall ( pneumatosis)
> DDx for abnormal bowel gas pattern: ileus or mechanical obstruction
• Ileus: typically seen in post -operative patients (gas is present in sigmoid colon/rectum)
• Mechanical obstruction: sick patients (no gas in the sigmoid colon/rectum, unless distal obstruction)
Bowel
• Carefully look for bowel wall thickening and narrowing of the lumen, as well as air in bowel wall
> Small bowel diameter < 3.5 cm; large bowel diameter < 6 cm ( variable); cecal diameter < 9 cm
Bones
• Begin with the spine, then study the ribs, followed by the pelvis, and finally the upper femurs
• Determine the proper alignment of the vertebral bodies, pedicles, and spinal/transverse processes
• Evaluate for signs of osteoarthritis, scoliosis, and other degenerative disease in the vertebral column
• Overall, carefully examine the bones for any fractures, lytic/blastic lesions, and/or metastatic disease
> Note: bowel gas patterns, in particular around the pelvis, may closely resemble lytic patterns
Organs/Soft Tissues
• Try to visualize liver, stomach, spleen, kidneys, bladder, psoas margins
• Plain X - ray films are generally not used to examine subtle changes in organs. For instance, the liver ’s radiological shadow is very
misleading as an index of its size, unless there is extreme hepatomegaly
• Useful for obvious changes such as masses, presence/absence of organs, calcifications/calculi, etc.
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I INTERPRETATION OF ABG
u Current Editor: Hana Yu MSc MD
BASICS
• Patient ID/date of test
• .
Patient demographics: age gender, ethnicity
• Pre -test data: determine if the test was performed with patient on room air or 02 flow
• Compare: previous ABGs if available
DIFFERENTIAL DIAGNOSIS
SELECTED CAUSES OF ACID- BASE DISORDERS
Respiratory Wide Anion Gap Normal Anion Gap Metabolic
Respiratory Alkalosis
Acidosis Metabolic Acidosis Metabolic Acidosis Alkalosis
• Respiratory center • Acute/chronic • M - methanol • H - hyperalimentation • Exogenous alkalis
depression hypoxemia • U - uremia • A - acetazolamide • Diuretics
• Neuromuscular • Respiratory center • D - DKA • R renal tubular acidosis • Post -hypercapnea
disorders stimulation • P - paraldehyde • D - diarrhea • Mineralocorticoid effect
• Airway obstruction • Mechanical
• I - isopropyl alcohol • U - ureteric shunt • Hypercalcemia
• Lung parenchymal hyperventilation
• L - lactic acidosis • P post -hypocapnea
- • Vomiting
disease
• E - ethyleneglycol •S spironolactone • Volume contraction
• Mechanical
hypoventilation • S salicylates
BASICS OF INTERPRETATION
What is the clinical context?
• Past medical history: CHF, COPD, renal disease, acute overdose, etc .
• Stable or unstable condition
• .
Is this patient being ventilated? If so how is 02 being delivered ?
How is the patient ventilating? ( PaC02)
• PaC02 < 35 mmHg then suggests hyperventilation
• PaC02 > 45 mmHg then suggests hypoventilation
.
• PA02 is calculated Pa02 is measured
> Alveolar air equation: PA02 = [ FI02( PB - 47) ] - ( PaCO 2/0.8 ]
• FI02 = fraction of inspired 02
• -
PB = barometric pressure ( 760 mmHg at sea level)
• Consider A- aD02 when patient is on room air
• Consider Pa02/ PA02 when patient is on supplemental 02
> Hypoxemia with normal A -aD02 - suggests hypoventilation or high altitude ( atmospheric p02)
^
> Hypoxemia with A - aD02 or|Pa02/ PA02 - suggests ventilation- perfusion mismatch, shunt, or low DLCO
^
Partially
PaC02 44 44 4 4
Compensated pH 4 4 4 4
Base Excess Positive Negative Negative Positive
PaC02 44 44 44 44
Fully Compensated pH Normal Normal Normal Normal
Base Excess Positive Negative Negative Positive
COMPENSATION RULES
Acid/ Base Disorder Compensation Rule
Acute respiratory acidosis 4 PC02: 4 HC03 = 10:1
Chronic respiratory acidosis 4 PC02: 4 HC 03 = 10:4
Acute respiratory alkalosis + PC02 lHC03
: = 10:2
Chronic respiratory
iPC02:
alkalosis
Metabolic acidosis
^ HC03 = 10:5
INVESTIGATIONS
Blood Work (if not already obtained from ABG)
• Hgb, electrolytes, glucose, urea
Anion Gap
• Anion gap = ([ Na+]) - ( [ HC03- ] + [Cl - ])
• Normal anion gap is 10 - 14 mEq/ L
• Anion gap is dependent on albumin and serum phosphate
•Normal Anion Gap = 0.2 x ( albumin (g/ L)) + 1.5 x (phosphate ( mmol/L))
• Most of the time we can estimate expected anion gap as -
Albumin ( g/ L) /4, ignoring phosphate
• Increased anion gap suggests an increased number of unmeasured anions
Osmolar Gap
• Osmolar gap = measured osmolality - calculated osmolality
• Calculated osmolality = 2[ Na+] + [urea ] + [glucose ]
• Normal osmolar gap < 10 mmol /L
• Osmolar gap >10 mmol /L suggests potential toxic osmole ingestion
Note: The approach to interpretation presented here focuses on a single acid - base disorder. Real - world clinical scenarios often
involve multiple acid -base disorders and should be interpreted in the context of clinical information.
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INTERPRETATION OF CHEST RADIOGRAPH
Current Editor: Edwin Cheng MD
u
HISTORY AND CONTEXT
Determine the following prior to acquiring/reading the radiograph
• Patient ’s name, age, gender, date of image, and previous imaging available for comparison
• HPI: acute/chronic, reason for chest x - ray, clinical question
• Determine the projection and patient positioning for the image (e.g., supine/upright / PA/AP/lordotic /decubitus)
> Normally, chest x - rays are done in PA and lateral views
> AP view for bedridden patients (portable X-ray), lordotic view to image lung apices, decubitus to assess loculation of effusion
INTERPRETATION
Technical quality
• Level of penetration and exposure
> Normal penetration: intervertebral discs and vascular lung markings behind L heart are clearly visible
> Under -penetration (CXR : too white): overaccentuation of lung vascular markings: may be mistaken for pulomonary edema
> Over - penetration (CXR : too dark ): difficult to discern vascular markings; false detection of pneumothorax or emphysema
• Adequacy
> Inclusion: ensure lung fields are complete - the apices to the costophrenic angles should be imaged
> Symmetry/Rotation: space between medial aspect of the clavicle and midline spinous process should be equal
> .
Inspiration: in adult patients 9- 10 posterior ribs or 6 anterior ribs visible above diaphragm
Inspection ( systematically work from inside to outside)
• Comment on any lines, iatrogenic devices, and/or tubes present (central line, chest tube, pacemaker, NG tube, ECG leads, etc.)
• Trachea
> Check position: if shifted from midline, consider tension pneumothorax or mediastinal mass
• Mediastinum
> Width > 8 cm PA CXR - " widened mediastinum” DDx: aortic dissection, aortic aneurysm, mediastinal mass
• Great vessels
> Assess pulmonary trunk, aortic arch, and descending thoracic aorta for any enlargement and/or calcification
• Lungs
> Ensure examination of the entire lung field, side - to - side comparison
> Airspace disease: DDx: pneumonia ( pus), pulmonary edema ( fluid), hemorrhage (blood), tumor
> Interstitial disease ( lung markings thicker /more prominent ): DDx : pulmonary edema, viral pneumonia, inflammation
> Obvious masses: consider lung cancer, tuberculosis, pulmonary nodules
• Pleura
> Blunting of costophrenic angles, suspect pleural effusion
> Look for any abnormalities in the diaphragm (e.g., excessive elevation)
> Pleural calcifications/thickening, pleural- based mass and calcified plural plaques often 2° to asbestos exposure
• Diaphragm
> Right hemidiaphragm often slightly higher than the left 2° to the liver
> Check for free air under the diaphragm on upright projection for pneumoperitoneum
• Bones and soft tissues
> Examine bones: look for fractures, lytic/ blastic bone processes, or any distortion of normal bone contour
> Cervical and thoracic spine: look for the contour and height of the spinous processes and pedicles
> Examine soft tissues: breast tissues, axillae, subdavicular areas, etc. Check for subcutaneous emphysema, axillary masses,
surgical staples.
> Bilateral breast shadows: axillary staples ± ipsilateral loss of a breast shadow
• .
Confirm pathology seen on PA view and determine posterior - anterior location
COMMON RADIOGRAPHIC FINDING: I
• Pulmonary edema
> Vascular redistribution to the upper lobes, interstitial edema ( thickening of interstitial markings Kerley B lines,
peribronchial cuffing, visualization of fissures), alveolar edema, pleural effusions, cardiomegaly
> .
DDx: CHF renal failure
• Pneumonia (silhouette sign)
> R hemidiaphragm not visualized = RLL pathology: R heart border not visualized = RML pathology
> L hemidiaphragm not visualized = LLL pathology: L heart border not visualized = Lingular pathology
• COPD
> .
Frontal: hyperinflated lungs ( > 10 posterior ribs visualized), flattened hemidiaphragms bullae
> Lateral: increased retrosternal air space and flattened hemidiaphragms
> .
In COPD increased risk of apical pneumothorax
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111INTERPRETATION OF CBC-P
u Current Editor: Bradley Brochu MD
HISTORY
• Infection ( fever, chills, cough, diarrhea, dysuria, headache, skin infection) & inflammation (joint redness /swelling and rash)
• Malignancy (constitutional symptoms: unintended wt loss, unexplained fevers and night sweats)
• Anemia (SOB, presyncope, sources of blood loss)
• Easy bruising or bleeding
.. ..
• Identify those patients in need of urgent care [e g , shock (i e , tachycardia, hypotension, poor peripheral vascular perfusion),
respiratory distress, cardiac ischemia /infarction, and decreased LOC ]
PHYSICAL
.
• Inspection: pallor, jaundice, petechiae purpura, ecchymosis, joint redness/swelling, skin rash, local signs of infection
• Palpation: lymph nodes, liver, spleen: digital rectal exam is contraindicated if neutrophil count < 1.0, inspect the area only
• Percussion: Castell' s sign/Traube’s space ( splenomegaly), liver margin
• Auscultation: flow murmur (high cardiac output in anemia, fever )
Red Flags
• Combined abnormalities including pancytopenia ( anemia, thrombocytopenia, and neutropenia)
.
• Fatigue, recurrent infections, abnormal bleeding Wt loss, night sweats
POLYCYTHEMIA
Primary • Polycythemia vera
• Hemoconcentration (dehydration, burns, V/ D), response to hypoxia ( sleep apnea
.
Secondary other cardiopulmonary disease, smoking CO poisoning, renal artery stenosis, high oxygen-
. COPD and
affinity hemoglobinopathy), and autonomous EPO secreting conditions and tumors
ANEMIA
• TAILS: Thalassemia
anemia
. Anemia of chronic disease, Iron deficiency. Lead intoxication. Sideroblastic
MICROCYTIC (MCV <80 FL)
• Note: elevated RDW suggests iron deficiency anemia
NORMOCYTIC (MCV 80- 100 FL)
• t reticulocytes ( > 2% of RBC) .
• Bone marrow response to the 4Hs ( Hemorrhage Hypoxia . Hematinics, and Hemolysis)
kVJ a 11H:] •
!•]m11f 1VJ:w COUNT
•
•
*
Actual number of WBCs per volume of blood; normal values: 4-11 x 109/L
Increased: infection, inflammation, tissue ischemic/infarction, corticosteroids, general physiologic stress response, hematologic
disorders (e.g., leukemia, lymphoma)
• Decreased: production ( aplastic anemia, folate or B12 deficiency, drugs); increased breakdown/consumption (hypersplenism
sepsis, drugs)
.
NEUTROPHILIA .
lithium, catecholamines G-CSF and GM - CSF), tissue ischemia and infarction (Ml. stroke), smoking,
pregnancy, post - splenectomy, metabolic (uremia, ketoacidosis) , general physiologic stress response,
leukemia and myeloproliferative disease, and hereditary (extremely rare)
NEUTROPENIA
Increased • Infection/sepsis, inflammation, autoimmune, drugs
Destruction
Decreased • Drugs, chemotherapy, bone marrow failure and /or infiltration (including aplastic anemia), cyclic, hereditary
Production • Immunodeficiency
Sequestration • Hypersplenism
LYMPHOCYTES
Role in adaptive immunity: normal values: 1- 4.5 x 109/L; reactive lymphocytes in EBV infection
• Viral infection (infectious mononucleosis), pertussis, drugs, endocrine disorders ( thyrotoxicosis, adrenal
LYMPHOCYTOSIS insufficiency), allergic reactions, autoimmune disease, lymphoproliferative disorders (CLL=classic), smoking,
and transient stress lymphocytosis
• Immune deficiency syndromes (including HIV), acute/chronic illness, immunosuppressive therapies
LYMPHOPENIA (chemotherapeutic agents, radiation), bone marrow failure and malignancy, idiopathic
MONOCYTES
Role in innate immunity: normal values: 0-1.1 x 109/ L
MONOCYTOSIS
• Chronic .
infection ( such as TB fungal, bacterial, viral, etc.), inflammatory ( sarcoidosis, IBD, collagen vascular
disease), neoplasms ( hematologic and non- hematologic), post - splenectomy
EOSINOPHILS
Role in response to parasites (especially helminths) and allergic response: normal values: 0-0.7 x 107L
• Allergic /hypersensitivity reactions, drug reactions, parasite infestation, autoimmune and collagen vascular
disease, cutaneous (pemphigus, eczema, atopic dermatitis), pulmonary ( sarcoidosis, bronchiectasis,
EOSINOPHILIA
.
pneumonia, cystic fibrosis) and Gl disorders (celiac disease, IBD) , neoplasms (Hodgkin’s lymphoma T cell
lymphomas, carcinomas), and certain drugs (cytokine and interleukin therapy)
BASOPHILS
• Role mostly unknown, likely in allergic response: normal values: 0- 0.3 x 109/ L
.
• Basophilia: allergic / hypersensitivity, inflammatory, endocrinopathy ( DM hypothyroidism), chronic renal disease, and
myeloproliferative disorders (especially CML)
PLATELET COUNT
Actual number of platelets per volume of blood: normal values: 150- 400 x 109/L
THROMBOCYTOSIS
Primary • Essential thrombocytosis/thrombocythemia
• Hemorrhage, iron deficiency, surgery, splenectomy/hyposplenism, malignancy, acute or chronic
Secondary
inflammatory disease, general physiologic stress response
THROMBOCYTOPENIA
• Severe nutritional deficiency, infection and inflammation, chemo and radiation therapy, bone
Decreased PLT Production marrow failure (including aplastic anemia) or infiltration (primary hematologic or metastatic
disease), hereditary
• Immune ( UP, EBV, SLE) and non- immune mechanical ( MAHA: TTP, HUS, DIC, HELLP) and
Increased PLT Destruction
.
mechanical (cardiopulmonary bypass IABP and ECMO)
Sequestration • Splenomegaly, massive transfusion
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111INTERPRETATION OF CREATININE
LU .E
u Authors: Kimberley Krueger MD, Jason Kiser MD, Mark Joffe MD FRCPC
DIFFERENTIAL DIAGNOSIS
Serum Cr increase
. .
• ARF: pre-renal (decreased ECFV renal artery vasoconstriction); renal ( ATN, acute interstitial nephritis GN. small vessel disease);
post -renal ( BPH. neurogenic bladder, anticholinergic medications, malignancy, bilateral nephrolithiasis)
.
• CRF: DM. HTN, PCKD. GN drug-induced, multiple myeloma, prolonged ARF
• Falsely high in drug interference with assay (cefoxitin, flucytosine)
Serum Cr decrease
• Decreased muscle mass, pregnancy
BASICS OF INTERPRETATION
• .
Normal values for serum Cr: 50- 110 pmol/L. Note: normal value depends on individual patient (e.g. body mass, age; previous
creatinine values are needed to interpret value).
• Cr produced from skeletal muscle metabolism, concentration proportional to body mass
• Serum Cr can be used to estimate GFR (endogenous Cr is freely filtered through the glomerulus with minimal tubular secretion
-
and excreted from muscle at a relatively constant rate): GFR is inversely proportional to Cr
• Limitations in ability to estimate GFR exist because:
.
> Cr values are influenced by age muscle mass, and dietary intake
> Contribution of tubular Cr secretion increase with increasing renal impairment
> GFR must fall considerably before serum Cr has a notable increase ( 50% fall in GFR doubling of serum Cr)
> Patient must be in steady state for Cr values to be used
sCrALCULATIONS
Clearance (CrCL
TO ESTIMATE GFR
)
• CrCL (mL/min) = (urine Cr x urine volume over 24 hrs) /(serum Cr x 140)
• Has the potential to overestimate GFR in patients with advanced kidney impairment
Cockcroft -Gault
• CrCL ( mL/min) = ( 140 - age) ( Wt in kg) / ( serum Cr in pmol/ L ) [ Note: multiply by 1.2 for males]
• .
Accounts for age body weight, and gender influences on GFR
Modification of Diet in Renal Disease (MDRD)
• Complex formula to estimate GFR (reported as mL/min/ 1.73m:body surface area)
. . .
• Uses the following indices: age sex serum Cr African descent
CKDEPI
• Formula used to estimate GFR in Alberta labs since 2012
• Uses the following indices: age, sex . .
serum Cr African descent
INVESTIGATIONS
Volume Status (pre- renal failure)
Blood Work
• Electrolytes, osmolality, CBC, urea ( to differentiate between causes of ARF)
Radiology/Imaging
• Renal U/S (assess kidney size, rule out post renal causes, rule out renal artery stenosis with Doppler )
Special Tests
. .
• Urinalysis (hematuria, proteinuria, casts) U/O urine electrolytes /osmolality/creatinine to calculate fractional excretion of sodium
.
( to differentiate between causes of ARF) foley catheter (prostatic obstruction)
Surgical/Diagnostic Interventions
• Renal Bx
Fractional Excretion of Sodium
FENa = (UrineNa x SerumCr ) / ( SerumNa x UrineCr )
Treat underlying cause ( see ARF and CRF [ in Internal Medicine - Renal Failure ] ) tn
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Emergent: to
• Follow Cr and watch for development of uremic symptoms or other indications for urgent dialysis ( acidemia, hyperkalemia,
volume overload) in those patients with renal failure
• Uremic symptoms tend to develop once serum Cr > 530- 710mmol /L or CrCL < 10 mL/min
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Authors: Brendan Diederichs MD Katherine Leung MD Tom Yeo MD FRCPC
BASICS
Name the study and orientation ( e.g., lateral, AP, odontoid)
Identify the patient and date
Comment on technical quality
Ask if previous studies are available for comparison
LATERAL
Mnemonic: All Able- Bodied Premeds Do Anatomy
• Adequacy: assessed by counting the vertebral bodies
> If you cannot see the top of T1, order a swimmer ’s view
• Prevertebral space
> 7 at 3.21 at 7 rule: normal width of the prevertebral line at C 3 ( 7 mm) and C 7
( 21 mm): widening may suggest pathology
• Intervertebral disc spaces
> Narrowing may be suggestive of degenerative disc disease
-
> Absence of midline C spine tenderness
Able to actively rotate neck 45° left and right ? ( if no - • radiographic imaging is indicated)
•
*
• Note: Rule not applicable if:
> Non- trauma cases
> GCS < 15
> Unstable vital signs
> Age < 16
> Acute paralysis
> Known vertebral disease
> Previous C-spine surgery
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INTERPRETATION OF CT
u Current Editor: Edwin Cheng MD
inISTOI
Name the study and orientation (e.g.. axial images from non-contrast CT head)
Identify the patient and date along with clinical question and relevant history
Determine if previous studies are available for comparison
L9L BASICS
CT scans are generally viewed in axial sections as viewed from the feet ( see figures below)
• Coronal (similar in orientation to a PA CXR ) and sagittal reformats are common
• IV contrast studies have vessels appearing white (approaching the attenuation of bone)
> In the arterial phase, the arteries are brighter than the veins
> In the portal venous phase, the arteries and veins are both bright
Anterior
pancreas
gall bladder
intestines
Right
Posterior
• Oral contrast may also be given to enhance the bowel
• Common contraindications for IV contrast include allergy and renal disease (check creatinine before administering contrast )
• Non- contrast studies have darker vessels ( approaching the attenuation of soft tissue)
CT ABDOMEN
• CT Abdomen studies typically include slices from just above the diaphragm to the iliac crests
• Be systematic (system or organ based approach) and scroll through image set several times
Abdominal Wall and Intra-abdominal Fluid
• Check for defects in the abdominal wall (e.g., hernias), thickening/ irregularities of the peritoneum, and fluid collections .
( indicates ascites, hemorrhage, abscess). Also assess for lymphadenopathy.
Bone
• In bone window, assess for fractures, degenerative changes, lytic /blastic lesions, decreased mineralization, symmetry.
Free Air
• In lung window, assess for free air under the anterior wall of the abdomen ( if scan was obtained with patient supine).
Stomach, and Small and Large Intestines
• Follow the Gl tract from distal esophagus to mid small bowel. Then start at the rectum and work your way up to the ileocecal valve.
• Assess for masses, polyps, wall thickening and other irregularities.
• Assess for distension, obstruction, inflammation, and air in the lumen wall (pneumoperitoneum).
• Look for diverticulae and the appendix (blind ending pouch) by finding the ileocecal valve and scrolling a few slices lower.
.
Liver, Biliary Tract Spleen, and Pancreas
• If looking for hepatic lesions, you will often need an arterial phase and portal venous phase.
• Assess the overall density of the liver to look for fatty infiltration.
• Look for masses, cysts, scarring, and enlargement.
in
3
.
• Assess for normal pancreatic duct Look for masses, abscesses or signs of pancreatitis including peripancreatic 7T Qj
Pleura
• Look for pleural plaques or masses. Look for pneumothoraces and pleural effusions.
Airways and Lung Parenchyma
• Assess for obstructions, masses, consolidation, atelectasis, nodules, bullae, bronchiectasis, ground glass opacity, emphysema,
honeycombing, etc.
CTHEAD
• CT head consists of axial views from the vertex to the skull base
• Medical history can help focus search ( trauma, new neurological deficits, query stroke, etc.)
• Start from the bottom and work up to the top (or vice versa)
V V
*V
• Is there loss of space (effacement/edema) or excess space ( atrophy, hydrocephalus) ?
• Is the ventricular system normal? Any dilatation, shift, compression, or asymmetry?
• Are the basal cisterns patent? Is there blood (bright if recent) in the cisterns?
Examine the brain parenchyma
• Move from central structures outward, ensuring each major area of the brain is symmetrical and without lesions ( any soft tissue
asymmetry may indicate mass effect).
• Examine for midline shift/mass effect, masses, bleeds, or infarcts.
• Examine grey - white matter differentiation, look for changes suggesting edema .
Examine the contours of the calvarium
• Are there any areas of attenuation in keeping with a subdural (lens shaped, crosses sutures) or an epidural (crescentic, within
sutures) hematoma?
Examine the bones (using the bone window )
• Also look at the sinuses ( air/fluid levels, fractures), the orbits, and mastoid air cells.
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INTERPRETATION OF ECG
u Current Editor: Derek Chan MD MBA CHE
GENERAL
Ensure correct patient ID
Compare with previous ECGs if available
RATE
Each thick line (5 mm box ) represents 0.2 secs. Find a QRS that lands on a thick line and use the count off method for
successive thick lines (300- 150- 100- 75 -60- 50)
• If there is an irregular rate, count the number of QRS complexes in the entire strip and multiple by 5 (each strip is 12 secs)
• Bradycardia = < 60 bpm
• Normal = 60- 100 bpm
• Tachycardia = > 100 bpm
RHYTHM
Regularity
• .
Sinus rhythm: P wave before every QRS QRS after every P wave, P waves upright in leads 11 and aVF
• Regular or irregular?
• If irregular, is it regularly irregular, or irregularly irregular ?
> Regularly irregular rhythms include 2nd degree heart block and ventricular bi/trigeminy
> Irregularly irregular rhythms include atrial fibrillation, multifocal atrial tachycardia, or wandering atrial pacemaker
Vectors Method
• Lead aVF for vertical vector
> If QRS is positive, axis points down toward + 90° Determining Axis
> If QRS is negative, axis points up toward - 90°
> The more positive the QRS, the more the overall vector points toward + 90°
-90°
• Lead I for horizontal vector
> If QRS is positive, axis points right toward 0°
> If QRS is negative, axis points left toward 180° Extreme
Left Axis
.
> The more positive the QRS the more the overall vector points toward 0° Right Axis
l (-) avF (-)
I (+) avF (+)
• Combine the vertical and horizontal elements to estimate the axis
180° 0°
Isoelectric Lead Method
• Determine the quadrant for the axis (see figure) Right Axis Normal
> Determine if QRS in lead I and lead aVF is positive or negative -
I( ) avF (+) K+) avF (+)
• Look at the 6 limb leads and decide which one is closest to being the
isoelectric lead (positive and negative components of the QRS are equal)
> Draw a line perpendicular to the isoelectric lead vector toward the
appropriate quadrant - this estimates the axis to the nearest 30°
90°
Interpretation
• Normal axis is between - 30° and +90°
.
• Note: if QRS is positive in lead I and lead II then axis is within normal range
n
INTERVALS
PR Interval-Normal: 0.12-0.20s CO d
• Shortened PR Interval
?r a)
.
> Fast conduction along an accessory pathway (pre - excitation Wolf - Parkinson - White) V)
> Junctional rhythms with retrograde P waves ( P waves occur within the QRS complex )
• Lengthened PR interval indicates delayed AV conduction
> Regular rhythm: 1° heart block
> Irregular rhythm: 2° or 3° heart block, wandering atrial pacemaker, multifocal atrial tachycardia
QRS Interval-Normal: < 0.12s
• Many causes of wide QRS complexes are life- threatening, always consider VT
> Consider LBBB, RBBB, hyperkalemia, interventricular conduction delay
.
> New LBBB and dynamic ST changes ( Ml) RBBB and S1Q 3T3 ( PE), third degree heart block (Ml), fascicular block
-
QT Interval — Normal: < Vi of preceding R - R interval, QTC < 460ms (male) or 480ms ( female)
• Calculate QTc as the QT/ VRR interval (0.38 - 0.42 s )
• Shortened QT interval
> Hypercalcemia, digitalis
• .
Lengthened QT interval (mnemonic: DIE because the most serious complication is torsades de pointes)
> Drugs: amiodarone, quinidine, procainamide, sotalol, TCA antidepressants, antihistamines, macrolides, cocaine
. .
> Injury: myocardial infarction, myocarditis, head injury, hypothermia HIV anorexia nervosa
.
> Electrolytes: decreased K * Mg' or Ca 2 *
> A lengthened QT interval may also be congenital (common)
HYPERTROPHY
Atrial Enlargement
• Left atrial enlargement
-
P - mitrale is a “ m shaped" P wave > 0.12s wide with > 0.04 s between peaks ( most common in leads I and II)
>
Negative component of P wave in VI is greater than or equal to lxl small boxes
>
• Right atrial enlargement
> P -pulmonale are peaked P waves > 2.5 mm tall (most common in leads II and III)
Ventricular Enlargement
• Left ventricular hypertrophy
> There are multiple criteria with varying sensitivity and sepcificity for chamber hypertrophy
> Deepest S wave of VI or V 2 + tallest R wave of V 5 or V6 > 35 mm ( Sokolow Lyon criteria)
> S wave of V3 + R wave of aVL > 28 mm in men or 20 mm in women (Cornell voltage criteria)
• Right ventricular hypertrophy
> R:S ratio is > linVlorV 2
. .
> May see evidence of posterior Ml or RBBB RAD ( axis > 90 degrees) R wave in VI > 7 mm (not R ' of RBBB)
PATHOLOGICAL FEATURES
T waves
•
•
. .
T waves should be positive in leads I II and V3-V6, and negative in aVR
Abnormal T waves: inverted, symmetrical, peaked, or tall ( > 2/ 3 of R wave)
ST segment
• Elevation >1mm in 2 contiguous leads from baseline (defined as the TP segment ) indicates acute transmural ischemia
• Depression >1mm in 2 contiguous leads from baseline indicates subendocardial ischemia
• Concave segments are classic for strain pattern: ST elevation with tombstone segments are classic for acute infarction
Q waves
• Signify necrosis: significant Q waves are 0.04 s (1small square) wide or >1/ 3 amplitude of QRS
Special Circumstances were an ECG is Difficult to Further Interpret
• LBBB: a new LBBB shown on an ECG is alway pathological and may be an indication of Ml, but this is not diagnostic. In a LBBB
ST segments and T waves are shifted in a discordant direction and can either mimic or hide a Ml. LV hypertrophy produces
an ECG pattern similar to LBBB with a widened QRS and ST depression or T wave inversion on lateral leads. Therefore, any
diagnosis of LBBB may also include a differential diagnosis of Ml and LV hypertrophy.
• Right Ventricular Paced Rhythm: a right ventricular paced rhythm results in a morphology similiar to LBBB on ECG. This
results in similar difficulty diagnosing an acute Ml to a new LBBB on ECG with ST segments and T waves shifted in discordant
directions.
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— INTERPRETATION OF ELECTROLYTES: CALCIUM
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sORRECTED CALCIUM AND PARATHYROID HORMONE
Measured serum calcium must be corrected because serum albumin influences ionized calcium to bound calcium ratio
Corrected calcium ( mmol/L) = measured serum calcium + 0.02 * ( 40 - serum albumin)
• If in doubt whether serum calcium reflects ionized calcium, can measure ionized calcium directly
• -
Ionized calcium normal range is usually 50% of serum calcium
HYPOCALCEMIA - PIAGNOSTIC APPROACH
Hypocalcemia (< 2.2 mmol/L)
Vitamin D
deficiency*
_ Yes Low 25-OHD?
Yes 1
Elevtated PT11?
No Low
Magnesium?
Yes
Hypomagnesem ia
No No
HYPOCALCEMIA - HISTORY
HPI: diet and medications (calcium and Vit D deficiency)
PMHx: renal disease, autoimmune disorders, Gl absorption disorders
SHx: head and neck surgeries (parathyroid injury)
FHx: familial hypocalcemia, polyglandular autoimmune syndromes
HYPOCALCEMIA - INVESTIGATIONS
Routine labs
.
• Electrolytes, magnesium, calcium, albumin, phosphate Vit D . PTH, ALP. creatinine, urea
Special tests
• 24 hr urine calcium: decreased in hypoparathyroidism and Vit D deficiency
HYPOCALCEMIA - TREATMENT
.
Emergent (calcium < 1.0 mmol/L acutely symptomatic)
• IV calcium gluconate, correct other electrolyte abnormalities (hypomagnesemia)
Chronic
• Treat underlying disease, diet and lifestyle modification
• Oral calcium and/or Vit D supplementation as appropriate
PHPTH*
Yes Elevated urinary Ca: ? Yes
J
Elevated PTH ?
No
Elevated PTHrP?
Yes Consider
t/>
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cr.
No No
I
Elevated Vitamin D?
Yes Consider
FFH lymphoma .
sarcoidosis
HYPERCALCEMIA - SYMPTOMS
" Bones, stones, groans, and psychic overtones"
Note: Symptoms are non-specific and many patients are asymptomatic at time of diagnosis
• CNS: confusion, depression, fatigue
• CVS: hypertension, shortened QT syndrome, arrhythmias
.
• Gl: abdominal pain N/V, anorexia, constipation, peptic ulcer disease, pancreatitis
• GU: renal calculi, polyuria, polydipsia, renal failure
• MSK: weakness, bone pain, arthritis, osteoporosis, fractures
HYPERCALCEMIA - INVESTIGATIONS
Routine labs
• . . . .
Electrolytes, magnesium, calcium, albumin, phosphate Vit D PTH ALP creatinine, urea
Special tests
• 24hr urine calcium: distinguish FHH from primary hyperparathyrodism. FHH is typically associated with low 24 hr urine calcium
excretion whereas primary hyperparathyroidism is often associated with elevated calcium excretion.
• Can consider spot urine calcium to creatinine ratio as a surrogate for 24 hr urine calcium excretion
HYPERCALCEMIA - TREATMENT
.
Emergent (calcium > 3.0 mmol/ L acutely symptomatic)
. .
• IV fluids with goal urine output being roughly 100- 200 cc /hr bisphosphonates calcitonin, correct other electrolyte
abnormalities
• Loop diuretics to promote excretion of calcium should only be used after dehydration is corrected and only if patient appears fluid
overloaded (most patients are in fact dehydrated)
Chronic
• Treat underlying disease, stop offending medications, diet and lifestyle modification, consider surgery if applicable
43 </>
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INTERPRETATION OF ELECTROLYTES: POTASSIUM
Current Editor: Hana Yu MScMD
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HYPOKALEMIA - DIFFERENTIAL DIAGNOSIS AND INVESTIGATIONS
Decreased intake ( uncommon): starvation or clay ingestion
.
• Redistribution into cells: acid - base (alkalosis), hormonal (insulin 02 adrenergic action), anabolic ( B12 or folate administration. TPN,
granulocyte -macrophage colony - stimulating factor), other ( hypokalemic periodic paralysis)
Extrarenal losses (urine K * < 20mmol/d)
• Gl losses: vomiting, diarrhea, tube drainage, laxative abuse
• Skin loss: excessive sweating
HYPOKALEMIA - TREATMENT
Recognize signs/symptoms of hypokalemia (see box)
-
1mEq/ L decrease reflects 200 meq total body loss
Redistribution
•
Acidosis
before collection
i Pseudohyperkalem
-hemolysis
•B-blockers K ' shift out of cells? after collection -leukocytosis
•cellular necrosis -thrombocytosis
•insulin deficiency No
•digitalis overdose
•rhabdomyolysis
high low
Urine K ' collection TTKG
bums
•
f
Increased intake
•diet
- KCI tabs/ I V > 10 I
Reduced tubular flow
<6
Decreased aldosterone
- kidney failure activity
- reduced ECV
[
Normal aldosterone/ Low aldosterone Low aldosterone
tubular resistance low renin normal renin
-K sparing diuretics - DM - ACEi
-pentamidine -NSAIDSs - ARB
43 Edmonton Manual of Common Clinical Scenarios
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Cellular Shift • Acidosis, insulin deficiency, beta -blockers, tumor lysis, burns, hemolysis U)
Note: Need to rule out pseudohyperkalemia via repeat serum K level before treatment if value does not match clinical scenario
HYPERKALEMIA TREATMENT
K * < 6.0
and • Treat underlying cause
normal ECG • Stop K * intake and meds that increase K *
• Promote K * loss ( see " Remove K * ” below)
K * > 6.0 • Antagonize effects of K * on myocardium ( 10 mLs of 10% calcium gluconate IV over 2 - 3 mins)
and/or • Shift K + into cells:
ECG changes *
> Insulin + glucose (e.g., 10 units of rapid acting insulin + 50 mL of 50% glucose solution IV as a
bolus followed by an infusion of glucose - containing solution) - Always give the glucose before the
insulin!!
A MEDICAL EMERGENCY: >
If patient is significantly hyperglycemic, insulin alone can be provided
TREAT URGENTLY •|i-
agonist ( Ventolin)
> Bicarbonate
• Remove K *
> Loop diuretics ( furosemide)
> Cation exchange resin (e.g., Na or calcium polystyrene sulfonate = Kayexylate®); give with lactulose
to promote osmotic diarrhea and prevent sticking
> Hemodialysis
7.0 8.0
Hyperkalemia
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INTERPRETATION OF ELECTROLYTES: SODIUM
. .
Authors: Kimberley Krueger MD Jason Kiser MD Mark Joffe MD FRCPC
mi
T1 YPQ 1 jraiaiiilfeMSIFFERE1
.
bo-osmolar -
Hyper osmolar
Hypo-osmolar
Urine Na <10mEq/L Urine Na> 20 mEe/ L Urine Na < 20mEq/L Urine Na >20mEq /L
l I
Extrarcnal losses Renal losses Water intoxication' Extrarenal Renal
.
(GI, skin , lung ( diuretics, salt - polydipsia (Cl IF, cirrhosis, ( ARF, CRF)
3rd spacing ) wasting nephropathy, SIADH nephrosis)
adrenal insufficiency Glucocorticoid de ficiency
bicarbonaturia, ketonuria Hypothyroidism
Stress
MANAGEMENT OF HYPONATREMIA
Recognize signs/symptoms of hyponatremia
• Headache Complications of Hyponatremia
• N/V • Seizures
• Anorexia
• Coma
• Lethargy
• Respiratory arrest
• Seizures
• Brain damage
• Decreased LOC
• Coma • Brainstem herniation
• Death
Order basic investigations
• If correction too rapid: osmotic
• .
Serum electrolytes, glucose Cr, BUN osmolality . demyelination of neurons
• Urine sodium, osmolality
• Consider ordering: TSH, free T 4, cortisol level
GENERAL MANAGEMENT
Acute hyponatremia ( < 24 hrs) • Rapid correction in symptomatic patients or those with large drop in sodium
Slow correction ( < 8mM/ 24 hours correction) as rapid correction can cause osmotic
Chronic hyponatremia ( > 24 hrs )
demyelination syndrome
GENERAL CHOICE OF IV FLUID (IN HYPOOSMOLAR HYPONATREMIA )
Asymptomatic • Normal saline
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\ - ves
I
Hypervolemic? no Small volume of >K00m()sm /kg urine?
CO
(Iatrogenic, Cushings,
hyperaldostcranism) <250m()sm/kg urine ? no
i \ es
no yes I
i offree water/
Exlrarenul losses
Drug induced Response lo ADI17 volume contracted
Osmotic diuresis yes < I
> no (Insensible, respiratory.G1 and
i I skin losses )
Central Diabetes Insipidus Nephrogenic Diabetes Insipidus
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P INTERPRETATION OF LFTS & ENZYMES
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Authors: Mackenzie Lees MD Simon Turner MD Gordon Lees MD FRCSC
I
INTRODUCTION
Liver enzyme abnormalities are common
1:10 Canadians will have at least one elevated liver enzyme during routine screening
Normal LFTs do not exclude the possibility of chronic liver disease
lij PES OF LIVER FUNCTION TESTS
Hepatocyte damage/inflammation (increased transaminases = cell death)
• ‘ALT: sensitive and specific marker of liver injury/inflammation
> Normal range: < 50 U/L
• Ischemic injury, toxicinjury, acute viral hepatitis,
> Nonhepatic increases: severe rhabdomyolysis, AST, ALT
acute biliary obstruction, autoimmune hepatitis
systemic myopathies > 1000
( less common)
> Can remain elevated weeks to months following
liver injury AST >500 • Unlikely to be EtOH-related liver disease
> Can be normal in presence of liver disease ( EtOH,
chronic HCV or inactive cirrhosis)
• 'AST: less sensitive and specific marker, useful as a screening test to determine AST/ALT ratio
> Normal range: < 40 U/ L
. .
> Nonhepatic increases: Ml, extensive surgery PE rhabdomyolysis
> AST/ALT <1: viral hepatitis, autoimmune liver disease
> .
AST/ALT > 2: EtOH liver disease, biliary obstruction NAFLD
> Decreasing AST/ALT ratio over time: can indicate progression to cirrhosis
> AST/ALT ratio is not useful in fulminant liver failure
Biliary function
• Bilirubin: usually increased in bile duct injury, cholestasis, and severe hemolysis
> Normal range: 1- 20 mmol /L
> Normal bilirubin is 70% unconjugated and 30% conjugated: hyperbilirubinemia is considered unconjugated if > 85% of bilirubin
is unconjugated.
> Test for indirect /unconjugated ( RBC lysis) vs. direct /conjugated (biliary): determine cause of high total bilirubin
> An increased bilirubin due to hepatic cause usually indicates advanced liver disease
• *ALP: Elevated in all forms of cholestatic liver disease, mild elevation in cirrhosis
> Normal range: 25 - 110 U / L
> Can also be high in pregnancy (placental ALP), bone disease, renal disease
• GGT: useful to confirm that high ALP reflects hepatobiliary disease (order GGT when elevated ALP)
> Normal range: < 65 U/ L
> Specific, with poor sensitivity: can be high following recent EtOH ingestion, secondary to antiseizure medications, renal
disease, pancreatitis, DM, CAD, prostate cancer
Liver synthetic function
• Coagulation factors (INR): PT-INR, measures extrinsic QUICK LFT REFERENCE FOR JAUNDICE
.
pathway Factor VII dependent ( synthesized by the liver )
-
Pre hepatic -
Post hepatic
> Normal range: 0.8 - 1.2 Hepatic
> Can be high with Vit. K deficiency
..
(i e , hemolysis) ..
(i e , biliary)
AST, ALT Normal /unchanged
• Albumin: major plasma protein ( synthesized by the liver )
ALP Normal /unchanged
> Normal range: 33 - 49 g/ L
orf
> Can be low in liver disease, malnutrition, diarrhea, iron
deficiency, infection
BILI
*
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Routine annual evaluation of patients with risk factors for liver disease in
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• Risk factors: obesity, DM, dyslipidemia, Hx of autoimmune disease, Hx of nephrotic syndrome, family Hx of liver disease, high- risk
.
behaviors (IVDU EtOH, sexual promiscuity, tattoos, non- sterile ear or body piercing, residence or travel to developing countries,
tn
occupational exposures)
• Hx of unexplained RUQ pain, dark urine, acholic stools, jaundice
• Findings on physical exam: unintentional Wt loss, stigmata of liver disease, impaired cognitive function
0PPROACHTOORDERING LFTS
Initial screening tests: ALT, AST, ALP, bilirubin, INR, +/- GGT, albumin
Use pattern of liver enzyme/LFT abnormality along with patient history and clinical context to guide further
investigations and treatment ( see table below)
• Prolonged INR
Cholestatic cause
• Very high ALP and bilirubin (direct )
• Normal ALT, unless severe
> Similar increase in ALP and AST (e.g., 4 x normal) likely cholestatic cause
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*43 to
111INTERPRETATION OF LIPIDS
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Authors: Adarsh Rao MD Carol Chung MD Arnold Voth MD FRCP
BASICS
.
The lipid profile includes: total cholesterol ( TC ), high - density lipoprotein (HDL) low - density lipoprotein ( LDL), and
triglycerides (TG).
1. Decide who to screen with lipid panel
2. Estimate risk for major adverse cardiac events based on risk factors
3. Classify patients into low, intermediate, or high risk
4. Treat according to risk category
Recommendations made are based on the 2016 Canadian Cardiovascular Society guidelines.
RISK FACTORS FOR CAD
Male > 45 years old or female > 55 years old LIPID SCREENING GUIDELINES
• All patients with the following conditions
Cigarette smoking
regardlessof age:
DM • Clinical evidence of atherosclerosis
High cholesterol (TC, LDL- C, or apoB) • Abdominal aortic aneurysm
Men > 40 years of
age; women > 40 • Diabetes
Low HDL-C years of age (or • Arterial hypertension
postmenopausal)
HTN • Current cigarette smoking
Consider earlier • Stigmata of dyslipidemia ( arcus cornea,
Family Hx of premature CAD screening in xanthelasma or xanthoma)
( male < 55 years old, female < 65 years old) ethnic groups
at increased • FHx of premature CVD or dyslipidemia
Elevated inflammatory biomarkers risk such as • Chronic kidney disease
South Asian and
(especially hs - CRP) First Nations • Obesity ( BMI > 30 kg/m2)
individuals • Inflammatory bowel disease
Overweight /obese
• HIV infection
Physical inactivity • Erectile dysfunction
• Chronic obstrucive pulmonary disease
• Hypertensive diseases of pregnancy
INVESTIGATIONS
History and Physical
• PMHx: angina, DM, HTN, chronic kidney disease RA SLE . .
.
• Lifestyle: obesity, sedentary lifestyle EtOH, smoking
• Family Hx of premature CAD
• .
Signs of hyperlipidemia include atheromata xanthoma, tendinous xanthoma, corneal arcus
Blood Work
• . . .
Screen patients with lipid profile (TC LDL HDL and TG) as part of global CVD risk estimation
• Non fasting lipid profile is considered reliable and acceptable as long as triglycerides are less than 4.5 mmol/L
• Research does not support use of biomarkers in risk assessment at this time
• . .
Screen for secondary causes if indicated by clinical scenario, e g. hypothyroidism, chronic kidney disease, drugs ( tamoxifen,
glucocorticoids, ft -blockers), nephrotic syndrome, DM, liver disease
. . .
> hs - CRP, TSH, fasting glucose, Cr electrolytes, urea GGT (if EtOH suspected) HbAlC, apoB
Risk Estimation
• Use a risk calculator every time lipid testing is performed, e.g., Framingham. QRISK 2
.
• Sum of scores for multiple risk factors: age sex. total cholesterol, tobacco use, HDL, BP ( both sBP and dBP). presence of diabetes
used to estimate 10-yr risk of CAD and stratify risk for treatment decisions
.
• Presence of some conditions put a patient in the high risk category irrespective of measured LDL arguing for pharmacotherapy
• In general, match the intensity of preventative effort to the patient ’s absolute risk estimate
01
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> 10- 19% • Discuss and offer statins ( preferably moderate intensity)
< 10%
• Re - test lipids in five years with risk estimation. Repeat sooner if other CVD risk factors
develop.
Recommend lifestyle changes for all patients: Mediterranean or DASH diet, exercise, Wt loss, smoking cessation,
moderation of EtOH intake
Manage additional medical risk factors to|CAD risk ( treat HTN and DM)
Pharmacologic therapies
• Treat to target if pharmacotherpay is started: LDL < 2 mmol/L or > 50% LDL reduction. Repeat cholesterol panel 3 months after
therapy change.
• Statins
> First line of treatment for all patients when drug therapy is warranted
> Statin can be expected to lower relative risk of CVD by 25 - 35%
> HMG- CoA reductase inhibitors slow cholesterol formation by inhibiting rate -limiting enzyme
> Major side effects include myalgia, elevated ALT, CK elevation, myopathy, rhabdomyolysis ( rare) , liver failure (very rare)
> Monitor CK and ALT in symptomatic patients and those at high risk of adverse events
> E.g., atorvastatin 10 - 80 mg po daily, rosuvastatin 2.5 - 40 mg po daily, simvastatin 5 - 40 mg po daily
<n
‘43 co
111
.
LU
INTERPRETATION OF PFT
E Current Editor: Bradley Brochu MD
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BASICS
. . .
Patient ID age gender, ethnicity, Ht Wt, BMI (used to calculate reference values)
Test information
• Date of test
-
• Pre test data
> Pre-test medications taken
> Smoking and past medical history
• Compare with patient ’s previous PFTs (if available)
• Contraindications
> Respiratory distress, angina, pneumothorax, ongoing hemoptysis, active TB
DIFFERENTIAL DIAGNOSIS
Approach to abnormal PFTs
/ \
N DLCO dec. DLCO
Not responsive to
I
Neuromuscular, ILD, CHF
Responsive to
bronchodilator bronchodilator Pleuraldz,
obesity
Normal spirometry and lung
COPD Asthma volumes with abnormal DLCO
/ \ / \
N DLCO dec. DLCO inc. DLCO dec. DLCO
I
T
Broncholitis Emphysema* Polycythemia, mild CHF PE, Anemia , Pulmonary HTN
Early ILD, increased COHb
SPIROMETRY
Quality
• .
Acceptability: requires 3 artifact - free maneuvers (e.g., no cough within 1 sec no glottis closure)
> Note: a minimum of 6 secs of sustained expiration on each maneuver is required
• Repeatability: requires 3 maneuvers where the two largest values of FEV1are within 0.150L of each other and the two largest
values of FVC are within 0.150L of each other
Flow-volume loop
•Right displacement of tidal flow loop and tidal flow curve approaching maximum expiratory flow curve is suggestive of airflow
limitation
• Flattening of the inspiratory or expiratory flow curve is suggestive of a thoracic airway obstruction. This could be either variable
.
or fixed and either intra or extra thoracic in origin (e.g. tumor, thyroid goiter).
Diagnostic criteria for airflow obstruction and significant reversibility
• Is there obstruction?
> FEV1/ FVC <0.7 - yes
> FEV1/FVC >0.7 - no
• How severe is the obstruction?
> Mild: FEV1>70%,
> Moderate: FEV160- 69%,
> Severe: FEV135 - 49% .
> Very Severe: FEV1< 35%
airflow obstruction 7T Qj
• COPD in
> Post - bronchodilator FEV1/FVC < 0.7 AND FEV1 < 80% predicted. Airflow obstruction is not fully reversible.
• Asthma
> FEV1/FVC ratio less than lower limit of normal based on age, sex, height, etc. AND increase in FEV1post bronchodilator > 12%
volume
A) normal flow -volume loop B) typical obstructive C) typical restrictive defect D) typical mixed
defect with FEV1 < lower withTLC < lower limit obstructive and restrictive
limit of normal of normal defect
LUNG VOLUMES
Quality vital capacity measured by lung volumes ( slow expiration) should be > FVC measured by spirometry (forced
expiration), especially in obstructive disease
• TLC measured by lung volumes should be > VA measured by diffusion capacity
Total Lung Capacity: may be measured using either N 2 dilution method or body plethysmography
• > 120% predicted suggests possible hyperinflation (emphysema)
03
'43 in
LU
I INTERPRETATION OF URINALYSIS Authors: Aamir Bharmal,Cathy Lu MD, Valerie Luyckx MBBS
u
INDICATIONS
UTI, pyelonephritis
Renal calculi
DM
Acute or chronic renal failure
Pregnancy
Hematuria
Undifferentiated abdominal or flank pain
PPEARANCE
CLEAR, LIGHT
• Normal variation with different physiological states of hydration
TO DARK YELLOW
COLORLESS • Diabetes insipidus, diuretics, excess fluid intake
CLOUDY .
• UTI amorphous phosphate salts, blood, mucus, bile
PINK/RED
• Blood Hgb . . sepsis, dialysis, myoglobin food coloring beets, sulfa drugs, nitrofurantoin, salicylates,
, ,
laxatives (phenolphthalein)
ORANGE/YELLOW • Dehydration, phenazopyridine ( pyridium), bile pigments, drugs (rifampin)
BROWN/BLACK • Myoglobin, bile pigments, melanin, cascara, iron, nitrofurantoin, alkaptonuria, metronidazole
HEMATURIA
Type 4 Free Hgb, myoglobin 4 Whole cell (erythrocyte)
• Differentiate free Hgb from • Transfusion reaction, intravascular • Neoplasm, coagulopathy, menses
RBCs by centrifuging urine hemolysis, burns, crush injury, (contamination), glomerulonephritis,
• (supernatant is colored if pigment is free) tissue ischemia foreign body (especially Foley catheter ) ,
stones, renal infarct
‘ To further delineate the nature of hematuria, analyze the nature of the sediment microscopically
Glucosuria
ENDOCRINE • DM . pheochromocytoma. Cushing's disease, hyperthyroidism pancreatitis
,
RENAL ..
• Defects in tubular reabsorption mechanisms (e g , Proximal Renal Tubular Acidosis)
IATROGENIC • SGLT - 2 inhibitors; false positive with large doses of aspirin, ascorbic acid, cephalosporins
Ketonuria
ENDOCRINE • DKA, hyperthyroidism
METABOLIC • N /V/D, starvation
LEUKOCYTE ESTERASE
Dependent on the presence of esterase from granulocytic leukocytes, used to detect 5 WBCs/HPF or lysed WBCs
.
May not be reliable in children with UTI generally detects pyuria, not bacteriuria
When combined with the nitrite test, leukocyte esterase has a PPV of 74% for UTI if both tests are +ve and a NPV of
.
> 97% if both tests are - ve ( therefore, seen as surrogate markers for bacteria )
PROTEIN
Normal protein excretion is < 150 mg/ 24 hrs ( 10 mg/100 mL in a spot specimen);
proteinuria on dipstick requires quantification with 24hr urine studies
Dipstick protein detection is limited to albumin primarily and will not detect immunoglobulins (urine protein
electrophoresis must be utilized to detect immunoglobulins)
DDx includes benign and pathological causes (see Proteinuria ( in Internal Medicine ])
FPECIFIC GRAVITY
< 1.016 1.016 - 1.022 > 1.022
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Preparation Epiglottis
• Sedation: midazolam, propofol, ketamine
• Neuromuscular blockade: succinylcholine - Glottic opening
• Opioid: fentanyl
Vocal cords
• Equipment
> Cuffed ETT: usually 8.0 - 8.5 mm for adult male; 7.5 - 8 mm for adult female
> Laryngoscope (usually Macintosh blade size 3 or 4)
> Suction
> Adjuvants, such as bougies, glidescopes, or lightwands
Evaluation - LEMON
• Look - foreign object, neck size, teeth, jaw
• .
Evaluate using 3:3:2 rule - 3 fingers in mouth (TMJ mobility) 3 fingers from mentum to hyoid bone (mandible length), 2 fingers
from hyoid to thyroid (neck length)
• Mallampati classification
• Obstruction - soft tissue swelling, foreign body, excessive soft tissue (obesity), burn / inhalation injury
• Neck mobility
Procedure
• Pre -oxygenate the patient with 100% 02. unless patient is at high risk of aspiration with bag mask ventilation
• Position the patient
> Ensure the patient ’s head is level to the umbilicus of the intubator
> Take appropriate precautions to minimize neck movement when intubating a patient with a potential C- spine injury
> Elevate the head to the " sniffing position”, so that the tragus of the ear is in the same horizontal plane as the sternal notch.
This will maximize view of glottis opening.
• Hold the laryngoscope in the left hand and insert into the right side of the oropharynx; the tongue will shift to the left and up
into the floor of the pharynx
• Advance the blade into the vallecula and apply force upward and forward
toward opposite junction of wall and ceiling to elevate epiglottis.
Do not rotate the laryngoscope using your wrist as this increases
the likelihood of dental damage.
• Hold the endotracheal tube with the right hand and pass the tip
through the abducted vocal cords, into the upper trachea and past
the larynx. The tube should be at approximately 23 cm at the
teeth for a male and 21cm at the teeth for a female.
• Withdraw the laryngoscope and inflate the cuff
• Secure the endotracheal tube
Post Intubation
• Confirm proper ETT placement
> Exam for symmetrical chest rise and tube condensation
> Listen for equal breath sounds and absence of epigastric
sounds .
If breath sounds are louder on the right side than the left, this
could indicate right mainstem bronchial intubation.
> Check return of ETC02
Chest X- ray should be performed after emergency intubation
UMBAR PUNCTURE
Indications CT Head prior to LP recommended if:
..
• Suspected CNS infection ( e g , meningitis)
• Suspected subarachnoid hemorrhage • age > 60
..
• Suspected CNS disease (e g , Guillain- Barre syndrome, carcinomatous meningitis) • immunocompromised
• Therapeutic relief of pseudotumor cerebri • history of CNS disease
• Administration of intrathecal therapy • seizures within the past 1week
Contraindications • focal neurologic abnormalities
• Absolute • papilledema
> Infected skin at intended site of needle entry • obtunded or unconscious
» Unequal pressures between the supratentorial and infratentorial compartments
(identified through CT head)
• Relative
> Signs of increased intracranial pressure
> Coagulopathy (anticoagulation therapy or disorder, bleeding diathesis)
> Brain abscess
Procedure
Position
•
> Lateral recumbent position: patient should be requested to adopt the fetal position, with back flexed, in order to widen the
gap between the spinous processes
> Sitting position: alternative position, may be preferred in patients who are obese; patient should be requested to lean forward
to open the interlaminar spaces
• Landmarking
> Palpate the posterior iliac crest and visually draw a line between the superior borders of the posterior iliac crests; this line will
intersect the L4 spinous process
> Using this landmark, identify the L4- L 5 interspace for your needle insertion site ( L 3 - 4 interspace may also be used )
> Remember that the spinal cord normally ends at around L1- L2 levels
• Preparation
> Apply mask, gown, and gloves using sterile technique
> Cleanse the skin with chlorhexidine three times
> Drape the area with a sterile cloth
> Ensure that the needle insertion site is blotted dry with a gauze pad
• Anesthesia
> Administer local anesthesia with injection of 3 - 5 mL of 1% lidocaine: retract the plunger to ensure no blood
• Collection
> Advance needle with stylet in place, aiming towards patient ’s umbilicus; bevel parallel to spinal column: feel for a “ pop” as the
dural membrane is pierced
> Remove the stylet to check for CSF during advancement if unsure
> Use a manometer to measure opening pressure ( N = 7 - 15 cm H20)
> Collect 4 - 10 mL of CSF; approximately 10 drops per tube
.
> Tube 1: cell count; Tube 2: gram stain, C+S +/- fungal: Tube 3: glucose, protein; Tube 4: cell count; Tube 5: virology, mycology,
cytology
• Removal of needle
> Reinsert the stylet to avoid entrapment of a nerve root Post LP Headache
in the dura as the needle is removed • Most common complication
• Occurs in 10 -30% of patients
Complications
• Post procedure headache • More common in women of younger age
• Infection ( meningitis, discitis, vertebral osteomyelitis) • Usually begins within 48 hrs of the procedure
• Bleeding • Headache is often positional: worse when upright,
• Cerebral herniation (most serious complication) better when supine
• Radicular symptoms and lower back pain (not uncommon)
• Treat with caffeine and/or analgesics
• Epidermoid tumor (occurs years after the procedure is performed)
• In case of failure of above therapies, epidural blood
• Abducens palsy
patch may be offered
• Trauma to nerve roots or conus medullaris
Edmonton Manual of Common Clinical Scenarios 56
in
.2
• Autosomal dominant: M = F; only one copy required to express phenotype; on average, half the offspring of an affected parent
may also be affected: may “ skip” a generation if incomplete penetrance
> e.g., familial hypercholesterolemia, hereditary colon cancer, polycystic History SCREEN
.
kidney disease Huntington’s disease, neurofibromatosis
• SC: Is there Some Concern of a familial disease?
• X- linked: M > F; son of carrier female has 50% probability of being
affected, daughters of affected males are obligate carriers, daughters of
.
• R: Are there Reproductive issues ( i.e. miscarriages,
infertility) in the family?
carrier females have 50% chance of being a carrier, carriers usually do • E: Early deaths/disease onset in family members
not express affected phenotype or have a mild form of disease
> e.g., Duchenne muscular dystrophy, hemophilia A
.
• E: Et hnicity (e.g., Ashkenazi Jews French Canadians)
• N: Non-genetic risk factors
Multifactorial
• Most common form of inheritance: arises from interaction between
multiple genes ± environment
> Neural tube defects, DM HTN .
Chromosomal disorders
• Number of chromosomes
. .
> e.g. Down syndrome ( trisomy 21) Klinefelter syndrome ( XXY)
HISTORY
ID • Patient ’s name, age, gender, ethnicity
PO&GHX • Multiple spontaneous abortions or stillbirths, infertility, maternal age, triple test results ( AFP, pHCG estriol), .
abnormalities detected on U/S
FHX ..
• Sibling/offspring with known chromosomal abnormality, consanguinity (i e , parents related to each other by
blood), early onset of disease/death in family members, reproductive concerns in multiple family members
SOCIAL • Adoptions, non -paternity, EtOH and tobacco use
PEDIGREE CONSTRUCTION
Pedigree Conventions
•
•
Mark the proband (index case) and consultands
( individuals seeking genetic counseling)
Organize family by generations - each generation on
i o 3
o
4
in a generation line
•
•
In a subline, arrange individuals from eldest to youngest
In unions, the male is on the left wherever possible
in A 2 P 3 4
o
cn
Female by phenotype Male by phenotype
o Sex not specified
>
(/
QJ
A Spontaneous abortion
Spontaneous abortion
( affected) A Termination of pregnancy
<s> Pregnancy
<5> Pregnancy ( affected)
Multiple individuals
(unknown number )
Multiple individuals
(known number )
Egg/sperm donor
© Surrogate
03EATMENT
Emergent
• Varies according to condition (e.g., neurosurgical evaluation in patient with osteogenesis imperfecta with neurological changes,
dietary interventions for patients with metabolic disorders such as PKU)
Treatment options
• Medical: enzyme replacement, pharmacological
.
• Surgical: Plastic Surgery ( e g., cleft palate), tumor resection, organ/bone marrow transplant
03
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IIu
III
PRE- OPERATIVE EXAM
. .
Authors: Imran Raghavji MD Eric Chou MD Surita Sidhu MD
BACKGROUND
Anesthesia is required for surgical interventions in order to provide analgesia, anxiolysis, amnesia, areflexia, and
hemodynamic stability. The pre - operative assessment should identify the presence of any factors which may increase the
risk of perioperative mortality and morbidity, with particular attention paid to cardio- respiratory reserve. The physical
exam emphasizes airway anatomy.
A pre - operative Internal Medicine assessment prior to surgery would focus on cardiac risk ( would a patient benefit from
cardiac investigation +/- cath), perioperative diabetes, anticoagulation, other medication management, etc.
HISTORY
ID • Patient’s name, age, gender
SURGERY • Anatomical region
INDICATION • Emergent or elective
PAST SURGICAL/
• Surgical procedure and history of perioperative course (especially related to anesthesia)
ANESTHETIC HX
PAST MEDICAL
HX
Seizure history
Stroke and residual deficits
CNS Increased ICP
Spinal cord disease, especially high cord lesions and autonomic dysreflexia
Neuromuscular disease (myasthenia gravis, dystrophy)
CAD
Previous Ml and any interventions
CHF
CV Systemic or pulmonary HTN (resting BP)
Valvular disease, especially aortic stenosis
Arrhythmias
Exercise tolerance ( ability to climb 1flights of stairs = 4 METs)
Asthma ( severity, treatment)
COPD (home 02)
RESP OSA (useofCPAP)
Restrictive lung disease
Recent infections
GERD
Gl
Hepatic disease
Renal disease
RENAL
Dialysis ( type, frequency, last run)
Diabetes and systemic manifestations
Adrenal insufficiency
ENDOCRINE
Thyroid disease
Exogenous steroid use
Anemia
HEMATOLOGIC Coagulopathy
Bleeding diathesis
Osteoarthritis (neck and back)
MSK
Diseases affecting airway manipulation: rheumatoid arthritis, ankylosing spondylitis, Down syndrome
scleroderma
.
Cervical tumor/infection
General Approach
• . .
VS ( BP. HR. RR, Temp. Sa02) Ht Wt. BMI
• Established IVs and potential sites for invasive monitoring/regional anesthesia
Airway Exam
Class I Class 3 Class 4
• Mallampati score ( see figure)
• Dentition ( prostheses, caps, crowns, chips)
• Mouth opening ( > 2 finger breadths ideal)
• Thyromental distance: mentum to thyroid notch ( > 6cm)
• TMJ ROM (ability to protrude lower jaw)
• Neck
• Length, circumference, cervical anatomy
Cardio - Respiratory
• Inspect: JVP, WOB ( work of breathing)
• Palpate: radial and carotid pulse for rate, rhythm, quality Indications for Investigations
• Auscultate for breath sounds and adventitious lung sounds, • Major surgery: cardiovascular, renal,
heart sounds, murmurs CBC pulmonary or hepatic disease:
Other malignancy, hematologic disorder
11 kTi »1 B [cfiTlWCFB
ELECTROLYTES - Hypertension; renal disease; diabetes;
^
Blood Work
CR
FASTING
adrenal disease; diuretic use
• Diabetes
• CBC ± type & screen; electrolytes, glucose, Cr; LFTs; GLUCOSE
coagulation studies; G- HCG PREGNANCY
• Women of childbearing age
Imaging TEST
• ECG; chest x -ray; echocardiogram; PFTs, or spirometry • Heart disease; hypertension; diabetes:
ECG men > 40 y/o, women > 50 y/o;
RISK CLASSIFICATION cerebral trauma; CVA
GENERAL
To minimize medical error, avoid using abbreviations that can be misinterpreted
• Use “daily " instead of "qd"
• Use "alternate daily" instead of "qod ”
. .
• Write “ 2" instead of " 2.0 ” and "0.1” instead of “ 1"
• Use " meg" instead of “ug"
PRESCRIPTIONS
The following information should be on a prescription
1. Date
• Time must be included if in hospital
2. Patient name and address
• Consider writing out to prevent patient removing stickers to sell Rx ’n
l Ntme Joh*vVo& DOB 14/3/85
3. Medication Information 2 Addnss 111 82 Ave' Due 10/11 /15
• Name of drug or ingredient (s)
> Generic name unless using combination product
> Spell the drug name correctly and write legibly
• Strength
> Include patient Wt for Wt - based dosages
• Dosage form
.
> Caps tabs, gtt (drops), erm (cream) , etc.
3 2 ) A m&xicillitv 500mg Copy PO TID x.10 dayy
> Consider putting parentheses around dosages and writing out
numbers so they cannot be easily altered (e.g., consider "( 30) ( thirty)
MUte: 30 (thirty )
tabs" rather than " 30 tabs") 2 ) Gentu*nycCm .5tng /kg' IV Q8K
> When writing dosages in mg/kg (especially in pediatrics) also write X 7 Dayy
total dosage (e.g., gentamycin 82.5 g (1.5 mg/kg) IV q8h x 7d, Pt Wt
55 kg Patient weight = 55kg
• Route of administration
. .
> PO (oral) IV (intravenous), IM (intramuscular ) SC (subcutaneous) PR
(per rectum)
. 4 MO REFILLS
.
Date, time, patient ID, age gender, admission presentation (diagnosis if known), Hx (significant comorbidities), if surgery
- include # of post -operative day and any surgical complications
5 - Subjective
• Symptomatic information: how the patient feels, how they are coping
• Historical information: changes since last note, new symptoms ( shortness of breath, chest pain)
• Caregiver information: events in the past 24 hrs (from nurse and family members)
• General review: behavior, activity, sleep, appetite (N/V), bowel/bladder routine, pain control
O - Objective
• . . .
VS ( BP HR, RR. Temp Sa02 ) (on RA or on 02) T-max, daily Wt
• General appearance (acutely ill, appears well, etc ) .
• . .
Physical exam findings ( FOCUSED: usually include CVS RESP ABDO)
• If applicable: incision/ wound (clean/dry/ intact ), dressings
• Ins & Outs including drains (number of /output/character)
• New laboratory results, microbiology (culture report ) , x -rays, pathology reports
• Allied health updates/consult reports
A - Assessment cn cr
QJ
.
• One line summary of patient ' s status ( improving, worsening, same)
(/>
• Summary of known medical problems (optionally can add inactive issues)
• Short DDx
P - Plan
• Evaluation: additional laboratory studies and procedures needed for management of each problem
• Therapy: medical treatment, education, etc.
• Disposition: Plan for patient discharge (home, long term care, etc ) .
• Note: Assessment and plan are often combined ( see example)
Signature
• Sign and print name, include level of training (e.g., SI - 3 for third year intern, PGY- 4 for fourth- year resident ) , and pager number
Patient ID: 70 y/o male admitted for delirium secondary to infection (urosepis vs. peri - rectal abscess) ± opioid toxicity.
.
PMHx - rectal tumor (currently actively being investigated, followed by Dr. Smith), rectal fistulas/abscesses, HTN GERD, PVD.
Lives independently.
S: Patient ' s rectal pain still present but has decreased in severity. Mentation improving. Continued delirium (says someone was trying
to sell him "dope" yesterday in hospital). No overnight concerns from caregivers and family. Patient had one bowel movement yesterday
(no hematochezia or melena), normal urine output, and slept for 8 hours.
O/ E: VS - BP = 137/ 62, Sp02 = 96% 2L, HR = 110, RR = 20, T 36.4. General - Alert. Oriented to person (not time or place). CV N SI/ -
S 2. No S3/S4/murmurs. RESP AE = AE. No adventitious sounds. Gl - BS +, abdo soft, non- tender. No organomegaly.
-
U/O - 2000mL/ 24hrs ( > 30cc/hr )
Labs/Investigations: Blood culture pending. Urine culture - no growth (post antibiotics) /urine culture ( Sep 17th pre- ATBx) - E. coli,
CFU108/ CT abdo/pelvis ( Sep 22nd) - no intra- abdominal hemorrhage. Invasion of rectal tumor into right levator ani muscle. R inguinal
LN spread of tumor. R ischiorectal fluid representing possible ischiorectal abscess.
Abnormal labs: CI-: 109. HCQ3: 22. ALT: 53. AST: 86. Hb: 98. Pit: 521. WBC: 23.9. Ca 2+:2.02
A/ P
Active Issues
>Delirium - Improving. Secondary to urosepsis/rectal abscess /opioid toxicity. Infections being treated with meropenem (see
below). Dilaudid decreased to hydromorph contin 3 mg po bid and hydromorphone 2-4mg po q4h PRN.
> Urosepsis - ESBL positive. Has had ESBL positive urine for mos. Being actively treated and followed by Dr. Johnson in
community. ID consulted, being treated with meropenem 500mg IV q6h.
> Rectal abscess - Elevated white count and CT suggests current active rectal abscess. ID consulted, being treated with
meropenem 500mg IV q 6h. Multiple rectal fistulas, abscesses and surgeries since 2005. Followed by Dr. Smith.
> Rectal tumor - diagnosed July 2013. Being followed by Dr. Anderson (Oncology) and Dr. Smith (Surgery). Currently the patient
is in the process of being appropriately staged. Treatment plan is still under discussion.
> Anemia - 2 units pRBCs transfusion on admission. Cause unknown.
> Code Status - Full code
> Disposition - home once delirium has cleared
Inactive Issues
> HTN - stable. On Adalat XL 60mg po daily.
> GERD - stable. On pantoprazole 40mg po daily.
-
> PVD treated with femoral - femoral bypass graft in past.
.
Jane Doe SI - 3
969 - 9999
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PROCEDURE & WARD CALL NOTES
u .
Authors: Ryan Gallagher MD Carrie Ye MD
PROCEDURE NOTE
Date and Time
Who: who was present for the procedure, including supervising staff if applicable; with pelvic & other sensitive exams,
make sure to document other staff present in the room
Consent: comment on whether consent was obtained ( was patient alert or unconscious), and if complications/risks
explained
Indication: purpose of the procedure
Preparation: materials, positioning, sterility, relevant investigations
.
• e.g., aseptic technique, freezing application INR
• Vital signs
• When and why you were called
• Progression of problem
• .
ID: one line summary of patient age gender, reason for admission
• Patientinformation (e.g., SAMPLE Hx )
• Medical Hx: quick list of active medical issues + relevant PMHx • What has been initiated
.
• S: Event details HPI from patient / family/staff • Who else has been called
• O: VS and relevant physical exam
• A: Impression (include DDx) While Walking There
• P: Plan • Thinkof differential for concern
> Actions taken • Review management of problem
A: 57 y/o M with multiple cardiac risk factors, admitted with pneumonia, now experiencing 5/ 10 atypical chest pain.
• DDx: Acute coronary syndrome, esophageal spasm, pleuritis secondary to pneumonia, GERD
P: ECG stat, trops/CK, Nitrospray, CXR. repeat CBC-D. electrolytes
.
June 2nd 2017; 2145h; Follow -up Note
S: Patient ’s pain decreased with nitrospray. Now 1/10.
O: Repeat VS: unchanged except HR now 85
• . .
CXR : unchanged ECG: NSR no T wave or ST changes compared with previous, 1st trop ( -)
• Rest of blood work pending
A/P: Patient 's pain resolving, no evidence of ACS on first ECG/trop
• Repeat ECG and trop in 8 hrs
• Nitrospray PRN for pain
• Consider Cardiology consult in AM for risk stratification ( MIBI or EST)
2
•
IITTJNDERSTANDIN ARTIBIOTICS
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BASIC PRINCIPLES
ATBx only effective against bacteria
^ Author: Maleka Ramji MD
.
• Certain ATBx contraindicated (e.g. tetracycline in renal failure, chloramphenicol in babies due to inability to glucuronidate)
Medication history
• Allergies, interactions
Setting of acquisition of infection
• Country/region
.
• Community vs hospital acquired, ward vs . ICU
• Contact with animals
05
to
m 03 CLASS OF ATBX MOA EXAMPLES SPECTRUM OF ACTIVITY THERAPEUTIC INDICATIONS
in O
F
tn
LU .E Cephalosporins • Bind transpeptidases, First Generation • Increased stability to beta - • Surgical prophylaxis, softtissue
U disrupt cell wall • Cefazolin (IM/IV) lactamases produced by and skin infections (impetigo,
synthesis, activate
• Cephalexin ( PO)
Staph (not active vs MRSA) cellulitis erysipelas caused by
autolytic enzymes • Moderate activity vs Strep MSSA) and bony infections
and cause bacterial • More activity vs. Gram -
like osteomyelitis and septic
cell lysis . .
(E. coli P. mirabilis K. arthritis
• Bactericidal .
pneumonia Moraxella sp.)
• NOT active vs
.
enterococci Chlamydia
and Mycoplasma, or
Haemophilus species
Aminoglycosides • Inhibit
protein • Gram-
• Gentamicin ( IV/IM/ • UTI
biosynthesis by OTIC /OPTH) • Pseudomonas • Synergistic with wall active
binding to 30S • Tobramycin ( IV/IM/ • No activity vs. anaerobes agents
ribosome: Bactericidal OPTH)
Macrolides • Inhibits protein • Erythromycin ( PO/ • .
Staph Strep, anaerobes • Alternative in acute pharyngitis
synthesis by binding IV/TOP/OPTH) (excluding B. fragilis), • 3rd linefor otitis media .
reversibly to the 50S • Clarithromycin( PO) • N. gonorrhea, atypical .
AECOPD sinusitis
ribosomal subunits
of susceptible
• Azithromycin (IV/ .
(legionella mycoplasma, • Alternative for superficial
PO) chlamydia), Bordetella S. aureus infection, acne
microorganisms pertussis . .
vulgaris CAP whooping
.
cough Chlamydia trachomatis
& prophylaxis of ophthalmia
neonatorum due to
N. gonorrhea or C. trachomatis
67 .
Edmonton Manuil of Common Clinical Seena
n
5* m
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CLASS OF ATBX MOA EXAMPLES
SPECTRUM OF
ACTIVITY
THERAPEUTIC INDICATIONS —
( )
cn =cr.
J
Cholera. Brucella
• malaria prophylaxis
• Alters the cytoplasmic
membrane causing
leakage
Lincosamide • Bindsto 50S ribosomal • Clindamycin ( PO/IV/ • Gram+ .anaerobes • Mixed skin infections .
subunit of susceptible IM/TOP)
bacteria, reducing the
including B.
.
fragilis Clostridium
• 3rd line acute pharyngitis . Group
A Strep necrotizing faciitis ( in
rate of nucleic acid ( excluding C. difficile)
Gardnerella vaginalis
. combo with penicillin), bacterial
synthesis and ceases vaginosis
protein synthesis
Metronidazole • Reduced substrate, • Metronidazole ( PO/ IV/ • Anaerobes including • Anaerobic infections
activated by TOP) B. fragilis, C. difficile • mixed infections, C. difficile
nitroreductase, affects • Some H. pylori, diarrhea or pseudomembranous
anoxic or hypoxic cells
causing loss of the
amoeba and parasites colitis, bacterial vaginosis .
(Trichomonas Trichomonas,
DNA helix and form .
vaginalis Entamoeba • PUD triple therapy
and impairment of
cellular function
.
histolytica Giardia
lambia)
Sulfonamides/ • Inhibits folic • TMP/SMX ( PO/IV) • Gram+, Gram-, • UTI, prostatitis, traveler ’s
Trimethoprim acid synthesis .
plasmodia, Chlamydia, diarrhea PJP prophylaxis
by competitively toxoplasma,
inhibiting actinomyces,
dihydrofolate mycoplasma,
reductase and other Pneumocystic jiroveci
steps in the pathway (carinii) pneumonia
( PJP)
• No enterococci or
anaerobes
Vancomycin • Inhibit peptidoglycan • Vancomycin ( PO/ IV ) • ONLY Gram+ • Severe or life - threatening
wall synthesis by
binding to precursor
• MRSA . penicillin staphylococcal infections when
MRSA is suspected (cloxacillin
highly resistant
S. pyogenes/S. is the drug of choice for Staph
pneumonia E. . aureus)
faecalis, E. faecium, • Vancomycin PO ONLY for the
anaerobes (excluding treatment of antibiotic associated
B. fragilis) pseudomembranous colitis
produced by C. difficile
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-
PRE & POST- OPERATIVE ORDERS
.
Authors: Patricia Lee MD Sarah Lai MD, Kamran Fathimani MD FRCSC
• Consent ( informed): discuss potential benefits, risks, and alternatives of surgery with patient and family
.
> Consults (if indicated): Anesthesia Internal Medicine ICU Cardiology. .
• Drugs: previous medications, cardiac medications (continue B-blockers and statins: hold diuretics and ACE inhibitors),
. . .
anticoagulation (hold Coumadin ASA Plavix therapeutic IV heparin/SC LMWH)
• Eating/drinking: NPO after midnight
• Fluids: IV NS or RL maintenance ( 4:2:1 rule: approximately 100- 125 cc /hr )
• Glucocorticoids: If patient on long- term steroids give stress dose steroids
• Heparin: DVT prophylaxis ( Heparin 5000 units SC 2h before OR ): hold if neuraxial anesthesia is expected
• Imaging
> CXR : > 50 y/o or previous abnormal within 6 mos
> ECG: > 50 y/o or as indicated by history
.
• IV: NS RL, etc.
.
> l& O: q 2h q4h, qshift
> Investigations: (depending on surgical procedure)
.
• CBC- D electrolytes BUN, Cr .
. . .
• LFTs: AST ALT ALP bilirubin, lipase
• INR PTT.
• CXR or necessary imaging
• Drugs:
CNS • Antiemetics, analgesics
ID • ATBx
DVT
• Prophylaxis: heparin or LMWH pneumatic stockings .
• Dressings:
> Closed wound: dry dressing PRN
> Open wound: saline soaked gauze bid / tid
• . .
Drains: JP to bulb suction NG to low intermittent suction Foley to urometer, chest tube - 20 cm H20 suction
tn
D
7T £U
Current Editor: Joseph Andrews MD
to
2 0.04 s
Notched R wave Is > 5 wave
> 35mm
20.2mV
P - wave
Lengthening PR interval until dropped beat ( R R interval drops with each beat )
Missed beat
A
Grouped beats with dropped beat between groups Atria and ventricles are firing separately
-
No P waves, irregularly irregular QRS
PR depression and diffuse ST Delta waves and shortened PR Wide flat P waves and peaked T waves
z i /3
QRS
Essential Dermatology
. .
Habif TP Campbell JL. Quitadamo M J Zug KA. Skin Disease Diagnosis and Treatment. Missouri: Mosby Inc.: 2001.
Schwarzenberger K. The essentials of the complete skin examination. Medical Clinics of North America. 1998:82:981-999.
.
Kasper DL. Braunwald E. Fauci AS. Hauser SL Longo DL. Jameson JL. Harrison' s Principles of Internal Medicine. 16th ed. New York : McGraw - Hill; 2005.
Fluid Resuscitation
.
Ahrens W. Chapter 132: Fluid and electrolyte therapy. In Tintinalli JF.. Kelen GD. Stapczynski JS eds. Emergency Medicine: A Comprehensive Study Guide. 6th
ed. New York: McGraw -Hill: 2004.
Capital Health. Clinical Guide to Blood Transfusion |Internet ]. Edmonton (CA): March 16.2010. Section 10,
MassiveTransfusion; [cited 20100ct 91; p.1- 5. Available from: http:// www.capitalhealth.ca/NR/rdonlyres /enupoxpjc 6ucke7lrnuy
jesyq6ibkxmb3sjhor 3 t 65pj27htq 5nnws6h2nnufkm6q 3rxmpkehkklwmidrwbgkzhglppd /Section 10March2010.pdf
.
Ganter MT Hofer CK. Pittet JF. Chapter 88: Postoperative intravascular fluid therapy. In Miller RD. ed. Miller ' s Anesthesia. 7 th cd. Philadelphia: Elsevier ;
2009 .
Morgan GE. Jr.. Mikhail MS. Murray MJ. eds. Clinical Anesthesiology . 4 th ed. New York: McGraw- Hill: 2006.
Manning JE. CHapter 31: Fluid and blood resuscitation. In Tintinalli JE. Kelen GD. Stapczynski JS. eds. Emergency Medicine: A Comprehensive Study Guide. 6th
ed. New York: McGraw -Hill; 2004.
.
Weil MH. Chapter 67: Shoc < and fluid resuscitation. In Beers MH. Porter RS Jones TV. Kaplan JL . Berkwits M. eds. Merck Manual of Diagnosis and Therapy.
18th ed. Whitehouse Station. N J: Merck; 2006.
Interpretation of ABG
.
DuBose TD. Chapter 48: Acidosis and Alkalosis. In Fauci AS. Braunwald E. Kasper DL. Hauser SL. Longo DL. Jameson JL. Loscalzo J eds. Harrison s Principles
'
Interpretation of CBC- D
.
Fauci AS, Braunwald E. Kasper DL. Hauser SL. Longo DL. Jameson JL Loscalzo J. eds. Harrison' s Manual of Medicine. 17th ed. New York: McGraw - Hill: 2009.
Interpretation of Creatinine
.
Fauci AS. Braunwald E Kasper DL. Hauser SL. Longo DL. Jameson JL. Loscalzo J. eds. Harrison s Manual of Medicine . 17 th cd. New York: McGraw -Hill; 2009.
*
03 j
43 to
c
*. Interpretation of C- Spine Imaging
<D 03
Ouellette H. Tetreault P. Clinical Radiology Made Ridiculously Simp ,e. Miami: Medmaster ; 20C
p
LU
i/> '
.E .
Stiell IG Wells GA. et al. The Canadian C- Spine rule for radiography in alert and stable trauma patients. JAMA 2001 Oct:286(15):1841- 1848.
Steill IG. Clement CM. et al. The Canadian C- Spine rule versus the NEXUS low - risk criteria n patients with trauma. NEJM . 2003 Dec:349( 26):2510- 2518.
u Stobbe K. The Occasional C- spine X - ray. CJRM 2004;9(l):38 - 42.
Interpretation of CT
Hofer M. CT Teaching Mcnual : A Systematic Approach to CT Reading. 2nd ed. New York: Thieme: 2007.
.
Fox JC Westin JJ. How to Read an Abdominal Computed Tomography Scan. Emergency Medic ne Reports. Atlanta: 2008.
CT Chest image obtained from Radiological Anatomy of Heart and Vessels of Thorax For N< >n Radiologists. Chandrasekhar HV and Chandrasekhar AJ.
Interpretation of ECG
Casale PN. Devereux RE. Alonso DR. Campc E. Klingfield P. Improved sex - specific criteria of left ventricular hypertrophy for clinical and computer
interpretations of electrocardiograms: Validation with autopsy findings. Circulation. 1987 Mar;75( 3):565 - 572.
Garcia TB. Holtz NE. 12- lead EKG: The Art of interpretation. Sudbury: Jones and Bartlett Pub Jshers: 2001.
Interpretation of Lipids
Toward Optimized Practice (TOP) Cardiovascular Disease Risk Working Group. 2015 February. Prevention and management of cardiovascular disease risk
in primary care clinical p'actice guideline. Edmonton. AB: Toward Optimized Practice. Avail, ible from: http://www.topalbertadoctors.org
. . . . .
Stone NJ Robinson J. Lichtenstein AH Bairey Merz CN. Blum CB. Eckel RH Goldberg AC jordon D. Levy D Lloyd Jones DM. McBride P. Schwartz JS.
-
.
Shero ST. Smith SC Jr. Watson K Wilson PWF. 2013 ACC /AHA guideline on the treatment of blood cholesterol to reduce atherosclerotic cardiovascular risk
in adults: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2013.
Interpretation of PFT
ATS Documents: Statements. Guidelines & Reports [ Internet ]. New York: American Thoracic Society:c 2009 [ cited 2009 Nov 23|. Available from httpY/ www.
thoracic.org/sections/publications/statements/index.html.
.
Miller MR . Hankinson J. Brusasco V. Burgos F Casaburi R. Coates A. et al. Standardisation of spirometry. Eur Respir J. 2005 Aug;26( 2):319 - 338.
Pellegrino R. Viegi G. Brusasco V. Crapo RO. Burgos F. Casaburi R. et al. Interpretative strategies for lung function tests. Eur Respir J. 2005 Nov:26( 5):948 - 68.
ATS - COPD
Celli BR , MacNee W. ATS / ERS Task Force. Standards for the diagnosis and treatment of pat lents with COPD: A summary of the ATS/ERS position paper. Eur
Respir J. 2004 Jun;23(6):932 - 46.
West JB. Pulmonary Pathophysiology: 7 he Essentials . 6th ed. Philadelphia: Lippincott William . & Wilkins: 2003.
1
Interpretation of Urinalysis
Stoller ML. Kane CJ. Meng MV. Chapter 23: Jrologic Disorders. In Tierney LM. McPhee SJ Papadakis MA. eds. Current Medical Diagnosis & Treatment. 47th
ed. New York: McGraw -Hill: 2009.
Bennett RL. Steinhaus French K. Resta RG. Doyle L. Standardized human pedigree nomenclature: Update and assessment of the recommendations of the 7T Q)
National Society of Genetic Counselors. J Genet Counsel . 2008:17:424 - 433.
in
linkTo? type = bookPage& isbn = 978 -0- 443 - 06959- 8&eid ^ 4 -ul.0 - B978 - 0 - 443 -06959- 8..00050- 9 s0310
"
KR
How to Write a Good Prescription. University of Alberta Pediatrics Clerkship Notes, [nd ] Understanding Antibiotics
.
Management of community acquired pneumonia in adults. [ Internet ). Alberta: Toward Optimized Practice. c 2009 ( updated 2008 Jan cited 2009 Oct 29 ).
Available from: http:// www.topalbertadoctors.org
Summary of the Alberta clinical practice guideline for acute otitis media. [ Internet ]. Alberta: Toward Optimized Practice. c 2009 updated 2008 Janxited
2009 Oct 29 ). Available from: http://vwwv.topalbertadoctors.org.
Guideline for the diagnosis and prevention of acute pharyngitis. [ Internet ]. Alberta: Toward Optimized Practice. c 2009 [ updated 2008 Janxited 2009 Oct
29 ]. Available from: http:// wvwv.topa! bertadoctors.org.
. .
Summary of the Alberta clinical practice guideline for acute bacterial sinusitis [ Internet ] Alberta: Toward Optimized Practice. c 2009 [ updated 2008
Janxited 2009 Oct 29 ] , Available from: http://vwvw. topalbertadoctors.org
Guideline for the management of acute exacerbation of chronic obstructive pulmonary disease [ Internet ]. Alberta: Toward Optimized Practice. c 2009
[ updated 2008 Janxited 2009 Oct 29 ], Available from: http://vwwv.topalbertadoctors.org.
Blondel- Hill E. FrytersS. Bugs & Drugs lsted. Edmonton: Capital Health: 2006.
,
.
Sabatine MS. Pocket Medicine: The Massachusetts General I lospital Handbook of Internal Medicine. 3rd ed. Philadelphia:Wolter Kluwer: 2008.
Canadian Pharmacists Association [ Internet ] Ottawa (ON) : e - Compendium of Pharmaceuticals and Specialities.: c 2009 [updated 2009 Oct 29: cited 2009
Oct 29]. Available from: http://vwwv.etherapeutics.ca
Edit 74
. PHYSICAL EXAM
Introduction 76
Abdominal Exam 77
ro _ Blood Pressure Measurement 78
.«y/ E
) TO
>X Cranial Nerve Exam 79
-CLCLU Diabetic Foot Exam 81
Examination for Liver Disease 82
Eye Exam 83
Female Genitourinary Exam 84
Fland Exam 85
FIEENT Exam 86
Flip Exam 87
JVP Exam 88
Knee Exam 89
Lymphadenopathy and Spleen Exam 90
Male Genitourinary Exam 91
Neurological Exam 92
Precordial Exam 96
Respiratory Exam 98
Shoulder Exam 99
Thyroid Exam 101
Station Contributors 102
References 103
75 Edmonton Manual of Cc I
INTRODUCTION
Welcome to the physical exam section! Here you will learn some of the common exams that you will
utilize during medical school and throughout your career. While it is tempting to rely solely on tests
such as ECGs and ultrasound to guide clinical decision- making, a properly - performed physical exam "O
can be invaluable in patient diagnosis and management. Furthermore, you will never have to wait on m zr
x) *<
0 in
the results of a physical exam and they can be performed with little to no equipment. 3o QJ
With this in mind, we strongly suggest that you avoid just “ going through the motions” while examining
your patients. Focus on what you are doing, and how pertinent positives and negatives suggest
what pathology may be occurring. For example, a full respiratory exam is much more than simply
auscultating the lungs and then ordering a CXR or PFT. Details such as nicotine stains on the fingers,
accessory muscle use, and breath sounds can not only help refine you Ddx, but also give you clues as
to the severity of the patient ’s condition. This will assist you with not only initial management, but
also in ordering appropriate investigations later.
A good question to ask yourself is if you make a reasonable management plan based on your physical
exam findings. This will help you perform a thorough exam, along with adjusting your differential
based on your findings. While not all conditions are diagnosable on physical exam, the majority of
them have exam findings that will get you pointed in the right direction.
A final piece of advice is regarding OSCEs. Students often find the format of these exams to be
uncomfortable and are unsure of how to demonstrate their expertise. For these situations, it is often
best to pretend you have two examiners. One of these examiners is blind, and the other is deaf. For
the deaf observer you need to demonstrate that you can properly and efficiently perform your exam
and any maneuvers required. For the blind observer, you must audibly explain what you are doing,
what you are looking for, and what pertinent positives and negatives suggest. By including all of these
aspects in your OSCEs, you can communicate that you know what you are doing and why you are
doing it.
We hope that you find these suggestions and the following exams useful not only in your OSCEs, but
throughout your training and career.
Sincerely,
Edmonton Manual team
Edmonton Manual Dt ( or 76
ABDOMINAL EXAM
Current Editor: Nikhil Raghuram PhD
Basics
Introduce yourself, ask for permission to perform physical examination, wash hands /perform hand hygiene
03
. . . . .
ABCs VS ( BP HR RR Temp, Sa02), IV monitors. Assess if the patient is hemodynamically stable, febrile, tachycardic, or dyspneic.
.yV) E03 PHYSICAL
> X General Approach - Patient ’s name, age
SZ LU
CL • General appearance: Check .
for pallor, jaundice, cachexia Wt loss. Is the patient in discomfort, diaphoretic, agitated, or
motionless? A patient who is still with flexed knees and rigid abdomen may have peritoneal inflammation. Restless patients who
are unable to get comfortable may have renal colic.
Exposure/Draping
• Examine patient from the right side of the bed. The patient should be supine, knees flexed, hands at sides. Cover the patient ’s legs
up to the pubic bone and to lower part of chest.
Inspection
.
• From the foot of the bed note any asymmetry of the abdomen and thorax
• Obvious organomegaly, masses, bulging flanks/ascites? hernias?
• Distension, scars, erythema, rash, hernias, engorged veins (suggestive of portal hypertension): ecchymosis (suggestive of
subcutaneous blood from intra/retroperitoneal hemorrhage: Turner’s sign - flank ecchymosis; Cullen’s sign - periumbilical
ecchymosis
Auscultation
•Listen over 4 quadrants: listen for 1minute prior to commenting on absence of bowel sounds. Comment on pitch and frequency.
> Aortic, renal, iliac, or femoral bruits
> Listen for friction rubs over the liver and spleen
Percussion
• Percussion tenderness: evaluate for acute abdomen/peritonitis (inflammation or perforated viscus) / bowel obstruction
• Percussion of liver: percuss at mid-clavicular line from third intercostal space downwards; asses each rib space looking for change
from resonance to dullness to obtain superior margin of liver
• Percussion for splenomegaly: Castell’s point ( most sensitive test ) - last intercostal space on anterior axillary line
• Percussion to evaluate for presence of ascites: flank dullness, shifting dullness, fluid wave
• Percussion over bladder for suprapubic dullness ( bladder distension)
Palpation
• All four quadrants, light (1cm depth) and deep ( 4 - 5 cm depth) palpation
• Palpate for guarding, rigidity, rebound tenderness.
• Palpation for hepatomegaly: palpate upwards from RLQ to RUQ in mid- clavicular line: move fingers up 2 cm with expiration to
determine inferior border of liver - comment on liver span given superior border identified by percussion
> Note that palpable liver edge is present in a number of normal patients
> If liver edge is palpable, comment on firmness, nodularity, pulsatility, and tenderness
.
• Palpation for splenomegaly: palpate from RLQ obliquely to LUQ moving with expiration with patient supine
• Palpate for distended bladder, hernias (reducible or incarcerated), stool
• Masses: location, size, shape, consistency, mobility, pulsatility
• Palpate away from area of tenderness, look for rebound tenderness and guarding
Other tests - an abdominal exam should also include a DRE ( look for blood, masses, pain, anal sphincter tone) and genital
exam ( look for discharge, cervical tenderness, blood)
Special Tests Indicated for LR + Definition/Procedure
McBurney's Appendicitis 3.4 Tenderness at McBurney 's point (l/3rd of the distance from ASIS to umbilicus)
Rovsing’s Appendicitis 2.3 Apply pressure on LLQ. Patient should experience pain in RLQ.
Obturator Appendicitis NS Flexion of the right hip and knee, followed by internal rotation of the right hip
Psoas sign Appendicitis 2.0 With patient lying on their left, hyper - extend the right hip. Positive if painful.
Rebound Peritonitis 2 Apply steady pressure over an area of tenderness. Test is positive if patient experiences
tenderness pain upon abrupt withdrawal of hand.
Rigidity Peritonitis 3.7 Involuntary reflex contraction of abdominal muscles
Murphy Cholecystitis 3.2 Sudden cessation of inspiration when the examiner ’s hands are hooked below the
hepatic margin
Fluid wave Ascites 5.0 Place edge of patient ’s hand on umbilicus tightly, tap on one side of abdomen, and feel
for fluid wave on opposite hand
Adapted from Evidence - Based Physical Diagnosis and The Rational Clinical Examination: Evidence - Based Clinical Diagnosis
77 Edmonton Manual of Common Clinical Seer
BLOOD PRESSURE MEASUREMENT
. Current Editors: Nathan Hoy MD. Yang Li MD Brian Sonnenberg MD FRCPC
PHYSICAL
Basics "
U
m IT
• Introduce self, wash hands/perform hand hygiene, ask for permission to do PE x<
«/>
. .
• ABCs VS ( BP, HR, RR, Temp Sa02), IV, monitors
Qj
3 n
a>
Patient: ask if patient has smoked, drank caffeine, or exercised in the past 30 minutes. Have patient sit quietly with back
supported and legs uncrossed for 5 minutes.
Equipment: accurate sphygmomanometer with appropriate cuff size ( bladder width > 40% of arm circumference, bladder
length 80- 100% of arm circumference)
Position: apply collapsed cuff around patient’s upper arm so lower end of cuff is 2 cm above antecubital fossa, and bladder
(denoted by an arrow) is above brachial artery. Support patient ’s supine arm at the mid- elbow so antecubital fossa is level
with heart and manometer is at eye level.
Performance:
• .
While palpating radial artery of same arm inflate cuff until radial pulse is no longer palpable. Decrease the pressure
approximately 2mm Hg/sec until the radial pulse is palpable again, note this pressure, then deflate cuff. Allow patient to relax
for 1 minute.
• With the supported antecubital fossa level with the heart, place the diaphragm of stethoscope over the brachial artery and
inflate the cuff to a pressure 20- 30mmHg above the pressure at which the radial pulse disappeared on palpation.
• Slowly decrease pressure by 2mmHg/sec and listen for the first time consecutive tapping sounds are heard ( Korotkoff sounds).
This is the systolic BP (round to the nearest 2 mmHg on the manometer). If Korotkoff sounds disappear during inhalation .
go up 30mmHg and decrease cuff pressure even slower, allowing at least 1respiratory cycle/ 2mmHg to see when Korotkoff
sounds first appear ( only on exhalation) and then are heard throughout respiration (even on inhalation). Difference between
these pressures = pulsus paradoxus ( in mmHg).
• Continue to decrease pressure and Korotkoff sounds will diminish in audibility, muffle, and disappear. Pressure at which
.
sounds disappear is the diastolic BP. If sounds are heard all the way down to OmmHg point at which sounds muffle should be
taken as diastolic BP.
• Slowly decrease pressure at same rate for lOmmHg to ensure no further sounds are heard, then rapidly deflate the cuff and
remove. After 1minute, repeat procedure in same arm.
Recording: average the two readings and report the final averaged BP as systolic BP over diastolic BP: repeat procedure
with opposite arm
Significant Signs
1. Orthostatic Hypotension: decrease in systolic BP by 20mmHg or more within 2 minutes of changing from recumbent to
standing position; indicates decreased blood volume, vascular tone or venous return, or abnormal BP reflexes (autonomic
neuropathy/anti- hypertensive meds)
2. Widened Pulse Pressure: pulse pressure (systolic BP - diastolic BP) > 80mmHg; indicates increased systolic pressure and/or
decreased diastolic pressure (i.e., aortic regurgitation, vasodilatory state, or hyperthyroidism)
3. Narrowed Pulse Pressure: pulse pressure < 25 mmHg, indicates decreased stroke volume or decreased ventricular contraction
rate ( i.e., cardiac tamponade or other low output )
4. Pulsus Paradoxus: systolic BP disappears on inhalation until much lower BP reached. Pressure when Korotkoff sounds first
audible on exhalation - pressure when Korotkoff sounds audible throughout respiration > lOmmHg ( i.e., increased work of
breathing: classic for cardiac tamponade > pericardial constriction)
Basics
03 Introduce yourself, ask for permission to perform PE, wash hands/perform hand hygiene
.in
y E
03 .
ABCs, VS (BP, HR. RR Temp. Sa 02), IV, monitors
>X
-C LU
CL Cranial Nerve Mnemonics
I III IV V VI VII VIII IX X XI XII
Olfactory Optic Oculomotor Trochlear Trigeminal Abducens Facial Vcstibulococh. Glossopharyngeal Vagus Spinal acc. Hypoglossal
Oh Oh Oh To Touch And Feel Very Good Velvet Such Heaven
Sensory Sensory Motor Motor Both Motor Both Sensory Both Both Motor Motor
Some Say Marry Money But My Brother Says Big Brains Matter More
PHYSICAL
CN I (olfactory, sensory only - smell)
•Smell test with one nostril closed (use cloves, peppermint oil, or coffee beans); prompt patient to name odor
•Abnormal unilaterally: brain lesion at olfactory bulb/tract (rare), deviated septum, blocked nasal passage
• Abnormal bilaterally: rhinitis, cribriform plate damage after head injury, Alzheimer 's and Parkinson’s
CN II (optic, sensory only - vision)
• Visual acuity (use best corrected, Snellen eye chart, ideally placed 6m/ 20 ft away )
• Visual fields ( 4 quadrants, arm' s length away ) tested by confrontation: finger movements or light stimulus
> Lesion anterior to optic chiasm - ipsilateral monocular visual loss
> Lesion at optic chiasm - bitemporal hemianopsia
> Lesion posterior to chiasm - homonymous hemianopsia (contralateral)
• Fundoscopy
• Color test (optic neuritis can have red desaturation)
.
• Motor (Note: LMN lesion (e.g , Bell’s palsy ) will affect forehead muscles, UMN is forehead sparing):
> Raise eyebrows ( frontalis)
> Close eyes tight (orbicularis oculi)
> Show teeth ( buccinator )
> Puff cheeks out forcefully (orbicularis oris)
> Tense neck muscles (platysma)
CN VI 11 (vestibulocochlear, sensory only -
hearing/balance):
-
• Auditory acuity (whispered speech test ) mask other ear by moving tragus
• If abnormality detected or patient complains of a specific ear, can elucidate further with Rinne ± Weber
• Rinne test ( tuning fork on mastoid process, when patient no longer hears sound, place fork close to ear )
• Normal = AC > BC
• CHL = BC > AC
• SNHL = AC > BC, both conduction decreased
• Weber test ( tuning fork on forehead midline)
• Normal = Left and right hear equally
• Sound localized to one ear (ipsilateral = CHL or contralateral = SNHL )
CN IX/ X ( glossopharyngeal: sensory -
posterior 1/ 3 taste, motor - palate elevation/Vagus: motor and sensory
swallowing/phonation, PS innervation to viscera)
•Motor:
> Patient says "Ah" - uvula deviates away from lesion, palate falls toward lesion
> Patient drinks water to assess swallowing
> Patient says “ Ka” and "Go" sounds to assess palatal speech
• Sensory:
> Taste to posterior 1/ 3 of tongue
• Reflexes:
> Gag - absence can be normal
CN XI ( spinal accessory: motor only - SCM /trapezius)
Motor:
•
> Shrug shoulders: scapular elevation ( trapezius)
> Turn head side to side ( SCM), repeat with resistance ( SCM helps turn head to opposite side)
CN XII (hypoglossal: motor only - tongue mm)
• Inspect:
> Tongue - fasciculations, atrophy, midline shift
• Motor:
> Stick out tongue (keep stationary) - tongue deviates toward side of lesion ( if facial weakness, watch tongue protrusion in
relation to front teeth)
> Patient pushed tongue to cheek
. . . . .
> If speech problems, have patient say " Ma Ma, Ma” (CNVII) "Ka Ka Ka” (CNIX / X ), “ La, La La" (CNXII)
80
DIABETIC FOOT EXAM
.
Current Editors: Arabesque Parker MD, Stephanie Mullin MD Laurie Mereu MD FRCPC
INSPECTION
ro Shoes
.ty/l -
E
CD
• Is there ample room for the toes?
>X • Are there arch supports and a cushioned sole?
Q
_
JZ LU
Skin
• Is the inside clear of stones and sharps?
• Hammertoes
• Flat feet
• Charcot foot: bony deformities of the foot secondary to
neuropathy and subsequent bone weakening
81 Edmonton M,
Current Editor: Grace Wong MD
Basics
TJ
• Introduce yourself and ask for permission to perform physical examination, wash hands/perform hand hygiene $3
Qj CO
. . . . .
ABCs VS ( BP. HR. RR, Temp Sa 02) IV monitors 3n
PHYSICAL
03
.y E
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General Approach
• Explain purpose and process of exam. Obtain consent and wash hands before initiating exam.
>X
JC LU Inspection
CL
• Deformities/swelling around orbit
• Eyelid symmetry and ptosis
• Ocular symmetry
• Sclera colour
• Conjunctiva
• Pupils ( size, shape, symmetry )
Visual Acuity
• Use a Snellen eye chart ( 20 feet away ) and test each eye separately
> Pinhole testing can determine if any deficits are refrative in nature
Colour Vision
• Assess each eye separately using Ishihara charts
Visual Fields
• With the patient sitting about one meter away and facing you, have them cover one eye. Cover your own eye (mirroring patient )
to compare your visual field with theirs. First determine if they see your entire face and it is not distorted (the inability to see
entire face suggests central visual field loss)
• Assess the size of the patient ' s blind spot relative to your own with a brightly -colored pen ( an enlarged blind spot suggests a
swollen optic disk )
• Assess peripheral vision relative to your own by bringing he pen from the periphery into view for all four quadrants
• Repeat testing on the other eye. Counting fingers in all four quadrants may also be done.
Pupil Reflexes
• Direct pupil reflex (sluggish or absent constriction suggests optic nerve/brainstem damage, drugs)
• Consensual pupil reflex
• Swinging light test ( assesses for relative afferent pupillary defect ( RAPD) )
• Accommodation reflex
Extraocular Eye Movements
• Have the patient follow your fingers or the tip of a pen without moving their head, and check for movement restictions of
nystagmus while moving in an H shape
• Ask patient to report any opthalmoplegia or diplopia ( if diplopia or other neurological symptoms reported perform a full cranial
nerve exam (refer to page 79)
Special Tests
• Opthalmoscopy: Darken room and administer short - acting mydriatic drops
> Observe cornea and conjunctival epithelium for damage and white opacities
> Assess red reflex (missing suggests cataracts in adults and retinoblastoma or detached retina in children)
> Assess optic disk (colour, margin, and cupping)
> Assess retinal vessels (hemorrhage, neovascularization, wool spots, AV nipping)
.
> Have patient look directly at light and assess macula (cherry red spot , drusen hard exudate)
PHYSICAL
D
"
External Exam
• Assess sexual maturity ( Tanner staging)
• Inspect: mons pubis, labia majora /minora, clitoris, urethral meatus, vaginal introitus, perineal and perianal regions
• Note: inflammation, lesions ( including nevi, ulcers, pustules, warts, rashes), signs of infection, swelling, tenderness,
erythema, atrophic skin changes or discoloration, and signs of trauma ( bruising, lacerations)
Internal Exam
• .
Lubricate and gently insert speculum at a downward angle (ensure proper size to not cause discomfort ) Insert the speculum to
a depth of 4cm. Open the speculum blades and identify the cervix.
• Note: a small amount of water - based lubricant does not affect Pap smear results
• Examine vagina /vaginal walls, cervix, uterus, ovaries, pelvic muscle strength ( any tenderness), and rectovaginal wall
• Check cervix location, color, surface mucosa, cervical os, and fix speculum in place
• Note: ulcers, lesions, masses, dysplasia, bleeding or discharge
• Pap smear (see Pap Test ) and collection of swabs ( if indicated)
• Remove speculum: slowly close the speculum while removing ( avoid pinching) and assess the support of the vaginal wall (note
any cystocele or prolapse)
Bimanual Exam
• Lubricate index and middle finger and gently insert fingers (only insert index if there is pain or never had vaginal delivery)
> Note: cervical motion tenderness or masses of vaginal wall
• Palpate the cervix: shape, mobility, tenderness, regularity
• Palpate the uterus: using other hand palpate umbilicus and move down to pubis, press into abdomen, and elevate cervix
anteriorly, pushing the uterus between both hands
» Note: masses, nodules, shape, size and mobility, identify any tenderness: assess retroversion/anteversion
• Palpate ovaries/adnexa: place hand on the lower quadrant and the corresponding lateral fornix
> Feel for size, shape, consistency, mobility, and tenderness; repeat for both ovaries
Rectovaginal Exam
• Perform if indicated: to palpate retroverted
uterus, screen for colorectal cancer in women
50 years or older, or assess pelvic pathology Ovary H
• Withdraw middle finger, tell patient, verify
consent
Fallopian tube — Rectum
• Introduce middle finger into rectum to assess Uterus
posterior vaginal wall and check for colorectal
Cervix
masses Urinary bladder
Urethra
Clitoris
11 Vagina
RANGE OF MOTION i
• Assess active ROM for all joints in the hand: assess passive ROM for any abnormal movement detected
• Quick screen: ask patient to make a fist then straighten fingers: visualize dorsal/volar surfaces looking for rotation, scissoring,
decreased /abnormal flexion/extension; assess for pain against resisted flexion/extension; also adduct and abduct fingers
• Determine ROM isolating each tendon
Ulnar Finger tip of little finger ( D 5) Abduction of index finger - First Dorsal
Flexion of DIP on little finger ( FDP)
Interosseous (FDI)
With palm facing down on table, extend thumb toward None
Radial Dorsal first webspace (Dl)
ceiling - Extensor Pollicus Longus (EPL )
Tinel’ssign Carpel Tunnel syndrome Tap over the median nerve in the wrist. Paresthesia radiating distally into the hand (in the
distribution of median nerve) is a positive test.
Finkelstein test DeQuervain’s Patient fully flexes their thumb into the palm. The wrist is then actively forced towards the ulna.
tenosynovitis Sudden severe pain is a positive test.
85 iton Manual
HEENT EXAM
Current Editor: Lundy McKibbin
PHYSICAL
Head “0
• Inspection m or
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(f)
> Head: symmetry, size, shape, masses, and involuntary movements QJ
03
_ PHYSICAL
Inspection
.y/>
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E
03
• With patient standing, examine the alignment of the lower extremity
• Inspect from front and from behind for pelvic tilting, rotational deformity, masses, scars, lesions and atrophy, joint swelling,
>X
-C LU
CL
redness
• Measure thigh circumference to detect muscle atrophy ( 10 cm above the patella)
> Measure leg length, both true and apparent
- True leg length is measured from the ipsilateral iliac crest or anterior superior iliac spine (ASIS) to the medial malleolus
- Apparent leg length is measured from the umbilicus or xiphisternum to the medial malleolus
• Examine gait : observe smoothness, time in stance and swing phase, toe - off, heel strike, and step /stride length. Observe for
abnormal gait patterns such as:
> Antalgic gait: a limp with less time spent in stance phase on affected limb: usually with short, quick steps ( indicates pain in hip,
pelvis, or lower back )
> Pelvic wink: greater than 40 degrees of rotation in the axial plane toward the affected hip during terminal extension ( indicates a
hip flexion contracture in the setting of lumbar lordosis or forward- stooped posture)
> Trendelenburg gait: a lurching of the trunk toward the affected side, to prevent pelvic sagging (indicates abductor pathology)
> Waddling gait: bilateral Trendelenburg
> Excessive pelvic internal rotation with decreased external rotation signifies femoral anteversion
> Circumduction gait : circumduction or vaulting of leg to clear it off the floor (indicates leg length discrepancy)
Palpation
• Palpate joint for warmth, tenderness, crepitus
• Palpate anterior structures: iliac crest, greater trochanter, trochanteric bursa, Anterior Superior Iliac Spine ( ASIS), inguinal
ligament, femoral triangle, symphysis pubis, hip flexors, adductor /abductor mm
• Palpate posterior structures: iliac crest, posterior superior iliac spine, ischial tuberosity, greater trochanter, sacroiliac,
lumbosacral, sacrococcygeal joints
Movement and strength
• Observe patient ’s passive flexion, extension, abduction, adduction, and external and internal rotation of the hip
• Normal ROM: flexion 120° with knee flexed: or 90° with knee extended, extension 10 - 20 , abduction 40 , adduction 25 , internal
° ° °
rotation 40°, external rotation 45° 90
> With the patient in supine position, test resisted hip flexion, extension, adduction, and abduction
» Observe for movements that cause pain or demonstrate weakness
Special tests
.
• Perform the Trendelenburg test: Keeping your index fingers on each ASIS ask the patient to stand on one leg. A positive
Trendelenburg sign is a pelvic drop of more than 2 cm on the unsupported side, indicating abductor pathology on the ipsilateral
(stance leg) side.
• Conduct the FABER test to assess for intra - articular hip pathology
> FABER: Flexion, ABduction, External Rotation of the leg
> Posterior pain indicates SI joint involvement, lateral pain indicates lateral impingement, and anterior /groin pain indicates
iliopsoas pathology
• Log Roll test: With the patient supine, passively rotate the leg (internally and externally) while stabilizing the knee and ankle .
Ensure that the rotation occurs at the level of the hip. A positive test reproduces pain in anterior or lateral hip.
• Anterior impingement test: With the patient in the supine position, pain with forced flexion, adduction, and internal rotation is a
positive test and the most sensitive for subtle intra - articular hip pathology ( e.g., femoroacetabular impingement )
• Posterior impingement test: In the supine position, pain with extension and external rotation is a positive test and indicates
.
posterior labral pathology, excessive acetabular anteversion and /or degenerative changes
• To assess for radiculopathy, perform the straight leg raise and femoral stretch tests
> The straight leg raise is positive if the patient experiences unilateral leg pain at 60° or less of hip flexion, and is indicative of L 5 -
S1nerve root compression
> Femoral stretch test: With the patient prone, flex the knee to 90 degrees and extend the hip. Radicular pain is suggestive of
L2-4 nerve root compression.
INSPECTION
• Location - The internal jugular vein runs deep to the sternocleidomastoid (SCM)
muscle within the carotid sheath. It may be visible anterior or posterior to the SCM 9cm
or between its two heads near the sternoclavicular junction. It provides a direct
5cm
measurement of right atrial pressure ( RAP).
• Distinguish from carotid - Carotid artery (CA) is adjacent and medial to IJV. The
most reliable way to distinguish the carotid and IJV is to palpate the left carotid
with your thumb while observing the right neck for the JVP; the carotid pulse
and JVP wave do not occur simultaneously. It is important to note that other
commonly taught differentiating features are unreliable with abnormal cardiac
physiology, e.g., biphasic waveform may be lost in atrial fibrillation due to absent
a - wave and x - descent.
• Describe waveform - Observe for biphasic waveform. For a normal patient -
.
a - wave followed by the palpable carotid pulse, and then the v-wave; under normal conditions, the c - wave cannot be seen.
.
• If one cannot find the top of the JVP it may be either low or high:
.
> If JVP is too low to see lower the head of the bed to visualize
> If JVP is too high to see, raise the head of the bed to visualize
• If you cannot detect the right IJV after changing the bed angle, it is possible that it is occluded from prior intervention. Before
reporting the JVP as not seen, be sure to inspect the left IJV using the method above.
MEASUREMENT
• Locate the sternal angle of Louis continuous with the 2nd rib and below the manubrium
-
• Place one ruler vertically at the sternal angle (angle of Louis) and the other horizontally at the top of the JVP. Measure the
maximum height of the JVP. A JVP 0- 4 cm above the sternal angle is considered normal.
• Add 5 cm to the height of the JVP to give right atrial pressure (this reflects the estimated height of the sternal angle above the
.
right atrium), e g., if JVP height above sternal angle is 4 cm, RAP = 4 cm + 5 cm = 9 cm above right atrium.
• Note that calculating the height of the JVP above the right atrium is of academic interest only; in common practice JVP is charted .
as the number of cm above the sternal angle
SPECIAL TESTS
Hepatojugular Reflux ( Abdominojugular Test)
• Ensure that the patient 's abdomen is non -tender - performing this maneuver in a patient with a tender abdomen will result in
Valsalva and an inaccurate result
• Press down with approximately 35 mmHg of pressure over the RUQ or mid- abdomen (either location is acceptable). You can
place a semi-inflated blood pressure cuff over the abdomen and press down on it to ensure you are applying sufficient pressure.
Instruct the patient to breathe normally through the mouth.
.
• While observing the JVP maintain pressure for at least 10 secs
• Normal response - transient rise in JVP followed by a decrease to baseline
• Abnormal response - sustained rise in JVP > 3 cm over entire 10 second period; correlates with an elevated left atrial pressure
• Note that this maneuver is only useful if the JVP is not elevated at rest
JVP Waveform (V
Waveform Heart Action Cartoid pulse
a
A "a wave" Atrial contraction
X "x descent" Atrial relaxation v
x\ c
C “C WAVE” Tricuspid bulges Interna! cartoid artery
(right ventricular External cartoid artery
contraction) x' y
Interna! Jugular vein
X‘ “ x descent” Descent of the External Jugular vein
base of the heart Common cartoid artery
V “v wave" Atrial filling Internal jugular vein Sternocleidomastoid
SI S2 muscle
Y “y descent ” Tricuspid opening/
atrial emptying +
Edmonton Manual of Common Clinical Scenarios 88
KNEE EXAM
Current Editor: Ameet Singh MD
.y E
V OJ
) Inspection: (SEADS)
Lateral collateral
ligaments
>X
C UJ • Gait: normal gait is smooth and rhythmic, rule out pain or instability
.
0 • Swelling: in medial/lateral hollow around patella
Lateral meniscus ^ Medial meniscus
• Erythema
• Atrophy: quadriceps, measured ~10 cm above patella
• Deformity: alignment ( valgus /varus /recurvatum), symmetry - Medial collateral
ligaments
• Skin: warmth, scars, lesions, wounds, discoloration
• Request knee flexion, measure angle with goniometer and knees as well as structural integrity
distance of heel from buttocks
Passive Flexion • Apply gentle pressure to max flex without pain • Evaluates structural integrity: normal 135° -
Active Extension • Patient sits on the edge of examination table with knee flexed • Evaluates quadriceps muscular control and
• Request knee extension and measure structural integrity
Passive Extension • Apply gentle pressure to max extend without pain • Evaluates structural integrity: normal -0 - 5°
Jo nt Stability (Grade I laxity = 3- 5 mm translation, Grade II = 5- 10 mm, Grade 111 = > 10 mm)
Test Procedure Evaluation/Results
Integrity of MCL: • Hold patient ' s ankle with one hand, other hand on lateral • Asymmetrical opening medially = laxity
Medial stability in aspect of the knee. Force is applied from the ankle with • Laxity often due to ligament injury on medial side
extension the hand at the knee as a fulcrum (valgus stress). and/or femoral - tibial wear (pseudolaxity)
(Valgus stress) • Test in full extension and 30° flexion
Integrity of LCL: • Hold patient ’s heel with one hand, while other hand • Asymmetrical opening laterally = laxity
Lateral stability in holds medial side of the knee and acts as a fulcrum • Laxity often due to lateral ligament injury and/or
extension ( varus stress) femoral- tibial wear ( pseudolaxity)
( Varus stress) • Test in full extension and 30° flexion
Integrity of ACL:
Anterior stability
• Patient supine, knee flexed -
30°, heel resting on stretcher • Softendpoint or 4 anterior translation indicative
• Secure thigh with one hand and apply anteriorly directed of tear
(Lachman test ) force to proximal calf from posterior
Integrity of ACL:
Anterior Stability on table
.90°, feet flat
• Patient supine, flex hips to 45° knees to • Ifthe tibia can be moved anteriorly without
abrupt stop, referred to as discrete end point,
( Anterior drawer • Cup hands around knee with thumbs on medial and lateral this is considered a positive anterior drawer test
test ) joint line
• Pull the tibia forward and observe if it slides forward from
under the femur
• Always compare with other knee
Integrity of PCL: • Patient supine, knee 70- 90° flexion • Loss of medial tibial step -off or 4 posterior
Posterior stability • Palpate medial tibial step - off translation indicates injury to PCL
( Posterior drawer proximal
• Apply posteriorly directed force on tibia
test)
Special Tests
Test Clinical Association Procedure Results/Evaluation
McMurray Meniscal pathology Patient supine, knee fully flexed passively + ve test includes palpable or auditory
then passive rotatory pressure while flexing/ click with tenderness along joint line
extending knee and palpating medial /lateral
joint lines
Patellofemoral Chondromalacia Patient supine, push patella into trochlear Irregular movement/crepitation =
Grind patella .
osteoarthritis
groove, patient to tighten quads patellofemoral articular pathology
Apley’s Grind Meniscus pathology Patient prone with knee flexed to 90° followed +ve test indicated by pain
by axial loading and rotation
Apprehension Test Dislocating patella Patient supine with knee flexed 20- 30°. Apply + ve if pt becomes apprehensive with
lateral force to medial edge of patella ( and vice feeling impending dislocation
versa).
89 Edmonton Manual of ( ommon Clinical Seen.
*
LYMPHADENOPATHY AND SPLEEN EXAM
Current Editor: Lance Frieburger MD
DIFFERENTIAL DIAGNOSIS
• Diagnostic criteria
> Lymphadenopathy: generalized or localized palpable lymph nodes > 1cm in size “U
.
> Splenomegaly: palpable spleen (not normally palpable) + Castell's sign/Traube’s space tests m =r
x) <
O /<>
PHYSICAL 3 n
QL)
Examine the spleen: Stand to the right of supine patient, begin palpating abdomen in the RLQ with right hand pressed
firmly flat and then roll hand so that angled pads of fingers press down firmly on abdomen
Differential Diagnosis Based on Physical Findings
Finding Differential Diagnosis
LOCALIZED • . .
Broad and includes infection in tissues drained by lymph node group, lymphoma TB metastatic
LYMPHADENOPATHY cancer /neoplasia, and EBV
GENERALIZED • Systemic . . . . .
infections ( typhoid fever HIV EBV syphilis, etc.), medications SLE, sarcoidosis 2° to liver
disease: many other causes
LYMPHADENOPATHY
SPLENOMEGALY ONLY • Hematologic disorders (ITP, AIHA ). infective endocarditis, or chronic inflammation
03 _
M E General Approach
to 03 • Explain process and purpose of exam ( especially if nervous or first exam), offer chaperone, and check patient comfort
> X
throughout exam. Position patient so initially they are lying supine and then standing up at the end of the exam. The patient
-
C LU
CL should be exposed from the waist down.
Inspection
• Penis:
> Tanner staging: pubic hair pattern, testicular size
> Prepuce ( foreskin): phimosis, paraphimosis, balanoposthitis
> Gians and urethral meatus:
- Presence of chancres, sores, warts, ulcerative/exophytic lesions, growths
- Hypospadias, epispadias, or meatal stenosis
- Discharge (usually due to gonorrhea)
Commonly Seen Genital Ulcers
Condition Number of Ulcers Detected Pain Lymphadenopathy
Syphilis .
Usually one multiple possible No Bilateral
Chancroid Multiple, usually tender Occasionally Bilateral
Granuloma inguinale Usually one No No
Herpes simplex Multiple (initially vesicular) Yes No
Cancer Usually single/one Not initially Not initially develops later
.
> Varicocele ( " bag of worms"): have patient stand and lay down to determine grade (Grade 1: palpable only with valsalva Grade 2:
.
non-visible on inspection but palpable upon standing Grade 3: visible with superficial inspection)
Hernias
• Ask patient to valsalva and compare the two sides (presence of a bulge - possibly inguinal/femoral hernias)
• Finger into the inguinal ring and ask pt to cough (mass felt at the fingertips - possible inguinal indirect hernia)
Lymph Nodes
• Palpate inguinal lymph nodes ( signs of local infection)
• Palpate supraclavicular lymph nodes ( testicular cancer metastases )
General Approach
Explain purpose and process of exam to obtain informed consent. Note the patient 's appearance and level of consciousness. Is there "O
signs of muscle rigidity, tremors, or dystonia? Be aware of the signs of meningeal irritation (nuchal rigidity, photophobia, headache). m zr
x<
JD />
(
Scores of 20- 29 indicate minor cognitive impairment, and scores under 20 indicate more severe cognitive impairment
Cranial Nerve Exam (refer to page 79)
While performing the exam observe for asymmetries and general function
Motor Exam
There are five components to the motor exam : inspection, tone, power, reflexes, and special tests
Inspection
• Bulk (or muscle wasting), involuntary movements - tremors, tics, fasciculations
Tone
• Assess for spasticity and rigidity, in both upper and lower extremities
• Note: Spasticity is a velocity - dependent increase in tone, while rigidity is a velocity -independent increase in tone
• Upper extremities - With patient relaxed and either supine or sitting upright, support their elbow while moving the forearm
.
back and forth to assess for rigidity. When arm is flexed, quickly extend arm fully to assess for spasticity Repeat on opposite
side.
• Lower extremities - With the patient supine with legs relaxed and extended, assess for spasticity by rapidly flexing the knee
upwards. Repeat on opposite side .
Edmonton Manual of Common Clinical Scenarios 92
Reflexes
Deep Tendon Reflexes (DTR ) Grading Reflexes
03
O £ Reflex Root Grade Observed Reflex
cn 03
> X Biceps Tendon C 5/6 0 Nil
-
C LU
CL Brachioradialis C 5/6 1 Requires reinforcement
Triceps Tendon C 7/8 2 Normal
Prepatellar Tendon L 3/ 4 3 Spreads to adjacent muscle groups
Achilles Tendon Sl/ 2 4 Sustained clonus ( > 3 beats)
Hoffman’s Sign Corticospinal
Babinski'sSign Corticospinal ( L 5 /S1)
Sensory
Dermatome Landmarks
Root Anatomical Location Root Anatomical Location
C2 Occiput T10 Umbilicus
C3 Neck T12 Pubic bone
C4 Lower neck/supraclavicular LI Inguinal ligament
C5 Lateral upper arm L2/ L3 Thigh
C6 Thumb L4 Knee, medial foreleg
C7 Index/ long finger L5 Big toe, dorsum of foot
C8 Little finger SI Heel, lateral foot
T4 Nipples S 2/ 3 Genitals
T5 Inframammary fold S4/5 Perineum
T6/7 Xyphoid process S5 Anus
Motor System
ACTION MUSCLES NERVES ROOTS
Upper Extremity
Arm abduction Deltoids Axillary C 5 /C6
Elbow flexion Biceps Musculocutaneous C 5/C 6
Elbow flexion BR Radial C 5 /C6
Elbow extension Triceps Radial C 6/7/ 8
Wrist flexion FCR Median C6/7
Wrist extension ECRB Radial C 5 /C6
Wrist ulnar deviation FCU Ulnar C 7/ 8/T1
Wrist radial deviation ECRL Radial C 5 /C6
Flex PIPJ D2/ 3/4/ 5 FDS Median C 7/C8/T1
Flex PIPJ D2/3 FDP D2/3 Median C7/C8
Flex PIPJ D4/ 5 FDP D4/ 5 Ulnar C7/C8
Ext D2/ 3/4/ 5 . .
ED El EDM Radial ( PIO) C7/C8
D2/ 3/4/ 5 adduction Palmar 10 Ulnar C8/T1
D2/ 3/4/ 5 abduction Dorsal IO ADM. Ulnar C8/T1
D1opposition OP Median C8/T1
D1adduction/ flexion MCPJ AdP Ulnar C8/T1
D1abduction/extension MCPJ AbPL Radial ( PIO) C7/C8
D1abduction (palmar ) AbPB Median C8/T1
Lower Extremity
Hip flexion IP Femoral Ll/ 2/ 3 roots. Ll/ 2/3/4
Knee flexion Hamstrings ( ST SM . .
Sciatic L 5 /S1/ 2
BF)
Knee extension Quads Femoral L 2/ 3 /4
Leg adduction . .
OE AdL AdM AdB . .
Obturator L 2/ 3/4
Gracilis
Leg abduction .
Gmed Gmin TFL . Superior gluteal L4/ 5 / S1
Footdorsiflex TA Deep peroneal L4/ 5
Foot plantarflex .
Gastrocs Soleus Tibial Sl/ 2
Foot inversion TP Tibial nerve L4/ 5
Foot eversion PL PB. Superficial peroneal L 5 / S1
Toe dorsiflex .
EHL EDL Deep peroneal L 5 / S1
Toe plantarflex . .
FHL FDL FDB Tibial (m plantar nn) S1/S 2
.
• Lower extremities - suggested reflexes: patellar, ankle Babinski
• Clonus - if reflexes are hyperactive, test for ankle clonus. With the patient 's knee in a partially flexed position, briskly dorsiflex
the foot, maintaining the foot in flexion. Absence of rhythmic oscillations between plantar flexion and dorsiflexion is normal.
Sensory Exam
.
Perform a complete primary modality sensory exam on specific dermatome( s) ensuring they are tested on both sides
• Light touch - patient 's eyes closed, touch gently with cotton wasp or tissue. Ask patient if they feel sensation and check if it ’s the
equivalent bilaterally.
• Pain - same as above but using a sharp point or tissue paper. Ask if patient can differentiate between the two and check if it ’s
equivalent bilaterally.
-
• Temperature same as above but using a tissue paper versus cold tuning fork. Ask them if it feels warm or cold. Check to see if it's the
same on both sides.
- .
• Vibration sense using 128 Hz tuning fork, apply it to patient 's index finger and large toe Ask the patient to tell you when the
vibrations are experienced and when the vibration is no longer felt. Note the time it takes for vibrations to cease being felt.
• Position sense (proprioception) - select a joint in either the fingers or toes. With patient ’s eyes closed, use one hand to stabilize joint
and with the other move the distal segment up or down and ask patient to tell you which direction it has moved.
PHYSICAL
• Chest wall deformities ( pectus excavatum or carinatum), surgical scars (sternotomy) T)
m zr
• Visible heaves or lifts and visible apical impulse x) <
Palpation Q /<>
3n
0)
• Thrills: palpable murmurs - with patient supine, palpate with finger pads over each valve location
• Lifts/heaves: RV overload /hypertrophy - rest heel of hand just left of the sternum and feel for lift
• Other impulses: subxyphoid impulse - palpate with finger pads below xyphoid process. Impulse may arise from RV (caudally
directed, suggests RV overload or hypertrophy), or aorta (anteriorly directed, normal in thin patients, may suggest aortic
aneurysm).
• Apical impulse: examine for apex with patient in left lateral decubitus position, or at end expiration. Palpate with finger pads.
Describe location, amplitude, size, and duration. A displaced apex, enlarged diameter, or sustained duration suggest LVH or
cardiac dilatation.
> Normal location - 5 th intercostal space at or just medial to mid - clavicular line
> Normal amplitude - gentle tap
> Normal size - < 2.5 cm, or about the size of a nickel
> Normal duration - about 2/ 3 of duration of systole
• Point of maximal impulse ( PMI): Determine which palpable impulse has the greatest amplitude. Should be the apex in a normal
patient, e.g., a PMI at left parasternal border suggests RV hypertrophy.
Auscultation
• Diaphragm
> While palpating the carotid pulse, auscultate over each valve area with the diaphragm
> Assess the presence, volume, and character of SI and S2
> Assess for any extra sounds (i.e., clicks, murmurs)
> If a murmur is noted, assess for location, timing in systole or diastole, intensity, character, and radiation
> Auscultate carotids for bruits and for radiation of the murmur of aortic stenosis
> Auscultate the axillae for radiation of the murmur of mitral regurgitation
• Bell
> While palpating the carotid pulse, auscultate over each valve area with the bell
> If present, describe the location and volume of S3 or S4 heart sounds
> S3 and S4 are low pitched sounds and are thus better heard with the bell
• Maneuvers
> To help differentiate certain murmurs, maneuvers can be performed while auscultating
> Inspiration - Increases most right - sided murmurs
> Expiration - Increases most left - sided murmurs
> Valsalva - Increases hypertrophic cardiomyopathy, increases mitral valve prolapse
> Standing - Increases hypertrophic cardiomyopathy, increases mitral valve prolapse, decreases most other murmurs
> Squatting - Increases aortic stenosis, decreases hypertrophic obstructive cardiomyopathy, decreases mitral valve prolapse
> Hand grip - Increases mitral regurgitation, increases aortic regurgitation, increases ventricular septal defect
Anatomical Location to Listen for Each Heart Valve Murmur Grade and Intensity
z Variably Split S 2 Changes in intrathoracic pressures during the respiratory cycle causes a softer pulmonary valve
closure sound ( P 2) to occur after the louder aortic valve closure ( A 2)
Loud SI Mild to moderate mitral stenosis, tachycardia or high cardiac output state, shortened PR interval
Soft SI . . .
Severe MS severe AS MR prolonged PR interval
Loud S2 Pulmonary hypertension ( loud P 2) or systemic hypertension ( loud A 2) a
0)
O
Widely split S 2 RBBB, pulmonary stenosis ( PS), pulmonary hypertension ir
2
Fixed split S 2 .
Atrial septal defect RV failure OQ
5
Aortic Stenosis ( AS) Mid systolic crescendo -decrescendo murmur at RUSB may .
radiate to clavicle and carotids
TO
E
Aortic Regurgitation
( AR )
.
Early diastolic murmur at RUSB may radiate to apex
o
r
JO Mitral Regurgitation Holosystolic murmur at apex, may radiate to axilla
< ( MR )
Mitral Stenosis ( MS) Low pitched mid - diastolic murmur at apex, usually no radiation,
may have early - diastolic opening snap
S3 Low pitched, early diastolic sound, usually heard at apex ( MON-TRE- al)
Abnormal in most adults; suggests heart failure and/or volume overload
May be normal in some children and pregnant women co
n
S4 Low pitched, late diastolic sound, usually heard at apex ( tor - ON- to)
Caused by atrial contraction into a non- compliant ventricle
Suggests ventricular hypertrophy
B .¥
Aortic stenosis
C
— iV"
Mitral regurgitation
Aortic regurgitation
E rf“ 1
*
•
i i Mitral stenosis i
Percussion
• Have patient cross arms in front of chest, then percuss over lung fields, noting flatness, dullness, resonance, hyperresonance
• Estimate diaphragmatic excursion by percussing lower lung border in expiration then inspiration (normal is 3 - 5 cm)
Auscultation
• Listen for at least one whole breath cycle in each location; inspiration should be 1/3 of expiration, characterize if prolonged
• Breath sounds: equal bilaterally? characterize as vesicular, bronchovesicular, or bronchial breath sounds
• Adventitious sounds ( wheezes, coarse /fine/ velcro crackles, pleural friction rub, mediastinal crunch)
• Special exams ( provide further support to suspected consolidation)
> Egophony ( when patient says "eee”, sounds like " aaah" on auscultation)
> Whispering pectoriloquy ( whisper "1- 2- 3 ”) sounds more clearly over area of consolidation
PHYSICAL
3E The shoulder is made up of three joints: the sternoclavicular, acromioclavicular ( AC), and the glenohumeral joints.
Always state that you will complete your exam by assessment of the joint above and below (cervical spine, elbow)
t/> OJ
>x
-CLC LU
Taw map>
Synovial membrane
Fibrous membrane •
N Hoad of humerus
LatowiTua darn Humerus
(nwr it orpn)
*
S ntt
*
Tnoac bract, later *! »ai
* *
MgHaaiBg
• Swelling over joints
• Erythema, bruising
• Atrophy of muscles of the pectoralis, deltoid, supraspinatus, infraspinatus, trapezius
• Step deformity of the clavicle or acromioclavicular joint
• Asymmetry of the shoulders
• Winging of the scapula (occurs due to injury to the long thoracic nerve)
PALPATION
• Palpate each of the three joints for warmth and/or tenderness
• Palpate over trapezius, supraspinatus, infraspinatus, deltoid, triceps, biceps muscles for tenderness
• Palpate for crepitus as the patient moves their shoulder
SPECIAL TESTS
SupraspinatusTear: TJ
m zr
• Drop arm test: watch for sudden dropping of the arm as the patient brings their arms back down from position of x<
O) />
(
abduction; positive test indicates supraspinatus tear 3 n
£U
Subacromial Impingement Syndrome Testing:
• Painful Arc Test: pain with abduction to 120o
• Neer ' s Test: pain with passive movement by the examiner of the patient 's arm upwards above the head
• Hawkins - Kennedy Test: shoulder and elbow at 90o; rotate the forearm clockwise while stabilizing the shoulder; pain
indicates a positive test
• Empty Can Test: arms held parallel to ground and shoulder internally rotated as if emptying a can with thumbs
downwards; examiner pushes down on arm and patient resists; if there is pain at shoulder this is a positive test
Bicipital Tendonitis:
• Speed ’s Test: extend elbow with arm supinated and bring arm forward 45 o; examiner presses down on forearm while
patient resists; pain at biceps tendon indicates positive test
• Yergason’s Test: arm at side with elbow at 90o; hold wrist and try to pronate the arm while patient tries to supinate;
pain at biceps tendon indicates positive test
AC Joint Abnormality:
• Scarf test : place patient ’s hand on opposite shoulder and push arm into the body; pain at AC joint is positive test
Shoulder Instability:
• Apprehension Test: have patient lie supine; abduct and externally rotate arm to 90o; apply upward pressure against
head of humerus as if you are dislocating it outwards and look at patients face for sign of apprehension/pain
• Relocation Test: Continue from where you left off on apprehension test, but now apply downward pressure to humeral
head as if you are relocating the humeral head
• Anterior Release Sign: Continue from where you left off on the relocation test, and remove the posterior force and
again look for signs of apprehension and pain on patient ’s face
Rotator Cuff Muscles:
• Supraspinatus: Empty can test as above
• Infraspinatus & teres minor: elbows at patient ’s side and 90o, ask patient to resist you as you attempt to push their
forearms in towards body
• Subscapularis: Liftoff test; bring arm behind back with elbow at 90o and palm facing outwards; ask patient to push off
against you, as you press against their palm
PHYSICAL
Inspection
• Patient should be seated, with neck and thyroid easily observable
.toy E
03
• From the front and side (tangential lighting useful)
>X Tip patient ’s head back and inspect region below cricoid cartilage for the thyroid. This makes a thyroid goiter more prominent
> .
-C LU with and without swallowing ( thyroid cartilage, cricoid cartilage, and thyroid gland rise with swallowing then return to
> Inspect
CL
resting position)
• A positive Pemberton' s sign could indicate an obstructive goiter ( facial flushing, distended neck and head superficial veins,
inspiratory stridor upon raising of the patient ’s both arms above his/her head simultaneously)
• General exam: Head and Neck Inspection
> Muscle bulk/symmetry
> Atrophy/hypertrophy
> Discoloration
> Scars
> Swelling/asymmetry
> Deviation from midline
> Exophthalmos
Goiter
>
Palpation
• Note the size, shape, and consistency of the gland ( normal size is 15 mg)
• Check for any nodules or tenderness
• Posterior approach: ask patient to turn their head upwards and towards the side being palpated
> With finger pads of one hand, find the thyroid cartilage and the cricoid cartilage, move interiorly to find the isthmus (usually
overlies the 2nd / 3rd/4 th tracheal rings). The isthmus lies just below the cricoid cartilage.
> Work laterally into the gutter between the trachea and the sternocleidomastoid muscle to feel one thyroid lobe for masses. An
enlargement of a lobe can be assessed (or estimated) if it ’s larger than the distal phalanx of the patient’s thumb.
> Get the patient to swallow and feel for masses ( thyroid should move up): repeat for other lobe
> Repeat the procedure using an anterior approach
Auscultation
• Auscultate for bruits using bell of stethoscope (localized or continuous bruit may
be heard in Graves hyperthyroidism)
Thyroid Eye Exam
.
• Inspect anteriorly for lid lag stare, periorbital edema, upper or lower lid retraction, and conjunctivitis
.
• With patient seated, inspect from above for exophthalmos Graves ophthalmopathy
.
• Assess EOM by having patient follow your finger making a wide " H" in the air paying focus to lid lag and assess for double vision
• Assess convergence by asking patient to follow finger as it is moved closer to the bridge of their nose
• Assess if patient experiences pain during eye movements or visual changes (compressive optic neuropathy )
101 Edmontc
3 FAMILY MEDICINE
Introduction 108
Adult Periodic Health Exam 109
Constipation 111
Cough 113
Diarrhea 115
0) Dyspepsia 117
>c
u Dysuria
Ez -a 119
< Q)
.
Li Erectile Dysfunction 121
2
Fatigue 123
Fever 125
Headache 127
Hypertension 129
Insomnia 131
Lower Back Pain 133
Nausea & Vomiting 135
Obesity 137
Respiratory Tract Infection 139
Sexual & High- Risk Infections 141
Skin, Hair, & Nails 143
Smoking Cessation 145
Sore Throat ( Pharyngitis) 147
Urinary Incontinence 149
Weight Loss 151
Station Contributors 153
References 154
Welcome to the family medicine section! The specialty of family medicine is truly broad and for many
students seems overwhelming. The discipline covers every facet of medicine, over all demographics.
A comprehensive, competent family physician embodies a solid understanding of diagnosis and
treatment of conditions, is skilled in the art of mindful conversation with patients, and is able to
facilitate coordinated care with other health professionals and the health care system.
Demonstrating competence in history - taking and physical examination skills is fundamental in OSCEs.
As always, one must remember to maintain a standardized approach in this regard; going about it in a 2 T1
to 0)
systematic manner helps to avoid memory lapses often seen in OSCE type situations. It is important CL
in family medicine ( and in OSCEs as well) to understand the patient' s perspective ( this includes social n• 3.
mm -
mmm
history, stressors, work /school, lifestyle behaviors, beliefs, etc.). Perhaps the patient has not been
D
to
<
taking the prescribed medications because finances are tight. Perhaps the patient 's migraines are
getting worse because of marital discord. Exploring these aspects of the patient ’s history will not only
earn you check marks on the OSCE marking sheet, they will also heighten the medical interaction with
increased understanding, resulting in an effective management plan and increased patient compliance.
I hope that this book will not only help you succeed in your OSCE preparations but help you in your clinical
practice in the years to come.
OSCE TIPS:
counsel a patient).
• Also, if during that station you are lost, please look at the station task again — it will be in the OSCE
KEY POINTS
• There is no evidence - based approach to the periodic health history and physical exam - both should be tailored to the patient
population and personal preferences of the physician and patient
• Key component of periodic health exam is counselling patients on preventative medicine and healthy living
.
• Screening tests should be considered based on age demographics, and risk factors
HISTORY
ID .
• Age gender, and ethnicity
CC • Any changes in health or health complaints since last visit
CD
> C RED FLAGS • Unintentional weightloss, night sweats, anorexia, mass, bowel/bladder dysfunction, new onset/change in
u headaches, blood in urine/stools
E T3
nj PMHX • Previous medical diagnoses, prior hospitalizations
LL CD
2 PSHX ..
• Previous surgeries (e g , abdominal surgery, CABG, appendectomy, cholecystectomy, hysterectomy)
MEDS • Update records of patient ’s medications including supplements, patient compliance, medication side effects
and modifications if needed
• Immunization status
LiHYSICALEXAM
. . . . .
General: VS ( BP HR, RR Sp02, Temp) Ht Wt BMI Counseling Topics
Note: Age and interval of screening maneuvers may need to be altered based on individual patient 's past medical history and family history.
KEY POINTS
• Constipation - passage of hard stools with straining (stool water < 50mL/day) or a decrease in bowel movement frequency (< 3 x/
week )
• In the absence of secondary causes, constipation is considered functional or due to lack of fiber or changes in diet
• Obstipation - failure to pass flatus or stool
• Must palpate abdomen and consider performing a digital rectal exam ( DRE)
• Intractable constipation refractory to therapy - > intestinal obstruction
DIFFERENTIAL DIAGNOSIS
Q)
>C Primary Secondary
ill2
.
Li
Functional/normal colonic transit
• Chronic idiopathic
Neurologic
• Dementia
Prescription Medication
• Anticholinergics
• Constipation - predominant IBS • Cerebrovascular accident • Opiates
• Multiple sclerosis • Antidepressants
• Parkinson's
HISTORY
ID • Age, gender
• Sense of incomplete emptying ( tenesmus), difficulty emptying bladder (weak stream, nocturia)
• Abdominal pain, bloating, N/V
• Diet: recent changes, dietary fiber intake
RED FLAGS • Change in bowel habit, change in stool caliber, bleeding, wtloss, obstructive symptoms ( severe constipation can
result in fecal impaction and obstipation, which can progress to bowel obstruction)
PMHX • Neuro: Parkinson’s disease .
MS
.
disease Hirschsprung’s disease
• Gl: IBS, diverticular
• Metabolic: Diabetes, hypothyroidism, electrolyte abnormalities (hypercalcemia, hypermagnesia)
• Neoplastic: colorectal cancer, anal cancer, prostate cancer / BPH
• Psych: depression, anxiety
• Collagen/vascular disease: scleroderma, amyloid
• Anatomic abnormality: prolapse, rectocele
PHYSICAL
General Approach
.
• VS: BP HR, RR , Temp, Sp02
ABDO
• Inspect for surgical scars and distention
• Auscultate for bowel sounds ( absence of bowel sounds or high-pitched tinkling indicate obstruction)
• Palpate for rebound tenderness /guarding, masses, hernias
GU
• Inspect rectum for fissures, hemorrhoids, fistulas, or prolapse
• DRE for masses, blood, stool impaction, sphincter tone and stricture 2 -n
NVESTIGATIONS 2
2
O=
Investigations are not typically required for patients who are not suspected to have secondary causes of constipation or who do not
present with red flag Sx
3•
3' <.
fl>
—
Laboratory Investigations
. . . .
• CBC- D electrolytes, glucose Ca Mg, Cr TSH, ± FIT
Radiology/Imaging
• AXR x 3 views (supine, upright, lateral )
• Consider air or water soluble contrast enema (if chronic constipation in setting of any obstruction)
• Consider abdominal CT scan (if intra -abdominal process suspected)
Special Tests (indicated for patients with severe constipation or red flags)
• Colonoscopy, colonic transit studies, defecating proctography, anorectal manometry
L REATMENT
Emergent
• IV fluids (if dehydrated)
• If obstruction suspected, NPO for bowel rest and NG tube to decompress the stomach
.
• If obstruction ruled out consider enema or suppository
Treatment Options
• Lifestyle
> Increase dietary fiber, fluids, exercise
• Medication
> Softener (e.g., Colace)
> Stimulant (e.g., Senokot )
> Osmotic agent (e.g., PEG)
> Enema (e.g., Fleet)
• Medication induced: stop offending agent and watch for any changes
• Surgical: correction of obstruction, volvulus or persistent failure of medical treatment for slow colonic transit
Referrals
• General Surgery if symptoms and signs of obstruction
KEY POINTS
• .
Characterized by duration: acute: < 3 wks, subacute: 3 - 8 wks chronic > 8 wks
• .
Determining etiology of cough is largely dependent on Hx and PE - investigations (CXR. PFTs esophageal pH studies, and /or sinus
radiography ) are performed to confirm a suspected diagnosis
• Must auscultate the chest on PE
DIFFERENTIAL DIAGNOSIS
ACUTE ( < 3 WEEKS) SUBACUTE (3- 8 WEEKS) CHRONIC ( >8 WEEKS)
0)
Life Threatening: Post -infectious: Cough:
11
2 2^
• Pneumonia
• Anaphylaxis
• FB aspiration
• Bronchitis /viral URTI
• Pneumonia
• Pertussis
• Asthma
• GERD
• Upper airway cough syndrome
• Environmental
Bolded items indicate the most common conditions
HISTORY
ID .
Age gender
CC Cough
HPI .
Duration: acute (< 3 wks) subacute ( 3 - 8 wks), chronic ( >8 wks)
Timing and frequency: time of day (associated with meals, night time) , paroxysmal
Character of cough: severity, dry or productive, sputum purulent or clear, hemoptysis, change from previous cough
Precipitating factors: positional, chemical irritants, smoke, allergies, pets, foods (e.g., milk ) , position changes (eg.
Worse after laying down in GERD)
Alleviating factors:rest, puffers, antacids
.
Associated symptoms: constitutional symptoms, wheezing SOB, nasal symptoms, sore throat, chest pain, reflux
Sick contacts
RED FLAGS .
Dyspnea, hemoptysis, weight loss, chest pain TB or HIV risk factors, stridor
PMHX .
Resp: infections (URTI pneumonia, TB, pertussis, bronchitis, CF), upper airway cough syndrome, COPD asthma, .
sinusitis
.
Cardio: CHF mitral stenosis, pulmonary HTN
.
Other: PE/DVT, GERD sarcoidosis
MEDS ACEi, G-blockers, inhalers: ask about meds that improve cough
ALLERGIES Environmental
FHX Atopy: asthma, eczema, allergic rhinitis/hay fever
SOCIAL Smoking, EtOH, pets, home and work environment, travel hx, immunizations
ROS Complete general ROS with focus on respiratory system
RISK COPD, asthma, allergies, immunocompromised (e.g., HIV), environmental triggers (e.g., smoke, chemical irritants)
FACTORS
n 3
INVESTIGATIONS 3 <
Laboratory Investigations
• If considering an infectious etiology: CBC- D, ESR /CRP, sputum cultures, nasopharyngeal aspirate, viral panel swabs
Radiology/Imaging
• CXR : to help with identifying an overt obstructing/infiltrating mass, infectious consolidation or fluid accumulation
Special Tests
• Consider for suspected pulmonary causes: PFTs or methacholine challenge ( Asthma), sputum studies (cytology, gram stain,
culture), d - dimer & chest CT ( PE), sinus CT (chronic sinusitis), bronchoscopy ( atypical/indolent infections), ABGs, AFB (TB)
.
• Consider for suspected GERD: modified barium esophagography 24 hr pH probe and if still unrelenting - HP Breath Test
• Consider for suspected cardiac causes: ECG, echocardiogram
TREATMENT
Emergent
.
• ABCs, observe airway for swelling, secretions, FB and obstruction; assess work of breathing and mental status
Please refer to Congestive Heart Failure, Dyspnea, and Respiratory Tract Infections sections
Follow -up
• Arrange for follow -up or refer based on etiology for worsening, unrelenting cough
• Smoking cessation leads to resolution of chronic cough in 90% of smokers
KEY POINTS
• The initial approach to diarrhea begins with distinguishing between acute vs. chronic diarrhea
• Acute diarrhea is primarily infectious in nature while chronic diarrhea has a number of different etiologies
.
• Fecal impaction can manifest with diarrhea (i.e. overflow diarrhea); hence, always ask about prior chronic constipation
DIFFERENTIAL DIAGNOSIS
ACUTE: > 3 stools/ day or > 200 g of stool/day for < 4 wks
Infectious Setting
Causes Community Institution Travel
Bacterial Small bowel ( watery ): Colonic (bloody ): • Shigella • ETEC ( most common)
• Enterotoxigenic E . Coli • Salmonella • Clostridium difficile • Vibrio cholera
• Vibrio cholera • Shigella • Bacteroides fragilis • Campylobacter
• Clostridium difficile . EHEC 0157:H7 • Salmonella
• Campylobacter • Campylobacter • Shigella
• Yersinia • Yersinia
Viral • Norovirus • Norovirus • Norovirus
• Rotavirus (most common cause in children) • Astrovirus • Rotavirus
HISTORY
ID • Age. gender
CC • Diarrhea
115 Edmonton
HPI • Onset: abrupt (meds, infection) vs . insidious (chronic illness)
• Urgency: urgent defecation usually indicates rectal involvement
• Frequency: change with fasting (secretory vs. osmotic), alternating constipation and diarrhea (IBS)
.
• Quantity: large bowel (small vol BM frequent, + blood, mucous/pus) vs . small bowel (large vol and infrequent BM)
• Quality of BM: large bowel (bright red blood) vs. small bowel ( watery); UGIB (melena = black, tarry stools);
malabsorption (mucous, foul smell, floating/oil drops)
• Risk factors: exposure ( travel, childcare, HCW, camping/ well water ), recent abx use, immunosuppression,
malignancy, anal intercourse, laxative abuse, foods (outbreaks, undercooked poultry, spoiled dairy, hamburger,
pork, seafood, mayonnaise at room temp), exotic pets
• Associated symptoms: fever, abdominal pain, tenesmus, vomiting, cough, arthalgia, myalgia, sore throat
RED FLAGS • Constitutional symptoms, age > 50, hematochezia, change in bowel habits (CRC)
• Vomiting, fever, arthritis, skin rash, anorexia
• Chronic diarrhea, nocturnal symptoms, cramping, wt loss, ± hematochezia (IBD)
• High Mortality/Morbidity - electrolyte abnormalities (most common is metabolic acidosis or hypokalemia), 2 Tl
cancer, IBD, malabsorption syndromes CD «i
a>
PSHX • Bowel resection ( short gut), cholecystectomy (bile acid wasting)
MEDS • Prior antibiotic use, laxative, chemotherapy, colchicine, antacids that contain Mg, PPI, SSRIs, metformin, and
NSAIDs
FHX • Colon cancer, celiac disease, IBD
.
SOCIAL • Drugs EtOH, caffeine, sexual Hx, exposures including sick contacts and travel
ROS • HEENT: uveitis (IBD), proptosis (hyperthyroidism), oral ulcers (Crohn’s), postural light -headedness
• CV: palpitations (hyperthyroidism), tachycardia (intravascular volume depletion)
• RESP: viral/bacterial infection (URTI)
miEATMENT
Emergent
• IV fluids and electrolytes (depending on volume status)
• Moderate to severe pyrexia or systemic toxicity - treat empirically or with quinolone
Treatment (dependant on underlying condition)
• Do NOT empirically prescribe anti -diarrheal, especially with fever or hematochezia
.
• Abx - generally not required unless pt high risk or has severe Sx ( >6 episodes/day, hematochezia febrile >1wk ). Metronidazole or
vancomycin ( C. difficile ) , metronidazole (Giardia), ciprofloxacin [ Shigella, Salmonella, Campylobacter, E. coli ; * * not EHEC because of|
progression to HUS and TTP)
Referrals: Gastroenterology when etiology of diarrhea is unclear despite multiple investigations (endoscopy for malabsorption or IBD).
Oncology, general surgery if suspect colorectal cancer
Edmonton Manual of Common Clinical Scenarios 116
DYSPEPSIA
.
Current Editor: Trent Schimmel BSc Cailey Turner BSc
KEY POINTS
• Constellation of symptoms : post -prandial fullness, early satiety, epigastric pain or burning
• Majority of the patients (75%) have the above symptoms with no evidence of organic /structural disease to explain their symptoms
(functional dyspepsia)
• 25% of patients with dyspepsia have an underlying organic cause for their symptoms
• Patients with alarm features and > 55 y must undergo an upper endoscopy; patients with GERD or NSAID induced dyspepsia should -
first be treated empirically with a PPI
DIFFERENTIAL DIAGNOSIS
Gastrointestinal (40%) Cardiac Metabolic Rheumatologic
O
>* C Gastric /duodenal ulcers (H. • Angina • DKA* * • SLE
.
•
u
E T3
Pylori NSAID EtOH) . • Ml • • Hypothyroidism • Scleroderma
05 ) > Perforating ulcer ” • Aortic dissection* * • Hypercalcemia • Rheumatoid arthritis
LL d
2 • GERD/ NERD • Pulmonary embolism* * • Hyperparathyroidism • Sarcoidosis
• Esophagitis (erosive EtOH
eosinophilic, infectious
. . • Pleurisy (pneumonia, pleural • Uremia
effusion)
.
[Candida HSV ]) • Pericarditis
• Gastritis
• Myocarditis
• Upper Gl bleed
• CHF
• Lactose intolerance
• Cholelithiasis, cholecystitis,
choledocolithiasis
cholangitis’ *
.
• Pancreatitis
• Celiac disease
• Diabetic gastroparesis
• Achalasia
• Inflammatory bowel disease
CC • Constellation of symptoms: post -prandial fullness, early satiation, epigastric pain or burning
HPI • Pain onset, quality, location, radiation, severity, frequency, association with position, meals or dietary factors
• Night - time symptoms: cough, pain, acid taste
• Symptomatic improvement .
with antacids H2 RA, or PPI
• Associated symptoms: odynophagia, heartburn, or regurgitation
. .
• Rule-out cardiac causes: retrosternal chest pain, radiation to shoulders/neck, diaphoresis SOB and exacerbation
with exertion
RED FLAGS • Acute dyspnea, tachycardia, diaphoresis
• Age > 55 and new onset dyspepsia, anorexia, wt loss, persistant N/V, progressive dysphagia, odynophagia, signs
. .
of Gl bleeding (hemetemesis melena bright red blood per rectum, unexplained Fe deficiency anemia), jaundice,
.
palpable mass or lymphadenopathy FHx upper Gl cancer, no improvement on H2RA or PPI
PMHX • Previous peptic ulcer disease. CAD/dyslipidemia. cancer/radiation, anxiety. DM. thyroid disease
PSHX • Appendectomy, cholecystectomy
JAMA 2006: Clinical impression based on Hx and exam do not distinguish between organic and functional dyspepsia
American J Gastroenterology 2001: Hx and physical exam in patients with no red flags not good predictors of endoscopic findings
INVESTIGATIONS
Laboratory Investigations
.
• CBC- D. electrolytes, Cr, urea, glucose, Ca2‘, albumin, lipase, troponin, CK INR. B - HCG
Imaging
• Upper Gl series or EGD ± Bx
.
• Indications for endoscopy: red flags (see above) , epigastric mass NSAID use, PMHx PUD
Special Tests
• Urea breath test: no alarm symptoms, age < 45 -
treat if H. pylori + ve
.
• Esophageal manometry: normal EGD and symptoms suggestive of motility disorder (e.g. achalasia, esophageal spasm)
• Ambulatory 24- hr esophageal pH monitoring: normal gastroscopy and suspicion of GERD
• Fasting serum gastrin levels or serum secretin test ( Zollinger - Ellison syndrome)
OEEATMENT
Emergent: suspect UGI bleed if hemodynamically unstable
.
• ABC monitors 2 large bore IVs, Pantoprazole 80 mg IV bolus then 8 mg/hr and volume resuscitate
• Crossmatch/ transfuse blood
• Proceed to therapeutic EGD
Treatment Options: stable, out - patient setting
• Lifestyle
Discontinue NSAIDs or triggering meds
Smoking/EtOH cessation, manage anxiety/depression
Wt loss, reduction of fatty foods or triggering foods, smaller meals, no eating 2 - 4 hrs prior to sleep, elevate head of bed
(decreases pH exposure nocturnally but no effect on symptoms)
• Medical
> .
PUD: Omeprazole 40 mg po OD x 8 wks then 20mg OD after healing
> Non-ulcer dyspepsia: Omeprazole 20 mg po OD or Lansoprazole 15 mg po OD
> Functional dyspepsia: Omeprazole 20 mg OD or Itopride 50 - 100 mg po tid ± Amitriptyline 50 mg qhs
> H. pylori : eradication of infection is controversial for certain conditions - use quadruple therapy x 2 wks ( see box above), then
treat as PUD
• Surgical: distal subtotal gastrectomy (reserved for complicated gastrointestinal bleeding unresponsive to endoscopic therapy )
KEY POINTS
The demographics are key to this station
.
• Sexually active females - cystitis due to coitus STIs
.
• Post - menopausal females - estrogen deficiency, incontinence, diabetes, cystoceles previous GU surgery
• Males - prostatic hypertrophy, anatomical abnormalities, sexual activity, catheter - associated
DIFFERENTIAL DIAGNOSIS
Common Presentation Other Considerations
Q) Conditions
c
Cystitis .
Dysuria urgency, frequency, hematuria, Most common bacteria causing UTIs ( KEEPS): Klebsiella,
£ change in urine color /odor, suprapubic .
Escherichia coli Enterococcus , Proteus mirabilis / Pseudomonas,
£52
pain; fever generally absent Staphylococcus saprophyticus /Serratia marcescens (Note: 95%
of uncomplicated cystitis in young women is due to E. coli )
Urethritis/ May be identical to cystitis, except Offer testing for STIs, including chlamydia and gonorrhea
Cervicitis urethral discharge may be present
Vaginitis Vaginal discharge, itch, foul smell DDx: Candida, trichomoniasis, bacterial vaginosis
Prostatitis Similar to cystitis except perineal pain, Tenderness +/- fullness on DRE
fever, urinary hesitancy, poor stream Urine culture to guide antimicrobial treatment if positive
Pyelonephritis Fever, chills, flank or back pain, Same pathogens as cystitis
nausea, vomiting, diarrhea Can progress to urosepsis (high mortality)
Renal abscess Similar to pyelonephritis, but persistent Consider ultrasound +/- CT to investigate for
pain and fever despite appropriate abx abscess in those who do not respond to abx
Benign Prostatic Urinary frequency, urgency, hesitancy, 50% of men > 70 years with clinical symptoms
Hypertrophy dribbling, incomplete voiding
HISTORY
ID • Age. sex F M
( > )
CC • Difficulty voiding, frequency, urgency, nocturia, pain on urination, hematuria, discharge, hesitancy, straining,
incomplete emptying, incontinence, intermittency, poor stream, delirium and falls (in the elderly), behavior
changes, constipation, and abdominal pain (elderly and pediatrics)
HPI • Onset, provoking/relieving factors, quality of pain, region and radiation of pain ( flank, scrotum, back, perineum,
rectum), changes in frequency of urination, discharge, burning, abdominal fullness, color of urine
.
RED FLAGS • Fever/chills, N/V diarrhea, gross hematuria
PMHX • Frequent . .
UTIs, DM immunosuppression, renal stones BPH, incontinence
PSHX • Recent instrumentation of GU tract (cystoscope, catheter), surgeries for incontinence (pessaries, sling, etc.)
PO&GHX • Current pregnancy, post -menopausal, prolapsed pelvic structures
MEDS • Anticholinergics, herbals, CAM
FHX • Immunosuppressive disorders, urological malignancy, structural anomalies, congenital anomalies, renal stones
SOCIAL • Sexual hx: number and genders of partners, types of sexual contact (oral, vaginal, anal), contraceptives, age of
sexual debut, foreign bodies, previous STIs
ROS • HEENT: uveitis, pharyngitis, grouped lesions on face
• Gl: abdominal pain
• GU: gross hematuria, stone passage, genital ulcers, presence of discharge
• MSK/DERM: arthritis, skin lesions/swelling/pain/rash in groin area
RISK • Sexually active females, risky sexual behavior, congenital anatomical GU aberrancies
FACTORS
PHYSICAL
General Approach
• ABCs, vitals, well vs. unwell
HEENT
• Inspection: uveitis/conjunctivitis (reactive arthritis), pharyngitis, mucosal lesions
INVESTIGATIONS
Choice of investigations guided by history and physical exam
Laboratory Investigations
2 -n
. . 2 Q>
• CBD- D lytes, urea Cr
• Blood cultures (if pyelonephritis or urosepsis suspected )
£ 3—
O •
.
• Urinalysis ( for cystitis) - nitrite or leukocyte esterase (sens 75% spc 82%), pyuria (sens 95%, spc 71%) , bacteria (sens 40 - 70%, spc a>
85 -95%), hematuria
• Urine C & S: significant if > 106 CFU/mL ( not always needed in symptomatic, uncomplicated women)
> > 3 mixed organisms is probably a contaminated collection
• Urine PCR ( for Gonorrhea/Chlamydia)
• Swab of vaginal discharge for: hyphae and budding yeast (Candida), motile trichomonads (trichomoniasis), clue cells ( bacterial
vaginosis)
Radiology/lmaging
• Renal U/S Klebsiella assess for renal abscess
> After 1st febrile UTI in children < 2 y +/- VCUG if US abnormal
• KUB x -ray or spiral CT/ KUB - assess for stones
Surgical/ Diagnostic Intervention
• Cystoscopy if gross hematuria (if no current infection)
TREATMENT
• Emergent if signs and sx of sepsis: IV fluids, admission to hospital, empiric abx
• Only treat cystitis if + ve UCx, pt symptomatic, or pt meets CAM delirium criteria with unreliable hx
-
Low dose or post coital abx (e.g., TMP/SMX 1tab PO Urologic workup recommended. Consider chronic
pericoitus) or 3 times / wk prostatitis.
Recurrent cystitis (consider investigating cystocele or bladder
diverticulae in post -menopausal women)
Asymptomatic Treat if pregnant: (e.g., cefixime 400 mg PO daily x 5 d with post -treatment urine culture)
bacteriuria Treat if prior to surgery or urological instrumentation: (e.g. cefixime 400 mg PO single dose pre -op)
Prostatitis Ciprofloxacin 500- 750 mg PO BID x 2 - 4 wks. If chronic symptoms > 3 months treat for 4-6 weeks.
Pyelonephritis
• Amoxi -dav 875mg po bid x 10 d (or cefixime. cipro. TMP/SMX) - do not use nitrofurantoin or fosfomycin
-
• If hospitalized/septic treat: empiric Ceftriaxone 1 2 g IV daily x 10
testicles and relieve pain. NSAIDs or acetaminophen for analgesia
• Special sling to elevate
Epididymitis/ • For older men: Ciprofloxacin 500 mg PO BID xlO d
Orchitis • For sexually active men with suspected /confirmed STI: Ceftriaxone 250 mg IM x 1dose + Doxycydine 100 mg PO bid
x 10- 14 d
* ln cases where urine C & S has been sent, ensure that empirically chosen abx has adequate coverage
• Follow - up if no resolution of symptoms after culture -guided therapy
• Referrals: Urology (if BPH refractory to medical management, anatomical GU aberrancies suspected, renal stones ): Nephrology:
Infectious Diseases for antimicrobial guidance/stewardship
KEY POINTS
• Differentiate between organic and psychogenic etiologies of ED
• Remember to evaluate for underlying etiology of organic ED
• Psychogenic component is present in majority of cases, so important to consider patient and partner
DIFFERENTIAL DIAGNOSIS
Organic Etiologies
Vascular • DM, CVD/ PVD, HTN, pelvic or retroperitoneal irradiation, smoking
0) Anatomical / Structural • Cavernous fibrosis, Peyronie's disease, hypospadias /epispadias, pelvic trauma/surgery
> C
E
Neurogenic . Alzheimer’s, Parkinson's disease, spinal cord injuries, peripheral neuropathy, local surgeries
• MS, stroke
HISTORY
ID Age
CC Inability to attain or maintain penile erection adequate for satisfactory sexual activity
HPI Distinguish organic ED vs. psychogenic ED
Onset: sudden (reversible causes such as meds, psych, trauma) vs. gradual/progressive (organic)
Non- sustained erection (anxiety, vascular leak )
Presence of nocturnal and morning penile erection (psych)
Difficulty with arousal, ejaculation, and orgasms ( self stimulation vs. with partner ), loss of libido
Prior treatments or diagnostic testing for ED
Sexual Hx: stable or new relationship (adjustment ), duration of relationship, age disparity, health of the partner,
alternative sexual activities, condoms, previous STIs, past or present sexual abuse
Psychosocial Hx: difficulties in relationship, anxiety about sexual performance, stressors at work or life, depression,
fatigue
Consider interviewing pt ’s partner
RED FLAGS Lack of rigid nocturnal erections suggests vascular or neurogenic etiology
Rule out Cauda Equina symptoms
PMHX Metabolic syndrome: DM, HTN, dyslipidemia, obesity
CVD, PVD, obstructive sleep apnea, neuro/psych /endocrine disease
Previous cancers, chemotherapy/radiation, brachy therapy, prostatectomy
PSHX Pelvic surgery, radiation Tx, retroperitoneal surgery, urological surgery, vasectomy
MEDS Anti- androgens, anti - HTN, anti-arrhythmics, antidepressants
FHX . . .
ED CVD, PVD DM obesity, dyslipidemia HTN .
SOCIAL .
EtOH smoking, recreational drug use (marijuana, cocaine, heroin), sedentary lifestyle, relationship issues/stress
ROS HEENT: headache, trauma
.
CV: evidence of vascular disease, chest pain, claudication, HTN SOBOE
Endocrine: gynecomastia, nipple discharge, heat or cold intolerance, palpitations, sweating, hair or skin changes
Gl: diarrhea or constipation
.
GU: previous genital trauma or surgery, retention, dysuria painful ejaculationhhtt
NEURO: Hx of stroke or trauma, visual field changes
PSYCH: depression, anxiety, abuse
RISK ED is a strong predictor of CAD, stroke, and mortality. CV risk assessment should be performed .
FACTORS
INVESTIGATIONS
Laboratory Investigations
.
• CBC, urea, creatinine, HbAlC lipid profile
• Morning total testosterone, prolactin TSH.
• Urinalysis (renal disease or infection), urine G + C
Imaging (usually not necessary)
• Ultrasound, arteriography, cavernosography
Special Tests
• Psychiatric evaluation
• Neurophysiologic testing: EMG, bulbocavernous reflex latency: cavernosal EMG: somatosensory evoked potential test
• Nocturnal penile tumescence testing
QREATMENT
Conservative Management
• Psychosocial: patient or couple counseling
.
• Lifestyle modification: wt reduction if obese, smoking cessation, reduce EtOH increase physical exercise, reduce cholesterol/ fat
• Drugs: remove causative agents and replace with alternatives: improve compliance with DM and CVD medications
Medical Management
• First line: Phosphodiesterase type 5 (PDE 5) inhibitors (contraindicated with nitrate drugs)
• Second line: intracavernosal injection and transurethral therapy: PGE 1(alprostadil), alpha agonist, educate about priapism
• Vacuum constriction pump: contraindicated in sickle cell anemia, blood dyscrasias, and in patients on anticoagulation medications
Hypogonadism
.
• Testosterone replacement therapy: IM patch, or transdermal gel - used only for patients with documented hypogonadism
• Monitoring includes surveillance for prostate cancer ( annual DRE with PSA), detection of polycythemia (Hb q6 - 12mo)
Surgical Management
• Penile prostheses (last resort) - semi -rigid ( fixed) vs. inflatable with scrotal pump
Cardiovascular Assessment
• ED is a strong predictor of CAD and may precede CV event by 2 - 3 yrs: sentinel marker for prompting discussions on promotion of
CV risk stratification and modification
Causes
Cardiopulmonary Post-MI, obstructive sleep apnea, CHF **, COPD **, angina **, critical aortic stenosis
Endocrine DM, hypothyroidism, Addison's disease
Gl Malignancy " *, celiac disease, chronic liver disease
Renal Chronic kidney disease
Hematologic Anemia , lymphoma, leukemia, autoimmune disease
Infectious Viral illness, HIV * *, viral hepatitis, subacute bacterial endocarditis, TB, EBV
Musculoskeletal Rheumatoid arthritis
Neurological Cerebrovascular disease, MS, ALS, myasthenia gravis, Parkinson's disease
Psychiatric Depression, anxiety, dementia, chronic fatigue syndrome, fibromyalgia, chronic pain syndrome
Other Disordered sleep, medication, malignancy, systemic lupus erythematosis, pregnancy
Bolded items indicate common conditions ‘•Asterisk indicates life - threatening conditions
HISTORY
ID • Age, gender
CC • Fatigue
PMHX • Chronic diseases, cancer, recent Ml .CHF. COPD.DM. hypothyroidism liver disease psychiatric history, etc.
, ,
ROS • CV/RESP: chest pain. SOB. edema, syncope/presyncope, daytime sleepiness, snoring
• ENDO: polyuria, dry skin, goiter, hyperpigmentation
• Gl: changes in bowel pattern, black/bloody stool, abdo pain, ascites
• RENAL: edema, nausea, emesis, anorexia, pruritus
• HEM: SOBOE, petechial rash, lymphadenopathy
• INFECTIOUS: constitutional sx, travel, social risk factors
• MSK: joint pain, swelling
• NEURO: vision changes, weakness, paresthesias, vertigo, ptosis, atrophy, fasiculations
• PSYCH: SIGECAPS, excessive worry, panic, anxiety, memory changes .SI/HI
• Other : constitutional Sx . CAGE, sleep habits, rash, menstrual Hx
123 Edmonton Manual of Common Clinical Scen.n
uHYSICALEXAM
Perform a head-to-toe P/E. Focus particularly on symptoms elicited on Hx, whilst seeking evidence of life -threatening illness.
General Appearance: unwell appearance, abnormal VS, cachectic, edematous, body habitus
HEENT
• ptosis, goiter, pharyngitis, pallor, lymphadenopathy
NEURO
• focal neurologic deficits, nystagmus, papilledema, fasciculations, abnormal gait , tremor, asterixis
CV
.
• new /changed murmur, displaced apex, extra heart sounds, arrhythmia, elevated JVP pulsus parvus et tardus
RESP
• crackles, wheeze, dullness to percussion
ABD
• scaphoid abdomen, ascites, splenomegaly, hepatomegaly, abdominal tenderness, DRE if indicated
DERM
.
• jaundice, petechial rash SLE rashes ( malar, oral ulcers, photosensitivity, discoid) , dry or oily skin or hair, cutaneous manifestations of
liver disease (palmar erythema, spider nevi, telangiectasias, nail abnormalities)
2 n
2. w
Q
-
n 3
MSK
3 *<
• muscular atrophy, wasting, clubbing a>
PSYCH: MSE
Other: breast or genital exam if indicated by clinical history
INVESTIGATIONS
Select based on Hx, risk factors, and PE findings. In the absence of concerning Hx or PE findings, investigations are unlikely to be useful.
Laboratory Investigations:
. . .
• CBC- D, lytes, Ca, P04, Cr, AST, ALT ALP, GGT INR / PTT, iron studies ( Fe. ferritin TIBC, % saturation), B12, glucose /HbAlc TSH .
.
• ESR CRP, anti -CCP, ANA, HIV, hepatitis serology, TB skin test, AFB in sputum, lyme serology, albumin, total protein
• U/A, BHCG
Imaging:
• CXR if lung pathology suspected
• XR of affected joint ( s ) if inflammatory arthritis suspected
• XR areas of bone pain if metastatic disease suspected
• Mammography if breast mass present
Other:
• Colonoscopy ( Fe deficiency anemia in women > 50 y/o and any man)
• ECG, echo, cardiac stress test
• Fine needle aspiration or exicional bx of mass or enlarged lymph nodes
MANAGEMENT
If an underlying cause is identified, treat the underlying etiology. If no organic cause is identified, the following interventions may be useful:
Lifestyle -
• Sleep hygiene ensure adequate sleep duration, consistent sleep / wake times, dark room, no TV/electronics in
Changes bedroom, no caffeine after noon, avoid food or exercise late in the day, avoid naps
• Stress reduction - mindfulness exercises (meditation), reduction of work hours, hobbies, counseling
• Exercise - regular, structured exercise (e.g., daily 30-minute walk)
• EtOH /substances .
- reduce or eliminate substance use offer community resources
Pharmacologic •A 6 - week trial of an SSRI may be appropriate if a diagnosis of depression is being considered
•A short course of treatment with a hypnotic (e.g., Zopiclone) may be appropriate for insomnia
Referrals • Consider referral for psychiatric assessment - psychotherapy, group therapy, etc.
KEY POINTS
• The differential diagnosis of fever of unknown origin (FUO ) can be broken down into five major subgroups: infections, malignancies,
autoimmune conditions, post - surgical , and miscellaneous
DIFFERENTIAL DIAGNOSIS
Diagnostic Criteria
• Fever: T > 38.3°C Post Surgical (5 Ws)
• FUO: T > 38.3°C for > 3 wks duration, no known cause after 1 wk of Post - Operative
Days
Causes
investigation
Etiologies (bolded items indicate most common causes) Wind 1- 2 atelectasis, pneumonia
<D • Infection Water 3- 5 UTI
>C > External and localized (e.g.. cellulitis)
!
.
l
Li W
> Internal and localized (e.g.. intra - abdominal abscess associated with
perforated hollow viscera following appendicitis, diverticulitis)
Walking
Wound
4- 6
5- 6
DVT. PE
surgical wound infection
Wonder
> Systemic (i.e., bacteremia ) 74- anesthetic , transfusion rxn
Drug
• Malignancy
> Leukemia , lymphoma , myelodysplastic syndromes, metastatic cancer SIRS Criteria
• Autoimmune and Inflammatory Disorders (any 2 of the following)
> Vasculitis, rheumatoid arthritis T > 38cC or < 36°C
> IBD, sarcoidosis
RR > 20 or paC02 < 32mmHg
> Endocrine: thyroid disease
• Post - surgical ( 5 Ws - see table to the right )
HR > 90
HISTORY
ID • Age, gender
CC • Feeling warm or cold , sweating, rigors/chills, change in LOC. Clarify “ tactile temp" versus measured fever.
HPI • Timing: onset in relation to medical condition, duration, recorded variations throughout the day
• Otherrelated symptoms: general malaise, N/V. diarrhea, pain, rash
• Recent travel to areas of high risk infection, exposure to farm animals , blood transfusion. IVDU ( amphetamines ) ,
trauma , time in sun or hot environment , sick contacts
RED FLAGS • Change in LOC, neutropenic /immunosuppressed, B sx, constitutional sx, recent travel to tropical area
PMHX • Recent acute or chronic infections, rheumatoid arthritis. Hx of cancer, vaccination Hx. recent abx use
PSHX • Recent surgery
PO&GHX • Immobilization, recent delivery, recent instrumentation (i.e., D&C)
FHX • Malignancies, fever disorders
SOCIAL HX • Occupation (e.g., health care professional working in an ID clinic )
MEDS • Chemotherapy, diuretics, pain medication, anti- arrhythmic drugs, steroids, immunosuppresive agents, medication
misuse , recent medication change/discontinuation
ROS • HEENT: lymphadenopathy, sweating, goiter, nuchal rigidity
• CV: palpitations, tachycardia , chest
pain, BP
• RESP: increased work of breathing, sputum production, coryza , cough
• NEURO: headache
INVESTIGATIONS
Investigations based on clinical suspicion according to Hx and PE:
Laboratory Investigations
• CBC-D, electrolytes, urea, Cr
• AST, ALT, ALP, bilirubin, albumin, INR, lipase
. .
• TSH /T3 /T 4 ESR, CRP, ANA anti- CCP
• Blood culture, serum lactate, venous gas (acidosis from sepsis )
.
• UA urine C & S, urine metanephrines, throat swab, monospot, sputum C& S
Radiology/Imaging
• CXR: pneumonia, TB, metastasis
• US: possible infective sites, abscesses, visualization of abdominal organs
• Echo for endocarditis
• CT head, chest, abdomen, pelvis if needed
• Bone scan: metastasis, osteomyelitis
Surgical/Diagnostic Interventions
• Mass or lymph node Bx/excision. bone marrow Bx, percutaneous fluid aspiration, LP
TREATMENT
Emergent
• ABCDEs and GCS . IV fluids. 02. treat underlying cause of fever
• Broad spectrum IV abx if sepsis is suspected - try to draw BCx first, but do not delay abx treatment
• Cooling ifT > 40°C with antipyretics and cooling blankets
• Source control: e.g., surgical excision of intra- abdominal abscess
Treatment Options
• Fever should not necessarily be treated and most people recover without medical attention
• Antipyretics to lower the raised hypothalamic temperature set point: acetaminophen, ASA, NSAIDs
.
• Treat underlying cause with the appropriate medical management: abx steroids, anticoagulation
Surgical
• Specific conditions where surgical Tx is curative (e.g., necrotizing fasciitis, abscess drainage)
• May also be diagnostic via pathology, organism identification, etc.
KEY POINTS
• There are two major categories of headaches: primary and secondary
• Always rule out secondary headaches prior to making a diagnosis of primary headache: this is usually done based on Hx
DIFFERENTIAL DIAGNOSIS
Primary Headaches ( 90% ): no identifiable cause
Headache Type Duration Quality Associated Symptoms Aggravating Factors
-
• Bilateral, mild moderate None usually Stress, muscle tension, poor posture
Tension 30 min - -
intensity, fronto occipital or
Q)
(most common) 7d generalized, pressure or tight
>C band across forehead
u • Unilateral, severe intensity, N/V, photophobia, phonophobia, Physical activity, sleep disturbances,
E pulsatile .
osmophobia scintillating scotoma motion sickness, foods/smells
nj
u
(
LL
2 -
Migraine (+/ aura) 4- 72 hrs • Often preceded by aura: < 60 min
of fully reversible visual, sensory,
or speech sx
• Several headaches occur in Ipsilateral autonomic sx: conjunctival Smells, exercise, smoking, EtOH
clusters, lasting wks - mos infection, lacrimation, nasal conges-
15 -180 tion, rhinorrhea, sweating, ptosis,
Cluster • Sharp, often unilateral in the
min eyelid edema
retro- orbital area, severe
intensity, hyperesthesia
HISTORY
ID • Age, gender
CC • Headache
INVESTIGATIONS
The Hx and PE guide the investigations ordered
Laboratory Investigations
• CBC- D (infection)
• INR, PTT ( vascular causes)
• ESR /CRP ( temporal arteritis)
• ABG (hypoxia /hypercapnia)
.
• CBC, LFT, Cr U/A (pre- eclampsia)
Radiology /lmaging
.
• Imaging can be considered in the presence of red flags, age ( > 50 yrs) unresponsive to conventional therapies, or recent significant
changes in headache
.
> Non- contrast CT (SAH epidural or subdural bleed, mass, increased ICP. focal neurological deficits)
> MRI (space occupying lesion)
Special Tests
• LP if meningitis, malignancy/metastasis, or SAH suspected ( ensure ICP is not elevated based on PE and Hx ( focal neurological signs,
drowsiness, papilledema, etc ])
• Tonometry (glaucoma)
• Temporal artery Bx for temporal arteritis
TREATMENT
Emergent: ABCs, GCS, empiric therapy with 3 rd gen cephalosporins + vancomycin for suspected meningitis
For secondary headaches, treat underlying cause
Migraine • NSAIDs, acetaminophen • Lifestyle - limit caffeine intake, sleep, eat and drink regularly, exercise
• Triptans • Propranolol
• Neuroleptics - Maxeran. Stemetil • Topiramate
• TCA
• Botox
Cluster • Oxygen 100% • EtOH avoidance
• Triptans • Verapamil
• Ergotamine • Topiramate
• Lithium
. .
Referral if refractory to treatment: Neurology Neurosurgery (SAH mass lesions, refractory cluster headaches)
KEY POINTS
• Hypertension is the leading cause of death and disability worldwide
. .
• End organ damage includes: CVD CHF stroke, renal failure, retinopathy
• The Hx is valuable in assessing symptoms suggestive ofa secondary cause and other risk factors for CVD (smoking DM) .
• The recommendations for diagnosing hypertension have changed recently, and now include a focus on automated blood pressure
measurement as the preffered in - office method
DIFFERENTIAL DIAGNOSIS
• Primary hypertension ( > 90% of cases)
<D • Secondary hypertension: ABCDE Mnemonic
>. c > A: Apnea ( sleep apnea), Aldosteronism Accuracy .
E TJ
u
> .
B: Bruits Bad Kidneys ( Renal Parenchymal Disease)
nj
.
Li
Q) > .
C: Catecholamines Coarctation of the Aorta Cushing's syndrome .
2 > .
D: Drugs Diet
> .
E: Erythropoietin Endocrine Disorders (Example: Pheochromocytoma)
2017 CHEP RECOMMENDATIONS:
Elevated BP reading at office, home, or pharmacy
.
Mean Office BP 2 180/ 110 at dedicated office visit
No
fes
No Diabetes Diabetes
No l. AOBP 2 135/85 (preferred ) AOBP or non AOBP 130/80
No Hypertension Hypertension
OR
2. Non- AOBP 2 140/ 90
Yes
Target Blood Pressures (CHEP 2017 Guidelines): Diabetes - Systolic < 130 and Diastolic <80, Renal disease (not diabetic) - Systolic < 140 and Diastolic <90
‘Hypertensive urgencies/emergencies include asymptomatic DBP > 130 or elevated blood pressure in the setting of hypertensive encephalopathy, acute aortic
dissection, acute coronary syndrome, acute kidney injury, intracranial hemorrhage or ischemic stroke.
Previously, the CHEP Guidelines recommended a series of "Hypertension Visits". These are now reserved for cases where AOBP or Ambulatory BP are unavail-
able ( www.hypertension.ca for details). Figure adapted from the CHEP 2017 guidelines: Criteria for Diagnosis of Hypertension and Guidelines for Follow - up
HISTORY
ID • Age and gender
CC • Hypertension +/- signs of end organ damage
HPI • Presence of .
symptoms related to target organ damage (orthopnea PND, angina, headaches, neurological deficits,
PVD, decreased visual acuity, hematuria)
RED FLAGS • New -onset headache, neurologic deficits, angina, visual disturbance, delirium, altered LOC, intermittent
palpitations, heart failure
PMHX • Complications of .
hypertension (CAD stroke PVD, CHF, AF) .
• Other: CAD risk factors (dyslipidemia, smoking. DM FHx ) .
PSHX • Cardiac, renal, vascular surgery
PO&GHX • Pre - eclampsia, PIH
MEDSAND • Prior use of anti-hypertensive medications
OTHER • Medications that increase BP (contraceptives, decongestants. NSAIDs)
DRUGS • Recreational drug use (cocaine, amphetamines)
FHX • CV disease, HTN DM .
PHYSICAL
Vital signs, including BP in both arms, HR, Sp02, and temp
Inspection
• JVP, precordial surgical scars
• Body habitus, short neck , and crowded oropharynx (obstructive sleep apnea)
• Diaphoresis and flushing (pheochromocytoma)
• Fat redistribution, facial plethora, striae, rapid weight gain (Cushing’s syndrome)
• Fundoscopy for signs of retinopathy
Palpation
• Assess bilateral peripheral (radial) and central (carotid) pulses
• Note rate and rhythm, as well as contour (central pulses only)
• Assess brachial - femoral pulse delay (coarctation)
2 n
2. w
Q
-
• Cardiac apex for sustained or diplaced PMI (LVH) n 3
Percussion 3
n>
<
• Percussion for pleural effusions (if CHF suspected)
Auscultation
• Precordial auscultation for normal heart sounds and presence of S3 ( heart failure) and S4 ( LVH)
• Chest auscultation for crackles (CHF)
• Carotid auscultation for bruits (cardiovascular disease )
• Deep abdominal auscultation for renal artery bruits (renal artery stenosis )
INVESTIGATIONS
Routine Investigations (to be repeated based on clinician judgement )
• Potassium, Sodium, serum creatinine, fasting blood glucose or HbAlc, lipid profile ( fasting or non- fasting)
.
• Urinalysis Urinary albumin excretion ( only in patients with DM)
• 12- lead electrocardiogram
Special Diagnostic or Prognostic Tests
• Echocardiogram ( LVEF and LVH)
• 24- hour urinary cortisol and dexamethasone suppression test (Cushing's syndrome)
• Renal ultrasound with doppler or MR angiogram (renal artery stenosis, fibromuscular dysplasia)
• Sleep study (obstructive sleep apnea)
• 24- hour urine metanephrines (pheochromocytoma)
• TSH + T3 /T4 ( thyroid disease)
• Renin, aldosterone (hyperaldosteronism)
TREATMENT
Non-Pharmacologic Treatments
• Wt loss if overweight (target BMI < 25 kg/m2)
• Healthy diet - high in fruits, vegetables, soluble fibre, low - fat dairy products, low in saturated fats and sodium (e.g., DASH diet)
• Regular, moderate intensity cardiorespiratory physical exercise for 30 - 60 minutes on most days
. .
• Low EtOH intake (0- 2 drinks /day < 8 drinks/ week for women < 14 drinks / week for men)
• Smoking cessation
Pharmacologic Treatments
• Consider initiating pharmacologic treatment once diagnosis of hypertension is established. Initial therapy is recommended to be
either monotherapy or single pill combination therapy
.
• First line agents include thiazide diuretics ACEi ( non-black patients), ARBs, beta -blockers ( patients < 60 yrs), or long- acting CCBs
• A combination of 2 first line drugs may be considered if target blood pressure levels are not achieved with standard - dose
monotherapy. The combination of ACEi and an ARB is not recommended
• Commerically available combination tablets ( such as ACEi/thiazide) may increase patient adherence
• Recent RCT evidence suggests that an aggressive BP target of less than 120/ 80 mmHg improves cardiovascular outcomes;
however, consider the risks of adverse events, such as symptomatic hypotension and acute kidney injury
• In elderly patients who do not have diabetes or target organ damage, more conservative diagnostic ( SBP >160 mmHg) and
treatment ( SBP < 150 mmHg) thresholds may be appropriate
• If blood pressure is not adequately controlled on 3 or more full -dose antihypertensive agents, referral to a specialist should
be considered
Follow up should occur every 1 - 2 months until BP readings on 2 consecutive visits are below target and every 3 -6 months thereafter
Some secondary causes of hypertension also require specialist referral for definitive management, including pheochromocytoma, Cushing's
syndrome, and coarctation of the aorta.
KEY POINTS
• Insomnia: a persistent difficulty with falling asleep or staying asleep lasting for >1month and resulting in daytime impairment
• Can be primary (no other cause present ) or secondary (caused or affected by an underlying condition)
• Management of primary insomnia includes sleep hygiene, pharmacologic, and non -pharmacologic therapies. Management of
secondary insomnia is based on treatment of underlying disorder
DIFFERENTIAL DIAGNOSIS
Primary Insomnia - diagnosis of exclusion: no underlying condition
Secondary Insomnia - caused by an underlying medical condition
<D
> C Medical Conditions CHF, COPD, asthma, neurodegenerative diseases (Parkinson's, Alzhiemer 's, stroke), hyperthyroidism, GERD, rheumatoid
|IJr
«u
LL
Qj
Psychiatric
arthritis, osteoarthritis, fibromyalgia, headaches
Depression, anxiety, PTSD, bipolar manic episode
2 Conditions
Sleep Disorders Restless legs syndrome, periodic limb movement disorder, sleep apnea, circadian rhythm disorders, parasomnias
( sleep walking), nightmares
EDSTORY
ID • Age and gender
CC • Difficulty sleeping
HPI -
• Duration - short term ( < 3 months), chronic (occurring at least 3 nights / wk for > 3 months)
-
• Sleep wake routine: hours of sleep per night, sleep schedule, difficulty falling/staying asleep, nighttime awakenings
(frequency, length, possible cause)
-
• Daytime symptoms sleepiness, difficulty concentrating, irritability, naps, functional impairment, safety concerns
• Snoring, apneic episodes at night, difficulty breathing when lying flat
• Leg movements at night, difficulty lying still, pain that prevents /interrupts sleep
-
• Sleep hygiene sleep schedule, sleep environment, bedtime routine, caffeine/exercise/TV at night
• Psychiatric symptoms- low mood, anxiety . PTSD. adjustment disorder, nightmares
PMHX • Medical conditions: (CHF, COPD
fibromyalgia)
. asthma, neurodegenerative diseases,hyperthyroidism GERD. RA. OA.
,
.
SOCIAL • Smoking, EtOH ilicit drug use, caffeine intake
• High stress occupation, shift work, travel/jet lag, recent psychosocial stressors
RISK • Female sex, advanced age, depressed mood, snoring, low levels of physical activity, comorbid medical conditions,
FACTORS nocturia, regular hypnotic use, previous hx of insomnia, high level of perceived stress
PHYSICAL
General Approach
.
• VS: BP, HR, RR Temp, Sp02
• General inspection for obesity (BMI > 30 increases risk of sleep apnea) , fatigue, well/unwell
HEENT
.
• Inspect for signs consistent with sleep apnea (enlarged neck circumference > 40 cm crowded oropharynx, nasal swelling)
• Thyroid exam ( for signs of hyperthyroidism)
CVS/ RESP
• General exam for signs of COPD CHF .
Mental Status Exam
• Appearance, speech, emotion, perceptions, thoughts, insight / judgment, cognition
• Provides information about the patient ’s mood, level of alertness, concentration, and overall functioning
131 Edmonton t
INVESTIGATIONS
Laboratory Investigations
• Based on suspected etiology, help to rule out underlying medical conditions
. .
• CBC + D TSH ferritin (restless legs syndrome)
Special Tests
- . .
• Polysomnography (overnight sleep study) EEG ECG Sp02, resp effort, and leg movements are recorded while patient sleeps
> Always screen for sleep apnea, depression, anxiety
• Sleep Diary - record bedtime, sleep latency, total sleep time, awakenings, and quality of sleep every morning for 1- 2 weeks
• “ Sleep Disorders Questionaire” or “ Insomnia Severity Index ”
TREATMENT
Treatment of Primary Insomnia
• Stimulus Control + Sleep Hygiene - 30% of patients will improve with basic sleep hygiene alone
KEY POINTS
• Physical exam and focused neuro-muscular exam are essential to delineate the source of lower back pain (mechanical vs. non-
mechanical). Pain history may be used to distinguish mechanical from neuropathic pain.
DIFFERENTIAL DIAGNOSIS
Mechanical (80- 90%) Neurogenic ( 5 -15%) Non-mechanical (1%) Visceral Disease
• Lumbar strain/sprain • Herniated disc • Neoplasia • Pelvic organs
• Degenerative disease • Spinal stenosis • Multiple myeloma • Prostatitis
• Spondylosis (discs) • Osteophytic nerve root • Lymphoma and leukemia • Endometriosis
<D • Osteoarthritis • Spinal cord tumors • Chronic pelvic inflammatory
>C
mmm mtmm
compression
• Retroperitoneal tumors disease
Spondylolisthesis
E - t!
' •
• Metastatic carcinoma • Renal disease
• Osteoporosis
LX . 2" • Fractures
• Infection
• Osteomyelitis
• Nephrolithiasis
• Pyelonephritis
• Osteoporotic fracture • Septic discitis Perinephritic abscess
•
Traumatic fracture
•
• Paraspinous abscess • Abdominal aortic aneurysm
• Congenital disease
• Epidural abscess
• Gastrointestinal disease
• Severe kyphosis • Bacterial endocarditis
• Scoliosis • Pancreatitis
• Herpes zoster
• Cholecystitis
• Spondyolysis • Inflammatory arthritis
• Penetrating ulcer
• Facet joint asymmetry • Ankylosing spondylitis • Fat herniation of lumbar spine
• Psoriatic spondylitis
• Reactive arthritis
• Inflammatory bowel disease
• Scheuermann disease
(osteochondrosis)
• Paget 's disease
HISTORY
ID • Patient ' s name, gender, age ( special consideration for pediatric populations)
CC • Back .
pain - distinguish between acute, subacute ( < 12 wks) and chronic ( > 12 wks)
HPI /legs /feet; unilateral vs.
• Onset /duration ( trauma/ injury), site, quality and severity, radiation (hip/buttocks
.
bilateral), timing (morning stiffness [OA ] constant pain at night [neoplasm/infection/inflammation]), previous
episodes, alleviating and aggravating factors
• Associated symptoms: fever, wt loss, bowel/bladder/sexual dysfunction
RED FLAGS • Cauda Equina Syndrome: sudden loss of bladder/bowel control, saddle anaesthesia ( surgical emergency)
• Severe worsening pain at night or when lying down ( > 2- 6 wks)
• Wt loss, hx of cancer, fever
• Use of steroids or intravenous drugs
• Patient with first episode at age > 50 yrs (malignancy risk )
• Widespread neurological signs
• Significant trauma
PMHX • OA . . .
osteoporosis, vertebral prolapse, spina bifida DM cancer, ankylosing spondylitis, previous infection (IVDU,
immunocompromised)
PSHX • Spine, hip. lower extremity: trauma or fractures: epidural catheters or spinal anaesthesia
MEDS • Chronic steroid use; analgesia (route/ frequency/dose)
.
SOCIAL • Substance use including IVDU
• Low mood, social withdrawal, poor coping skills, hx of back pain, lack of support, belief that pain and activity are
harmful
• Occupation and working conditions, problems with claims/compensation
• Unrealistic treatment expectations
ROS • CV/ RESP: previous hx of aortic aneurysm
• GI/GU: dysuria . frequency and urgency of urination, bladder and bowel retention/incontinence
• MSK / DERM: rash, morning stiffness, response of pain to activity
RISK
FACTORS
• Age, smoking, substance use/lVDU . obesity, female gender psychosocial barriers (yellow flags)
,
133 Edmonton M
PHYSICAI
General Approach
• Ensure spinal precautions for acute back injury
. .
• VS ( HR BP RR, Temp, Sp02)
• The abdominal exam can be useful to rule out any visceral organ disease that might be causing low back pain
-
MSK Lumbar Back Exam
• Inspection
> Check for skin markings, dimples, scars, deformities or swelling; inspect for scoliosis, lordosis, kyphosis, gait, and total spinal
posture (inability to walk heel to toe and squat and rise indicates cauda equine syndrome or neurological compromise)
• Palpation
.
Palpate for vertebral tenderness (metastases/infection/fracture) altered temperature, muscle spasms,paravertebral muscles
>
Anterior (patient supine) - palpate umbilicus, inguinal areas, iliac crests, symphysis pubis; Posterior (patient prone) - palpate
>
spinous processes (spondylolisthesis), sacrum, sacroiliac joints, coccyx, iliac crests, ischial tuberosities
• Range of Motion - pain with forward flexion ( mechanical causes ) , extension (spinal stenosis), side flexion, rotation, chest expansion
2 -n
• Special Tests fD
S= 3
> Schober ' s test (lumbar flexion): mark 10 cm above and 5 cm below dimples of Venus - should increase to > 20 cm during flexion
( limited flexion in ankylosing spondylitis)
o
*
D *
—
<
•
> Straight leg raise: raise leg until radicular pain felt ; + ve: pain in sciatic L 4 - S 3 at 30 - 70° passive flexion (indicates radiculopathy) O
> Cross straight leg: raise asymptomatic extremity in similar fashion to straight leg test; + ve: pain on contralateral ( affected) side
( indicates radiculopathy)
> -
Bragard’s test: if pain is generated with straight leg raise lower symptomatic extremity until pain disappears, dorsiflex ankle at
point when pain disappears to reproduce pain - test + ve for possible lesion in lumbosacral, sacroiliac joint, or hamstring regions
(L4 - S1)
> Prone straight leg: with extension of extremity, if pain moves more anteriorly in the thigh, likely L2 / L 3
.
> Patrick Test (SI joint pain): Flexion Abduction, External Rotation ( FABER)
NEURO
• Perform a full neurological exam of the lower limbs including sensation, strength, and reflexes
Root Pain Sensory Loss Weakness Stretch Reflex Loss
LI Inguinal Inguinal Rarely hip flexion None
L2- 4 Back, radiating into anterior Anterior thigh, occasionally Hip flexion/adduction Patellar tendon
thigh or medial lower leg medial lower leg Knee extension
L5 Back , radiating into buttock , Lateral calf, dorsum foot, web Hip abduction, knee flexion, Semitendinosus /
lateral thigh, lateral calf, space between 1st and 2 nd toe .
foot dorsiflexion toe extension/ semimembranosus (internal
dorsum foot, great toe flexion, foot inversion/eversion hamstrings) tendon
SI Back, radiating into Posterior calf, lateral/ Hip extension, knee flexion, Achilles tendon
buttock, lateral /posterior plantar aspect of foot plantar flexion of the foot
thigh, posterior calf,
lateral /plantar foot
S2-4 Sacral or buttock pain Medial buttock, perineal, Possible urinary and fecal .
Bulbocavernosus anal wink
radiating into posterior perianal regions incontinence, sexual dysfunction
aspect of leg/perineum
INVESTIGATIONS
.
Laboratory Investigations ( individualize to patient presentation) - CBC- D, ESR CRP (infection/neoplasia); Ca 2 \ P04 ( Paget ' s disease);
albumin +/- urine/serum electrophoresis (multiple myeloma); urinalysis
.
Radiology/Imaging - Lumbar spine XR ( pain > 6 wks or red flags) CT or MRI ( soft tissue changes, nerve impingement), bone scan ( in-
.
fection malignancy), skeletal survey (multiple myeloma)
Special Tests - EMG (skeletal muscle activity)
REATMENT
Pain Type Lifestyle Medication
Acute & • Alternating cold • 1st line: acetaminophen
Subacute and heat .
• 2 nd line: NSAIDs (ibuprofen diclofenac )
"
‘Cauda Equina Syndrome requires urgent Neurosurgery consult to preserve bowel and bladder function and prevent paraplegia
KEY POINTS
• Acute nausea & vomiting ( < 1month) can be due to infectious, inflammatory, or iatrogenic (chemo, post - surgical) causes
• Chronic nausea ( >1month) is a pathological response to a host of conditions and may need further investigation
• Etiology can usually be identified by history and physical exam
DIFFERENTIAL DIAGNOSIS
TOXINS Chemo /radiotherapy, opioids, anticonvulsants, abx, arsenic, organophosphates, EtOH
Gl Gastroenteritis, GERD, achalasia, esophageal dysfunction, food intolerance, gastric outlet obstruction, PUD * *,
obstruction * *, ileus, inflammatory (pancreatitis **, appendicitis* *, cholecystitis), constipation, gastroparesis, IBD,
OJ
>- C volvulus, varices, hepatobiliary disease
u
E CNS Central: increased ICP** (CVA, mass lesion, hydrocephalus, meningitis* 7encephalitis* *), brainstem lesions, MS,
«V Ql neurosyphilis, complex migraine, advanced Parkinson's Disease, closed head injury
LL JZ
2 Peripheral: otitis media, BPPV, Meniere's disease, labrynthitis, vestibulitis, acoustic neuroma, acute glaucoma
ENDO Hyperthyroidism, DKA, adrenal insufficiency, hypercalcemia, pregnancy, uremia
PSYCH Bulimia or anorexia nervosa, anxiety, depression, conversion disorder, cyclical vomiting syndrome
MISC Emotional response to unpleasant smells /tastes, motion sickness, acute myocardial infarction**, nephrolithiasis, excess
pain, HTN emergency**
“Asterisk indicates high morbidity/mortality causes
HISTORY
ID • Age, gender
HPI • Onset of symptoms: acute (<1mo) vs. chronic ( >1mo), post prandial (immediate vs. 1-4 hrs after eating),
predictable
• Vomited material (undigested, bilious, feculent ( obstruction], bloody)
• Aggravating/alleviating factors
• Associated symptoms: headache (migraine), focal neuro symptoms, decreased LOC, abdominal pain ( severity,
location, radiation), early satiety, constitutional symptoms, vertigo (labrynthitis, BPPV), infectious sx: fever,
diarrhea, sick contacts (gastroenteritis)
.
RED FLAGS • Worse with supine position ( increased ICP) focal neurological symptoms, pain that migrates to RLQ
(appendicitis), abdominal distention/pain/feculent or bilious emesis (obstruction), severe epigastric pain
(pancreatitis), decreased LOC, severe dehydration (adrenal insufficiency)
PMHX • DM, cancer, systemic sclerosis, pancreatitis, adrenal . .
insufficiency, IBD hernia Parkinson's disease
PSHX • Prior abdominal surgery
PO&GHX • Last normal menstrual cycle, menstural regularity, current pregnancy
» Brudzinski's sign - spontaneous flexion at hips during passive flexion at neck (meningitis or SAH)
CV
• Tachycardia, S4, pericardial rub, low JVP (dehydration)
ABDO z T|
• Inspection: scars, bulging flanks, distention, hernias
• Auscultation: bowel sounds, succession splash (gastric outlet obstruction)
2
n
-3
Q. wi
• Percussion: tenderness
D <
o
•Palpation: guarding/rigidity, ascites, hernias, palpable mass, organomegaly
• Special tests:
> Murphy ’s sign - RUQ tenderness and arrested inspiration due to tender gallbladder (cholecystitis)
> McBurney ’s sign - localized pain 1/ 3 the distance between the right anterior superior iliac spine and umbilicus ( appendicitis)
> Asterixis - tremor during wrist flexion that occurs with decompensated liver failure or metabolic encephalopathies
MSK/DERM
• Grouped papulovesicles, joint swelling, telangiectasia, purpuric skin rash, jaundice, skin tightening, dorsal hand surface calluses, gait
GI/GU
• DRE ( tone / blood)
INVESTIGATIONS
Routine investigations not indicated if the cause of N/V determined by Hx and physical
Blood Work
.
• Initial labs: CBC- D (leukocytosis - infection/inflammation), electrolytes B-hCG (pregnancy)
• If abdo pain/ jaundice: AST/ALT, ALP, bilirubin, lipase (pancreatitis)
.
• ANA troponin, TSH
Radiology/Imaging
• AXR 3 views ( R /O obstruction - free air, volvulus, air - fluid levels)
• Abd US ( RUQ pain - hepatic /pancreatic /gallbladder pathology)
• CT abdomen
. .
• CT head ( focal neuro Sx decreased LOC , papilledema Sx of meningismus /encephalitis)
Special Tests
• Esophagogastroduodenoscopy ( EGD): chronic N/V with no cause ID'd after routine workup
3EATMENT
Emergent - IV fluids to correct dehydration (NS bolus) , correct electrolyte abnormalities
Medical (treat underlying cause)
> Gastroenteritis (i.e., cipro if mod/severe)
> Migraine: pain control ( i.e., tryptan)
> GERD. PPI
> Medication side effect ( titrate dose or change to alternative agent )
• Symptom control
> Ondansetron 8 mg PO/IVq8h
> Metoclopramide 5 - 10 mg PO/IV q 6h (contraindicated in complete bowel obstruction)
> Dimenhydrinate 25 - 50 mg PO/IV/ IM q6h ( best for vestibular causes of N/V)
> Diclectin ( if pregnant)
> Analgesia as needed
• Nasogastric tube decompression for mechanical small bowel obstruction if associated with significant N/V or distension
Interventional
• Therapeutic EGD for PUD or GIB
• Air enema for volvulus
• Surgery for bowel obstruction, appendicitis, cholecystitis
KEY POINTS
• . . . .
Obesity is a complex multifactorial condition that can exist with other comorbidities such as HTN CAD DM OA depression .
.
GERD and obstructive sleep apnea
• BMI and waist circumference are most commonly used clinically to assess obesity
• Management of obesity can include both pharmacological and non- pharmacological modalities - counselling an obese patient is of
utmost importance
DIFFERENTIAL DIAGNOSIS
Common Conditions
• Exogenous
V
>* c > Excess energy intake, insufficient energy expenditure
u > Iatrogenic ( antidepressants, anti - epileptics, antipsychotics, glucocorticoids, insulin, hypoglycemics)
E T3
Li. 0»
flj • Endogenous
2 . . . .
> Endocrine ( Hypothalamic syndrome Cushing' s syndrome Hypothyroidism PCOS DMT 2, hypogonadism)
.
> Genetic (e.g. Prader - Willi)
> Fluid retention: edema, ascites, effusion
DIAGNOSTIC CRITERIA
Class BMI (kg/m2) Obese Waist Circumference (cm)
Underweight < 18.5 Ethnicity Men Women Men ^ Waist to Hip Ratio
>0.9
Healthy Wt 18.5 - 24.9 European > 94 > 80 Women >0.85
Overweight 25 - 29.9 .
South Asian Chinese > 90 > 80
HISTORY
ID .
Age gender
CC Wt gain
HPI Onset, duration, amount, and rate of Wt gain
Location of Wt gain: generalized vs. central
Eating and exercise frequency, amount/intensity, and timing
Assess readiness to change Wt and obstacles for Pt
Assess for eating disorder or depression
Fatigue,cold intolerance, constipation (hypothyroid)
Easy bruising, myopathy (Cushing’s syndrome)
Menstrual changes, infertility, hirsuitism ( PCOS)
Congenital disease
PSHX Bariatric surgery
Hypothalamic surgery
Thyroid surgery
MEDS Look for causes of wt increase
FHX Obesity, cardiovascular (Ml, TIA) , endocrine disorders, eating disorders, autoimmune disorders
SOCIAL Support network for healthy eating and exercise
. .
Smoking EtOH or illegal drug use
PMHX CV: HTN, CAD, CHF, varicose veins, stroke, edema
RESP: dyspnea, sleep apnea
Gl: GERD, hepatic steatosis, NAFLD, cholelithiasis, hernias
ENDO: DM, hypothyroidism, Cushing's, hyperlipidemia, hyperuricemia
MSK/DERM: OA
PHYSICAL
General Approach
.
• VS: BP. HR RR. Temp Sp02 . 2 T|
BMI (Wt/Ht2) (kg/m2)
• Waist circumference (measured at top of iliac crest)
• Waist - to - hip ratio (hip measured at widest diameter around the buttocks)
Q
-
2. wi
INVESTIGATIONS
Laboratory Investigations
• Assess comorbidities
> Fasting glucose, HbAlC
.
> Lipid profile ( total cholesterol, TG LDL, HDL, total cholesterol)
• Look for endogenous causes when clinically appropriate
> TSH
> Overnight low - dose dexamethasone suppression test
.
> Free testosterone LH /FSH ratio, DHEAS
TREATMENT
Treatment Options
• Lifestyle modification ( all BMIs): nutrition therapy, physical activity, cognitive behavioral therapy
• 5 As Strategy for behavior change:
> Ask - explore readiness to change - "Are you concerned about your weight and its effects on your quality of life? "
> Assess - health, effects of obesity on psychosocial factors, complications of obesity
> Advise - plan of action, treatment options, medications, low - calorie diet, surgery
> Agree - negotiate treatment plan agreement respectfully - emphasize that even modest weight loss ( 5 - 10%) has significant
health benefits
> Assist - identify facilitators and barriers to treatment plan - provide resources and follow -up with physicians and other health
professionals
• Dietary interventions - dietary adherence and caloric restriction most important. Mediterranean diet has strongest evidence for
improving health outcomes (decreased cardiovascular events and death vs. low fat diet ). No clear benefit of low fat vs. low carb.
• Physical activity interventions - 30 - 60 min of moderate intensity exercise /day - greater efficacy when combined with dietary
interventions
• Pharmacotherapy ( for select patients who have failed lifestyle interventions or who have a BMI > 27 + risk factors, or BMI > 30)
.
- orlistat sibutramine, liraglutide injection
• Bariatric surgery ( BMI > 35 + risk factors or BMI > 40) - Gastric bypass, laparoscopic adjusted gastric banding
Follow -up
• Regular assessment of obesity comorbidities and emphasize healthy lifestyle change as the goal rather than amount of weight loss
• Wt maintenance and prevention of Wt regain ( = chronic illness)
Referrals as indicated
.
• Registered Dietitian, Psychologist or Psychiatrist (if clinically indicated), Endocrinologist for endogenous causes Bariatric Surgeon,
exercise health professional
EY POINTS
• An anatomic approach is useful for classifying and diagnosing respiratory tract infections
• Most infections are caused by viruses and are self -limited
• Treatment should be aimed at alleviating severity and duration of symptoms
• It is difficult to differentiate bacterial from viral infections based on clinical evaluation
DIFFERENTIAL DIAGNOSIS
Definition Differential Diagnosis
<u Upper respiratory tract infection Occurs above the level of the glottis Common cold, sinusitis, pharyngitis,
>c (URTI ) (mouth, nose, sinuses, throat ) tonsillitis, laryngitis, influenza
E T3
TO
Lower respiratory tract infection Occurs below the level of the glottis Pneumonia, bronchitis, bronchiolitis, influenza
( LRTI ) ( trachea, bronchi, alveoli)
u. <D
2
Common Conditions
Condition Microbiology Symptoms Other Considerations
• Rhinovirus 30 - 50%, Coronavirus 10- Nasal congestion/nasal discharge, Usually self -limited in 5 - 14 d
Viral URTI
( common cold ) .
15% Influenza viruses 5 - 15% sore throat, cough, H/ A, malaise,
fever
• Unknown 20%
• Viral 90% Sore throat, fever Treat within 9 d of symptom
Acute Pharyngitis
• GAS . R-haemolytic streptococci (Group • Absence of cough, rash (bacterial) onset to prevent acute
rheumatic fever if swab
C and G) • Coryza, conjunctivitis, cough,
hoarseness, diarrhea (viral) positive for GAS
• N. gonorrhea
• Viral Persistent URTI sx: nasal congestion/ Treat with abx for Sx > 10 d or
.
• S pneumoniae, H. influenzae, M . purulent nasal discharge, facial pain, worsening Sx after 5 -7 d
Sinusitis fever, maxillary toothache, and/or
catarrhalis
facial swelling
• Anaerobes if chronic
Influenza A, B, and C viruses High fever, H/ A, extreme fatigue, sore Lasts 3 d-2 wks
Influenza throat, cough, N/V, myalgias and/or
diarrhea
Primarily viral ++ Coughing ( up to 3 wks - can be Self-limited; often need to rule
Acute Bronchitis productive), fever, constitutional out pneumonia by CXR
symptoms
• Typical pneumonia: S. pneumonia. H. Fever, productive cough, dyspnea,
Crackles on exam and
influenzae, S. aureus tachypnea, and/or pleuritic chest
consolidation/infiltrate on CXR
Pneumonia pain
• Atypical pneumonia: Legionella sp., C.
pneumoniae, Mycoplasma pneumoniae
High Mortality/Morbidity: epiglottitis, pneumonia, retropharyngeal abscess, submandibular space infections, HIV
HISTORY
ID • Age, gender
CC • Nasal discharge/congestion, cough, sore throat, facial pain, H/A
HPI • Characterize onset, duration, and course
• Nasal discharge /congestion: color, triggers (e.g„ seasonal or exposure to allergens [allergic rhinitis])
• Facial pain ( worse with leaning forward/valsalva maneuver ), facial swelling, tooth pain, hyposmia/anosmia
(sinusitis)
• Sore throat, tender cervical adenopathy, voice change (" hot potato voice"), trismus
• Cough: severity, frequency, any triggers, sputum production, color of sputum, post - tussive emesis (pertussis)
• Fever: temperature measurement, Tylenol/Advil use and last dose used
• Other associated symptoms: dyspnea, pleuritic chest pain, vomiting, malaise, anorexia
• Recent exposure to sick contact (daycare, school, work, home), travel Hx (fungal or tuberculosis)
RED FLAGS • Epiglottitis (stridor, drooling, febrile, unvaccinated against
HiB), retropharyngeal abscess (neck pain, febrile,
dysphagia, hx penetrating trauma), submandibular space infection (febrile, mouth pain, drooling, swollen+tender
.
floor of oropharynx, woody induration to submandibular area) HIV (painful ulcers, risk factors)
PMHX • Immunizations up to date ( pertussis booster ) ; chronic illness (CHF, COPD, asthma, CF, CRF, liver disease), lung
cancer, immunocompromised (HIV, DM), recurrent strep pharyngitis, vaccinations, hospitalization (last 3 mos)
ROS • HEENT: problems hearing, sinus problems, allergies ( seasonal), hoarseness, anosmia
• CV/RESP: palpitations, dyspnea, SOB, wheeze
.
• Gl: N/V/D abdominal pain, anorexia
• MSK/DERM: myalgia, rashes (mycoplasma)
PHYSICAL
General Approach
• If signs of severe distress: ABCs, call for help (epiglottitis - experienced person to intubate)
• Assess for respiratory distress: cyanosis, nasal flaring, stridor, audible wheeze, pursed lip breathing, use of accessory muscles,
splinting, tripoding, unable to complete a sentence in one breath 2 -n
HEENT 2 a>
Q. i
• Inspection: perioral cyanosis, periorbital edema,
Mclsaac Classification for Strep Throat n 3
facial swelling, nasal erythema/swelling, tympanic 3 •<
membrane (bulging or opacification), oropharynx/ Mclsaac Classification Mclsaac Modification of the Centor Strep Score3
tonsils (erythema, exudate), displaced uvula
Hx of fever ( > 38.3°C) (+1) Total Points Likelihood Ratio
(peritonsillar abscess), mouth ulcers
• Palpation : tenderness over paranasal sinuses or Tonsillar exudate (+1) - 1 toO 0.05
maxillary teeth (sinusitis), palpable and/or tender Cervical lymphadenopathy (+1) 1 0.52
cervical LNs
RESP Absence of cough (+1) 2 0.95
• Inspection: AP diameter Age < 15 y/o (+1) 3 2.5
• Percussion: lung fields for consolidation,
Age > 45 y/o (-l) 4 or 5 4.9
diaphragmatic excursion
• Palpation: chest wall tenderness, tactile fremitus
• Auscultation: decreased AE, localized crackles, bronchial breath sounds, whispering pectoriloquy, egophony, pleural rub
( pneumonia)
INVESTIGATIONS
Laboratory Investigations
. .
• CBC- D, electrolytes, glucose Cr ALT, blood cultures ( Hx of chills /rigors)
• GAS throat culture if > 2 points on Mclsaac ’s Classification ( see table)
• ABG: 02 sat < 90%, COPD, chronic 02 use
• Sputum gram stain and culture ( productive cough and suspected pneumonia /bronchitis)
• Monospot ( if infectious mononucleosis suspected)
Radiology/ lmaging
• CXR: PA and lateral views (if abnormal lung auscultation/pneumonia suspected)
• Lateral neck XR (if epiglottitis or retropharyngeal abscess suspected)
• Laryngoscopy (if epiglottitis suspected)
UREATMENT
Emergent:
• 02 if hypoxic. Ensure adequate hydration, analgesics /antipyretics for pain and fever.
Assess need for hospitalization for pneumonia: CURB - 65 or Pneumonia Severity Index ( PSI)
Condition Treatment
Viral URTI OTC for Sx control (not approved in children 2 y/o)
GAS Pharyngitis Delay abx until culture confirms GAS
Penicillin VK or macrolides x 10 d to prevent acute rheumatic fever; clindamycin if B -lactam allergy
Sinusitis Amoxicillin x 5 -7 d
Influenza OTC for Sx control
Consider oseltamivir or zanamivir x 5 d in high risk populations and very ill
Acute Bronchitis Humidity/ smoking cessation; may use bronchodilators for Sx control
Pneumonia Community acquired: doxycycline +/- amoxicillin
Moderate/ severe or hospitalized: ceftriaxone + doxycycline or macrolides
:ollow -up
• Persistence of high fever and severe symptoms for > 2- 3 d
• Routine F/U in asymptomatic patients is not required for acute pharyngitis or bacterial sinusitis
. .
• Post therapy CXR ( at 6 wks) for extensive/necrotizing pneumonia, smoker EtOH. COPD > 5% Wt loss in past mo and > 50 y/o
.
Prevention: hand -washing, vaccinations (Influenza Pneumococcal, H. influenza if < 4 y/o)
KEY POINTS
• Understanding the epidemiological trends in STIs and risk factors for transmission and infection is key to this station
• Management of STI and contraception are closely related - screening for high risk behavior may be warranted when patients
present for contraceptive advice. Remember to use simple, non- judgmental language.
DIFFERENTIAL DIAGNOSIS
Organism Incidence Affected Populations
C. trachomatis Most common bacterial STI f 20- 29 y/o . 9 15-24 y/o
>C
<D .
N gonorrhea 2nd most common bacterial STI C 20 - 29 y/o
(2/3 of cases in
. 9 15 - 24 y/o
'
)
u
E T3 HPV Very common V and
;
of all ages
<Z Q )
LL HSV-1and HSV- 2 Common > K , affects adolescents and adults
2 ;
HISTORY
ID .
Age gender
CC .
Genital symptoms associated with STI (discharge, dysuria abdo pain, testicular pain, rashes, lesions, dyspareunia)
Systemic symptoms associated with STI (fever, wt loss, lymphadenopathy, joint pain)
HPI Onset and duration of symptoms
Date of last sexual contact, methods of protection
Previous STI/HIV testing
Previous episodes of STIs and treatment
RED FLAGS .
HIV hepatitis co-infection
PID, sepsis
STI in pre - pubertal child: evaluate for sexual assault
PSHX Blood transfusions
PO&GHX .
Last normal menstrual period, last Pap test GTPAL
MEDS OCP (+ other methods of birth control)
Vaccinations: Hep A/B HPV.
ALLERGIES Especially to abx, including penicillin/cephalosporin
SOCIAL & .
Intercourse with men women, both? Regular sexual partner? Number of sexual partners in the past 2 mos? Past
SEXUALHX yr?
Sexual acts: perform/receive, oral/vaginal /anal sex
Risk assessment: sexual encounters with foreigners, trade sex for money/drugs/shelter, paid for sex or been paid
.
for sex condom use
Use of EtOH/drugs/lVDU (shared injection equipment ), tattoos or piercings, sterile equipment
. .
Homeless? (If so where does the patient sleep?); If not who does the patient live with?
ROS .
HEENT: throat lesions, conjunctivitis LNs
CV/RESP: signs of tertiary syphilis (gummas, neurosyphilis)
.
Gl: RUQ pain ABD pain, bowel symptoms ( dyschezia diarrhea).
.
GU: dysuria frequency, urgency, change in vaginal discharge, urethral discharge, genital sores, hematuria
MSK / DERM: rashes, joint inflammation (Reiter ’s/reactive arthritis)
141 nton M.
PHYSICAL
General Approach
.
• VS: BP, HR, RR Temp, Sp02
• Systemic signs: Wt loss, enlarged LNs
Inspection
• Mucocutaneous regions including the pharynx
• Eyes: uveitis, conjunctivitis
• External genitalia: cutaneous lesions, inflammation, genital discharge, anatomical irregularities
• Rectal/anal exam ( when relevant hx given - e.g., anal sex )
Examination of Males
• Palpate scrotal contents with attention to the epididymis ( tenderness): retract foreskin to inspect glans (inflammation, lesions /
chancre, discharge)
Examination of Females
• Expose and visualize vaginal orifice ( swelling, inflammation, discharge): illuminated speculum exam of vaginal cavity (obtain
specimens if necessary): bimanual pelvic exam to detect uterine or adnexal masses or cervical motion tenderness 2n
2
INVESTIGATIONS
Laboratory Investigations
n
5’<
a>
— •
f
• CBC- D ( WBCs), G - HCG
.
• EIA: Syphilis anti-HIV Ab, HBsAg, anti - HepB Ab, anti-HepC Ab
Swabs
.
• Endocervical: for C. trachomatis (NAAT, antigen detection tests) and N . gonorrhea ( NAAT culture). Include pharyngeal and anal swabs
if indicated.
• Lesion: swab the lesion bed ( HSV) or ulcer base
( T. pallidum - dark - field microscopy or DFA testing)
Urinalysis
• NAAT for C. trachomatis and N. gonorrhea
(First catch urine >120 min post last void)
.
• R & M C & S if urinary symptoms
TREATMENT
Treatment Options (see table)
Treatment Options for Common STIs
Further Workup: Rx Route Duration
• Post - test counseling Azithromycin 1 g PO Single dose
> Safer sex practices Chlamydia
> Case reporting requirements (to health unit and Doxycydine 100 mg PO bid x 7 days
sexual partners) vary by provinces and territories
Cefixime 800 mg
> In Canada, nationally reportable STIs: Chlamydia, PO Single dose
Plus Azithromycin Ig
gonorrhea, infectious syphilis, HIV
Gonorrhea IM
> Partner notification through either the index case, the Ceftriaxone 250 mg
physician or a public health official Single dose
Plus Azithromycin Ig
PO
• Immunization against HepB and HPV, if not already
administered Penicillin B 2.4 mu IM Single dose
Syphilis
• In at -risk population (e.g„ MSM, sex trade), consider Doxycydine 100 mg PO bid x 17 days
HepA vaccine
Herpes Acyclovir 200 mg PO 5 / day x 5 - 10 days
Follow-up
• Re - evaluation at 3- 4 wks if: Simplex Valacyclovir lg PO bid x 10 days
> Symptoms do not resolve
bid x 3 days, 4 days
> Non-compliance with therapy Podofilox 0.5% solution Topical
off, repeat 4 wks
> Patient is an adolescent or pregnant woman
.
• If immune compromised HIV +ve
HPV
Imiquimod ( Aldara) 5%
Topical
3 / week (max 16
> Refer to Infectious Disease cream wks)
Cryotherapy,
electrocautery, laser, Provider administrated
surgery
KEY POINTS
• It is important to differentiate primary causes from secondary manifestations of systemic disease
• Physicians must be able to clearly communicate and describe skin lesions
• Many skin/hair /nail conditions are first found by physicians; therefore, it is important to perform a complete skin/hair/nail exam
DIFFERENTIAL DIAGNOSIS
Primary Skin Disease Cutaneous Manifestations of Systemic Disease
Infections
Cellulitis, folliculitis, impetigo, dermatophytosis Endo .
Addison's Cushing's, thyroid disease DM .
( tinea), candidiasis, pityriasis versicolor
Peripheral vascular disease,
<D Vesiculobullous Pemphigus, herpes simplex, herpes zoster, varicella
CV
congenital heart disease
>C
u Dermatitis, Atopic dermatitis, seborrheic dermatitis, ID HIV, sepsis, viral exanthem
E Eczema lichen simplex chronicus
.2
Li <D GU Renal dysfunction. PCOS
Papulosquamous Psoriasis, pityriasis rosea, lichen planus
Gl . .
Liver dysfunction IBD celiac disease
Erythema
.
Urticaria
Allergic urticaria, erythema nodosum, rosacea Connective tissue disorders ( SLE,
MSK
.
dermatomyositis scleroderma) RA .
Skin Cancer Melanoma, basal cell carcinoma, squamous cell carcinoma
Malignancy Hodgkin’s disease
Acne vulgaris Mild, moderate, severe; with or without scarring
Stevens -Johnson syndrome,
Acrochordon ( skin tag), scabies, vasculitis, vitiligo DrugRxn .
angioedema erythema multiforme,
Other Systemic disease: acanthosis nigricans (insulin resistance), urticaria, vasculitis, dermatitis
dermatitis herpetiformis (celiac), pretibial myxedema (Grave's)
HISTORY
ID • Age, gender, ethnicity, occupation
CC • Lesion of skin or nails; change in hair growth
HPI • Onset, location, duration of lesion, persistent vs. intermittent
• Associated symptoms: pruritus, pain, burning
• Changes in lesion over time (color, size, bleeding, pain)
• Previous treatments if previous or recurrent episodes
• Aggravating and alleviating factors: sunlight, temperature, medication, herbals
• Recent illnesses or stressors (hospitalization, pregnancy), exposure to toxins or chemicals, chemotherapy, trauma
• Cracking, ridging, brittleness of nails
• Pattern, duration of hair growth or loss
RED FLAGS • Constitutional symptoms ( fever, chills, wt loss, malaise), chronic or atypical infections (HIV), arthralgias
PMHX • Allergies, atopy, skin cancer, chicken pox, measles, other skin conditions
.
• Chronic disease: DM, rheumatologic thyroid, collagen, vascular
LaHYSICAL
General
Simple Screen for Dehydration
• ABCs if unstable, level of consciousness
• Drugs (e.g., diuretics)
• Vital signs, including orthostatic BP (decrease in SBP > 20 mmHg , DBP > 10mmHg) and pulse
• End of life
(increase in HR by >30 bpm* ), TRR , postural dizziness that leads to an inability to stand’, urine
• High fever
output - *evidence- based high value physical signs for acute blood loss
• Yellow urine turns dark
HEENT: inspect for dry and sunken eyes, dry mucous membranes, longitudinal furrows on • Dizzy (orthostatic hypotension)
tongue, low JVP • Reduced oral intake
MSK / DERM: inspect for obvious bleeding, dry axilla, skin turgor, wet/clammy skin , draining • Axilla dry CD
wounds/ulcers, collapsed veins; palpate for skin turgor ( forearm or subclavian), capillary refill • Tachycardia .
Q fD
0.5
. Cap refill T
Confusion NS
Weakness NS NS Try oral rehydration first if 5% or less
Adapted from Evidence- Based Physical Diagnosis. 3rd ed.. Steven Adapted from The Rational Clinical Examination: Evidence-
McGee. MD and The Rational Clinical Examination: Evidence-
.
Based Clinical Diagnosis David L.Simel Drummond Rennie
.
Based Clinical Diagnosis David L. Simel Drummond Rennie
INVESTIGATIONS
Laboratory Investigations
• CBC ( Hgb. Hct ) , electrolytes. Ca 2 * . creatinine , urea , glucose
• Water deficit = [0.45 x basal body Wt (kg) ] - [ 140 mmol / L x basal body Wt ( kg ) x 0.45 ]
serum Na * (mmol /L)
‘Note: Water deficit equation only used in cases of pure water loss such as diabetes insipidus
Special Tests
• Consider urinalysis, urine Na * . urine osmolality
• Swallowing assessment (if indicated)
L REATMENT
• Ifsevere dehydration or blood loss (shock): 2 large-bore peripheral IV lines, start crystalloid fluids, consider blood transfusion
• Replenish deficits and ongoing losses using PO. IV, or SC rehydration therapy
• Address and correct any electrolyte imbalances
KEY POINTS
• Remember to take a good functional history including ADLs /IADLs .
• In addition to speaking with the patient, try to obtain history from caregiver /family.
.
• Use the physical exam to identify the cause of dementia (e.g. to confirm idiopathic PD vs. Parkinson Plus Syndrome).
• Pay attention to red flags regarding patient safety.
• Always rule out elder abuse.
DIFFERENTIAL DIAGNOSIS
Definition of Dementia:
• Chronic acquired decline in at least one cognitive domain (learning/memory, complex attention, language, visuospatial, executive)
• Impairment of social, occupational, or personal function
• Not due to other psychiatric or systemic illness
Alzheimer ’s Dementia ( AD) Gradual onset memory ( temporal) and visuospatial ( parietal) impairment
Vascular Dementia Acute onset, stepwise deterioration
Lewy Body Dementia (LBD) Visual hallucination, gait instability/falls, neuroleptic senstivity
—ro c CD
Fronto Temporal Dementia ( FTD) Pick ’s - personality, language, executive dysfunction
E :g
CD “O
Normal Pressure Hydrocephalus Gait instability, apraxia, incontinence, dementia
( NPH)
C CD
-2 Infections HIV. CJD (myoclonus, rapidly progressive dementia), syphilis
Metabolic B12 deficiency, thyroid, parathyroid, CKD, cirrhosis
Inflammatory Multiple sclerosis
Other Neoplasm, alcohol, trauma, chronic SDH, drugs ( anticholinergics), depression, delirium
HISTORY
ID • Patient ' s name, age, gender
CC • Forgetfulness, wandering, behavioural changes, incontinence, falls
HPI • Determine patient's baseline cognitive status
• Pattern of decline ( smooth or stepwise)
• Hallucinations
• Parkinsonian features (hypomimia
abnormal gait)
. . .
hypophonia drooling, tremor, rigidity, bradykinesia micrographia, falls,
.
RED FLAGS • Memory ( wandering, doors unlocked, stove on losing objects)
• Driving ( traffic violations, accidents/near misses, injury, death)
• Agitation and behavioral changes:
» Aggression/agitation (verbal, physical, sexual)
> Hallucinations ( visual, auditory), delusions
> Coarsening (exaggeration of pre -morbid character traits)
NEURO
.
• CN tone, strength, reflexes, sensation (esp. loss of sensation in lower extremities)
• Hearing ( whispered voice and otoscope) and vision ( Snellen chart ) assessment
• Gait and balance (Romberg, sternal nudge, unipedal stance, tandem stance)
• Timed "Up and Go Test ” - allow patient the use of their mobility aid
.
> Begin with patient seated in chair. Ask patient to stand up walk 3 m, turn, and return to chair
> > 12 s indicates high risk for falls
• Frontal release signs: glabellar tap, grasp reflex, snout reflex, palmomental sign
• Look for signs of parkinsonism: masked face, pill rolling 3 Hz resting tremor, bradykinesia, cogwheel rigidity, postural instability,
gait abnormalities ( shuffling gait, fenestration, reduced arm swing, en-bloc turning)
HEENT - Thyroid exam, lymphadenopathy
.
Other - Routine CVS Resp, Gl, MSK (note reduced ROM and/or pain limiting mobility), skin exam ( note any sacral ulcers)
INVESTIGATIONS
Investigations should be used to rule out reversible dementias and common causes of delirium.
Laboratory Investigations
. . . . . .
• CBC, lytes, BUN Cr Ca.Mg.P04, glucose/HbAlc TSH LFTs alb B12, INR / PTT, lipids Sir
. .
• Consider (guided by history and physical) - ESR, urine and blood cultures, heavy metals, ferritin, ceruloplasmin, cortisol RPR HIV (0D
--
Q. n>
r t
onEATMENT
Non- Pharmacologic
• Refer to a Geriatrician: Geriatric Day Care
• Issues to consider: failure to cope, driving ( need to inform ministry), advanced /personal directives (health care), power of attorney
.
( financial matters), caregiver education (respite/day programs, home support, nursing homes Alzheimer ’s society)
• Home OT assessment
• Nutrition: have the largest meal of the day in the morning ( AD patients eat more in the am): supplementation more effective if
given between meals rather than with meals
• High- Intensity resistive exercise and strength training: counteracts muscle weakness and physical frailty in very elderly patients
Pharmacologic
• .
Treat reversible causes - depression, thyroid B 12, vascular risk factors, alcohol abstinence
• .
Avoid anti -cholinergics benzodiazepines
• Cognitive enhancement ( DLB, mild -moderate AD)
.
• Acetycholinesterase inhibitors (e.g. donepezil ) - can take 3 months before therapeutic effects
.
> Mild -moderate AD - shown to improve cognitive function and some behavioural sx not disease modification
• Vitamin E and Selegine
DIAGNOSTIC CRITERIA
Diabetic Ketoacidosis ( DKA)
• No definitive criteria. Typically, arterial pH < 7.3, serum bicarbonate < 15 mM. anion gap > 12 mM and BG > 14 mM. Usually T1DM.
.
• Common triggers ( 61's): insulin missed, infection, infarction (Ml CVA ), iatrogenic ( steroids), intoxication ( EtOH), initial dx
Hyperosmolar Hyperglycemic State ( HHS)
• Hyperglycemia, increased plasma osmolality, but negative ketones. Usually T 2DM.
Hypoglycemia
• Autonomic and/or neuroglycopenic symptoms with blood glucose < 4.0 mM. with symptoms responding to glucose in treated DM.
SIISTORY
ID • Patient name, age, gender
CC • DKA: Polyuria, polydipsia, polyphagia, wt .
loss, blurry vision, nocturia, abdominal pain N/V, and altered LOC
• HHS: Intercurrent illness, stress, surgery, altered LOC, confusion, seizures, stroke-like state
• Hypoglycemia: trembling, palpitations, sweating, hunger, nausea, weakness, vision changes, difficulty speaking
_
(TJ
<D
C
HPI • Type 1.2 . or gestational DM. Age of onset, manner of diagnosis (symptoms lab values)
• Self management
,
PMHX .
• Hypoglycemia unawareness, pancreactomy gastroparesis, liver /renal failure, recurrent UTIs, yeast/sinus
infections, autoimmune conditions
MEDS • Oral hypoglycemics, insulin
• Precipitating meds: glucocorticoids, atypical antipsychotics, diuretics, lithium, propranolol, and phenytoin
PHYSICAL
General - ABCs
• Airway: GCS < 9, consider intubation and transfer to ICU
• Breathing: RR, monitor for Kussmaul breathing ( rapid and deep respiration) , fruity acetone breath ( DKA)
• Circulation: postural BP and HR ( if possible), assess JVP, mucous membranes, urine output, and capillary BG
INVESTIGATIONS
Laboratory Investigations:
• ABG ( switch to VBG for subsequent monitoring if pH > 7.0), serum glucose, lytes, urea, creatinine, CBC diff, plasma osmolality,
- .
beta hydroxybutyric acid, urinalysis/urine ketones, TSH troponin, and septic workup if suspect infection
Radiology/Imaging:
• CXR and EKG
EEEATMENT
Orders for Hypoglycemia - Rule of 15 s
• Mild (autonomic symptoms) to moderate (autonomic and neuroglycopenic) hypoglycemia
> Oral ingestion of 15 g of fast carbs (glucose tabs, 3 packs of sugar, A cup of orange juice, 6 LifeSavers, or 1tbsp of honey)
3
> .
Recheck BG in 15 mins. If < 4.0 mM retreat with another 15 g until BG in safe range
• Severe (requires assistance) or unconscious hypoglycemia and > 5 y/o
> .
1mg glucagon SC or IM or 10- 25 g glucose IV (1amp D50W)
Time Intervals:
• Blood gluscose Q1H until DKA resolved
• Electrolytes Q1- 2H until DKA resolved
• 0.45%NaCI • 0.9%NaCI
DKA resolution = BG <14 mM, bicarbonate > 15 mM, venous pH >7.3 and anion gap <12 mM
186
DIABETES - CHRONIC MANAGEMENT .
Current Editors: Elaine Chiu RD CDE Tammy McNab MD FRCPC
HISTORY
ID .
• Patient name, age gender
HPI .
• Type 1.2, or gestational DM Age of onset, manner of diagnosis (symptoms, lab values)
• Metabolic syndrome .
- elevated waist circumference BP. BG, TG, and reduced HDL
• Self management - recent illness, infection, pregnancy, ETOH, drugs, or hospitalizations
_ CD
OJ C
• Therapy - lifestyle, oral hypoglycemic agents (OHAs), insulin
• Glucose monitoring - tracking, insulin noncompliance, frequency, typical glucose/HbAlC measurements
• Chronic complications - microvascular (retinopathy, nephropathy, neuropathy); macrovascular (CAD, stroke,
c u PVD)
CD T3
-M
r-
ni • Foot care - regular foot exams?
-2 RED FLAGS • Hypoglycemia: unawareness or recurrent hyperglycemia
.
• Proliferative retinopathy, progressive nephropathy with signs of decompensation (edema HTN), foot ulcers/
amputations, dysesthedia/abnormal sensation, loss of vibration sense, inability to sense 10 g monofilament
PMHX • CVD . HTN, dyslipidemia. peripheral arterial disease. PCOS, erectile dysfunction. CKD, psych, and smoking
MEDS • OHAs, insulin
• ACE -i/ARBS, statins. ASA. influenza/pneumococcal vaccine
FHX • DM and associated complications
. .
• Ht Wt BMI
.
• Vital Signs: BP/orthostatic hypotension (diabetic autonomic neuropathy) HR /delayed postural HR response, RR
HANDS
• Stiff hands with + Prayer sign (limited joint mobility or diabetic cheiroarthropathy) , Dupuytren’s contracture
• Assess for burning, paresthesias, sensory loss in the median nerve distribution, and positive Tinel' s and Phalen' s test (carpal tunnel
syndrome or median nerve mononeuropathy )
DERM
• Inspect for presence of infections ( folliculitis, cellulitis, ulcers, necrobiosis)
HEENT
.
• Inspect for Acanthosis nigricans (can also be present in Cushing’s, obesity PCOS) JVP .
EVES
.
• Pupillary response to light EOM, and fundoscopy. Should see ophthalmology for comprehensive exam of diabetic retinopathy.
CV
• Palpation - assess for carotid & femoral artery bruits; peripheral artery pulses, displaced apex
INVESTIGATIONS
Individualize treatment targets
• HbAlC 7.1- 8.5 % more appropriate if multiple morbidities, limited life expectancy, hypoglycemia unawareness or high level of
functional dependency
• HbAlC < 7.0%, FPG 4.0- 7.0 mmol /L , 2 hr postprandial 5.0- 10.0 mmol / L and if HbAlC target not met then 5.0 - 8.0 mmol/ L
MANAGEMENT
Care Investigations Targets Follow Up
• Blood Pressure • Postural BP • BP < 130/80 • Baseline BP at diagnosis
• Check BP at every diabetes visit and target to treat
• Dyslipidemia • . . .
TC TG HDL calculated • Primary: LDL < 2.0 • Baseline investigations at diagnosis
LDL mmol/L • If meds not initiated, yearly investigations
• If meds started, initially monitor at 3 months and intensify
regime if target not met
• Coronary • Baseline ECG and • .
Optimize BP glycemic • Stress test if angina, peripheral arterial disease, carotid bruits.
Artery Disease Q2years if > 40 y/o, end control, and lifestyle. TIAs, stroke, resting abnormalities on ECG
(CAD) organ damage, cardiac • Statin therapy if > 40 y/o OR macro /microvascular disease OR
risks, or > 30 y/o with DM long duration of DM ( > 15 yrs and > 30 y/o)
duration > 15 yrs
• Chronic Kidney
Disease (CKD)
• Random urine ACR - 2/ 3
samples in 3 months
• Normal ACR < 2.0 mg/
mmol /L
• T1DM - exam 5 years post Dx and annually if no CKD
• T 2DM - exam at Dx and annually if no CKD
SET
(V
• .
Serum creatinine eGFR. • Normal eGFR > 60 ml/ • ACEi or ARB with either HTN or albuminuria
CL fD
and urinanalysis min • 24 hr urine collection for protein/albumin is gold standard but S3
cumbersome. Consider if suspect ACR is falsely positive. D CD
<D “
• Retinopathy • N /A • Early detection and treat • T1DM - exam 5 years post Dx and then annually
• .
T 2DM - exam at Dx then 1- 2 years if no retinopathy
• Neuropathy • Foot exam (see below) • Early detection and treat • T1DM - exam 5 years post dx and then annually
(Foot exam) • T 2DM - exam at Dx and then annually
Additional Interventions
• Lifestyle: healthy weight , regular exercise, smoking cessation, healthy eating
• T1DM: Insulin
• T 2DM: Oral hypoglycemic agents + /- insulin for T 2DM
• Pneumococcal vaccine if > 65 y/o and annual influenza vaccine
KEY POINTS
•Always remember Airway, Breathing, and Circulation when you are assessing a patient. If there is an abnormality, stop your
physical exam immediately - your patient may urgently need more invasive procedures
• Timeline is important when thinking about the differential diagnosis
• Always get a CXR and compare with previous CXR for changes
• Conduct your exam in an organized manner ( from periphery to central).
DIFFERENTIAL DIAGNOSIS
Time of Onset Respiratory Cardiac Other
• Asthma • CHF • Anaphylaxis
• PE • .
Ml angina • Panic attack
Acute • FB aspiration • Arrhythmia • Hyperventilation syndrome
(min) • Hemo/pneumothorax • Rupture or dysfunction of
• Toxic airway damage papillary muscle
• Aortic dissection
• Infection: pneumonia, • CHF • Anemia
Subacute bronchitis • Pericardial effusion/
—
OJ C
CD (hrs-days) • AECOPD tamponade
• Stable angina
E :C
CD ~0
• Asthma
• COPD • CHF • Anemia
<D • Pleural effusion • Stable angina • Deconditioning
Chronic • Restrictive lung disease
(days- yrs) • Interstitial lung disease
• Cystic fibrosis
• Lung cancer
HISTORY
. .
Note: If patient is unstable, proceed with ABCs first, then obtain SAMPLE Hx: (Symptoms (related) Allergies Medications PMHx .
relevant), Last meal, Events prior to presentation)
ID • Patient name, age, gender, occupation
CC • SOB
HPI • OPQRST (onset, palliating/aggravating factors, quality, radiation, severity ( at rest or with exertion), timeline) of
SOB, previous episodes of SOB
• Chest pain (pressure -like angina vs pleuritc vs MSK -related)
• Orthopnea, PND, leg swelling for cardiac etiology
• Hemoptysis, leg swelling/pain/erythema, recent surgery/immobilization for DVT/ PE
• Trauma: penetrating or crush trauma ( with blood loss)
• .
PreviousURTI (OPQRST),rhinorrhea,pharyngitis cough ± sputum, swallowingdysfunction,sick contacts, travel
hx for pneumonia or URTI
• Environmental exposures: asbestos, allergens, chemicals, cold, smoke ( tobacco, marijuana, e -cigarettes)
RED FLAGS • Fever, night sweats, change in wt (malignancy) syncope ( PE), chest/shoulder /arm pain ( Ml), hemoptysis
PMHX . .
• Asthma, COPD CHF malignancy, previous DVT/PE, cardiac risk factors
PSHX • ..
Thoracotomy, cardiac surgery (e g. phrenic nerve paralysis secondary to surgery)
PO & GHX • Pregnancy
MEDS • ILD risk ( amiodarone, bleomycin, methotrexate, nitrofurantoin), OCP ( VTE), immunosuppressive drugs,
.
coumadin, heparin, immunizations (influenza) IVDU (talc lung)
ALLERGIES • Environmental, food, medications
.
• Palpation: tracheal deviation, tracheal tug lymphadenopathy laryngeal . McGee. MD and The Rational Clinical Examination :
Clinical Diagnosis David L. Simel. Drummond Rennie
Evidence - Based
.
> Kussmaul 's sign = paradoxical rise in JVP with inspiration, seen in constrictive pericarditis, restrictive CM massive PE. R - CHF
S 3
RESP
3 Q
n> —
)
.
• Inspection: thoracic AP diameter ( barrel chest - COPD) asymmetry, deformities, scars, intercostal indrawing, diaphragm motion
• Palpation: chest wall deformities, mass, tenderness, chest wall expansion, tactile fremitus (increased with consolidation, reduced with
pleural effusion)
• Percussion: lung fields (do not forget upper lobes on anterior chest wall) for hypo/ hyper - resonance, diaphragmatic excursion
• Auscultation: all lung lobes ( R vs L ) comment on air entry, crackles, wheeze, stridor, prolonged expiration phase ( < 3 sec normal:
*
.
> 9 sec COPD) broncophony and egophony (consolidation)
CV
• Inspection: pacemaker insertion scars, visible pulsations, edema in all limbs and sacrum
• Palpation: palpable thrills, heaves, apical beat (diameter, displacement, amplitude, duration)
• Auscultation: S3/S 4, murmur, rhythm ( AF)
.
• If clinically indicated: echo CTPE/VQ scan HR > 100 bpm 1.5
Special Tests (if patient stable and clinically warranted) Hemoptysis 1
.
• PFT/ PEFR methacholine challenge test, shunt test ( see if Sa02 improves with Malignancy 1
administration of 02), oximetry, sleep study
Clinical Probability: Low (0- 2) 3%:
Surgical/Diagnostic Interventions Intermediate ( 3 - 6) 28%: High ( > 6) 78%
• Thoracocentesis (pleural effusion), needle decompression + chest tube (tension
Modified Wells: > 4 PE likely: < 4 PE unlikely
pneumothorax ) , bronchoscopy if indicated
Adapted from J Thromb Hemost 20C0;83:416-420, 2008:6:772 &
PE Rule - Out Criteria ( PERC): Acute PE can be excluded without further diagnostic JAMA 2006
testing if the patient meets all PERC criteria AND there is a low clinical suspicion.
. . . . .
• Age < 50 y HR < 100 bpm 02 Sat > 95% and absence of hemoptysis, estrogen use prior DVT/ PE unilateral leg swelling, and surgery/
trauma requiring hospitalization within the past 4 weeks
TREATMENT
.
Emergent: High flow 02 mask NIV, personnel and equipment for intubation (if GCS < 8, then intubate): cardiac and Sa02 monitors
.
Treatment options: medical and surgical Tx dependent on etiology e.g. needle decompression for tension pneumothorax,
.
bronchodilators and NIV for AECOPD diuretics for CHF
Follow-up: especially with disease where frequent exacerbations affect long- term outcome ( asthma, COPD)
Psychosocial support, breathing control, use of coping strategies (i.e., relaxation techniques) may reduce dyspnea
KEY POINTS
• Falls are often multi - factorial in nature - keep assessment broad to prevent missing additional contributors to falls
• Multiple falls in a patient can be a sign of underlying chronic disease or functional disability
• Organize your differential diagnosis into intrinsic, extrinsic, and contributing factors
• Focus on global risk reduction, education, and treatment for specific diseases causing falls
DIFFERENTIAL DIAGNOSIS
Common Etiologies of Falls
Intrinsic Causes Extrinsic Causes Contributing Factors
• -
Syncope /pre syncope: vasovagal, • Drugs: anticholinergics, • Sensory: visual impairment (use
cardiac (conduction, valvular, vascular, .
antihypertensives, diuretics EtOH of glasses), auditory impairment,
peri/myocardial diseases) • Environment: thick rugs, furniture peripheral neuropathies
• Dizziness: postural dizziness, vertigo • Poor Footwear • Motor: weakness, pain, deconditioning
( BPPV, Meniere disease, labrynthitis . • Cognition: delirium, dementia
.
brainstem CVA) disequilibrium
. . .
• MSK: OA RA OP spinal stenosis,
deconditioning
—ns 0)
.
• Neurogenic: CVA seizures .
£D !y
C
.
Parkinsonism ALS, NPH
< T3
c| HISTORY
ID • Patient ’s name, age, gender
CC • Fall ( s)
HPI •S -
- Symptoms associated with falls: nausea, warmth, diaphoresis (pre syncope), chest pain, dyspnea
(cardiovascular ), no warning and immediately aware following fall (cardiac conduction) , dehydration, bleed,
anemia (orthostatic ), perception of movement/spinning (vertigo), post -ictal confusion (seizure), leg pain /
. .
immobility (MSK) unilateral weakness (CVA) impaired gait, incontinence, confusion ( NPH)
• P - Previous falls
• L - Location: home environment, outdoor
• A - Activity preceding fall: exertional (cardiac), up from sitting/laying (orthostatic), pre -ictal deja vu (seizure),
stressful situation (vasovagal)
• T - Time of fall and time on ground: long time spent on ground a risk factor for rhabdomyolysis
• T - Trauma: cause of fall, characterize resulting injuries (OPQRST hx) associated symptoms, timeline
RED FLAGS • Loss of consciousness
• Chest pain and/or dyspnea
• Dysarthria, difficulty swallowing, unilateral weakness
• Bowel and /or bladder incontinence, tongue biting
PMHX • Ask about DDx conditions, as well as CV risk factors (DM, HTN, Afib, dyslipidemia)
PSHX • Fracture repair, cardiac valve repair, pacemaker, coronary bypass /stenting
MEDS .
• SSRIs, TCAs, sedatives, anti -psychotics anti - epileptics, benzodiazepines, antiarrythmics, hypoglycemics
.
• Gl: N/V, diarrhea, hematemesis, melena hematochezia
.
• GU: dysuria nocturia ( assess for UTI/incontinence)
• MSK/ DERM: muscle weakness, joint stiffness, gait disturbance
PHYSICAL
General
. .
• Timed Up & Go test (mobility) 10 ft return from seated in chair, further evaluation if > 20s < 10 s normal
• Areas of skin bruising
INVESTIGATIONS
. .
Laboratory Investigations - CBC- D electrolytes, creatinine, glucose, troponin B12, TSH, CK
13
.
Radiology/Imaging - Extremities X - ray ( suspected fracture) CXR, CT head
0)
Q. n>
. . .
Special Tests - ECG (cardiac) Holter (dysrhythmia), toxicology screen ( substance use) EEG (seizure) EMG/NCS (peripheral nerve £3
dysfunction) D Q)
CD —
L REATMENT
Emergent - Ensure patient is stable
.
> If prolonged time spent on ground, consider hypovolemia risk AKI, and rhabdomyolysis start IV fluids immediately
Treatment Options
• Prevent future occurrence by multifactorial risk assessment and intervention:
> Stop/taper potentially offending meds
> Educate on good fluid intake to decrease hypovolemia risk, 1.5 - 2L/day
> Encourage standing slowly and pausing before walking if orthostatic hypotension
> Optimize home environment: remove loose rugs, install bath/stair rails, adequate lighting, bedside floor mats, low bed
> Encourage hard - soled, wide based shoes, grippy socks
> Balance retraining/group exercise programs (e.g., tai chi)
• Treat underlying etiology
> Cardiac: bradyarrhythmia (pacemaker ) , tachyarrhythmia ( intracardiac device) , valvular repair
.
> Vertigo: vestibular rehabilitation (BPPV) conservative therapy ( labyrinthitis)
> MSK : physiotherapy, anti -inflammatories
.
> Neurological: anticonvulsant (epilepsy) , tPA ( acute CVA when indicated), referral to neurology
Follow - up / Referrals
. .
• Depends on injuries sustained, cause of fall. PT OT Home Care, home hazard assessment.
KEY POINTS
• Rule out red flag signs /symptoms of cauda equina syndrome and stroke before proceeding to detailed history and examination
neurogenic gait disturbance
• A full neurological exam and gait assessment are required to narrow the differential for
• Do not neglect to perform a focused MSK exam to rule out mechanical pathology
DIFFERENTIAL DIAGNOSIS
Neurogenic Etiology Non-neurogenic Etiology
-
• Extra pyramidal: Parkinson's disease • Orthopedic issues
• Frontal lobe: any frontal lobe lesion including NPH and cerebrovascular disease • Visual disturbance
• Weakness: UMN .
( MS stroke) vs. LMN (cauda equina syndrome, mononeuritis) • Muscle disease
• Spasticity: UMN (post - stroke, cerebral palsy, spinal cord lesion) • Pain
.
• Sensory deficit (proprioception): DM syphilis, Vit B12 deficiency, posterior column spinal cord lesion • Psychogenic
.
• Cerebellar: EtOH, stroke, mass lesion, MS hypothyroidism
• Vestibular dysfunction
HISTORY
—05 C<D ID • Patient name, age, gender
EQJ 2 CC • " Trouble walking”
U
C <D
-2 HPI • Ask patient or patient 's family to describe the gait disturbance ( higher order gait disorders exhibit freezing
feet sticking to the ground)
.
• Duration/onset /precipitant (stroke, EtOH head trauma, injury to extremities)
• Exacerbating factors (darkness, uneven surfaces, going through doorways)
• Weakness (difficulty getting out of the chair or reaching for items); sensory deficits (numbness, not knowing
where their feet are); vertigo
• Tremor (Parkinsonism)
• Falls: frequency, major injuries, pre - syncope
• Previous episodes of sensory/motor deficits ( MS, cerebrovascular )
• Cognition
PHYSICAL
General
Strength Grading System
. . . .
• Vital Signs ( BP HR RR Temp Sa02) and GCS
0/5 No muscle activity
• Cognitive status
NEURO 1/ 5 Muscle twitch
• Cranial nerves: impaired EOM & ptosis ( myasthenia), vertical gaze palsy ( PSP), 2/ 5 Movement in absence of gravity
nystagmus(cerebellarmulti -systematrophy),dysarthria (cerebellarvascularstroke),
tongue fasciculations and jaw jerk ( ALS) 3/ 5 Against gravity
• Motor: 4/ 5 Some resistance
> Muscle bulk , fasciculation ( LMN lesion) 5/ 5 Normal strength
> Tone: lead - pipe /cog- wheel rigidity ( Parkinsonism) , spasticity ( UMN lesion)
> Strength: proximal - myopathy vs. distal - neuropathy
f
> Reflexes: with UMN .
I .
with LMN positive Babinski’s with UMN
.
• Cerebellar : fmger - nose/heel - shin dysmetria, and finger - tapping dysrhythmia, ataxia
• Posture and Gait:
Gait Syndromes
Type Description Cause
Antalgic Limited range of motion, limping, non - wt bearing Degenerative joints, trauma
Ataxia (cerebellar) Staggering, wide - based .
EtOH MS, stroke
Ataxia (sensory) Unsteady, worse with poor visual input (i.e., night) Neuropathy, dorsal column dysfunction
Ataxia (vestibular) Deviating to one side, nausea, vertigo Meniere's, acute labyrinthitis
Frontal gait disorder Magnetic ( start /turn hesitation), freezing Frontal lobe degeneration/infarct NPH .
Hemiparetic/spastic .
Narrow based, toes turned in hyperreflexia UMN ( stroke, cerebral palsy )
Parapetic Adduction, scissoring of both legs, stiffness Bilateral UMN ( spinal, cerebral lesion) 2
o> D ^
Parkinsonian Shuffling, stooped, little arm swing, festinating Parkinson’s disease CL a>
Psychogenic Bizarre, lurching, rare fall /injury, no neurologic signs Factitious, somatoform disorder £3
D Q)
Steppage Excessive knee/hip flexion when walking, footdrop LMN (motor neuropathy) 0> ““
Waddling Trendelenburg, swaying, symmetric, wide based - .
Weak gluteus medius myopathy,
hip osteoarthritis
INVESTIGATIONS
Laboratory Investigations
• CBC -D, electrolytes, urea, creatinine
• . . .
B12 fasting glucose, syphilis serology ESR/CRP TSH, EtOH level
Radiology/ lmaging
• X - ray of affected joint(s)
• CT/MRI head and spine is often required
• Bladder scan for retention
UREATMENT
Emergent
• Fall precautions: treat injuries of fall
• Stroke: consult Neurology: thrombolysis or thrombectomy if acute ischemic
• Cauda equina: consult Neurosurgery, imaging, surgical decompression
• Think myelopathy for bilateral UMN findings with no cranial findings, image appropriate level (i.e., cervical spine)
Treatment Options
• Most patients will need long- term multidisciplinary team for rehab: home care can provide assistance if subacute
• Treat underlying cause:
> Parkinson's - levodopa /carbidopa
> MS - multidisciplinary approach with neurorehab, steroids for acute episodes, drugs to prevent relapses
> Foot drop - brace
> Vit B12 deficiency: B 12 replacement
Surgical: surgical fixation of fractures, tumor resection
Referrals: Neurology, orthopedic surgery, physical therapy
Finding Target Disease LR + LR -
Able to perform 10 tandem steps PD in patients with Parkinsonism 5.0 0.1
Intact gait or balance Alzheimer ’s dementia 3.4 0.2
Parkinsonian gait Lewy body/ PD dementia 8.8 0.2
Frontal gait Vascular dementia 6.1 0.5
.
Adapted from Evidence- Based Physical Diagnosis. 3rd ed.. Steven McGee MD and
The Rational Clinical Examination: Evidence- Based Clinical Diagnosis
.
David L. Simel Drummond Rennie
194
into imon inical Scenarios
HEARING LOSS & DEAFNESS
.
Current Editors: Samapti Samapti MD Jennifer McCombe MD MPH FRCPC
DIFFERENTIAL DIAGNOSIS
Conductive Hearing Loss Sensorineural Hearing Loss
• External ear: obstructed canal (cerumen • Congenital/hereditary: teratogens (quinine, retinoids), infections (TORCH,
impaction), otitis externa, tumor, trauma, .
mumps, measles) Alport syndrome
congenital .
(e.g. aminoglycosides, furosemide)
• Adult: presbycusis, noise, ototoxic drugs .
• Middle ear: congenital, otitis media, tumor, . .
Meniere’s MS acoustic neuroma, cerebrovascular accident, syphilis,
otosclerosis, tympanic membrane perforation .
autoimmune ( SLE RA). trauma ( temporal bone number, barotrauma)
HISTORY
ID • .
Patient name, age gender, occupation
CC • Hearing loss
HPI • Trouble with background noise, misunderstanding conversations,asking people to repeat, turningupTV volume
• OPQRST (onset,palliating/aggravatingfactors,qualityofpain,radiation,severity/associatedsymptoms,timeline)
• Unilateral vs. bilateral; sudden vs. progressive
—<TJ C<D • Otalgia or otorrhea, association with tinnitus, vertigo, or disequilibrium
C u • Trauma - head trauma, barotrauma, foreign body, or noise exposure
Q) "O
• Recent illness - otitis externa, otitis media, sinusitis
QJ
-2
C
RED FLAGS • Recurrent ear infections, temporal bone trauma, sudden hearing loss
PMHX • . .
Unusual ingestions DM stroke, heart disease, autoimmune disease, TORCH infection, ear /craniofacial
abnormalities, recurrent otitis media, psychiatric illness
• Ear surgery
INVESTIGATIONS
Laboratory Investigations (not routine, for unclear etiology)
• CBC- D, TSH, blood glucose, serum aminoglycosides (if indicated), syphillis EIA/ RPR (if indicated)
• Autoimmune workup; ESR/CRP, RF, ANA ( if progressive and bilateral sensorineural hearing loss)
Radiology/ lmaging
• CT not recommended for initial evaluation of sensorineural hearing loss
• CT of posterior fossa & internal auditory canal: indication for progressive asymmetric sensorineural hearing loss ( acoustic neuroma)
• CT of temporal bone: indication for head trauma (especially to temporal area)
• MRI + gadolinium: > 15 dB difference between left and right ears on bone conduction ( gold standard for internal auditory canal imaging
and retrocochlear pathology)
Special Tests
CD
• Consider auditory brainstem response test if persistent and undiagnosed hearing loss CL ft)
TREATMENT G. D
Emergent
=CD3 ~
QJ
Treatment Options
• Medical
> Meniere' s disease: IV fluids, anti- emetics, anti - vertigo medication (e.g., meclizine, droperidol), low Na * and calorie diet, diuretic;
destructive Rx 'n: intratympanic gentamicin and labyrinthectomy. Nondestructive Rx 'n: Meniett device & intratympanic steroid
( monitor regularly)
> Otitis media ( see also Ear Pain): amoxicillin
> Cerumen obstruction: physically remove cerumen with cerumen-softening drops, irrigation
> ldiopathicsensorineuralhearingloss:often resolves spontaneously; 10dprednisone ( 60 -80mg) couldbeused;ifnoimprovementon
audiogram, intratympanic steroids can be considered
> Hearing aid is not recommended until underlying pathology is treated
• Surgical: acoustic neuroma or otosclerosis
Follow -up
.
• Acute conditions (infection Meniere’s, trauma): 1- 4 wks serial audiograms and otoscopic exam until hearing loss resolves
• Prevention:
> Monitor drug levels and take baseline audiogram with ototoxic drugs
> Screen high-risk individuals and provide patient education (ear protection, safety issues with vertigo)
> Patient with otorrhea should keep water out of ears while draining
> Earplugs
Referrals - Audiologist for audiogram followed by an Otolaryngologist if etiology unclear
KEY POINTS
• Hematologic malignancies may be classified as:
> Acute or chronic ( depending on the clinical onset ):
> Myeloid or lymphoid (depending on the cell lineage from which the disease arises)
• Leukemia primarily affects the peripheral blood and bone marrow: lymphoma primarily affects lymph nodes or other extramedullary
tissues (e.g. Gl tract, skin, spleen, etc.)
• Acute leukemias tend to be rapid in onset (days to weeks) and symptoms relate to complications of bone marrow failure and cytopenias
. .
(i.e. bleeding DIC febrile neutropenia, tumor lysis syndrome, leukostasis, etc.)
-
• Chronic leukemias (e.g. CLL) tend to be more indolent in presentation and onset may bediscovered incidentally on blood work or other
testing
• Lymphomas may be clinically indolent or aggressive. Aggressive lymphoma may be associated with medical emergencies, including
.
tumour lysis syndrome SVC syndrome, spinal cord compression, cardiac tamponade, splenic rupture, etc.)
DEFINITIONS
Hematopoiesis begins with undifferentiated stem cells in the bone marrow, which can proceed along either myeloid or lymphoid path-
ways. Precursor cells are immature and are called “ blasts”
• End result of myeloid pathway: platelets, red blood cells, granulocytes (basophils, eosinophils, neutrophils), monocytes /
macrophages, mast cells
.
• End result of lymphoid pathway: T cells B cells, and NK cells
—
03 C
C u
Q) Location of hematopoeisis:
• Myeloid precursors stay in the bone marrow
• Lymphoid precursors start out in the bone marrow but then mature in the thymus, lymph nodes, and spleen, and then out into the blood
0 "O
QJ Errors in the hematopoiesispathway cancausecells tolose theabilitytodifferentiate/mature past acertain point.Inacute leukemia, thecells
fail to differentiate beyond theblast stage and begin to multiply and replace normal hematopoiesis. Results in large numbers of blasts in the
bone marrow which often spills over into the peripheral blood.
Classification of Leukemias
1. Myeloid vs. Lymphoid
2. Mature cells vs. Immature cells undergoing clonal proliferation
• Proliferation of more immature cells translates to aggressive, acute disease ( acute leukemias, high grade lymphomas)
• Proliferation of more mature cells translates to less aggressive, chronic disease (chronic leukemias, myelodysplastic syndromes,
myeloproliferative neoplasms, indolent lymphomas, multiple myeloma)
Lymphomas are classified as Hodgkin Lymphoma or Non - Hodgkin Lymphoma.
.
• Common examples of NHL' s are CLL, follicular lymphoma, diffuse large cell lymphoma Burkitt lymphoma, and multiple myeloma, etc.
Chronic disease can transform into acute, aggressive disease if additional mutations accumulate over time
Myeloid Lymphoid
Acute Acute myeloid leukemia ( AML) Acutelymphoblasticleukemia ( ALL)
Aggressive lymphoma
Chronic Myeloproliferative neoplasms and Chroniclymphocyticleukemia (CLL)
myelodysplastic syndromes
and other indolent lymphomas
HISTORY
ID • Patient 's name . age. gender, ethnicity
CC • Fatigue, fever, weight loss, incidental lab abnormality
HPI • Timing of symptom onset ( acute vs. chronic)
• Course (progressive, fluctuant, improving)
• Change in weight
• Abdominal pain, change in appetite, early satiety
• Bruising, bleeding, petechiae
• Lymphadenopathy
PMHX • Down syndrome, previous cancers, immunodeficiencies (esp. HIV .
transplant ), recurrent infections, history of MDS or
myeloproliferative disorder (essential thrombocytosis, polycythemia vera, myelofibrosis)
PSHX • Any previous cancer -related surgeries or transplants
FHX • Malignancies, esp. heme malignancies
.
MEDS • Chemotherapies, immunosuppression, radiation G-CSF, herbals
SOCIAL • EtOH/drug use ( present and past ), smoking, diet, travel history, occupational exposures (benzenes, dyes)
197 dr
ROS • General: fatigue,fever, weightchanges,night sweats, altered mental status,weakness,noticeable lumps/bumps (may be
painful after EtOH in some lymphomas)
• HEENT: gingival/nose bleeding, gingival hyperplasia, headaches
.
• CV/ Resp: chest pain SOB, cough
• GI/GU: changes in stool or urine, N/V, anorexia, testicular
• MSK /Derm: jaundice, rashes ( leukemia cutis), pruritus, bruising, arthralgia ( gout fromTLS), bony pain
PHYSICAL
General:
• Vital Signs: may have fever ( febrile neutropenia), tachycardia (esp. if bleeding)
• Stable or unstable
.
• Cachectic, obvious masses / lymphadenopathy altered LOC, distressed
Lymph Node Exam:
.
• Head /neck: pre -/post - auricular occipital, submandibular, anterior cervical, posterior cervical, supraclavicular, infraclavicular
• Upper extremity: axillary, epitrochlear
• Lower extremity: superficial inguinal, deep inguinal, popliteal
HEENT: dry mucous membranes, gingival hyperplasia, tonsillar hypertrophy, ulcers/mucositis, thrush
CV/ RESP: especially for pneumonia and pleural effusions
ABDO:
• Inspection: abdominal distension
.
• Palpation /percussion: hepatosplenomegaly fluid wave, shifting dullness (may have malignant ascites)
-
• Do NOT do a DRE in any neutropenic patient ( risk of causing bacterial translocation)
Laboratory Investigations G. 3
13 QJ
• CBC and differential: anemia, thrombocytopenia, variable white blood cell count: may have blasts in the blood ( watch for fD —
neutropenia / febrile neutropenia)
. .
• INR PTT fibrinogen ( for DIC)
. .
• LDH uric acid, phosphate, calcium, electrolytes Cr ( for possible tumour lysis syndrome)
.
• Bilirubin, haptoglobin DAT ( for associated autoimmune hemolytic anemia)
• Peripheral blood smear ( for circulating blasts), Auer rods ( for AML)
• Panculture if febrile neutropenia
Radiology/Imaging
• Depends on presentation:
> e.g., if febrile neutropenia, requires chest x -ray as part of septic workup
.
> e.g., if symptoms of mass effect, image affected area with U/ S, CT or MRI
Biopsy
• Always biopsy bone marrow if suspected leukemia
> > 20% blasts diagnostic of acute leukemia (normal < 5%)
> Further testing done for molecular markers and genetic abnormalities can help in prognostication and guiding treatment
> For staging in certain lymphomas
•Biopsy of lymph nodes/extranodal masses: excisional lymph node biopsy required for lymphoma
Lumbar puncture to assess for CNS involvement in leukemia (high- risk patients only)
L REATMENT
Emergent
• Can present with sepsis, critical illness - fluid resuscitation, septic workup, appropriate consultation as necessary
• If febrile neutropenia, prompt initiation of broad - spectrum antibiotics as per your institution's protocol (usually piperacillin -
tazobactam +/- aminoglycoside) - AFTER cultures drawn
Chemotherapy
• Acute leukemias: rapidly fatal without chemotherapy
• Chronic leukemias: therapy depends on stage of disease
• Lymphomas: watchful waiting if indolent: chemotherapy if active
• Do not give any steroids until biopsies taken (can cause false negative results)
DIFFERENTIAL DIAGNOSIS
• Transient ischemic Attack: brief neurological deficit caused by ischemia without infarction ( usually less than one hour )
• Ischemic stroke: 80% of strokes
> Thrombosis ( atherosclerosis, dissection, fibromuscular dysplasia, vasoconstriction)
. .
> Embolism ( atrial thrombus AF endocarditis); Hypoperfusion ( cardiac arrest, PE, pericardial tamponade)
• Hemorrhagic stroke - 20% of all strokes
.
> Intracerebral hemorrhage ( aneurysm rupture is most common HTN, trauma, amphetamines, cocaine)
> Subarachnoid hemorrhage ( arterial aneurysm, vascular malformation)
• Most common stroke mimics: seizure, migraine, systemic infection, brain tumor, hyponatremia and hypoglycemia, positional
vertigo, conversion disorder
HISTORY
ID • Patient’s name, age, gender
CC • Acute hemiparesis, acute loss of sensation
HPI • Onset: time of onset is a critical decision point for therapy
_<
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D
• Progression
• Distribution: location of paralysis or sensory loss, unilateral or bilateral, proximal or distal
c u .
• Character: true paralysis or weakness, complete vs partial loss of sensation
a) -a
4
—* CD
• Associated symptoms: visual/speech impairments, hearing changes, vertigo, seizure, fever
RISK • Use theCHADS2 score toassessrisk (in non-rheumatic,non - valvularAF):CHF, HTN consistently above 140/90 mmHg,
FACTORS age > 75 yrs, DM,prior stroke or Tl A; the annual stroke risk increases with these risk factors; othersrisk factors include
smoking, dyslipidemia
.
> If using thrombolysis sBP < 185 mmHg and dBP < 110 mmHg
» Note that ICH and SAH have different blood pressure targets
» If must lower, use IV labetolol and avoid decreasing by more than 15% per 24 hrs
• Determine etiology with a non-contrast CT head
• In hemorrhage:
» Patients < 55 yrs: higher yield for angiography to look for aneurysm
> Patients > 55 yrs with hypertension: likely HTN - related. angiography low yield
» Patients > 65 yrs with dementia: likely amyloid angiopathy, angiography low yield
• In ischemic:
* Medical management: Tissue plasminogen activator only within 4.5 hrs of symptom onset
* Surgicalmanagement:endovasculartherapyforanyonewithsxwithinl 2- 24h;carotidendarterectomyifsignificantcarotidstenosis
( > 50%)
KEY POINTS
• Hemoptysis largely results from pulmonary causes (airway, parenchyma, or vascular) rule out mimics, such as epistaxis and UGIB
*
• Quantify the volume of bleeding to determine if the patient has massive hemoptysis (definition: > 100 - 600ml/ 24 hours)
.
• Investigations to determine etiology include CXR CT chest, bronchoscopy
• If patient experiences massive hemoptysis, assess ABCs and if the side of bleeding is known, they should be placed with the
compromised lung down
DEFINITIONS
• Hemoptysis: expectoration (expulsion) of blood from the lower respiratory tract
• Massive hemoptysis: 100- 600 mL of expectorated blood over 24 hrs
• Sources of hemoptysis include the upper or lower airway
> Bronchial arteries: supply blood to lung parenchyma at systemic pressure, a source of massive hemoptysis ( 90% of the time)
> Pulmonary arteries: carry entire blood supply at a lower pressure for oxygenation
DIFFERENTIAL DIAGNOSIS
Pulmonary
• -
Airway acute/chronic bronchitis, bronchiectasis, cancer (primary bronchogenic or metastatic), trauma, foreign body
—c
nj
CD • Parenchyma -
infectious (TB. bacterial pneumonia ( S. pneumoniae/ S. aureus), abscess, fungal), cancer (bronchogenic, metastatic),
.
alveolar hemorrhage (vasculitis - GPA EGPA: pulmonary capillaritis)
E
0)
3 .
• Vascular - PE arteriovenous malformations, pulmonary HTN, iatrogenic
T3
C CD Cardiac: CHF, mitral stenosis
-2 Hematologic: thrombocytopenia, coagulopathy, anticoagulation
Pseudohemoptysis: blood originating from the upper respiratory tract and /or upper Gl tract (epistaxis hematemesis) .
HISTORY
ID • Patient ’s name . age. gender
CC • Coughing blood
HPI • Onset, frequency, progression, aggravating/relieving factors, timing, previous episodes of hemoptysis
• Quantity of blood: massive ( 100- 600 mL/ 24 hrs)
• Color: bright red, dark red .
coffee grounds, pink, rust -tinged sputum, clots, purulent, frothy
• Recent or .
past respiratory infections, infectious contacts TB risk factors (incarceration, travel to endemic
.
regions, recent immigrant, IVDU homelessness, HIV)
• Previous or chronic cough
• Dyspnea
• Epistaxis
• Chest pain, palpitations, symptoms of CHF
• Immunosuppression
• Joint inflammation, rash, bruising or other signs of bleeding diathesis
• Gl: N/V, abdominal pain, hematemesis . melena/hematochezia
( tea -colored urine suggests glomerular etiology)
• GU: hematuria
PMHX • Previous cancer (primary or mets to lung) or chemotherapy ( Bevacizumab), lung disease (CF emphysema, chronic .
bronchitis, bronchiectasis), cardiac disease, thromboembolic disease, infectious risk factors (HIV TB), peptic .
.
ulcer disease, vasculitic and granulomatous disease (granulomatosis with polyangitis) Goodpasture’s syndrome,
connective tissue disease (e.g., SLE)
PSHX • Recent surgery ( PE), recent procedures to upper or lower respiratory tract
FHX • Lung cancer, autoimmune disorders
SOCIAL • EtOH, smoking, inhalation of chemicals, crack cocaine, travel hx, occupation, place of birth, incarcerations
HEENT
• Nasopharyngeal bleeding, oropharynx bleeding ( any obvious lesions), lymphadenopathy (cervical, supraclavicular, axillary) JVP .
RESP
• Inspection for clubbing and capillary refill in fingers: tracheal shortening or deviation in the neck: deformities, scars, asymmetric chest
expansion
• Palpate for chest tenderness, masses, assymetric chest expansion, tactile fremitus
• Percuss for dullness or resonance, diaphragmatic excursion
• Auscultate for breath sounds, adventitious sounds ( wheeze, crackles), vocal resonance (bronchophony, egophony, whispering
pectoriloquy)
CV
• Inspection: pacemaker insertion scars, visible pulsations, peripheral edema
• Palpation: peripheral pulses, palpable thrills, heaves, apical beat (diameter, displacement, amplitude, duration)
• Auscultation: rhythm, S 3/S4, murmurs
Abdominal exam
• Cirrhosis: palpate and percuss for hepatomegaly and splenomegaly 2 =7
to 3
MSK / DERM
- --
rt
Q 05
.
• Inspect for petechiae ecchymosis, rashes, joint inflammation, signs of DVT ( > 3 cm difference between calves, erythema, warmth,
£3
tenderness to palpation) 3 O)
05 “
INVESTIGATIONS
Laboratory Investigations
• CBC . .
-D. lytes, LFTs. liver enzymes Cr, INR PTT. consider D - dimer (only if low suspicion of PE), urinalysis
• Type/screen and cross -match if significant bleeding
• Microbiology: sputum gram stain and culture, acid - fast stain, sputum cytology if risk factors for cancer, blood cultures
Radiology/ lmaging
• CXR ( PA and Lat ) - the best initial investigation for hemoptysis
.
• CT:useful for diagnosing bronchiectasisand evaluating mass /nodule found on CXR helpful if CXR normalbut patient has risk factors for
cancer
• Doppler US. CT angiography /VQ scan (if suspicous of PE )
Special Tests
• ABG if respiratory distress
. .
• Vasculitis screen: CRP ANCA anti - GBM. ANA. ENA
• Consult respirology for flexible bronchoscopy: indications are hemoptysis with a normal CXR in males . > 50 yrs, > 40 pk yrs
TREATMENT
Emergent
• .
ABCs, cardiac and respiratory monitoring 2 large bore IVs
> Airway: prepare to secure airway if massive hemoptysis, difficulty protecting airway, or GCS < 8
> Breathing: assess oxygenation and ventilation, consider intubation if clinically warranted. Position patient in lateral decubitus
position with bleeding lung on bottom to protect functioning lung if compromised.
> Circulation: if massive hemoptysis, assess for hypotension, need for transfusion
• Note: Hemoptysis morbidity is more from asphyxiation than from exsanguination
Treatment options
• Treat underlying cause
• Correct coagulopathy
• Transfusions as needed
• Bronchoscopy
• Treat infection with appropriate anti-microbials and source control
• Malignancy - dependent on type and stage: includes radiation, chemotherapy, and /or surgical resection
• CHF - diuresis, rate control
• Vasculitis - immunosuppression (steroids initially with consideration of other immunosuppressants)
• Pulmonary arteriography with embolization as needed
DIFFERENTIAL DIAGNOSIS
Clinical Scenario Etiology
Community - acquired .
S. pneumoniae, M . pneumoniae , C. pneumoniae Chlamydia, viral, H. influenzae , M. catarrhalis , S. aureus
Hospital- acquired GNB (pseudomonas, klebsiella, E. coli ) , S. aureus , MRSA
Immunosuppressed . .
Pneumocystisjiroveci , CMV HSV, atypical mycobacteria, fungal infections Legionella
Aspiration Chemical pneumonitis (aspiration gastric contents), bacterial pneumonitis > 24-72 hrs later ( anaerobes)
HISTORY
ID • Patient ’s name, age, gender
HPI • Cough, fever, pleuritic CP, dyspnea /SOB, sputum production, hemoptysis
• Duration of symptoms, preceding viral infection, rigors, diaphoresis
• Recent exposure to sick contact (e.g., daycare, school, work, home)
• Recent travel Hx (endemic regions for fungal or tuberculosis)
—E :S
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RED FLAGS
• Associated symptoms: headache, abdominal pain, anorexia, vomiting, myalgias, malaise
• Elderly: Hx of falls, confusion, altered LOC ( increased aspiration risk )
• Cyanosis, clinical signs of respiratory distress
-! TCD3
()
M
PMHX • Chronic illness (CHF, COPD, CF, DM, asthma, CKD, liver disease)
• Lung cancer
• Immunocompromised ( AIDS patients, transplants, chronic steroid use, neutropenia)
• Dementia, recent hospitalization ( 3 mos), past splenectomy
PHYSICAL
General
Findings for Pneumonia LR + LR -
• Vital Signs: hypotension, tachycardia, tachypnea, oxygen saturation, temperature
(elderly are often euthermic/ hypothermic ) Asymmetrical chest 44.1 NS
• Signs of respiratory distress: cyanosis, diaphoresis, inability to speak in full sentences, expansion
accessory muscle use, intercostal indrawing, diaphragm motion, nasal flaring Percussion dullness 3.0 NS
HEENT Diminished breath sounds 2.3 0.8
.
• Central cyanosis, carotid pulse, JVP skin turgor (dehydration), dentition
Bronchial breath sounds 3.3 NS
CV
Egophony 4.1 NS
• Check cap refill, peripheral pulses
• New murmurs (endocarditis)
Crackles 1.8 0.8
INVESTIGATIONS
Laboratory Investigations
• CBC- D, electrolytes, urea . . . . .
Cr AST ALT ALP bilirubin, urinalysis
• Microbiology: blood cultures ( before abx), sputum Gram stain and culture, sputum AFB & fungal if applicable.
.
• ABG if in respiratory distress ( Sa02 < 90% COPD supplemental 02) .
• CXR ± CT chest
. .
Bronchoscopy: if severe CAP immunosuppressed not responding to therapy
Nasopharyngeal swab: if viral infection suspected
Thoracentesis: if significant pleural effusion
UREATMENT
.
Acute: ABCs, supplemental 02 consider bronchodilators
.
Antibiotics: choice influenced by recent abxuse recent stay in health care institution, hospital flora, cultured organisms (e.g.,blood sputum) .
n> rr
Clinical Scenario Treatment CL ( D
• No comorbid factors *: ( amoxicillin ± doxycycline) or ( amoxicillin + ( azithromycin or clarithromycin) ]
.3
Out-patient
• Comorbid factors': ( amoxicillin or amoxicillin-clavulanate) + (doxycycline or azithromycin or clarithromycin)
D 0)
n> —
Community-acquired, • (Ceftriaxone + (doxycycline or azithromycin or clarithromycin) ] or levofloxacin
ward inpatient
Community- acquired, • Ceftriaxone + azithromycin
ICU inpatient • If MRSA suspected, add vancomycin or linezolid
Hospital-acquired • Nomulti - drugresistance ( MDR ) riskfactors * *:ceftriaxoneorampicillin-sulbactamorlevofloxacinorertapenem
• MDR risk factors’*: antipseudomonal cephalosporin ( cefepime or ceftazidime) or antipseudomonal
carbepenem (imipenem or meropenem) or piperacillin- tazobactam
• Plus antipseudomonal fluoroquinolone (ciprofloxacin or levofloxacin) or aminoglycoside (gentamicin or
tobramycin or amikacin) (if indicated based on past cultures and/or local microbiology data)
• Plus vancomycin or linezolid for MRSA ( if suspected or high local incidence)
Immunosuppressed • As above ± TMP - SMX ± steroids to cover PCP
Aspiration • (Cetriaxone or levofloxacin) ± metronidazole
Administration • Start with IV abx for inpatients, switch to oral once clinically responding and able to take oral
‘Comorbid factors: smoking, malignancy, diabetes, chronic heart, lung, renal, or liver failure, chronic corticosteroid use /immunosuppressive
. .
therapy HIV/immunosuppression, malnutrition or acute Wt loss ( > 5%) hospitalization in past 3 mos
.
“MDR risk factors: ATBx use within last 90d. current hospitalization > 5 d (or previous hospitalization > 2d within last 90d) high frequency of
.
antibiotic use in community or hospital unit, immunosuppressive disease and/or therapy IV tx/wound care/hemodialysis within last 30d family .
member with MDR pathogen, residence in nursing home or long- term care facility
Non-pharmacologic: vaccinations (influenza yearly, pneumococcal booster every 5 yrs), chest physiotherapy
. .
Follow -up: 48 -72 hrs for out - patients CXR at 6 wks if pneumonia, smoker, alcoholism COPD, > 5% Wt loss, > 50 yrs old
DIFFERENTIAL DIAGNOSIS
Infectious
• Septic arthritis ‘until proven otherwise
.
S. aureus , H . influenzae, S pneumo , gram -ve bacilli, enterococcus, anaerobic )
>
> Gonococcal (may be culture - negative tap)
> Lyme disease
> Less common: mycobacterial ( tuberculosis and atypical mycobacterial), viral, fungal
Inflammatory
• Crystal induced arthropathy - gout (uric acid crystals), pseudogout (calcium pyrophosphate arthropathy)
.
• Seronegative spondyloarthropathies - reactive arthritis, psoriatic arthritis IBD-associated arthritis, osteoarthritis
Trauma
• Hemearthrosis - non- articular, peri - articular (olecranon bursitis, prepatellar bursitis, sarcoidosis)
HISTORY
—c c
OJ
CD
ID • Patient’s name, age . gender
u
CD "O CC • Joint swelling, pain, can' t Wt -bear, restricted range of motion
CD
HPI • History of trauma to joint ’differentiate articular vs non/peri- articular pain*
• Onset (gradual vs. acute), progression: previous episodes
• Which joint(s), affected ( pattern)
• Hx travel (Lyme), risk factors for STI
• Extraarticular features: fever (infection, crystal), urethritis/cervicitis (gonococcal), rashes, symptoms suggesting
. .
inflammatory arthritis (oral ulcers, uveitis GU/GI symptooms, enthesitis dactylitis, back involvement with morning
stiffness), recent diarrheal illness (reactive)
RED FLAGS • Immunocompromised, febrile, rapid onset/progression, trauma, prosthetic joint/recent instrumentation of joint
PMHX .
• IBD, psoriasis, DM immunosuppression, renal disease . HTN. myeloproliferative disease. TB, hemophilia
PSHX • Joint prosthesis, recent open wound/ joint debridement or joint injection
MEDS • Can trigger gout: cyclosporine, diuretics, low dose ASA, chemotherapy, allopurinol, niacin
• Long - term steroids ( AVN risk ), anticoagulants (hemarthrosis)
ALLERGIES • General inquiry
RISK • Septic arthritis: age > 80 (LR + 3.5 * ) , DM ( LR + 2.7 * ), RA ( LR +2.5 * ), immunocompromised, prosthetic joint ( LR +3.1* ),
. .
FACTORS recent joint surgery (LR + 6.9 * ), IVDU HIV ( LR + 1.7 *), EtOH. skin infection ( LR + 2.8 * with hip/knee prosthesis LR
+15’) ' Likelihood ratios for septic arthritis
. .
• Gout: renal disease, chemotherapy EtOH obesity, OA, meds (see above)
[PHYSICAL
Vital Signs - BP. HR. RR. Temp. Sa02
Skin & Nails:
.
• Rashes: pustular lesions (disseminated gonococcal infection), erythema migrans ( Lyme) erythema nodosum (IBD sarcoidosis), .
psoriasis/nail pitting/onycholysis ( psoriatic)
• Tophi (gout )
• Lesions on glans penis (reactive arthritis)
.
• Examine peri- articular structures for point tenderness (enthesitis tendonitis, bursitis). Evaluate other joints patient may be unawareof
(including spine if suspecting seroneg.) .
• Range of motion: active then passive - active ROM is reduced in bursitis, tendonitis, or injury to the muscle; active and passive ROM is
reduced in synovitis or structural deformities
Hematological - lymphadenopathy, hepatosplenomegaly
INVESTIGATIONS
Blood Work
. . . . .
• CBC-D electrolytes Cr BUN ESR. CRP blood cultures; urinalysis, culture, gonorrheal swab
.
Joint Aspiration/Arthrocentesis - send for 3Cs: Cells Culture Crystals .
• Contraindications: local infection over site/needle path (could seed joint )
• ALWAYS rule out septic joint - can co -exist with gout ( i.e., presence of uric acid crystals does not rule out septic joint)
2 3-
• Gout - needle- shaped, strong negatively - birefringent crystals intra -cellular in acute attacks, extracellular in chronic gout
• CPPD - rhomboid, weakly positively - birefringent crystals = CPPD a> =
r-t-
-
Q rt>
Disease Appearance Viscosity WBC count %PMNs Other S3
Normal Clear Viscous < 200 < 25%
D
rt> —
Non- lnflammatory
Clear Viscous 200- 2000 < 25%
(e.g., osteoarthritis, trauma)
Crystals: (- )
Inflammatory Yellow, turbid 2000-
Thin > 50% ve birefringent = uric acid ( +)
.
(e.g., crystals, RA seronegative spond.) to opaque 50.000 ve birefringent = CPPD
Radiology/ lmaging:
• Consider X - ray of joint and contralateral limb ( for baseline, chondrocalcinosis, osteonecrosis, osteomyelitis, adjacent bone)
TREATMENT
Emergent: ABCs, arthrocentesis. Rule out septic arthritis (high risk of rapid joint destruction).
> If involving prosthetic joint: immediate referral to Orthopedics for aspiration & management
Supportive treatment: rest, ice, splinting to reduce pain. Refer to Physio once settling.
Treatment & follow - up (by differential):
• Septic arthritis:
.
> Percutaneous arthrocentesis daily with saline irrigation, analgesia (codeine - no NSAID) IV ATBx x 2 wks, then PO ATBx x 3 - 4 wks
as per clinical response and gram stain/sensitivities. Limit Wt bearing, encourage passive motion. Consult Orthopedic Surgery for
lavage/debridement.
.
> Gonorrhea: ceftriaxone IV + azithromycin (single dose: cross cover for chlamydia). Screen for syphilis HIV; screen contacts.
> Lyme: doxycycline x 14 - 21 d in early stages. Ensure IM/ID follow -up for cardiac, neuro manifestation if later stages.
• Crystals
> Gout : colchicine (0.6 mg PO bid or 1.2mg PO and then 0.6mg PO lhr later ) - esp if < 24 - 48 hrs or NSAIDs contraindicated. Consider
intraarticular steroid if mono/ systemic if polyarticular. NSAIDs if no Cl x 2 weeks. Chronic management : risk reduction - Wt loss,
minimize EtOH, hydration, Vit C 500 mg po daily, start allopurinol ( 2 wks after acute attack ) to reduce urate level < 360 mmol with
prophylactic NSAID/colchicine 0.6 mg po bid. Follow -up with Family Doctor.
> CPPD: NSAIDs, colchicine ( similar to gout ) & referral to Rheumatology
• Trauma: analgesia & refer to Orthopedics for definitive management
• Seronegativespondyloarthropathies:NSAIDx 2 - 3 weeksifnoCI.Considerintraarticularsteroid (monoarthritis) orsystemicsteroid(poly).
Follow -up with Rheumatology.
DIFFERENTIAL DIAGNOSIS
• The first and most important step is to localize the lesion, then think about the etiology
• High Mortality/ Morbidity: stroke, cord compression (+/- Cauda Equina Syndrome) , Guillain- Barre Syndrome
_ro QJ
C
Spinal Cord (central
cord lesion) Weakness of hands bilaterally Loss of pain/temp across upper back, shoulders, upper
arms (’cape -like distribution’), sacral sparing
UMN/
LMN
C U Spinal Roots
(radiculopathy) Weakness following myotomal distribution Sensory deficit following dermatomal distribution LMN
QJ *o
Plexopathy Brachial (C 5 -T 1) or Lumbosacral (T12- L4) affecting Sensory deficit according to plexus
nerves of respective plexus LMN
Peripheral Weakness beginning in feet, progressing up to legs, Sensory deficit in stocking-glove distribu LMN
Neuropathy hands, then arms (’stocking-glove distribution’)
Mononeuropathy Weakness following peripheral nerve distribution Sensory deficit following peripheral nerve distribution LMN
Neurological
Central Nervous System Peripheral Nervous System Non- Neurological
Cortex, Thalamus, Mononeuropathy Psych
Brainstem
• Stroke, MS,
.
• Common: trigeminal neuralgia Carpal Tunnel Syndrome (median nerve), Saturday
Night Palsy (radial nerve), ulnar nerve palsy, meralgia paresthetica (lateral cutaneous
• Conversion disorder
Other Organs
inflammation, mass
lesion ( tumor, mets .
nerve of the thigh), peroneal nerve palsy, femoral nerve compression
Radiculopathy
.
• Referred pain eg. Ml .
vascular claudication
.
abscess) EtOH • Disc herniation, osteophytes, infections, epidural abscess, arachnoiditis, herpes
Spinal cord zoster
• Trauma, compression Polyneuropathy
. . . . .
(disc, tumor, mets • DM uremia, vasculitis, amyloidosis, hypothyroidism Sjogren’s syndrome
abscess) MS infection
. . .
(e g., HIV syphillis)
. .
• Syphilis HIV Lyme disease EBV, CMV .
.
• EtOH vit B 12 deficiency, vit B 6 toxicity, critical illness polyneuropathy,
cord infarction, vit B 12
deficiency
. .
paraneoplastic GBS hereditary neuropathies
Drugs
• ChemotheraDV. heavy metals, metronidazole
HISTORY
ID • Patient’s name, age, gender . BMI
CC • Numbness/paresthesias/altered sensation
207 mmc
FAMHX • As with PMHx, especially if
polyneuropathies
.
early onset ( < 60 y/o) autoimmune disease, thyroid disease, hereditary
. . .
.
• Hematology (CBC, glucose HbAlc ), biochemistry ( vit B12, TSH, urea) , rheumatologic screen
.
( ANA ANCA, RF anti-SSA anti- SSB, ESR/CRP), infectious screen (HIV HepBsAg, HCV Ab . S2 Posterior thigh
syphillis EIA/ RPR ), toxin screen (heavy metals), malignancy screen ( SPEP, UPEP) S3/4 Perneum
Radiology/ lmaging S5 Anus
• Central ( UMN) lesions: MRI, MRA, CT ± contrast, CTA
• Spinal cord lesions: MRI of brainstem down to the spinal sensory level
• CT chest /abdo/pelvis for primary malignancy
Special Tests
• Peripheral ( LMN) lesions:
» EMG, nerve conduction studies
> Muscle and/or nerve Bx
• LP (Guillian Barre Syndrome - albuminocytologic dissassociation ( high protein, low WBC ]: MS - oligoclonal bands: SAH -
xanthocromia, RBCs)
TREATMENT
Emergent Neurology or Neurosurgery consult, if clinically indicated e.g., stroke, SAH
Non- emergent: treat underlying cause (see table below): consult refer to Neurology if indicated
Sciatica
Sciatic n. compression: disc .
Activity modification NSAIDs, PT, pain control, open
herniation or spinal stenosis discectomy/microdiscectomy, muscle relaxants
DIFFERENTIAL DIAGNOSIS
Disease State History Diagnostic Criteria
COPD • > 10 pack yr smoking Hx or significant second hand • Spirometry: post bronchodilator FEV1/FVC < 0.70
smoke exposure • GOLD Criteria to categorize severity of airflow
• Exertional dyspnea, cough, sputum limitation (post -bronchodilator administration).
• Previous COPD exacerbations .
> mild FEV1< 80% ofpredicted moderate 50- 80% .
severe 30- 50%, very severe < 30%
• Chronic bronchitis: spirometric confirmation
of COPD + productive cough for > 3 mo for > 2
consecutive years
• Emphysema: destruction of airspace walls distal to
terminal bronchioles
Asthma • Early onset (often rapid) • Spirometry: FEV1/FVC < 0.70 AND post -
• Maybe atopic, allergic, or exercise- induced bronchodilator improvement in FEV1> 12% and 200
• Wheezing or copious coughing mL
—c <
OJ C
U Bronchiectasis
.
(e.g., cystic fibrosis
• ++ purulent sputum
• Oftenassociatedwithrecurrentbacterialinfections
• High - resolution CT scan: bronchial dilation,
bronchial wall thickening, signet ring sign, lack of
u ILD) • Coarse crackles, nail clubbing bronchial tapering
IHISTORY
Asthma COPD
HPI • Triggers of symptoms: strenuous activity, smoke/ inhalants, • Chronic bronchitis ( Blue Bloaters) vs. emphysema ( Pink
pollen, dust, cold air Puffers) symptoms
• Worsening sputum production • Cough, sputum, chest pain, hemoptysis, edema
• Increasing frequency of daytime symptoms, nocturnal • Previous exacerbations, hospitalizations, antibiotic /
symptoms, audible wheezes, increased use of rescue meds prednisone use
.
(e.g. short - acting |32-agonist ) • Previous /increasing home 02 requirements
• Limitation of daily activities (e.g., dyspnea while walking, going • Inhaler compliance and technique
up stairs, rest ) , days missed from work /school
PMHX . ..
• Childhood symptoms (e g chronic cough, nocturnal cough in • . .
NotepreviousEDvisits hospitalizations lCUadmissions .
the absence of a respiratory infection, hospitalizations) exacerbations requiring intubation
• Childhood diagnosis of " recurrent bronchitis" or " wheezy • Pulmonary or cardiovascular co - morbidities (notably
bronchitis" upper airway obstructions)
• Vaccination Hx ( pneumonia, influenza)
• Pulmonary rehab
• Lung resection or lung transplant
> Diaphragmatic excursion: percuss posterior chest wall during maximal inspiration/expiration ( norm ~ 6 cm)
• Auscultation: reduced breath sounds ( LR + 3.5 * ): bronchial/ vesicular breath sounds, length of inspiratory/expiratory phase
> Adventitious sounds: early inspiratory crackles (LR + 14.6 * ), wheezes, stridor, rhonchi
> Forced expiratory time (FET) > 9s (LR + 4.1* ), FET < 3 seconds ( LR + 0.2 * ), breath sound score ( < 9 i.e., soft breath sounds) ( LR + 10.2’)
INVESTIGATIONS
Laboratory Investigations
. .
• CBC- D:increasedHCT (compensationfordecreasedPa02) eosinophils(allergycomponent ) elevatedWBC (pneumoniacausingAECOPD)
.
• ABG ( Pa02 for 02 treatment assessment PaC02 to assess for C02 retention/need for NIPPV during acute exacerbation)
Z =r
Radiology/Imaging 3
-
ft) r f -
CL (D
• CXR : may appear normal or show increased bronchial markings and /or hyperinflation, flat diaphragm, increased retrosternal airspace,
bullae - may show pneumothorax, pulmonary edema, or pneumonia in acute exacerbation S 3
3 0 )
• ECHO ( in the context of signs and symptoms of right ventricular dysfunction and PHTN), ECG ft) ~
Special Tests
• PFT/ Spirometry ( see Diagnostic Criteria above) , allergy testing, BMD (chronic inhaled corticosteroid use), sputum induction,
methacholine challenge (reduced breath sounds LR + 4.2', presence of wheezing LR + 6.0*) if normal spirometry and asthma is still
suspected
TREATMENT
Emergent
• ABCs: in chronic C02 retainers, 88 - 92% is appropriate saturation target
> Short - acting p 2 - agonist. long acting bronchodilators, inhaled corticosteroids, systemic corticosteroids, home 02, etc.
• Surgical: lung resection, lung transplant
Follow -up
• Allergy skin testing (identify triggers), specific inhalation challenge (occupational triggers) , cardiopulmonary exercise test. Strongly
encourage scheduled vaccinations (pneumococcal and influenza).
Referrals
• Occupational Health and Social Work if applicable
• Counseling for smoking cessation (e.g., AADAC), pulmonary rehabilitation programs
Palpitations are unpleasant perceptions of cardiac activity, which may result from arrhythmias, increased sinus heart rate, or from a
heightened awareness of normal cardiac activity.
DIFFERENTIAL DIAGNOSIS
Classification of Arrhythmias of Cardiac Origin
Common & Benign Arrhythmic Cause Premature atrial contractions ( PACs), premature ventricular contractions
( PVCs)
Commonfit Serious Arrhythmic Cause . . . .
ProlongedQT’ VT’ Afib paroxysmalSVT atrioventricularnodalre - entrytachycar -
dia, bradyarrhythmias/heart block
Non- Arrhythmic Cause .
IHD’ hypertrophic cardiomyopathy’, CHD, valvular heart disease, conduction
system disturbances
. .
In the out -patient setting, the most common etiology of palpitations are anxiety and panic attacks ( 31%) cardiac (43%) and miscellaneous
(10%). In the emergency department, a cardiac origin of palpitations is more likely and must be ruled out.
HISTORY
ID Patient’s name, age, gender
CC Forceful, rapid, or irregular heart beat
HPI Onset (gradual onset: most common causes: sudden onset: tachycardia due to reentry)
Duration of episode (Intermittent, brief - PACs/ PVCs; Sustained - Afib, psychiatric etiologies)
Precipitating (pain, exercise, EtOH withdrawal) and relieving (valsalva) factors
HR and rhythm (regular /irregular) during episode and at rest
.
Associated chest pain, SOB syncope/presyncope, dizziness, diaphoresis, N/V, tingling
RED FLAGS Associated chest pain, syncope/presyncope (hypotension), dyspnea
New onset of irregular rhythm
Hx of cardiac disease
Episodes: > 5min duration, > 120 BPM or < 45 BPM at rest
Significant FHx (especially of sudden death)
PMHX Cardiac risk factors (smoking, DM, HTN, dyslipidemia FHx) .
.
Hx of AF, WPW, arrhythmias CAD, CHF, DM, stroke, TIA, syncope
. .
CVD (angina Ml, TIA stroke, valvular disease, pericarditis, rheumatic heart disease)
Psychiatric Hx ( anxiety or panic disorder, depression)
Endocrinopathy (thyroid, DM/hypoglycemia, MEN)
Fever or infection
Severe vomiting or diarrhea (electrolytes disturbances)
Wt loss (hyperthyroidism)
Recent surgery or immobilization ( PE)
Episodic pallor, tremor, headache, diaphoresis (pheochromocytoma)
PSHX Cardiac surgery
MEDS .
S-agonists, stopping a B - blocker, vasodilators, anti-cholinergics, synthroid insulin, theophylline, digitalis,
antiarrhythmics, pseudoephedrine, TCA herbals .
FHX .
Syncope, sudden death, especially cardiac in 1° relatives (male < 65 yrs female < 55 yrs), serious arrhythmias,
cardiomyopathies
SOCIAL .
Caffeine, smoking, EtOH recreational drugs: cocaine, amphetamines, opiate withdrawal, EtOH withdrawal
PHYSICAL
General
. .
• Stable vs. unstable: ABCs, VS ( BP HR, RR Temp Sa02).
• General inspection: diaphoresis, pallor, LOC, obvious discomfort/pain
Physical Exam
• Hands - look for tremors (increased adrenergic activities from thyroid, beta -agonist, caffeine, sympathomimetics)
• Wrists - palpate radial pulse for rhythm (Irreg. pulse LR + 3.3, LR - 0.1 for AFib, chaotic pulse LR + 24.1 for AFib), character, rate
• Neck - inspect for goiter (hyperthyroidism)
> Palpate JVP (not reliable for intracardiac pressure in Afib), thyroid size and nodules
• Eyes/ Face - inspect for exopthalmos (Graves), flushing, diaphoresis, conjunctival pallor ( anemia)
• Cardiac exam:
> Inspection - scars, pacemaker
INVESTIGATIONS s =r
n>
Laboratory Investigations CLO
r -r
.
• CBC- D, troponin, CPK, glucose, electrolytes TSH, Cr, INR, Ca, Mg S 3
D 0 )
Radiology/Imaging n>
• CXR
Special Tests
• ECG for any patient with suspicion of cardiac disease
• Echo for structural cardiac abnormalities
• Holter monitor for patients with paroxysmal palpitations, syncope/presyncope, suspected mild ischemia
• Urine metanephrines if pheochromocytoma suspected
Surgical /Diagnostic Interventions - electrophysiologic study if ECG or Holter reveal serious arrhythmia
L REATMENT
Emergent
• ABCs
.
• Treat underlying causes, continuous cardiac monitor Cardiology consult
• Asynchronous defibrillation for VF or pulseless VT
• Unstable patient with atrial fibrillation or other narrow complex tachy -arrhythmia: synchronized cardioversion
Li!EY POINTS
• Mnemonic for etiology: "I GET SMASHED"
• Alcohol and gallstones are the most common causes in North America.
• Think of pancreatitis in your differential when someone presents with severe, acute onset epigastric pain.
• A thorough history (to look for etiology ) and physical exam is key.
• Mainstay of treatment is FLUIDS and pain control .
.
• Pancreatitis can be life threatening. There are tools such as Ranson' s Criteria. BISAP Score APACHE II etc for prognostication. .
• Look for complications and manage accordingly.
DIAGNOSTIC CRITERIA
2 of 3 criteria:
Acute, severe, persistent epigastric pain (often radiating to the back )
• Elevated serum lipase ( 3 x upper limit of normal)
.
• Findings on CT U/S or MRI characteristic of acute pancreatitis
DIFFERENTIAL DIAGNOSIS
Acute Pancreatitis
— c<u .
• Obstructive: cholelithiasis (gallstones), biliary sludge, pancreatic divisum malignancy (pancreatic adenocarcinoma, lymphoma)
OJ
ES
• Traumatic: blunt or penetrating trauma post - ERCP .
• Metabolic: hypertriglyceridemia, hypercalcemia
0 O
)"
0) . . . .
• Infectious: coxsackie mumps VZV. CMV hepatitis B, mycoplasma, legionella salmonella, ascaris toxoplasma .
. . .
• Drugs/ toxins: ethanol, methanol, azathioprine valproic acid, pentamidine, steroids 5 - A 5 A metronidazole, salicylates, scorpion
sting
• Other: autoimmune, ischemia, vasculitis
Mnemonic for etiology: "I GET SMASHED"
. . . . . .
• Idiopathic Gallstones EtOH Tumors Scorpion sting Microbiological/ infectious. Autoimmune Surgery/ trauma Hypertriglyceridemia . .
.
Embolic/ ischemia Drugs/toxins
nISTORY
ID • Patient ’s name . .
age gender
CC • Epigastric pain
HPI • Location: usually epigastric, less commonly RUQ .
DDx RUQ pain: biliary colic, acute cholecystitis, acute cholangitis, hepatitis, pyelonephritis, pneumonia
>
> DDx epigastric pain: myocardial infarction, peptic ulcer disease/perforation, ruptured AAA gastritis . .
GERD DKA .
• Onset: acute vs. chronic (usually acute)
.
• Precipitants: EtOH anti-hyperglycemics, ERCP
• Position: pain often relieved sitting forward, worse leaning back
HEENT
• Jaundice ( scleral icterus)
RESP
• Decreased airway entry may suggest pleural effusions: bilateral rales may suggest acute respiratory distress syndrome (severe cases)
ABDO
. .
• lnspection: distension ecchymosisaroundumbilicus (Cullen’ssign - hemorrhagicpancreatitis ectopic),ecchymosisalongtheflank (Grey
Turner 's sign - hemorrhagic pancreatitis, ectopic pregnancy)
• Auscultation: bowel sounds (hypoactive may suggest ileus)
• Percussion: tenderness to percussion (peritonitis), hyperresonance ( suggests ileus)
.
• Palpation: epigastric tendernes guarding, rigidity, rebound tenderness (peritonitis)
> Murphy's sign - press firmly on RUQ while pt inspiring - test is positive test if pt stops inspiring (acute cholecystitis)
Laboratory investigations
. . . .
• CBCd INR PTT, electrolytes BUN creatinine, blood glucose, calcium CRP .
• Lipase CD
. .
• Liver enzymes ( ALT AST ALP)
CL fl>
Q. 3
.
• LFTs (INR bilirubin, albumin)
3 Q>
.
• Triglyceride level lgG4 level (if clinically indicated) D
( —
Radiology/ lmaging
• Abdominal X -ray: usually normal: may see colon cut -off sign (sentinel loop)
• Chest X - ray: usually normal: may see free air (perforation) , pleural effusions, bilateral pulmonary infiltrates ( acute respiratory distress
syndrome)
• Abdominal U/S:pancreatitis - enlarged,hypoechoicpancreas;cholecystitis /choledocolithiasis - cholelithiasis,gallbladderwallthickening
( > 3mm) , pericholecystic fluid, dilated CBD: pancreatitis complications ( thrombosis, pancreatic necrosis)
• Contrast enhanced CT abdo: pancreatic inflammation, enlargement, fluid extravasation +/- complications of pancreatitis (pancreatic
necrosis, hemorrhage, abscess, calcification)
• MRI abdo: diffuse enlargement, edema of the pancreas +/- complications of pancreatitis
TREATMENT
. .
Initial - ABCs, establish IV access 02 cardiac monitors
Fluids
• IV crystalloid (some evidence Ringer 's lactate may be preferred) - initially at 5 - 10 mL/kg/hr
> In acute pancreatitis caused by hypercalcemia, Ringer ' s lactate is contraindicated because of the calcium content.
• Close monitoring of vital signs
• Urine output 0.5 to 1mL/kg/hr
.
• Frequent monitoring of vitals IV fluids, and urine output
Pain control - Opioids
-
Early nutrition Oral or enteral nutrition preferred. Timing of initiation depends on severity of pancreatitis, nausea, and pain control .
Monitor for complications - pancreatic pseudocyst,abscess formation, splenic/portal vein thrombosis,bleeding (gastric varices secondary
to splenic vein thrombosis, pseudoaneurysm of splenic artery, duodenal ulcer secondary to enlarged pancreas compressing duodenum),
multiorgan failure, hypoglycemia
.
Consults - Gastroenterology General surgery
PROGNOSTICATION
APACHE II Score
Ranson’s Criteria
BISAP Score
DIFFERENTIAL DIAGNOSIS
Features of Parkinsonism:
• TRAP:
> Tremor ( 4 - 6 Hz resting tremor - ’pill - rolling' hand movement, often asymetric, inhibited during sleep and voluntary movement,
increased by emotional distress)
> Rigidity ( 'cog- wheel ' rigidity)
> Akinesia /bradykinesia
> Postural instability
1. Parkinsonism versus Essential Tremor
2. Causes of Parkinsonism
—<
OJ C
D
Cause Clinical Manifestations
E
Q)
:S u
-
Drug induced Parkinsonism
(neuroleptics, lithium
• Bilateral bradykinesia or tremor
• Symptoms usually improve with drug discontinuation
CD carbonate, metoclopramide,
-2
C
valproate)
Progressive Supranuclear Palsy . early postural instability (<1y of onset)
• > 40 y
• Vertical gaze dysfunction (initially downward gaze, then upward gaze limitation)
• Symmetrical axial bradykinesia + rigidity, tremor uncommon
• Frontal lobe- type dementia
Corticobasilar Degeneration .
• > 45 y assymetric Parkinsonism
.
• Cortical (apraxis difficulty naming objects) and basal ganglia (rigidity in one arm) dysfunction
• 'Alien limb phenomenon' - involuntary, purposeful movement of limb
• Frontotemporal dementia/progressive aphasia
Vascular Parkinsonism • Akinesia + rigidity, lower body Parkinsonism (confined to legs), no tremor
• .
UMN signs (hyperreflexia spasticity), pseudobulbar palsy, dementia
• Poor response to levodopa
HISTORY
.
ID • Patient's name, age gender
CC • Tremor or movement abnormality (common CC is falls in the elderly)
HPI • Acute vs. chronic onset, characterize tremor ( frequency, involved body parts, pronation- supination vs flexion-
extension)
• Provoking/palliating factors: distraction, concentration, rest, posture, EtOH, caffeine, uneven surfaces, dim light
• Presence of other Parkinsonism features:bradykinesia ( slow movements/reaction times, trouble turning over in bed
.
(LR +13‘),troubleopeningjars (LR +6.1,LR -0.26 * ) doingupbuttons ( LR +3,LR - 0.33 *),worsenswhenpatientexcitedi.e.
patient unable to make quick movement to catch a ball), rigidity (painful shoulder common manifestation), postural
.
dysfunction ( feet freezing in doorway ( LR + 4.4 * ), difficulty rising from chairs, falls)
• Functional hx: ADLs, iADLs, decline in function, safety ' Indicates likelihood ratios for Parkinson' s Disease
. .
PMHX • Hyperthyroidism, DM CVA, head trauma CV risk factors, encephalitis, unexplained liver disease (Wilson's
disease)
PSHX • Intracranial surgery
IIREATMENT
PD: trial of levodopa, response to Tx is suggestive of Parkinson's Disease
Indications for hospitalization: neuropsychiatric disturbance, delirium, frequent falls, failure to cope at home
.
Referrals: Neurology if there is diagnostic uncertainty, for help with initiating/adjusting Tx and for follow - up
DIFFERENTIAL DIAGNOSIS
Diagnostic Criteria
• Arterial insufficiency
.
> Classic Hx: exercise - induced,reproducible walkingdistance, rapid relief with rest crampingorachinginspecificareaof leg (buttock,
hip, thigh, calf, foot ) corresponding to occluded vessel
> Atherosclerotic risk factors
> Fontaine’s stages: asymptomatic (I), mildclaudication (Ila), moderate - severe claudication (Ilb), ischemic rest pain ( 111), ulceration or
gangrene (IV)
Common Conditions
• Neurogenic: nerve root compression, spinal stenosis, diabetic neuropathy
• Inflammatory: arthritis, myositis, mechanical muscle pain
• Vascular: arterial embolism, vasculitis, thromboangiitis obliterans ( Buerger ' s Disease)
• Anatomic: compartment syndrome, Baker ' s cyst, popliteal entrapment syndrome
High Mortality/Morbidity
• Acute limb ischemia
Q) > Sudden onset
ro c > 6 Ps ( in temporal order ): pain, pallor, pulselessness, poikilothermia, paresthesia, paralysis
c u
• DVT
<U T3
^ <D BHISTORY
-2 ID • Patient ’s name, age, gender
CC • Lower extremity discomfort or pain with activity
HPI • Aching/cramping/tightening pain in calves ± thighs ± hips ± buttocks (but NEVER in shins)
• Pain onset after fairly fixed distance (claudication distance), relief with rest (< 10 min)
RED FLAGS • Rest pain, non-healing ulcers, gangrene - indicate critical ischemia
PMHX • Atherosclerosis, DM, dyslipidemia, HTN, trauma, vasculitis, RA . Raynaud’s, clotting disorder, stroke, CHF, renal
failure, radiotherapy
PSHX • Bypass graft or stent placement, carotid endarterectomy
FHX • Atherosclerosis and associated sequelae, non -cerebral aneurysm, clotting disorders
SOCIAL • Smoking, drugs
ROS •HEENT: headache (rule out temporal arteritis), vision change
•CV: angina, chest pain
• MSK/ NEURO: focal weakness, focal paresthesias
I I i i II 1
.
Vitals - BP, HR RR , Temp, Sa02, bilateral BP (comment on asymmetry)
Inspection
• Presence of wounds/sores on foot ( LR + 7.0 * ), discoloration (LR + 2.8 * ), atrophic skin ( LR + 1.7 * ), absent lower
limb hair ( LR + 1.7 *)
• Signs of insufficiency
> Arterial: pallor on elevation, dependent rubor, loss of hair, skin may appear shiny/thin, thickened toenails, digital gangrene
> Venous: venous dermatitis (dark pigment, oozing ulcers), edematous
Auscultation
• Listen for carotid, abdominal, renal, and femoral bruits bilaterally: presence of limb bruit ( femoral / iliac/popliteal) ( LR + 7.3 * )
Special Tests
• Role of posture and pain on standing ( to distinguish from spinal stenosis)
• Ankle -brachial index ( ABI)
> Use Doppler to find lower limb vessels
( waveforms - tri/ bi -phasic: normal: monophasic: proximal arterial obstruction)
.
* Ankle BP (highest value of posterior tibial dorsalis pedis, and peroneal arteries) / Brachial BP
. . .
* As compared to angiography ABI is 89% sensitive 99% specific, accuracy of 98% threshold of 0.9 at detecting luminal
stenosis of > 50%
> Note: ABI may be falsely high where vessels are incompressible due to severe atherosclerosis
• Buerger ' s Test - pallor on limb elevation, rubor on limb dependency suggests arterial insufficiency
• DeWeese’s Test - disappearance of previously palpable (or by Doppler ) pulses after walking or climbing stairs
0)
• Venous filling time - With the patient supine, identify a vein on the foot (dorsum), elevate the leg at 45 deg for 1min to empty the
.
-
Q fl>
vein. After a min ask patient to dangle foot at the edge of the bed and measure the amount of time taken to refill the vein ( time > 20 G. D
seconds LR + 3.6 *).
rt> ““
INVESTIGATIONS
Laboratory Investigations
. . . .
• CBC-D glucose Cr electrolytes, clotting profile ESR CRP (if suspicious of inflammatory vasculitic cause), fasting lipid profile, and
fasting glucose
Radiology/ lmaging
• Duplex US
• CT or MR angiography + digital subtraction angiography ( arranged by vascular surgery)
Special Tests
• Treadmill exercise test and ABI pre/post exercise (differentiate neurogenic pseudoclaudication vs. true vascular claudication)
L REATMENT
Emergent
• Acute limb ischemia
.
» Generally. 1/ 3 improve with exercise 1/ 3 stay the same, 1/ 3 deteriorate
• ASA 81- 325 mg daily or clopidogrel 75 mg daily for prevention
• Pentoxifylline (questionable benefit) or cilostazol for claudication symptom relief
Surgical Treatment
• Indicated in patients with severe limb ischemia, significant functional disability, unresponsive to exercise /pharmacotherapy, or have
a reasonable likelihood of symptomatic improvement with surgery
•Type of intervention dependent on extent of disease: balloon dilation, stent placement, grafting, or bypass
• Sympathectomy or amputation considered with risk of sepsis from gangrene, intractable pain at rest, or revascularization not
possible
Follow up -
• Annual follow - up for patients with claudication, assess progression and risk reduction compliance
Referrals
• Vascular Surgery
* Indicates likelihood ratios for peripheral vascular disease
ISTORY
ID • Patient’s name, age, gender
—
OJ C
ES
<D TJ
<D
CC
HPI
• Dyspnea (most common), pleuritic chest pain
• Symptoms: OPQRST, previous episodes
• Exertional
dyspnea, PND, orthopnea, leg swelling (CHF)
<D . fever), hx of aspiration (pneumonia)
• Cough, hemoptysis, infectious symptoms (ex
-2
C
• Constitutional symptoms and risk factors for malignancy
• Jaundice,ascites,easy bruising,fatigue,weight loss,riskfactorsfor livercirrhosis(EtOH use,Hxhepatitisorfatty liver)
• Recent immobility (surgery, travel), hypercoaguability (pregnancy, hormone use, malignancy), unilateral leg swelling,
hemoptysis, previous DVT/PE
• Recent infections, exposure to infectious /TB contacts, travel Hx, chest trauma
RED FLAGS • Always consider PE (75% of patients with PE - induced pleural effusions have unilateral effusions and pleuritic CP; PE
cannot be diagnosed by pleural fluid aspiration)
PMHX • Cancer
• Pneumonia . TB. other lung infections/conditions
• Liver disease: NAFLD . alcoholic liver disease, chronic hepatitis hemochromatosis
,
• Organ failure: heart, liver, kidneys
..
• Collagen vascular disease e g , RA, SLE
• Pancreatitis
• Thyroid disease
PSHX • CABG/valve surgery, any recent surgery ( PE)
FHX • Cancer
PHYSICAL
General Findings ( for pleural effusion) LR + LR -
• ABCs - is the patient stable, gasping for breath, anxious?
Asymmetrical chest expansion on inspection
. .
• VS: BP HR, RR Temp Sa02 . Decreased tactile fremitus
8.1
5.7
0.3
0.2
HEENT
Dullness on percussion 4.8 0.1
• Inspection: accessory muscle use +/- tracheal deviation (large effusion)
• Palpation: lymphadenopathy (TB malignancy). . Reduced breath sounds on auscultation 5.2 0.1
RESP Reduced vocal resonance on auscultation 6.5 0.3
• Inspection: asymetric chest expansion Absence of crackles 1.5 NS
• Percussion: dullness to percussion Pleural rub NS NS
• Palpation: decreased tactile fremitus.
. .
Adapted from Evidence - Based Physical Diagnosis 3rd ed. Steven
• Auscultation: vocal resonance (bronchophony, whispered pectoriloquy, .
McGee MD and The Rational Clinical Examination: Evidence-
egophany), lung sounds (see table) .
Based Clinical Diagnosis. David L. Simel Drummond Rennie
ABDO
• Inspection: jaundice, caput medusae
• Percussion: ascites, hepatosplenomegaly
• Palpation: liver edge
EXTREMITIES
• Unilateral leg swelling ( PE): pedal edema (CHF)
• Crackles
• Whispered pectoriloquy
• Egophony
INVESTIGATIONS 2 13
Laboratory Investigations
=r
fl>
CL 0)
.
• CBC- D, electrolytes, serum LDH total protein, glucose, LFTs, liver enzymes, creatinine
• Further investigations determined by suspected etiology
Radiology/lmaging
D 0)
fD —
• CXR: PA and Lat blunting of costophrenic angles initial sign of small effusion (Lat more sensitive): lateral decubitus
determine if effusion is loculated and to assess for safety of thoracentesis ( must be > 20 mm in height)
• US: to landmark or perform US - assisted thoracentesis, diagnose small effusions, or differentiate effusion from pleural thickening
• CT: to help with identifying etiology by visualizing lung parenchyma and mediastinum
Special Tests
• Thoracentesis for pleural fluid analysis
.
> Do not perform if < 20 mm or clinically a transudate that improves with Tx (CHF post -surgical)
. .
> Fluid analysis: appearance LDH, protein, glucose, pH cell count and differential, gram stain and culture, TB and fungal
cultures, cytology, AFB. adenosine deaminase ( ADA) (if TB suspected), amylase (if pancreatitis suspected)
• Bronchoscopy, needle Bx, or thoracostomy for tissue diagnosis if neoplasm suspected
• ± Pleural Bx
UREATMENT
Treatment Options
• Thoracentesis symptomatic effusions should be drained independent of the cause: indwelling catheter for recurrent effusions
• Tube thoracostomy - .
if associated pneumothorax, empyema, hemothorax, chylothorax or complicated parapneumonic effusion
• NB be cautious * risk of iatrogenic pneumothorax
Further Workup
.
• Manage underlying cause of effusion (e g., abx for infectious, diuresis for heart failure, anticoagulation for PE)
Surgical
• Pleurodesis for recurrent effusions
• Intrapleural fibrinolysis for loculated effusions
• Thorascopic surgery for certain cases of complicated empyemas and parapneumonic effusions - adhesion breakdown, chest tube
placement, decortication
DIFFERENTIAL DIAGNOSIS
Differential Diagnosis Classic Symptoms/Signs
Mechanical Osteoarthritis Bouchard/Heberdon's nodules, pain worse with activity, obesity, spares MCPs
Inflammatory Rheumatoid arthritis AM stiffness, worse with inactivity, constitutional symptoms, tends to affect the small
peripheral joints, spares DIPs
Spondyloarthropathies (ankylosing AM stiffness, worse with inactivity, constitutional symptoms, buttock/lower back pain,
.
spondylitis, reactive arthritis IBD - dactylitis, uveitis, preceding GI/GU infection, known IBD. plaque psoriasis, nail changes
.
associated psoriatic)
-
Crystal induced arthropathy (gout ,
pseudogout ) meals
.
Episodic, typically older, men > women associated with diuretic use and high protein
Connective tissue diseases ( SLE. SLE: malar rash, discoid rash, oral ulcers, alopecia, hematuria
Sjogren's scleroderma, myositis
MCTD)
. Sjogren's: xerostomia, sicca
—-
OJ C
C
<D
<D
u
0 Vasculitis
. .
Scleroderma: sclerodactyly telangiectasias. calcinosis Raynaud 's, dysphagia
.
Myositis: proximal muscle weakness Gottren’s papules, heliotrope rash, shawl sign
.
Small vessel: purpura/petechiae hematuria, hemoptysis, saddle -nose deformity
0) Medium vessel: mononeuritis multiplex, hematuria
Large vessel: stroke, peripheral vascular disease, abnormal pulses, jaw claudication, scalp
tenderness
Infectious Septic arthritis (usually mono- or
oligoarticular )
.
Fever, prosthetic joints IVDU. recent gonococcal infection
.
Systemic viral infections (HIV HBV. Constitutional symptoms, IVDU
. .
HCV, EBV CMV parvovirus, rubella)
Lyme and other tick - borne illnesses Travel history, history of tic bite
Endocrine/ Hypo/hyperthyroidism (see stations on thyroid disease)
Metabolic
Hyperparathyroidism (see station on hypercalcemia)
Hemochromatosis Frequent transfusions
Wilson's disease Kaiser -Fleishcer rings, confusion
Malignancy Multiple myeloma Fatigue, bony pain
Bone metastases Esp. breast, lung, prostate Ca
Paraneoplastic syndromes Known lung cancer
Miscellaneous Polymyalgia rheumatica Proximal muscle pain
Sickle cell disease
Sarcoidosis .
SOB erythema nodosum
Amyloidosis
Fibromyalgia, chronic fatigue .
Depression, anxiety, other chronic pain syndromes ( IBS chronic pelvic pain)
Hemarthroses Anticoagulated, known bleeding diathesis, trauma
HISTORY
. .
ID • Patient 's name age gender, ethnicity
CC • Joint swelling, joint pain, decreased range of motion
HPI • Timing of onset (acute vs. chronic vs. episodic)
• Identify involved joints
• Features ofinflammatory arthritis: AM stiffness, pain worse at rest, constitutional symptoms
• Features of osteoarthritis: no AM stiffness, pain worse with activity
• Improvement with NSAIDs
RED FLAGS • Abnormal vitals, symptoms > 6 weeks, immunocompromised, rapid onset /progression
bearing, constitutional symptoms
. STI/IVDU, non-weight
PMHX • Recent GI/GU infection (reactive arthritis). IBD. psoriasis, vasculitis, connective tissue disease. OA. malignancy,
autoimmune disease, previous trauma. depression/IBS (associated with fibromyalgia)
SOCIAL • EtOH, smoking . IVDU, camping/travel occupation, insurance coverage (for biologies)
,
PHYSICAL
General: Vitals signs and general appearance
HEENT
• Malar rash, oral/nasal ulcers, heliotrope rash, alopecia, telangectasias, conjunctivitis (connective tissue diseases )
• Scalp tenderness, abnormal temporal pulse ( GCA / PMR), Kaiser - Fleisher rings ( Wilson’s disease), saddle - nose deformity (GPA ) .
tophi on ears (gout)
CV/RESP: Systemic features of connective tissue disease and vasculitis include: pericardial rub, dullness to percussion (pleural
effusion), crackles (interstitial lung disease) O 13
ABDO: Signs of ascites, masses, hepatosplenomegaly) -
Q CD
MSK G. 3
D CD
• Examine all painful/swollen joints (compare them opposite side, and exam the joint above and below) fD “
• General approach to joint exam:
> Inspection: SEADS [ ( S) welling, (E) erythema/ecchymosis, ( A ) trophy/asymmetry, ( D) deformity /distribution, (S) kin changes /scars]
> Palpation: warmth, tenderness, effusion ( wipe- bulge sign for small knee effusion and ballotment /patellar tap for mod -large
knee effusion), subcutaneous nodules, crepitus
> Range of motion: active first, then passive if needed
• Special tests: joint -specific, tender points (especially knees - > fibromyalgia), peripheral neurological exam (motor, sensory, reflexes)
INVESTIGATIONS
Laboratory Investigations
• CBCd (may have anemia of chronic disease, leukocytosis/leukopenia, thrombocytosis/thrombocytopenia)
• Electrolyte, Cr, CRP/ESR, liver enzymes, urinalysis, serum urate
• If suspected RA: RF, anti- CCP
.
• If suspected connective tissue disease: ANA, anti -dsDNA, ENAs C 3 /C4, urine protein- Cr ratio CK .
• If suspected seronegative spondyloarthropathy: HLA-B 27
• If suspected vasculitis: ANCA, anti - GBM
• Others as clinically indicated (blood cultures, iron studies, TSH, Ca / PTH, SPEP/ UPEP)
.
Radiology/ lmaging: CXR, joint X - ray ( target affected joints) MRI (more specific then x -ray, use if diagnosis uncertain /needed)
.
Arthrocentesis with synovial fluid complete cell count + differential Gram stain, culture, crystals
• Septic arthritis: WBC > 50,000
• Inflammatory arthritis: WBC 2,000- 25,000
L REATMENT
Emergent
• Septic arthritis: empiric IV abx, debridement PRN
• Pericardial /pleural effusion: consider systemic high dose steroids (e.g., prednisone 1mg/ kg PO)
Treatment Options (out -patient )
• Rheumatoid arthritis
> Non- pharmacologic: exercise, education, consult PT/OT
> Symptom control: NSAID ( topical /oral), low dose oral steroids ( < 15 mg/d) once diagnosed, or intraarticular steroid
> DMARD: Methotrexate ( first line) ± hydroxychloroquine, sulfasalazine, or azathioprine
.
> Biologic anti -TNF ( infliximab, adalimumab, etanercept), anti- CTLA - 4 ( abatacept ) anti - CD20 (rituximab)
• Osteoarthritis
> Non -pharmacologic: Wt loss, exercise, education, physiotherapy, walking aid
.
> Symptomatic relief using analgesia: acetaminophen, acetaminophen around the clock, NSAIDs intraarticular steroid injection
> Orthopedic Surgery referral for potential replacement
DIFFERENTIAL DIAGNOSIS
Proteinuria Gold Standard: >150 mg/ 24 hr Urine (UrPnUrCr > 13mg/mmol random sample)
Dipstick Positive Dipstick Negative, Positive PCR Dipstick Negative, Positive ACR
—<
TJ C
0)
Primary Glomerular Secondary Glomerular Many Peaks Monoclonal
CD *o)
C 0 Renal disease Systemic disease
" 2 Nephrotic • Diabetes Tubular Overflow
• Membranous GN (elderly) • Lupus Impaired tubular Increased low-
• Minimal change disease ( < 15 yr, > 50% • Infection: (typically reabsorption <1- 2 g/day molecular
.m .
membranous) HIV Hep B and C . .
(i.e. Fanconi Syndrome . weight protein
Nephritic
•
endocarditus, syphilis
Malignancy (breast, colon, lung)
ATN AIN). production (i.e..
multiple myeloma,
• IgA Nephropathy ( < 10% pure nephrotic)
.
• Anti GBM Ab ANCA, Lupus
•
•
Amyloidosis
.
Meds (NSAIDs penicillin, cold)
amyloidosis,
rhabdomyolysis)
HISTORY
ID • Patient 's name . age. gender
CC • Lower extremity or periorbital edema, abdominal swelling, foaming urine
HPI • Dysuria, urinary frequency, fever, unwell, peripheral/generalized edema
• Vasculitis (rash, joint pain)
• Polydipsia , polyurea , weight loss, new diagnosis of DM
• Connective tissue disease ( Raynaud 's, photosensitivity, oral ulcers)
• PE or DVT, infection (complications)
PMHX • DM , HTN, lupus, collagen vascular disease , malignancy, glomerulonephritis, illnesses associated with|serum
protein levels (multiple myeloma, amyloidosis, macroglobulinemia, leukemia )
FHX • Hereditary nephropathies ( Alport 's/PKD)
MEDS • Nephrotoxic substances (NSAIDs), contrast dyes
ROS • DM - retinopathy, neuropathy, poor wound healing, foot ulceration
• CV disease (proteinuria is a risk factor )
CV
• pericardial rub (uremic pericarditis) - found in renal failure
RESP
• pleural effusion and crackles with volume overload
ABDO
.
• Ascites, attempt kidney palpation (rare, may be enlarged in amyloidosis DM, HIV, PKD)
DERM
• Rash, pallor if anemic (secondary to chronic renal disease), generalized edema ( anasarca) in nephrotic syndrome
INVESTIGATIONS
Laboratory Investigations Nephritic Nephrotic
• CBC- D (low Hb in chronic kidney disease)
• Hematuria (microscopic) • Edema
.
• SrCr Urea, electrolytes
• RBC casts • Lipid casts, hyperlipidemia
.
• Glucose HbAlc (diabetic control) • Dysmorphic RBCs • Hypoalbuminemia
• Albumin, fasting lipid profile (nephrotic syndrome) • Minimal - to -moderate • Massive proteinuria
• ESR , urate; B - HCG ( women of childbearing age) proteinuria ( 3g/ 24h or greater )
Urine
0)
• Urinalysis: UA dipsticks mostly detects albumin (1+ to 4+ with albumin cone.; 3+ correlates with ~3g/L)
f .
Q 0)
• Spot urine protein/Cr ratio ( PCR ): correlates well with 24hr urine collection S 3
• 24hr urine collection for protein and Cr (gold standard but inconvenient)
.
• Examine urine sediment RBC casts/ fatty casts and lipiduria (renal injury)
D Q
CO —
)
Radiology/ lmaging
• Consider renal US to assess for structural kidney disease
• Consider CXR for systemic disease (e.g., sarcoidosis)
Special Tests
• Split 24hr urine collection ( - ve ->- benign positional proteinuria)
• Urine and serum protein electrophoresis (multiple myeloma; overflow proteinuria to determine type)
. . . . .
• Serology: ANA RF p - ANCA, c -ANCA cryoglobulins, complements (C 3 + C 4) , Hep B Hep C, HIV ASOT (post - strep infx), blood
culture, peripheral smear
Surgical/Diagnostic Interventions
• Consult Nephrology and discuss renal Bx with patient
• Consider renal Bx when persistent proteinuria of unknown origin ± abnormal renal function (e.g., renal Bx results may help
determine Tx course for a suspected GN)
LLiEATMENT
If asymptomatic and renal function normal, repeat test in 1- 2 wks
.
• If repeat - ve then proteinurea likely transitional/physiological and does not require follow-up
• Asymptomatic proteinuria without associated disease should be followed closely
• Treat underlying systemic disease and/or look for offending agents
.
If DM with proteinuria, start ACEi or ARB follow K * and Cr after drug initiation
• Screen annually for glomerular dysfunction and subsequent microalbuminuria with spot urine albumin/Cr ratio ( > 30 mg/mmol
early sign of diabetic nephropathy)
Follow -up
.
• Urine dipstick PCR. and ACR should be repeated at each visit until persistently - ve
• Nephrology referral if proteinuria persists, signs or symptoms of decreased renal function
DIFFERENTIAL DIAGNOSIS
DRUG- RELATED • Clonidine, opiates, ASA, calcitriol, QCP (cholestatic ), antifungals, any drug allergy
SKIN DISEASE • Dry skin ( xerosis ), atopic dermatitis (eczema), contact dermatitis, fungal skin infections, psoriasis, scabies, lice
SYSTEMIC .
• Allergy/atopy, cholestasis, thyroid dysfunction, renal failure HIV, neuro (MS, neuropathy), Fe deficiency anemia,
DISEASE hepatic failure or impairment, psychiatric illness
High mortality: malignancy (especially Hodgkin’s lymphoma)
HISTORY
ID Patient 's name, age, gender
HPI Onset, duration ( acute = better prognosis), location of symptoms, migration
Pattern of itch (nocturnal, diurnal, seasonal variation)
Precipitating and palliating factors
Recent exposure to new substances (cosmetics, drugs, foods)
Associated symptoms: inflammation, excoriation/infection at itch site, abdominal pain/ jaundice
Rash Hx (distribution, presence/absence dermatitis, palm/sole involvement)
0)
03 C RED FLAGS Wt loss/fatigue/night sweats (cancer), older age (increase risk systemic disease)
E 2
CD “ PMHX Eczema, dry skin, recurrent skin infections, dialysis, cancer being treated with chemotherapy, psych ( Dx of
O
C D
( exclusion)
«
2 FHX Atopy, food allergy, asthma
MEDS .
Use of any oral (opioids ASA) and topical (hydrocortisone, benadryl, moisturizers) medications
ALLERGIES Medication, foods, and environmental (including animals)
SOCIAL Work environment, exposure to plants, animals, or chemicals, recent travel, smoking, EtOH
ROS Neuro: intermittent weakness, numbness and parasthesias ( MS)
HEENT: visual disturbances (MS)
CV: palpitations, diaphoresis (hyperthyroidism)
Gl: RUQ, steatorrhea (cholestasis)
GU: urinary frequency with excessive thirst and Wt loss (DM)
MSK/DERM: pica with hair thinning
PHYSICAL
General
. .
• Vitals - BP, HR RR, Temp Sa02 (especially if allergic reaction suspected)
• Palpate for lymphadenopathy in head, neck , axillary, inguinal regions - comment on presence, location, size, texture, tenderness,
mobility of LN ( local infection, Hodgkin' s lymphoma)
DERM
-
• Inspect for any erythema, swelling, warmth, and yellow with honey crusting (impetigo) comment on presence, morphology,
borders, extent, and distribution of lesions
• Obvious skin lesions/excoriatins/infections ( indicates derm cause)
• Jaundice, scleral icterus (cholestasis)
ABDO
• Examine liver and spleen size for organomegaly, tenderness, obvious masses
NEURO
• Screening for MS: assess strength, tone, and sensation in the upper and lower limbs
INVESTIGATIONS
Blood Work
• CBC ( Fe deficiency anemia)
• Cr, bilirubin, albumin, ALP (cholestasis)
• TSH (hypo and hyperthyroid)
• Fasting glucose ( DM)
• HIV serology
• G - HCG ( in women of childbearing age)
Special Tests
• Skin testing for specific allergens
• If skin lesion present, scrapings for tinea and culture ( fungal, bacterial, viral )
iEEATMENT
Emergent
• Antihistamines and supportive Tx
Non- Emergent
• Skin care with cool or lukewarm water, limit use of soap, use of moisturizers and emollients
• Avoidance of irritating/tight clothing and contact irritants ( i.e., wool clothing) may also be helpful
• Topical medications (corticosteroids) are effective in relieving itch caused by inflammation in the short term
• Systemic medications for generalized itching or local itching resistant to topical agents
• Treat underlying cause for systemic illnesses
Further workup as indicated by suspected etiology and clinical presentation
2=
n>
Referrals
Q. o>
• Dermatologist if symptoms progress despite topical and systemic interventions or if Dx uncertain
D ID
a> —
KEY POINTS
• Differentiate between pre-renal, renal, and post - renal causes of renail failure
• Recognize indications for urgent dialysis ( AEIOU mnemonic)
• Baseline kidney function (MDRD used in Alberta; other equations include CrCI CKD - EPI, Cockcroft -Gault) .
Renal Failure
Assess Renal Function via • AKI: Increase inSCr by > 30 umol/L within 48 hrs increase in SCr by > 1.5 x .
Cockcroft -Gault Formula .
baseline within 7d or urine volume < 0.5 mUkg/h for 6 hrs
—
C
QJ
CO C
Fractional Excretion
of Na * (FENA) Pre Renal Renal Post Renal
u
<D -a [ (UNa /PNa) + (UCr / Investigations specific to etiology: Post - void residual > 200
C <D
•
-2 PCr )] (interpret with • UNa < 20 mmol / L • ATN: UNa > 40mmol/L FENa > 2%, . cc. Renal U/S may show
caution in diuretic use) • FENa < 1% hemegranular casts hydronephrosis
• BUN: SrCR > 20:1 • Consider GN workup in nephritic
• Estimates what
proportion of filtered Na *
• Bland U/A patients (C 3/C4, HBV/ HCV anti-strep .
Ab, ANA. ANCA. anti - GBM Ab)
is reabsorbed via tubules
Tubular
Hypovolemia
• ATN: ischemia, sepsis, contrast, toxins
.
• Hemorrhage Gl loss, renal
(drugs: aminoglycosides, ampho .
loss (overdiuresis, osmotic pigments: myoglobin) • Ureter: stones, clot, tumor,
e.g., DKA), skin loss (burns), • Intratubular obstruction: crystals fibrosis
decreased PO intake
Decreased ECFV
.
(uric acid, MTX acyclovir ), light chains • Bladder: outlet obstruction,
neurogenic bladder,
(multiple myeloma)
Drugs to Stop in ARF • Cardiogenic/septic shock. CHF . Glomerular malignancy
• NSAIDs
cirrhosis (hepatorenal) 3rd . • Nephritic: anti-GBM antibody, immune
• Urethra: stricture, cervical
• ACEi/ARBs
spacing, hypoalbuminemia
.
complex (SLE IgA cryos post - . . cancer, enlarged prostate,
• Contrast
• Decreased flow through renal
infectious, HBV/ HCV) pauci-immune . misplaced Foley
artery
Stenosis: RAS. FMD RVT . .
(GPA EG PA MPA ) .
• Other
substances
nephrotoxic •
• Offending agents: NSAIDs.
• Nephrotic: systemic ( DM SLE, cryos, .
amyloidosis), primary renal disorders
’Adjust dose for abx and
.
ARBs/ACEIs calcineurin
.
(FSGS membranous MCD MPGN) . .
inhibitors, cocaine
DM meds Interstitial
.
• AIN: meds infections (pyelonephritis),
infiltrative ( Sjogren's, sarcoid), idiopathic
• Vascular: thrombotic microangiopathies
(malignant HTN TTP/ HUS cholesterol. . Treatment:
emboli)
• Resolve obstruction*
Treatment:
• Lower Tract: Foley/suprapubic
• Discontinue nephrotoxins Treatment:
catheter
• Restore perfusion and • Discontinue nephrotoxins
• Upper Tract: Stent (urology) or
correct volume deficits • Prevent hypoperfusion and
nephrostomy tube (radiology)
( fluid resuscitation, treat dehydration
• Monitor for post -obstructive
underlying cause) • Consider Nephro consult diuresis
HISTORY
ID • Patient ’s name, age, gender
• Often asymptomatic
.
CC • Uremic symptoms (weakness, fatigue N/V, poor appetite, pruritis, confusion, restless legs/nocturnal leg cramps,
SOB, chest pain (pericarditis))
• Prerenal: volume depletion (dehydration, diarrhea, diuretics, vomiting); causes of decreased ECFV (CHF
symptoms - SOB, PND, orthopnea, edema), drugs ( ACEi/ARB/NSAIDs)
.
• Renal: flank pain, edema HTN, Hx of dialysis/transplant, vasculitis (rash, joint pain, gross hematuria), muscle injury
(rhabdomyolysis), recent scans (contrast -induced nephropathy), recent infections ( PIGN), recent meds ( AIN - also
HPI
fever, rash)
• Post-renal: dribbling, weak stream, hesitation, frequency, nocturia, urine retention, dysuria
• Generic: U/O, edema
PMHX
• DM, CAD .
CHF, HTN, liver disease (hepatorenal), pregnancy (TMA ), vascular disease (emboli), structural (solitary
kidney, BPH) scleroderma, SLE, vasculitis, Goodpasture’s, streptococcal infections
3
PSHX • Genitourinary tract procedures, nephrectomy, donation/ transplant CD
-
Q rt>
FHX • Polycystic kidney disease, Alport syndrome, deafness, end stage renal disease .
G 3
MEDS • Nephrotoxic .
substances (aminoglycosides, other abx, furosemide contrast, NSAIDs, ARB, ACEi)
3 O)
to
.
SOCIAL • Smoking EtOH, IVDU, cocaine
• General: infectious symptoms, weight changes, fatigue, poor sleep, difficult concentration
General
• Vital signs, level of consciousness
Volume status
• Overloaded: engorged neck veins, pretibial/sacral edema, respiratory crackles S3 .
• Hypovolemic: flat neck veins, poor skin turgor, dry oral mucosa/tongue furrows, dry axillae
DERM
• Uremic frost (rare) , diffuse rash ( AIN or CTD) , livido reticularis, needle / track marks, crush injuries/ fracture ( ATN or hypoperfusion)
CV
• S3, pericardial rub (uremia)
RESP
• Crackles (volume overloaded)
ABDO
• Palpate for ascites ( bulging flanks, flank dullness, shifting dullness, fluid wave) , hepatomegaly, ballotable kidneys ( PCKD), distended
bladder (obstructive, post renal)
• Percuss for CVA tenderness
• Auscultate for renal bruits
GU
• Pelvic exam (cervical cancer ) or DRE (prostatic enlargement )
TREATMENT
• Goal: to achieve euvolemia and normotension
• Avoid further nephrotoxins and hypotension ( stop NSAIDs, ACEi/ARBs, other nephrotoxins); avoid contrast if possible: ensure renal
dosing of all medications especially antibiotics and diabetic medications
• Renal Bx when cause not found and /or renal cause suspected
• Treat complications ( fluid overload with NaCI restriction and loop diuretics, hyperkalemia with IV Ca if indicated, agents to shift and
eliminate K)
• Critically ill: admit to ICU
• Follow -up to ensure resolution of acute process
• Referrals to nephrology ( for dialysis planning) or urology (obstructive)
KEY POINTS
• Cardinal spirometry findings of restrictive lung disease: normal FEV1/FVC and low VC and TLC
• If reduced DLCO: intrinsic ( intraparenchymal). If normal DLCO: extrinsic (chest wall, neuromuscular)
• Idiopathic pulmonary fibrosis has high morbidity/mortality
• CXR is the most important initial investigation. Consider lung Bx for further workup if Dx unclear and refer to respirologist
• Treatment is dependent on the pathology of the fibrosis and clinical condition
DIAGNOSIS
Diagnostic Criteria:
• Characterized by reduced lung volume and reduced lung compliance: total lung capacity (TLC): < 80% of predicted . fo reed vital
.
capacity ( FVC) and T forced expiratory volume in 1sec ( FEV1) normal FEV1: FVC ratio ( >0.75)
• Normal airway resistance with no airway obstruction
• DLCO usually decreased if caused by parenchymal lung disease
High Mortality/Morbidity:
• Idiopathic pulmonary fibrosis ( IPF) is most common idiopathic etiology. Median survival time is < 3 yrs
• Poor outcome predictors/risk factors: male, old age, severe dyspnea, cigarette smoking Hx, severity of fibrosis on imaging
—ca c d) Differential Diagnosis:
• Anatomic Approach (1) Parenchymal ( 2) Pleura ( 3) Chest Wall ( 4) Neuromuscular
Ely
CD xi . . . .
• 6 Is of ILD: Inflammatory Immunologic Infiltrative Inhalational Iatrogenic. Idiopathic
QJ
CLASSIFICATION OF RESTRICTIVE LUNG DISEASE
Intrinsic Lung Disease Extrinsic Lung Disease
Idiopathic e.g.lPF,otheridiopathicinterstitialpneumonias (e.g. Chest Wall e.g., kyphoscoliosis, morbid obesity,
Interstitial desquamative,cryptogenic organizing pneumonia) Deformity ankylosing spondylitis, trauma
Pneumonias e.g., Muscular dystrophy, Guillain-
Neuromuscular
Inflammatory/ e.g., sarcoidosis, vasculitis, connective tissue Barre syndrome,myasthenia gravis,
.
Immunologic diseases (e.g. SLE, RA systemic sclerosis)
Weakness
ALS, diaphragmatic paralysis
Infiltrative
e.g., lymphangitic carcinomatosis,
Pleural Disease
.
e.g. large pleural effusion,
lymphoma, amyloidosis pleural plaques, mesothelioma
Inhalational
.
e.g., asbestosis silicosis, hypersensitivity .
CNS e.g., Parkinson's MS, post -polio
pneumonitis (Farmer ' s lung, bird fancier’s disease)
Iatrogenic
.
e.g. chemotherapeutics, radiation
fibrosis, medication- induced
HISTORY
ID • Patient ’s name, age, gender, occupation
CC
• Progressive dyspnea, dry cough, iexercise tolerance
HPI • Duration: acute < 3wks, subacute 4 - 12wks, chronic > 12wks . or episodic
• Aggravating and relieving factors, pleuritic chest pain
• Hemoptysis (vasculitis . anti-GBM . fever pulmonary infection inflammatory
) ( , )
• Sleep - disordered breathing (neuromuscular), chest/spinal deformities,Hx of trauma
RED FLAGS • Severe dyspnea, hemoptysis, Wt loss, fatigue, night sweats
PMHX • Connective tissue disease, neuromuscular disease, recurrent pulmonary infections, immunosuppression/
immunodeficiency, cancer, previous radiation
-
MEDS • Drug induced ILD (chemotherapeutics, immunologics /DMARDs, antiarrhythmics, abx), herbals
ALLERGIES • Hypersensitivity to dust, pollen
FHX • Sarcoidosis. Most patients with IPF have no family Hx
SOCIAL • Occupational and domestic Hx - job duties, hobbies, exposure to environmental substances (asbestos, silica,
coal)
• Smoking Hx ( IPF, desquamative interstitial pneumonia). Smokers less likely to have sarcoidosis or hypersensitivity
pneumonitis
• Travel Hx . HIV risk factors, illicit drug use
229 on M
ROS • CV: cyanosis, pulses, cardiac function
• GI: GERD
• NEURO: generalized weakness, numbness, fatigue, proptosis, diplopia
• RHEUM: rash, joint pain, eye symptoms
PHYSICAL
General
. . . .
• ABC VS (BP HR RR Temp Sa02) .
.
• Respiratory distress ( accessory muscle use nasal flaring: especially in NMD)
• Body habitus (obesity)
HEENT
.
• Inspection: Central cyanosis, uveitis ( sarcoidosis or CTD) malar rash ( SLE), heliotrope rash (dermatomyositis)
• Palpation: Lymphadenopathy (sarcoidosis)
CV
• Palpation: Right - sided heave (cor pulmonale 2° to advanced pulmonary fibrosis)
• Auscultation: Cardiac arrhythmias (sarcoidosis), loud P2 and/or right sided gallop (cor pulmonale)
Respiratory
• Inspection: Chest wall deformity, kyphoscoliosis
• Palpation: Asymmetrical chest expansion, decreased tactile fremitus (pleural effusion 2° to asbestosis, drug-induced ILD, CTD)
. .
• Percussion: Dullness to percussion (pleural effusion 2° to asbestosis drug- induced ILD CTD)
• Auscultation: Symmetric and dry “ Velcro"-like inspiratory crackles ( > 90% of patients with IPF, CTD), wheeze/inspiratory squeak
( sarcoidosis, hypersensitivity pneumonitis, bronchiolitis)
DERM/MSK
.
• Inspection: Peripheral cyanosis, clubbing (IPF) Raynaud’s phenomenon (systemic sclerosis ), erythema nodosum (sarcoidosis) 2 13
=r
fD
.
• Palpation: Joint swelling ( RA CTD) Q fD -
INVESTIGATIONS G.3
D CO
Laboratory Investigations fD “
. . . . . . . . . .
• CBCdiff lytes Cr BUN LFTs CRP,e!evatedCa(sarcoidosis) elevatedCK:(myositis) antibodies( ANA ENA ANCA RF,anti- CCP,anti- dsDNA)
Radiology/Imaging
• CXR
> Most common abnormality is reticular pattern in fibrosis
> Honey combing/ground glass (advanced fibrosis)
.
> Upper lung involvement ( sarcoidosis, silicosis, hypersensitivity pneumonitis) vs. lower lung involvement ( IPF, CTD asbestosis)
.
> Pleural disease (CTD, asbestosis sarcoidosis, radiation-induced)
> Bilateral hilar lymphadenopathy + reticulonodular pattern (sarcoidosis)
> Cobb Angle > 100° indicates severe deformity in scoliosis
• CT Scan
> Assists with identifying underlying etiology i.e., bibasilar involvement and peripheral infiltration in IPF: bilateral cysts /nodules,
reticular fibrosis, and air spaces in ILD
Special Tests
• Pulmonary Function Test
.
> Reduced TLC ( amount determines severity) FRC, and Residual Volume (RV)
.
> Decreased FEV1and FVC thus normal or increased FEV1/FVC ratio
> Please refer to station Pulmonary Function Tests station for more details
> Concurrent obstructive and restrictive pattern on PFT characteristic of sarcoidosis or combined obstructive/restrictive diseases
Surgical/ Diagnostic Interventions
• Bronchoalveolar lavage ( BAL): May see malignant cells, asbestosis bodies, eosinophils, hemosiderin macrophages
• Transbronchial or surgical lung Bx for definitive Dx, exclusion of malignancy or infection to predict prognosis
TREATMENT
Emergent
.
• Airway management: high flow 02. BIPAP intubation with respiratory therapy present
• ICU consult
Treatment Options - specific treatments depend on etiology
• IV corticosteroids, immunosuppresive medication, based on the etiology
.
• Correct ventilation problems in chest wall deformities: +ve pressure mask, tracheotomy Wt loss
.
• Consider lung transplant if no response to Rx severe functional impairment, deteriorating course or 02 dependent
• Counselling on smoking cessation
Referrals
• Respirology
KEY POINTS
• A thorough history of symptoms before, during, and after the event is key to distinguish seizures from seizure mimics
• In patients presenting with first time seizures, always order Na, glucose, and CT head
• Immediate treatment of status epilepticus (seizure lasts > 5 min) is key for reducing mortality
DIFFERENTIAL DIAGNOSIS
Definitions
• Seizure: abnormal and unregulated electrical neural discharge that interrupts normal brain function and causes altered awareness,
abnormal sensations, involuntary movements, and /or convulsions
• Seizures can be epileptic or non - epileptic:
> Epileptic seizure disorder ("epilepsy ”): a chronic brain disorder involving recurrent ( > 2) seizures without a reversible disorder
or stressor
.
> Non -epileptic seizures: caused by a temporary disorder or stressor (e.g.. metabolic disorders CNS infections CV disorders,
drug toxicity/ withdrawal)
.
Common Conditions
• Drugs: EtOH/ benzodiazepine withdrawal,
cocaine, LSD, methanol, ethylene glycol .
—Ely<
(TJ
D
C
.
TCAs insulin, prescription drugs
• Infections: febrile seizure, meningitis,
encephalitis
<D TD • Metabolic: hypoglycemia, hyponatremia,
CD
hypocalcemia, non- ketotic hyperglycemic
hyperosmolar coma ( NKHHC),
hyperthyroidism
• Structural: mass (tumor, abscess, blood) ,
stroke, trauma, congenital malformations
Seizure Mimics
• Migraine, syncope, stroke /TIA, psychogenic, movement disorders, night terrors, panic attacks
• Absence of post -ictal phase suggests seizure mimic
Complications
• Aspiration, hypoxia -
hypoxic brain injury, aspiration pneumonitis/pneumonia
• Lactic acidosis, rhabdomyolysis - ARF
• Status epilepticus: > 30min of continuous seizure activity (or recurrent seizures without full recovery). If seizure > 5 min, consider
status epilepticus and treat immediately.
HISTORY
ID • Patient’s name, age, gender
HPI • Pre -ictal:
• Aura (simple partial), automatisms (complex partial)
• Triggered by intense emotion/exercise, pallor, lightheadedness, diaphoresis (syncope)
• Ictal:
• Loss of awareness, aura, abnormal motor activity ( tonic , clonic, atonic), muscle tone (rigid vs. flaccid), facial
involvement (head or eye deviation, tongue biting, excess blinking), symptom lateralization (one eye, one side
of face, one limb affected), incontinence, tongue -biting, automatisms
• Numbness, weakness, CV risk factors (TIA)
• Visual aura, N/V, pounding hemi- cranial headache (migraine)
• Waxing/ waning movements, pelvic thrusting, sobbing or moaning during event (psychogenic)
• Post -ictal:
• Disorientation, lack of awareness
• Hemiparesis and hemiplegia (Todd's paralysis suggests focal onset)
• Events prior to incident: infection, fever, trauma, medication /drug use
• Triggers: sleep deprivation, flickering lights, menses, hyperventilation, voiding/defecation
RED FLAGS • Status epilepticus (seizure lasting > 5 min)
• Sudden or "worst ever " headache ( SAH)
• Stiff neck, fever (meningitis)
• Focal neurological signs
PMHX .
• Prior seizures or dx of epilepsy ( age of onset, duration of event ( s) frequency of event ( s )), CNS ( infection, neoplasm,
injury), cerebrovascular disease DM .
231 Edmonton Manual of Common Clinical Sccn.n
FHX • Epilepsy, neurologic or developmental disorders
PO&GHX • If pregnant: hx of gestational HTN, pre -eclampsia, eclampsia
MEDS • Psychotropics, benzodiazepines, theophylline, bupropion, meperidine
SOCIAL • EtOH .
( withdrawal), other drug use occupation, motor vehicle license
ROS • HEENT: fever, headache, stiff neck
• CV: chest pain, palpitations
• RESP: shortness of breath
PHYSICAL
General
• Assess ABCs and GCS - confusion/memory disturbances can be present post - seizure
.
• VS: BP HR, RR, Temp, Sa02
> HR (irregular may suggest syncope)
> BP ( fin i
stroke, in cardiogenic syncope transiently), fever (infection), hypoxia (hypoxic seizure)
Neurologic
• Often normal, focal neurologic findings suggest local pathology
• CN: asymmetry, speech difficulties, pupil asymmetry (SAH)
• Tone: spastic (cerebral palsy post -stroke)
• Strength: grade from 1- 5 , look for lateralizing weakness ( Todd’s paralysis - transient paralysis lasting < 48 h vs. stroke)
.
• DTR : grade from 1- 4 ( UMN, hyperthyroid) ( LMN), symmetric vs. asymmetric 2) =Dr
0
• Sensory 0.0
• Cerebellar/Gait Assessment Q. o
D Q)
INVESTIGATIONS n>
Blood Work
.
• CBC-D, electrolytes: Na \ Ca24 glucose, troponin, Cr, urea ( renal failure)
. . . .
• CK (rhabdomyolysis), TSH INR, AST ALT, bilirubin ALP ( liver failure), G - HCG toxicology
• Prolactin measured 10- 20 min after event. If elevated, it ’s helpful in distinguishing generalized tonic clonic or complex partial
symptoms from psychogenic non-epileptic seizure. PRL cannot be used to distinguish seizure from syncope,
Radiology/Imaging
• CT head
Special Tests
• LP: if signs of infection or immunocompromised patients
• EEG: emergent for status epilepticus, recommended for all patients with new onset seizure (may be done as outpatients)
L REATMENT
Emergent
. .
• ABCs VS and prevent injury/aspiration
• Acute seizure
Education
• Seizure precautions - no swimming/ bathing alone, avoid heights, avoid baths, no fire
• No driving until evaluated by neurologist ( should have a normal CT head and EEG)
Referrals
• Neurology follow -up as an out -patient for assessment of possible epilepsy
• Radiology for MRI to further delineate intracranial pathologies
Diagnostic Criteria
• T tissue perfusion, with possible end organ failure or dysfunction (most important aspect of shock to consider)
• Hypotension ( sBP < 90 mmHg)
• Tachycardia ( HR > 100 bpm)
• Bradycardia (neurogenic or decompensating)
DIFFERENTIAL DIAGNOSIS
Types of Shock:
• Hypovolemic (H): insufficient circulating volume due to fluid loss
.
> External hemorrhage, Gl bleed, dehydration N/V/ D, pancreatitis, severe burns
• Obstructive (O): circulation impeded due to obstruction of heart or great vessels
.
> PE caridac tamponade, tension pneumothorax, constrictive pericarditis
• Distributive (D): insufficient intravascular volume due to redistribution
.
> Sepsis, anaphylaxis Addison' s crisis, myxedema coma, neurogenic shock
• Cardiogenic (C): circulation impeded due to failure of the heart to pump effectively
. .
> Ml, CHF arrythmias hypertrophic cardiomyopathy, aortic stenosis, aortic dissection B blockers .
—Ely
QJ
05 C • ’Combined: can have two or more types of shock (e.g., a trauma patient may have both hypovolemic and distributive shock)
High Mortality/Morbidity
GJ U • If untreated could lead to death
GJ
• Most common cause is hypovolemic
• Shock in a trauma patient is considered hemorrhagic/ hypovolemic until proven otherwise
HISTORY
Note: If patient is unstable, manage ABCDEs first and then proceed with emergency SAMPLE Hx ( Symptoms (related) Allergies . .
. . .
Medications Past medical Hx (relevant) Last meal Events prior to presentation)
ID • Patient 's name, age, gender
ROS • HEENT: lightheadedness, altered LOC . vision problems, throat closing, eyes swollen shut
• CV: palpitations, cold extremities, chest pain
• RESP: SOB
• Gl: distension, bleeding, pain
• GU: bleeding, pain
• MSK/DERM: rashes ( anaphylaxis), unable to feel/move limbs, obvious pain/trauma, sacral sensation
PHYSICAL
General
.
• ABCDE vital signs (including orthostatic VS) GCS C / S . .
• Examine for signs of distress
DERM/ MSK
• Expose entire body: chest, abdomen, back , extremities
..
• Examine for signs of trauma, hives, rashes (i.e pruritic rash/bruising, urticaria, cellulitis, open wounds /ulcers [ esp sacral and foot
ulcers ])
NEURO
• Hyperreflexia .istrength of limbs, lack of sensation in perianal area
vasodilation) fD ~
Cardiogenic Cool extremities High JVP Crackles on chest auscultation
.
(pleural effusion) S3 gallop
INVESTIGATIONS
Blood Work
• I f
ABG ( 02 perfusion measured by lactate, metabolic acidosis, and base excess) f
• . . . . . .
CBC- D, electrolytes Cr / BUN AST ALP glucose, lipase, amylase INR/ PTT, fibrinogen, blood type and screen D-dimer T& C . .
. .
troponins, blood culture, cortisol CK. EtOH/ tox screen, B - hCG urinalysis, lactate (prognostic marker )
Radiology/ lmaging
. .
• Plain films: CXR AXR, C /T/ L spine XR XR limbs
• CT ( head, thorax, abdo)
• FAST, abdo US
.
• Echo EKG
Special Tests
• Culture potential sites suspicious for infection ( blood, urine, sputum, LP)
• FAST, pulmonary artery catheterization for pressures
Surgical/Diagnostic Interventions
• Diagnostic laparotomy, thoracotomy, decompression
[ TREATMENT
Emergent Resuscitation Fluid Examples
.
• ABC c -spine collar .
Normal Saline Ringer ’s
. .
• For all cases of shock: 2 large bore for IV resuscitation 02 monitors, Crystalloid
Lactate
identify underlying cause
.
• Foley (unless urethral trauma) C- spine collar
Colloid . .
Albumin FFP Dextran
Blood pRBC
Treatment Options
• Anaphylactic: epinephrine, benadryl, H 2 blocker, steroids, supportive care,
find causative agent
• Distributive: locate and treat underlying cause ( antibiotics /Epi -pen until sepsis or anaphylaxis is ruled out ), vasopressors, supportive
care
. .
• Cardiogenic: cath lab or thrombolysis, be careful of fluid overload IABP ionotropes
.
• Hypovolemic: fluid resuscitation/blood products, monitor 02 locate and treat underlying cause
. .
• Obstructive: remove obstruction (pericardiocentesis embolectomy needle decompression) , supportive care
Surgical
. .
• Source control i.e. stop bleeding, treat infection sources (e.g. remove abscess, excise necrotic bowel)
KEY POINTS
• Differentiate causes of sleep- disordered breathing
• Differentiate between OSA and CSA
.
• Lifestyle modification (e g. . Wt loss, avoid alcohol) and non-invasive ventilation (e.g., CPAP) are the main treatments for OSA
DIFFERENTIAL DIAGNOSIS
Disease State History Diagnostic Criteria
Obstructive • Daytimesleepiness • Determined by the Apnea / Hypopnea Index ( AHI) on a sleep study:
Sleep Apnea • Morningheadache • Mild: AHI 5 - 15
• Unrefreshed sleep • Moderate: AHI 15 - 30
• Witnessed apneas • Severe: AHI > 30
• Snoring • One or more of the following are required if AHI < 15:
• Requires daytime • Sleepiness, nonrestorative sleep, fatigue, or insomnia symptoms
naps • Waking up with breath holding, gasping, or choking
• Sleepy while • Habitual snoring, breathing interruptions, or both (noted by a bed partner or other
in social observer)
— <u
(Z
C
D
C
circumstances
• Hypertension
• Hypertension, mood disorder, cognitive dysfunction, coronary artery disease, stroke,
congestive heart failure, atrial fibrillation, or Type 2 diabetes mellitus
CD Central Sleep • Disrupted sleep • Polysomnography ( PSG) reveals > 5 central apneas and/or central hypopneas per hour of
0) Apnea • Bed partner may sleep: the number of central apneas and/or central hypopneas is > 50 percent of the total
( Primary / report episodic number of apneas and hypopneas: and there is no evidence of Cheyne - Stokes breathing
Secondary) hyperpnea, • The patient reports sleepiness, awakening with shortness of breath, snoring, witnessed
hypopnea and . apneas, or insomnia (difficulty initiating or maintaining sleep, frequent awakenings, or
apneic periods nonrestorative sleep)
• Daytimesleepiness • There is no evidence of daytime or nocturnal hypoventilation
• Insomnia, • The patient is taking an opioid or other respiratory depressant (CSA due to medication or
inattention, poor substance)
concentration • The breathing pattern is associated with atrial fibrillation/ flutter, congestive heart failure,
• History of CHF or a neurological disorder and three consecutive central apneas and /or central hypopneas
• Medicationhistory separated by crescendo- decrescendo breathing with a cycle length of at least 40 seconds
.
(opioids especially (CSA with Cheyne- Stokes breathing)
methadone)
Periodic limb • Recurrent jerks of • The minimum number of consecutive limb movement (LM) events needed to define a PLMS
movements of the legs and arms series is 4 LMs
sleep (PLMS) that can occur in • The minimum period length between LM (defined as the time between the onsets of
association with • consecutive LMs) to include them as part of a PLMS series is 5 seconds
arousals • The maximum period length between LMs to include them as part of a PLM series is 90
• Insomnia or seconds
daytimesleepiness
Respiratory • Sudden • Patients with COPD,restrictive lung disease,or poorly controlled asthma,or neuromuscular
diseases awakenings and disease with failure to use muscle to assist breathing during REM sleep may present sleep -
dyspnea related desaturation, sudden awakenings, and dyspnea that imitate OSA
• Not qualified for diagnostic criteria of either OSA or CSA
. ziamttt
OSA CSA
HPI • Snoring, choking/gasping, witnessed apneas, recurrent • PND
awakenings
• Fatigue, unrefreshing sleep, daytime somnolence, morning
• .
Bed partner reports episodic hyperpnea hypopnea and
apneic periods
.
headache • Compared with OSA, symptoms of poor sleep quality are
• Irritability, impaired concentration usually subtle
• Poor short term memory
• ‘Use STOP- Bang questionnaire for screening
PMHX • Majority related to obesity & metabolic syndrome • Heart failure, stroke, acromegaly, renal failure, low cervical
• Hypothyroidism, acromegaly, renal failure, restrictive lung
disease ( scoliosis), neuromuscular disease ( postpolio),
.
tetraplegia Afib, primary mitochondrial diseases
heart failure
PHYSICAL
General
Level of consciousness, mental status, obesity/high BMI
•
.
VS: BP (hypertension) HR ( bradycardia due to increased vagal tone), RR (tachypnea), temp, Sa02 ( hypoxia), respiratory patterns
•
HEENT
• Inspection:
> Face / Mandible - Facial plethora, retrognathia, micrognathia, overbite
Nose- Nasal obstruction ( polyps, deviated septum, rhinitis),
.
Mouth - Macroglossia ( Down syndrome,amyloidosis,acromegaly) Mallampati score, tonsillar or uvula hypertrophy, low soft palate
Neck - Neck circumference ( > 43 cm male, > 40 cm female), thyromental distance (normal > 6.5 cm)
•
Palpation .
:Nose - Palpate thenasal bone and cartilage to assess for alignment (nasal obstruction), or tenderness JVP (elevated, positive
• Auscultation Nose - Occlude each nostril one at a time and have the patient breath through his nose with his mouthclosed to listenand
assess for nasal patency
RESP SET
CD
• Inspection: cyanotic, symmetrical chest wall movements, stridor ( airway obstruction) .
Q rD
• Palpation: equal chest expansion. S3
• Auscultation: equal air entry, wheeze, crackles D 0 )
cv fD “
• Inspection: Signs of peripheral edema, jugular venous pressure and distension (cor pulmonale/right heart failure which are common in
OSA or CSA)
• Palpation: apex beat (cardiomegaly - heart failure common in CSA)
• Auscultation: Loud P 2 (pulmonary hypertension common in OSA or CSA )
Causes:
. .
• Acromegaly: macrognathia, macroglossia frontal bossing, widely - spaced teeth, hirsutism, hyperhidrosis, goiter LVH /CHF, HSM,
• large/swollen hands / feet, skin tags, thick skin CTS, visual fields, acanthosis
.
• Hypothyroidism: goiter, peripheral signs
• Amyloidosis: periorbital ecchymoses, shoulder pad sign (enlargement of anterior shoulder )
.
• Cushings: central obesity, facial plethora, hirsutism, prominent dorsocervical fat pad cushingnoid facies
Consequences:
• RESP: Consolidation, clubbing, cyanosis
• CV: hypertension, pulmonary hypertension, cor pulmonale, Afib, Ml
> Peripheral edema, hepatomegaly, pulsatile liver, ascites
.
> Elevated JVP positive AJR
> Inspection: RV heave, subxiphoid impulse
> Palpation: palpable P2, RV heave, displaced or sustained apex
. . . .
> Auscultation: Afib loud P 2 wide split 2 TR murmur PR murmur, R S3/S4. L S4
• NEURO: TIA/stroke. depression, impaired concentration
> Focal deficits, MMSE
• ENDO: diabetes
> Acanthosis nigracans
INVESTIGATIONS
• Sleep study: Level 3 home study can be initial study if OSA is primary diagnosis being considered. Otherwise a Level 1 PSG is
recommended
• TSH, ABG ( high C02), ECG
.
• Head CT if query stroke
• Echocardiogram, if query CHF
• Chest X -ray or CT if presenting with respiratory distress
TREATMENTS
1. Pulmonary consultations for sleep study. If urgent sleep study not available, try overnight oximetry monitoring first.
2. Advise patient not to drive or operate machinery if high risk or very symptomatic.
3. Warn patient about anesthetic risk:need tostartCPAP prior to surgery,continue after surgery,and monitor with pulse oximetry post -op.
4. Nonpharmacologic managements: weight loss in overweight patients, avoid all CNS depressants, treat nasal congestion, proper sleep
hygiene, positional therapy
.
5. Device Therapy: CPAP if AHI > 15 for OSA. If other diagnosis, such as PLM CSA then other treatments will be necessary
6. Surgical Options: for patients with enlarged tonsils, offer consultation for potential tonsillectomy
7. Treat underlying diseases
KEY POINTS
• A thorough yet concise history is paramount to quickly distinguish syncope from a variety of other diagnoses: collateral history is
vital
• Be cognizant of cardiac causes (increased mobidity/mortality); ensure to perform cardiac workup and ECG where appropriate
.
• Characterize pre-ictal, ictal and post -ictal phases
• Differentiate syncope from hypoglycemia, seizures, stroke
DIFFERENTIAL DIAGNOSIS
Definition: Syncope is a sudden, transient, self -limited LOC from global cerebral hypoperfusion with spontaneous recovery
1. Differentiate syncope from other causes of transient LOC
• Seizure - preceding aura, tonic - clonic movements, tongue biting, urinary incontinence during episode, post - ictal state (confusion
> 5 min after event vs rapid return of consciousness with syncope)
.
• Stroke ( bi-hemispheric,brainstem, posteriorcirculation) - weakness, numbness, visual changes CNsx (diploplia dysphagia dysarthria) . . .
. . .
other focal neuro deficits CVA risk factors (HTN CAD DM DLD, Ahb obesity) . .
.
• SAH - sudden onset, severe H/A ( ' thunder - clap H/A'), N/V, photophobia CN palsy (III, IV )
• Metabolic - hypoglycemia (insulin and other anti -hyperglycemic use, change in mental status, diaphoresis, palpitations), Na, K, Ca, Mg
abnormalities
• Psychogenic pseudosyncope - diagnosis of exclusion: assess by picking up pt ' s hand and dropping it on pt 's face - pt will move arm to
—05 C<D avoid hitting face
2. Determine cause of syncope
E !£
CD " O
<D Etiology Clinical Symptoms
Neurally - Vasovagal (most common) • .
Preceding NA/ abdo discomfort, diaphoresis, blurry vision
mediated
(reflex )
• .
Triggers: fear, heat pain, stress
Situational • Triggers: coughing, defecation, micturition, prolonged standing, after exercise, hx similar episodes
Carotid sinus hypersensitivity • Triggers: head rotation/pressure on carotid sinus (shaving, tight collar)
Cardiac Arrythmia (brady, SVT, VT . • Usually sudden and unprovoked (may have preceding palpitations)
.
Afib channelopathies) • .
FHx sudden death PMHx cardiac risk factors
Obstructive (HOCM. AS. • Sudden-onset syncope during exertion (HOCM) or when supine - may have CP. dyspnea,
valvular disease) palpitations
• FHx sudden death PMHx HTN.
.
Other (Ml aortic dissection, • .
Chest pain radiating to shoulder / jaw SOB N/V, epigastric discomfort (Ml), sharp severe CP
tamponade) radiating to back, hypotension (aortic dissection)
• PMHx cardiac risk factors
Orthostatic Hypovolemia • .
Acute blood loss (GIB. ectopic pregnancy), anemia. N/V/D inadequete intake
• Pre- syncope/syncope upon sitting/standing quickly
ANS dysfunction •
•
. .
Focal neuro deficits (MS MSA PD. DM)
Pre- syncope/syncope upon sitting/standing quickly
Drugs • Anti -HTN (diuretics, nitrate. ACEi). - slowing drugs ( B blocker digoxin. amiodarone). QTc -
rate ,
prolonging drugs phenothiazine, quinidine. psych meds)
(
Other Pulmonary embolism • Sudden onset syncope + dyspnea
• .
Hx of unilateral tender swollen leg recent immobilization/surgery, malignancy, hemoptysis
HISTORY
ID • Patient 's name . age. gender
CC • Sudden LOC
HPI • Pre - . . .
ictal: diaphoretic N/V, light -headed, CP, SOB palpitations, supine position, aura, H/A focal neuro deficit
• Ictal: complete LOC with rapid onset, short duration, loss of postural tone, hx of previous syncopal episodes
(high liklihood of syncope), tonic -clonic movements, automatisms, incontinence, tongue biting ( seizure) may -
have brief limb- jerking movements with syncope
• Post -ictal: recovery time (rapid, spontaneous recovery suggests syncope), prolonged confusion (seizure), head
injury, recall of event
• Precipitating factors: coughing, sneezing, prolonged standing, emotional stimulus, pain, head movement /
shaving, standing quickly, exertion, prolonged standing
RED FLAGS • Exertional onset, chest pain, palpitations, dyspnea, syncope without warning, headache, focal neuro deficits
PMHX • Dementia, EtOH, PD . DM (autonomic dysfunction), underlying structural heart disease (congenital heart
.
disease, valvular disease, left venticular dysfunction), arrhythmias, IHD, HTN epilepsy, psych disorder
MEDS • Anti . . .
-HTN (diuretics, nitrate ACEi) rate - slowing ( B blocker, digoxin, amiodarone) QTc -prolonging drugs
(phenothiazine, quinidine, psych meds), alpha antagonists
FHX • Cardiovascular disease, sudden death (esp at young age), intracranial aneurysm, neurologic disorders
.
• Resp: SOB hemoptysis
.
• Gl: melena, hematochezia hemetemesis
• GU: menorrhagia
.
• MSK /Derm: brittle nails /hair unilateral leg swelling, erythema, tenderness
• Neuro: weakness, numbness, diploplia, dysphagia, dysarthria, facial droop
RISK FACTORS .
• Major - abnormal EKG Hx of heart disease/CHF, hypotension (sBP < 90 mmHg)
• Minor - age > 60 y/o, dyspnea, anemia, HTN/CAD
PHYSICAL
Initial Examination
. . .
• VS ( BP, HR RR Temp Sa02) including orthostatic vitals (measure BP and HR while supine, then 5 min after standing up - decrease
. .
in SBP > 20 mmHg, DBP > 10mmHg or increase HR by > 30 bpm is positive) and BP in both arms ( > 20mmHg mismatch - aortic
dissection)
• Measure glucometer reading
.
• If unstable - resuscitation orders: 2 large bore I Vs, fluid resuscitation, 02 glucose administration 0) D
CL fl>
EXTREMITIES
S3 3CU
• Pulses, capillary refill, warmth, peripheral cyanosis
• Calf swelling, erythema, tenderness to palpation
HEENT
=—
0)
• Conjunctival pallor, central cyanosis, diaphoresis, JVP assessment, carotid pulse, carotid bruits
CV
• Palpation
> .
Systolic thrill in the RUSB sustained cardiac impulse, parvus et tardus carotid pulse ( AS)
) Apical impulse with a sustained systolic thrust, spike and dome carotid pulse (hypertrophic cardiomyopathy)
•Auscultation
. . .
> Mid - systolic ejection click, harsh crescendo - decrescendo medium/harsh-pitched murmur in RUSB S3 S4 paradoxical or
single S 2 ( AS)
.
> Mid - systolic, harsh, crescendo- decrescendo, mid - pitch murmur at LUSB. wide split S 2 S4 ( PS)
> Diastolic decrescendo low -pitched rumble at the apex ( MS)
> Crescendo - decrescendo murmur at the LLSB (louder while standing - hypertrophic cardiomyopathy)
NEURO ( focused exam)
• Cranial nerves, motor (bulk, tone, power ), reflexes, sensory
INVESTIGATIONS
Laboratory Investigations
.
• CBC- D, electrolytes, Mg2 *, Ca2 * creatinine, glucose
Radiology/ lmaging
• CT head, if clinically indicated ( focal neuro deficits, seizure activity)
• Echocardiogram, if clinically indicated ( structural or valvular heart disease evaluation)
Special Tests
• EKG should be performed on all patients who present with syncope
> Can consider continuous EKG or outpatient portable Holter monitoring, although low yield
• Carotid massage
• EEG for detection of seizures
• Exercise stress test (if concerned about exercise -induced arrythmia)
IIREATMENT
Medical
• Vasovagal /situational syncope: avoidance of triggers, compression stockings, discontinue offending meds
• Orthostatic hypotension: fluids, compression stockings
Surgical
• Valve replacement ( AS, MS, PS)
• Implantable cardioverter defibrillator (ventricular tachyarrhythmia)
• Permanent pacemaker (bradyarrhythmias, SSS)
.
• Catheter ablation (SVT atrial flutter /tachycardia)
KEY POINTS
• Bleeding associated with thrombocytopenia is often mucocutaneous and immediately after trauma/surgery
• The most common causes of isolated thrombocytopenia include UP, medications, and alcohol
• Suspect ITP in the well-looking individual with severe isolated thrombocytopenia ( platelets < 10)
• Thrombocytopenic emergencies such as HITT. MAHA, and acute leukemia must be ruled out
• If multiple cell lines are low and no obvious cause is identified, then bone marrow biopsy is indicated
DIFFERENTIAL DIAGNOSIS
Mechanism Common Conditions
Decreased Production • Primary BM failure (Faconi anemia , other inherited marrow failure syndromes)
• BM infiltration ( MDS. leukemia , lymphoma , metastatic malignancy )
• Viral and other infections (e.g.. HIV. CMV, EBV, varicella, parvo. mumps, rubella )
—c
OJ
0) • Drugs and toxins (chemotherapy, radiation. ETOH)
• Nutritional ( Vit B 12. folate deficiency)
E
0)
:S -a Increased • Immune (ITP: primary & secondary * ; NAIT, PTP)
H Destruction/Consumption •
•
•
Viral infections (HCV. HIV. EBV. CMV. varicella , rubella, measles, mumps)
Drugs (HIT. sulfas, clopidogrel. quinine, valproate, rifampin, vancomycin)
Massive hemorrhage
• Microangiopathic Hemolytic Anemia (TTP. HUS. DIC. HELLP)
Sequestration/dilution • Splenomegaly/hypersplenism
• Pregnancy
• Massive transfusion
• ECMO/bypass/intra- aortic balloon pump
Pseudothrombocytopenia • Platelet clumping
• Platelet satellitism
"Common causes of secondary ITP: autoimmune disease ( SLE, antiphospholipid syndrome, thyroid disease, Evans syndrome), lymphoprolif-
erative disorders (CLL, lymphoma), infections (HIV, HCV, H. pylori)
HISTORY
ID • Patient ’s name age. . gender
CC • Bleeding, asymptomatic (routine lab work )
PMHX . . . . .
• Malignancy (especially heme), viral infections (esp HIV EBV CMV, HBV, HCV) ITP autoimmune disease (SLE,
.
RA APLA), liver disease, sepsis, recent diarrheal illness, recent transplant or transfusion
PSHX • Hx excessive bleeding with minor procedures (especially dental)
PO & GHX • Current or recent pregnancy, hx of pregnancy complications
FHX • Familial hematologic disease, leukemias, malignancies
SOCIAL • EtOH and drug use, occupational exposures, diet, herbals and nutritional supplements
MEDS • Heparin, antibiotics (esp . B- lactams, TMP-SMX, vanco. rifampin), chemo, radiation, anti-epileptics, quinine
——
ROS • Gl: early satiety (splenomegaly)
• MSK /DERM: joint pain, rash (rheumatologic disease)
II i Ml > I
.
VITALS: Fever (sepsis, DIC, malignancy) , hypertension ( HELLP intracranial bleed), hypotension and tachycardia (sepsis, ongoing
bleeding, concomitant anemia)
Laboratory Investigations
.
• CBCd ( to assess for other cytopenias) PBS ( looking for schistocytes, blasts, large platelets, hypersegmented PMNs), creatinine
(consider AKI in MAHA), liver enzymes (if suspected liver disease or HELLP)
Radiology/ lmaging
• U/ S or CT abdomen to assess for hepatosplenomegaly/lymphadenopathy 2=
(T>
Special tests:
. . . . .
Q
- n>
• Anemia or suspicion for DIC/TTP/HUS: reticulocyte count LDH haptoglobin, DAT bilirubin INR PTT, fibrinogen, anti-
ADAMTS13 (if available) 53: 3
• Liver disease or hepatosplenomegaly: liver enzymes, abdominal U/S or CT fibroscan
. . .
• Infection suspected: HIV HCV EBV H. pylori serology, stool for Shiga toxin -
. <D
CD
—
• Malignancy suspected or blasts on PBS: bone marrow biopsy ± other tissue biopsies
• Associated rheumatologic symptoms: ANA. antiphospholipid antibodies
4 T Score for HIT:
Thrombocytopenia Platelet count fall >50% and platelet nadir 220 2
Platelet count fall 30- 50% or platelet nadir 10- 19 1
Timing of platelet Clear onset between 5 - 10 days or si day if prior heparin exposure within 30 days 2
fall Consistent with days 5 - 10 but not clear, onset after day 10, or si day if exposure 30- 100 days ago 1
Platelet count fall < 4 days in the absence of recent heparin exposure 0
Thrombosis New thrombosis or skin necrosis, acute systemic reaction post IV heparin bolus 2
Progressive or recurrent thrombosis, non- necrotising skin lesion or suspected thrombosis 1
None 0
ITP .
Initiate when platelets < 30 or bleed (1st line = glucocorticoids IVIG; 2nd line = splenectomy, rituximab, eltrombopag)
HITT Stop all LMWH/UFH (including heparin locks and DVT prophylaxis), use non -heparin anticoagulation ( argatroban lepirudin, .
.
fondaparinux) and transition to warfarin once platelets > 150: lifetime avoidance of heparin
TTP Urgent treatment = plasma exchange and steroids: if refractory, consider rituximab and splenectomy
DIC Treat underlying cause (e.g. if bleeding, give cryoprecipitate/plasma/platelets; if clotting, give heparin)
DIAGNOSIS
• Hypothyroidism
> Primary: elevated TSH
> .
Secondary: normal or low TSH low free T4
• Hyperthyroidism
.
> Primary: low TSH elevated free T4 & free T 3
.
> Secondary: elevated TSH elevated free T4 & free T3
• Thyroid Nodules /Goiter/Cancer: Please refer to Neck Mass /Goiter station
DIFFERENTIAL DIAGNOSIS
Hypothyroidism Hyperthyroidism
Primary Primary
• Hashimoto’s thyroiditis: subacute thyroiditis • Grave’s disease
• Post -partum thyroiditis • Thyroiditis: subacute, post -partum
• Drugs ( lithium, amiodarone); iodine deficiency • Toxic multinodular goiter, toxic adenoma
—
03 C
0) • Iatrogenic (iodine ablation, thyroidectomy, radiation)
• Absent/ectopic thyroid gland
.
• Drugs ( amiodarone levothyroxine)
• Excess iodine (seaweed, supplements)
ED 2 Secondary: hypopituitarism (pituitary adenoma, pituitary Secondary: TSH - secreting pituitary adenoma, gestational
< “O
0» surgery/radiation/destruction); hypothalamic disorders thyrotoxicosis
High Mortalty/Morbidity
• Myxedema coma (hypothyroid)
• Thyroid storm (hyperthyroid)
• Thyroid cancer and /or metastases (euthyroid)
HISTORY
ID • Patient ’s name . age. gender
CC • Symptoms associated with hyper /hypothyroidism, neck mass
RED FLAGS • Fever, altered LOC, B symptoms ( weight loss, fever, night sweats), dysphagia, stridor
PMHX • Previous neckmasses, thyroid disease, head and neck cancer, Hodgkin' s lymphoma treated with radiation
therapy, psychiatric illness
PSHX • Neck surgery, thyroidectomy, parathyroidectomy
FHX • Thyroid disease, thyroid cancer, auto - immune diseases (adrenal insufficiency. Type I diabetes)
SOCIAL • Diet (e.g., seaweed), caffeine intake, smoking, EtOH, radiation exposure
MEDS • Levothyroxine (Synthroid), amiodarone . lithium, herbals
ALLERGIES • General inquiry
RISK FACTORS -
• Previous radioactive iodine or anti thyroid drug therapy, radiation of neck, thyroid/neck surgery
. . .
> TSH free T4 free T 3. TSH receptor antibodies anti -TPO antibodies
> Thyroid scan or 24 hr radioactive iodine
• Thyroid Nodules: U/S plus FNA for nodules greater than 1.0 cm ( Please refer to Neck Mass / Goiter station for additional details)
LLJEATMENT
Emergent
• Thyrotoxicosis ( thyroid storm)
) .
(3- blocker (e.g. propranolol) to control symptoms
)
.
PTU 1g PO STAT then 300 mg PO q6h
> Iodine drops 2- 3 PO q 6 h after each dose of PTU
) Dexamethasone 2 mg ! Vq6h
> IVF, cooling blanket, acetaminophen, correct electrolytes
. .
> Tx precipitating event (sepsis. DKA PE bowel infarction)
• Myxedema coma
.
> L- thyroxine 500 meg IV then 100 - 300 meg IV daily
> Hydrocortisone 100 mg IV q6h
> Dextrose- containing intra - venous fluids, warming blanket, correct electrolytes
.
> Tx precipitating event (infection Gl bleed, overdose CHF).
Treatment Options
• Hypothyroidism: synthetic levothyroxine, thyroidectomy for goitre (especially if causing compressive symptoms)
• Hyperthyroidism: anti- thyroid medications ( i.e., propylthiouracil or methimazole)
.
> Once hyperthyroidism is stabilized, may consider continued methimazole iodine ablation, or thyroidectomy
Referrals
• All cases of hyperthyroidism and thyroid disease during pregnancy, severe cases of hypothyroidism, thyroid masses, and
complicated or medication- refractory thyroid disease warrant referral to Endo. Grave’s should be referred to Ophthalmology
Edmonton Manual of Common Clinical Scenarios 242
TRANSFUSION COUNSELING
Current Editors:Minju Park MD, Kathleen Wong MD FRCPC
KEY POINTS
• Indications for transfusion and benefits of transfusion
• Risks of transfusion ( infectious vs. non - infectious)
• Alternatives to transfusion
• Documentation of provided consent
INDICATIONS
Cellular product transfusion is indicated in the following situations:
• Hemodynamically unstable or symptomatic acute hemorrhage
• Severe or symptomatic anemia if other non - transfusion therapies or observation would not be effective
• Procedures/perioperative indications
• ECMO/cardiac bypass
• Coagulopathy and bleeding
SKSOlSEEEHSiEEE
Infectious Risks:
Infection Estimated Risk
Human Immunodeficiency Virus 1 in 21 million
Hepatitis C Virus 1 in 13 million
Hepatitis B Virus 1 in 7.5 million
West Nile Virus <1 in 1 million
-
Human T cell Lymphotrophic Virus 1 in 7.6 million
Symptomatic bacterial sepsis 1 in 10,000
(per unit of pooled platelets)
ALTERNATIVES TO TRANSFUSION
• Hematinic therapy with iron supplementation, Vit B12, and/or folate as required
• Erythropoietin
• Preoperative autologous blood donation
• Intraoperative blood salvage
• Antifibrinolytic agents (i.e., tranexemic acid)
• Stop medications that promote bleeding
• Observation and monitoring
KEY POINTS
• Edema can be classified as either pitting or non -pitting - helps to distinguish etiologies
• .
Unilateral leg edema is normally attributed to a local cause ( DVT venous insufficiency, lymphedema)
.
• Bilateral leg edema can be caused by a local or systemic cause ( HF kidney disease, liver disease)
• Generalized edema ( arms and legs) is always caused by a systemic disease
. . ..
• As opposed to unprovoked DVT provoked DVT is usually caused by a known event (e g surgery, hospital admission, travel)
High Mortality/Morbidity
• .
DVT leading to PE necrotizing fasciitis, compartment syndrome
HISTORY
ID • Patient 's name, age, gender
RED FLAGS • Sudden onset ( < 72 hrs) of leg swelling, painful, discolored (rule out DVT)
• Rapidly growing area of erythema (necrotizing fasciitis)
• Pain out of proportion (necrotizing fasciitis, compartment syndrome)
PMHX • Hx of .
malignancy, blood clots, hypercoaguability recurrent cellulitis, systemic disease (heart, liver, kidney)
PSHX • Hx of immobilization after surgery
PO&GHX • Pregnancy, prolonged bed rest
MEDS • CCB, prednisone, and anti - inflammatory drugs are common causes of leg edema: OCP (highest risk of clots in 1st
year )
FHX • Hypercoaguability disorders .
( Factor V Leiden, Protein C Protein S, ATIII deficiency)
SOCIAL • Smoking, travel to tropical areas or mosquito bites
ROS • General: fevers, chills, night sweat, decrease weight (cellulitis /infection, malignancy)
• RESP: dyspnea, hemoptysis, pleuritic chest pain
• MSK/DERM: trauma, muscle injury
RISK FACTORS • DVT: Virchow’s triad, prior DVT . recent surgery/trauma malignancy, immobilization
,
.
• Venous insufficiency: age obesity, smoking, history of varicose veins/trauma to LE/previous DVT pregnancy,
cardiovascular disease
.
rare
Vital Signs
.
|HR, RR .102 sat ( PE), fever (cellulitis, necrotizing fasciitis)
• BP
Inspection ^
245 Edmonton Manual of Common Clinical Scot
• Skin changes, ulceration (often malleolar, flat), brown Well’s Score for DVT
hemosiderin deposits (venous insufficiency)
• Active cancer +1
• Erythema with demarcated border (cellulitis)
• Swelling • Bedridden recently > 3 days or major surgery within 4 wks +1
• Collateral superficial veins • Calf swelling > 3 cm compared to other +1
Palpation • Collateral (nonvarciose) superficial veins present +1
• Pain on palpation, warmth
• Distal pulses, capillary refill (arterial disease)
• Entire leg swollen +1
• Pain with passive range of motion ( compartment syndrome) • Localized tenderness along the deep venous system +1
• Tenderness along deep veins • Pitting edema, greater in symptomatic leg +1
• Unilateral vs. bilateral pitting edema
• Paralysis, paresis, or recent plaster immbolization of LE +1
Auscultation
• Previously documented DVT +1
• CHF findings ( arrhythmias, lung crackles, pleural rub)
> LMWH with simultaneous warfarin therapy ( 5 mg po daily) until oral anticoagulation target INR 2.0 - 3.0 established for 48 hrs .
then discontinue LMWH
> Total duration of therapy 3 - 6 months to lifelong depending on risk of recurrent VTE vs. bleeding risk ( HAS - BLED score)
.
> LMWH: Dalteparin ( 200 u/kgQD), Tinzaparin ( 175 u/kgscdaily ) orEnoxaparin ( lmg/ kgscQ 12H) IV/ Sc Unfractionated Heparin is
also available if renal impairment present
• DOACs: Direct thrombin inhibitor ( Dabigatran preceded by LMWH for 5 - 7 days) or Factor Xa inhibitor ( Rivaroxaban or Apixaban)
• I VC filter if anticoagulation is absolutely contraindicated in acute phase ( < 3 months) - usually inserted for a short period
• If massive ileofemoral DVT ( with phlegmasia), consult vascular surgeon and interventional radiology for surgical thrombectomy
Compartment Syndrome
• Remove constrictive dressings, elevate limb, fasciotomy to release compartments
Necrotizing Fasciitis
• Urgent surgical debridement of all necrotic tissue
• Penicillin 4 million IU IV q4h +/- Clindamycin 900mg IV q 6h and urgent ID consultation
Cellulitis
• Cephalexin 500mg PO QID x 10 - 14 d
KEY POINTS
• Divide approach into acute (seconds to days) and chronic (weeks to months)
• Break down acute vision loss into transient (< 24 h) or persistent ( > 24 h)
• Go through your differential anatomically: pre - retinal, retinal, post - retinal, CNS
• Look for red flags: sudden onset, progressive, neurologic findings
DIFFERENTIAL DIAGNOSIS
Acute vs. Chronic Vision Loss
Acute Vision Loss Chronic Vision Loss
Pre-retinal problems Pre - retinal conditions
• Infectious/inflammatory: corneal edema, keratitis, uveitis • Corneal disorders: corneal opacity
• Angle -closure glaucoma: elevated intraocular pressure • Lens disorders: age - related, traumatic, or steroid-induced
—c
OJ
QJ
Retinal detachment: curtain of vision loss
•
Optic nerve dysfunction
control or long duration of DM
• Vascular insufficiency
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.
• Optic neuritis: pain with EOM pupil/color vision dysfunction • Tumors
• Papilledema: increased ICP • Macular degeneration or dystrophy: often have + ve FHx
Q)
C
• Anterior ischemic optic neuropathy ( arteritic vs. non-arteritic) Central lesions
Chiasmal conditions • Ischemia, neoplasm
ROS • HEENT: symptoms of temporal arteritis (scalp tenderness, temporal pain, jaw claudication), herpetic rashes
• CV: CVD, stroke
PHYSICAL
Vital Signs - hypertension
Eye Exam
• Inspection
> Ptosis (measure interpalpebral fissures with eyes open), exophthalmos/proptosis, enophthalmos
> .
Pupils: symmetrical or anisocoric, equal and reactive to light RAPD ( pre - chiasmal lesion), red reflex (retinal disorders)
> Visual acuity, colour vision
> EOMs, confrontational visual fields (chiasmal lesion, neuropathy)
> Fundoscopy (papilledema, hemorrhage, vascular occlusion)
• Palpation
> Temporal arteritis: prominent temporal artery (+ pulse), pain on temporal/scalp palpation, TMJ palpation with jaw mobility for
claudication
NEURO
• Orientation, focal deficits
INVESTIGATIONS
Laboratory Investigations
• Temporal arteritis: stat ESR and CRP
• Uveitis: infection and/or inflammatory work up
.
• CBC-D, syphilis EIA and VDRL, TSH, T 4, T3 lipid profile, fasting glucose
Special Tests
• Intra - ocular pressure
• Temporal artery Bx if temporal arteritis suspected
• CT scan if suspected intracranial hemorrhage, mass, or ischemic stroke
TREATMENT
Emergent Treatment:
• Acute central retinal artery occlusion/ intraocular pressure > 40mmHg: lower intraocular pressure ( i.e„ timolol eyedrops)
.
• Temporal arteritis: steroids while awaiting temporal artery biopsy (methylprednisone lOOOmg IV daily x 3 then lmg/kg PO daily
[ max. = 60mg])
• Keratitis: if infectious etiology suspected, consider fluoroquinolone (moxifloxacin) drops
• Referral to ophthalmology if suspected ocular related etiology
Definitions:
• Localization: UMN (corticospinal tract, extrapyramidal lesions). LMN ( NMJ, muscle myopathies, peripheral, mono or polyneuropathies)
• Fatigue (“ weakness " without an anatomic or temporal pattern, being " weak all the time and everywhere”) vs. weakness ( specific anatomic or
temporal pattern, complains about inability to perform specific tasks and associated with objective findings on physical exam)
DIFFERENTIAL DIAGNOSIS
Localizing the Lesion
HISTORY
ID • Patient ’s name, age . gender
CC • Weakness
HPI • Onset
Sudden/progressive, duration, intensity, fluctuation (cyclic/episodic)
>
Preceding illness, trauma, toxic ingestion, immobility
>
• Precipitating/ Palliating factors
> AM / PM, exercise ( worsens - myasthenia gravis: improves - Lambert Eaton)
> Worsens with heat ( MS)
• Distribution of weakness
» Diffuse, focal, unilateral/ bilateral, proximal /distal, hemiparesis vs. para /quadriplegia
• Severity
> Trouble rising from chair/ brushing hair, difficulties with ADLs
• Associated Symptoms
.
Neurologic: numbness, tingling, diploplia vision loss, lid droop, dysphagia, dysarthria, drooling
>
Constitutional: fever, Wt loss (malignancy)
>
Autoimmune: arthritis/arthralgias, skin rash ( SLE, dermatomyositis)
>
Endocrine: cold intolerance (hypothyroid)
>
• Speech becomes unintelligible after prolonged speaking: drooling, chewing, swallowing difficulties (+ LR 4.5, -LR
0.61 for myasthenia gravis)
PHYSICAL .
UMN vs LMN Lesions
General LMN
. .
• VS ( BP HR RR. Temp Sa02) .
• General appearance - posture, facies Power
UMN
UEflex >
fD D
Motor Exam (see tables)
• CN: bulbar involvement
.
extend
LE extend > flex ^ /absent Q O)
G
-
.3
• Inspection: muscle bulk/atrophy, fasciculation ( LMN) tremor, myoclonus
.
• Tone: rigidity (lead-pipe, cog- wheel) , spasticity ( UMN) flaccid ( LMN)
Tone Spastic flaccid =
J 0)
Plantars
^ /absent
.
(UMN lesion LR + 9.6 LR - 0.3 for unilateral cerebral hemispheric disease)
• Deep tendon and plantar reflexes (Babinski reflex highly specific for Fasciculations Absent ±
.
corticospinal tract lesion LR + 8.5 for unilateral cerebral hemispheric disease )
Atrophy Late Early
Systemic exam (if above exam is not suggestive of a lesion)
. . .
• CV RESP Gl DERM looking for signs of systemic disease
• Further neurological testing including sensation, coordination, gait
Special Tests ( for myasthenia gravis)
• Ice pack test: place ice on eyelid for 2 min, improvement in ptosis suggests
.
myasthenia gravis ( LR + 24 LR - 0.16) Muscle Strength
• Peek sign: within 30s of complete apposition of lid margins, patient 0 No visible muscle activity
.
involuntarily starts to separate the lids and sclera starts to show ( LR + 30 LR - 0.
1 Visible muscle twitch
88 )
2 Movement but not against gravity
INVESTIGATIONS
Laboratory Investigations 3 Movement against gravity, not resistance
. ,
.
• CBC- D electrolytes, glucose Ca2 (corrected). Mg, P04, TSH 4 Movement against some resistance
• CK (myopathy, rhabdomyolysis)
.
• ESR, ANA ( SLE) HBV/HCV serology, cryoglobulin 5 Full strength
Radiology/ lmaging
• CXR ( paraneoplastic syndrome from lung CA ) CT/MRI.
LP for Guillain - Barre Syndrome ( albuminocytologic disassociation - high protein, normal WBC)
Special Tests
• Electromyography (differentiates neuropathy and myopathy)
• Erdrophonium test : anticholinesterase inhibitor injection results in symptoms improvement within 30s in myasthenia gravis (+ LR
15)
• Acetylcholine receptor antibody testing (myasthenia gravis)
Surgical /Diagnostic Interventions
• Muscle Bx (necessary for diagnosis for poly - /dermatomyositis)
UREATMENT
Emergent
• CVA: thrombolysis (consult stroke neurology )
.
• Respiratory failure: appropriate respiratory support (02 mechanical ventilation, intubation)
Treat underlying disorder:
• Polymyositis: prednisone. Myasthenia gravis: pyridostigmine/ Mestinon, thymectomy if thymoma. Eaton Lambert: treat
underlying malignancy ( associated with small cell lung cancer ). ALS: antiglutamate. GBS: IVIG
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Reamy BV Bunt CW. Fletcher S. A diagnostic approach to pruritus. Am Fam Physician. 2011:84( 2):195 - 202.
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Adams SM, Knowles PD. Evaluation of a first seizure. Am Fam Physicians. 2007 May 1:75(9):1342 - 1347.
.
Chen DK So YT. Fisher RS. Use of serum prolactin in diagnosing epileptic seizures: Report of the Therapeutics and Technology Assessment
Subcommittee of the American Academy of Neurology. Neurology. 2005 Sep;65( 5 ):668 - 675.
n>
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Hoffman LH et al. First Exposure Emergency Medicine. New York: McGraw - Hill: 2008.
Q fD
-
The Merck Manual of Diagnosis and Therapy . 19th ed. Chapter 176: Seizure Disorders. 2011. . 3a
Shock
.
Gaieski D. Shock in adults: Types, presentation, and diagnostic approach [ Internet ]. Parsons P. Wilson K eds. UpToDate; updated 2008 Aug 6. cited 2009
D
fD —
>
_
Dec 15. Available from: http:// www.uptodate.com/online/content /topic.do? topicKey= cc medi/ 11364&selectedTitle=l%7E 150&source = search _result.
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Harbrecht B„ Forsythe R. Peitzman A Chapter 13:Management of shock. In Feliciano D Moore E Mattox K, eds. Trauma. 6 th ed. New York: McGraw
Hill: 2008.
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Peitzman A Harbrecht B. Billiar T. Chapter 4: Shock. In Brunicardi F ed. Schwartz Principles of Surgery . 8th ed. New York: McGraw Hill: 2005.
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Tintinalli JE. Kelen GD Stapczynski JS. eds. Eme' gency Medicine: A Comprehensive Study Guide. 6 th ed. New York: McGraw- Hill: 2004.
Thrombocytopenia
Bain BJ. Blood Cells: A Practical Guide. 5 th ed. Malden, MA: Wiley Blackwell; 2015.
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Cines DB Liebman H. Stasi R. Pathobiology of secondary immune thrombocytopenia. Semin Hematol. 2009;46:S2 - 14.
Gauer RL. Braun MM. Thromocytopenia. Am Fam Physician. 2012;85(6):612 - 622.
George JN. Arnold DM. Approach to the adult with unexplained thrombocytopenia. In Leung L. ed. Waltham MA: UpToDate. Accessed on June 27.2016
Stasi R. Howto approach thrombocytopenia. Hematology . 2012:2012(1):191- 197.
Thyroid Disease
.
Fauci AS et al. Harrison' s Principles of Internal Medicine. 17th ed. New York: McGraw - Hill: 2008.
.
McPhee SJ Papadakis MA Current Medical Diagnosis & Treatment . New York: McGraw - Hill: 2011.
McGee S. Evidence- Based Physical Diagnosis. 3rd ed. Philadelphia: Elsevier; 2012:192 - 209.
Transfusions Counseling
Acute Transfusion Reaction Chart. (2013. March). Retrieved June 20.2016 from httpY/www.albertahealthservices.ca /assets / wf /lab/ wf - lab-clin- tm- trsn-
algrthrrLpdf
Callum JL. Bloody Easy 3: Blood Transfusions. Blood Alternatives , and Transfusion Reactions: A Guide to Transfusion Medicine. Toronto: Ontario Regional Blood
Coordinating Network; 2011.
Choosing Wisely Canada. Transfusion Medicine: Ten Things Physicians and Patients Should Question. CSTM. Released October 29.2014 (1- 5) and une
2.2015 (6- 10). Retrieved from: http:// www.choosingwiselycanada.org/recommendations /transfusion-medicine/
-
Edmonton Manual of Common Clinical Scenarios 256
card-risks - and - consent .pdf
-
Major Evaluated Risks of Blood Transfusion. Retrieved June 21.2016 from http://rnyahs.ca insite/assets /picuc/tms - picuc -nursing resources - transfusion -
O'Brien SF. Yi QL. Fan W, Scalia V. Fearon MA, Allain JP. Current incidence and residual risk of HIV. HBV and HCV at Canadian Blood Services. Vox Son#.
2012 Jul;103(l):83- 86.
Vision Loss
Corbett J J. Approach to the patient with visual loss. In Biller J. ed. Practical Neurology . Philadelphia: Lippincott Williams & Wilkins: 2009:117 - 130.
Hoffman LH. et al. First Exposure Emergency Medicine. New York: McGraw - Hill: 2008.
Eye diagram: http:// www.healthpages.org/ health - a - z/human - eye - anatomy - surgery - types/
_< D
Weakness
.
Schere K. Bedlack RS Simel DL. Does this patient have myasthenia gravis? JAMA. 2005:293 15):1906 - 1914.
05 C
.
Blumenfeld H. ( 2010) Neuroanatomy through clinical cases. Sunderland Mass: Sinauer Associates.
53
<D U
McGee S. Evidence - Based Physical Diagnosis. 3rd ed. Philadelphia: Elsevier; 2012.
Hui D. Approach to Internal Medicine: A Resource Book for Clinical Practice. 4th ed. New York : Springer; 2016.
0)
Figure for caput medusa adapted from East Tennessee State University Medical Mysteries http://www.etsu.edu/com/medicalmyste'y/
CAPUTMEDUSA.aspx
Hand Exam
Janis JE. Essentials of Plastic Surgery. St. Louis: Quality Medical Publishing: 2C07.
Bickley LS. Bates ' Guide to Physical Examination and History Taking. 10th ed. Philadelphia: Lippincott Williams & Wilkins: 2009.
HEENT EXAM
Bickley LS. Bates " Guide to Physical Examination and History Taking. 10th ed. Philadelphia: Lippincott Williams & Wilkins; 2009.
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University of Virginia School of Medicine ( Internet ). HEENT exam; 1998 - 2005. ( cited Sept 10.2010). Available from: http:// www.med -ed .
virginia.edu/.ourses/poml/pexams/HEENT/
JVP EXAM
Hurley K. Cardiovascular system. In OSCE and Clinical Skills Handbook. 2nd ed. Toronto: Elsevier / Saunders; 2011.
McGee S. Inspection of the neck veins. In Evidence- based Physical Diagnosis. 3rd ed. Philadelph a: Elsevier /Saunders: 2012.
Orient JM. The Abdominojugular Test (Hepatojugular Reflux). In Sapira ’s Art and Science of
Bedside Diagnosis. 4 th ed. Philadelphia: Lippincott Williams & Wilkins: 2009.
Applefeld MM. The jugular venous pressure and pulse contour. In Walker HK Hall WD. .
Hurst JW. eds. Clinical Methods: The History Physical, and Laboratory .
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Examinations. 3rd ed. Boston MA: Butterworths; 1990. http://www.ncbi.nlm.nih.gov/bookshelf /br.fcgi?book = cm&part = A 622
Knee Exam
Hoppenfeld S. Physical Examination of the Spine and Extremities, lsted. Prentice - Hall: 1976.
.
Nett MP Pedersen HB. RoehrigGJ. Tria AJ Jr.. Scott WN. Clinical examination of the
knee. In Insall & Scott Surgery of the Knee. Chapter 3.47 - 60.
McRae R. Clinical Orthopaedic Examination. 6th ed. Churchill Livingston Elsevier ; 2010.
.
Sood R Achauer BM. Achauer and Sood ' s Burn Surgery: Reconstruction and Rehabilitation. Philadelphia: Elsevier ; 2006.
Johnson MW. Figure adapted from Acute Knee Effusions: A Systematic Approach to Diagnosis. Am Fam Physician. 2000 Apr
15;61( 8):2391- 2400.
Neurological Exam
Blumenfeld H. Neuroexam.com. [ Online ]. 2001 [cited January 14.2010 ]; Available from: URL:http://www.neuroexam.com/index.php
Gelb D. The detailed neurological examnation in adults. [Online ]. October 1st 2009 [cited January 14.2010 ]; Available
from http:// www.uptodate.com/online/content/topic.do?topicKey = genneuro/ 2959&selectedTitle=l~ 150& source
Brain. Aids to the Examination of the Peripheral Nervous System. 4 th ed. Edinburgh: W.B. Saunders; 2000.
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Bickley LS Szilagyi PG. Bates Guide to Physical Exam anc History Taking. 10th ed. Philadelphia:
Wolters Kluwer Health/ Lippincott Williams and Wilkins; 2009.
. .
Maranhao ET Maranhao-Filho P. Lima MA Vincent MB. Can clinical tests detect early signs
of monohemispheric brain tumors ? J Neurol Phys Ther. 2010:34:145 - 149.
. .
Teitelbaum JS Eliasziw M Garner M. Tests of motor function in patients suspected of having
mild unilateral cerebral lesions. Can J Neurol Sci. 2002:29:337 - 344.
. . .
Anderson NE Mason DF Fink JN et al. Detection of focal cerebral hemisphere lesions using the
neurologic examination. J Neurol Neurosurg Psychiatry. 2005:76:545 - 549
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Sawyer RN Hanna JR Ruff RL. Leigh RJ. Asymmetry of forearm rolling as a sign of
unilateral cerebral dysfunction. Neurology. 1993:43:1596 - 1598.
. . .
Daroff RB Fenichel GM JJankovic J Mazziotta JC. Diagnosis of neurological disease in Bradley 's neurology. In Clinical Practice. 6th ed.
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Andreoli TE Benjamin IJ Griggs RC. Wing E J. Chapter 112: Neurologic evaluation of the patient In Andreoli
and Carpenter ' s Cecil Essentials of Medicine. 8 th ed. Philadelphia: Elsevier Saunders; 2010.
Precordial Exam
Badgett RG. Mulrow CD. Lucey CR. Original article: Can the clinical examination diagnose left -sided heart failure in adults? In Simel
DL. Rennie D. eds. The Rational Clinical Examination: Evidence - Based Clinical Diagnosis. New York . NY: McGraw- Hill;
2009. http://vwAv.jamaevidence.com.login.ezproxy.library.ualberta.ca/content /3478756. Accessed 10/11/ 2014
Blaufuss Multimedia - Heart Sounds and Cardiac Arrhythmias (n.d.). Retrieved October 12.2014. from http://www.blaufuss.org
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Filate W. Leung R. Ng D. Sinyor M. Essentials of Clinical Examination Handbook. 5 th ed. University of Toronto Medical Society: 2005.
Armitage JO. Goldman: Cecil Medicine. 23rd ed. Elsevier: 2007.
Hui D. Padwal R. eds. Cardiac Examination in Approach tc Internal Medicine: A Resource
Book for Clinical Practice. 3rd ed. New York : Springer: 2011.
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McGee S. Palpation of the heart and auscultation of the heart. In Evidence -based
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Williams & Wilkins; 2009.
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Warnica JW. Canadian mnemonics for heart sounds. CMAJ. January 2.2007:176(1) doi: 10.1503/cmaj.l060180
Figure adapted from Wikipedia - Phonocardiograms from normal and abnormal heart sounds, author Madhero88. retrieved on 23
.
May 2015 and from Netters Cardiology. Marschall S. Runge George A. Stouffer. Cam Patterson. Chapter: The History and Physical
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7th ed. Philadelphia: Lippincott Williams & Wilkins: 1999.
Jarvis C. Physical Examination & Health Assessment. 4 th ed. St. Louis: Saunders: 2004.
.
Munro J Edwards CRW. Macleod's Clinical Examination. 9 th ed. Edingurgh: Churchill Livingstone: 1995.
Thyroid Exam
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Bickley LS Szilagyi PG. Bates' Guide to Physical Examination and History Taking. 10th ed. Philadelphia: Lippincott Williams & Wilkins: 2009.
McGee S. In Evidence-based Physical Diagnosis. 3rd ed. Philadelphia: Elsevier /Saunders: 2012:192- 209.
Obstetrics and Gynecology is a unique combination of medical and surgical issues that span the entire
spectrum of a woman' s life. This section begins with the pediatric female infant through to adolescence,
pregnancy, and mature women’s health.
When taking a history from postpubertal women, it is important that a gynecological history be taken as
a standard procedure. Just as you ask someone' s age, you would also ask about the last menstrual period
and history of any prior pregnancies, as a matter of routine. With your pregnant patients, last menses and
how the date of confinement is established is crucial. Knowledge of the earliest ultrasound performed
is essential, and is the basis of how gestational age is established. Accurate knowledge of gestational
age impacts many outcomes in Obstetrics, including timing of prenatal screening and ultrasound. It
also impacts management in situations where delivery is a possibility, such as the patient with severe
preeclampsia or the patient with preterm labor. If the gestational age is extremely premature, this has a
significant impact on the morbidity and mortality of the infant.
When asking about medications, it is important to remember that many women do not consider oral
contraception as medication so you must ask about this specifically. For adolescents who come in
with their parents, you will need to be sensitive to the fact that matters related to sexual activity and
contraception may not easily come out in the interview; it is important that your adolescent patient has
the opportunity to discuss obstetrical and gynecological matters in a private setting. OO
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Most OSCE examinations will focus on history - taking skills and talking through the mechanisms of a 2.2.
pelvic examination with a simulated patient rather than an actual patient. When faced with having to o p
demonstrate a pelvic examination on a pelvic model, it is important to refer to appropriate draping of the
patient and demonstrate clear communication during the examination.
There are several ethical and advocacy issues unique to Obstetrics and Gynecology that may appear on
examinations. Specific areas requiring a working knowledge include: intimate partner violence, prenatal
diagnosis, and pregnancy termination. It is important to recognize that for emergency management
of the pregnant patient, stabilizing the mother is always the first priority before focusing on the fetus.
Generally, however,formostsituationsyouwillencounterinObstetricsandGynecology,you,asa medical
student, will need to demonstrate that you are able to manage looking after both mother and fetus.
Ensure you have a standardized approach to taking a history from a pregnant patient and a menstrual
history for any female patient you see. I hope these tips will hold you in good stead regardless of your
eventual area of practice.
Good luck !
.
Edmonton Manual of CommonClniic il Scenarios 260
Current Authors: Helen Yang MD. Shawna Jensen MD
DIAGNOSTIC CRITERIA
• Primary Amenorrhea: Absence of menses at 16 y/o with secondary sexual characteristics or no menses at 14 y/o with absent secondary
sexual characteristics
• Secondary Amenorrhea: Absence of menses in a woman who previously was menstruating for >6 mos or 3 cycles
.
‘Sources of estrogen ( ives rise to secondary sexual characteristics ) ovanes adiposetissue ( theca- lutein
cells produce
COMMON CONDITIONS
^ ^ ^
CONCEPTION • Pregnancy ( intrauterine and ectopic)
. .
OTHER • Hypothyroidism Cushing's, non-classical CAH 17 hydroxylase deficiency, androgen insensitivity
2u O$ • Androgen secreting tumor ( adrenal or ovarian)
• Androgen insensitivity syndrome
o
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8
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X)
ID • Patient ’s name, age
.
• Sexual Hx ( vaginal intercourse), contraception, dyspareunia STI Hx, possibility of pregnancy, sexual abuse
. . .
MEDS • OCP IUD depo provera, steroid use antipsychotics, metoclopramide
FHX • Delayed menarche/puberty, PCOS . endocrine disorders, males with learning difficulties
. .
SOCIAL • Smoking EtOH, recreational drug use occupation, stressors, exercise, anabolic steroid use, relationships,
breastfeeding
HISTORY
. .
ID Patient 's name age GTPAL, GA ethnicity .
CC Possible pregnancy, first prenatal visit, or ongoing prenatal care
HPI Initial prenatal visit (6-12 wks GA):
• Establish EDC: Based on earliest US between 7-23 wks GA (most accurate regardless of LMP)
• Naegle’s Rule: 1st day of LMP + 7 days - 3 mo ± days above/below 28 - day cycle
• Full past medical, surgical, family, OBGyn, social, and current medication history
• Planned or unplanned pregnancy ( tactfully assess desire to continue with pregnancy and be supportive of
patient ' s choice)
. .
• Symptoms of pregnancy: amenorrhea, breast tenderness N/V fatigue, urinary frequency
• Discuss pregnancy blood work and investigations (see below)
Subsequent prenatal visits:
• Inquire about patient 's well being, routine and special investigations, monitor for fetal well being, monitor
for signs of pregnancy complications
• DO NOT change the assigned GA (most accurate in First Trimester, margin for error increases as pregnancy
continues)
• 4 cardinal symptoms ( ABCD): fetal activity (beginning at 18 - 20 wks), bleeding, cramping, fluid discharge
RED FLAGS Absence or decrease of fetal movement >20 weeks GA, bleeding, contractions, HTN, maternal illness
PMHX • CVD: HTN, cardiac disesase, valvular disease, obesity
• Endocrine: DM, thyroid, adrenal
• . .
MSK/Rhum: SLE APLAS Sjogren
• .
Neuro: MS, migranes ONTD
• Heame: Bleeding disorders VTE .
<2 > • GI/GU: IBD, renal stones, liver disease
OJO
U o • Renal: CKD
H O • Psych: Mood disorders, anxiety
Q) QJ
u • .
Infectious: HIV Hep B/C, TORCH infections, influeza (encourage vaccine use in pregnancy), varicella, travel
IS)C Hx (Zika Virus)
-O > - .
PSHX C sections, anesthetic problems, abdominal, back, pelvic. CNS eye (Cl to Valsalva), or cervical surgery
POHX & GHX OB Hx
. .
• Previous pregnancies: date of delivery GA at delivery, delivery type, gender, birth Wt complications during
pregnancy, delivery, or postpartum for mother or infant, child’s health, abortions (spontaneous or therapeutic)
• GHx
• Date of last Pap test, abnormal Pap tests & outcome
• Previous or currently at high risk of STI
MEDS • Folic acid, prenatal vitamins, Vitamin D, calcium (best 3 months preconception FA use)
• Teratogens: Stop and substitute ASAP, document exposure history, and timing, goal use of the safest drug,
at the lowest dose, at the safest time in pregnancy
• e.g.: ACEi, warfarin, tegretol, isoretinoin , NSAIDs (> 20 weeks) */V8:not complete list
. .
• Previous Pregnancy Risk Classification (i.e. A, B, C D, X Criteria) has been abandoned by the FDA to be .
.
replaced by drug specific (1. Risk Summary 2. Clinical Consideration 3 Data Summary) to improve risk benefit
counseling for patients
ALLERGIES • Medication (especially analgesics), environmental : note specific reaction
. .
FHX • HTN, DM VTE multiple gestations, stillbirth, chromosomal, structural, syndrome and genetic abnormalities
.
DM multiple gestation, stillbirth, chromosomal or genetic abnormalities
SOCIAL • Occupation (mother, father, and those at home)
• EtOH, smoking, drug abuse (access aids to reduce/stop in pregnancy)
• Partner information, stability, current living situation, safety at home (domestic violence)
• Diet, caffeine (recommend < 300 mg/day), exercise
. .
RISK FACTORS • Maternal Factors: Age < 17 or > 35, pre -existing medical disorders (especially: HTN DM CKD SLE APLAS) . .
THAT INCREASE poor or lack of prenatal care, previous cesarean section
COMPLICATIONS .
• Fetal Factors: Multifetal gestation, ART use placenta previa
UREATMENT
Identify patient at high risk of pregnancy complication (see Risk Factors on previous page)
Common Issues and Treatment Options:
• Nutrition: prenatal vitamin, folic .
acid 0.4 mg/d (1mg/d for smoking DM, epilepsy, daily use ASA or antacids, 4 mg/d if prior NTD)
• Constipation: dietary modification ( increase fiber/ water ), bulk - forming agent (psyllium fiber), stool softeners (PEG 3350)
.
• Heartburn: avoid lying down after meals, elevate head of bed calcium carbonate antacids, antihistamines
.
• N/V: small frequent meals, avoid triggering foods Diclectin ( Vit B6/doxylamine) , gravol
• Rh ( - ): Rh IgG 300 meg routinely at 28 wks and with episodes of antepartum hemorrhage: re -administer at 40 wks if undelivered
and then post partum if required (usually circulating anti-D titres and not required if given at 40 GA)
• Growth: Third Trimester ultrasound
-
• Patients high risk Pre eclampsia: Daily 81 mg ASA QHS starting at 12 weeks, inc Calcium intake to 1g/day if low daily dietary
intake ( < 600 mg/day)
• Counsel Signs and Sx PTB: Screen for UTI and BV (if symptomatic ), cervical length screening for those with RFx (prev history. Cx
conealization)
• Leg Swelling: Graded compression stockings, elevation of legs
• Bed rest has been shown NOT to be therapeutic in treating/preventing PTL and GHTN, and may be harmful
Follow-up ( using provincial prenatal visit guidelines)
Referrals
• Obstetrics/Gynecology or Maternal Fetal Medicine
• High risk pregnancy: multiple gestation, pre - existing maternal illness, pregnancy related complications (pre -eclampsia) and fetal
conditions (IUGR , oligohydramnios, non-reassuring fetal status, abruption)
DIFFERENTIAL DIAGNOSIS
'Note: 4 - 5 % of pregnancies are Complicated by APH
Differential Placental Placenta Previa Placenta Uterine Rupture Preterm Labour/ Cervical /
Abruption ( 20%) Accreata Cervical Vaginal
( 30%) Spectrum Insufficiency Pathology
Types • Apparent • Complete (over os) • Placenta
• Concealed • Marginal ( touching accreta
internal os) • Placenta
• Low lying placenta increta
(< 2 cm from • Placenta
internal os) percreta
• Vasa previa ( fetal
vessel overlying
Cx )
Presentation • Painfulvaginal • Painless vaginal • Post • Fetal heart rate • Asymptomatic • Observed
bleeding bleeding partum abnormalities in cervical dilation onj
I
retained labour ( may also < 37 weeks GA speculum
placenta occur outside • Painful uterine exam
• PPH labour) contraction < 37
weeks GA
Major Risk • Previous AMA • PreviousCS • Previous uterine • Previous cervical • HPV
Factors History (4 - 8% Previous CS incision procedures • Idiopathic
recurrence) Multiparous • Instrumentation • UTIs
• Smoking Multiples • BV
• Drug use in Smoking • Previous history
pregnancy ART of PTB
• Hypertensive
disorders
u 0_ • Trauma
• ART
H O • PPROM
<D <o
U
w c HISTORY
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ou . . .
ID Patient 's name, age GTPAL GA ABO Rh status .
CC Vaginal bleeding
HPI First Trimester Second and Third Trimester
• Bleeding with associated cramping or abd pain • Trauma to abd
• Pain (OPQRST) • Falls
• Leakage of fluid • Sexual intercourse
• Vaginal discharge • Physican cervical checks
• Recent transvaginal U/S
• Pain (OPQRST )
• Leakage of fluid
• Decreased FM
• Vaginal Discharge
PMHX • APLAS
• DM
PSHX • Previous abd or pelvic surgery • CS, abd, pelvic, or cervical surgery
MEDS/ALLERGIES • Routine
• HTN
• Pre -eclampsia
SOCIAL • Smoker • Smoker
• Drug use
• Domestic abuse
RISK FACTORS • Young or advanced maternal age
THAT INCREASE • Previous bleed with adverse outcome
COMPLICATIONS • Poor follow -up
• Maternal coagulopathy
£
General Approach
• ABCs, Vital signs
• Assess skin for signs of bleeding diathesis ( petichea, bruising)
• Fetal heart rate tracing non- stress test
Palpation
• Abd tenderness
• Uterine resting tone ( most predictive of adverse outcome
• Fetal lie (leopolds)
Special Exam
• Speculum exam: Assess for active bleeding, source of bleeding, associated leak of fluid, vaginitis, cervical polyp, or ectropion
• Digital cervical exam if associated with contractions or pain
> NOTE: Do not do a digital cervical exam in a pregnant woman with vaginal bleeding without an U/S to confirm the position of
the placenta (rule out placenta previa)
INVESTIGATIONS
Ultrasound
• Can be used to assess placental location
• Does not rule out placental abruption
-n< o
3
O’
_n
CD
• Sensitivity 25 - 50% n
o j
• PPV 88% n
O
Labs
• .
CBC, PT PTT, T& S if significant bleed
• Kleihaur Betke: Not sensitive in Dx abruption but helpful with maternal fetal hemmorrhage
• RhoGam Rh IgG re - administer, use titre form Kleihaur to dose
Placenta Previa
•Pelvic rest ( no intercourse, no digital vaginal exams)
•Monitor for growth
• Possibility will resolve as lower uterine segment develops (only 0.3 - 0.4 % of placenta previa’s diagnosis in second trimester remain)
• If not resolved by 28 weeks, plan for CS at ~ 38 weeks
Vasa Previa
• High risk for rupture of fetal vessels with ROM
• Often observed as in patient until elective delivery at 35 weeks via CS
Referrals
• Obstetrics /Gynecology and maternal fetal health, as APH classified as a hig- risk pregnancy
• Post coital bleed or ectopion can be managed expectantly with no changes to management
HISTORY
ID • Patient 's name, age
• Date of last Pap and pelvic exam, past abnormal Paps and gynecological procedures
• GTPAL
• Current breastfeeding
• Childbearing goals and attitude towards accidental pregnancy
PHYSICAL
.
VS: BP, HR , RR Temp, Sp02
Gynecological Exam (if due or Hx suggests STI; otherwise, NOT necessary to prescribe contraception)
• Exclude presence of pregnancy
• Pelvic examination ( speculum and bimanual) if suspicion of STI or PID (may defer if not sexually active)
• Pap test if due (see Pop Test section)
INVESTIGATIONS
Blood Work
• G- HCG (if suspicion of pregnancy or if choosing IUD)
Special Tests
.
• STI testing: swabs /urine for N. gonorrhea and C trachomatis , syphilis (if high risk, patient requests, or choosing IUD)
• U/S if pregnant or to evaluate anatomy of uterus ( if suspecting anomalies)
iiifA«!igwaim:ujadja
PMS • Affective and somatic symptoms during the luteal phase for 3 consecutive cycles
• Symptoms do not occur at other times of the cycle
• Symptoms interfere with daily life and/or relationships
PMDD • Severe form of PMS with specific DSM - 5 diagnostic criteria
Common Conditions
• .
PMS 1* dysmenorrhea, endometriosis
ISIMMOT
ID • Patient ’s name, age
_
u 0
• Menstrual Hx: LMP, menarche, length of cycle, length of menstruation, amount of bleeding, clots, regularity,
moliminal symptoms (breast tenderness, increased appetite, altered mood, fatigue), premenstrual spotting
H O • Effect on function and/or quality of life
0
u
Q)
u» C .
• Sexual Hx: # of partners, practices, STI Hx pregnancy risk, dyspareunia, contraceptive use
• DYSMENORRHEA:
oo .
» Associated symptoms: low back pain, dyspareunia infertility, pelvic pain/congestion, discharge, AUB,
changes in bowel movements (diarrhea premenstrally), nausea, fatigue, dizziness, headache
> Reproductive Hx: PO&GHx, infertility, contraceptive use, sexual Hx, STI Hx
• PREMENSTRUAL SYNDROME:
> Affective symptoms: depression, irritability, mood lability, anxiety, confusion, social withdrawal,
difficulty concentrating, feeling overwhelmed, sleep disturbance, change in appetite
> Somatic symptoms: breast swelling/tenderness, bloating, headache, edema, Wt gain
RED FLAGS • DYSMENORRHEA: ifdoes not appear to be 1° dysmenorrhea by clinical presentation or if treatment for 1°
does not resolve pain, further investigation is warranted
• PMS: symptoms severe enough to seriously interfere with daily life and/or relationships
PMHX • HTN, stroke, DVT, CVD, depression, other neuropsychiatric disorders
PSHX • Pelvic or abdominal
.
PO&GHX • GTPAL obstetrical Hx, Pap Hx, endometriosis, menorrhagia
MEDS • Hormonal contraception, pain medication
FHX • Endocrine disorders, gynecologic cancer, infertility, depression/neuropsychiatric disorders
.
RISK FACTORS • Major depression 1° dysmenorrhea: age (adolescent), early menarche menorrhagia .
269 .
Edmonton Mnnuil of Comrnoi inr
PHYSICAL
General Approach
.
• VS ( BP, HR RR, Temp, Sp) , Wt . BMI, WC
• Abdominal exam
• Masses
Pelvic Exam
• External genitalia, speculum, bimanual ( check for masses)
• Not required for mild 1° dysmenorrhea in adolescent who has never engaged in sexual activity
INVESTIGATIONS
General
• Diary of PMS symptoms (including type, frequency, severity, and timing of symptoms)
Laboratory Investigations
• TSH ( because PMS is a diagnosis of exclusion)
Radiology/ lmaging
• Transvaginal U/S if suspect 2° dysmenorrhea
Special Tests
• Pap test, vaginal and cervical swabs, urine for N. gonorrhea and C. trachomatis
• Surgical /diagnostic interventions
• Laparoscopy if endometriosis is suspected and/or pain is not controlled
nsEATMENT
Treatment Options
PMS/PMDD • Reassurance, diet, exercise, stress sleep hygiene, stop tobacco /EtOH/drugs
• Pharmacological
.
> Continuous use of combined OCP 24 - 4 dosing of combined OCP
> SSRI: fluoxetine, sertraline, paroxetine taken during the luteal phase CBT.
.
> Symptoms specific: buspirone calcium carbonate, spironolactone oo
1° DYSMENORRHEA • Reassurancethat the condition is common
• Pharmacologic
NSAIDs to decrease inflammation and pain; hormonal contraception: atrophy of endometrium-
O
O
a
.
decrease prostaglandins, reduce menstrual flow (OCP mirena, depo - provera) O n
*
Follow -up
• If patient does not respond to Tx for 1° dysmenorrhea, look for another cause of the pain
• .
Address any associated issues (dyspareunia social and psychiatric factors, etc.)
Referrals
• Gynecology
• Psychiatry
• Pain management clinic
• Pelvic floor physiotherapy ± acupuncture
Definitions
• Recurrent or persistent pain associated with vaginal intercourse
> Primary - Occuring with first intercourse
> Secondary - Begnning after previous non- painful sexual activity
Localization
• Entry - Pain with initial penetration of vaginal introitus
• Deep - Pain with deep vaginal penetration
• Congenital anomaly
• Psychogenic
<Z >
W)
u O 'Leading cause in women over 50
o "Leading causes in women under 50
2is> *
C
-Q >* HISTORY
ID • Patient ’s name, age, GTPAL
• Use of lubricants
• Dysuria or vaginal discharge
PHYSICAL
Complete Pelvic Exam
• Vulvar Examination
> External genitalia, perineum, perianal area, skin of groin and pubic
mons rudmdjlOfft
INVESTIGATIONS
Bloodwork
• FSH, LH, and estrogen levels
• . .
Neisseria Gonorrhea; Chlamydia Trachomatis Trichomonas vaginalis Genital herpes
oo
• Candida albicans cr
<
*
D <
• Urine culture 5.
(D
n n>
Imaging
• U/ S is the initial study of choice to image the pelvis in women with deep dysparunia
O
on
-i
Special Tests
• Vaginal pH and microscopy if chronic vaginal discharge
• Vaginal bacterial cultures if indicated
Surgical Intervention
• Visible lesions require biopsy if neoplasia is suspected
• Diagnostic laparoscopy
uREATMENT
INADEQUATE • Management of the underlying disorder (physical or psychiatric)
LUBRICATION • Avoiding causative medications (anti-estrogens such as Tamoxifen and aromatase inhibitors; antihistamines
and anticholinergics)
• Use of topical moisturizers and personal lubricants
VAGINISMUS • Myofascial release of muscle tension in muscles of the pelvic floor, thighs, and abdomen
• Desensitization techniques including Kegel exercises, use of dilators
• Other possible therapies include sex therapy, electromyography, use of benzodiazepines, and botulinum
toxin
•Referral to sexual health therapist
VULVOVAGINITIS • Treat underlying infection
POSTPARTUM • Surgical correction of distorted anatomy
• Ablation of granulation tissue
• Physical therapy
Edmonton Manual of Common Clinical Scenarios 272
FETAL DISTRESS
Current Author: Rachel Wang MD
[CLINICAL MANIFESTATIONS
• Fetal tachycardia ( > 160 bpm over 30 minutes)
• Fetal bradycardia ( < 110 bpm)
• Minimal FHR variability ( < 5 bpmover 40 to 80 minuites)
• Late decelerations
• Complicated variable decelerations
• Fetal acidosis on fetal scalp sampling or card gases ( pH < 7.10)
rs
£:OMMON RISK FACTORS
_o/
( ) • Post -dates
> • Cord prolapse
o <J
SIISTORY
ID • . .
Patient’s name, age, GTPAL, GA, Rh factor GBS status EDC
HPI • Cardinal questions: contractions ( frequency, onset). ROM (length, meconium), vaginal bleeding (clots,
++amount ), fetal movement (decreased frequency)
• New onset of abdominal pain, visual changes, nausea/vomiting/diarrhea, headache. RUQ pain, chest pain,
shortness of breath, cough, fever, polyuria/polydipsia, edema/weight gain
RED FLAGS • Decreased fetal movements ( < 6 kick counts/ 2 hrs), low biophysical profile (score 4 or lower), fetal
bradycardia/tachycardia +/- late decelerations +/- loss of FHR variability, metabolic acidosis ( cord blood
gas)
PMHX • Gestational / Pre - existing DM. gestational/essential. HTN/ pre - eclampsia, eclampsia, thrombophilia, existic
chronic diseases.
PSHX • C- section, hysterotomy, pelvic or abdominal surgery
. .
PO&GHX • Previous pregnanies (gestational age type of delivery, complications, weight of baby APGAR scores), blood
transfusions post-delivery
• Last pap and results, history of STI, previous LEEP/cone biopsy
MEDS • Insulin, metformin, anti -hypertensives, anti - coagulants, prenatal vitamins, OTCs
ALLERGIES • Drug and enviromental allergies, note reaction type (i.e. anaphylactic )
FMHX • HTN . DM, multiple pregnancies, congenital malformations
SOCIAL • Smoking, EtOH, recreational drug use prior and during pregnancy, current living situation, information about
partner, domestic abuse
Laboratory Investigations
• Urinalysis (glucosuria, proteinuria)
• Urine C& S (asmyptomatic UTI)
• .
Urine for gonorrhea and chlamydia ( if high suspected) GBS swab (if not done)
Radiology/Imaging
• .
Obstetrical U/ S ( assess estimated fetal weight AFI, cervical length), biophysical profile
Special Tests
• NST/ electronic fetal monitoring ( EFM), nitrazine test, ferning, fetal scalp blood sampling, contraction stress test
MANAGEMENT
Emergent OO
cr
'C
• .
Reposition women (increase uteroplacental perfusion, relieve cord compression) , continuous monitoring IV fluids (if signs of £
3
».
•
maternal hypovolemia), oxygen at 8 - 10L/min (if signs of maternal hypotension), emergent caesarean if term/post - term and/or n
O 25
risks to maternal +/- fetus outweigh s benefits of not delivering ’
O n
Non- Emergent:
• .
Delivery at term NST or continuous FHR monitoring, follow - up biophysical profiles, treat underlying medical conditions (ie.
. .
hypertension, diabetes UTI) consider betamethasone x 2 doses ( < 34 weeks), consider MgS04 for neuroprotection (< 32 weeks),
consider GBS prophylaxis if rupture of membrane and indicated, consider tocolytics to achieve steroid benefit or transfer to
tertiary facility
Consults
• Maternal Fetal Medicine, NICU
DEFINITIONS
• Small for Gestaional Age ( SGA): estimated fetal weight less than the 10th percentile
> Includes constitutionally grown fetuses and growth restricted fetuses
• Fetal Growth Restriction ( FGR ): failure to meet growth potential because of an underlying pathological process
• Large for Gestational Age ( LGA): estimated fetal weight greater than the 90 th percentile
DIFFERENTIAL DIAGNOSIS
Small for Gestational Age or Fetal Growth Restriction:
MISC FETAL PLACENTAL* MATERNAL
• Incorrect Dating • Chromosomal 5 - 20%: • Placental vasculopathy: • Familial/ethnicity
• Constitutionally small .
aneuploidy (T 21 T18 . preeclampsia, abruption .
• PMHx: chronic HTN GHTN, CKD DM SLE . . .
baby but appropriate .
T13) triploidy • Cord abnormalities: .
APLS, cyanotic heart disease COPD chronic .
growth potential • Genetic: e.g.. osteogenesis .
2 VC previa, .
anemia, sickle cell Gl malabsorption, eating
(e.g., small parenteral .
imperfecta Russell Silver .
velamentous marginal . d/o
stature) Smith Lemli Opitz cord insertion • Uterine anomaly: bicornuate uterus
• Congenital Infection • Placental abnormalities: • Previous pelvic radiation
5 -10%: CMV, toxo, bilobed, circumvallate, • Modifiable riskfactor: alcohol, smoking, drug,
rubella, varicella - zoster, placental hemangiomas
malnutrition
syphilis, HSV, malaria • Abnormal maternal
• Teratogen: warfarin, valproate, chemo, anti -
• Congenital anomalies (e.g., serum analytes (e.g. . folate meds
CVS) high AFP)
• High altitude
• Multiple gestation • ’typically asymmetrical
• Short interpregnancy interval
IUGR due to late onset
• Maternal age (< 18. >40)
taISTORY
ID . . . .
Patient’s name age GTPAL, GA blood type Rh status EDD .
CC PPH or postpartum fever
HPI GA at which growth discrepancy was noted and how
Prenatal care received, U/S findings
Any prenatal genetic screening or testing and results
Symptoms of TORCH infections (asymptomatic, fever, malaise, rash)
PMHX See tables above for maternal conditions
PSHX C- sections, abdominal or pelvic surgeries
PO&GHX Previous pregnancies: GA, mode of delivery, complications, sex, birth weight, child’s present health and
development
. .
Previous abortions, stillbirths SGA/IUGR/ LGA GDM/GHTN/PEC
. .
STI (syphilis HSV) paps, menstrual cycle, use of ART
MEDS Anticoagulants/antiplatelets, seizure medications OTC PNV . .
ALLERGIES Medication/environmental: note specific reaction
SOCIAL Occupation, living situation, partner, domestic safety, nutrition status
EtOH, smoking, drugs
RISK See above tables
FACTORS Any medical conditions affecting maternal vasculature and oxygen delivery to the fetus
DM can cause SGA ( placental insufficiency) or LGA (hyperinsulinemia)
275 .
E dinonton Manual of Common Climc il Sc
PHYSICAL
General Approach:
. .
• Maternal BP HR RR, temperature
• Fetal HR ( with Doppler ) or NST
Cardiopulmonary
• Heart sounds
• S3 /S4
• Air entry
Abdominal
• SFH
• Leopold’s
• Abdominal pain
Dermatologic
• Skin rash (TORCH)
• .
Genital ulcers ( HSV syphilis)
• Acanthosis nigricans (insulin resistance)
INVESTIGATIONS
Bloodwork
. SGA
> Infection: TORCH infection, syphilis RPR
> Screen for common trisomies: MSS NIPT.
> . . . . . . .
If preeclampsia: CBC-D INR, PTT, Cr urea AST ALT urate LD urine protein-cr ratio
• LGA
> 2 hourOGTT
Invasive Prenatal Testing
• . .
Offer amniocentesis: Rapid Aneuploidy Test ( RAD) for T21 T 18 T 13.45 X, and Microarray
> esp. for early onset, symmetric SGA
> amniotic fluids can be sent for TORCH infections no
• Consider CVS if evidence of SGA before 14 weeks
Imaging n «
O
• Detailed anatomical U/S O n
*
OSEATMENT
Refer to Maternal Fetal Medicine at Tertiary Center
SMALL FOR GESTATIONAL AGE LARGE FOR GESTATIONAL AGE
• Depends on etiology and severity • Counsel on pregnancy weight gain
.
• Optimization of maternal medical conditions, nutrition smoking/EtOH/ • Management of diabetes: referral to DM clinic,
drug cessation initiation of insulin if necessary, glycemic targets for
• Termination of pregnancy may be discussed if abnormal genetic testing, fasting and postprandial levels
severe TORCH infection, severe structural anomalies, or maternal • Induction at 39 weeks
request. -
• May offer C section if EFW >4500 g and maternal
• Plan delivery if signs of fetal distress or: DM or > 5000 g and not diabetic
> Normal interval growth + Normal UA/ MCA Doppler in the absence
of other risk factors: deliver 39 -40 wk
.
> Abnormal interval growth Increased PI or S/ D in UA or Decreased
PI in MCA = deliver 37- 38 wk
> Absent or reverse end diastolic flow = deliver at 32 - 34 wk
• Consider betamethasone for fetal lung maturity x 48 hours prior to
delivery < 34 wk
• Consider MgS04 for neuroprotection x at least 4 hours prior to delivery
< 32 wk
• NICU consult
LESS COMMON
Adrenal ( high mortality/morbidity)
• Cushing’s Syndrome
> .
increase in ACTH production ( +) dexamethasone suppression test
• CAH ( 17 - OH -progesteronase deficient )
> .
HAIR -AN: hyperandrogenism insulin resistant, and acathosis nigricans
• Non- classical CAH
• Androgen secreting adrenal/ovarian adenoma
> Rare, rapid onset, severe symptoms, including DHEA - 5
Other
u O • Hypothyroidism
H O
<D u • Hyperprolactinemia
o
t/> C
JD > HISTORY
ID • Patient ’s name, age
CC • Excessive hair .
growth (lower abdomen, nipple, chin, upper lip breasts, thighs)
HPI • Age of onset, location/quality/pattern of hair growth, rate, progression, severity, acuity
• Effect on quality of life, methods of hair removal ( frequency)
• Reproductive Hx: infertility issues
• Wt 4|/ , change in fat distribution ( android vs. gynecoid)
• Moderate to severe acne, andrenarche, puberty
RED FLAGS • Acute onset, rapid progression with other signs of virilization or Cushingoid disease
• Androgenic alopecia, deepened voice. muscle bulk , clitoromegaly
4
PMHX • DM -T2/glucose intolerance, HTN, dyslipidemia, CVD
• CAH, Cushing's or thyroid disease, adrenal/ovarian tumor
PO&GHX • Menstrual/obstetrical/infertility Hx
. .
• Menstrual cycle: age of menarche oligo/amenorrhea cycle/menses length, moliminal symptoms
PSHX • Adrenal/pelvic/thyroid surgery
. . .
FHX • Excessive hair growth, endocrine disorders, DM, CVD HTN hyperlipidemia PCOS, menstrual problems
MEDS • Androgenic: testosterone, dehydroepiandrosterone ( DHEA -S), danazol, corticotropin (ACTH). high-dose
.
corticosteroids, androgenic progestins (component in OCP) acetazolamide, Provera, danazol ovral
• Nonandrogenic: cyclosporine, phenytoin, diazoxide, triamterene/hydrochlorothiazide, minoxidil,
.
hexachlorobenzene, penicillamine, psoralens, metoclopramide, methyldopa, reserpine
SOCIAL • Anabolic steroid use, smoking, EtOH, recreational drugs
RISK FACTORS • FHx of excessive hair growth, obesity, ethnicity
INVESTIGATIONS
Blood Work
Testosterone ( tumor ), LH - FSH ratio (may be helpful with PCOS, but limited
*
•
sensitivity)
• DHEA- S
> ACTH if above elevated (CAH, adrenal neoplasm)
• TSH (hypothyroidism)
• Fasting glucose, fasting insulin, fasting lipid profile ( familial/ PCOS)
Radiology/Imaging
• Pelvic U/ S for suspected polycystic ovaries or ovarian tumor
• CT/ MRI for suspected adrenal neoplasm or pituitary adenoma oo
Special Tests
n
• 24 hr urine cortisol or dexamethasone suppression test if suspect Huvutlvm O 2 .
Cushing' s Syndrome o n*
TREATMENT
• The most effective therapy for hirsutism usually involves a combination of lifestyle modifications, mechanical hair removal, and
medical therapy (after ruling out other treatable causes)
.
• General: treat underlying disorder (i.e , surgical removal of tumor)
• Wt * exercise, proper nutrition
• Mechanical: hair removal treatments such as shaving, electrolysis, laser hair removal
• Pharmacologic: Tx dependent on etiology - Familial + idiopathic = OCP +/- antiandrogen: PCOS = Metformin, OCP
+/-antiandrogen ( antiandrogens should be stopped at pregnancy to prevent feminizing of male fetus)
Follow -up
• .
Regarding associated risk factors or complaints: infertility AUB, endometrial hyperplasia, Wt gain, DM, CVD, HTN,
hyperlipidemia, metabolic syndrome, and smoking cessation
Referrals if signs of virilism, Cushing’s syndrome, or hyperandrogenism
• Endocrinology
• Gynecology
HELLP • H: Hemolysis . EL: elevated liver enzymes. LP: low platelet count (< 100 x 109/L)
ADVERSE CONDITIONS
Severity End Organ Damage CNS
• SBP > 160mmHg Kidney • Convulsions
RED FLAGS • Irritability, somnolence, visual disturbances ( scotomata), frontal HA . dyspnea and/or chest pain. N/V,
. .
epigastric/RUQ pain, seizures|U/O edema, Wt gain, bleeding
PMHX • Medical disease (HTN, DM, cardiac, renal, thyroid, asthma, thrombophilias, connective tissue disease)
PSHX •C- sections, abdominal or pelvic surgeries
POBSHX • Previous pregnancies: date . .
GA reached, delivery type ( SVD C-section, use of vacuum/forceps),
complications (in pregnancy, delivery, or postpartum), sex, birth Wt, child’s present health
• Previous gestational HTN/preeclampsia, gestational diabetes
PGYNEHX • STI Hx, abnormal Paps, regularity of menstrual cycle, last use of contraception
MEDS • Prescription . OTC, prenatal vitamins
ALLERGIES • Medication/environmental : note specific reaction
FHX • HTN, DM . Hx of gestational HTN/preeclampsia
SOCIAL • Occupation, current living situation, information about partner, domestic abuse
• Recreational drugs, EtOH, smoking during pregnancy
Chemistry 8O 2ft.
• Urinalysis for proteinuria ( >0.3 g/d in a 24 hr collection or > 30 mg/mmol protein creatinine ratio) O o
’
Follow-up
• .
BP should be measured during the time of peak postpartum BP at 3 - 6 days after delivery
• Gestational HTN usually resolves by 6 wks postpartum, but women with severe preeclampsia may remain hypertensive for up to
3- 6 mos
DIAGNOSTIC CRITERIA
• Infertility: no conception after 12 mos of unprotected and frequent intercourse
> Primary: without any previous pregnancy
> Secondary: after previous conception
• Investigations can begin after 6 mos of unprotected and frequent intercourse if female > 35 y/o
Unexplained ( 15%)
HISTORY
ID • Patient ’s name, gender .
( 9 /cJ) age, GTPAL
m ?
u O
I cc • Infertility
o
2a
to C
HPI
• Length and type of infertility
$: Female cJ: Male
• Length and type of infertility
JQ >
oo • Fertility in current or previous relationships • Fertility in current or previous
relationships
• Number and outcome of prior pregnancies (including ectopic and
miscarriages) • Coital frequency, intercourse timed
• Coital frequency, intercourse timed around ovulation, use of around ovulation, use of lubricants ( which
lubricants ( which may be toxic to sperm) may be toxic to sperm)
.
• Menstrual Hx: LNMP cycle, length, regularity, moliminal symptoms, • Boxers vs. briefs ( testicular
4
temperature), erections, ejaculations,
cyclical pelvic pain
• Symptoms of PCOS: hirsutism, acne, alopecia, weight gain libido, androgen supplementation/steroid
use
• Symptoms of POI: hot flashes, vaginal dryness
• Symptoms of prolactinoma: headache, vision change, galactorrhea
• Symptoms of endometriosis: dysmenorrhea, dyspareunia, dyschezia
GU Exam • Inpect: Hair distribution, clitoris size, stigmata of STI • Hypospadias (hypogonadism . Kallmann)
.
• Speculum exam: Pap vaginal/cervical swabs for STIs • Surgical scars
• testicular size with orchidometer (hypogonadism,
• Bimanual exam: masses, irregularily shaped
uterus, or fixation of uterus/adnexa ( adhesions, Kallmann)
endometriosis) • Decent of testes (cryptorchidism)
• Varicocoele
• Rectovaginal exam: nodularity of uterosacral
ligaments (endometriosis) • Presence of hernias
• Presence of masses
INVESTIGATIONS
Blood Work
9 CBC ( infection), TSH. prolactin level, free androgen level ( PCOS). FBG/HbAlc ( PCOS) DO
(
•
• ; assess ovulation: day 3 LH/FSH /PRL/TSH/estradiol/DHEA. day 21 progesterone Infertility Basic Workup
• 9 Rubella and varicella status (if not immune, then vaccinate before pregnancy) Ovulation (day 3 and day 21)
o ®
• $ CBC (infection). TSH. FSH/LH
t O 2.
*
• Genetic testing (as indicated by Hx/ PEx )
Tubes (HSG) O n
Sperm (semen analysis)
Radiology/Imaging
• 9 pelvic U/S: assess for uterine myomas and ovarian cysts
• 9 HSG: assess tubal patency and uterine cavity, can also be therapeutic as it can clear the fallopian tubes
• 9 hysteroscopy: directly visualize uterine cavity if HSG is abnormal
Special Tests
• 9 basal body temperature monitoring ( to assess ovulation): LH ovulation prediction monitors /kits
• 9 cervical mucous analysis: assess post -intercourse for presence of motile sperm
• .
Assessment of ovarian reserve, i.e., Day 3 antral follicle count anti - Mullerian hormone, and inhibin levels in women > 35 yrs of age
• o semen analysis: liquification, count, motility, volume, morphology, pH, WBC count
Surgical /Diagnostic Interventions
• ) diagnostic laparoscopy: allows for direct view of pelvis when looking for endometriosis or other pelvic pathology
TREATMENT
General Education
• time intercourse to 6d prior to presumed ovulation day;
• sperm live 48 - 72 hrs; therefore should have intercourse every 2 - 3 days
• Counsel about adoption options, referral for psychological counseling/emotional support
9
• Ovulation Induction:
PCOS: wt. loss, clomiphene letrozole/gonadotropins/metformin
Prolactinoma: bromocriptine
• Tubal disease: tuboplasty, or IVF
• Endometriosis /Abdo. Adhesions: surgical lysis of adhesions
• Unexplained infertility: clomiphene citrate with IUI, or IVF
c?
• Azoospermia: therapeutic donor insemination
• Oligospermia: IVF with ICSI
• Sperm Motility Problem: IUI
HISTORY
ID • Patient ’s name, age, GTPAL, GA
CC • Signs of fetal distress or risk factors for adverse outcomes
HPI • Vaginal bleeding, contractions/cramping, leak of fluid, meconium, Rh status
• Fetal movement, chronic abruption, placenta previa/low lying placenta, cord abnormalities
• Maternal symptoms: infection, systemic, chronic disease
RED FLAGS • Fetal distress: decreased/absent fetal movement, vaginal bleeding, severe uterine pain
.
PMHX • DM, HTN, HIV, thyroid or Gl disease, infections STIs, thrombophilias, anemia
PSHX • C-section, pelvic or abdominal surgery, need for blood transfusions
PO& GHX • Current ObsHx: LMP, EDC, results of recent U/ S (dating, placental position, fetal anatomy), complications (HTN,
GDM, PPH), fetal growth
• GA at delivery, type/complications of delivery, Wt of baby, complications with previous pregnancies
.
• Pap abnormalities STIs, brief menstrual Hx
2 1o»
*u • RESP: Cough, wheezing, pharyngitis, shortness of breath
• Gl: Diarrhea, vomiting, constipation
H O
<L> u
<u • GU: Diabetic nephropathy, vaginal discharge, vaginal irritation
_
V)
Q
c
>* • MSK /DERM: Arthritis, butterfly rash, petechiae
RISK • Maternal conditions, umbilical cord abnormalities, placenta previa, placental insufficiency, abruption or placental
FACTORS infarction, fetal anemia or infection, uterine hyperstimulation, obesity
PHYSICAL
General Approach
• Maternal VS: BP, HR, RR. Temp Sp02 .
Inspection
• ABD: assess for uterine masses
• Pelvic exam: may be warranted if PROM or bleeding is being Transducer for sensing
investigated uterine contractons .
Transducer for sensing
Palpation , fetal heart rate
• ABD: tenderness (primarily uterine) , size of the uterus, SFH,
Leopold's Maneuvers
• .
Pelvic exam: cervical effacement consistency, dilation and fetal
station
ELECTRONIC FHR MONITi r
• External or Internal lead f
Potential causes of inadequate tracings
• Interpretation of NST
must take into account • High maternal BMI
overall clinical picture • Poly/oligohydramnios
Baseline Variability
• Definition: beat - to- beat fluctuations in the baseline FHR as seen in a section without
accelerations or decelerations
• Normal variability 5 - 25 bpm is a good indicator of a healthy fetus
• Flat baseline DDx: acidosis, sleeping, maternal sedative use
Accelerations
• Definition: 15 bpm above baseline for > 15 secs
• < 32 wks GA: 10 bpm above baseline >15 secs
»
Decelerations »
• Definition: decrease in FHR relative to baseline i
TYPE OF
DECELERATION CAUSE PATTERN OBSERVED PATHOLOGIC
oOcr
Head compression when Mirror image of No: still has good beat - to - beat variability <
3 &
Early
head is engaged uterine contraction and returns to baseline n
O
a
Severity proportional to duration
Umbilical cord No relation to uterine Mild: < 30s, Moderate: 30- 60 s o n*
compression and contractions, Severe/Complicated: > 60 s, drop by > 60 bpm
Variable
subsequent decrease in length depends on duration of .
and FHR < 60 bpm repetitive, loss of " shoulder "
fetal BP cord compression acceleration, slow recovery, loss of short term
variability
Yes: Severity of fetal hypoxemia and acidosis are
Inadequate fetal 02 Shifted to the right relative to
proportional to amplitude of FHR drop below
Late due to uteroplacental the uterine contraction, later
baseline: Mild < 15 bpm; Moderate 15 - 45 bpm; Severe
insufficiency onset, minimum and recovery
> 45 bpm
L REATMENT
• If normal, continue to monitor as the clinical situation dictates
• If atypical and not labouring patient, not predictive of fetal acid-base status: continue monitoring, perform a BPP
. . .
• If abnormal BPP or U/S alter maternal position 100% 02 by face mask D/C induction agents, further testing; urgent delivery
may be indicated
Referrals: Obstetrics/Gynecology or maternal fetal medicine specialist if increased fetal surveillance during labor / NSTs required
Diagnostic Criteria Regular, frequent , painful uterine contractions and cervical change (dilatation and effacement )
• First Stage
.
> Latent phase: cervical dilatation < 3 - 4 cm uterine contractions irregular
> Active phase: rapid cervical dilatation ( 4 - 10 cm) , regular contractions
• Second Stage: from full dilatation to delivery
Common Conditions Braxton Hicks contractions: irregular, less painful, no A frequency/intensity, no cervical change
Abnormal Conditions • Abruption ( ABD pain, vaginal bleeding) • Preterm labor
• Placenta previa (painless, vaginal bleeding) • Preterm ROM
HISTORY
ID • Patient ’s . . . .
name age GTPAL GA GBS swab results, blood type and Rh status
CC • Suspected labor: ROM contractions .
HPI • Spontaneous onset vs. induction of labor (reason for induction, method used)
• EDC (document whether established by LMP or early U/S)
.
• Prenatal care received, complications, abnormal or repeat U/S low lying placenta, last internal exam,
steroids, diabetic screen results HTN .
. .
• HIV HepB syphilis, rubella, varicella status
•2 O85 .
• ABCD: Activity Bleeding, Contractions, Drench/ Discharge
u ( A ) Fetal movement: decreased?
H O ( B) Bleeding: onset, quantity, color, prior bleeding
0) u
_
Q>
<u
V) C
(C) Contractions: onset, regularity, duration, interval between contractions, severity
(D) Fluid leakage/rupture of membranes: onset, color, consistency, quantity, odor, meconium
QO
• Pain: OPQRST
.
complications (in pregnancy, delivery or postpartum), gender, birth Wt child’s present health
PGYNEHX • Date of last Pap test, abnormal Pap tests + outcome
• Menstrual cycle regular before pregnancy, contraception use + stop date
.
• Previous STIs whether at risk for STIs currently ?
MEDS • Rx ’n, OTC, CAM . known teratogens (e.g.. coumadin. antiepileptics. ARB) & vitamins (folic acid)
ALLERGIES • Medication/environmental: note specific reaction
FHX • HTN . DM, multiples, congenital malformations
.
SOCIAL • EtOH smoking, recreational drugs
• Occupation, partner information, current living situation, safety at home (domestic violence)
• Patient ’s desires and expectations for intrapartum care and analgesia
ROS • Focus ROS on areas where Hx suggests relevant findings (e.g., visual changes, SOB RUQ pain N/V,
-
edema for pre eclampsia)
. .
285
PHYSICAL
General Approach
• Maternal VS ( BP, HR. RR, Temp, Sp02), NST. and contraction pattern (quality, duration, frequency)
• Maternal Wt and FHR
Inspection and Palpation
• ABD: assess uterine tone, tenderness, palpate contractions
> SFH: uterine fundus to pubic symphysis ( within 2 cm of GA at 20- 37 wks)
.
Leopold’s Maneuvers: systematic palpation of abdomen to determine lie position, and presentation of fetus
>
• Pelvis: Inlet ( AP diameter), mid - pelvis (ischial spines), outlet
• Cervix: Internal examination, comment on each of the following:
Special Tests
• Sterile speculum exam: to verify ROM
> Pooling of clear fluid in posterior fornix, (+) nitrazine, (+) ferning
• Urine R & M: proteinuria, UTI; swab for GBS if unknown
usEATMENT
Emergent ( see Fetal Distress)
Treatment Options
• GBS prophylaxis (Indications: GBS +, GBS bacteriuria any time in current pregnancy, unknown, or previous infant with invasive
GBS)
> Penicillin G 5 million units IV x 1dose then 2.5 million units q4h until delivery
> Clindamycin or vancomycin if menicillin allergic
• Pain management
> Non - pharmacological: continuous labor support, baths, maternal movement /positioning
> Nitrous oxide: self -administered, inhale deeply at the onset of contraction
> Narcotics: morphine, fentanyl ( avoid meperidine which has a longer y2 life)
> Pudendal nerve block: local anesthetic for the perineum useful during 2nd stage or forceps
> Epidural block: relief throughout all stages of labor, may prolong 1st and 2nd stage
• Labor dystocia: assess 4Ps-power (contractions), passenger ( fetal position), passage (pelvis), psychologic (effort)
> Consider interventions: amniotomy, oxytocin augmentation C-section .
• Cardinal movements of delivery: engagement, descent, flexion, internal rotation, extension (delivery of head), restitution, external
rotation, expulsion, delivery of the shoulders (anterior, then posterior) and body
• 3rd stage management ( separation and expulsion of placenta, < 30 min)
> Oxytocin: 10 units IM, or IV infusion of 20 - 40 units in 1000 mL , RL at 150 mL/hour with delivery of anterior shoulder
> Gentle umbilical cord traction and counter traction on uterine fundus
> Signs of placental separation ): gush of blood, cord lengthens, fundus rises in ABD and uterus becomes globular
• Laceration repair (1- 4 degree) ^
> Absorbable sutures, continuous locking above hymenal ring, interrupted sutures for perineal fascia
EIAGNOSTIC CRITERIA
• Physiologic: 12 months of amenorrhea in absence of other biologic or iatrogenic causes
• Premature ovarian insufficiency (< 40 yrs) (radiation or chemotherapy)
• Induced (hysterectomy, oophorectomy, radiation therapy)
CC • Cessation of menses
HPI • Decrease in amount and duration of menstrual flow
• Onset of amenorrhea (12 mos is diagnostic)
• Symptoms associated with vaginal changes
Discharge, bleeding with coitus, vaginal pruritis, excessive dryness, vaginal burning, dyspareunia
• UTI symptoms
> Incontinence (changes in urgency, frequency) and/or diagnosed recurrent UTIs
• Changes in breast size, hot flashes, skin and hair changes, insomnia, depression, aches/pains
• Use of HRT, OCP
• Contraindications to HRT
JQ > > CVD, previous stroke
O
> Acute liver disease
> Undiagnosed vaginal bleeding
> Cancer ( breast, uterine)
> DVT (past thromboembolism)
• Osteopenia or osteoporosis
• HTN ( RF for CVD)
MEDS • Steroids, HRT, herbals and vitamins, dietary interventions such as soy
Charateristics of Murmurs:
1.Location +/- radiation
2.Timing in the cardiac cycle ( systolic or diastolic)
3. Intensity (Grade l-VI)
4. Variation with patient position
5.Quality: harsh, musical, blowing
6. Associated extra heart sounds
Innocent Murmurs
• Child age >1year, asymptomatic, abscence of risk factors for structural heart disease, normal P/E otherwise, and murmur has
Common Conditions
Type Characteristics Age
HISTORY
ID • Name, age, gender, ethnicity, home
CC • Murmur
HPI • Cardiac symptoms: chest pain, palpitations, cyanosis, pre -syncope /syncope, dyspnea (particularly on
exertion)
• Constitutional symptoms: diaphoresis ( with feeds or exercise), fatigue, poor exercise tolerance or capacity
.
for play, poor growth or FTT developmental delay
• Respiratory symptoms: chronic cough and dyspnea
RED FLAGS • Feeding difficulties and FTT in infants
• Fatigue, poor exercise tolerance in children
339
PMHX • Prenatal: prenatal care, U/S frequency (cardiac anomalies on U/ S), EtOH and other toxin ingestion,
medication exposure ( SSRI, lithium, valproate), maternal illness (particularly infection or DM)
.
• Perinatal: gestational age mode of delivery, complications, birth Wt, APGAR scores
• Postnatal: neonatal complications, NICU admission, newborn metabolic screen
..
• Medical Hx: genetic syndromes (e g Trisomy 21, Turner Syndrome, Marfan Syndrome), frequent
respiratory infections (due to pulmonary congestion secondary to CHF), Kawasaki disease, rheumatic
fever
PSHX • Previous surgeries and complications
—— —
ROS • Gl: nutrition, nausea /vomiting, diarrhea, abdominal distention
• GU: urine output, edema
I I i i IIM I
General Approach ^^1
• VS ( BP . HR. RR, T. pre/post ductal Sp02), growth charts (Ht/Wt/HC)
• Four -limb BP measurements (coarctation of the aorta may produce a pressure gradient > 20mmHg between the upper and lower
extremities)
• General appearance ( distress), dysmorphic features
HEENT: dysmorphic features, pallor, cyanosis, prominent neck vessels, abnormal pulsations
RESP: evidence of respiratory effort, crackles suggest pulmonary edema
CVS:
• Inspect for clubbing, scars on the chest, pectus excavatum or carinatum
• Palpate for peripheral perfusion (distal pulses, capillary refill, peripheral temperature), precordial heaves or thrills, apical impulse,
femoral pulse, edema
• Percussfor cardiac dullness
• Auscultate for SI and S 2, murmur (characterize as above) , extra heart sounds (e.g. fixed S 2 split in ASD, S 3 in LV dilation and
.
dysfunction S4 in hypertrophic cardiomyopathy), ejection clicks (e.g. aortic stenosis)
ABDO: hepatomegaly, ascites
INVESTIGATIONS "U
Radiology/ lmaging n>
Q.
• CXR ( routine use is discouraged as if normal this does not rule out structural heart disease) &>
• Echocardiography ( test of choice) 2
n
.
ECG: (routine use is discouraged as if normal this does not rule out structural heart disease) in
L REATMENT
Referrals
• All newborn murmurs ( < 1 year ) and pathologic murmurs (at any age) should be referred to a pediatric cardiologist
Follow - up
• Document and continue to follow any murmur (even an innocent one): continue to monitor for resolution (innocent murmurs) or to
ensure that it does not change over time (innocent or pathologic murmurs)
HISTORY
ID • Name . age. gender, ethnicity, home
CC/HPI • Inquire about and discuss patient and parental concerns regarding immunizations
RED FLAGS .
• Previous anaphylactic reaction to vaccine (urticaria, angioedema respiratory distress, shock ), recent
steroids, or blood product transfusions
PMHX .
• Current state of health, primary immunodeficiency Hx of immunoglobin or blood product transfusion,
.
chronic disease, functional hyposplenia, HIV Guillain-Barre Syndrome, seizures
13 • Prematurity, maternal serology (e.g., anti - HBsAg), requirement for IVIG/vaccinations at birth
•MM
-n<v
U MEDS • Immunosuppressive drugs (chemotherapy, organ transplantation, biologic agents), systemic steroids, recent
administration of IVIG
CL
• Other prescriptions .
OTC, vitamins, CAM
ALLERGIES • Medication, food, environmental, specifically to eggs . ABTx, latex,or gelatin
IMMUNIZATIONS .
• Routine IUTD special
• Date of last immunization, adverse reactions or anaphylaxis to previous vaccinations
FHX • Seizure disorders, severe reactions to a vaccine
SOCIAL • Ethnicity, recent immigration, travel Hx . community outbreaks
PATIENT AND PARENT COUNSELING
Vaccine Preparations and Additives
• 3 types: live -attenuated, whole inactivated, or subunit (organism parts, protein/toxoid, polysaccharide ± conjugate)
> Live attenuated vaccines include MMRV. oral typhoid, yellow fever, and BCG; these are given subcutaneously
• Except for live vaccines, most are intramuscular, and some shots contain multiple vaccines
> .
± adjuvant to enhance immune response (e.g. aluminum salt )
> .
± preservative (e.g. thimerosal)
> .
± stabilizers (e.g., albumin, gelatin, lactose) or trace components from manufacturer (e.g. egg protein, formaldehyde)
Common Misconceptions About Immunizations
• Acknowledge and respect parental concerns; always provide current information and let them make the decision
.
• Safety of multiple vaccines early in life: all vaccines are tested prior to use and early vaccination builds immunity against vaccine -
preventable illnesses before children are likely to be exposed to the causal organisms
341
• Autism and the MMR: The 1998 study in The Lancet claiming this link was fraudulent and has since been refuted by numerous
studies
• Safety of thimerosal: there is no legitimate safety reason to avoid the use of vaccines that contain thimerosal
Benefits of Immunization
• Emphasize to parents that an unimmunized child is at risk of serious infection
• Vaccines prevent infections that may result in serious illness or death (e.g., epiglottitis, measles, encephalitis, whooping cough,
poliomyelitis, meningitis, pneumonia, tetanus, hepatitis/cirrhosis, cervical cancer)
• Herd immunity: high rates of immunization reduce infection risk in individuals who cannot be immunized
> Treatment: 10 - 15 mg/ kg acetaminophen q4H PRN ( max 5 doses /d) for fever or pain, prophylactic use controversial
• Less common, moderate: seizure, hypotonic unresponsive state, inconsolable crying (DTaP - IPV), fever, arthralgias, parotitis (MMR)
SPECIAL CONSIDERATIONS
Contraindications
• Previous anaphylactic reaction to vaccine or one of its components
> Previous vaccine
-
» Neomycin ( IPV, DTaP IPV - Hib, MMR . varicella)
> .
Gelatin ( varicella MMR )
> Baker ’s yeast (Hepatitis B )
> Eggs ( influenzae, yellow fever )
> Streptomycin ( IPV)
• Immunodeficiency or active immunosuppressive therapy: generally, all live vaccines are contraindicated
> Following solid organ transplant: resume non - live vaccinations in 6 - 12 mos, consider live in 2 + yrs
> HIV: vaccinate early in disease when CD 4 counts are still high
> High dose systemic steroids for > 2 wks: defer all vaccines until off steroids for 1 mo
• Pregnancy: defer live vaccines until immediate postpartum (breastfeeding is not a contraindication)
• Take precautions with vaccine administration under these circumstances
> All vaccines: moderate to severe illness, severe bleeding disorder
> Live vaccines: recent administration of IVIG or blood products. Wait 3 - 11 mos ( generally 6 mos).
Missed Immunizations: no need to restart immunizations if one is missed; patients can pick up where they left off
• If there are inadequate immunization records (e.g., immigrants), restart on immunization protocol based on age u
fD
Prematurity: immunizations should be given on the regular schedule if a child is premature, not delayed to corrected age Q.
(e.g., first set due at 60 days from birth) ft
*
Hyposplenia and asplenia (congenital, surgical, or functional): no contraindications to any vaccines n
.
• Increased risk for encapsulated bacterial infections (S. pneumoniae , Hib N. meningitides )
</>
• Ensure IUTD, children > 2 y/o should receive additional vaccines against encapsulated bacteria
DIFFERENTIAL DIAGNOSIS
CATEGORY Condition Distinguishing Characteristics
INFECTIOUS Septic Arthritis Acute, febrile, warm/swollen/painful joint
Osteomyelitis Commonly preceded by trauma, febrile, bone pain
Cellulitis Soft tissue swelling, warmth, redness, infection entry point
INFLAMMATORY Transient (toxic) Synovitis of the Hip .
Common, age 3-10 yrs, recent URTI afebrile, well, onset 1- 2 d
Juvenile Inflammatory Arthritis ( JIA) .
Gradual onset AM stiffness, polyarthritis, systemic symptoms
Henoch-Scholein Purpura ( HSP) Migratory polyarthralgias, purpuric rash, abdo pain, nephritis
Bursitis Overuse in athletes
Reactive Arthritis Enteric/GU infection 1-4 wks before oligoarthritis
Kawasaki Disease . .
Arthralgias, patient < 5 yrs fever > 5 d conjunctivitis, lip cracking,
cervical lymphadenopathy, rash, redness of hands and feet
MALIGNANCY Leukemia, Bone Tumors. Systemic symptoms, night pain, abnormal bruising/pallor
Metastasis Unilateral pain, worsens over time
TRAUMA Traumatic injury Hx of trauma
OTHER -
Legg Calve - Perthes Disease ( LCPD) 4- 8 y/o, persistent pain, limited internal rotation of hip
Slipped Capital Femoral Epiphysis ( SCFE) Adolescent, obese males, vague, persistent pain,
limited internal rotation of hip
Osgood-Schlatter Disease .
11- 13 y/o athletes or rapid growth spurt, anterior knee pain
(patellar tendon insertion) that gradually worsens
Developmental Dysplasia of the Hip Breech presentation, first born, female, oligohydramnios,
( DDH) family history
Growing Pains .
2- 12 y/o pain disrupts sleep, bilateral, no limitation of activity
CC • Limp: any alteration in child’s normal gait (due to pain, weakness, or deformity)
IS)
u HPI • Onset: acute/chronic, recent . .
trauma, recent URTI/illness getting worse/better overuse prior episodes .
• Palliating/precipitating: effect of activity/rest, prolonged sitting/kneeling . NSAIDS
a • Quality: painful or painless limp, continuous or intermittent, sharp or dull/vague
Q)
a. • Radiation/region: monoarticular vs . polyarticular, focal/hip/groin/knee/foot, unilateral vs. bilateral, migratory
• Severity: wt bearing, activity level, subjective description
• Timing: AM stiffness or limping, pain at night or wakes from sleep
• Mechanical: catching, clicking, snapping
• Systemic symptoms: fever, night sweats, decreased appetite, wt loss, fatigue, lethargy, irratibility
• Other: sore throat, rashes, abdominal pain, diarrhea, back pain, incontinence, sciatica
• High suspicion of child abuse
RED FLAGS • Constitutional .
symptoms, ill/lethargic, night pain, refusal to wt -bear back pain, incontinence
PMHX .
• JIA chronic illness, sickle cell gene, endocrinopathy . bleeding disorder
.
• Prenatal, perinatal or neonatal complications, gestation GTPAL, delivery, presentation, birth wt
FHX .
• RA SLE, psoriasis, IBD, hematological disorder, sickle cell, leukemia, DDH
SOCIAL • Home environment, psychosocial situation (parental neglect, abuse, sexually active)
» Galeazzi test for DDH: positive if knees different height when supine with ankles buttocks (knees flexed )
. .
NEURO: muscle strength, bulk, tone DTR sensation (dermatomes/peripheral nerve distributions)
INVESTIGATIONS
Radiology/ lmaging
• X - ray: AP, lateral, frog leg views of pelvis (beware, initial XR CONDITION EXPECTED FINDINGS
negative in some fractures, AVN, OM, septic joint)
Septic Arthritis
.
High ESR /CRP high WBC > 75% PMN
> Limp + acute hip pain look for: SCFE, osteomyelitis, stress synovial fluid
fracture High ESR/CRP, high WBC blood C& S,
Osteomyelitis
• Technetium bone scan or MRI if suspicion, despite normal normal X - ray, bone scan/MRI to Dx
.
x -ray for: spine pathology OM, stress fracture, early AVN) Transient
Minimal findings (clinical diagnosis)
Laboratory Investigations Synovitis
•Indicated if fever, persistent limp, or etiology uncertain LCPD
.
Limited internal rotation of hip normal
labs, x -ray is diagnostic
following Hxand PE
• If suspicious, must rule out septic joint with joint aspiration: SCFE
Limited internal rotation of hip. -o
X - ray is diagnostic (frog-leg views) n>
send joint fluid for WBC, differential, gram stain, cultures, .
protein, glucose JIA . .
High ESR/CRP -ve RF + ve ANA ( 50%)
Q
.
• CBC-D ESR/CRP, blood C& S if worrisome joint swelling
• If suspect post -infectious etiology, consider strep antigen test,
. .
lyme titer, DNAse B, throat swab, urine C& S R & M FOBT stool .
Neoplasm
.
Low Hb, WBC Pit, X -ray (poorly defined
margins, onion skin/sun burst appearance
without sclerosis
-
n)
V
i
C& S/O& P
Special Tests:ANA ( SLE), HLA - B 27 (Reactive Arthritis, Psoriatic Arthritis), sickle cell, viral serologies, complement, immunoglobulins
TREATMENT
Treatment dependent on etiology
• . .
Trauma: supportive RICE (rest, ice, compress, elevate) NSAIDs
- ..
• Infection: IV ABTx (start empirically e g cefotaxime + gentamicin, add vancomycin if MRSA is suspected, then narrow base on C&S)
and irrigation and debridement
• .
JIA: NSAIDS methotrexate, biologies
• Transient Synovitis: NSAIDs and AAT
• SCFE: avoid wt - bearing, prompt referral to orthopedic surgeon, operative repair
Follow-up: Ensure mobility, resolution of infection
Referrals: Pediatric Rheumatologist, Orthopedic Surgeon, Pediatric Oncologist as needed
KEY POINTS
• Do a thorough history, pay attention to systemic symptoms and remember to ask about concurrent infections
• For physical exam, expose both lower limbs. It is important to address the entire lower limb as what hurts can be the result of an
abnormality somwere else.
• If septic arthritis is suspected, a joint aspiration should always be done
• Remember non-muscoloskeletal conditions can cause a limp
DIFFERENTIAL DIAGNOSIS
Etiology of Unconjugated Hyperbilirubinemia
Pathologic
Physiologic
Hemolytic Non-Hemolytic
Intrinsic Extrinsic
• Red cell membrane defects
• Drugs
Spherocytosis
>
Vit K • Hemorrhage / hematoma (e.g.,
• Breast feeding • Sepsis cephalohematoma)
> Elliptocytosis
jaundice • Splenomegaly • Polycythemia
• Erythrocyte enzyme defects
• Breast milk • Isoimmune -mediated • Gl obstruction/ileus
jaundice > G6PD deficiency
> Pyruvate kinase deficiency
> ABO, Rh(D), or • Crigler - Najjar syndrome
• Jaundice of
other minor antigen • Gilbert syndrome
prematurity > Congenital erythropoietic
incompatibilities • Congenital hypothyroidism
porphyria
• Hemoglobinopathies
-
> a Thalassemia
Common Conditions
10 • Unconjugated hyperbilirubinemia: breast feeding jaundice, breast milk jaundice
u
High Mortality/Morbidity
• Biliary atresia, acute bilirubin encephalopathy, sepsis
TJ
.
QJ
Q HISTORY
ID • Name, age, gender, ethnicity, home
CC • Jaundice
ROS .
• Hypo/hypertonia, seizures, decreased LOC, cough/ wheeze, apnea ( ALTE) respiratory distress, abdominal
distention, bleeding, rash/ lesions
RISK FACTORS .
• ABO incompatibility (mother type O infant type A or B), prematurity, sibling with severe hyperbilirubinemia,
birth trauma, male, mother > 25, Asian/European ethnicity, infection, breastfeeding, macrosomic infant of
. .
diabetic mother, poor feeding, TPN sepsis risk factor (GBS+ PROM/ PPROM, chorioamnionitis)
PHYSICAL
General Approach
• ABCs . VS (BP.HR. RR. T. Sp02).LOC/vigor/pallor
HEENT
• Bulging/sunken fontanelles, jaundice ( sclera, mucous membranes, tip of nose), cataracts, abnormal facies (e.g. triangular in Alagille
syndrome), cephalohematoma
CVS/RESP
• Murmurs or extra heart sounds, delayed capillary refill
• Breath sounds
Gl
• Hepatosplenomegaly, abdominal mass and/or distention
MSK
• Birth trauma (e.g. clavicles), hematoma’s
DERM
• Jaundiced palmar creases, bruising/petechiae
NEURO
• Hyper /hypotonia, primitive reflexes
INVESTIGATIONS
Blood Work (as indicated by Hx and PE )
• Total serum/conjugated/unconjugated bilirubin ( fractionate if jaundice > 2 wks or markedly elevated TSB)
• Cord blood for blood group and DAT (Coombs test) if early jaundice or mother ’s T& S unknown
• Blood smear, reticulocyte count
.
• Septic workup: CBC- D, blood/urine C & S ± CXR , ± LP if indicated, TORCH screen, hepatitis serology
.
• Screening for G6PD deficiency if severe hyperbilirubinemia or high risk based on ethnicity TSH screen
. .
• If conjugated hyperbilirubinemia - AST, ALT, ALP PT/INR PTT, albumin, ammonia, sweat chloride test as well as metabolic and
TJ
.
genetic screens ( serum r - antitrypsin RBC GALT assay for galactosemia, etc.) O
Radiology/ lmaging ^ Q.
0)
• Abdominal U/ S. HIDA scan (normal clearance excludes atresia and stasis) if conjugated hyperbilirubinemia
Surgical/ Diagnostic Interventions n
V )
Emergent
• ABCs, fluids, ABTx if septic
• Exchange transfusion immediately if signs of acute bilirubin encephalopathy (rare)
Treatment Options
• Mild to moderate unconjugated hyperbilirubinemia: breast feeding support, phototherapy (nomogram guides usage)
• Breast feeding should not be stopped for breast feeding or breast milk jaundice
•Immune hemolytic jaundice: IVIG ± exchange transfusion
•Severe hyperbilirubinemia: phototherapy, exchange transfusion
Surgical
• Biliary atresia: Kasai procedure (hepatoportoenterostomy) ± liver transplant
Follow - up
• Reassess in 24 - 48 hrs: close monitoring of Wt gain & serum bilirubin: repeat Hb at 2 and 4 wks for infants with isoimmunization
• After exchange transfusion, close follow -up and hearing test with brainstem evoked auditory potentials
Referrals
• Lactation Consultant, General Pediatrics . NICU. Surgery. Hematology, Genetics as required
Common Conditions
Pulmonary Causes of Respiratory Distress
Causes X -ray Findings Treatment
TTN
Streaky interstitial infiltrates ( mostly perihilar )
hyperinflation, fluid in interlobar spaces
. .
Supportive Tx (02 neonatal CPAP, fluid restriction ±
nutrition usually sufficient
RDS Reticulonodular, air bronchograms, deer, lung volume Surfactant, supportive (often intubated)
MAS
Patchy atelectasis/infiltrates, air trapping, often
hyperinflation, Rule out pneumothorax (up to 20%)
. .
Supportive ± surfactant ± inhaled nitric oxide ( iNO) ± .
ABTx
Pulmonary
atresia
Cyanosis in neonatal period after .
Distress, loud single S2 ± VSD/ PDA PGE1, surgery (systolic pulmono -
ductus arteriosus closes murmurs aortic shunt, complete repair )
Birth - infancy (85% before 2 mos),
Tricuspid cyanosis (deer, pulmonary blood Single S 2 ± VSD/ PDA/systolic - PGE1, surgery (depends on pulmonary
atresia . .
flow) CHF/ FTT (incr pulmonary pulmonary collateral murmurs blood flow)
blood flow)
Truncus
Cyanosis in newborn, but more
commonly CHF ( worsens as
SEM (truncal flow) ± diastolic
.
murmur (regurgitation) L precordial
.
Surgery (close VSD commit LV to
trunk, reconstruct right ventricular
arteriosus
pulmonary vascular resistance deer.) bulge, hyperactive precordium outflow tract )
Ebstein Newborn to teenage/adult yrs Fatigue, holosystolic murmur over
anomaly depending on severity PGE1, surgery
left precordium (TR )
[£ISTORY
ID . .
• Name age gender, ethnicity, home
HPI • Onset of respiratory distress or cyanosis (rapidity, day of life), course/progression, duration
• Cyanosis worse with crying, activity, or position
347
RED FLAGS • Poor perfusion, cyanosis, poor respiratory effort or apnea, gasp/choke/stridor, worsening condition
PMHX • Medical conditions: prior episodes of cyanosis, respiratory distress, stridor, intubation, immune status
• Prenatal: prenatal care, U/Sfrequency, maternal illness /exposure to toxins (smoking/EtOH/drugs)
• Perinatal: GA, complications of delivery, birth Wt, APGARs, asphyxia
• Postnatal: neonatal complications, NICU admission, newborn metabolic screen
FHX • Congenital heart / lung disease, genetic -metabolic syndromes, SIDS/early death, immunodeficiency
SOCIAL • Second hand smoke, SES, sick contacts, trauma
ROS • HEENT: cough, rhinorrhea, red/purulent eye, blue trunk /face /lips, choking
• CV/RESP: diaphoresis/ tachypnea with feeds, wheeze, cough, SOB, stridor, gasping, apnea
• Gl: feeding changes, regurgitation/vomiting (esp bilious), diarrhea, failure to pass meconium
RISK FACTORS • Intubation, immunodeficiency, craniofacial malformation (or FHx of same), preterm delivery
PHYSICAL
General Approach
• .
ABCs, VS: BP (in all 4 limbs), HR. RR, T Sp02 (on and off of 02: Sp02 in R hand and foot to assess for flow through ductus
.
arteriosus); capillary refill; growth charts (Ht /Wt /HC) APGARs for neonates
• Signs of impending collapse: obstructive airway (gasp/stridor ), poor /no resp effort, cyanosis /dusky / bradycardic = get help
HEENT/NEURO
.
• Craniofacial abnormalities, e.g. depressed nasalbone, cleftpalate, micrognathia, macroglossia
• Tone + primitive reflexes
RESP
• Nasal flaring, grunting, chest retractions ( supraclavicular suggests upper airway obstruction), symmetry of chest movement, chest
expansion, head bobbing ( accessory muscle use), paradoxical breathing (chest in and abdomen out during inspiration, may be seen in
healthy newborns as well), tracheal tug
• Air entry, stridor, wheeze or cough, crackles
CVS
• Precordial heaves, point of maximal impulse, thrills
.
• Murmurs, extra heart sounds (S3, S4, pericardial rubs etc.), central and peripheral pulses
ABD U
scaphoid abdomen (congenital diaphragmatic hernia or proximal Gl obstruction), bowel sounds in chest
o
• Q -
• Peritonitis P
INVESTIGATIONS n
t/>
Blood Work ( as indicated by Hx and PE)
• CBC- D, electrolytes, blood glucose, blood C& S ± LP ABG .
Radiology/ lmaging
.
• CXR (inspiratory, expiratory, lateral) , echo ( structural heart disease) EKG
Special Tests
• Tracheal secretions, hyperoxia test ( Pa02 < 150 mmHg on 100% Fi02 suggests cyanotic lesion/severe PPHN - only used if Echo not
available)
TREATMENT
Emergent treatment
• Maintain patency of ductus arteriosus with PGE1if suspected duct dependent lesion, 02 to maintain Sp02 > 90% consider .
bronchodilators and nebulized epinephrine, monitor BP and HR to ensure adequate tissue perfusion, vetilation if respiratory failure,
empiric antibiotics if suspecting sepsis
Treatment options ( see tables on previous page)
Referrals
• . .
Pediatrics Pediatric Cardiology, Respirology, Surgery NICU/PICU as required
DIFFERENTIAL DIAGNOSIS
Traumatic Causes Medical Causes
Accidental Injury Coagulation Disorders
Inflicted injury/child
abuse* Infectious Meningococcemia'/septic shock
Immune Inflammatory/
Henoch - Schonlein purpura (HSP) .
Other Causes
Acquired Thrombocytopenia Autoimmune
Gardner - Diamond syndrome .
Hemolytic Uremic syndrome (HUS)
(ITP)
Mongolian blue spots
Malignancy .
Leukemia * Neuroblastoma *
or slate - grey nevi Severe Systemic Disseminated Intravascular
Hemangiomas
Illness Coagulopathy (DIC) *
Von Willebrand’s
Skin staining from dyes disease
or other discolourations
Hemophilia A
Striae
Eczema
Inherited ( Factor VI11 deficiency ) Nutritional
Deficiencies .
Vitamin K Vitamin C
Hemophilia B
Cultural practices such (Factor IX deficiency)
as coining or cupping Platelet Abnormalities
CC • Bruising
PSHX • Prior surgeries and any complications such as prolonged bleeding or requiring transfusions
MEDS .
• Prescriptions OTC, vitamins, complimentary and alternative medicines
ALLERGIES • Medication, food, environmental
PHYSICAL
General Approach
. . . . . .
• ABCs, VS ( BP HR RR T Sp02) general appearance LOC /vigor
Oropharynx
• Signs of bleeding, trauma
Skin
• Entire skin surgface should be examined, with special attention to the neck, trunk, buttocks, genitalia, anterior and posterior pinnae,
and feet. Recognize life threatening conditions such as meningococcemia.
Minor Accidental Injury Inflicted Injury
• Relatively small, oval /round in shape with nondistinct borders • Bruises in babies not cruising
Above or near bony prominences on front of body (forehead, • Bruises on ears, neck, feet , buttocks, or torso ( torso includes
knees, shins) chest, back, abdomen, genitalia, posterior surfaces) - not on
• Recognizable shape or pattern front of body or overlying bone
• Bruises that do not fit the causal mechanism described,
unusually large or numerous
• Patterned, bilateral, or clustered bruises; may include
handprints, loop or belt marks, bite marks
MSK
• Bony deformities, joint hypermobility, fractures
Abdomen
• Hepatosplenomegaly
NEURO
. .
• Meningismus CNs strength, sensation, reflexes, focal neurological signs
Cardiac and respiratory
• Routine exam
INVESTIGATIONS
Only required if history not consistent with accidental trauma
T7
If the DDx includes inflicted trauma, malignancy, or infection, the following investigations should be strongly considered: ro
Q .
Blood Work ( to rule out medical causes) CL)
• CBCD (blood culture if febrile), peripheral blood smear, INR / PTT
UREATMENT
Emergent
• ABCs, IV fluids, transfuse if continued bleeding or hemodynamically unstable
Referrals
• Hematology if suspecting coagulation disorder
• Oncology if suspecting malignancy
• Ensure the child’s safety if inflicted injury is strongly suspected, involve Child Protective Services
HISTORY
V)
u ID • Name, age, gender, ethnicity, home
351 .
Edmonton Manual ot CommonClinical Scen n
PHYSICAL
General Approach
. . .
• ABCs Vitals ( BP HR. RR Sp02 Temp) .
• Increased thirst, irritability, lethargy, pallor, jaundice
HEENT
• Dry mucuous membranes, decrease in tear production, sunken fontanelles in newborns, sunken eyes, lymphadenopathy fruity odor .
in breath (diabetic ketoacidosis)
ABDO
• Abdominal distension, blood/mucous in stool, abdominal tenderness, olive -sized mass in RUQ (pyloric stenosis), hepatomegaly
RESP
• Deep respirations, cyanosis, adventitious sounds
GU
• Decreased urine output, flank pain, ambiguous genitalia in females (congenital adrenal hyperplasia)
CVS
• Delayed capillary refill time ( > 3 sec), weak or absent peripheral! pulses
DERM
• Increased skin turgor, rash (viral, meningococcal), burns
INVESTIGATIONS
Blood Work
• Unnecessary for mild to moderate dehydration
• . . . .
Serum electrolytes BUN creatinine, urinalysis, blood gas lactate, glucose CRP/albumin (autoimmune conditions), plasma and
urine osmolality ( diabetes insipidus)
• If dysnatremic: urine sodium and creatinine, urine specific gravity, blood sodium and creatinine
• Septic workup (CBCd, blood culture, urine culture) +/- CSF if child appears toxic or is a neonate
.
• Stool culture and sensitivity Clostridium difficile (C. diff ) toxin if bloody stools or recent antibiotic use/ hospital stay.(not
recommended in children < 12months)
Imaging
• Not routinely ordered
• Abdominal X- ray (e.g. ileus, obstruction, toxic megacolon)
• Ultrasound (e.g. pyloric stenosis, renal anomalies)
L REATMENT
Emergent Management (Severe Dehydration)
• Restore intravascular volume
1. Normal Saline 20ml /kg over 20 minutes Q .
2. Repeat as needed
3. If vital signs and end organ perfusion fails to respond after a total of 60ml/kg, start colloid solutions “T
o
• Consider packed red blood cells in cases of blood loss
• Sample calculation for a patient who weighs 10kg and was 5% dry and got a 20ml/kg bolus
1.Calculate a deficit : 10kg x 0.65 L/kg x 0.05 = (Total body water ) x (0.05) = deficit
2.Calculate ongoing needs using maintenance: (4- 2-1) 4ml/ kg/ hr x 10kg x 24hr = needs
3.Substract volume which has already been administered: 20ml / kg x 10kg = already adminstered bolus
4.Fluids to be administered over 24hr: deficit + needs - bolus = 325 ml + 960ml - 200ml = 1085 ml
• Note: the above calculations and principles of fluid replacement apply only to isotonic dehydration
Etiology - Specific Considerations
. .
• Sepsis UTI, bacterial gastroenteritis C. difficile = antibiotics
• Toxins = remove offending agents
• Congenital heart disease, pyloric stenosis = surgical repair
• Congenital adrenal hyperplasia = hydrocortisone and fludrocortisone
• Food protein induced enterocolitis = remove offending protein (commonly cow' s milk protein)
• Diabetic ketoacidosis = insulin, glucose, slow rehydration, monitor for cerebral edema
.
• Diabetes insipidus = low solute diet, desmopressin, investigate the cause (central vs nephrogenic)
Definition
• Shock: inadequate oxygen/nutrient delivery to meet metabolic demands
> Pediatric response to hypovolemia: hypotension is a late finding and quickly progresses to cardiovascular collapse
> Infants may become bradycardic rather than tachycardic
Common Conditions
• . .
Status epilepticus, status asthmaticus, croup, bronchiolitis, DKA trauma FB aspiration, sepsis /systemic inflammatory response
syndrome, meningitis, hypovolemia
High Mortality/Morbidity
• Trauma, bacteremia, respiratory distress, burns, head injuries, submersion, poisoning, anaphylaxis
• Suspected physical abuse
> Abusive head trauma (shaken baby syndrome): subdural hemorrhage, retinal hemorrhage, posterior rib fractures, metaphyseal
fractures
> Burns: glove and stocking distribution
» Bruises: inaccessible locations, patterned
> Any presentation inconsistent with developmental capabilities or history
HISTORY
ID • Name . age. gender, ethnicity, home
CC • Trauma, altered LOC . respiratory distress
HPI • Signs and symptoms. Allergies. Medications. Past medical Hx. Last meal, Events leading up to.
(SAMPLE) Interventions en-route
IMMUNE • Routine IUTD. special
FHX • Pertinent FHx and sick contacts
RED FLAGS • Patient brought in by EMS, unresponsive, altered mental status, unstable vital signs
“a
> Approach to airway management : suction, reposition NPA/ _ 0-3 m 85-160 60- 90
. 40- 50 2.0 mL/kg/h
<U
CL
OPA, dislodge FB ( <1y/o-back slaps /chest thrusts >1y/o- . 3 m- 2 y 100- 160 75 - 105 24-40 1.5 mL/ kg/h
abdo thrusts), intubation with laryngeal mask airway ( LMA) or
2- 10 y 60- 120 85 - 112 12- 30 1.0 mL/ kg/h
endotracheal tube (ETT)
.
• Breathing: rate, rhythm 02 saturation, effort, skin color > 10 y 60- 100 97- 112 12- 20 0.5 mL/kg/h
> Approach to breathing management: 02 ventilation .
• Circulation: assess pulses, blood pressure, skin color /temperature, Pediatric Airway Management Considerations
capillary refill, mental status
Estimation of ETT Size Anatomic Differences
> Follow pediatric advanced life support algorithms for septic shock,
tachycardia, bradycardia, or pulseless arrest ( may involve chest
(l10 y)
• Uncuffed = age/ 4 + 4
- ( from Adult Airway )
• Narrow nasal passages
compression, defibrillation, resuscitation drugs)
> Establish vascular access ( peripheral, central, intraosseous) • Cuffed = age/ 3 + 4 • Large occiput, large tongue
.
> Draw blood for CBC electrolytes, calcium, blood glucose, ABG/ • Emergency drugs
that can be given
• Superior larynx at C 3 (C 4/ 5
in adults)
VBG (lactate, mixed venous 02 sats)
> Volume resuscitation: 20 ml/kg 0.9%NaCI or RL no maximum
(
by ETT: lidocaine
epinephrine,
.
• Narrowest at subglottic area
(narrowest at vocal cords in
volume), consider pRBCs if not responding atropine, naloxone, adults)
• Continue post -resuscitation monitoring: cardiac monitor . salbutamol • Anteriorly slanted cords
.
VS q5 - 15 min volume status, urine output (perpendicular to trachea in
• Disability: assess LOC, (GCS/AVPU scales), pupil size/reactivity, adults)
movement of extremities
• Exposure: undress patient, log roll, palpate spine /extremities for
deformities/pain, DRE, warming measures
• Empiric: broad - spectrum ABTx ( < 1hr ideal, sooner is better )
if suspect septic shock
INVESTIGATIONS
Blood Work
•Blood work depending on presentation; may include full septic workup ( blood and urine cultures, do not LP if unstable), liver and
. . .
kidney function VBG, lactate, INR, PTT T&S crossmatch
Radiology/ lmaging dependent on presentation
Special Tests as indicated by Hx and PE
• Lumbar puncture as part of septic workup
• EEG and anticonvulsant levels
• Toxicologic and metabolic workup
UREATMENT
MENINGITIS STATUS EPILEPTICUS SICKLE CELL DISEASE STATUS ASTHMATICUS
• Bacterial meningitis: • Maintain patent UAW • Pain management for vaso - • Inhaled short acting p-agonist:
• Neonatal: ampicillin .
(suction/position) 02 occlusive crisis (morphine) nebulized salbutamol 0.1 mg/ kg x 3
+ gentamycin/ • Anti -epileptic drugs • Fluid bolus followed by 1.5 x • Inhaled short acting anticholinergic:
cefotaxime ± acyclovir ( AED): maintenance nebulized ipratropium bromide
• 1- 3 mos: ampicillin • Lorazepam 0.1 mg/ kg • If febrile, empiric IV ABTx 250 meg x 3
+ cefotaxime ± IV/SL/ PR q5 min (ceftriaxone ± vancomycin if • Systemic corticosteroids:
• Do not agitate or attempt 100 mg/m 2/d divided • Nebulized L- epinephrine 5 mL • Bronchodilators: salbutamol if
to secure an airway on 4 -6 h 1:1000 ( 5 mg) q 20- 30 min PRN bronchospasm
your own • Intubation as last resort • Antihistamines: diphenhydramine
• 02 by mask if tolerated ( smaller tube than estimated 1- 2 mg/kg IV
• Cefuroxime x 10 days based on size) • Ranitidine 2 - 6 mg/ kg/d IV q6-12 h
( 2nd/ 3rd generation • If bacterial tracheitis: 3rd • Corticosteroids: hydrocortisone
.
cephalosporin GAS and generation cephalosporin + 5 - 10 mg/ kg IVq4 - 6h
S. aureus are now more vancomycin
• Observe vs. admit depending on
common than Hib) severity
DIFFERENTIAL DIAGNOSIS
Vomiting in the Newborn Period
• Esophageal atresia + TE fistula: excess salivation, regurgitation, respiratory distress, failure to pass NG/OG tube, VACTERL defects
• Pyloric stenosis: 3 wks - 3 mos: 3 Ps-non - bilious projectile emesis, visible gastric peristalsis, palpable olive-shaped mass
• Duodenal atresia: bilious emesis ( 80%), scaphoid abdomen, high association with Down syndrome, polyhydramnios,
“ double - bubble" on AXR
• Jejunoileal atresia: polyhydramnios, bilious emesis, jaundice, abdominal distension, failure to pass meconium
• Meconium ileus: clear then bilious emesis, abdominal distension, visible and palpable loops of bowel, failure to pass meconium,
associated with CF
• Malrotation with midgut volvulus: bilious emesis, abdominal distension (late), bloody emesis/diarrhea/signs of shock if bowel
compromised. Child often looks completely well early in disease.
• Colonic atresia: marked abdominal distension, respiratory distress, failure to pass meconium
• Hirschsprung's disease: failure to pass meconium, abdominal distension, feeding intolerance, non- bilious followed by bilious emesis
• Meconium plug syndrome: delayed passage of meconium, transient
• Imperforate anus: may be high (no opening on perineum) or low ( fistula opening on perineum but in abnormal position)
• Necrotizing enterocolitis: disease of prematurity, feeding intolerance, emesis, temperature instability, bloody stools, abdominal
distension, abdominal wall edema /discoloration, hemodynamic changes ( late), pneumatosis and /or pneumoperiteoneum on AXR
Vomiting after the Newborn Period
• Overfeeding
• GERD: non- bilious vomiting soon after feeding, water brash, FTT, feeding intolerance, respiratory symptoms ( asthma, with atypical
symptoms), ALTE
• Infectious Gl: gastroenteritis, appendicitis, hepatitis, cholecystitis
-
• Infectious non GI: meningitis, otitis media, pneumonia, UTI, pyelonephritis RULE OUT OBSTRUCTION
• Intussusception: emesis, paroxysms of abdomindal pain with leg raising, " red currant 1. Maternal polyhydramnios
jelly" stool, palpable abdominal mass, lethargy 2. Bilious emesis
• Incarcerated hernia 3. Abdominal distension
• Malrotation with midgut volvulus: bilious emesis, abdominal distension, bloody 4. Failure to pass meconium
emesis/diarrhea/signs of shock if bowel ischemia
• Ingestion: poisons, drugs, toxins, food allergy FB.
• CN: increased ICP, migraine
• Psychogenic: anorexia /bulimia
V) • Inborn errors of metabolism
u
HISTORY
T3
<D
.
ID • Name, age gender, ethnicity
Q. .
CC • Vomiting FTT, irritability
HPI • Emesis: onset, course, duration, quantity, quality/color (bilious vs non -bilious, bloody vs non-bloody)
• Regurgitation, choking, or excess salivation
• Abdominal pain/distension, obstipation/constipation, diarrhea, blood in stool
• Lethargy, number of wet diapers
• Recent ingestion: FB, poisons, toxins, drugs
RED FLAGS • Bilious emesis ( Rule out malrotation/volvulus), bloody stools ( Rule out ischemia/necrosis)
• Lethargy, inconsolability, fever
.
ROS • General: energy, irritability, fever Wt loss
• HEENT: focal neurological deficits, headache, neck stiffness, photophobia, change in mentation
• RESP: cough, wheeze, SOB
• GU: suprapubic/flank pain, irritative urinary symptom, decreased U/O
.
• Nutrition: breast / formula fed frequency/volume of feeds
General Approach
• . .
ABCs and VS ( BP HR RR, T, Sp02)
• Growth parameters (HC, Ht Wt) .
• General appearance: toxic, hydration status, irritability, lethargy
HEENT
.
• CN papilledema, photophobia, TMs, oropharynx
• Anterior fontanelle, lymphadenopathy, nuchal rigidity
CVS/ RESP
• Increased SOB . .
decreased AE adventitious sounds (crackles, wheeze)
• Tachycardia, murmurs
• Central and peripheral pulses, capillary refill, skin turgor
ABD/GU
• Scars, distension, scaphoid abdomen, hernias, visible gastric peristalsis (pyloric stenosis)
• Bowel sounds
• Soft / firm, peritonitis, guarding, rebound, palpable mass, palpable hernia, organomegaly, percussion tenderness, CVA tenderness
• Anal opening, rectal tone ( spastic in Hirschsprung’s) , blood/stool in rectum
Special Tests
• Murphy ’s sign, McBumey’s / Psoas /Obturator /Rovsing's sign, Kernig’s / Brudzinski's sign
INVESTIGATIONS
Blood Work: CBC-D, electrolytes, urea, creatinine, glucose
• If indicated: AST . ALT. ALR bilirubin (direct and indirect ), lipase, CRP. lactate
Radiology/ lmaging
• .
AXR ( 3 views): dilated loops of bowel, air - fluid levels, free air double bubble sign (duodenal atresia), soap bubble appearance
(meconium ileus), absence of gas, coiled nasogastric tube ( EA)
“0
-
• Abdominal U/S: pi sign 3 mm thick and 14 mm long pylorus (pyloric stenosis), target sign (intussusception) fl>
• UGI barium: intestinal atresias, malrotation Q .
• Barium enema: microcolon (atresia), inspissated plug (meconium ileus) , transition point of colon ( Hirschsprung’ s)
• Air enema: intussusception —
o)•
V
»
L REATMENT
Emergent
• .
ABCs IV fluids to correct dehydration
Medical
• .
Analgesia (avoid narcotics in neonates due to high risk of apnea), antiemetics ABTx as needed
• NG tube decompression for obstruction/atresia
• PPI for GERD
Surgical/Procedural
• Malrotation: emergent laparotomy + Ladd’s procedure (surgical emergency!)
• Intussusception: air /contrast enema with emergent laparotomy if not successful
• Pyloric stenosis: Pyloromyotomy (after rehydration and correction of electrolyte abnormalities)
• Meconium ileus: gastrograffin enema + Mucomyst via nastogastric tube
• Hirschsprung' s: endorectal pull-through +/- leveling colostomy (depends upon ability to decompress from below)
Referrals
• Pediatric General Surgery, Gastroenterology as required
Diagnostic Criteria
• Seizure: abnormal electrical activity in the brain, which may cause a change in motor activity and/or behavior
• Epilepsy: two or more unprovoked seizures
• Status epilepticus: continuous or intermittent seizure activity for > 5 minutes without regaining consciousness
> Give fosphenytoin or phenytoin first, then consider phenobarbital if ongoing seizure activity
PMHX • Medical conditions: acquired brain injury, neurological disease, metabolic disease
• Prenatal: prenatal care, U/ S frequency, maternal illness /exposure to toxins (smoking/EtOH/drugs)
.
• Perinatal: GA complications of delivery, birth Wt, APGARs, asphyxia
• Postnatal: neonatal complications . NICU admission, newborn metabolic screen, complications in first month of
life (jaundice,kernicterus)
PSHX • Cranial surgeries
PHYSICAL
General Approach
. .
• ABCs, general appearance (toxic) VS (BP. HR. RR T. Sp02). growth charts (Ht /Wt / HC)
HEENT
• Dysmorphism, microcephaly, tongue -biting, signs of trauma, nuchal rigidity
CVS/RESP
•S1/ S 2, extra heart sounds, arrhythmia, peripheral pulses
•AE, adventitious sounds (crackles, wheeze)
MSK /DERM
• cafe - au -lait spots or port wine stains indicating neurocutaneous disorders, rash ( viral exanthems, purpura)
NEURO
• Meningismus . CNs, strength, sensation reflexes focal neurological signs
, ,
-o
fD
INVESTIGATIONS Q .
Blood Work
• If .
indicated (e.g., V/D dehydration or failure to return to baseline alertness), consider CBC- D, glucose, electrolytes, calcium, 2.
n
. . .
magnesium BUN creatinine. LFTs and metabolic workup to
Imaging
• Recommended for afebrile, first - time seizures, although urgency depends on various factors
> Neonatal, significant head trauma, focal/complex partial, generalized tonic clonic with focal deficits that do not resolve quickly
.
or failure to return to normal consciousness within a few hrs underlying medical condition predisposing to intracranial masses
(e.g., tuberous sclerosis, neurofibromatosis)
> Remember that abusive head trauma rarely has any visible injuries
Special Tests
• EEG to classify seizure type and predict recurrence risk with hyperventilation and photostimulation to induce absence seizure
• Lumbar puncture if CN infection is suspected and child is in stable condition
uREATMENT
Counseling
• First unprovoked seizure with a normal MRI: 30% chance of having recurrent seizure: rarely requires longterm AED
• Reassure parents that children without underlying developmental problems do not seem to have lasting neurologic deficits
following febrile seizures
• Risk of epilepsy after an initial simple febrile seizure is approximately 2%
Referrals
• Urgent Neurology referral if status epilepticus refractory to treatment
• .
Pediatrics Neurology for recurrent seizure
> Warm- fever > 5 days More extensive cases require oral cloxacillin.
TJ
> Conjunctival injection (bilateral) O
> Rash, blotchy erythematous coalescing macular eruption; Scarlet Fever
Q.
a
> Edema or Erythema of hands / feet • Caused by S. pyogenes (GAS) *
> Adenopathy, cervical • Finely punctate erythematous “ sandpaper -like” eruption that n
starts on the upper trunk and progresses downward. Red tn
> Mucous membrane changes, such as red fissured lips
strawberry tongue results from brightly erythematous swollen
and strawberry tongue papillae.
• Immediate IVIG and aspirin; complications include coronary
• Penicillin is ATBx of choice; symptomatic management for
artery aneurysm and death
fever and/or pain
Atopic Dermatitis
Cellulitis
• Condition characterized by dry skin and pruritus . Associated • Caused by S. aureus, GAS, Hib
with asthma and hay fever.
• Ill- defined, warm, tender, erythematous plaques
• Ill-defined, erythematous patches and plaques; with scratching,
lesions become lichenified and often impetiginized • 1st generation cephalosporin is first - line Tx (cefalexin po or
• Treatment includes frequent application of moisturizer, topical
cefazolin IV)
corticosteroids or calcineurin inhibitors, anti - histamines, topical FUNGAL
and systemic ABTx Diaper Dermatitis
• Caused by Candida albicans
Others;Erythema toxicum neonatorum, seborrheic • Brightly erythematous, well - demarcated, eroded plaque with
dermatitis "satellite pustules" in the diaper area of an infant
• Topical antifungal (e.g., nystatin) bid or tid
DEFINITIONS
• Wheeze: continuous high - or low - pitched sound due to intra- thoracic airway narrowing. It can be inspiratory or expiratory but is
usually heard during expiration.
• Stridor: harsh, high-pitched sound due to extra - thoracic airway narrowing. It can be inspiratory or expiratory but it is usually heard
during inspiration.
OMMON CONDITIONS
• Acute wheeze
.
> Infection (e.g. viral bronchiolitis - common in infants)
.
> Mechanical obstruction (e.g. FB aspiration)
Anaphylaxis
>
> Acute asthma exacerbation
• Chronic or recurrent wheeze
.
> Pulmonary disease (e.g. asthma, cystic fibrosis)
> Feeding/swallowing dysfunction (e.g., aspiration GERD) .
HISTORY
ID . .
• Name age gender, ethnicity, home
CC • Wheeze
PMHX • Prenatal: prenatal care . U/S frequency maternal illness/exposure to toxins (smoking/EtOH/drugs)
,
.
• Perinatal: GA complications of delivery, birth Wt . APGARs. asphyxia
• Postnatal: neonatal complications .
NICU admission, respiratory problems or wheezing since birth (suggests
congenital abnormality), newborn metabolic screen
• Medical conditions: asthma, eczema, infections, cystic fibrosis, congenital heart disease, previous admissions or
ED visits for asthma, oral steroid use, Hx of pneumonia or protracted course of viral URTIs
PSHX • Upper respiratory tract or thoracic surgery
MEDS • Prescriptions (response to asthma medications), OTC, vitamins, CAM
RISK • Complicated perinatal health, smoking in the home, low SES . domestic violence, parental mental health
FACTORS
RESP
• Inspection: respiratory distress, central and peripheral cyanosis, clubbing, nasal exam (e.g.. signs of rhinitis, nasal polyps), structural
.
chest abnormalities (e.g. increased A- P diameter )
.
• Palpation: cervical lymphadenopathy subcutaneous emphysema
• Percussion: diaphragm position, differences in resonance among lung regions
• Auscultation: define characteristics and location of wheeze, stridor, crackles, prolonged expiration
CVS
• Inspection: chest wall deformities, surgical scars, visible heaves or thrills
• Palpation: apical impulse (normally located in 4 th- 5 th intercostal space in midclavicular line) impulses, thrills, parasternal heave
• Auscultation: murmurs, extra heart sounds
• Signs of heart failure
DERM
• eczema, urticarial rash
INVESTIGATIONS
Blood Work
.
• Rarely ordered; if relevant, consider CBC- D sputum cultures, immunoglobulin levels
Imaging
• CXR is recommended for the first presentation of wheeze but not always necessary for every incidence afterward, especially for a
typical presentation of asthma or bronchiolitis; for FB aspiration, need both inspiratory and expiratory views
• Barium swallow with VFSS will be helpful when conditions like vascular rings, swallowing dysfunction, and GERD/aspiration are
suspected
Special Tests
• Sweat chloride test if suspect CF
• PFT: to assess presence, degree, and location of airway obstruction in cooperative, older children as well as response to
bronchodilators (impractical in children < 6 yrs old). Methacholine challenge and exercise testing can confirm hyper -reactive
airways.
• Bronchoscopy; to assess patients with suspected FB aspiration, persistent symptoms, or unresponsive to therapy
• Bronchioalveolar lavage (BAL) culture can be used to diagnose atypical pneumonia
UREATMENT
Management “0
.
• Asthma exacerbation: 02, bronchodilators (B 2 - agonist anticholinergics) , corticosteroids (oral /IV), magnesium sulfate
<D
Q .
• Anaphylaxis: epinephrine 0.01 mg/kg IM ( max 0.5 mg/dose), high flow 02, NS bolus, diphenhydramine, ranitidine,
methylprednisolone
• Bronchiolitis: supportive care, maintain oxygenation and hydration +/- nebulized hypertonic saline in those requiring hospitalization 5
• GERD: nonpharmacologic (milk - free diet, thickening feeds, positioning therapy), may consider pharmacotherapy in children >1year
I:OMMON CONDITIONS
"
i
T
ISTORY
ID • Name, age, gender, ethnicity, home
IMMUNE .
• Routine IUTD, special (e.g , RSV Ig); see Immunizations
FHX • Congenital heart disease, autoimmune disorders, bleeding/clotting disorder, congenital anomalies, genetic
syndromes, learning disabilities, perinatal deaths, SIDS, other pertinent familial disease
SOCIAL -
• Primary caregiver, infant parental attachment, parental stress/mood, parental support, family’s financial situation,
siblings, drug plan
• Safety: see counseling topics
• Second - hand smoke, pets
DEVT. HX • Review GM . FM, speech/language, social, and cognitive development
ROS • Fevers, Wt loss or poor gain, jaundice, irritability, fatigue/lethargy, floppy, jittery
• CV: cyanotic spells, puffy eyelids, diaphoresis/dyspnea with feeds
• RESP: distress, tachypnea, stridor, wheeze, cough/coryza
(arches back, irritable) aspiration, choking or crying with feeds, vomiting (projectile/bilious), blood/
• Gl: reflux
mucus in stool, age at first meconium
RISK • Complicated perinatal health, second-hand smoke, low SES, family conflict /domestic violence, parental mental
FACTORS health
HEAD . .
• Size/shape of skull ( micro/macrocephaly plagiocephaly etc), size/fullness of fontanelles ( anterior and
posterior), dysmorphic facial features, symmetry of head and face, caput succedaneum, cephalohematoma
EYES
• Spontaneous eye opening, red reflex, corneal light .
reflex, cover -uncover test EOM, subconjunctival
hemorrhage, discharge, conjunctival pallor
EARS • Skin tags /pits, pinna shape, proper positioning, tympanic membrane
MOUTH • Hard and soft palate abnormalities ( palpate for cleft palate), tongue and chin size/shape, suck, teeth
NECK • Goiter, cysts, full ROM . neck webbing, assess neck stability for development
CV • Murmurs, extra heart sounds, heaves/thrills, pulses (peripheral, femoral), cap refill
• Symmetry, pectus deformity, cyanosis, gasping/grunting/ wheeze, crackles, paradoxical abdominal
RESP
.
movement, accessory muscle use equal breath sounds bilaterally, adventitious sounds on auscultation
• Distension/ indentation, masses, hepatosplenomegaly, bowel sounds, umbilical cord appearance (granulation
Gl
tissue, bowel tissue), perforate anus
• Presence of normal genitalia, descended testes, penis size, foreskin care, clitoromegaly, urethral opening,
GU
symmetry, masses
• Equal and spontaneous limb movements, hip dysplasia ( Barlow, Ortolani, and Galeazzi test), additional
MSK /DERM limbs/digits, palmar /plantar creases and nail abnormality, presence of lesions /rash on skin, birthmarks
(hemangiomas, port wine stain, Mongolian spots, nevi), spine curvature, dimpling, hair patches
NEURO . .
Moro palmar /plantar grasp, Galant, tonic neck, Babinski), deep
• CNs, tone, primitive reflexes ( suck, root
tendon, superficial reflexes ( abdominal, anal wink )
ICOMMON CONDITIONS
• Developmental delay ( see Developmental Delay )
• Learning disorder /ADHD (see ADHD/ Learning Disorder )
• Asthma
• Eczema
• Sleep issues
• Nutritional issues ( most commonly picky eaters)
HISTORY
ID • Name, age . gender, ethnicity, home
CC • Periodic health exam; other chief complaints
HPI • Discuss specific medical or psychosocial concerns
• Nutrition: Canada' s Food Guide; vegetarian diet, beverages (milk/juices /etc.)
• Sleep: night wakening, naps, snoring, apneas
• Output: void frequency, toilet training, incontinence
FHX • Obesity, asthma, eczema, atopy, chronic medical conditions, psychiatric disorders, pertinent familial disease
in SOCIAL • Primary caregivers, living situation, financial concerns, drug plan, second - hand smoke, pets
u • School/daycare, school performance, bullying, extracurricular activities, socialization)
re • Safety: car seat, bicycle helmet, etc .
T3
Q)
DEVT. HX • Review GM, FM, speech/language, social and cognitive development
CL ROS • Optometry and dental assessment/follow -up
.
• HEENT: vision, hearing, dental problems, frequent infections (pharyngitis AOM, sinusitis)
• CVS/RESP: cyanosis, cough, wheeze, stridor, exercise tolerance, apneas
• Gl: vomiting, regurgitation, reflux, abdominal pain, bowel movements, encopresis
• GU: toilet training, enuresis, precocious puberty
• DERM: eczema, diaper rash
RISK • Second -hand smoke, low SES, family conflict/domestic violence, complicated perinatal course
FACTORS
365 EdmontonManual of C
PHYSICAL
General Approach
• . . .. .
VS (BP HR RR T Sp02) growth charts (Ht/Wt/HC)
•General appearance
. .
• Developmental domains: GM FM social, cognitive, language (observe during Hx and PE)
• Child - caregiver interaction (observe during Hx and PE)
Systems - Based Physical Exam
. . .
• HEENT: eyes ears nose, throat, dentition, tonsils, lymphadenopathy thyroid
• CVS: heart sounds, murmurs, pulses, skin color, temperature
• RESP: equal breath sounds bilaterally, crackles, wheeze
• ABD: appearance, bowel sounds, tenderness, masses, organomegaly
• GU: normal female/male genitalia: descended testicles in males, circumcision
• MSK: bony abnormalities, focal deficits, strengths, coordination, gait, scoliosis screen
• NEURO: tone, CNs, deep tendon reflexes, sensory or motor deficits
• DERM: rashes, birthmarks, abnormal skin findings
[COMMON CONDITIONS
•
.
• Pregnancy STIs (chlamydia, gonorrhea, syphilis, etc )
Substance abuse ( tobacco, alcohol, marijuana, illicit drugs)
• Mood disorders ( anxiety, depression, etc.)
.
Current Editor: Helena Liu
-
I
—
Disturbance does not occur exclusively
V
during episodes of anorexia nervosa
Subtypes Restricting or binging/purging Purging or non- purging
I II II I i
^
Confidentiality statement: everything discussed will be remain confidential except SI HI and abuse . .
ID • Name age. . gender ethnicity home
, ,
CC • Periodic health exam: other chief complaints
HPI • Discuss specific medical or psychosocial concerns
RED FLAGS • Homelessness, absence from or failure in school, abnormal eating behaviors, distorted body image, depression,
i/ )
substance abuse, risky sexual behavior, self harm, safety ( SI abuse).
u
PMHX • Medical: chronic medical conditions, other medical concerns
n • Prenatal/perinatal/postnatal
u PSHX • Prior surgeries and complications
0)
CL
MEDS • Prescriptions (oral contraceptive pill) . OTC. vitamins, CAM
ALLERGIES • Medication, food, environmental
367
PHYSICAL
General Approach
• VS ( BP . HR. RR. T. Sp02). growth charts (Ht/Wt/HC)
Systems- Based Physical Exam
. .
• HEENT: eyes ears nose, throat, TANNER STAGING
lymphadenopathy, thyroid FEMALE MALE/FEMALE MALE
• CV: heart sounds, murmurs, pulses,
STAGE
BREAST PUBIC HAIR GENITALIA
skin color, temperature 1 Pre -pubertal Pre - pubertal Pre -pubertal
• Breasts: Tanner staging in females
Sparse hair along base of
• RESP: breath sounds bilaterally, 2 Breast bud Scrotal/testes enlargement
penis/labia
crackles, wheeze
• ABD: appearance, bowel sounds,
3 Bud enlarges Hair over pubis |in length of penis
tenderness, masses, organomegaly Areola + papilla Further|in length and
4 Coarse adult hair
• GU: Tanner staging in males and female:
Secondary mound breadth of penis
• NEURO: CNs, deep tendon reflexes, Areola recedes
sensory or motor deficits 5 Adult size and Extends to medial thigh Adult size and shape
shape
• DERM: rashes, birthmarks, abnormal
skin findings
CRAFFT Substance Abuse Screening Test for Adolescents
C Have you ever ridden in a car driven by someone (including yourself) who was “high” or had been using alcohol or drugs?
R Do you ever use alcohol or drugs to relax, feel better about yourself, or fit in?
A Do you ever use alcohol or drugs while you are by yourself, alone?
F Do you ever forget things you did while using alcohol or drugs?
F Do your family or friends ever tell you that you should cut down on your drinking or drug use ?
T Have you ever gotten into trouble while you were using alcohol or drugs?
*A CRAFFT score of 2 or higher was optimal for identifying substance abuse problems, disorders, and dependence.
Definitions
• -
Speech The articulation of speech sounds, fluency, and/or voice
Articulation - Pronunciation of speech sounds
>
> Fluency - Flow and pattern of speaking
> Voice - Production of sound including vocal quality, pitch, loudness, resonance and duration
> Phonology - Knowledge of speech sounds and their rules
• Language - Comprehension and use of spoken, written, and/or other communication systems
DIFFERENTIAL DIAGNOSIS
Speech Disorders
• Articulation Disorders - Incorrect production of speech sounds
Hearing impairment
>
Dysarthria - e.g., stroke, brain tumor, cerebral palsy
>
> Apraxia
.
> Structural defects - e.g. cleft lip and palate, ankyloglossia
> Lisp
• Fluency Disorders - Disrupted flow of speech
> Stuttering
• Voice Disorders - Abnormal sound production
.
> Hoarseness - e.g. vocal cord nodules, laryngitis
> Hypernasality - e.g., velopharyngeal insufficiency
.
> Hyponasality - e.g. enlarged adenoids, nasal polyps
• Phonological Disorders
HISTORY
ID • Name age . . gender, ethnicity, home
CC • Teacher /caregiver concern: speech delay, poor social skills
HPI • Speech: articulation, fluency, voice, phonology, intelligibility
-
• Language: receptive +/ expressive
• Onset: when/how it was noticed and by whom, multiple settings
• Difficulty hearing: responds to sounds, recurrent AOM/OME
.
• School Hx: academic performance, hyperactivity, impulsivity homework, psychoeducational tests
-
• Social Settings: age appropriate interactions, teasing/ bullying by peers
• Autism Spectrum Disorder features: poor social communication, restricted/repetitive interests
PMHX • Prenatal: prenatal care . U/S results, maternal illness, drug/EtOH exposure
• Perinatal: GA, complications of delivery, birth Wt, APGAR scores, asphyxia
• Postnatal: neonatal complications, NICU admission, length of stay, newborn metabolic screen
.
• Head trauma, chronic illness AOM/OME, cleft palate, ankyloglossia, child abuse/neglect, meningitis, seizures
SOCIAL • Family unit, SES, health insurance, languages spoken at home, parental education/employment
• Child abuse/neglect
DEVT. HX • See Developmental Delay chapter
PHYSICAL
• Growth charts (Ht /Wt /HC)
• GENERAL
Wellbeing
>
Behavior: alertness, attention span, impulsiveness, attentiveness, hand - wringing, hand- flapping
>
> Social Interaction: eye contact, speech/language, play
> Dysmorphic features
> Signs of abuse/neglect
.
• HEENT: TM (evidence of OME), shape of pinna, pre - auricular cysts/tags / fissures oropharynx (ankyloglossia, cleft lip/palate,
tonsils)
• NEURO: CNs, strength, muscle tone, reflexes, coordination, gait, limb movements
INVESTIGATIONS
Adjunctive Clinical Assessments
“0
• Audiology o
• Formal developmental screening: ASQ or PEDS, M-CHAT for Autism Spectrum Disorder Q.
Multidisciplinary Services
. . .
• If clinically indicated (e.g., Audiology Speech Language Pathology Educational support Psychology)
Referrals
• If clinically indicated (developmental pediatrics for complex developmental problems, ENT for articulation/resonance problems)
Follow-up
• Regular appointment with pediatrician or family physician to monitor progress and growth
Definitions
• Wheeze: continuous high - or low -pitched sound due to intra-thoracic airway narrowing. It can be inspiratory or expiratory but is
usually heard during expiration.
• Stridor: harsh, high -pitched sound due to extra - thoracic airway narrowing. It can be inspiratory or expiratory but it is usually heard
during inspiration.
Common Conditions
• Laryngomalacia: most common cause of .
chronic stridor, infants (onset at 1 wk to 3 mos) constant/intermittent, worse when supine
• Croup: most common cause of acute stridor, barky cough, hoarse voice, 1- 3 day viral prodrome, usually clinical Dx
.
• FB: often clear Hx of choking, cyanosis, wheezing; CXR may show radio - opaque FB expiration views may show hyperinflated
section of lung distal to FB
• Laryngotracheal FB (LTFB): often severe, acute, drooling, dysphagia. If suspected, only minimal manipulation of patient with
immediate ENT referral for removal with rigid bronchoscopy.
High Morbidity/Mortality
• Epiglottitis: acutely toxic, high fever, drooling, dysphagia, muffled voice, tripod position
• Bacterial tracheitis: like severe croup, but toxic appearing, higher fever, deteriorate despite therapy for presumed croup
. .
• Anaphylaxis: usually systemic symptoms (urticaria /itching N/V) along with appropriate Hx
Emergent Treatment
.
• If patient is unstable, in respiratory failure, or severely obstructed ABCs and call ENT/Anesthesia STAT
• Airway: comfortable position (head tilt - chin lift / jaw thrust) , remove visible FB. intubate if in respiratory failure
.
• Breathing: assist ventilation, high - flow 02 monitor pulse oximetry, rate, rhythm, respiratory effort
• Circulation: monitor HR /rhythm, vascular access as needed ( avoid agitation if possible)
HISTORY
ID • Name . age. gender, ethnicity, home
CC • Stridor
HPI -
• Onset: age ( first wks of life suggests congenital, 6 mos 3 yrs high risk for FB)
• Progression: sudden onset (FB, anaphylaxis), insidious/slow progression (croup), recurrent/chronic (vocal cord
dysfunction, compression with rings, tumors, stenosis, etc ) .
• Provoking: sleep (pharyngeal obstruction), exercise/wakefulness (LTFB), feeding (reflux/aspiration)
• Quality: describe sound (inspiratory/expiratory/biphasic . high pitched, musical)
• Severity: cyanosis, respiratory distress, gasping, ill/toxic, lethargic, altered mental status
a • Timing: recent allergic exposures, FB in mouth/choking episodes, URTI prodrome
• Assoc, symptoms: fever, URTI symptom (cough, coryza, red eyes), voice change, drooling, dysphagia, nasal
T3 regurgitation/coughing with feeds, allergic symptom (urticaria, itching, N/V, flushing, facial swelling), reflux
V
Q. RED FLAGS • Drooling, increased respiratory effort, tripod posture, cyanosis
PMHX .
• Antenatal: prenatal care U/S, medication exposure, maternal infection (TORCH), complications
• Perinatal: gestation, route and complications of delivery, APGARs, resuscitation (intubation/ventilation), birth
Wt, cyanosis/distress, congenital anomalies (nasal patency, macroglossia, micrognathia, etc ) .
• Previous intubations, admissions for respiratory distress, episodes of stridor
• Recurrent / frequent infections, cardiac, respiratory, neurologic, metabolic, genetic disease
• Caustic ingestion, inhalation injury, facial/neck trauma, burns
SOCIAL • Smoke exposure, home and environmental allergen exposures, sick contacts
RISK FACTORS • Previous intubations or hospitalizations, allergies, immunocompromised state, craniofacial malformations
371
PHYSICAL
General Approach
• General appearance (toxic, tripoding), VS ( BP . HR. RR. T. Sp02), growth charts (Ht/Wt/HC)
HEENT
• Upper airway patency: stridor, drooling, cough, ability to speak full sentences
• Surgical scars, neck bruising/edema, hemangioma /neurofibroma, tongue/mandible size /position, refusal of neck movement
( retropharyngeal abscess ( RPA)), tonsillar hypertrophy, peritonsillar mass/trismus (peritonsillar abscess, PTA ) , visible blood/
secretions
• Palpation: cervical lymphadenopathy, tracheal tenderness
RESP
.
• Respiratory distress: nasal flaring, retractions, tracheal tug accessory muscle use, tripod posture, paradoxical breathing (older
children)
• Respiratory failure: cyanosis, obtunded, decreased chest wall movement, bradypnea or extreme tachypnea
•Percussion: lung fields for dullness, asymmetry, respiratory excursion
• Palpation: chest expansion bilaterally, tactile fremitus, subcutaneous emphysema
.
• Auscultation: inspiratory, expiratory or biphasic stridor, audible crackles or wheeze AE bilaterally. Listen over mouth/neck for
snoring/ low -pitched sounds, barky cough.
INVESTIGATIONS
Blood Work
• CBC- D, blood /throat cultures if suspected bacterial source (epiglottitis, retropharyngeal/peritonsillar abscess), VBG
• Do not attempt throat exam/throat swab with a tenuous airway
Radiology/ lmaging
• Inspiratory/expiratory CXR if suspect FB aspiration
Special Tests
• Culture of tracheal secretions
• Lateral decubitis simulates expiratory film if young/uncooperative
L REATMENT
• Intubation if unstable/impending respiratory failure "D
to
• Medical CL
. .
Croup: supportive 02/cool mist PO dexamethasone nebulized epinephrine
.
Bacterial tracheitis/epiglottitis/RPA/ PTA: IV ABTx drain abscess, supportive
n
Monitor child with laryngomalacia, usually improves without intervention VI
• Surgical
.
fdmonton Manual of CommonClinic il Scenarios 372
STATION CONTRIBUTORS
Abnormal Sexual Maturity Chris Gerdung MD. Gary Galante MD, Melanie Lewis BN MEd MD FRCPC
Abnormal Stature Chris Gerdung MD. Gary Galante MD. Melanie Lewis BN MEd MD FRCPC
ADHD/Learning Disorders Peter Gill PhD. Gary Galante MD. Melanie Lewis BN MEd MD FRCPC
Anemia (Pediatric) Peter Gill PhD. Gary Galante MD. Melanie Lewis BN MEd MD FRCPC
Childhood Communicable Diseases Peter Gill PhD. Gary Galante MD. Melanie Lewis BN MEd MD FRCPC
Depressed Newborn Peter Gill PhD. Gary Galante MD. Melanie Lewis BN MEd MD FRCPC
Developmental Delay Peter Gill PhD, Gary Galante MD. Melanie Lewis BN MEd MD FRCPC
Down Syndrome Peter Gill PhD. Gary Galante MD. Melanie Lewis BN MEd MD FRCPC
Ear Pain Chris Gerdung MD. Gary Galante MD. Melanie Lewis BN MEd MD FRCPC
Enuresis Chris Novak BSc MD. Darcie Kiddoo MD FRCSC
Failure to Thrive Lauren Kitney MD. Gary Galante MD. Melanie Lewis BN MEd MD FRCPC
Fever Without a Source in a Child < 3mo Peter Gill PhD. Gary Galante MD. Melanie Lewis BN MEd MD FRCPC. Lundy McKibbin
Heart Murmurs Emma Heydari MD. Melanie Lewis BN MEd MD FRCPC
Limping Child Michelle Ruhl MD. Peter Gill PhD. Chantelle Champagne MD. Gary Galante MD. Melanie Lewis BN MEd MD FRCPC
Pediatric Nausea and Vomiting Lillian Du MD. Allison Hobbs MD. Bryan J Dicken MD FRCSC FAAP
Pediatric Wheeze Christina Vang MD. Mark Enarson MD FRCPC
Newborn Jaundice Lauren Kitney MD. Gary Galante MD. Melanie Lewis BN MEd MD FRCPC
Newborn Respiratory Distress/Cyanosis Chris Gerdung MD. Gary Galante MD. Melanie Lewis BN MEd MD FRCPC
Pediatric Nausea and Vomiting Ashlee Yang. Melanie Lewis BN MEd MD FRCPC
Pediatric Dehydration Nikytha Anthony BHSc. Jessica Foulds MD FRCPC
Pediatric Emergency Lauren Kitney MD. Gary Galante MD. Melanie Lewis BN MEd MD FRCPC
Pediatric Seizure Christina Yang MD. Mark Enarson MD FRCPC
Pediatric Rash Russell Wong MD. Tiffany Kwok MD. Loretta Fiorillo MD FRCPC
Periodic Health Exam of a Newborn Helena Liu MD. Chris Gerdung MD. Gary Galante MD. Melanie Lewis BN MEd MD FRCPC
Periodic Health Exam of a Toddler /Child Helena Liu MD. Lauren Kitney MD. Gary Galante MD. Melanie Lewis BN MEd MD FRCPC
Periodic Health Exam of a Adolescents Lauren Kitney MD. Gary Galante MD. Melanie Lewis BN MEd MD FRCPC
V)
Speech & Language Abnormalities Peter Gill PhD. Gary Galante MD. Melanie Lewis BN MEd MD FRCPC
u Stridor Lauren Kitney MD. Gary Galante MD. Melanie Lewis BN MEd MD FRCPC
as
-a<
D
CL
373
Abnormal Sexual Maturity
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Bramswig J Dubbers A. Disorders of pubertal development. Continuing Medical Education. 2009;106( 17):295 - 304 .
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Nebesio T Eugster E. Current concepts in normal and abnormal puberty. Current Problems in Pediatric and Adolescent Health Care. 2007;37 { 2):53 - 72.
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Traggai C Stanhope R. Delayed puberty. Best Practice & Research Clinical Endocrinology & Metabolism. 2002:16( 1):139- 151.
Crowley WF Pitteloud N. Diagnosis and treatment of delayed puberty. In UpToDate, Basow DS. ed. UpToDate: Waltham MA; 2012. .
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Saenger P. Definition, etiology, and evaluation of precocious puberty. In UpToDate. Basow DS ed. UpToDate: Waltham MA: 2012.
Abnormal Stature
Nwosu BU. Lee MM. Evaluation of short and tall stature in children. American Family Physician . 2008:78( 5 ):597- 604.
Rogol AD. Diagnostic approach to short stature. In UpToDate. Basow DS. ed. UpToDate: Waltham. MA; 2012.
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Richmond EJ. Rogol AD. The child with tall stature or abnormally rapid growth. In UpToDate. Basow DS ed. UpToDate: Waltham. MA: 2012.
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Rogol AD. Causes of short stature. In UpToDate Basow DS. ed. UpToDate: Waltham. MA; 2014.
Anemia (Pediatric)
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Hay W, Levin M, Sondheimer J Deterding R. Current Diagnosis & Treatment : Pediatrics. 18th cd. New York: McGraw - Hill: 2007 .
. . . .
Pearson H Dallman P. Anemia: Diagnosis anc classification. In Rudolph C Rudolph A. Hostetter M Lister G Siegel N. eds. Rudolph' s Pediatrics. 21st ed. New
York: McGraw -Hill: 2003 .
Childhood Communicable Diseases
Otsu S. Reed Z. Lee CK. Tuan LV. Singh H. Zhou W. A Guide to Clinical Management and Public Health Response for Hand. Foot , and Mouth Disease. World
Health Organization. 2011
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Kleigman RM. Marcdante KJ. Jenson HB Behrman RE. Nelson Essentials of Pediatrics. 5 th cd Philadelphia. Elsevier: 2006.
. . . .
Zorc JJ. Alpern ER. Brown LW Loomes KM Marino BS. Mollen CJ Raffini L J eds. Schwartzs Clinical Handbook of Pediatrics. 4 th cd. Philadelphia: Lipppincott
Williams & Wilkins: 2009.
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Red Book: 2006 Report of the Committee on Infectious Diseases 27th ed. Elk Grove, IL: American Academy of Pediatrics; 2006.
Cheung A. Williams BA. Sivarajan BV, eds. The HSC Handbook of Pediatrics. 10th cd. Philadelphia: Elsevier: 2003.
Depressed Newborn
. .
Kleigman RM Marcdante KJ Jenson HB. Behrman RE. Nelson Essentials of Pediatrics. 5th ed Philadelphia: Elsevier: 2006.
Zorc JJ. Alpern ER. Brown LW. Loomes KM, Marino BS. Mollen C J, Raffini LJ. eds. Schwartz' s Clinical Handbook of Pediatrics. 4 th ed. Philadelphia: Lipppincott
Williams & Wilkins: 2009.
i/> Kattwinkel J. et al. Neonatal resuscitation: 2010 American Heart Association guidelines for ardiopulmonary resuscitation
u
and emergency cardiovascular care. Pediatrics . 2010;126( 5):1400- 1413.
flj
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Cheung A Williams BA. Sivarajan BV. eds. The HSC Handbook of Pediatrics. 10th ed. Philadelphia: Elsevier: 2003.
T3
0) Developmental Delay
Q
- Zorc JJ. Alpern ER. Brown LW. Loomes KM, Marino BS. Mollen CJ. Raffini LJ. eds. Schwartzs Clinical Handbook of Pediatrics . 4 th ed. Philadelphia: Lipppincott
Williams & Wilkins: 2009.
Shevcll M. Global developmental delay and mental retardation or intellectual disability: Conceptualization, evaluation, and etiology. Pediatr Clin N Am.
2008:55( 5):1071- 1084.
Gerber RJ. Wilks T. Erdie - Lalena C. Developmental milestones: Motor development . Pcdiati cs in Review. 2010:31( 7):267 276.
Council on Children With Disabilities. Identifying infants and young children with developmental disorders in the medical home: An algorithm for
developmental surveillance and screening. Pediatrics. 2006:118(l):405- 420.
Down Syndrome
Davidson M. Primary care for children and adolescents with Down syndrome. Pediatric Clinics of North America. 2008:55( 5 ):1099 - 1111.
Edmonton Down Syndrome Society. Clinical guidelines for the down Syndrome population, http:// www.edss.ca/7q = node/ 50
Harrison A. Down Syndrome (pediatrics). ACP PIER & AHFS Dl ® Essentials"* ( Internet ). American College of Physicians: STAT.Ref Online Electronic
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Medical Library ( US); c 2010. Available from; http://online.statref.com.login.ezproxy.library.i. alberta.ca /document.aspx ?fxid - 92&docid 1305
Ear Pain
Forgie S, Zhanel G. Robinson J. Management of acute otitis media. Pacdiatr Child Health. 2009;14( 7):457 - 460.
.
Leung AKC, Fong JHS Leong AG. Otalgia in children. Journal of the National Medical Association. 2000 May:92:254 - 260.
.
Majumdar S. Wu K. Bateman ND Ray J. Diagnosis and management of otalgia in children. Arch. Dis. Child. Ed. Pract . 2009:94:33 - 36.
Failure to Thrive
Cole SZ. Lanham JS. FTT: An update. Am Fam Physician. 2011 April 1; 83( 7):829 - 834.
. .
Hay W Levin M Sondheimer J. Deterding R . Current Diagnosis & Treatment in Pediatrics. 18th ed. New York: McGraw - Hill; 2007.
Vojvodic M. Young A. Toronto Notes (2014). 30th ed. Toronto: Toronto Notes for Medical Students: 2014.
Heart Murmurs
.
Frank J Jacobe K. Evaluation and management of heart murmurs in children. American Family Physician. 2011:84( 7):793 -800.
.
Miyamoto S. Sondheimer H Fagan T. Collins K. Cardiovascular diseases. Current Diagnosis & Treatment : Pediatrics . 20th ed. New York: McGraw -Hill: 2011.
Immunizations
National Advisory Committee on Immunization Canadian Immunization Guide. 7th ed. Tornoto: Public Health Agency of Canada: 2006. Routine immunization
Schedules. Government of Alberta. 2012. http://vvvAv.health.alberta.ca/health- info/imm - routine-schedule.Html
Update on human papillomavirus (HPV ) vaccines. Public Health Agency of Canada. 2012. http://www.phac -aspc.gc.ca/publicat/ccdr - rmtc/ 12vol38/acs-
dcc -l/index -eng.php# a 5
Influenzae Information Package. Alberta Health Services. 2012. http://vAvw.albertahealthservices.ca/ 5664.asp
Limping Child
Kleigman RM. Marcdante KJ. Jenson HB. Behrrnan RE. Nelson Essentials of Pediatrics. 5 th ed. Philadelphia. Elsevier: 2006.
Miall L. Rudolf M. Levene M. Paediatrics At A Glance. 2nd ed. Oxford. New York: Blackwell Publishing: 2007.
Hay WW. Levin MJ. Deterding RR. Abzug MJ. Sondheimer JM. Current Diagnosis & Treatment : Pediatrics. 21st ed. New York: McGraw -Hill: 2012.
Kienstra AJ. Macias CG. Osgood - Schlatter Disease. In UpToDate. Basow DS. ed. UpToDate: Waltham. MA: 2012.
Rosenfeld. SB. Clinical features and diagnosis o* developmental dysplasia of the hip. In UpToDate. Basov/ DS. ed. UpToDate: Waltham. MA; 2012.
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Lehman TJA. Growing pains. In UpToDate Bascw DS ed. UpToDate: Waltham. MA; 2012.
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Yu DT. Reactive arthritis ( formerly Reiter Syndrome). In UpToDate. Basov/ DS ed. UpToDate: Waltham. MA: 2012.
Neonatal Jaundice
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Candian Paediatric Society. Guidelines for detection, management and prevention of hyperbilirubinemia in term and late
preterm newborn infants ( 35 or more wks' gestation). Paediatric Child Health. 2007:12( 5):401- 407 .
.
Wong R Bhutani V. Pathogenesis and etiology of unconjugated hyperbilirubinemia in the newborn. In UpToDate desktop 17.2 2009 . .
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Abrams S Shulman R . Causes of neonatal cholestasis In UpToDate desktop 17.2 2009 . .
Newborn Respiratory Distress/Cyanosis
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Bernstein D. Chapter 430- 431: Cyanotic congenital heart lesions Lesions associated with decreased pulmonary blood flow. Nelson Textbook of Pediatrics.
Philadelphia: Saunders Elsevier: 2007.
Steinhorn RH. Evaluation and management of tie cyanotic neonate. Clinical Pediatric Emergency Medicine. 2008: 9:169 - 175.
Flidel - Rimon O. Shinwell ES. Respiratory distress in the term and near - term infant. NeoReviews. 2005 June;6( 6):289 - 297.
Fernandes CJ. Pulmonary air leak in the newborn [ Internet ). 2014 [ cited 2016. July 23 ]. Available from: www.uptodate.com T>
Martin R. Overview of neonatal respiratory distress: disorders of transition [ Internet ], 2016 [ cited 2016. July 23]. Available from:www.uptodate.com 0>
Eichenwald EC. Overview of cyanosis in the newborn [ Internet ]. 2016 [ cited 2016, July 26 ]. Available from:www.uptodate.com —
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Iserson KV. Chapter 11: Dehydration/Rehydration. In Iserson KV ed. Improvised Medicine: Providing Care in Extreme Environments. New York:
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Fakhoury K. Redding G TePas E. Approach to wheezing in children. UpToDate online versionl8.2: May 2010.
Ralston S, et al. Clinical practice guideline: The diagnosis, management, and prevention of bronchiolitis. Pediatrics. 2014;134( 5):el474-el 502.
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.
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u
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Welcome to the Psychiatry section of the Edmonton Manual. Many of the key elements important to
successful completion of a psychiatry -based OSCE will have already been covered in this manual-
effective communication, patient centeredness, and history - taking. Psychiatry - based OSCE stations
are somewhat unique in that there will be limited opportunity for procedural examination in the form
of a physical exam and, as such, most stations will be focused on history -taking and communication.
Patient presentation may take the form of a specific psychiatric symptom, but most psychiatric OSCE
stations will begin with a non -specific complaint. In the history, it will often become clear that there
is a separate or parallel process that requires a more specific biopsychosocial focus. The focus may be
physical mimics of psychiatric disorders such as weight loss, memory impairment, poor concentration,
perceptual disturbance, or psychosocial issues such as substance use, interpersonal conflict, or poor
social /occupational functioning.
It is important that students have a clear understanding of the formal mental status examination as
this will play a role in most psychiatry - based OSCE stations. A formal mental status assessment not
only includes descriptions of behavior, mood/affect, and thought, but may require a complete Folstein
Mini Mental Status Exam or other such cognitive screening tool. The mental status exam may also be
required in stations that initially appear to be surgery or medicine specific. Safety is a very important
issue to address, both in the form of self - harm and /or harm to others. Harm to self may manifest itself
as lack of capacity to appreciate the danger in refusing medical treatment or discharge from care
prematurely.
Management portions of psychiatric stations should follow a biopsychosocial framework. This will
allow for a clear and concise approach to management that will score you points even if you do not
recall the specifics of treatment. If you are unsure of your answer, be honest.
I hope the following section covering psychiatric OSCE stations will be helpful not only in exam
preparation, but also to remind you of the ubiquitous nature of psychiatric disorders in medicine.
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.
I dmonton Manuil of Common Clinical Scenarios
.
380
MENTAL STATUS EXAM
.
Authors: Muhammed Dhalla MD Jasmine Pawa MD • Current Editor: Mim Fatmi MD
Thoughts
• Thought Form: the fluidity and focus of thought
> Linear: completes a given idea before moving on to the next
Circumstantial: moves on to related topics but eventually returns to original topic
>
Tangential: moves on to related topics but never returns to original topic
>
> Loosening of associations: no logical connection between sequence of thoughts
> Word salad: no logical connection between words TJ
i/>
> Flight of ideas: rapid movement from topic to topic without completing each train of thought (usually manic)
BASICS
Definitions
• Neglect: failure or refusal to Partner Violence Screen ( PVS)
provide basic emotional or
physical needs
.
• Have you been hit kicked, punched, or otherwise hurt by someone in the past year ? If so. by whom?
• Do you feel safe in your current relationship?
• Physical Abuse: physical • Is there a partner from a previous relationship who is making you feel unsafe now?
harm causing pain or injury • > 1positive answer denotes abuse with sensitivity 0.35 -0.71, specificity 0.80 - 0.94
• Emotional/ Psychological
Abuse: includes intimidation,
isolation, manipulation, coercion, or threats
• Sexual Abuse: any nonconsensual sexual contact: age of consent in Canada is 16
• Elder Abuse: physical, emotional, financial, sexual abuse, or neglect of a vulnerable elder by person in trusted relationship
• (Munchausen) Factitious Disorder imposed on another: mentally well caregiver producing/ fabricating symptoms in another under
their care, often their child, with no gains aside from assuming sick role
DDx
• . .
T: depression, anxiety PTSD somatoform disorders, substance abuse, personality disorders, psychosis (paranoid delusions),
dementia, or other cognitive disorders
• Other: accidental trauma, bleeding diathesis, vascular malformations, vasculitis, skeletal pathology, benign dermatological
conditions ( photodermatitis or hypersensitivity reactions), animal bites, chronic pain syndromes
HISTORY
ID • Name, age, sex/gender, ethnicity, occupation or education, source of income, living arrangements, caregivers
CC/HPI • Chiefcomplaint may directly indicate abuse or may present with non-specific unrelated complaints
• PVS: onset, identity of assailant, time and place, description of event, frequency, severity, recent change in
frequency/severity, use of weapon, specific physical injuries
• Vaginal, oral, and/or anal penetration, bath/shower or change of clothing since event, time of last consensual
intercourse
.
• Risk factors: children and elderly, cognitive/physical disability, mental illness, low SES isolation (recent
immigrants or'recently relocated), pregnancy, previous Hx of abuse, caregiver burnout
• Safety: assess basic needs ( food, clothing, safe shelter, medications), feeling unsafe at home/school /work, SI self. -
harm, identify others who may be in danger, abuser’s access to victim or weapons, threats HI .
.
• Substances:EtOH stimulants, nicotine, marijuana, IVDU:evidence of drug- facilitated abuse such as memory loss
or intoxication inconsistent with EtOH consumption; abuser 's use of substances
• Signs and symptoms screen: mood, anxiety, psychosis, feelings of guilt or shame
RED FLAGS • Partner refuses to leave room during interview; partner answers questions for patient; caregivers present
themselves as highly knowledgeable, overly friendly with medical staff
• Delayed presentation, description of injury inconsistent with mechanism
PMHX • Chronic medical conditions, previous abuse, injuries related to abuse, previous ER visits or admissions (especially
>• for multiple unexplained physical symptoms), failure to thrive, malnutrition, recurrent UTIs
. . .
• Fibromyalgia, chronic pain IBS migraines, chronic fatigue, leukemia, sepsis, UP hemophilia/vWB vascular .
•
(Z
MB
. .
malformations, vasculitis, osteogenesis imperfecta Rickett ’s, osteoporosis Ehler ’s Danlos, congenital syphilis,
-u
C sunburns, hypersensitivity reactions, animal bites, hemangiomas, erythema multiforme, Mongolian spots, seizure
>
on
disorder, falls/immobility, previous fractures
Q- PO&GHX • Previous pregnancies, therapeutic abortions, miscarriages
• LNMP, chronic pelvic pain, dyspareunia, contraception
P‘FHX • Any psychiatric illnesses, previous admissions for psychiatric reasons, psychiatric follow-up
• PTSD, depression, substance abuse, phobias, dissociative disorders, psychosis, conduct disorder
personality disorders, eating disorders, somatoform disorders
. ADHD,
MEDS • Screen for prescription drug abuse, failure to be given or being given inappropriate medications
SOCIAL HX • Relationships with family members, other close relationships, social support network, source of income and
financial dependence on abuser, financial abuse by caregiver, childhood abuse, childhood development
FHX • Patterns of abuse, psychiatric illness, substance use
• Bleeding disorders, bone disorders, vascular disorders
ROS • Headaches, memory loss, disordered sleep, poor concentration, avoidant behavior, weakness/dizziness, chronic
pain, palpitations, tachycardia, chest pain, hyperventilation, abdominal pain, bleeding
Appearance: may appear withdrawn, frightened, hyperalert, aggressive, or display sexual behavior, psychomotor
agitation/retardation, layers of clothing to hide signs of abuse, inappropriate dress for weather, poor eye contact ,
poor hygiene
Emotions: low mood, irritable, worried, fearful, guilt, shame; affect may be labile, may be flat, euthymic , angry
Thoughts: ambivalence regarding disclosure, themes of worthlessness and guilt, SI/HI, may have detailed knowledge of
sexual acts inappropriate for age
Insight /Judgment: may not be intact or may be sympathetic to abuser if recurrent pattern, unwilling to escape
PHYSICAL EXAM
Examine in a private setting, consider chaperone, attention to compassionate care, careful draping, explain reasoning
behind maneuvers to put patient at ease. Examine head - to - toe and document bruises, lacerations, or specific injuries.
.
General GCS, ABCs, VS obvious bleeds, signs of distress, signs of dehydration and malnourishment
HEENT
.
Facial fractures/ bruising, torn lips, retinal hemorrhage, loose or lost teeth TM perforation, temporal
wasting, changes in voice, laryngeal swelling, finger marks / bruises /abrasions from asphyxiation
Heart sounds, peripheral pulses, peripheral edema, wheezing/stridor,
Chest
important to examine breasts for signs of assault
Gl Abdominal tenderness, hepatosplenomegaly
Muscle wasting; injuries with characteristic patterns (cigarette burns, bite marks, belt / whip marks);
MSK/Derm/
sprains/dislocations/fractures consistent with attempted defense; bruises at multiple stages of
Extremities
healing and atypical locations; petechiae or purpura, benign nevi, Mongolian spots, dermatitis
Neurologic Focal neurologic findings secondary to head injury, cognitive dysfunction
GU Perineal lacerations or abrasions, speculum exam in females, vaginal or cervical secretions or lacerations
INVESTIGATIONS
Blood Work/Urine
.
• CBC- D (anemia, thrombocytopenia, leukopenia), AST/ALT/ALP. PT/ PTT/albumin, electrolytes, Cr, BUN blood glucose, ESR /CRP if
suspicious of vasculitis, type and screen in case of transfusion
• ABGs
• Urine/serum toxicology (if clinically suspicious)
.
• B -HCG, STI testing (chlamydia, gonorrhea HBV, HCV, HIV, syphilis)
Radiology/ lmaging
• CT head if head injury with neurologic deficits ( suspected intracranial bleed or retinal hemorrhage)
• Limb X- rays. AXR or FAST (focused assessment with sonography for trauma) to assess internal hemorrhage/organ trauma
U REATMENT
Emergent
• Stabilize ABCs “U
t/>
• Legal obligation to report to Child Services if reasonable or probable suspicion of child abuse <
Treatment n
IT
PSYCHOSOCIAL QJ
BIOLOGICAL
NEGLECT • Restore nutritional status (dehydration, • Victim: ensure victim’s safety by admission to hospital or shelter <
•
starvation, electrolyte imbalances) • Social Work for information about shelters, legal services, financial
• 4* comorbidities support, childcare options, employment, and counseling
• Elimination of environmental stressors
PHYSICAL • Wound care (clean site, suture,
• Provide reassurance and validation
dressing) , photographic documentation,
• Report to appropriate agency and assess risk to others in home such
•4' comorbidities as siblings or children
EMOTIONAL • Treat comorbid 4' conditions • Full
'1' assessment especially for emotional or behavioral disturbances,
SEXUAL • Notify sexual assault response developmental delay; close follow -up
team, emergency contraception . . .
• Group and family therapy CBT victim support groups
STI prophylaxis; photographic • Psychotherapy for parents
documentation . • Abuser: monitoring, education, psychotherapy, substance abuse
• 4' comorbidities counseling
BASICS
Definitions
• Anxiety: excessive fear and worry that manifests via cognitive distortions or somatic complaints or both
• Generalized Anxiety Disorder (GAD): excessive anxiety in >1domain (occupation, social, etc.): difficult to control; > 6 mos of > 3 of blank
mind, easily fatigued, sleep disturbance, keyed up/restless, irritability, muscle tension (mnemonic: BE SKIM): not due to medications/
drugs or other medical conditions, including ? conditions
• Panic Attack: acute onset of intense fear or discomfort with > 4 of sweating, trembling, unsteadiness/ dizziness, depersonalization/
. . . .
derealization excessiveHR /palpitations nausea tingling/parasthesias SOB. fearof dying/losingcontrol/goingcrazy chest pain/chills/ .
choking (mnemonic: STUDENTS Fear the 3 Cs)
• Panic Disorder: recurrent unexpected panic attacks with >1attack followed by > lmo of persistent concern of having another attack /
worry over implicationsof attack and /or maladaptivechange in behavior toavoid further attacks: not due to medications /drugsorother
medical conditions, including other ? conditions
• Agoraphobia: fear and anxiety lasting > 6 mos of > 2 from public transportation, open spaces, enclosed spaces, standing in line/crowd,
outside home alone: active avoidance of places where escape is difficult if panic attack occurred or requiring companion; fear out of
proportion to risk / hazard/sociocultural context: functional impairment; not due to medications /drugs or other medical conditions,
including other 3 conditions
• Social Phobia: persistent fear of social performance situations and fear of humiliation causing distress or impaired functioning > 6 mos
• Specific Phobia:persistentfearoravoidancethatisexcessive /unreasonable,associatedwithspecificobjectsorsituationscausingdistress
>6 mos
• Obsessive - Compulsive Disorders: presence of obsessions (recurrent and persistent intrusive thoughts/urges /images), compulsions
(excessive repetitive behaviors to suppress or neutralize obsessions to reduce anxiety) or both that are time consuming ( > lhr /d) ;
causing distress or impaired functioning, not due to medications /drugs or other medical conditions, including other ?i conditions
Risk Factors
• Female sex, low education level, few social supports, chronic medical illness, family Hx or personal Hx of anxiety or mood disorder,
childhood stressful event
DDx
• ?: mood disorders (unipolar .
and bipolar ) , psychosis, personality disorders (OCPD) somatoform disorder, substance use disorder .
.
ADHD. PTSD separation anxiety disorder
.
• Systems-based (critical): Endocrine (hyperthyroidism, hyperparathyroidism. hyper -/hypoglycemia pheochromocytoma) ; CVS
. . . .
(Ml pulmonary embolus CHF arrhythmias, mitral prolapse); Respiratory ( anaphylaxis, asthma COPD pneumonia); Metabolic .
.
(substance - induced intoxication/ withdrawal Vit B12 deficiency): Neurology ( temporal lobe epilepsy, encephalitis, neoplasm)
HISTORY
ID • Name, age . sex/gender, ethnicity occupation or education source of income, living arrangements
, ,
CC/HPI • Onset, duration, intensity, frequency of symptoms ? panic, fear, anxiety, agoraphobia, discomfort SOB . . sweating,
chest pain, flashbacks, nightmares, maladaptive behaviors and avoidance patterns, somatic symptoms
• Triggers: social situations, environmental (e.g. animals, insects, storms), circumstantial ( airplanes, heights), past
experiences
>-
03
• Functional impairment: social, occupational, relationship/ interpersonal
.
• DSM-Vcriteria: BE SKIM (GAD) STUDENTS Fear CCC ( PD)
• Stressors: biopsychosocial approach, health, finances, relationship, divorce, death in family, loss of job, illness,
non- compliance with medications
U
>
.
• Safety: self -harm, SI HI
a.
*
. .
• Substances: cannabis, cocaine MDMA, methamphetamine ecstasy, caffeine, nicotine, EtoH, energy drinks OTC
decongestants, benzodiazepines
.
• Signs and symptoms screen: mood, psychosis (hallucinations, delusions), intrusive thoughts, concurrent/pre -
existing/new medical conditions
RED FLAGS iSpQ2
• Pain with exertion, crushing chest pain,
PMHX • CAD . CHF. arrhythmia, mitral valve prolapse, asthma. DM. hypo-/hyperthyroid, COPD, neoplasm, surgeries, in
particular chronic medical illness
P'l'HX • Other psychiatric illnesses, psychiatrist/psychologist/ therapist .
follow -up previous admissions, suicidal attempts
including means of attempt and I C U f l admission because of the attempt
SOCIAL HX • Relationships, social support network, abuse/neglect, development through childhood, legal problems
OCD
.
SNRIs SSRIs, clomipramine is gold standard in severe disease CBT including exposure response 0)
prevention component
<
. i .
PTSD SSRIs, SNRIs Propranolol PTSD if given after initial stressor SSRIs, SNRIs Propranolol PTSD
^
if given after initial stressor
SSRIs/SNRIs. benzodiazepines/MAOIs second - CBT - restructure and challenge problematic
Social Phobia
line: propranolol for physical symptoms thoughts + exposure therapy
Specific Long- term medication rare, benzodiazepines Exposure based treatment - in vivo or virtual
Phobia for acute symptom relief
Follow - up
• Follow - up in two weeks if starting new SSRI /SNRI to assess for response to treatment and suicidality
BASICS
Definitions
• Manic Episode: elevated, expansive or irritable mood > 7 davj or hospitalization plus > 3 (4 if irritability) of DIG FAST (distractibility .
f
impulsivity/irritability, grandiosity, flight of ideas, activity, sleep, talkative)
• Hypomanic Episode: elevated/irritable mood like mania, but < 4 days and no marked impairment /psychotic symptoms/
hospitalization
• Major Depressive Episode: > 14 days of one or both of mood or interest AND must have > 4 of MSIGECAPS ( T mood, sleep
. .
changes interest, guilt T energy, t concentration, appetite changes, psychomotor retardation/agitation, suicidality)
• Mixed Episode: meets criteria for manic and major depressive episode for majority of >1week (only specifier now in DSM - 5)
DDx
• *F: primary depressive disorders ( with or without psychotic history), bereavement, primary psychotic disorder, drug induced,
premenstrual dysphoric disorder, postpartum psychosis, personality disorders (especially borderline/narcissistic), anxiety disorder,
.
delirium ADHD, eating disorder, somatoform disorders
• Other: hyperthyroidism/hypothyroidism, traumatic brain injury, dementia (especially Fronto - temporal dementia), neurosyphilis,
heavy metal poisoning
• Substance related: stimulant ..
intoxication; withdrawal; psychosis (i e. cocaine, methamphetamine), prednisone use
HISTORY
ID • Name . age. gender, ethnicity, occupation or education, source of income, living arrangements
CC/HPI • Onset, duration, time of the day affected
• DIG FAST. MSIGECAPS
• Previous episodes, recent change in psychotropic medications, especially increase in antidepressant dosage
• Recent impulsive activity and aggression, including sexual promiscuity, drug use, extravagantspending, criminal
activity, reckless driving
• Impairment in function: occupational, social, and interpersonal
• Last time they felt well (euthymia >1week ); premorbid mood and personality
• Loss of a loved one < 2 mos ago (bereavement)
387
MENTAL STATUS EXAM
Appearance: bizarre/socially and culturally inappropriate clothing/makeup, restless, aggressive, distractable, tremor,
psychomotor agitation
Speech: pressured, rapid, loud, may display clanging/rhyming, flight of ideas
Emotions: mood may be elated, euphoric, depressed, irritable; affect may be labile
Perception: hallucinations, illusions, dissociative symptoms
Thoughts: expansive, overinclusive, may be tangential or circumstantial, delusions (especially grandiose)
Insight/Judgment: impaired, reckless behavior, depends on severity
Cognition: poor concentration and attention, poor memory
PHYSICAL EXAM
General PE to rule out other causes
INVESTIGATIONS
Blood Work/Urine
• CBC- D . electrolytes. Cr. urea (renal failure). TSH (lithium may induce hypothyroidism), random blood glucose. B12 (esp. if MCV
> 100)
• Urinalysis, urine toxicology ( amphetamines, cannabis, or cocaine)
• STI tests/VDRL (infection)
.
• EtOH acetaminophen, salicylates (contributions to mood, toxic ingestions, suicide attempt)
• Serum lithium, valproate levels
Radiology/ lmaging
• May consider CT
• EKG
03EATMENT
Emergent
• Admit to hospital if mania, mixed episode, acute danger to self or others: may require certification
• Benzodiazepines if agitated
Treatment for bipolar disorders
BIOLOGICAL PSYCHOSOCIAL
Referrals
• Psychiatry: mania, treatment resistant, severe, psychosis, unsure of diagnosis
•fcMKflifeujai :
DISORDER ABBREVIATED DSM- 5 SYMPTOMS TIMELINE AND OTHER CRITERIA
Major Depressive
i i
Episode
> 5 of
^
MSIGECAPS ( mood, sleep changes, interest, guilt, energy 1
concentration, appetite changes, psychomotor retardation/agitation,
,
>14 days
.^
suicidality; must include mood or decreased mood or anhedonia
i .
interest ) ± psychotic symptoms ± postpartum onset
Major Depressive >1major depressive episode, no manic, hypomanic or mixed episodes functional impairment
Disorder
Persistent depressed mood for majority of day; no MDEs no manic/. majority of days for > 2 yrs
Depressive Disorder .
hypomanic/mixed no cyclothymia, no psychosis, not suicidal
DDx
• 4*: anxiety, bipolar disorder, cyclothymia, adjustment disorder with depressed mood, seasonal affective disorder, postpartum
depression, premenstrual dysphoric disorder, primary psychosis, substance use (EtOH, opioids, benzodiazepines /sedatives),
withdrawal ( stimulants), personality disorder (especially borderline), somatoform disorders
• Other; endocrine abnormalities (hypothyroidism), anemia, infection, renal failure, lupus, neurocognitive disorder, stroke
Parkinsonism, cardiac, chronic debilitating illness, chronic pain, MS on interferon or Hep C on interferon, treatment with prednisone
.
ID • Name, age, sex/gender, ethnicity, occupation or education, source of income, living arrangements
CC/HPI • Onset, duration, time of the day affected
• MSIGECAPS
• Previous episodes
• Impairment in function: occupational, social, and interpersonal
• Last time they felt well (euthymia >1week ); premorbid personality
• Loss of a loved one < 2 mos (bereavement)
. .
• Stressors: premenstrual post partum seasonal, relationships, occupation
*
.
• Safety: self -harm, SI (plan, means, intent) HI (plan, means, intent, name of person/people)
• Substances: cocaine, amphetamines, cannabis, caffeine, EtOH, smoking, hallucinogens, opioids, benzodiazepines;
recent withdrawal, longest time sober ( what was mood like then? - R/O substance -induced mood disorder )
.
• Signs and symptoms screen: anxiety, psychosis GMC - concurrent /pre - existing/new
CD
MEDS • Antihypertensives (e g. .
. metoprolol, reserpine), steroids, OCP, clonidine, levodopa, antiepileptics, analgesics,
antipsychotics, mood stabilizers, chemotherapy
-C
U SOCPERSHX • Relationship, social support network, childhood abuse, childhood development
>
</ ) FAMHX • Psychiatric illness especially mood disorders, suicide, substance use . Hx of abuse
CL
ROS .
• Skin changes, cold intolerance, hair loss, muscle pain/ weakness, loss of libido Wt changes
Appearance: dress, grooming, and self - care often neglected in depression, psychomotor agitation or retardation,
tearfulness
Speech: reduced volume, tone, rate, spontaneity, poverty of speech
Emotion: mood depressed, anxious, or irritable; affect may be flat or dysphoric
Perceptions: may have mood-congruent hallucinations (especially in severe depression, post - partum depression)
Thoughts: process may be linear or abnormal, themes of guilt, hopelessness, persecution, content may involve mood '
congruent delusions (guilt, nihilistic)
Insight/Judgment: both may be impaired
389
Cognition: cognitively impaired, reduced memory and concentration
Safety: SI ( thoughts, plan, time frame) in depression
PHYSICAL EXAM
General PE to rule out other causes
INVESTIGATIONS
Blood Work/Urine
.
• CBC- D, electrolytes, Cr urea (renal failure). TSH, random blood glucose, B12
• Urinalysis (infection), urine toxicology
• EtOH, acetaminophen, salicylates
Radiology/ lmaging
• May consider CT/ MRI to rule out organic brain syndrome
• EKG
uSEATMENT
Emergent
• Admit to hospital if acute danger to self or others, may require certification
- -
• Neruostimulation ECT/rTMS if contraindications to meds and delivered therapy
moderate to severe or if pregnant
• Promote regular excercise /healthy diet
Referrals
• Psychiatry: if treatment resistant, severe, psychosis, unsure of diagnosis
T>
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QJ
Definitions
• Anorexia nervosa ( AN)
> Restriction of energy intake leading to a significantly lower body weight, intense fear of gaining Wt or becoming “ fat " despite
being underweight, disturbance in self evaluation and experience of body Wt or shape, denial of seriousness of condition
> Subtypes: restricting type, binge -eating/purging type: severity classified from “ mild" to “extreme" based on BMI
> Prevalence 0.5 -1% for young women and 0.1% for adolescent males, average age of onset 15 - 17 ( female) 12- 13 (male)
• Bulimia Nervosa (BN)
.
> Recurrent episodes of binge eating, recurrent inappropriate compensatory behavior to prevent Wt gain, binge eating and
.
compensation occur once a week for > 3 mos, self evaluation is unduly influenced by body shape and Wt disturbance not only
during episodes of AN
> Severity classified from “mild" to "extreme" based on frequency of inappropriate compensatory behavior
> Prevalence 2 - 4% for young women and 0.1% for males
• Other Eating Disorders:
> Avoidant/ Restrictive Food Intake Disorder: avoiding or restricting intake with failure to meet nutritional needs, not due to
.
food availability or cultural practices,not only during courses of AN or BN without distortion of body Wt/shape
> Binge Eating Disorder: recurrent binge eating episodes without compensatory behavior, not only during courses of AN or
.
BN severity classified from “ mild ” to "extreme" based on number of binge eating episodes per week
.
> Pica: recurrent episodes of non- food substances for >1mo inappropriate for developmental/cultural/social context
.
> Rumination Disorder: recurrent food regurgitation for >1mo not due to medical illness (e.g., GERD). not only during course
of any other eating disorder
• Unspecified Feeding or Eating Disorder
> Symptoms of an eating disorder causing distress, without meeting the full criteria for a specific disorder
DDx
• . .
*F: depression, anxiety (social anxiety GAD panic disorder, OCD), substance use disorder (specifically stimulant use disorder ),
psychosis, personality disorders (cluster C more common for restrictive types, cluster B more common in binge/purge subtypes)
. .
• Other: hyperthyroidism DM IBD, celiac, malabsorption, malignancy
HISTORY
ID • Name, age, sex /gender, ethnicity, occupation or education, source of income, living arrangements
CC/HPI • Onset, Wt loss/gain, amenorrhea, fatigue: family/ friend may bring patient to medical attention
. .
• SCOFF Questionnaire (sick, control, one stone (14 lbs/ 6.5 kg ), fat food)
• Eating behaviors: types of food avoided or preferred, guilt about eating, typical day, typical meals, calories/d,
binging, binge foods and frequency, bowel habits, fluid intake restriction to decrease Wt or increased intake to
hide Wt loss
• Wt: maximum/minimum/ideal Wt, feelings about current Wt/food and Wt gain
• Compensatory behaviors: exercise, enemas, laxatives, purging, appetite suppressants and how often, fasting,
chewing and spitting
• Menses
• High risk: adolescent .
females especially of higher SES ballet dancers, gymnasts, models, DM-Type 1 medical
professionals, gay males
.
+>-
OJ • Stressors: relationships (parents, friendship circle, romantic): bullying re: appearance, difficulties with work or
school: abuse; unwanted sexual attention
u • Safety: self -harm, SI/HI
>
to • Substances: cocaine, amphetamines, cannabis, caffeine, smoking, EtOH, energy drinks
Q. • Signs and symptoms screen: mood, psychosis, GMC - concurrent/pre - existing/new
RED FLAGS • Suicidal references, self-harm, palpitations, malnutrition (significant Wt loss/poor growth in children,
nutritional deficiencies, impaired psychosocial functioning)
PMHX • Gastrointestinal
delay, coma
.
illness including surgeries, thyroid problems DM, falls, seizures, dehydration, developmental
P'FHX .
• Any psychiatric illnesses, therapist, follow -up personality disorder, admissions for eating disorders,
substances, suicide attempts, previous eating disorder, day treatment programs, etc.
MEDS • Laxatives, levothyroxine, insulin. SSRIs
SOCPERSHX • Social support network, source of income, abuse/neglect, development through childhood, high achievers,
maladaptive personality patterns, legal problems
FAMHX • Any psychiatric illness, eating disorders, suicide, substance use
HEENT
Scalp hair thinning, temporal wasting .
Temporal wasting, periocular /palatal petechiae parotid
hypertrophy, perioral skin irritation, worn enamel, caries
Cardiac .
Arrhythmias CHF
Respiratory Aspiration pneumonia
Gl
Decreased bowel sounds, bloating, abdominal pain .
Decreased bowel sounds GERD
symptoms, muscular abdomen
Lanugo, dry/cold skin, hair loss, yellow skin Russell’s sign (calluses over knuckles), muscle wasting
MSK /Derm/
( from carotene), muscle wasting, fractures,
Extremities
pain in extremities, brittle nails
Abnormal taste sensation, weakness, Changes in reflexes, loss of gag reflex, weakness,
Neurologic
neuropathies, cognitive dysfunction neuropathies, decreased LOC, cognitive dysfunction
INVESTIGATIONS
Blood Work /Urine
• CBC- D ( anemia, leukopenia), electrolytes (hypophosphatemia, hypokalemia, hypochloremia, metabolic alkalosis if vomiting) Cr . .
. . .
BUN blood glucose (hypoglycemia), LFTs, TSH, T3 T4 (hypo or hyperthyroid), LH FSH ( to rule out other causes of amenorrhea),
estrogen, progesterone, cortisol
ABGs
• Urine/serum toxicology ( if clinically suspicious)
Radiology/ lmaging
• CXR (if complains of SOB)
Special Tests
T7
• EKG ( long QT and arrhythmias) c/>
REATMENT o
3t*
mmm
BASICS
Definitions
• Gender Identity: personal identification as male or female: gender role is stereotypical observable manifestations such as behavior
and appearance, often outward expression of gender identity
• Sex: biologic, defined by phenotype and genotype
• Gender Dysphoria: results when gender identity and sex are incongruent
Diagnostic Criteria
• Strong and persistent cross -gender identification:
.
Children must display at least 6 characteristics of insistence that he /she is other sex preference for wearing stereotypical
>
.
clothing of opposite sex persistent preferences for cross-sex roles in make-believe play and fantasies, intense desire to
.
participate in stereotypical activities of opposite sex prefers playmates of opposite sex
> Adolescents and adults often display stated desire to be other sex, passing as the opposite sex, desire to live or be treated as
.
opposite sex,conviction that he /she has typical feelings /reactions of opposite sex strong dislike of one’s sexual anatomy
• Persistent discomfort and an overwhelming sense of inappropriateness in the gender role of an individual’s sex
• Not concurrent with a physical intersex condition
• Disturbance in gender causes significant impairment or distress in social, occupational, or other important areas of functioning
DDx
•
'1': transvestite fetishism, psychosis (delusion of belonging to opposite sex ), body dysmorphic disorder (excessive preoccupation
.
with imaginary/minor defect in appearance), OCD Borderline Personality Disorder
• Other: Turner syndrome (lack of secondary sex characteristics and infertility may lead to feelings of inadequacy and questioning
identity) , ('new specifier of Gender Dysphoria: ’Disorder of Sexual Development: CAH’ [ particularly completely virilized ], androgen
insensitivity, gonadal dysgenesis, 5 - alpha reductase deficiency)
• Normal conformity to stereotypical sex - role behavior
HISTORY
ID preferred name and preferred gender pronoun, age, biological sex, ethnicity, occupation or education,
• Clarify
source of income, living arrangements
CC/HPI • First onset of dysphoria with sex, toys/play as child, sex of majority of friends, fears of developing as certain sex,
desire to alter /eliminate secondary sexual characteristics
• Gender atypical behaviors including clothing preferences, activities, attempts to alter appearance including
hair removal, previous management including counseling/ investigations/hormone therapy/surgery, if /how long
passing ( living/dressing) as oppositive sex
• Impaired function: social, occupational, relationship/interpersonal
.
• Stressors: biopsychosocial approach, health, finances, relationships, loss of job illness
• Safety: self -harm, SI (higher rates of suicide with this population), safety at home/ work/school, victimization
.
(bullying, verbal abuse, hate crimes) HI
. .
• Substances: nicotine EtOH steroids, cannabis, estrogen
• Signs and symptoms screen: mood, anxiety, delusions/hallucinations, GMC - concurrent/pre -existing/new .
somatic symptoms
RED FLAGS • Self -mutilation, especially genital damage
CO PMHX • Chromosomal abnormalities, metabolic/hormonal deficiencies, past surgery/ hormone therapy
•
-U•
MM
C
P'I'HX • Comorbid depression, anxiety, substances, personality disorder, psychosis, other identity disturbances
>
to -
•Therapist, follow up, admissions, SI
CL • Hormones ( testosterone, estrogen, GnRH analogues ) , steroid use
MEDS
SOCPERSHX • Childhood relationships and development, legal problems, acceptance by family/work
• Take thorough sexual Hx (relationships, sexual preferences)
• Hx of sexual or physical abuse
Special Tests
• EKG
• Consider BMD if on estrogen therapy
• Genetic screening if suspicious for genetic syndrome
nsEATMENT
Emergent
• Treatment for acute safety concerns
Treatment Options
Biological
Psychosocial
Medical Surgical
“O
m
<
O
CD
<
*
BACKGROUND
• Rare, potentially fatal, idiosyncratic reaction to antipsychotics due to excessive dopamine receptor blockade, can also
• occur with dopamine agonist withdrawal
• Key .
features are hyperthermia, rigidity, altered LOC, autonomic instability, elevated CK treatment is mainly supportive
• Significant similarities to serotonin syndrome, catatonia EPS.
.
• 0.01%- 2% of those treated with antipsychotics, mortality as high as 20% or higher if injectable
DIFFERENTIAL DIAGNOSIS
• Serotonin Syndrome vs NMS
> .
both: fever, altered LOC autonomic NEUROLEPTIC MALIGNANT SYNDROME DIAGNOSTIC CRITERIA
instability • Exposure to dopamine antagonist or dopamine agonist withdrawal
.
> SS: rapid onset ( vs days) Gl symptoms • Hyperthermia
( vs none), hyperreflexia/restlessness ( vs • Rigidity
rigidity/bradykinesia) •Reduced/ fluctuating LOC
• Other pharmacologic: EPS, lithium,
anticholinergics, interactions, •CK elevation
withdrawal, malignant hyperthermia • Autonomic instability ( > 2 of ) ng:
• Other: heatstroke
Hypothesized Pathophysiology
• Excessive D 2 blockade or withdrawal
> Tuberoinfundibular dopamine pathway
= hyperthermia
> Nigrostriatal dopamine pathway = rigidity
> Mesolimbic/mesocortical dopamine pathways = altered LOC
> Brainstem/spine = autonomic instability
• Excessive sarcoplasmic reticulum calcium release leading to muscle contraction
HISTORY
ID • Name, age, sex/gender, occupation or education, source of income, living arrangements, relationship, children
HPI • Orientation to person, time, and place
• Onset usually within 4- 14 days of medication change, but can occur at any time, generally progresses over 24-72
hours
• Confusion, muscle stiffness, fever, sweating
£ • Rule out SS: rapid onset, restlessness, Gl symptoms of N/V/D/abdo pain
CTJ • Sick contacts, toxic exposures, heat exposure, physical restraints
-u
C . .
• Safety: overdose SI self -harm. HI
• Substances: cigarettes, alcohol, cocaine, amphetamines, cannabis, hallucinogens, opioids, benzos, history of
>
in withdrawal
CL
• Signs and symptoms screen: for mood disorders, anxiety, psychosis
INVESTIGATIONS
Blood Work /Urine
.
• CBC- D (leukocytosis in 70- 98% of NMS), electrolytes Ca. Mg, P04, Cr, urea (dehydration), liver function tests
• CK (( f in 50- 100% of NMS) , LDH, serum iron (commonly |in NMS)
•ABG (metabolic acidosis), urine myoglobin (rhabdomyolysis)
•Rule out infectious cause: consider blood cultures, CXR ( aspiration pneumonia), urinalysis, LP ( meningitis)
• Rule out metabolic cause: TSH, glucose
• Rule out toxic cause: urine toxicology screen, consider heavy metal
Radiology/Imaging
• Rule out neurologic cause: consider CT/MRI head to rule out lesions/mass/trauma
mEATMENT
Emergent
• .
Airway, breathing, circulation, oxygen IVs, monitoring
• Admit to hospital, preferably ICU for monitoring and management
• Most important intervention is to discontinue antipsychotics /reintroduce dopamine agonists with slightest suspicion of NMS
Safety
• May require certification
Biological
• Treatment is mainly supportive
> Hyperthermia: aggressive cooling measures such as ice packs or cooled IV fluids/blankets, antipyretics (less likely to be
effective in NMS), reducing rigidity
> Rigidity: mixed evidence for dantrolene/lorazepam (muscle relaxant ) and bromocriptine ( dopamine agonist)
> Respiratory: oxygen, elevate head of bed to minimize aspiration risk, monitor for respiratory failure, consider intubation/
ventilation for low LOC /sialorrhea/dysphagia
> Circulatory: hemodynamic stabilization, fluids for hydration/hypotension, antihypertensives if necessary (CCBs may also
"O
improve rigidity), risk of clotting if immobile t/>
> Rhabdomyolysis: avoid /minimize physical restraints, aggressive hydration, slightly alkalotic pH to minimize risk of renal failure, <
n
correct electrolytes, glucose, other metabolic abnormalities
.
• ECT may improve hyperthermia, catatonic symptoms, altered LOC and underlying psychiatric condition — »
•
• Reinstituting antipsychotics: consider ECT instead, or give a 2 week washout period, use low D 2 affinity antipsychotic such as
quetiapine, slow titration, and avoid injectables <
Psychosocial
• Collateral from family/previous records, liaise with allied health professionals /care providers, followup/referrals as necessary
ASICS
Personality Disorder: Pattern of behavior that deviates markedly from the expectations
of the individual’s culture, involving cognition, affectivity, interpersonal function, impulse
control ( since adolescence/early adult ) causing distress and impairment
Cluster Disorder DSM Criteria
A Schizoid DISTANT: > 4 detached affect, indifferent to praise/criticism, sex of
little interest , tasks solitary, absence of friends, neither desires or
“Mad" enjoys close relationships, takes pleasure in few activities
Defenses: projection, Schizotypal ME PECULIAR: > 5 magical thinking, experiences unusual perceptions,
denial, rationalization, paranoid, eccentric behavior /appearance, constricted affect, unusual thinking/
fantasy, distortion speech, ideas of reference, anxiety socially, rule out psychosis/PDD
Links: familial Paranoid SUSPECT: > 4 suspects infidelity, unforgiving, suspicious, perceives
psychotic disorders attacks/reacts quickly, "enemy vs. friend" (doubts loyalty), confiding
little in others, threats perceived in normal events
B Antisocial CORRUPT: evidence of conduct disorder before 15 yrs + > 3 criminal
behaviors /can' t conform, obligations ignored, reckless disregard for
"Bad"
safety, remorseless, untrustworthy, poor planning, temperamental
Defenses: splitting, Borderline AM SUICIDE: > 5 abandonment fear, mood unstable, suicidal /self -
idealization/ .
harm unstable relationships, impulsive, control of anger poor, identity
devaluation, acting disturbance, dissociative symptoms, emptiness feelings
out, denial, distortion,
Narcissistic SPECIAL: > 5 special/unique, preoccupied with fantasies, envious/believes
dissociation,
envied, entitlement, excessive admiration required, conceited (grandiose self
repression, regression
importance), interpersonal exploitation, arrogant behavior, lacks empathy
Links: familial Histrionic PRAISE ME: > 5 provocative behavior, relationships considered more
mood disorders intimate than reality, attention (uncomfortable when not center of attention),
influenced easily, speech impressionistic/ lacks detail, emotions shallow and
rapidly shift, made up to draw attention to self, exaggerated emotions
C Obsessive - LAW FIRMS: > 4 loses point of activity/preoccupied with detail, abilities hindered
Compulsive perfectionism, worthless objects kept, friendships excluded due to work, inflexible/
"Sad ”
overconscientious morally, reluctant to delegate, miserly, stubborn/rigid
Defenses: isolation, Avoidant CRINGES: > 4 certainty of being liked required, rejection preoccupied
avoidance, thoughts, intimate relationships strained due to fear, new relationships
hypochondriasis, inhibited, gets away from interpersonal contact at work, embarrassment
idealization, prevents new activities, self viewed as inferior/ inept /unappealing
regression,
Dependent RELIANCE: > 5 reassurance required for decisions, expressing disagreement
rationalization
feared, life responsibilities done by others, initiating projects difficult
> Links: familial because unconfident. alone uncomfortable, nuturing needed, companionship
anxiety disorders sought urgently, exaggerated fears of being left to care for self
a
JO DDx:
u • P: mood disorders, anxiety disorders, adjustment disorder, somatic symptom disorders, developmental delay, neurocognitive
‘
disorder, substance use disorder, autism spectrum disorders, impulse control disorders, ADHD, primary psychotic disorder, eating
cn
CL disorders
• Other: CNS insult, metabolic, endocrine, hepatorenal, vitamin deficiency, delirium, chronic or debilitating medical condition
ISTORY
ID • Name, age . sex/gender ethnicity occupation or education source of income, living arrangements
, , ,
CC/HPI • Mood complaints . SI. anxiety, anger, troubled relationships somatic symptoms, social withdrawal: may present
suicidal, violent, bizarre behavior criminal activity within
,
, , context of medical encounter
. .
^
• Mood: or T how long, last time felt euthymic stability, angry outbursts: Hx of true manic episode
• Impaired function: social, occupational, relationship/interpersonal
• Stressors: relationships, work /school stresses, finances, death in family, illness; Safety: SI (borderline has 10%
suicide rate), plan, intent, means, time frame, parasuicidal attempts, HI: Substances: cocaine, amphetamines,
cannabis, hallucinogens, caffeine, nicotine, EtOH, energy drinks: Signs and symptoms screen: mood, psychosis,
anxiety, GMC - concurrent/pre - existing/new
397
RED FLAGS • SI with plan, intent, means . HI with plan, intent, means (i.e., access to firearms)
PMHX .
• DM thyroid problems, traumatic brain injury, neurocognitive disorder, chronic pain/ fatigue syndromes, epilepsy,
. .
heavy metal poisoning, neurosyphilis, AIDS, CNS tumors MS Huntington’s, Parkinson's
PM'HX • Any psychiatric illnesses, therapist, follow -up, admissions, suicidal ideation; repeat ER visits for Sl/suicide
attempts/parasuicidal behaviors; multiple presentations for somatic complaints
MEDS • Levothyroxine, SSRIs, steroids, sympathomimetics . anticholinergics, benzodiazepines, opiates
SOCIAL HX • Childhood abuse/neglect, loss of parent, family violence, family dynamic, childhood development
• Relationships: nature, length, and stability of relationships and friendships from childhood, and means by which
they ended, ease of social interactions
• Occupation: length and stability of current and past careers
• Education: how far, level of success, interaction with others, frequency of disciplinary actions
• Legal: nature, age of first offense, total number of criminal events
FAMHX • Any psychiatric illness, substance use disorder, completed suicide
INVESTIGATIONS
Blood Work /Urine
• CBC -D, electrolytes. Ca2 \ Mg. glucose. B12. TSH. ALT. AST. Cr, Urea
• Urinalysis . .
EtOH salicylates, acetaminophen, urine toxicology, heavy metals
•STI testing (CNS infection such as neurosyphilis or HIV)
Radiology/ lmaging
• CT/ MRI brain if suspect organic brain disorder, personality change secondary to head injury
Special Tests
“U
• EEG ( rule out temporal lobe epilepsy) cn
<
n
UREATMENT
o>•
»
BASICS
Definitions
•Peripartum Depression
> maternal mood alterations during pregnancy and/or postpartum that range from transient mild mood changes to severe
depressive episodes
• Major Depressive Disorder with Peripartum Onset
> onset of mood symptoms occurs during pregnancy or in the 4 weeks following delivery
Screening
• Regularly enquire about depressive symptoms during prenatal and postnatal doctor ’s visits
consider normalizing, nonjudgmental questioning such as, "It is common for women to feel overwhelmed by the ( anticipated)
>
.
birth of a new baby Do you ever feel that way?”
• No consensus regarding universal screening in pregnancy, though enquiring about mood, sleep, energy, appetite and feelings
should be a part of an initial history/assessment
> If screening, use Edinburgh Postnatal Depression Scale
Risk Factors
• Major Risk Factor: past history of diagnosed mood disorder +/- anxiety disorder (historic, perinatal, current)
• Family history of psychiatric conditions, especially major depressive disorder, bipolar disorder, primary psychotic disorder,
completed suicide
• Personal life stressors
.
> Pregnancy (e.g. unintended pregnancy, traumatic birth experience, hyperemesis gravidarum)
.
> Infant (e.g., preterm birth NICU admission, overall health)
> Relationships (e.g., young age, single marital status, specifically, a lack of perceived support , domestic violence)
Severity
Considered part of normal spectrum Persistent and severe symptoms,
impairment in daily functioning
First few days after childbirth Anytime in pregnancy, up to 4 weeks after birth of
Onset
the child. Usually starts 1- 3 weeks after birth .
Intermittent, self - limited, usually resolves Persists >2 weeks and meets criteria for
Duration
in 1- 2 weeks without treatment Major Depressive Disorder
• Tearfulness, sadness • Unable to sleep even when baby sleeping
• Mood lability, irritability, anxiety • Statements of guilt or worthlessness as a parent
• Increased sensitivity to criticism • Thoughts of harm to self and/or baby which may be
• Trouble sleeping, eating, and making intrusive or frightening
Symptoms
decisions • Suicide ideation or need to "escape"
• Increased concern over own health and • decreased mood: decreased interest
PMHX • Hyperthyroidism, hypothyroidism, Cushing's, DM . malignancy autoimmune, CAD/CVA Vit B12 deficiency, chronic
, ,
infection, renal failure, chronic medical condition
P'i'HX • Psychiatric diagnoses, treatments, past episodes, mania, hypomania, prior suicide attempts, current psychiatrist,
next appointment/last appointment
MEDS • Current and past meds including antidepressants, mood stabilizers, antipsychotics . Current thoughts on
medications; who prescribed them; how long has pt been taking them; SEs .
ALLRG • Any drug reactions, anaphylaxis
SOCPERSHX • Tobacco/EtOH/drugs; financial stressors; relationships and social support; screen for domestic violence and abuse
FAMHX • Any psychiatric illness, completed suicide, substance use, history of abuse
5HYSICAL
Conduct Mental Status Exam
General Physical to rule out other causes of depressed mood
IEEATMENT
Emergent
• Admit to hospital if acute danger to self/ baby/others or evidence of mania /psychosis, may require certification
Non- Emergent
• Important to discuss options for accessing care in urgent manner if symptoms persist (e.g., call pediatrician/family doctor /
obstetrician/psychiatrist, go to emergency department or call local crisis line)
Biological Psychosocial Social
1. Antidepressants: use minimum number of 1. Psychotherapy: 1. Education: patient and family
psychotropic meds at lowest effective dose interpersonal or
cognitive behavioural 2. Resources:
• 1st line: continue medication used to achieve euthymia or financial/social support
SSRI if starting new medication (including domestic violence)
• Sertraline/ Zoloft = min. known risk of harm and
considered safest choice in mothers who plan to
breastfeed
2. ECT: considered safe, used in cases of failed medical
management or when rapid response needed
(e.g., acute psychosis, suicidal /homocidal)
BASICS
Diagnostic Criteria
• HDSBN: DSM psychotic symptoms are hallucinations, delusions, speech disorganized, behavior disorganized/catatonic, negative
. .
symptoms ( affective flattening, alogia avolition) delusions
Delusional Disorder delusions, criteria for schizophrenia not met >1month if present, 2°
Substance - induced presence of at least one or both of Developed during (or variable
Psychotic Disorder hallucinations or delusions < 1month following)
intoxication/ withdrawal
or after exposure to
medication
2° to Mood Disorder Occurs within ongoing mood disorder, Unspecified 1°
hallucinations or delusions often mood
congruent
DDx
• '1': mood disorders, personality disorders ( paranoid, borderline, schizotypal, schizoid), somatoform disorder, substance abuse/
withdrawal, neurocognitive disorder, delirium, dissociative disorders, anxiety disorders
• Other: partial complex . .
seizure, temporal lobe epilepsy, neurosyphilis AIDS. CNS tumor CNS infection, increased ICP stroke, heavy .
metal poisoning, nutrient deficiency, endocrine, liver failure, renal failure, medications
HISTORY
ID . . sex/gender ethnicity, occupation or education source of income, living
• Name age , , arrangements
CC/HPI • Onset, duration, intensity, frequency, course
• HSBND: hallucinations (mood - congruent or not), impaired functioning; collateral may report bizarre/eccentric /
suspicious ideas and behavior, aggression, agitation, social withdrawal
• Premorbid function: school / work, social, home; prodromal symptoms of irritability, isolation, anxiety
• Stressors: health, finances, relationships, death in family, loss of job, illness, med non- compliance
• Safety: self -harm, SI (Dx of schizophrenia >10% of successful suicides), HI, Hx of violence or aggression, enquire
03 about command hallucinations
-Cu .
• Substances: cocaine, cannabis, MDMA, ecstasy, mushrooms, LSD caffeine, nicotine, EtOH intoxication/
.
withdrawal, ketamine PCP, steroids
• Signs and symptoms screen: mood, anxiety, concurrent/pre - existing/new
Q.
RED FLAGS • Focal neurological signs, febrile, meningismus, command hallucinations, hypoxia
PMHX • Recent or chronic major illness, malignancy, HIV, CVA, dementia, seizures, hyperthyroid, hypothyroid
("myxedema madness”) , parathyroid dysfunction, Cushing’s, hepatorenal pathology, lupus
PTHX
means, need for ICU admission as a result)
.
• Personality disorders, any psychiatric illnesses, therapist, follow -up admissions, suicide attempts (lethality,
401
MENTAL STATUS EXAM
Appearance: many appear normal, style of dress may be "odd", eye contact often poor (if responding to perceptual
disturbance), socially awkward, withdrawn, movement may reveal agitation or catatonia ( stupor, mannerisms); assess
presence of EPS ( akathisia, tardive dyskinesia, dystonia, Parkinsonism)
Speech: echolalia, neologisms, poverty of speech
Emotion: depressed, anxious, irritable, euphoric: Affect: inappropriate, blunted, or incongruent
Perceptions: illusions and hallucinations common (primarily tactile in substance etiology. auditory > visual in
schizophrenia), can also report olfactory, gustatory, or somatic - consider substance or general internal medical etiology if
reported
Thoughts
• Thoughts may be very concrete or mystical /pseudoscientific; thought process may be disorganized, ranging from loosening of
associations to word salad or thought blocking; though insertion, broadcasting or thought withdrawal
• Delusions can be primary vs. secondary (one that arises from a previous abnormal idea or experience), bizarre vs. non-bizarre,
( types include persecutory, paranoid, grandiose, nihilistic, jealousy, erotomanic, religious, thought insertion / withdrawal/
broadcasting, ideas, and delusions of reference)
.
• Self -harm: elicit reasons for (i.e., to remove microchip 2° to command hallucination) ; SI and /or HI (elicit plan: intent: means)
Insight/Judgment: often impaired, many unwilling to accept their illness and refuse treatment. Note that if insight is
preserved, the patient is at high risk of suicide as they realize the effect of the diagnosis on his/her entire life (especially SZP).
.
Cognition: may have poor orientation MMSE may reveal deficits, poor concentration and executive function
PHYSICAL EXAM
VS: include Ht, Wt , and waist circumference to track metabolic side effects of antipsychotic medications
General: watch for catatonia, Wt gain, perform general PE to a) rule out other reasons for psychotic symptoms; b) assess
general state of health as often persons with chronic mental illness do not routinely seek medical attention
NEURO: PCRST (power, coordination, reflexes, sensation, tone), primitive reflexes/abnormal stereognosis/
dysdiadochokinesis
nsEATMENT TD
(/)
Biological Psychosocial O
• Stabilize medically, reassess once suspected substance out of system • consider certification under Mental
Emergent • Rule out neuroleptic malignant syndrome (NMS) Health Act
• Duty to warn? Children at risk ?
• Antipsychotics /benzodiazepines for agitation <
• Antipsychotic: atypicals treat positive and negative Sx; typicals • Consider neuropsych testing
treat positive Sx: clozapine reserved for treatment resistance due to • Patient and family education (relapse
agranulocytosis SE ( < 1%) greater when family unsupportive)
• Depots .
for noncompliance (risperidone, palliperidone zuclopenthixol . • Social Work. OT and other community
etc.): antidepressants as adjunct for negative symptoms: ECT for severe services: assistance with med
mood symptoms or catatonia adherence: vocational training and
Long- term • Side effects of antipsychotics: benztropine for EPS ( typicals > atypicals); supportive employment
metformin/nutrition counseling for Wt gain/DM ( atypicals > typicals); • Day programs, residential programs
qhs dosing for sedation: minimize risk factors for cardiovascular / .
• Joint crisis plans with patient, family
cerebrovascular: discontinue antipsychotics and provide continuous Psychiatrist
supportive care for NMS • Addictions support
• If patient's first episode, then recommend follow -up 4 wks after decreasing • Lifestyle management education and
dose, may trial discontinuation of meds after 6 mos in remission support (diet, exercise, sleep)
BASICS
Definitions and Diagnostic Criteria
• Tolerance: requires increasingly larger doses for original effect
• Withdrawal: substance specific syndrome resulting from cessation or reduction following heavy or prolonged use: 20% mortality
associated with untreated EtOH withdrawal
• Intoxication: reversible syndrome affecting mental, behavioral, social,
occupational functioning CAGE-AID Questionnaire
DSM - 5 Substance Use Disorder • Have you ever felt you ought to CUT DOWN on your
drinking or drug use?
Substance use with > 2 of :
• Using more than intended • Have people ANNOYED you by criticizing your
‘ Substance use disorders are categorized by severity: Mild = 2- 3 symptoms; Moderate = 4 - 5 symptoms; Severe = 6 or more symptoms
Categories of Commonly Abused Substances
. .
• Opioids (heroin, morphine, oxycodone) Stimulants ( amphetamines, cocaine MDMA, phencyclidine); Depressants ( EtOH, sedatives,
. . . . . . .
hypnotics) Hallucinogens (marijuana LSD mushrooms) Volatile inhalants (glue NO amyl nitrate) Nicotine, other (e.g. ketamine) .
HISTORY
. .
ID • Name age sex/gender, ethnicity, occupation or education, source of income, living arrangements
CC • Substance use/ withdrawal, bizarre behavior
HPI • Quantity/ frequency of past and recent abuse, drugs used ( all substances and routes: e.g .. cough syrup. IVDU)
• CAGE -AID
• Severity (blackouts, withdrawal . DTs, seizures, admissions to hospital for intoxication/withdrawal)
• Consequences: assault, impaired driving, incarceration, frequent injuries, compulsive use . loss of control
• Amount on average per day/wk/month; “normal" = females: 2/day or 10/wk; males: 3/day or 15/ wk
• Readiness to change versus denial; substance abuse rehab programs (out -patient or inpatient/residential)
>-
OJ
• Stressors: reasons for substance use ( peer pressure, availability, relieving physical symptoms)
. . .
• Safety: Self -harm SI HI use of contaminated needles, use during pregnancy
• Signs and symptoms screen: for mood disorders, anxiety, psychotic illness
u . .
RED FLAGS • Autonomic instability, decreased LOC, agitation, active psychosis SI/HI Wernicke’s encephalopathy, DTs
>-
in
CL
• Early refills, visits to multiple health care providers
PMHX • Chronic pain, progressive debilitating conditions such as MS or cancer, seizure disorders, head injuries
.
• Liver disease ( Hep B and Hep C cirrhosis), PUD, gastritis, pancreatitis, diarrhea, DM
. . .
• Infectious endocarditis /skin infections /osteomyelitis COPD HIV cardiomyopathy and Mis, dementia
PfflHX • Mood and anxiety disorders, Hx of substance induced psychosis, personality disorders
MEDS • Prescription meds with the potential for abuse (narcotics, stimulants, opioids, benzodiazepines, insulin);
increases in meds
SOCPERSHX • Relationships, support network, close contacts with substance issues, abuse/neglect, childhood development,
legal problems
FAMHX • Substance use, psychiatric illness
ROS • Auditory/visual disturbances, headache, agitation, amnesia, insomnia, sneezing, yawning, lacrimation
palpitations, chest pain, SOB, N/V/D, cramping, anorexia, paroxysmal sweats, flushing, tremor, skin infections
.
*
Sedative / N
Hypnotics
HEENT: sneezing, yawning, lacrimation, myosis/mydriasis, tongue lacerations ( seizures), head trauma, odor, temporal
wasting, dentition, parotid swelling
CV and RESP: palpitations, murmurs, arrhythmias, pericardial rub in endocarditis, abnormal respiratory patterns,
consolidation (aspiration pneumonia)
Gl: N/V/D, cachexic appearance, abdominal pain/cramping, ascites ( shifting dullness, fluid wave, edema), hepatomegaly
MSK /DERM: paroxysmal sweats, flushing, tremor, skin infections, piloerection, rash, stigmata of liver failure (caput
medusae, jaundice), IVDU track marks, signs of infection, pallor, cyanosis, diaphoresis
NEURO: reflexes, motor /sensory exam, gait
NVESTIGATIONS
Blood Work /Urine
. .
• CBC- D, electrolytes, Ca, Mg, P04, Cr urea (metabolic disturbance), ALT, AST ALP, GGT, bilirubin, lipase (liver damage, pancreatitis),
albumin ( liver function, nutritional status)
• ABG, osmolality, osmolar gap, urinalysis
.
• EtOH ASA and acetaminophen levels: urine toxicology (cannabis, amphetamines, cocaine, barbiturates, benzodiazepines, opioids,
MDMA)
Imaging/Other
• CXR . AXR. EKG
• CT head if suspect head injury
OHEATMENT
Emergent
• ABCs, IV access, intubation and mechanical ventilation if GCS < 8 or falling
.
• Supportive care (hydration, electrolytes), universal antidotes for suspected poisoning " DONT ” ( D 50W, 02 naloxone, thiamine)
• . .
Optimize nutrition - high dose IV thiamine: if investigations point to starvation state (i.e. low P04) need to monitor for refeeding
syndrome
Biological
• Monitor for respiratory depression and cardiac arrest: intubate if needed
OPIOID • Naloxone for acute overdose
• Methadone or buprenorphine long term for opioid dependence, manage chronic pain
• Closely monitortemperature and use aggressive cooling measures if hyperthermia for MDMA: monitor for
“O
STIMULANTS arrhythmias and signs of hypertensive crisis or Ml; monitor and treat serotonin syndrome in
• Benzodiazepines to THR and BP and for seizures
n
lOOmg once daily + multivitamin if withdrawal (high dose thiamine before glucose prevents
• Thiamine
IT
Wernicke’s encephalopathy): folic acid 5 mg once daily Hi
• Clinical Institute Withdrawal Assessment for EtOH. Revised ( CIWA- Ar ): if score > 8 give benzodiazepines
ETOH
-
( Lorazepam 2- 4 mg IV g 15 20 min/ Diazepam 10 -15 mg IV g 10 - 15 min in emergency): benzodiazepines for <
DTs and to prevent seizures: antipsychotics and anticonvulsants if necessary
• Assess for and treat autonomic dysfunction
• Gradual taper
BENZODIAZEPINE
• Flumenazil ( benzodiazepine antagonist ) 0.4 - lmg reverses effects of overdose
Psychosocial
• Counsel patients using principles of motivational interviewing
• Psychotherapy, behavioral modification, self -help, residential or outpatient treatment programs
.
• Detox centers, halfway houses, Alcoholics Anonymous Narcotics Anonymous Moderation Management.
• Consider consulting Psychiatry if patient on in - patient unit and history and appropriate screening suggest possible comorbid mood,
anxiety, psychotic or personality disorder
• If hospital has separate addictions service, consider consulting as well, though Psychiatrists are trained in addictions
HISTORY
ID • Name age
status
. . sex /gender, ethnicity, occupation or education source of income, living arrangements, relationship
,
>* PMHX • Chronic or debilitating illnesses, chronic pain/chronic fatigue syndromes, epilepsy, liver failure, medication side
ro effects, endocrine abnormalities, malignancy, vitamin deficiencies
JZ
u
MEDS • Medications . .
that may be used in a suicide attempt (e.g. acetaminophen, TCAs MAOIs)
> FAMHX • Suicide attempts and completion, psychiatric illness, substance use
Q. SOCIAL HX • Assess support systems
• Social isolation is risk factor ( immigrants, low SES, unemployed, living alone, divorced/ widowed/single)
• Legal Hx
• Domestic partner /family violence, young children at home
• Childhood abuse
405
MENTAL STATUS EXAM
Interview patient when medically stable and ideally when sober to properly assess intent and plan
• Appearance: general appearance may be withdrawn with poor grooming and hygiene, psychomotor agitation or retardation,
restlessness, poor eye contact, tearfulness; note if clinically intoxicated, may have decreased LOC if overdose ingestion
• Emotions: mood often depressed, anxious, frustrated, with restricted affect
• Perceptions: mood congruent hallucinations (high risk), dissociative symptoms, command hallucinations (high risk )
• Thoughts: stream often linear, may have poverty of thought, may perseverate on themes of hopelessness, worthlessness, guilt,
mood congruent delusions (high risk)
• Insight /Judgment: in schizophrenia, greater insight is associated with higher suicide risk; assess impulsivity (high risk factor )
• Safety: active vs. passive suicidal, homicidal, or infanticidal ideation
Admission Certification - Form 1
PHYSICAL Alberta - specific Legislation
.
VS GCS if patient has attempted suicide
• Holds Patient in hospital up to 24 hrs for assessment
General PE • Requires all three of the following:
• Inspection: scars on flexor surface of wrists (cutting or burning), • Suffering from a mental disorder
bruising/ scars around neck hanging old blunt
( ), trauma
• Likely to cause harm to self or others or to suffer
(fall, car crash), signs of head trauma or increased ICP. Observe for
substantial mental or physical deterioration
toxidrome patterns ( anticholinergics, opioids)
• Unsuitable for admission to a facility other than as
INVESTIGATIONS formal patient
Blood Work/Urine .
• Within 24 hrs 2nd certificate may be completed allowing
involuntary admission for up to one month
. . .
• CBC- D electrolytes, urea Cr ammonia (metabolic disturbance)
. . . .
• glucose (medical cause of altered behavior ) ALT AST ALP GGT (liver disease)
• TSH (hypo - or hyperthyroidism)
• Urinalysis ( infection)
• EtOH, salicylate, and acetaminophen levels (potential toxic ingestions)
Imaging/Other
• EKG
• Consider CT/MRI brain if suspect organic brain syndrome, head trauma, intracranial tumors
• CXR if overdose to rule out aspiration pneumonia
ULEATMENT
Psychosocial Biological
• Involuntarycertification ( see box above)
with close observation
• Involve family members /other supports • Stabilize medically, wait until sober if intoxicated to assess
Emergent
early on; provide sucidine hotline number • Antipsychotics, benzodiazepines if agitated /psychotic
• Important to document reasons if not
certifying/admitting
• Psychotherapy for underlying disorders; • Treat underlying psychiatric disorders/substance issues
CBT has evidence for secondary ( avoid meds such as TCAs and MAOIs with high fatality if
prevention of suicide ingested)
• If personality disordered, suicidal thought /
“D
self harm diary
Long-term Medications with evidence for decreasing risk of suicide: n
.
• Refer to support groups Social Work, and
other community services
• Substance abuse counseling
• Lithium in bipolardisorder
• Atypical antipsychotics especially clozapine in
—
ir
QJ
•
schizophrenia
• Contracts to safety often used in practice
but may not influence outcome
• SSRIs/ SNRIs in depression
Anxiety Disorders
.
American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 5 th ed. Washington DC: American Psychiatric Association. 2013.
. .
Crippa JA Derenusson GN et al. Neural basis of anxiolytic effects of cannabidiol (CBD) in generalized social anxiety disorder: A preliminary report. Journal
of Psychopharmacology. 2011:25(1):121- 130.
..
Geddes J. Price J McKnight R. Psychiatry . 4th ed. New York: Oxford University Press: 2012:284 - 304.
.
Sadock B J Sadock VA. Kaplan & Sadock ' s Synopsis of Psychiatry. 10th ed. Philadelphia: Lippincott Williams & Wilkins: 2007:597- 633.
. .
Schier AR. Ribeiro NP et al. Cannabidiol a Cannabis sativa constituent, as an anxiolytic drug. Revista Brasileira de Psiquiatria. 2012;34 (Supp 1):S104 - S117.
Bipolar Disorder
American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 5 th ed. Washington. DC: American Psychiatric Association. 2013.
. ..
Geddes J Price J McKnight R. Psychiatry. 4 th ed. New York: Oxford University Press; 2012:221- 245.
.
Sadock BJ Sadock VA. Kaplan & Sadock ' s Synopsis of Psychiatry . 10th ed. Philadelphia: Lippincott Williams & Wilkins: 2007:527 - 578.
Depressive Disorders
American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 5 th ed. Washington. DC: American Psychiatric Association. 2013.
Geddes J. Price. J. McKnight R. Psychiatry. 4th ed. New York: Oxford University Press: 2012:221- 245.
221-245.
.
Sadock BJ Sadock VA. Kaplan & Sadock' s Syropsis of Psychiatry . 10th ed. Philadelphia: Lippincott Williams & Wilkins: 2007:527 - 578.
Eating Disorders
.
American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 5 th ed. Washington. DC: American Psychiatric Association 2013.
. .
Morgan JF Reid F Lacey JH. The SCOFF questionnaire: Assessment of a new screening tool for eating disorders. British Medical Journal.
1999:319( 7223):1467- 1468.
.
Sadock BJ Sadock VA. Kaplan & Sadock ' s Synopsis of Psychiatry. 10th ed. Philadelphia: Lippincott Williams & Wilkins; 2007:727 - 748.
Gender Dysphoria
American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 5 th ed. Washington. DC: American Psychiatric Association. 2013.
.
Geddes J. Price J. McKnight R. Psychiatry . 4th ed. New York: Oxford University Press; 2012:434- 436.
Sadock BJ. Sadock VA. Kaplan & Sadock ' s Synopsis of Psychiatry. 10th ed. Philadelphia: Lippincott Williams & Wilkins: 2007:718- 726.
Peripartum Depression
American Family Physician. Indentificationand Management of Peripartum Depression. 2016. Available at http://www.aafp.org/afp/ 2016/0515/p852.html
American Congress of Obstetricians and Gynecologists. Screening for Perinatal Depression. 2015. Available at http:// www. acog.org/Resources- And-
Publications/Committee- Opinions/Committee-on- Obstetric - Practice/Screening- for - Perinital -Depression
BC Reproductive Mental Health Program & Perinatal Service BC. Best Practice Guidelines for Mental Health Disorders in
the Perinatal Period 2014. Available at http:// www.perinatalservicesbc.ca/ Documents/Guidelines - Standards/ Maternal/
MentalHealthDisordersGuideline.pdf
.
Sadock B J Sadock VA, Ruiz P. Kaplan and Sadock 's Synopsis of Psychiatry: Behavioral Sciences/Clinical Psychiatry. 11th ed. Philadelphia:
Wolters Kluwer ; 2015.
Suicidal Behavior
.
American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 5 th ed. Washington. DC : American Psychiatric Association 2013.
.
Geddes J Price. J. McKnight R. Psychiatry. 4th ed. New York: Oxford University Press: 2012:61- 75.
Sadock B J. Sadock VA. Kaplan & Sadock ' s Synopsis of Psychiatry . 10th ed. Philadelphia: Lippincott Williams & Wilkins: 2007:897- 923.
STATION CONTRIBUTORS
Mental Status Exam Muhammed Dhalla MD. Jasmine Pawa MD. Mim Fatmi MD
Abuse Jonathan Hamill MD. Cindy Liu MD, Jorge Perez- Parada MD FRCPC
Anxiety Disorders Jonathan Hamill MD. Cindy Liu MD. Jorge Perez - Parada MD FRCPC
Bipolar Disorders Jonathan Hamill MD. Cindy Liu MD. Jorge 3erez - Parada MD FRCPC
Depressive Disorders Jonathan Hamill MD. Cindy Liu MD. Mim Fatmi MD Jorge Perez- Parada MD FRCPC
Eating Disorders Jonathan Hamill MD. Cindy Liu MD. Jorge Perez- Parada MD FRCPC
Gender Dysphoria Jonathan Hamill MD. Cindy Liu MD. Jorge Perez - Parada MD FRCPC
Neuroleptic Malignant Syndrome Rejish Thomas MD. Jonathan Hamill MD. Sudhakar Sivapalan MD FRCPC
Personality Disorders Jonathan Hamill MD. Cindy Liu MD. Jorge Perez Parada MD FRCPC
Peripartum Depression Michaela Iverson. Amanda Aiken MD FRCPC. Melanie Marsh- Joyal MD FRCPC
Schizophrenia Spectrum Disorders Ameet Singh MD. Jonathan Hamill MD. Cindy Liu MD. Jorge Perez - Parada MD FRCPC
Substance Use Disorders Ameet Singh MD. Jonathan Ham II MD. Cindy Liu MD. Daniel Friedman MD Jorge Perez - Parada MD FRCPC
Suicidal Behavior Jonathan Hamill MD. Cndy 1 iu MD, Mim Fatmi MD Jorge Perez - Parada MD FRCPC.
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The Surgery section in the Edmonton Manual provides a focused approach to workup and
management of common surgical conditions. It is also an excellent study resource for your Surgery
OSCE and future postgraduate Surgery rotations.
You will have an excellent learning experience during your Surgery rotation.
Good luck !
DIFFERENTIAL DIAGNOSIS
RUQ • Biliary
cancer
-
tract cholecystitis, choledocolithiasis .
• Renal - cancer
RUQ EPIGASTRIC LUQ
• Liver - hepatomegaly, hepatitis, abscess, cancer Eiophagus
Uterus
Bladder
• Inguinal hernia
ISTORY
HPI • Characterize mass: size, location, onset, growth rate, associated pain, pulsatile ( AAA ), reducibility (hernia)
• N/V, bloating
• Early satiety, fatigue, jaundice ( hepatocopancreaticopilary malignancy)
• Pain: characterize onset, aggravating/alleviating factors, quality, radiation, change with bowel movements or
with meals
• Female: possibility of being pregnant
RED FLAGS • Constitutional symptoms: fever, Wt loss, night sweats
• Blood in stools: melena (black tarry feces), hematochezia (bright red blood per rectum), is the blood mixed in
with the stool or outside the stool, dripping into the toilet bowl, etc.
• Change in bowel or bladder habit
• Pulsatile mass
PMHX • Cancer, liver disease, cysts, cardiac events . Crohn’s or ulcerative colitis
PSHX • GI/GU surgeries, other cancer surgeries
Auscultation
• Gl: bowel sounds /high pitched peristalsis not related to pain episodes ( gastroenteritis, dysentery, active UC)
• Bruits ( AAA)
Percussion
•
, .
Gl: tenderness, dullness, liver size ( normal = 9 - llcm at the MCL), Castell’s sign (10 h ICS at L. anterior - axillary line) Traube's space
( splenomegaly), shifting dullness (ascites)
Palpation
• Gl: Palpate all 4 quadrants . Look for rigidity, tenderness, palpable masses, reducible vs. incarcerated hernias, pulsatile mass,
hepatosplenomegaly.
Special Tests
• DRE, bimanual examination (ovarian cyst, fibroid)
INVESTIGATIONS
Blood Work
. . . . . .
• CBC- D. BUN electrolytes Cr ALT. AST bilirubin, albumin, PT, PTT. ALP lipase (J - HCG. urinalysis
Radiology/ lmaging
• Abdominal/pelvic U/S, AXR . ± CT scan or ERCP/ MRCP if warranted
Special Tests
• Gastroscopy ( gastric tumor ), colonoscopy ( CRC . polyp), barium enema (CRC)
Further Workup
.
• Thrombocytosis ( splenomegaly), amylase /lipase (pancreas) , prostate Bx CEA (CRC screening baseline)
CRC Screening
Above Average • Asymptomatic, one 1st degree relative > 60 • FIT ql - 2 years starting at age 40
years of age at diagnosis of CRC and/or high • If FIT ( +) then colonoscopy
risk adenoma • If normal scope, wait 10 years then restart FIT
High • Family Hx of Lynch syndrome (HNPCC) • Colonoscopy q1- 2 years starting at age 20 or 10 years younger than
• Family Hx of Familial adenomatous polyposis earliest family case
(FAP) • Flexible sigmoidoscopy ql years from age 10 -12 years
• Personal Hxof IBD • First screening colonoscopy 8 - 10 years after disease onset
• Subsequent surveillance with colonoscopy ql- 2 years
in
C
Treatment of CRC era
• Radiotherapy/Chemotherapy rt>
> Not curative alone: used as adjuvant or neoadjuvant therapy in advanced stages ( Stage 3 or 4)
• Surgery
DIFFERENTIAL DIAGNOSIS
RUQ Epigastric LUQ RLQ Periumbilical LLQ
• Biliary disease • GERD • Pancreatitis • Appendicitis • Early appendicitis • Diverticulitis
• Pancreatitis • Gastritis • Gastritis • Inguinal hernia • Gastroenteritis • Inguinal hernia
• Hepatitis • Dyspepsia • PUD • Renal colic • Bowel obstruction • Renal colic
• Pyelonephritis • Pancreatitis • Pyelonephritis • IBD • Ruptured AAA* • Sigmoid volvulus
• RLL pneumonia • Pericarditis • LLL pneumonia • Mesenteric • IBD
• Subdiaphragmatic • Esophagitis • Splenomegaly adenitis • IBS
abscess • PUD * • Splenic abscess • Ovarian cyst • Ovarian cyst
• Rightsided PE * • Ruptured AAA * • Splenic infarct • PID • PID
. Ml * . Ml * • Ml * • Ectopic • Ectopic
• Aortic
pregnancy * pregnancy *
dissection*
• Ovarian torsion* • Ovarian torsion*
Diffuse: gastroenteritis, metabolic (porphyria, lead poisoning), bowel obstruction, constipation IBD. IBS. DKA \ mesenteric
ischemia *
’Indicates high morbidity/mortality
HISTORY
ID • Patient 's name age . . gender, ethnicity
CC • Abdominal pain
HPI • Onset: sudden (organ perforation or ischemia, obstruction of small tubular structure, vascular emergencies),
gradual (inflammatory or infectious process, obstruction of a larger tubular structure)
• Aggravating and alleviating/palliating factors: change with eating, bowel movements, emesis, urination,
position, deep breaths, going over bumps (peritonitis)
• Quality: burning (ulcer ), tearing ( aortic dissection), colicky (distention of a hollow tube)
• Radiation/referred pain: shoulder pain (duodenal ulcer, pancreatitis, post -op abd air ), R. subscapular area
(gallbladder disease) , back ( pancreatitis, ruptured AAA), groin ( renal colic, hip pain), periumbilical to RLQ
(appendicitis)
Site (refer to Differential Diagnosis above)
Timing: duration, constant vs. intermittent
Type of pain: visceral pain (ischemia, inflammation, distention of hollow organs or capsular stretching of solid
organs), parietal pain (ischemia, inflammation or stretching of the parietal peritoneum), referred pain
RED FLAGS Severe pain
Signs of shock (hypotension, oliguria, abnormal mental status, metabolic acidosis, cool/clammy skin)
Peritoneal signs (direct/rebound tenderness, hypoactive bowel sounds, new or worsening ascites, fever/chills)
Abdominal distention (bowel obstruction)
Blood in stool (colon cancer) or urine
Anorexia and Wt loss
Abdominal mass or organomegaly
Fever
Jaundice (biliary obstruction)
Awakening pain, nocturnal pain
PMHX GI/GU conditions, CV risk factors
PSHX Abdominal surgery ( RF for adhesions - bowel obstruction), gyne surgery
>•
<D PO& GHX LNMP, GTPAL, sexually active, method of birth control
W>
MEDS Steroids and immunosuppressants (inhibit inflammatory response to perforation/peritonitis), anticoagulants
D
LO .
(increased risk of bleeding) EtOH (hepatitis, pancreatitis)
FHX .
IBD GI/GU cancer
SOCIAL Smoking EtOH.
ROS . . .
CV: CV risk factors CAD PVD atrial fibrillation
RESP: SOB cough .
. .
Gl: constipation, diarrhea, vomiting, mucus or blood in stool GERD jaundice, anorexia/Wt loss, obstipation
GU: hematuria, dysuria, vaginal discharge
413 Edmonton Manual of Conn
PHYSICAL
General Approach
• Wash hands/perform hand hygiene, proper draping
• VS ( BP . . .
HR RR Temp Sa02) .
Inspection
• Appearance: well vs. unwell, lying still ( appendicitis/peritonitis) , rolling in pain ( biliary or renal colic), leaning forward ( pancreatitis),
jaundice ( obstruction of biliary tree)
.
• ABD: abdominal distention (bowel obstruction), surgical scars, hernias, obvious masses Cullen’s sign (ectopic pregnancy) Grey .
Turner's sign (pancreatitis), visible peristalsis (bowel obstruction)
Auscultation
• ABD: presence or absence of bowel sounds, aortic or renal bruits
Percussion
• Abdominal tenderness, costovertebral angle tenderness (pyelonephritis), flank dullness ( ascites), shifting dullness (ascites)
Palpation
• Peritoneal signs (involuntary guarding, rigidity, rebound tenderness), masses, hernias, pulsatile mass ( AAA )
Special Tests - Directed by History
• DRE - ( fecal impaction, palpable mass, occult blood in stool, or retrocecal appendix if tender and fullness on right side)
• Examination for inguinal hernias - (examine patient laying down and standing, have them cough while you palpate)
• Testicular exam in men and pelvic exam in women with lower abdominal pain
• Carnett ’s sign (patient flexes abdominal muscles - increasing/unchanged pain is a positive sign, suggests abdominal wall pain, pain
decreasing with tensing abdomen is a negative sign suggesting intra- abdominal source)
• Murphy 's sign (palpation of RUQ on deep inspiration causes arrest of breath - sensitive for acute cholecystitis)
• Obturator sign (pain with hip flexed at 90° and internal rotation). Psoas sign - pain with passive hip extension or flexion of hip
against resistance. Rovsing’s sign - pain in RLQ with LLQ palpation ( appendicitis)
INVESTIGATIONS
Blood Work /Urine Investigations
. .
• CBC- D, electrolytes, urea Cr, glucose (1-HCG ( all women of childbearing age)
.
• Upper - or mid - abdominal pain: AST. ALT, ALP bilirubin, lipase
• Urine R & M
• Blood and urine culture (in the presence of fever and unstable VS)
• INR . .
PTT cross - match ( if OR imminent )
Radiology/ lmaging
• CXR: more sensitive than AXR for free air (bowel perforation)
• AXR: bowel obstruction, volvulus, pneumatosis, biliary tree air. calcification, colitis
• U/S: unstable patients with suspected AAA. gallbladder disease, renal disease, pancreatitis, venous thrombosis, hemoperitoneum.
peritonitis, pelvic disease, imaging of choice during pregnancy
.
• CT: stable patients with suspected AAA acute appendicitis, bowel obstruction
• CT angiography: mesenteric ischemia
L REATMENT
Emergent
• . . .
ABCs: VS IV fluids Foley catheter (monitor Ins/Outs) IV ATBx (abdominal sepsis or on call to OR )
Treatment Options
• The surgical abdomen usually requires a surgical approach
• Small bowel obstruction: NPO. NG tube, analgesia, antiemetics, surgery consult
• Renal colic: most stones will pass spontaneously, analgesia, imaging to estimate size of stone, lithotripsy, ureteric stents
• Biliary colic: analgesia, usually able to see General Surgery as an out - patient for elective surgery: changes in liver enzymes or an
unstable patient requires immediate referral
• . . .
Ectopic pregnancy: frequent reassess VS type & screen Rhogam Gyne consult for evaluation - may need medical or surgical
management (oophorectomy or salpingectomy) (/ >
• Functional abdominal pain is mainly a diagnosis of exclusion and requires a multidisciplinary approach to treatment C
Referrals QTQ
. n>
• . . .
General Surgery Vascular Surgery Gynecology Gastroenterology Internal Medicine
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DIFFERENTIAL DIAGNOSIS
Common Conditions
Ankle Foot
TRAUMATIC/ • Ligament sprain • Metatarsal fractures
ACUTE • Fibular fracture • Midfoot fractures
• Fibial avulsion fracture • Calcaneal fractures
• Dislocations
• Morton’s neuroma
• Cellulitis, ingrown nail
• Calluses, corns, warts
High Mortality/Morbidity
• Pathological fracture with underlying etiology including metastatic lytic lesion, bone tumor, or osteopenia/osteoporosis
• Compartment syndrome ( Pain out of proportion .
Paraesthesia, Pallor, Pulseless, Poikilothermia)
HISTORY
ID • Patient ’s name, age, gender
RED FLAGS • Fever /chills, night sweats, Wt loss, high energy mechanism (look for further injuries)
PMHX • Bleeding disorders, arthritis, heart disease, IBD, DM
ALLERGIES • Specifically to ATBx and pain medications (NSAIDs, acetaminophen, codeine, opioids, etc ) .
FHX • Arthritis , IBD, cancer
SOCIAL • EtOH use, IVDU, physical abuse, falls (baseline gait, ambulating aids)
ROS • HEENT: headaches, vertigo, visual disturbances, fever, mental status changes, conjunctivitis
CD • CV/ RESP: palpitations, chest pain, SOB
W> • Gl: change in bowel habits, diarrhea, blood in stool, abdominal pain, cramping, anorexia
D • MSK /DERM: rash, psoriasis, sensation and motor function in ankle and foot
C/>
RISK FACTORS • Fractures: osteopenia, osteoporosis, cancer (bone mets or tumors)
02EATMENT
Emergent
• .
ABCDE life before limb, once stable tend to injuries that are not life threatening
Treatment Options
• Medical
> .
Reduce swelling ( PRICE): Pain, Rest Ice, Compression, Elevation
> Reduce fracture/dislocation ( ASAP to prevent neurovascular injury then X - ray and re -check neurovascular status)
> Tetanus prophylaxis if not up- to - date (open fracture)
> Irrigation, debridement, and ATBx (open fracture)
> Manage pain: analgesic medications
> Immobilization: ambulation aids and instruction ( if required)
> Further workup (may be required for insidious onset etiologies)
• Surgical
DIFFERENTIAL DIAGNOSIS
BENIGN • Pruritus Ani
• Anal fissure
• Hemorrhoid
Abscesses Fistula
> Internal Supralevator tracts
> External thrombosed
• Prolapse Intersphincteric
INFLAMMATORY • Crohn' s Disease Ischiorectal
• Ulcerative Collitis
Perianal
INFECTIOUS • Fourner ' s Gangrene
• Anorectal Abscess
• Gonorrhea / Chlamydia / Herpes
• Anorectal condylomas
• Enteric Infectious Intersphincteric :t s
• Proctitis Trans sphincteric® (3) @ Extrasphincteric
-
MALIGNANT • Anal Cancer Suprasphincteric
• Rectal Cancer
[HISTORY
ID • Patient ’s name, age . gender
CC • Anorectal pain
HPI • Characterize pain: onset, precipitating/aggravating factors, quality, radiation, associated symptoms and
.
timeline, pain with defecation ("shards of glass" - fissure) , how long pain lasts after defecation
• Acute ( < 3mos) vs. Chronic ( > 3mos)
.
• Associated rectal bleeding and /or mucoid discharge? if so characterize episodes
• Recent constipation or diarrhea
• Visible sores on anus
• Fevers, fluctuant masses, purulent discharge ( abscesses)
FHX .
• IBD cancer
SOCIAL .
• Smoking, sexual practices (men/ women/both, anal sex foreign body use, safe sex )
uREATMENT
Emergent
• Ensure patient is stable
• Rule out emergent and high mortality cases
• Fournier ’s gangrene - start high - dose ATBx and consult Surgery for surgical debridement
• Thrombosed external hemorrhoids may require surgical evacuation of the hemorrhoid clot with excision of the overlying skin
• Anorectal abscess requires incision and drainage of abscess
Treatment Options
• Depend on etiology:
* Functional/ fissure: Sitz bath, antispasmodic medication, stool softener, low residue diet
.
> Infectious enteric: ATBx if rare infection consider possibility of patient being immunocompromised
> Ulcerative colitis: Gl consult
> Abscess: incision, drainage, irrigate and pack. ATBx are provided for selected patients (immunocompromised).
> Gonorrhea: ceftriaxone or doxycycline
> Chlamydia: azithromycin or doxycycline
> Herpes: antiviral
.
• Surgical: thrombosed external hemorrhoid Fournier ’s gangrene, cancer, fistula, anorectal abscess, anal fissure
Follow - up
• Dependent on condition
Referrals t/>
C
• Colorectal Surgery if rectal lesion/symptomatology suspected
OQ
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DIFFERENTIAL DIAGNOSIS
Orthopedic Injury Classification Fracture Classification
Strain Tearing injury to muscle fibers
Normal bone strength but excess load
Tearing injury to one or more
Sprain Traumatic • Direct blow, axial loading, angular forces, torque
ligaments of a joint
( twisting), or combination
Normal load but weak bone
Complete disruption of a joint; loss of
Dislocation Pathologic • Neoplasms, osteoporosis, osteogenesis
contact between articular surfaces of bones
.
imperfecta Paget 's disease
Partial disruption of a joint; Repetitive forces on unadapted bone
Subluxation preservation of some degree of Stress Injury • Classically soldiers marching, long distance
contact between articular surfaces runners, patients on chronic steroids
[HISTORY
ID • Patient ' s name . age. gender, functional status occupation, handedness (for upper extremity injuries)
,
CC • Break in continuity of bone resulting in pain, instability, det reased range of motion, immobility, and possible
associated soft tissue injury (neurovascular structures, skin, muscle/ tendon, ligamentous structures)
HPI • Mechanism of injury: How did the injury occur ? High or low energy? What was patient doing? What did
.
patient hear feel, or see? What part of body was used to support the fall?
• Pain; onset, progression, quality, radiation, severity, timing, alleviating factors
• Paresthesias, numbness, cold skin
• Associated soft tissue injury: visible wounds or signs of injury (bruise, hematoma)
• Change in physical activity regimen
• Ability to Wt bear (both immediately and at presentation) , change in ROM
• Hx of previous trauma, fracture, injury, or surgery
PHYSICAL
General Approach:
• If high energy trauma, follow Advanced Trauma Life Support ( ATLS) guidelines for assessment of associated injuries: primary survey
. . . .
( Airway Breathing Circulation Disability Environment)
. .
• Stable Patient: VS (BP HR, RR, Temp Sa02), general appearance: in distress, sweating, dyspnoeic, mental status, unnatural movement
Percussion:
• Relevant for associated injuries
Range of motion:
• Active and passive ROM of joint above and below
• No need for significant ROM testing if acute fracture with pain and instability
Neurovascular status:
Open (compound) Closed Transverse
• Must be checked in all fractures pre - and post -reduction
• Strength and sensation testing, peripheral pulses, capillary refill
INVESTIGATIONS
X-ray
• At least2 orthogonal views of fracture site, with imaging of joint above N m
and below fracture. Note: ensure post - reduction X -rays also completed
• Non- Wt bearing vs. Wt bearing
Oblique Spiral Comminuted
• Negative report does not exclude injury
CT
• For better pre - op planning with complex intra - articular fractures
• For undisplaced fractures not visualized on plain XR but strongly suspected
• For pathologic fractures secondary to neoplasms
• Negative report does not exclude injury
o w
MRI
AvuHion Impaction S«9»r>«ntal
• Soft tissue visualization (assessment of ligamentous structures), undisplaced
.
fractures as with CT or osteochondral lesions
• For pathologic fractures secondary to neoplasms
u/s
• May .
be helpful for associated soft tissue injuries (e.g., rotator cuff Achilles tendon rupture)
Note: in suspected pathologic fractures, look for signs of osteopenia and malignant tumors
L REATMENT
High energy: ATLS ( ABCs); low energy: treat cause of fall (e.g., AECOPD, CHF, Ml)
.
Control pain and swelling: analgesics/anti-inflammatories (NSAIDs) narcotics (morphine), cold, elevation
Reduction of Fracture
• In ED, closed reduction under procedural sedation should be attempted
• May or .
may not require open surgery (e.g. fractures into joints require precise reduction to prevent arthritis)
-
• Ensure complete neurovascular exam of extremity pre- and post reduction and splinting
Immobilization of Fracture
• Immobilization of limb (including joint above and below fracture) with splinting (plaster, fibreglass) in ED
• Surgery: internal or external fixation, percutaneous pinning, arthroplasty (e.g., hip replacement )
Open fractures (in addition to above)
• Early ABx: Cefazolin 2g IV pre op x 1dose then 2g IV Q8h x 24 - 48h post op
• Ensure up - to -date tetanus and moist dressings
tn
• Irrigation and debridement in OR prior to operative fixation c
• Neurovascular repair era
Treat associated injuries: sprain, subluxation, dislocation CD
.
Rehabilitation: Physiotherapy Occupational Therapy <
Patients with functional impairment ( e.g., elderly patients ): geriatric /cognitive assessment, increased level of care
as required
Follow - up with Orthopedic Surgeon for union/mal - union until fracture healed and adequate return to function
DIFFERENTIAL DIAGNOSIS
Biliary Conditions
• Biliary colic: brief intermittent obstruction of the cystic duct by gallstones
> Acute onset, steady, moderate to severe RUQ pain, usually peaks at lh and decreases over l- 5 h, worse after fatty/greasy/spicy
meals, worse at night and wakes patient up. negative Murphy ’s sign, cholelithiasis on U/S. patient presents electively in clinic
• Cholecystitis: gallstone/ biliary sludge has obstructed the cystic duct leading to inflammation of the gallbladder
> Constant epigastric pain migrating to RUQ ± radiation to tip of right scapula ± worse post - fatty/greasy/spicy meal ± Hx of
biliary colic
> RUQ tenderness, positive Murphy 's sign. U/S findings ( see investigations) ± low -grade fever, anorexia, nausea, vomiting
• Choledocolithiasis: obstruction of common bile duct by gallstones
> Intermittent RUQ pain, jaundice, dark urine, acholic stools, pruritis. gallstone pancreatitis
• Cholangitis’: obstruction of the common bile duct that leads to biliary stasis, bacterial overgrowth, and biliary sepsis
> Charcot ’s triad ( RUQ pain, jaundice, fever ). Reynolds pentad (Charcot ’s + hypotension + altered mental status)
Non-Biliary Conditions
• Pancreatic cancer ’
• Pancreatitis *
’Indicates high morbitity/mortality
HISTORY
ID .
Patient 's name, age gender, ethnicity
CC RUQ or epigastric pain
HPI Hx pain: OPQRST/AAA pain assessment
Food: onset post -meal, specific types of food (fatty/greasy/spicy)
Change in stool color (pale), urine color (dark )
N/V, anorexia, diaphoresis, pruritis
RED FLAGS High-grade fever is usually only present in cholangitis (medical emergency)
PMHX Biliary colic
PSHX Abdominal surgeries
FHX Gallstones/cholecystectomy, IBD
SOCIAL .
EtOH smoking
ROS General: fever /chills, malaise, lethargy
HEENT: signs of jaundice
.
RESP: tachypnea SOB
CV: tachycardia
.
Gl: last meal, last normal bowel movement N/V, diarrhea, pale stools
MSK / DERM: pruritis, jaundice
RISK FACTORS .
Biliary colic more common in the 4 Fs: Female, Fertile, Fat and over Forty
Family history
Rapid weight loss
Total parenteral nutrition (TPN)
Prolonged fasting
Low physical activity
>
CD
OJO
3
to
421
PHYSICAL
General Approach
• Introduction, wash hands /perform hand hygiene, ask permission
INVESTIGATIONS
Blood Work
• CBC- D: normal in biliary colic. ± f WBC in cholecystitis, f WBC in cholangitis
• Cr /urea/electrolytes
• . f f
TSB LFTs / liver enzymes: normal in biliary colic: TSB and ALP mildly in cholecystitis: marked in LFTs in cholangitis
• Lipase: rule out pancreatitis, possibly increased in cholecocholithiasis if causing gallstone pancreatitis
Radiology/ lmaging
fluid, sonographic Murphy ’s sign, gallbladder
• Abdominal U/ S: biliary dilatation, wall thickening, gallstones, pericholecystic
distention
Special Tests
• ERCP for Dx and Tx intervention for choledocolithiasis. MRCP to image biliary tree, endoscopic U/S. CT abdomen. HIDA scan
UREATMENT
Biliary colic
• Hydration and analgesia during episode, elective laparoscopic cholecystectomy
Cholecystitis
• NPO for OR. IV fluids, analgesia, antibiotics, cholecystectomy or percutaneous cholecystostomy if poor surgical candidate
Choledocholithiasis:
• ERCP and sphincterotomy, elective cholecystectomy after ERCP
Ascending cholangitis
• . .
Emergency - ABCDE NPO IV fluids, analgesia, antibiotics, urgent ERCP or cholecystectomy for removal of stones, consider
percutaneous cholecystostomy if unstable
Follow- up
..
• Watch medically treated biliary patients for recurrence: surgical patients for complications (e g , infection)
Referrals
.
• General Surgery Gasteroenterology
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C
00
CO
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DIFFERENTIAL DIAGNOSIS
Human Bites
.
Streptococcus spp Staphylococcus aureus, Eikenella spp , and oral anaerobes
Animal Bites
• Cats: Pasteurella multocida , Staphylococcus spp, Streptococcus spp, and oral anaerobes
» Bartonella henselae may cause “cat scratch disease" 1- 2 wks following bite
• Dogs: S. aureus, S. viridans, P. multocida, and oral anaerobes
RISK • Cat bites: more likely to cause abscess due to deep penetration, heavily contaminated (up to 80% infection rate)
FACTORS • Dog bites: most common animal bite, up to 50% infection rate
• Human bites: most contaminated, highest infection risk
• Fight bite (closed- fist injury): often have laceration over knuckle with high rate of infection and possibility of septic
arthritis of underlying joint
• Tetanus-prone wounds ( see box below - tetanus prophylaxis)
• Rabies: fatal if untreated, important to know treatment algorithm
• If animal unknown and possible carrier, must observe animal or start rabies prophylaxis
General Approach
. .
• ABCs and VS ( BP HR RR. Temp Sa02) . KANAVEL’S CARDINAL SIGNS
Inspection Fusiform swelling
• Wound: location, size, obvious contaminants / foreign bodies, surrounding erythema, Pain on passive extension of the digit
discharge, exposed vital structures (e.g., tendon, bone)
Partially flexed posture of the digit
Palpation
• Vascular integrity: palpate peripheral pulses, check capillary refill, skin color,
Tenderness over flexor tendon
sheath
temperature
• Joints: examine ROM, ask about pain associated with active and passive movement
• Motor function: examine strength
• Sensory function: check sensation in superficial nerve distributions
• Tendons: check integrity of tendons near injury site (especially important in the hand), rule out suppurative flexor tenosynovitis
( Kanavel's Cardinal Signs)
> »
<v
W)
D
CO
INVESTIGATIONS
Laboratory Investigations
.
• CBC- D gram stain . C& S of wound site after topical decontamination
• Blood cultures if signs of systemic infection (prior to initiation of ATBx )
Radiology/Imaging
• X -rays of the affected body part to look for retained foreign body ( e.g., tooth fragment) or fractures
• Bone scan or MRI if osteomyelitis suspected
Diagnostic Interventions
• Aspirate of synovial fluid if septic arthritis suspected
L REATMENT
General Approach
• Irrigate wound deeply with copious NS via angiocatheter
• Under local anesthesia, debride devitalized tissue, drain any fluid collections
. .
• Determine if tetanus prophylaxis is indicated; if ATBx are indicated; if rabies Ig HepB Ig HepB vaccine or HIV prophylaxis are
indicated
• Primary closure is not recommended for extensive crush or puncture wounds, human bites or wounds > 12 hrs old (except on the
face)
• Saline soaked gauze packing dressings ( daily or twice daily )
Treatment options for cat, dog, and human bites
• Prophylaxis: amoxicillin- clavulanate 500mg PO tid or 875 mg PO bid x 3 - 5 d
• Infection: amoxicillin-clavulanate 875 mg PO bid x 7- 10d
• Beta -lactam allergy: doxcycline lOOmg PO bid ( 3- 5 d for prophylaxis, 7- 10d for infection)
• Longer treatment durations in osteomyelitis ( 4 - 6wks) and septic arthritis ( 3 - 4 wks)
.
• Severe infections warrant broad spectrum ATBx (e.g., ertapenem piperacillin- tazobactam) and consultation with ID specialists
Referral
•Surgical consultation warranted if:
> Deep wound with bone, tendon, or joint injury
> Wounds resulting in neurovascular compromise of distal extremity
> Complex infections
> Complex facial lacerations
Follow-up
• 2 days following initial consultation to evaluate wound and examine for complications
• Bite wound infections tend to develop early ( first 24- 48 hrs)
cn
c
cro
CD
3
Adult • Neuropathic bladder: spinal cord injury, MS, tumor, iatrogenic, medication-induced urinary retention .
Guillain- Barre syndrome
(Bladder Abnormality) • Bladder stone, blood clot, fungi, or sloughed papillae
Female Adult • .
Organ prolapse (cystocele rectocele uterine prolapse)
• Pelvic mass (tumor, fibroid, ovarian cyst), retroverted gravid uterus
(Outflow Tract • Urethral stricture/contracture: following instrumentation of urinary tract
Obstruction) • Other: urethral trauma, vaginal lichen planus or lichen sclerosis, cystitis
High Mortality/Morbidity
• Prostate cancer: spinal cord compression: acute urinary retention from any cause can lead to renal failure
Prostate Cancer - 95% Adenocarcinoma.
Diagnosis - PSA > 4.0 and irregular DRE both suggest cancer - perform transrectal U/S guided biopsy ( TRUS) to obtain
tissue samples
• Screening very controversial: screening with PSA and DRE is not recommended by current guidelines. For men 55+ screening should
be based on patient preference after discussing risks of false positive.
• .
Other factors may raise clinical suspicion about prostate cancer such as: PSA velocity % free PSA. family Hx
• Gleason grading system for core biopsy: based on prostatic cell architectural features ( not cytologic features)
> Grade 2 - 4: well differentiated, low grade. Active surveillance recommended for localized prostate cancer.
> Grade 5 - 6: moderately differentiated, mid - range grade. For localized prostate cancer, active surveillance recommended but
consider local therapy based on disease volume, patient preference, and ethnicity (see Treatment section).
> Grade 7- 10: poorly differentiated, high grade. Definitive local therapy recommended, (see Treatment section).
HISTORY
ID • Patient’s name, age, gender, ethnicity
CC • Difficulty voiding: patient may be asymptomatic with prostate cancer
HPI . . .
• Obstructive Sx (SHIP: Straining, Hesitancy Intermittency Poor stream) vs irritative Sx (FUND: Frequency .
.
Urgency Nocturia, Dysuria)
• Other symptoms including pain/dysuria, hematuria, hemospermia, incontinence (possible overflow incontinence)
RED FLAGS • Anuria, prostate cancer (bony pain, fever, night sweats, Wt loss)
• Cauda equina syndrome/spinal cord compression ( leg weakness, absent perineal sensation, fecal incontinence,
urinary retention), autonomic dysreflexia (complete spinal lesion lower than T6 - HTN, bradycardia,
vasodilation above lesion, vasoconstriction below)
• Pyelonephritis in the setting of nephrolithiasis
• Hematuria (nephritic syndrome of neoplasm)
PMHX • HTN . .
congenital abnormalities of GU tract, neurological disease, prior urologic treatments for BPH prostatitis,
retention, recurrent UTIs, trauma, stricture
PSHX • Instrumentation to the GU tract
PO&GHX • Number of vaginal deliveries, prolapsed pelvic structures
<L>) .
MEDS • Anticholinergics, antihistamines, antidepressants, antiarrhythmics anti-hypertensives, sympathomimetics,
Ctf
a-blockers, 5 -a-reductase inhibitors, ATBx
D
LO FHX • Prostate cancer
SOCIAL « Diet, EtOH, previous STIs, voiding habits, smoking
ROS • MSK/ DERM: signs of spina bifida (dimple/tuft of hair midline on the back )
RISK • Advancing age, race ( African American/Jamaican > Caucasian > Oriental), family Hx of prostate cancer
FACTORS
Percussion
• GU: suprapubic/flank tenderness
Palpation
• .
Palpable bladder, abdominal masses, supraclavicular / inguinal lymphadenopathy bony metastasis assessment
Special tests
• DRE: recommend patient lie on side curled in fetal position (higher knees = easier exam), have gloves /lubricating jelly/ tissue at
bedside
Inspection: note perineal abnormalities such as fissure, hemorrhoid, rash
Palpation: note rectal tone, presence of anal wink, do full 360° sweep of finger prior to prostate palpation: then palpate
prostate commenting on size (normal = walnut sized), firmness ( should be consistency of tip of nose: hard like a stone indicates
prostate cancer ), symmetry, and tenderness. Tenderness suggests prostatitis. Firm, irregular asymmetric prostate suggestive of
prostate cancer. Reduced rectal tone in cauda equina.
Check for blood on glove after exam ( possible Gl neoplasm)
INVESTIGATIONS
Blood Work
• .
Recommend: PSA CBC- D, electrolytes, urea Cr.
.
> Note: PSA can be falsely elevated after DRE after sex /masturbation, during/shortly after bout of prostatitis
Radiology/Imaging
• Bladder scan to assess post -void residual/bladder capacity
•Renal and/or abdominal U/ S looking for hydronephrosis/bladder pathology
Special Tests
.
• U/A. urine C& S; uroflowmetry, urodynamics cystoscopy can be done for complex cases
Surgical/Diagnostic Interventions
• TRUS ( trans - rectal U/S - guided Bx ) for all men with +ve prostate screen
L REATMENT
Emergent
• Relieve obstruction with urethral catheter (suprapubic catheter rarely needed)
• Continued obstruction may lead to ARF and /or urosepsis if infection develops
• Treat UTI if present
.
> Trimethoprims/sulfamethoxazoles (e.g., Bactrim) or fluoroquinolones (e.g. ciprofloxacin)
Treatment Options
• BPH
> Lifestyle: decrease fluid/caffeine/EtOH intake prior to bed to decrease frequency and nocturia
> Medical: alpha -l- adrenergic antagonist ( tamsulosin) or 5 alpha -reductase inhibitor ( finasteride)
> Surgical: symptomatic men failing lifestyle + medical management who have chronic /'recurrent infections or renal sequelae 2°
to obstruction/hematuria/bladder stones - Transurethral Resection of Prostate (TURP)
> If not a surgical candidate - indwelling catheter or clean intermittent catheterization (careful of UTIs)
• Prostate cancer
.
> Depending on PSA Bx Gleason grade, clinical stage as determined by DRE and considering the patient' s life expectancy, the
patient should be counseled by a Urologist regarding:
CO
1. Watchful waiting, especially if low -risk disease or short ( < 5 year) life expectancy c
2. Active surveillance with local disease and Gleason < 6, especially if low volume disease or age < 55 QTQ
(D
3. Local definitive therapy via radical prostectomy or radiation therapy (external beam radiation and /or brachytherapy) for
.
patients with intermediate or high- risk localized prostate cancer > 10 year life expectancy, and no serious comorbidity
4. Androgen deprivation therapy in combination with definitive therapy, as a monotherapy in patients with significant co -
morbidities ineligible for radiation/surgery, or as part of systemic treatment of disseminated disease. Androgen deprivation
can be achieved via surgical castration or chemical castration (e.g., GnRH agonists).
Referrals
• . .
Urology Nephrology Gynecology
.
vl miml of Cor limca Scenario 426
BREAST LUMP & CANCER SCREENING
Current Editor: Cindy Kao MSc MD
DIFFERENTIAL DIAGNOSIS
Common Conditions
DISTINGUISHING FEATURES
DIFFERENTIAL NUMBER , SHAPE,
ONSET AGE ( Y/O) CONSISTENCY, TENDERNESS RETRACTION
MOBILITY
CYSTS
Majority > 35 . Single or multiple, round, Soft or firm, elastic, usually tender,
Absent
peri - menopausal mobile may be non-tender
Most common benign Usually single, round, very
FIBROADENOMA Usually firm, rubbery, non- tender Absent
mass < 30, uncommon > 45 mobile
Usually single, irregular, may Very hard, skin changes present, May be
BREAST CANCER Incidence increases > 50
be fixed usually non- tender present
FIBROCYSTIC Common 40- 50, Usually firm, non - elastic, usually very
Nodular, ropelike, mobile Absent
CHANGES fluctuates with menses tender (pain common)
INFECTIONS
Erythema, swelling, pain, tenderness, must rule out inflammatory breast cancer (mammography, breast U/S Bx of .
-
2- 3 areas, including skin). Note: 50% of inflammatory breast cancer undetected on imaging.
High Mortality/Morbidity
• Breast cancer ( average risk 1in 8 women during lifetime)
HISTORY
ID • Patient’s name, age . gender
CC • Palpable breast mass, nipple discharge, nipple retraction, skin changes, breast pain
HPI • Onset ( when and how breast lump was discovered)
• Change in size ( fluctuates with menses - usually benign cystic change, rapid growth poor sign)
• Nipple discharge (bloody < 10% cancer, majority benign intraductal papilloma), unilateral vs. bilateral,
.
spontaneous vs induced, frequency & duration
• Presence of pain or skin changes
.
RED FLAGS • Bony pain, anorexia Wt loss, dyspnea, chest pain, hemoptysis, signs of metastasis
PMHX • Previous mammograms
• Breast cancer, benign breast disease, prior cancer radiation to breast or axillae, previous breast Bx (atypical
. .
hyperplasia DCIS, LCIS) ovarian/endometrial cancer
PSHX • Cyst drainage, lumpectomy, mastectomy, hysterectomy ± oopherectomy
PO& GHX • LMP/ LNMP, normal menstrual Hx
• Time of menarche (early < 12 y/o) & age of menopause ( late > 55 y/o)
• Nulliparity or 1st pregnancy > 30 y/o ( breast feeding Hx)
• OCP/HRT (estrogen ± progesterone)
MEDS • Rx ’n, OTC, CAM
FHX • lil degree relative with breast or ovarian cancer (age of onset, details of cancer type)
SOCIAL • Smoking . EtOH, sedentary lifestyle,high fat diet
ROS • CV: CP
• RESP: dyspnea, hemoptysis
<D
W>
• Gl: Wt loss, change in bowel habit, abdominal distension BRBPR/melena .
• GU: Pap test
3 • MSK /DERM: bony pains
CO
RISK FACTORS • Family Hx .BRCA gene mutation, personal Hx of breast cancer, older age, female gender, significant radiation to
the chest, late menopause ( > 55), early menarche (< 12), late first gestation ( > 30), nulliparous, postmenopausal
HRT/OCP x > 5 yrs (estrogen only), moderate EtOH intake ( > 2 - 3 drinks/day), smoking, sedentary lifestyle
INVESTIGATIONS
Radiology/ lmaging
• Bilateral diagnostic mammography
• Breast U/S (useful for identifying benign cysts /monitor and guided core Bx)
• MRI for "difficult to characterize" lesions
Special Tests
•BRCA1and BRCA 2 genetic testing (FHx, male breast cancer, known gene mutation, bilateral disease, age < 35 at diagnosis)
•HER - 2 and hormone receptor testing if mass is cancer ( triple negative - refer for BRCA testing)
Surgical / Diagnostic Interventions
TEST INDICATION INFORMATION
• If fluid is non - bloody and lump completely disappears: consistent with
FNA benign cystic disease (discard fluid)
All lesions likely to be cysts
(NOT DIAGNOSTIC) • If bloody or if lump remains/solid lump: formal core or excisional biopsy
recommended
CORE BX Clinically suspicious lesion:
(DIAGNOSTIC)
• Distinguish in -situ from invasive lesions
not cyst by U/ S or FNA
IIREATMENT
Treatment Options
• Radiation, chemotherapy, or combined modalities
MEDICAL
• Hormone and biological therapy ( for hormone receptor +ve cancers)
. .
• Modified radical mastectomy ( > 5 cm multiple nodes +ve large tumor in small breast, tumor - free margin not
anticipated with lumpectomy, contraindication to radiation)
SURGICAL • Lumpectomy with radiation
• Sentinel lymph node Bx. Axillary node dissection if sentinel node is + ve.
Follow-up/Referrals
• Immediate follow -up if any change in size, consistence, or appearance
• Clinical breast exam every 4- 6 wks if cystic
. . .
• Referral to General Surgery Medical Oncology Radiation Oncology Gyne if considering hormone therapy ( risk of endometrial ca)
SCREENING
SCREENING MODALITY AGE ( Y/O) RECOMMENDATION (FOR WOMEN)
CLINICAL BREAST EXAM > 40 Every yr (complimentary to mammographic screening)
< 40 Routine screening not recommended
40- 49 Assess risks and benefits on case - by -case basis
cn
50-74 Screening recommended at least every 2 yrs c
MAMMOGRAPHY
> 75 Continue screening considering comorbidities and life expectancy era)
0
Strong FHx
Screening mammograms every yr starting 40 y/o,
or 5 -10 yrs prior to the age of onset in 1st degree relative
2
BREAST SELF- EXAM ( BSE) Not generally recommended
BREAST MRI AND U/S Generally non - effective screening tools
KEY POINTS
• Use the rule of nines to estimate the total body surface area of a burn
• Be able to identify burns of different depths
• Look for signs of inhalational injury
• Determine initial fluid management using the Parkland formula 9%
• Know inidications for transfer to a burn centre 14%
18 '
•1IFFERENTIAL DIAGNOSIS
Burn Types Lund -Browder Estimation of Total Body
Surface Area of Burn (%TBSA)
• Chemical: acid, alkali • Adults (rule of .
9s): arm (9%), leg (18%) head
• Electrical: low/high voltage, . .
& neck ( 9%) ant. trunk (18%) post, trunk
lightning .
( 18%) genitalia (1%)
• Thermal: flame, contact, scald .
• Pediatrics ( < 9yrs): arm ( 9%) leg ( 13.5%),
• Radiation: medical,
.
head & neck ( 18%), ant. trunk (18%) post,
therapeutic, UV trunk (18%), genitalia (1%)
-
• Palm rule: the patient's palm is 1% TBSA
sLASSIFICATION OF BURNS
Depth Appearance Blanches Blisters Damage Surface Sensation Healing/Treatment
Superficial (1°) Pink , red Yes No Epidermis Dry Painful 3- 5 d
Superficial partial Epidermis, Very
Pink, red Yes Yes Moist 7-14 d
thickness ( 2°) papillary dermis Painful
.
Deep partial
thickness ( 2°)
Red or white No Yes
Epidermis, entire
dermis and
appendages
Moist None
> 21 d
^ incidence of
hypertrophic scar,
excision & grafting gives
best aesthetic result
White or Epidermis, dermis . Dry.
Full thickness (3°) brown, No No ± underlying None Early excision and grafting
leathery
charred structures
HISTORY
ID • Patient ’s name, age, gender
CC • Burn
HPI • Date, time, location of incident
• Mechanism of burn: thermal, electrical, chemical
• Duration of exposure
•Electrical burn: voltage, tetany, palpitations
• Chemical burn: acidic vs. basic, name of chemical
• Inhalation injury ( suspect if burned in closed space, altered LOC . carbonaceous sputum)
. ..
• Associated trauma (e g explosion, fall)
• Treatment received from time of incident to presentation
CD
W) REDFLAGS • Indications for transfer to a burn center:
=
tn
5 • 2° to >10% TBSA
• Any 3° burns
• Burns involving face, hands, feet, genitalia, or major joints
• Chemical or electrical burns (including lightning)
• Inhalation injury
• Presence of significant co- morbid illness or concomitant trauma
• Hospitals lacking qualified personnel or equipment for the care of burned children
IMMUNIZATIONS • Tetanus
SOCIAL • Occupation, place of residence, social support network, EtOH . smoking, illicit drugs
PHYSICAL
Primary survey ( ABCDE) including VS (BP, HR , RR, T. Sa02) followed by secondary survey
General Approach: remove clothing and jewelry as needed: initial dressing with plastic wrap appropriate (protects wound
but allows for examination by burn team)
• Classify burn depth and fill out burn diagram
•Estimate size of burn: rule of 9s or palm rule
•Inspection: obvious deformity, singed hairs, pharyngeal swelling, tongue edema
• Listen for stridor, hoarseness
Consult Burn Surgeon for potential transfer if any red flags present
ROS
• CV: rhythm (electrical burns may cause arrhythmias)
• RESP: carbonaceous (black) sputum, normal air entry, respiratory distress
• Gl: abdominal distension
• GU: accurate urine output, color of urine (dark brown -- > consider rhabdomyolysis)
• M5K: rule out compartment syndrome especially for electrical injuries; assess need for escharotomies
INVESTIGATIONS
Laboratory Investigations:
• CBC- D, electrolytes, urea. Cr. CK. Ca:*
• ABGs: pH and COHb ( > 10% suggests inhalation injury for non smokers )
.
• CXR EKG
Bronchoscopy (if you suspect inhalation injury)
Compartment pressure (if you suspect compartment syndrome)
DREATMENT
Primary Survey: ABCDEF
• Airway: intubation if significant inhalation injury
• Breathing: provide humidified 02 via face mask
• Circulation:
> Fluid resuscitation is required for adults with burns to > 10% TBSA ( 2 & 3° only)
> Initial resuscitate with NS or RL using Parkland formula ( 4cc / kg/%TBSA); give 1/ 2 over the first 8 h, and 1/ 2 over next 16 h
> Beyond 24h, titrate fluid infusion to U/O (0.5 cc / kg/hr in adults; lcc /kg/hr in children) and BP ( MAP > 70)
.
• Disability: assess neurologic status (GCS) orientation to person, place, time, event
• Exposure: remove all clothing to assess gross injuries and burn severity
• Keep patient warm: prevent hypothermia by increasing room temperature, infusing warm IV fluids, blankets, etc.
Secondary Survey
• CVS: electrical injuries require continuous cardiac monitoring at least 6 h post - injury
• Gl: high protein, high calorie nutrition ( via NG tube if necessary), watch for abdominal compartment syndrome with massive fluid
resuscitation
• GU: accurate U/O via Foley catheter (if rhabdomyolysis U/O goal to 200 - 300cc /h, consider adding NaHC03)
• ID: tetanus, start ABx only if evidence of infection (no role for prophylactic ATBx )
• MSK: monitor for compartment syndrome (pain with passive stretch, tightness, paresthesia)
• RESP: if CO poisoning, provide 100% 02 and nebulized bronchodilators
Wound Care
• After initial resuscitation, the care of burn patients is largely supportive. Surgery may be indicated to optimize healing and CO
aesthetic outcomes. c
• Small burns: polysporin + non - stick gauze usually sufficient CTQ
. . .
• If TBSA > 20%: topical antimicrobial dressings (e.g. silver nitrate Acticoat Sulfamylon)
CD
• Superficial burns will heal with daily dressing changes <
• Deep burns may require debridement and skin grafts
• Escharotomy may be required for deep, circumfernential burns resulting in compartment syndrome (rarely required in first 8hr )
• Chemical burns require copious irrigation
DIFFERENTIAL DIAGNOSIS
Common Conditions
• Monocular diplopia:
> Refractive error, keratoconus, cataract, decompensated congenital eso /exo -tropia, functional, dislocated lens
• Binocular diplopia:
> .
Oculomotor nerves (CN III, IV VI): ischemia. DM, aneurysm, hemorrhage, trauma, tumor
> Neuromuscular junction ( myasthenia gravis)
> EOM restriction/entrapment: thyroid related, inflammation/infection, tumor, orbital fracture
>Strabismus
High Mortality/Morbidity
• Aneurysm in Circle of Willis CN III palsy, unilateral pupil dilation (typically aneurysm of PCA)
> Pupil constriction fibers run on top of CN 111 — compressive lesion (aneurysm or neoplasm) will involve the pupil, whereas
ischemia of CN III leaves the pupil unaffected
> Association of CN VI and CN VII lower Pontine lesion
HISTORY
ID • Patient’s .
name, age gender, ethnicity
CC • Double vision
HPI • OPQRST-AAA
. . ..
• Onset: gradual vs sudden onset: any precipitating mechanisms (e g trauma)
• Pain: headaches, temple, eyebrows, scalp tenderness, TMJ pain secondary to claudication with chewing
• Quality: constant or intermittent
• Region: monocular (diplopic with only one eye open) vs. binocular (diplopia resolves if one eye closed)
-
• Severity: out of 1 10 (10 is worst)
• Timing: ability to fuse images for set amount of time
• Aggravating/alleviating factors: aggravated by certain directions of gaze; alleviated by head tilted to one side:
Associated: focal neurological symptoms
RED FLAGS • Sudden onset is suggestive of ischemia/infarct
• Involvement of multiple CNs suggests f
ICP
• Gradually worsening could suggest tumor or inflammation
• Pupillary involvement of any degree suggests a compressive lesion (rather than nerve ischemia)
• Any neurological symptoms
• Proptosis (rule out cavernous sinus fistula or thrombosis)
• Pain, headache, scalp tenderness, Wt loss, fever, chills, night sweats, jaw claudication ( temporal arteritis may
present as an extraocular muscle palsy)
PMHX • Thyroid disease, myasthenia gravis, DM, MS
• Past strabismus, amblyopia, or diplopia
• Orbital tumors, inflammation, infection, trauma
Palpation
• Temporal arteritis: palpable, bead -like temporal artery, temporal pain, scalp tenderness . TMJ pain
ROM
• EOMs: observe for limitation of movements, comparing movement of L vs. R to
determine if there is asymmetry or worsening in specific directions
.
• Assess which CNs are involved (lateral rectus - CN VI superior oblique - CN IV,
remaining - CN III)
• EOM fatigue with repeated use (myasthenia gravis): have patient gaze upwards for
60 secs
• Diplopia on R /L head tilt
Special Tests
• Determine whether diplopia is present in one eye or both: cover one eye at a time
and see if diplopia resolves ( binocular diplopia only present with both eyes open)
• Visual acuity, pupillary reactivity (light /dark ) to look for anisocoria and RAPD, visual
fields by confrontation
• Lid lag if thyroid pathology suspected
INVESTIGATIONS
Blood Work
• Thyroid testing if
signs /symptoms of thyroid disease
• Acetylcholine receptor antibody if considering myasthenia gravis
• Glucose and HgbAlC
Radiology/Imaging
• Older patients with CV risk factors and a unilateral, single CN palsy with no pupillary involvement and no other signs/symptoms
observe ( many will resolve spontaneously, if no resolution within 2 - 3 mos, should be further evaluated with CT/MRI)
.
• All other patients: CT/MRI for orbital, CN or other neurological abnormalities
• Clinical suspicion of infection, aneurysm, or acute CVA ( < 3 h) — urgent imaging, angiography
Special Tests
• Tensilon test ( for myasthenia gravis): tensilon ( edrophonium, an acetylcholinesterase inhibitor ), is given IV
• Prior to its injection, atropine may or may not be given: +ve test fatigue would disappear with tensilon ( if atropine given prior,
fatigue should not disappear )
.
• ESR CRP for temporal arteritis
L REATMENT
Emergent
• Ischemia /infarct, aneurysms, bleeds: full stroke workup, control for risk factors
Treatment Options
• As per cause
• Note: Inform patient that driving is not permitted until diplopia has resolved
Referrals
• Monocular diplopia, fractures/tumors/thyroid eye disease, binocular diplopia not due to myasthenia gravis or infarct/ischemia:
Ophthalmology
• Myasthenia gravis, or any patient with suspected ischemia/infarct: Neurology cn
• Bleed, stroke, mass: Neurosurgery c
• Facial fractures: craniofacial team ( ENT or Plastic Surgery as per hospital) 0Q
CO
3
DIFFERENTIAL DIAGNOSIS
Type Symptoms Causes/Differential Diagnosis
Feeling faint, lightheaded, • Postural hypotension
Presyncope sweating, clouded vision • Vasovagal response
• Cardiac pathology ( aortic stenosis, CHF, cardiac arrhythmias, etc.)
Feeling off - balance or unsteady • Peripheral neuropathy (often secondary to diabetes)
Disequilibrium when standing or walking • Cerebellar . .
disorder ( e.g. Ataxias Parkinsonian)
• Visual impairment
Central Vertigo Peripheral Vertigo
(often with neurological (no neurological symptoms)
symptoms)
The illusion of motion at rest; feeling • Tumor • Benign paroxysmal positional vertigo
True Vertigo ( BPPV) (vertigo lasts seconds - minutes)
as if the room is spinning around • Stroke
• MS • Meniere’s disease (vertigo lasts minutes -
• Migrainous vertigo
hrs)
• Vestibular neuronitis /labyrinthitis
(vertigo can last for days)
May be any combination • Anxiety disorder
High Mortality/Morbidity
• Cerebrovascular accident, aortic stenosis, arrhythmias, high ICP
HISTORY
ID • Patient ’s name, age, gender
CC • ‘' Dizziness," " spinning," "lightheadedness," “ unsteadiness"
HPI • Ask patient to use any other word than "dizziness" (very non- specific term)
• Onset, presence when sitting, severity, timing, direction of spinning, duration (seconds, hours, days)
• Associated otologic symptoms: tinnitus /aural fullness/hearing loss, occur only with vertigo episode or always
present
• Associated neurological symptoms: dysarthria /dysphagia .
LOC, headaches, ataxia, falls (central etiology)
• Recent . .
URTI otitis media, trauma N/V
• Travel, sick contacts, rashes, tick bites
• Presyncope, palpitations, SOB
• Changes in vision, hearing, eyes movements ( superior semi - circular canal dehiscence), oscillopsia
RED FLAGS • Syncope, angina, focal neurologic deficits, headache, diplopia
£
CD
PSHX • Any head or neck surgery
PO&GHX • LMP, if currently pregnant
W>
FHX • Stroke /TIA, brain cancer, vertigo, Meniere’s disease
CO
MEDS • ASA, aminoglycosides, loop diuretics, anticonvulsants, hypnotics, EtOH, caffeine
. .
SOCIAL • Smoking EtOH IVDU, STIs, degree/frequency of exposure to high noise levels
ROS • HEENT: ear pain/fullness, effusion, tinnitus, diplopia, facial droop, dysphagia, anxiety/depression
• CV: palpitation, signs of valve disease (low and slow pulse)
• RESP: difficulty breathing (anxiety vs. SOB)
• MSK/DERM: numbness/ weakness, uncoordinated, bull’s eye/target rash ( Lyme)
.
• Vestibulo - ocular reflex - maintains visual fixation during head movements through CN III IV. VI
.
• Cerebellar exam: finger to nose, heel shin, dysdiadochokinesis Romberg and tandem rhombus ( isolates vestibular system) , tandem
gait
• Fundoscopy to look for high ICP
• Cardiovascular examination
Special Tests
• Dix - Hallpike position test (diagnostic of BPPV): The clinician holds patient ’s head while moving patient rapidly from a sitting to
supine position, with the patient 's head hanging off the edge of the examination table - first, with the head turned 45 degrees to
one side and then repeating the maneuver on the other side. In BPPV. patient will show rotatory nystagmus lasting < 2 - 3min with
the head turned towards the affected ear.
INVESTIGATIONS/TREATMENT
Peripheral Vertigo .
• TSH syphilis screen • BPPV: Epley’s maneuver
semicircular canal)
(displaces otolith from
• Videonystagmography ( VNG)
• Dix -Hallpike maneuver . .
• Meniere’s: avoid triggers (caffeine EtOH salt
intake), supportive treatment during acute attacks
( antihistamines, antiemetics, anticholinergics), diuretics
to reduce endolymphatic fluid, surgical treatment as
last resort
• Vestibular neuronitis/ labyrinthitis: usually self -
limiting: supportive treatment ( antihistamines,
.
antiemetics) +/- short - term vestibular suppressant
(e.g. benzodiazepines)
underlying etiology - treat vestibular lesion via
Central Vertigo
• CT. MRI, carotid Doppler. EEG • Treat
surgery or radiation therapy
Psychogenic Dizziness • Clinical diagnosis /exclusion • Treat underlying psychiatric disorder
in
c
era
rD
^5
DIFFERENTIAL DIAGNOSIS
Common Conditions
Main Symptom Food Gets Stuck on the Way Down Trouble Initiating Swallowing
Type of Dysphagia Esophageal
Oropharyngeal
Sub -Type Mechanical Motor
• Progressive • Intermittent • Coughing, choking, drooling
• At first only trouble swallowing • No difference in symptoms • Nasal regurgitation
Secondary Symptoms solids, progresses to liquids between solids and liquids
• No difference in symptoms • Extremes in temperature tend
between hot or cold foods to aggravate symptoms
Neurological: stroke,
Differential Diagnosis
.
Stricture, neoplasm Schatzke’s .
Achalasia GERD, esophageal MS, myasthenia gravis .
ring, eosinophilic esophagitis spasm, scleroderma Parkinson's, cranial
nerve dysfunction
High Mortality/Morbidity
• Esophageal carcinoma, resulting aspiration pneumonia
HISTORY
ID • Patient ’s name, age, gender
CC • Trouble swallowing
HPI • Upper aerodigestive symptoms: cough, drool, nasal regurgitation, snort /sputter /sneeze with swallowing,
throat pain, odynophagia, voice changes, difficulty breathing, hemoptysis, hematemesis
• Swallowing symptoms: trouble initiating vs . food getting stuck on the way down: where does the food stick
• Intermittent (motility disturbance), constant (mechanical obstruction), occur with liquids (motility
disturbance), with solids ( mechanical), both
• Symptoms worse with hot/cold ingestions (esophageal spasm), ask about reflux symptoms
Palpation
• Head, neck, and supraclavicular lymph nodes (infectious pharyngitis, carcinoma) and muscle tenderness
• Neck masses: thyroid (goiter, nodule( s) - external esophageal compression: other masses -
external compression)
Auscultation
• Respiratory: bronchial breath sounds, tactile fremitus ( focal consolidation, pulmonary aspiration)
Special Tests
• NEURO
> Gross neuro: proximal skeletal weakness, tremor, polymyositis, cogwheeling, rigidity, shuffling gait
> .
CNS: deficits of sensory branches of V, IX, X and motor branches of V, X XI, XII involved in swallowing suggest oropharyngeal
dysphagia
> .
Check for easy fatiguability by asking patient to perform repetitive motion (e.g. eye blink, counting aloud)
» Assess patient 's balance/gait
INVESTIGATIONS
Blood Work
• CBC- D. electrolytes, urea. Cr, albumin for nutrition assessment
• Anemia is a red flag in men > 50 y/o and in post -menopausal women
Radiology/ lmaging
• Videofluoroscopic swallowing study or modified barium swallow ( for obstruction or aspiration)
• CT and MRI to evaluate suspected CNS etiologies and neck /chest tumors
• CXR (if suspecting aspiration or mediastinal mass)
Special Tests
• Reflex cough test - done at bedside to assess aspiration risk
• Esophageal pH monitoring ( GERD)
• Esophageal manometry ( to diagnose achalasia)
Surgical/Diagnostic Interventions
• Endoscopy (especially if barium swallow positive)
OEEATMENT
Emergent
• Food impaction/FB obstruction: attempt /perform Heimlich: push or pull the food bolus with forceps or endoscopy
Treatment Options
• Medical
.
Dietary modification: different food consistencies, enteral feeding NG tube feeds if unable to tolerate swallowing
Lifestyle modification: head tilt while swallowing, elevate head of bed
• Surgical
> Endoscopy with dilatation for webs and strictures
> Heller myotomy, endoscopic dilatation or botulinum toxin injection for achalasia
> Surgical resection, chemotherapy, radiotherapy for cancer: laryngectomy for intractable aspiration
Referrals
• . . . . . .
Otolaryngology Neurology Gastroenterology General Surgery Oncology Thoracic Surgery Speech Pathology Occupational . CO
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DIFFERENTIAL DIAGNOSIS
Differential Diagnosis
• Anterior epistaxis ( Kiesselbach's area)
•Posterior epistaxis
•Other upper airway or Gl bleeds
Common Conditions
• Nasal trauma
• Dry nasal mucosa
• Rhinosinusitis
• Hypertension
High Mortality/Morbidity
• Posterior epistaxis
HISTORY
.
ID • Patient 's name, age gender
CC • Nose bleed
HPI • Onset (sudden vs . gradual)
• Precipitant: trauma (nose picking/ blowing, nasal fracture), dry nasal mucosa (low humidity), topical nasal
medications ( antihistamines, steroids, illicit drugs)
• Palliating: attempts to stop bleeding if present and how long it takes to stop
• Quality (color /consistency of blood): bright, dark, clots, mucous
• Region: unilateral/bilateral discharge ( anterior epistaxis is most often unilateral)
RED FLAGS • Signs of hypovolemia ( tachycardia, hypotension, altered LOC)
• Epistaxis that does not stop with 15 mins of direct pressure
• Recurrent epistaxis
• Use of anticoagulants
• Signs of bleeding disorder (bruising, excessive bleeding from minor injuries or brushing teeth)
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Address ABCs as necessary : IV access, blood transfusions, intubation to maintain airway, etc.
Pressure
• Direct pressure (pinching soft area of nose) maintained continuously for 10 - 15 mins
Pledgets soaked with vasoconstrictive agents
Cautery (anterior bleeds only): silver nitrate sticks can be applied when bleeding site is easily visualized
Packing
• Nasal tampons
• Vaseline - soaked gauze
• Posterior foley tamponade ( Requires ENT consult)
Embolization/Surgical Ligation (Requires ENT consult )
Referrals: Otolaryngology Head and Neck Surgery
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DIFFERENTIAL DIAGNOSIS
LOWER Gl BLEED
CLASSIFICATION Bleeding distal to ligament of Trietz
ISTORY
ID • Patient’s name, age . gender
CC • Blood in the stool
HPI • Characterize bleeding onset, duration, severity, where observed (on wiping, mixed with stools, on surface
of stools, in toilet bowl),colour/consistency of stools ( black and tarry = melena, bright red = hematochezia
which is more indicative of LGIB), with every BM or episodic in nature, associated with straining
• Change in bowel habits (constipation, diarrhea, shape of stools, caliber of stool)
• Abdominal pain ( painless = diverticulosis, angiodysplasia, CRC; painful = perforation, ischemic bowel, fissure,
abscess, hemorrhoids) or mass
• Associated symptoms: constitutional symptoms, fatigue, anorexia, presyncope, dizziness, diaphoresis
PMHX • Gl bleeds
• Bleeding diathesis
• Liver dysfunction, portal hypertension
• Hemorrhoids
• IBD
• Cancer, radiation exposure
MEDS • NSAIDs, ASA, Plavix, steroids, anticoagulants, iron supplements, Pepto Bismol
.
RISK FACTORS • Long-term NSAID use, multiple comorbidities Hx of Gl bleeds
Auscultation
• Gl: presence or absence of bowel sounds
Percussion
• Gl: ascites, hepatomegaly, tenderness, gaseous distension
Palpation
.
• Gl: guarding (peritonitis: intraperitoneal bleed, perforation, ischemic bowel), hepatosplenomegaly masses, perianal inspection
• DRE ( fissures, hemorrhoids, rectal mass, melena, bright red blood on glove)
INVESTIGATIONS
Laboratory Tests
. CBC-D, INR, PTT, T& S
• .
Electrolytes BUN, Cr, liver enzymes
Radiology/ lmaging
• 3 viewsAXR
• CT abdomen
Surgical/Diagnostic Inverventions
• Colonoscopy
Special Tests
• Angiography
• RBCscan
EEEATMENT
Resuscitation
• Airway: intubate if patient unable to protect airway
• Breathing: oxygen to maintain Sa02, ventilate if prevent hypoxia
• Circulation: 2 large bore IVs, optimize hemodynamic status with fluids
>
disease.
.
Consider transfusion of PRBCs especially if unstable, Hgb < 70 g/ L, Hct < 30% pit < 50. Consider Hgb target of 90 if coronary
Out -patient Treatment ( for stable patients who do not require admission or ugent intervention)
• Colonoscopy ± endoscopy as a diagnostic and therapeutic intervention
Referrals
• Gastroenterology
• General Surgery
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DIFFERENTIAL DIAGNOSIS
Diagnostic Criteria/Common Conditions
.
• Upper Gl bleed vs. lower Gl bleed (proximal or distal to the ligament of Treitz respectively)
UPPER Gl BLEED
CLASSIFICATION Above Ligament of Treitz
SIGNS .
• Hematemesis hematochezia (rapid bleed), melena
Inflammatory
• Esophagitis
• Gastritis
COMMON
ETIOLOGY Vascular
• Arteriovenous malformation
• Dieulafoy lesion
• Aorto - enteric fistula
Trauma
• Mallory - Weiss tear
• Boerhaave's syndrome
Upper intestinal neoplasm (benign or malignant )
HISTORY
ID Patient’s name, age, gender
CC Bloody emesis
Black, tarry stools
HPI Onset - acute vs. chronic
Precipitant: vomiting/retching, trauma
.
Quality: bright red dark, presence of clots, coffee ground emesis
Severity: volume of blood in the emesis
Painless (varices, angiodysplasia, carcinoma)
Painful: sudden severe (perforation), epigastric ( PUD)
Associated symptoms: weight loss, fatigue, anorexia (malignancy), melena stools, hematochezia (brisk UGIB)
presyncope
.
RED FLAGS Recent frequent vomiting and /or retching followed by pain then blood (M-W tear)
Signs of hypovolemic shock: tachycardia, diaphoresis, altered mental status, syncope, hypotension
Unexplained Wt loss over mos or yrs (may suggest malignancy)
PMHX . . .
Previous UGIB PUD GERD H. pylori infection
Liver disease/cirrhosis
Bleeding disorders
Underlying malignancy
Recent hospitalization (significant source of stress)
> PSHX .
Gastroenteric anastomosis (marginal ulcers) AAA repair/graft ( aortoenteric fistula)
<D MEDS NSAIDs, ASA, PPI, steroids, anticoagulants, thrombolytics, OTC antacids, iron supplements, Pepto Bismol
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FHX .
Bleeding disorders, gastric malignancies H. pylori (’’runs" in the families)
to SOCIAL . .
Smoking EtOH, travel Hx diet (iron, beets, licorice, spinach)
ROS CV/ RESP: presyncope, dizziness, SOB
.
NEURO: confusion - acute (hypovolemia) vs chronic ( hepatic encephalopathy)
ABDO: increasing distension (ascites, suggestive of portal HTN)
Constitutional symptoms
RISK FACTORS Long- term NSAID use, multiple comorbidities, Hx of Gl bleeds
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PHYSICAL
General Approach
• . . . .
ABCs (resuscitation with IV fluids or PRBCs if indicated), VS (BP HR RR Temp Sa02)
• General appearance: anxious, pale, diaphoretic, active bleeding, signs of shock
Assess for signs of acute bleed, anemia, and hypovolemia
• VS: sinus tachycardia, supine hypotension (sBP less than 95mmHg)
• Orthostatic .
VS: postural pulse increment (greater than 30 bpm) postural hypotension ( greater than 20 mmHg)
• NEURO: mental status and orientation
• HEENT: facial and conjunctival pallor, dry mucous membranes
• CVS/ RESP: flow murmur
•ABDO: palpation for tenderness, rebound, guarding, peritonitis
•DRE: frank blood or melena
• MSK: palmar pallor
Assess for stigmata of chronic liver disease
• HEENT: scleral icterus, jaundice of frenulum, xanthomas/ xanthelasmas, fetor hepaticus, temporal muscle wasting
• MSK: palmar erythema, leukonychia, clubbing, Dupuytren’s contracture, asterixis
• Telangiectasia, spider angiomas, gynecomastia, testicular atrophy, peripheral edema
• ABDO: caput medusae, ascites
IONS
Laboratory Investigations
.
• CBC + differential, electrolytes, urea, Cr glucose
• INR , PTT, type and screen, cross - match if appropriate
• AST. ALT. ALT. bilirubin, albumin
Radiology/ Imaging
• 3 views AXR if peritonitis
UREATMENT
Resuscitation
• Airway: clear vomitus if present and intubate if patient unable to protect airway
• Breathing: oxygen to maintain Sa02, ventilate if prevent hypoxia
• Circulation: 2 large bore IVs, optimize hemodynamic status with fluids
. Consider Hgb target of 90 if coronary
> Consider transfusion of PRBCs especially if unstable, Hgb < 70 g/ L, Hct < 30%, pit < 50
disease.
> Insert foley to urometer ( monitor to U/O and response to fluids)
• NG tube and suction (determine UGIB vs. LGIB. caution if suspected variceal)
Medical Management
• NPO until gastroscopy or Gl consult
• Non - variceal bleeding/ulcer: Pantoprazole 80 mg IV bolus, then 8 mg IV per hour, some evidence to suggest now 40 mg IV BID
• Variceal bleeding: Octreotide 50 meg IV bolus, then 50 meg IV per hour. Ceftriaxone 1g IV daily (or ciprofloxacin)
• Hold antihypertensives, diuretics, NSAIDs
• If on anticoagulants, consider reversal:
> Vitamin K ( lOmg po/IV). FFP ( 2- 4 units IV). prothrombin complex concentrate (octaplex )
> Protamine if on heparin ( Img for every 100 units of heparin)
Interventional/surgical management
• Consult gastroenterology for EGD
> Ulcers: endoscopic hemostasis achieved with coagulation/fibrin, sealant /endoclips, epinephrine injection
> Varices: ligation/band/glue/sclerotherapy +/- balloon tamponade
Referrals CO
• Gastroenterology c
• Consult General Surgery if hemodynamically unstable despite resuscitation, shock, failed endoscopy, or high-risk endoscopic lesion QTQ
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DIFFERENTIAL DIAGNOSIS
PHYSIOLOGIC Occurs in infants, pubescent, obese, and elderly patients; often asymptomatic; may complain of pain/tender -
ness (due to proliferation); generally lasts less than 6 mos and then regresses
IDIOPATHIC Unknown cause
PHARMACOLOGIC Medications that increase estrogen or decrease testosterone; common medications include: ketoconazole,
GnRH analogues, GH, hCG, spironolactone, 5 - a-reductase inhibitors, and estrogen therapy used in prostate
cancer
CHRONIC DISEASE Due to malnutrition (renal failure, CF) or impaired hormone production/metabolism (liver disease, renal
failure, hyperthyroidism)
.
PRIMARY 5 -a-reductase inhibitors 5 - a -reductase deficiency, androgen insensitivity syndrome, congenital anorchia .
.
HYPOGONADISM hemochromatosis Klinefelter syndrome, testicular torsion, infectious orchitis, testicular chemotherapy/
radiation
TUMORS Estrogen secreting tumors ( Leydig cell tumor, Sertoli cell tumor, adrenal tumor), hCG secreting tumor (gas -
tric, lung, and renal cancers), pituitary tumor
SECONDARY Kallmann syndrome, hypopituitarism
HYPOGONADISM
PSEUDO- Enlargement of breast/chest wall for other reasons such as: lipomastia cyst, mastitis .
GYNECOMASTIA
BREAST CANCER 1-2% of breast cancer occurs in males, associated with skin dimpling, nipple retraction, nipple discharge, and
a hard, immobile mass
ISTORY
ID • Patient 's name, age (pubertal, older age)
CC • Nipple swelling/breast mass/increased breast tissue
HPI • Onset
• Change in size, fluctuations
• Nipple discharge
• Pain (unlikely in carcinoma)
RED FLAGS • B symptoms, bloody nipple discharge, fixed/hard lump ( breast cancer )
-
MEDS • Estrogens, estrogen synthesis enhancers (exogenous testosterone), anti androgens (spironolactone,
chemotherapeutics), digoxin, and any OTC or herbal medications, long- acting psychotropics
FHX • Gynecomastia (present in 1/ 2 of .
physiological cases), breast cancer BRCA 2 mutation
SOCIAL • Anabolic steroids, marijuana, EtOH, opioids
• Malnutrition (refeeding gynecomastia)
• Occupational, dietary exposure to estrogen
> ROS • HEENT: headache, visual changes, diaphoresis
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• RESP: dyspnea, hemoptysis
• Gl: abdominal pain, change in bowel habit (hyperthyroid)
• GU: testicular pain/trauma/enlargement, libido, erectile dysfunction
• MSK/DERM: jaundice (liver disease), bony pain/back pain (metastatic cancer )
• Other: heat intolerance, nervousness, tremors (hyperthyroid)
.
RISK FACTORS • Adolescence, obesity, elderly, liver disease, renal disease, hyperthyroid Klinefelter ’s syndrome, recreational
drugs
> True breast tissue is characterized by concentric rubbery/ firm tissue around the areola
> Hard, immobile masses and/or lymph nodes raises suspicion for breast cancer
HEENT • Inspect for signs of hyperthyroidism (exophthalmos, goiter ) , cirrhosis (scleral icterus, jaundice)
• Palpate thyroid, cervical lymph nodes
• Assess breath sounds (metastatic lung cancer rarely presents with abnormal breath sounds)
CVS/Resp • Inspect for signs of liver disease (ascites, caput medusae, telangiectasias)
• Palpate for enlarged liver and spleen, assess for shifting dullness if ascites suspected
Abdo • Inspect for testicular enlargement/atrophy, ambiguity
• Palpate for testicular tenderness, masses, size
GU • If pubertal/pre -pubertal: assess Tanner staging
• Look for signs of androgen insufficiency: signs of anemia and muscular atrophy
• Look for signs of feminization: spider nevi, palmar erythema, loss of eustachian hair
INVESTIGATIONS
Blood Work (individualize to patient presentation)
In adolescent males, investigations are
• Testosterone ( total and free)
not warranted unless:
> If low, look at SHB
> Primary hypogonadism: low T, high FSH/ LH • Breast mass > 4cm or rapid progression
Radiology/ lmaging
Breast U/S and mammography if breast cancer is suspected
•
.
See above indications for testicular U/S CXR, abdominal CT
•
Surgical/Diagnostic Interventions
• Fine needle aspiration, core Bx if cancer suspected
TREATMENT
Medical
• Surveillance of otherwise healthy adolescent boys
• Discontinuation of offending drugs
• If due to low testosterone: androgens (testosterone), anti-estrogen (clomiphen) , estrogen antagonist ( tamoxifen) Note: most .
effective if initiated within 1year of onset.
• If due to chronic disease, treat underlying cause
Surgical
• Consider for cosmetic purposes
Follow -up
• Asymptomatic and pubertal gynecomastia require reassurance and reevaluate in 6 mos
• If patient on medical therapy, reevaluate and assess response to therapy (e.g., follow -up in 3 mos with tamoxifen)
Referrals
• General Surgery, Endocrinology, Urology, Neurosurgery in
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Non- trauma
• Joints: osteoarthritis, RA
• Nerves: carpal tunnel syndrome
• Tendons: DeQuervain’s tenosynovitis, trigger finger
• Other: ganglion cyst, Dupuytren's contracture
HISTORY
ID • Patient 's name, age, gender, occupation, hand dominance
CC Trauma Non-Trauma
HPI • When, where, how did the injury occur? • Pain Hx (onset, provoking/palliating factors, quality, region/
• Any unusual sounds or sensations? radiation, severity, time of day, treatments)
• Dominant or non- dominant hand injured? • Progression of symptoms, in what order?
• Other injuries or open wounds? • Any other joints affected?
• What treatment has been administered? • How is function affected?
• Tetanus status
PMHX • Previous trauma to hand/ wrist • Arthritis, bleeding diathesis, diabetes, thyroid
PHYSICAL
General Approach
• . . ..
ABCs VS ( BP, HR RR T Sa02), general appearance of the patient Important Things to Rule Out
• Expose hands, forearms adequately (remove splints, casts, dressings, etc.) • Skeletal instability/ joint dislocation
Inspection • Compartment syndrome
• Posture/resting cascade of the hand
• Actual or threatened skin loss
• . .
SEADS: Swelling, Erythema Atrophy Deformities Skin changes . •
•
Neurovascular injury
Tendon injury or infection
• Bony alignment, lacerations, surgical scars
If present, seek specialized care
Palpation (i.e., Plastic Surgeon)
• Vascular: radial and ulnar pulses, capillary refill, temperature, color of the skin
• Motor : check strength of muscles supplied by median, ulnar, and radial nerves
• Sensory: check sensation in territories supplied by median, ulnar, and radial nerves
• Joints: palpate for bony deformities, effusions, tenderness: assess pain with axial loading
• Tendons: palpate for fibrosis, nodules, tenderness, flexion/extension
• Ligaments: assess joint stability
ROM
• Check active ROM for all joints in the hand
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OJO > Quick screen: ask patient to "make a fist ” then " straighten out your fingers": visualize dorsal and volar surfaces looking for
D rotation, scissoring, decreased or abnormal flexion/extension, assess for pain against resisted flexion/extension
CO • Check passive ROM if there was any abnormal movement on active ROM
• Isolate FDP/FDS tendons in each finger and test function ( flexor digitorum profundus / flexor digitorum superficialis)
OSTEOARTHRITIS • Bony enlargement of PIP/DIP joints ( Bouchard/Heberden nodes), stiffness, I • Hand X -ray ( 3 views)
ROM: pain/stiffness exacerbated by activity, relieved by rest
RHEUMATOID • Swelling of PIP and MCP joints, usually > 1 joint, symmetric, morning stiffness . • Clinical diagnosisESR . .
serologies (RF etc.), hand
ARTHRITIS ROM X -rays
NERVE
CARPAL TUNNEL • Sensory changes and weakness in median nerve distribution: positive Phalen's • Nerve conduction studies .
SYNDROME or Tinel’s signs EMG
BOUTONNIERE
DEFORMITY
• PIP in flexion . DIP hyperextended • Clinical diagnosis
DEQUERVAIN’S • Positive Finkelstein test: knife - like pain just proximal to the radial styloid when • Local anesthetic block at
TENOSYNOVITIS thumb is clasped in palm and wrist forced into ulnar deviation radial styloid should T pain
MALLET FINGER • DIP held in flexion: inability to actively extend • Clinical diagnosis
TENDON
STENOSING • Local anesthetic block
• Loss of smooth motion of PIP joint: catching, snapping or locking: palpable at flexoc tenosynovium
TENOSYNOVITIS
nodule proximal to MCP joint
( “TRIGGER FINGER ") should pain *
SWAN NECK
DEFORMITY
• .
PIP hyperextended DIP in flexion • Clinical diagnosis
DUPUYTREN'S • Nodular thickening of palmar fascia, flexion contracture, palmar pits, knuckle
• Clinical diagnosis
CONTRACTURE pads (commonly D5 > D4 > D3)
OTHER
GANGLION CYST • Cystic swelling usually on dorsal aspect of hand / wrist
• Trans -
illumination or cyst
aspiration
INVESTIGATIONS
Blood Work: CBC- D, ESR, rheumatoid factor Position of Safety
Radiology/ lmaging MCP joints in 70- 90° of
• Hand X -ray with AP, lateral, and oblique views flexion
• CT/ MRI wrist for complex carpal fractures and dislocations IP joints in extension
Special Tests: nerve conduction studies, electromyography (EMG) Wrist in 20- 30° extension
L REATMENT
Emergent: ABCs, life before limb
Medical Treatment
• Reduce fractures or dislocations ASAP to prevent neurovascular injury
• Irrigation, debridement, ± antibiotics for lacerations and open fractures
• Tetanus prophylaxis if indicated
• Analgesics, anti -inflammatories
• Reduce swelling: Rest. Ice, Compression. Elevation
• Splinting: depends on type of injury: when possible, use position of safety ( see box )
• Early motion is often crucial to rehabilitation so physiotherapy recommended cn
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Surgical Treatment
OQ
• Complex dislocations and fractures may require CRPP (closed reduction and percutaneous pinning) or ORIF (D
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HEAD TRAUMA
Current Editor: Isabelle Colmers
DIFFERENTIAL DIAGNOSIS
• Traumatic brain injury
• Skull fractures (linear vs. depressed vs. penetrating; orbital, facial, basilar)
• Contusion/hemorrhage/hematoma (epidural, subdural, subarachnoid)
HISTORY
ID • Patient ’s name, age, gender, handedness, occupation
CC • Head trauma
RED FLAGS • Depressed or changing mental status, focal neurological deficits, depressed skull fracture, penetrating
head injury, seizures
• Abnormal VS, including hypo /hypertension
• Cushing’s triad (increased ICP): systolic hypertension, bradycardia, respiratory depression
PMHX • Previous seizure or other neurological/psychiatric disorders
• Bleeding diathesis
PO&GHX • Pregnancy status
MEDS • Anticoagulants, vaccination status ( tetanus)
> Mental status examination: assess LOC using GCS, (orientation x 4 - person, place, time, event ), perform MMSE if appropriate
> Cranial nerve exam: pupillary response, corneal reflexes, extraocular movement, conjugate gaze, oculocephalic (doll’s eyes)
reflex, oculovestibular reflex (cold caloric test), gag reflex, response to central pain
> Gross/fme motor evaluation: muscle power, tone, bulk: decorticate ( flexor ) or decerebrate ( extensor ) posturing
.
> Reflexes: superficial and deep tendon reflexes: pathologic reflexes ( Hoffmann's Babinski’s, clonus, frontal release signs)
> Sensory: pain, light touch, vibration, temperature, proprioception: dermatomal distribution of deficits
.
> Cerebellar: dysdiadochokinesis, finger - to -nose heel -shin draw, Romberg’s test
> Gait evaluation: stance, pathologic gait ( festering, wide - based, antalgic, slapping), tandem walking
• CV: auscultate for dysrhythmia, muffled heart sounds, sustained JVP (if pericardial effusion)
• RESP: respiratory pattern, inspect for signs of associated chest trauma
• Gl: bowel sounds, abdominal tenderness, distension, guarding, rigidity
• MSK: inspect and palpate for evidence of external trauma ( fractures, hemorrhages, IV drug abuse)
INVESTIGATIONS
Laboratory investigations
• CBC- D, electrolytes, urea, Cr, glucose, INR , PTT, fl- HCG
• Consider EtOH /toxscreen, Mg, Ca, P04, troponin, CK -MB, lactate
Diagnostic Imaging
• C- spine X -ray (refer to Canadian C- Spine Rules for clinical decision making protocol)
• CT head ( refer to Canadian CT Head Rules)
> Unstable patients cannot go to CT scanner
> Epidural hematoma on CT: immediately visible (epidural hematoma from middle meningeal artery) vs. delayed presentation
(epidural or subdural hematoma from venous injury)
> Repeat CT in 4 - 8 hrs if any intracranial hemorrhages, coagulopathies, or if patient fails to improve, or sooner if patient
deteriorates
uSEATMENT
Primary Survey: ABCDE and continued assessment of VS ( BP, HR, RR, Temp, Sa02)
• Airway: Intubation if patient unable to protect airway: C- spine precautions
.
• Breathing: Provide oxygen to maintain Sa02 ventilate if intubated to prevent hypoxia
• Circulation: Obtain vascular access ( 2 large bore IVs) and optimize hemodynamic status with fluids and vasopressors if necessary,
cardiac monitoring, control bleeding
• Disability: Assess neurologic status (GCS), ensure C-spine precautions
• Exposure: Expose patient as necessary to allow for assessment and management of associated injuries
Specific therapy is directed at the underlying injury
• Pain control and sedation as necessary
• Elevated ICP: mannitol lg/kg IV
• Seizures: Dilantin, phenytoin, or divalproic acid
• Reverse anticoagulation: warfarin - give Vit K, prothrombin complex concentrate (Octaplex), FFP
• Open skull fractures/burr hole /subdural hematoma: ATBx (cefazolin) in
• Any laceration: tetanus toxoid (if not immune or if unsure) c
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KEY POINTS
• Hematuria is a broad differential diagnosis
• History and symptoms may point to common, treatable conditions
• Persistent hematuria or high-risk patient factors necessitate further investigation
DIFFERENTIAL DIAGNOSIS
• Gross hematuria: visible to the naked eye
• Microscopic hematuria: RBCs visible only microscopy (considered abnormal if > 3 per HPF present in 2 or 3 samples)
• . .
Glomerular hematuria: Proteinuria ( > 500mg of protein/day in urine) > 80% dysmorphic RBCs red cell casts, brown cola - colored
urine with gross hematuria
• Positive dipstick without cells on microscopy: myoglobinuria ( rhabdomyolysis) or hemoglobinuria ( intravascular hemolysis)
• Dark urine with negative dipstick and no cells on microscopy: beets, food dyes, drugs (e.g. rifampin) , porphyrin, alkaptonuria,
bilirubinuria
• Presence of blood clots highly suggestive of a non- glomerular cause of hematuria
Common Conditions
Pre-renal Glomerular Upper Urinary Tract Lower Urinary Tract
• Exercise hematuria • IgA nephropathy * • Renal cell cancer • Bladder cancer
• Anti -coagulation • Thin basement membrane • Nephrolithiasis * • Prostate cancer
• Neoplasm • Hereditary nephritis • Pyelonephritis • BPH *
• Thromboembolism • Focal glomerular nephritis • Polycystic kidney • Cystitis *, prostatitis,
• Coagulopathy • Post -infectious • Ureteral stricture urethritis
glomerulonephritis • Renal trauma • Polyps
• Anti- GBM disease • Sickle cell • Schistosomiasis
.
• Systemic ( vasculitis SLE) • Papillarynecrosis • Urethral strictures
.
• Infection (TB STIs * ) • Trauma
• Trauma
HISTORY
ID . .
• Patient 's name age gender
CVS
• Renal bruits ( RAS)
Gl
• Abdo exam: R or L sided tenderness (ureteric stone) , suprapubic tenderness (cystitis)
• DRE ( prostate Ca)
GU
• Flank tenderness (pyelonephritis)
• Palpation of kidneys ( renal cysts, polycystic kidney disease)
• External genitalia: pelvic exam ( women)
MSK
• Bony tenderness ( metastases)
• Lymphadenopathy, esp. inguinal nodes
INVESTIGATIONS
Laboratory Investigations
• CBC -D, electrolytes, urea, Cr, PTT, INR
Urine
• Urine dipstick: to diagnose microscopic hematuria, pyuria, proteinuria
• Urine microscopy: to confirm presence of intact RBCs and RBC casts
• Quantification of proteinuria ( 24 hr urine protein or spot urine protein: creatinine ratio)
• Urine C & S: if urinary infection is suspected
• Urine cytodiagnostics: examination of exfoliated cells in urine for transitional cell carcinoma (recommended in all adult patients
with unexplained hematuria), detects presence of dysmorphic RBCs
Radiology/ Imaging
• Multi - detector CT urography: preferred imaging technique of the upper tracts for patients > 40 yrs or those < 40 yrs with known risk
factors for genitourinary malignancies
• U/ S: indicated in low risk patients, pregnant women, and those with a contraindication to iodinated contrast administration
• KUB: can be used in low - risk patients
Special Tests
..
• Cystoscopy: recommended in all high- risk patients with unexplained hematuria (i e , those with any red flags)
• Renal Bx: patients with signs of glomerular disease (refer to nephrology)
DEEATMENT
Common Conditions
•Nephrolithiasis - majority of stones pass on their own (especially if < 5 mm in diameter )
> Analgesia +/- alpha blocker (i.e., tamsulosin)
> Urologic intervention occasionally required: shockwave lithotripsy, laser lithotripsy, ureteroscopy, percutaneous
nephrolithotomy
• STIs - test and treat if suspicion
swab or urine culture, abstain from intercourse during treatment, notify public health (contact tracing)
> Chlamydia: azythromycin lg PO xl or doxycycline lOOmg PO BID x 7 days
Gonorrhea: cefixime 800mg PO xl or ceftriaxone 250mg IM xl
• BPH - a- adrenergic antagonists (i.e., tamsulosin) , 5 - a -reductase inhibitors ( i.e., finasteride) , TURP
.
• Cystitis - urinalysis, C & S appropriate ATBx accordingly
(/ >
• IgA nephropathy - may or may not require treatment: BP control, ACEi/ARB to slow progression, glucocorticoids / C
immunosuppressive therapies
CTO
Follow - up CD
• Patients with asymptomatic microscopic hematuria and negative radiology, cytology, and cystoscopy should be followed up with
urine cytology and urinalysis at 6, 12, 24, and 36 mos.
• Some centers recommend repeat U/S and cystoscopy at one year in high- risk patients with persistent hematuria
Referrals
• Glomerular disease: Nephrology; other causes of hematuria: Urology
DIFFERENTIAL DIAGNOSIS
Diagnostic Criteria
Epigastric Hernias
• Hernia: A weakness or defect through which there may be an abnormal
.
protrusion of an organ (e.g. bowel).
> Reducible: hernia contents are capable of being returned to their usual Incisional
anatomic site either spontaneously or manually
> Incarcerated: unable to reduce hernia, may cause obstruction Umbilical
> Strangulated: vascular supply of bowel is compromised ( ischemia)
• Rule out mimicking conditions Indirect-
inguinal
> Ventral hernias: rectus diastasis (a weakening of the linea alba and stretching
of the rectus abdominus muscles, there is no fascial defect ), tumor (e.g.. Direct -
Desmoid tumour, abdominal wall sarcoma), hematoma inguinal
> Groin hernias: testicular torsion, epididymitis, adenopathy, ectopic testes,
lipoma, testicular tumour, varicocele, hydrocele, spertmatocele round. Femoral
TT
JL 1STORY
ID . . gender, ethnicity
• Patient 's name age
CC • Swelling, fullness, or aching at the hernia site
HPI • Site of hernia
• Onset, precipitating events (heavy lifting .
Valsalva maneuver), evolution (growing in size, stable), size changes
during the day
• Associated pain: OPQRST and effect on daily activity
• N/V, change in bowel habits, presence of flatus, hematochezia, melena stools
RED FLAGS • Severe abdominal pain, focal peritonitis, fever, overlying skin is warm and erythematous (strangulation)
• N/V, constipation, obstipation (obstruction)
PMHX • Chronic cough, constipation, obesity, ascites (increased intra -abdominal pressure)
• Previous hernia
• Chronic disease (cardiac, respiratory, renal .HTN, DM), bleeding diathesis (surgical considerations)
PSURGHX • Previous abdominal surgery, gyne surgery, inguinal surgery, herniorrhaphies
PO&GHX • GTPAL, previous /current pregnancies
MEDS • Anticoagulants, steroids (surgical considerations)
<D)
W FHX • Hernias, connective tissue disorders
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SOCIAL • Smoking (cough) . EtOH. occupation (heavy lifting)
RISK FACTORS • Increased intra-abdominal pressure - chronic cough, heavy lifting, Valsalva maneuver, obesity, pregnancy,
constipation, ascites
• Previous hernia repair
• Congenital abnormality - patent processus vaginalis
Palpation
• Palpate the hernia sac with finger pads, assessing size, shape, consistency, and warmth; ask the patient to cough or strain ( a soft
impulse tapping against fingers is indicative of a hernia)
• Determine relationship of hernia sac with respect to inguinal ligament by palpating from ASIS to pubic tubercle, and with respect to
the external inguinal ring in males by digital inspection via the scrotum
> palpable mass below the inguinal ligament is most likely a femoral hernia
> palpable mass in the inguinal canal is most likely an inguinal hernia
• Assess whether hernia is reducible or not
Auscultation
• Absent or high - pitched bowel sounds may indicate an obstruction
Special Tests
• DRE to rule out other pathologies
• Testicular transillumination (rule out hydrocele)
INVESTIGATIONS
As needed directed by history and physical (not necessary in most cases)
Laboratory Investigations
• CBC- D: leukocytosis with left shift may occur in strangulation
Radiology/Imaging
• CXR: looking for free air under the diaphragm (if incarcerated or strangulated hernia is suspected)
• AXR: to diagnose small bowel obstruction or identify areas of bowel outside of the abdominal cavity
• U/S: differentiate masses in the groin vs. abdominal wall vs. testicular source of swelling
• CT: if unable to appreciate hernia on physical exam due to body habitus
uiiEATMENT
Conservative
• Hernia belt: maintains hernia in reduced state, alleviates pain to allow for activity while awaiting consultation/treatment
Elective surgery
• Elective surgery indicated for symptomatic hernias -
pain/discomfort
• Goal isto prevent strangulation, provide symptom relief and cosmesis
-
• Dependant on risk benefit assessment
• Note: femoral hernias should be eventually repaired in patients who are fit for surgery due to high risk of strangulation
Referrals
• General Surgery CO
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CD
2
DIFFERENTIAL DIAGNOSIS
Common Conditions
Groin/Anterior Thigh Pain Posterior Hip Pain Lateral Hip Pain Non- hip Pain
• OA . RA • Lumbar degenerative disc • Trochanteric bursitis • Inguinal hernia
• Osteonecrosis disease • Hip abductor weakness • Gl pathology ( appendicitis,
• Hip fracture, dislocation • Facet arthropathy, spinal
stenosis
(especially gluteus medius) .
diverticulosis IBD)
• Pelvic, femoral fracture • Meralgia paresthetica • GU pathology ( UTI,
• SI joint pathology • Iliotibial band syndrome nephrolithiasis, prostatitis)
• Acute synovitis
• Hip extensor or rotator • Referred from lumbar spine
• Septic arthritis
muscle strain • Aortoiliac vascular occlusive
• Osteomyelitis
disease ( Leriche’s syndrome)
• Femoroacetabular impingement
• Labral pathology
. .
Note: In pediatric patients, must consider: SCFE hip dysplasia Legg-Calve - Perthes disease
ISTORY
ID • Patient 's name, age, gender, occupation
CC • Groin pain, anterior thigh pain, lateral hip pain, buttock pain, inability to Wt bear
HPI • Mechanism of injury
• Onset/duration of pain (acute, chronic, progressive)
• Provocative and palliating factors (OA worse with activity, relieved by rest )
• Radiation (distally down the femur or up to the pelvis)
• Severity ( affect on ADLs)
• Site (groin and anterior thigh, posterior hip .
lateral hip)
• Timing: morning stiffness of lessthan 30- 60 mins (osteoarthritis), constant pain especially at night
(infection/ inflammation/ neoplasm),"start up pain" ( trochanteric bursitis/loosening of the cup or stem
from previous THR)
• Associated symptoms: fever, chills, sweats, fatigue, Wt loss, involvements of other joints
RED FLAGS • Systemic symptoms, Hx of cancer, Hx of significant trauma
PMHX • Developmental dysplasia of .
the hip osteoarthritis, inflammatory arthritis, previous femoral /pelvic
fractures, previous hip dislocations, trauma, pelvic irradiation, thrombophlebitis, syncope PVD .
PSURGHX .
• Previous THR hip surgery, spinal surgery
laHYSICAL
General Approach
• Ask permission to perform physical exam, wash hands/perform hand hygiene, proper draping and exposure
• . . . .
VS ( BP HR RR Temp Sa02)
Inspection
> .
• Gait: antalgic. Trendelenburg, short leg limp non- Wt bearing
• Note any leg length discrepancy, obvious deformity, shortening, rotational deformity, pelvic tilting, degree of lumbar lordosis, spinal
0) scoliosis, muscle atrophy
bo
• Check pelvic obliquity: asymmetry of iliac crests seen with leg length discrepancy, pelvic fracture, scoliosis, unilateral paraspinal
D
CO muscle spasm
. .
• Remember SEADS: Swelling Erythema / Ecchymosis. Atrophy/Asymmetry of muscle Deformity Skin changes /Scars .
• Inability to change position (e.g., climbing the examination table) suggests severe hip arthritis, osteonecrosis, metastatic disease,
dramatic muscle weakness, dramatic radiculopathy or infection
Sensory
• Paresthesia /hypoesthesia of the anterolateral thigh without impaired reflexes or muscle weakness ( meralgia paresthetica)
Reflexes
• Impaired reflexes ( radiculopathy )
Special Tests
• Trendelenburg test: positive test indicates hip abductor weakness, hip joint pathology
• Patrick ’s test ( FABER): positive test indicates hip joint pathology, SI joint pathology, or iliopsoas spasm
• Impingement test ( FADIR ) for anterior and posterior impingement is highly sensitive for femoral acetabular impingement
• Always examine the joint above and below and in case of fracture; always examine other extremities, pelvis, and spine looking for
other fractures/injuries
INVESTIGATIONS
Laboratory Investigations
• In the presence of systemic symptoms: CBC- D. ESR, CRP
• In trauma: follow ATLS protocol
Radiology/ lmaging
• AP pelvic X -ray: identify fractures, dislocations, osteoarthritis, osteonecrosis, lytic bone lesions
• AP/cross- table lateral hip X-ray: identify fractures, dislocations, osteoarthritis, osteonecrosis, lytic bone lesions
• CT: identify fractures, dislocations, infiltrative bone lesions
• MRI: identify soft - tissue injuries, stress fractures, osteomyelitis, osteonecrosis, tumor, labral pathology
• Bone Scan: useful in suspected fracture or AVN not seen on plain X -ray, when MRI not available/contraindicated
• Ultrasound: helpful for bursitis, joint effusions, functional causes of hip pain, therapeutic imaging guided hip injections and
aspirations
Surgical/Diagnostic Interventions
• Hip aspiration: recommended with acute and severe hip pain or other evidence suggestive of infection
IIREATMENT
Condition Treatment /Medications
Osteoarthritis • Exercise program (cardiovascular, Tai Chi), thermal agents, Wt loss counseling, patient education,
analgesia, intra - articular corticosteroid injection
in
Hip Dislocation/ • Analgesia, reduction, rehabilitation and physical therapy c
Fracture • Nonsurgical (stable fracture/patient too unstable): analgesa, bed rest era
• Surgical (based on type offracture): reduction + percutaneous pinning (intracapsular), compression hip <T>
screw/itramedullary nail (intertrochanteric), IM nail (subtrochanteric), rehabilitation 2
Bursitis • Activity modification, NSAIDs, walking aids, physical therapy, intrabursal corticosteroid injection
Septic Arthritis • Cloxacillin 2g IV Q4hr x 2-4 weeks +/- Ciprofloxacin 750mg po BID. Aspiration of joint.
Referrals
• . .
Orthopedic Surgery Rheumatology Sports Medicine, Internal Medicine (e.g., fall in elderly )
DIFFERENTIAL DIAGNOSIS
Clinical jaundice does not occur until serum bilirubin > 40 pmol/L (twice upper limit of normal)
HISTORY
ID • Patient ’s name, age, gender
RED FLAGS jaundice in elderly with constitutional symptoms (cancer ) , febrile jaundice, altered mental status,
• Painless
Gl bleeding (gross/occult), severe RUQ pain
PMHX • Hepatitis, cirrhosis, gallstones, hemoglobinopathy, G6PD deficiency, IBD, infiltrative disorders, HIV, travel
Hx, blood transfusion ( before 1990), autoimmune disease
PSURGHX • Abdominal surgery (especially gallbladder surgery)
PO&GHX • Gravid female
MEDS • Drugs and toxins that affect the liver including herbal medications, acetaminophen, methotrexate,
amoxicillin, amiodarone, statins, rifampicin
FHX • Liver disease, gallbladder disease, hemolytic disorders, autoimmune disease
SOCIAL • EtOH, exposure to .
toxic substances, hepatitis/HIV risk factors (i.e , IVDU, sexual Hx, needlestick exposure,
tattoos, and piercings), place of birth/ travel to endemic areas
ROS • Changes in mental status ( hepatic encephalopathy)
• Constitutional symptoms (primary or secondary liver /pancreatic cancer)
0)
&J0
D
CO
Inspection
• Jaundice of sclera, frenulum, skin
• Assess for stigmata of chronic liver disease
INVESTIGATIONS
Blood work
• CBC- D, urea, electrolytes, Cr
• Serum bilirubin ( total, unconjugated) Interpreting Liver Enzymes, LFTs
• .
AST ALT, ALP, albumin, INR PTT. • Liver enzymes: ALT AST, ALP, GGT
• Consider the following
> Hemolysis: LDH, haptoglobin, peripheral smear, retie count,
• Liver function tests: albumin, bilirubin, INR
.
bilirubin DAT • Predominantly hepatocellular: AST and ALT elevation
• Predominantly cholestatic: ALP and GGT elevation
» Hepatitis: HAV IgM and IgG, HBsAG, HBsAB, HBcIgM, anti-
.
HCV CMV EBV . • AST: ALT > 2: alcoholic liver disease
• AST: ALT > 4: Wilson’s disease
» Autoimmune: ANA , anti- smooth muscle antibody, anti-
mitochondrial antibody • AST: ALT > 1000: drug/toxin, vascular (ischemic
DIFFERENTIAL DIAGNOSIS
Anatomical Approach:
• Ligament: anterior/posterior cruciate ligaments, medial /lateral ligaments Patella ( knee cap)
• Muscle /tendon: tendonitis, quadriceps rupture, patellar tendon rupture Lateral collateral
^
• Patella: subluxation, dislocation, fracture, patellofemoral syndrome ligaments
Lateral meniscus x Medial meniscus
• Bursa: bursitis
.
• Vascular: DVT popliteal aneurysm
• Joint: osteoarthritis, Baker ’s cyst, inflammatory arthritis, septic arthritis, osteochondral - Medialcollateral
ligaments
injury, osteochondritis
• Bone: fracture, neoplastic ( metastatic vs. primary ) , osteoporosis, avascular necrosis
• Other: iliotibial band syndrome, Osgood - Schlatter disease, referred pain (hip pathology)
HISTORY
ID • Patient 's name, age, gender, mobility aids
CC • Knee pain
• OPQRST
• Acute: establish mechanism of injury: high vs. low energy, contact vs. non-contact, plant and pivot, land
from jump, rapid deceleration, varus/valgus stress, rotation, audible pop
• Swelling, stiffness, locking or catching (meniscal pathology), crepitus, instability or giving way (ligament
pathology), stiffness (duration and timing), night pain, activity limitations ( squatting, twisting)
. .
• Changes in sensation, strength ROM and ability to wt bear
RED FLAGS • Constitutional symptoms, night pain, fragility fracture, pain on wt bearing prior to injury sugests
neoplastic or systemic patholgy
PMHX • Previous trauma or pathology of joints or bones
• Inflammatory .
arthritis DM, bleeding disorders, neurologic disorders, previous malignancy
• Falls: explore etiology to attempt prevention ( syncope/presyncope/ weakness/seizure)
PHYSICAL
General Approach
• Self -introduction, ask permission to perform physical exam, wash hands /perform hand hygiene
CD
W) • . .
VS ( BP. HR RR Temp, Sa02) and general appearance
• Remove clothing/splints /casts/dressings /etc. from the affected area and drape the patient appropriately
D
t/> Inspection
.
• Alignment (genu varus/valgus/recurvatum) limb length discrepancy, internally/externally rotated, equal wt bearing
• Gait: shuffling, antalgic, foot drop
• Ability to squat and duck walk
• SEADS ( swelling, erythema, atrophy, deformity, scars) compared with contralateral joint
457 .
E 'lmonton Manual of Common Clin c .H Scr
Palpation
• M5K: with knee bent at 90°
> Patella tendon - tenderness suggestive of tendinitis
Tibial tuberosity - tenderness suggestive of Osgood - Schlatter disease
>
> Joint line - tenderness may suggest meniscal tear
> Head of the fibula
> Collateral ligaments
> Popliteal fossa - Baker cyst
• VASC: color, hair atrophy, pulses ( popliteal, posterior tibialis, dorsalis pedis ) , capillary refill, and temperature difference
• NEURO:
> Sensation: dermatomes and peripheral nerves including saphenous, sural, superficial and deep peroneal, and tibial
> Muscle strength / function (quads, hamstrings)
> Reflexes (patellar, Achilles, Babinski)
ROM
• Active and passive (heel to buttocks, knee to chest ): also assess joint above and below (hip and ankle)
Special Tests
• Effusions
> Swipe/bulge test (small effusions): sweep fluid upward along medial side, stroke down lateral side: positive with medial bulge
> Patellar tap /ballotment test for large effusions: compress suprapatellar pouch and press patella into femur: positive if patella
rebounds when pressure removed
• Cruciate ligament injuries
Anterior/posterior drawer test *
>
Lachman (most sensitive for ACL) *
>
> Pivot -shift (most specific for ACL): valgus and internal rotation to extended knee, flex past 30°: positive if posterior
subluxation of tibia
• Meniscus injuries:
Ottawa Knee Rules
> McMurray test’
• Collateral ligaments: Knee X - ray series only required for knee injury
> Valgus /varus stress *
patients with any of the following features:
‘See Knee Physical Exam • > 55 yrsold
• Isolated tenderness of the patella
INVESTIGATIONS
• Tenderness of the head of the fibula
Radiology
• Inability to flex to 90°
•XR knee AP, lateral, skyline ( patella)
• Inability to Wt bear for 4 steps both at time of
•XR hip and ankle injury and in ED
• CT or bone scan if pathologic fracture suspected
• MRI if ligamentous or meniscal pathology suspected
Laboratory investigations
. . . . .
• Metastatic workup: TSH calcium PTH, ALP SPEP UPEP PSA Inflammatory: ESR, CRP CBC RF ANA . . .
Special tests
• Bone mineral density (osteoporosis)
• Bone scan (osteomyelitis, bone mets, bone tumors)
• Diagnostic arthrocentesis for effusions
.
> Send aspirate for 4Cs : Cell count, Culture Cell Gram stain. Crystals
UREATMENT
Emergent
• ABCDE, life before limb: reduce open fractures to prevent neurovascular injury Malignancies that Metastasize to Bone
Conservative Treatment • Top 4: " Mets . mets, mets. primary”
. .
• PRICE: protection, rest ice compression, elevation • " BLT Kosher Pickle Mustard Mayo’: C/>
• Immobilize appropriately: splint, half cast, full cast, hinged brace > Breast c
• Ambulation aids and instruction (if required) > Lung era
0>
Surgical Management > Thyroid
• Fixation, arthroscopy, arthroplasty, ligament reconstruction, irrigation and > Kidney <
•
debridement > Prostate
Follow - up: if increased swelling, redness, cyanosis, increased pain, or > Multiple myeloma
decreased sensation
• DVT .
pulmonary embolus, fat embolus, ischemic contracture, nonunion,
. . .
malunion joint stiffness, traumatic arthritis AVN osteomyelitis, septic arthritis, compartment syndrome, amputation
458
NECK MASS / GOITER
Current Editor: Alexandria Webb BSc MD
HISTORY
ID • Patient ’s name, age . gender, ethnicity
CC • Lump/mass in neck
• Constitutional symptoms: Wt. night sweats, chills/fevers, palpitations. EtOH exacerbation + steroid
regression = lymphoma
.
RED FLAGS • Dysphagia, odynophagia, hoarseness SOB/stridor/wheeze, hemoptysis, halitosis, night sweats, chills/fevers
• Weight loss, palpitations
Auscultation (only if mass is pulsatile, then auscultate the mass and do a CV exam)
• Heart sounds, murmurs, thyroid/carotid bruits (rule out these causes)
Special Tests
• Tongue protrusion - elevation of thyroglossal duct cyst
• Swallow - elevation of thyroid mass
• Valsalva - expansion of laryngocoele
'Red Flag for Neoplasm
INVESTIGATIONS
Thyroid
• Blood Work: TSH . free T3/T4. anti-TPO. Ca . PTH
2*
• Imaging:
>Thyroid U/ S for size and anatomy
>Thyroid scintigraphy ( 1231 or technetium- 99m pertechnetate) for function
• Bx: fine needle aspiration
Neck Mass
• Imaging: U/S, CT neck, MRI, upper airway endoscopy
• Bx: U/ S guided fine needle aspiration (do not open Bx in office)
• Blood work: CBC- D, PTH, serology for HIV or EBV, monospot, blood smear
• Throat swab, Mantoux skin
.
• Autoimmune workup: ANA ESR, CRP, RF, c - and p - ANCA
L REATMENT
Emergent
• Airway obstruction due to mass effect requires emergent intubation or tracheostomy
Specific Options
• Reactive lymph node: antibiotics x 2 wks then reassess
• Suspicious neck mass: refer to Otolaryngologist for upper airway endoscopy and Bx
• .
Thyroid mass/nodule: serial U/S repeat FNA or surgery if symptomatic or suspicious cytology
• .
Graves' disease: beta block. MMI or PTU corticosteroids, radioiodine ablation, thyroidectomy
• Hashimoto's thyroiditis: corticosteroids, beta blocker, thyroid hormone replacement
• Congenital: surgical cystectomy to prevent recurrent infection
in
Follow-up c
• Neck masses > 4 cm, persisting > 2 wks or causing upper aerodigestive tract symptoms should be referred OQ
Referrals CO
• .
Otolaryngology Head and Neck Surgery Infectious Diseases <
DIFFERENTIAL DIAGNOSIS
Diagnostic Criteria
• Unilateral or bilateral pupillary abnormality
High Mortality/Morbidity
• CN III palsy with pupil dilation (extrinsic compression - often due to intracranial aneurysm), brainstem stroke, angle closure
.
glaucoma Horner 's syndrome
HISTORY
ID • Patient's name, age, gender
CC • Photophobia
• Visual changes
• Asymmetrical pupils
• Pain
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461 .
Edmonton Manual of Common Clinical Scen v 105
PHYSICAL
General Approach
• General vision testing foreach eye
»Visual acuity, pupil reactivity, tonometry, visual fields, extra - ocular movements, diplopia, ophthalmoscopy
• Determine nature of pupil abnormality - idiopathic, problem with afferent /efferent pathways, damage/defect in iris
» Important question: are pupils more asymmetric in light or dark ? - helps elicit if issue is with mydriasis or miosis
> Assess pupil size, shape, and reactivity in room light, to a bright stimulus, in dim light, and to an accommodative target
• Screening neurological and CN exams
Special Tests
• Swinging flashlight test: assesses for RAPD
> Shine focused light source on one eye for 1- 2 secs, then swing light to contralateral eye; repeat as needed
> Normal response: pupil constricts slightly when light is shone in eye
> Abnormal response: pupil dilation when light is shone in eye: RAPD present on abnormal side
> Note: RAPD needs to be differentiated from hippus, a normal rhythmic dilation - constriction of the pupils ( which, if present , will
be occur equally in both eyes)
• Pharmacological testing (administered as eye drops during assessment by Ophthalmologist )
INVESTIGATIONS
Blood Work
• Indicated if features suspicious for systemic disease are present on exam
Radiology/ lmaging
• MRI - suspected intracranial tumor
• MR /CT angiogram - suspected intracranial aneurysm
• CT head/orbits - trauma
L REATMENT
Emergent
• Cerebral aneurysm/intracranial tumor - Neurosurgery referral
• . .
Angle closure glaucoma: pilocarpine/ beta blocker eye drops IV acetazolamide iridotomy as appropriate
Treatment Options
• Dependent on etiology of pupillary abnormality
Referrals
• Neuro -ophthalmology, Neurology. Ophthalmology, Neurosurgery as appropriate
m
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3
DIFFERENTIAL DIAGNOSIS
Anatomic Common Conditions Emergent Conditions
Location
Eyelid Bacterial (blepharitis, hordeolum, chalazion, preseptal cellulitis)
Inflammatory (contact dermatitis, atopic dermatitis)
Lacrimal System .
Dry eye (meds, naso-lacrimal duct obstruction Sjogren’s. RA)
Infectious (dacryoadenitis, dacryocystitis)
Orbit Thyroid orbitopathy Orbital cellulitis, retrobulbar hemorrhage
Globe Ruptured globe
Conjunctiva Bacterial conjunctivitis, viral conjunctivitis, allergic Chemical toxicity, burn, blunt/penetrating
conjunctivitis, pinguecula, pterygium, neonatal trauma
conjunctivitis, subconjunctival hemorrhage
Sclera Episcleritis, scleritis Necrotizing scleritis
Cornea HSV, HZV, fungal keratitis, peripheral ulcerative Bacterial keratitis (staph, pseudomonas,
keratitis, contact lens keratopathy, abrasion, strep, Moraxella), acanthamoeba keratitis
recurrent erosion, FB, flash burn
Uvea . .
Uveitis: idiopathic, HLA- B27 syndromes ( AS IBD psoriatic
arthritis.
. .
reactive arthritis), HSV HZV. syphilis TB,
fungal, toxoplasmosis, trauma
Other Cluster headaches Endophthalmitis, angle closure glaucoma,
carotid - cavernous fistula
HISTORY
ID Patient ’s name, age, gender, occupation
CC Red eye
HPI Characterize onset, duration, symptoms of red eye, deep or superficial
Trauma: FB, abrasion, chemical exposure, sun, ultraviolet or arc light exposure
Decreased visual acuity, photophobia, constricted pupil, halos around light
Conjunctival discharge: purulent, watery
Bilateral/unilateral onset, redness, irritation, burning, gritty, pruritis, pain (sharp or dull), radiation, HA, N/V
Contact lens use
Sick contacts
RED FLAGS Severe ocular pain, acute visual loss, traumatic etiology, chemical burn, fixed pupil
PMHX . .
RA AS, psoriasis, IBD, reactive arthritis, sarcoidosis, TB Behcet 's, HZV, Ehlers - Danlos
PSHX Eye surgery, intravitreal injections
PO& GHX Chlamydia, herpes simplex, gonorrhea, syphilis
MEDS Any medications, including eye drops
ALLERGIES Hay fever, giant papillary and contact conjunctivitis, allergies to eye drops
FHX Autoimmune conditions, glaucoma (especially angle closure glaucoma)
> SOCIAL Contact lens Hx: hard or soft lens, disposable, weekly or monthly, length of actual wear, sleep in contacts,
CD
W) swim or hot tub in contacts, method of lens cleaning (solution or water)
13 ROS HEENT: recent URTI
to CV: hypertension, bleeding disorder
RESP:URTI
Gl: IBD, IBS symptoms
GU: urethritis, STIs
MSK/DERM: psoriasis, skin rash, arthritis, lower back pain
RISK FACTORS Contact lens wear, chemical/allergen exposure, trauma, infections/conditions above, surgery
INVESTIGATIONS
Depends on Hx and DDx
• Conjunctivitis: C& S
• Infectious keratitis: refer to Ophthalmology for corneal scraping for C&S
• Uveitis, scleritis, episcleritis: refer to Ophthalmology for appropriate workup
• Orbital cellulitis, thyroid - related orbitopathy, and retrobulbar hemorrhage: CT orbits
• Trauma: orbital X - ray, CT orbits
• Endophthalmitis: refer to Ophthalmology for vitreous tap
UuiEATMENT
Emergent
• Globe rupture: refer to Ophthalmology
• Acute angle closure glaucoma: refer to Ophthalmology for pilocarpine/ beta blocker drops, IV acetazolamide, iridotomy
• Infectious keratitis, especially in contact lens wearers: refer to Ophthalmology
• Chemical burn: flush eye with Morgan lens and NS or RL to normal pH 7
• Endophthalmitis: refer to Ophthalmology for ATBx injection ± vitrectomy
• Orbital cellulitis: refer to Ophthalmology for IV ATBx
Non-emergent
.
• Dry eye: warm compresses, tear drops QID tear gel QHS
• Conjunctivitis: viral (cold compresses, hand hygiene), bacterial ( Polysporin drops QID x 5 /7), allergic (cold compresses,
antihistamines), chemical ( withdraw aggravating agent, tears)
.
• FB on cornea: remove with burr or needle tip Polysporin drops QID x 5 / 7; refer to Ophthalmology if unable to remove
• Preseptal cellulitis: appropriate oral ATBx depending on offending bacteria
• Marginal keratitis: refer to Ophthalmology
• Uveitis, scleritis, episcleritis: refer to Ophthalmology for treatment and workup
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DIFFERENTIAL DIAGNOSIS
Differential Diagnosis
SpcrmjtK ctxd
Location Painful Painless
Intratesticular • Orchitis • Tumor
• Epididymitis * • Spermatocele
Pampiniform
• Fournier ’s gangrene • Scrotal edema pl«ius
Appendix of
• Strangulated inguinal hernia’ • Inguinal hernia rpkfldymit
• Torsion of testicular appendage* ( non-strangulated) * Eptdidyrm «,
• Referred ( STI, ureteric colic, etc.)
'Common conditions
Testn
( covered by visceral
High Mortality/Morbidity layer of tunica
vaginalis testisl
• Testicular torsion: must be ruled out in the setting of scrotal pain
• Testicular malignancy
Parietal layer of
• Fournier 's gangrene tunica vaginalis testis
• Strangulated inguinal hernia
HISTORY
ID Patient 's name, age, gender
CC Painless scrotal mass /heaviness vs. scrotal pain
HPI Onset (suddenly over hrs vs. days vs. chronic)
Delay in presentation is a common issue (Note: commonly a tumor is noted post trauma or in shower)
Painful (epididymitis, orchitis, trauma, torsion, hemorrhagic tumor ) vs. painless ( tumor, hydrocele, varicocele,
spermatocele)
If painful: radiation ( to back, tip of penis), timing (with urination)
Describe size, position, hard vs. soft, unilateral vs. bilateral, intra - vs. extra - testicular
Associated Sx: N/V
RED FLAGS Acute onset, diffusely tender scrotum, Hx of minor trauma, pain woke from sleep (torsion)
.
Fever, Wt T night sweats (malignancy)
PMHX Undescended testicle at birth (cryptorchidism)
PSHX Hernia, orchiectomy, orchiopexy
FHX FamHx of testicular cancer
SOCIAL Family planning and fertility (past and future plans)
Prior sexual Hx and contacts, and Hx of STIs
ROS HEENT: testicular metastasis may present as neck mass, mumps (orchitis may be associated with parotid
gland enlargement)
CV: heart failure can lead to generalized scrotal edema
RESP: TB/metastatic disease may cause cough/SOB/hemoptysis
.
Gl: change in BM (herniated bowel), N/V hepatomegaly
GU: difficulty with urination, pain with urination, blood in urine, change in erection, pain with ejaculation,
amount of ejaculate, blood in ejaculate, urethral discharge
> MSK/DERM: bone pain, gynecomastia, arthritis, rash, chancres
(U
RISK FACTORS Malignancy: cryptorchid testis (undescended testis), exogenous estrogen exposure to mother during
bJO
pregnancy, previous testicular cancer
D Torsion: bell -clapper deformity (congenital absence of posterior anchoring of the gubernaculum)
CO
> Trans - illumination: hydrocele /spermatocele will trans -illuminate but tumors/varicocele /blood will not
> Valsalva, cough or standing: will enlarge hernia or varicocele if present with subsequent resolution in supine position
> Cremasteric reflex: usually absent in testicular torsion
• Blue dot sign: tender nodule with blue discoloration at upper pole of testis in torsion of testicular appendage
• Gians penis and urethral meatus: discharge, chancres, sores
MSK /DERM
• Peripheral leg edema ( secondary to retroperitoneal mass)
INVESTIGATIONS
Blood Work
• AFP, fl-HCG. and LDH
UREATMENT
Emergent
• IV fluids to correct dehydration if N/V
• Surgical exploration if torsion suspected clinically
Treatment Options
• Symptom control:
> Analgesics, antiemetics
• Torsion: emergent surgical detorsion and bilateral fixation of testes, manual detorsion (rotate medial to lateral) may be attempted if
surgery delayed
• Epididymitis/orchitis: ATBx, scrotal support, bed rest, ice, analgesia
cn
• Strangulated inguinal hernia: immediate surgery c
• Torsion of testicular appendage: analgesia
era
• Malignancy: orchiectomy with active surveillance, chemotherapy or radiotherapy depending on stage and type CD
• Hydrocele: conservative, needle drainage, surgical 3
• Varicocele: conservative, surgical ligation of testicular veins, percutaneous vein occlusion
Referrals
• Urology, Oncology
KEY POINTS
• Shoulder pathologies can be divided into acute and chronic. Further approach the differential using an anatomic approach.
• There are many special tests for the shoulder. Use your history to narrow down your differential and focus your physical exam.
. .
• As with all joints, always obtain three views of the shoulder when ordering X -rays ( AP axillary/Velpeau, scapular ( Y ) lateral)
• Most chronic shoulder pathologies may be treated with analgesia, physiotherapy, and cortisone injections. Consider surgery if the
patient fails conservative management.
DIFFERENTIAL DIAGNOSIS
Shoulder
Bones: fracture (clavicle, scapula, humeral head/neck )
Acute Tendons: rotator cuff tear, proximal biceps tendon rupture
Joints: glenohumeral dislocation, acromioclavicular separation
Bones: osteoarthritis (glenohumeral, acromioclavicular), inflammatory arthritis, primary bone tumour or metastatic lesion
Tendons: rotator cuff tendinitis/impingement, biceps tendinitis
CC • Shoulder pain
HPI • OPQRST
• Trauma: mechanism of injury ( if low energy, think pathologic or fragility fracture)
• Changes in sensation, strength, ROM
• Crepitus, repetitive use ( osteoarthritis)
• Morning stiffness that improves with use, >1 joint involved (inflammatory arthritis)
• Prolonged shoulder immobilization (adhesive capsulitis)
• Joint above and below (C spine and elbow) concerns
ALLERGIES .
• Specifically to antibiotics and pain medications (NSAIDs, acetaminophen, codeine, opioids, etc )
Q)
W>
FHX • Inflammatory Arthritis . IBD. malignancy
3
SOCIAL • Smoking, EtOH use . IVDU. physical abuse
CO • Occupation and handedness
ROS • CV/ RESP: chest pain, SOB . dizziness, diaphoresis (Ml)
• Gl: abdominal pain . N/V (diaphragmatic irritation)
• MSK/ DERM: rash (inflammatory arthritis)
RISK FACTORS .
• Osteopenia / osteoporosis ( fractures), FHx of malignancy, Prev Cancer (bone mets or tumors)
INVESTIGATIONS
Radiology/ lmaging
• X -ray of shoulder ( 3 views: AP. axillary/Velpeau, scapular Y lateral); Zanca view ( acromioclavicular joint); AP bilateral shoulders
(clavicle)
• CT shoulder (if complex fracture or for preoperative planning)
-
• Ultrasound +/ arthrography +/- MRI (rotator cuff tendinitis /impingement )
Special Tests
• Bone scan ( malignancy )
UREATMENT (/)
Emergent C
Treatment Options (common/life threatening conditions) era
• Fracture/dislocation: primary and secondary survey, reduce, immobilize, analgesia, consider consulting orthopedics
n>
• Rotator cuff tendinitis/impingement, osteoarthritis, adhesive capsulitis: analgesia, physiotherapy, cortisone injection, consider <
*
DIFFERENTIAL DIAGNOSIS
Subjective
• Otologic: Hearing loss . Acoustic neuroma. Meniere' s disease
Sensorineural hearing loss: presbyscusis (age- related hearing loss), noise- induced hearing loss
>
> Conductive hearing loss: cerumen impaction, middle ear effusion, otosclerosis
Objective
• Pulsatile: vascular ( AVMs, acquired shunts, aneurysms, glomus tumor, carotid stenosis)
• Intermittent ( TM J crepitus with eating ) vs. continuous ( patulous Eustachian tube, palatal myoclonus, stapedial muscle spasm )
Common Conditions
• Presbycusis, noise- induced hearing loss. Meniere' s, drug- induced ototoxicity, trauma , aging
High Mortality/Morbidity
• Meningitis, increased ICP, aneurysms, malignancy
HISTORY
ID • Patient’s name, age (prevalent 40- 70 y/o , sometimes in children), gender
CC • " Ringing" in the ear ( s) / tinnitus
RED FLAGS • Bruit over ear/skull , unilateral tinnitus, neurologic signs (e.g., vertigo, syncope), neck stiffness/rash, fever
PMHX • Uni/bilateral hearing loss, trauma/whiplash, infections /meningitis, vascular ischemia, Meniere’s, TMJ
dysfunction, CHF, CRF, anxiety/depression, MS, malignancy, Paget’s, thyroid pathology. Chiari malformations,
Hxof syphilis
PSHX • Chiari malformation surgery, ear surgery
PO&GHX • Currently pregnant , previous pregnancies, better / worse with pregnancy
MEDS • Aminoglycosides, ASA, NSAIDs, loop diuretics, cisplatin, anticonvulsants, hypnotics, chloroquine
>* ssEBsmm
General Approach
0)
txo • Introduce self and ask permission to proceed , wash hands/perform hand hygiene
D • ABC. IV. VS (BP. HR. RR. Temp , Sa02)
Inspection
• Inspect behind ear. pinna, canal, anterior rhinoscopy, oropharynx for pulsatile mass, patent Eustachian tubes
• Otoscopy: wax . foreign bodies , perforation, retracted/ bulging TM/OM/OE . reddish hue on TM: Schwartze’s sign, pulsatile mass
INVESTIGATIONS
Blood Work
. .
• CBC- D, electrolytes. Cr urea TSH. lipid profile, glucose. VDRL ( syphilis)
Radiology/ lmaging
• MRA head, carotid Doppler for pulsatile tinnitus
• Gadolinium- enhanced MRI of posterior cranial fossa to rule out retrocochlear lesions /acoustic neuroma
EPECIAL TESTS
Audiogram = first test of choice (often all that is necessary )
VNG for vestibular dysfunction
Pre- op angiogram with embolization, urine catecholamines for carotid body tumor /paraganglioma
Emergent
• ATBx ( meningitis)
f
• Burr hole + catheter ( ICP)
• Neurosurgery ( aneurysms/malignancy)
Treatment Options
• Lifestyle: noise exposure, decrease salt intake (Meniere’s).
BP, glucose, thyroid control
• Stop ototoxic factors
• Treat anxiety/depression, allergic rhinitis
• Hearing aids /tinnitus maskers, wax removal
• Cognitive behavioural therapy / tinnitus retraining therapy
Surgical
• Resection of tumor, repair of malformation/shunt, myringotomy + tube insertion, tympanoplasty
Follow - up
• If symptoms persist or if chronic problem
Referrals
• Neuro - otology, Otolaryngology. Neurosurgery
CO
c
era
n>
Objective: To evaluate a trauma patient in accordance with Advanced Trauma Life Support basics
\k RIMARY SURVEY
Survey Query Assessment Red Flags Management
• Airway patent ? Have patient talk No speech • Chin lift/ jaw thrust
Stridor, hoarseness • -* 0 chin lift if C-spine injury
• Airway protected? GCS GCS < 8 • Suction
• “GCS < 8 = Intubate" (ETT)
• Airway at risk for Assess for injury - burn, ++ airway edema
decline? inhalation, facial trauma • Surgical airway
Frank injury/deformity
AIRWAY
Assess for obstruction -
. ..
(i e cricothyrotomy)
Large FB
.
FB fluid, swelling
Massive hemoptysis
-
• C spine fracture? Mechanism of injury Hxof head trauma •C -spine protection - collar or in -
-
C spine palpation Midline tenderness line stabilization
Neurologic symptoms Limb weakness /tingling
• Can patient .
RR Sp02 Tachypnea • Supplemental 02 (nasal cannula
ventilate and Look for chest rise Hypoxia, cyanosis -* simple mask -* non-rebreather
oxygenate? mask)
Listen for breath sounds Asymmetric chest rise
Feel for exhaled air 0 breath sounds -
• Non invasive mechanical
..
ventilation (i e , BiPAP)
• Flail segment ? Inspect chest wall Paradoxical chest rise • Invasive mechanical ventilation
Palpate chest wall SubQ emphysema (BVM ± ETT)
Frank rib deformities
BREATHING • (Tension) Inspect trachea Tracheal deviation • Needle decompression (2nd ICS .
Pneumothorax ? Palpate chest wall SubQ emphysema mid-clavicular line, superior to
R * L hyperresonance inferior rib) (immediate Tx)
Percuss for resonance
• Chest tube (definitive Tx)
Auscultate for breath R * L breath sounds
sounds 0 breath sounds
• Hemothorax ? Percuss for resonance Focal dullness • Chest tube
Auscultate for breath R * L breath sounds
sounds
• Shock ? .
LOC BP. HR 1 LOC • t intravascular volume
Central pulses (carotid . .
sBP < 90 dBP < 60 .
• 18 gauge IV x 2 then 1-2 LIV NS
femoral) Tachycardia bolus, then fluids PRN
Peripheral pulses (radial,
pedal), skin temp + colour
0 peripheral pulses, cold
peripheries. T cap refill
• pRBC if still hypotensive
if female) if no T&S
— 0+ (O -
• Unseen injuries • Remove all clothing • Penetrating chest trauma in • Tx hypothermia with warm
on back or under • Log -roll patient cardiac box blankets, ambient heaters, warm
clothes? • BRBPR (? bowel injury) IV fluids
• Palpate spine for
EXPOSURE
tenderness • 1 anal tone (? spinal injury) -
• Remove backboard during log roll
• DREfor BRB, tone, • High -riding prostate = 0 Foley • Pressure + dressing to all wounds
prostate insertion
SECONDARY SURVEY
• The secondary survey is a Hx + head - to - toe PE to evaluate for all possible injuries in a trauma patient
• The secondary survey should not begin until the patient is clear per primary survey, VS are in acceptable limits, and resuscitation is
well underway
. .
eyes Battle's sign CSF rhino / otorrhea) • Lytes, glucose, urea + Cr, CK
HEENT • Assess face for signs of facial fracture (purpura, swelling, step deformity, tenderness) .
• AST + ALT ALP + bili, lipase o ABG
• EKG
• Inspect neck for penetrating trauma, possible vascular injury, and palpate for crepitus
-
• Inspect C-spine for frank deformity, palpate for midline tenderness * clear C spine if - • CT head if head trauma, neuro
possible ( see CCSR) deficits, signs of t ICP -* can use
Canadian CT Head Rule to help
• Inspect entire chest wall for signs of penetrating or blunt trauma, asymmetric chest decide if minor trauma
rise, paradoxical movements
• CXR -* CT chest if major chest
• Palpate entire chest wall for deformities, tenderness, crepitus trauma
CHEST • Percuss all lung fields for hyperresonance or dullness • CT abdo if major abdo trauma, or
• Auscultate all lung fields for breath sounds, wheezes, crackles peritoniticO/ E
• Auscultate all heart bases for heart sounds, murmurs, rubs • CT pelvis if major pelvic trauma,
• Inspect for external injuries (lacerations, penetrating trauma, blunt trauma) & signs of
unstable pelvis, or gross hematuria
ABDOMEN
. .
internal injuries (distension, purpura Grey -Turner’s Cullen's, seatbelt sign) • CT spine if large mechanism of
injury, vertebral tenderness, or
• Auscultate for bowel sounds
neuro deficits
• Palpate entire abdo for tenderness & peritoneal signs
• XR any extremities with swelling,
• Assess pelvic stability with anterior -posterior stress, lateral stress, and cranial-caudal deformity, tenderness
PELVIS stress
• Inspect for GU bleeding, esp. at urethral meatus
EXTREMITIES • Assess all extremities for swelling, deformity, tenderness, pulses + perfusion
• Assess all joints for swelling, deformity . ROM. tenderness
• Administer tetanus toxoid if patient not up- to date -
-
• Log roll (with DRE & removal of backboard) if not already done
.
Chapman MD Robert Chan MD FRCSC
.
Knee (Pain, Fractures, & Dislocations) Babak Maghdoori MD. Khaled Al - Mansoori MD. Nadr M Jomha MD PhD FRCSC, Kevin Zuo MD Chris
Neck Mas / Goiter Shawna Pandya MD. Kevin Zuo MD. Jerry Dang MD. Kal Ansari MD FRCSC ABO ABFPRS
.
Pupil Abnormalities Terence Kwan-Wong MD. Chris Hanson MD Christopher J. Rudnisky MD MPH FRCSC
Red Eye Darwin Wan MD, Christopher Hanson MD. Christopher J. Rudnisky MD MPH FRCSC
Scrotal Mass & Scrotal Pain Brendan Diederichs MD. Winston Teo MD
Shoulder Joffre Munro MD. Yang Li MD. Darren Nichols MD CCFP. Brianne Tetz MD
Tinnitus Shawna Pandya MD. Kal Ansari MD FRCSC ABO ABFPRS. Krista Lai MD
Trauma Kelvin MH Tran MD. Ashraf Kharrat MD. James Keay MD CCFP
<D
W>
Z3
CO
Abdominal Pain
. -
Beers MH Porter RS. Jones TV. Kaplan JL. Berk wits M. eds. Chronic and recurrent abdominal pain. In The Merck Manual . 18 th ed. Whitehouse Station. N J:
Merck Research Laboratories: 2006.
Fishman MB. Aronson MD. Differential diagnos s of abdominal pain in adults. In Fletcher RH. ed. UpToDate. Waltham. MA: 2009.
Kendall JL. Moreira ME. Evaluation of the adult with abdominal pain in the emergency department. In Hockberger RS. ed. UpToDate. Waltham. MA; 2009.
Wagner JM. McKinney WP. Carpenter JL. Original article: Does this adult patient have appendicitis? In Simel DL. Rennie D. eds. The Rationil Clinical
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Examination: Evidence - Based Clinical Diagnosis. New York: McGraw Hill; 2009.
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Cartwright SL Knudson MP. Evaluation of acute abdominal pain in adults. Am Earn Physician. 2008 Apr l;77 ( 7):971- 978.
Anorectal Pain
Kornbluth A. Sachar DB, Practice Parameters Committee of the American College of Gastroenterology. Ulcerative colitis practice guidelines in adults
(update): American College of Gastroenterology. Practice Parameter Committee. Am J Gastroenterol. 2004;99( 7):1371- 1385.
Lacy BE. Weiser K. Common anorectal disorders: Diagnosis and treatment. Curr Gastroenterol Rep. 2009:11( 5):413- 419.
_ _
Image: http://suncoastsurgicalassociates.com/ wp- content /uploads / 2013/12/anal fistula 002.jpg
Approach to Fracture
. .
Stone CK Humphries RL. Chapter 4: Sports Medicine Chapter 28: Orthopedic Emergencies. In Current Diagnosis & Treatment Emergency Medicine. 7th ed.
New York: McGraw - Hill: 2011.
. -
Swales C. Bulstrode C. Rheumatology Orthopedics and Trauma at a Glance. 2nd ed. Hoboken. NJ: Wiley Blackwell; 2011.
. .
Tintinalli JE. Stapczynski JS Cline DM. Ma OJ, Cydulka RK Meckler GD. Section 22: Injuries to Bones and Joints. In Tintinalli' s Emergency Medicine: A
Comprehensive Study Guide. 7 th ed. New York: McGraw - Hill: 2011.
Burns
Janis JE. Essentials of Plastic Surgery . St. Louis: Quality Medical Publishing: 2007.
.
Kao CC Garner WL. Acute burns. Plastic ana Reconstructive Surgery' . 2000;105:2482- 2493
. .
Sood R Achauer BM. Achauer and Sood ' s Burn Surgery Reconstruction and Rehabilitation. Phil ideiphia: Elsevier: 2006.
Diplopia
Bradford CA. Basic Ophthalmology for Medical Students and Primary Care Residents. 8th ed. San Francisco: American Academy cf Ophthalmology; 2005.
Dizziness/Vertigo
.
Tintinalli JE et al. Tintinalli ' s Emergency Medicine: A Comprehensive Study Guide. 6th ed. New York: McGraw - Hill; 2004 .
Dysphagia
DiMarino MC. Dysphagia. Merck Manual Online. 2009 Jun [ cited 2010 Sep 24 ). Available from: http:// wvvw.mcrck.com/mmpe/sec02/ch012/ch012 b.html
Paik NJ. Dysphagia. E - medicine. 2008 Jun [ cited 2010 Sep 24 ). Available from: http://emedidne.medscape.com/article/324096-overview
Epistaxis
. . . . .
Kaplan JL Beers MH Berkwits M Porter RS Jones TV eds. Nose and paranasal sinus disor lers. In The Merck Manual of Diagnosis and Therapy . 18th ed.
.
( 2006). http://online statref.com.login.ezproxy.library.ualberta.ca/document .aspx ?fxid = 21& locid = 372.
. .
Schlosser RJ Epistaxis N Engl J Med. 2009 Feb 19;360(8):784 - 789 .
. . .
Waters TA Peacock IV WF. Chapter 241: Nasal emergencies and sinusitis. In Tintinalli JE e! al eds. Tintinalli ' s Emergency Medicine: A Comprehensive Study
. .
Guide 6 th ed Available from: http:// www.accessmedicine.com.login.ezproxy.library.ualberta.ca/contcnt.aspx ?alD :609033
;
Gynecomastia
Alice MR. Baker MZ. Gynecomastia. Last updated 2009 Sep 23. Available from: http://emec cinc.medscape.com/article/ 120858 - overview
Braunstein GD. Gynecomastia. N Engl J Med . 2007 Sept 20:357:1229 - 1237.
Federman DD. Nabcl EG. eds. Gynecomastia. New York: ACP Medicine: 2010.
Ma NS. Geffner ME. Gynecomastia in prepubertal and pubertal men. Curr Opin Pediatr . 2008 Aug;20( 4):465 - 470.
Narula HS. Carlson HE. Gynecomastia. Endocrinol Metab Clin North Am. 2007 Jun:36(2):497 - 519.
in
Hematuria
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Blondel-Hill E. Fryters S. Bugs & Drugs : An Antimicrobial / Infectious Diseases Reference. Ecmonton AB: Alberta Health Services: 2012.
Cattran DC. Appel GB. Treatment and prognosis of IgA nephropatny. In Glassock RJ. Fervenza FC. eds. UpToDate. Walthham. MA: 2014.
Cunningham GR . Kadmon D. Medical treatment of benign prostatic hyperplasia. In O'Leary MR ed. UpToDate. Waltham. MA; 2014.
Grossfeld GD. Wolf JS Jr.Litwan MS. Hricak H. Shuler CL. Agerter DC. Carroll PR. Asymptomatic microscopic hematuria in
adults: Summary of AUA best practice policy recommendation. Am Fam Physician. 2001:63:1145 - 1154.
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Preminger GM. Options in the management of renal and ureteral stones in adults. In Goldfarb S. O'Leary MP eds. UpToDate. Waltham. MA: 2014.
. . .
Rose BD Fletcher RH. Evaluation of hematuria in adults. In Glassock RJ. O'Leary. MP eds. UpToDate Waltham. MA; 2009.
Wein A J. Kavoussi LR. Novick AC. Partin AW. Peters CA. eds. Campbell -Walsh Urology. 9th ed. Philadelphia: Saunders Elsevier: 2007.
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Wollin T. Laroche B Psooy K . Canadian guidelines for the management of asymptomatic miscroscopic hematuria in adults. Canadian Urology Association
Journal . 2009 Feb:3 (l):77- 80.
Cohen RA. Brown RS. Microscopic hematuria. New England Journal of Medicine. 2003:348( 23):2330 - 2338.
Hernia
. . . .
Beers MH Porter RS Jones TV Kaplan JL Berkwits M. eds. Abdominal wall hernias. In The Merck Manual of Diagnosis and Therapy . 18th ed. Whitehouse
Station. NJ: Merck; 2006.
.
Brooks DC. Abdominal wall hernias. In Turnage R ed. Waltham. MA: UpToDate; 2009.
.
Lawrence PF ed. Abdominal wall, including hernia. In Essentia /s of General Surgery . 4th ed. Baltimore: Lippincott Williams & Wilkins; 2006.
Nicks BA. Askew K. Hernias. McdGenMed. 2010. http: //emedicine.medscape.com/article/775630- overview. Accessed September 06.2010
Brooks DC. Overview of abdominal wall hernias in adults. In Rosen M. ed. Waltham, MA: UpToDate; 2016.
.
Brooks DC Hawn M. Classification, clinical features and diagnosis of inguinal and femoral hernias in adults. In Rosen M. ed. Waltham. MA: UpToDate: 2016.
Brooks DC. Overview of treatment for inguinal and femoral hernia in adults. In Rosen M. ed. Waltham. MA: UpToDate: 2016.
Jaundice
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Beers MH Porter RS. Jones TV. Kaplan JL. Berkwits M eds. Jauncice. The Merck Manual of Diagnosis and Therapy . 18th ed. Whitehouse Station. NJ: Merck:
2006.
Chowdhury NR. Chowdhury JR . Diagnostic approach to the patient with jaundice or asymptomatic hyperbilirubinemia. Chopra S. ed. Waltham. MA:
UpToDate: 2013.
Hui D. Leung AKC. Padwal R. Jaundice. In Approach to Internal Meaicine: A Resource Bock for Clinical Practice. 3rd ed. New York: Springer; 2011.
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Schrier SL. Approach to the diagnosis of hemolytic anemia in the adult. Mentzer WC. Landaw SA. eds. Waltham MA: UpToDate: 2014.
Neck Mass/Goiter
Lalwani AK. Chapter 27: Neck Masses. In Current Diagnosis & Treatment in Otolaryngology: Head & Neck Surgery . New York: McGraw - Hill: 2011.
Ross DS. Diagnostic approach to and treatment of thyroid nodules. In Post TW. ed. Waltham. MA: UpToDate: 2014.
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Ross DS. Treatment of Graves' hyperthyroidism in adults. In Post TW. ed. Waltham. MA: UpToDate: 2014. c
Schwetschenau E. Kelley DJ. The adult neck mass. Am Fam Physician. 2002 Sep 1:66( 5):831- 838.
Fried MP. Neck mass. The Merck Manual ( internet ]. Kenilworth. NJ: Merck: 2016. Accessed July 4.2016. era
CD
Pupil Abnormalities
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Friedman Dl Trobe J. Pupillary abnormalities MedLink Neurolog'/: 2010.
Riordan- Eva P. Hoyt WP. Neuro- ophthalmology. In Riordan-Eva P. Whitcher J. eds. Vaughan & Asbury 's General Ophthalmology. 17thed. New York:
McGraw -Hill: 2007.
Tinnitus
Crummer RW. Hassan GA. Diagnostic approach to tinnitus. Am Fam Physician . 2004 Jan l;6'/ ( 1):120 - 126.
Tucci DL. Tinnitus. Merck Manual Online. 2009 Jan. [cited October 7.2010 ], Available from: IItp:// www.merck.com/mmpe/sec08/ch084/ch084d.ht ml
Trauma
. .
MacKinnon D Brzozowski M. Hans L. Trauma resuscitation. In Hans L. Mawji Y eds. ABCs of Emergency Medicine. 12 th ed. Toronto: University of Toronto:
2012:206 - 214.
Marx JA. et al. Rosen s Emergency Medicine: Concepts and Clinical Practice. 7th ed. Philacelphia Mosby Elsevier; 2010:247 - 250.
.
Raja A. Zane RD. Initial management of trauma in adults. Waltham MA: UpToDate.
Stiell IG.et al. The Canadian C- Spine rule versus the NEXUS low - risk criteria in patients with trauma. New Engl J Med . 2003:349:2510- 2518
Dries DJ. Perry JF. Initial evaluation of the trauma patient. Last updated 2008 Aug 19. Available from:
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Hoffman LH. et al. First Exposure Emergency Medicine. New York: McGraw - Hill; 2008.
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Introduction 430
Approach to End of Life Care & Bereavement 481
Approach to Medical Literature 483
Capacity Assessment 485
Clinical Epidemiology 436
Confidentiality 487
Doctor -Patient Relationship 438
Informed Consent 439
Medical Assistance in Dying 490
Personal & Professional Conduct 491
Research Ethics 492
Resource Allocation 493
Sexual Health History 494
Truth Telling 495
Station Contributors 496
References 497
o
LU
I
CL
This section of the manual addresses a number of topics that are not directly tied to specific medical
disciplines or organ systems, but rather addresses other knowledge which is essential for the practice
of medicine. In an OSCE station, this material may represent an important component of being able
to manage the medical problem at hand. For example, it is important to understand the concepts of
relative risk and number needed to treat if you are asked to discuss the pros and cons of starting a
cholesterol - lowering medication with a patient. Alternately, you will also encounter OSCE stations
that focus on this material as the primary topic. Common examples include breaking bad news,
obtaining consent for a surgical procedure, or counseling a patient before HIV testing.
Often this material is dismissed by students as being " soft ” or less important than the biological
content of medical school. However, once out in practice, many physicians will agree that these
topics present some of the most challenging aspects of patient care. It is relatively easy to look up
treatment for a given disease or the appropriate workup for an abnormal lab value, but harder to
know how to solve an ethical dilemma or a difficult medico - legal situation. Giving these topics the
attention they deserve as you prepare for exams will save you great time and stress in your future
training and practice.
In an OSCE, just as in real life, it is important to remember that you cannot know everything, but
you should have an idea of what resources are out there for the times when you need help. If you
are unsure if you really should be giving out confidential information, or if a certain action could be
considered unprofessional, it is best to stop and defer the decision until you can find out. Being able
to tell your OSCE examiner, " I don' t know, but this is who I would call (or consult with) to find out ”
is better than guessing and risking a critical error.
“D
ZE
m
O
Edmonton Manual of Common Clinical Scenarios 480
APPROACH TO END OF LIFE CARE & BEREAVEMENT
Current Editor: Caitlyn Collins BSc MD
End of life care can be challenging for patients, their families, and the health care team. To provide high quality care, it is necessary to
inquire about and understand patients’ wishes for the end of life, ideally while they are still well. As part of holistic care for a patient
and their families during the dying process, the emphasis should be placed on patient comfort. This includes symptom management ,
as well as the integration of an interdisciplinary team to address spiritual care and provide emotional support. Families are often
unsure what to expect in the period of imminent death and how they can interact with their loved ones. As health care practitioners,
it is our role to help prepare families and assist them in understanding what is happening to their loved ones and begin the grieving
process.
S.P.I.K.E.S.
•S — Setting:
Ideally, try to ensure there is a quiet , private space available to have a discussion. Focus your attention on the patient and their
families, and avoid distractions such as cell phones and pagers. Create a safe and welcoming environment by positioning yourself
so that all members of the conference are in view. Sit down during the encounter to ensure you are speaking on the same level as
the patient and family.
•P — Perception:
Next, try to gain understanding of what the patient and their family already know. Ask open-ended questions such as " What do
you know about the illness/situation thus far ? What is your understanding of the current situation? ”
.
•I — Invitation:
.
The amount of information desired about the situation varies between individuals. Ask questions such as " Would you like all the
information today ? Are you the type of person who likes to know everything that is going on presently? Would you prefer to have
a family member present ? ” to understand how and when to deliver the details of the bad news.
•K - Knowledge and Information:
For most , this is the most challenging part of delivering bad news. Before you actually deliver the news, warn the patient; for
. .
example "Unfortunately I have bad news to deliver today.” Speak slowly and confidently. Use simple and concise language, and
avoid medical jargon. Be direct and clear in what you are saying. Portray empathy with your phrasing, but ensure you provide all
the information the patient and family needs to know. Be sure to intermittently check for the patient 's /family ’s understanding of
information.
•E — Empathy and Emotions:
Be reactive to the patient 's feelings. Have tissues nearby. Acknowledge their emotions through your body language and words.
Body language is key: for example, lean forward and uncross your arms and legs. Validate what the patient is feeling, no matter
.
what that may be. There may be tears - don’t be scared! Take a breath, pause, and allow the patient to cry or think You don’t have
to fill the silence.
•S — Summary:
Make sure you have a plan in place for the patient. Summarize key things from the encounter. Allow plenty of time for the patient
and/or family to ask questions. If not already known, it is important to identify the patient ’s goals from this point forward; for
example, aggressive therapy vs. palliation. Be sure to offer follow - up to address additional questions the patient and /or family may
have.
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KUBLER -ROSS 5 STAGES OF GRIEF
1. Denial and Isolation
2. Anger
3. Bargaining
4. Depression or Sadness
5. Acceptance
These stages may occur sequentially or overlap in any order or combination. For every stage, the same approach to the patient should
be used:
• Be sensitive toward the patient ’s feelings about death
• Watch for cues that indicate the patient is willing to speak/share
• Allow time for the patient to ask questions
• Explore patient concerns and provide information that they request
• Demonstrate a commitment of support for the duration of the illness
• Maintain open communication with patient/ family to address demands for inappropriate treatment
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APPROACH TO MEDICAL LITERATURE
Current Editor: Conrad Tsang BHSc MD
HIERARCHY OF EVIDENCE
Systematic Review: compilation of results from multiple studies
• Meta - analyses can quantify the overall treatment effect across multiple studies, but only if the studies are homogeneous (they use
methodology that is similar enough to allow results to be combined)
Randomized Control Trial (RCT): patients are randomly assigned to the treatment or a comparison group
• Minimizes bias as statistically the treatment and comparison groups should be balanced in prognostic factors
Cohort Study: groups patients according to exposure status / risk factors and assesses the likelihood of outcomes
..
• Conceptually is similar to a RCT without the randomization step (e g , in adults who work in construction versus other settings,
how many from each group will be diagnosed with asthma?)
> Prospective: enroll patients and follow them for development of outcome
> Retrospective: use previously collected data on risk factors but still look forward in time for development of outcome
Case-control: groups patients according to outcomes and assesses who had risk factors of interest
• For example, in adults who have been diagnosed with asthma, how many worked in construction compared to other settings?
• By definition, these must be retrospective studies
Cross- sectional: assess both exposure and outcome prevalence simultaneously in an assembled population of exposed
and unexposed patients: data captures the population in a “snapshot in time"
Case Series and Case Reports: descriptions of multiple or single patients with no control group
—
neously ulation and not just those seeking medical association
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Internal Validity: methodological quality of a study to support its conclusions
External Validity: generalizability to patients outside the study (e.g., are the patients in the study group similar to your patient?)
483 Edmonton Manual of Common Clinical Scenarios
RCT VALIDITY CONSIDERATIONS
Note: aspects not concerning the randomization protocol also apply to cohort studies
Population Selection
• To answer the study question, appropriate inclusion and exclusion criteria for subjects should be used - will affect external validity
Allocation Sequence (protocol for randomization)
• Should assign subjects to intervention or comparison groups completely randomly (e.g., using a computer - generated sequence)
Allocation Concealment
• Allocation sequence is hidden from investigators to minimize selection bias (e.g., hiring an independent group to randomize
subjects); this safeguards the allocation sequence before and until allocation
• Unlike blinding, can be fully implemented in any RCT and therefore should always be done
Balance of Prognostic Factors
• Based on probability, the randomization process should have balanced the potential prognostic factors between groups, and
studies should report this
Blinding
• Whenever possible, it is preferable that individuals involved with the study do not know whether patients are in the intervention
or comparison group. Consider blinding patients, clinicians, outcome adjudicators, and data collectors /analysts.
• Safeguards the allocation sequence after allocation has occurred
• Cannot always be implemented (e.g., in a study comparing two surgical techniques, it would be impossible to blind the surgeons)
Intention- to- treat Principles
• Patients are analyzed according to the group they were originally randomized to, not based on whether they ended up receiving
the intervention or comparator
•Preserves the prognostic balance between the groups and minimizes the risk of bias, as there may have been a systematic reason
Completeness of Follow-up
• Authors should assess why data is missing (e.g., are patients are dropping out of a group because there are too many side effects?)
Study Selection
• A wide variety of sources were used to ensure an exhaustive search was completed, including using databases, trial registries,
funding agencies, unpublished data (e.g., negative results are less likely to be published), hand- searching, etc.
• Based on inclusion and exclusion criteria, abstracts are reviewed by at least two reviewers; full articles are read when reviewers
agree they are relevant to the clinical question
• An appropriate method is used to resolve conflicts in abstract review (e.g., use a third reviewer to decide)
When individually assessed, the included studies were of high methodologic quality.
Results were relatively similar from study to study
• Data can be pooled into a meta - analysis if statistical tests indicate low heterogeneity, both clinically (patients /diseases) and
methodologically (study design and execution). The I2 test is commonly used to assess for heterogeneity.
• Forest plots may be used to visually show individual trial results and the pooled result
a UDY ENDPOINTS
Patient -important: the preferred reported outcomes used in clinical decision - making ( e.g., risk of stroke, quality of life)
.
Composite: outcome is comprised of several other events (e.g., cardiovascular events including Ml hospitalization, and death)
• Allows studies to have smaller sample sizes and shorter follow - up periods. Need to be interpreted with caution as interventions
will not have the same effect across different events, and the composite endpoints may not have similar importance to patients.
Surrogate: outcome is a substitute lab/physiologic variable or subclinical disease measure for patient -important
outcomes (e.g., bone mineral density as a surrogate for fracture risk )
• May be more convenient for data collection; also allows smaller sample sizes and shorter follow -up periods
• Surrogate outcomes should be correlated to patient -important outcomes to be valid measures
INTERPRETING RESULTS
• Is this result statistically significant? By convention, statistical significance is usually set at p < 0.05, meaning there is < 5% chance
the results are due to chance
• How statistically precise is the result ? Are the confidence intervals narrow, meaning the data is convincing that the treatment
effect is close to the point estimate?
• Is this result clinically important and does it change outcomes that matter ?
• Is the treatment worth the potential harms or costs? Are there other patient - important outcomes that were not reported? u
• Can I apply these results to my patient? Did they fit well into the population that was studied?
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CAPACITY ASSESSMENT
Current Editor: Daniel Friedman MD
HAT IS CAPACITY?
• Capacity is defined as the ability to understand the information that is relevant to making a personal decision and the ability to
appreciate the reasonable foreseeable consequences of the decision
• Capacity is assessed for a specific decision and is not "all - or - nothing" (e.g., a patient may be able to make most decisions but
cannot make some complex healthcare decisions unassisted)
• Continuum of capacity: full -* impaired -* temporary loss
—
• Capacity is not a medical diagnosis but rather a professional opinion
permanent / long- term loss
• Making a risky decision or against medical advice isn’ t necessarily incapable ( the process, not the decision, dictates capacity)
> Initial assessment: gather collateral history, assess risk of decision to patient /others, identify domain( s) in which the
patient ' s decision - making is questioned (e.g., healthcare, finance, legal matters, accommodation, social activities, education,
employment activities)
> Assessment in depth: test and remove barriers to functioning ( e.g., poor vision, delirium, language barrier )
> Formal capacity interview: structured interview guided by a government -provided interview worksheet
> Assessor can formulate a clinical opinion of patient ' s current level of capacity in a specific domain
• To regain capacity, both the assessor and ADM agree that the patient has improved and regained capacity (if there is a
disagreement, a separate physician/psychologist and another assessor must independently assess patient)
> Guardian: make non- financial decisions if an ADM is required and no previous personal directive is prepared
> Trustee: make financial/property decisions if an ADM is required and no ePOA has been prepared
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KEY DEFINITIONS
Incidence: new cases of disease during a time interval in a given population
Present A B
Prevalence: number of existing cases of disease in a given population
Absent C D
Attack Rates: the proportion of those who became ill after a specific exposure:
used in epidemics
Case Fatality Rates: ratio of number of deaths due to a specific disease/number of
people affected by disease over a defined period of time
Relative Risk ( RR ): ratio of events occurring in exposed vs. unexposed group: differentiate from absolute risk
• RR = risk in exposed/risk in unexposed = Positive Predictive Value/(1- Negative Predictive Value) = A/ ( A+ B ) + C/ (C+D)
Odds Ratio (OR ): ratio of odds that event will occur in exposed vs. unexposed groups; when prevalence of disease is low.
OR approximates RR
" OR = A/B T C/D
Absolute Risk ( AR ): amount of risk that is due to exposure
. AR = A/( A + B) - C/(C+D)
Number Needed to Treat ( NNT): number of patients who need to be treated to prevent one adverse outcome
• NNT = 1/Absolute Risk Reduction ( where ARR = Control event rate - Experimental event rate )
Specificity: proportion of patients without the disease who test negative: high specificity = positive test rules IN (SpIN)
• Specificity = TN/ (TN+FP)
Sensitivity: proportion of patients with the disease who test positive; high sensitivity = negative test rules OUT ( SnOUT)
• Sensitivity = TP/(TP+FN )
Likelihood Ratio: provides a direct estimate of how much a test result will change the odds of having a disease
• + ve LR = Sensitivity/ ( 1- Specificity )
• - ve LR = (1- Sensitivity)/Specificity
Positive Predictive Value: proportion of patients with positive test who have the disorder = TP/ ( TP+FP)
Negative Predictive Value: proportion of patients with negative test who do not have the disorder = TN/( TN+FN)
False Positive Positive predictive value ( PPV ) = True
Positive True Positive ( Type I error ) positive / 1Test outcome positive
False Negative Negative predictive value ( NPV ) = True
Negative True Negative
(Type II error ) negative / S Test outcome negative
Sensitivity = True positive Specificity = True negative
/ 2 Disease present /1 Disease absent
Standardization: adjusting raw measurements to a ' standard population' to minimize bias due to varying demographics
A screening test must detect disease before clinical diagnosis; test must be acceptable to population, facilities for
diagnosis should exist, and treatment is acceptable and effective
Pre - test Probability: based on clinician’s experience and interpretation of patient ’s signs/symptoms
Post - test Probability pre- test probability x likelihood ratio; calculate with nomogram
Bias
• Lead- time: earlier detection, longerapparent survival
• Length- time: preferentially detect disease with slower progression
• Volunteer: volunteers are usually healthier people
• Sampling: non-representative sample chosen (e.g.. characteristics of larger population not reflected )
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CONFIDENTIALITY
Current Editor : Patricia Lee MD
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PHYSICIAN OBLIGATIONS
The physician must place the best interests of the patient first.
The physician must follow through on undertakings made to the patient in good faith.
The physician must disclose to the patient any limitations, whether it be personal beliefs, values, or inclinations that
would limit the treatment the physician is able to provide.
SSJFLICTS OFINTEI
The physician must always act in the patient 's best interest.
Any conflict of interest should be managed by the physician so as not to compromise what is considered to be in the
best interest of the patient.
The physician should not act for personal advantage- financial, academic, or other.
It is therefore a physician’s duty to recognize any conflict of interest, ensure that the patient ’s best interest remains
central, and, if necessary and appropriate, disclose the conflict of interest to the patient.
PROFESSIONAL BOUNDARIES
The physician should respect and maintain professional boundaries with the patient.
This applies to physical, social, emotional, and sexual boundaries.
I a:MM AN AND PATIEIziMUMaj
The physician has the right to refuse or accept patients requesting care
• without consideration of race, age, gender, sexual orientation, financial means, religion, or nationality
• without arbitrary exclusion of any particular group of patients, such as those known to be difficult, or afflicted with serious disease
• cannot refuse care in emergency situations, in which case care must be provided
Once having accepted a patient into care, the physician may terminate the relationship, but must ensure the following:
• 1) that care has been transferred to another physician or 2) adequate notice has been offered to the patient to make alternate
arrangements
• without consideration of race, age, gender, sexual orientation, financial means, religion, or nationality
SARE OF FAMILY
Physicians should not diagnose or treat family members except for minor conditions or emergencies, where they are the
only available physician.
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INFORMED CONSENT
Author: Mackenzie Lees MD
• Voluntary agreement given by a patient or responsible proxy (e.g., patient ’s parents) for a medical treatment, participation in a
study, invasive procedure, etc., done for any reason
• Must be specific, informed, and freely made (not coerced or made under duress)
• Based on principles of autonomy and beneficence
• A necessary part of a physician's duty to care for their patient
• Legal consequences if not properly obtained
kViil4in:L«IH!»x«]ill
. «i iISENT?
.
—
• Note: Should be made in advance and should be well documented
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Exact nature of the procedure and any alternatives ( including ’ zero option’ = do nothing)
• Prognosis ( with and without treatment)
• Associated risks and benefits of treatment and alternatives, including serious risks (even if rare)
• Answers to patient ’s questions, if any
• Patients only need the relevant information that will allow them to make a decision consistent with their values /beliefs
• Reasonable -person standard": disclose what a reasonable person in the patient ’s situation would want to know in order to make a
decision about the intervention
HOW TO OBTAIN INFORMED CONSENT
• Explain simply, clarify when/if necessary, word the information appropriately, and use translators and/or pictures /diagrams to help
explain procedures
• Define the options clearly
• Encourage patient to ask questions and ensure ample time for a decision
• Ask patient to explain in their own words what was discussed to ensure their comprehension
• Consent can be withdrawn at any time (halt procedure, unless doing so would cause serious harm ), but if the procedure is
continued, the onus is on the physician
• Keep in mind that obtaining consent does not mean getting the patient to sign a consent form, but is rather a complex, important
process as outlined above
IEXC1
• Patient waiver or patient incapacity (consent must come from a properly informed proxy decision maker )
• Emergencies: immediate treatment required to preserve life or health, patient ’s or proxy’s consent cannot be obtained, no
evidence of prior competent refusal and /or treatment prescribed under legislation (e.g.. The Mental Health Act: The Public Health
.
Act; The Child Youth, and Family Enhancement Act)
> Exceptions to this exception: suicide notes and if the patient previously refused the same treatment
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As of 2015, the Canadian Supreme Court of Justice deemed it is no longer a criminal offence for Canadian physicians to
assist in certain individuals in ending his/her life. Federal Bill C- 14 took effect June 2016, and outlines specific criteria
m
and safeguards for Medical Assistance in Suicide (MAID)
HAT IS MEDICAL ASSISTANCE IN DYING
MAID is when a physician or nurse practitioner administers or prescribes a substance to the patient, at their request,
that causes death. The substance can be self - administered by the patient. MAID does not encompass palliative care or
—
pallitive sedation
ETHICS, LAW & POLICY
MAID provides the patient with autonomy in life and dignity in death. The Canadian Medical Association acknowledges
that physicians are not obligated to provide MAID. They may refer to a practitioner who administers MAID. Each health
jurisdiction may have its own policy. Some, such as Alberta Health Services have a MAID consulting team.
i HI ii ilmJ IInIIM
( from Bill C- 14)
• Eligible for Canadian funded health services
• Must be 18 years or older with full capacity
• Must have palliative medical diagnosis
• Request for MAID must be voluntary and without external pressure
• Must provide consent for MAID after being fully informed of MAID and other options including symptom relief via Palliative care
HPPROACH TO MAID
Generally, the patient must be assessed by two separate physicians/nurse practitioners, fulfill the eligibility criteria,
and deemed appropriate for MAID. A written and signed request/form must be made by the patient before two
.
independent witnesses The practitioners must also fill out a MAID form. After a period of 10 clear days, MAID can be
carried out at the patient 's desire. Time of death can be decided by the patient. The patient may rescind their decision
.
at any time The drugs are dispensed, and administered ( by self or practitioner). A death certificate is issued, and some
jurisdictions may request a coroner consult post -mortem.
• Ensure the patient ' s request for MAID is not due to poorly controlled palliative symptoms.
• The ESAS - r can be used to assess the progression of the symptoms. Symptoms should be optimally controlled first.
• Capacity assessment
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PERSONAL & PROFESSIONAL CONDUCT
Current Editor: Jonathan Yang MD
Practicing medicine requires maintaining a high degree of integrity, honesty, professionalism, and adherence to
fundamental ethical values. To accomplish such objectives, the MCC and CPSA have outlined the following expectations:
Accountability
• Promote safe, high quality patient care and effective collaboration with others on the health care team
• Maintain high standards of personal and professional honesty and integrity
•Take responsibility for one’s behavior and ethical conduct
• Record/report accurately and in a timely way clinical information, research results, assessments, and evaluations
• Communicate with integrity and compassion
• Accurately attribute ideas developed with others and credit work done by others
• Deal with conflicts of interest openly and honestly
• Engage in lifelong learning
Confidentiality
• Respect the confidentiality and privacy of patients, research participants, and educational participants
• Limit discussion of patient information to settings appropriate for clinical or educational purposes and to caregivers, unless given
explicit patient consent, or permitted by legal and ethical principles
• Know and comply with legislation regarding confidentiality and health information
Respect for Others
• Treat patients, families, and members of the health care team with respect and dignity
• Refrain from conduct that may be considered offensive to others or disruptive to the workplace
• Respect patient autonomy by appropriately discussing investigation and treatment options with the competent patient and, only
with the patient ' s consent, identified other persons
• Ensure appropriate consultation occurs when a patient lacks the capacity to make treatment decisions, except in emergency
circumstances
• Respect the personal boundaries of patients by refraining from sexual behavior and physical contact outside the proper role of a
physician
• Avoid any forms of discrimination based on age, gender identity, gender expression, race, ethnic origin, beliefs, sexual orientation,
or any other protected grounds, as defined by human rights legislation
• Allow colleagues to disagree respectfully without fear of punishment, reprisal, or retribution
• Recognize the important contributions of colleagues
Responsible Behavior
• Attend to personal health, recognize self - limitations, and seek help when personal knowledge, skills, or health is inadequate
• Avoid substance misuse or other factors that could impair the ability to provide safe care to patients
• Maintain professional boundaries by minimizing self - disclosure and refraining from providing care to individuals where objectivity
may be compromised
• Participate in professional development, assessment processes, and quality improvement projects to deal with errors, disclosure of
events, and close calls
• Avoid exploitation of others for emotional, financial, research, educational, or sexual purposes
• Teach and model professional behavior in research, clinical practice, educational encounters, and in all public settings (including
online settings)
• Address breaches of professional conduct by another colleague by direct discussion with that person or. if necessary, reporting to
the appropriate authorities
• Know and adhere to the CPSA Standards of Practice
• Respect the authority of the law and understand professional and ethical obligations
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RESEARCH ETHICS
Current Editor: Conrad Tsang BHSc MD
i n:w h\ z an 1 »
Evidence shows that clinician- researchers may conflate their practice with research trials and be overly optimistic about
experimental interventions. They should remember their expectations as clinicians and communicate with patients
appropriately.
They should take all necessary measures to separate their roles, if possible (e.g., hire an individual to recruit participants).
—
ethical dilemmas and conflicts can arise.
Current Editor: Jaspreet Mangat MD
Our aging population, demand for new medical therapies, increasing financial strain on the health care system, and
rising public expectations make resource allocation a relevant topic. Maximal benefit with minimal cost is the mentality
surrounding scarce resource allocation. However, health care providers are expected to abide by their patients and
ensure the best care possible regardless of costs. At times, this balance is difficult to maintain and, as a result, many
Resource allocation is the distribution of goods and services to programs and people. In the context of health care,
resource allocation can be divided into three major concepts: macro, meso, and micro allocation:
• Macroallocation: resources provided by all levels of the government -federal, provincial, and municipal
• Mesoallocation: involves the individual hospital's allocation of finances and services to its programs
• Microallocation: is the deliverance of resources to every individual patient
Resource allocation is a broad term and includes things such as finances, human resources, and services offered (cancer
therapy, dialysis, organ availability, etc.).
h\‘J U : •<
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• Select therapies, tests, and exams with proven cost effectiveness and beneficial outcomes.
• Decrease use of ‘marginally ’ beneficial and unnecessarily repeated tests /exams.
• Advocate and meet your patient ’s needs first, but also be open with them regarding providing cost - effective care, particularly if it
will not alter management plans.
• Unacceptable shortages in medical resources need to be brought up v/ ith individuals and administration responsible for macro-
and mesoallocation.
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BASICS
• Sexual health and sexuality (SHS) can have a significant impact on overall health and quality of life; identity and self -esteem may
be impacted by poor sexual health.
• Clinicians should approach SHS in an open, respectful, and non- judgmental manner. Do not make assumptions based on patients '
age.
• Always screen for high- risk behaviours and red flags.
HISTORY
Patient may be uncomfortable; provide privacy, respect and confidentiality. Maintain a non - judgemental,
respectful and neutral manner. Introduce the topic by normalizing SHS and asking for an invitation to Special Groups
discuss the topic. Extremes of age
For example; "I would like to ask you about SHS. It is something I talk to with all of my patients and Cognitively Impaired
important for health. Would that be alright ?" Physically Disabled
Sexual Minorities
• For teenagers; emphasize patient confidentiality, normalize sexuality and encourage questions. Assault Survivors
• For adults: an active sex life is a normal part of aging Sex trade workers
• Acknowledge the patient ' s discomfort. If the patient does not consent, consider the discussion again
at a later date if time allows.
ID .
• Patient name, age gender (male, female, trans, fluid, etc ).
HPI patient has specific complaints, approach with PQRSTAA
• If
• The five Ps
• Sexual function and cycle
• Screen for red flags and intimate partner violence
RED FLAGS • High -risk behaviours, addiction, multiple STIs, sex- trade workers
• Positive intimate partner violence screen
PMHX • Chronic conditions: DM, HTN, CVD, cancer
• Infections: past Hx of STI, UTI, PID (in women)
PO&GHX • Menstrual cycle, obstetrical history
LEGAL BASIS
• Standard for disclosure is what a reasonable person in the
patient ’s circumstances would want to know (i.e., purpose
ABCDE of Breaking Bad News
and implications of investigation, disease and prognosis, • Advance preparation
risks and benefits, health risks of test ); consult CMA Code of ( ask what they already know, arrange time and place for
Ethics or CMPA if unclear meeting, prepare emotionally)
• Obtaining informed consent is a legal obligation and failure
to do so may result in legal action. Obtaining consent • Build a therapeutic environment/relationship (quiet place
with incomplete or false information can be considered without disturbances, sit close enough to touch if necessary,
negligence. reassure about suffering/pain)
• Disclosure is a vital component of obtaining full consent from
a patient • Communicate (be direct; no jargon, acronyms, or euphemisms;
allow silence; use 'death' and 'cancer ' and ask them to repeat
DIFFICULTIES ENCOUNTERED IN PRACTICE their understanding of news)
• Bad news may harm the patient, thus conflicting with the
obligation of non- maleficence (see Approach to End of Life • Deal ( with patient and family reactions; assess patient
Care & Bereavement station) reaction ( e.g., withdrawal, disbelief, anger ); listen actively,
• Uncertainty about the diagnosis empathize, and support the patient )
• When a medical error occurs: disclose error without
suggesting it resulted from negligence; negligence is a • Encourage (correct distortions, address further needs, offer
finding made in court and not by the physician to tell others on patient behalf, develop a plan for near - and
• Patient 's family is opposed to truth telling - counsel them long- term, assess suicide risk, arrange referrals and follow -
about truth telling as you would any other medical problem .
up be aware of own feelings)
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IM
Approach to End of Life Care & Bereavement *
Bailea W.. Buckmanb R.. Lenzia R . . Globera G.. Bealea E. Kudelkab A. SPIKES- A six -step protocol for delivering bad news: Application to the patient with
cancer. The Oncologist . 2000;5 ( 4):302 311.-
Bailey F. Harman B. Palliative care: The last hours and days of life. In Savarese D. ed. UpToDate. 2014. Retrieved from http://uptodate.com/home
.
Bickley LS Szilagyi PG. Bates' Guide to Physical Exam and History' Taking. 10th ed. Philadelphia: Lippincott Williams & Wilkins; 2009.
Singer PA, MacDonald N Bioethics for clinicians: Quality end of life care. CMAJ . 1998:159 2): 159- 162.
,
'
Canadian Hospice Palliative Care Association ( Internet ]. Ottawa: c 2010. [cited Oct. 1.2010]. Available from: http://www,chpca.net
Hui D. Approach to Internal Medicine: A Resowce Book for Clinical Practice. 3rd ed. New York: springer: 2011:389 - 400.
Pereira J. The Pallium Palliative Pockctbook . 1st ed. Ottawa: Pallium Canada: 2013.
.
Meier D. McCormick E. Palliative care: Benefits, services, and models of care. In Dizcn D ed. UpToDate. 2014. Retrieved from http://uptodate.com/home.
Capacity Assessment
Alberta Office of the Public Guardian. Guide to capacity assessment under the Personal Directive Act. 2008. Retrieved from Alberta Human Services
website: http:// www.humanservicc 5.alberta.ca/documents/opg - personal -directives -public.ition- opgl642.pdf
.
Covenant Health. Capacity Assessment Retrieved from https://medicalstaff .covenanthealth.ca/clinicaTsupport - services /capacity - assessment. Accessed
June 24.2016.
Clinical Epidemiology
.
Guyatt G Rennie D. Users ' Guides to the Medical Literature: A Manual for Evidence - Based Clinical Practice. 1st ed. Chicago: JAMA: 2005.
. . .
Goodman KJ Phillips CV The Hill criteria of causation In Encyclopedia of Statistics in Behavioral Sciences. London: Wiley: 2005.
Confidentiality
CMACode of Ethics. 2C04. Retrieved from: http://policybase.cma.ca /dbtw - wpd/PolicyPDf / PD04 - 06.pdf
Informed Consent
Hebert PC. Doing Right: A Practical Guide to Ethics for Medical Trainees and Physicians. 2nd ed Don Mills. ON: Oxford University Press: 2009.
MAID
Medical Assistance in Dying |AHS Policy HCS- 165 - 01]. ( 2017). Alberta Health Services. Medical Assistance in Dying [ CMA policy ]. (February 6.2016).
. .
Canadian Medical Association. Medical Assistance in Dying [ Standard of Practice ]. ( 2016. July 16 ) . Yukon Medical Council S. C - 14 ( 2016) (enacted)
Medical Assistance in Dying
Research Ethics
Canadian Institutes of Health Research. Natural Sciences and Engineering Research Couni il of Canada, and Social Sciences and Humanities Research
Council of Canada. Tri- Council Policy Statement: Ethical Conduct for Research Involving Humans. December 2010.
Canadian Medical Association. CMA Policy: Code of Ethics. 2004.
Lerrmens T. Singer PA. Bioethics for cliniciars: 17. Conflict of interest in research, education and patient care. CMAJ . 1998:159(8):960- 965.
Weijer C. Dickens B. Meslin EM. Bioethics for clinicians: 10. Research ethics. CMAJ . 1997:156( 8):1153 - 1157.
Resource Allocation
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McKneally MF Dickens BM Meslin EM Singer PA. Bioethics for clinicians: Resource allocation. CMAJ. 1997 Jul 15:157( 2) :163 - 167.
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LU Heber PC. Hoffmaster B. Glass KC. Singer PA. Bioethics for clinicians 7. Truth telling. Can Med Assoc J . 1997 Jan 15;156( 2):225 - 228.
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Minichiello TA. Ling D Ucci DK. Breaking bad news: A practical approach for the hospitalist Journal of Hospital Medicine. 2007 Nov:2( 6):415 - 421.
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Edmonton Manu il of Common Clinical S
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APPENDIX A: ABBREVIATIONS
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- A ARB angiotensin II receptor blockers
ARDS acute respiratory distress syndrome
aa artery ARF acute renal failure
AAA abdominal aortic aneurysm AMD age related macular degeneration
A- aD02 alveolar -arterial oxygen gradient AS aortic stenosis
AAT activity as tolerated AS ankylosing spondylitis
A &O alert & oriented ASAP as soon as possible
ABCDE airway breathing circulation disability exposure ASC-H atypical squamous cells cannot exclude high grade
aBd abduction intraepithelial lesion
ABD abdomen
ASC- US atypical squamous cells of undetermined significance
ABG arterial blood gas
ASD atrial septal defect
ABI ankle brachial index ASIS anterior superior iliac spine
AbPB abductor pollicis brevis muscle ASOT antistreptolysin-0 titres
AbPL abductor pollicis longus muscle
ASQ ages & stages questionnaire
Abx antibiotics AST aspartate transaminase
AC air conduction
ATLS advanced trauma life support
ACEI angiotensin converting enzyme inhibitors
ATN acute tubular necrosis
ACLS advanced cardiac life support
ACTH adrenocorticotropic hormone
-
ATTG anti transglutaminase
AUA American Urology Association
AD Alzheimer’s disease
AUB abnormal uterine bleeding
ADAMTS13 a disintegrin and metalloproteinase with a
AV atrioventricular
thrombospondin type 1motif, member 13
A-V arteriovenous
AdB adductor brevis muscle
AVM arteriovenous malformation
aDd adduction
AVN avascular necrosis
ADH anti-diuretic hormone
A-V02 arteriovenous oxygen
ADHD attention deficit hyperactivity disorder
AXR abdominal Xray
ADL activity of daily living
AdDM adductor digiti minimi muscle
AdL adductor longus muscle B
AdM adductor magnus muscle BADL basic activity of daily living
AdP adductor pollicis muscle BAE bronchial artery embolism
ADR adverse drug reaction BBB bundle branch block
ad lib as much as needed BC bone conduction
AECOPD acute exacerbation chronic obstructive pulmonary disease BCC basal cell carcinoma
AED Anti - epileptic drugs BE barium enema
AF atrial fibrillation BF biceps femoris muscle
AFB acid - fast bacilli B - hCG beta human chorionic gonadotropin
AFP alpha - fetoprotein bid twice a day
AGC atypical glandular cells BKA below the knee amputation
Al aortic insufficiency BM bone marrow, bowel movement
AIHA autoimmune hemolytic anemia BMD bone mineral density
AIO anterior interosseous BMI body mass index
AIS adenocarcinoma in situ BP blood pressure
AKA above the knee amputation BPH benign prostatic hypertrophy
ALD alcoholic liver disease BPM beats per minute
ALL acute lymphocytic leukemia BPP biophysical profile
ALP alkaline phosphatase BPPV benign positional paroxysmal vertigo
ALS amyotrophic lateral sclerosis BR brachioradialis muscle
ALT alanine transaminase Br branches
ALTE apparent life threatening event BRBPR bright red blood per rectum
amb ambulate BRCA breast cancer gene
AMDA American Medical Directors Association BRP bed rest with bathroom privileges
AML acute myelogenous leukemia BS bowel sounds
ANA antinuclear antibody BSA body surface area
ANS autonomic nervous system BSO bilateral salpingo - oophorectomy
anti-GBM anti-glomerular basement membrane BUN blood urea nitrogen
AODM adult onset diabetes mellitus BV bacterial vaginosis
AOM acute otitis media BW body Wt
AP anteroposterior Bx biopsy
AR autosomal recessive
x
x 2d times 2 days
XL extended release
XM crossmatch
XOM extraoccular movements
XRT X - ray therapy (radiation therapy)
xULN times upper limit of normal
Y
YF yellow fever
y/o years old
yryear
ytd year - to - date
z
ZEZollinger - Ellison
NUMERIC
# fracture
-ve negative
+ ve positive
17-OHP 17 hydroxyprogesterone
Hemolytic uremic syndrome O'Donoghue triad (rotational force in a Wt- bearing knee)
anemia medial collateral ligament injury
thrombocytopenia anterior cruiciate ligament injury
renal failure medial meniscus injury
Kwashiorkar Rubella
growth retardation patent ductus arteriosis
mental changes deafness
edema cataract
Triad of Luciani (cerebellar disease) Saint’s triad
asthenia gallstones
atonia diverticulosis
astasia hiatus hernia
Mayer- Rokitansky- Kuster- Hauser syndrome Samter ’s triad
absent vagina aspirin allergy
-
non functional uterus
bronchial asthma
normal XX female nasal polyp
Melkersson- Rosenthal syndrome Triad of Schultz
recurrent facial palsy jaundice
plication of tongue gangrenous stomatitis
facial edema leukopenia
Vogt ’s triad
epilepsy
mental retardation
adenoma sebaceum
Weil’s disease
hepatorenal damage
bleeding diathesis
pyrexia
Young' s syndrome
sinusitis
bronchiectasis
azoospermia
Tetralogy of Fallot
atrial septal defect
overarching aorta
pulmonary stenosis
right ventricular hypertrophy
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The Edmonton Manual of Common Clinical Scenarios: Approach to the OSCE
*
The Edmonton Manual is a Canadian guide for medical students and residents that provides
a quick, efficient, and up- to-date approach to over 140 common clinical scenarios. Based on
the Medical Council of Canada Qualification Examination ( MCCQE) objectives, the Edmonton
Manual is a valuable study resource for medical trainees preparing for Objective Structured
Clinical Examinations (OSCE) including the MCCQE Part II.
Organized by medical specialty, each common clinical scenario is presented in a concise and
easy to read two-page format. Key details including diagnostic criteria, differential diagnoses,
focused history and physical exam, relevant investigations, and management are provided
for each clinical scenario. Reviewed by expert physicians, the Edmonton Manual is a reliable
resource for quick review prior to patient encounters in the clinic, on the wards, or in the
emergency room. With additional chapters, essential clinical skills (electrocardiography,
blood-work, radiology) and physical examination techniques, the Edmonton Manual is an
important bedside tool for all physicians in training.
e O
. • Special chapters on essential clinical skills, physical examinations, population health, and
••
'
• -M the ethical, legal and organizational aspects of medicine ( PHELO)
• At-a -glance page format that summarizes focused histories and physical exams, and
provides relevant workups for common presentations.
The Edmonton Manual is a collaborative initiative involving input from students, residents, and
staff physicians at the University of Alberta. The book remains a not - for - profit endeavor from which
proceeds go to charity works and the University of Alberta Medical Students Association.
a P &
9 780986 487460
www.edmontonmanual.com