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Edmonton Manual 6th Edition

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0% found this document useful (0 votes)
1K views

Edmonton Manual 6th Edition

Uploaded by

jane
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd
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tDI I ION

TH
EDITION

APPROACH TO THE OSCE

EDITORS- IN- CHIEF


Patrick Vallance BSc ( Hons )
Colin Andrews MD

Parnian Riaz MD
SENIOR EDITORS
Nazlin Karmali BSc
Cailey Turner BSc

JUNIOR EDITORS
Scott Wong MSc
Trent Schimmel BSc

SENIOR DIRECTOR OF MARKETING & SALES


Patrick Vallance BSc ( Hons)
JUNIOR DIRECTOR OF MARKETING & SALES
Trent Schimmel BSc
Approach to the OSCE: The Edmonton Manual of Common Clinical Scenarios
1st edition ( 2010)

Approach to the OSCE: The Edmonton Manual of Common Clinical Scenarios


2nd edition ( 2011)

Approach to the OSCE: The Edmonton Manual of Common Clinical Scenarios


2nd edition Text Revision ( 2011)

Approach to the OSCE: The Edmonton Manual of Common Clinical Scenarios


3rd edition ( 2013)

The Edmonton Manual: Approach to the OSCE


4 th edition ( 2015)

The Edmonton Manual: Approach to the OSCE


5 th edition ( 2017)

The Edmonton Manual: Approach to the OSCE


6th edition ( 2018)

Copyright © 2018 University of Alberta Medical Students' Association

All rights reserved.


No part of this book may be reproduced in any form without explicit permission from the copyright owner.

Printed in Canada.

ISBN: 978 - 0- 9864874- 6- 0

We look forward to improving this resource annually.


Please send your comments, feedback, errors, or omissions to us by post or email.

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

Edmonto ual of Common Clinical See


PLEASE READ THE FOLLOWING STATEMENTS CAREFULLY

By using this book, you understand and agree to the following:

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.

Edmonton Manual of Common Clinical Scenarios


CONTRIBUTORS
Editorial Team
Editors - in - Chief Patrick Vallance BSc ( Hons) MD Candidate ( 2019) ( Senior Director of Marketing & Sales)

Senior Editors Nazlin Karmali BSc MD Candidate ( 2020)


Cailey Turner BSc MD Candidate ( 2020)

Junior Editors Scott Wong MSc MD Candidate ( 2021)


Trent Schimmel BSc MD Candidate ( 2021) ( Junior Director of Marketing & Sales)

Staff Section Editors:

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
,

Jennifer McCombe MD MPH FRCPC Associate Professor. University of Alberta


,

Kathleen Wong MD FRCPC Assistant Clinical Professor, University of Alberta


,

Mohit Bhutani MD FRCPC. Associate Professor. University of Alberta

Obstetrics & Gynecology . .


Rahim Janmohamed MD FRCSC Associate 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

Essential Clinical Skills . .


Dr. Helly ( Rachel) Goez MD FRCPC Assistant Dean 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

Cover designed by Sharon Liu

Student Section Editors


ECS: Cailey Turner BSc MD Candidate ( 2020)
Physical Exam: Scott Wong MSc MD Candidate ( 2021)
Family Medicine: Trent Schimmel BSc MD Candidate ( 2021)
Internal Medicine: Parnian Riaz MD
Obstetrics & Gynecology: Nazlin Karmali BSc MD Candidate ( 2020)
Pediatrics: Cailey Turner BSc MD Candidate ( 2020)
Psychiatry: Colin Andrews MD
Surgery: Patrick Vallance BSc ( Hons) MD/ MBA Candidate ( 2019)
PHELO: Nazlin Karmali BSc MD Candidate ( 2020)

Edmonton Manual of Common Clinical Scenarios


TABLE OF CONTENTS
1 Essential Clinical Skills
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

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

Edmonton Manual of Common Clinical Scenarios


Lower Respiratory Tract Infection 203
Monoarticular Joint Pain 205
Numbness & Parasthesias 207
Obstructive Lung Disease 209
Palpitations & Arrhythmias 211
Pancreatitis 213
Parkinson’s & Movement Disorders 215
Peripheral Vascular Disease 217
Pleural Effusion 219
Polyarticular Arthritis & Joint Pain 221
Proteinuria 223
Pruritus 225
Renal Failure 227
Restrictive Lung Disease 229
Seizures 231
Shock 233
Sleep - Disordered Breathing 235
Syncope 237
Thrombocytopenia 239
Thyroid Disease 241
Transfusion Counseling 243
Unilateral Swollen Leg 245
Vision Loss 247
Weakness 249
5 Obstetrics & Gynecology
Introduction 260
Amenorrhea 261
Antepartum Care 263
Antepartum Hemorrhage 265
Contraception 267
Dysmenorrhea & PMS 269
Dyspareunia 271
Fetal Distress 273
Fetal Growth Disorders 275
Hirsutism 277
Hypertension in Pregnancy 279
Infertility 281
Interpretation of Fetal Heart Rate 283
Intrapartum Care 285
Menopause 287
Pap Test 289
Pelvic Mass 291
Pelvic Organ Prolapse 293
Pelvic Pain 295
Postpartum Complications 297
Post Term Pregnancy Complications 299
Pregnancy Loss 301
Preterm Labor 303
Vaginal Bleeding 305
Vaginal Discharge 307

Cdmonton Manual of Cum;non Clinical Scenarios


6 Pediatrics
Introduction 314
Abnormal Sexual Maturity 315
Abnormal Stature 317
ADHD/ Learning Disorder 319
Anemia ( Pediatric ) 321
Childhood Communicable Diseases 323
Depressed Newborn 325
Developmental Delay 327
Down Syndrome 329
Ear Pain 331
Enuresis 333
Failure to Thrive 335
Fever without a Source in a Child < 3 Months 337
Heart Murmurs 339
Immunizations 341
Limping Child 343
Neonatal Jaundice 345
Newborn Respiratory Distress /Cyanosis 347
Pediatric Bruising 349
Pediatric Dehydration 351
Pediatric Emergency 353
Pediatric Nausea & Vomiting 355
Pediatric Seizure 357
Pediatric Rash 359
Pediatric Wheeze 361
Periodic Health Exam of a Newborn 363
Periodic Health Exam of a Toddler /Child 365
Periodic Health Exam of an Adolescent 367
Speech & Language Abnormalities 369
Stridor 371

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 !

How to Excel at the OSCE


Approach theOSCEasyou would approach an interview: "beyourself ... butaslightly more refined you! ” Thistiponly works if you adhere
to thelessonslearned in medical school (e.g., palpating the radial before taking theblood pressure) with your real - life patients. For more
thoughts on how to excel at the OSCE as it applies to the specific specialties, please see theintroductions by each of the sectioneditors.
Good luck !

Figure adapted from:


Miller GE. The assessment of clinical skills/competence/performance. Acad Med. 1990 Sep;65 ( 9 Suppl):S63 - 567.

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.

Edmonton Manual of Common Clinical Scenarios


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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

Staff Section Editors


Helly Goez MD FRCPC
Division of Pediatrics Neurology
. .
Assistant Dean Associate Professor Diversity. Faculty of Medicine and Dentistry
Stollery Children Hospital. Glenrose Rehabilitation Hospital, Edmonton Clinic Healthy Academy

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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

16
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Authors: Shawna Pandya MD. Brian Yong MD Darren Nichols MD CCFP

Orders ( DAD -DAVID)


• The traditional DAD - DAVID format, with some examples of common orders, is included below:
D - A- D
• Date/Time
• Admit to ( ward/service) /Allergies
• Diagnosis
D
• Diet
> Diet as tolerated ( DAT)
> .
NPO ± ice chips (e.g. pre - op, aspiration risk ), clear fluids, full fluids, thickened fluids (dysphagia diet )
> Advancing diet ( NPO sips CF FF DAT)
.
> Canadian Diabetes Association: diabetic diet ( small - 1600kcal med- 1800kcal, lrg- 2000kcal)
> Cardiac /heart healthy diet, Mediterranean diet
> Fluid restrictions, salt restrictions
> Consider Speech Language Pathologist consult for dysphagia, aspiration risk, swallowing study
> Consider Dietary consult for content, consistency, and quality
A
• Activity
> Activity as tolerated ( AAT)
> Ambulation orders: if necessary consult OT/ PT
> Up in chair for meals
> Non- weight bearing (NWB), weight - bearing as tolerated ( WBAT), full weight -bearing ( FWB )
.
> Bed rest ( BR ) bed rest with bathroom privileges ( BRwBP)
> Bed/chair alarms
> Elevate head of bed (HOB) to 30 degrees
> Precautions: fall, seizure, spinal, etc.
> DVT prophylaxis, compression stockings
V
• Vital Signs
.
> Clarify what routine VS are for each service, add on as necessary ( i.e., HR, BP RR, Temp, Sa02)
> Include on - call orders: set parameters (e.g., call MD if sBP > 180 mm Hg)
. . .
> Specify frequency, e.g. qlh q4h, close observation (q15 min) nurse in room, constant security (psychiatry, geriatrics), routine/
regular observation (pediatrics), when awake
> Neurovitals (GCS and pupils)
> Peripheral pulses/doppler ( vascular patient)

> Capillary glucose


I
• IV
> Fluid, route, rate
> Replace NG losses 1:1with 1/ 2 NS + KCI 10 mEq/ L
.
> Pediatrics: consider Wt age, deficit, maintenance, and ongoing losses
> Parameters for locking IV when patient drinking well
> Saline or heplock
> Emphasize oral route when possible
• Ins/Outs
> Ins/Outs with shift change ( surgery, volume status patients, heart failure)
> Foley catheter
> Daily weights
• Infection Control
> Droplet
> Contact
> Droplet and contact
> Airborne
> Significant organism

17 Ldinonton Manual ommon Clinical See


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• Investigations n cn
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> Blood - Hematology: CBC-D reticulocyte count, PT/INR + PTT. crossmatch, type & screen cn
. . .
> Blood - Biochemistry: liver function tests, liver enzymes ( AST ALT, ALP) , urea, Cr electrolytes ( Na * K +, CI -, HC03-), glucose, 7T Qj

. . . . .
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.

Edmonton Manual of Common Clinical Scenarios 18


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APPROACH TO ACUTE & CHRONIC PAIN
Current Editor: Hana Yu MSc MD
u
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,
n
3 . -
*7 Adjuvant

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

and the analgesic ladder


Drug Equi- analgesic dose (mg)
• Multimodal Analgesia:
Parenteral Oral
> Involves the use of medications from different pharmacological categories
for synergistic analgesic effects while minimizing the side effects of Morphine 10 30
approaching the dose ceiling of individual medications Codeine 130 200
• Analgesic Ladder: Fentanyl 0.1
> Initially developed by the World Health Organization to address cancer
pain. Has now been adapted as a stepwise approach to the management of Hydromorphone 1.5 - 2 6 - 7.5
pain from any etiology Methadone 10 20
> Start with non- opioid medications and then sequentially add increasingly .
From Miller. Eriksson. Flasher.V / icner - Kronish f Young. 2010. p. 2774
potent medications until pain is relieved. Adjuvant therapy may be added at
any point of treatment

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• Definition: a transient exacerbation of pain that occurs in the context of otherwise stable baseline pain
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> 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)

Pain history and functional assessment


Discuss Rx options
Reassess pain with each Rx failure
Consider further investigations.

Non- pharm and pharm Rx

Explore adjuvant therapy such as steroid


.
injections for arthritic pain

Edmonton Manual of Common Clinical Scenarios 20


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ESSENTIAL DERMATOLOGY
Current Editor: Yan Fci Chen
u
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)

21 Edmonton Mam
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BOX 2: Primary Lesions BOX 3: Secondary Lesions
in cr.
• 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>

• Papule: palpable lesion, elevated above the skin, <1cm


• Erosion: loss of epidermis, heal without scarring (e.g. .
(e.g., molluscum contagiosum, acne vulgaris) dermatophyte infection)
• Ulcer: loss of epidermis and dermis, heal with scarring (e.g.,
• Plaque: palpable lesion, elevated above the skin, >1cm
(e.g., psoriasis) stasis ulcer)
• Fissure: linear loss of epidermis and dermis
• Vesicle : < 1cm blister ..
(e g , varicella, contact dermatitis)
• Atrophy: thinning of epidermis or dermis causing depression
• Bulla : > 1cm blister (e.g., bullous pemphigoid) (e.g., morphea)
• Pustule: superficial cavity of the skin that contains a purulent • Scarring: abnormal formation of connective tissue after
exudate (e.g., folliculitis) dermal injury (e.g., keloid)
• Nodule: < 1cm deep palpable solid lesion within the skin; depth
• Special Lesions:
and size differentiate a nodule from a papule: often better felt than
seen (e.g., lipoma)
• Excoriation: scratch mark; if lesions occur at site of
scratching it is called Koebner’s phenomenon
• Tumor: > lcm nodule • Comedone: hair follicle plugged with sebaceous and
• Cyst cavity containing fluid or semi- solid (e.g., pilar cyst) keratinous material (e.g., acne)
• Petechiae: <0.5 cm deposits of extravasated red blood cells
• Wheal: rounded or flat - topped papule or plaque that is evanescent
( RBC) suggestive of vasculitis
.
due to edema of the dermis (e.g. hives, angioedema)
• Purpura: >0.5 cm petechiae (e.g., senile traumatic purpura)
• Telangiectasias: dilated superficial blood vessels (e.g.,
rosacea, basal cell carcinoma, CREST syndrome)
INVESTIGATIONS (BASED ON CLINICAL SUSPICION1
Investigations
• CBC, ESR , CRP; ANA if suspicious of connective tissue disease
BOX 4: Hair, Scalp, and Nail Examination
• TSH, fasting glucose, blood culture; LFTs and organ specific
labs if suspicious of other systemic disease • Hair and Scalp: texture, scars, thinning, absence ( alopecia)
• Imaging as relevant for systemic disease or melanoma staging or excess ( hypertrichosis) , infestations ( lice), masses (on
• CXR (heart or lung pathology ) scalp), plaques, crusting
• Skin scraping for fungal KOH test • Nails: clubbing, thickness, pitting (psoriasis), separation
• Wood’s lamp for depigmented lesions from nail bed (onycholysis), yellow discoloration of nail bed
• Surgical/ Diagnostic Interventions (oil drop sign for psoriasis), other discoloration, periungual
• Biopsy: shave (epidermal) , punch (extends into dermis and erythema, splinter hemorrhages (endocarditis)
subcutaneous tissue), or excisional
• Biopsy is indicated in lesions suspected of neoplastic, bullous
disorders or unclear diagnosis with clincial exam alone

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

Edmonton Manu. Zommon Clinical Scenarios 22


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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

Compensation in Hypovolemic States first 10 kg 4


• Initially: sympathetic outflow - vasoconstriction, tachycardia next 10 kg 2
• Over hours: extravascular - intravascular shift each kg > 20 kg 1

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)

COLLOID • Large molecules maintain plasma oncotic pressure

f vascular permeability): given as 1:1ratio of volume deficit


• Mostly intravascular ( altered if
• Use: severe intravascular deficits prior to arrival PRBC, large protein loss (e.g., burns)
• Caution: prepped in NS (hyperchloremic acidosis), allergic reactions, antiplatelet effects, possible renal injury
from excessive colloid use
> Blood derived: albumin ( 5% and 25%), plasma protein fraction ( 5%)
,M
.
> Synthetic: Dextran ( 40 and 70) , Hetastarch ( 6%) Pentaspan (pentastarch), Voluven (hydroxyethyl starch)

BLOOD • PRBC: compensate for anemia, not volume deficit


• Give when anemia risks > risks of transfusion ( Hgb 70- 80 g/L)
• 1unit: Hgb 110 g/L, warm to > 37° if need >1-2 units

COMMON CRYSTALLOID SOLUTIONS

Tonicity pH Na Cl K HCQ 3 Ca Mg Glucose


Solution (mOsm/L) Caution
(mEq/ L) (g/L)
Intravascular 290 7.4 140 105 4 24 2.4 2 0.7-1.1
NS (0.9%) 308 5.5 154 154 hyperchloremic acidosis
Ringer 's 273 6.5 130 109 4 28 * 3 lactic acidosis
Plasmalyte 294 7.4 140 98 5 3
D5 W 253 5.0 50 hyperglycemia
1/ 2 NS 154 5.5 77 77 hyponatremia
3% Saline 1026 5.0 513 513 hypernatremia, hemolysis
‘converted from lactate

.
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)

23 Edmonton Manual of Common Clinical Scenarii


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FLUID THERAPY (ORAL


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• 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 %
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• 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)

SESSMENT AND TREATMENT


. . .
Initial Assessment: ABCs, VS ( BP. HR RR Temp Sa02), IV, monitor, SAMPLE Hx
• Assessment of severity ( see table)
> Consider DDx (see Trauma ( in Surgery ] and Shock [ in Internal Medicine])
• Fluid resuscitation goals: restore vital organ perfusion, maintain adequate oxygen delivery, limit ongoing loss of RBC

HEMORRHAGIC SHOCK CLASSIFICATION


Blood Loss
Class Blood Loss (mL) HR BP RR U/O (mL/h) Mental Status
(% blood vol)
I < 750 < 15% N N N N slightly anxious

II 750- 1500 15 - 30% > 100 N 20- 30 20- 30 mildly anxious

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 .

Edmonton Manual of Common Clinical Scenarios 24


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INTERPRETATION OF ABDOMINAL RADIOGRAPH
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Authors: Babak Maghdoori MD Christopher Fung MD Ed Wiebe MD FRCPC

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)

> DDx for small bowel obstruction: adhesions, hernia, tumor


> DDx for large bowel obstruction: tumor, diverticulitis, volvulus (sigmoid or cecum)
• Extraluminal air:
> Rigler /double wall sign: sign of pneumoperitoneum with air outlining both sides of the bowel wall
> Evaluate underneath the hemidiaphragms for possible free air
> Pathologically significant unless recent intra - abdominal surgery (up to 5 - 7 days post op)
> DDx: perforated ulcer, diverticulitis, perforated ischemic bowel, etc.

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

Calcifications and Abnormal Densities


• DDx: GU stones, gallstones, chronic pancreatitis, calcified lymph nodes, fibroid tumors, calcified arteries, calcified wall of aortic
aneurysm, etc. Note that phleboliths are commonly seen and generally not clinically significant.

25 Edmonton Manual o'* Common Clinical 5 : : w


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• Free fluid may be due to an exudative, transudative, or bleeding process t/> d;


• The distance between flank fat pads and the colon may be used as a diagnostic measure 7T CU
> If the distance >1cm then increased possibility of free fluid in the paracolic gutters on

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.

Normal Supine Abdominal X- ray Legend


1. Liver 10. Gas in splenic flexure
2. Spleen 11. Ilium
3. T 12 vertebral body 12. Sacroiliac joint
4 . Pedicle 13. Bladder
5. Spinous process 14. Acetabulum
6. Right kidney 15. Femoral head
7. Right psoas margin 16. Femoral neck
8. Gas in stomach 17. Greater trochanter
9. Gas in hepatic flexure 18. Lesser trochanter

Edmonton Manual of Common Clinical Scenarios 26


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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

What is the patient’s arterial oxygenation? ( Pa02)


• Normal Pa 02 is 80 - 100 mmHg depending on age (Pa021with age)
• Causes of low Pa02 include
> High alveolar PaC02 from hypoventilation
> 'f atmospheric 02 content and/or atmospheric pressure
> Ventilation /perfusion mismatch

Are the lungs working as normal oxygenators? (A - aD02 or Pa02/PA02)


• A - aD02 determined by PA02 - Pa02 (normal < 15 mmHg)
• Normal Aa gradient is age dependent. Expect Aa gradient = Age/ 4 + 4

.
• 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
^

27 Edmonton Manual of Common Clinical Scon n . •


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CLINICAL APPROACH TO INTERPRETATION


Does the patient have acidosis or alkalosis?
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• pH < 7.35 = acidosis


tn
• pH > 7.45 = alkalosis

Is it a primary respiratory (PaC02) or metabolic (HC03) problem?


Is it acute, partially compensated, or fully compensated? (Base- excess and HC03)
Respiratory Respiratory
Summary of ABG Findings in Respiratory Respiratory Metabolic Metabolic Acidosis + Alkalosis +
Acid- Base Disorders Acidosis Alkalosis Acidosis Alkalosis Metabolic Metabolic
Acidosis Alkalosis
PaC02 44 44 Normal Normal 44 44
Acute pH 4 44 44 44 44 44
Base Excess 0 0 Negative Positive Negative Positive

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

Expected PCQ 2 = 1.5 ( HC03) + 8 ± 2


Metabolic alkalosis Expected PCQ 2 = 0.7( HCO 3) + 20 ±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.

Edmonton Manual of Common Clinical Scenarios 28


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INTERPRETATION OF CHEST RADIOGRAPH
Current Editor: Edwin Cheng MD
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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

• Hila/ Lymph nodes


> Assess for lymphadenopathy
> If thickness of superior vessels > inferior vessels .
vascular redistribution (DDx: edema, effusion CHF, etc.)
• Heart
> Determine cardiothoracic ratio: lateral width of heart relative to thoracic cage in PA view < 50% normal
.
> If enlarged ( > 50%) possible DDx: cardiomegaly, pericardial effusion
> Visualization of right and left heart border (see "Pneumonia" on following page)

• 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

29 Edmonton Manual of Common Clinical Scenr .


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5’ m
LATERAL VIEW _
n ro
OJ
£
• Examine anatomy as described above, focusing on spine: assess the contour and height of the vertebral bodies to 2:
x" QJ
• Follow peripheral parenchyma along spine superior to inferior: lung fields should darken inferiorly. Whitening of lung fields
V)
inferiorly (the “ spine sign") suggests pathology (e.g., lower lobe pneumonia).
• Assess the hemidiaphragms for evidence of hyperinflation ( flattening)

• .
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

Normal Chest X- Ray Legend


1. Trachea
2. Mediastinum
3. Right heart border
4. Left heart border
5. Aortic arch
6. Lung fields
7. Costophrenic angles
8. Hemidiaphragms
9. Breast shadows
10. Spinous process
11. Humeral head
12. Scapula
13. Acromioclavicular joint
14. Clavicle
15.
,
8 h posterior rib
16. 4th anterior rib

Edmonton Manual of Common Clinical Scenarios 30


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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

RED BLOOD CELL INDICES


-
• Red Blood Cell Count ( RBC ): number of RBCs per volume of blood; normal values: AA- 5.7 X 1012/L ( < ), 4.0 5.2 X 1012/L ( 2 )
5
• Hemoglobin (Hgb): amount of oxygen carrying protein in blood; normal values: 130 - 175 g/L ($), 120 - 160 g/L ($)
.
• Hematocrit ( Hct ): % of whole blood volume occupied by packed RBCs, Hct = RBC x MCV; normal values: 41- 52% ( ’) 36 - 46% ( ; )
• Mean Corpuscular Volume (MCV): average size of RBCs; normal values: 80- 100 fL
• Mean Corpuscular Hemoglobin Concentration ( MCHC): average concentration of Hgb inside RBCs, MCHC = Hgb/(MCV x RBC ),
- .
normal values: 32 36% Increased: spherocytosis, autoagglutination, lipemia
• Red Blood Cell Distribution Width ( RDW): normal RDW is < 15%; increased indicates red cell size and /or shape variability and is
most commonly related to iron deficiency

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)

• I reticulocytes ( < 1% of RBC )


• Bone marrow suppression or .
infiltration ( severe nutritional deficiency ACD, aplastic anemia,
bone marrow failure from primary hematologic or metastatic malignancy)
• Megaloblastic anemia ( B12/ folate deficiency) , liver disease, EtOH abuse, myelodysplasia,
MACROCYTIC (MCV > 100 FL )
.
thyroid dysfunction, reticulocytosis anti- DNA and folate drugs, some cases of aplastic anemia

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)
.

31 Edmonton Manual of Common Clinical Sc


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NEUTROPHILS
Role in innate immunity, ANC; normal values: 1.8 -7.5 x 109/L, ANC < 1.0 increases general infection risk
tn cr
7T 0)
.
• Infection (primarily bacterial ) , inflammatory disorders (gout, autoimmune, collagen vascular), drugs (steroids, in

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

32
V)

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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 )

33 Edmonton Manual ot < .ommon Clinic at hm i 1


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Treat underlying cause ( see ARF and CRF [ in Internal Medicine - Renal Failure ] ) tn
7T QJ
13
d .
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

Edmonton Manual of Common Clinical Scenarios 34


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1/1 u
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LU
u . .
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

• Alignment should then be commented on in the lateral view; disruption of the


normal contour of these lines may indicate fracture/dislocation
> 1: anterior vertebral line (in image)
> 2: posterior vertebral line
> 3: spinolaminar line
> 4: spinous process line
• Bones: Each vertebra should be examined for fracture
> Look for wedge shaped defects indicating compression fracture
> Examine each spinous process for fracture line

• 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

• Atlanto - axial joint


> Look at the space between the atlas (Cl) and the odontoid process of C 2 to ensure there is no ligamentous damage resulting
in instability
> This space ( atlantodental distance) should be < 3 mm in width for adults

Focus on the vertebral bodies


• Look for fractures of the pedicles and facets, as any asymmetry may be pathologic and should be noted
• Examine the spinous processes for alignment and spacing
Examine the soft tissue for any masses or calcifications
ODONTOID
This figure provides an AP view of the odontoid
• Alignment
> Look for the lateral sides of the atlas to align with the edges of the axis
> Look for equal spacing bilaterally between the axis and the atlas
• Fracture lines through the dens Odontoid
> Type 1: through the cephalic dens
> Type 2: evenly through the base of the dens (most unstable)
> Type 3: descending into the base of the dens

35 Edmonton Manual o* Common Clinical S


n
5* m
m
n in
EBL1QUE VIEWS ID fD
D
CD
Oblique views may not be available depending on local imaging protocols 7T ID
(not typically performed in acute trauma setting)
in
• Examine the foraminae
> Each vertebral body should have a patent foramina; otherwise, suspect fracture with
angular distortion, poor positioning, or degenerative uncovertebral joint and/or facet
joint changes
• Examine the alignment of facet joints Odontoid
> Commonly described as " shingles on a roof " in this view
> Disruptions of the " shingles" may indicate dislocations of the facet joints

• Examine the pars interarticularis


(region of vertebra between superior and inferior facet joints)
> Scotty dog sign: pars interarticularis fracture in spondylolysis - vertebral body slips
anteriorly and compresses the vertebral canal

COMMON EPONYMOUS FRACTURES


• Jefferson’s fracture (unstable)
Dens (odontoid)
> Classically seen in the odontoid view as the lateral edges of the atlas extend
beyond the lateral edges of the axis (Cl ring has broken open)
• Hangman’s fracture (unstable)
> Due to hyperextension of the neck resulting in bilateral C 2 pedicle fracture
> Often seen in motor vehicle accidents (MVAs)
• Clay - Shoveler’s fracture ( stable)
> Avulsion fracture of the lower C- spine (C6 or C 7) spinous processes
> Caused by sudden flexion force of neck and back muscles
[CANADIAN C-SPINE RULE
Used for alert (GCS 15) and stable trauma patients in whom C- spine injury is
suspected: 99.4% sensitive and 45.1% specific for C- spine injury (P < 0.001)
• High risk? (if yes radiographic imaging indicated)
> Age 65
> Dangerous mechanism
• Fall > 3 feet/ 5 stairs, axial load to head, MVA high speed ( >100 km/hr )
or rollover or ejection, motorized recreational vehicle, bicycle collision
> Paresthesia in extremities

• Factors allowing ROM assessment ? (if no radiographic imaging is indicated)


> Simple rear - end MVA
• Exceptions: pushed into traffic, rollover, hit by bus/ large truck /high speed vehicle

> Sitting in emergency department


> Ambulatory at any time
> Delayed onset of neck pain

-
> 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

Edmonton Manual of Common Clinical Scenarios 36


to

03
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to
to
LU
03
U
C
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

left adrenal gland


right kidney

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)

> Especially important for identifying renal calculi


• CT images should be windowed according to what you are examining
> Windows are often preset and described as " Lung", " Bone", " Soft tissue", etc.
• Beam attenuation is measured in Hounsfield Units ( HU)
> Air ( - 1000 HU) < Fat ( - 100 HU) < Water (0 HU) < Muscle ( 40 HU) < Bone ( 1000 HU)

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.

37 Edmonton Manual of Common Clinical Scenar lOS


n
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w
• Assess the hepatic duct and common bile duct for dilation, the gallbladder for stones /inflammation/masses . n !CD8
• Assess the splenic volume and contours .
fluid.
— zT.
QJi

in
3
.
• Assess for normal pancreatic duct Look for masses, abscesses or signs of pancreatitis including peripancreatic 7T Qj

Kidneys and Adrenals U)

• Look at both adrenals and assess for masses.


• Look at both kidneys for size and shape. Look for masses and cysts. Look for hydronephrosis and hydroureter.
Follow the ureter to the bladder, looking for ureteric calculi or a bladder mass
Vasculature
• Assess the aorta and its vessels for aneurysms, dissections, and calcifications
CT CHEST
• The CT chest series will include images from the lower neck to the diaphragm.
• A systematic approach is key to successful interpretation. Review medical history to attune focus.
• The use of contrast enhancement will allow better assessment of the vessels, heart, thyroid, and lymph nodes.
• The commonly used “CT PE Protocol" uses IV contrast timed when the contrast is in the pulmonary arteries and allows for
visualization of pulmonary emboli.
Soft Tissues
• In soft tissue window, look at the thyroid gland, thymus, and breasts. Assess for any masses or lymphadenopathy.
Bone
• In bone window, assess for any fractures, lytic or blastic lesions, and masses.
• Look at the ribs, humerus, scapula, and clavicles. Assess the vertebrae and sternum.
Mediastinum
• Look at the different heart chambers, valves, and pericardium. Assess for any lymph node enlargement. Look for masses.
Vessels
• Assessed best with IV contrast. Look at the aorta for dissection, aneurysm, or calcification.
• Look at the branches of the aortic arch. Assess the vena cava.
• Look at the pulmonary arteries, and follow individual arteries in the CT PE Protocol to find emboli.

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)

Examine the CSF spaces


Normal Subdural Epidural

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.

Edmonton Manual of Common Clinical Scenario 38


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43 LO
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in
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TO
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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

Important Differentiating Questions


• P - waves ( PQRS mnemonic)
> P: Are P waves Present ? (e.g., atrial fibrillation)
> Q: What is the relationship between the P waves and the QRS? (e.g., sinus rhythm)
> R: Is the PR interval constant or different ? Does the PR interval get progressively prolonged? (e.g., 2 nd degree Mobitz I)
> S: Are the P waves the same Shape? (e.g., multifocal atrial tachycardia or wandering 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

DDx of Right Axis Deviation DDx of Left Axis Deviation


Right ventricular hypertrophy Left ventricular hypertrophy
RBBB LBBB
Left posterior hemiblock Left anterior hemiblock
Lateral infarct Inferior infarct

39 Edmonton Manual of Common Clinical Scenar


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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.

Location of Infarct Leads Showing Ischemic Changes Coronary Arteries

Septal Viand V 2 LAD


Anterior Wall V 3 and V4 LAD
Lateral Wall .
I aVL, V 5, V6 LAD, LCx
Inferior Wall .
II, lll aVF RCA, LCx
Posterior Wall VI-V 3 (ST-dcpfessloo), V7-V 9 RCA
Right Ventricle .. .
V4R II lll aVF RCA

Edmonton Manual of Common Clinical Scenarios 40


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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

Chronic renal Yes Low l,25(OH),D? 1 lypoparathyroidism *


insufficiency*
No
25-OHD = 25- hydroxy-vitamin D ( inactive )
Pseudohypoparathyroidism 1.25( OH ) ,D - 1 ,25 -dihydroxy-vitamin D ( active )
( PTH resistance ) *dcnotes common causes

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 - SIGNS AND SYMPTOMS


CN5: confusion, depression, psychosis, seizures, personality changes
CVS: hypotension, prolonged QT interval, arrhythmias
MSK/NEURO: tetany, spasms, myopathies, paresthesias, circumoral numbness
Special tests (T&C signs)
• Trousseau's sign: carpopedal spasm ( wrist and fingers flex and draw together ) when BP cuff inflated over arm for 2- 3 minutes
• Chvostek ’s sign: facial spasm when facial nerve tapped over the parotid

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

41 Edmonton Manual of Common Clinical Seen.


n
=• m
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Hypercalcemia (>2.6 mmol/L) Q) fi)

PHPTH*
Yes Elevated urinary Ca: ? Yes
J
Elevated PTH ?
No
Elevated PTHrP?
Yes Consider
t/>
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cr.

(>200mg in 24h ) malignancy*

No No
I
Elevated Vitamin D?
Yes Consider
FFH lymphoma .
sarcoidosis

PTHrP = parathyroid hormone related peptide


No
\
Consider other causes
PHTPH = primary hyperparathyroidism .
( e.g., Thiazides* , milk -alkali syndrome TPN, endocrine
FHH = familial hypocalciuric hypercalcemia disorders , etc. )
‘denotes common causes
HYPERCALCEMIA - HISTORY, SYMPTOMS, INVESTIGATIONS, AND TREATMENT
.
HPI: diet (milk and antacids), drugs (thiazides, lithium, Vit D) bone pain, abdominal pain
PMHx: endocrine disorders, malignancies
FHx: hypercalcemia or MEN syndromes, cancers

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

• Serum and urine protein electrophoresis: if multiple myeloma is suspected

• Parathyroid Sestamibi scan: hyperparathyroid lesions

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

Edmonton Manual of Common Clinical Scenarios 42


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INTERPRETATION OF ELECTROLYTES: POTASSIUM
Current Editor: Hana Yu MScMD
u
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

Renal losses ( urine K * > 20mmol/d)


• Hypertensive (mineralocorticoid excess): primary or secondary hyperaldosteronism, Cushing' s, CAH
• Hypotensive or normotensive:
> Acidemic: DKA/renal tubular acidosis ( Types 1& 2)
> Alkalemic: diuretics
> Variable: vomiting/hypomagnesium/drugs (amphotericin)

HYPOKALEMIA - TREATMENT
Recognize signs/symptoms of hypokalemia (see box)

Calculate transtubular potassium gradient (TTKG): Signs/Symptoms of Hypokalemia


• TTKG = ( K 'urine) (Osmserum) /( K‘serum) (Osmurine) • Nausea, vomiting
.
= > 4 (renal loss) < 2 (extrarenal loss) • Muscle weakness ( if severe:
Treat underlying cause and/or remove offending medication ascending paralysis, ileus, respiratory
failure, rhabdomyolysis, arrhythmias)
Replace K * slowly: oral preferred over IV KCI ( max dose 20 - 40 mEq oral, max infusion
• ECG changes: flattened T wave, ST
20mmol/h IV): never bolus K *
segment depression, high U wave
Check serum K * frequently to avoid over -correcting
Consider role of K ’- sparing diuretics in treatment plan

-
1mEq/ L decrease reflects 200 meq total body loss

Hyperkalemia (>5.0 mmol/L)

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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HYPERKALEMIA - DIFFERENTIAL DIAGNOSIS AND TREATMENT n


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HYPERKALEMIA DIFFERENTIAL DIAGNOSIS


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Cellular Shift • Acidosis, insulin deficiency, beta -blockers, tumor lysis, burns, hemolysis U)

Decreased Excretion • Renal failure, hyperaldosteronism


Drugs • TMP . .
- SMX, succinylcholine K - sparing diuretics (e.g. spironolactone)

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

ECG Changes - Hypokalemia


.
PR interval lengthens ST segment
.
depresses T wave inverts, and U
wave is appears and becomes more
pronounced .
/\
i a —
1.7
Hypokalemia

rziip ECG Changes - Hyperkalemia


Progression from tall peaked T waves
( 5.5 - 6.5 mM), to a loss of a P wave (6.5 -
7.5mM), to a widened QRS complex
( 7.0- 8.0mM) , then a sine wave pattern
( >8.0)

7.0 8.0
Hyperkalemia

Edmonton Manual of Common Clinical Scenarios 44


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INTERPRETATION OF ELECTROLYTES: SODIUM
. .
Authors: Kimberley Krueger MD Jason Kiser MD Mark Joffe MD FRCPC
mi
T1 YPQ 1 jraiaiiilfeMSIFFERE1
.

Hyponatremia (<135 mmol /L)

bo-osmolar -
Hyper osmolar

Hypo-osmolar

Pseudohyponatremia ( usually due to Hyperglycemia


hypcrlipidemia/ protcmemia ) Hypertonic infusion
Isotonic in fusion

Hypovolemic Euvolcmic Hypervolemic

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 treatment guidelines


• Fluid restrict to lL/day (if hypovolemic give NS)
• Treat underlying cause
• Monitor both serum sodium and urine output to ensure appropriate correction rate

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

Symptomatic/seizing • Hypertonic 3% saline; consider demeclocyline if patient refractory to treatment

45 Edmonton Manual of Common Clinical Sccnar if


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HYPERNATREMIA - DIFFERENTIAL DIAGNOSIS AND INVESTIGATIONS £U fD

Hypernatremia (> 145 mmol/l.) </> = J

7T Q>

t a gam ( rare )
\ - 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

HYPERNATREMIA - SIGNS, SYMPTOMS AND TREATMENT


Recognize signs/symptoms of hypernatremia H ?Q Deficit
• Thirst
• Weakness H20 deficit = [ TBW x ( serum Na* - 140) ]/140
• Altered mental status
• Convulsions TBWr ,, = 0.6( Wt)
,

• Coma TBwH 0.5 Wt = ( )

General treatment guidelines


• Give free water (POor IV) Complications of Hypernatremia
• Restrict salt • Increased risk ofvascular rupture (can lead
• Treat underlying cause
to intracranial hemorrhage)
• Monitor the serum sodium regularly to ensure < 0.5 mmol/ L/hr of correction
• If correction too rapid: cerebral edema
• H20 deficit = [ TBW x ( serum Naffl - 140) ]/140
• TBWnule= 0.6( Wt); TBWfemale =0.5 ( Wt )

If hypovolemic: follow general guidelines


If hypervolemic: remove excess Na * with diuresis/dialysis and replace water deficit with free water

Edmonton Manual of Common Clinical Scenarios 46


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c
P INTERPRETATION OF LFTS & ENZYMES
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u . .
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
*

47 -
F.dmonton Manual of Common Clinical Scc nari'
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i7JHINTO USE LFTS =
n %
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Routine annual evaluation of patients with risk factors for liver disease in
7T QJ
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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)

PATTERN OF LFT ABNORMALITIES


Hepatocellular cause
• Very high ALT (e.g., 200 - 2000 + U/L)
• Moderately high ALP, unlikely > 2x normal
> Elevated AST and ALT > 2 x in ALP - likely hepatocellular cause
• Variable bilirubin, with degree of elevation proportional to severity of damage

• 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

Test Result Possible Cause Initial Action Management


Liver damage • Perform additional blood tests ( 2nd line • Treat underlying cause
• Viral LFTs, HCV/HBV serology, autoimmune • Specialist referral
panels, iron saturation, ceruloplasmin, al-
• EtOH
4 AST/ALT < 1.0 anti-trypsin)
• Autoimmune
• Abdominal U/ S
• Heritable disorders
• Liver Bx
• EtOH • Recheck LFTs q3 - 6 mos • Reduce EtOH ingestion

• Obesity • Change hepatotoxic meds

4 AST/ALT >2.0 • Hepatotoxic drugs • Lose weight if BMI > 25


• Specialist referral ifLFT >1.5 x
.
normal 2 x 6 mos apart
Cholestatic • Additional testing: autoimmune panels, • Treatunderlying cause
• Biliary obstruction viral serology, abdominal U/ S, liver Bx • Specialist referral

• Primary biliary cirrhosis


4 ALP AND GGT
± 4 BILIRUBIN • Primary sclerosing
cholangitis
• Autoimmune hepatitis

• Hemolysis • Check direct / indirect bilirubin Indirect


• Biliary obstruction • Look for cause of hemolysis

4 BILIRUBIN ONLY Direct


• Likely Gilbert ’s syndrome
• No further treatment necessary

• EtOH ingestion • Review patient ’s PMHx • Treat underlying cause


• Antiseizure medications • Identify risk factors
• Renal disease
• Pancreatitis
4 GGT ONLY • DM
•CAD
• Prostate cancer

Edmonton Manual of Common Clinical Scenarios 48


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*43 to

111INTERPRETATION OF LIPIDS
u . .
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

49 Edmonton Manual of Common Clinical Scenarios


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[INTERPRETATION OF LIPID PANEL =. £D
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If TC > 6 mM or LDL > 5 mM, suspect familial hypercholesterolemia



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IfTG > 5 mM, suspect familial hypertriglyceridemia V)

If fasting TG are > 5 mM - TG will be increased in non-fasting states


U REATMENT

THERAPY BASED ON CVD RISK


10-Year CVD Risk Recommendation
> 20% • Discuss and strongly encourage statin (preferably high intensity)

> 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

• Non- statin lipid lowering agents


> Additional agents are considered in patients who are not at target despite statins
> Ezetemibe is second line to reach target LDL. Niacin, fibrates, and bile acid sequestrants can be used if LDL is NOT at target.
Addition of second line agents not useful if LDL is at target.
• ASA
> Consider after statin therapy in high risk individuals with low risk of bleeding
> Relative benefit approximately 10%
> Annual risk of major bleed approximately 0.5%

EXAMPLE IF BASELINE RISK ESTIMATED AT 20% OVER 10 YEARS


ESTIMATED
THERAPY BENEFIT
(RELATIVE RISK Absolute Risk Number Needed
New Risk Estimate
REDUCTION) Reduction to Treat (NNT)

Smoking Cessation Recalculate 9% 12 11%


without smoking
Mediterranean Diet 30% 6% 17 14%
Exercise 30% 6% 17 14%
Low 25% 5% 20 15%
Statin
Moderate 30% 6% 17 14%
Intensity
High 35% 7% 15 13%
ASA 12% 2% 50 18%
• Note: Example used a 53 year old male smoker with total cholesterol 5, HDL 1.2 and systolic BP 128, estimated risk from
Framingham ( from http://cvrisk.mvm.ed.ac.uk /calculator /calc.asp andhttp://chd.bestsciencemedicine.com/calc 2html # basic) to
attain a 20% risk over 10 years.

Edmonton Manual of Common Clinical Scenarios 50


CO

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‘43 co

111
.
LU
INTERPRETATION OF PFT
E Current Editor: Bradley Brochu MD
u
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

Obstructive pattern Restrictive pattern

/ \
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%

51 Edmonton Manual of Common Clinical Sc t I ..I f


n
* m
5.
2 «/ »
n £
• Is there bronchodilator response ?
> >12% and > 200 mL improvement in FEV1post - bronchodilator indicates a significant bronchodilator response, i.e., reversible — c?.
QJ «D
cn
D
*

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%

Selected Examples of Flow -Volume Loops


Obstructive
Normal Obstruction Restriction + Restrictive

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)

• < 80% predicted suggests possible restrictive ventilatory defect


• TLC may be underestimated if using the N2
dilution method (measures only ventilated lung Lung Volume Guide
volume); using body plethysmography is the best • Volume ofair moved into or out of lungs
TIDAL VOLUME (TV)
method as it measures total lung volume during normal quiet breathing
> If TLC measured by body plethysmography FORCED VITAL • Maximum volume of air forcibly expired
is greater than N2 dilution,it suggests the CAPACITY (FVC) after maximal inspiration
presence of bullous lung disease
FUNCTIONAL
Residual Volume (RV) • Volume remaining in lungs after normal
RESIDUAL CAPACITY
breath
• >120% predicted suggests gas trapping due to (FRC)
poor patient effort or obstruction
TOTAL LUNG CAPACITY
• Volume of air at maximal inflation
Expiratory Reserve Volume (ERV) and Functional (TLC)
Residual Capacity (FRC ) • Maximum volume of air exhaled after
VITAL CAPACITY ( VC)
• In obese patients, both ERV maximal inspiration
and FRC are decreased RESIDUAL VOLUME air remaining in the lungs after
• Volume of

DIFFUSION CAPACITY ( RV) maximal exhalation

Check for DLCO correction for Hgb or VA (alveolar


volume)
Decreased DLCO adjusted for VA suggests reduced diffusion capacity due to parenchymal abnormalities, abnormal
concentrations of hemoglobin or carboxyhemoglobin, or the presence of pulmonary vascular disease
lAIRWAY RESISTANCE
Increased airway resistance suggests turbulent airflow (airway constriction, edema, etc.)

Edmonton Manual of Common Clinical Scenarios 52


V)

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

DARK • Acute intermittent porphyria, advanced malignant melanoma, cholestasis

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

GREEN/BLUE • Urinary bile pigments, indigo carmine, methylene blue

FOAMY • Proteinuria, bile salts

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
,

MEDICATIONS, BURNS • Steroids

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

MEDICATIONS • Parkinsonian medications, stimulant laxatives


‘Used primarily to detect acetone and acetoacetic acid, does not detect {3 -hydroxybutyric acid

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 )

53 Edmonton Manual of Common Clio


n
5’ m
n IB
Qi £
NITRITE
Coagulase - splitting bacteria convert nitrates to nitrite, urine must be in the bladder for > 4 hrs prior to voiding for
—tn =J
7T QJ
conversion, nitrates must be present
Some bacteria do not produce nitrite (E. faecalis )
Morning sample is preferred ( stasis)
False negatives - dilute urine, non-nitrate reducing bacteria, insufficient bacterial counts

Range 4.6 - 8.0 (utility is often limited to select clinical situations)


Acidic Basic
• High- protein (meat) diet • UTI
• Metabolic alkalosis
• Acidosis ( secondary to ketoacidosis in starvation, diabetes)
• Renal tubular acidosis

• Uric acid stones


• Diet .
(high vegetable diet milk, immediately after meals)
• NaHC03 therapy, vomiting

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

• Diabetes insipidus (central or


• Average with normal fluid intake . • Volume depletion, CHF .
adrenal insufficiency DM, .
• isosthenuria: SG fixed at 1.010, SI ADH, 4 proteins (nephrosis) , newborn state
nephrogenic), pyelonephritis,
regardless of intake • if markedly 4 ( 1.040- 1.050), artifact or recent
glomerulonephritis, water load
• suggests renal tubular administration of plasma expanders
with normal renal function
dysfunction • radiographic contrast media

Note: Interpret in light of relative fluid status

UROBILINOGEN AND BILIRUBIN


Limited utility (dipstick analysis), bacteria in gut utilize conjugated bile to form urobilinogen cleared by the liver
Normal, low level of urobilinogen excreted in the urine daily, but hemolytic processes or hepatocellular disease can lead to increased
urinary levels
Complete biliary obstruction - absence of urobilinogen in the urine
1% of conjugated bile is filtered and usually undetectable . 4 levels associated with states of conjugated hyperbilirubinemia
ICROSCOPIC EXAMINATION OF THE URINARY SEDIMENT
BACTERIA OR .
• > 5 WBCs /HPF indicates significant pyuria ( DDx: infection, neoplasm, calculus disease, etc )
LEUKOCYTES
• > 5 RBCs /HPF on one occasion or > 3/HPF on multiple warrants further investigation (DDx: glomerular
ERYTHROCYTES
disease, neoplasm, trauma)
• Normal patients and stone - formers will both form uric acid, phosphate and oxalate crystals: preferential
CRYSTALS
formation of stones based on the acidity or alkalinity of the urine
• Hyaline .
(commonly benign), hemegranular ( ATN), WBC ( AIN pyelonephritis, glomerulonephritis), RBC
CASTS .
( glomerulonephritis), fatty casts (nephrotic syndrome. DM damaged renal tubular epithelial cells),
.
epithelial ( tubular damage, nephrotoxin, virus), waxy (severe CRF amyloidosis)

Edmonton Manual of Common Clinical Scenarios 54


to

nj

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‘ 3 LO

51 INTUBATION & LUMBAR PUNCTURE


CO
to
LU
. Authors: Maleka Ramji MD Keir Peterson MD CCFP
u
INTUBATION
Indications
• Depressed level of consciousness such as in head trauma or after administration of general anesthetic
• Actual or impending airway obstruction
• Clinical signs of respiratory failure or fatigue; Hypoxemia
• Failure to achieve adequate ventilation with non -invasive means

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

55 Edmonton Manual o* Common Clinical Scenar


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=• m
n to
Complications of intubation a> 0)
• Recurrent laryngeal nerve injury c/)
3
7T Q)
=
zr.
• Hemorrhage
• Aspiration secondary to esophageal intubation U)
• Tracheal stenosis
• Dental fractures
• Dislocation of arytenoid cartilage
• Vocal cord injury

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

LU .E I FAMILY HISTORY & PEDIGREE


.
Authors: Christina Beach MD Norma Leonard MD FRCPC
u
BASICS
Mendelian Inheritance
• Autosomal recessive: M=F; trait expressed with inheritance of two mutated copies of gene
> e.g., cystic fibrosis, sickle cell anemia, Tay Sachs disease

• 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)

Rearrangements: translocations, inversions


> e.g., CML

HISTORY
ID • Patient ’s name, age, gender, ethnicity

CC • As per concern prompting clinic visit


HPI • Age of onset of condition, details of diagnosis, genetic and medical tests previously performed
RED FLAGS socially isolated populations, congenital anomalies, family history of early onset cancer or disease,
• Physically or
presence of disease in an unlikely individual (e.g., male family member with breast cancer ), unexplained mental
retardation or developmental delay, advanced parental age (mother > 35 y/o, father > 50 y/o)
PMHX ..
• Hx of pregnancy (e g , prenatal care, teratogen exposures), birth, development history, past illnesses

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

a separate line and designated by Roman numerals


from top to bottom
• Label individuals with Arabic numerals from left to right
II 0 2 i (

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

57 Edmonton Manual of Common Clinical See


n
=2.• m
<>
/
n £
QJ <T>
PEDIGREE SYMBOLS
— D

o
cn
Female by phenotype Male by phenotype
o Sex not specified
>
(/
QJ

Affected individual Carrier (obligate)


CD Asymptomatic /
presymptomatic

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

Deceased Proband Consultand


/
—o Relationship DO
Relationship no longer
exists = o Consanguinous relationship

d>^b Monozygotic twins Dizygotic twins Twins (zygosity unknown)

°s° Biological parents Infertility


No children by choice/
reason unknown

Adopted in Adopted out


( ]
INVESTIGATIONS
Blood Work
• Newborn screening panel (in Alberta: endocrine, amino acid, organic acid, fatty acid oxidation disorders
.
+ biotinidase deficiency CF). As with any protocols, check with your provincial/national guidelines.
Radiology/ lmaging
• Prenatal: U/S ( 18 - 20 wks)
• Postnatal: U/S, X -ray
Special Tests
• DNA sequencing. PCR. karyotyping, fluorescence in situ hybridization ( FISH)
Diagnostic Interventions
• Prenatal: MSS, amniocentesis, chorionic villus sampling, preimplantation genetic diagnosis (during in vitro fertilization), fetal
blood sampling by cordocentesis

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

Follow- up with genetic counselor and multidisciplinary team as needed


Referrals
• . .
Genetic counselor Dietician, neurodevelopmental clinic, support groups Psychologist, specialist physician (e.g.. Endocrinologist)

Edmonton Manual of Common Clinical Scenarios 58


l/>

03
CO

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

59 Edmonton Manual of Common Clinical Scenarios


n
=.• m
=
n V)
(D
• All medications a)
D
• Peri -operative management CD
7T IU
CURRENT > Anti -coagulants/anti -platelets and last dose
in
MEDICATIONS > Oral hypoglycemic agents
> Steroids in last 6 weeks
> G -blockers, ACEi, ARB, diuretics

ALLERGIES • Medication and specific reaction, latex

SOCIAL HX • EtOH, smoking (pack years), drugs


• Malignant hyperthermia
FAMILY HX
• Cholinesterase disease (pseudocholinesterase deficiency)

OTHER • Pregnancy, obesity

FASTING • Last time of ingestion of food or drink

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

• ROM ( flexion and extension)

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

• Neurologic exam if indicated through surgery, history, or • Hepatic disease: anticoagulant


utilization of regional anesthesia technique PTT/INR therapy; bleeding diasthesis

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

American Society of Anesthesiologists CXR


• Cardiac or pulmonary disease;
malignancy; age > 60 y /o
-
• ASA I healthy, fit patient
• ASA II - patient with mild systemic disease with no
functional limitation (controlled HTN)
• ASA III - patient with severe systemic disease causing functional limitation (stable CAD)
-
• ASA IV patient with severe systemic disease causing constant threat to life (unstable angina)
-
• ASA V moribund patient not expected to survive > 24 hrs with or without surgery (ruptured AAA with shock )
• ASA VI - organ donor
• Add the E classification for patients undergoing emergency procedures

Edmonton Manual of Common Clinical Scenarios 60


03
CO
c
0
10
to
LU
03
U
c PRESCRIPTIONS & PROGRESS NOTES
u . .
Authors: Shawna Pandya MD Brian Yong MD Darren Nichols MD CCFP

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

Directions for use



. .
> Daily, bid ( twice/day) tid ( thrice/day ) qid ( four times /day)
> PC ( after meals), AC (before meals), qHS ( at bedtime), qAM (daily
before noon), qad (every other day)
> PRN (as needed) 5 MD Mike' Smith' HD ( 567 -112 -2334 )
. . .
> q # h (e.g. q4h q 6h etc.)
• Quantity (especially for PRN dosing)
6 Sipuairc

> Mitte ( send): number of caps, pills, etc.


4. Number of refills authorized ( write out and circle); interval between each refill
5. Prescriber’s name and phone number
6. Preserver's signature
• Orders written by medical students must be approved/co -signed by a physician before implementation
• Printout name under the signature
.
7 Draw a line under last Rx 'n to prevent others from adding additional drugs
8. Outside of hospitals - controlled drugs (e.g., narcotics) require triplicate prescriptions

.
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

61 Edmonton Manual of Commo


n
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n
• Review medications, do not rewrite. Assess whether any need to be added or discontinued. Q)

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

Medicine SI Progress Note Jan 1, 2015 1400h

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

Edmonton Manual of Common Clinical Scenarios 62


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0
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CO
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u
C
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

Description: technique, attempts


Findings
Complications
Outcome
Specimens taken (e.g., Bx for pathology)
Instructions given to patient, family
Signature

Example: Lumbar Puncture


June 5, 2017; 1315h; Lumbar Puncture Procedure Note
• This procedure was supervised by house staff Dr. [ Name]
• Written consent obtained and potential complications explained
• Indication for LP: fever and headache
.
• INR PTT, and PLTs normal
• Patient in seated position and prepped using sterile technique: landmarking for L4/ 5 interspace done using iliac crest palpation
• 3 cc of 1% lidocaine was used for anesthetic
• 20 gauge spinal needle was introduced successfully into the arachnoid space on 1st attempt
• CSF fluid was light yellow and clear; 5 cc CSF collected in 5 tubes
.
• Tubes sent for: cell count and differential, gram stain and culture, glucose, protein HSV PCR
• Patient tolerated procedure well; no complications
• John Doe SI - 4

63 Edmonton Manual of Common Clinical Scenario


n
S
n
B1 cn
ErARD CALL NOTE 0) CD
3
Common calls: chest pain, shortness of breath, urinary (/) zl.
What to ask for on the Phone 7T QJ
incontinence/retention, pain medications, drug reaction
.
• Date time, service you represent • ID: name . ID #, age. location V)

• 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

> Investigations ordered


> Medications given
> Outstanding issues /results for day staff to follow up on
• Note: every good note is followed by a turnover to corresponding staff in A.M.
• Remember to write a follow -up note once the results of the investigations ordered come back and patient has been re - evaluated

Example: Chest Pain


June 2nd. 2017; 2115h; GIM Student Intern On-call
Called at 2100h by patient 's nurse re: acute onset chest pain
Pt ID: 57y/o M admitted May 28 th with confusion, found to have bilateral pneumonia, currently treated with IV levofloxacin
.
PMHx: DMT2 HTN, BPH, smoker
. . .
S: New onset chest pain around 2040h gradually worsening- left anterior chest 5/10 no radiation. Was lying in bed at onset of pain.
No change with deep inspiration/cough/position. Has had similar pain before but has not sought medical attention. No leg swelling/
SOB/palpitations. No metallic taste in mouth.
. . . .
O: VS: HR 101 & regular BP 135/82 Sp02 94% on 2L 02 (unchanged) T 37.2 RR 18, GCS 15/15
. . .
• CVS: radial pulses strong/regular bilaterally JVP 3 cm ASA normal S1/S 2 no murmur /S 3 / S4, pain not reproduced on palpation
• RESP: breath sounds equal bilaterally. No adventitious sounds.
• ABDO: soft, non- tender, no masses
• Investigations:
> This AM: Hgb 140, platelets 210, WBC 13, neutrophils 10.9. Lytes normal ( K = 4.1)
> CXR ( Nov 2): bilateral airspace disease, no pleural effusion/pneumothorax
> ECG ( May 28th): NSR

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)

Edmonton Manual of Common Clinical Scenarios 64


>
(/

2

IITTJNDERSTANDIN ARTIBIOTICS
LU
u
BASIC PRINCIPLES
ATBx only effective against bacteria
^ Author: Maleka Ramji MD

Need effective concentration at the site of infection


Need appropriate duration of therapy
Inappropriate use contributes to the development of resistance
For most infections, the goal of treatment is concentration > minimum inhibitory concentration (MIC ) except where host
defense is inadequate. In this case, concentration must be > minimum bactericidal concentration (MBC ).
ONSIDERATIONS FOR ANTIBIOTIC SELECTION
Site
• .
E.g. eye/brain/prostate = non- fenestrated capillaries, which impede drug diffusion
• Low pH in abscesses inactivate aminoglycosides and erythromycin
• .
Ability to reach site (e.g. aminoglycosides not absorbed orally; endocarditis creates huge vegetative growths, therefore longer
duration required; foreign objects such as catheters and joint replacements are prone to biofilm production, which provides a
mechanism of resistance)
Immune status
..
• May determine the organism (e g , Pneumocystitis carinii in HIV patients)
..
• May determine antimicrobial agent and dose (i e , 'big guns' in immunosuppressed patients)

Hepatic and renal function


• If decreased, may require dose adjustment (drugs either renally or hepatically metabolized)

.
• Certain ATBx contraindicated (e.g. tetracycline in renal failure, chloramphenicol in babies due to inability to glucuronidate)

Pregnancy and breastfeeding


• Teratogenicity of certain ATBx
• Altered pharmacokinetics because of increased maternal volume of distribution, cardiac output and clearance

Medication history
• Allergies, interactions
Setting of acquisition of infection
• Country/region
.
• Community vs hospital acquired, ward vs . ICU
• Contact with animals

65 Edmonton Manual of Common Clinical Scenar


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= CO
n
tu rt>
CLASS OF ATBX MOA EXAMPLES SPECTRUM OF ACTIVITY THERAPEUTIC INDICATIONS D
in
7T Qj
Penicillins • Interfere with the • Streptococci
synthesis of cell wall • some enterococci t/>
peptidoglycan •N . meningitidis
• Results in formation
• Many anaerobes (excluding
of defective cell B. fragilis)
walls that lyse and
result in death of • Spirochetes (Treponema)
the organism • Corynebactium diphtheriae
• Bactericidal
• Pen G (IM/IV) • Most active against non • Acute Pharyngitis (Group A Strep),
• PenVK ( PO) R - lactamase producing Group B Strep .
Gram+ organisms, anaerobes • Syphilis Listeria Actinomyces
and selected Gram- cocci
. .
• Cloxacillin ( PO/IV/ • Bulky side chain provides • Staphylococci skin infections
IM) increased activity against ( excluding MRSA)
B-lactamase producing
staphylococci

• Amoxicillin ( PO) • More activity vs . • Streptococcus pneumoniae


• Ampicillin (IV/IM) enterococcus, Listeria
monocytogenes, increased
. .
infections ( sinusitis, otitis CAP
• Covers the same AECOPD) (beware that resistance
Gram- ( E. coli, H. influenzae . to penicillins is increasing),
organisms as
penicillin, but also
Shigella)
.
P. mirabilis Salmomella, H.pylori eradication in triple
covers additional therapy, prevention of infective
gram - negative endocarditis in susceptible patients
organisms

• Ticarcillin - • Increased spectrum to • Similar -


to Pip Tazo
clavulanate (IV) include P. aeruginosa P. .
mirabilis. Enterobacter some
serratia, some B. fragilis
.
• Activity vs. non- G -lactamase
producing E. coli, H.
.
influenzae N. gonorrhea

• Piperacillin • Excellent activity vs. • Severe intra - abdominal infections


• Pip-Tazo Nisseria, H. influenzae. • Severe nosocomial infections
( Piperacillin + enterobacteraciae
pseudomonas
. • Empiric therapy in high risk
Tazobactam) febrile neutropenic patients +
• Gives broad • Used in combination with aminoglycoside
coverage tazobactam for activity
against G - lactamase
producing Gram- and Gram+
organisms

• Imipenem - cilastin • Broadest spectrum • Most Gram+ & Gram- bacteria


(IV) • Ertapenem advantage once • Severe intra -abdominal infections
• Meropenem (IV) daily dosing • Severe polymicrobial skin and soft
• Ertapenem (IV) • Most Gram+ (excluding tissue infection
.
MRSA enterococci) Gram-
(including Pseudomonas) ,
. • Fournier ’ s gangrene
• Severe ventilator - associated
most anaerobes ( except C. pneumonia where Pseudomonas
difficile) and S. aureus coverage is needed
• Resistant to most beta -
lactamases

Ldmonton Nianual of Common Clinical Scenarios 66


in

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

Second Generation • Slightly decreased


activity vs. Gram+ cocci,
• CAP . otitis, sinusitis
• Cefuroxime ( PO/ • Abd/pelvic infections, surgical
IV) increased vs. Gram- rods, 2 prophylaxis
subgroups:
• Cefprozil ( PO)
> Respiratory: increased
• Cefoxitin (IM/IV)
activity vs. H. influenzae
• Cefotetan (IM/IV)
& M. catarrhalis
> GI/GU: increased activity
vs. B. fragilis

Third Generation • Enhanced activity against • Sepsis, meningitis (penetrate


• Cefotaxime (IM/IV) aerobic Gram- organisms the blood brain barrier ), hospital
• Ceftriaxone (IM/IV)
such as Enterobacteriaceae; acquired pneumonia
while retaining good • Ceftriaxone DOC for Lyme
• Ceftazidime (IM/IV)
activity against streptococci disease
• Cefixime ( PO) (except enterococci),
• Cefixime DOC for
it is less active against uncomplicated gonorrhea
staphylococci
• Cefazidime active vs.
Pseudomonas but not good
for Strep pneumoniae
Fourth Generation • Good Gram+ & Gram- • Similar to 3r <1 gen .
• Cefepime (IV/ IM) coverage • MonoRxfor nonlocalizing
• Increased resistance to febrile neutropenia
beta - lactamases (inclusive
of Staph and Enterobacter )
• Lacks coverage of B. fragilis

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
n\ fD
CLASS OF ATBX MOA EXAMPLES
SPECTRUM OF
ACTIVITY
THERAPEUTIC INDICATIONS —
( )

cn =cr.
J

Tetracycline • Inhibits bacterial .


• Tetracycline ( PO .
• Gram+ Gram-, • CAR AECOPD . acne, chlamydia
)Q

protein synthesis by OPTH) .


anaerobes Chlamydia, trachomatis, rocky mountain cn
binding to 30Sandto • Doxycycline ( PO) Mycoplasma . spotted fever
some extent the 50S
ribosomal subunits
• Minocycline ( PO)
Plasmodium. Vibrio
.
Nocardia, Rickettsiae .
• brucellosis Lyme disease

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

Nitrofurantoin • Reactive intermediates • Nitrofurantoin ( PO) • Enterococci and E. coli • UTI


alter bacterial
ribosomal proteins and
macromolecules

Quinolones • Inhibits bacterial


DNA synthesis by
• Ciprofloxacin ( IV/ PO/
OTIC /OPTH)
• Enteric Gram-
atypical (Cipro
and • UTI.refractory prostatitis,
bacterial diarrhea, respiratory
targeting types II and • Norfloxacin ( PO) has activity vs. tract infection with penicillin/
IV topoisomerases • Ofloxacin ( PO/OPTH)
pseudomonas)
, macrolide resistant S. pneumonia .
• Causes arrest of • 3rd and 4 hgen have AECOPD
• Levofloxacin (IV/ PO)
DNA replication and increased activity vs
subsequent cell death • Moxifloxacin (IV/ PO/ Gram+
OPTH)
• Gatifloxacin ( OPTH)
• Gemifloxacin ( PO) D/C
2009

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

Edmonton Manual of Common Clinical Scenario? 68


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u
-
PRE & POST- OPERATIVE ORDERS
.
Authors: Patricia Lee MD Sarah Lai MD, Kamran Fathimani MD FRCSC

PRE-OPERATIVE ORDERS: ABCDEFGHI MNEMONIC


Date, time, planned procedure, diagnosis
• .
Antibiotics: Ancef (Cefazolin) ± Flagyl ( Metronidazole) Clindamycin ± Ciprofloxacin (on call to OR vs. STAT)
• . . . . .
Blood Work : CBC- D electrolytes, BUN Cr INR PTT type & screen or cross -match
> Bowel prep: laxatives, enemas, suppositories
> Booking the case: call OR

• 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

POST-OPERATIVE ORDERS: AD-DAVID MNEMONIC


Date, time, admit to surgery, diagnosis
• Admit to surgery under Dr.
• Diagnosis
• . . . . . .
Diet: NPO ice chips /popsicles TPN PPN, CF FF DAT tube feeds, diabetic diet, cardiac diet, renal diet
• Activity: AAT . . .
NWB WBAT bed rest, full spine precautions HOB > 30° .
.
• VS: q2h q4h, routine

.
• 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

CVS • Anti -hypertension, cardiac meds


RESP • Inhalers . Oj, incentive spirometry
Gl • Bowel routine, PPI

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

69 Edmonton Manual of Common Clinical Sect


n
5' m
n £
ECG (EXAMPLES) — cr.
QJ iD

tn
D
7T £U
Current Editor: Joseph Andrews MD
to

P-Pulmonale P- Mitrale Right Ventricular Hypertrophy Left Ventricular Hypertrophy


(right atrial enlargement ) ( left atrial enlargement )

2 0.04 s
Notched R wave Is > 5 wave
> 35mm
20.2mV
P - wave

Lead II & III 20.12 s Lead V 1 orV2 VI orV2 V 5 or V6

First Degree AV Block Mobitz I Second Degree Heart Block ( Wenckebach)


Missed beat

Lengthening PR interval until dropped beat ( R R interval drops with each beat )

Mobitz II Second Degree Heart Block Third Degree Heart Block

Missed beat

A
Grouped beats with dropped beat between groups Atria and ventricles are firing separately

Atrial Fibrillation Ventricular Tachycardia Ventricular Fibrillation

-
No P waves, irregularly irregular QRS

Acute Pericarditis WPW Syndrome Hyperkalemia

PR depression and diffuse ST Delta waves and shortened PR Wide flat P waves and peaked T waves

Premature Ventricular Complex Ischemia and Infarction

z i /3
QRS

Compensatory > 0.04 s —1

Flipped,symmetrical T-wavcs Pathological Q waves ST Elevation ST Depression

Edinonion Manual of Common Clinical Scenarios 70


</>
03
'
^v3 7tO
to
in
°
C STATION CONTRIBUTORS
LU
u
Approach to Acute and Chronic Pain Kirles Bishay MD. Kirsten Biefer MD Maryam Soleimani MD
Essential Dermatology Nathan Hoy MD. Isaiah Day MD. Alain Brassard MD FRCPC
Intrepretation of ABG Charles Lim MD. Edward James PLT, Janjeevan Deol MD. Dilini Vethanayagam MD FRCPCC
Intrepretation of Chest Radiograph Babak Maghdoori MD. Christopher Fung MD. Ed Wiebe MD FRCPC
Interpretation Of CBC- D Kimberely Krueger MD. Jason Kiser MD. Mark Joffe MD FRCPC
.
Interpretation of CT Brendan Diederichs MD. Katherine Leung MD Ed Wiebe MD FRCPC
Interpretation of Electrolytes: Calcium Charles Lim. Craig Domke MD. Lucille Lalonde MD FRCPC
.
Interpretation of Electrolytes: Potassium Kimberely Krueger MD Jason Kiser MD. Mark Joffe MD FRCPC
.
Interpretation of ECG Charles Lim. Craig Domke MD Lucille Lalonde MD FRCPC
.
Interpretation of PFT Maleka Ramji MD Mohit Bhutani MD FRCPC
. .
ECG Examples Odell Pui MD Sabira Suleman MD James Huang MD

71 LdmoiUon Manual of Common Clin


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Admission & Daily Orders
Blackbourne LH. Surgical Recoil . 5 th ed. Baltimore: Wolters Kluwer: 2009.
_ _
Writing on Effective Daily Progress Note. http://www.medidne.ufl.edu / 3rd yr _clerkship/documonts/writing an _effectivc _ daily _progress_note.pdf

Approach to Acute and Chronic Pain


American Society of Anesthesiologists. Practice guidelines for acute pain management in the perioperative setting. Anesthesiolog / . 2012;116.248 - 273.
Bennet: D. Burton A. Fishman S. Fortner B. Barash PG. Cullen BF. Stoelting RK, Cahalan MK. Stock MC. Clinical Anesthesia . 6 th ed. Philadelphia; Lippincott
Williams & Wilkins; 2009.
McCarberg B. Miaskowski C. Consensus panel recommendations for the assessment and management of breakthrough pain. Pharmacy and Therapeutics
Journal . 2005:30:354- 361.
Carr DB, Goudas LC. Acute pain. Lancet . 1999:353:2051.
. .
Miller RD. Eriksson LI. Fleishcr LA Wiener - Kronish JP. Young WL. Miller ' s Anesthesia. 7th ed. Philadelphia PA: Churchill Livingstone; 2010.
.
Moulin D. Clark A. Gilron I. Ware M. Watson C Sessle B. et al. Pharmacological management of chronic neuropathic pain: Consensus statement and
guidelines from the Canadian Pain Society. Journal of the Canadian Pain Society . 2007:12:13 - 21.
Rosenquist E. Overview of the treatment of chronic pain. Retrieved October 2014. from UpToDate: http://wvAv.uptodate.com/contents/overview - of - the-
treatment -of -chronic - pain?sourcc = search_ result &search=chronic +pain&selectedTitle =l%7E 150
Sullivan P. Ottawa Anesthesia Primer . Echo Book Publishing: 2012.
.
Todd K Ducharme J. Manon C. Crandall C. Fosnocht D. Homel P. et al. Pain in the Emergency Department: Results of the Pain and Emergency Medic ne
Initiative (PEMI) Multicentc-r Study. The Journal of Pain. 2007:8:460- 466.
World Health Organization. WHO' s cancer pain ladder for adults. Retrieved October 2014. from World Health Organization Web site: http://wvAv.who.int /
cancer/palliative/painladder /en/

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 Abdominal Radiograph


Novclline RA. Squire' s Fundamentals of Radiology . 6 th ed. Boston: Harvard: 2004 .
Chen MM, Pope TL. Ott DJ. Basic Radiology . 2nd ed. New York. NY: McGraw -Hill: 2011.
.
Abdominal X - ray courtesy of Dr. Edward Wiebe. Department of Radiology and Diagnostic Imaging University of Alberta.

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
'

of Internal Medicine. New Yo'k: McGraw - Hill: 2008.


Williams AJ. ABC of oxygen Assessing and interpreting arterial blood gases and acid - base balance. BMJ. 1998 Oct 31:317( 7167):1213- 6
West JB. Pulmonary Pathophysiology: The Essentials.6th ed. Philadelphia: Lippincott Williams & Wilkins: 2003

Interpretation of Chest Radiograph


Novelline RA. Squire' s Fundamentals of Radiology . 6th ed. Boston: Harvard: 2004.
.
Chest Radiograph courtesy of Dr. Edward Wiebe. Department of Radiology and Diagnostic Imaging University of Alberta.

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.

Edmonton Manual Clinical SeeI Id! »U> 72


to

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43 to
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*. Interpretation of C- Spine Imaging
<D 03
Ouellette H. Tetreault P. Clinical Radiology Made Ridiculously Simp ,e. Miami: Medmaster ; 20C
p
LU
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.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 Electrolytes: Calcium


.
Carroll MF Schade DS. A practical approach to hypercalcemia. Am Fam Physician. 2003 May 1:67( 9):1959 - 1966.
.
Cooper MS Gittoes NJ. Diagnosis and management of hypocalcemia. BMJ. 2008 Jun 7:336 ( 7656):1298- 1302.
. . . .
Fauci AS Braunwald E. Kasper DL. Hauser SL Longo DL Jameson JL. Loscalzo J eds Harm on s Principles of Internal Medicine. New York: McGraw -Hill; 2008.
.
Ferri FF. Cooper E McClure M. Practical Guide to the Care of the Medical Patient . 7 th ed. Philadelphia: Elsevier Mosby; 2007.
Longmore M. Wilkinson IB. Davidson EH. Foalkes A. Mafi AR. Oxford Handbook of Clinical M dicine. 8th ed. New York: Oxford University Press: 2010.

Interpretation of Electrolytes: Potassium


Fauci AS. Braunwald E. Kasper DL. Hauser SL. Longo DL. Jameson JL. Loscalzo J. cds Harm on s Manual of Medicine. 17th ed. New York: McGraw- Hill 2009. .
Interpretation of Electrolytes: Sodium
.
Fauci AS. Braunwald E. Kasper DL. Hauser SL Longo DL. Jameson JL. Loscalzo J. eds Harrison's Manual of Medicine. 17thcd. New York: McGraw -Hill; 2009.

Interpretation of LFTs & Enzymes


Minuk GY. Canadian Association of Gastroenterology Practice Guidelines: Evaluation of abnormal liver enzymes tests. Con J Gastroenterol. 1999
Sep;12( 6):417 - 421.

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.

Intubation and Lumbar Puncture


Bowers RC. Weaver JD. Chapter 8. Compromised Airway. In: Stone CK. Humphries RL: CURRENT Diagnosis & Treatment: Emergency Medicine. 6e: http://
www.accessmedicine.com.login.ezproxy.library.ujlberta.ca /content.aspx ?alD = 3118968.
. . .
White SJ Levitan RM. Stack LB. Chapter 22: Airway Procedures. In Knoop KJ Stack LB. StorrowAB Thurman RJ. cds. The Atlas of Emergency Medicine. 3rd
ed. http:// www.acccssmedicine.com.login.czproxy.library.ualberta.ca/content.aspx 7alD 6007352
Gomella LG. Haist SA. Chapter 20: Critical Care. In Cornelia LG. Haist SA, eds. Clinician' s Po - kct Reference: The Scut Monkey . 11th ed. http://www.
accessmedicine.com.login.ezproxy.library.ualberta.ca /content.aspx ?alD= 2695577
Johnson KS. Sexton DJ. Lumbar puncture: Technique: indications: contraindications: and complications in adults [ Internet ], Aminoof MJ .
Wiltcrdink JL: UpToDate: [updated 2010 June 02: cited 2010 October 01]. Available from http:// www.uptodate.com/paticnts /content/topic.
do?topicKey = ~05iLljyWVqRVe 5
Roboins E. Hauser SL. Chapter e 32: Technique of Lumbar Puncture. In Fauci AS. Braunwald E. Kasper DL. Hauser SL. Longo DL. Jameson JL. Loscalzo J. eds.
Harrison s Principles of Internal Medicine 17th ed. http:// www.accessmedicine.corn/content aspx 7alD = 2886062
Gomella LG. Haist SA. Chapter 13: Bedside Procedures. In Gomella LG. Haist SA. eds. Clinician' s Pocket Reference: The Scut Monkey . 11th ed. http:// www.
accessmedicine.com/content.aspx 7alD - 2694363
.
T int nalli JE Kelen GD. Stapczynski JS. Ma C J. Cline DM. Tintinalli s Emergency Medicine: A Comprehensive Study Guide. 6th ed. http:// www.accessmedicine.
com.login.ezproxy.library.ualberta.ca/content.aspx ?alD = 615534
73 I dmontori Manual of Common (
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Family History & Pedigree QJ < >
.
Hinton RB. The family Hx: Re-emergence of an established tool. CritCare Nurs Clin N Am. 2008;20:149 - 158. — .
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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

Pre- Operative Exam


Sullivan P. Anesthesia for Medical Students . Ottawa: Department of Anesthesia, Ottawa Civic Hosital; 1995 .
Canadian Anesthesiologists' Society. Guidelines to the Practice of Anesthesia: Revised Edition 2012. Can JAnesth. 2012:59( 1).
Miller R. Eriksson L. Fleisher L. Wiener - Kronish J. Young W. Miller s Anesthesia . 7 th ed. Philadelphia: Churchill Linvingston; 2010. Web. books /
'

linkTo? type = bookPage& isbn = 978 -0- 443 - 06959- 8&eid ^ 4 -ul.0 - B978 - 0 - 443 -06959- 8..00050- 9 s0310
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Prescriptions & Progress Notes


Blackbournc LH. Surgical Recall. 5 th ed. Baltimore: Wolter Kluwer; 2009.
_ _ _
Writing an Effective Daily Progress Note. http://www.medicine.ufl.edu/ 3rd_ yr clerkship/documents/Writing an Effective Daily _Prcgress _ Note.pcf eier
,

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

Pre- & Post - Operative Orders


.
Gomel la LG Haist SA. Clinician' s Pocket Reference: The Scut Monkey . 11th ed.
Vojvodic M. Young A. Toronto Notes 2014.30th ed. Toronto: Type and Graphics Inc: 2014.
White J. Medical Student ' s Guide for Surgery and Anesthesiology Clerkship.accessmedicine.com /contcnt.aspx 7al D 2694363
.
Tintinalli JE. Kelen GD, Stapczynski JS Ma OJ. Cline DM. Tintinalli' s Emergency Medicine: A Comprehensive Study Guide. 6 th ed. httpY/vAvw.accessmedicinc.
com.login.ezproxy.library.ualberta.ca/content.aspx?alD= 615534

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

Staff Section Editor


Laurie Mereu MD FRCPC
Professor
Division of Endocrinology
University of Alberta

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)

immon Clinical Scenario 78


CRANIAL NERVE EXAM
.
Current Editors: Michael Driedger MD. Usha Ramanthan MD George Elleker MD FRCPC

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)

CN 11l/IV/VI (oculomotor/trochlear /abducens, motor only - eye movements):


• " LR 6S 04 " rule, all other movements are CN III
• Pupils
.
> Pupil size (- 3mm in diameter ) /shape/symmetry ptosis, alignment
> Accommodation ( near response or constriction on attempted convergence)
> Pupillary light reflex ( afferent is CNII ) - A consensual response (constriction of both pupils upon illumination of one pupil)
must be noted
> Swinging flashlight test - Marcus Gunn pupil ( relative afferent papillary defect (can be due to optic neuritis)
- The affected pupil constricts less ( therefore appears to dilate) when a bright light moves from the unaffected eye to the affected
.
eye
Argyll Robertson pupil ( accommodates but does not react to light ): sign of syphilis
>
• Eye lids and orbits
> Drooping of the eye lid ( ptosis), or abnormal protrusion of eye ( proptosis) should be noted
• Eye movements
> Follow " H" pattern ( the 6 cardinal eye movements), saccadic movement: quick eye movements
> Monocular diplopia is a local problem ( refractive/corneal problems); binocular diplopia in neuropathy, eye muscle disease
• Ocular oscillations
> Nystagmus - involuntary jerking eye movement that may be congenital or acquired. Occurs at the extremes of voluntary gaze.
CN V ( trigeminal, sensory Vl/ 2/ 3, motor only - mastication)
• Inspection:
> Atrophy (masseters or temporalis muscles), lateral deviation of jaw to side of lesion
• Sensory ( touch, temperature, pinprick tests)
> VI forehead
> V 2 upper lip/cheek
> V 3 lower lip/chin ( touch, temperature, pinprick tests)
• Motor:
> Clench teeth ( palpate masseter / temporalis)
> Move jaw side to side ( pterygoids)
> Open mouth jaw deviates toward weak side, repeat against resistance

79 Edmonton Manual of (_i) f nrr


.
Reflexes: Corneal ( afferent VI, efferent VII), normal = bilateral blink, Jaw jerk ( afferent V 2, efferent V3) pseudobulbar palsy =
>
increased response
CN VII ( facial, sensory - EAC and anterior 2 /3 tongue taste, motor - facial expression)
• 5 branches:
> " To Zanzibar By Motor Car " ( temporal, zygomatic, buccal, mandibular, cervical )
• Inspection:
Asymmetry, flat nasolabial fold, mouth droop, involuntary facial movements, retracted eyelid
> m zr
-u
• Sensory:
X
Q)
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</>
> Taste on anterior 2 / 3 of tongue 3n
O )

.
• 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?

• Be sure to look between toes and along the sole


• Texture: dry and atrophic ?
• Color
• Hair growth
• Calluses, fissures, cracks, evidence of tinea pedis
• Necrobiosis lipoidica diabeticorum: central reddish-brown
O O
pigmented plaque with central atrophy (associated with
diabetes but not related to diabetic control)
• Diabetic dermopathy: thin, atrophic skin with shiny brown
spots
O
Amputations
Ulcers ( see table below)
O
• Type: neuropathic, arterial, venous stasis
• Any gangrene?
Bony deformity
•// o

• Hammertoes
• Flat feet
• Charcot foot: bony deformities of the foot secondary to
neuropathy and subsequent bone weakening

Arterial Ulcer Venous Ulcer Neuropathic Ulcer


Usual Location Along the shins and feet Medial malleolus Pressure points on the plantar feet
.
Appearance Red punched out Hyperpigmented. ragged border .
Red often associated with callus
History Very painful Due to venous stasis Tingling, numbness, usually painless
CIRCULATION Screen for Diabetic Neuropathy
Color with 128 Hz Vibration Tuning Fork
Temperature 1. Strike the tuning fork and apply it to the patient’s sternum
• Check temperature of each foot, compare bilaterally to ensure understanding of the vibration sensation
Pulses: strength, compare bilaterally 2. Have the patient close eyes and indicate both when
• Dorsalis pedis vibration is felt and when it has stopped
• Posterior tibial 3. Begin on the bony prominence on the dorsum of the first
Ankle/Brachial Index .
toe proceed to proximal joints if vibration is not sensed
• Indicator of PAD (if ABI < 0.8) 4. After the patient no longer senses vibration, apply the
Check for pitting edema tuning fork to own thumb and measure how long it takes to
no longer sense the vibration
NEUROLOGIC AND MUSCULOSKELETAL Normal response is being able to feel the vibration in the
Pressure sensation: lOg monofilament screen for diabetic hand for up to 10 seconds longer than in the patient ’s
neuropathy foot: beyond 10 seconds implies loss of vibration sense
Vibration sensation: 128 Hz vibration tuning fork screen for
neuropathy
Proprioception ( severe neuropathy ): Start at peripheral joints, move proximally if proprioception not intact ( move joint up
or down, ask patient which direction)
Temperature sensation: A cold metal tuning fork can be used to assess whether quality of temperature sensation is equal
in both feet and legs
Reflexes: Achilles reflexes
Range of motion: Move the ankle, subtalar joint, metatarsal, and phalangeal joints through their normal ROM
Power: Assess dorsiflexion and plantar flexion

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

General Approach - Patient 's name, age


• Patient ’s general appearance: evidence of Wt loss or cachexia, muscle atrophy, pallor, jaundice
• Encephalopathy: orientation x 4 ( person, place, time, event); affect
Any LOC. delerium coma.
Systems - Based Approach
• HEENT: scleral icterus, check tongue/frenulum for jaundice, parotid hypertrophy ( mostly EtOH), fetor hepaticus
. .
• DERM: jaundice, spider nevi (especially on chest, back, and neck ) , facial telangiectasia, petechiae ecchymoses excoriations from
.
pruritis and loss of facial/body hair in sex hormone dependent areas
• BREAST: gynecomastia in males
.
• MSK / EXTREMITIES: peripheral edema, proximal muscle atrophy/ weakness, palmar erythema, clubbing Dupuytren’s
.
contractures Terry ’s nails ( leukonychia - white nails), asterixis ( hepatic encephalopathy)
•ABD:
> Inspection: ascites (bulging flanks, everted umbilicus), caput medusa, splenomegaly, external hemorrhoids
Percussion:
- Identify liver size:
Percuss upwards from the RLQ along the mid - clavicular line for liver dullness
Percuss downwards from chest along the mid - clavicular line for liver dullness
Describe liver span and size ( normal < 12 cm)
- Castell's sign: percussion in lowest left intercostal space on anterior axillary line. Dullness any time during
respiration or on inspiration is abnormal (should be resonant at all times) and indicates splenomegaly (LR + 1.7)
. .
- Traube space is demarcated by the left anterior axillary line 6th rib and left coastal margin. Percussion over this space
should be resonant ( lungs). Dullness could indicate splenomegaly (or pleural effusion)
Palpation: Feel liver edge in RUQ along subcostal margin
- Comment on liver edge, consistency, nodules, pulsatile
- Palpate the spleen using 2 hands starting at RLQ moving to LUQ
Auscultation over liver and spleen: bruits, venous hums
• GU: testicular atrophy in males
Special Tests for Ascites:
• Shifting dullness ( LR + = 2.3)
Percuss medially to laterally while supine for line of dullness, roll patient on side and repeat: does line of dullness move?
Positive if line of dullness changes > 2 cm
• Fluid wave ( LR + = 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

Spider nevi Caput medusa Dupuytren's contracture

Edmonton Manual of Cot linical Scenario 82


EYE EXAM
.
Current Editors: Scott Wong MSc Dominic Mudiayi MD

PHYSICAL
03
.y E
U ) 03
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)

MUSCLE Movement Innervation


Superior Rectus Elevation + minor adduction Oculomotor nerve (CN3)
Medial Rectus Adduction Oculomotor nerve (CN3)
Inferior Rectus Depression + minor adduction Oculomotor nerve (CN3)
Lateral Rectus Abduction Abducens nerve (CN6)
Superior Oblique Abduction, depression, medial rotation Trochlear nerve (CN4)
Inferior Oblique Abduction, elevation, lateral rotation Oculomotor nerve (CN3)

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)

83 Edmonton Manual of Coi


FEMALE GENITOURINARY EXAM
Current Editor: Amanda Klinger

PHYSICAL
D
"

General Approach m •zr


x <
• Explain process and purpose of exam (especially if nervous or first exam), offer chaperone, check patient comfort 0} (/>
throughout exam 3n Cl)
• Position patient: The pelvic examination is performed in the dorsal lithotomy position. The patient should be draped mid -
abdomen to knee. Position patient supine with head and shoulders elevated, feet in footrest, and instruct to slide down until
buttocks at edge of exam table and relax leg and abduct knees (ensure eye contact with patient and have patient position self ).

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

Labia minora Perianal region


Labia majora
f
I I
Urinary introitus Vaginal introitus

Edmonton Manual of Common Clinical Scenarios 84


HAND EXAM
.
Current Editors: Hollie Power MD. Regan Guilfoyle MD Michael Morhart MD FRCS

GENERAL APPROACH Common Hand Deformities


• Expose hands, forearms adequately (remove splints, casts, dressings) • Bouchard and Heberden’s nodes: bony
03
.a E03
to
• Shoulder relaxed, elbow flexed at 90° enlargement of PIP and DIP joints in OA
• Boutonniere deformity: PIP in flexion, DIP
>X INSPECTION
-QC. LU • Posture/resting cascade of the hand; compare with opposite hand
hyperextended
• Claw hand: hyperextension of MCPs and
• Skin; bruising, erythema, hair, pallor, rashes, lacerations, scars
• Nails: clubbing, infection, leukonychia, onycholysis, pitting, splinter
flexion of the PIPs and DIPs
• Dupuytren’s contracture: flexion
hemorrhages
• Joints: swelling, dislocation, subluxation
deformity at MCPs, IPs with nodular
thickening of palmar fascia; palmar pits,
• Deformities ( see box )
knuckle pads
• Other: muscle atrophy, masses
• Mallet finger: DIP held in flexion; inability
PALPATION to actively extend
Vascular • Swan neck deformity: PIP hyperextended .
• Palpate radial and ulnar pulses DIP in flexion (many causes)
• Ulnar deviation of MCPs ( RA )
• Assess temperature of the skin, capillary refill ( should be ~ 2 - 3 sec)
• Perform Allen’s test
Joints
• Palpate individual MCP joints for pain, swelling, deformity, instability ( 2
finger method) Median nerve
• Palpate IP joints using the 4 finger method to check for ballottement
Motor function
•Assess strength of intrinsic and extrinsic muscle groups (see table) Ulnar nerve Ulnar nerve
•Assess grip strength
Sensation ( see table and figure - dermatomes) Radul nerve
• Assess sensation of median, ulnar, and radial innervated territories
• Assess 2- pt discrimination on pads of fingertips (normal ~ 2- 3 mm)
Soft tissue Dermatomes in the hand
• Palpate soft tissues for any masses
Tendons
• Palpate for fibrosis, nodules, tenderness

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

Screening Exam for Peripheral Nerve Function in the Hand


Nerve Sensation Extrinsic Motor Function Intrinsic Motor Function

Median Finger tip of index finger (D2)


Flexion of DIP on index finger • Flexor Digitorum With palm facing up. point thumb to
Profundis (FDP) ceiling - Abductor Pollicus Brevis ( APB)

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 )

Special Tests Indication Procedure


Allen's test Collateral blood supply to Occlude the radial and ulnar arteries while the patient ’s hand is clenched. Release one artery and
the hand note color in patient 's hand. Test is positive for that artery should color not return.
Phalen's sign Carpel Tunnel syndrome Have the patient hang wrists downward in a palmar - flexed position. Positive if patient symptoms
reproduced/ worsened.

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
x<
(f)
> Head: symmetry, size, shape, masses, and involuntary movements QJ

> Hair: quantity, texture, distribution, and pattern of hair loss 3 fi


CD
> Scalp: redness, scaling, lumps, lesions, scars, nits
> Face: expression, lesions, scars, pigmentation, hair
• Palpation
> Scalp and skull : for masses or tenderness

> Temporal arteries: thickening, tenderness, or absent pulse


Eyes
• Visual Acuity: test each eye individually at 20 feet with a Snellen eye chart, with and without glasses/contacts
• Visual Fields
> Test visual fields one eye at a time: Facial description - " Is any part of my face distorted or missing?"; Static technique (1, 2, or 5
fingers); Kinetic technique - wiggle finger minimally and move inwards (ask - “how many fingers do you see?”)
> Screen for field defects such as homonymous hemianopsia ( blindness on one half of field in both eyes ) , bitemporal hemianopsia
( blindness in half of field nearest the temples bilaterally), and quadrantic defect (blindness in V field bilaterally)
*
. .
> Test extraocular movements (lid lag CN III, IV VI; diplopia, amblyopia, nystagmus, cover -uncover test )
• Inspection
> Eyes: position/alignment, eyebrows, eyelids, lacrimal apparatus, conjunctiva, sclera, cornea, lens and iris, corneal light reflex,
proptosis
> Pupil: size, shape, symmetry, reaction to light, swinging light test ( relative afferent pupillary defect )
• .
Ophthalmoscopic examination: red reflex, examine optic disc, physiologic cup arterioles, veins, macula, fovea
Ears
• Inspection: auricle for size, position, symmetry; lumps, inflammation, discharge, or any skin lesions
• Palpation: palpate mastoid for mastoiditis, lymph nodes (occipital, pre/post - auricular, parotid, tonsillar, sub - mental,
submandibular, anterior and posterior cervical, supraclavicular

Otoscopic Exam Findings for Different Ear Pathologies


Otitis Media . grey, or yellow bulging tympanic membrane, loose landmarks, inflammation; may have pain at
• Red
mastoid bone. Pneumatic insufflator is a gold standard (Strep pneumonia. H. Influenzae. M. Catarrhalis)
Otitis Externa .
• Swollen, moist, pale/reddened and tender canal (if chronic, canal is often thickened, red itchy)
• The tug test is painful in acute otitis externa (Pseudomonas aeruginosa)
Serous Effusion • Amber .
color behind TM may visualize air bubbles
Retracted • Drum pulled medially, sharply outlined malleolar folds, protruding short process, short/horizontal
Eardrum malleus handle
Nose
• Inspection
> Anterior /inferior surfaces: asymmetry, deformities, nostril patency
> Mucosa: swelling, bleeding, exudate, ulcers, or polyps ( Note: nasal mucosa is somewhat redder than oral mucosa)
> Nasal septum: deviation, inflammation, perforation
• Palpation:
> Frontal and maxillary sinus: tenderness and transillumination
Throat
• Inspection
> Lips: symmetry, color, moisture (note any ulcers, cracking, scaling, or masses), vermillion border size, philtrum
> Oral mucosa (employ use of light and tongue blade): color, ulcers, nodules, or white patches
> Gums: inflammation, gingival margins /interdental papillae for ulceration/swelling, and palate
> Teeth: missing teeth or discoloration
> Tongue: movement, symmetry, ulcers on sides or floor of mouth
• Pharynx
> Uvula: when patient saying “ah” or yawning, soft palate should rise symmetrically ( test of CN X ) and uvula stay mid - line
» Anterior /posterior pillars, tonsils: color, symmetry, swelling, exudates, ulcerations

Edmonton Manual of Common Clinical Scenarios 86


HIP EXAM
Current Editor: Arif Ismail

03
_ PHYSICAL
Inspection
.y/>
l
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.

87 Edmonton Manual of Common Clinical Scenaric


JVP EXAM
Current Editors: Christine East MD, Dylan Taylor MD FRCPC FACC CHE

POSITIONING OF THE PATIENT


• Patient supine at 30- 45° angle, chin lifted and head turned slightly to the left
TJ
• Drape to reveal neck and upper chest m rr
• If available, use a tangential light source to improve visualization of the neck veins x<
Q) (/>
• The angle of the bed may need to be adjusted if the top of the Internal Jugular Vein
(IJV) pulsation is not appreciated - see below
3 nO
)

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

Patella (knee cap)


PHYSICAL
OJ
_ General Approach: compare bilaterally and examine hip, ankle, and back '
Articular cartilage

.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

Palpation: tenderness, effusion ( wipe for small: ballottement for large),


swelling, temperature, crepitation, popliteal fossa crepitation, popliteal fossa

Active and Passive Range of Motion Tests


Test Procedure Evaluation/Results
Active Flexion • Patient supine with legs extended • Evaluates hamstring muscle control around

• 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

MASSIVE SPLENOMEGALY • Visceral Leishmaniasis . CML. tropical splenomegaly syndrome, or shistosomiasis


• Continue palpating in this manner in a smooth fashion moving diagonally across the abdomen toward the left costal margin,
asking the patient to inspire deeply with each palpation
• Castell’s sign: percuss the lowest left intercostal space at the anterior axillary line ( AAL) on patient ’s left side continuously while
patient breathes deeply: a change in percussion note from tympany to dullness on inspiration suggests splenomegaly
. .
• Traube' s space: landmark the triangle bordered by 6th rib left costal margin and AAL percuss space while patient breathes
deeply; if any dullness is found, splenomegaly should be suspected
Lymph nodes
• Palpate lymph nodes by moving pads of fingers in a circular motion
• Begin from palpating the occipital lymph nodes and then move to the auricular lymph nodes, submandibular, and submental
lymph nodes
• Other locations of commonly found lymph nodes (and a few of their causes) include: axillary (cat -scratch fever, breast cancer ),
epitrochlear ( lymphoma, sarcoidosis), inguinal ( STI) and popliteal (foot infections)
• Virchow ’s node: important node in the left supraclavicular space that, when palpable, suggests metastases from upper abdomen

Characteristic Benign ( likely Worrisome


infectious) (malignant)

Size <1cm >l c m


Anterior auricular Shape regular, round irregular
Mobility mobile immobile/
stuck down
Consistency soft/rubbery rubbery/ hard
Tenderness tender non- tender

Lymph nodes Drainage Common diseases


Suboccipital LN Back of scalp Scalp ringworm
Occipital + head

Posterior auricular Post auricular LN Acoustic Bacterial infection


(behind ear)
meatus
Submental
Preauricular LN Eyes, temporal Basal cell carcinoma
Posterior cervical Submandibular skin
Parotid Anterior cervical Tongue Infection/
Tonsilar neoplasm of tonsils,
( jugulodigastric) node
thyroid cancer
‘ Anterior cervical Deep cervical Thorax Intrathoracic
- Supraclavicular disease/neoplasm

lcl nonton Manual of Common Clinical Scenarios 90


MALE GENITOURINARY EXAM
. . .
Current Editor: Derek Chan MD MBA CHE

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

• Scrotum: swelling, ulcers, hydrocele, tumor, or varicocele


Palpation
•Retract foreskin and inspect urethral meatus (reduce foreskin following to prevent paraphimosis)
• Palpate the penile shaft for any fibrotic plaques if there is concern about curvature
• Palpate the testicles and epididymis for any swelling ( hydrocele, spermatocele, tumor), and tenderness ( testicular torsion, torsed
appendix testis, epididymitis, or orchitis)
• Assess testicular size
• Transilluminate swelling if present: shine light behind the scrotal swelling
> Red glow through the testicle - collection of fluid (e.g., a hydrocele/epididymal cyst)
.
> Absence of glow - solid mass (e.g. tumor )
• Palpate the spermatic cord: normally a thick, cord -like structure: palpate from inguinal canal to the testes bilaterally

.
> 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 )

Digital Rectal Exam (DRE)


-
• Have the patient standing and bent over the examining table or laying on their left side in the knee chest position
• Insert a single gloved, lubricated finger and move toward the anterior aspect of the patient palpate for the enlargement,
tenderness, texture, and softness/hardness of the gland
Special Tests
• Prehn’s sign: Traditionally used to distinguish between testicular torsion ( a surgical emergency ) and epididymitis
> Lifting the affected testicle results in pain relief in epididymitis, but not in torsion
• Cremasteric reflex: Swipe the medial thigh to see if the ipsilateral testicle elevates: can be absent in testicular torsion

91 Edmonton Manual of Common Clinical Scen.ii K


NEUROLOGICAL EXAM
Current Editor: Dominic Mudiayi MD

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 />
(

Assess level of consciousness of the patient 3n CD


• Mental status may be assessed while obtaining patient history.
• Several tools that also allow assessment of consciousness, such as the Glasgow Coma Scale (GCS).

Points Eyes Verbal Motor


1 No eye opening No verbal response No motor response
2 Eyes open with pain Incomprehensible sounds Extension to pain (decerebrate)
3 Eyes open to verbal command Inappropriate words Flexion to pain (decorticate)
4 Eyes open Confusion Withdrawal from pain
5 Oriented Localizes pain
6 Obeys commands

Mini Mental Status Exam


Orientation .
Year, month, day date, season /5
Country, city, province, hospital, ward /5
Registration Examiner names three objects (book, table, pen)
Patient asked to repeat objects /3
Attention Serial subtraction of 7 from 100 ( 93, 86...)
Alternatively, spell WORLD backwards /5
Recall Ask for the names of the objects mentioned earlier /3
Language Point towards objects and name (pen/watch) /2
Repeat " No ifs ands or buts ” /1
Write a sentence /1
Follow a 3 - step command " take a paper in your right hand, fold it in half, and drop it on the floor ” /3
Read and obey the following "close your eyes" /1
Copying Copy intersecting pentagons /1
Total /30

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

Localizing the Lesion


CNS Location Motor Sensory DTR
CEREBRAL Contralateral UMN weakness
Contralateral sensory loss in
CORTEX
UE (strength): arm flex > extension: LE: plantar flexion >
dorsiflexion, leg externally rotated
limb/ trunk t
Variable weakness /spasticity + CN deficits
BRAINSTEM
± “crossed" cranial nerve signs Variable t
Bilateral deficit at lesion,
Weakness/spasticity I sensation below
SPINAL CORD Bilateral with bilateral damage: paraplegia /quadriplegia
Bladder / bowel dysfunction
Hemicord lesion - loss of t
vibration ipsilateral, loss of
paincontralaterally
BASAL GANGLIA .
Bradykinesia rigidity, tremor Sensation not affected N/A

PNS Location Motor Sensory DTR


ANTERIOR HORN Focal weakness, atrophy, fasciculations Sensation not affected
Root innervated pattern weakness, atrophy, Corresponding dermatome
SPINAL ROOTS
± fasciculations deficit I
Peripheral nerve distribution - pattern atrophy, Sensory deficit in nerve
MONONEUROPATHY
weakness. ± fasciculations distribution iif nerve involved
POLYNEUROPATHY Symmetrical distal weakness Reduction, loss of
Stocking glove distribution
distal reflexes

93 Ldmonton Manual of Common Clinical Scenarios


Grading Power UMNvs. LMN
Grade Feature UMN LMN TD
m IT
0 No contraction Power UE flex > ext and LE ext > flex "
/absent X <
QJ V)
1 Muscle contraction Tone Spastic Flaccid 3 n
2 Movement with gravity eliminated DTR
3 Against gravity Plantars Up going Down going
4 Against resistance Fasciculations Absent ±
5 Normal strength Atrophy Late Early

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

Edmonton Manual of Common Clinical Scenarios 94


Power
• Select a specific motor action/muscle group that can be assessed depending upon patient presentation/complaint
• Once complete, grade the power (see table) and state what nerves were tested
> Upper extremities
- Assess: deltoids, biceps, triceps, wrist extensors, finger flexors/extensors, thumb abduction/extension/adduction
> Lower extremities
nj
.102 EOJ * Assess: hip flexion/extension/abduction/adduction, knee extension/ flexion, ankle plantar flexion/dorsiflexion/

eversion/inversion, and big toe extension


>X
-CL
C LU
Reflexes
Ensure the patient is relaxed. If unable to elicit reflexes, re - attempt with accentuation techniques such as teeth clenching. After
performing reflex, grade reflex and state what nerves were tested
• Upper extremities - suggested reflexes: biceps, triceps, brachioradialis

.
• 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.

Cortical sensory modalities


• Two - point discrimination
> With patient ’s eyes closed, using an unfolded paper clip, touch their index finger pad with the paper clip points ( 2- 4 mm
apart) and ask if they feel 1or 2 points

• Stereognosis
> With patient 's eyes closed, place an object in their hand and ask them what it is
• Graphesthesia
> With patient 's eyes closed, trace a number on their hand and ask them what number you traced. Repeat on opposite side.
• Bilateral Simultaneous Stimuli
> Visual: With eyes open, ask patient to look at your nose with both of your hands out to the side. Patient identifies which hand
is moving. Check each side individually first and then simultaneously.
» Auditory: By rubbing your fingers together, check each ear 's hearing individually, then simultaneously.
> Tactile: With patient ' s eyes closed, ask patient to identify which side you are touching. Touch each side individually and then
both simultaneously.
Gait, balance, and cerebellar tests
Ask the patient to take a few steps along a hallway. Observe their spontaneous gait for stance, cadence, arm swing, base. Heel-toe
walking can be used to further assess balance.

Tests for unilateral cerebral lesions


• Pronator drift - ask patient to stretch their arms out in front of them and close their eyes for 45 s. Test is positive if one of the
arms pronates (pronating arm is contralateral to the lesion).
• Finger/ forearm rolling test - ask patient to rapidly roll their fmgers/arms around each other. Test is positive for unilateral cerebral
lesion if one finger remains still while the other rolls around it. The still finger/arm is contralateral to the lesion.

Coordination tests for cerebellar function


• Perform 1upper extremity and 1lower extremity coordination exam (rapid rhythmic alternating movements)
> Upper extremity - finger to nose, rapid hand supination- pronation, rapid finger to thumb apposition
> Lower extremity - sliding heel along shin, rapid knee taps
Romberg Test
Ask the patient to stand with their eyes closed, feet together, and arms at their sides. The inability to stand for 60 seconds with feet
together and eyes closed is a positive Romberg test indicating a proprioceptive or vestibular lesion.

95 Edmonton Manual of Common Clinical Sc


-
PRECORDIAL EXAM
Current Editor: Christine East MD

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

Valve Location Grade Intensity

Aortic ( AV) Right upper sternal border 1 Barely audible


-1- ( RUSB)
2 Consistently audible
2nd ICS right of the sternum
Pulmonary ( PV) Left upper sternal border Loud without thrill
3
- 2- ( LUSB)
2nd ICS left of sternum 4 Loud with thrill
Tricuspid (TV) Left lower sternal border (LLSB)
-3- .
3rd 4 th, and 5 th ICS left of 5 Heard with stethoscope
partially off the chest
sternum
Mitral (MV) 5 th intercostal space in 6 Heard without
-4- the mid - clavicular line stethoscope

Edmonton Manual of Common Clinical Scenarios 96


Selected Heart Sounds and Common Murmurs
Sound Description and Etiology (/ >
03 £
.l»/ E =
ft
to r
> 03
>
C UJ
X
o
- o
CL ft>

Normal SI Closure of mitral and tricuspid valves


n
E Normal S 2 Closure of aortic ( A 2) and pulmonary ( P 2) valves
c-
L

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

Diastole Systole Diastole Systole


1 st i 2nd 3rd Atrial
A IfM- Normal

B .¥
Aortic stenosis

C
— iV"
Mitral regurgitation

Aortic regurgitation

E rf“ 1
*

i i Mitral stenosis i

97 Edi inton Manual of Common Clinical S( n


r RESPIRATORY EXAM
Current Editor Lance Frieburger MD

Signs of Increased WOB


GENERAL APPROACH ( work of breathing)
Introduction “U
Pursed lips m 3"
• Ask patient to wear a gown with the back open, then drape appropriately during the exam
x<
• Examine peripheral to central (or vice versa), compare side- to-side, do posterior first then anterior Nasal flaring O
)

General Inspection Tripoding 3n


&>
• Respiration: rate, rhythm, depth, pattern ( Kussmaul’s, ataxic, apneustic, paradoxical) and WOB Accessory muscle use
( work of breathing) ( see table) , pulsus paradoxus as a sign of diaphragmatic fatigue
• .
Chest shape: barrel chest, traumatic flail chest, pectus excavatum pectus carinatum, Intercostal muscle
indrawing
kyphoscoliosis
• Fingernails: clubbing ( Shamroth’s sign), nicotine stains ( COPD) Tracheal tugging
• Cyanosis: peripheral ( fingers) and central (lips, mouth, underneath tongue)
• Trachea: deviation, cricosternal distance, and Hoover’s sign ( hyperinflation)
.
• Accessory muscle: sternocleidomastoid, platysma, scalenes or intercostals during inspiration
• Observe at bedside for additional sounds (cough, wheeze, stridor )
• A aximum laryngeal height of 4cm or less ( LR + 3.6)
• Increased forced expiratory time ( FET) of more than 9 seconds ( LR + 4.1 for COPD) are the most sensitive measures for
hyperinflation/obstructive disease

POSTERIOR CHEST EXAMINATION


Inspection
• Shape and movement of the chest, noting deformities, asymmetry, impairment, position, or retraction
Palpation
• Deformities, lumps, masses, or tenderness, subcutaneous emphysema
• .
Confirm symmetrical lung expansion during inspiration by placing hands on 10 th rib with thumbs meeting at midline, and
checking that thumbs separate symmetrically
• Vocal tactile fremitus in all fields with ulnar edge of palms, and asking patient to repeat " boy oh boy " or " ninety -nine"

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

ANTERIOR CHEST EXAMINATION


Inspection, Palpation, Percussion, Auscultation
• As above, disrobing only as appropriate for females; do not percuss over the breast in females. Examine around the heart on
anterior examination of the left chest
Test Signs/Findings Possible Causes
Tactile fremitus Increased transmission Consolidation (pneumonia)
Decreased transmission (unilaterally) Atelectasis, pleural effusion, pneumothorax
Decreased transmission (bilaterally) COPD, bilateral pleural effusion
Chest percussion Flatness Large pleural effusion
Dullness Lobar pneumonia, pleural effusion,
hemothorax, empyema, atelectasis, tumor
Hyperresonance Emphysema, pneumothorax , asthma
Tympany Large pneumothorax
Tracheal deviation Ipsilateral Atelectasis, fibrosis, lung collapse
Contralateral Pleural effusion, hemothorax, tension pneumothorax

Edmonton i, l of Common Clinical Scenarios 98


SHOULDER EXAM
Current Editor: Maryam Soleimani MD

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

Clavicle Acromioclavicular ligament

Tendon of Acromion of scapula


supraspinalus
muscle
Coracoacromial
Glenoid labrum ligament
Subacromial bursa
«
( 1
(toll
or mi lataunu tm
Mar w «)
* * (ponanrr .
»«
Glenoid cavity
Articular capsule
Scapula Tendon sheath
Tarai miro» SuC» Mp> natu*
Kull o»
Tendon of biceps
d
-
Co»»cori p oc***
Madion
Articular cartilage
brachii musdes
(long heed)
Articular capsule:
-
Pede<m»»
suc» le>/|

Taw map>
Synovial membrane
Fibrous membrane •
N Hoad of humerus
LatowiTua darn Humerus
(nwr it orpn)
*
S ntt
*
Tnoac bract, later *! »ai
* *

lartarw Mam ,*«ma)Ml tnouda


(C|Oaafi ruaiM e
*
( 31 Daae >ucM d Iba la»lifojttr
IpoaMnv n»»i

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

RANGE OF MOTION (M)


• Perform active ROM first and if any abnormalities, perform passive ROM
• If active ROM abnormal but passive is normal, indicate potential neurologic impairment
• If both active and passive ROM are limited, indicate joint pathology
• Abduction: move arms up in an arc above head; pain may indicate AC joint problem, supraspinatus tendonitis,
subacromial impingement
• Adduction: bring arms back down after abduction and cross in front of body
• Flexion: bring arms straight out front to 180o
• Extension: bring arms straight back behind to 60o
• External rotation: elbows at side and flexed to 90o, move forearms away from body
• Internal rotation: elbows at side and flexed to 90o, rotate forearms toward body and behind back as if to touch
between scapulae

99 Edmonton Manual of Common Clir


POWER ASSESSMENT
Ask the patient to resist you on movements of flexion, extension, abduction, and adduction as outlined above while you
apply a force

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

Edmonton Manual of Common Clinical Scenarios 100


THYROID EXAM
.
Current Editors: Suqing Li Todd McMullen MD

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

Common Systemic Signs of Thyroid Disease


Hypothyroidism Hyperthyroidism
General appearance: dulled expression, slow and General Appearance: nervousness, Wt loss
.
thick speech Wt gain Eye signs: lid lag, lid retraction, exophthalmos. Graves
HEENT: periorbital puffiness, loss of lateral one- third ophthalmopathy ( specific for Graves): periorbital edema,
of eyebrow diplopia, limited extraocular movements, conjunctival swelling/
.
Skin: dry cool, coarse, myxedema, cold intolerance chemosis, exophthalmos ( bulging of the eye).
Cardiovascular: bradycardia, swelling of face, hands, Skin: warm, smooth, moist, excessive sweating and heat
and legs ( non-pitting edema) intolerance
Neuro: delay in the relaxation phase of reflexes Hands: onycholysis, acropachy, aplmar erythema
( Achilles reflex) Cardiovascular: tachycardia, palpitations
Neuro: weakness, fine tremor of the outstretched hands, brisk
reflexes ( Achilles)

• 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

Staff Section Editors


Sheny Khera MD CCFP MPH
Jennifer Ringrose MD FRCPC

With Special Thanks To:


Selina Liu MD
Alex KnebelMD
Barbara Osswald MD

107 Edmonton Manual of Common Clinical Scerui IOS


INTRODUCTION
Sheny Khera MD CCFP MPH

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:

1. Practice with others. Practice aloud.


is one thing to have an approach to a condition/physical exam component, but a totally different
• It
matter to be able to say what you are doing and to conduct the actual history and perform the
physical exam maneuver.

2. Get a good night 's sleep.


• The exam is long and tiring. Getting a sound sleep the night before will allow you to be fresh and
alert for a long day.

3. Read the scenario/OSCE station task very carefully.


• Make sure you know what you are to do for that station (e.g., take a history; demonstrate a skill;

counsel a patient).
• Also, if during that station you are lost, please look at the station task again — it will be in the OSCE

station room as well.

4. Treat the OSCE station/standardized patient as a REAL life situation.


• When you approach it this way, you will naturally be more patient -centric and focused.

n Manual of Common Clin Scenarios 108


ADULT PERIODIC HEALTH EXAM
Current Editor: Stephanie Wickersham Napier MD

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

ALLERGIES • Medication, environmental and food allergies

FHX • Cancer, cardiac, psychiatric, rheumatoid/autoimmune, any chronic disease

SOCIAL • Smoking, EtOH . recreational drug use


• Diet, physical activity, sleep
• Current employment, living arrangements, financial situation, relationships
• Sexual hx: new partners, types of .
sexual practise (vaginal, anal oral), contraception, previous STI
ROS • HEENT - H/A, vision changes, nose/ear problems
• CV - chest pain, palpitations, dizziness, peripheral edema. SOBOE
• RESP - dyspnea
• Gl . .
- dysphagia N/V abdo pain, changes in stool pattern/color /consistency, blood in stool
• GU - for men: sexual function, screen for LUTS (polyuria, urinary retention, nocturia, urgency, hesitancy weak,
stream/dribbling) ; for women: menses, sexual function, screen for incontinence
-
• MSK arthralgias/arthritis, myalgias, recent falls (in elderly)
• DERM - new /changing lesions
• NEURO - weakness, numbness, paresthesias
• PSYCH - depression, anxiety, cognitive impairment for elderly

LiHYSICALEXAM
. . . . .
General: VS ( BP HR, RR Sp02, Temp) Ht Wt BMI Counseling Topics

HEENT • Smoking cessation


• Inspection: skin lesions, throat / tonsils /uvula, otoscopic and ophthalmoscopic exam • Alcohol consumption
o
• Palpation: sinuses, lymph nodes, thyroid l/t
fZ • Brushing/ flossing teeth
o
NEURO
• Only if indicated based on history
.Q52 • Exercise & diet, weight loss
• Hearing protection
CV
• Inspection: chest wall deformities, heaves, scars • Sun exposure
• Palpation: apical impulse, thrills, heaves, peripheral edema, peripheral pulses • Helmets
.
• Auscultation: S1/S 2 character and presence of murmurs and S 3 /S4
E
01
T3
• Seat belts
RESP u • Drinking and driving
u
• Inspection: breathing pattern, chest shape
< • Smoke detectors
• Palpation: deformities, tenderness, and symmetrical lung expansion
• Percussion: dullness or hyperresonance to percussion • STI education
• Auscultation: equal air entry bilaterally and adventitious sounds (crackles, wheezes) • Varicella vaccination
ABDO c • Yearly influenza
• Inspection: bruising, scars, hernias, and bulging flanks/ascites .2 vaccination
• Auscultation: bowel sounds in 4 quadrants, abdominal bruits a • Tetanus vaccine q10 yrs
• Percussion: tenderness, liver and spleen size, ascites c
• Pneumococcal vaccination
• Palpation: tenderness, masses, abdominal aneurysm, hepatosplenomegaly
if at risk
• TB and HIV testing if at risk

109 Edmonton Manual of Common Clinic


GU
• Only if indicated based on history
DERM
• Inspection: atypical skin lesions
OTHER
• Fall Assessment in Elderly

SUMMARY OF SCREENING MANEUVERS IN ADULTS


Screening Maneuver Age ( years ) Interval forGeneral Population
Blood Pressure 18+ Annual
Weight 18+ 3 years
Exercise Assessment 18+ Annual
Tobacco Assessment 18 + Annual 2 T|
(T)
0)
Influenza Assessment 18+ Annual
n 3
~
Pap Test • Start screening at age 25 or 3 years after onset of 3 years
sexual activity, whichever occurs later
3 <
<T>
• Discontinue screening after age 70 if > 3
consecutive normal Pap tests at any interval

Mammography Females 50 - 74 2 years


Colorectal Cancer - one of: 50 - 74 2 years
• FIT 5 years
• Flex sigmoidoscopy
10 years
• Colonoscopy
Prostate Cancer ( PSA and DRE) Males 50+ 1 - 2 years
Note: no indication for routine population
screening; only screen after discussing risks and
benefits of screening tests with patient
Lipid Profile (TG, total cholesterol, LDL, HDL) Males 4 0 - 7 4 5 years
Females 5 0 - 7 4
CV Risk Calculation Males 40 - 74 5 years
Females 5 0 - 7 4

Diabetes Screen - one of: 40+ 5 years


• Fasting glucose
• HbAlc
• DM risk calculator
Abdominal Aortic Aneurysm (Ultrasound) Males 65 -80 One Time only

Note: Age and interval of screening maneuvers may need to be altered based on individual patient 's past medical history and family history.

iual of Common Clinical Scenarios 110


.
Current Editor: Telford Yeung MD PhD

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

Outlet Dysfunction Endocrine/Metabolic Over The Counter Medication


• Colorectal tumor /polyp • Diabetes • Iron and calcium supplements
• Diverticulosis • Hypothyroidism • Antacids
• Stricture • Abnormal serum calcium, magnesium, • NSAIDs
• Rectocele potassium Lifestyle
• Hirschsprung’s • Cystic fibrosis • Low fiber
Slow colonic transit Connective Tissue /Vascular Disease • Dehydration
• Scleroderma • Sedentary
• Dermatomyositis
• Amylodosis
Bolded items indicate most common conditions

HISTORY
ID • Age, gender

CC • Constipation, pain with defecation, tenesmus, straining

HPI • Frequency of bowel movements


• Bleeding: where / when noticed ( toilet paper, toilet bowl, on stool surface, mixed in the stool), dark /tarry melena
.
(upper Gl) vs bright red blood ( lower Gl)
• Pain: relieved by defecation, hard stools, straining, manual maneuvers used, hemorrhoids

• 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

PSHX • Recent abdominal or pelvic surgeries


PO&GHX • Current pregnancy

MEDS • Anticholinergics, opioids, antidepressants, anticonvulsants, iron supplements


FHX • Malignancy (especially colorectal), diabetes

111 Edmonton Manual of Common Clinical Scenario


ROS • HEENT: vision changes (DM, MS)
• CV: palpitations/bradycardia (hypothyroid, electrolyte abnormalities)

• Constitutional symptoms ( wt loss, night sweats, fevers)

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

Edmonton Manual of Common Clinical Scenarios 112


. .
Current Editor: Mihai Sfranciog BSc ( Hons ), MD

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

• Exacerbation of asthma or COPD • Chronic bronchitis


• Pulmonary embolism Non-post Infectious: • Tuberculosis
• GERD • CHF
Non- life Threatening: • Asthma • Malignancy
• Bronchitis / viral URTI • Upper airway cough syndrome Chemical Irritants:
• Upper airway cough syndrome • Smoking/inhalants
• Environmental • ACE - inhibitor induced

• 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

113 Edmonton Mai mm<


PHYSICAL
General Approach
. . .
• VS: BP HR, RR Temp Sp02
HEENT
• Inspect for nasal bogginess, nasal polyps, oropharynx erythema, and tonsillar enlargement/exudate
• Palpate for tenderness over sinuses and lymphadenopathy
RESP
.
• Inspect for patient positioning ( tripoding) ease of speech ( full sentences or broken phrases), grunting, stridor, and use of accessory
muscles
• Percuss for dullness (consolidation)
• Palpate trachea position, chest expansion, and tactile fremitus
• Auscultate for equal air entry, bronchial breath sounds, wheezes, crackles, egophony, whispered pectoriloquy
CV
• Inspect for central cyanosis and digital clubbing
• Palpate for regular and equal pulses, cardiac apex, and peripheral edema 2 -n
• Auscultate for heart sounds, murmurs, and rubs 2
CL -
ft
)
i

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

Treatment Options (limited data regarding efficacy)


• Cough suppression

> Consider: narcotics (e.g., codeine), non-narcotics (e.g„ dextromethorphan, diphenhydramine)


> Pregabalin or gabapentin for chronic cough refractory to other measures

Treatment for Common Causes of Cough


Common Causes of Cough Suggested Treatment of Underlying Cause
Common Cold Sx control ( fluids, analgesics, lozenges) , cough suppressants NOT recommended
Influenza .
Sx control, antivirals (e.g. oseltamivir ) in select cases
Allergic Rhinitis Avoid triggers, oral +/- nasal antihistamines, oral leukotriene receptor antagonists. See post -nasal
drip.
(avoid antihistamines for chronic cough in children)
Bacterial Sinusitis .
Abx (e.g. amoxicillin). See post -nasal drip.
Asthma /COPD . .
Inhaled corticosteroids SABA LAMA. Refer to obstructive pulmonary disease section.
Post- nasal Drip .
Oral decongestants (e.g., pseudoephedrine) nasal steroids, nasal saline rinses;
Treat underlying cause of post -nasal drip (e.g., allergy, vasomotor, bacterial)
GERD Lifestyle changes, PPIs, H2RAs
(insufficient evidence to show if treating GERD for chronic cough is any better than placebo)
Medication Induced Discontinue med or replace with alternative ( e.g., change ACEi to ARB)

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

Edmontor Mar Clinical Scenaric 114


Current Editor: Nikhil Raghuram PhD

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

Parasitic • Cryptosporidium • Cryptosporidium • Entamoeba

• Giardia • Giardia • Cyclospora


• Giardia

CHRONIC: timeline > 4 wks

Type Features Causes


Osmotic • Diarrhea stops with fasting/ • Lactase deficiency
restricting intake of offending • Ingestion of a non- absorbable osmotically active substance
substance (e.g., rarely at night) • Carbohydrates - lactose, fructose, mannitol, sorbitol (chewing gum diarrhea),
• Minimal cramps and pain lactulose
• Divalent .
ions - magnesium ingestion ( antacids Epsom salts)
• Fat malabsorption (e.g., celiac disease, pancreatic insufficiency)
• Carbohydrate malabsorption - short bowel syndrome

Secretory • Large volume watery stools • Laxatives


• Diarrhea persists despite • Small bowel bacterial overgrowth
fasting • Medications
• Minimal cramps and pain • Bacterial enterotoxins ( note: these are usually acute diarrhea syndromes)
• Bile salt wasting diarrhea (previous cholecystectomy)
• Toxins: EtOH, Arsenic
• Secretagogues: VIP ( Pancreatic Cholera Syndrome), calcitonin (med. ca of
thyroid), gastrin ( ZES)
Inflammatory • Systemic symptoms • Invasive infections: Shigella
(0157)
. Campylobacter, Salmonella, enteroinvasive E. coli
• Visible blood in stools
• Significant cramps and pain • Radiation Tx
• PMNs on stool microscopy • Inflammatory .
bowel disease - ulcerative colitis Crohn’s disease
Increased Gut stools, porridge like
• Soft • Irritable bowel syndrome
Motility (++pain/cramps) • Hyperthyroidism
• Post - surgical diarrhea - vagotomy, resection of ileocecal valve

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

PMHX • Hyperthyroidism, Addison's, AIDS, Celiac


fibrosis, incontinence
. .
, IBD, IBS, CRC lactose intolerance, DM pancreatic disease, cystic S'l mmmm

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)

• GU: impotence (autonomic neuropathy)


• MSK/DERM: myalgias and arthritis (reactive or IBD), erythema nodosum (IBD)
PHYSICAL
. . .
General Approach - VS: BP, HR RR Temp Sp02, orthostasis
Volume Status - mucous membranes, capillary refill, skin turgor, JVP
ABDO
• Inspection - abdominal distension, scars
• Auscultation - bowel sounds, high pitched sounds/ borborygmi (gastroenteritis, dysentery, active ulcerative colitis)
• Percussion - dullness, tenderness, liver span (normal: 9-11cm at the MCL), Castell’s sign (dullness during inspiration at the 9th ICS at the
L. anterior -axillary line - indicates splenomegaly)
• Palpation - abdominal tenderness, masses, guarding, and rebound tenderness (peritonitis), DRE: skin ( fissures, hemorrhoids) tone,
mass, blood, stool, perianal excoriation
INVESTIGATIONS
Most episodes of diarrhea are self-limited - investigate patients with red flags
Laboratory Investigations
• CBC-D , electrolytes, ( low Hb for bloody diarrhea, high WBC for infection), Cr, urea ( fluid status)
• Anti- transglutaminase antibody and IgA level (Celiac disease), TSH (hyperthyroidism)
Microbiology
.
• Stools: C& S, O& P, C. difficile toxin, fat WBC (inflammatory), phenolphthalein ( laxative abuse), stool osmolality (secretory vs.
osmotic diarrhea)
• PCR (noroviruses), electron microscopy ( noroviruses and rotaviruses)
Special Tests
• Check for occult blood in stool ( FIT)
• Barium enema + sigmoidoscopy (Crohn's, colorectal cancer ), Abdo XR or Abdo CT to rule out obstruction
.
• Colonoscopy if chronic (Crohn’s, UC colorectal cancer )

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

• Zolliinger - Ellison syndrome


• Ischemic bowel * *
• Esophogeal / intestinal
dysmotility
Psychiatric Infectious Malignancy Other
• Mood disorder •H - pylori • Esophogeal cancer * * • Functional (no etiology
• Anxiety • TB • Gastric cancer * * found)
• Conversion disorder • Sepsis • Pancreatic cancer ” • Post -immobilization
• Hypochondriasis • Intestinal parasites
Cryptosporidium)
(Giardia . • Post - vagotomy
• Dumping syndrome

”High mortality/ morbidity


Bolded items are most common
HISTORY
ID • Age, gender, ethnicity

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

117 Edmonton M.i f Commor


MEDS • NSAIDs . steroids, recent abx
FHX • IBS . esophageal or gastric cancer
SOCIAL • Smoking. EtOH, caffeine, travel Hx, diet (hot foods, Betel nuts)
ROS • General: fatigue, wt gain/loss, energy
• CV: pallor, dependent edema, orthopnea, paroxysmal nocturnal dyspnea, palpitations
• RESP: cyanosis, dyspnea, sputum, cough, hemoptysis, Hx TB or pneumonia
• Gl: bowel function, jaundice
• GU: decreased urine output
• MSK/DERM: arthralgia/myalgia, rash . Raynaud's phenomenon
PHYSICAL
General Approach
. . .
• ABCs, VS: BP HR RR. Temp Sp02 (+ orthostatic vitals if significant blood loss or dehydration suspected)
HEENT 2 T!
ro
• Inspection: oral cavity for dental erosions, oral ulcers /candidiasis, halitosis
5
n= 3
• Palpation: thyroid, lymphadenopathy (+ Virchow 's node)
CV/RESP
Quadruple Therapy for H. pylori Eradication — •

1) Omeprazole 20 mg BID x 14 d <T>


• Inspection: JVP
2) Clarithromyan 500 mg BID x 14 d
• Palpation: chest tenderness, pitting peripheral edema
3) Amoxicillin lg BID xl4 d
• Auscultation: cardiac and respiratory sounds 4) Metronidazole 500 mg BID xl4d
ABDO
• Inspection: bulging flanks ( ascites), masses
• Auscultation: bowel sounds, succussion splash (gastroparesis)
• Percussion: tenderness ( peritonitis), tympany (obstruction)
• Palpation: abdominal tenderness /rebound /guarding, palpable gallbladder, masses + DRE
DERM
.
• Signs of scleroderma ( sclerodactyly, tightened / thickened skin, hyper /hypopigmentation telangiectases, calcinosis, ulceration), SLE
( malar rash, discoid rash, alopecia, photosensitivity), synovitis

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 )

onton Ma lot C( on Clinical Scenario! 118


DYSURIA
Current Editor: Lindsay Drummond BSc BEd

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

119 Edmonton Manual of Common Clir


ABDO
• Percussion: CVA tenderness ( pyelonephritis)
• Palpation: bladder ( suprapubic tenderness) , kidneys
• DRE in men to examine prostate (prostatitis or BPH)
GU
• Men: examine testes, epididymis, glans penis and prepuce (balanitis). Palpate testes and scrotum for tenderness. Palpate inguinal,
iliac, supraclavicular LN (prostate/testicular tumor). +/- Prehn's sign (relief of pain with elevation of testicle suggests epididymitis) .
• Women: exam pelvic area +/- sterile speculum exam if hx suggests STI
• In both, look for: skin changes, abnormal discharge, trauma, infective lesions
Extremities
• Palpate joints for arthritis /tenderness (reactive arthritis)
• Determine if extremities are cool/clammy or warm (signs of shock )

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

Diagnosis Female Male

Uncomplicated Fosfomycin 3 g PO x 1dose TMP/5MX IDS tab PO BID x 10 d


Cystitis or Nitrofurantoin 50- 100 mg PO qid x 5 d or Cefixime 400 mg PO daily x 10 d
Gonorrhea Cefixime 800 mg PO single dose or Ceftriaxone 250 mg IM single dose PLUS rx for chlamydia
Azithromycin Ig PO single dose or Doxycydine 100 mg PO bid x 7 days (report to public health to treat sexual
Chlamydia contacts)

-
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

Edmonton Manual of Common Clinical Scenarios 120


ERECTILE DYSFUNCTION
.
Current Editor: Tianru Sui MD

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

Metabolic/ Endocrine • Hypogonadism, hyperprolactinemia, hypothyroidism or hyperthyroidism


2 £2
Medication • Antihypertensives: CCB, beta - blockers, thaizide diuretics, spironolactone
• Antidepressants: SSRIs, TCAs, MAOIs
• Antipsychotics
• Recreational drugs: EtOH, marijuana
Psychogenic Etiologies
Performance anxiety Depression/anxiety Traumatic past experiences
History of sexual abuse Marital or relationship discord Stress

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

121 Edmonton Manual of Common Clii


PHYSICAL EXAM
.
General Approach - VS: BP, HR, RR Temp, SpCh, BMI
CV
• Precordial examination, heart sounds, femoral ( femoral bruits) and peripheral pulses
Endocrine
• Secondary sexual characteristics (hypogonadism): gynecomastia, nipple discharge, decreased male hair distribution, testicular
atrophy
• Hypothyroidism or hyperthyroidism: hair and skin changes, goiter, deep tendon reflexes
NEURO
• Visual field defects (pituitary tumors), pinprick and touch sensation of the penile shaft and perineum, screening neurologic exam
. .
( CVA MS PD)
GU
.
• Evaluate penis for size, scars, fibrosis /plaques urethral meatus (hypo /epispadias), elasticity ( foreskin phimosis ), curvature
(Peyronie’s disease)
• Evaluate scrotum for testicular size and consistency 2n
Gl JD- w
Q
• DRE: size, consistency and tenderness of prostate: if considering starting testosterone therapy, assess for contraindications n 3
(prostate cancer ) 3 *
n>
<
Special Tests
• Bulbocavernous reflex: anal sphincter contraction in response to squeezing glans penis ( neurogenic ED)
• Cremasteric reflex: elevation of ipsilateral testicle in response to stroke of medial thigh ( thoracolumbar erection center integrity)

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)

Time b/w dosing Duration


Drug Standard dose Onset
and intercourse

Sildenafil ( Viagra) 25 - 100 mg 1hr 14 - 60 min Up to 4 hrs


Tadafanil (Cialis) 5 - 20 mg 1- 12 hrs 16 - 45 min Up to 36 hrs
Vardenafil (Levitra) 5 - 20 mg 1hr 25 min Up to 4 hrs

• 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

Edmonton Manual of C imon Clinical Scenarii 122


Current Editor: Christine East MD
KEY POINTS
• The differential diagnosis for fatigue is broad - effective assessment requires a thorough Hx and PE
• A systems - based approach provides structure and ensures that important causes are not overlooked
• Eliciting what the patient means by " fatigue" is key to assessment and diagnosis. Fatigue must be differentiated from the similar or
related complaints defined below:
Fatigue: 1. Perceived generalized weakness causing inability to initiate some activities;
2. Increased fatigability reducing the ability to maintain activity;
3. Mental fatigue causing poor concentration, memory impairment, and emotional instability
Somnolence: Abnormal sleepiness
Muscle True muscular weakness, wherein the strength of muscles is less than expected (differentiate from perceived
Weakness: muscular weakness, where patient feels that more effort is required than normal, but muscle power is normal)

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

HPI • Characterize fatigue vs. somnolence vs. muscle weakness


• Onset, duration, pattern, severity, aggravating and alleviating, course (stable, worsening)
. .
• Associated symptoms (may suggest a diagnosis, e g. SOB in CHF or COPD)
- ability to work, socialize, participate in family activities
• Impact on daily life
• Constitutional symptoms - unintentional wt loss, fevers, night sweats (infection, inflammation, cancer)

PMHX • Chronic diseases, cancer, recent Ml .CHF. COPD.DM. hypothyroidism liver disease psychiatric history, etc.
, ,

PSHX • Thyroidectomy, cardiac surgery

FHX • Cancer.CAD, autoimmune disease


MEDS ..
• Medications associated with fatigue (e g , beta -blockers, benzodiazepines)
• New medications or recent dose changes
.
• OTC, herbals CAM

SOCIAL • Tobacco use .EtOH. IVDU, recreational drug use


• Social stressors, living situation (e.g.. homeless, prison), abuse and intimate partner violence
• Recent travel or emigration (endemic infections)
• Sexual history (HIV. viral hepatitis)

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:

General • BATHE mnemonic for patient counseling:


Approach Background factors
>
> How is this Affecting you?
» What about this Troubles you the most ?
> How are you Handling this?
-
> Empathize and Empower elicit patient ’s resources and coping mechanisms
• Ensure frequent follow - up (e.g., monthly) to monitor symptoms; continue to screen for red flags
• Consider alternate diagnoses if chronic and no organic causes identified (e.g., CFS, fibromyalgia)

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.

Edmonton Manual of Common Clinical Scenarios 124


Current Editor: Jamie McIntyre MD

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

• Miscellaneous WBC > 12 or < 4 or > 10% band cells


> Allergic reaction, idiopathic/familial. EtOH withdrawal, transfusion
reaction
> Drug induced: overdose or side effect

> Environmental: heat stroke


High Mortality /Morbidity
• Sepsis: SIRS criteria AND an infectious source ( see table to the right )
• Severe sepsis: sepsis AND increased lactate or SBP < 90mmHg
• Septic shock: severe sepsis AND hypotension despite adequete fluid resuscitation

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

• Gl: constipation or diarrhea , abdominal distention or pain, ascites, jaundice

• GU: dysuria, discharge


• MSK / DERM: muscle cramps or weakness , joint pain or swelling, rash, masses

• NEURO: headache

125 Edmonton Manual of C


PHYSICAL
General Approach
. . . .
• ABCDE VS ( BP, HR. RR Temp, Sp02 GCS chemstrip, localize cause of fever (head to toe exam)
• Does the patient look toxic ?
Head-to-toe exam to locate source of infection:
HEENT
• Inspection: tympanic membranes ( middle ear infection) , frontal and maxillary sinuses ( sinusitis), temporal arteries (giant cell
.
arteritis), nasal discharge, oropharyngeal inflammation or oral candidiasis, nuchal rigidity Kernig’s, Brudzinski ’s sign (meningitis),
conjunctivitis
• Palpation: thyroid nodules, lymphadenopathy
CV
• Inspection: splinter hemorrhages and Janeway lesions (hemorrhagic macules on palms and soles indicative of infective
endocarditis)
• Palpation: pulse (tachycardia)
• Auscultation: new or changed murmurs, friction rubs 2 n -
n<.
O )
RESP
• Percussion: evidence of consolidation (pneumonia) or effusion (empyema) mm • MM

• Auscultation: crackles, wheezes, whispering pectoriloquy, egophony 3


rt>
ABDO
• Inspection: ascites, surgical wounds
.
• Percussion: peritonitis, hepatomegaly, splenomegaly (percussion over Traube's space Castell ' s sign)
.
• Palpation: tenderness, hepatomegaly, splenomegaly, peritonitis, Murphy ' s sign Rovsing's sign
• Auscultation: lack of bowel sounds
GU
• Inspection: genital ulceration or discharge
MSK
• Inspection: joint swelling or erythema, signs of tenosynovitis
DERM
.
• Inspection: erythema (mark outline to monitor rate of spread ) , pus rash, tender, swollen skin, streaking lymphangitis, surgical
wound sites: in hospitalized patients, look for signs of inflammation at site of IV lines or catheters
• Palpation: any lesions / wounds: redness, swelling, pain, tenderness, warmth, fluctuance ( abscess)

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.

Edmonton Manual of Common Clinical Scenarios 126


Current Editor: Parnian Riaz BSc (Hons)

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

Secondary Headaches: underlying etiology present


Headache Type Symptoms Causes
Increased ICP Constantly present, worse in AM, when supine, and with valsalva, blurred Space - occupying lesion, HTN emergency,
vision, papilledema signs venous sinus thrombosis, hydrocephalus,
idiopathic intracranial hypertension
Thunderclap Acute onset, reaches max intensity in minutes, worse with exertion SAH, arterial dissection
Infection Fever / chills, nuchal rigidity, N/V, confusion/ altered LOC, purpuric rash, immu- Meningitis, encephalitis
nocompromised
Vasculitic Age> 50, unilateral scalp tenderness, jaw claudication, blurred vision, fever / Temporal arteritis
chills
Focal neurological deficits Negative sx: weakness, clumsiness, numbness, vision loss Space -occupying lesion, AV malformation,
arterial dissection (stroke mimic),
encephalitis
Other causes: medication overuse (rebound H/ A ), infection ( sinusitis, mastoiditis, dental infx ), trauma, pre -eclampsia, post - LP, intracranial abscess,
glaucoma, optic neuritis, neuralgia, TMJ, C-spine OA, hypoxia / hypercapnia, drugs /toxins

HISTORY
ID • Age, gender

CC • Headache

HPI • Onset, location (unilateral/bilateral), progression, frequency


.
• Provoking factors (trauma, head position, time of day sleep, physical activity, chewing, lights, sounds, valsalva),
palliating factors, known triggers
• Quality (throbbing, constant, intermittent, pressure)
• Radiation (to cervical musculature)
• Severity (especially in comparison to previous headaches)
• Timing (events leading up to the headache, headache progression, relation to menstruation)
• Associated Symptoms: N/V, aura, visual disturbances, vertigo, dizziness, focal neurological symptoms LOC
(intracranial bleed), jaw claudication, TMJ clicking
.
.
RED FLAGS • Papilledema, altered LOC fever, meningismus, focal neurological deficits, signs of head trauma
PMHX .
• Pregnancy, migraine/tension/cluster headaches, HTN HIV, cancer, recent trauma, seizure, glaucoma, polymyalgia
rheumatica, vasculitis or other rheumatological conditions
PSHX • Recent LP, previous cancer,intracranial surgery
. .
FHX • Migraines SAH aneurysms, stroke, seizures, motion sickness
MEDS • Nitroglycerin, analgesics ( frequency of use), OCP, caffeine use

127 Edmonton Manual of Commoi cenar


ALLERGIES • Medical or environmental
SOCIAL • Illicit drug use, smoking, EtOH, stress, recent travel
ROS • HEENT: jaw claudication, scalp/ temporal tenderness ( temporal arteritis), photophobia/phonophobia, neck pain,
aura, scintillating scotomas (meningitis), neurovisual disturbances, eye pain and halos around objects (glaucoma),
ipsilateral autonomic dysfunction (cluster ), rhinorrhea (sinusitis), tinnitus (idiopathic intracranial hypertension, AV
malformation), seizures (encephalitis, space occupying lesion)
•Gl: N/V/D
• MSK/ DERM: weakness/paresthesia, stiffness, myalgias (temporal arteritis)

• Other: fever, depression (cluster) . B symptoms (metastasis)


.
RISK • HTN, DM, smoking, low physical activity, age, obesity, hypercholesterolemia Ml, OCP, previous thrombosis
FACTORS (venous sinus thrombosis)
PHYSICAL
.
Vitals: BP (high BP - HTN emergency ), HR, RR Temp ( infection), SpOi, GCS
.
• Cushing’s response: HTN bradycardia, irregular respiration (high ICP) 2 1
n> J
HEENT Q.
• Inspection: visible trauma, tympanic membrane (otitis media), fundoscopy ( papilledema), dental exam, visibly swollen temporal o 3
artery, purpuric rash (meningitis), lacrimation, conjunctival injection (cluster ) 3 *<
n>
.
• Palpation: tenderness over frontal/maxillary sinuses (sinusitis), paraspinal muscles (tension H/A ) TMJ, temporal artery (temporal
arteritis), nuchal rigidity (meningitis), "clicking" during TM J movement
.
• Auscultation: bruit at neck eyes, head ( AV malformation), temporal artery ( temporal arteritis)
NEURO
• Assymetry/focal deficits of CN, tone, strength, reflexes, sensation, gait (CNS lesion)
• Kernig’s sign: pain with passive extension of flexed knee (meningitis)
• Brudzinski's sign: hip flexion with passive neck flexion (meningitis)

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

Headache Type Abortive Prophylaxis


Tension • Acetaminophen • Stress/triggeravoidance
• NSAIDs • Relaxation exercises
• Muscle relaxants, heat, massage • TCA antidepressants

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)

Edmonton Manual of Common Clinical Scenarios 128


Current Editor: Lisa Weger MD

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

Out -of - office Measurement Yes


1. ABPM ( preferred)
Daytime Mean 135/85
24 - hour mean 130/80
OR
2. Home BP series Mean 135 /85
] NO
White Coat Hypertension

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 .

129 Edmonton Manual of Common Clinical


SOCIAL • Na * consumption ( > 4 g/day), smoking, EtOH, physical activity
RISK • Age, smoking, physical inactivity, obesity ( BMI > 30 kg/m2), FHx of CVD ( < 55 yrs male, < 65 female), excess intake
FACTORS of dietary Na+ and /or EtOH, previous CV event

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.

iton Manual of Common Clinical Scenarios 130


Current Editor: Leah Brown

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

Medications Antidepressants, corticosteroids, beta - agonists, stimulants, decongestants


Substance Use Caffeine, alcohol, nicotine, cocaine

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.
,

• Psychiatric conditions: mood disorders, PTSD. anxiety, bipolar disorder


• Previously diagnosed sleep disorders
MEDS • Medications that affect sleep: antidepressants, corticosteroids, beta -agonists, stimulants, decongestants
• Sleep aids: melatonin, hypnotics, benzodiazepines (confirm frequency and dose)

FHX • Sleep, psychiatric, and general medical disorders

.
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

> Maintain regular sleep schedule (bedtime and wake - time)


> Go to bed only when sleepy; get out of bed if unable to sleep after 15 - 20 mins and return later
2 Tl fti
Q.
> Adjust bedroom environment to promote sleep (quiet, dark, cool); use bedroom only for sleep
n 3
> Avoid caffeine, alcohol, nicotine, and exercise in evening; avoid naps in daytime 3 <
> Avoid prolonged use of light -emitting screens (computer. TV. smartphones)
CD

• Non- Pharmacologic Therapies


> Stress reduction techniques, regular exercise, meditation
> Cognitive behavioral therapy - online CBI courses or books available if none in community. For chronic insomnia, combine
medication and CBI ( while tapering medication).
> Sleep restriction therapy - consolidate total time in bed to match total time sleeping, then increase time in bed
by 15 - 30 min/ wk
• Pharmacologic Therapies - consider short term/intermittent dosing with close follow -up
> Melatonin - hormone that is naturally secreted during darkness; signals sleep onset. Available OTC; 2 mg PO 1- 2 hrs before
bedtime. Some evidence of modest effect.
.
> Benzodiazepines - use at lowest possible dose, should only be used short term due to risk of dependence; e.g. lorazepam,
temazepam
> Trazadone - less risk of tolerance/dependence, less "morning hangover ". Consider in sundowning dementia pts.
Give 25 -100 mg.
> Non-benzodiazepines (" Z-hypnotics") - e.g., zopiclone, zolpidem - risk of tolerance/dependence, may induce complex
sleep -related behaviors
> L- tryptophan 500 mg - 3 g PO qhs for sleep and mood
> . .
Sedating antidepressants/antipsychotics - e.g., quetiapine olanzapine. Taper sedating meds for 2 - 6 wks at no more than 25%/
wk , when discontinuing (do not stop abruptly). Follow up regularly if on long- term sedatives to discuss dependence, side effects,
.
and comorbid conditions Do not suggest OTC sleep aids (esp. antihistamines) in elderly due to side effects.
> Doxepin (low dose), melatonin, Z -hypnotics (low dose) considered safe in elderly
> Limit medications in pregnancy/breastfeeding

Treatment of Secondary Insomnia


Common Causes of Insomnia Suggested Treatment of Underlying Cause
Obstructive Sleep Apnea CPAP or devices to improve airway (mandibular advancement device, nasal dilators),
weight loss, nasal steroids
If swelling present, consider referral to sleep specialist.
Restless Leg Syndrome Check ferritin, non-drug treatments (massage, exercise, warm baths), non-ergot dopamine
antagonists
Circadian Rhythm Disorder Melatonin 4- 5 hrs before bed, natural light exposure during day, avoid shift work
Depression / Anxiety Antidepressants/anxiolytics, CBT
Physical Symptoms ( pain, dyspnea ) Symptom control (analgesia), treat underlying condition
Alcoholism Reduce alcohol intake, promote abstinence, enroll in treatment program
Illicit Drug Use Reduce drug intake, promote abstinence, enroll in treatment program
Parasomnias ( sleep walking, sleep talking, Safety precautions, consider referral to sleep specialist
night terrors, nightmares )

Edmonton M ial of Cc in Clinical Scenario! 132


LOWER BACK PAIN
Current Editor: Shalini Reddy BSc (Hons) MBBS

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 )
"

• Physiotherapy • Add: cyclobenzaprine for muscle spasms


and exercise
• If already on controlled- release opioid: add short - acting opioid or increase controlled release by 20- 25%
• Mechanical back pain resolves in < 6 wks - otherwise, further investigations required

Chronic • Encourage as • 1st and 2nd lines: see acute pain


above • 3rd line: TCA (amitriptyline, nortriptyline), weak opioids (codeine)
• Community • 4 th line: tramadol
rehab/chronic
pain programs . .
• 5 th line: strong, controlled- release opioids (hydromorphone HCL oxycodone HCL fentanyl patch)

‘Cauda Equina Syndrome requires urgent Neurosurgery consult to preserve bowel and bladder function and prevent paraplegia

Edmonton Manual of Common Clinical Scenarios 134


NAUSEA & VOMITING
Current Editor: Britney Jones MD

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

CC • Nausea and vomiting

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

MEDS • Steroids, chemotherapy/radiation therapy, NSAIDs, opioids, SSRIs, anticonvulsants, antiarrhythmics


SOCIAL • EtOH, IVDU, marijuana use, sexual history
ROS • HEENT: vertigo, acute changes in vision, red color (MS)
• CV: chest pain
• GU: testicular pain, urinary changes
• MSK/ DERM: rash, arthralgia

135 Edmonton Manual of Common Clinical Scenario'


PHYSICAL
Focus exam based on likely etiology
General
.
• ABCs, VS: BP, HR RR, Temp, Sp02, ( fever, orthostatic hypotension), diaphoresis, increased work of breathing
HEENT
• Dental enamel erosion, dry mucous membranes, tongue furrows, lymphadenopathy, oral ulcers, thyroid exam
NEURO
• Focal neurologic signs, nystagmus, papilledema
• Meningismus:
> Nuchal rigidity
> Kernig’s sign - pain on knee extension (leading to resistance) with hip flexed to 90 degrees (meningitis or SAH)

» 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

Edmonton Manual of Common Clinical Scenarios 136


OBESITY
Current Editor: Arabesque Parker MD

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

Obese Class 1 30- 34.9 Japanese > 85 > 90

Obese Class 2 35 - 39.9


Obese Class 3 > 40

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

137 Edmonton Manual of Common Clinical Sc


ROS • CV - chest pain on exertion
• RESP - SOBOE
• Gl - heartburn, constipation
• ENDO - cold intolerance, fatigue
• MSK - joint pain, back pain, pain with exercise
• DERM - appearance of striae, skin infections, skin/hair changes, excess hair growth

• GYN - menstruation changes, infertility


• PSYCH - depressed mood, guilt about excessive eating

RISK • Female gender, insulin resistant . .


states PCOS, FHx of obesity, lower SES depression, shift work
FACTORS

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

• General fat distribution: truncal vs. generalized vs. localized


<
HEENT
• Thyroid exam, fundoscopy
CV/ RESP
.
• Signs of CHF cardiomegaly, arrhythmias, edema, vascular bruits
ABDO
• Hepatomegaly, ascites, abdominal pannus
MSK
• Decreased ROM associated with OA
DERM
• Acanthosis nigricans, xanthomas, hirsuitism, venous stasis changes, intertrigo, purple striae

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

Edmonton Manual of Common Clinical Scenarios 138


RESPIRATORY TRACT INFECTION
Current Editor: Parnian Riaz BSc (Hons)

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)

139 Edmonton Manual of Common Clinical Scenarios


PO&GHX • Current pregnancy

MEDS • Recent Abx use, chronic corticosteroid use


ALLERGIES • Drugs (especially Abx), environmental
SOCIAL • Smoker, EtOH, dentition, occupation, home environment, nursing home, sick contacts, travel

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)

Idmonton Manual of Common Clinical Scenarios 140


SEXUAL & HIGH-RISK INFECTIONS
Current Editor: Cassandra Hirt MD

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 ;

Hepatitis B Low to moderate


.
Infants of HBsAg+ mothers IV drug users, multiple sex
partners, endemic regions, sexual and household contacts of
acute or chronic carrier
Infectious Syphilis (T. palladium) Previously rare, increasing MSM, sex workers (+ clients), endemic regions

HIV Rare, increasing


MSM. IV drug users, endemic regions .
9 15-19 y/o
Chancroid, Granuloma inguinale,
Very rare Endemic regions
Lymphogranuloma venereum

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

Ecimo Manual of Common Clinical Sc 142


SKIN, HAIR, & NAILS
Current Editor : Briannc Tetz MD

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)

Hair Loss Hair Gain


Androgenic alopecia: normal in both males and females, but
Endocrine consider PCOS or other source of androgens if female with male Hirsutism in females (hyperandrogenism)
pattern and menstrual irregularities, acne, hirsutism, deep voice

Autoimmune Alopecia areata: patchy hair loss


Infectious Tinea capitis, secondary syphilis
Psych Trichotillomania
Telogen effluvium (resting phase of hair follicle), anagen effluvium, Hypertrichosis: generalized increase in growth of
Other
drugs, chemicals, trauma, cicatricial alopecia, pediculosis (lice) fine, non-pigmented hair, in a non-sexual pattern
Nail Pathology
Onychomycosis (Tinea unguium), green nail syndrome (Pseudomonas), paronychia (S. aureus -
Infections
resolves with Abx, unlike onychocryptosis which can require surgical procedure)
Dermatologic Psoriasis, lichen planus
Onychocryptosis (ingrown nail), onycholysis, nail dystrophy, yellow nail, clubbing, splinter hemorrhages,
Structural
.
koilonychia (spoon nails) Beau lines, leukonychia, nail plate pitting, longitudinal melanoychia (pigmented bands)

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

143 Edmonton Manual of Common Clinic . t


MEDS Abx: beta -lactams (penicillins, cephalosporins), tetracyclines (photosensitivity)
Anticonvulsants (phenobarbital, phenytoin, carbamazepine)
Sulfonamides ( Stevens - Johnson syndrome)
Androgens /estrogens
Chemotherapy
ROS • HEENT: dry mouth, dry eyes
• CV/RESP: palpitations, SOB, cough, chest pain (complication of hypovolemia)
• Gl: rapidwt loss, vomiting, diarrhea, constipation, blood in stool/melena, ostomy
• GU: UTI symptoms (i.e., dysuria ), excessive/decreased urine output, dark colored urine

• MSK/DERM: diaphoresis, burns, dermatological conditions


• CNS: change in mental status (confusion, incoherent speech, irritability), seizures
• Other: fever, dizziness, fatigue, lethargy, weakness

RISK FACTORS • Cognitive impairments (dementia /delirium), depression


• Dependence on feeding assistance, dysphagia /odynophagia . NPO/ fluid restriction
• Chronic illnesses, infection
• Previous episodes of dehydration
• Risk factors for hypovolemia in the elderly: female sex , > 85 yrs, > 4 chronic medical conditions,
> 4 medications, being confined to bed

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

> 3 s, strength in extremities • Incontinence ( fear of ) 0. 3


D CD
• Oral problems/sippers 0) “
CV: palpate peripheral pulses; auscultate for murmurs and EHS • Neurological impairment
ABDO: inspect for abdo distention, signs of cirrhosis; auscultate for bowel sounds; DRE for blood • Sunken eyes

Severity of Dehydration - Body Weight Loss (%)


Finding ( for Hypovolemia ) LR + LR -
5% 10% 15%
Dry mucous membrane (mouth/nose) 3.1 0.4
• VS normal • BP normal • Reduced LOC
Abnormal skin turgor ( subclavicular area) 3.5 0.3
BP|
Sunken eyes
Dry axillae
NS
2.8
0.5
NS


U/O normal
MM moist
. HR
. u/oi

^
MM dry



HRf
Anuria /oliguria

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

• Serum osmolality ( mmol/ L ) = 2 x Na * + 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

• Closely monitor and reassess volume status throughout rehydration period

Edmonton Manual of Common Clinical Seenanc 182


.
Current Editors: Prabhpreet Dhaliwal MD Vijay Daniels MD FRCPC

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)

• Memory loss (short -term, long- term)


• Language, orientation, attention

• Hallucinations
• Parkinsonian features (hypomimia
abnormal gait)
. . .
hypophonia drooling, tremor, rigidity, bradykinesia micrographia, falls,

• Autonomic symptoms (postural dizziness, diaphoresis)


PMHX • Stroke, vascular disease
FHX • Dementia in 1st degree relative
FUNCTIONAL • ADLs - bath (1st to go), dress, toilet, transfer, continence, eating (last to go)
HX • lADLs - phone, shop, transportation, meds, budget, cooking, housekeeping
• Assistive devices (walking/bathroom aids) and services (meal delivery, lifeline)
MEDS • Especially CNS- toxic drugs (psychotropics, benzodiazpines, anticholinergics)
SOCIAL • Living situation, social supports (network , relationships, family), legal ( finances, abuse, neglect, POA)
• Smoking, drugs
RISK FACTORS • Risk factors (DM, dyslipidemia, HTN)
• Protective factors (e.g., higher education)

.
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)

183 LcJmonton Manual of Common Clinical Scenarios


PHYSICAL EXAMINATION
General
• Vital signs and orthostatic vitals for all patients
.
• MMSE (+ LR 6.3, -LR 0.19) Clock, Frontal Lobe Testing (similarities, proverbs)

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

CT Head - if any one of the following are present:


5:3
• Age < 60
• Rapid decline in mental or physical function (1- 2 months) or short duration ( < 2 years )
3 U
CO —
• Recent head trauma, anti- coagulant, or bleeding disorder
• Unexplained neurologic symptoms (e.g., severe headache) , or new localizing signs (e.g., seizures, weakness )
• History of cancer (especially type that met to brain - lung, breast, colon, kidney)
• History of incontinence or gait disorder early in dementia ( NPH)
.
• Unusual or atypical presentation (e.g. progressive aphasia)

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

> Moderate AD - may delay progression


.
• NMDA receptor antagonist (e.g. memantine)
> Moderate -Severe AD - shown to improve global function and cognition
.
• Specific to Lewy Body Dementia - acetylcholinesterase inhibitors Levodopa ( for associated Parkinsonism)
• Specific to Normal Pressure Hydrocephalus - ventriculo - peritoneal or ventriculo- atrial CSF shunting
Behavioral or Psychotic Symptoms of Dementia (BPSD)
• Non - pharmacologic interventions
> Environmental: light/pet/activity therapy, " white noise”
> Behavioral modifications / behavioral techniques
• Pharmacotherapy (low dose trial - short term; not for LBD)
> Agitation, aggression, or psychotic behavior - quetiapine
> Sleep disturbances - trazodone

. Common Clinical Scenarios 184


DIABETES - ACUTE COMPLICATIONS
.
Current Editors: Elaine Chiu RD CDE Tammy McNab MD FRCPC

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
,

- current illness/infection, pregnancy. ETOH. drugs, or hospitalizations


E :S
Q “
) O
• Therapy - lifestyle, oral hypoglycemic agents (OHAs), insulin
• Glucose monitoring - tracking, insulin noncompliance, frequency, typical glucose/HbAlC measurements
<D • Hypoglycemia - frequency, threshold for detection, hypo protocol, major hypo events (req external
intervention)
RED FLAGS • DKA/HHS: GCS< 9, seizures, severe neurological features, hypotension, renal failure, and end organ damage
• Hypoglycemia: neuroglycopenic symptoms, acute coronary syndrome, arrhythmias

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

FHX • Automimmune conditions (e.g. . DM)


RISK FACTORS • Poor glycemic control, illness, medication changes, and omission of insulin

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

DERM: hyperpigmentation of the skin (r /o Addison's disease)


ABDO: abdominal tenderness ( more common in DKA)
NEURO: focal neurological symptoms

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)

185 Edmonton Manual of Comm .


Orders for DKA
• Admit to Internal Medicine or ICU with diagnosis of DKA
• Diet: NPO
• Activity: Limit to bed rest until resolution of DKA
.
• Vitals & Neuro Vitals: q30min for 1st hour Q1H for next 4 hours, then Q2-4H until resolution of DKA
• Ins/Outs: See below for IV fluids K \ and HC03- .
• Accurate ins /outs +/* foley catheter
• When BG 12 - 14 mM, insulin infusion may be 50% decreased as 5% dextrose in 0.45% NaCI added
• Drugs: Continuous IV infusion of regular insulin ( Humulin R or Novolin R ) as per protocol below

General Treatment Approach - DKA


Utilizing a chart to monitor patients progress while closing the metabolic acidosis gap can be useful
Time pH BG Na+ K+ Anion Gap HC03- Lactate Insulin Urea Creat Serum Serum
Ketones Osmolality

Time Intervals:
• Blood gluscose Q1H until DKA resolved
• Electrolytes Q1- 2H until DKA resolved

DKA in Adults - General Approach 2D


> Best monitored in ICU or step down unit with specialist IM care fl>
CL rD
> Requires close monitoring of lab values and vitals
£3
D O
fD —)

IV Fluids Insulin Potassium

• Determine hydration status • Rule out hypokalemia • Assess renal function


• Assess cardiac, kidney status to • < 3.3 mM • Check serum K+ Q1-2H for first
prevent fluid overload. • Start regular insulin IV 0.1U/kg/hr 5 hours with insulin initiation

• Hypovolemic shock • Mild/moderate • Check BG hourly


dehydration • If BG does not fall > 3 mM
K>5.5 mM
• .
in 1st hr check hydration level and K < 3.3 mM K between
3.3 - 5.5 mM
double insulin every hour until BG
• 0.9% NaCI • 0.9% NaCI 500 ccX 4hr drops 3 - 4 mM per hour
-
• @1 2 L/hr until stable then 250 c c X 2h r
• .
When BG 12 -14 mM reduce
IV insulin by 50%
• Euvolemic • Add 5% dextrose to fluids

• Hold insulin • Give 20 - 30 mM • Do not give K +


• Corrected Na > 145 mM • Corrected Na < 145 mM K +/L of IV fluid to
• Give 40mM
• Fall of plasma osmolality • Fall of plasma osmolality keep K level at 4- 5
> 3 mM/kg/hr
• K+/Lof IV fluid
< 3 mM/kg/ hr until K > 3.3mM mM ( less aggressive
if renal failure)

• 0.45%NaCI • 0.9%NaCI

• When BG 12 - 14mM. switch to 0.45% pH < 7.0, 44.6 mM of sodium


• If
NaCI + 5% dextrose @ 250 cc /hr
bicarbonate in 200 cc of sterile water
• -
DKA resolution check BGQ4H
and infuse at 200 cc/hr Q 2H until pH
• Initiate SC insulin, overlap IV insulin
with basal SC for 2 hr > 7.0

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

DIAGNOSTIC CRITERIA (CANADIAN DIABETES ASSOCIATION


Any 1of the following, with confirmation Prediabetes
on another day if asymptomatic ( single measurement)
1. Random plasma glucose >11.1 mmol / L 1. Impaired fasting glucose: 6.1- 6.9 mmol/L
2. Fasting plasma glucose (FPG) > 7.0 mmol /L .
2 Impaired glucose tolerance: 7.8 - 11.0 mmol /L with 75 g
3. 2 h plasma glucose >ll.lmmol/L after 75 g tolerance test (OGTT) 2 hr post - challenge
4. HbAlC > 6.5% 3. HbAlC: 6.1-6.4%

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

• Metabolic syndrome, vascular disease, HTN, dyslipidemia

ROS • General: wt loss, fatigue, dehydration, infections


• HEENT: blurred vision, fruity breath, cataracts
• CV: angina, orthostatic hypotension, claudication, foot ulcers, amputation
• Gl: polydipsia, polyphagia, N/V, abdominal pain, gastroparesis (bloating, early satiety)
• GU: polyuria, nocturia, urinary retention, erectile dysfunction
• MSK/ DERM: Dupuytren’s contracture, bone demineralization, frozen shoulder
• NEURO: sensory changes in hands / feet

RISK FACTORS • DM -T2: Age > 40 yrs . .


FHx member of high risk ethnic population, hx of IGT or IFG, vascular disease, hx of
gestational DM, hx of macrosomic infant, metabolic syndrome, PCOS, psychiatric conditions HIV OSA . .
PHYSICAL
General

. .
• 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

187 F .'monton Manual of Common Clinical Seer


i
• Auscultation - listen for S 3/ S4 , ventricular dysfunction (diabetic cardiomyopathy )

FEET - See Diabetic Foot Exam station

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

• Medications: self monitored blood glucose > 3 x/day if on insulin

• T1DM: Insulin
• T 2DM: Oral hypoglycemic agents + /- insulin for T 2DM
• Pneumococcal vaccine if > 65 y/o and annual influenza vaccine

Exam Findings Target Disease LR+ LR -


Foot exam Insensitivity to 10 g monofilament Predictor for foot ulceration 2.4 0.5
Ulcer size > 4 cm2 Predictor of osteomyelitis 7.3 0.4
Ulcer depth > 3 mm/bone exposure Predictor of osteomyelitis 3.9 0.3
Wound age > 2 mon, > 2 cm2, exposed /necrotic tissue Non- healing wound by 20 wks 3.5
Direct ophthalmoscope Macular edema/proliferative changes on dilated pupils Diabetic retinopathy 10.2 0.4
Palpation Absent post tibial AND dorsalis pedis pulses Peripheral Vascular Disease 14.9 0.3
.
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

Edmonton M, ual of Common Clinical Scenari< 188


DYSPNEA
Current Editors: TaeEun Ahn, Mohit Bhutani MD FRCPC FCCP

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

FHX • Malignancy . Ml, hypercoaguability, asthma, allergies,a-1antitrypsin deficiency. CF


SOCIAL • Smoking, anxiety disorders, IVDU ( talc lung) . EtOH, medication overdose occupation (silicosis, asbestosis)
,

ROS • HEENT: neck masses


• CV: CHF (pulmonary hypertension)
• RESP: cough, fever, chills
• .
GI/GU: bowel/bladder function, bleeds (i.e , dark stools, coffee ground emesis, tea colored urine)
• MSK/DERM: structural (scoliosis), rheumatologic (ankylosing spondylitis, SLE)
RISK FACTORS • Obesity, smoking, occupational exposure, aspiration, decreased mobilization

189 Edmonton Manual of Commor


PHYSICAL
General Findings (for Pulmonary Embolism) LR + LR -
• Isthe patient well vs. unwell, in distress, anxious Pulmonary crackles NS NS
• Assess for signs of respiratory distress: pallor, difficulty talking, increased
work of breathing, tripod positioning, accessory muscle use. cachexia Wheezes 0.4 NS
• ABCs and vital signs - assess airway, breathing ( rate, resp pattern. Sa02, Elevated JVP 1.7 NS
use of supplemental 02 or assisted ventilation), circulation ( BP, HR ) Left parasternal heave 2.4 NS
> BP: pulsus paradoxus (asthma. COPD. tamponade), hypotension
Unilateral calf pain/swelling (DVT) 2.2 0.8
( tension pneumothorax, Ml, sepsis)
High Wells score DVT ( ) 6.7
EXTREMITIES
• Inspection: skin for urticaria: fingers and hands for acrocyanosis, cold / Pleural friction rub NS NS
clammy skin, clubbing (ILD. cancer: not present in COPD alone), edema, Loud P 2 or S 3 or S4 NS NS
nicotine stains: calves for unilateral swelling, erythema, tenderness Tachypnea ( > 30 breaths/min) 2.0 0.9
• Palpation: cap refill and radial pulse
Sudden dyspnea 2.4
HEENT
Syncope 2
.
• Inspection: central cyanosis (under tongue) , angioedema pursed lip
breathing, supraclavicular fossa indrawing, accessory muscle use ( scalenes, Hemoptysis 1.9
SCM, trapezius, pectoralis, intercostal, abdominal muscles, diaphragm) Adapted from Evidence-Based Physical Diagnosis. 3rd ed„ Steven

.
• Palpation: tracheal deviation, tracheal tug lymphadenopathy laryngeal . McGee. MD and The Rational Clinical Examination :
Clinical Diagnosis David L. Simel. Drummond Rennie
Evidence - Based

height (distance from thyroid cartilage to sternal notch: < 4 cm suggestive of


COPD)
.
• Auscultation: forced expiratory time (if stable, ask patient to take large breath in and breathe out air as quickly as possible) - > 9 sec 2
0) =
suggestive of COPD
• Assess JVP assessment and hepatojugular reflex
-
Q fD

.
> 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)

INVESTIGATIONS Well’s Criteria Score


Laboratory Investigations Clinical signs of DVT 3
. .
• CBC- D ( infection, inflammation, anemia), lytes Cr urea, glucose, troponin CK . .
Not likely alternative Dx (H& P CXR ECG) . . 3
ABG ( A - a gradient, hypoxia, hypercarbia): consider D-dimer to rule out PE
Immobilized/surgery in the previous 4 weeks 1.5
Radiology/ lmaging
.
• CXR EKG Hx of PE/ DVT 1.5

.
• 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

nton Manual of Common Clinical Scenarios 190


.
Current Editors: John Stimson MD Selina Dobing MD FRCPC

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

FHX • Osteoporosis, cardiac conditions (HOCM . Brugada syndrome, early Ml)


SOCIAL • EtOH, street drugs
• Living situation, environmental hazards (home layout, lighting, stairs, footwear), possible abuse
• Nutrition: Vit B 12 deficiency (neuropathy), iron ( anemia), calcium and Vit D (osteoporosis)
ROS • HEENT: blurry vision/vision changes, head injury, cognitive issues (dementia, encephalopathy), issues with
balance/proprioception, vestibular dysfunction (vertigo, hyperthyroidism)
• CV: palpitations, chest pain, fatigue, lightheadedness, orthostatic hypotension
• RESP: SOB(OE), 02 requirements

.
• Gl: N/V, diarrhea, hematemesis, melena hematochezia
.
• GU: dysuria nocturia ( assess for UTI/incontinence)
• MSK/ DERM: muscle weakness, joint stiffness, gait disturbance

PHYSICAL
General

191 Edmonton Manual of C


• Vital Signs: dysrhythmias, postural BP and HR (orthostatic hypotension), fever ( precipitating cause)
• Assess patient ’s stability and cognitive status (delirium/dementia, substance use)
CV/RESP
• Inspect mucous membranes, JVP .
skin turgor (dehydration)
•Palpate peripheral pulse and carotid pulse (note rhythm, upstroke, contour ), auscultate for murmurs and carotid bruits
• Auscultate for adventitious sounds
NEURO
.
• CNs check visual acuity, hearing
• Extremities (strength, tone, sensation, reflexes)
• Finger -nose test, heel - to - shin test, ataxia (cerebellar )
• Romberg (proprioception, vision, and vestibular assessment )
• MMSE/MoCA (dementia/delirium)
• Dix Hallpike ( BPPV)
MSK /DERM
.
• Circumducting gait (CVA ) shuffling gait ( Parkinson's disease), wide gait (cerebellar / EtOH)
• Strength in hip and knee extension, joint exam ( arthritis), range of motion, rule out bony tenderness ( fracture)
• Examine feet and footwear for poor fitting, foreign bodies ( DM)

. .
• 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.

Finding Target Disease LR + LR -


Dementia/previous stroke Predictor for at least one fall 16 0.9
in the ensuing year
Unable to rise from a chair without using arms 4.3 0.8
Failure to tandem walk 1.7 0.7
One fall in the past month 3.8 0.8
Cognitive impairment 4.2 0.9
Mobility problem ( self -perceived) 1.8 0.7
Dementia Predictor for frequent falls 13 0.9
in the ensuing year
Fear of falling 2.6 0.7
History of >1falls in the past year 2.3 0.6
Slow gait/absence of vibratory sensation 2 0.7
. .
Adapted from Evidence - Based Physical Diagnosis 3rd ed. Steven McGee, MD and The Rational Clinical
.
Examination: Evidence Based Clinical Diagnosis Diagnosis David L. Simel Drummond Rennie

Edmonton Manual of Common Clinical Scenarios 192


GAIT DISTURBANCE
.
Current Editors: Albert Vu MD Jennifer McCombe MD MPH FRCPC

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

RED FLAGS • Bowel or bladder incontinence/saddle anesthesia (cauda equina syndrome)


• Urge incontinence (normal pressure hydrocephalus or vascular )
• Acute onset lateralizing weakness, dysarthria, confusion/headache (stroke)

PMHX • Strokes (risk .


factors), MS cancer (CNS metastasis, including spinal), DM, dementia, Parkinson's disease,
Huntington' s disease
PSHX • Back surgery
MEDS • Antipsychotics (can cause Parkinsonism), change in medications (dosing, type)
SOCIAL • Living situation/safety, EtOH use

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:

193 Edmonton Manual o* Common Clinical S:


> Romberg (proprioception, vision, vestibular assessment )
> Tandem walking (neuropathy or midline cerebellar )
> .
Trendelenburg test: wt - bearing on one leg pelvis tilts down on contralateral side) - weakness of gluteus medius
> Gait ( also observe ability to get up from a chair ): station, initiation, base width, stride length, symmetry and turning
MSK
• Inspection: joint swelling, erythema, muscle atrophy, deformities, bruising and skin changes. Observe posture, spinal alignment , pelvis
( symmetry of iliac spines and gluteal folds), knees (genu varus /valgus), feet ( foreign bodies, plantar warts, pes cavus /planus)
• Range of Motion: hip internal/external rotation, knee flexion/extension, foot supination/pronation/dorsiflexion/plantar flexion
• Palpation: joint effusions, warmth, localized tenderness, crepitus
• Special Tests: tailor based on patient complaints

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

FHX • Hearing loss especially < 50 y/o


MEDS • Hx of use of aminoglycosides & other ototoxic drugs
• Check for recent change in medications
SOCIAL • Work -related noise exposure, frequent excessive noise exposure
ROS • HEENT: head trauma, headaches, dry eyes, dry mouth, oral ulcers, photosensitive rash
• MSK/ DERM: myalgia, arthralgia
RISK FACTORS • Familial, excessive noise ( 85 dB for >8 h/d) 2, drugs, congenital, complications at birth
• Regular screening (pure-tone audiometry, speech discrimination, tympanometry) for excessive noise
. . .
exposure FHx < 50 y/o >65 y/o smoking DM .
PHYSICAL
General
. . .
• VS: BP HR RR Temp Sa02 .
• Inspection - Rashes, scars, facial asymmetry, nystagmus, unilateral weakness, craniofacial and pigmentary anomalies
Cranial nerve exam
Nasopharyngeal exam: inspect for masses
Ear exam
• Precense of discharge, mass, erythematous/bulging TM, TM perforation, visibility of ossicles
• Otoscopy: distorted anatomy, membrane discoloration, foreign body, mobility of TM
• Special Tests (hearing tests)
> Whisper test: cover one ear and whisper into the other
.
> Rinne test: 512 Hz tuning fork on mastoid process of affected ear ( BC) patient hears no sound; move fork to pinna ( AC) , patient
.
should normally be able to hear sound. If not it ’s conductive hearing loss.
> Weber test: 512 Hz tuning fork on forehead in midline ( if louder in affected ear it ’s conductive hearing loss)
• Formal audiologic assessment, speech audiometry, impedance audiometry can be considered

195 Edmonton Manual of Common Clmii


Hearing Test Interpretation
Type RinneTest Weber Test Pure Tone Audiometry
Normal AC > BC, bilateral -ve = bilateral Normal
BC > AC in affected BC normal; AC outside normal range;
Conductive Sounds louder on the bad side
ear AC- BC threshold gap > 10 dB ( air -bone gap)
AC > BC in affected AC + BC below normal;
Sensorineural Sounds softer on the bad side
ear AC- BC threshold gap < 10 dB (no air - bone gap)
AC = air conduction, BC = bone conduction

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

• Trauma and hearing loss: hospitalization with full trauma workup

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

Finding Target Disease LR+ LR -


Abnormal whisper voice test Hearing loss 6.0 0.03
Unable to hear strong finger rub 355.4 0.4
Unable to hear faint finger rub 3.9 0.02
Rinne test Conductive hearing loss 16.8 0.2
Weber test, lateralizing to bad ear NS 0.5
Weber test, lateralizing to good ear Neurosensory loss 2.7 NS
. .
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

Edmonton Manual of Common Clinical Scenarios 196


HEMATOLOGIC MALIGNANCIES
.
Current Editors: Daniel Friedman MD Kathleen Wong MD FRCPC

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)

MSK / DERM: rashes, petechiae, purpura, bruising, jaundice 2=


INVESTIGATIONS -
Q n>

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)

Potential for bone marrow transplant


• Chemotherapy destroys the bone marrow: bone marrow transplant can replace it
• Requires a donor -recipient match and the recipient then must be immunosuppressed
• Healthy donor stem cells then repopulate the patient ' s bone marrow, while the donor T- cells aid in fighting the leukemia
• Donor T- cells are also responsible for graft versus host disease in the recipient

Edmonton Manual of Common Clinical Scenarios 198


HEMIPLEGIA / HEMISENSORY LOSS Current Editors: Jenny Shi, Jennifer McCombe MD MPH FRCPC

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
_<
OJ C
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

RED FLAGS • Fever, associated thunderclap headache ( SAH), acute onset


PMHX . .
• Strokes/TIA,CVD DM,dyslipidemia,HTN,AF hypercoagulablestates .bleedingtendency.seizure.migraines,aneurysm ,
. .
tumors, valvular disease MS immunocompromised, migraine
PSHX • Brain surgery, cardiac surgery, endovascular procedures
FHX • Cerebrovascular disease, aneurysms ( two first degree relatives is significant), HTN, DM, coagulopathies, AVMs

MEDS • Anticoagulants, antiplatelets, anti-hypertensives, OCP


SOCIAL • Smoking, EtOH, recreational drugs (amphetamines, cocaine, heroin)
ROS • HEENT: fever, meningismus, headache, seizure, ageusia (for Bell’s palsy)
• CV: AF, palpitations, pericarditis
• RESP: SOB
• Gl: N/V
• MSK/ DERM: petechiae, purpura, pain

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

PHYSICAL Grade Power Reflexes


General
0 No movement Nil
. .
• Assess ABCs, VS ( BP HR, RR, Temp Sa02 ), GCS
1 Fasciculations Present with
> KeepSa02 > 92%
reinforcement
> Monitor BP rigorously. BP is only initially treated if the systolic BP > 220
maneuvers
mmHg, unless considering tPA. BP > 220 has a high LR + 4.0 for hemorrhagic
stroke 2 Gravity removed Normal
> If tPA administered or if a hemorrhagic stroke, then treat 3 Against gravity High normal
if systolic BP > 180 mmHg
4 Against Clonus ( > 3
> If febrile consider an infectious diagnosis
resistance beats)
General Inspection
5 Full strength
• Airway - Intubate any patient whose GCS < 8 and cannot protect airway
• Breathing - Assess saturation, look in mouth for obstruction or vomiting
• Circulation - Check blood pressure

> Hypertension is expected in acute ischemic or hemorrhagic stroke


> Hypotension may point to decreased cerebral perfusion pressure as etiology
• Appearance - Remark on patient ' s color, diaphoresis, distress level, LOC, presence of posturing, rashes ( meningococceal)
• Cushing reflex ( indicates high ICP ): sympathetic nervous system response that leads to Cushing’s Triad ( hypertension ( widened
pulse pressure), irregular respirations, bradycardia)

199 Edmonton Manual of Common Clinical Set


cv UMN vs LMN .
• Blood pressure taken from both arms (mismatch may indicate aortic dissection)
• Inspection: capillary refill on hands for perfusion Findings UMN LMN
• Palpation: peripheral pulses for rate, rhythm, character ( atrial fibrillation) Power UEflex > ext Flexors and
• Auscultation: carotids bilaterally for bruit (carotid stenosis) and precordium as extensors
LEext > flex equallyweak
per standard cardiac exam (murmurs - endocarditis)
NEURO Tone Spastic/ Flaccid
hypertonic
• GCS: check patient ’s responsiveness /orientation x 4 ( who / where / when /event )
• Language: dysarthria - motor inability to form words DTR Hypereflexic / Hyporeflexic
. .
> Broca'saphasia - non - fluent poorsentenceconstruction canfollowinstruction
clonus
( impaired language production) Plantars Upgoing Downgoing
> Wernicke's aphasia - very fluent, non - sensical, cannot follow instruction ±
Fasciculations Absent
( impaired language comprehension)
• HEENT: facial symmetry - nasolabial folds, ability to raise eyebrows, smile, bare Atrophy Late Early and
teeth pronounced
Cranial nerve exam
Finding (for Unilateral Cerebral LR + LR -
> Signs of trauma
Hemispheric Disease)
> Assess nuchal rigidity: Jolt test is the most sensitive for meningeal
irritation ( worsening headache with rapid turning of head in side- Hemianopia 4.3 0.8
to - side motion). Neck stiffness has a high LR + 5.4 for hemorrhagic Pronator drift 9.6 0.3
stroke.
Forearm rolling test 15.6 0.6
• Limbs: Assess upper extremity and lower extremity strength in flexion
and extension at each joint ( see table for UMN vs. LMN) Index finger rolling test 6.0 0.7 CD
CL fl>
• Assess pronator drift ( ask patient to hold UE extended in front of them,
palms upwards, with eyes closed - watch for drift )
Hemisensory loss NS 0.7 .3
D O)
• Arm rolling test ( patient rapidly rotates both forearms around each
Hyperreflexia 5.3 NS CD
other for 5 s in each direction), finger rolling test ( rotate index finger Babinski 8.5 NS
around each other ) .
Adapted from Evidence-Based Physical Diagnosis 3rd ed. .
• Assess chronicity of deficiency: decreased muscle bulk, fasciculation,
hyperreflexia indicate long standing deficits
.
Steven McGee MD and The Rational Clinical
Examination: Evidence- Based Clinical Diagnosis
• Assess sensory loss: first assess sensation to gross touch, and if intact, .
David L. Simel Drummond Rennie
assess cortical sensations (extinction, two point discrimination (use an unfolded paper clip) , light touch ( with a piece of
cotton) ( see table below )
• Note: The three most specific examination findings for acute stroke are facial paresis, arm drift, and language abnormalities (if all
three present, LR + 14; if any two present LR + 4.2 )
TREATMENT
• ABCs and glucose
> Hyperglycemia is common in acute stroke and evidence is unclear whether treatment of glucose > 7.8 mM improves outcomes;
hypoglycemia can mimic stroke symptoms
• Fever: may indicate an underlying etiology of hemiparesis or a damaging side effect of stroke
> Consider acetaminophen antipyresis in T > 37.8 C (evidence inconclusive)
• No evidence for induced hypothermia in acute stroke
• Consider meningitis if Jolt test positive & patient does not have RF for acute stroke
• Hypertension: expected in acute stroke
> Allow sBP up to 220 mmHg and a dBP up to 120 mmHg

.
> 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%)

Edmonton Manual of Common Clinical Sceiarios 200


HEMOPTYSIS
.
Current Editors: Ashley Tse Mohit Bhutani MD FRCPC FCCP

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

MEDS • Anticoagulants and coagulants ( PE)

SOCIAL • EtOH, smoking, inhalation of chemicals, crack cocaine, travel hx, occupation, place of birth, incarcerations

201 Edmonton Manual of Common Clinical Scenar ms


PHYSICAL
General
• Assess ABC' s
.
• Signs of respiratory distress: cyanosis, diaphoresis, inability to speak in full sentences, accessory muscle use intercostal indrawing,
diaphragm motion, nasal flaring
• Vital Signs: hypotension with massive hemoptysis

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

nical Scenario 202


LOWER RESPIRATORY TRACT INFECTION
.
Current Editors: Stephanie Urn Mohit Bhutani MD FRCPC FCCP

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
OJ C
<D
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

MEDS • Chronic corticosteroid use . recent abx hx (3 mos). immunosuppressants


IMMUNIZATIONS • Annual influenza, pneumococcal vaccine and booster, splenectomy vaccines (pneumococcal, meningococcal,
haemophilus)
SOCIAL • Smoking . EtOH, IVDU, home environment place of residence (e.g., nursing home),occupation
,

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

RESP Wheezes 0.8 NS


• Inspection: chest wall deformity, scars Tachycardia 1.7 0.8
• Palpation: decreased chest expansion, tactile fremitus (increased in consolidation,
Tachypnea ( >28 2.7 0.9
decreased in pleural effusion) breaths/min)
• Percussion: dullness to percussion over consolidation and pleural effusion
Febrile ( temp > 37.8 C) 2.2 0.7
• Auscultation: decreased breath sounds, crackles, wheeze, stridor (upper airway
pathology) Any vital signs abnormal 2.2 0.3
> Bronchial breath sounds, bronchophony, whispering pectoriloquy, egophony Oxygen saturation < 95% 3.1 0.7
present in consolidation
Cachexia 4.0 NS
5 findings on CURB 65 11.2
2 findings on CURB 65 NS
Adapted from Evidence - Based Physical Diagnosis .
. .
3rd cd. Steven McGee MD and The Rational Clinical
.
Examination: Evidence- Based Clinical Diagnosis David
.
L. Sirnel Drummond Rennie

203 dmonton Manual of Common (


CURB- 65 Pneumonia Severity Score
• Confusion - 1point • 0 -1points: low severity ( < 3% risk of death), out - patient treatment
• Urea > 7 mmol /L - 1point • 2 points: moderate severity ( 9% risk of death), consider hospitalization
• RR > 30 -1point • 3 - 5 points:highseverity ( 15 - 40%riskofdeath) ,hospitalizationindicated ( if 4- 5
• sBP < 90 mmHg or dBP < 60 mmHg - 1point points, assess for ICU admission)
• Age > 65 y -1point

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

Edmonton Manual of Common Clinical Scenarios 204


MONOARTICULAR JOINT PAIN
.
Current Editors: Larissa Petriw Selina Dobing MD FRCPC

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)

High Mortality/Morbidity - septic arthritis, osteomyelitis/osteonecrosis

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

FHX • Gout, seroneg . spondyloarthropathies, hemophilia


SOCIAL • EtOH, IVDU, travel/camping in tick -infested areas
• Sexual Hx & contacts
ROS • General: constitutional symptoms
• HEENT: eye pain/photosensitivity, red eye, oral ulcers
• RESP: tachypnea, SOB/OE
• Gl: abdominal pain, change in bowel habits, blood/mucous in stool
• GU: dysuria, discharge, dyspareunia
• DERM: new rash, lumps nodules

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)

205 Edmonton Manual of Comm'


HEENT: red eye/iritis ( seronegative spond.), oral ulcers - painless (reactive) vs.painful ( IBD- associated )
MSK Inspection: SEADD
PULM & CVS: aortic insufficiency (uncommon sequelae of longstanding seronegative
• Swelling
spondyloarthropathies)
• Erythema/ecchymosis
MSK/ joint: - Key features suggestive of synovitis include - soft tissue swelling, warm joints, and joint • Atrophy/asymmetry of
effusion muscle
• Inspection: SEADD . overlying infection • Deformity
•Palpation: heat, effusion, tenderness, warmth, effusion, synovial thickening, subcutaneous • Distribution (MCP/ PIP vs .
crepitations DIP)
• Special tests: wipe bulge test ( small effusion), ballotment /patellar tap

.
• 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

Septic / Bacterial Opaque Varies > 50.000 > 75%


.
Gram: G + cocci G- rod; Culture
sens: 50% (less if gonorrhea)
Bloody/
Hemorrhagic (e.g., trauma, hemophilia) Varies Varies Varies
Sanguinous

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.

dmonton Manual of Common Clinical Scenarios 206


NUMBNESS AND PARESTHESIAS
.
Current Editors: Parnian Riaz MD Jennifer McCombe MD MPH FRCPC

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

Localizing the Lesion

Lesion Location Motor Sensory UMN/


LMN
Cerebral Cortex Contralateral weakness Contralateral sensory loss in face limb. & trunk . UMN
Ipsilateral CN weakness ( facial droop, ptosis, dysarthria .
Brainstem . .
dysphagia) contralateralbodyweakness:cerebellarataxia Sensorydeficitintheipsilateralfaceandcontralateralbody
Horner 's syndrome
UMN

Thalamus Contralateral loss of all sensory modalities UMN


SpinalCord(complete Bilateral weakness -
paraplegia/quadriplegia urinary . Sensory deficit below specific spinal level
cord lesion) incontinence/retention (LMN findings at level of lesion, Dissociated sensory loss UMNUMN
UMN findings below level of lesion)
Spinal Cord (hemi* Ipsilateral loss of proprioception/vibration, contralateral UMN/
cord lesion) Ipsilateral weakness
loss of pain/ temp LMN

_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

HPI • OPQRST, pattern of sensory loss


.
• +ve sensory sx: paresthesia dysesthesia, or hyperesthesia
• -ve sensory sx: hypoesthesia, anesthesia, sensory ataxia
• Other neurological symptoms: cranial nerve sx (dysarthria, dysphagia, diploplia), cerebellar sx ( ataxia, gait
imbalance), motor sx ( weakness), language, cognition
• Hx of trauma, infection, recent medication change, systemic symptoms
RED FLAGS • Urinary retention, reduced rectal tone/fecal incontinence, saddle anaesthesia - Cauda Equina Syndrome
• Acute, rapid, ascending weakness/numbness -
Guillian Barre Syndrome
• Constitutional symptoms, fever, recent infection
• Amaurosis fugax ( transient, painless vision loss)
• Sudden onset, severe headache (’thunderclap headache’) ± focal neuro sx (CN III, VI palsy) SAH -
-
• Lhermitte’s phenomenon cervical spinal cord

PMHX • CAD, CVD, PVD, hyperlipidemia, T2DM, HTN, autoimmune disease, MS


• Cancer and its treatment
MEDS • Recent vaccinations ( may provoke auto -immune demyelination), new meds, statins, diuretics

207 mmc
FAMHX • As with PMHx, especially if
polyneuropathies
.
early onset ( < 60 y/o) autoimmune disease, thyroid disease, hereditary

SOCIAL • Smoking . EtOH, IVDU


ROS • HEENT: headache, vision problems, cognitive sx, optic neuritis ( vision loss, eye pain, afferent pupillary defect)

• CV/RESP: chest pain, SOB . rheumatic heart disease/valve replacement, palpitations/AFib


• GI/GU: bowel dysfunction, bladder dysfunction
• MSK /DERM: neglect, back pain

PHYSICAL Important Dermatomes


General Root Anatomical Landmark
.
• General appearance, vital signs GCS, MMSE
C2 Occiput
Cranial nerve exam
C3 Neck
Motor exam (UMN vs LMN)
C4 Supraclavicular
• Involuntary movements: tremor, myoclonus, chorea, athetosis, ballismus, tics, dystonia
.
• Inspection: muscle bulk ( atrophy - early and pronounced in LMN late from disuse in UMN), C5 Lateral arm
fasciculations ( LMN) C6 Thumb
.
• Muscle tone: hypertonic /spastic (UMN) vs hypotonic /flaccid ( LMN) rigidity, paratonia
C7 Index/Long finger
• Muscle strength - assess for asymmetry
C8 Little finger
> Upper limb flexors stronger than extensors and lower limb extensors stronger than flexors
(UMN) vs flexors and extensors equally weak ( LMN) T4 Nipples
• Reflexes - assess for asymmetry: increased (UMN) vs decreased ( LMN)
2 =r
T5 Inframammary fold n> 3
.
• Pronator drift (UMN lesion) Babinski’s (upgoing in UMN, downgoing in LMN)
T6/7 Xiphoid process
QL ( D
.
• Cerebellar: dysmetria finger tapping, rapid alternating movements, finger - to -nose, heel -to- shin
testing, trunchal/appendicular ataxia
• Gait: perform heel /toe/tandem walk: assess for asymmetry of movement, festination
T10
T 12
Umbilicus
Pubic bone
3 ID
0> —
Sensory exam: have patient map out areas of sensory alteration LI Inguinal ligament
• Primary sensory modalities: spinothalamic tract (pain, temperature) , dorsal column medial L2 Lateral thigh
lemniscus tract (proprioception, gross touch, vibration)
L3 Medial knee
• Cortical sensory modalities (stereognosis, graphesthesia, localization, point discrimination, and
extinction) L4 Above medial
malleolus
.
Special Tests: e.g. Phalen's test and Tinel’s test for carpal tunnel syndrome
INVESTIGATIONS L5 Dorsum of medial foot
Laboratory Investigations ( targeting narrowed DDx after lesion localization) SI Heels

. . .
.
• 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

Neuropathy Description Treatment


Carpal Tunnel Wrist splinting, glucocorticoid injections, oral glucocorticoids,
Compressionofmediann.at wrist surgical decompression
Syndrome : NSAIDs NOT useful
Compression of ulnar Avoid leaning on elbows and prolonged elbow flexion, splinting,
UlnarNeuropathy n. padding, surgical decompression/transposition
at wrist or elbow
Trigeminal Trigeminal n. root dysfunction Medical therapy (carbamazepine. gabapentin, lamotrigine, etc.),
Neuralgia microvascular decompression, rhizotomy, gamma knife radiosurgery
Diabetic Hyperglycemic axonal Glycemic control: pain control: foot care: medications
Neuropathy degeneration and demyelination (gabapentin, pregabalin, amitryptyline)

Sciatica
Sciatic n. compression: disc .
Activity modification NSAIDs, PT, pain control, open
herniation or spinal stenosis discectomy/microdiscectomy, muscle relaxants

Edmonton Manual of Common Clinical Scenarios 208


OBSTRUCTIVE LUNG DISEASE
Current Editors: Mihai Sfranciog MD. Mohit Bhutani MD FRCPC FCCP

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

SHx home, smoking history and second hand


• Occupation, pets at .
• Smoker ( > 40 pack years LR + 12 * ) smoking cessation,
.
smoke, marijuana use age of house occupational exposures, indoor /outdoor pollution
Meds • ISC, ISC / LABA, LTRA' s, rescue meds .
(e.g. short - acting (32 - • Long - acting bronchodilators. ICS/LABA, SABA
agonists)
Allergies • Dust mites, molds, furry animals, cockroaches, pollen ASA . • Medication allergies and environmental triggers
hypersensitivity, environmental triggers
FHx • Atopy (allergies, asthma, eczema), respiratory diseases • Family Hx of COPD and second hand smoke
ROS triad ( asthma, nasal polyps, and ASA sensitivity),
• Samter 's • HEENT: rhinitis, sinusitis, oral thrush (chronic inhaled
eczema, rashes corticosteroid use)
• HEENT: rhinitis, sinusitis, oral thrush (chronic inhaled
corticosteroid use)
.
Asthma red flags: daytime sx > 4 days / wk night - time sx >1night / wk, inability to perform normal physical activity, frquent/severe
. .
exacerbations, absence from work/school > 4 doses SABA needed/ wk FEV1< 90% of personal best, > 10- 15% PEF diurnal variation,
> 2 - 3% sputum eosinophils
COPD red flags: worsening symptoms /requirements (home 02 steroid usage . . > 4 episodes/yr, high MRC score)
i -jirc.-ifrE
General * indicates likelihood ratios for COPD: * indicates likelihood
ratios for asthma

209 Edmonton Manual of Common Clinical


• .
ABCs LOC, mental status
• Vital Signs - pulsus paradoxus, BMI
• Signs of respiratory distress: fragmented speech, tri - podding, pursed lip breathing (LR + 2.7 * ), nasal flaring, tracheal tug, intercostal
indrawing, reduced breath sounds (LR + 3.2 * )
EXTREMITIES
• Peripheral /central cyanosis, digital clubbing, smoker 's fingers, eczema, signs of cor pulmonale (elevated JVP, chest pain, wheezing/
coughing with crackles and peripheral pitting edema * seen in COPD)
RESP
• Inspection: AP/ lateral diameter > 0.9 (barrel chest, LR + 2.0 * ), chest wall deformities, accessory muscle involvement ( LR + 3.3 * )
• Palpation: chest expansion, Hoover ’s sign ( LR + 4.2 * ), maximum laryngeal height < 4cm (LR +3.6 * ), tracheal deviation, tactile fremitus
( AECOPD from pneumonia) , subxiphoid cardiac impulse ( LR + 7.4 * )
• Percussion: hyperresonance (LR + 7.3 * ) or loss of cardiac dullness due to acute asthma /COPD ( LR + 11.8 * )

> 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

> 02 supplementation if hypoxic


> BiPAP for increased work of breathing
> Intubate: respiratory failure, fatigue, unable to maintain adequate oxygenation
. .
• lnhaledmedications (e.g., salbutamol,ipratropium corticosteroids),systemiccorticosteroids (e.g. prednisone),abxifinfectiousbacterial
triggers
Treatment Options
• Social: environmental control of allergens and triggers, smoking cessation ( patient AND household ), medication compliance
• Medical: Step - up or step - down medical therapy as needed to achieve adequate symptom control in stable patients

> 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

Edmonton Manual of Common Clinical Scenarios 210


PALPITATIONS & ARRHYTHMIAS
.
Current Editors: Alanna Chomyn Selina Dobing MD FRCPC

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

’ Life threatening conditions

Non- Cardiac Etiologies of Palpitations


Endocrine Thyrotoxicosis, pheochromocytoma, hypoglycemia
_c
nj
CD Psychiatric Anxiety, panic attacks
C u Medication Intoxication (cocaine, amphetamines), withdrawal (EtOH, opiates), levothyroxine. beta agonists,
<D “U stimulants (caffeine, energy drinks. OTC pseudoephedrine)
c CD Other .
Hypovolemia, fever PE, idiopathic

. .
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

211 Edmonton Manual of Commoi


ROS • RESP: asthma, lung disease
f
• GU: pregnancy ( cardiac output)

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

> Palpation - palpate apex for size, length of beat - cardiomyopathy/cardiomegaly


. .
> Visible impulses - apical (LV) parasternal ( RV) upper sternal borders ( aortic and pulmonary artery)
> Auscultation - valve abns, rhythm, extra sounds (cardiomyopathy/cardiomegaly), ask to valsalva while auscultating
> Mid -systolic click - mitral valve prolapse classically presents with anxiety and palpitations
• Abdomen - palpate for masses (pheochromocytomas)

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

Condition Medical Therapy Other Interventions


SVT/Narrow Vagal maneuvers first (carotid sinus massage, valsalva)
complex if not successful - Adenosine IV push (avoid in suspected WPW)
Tachycardia if still not successful IV beta - blocker or non-
dihydropyridine CCB (Verapamil)
VT/Wide Complex Synchronized electrical cardioversion
Tachycardia If not successful - amiodarone, procainamide IV, or lidocaine
AFib < 48 hrs: pharmacologic cardioversion (amiodarone or sotalol) < 48 hrs: Electrical cardioversion
Recurrent: rate vs. rhythm control > 48 hrs: Electrical cardioversion
• Rate: beta -blocker or non-dihydropyridine CCB only after 3 weeks anticoagulation
• Rhythm: amiodarone if structural heart disease, Propafenone or rule out atrial clot with TEE
or flecainide if no structural heart disease
Apply CHADS2 decision for anticoagulation
Paroxysmal Afib Same long- term stroke risk as continuous Afib; Catheter ablation
apply CHADS2 decision for anticoagulation

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

Treatment options in stable patients


• Consider Cardiology consultation, electrophysiologic studies or ablation, pacemaker or AICD if indicated

Edmonton Manual of Common Clinical Scenarios 212


.
Current Editors: Parnian Riaz MD Vijay Daniels MD FRCPC

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

• Quality: sharp +/- colic


• Radiation: often to the back
• Severity
• Associated symptoms: nausea, vomiting, anorexia, change in bowel habits, SOB presyncope /syncope .
PMHX .
• Previous episodes of pancreatitis, gallstones, recent procedures (ERCP) recent trauma, hypertriglyceridemia,
hypercalcemia, pancreatic divisum SLE .
MEDS • Ethanol, methanol, azathioprine, valproic .
acid, pentamidine, steroids 5 - ASA, metronidazole, salicylates
FHX • Gl malignancy
SOCIAL • Alcohol use, smoking
• Recent travel
ROS • HEENT: scleral icterus/ jaundice
• MSK/ DERM: bruising

213 Edmonton Manual of Common C In


PHYSICAL
General
• Assess airway, breathing, circulation
.
• Vital signs ( BP.HR.RR Temp. Sa02) - tachycardia,tachypnea,hypoxia (acuterespiratorydistresssyndromeinseverecases) hypotension .
(shock )
• General appearance: diaphoretic, signs of shock

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

Edmonton Manual of Common Clinical Scenarios 214


i :< i:L-M: i PI
.
Current Editors: Parnian Riaz MD Jennifer McCombe MD MPH FRCPC

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

Parkinsonism Resting Tremor Essential Tremor


• Affects UE > jaw > LE (rarely involves head or neck ) • Affects UE >head > LE > tongue
• Low frequency ( 4 - 6 Hz), pill rolling
• Worse with rest and while distracted
.
• High frequency 6-12 Hz fine tremor
• Worse with sustained poture (outstretched arms), concentration
• Associated with above Parkinsonism sx • Often have positive FHx

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

Multple System Atrophy .


• > 30 y not responsive to levodopa
• Early speech and postural instability
• Significant autonomic dysfunction (orthostatic hypotension, diaphoresis, leg swelling, urinary incontinence)
• Symmetric parkinsonism, cerebellar signs (ataxia, nystagmus)

Vascular Parkinsonism • Akinesia + rigidity, lower body Parkinsonism (confined to legs), no tremor
• .
UMN signs (hyperreflexia spasticity), pseudobulbar palsy, dementia
• Poor response to levodopa

Lewy Body Dementia • Cognitive dysfunction within 1 year of Parkinsonism development


• Prominent visual hallucinations, diurnal variation, fluctuating alertness
• Neuroleptic sensitivity
.
Other causes: Wilson's disease (must rule out in patients < 40y with Parkinsonism) Huntington' s disease, prion disease, late Alzheimer's disease,
. . .
toxins (CO MPTP. manganese, cyanide), infection (HIV neurosyphillis post -encephalitis)

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

FHX • Tremor, dementia . Parkinson’s. Huntington’s, Wilson’s


215 Edmonton Manual of Common Clinical Scenarn
MEDS • Recent med changes, anti-dopaminergic exposure (esp. neuroleptics)
SOCIAL • Smoking, EtOH, living situation, work, toxin exposure (Mn, CS2, MPTP, Hg, Pb, As), recent travel
ROS i
• CNS: memory, visual disturbances, loss of smell ( anosmia), small writing (micrographia)
• HEENT: diaphoresis, soft voice (microphonia)
• CV: pre -syncope/syncope, falls (often first sx in PSP)
• Gl: dysphagia, dysarthria ( MSA ) , constipation, sialorrhea
• GU: sexual difficulties, urinary incontinence /urgency
• PSYCH: personality changes, disordered sleep, restless leg syndrome, daytime sleepiness, vivid nightmares /
dreams, hallucinations ( LBD), depression
PHYSICAL EXAMINATION
General Examination - use the physical exam assess idiopathic PD vs. Parkinson Plus Syndromes
• VS: ( BP, HR, RR, Temp, Sa02), including orthostatic vitals for orthostatic hypotension
• General appearance: general poverty of movement (bradykinesia) , depressed affect
HEENT: expressionless, " masked" facies (hypomimia), T blinking rate, soft and quiet voice (hypophonia) (LR + 3.2 * ) , drooling ( sialorrhea
- caused by t swallowing frequency), head tremor ( Titubation)
ABDO: enlarged liver (Wilson's disease), gastric dysmotility, constipation
.
DERM: facial seborrhea (dry flaking skin), excessive sweating
NEURO
.
• Mental status LOC, orientation, language assessment ( aphasia in CBD), consider cognitive screening test ( MMSE or MoCA) for
LBD
• Cranial Nerves - EOM: impairment of eye convergence and vertical gaze ( PSP) , delayed initiation of gaze movements, slowing of
conjugate movements, dysarthria ( MSA) CD
Motor Examination O fD -
• Tremor (LR + 1.5, LR - 0.5 *) : Note frequency, amplitude, body parts involved, resting or action tremor G. 3
ZJ 0)
> PD: pill -rolling, slow frequency ( 4 - 6 Hz ) resting tremor n>
.
• Tone (rigidity LR + 2.8 LR - 0.4 *): test elbow flexion/extension, rapid forearm supination, slow wrist circumduction
> Velocity -independent (rigidity) or velocity - dependent (spasticity)
> Is the rigidity constant and smooth (lead - pipe) or ratchet -like (cog- wheel)?
> PD: cog- wheeling rigidity: best seen with slow wrist circumduction, accentuated by complex movements of opposite limb
. .
(e.g. trace circles in air touch each finger to thumb in sequence), rigidity with bradykinesia
• Power: should not be altered in an extrapyramidal (BG) lesion: if affected may indicate MSA
Reflexes
• Deep tendon reflexes, plantar responses should not be altered in an extrapyramidal ( BG) lesion; if increased may indicate MSA
• PD: inability to suppress blinking on tapping glabella (+ve glabellar tap/ Myerson sign LR + 4.5, LR - 0.13 * )
Coordination/Cerebellar Function
• Coordination: presence of dysmetria on finger - to -nose or heel - shin testing, suspect MSA
• Diminished rate and amplitude of repetitive movements such as tapping fingers in sequence, pinching motions of thumb and index
finger, twiddling hands, tapping heel on floor (bradykinesia)
> Contrast to failure to perform rapid alternating movements, a sign of a cerebellar lesion
Sensory Examination: unilateral cortical sensory loss may indicate CBD
Posture/Stance/Gait Assessment
• Observe patient rise from a chair, walk across room, turn around, and return to chair
• Gait in PD: Flexed /stooped posture, narrow stance width
> Slow small shuffling steps, arm swing, "en bloc ” turn, festination (involuntary acceleration of gait, may lead to a fall)
• Romberg test: not expected to be + ve (as there is no sensory deficit)
• Pull test: ensure patient safety-do not drop your patient
> Normal is to regain balance with perhaps one backward step. Multiple backward steps ( retropulsion) or an uncontrolled fall
indicates postural instability .
INVESTIGATIONS
Blood Work: generally not indicated (PD is a clinical diagnosis), but may rule out other causes of tremor /abnormal movements
• TSH ( hyperthyroidism) , serum ceruloplasmin/ 24 hr urine Cu2* ( Wilson's Disease)
Radiology/ lmaging
• CT/MRI brain: not indicated for PD, order if suspected infarct/structural lesion
.
• [ 18F ] - fluorodopa PET scan: research use only T uptake of F -dopa at dopaminergic terminals in caudate and putamen correlates
with severity of neurodegeneration in substantia nigra
.
Psychiatric - high rate of depression in PD, consider screening (e.g. Geriatric Depression Scale)

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

Edmonton Manual of Common Clinical Scenarios 216


PERIPHERAL VASCULAR DISEASE
.
Current Editors: Charles Lim MD Lucille Lalonde MD FRCPC

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)

• Rest pain is a sign of critical limb ischemia


• Pain at night with legs horizontal, relieved in dependent position suggests arterial cause
• Cold extremities and difficult to warm

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

RISK FACTORS • Advanced age, smoking, DM, dyslipidemia, HTN, hyperhomocysteinemia

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

Type of Ulcer Pain Appearance Location


Arterial Painful Pale base with dry eschar, "punched out ” Toes, sites of trauma/pressure
Venous Painless Wide base, bronze discoloration of skin Malleolar, sites of venous stasis
Neurogenic Painless Deep, repeated trauma Plantar surface of metatarsal heads, lateral 5 th metatarsal
head

217 Edmonton Manual of Common Clinical Seer


Palpation Ankle Brachial Index
• Comment on asymmetry in amplitude, contour, and upstroke: cool skin (asymmetry in
>0.90 Normal
foot temperature LR + 6.1*)
• Dorsalis pedis pulse may be absent in up to 12% of normal population and posterior 0.71- 0.90 Mild obstruction
tibial pulse may be absent in up to 10% of the population. Absence of both posterior 0.41- 0.70 Moderate obstruction
. .
tibial and dorsalis pedis pulse ( LR + 14.9 LR - 0.3 *) absent femoral pulse ( LR + 6.1*).
< 0.40 Severe obstruction
• Palpate abdominal aorta using both hands to " trap” the pulsation in abdomen and
estimate size
.
• Prolonged capillary refill ( N < 2 s) abnormal if > 5 s

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

* Immediate neurovascular assessment


* Refer to Vascular Surgery for assessment of limb viability ( Doppler ) and revascularization
» Consider local thrombolysis or surgical embolectomy, ensure anticoagulation post - op
Conservative Treatment
. .
• Control atherosclerotic risk factors: HTN. DM dyslipidemia encourage smoking cessation
• Exercise
.
> Supervised program for patients with intermittent claudication ( 30 - 45 min 3x / wk for 12 wks)

.
» 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

Ldmonton Manual of Common Clinical Scenarios 218


PLEURAL EFFUSION
.
Current Editors: Bethea Shute MD Mohit Bhutani MD FRCPC FCCP

Effusion Types ( based on pleural fluid analysis): Light’s Criteria


• Transudate vs. exudate: Light’s criteria ( see below) Any one of the following suggests exudative effusion
>Complicated exudative effusion = pH < 7.2, glucose < 3.3 mmol Pleural /serum protein ratio >0.5
>Empyema = pus + microorganisms on gram stain or culture
Pleural /serum LDH ratio >0.6
• Hemothorax: pleural/serum HCT >0.5
• Chylothorax: triglycerides > 1.2 mmol/L, chylomicrons
Pleural LDH > 2/ 3rds the upper
limit of normal
DIFFERENTIAL DIAGNOSIS for serum LDH
• Common Etiologies:
> Transudate: CHF (most common), liver cirrhosis (causing hypoalbuminemia or hepatic hydrothorax), nephrotic syndrome,
hypothyroidism, cardiac valvular disease, peritoneal dialysis
>
diseases, asbestos exposure
.
Exudate: pneumonia,( mostcommon) , malignancy (esp. lungcarcinoma breastcarcinoma, and lymphoma),TB,PE,connective tissue

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

MEDS • Amiodarone, nitrofurantoin, phenytoin, methotrexate (commonly implicated in pleural effusions)


ALLERGIES • General inquiry

SOCIAL • Smoking, EtOH, occupational exposures


ROS • Symptoms of metastatic disease (bone pain, neuro symptoms), symptoms of liver cirrhosis

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

219 Edmonton Manual of ali


cv
• Inspection: JVP ± abdominojugular reflex . Cheyne-Stokes breathing (rapid, shallow breaths alternating with apneic episodes)
• Palpation: apical impulse (location & diameter )
• Auscultation: presence of S 3 &/or S4

ABDO
• Inspection: jaundice, caput medusae
• Percussion: ascites, hepatosplenomegaly
• Palpation: liver edge
EXTREMITIES
• Unilateral leg swelling ( PE): pedal edema (CHF)

Physical findings to differentiate effusion from consolidation


Pathology Percussion Palpation Auscultation over Affected Area Special Tests
iTactile fr mitus Ior absent breath sounds

Effusion Dull

I
• IpsilateralT chest wall
expansion
• Bronchial breathing at
effusion
top of
•Ivocal resonance at top of effusion,
vocal resonance over effusion

IAir entry • Bronchophony


Consolidation Dull

^Tactile fremitus
• IpsilateralT
expansion
chest wall

• Bronchial breathing

• 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

Edmonton Manual of Common Clinical Scenarios 220


POLYARTICULAR JOINT PAIN
.
Current Editors: Daniel Friedman BSc MD Selina Dobing MD FRCPC

• Etiologies of high morbidity/mortality = infectious, vasculitis, malignancy, connective tissue disease


• Investigate based on Hx and physical, as "autoimmune work - up" is non-specific and may lead to false positives

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)

221 Edmonton Manual of Common Clinical Scenar


PSHX • Joint replacements, previous fractures
.
PO&GHX • Gonococcal/chlamydial infection GPTAL status
MEDS • NSAIDs . steroids, allopurinol, DMARDs. immunomodulatory, diuretics (associated with gout flare), colchicine,
chemotherapy, hydralazine (drug-induced lupus )
FHX • Gout, autoimmune conditions, sickle cell disease

SOCIAL • EtOH, smoking . IVDU, camping/travel occupation, insurance coverage (for biologies)
,

ROS • General: fatigue, fever, weight changes, night sweats


• HEENT: dry mouth/eyes, photophobia, facial swelling, scalp tenderness, jaw claudication, tinnitus, oral /nasal
ulcers
.
• CV/ Resp: chest pain SOB, palpitations, pre - syncope
• GI/GU: diarrhea, hematochezia, abdominal pain, hematuria, dysuria, urethral discharge, genital ulcers,
dyspareunia
• Neuro/ MSK/Derm: change in mental status, neck stiffness, rashes, foot drop, proximal muscle weakness,
arthralgia, Raynaud’s, claudication, dactylitis, tenosynovitis, plaques

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)

DERM: digital ulcers, petechiae, purpura, bruising, jaundice, bronzing

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

Edmonton Manual of Common Clinical Scenarios 222


.
Current Editors:Cassandra Hirt MD Selina Dobing MD FRCPC

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

Transient/Physiological Peristent ( > 2 x ) - Pathological


• Any acute illness
(retest when well)
Microalbuminuria ( > 20 mg) - Diabetes
.
• Fever, excessive CHF UTI . Quantify ( 24 Ur) or Spot Protein: Cr
• Orthostatic - resolves overnight
• Idiopathic

> 3 g/day ( 24 Ur) < 3 g/day (24 Ur)


Glomerular UrPrrUrCr >300 mg/mmol UrPnUrCr < 300 mg/mmol
Inc. glomerular permeability ( > 3.5 g/ 24
-
hrs) +/ Nephrotic Syndrome, edema,
.
hypoalbuminemia hyperlipidemia >70% Albumin SPEP/ UPEP to determine content

—<
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)

Risk of Adverse Outcomes


False +ve/- ve Dipstick Common Conditions:
( < 2% pts with proteinuria):
• False +POS: very concentrated urine: immersed too long • Transient proteinuria (if < 30 yrs Presence of active urine sediment (active
• False - NEG: very dilute urine: non-albumin protein and normal renal function) inflammation) with uncontrolled HTN may
• DM Nephropathy suggest nephritic syndrome
• HTN
• Diabetic Measurements
• Dipstick NOT sensitive enough to pick up
• Minimal Change Disease (peds) f risk of thrombosis/infection/
malnutrition/ hyperlipidemia with severe
microalbuminuria proteinuria and Sr Albumin < 20

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)

RED FLAGS • HTN, active urine sediment , ARF| f


, albumin, cholesterol

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 )

223 Edmonton Manual of Common Clinical Scenarios


PHYSICAL
. . .
Vitals - BP, HR RR Temp Sa02 (HTN typically associated with nephritic syndrome)
HEENT
• Periorbital edema, volume status - assess JVP (low in nephrotic and high in nephritic)

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

Edmonton Manual of Common Clinical Scenario* 224


Current Editors: Michael Samycia MD. Parbeer Grewal MD

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)

225 Edmonton Mai


• Note: Cholestasis of pregnancy may cause pruritis in 2nd/ 3rd trimester, while atopic eruption is more likely in lvt trimester
Radiology/Imaging
• CXR for Hodgkin' s lymphoma (if presence of constitutional symptoms)
• MRI of the brain and/or spinal cord ( to rule out MS if neurological symptoms present )
• US of liver ( if cholestatic picture)

Special Tests
• Skin testing for specific allergens

• If skin lesion present, scrapings for tinea and culture ( fungal, bacterial, viral )

Surgical/ Diagnostic Interventions


• Bx skin lesions if diagnosis still uncertain/worrisome

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> —

non Manual of Common Clinical Scenarios 226


RENAL FAILURE
.
Current Editors: Shannon Fong MD Vijay Daniels MD FRCPC

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

GFR = [ (140- age) x ( Wt


• .
CKD: GFR < 60 mL/min or evidence of kidney damage present for > 3 mo

in kg) x ( 1.2 if female) ) / General Evaluation


( SrCr (pmol/l]) • Hx and PE (including urine output )
• Investigations: CBCD, SrCr ( +baseline if available ), urea, lytes (monitor for hypcrK , met.acidosis), urinalysis,
• To calculate estimated
.
CrCI estimate GFR
.
urine lytes/osmo ECG (may see changes if hyperK )
• Consider: FeNa (in AKI). post - void residual +/- catheterization (if suspect obstructive etiology), renal U/S


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

Limitations of SrCr Estimation of GFR Indications for Urgent Dialysis


• Need steady state - dependent on muscle % and body mass • Acidosis (metabolic )
• GFR must fall before see SrCr f • Electrolytes (hyperkalemia)
• Hyperfiltration: GFR is preserved but not representative of .
• Intoxication ( ASA lithium, methanol, ethylene glycol)
structural damage • Overload ( volume overload)
• Tubular component of secretion
• Uremia (encephalopathy, pericarditis)

227 Edmonton Manual of Common Clin;


DIFFERENTIAL DIAGNOSIS
Common Conditions
I
• Prerenal: volume loss, renal perfusion
• Renal: ATN, DM nephropathy
• Post Renal: obstruction uropathy (enlarged prostate), stones

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

RED FLAGS • Acute indications for dialysis ( AEIOU)

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

ROS • Gl: N/V


• MSK/DERM: rash, pruritis, petechiae, leg cramps

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)

Edmonton Manual of Common Clinical Scenarios 228


RESTRICTIVE LUNG DISEASE
.
Current Editors: Albert Vu MD Mohit Bhutan! MD FRCPC FCCP

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

Edmonton Manual of Common Clinical Scenaric 230


.
Current Editors: Parnian Riaz Vijay Daniels MD FRCPC

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

> Ensure safe environment, put patient in recovery position, provide 02


> Anti- epileptics (benzodiazepines +/- phenytoin)
Treatment Options
• Treat underlying cause if identified

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

Edmonton Manual of Common Clinical Scenarios 232


SHOCK
.
Current Editors: Jamie McIntyre MD Matthew Inwood MD CCFP-EM

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

CC • Hypotension, oliguria, altered LOC

HPI • Obtain collateral Hx if necessary


• SAMPLE Hx once patient is stable
• Trauma (H, O. D, or mixed)
RED FLAGS • Severely hypotensive, shifting from tachycardia to bradycardia, altered LOC or unconscious, arrhythmia, CP.
resp distress. SOB with minimal activity or at rest, rapid deterioration
PMHX • Ml (past 24 hrs), coagulopathy, infection, pancreatitis, Addisonian crisis, myxedema coma, bleeding
PSHX • Recent surgeries in abdomen 3rd spacing or bleed, vascular surgeries
PO&GHX • Recent pregnancy with bleeding

MEDS •B - Blockers. steroids, chemotherapy, drug intoxication


ALLERGIES • Anaphylaxis

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 ])

233 Edrrn n Manual of Co


• Inspect for brocken bones, palpate for spine step deformities or tenderness
EXTREMITIES
• Peripheral cyanosis, palpate extremities (cool vs warm) , peripheral pulses, cap refill
• Calf swelling, erythema, tenderness
HEENT
• Inspect for angioedema, central cyanosis, tracheal deviation
• JVP assessment • low vs high
CV/ RESP
• Inspect for assymetric chest movement, apnea
• Percuss for hyperresonance ( pneumothorax ), dullness (consolidation, hemothorax)
• Auscultate for cardiac friction rub, breath sounds (present, absent, reduced), crackles, or other adventitious breath sounds
ABDO
• Inspect for abdo distension, bruising around umbillicus (Cullen' s Sign) or flanks ( Grey Turner Sign)
• Palpate for rigid/tender abdomen, masses
• DRE for tone, blood, high -riding prostate

NEURO
• Hyperreflexia .istrength of limbs, lack of sensation in perianal area

Physical Exam Findings


Peripheral Palpation JVP Other Findings
Low JVP Tachycardia
S =3T
Hypovolemic Cool extremities 0)

Cool extremities High JVP No crackles on chest auscultation -


Q 0>
Obstructive
Distributive Warm extremities ( severe peripheral Low JVP
S
D O
3 )

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)

Edmonton Manual of Common Clinical Scenarios 234


-
SLEEP DISORDERED BREATHING
Current Editors: Derek Chan MD MBA CHE. Mohit Bhutani MD FRCPC FCCP

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

235 Edmonton Manual of Common Clinical Scenarios


OSA CSA
SHx • Smoking, alcohol/sedatives, obesity • Smoking, alcohol/sedatives
Meds • Sedatives • Opioids, especially methadone
FHx • Metabolic disease, heart disease • Metabolic disease, heart disease
ROS • Hypertension, right and left ventricular dysfunction, • Hypertension, heart failure, myocardial infarction
myocardial infarction, arrhythmias ( Afib), pulmonary arrhythmias ( atrial fib) , pulmonary hypertension, stroke,
hypertension, stroke, driving accidents (7 times more . .
driving accidents (7 times more likely) GERD diabetes
likely ), GERD, diabetes, depression

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

Edmonton Manual of Common Clinical Scenarios 236


SYNCOPE
.
Current Editors: Parnian Riaz MD Selina Dobing MD FRCPC

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

237 Edmonton Manual of Common Clin


PO&GHX .
• Current pregnancy, previous ectopic pregnancy/ PID eclampsia

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

SOCIAL • EtOH, street drugs (e.g., cocaine), occupation, driving


ROS • HEENT: pallor
• CV: peripheral edema

.
• 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)

mton Manual of Common Clinical Scenar 238


THROMBOCYTOPENIA
.
Current Editors: Bryan Duong MD Kathleen Wong MD FRCPC

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

Definition: Platelet count < 150 xlOVL


Bleeding risk ( based on expert opinion rather than evidence- based trials):
• > 50 very unlikely to spontaneously bleed and fit for most surgeries (often neurosurgery prefers > 100)
• < 10 high risk of spontaneous life - threatening bleeds

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 )

HPI • Onset and origin of bleeding (epistaxis, gingival, hematemesis .


melena, menorrhagia, petechiae, bruises)
• Cause or trigger of bleeding ( spontaneous, traumatic, recent infection/procedure/medication use)
• Duration, volume, and frequency of bleeding
• Resolution of bleeding with or without intervention
• Symptoms of anemia/neutropenia ( fatigue, shortness of breath, chest pain, infections)
• Symptoms of malignancy or systemic illness ( fevers, weight loss)

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)

239 Edmonton Manual of Common Clinical Scenar n


HEENT Differentiating ITP, DIC, and TTP
• Inspect skin and eyes for jaundice and scleral icterus (liver disease) ITP DIC TTP
• Inspect oral cavity, pharynx, and nasal mucus membranes for
petechiae, gingival bleeding, tonsillar enlargement Platelet Low /Very Low Low Low
• Palpate anterior /posterior cervical and submandibular LNs for
lymphadenopathy INR/ PTT Normal Prolonged Normal
ABDO Fibrinogen Normal Low Normal/high
• Inspect for bulging flanks, percuss for flank dullness and shifting Schistocytes None Variable Present, may
dullness ( ascites/liver disease) be many
• Palpate/percuss liver edge for hepatomegaly
• Percuss for dullness over Traube’s space or for Castell ' s sign
(splenomegaly)
DERM
. . . .
• Inspect skin for petechiae purpura (ITP TTP) bruising, ecchymoses palmar erythema ( liver disease), rash ( rheumatologic disease)
• Palpate axillary and inguinal LNs for lymphadenopathy
NEURO
• Examine for lateralizing signs (intracranial bleed), peripheral neuropathy (vitamin B 12 deficiency), hyperreflexia (pre - eclampsia,
HELLP)

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

Platelet count <30% or platelet nadir < 10 0

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

Alternate cause of None apparent 2


Thrombocytopenia 1
Possible
Definite 0
•Score: s 3 = low probability, 4 - 5 = intermediate probability, 6-8 = high probability
TREATMENT
General comments
• Platelet transfusion is considered if platelets are < 50 with major bleeding or in the setting of an invasive procedure or surgery
• Also consider platelet transfusion if there is major bleeding in the setting of antiplatelet agents, regardless of platelet count
• Avoid contact sports when platelets are < 10
• Treat any underlying conditions (e.g. if lupus, give anti - SLE therapy: if HIV give HAART) .
• Stop offending agents and alcohol

Disease specific treatments:

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)

nonton Manual of Common Ciinical Scenarios 240


THYROID DISEASE
.
Current Editors: Joffre Munro MD Laurie Mereu MD FRCPC

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

HPI Hypothyroidism Hyperthyroidism


• General: fatigue, cold intolerance • General: anxious, irritable, heat intolerance
• HEENT: impaired hearing, hoarseness • HEENT: eye irritation, diplopia
• CV/ RESP: dyspnea • CV/RESP: palpitations
.
• Gl: constipation, Wt gain appetite
f
• Gl: diarrhea, Wt loss, appetite
• GU: menorrhagia • GU: polyuria, oligomenorrhea, loss of libido
• MSK / DERM: weakness, arthralgia, myalgia, • MSK / DERM: weakness, onycholysis
paresthesia, dry/itchy skin • CNS: dysphoria, tremor
• CNS: depression, poor concentration/memory

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

241 Edmonton Manual of Common Clinii


PHYSICAL
Vital Signs ( BP, HR, RR, Temp, SaQ 2)
Hypothyroidism Hyperthyroidism
• Vitals: diastolic HTN (decreased pulse pressure), bradycardia • Vitals: systolic HTN ( increased pulse pressure),tachycardia, Afib
• General Appearance: flat affect, slow speech ( 10 - 20% of hyperthyroid patients)
• Extremities: thin/brittle nails, jointeffusions • General Appearance: irritable/anxious, thin, diaphoretic, muscle
• HEENT: periorbital edema, loss of out 2 / 3 of eyebrow; irregular,
wasting
firm thyroid gland in Hashimoto's thyroiditis • Extremities: clubbing (Grave' s disease), onycholysis, palmar
• Derm: dry/cool /coarse skin, diffuse alopecia, myxedema . erythema
• HEENT: Grave' s ophthalmopathy (lid retraction, lid lag .
• Neuro: decreased muscle strength, delayed relaxation of deep
conjunctival injection, diploplia, proptosis), periorbital edema,
reflexes, positive Tinnel's/Phalen's test
hair loss, alopecia areata ( autoimmune disorders), diffusely
enlarged, firm thyroid gland +/- bruit in Grave' s disease
• Derm: moist / warm skin, pretibial myxedema (Grave' s disease),
vitiligo
• Neuro: impaired concentration, fine tremor, proximal muscle
weakness, hyperreflexia

Thyroid Examination ( Refer also to PE Thyroid ) Thyroid Storm


• .
Inspection: obvious masses, symmetry of STM tracheal deviation. Signs Lab Findings
> Have patient sit up with a cup of water in their hand - ask
f
them to swallow water and look for movement of thyroid
gland and obvious masses (no movement indicates fixed mass,
^
HR: BP: widened pulse
pressure: fever: ILOC
; shock
f f f
T4; FT 4; glucose:
fWBC + f
; Hgb; Ca K'
^+
2
fD =
Q. rt>
possible malignancy or retrosternal goitre)
(severe cases)
0.3
3 Q)
• Palpation: palpate thyroid gland (isthmus and both lobes) while Myxedema Coma
standing on each side of the patient - comment on size, texture,
nodularity, symmetry, tenderness, masses, mobility while patient Signs Lab Findings
i I
swallowing water
> Palpate for lymphadenopathy in head and neck region + + +
HR ; BP; RR; ^
T4; FT4; glucose:
i
I
hypothermia; LOC
WBC; Hgb:
Na»|
; CK t
Screen for Thyroid Disease: TSH
• Hypothyroidism:
.
> TSH anti-TPO antibodies ( +ve in > 90% of patients with autoimmune hypothyroidism)
• Hyperthyroidism:

. . .
> 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

Uu PES OF BLOOD PRODUCTS


—c
OJ
O) Cellular Products:
• Red blood cells
• Platelets (pooled or apheresis)
0) ~o
• Frozen plasma
OJ
-c 2 • Cryoprecipitate
Fractionated Products:
• Coagulation factors and concentrates
. .
• Immune globulin (e.g., IVIG RhIG, Hepatitis B IG Varicella Zoster IG)
• Albumin

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)

Symptomatic bacterial sepsis 1 in 250,000


(per unit of RBCs )

243 Edmonton Manual of Common Cl


Non- infectious Risks:
Type of Reaction Prevalence Signs & Immediate Actions Investigations Management
Symptoms
Febrile non-hemo - RBC 1 / 300 Fever 1. Stop transfusion None 1. Acetaminophen
lytic transfusion Platelets 1/ 20 2. Restart transfusion
reaction (FNHTR) 2. Check vitals
ABO Incompatibility 1 /40,000 Fever CBC, lytes, 1. Acetaminophen
3. Verify correct
Tachycardia Cr, bilirubin, 2. Do not restart transfusion
(< 10% result Hypotension blood was given haptoglobin, 3. Aggressive IV fluid hydration
in fatality) Nausea/ vomiting LDH, INR, PTT,
4. Inform blood
Dyspnea fibrinogen, DAT,
Back/ flank pain bank/transfusion urine dipstick
Bleeding medicine
Hemogloinuria
Mild hypersensitivity 1/100 Urticaria None -
1. Diphenhydramine 25 50 mg PO/
Pruritus IV
2. Restart transfusion slowly if:
- the urticarial rash involves <2/3 of
the body surface area; and
- there are no symptoms suggesting
severe allergic reaction
1. Do not restart transfusion 2
Anaphylaxis 1 /40,000 Urticaria Chest x -ray
2. Administer epinephrine,
0> =
Pruritus
Bronchospasm/
ABG
corticosteroids, diphenhydramine,
Q
- n>
O. 3
dyspnea
Angioedema
vasopressors and supportive care as
required, according to current local
D £1)
n> —
Hypotension guidelines/protocols
Hypoxia 3. Resuscitate and activate medical
emergency/ code blue team as
required
Transfusion 1/ 100 Dyspnea Chest x -ray 1 . Diuretics (Furosemide 40 mg IV )
Associated Hypoxia ABG 2. Restart transfusion at a reduced
Circulatory Overload CHF (orthopnea, infusion rate
( TACO) PND, JVP disten- 3. Diuretics between transfusions
tion, pedal edema) for future transfusions
Transfusion Related 1 / 10,000 Acute onset dys- Chest x -ray 1. Do not restart transfusion
Acute Lung Injury pnea and hypox - ABG 2. Resuscitate and activate medical
(TRALI) emia emergency/ code blue team as
Bilateral lung required
infiltrates 3. Oxygen support (including me -
No evidence of cir - chanical ventilation if required)
culatory overload
Other notes:
- Chronically transfused patients are at increased risk of iron overload
- Despite rigorous testing and research, there are still unknown risks associated with transfusion due to infectious agents yet to be
identified and known diseases that cannot be screened

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

Eelmonte Manual of C mmon Clinical S 244


UNILATERAL SWOLLEN LEG
.
Current Editors: Mohammad Refaei MD Mohit Bhutani MD FRCPC FCCP

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)

Causes of pitting unilateral leg edema:


• DVT: presents as acutely swollen, discolored, painful leg
• Venous:
> Insufficiency (due to risk factors or post - thrombotic syndrome)
> Obstruction ( tumor, hematoma, lymphoma)
• Infectious /Inflammatory: cellulitis, myositis, fasciitis
• Trauma /muscle injury: hip / femur fracture (especially post op), ruptured gastrocnemius muscle
• Ruptured Baker’s cyst: obstruction of poplilteal vein

—ac c CD • Compartment syndrome


• Lymphatic obstruction
u • Reflex sympathetic dystrophy syndrome ( RSDS)
0 -0a Causes of non - pitting unilateral leg edema:
.
• Lymphatic obstruction (often painless: due to recent surgery LN dissection, parasitic infection, tumor, or trauma)
• Pretibial myxedema (secondary to hyperthyroidism)

High Mortality/Morbidity
• .
DVT leading to PE necrotizing fasciitis, compartment syndrome
HISTORY
ID • Patient 's name, age, gender

HPI • Duration of swelling: acute (< 72 hrs) vs. chronic


• Associated symptoms: painful, warm, red
• Does the edema improve overnight ? ( venous more likely to improve than lymphedema)
• Recent trauma or extreme activity, e.g., popping sensation after physical activity
• Recent immobilization: surgery, paralysis, cast, travel > 4-8 hrs

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)

Special Tests • Alternative Dx to DVT as likely or more likely -2


• Homan’s sign - discomfort or pain behind the knee upon £ 3 = high prob ( 53%); 1 - 2 = moderate ( 17%); 0 = low risk (3%)
forced dorsiflexion of the foot by the examiner as a test for Adapted from thrombosiscanada.ca and Wells PS et al Lancet 1997
DVT (likelihood ratio not significant )
Findings (for DVT) LR+ LR-
Laboratory Investigations Asymmetrical calf swelling 2.1 0.5
• CBC, urinalysis. CK. electrolytes, creatinine, blood sugar. TSH. albumin, liver enzymes ( > 2 cm difference)
• Serum albumin < 20 g/ L leads to edema from liver disease, nephrotic syndrome
Superficial venous dilation 1.6 0.9 CD D
Radiology/ lmaging CL (D
Swelling of the entire leg 1.5 0.8
• Doppler US (determine deep vs. superficial; proximal vs. distal) oZ5! 3
.
• Spiral CT angiogram for suspected PE V/Q scan useful if CT angio not available Erythema /superficial NS NS
CD
D
)

• CXR: useful to look for other causes thrombophlebitis


Special Tests Tenderness on palpation NS NS
• D - dimer: high sensitivity, makes it useful in ruling out DVT in low risk patients. Elevated Asymmetrical skin temp 1.4 NS
D- dimer should be followed up with Doppler US
Homan' s sign NS NS
• For unprovoked DVTs, perform age - appropriate screening for cancer unless clinical
presentation pointing to a specific focus of malignancy - no utility of over -investigating Well’s score ( low risk ) 0.2
for malignancy ( SOME trial) Well’s score ( high risk ) 6.3
[EEATMENT [Adapted from Evidence-Based Physical Diagnosis.
3rd ed., Steven McGee.MD and The Rational Clinical
Acute Management ( if unstable or signs of respiratory distress) .
Examination: Evidence- Based Clinical Diagnosis David
.
• Immediate stabilization IV access: 2 large bore IVs, oxygen L. Simel, Drummond Rennie
• Consider thrombolytic ( tPA) treatment followed by LMWH/UFH if high clinical
suspicion for PE
DVT/ PE
• Avoid anticoagulation if platelet < 50x109
• LMWH recommended for hemodynamically unstable patients and for cancer - associated VTE
• Bridging anticoagulation

> 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

Chronic Venous Insufficiency


• Lifestyle modification, leg elevation, and knee - high compression stockings that provide 30 - 40 mmHg pressure at ankle
• ABI if arterial insufficiency is a concern to determine if compression stockings are contraindicated

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

jmonton t malofCc Clinical Scenarios 246


'
VISION LOSS
.
Current Editors: Taurian Guinand MD Jessica Ting MD FRCPC

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

• Vitreous hemorrhage: seen on fundoscopy cataracts


Open- angle glaucoma: primary, secondary

Retinal dysfunction
Retinal dysfunction
Retinal artery/vein occlusion: seen on fundoscopy

• Diabetic ( retinal edema, retinopathy): Hx of poor diabetic

—c
OJ
QJ
Retinal detachment: curtain of vision loss

Optic nerve dysfunction
control or long duration of DM
• Vascular insufficiency
£5
<D T3
.
• 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

• Pituitary apoplexy, compressive chiasmal lesion • Multiple sclerosis


Post -Chiasm problems Other
• Occipital infarct/hemorrhage: central neuro signs/ symptoms .
• Toxic/nutritional: nutritional deficiencies tobacco/EtOH

Other amblyopia, methanol


• Hereditary optic neuropathies
• Functional loss: no organic cause found, often past psych Hx
and /or significant stress (diagnosis of exclusion)
ISTORY
ID • Patient ’s name, age . gender
CC • Loss of vision (acute vs. transient vs. chronic)
HPI • Sudden or gradual: one eye or both (peripheral vs. central origin): painful or painless
• Transient (amaurosis fugax, migraine, seizure) or persistent
• Photophobia (keratitis, iritis, migraine)
• Total or partial visual decrease; degree of loss; central or peripheral
• Other visual disturbances: flashing lights, floaters, zig-zag lines (retinal tear /detachment )
• Associated headache or other neurological symptoms (glaucoma, raised ICP, post -ictal, CNS lesion)
• Trauma (blunt /penetrating, foreign body, chemical exposure, UV radiation)
• Infectious/inflammatory symptoms: redness, irritation, photophobia, discharge
RED FLAGS • Sudden, painful vision loss ( angle-closure glaucoma, endophthalmitis, optic neuritis, uveitis)
• Sudden, painless vision loss (retinal vascular occlusion, retinal detachment, vitreous hemorrhage, ischemic
optic neuropathy)
PMHX • Vascular risk factors: HTN, DM . .
CAD hypercoagulable, sickle cell disease
• Migraines and other
neurological conditions: CVA, MS
• Glaucoma, high myopia ( > 6.00D)
• Contact lens wear
• Ocular trauma
PSHX .
• Ocular surgery (i.e. cataract surgery)
MEDS .
• Eye drops CVD medications, anticholinergics, topiramate (angle closure glaucoma), bisphosphonates
(keratitis, uveitis)
ALLERGIES • Topical and oral medications
FHX • Ocular . .
Hx, CVD Hx DM migraines

247 Edmonton Manual of CommonCli


SOCIAL • Drug use, smoking Hx

ROS • HEENT: symptoms of temporal arteritis (scalp tenderness, temporal pain, jaw claudication), herpetic rashes
• CV: CVD, stroke

RISK FACTORS • Previous ocular Hx, DM, HTN

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

Special Tests: SET


n>
• Ophthalmoscopy C L (D
> Examine optic disc for any abnormalities (e.g., papilledema, hemorrhage, optic disc pallor ) G. 3
D a>
> Examine retinal vasculature for any visible clots /bleeds ( lack of view may point to retinal detachment, endophthalmitis, or
vitreous hemorrhage)
CD —
• Amsler grid (each eye separately) to identify any abnormalities that may suggest retinal pathology
- -
• Slit lamp exam: to view the anterior segment of the eye +/ foreign body retrieval
• Fluorescein staining: Keratitis, corneal abrasion

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

nonton Manual of Common Clinical Scenarios 248


.
Current Editors: Michael J Kapusta MD Jennifer McCombe MD MPH FRCPC

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

Lesion Location Motor Sensory UMN/


LMN
Cortical/
subcortical Contralateral weakness . .
Contralateral sensory loss in face limb & trunk UMN
Ipsilateral CN weakness ( facial droop, ptosis, dysarthria,
Brainstem dysphagia), contralateral body weakness: cerebellar ataxia
Horner 's syndrome
. Sensory deficit in the ipsilateral face and contralateral
body UMN

Spinal Cord Bilateral with bilateral cord damage -paraplegia /


quadriplegia; LMN at level of lesion and UMN below level of Sensory deficit below specific spinal level UMN/
(myelopathy) Dissociated sensory loss, sacral sparing LMN
lesion
Anterior Horn .
Dysarthria, dysphagia (bulbar, not oculobulbar weakness),
bilateral (often asymmetric ) weakness: mixed UMN and LMN UMN/
Cell LMN

03 C
0
Spinal Roots
signs
.
Areflexia weakness ± fasiculations following dermatomal Sensory deficit corresponding to dermatomal
LMN
ES
0 “U
(radiculopathy) distribution distribution
Plexopathy Brachial (C 5 -T1) or Lumbosacral (T12- L4) affecting nerves of Sensory deficit according to plexus LMN
C 0
-2 Peripheral
respective plexus
Weakness beginning in feet, progressing up to legs, hands, Sensory deficit in stocking-glove distribution LMN
Neuropathy then arms ('stocking-glove distribution')
.
Mononeuropathy Areflexia atrophy, weakness ± fasiculations following
peripheral nerve distribution
Sensory deficit following peripheral nerve distribution LMN
Neuromuscular Fluctuating, fatiguable ocubulbar weakness (diploplia
Junction dysarthria, dysphagia, drooling, ptosis)
. LMN

Myopathy Proximal symmetric weakness (shoulder /hip girdle) LMN


Etiology ( * indicates high, early mortality/morbidity)
. . .
• Infectious: influenza. EBV CMV. Lyme disease HIV rabies *
.
• Inflammatory: polymyositis, dermatomyositis inclusion body myositis, lupus
. . .
• Neurologic:cerebrovasculardisease‘( stroke.TIA).demyelinatingdisorders (MS Guillain - Barre * ) spinalcordinjury neuromuscularjunction (myasthenia
. .
gravis Lambert Eaton, botulism), anterior horn cell ( ALS poliomyelitis)
. .
• Metabolic: K
^ ^
.
Ca. / T Na Vit B 12 deficiency
.
• Endocrine: DM hypothyroidism Cushings, acromegaly
. .
• Drugs: steroids, methotrexate, chemotherapy, statins EtOH cocaine, interferon

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)

249 Edmonton Manual of Common Clinical Scenarios


RED FLAGS • Sudden onset, one- sided weakness (CVA) , ascending paralysis (rabies, GBS)
• Weakness that becomes severe within a few days
• Dyspnea ( impending resp failure)
• Bulbar symptoms (dysarthria, dysphagia, facial weakness, ocular impairment )

PMHX • Recent orchronic infections (HIV, CMV, influenza)


.
• Metabolic disorders: hypothyroidism, DM adrenal disorders
• Malignancy (paraneoplastic syndrome and metastatic disease) , depression

PSHX • Back, brain

MEDS • Steroids, statins, interferon, recent immobilizations

FHX • Myasthenia gravis, muscular .


dystrophy, autoimmune disease, collagen vascular disease ALS
SOCIAL • Occupation: possible occupational injury or exposures (organophosphates used in farming)
• EtOH, smoking, recreational drugs (cocaine), exposure to lead

ROS • HEENT: headache


• CV/RESP: palpitations, chest pain, claudication, SOB
-
• MSK / DERM: joint pain, muscle pain, neck pain, rash (malar /discoid rash lupus: heliotrope/shawl rash, Gottren
papules - dermatomyositis)

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)

• Strength (note pattern): proximal weakness ( myopathy/Guillain- Barre ) vs.


distal weakness (neuropathy)
• Pronator drift: outward drift ( muscle weakens ), pronation and downward drift
DTR

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

Edmonton Manual of Common Clinical Scenarios 250


STATION CONTRIBUTORS
Ascites Charles Lim MD, Craig Domke MD. Lucille Lalonde MD FRCPC
Abnormal Heart Sounds Alim Nagji MD, Jamil Kanji MD. AmmaraSadiq MD FRCPC
Acute Confusion Joffre Munro MD, Yang Li MD, Darren Nichols MD FFCP, Vijay Daniels MD FRCPC
.
Acute Liver Injury Jason An MD Vijay Daniels MD FRCPC
Allergic Reactions Mohammed Osman MD PhD, Michael Chu MD, Vijay Daniels MD FRCPC
Altered Level of Consciousness Ashraf Kharrat MD. James Keay MD CCFP. Vijay Daniels MD FRCPC
Numbness and Paresthesias Gavin Chu, Pen Li MD, Gregg Blevins MD FRCPC
Anemia Debraj Das MD, Robinder Sidhu MD, Todd Penney MSc MD, Henry Conter MD, Ryan Cooper MD MPH FRCPC
Bleeding Disorders Janna Tram MD. James Yeung MD, Matthew Wong MD CCFP
Cardiac Chest Pain Charles Lim MD. Craig Domke MD. Lucille Lalonde MD FRCPC. Vijay Daniels MD FRCPC
Congestive Heart Failure Alim Nagji MD. Jamil Kanji MD, Ammara Sadiq MD FRCPC
Dehydration/Hypovolemia Joffre Munro MD, Yang Li MD, Darren Nichols MD CCFP, Vijay Daniels MD FRCPC
Dementia Prabhpreet Dhaliwal MD. Vijay Daniels MD FRCPC
Diabetes - Acute Complications Elaine Chiu RD CDE, Tammy McNab MD FRCPC
_ C
CD
Diabetes - Chronic Management Elaine Chiu RD CDE. Tammy McNab MD FRCPC
Dyspnea Kamal Abdulwahab MD, Abraam Isaac MD. Kourosh Dinyari MD, Mohit Bhutani MD FRCPC FCCP
C u
QJ U
C
-
Q)
Falls Aamir Bharmal MD. Cathy Lu MD. Marjan Abbasi MD CCFP
Gait Disturbance Carrie Ye MD. Richard Camicioli MD FRCPC
“ 2 Hearing Loss & Deafness Samapti Samapti MD
.
Hematologic Malignancies Antonia Johnson MD Jeffrey M. Patterson MD FRCPC
Hemiplegia/Hemisensory Loss Scott McLeod MD, Francois Jacob MD. D. B. Sinclair MD FRCPC
.
Hemoptysis Zoe Wolf MD, Ashley Gillson MD Mohit Bhutani MD FRCPC FCCP
Lower Respiratory Tract Infection Stephanie Lim, Neeja Bakshi MD
.
Monoarticular Joint Pain Mohammed Osman MD PhD MichelleTeo MD FRCPC. Elaine Yacyshyn MD FRCPC
Obstructive Lung Disease Kamal Abdulwahab MD. Abraam Isaac MD, Kourosh Dinyari MD, Mohit Bhutani MD FRCPC FCCP
Palpitations & Arrhythmias Michael J Kapusta MD. Christopher Fung MD. Ashraf Khan MBChB CCFP
Pancreatitis Caitlyn Collins MD. Vijay Daniels MD FRCPC
Parkinson's & Movement Disorders Samapti Samapti MD. Tom Nowacki MD
Peripheral Vascular Disease Charles Lim MD. Craig Domke MD, Lucille Lalonde MD FRCPC
.
Pleural Effusion Zoe Wolf MD, Ashley Gillson MD Mohit Bhutani MD FRCPC FCCP
Polyarticular Arthritis & Joint Pain Mohammed Osman MD PhD. Michelle Teo MD FRCPC, Elaine Yaccyshyn MD FRCPC
Proteinuria Cassandra Hirt MD. Stephanie Thompson MD. Valerie Luyckx MBBCH
Pruritus Michael Samycia MD, Parbeer Grewal MD
Renal Failure Cassandra Hirt MD. Stephanie Thompson MD. Valerie Luyckx MB ChB. Vijay Daniels MD FRCPC
Restrictive Lung Disease Timothy Chan MD. Mohit Bhutani MD FRCPC FCCP
Seizures Ashraf Kharrat MD, James Keay MD CCFP. Vijay Daniels MD FRCPC
Shock Jamie McIntyre MD, Craig Domke MD. Matthew Inwood MD, CCFP-EM
Sleep-Disordered Breathing Peng Wang MD PhD. Mohit Bhutani MD FRCPC FCCP
Syncope Timothy Chan MD, Gabor Gyenes MD FRCPC. Vijay Daniels MD FRCPC
Thrombocytopenia Daniel Friedman MD, Kathleen Wong MD FRCPC
Thyroid Disease Joffre Munro MD, Carrie Ye MD, Laurie Mereu MD FRCPC
Transfusions Counseling Minju Park MD. Kathleen Wong MD FRCPC
Unilateral Swollen Leg Timothy Chan MD. Mohammad Refaei MD. Mohit Bhutani MD FRCPC FCCP
Vision Loss Ashraf Kharrat MD. James Keay MD CCFP, Vijay Daniels MD FRCPC
Weakness Michael J. Kapusta MD, Carrie Ye MD. Ashraf Khan MBChB CCFP

251 Edmonton Manual of Common Clinical Scenarios


REFERENCES
Ascites
.
Barkun AN. Camus M. Green L et al. The bedside assessment of splenic enlargement. Am J Med. 1991;91:512 - 518.
Chongtham DS, Singh MM. Kalantri SP. Pathak S. Accuracy of palpation and percussion manoeuvres in the diagnosis of splenomegaly. Indian J Med Sci.
1997:51( 11):409 - 416.
.
Simel DL Rennie D. Liver disease and cirrhosis. In Simel DL. Rennie D. eds. The Rational Clinical Examination: Evidence- Based Clinical Diagnosis . New York:
McGraw - Hill; 2009.
.
Longmore M. Wilkinson IB Davidson EH. Foulkes A , Mafi AR. Oxford Handbook of Clinical Medicine. 8 th ed. New York: Oxford University Press; 2010
McCormick PA. Nolan N. Palpable epigastric liver as a physical sign of cirrhosis: A prospective study. Eur J Gastroenterol Hepatol. 2004;16.
.
Cummings S Papadakis M. Melnick J. et al. The oredictive value of physical examination for ascites. West J Med. 1985:142:633 - 636.
.
Dubey S, Swaroop A Jain R. et al. Percussion of Traube's space: A useful index of splenic enlargement. J Assoc Physicians India. 2000;48:326 - 328.
.
Sullivan S Williams R. Reliability of clinical techniques for detecting splenic enlargement. Br Med J. 1976:2:1043 - 1044.
. .
Schenker S Balint J Schiff L. Differential diagnosis of jaundice: Report of a prospective study of 61 proved cases. Am J Dig D/ s. 1962:7( 5):449- 463.
McGee S. Evidence- Based Physical Diagnosis. 3rd ed. Philadelphia: Elsevier: 2012:428 - 440.

Abnormal Heart Sounds


.
Braunwald E. Chapter 219: Approach to the patient with possible cardiovascular disease. In Fauci AS Braunwald E. Kasper DL. Hauser SL.
Cescon D. Etchells E. Harrison' s Manual of Medicine. New York: McGraw- Hill.
.
Simel DL Rennie D. Update: Murmur Systolic In Simel DL. Rennie D. eds. The Rational Clinical Examination: Evidence - Based Clinical Diagnosis. New York:
McGraw - Hill; 2009.
.
Forssell G Jonasson R. Orinius E. Identifying severe aortic valvular stenosis by bedside examination. Acta Med Scand. 1985:218:397- 400.
Lilly LS. Pathophysiology of Heart Disease. 4th ed. Lippincott Williams & Wilkins: New York; 2007.
Buss J. Thompson G. eds. Auscultation Skills : Breath and Heart Sounds. 4 th ed. New York: Springhouse: 2009.
.
Longo DL. Jameson JL Loscalzo J. eds. Harrison' s Principles of Internal Medicine. New York: McGraw -Hill: 2008.
Otto CM. Valvular aortic stenosis: Disease severity and timing of intervention. JACC. 2006:47(11) : 2141- 2151.
.
Grayburn PA. Smith MD. Handshoe R et al. Detection of aortic insufficiency by standard echocardiography, pulsed Doppler echocardiography, and
auscultation: A comparison of accuracies. Ann Intern Med. 1986:104:599 - 605.
SET
fD -
ft

McGee S. Evidence- Based Physical Diagnosis. 3rd ed. Philadelphia: Elsevier: 2012:320 - 412.
CL fD
Aronow WS, Kronzon I. Correlation of prevalence and severity of aortic regurgitation detected by pulsed Doppler echocardiography with the murmur of Q. 3
aortic regurgitation in elderly patients in a long term health care facility. Am J Cardiol. 1986:63:128 - 129.
-
Z3 QJ
fD ““
Acute Confusion
.
Fauci AS et al. Harrisons Principles of Internal Medicine. 17th ed. New York: McGraw - Hill; 2008.
.
Tintinalli JE et al. Tintinolli's Emergency Medicine: A Comprehensive Study Guide. 6th ed. New York: McGraw - Hill: 2004.

Acute Liver Injury


Hui D. Approach to Internal Medicine: A Resource Book for Clinical Practice. 3rd ed.New York: Springer; 2013:128- 130.
Sabatine MS. Pocket Medicine: The Massachusetts General Hospital Handbook of Internal Medicine. 5 th ed. New York: Lippincott Williams & Wilkins: 2014:3 -
16.

Allergic Reactions
Simel DL. Rennie D. eds. The Rational Clinical Examination: Evidence- Based Clinical Diagnosis. New York: McGraw - Hill; 2009.
UpToDate: Anaphylaxis: rapid recognition and treatment [ Online] ( 2010). Available from: http:// www.uptodate.com
. .
Salkind AR , Cuddy PG Foxworth JW. Is this patient allergic to penicillin? In Simel DL. Rennie D eds. The Rational Clinical Examination: Evidence- Based
Clinical Diagnosis. New York: McGraw -Hill: 2009.
Simons FE. Anaphylaxis . J Allergy Clin Immunol. 2010 Feb:125( 2 Suppl 2):S161- 181.

Altered Level of Consciousness


ACP PIER & AHFS Dl Essentials: Delirium. http://online.statref.com/document.aspx?fxid= 92&docid= 1146. Posted:10/8/2009.
.
Bickley LS Szilagyi PG. Botes ' Guide to Physical Examination and History Taking. 9th ed. Philadelphia: Lippincott Williams & Wilkins: 2007.
Fauci AS. Kasper DL. et al. Harrison's Principles of Internal Medicine. 17th ed. New York: McGraw -Hill; 2008.
Hoffman LH. et al. First Exposure Emergency Medicine. New York: McGraw - Hill: 2008.
.
Moore EE Feliciano DV. Mattox KL. Diagnostic and interventional radiology. In Trauma. 6th ed. New York: McGraw Hill: 2008.
Ropper AH. Samuels MA. Adams and Victor ' s Prnciples of Neurology . 9th ed. New York: McGraw - Hill: 2009.
-
.
Stone KC Humphries R. Current Diagnosis & Treatment Emergency Medicine. 6th ed. New York: McGraw - Hill; 2008.
.
Tintinalli JE Kelen GD. Stapczynski JS. Emergency Medicine: A Comprehensive Study Guide. 6th ed. New York: McGraw - Hill; 2004.

Numbness and Paresthesias


American College of Physicians. ACP PIER & AHFS Dl Essentials: Stroke and Transient Ischemic Attack. http://online.statref.com.lcgin.ezproxy.library.
ualberta.ca /document.aspx ?fxid =92&docid = 3539
.
Federman DD. Nabel EG. ACP Medicine: Neurology ( VI. Neoplastic Disorders ) New York; 2009.
Misulis KE. Chapter 28: Sensory abnormalities of the limbs, trunk, and face. Daroff: Bradley ' s Neurology in Clinical Practice. 6th ed. Available from http://
mdconsult.com
.
Ropper AH Samuels MA. Adams and Victor ' s Principles of Neurology . 9 th ed. New York : McGraw-Hill; 2009.
UpToDate: Approach to the patient with sensory loss [ Online ] ( 2012). Available from: http:// www.uptodatc.com

Anemia
Bain BJ. Blood Cells : A Practical Guide. 5 th ed. Malden, MA: Wiley Blackwell; 2015.
Crover SA. Barkun AN. Sackett DL. The rational clincial examination: Does this patient have splenomegaly ? JAMA. 1993 Nov;270(18):2218 - 2221.
Hui D. Approach to Internal Medicine: A Resource Book for Clinical Practice. 3rd ed. New York: Springer: 2011: 144 - 146.
Hoffman R. et al. Hematolcg )' : Basic Principles and Practice. 5 th ed. Philadelphia: Churchi I Livingstone: 2008.
. .
Sabatine MS ed. Pocket Medicine. 3rd ed. New York: Wolters Kluwer /Lippincott. Williams & Wilkins: 2008:1- 6.
McGee S. Evidence - Based Physical Diagnosis. 3rd ed. Philadelphia: Elsevier: 2012:74- 75.

Bleeding Disorders
. . .
Fogarty PF. Chapter 14: Disorders of hemostasis, thrombosis, and antithrombotic therapy In McPhee SJ Papadakis MA eds.Current Medical Diagnosis &
Treatment. New York: McGraw -Hill: 2016 .
Edmonton Manual of Common Clinical Scenarios 252
Cardiac Chest Pain

.
Examination: Evidence-Based Clinical Diagnosis New York: McGraw - Hill; 2009.
.
Panju AA. Hemmelgarn BR . Guyatt GH. Simel DL. Is this patient having a myocardial infarct on? In Simel DL. Rennie D eds. The Rational Clinical

.
Herlitz J Karlson BW. Karlsson T. et al. A description of the characteristics and outcome of patients hospitalized for acute chest pain in relation to
whether they were admitted to the coronary care unit or not in the thrombolytic era. Int J Cardiol. 2002:82:279- 287.
Lee TH. Goldman L. Evaluation of the patient with acute chest pain. N Engl J Med. 2000 Apr 20:342( 16):1187 - 1195.
Longmore M. Wilkinson IB. Davidson EH. Foulkes A. Mafi AR. Oxford Handbook of Clinical Medicine. 8th ed. New York: Oxford University Press: 2010.
. . -
Thygescn K Alpert JS White HD. Universal definition of myocardial infarction. J Am Coll Ca diol. 2007 Nov 27;50( 22):2173 -2195.
McGee S. Evidence- Based Physical Diagnosis. 3rd ed. Philadelphia: Elsevier: 2012:413 - 422.
Tierney WM. Fitzgerald J. McHenry R. et al. Physicians' estimates of the probability of myocardial infarction in emergency room patients with chest pain.
Med Decis Making. 1986:6:12 - 17.

Congestive Heart Failure


. . .
Davie AP Caruana FL Sutherland GR McMurray J JV. Assessing diagnosis in heart failure: which features are any use? Q J Med. 1997;90:335 - 339 .
.
Arnold JMO ed. Heart failure. Merck Manual Professional. 18 th ed. New Jersey: Merck Publishing: 2006.
. . . .
Faris RF Flather M Purcell H Poolc - Wilson PA. Coats AJS Diuretics for Heart Failure. Cochrane Library. 2009:1- 33 .
.
.
Longmore M. Wlkinson I. Turmezei T Cheung C K. Oxford Handbook of Clinical Medicine. 7th ed. New York: Oxford University Press: 2008
. . .
.
Gadsboll N Hoilund - Carlsen PF Nielsen GG et al Interobserver agreement and accuracy of bedside estimation of right and left ventricular ejection
fraction in acute myocardial infarction. Am J Cardiol. 1989;63:1301- 1307.
McGee S. Evidence - Based Physical Diagnosis. 3rd ed. Philadelphia: Elsevier: 2012:405 - 412.
- .
Fahc y T Jeyaseelan S, McCowan C, et al. Diagnosis of left ventricular systolic dysfunction (LVSD): Development and validation of a clinical prediction rule
.
in primary care Fam Pract . 2007:24:628 - 635 .
. .
Wang CS et al. Does this dyspneic patient in the emergency eepartment have congestive heart failure? In Simel DL. Rennie D eds.The Rational Clinical
.
Examination: Evidence- Based Clinical Diagnosis. New York NY: McGraw-Hill: 2009 .
Dehydration/ Hypovolemia
American Medical Directors Association ( AMDA ). Clinical Practice Guideline: Dehydration ana Fluid Maintenance. Columbia. MD: AMDA; 2001.
— <D
05 C
Gross CR. Lindquist RD. Woolley AC.et al. Clinical indicators of dehydration severity in eldc rly patients. J Emerg Med . 1992:10:267 - 274.
.
Chassagne P. Druesne L Capet C. et al. Clinical presentation of hypernatremia in elderly pat ents: A case control study. J Am GeriatrSoc . 2006:54:
ED ":
< =
O
O)
1225 - 1230.
. .
Simel DL. Rennie D. Hypovolemia Adult . In Simel DL. Rennie D eds. The Rational Clinical Examination: Evidence - Based Clinical Diagnosis. New York:
McGraw - Hill; 2009.
c
2 McGee S. Evidence - Based Physical Diagnosis. 3rd ed. Philadelphia: Elsevier: 2012:76- 77.
.
Thomas DR et al. Understanding clinical dehydration and its treatment. JAm Med Dir Assoc. 2008:9:292 - 301.

Diabetes - Acute Complications


.
Chiasson JL et al. Diagnosis and treatment of diabetic ketoacidosis and the hyperglycemic hyperosmolar state. Canadian Medical Association Jounxil.
2003:168:859- 866.
Goguen J. Gilbert J. Hyperglycemic emergencies in adults. Canadian Journal of Diabetes. 201i:37:S 72 - S 76.
Stoner GD. Hyperosmolar hyperglycemic state. American Family Physician. 2005:71:1723- 1730.
Trachtenberg DE. Diabetic ketoacidosis. American Family Physician. 2005:71:1705 - 1714.

Diabetes - Chronic Management


Canadian Diabetes Association. Appendix 2: Sample diabetes patient care flow sheet for adults. Canadian Journal of Diabetes. 2013:37:S 197- S212
Canadian Diabetes Association. Definition, classification and diagnosis of diabetes, prediabc-res and metabolic syndrome. Canadian Journal of Diabetes.
2013;37:S8 - S11.
Canadian Diabetes Association. Screening for type 1 and type 2 diabetes. Canadian Journal of Diabetes . 2013:37:S 12 - S15.
McGee 5. Evidence- Based Physical Diagnosis . 3rd ed. Philadelphia: Elsevier: 2012.

Dyspnea
.
Bickley LS Szilagyi PG. Bates' Guide to Physical Examination and History Taking . 9 th ed. Philadelphia: Lippincott Williams & Wilkins: 2007.
.
Bredin M et al. Multicentre RCT of nursing intervention for breathless in patients with lung rancer. BMJ . 1999 Apr 3:318 ( 7188):901- 904.
. .
Chen J Y Chao TH Guo YL. et al. A simplified clinical model to predict pulmonary embolism ii i patients with acute dyspnea. Int Heart J. 2006:47:259 - 271 .
. . .
Kline JA Mitchell AM Kabrnel C Richman PB. Courtney DM. Clinical criteria to prevent unnecessary diagnostic testing in emergency department
patients with suspected pulmonary embolism J Thromb Haemost . 2004 Aug:2(8):1247- 1255
.
Stein PD Beemath A Malta F, et al. Clinical characteristics of patients with acute pulmonary embolism: Data from PIOPEDII. Am J Med. 2007:120
871- 879.
McGee S. Evidence- Based Physical Diagnosis. 3rd ed. Philadelphia: Elsevier: 2012:283-287
The Merck Manual of Diagnosis and Therapy . 19thed. http://online.statref.com [ internet ]. New Jersey: Merck Sharp & DohmeCorp; 2011. Accessed
10/ 25 / 2012.
Hoellerich VL. Wigton RS. Diagnosing pulmonary embolism using clinical findings. Arch Intern Med. 1986:1 16: 1699 1704.
/

Falls
Fuller GF. Falls in the elderly. Am Fam Physician. 2000:61( 7):2159- 2174.
.
Simel DL. Ganz DA. Bao Y Shekcllc PG. Rubenstein LZ. Falls, older adults. In Simel DL. Rennie D. eds. The Rational Clinical Examination: Evidence - Based
Clinical Diagnosis. New Yo'k.: McGraw - Hill; 2C09.
Van Voast Moncada L. Managment of falls in cider persons: A prescription for prevention. Am Fam Physician. 2011:84:1267 - 1277.
UpToDate: Falls in Older Persons: Risk Factors and Patient Evaluation. 2018. Available from http:// www.uptodate.com
Hui D. Approach to Internal Medicine: A Resource Book for Clinical Practice. 3rd ed. New York: Sr ringer: 2011.

Gait Disturbance
Allanl.M. Ballard CG. Burn DJ. Kenny RA. Prevalence and severity of gait disorders in Alzheimer 's and non - Alzheimer 's dementia. J Am Geriatr Soc.
2005;53:1681- 1687.
Salzman B. Gait and balance disorders in older adults. Am Fam Physician. 2010:82:61- 68.
McGee S. Evidence- Based Physical Diagnosis. 3rd ed. Philadelphia: Elsevier ; 2012:619 - 623.
.
Alxlo WF Bonn GF. Munncke M. et al. Ten steps to identify atypical parkinsonism. J Neurol Neurosurg Psych. 2006:77:1367- 1369.

Hearing Loss & Deafness


.
ACP PIER & AHFS Dl. Essentials: Hearing Loss, http://online statref.com. Posted: 04 /25/ 2012: Accessed: 10/ 24/ 2012.
.
Hay WW. Levin M J Sondheimer JM. Deterding RR . Current Diagnosis & Treatment Pediatrics. 19th ed. New York: McGraw-Hill: 2009.

253 Edmonton Manual of Common Clir


Stankievvicz JA. Mowry HJ.Clinical accuracy of tuning fork tests. Laryngoscope. 1979;89:1956- 1973.
Burkey JM. Lippy WH. Schuring AG. Rizer FM. Clinical utility of the 512- Hz Rinne tuning fork test Am J Otol . 1998:19(l):59 - 62.
Chole RA. Cook GB. The Rinne test for conductive deafness: A critical reappraisal.Arch Otolaryngol Head Neck Surg. 1988:114:399- 403.
Stachler RJ. et al. Clinical practice guideline: Sudden hearing loss. Otolaryngol Head Neck Surg. 2012: 146:S 1- S 35.
McGee S. Evidence - Based Physical Diagnosis. 3rd ed. Philadelphia: Elsevier; 2012:186 - 191.
UpToDate: Etiology of Hearing Loss in Adults. 2010. Available from: http://wvvw.uptodate com.
Up IoDate: Evaluation of Hearing Loss in Adults. 2010. Available from: http://wvAV.uptodate.com
'

Hematologic Malignancies
Woodford. Curtis and Yao. Christopher. The Toronto Notes 2013 : Comprehensive Medical Reference and Review for the Medical Council of Canada Qualifying
Exam Part 1 and the United States Medical Licensing Exam Step 2.29th edition / Toronto: Toronto Medical Notes for Students Inc. 2013.
Hui. David. Alexander A Leung, and Raj Padwal. Approach to Internal Medicine : a Resource Book for Clinical Practice. Fourth edition, substantially updated.
Cham: Springer. 2016.
Zhu. Nancy. Approach to Hematologic Neoplasmsand Bone Marrow Disorders. Rotating Hematology Residents' Teaching. 4 Jan 2016. University of Alberta
.
Hospital Edmonton. Alberta. Canada.
. .
. .
Peters Anthea. Lymphoprolifcrative Disorders. Rotating Hematology Residents' Teaching 7 Jan 2016. University of Alberta Hospital. Edmonton Alberta
Canada.
Hemiplegia/Hemisensory Loss
American College of Physicians. ACP PIER & AHFSDI Essentials: Stroke and Transient Ischemic Attack.
Bcnavente O. Hart RG. Stroke: Part II. Management of acute ischemic stroke. AAFP. 1999 May 15:59( 10):2828 - 2834.
.
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 pat ents suspected of having mild unilateral cerebral lesions. Can J Neurol Sci .
2002:29:337- 344.
NIH Stroke Scale. www.ninds.nih.gov/doctors/NIH _ Stroke _Scale.pdf
Anderson NE. Mason DF. Fink JN. et al. Detection of focal cerebral hemisphere lesions using the neurologic examinat ion. J Neurol Neurosurg Psychiatry.
2005:76:545- 549.
.
Sawyer RN. Hanna JP. Ruff RL Leigh RJ. Asymmetry of forearm rolling as a sign of unilateral cerebral dysfunction. Ncuro/cyy. 1993:43:1596 - 1598.
McGee S. Evidence - Based Physical Diagnosis . 3rd ed. Philadelphia: Elsevier: 2012:550 - 566.
2 =r
(D

Hemoptysis
-
Q 0)

Bidwell JL. Pachner RW. Hemoptysis: Diagnosisand management. Am Fam Phys. 2005:72( 7):1253- 1260. 3 0)
Corder R. Hemoptysis. Emerg Med Clin NAm. 2003:21:421- 435. CD “
Hui D. Approach to Internal Medicine: A Resource Book for Clinical Practice. 3rd ed. New York: Springer: 2011:13.
.
Knott -Craig C J. Oostuizen JG Rossouw G. Joubert JR. Barnard PM. Management and prognosis of massive hemoptysis: Recent experience with 120
patients. J Thorac Cardiovasc Surg. 1993:105:395 - 397.
.
O' Neil KM Lazarus AA. Hemoptysis: Indications for bronchoscopy. Arch Intern Med . 1991:151: 171- 174.
Weinberger. SE. Etiology and evaluation of hempotysis in adults. [ Online]. June 1.2016 [ cited July 1.2016 ]: available from: https:// wvAV.uptodate.com/
_
contents/etiology - and - evaluation - of - hemoptysis - in- adults?source= scarch result & searctrhemoptysis£< selectedTitle - 1-150

Lower Respiratory Tract Infection


Capelastegui A. Espana PP, Quintana JM. et al. Validation of a predictive rule for the management of community - acquired pneumonia. Eur Respir J.
2006:27:151- 157.
.
Fedullo AJ Swinburne AJ. Relationship of patient age to clinical features and outcome for in-hospital treatment of pneumonia. J Gerontol . 1985:40:29 - 33.
.
Starczewski AR. Allen SC Vargas E. Lye M. Clinical prognostic indices of fatality in elderly patients admitted to hospital with acute pneumonia. Age Ageing.
1988:17:181- 186.
American Thoracic Society. Guidelines for the management of adults with hospital-acquired, ventilator - acquired, and health care associated pneumonia.
American Journal of Respiratory and Critical Care Medicine. 2005:171:388 - 416.
.
Blondel - Hill E . Fryters S. Bugs & drugs: An antimicrobial / infectious disease reference. Edmonton AB: Alberta Health Services: 2012.
.
Aujesky D. Auble TE. Ycaly DM et al. Prospective comparison of three validated prediction rules for prognosis in community -acquired pneumonia. Am J
Med. 2005:118:384 - 392
Conte HA. Chen YT. Mchal W. et al. A prognostic rule for elderly patients admitted with community -acquired pneumonia. Am J Med. 1999:106:20- 28.
Melbye H. Straume B. Aasebo U. Brox J. The diagnosis of adult pneumonia in general practice. Scand J Prim Health Care. 1988:6:111-117.
Hessen MT. Thompson A. Murphy P. Pearson RL. Community - acquired pneumonia in adults. MD Consult . Philadelphia: Elsevier; 2011.
Hui D. Approach to Internal Medicine: A Resource Book for Clinical Practice. 3rd ed. New York: Springer: 2012.
.
Lim WS. van der Eerden MM. Laing R et al. Defining community acquired pneumonia severity on presentation to hospital: An international derivation and
validation study. Thorax. 2003:58( 5):377 - 382.
Ananda - Rajah MR. Charles PG. Melvani S, et al. Comparing the pneumonia severity index with CURB - 65 in patients admitted with community acquired
pneumonia. Scand J Infect Dis. 2007:40:293 - 300.
Dichr P. Wood RW, Bushyhead J et al. Prediction of pneumonia in outpatients with acute cough: A statistical approach. J Chron Dis. 1984;37 ( 3):215 - 225.
. . .
Gennis P Gallagher J Falvo C et al. Clinical criteria for the detection of pneumonia in adults: Guidelines for ordering chest roentgenograms in the
emergency department. J Emerg Med . 1989:7:263- 268.
Heckerling PS. Tape TG. Wigton RS. et al. Clinical prediction rule for pulmonary infiltrates. Arm Intern Med. 1990;113:664 - 670.
McGee S. Evidence - Based Physical Diagnosis. 3rd ed. Philadelphia: Elsevier: 2012:271- 276.
Lim WS. Macfarlane JT. Boswell TC. et al. Study of community acquired pneumonia aetiology ( SCAPA) in adults admitted to hospital: implications for
management guidelines. Thorax. 2011:56:296- 301.

Monoarticular Joint Pain


.
Kocher MS Mandinga R. Zurakowski D. Barnewolt C. Kasser JR. Validation of clinical prediction for the differentiation between septic arthritis and
transient synovitis of the hip in children. J Bone Joint Surg Am. 2004:86( A8):1629 - 1635.
Margaretten ME. Kohlwes J. Moore D. Bent S. Docs this adult patient have septic arthritis? JAMA. 2007:297 ( 13 ):1478 - 1488.
Mathews CJ, Weston VC, Jones A. Field M. Coakley G. Bacterial septic arthritis in adults. Lancet. 2010:375( 9717):846 - 855.
Rott KT. Agudelo CA. Gout . JAMA . 2003:289:2857 - 2860.
.
Hui D, Approach to Internal Medicine: A Resource Book for Clinical Practice. 3rd ed New York: Springer; 2011:273 - 276.

Obstructive Lung Disease


ATS Documents: Statements. Guidelines & Reports [ Internet ]. New York: American Thoracic Society; 2009. [cited 2009 Nov 23 ]. Available from http://
www. thoracic.org/sections /publications/statements/index.html.
Cclli BR. MacNee W. ATS/ ERS Task Force. Standards for the diagnosis and treatment of patients with COPD: A summary of the ATS/ERS position paper.
Eur Respir J. 2004 Jun:23(6):932-946.
.
Lougheed MD. Leniere C. Ducharme FM. Licskai C Dell SD. Rowe BH. et al. Canadian thoracic society 2012 guideline update: diagnosis and

Edmonton Manual of Common Clinical Scenarios 254


management
of asthma in preschoolers, children and adults: executive summary. Can Respir J. 2012:19 ( 6 :e-81- 8.
.
O'Donnell DE et at. CTS recommendations for management of COPD: 2008 update: Highlights for primary care. Can Respir J . 2008:15 Suppl A.
.
Pellegrino R. et al. Interpretative strategies for lung function tests. Eur Respir J 2005 Nov;26( 5 ):948- 968.
Straus SE.McAlister FA. Sackett DL. Deeks J J. The accuracy of patient history, wheezing, and laryngeal measurements in diagnosing obstructive airway
disease. JAMA. 2000:283:1853- 1857.
.
Simel DL. Update: Chronic obstructive airways disease. In Simel DL. Rennie D eds. The Rational Clinical Examination: Evidence- Based Clinical Diagnosis.
New York: McGraw - Hill: 2009.
McGee S. Evidence- Based Physical Diagnosis. 4 th ed. Philadelphia: Elsevier: 2017.
From the Global Strategy for the Diagnosis. Management and Prevention of COPD. Global nitiative for Chronic Obstructive Lung Disease ( GOLD) 2017.
Available from: https://goldcopd.org.

Palpitations & Arrhythmias


.
Bollinger BC. Heidenreich J. Chapter 33: Cardiac arrhythmias. In Stone CK Humphries RL. -ids. Current Diagnosis & Treatment Emergency Medicine. 6th ed.
New York: McGraw - Hill: 2008. http://www.accessmedicine.com.login.czproxy.library.ualberta.ca/contcnt.aspx ?alD= 3107067
.
Gonzales R . Nadler PL. Chapter 2: Common symptoms. In McPhee SJ Papadakis MA. Tierney LM Jr. eds. Current Medical Diagnosis & Treatment . New
York: McGraw-Hill; 2009. http:// www.accessmedicine.com.login.ezproxy.library.ualberta.ca/ Content.aspx 7alD - 79
Hurley KF. OSCE and Clinical Skills Handbook . Toronto: Elsevier: 2005.
The Merck Manual of Diagnosis and Therapy . 19th ed. Chapter 206: Approach to the Cardiac Patient. Palpitations. 2011.

Pancreatitis
DynaMed. Acute pancreatitis. http://web.ebscohost.com.login.ezproxy.library.ualberta.ca/d\ named/detail?vid = 3&sid = 694aalc 9 -b8ee- 4776-a 564 -
del 64e2b6706%40sessonmgr 4005&hid = 4204& bdata = JnNpdGU9ZHIuYWllZClsaXZLnNjb3BIPXNpdGU%3d# db = dme& AN - 127664. Accessed
January 20, 2014.
Kim YS. Kim Y. Kim SK. Rhim H. Computed tomographic differentiation between alcoholic and gallstone pancreatitis: Significance of distribution of

_
ro c
<D
infiltration or fluid collection. World J Gastroenterology . 2006;12 ( 28):4524 - 4528.
Sabatine M. Pocket Medicine: The Massachusetts General Hospital Handbook for Internal Medicine. 4 th ed. Philadelphia: Lippincott Williams & Wilkins:
2011:2.
. . .
Park JY. Jeon TJ Ha TH Hwang JT. Sinn DH Oh TH. Shin WC. Choi WC. Bedside index for severity in acute pancreatitis: comparison with other scoring
systems in predicting severity and organ failure. Hepatobiliary & Pancreatic Diseases International. 2013:12(6 ):645 - 650.
E
0)
: =
T3
Santhi SW. Clinical manifestitations and diagrosis of acute pancreatitis. In Whitcomb DC.ec UpToDate: 2013. Available from http:// www.
uptodateonline.com. Accessed January 20.2014 .

Santhi SW. Etiolooy of acute pancreatitis. In Whitcomb DC. ed. UpToDate: 2013. Available from http:// www.uptodateonline.com. Accessed January 20 .
C
CD
2014 .
Santhi SW. Management of acute pancreatitis. In Whitcomb DC. ed. UpToDate: 2013. Availaole from http:// www.uptodateonline.com. Accessed January
20.2014.
. .
Tenner S Baillie J DeWitt J. Vege SS. American College of Gastroenterology guideline: Management of acute pancreatitis. American College of
Gastroenterology. 2013:108( 9):1400- 1415.
McGee S. Evidence- Based Physical Diagnosis. 4 th ed. Philadelphia: Elsevier ; 2017.
UpToDate: Clinical manifestations and diagnosis of acute pancreatitis. 2018. Available from http://uptodate.com
UpToDate: Management of Acute Pancreatitis. 2018. Available from http://uptodate.com

Parkinsonism
Albanese A. Colosimo C. Bentivoglio AR. et al. Multiple system atrophy presenting as parkinsonism: Clinical features and diagnostic criteria. J Neurol
Neurosurg Psychiatry . 1995:59:144 - 151.
. .
Hughes AJ Ben - Shiomo Y. Daniel SE Lees A J. What features improve the accuracy of clinical diagnosis in Parkinson's disease: A dinicopathologic study.
Neurology . 1992:42:1142 - 1146.
Ropper A. Samuels M. Adams and Victor ' s Principles of Neurology . 9th ed. New York: McGraw - f till: 2009.
ACP PIER & AHFS Dl Essentials: Parkinson's Disease, http: //online.statref.com.login.ezproxvlibrary.zualberta.ca/document.3sox ? fxid= 92&docid= 2721
Posted: 11/10/2009.
.
Daroff RB. Jankovic J Mazziotta JC. Pomeroy SL. Bradley ' s Neurology’ in Clinical Practice. 5 th ed. New York: Elsevier ; 2008.
.
Wenning GK. Ben- Shlomo Y Hughes A, et al. What clinical feaures are most useful to distinguish definite multiple system atrophy from Parkinson's
disease?
J Neurol Neurosurg Psychiatry . 2000:68:434 - 440.
Yamanouchi H, Nagura FI. Neurological signs and frontal white matter lesions in vascular parkinsonism: A dinicopathologic study. Stroke.
1997;28( 5):965-969.
.
Litvan I, Goetz CG. Jankovic J et al. What is the accuracy of the clinical diagnosis of multiple system atrophy? A dinicopathologic study. Arch Neurol .
1997:54:937- 944.
.
Litvan I Jankovic J. Goetz CG. et al. Accuracy of clinical criteria for the diagnosis of progressive supranuclear palsy (Steele - Richardson- Olszewski
syndrome). Neurology. 1996:46:922 - 930.
Winikates J, Jankovic J. Clinical correlates of vascular parkinsonism. Arch Neurol. 1999:56:98 - 102.
Demirkiran M. Bozdemir H. Sarica Y. Vascular parkinsonism: A distinct, heterogeneous clinical entity. Acta Neurol Scand . 2001;104:63- 67.
.
Rao G. Fisch L et al. Does this patient have Parkinson disease? JAMA. 2003:289:347 - 353.
McGee S. Evidence- Based Physical Diagnosis. 3rd ed. Philadelphia: Elsevier; 2012.
UpToDate: Diagnosis and Differential Diagnosis of Parkinson disease. 2018. Available from https://uptodate.com

Peripheral Vascular Disease


Hiatt WR. Medical treatment of peripheral arterial disease and claudication. N Engl J Med. 2001 May 24:344( 21):1608 - 1621.
. .
Longmore M Wilkinson IB Davidson EH, Foulkes A. Mafi AR. Oxford Handbook of Clinical Mecicine. 8 th ed. New York: Oxford University Press; 2010.
Olin JW. Sealove BA. Peripheral artery disease: Current insight into the disease and its diagnosis and management. Mayo Clin Proc. 2010 Jul:85 ( 7):678-
692.
McGee S. Evidence - Based Physical Diagnosis. 3rd ed. Philadelphia: Elsevier; 2012:459- 465.

Pleural Effusion
Liight RW. MacGregor Ml. Luchsinger PC. Ball WC. Pleural effusions: the diagnostic separationof transudates and exudates. Ann Intern Med .
1972:77:507- 513.
Light RW. Pleural effusion due to pulmonary emboli. Curr Opin Pulm Med. 2001:7:198 - 201.
Light RW. Pleural effusions. Med Clin N Am. 2011:895:1055-1070.

. -
Maskell NA. Butland RJA. BTS guidelines for the investigation of a unilateral pleural effusion in adults. Thorax. 2003:58(Suppl Il):ii8 iil7.
Kalantri S. Joshi R. Lokhande T et al. Accuracy and reliability of physical signs in the diagnosis of pleural effusion. Respir Med . 2007:101:431- 438.
McGee S. Evidence - Based Physical Diagnosis. 3rd ed. Philadelphia: Elsevier: 2012:288 - 290.
Yataco JC. Dweik RA. Pleural effusions: Evaluation and management. ClevCIin J Med. 2005:72 ( 10):854 - 872.

255 I dmonton Manual of Common Clinical Scenario * .


Polyarticular Arthritis & Joint Pain
Felson DT. Clinical practice: Osteoarthritis of the knee. N. Engl J Med. 2006;354 ( 8):841-848.
.
Grassi W De Angelis R. Lamanna G. Cervini C. The clinical feature of rheumatoid arthritis. Eur. J Radiol. 1998;27(l):S18- 24.
Klareskog L. Catrina Al. Paget S. Rheumatoid arthritis. Lancet . 2009;373( 9664):659- 672.
O'Dell JR. Therapeutic strategies for rheumatoid arthritis. N. Engl. J Med. 2004;350( 25):2591- 2562.
Richie AM. Francis ML. Approach to polyarticular joint pain. Am Fam Physician. 2003;68:1151- 1160.

Proteinuria
Kashif W. Siddiqi N. Diner AP. Hirsh S. Proteinuria: How to evaluate an important finding. C/e Cli J Med . 2003; 70(6):535 - 547.
.
Naderi AS Reilly RF. Primary care approach to proteinuria. J Am Board Fam Med . 2008 Nov - Dec;21( 6):569- 574.
.
Wango CS Clapp WL. Proteinuria: Potential causes and approach to evaluation. Am J Med Sci . 2000;320( 3) : 188 - 194.

Pruritus
Berger TG. Dermatological disorders. In McPhee SJ. Papadakis MA. eds. Current Medical Diagnosis & Treatment . New York: McGraw - Hill: 2009.
.
Reamy BV Bunt CW. Fletcher S. A diagnostic approach to pruritus. Am Fam Physician. 2011:84( 2):195 - 202.

Renal Failure
Needham E. Management of acute renal failure.Am Fam Physician. 2005:72:1739 - 1746.
Khalil P. Murty P. Palevsky PM. The patient with acute kidney injury. Prim Care. 2008;35( 2):239 - 264.vi.

Restrictive Lung Disease


Damant R. Restrictive and Interstitial Lung Diseases. [ Lecture ], University of Alberta. Katz 1080.2011 March 30.
.
Kanaparthi L Mosenifar Z. Restrictive Lung Diseases. Emcdicine. http://emedicine.medscape.com/article /3C 1760 -overview
Hui D. Approach to Internal Medicine: A Resource Book for Clinical Practice. 4th ed. New York: Springer: 2016.

Seizures
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>
.
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.
.
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.
. .
Peitzman A Harbrecht B. Billiar T. Chapter 4: Shock. In Brunicardi F ed. Schwartz Principles of Surgery . 8th ed. New York: McGraw Hill: 2005.
.
Tintinalli JE. Kelen GD Stapczynski JS. eds. Eme' gency Medicine: A Comprehensive Study Guide. 6 th ed. New York: McGraw- Hill: 2004.

Sleep- Disordered Breathing


. .
American Academy of Sleep Medicine. International Classification of Sleep Disorders 3rd ed. Darien IL: American Academy of Sleep Medicine: 2014 .
. . . .
Berry RB Brooks R Gamaldo CE et al.The AASM Manual for the Scoring of Sleep and Associated Events : Rules Terminology and Technical Specifications , ver.
.
2.0. Darien IL: American Academy of Sleep Medicine: 2012.
UpToDate. Clinical Presentation and Diagnosis of Obstructive Sleep Apnea in Adults .
Syncope
Cardiovascular Society Position Paper. Canadian Journal of Cardiology . 2011:27:246 - 253. [ Medline ]
Carlson MD. Grubb BP. Chapter 48: Diagnosis and management of syncope. In Fauci AS. Braunwald E. Kasper DL. Hauser SL. Longo DL. Jameson JL.
Loscalzo J. eds. Harrison' s Principles of Internal Medicine.17th ed. New York: McGraw - Hill; 2008.
. .
Carlson MD. Chapter 21: Syncope. In Fauci AS. Braunwald E. Kasper DL. Hauser SL. Longo DL Jameson JL. Loscalzo J eds. Harrison s Principles of Internal
Medicine.17th ed. New York: McGraw - Hill; 2008.
MCC Objectives Online. http: //www.mcc.ca/objecties /online/objectives.pl?lang= english& loc = obj&id = 106 - E
.
Moya A Sutton R. Ammirati F et al. Guidelines for the diagnosis and management of syncope ( version 2009): The Task Force for the Diagnosis and
Management of Syncope of the European Society of Cardiology ( ESC ). Eur Heart J. 2009 Nov;30( 21):2631- 2671. [ Medline]
-
Fuster V. O ' Rourke RA. Walsh RA. Poole - Wilson P. eds. Hurst ' s The Heart . 12 th ed. New York: McGraw Hill: 2007.
.
Sheldon RS. Carlos AM Krahn AD. et al. Standardized approaches to the investigation of syncope: Canadian Cardiovascular Society position paper. Can J
Cardiol. 2011;27(2):246- 253.
Hui D. Approach to Internal Medicine: A Resource Book for Clinical Practice. 4 th ed. New York: Springer ; 2016.
UpToDate: Syncope in Adults: Clinical Manifestations and diagnostic evaluation. 2018. Available from http://uptodate.com.

Thrombocytopenia
Bain BJ. Blood Cells: A Practical Guide. 5 th ed. Malden, MA: Wiley Blackwell; 2015.
.
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.

Unilateral Swollen Leg


.
ELy JW. Osheroff JA, Chambliss ML Ebell MH. Approach to leg edema of unclear etiology. Journal of the American Board of family Medicine. 2006 March:
19( 2):148- 160.
McGee S. Evidence - Based Physical Diagnosis. 3rd ed. Philadelphia: Elsevier: 2012:470 476.
Sterns RH. Clnical manifestations and diagnosis of deem in adults. UpToDate. Accessed Jur 113.2016.
. .
Carrier M. Lazo Langner A. Shivakumar S Tagalakis V. Zarychanski R. Solymoss S et al. Sere ening for occult cancer in unprovoked venous
*

thromboembolism. N Engl J Med. 2015:373:697 - 704.


.
Kearon C Akl EA. Ornelas J. Blaivas A, Jimerez D. Bounameaux H. et al. Antithrombotic the rapy for VT [ disease: CHEST guideline and expert panel
report. Chest . 2016:149 (2):315 - 352
Kearon C. Akl EA. Duration of anticoagulant therapy for deep vein thrombosis and pulmonary embolism. Blood . 2014;123( 12): 1794 - 1801.
Guyatt GH. Akl EA. Crowther M. Gutterman DD. Schuunemann HJ. Executive Summary: Ai itithrombotic Therapy and Prevention of Thrombosis 9th cd:
American College of Chest Physicians Evidence - Based Clinical Practice Guidelines. Chest . 1012:141( 2 Suppl):7s- 47s.
.
.
Wells PS. Anderson DR . Bormanis J et al. Value of assessment of pretest probability of doei > - vein thrombosis in clinical management. Lancet .
1997 Dec 20-27:350( 9094 ):1795 - 1798.
http://thrombosiscanada.ca/ provides great online tools for diagnosis and management of Y TE. including newer agents, updated by experts in the field. A
mobile app is also available.

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)

257 Edmonton Manual of Common Clinical So


Li STATION CONTRIBUTORS
Abdominal Exam Patricia Lee MD, Vijay Selvarajah MD. Clarence Wong MD FRCPC
Examination of the Hip Maleka Ramji MD. Christopher Gee MD. Sheny Khera MD CFPC MPH
Examination for Liver Disease Patricia Lee MD, Vijay Selvarajah MD. Clarence Wong MD FRCPC TJ
Eye Exam Scott Wong m IT
X
QJ tO
Female Genitourinary Exam Cassandra Hirt MD, Amanda Aiken MD. Jonathan Tankel MBBCh FRCSC
3n
HEENT EXAM Michael Driedger MD. Usha Ramanthan MD. George Elleker MD FRCPC
Knee Exam Babak Maghdoori MD, Khaled Al- Mansoori MD. Nadr M Jomha MD PhD FRCSC
Lymphadenopathy & Spleen Exam Todd Penney MSc MD, Henry Conter MD, Ryan Cooper MD MPH FRCPC
Neurological Exam Wallace Wee MD. Wasif Hussain MD. Jennifer McCombe MD
Precordial Exam Debraj Das MD. Olga Toleva MD. Michael Tjandrawidjaja MD. Paul W. Armstrong MD FRCPC
Respiratory Exam Darwin Wan MD. Jason Soo MD. Dilini Vethanayagam MD FRCPC
Thyroid Exam Mackenzie Lees MD, Simon Turner MD, Gordon Lees MD FRCSC

Edmonton Manual of Common Clinical Scenarios 102


Abdominal Exam
.
Tintinalli JE et al. Tintinalli 's Emergency Medicine: A Comprehensive Study Guide. 6th ed. New York : McGraw -Hill: 2004.
.
Singer AJ McCracken G. Henry MC. et al. Correlation among clinical, laboratory, and hepatobiliary scanning
03 findings in patients with suspected acute cholecystitis. Ann Emerg Med. 1996;28 ^ 3):267 - 272.
.ly/ E Arnbjornsson E. Scoring system for computer - aided diagnosis of acute appendicitis: the value of
> 03 prospective versus retrospective studies. Ann Chir Gynaecol. 1985: 74:159 - 166.
>• X
-CLC LU . . .
Fenyo G Linberg G Blind P et al. Diagnostic decision support in suspected acute appendicitis:
Validation of a simplified scoring system. Eur J Surg. 1997:163:831- 838.
.
Jahn H. Mathiesen FK. Neckelmann N et al. Comparison of clinical judgment and diagnostic ultrasonography in the
diagnosis of acute appendicitis: Experience with a score -aided diagnosis. Eur J Surg. 1997:163:433 - 443.
.
John H. Neff U Kelemen M. Appendicitis diagnosis today: Clinical and ultrasonic deductions. World J Surg. 1993:17:243 - 249.
. .
Teicher I. Landa B Cohen M et al. Scoring system to aid in diagnoses of appendicitis. Ann Surg. 1982:198:753 - 759.
. .
Fernandez JAN Lopez PJT, J Montes JAR Cara MAL. Validity of tests performed to diagnose acute abdominal pain
in patients admitted at an emergency department. Rev Esp Enferm Dig ( Madrid). 2001;101( 9):610- 618.
. .
Golledge J Toms AP. Franklin I J et al. Assessment of peritonism in appendicitis. Ann R Coll Surg Engl. 1996:78:11- 14.
. .
Dixon JM Elton RA. Rainey JB Macleod DAD. Rectal examination in patients with pain in
the right lower quadrant of the abdomen. Br Med J. 1991:302:386- 388.
. . .
Izbicki JR Knoefel WT Wilker DK et al. Accurate diagnosis of acute appendicitis: A retrospective
and prospective analysis of 686 patients. Eur J Surg. 1992:158:227 - 231.
. .
Staniland JR Ditchburn J De Dombal FT. Clinical presentation of acute abdomen: Study of 600 patients. Br Med J. 1972:3:393- 398.
.
Berry J Malt RA. Appendicitis near its centenary. Ann Surg. 1984:200:567 - 575.
.
Mills LD. Mills T Foster B. Association of clinical and laboratory variables with ultrasound findings
in right upper quadrant abdominal pain. South Med J. 2005:98( 2):155 - 161.
. .
Leb ond RF Brown DD DeGowin RL. DeGowin's Diagnostic Examination. 9 th ed New York: McGraw - Hill: 2009.
.
Eskelinen M Ikonen J. Lipoponen P. Clinical diagnosis of acute appendicitis: A prospective
study of patients with acute abdominal pain. Theor Surg. 1992;7:81- 85.
. .
Alshehri MY Ibrahim A Abuaisha N. et al. Value of rebound tenderness in acute appendicitis. East Afr Med J. 1995:72(8):504 - 507.
.
Adedeji OA McAdam WA. Murphy 's sign, acute cholecystitis and elderly people. J R Coll Surg Engl.1996:41:88 - 89.
. .
Andersson RE Hugander AP Ghazi SH. et al. Diagnostic value of disease history, clinical presentation,
and inflammatory parameters of appendicitis. World J Surg. 1999:23:133- 140.
. .
Brewer RJ Golden GT, Hitch DC et al. Abdominal pain: An analysis of 1000 consecutive cases
in a university hospital emergency room. Am J Surg. 1976:131:219 - 223.
.
Lane R Grabham J. A useful sign for the diagnosis of peritoneal irritation in the right iliac fossa. Ann R Coll Surg Engl. 1997:79:128- 129.
McGee S. Evidence- Based Physical Diagnosis. 3rd ed. zPhiladelphia: Elsevier: 2012:441- 452.
. . .
Simel DL Rennie D. Appendicitis Adult. In Simel DL. Rennie D eds. The Rational Clinical Examination: Evidence-Based Clinical Diagnosis.
New York: McGraw - Hill: 2009.

Blood Pressure Measurement


LeBlond RF. Brown DD. DeGowin RL. Chapter 4: VS. Anthropometric Data, and Pain.
LeBlond RF. Brown DD. DeGowin RL. DeGowin's Diagnostic Examination. 9th ed http:/Avww.
accessmedicine.com.login.ezproxy.library.ualberta.ca/content.aspx ?alD = 3658971.google
Canadian Hypertension Education Program Recommended technique for measuring blood pressure (Internet ] Blood Pressure Canada,
(updated 2010, accessed 2010 Sept . 5 ]. Available from: http://hypertension.ca/chep/recommendation - tables/ # tablel

Cranial Nerve Exam


DeMeyer W. Technique of the Neurological Examination. 5 th ed. New York: McGraw Hill: 2003.
.
Federman DD Nabel EG. ACP MEDICINE : Neurology (VI. Neoplastic Disorders). New York : McGraw - Hill; 2009.
Hohol MJ. The Neurological Exam: Cranial Nerves. Toronto: University of Toronto, http://neuroexam.rned.utoronto.ca/
.
Bickley LS Szilagyi PG. Bates Guide to Physical Examination and History Taking. 9th ed. Philadelphia: Lippincott Williams & Wilkins; 2007.
'

Diabetic Foot Exam


Caradian Diabetes Association. Canadian Diabetes Association 2008 Clinical Practice Guidelines for the
prevention and management of diabetes in Canada. Canadian Journal of Diabetes. 2008:32.
.
Armstrong DG Lavery LA Figure adapted from Diabetic Foot Ulcers: Prevention. Diagnosis
and Classification. Am Fam Physician. 1998 Mar 15: 57( 6):1325 - 1332.

103 Edmonton Manual of Common Clinical Scenarios


Examination for Liver Disease
. .
Simel DL .Halvorsen RA .Feussner JR. Quantitating bedside diagnosis: Clinical evaluation of ascites. J Gen Intern Med. 1998:3:423 - 428.
. .
Cattau EL Benjamin 5B. Knuff TE Castell DO. The accuracy of the physical examination
in the diagnosis of suspected ascites. JAMA. 1982:247:1164- 1166. TD
m zr
.
Greenburger J. Current Diagnosis and Treatment: Gastroenterology Hepatology and Endoscopy. 3rd ed. New York: McGraw Hill; 2009. x<
. .
Cummings S Papadakis M Melnick J etal. The predictive value of physical examination for ascites. West J Med. 1985;142:633 - 636.
. 0) l/>
3 fi
McGee S. Evidence - Based Physical Diagnosis. 3rd ed. Elsevier: 2012:428 - 440. O )

Figure for caput medusa adapted from East Tennessee State University Medical Mysteries http://www.etsu.edu/com/medicalmyste'y/
CAPUTMEDUSA.aspx

Examination of the Hip


. .
Brooks AG Redmond J Domb BG. Hip Diagnosis and Decision Making. In DeLee, Drez. eds. Orthopaedic
.
Sports Medicine: Expert Consult - Online By Mark D. Miller Stephen R. Thompson .
.
DeGowin’s Diagnostic Examination 9th ed. Chapter 13. The Spine. Pelvis and Extremities.
Fernando Checo. Mark Shekhman. Alex Goldstein, and Andrew S. Erwteman. Hip and Thigh in " Musculoskeletal
.
Emergencies" By Bruce D. Browner Robert P. Fuller. Elsevier Health Sciences Sep 7.2012. .
.
McPhee SJ Papadakis MA. Current Medical Diagnosis and Treatment 2010.49 th ed. New York: McGraw - Hill; 2009.
. . .
Lincoln M McSheffrey G Tran C Wong D. eds. Essentials of Clinical Examination Handbook. 6 th ed.
.
Toronto: The Medical Society Faculty of Medicine University of Toronto; 2010. .
Margo K Drezner J Motzkin D. Evaluation and management of hip pain: An algorithmic approach. J Fam Pract . 2003;52( 8):607 - 619.
. .
Eye Exam
Jason DR. 8 Point Eye Exam ( online). 2017 (cited March 16 th. 2018 ); available from https://www.aao.org/
,

young-ophthalmologists/yo-info/article/how- to- conduct -eight -point - ophthalmology- exam


Netter FH. Atlas of Human Anatomy. 6 th ed. Philadelphia: Elsevier /Saunders: 2014

Female Genitourinary Exam


.
Edelman A et al. Pelvic Examination. New England Journal of Medicine. 2007;356:e 26.

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.
.
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 .
.
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.

Lymphadenopathy & Spleen Exam


. .
Grover SA Barkun AN Sackett DL. The rational clinical examination. Does this patient
have splenomegaly? JAMA. 1993 Nov 10:270( 18): 2218 - 2221.
. . .
LeBlond RF Brown DD. DeGowin RL. Chapter 5: Non- Regicnal Systems and Dzs. In LeBlond RF Brown DD DeGowin RL eds. DeGowin’s .
Diagnostic Examination. 9 th ed: http:// www.accessmedicine.com.login.ezproxy.library.ualberta.ca/content.aspx ?alD = 3659310
Edmonton Manual of Common Clinical Scenarios 104
Hui D. Padwal R. eds. Approach to Internal Medicine: A Practical Guide to Clinical Problem Solving. 2nd ed.
.
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.
McGee S. In Evidence-based Physical Diagnosis. 3rd ed. Philadelphia: Elsevier/Saunders: 2012:215 - 226.
Additional information - from Stanford 25 videos online - Dr. Saul Rosenberg http://stanfordmedicine25.stanford.edu/ the 25/ lymph.ht ml
. .
Figure adapted from Evaluation of peripheral lymphadenopathy in adults Uptodate Author Robert H Fletcher

03 Male Genitourinary Exam


.a E03 Orient JM. Sapira's Art and Science of Bedside Diagnosis. 4 th ed. Wolters Kluwer / Lippincott Williams and Wilkins: 2010.
>X
JC LU Eyre RC. Evaluation of nonacute scrotal conditions in adults. Uptodate.
CL

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.
.
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
.
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.
. .
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
,

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.
Hurley K. Cardiovascular system. In OSCE and Clinical Skills Handbook. 2nd ed. Toronto: Elsevier /Saunders; 2011.
McGee S. Palpation of the heart and auscultation of the heart. In Evidence -based
Physical Diagnosis. 3rd ed. Philadelphia: Elsevier / Saunders: 2012.
Orient . JM. Precordial examination. In Sapira's Art and Science of Bedside Diagnosis. 4 th ed. Philadelphia: Lippincott
Williams & Wilkins; 2009.
.
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
Examination, p. 12.

Respiratory Exam
Bickley LS. Hoekelman RA. Bates ' Guide to Physical Examination and History Taking.
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
.
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.

105 Edmonton Manual of Common Clinical Sconar IOS


5 OBSTETRICS & GYNECOLOGY
Introduction 260
Amenorrhea 261
Antepartum Care 263
Antepartum Hemmorrhage 265
Contraception 267
Dysmenorrhea & PMS 269
Dyspareunia 271
Fetal Distress 273
Fetal Growth Disorders 275
Flirsutism 277
Hypertension in Pregnancy 279
Infertility 281
Interpretation of Fetal Heart Rate 283
Intrapartum Care 285
Menopause 287
^ S>
u o Pap Test 289
H O
u
0 0 Pelvic Mass 291
U c
)
.n > Pelvic Organ Prolapse 293
Q <J
Pelvic Pain 295
Postpartum Complications 297
Post Term Pregnancy Complications 299
Pregnancy Loss 301
Preterm Labor 303
Vaginal Bleeding 305
Vaginal Discharge 307
Station Contributors 309
References 310

Staff Section Editor


Rahim Janmohamed MD FRCSC
Department of Obstetrics & Gynecology
University of Alberta

259 Edmonton Manual of Common Climca


INTRODUCTION
Sujata Chandra MD FRCSC

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
<3 cr
=
<D
n rt>
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)

HYPOTHALAMUS • Anorexia/stress/systemic illness /excessive exercise ( functional)


• Tumor, injury, drugs, infection
• Kallman’s syndrome (congenital absence of GnRH)

PITUITARY • Tumor (prolactinoma, acromegaly )


• Hypopituitarism(Sheehan’ssyndrome/postpartumpituitarynecrosis,emptysellasyndrome.pituitaryirradiation
or infection)
OVARIES, UTERUS • PCOS
• Premature ovarian insufficiency, (idiopathic, infection, radiation, chemotherapy, Turner’s syndrome
FMR 1 gene mutation)
. Fragile X/
• Anatomical (e.g., Asherman' s. imperforate hymen, mullerian agenesis)
• Menopause
• Asherman’s (intrauterine adhesions 2 o to trauma /surgery)

. .
OTHER • Hypothyroidism Cushing's, non-classical CAH 17 hydroxylase deficiency, androgen insensitivity
2u O$ • Androgen secreting tumor ( adrenal or ovarian)
• Androgen insensitivity syndrome
o
«
in C
8
oo>-
X)
ID • Patient ’s name, age

CC • Primary or secondary amenorrhea


HPI • Signs of pregnancy: Wt gain, nausea, mood changes, moliminal symptoms
• Sexual development: age at thelarche, development of axillary /pubic hair, sweat glands, growth spurt
. . . .
• Menstrual Hx:ageatmenarche lengthof cycle lengthofmenses LMP cyclicdysmenorrhea,menorrhagia,PMS/
moliminal symptoms, regularity
• Symptoms of athletic female triad: diet, exercise, recent Wt gain or loss, change in body habitus, psychological
stress
• Signs of hypoestrogenism ( primary ovarian insufficiency or menopause): hot flashes, night sweats, mood
changes, vaginal dryness, word finding difficulties, early morning awakenings
.
• Hyperandrogenism symptoms: hirsuitism androgenic alopecia, acne
• Signs of pituitary adenoma (including prolactinoma): galactorrhea, headaches, visual changes
• Symptoms of thyroid/Cushing' s syndrome

.
• Sexual Hx ( vaginal intercourse), contraception, dyspareunia STI Hx, possibility of pregnancy, sexual abuse

RED FLAGS • Virilization, visual field changes, headache


PMHX .
• Radiation, chemotherapy, neonatal Hx (congenital adrenal hyperplasia), thyroid Dx Cushing’s

PSHX • Pelvic surgery . .


and/or trauma: hysterectomy, oophorectomy D&C therapeutic abortion PPH .
.
PO&GHX • GTPAL Pap Hx, menstrual Hx, obstetrical Hx STI Hx .
• Reproductive Hx: problems with infertility
• Obstetrical Hx: breastfeeding, failure to lactate

. . .
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

261 Edmontc al of Comi


PHYSICAL
General Approach
• . . .
VS (BP HR RR. Temp. Sa02) height, weight BMI .
• Degree of sexual maturity (Tanner Staging)
Inspection
• Hyperandrogenism: hirsutism, acne, androgenic alopecia
.
> PCOS ( Acanthosis nigricans, acrochodons) androgen secreting tumour Cushing’s CAH . .
.
• Stigmata of Cushing's: dorsal fat pad moon face, purple striae, large abdomen
• Stigmata of Turner 's: short stature, shield chest, webbed neck, wide spread nipples
• Anorexia (increased lanugo, bradycardia, hypotension, fixation with Wt and fear of Wt gain)
Thyroid Exam
Breast Exam
• Tanner staging, galactorrhea
Abdominal Exam
• Masses, tenderness
Pelvic Exam ( speculum and bimanual)
. . .
• Externalgenitalia clitoromegaly imperforatehymen patentvagina transversevaginalseptum
mucous, adnexal pathology, masses, presence of uterus
. .vaginalatrophy.cervicalstenosis,cervical
Visual Field Testing (pituitary adenoma)
INVESTIGATIONS
Blood Work
. . . .
• CBC lytes Cr BUN glucose, liver panel (to r /o chronic Dz)
. . .
LH 17-OH-progesterone
• Sex hormones: B - HCG, estradiol FSH
.
• Other: TSH PRL
Radiology/ lmaging oo
.
• Transvaginal U/ S ( to ax uterus, cervix, vagina, ovaries) . MRI pelvis (if concern re: mullerian agensis)
• MRI head ifthere are signs of intracranial pathology or prolactinoma 8O -2-
t
.
• Hysterosalpingogram, sonohysterogram hysteroscopy if suspect uterine malformation or adhesions op
Special Tests
.
• Testosterone DHEA - S (if hyperandrogenism)
• Progesterone challenge test
> withdrawal bleed = adequate estrogen, patent outflow tract
> no withdrawal bleed = uterine/vaginal defect, inadequate estrogen, high androgens
. . . . .
• Karyotype: r /o Turner's ( 46, X ), can r /o AIS ( 46 XY) mullerian agenesis (46 XX ) gonadal dysgenesis (46 XY or XX ) FMR1Gene testing .
• 24 hr urine cortisol or dexamethasone suppression test (Cushing’s )
TREATMENT
’Treat according to the underlying cause of the amenorrhea, desire for fertility, and to prevent complications.
General: Wt increase/decrease, exercise control, adequate diet and nutrition, stop causative medications
Medical
• Hormonal: to normalize cycle, reduce symptoms of hypoestrogenism (OCP/ HRT) , prevent endometrial ca (progestin), fertility
(induce ovulation via clomiphene citrate /aromatase inhibitor, etc.)
• Underlying causes example:
.
> PCOS: OCP/IUD ( to prevent endometrial hyperplasia), control for dyslipidemia / diabetes CVD risk Wt loss, clomiphine citrate
( fertility)
.
> Hypothyroidism: synthroid
. .
• Prevent risks associated with low estrogen: osteoporosis ( Vitamin D calcium) CVD (e.g. statin for dyslipidemia) .
Surgical: correct anatomical abnormalities (e.g., imperforate hymen - hymenotomy)
Follow - up regarding associated complaints and risk factors
.
• Infertility, hirsutism, endometrial hyperplasia Wt decrease, osteoporosis, DM, heart disease . HTN. hyperlipidemia, metabolic
syndrome, smoking cessation, mental illness
Referrals ( as needed) to:
. .
• Endocrinology Obstetrics/Gynecology Neurosurgery. Psychiatry, Pediatric Gynecology

i.- dmonton Manual of Common Clinical Scenarios 262


ANTEPARTUM CARE
Current Author Cassandra Hirt -Walsh MD

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

263 Edmonton Manual of Co:


PHYSICAL
General Approach - Initial visit requires a complete PE
Expected Weight Gain by Starting BMI
•Measure baseline BMI
. .
• BP, HR, HEENT breast RESP, CV, abdo, reflexes, varicosities /extremities, BMI < 18.5: 12.5 -18kg
perineal/pelvic exam BMI 18.6 - 24.9: 11.5 -16kg
General Approach - Subsequent prenatal visits BMI 25 - 29.9: 7- 11.5kg
> Measure Wt and BP (expected Wt gain varies based on starting BMI)
BMI > 30: 5 - 9kg
• SFH: pubic symphysis to uterine fundus ( ± 2 cm of GA at 20 - 40 wks), plot SFH
on prenatal growth curve
28- 32 wks): Leopold’s Maneuvers to determine lie/presentation of fetus, confirm presentation of fetus at
• Fetal position (starting at
36 weeks
• Determine FHR (starting at 12 wks) using Doppler U/S
• Cervical exam at 37 weeks in case require IOL ( to decrease incidence of IOL for Post Dates Pregnancy)
NOTE: Do not do a digital vaginal exam in a pregnant woman with vaginal bleeding without an U/S to confirm the position of the
placenta (rule out placenta previa).
[INVESTIGATIONS
Blood Work
Confirmation of pregnancy: serum p - HCG

Initial visit ( 6-10 wks):

. . . .
> Routine: CBC, ABO/ Rh, blood antibodies HBsAg syphilis serology HIV serology, rubella titre varicella immune status U/S to .
assess fetal anatomy 18- 22 wks
> Patient choice: explain maternal aneuploidy screening options (to be offered to ALL patients regardless of age or baseline risk ):
1. First Trimester Combined Screening and NT at 11- 13 wks (NT, p- HCG, and PAPP-A) followed by T2 maternal serum AFP
2. QUAD screen at 15 - 20+ 6 wks (unconjugated estriol, p - HCG + inhibin A, AFP)
3. NIPT at 9+ wks ( maternal serum)
* Funding depends on location, and is designed to detect T 21 Vaccine Safety in Pregnancy
• Subsequent prenatal visits: Recommend give routine to all:
> 24 - 28 wks: CBC, gestational DM screen • Inactivated Influenza Season Flu CIO
• DTaP (vaccinate between 27 - 36 weeks) in
Radiology/ lmaging - U/S each pregnancy
0_ "
• 7 - 12 wks: dating U/ S, viability, intrauterine pregnancy, GTN, multiples
• 11-16 wks: FTCS- NT if appropriate
Safe and give if required: 8 2.*
• Hep A O <">
• 18 - 22 wks: routine for fetal anatomy and growth, placental position, • HepB
multiple gestations • Meningococcal ( polysaccharide or conjugate)

Special Tests • Pneumococcal


. .
• Initial visit: urine R&M, C & S Pap test (if needed ) Urine NAAT G/C Contraindicated (but give post partum if
required):
• Subsequent visits: urine dipstick for protein/glucose
• 35 - 37 wks: GBS vaginal/anal swab
. HPV
• MMR
• Additional screening based on ethnicity

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)

Ldmonton Manual of Common Clinical Scenarios 264


ANTEPARTUM HEMORRHAGE
Current Authors Cassandra Hirt -Walsh MD

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
JO >
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

RED FLAGS • Abd pain • Absence or decrease of FM


• Amenorrhea and +BHCG • Abd pain
• Vaginal spotting • Large bleed with maternal hemodynamic instability

PMHX • APLAS
• DM
PSHX • Previous abd or pelvic surgery • CS, abd, pelvic, or cervical surgery

POHX & GHX • Previous ectopic pregnancy • Placental abruption


• Recurrent pregnancy loss • Preterm birth
• Infertility • Placenta location this pregnancy
• Tubal disease • Previous bleeds this pregnancy
. Previous PID/STI • GHTN or pre -eclampsia
• Abn Pap test • Multifetal gestations
• Oligohydramnios/polyhydramnios
• PPROM

MEDS/ALLERGIES • Routine

265 Edmonton Manual of Commc


FHX • Recurrent pregnancy loss • Bleeding disorders

• 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

L REATMENT AND COMPLICATIONS


Placental Abruption Maternal Fetal
• No identifiable treatment options for idiopathic abruption Anemia Hypoxia and non
prevention or therapy
Complications • •
• Shock reasurring fetal
• Monitor for fetal growth and wellbeing with serial ultrasounds, • Blood status
high risk to extend abruption transfusion • IUGR
.
• Recommend smoking and drug cessation BP control • PPH
• CS


Prematurity
Intrauterine fetal
• Monitor for PTL, consider antenatal steroids if risk for preterm demise
• Infection
birth high ( < 34 wks) • Renal failure

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

Manual of Common Clinical See 266


CONTRACEPTION
Current Author: Larrisa Petriw

HISTORY
ID • Patient 's name, age

CC • Patient wants to learn about contraceptive options


SEXUALHX • Previous and present use of contraception, compliance, side effects experienced
• Sexual orientation and practices
• Present and past number of partners, concurrent partners
• Current relationship (monogamous?, health, and age of partner)
(consider for very young patients and note the legal age of consent in province of practice)
• STIs present and past (consider screening for current symptoms - sores, discharge, etc.)
• Possibility of current pregnancy

PO&GHX • Age of menarche


• Menstrual cycle - length, regularity, total days, amount of bleeding
• Premenstrual symptoms PMS/ PMDD .
• Dysmenorrhea, pelvic pain, dysfunctional uterine bleeding

• Date of last Pap and pelvic exam, past abnormal Paps and gynecological procedures
• GTPAL
• Current breastfeeding
• Childbearing goals and attitude towards accidental pregnancy

RED FLAGS • Absolute and relative contraindications to combined estrogen-progesterone contraceptives,


progesterone-only contraceptives, and lUDs ( see table)
PMHX • HTN
> • Liver: cirrhosis, adenoma /hepatoma
in w> Thromboembolic disease: IHD, CVA, DVT/ PE
u O •
'C
O • Cancer: breast, uterine, ovarian

Ss • Migraines with focal neurological findings, aura

J3 £ MEDS • Note potential interactions (anticonvulsants), ATBx


OV
FHX • Cancer: breast, uterine, ovarian, liver; Hx of DVT/PE in family
SOCIAL • Smoking
• EtOH, illicit drugs

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)

267 Edmonton Manual of Common Clinical Scenar io -


FACTORS TO CONSIDER WHEN CHOOSING CONTRACEPTIVE MEASURES
Method Absolute Contraindications Pros/Cons
• Pregnancy • 99.9% efficacy
• Unexplained abnormal vaginal bleeding • Pros:
> Most effective reversible form of birth control,
• Cervical, uterine, or salpingeal infection, current lasts 5 + years
or recurrent PID or STIs in past 3 mos > Copper IUD: can be inserted for emergency
• Immediately post -septic abortion, puerperal contraception up to 7 days post -coitus
sepsis > Levonogestrel IUD: significantly improves
menorrhagia & dysmenorrhea
IUD • Cons:
• Malignant trophoblastic disease
(copper, hormonal)
• Copper allergy or Wilson’s disease (copper IUD) > Small risk of uterine perforation (0.6- 1.6/1000),
• Current breast cancer (levonoroestrel IUD) pain or dysmenorrhea. Irregular bleeding is
common in first few months (decreases over
• Severely distorted uterine cavity
time)
> Possible increased risk of PID around month of
insertion
> Small risk of expulsion (more in first year )
> Rule out ectopic pregnancy if become pregnant
with IUD
.
• Previous PE, DVT CVA, IHD/CAD • 99.9% efficacy perfect use, user failure rates 3- 8%
• Smoker > 35 y/o ( > 15 cigarettes/d) • Pros:
Non-contraceptive benefits: improved cycle
• Current breast, endometrial, or cervical cancer regulation, decreased menstrual flow, improved
• Unexplained abnormal vaginal bleeding acne, hirsutism, dysmenorrhea and perimenopausal
symptoms
• Severe cirrhosis, liver adenoma/hepatoma
Decreased risk of ovarian, endometrial,and colon
cancer, benign breast disease, fibroids, and ovarian
• Pregnancy cysts
Combined
• < 6 weeks postpartum if breastfeeding
Estrogen-Progestin • Cons:
• Uncontrolled HTN ( > 160/100) > Must take pill daily (compliance), patch/ring
Contraceptives
• Migraine headaches with aura changed less often
(OCP, ring, patch) OO
• Complicated valvular heart disease > Irregular bleeding common for first few cycles
(10- 30%): tends to improve with time <J cr
• Diabetes with retinopathy, nephropathy, or
neuropathy > Slight increase in VTE risk compared to non-
=
ft)
n fD
£
.
users highest in first year of use o -i
> Common minor side effects: nausea, breast O n
tenderness, headache OQ t/>
> Increased risk of Wt gain and mood changes -
<
* Q?
NOT supported by evidence
• Pregnancy • 99.5% efficacy perfect use, typical use: 5-10% failure
• Current breast cancer rate
Progesterone - only • Relative contraindications: acute viral hepatitis,
• Pros:
Contraceptives liver tumors > Can be used in breastfeeding women or in
patients with contraindications to estrogen -
containing OCP

‘Ensure normal blood pressure before starting OCP


Emergent
• Treat STI or PID if tests positive or high clinical index of suspicion
Treatment Options
• Discuss available methods of contraception (see table above) , risks, and contraindications
. . . .
• Discussefficacy convenience durationofaction reversibilitytimetoreturnoffertility.riskofadverseevents effectonuterinebleeding/non-
contraceptive benefits, cost, potential complications and drug interactions, and correct usage of contraception
• StartingOCP:(l) Quickstart method - patienttakesfirstpill thatday after rulingout pregnancy. Requiresbackupbarriercontraceptionforl
wk but improves compliance.( 2) Time with next cycle (first 5 days of menses) or the Sunday after menses.If started in first 5 days, no backup
necessary.
• Counsel regarding adjustment of OCP if missed pill
• Discuss need for barrier method for STI protection and encourage safe- sex practices
• IUD:ProvideRx ’nandbookappointment for insertion. Canadvisetotime with next menstrualcycleifconcernedaboutcervicalopening.but
not necessary (use dilator on insertion and NSAIDs day -of for pain). If > 7d after menses, use back -up contraceptive for 7d.
Follow - up
• If new OCP prescription, book follow - up in 3 mos
• For IUD insertions, book follow -up 4-6 wks after procedure to check strings

[ dmonton Manual of Common Clinical Scenarios 268


DYSMENORRHEA & PMS
Current Author: Sarah Wozney MD

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

DYSMENORRHEA PRIMARY (IDIOPATHIC: NO PELVIC PATHOLOGY ) SECONDARY (ORGANIC PATHOLOGY PRESENT)


• Pain beginning within a few hrs of onset of • Pain is less related to the first few days of menses, more
.
menstruation, lasting < 48-72 hrs associated with likely premenstrual or postmenstrual symptoms
change BM nausea . • Onset is usually in 30- 40 y/o age group
• Onset generally within first 2- 3 yrs of menarche • DDx:endometriosis (up to 70% of women who present
• Crampy pain strongest over lower abdomen with with chronic pelvic pain), cervical occlusion/stenosis,
radiation to inner thighs/back adenomyosis, fibroids, ovarian cyst, pelvic congestion
• Related to ovulation, recur prior to menstruation .
syndrome IBS, foreign body, infection, PID

Common Conditions
• .
PMS 1* dysmenorrhea, endometriosis
ISIMMOT
ID • Patient ’s name, age

CC • Pain with menses, mood changes, physical symptoms prior to menses


HPI • Onset, timing, and severity of symptoms, and relationship to menses ( where symptoms are cyclic)

_
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

SOCIAL • Smoking, EtOH . recreational drug use


.
• Occupation, family life, stressors Hx of abuse

.
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
*

High- frequency TENS, acupuncture, psychotherapy, heat for symptomatic Tx


2° DYSMENORRHEA • Treat .
the underlying cause as indicated GnRH analogues
• Can try treatments for 1° dysmenorrhea for symptomatic relief

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

Edmonton Manual of Common Clinical Scenarios 270


DYSPAREUNIA
Authors: Arielle Cantor MD.

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

VAGINA /VULVA/VESTIBULE URETHRAL/ BLADDER PERINEUM/ANUS PELVIS


• Inadequate lubrication • Urinary tract infection • Dermatitis • Retroverted uterus
• Vulvovaginitis or inflammitory vaginitis • Urethral diverticulum • Inflammatory bowel • Fibroids
• Dermatologic disease (lichen planus, lichen • Interstitial cystitis disease • Endometriosis /
sclerosus, psoriasis, dermatitis, herpes simplex ) • Rectocele Adenomyosis
• Postpartum dyspareunia • Episiotomy • PID
• Urogenital atrophy * • IBS
• Vaginismus • Adnexal pathology
• Localized provoked vulvodynia" • Pelvic adhesions
• Generalized vulvodynia
• Radiation
• Bartholin cyst /abscess

• 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

CC • Painful vaginal intercourse

HPI • Visible lesions, burning, itching, dryness, odor

• Use of lubricants
• Dysuria or vaginal discharge

• Urinary tract symptoms ( frequency, urgency, recurrent infection)


• Difficulty achieving entry into the vaginal cavity
• Sexual pain history (Did you have pain with your
first sexual experience? Was there a period of enjoyable intercourse?
Was the onset of pain with a specific event?)
• Characteristics of pain OPQRST
PMHX • Diabetes,atherosclerosis, autoimmune disorders,chronic pelvic pain,urinary (interstitial cystitis,urethral disorders)
or gastrointestinal conditions (IBS. constipation, IBD, diverticulitis), musculoskeletal conditions, hypertension,
psychosocial issues (depression, anxiety, trauma)
PSHX • CS. pelvic or vaginal surgery, use of mesh, female circumcision
PO&GHX • Mode of delivery, episiotomy or lacerations, breastfeeding, infertility
• Menstrual history (regularity,dysmenorrhea),menopausesymptoms, history of pelvicinfections ( candidiasis, herpes,
gonorrhea, chlamydia, PID), endometriosis,uterine fibroids, ovarian cysts, pelvic organ prolapse, retroverted uterus
MEDS .
• Pelvicradiationorchemotherapy contraception .
anticholinergicsandantihistamines(causedryness),anti -depressants,
. .
immunosuppressants/antibiotics (Candida) spermicides aromatase inhibitors GnRH agonists Tamoxifen (induce
atrophy) anti -hypertensives
ALLERGIES • Medication/environmental, atopy; note specific reaction
FHX • Anxiety, depression

SOCIAL • History of trauma or abuse


.
• Recreational drugs, EtOH smoking

271 Edmonton Manual of Common Clinical Sc


RISK • History of PID
FACTORS • Mental illness - depression, anxiety, stress
• History of sexual abuse
• Age - Peri/post - menopausal status; younger age

PHYSICAL
Complete Pelvic Exam
• Vulvar Examination
> External genitalia, perineum, perianal area, skin of groin and pubic
mons rudmdjlOfft

Inspect for ulcers, skin coloration, atrophy, erythema, thickening,


>
of cicorn
abrasions
> Gentle palpation for fissures, scarring, localized pain, masses Optrwtpof [ ttmdiMdrjl
pw«ur tfv «l duett
> Q - tip test: Assess for localized vulvodynia by using a moist cotton-
*
OCWWQCrf
tipped swab to determine if there is pain with pressure around the tortftofent gland
vestibule Vrttfeuiarfeuj
• Speculum Examination
> Evaluate the vagina for anomalies, discharge, fissures, erosions,
Vagatalcptnang '
thinning
• Bimanual and rectovaginal examination Ptnrwlfjpt
*
> Evaluate vaginal sidewalls, rectovaginal septum, cervix, uterus,
adnexa, retroversion, masses, nodularity, sensitivity
Abdomen Exam
• Inspect palpate and percuss for pain

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

• Increasing amount of foreplay, frequent vaginal intercourse


UROGENITAL • Non-hormonal treatments include moisturizers (Hyaluronic acid) and lubricants
ATROPHY • Low dose local estrogen
LOCALIZED OR • Topical lidocaine ointment or EMLA (lidocaine -prilocaine) cream applied to the vestibule before and after
GENERALIZED intercourse
PROVOKED • Physical therapy for pelvic floor muscles
VULVODYNIA

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

PLACENTAL • Placental abruption


• Placental previa .
• Vasa previa
MATERNAL • Gestational DM
• Gestation HTN/ pre - eclampsia / eclampsia
• Advanced maternal age
.
• Trauma
• Uterine rupture
• Prolonged rupture of membrane/chorioamnionitis
FETAL • Oligohydramnios .
• Polyhydramnios .
• IUGR
• Prematurity .
• Abnormal umbelical artery dopplers
• Multiple pregnancy
,< j o • loimmunization
-
J o
Sc g • TORCH infections

_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

273 Edmonton Manual of Cor


PHYSICAL
General Approach
• General appearance ( well/unwell)
• . .
Maternal VS: BP HR RR. Temp, Sp02
• FHR as per NST/EFM
Abdominal exam
• .
Previous surgical incisions, abdominal pain (note specific quadrant, ie. RUQ vs. diffuse peritonitis) Leopold maneuver cephalic
vs. breech), palpable contractions
Pelvic exam
• Sterile speculum ( pooling, blood, meconium), bimanual exam (ensure no previa prior to VE), cervical assessment (calculate Bishop
score based on extent of cervical dilation, effacement, consistency, length and head station).
INVESTIGATIONS
Blood Work
.
• CBC- D electrolytes, urea, type and screen ( if high suspicion of antepartum or postpartum hemorrhage), INR / PTT. fibrinogen (if
high suspicion of DIC), blood cultures (if high suspicion of sepsis)
• Consider pre - eclampsia workup as indicated.

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

Edmonton Mam I of Common Clinical Scenarios 274


FETAL GROWTH DISORDERS
.
Current Authors: Cindy Kao MD MSe

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)

ujD Large for Gestational Age:


o
2a MISC GENETIC MATERNAL
• Incorrect dating • Syndromes: Beckwith -Wiedemann, • Diabetes
OO • Constitutionally large baby ( tall Simpson - Bolabi- Behmel etc. . • High pre -pregnancy weight
maternal stature, proportionate growth • Race/ethnicity • Excessive weight gain
• Multiparity
• Post - term

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
*

• Fetal echocardiography if DM or suspect CV defect


• Ultrasounds to assess fetal growth in 2nd and 3rd trimesters are indicated if SFH deviates by > 2cm or risk factors for SGA/ LGA
.
• If LGA: Assess for organomegaly (e.g. Beckwith-Wiedemann)
. .
• If SGA:Serial ultrasounds to monitor BPP Dopplers (UA MCA DV) AFV . .
> Frequency depends on degree of severity

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

Edmonton Manual of Common Clinical Scenario 276


Current Authors: Cassandra Hirt MD

AREA OF HAIR GROWTH


Hirsutism: Terminal Hair Growth in Male Pattern Hypertrichosis: Non- sexual Pattern
COMMON Drugs
PCOS (85%) Ideopathic/ familial
• 2/ 3
Rotterdam Criteria: (1) polycystic ovaries on U/ S: ( 2) oligio/ Systemic illness
amenorrhea: (3) signs of hyperandrogenism
Hypothyroid
Familial
Anorexia/malnutrition
Drugs
• Anabolic steroids or Danazol
Idiopathic
• Regular menses and no increase in circulating androgens

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

277 Edmonton Manual of Common Clinical Sconan -


PHYSICAL
General Approach
. .
• VS: BP HR, RR Temp, Sp02, BMI, WC
Hyperandrogenisim
• Establish presence of hirsutism ( vs. hypertrichosis) and look for other signs of hyperandrogenism
• Temporal hair recession
HEENT
• Oily skin
• Acne, temporal hair recession, oily skin, deepened voice
• Deepened voice
• Thyroid exam
• Well - developed muscles
ABD • Clitoral enlargement
• Male pattern hair, signs of Cushing’s syndrome (striae, bruises, fat distribution) , masses • Irregular periods
GU Exam
• Clitoromegaly
MSK /DERM
• Well -developed muscles ~
• Hair growth: location ( abdomen, lip. chin, chest, back ), quality of hair, degree of rJ
hirsutism, male pattern
• Acne, acanthosis nigricans, striae, bruises, oily skin

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

Edmonton Manual of Common Clinical Scenarios 278


HYPERTENSION IN PREGNANCY
Current Authors: Gabriela Pelinska MD

IM l " ill I I lii i >


• .
Diastolic BP of > 90 mmHg based on the average of 2 measurements, taken using the same arm
• Severe HTN should be defined as a systolic BP of > 160 mmHg or a diastolic BP of > 110 mmHg
PRE-EXISTING HTN • Diagnosed before 20 wks gestation

GESTATIONAL HTN • Develops after 20 wks


WITHOUT PREECLAMPSIA • .
24hr urine protein excretion < 0.3 g/d no adverse conditions
WITH PREECLAMPSIA • With proteinuria ( 24hr urine protein excretion > 3 g/d) or one or more adverse conditions
SEVERE PREECLAMPSIA • Onset < 34 wks and proteinuria ( 3 - 5 g/d in 24hr urine) or one or more adverse conditions

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

• DBP > 110mg Hg • Oliguria (< 500 ml/24hr ) • Severe HA


• Proteinuria > 5 g/ 24hr • Elevated serum Cr • Visual disturbances

• IUGR Liver Placenta


• Intrauterine fetal death • Epigastric or RUQ pain/tenderness • Absent or reversed umbilical artery end
• Oligohydramnios . .
• Elevated AST ALT or LDH diastolic flow
• Serumalbumin < 200 g/ L • Placental abruption
•Severe N/V
HELLP • Thrombocytopenia ( PLTs < 100 x 109/L) Heart
• Pulmonary edema
• Chest pain/ SOB
y O
H O
u
Siin 5 E HISTORY
C
JD >1 ID • Patient 's name, age . .
GTPAL, GA blood type and Rh status, GBS status, EDD ( whether established by LMP or
oo .
U/S), LMP if known HIV/Hep B status
cc • HTN

HPI • Onset of HTN ( whether > 20 wks gestation)


.
• Prenatal care received, pregnancy complications U/S findings, baseline blood pressure
• Cardinal obstetric symptoms: contractions, leaking of fluid, vaginal bleeding, fetal movement
• Pain: OPQRST

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

RISK FACTORS • Demographics: maternal age < 18 or > 40 y/o, lower .


SES ethnicity: Black, South Asian
-phospholipid antibodies, heritable thrombophilias, pre - existing
• Previous preeclampsia ( 25% recurrence), anti
medical disease (HTN, renal & DM), BMI > 35, multiple pregnancy, primigravida, inter-pregnancy interval > 10
yrs, family Hx of preeclampsia, new partner

279 Edmonton Manual of Common Clinical Scena


Complications
.
• Maternal: stroke (high risk if sBP > 160 mmHg) seizure ( 2% preeclamptics get ecclampsia - 50% antepartum, 25% intrapartum, 25%
postpartum). DIC. HELLP. pulmonary edema secondary to left ventricular failure, acute kidney failure and hepatic dysfunction
• Fetal: oligohydramnios. IUGR, prematurity, stillbirth
• Placenta: abruption
PHYSICAL
General Approach
• . . . .
VS (maternal: BP HR RR Temp Sp02) and FHR
HEENT
• cranial nerve exam, fundoscopy (papilledema)
CV:
• assess heart sounds, S3/S4
RESP:
• air entry, crackles (pulmonary edema)
ABD:
• .
epigastric/RUQ pain, SFH Leopold's Maneuvers
NEURO:
• reflexes ( hyperreflexia, clonus)
DERM:
• petechiae, pitting edema
Pelvic Exam:
• external inspection, sterile speculum exam, bimanual exam, and cervical assessment
INVESTIGATIONS
Blood Work
• Hematology: CBC-D. DIC: INR & PTT fibrinogen| .
( in DIC)
• Renal: Cr and uric acid
.
• Liver: AST, ALT bilirubin, albumin no
• Hemolysis: blood film and LDH

Chemistry 8O 2ft.
• Urinalysis for proteinuria ( >0.3 g/d in a 24 hr collection or > 30 mg/mmol protein creatinine ratio) O o

• Urine dipstick of > 1+ protein is often considered a positive sign


Imaging
• Fetal monitoring: NST (baseline, variability, accelerations, number and description of decelerations)
• BPP with amniotic fluid index, estimated fetal Wt and umbilical artery Doppler for increased resistance, absent or reversed end-
diastolic flow
EATMENT
• Gestational HTN without preeclampsia: bed rest in left lateral decubitus, fetal surveillance, monitor for progression
• Severe HTN or .
preeclampsia: stabilize and deliver; maternal monitoring: NVS qlh U/O qlh, UA ql2h; type and screen; repeat
blood work q 6 - 8h; continuous fetal monitoring
.
> Treatment for HELLP: consider ordering blood products, including PLTs when PLT count is < 50 * 109/L
• Antihypertensive therapy: for sBP >160 mmHg and dBP > 110 mmHg; GOAL: for women with no comorbidities, therapy should be
used to keep sBP within 130- 155 mmHg and dBP within 80- 105 mmHg
• Anticonvulsant therapy: increases seizure threshold

> MgS04 4 g IV bolus over 20 min, then IV 1g/ hr


> Monitor for Mg toxicity| . .
^
( DTRs RR CNS depression)
> Antidote: calcium gluconate lOmL of 10% sol 'n over 10 min
• Antenatal corticosteroid treatment: for all women who present with preeclampsia before 34 wks GA

> Betamethasone: 2 doses of 12 mg IM 24 hrs apart

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

Edmonton Manual of Common Clinical Scenarios 280


INFERTILITY
Current Authors: Olivia Guerra MD

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

Q : Female (50%) 6 : Male ( 35%)


• Fallopian Tube: PID, endometriosis, adhesions, previous tubal • Sperm Production:
pregnancy, uterine anomaly, retained IUD >Pre -testicular: Kallmann, hyperprolactinemia,
• Uterus: Fibroids/polyps, Asherman' s syndrome, congenital hypothyroidism, drugs, tumor, infection, trauma,
anomalies, adenomyosis, unfavourable cervical mucous, cervical anabolic steroids
stenosis > Testicular - genetic abnormality (e.g. Klinefelter, .),..
• Ovary: cryptorchidism, varicocele, mumps orchitis, radiation,
> Low FSH: weight loss /malnutrition, excessive exercise, infection, drugs, trauma, torsion
stress /psychosis, systemic disease, hypothyroidism, • Sperm Motility: Ab from infection
hyperprolactinemia, tumors (e.g. prolactinoma) • Sperm Transport: vasectomy, CF gene mutation, post -
> Normal FSH: PCOS, obesity infectious obstruction, ejaculatory duct cyst (e.g. prostate)
Kartagener syndrome
.
> High FSH: POL Turner, premenopausal changes
• Sexual Dysfunction

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

PMHX • Thyroid disease, Cushing’s . Turner syndrome, Hx of chemotherapy/ • DM .


( possible ED) Hx of chemo/radiation,
radiation .
infections ( STIs mumps, TB), testicular
trauma
PSHX • Abdominal or pelvic surgery, especially for ruptured appendicitis (4 • Testiculartorsion not repaired within 6
chance of adhesions) or surgery for endometriosis hrs, hernia repair, vasectomy with reversal
PO&GHX • Pap Hx (cervical dysplasia)
• Hx of Cone biopsy, LEER cervicitis ( alters cervical structure or
mucous)
. .
• Previous IUD use past Hx of STIs/ PID, previous ectopic (4 risk of
tubal disease)
• Hx of fibroids, previous D& C
• Hx of abnormal anatomy

FHX • Infertility, congenital /chromosomal anomalies, miscarriages


MEDS • Pre -conception folic acid to decrease neural tube defect
ALLERGIES • Medication/environmental; note specific reaction

SOCIAL • Smoking . EtOH, drugs • Smoking .


EtOH. drugs (especially
marijuana)
• Excessive exercise or emotional stress
281 Edmonton Manual of Common Clinical Sccr
HYSICAL
$ <?
General . HR. RR, Temp. Sp02)
• VS ( BP . . .
• VSIBP HR, RR Temp Sp02)
Approach • BMI (overweight/underweight /stature) • BMI (overweight /underweight /stature)
• Hirsutism, acne, alopecia ( PCOS) • Tall, thin, gynecoid appearance ( XXY )
• Short stature, webbed neck, low hairline (Turner)

HEENT • High- arched palate, ptosis, strabismus amblyopia, • Exopthalmos (Graves )


auricles posteriorly rotated/ low set (Turner ) • Enlarged/nodular thyroid ( hypo / hyperthyroidism)
• Exopthalmos (Graves)
• Enlarged/nodular thyroid (hypo /hyperthyroidism)

Chest exam breast development, cardiac


• "Shield chest ", absent • Cardiac murmurs ( Kallmann XXY).
murmur (Turner )
• Galactorrhea (hyperprolactinemia)

Abdominal • Abdominal scars from previous surgery • Gynecomastia .


cannabis, steroids)
.
(hyperPTH hypothyroidism XXY drugs, . .
Exam • Abdominal masses or tenderness
.
• Lack of body hair ( XXY Kallmann, hypogonadism

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

M immon Clinical Scenarios


. 282
INTERPRETATION OF FETAL HEART RATE
Current Authors: Jessica Nicoll MD

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

MEDS • Insulin, metformin, antihypertensive medications, anti- coagulants, contraindicated meds


ALLERGIES • Medication/environmental: note specific reaction

FHX • Fetal or maternal RFs listed

SOCIAL • Smoking, EtOH, recreational drugs, stress

ROS • HEENT: Diabetic retinopathy, goiter


• CV: Dizziness, decreased exercise tolerance, fatigue and decreased energy

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

• GA, Hx of current • Detection of maternal pulse


pregnancy, risk factors, • Maternal movement
and stages of labor • Very active fetus
• Intrauterine death
• Fetal cardiac dysrhythmia
• Fetal position

283 Edmonton Manual of Common Clinical Scenarios


APPROACH TO FHR MONITORING
Quality of Tracing and Paper Speed
• Strip must be at least 20 min long Nadir Recovery
• Scale: small squares are 0.5 cm: Paper speed: if 1cm/min, 2 squares = 1 min
i
Uterine Activity p
1
210
Onset
• The tracing recorded below FHR (must not be in labor or is not an NST)
.
• Measures contraction duration and frequency NOT strength (palpate for strength)
i
> 30 sec - i
i
i
150
• Frequency: number of contractions in a 10 min strip ( > 5 is tachysystole)
120
• Duration: count the number of squares under the curve of the contraction i

• Pattern: note coupling/ tripling of contractions


i '
i
90
Baseline Heart Rate
60
• Definition: approximate mean FHR during a 10 min segment of tracing
• Normal: 110- 160 bpm at term; Tachycardia: > 160 bpm; Bradycardia: < 110 bpm 30

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

• Classification: early, variable, late, mixed

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

sLASSIFICATION AND TREATMENT OF NST


PARAMETER NORMAL ATYPICAL ABNORMAL
100- 110 bpm < 100 bpm or
Baseline 110- 160 bpm > 160 bpm for < 30 min > 160 bpm for > 30 min
Rising baseline Erratic Baseline
6 - 25 bpm > 25 bpm for > 10 minutes or < 5 bpm for > 80 min
Variability <5 bpm for 40 - 80 min
< 5 bpm for < 40 min Sinusoidal
< 2 in 40 - 80 min
> 2 normal accelerations < 2 in 80 min tracing
Accelerations None with fetal scalp electrode
in < 40 mins stimulation
Severe/complicated variables
Early or occasional, Variable decelerations 30- 60 s
Decelerations Late decelerations
mild variables in duration Prolonged decelerations: > 3 min

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

Edmonton Manual of Common Clinical Seenar 284


INTRAPARTUM CARE
Current Authors: Gabriela Pelinska MD

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

• Third Stage: separation and expulsion of the placenta


• Fourth Stage: first - hour postpartum (carries high risk of postpartum hemorrhage)

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

• Chorioamnionitis ( ABD pain, fever, leukocytosis) • ROM > 24 hrsatterm

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

RED FLAGS • Preterm, or post term (< 37 or > 42 wks GA) .


ROM > 24 hrs at term
.
•HTN scotomata or . . .
blurred vision, headache N/V SOB RUQ/epigastric pain, seizures|urine output .
• Vaginal bleeding in labor| .
fetal movement, multiples, breech, vaginal birth after C-section
PMHX • Medical ( HTN . DM. cardiac, renal, thyroid, asthma, connective tissue/SLE). trauma or MVA
.
PSHX • C- sections anesthetic problems, abdominal or pelvic symptoms, procedures to cervix (LEEP, Cone Bx )
POBSHX . .
C- section vacuum/ forceps),
• Previous pregnancies: date, hospital/city, GA reached, delivery type ( SVD

.
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:

EXTERNAL • Examine for edema, skin lesions, bleeding


GENITALIA
DILATATION • Use fingers to assess the diameter of the internal os (10 cm = fully dilated)
EFFACEMENT • Length of the cervix (4 cm = 0%, 0 cm = 100%)
POSITION • Relationship of presenting part to maternal pelvis (e.g., Left Occiput Anterior ( LOA))
CONSISTENCY • Soft, medium, firm

STATION • Level of presenting part in relation to ischial spines ( - 5 to + 5 ) ( - 2 = 2 cm above, 0 = spine, +2 = 2 cm


below)
FETAL • Part of the fetus at the cervical opening (e.g., breech, vertex, shoulder )
PRESENTATION
• Active first stage of labor ( dilated 3 cm if nulliparous or 4 cm if primiparous/multiparous, regular contractions)
• Use a Friedman curve (partogram) to follow labor progress and identify labor vs. dystocia (dilatation of < 0.5 cm/hr x 4 hrs during
active 1st stage or 1hr with no decent during the 2nd stage)
Special Tests
• Continuous vs. intermittent fetal heart rate monitoring (see Interpretation of Fetal Heart Rate): uterine contractions monitoring
• External fetal and uterine monitoring using tocometer (most commonly indicated) vs. internal fetal monitoring using scalp
electrode and Internal Uterine Pressure Catheter (IUPC) ClO
INVESTIGATIONS
Radiology/ lmaging
O
O
a
*
on
• U/ S: as needed to confirm fetal presentation, position of placenta, or amniotic fluid index

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

Edmonton Manual of Common Clinical Scenarios 286


Current Authors: Victoria Cook MSc MD

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)

Differential diagnosis for amenorrhea:


• Pregnancy ( 12 - HCG)
• Hypothalamic ( anorexia, nutritional deprivation, extreme stress or systemic illness, tumors)
• Pituitary tumor
• Ovarian ( PCOS, ovarian/adrenal hormone secreting tumors) POI .
Common conditions
• Normal physiologic menopause most common
HISTORY
ID • Patient ’s name, age

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

u o • Early morning awakenings, difficulty concentrating, word - finding difficulties


o
2a
W C
RED FLAGS
PMHX
• Hx of low or no-impact fractures

• 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)

PSHX • Hysterectomy, oopherectomy


PO&GHX • Age at menarche, duration of menstrual cycle
• Duration and character of previous menses, recent changes
• Premenstrual molimina

MEDS • Steroids, HRT, herbals and vitamins, dietary interventions such as soy

FHX • Age of menopause and associated symptoms in direct female relatives


• Breast cancer
SOCIAL • Married/partners? Explore impact on sexual relationships
ROS • HEENT, CV . RESP. Gl, GU. MSK/DERM
RISK • Smoking (reduces age of menopausal onset)
FACTORS

287 Edmonton Manual of Common Clinical Scenar > os


HEART MURMURS
Current Editor: Cynthia Gunaratnam BSc MD

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

innocent characteristics and lacks pathological characteristics


Innocent (The Sevens) Pathologic
Location +/-
Small area, no radiation Loudest atLUSB
Radiation
Timing Short Systolic Holosystolic, diastolic, or continuous
Intensity Soft Grade III or higher
Quality Sweet Harsh
Unchanged with position; increased with
Variation Sensitive
standing, squatting, or passive leg raise
Extra Sounds Single (no associated clicks or gallops) Extra heart sounds (e.g., abnormal S 2)

Common Conditions
Type Characteristics Age

Peripheral Pulmonary Stenosis .


LUSB radiates to axillae and back, systolic Newborns, disappears
.
ejection murmur, low -pitched Grade Ml by age 2
Aortic Flow Murmur RUSB, systolic ejection murmur Adolescents

Pulmonary Flow Murmur .


LUSB systolic ejection murmur, rough, dissonant quality,
Vi
u .
Grade II loudest supine, quiet when upright and holding breath
> 3 yrs

Supraclavicular /Brachiocephalic Supraclavicular, radiating to neck, systolic ejection Childhood to young


<u Systolic Murmur murmur, decreased with shoulder hyperextension adulthood
T3
o Venous Hum Infraclavicular, R > L, continuous hum 3 - 8 yrs
CL
.
Systolic ejection murmur, musical Grade l ll, -
Still ' s Murmur loudest supine, disappears when standing,
increased with fever, anemia, or tachycardia

Causes of Pathological Murmurs:


.
• Bacterial endocarditis: sick child, febrile 2 x positive blood cultures and a new murmur
• Pathological conditions without a murmur: transposition of the great arteries, coarctation of the aorta, hypoplastic left heart
syndrome

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

MEDS • Prescriptions, OTC, vitamins, CAM

ALLERGIES • Medication, food, environmental

IMMUNIZATIONS • Routine IUTD . special


FHX • Congenital heart disease, sudden cardiac death, hypertrophic cardiomyopathy . SIDS
SOCIAL • Financial situation, drug plan

—— —
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)

Edmonton Manual of Common Clinical Scenarios 340


IMMUNIZATIONS
VACCINE- PREVENTABLE ILLNESSES ROUTINE IMMUNIZATION SCHEDULE
IN ALBERTA
Viral AGE Immunization
• Polio (IPV, inactivated polio vaccine) 2 MOS DTaP-IPV- Hib
• Measles-Mumps - Rubella -Varicella zoster (MMRV, a live vaccine) Pneumococcal conjugate
• Hepatitis B Meningococcal conjugate
>3 doses over 6 mos; given at birth ( along with HepBIG) if maternal serology 4 MOS -
DTaP IPV- Hib
is HBsAg+ or unknown; routine schedule is in Grade 5 Pneumococcal conjugate
• Human papillomavirus Meningococcal conjugate
> Protects against HPV 16 and 18 (Gardasil and Cervarix; these cause 70%
of cervical cancer) and HPV 6 and 11 (Gardasil only; these cause 90% of
6 MOS -
DTaP IPV-Hib
Pneumococcal conjugate
anogenital warts)
> 6 MOS Influenzae (annual)
.
> 3 doses given over 6 mos approved for use in 9 - 45 y /o females and
12 MOS MMRV
9 - 26 y/o males
• Influenzae ( annual ): IM injection ( inactivated) or nasal spray ( live attenuated)
Pneumococcal conjugate
Meningococcal conjugate
Bacterial
DTaP- IPV- Hib
.
• Diptheria -Tetanus ( acellular ) Pertussis ( DTaP dTap . and Td boosters) 18 MOS
4 - 6 YRS DTaP- IPV. MMRV
• Streptococcus pneumoniae (pneumococcal conjugate)
• Haemophilus influenzae serotype B (Hib) GRADE 5 Hep B. HPV
• Neisseria meningitidis (meningococcal conjugate) GRADE 9 .
dTaP MCV4
ADULTS Td (q lOyrs)

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

PSHX • Splenectomy, organ transplant, hematopoietic stem cell transplant

-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

Risks and Side Effects of Immunizations


• Common, mild: pain, erythema, and swelling at injection site, irritability, rash, fever

> 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)

> Hx of these adverse events is NOT a contraindication for future immunizations


- .
• Rare, life threatening: anaphylaxis ( 1- 2 out of 1million) Guillain- Barre rate following influenzae vaccination may be higher than
background rate of 1additional case per million vaccinated

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

> Pneumococcus booster q 2 - 5 yrs


> Meningococcus booster q 3 - 5 yrs
> Hib booster for all asplenic patients > 5 y/o
Additional Immunizations
• Influenzae: seasonal inactivated vaccine (IM injection) or live attenuated ( nasal spray ) is recommended for all Albertans 6 mos and
older (nasal spray must not be given if anyone in the household is immunocompromised)
• Travellers
.
Consider Rabies, Typhoid Fever, Yellow Fever, Hepatitis A and Cholera ( Dukoral) vaccines
>
>Advise patient to speak to public health or travel clinic for more information
• BCG vaccine: should be given to infants of parents with infectious TB at time of delivery, high risk populations ( Aboriginal reserves),
and health care workers at risk (only given to individuals with a negative Mantoux test )
• Respiratory Syncytial Virus ( RSV) Ig ( Palivizumab): monthly IM injection recommended entering RSV season ( Nov -Apr ) for all who
are < 2 y/o with chronic lung disease, hemodynamically significant congenital heart disease, infants <1year with Down syndrome, or
premature infant < 6 mos of age (e.g., < 32 wks or ex - < 36 wks and living in a remote community); affords passive immunity

Edmonton Manual of Common Clinical Scenarios 342


LIMPING CHILD
Current Editor: Stephanie Napier MD MSc BSc

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

ID • Name, age, gender, ethnicity, home

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

PSHX • Joint repair, fractures, splenectomy


MEDS .
• Prescriptions, OTC vitamins, CAM

ALLERGIES • Medications, food, environmental

IMMUNE • Routine IUTD, immunocompromised, additional immunizations (e.g. travel)

FHX .
• RA SLE, psoriasis, IBD, hematological disorder, sickle cell, leukemia, DDH

SOCIAL • Home environment, psychosocial situation (parental neglect, abuse, sexually active)

DEVT. HX • Gross motor, fine motor, language, cognitive, personal -social


ROS • Diet /nutrition, level of activity

343 Edmonton Mdiiuol «:


PHYSICAL
.
General: ill or toxic appearing, VS ( BP, HR. RR. T Sp02), growth charts (Ht /Wt/HC)
HEENT: conjunctivitis, pallor, tonsillar exudates, mucosal lesions, lymphadenopathy. tympanic membranes, rhinitis
.
CV: new onset murmur (rheumatic fever), tachycardia CHF (myocarditis)
Gl: signs of peritonitis, hepatosplenomegaly, abdominal mass or tenderness
DERM: rashes, subcutaneous nodules, swollen hands/feet + desquamation
MSK: spine, lower extremities
• Inspection
.
Observe gait: smooth versus antalgic Trendelenburg, toe - walking, circumduction
>
Walk on toes, walk on heels, jump on one foot, inspect swing/stance, look for asymmetry
>
Examine spine: curvature, midline abnormalities
> Examine each limb: swelling, erythema, atrophy, deformity, skin changes ( bruising, scars)
Look for effusions, leg- length discrepancy, ingrown toe nails, poorly fit shoes
• Palpation

> Landmarks /anatomy, effusion, swelling, temperature, crepitus


> Pain / tenderness over tendon insertion (apophysitis), bony points (osteomyelitis, tumor ), muscle
> Presence of Baker ' s Cyst (septic arthritis)
• ROM ( active/passive)
> Back, knee, hip, spine and ankle: look for limitation, guarding, discomfort
• Special Tests
» Faber test for SI joint pathology: hip Flexion, ABduction, and External Rotation: positive if pain

» 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

Edmonton Manual of Common Clinical Scenarios 344


NEONATAL JAUNDICE
Current Editor: Menglin Yang BSc MD MSc

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

Etiology of Conjugated Hyperbilirubinemia


Hepatic Post - Hepatic
.
• Infection: TORCH, hepatitis, E. coli UTI • Biliary atresia
• Genetic/metabolic/endocrine: galactosemia, fructose intolerance, tyrosinemia . • Choledochal cyst
ul-antitrypsin deficiency, hypopituitarism, hypothyroid, neonatal hemochromatosis, • Inspissated bile/mucus: cystic fibrosis
Alagille syndrome • Spontaneous perforation of extra -hepatic
• Drugs: carbamazepine, rifampin, antiretrovirals, ABTx (ceftriaxone, sulfa) bile ducts
• Total parenteral nutrition • Tumor /mass
• Idiopathic neonatal hepatitis
• Inspissated bile/mucus: cystic fibrosis

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

HPI • Gestational age, onset, duration, evolution/progression


• Nutrition: breastfed vs . formula, amount, frequency, difficulties, vomiting. Wt loss > 10% of birth Wt
• Sleep (duration, frequency) .
high pitched cry inconsolable/temperament change, lethargy, fever
• Voids (dark urine, number of wet diapers /d), bowel movements (frequency, consistency, pale color)
RED FLAGS • Onset < 24 h after birth, prolonged ( > 1- 2 wks), pale stools, dark urine, hyper /hypotonia, dehydration
PMHX • Medical conditions: course since birth, infections
• Prenatal: prenatal care, U/S frequency, complications (GDM, HTN, infections, rash, fever ), GBS status,
exposures to toxins /teratogens (smoking/EtOH/drugs), IUGR, WinRho
• Perinatal: GA , complications of delivery, birth Wt, APGARs, asphyxia
• Postnatal: complications ( fever, shock, hypotonia, seizures), NICU, newborn metabolic screen
PSHX • Prior surgeries and any complications
. .
MAT OBS HX • GTPAL, previous pregnancies with hyperbilirubinemia, maternal fever/illness, result of mother’s ABO and Rh
(D) blood type and red cell antibody screen during pregnancy
MEDS • Prescriptions . OTC. vitamins. CAM
ALLERGIES • Medication, food, environmental

345 I dmonton Manual of Common Clinii


FHX • Consanguinity, anemia, jaundice (newborn/other age), hepatobiliary disease, G 6PD deficiency, splenectomy,
miscarriages, hemoglobinopathies, autoimmune disease, CF
SOCIAL • Primary caregiver, financial situation, drug plan

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 )

• Liver Bx (undiagnosed conjugated hyperbilirubinemia), intra -operative cholangiogram ( biliary atresia)

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

Edmonton Manual of Common Clinical Scenar 346


NEWBORN RESPIRATORY DISTRESS/CYANOSIS
DIFFERENTIAL DIAGNOSIS
• Pulmonary: transient tachypnea of the newborn (TTN) , respiratory distress syndrome ( RDS), meconium aspiratory syndrome
(MAS), pneumothorax, pneumonia, congenital upper airway obstruction, congenital pulmonary airway malformation (CPAM),
diaphragmatic hernia
Current Editor: Nikytha Antony
-
I
•Cardiac: persistent pulmonary hypertension of the newborn ( PPHN), cyanotic heart disease, acyanotic obstructive/regurgitant
lesions (not left - to-right shunts)
• Systemic/metabolic: sepsis (especially GBS), hypoglycemia, inborn errors of metabolism
• Neurologic:CN damage (hypoxic-ischemic encephalopathy, intraventricular hemorrhage), drug withdrawal

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

PPHN Normal, may see increase in hilar markings . .


Tx cause 02 correct acid-base, inhaled nitric oxide (iNO),
high frequency ventilation
CPAM Air trapping, cysts Supportive, surgery (resection)
Pneumonia Hazy/distinct infiltrates, may see pleural effusion . .
Oxygen ABTx ± vasopressors ( sepsis)
Air in the pleural space;
Pneumo - If tension: mediastinal shift away from the
Supportive Tx (02 supplementation) if mild/asym.
thorax Consider thoracentesis or chest tube if severe/ tension
pneumothorax

Congenital Cardiac Causes of Cyanosis


(Unresponsive to 02 - which can promote ductus closure)
Causes Age of symptom onset Exam Findings Treatment
co
u Tetralogy of .
25% at birth (cyanosis) 75% by lyr
Exertional dyspnea, single S2, PGE1, surgery (right ventricular
.
.
V Fallot (Tet spells/squatting FTT) . harsh SEM at LSB, (right ventricular
outflow tract obstruction)
outflow tract obstruction repair
VSD closure)
f0
TJ Transposition Cyanosis in hrs- days (as foramen Distress, other findings variable
Q)
Q. of the great ovale and ductus arteriosus close) or ( sternal heave, single S 2, ± murmur
PGE1, septostomy if no VSD .
arteries CHF in few wks if VSD present if VSD/PDA) definitive surgery ( arterial switch)

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

PSHX • Any previous surgeries, especially cardiothoracic


MEDS • Prescriptions, OTC, vitamins, CAM

ALLERGIES • Medication, food, environmental

IMMUNE • Routine IUTD, special

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

Edmonton Manual of Common Clinical Scenarios 348


PEDIATRIC BRUISING
.
Ashlee Yang Melanie Lewis BN MEd MD FRCPC

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

ID • Name, age . gender, ethnicity home


,

CC • Bruising

HPI • Onset and progression of bruising


• Associated symptoms
• Any known injury events
• Bleeding or .
bruising elsewhere (e.g. in stools, urine, epistaxis)
i/i RED FLAGS • Fever, story incompatible with developmental age of child, bruising in babies not yet cruising, bruises that do
U
not fit the causal mechanism described
<TJ
*U
PMHX • Pregnancy and birth history: prenatal care, complications in pregnancy, exposure to toxins/teratogens GA at
birth, delivery complications, postnatal complications, NICU, newborn metabolic screen
.
0)
Q. • Medical conditions: course since birth
• Developmental history and milestones reached ( with particular attention to gross motor skills to corroborate
described mechanism of injury )
• Hx of previous similar bruises/injuries
• Easy bruising
• Bleeding Hx: difficulty stopping bleeding, mucocutaneous bleeding ( gingival), bleeding from minor wounds,
epistaxis spontaneous and/or lasting >10 mins or requiring medical treatment, joint swelling with minor injury
• Unexplained anemia, history of blood transfusions
• Infant - post circumcision bleeding, umbilical stump bleeding, birth cephalohematoma

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

IMMUNE • Routine IUTD, special ( HPV for males and females)


FHX • Coagulation disorders ( von Willebrand disease, hemophilia A and B, platelet abnormalities) or other heritable
medical disorders that predispose to bleeding
• Consanguinity, hx of postoperative bleeding, need for transfusions or recurrent and severe epistaxis in family
members

349 Edmonton Mamial of Common Cluneal


SOCIAL • Detailed social history of home situation including primary caregiver, persons in the home, financial situation,
stressors, previous involvement with child protective services
DEVT. HX urine, fever, decreased LOC /lethargy, constitutional symptoms ( weight loss, decreased
• Blood in stool or
appetite, night sweats), rash/other lesions

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

If a bleeding disorder is suspected, add in the following investigations: Q


• Fibrinogen, Von Willebrand studies, type and and screen, Factor VIII and Factor IX levels, liver function tests and renal function
tests ( secondary platelet dysfunction)
Radiology/ lmaging
• Skeletal survey/bone scan for all children younger than two years of age with suspected physical abuse injuries (can also consider
CT head and optho assessment )
Child Protective Services
• If suspecting inflicted injury, involve child protective services to investigate. Carefully document clinical information and physical
exam findings.

UREATMENT
Emergent
• ABCs, IV fluids, transfuse if continued bleeding or hemodynamically unstable

Management according to underlying etiology


• Admission to hospital if severe physical injuries or medical illness, e.g., meningitis, HUS, DIC
• IV antibiotics and further septic workup if suspecting infection

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

I dmonton Manual of Common Clinical Scenarios 350


PEDIATRIC DEHYDRATION
Current Editor: Cynthia Gunaratnam BSc MD

Clinical Signs Mild (3%) # Moderate (6%) * Severe ( 9%) *


Systemic Increased Thirst Irritable Lethargic
Urine Output Decreased Decreased ( lml/kg/hr) Decreased ( anuria)
Mucous Membranes Tacky Dry Parched
SkinTugor Normal Reduced Tenting
Capillary Refill Normal Mildly Delayed Markedly Delayed

Anterior Fontanelle Normal Sunken Markedly Sunken


Heart Rate Normal Increased Markedly Increased

Blood Pressure Normal Normal Low


‘Note for 2 years of age, loss of 5%, 10%, and > 15% of total body weight is defined as mild, moderate, and severe dehydration
respectively
Dehydration

Fluid shifts: Inadequate Intake Excessive


-CHF Output
- Liver Failure Gl Losses Renal Losses Other Losses
- Sepsis - Diarrhea/vomiting - UTI - Burns
- Nephrotic Syndrome - Gastroenteritis - Polyuric ATN - Hyperthemia
- IBD - DKA - Hemorrhage
- FPIESand IEOM Diabetes Inspidus
Example fluids calculation: A 10 kg child is brought in with severe dehydration of 10%. The deficit calculation is 10 X 10
_
mL/kg so it is 100 ml /kg. -> 10 kg X 100 mL/kg = 1000 mL. The maintenance amount would be 4 mL/kg X 10 kg = 40 mL/hr,
The total IV fluid would be maintenance + deficit = 40 mL/ h + (1000 mL/ 24h) which is 81 mL/ hr for 24 hours. If the patient
received any IV bolus you would subtract this from the 1000 mL deficit prior to dividing it by 24 hours to get the hourly rate.

HISTORY
V)
u ID • Name, age, gender, ethnicity, home

nj CC • Lethargy, increased thirst, nausea/vomiting/diarrhea, bleeding


-u
0) HPI • Onset, duration
.
Q • Fluid intake ( breastfeeding, bottle- feeding, water, juice), polydipsia
• Fluid output (vomiting, diarrhea, number of wet diapers/saturation), polyuria, oliguria
• Insensible losses (skin burns, sweating)
• Food intake in older child, changes in diet
• Assessment of severityraltered level of consciousness, anuria, orthostatic symptoms, syncope
• Associated Gl symptoms: nausea, abdominal pain, anorexia, jaundice
• Associated GU symptoms: edema, dysuria, hematuria, tea -colored urine, frothy urine (proteinuria)
• Exposures: trauma /bleed, toxic ingestions, fever, travel, antibiotic use, weight loss
RED FLAGS • Infants < 3 months, immunocompromised, recent travel
PMHX • Prenatal Hx: oligohydramnios, prenatal ultrasounds specifically heart and kidney abnormalities
.
• Perinatal Hx: GA mode of delivery, BW, APGARs, complications . NICU, jaundice
• Postnatal Hx: feeding pattern, growth
• Medical Hx: diabetes insipidus, diabetes mellitus, metabolic disorders, previous hospital admissions, failure to
thrive
PSHX • Prior surgeries and complications
ALLERGIES • Food allergies /sensitivities, medications, environmental

IMMUNE • Routine IUTD . special


FHX • Consanguinity, diabetes, inborn errors of . .
metabolism, genetic syndromes IBD renal abnormalities
SOCIAL • Smoking, alcohol, toxin exposures, food and water sources, daycare, malnutrition

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

Fluid Replacement for Isotonic Dehydration


• Replace remaining deficit and on-going needs over 24 hours using isotonic solution
• Option for fluids
• In neonates use 10% dextrose NS + 20mEq/L KC and in children use 5% dextroseNS + 20mEq/ L KCI
.
• Leave out the KCI if the patient is anuric until the patient is voiding
.
• Oral fluid options include: pedialyte, enfalyte, oral rehydration solutions. Juice, tea water are hypotonic and shouldn' t be used

• 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)

Edmonton Manual of Common Clinical Scenarios 352


PEDIATRIC EMERGENCY
.
Lauren Kitney MD Gary Galante MD. Melanie Lewis BN MEd MD FRCPC

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

PHYSICAL EXAM AND EMERGENT TREATMENT


Primary Survey
.
• VS ( BP HR , RR. T, Sp02), general appearance Normal Vital Signs in Children
• C- spine precautions
l/l
u
Heart Systolic Respiratory Urine
• Airway: trauma to airway or signs of upper airway obstruction Age
Rate BP Rate Output
(abnormal or no sounds), airway patent

“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

353 fc dm tiioi't Manual of


'

> nmon Clinic il .


Secondary Survey (Head- to-Toe Exam)
• HEENT: fontanelles (bulging/sunken), suture lines, scalp lacerations, hematomas), pupils (size, symmetry, reactivity), fundoscopy
(papilledema, hemorrhages). EOM. nystagmus. TMs. discharge from ears, nose (position, discharge) mouth ( tongue biting,
.
oropharynx, swelling of lips or tongue, blood), facial bones (symmetry, bony deformities, pain), lymphadenopathy clavicles
• CV: murmurs, extra sounds, capillary refill, peripheral pulses
• RESP: stridor, increased work of breathing (nasal flaring, retractions), tracheal position, flail segments, subcutaneous emphysema,
symmetry of breath sounds, adventitious sounds. Beware of bradypnea without improvement !
• ABD: shape, bowel sounds, rigidity, peritonitis, masses, hepatosplenomegaly
• GU: scrotal hematoma or blood at meatus/vaginal bleeding
• MSK: pelvic instability, extremities (deformities/ bleeding/swelling), movement of extremities bilaterally
• NEURO: primitive reflexes, CNs, reflexes, strength, tone, sensation
.
• DERM: rashes, urticaria /angioedema purpura, petechiae, abnormal skin findings

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:

vancomycin • Phenytoin 20 mg/kg severely ill) methylprednisolone 1- 2 mg/kg


• > 3 mos: ceftriaxone/ IV over 20 min OR • Evaluate for acute chest IV divided q6h or hydrocortisone
syndrome, aplastic/splenic 4- 6 mg/kg IVq4- 6h
cefotaxime ± • Phenobarbital 20
vancomycin mg/kg IV/IM over 20 sequestration crisis, shock, • Magnesium sulphate 20- 50 mg/ kg
meningitis, sepsis, etc.; tailor IV over 20 min "U
• Viral meningitis: min(preferred 2ndline a>
workup/treatment accordingly • Intravenous p - agonist: salbutamol CL
supportive, acyclovir for in neonates)
(start at 1- 2 meg/kg/min IV) a
HSV • If refractory, rapid *
sequence intubation
PICU
. n
to

EPIGLOTTITIS ADRENAL CRISIS CROUP/ BACTERIAL ANAPHYLAXIS


TRACHEITIS
• Call PICU .
anaesthesia,
ENT to secure airway
• Hydrocortisone
m2 IV bolus then
100 mg/ • Dexamethasone 0.15 - 0.6 mg/
kgx 1PO IM q5min PRN
1:1000 epinephrine
• 0.01 mg/ kg of

• 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

tdmenton Manual of Common Clinical Scenarios 354


PEDIATRIC NAUSEA & VOMITING
. .
Lillian Du MD Allison Hobbs MD Bryan J Dickon MD FRCSC FAAP

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

PMHX • Previous similar episodes of emesis, stool Hx


..
• Chronic medical conditions, syndromes (e g , CHARGE syndrome)
PSHX • Previous abdominal surgeries
MAT. OBS. HX • Prenatal: prenatal ultrasounds, poly/oligohydramnios, maternal health, maternal exposures
• Perinatal: APGAR scores, mode of delivery, GA (term vs. preterm)
• Postnatal: neonatal complications, passage of meconium, neonatal metabolic screen

FHX • Genetic syndromes, Gl tract atresias, Hirschsprung's disease, pyloric stenosis

MEDS • Prescriptions, OTC, vitamins, CAM

355 Edmc on Manual of


ALLERGIES • Medication, food, environmental

IMMUNIZATIONS • Routine IUTD, special

.
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

Ldmonton Manual of Common Clinical Scenarios 356


PEDIATRIC SEIZURE
.
Christina Yang MD Mark Enarson MD FRCPC

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

Common Seizure Mimics ( non- epileptic )


• Breath - holding spells Causes of Seizures
• Syncope .
(e.g. cardiac causes, vasovagal) “DIMS”
• Migraine Drugs
• Benign paroxysmal vertigo
Infection
Metabolic
High Mortality/Morbidity
Structural
• Non-accidental injury
• Cerebrovascular accident
• Hypoglycemia, hyponatremia, toxic ingestion Typical Febrile Seizures
• Brain tumor 1. Age 6 mos to 5 yrs
• Encephalitis, meningitis 2. Lasts < 15 min
INITIAL MANAGEMENT 3. No underlying neurological
Emergent disorder
4. Generalized tonic - clonic seizure
• . . . ..
ABCDFG ( Don' t Forget Glucose) LOC. VS (HR BP RR T Sp02)
5. No recurrence in 24 h
• Identify and treat life- threatening conditions
> Aspiration, head injury, meningitis, metabolic derangements
(e.g., lactic acidosis, hypoxia, hyperthermia, hypoglycemia)
Stop the seizure
• First line anti- epileptic agents (benzodiazepines)

> Lorazepam 0.1 mg/kg IV or IO ( max 4 mg/dose) OR diazepam 0.2 mg/kg IV or IO


( max 8 mg/dose) OR midazolam 0.1- 0.2 mg/ kg IM (max 6 mg/dose)
> Second dose at 5 - 10 minutes as needed
• Second line anti- epileptic agents

> Give fosphenytoin or phenytoin first, then consider phenobarbital if ongoing seizure activity

VI • Note: phenobarbital + benzodiazepine = respiratory depression (be prepared to intubate)


u
<TJ
HISTORY
TJ ID • Name, age, gender, ethnicity, home
<D
CL
CC • Suspected seizure
HPI • Note duration of each stage, symmetry/spread, time of day (e.g., upon waking, nocturnal)
• Pre-ictal symptoms: Aura, usually associated with focal /partial seizures
> Younger child: irritability, behavioral changes, somnolence, clinginess
Older child: epigastric sensation, dej -vu/ jamais -vu, and anxiety all suggest temporal lobe involvement:
>
^
also note paresthesia, weakness, fearful look, headache, and visual phenomena
> Provoking event
• Ictal event: note whether suppressible or not, incontinence, level of consciousness

> Tonic: rigidity and extension of extremities


> Clonic: rhythmic flexion and extension of extremities, less jerky than myoclonic
> Tonic followed by clonic
> Myoclonic: jerky muscle contractions
> Atonic: loss of muscle tone, may be referred to as "drop attack ”
> Non - motoric: abnormal eye movement, staring, lip -smacking, automatisms, behavioral arrest
• Post -ictal symptoms: note LOC and degree of recollection of event (Oriented x 4 - person, place, time, event )
> Length of time to return to baseline (e.g., seconds with breath-holding spell, hours with seizure)
.
• Headache Todd's paralysis, somnolence, weakness, behavioral changes (e.g., aggressiveness, persistent crying)
• Provoked seizure: head trauma, infection, intoxication, dehydration, hypoglycemia, stroke (e.g., sinus venous
thrombosis), brain tumor, minor trauma, behavioral event, hyper /hyponatremia, hyperventilation
• Febrile seizure: associated with fever, occurs in children of 6 mos to 6 yrs old

357 Edmonton Manual ot


RED FLAGS • Significant head trauma • If suspicious mechanism, inconsistent Hx, or delayed
• Persistent focal deficits presentation, suspect inflicted head trauma
• Unwell child (e.g., significant intercurrent • Persistently altered LOC
illness, signs of meningitis) • Developmental regression

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

MEDS • Prescriptions (recent ATBx use, anticonvulsants) . OTC, vitamins, CAM


ALLERGIES • Medication, food, environmental

IMMUNE • Routine IUTD, special

FHX • Seizures, epilepsy, stroke, thrombotic events, bleeding/clotting disorders


• Unexplained infantile deaths, developmental delay, congenital or developmental syndromes, cardiac
.. .
conditions (e g ,arrhythmias WPW, long QT)
SOCIAL • Safety at home, daycare, and school
• Parental education regarding seizure management

DEVT. HX • Milestones, regression, developmental delay

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

Edmonton Manual of Common Clinical Scenarios 358


PEDIATRIC RASH
. .
Russell Wong MD Tiffany Kwok MD Loretta Fiorillo MD FRCPC

DERMATOLOGY gt Al =KM Jifrf J :J =1


^
PRIMARY LESIONS SECONDARY LESIONS
Flat Lesions Surface Changes
• Macule: flat lesion < 1cm diameter • Scale: flakes of keratin, usually white
• Patch: flat lesion >1cm diameter • Crust: dried blood, serum, or exudate
• Petechiae ( < 3 mm) /purpura ( 3 - 10 mm) /ecchymosis ( >10 • Excoriation: linear abrasions from scratching
-
mm):non blanchable, red to violaceous lesions secondary to • Fissure: linear crack extending to dermis
RBC extravasation
• Lichenification: thickening of skin with accentuated skin folds
• Eschar: black crust indicating tissue necrosis
Elevated Lesions
• Atrophy: thinning of skin; may appear wrinkled, translucent, or
• Papule: elevated lesion < 1cm diameter depressed
• Plaque: elevated lesion >1cm diameter • Telangiectasia: permanent dilatation of surface blood vessels
• Nodule: papule with similar depth to its width, usually <1cm • Erythema: blanchable, pink to red color
• Tumor: nodule >1cm diameter • Erosion: depressed lesion lacking epidermis
• Wheal: smooth, erythematous, edematous plaque, often with
central clearing, usually lasting < 24 hrs
Deep Changes
• Ulcer: deeper lesion lacking at least upper dermis
Fluid-filled Lesions
• Sclerosis: bound-down induration of skin from dermal fibrosis
• Vesicle: fluid - filled cavity <1cm diameter
• Bulla: fluid - filled cavity >1cm diameter
• Pustule: papule with purulent core
• Furuncle: deep collection of pus in a hair
follicle
• Carbuncle: coalescence of multiple furuncles
• Abscess: accumulation of pus in a cavity deep in the dermis
or below the dermis
• Cyst: encapsulated cavity containing fluid or semisolid
material
OTHER TERMS
Shape or Configuration Distribution
to
u • Annular: ring- like, with central clearing • Exanthem: skin involvement
• Nummular /discoid: solid, round, coin- shaped • Enanthem: mucous membrane involvement
ro • Polycyclic: coalescing circles or rings • Unilateral /bilateral
T3
Q) • Arcuate: arc - shaped • Symmetric/asymmetric
CL • Linear: in a straight line • Dermatomal: unilateral and in the distribution of a single nerve
• Reticular : net -like or lacy pattern root
-
• Targetoid: bulls eye - like target with three zones • Sun -exposed: on areas not covered by clothes
• Whorled: like marble cake • Acral: distallimbs ( hands, feet )
• Extensor: over the dorsal limbs
Arrangement • Flexor /ventral: over the flexor aspect of limbs

• Herpetiform: lesions clustered in a group • Intertriginous: in the folds (axillae, groin)


• Scattered: irregularly distributed
• Linear, annular

359 Edmonton Manual of Common Clinic j| Srenarn.s


s:OMMON AND IMPORTANT PEDIATRIC CONDITIONS
Dermatological Emergencies Infectious
Staphylococcal Scalded -Skin Syndrome VIRAL
• Caused by exotoxin of Staphylococcus aureus, typically Erythema Infectiosum (Fifth disease)
affecting infants and immunocompromised • Caused by human parvovirus B19 infection
• Presentation; febrile child with diffuse, tender erythema that • Edematous erythematous plaques on the cheeks (" slapped
progresses to sloughing of superficial epidermis with sparing cheeks ”) and reticular erythema on the trunk and extremities;
of mucous membranes may be associated with arthralgias, arthritis
• Management includes systemic ABTx against S. aureus • Self - limited, symptomatic management; in pregnant women -
risk of transmission to fetus, hydrops fetalis
Purpura Fulminans
•A presentation of disseminated intravascular coagulation, Varicella (Chickenpox)
often due to a complication of meningococcemia or congenital • Caused by varicella - zoster virus infection
protein C or S deficiency • Polymorphic eruption consisting of pruritic papules, vesicles,
-
• Clinically appears as rapid onset petechiae, purpura, and pustules, and crusted erosions; characteristic "dewdrops on
ecchymosis and may progress to hemorrhagic bullae and a rose petal" refers to vesicles with surrounding erythema;
necrosis palms and soles typically spared
• Vesicles in multiple stages of eruption
Eczema Herpeticum • Self -limited, symptomatic management
• Disseminated cutaneous HSV infection in a child with atopic
dermatitis Molluscum Contagiosum
• Presents as innumerable small discrete vesicles and crusted • Caused by poxvirus infection
erosions on erythematous skin; child may also have a fever, • Skin colored to pink, dome - shaped papules with central
lymphadenopathy, and irritability
umbilication
• Management includes systemic acyclovir, control of eczema,
• Self - limited, but may take up to 2 yrs to resolve
and treatment of associated superficial bacterial infections, if
any • Treatments include cryotherapy and topical cantharadin

Others: Stevens - Johnson syndrome (SJS), toxic epidermal BACTERIAL


necrolysis (TEN), necrotizing fasciitis Impetigo
INFLAMMATORY • Infection ofthe epidermis by S. aureus or Group A
streptococci (GAS)
Kawasaki disease • Presents as golden - yellow crusting on erythematous erosions;
• Acute febrile illness in infants and children may present as bullae in neonates or infants
• Clinical findings (" Warm CREAM") • Treatment is topical mupirocin to affected skin and nares.

> 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

Ldmonton Manual of Common Clinical Scenarios 360


PEDIATRIC WHEEZE
Current Editor: Raisa Kanji

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

HPI • Onset: age and course (acute vs . chronic: intermittent/constant/progressive)


• Acute
• SOB . cough anxiety. Hx of choking
,
• Chronic
• Rule out congenital or structural abnormalities, bronchial compression by mass, interstitial lung disease
• Associations
• Seasonal variation and common triggers including URTI, exercise, cold, allergens ( suggests asthma)
• Association with feeding or vomiting (suggests GERD)
• Urticarial rash ( rule out anaphylaxis)
• Other:
• Poor Wt gain and recurrent ear or sinus infections (suggests cystic fibrosis, immunodeficiency)
i/>
u
• Progressive dyspnea, exercise intolerance .
FTT (suggests interstitial lung disease)
RED FLAGS • Hx of choking and wheezing with minimal cough (suggests FB aspiration)
ro • Decreased LOC
"G
• Toxic appearance
o>
Q
- • Significant
• Cyanosis
respiratory distress

• Silent chest ( absent breath sounds)

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

ALLERGIES • Medication, food, environmental

IMMUNE • Routine IUTD, special

FHX • Asthma, atopy, cystic fibrosis


SOCIAL ..
• Environment (e g , type of heating, rugs, mould, infestations), daycare, smoking, pets

RISK • Complicated perinatal health, smoking in the home, low SES . domestic violence, parental mental health
FACTORS

361 [ clmonton Manual of Common t lim


PHYSICAL EXAM
General Approach
.
• ABCs, appearance ( toxic), VS ( BP. HR. RR. T, Sp02) growth charts (HtA/Vt /HC)

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

Follow-up ( dependent on etiology)


-
• Regular follow up to assess asthma control
Referrals
• . .
Pulmonary for poorly controlled asthma CF or undiagnosed wheeze

nonton mon Clinical Scenario: 362


PERIODIC HEALTH EXAM OF A NEWBORN
Current Editor: Epsita Shome

I:OMMON CONDITIONS
"
i

• Inadequate nutrition (breastfeeding difficulty)


• FTT (see Failure To Thrive )
• Congenital anomalies
• Eczema
• Colic

T
ISTORY
ID • Name, age, gender, ethnicity, home

CC • Periodic health exam

HPI • Discuss specific medical or psychosocial concerns with caregiver


• Feeding Hx: breastfed, formula fed, solids
>If breastfed: breast problems (latching, cracked/sore nipples, mastitis, thrush, etc), milk supply ( feeds
from both breasts, let - down, change in congestion), frequency/duration of feedings Vit D .
.
supplementation (400 lU/day 800 lU/day in high- risk infants)
> If formula - fed: formula used (how much/how often/how is it mixed)
> Introduction of solids at 6 months of age (see counseling topics)
> Reflux, colic, choking, diaphoresis, grunting with feeds, or projectile vomiting
• Elimination Hx: number of wet diapers /day, BM frequency and color
• Sleep Hx: waking to feed at night, able to fall back to sleep, location ( with parents, crib)
• Hearing inquiry
• Teething (6 months and onwards); irritibility, fever
RED FLAGS • Lack of maternal-infant bonding, neglect, no social smile by 6 wks
• < 6 wet diapers/day . Wt loss >10% of birth Wt. fever, failure to regain birth Wt by 2 wks, jaundice at 2 wks
PMHX • Prenatal: prenatal care . U/S frequency, maternal illness/exposure to toxins (smoking/EtOH/drugs)
• Perinatal: GA . complications of delivery, birth Wt, APGAR scores, asphyxia
• Postnatal: neonatal complications, NICU admission, length of stay, jaundice, meconium passage, newborn
metabolic screen
</> • Medical: chronic medical conditions, prior hospitalizations/emergency visits
u
PSHX • Surgeries at the time of delivery and/or postnatally for mother and/or child (including circumcision)
"O MEDS • Maternal: Prescriptions , OTC, vitamins, CAM
Q.
0) • Newborn: Prescriptions, OTC, vitamins ( Vit D if breastfeeding), CAM
ALLERGIES • Medication, food, environmental
. .
• IgE and non- lgE "allergies" (e g. cow’s milk protein intolerance)

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

363 Edmont iManual of Cccrm


PHYSICAL
General Approach
.
• VS ( BP. HR RR. T. Sp02). growth charts (Ht / Wt /HC)
• General appearance: dysmorphic features, distress, grunting, lethargy, tone
• Observe: child- caregiver interaction, developmental domains
• Opportunisitic exam: auscultation while child is settled before head to toe review

Systems- Based Physical Exam

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 )

PSCOUNSELING TOPICS AND ANTICIPATORY GUIDANCE


kJ!
• CPS recommends Rourke Baby Record as an evidence -based health supervision guide for children < 5
• Immunizations (see Immunizations )
• Nutrition
Encourage exclusive breastfeeding until 6 months of age
Newborn infants typically feed every 2- 3 hours: frequency decreases and feed amount increases with age 13
CD
Diet should be supplemented with Vit D if breastfeeding (400- 800 lU/day) Q .
Solid food should be initiated at 6 months of age due to depletion of Fe stores - introduce one new food at a time with a few fl)
days in between to assess for reaction 2 .
Do not delay introducing allergenic foods to prevent food allergy ct
Honey should be avoided in the first year of life due to the risk of botulism
By 1 yr, diet should contain foods from all food groups
• Safety
> Car seat ( infant)
> Electrical plugs/cords
> Falls ( stairs, change table, unstable furniture, no walkers)
> Safe sleep (position, room sharing, avoid bed sharing, crib safety)
> Poisons (Poison and Drug Information Service number )
> Firearm safety
> Carbon monoxide and smoke detectors
> Bath safety (hot water heater set to < 49° C)
> Choking/safe toys
> Second - hand smoke
> Sun exposure - no sunscreen < 6 months
> High-risk infants assess need for home visit
• Screen for parental fatigue and postpartum depression
. . . . .
• Follow - up with family physician or pediatrician at 1- 2 wks 6 wks 3 mos, 6 mos 9 mos, 12 mos 18 mos and annually thereafter

Ecmonton Manual of Common Clinical Scenarios 364


PERIODIC HEALTH EXAM OF A TODDLER/CHILD
Current Editor: Epsita Shome

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

• Exercise: physical activity, able to keep up with peers

RED FLAGS • FTT. developmental delay, regression, signs of abuse/neglect


PMHX • Prenatal: prenatal care . U/S frequency maternal illness/exposure to toxins (smoking/EtOH/drugs)
,
• Perinatal: GA . complications of delivery, birth Wt. APGAR scores, asphyxia
• Postnatal: neonatal complications, NICU admission, length of stay, newborn metabolic screen
• Medical: chronic medical conditions, prior hospitalizations/emergency visits, other concerns
PSHX • Prior surgeries and complications
MEDS .
• Prescriptions OTC, vitamins CAM.
ALLERGIES • Medication/food/environmental/previous reactions, allergy skin testing, ask about reaction ( specifically
anaphylaxis - Epipen)
IMMUNE .
• Routine IUTD special

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

COUNSELING TOPICS AND ANTICIPATORY GUIDANCE


• CPS recommends Rourke Baby Record as an evidence-based health supervision guide for children < 5
• Immunizations (see Immunizations )
• Vision: recommend checking visual acuity at 3- 5 years
• Dental: supervised brushing with fluoride between 3 - 6 years, parental brushing with fluoride < 3 years
• Growth (Ht / Wt /HC)
• Nutrition
> Homogenized milk ( 16 oz/day)
> Choking/safe foods
> Avoid sweetened juices / liquids to prevent early dental caries
> Promote open cup instead of bottle
> Inquire re: vegetarian diets
• Safety/Injury Prevention

> Car seat ( Wt appropriate)


> Childproof electrical plugs/cords
> Falls ( stairs, change table, unstable furniture, no walkers)
> Poisons (provide Poison and Drug Information Service number )
> Firearm safety
> Carbon monoxide and smoke detectors
TJ
> Bath safety (hot water heater set to < 49° C) rt>
> Pacifier use ( wean at 18 mos)
Q .
> Choking/safe toys
> Bike helmet, water safety, matches (discuss at 2 yrs+) n)
V
> High risk child assess need for home visit
• Environmental
> Second -hand smoke
> Sun exposure, sun screen, insect repellent
• No OTC cough medicine
• Fever advice/thermometers
• Encourage reading
• Toilet learning ( begin discussion at 18 mos)
• Parental support, if needed
• Annual follow -up with Pediatrician or Family Practitioner, or sooner if warranted

Edmonton Manual of Common Clinical Scenarios 366


PERIODIC HEALTH EXAM OF AN ADOLESCENT

[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

• Eating disorders (anorexia nervosa, bulimia nervosa)


.
• Obesity: BMI = Wt (kg) /Ht 2 ( m 2). OverWt ( 25 - 30) Obese ( > 30)

DSM-V Diagnostic Criteria for Anorexia Nervosa and Bulimia Nervosa


Criteria Anorexia Nervosa Bulimia Nervosa
I < 85% of ideal body Wt Recurrent episodes of binge eating
Recurrent, inappropriate compensatory behavior to prevent Wt gain
II Intense fear of gaining Wt ( laxatives, vomiting, diuretics, fasting, excessive exercise)
Disturbance in the way body Wt or shape is
experienced, undue influence on Binge eating and inappropriate compensatory behaviors
III
self - evaluation, denial of seriousness of occur at least lx/ week for 3 mos
low body Wt
IV Self - evaluation unduly influenced by body shape and Wt


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

IMMUNE • Routine IUTD . special (HPV for males and females)


FHX • Eating disorders, substance abuse, suicide, depression, abuse, pertinent familial disease, delayed puberty
SOCIAL •H -Home situation: where living, who with, getting along discipline
,

(HEEADSSS) • E-Education/Employment: attending school, grades, stress/balance, financial stressors


• E-Eating: eating behaviors, body image, nutrition, dietary restrictions
•A -Activities: interests, physical activity, interactions with family and peers, social network
•D -Drugs: alcohol, tobacco, marijuana and other recreational drugs, friends using, how much, how often,
when, why, driving under the influence
•S — Sexuality: sexual preference, sexual activity - oral, vaginal, anal, age of partner, multiple partners,
.
consensual, protection from STIs contraception
• S-Suicide and depression: mood, self harm, suicidality
• S — Safety: home/school / work/community, bullying, bicycle and automobile safety

ROS • Ophthalmology and dental follow -up . concerns re: hearing


• Menstrual/gynecological Hx in females, pubertal development
• Sleep

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.

[COUNSELING TOPICS AND ANTICIPATORY GUIDANCE


• Sexuality, sexual health, counseling to protect against STIs
• Healthy eating behaviors
• Substance use
• Smokers: counsel on smoking cessation
• Injury prevention ( bike helmet )
• Mental health
-o
o
• Environmental
Q .
55’
> Second-hand smoke
> Sun exposure, sunscreen n
in
• Seat belt use
• Dental hygiene (cleaning, fluoride, dentist )
• Adjustment and coping skills for adolescents with chronic illness
• Annual follow - up with Pediatrician or Family Practitioner, or sooner if warranted

Edmonton Manual of Common Clinical Scenarios 368


SPEECH & LANGUAGE ABNORMALITIES
.
Current Editors: Chris Novak BSc MD Debra Andrews MD FRCPC

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

> Receptive - Ability to understand others


> Expressive - Ability to communicate information

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

> Associated with language-based learning disabilities


> Language disorders
• Isolated Language Impairment
> Specific language impairment
> Learning disabilities - may also have impaired oral speech skills
IS) > Selective mutism
u
> Acquired aphasia
ro > Landau Kleffner syndrome - epilepsy syndrome (high morbidity )
"O
• Broader Developmental Impairment
0)
CL . . .
> Global Developmental Delay ( < 5 yrs old) Intellectual Disability ( > 5 yrs old IQ < 70 poor adaptive function)
> Autism Spectrum Disorder
. .
> Degenerative neurological disorders (high morbidity) - e.g. Rett syndrome Leigh encephalopathy, inborn errors of metabolism
> Neglect and abuse
> Head injury

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

369 Edmonton Manual of Gui


RED FLAGS • Regression: loss of previously attained skills: consider Rett syndrome or Landau - Kleffner syndrome
• Dysphagia, excessive drooling, poor suck, choking
• Language: no babbling at 9 mos, no consistent words at 18 mos, no two - word phrases at 2 yrs
• Speech: unintelligible to parents at 2 yrs and strangers at 3 yrs

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

PSHX • CN surgeries ( shunt, tumor ) . LP


MEDS • Prescriptions, OTC, vitamins, CAM

ALLERGIES • Medication, food, environmental

IMMUNE • Routine IUTD, special

FHX • Autism spectrum disorder


disorder, stutter, anxiety
.
Rett syndrome, deafness, developmental delay/intellectual disability, neurologic

• Consanguinty: create three generation pedigree

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.

• Speech Language Pathology referral: highly skilled at diagnosis


• Broad cognitive assessment
Blood work 8
.
• If clinically indicated (e.g., CPK, TSH, metabolic workup, karyotype Fragile X testing, and other genetic testing)
Radiology/ lmaging
•Neuroimaging: if micro/macrocephaly, loss of psychomotor skills, neurologic signs
•EEG: if seizures or regression
• MRI preferable to CT scan except for intracranial calcifications (TORCH, tuberous sclerosis)
For investigations for broader developmental impairment see Developmental Delay chapter
L REATMENT
Family - Centered Care
• Tailor plan to child and family’s needs. Should address short and long- term goals.

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

( dmonton Manual or Common Clinical Scenarios 370


.
Lauren Kitney MD Gary Galante MD, Melanie Lewis BN MEd MD FRCPC

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

PSHX • Previous neck, thoracic, or cardiac surgeries


MEDS • Prescriptions, OTC, vitamins, CAM

ALLERGIES • Medication, food, environmental

IMMUNE • Routine IUTD (especially H . influenzae type B), special


FHX • Pediatric cancer, allergy, asthma, hereditary angioedema

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

> Hyperinflation, contralateral mediastinal shift, atelectasis, post - obstructive pneumonia


• AP and lateral neck XR
• Retropharyngeal abscess: widened retropharyngeal space
• Croup: steeple sign with narrowed upper trachea on AP or subglottic haziness on lateral
• Epiglottitis: thumb sign with epiglottic edema

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

Cricothyrotomy if intubation unsuccessful or impossible


Rigid bronchoscopy/ laryngoscopy may be diagnostic and/or therapeutic
Tracheotomy or laryngoplasty for severe laryngomalacia
• Referrals
Consider PICU, Anesthesia, ENT, Pulmonary

.
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
.
Bramswig J Dubbers A. Disorders of pubertal development. Continuing Medical Education. 2009;106( 17):295 - 304 .
.
Nebesio T Eugster E. Current concepts in normal and abnormal puberty. Current Problems in Pediatric and Adolescent Health Care. 2007;37 { 2):53 - 72.
. .
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. .
. .
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.
.
Richmond EJ. Rogol AD. The child with tall stature or abnormally rapid growth. In UpToDate. Basow DS ed. UpToDate: Waltham. MA: 2012.
.
Rogol AD. Causes of short stature. In UpToDate Basow DS. ed. UpToDate: Waltham. MA; 2014.

ADHD/ Learning Disorder


Cheung A. Williams BA. Sivarajan BV. eds. The HSC Handbook of Pediatrics. 10th ed. Philadelphia: Elsevier: 2003.
Miall L. Rudolf M. Levene M. Paediatrics At A Glance. 2nd ed. Oxford. Now York: Blackwell Publishing; 2007.
.
Krull KR . Attention deficit hyperactivity disorder in children and adolescents: Clinical features and evaluation. In UpToDate Basow DS. ed. UpToDate:
Waltham. MA; 2014.

Anemia (Pediatric)
.
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
.
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.
.
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
.
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
' -
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.

375 Ldmonton Manual of Common Clinical Scenario


Fever Without a Source in a Child < 3 Months
.
Kleigman RM, Marcdante KJ. Jenson HB Behrrnan RE. Nelson Essentials of Pediatrics. 5th ed. Philadelphia. Elsevier; 2006.
Cheung A. Williams BA. Sivarajan BV. eds. The HSC Handbook of Pediatrics . 10th ed. Philadelphia: Elsevier: 2C03.
Robinson. J. Fever without a source. ( November 2013 ). Lecture presented in Pediatrics Clerkship. University of Alberta. Edmonton. AB.

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.
'

. .
Lehman TJA. Growing pains. In UpToDate Bascw DS ed. UpToDate: Waltham. MA; 2012.
.
Yu DT. Reactive arthritis ( formerly Reiter Syndrome). In UpToDate. Basov/ DS ed. UpToDate: Waltham. MA: 2012.

Pediatric Nausea & Vomiting


. . .
Arensman RM. Bambini DA Almond PS eds. Pediatric Surgery. Georgetown TX: Landes Bioscience: 2000.

Neonatal Jaundice
. . . . .
Hay W Levin M Sondheimer J Deterding R. Current Diagnosis & Treatment: Pediatrics 18 th ed New York: McGraw - Hill: 2007.
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 . .
. .
Abrams S Shulman R . Causes of neonatal cholestasis In UpToDate desktop 17.2 2009 . .
Newborn Respiratory Distress/Cyanosis
.
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 —
CL
tu

Pediatric Dehydration n
in
Somers MJ. Clinical assessment and diagnosis of hypovolemia (dehydration) in children [ Internet ]. 2015 [cited June 18.2016 ] Available
from: www.uptodate.com
.
Iserson KV. Chapter 11: Dehydration/Rehydration. In Iserson KV ed. Improvised Medicine: Providing Care in Extreme Environments. New York:
McGraw -Hill: 2012.
Freedman SB. Thull-Freedman JD. ( 2016) Vomiting, diarrhea, and dehydration in infants and children. In Tintinalli JE. Stapczynski J Ma O . .
. . .
Yealy DM Meckler GD Cline DM eds. Tintinalli ' s Emergency Medicine: A Comprehensive Study Guide. 8 th ed. New York : McGraw - Hill; 2016.
. .
Stephan M Carter C. Ashfaq S. Chapter 50: Pediatric emergencies. In Stone C Humphries RL. eds. Current Diagnosis & Treatment Emergency
Medicine. 7 th ed. New York: McGraw - Hill; 2011.
Bischoff M. Lewis M. Dehydration in children [ Internet ]. 2010 [cited Jul 2.2016 ] Available from: www.pedscases.com
Jeha GS. Haymond MW. Treatment and complications of diabetic ketoacidosis in children[ lnternet ]. 2015 [cited July 2.2016 ] Available
from: www.uptodate.com
Blondel -Hill E. Fryters S Clostridium difficile. In Bugs and Drugs. 2012. Retrieved on July 2.2016.

Pediatric Emergency
. .
Rubin M Sadovnikoff N. Pediatric airway management. In Tintinalli J Kelen G. Stapczynski S. eds.Tintinalli ' s Emergency Medicine: A Comprehensive Study
Guide. 6th ed. New York: McGraw - Hill: 2004.
Dipchand A. Friedman J. The Hospital for Sick Children Handbook of Pediatrics. 11th ed. Toronto: Elsevier Canada: 2009.

Edmonton Manual of Common Clinical Scenarios 376


Pediatric Seizure
.
Chu- Shore CJ Tseng BS. First seizure, pediatric perspective. eMedicine: 2010.
Marshall RS. Mayer SA. On Coll Neurology. 3rd ed. Philadelphia: Saunders Elsevier;2007: 45 - 56.
Baumann RJ. Febrile seizures. In Medscape Reference. Kao A. ed. WebMD: 2012. http://emedicine.medscape.com/article/ 1176205 -overview
Graves RC, Oehler K. Tingle LE. Febrile seizures: Risks, evaluation, and prognosis. Am Fam Physician. 2012 Jan 15;85(2):149-153.
Wilfong A. Management of convulsive status epilepticus in children. In UpToDate. Nordli DR. ed. UpToDate. Waltham. MA. ( Accessed on February 5.2015)

Pediatric Rash
.
Schalock P Hsu J. Arndt K. Lippincott ' s Primary Care Dermatology . Philadelphia: Lippincott W iliams & Wilkins: 2011.
Wolff K. Johnson R. Fitzpatrick ' s Color Atlas and Synopsis of Clinical Dermatology . 6 th ed. New York: McGraw - Hill: 2009.

Pediatric Wheeze
Majaesic C. Approach to the wheezy child. PowerPoint presentation. 2009.
.
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.

Periodic Health Exam of a Newborn


.
Heird WC. Chapter 42: The feeding of infants and children. In Kliegman R. Behrman R. Jenson H. Stanton B eds. Nelson Textbook of Pediatrics. 18th ed.
Philadelphia. Saunders Elsevier: 2007.
.
Lowe MC Woolridge DP. The normal newborn exam, or is it ? Emergency Medicine Clinics of North America. 2007; 25:921- 946.
. . .
Stoll BJ. Chapter 94: The newborn infant. In Kliegman R Behrman R. Jenson H Stanton B eds. Nelson Textbook of Pediatrics. 18th ed. Philadelphia. Saunders
Elsevier: 2007.
Rourke L, Leduc D, Rourke J. Rourke baby record: evidence - based infant/child health maintenance guide. 2014 Nov 29. Retrieved from http:// www.
rourkebabyrecord.ca/pdf /RBR 2014 _onepage.pdf

Periodic Health Exam of a Toddler/Child


. .
Rourke L Leduc D Rourke J. Rourke baby record: evidence -based infant/child health maintenance guide. 2014 Nov 29. Retrieved from http://www.
rourkebabyrecord.ca/pdf /RBR 2014_onepage.pdf

Periodic Health Exam of an Adolescent


.
Golcenring JM Rosen DS. Getting into adolescent heads: An essential update. Contemporary Pediatrics. 2004 Jan:21(l):64 - 90.
.
American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders: DSM 5 . Washington DC: American Psychiatric Association; 2013.
.
Knight JR. Sherritt L. Shrier LA. Harris SK Chang G. Validity of the CRAFFT substance abuse screening test among
adolescent clinic patients. Archives of Pediatrics & Adolescent. 2002:156(6):607-614.

Speech & Language Abnormalities


.
Zorc JJ. Alpern ER. Brown LW. Loomes KM. Marino BS Mollen C J. Raffmi LJ. eds. Schwartz' s Clinical Handbook of Pediatrics. 4th ed. Philadelphia: Lipppincott
Williams & Wilkins: 2009.
.
Cheung A. Williams BA. Sivarajan BV eds. The HSC Handbook of Pediatrics. 10th ed. Philadelphia: Elsevier: 2003.

in
u Stridor
.
Babin E et al. How we do it: Management of tracheobronchial foreign bodies in children. Clin Otolaryngol Allied Sci. 2004;29:750- 753.
Boat TF. Green TP. Chapter 381: Chronic or recurrent respiratory symptoms. In Kliegman R. Behrman R. Jenson H. Stanton B. eds. Nelson Textbook of


T3 Pediatrics. 18th ed. Philadelphia. Saunders Elsevier: 2007.
<U Roosevelt GE. Chapter 382: Acute inflammatory upper airway obstruction (croup. epiglotti:is. laryngitis, and bacterial tracheitis). In Kliegman R. Behrman R.
.
Q .
Jenson H Stanton B. eds. Nelson Textbook of Pediatrics. 18 th ed. Philadelphia. Saunders Elsevier: 2007.

377 Edmonton Manual of Common Clinical Scenarios


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
References 407
Station Contributors 408

Staff Section Editor


Melanie Marsh-Joyal MD FRCPC
Department of Psychiatry
University of Alberta

Jorge Perez - Parada MD FRCPC


Department of Psychiatry
University of Alberta

Jonathan Hamill MD FRCPC BMus ARCT


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OJ

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379 Edmonton Manual of Common Clinical Scenarios


INTRODUCTION
Melanie Marsh- Joyal MD FRCPC

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

The MSE is an essential part of the physical exam.


The MSE should start with a brief introductory statement that identifies the patient and flows into the MSE. For example:
"Pt. X is a 65 year old female who ... etc.”

A mnemonic for the MSE is ASEPTIC:


Appearance
.
• General Appearance: apparent age dress ( cleanliness, appropriateness), and personal hygiene, distinguishing features ( scars,
tattoos, hair colour, etc.) , signs of self harm ( scars / bruises on flexor surfaces of wrists), signs of abuse or involvement in a physical
. .
altercation ( black eye split lip etc.)
• Behavior: posture, eye contact, emotional expression, degree of cooperation
• Movements: tics, psychomotor agitation or retardation, tremor (resting or intentional), signs of extrapyramidal symptoms
Speech
• Rate (slow, rapid but easily interrupted, pressured), rhythm ( slurring, stuttering), volume, quantity ( poverty of speech), spontaneity,
latency
• Observe for pecularities such as word finding difficulty, echolalia, signs of Broca' s or Wernicke's aphasia
Emotion
• Mood is subjective and describes patient 's internal state; use patient 's own words (sad, depressed, frightened, anxious). If patient is
not able to describe subjectively, offer scale of 1 to 10 .
> Be consistent when assigning value ( i.e., 1 = worst mood ever and 10 = feeling great ), and identify the same for the reader
• Affect is objective outward emotional state that examiner observes
> Quality: elated, euphoric, irritable, euthymic ( neutral), dysphoric
> Range: full vs. restricted
> Lability: labile vs. stable
> Intensity: flat, blunted, exaggerated
• It is very important to document what you observe and if it is congruent with what the patient says (i.e., patient reported auditory
hallucinations but did not appear distracted or preoccupied during assessment)
Perceptions
• Hallucinations: perceptions in the absence of sensory stimuli in any of the five senses: note if congruent with delusions
• Illusions: misperceptions of apparent stimuli; either a misinterpretation or clear error in perception (e.g., patient feels as though a
clock has eyes or that wind blowing is whispers)
• Dissociation: derealization, depersonalization

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)

> Perseveration: persistent inappropriate repetition of same thoughts n


• Thought Content: the overarching themes present in thought
zr
O)
> Worries, obsessions, themes such as abandonment/hopelessness/guilt
> Safety: suicidal ideation ( SI) (active vs. passive) and homicidal ideation ( HI) (intended victims vs. nonspecific threats); assess
plan, intent, means
> Overvalued ideas: false beliefs but redirectable
> Delusions: fixed false beliefs (religious, grandiose, nihilistic, persecutory, erotomanic); abnormal thoughts, not perceptual
abnormalities; determine if bizarre ( strange and implausible) vs. non-bizarre and if mood congruent
Insight/Judgment
• Insight: awareness of illness and understanding of need for treatment; strong predictor of prognosis, as patients with insight are
more likely to seek/cooperate with treatment
• Judgment: actions and future plans that reflect ability to make sound, reasonable, socially appropriate decisions; includes impulse
control (strong predictor of safety)
..
• Judgement and insight can differ from each other (i e , insight can be poor and judgement can be fair )
Cognition
• LOC, intelligence, may use MoCA, MMSE to assess attention, concentration, memory, orientation, executive function

Edmonton t 'lidI of Common Clinical Scenarios 382


. .
Authors: Jonathan Hamill MD Cindy Liu MD Jorge Perez - Parada MD FRCPC

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

383 Edmonton Manual of Common Clinical Sc


[MENTAL STATUS EXAM

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

Edmonton Manual of Common Clinical Scenarios 384


ANXIETY DISORDERS
.
Current Editor: Hely Shaw MD Jorge Perez - Parada MD FRCPC

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

385 inton Manual of C r»mc


MEDS • Levothyroxine, synthroid, SSRIs/SNRIs, steroids, dextroamphetamine, methylphenidate, anticholinergics,
benzodiazepines, decongestants
• Confirm recent dose changes and compliance
ALLRGIES • Any drug reactions, anaphylaxis

SOCIAL HX • Relationships, social support network, abuse/neglect, development through childhood, legal problems

FAMHX • Any psychiatric illness, in particular of mood or anxiety disorder


ROS • Fluctuant .
LOC, headache, dyspnea, diaphoresis, chest pain, SOB unilateral leg swelling/erythema/calf pain

M ENTAL STATUS EXAM


• Appearance and Behavior: agitation/ hyperactivity/aggressiveness, restlessness, tremor, diaphoresis, avoidant eye
contact, uncooperative
• Speech: tangential, pressured

• Emotions ( mood and affect) : may be depressed, tearful, irritable, or euthymic

• Perceptions: hallucinations, derealization, derealization/ depersonalization

• Thought content and process: obsessions, delusions, paranoia, grandiosity, SI/HI


• Insight and judgement: could be poor or absent depending on severity and/or compliance with treatment
• Cognition: alert, orientated, attentive, impaired memory
PHYSICAL EXAM
VS|
: BP| .
, HR, RR Temp, TSp02
General: diaphoresis/hyperhydrosis, mydriasis
.
HEENT: mydriasis, Graves’ ophthalmopathy (lid lag upper eyelid retraction), neck mass (goiter / nodules)
CVS: arrhythmia, murmurs, ankle edema
RESP: distress, hyperventilation, rapid/shallow breaths, signs of asthma/COPD/pneumonia
ABD: tenderness, change in bowel sounds
NEURO: tremor, hyperreflexia, tingling
MSK: calf tenderness, clinical signs of DVT
INVESTIGATIONS
Choose wisely, select and order investigations according to your differential diagnosis. Depending on setting no
investigatriions may be required
TREATMENT
Emergent
• Low dose Lorazepam (or other rapid onset benzodiazepine)
Treatment Options
Biological Psychosocial
SSRIs/SNRIs first line, short -term benzodiazepines CBT (individual or group) or arousal management
GAD
via mindfulness techniques, +/- Bibliotherapy “O
in
Panic SSRIs /SNRIs, short - term benzodiazepines CBT + /- exposure component if with agoraphobia
Disorder n

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

Edmonton Manual of Common Clinical S narios 386


BIPOLAR DISORDERS
. .
Current Editor: Jonathan Hamill MD Cindy Liu MD Jorge Perez - Parada MD FRCPC

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)

DISORDER ABBREVIATED DSM- 5 SYMPTOMS


Bipolar I >1manic .
or mixed episode ± depressive episode ± psychotic symptoms; Bipolar I A A
affects function
Bipolar II >1major depressive episode and >1hypomanic
Bipolar II
episode; no manic or mixed episodes
Cyclothymia .
> 2 yrs multiple periods of hypomanic symptoms and
U V
depressive symptoms that don’t meet criteria for MDE
Cydothemia

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)

• Stressors: premenstrual, postpartum, seasonal, relationships, occupation


• Safety: self - harm; SI /HI: plan, means, intent, name of person/people if HI
fO • Substances: cocaine, MDMA, ecstasy, cannabis (specificaly Shatter - ultraconcentrated THC that can
_c .
produce a manic episode usually with psychotic features) , caffeine EtOH, smoking, hallucinogens, opioids,
benzodiazepines, energy drinks; recent withdrawal
u
>*
V)
QL
.
• Signs and symptoms screen: anxiety, psychosis GMC - concurrent/pre- existing/new

RED FLAGS • SI/HI with plan and access to means, delusions


PMHX • Hyperthyroidism/hypothyroidism . Cushing’s. DM. autoimmune disorders. CAD/CVA. Parkinson’s, dementia,
.
brain injury, epilepsy HIV
PTHX • Psychiatric illness including past
episodes of depression/mania/hypomania/mixed episode, substances,
.
admissions, ADHD, previous therapy and follow -up trials of medications
MEDS • Antidepressants, mood stabilizers, dextroamphetamine, methylphenidate, bromocryptine, captopril, steroids,
cyclosporine, levodopa
SOCPERSHX • Relationships, social support network, childhood abuse, childhood development
FAMHX • Psychiatricillness, especially mood disorders, suicide, substance use. Hx of abuse
ROS • Skin changes, diaphoresis, heat intolerance, fever, increased libido, Wt changes

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

LONG-TERM Lithium, valproate Family therapy, CBT, interpersonal


PROPHYLAXIS therapy
Lamotrigine ( prevents depressive relapses in Bipolar II)
Patient education to identify new
Carbamazepine ( 2nd line) episodes early
Antipsychotics (olanzapine, quetiapine (Bipolar II),
risperidone)
MANIA Lithium, valproate, carbamazepine ( 2nd line) ± lithium/ • CBT
divalproex • Interpersonal psychotherapy
Atypical antipsychotic monotherapy • Education of patient and family
ECT ( 2nd line) • Establish a therapeutic alliance “O
in
DEPRESSION Lithium or lamotrigine or antipsychotic + lithium/ n
divalproex ir
ECT CD

Quetiapine monotherapy <


MIXED Atypical antipsychotic ± mood stabilizer
Mood stabilizer monotherapy (lithium, valproate)
Add antidepressant only if depressive symptoms
predominate
ECT
Follow-up
• Follow -up in 2 wks to assess response to treatment, side effects, and safety assessment

Referrals
• Psychiatry: mania, treatment resistant, severe, psychosis, unsure of diagnosis

Edmonton Manual of Common Clinical Scenarios 388


DEPRESSIVE DISORDERS
.
Current Editor: Sarah MacArthur MD Jorge Perez - Parada MD FRCPC

•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

One symptom must be either

.^
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

RED FLAGS • Suicidal ideation, Homicidal Ideation


PMHX • Hyperthyroidism or hypothyroidism, Cushing's, DM, malignancy, autoimmune, CAD/CVA, Parkinson’s, Vit B12
deficiency, neurocognitive disorder, chronic pain, renal failure, chronic medical condition
PM'HX • Psychiatric illness, previous suicide attempts and treatments; past episodes of depression, mania, hypomania,
mixed episodes; previous M * hospital admission, previous therapy or antidepressant trials (what was most helpful?)

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

Treatment for MDD


BIOLOGICAL PSYCHOSOCIAL SOCIAL

Pharmacological • Psychotherapy • Education of patient and family


•1st line: antidepressant .
(SSRIs, SNRIs, Bupropion Mirtazapine),
(interpersonal, cognitive
behavioral, supportive,
• Establish a therapeutic alliance,
book regular follow -up
• 2 nd line: TCAs, trazodone, quetiapine; augmentation with lithium,
psychodynamic)
atypical antipsychotics, anticonvulsants: • Offer assistance of social work,
• Mindfulness based support groups, suicide hotline
• 3rd line: MAOIs
cognitive therapy number
Non Pharmacological • Internet /computer

- -
• Neruostimulation ECT/rTMS if contraindications to meds and delivered therapy
moderate to severe or if pregnant
• Promote regular excercise /healthy diet

Special Populations - Geriatrics


• Consider overlapping triad of Delirium/Depression/Dementia - onset and course often helpful in differentiation.
• Cognitive testing - MMSE/MOCA
• Address polypharmacy: unnecessary or sedating medications.
.
• With antidepressants - start low go slow.
Follow - up
• Follow -up in 2 wks to assess response to treatment, side effects ( weight gain, sexual dysfunction), and safety assessment

Referrals
• Psychiatry: if treatment resistant, severe, psychosis, unsure of diagnosis
T>
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Edmonton Manual of Common Clinical Scenarios 390


EATING DISORDERS
.
Current Editor: Jonathan Hamill MD Jorge Perez - Parada MD FRCPC

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

391 Edmonton Manual of (


ROS • Syncope, headache, dizziness, palpitations, seizures, fatigue, change in sleep pattern, decreased
concentration/memory/slow mentation, loss of libido, muscle pain/ weakness, reflux, constipation/bloating/
abdominal pain, cold intolerance, skin changes, hair loss, lanugo

MENTAL STATUS EXAM


Appearance: checking in mirrors, layers of clothing to hide Wt or for cold intolerance
Emotions: low mood, embarrassment, guilt
Perception: disturbed body image (what does the patient see when they look in the mirror )
Thoughts: overvalued ideas about food and Wt, suicidal ideation
Insight /Judgment: aware or may deny symptoms and severity
Cognition: may be altered
PHYSICAL EXAM
Restriction Binging/Purging
VS iBP/HR /RR, assess HT, Wt, BMI, orthostatic changes, hypothermia
Cachexia, edema, signs of hyperthyroidism, Normal or slightly over -Wt, signs of
General
cold intolerance, cyanosis, signs of self -harm hypovolemia, signs of self - harm

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

Bio Psychosocial a>


• Restore nutritional status (dehydration, starvation, electrolyte imbalances) - slow and steady to avoid refeeding
syndrome
Emergent
for admission: significant electrolytes abnormalities, seizures, decreased LOC, syncope, arrhythmias,
• Indications
prolonged QT, < 80% expected body Wt, SI or self -harm
limited role and should only be started once
• Medications have a • Treat comorbid '1' conditions,
medically stable. Fluoxetine, atypical antipsychotics, topiramate may supervision of meals and post - meal,
help with binging: atypical antipsychotics (especially olanzapine) have restricted access to bathrooms
evidence for anorexia. • Individual / family/group psychotherapy,
• Avoid buproprion as decreases seizure threshold patient/family education, support
Long- term
.
• Daily Wts/electrolytes dietician consult, daily intake of 500 calories groups, partial hospitalization, day
program
greater than maintenance divided in small feedings throughout day
± liquid nutrition supplements, metoclopromide to promote gastric • Social work involvement, addictions
emptying, multivitamins counseling
• Monitor for refeeding syndrome

Edmonton Manual of Common Clinical Scenarios 392


GENDER DYSPHORIA
.
Current Editor:Cindy Liu MD Jorge Perez - Parada MD FRCPC

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

FAMHX • Psychiatric illness, genetic/hormonal pathology

MENTAL STATUS EXAM


Appearance: dress as opposite gender, stereotypical mannerisms/posture of opposite gender
Speech: vocal changes to match opposite gender
Emotions: mood and affect highly variable, feelings corresponding with degree of acceptance
Thoughts: content may reflect cross - gender identification and pervasive disturbance in self - perception
Insight /Judgment: generally intact
393 Edmonton Manual of Common Clinical
PHYSICAL
VS
General: secondary sexual characteristics, hair distribution. Tanner staging, dysmorphic features consistent with genetic
.
anomalies, signs of self -harm, signs of steroid use signs of abuse
Genital exam may be deferred to GP or Endocrinology (undescended testes, ambiguous genitalia, signs of surgery or self -
mutilation/autocastration)
INVESTIGATIONS
Blood Work
. .
• CBC- D, electrolytes. BUN Cr, LFTs /liver enzymes TSH. B 12, folate (rule out medical causes of psychiatric symptoms )
• Hormone assays ( testosterone, estradiol, progesterone. 17 - hydroxyprogesterone)

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

Referral to Endocrinology Laser /electrolysis hair Referral to community resources


removal ( transgender support groups)
GnRH analogues in children to
delay onset of puberty Removal of testes and Psychotherapy ( assessment,
penis adjustment and exploration of
Male- to-Female Spironolactone or cyproterone
( block effects of testosterone) Breast implants, preferred gender role)
Estrogen and progesterone
vaginoplasty Treat comorbid disorders
Education for family and school/
Changes reversible
work
Referral to Endocrinology Breast reduction and Reassurance and validation
male chest contouring
GnRH analogues in children to
Female- to- Male delay onset of puberty Hysterectomy .
Testosterone
oophorectomy
phalloplasty
.
Changes irreversible
Follow -up
• Require >1 yr of psychiatric follow -up prior to sexual reassignment surgery
• Must spend 6 mos living as preferred gender role before hormones initiated

“O
m
<
O

CD

<
*

cimonton r nC Scenario 394


NEUROLEPTIC MALIGNANT SYNDROME
Current Editor: Jonathan Hamill MD BMus ARCT

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:

• Infectious: sepsis, meningitis, > BP elevation


encephalitis, brain abscess, tetanus > BP fluctuation
• Metabolic: thyrotoxicosis, > diaphoresis
pheochromocytoma
> urinary incontinence
• Neurologic: delirium, catatonia,
• HR and RR increase
epilepsy, lesions/mass/trauma
• Toxic: substances, heavy metals • Negative infectious/metabolic/neurologic/ toxic workup

• 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

RED FLAGS • Recent start/change /increase of antipsychotic or discontinuation of dopamine agonist


• Fever > 38.0o C not responsive to antipyretics, respiratory distress, delirium, dystonia, dysphagia
PMHX • See DDx above, heart/lung/kidney disease, Parkinson' s
PM'HX • NMS, SS . catatonia, .
psychotic disorders, mood disorders, admissions, psychiatrist, therapist GP
MEDS • Dopamine antagonists ( antipsychotics, oral and injectable), dopamine agonists (levodopa - carbidopa,
dextroamphetamine), mood stabilizers (lithium), antidepressants, anticholinergics, metoclopramide
ALLRG • Medication/environmental, note specific reactions

395 Edmonton Manual of Common Clinical Scenarios


PHYSICAL EXAM
General inspection: diaphoresis, disorientation, delirium, GCS for altered LOC, consider MMSE for cognitive screen/
baseline
.
Vitals: t /fluctuating BP. fHR, fRR TTemp,|Sp02
HEENT: sialorrhea, thyroid exam ( thyrotoxicosis), lymph node exam (infectious)
CVS/RESP: cardiac, respiratory distress/infection/aspiration
Gl: abdominal pain ( SS)
Neuro:
• Full neurological exam: power, coordination, reflexes, sensation, tone, focal neurologic signs (brain lesions), Kernig' s and
Brudzinski’s signs ( meningitis)
• Common NMS findings: generalized /symmetrical hypertonia, rigidity, tremor
• Distinguish from SS: "lead pipe" rigidity vs hyperreflexia (SS), bradykinesia vs restlessness (SS)
• Note overlap with EPS: dystonia, akathisia, Parkinsonian symptoms, tardive dyskinesia ( antipsychotic side effects)
• Note overlap with catatonia: psychomotor disturbance with > 3 features of decreased activity/engagement or excessive /
• peculiar motor activity, ranging from unresponsiveness to repetitive/purposeless movements (stereotypies) or agitation

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

LcJmonton Manual of Common Clinical Scenarios 396


PERSONALITY DISORDERS Current Editor: Jonathan Hamill MD, Jorge Perez - Parada MD FRCPC

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

MENTAL STATUS EXAM


Appearance: posture ( aggressive, withdrawn) and attire (eccentric, SAPAS Personality Disorder Screen
fanciful, excessive, revealing), evidence of child- like coping (i.e., teddy 1. In general, have you experienced difficulty
bear ), overly familiar or suspicious attitude, tearful making and keeping friends?
Speech: dramatic, impressionistic (Cluster B) 2. Would you describe yourself as a loner or as
having a preference to be alone?
Emotions: mood may be fluctuating or incongruent; affect may be
3. In general, do you trust other people?
incongruent with mood, inappropriately extreme given context, may be
4. Are you one to easily lose your temper?
irritable, anxious, dysphoric
5. Would you describe yourself or would others
Thoughts: process linear, content may demonstrate entitlement or describe you as impulsive?
self importance, black & white thinking/splitting ( Borderline), rigid, 6. Would you describe yourself as a worrier ?
paranoia/magical thinking (Cluster A ), may have pervasive themes of 7. In general, do you depend on others to help
abandonment, suspicion, catastrophizing you with decision making?
Insight/Judgment: may be impaired 8. In general, are you a perfectionist?
> 3 YES ( except NO in question 3) has a
PHYSICAL EXAM sensitivity of 0.94 and a specificity of 0.85
General PE to rule out other causes in identifying DSM - IV PDs

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>•
»

Biological Psychosocial Social


• Admit to hospital if significant and acute risk to self or others, may require certification
Emergent
• Remember to rule out and treat any co - morbid psychiatric or general medical illness
• No specific medication for personality disorders directly • Dialectical Behavior • Life skills training
• Some medications can be used to treat specific symptoms Therapy (particularly for • Maintaining connections
Borderline PD ) with family/ friends
• SSRIs: irritability, depressive symptoms, anger,
impulsivity .
• CBT psychodynamic • Pro - social activities
therapy, group therapy,
Treatment • Lithium/carbamazepine: mood instability, irritability tailored to the individual
Options • Antipsychotics: impulsivity. mood instability • Validate and praise
• Anxiolytics: anxiety adaptive behaviours and
decision making
• Therapy likley necessary
long term

Edmonton Marumi of Common Clinical Scenarios 398


. .
Current Editor: Michaela Iverson MD Amanda Aiken MD FRCPC Melanie Marsh - Joyal MD FRCPC

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)

> Finances (e.g., difficulty maintaining employment, low SES)

“Baby Blues” Major Depressive Disorder with Peripartum Onset

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

> health of baby • altered appetite (increased or decreased)


• Angry with new baby, partner, and /or other • decreased focus and concentration
03 children
• Predominant mood overall is happiness
U
in rr ISTORY
CL la.
ID • Name, age, sex/gender, ethnicity, occupation or education, source of income, living arrangements
CC • Depressed mood/not feeling the way “ should be feeling”
HPI • MSIGECAPS
• Onset, duration, frequency
• Prior episodes
• Impairment in social, occupational, or other areas of functioning
• Safety: SI, HI, infanticide
RED FLAGS • SI, HI . infanticidal ideation
• Psychotic symptoms
• Manic /Hypomanic symptoms (remote, current )

399 Edmonton Manual of Common Cl:


HX OF • Wanted vs. unwanted
PREGNANCY • Maternal health during pregnancy
• Birthing experience (e.g., complications from delivery)
• Support/sense of feeling supported during pregnancy
• Health of new infant
• Breastfeeding

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)

3. Counseling on lifestyle management


“U
to
Counseling on SSRI
n
Benefits Risks
D-
SD
Psychologically healthy mom can provide an emotionally secure In Utero: Known to cross placenta, low risk of
relationship and environment for her baby to fluorish congenital defects (exception: Paxil associated
with 2x risk of cardiac malformation), risk of
transient withdrawal syndrome at birth
Risk of relapse if treatment discontinued. Recommend Breastfeeding: low levels found in breast milk,
minimum 9 - 18 months of therapy to prevent relapse. psychotropic meds are not a contraindication
to breastfeeding, considered safe
* History of hypomania /mania considered a relative contraindication to antidepressant mono - therapy as this may trigger a relapse.
Referral to psychiatry should be pursued!

Edmonton Manual of Common Clinical Scenaric 400


SCHIZOPHRENIA SPECTRUM DISORDERS
.
Current Editor: Cindy Liu MD Jorge Perez - Parada MD FRCPC

BASICS
Diagnostic Criteria
• HDSBN: DSM psychotic symptoms are hallucinations, delusions, speech disorganized, behavior disorganized/catatonic, negative
. .
symptoms ( affective flattening, alogia avolition) delusions

DISORDER PSYCHOTIC SYMPTOMS TIMING MOOD SX


Brief Psychotic Disorder >1positive psychotic symptom .
>1day < 1month if present 2° .
Schizophreniform Disorder > 2 of HDSBN with at least 1of HDS 1- 6 mos if present 2° .
Schizophrenia > 2 of HDSBN with at least 1of HDS >6 mos if present 2° .
DSM - 5 does NOT identify subtypes for diagnosis:
disorganized, paranoid, catatonic, undifferentiated, residual
Schizoaffective > 2 of HDSBN with superimposed major > 6 mos disturbance ( with present
depressive, manic, or mixed episode >1month > 2 HDSBN)

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,

MEDS • Mood stablizers /anticonvulsants, antipsychotics, antidepressants, levothyroxine . corticosteroids,


. .
benzodiazepines, dextroamphetamine, methylphenidate anticholinergics anti- Parkinsonian, recent changes
SOCPERSHX • Developmental delay, learning disabilities, autism, social support network, abuse/neglect, development through
childhood, legal problems
FAMHX •1 .
° psychotic disorder, schizotypal PD any mood disorder, substance use disorder, completed suicide, movement
disorder (i.e., Huntington's)

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

Blood Work /Urine


• . . . . .
CBC-D, electrolytes, Ca 2 \ Mg, glucose B 12 TSH ALT AST Cr, urea
• Urinalysis, STI testing (infection causing delirium or CNS infection such as neurosyphilis or HIV)
• EtOH, salicylates, acetaminophen, urine toxicology, heavy metals
Radiology/ lmaging
• Consider CT/ MRI brain if focal neurologic symptoms: older age at onset ; presence of fever: fluctuating level of cognition
Special Tests
• LP if suspect meningitis, encephalitis
• ECG - baseline, especially if considering antipsychotic treatement that can prolong QTc interval .
• EEG (rule out temporal lobe epilepsy)
• MoCA - if older age and suspect neurocognitive disorder

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)

Edmonton Manual oi mmon Clinical Scenario 402


SUBSTANCE USE DISORDERS
.
Current Editor: Daniel Friedman MD Jorge Perez - Parada MD FRCPC

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

• Unsuccessful attempts to cut down on use


drinking or drug use?
• Tolerance • Have you felt bad or GUILTY about your drinking or
• Withdrawal
drug use?
• Have you ever had a drink or used drugs first thing in
• Craving or urge to use substance
the morning (EYE - OPENER ) to steady your nerves/
• Excessive time related to substance (obtaining, hangover)
get rid of a hangover ?
• Impaired social or work activities due to substance use
• > 2 is cutoff, pursue further questioning
• Giving up of social or work activities
• Recurrent substance use despite failure to fulfill major roles at
work or at home
• Use despite physical or psychological consequences

• Use of substance in situations that are physically hazardous

‘ 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
.

403 Edmonton Manual of Common ( lin


\sHYSICAL & MENTAL STATUS EXAM
.
VS: including HR, BP, RR, T, Sp02 glucose, GCS
Intoxication HR BP RR Temp Eyes Mental Status Gl Derm

Opioids l/N +/N I +/N


myosis confusion, lethargy,
euphoria
decreased bowel sounds dry

agitation, delirium, hyperactive bowel diaphoretic


Stimulants t mydriasis
psychosis, seizure sounds, emesis
l/N i/N depressed mental status N/decreased bowel sounds N

*
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

Edmonton Manual of ( on Clinical Scenarios 404


SUICIDAL BEHAVIOR
Current Editor: Antonia Capella MD FRCPC

Definitions Risk Factors for Suicide


• Suicidal ideation: thoughts of suicide, can be active ( thoughts of actively ending own life)
or passive ( thoughts of wanting to be dead but no thoughts of actively ending life)
• Sex (male)
• Age ( >60 y/o, 15 - 24 y/o)
• Suicidal intent: can be assessed based on planned vs. impulsive attempt,
• Depression
precautions against being found, seeking help after act, dangerousness of
• Previous attempts
method and presence of " final act " such as note or will; intent is risk factor
• EtOH and substance abuse
for suicide and can be assessed using the Beck Suicide Intent Scale • Rational thinking loss
• Parasuicidal behavior: deliberate self - harm, often impulsive and usually without • Suicide in the family
suicidal intent, but increases risk for suicide (e.g., cutting, burning, scratching, swallowing) • Organized plan
Common Conditions • Nospouse/supportsystems/job
• M : mood disorders, anxiety disorders, psychosis, substance abuse/ withdrawal, eating • Serious illness /intractable pain
'
disorders, adjustment disorder, personality disorders, conduct disorder, dementia
• Other: delirium, chronic medical illness, epilepsy, chronic pain, medication side effects

HISTORY
ID • Name age
status
. . sex /gender, ethnicity, occupation or education source of income, living arrangements, relationship
,

CC/HPI • Hx of risk factors (SADPERSONS); high risk for Aboriginals on reserves


• Suicidal behavior (suicide note, social isolation, preparing a will, giving away possessions, purchasing a burial plot,
feelings of hopelessness, suicide attempt )
• Symptoms: Hopelessness, anhedonia, insomnia, anxiety, psychomotor retardation/agitation, panic attacks,
psychosis (especially command hallucinations)
.
• Safety: SI (content, duration, frequency), parasuicidal behavior, HI infanticide in postpartum patients
• Stressors: changes in health, finances, job loss, relationship dissolution/divorce, sexual orientation, death in
family
.
• Substances: recent overdose; cocaine, amphetamines, hallucinogenics, cannabis, EtOH smoking, opioids, energy
drinks
• Plan: lethality, rehearsal, access to means (e.g., firearm at home), intent, presence of suicide note
• Protective factors including religious beliefs, children in the home, spouse/partner, pets
RED FLAGS • Hxof attempted suicide, major depression, bipolar disorder, anxiety spectrum disorders, substance abuse,
agitation, violence toward others, impulsiveness, hopelessness, detailed plan
PTHX • Prior suicide attempts: severity and outcome of previous suicide attempts, parasuicidal behaviors
• Depression, anxiety, psychotic disorder, other psychiatric illness (schizophrenia alone carries a 10% lifetime risk
for suicide completion)
• Personality disorder (present in 1/ 3 of suicidal patients)

>* 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

Ldrnonton Manual of Common Clinical Scenarios 406


Abuse
.
American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 5th ed. Washington DC: American Psychiatric Association. 2013.
.
Geddes J Price. J. McKnight R. Psychiatry . 4 th ed. New York: Oxford University Press: 2012:166 - 170.
Rabin RF. Jennings JM. et al. Intimate partner violence screening tools: A systematic review. American Journal of Preventive Medicine. 2009:36( 5):439 - 445.
.
Sadock BJ Sadock VA. Kaplan & Sadock ' s Synopsis of Psychiatry . 10th ed. Philadelphia: Lipphcott Williams & Wilkins: 2007:874 - 886.

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.

Neuroleptic Malignant Syndrome


. .
American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 5th ed. Washington DC: American Psychiatric Association 2013.
Balzan MV. The neuroleptic malignant syndrome: A logical approach to the patient with temperature and rigidity. Postgrad Med. 1998; 74:72 - 76.
. .
Gurrera RJ. Caroff SN. Cohen A. Carroll BT. DeRoos F. Francis A. Frucht S Gupta S. Levenson JL. Mahmcod A, Mann SC Policastro MA. Rosebush PI.
. . .
Rosenberg H Sachdev PS Trollor JN. Valamoor VR. Watson CB Wilkinson JR. An international consensus study of neuroleptic malignant syndrome
diagnosticcritieriausingthe Delphi method. JCUn Psychiatry . 2011 Sep;72(9):1222 - 1228.
Gelenberg AJ. Bellinghausen B. Wokcik JD. A prospective survery of neuroleptic malignant syndrome diagnostic criteria in a short term psychiatric hospital.
Am J Psychiatry. 1988;145( 4):517 - 518.
Sadock BJ. Sadock VA. Ruiz P. Kaplan and Sadock ' s Synopsis of Psychiatry. Behavioral Sciences/ Clinical Psychiatry. 11th ed. Philadelphia: Wolters Kluwer ;
CO 2015:925.
-u
C Pileggi DJ. Cook A. Neuroleptic Malignant Syndrome: Focus on Treatment and Rechallenge. Annals of Pharmacotherapy. 2016: 50( 11): 973- 981.
.
Tse L. Barr AM. et al. Neuroleptic Malignant Syndrome: A Review from a Clinically Oriented Perspective. Current Neuropharmacology 2015: 13 ( 3): 395 -
>* 406.
CL
Personality Disorders
American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 5 th ed. Washington DC: American Psychatric Association. 2013.
Sadock B J. Sadock VA. Kaplan & Sadock 's Synopsis of Psychiatry. 10th ed. Philadelphia: Lipincott Williams & Wilkins; 2007.
.
Biskin. R. Paris. J. Management of borderline personality disorder. CMAJ 2012: 184: 1897 1902.
Goldbloom. D. Psychiatric Clinical Skills. Toronto (ON): Mosby;2006. pp. 91- 107.

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.

407 Edmonton Manual of Common Clinical Scenarios


Schizophrenia Spectrum Disorders
. .
American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 5th ed. Washington DC: American Psychiatric Association 2013.
.
Geddes J Price. J. McKnight R. Psychiatry. 4th ed. New York : Oxford University Press: 2012:246- 262.
Sadock BJ. Sadock VA. Kaplan & Sadock ' s Synopsis of Psychiatry . 10th ed. Philadelphia: Lippincott Williams & Wilkins: 2007: 467- 526.

Substance Use Disorders


.
American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 5th ed. Washington. DC: American Psychiatric Association 2013.
Geddes J. Price. J. McKnight R. Psychiatry . 4th ed. New York: Oxford University Press: 2012:376- 407.
Mdege ND. Lang J. Screening instruments for detecting illicit drug use/abuse that could be useful in general hospital wards: A systematic review. Addictive
Behavours. 2011:36( 12):1111- 1119.
Sadock B J. Sadock VA. Kaplan & Sadock ' s Synopsis of Psychiatry . 10th ed. Philadelphia: Lippincott Williams & Wilkins; 2007:381- 466.

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.

TJ

n
—•
<

Edmonton Manual of Common Clinical Scenarios 408


8 SURGERY
Introduction 410
Abnormal Mass & CRC Screening Guidelines 411
Abdominal Pain 413
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
DizzinessA/ertigo 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
£
a
Tinnitus 469
>
W> Trauma 471
13
CO Station Contributors 473
References 474

409 Edmonton Manual of Common Clinical Scenar


INTRODUCTION
Kamran Fathimani BSc MD FRCSC FACS

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.

Here are the top 10 tips to ace the Surgery OSCE:


.
1 Review the learning objectives for the Surgery clerkship. Surgery OSCE stations are linked to the
clerkship’s learning objectives.
2 . Review the exam blueprint to anticipate common Surgery topics that may appear in the OSCE.
Common Surgery OSCE stations include approach to trauma, breast mass, neck mass, gastrointestinal
bleeding, and abdominal pain.
3 . Prepare for and anticipate a variety of potential Surgery OSCE stations such as history - taking,
physical exam, suturing, interpretation of diagnostic imaging or laboratory investigation results,
patient counseling, and writing management plans or physician orders.
4. See as many patient cases as possible in Surgery clerkship and read around these cases. This will
certainly help with studying for the OSCE.
5. Review and practice your approach to common Surgery OSCE scenarios with your classmates. Your
peers can provide feedback for strengths of your approach and critique areas needing improvement.
6. Read the OSCE station instructions carefully. Make a brief plan for how to approach each station prior
to entering the room.
.
7 Manage your time during the Surgery OSCE. Ensure you know how much time you have for each
station and you understand what the buzzer signals indicate during OSCE. Complete a focused
approach to the OSCE station without getting distracted.
8. Demonstrate professional behavior expected during a standardized patient encounter. Examples
include introducing yourself, washing of hands, appropriate patient draping, and respecting the
simulated patient.
9. For physical exam stations, demonstrate and verbalize your examination skills. State normal and/or
abnormal physical exam findings on the standardized patient.
.
10 Avoid egregious management plans. For example, a patient with acute abdomen and abdominal
X -rays showing pneumoperitoneum needs intravenous fluids, antibiotics, and urgent laparotomy. An
egregious management plan would be ordering CT scan of abdomen/pelvis.

You will have an excellent learning experience during your Surgery rotation.
Good luck !

Staff Section Editors


Daniel W Birch MSc MD FRCSC FACS
Department of Surgery CO
University of Alberta
C
era
.
Caroline Jeffery MD MPH FRCSC . o>
Department of Surgery 2
University of Alberta

iion Clinical Scenar 410


ABDOMINAL MASS & CRC SCREENING GUIDELINES
Current Editor: Siddharth Shinde

DIFFERENTIAL DIAGNOSIS
RUQ • Biliary
cancer
-
tract cholecystitis, choledocolithiasis .
• Renal - cancer
RUQ EPIGASTRIC LUQ
• Liver - hepatomegaly, hepatitis, abscess, cancer Eiophagus

EPIGASTRIC • AAA (abdominal aortic aneurysm) liver Stomach

• Pancreas - pseudocyst, cancer


• Stomach - cancer, pyloic stenosis

LUQ • Stomach - cancer f


• Spleen - splenomegaly, abscess, cancer Pancreas
Gall Bladder
ABD WALL • Hernias: umbilical, epigastric
ABDOMINAL WALL
RLQ • Intestine: Cancer .
Crohn’s disease, diverticular
abscess, appendiceal tumor
Small Intestine -
Large Inteitlne

• Intra -abdominal abscess (psoas abscess )


• Ovary - ectopic pregnancy, cyst, cancer
• Fallopian tube - ectopic pregnancy
Cecum
— Ovary

Uterus
Bladder
• Inguinal hernia

SUPRAPUBIC • Uterus - pregnancy, fibroids, tumor /cancer


• Bladder - distension, cancer
.
• Prostate - BPH cancer
Y7
LLQ • Intestine: stool, abscess, cancer, diverticular abscess
• Ovary - ectopic pregnancy, cyst, cancer
• Fallopian tube - ectopic pregnancy
• Inguinal hernia

ISTORY

ID • Patient’s name, age, gender


CC • Abdominal mass

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

PO&GHX • LNMP, ovarian pathology


2r
Q) ALLERGIES • Gluten/wheat (Celiac), lactose intolerance
ttf)
FHX • Cancer (especially CRC), cysts, polyps, Crohn's, ulcerative colitis
3
CO SOCIAL • Smoking, EtOH, recent travel (hepatic pathology)
ROS • HEENT: sore throat/difficulty swallowing (esophageal or EBV), aphthous ulcers (Crohn’s)
• RESP: SOBOE, difficulty breathing on inspiration (cholecystitis)
.
• Gl: early satiety (gastric), GERD painful /difficult swallowing, melena or bright red blood per rectum
• GU: menorrhagia, dysmenorrhea, dyspareunia, dysuria
• MSK /DERM: bone pain (cancer), jaundice, shoulder pain ( spleen/gallbladder /liver pathology)

411 Edmonton Manual of Common Clinical Scenarios


PHYSICAL
General Approach
• Introduce self, ask permission to perform exam, wash hands /perform hand hygiene, proper draping
• . . ..
VS (BP HR RR T Sa02)
Inspection
• Overall appearance: comfortable vs. distressed, still (peritonitic) vs. moving (renal colic), cachexic
• HEENT: mucus membranes yellow, scleral icterus (hepatic ), oral ulcers (Crohn's), enlarged tonsils (EBV), lymphadenopathy
(lymphoma/Virchow ' s node)
• CV: elevated JVP, dependent edema
• Gl: abdomen distended, surgical scars, discrete mass visible, caput medusae, ascites, hernias
• MSK / DERM: gynecomastia, petechiae, jaundice, spider nevi ( stigmata of chronic liver disease)

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

RISK DEFINITION OF RISK SCREENING TESTS AND INTERVALS


Average • -
Asymptomatic, age 50 74 -
• FIT q1 2 years
• If FIT (+) then colonoscopy
• If normal scope, wait 10 years then restart FIT

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

Moderate • Asymptomatic, one 1st degree relative s 60


years at diagnosis of CRC and/or high risk
• Colonoscopy at
earliest
.
age 40 or 10 years prior to index case, whichever is

adenomas OR two or more affected relatives • Repeat colonoscopy q5 years if normal


of any age

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

Edmonton Manual of Common Clinical Scenarios 412


ABDOMINAL PAIN
Current Editor: Alexandria Webb BSc MD

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
<

Edmonto ial of Common Clinical Scenarios 414


ANKLE St FOOT (PAIN, FRACTURES, & DISLOCATIONS)
Current Editor: Kate Bacon MD

DIFFERENTIAL DIAGNOSIS
Common Conditions
Ankle Foot
TRAUMATIC/ • Ligament sprain • Metatarsal fractures
ACUTE • Fibular fracture • Midfoot fractures
• Fibial avulsion fracture • Calcaneal fractures
• Dislocations

ATRAUMATIC/ • Arthritis • Arthritis


INSIDIOUS • Gout • Gout
• Tendonitis • Achilles tendonitis, bursitis
• Arterial insufficiency ulcer • Arterial insufficiency ulcer
• Osteomyelitis • Osteomyelitis
• Charcot joint • Neuropathy

• Avascular necrosis • Plantar fasciitis, bony heel spur

• 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

CC • Ankle or foot (heel, midfoot, toe) pain


HPI • OPQRST
• Mechanism of injury (low energy - think underlying pathological process)
• Previous problems with this site/joint or similar problems with other joints
• Response to activity and rest
• Hx of redness, swelling, or stiffness
• Changes in sensation, strength, ROM, ability to Wt bear

RED FLAGS • Fever /chills, night sweats, Wt loss, high energy mechanism (look for further injuries)
PMHX • Bleeding disorders, arthritis, heart disease, IBD, DM

• Falls: preceding factors .


- i.e., chest pain SOB, syncope/presyncope, focal weakness, seizure
• Osteopenia, osteoporosis, malignancy (pathological fractures)
• Previous injuries to the area
PSHX • Previous surgeries (specifically to site/ joint in question)
MEDS • Rx’n . analgesic use anticoagulation meds, ATBx
,

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)

415 Edmonton Manual of Common Clinical Set


PHYSICAL
General Approach
• . . . . .
ABCs VS ( BP HR RR Temp Sa02) general appearance of the patient
• Remove clothing/splints/casts /dressings/etc. from site of pain and drape properly MSK Inspection: SEADS
• Examine both the ankle and foot together as well as joints above and below area of concern
Swelling
• Look, move, and feel
Erythema/ecchymosis
Look Atrophy/asymmetry of muscle
• MSK: SEADS (comparison to opposite joint), open fracture, laceration, bleeding, observe gait Deformity
and alignment Skin changes/scars
Move
• Check active and passive ROM at ankle, foot, and metatarsals
• Reflexes ( ankle jerk, plantar)
Feel
• MSK: palpate for localized tenderness, deformities, warmth, or joint effusion (include palpation over tibia and fibula)
•NEURO: sensation and muscle strength supplied by
saphenous, peroneal, and tibial peripheral nerves Ottawa Ankle and Foot Rules
.
• VASC: pulses ( posterior tibial dorsalis pedis, Ankle X - rays required if pain in malleolar zone + one of:
popliteal), capillary refill, temperature difference Tender along distal 6 cm of posterior edge of tibia or tip of medial
malleolus
INVESTIGATIONS
Radiology/ lmaging/Blood Work Tender along distal 6 cm of posterior edge of fibula or tip of lateral
malleolus
• Ottawa Ankle and Foot Rules (see box )
> At minimum: AP + lateral views
Inability to Wt bear for 4 steps both at time of injury and in ED
> Consider knee and tibia/fibula X -rays Foot X - rays required if pain in midfoot zone + one of:
Special Tests Tender at base of 5 th metatarsal
• Bone scan (osteomyelitis, bone mets, tumors) Tender at the navicular bone
• Arthrocentesis (investigate joint effusion) Inability to Wt bear for 4 steps both at time of injury and in ED
Blood work may be considered as part of a
rheumatological/pathological/pre- operative workup

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

Fixation, manipulation, arthroscopy (if indicated)


Follow - up
• Instructions to return if increased swelling, cyanosis, significant increase in pain, decreased sensation
• .
Possible complications: nonunion, malunion joint stiffness, AVN, osteomyelitis
Referrals
• Urgent Orthopedic Surgery (compartment syndrome, neurovascular compromise, irreducible, open fracture, Salter - Harris
fractures grade 3 or higher, consider dislocations)
• Rheumatology, Infectious Diseases, Oncology ( if indicated) in
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*

Edmonton Manual of Common Clinical Scenarios 416


ANORECTAL PAIN
Current Editor: Patrick Vallance

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)

• Excoriated and itchy skin


RED FLAGS • ‘ B ’ symptoms: fever, wt loss, night sweats
• Change in bowel/bladder habits, incontinence
PMHX . .
• IBD cancer STIs

PSHX • GI/GU surgeries

PO& GHX • GTPAL, episiotomy/tearing with delivery

MEDS • ATBx, radiation therapy, enemas, immunosuppressants


ALLERGIES • Gluten intolerance

FHX .
• IBD cancer
SOCIAL .
• Smoking, sexual practices (men/ women/both, anal sex foreign body use, safe sex )

ROS • HEENT: oral ulcers (herpes . Crohn’s),pharyngitis (gonorrhea)


• GU: painless lesion (syphilis), painful genital lesion, dysuria (more likely STI), discharge
• MSK /DERM: bony pain (metastases ), other skin lesions ( melanoma)
Sr
<D
RISK FACTORS • Prior .
Hx of radiation therapy Diabetes
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417 Edmonton Manual of Common Clinical S.


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PHYSICAL
General Approach
• Introduce self, ask permission to perform exam, wash hands /perform hand hygiene, proper draping (left lateral decubitus, knees to
chest )
. . .
• VS (BP HR RR Temp, Sa02)

HEENT: oral ulcers, pharyngitis, anemic pallor


DERM: ulcers / lesions / rash
GU: genital/rectal discharge from vagina or urethra
Gl
• Inspection:: distended, external hemorrhoid, anal fissures, fluctuant masses, purulent discharge, erythematous skin, rectal prolapse
. .
( reducible/non-reducible): anal fistula openings (off midline suggest: atypical, crohn' s TB leukemia, HIV)
• Auscultation: bowel sounds
• Percussion: tenderness
• Palpation: tenderness (especially in LLQ). If patient is too tender to permit examination, may need to be examined under
anesthesia
SPECIAL TESTS
• DRE: check for blood, impacted stool, assess rectal tone, prostatic contour, palpable mass, abnormal amounts of pain elicited
• Patient may be too tender to permit DRE
INVESTIGATIONS
Blood Work
• CBC- D, BUN, electrolytes
Radiology/ lmaging
• If .
abscess not clinically evident : CT MRI, TRUS
• Colonoscopy
Special Tests
. .
• Stool for C& S, O& P C diff. toxin, culture from lesions ( gonorrhea and chlamydia) VDRL ( syphilis)
Surgical/ Diagnostic Interventions
• Dependent on underlying condition

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
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i dmonron Manual of Common Clinical Scenarios 418


APPROACH TO FRACTURE
Current Editor: Shalini Reddy BSc MBB5

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

Fracture Disruption in bone tissue

[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

RED FLAGS • Open fracture/significant soft tissue injury


• Circulatory compromise: vascular compromise (delayed capillary refill, pallor, decreased or absent pulses),
hemorrhage
• Neurologic deficit
• Compartment syndrome: early (pain out of proportion, uncontrolled by analgesics, exacerbated by passive
.
stretch of involved muscular compartments) vs late (paralysis, paresthesias)
. ..
• Severe associated injuries (high energy trauma, e g tension pneumothorax)

PMHX • Previous fracture, injury, pain, or surgery at site of injury


• Neoplasms, osteoporosis
• Endocrine: malnutrition, Vit D deficiency . Cushing's syndrome, hyperparathyroidism, hyperthyroidism, renal
osteodystrophy
MEDS • Drugs causing decreased bone mineral density: corticosteroids, anti- epileptics, dietary calcium and Vit .D
deficiency
FHX • Osteoporosis, neoplasms
SOCIAL - morbid mobility), living situation/environment, social supports,
• Occupation, functional status ( walking aids, pre
change in physical activity regimen, smoking, EtOH, illicit drugs or IVDU
<D ROS • CV: chest pain, claudication symptoms (cramp, ache, weakness)
W> • CNS: pre-existing paresthesias or weakness (i.e., secondary to previous stroke), confusion, fatigue
D • MSK: pre-existing muscle/joint pain
LO

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

419 LdmofUon Manual ot Common Clinical


Inspection:
MSK Inspection: SEADS
•Skin must be visualized circumferentially in all fractures
Swelling
• Open vs. closed fracture, soft tissue damage, bruising, old scars, bleeding, signs of wound infection,
Erythema/ecchymosis
other injuries
• Joint above and below
Atrophy/asymmetry of
muscle
Palpation:
Deformity
• Tenderness, deformity, warmth, swelling, crepitus
Skin changes /scars
• As pain may be referred, palpate well beyond location of pain described by patient
• Joint above and below

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

Edmonton Manual of Common Clinical Scenarios 420


BILIARY DISEASE: CHOLELITHIASIS
Current Editor: Alexandria Webb BSc MD

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
>
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to

421
PHYSICAL
General Approach
• Introduction, wash hands /perform hand hygiene, ask permission

ABCs and VS (BP. HR. RR. Temp, Sa 02)


Inspection
• General: well vs. unwell, discomfort/pain, dehydration, jaundice (choledocolithiasis or ascending cholangitis, leaning forward
(pancreatitis)
• Abdomen: contour of abdomen, masses, scars, stigmata of liver disease, ascites, hernias
Auscultation
• Bowel sounds - ’Note: auscultation is of limited use overall
Percussion
• Percussion tenderness for presence of ascites (both unlikely with cholelithiasis)
Palpation
• Light palpation: start furthest from most painful area and progress to most painful area
• Deep palpation if tolerated
• Murphy's sign: palpation of RUQ on deep inspiration causes arrest of breath
Special Tests
• DRE to check for masses, bleeding, tenderness, rectal tone

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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Edmonton Manual of Common Clinical Scenarios 422


BITES & DIRTY WOUNDS
. .
Authors:Hollie Power MD Jay Zhu MD James Wolfli MD FRCSC

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

ID • Patient’s name, age, gender


CC • Bite or cut
HPI • Location/date/time of incident, depth of wound
• Mechanism of wound ( scratch, laceration, crush, puncture)
• Agent involved ( human, dog, cat . insect, snake, foreign object)
RED FLAGS • Signs and symptoms suggesting:

• Sepsis (tachycardia, tachypnea, fever /chills, hypotension, decreased U/O, confusion)


• Septic arthritis (pain with passive ROM and axial loading of joint, swelling, erythema, warmth over affected bone or
joint)
PMHX • Immunization status
• Immunocompromised states (e.g., HIV, immunosuppressants post - transplant, asplenism, DM)

ALLERGIES • ATBx, local anesthetics

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)
> »

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423 Edmonton Manual of Common Clinical Scenarios


RECOMMENDATIONS FOR TETANUS PROPHYLAXIS
Previous Doses of Clean and minor wound Tetanus- prone wound
Adsorbed Tetanus
Toxin Tetanus toxoid * TIGA Tetanus toxoid * TIGA

< 3 or unknown Yes No Yes Yes

Only if last dose given Only if last dose given


>3 No No
> 10 yrs ago > 5 yrs ago

‘Tetanus toxoid: 0.5 ml IM


Tetanus immunoglobulin (TIG): 250 units IM

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)

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Edmonton Manual of Common Clinical Scenarios 424


BLADDER OBSTRUCTION & PROSTATE CANCER
Current Editor: Youness Elkhalidy BSc

DIFFERENTIAL DIAGNOSIS - URINARY RETENTION


Child • Posterior urethral valves
• Stricture
• Phimosis

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

Male Adult • Prostatic : BPH (most common), cancer, prostatitis


• Anatomical abnormalities: high bladder neck, compression from adjacent organ (rectum)
(Outflow Tract • Urethral stricture/contracture: following instrumentation of urinary tract
Obstruction) • Other: penile/urethral trauma, balanitis, cystitis

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

425 Edmonton Manual of Common Clinical Scerv i 10' .


PHYSICAL
General Approach
• ABCs and VS ( BP. HR. RR. Temp. Sa02)
Inspection
• Abdominal distension due to enlarged bladder or pelvic mass +/- concomitant large bowel obstruction
• Males: check phallus, comment on blood at the meatus ( trauma +/- meatal stenosis), urinary incontinence (possible overflow
incontinence), curvature to the penis ( penile trauma) and swelling/purulence of the foreskin ( balanitis)
• Females: pelvic exam is indicated to rule out pelvic mass. Examination of the vulva for lichen planus /sclerosis.

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

427 Edmonton Manual of CommonClmic.il Sc <


PHYSICAL
General Approach
• Effective clinical breast exam depends upon thorough examination of both breasts and all regional lymph nodes
• Gown patient and expose waist; presence of chaperone is recommended, provide feedback to comfort patient
Inspection
• Patient sitting bilaterally inspect breast, areola, nipple, axillae
• 4 positions: arms at side, arms over head, hands on hips, leaning forward
• Note: skin changes (erythema, edema, retraction, peau d’orange) . nipple changes (retraction, inversion, excoriation (Paget’s)), and
variation in symmetry and contour
Palpation
• Patient sitting - lymph nodes: axillary ( 5 groups), supraclavicular, infraclavicular, cervical
• Patient supine, arms behind head: bilaterally palpate breast areola, nipple, axillae
• Note: location/size/shape/consistency/ tenderness/mobility of breast mass

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

I of Common Clinical Scenario 1 428


Current Editor: Joshua Hefler MD

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

• 'Only count 2° and 3° burns;1° burns do not


count toward the 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

429 Idmonton Manual of Common Clir


PMHX • AMPLE trauma Hx (allergies, meds, PMHx, last meal, events)

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

niton Manual of Common Clinical Scenarios


. 430
DIPLOPIA
. .
Authors: Scott McLeod MD Francois Jacob MD DB Sinclair MD FRCPC

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

PSHX • Any ocular surgery, especially past strabismus surgery


. .
FHX • Family ocular Hx, autoimmune disease, thyroid disease DM, CVA, Ml aneurysms, polycystic kidney disease
SOCIAL • Smoking, recreational drugs (sympathomimetics/stimulants (e.g., cocaine)-mydriasis; opioid agonists-
pinpoint pupils)
ROS • HEENT: other CN symptoms
• CV: risk factors for CAD
CD • RESP: SOB
W)
• Gl: dysphagia
13
if ) • MSK / DERM: muscle weakness, fatigue

431 Edmonton Manual of Comm nical Scenar


PHYSICAL
General Approach
• Introduce self, wash hands /perform hand hygiene, ask for permission to examine patient
.
• VS ( BP HR, RR , T, Sa02)
Inspection
• Symmetry: ptosis (measure interpalpebral fissure height with patient looking comfortably in the distance), pupil size
• Signs of trauma, number
• Exophthalmos, enophthalmos

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

Edmonton Manual of Common Clinical Scenarios 432


DIZZINESS / VERTIGO Current Editor: Irum Rizwan

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

Psychogenic of above symptoms; often • Mood disorder

Dizziness difficult to describe/localize • Panic disorder

• Dizziness associated with hyperventilation

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

PMHX • Hearing loss, previous labyrinthitis, cholesteatoma, syphilis .


MS, Parkinson's, TlA, stroke, epilepsy, cancer
(possible metastases to brain), migraines, anxiety, depression, atrial fibrillation, carotid stenosis, aortic
. .
stenosis), head trauma, HTN CHF renal insufficiency, anemia, visual impairment, recent ATBx use

£
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)

433 Edmonton Manual of union C


PHYSICAL
General Approach
.
• ABCs VS ( BP. HR. RR. T. Sa02). orthostatic BP. GCS

Neuro - otologic exam for vertigo


• General appearance
• Cross examination:
> Ears (out to in)
> Nose (signs of URTI)
> Oral cavity/oropharynx ( signs of pharyngitis)
> Neck (masses/lymphadenopathy)
• CN: ll-XII
• Head shake and head thrust test
.
• Smooth pursuit (observe during CN III, IV VI exam)

.
• 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

Suspected Diagnosis Specific Investigations Treatment


Presyncope .
• CBC-D electrolytes, creatinine, trops . • Treat underlying etiology
CXR. EKG
• ECHO, stress test . Holter monitor
Disequilibrium
• Audiogram . Weber and Renne tests,
• Treat underlying etiology( peripheral neuropathy .
Parkinsonism, impaired vision)
vision testing, blood glucose
• Physiotherapy for strength and proprioception

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

Ldmonton Manual of Common Clinical Scenarios 434


DYSPHAGIA
.
Authors: Shawna Pandya MD Kal Ansari MD FRCSC ABO ABFPRS

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

• Progression: sudden vs. gradual onset


• Gurgling or regurgitation of undigested food ( Zenker's diverticulum)
RED FLAGS • Inability
to swallow anything, drooling, unexplained Wt loss, emesis, hematemesis, change in voice, drastic
change in reflux symptoms, new focal neurological deficit (especially new weakness)
PMHX • GERD, DM, scleroderma, Sjogren’s syndrome, AIDS, syphilis, poliomyelitis, stroke, achalasia, peripheral
.
neuropathy, myasthenia gravis, muscular dystrophy, MS Parkinson’s, cancer
• Previous endoscopies: indications and findings
PSHX • Laryngeal, esophageal, gastric, or spine surgery
MEDS • NSAIDs (mucosal injury), new medications (pill esophagitis)

FHX • Cancer of the upper aerodigestive tract, MS, autoimmune diseases


SOCIAL • Occupation (risk .
of environmental radiation), caustic ingestion smoking/EtOH use
ROS • HEENT: dry eyes, dry mouth, globus sensation, odynophagia, difficulty chewing, drooling
• NEURO: paresis, facial muscle fatigue, balance disturbance/ataxia, tremor, difficulty speaking
•CV: chest pain
• RESP: cough, SOB
• Gl: abdominal pain, heartburn, reflux
0)
W>
• MSK: atrophy, muscle/ joint pain .
• DERM: scleroderma, rash, swelling, skin thickening, Raynaud’s
D
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435 Edmonton Manual of Common Clinical S narios


PHYSICAL
General Approach
. . .
• Introduction, wash hands /perform hand hygiene, ask permission VS ( BP HR. RR. Temp Sa02). ABC IV. monitors .
Inspection
• Well vs. unwell
• Nutritionally replete, depleted, or emaciated
• Oral cavity: look for poor dentition, xerostomia, peritonsillar abscess, pharyngitis, tumor
• Skin: cutaneous lesions suggestive of CTD, Raynaud’s phenomenon (collagen vascular disease), rashes, sclerosis
• Muscles wasting, fasciculations

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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.
Therapy Dietician
CTQ
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2

Edmonton Manual of Common Clinical Scenarios 436


EPISTAXIS
. .
Authors: Michael J Kapusta MD Christopher Fung MD Ashraf Khan MBChB CCFP

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)

PMHX • Previous epistaxis ( ER visit required?)


• Bleeding disorders or conditions associated with coagulopathy (e.g., hemophilia, pregnancy, liver disease)
• Hypertension

PSHX • ENT surgeries


MEDS • Medications that . .
promote bleeding (e.g., ASA NSAIDs, clopidogrel heparin, warfarin)
FHX • Epistaxis or bleeding disorders

SOCIAL • Smoking . EtOH, cocaine use


• Exposure to low humidity environment
ROS • HEENT: headache, fever, sinus congestion, allergies
• MSK/DERM: bruising, petechiae

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437 Edmonton Manual of Common Clinical


PHYSICAL
ABCs: be sure patient can maintain airway
General Approach
• . . . .
VS: BP HR RR Temp Sa02 ( assess for potential hypovolemia)
Inspection
Anterior
ethmoid artery
Posterior
\
• Have patient in sitting position (reduces venous pressure) S
ethmoid artery
• Signs of nasal fracture ( swelling, ecchymosis, nasal deformity) Kiesselbach's
• Nasal speculum, headlamp, and suction to visualize source of bleed plexus
• Phenylephrine, two sprays of 0.5 - 1% solution, acts as a vasoconstrictor
and can assist visualization
• Fiberoptic endoscopy may be required for severe bleeding or to
visualize a posterior bleed
• Examine for other signs of infectious cause
-
^
'" Bleeding
INVESTIGATIONS 3
Blood Work Superior
Sphenopalatine artery labial artery
• Not routinely required unless there is a significant suspicion of anemia
from recurrent or prolonged episodes of epistaxis
• INR / PTT if coagulopathy is suspected

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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Edmonton Manual of Common Clinical Scenarios 438


Current Editor: Siddharth Shinde

DIFFERENTIAL DIAGNOSIS

LOWER Gl BLEED
CLASSIFICATION Bleeding distal to ligament of Trietz

SIGNS Hematochezia, fatigue, BRBPR, fever, dehydration,


abdominal cramping
Anatomic • Diverticulosis
• Meckels diverticulum
• Diverticulitis
• Anal fissure
Vascular • Angiodysplasia
• Ischemic colitis
COMMON • Radiation induced colitis
ETIOLOGY • Hemorrhoids
Inflammatory • Infectious colitis
• Crohn's disease
• Ulcerative colitis
Neoplastic • Polyps
• CRC

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

RED FLAGS • Hypotension, syncope, tachycardia, diaphoresis


• Constitutional symptoms

PMHX • Gl bleeds
• Bleeding diathesis
• Liver dysfunction, portal hypertension
• Hemorrhoids
• IBD
• Cancer, radiation exposure

PSHX • Gl, vascular, past colonoscopies

MEDS • NSAIDs, ASA, Plavix, steroids, anticoagulants, iron supplements, Pepto Bismol

FHX • Bleeding disorders


• Gl cancer, IBD
SOCIAL • Smoking, EtOH, travel Hx
• Diet (iron, beets, licorice)
Sr
<D ROS • HEENT: scleral icterus, jaundice, vertigo, light -headedness ( anemia from blood loss)
W>
• CV: palpitations
D • Resp: SOBOE
CO
• Gl; Abdo pain
• GU: Hematuria, menorrhagia
• MSK/DERM: jaundice, purpura, ecchymoses

.
RISK FACTORS • Long-term NSAID use, multiple comorbidities Hx of Gl bleeds

439 Edmonton Manual of Common Clinical Scenarios


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
Inspection
• Gl: distension, surgical scars, caput medusa
• DERM: stigmata of liver disease, petechiae. bruising, pallor, pyoderma gangrenousm

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

> Insert foley to urometer (monitor to U/O and response to fluids)


Emergent Treatment
• NPO until gastroscopy or Gl consult
colonoscopy/sigmoidoscopy
• Consider
management until etiology is confirmed
• Symptomatic

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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Edmonton Manual of Common Clinical Scenarios 440


Current Editor: Caitlyn Collins MD

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

Peptic ulcer disease (gastric or duodenal)


Portal hypertension
• Esophageal varices
• Portal hyperteensivegastropathy

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
W)
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

441 .
Edmonton Maiuiil of Common Clinical Seen,if
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

Invasive Diagnostic Interventions


• Esophagogastroduodenoscopy

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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3
*

linonton M ual of Common Clinical Seer 442


GYNECOMASTIA
Current Editor: Brianne Tetz MD

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)

• Trauma or irritation (mastitis)

RED FLAGS • B symptoms, bloody nipple discharge, fixed/hard lump ( breast cancer )

• Hemoptysis, dyspnea, bony pain (metastatic breast cancer )

PMHX •Hyperthyroidism, liver disease, renal disease, prostate cancer, Hx of hypogonandism

PSHX • Previous breast/chest surgery


PO&GHX • Infertility, reduced libido, sexual dysfunction, reduced nocturnal erections (suggests hypogonadism)
• Pubertal changes (precocious/delayed puberty), feminization, loss of secondary sex characteristics

-
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
0)
w> • CV: palpitations

=3
CO
• 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

443 Edmonton Manual of Common Clinical Scenario


PHYSICAL
General • Wash hands/perform hand hygiene, ask patient for permission to examine
• Assess patient's LOC, VS ( BP, HR, RR, Temp, Sa02), proper draping
Chest/Breast • Inspect for any obvious masses, asymmetry, skin changes, nipple discharge or nipple retraction
• Palpate both breasts ( start with normal) and axillary lymph nodes

> 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

>Secondary hypogonadism: low T, low/inappropriately normal FSH • Galactorrhea (hyperprolactinemia)


• Small testicles and lack of secondary
• Serum estradiol
sexual characteristics (hypgonadism)
> If high - urgent U/S of testicles for neoplasm
> If testicular U/S negative, an urgent CT scan to rule out adrenal neoplasm is required
• hCG, alpha - fetoprotein ( tumor markers)

> Elevated tumor markers require CXR (bronchocarcinoma) and testicular U/ S


• Serum prolactin
> Elevated prolactin requires MRI head (pituitary tumor )
• Cr, urea ( renal failure), LFTs (liver disease), TSH, free T4 /T4 (hyperthyroidism)

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
c
00
a>
3

Ldmonton Manual of Common Clinical Scenarios 444


HAND (PAIN, FRACTURES, & DISLOCATIONS)
.
Authors: Hollie Power MD. Regan Guilfoyle MD Michael Morhart MD FRCSC

Common Hand Pathologies:


Trauma
•Fractures: distal phalanx (most common), proximal /middle phalanx, metacarpal
•Dislocations: PIP (most common), DIP, MCP (rare)
• Ligaments: volar plate injury, ulnar collateral ligament tear ( skier ’s thumb)
• Tendons: boutonniere deformity, mallet finger, swan neck deformity (may also be non- traumatic, e.g., RA )

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

RED FLAGS • Signs of neurovascular compromise

PMHX • Previous trauma to hand/ wrist • Arthritis, bleeding diathesis, diabetes, thyroid

PSHX • Previous hand/ wrist surgery • Previous hand/wrist surgery

FHX • Collagen vascular disease • Arthropathies, collagen vascular disease


SOCIAL • Hobbies, smoking, EtOH • Hobbies, smoking, EtOH

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
0)
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)

445 Ldmoriton Manual of Common Clinical be iiru,


CONFIRMATION OF
CONDITION COMMON FINDINGS ON EXAMINATION
DIAGNOSIS
• PIP/DIP/MCP: dorsal dislocation most common (hyperextension injury)
DISLOCATIONS • Hand X -ray ( 3 views)
• May have subluxation with movement - implies severe ligamentous injury
border digits ( thumb and fifth finger )
• Most commonly affect
• Distal phalanx: often accompanied by soft
tissue injury, subungual hematoma
FRACTURES • Middle/proximal phalanx: rotation, scissoring (overlap of fingers while making • Hand X - ray ( 3 views)
a fist ), shortening
BONE • Metacarpal: loss of prominence of metacarpal head, scissoring

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
c
Surgical Treatment
OQ
• Complex dislocations and fractures may require CRPP (closed reduction and percutaneous pinning) or ORIF (D

• Repair of associated injuries to digital nerves, ligaments, tendons 3


Referrals
• Plastic Surgery. Physical Medicine and Rehabilitation, Rheumatology. Occupational Therapy. Physiotherapy

446
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)

Glasgow Coma Scale*


Points Best Eye Opening Best Verbal Best Motor
6 Follows commands
5 Oriented Localizes pain
4 Spontaneous Confused Withdraws from pain
3 To speech Inappropriate Flexor posturing
2 To pain Incomprehensible Extensor posturing
1 None None None
Categories of Head Injury
GCS score: Mild: 14- 15; Moderate: 9 - 13; Severe: GCS < 8 (indication to intubate)
’Note: Based on best effort. Not applicable if < 4 years old.

HISTORY
ID • Patient ’s name, age, gender, handedness, occupation

CC • Head trauma

HPI • Mechanism of injury:




.
MVA: velocity, use of seatbelt, airbags deployed, location in car ejection, prolonged extraction
Fall from height: distance fallen, position of landing, type of surface
• Timing of injury (serious complications much less likely if > 6 hrs and asymptomatic)
• Neurologic symptoms:

• Changing LOC, seizures


• Altered sensation, weakness or paralysis, saddle anesthesia, fecal or urinary incontinence
• Headache, nausea, vomiting, changes in vision, dizziness, photo -/phono - sensitivity, tinnitus
• Behavioral, emotional, or cognitive disturbances
• Other systemic injuries sustained
• Last meal

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)

FHX • Neurological disorders, bleeding/clotting disorders

SOCIAL • Drugs /EtOH (especially at .


time of injury), suicide Hx ( toxidromes) assaults
• Occupation, place of residence, social support network

>. ROS • HEENT: neck pain, deficits in facial/ ENT function


• GU: incontinence
<D
txo
D
LO

447 Edmonton Manual of Common Clinical be: -


PHYSICAL
. .
Primary survey ( ABCDE) including VS ( BP HR, RR, Temp Sa02), as per ATLS protocol
Secondary survey
• HEENT:
> Inspect for open or depressed skull fractures, obvious deformities, presence of scalp lacerations
> Identify signs of Basilar skull fracture: periorbital ecchymosis (raccoon eyes) , mastoid ecchymosis ( Battle’s sign) , CSF
.
rhinorrhea, rhinorrhagia CSF otorrhea, otorrhagia, hemotympanum
> Inspect for subconjunctival hemorrhage, hyphema, malocclusion
> Perform fundoscopic exam: papilledema
> Palpate for bony deformities, cervical tenderness
• NEURO:

> 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
QTQ
ro
3

Edmonton Manual of Common Clinical Scenari 448


Current Editor: Joshua Hcfler MD

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

'Denotes most common conditions

HISTORY
ID . .
• Patient 's name age gender

CC • Gross or microscopic hematuria


HPI • Onset, frequency, provoking, and palliating factors
• Quality: frankblood in urine, presence of clots
• Associated with pain: flank ( pyelonephritis) radiating to groin (nephrolithiasis), suprapubic (cystitis), perineal
.
• Urinary symptoms: dysuria pyuria, frequency, urgency ( UTI), changes to stream (i.e., weak, dribbling)
.
• Rule out: other sources of bleeding (Gl gyne), beets, fever, strenuous exercise
RED FLAGS • Smoking Hx or occupational exposure to chemicals/dyes
• Gross hematuria
• Age > 40
• Persistent irritative voiding symptoms
• Hx of pelvic irradiation
• Hx of chronic or recurrent UTI
• Analgesic abuse, previous exposure to cyclophosphamide (bladder cancer )
PMHX • Urological disorders, nephrologic conditions, urinary retention, recurrent UTI, malignancy, HTN
>•
<D PSURGHX • Instrumentation of GU tract
tXO • LMP (pseudohematuria)
PO&GHX
D
CO MEDS • Anticoagulants, medications that might cause nephritis ( ASA . NSAIDs)
FHX • Hereditary nephritis, polycystic kidney disease, sickle cell disease, renal stones, malignancy

SOCIAL • African American descent (sickle cell trait )


• Smoking Hx and industrial exposure to tetraethylchloride, benzene, and aromatic amines
ROS . -
• Headache ( HTN) recent URTI or impetigo (2- 3 days: IgA nephropathy, 2 3 wks: post streptococcal
glomerulonephritis), constitutional symptoms

449 Edmonton Manual of Common Clinical Sc ?nar > i


PHYSICAL
General Approach
•VS ( BP, HR, RR, Temp, Sa02)
•Alert vs. lethargic ( sepsis)
• Signs of recent weight loss / cachexia ( malignancy)
• Rashes ( authoimmune / post -infections) , bruising ( anticoagulation / coagulation disorder ), obvious trauam

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

Edmonton Manual of Common Clinical Scenarios 450


Current Editor: Alexandria Webb BSc MD

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

ligament varicosities ( women), ( pseudo) aneurysm of iliac or femoral arteries


Common Conditions
Groin Hernias Ventral Hernias
• Indirect inguinal hernia: protrusion through inguinal canal, exiting • Umbilical hernia: congenital or acquired ( secondary to
lateral to inferior epigastric vessels; due to persistent patency of the obesity, pregnancy, ascites)
processus vaginalis • Epigastric hernia: congenital or acquired, sac exits in the
• Direct inguinal hernia: protrusion through Hesselbach’s triangle, midline through the linea alba, superior to umbilicus
medial to inferior epigastric vessels; due to weakness of anterior • Incisional hernia: through previous abdominal surgery
abdominal wall incision
• Pantaloon hernia: inguinal hernia involving both indirect and direct • Spigelian hernia: through defect of the transversus
components straddling inferior epigastric vessels abdominis muscle, lateral to rectus sheath
• Femoral hernia: protrusion through femoral canal, medial to femoral
vein

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
D
CO
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

451 mton Manual omr


PHYSICAL
General Approach
• Wash hands, proper draping
• VS (BP, HR, RR, Temp, Sa02)
• Exam should be performed with the patient in both upright and supine positions
Inspection
• Previous surgical sites
• Visible masses that increase in size with Valsalva maneuver
• Overlying skin erythema (strangulation)

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

Urgent or Emergency Surgery


• Urgent surgery indicted for incarcerated hernias, to prevent strangulation
• Emergent surgery indicated for strangulated hernias, bowel perforation, and peritonitis, and should be performed within 6 hrs
.
> NPO for OR IV fluids, analgesia, antibiotics

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
c
OQ
CD
2

Edmonton Manual of Common Clinical Scenarios 452


HIP (PAIN, FRACTURES, & DISLOCATIONS)
Current Editor: Shalini Reddy BSc MBBS

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

MEDS -hypertensives (associated with hypotension and fall) Vit D


• Steroids ( associated with osteonecrosis), anti
deficiency, cancer, bisphosphonates (possible association with fractures of proximal femur)
.
SOCIAL • EtOH ( associated with osteonecrosis), smoking (associated with osteonecrosis), ambulatory status before
the injury, living situation

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

453 Edmonton Manual of Common Clinical Seen ) ' .


Palpation
• Palpate the iliac crest, greater trochanter, trochanteric bursa, ASIS, PSIS, ischial tuberosity, symphysis pubis, SI joint, lumbosacral
joint, sacrococcygeal joint, inguinal ligament
> Point tenderness over the trochanteric bursa ~ 2.5 cm posterior and superior to the greater trochanter indicates trochanteric
bursitis (also occult fracture, stress fracture, metastases to femur)
> Progressive lateral hip pain, worse with pressure and weight bearing suggests metastatic cancer to femur
• Palpate hip flexors, abductor muscles for signs of pathology
• Palpate lower extremity pulses: dorsalis pedis and posterior tibialis arteries ( in patients with suspected aortoiliac vascular occlusive
diease)
ROM
• Perform/measure full ROM of the hip noting patient ’s tolerance of the maneuver and any endpoint stiffness ( flexion: 120°, -
extension: ~ 15°, abduction: ~40°, adduction: ~30°, internal rotation: ~ 300- 40o, external rotation: ~30°-40°)
> Impaired ROM and severe pain at the endpoints suggest osteoarthritis, osteonecrosis, occult fracture, acute synovitis,
metastatic involvement of the femur
• Decreased internal and external rotation can be due to the loss of articular cartilage, outgrowth of acetabular osteophytes, acute
synovitis
• Decreased internal rotation ( < 15°) is the most sensitive sign of early osteoarthritis
• Patients with non-displaced fracture have a positive log-roll test (pain on internal and external rotation of the limb)
Motor
• Examine lower extremity myotomes for atrophy/ weakness (radiculopathy/myelopathy/myopathy)

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 )

F c ,monton Manual of Common Clinical Scenarios


.
454
Current Editor: Kevin Zuo MD, Thuc -Nhj Tran Dang MD

DIFFERENTIAL DIAGNOSIS
Clinical jaundice does not occur until serum bilirubin > 40 pmol/L (twice upper limit of normal)

Unconjugated hyperbilirubinemia Conjugated hyperbilirubinemia


Pre- hepatic (hemolysis) Hepatic Post-hepatic
Intracorpuscular Defects • Decreased uptake: Gilbert ’s, drugs • Gallstones: choledocholithiasis
• RBC membrane: spherocytosis, (rifampin, contrast ) • Cancer: pancreas, bile ducts, ampulla (of Vater )
elliptocytosis, paroxysmal nocturnal
hemoglobinuria
• Decreased conjugation: Gilbert ’s
Criggler -Najjar, hepatocellular
. • Biliary structures: post -cholecystectomy, PSC,
biliary atresia
• RBC enzymes: G6PD, pyruvate disease, drugs (chloramphenicol)
kinase deficiency • Decreased excretion (cholestasis ):
• RBC hemoglobin: sickle cell, Dubin - Johnson, Rotor ’s syndrome,
thalassemia benign recurrent cholestasis,
Extracorpuscular Defects cholestasis of pregnancy, drug-
• Blood: toxins, drugs, infections (i.e., induced cholestasis, PBC, PSC, TPN
viral hepatitis, malaria), immune • Mixed: hepatocellular disease, sepsis

• Vascular: TTP/HUS/DIC, HELLP,


malignant HTN, mechanical trauma
.
(i.e , malfunctioning valves, VAD)
• Ineffective erythropoiesis:
megaloblastic anemia

Unconjugated hyperbilirubinemia: overproduction, impairment of uptake or conjugation of bilirubin


Conjugated hyperbilirubinemia: decreased excretion into the bile ductules or backward leakage of bilirubin

HISTORY
ID • Patient ’s name, age, gender

CC • Yellow discoloration of skin, sclera, or mucus membranes


HPI • Timing: acute vs . sub-acute, previous episodes, relation to stress and fatigue
• Abdominal pain ( biliary colic), mass, Wt loss, appetite, fever
• Stool color ( acholic, i.e., pale or clay - colored), urine color (dark or cola -colored)
• Pruritus, ecchymoses, bleeding

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
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455 Edmonton Manual of Common Clinical Scenarios


PHYSICAL
General Approach
• Ask permission to perform physical exam, wash hands /perform hand hygiene, proper draping and exposure
• VS ( BP, HR , RR, Temp, Sa02)
• Mental status examination

Inspection
• Jaundice of sclera, frenulum, skin
• Assess for stigmata of chronic liver disease

> HEENT/CNS: asterexis, fetor hepaticus, parotid hypertrophy


> ABD: ascites, caput medusa, splenomegaly, surgical scars
> MSK : telangiectasia, spider angiomas, gynecomastia, Dupuytren’s contractures, leukonychia, palmer erythema, peripheral
edema
HEME: ecchymoses, petechia
GU: testicular atrophy
Auscultation
• Bowel sounds
Percussion
• Percuss for the edge and span of the liver, Castell’s sign/Traube's space, bulging flanks, shifting dullness
Palpation
• Abdominal tenderness, masses, hepatosplenomegaly, liver nodularity
• Courvoisier sign: non-tender palpable gallbladder in patient with jaundice (malignant obstruction of biliary tract)
• Murphy’s sign: arrest of inspiration with pressure over RUQ due to pain (cholecystitis)
• Virchow ’s node ( L. supraclavicular node) and Sister Mary Joseph's node (periumbilical node) associated with Gl malignancy

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

» Hemochromatosis: Ferritin, FE, transferrin, TIBC .


hepatitis Budd Chiari), acute viral hepatitis, acute
biliary obstruction, autoimmune
> Serum nl- antitrypsin
.
> Wilson’s: Ceruloplasmin 24 hr urine copper
> Toxicology screen: serum acetaminophen level
Radiology/Imaging
• Abdominal U/ S: intrahepatic vs. extrahepatic bile duct dilation/obstruction
•EUS, MRCP, ERCP: extrahepatic obstruction
•CT if suspect malignant obstruction
Liver Bx: persistent enzyme elevation with unclear diagnosis
U REATMENT
Gallstone disease: ERCP, cholecystectomy
Viral hepatitis: anti-viral medications, hepatoma screening, blood/sex precautions
Acetaminophen: NAC protocol if )
Alcoholic hepatitis: restrict EtOH use, vitamin supplementation ( thiamine) C
QTQ
Gilbert syndrome: benign, avoid unnecessary testing, no treatment necessary 0
Hemochromatosis: phlebotomy, iron chelation <

Edmonton Manual of Common Clinical Scenarios 456


KNEE (PAIN, FRACTURES, & DISLOCATIONS)
Current Editor: Orysya Svystun

DIFFERENTIAL DIAGNOSIS
Anatomical Approach:
• Ligament: anterior/posterior cruciate ligaments, medial /lateral ligaments Patella ( knee cap)

• Meniscus: tear Articular cartilage

• 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

HPI • Acute vs. chronic

• 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)

PSURGHX • Previous surgeries to joint or adjacent bone or soft tissue


MEDS • Analgesics ( Rx’n, OTC, herbal medications), calcium . Vit D deficiency, bisphosphonates
FHX • Inflammatory arthritis, connective tissue disorders

SOCIAL • Occupation, limitations on daily activity


• EtOH use . .
smoking IVDU
• Risk factors for physical abuse or STIs
ROS • HEENT: headaches, vertigo, visual disturbances, fever, mental status change, conjunctivitis
• CV: palpitations, chest pain
• RESP: SOB, cough
• Gl: changes in bowel habits, diarrhea, blood in the stool, abdominal pain, cramping, anorexia
• GU: urinary frequency, urethritis, hematuria
.
• MSK /DERM: sensation and motor function of leg rash, psoriasis

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

Etiology Common Examples


Inflammatory Lymphadenopathy (reactive, primary, autoimmune) , abscess TB . .
cat scratch, Kawasaki, infectious mononucleosis
Cystic Thymic, epidermal & sebaceous gland cysts, plunging ranula
Congenital Cysts ( thyroglossal duct, dermoid, branchial cleft), cystic hygroma, hemangioma, laryngocoele
Neoplastic Lymphoma, salivary gland tumor, metastatic SCC (oral cavity, pharynx, larynx, esophagus), thyroid cancer
Thyroid Autoimmune (Graves’ disease, Hashimoto’s thyroiditis), inflammatory ( subacute/radiation
.
thyroiditis), medullary Hurthle cell, anaplastic), goiter, benign thyroid nodules
Benign Schwannoma, neuroma, lipoma, sialolithiasis
Trauma .
Hematoma, post -operative seroma vascular aneurysm

NB: consider age group


• < 40 y/o: inflammatory > congenital > neoplastic
• > 40 y/o: neoplastic > inflammatory > congenital
> < 30 or > 60 years - new mass more concerning

HISTORY
ID • Patient ’s name, age . gender, ethnicity
CC • Lump/mass in neck

HPI • Location, onset, inciting event . .


(e.g. trauma URTI, HIV/TB), prior Hx of neck mass
• Growth: slow /fast, fluctuant/constant, pain/tenderness, uni/bilateral

• Pain or tenderness, response to ATBx, other lumps on body


• Upper
halitosis
. .
aerodigestive symptoms: dysphagia, odynophagia, hoarseness SOB stridor/ wheezing, hemoptysis,

• 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

• Hard fixed mass


PMHX • Radiation, cancer Hx: breast, lung, kidney, melanoma, head and neck, lymphoma
PSHX • Thyroidectomy or any neck surgery
PO&GHX • Pregnant or post -partum
.
MEDS • Thyroxine, propylthiouracil, Li \ allopurinol phenytoin, methimazole
FHX •Thyroid cancer, MEN-II, head and neck cancer, paraganglioma, neurofibromatosis
. . .
SOCIAL • Smoking, EtOH travel ( Lyme disease TB fungal infection, typhoid), sex (HIV), sawdust, chemical fumes,
beryllium, silicone, radiation, cat scratch
ROS • HEENT: diplopia, sensory changes, difficulty speaking. CN deficits
• CV: palpitations
• RESP: SOB/stridor, hemoptysis
• GU: nodal swelling in groin
>* • MSK/ DERM: skin lesion/melanoma ( sun exposed areas), tremors
<U
DJD
.
RISK FACTORS • FHx, cancer, radiation Hx smoking/EtOH, chemical fume exposure HPV .
13
CO

459 Edmonton Manual of Common Clinical Scenarios


PHYSICAL
General Approach
• Introduction, wash hands
• VS: BP, HR, RR . Temp. Sa02
Inspection
• Location ( midline, lateral, distal, intra - oral), symmetry
• Skin: lesions, overlying changes, ulceration, inflammation
• Rhinoscopy, otoscopy, oral cavity exam. CN exam
• Signs of hyperthyroidism: proptosis, lid retraction, irritability, hyperactivity, perspiration, tremor, thin skin, fine hair, pretibial
myxedema
• Signs of cachexia
• SOB
Palpation
•Size, mobility (mobile vs. fixed * to skin or deep structures), nodularity/consistency (rubbery/ hard * ), pulsatile, single/confluent
•Tender ( inflammation), non- tender * (cyst or tumour)
• Bimanual palpation of floor of mouth and tongue
• Assess for lymphadenopathy in other regions ( axillae, abdomen, groin)
• Hepatosplenomegaly (infectious mononucleosis)

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 <

non Manual of Common Clinical Scenarios 460


PUPIL ABNORMALITIES
.
Authors: Terence Kwan - Wong MD, Chris Hanson MD Christopher J. Rudnisky MD MPH FRCSC

DIFFERENTIAL DIAGNOSIS
Diagnostic Criteria
• Unilateral or bilateral pupillary abnormality

> Anisocoria: unequal pupil size


> Corectopia: displacement of pupil from its normal, central position
> Relative afferent pupillary defect ( RAPD)
Common Conditions
•Physiologic anisocoria
•Traumatic mydriasis
• Pharmacological (e.g., mydriatics, miotics, opioids)
• Adie’s tonic pupil

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

HPI • Problems with vision: acuity, nearvision, diplopia, color, glare


• Nature of visual changes: onset, duration, quality, aggravating/palliating, timing
• Ocular pain or redness
• Associated sympathetic dysfunction: ptosis, anhydrosis, flushing
• Ocular /head trauma
• Headache, constitutional symptoms, proximal muscle weakness
RED FLAGS • CN IIIpalsy with pupil dilation and diplopia - aneurysm ± rupture
• Symptoms consistent .
with angle closure glaucoma (red eye N/V, pain, headache, cloudy cornea, fixed, mid -
dilated pupil)
PMHX • Neurological symptoms
• Stroke/CV disease
• Ocular iritis, glaucoma, central retinal vein occlusion
• Recent illness Adie syndrome (viral origin)
• Vasculitis temporal arteritis, polymyalgia rheumatica
PSHX • Ocular e.g., cataract extraction, glaucoma
MEDS • Attempt to elicit full list of meds to rule out pharmacologic anisocoria
FHX • Ocular .
disease, CVA, Ml, DM glaucoma
.
SOCIAL • Recreational drug use smoking

Q)
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D
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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 )

> Cocaine - failure of eye to dilate = Horner 's syndrome


> Phenylephrine - can be used to directly test pupillodilator muscle function
> Dilute pilocarpine - pupillary contraction = denervation (suggestive of Adie's tonic pupil)
• Ophthalmoscopy - assess health of each eye and optic nerves
• Gonioscopy - assess ocular (cornea -iris) angle to help determine presence of glaucoma

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

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a>
3

Edmonton Manual of Common Clinical Scenarios 462


RED EYE
Current Editor: Matthew Benson MD

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

463 Edmonton Manual of Common Clinical Scenarios


PHY!
General Approach
• Ask permission to perform exam, wash hands /perform hand hygiene, properly position patient
• Focus physical exam according to the Hx
Tests
• Test visual acuity, pupil reactivity, tonometry, visual fields, extra - ocular movements
• Look for photophobia, signs of proptosis
• Examine from inside out: the skin and periorbita, slit - lamp exam to look at lids and lashes, conjunctiva, sclera, cornea, iris, anterior
chamber for cells and flare, fundoscopy
• Special tests: fluorescein staining, tonometry if available
Important Signs
• Look for signs of:
. . .
> Trauma (conjunctival laceration FB distorted pupil, hyphema Seidel sign)
> Infection ( severe mucopurulent discharge, corneal opacity or ulcer, hypopyon, uveitis)
> Irritation ( abrasion, fluorescein exam, localized conjunctival injection)
> Angle closure glaucoma ( high intraocular pressure, unreactive mid - dilated pupil, corneal edema)
> Orbital cellulitis (ophthalmoplegia, proptosis)

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

CO
c
GTQ
n>

Ldrnonton Manual of Common Clinical Scenarios 464


SCROTAL MASS & SCROTAL PAIN
Current Editor: Krista Lai MD

DIFFERENTIAL DIAGNOSIS
Differential Diagnosis
SpcrmjtK ctxd
Location Painful Painless
Intratesticular • Orchitis • Tumor

• Hemorrhagic tumor • Hydrocele *


Crenuurr mulct
Extratesticular • Testicular • Varicocele*
*
torsion* Vai deferent _ andfaoj

• 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

465 Edmonton Manual of Common Clinical


PHYSICAL
General Approach
• Ask permission to perform exam, wash hands /perform hand hygiene, VS ( BP, HR . RR. Temp. Sa02)
• Note Hxof Wt loss
HEENT
• Supraclavicular lymph nodes (Note: testicular tumors drain to the retroperitoneum)
• Parotid gland enlargement (mumps orchitis)
GU
• Gynecomastia
• Inguinal region: masses, nodes, pulses
•Bowel sounds may be auscultated in the scrotum in the setting of indirect inguinal hernia
• Signs oftrauma or infection to testicle(s) (erythema, discharge, ulcer, chancre, laceration, hematoma, swelling)
• Horizontal lying testicle may indicate torsion
• Bimanual exam of each testicle: hold testicle between finger and thumb with each hand, pinch the epididymis at the posterior aspect
of each testicle, start inspection and examine for any palpable masses
> To determine if intra - vs. extra - testicular, tenderness
• Testicle special test :

> 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

• CBC- D, electrolytes, urea, Cr


• U/A R & M, C& S
^
• 90% of testicular tumors will have either AFP or (3 - HCG

. urethral swab/genprobe if indicated


Radiology/ Imaging
• Scrotal U/S: hypoechoic intratesticular lesions ± demonstrable hypervascularity suggests testicular cancer, Doppler scrotal U/S for
torsion or epididymitis/orchitis
• If scrotal U/S positive for possible cancer, obtain CXR, CT abdomen and pelvis
Surgical/Diagnostic Interventions
• If torsion suspected on Hx alone, patient must go for surgical exploration within 6 hrs of onset
• Any primary intratesticular mass is a cancer until proven otherwise and necessitates radical orchiectomy
• Trans -scrotal Bx is contraindicated as lymphatic drainage of scrotum differs from testicles

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

hdmonton Manual of Common Clinical SccnariOb 466


SHOULDER (PAIN, FRACTURES, & DISLOCATIONS)
Current Editor: Teresa Li MD

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

Chronic Joints: adhesive capsulitis, glenohumeral


instability
Other MSK: subacromial bursitis, proximal myopathies (polymyalgia rheumatica, dermatomyositis)
. .
Non - MSK : referred pain (cervical spine Ml diaphragmatic irritation), thoracic outlet syndrome,brachial plexus neuropathy,
Pancoast tumour
High Mortality/Morbidity
• Pathologic fracture ( primary bone tumour, metastatic/hematologic lytic lesion)
• Compartment syndrome ( Pain out of proportion . . .
Paraesthesia, Pallor Pulseless Poikilothermia)
HISTORY
ID • Patient's name, age, gender

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

RED FLAGS • Fever /chills, night sweats, weight loss (malignancy)


• High energy mechanism (look for further injuries)
• Weakness (neurological)
PMHX / PSHX • Bleeding disorders, arthritis, immobilization ( adhesive capsulitis)
• Heart disease, lung disease, gallbladder /spleen issues (referred shoulder pain)
Falls: reason for fall (syncope/presyncope/focal weakness/seizure)
• Osteopenia, osteoporosis, malignancy (pathological fractures)
MEDS • Prescription, analgesic use, anticoagulants

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)

467 Edmonton Manual of Common Clinical Scenarios


PHYSICAL
General • Wash hands/perform hand hygiene, ask patient for permission to examine
CVS for vascular compromise in limb (skin color, cap refill): palpate peripheral
• Inspect MSK Inspection: SEADS
pulses ( brachial, radial), temperature of extremity
• Swelling
• General cardiac exam if indicated (suspected Ml)
• Erythema/ecchymosis
.
Neuro • Test sensory/motor function of C 5 -T1 radial, median, ulnar, and musculocutaneous
• Atrophy/asymmetry of
nerves, reflexes (C 5. C 6 = biceps, brachioradialis: C 7, C8 = triceps)
MSK • Inspection: SEADS muscle
• Deformity
• Active /passive ROM and strength: shoulder abduction, forward flexion, extension, • Skin changes /scars
internal/external rotation
• Palpation: bony landmarks ( sternoclavicular joint , clavicle, acromioclavicular joint,
coracoid process, scapular spine, humerus) , soft tissue landmarks (supraspinatus /
infraspinatus muscles, bicipital groove)
• Neurovascular : axillary nerve (motor: shoulder abduction: sensory: regimental badge
area): radial pulse
• Examine joint above and below (C spine and elbow)

Special Rotator cuff tendinitis/ impingement:


tests • Painful arc (supraspinatus): painful active abduction from 60° to 120°
• Jobe's sign ( supraspinatus): pain/ weak resistance to downward force ( patient 's arms fully extended, shoulders
abducted to 90° and forward flexed to 30°, and thumbs pointing down)
• Resisted external rotation (infraspinatus and teres minor ): pain/ weak resistance to external rotation (patient ’s elbow
.
flexed to 90° shoulder fully adducted, and forearm neutral)
• Belly press (subscapularis): examiner places dorsum of hand on patient 's abdomen: patient uses palm to press against
examiner’s hand, with shoulder maintained in internal rotation; positive test = patient ’s elbow moves posteriorly or
shoulder extends
• Neer ’s sign ( impingement): painful passive shoulder forward flexion with thumb pointing down > 90°
• Hawkins ' test (impingement): painful passive internal rotation with shoulder in 90° forward flexion and elbow in 90°
flexion
Biceps tendinitis:
• Speed’s test: pain in bicipital groove with resisted shoulder forward flexion ( patient ’s arm fully extended in anatomical
position)
• Yergason’s sign: pain in bicipital groove with resisted supination (patient ’s elbow flexed to 90° and shoulder in
adduction)
Glenohumeral instability:
• Sulcus sign (multidirectional instability): sulcus appears on superior aspect of humeral head with inferior force applied
to fully adducted shoulder
• Apprehension ( anterior instability ): apprehension with anterior force applied to humeral head ( patient supine with arm
in 90° abduction and full external rotation)
Proximal biceps tendon rupture:
• Popeye sign: biceps muscle belly bunched distally

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 <
*

surgery with failure of conservative treatment


.
• Biceps tendinitis: analgesia, physiotherapy, ice rest from overhead activity, surgery
Referrals
• Urgent Orthopedic Surgery (compartment syndrome, neurovascular compromise, irreducible, open fracture . Salter -Harris fracture
> grade 3. consider dislocations). Rheumatology. Infectious Disease. Oncology
468
.
Current Editor: Hana Yu MD Patrick Vallance

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

• Metabolic conditions ( weak evidence): Thyroid, hyperlipidemia. B 12 deficiency


• Neurologic: Multiple sclerosis, brainstem lesion

• Medication: Side effect of many medications and substance use

• Psychologic: anxiety/depression, fibromyalgia

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

HP! • Onset, location, unilateral vs. bilateral, duration


• Pattern, character (pulsatile, intermittent , constant ) pitch, ' whoosh,' pitch (high vs low), aggravating/
alleviating factors, pulsation
• Associations: hearing loss , vertigo, aural fullness, otalgia, otorrhea

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

ALLERGIES • Allergic rhinitis

FHX • Hearing loss, tinnitus, neurofibromatosis type 2


SOCIAL • Noise exposure, smoking, caffeine, EtOH, IVDU, heavy metals

ROS • HEENT: neck mass, visual changes, exophthalmos


• CV: chest pain. HTN
• RESP: SOB
• Gl: constipation, diarrhea
• MSK /DERM: numbness /weakness/asymmetry, rash on body

RISK FACTORS • Noise exposure, sudden air .


pressure change Hx CNS and ear infections/trauma , radiation to head, recent Wt
loss (patulous Eustachian tube), meds as above

>* 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

behind TM. blue mass behind TM (paraganglioma)


• Pneumatic otoscopy: movement of TM, does red mass /blue mass blanch ( paraganglioma )

469 Edmonton Manual of Common Clinical Scenario


Palpation
• Check neck for masses
• TMJ for crepitus
• Check if pressure on IJ / Carotid changes tinnitus
Auscultation
• Earcanal: listen for objective tinnitus, pulsation, clicking with stethoscope tubing (remove bell)
•Auscultate around the external ear and over neck and carotid artery and jugular vein for masses
Special Tests
.
• Neurological exam ( see physical exam section for details): CN ll - XII, peripheral strength, sensation, reflexes
• Tuning forks
> Use tuning forks at 512 to 1024 Hz frequencies
> Weber: " Weber on the header " (head);
> Sensorineural loss (sound lateralizes to the unaffected side)
> Conduction loss ( sound lateralizes to the affected side)
> Rinne: "Rinne under the pinne" ( Pinna - on the mastoid tip)
> (+ ) Rinne = AC > BC (normal/sensorineural loss)
> ( -) Rinne = BC > AC (conduction loss)

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>

Edmonton Manual of Common Clinical Scenarios 470


TRAUMA
Current Editor Kelvin MH Tran MD

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 -

Urine output Anuria


• Major Heart + lung auscultation R L breath sounds
* • Control sources of hemorrhage
hemorrhage? Abdo palpation Beck ’s triad • Ensure OR teams aware
Stress pelvis to query RUQ or LUQ tenderness • Direct pressure to active bleeds
fracture Unstable pelvis • Chest tube for hemothorax
CIRCULATION .
FAST for spleen lac liver Positive FAST exam • Thoracotomy for tamponade
.
lac pelvic bleed Large wounds, esp. if gushing blood or severe chest trauma (esp.
Assess for long bone penetrating)
fractures • Urgent OR for hemoperitoneum
Inspect for large wounds • Bind pelvis with bed sheet if
>* • Tamponade? Beck ’s triad . .
• i BP t JVP i heart sounds unstable
Q) • Reduce + splint long bone
W> Penetration to cardiac box
fractures
=3
CO • Non
shock ?
-hemorrhagic Obstructive • Pneumothorax, tamponade • Non-hemorrhagic shock managed
Neurogenic • Head or C spine trauma or shock + during secondary and tertiary
bradycardia surveys
Cardiogenic
Distributive • Blunt chest trauma
• Fever, swelling, warm peripheries

471 Edmonton Manual of Common Clinical Sc oi tar


Survey Query Assessment Red Flags Management

• Hypoglycemia? • Bedside glucose • BG < 4 • lampD50


• TICP? • GCS • i LOC • Mannitol, hypertonic saline
DISABILITY • Pupils • Hemiplegia • Steroids

• Strength arms + legs • Anisocoria • Urgent surgical decompression

• Mechanism of injury • Fixed dilated pupil (? herniation)

• 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

Survey Assessment Investigations


HISTORY • SAMPLE Hx (symptoms, allergies, meds . PMHx, last meal , event details) Investigations should be done
as part of the secondary survey,
• Assess pupils for size, response to light, gross visual acuity, anatomic deformities, and
including:
FB
• Assess entire skull for frank deformity, and signs of basilar skull fracture (raccoon
.
• CBCd + T&S PTT + INR

. .
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

• Inspect oral cavity for loose / broken teeth FB's . • Urinalysis

• 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

NEUROLOGIC • Assess orientation to name, place, time


.
• Complete neurologic exam, including CN strength + tone + reflexes, sensation,
cerebellar testing
(/)
FURTHER MANAGEMENT c
• Serial examinations, include repeat primary survey ± resuscitation, should be undertaken as clinical context dictates era
.
• Operative management may be required by General Surgery, Orthopedics Neurosurgery Plastics ENT for damage control. . o>
Tertiary Survey <
• The tertiary survey is a formal head- to - toe examination repeated within 24 hrs of presentation.
• All laboratory & radiologic results must be acknowledged during the tertiary survey.
• The aim of the tertiary survey is to identify any missed injuries or misdiagnoses that may have occurred during the more chaotic
primary & secondary surveys.

Edmonton Manual of Corr 3n C 472


STATION CONTRIBUTORS
Abnormal Mass & CRC Screening Guidelines Aamir Bharmal MD. Marta Broniewska MD. Daniel Schiller MD FRCSC
Abdominal Pain Armin Badre MD. Sayf Gazala MD. Adriana Lazarescu MD FRCPC
Ankle & Foot (Pain, Fractures, & Dislocations) Joffre Munro MD. Yang Li MD. Darren Nichols MD CCFP
Anorectal Pain Aamir Bharmal MD. Marta Broniewska MD. Daniel Schiller MD FRCSC
.
Approach to Fracture Kevin Zuo MD James Mclnnes MD. Robert Chan MD FRCSC
Biliary Disease: Cholelithiasis Shawna Pandya MD. Jonathan White MBBCh BAO MSc PhD FRCS
Bites & Dirty Wounds Hollie Power MD. Jay Zhu MD. James Wolfli MD FRCSC
Bladder Obstruction & Prostate Cancer Todd Penney MSc MD. Henry Conter MD. Ryan Cooper MD MPH FRCPC
Breast Lump & Cancer Screening David Lesniak PhD, Tamara Kuzma MD. Gordon Lees MD FRCSC
Burns Holie Power MD. JayZhu MD. James Wolfli MD FRCSC, Brianne Tetz MD
Diplopia Holie Power MD, JayZhu MD, James Wolfli MD FRCSC. Brianne Tetz MD
Dizziness/Vertigo Scott McLeod MD. Francois Jacob MD. DB Sinclair MD FRCPC
Dysphagia Shawna Pandya MD. Kal Ansari MD FRCSC ABO ABFPRS
.
Epistaxis Michael J Kapusta MD Christopher Fung MD. Ashraf Khan MBChB CCFP
Gastrointestinal Bleed (Lower ) Siddharth Shinde. Michael J. Kapusta MD. Christopher Fung MD. Ashraf Khan MBChB CCFP
Gastrointestinal Bleed ( Upper ) Caitlyn Collins MD. Michael J. Kapusta MD. Christopher Fung MD. Ashraf Khan MBChB CCFP
.
Gynecomastia Mackenzie Lees MD, Simon Turner MD Gordon Lees MD FRCSC
.
Hand ( Pain, Fractures, & Dislocations) Hollie Power MD Regan Guilfoyle MD. Michael Morhart MD FRCSC
Head Trauma Ashraf Kharrat MD. James Keay MD CCFP
Hematuria Armin Badre MD. Leyla Asadi MD. Alan McMahon MD FRCPC. Kate Bacon MD
Hernia Armin Badre MD. Sayf Gazala MD. Chris de Gara FRCS FACS
.
Hip ( Pain, Fractures, & Dislocations) Armin Badre MD. Colleen Weeks MD Carlo Panaro MD FRCSC
Jaundice Matthew Mazurek MD. Sarah Robbins MD FRCPC

.
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

473 Edmonton Manual of Com Clinical Scenarios


REFERENCES
Abnormal Mass & CRC Screening Guidelines
Brenner H. Kloor M. Pox CP. Colorectal cancer. Lancet . 2014:383( 9927):1490- 1502.
. .
Desch CE Benson AB 3rd. Somerfield MR. Flynn PJ Krause C. Loprinzi CL. et al. Colorectal cancer surveillance: 2005 update of an American Society of
Clinical Oncology practice guideline. JClin Oncol. 2005:23( 33): 8512 -8519.
. .
Leddin D. Hunt R Champion M, Cockeram A. Flook N. Gould M et al. Canadian Association of Gastroenterology and the Canadian Digestive Health
Foundation: Guidelines on colon cancer screening. Can J Gastroenterol. 2004:18( 2):93 - 99.
Toward Optimized Practice (TOP) Working Group for Colorectal Cancer Screening. Colorectal Cancer Screening: Clinical Practice Guideline. Edmonton. AB:
Toward Optimized Practice: 2013.

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
-
Examination: Evidence - Based Clinical Diagnosis. New York: McGraw Hill; 2009.
.
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

Ankle & Foot (Pain, Fractures, & Dislocations)


Bickley LS. et al. Bates ' Guide to Physical Examination and History Taking. 10th ed. Philadelphia: Lippincott Williams & Wilkins: 2009.
.
Tintinalli JE et al. Tintinalli' s Emergency Medicine: A Comprehensive Study Guide. 6 th ed. New York: McGraw-Hill; 2004.

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.

Biliary Disease: Cholelithiasis


Blumgart LH. ed. Surgery of the Liver. Biliary Tract , and Pancreas. 4 th ed. Philadelphia: Saunders Elsevier ; 2006.
Gilroy RK. Mukherjee S. Botha JF. Biliary Colic . E - Medicine. 2009 Dec 11. [ cited September 12.2010). Available from http://emedicine.medscape.com/
article / 171256 -overview
.
Gladden D Migala AF. Beverly CS. Wolff J. Cholecystitis. E - Medicine. 2010 May 19. [cited September 16.2010]. Available from: httpy/emedicine.medscape.
com/article/171886-overview
.
Rosh AJ. Manko J. Sally S. Cholangitis. E - Medicine. 2010 Jun 11. (cited September 16.2010 ]. Available from: http://emedicine.medscape.com/
article/774245 - followup
Abraham S. Rivero HG. Erlikh IV. Griffith LF. Kondamudi VK. Surgical and nonsurgical management of gallstone. Am Fam Physician. 2004 May
15;89( 10) 795 - 802.
Siddiqui AA Acute cholecystitis. Merck Manual [ internet ]. Kenilworth.NJ: Merck; 2016. Accessed July 4.2016.
Siddiqui AA Choledocholithiasis and cholangitis. Merck Manual [ internet ]. Kenilworth. NJ: Merck: 2016. Accessed July 4.2016.

Bites & Dirty Wounds


Blonde - Hill E. Fryters S. Bugs & Drugs. Edmonton: Capital Health; 2006.
.
Chao J J Morrison BA. Infections of the upper limb. In: Thorne CH. editor. Grabb and Smith s Plastic Surgery. 6 th ed. Philadelphia: Lippincott. Williams &
Wilkins: 2007. p. 817- 825.
Endom E. Initial management of animal and human bites. In: Danzl DF. Wiley JF. editors. Up to Date. Waltham: Up to Date; 2010

Bladder Obstruction & Prostate Cancer </>


. .
Barry MJ Fowler FJ Jr. O'Leary MP. et al. ( 1992). The American Urological Association symptom index for benign prostatic hyperplasia.
J Urol 148: 1549- 57.
C
era
.
Carroll P. Albertsen PC Greene K. Babian RJ. Carter HB. Gann PH et al. Prostate- specific antigen best practice statement update panel members. Prostate - CD
Specific Antigen Best Practice Statement: 2009 Update. American Urological Association Clinical Practice
Guideline 2009. Available from: http:// www.auanet .org/content/guidelines - and - quality -care/ciinical - guidelines.cfm. 2009.
3
. .
Carter HB. Mohamad EA, Partin AW. Diagnosis and staging of prostate cancer. In Wein AJ Kavoussi LR Novick AC . Partin AW, Peters CA. eds. Campbell -
Walsh Urology . 9th ed. Philadelphia: Saunders Elsevier ; 2007.
Prostate Cancer Screening Group. Use of PSA and the early diagnosis of prostate cancer. Toward Optimized Practice. Available from www.
_ .
topalbertadoctors.org/cpsg/prostate cancer html.2009
Reynard J, Brewster S. Biers S. Oxford Handbook of Urology . 2nd ed. New York: Oxford University Press: 2009.
Selius BA, Subcdi R. Urinary retention in adults: Diagnosis and initial management. Am Fam Physician. 2008;77( 5):643 - 50.

Edmonton Manual of Common Clinical Scenarios 474


Breast Lump & Cancer Screening
Alberta Medical Association. Early detection of breast cancer. Toward Optimized Practice [ internet ). c 2009 [ updated 2007 Mar ; cited 2009 Oct 30).
Available from: http:// www.topalbertadoctors.org/cpgs /breast _cancer.html
.
Bicklcy L5 et al. Bate s ' Gjicic to Physical Examination and History Taking. 10th ed. Philadelphia Lippincott Williams & Wilkins; 2009.
Pruthi S. Detection and evaluation of a palpable breast mass. Mayo Clin Proc. 2001 Jun 76( C t:641- 648.
U.S.Preventive Services Task Force. Screening for breast cancer; U.S. Preventive Sendees 1 isk Force recommendation statement. Ann Intern Med. Nov 17
2009;151(10):716- 726. W - 236.

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
;

Gastrointestinal Bleed (Lower )


Subramanian R. McCashland T. Gastrointestinal hemorrhage. In Hall JB. Schmidt GA. Wooc LDH. eds. Principles of Critical Care. New York: McGraw - Hill;
2005.
Kaplan JL. Beers MH. Berkwits M. Porter RS. Jones TV. eds. Gl Bleeding. In The Merck Manu il of Diagnosis and Therapy. 18 th ed. ( 2006).
http://online.statref.com login.ezproxy.library.ualberta.ca/document.aspx ?fxid = 21&docid = 41
.
Barnert J Messmann H. Management of lower gastrointestinal tract bleeding. Best Pract Re Clin Gastroenterol. 2008:22(2):295 - 312.
Laine L. Peterson WL. Bleeding peptic ulcer. N Engl J Med. 1994; 331( 11): 717- 727.
Zuckerman GR. Prakash C. Acute lower intestinal bleeding. Part II: etiology, therapy, and outcomes. Gastrointest Endosc. 1999;49{2):228 -238.

Gastrointestinal Bleed (Upper)


.
Hui D. Leung AKC Padwal R. Upper Gl bleed. In Approach to Internal Medicine: A Resource Book for Clinical Practice. 3rd ed. New York: Springer:
2011:118 - 120.
Longmore M. Wilkinson IB. Davidson EH. Foulkes A. Mafi AR. Upper gastrointestinal bleeding. In Oxford Handbook of Clinical Medicine. 8th ed. Oxford. UK:
Oxford University Press: 2010:252 - 255.
Subramanian R. McCashland T. Gastrointestinal hemorrhage. In Hall JB. Schmidt GA. Wood LDH. eds. Principles of Critical Care. New York: McGraw - Hill:
2005.
. .
Kaplan JL. Beers MH, Berkwits M Porter RS Jones TV eds. Gl bleeding. In The Merck Manual of Diagnosis and Therapy . 18 th ed. (2006).
http://online.statref.com.login.ezproxy.library.ualberta.ca /document.aspx ?fxid= 21&docid = 41

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.

Hand (Pain, Fractures, & Dislocations)


Anderson BC . Evaluation of the patient with hand pain. In Shmerling RH. Romain PL. eds. UpToDate. Waltham. MA: UpToDate: 2010.
Green DP. Hotchkiss RN. Pederson WC. Wolfe SW. Green' s Operative Hand Surgery. 5th ed. Philadelphia: Elsevier Churchill Liv ngstone: 2005.
<V Janis JE. Essentials of Plastic Surgery . St. Louis: Quality Medical Publishing: 2007.
W)

in

475 Edmonton Manual of Common Clinical Scenarios


Head Trauma
.
Hodgkinson S. Pollit V. Sharpin C Lecky F. Early management of head injury: Summary of updated NICE guidance. BMJ . 2014:348:gl04.
Hoffman LH. et al. First Exposure Emergency Medicine. New York: McGraw - Hill: 2008.
Stiell IG. Wells GA. Vandemheen KL. Clement CM. Lesiuk H. De Maio VJ, et al. The Canadian Cervical Spine Radiography Rule for alert and stable trauma
patients. Journal of the American Medical Association. 2001:286:1841-1848.
.
Stiell IG. Wells GA. Vandemheen K. Clement C. Lesiuk H. Laupacis A. Worthington J et al. The Canadian CT Head Rule for patients with minor beac injury.
Lancet. 2001:357:1391- 1396.

Hematuria
.
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.
.
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.
.
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.

Hip ( Pain, Fractures, & Dislocations)


Anderson BC. Evaluation of the adult with hip pain. In Fields KB. ed. Waltham. MA: UpToDate; 2009.
.
Burroughs KE Walker KM. Hip fractures in acults. In Eiff P. ed. Waltham. MA: UpToDate: 2009.
.
Greene WB ed. The pelvis, hip and thigh. In Netter ' s Orthopedics. 1st ed. Philadelphia: Elsevier: 2006.
Ortigjera CJ. Raposo JM. Groin pain. Epocrates online ( internet ]. San Mateo. CA: Epocrates; 2009. Accessed Sep. 10.2010.
Petrisor BA. Bhandari M. Hip fractures. Epocrates online ( internet). San Mateo. CA: Epocrates; 2009. Accessed Sep. 10.2010.
Hochberg MC. Altman RD. April KT. Americar College of Rheumatology 2012 recommendations for the use of nonpharmacological and pharmacological
therapies in osteoarthritis of the hand, hip and knee. Arthritis Care & Research. 2012 Apr:64( 4):465 - 474.
.
Fricker P. Evaluation of the adult with hip pain. In Fields KB. ed. Waltham MA: UpToDate; 2016.

Jaundice
. .
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.
. .
Luongo DL Fauci AS Kasper DL. Hauser SL. Jameson JL. Loscalzo J. Harrison's Principles of Internal Medicine. 18 th ed. New York: McGraw -Hill: 2012.
.
Schrier SL. Approach to the diagnosis of hemolytic anemia in the adult. Mentzer WC. Landaw SA. eds. Waltham MA: UpToDate: 2014.

Knee (Pain, Fractures, & Dislocations)


. .
Bickley LS et al Bates' Guide to Physical Examination and History Taking. 11th ed. Philadelphia: Lippincott Williams & Wilkins: 2011.
. . .
Henderson MC et al. The Patient History: An Evidence- Based Approach to Differential Diagnosis 2nd ed New York: McGraw - Hill: 2012.
.
Imdoben JB et al. Current Diagnosis and Treatment: Rheumatology . 3rd ed. New York: McGraw - Hill; 2013.
. .
Tintinalli JE et al. Tintinalli' s Emergency Medicine: A Comprehensive Study Guide. 7th ed. New York: McGraw - Hill: 2011

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.
IS)
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
.
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.

Edmonton Manual of Common Clinical Scenarios 476


Red Eye
Cronau H. Kankanala RR. Mauger T. Diagnosis and management of red eye in primary care.Am Family Physician. 2010 Jan 15:81( 2):137- 144.
.
Gerstenblith AT Rabinowitz MP. The Wills Eye Manual : Office and Emergency Room Diagnosis and Treatment of Eye Diseases. Philadelphia: Lippincott Williams &
Wilkins; 2012.
Mahmood AR. Narang AT. Diagnosis and management of the acute red eye. Emerg Med Clin N Am. 2008 Feb:26(l):35 - 55.
.
Sethuraman U Kamat D. The red eye: Evaluation and management. Clin Pediatr . 2009 Apr 8 48( 6):588 - 600.
Wirtelauer C. Management of the red eye fo' the primary care physician. AmJof Mea. 2006 Apr:119( 4):202 - 306.

Scrotal Mass & Scrotal Pain


Reynard J. Brewster S. Biers S. Oxford Handbook of Urology . 2nd ed. New York: Oxford University Press: 2009.
Wein AJ. Kavoussi LR. Novick AC. et al. Neopiasms of the testis.Compbell -Walsh Urology . 9tl ed. Philadelphia: Saunders Elsevier; 2007:2411- 2452.
.
Junnila J Lassen. P. Testicular masses. Am Fam Physician. 1998 Feb 15;57(4):685 - 692.
Shah AP. Painles scrotal mass. Merck Manual Online. 2013 Jul. (cited Oct 12.2014 ], Available from:
_ _ _
http:// www.merckmanuals.com/professional/genitourinary disorders/symptoms of.genitourinary disorders/painless_scrotal_ mass.html
Shah AP. Scrotal pain. Meek Manual Online. 2013 Jul. [ cited Oct 12.2014). Available from:
_ _ _
http:// www.merckmanuals.com/professional/genitourinary _disorders/symptoms of genitoiirinary disorders/scrotal pain.html_
.
Tiemstra JD Kapoor S. Evaluation of scrotal masses. Am Fam Physician. 2008 Nov 15:78 ( 10 :1165 - 1170.

Arm & Shoulder (Pain, Fractures, & Dislocations)


.
Bickley LS et al. Bates ' Guide to Physical Examination and History Taking. 10th ed. Philadelphia l ippincott Williams & Wilkins; 2C09.
Collcdge E. Di Santo L. Shoulder pain: Soft Tissue Injuries in Adults. The Foundation for Medical Practice Education. 2013 Aug:21( 9):l- 16.
Tintinalli JE. et al. Tintinalli ’s Emergency Medicine: A Comprehensive Study Guide. 6th ed. New York: McGraw -Hill; 2004.

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:
http://emedicine.medscape.com/article/434707-overview
Hoffman LH. et al. First Exposure Emergency Medicine. New York: McGraw - Hill; 2008.

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477 Edmonton Manual of Common Clinical Scenarios


9 PHELO
( PHELO) Population Health, and the Ethical, Legal, and Organizational Aspects of Medicine

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

Staff Section Editor


Laurie Mereu MD FRCPC
Professor
Division of Endocrinology
University of Alberta

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479 Edmonton Manual of Common Clinical St>


INTRODUCTION
Lisa J. Steblecki MD MPH CCFP

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.

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ZE
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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.

BREAKING BAD NEWS


As a medical student , resident, or physician, one of the most challenging encounters with patients and their families is in breaking
bad news. In this setting, it is imperative to have a systematic yet flexible process in providing key information and giving adequate
time to understand and ask questions. The mnemonic " S.P.I.K.E.S.” was developed to assist health care professionals deliver bad news.
However, it is more of an art than a science, and portraying empathy, understanding, and patience will facilitate trust and strengthen
the patient - physician relationship.

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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481 Hon M
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

END OF LIFE CARE


Control of Pain and Other Symptoms
• It is difficult to address the social, psychological, and spiritual issues without adequate pain and symptom management
• Involve a multidisciplinary team early to assist in proper pain regimes and adequate control of dyspnea, nausea, delirium, agitation,
and psychological distress
• Focus on quality of life
Advance Directive/Advance Care Planning
• The creation of an advance directive or advance care planning, as well as an enduring power -of - attorney, ensures that clinical care
is shaped by the patient 's preferences and ideals, particularly when the patient is no longer capable of making decisions
• The patient, family, and physician should be involved in this process
• The advance directive should be tailored to the specific clinical situation (e.g., DNR status and life- sustaining treatment )
• A substitute decision maker should be appointed in the action directive

• Maintain open communication with patient/ family to address demands for inappropriate treatment

Support Patients and Their Families


• Ask the patient and family what support they may need / want for a given situation
• Pay close attention to the psychosocial and spiritual needs-consult Social Worker. Pastoral Care Team, cultural liaisons, and/or
palliative care services as appropriate
• Follow up with family following death: pay attention to risk factors regarding poor adjustment to bereavement

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APPROACH TO MEDICAL LITERATURE
Current Editor: Conrad Tsang BHSc MD

ELEMENTS OF CLINICAL DECISION MAKING


Using the best available evidence in the literature
Leveraging the clinician’s expertise and experience
Incorporating the patient’s values and preferences

KING A CLINICAL QUESTION


Population: Who are the relevant patients or populations? Ideally, the literature you use should study a group of patients which
represents your current patient well.
Intervention: What intervention (treatment) will be used?
Comparison: What am I comparing the intervention to? This includes another treatment option, placebo, or no treatment at all.
Outcomes: What outcomes am I concerned about ? These can range from outcomes for the patient or society.

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

METHODOLOGICAL STRENGTHS AND WEAKNESSES OF STUDY DESIGN


Study Design Initiation Point Assessment Strengths Weaknesses
Systematic Depends on what studies were Effectively increases sample size, thus can Study quality depends on the quality of
review included greatly improve statistical power to detect individual studies that were included: differ-
significant results ences in study methodology (heterogeneity)
can make it difficult to combine results
RCT Exposure status Outcome Typically not vulnerable to biases: accounts Costly: highly selective patient populations
event status for both known and unknown prognostic used can affect external validity
factors
Cohort study Exposure status Outcome Appropriate for when exposures or Baseline prognostic factors likely will be
event status treatments cannot ethically be randomized unbalanced: risk for confounding, even after
statistical adjustment
Case - control Outcome event Exposure Starting from outcomes removes the Susceptible to biases: only able to determine
study status status temporal delay from exposure to outcome if the exposure is associated with the out -
onset: useful for rare outcomes come: cannot comment on causality
Cross - section Exposure status and outcome Inexpensive: useful to test initial Susceptible to a wide variety of biases:
study prevalence are measured simulta - hypotheses: results based on general pop - provides no information on direction of


neously ulation and not just those seeking medical association
o treatment

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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?)

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*
Eligibility Criteria for Study Inclusion and Exclusion
• An appropriate clinical question was asked to be able to define what is relevant to answering the question
• Search strategies should be published so assessments are reproducible

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)

E5HO CAN ASSESS CAPACITY?


By regulation, all physicians and registered psychologists may perform a capacity assessment. Nurses, OTs, and social workers may
become a Designated Capacity Assessor after completing specific training.

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•Every person is assumed capable until proven otherwise (the assessor must prove incapacity)
• Taking away a person's capacity is very intrusive and deemed a last resort -results in a patient ’s loss of autonomy
• A patient must be informed that a capacity assessment is occurring and patient must provide consent for assessment (if patient
refuses, it may proceed if the Court deems assessment is in the patient 's best interest )
• Criteria for initiating a capacity assessment:
> An event or circumstance puts a patient at risk
> This event seems to be due to impaired decision making
> This event requires investigation, problem solving, and possibly action on the part of the health care worker
• Stages of capacity assessment:

> 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)

HAT HAPPENS IF A PATIENT IS DEEMED INCAPABLE?


• An ADM is appointed to make a specific decision for the patient
• Documents prepared by patient beforehand:
> Personal directive: appoints an ADM for matters regarding healthcare, where to live, and social activities
> Enduring power of attorney (ePOA ): appoints an ADM for financial and property decisions
• Court - appointed agents:

> 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

5APACITY AND MINORS


• A mature minor doctrine: child's ability to understand nature of treatment have determinants beyond age
• Canadian Paediatric Society requires that the minor demonstrate comprehension of the magnitude of the intervention, the
probabilities of harm and benefit, and the consequences of consent or refusal
• If a minor is deemed incapable, the parents or legal guardians become the ADMs: if ADMs don' t act in child’s best interest, third

parties such as Children's Aid may be required to intervene

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CLINICAL EPIDEMIOLOGY
Current Editor: Alim Nagji MD

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

ETHICAL BASIS OF CONFIDENTIALITY


Patient autonomy
Patients have the right to control their personal information

> Confidentiality is a fiduciary duty (legal)
Confidentiality is not absolute — communicate to patients the limits of maintaining confidentiality
When interacting with families, maintain patient’s wishes as the priority, recognizing there may be exceptions
n SHE 11 MI fin^LiM
Legal duty arises ( directly and indirectly) from various sources including:
• Provincial and federal privacy legislation
• Court decisions (jurisprudence)
•Expectations from professional regulatory bodies (i.e., Codes of Ethics and Conduct)
•Hospital or site policies as grantor of privileges
Legal aspects are complex and most often require case- by - case determination
Some principles include:
• Cannot disclose patient information without patient consent unless under circumstances defined by statutory law
• Physicians who breach confidentiality may be sanctioned by the hospital, court, or regulatory authority
• Physicians who fail to report information in circumstances where required by law may be subject to professional and/or civil
actions
• Duties set out for collection, use, and disclosure of a patient ' s health information ( including safeguarding duties) as well as duties
for response to patient’s right to access and/or correct his/her health information
BREAKING CONFIDENTIALITY
Confidentiality may be broken in certain situations
•A child in need of intervention (e.g., child abuse/neglect) -report to Social Services
•Fitness to drive-report to provincial Ministry of Transportation
• Certain communicable disease (e.g., HIV, STIs) — report to Medical Officer of Health
• Inappropriate behavior by other health care professionals-report to professional regulatory body
• If clear risk of serious bodily harm/death or imminent danger to any individual, either by the patient or any other individual.
Includes patient self - harm.
Resources for Physicians
• Hospital ethics boards
• Local health authority
• CM PA
• Privacy commissioner
Appropriate Pre- test Counseling
• Remember to inform patients about situations in which confidentiality may be broken
> For example, before testing for STIs such as gonorrhea and chlamydia, counsel patient that if the test is positive, as mandated
by the Public Health Act, attempts are allowed to identify, locate, examine, and treat the contacts/partners of the patient

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DOCTOR- PATIENT RELATIONSHIP
Current Editor: Maleka Ramji MD

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

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.

• Whenever anything is done for a medical purpose for/to a patient


• Invasive procedures or procedures involving physical trespass need a higher form of consent (even when unconscious for a
procedure)


• Note: Should be made in advance and should be well documented

EIQNSENT SHOULD BE OBTAINED FROM WHOM?


• Competent patients or substitute decision makers
.
> Patient has appropriate capacity (e.g. the ability to communicate/understand information/reason and deliberate/choose)
> If patient is incapable of giving consent and/or they are incompetent, use substitute decision maker

mHO SHOULD OBTAIN THE CONSENT?


The treating physician or resident

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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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MEDICAL ASSISTANCE IN DYING (MAID
. .
Author: Tianru Sui BScN MD

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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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Tonton Manual of Common Clinical Scenarios 490
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

FRAMEWORK OF CORE PRINCIPLES


Honesty
• To strive for honesty in all scientific communications, whether to your patients, colleagues, or the public

Respect for persons


• To respect autonomy and to protect those with impaired or developing autonomy by allowing research participants and their
proxies to make informed choices without interference
• To commit to accountability and transparency in research

Concern for welfare


• Consideration of all aspects of a person's life, including physical, mental, and spiritual health; physical and economic circumstances;
social determinants, including housing, employment, security, and community membership; and privacy and control of information
Justice
• Obligations .
to treat people fairly ( i.e. respect and concern) and equitably (distributing benefits and burdens of research
participation so no population is burdened or denied benefits)
• This does not always mean treating people equally. Groups who are vulnerable or marginalized may be given special attention in
order to be treated justly.
CONSENT
Consent to enroll in a study is given voluntarily, and consent is an ongoing process
• There should be no undue influence or coercion
• Participants should have the right to decline and also to withdraw previously given consent at any time during the research
process with no negative consequences or prejudice
Consent should be informed
• Information must be provided on the purpose of the study, identity of the researcher, source of funding, nature and relative
probability of harms and benefits, nature of participation including any compensation, any pertinent conflicts of interest, and that
the study is approved by a research ethics board
Consent should precede collection or access of data.
Consent should be documented.
[STUDY DESIGN
Studies must ask an appropriate research question of sufficient value to justify exposing participants to potential risks.
There needs to be a genuine uncertainty regarding the effectiveness of an intervention; if it is unquestionably inferior,
then it would be unethical for participants to receive.
Studies must be designed so that the research question can be reliably answered and replicated. Sufficient participants
must be recruited in order to be able to statistically detect outcomes of relevance to patients.
Data must be stored safely to ensure privacy.
Findings should be reported accurately and in a timely manner.

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).

0PPROACH TO CONFLICTS OF INTEREST


Disclosure: researchers are expected to disclose their relationships ( e.g., industry relationships, financial ties, non-
monetary benefits).
Review and authorization: research ethics boards assess whether conflicts of interest affect proper conduct of research
trials or quality of patient care. Researchers should be aware of bias and decreased objectivity.
Prohibition: some conflicts of interest may be at high risk of negative consequences and therefore are not allowed.
PUBLISHING RESEARCH FINDINGS
Publications should be truthful and not be written in a misleading manner.
Collaborators should be appropriately credited for their contributions “D
• Authors should have: contributed substantially to study design, data collection, analysis, or interpretation; drafted or revised the I
manuscript; approved the final publication; and be accountable for all aspects of the work m
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Edmonton Manual of Common Clinical Scenarios 492
RESOURCE ALLOCATION
\ * i l I Vi \ IV
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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.).

ETHICS. LAW, AND POLICY


From an ethical standpoint , it is important to consider the concept of social justice: the best treatment should be
.
administered to every patient regardless of disease, sex, religion, level of education, age etc. Scarce resources, however,
force clinicians to make decisions and selectively distribute resources based upon each patient. Inevitably, important
questions arise:
• How much priority should we give to the sickest /oldest patients?
• Should there be a democratic process in determining allocation?
• Should modest treatment benefits go to a larger number of patients or should superior benefits go to a small number of patients?
These questions are only the tip of the iceberg in terms of the ethical dilemmas, but they outline the important
considerations clinicians must keep in mind. Balancing limited resources with your patient 's best interests is very often a
difficult and challenging task .
. .
From the perspective of Canadian law discrimination based upon age, sex religion, etc. is strictly prohibited. Breaching
this fundamental law may lead to legal consequences. Physicians juggle these patient characteristics with medical
therapy and prognosis. Each individual case is unique and courts are cautious about interfering with day- to- day practices
of clinicians. In the end, a physician’s primary responsibility is to the patient -not external administration. For a physician
to consider the financial implications of their decisions and for that to supersede patient care defeats the fundamental
responsibility of the medical profession.
Policy is commonly dictated by local hospitals or institutions in an attempt to standardize each clinician’s approach to
difficult decisions. Evidence- based care pathways and professional guidelines are commonly used. The Canadian Medical
Association (CMA ) has a distinct framework for physicians to follow in regards to decision-making centered around the
three major concepts of ethics, economics, and quality. In addition, the CMA's Code of Ethics clearly states that every
physician has the responsibility to " promote fair access to health care resources’’ as well as use health care resources
" prudently.’’

h\‘J U : •<
!( ]; II w
• 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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493 Edmonton Manual of Common Clinic


SEXUAL HEALTH HISTORY
Current Editor: Tianru Sui BScN, MD

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

PSHX • Hx of genitourinary and abdominal surgeries

MEDS • OTC ( including topical products), prescription (hormonal contraception)


SOCIAL • Smoking, EtOH, recreational drugs, disclosure of sexual assault

1) Ask about the five " Ps”:


• Partners: "male, female, or both?", number of partners in past 2 months and 12 months; partners' ages: for multiple partners,
. .
ask about patterns of condom use, partner ' s risk factors ( i.e , other partners, injection drug use history of STDs), safety in the
relationship
• Sexual Practices: oral /vaginal /anal sex - helps stratify risks and identify anatomical sites from which to collect specimens for STD
testing, masturbation, sharing of toys, fetishes. BDSM.
• Past History of STDs: when, what, treatment, resolution: recent past STDs indicate higher risk behavior and an increased risk of
repeat infection. Stratify high-risk populations. Frequency of STD screening.
• Pregnancy Plans/Prevention: current plans /desires regarding pregnancy, pregnancy prevention; ensure that patient understands
correct use of contraception.
• Protection from STDs: use of protection/contraception: type, frequency, consistency, patient /partner IV drug use.

2) If concerns re: sexual function/sexual cycle:


• Desire (interest, aversion, who initiates), arousal/excitement ( foreplay, sufficient duration and nature), orgasm ( ask if sex is
satisfying), resolution (does relaxation occur ? if not - what interferes?)
• Men: premature or delayed ejaculation, performance anxiety
• Women: Dyspareuria, vaginismus, vaginal dryness
3) Intimate Partner Violence Screen - " Because sexual violence is a serious problem in our society and can affect a person' s health and
well - being, I now ask all of my patients about sexual assault."
• In general, how would you describe your relationship ? A lot of tension, some tension, no tension?
• Do you and your partner work out arguments with great difficulty ? Some difficulty ?
• Has anyone ever forced you to perform sexual acts that made you uncomfortable? Do you ever engage in sexual activities that you
.
don’t want to or when you don' t want to? “O
4) Complete the interview by asking: " Is there anything else about your sexual practices that I need to know about to ensure your
m
good health care? Do you have any questions for me?”
• Review and reinforce positive, protective behaviors O
• Reinforce confidentiality
Edmonton Manual of Common Clinic,i 494
TRUTH TELLING
. .
Current Editor: Tianru Sui BScN MD

• The autonomy of the patient must be respected


• Truth telling establishes trust between the physician and patient, and avoids paternalism
• Patients need to make realistic life decisions
• Patients may find comfort in the fact that their physician can name their condition
• If a patient is unaware of their condition, they may not seek the medical attention they need
• A patient 's information is the property of the patient, not the physician

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)

• Patient waives right to information, must be capable of making decision


• Physician must ensure it is an authentic request and offer the patient a chance to be told important information (be sure to
document this process)
• Common reasons for refusal: disclosure would cause harm to the patient, cultural values, incapacitation, emergency
• If the request is authentic and contrasts with the family 's wishes, the physician must respect the patient 's wishes above the
family's
• " Therapeutic privilege”: physician withholding information on the grounds that disclosure would cause significant harm to the
patient; invoking this should be avoided as it is not a justifiable reason for non- disclosure in most Canadian courts

o
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Q.

495 Edmonton Manual o; Common Clinical S:


STATION CONTRIBUTORS
Clinical Epidemiology Nawaaz Nathoo MD. Ashnoor Nagji MD CCFP
.
Confidentiality Brendan Leier PhD Lisa Steblecki MD CCFP MPH
Doctor - Patient Relationship Lisa steblecki MD CCFP MPH
Informed Consent Simon Turner MD. Gordon Lees MD FRCSC
Personal & Professional Conduct Sujata Chandra MD FRCSC
Research Ethics Laurie Mereu MD FRCPC
Resource Allocation Daniel Birch MD FRCSC. Debraj Das MD. Olga Toleva MD. Michael Tjandrawidjaja MD. Paul W. Armstrong MD FRCP
Sexual Health History Cassandra Hirt MD. Amanda Aiken MD FRCSC. JonathanTankel MBBCh FRCSC. Julie Man MD. Graham Brassard MD
.
FRCSC Viktor Sekowski. BSc

Truth Telling Brendan Leier PhD

TJ
X
m
O
Edmonton Manual of Common Clinical Scenarios 496
- i l M : lH
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.

Approach to Medical Literature


. . .
Guyatt G Rennie D. Meade MO Cook DJ eds. Users ' Guides to the Medical Literature: A Man . ial for Evidence Based Clinical Practice. 2nd ed. New York:
McGraw - Hill; 2008.

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.

Personal & Professional Conduct


CP5A Code of Conduct. Retrieved June 5.2014 from:
_ _ _ _
http:// vwAv.cpsa.ab.ca/Libraries/res/CPSA Code of _Conduct - _Expectations of Professionalism.pdf

Doctor- Patient Relationship


Medical Council of Canada ( Internetl. CLEG: Objectives of the Considerations of the Legal Ethical and Organizational Aspects of the Practice of
Medicine: c 2010 (cited 2010 Sep 12 ). 4.8. Doctor Patient Relationship: Available from: http://vAvw.mcc.ca/objectives.online /objectives.

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
. . .
McKneally MF Dickens BM Meslin EM Singer PA. Bioethics for clinicians: Resource allocation. CMAJ. 1997 Jul 15:157( 2) :163 - 167.

Sexual Health History


SOGC Clinical Practical Guidelines: Intimate Partner Violence Consensus Statement. 200S
Hughes S. Tools and Techniques for Taking a Sexual History. 2010.
.
Masters W Johnson V. Kalpan HS. The Sexual Cycle. 1996.
.
Centers for Disease Control and Prevention: A Guide to Taking a Sexual History. Available from: http:// w vw.cdc.gov/std/treatment /sexualhistory.pdf

O Truth Telling
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.
.
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.
Q.
497 .
Edmonton Manu il of Common Clinical S
>
O
T3
APPENDIX A: ABBREVIATIONS
=J
Q
X
- 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

499 Edmonton Manual of unn


c CRTx chemoradiation therapy
C&S culture and sensitivity
>
T3
Clq complement subcomponent Iq *D
C3 complement component 3 CSF cerebrospinal fluid
CO
C4 complement component 4
Ca cancer
CT computerized tomography
CTx chemotherapy =CL
3

Ca2 * calcium CV cardiovascular X


CVD cardiovascular disease
-
CA 125 cancer antigen 125
CVA cerebrovascular accident
CABG coronary artery bypass graft
CAD coronary artery disease CVA costovertebral angle
CAH congenital adrenal hyperplasia CVP central venous pressure
CAM confusion assessment method, complementary and CXR chest X - ray
alternative medicine
c - ANCA circulating anti -neutrophil cytoplasmic antibody D
CAT computerized axial tomography D1thumb
CABG coronary artery bypass graft D2 index finger
CBC complete blood count D3 long finger
CBC-D CBC with differential D4 ring finger
CBD common bile duct D5 little finger
CBE clinical breast examination D5 W 5% dextrose in water
CBG capillary blood gas DAT diet as tolerated
CBT cognitive behavioural therapy DAT direct antiglobulin test
CC chief complaint dBP diastolic blood pressure
CCAM congenitial cystic adenomatoid malformation DBT dialectical behavioural therapy
CCBs calcium channel blockers DC discontinue
CCU cardiac care unit D& C dilation and curettage
CD conduct disorder DCIS ductal carcinoma insitu
CD4 CD4 T lymphocyte DDH developmental dysplasia of the hip
CDC Center for Disease Control DDx differential diagnosis
CEA carcinogenic embryonic antigen dflex dorsiflexion
CEA carotid endarterectomy DHEA dehydroepiandrosterone
CF cystic fibrosis, clear fluids Dl diabetes insipidus
CFS chronic fatigue syndrome DIA dimeric inhibin- a
CGL chronic granulocytic leukemia DIC disseminated intravascular coagulopathy
CHEP Canadian Hypertension Education Program DIP distal interphalangeal joint
CHF congestive heart failure DJD degenerative joint disease
CHL conductive hearing loss DKA diabetic ketoacidosis
Cl cardiac index DLCO diffusing capacity of the lung for carbon monoxide
CKD chronic kidney disease DM diabetes mellitus
CM cardiomyopathy DMARD disease modifying anti -rheumatic drug
CML chronic myelogenous leukemia DMT1diabetes mellitus type I
CMPA Canadian Medical Protective Association DMT2 diabetes mellitus type II
CMPI cows milk protein intolerance DNR do not resuscitate
CMV cytomegalovirus D/O disorder
CN cranial nerves DOE dyspnea on exertion
CNS central nervous system DPT diphtheria, pertussis, tetanus
CO cardiac output DRE digital rectal exam
C /O complaining of DSM -V Diagnostic and Statistical Manual of Mental Disorders V
COPD chronic obstructive pulmonary disease DTs delirium tremens
CP cerebral palsy DTR deep tendon reflexes
CPA costopherenic angle DVT deep venous thrombosis
CPAP continuous positive airway pressure DX diagnosis
CPC cancer and palliative care DZ disease
CPG Clinical Practice Guidelines
CPK creatine phosphokinase
CPPD calcium pyrophosphate deposition E
CPR cardiopulmonary resuscitation EA esophageal atresia
CPS Canadian Pediatric Society EAC external auditory canal
Cr creatinine EBL estimated blood loss
CrCL creatinine clearance EBV Epstein - Barr virus
CRC colorectal cancer ECF extracellular fluid
.
CREST calcinosis Raynaud's phenomena, esophageal dysmotility . ECFV extracellular fluid volume
EKG electrocardiogram
sclerodactyly, telangectasia
CRF chronic renal failure ECRB extensor carpi radialis brevis muscle
CRP C-reactive protein ECRL extensor carpi radialis longus muscle

Edmonton Manual of Common Clinical Scenarios 500


>
"U
ECT electroconvulsive therapy
ED erectile dysfunction
G
-o ED extensor digitorum muscle ( arm)
GA gestational age
n> EDC estimated day of confinement
GAD generalized anxiety disorder
3 GAS group A strep
Q. EDL extensor digitorum longus muscle (leg) GBS group B strep
X EDM extensor digiti minimi muscle GC gonorrhea
EGD esophagogastroduodenoscopy GCS Glasgow coma scale
EHB extensor hallicus brevis muscle GDD global developmental delay
EHL extensor hallicus longus muscle GDM gestational diabetes mellitus
El extensor indicis muscle GERD gastroesophageal reflux disease
EIA enzyme immunoassay GFR glomerular filtration rate
EMG electromyogram GH growth hormone
EMV eyes, motor, verbal response (Glasgow coma scale) GHB gamma hydroxybutyrate
ENG electronystagmogram Gl gastrointestinal
ENT ears, nose, and throat GIB gastrointestinal bleed
EOM extraocular muscles, extraocular movements GM gross motor
EPO erythropoietin Gmax gluteus maximus muscle
EPS extrapyramidal symptoms GMC generalized medical condition
ESR erythrocyte sedimentation rate Gmed gluteus medius muscle
ET endotracheal Gmin gluteus minimus muscle
ETDRS early treatment diabetic retinopathy study GN glomerulonephritis
ETT endotracheal tube GnRH gonadotropin releasing hormone
ERCP endoscopic retrograde cholangio- pancreatography
EtOH ethanol
.
GPTAL gravida, para term, abortion, living
gt or gtt drops
EUA examination under anesthesia GTT glucose tolerance test
ext extension GU genitourinary
GV growth velocity
F
FAP familial adenomatous polyposis H
FASD fetal alcohol spectrum disorder H2RA histamine 2 receptor antagonist
FAST focused assessment with sonography for trauma HA headache
FB foreign body HepA hepatitis A virus
FBA foreign body aspiration HepB hepatitis B virus
FBS fasting blood sugar HepC hepatitis C virus
FCR flexor carpi radialis muscle HBP high blood pressure
FCU flexor carpi ulnaris muscle HC head circumference
FDB flexor digitorum brevis muscle hCG human chorionic gonadotropin
FDL flexor digitorum longus muscle HCT hematocrit
FDP flexor digitorum profundus muscle HDL high density lipoprotein
FDS flexor digitorum superficialis muscle
FVC forced vital capacity
. . .
HEENT head eyes ears nose, throat
HF heart failure
FEV forced expiratory volume Hgb hemoglobin
FESS functional endoscopic sinus surgery HgbAlc hemoglobin Ale
FF full fluids HHS hyperosmolar hyperglycemic state
fFN fetal Fibronectin HI homicidal ideation
FFP fresh frozen plasma HIE hypoxic ischemic encephalopathy
FHR fetal heart rate HIV human immunodeficiency virus
FISH fluorescence in situ hybridization Hib Haemophilus Influenzae B
FIT fecal immunochemical test HJR hepatojugular reflex
flex flexion HLA histocompatibility locus antigen
FM fine motor HNPCC hereditary nonpolyposis colorectal cancer
FNA fine needle aspirate HOB head of bed
FOBT fecal occult blood test HOCM hypertrophic obstructive cardiomyopathy
FPG fasting plasma glucose HPF high powered held
Fr French size HPI history of present illness
FRC functional residual capacity HR heart rate
FSGS focal segmental glomerulosclerosis HRT hormone replacement therapy
FSH follicle stimulating hormone HSat bedtime
FSWU full septic workup hs -CRP high sensitivity C-reactive peptide
FTA-ABS fluorescent treponemal antibody absorbed test HSG hysterosalpingogram
FTT failure to thrive HSIL high grade squamous intraepithelial lesion
FU follow -up HSM hepatosplenomegaly
FUO fever of unknown origin HSP Henoch- Scholein purpura
FVC forced vital capacity HSV herpes simplex virus

501 £ drnonton Manual of Common Clinical Seer


HUS Hemolytic -uremic syndrome K >
Ht height K potassium T3
HTLV-III human lymphotropic virus, type III o
HTN hypertension
KUB kidneys, ureters, bladder n>
KVO keep vein open D
Hx history Q .
X
I L
L left
IABP intra - aortic balloon pump LABD long acting bronchodilator
IAC internal auditory canal LAD left axis deviation, left anterior descending
IADL instrumental activity of daily living LAE left atrial enlargement
IBD inflammatory bowel disease LAHB left anterior hemiblock
IBS irritable bowel syndrome LAP left atrial pressure
ICF intracellular fluid LBBB left bundle branch block
ICH intracerebral hemorrhage LCIS lobular carcinoma insitu
ICS intercostal space LCPDz Legg-Calve- Perthes disease
ICSI intracytoplasmic sperm injection LD learning disorder
ICP intracranial pressure LDH lactate dehydrogenase
ICU intensive care unit LDL low - density lipoproteins
ID infectious disease, identification LE lupus erythematosus, lower extremity
l& D incision and drainage LEEP loop electrosurgical excision procedure
IDDM insulin dependent diabetes mellitus LFT liver function tests
IFG impaired fasting glucose LGIB lower gastrointestinal bleed
IFN interferon LH luteinizing hormone
Ig immunoglobulin LLL left lower lobe
IGGR -nterferon- gamma release assays LLQ left lower quadrant
IGF insulin-like growth factor LMA laryngeal mask airway
IGFBP insulin-like growth factor binding protein LMN lower motor neuron
IGT impaired glucose tolerance LMP last menstrual period
ILD interstitial lung disease LMWH low molecular weight heparin
IM intramuscular LN lymph node(s)
Immun immunizations LNMP last normal menstrual period
INF intravenous nutritional fluid LOC level of consciousness
INR international normalized ratio LP lumbar puncture
IO interosseous LRTI lower respiratory tract infection
l& O intake and output LSB lower sternal border
IOP intraocular pressure LSIL low grade squamous intraepithelial lesion
IP iliopsoas muscle, interphalyngeal LTB laryrngotracheal bronchitis
IPF idiopathic pulmonary fibrosis LTFB laryngotracheal foreign body
IPJ interphalyngeal joint LTRA leukotriene receptor antagonist
ITinterthecal LUL left upper lobe
UP idiopathic thrombocytopenic purpura LUQ left upper quadrant
IV intravenous LV left ventricle
IVC inferior vena cava LVD left ventricular dilation
IVH intraventricular hemorrhage LVEDP left ventricular end diastolic pressure
IVP intravenous pyelogram LVH left ventricular hypertrophy
IVDUIV drug user
IUD intrauterine device
IUGR intrauterine growth restriction M
IUI intrauterine insemination MAHA microangiopathic hemolytic anemia
IUTD immunizations up to date MAL mid- axillary line
IVF in vitro fertilization MAS meconium aspiration syndrome
IVIG intravenous immunoglobulin MAO monoamine oxidase
lx investigations MAP mean arterial pressure
MAST medical antishock trousers
MCC Medical Council of Canada
j MCH mean cell hemoglobin
Jl A juvenile idiopathic arthritis MCHC mean cell hemoglobin concentration
JODM juvenile onset diabetes mellitus MCL mid - clavicular line
JP Jackson- Pratt drain MCV mean cell volume
JVD jugular venous distention MD muscular dystrophy
JVP jugular venous pressure MDEs major depressive episodes
MDR multi-drug resistance
MDRD modification of diet in renal disease
MEN multiple endocrine neoplasia

of Common Clinical Scenarios 502


>
T3
MG myasthenia gravis
Ml myocardial infarction
o
OB obstetrics
T3 mL milliliter
CD OC oral cavity
D mm muscle OCP oral contraceptive pill
Q

. MM multiple myeloma OD overdose
X MMA middle meningeal artery OD right eye
mmol millimole ODD oppositional defiant disorder
mmol /L millimoles/liter OE otitis externa
MMR measles, mumps, rubella OE obturator externus muscle
MMSE mini-mental state examination OGTT oral glucose tolerance test
MOCA Montreal cognitive assessment
Ol obturator internus muscle
MR mitral regurgitation OM otitis media, osteomyelitis
MR mental retardation OME otitis media with effusion
MRA magnetic resonance angiogram OP opponens pollicis muscle
MRCP magnetic resonance cholangiopancreatography
OPQRST onset, provoking/palliating factors, quality, region/
MRI magnetic resonance imaging radiation, severity, time/ treatments
MRSA methicillin- resistant Staphylococcus aureus O& P ova and parasites
MS multiple sclerosis OPV oral polio vaccine
MS mitral stenosis OR operating room
MSA multi -system atrophy OS left eye
MSAFP maternal serum alpha feto -protein OSA obstructive sleep apnea
MShCG maternal serum chorionic gonadotropin OT occupational therapist
MSuE3 maternal serum unconjugated estriol
OTC over the counter
MSL mid-sternal line
OU both eyes
MSM men who have sex with men
OME otitis media with effusion
MSS maternal serum screen
MSSA methicillin- sensitive Staphylococcus aureus
MSU mid - stream urine p
MVA motor vehicle accident PA posteroanterior
MVP mitral valve prolapse PAC premature atrial contraction
PAD peripheral artery disease
pANCA perinuclear anti-neutrophil cytoplasmic antibody
N PA02 partial pressure of alveolar oxygen
N nausea
Pa02 partial pressure of arterial oxygen
N normal
PAP pulmonary artery pressure
Na sodium PAPP- A pregnancy - associated plasma protein A
NAAT nucleic acid amplification test PAT paroxysymal atrial tachycardia
NAC protocol N- Acetylcysteine protocol
PB peroneous brevis muscle, palmaris brevis muscle
NAFLD nonalcoholic fatty liver disease
PBC primary biliary cirrhosis
NB newborn PBF pulmonary blood flow
NG nasogastric
PCA posterior communicating artery
NEC necrotizing enterocolitis
PCI percutaneous coronary intervention
NERD non- erosive esophageal reflux disease
PCKD polycystic kidney disease
NICU neonatal intensive care unit
PCOS polycystic ovarian syndrome
NIDDM non-insulin dependent diabetes mellitus PCR polymerase chain reaction
NKA no known allergies
PCWP pulmonary capillary wedge
NKDA no known drug allergies
PD Parkinson' s disease
NKHHC non -ketotic hyperglycemic hyperosmolar coma PDA patent ductus arteriosus
NMD neuromuscular disorders PDD pervasive developmental delay
NMR nuclear magnetic resonance PDE- 5 phosphodiesterase type 5
nn nerve
PE pulmonary embolus
N/P (swab) nasopharyngeal
PE physical exam
NPO nothing by mouth
PE pleural effusion
NPV negative predictive value
PEDS pediatrics
NRFS non-reassuring fetal status
PEDS parental evaluation of developmental status questionnaire
NS normal saline
PEEP positive end expiratory pressure
NSAID non- steroidal anti-inflammatory drug
PEFR peak expiratory flow rate
NSR normal sinus rhythm pflex plantar flexion
NST non- stress test
PFT pulmonary function tests
NT nasotracheal, nuchal translucency
PGE1prostaglandin El
NTD neural tube defect pH potential of hydrogen
N/V nausea /vomiting
PHTN pulmonary hypertension
NWB non - weight (Wt ) bearing
PICA posterior inferior cerebellar artery
NYHA New York Heart Association
PICU pediatric intensive care unit

503 Edmonton Manual of Common C linical Sccnar ios


PID pelvic inflammatory disease
PIH pregnancy - induced hypertension
R >
T3
R &M routine and microscopic ( urinalysis)
PIO posterior interosseous T3
R right 0)
PKU phenylketonuria RA rheumatoid arthritis D
PL peroneous brevis muscle
PL palmaris longus muscle
RA right atrium
RAD right atrial axis deviation
Q
X
-
PLT platelet RAE right atrial enlargement
PMDD premenstrual dysphoric disorder RAM rapid alternating movements
PMH previous medical history ( Hx ) RAP right atrial pressure
PMI point of maximal impulse RAPD relative afferent pupillary defect
PMN polymorphonuclear leukocyte (neutrophil) RBBB right bundle branch block
PMR polymyalgia rheumatica RBC red blood cell
PMS premenstrual syndrome RDS respiratory distress syndrome
PND paroxysmal nocturnal dyspnea RDW red cell distribution width
PNS peripheral nervous system RF risk factor
PO ( Latin per os ) by mouth RF rectus femoris muscle
POD post - op day Rh rhesus factor
POI primary ovarian insufficiency RhoGAM anti - Rhesus factor D immune globulin
PPD purified protein derivative RICE rest ice compress elevate
PPH postpartum hemorrhage RL Ringer 's lactate
PPHN persistent pulmonary hypertension of the newborn RLL right lower lobe
PPI proton pump inhibitors RLQ right lower quadrant
PPROM preterm premature rupture of membranes RML right middle lobe
PPV positive predictive value RNA ribonucleic acid
PR by rectum R /O rule out
PRBC packed red blood cells ROM range of motion, rupture of membranes
PRL prolactin ROS review of systems
PRN ( Latin pro re nata ) as needed RPA retropharngeal abscess
PROM premature rupture of the membranes RPR rapid plasma regain
PRS Pierre Robin syndrome RR respiratory rate
PS pulmonic stenosis RSD reflex sympathetic dystrophy
PSA prostate specific antigen RSV respiratory syncytial virus
PSC primary sclerosing cholangitis RT respiratory, radiation therapy
PSGN post - streptococcal glomerulonephritis RTA renal tubular acidosis
PSI pneumonia severity index rTMS repetitive transcranial magnetic stimulation
PSIS posterior superior iliac spine RTx radiation therapy
PSP progressive supranuclear palsy RUG retrograde urethogram
PT prothrombin time RUL right upper lobe
PT physical therapy RUQ right upper quadrant
PT peroneous tertious muscle RV residual volume
Pt patient RVH right ventricular hyperthrophy
PTA peritonsillar abscess RVOT right ventricular outflow tract
PTCA percutaneous transluminal coronary angioplasty RVOTO right ventricular outflow tract obstruction
PTH parathyroid hormone Rx prescription
PTHC percutanous transhepatic cholangiogram
PTSD post - traumatic stress disorder
PTT partial thromboplastin time s
PTU propylthiouracil SA sinoatrial, spontaneous abortion
PUD peptic ulcer disease SAAG serum-ascites albumin gradient
PV pulmonary valve SAH subarachnoid hemorrhage
PVC premature ventricular contraction SABD short - acting bronchodilator
PVD peripheral vascular disease SBE subacute bacterial endocarditis
PVR post - void residual SBE breast self - examination
SBFT small bowel follow through
SBI serious bacterial infection
Q SBO small bowel obstruction
q every
.
q4h, q6h every 4 hrs, every 6 hrs etc
qd every day
SBP spontaneous bacterial peritonitis
sBP systolic blood pressure
SC spinal cord
qh every hour SCC squamous cell carcinoma
qid four times a day SCFE slipped capital femoral epiphysis
qod every other day SCM sternocleidomastoid muscle
SCr serum creatinine
SD standard deviation

EdmontonManual of Common Clinical Scenarios 504


>
T3
SEM systolic ejection murmur
Sens sensitivity
TM tympanic membrane
T- max maximum body temperature recorded in a 24 - hr period
"D
SES socioeconomic status TMJ temporomandibular joint
fD
D SFH symphysis fundal height TMP/SMX trimethoprim and sulfamethoxazole
Q
X
- SGA small for gestational age
SGGT serum gamma glutamyl transpeptidase
TOF tetralogy of fallot
T.O.P. Toward Optimized Practice
SGOT serum glutamic oxaloacetic transaminase .
TORCH toxoplasmosis, other (syphilis), rubella CMV HIV.
SGPT serum glutamic pyruvic transaminase TP tibialis posterior muscle
SI sacroiliac TPN total parenteral nutrition
SI suicidal ideation TPPA T. pallidum particle agglutination
SIADH syndrome of inappropriate antidiuretic hormone TR tricuspid regurgitation
SIDS sudden infant death syndrome TS tricuspid stenosis
SIRS systemic inflammatory response syndrome TSB total serum bilirubin
SJS Stevens - Johnson syndrome TSEC tissue - selective estrogen xomplex
SL sublingual TSH thyroid stimulating hormone
SLE systemic lupus erythematosus TTE transthoracic echocardiogram
SLP speech language pathologist TTN transient tachypnea of the newborn
SM semimembranosis muscle TTP thrombotic thrombocytopenic purpura
SNHL sensineural hearing loss TURBT transurethral resection of bladder tumors
SNRI serotonin- norepinephrine reuptake inhibitor TURP transurethral resection of prostate
SOAP subjective, objective, assessment, plan TV tidal volume
SOB shortness of breath TVH total vaginal hysterectomy
SOBOE shortness of breath on exertion TVUS transvaginal ultrasound
Spec specificity Tx treatment
SPEP serum protein electrophoresis Tx transplant
Sp02 saturation of hemoglobin with oxygen as measured by pulse
oximetry
SQ subcutaneous
u
UA urinalysis
S/Sx signs and symptoms
UAC umbilical artery catheter
SSRI selective serotonin reuptake inhibitor
UAO upper airway obstruction
SSS sick sinus syndrome
UAW upper airway
ST semitendonosis muscle
STEMI ST elevated myocardial infarction UC ulcerative colitis
UE upper extremity
STAT immediately
UFH unfractionated heparin
STI sexually transmitted infection
SVD spontaneous vaginal delivery UGI upper gastrointestinal
UGIB upper gastrointestinal bleed
SVT supraventricular tachycardia
UMN upper motor neuron
Sx symptoms
U/O urine output
UPEP urine protein electrophoresis
T URTI upper respiratory tract infection
T temperature URQ upper right quadrant
TA tibialis anterior muscle U/S, US ultrasound
TAH total abdominal hysterectomy UTI urinary tract infection
TAPVR total anomalous pulmonary venous return
TB tuberculosis
TBW total body water v
TCA tricyclic antidepressant V vomiting
Td tetanus - diphtheria toxoid VI first division of trigeminal nerve
TEE transesophageal echocardiogram V 2 second division of trigeminal nerve
TEF tracheoesophageal fistula V3 third division of trigeminal nerve
VA alveolar volume
TENS transcutaneous electrical nerve stimulation
TENS toxic epidermal necrolysis
radial, limb
.
VACTERL vertebral, anal, cardiac TE fistula, esophageal, renal/
TFL tensorfascialata muscle
VBG venous blood gas
TG triglycerides
TGA transposition of the great arteries VC vital capacity
VCUG voiding cystourethrogram
THR total hip replacement
TlA transient ischemic attack VDRL venereal disease research laboratory ( test for syphilis)
TIBC total iron binding capacity VFSS videofluoroscopic swallowing study
tid three times a day VLDL very low - density lipoproteins
TIG tetanus immune globulin
VMA vanillymadelic acid
TIPS transjugular intrahepatic portosystemic shunt VNG videonystagmography
TKO to keep open
V/Q ventilation - perfusion
TLC total lung capacity VRE vancomycin resistant enterococcus
VSD ventricular septal defect

505 Edm it on Manual of C


VSR VS routine
VSS VS stable >
VT ventricular tachycardia
VTE venous thromboembolism
--o
o
fl>
vWF von Willebrand factor D
vWD von Willebrand disease
VZV varicella zoster virus
Q
X
-
w
WBC white blood cell (count )
WC waist circumference
WIAT Wechsler individual achievement test
WISC Wechsler intelligence scale for children
WOB work of breathing
WPW Wolff - Parkinson- White
Wt Weight
WU workup

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

Edmonton Manual of Common Clinical Scenarios 506


>
O
T3
APPENDIX B: TRIADS, TETRADS, &
fl)
D
CL
PENTADS

X Adrenomeduilary excess (catecholamines) Bezold ' s triad (otosclerosis)
tachycardia prolonged bone conduction (negative Rinne test)
vasoconstriction lessened perception of low tones
sweating negative Rinne’s test

Albinism Biotin deficiency


black locks glossitis
occulo -cutaneous albinism alopecia
deafness (sensorineural) dermatitis

Alkaptonuria Bochdaleck triad ( hernia )


ochronotic arthritis respiratory distress
ochronotic pigmentation apparent dextrocardia
urine darkens on standing scaphoid abdomen

Alport syndrome Carney ’s triad


sensorineural deafness functioning paraganglioma
progressive renal failure gastric leiomyosarcoma
ocular anomalies pulmonary chondroma

Anderson' s triad Charcot ’s triad ( billiary colic /cholangitis)


bronchiectasis pain
cystic fibrosis fever
Vitamin A deficiency jaundice

Aspergillosis ( bronchopulmonary) Charcot ' s triad ( multiple sclerosis)


bronchospasm scanning speech
hemoptysis intentional tremors
bronchiectesis nystagmus

Bartter syndrome Currarino’s triad (congenital anomalies in the


metabolic alkalosis anococcygeal region)
hypokalemia scimitar sacrum
normal or decreased BP presacral anterior meningocele, teratoma, or cyst
rectal malformations
Beck ’s triad (cardiac compression/cardiac tamponade )
muffled heart sound Dieulafoy’s triad
distended neck veins ( high venous pressure) hypersensitiveness of the skin
hypotension (low arterial pressure) reflex muscular contraction
tenderness at McBurney’s point in appendicitis
Beck ' s triad (renal cell Ca )
hematuria Fanconi syndrome
flank pain aminoaciduria
palpable flank mass proteinuria
phosphaturia
Behcet 's syndrome
recurrent oral ulcers Gradenigo' s triad
genital ulcers
sixth cranial nerve palsy
iridocyclitis
mastioditis ( persistent ear discharge)
deep- seated retro - orbital and temporal pain
Bergman' s triad (fat embolism )
petechial hemorrhages over chest
Grancher ’s triad (early pulmonary tuberculosis)
moderate rise in temperature
lessened vesicular quality of breathing
fall of hematocrit
skodaic resonance
increased vocal fremitus

507 Edmonton Manual of Common Clinical Scenario


Grawitz tumour (hypernephroma ) Multiple myeloma >
u
hematuria plasmacytosis > 10%
pain
O
hypergammaglobulinemia CD
palpable renal tumor lytic bone lesions =-
Q
3

Heerfordt syndrome Murphy’s triad ( acute appendicitis) X


uveitis pain
fever fever
parotid enlargement vomiting

Hemobilia Normal pressure hydrocephalus


melena dementia
obstructive jaundice urinary incontinence
biliary colic ataxia/gait apraxia

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

Hypernephroma Osier ’s triad (hereditary hemorrhagic telangiectasia )


pain telangiectasia
hematuria capillary fragility
renal mass hereditary hemorrhagic diathesis

Hutchinson’s triad (congenital syphilis) Paroxysmal nocturnal hemoglobinuria


mulberry molars hemolytic anaemia
interstitial keratitis venous thrombosis
labyrinthine disease (nerve deafness) deficient hemopoesis

Kartagener ' s syndrome Reiter ’s syndrome


bronchiectasis arthritis
recurrent sinusitis urethritis
situs inversus conjunctivitis

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

Meniere’s disease Tetany in children


vertigo stridor
tinnitus carpopedal spasm
sensorineural hearing loss convulsions

Edmonton Manual of Common Clinical Scenarios 508


“O
> Trotter ’s triad Pentalogy of Fallot
-a conductive deafness
immobility of homolateral soft palate
Tetralogy of Fallot
+ patent foramen ovale or atrial septal defect
0>
D trigeminal neuralgia
a. Reynolds ' pentad
X Urethral diverticulum Charcot ’s triad
dribbling of urine after voiding + sepsis
dysuria + mental status changes
dyspareunia
Pentad of TTP
microangiopathic haemolytic anaemia
Van der Hoeve syndrome
fever
blue sclera
multiple fractures disturbed neurological function
renal failure
otosclerosis
thrombocytopenia
Virchow ' s triad (predisposing to vascular thrombosis)
stasis
hypercoagulabilty
vessel injury

Vogt ’s triad
epilepsy
mental retardation
adenoma sebaceum

Weil’s disease
hepatorenal damage
bleeding diathesis
pyrexia

Wessel’s rule of threes ( colics in infants)


crying for > 3 hrs /day
crying for > 3 days / week
crying for > 3 wks

Whipple' s triad (insulin- producing tumors)


hypoglycaemia during attacks
serum glucose < 40 mg%
prompt relief on glucose administration

Young' s syndrome
sinusitis
bronchiectasis
azoospermia

Hemoplytic uremic syndrome pentad


microangiopathic hemolytic anemia
acute renal failure
thrombocytopenia
fever
hypertension

Tetralogy of Fallot
atrial septal defect
overarching aorta
pulmonary stenosis
right ventricular hypertrophy

509 Edmonton Manual o; Comrr


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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

The Edmonton Manual 6 th Edition features:


• Over 140 scenarios covering all major specialties including Family Medicine, Internal
Medicine, Surgery, Obstetrics and Gynecology, Pediatrics, and Psychiatry
< . • Revised " to the point ” content with new figures and tables for easy viewing
• Red flags and risk factors focus your attention on the “do not miss" differential diagnoses
• Likelihood ratios for physical exams help trainees ask specific questions and perform a
focused physical exam t

. • 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 &

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