OSCE Manual (Edmonton 2011)

Approach to the OSCE:
The Edmonton Manual of

Common Clinical Scenarios
A collaborative initiative ofstudents, residents,
and staffphysicians at the University ofAlberta
EDMONTON MANUAl
1
Approach to the OSCE:
The Edmonton Manual of • • .
Common Clinical Scenarios

A collaborative initiative ofstudents, residents,
ri and staffphysicians at the University ofAlberta
The Edmonton Manual is a unique Canadian guide for medical students to transform
their pre-clinical knowledge to useful skills for clerkship learning and objective
structured clinical examinations (OSCE).
Drawing on the experience of medical students, residents, and staff physicians at the
University of Alberta, this resource brings together an approac,h,to over 190 common
clinical scenarios.
Thisguide will help you focus your history and physical examination and quickly arrive to
relevant differential diagnoses. Abbreviated formatting allows for a quick review targeted
specifically for OSCE preparation.
Edmonton Manual Features:

• Over 190 common clinical presentations
• Covers all mjor-specialties: internal medicine, surgery, obstetrics & gynecology,
• pediatrics, and psychiatry.
• PLUS: Essential Clinical Skills (electrocardiography, radiology, blood work and more!)
• Easy to follow 2-page format summarizes your focused history and physical
• Red flags and risk factors focus your attention to sinister differentials
• Each presentation contains relevant workup for common diagnoses
New to the 2011 Edition:

• Physical Exam Section (abdominal, diabetic foot, hand, knee, thyroid and more!)
• PHELO Section (confidentiality, consent, research ethics, sexual health and more!)
• PLUS: Expansion and improvement of past sections (improved differentials, more tables
and images, updated content and evidence)
The Edmonton Manual will strengthen your”Approach to the OSCE”!
ISBN 978—0—9864874—1—5
0 M$A [: i
EDMONTON MANUAL
APPROACH TO THE OSCE:

THE EDMONTON MANUAL OF COMMON CLINICAL SCENARIOS
ND
2
EDITION 2011
-
EDITOR-IN-CHIEF
RYAN GALLAGHER
SENIOR EDITOR
JASMINE PAWA
JUNIOR EDITOR
DAVID LESNIAK
Edmonton Manual of Common Clinical Scenarios 1

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

d
2
Edition (2011)
Copyright © 2011 University of Alberta Medical Students’ Association
explicit permission from the copyright owner.

All rights reserved. No part of this book may be reproduced in any form without
Printed in Canada.
ISBN-i 3:978-0-9864874-1-5
errors or omissions to us by postal mail or e-mail.

We look forward to improving this resource annually. Please send your comments feedback,
Edmonton Manual
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feedback@edmontonmanual.com
information on this publication.

Additional copies of this publication may be purchased on-line. Our website also hosts more
www.edmontonmanual.com
2 Edmonton Manual of Common Clinical Scenarios

PLEASE READ THE FOLLOWING STATEMENTS CAREFULLY
By using this book, you understand and agree to the following:
This book is published by the University of Alberta Medical Students’ Association. ft 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 reasonable 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 guiding your 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.

CONTRI BUTORS
Editorial Team
Editor-in-Chief Ryan Gallagher
Senior Editor Jasmine Pawa
Junior Editor David Lesniak
Internal Medicine Section Editor: Vijay Daniels, MD, FRCPC

Assistant Professor
Division of General Internal Medicine
Obstetrics & Gynecology Section Editor Sujata Chandra MD FRCSC

Residency Program Director
Department of Obstetrics & Gynecology
Pediatrics Section Editor Melanie Lewis BN MD MEd FRCPC

Associate Professor
Department of Pediatrics
Psychiatry Section Editor Jorge Perez-Parada BSc MD MS FRCPC

Assistant Professor
Department of Psychiatry
Surgery Section Editor Jonathan White MB BCh BAO BMedSci(Hons) MSc(MedEd) PhD FRCS(Gen Surg)
Director of Undergraduate Surgical Education
Department of Surgery
Physical Exam and PHLEO Lisa J. Steblecki MD MPH CCFP

Associate Professor
Department of Family Medicine
Founding Members of EM Aaron Knox, Shaheed Merani, Ryan Gallagher, Jasmine Pawa
Design and Production

Resident Editor Team: Carrie Ye MD and Gary Galante MD
Director of Marketing and Sales Lina Wang and Marc Curial
Cover Design Penny Snell
Logo Design Mark Buller
Artists Odell Pui, James Huang, Christopher Fung, Aaron Banman (co-ordinator), Babak Maghdoori,
Cassandra Hirt, Nirupan Vipulananthan
Sub-committees:
Evidence based medicine: AIim Nagji and Scott McLeod
Finishing: Hollie Power (coordinator), Mackenzie Lees, Babak Maghdoori, Shawna Pandya,Casandra Hirt
Compare and Contrast Tables: Jessica Nicoll (co-oordinator), Shawna Pandya, Mackenzie Lees, Timothy Chan

Student Contributing Authors
Aamir Bharmal Daisy Hartmann Mackenzie Lees Sarah Wozney
Adarsh Rao Darwin Wan Maleka Ramji Scott McLeod
AIim Nagji David Lesniak Malgorzata Ejsmont Shawna Pandya
Arabesque Parker Debraj Das Michael Driedger Taryn Brown
Armin Badre Gabriela Pelinska Mike Samycia Terence Kwan-Wong
Ashraf Kharrat Hollie Power Mike Kapusta Timothy Chan
Babak Maghdoori Jamie Mcintyre Mohammed Osman PhD Todd Penney MSc
Brendan Diederichs Janna Tram Nathan Hoy Victoria Lam
Cassandra Hirt Jessica Nicoll PatriciaLee Victoria Cook MSc
Charles Lim Joffre Munro Peter Gill Zoe Wolf
Chris Gerdung Kamal Abdulwahab Ryan Gallagher
Christina Beach Kim Krueger Samapti Samapti
Christina Yang Lauren Kitney Sara Houlihan
Resident Contributing Authors

Abraam Isaac MD Christopher Gee MD Katherine Leung MD Simon Turner MD
Adam Dryden MD Christopher Hanson MD Khaled Al-Mansoori MD Stephanie Mullin MD
Amanda Aiken MD Colleen Weeks MD Leyla Asadi MD Stephanie Thompson MD
Anu Parhar MD Craig Domke MD Madhav Sarda MD Tamara Kuzma MD
Ashley Gillson MD Francois Jacob MD Marta Broniewska MD Tom Nowacki MD
Avi Aulahh MD Gary Galante MD Michael Chu MD Troy Schultz MD
Brian Yong MD Henry Conter MD Mohammad Almutawa MD Usha Ramanthan MD
Carol Chung MD isaiah Day MD Namdar Manouchehri MD Vijay Selvarajah MD
Carrie Ye MD James Yeung MD Nawaaz Nathoo MD WinstonTeo MD
Catherine Burton MD Janjeevan Deol MD Nicole Hubner MD Yang Li MD
Cathy Lu MD Jason Kiser MD Olga Toleva MD Michael Tjandrawidjaja MD
Chris Gee MD Jason Soo MD Parbeer Grewal MD Edward James PLT
Chris Hanson MD JayZhu MD Phil Bach MD
Christina Kerr MD Jeff Campbell MD Regan Guilfoyle MD
Christine Bentz MD Juliette Sacks MD Sarah Lai MD
Christopher Fung MD Kate Collins MD SayfGazala MD
Staff Physician Contributing Authors

Adriana Lazarescu MD FRCPC Daniel Schiller MD FRCSC Kal Ansari MD FRCSC Diplomate NadrMiomha MD PhD FRCSC
Alain Brassard MD FRCPC Darcie Kiddoo MD FRCSC (ABO) Diplomate (ABFPRS) Norma Leonard MD FRCPC
Alan McMahon MD FRCPC Darren Nichols MD CCFP(EM) Kamran Fathimani MD FRCSC Paul W. Armstrong MD FRCP
Ammara Sadiq MD Dilini Vethanayagam MD FRCP Keir Peterson MD CCFP (EM) Peggy Sagle MSc MD FRCSC
Arnold Voth MD FRCP Ed Wiebe MD FRCPC Laurie Mereu MD FRCPC Richard Camicioli MD FRCPC
Ashnoor Nagji MD CCFP Elaine Yacyshyn MD FRCPC Lisa StebleckiMD MPH CCFP Roger W.Turnell PhD MDCM
Ashraf Khan MBChB CCFP Eric Estey MD FRCSC Lucille Lalonde MD FRCPC MCEd FRCSC
Brendan Leier PhD Gabor Gyenes MD FRCPC Mansfield Mela MD FRCP Rohit Moudgil MD PhD
Brian Sonnenberg MD FRCPC George Elleker MD FRCP Marjan Abbasi MD CCFP, Dip. COE Ryan Cooper MD MPH FRCPC
Carlo Panaro MD FRCSC Gordon Lees MD FRCSC Mark Enarson MD FRCPC Sheny Khera MD CCFP MPH
Catherine Flood MD FRCSC James Keay MD CCFP Mark Joffe MD FRCPC Sujata Chandra MD FRCSC
Chris de Gara FRCS FACS James Wolfli MD FRCSC Matthew Wong MD CCFP Tarek Motan MB ChB CCFP FRCSC
Christopher J. Rudnisky MD MPH John Dewart MD FRCPC Matthew lngwood MBBChBAO Timothy Yeh MD FRCPC
FRCSC Jonathan Tankel MBBCh FRCSC Melanie Lewis BN MEd MD FRCPC Tom Yeo MD FRCPC
Clarence Wong MD FRCPC ABG Jonathan White BMedSci (Hons), Michael Morhart MD FRCSC Valerie Luyckx MBBCH
ABIM MB BCh BAO, FRCS (Gen Surg), Michel Donoff MD FRCPC Vijay Daniels MD FRCPC
Connie Switzer MD FRCPC MSc (Med Ed), PhD Michelle Teo MD FRCPC
D.B. Sinclair MD FRCPC Jorge Perez-Parada MD FRCPC Mohit Bhutani MD FRCPC FACP

1ABLE OF CONTENTS
Introduction
9 ACKNOWLEDGEMENTS 10
PREFACE
Primer Assesment in Medical Education 10
Section #1: Essential Clinical Skills

14 Interpretation of Electrolytes: Sodium 40
Admission and Daily Orders
16 Interpretation of LFTs and Enzymes 42
Essential Dermatology
Fluid Resuscitation 18 Interpretation of Lipids
20 Interpretation of PFT 46
Interpretation of a Abdominal Radiograph
22 Interpretation of Urinalysis 48
Interpretation of ABG
24 Intubation and Lumbar Puncture 50
Interpretation of a Chest Radiograph
26 Family History and Pedigree 52
Interpretation of CBC-D
28 Prescriptions and Progress Notes 54
Interpretation of Creatinine
30 Procedure and Ward Call Notes 56
Interpretation of C-Spine Imaging
32 Understanding Antibiotics 58
Interpretation of CT
34 Pre- and Post-operative Orders 62
Interpretation of ECG
36 ECG (Examples) 63
Interpretation of Electrolytes: Calcium
Interpretation of Electrolytes: Potassium 38
Section #2: Physical Exam 64

65 Jugular Venous Pressure (JVP) Exam 75
Abdominal Exam
66 Knee Exam 76
Back and Hip Exam
67 Lymphadenopathy and Spleen Exam 77
Blood Pressure Measurement
68 Male Genitourinary Exam 78
Cranial Nerve Exam
70 Precordial Exam 79
Diabetic Foot Exam
71 Neurological Exam 80
Examination for Liver Disease
72 Respiratory Exam 82
Female Genitourinary Exam
73 Thyroid Exam 83
Hand Exam
HEENT Exam 74
Section #3: Internal Medicine 84

85 Hearing Loss and Deafness 132
INTRODUCTION
86 Hemiplegia/Hemisensory Loss. 134
Abdominal Distention, Ascites, Liver Disease
88 Hemoptysis 136
Abnormal Heart Sounds
90 Hypertension 138
Acute Confusion
92 LowerBackPain 140
Allergic Reactions
94 Nausea and Vomiting 142
Altered Level of Consciousness
96 Obstructive Lung Disease 144
Altered Sensation (Numbness and Tingling).
A nomi, 98 Palpitations and Arrhythmias 146
.
100 Parkinsons and Movement Disorders 148

Arthritis and Joint (Monoarticular)
102 Peripheral Vascular Disease 150
Bleeding Disorders
104 Pleural Effusion 152
Chest Pain, Angina and Cardiac Arrest
106 Polyarticular Arthritis and Joint Pain.. 154
Congestive Heart Failure& Edema
108 Proteinuria 156
Cough
1 10 Pruritus 158
Dehvd ration 160
.112 Renal Failure
fli,rrhn .114 Respiratory Tract Infection. 162
116 Restrictive Lung flkc 164
flvcnpnci
118 C’S..’. 166
Dyspnea
120 Sexual and High Risk Infections. 168
Dysuria
122 Shock 170
Falls 172
Fatigue 124 Skin, Hair and Nails
126 Sleep Apnea and Insomnia 174
Fever 176
Gait Disturbance 128 Sore Throat (Pharyngitis)
130 Syn cope 178
Headache

.180 .188
i;;ri;len Leg .182 Weight Gain. .190
Urinary Incontinence . .184 Weight Loss. .192
Vision Loss .186
Section #4: Obstetrics and Gynecology 194

INTRODUCTION 195 Intrapartum Care 214
Amenorrhea 196 Menopause 216
AntepartumCare 198 PapSmear 218
Contraception 200 Pelvic Mass 220
Dysmenorrhea & PMS 202 Pelvic Organ Prolapse 222
Fetal Distress 204 Pelvic Pain 224
Hirsutism 206 Postpartum Complications 226
Hypertension in Pregnancy 208 Pregnancy Loss 228
Infertility 210 Vaginal Bleeding 230
Interpretation of Fetal Heart Rate 212 Vaginal Discharge 232
Section #5: Psychiatry 234

INTRODUCTION 235 Personality Disorders 244
Abuse 236 Psychosis 246
Gender Identity Disorder 238 Substance Abuse 248
Mood Disorders 240 Suicidal Behaviour 250
Panic and Anxiety 242
Section #6: Pediatrics 252

INTRODUCTION 253 Immunizations 278
Abnormal Sexual Maturity 254 Limping Child 280
Abnormal Stature 256 Neonatal Jaundice 282
ADHD/Learning Disorder 258 Newborn Respiratory Distress/Cyanosis 284
Anemia (Pediatric) 260 Pediatric Emergency 286
Childhood Communicable Diseases 262 Pediatric First Presentation of Seizure 288
Depressed Newborn 264 Pediatric Wheeze 290
Developmental Delay 266 Periodic Health Exam of a Newborn 292
Down Syndrome 268 Periodic Health Exam in a Toddler/Child 294
Ear Pain 270 Periodic Health Exam in an Adolescent 296
Failure to Thrive 272 Speech and Language Abnormalities 298
Fever Without a Source in a Child < 3 mo 274 Stridor 300
Genetic Concerns & Pedigree 276
Section #7: Surgery 302

INTRODUCTION 303 Gynecomastia .340
Abdominal Mass, CRC Screening Guidelines 304 Hand (Pain, Fractures, Dislocations) .342
Abdominal Pain 306 Head Trauma .344
Anal Pain 308 Hematemesis .346
Ankle and Foot (Pain, Fractures, Dislocations) 310 Hematuria .348
Arm and Shoulder (Pain, Fractures, Dislocations) 312 Hernia .350
Biliary Disease: Cholelithiasis 314 Hip (Pain, Fractures, Dislocations) .352
Bites and Dirty Wounds 316 Jaundice .354
Bladder Obstruction and Prostate Cancer 318 Knee (Pain, Fractures, Dislocations). .356
Breast Lump and Cancer Screening 320 Neck Mass/Goiter .358
Bright Red Blood Per Rectum and Melena 322 Pediatric Strabismus .360
Burns 324 Pupil Abnormalities .362
Constipation 326 Red Eye .364
Diplopia 328 Scrotal Mass and Scrotal Pain .366
Dizziness/Vertigo 330 Tinnitus .368
Dysphagia 332 -
.370
Epistaxis 334
Erectile Dysfunction 336
Gastrointestinal Bleed 220

Section #8: PHELO
INTRODUCTION 373 Informed Consent
374 Personal and Professional Conduct 381
Approach to Medical Literature
376 Research Ethics 382
Clinical Epidemiology
Confidentiality 377 Resource Allocation
Doctor-Patient Relationship 378 Sexual Health History
Dying Patient/Bereavement 379 Truth Telling

PREFACE
Thank you for choosing Approach to the OSCE: The Edmonton Manual of Common Clinical Scenarios. This “for-students by- students”
resource is a collaborative project of medical students at the University of Alberta, with resident and staff physician oversight. Our goal has
been to create a guide that will help medical students prepare for their clinical experience and for objective structured clinical examinations
(OSCE). This venue also serves as an opportunity for medical students at the University of Alberta to be involved in medical education and
publication at an early point in their academic careers.
Transforming knowledge of physiology, anatomy, biochemistry, and pathology into clinically useful skills requires both organization and
practice. This resource serves as a template which medical students can organize that transition and demonstrate clinical proficiency.
You will find herein two-page layouts addressing over 190 common clinical scenarios you may face during your clinical experience. Our aim is
to help you focus your knowledge to the common differential diagnoses as well as those diagnoses that are life threatening. Taking a focused
and patient-centered history, performing an appropriate physical examination, and ordering justified investigations will help you narrow the
differential diagnosis.
This book is divided into eight sections:
1. Essential Clinical Skills (ECS)

2. Physical Exam (PE)
3. Internal Medicine
4. Obstetrics and Gynecology
5. Pediatrics
6. Psychiatry
7. Surgery
8. Population Health, and the Ethical, Legal, and Organizational Aspects of Medicine (PHELO)
Most sections begin with a brief introduction written by one of our staff physician section editors each of whom is familiar with both
undergraduate medical education as well as examination of clerkship students.
We hope that the collective knowledge provided within The Edmonton Manual will be of use to you as you pursuit your clinical placements
and prepare for the OSCE. If you have any suggestions, comments, or feedback or are interested in becoming involved in this publication,
please contact us at feedback@edmontonmanual.com.

PRIME R ASSESMENT IN MEDICAL EDUCATION
MD, FRCPC
ay Daniels,
If you are reading this, you have been around long enough to know that assessment in medical
school is far different than assessment in high school or undergraduate courses which primarily used
multiple choice examinations, short answer or long answer essays. Why? Because these methods
assess mainly knowledge and not performance. Being a doctor is about doing, not just knowing. This
, which is a commonly used paradigm amongst
distinction is best demonstrated by the Miller pyramid
1
medical educators. The Knows level involves basic recall of thing 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 their clinical skills in a structured
environment (in-vitro). Finally the Does level involves the real-life or in-vivo performance of the /SHOWS
learner.
/
An Objective Structured Clinical Examination (or OSCE) is a method that assesses the Shows How level.
To contrast the Shows How and the Does we need not look that far: all of us as teachers have had the
medical student who, in an OSCE, palpates the radial before inflating the blood pressure cuff and then / KNOWS HOW
(c.mp4Inc.)
after finding the systolic blood pressure, reinflates to 20 mm Hg above the systolic. Yet, this same
medical student simply inflates the cuff to 300mm Hg on the real patient (this is at least better than
the student who says the nurse has not taken the blood pressure yet!).
Why an
OSCE?
/ KNOWS
PeLPewaTkfDrI1bIi
We have already examined what an OSCE is assessing: performance, not just knowledge. Next is how it assesses it. 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 how they examine one organ system in one patient. An OSCE involves multiple short samples of your clinical performance. It
should come as no surprise that multiple short samples of 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

I often tell students to approach the OSCE as you would approach an interview: “be yourself... but a slightly more refined you!” This tip only
works if you adhere to the lessons learned in medical school (e.g. palpating the radial before taking the blood pressure) with your real-life
—
patients. If not, then my tip to you is “do on an OSCE what you should be doing in real-life!” I hope it is a minority of you that have to take
that advice! For more thoughts on how to excel at the OSCE as it applies to the specific specialties, please see the introductions from each of
the section editor’s. Good luck!
ACKNOWLEDGEMENTS
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 those students who were involved in the initial conceptual design of the project through informal feedback during
who
hallway discussions as well as those who contributed to formal focus groups. It was the dedication and energy of our student authors
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.
Funding for this edition was provided by the University of Alberta Medical Students’ Association. The 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.
1. Miller GE. The assessment of clinical skills/competence/performance. Acad Med. 1990 Sep;65(9 Suppl):S63-7.

EDMONTON MANUAL
APPROACH TO THE OSCE:

THE EDMONTON MANUAL OF COMMON CLINICAL SCENARIOS
2ND EDITION 2011

-

v.
EDMONTON MANUAL
Section #i
ESSENTIAL CLINICAL SKILLS
Admission and Daily Orders .14 Interpretation of Electrolytes: Sodium 40

Essential Dermatology 16 Interpretation of LFTs and Enzymes 42
Fluid Resuscitation 18 Interpretation of Lipids .4A
Interpretation of a Abdominal Radiograph .20 Interpretation of PFT 46

Interpretation . .22 Interpretation of Urinalysis
Interpretation of a Chest Radiograph .24 Intubation and Lumbar Puncture
Interpretation of CBC-D .26 Family History and Pedigree
Interpretation of ,_reatinine ‘ Prescriptions and Progress Not CA
Interpretation of C-Spine Imaging 30 Procedure and Ward Call Notes.

Interpretation of CT 32 Understanding Antibiotics
Interpretation of :-t; 34 Pre- and Post-operative Orders. 62
Interpretation of Electrolytes: Calcium. .36 ECG (Examples)
Interpretation of Electrolytes: Potassium
12 Edmonton Manual of Common Clinical Scenarios I Essential Clinical Skills

INTRODUCTION
In this section you will find some of the basic skills you will need as a clinical clerk or intern. Your role of a medical student will transition
from preclinical to clinical years. In the former, your primary goal is that of gaining an understanding of normal human physiology and the
pathology, while in your clerkship experience you will be asked to act as an information gatherer (in the form of a patient history and physical
examination), and then as an interpreter: combining with 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 to your clinical team.
In an OSCE or clinical scenario, you may be asked to interpret basic clinical laboratory test or radiographic images to demonstrate your skill as
a diagnostician. The following pages discuss those skills in further details. Whatever the test, don’t 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 with your interpretation of
the test. That is, don’t 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 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 a clearly written prescription and orders will ensure that the care of your
patients is carried out and reduces medication errors.
On the ward, in clinic, and examination settings medical students are often asked to provide an oral summary of a patient interaction.
When a resident or staff physician asks you to present a case, organization is the 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. What is 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 demonstrates 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% is above the waters surface, and the vast majority below.
Similarly you presentation should present only the key findings, while keeping in your own mental reserve the other 70% of the detail should
you be 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 you find these essential clinical skills useful as you begin your clinical placements and prepare for OSCEs.
Sincerely,
The Edmonton Manual EditorialTeam
Essential Clinical Skills Edmonton Manual of Common Clinical Scenarios 13

ADMISSION & DAILY ORDERS
2011 Ed. Authors: Shawna Pandya, Erian Yong MD, Darren Nichols, MD CCFP(EM)
j
— OriginalAuthors: Sara Houlihan, Sarah Forgie MD FRCPC
Station Objective
To properly complete admission and daily orders.
Orders (Dad-david)
under each section.
The traditional DAD-DAVID format is included below, with common orders included
1. D-A-D
• Date/Time
• Admit to ward/service under Dr [Name]
• Diagnosis
2. 0
• Diet
• Include: content, consistency, quality, delivery method
thickened fluids (dysphagia diet), DAT: diet as
• NPO ± ice chips (e.g. pre-op, aspiration risk), CF (clear fluids), FF (full fluids),
tolerated
• Advancing diet (NPO -+ sips —* CF -. FF —* DAT)
• CDA: diabetic diet (small-i 600kcal, med-i 800kcal, lrg-2000kcal)
• Cardiac diet, renal diet (assessed by dietician or speech language pathologist)
3. A
• Activity
• AAT (activities as tolerated)
• Ambulation: up in chairTlD, ambulate BID
• NWB (non-weight bearing), WBAT (weight bear as tolerated), FWB (full weight bearing)
• BR (bed rest), Bed rest with BRP (bathroom privileges)
• Elevate head of bed to 30 degrees
• Precautions: fall, seizure, spinal etc.
4. V
• Vital Signs
• Clarify what routine vitals are for each service, add on as necessary
• Include on-call orders: set parameters. (Ex. Call MD if sBP 1 8OmmHg)
security (Psychiatry, Geriatrics), routine/
• Specify frequency, e.g. qlh, q4h, close observation (qi5min), nurse in room, constant
regular observation (Pediatrics), etc.
• HR,BP,RR,T,Sp0
2
• Neurovitals (GCS and pupils)
• Peripheral pulses/Doppler (vascular patient)
• Capillary glucose
5. I
• IV
• Fluid, route, rate
• NS or RL @ 125-150 mI/hr (depending on pt size and medical condition)
• Bolus IV NS @ 500ml/hr x 2 hrs
• Replace NG losses 1:1 with 1/2NS + KCL 10 mEq/L
• Pediatrics —* consider wt, age, deficit, maintenance and ongoing losses
• In/Outs
• I/O qshift (surgery, volume status patients)
• Foley —* call if u/o <6OmL over 2 hrs
• Pediatrics, renal failure, edematous/CHF: daily wts
• Infection Control
• Droplet
• Contact
• Droplet and contact
• Airborne
• Significant organism
• Investigations
• Blood — Hematology: CBC-Diff, reticulocyte count, PT/INR + PU, crossmatch, type, screen
(Na, K, CI, HCO3), glucose, Ca
’
2
• Blood — Biochemistry: Liver function tests, liver enzymes (AST, ALT, ALP), urea, Cr, electrolytes
, P0
2
Mg ,TSH, Vit Bi 2, folate, CK,
4 CKMB
• Blood — Culture: Viral serology, cultureu
14 Edmonton Manual of Common Clinical Scenarios Essential Clinical Skills

• Urine Urinalysis, culture, routine & microscopy
—
• Imaging X-ray, MRI, CT, bone scan

—
• Other ABG, EKG, echo

—
• Consults pharmacy, OT/PT, dietician, social work, pastoral care, other specialties
—
6. D
Drugs
• CHECK ALLERGIES! (Include latex, iodine and tape allergies)
• Include drug name, dosage, route, frequency and stoo date
• Antibiotics
• 6Ps:
• Pain (analgesia) always include a Tylenol order unless contraindicated
-
• 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 Meds (very important! do not forget!)
Drains
• Foley (to urometer)
• NG to low wall suction
• G tube or T tube to straight drainage
• Reprime JP/hemovac qshift and pm
Dressings
• Change dressing QD, pm; remove staples day x post-op
7. Signature
Signature, printed name, training (e.g. 51-3, PGY-4, etc.), pager number
NB Be sure to flag the patient’s chart once you have written your orders. Communicate any stat, important or nuanced orders to your
-
nursing colleagues.
References
Blackbourne LH. Surgical recall. ed. Baltimore: Wolter Kluwer; 2009.
2. “Writing an Effective Daily Progress Note:’ http//www.medicine.ufl.edu/3rd_year_clerkship/documents/Writing_an_Effective_Daily_Progress_Note.pdf
[online].

:
‘ ESSENTIAL DERMATOLOGY
20?? Ed. Authors: Nathan I-lay, Isaiah Day MD, Alain BrassardMD, FRCPC
Station Objective
To develop a structured approach to diagnosing common skin conditions
Differential Diagnosis
1. Common Conditions:
• Acne vulgaris, Atopic eczema, Psoriasis vulgaris, Actinic keratosis, Seborrheic keratosis, Basal cell carcinoma, Androgenetic
alopecia, Pigmentary disorders like Vitiligo and Melasma
2. High Mortality / Morbidity:
• Melanoma, Stevens-Johnson syndrome, Toxic Epidermal Necrolysis, Necrotizing fasciitis, Pemphigus vulgaris
History
ID Age, race, gender, ccupation (occupational/contact/allergic dermatitis)
HPI • Seven key questions: when, where (site of onset), symptoms (itch, pain, asymptomatic, systemic sx),
how has it spread, have the individual lesions changed, provocative factors (heat, cold, sun, exercise,
travel history, drug ingestion, pregnancy, season), which treatment(s) have been tried
RED FLAGS • Fever, malaise, flu-like symptoms, positive Nikoisky’s sign, painful rash with mucosal involvement
(Stevens-Johnson syndrome), weight loss, difficulty swallowing or breathing
PMHx • Previous skin cancers, shingles, psoriasis, thyroid disorders, diabetes
PSHx • Previous operations
PO&GHx • STI, pregnancy, sexual activity, HIV risk factors
Meds • Present and past medications (both topical and systemic), supplements
Allergies • Food but most importantly drugs
FHx Psoriasis, atopy (atopic dermatitis, allergies, allergic rhinitis), skin cancer, genodermatoses (eg. tuberous
sclerosis, neurofibromatosis)
Social • Sun/chemical exposure, smoking, EtOH, IV drugs, pets, travel history, hobbies
ROS • Done as indicated by the clinical situation with particular attention to possible connections between
signs and disease of other organ systems.
• Eg. a patient with a lesion suspicious for melanoma would require a complete ROS looking for any sign
of organ dysfunction suggesting metastases.
• Often neglected symptoms include myalgia, arthralgia, fever, oral ulcers and Raynaud’s phenomenon.
Remember to ask about hair and nail changes as many conditions that affect the skin also affect hair
and nails (eg. psoriasis)
Physical
Define lesions by:
Primary morphology (see Box 2)
• Secondary morphology: develop from scratching, infection, or evolution of primary lesion (Box 3)
• Arrangement- how the lesions are grouped (eg. annular, herpetiform), distribution (eg. extensor surfaces, dermatomal), color,
number of lesions
• Assess suspicious lesions for malignancy (Box 1)
• Examine the hair, scalp and nails (Box 4)
BOX 1: Assessing malignancy in lesions:

Asymmetry
Border irregularity
Color variation
Diameter (new lesion exceeding >6mm)
Evolution (changes in size, color, or bleeding)

BOX 2: Types of Primary Lesions: BOX 3: Types of Secondary Lesions and Special Lesions
1. Macule (flat, non-palpable lesions<5 mm), Patch (>5mm) eg. 1. Scales (excess keratin) eg. psoriasis
vitiligo, café au lait spot 2. Crusts (dried serum, scab) eg. impetigo -
2. Papule (<5 mm, palpable lesion, most of it is elevated 3. Erosion (loss of epidermis, heal without scarring) eg.
above the skin rather than deep within) eg. molluscum dermatophyte infection
contagiosum, acne vulgaris 4. Ulcer (loss of epidermis and dermis, heal with scarring) eg.
3. Plaques (>5 mm, plateau like elevation above the skin) eg. stasis ulcer
psoriasiS 5. Fissure (linear loss of epidermis and dermis) eg. chapping feet
4. Vesicle/Bulla (<5 mm blister)/ bulla (>5mm blister) eg. 6. Atrophy (thinning of epidermis or dermis causing depression)
varicella, contact dermatitis, bullous pemphigoid eg. morphea
5. Pustule (superficial cavity of the skin that contains a purulent 7. Scarring (abnormal formation of connective tissue after dermal
exudate) eg. folliculitis injury) eg. keloid
6. Nodule (deep palpable solid lesion within the skin)/tumor Special Lesions:
(large nodule). Depth and size differentiate a nodule from a 8. Excoriation (erosion due to scratching) eg. Atopic dermatitis
papufe. They are often better felt than seen eg. Lipoma 9. Comedone (hair follicle plugged with sebaceous and
7. Cyst (cavity containing fluid or semi-solid component) eg. keratinous material) eg. acne
pilar cyst 10. Purpura, >0.5cm and petechiae, <0.5cm (deposits of extravased
8. Wheal (rounded or flat topped papule or plaque that RBC in the skin) eg. Senile traumatic purpura
is evanescent due to edema of the dermis) eg. hives, 11. Telangiectasias (dilated superficial blood vessels) eg. rosacea
angioedema
BOX 4: Hair, Scalp and Nail Examination
Hair and Scalp:Texture, scars, thinning, absence (alopecia) or
excess (hypertrichosis), infestations (lice), masses (on scalp), plaques,
crusting
Nails: Pitting, separation from nail bed (onycholysis), Yellow

Investigation discoloration in nail bed (oil drop sign for psoriasis), other
Blood Work discoloration, Periungual erythema, splinter hemorrhages
1.
• CBC, ESR, CRP, ANA (if suspicious of connective tissue (endocarditis), clubbing, thickness
disease)
• TSH, fasting glucose, blood culture, LFT (If suspicious of internal pathology, order organ specific blood work)
1. Radiology/Imaging
• CXR (heart or lung pathology)
2. Special Tests
• Skin scraping for fungus, Wood’s Light to accentuate areas of depigmentation
3. Surgical/Diagnostic Interventions
• Skin Bx (shave, punch or excisional Bx) New lesions usually more useful than old lesions.
-
• Biopsy is indicated in all skin lesions that are suspected of being neoplastic, in bullous disorders, along with immunofluorescence,
and disorders in which Dx is not possible by clinical exam alone
Treatment
1. Emergent
• Stop offending agent if drug reaction (eg. Stevens-Johnson syndrome). Start antimicrobials for infection (eg. Cellulitis) or
immunosuppressive agent for immune mediated disease
2. Treatment Options
• Topical: Steroids, antibiotics, antifungals, emollients, retinoids, etc.
• Systemic medications: Immunosuppressives (methotrexate), retinoids, antibiotics, antimalarials
• Light: Narrow band Ultraviolet B, Ultraviolet A (PUVA), laser therapy
• Surgical: curettage, cryotherapy, electrotherapy, scalpel
3. Follow-up
• Monitor skin findings over time to evaluate progression, monitor for Rx medication side effects
4. Referrals
• Refer to appropriate specialty for cases requiring multidisciplinary approach
References
1. HabifTP, Campbell JL, Quitadamo Mi, Zug KA. Skin Disease Diagnosis and Treatment. Missouri: Mosby Inc.; 2001.
2. Schwarzenberger K. 1998.The essentials of the complete skin examination. Medical Clinics of North America 82:981-99.

FLUID RESUSCITATION
FRCPC
20 I I Ed. Authors: Malgorzata Ejsmont, Adam Dryden MD, 7imothy Yeh MD
Station Objective
on and
and their use in resuscitating during intravascular volume depleti
To understand the key concepts of fluid balance, IV and oral fluids
tissue hypoperfusion.
TBW 42 L
Fluid Balance ECF1/3
1CF23
1. Basics
• Fluid makes up 50-60%TBW Interstitial 3/4
• Water movement: mainly osmotic forces (Na, K)
2. Distribution (Figure 1)
• Note: Intravascular volume — ECF (plasma 3-3.5 L) + CF (RBC 2-2.5
L) in L ..t 4— Intravascular 1/4
Figure 1. Fluid Distribution
70kg male
3. Fluid Requirements
s)
• Total: maintenance + replacement (existing & ongoing deficit Table 1: Maintenance Fluids —
• Maintenance requirements: -2.5 L/day (4-2-1 rule: Table 1)
Weight mLlkg/hr
4. Compensation in hypovolemic states
• Initially: sympathetic outflow —* vasoconstriction, tachycardia first 10kg 4 —
• Over hours: extravascular —* intravascular shift next 10kg 2

each kg > 20kg 1
Fluid Therapy (IV)
Crystalloid Aqueous solution of salts +1-glucose (Table 2)
Equilibrate in entire ECF: given as 3 —4 X volume deficit
l perfusion
Initial resuscitation in hemorrhagic/septic shock, burns, maintain cerebra
0 and electrolyte deficit (distrib
Isotonic (replacement): if H
2 ute ECF)
•
• 0 deficit only (distribute ICFIECF)
Hypotonic: if free H
2
• Hypertonic: in severe hyponatremia (shift ICF —* ECF)
• Glucose: prevents hypoglycemia in fasting
Colloid • Large molecules maintain plasma oncotic pressure
ratio of volume deficit
• Mostly intravascular (altered if t vascular permeability): given as 1:1
scular deficit s prior to arrival pRBC, large protein loss (ex.burns)
• Use: severe intrava
c reactio ns, antipla telet effects
• Caution: prepped in NS (hyperchloremic acidosis), allergi
• Blood derived: albumin (5% & 25%), plasma protein fractio n (5%)
Voluven (hydroxyethyl starch)
• Synthetic: Dextran (40 & 70), Hetastarch (6%), Pentaspan (pentastarch),
Blood . Packed RBC: compensate for anemia, not volume deficit

• Give when anemia risks > risks of transfusion (Hg 70-80 g/L)
• 1 unit: Hg 1’ 10 g/L,warm to>37 if need >1-2 units
Table 2. Common Crystalloid Solutions

pH Na Cl K HCO3 Ca Mg Glucose
. Tonicity Caution
Solution (mEq/L) (gIL)
(mOsm/L)
7.4 145 105 4 24 3 2 0.7-1.1
Intravascular 290
154 154 hyperchloremicacidosis
NS(0.9%) 308 5.5 - - - - -
109 4 28* 3 - lactic acidosis

Ringers 273 6.5 130 -
7.4 140 98 5 3
294
-
-
Plasmalyte -
50 hyperglycemia
D5W 253 4 - - - - - -
77 hyponatremia
1/2 NS 154 5.5 77 - - - - -
513 513 hypernatremia,hemolysis

3%Saline 1026 5 - - - - -
*converted from lactate

Crystalloid vs. Colloid
tation with colloid vs. crystalloid
• Extensive meta-analysis found no difference in survival between resusci
loids (contro versial in some cases)
• The cost difference guides recommendations in favour of crystal

Fluid Therapy (oral)
Used mostly in pediatrics (in infants with mild-moderate dehydration: equivalent to IV therapy)
• Maintenance solutions (Pedialyte, Ricelyte): Na 45-50 mEq/L, glucose 2-3 %
• Rehydration solutions (WHO formulation, Rehydralite): t Na (60-90 mEq/L) —* improve water absorption
• Administer slowly to 1’ emesis: mild (50 mI/kg over 4 hrs), moderate (100 mI/kg over 4 hrs)
Assessment and Treatment

1. Initial Assessment: ABC, IV, °2’ monitor, SAMPLE Hx
• Assessment of severity (Table 3)
• Consider DDx (see Trauma and Shock)
• Fluid resuscitation goals: restore vital organ perfusion, maintain adequate oxygen delivery, limit ongoing loss of RBC
Table 3. Hemorrhagic shock classification
Blood Loss
Class Bloodloss(mL) HR BP RR U/O(mL/h) Mentaistatus
(% blood vol)
i <750 <15% N N N N slightlyanxious
II 750-1500 15-30% >100 N 20-30 20-30 mildlyanxious
III 1500-2000 30-40% >120 30-40 5-15 confused, anxious
IV >2000 >40% >140 1- >35 Anuric confused, lethargic
2. IV access
2 large bore IV (16/18) in peripheral veins —* investigations, type & crossmatch
• If severe shock or peripheral IV not achieved —* large catheter introducer (8-9 Fr) in femoral vein
• If major vascular injury in Abd/pelvis —* establish vascular access above diaphragm (subclavian/jugular)
3. Hemodynamic Assessment
• Continuous monitoring: HR, BP, RR,T, SpO , ECG.
2
• Frequent checks: mental status, peripheral perfusion signs
• Other: urine catheter (end organ perfusion), arterial line (serial ABG: once lactate t: several hrs to normalize), central venous
pressure (CVP - response to fluid), central venous oxygen saturation (ScVO
2 - 02 extraction, global perfusion)
4. IV therapy (also see Pediatric Emergency)
• Isotonic crystalloids: (RL or NS) x 2-3 L wide open
Table 4: IV Infusion Rates Isotonic Crystalloids
-
• Hemodynamics not stable: suggests >15-20% blood

volume lost or significant ongoing loss —* transfusion Access IV Gravity’ 2
Pressure
• Adequate response —* continue crystalloid, monitor (mL/min) (mL/min)
hemodilution Peripheral 18g 50-60 120-180
• Blood transfusion
169 90-1 25 200-250
• If not typed/crossmatched —* transfuse 0 (male), 0
(female) 14g 125-160 250-300
• Severe hemorrhagic shock —* transfuse initially Central Venous Introducer 8.5 Fr 200 400-5 00
• Bleed controlled —* target Hgb >70 g/L
• Hemorrhage, large volume resuscitated: dilutional ‘80cm hight,
2 300 mmHg
coagulopathy
• Massive Transfusion Protocol: 6u pRBC, 6u FFP, 1 pool platelets (Capital Health)
5. Referral
Surgery (control bleed), ICU
References
1. Ahrens W. Fluid and ElectrolyteTherapy. ln:Tintinalli JE, Kelen GD, Stapczynski JS, editors. Emergency Medicine: A Comprehensive Study Guide.6th ed.
USA: McGraw-Hill; 2004. Chapter 132.
2. Capital Health. Clinical Guide to Blood Transfusion [Internet]. Edmonton (CA); March 16,2010. Section 10, Massive
Transfusion; [cited 2010 Oct 9]; p.1-5. Available from: http://www.capitalhealth.ca/NR/rdonlyres/enupoxpjc6ucke7lmuy
jesyq6ibkxmb3sjhor3t6spj27htqsnnwsoh2nnufkm6q3rxmpkehkklwmidrwbgkzhglppd/sectionl OMarch2Ol 0.pdf
3. Ganter MT, Hofer CK, Pittet JF. Postoperative Intravascular Fluid Therapy. In: Miller RD. Miller’s Anesthesia. 7
th
ed. USA: Elsevier Inc.; 2009. Chapter 88.
4. Morgan GE, Jr., Mikhail MS, Murray MJ, editors. Clinical Anesthesiology. 4t1 ed. USA: McGraw-Hill; 2006
5. Manning JE. Fluid and Blood Resuscitation. ln:Tintinalli JE, Kelen GD, Stapczynski JS, editors. Emergency Medicine: A Comprehensive Study Guide.6th ed.
USA: McGraw-Hill; 2004. Chapter 31.
6. Well MH. Shock and Fluid Resuscitation. In: Beers MH, Porter RS, JonesTV, Kaplan JL, Berkwits M, editors. Merck Manual of Diagnosis and Therapy. 1 gth ed.
Whitehouse Station, NJ.: Merck & Co., Inc.; 2006. Chapter 67.
Essential Clinical Skills I Edmonton Manual of Common Clinical Scenarios 19

INTERPRETATION OF AN ABDOMINAL RADIOGRAPH
2011 Ed. Authors: Babak Maghdoori, Christopher Fung MD, Ed Weibe MD FRCPC
Original authors: Summit Sawhney, Karen Seland MD, Arlene Kanigan MD FRCPC
Station Objective
To offer a systematic approach for reading, interpreting, and analyzing abdominal radiographs.
History
Determine the following prior to acquiring/reading the radiograph:
• Pt’s name, age, gender, and date of image
• HPI: Acute/chronic, level of progression of the disease, etc.
• Determine the type of the image (supine/prone/decubitus)
• Ensure completeness of the abdominal film series, “the 3 views”: supine AXR, erect AXR, and a CXR,
• Note: if the Pt IS unable to stand for an upright abdominal radiograph, acquire a left lateral decubitus AXR
Interpretation
Basic approach: ABC
• Air (free air/gas pattern)
• Bones (fractures, metastatic disease)
• Calcifications (GU stones, gallstones, lymph nodes, calcified AAA wall)
Full Assessment:
1. Technical quality:
• Level of penetration:
• Normal penetration: Vertebral columns (lumbar and thoracic) can be seen clearly
• Under-penetration:The AXR is too white, leading to inability to distinguish between different densities
• Over-penetration: The AXR is too dark, leading to the loss of significant density differences
• Inclusion and adequacy:
• Inclusion: Ensure that the entire abdominal region, from the diaphragm to the proximal femoral head is included in the study
(additional images may be required).
2. Foreign/therapeutic objects:
• Comment on any lines, iatrogenic devices, and/or tubes present (foley, NG tube, ECG leads etc.)
3. Gas patterns:
• Normal: gas present in the stomach and a few loops of transverse colon/sigmoid colon/rectum
• In a healthy, ambulatory adult, who has not just eaten, the small bowel usually has very little or no air
• 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)
• DDx for abnormal bowel gas pattern —* ileus or mechanical obstruction.
• Ileus: typically seen in post-operative pts (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
• More pathologically significant than intraluminal air
• Evaluate underneath the hemidiaphragms for possible free air
• DDx: perforated ulcer, diverticulitis, perforated ischemic bowel, etc
• Post-operation free air is also common (5-7 days post-op)
4. Bowel:
• Carefully look for bowel wall thickening and narrowing of the lumen
• Small bowel diameter < 3.5 cm; Large bowel diameter < 6cm (variable); Cecal diameter < 9cm
5. 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 diseases 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, thus requiring careful attention
to avoid a misdiagnosis

6. Calcificatiofls and abnormal densities:
• DDx: GU stones, gallstones, chronic pancreatitis, calcified lymph nodes, fibroid tumors, calcified arteries, calcified wall of aOrtic
aneurysm, etc.
7. Free fluids:
• Free fluid may be due to an exudative, a transudative, or a bleeding process
• The distance between flank fat pads and the colon may be used as a diagnostic measure:
• If the distance> 1cm —* increased possibility of free fluid in the paracolic gutters
B. organs/Soft tissues:
• Try to visualize liver, stomach, spleen, kidneys, bladder, psoas margins
• Plain X-ray films are not generally 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.
3{
54
Normal Supine Abdominal X-ray Legend:
1. Liver
2. Spleen
3. Ti 2 vertebral body
4. Pedicle
5. Spinous process
6. Right kidney
7. Left psoas margin
8. Gas in stomach
9. Gas in hepatic flexure
10. Gas in splenic flexure
12 12 11. Ilium
12. Sacroiliacjoint
13. Bladder
14. Acetabulum
15. Femoral head
16. Femoral neck
17. Greater trochanter
18. Lesser trochanter
References
Novelline RA. Squire’s Fundamentals of Radiology. 6
th
ed. Boston: Harvard; 2004.
2. Abdominal Radiograph courtesy of Dr. Edward Wiebe, Assistant Professor and Undergraduate Medical Student Education Coordinator, Department of
Radiology and Diagnostic Imaging, University of Alberta.

INTERPRETATION OF ABG
MD FR
0) 20 I I Ed. Authors: Charles tim, Edward James PLI Janjeevan Deal MD, Dilini Vethanayagam
Station Objective
blood gas tests to determine a pt’s respiratory and
In this station you may be expected to use a systematic approach to interpreting arterial
oxygenation. The approach to interpretation presented focuses on a single acid-base
metabolic acid-base state, as well as a Pt’s arterial
be interpreted in the context of clinical
disorder, but real world clinical scenarios often involve multiple acid-base disorders and should
information.
Basics
1. Pt ID, date of test
2. Pt demographics: age, sex, ethnicity
3. Pre-test data: test performed with pt on room air or on flow?
4. Compare with previous ABGs if available
Table 1: Selected Causes of Acid-Base Disorders
Wide Anion Gap N Anion Gap Metabolic Metabolic
Respiratory Respiratory Alkalosis Metabolic Acidosis Acidosis Alkalosis
Acidosis
M-methanol • Exogenous alkalis
• Respiratory center •
. H-hyperalimentation
Acute / chronic U-uremia Diuretics
depression • A-acetazolamide
hypoxemia D-DKA Post-hypercapnea
. Neuromuscular •
• R-RTA
Respiratory center P-paraldehyde Mineralocorticoid
disorders • •
• D-diarrhea
stimulation 1-isopropyl alcohol effect
• Airway obstruction •
• U-ureteric shunt
Mechanical L-lactic acidosis Hypercalcemia
• Lung parenchymal dz •
• P-post-hypocapnea
hyperventilation E-ethylene glycol • Vomiting
• Mechanical • S-spironolactone
S-salicylates Volume contraction
hypoventilation
Basics of Interpretation
What is the clinical context of this pt?
• Known medical history? (eg. CHF, obstructive lung dz, renal dz, acute overdose, etc.)
• Stable or unstable condition?
• Is this pt being ventilated? If so, how is °2 being delivered?
2. How is the Pt ventilating? (PaCO
)
2
• 2 < 35 mmHg —* suggests hyperventilation
PaCO
• 2 >45 mmHg —* suggests hypoventilation
PaCO
3. How is the pt’s arterial oxygenation? (Pa0
)
2
• Normal Pa02 is 80— 100 mmHg depending on age (Pa0 2 4 with t age)
• 2 include:
Causes of low Pa0
• High alveolar PaCO2 from poor ventilation
• 4 atmospheric 02 content and/or atmospheric pressure
• Ventilation/perfusion mismatch
4. Are the lungs working as N oxygenators? 2 (A-aD
o r O2 /PAO
Pa0
)
• 2 determined by PAO
A-aDO 2 — Pa0 2 (normal < 15 mmHg)
2 is calculated, Pa0
PAO 2 is measured
• Alveolar air equation: PAO 2=8 (P —47) — PaCO
2
F10 /0.8
2
• F10 2 = fraction of inspired °2
• = barometric pressure
2 when Pt is on room air
Consider A-aDO
Consider 2 /PAO when Pt IS on 02 flow
Pa0
• Hypoxemia with normal A-aDO 2 —* suggests hypoventilation or high altitude (4 atmospheric p0 )
2
• Hypoxemia with t 2
A-aDO or 4 / PAO
Pa0
2 -+ suggests ventilation-p erfusion mismatch or shunt

Clinical Approach to Interpretation
1. Does the pt have acidosis or alkalosis? (pH)
• pH < 7.35 = acidosis
• pH > 7.45 = alkalosis
2. If an acid-base imbalance is present, is it respirator> metabolic or mixed? (pH and PaCO
)
2
• Refertotable2
3. If an acid-base imbalance is present, is it acute, partially compensated or fully compensated?
(Base-excess and HCO
)
3
• Refertotable2
Table2: Summary of ABG Findings in Acid-Base Disorders

Respiratory Respiratory
Respiratory Respiratory Metabolic Metabolic Acidosis + Alkalosis +
Acidosis Alkalosis Acidosis Alkalosis Metabàlic Respiratory
Acidosis Alkalosis
2
PaCO ft .4.4 Normal Normal ft
. Acute pH 4- ft ft U ft
Base Excess 0 0 Negative Positive Negative Positive
PaCO, tt .44. 4. t
Partially Compensated pH ‘I, t .4, t
Base Excess Positive Negative Negative Positive
PaCO, tt U tt - -
Fully Compensated pH Normal Normal Normal Normal - -
Base Excess Positive Negative Negative Positive - -
Further Investigations
1. Blood work
• Electrolytes (anion gap)
• Glucose (osmolar gap)
• Urea (osmolar gap)
2. Anion gap
• Anion gap = ([Nal) ([HCO
] + [Cl])
3
—
• Normal anion gap is 10—14 mEq/L

• t anion gap suggests an increased number of unmeasured anions
3. 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 EtOH ingestion
References
1. DuBose TD. Chapter 48: Acidosis and Alkalosis. In: Fauci AS, Braunwald E, Kasper DL Hauser SL, Longo DL Jameson JL, Loscalzo J, editors. Harrison’s
Principles of Internal Medicine. New York: McGraw-Hill; 2008.
2. Williams AJ. ABC of oxygen: Assessing and interpreting arterial blood gases and acid-base balance. BMJ. 1998 Oct31 ;31 7(71 67):1 213-6
3. West iS. Pulmonary Pathophysiology:The Essentials. 6 h
ed. Philadelphia: Lippincott Williams & Wilkins; 2003.

INTERPRETATION OF A CHEST RADIOGRAPH
201 I Ed. Authors: Babok Maghdoori, Christopher Fung MO, Edword Wiebe MO FRCPC
Original authors:Summit Sowhney, Karen Seland MD, Arlene Kanigon MO FRCPC
Station Objective
To offer a systematic approach for reading, interpreting, and analyzing chest radiographs.
History
Determine the following prior to acquiring/reading the radiograph:
• Pt’s name, age, gender, and date of image
• HPI: Acute/chronic, level of progression of the disease, reason for request, etc.
us)
• Determine the projection and patient positioning for the image (eg. supine/upright/PA/AP/lordotic/decubit
• Normally CXRs are done in PA and lateral views
of effusion
• AP view for bedridden pts, lordotic view to image lung apices, decubitus to assess loculation
Interpretation
Technical quality:
• Level of penetration and exposure:
visible
• Normal penetration: The intervertebral disk spaces and vascular lung markings are clearly
densities
• Under-penetration: The CXR is too white, leading to inability to distinguish between different
inability to identify vascular markings in lungs
• Over-penetration: The CXR is too dark, leading to the
• Inclusion and adequacy:
Inclusion: Ensure the lung fields are complete — the apices to the costophrenic angles
should be imaged
•
and the midline spinous process should be equal
• Symmetry: Space between the medial aspect of the clavicle
• Inspiration: Adult Pt: 9-10 posterior ribs visible above diaphragm
2. Inspection (working inside to outside)
ECG leads etc.)
Comment on any lines, iatrogenic devices, and/or tubes present (chest tube, pacemaker, NG tube,
• Trachea:
mass
• Check position: If shifted from the midline, consider tension pneumothorax and mediastinal
• Mediastinum:
mass
• Width >8cm PA CXR—*”widened mediastinum”—* DDx: aortic dissection, aortic aneurysm, mediastinal
• HilaILymph Nodes
• Assess for lymphadenopathy
effusion, CHF, etc)
• If thickness of superior vessels > inferior vessels consider vascular redistribution (edema,
• Heart:
<50% normal
• Determine cardiothoracic ratio: Lateral width of the heart relative to thoracic cage, in PA view
• If enlarged (>50%) — possible DDx: cardiomegaly, pericardial effusion
• Visualization of right and left heart border (see “Pneumonia” below)
• Great vessels:
calcification
• Assess pulmonary trunk, aortic arch, and descending thoracic aorta for any enlargement and/or
• Lungs:
• Ensure examination of the entire lung field, comparing side to side.
• Airspace disease —* DDx: pneumonia (pus), pulmonary edema (fluid), hemorrhage (blood), tumor
• Interstitial disease = linear markings —* DDx: pulmonary edema, viral pneumonia, inflammation
• Obvious masses: consider lung Ca, tuberculosis, pulmonary nodules
• Pleura:
• White line of visceral pleura in chest periphery (esp apex) = pneumothorax (if seen r/o tension pneumothorax)
• Blunting of costophrenic angles —* pleural effusion (decubitus film with effusion side down to r/o loculation)
• Look for any abnormalities in the diaphragm (e.g. excessive elevation)
• Pleural calcifications/thickening, pleural-based mass —* calcified plural plaques often 2° to asbestos exposure
• Diaphragm
• Right hemidiaphragm often slightly higher than the left 2° to the liver
• Visualize both hemidiaphragms clearly (see “Pneumonia” below)
• 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
Pt’s.
• Humeral heads, scapulae, acromioclavicular joints, sternum, and ribs; may not be visible in some
• Examine soft tissues: breast tissues, axillae, supraclavivu lar areas, etc.

• Check for subcutaneous emphysema, axillary masses and surgical staples
• Bilateral breast shadows: Axillary staples ± ipsilateral loss of a breast shadow —* highly suggestive of mastectomy/previous
breast cancer —* assess for metastatic advancement of the disease
Lateral View
• Examine anatomy as described above, focusing on spine: assess the contour and height of the vertebral bodies
• Follow peripheral parenchyma along spine superior —* inferior: lung fields should darken inferiorly. Whitening of lung fields
inferiorly suggests pathology (eg. Lower lobe pneumonia)
• Assess the hemidiaphragms for evidence of hyperinflation (flattening)
• Localize any pathology seen on PA to confirm posterior-anterior location
Common radiographic findings on a CXR

• Pulmonary edema
• Vascular redistribution to the upper lobes, interstitial edema (thickening of interstial markings —* Kerley B, 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, and bullae
• Lateral: increased retrosternal air space and flattened hemidiaphragms
• In COPD, increased risk of apical pneumothorax
Normal Chest X-ray Legend:

3 14 1. Trachea
‘ii. 1 2. Mediastinum
3. Right heart border
2 12 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. Acromioclavicularjoint
14. Clavicle
15. 8”' posterior rib
16. 4
th
anterior rib
References
Novelline RA. Squire’s Fundamentals of Radiology. 6” ed. Boston: Harvard; 2004.
2. Chest Radiograph courtesy of Dr. Edward Wiebe, Assistant Professor and Undergraduate Medical Student Education Coordinator, Department of
Radiology and Diagnostic Imaging, University of Alberta.

INTERPRETATION OF CBC-D
2011 EdAuthors: Kimberley Krueger, Jason KserMD, Marki ife MD FRCPC
OriginalAuthors: Kimberley Krueger, Carre Ye MD, Mark Joffe MD FRCPC
Station Objective
To interpret the Complete Blood Count and Differential Count (CBC-D) in context of the clinical setting, identify those in need of urgent care,
list other key laboratory findings for diagnosis and design appropriate management plan.
History and Physical

1. Question patient for symptoms of:
• Infection (fever, chills, cough, diarrhea, dysuria, headache, skin infection)
• Malignancy (weight L, drenching sweats)
• Anemia (SOB, presyncope, sources of blood loss)
• Easy bruising or bleeding
2. Identify those patients in need of urgent care (ABC’s: tachycardia, hypotension, hypothermia, 1- LOC)
3. Exam
• Lymph nodes, spleen, liver
• Petechiae, purpura
• Signs of local infection
• Pallor or jaundice
4. Be aware of combined abnormalities on the CBC-D
• Pancytopenia (decrease in all three hematopoietic lines): presents with fatigue, recurrent infections, bleeding issues, or may
present asymptomatically with findings on routine blood work
Red Blood Cell (RBC) Count, Hemoglobin (Hgb), Hematocrit (Hct)

1. RBC: number of RBCs per volume of blood —* N values: 4.3—6.0 x 1 0 /mm
3 (s),
3 ()
3.8-5.2 x 10 /mm
2. Hgb: amount of oxygen carrying protein in blood —* N values: 130—175 g/L (d’); 120-160 g/L ()
3. Hct: % of whole blood volume occupied by packed RBCs, Hct = RBC x MCV —÷ N values: 41-52% (cf), 36-46% ()
4. Increased: hemoconcentration (dehydration, burns, vomiting); extreme physical exercise; Polycythemia:
Primary I Polycythemia ruba vera
Secondary
I Poor tissue oxygenation/hypoxemia (COPD=classic), CO poisoning, inappropriate production of EPO/EPO secreting
I tumor, local renal hypoxia, hemoconcentration due to capillary leak syndromes
5. Decreased: Anemia
I Fe deficiency, lead intoxication, thalassemmia, sideroblastic anemia, anemia of chronic dz Use
Microcytic (MCV <80 ft.)
I Mentzer index to distinguish Fe deficiency from thalassemmia (MCV/RBC<1 3 in thalassemmia)
Normocytic (MCV 80-100 ft.)
• t reticulocytes (>2% of RBC) Hemolytic anemia, post hemorrhagic anemia
• Marrow invasion or suppression, anemia of chronic dz, endocrine disorders, liver failure, renal failure,
reticulocytes (<1% of RBC)
aplastic anemia
Megaloblasic anemia (B1 2/folate deficiency), liver dz, EtOH abuse, myelodysplasia, hypothyroidism,
Macrocytic (MCV >100 fL)
reticulocytosis
Mean Corpuscular Volume (MCV)

1. Size of RBCs —* N values: 80-100 fL
2. Increased/decreased: see above table
Mean Corpuscular Hemoglobin Concentration (MCHC)

1. Average concentration of Hgb inside RBCs —* MCHC = Hb/ (MCV x RBC), N values: 32-36%;
2. Increased: spherocytosis; autoagglutination, hemolysis, lipemia, cellular dehydration, xerocytosis
3. Decreased: Fe deficiency, chronic dz, chronic blood loss
Red Blood Cell Distribution Width (RDW)

Variability of RBC size —* N values: 11 — 15%; increased indicates variability and is nonspecifc
Mean Corpuscular Hemoglobin (MCH)

1. Amount of Hgb inside RBCs —* MCH = (Hb/RBC) x 10, N values: 27-32 pg/cell

2 increased: maCrOCYtOSiS due to any cause
3. Decreased: microcytOsis (.J,.Fe, thalassemia), hypochromia (Pb poisoning, sideroblastic anemia, anemia of chronic dz)
Count
White Blood Cell (WBC)
1. Actual number ofWBCs per volume of blood —* N values: 4.0— 11 x 1 0 /L
9
2. increased: infection, inflammation, major tissue damage, lympho/myeloproliferative disorders

3. Decreased: 1) Decreased production (aplastic anemia, folate or B12 deficiency, drugs); 2) Increased breakdown/consumption
(hyper5plefl15m sepsis, drugs)
NeutroPh i Is
values:1 .8—7.5 x 1 0
1L, ANC<0.5 X 1 0
9 /L=infection risk f
9
Role in innate immunity,ANCabsolute neutrophil count—> N
I Infection, (bacterial or early viral), stress (Ml), inflammation, drugs (steroids, lithium, catecholamines, G-CSF/GM
NeutrOPhilia (SF), malignancy, tissue necrosis, leukemia, myeloproliferative dz, hereditary, idiopathic
NeutrODeflia
.tdestructiofl Post-infection, drugs, transfusion, autoimmune, hemodialysis
...production Drugs, nutritional, hematological dz, marrow infiltration
. Sequestration Hypersplenism
Lymphocytes
/L; atypical lymphocytes in EBV infection
Role in adaptive immunity —* N values: 1 — 4.5 x 1 0
9
Viral infection (infectious mononucleosis), pertussis, drugs, endocrine disorders (thyrotoxicosis, adrenal insufficiency),
LymphOCytOSiS.
allergic reactions, autoimmune dz, lymphoproliferative disorders (CLL=classic)
.
Immune deficiency syndromes (including HIV), acute/chronic illness, immunosuppressive therapies (chemotherapeutic
Lymphopeflia.
agents, radiation), bone marrow failure, malignancy, idiopathic
Monocytes
Role in innate immunity —* N values: 0.0.— 1.1 x 1 0”/L
[Monocytosis: Inflammation, infection, malignancy, TB, myeloproliferative disorders
Monocytopenia: Overwhelming sepsis, glucocorticoid therapy, aplastic anemia, leukemia, chemotherapy
Eosinophils
Role in response to parasites (especially helminthes) and allergic response —* N values: 0.0. — 0.7 x 1 0
1L
9
Allergic and atopic reactions, parasitic infection, drug sensitivity reactions, polyarteritis nodosa, Hodgkins, cholesterol
Eosino ‘ hilia
emboli, collagen vascular dz, malignancy, hypereosinophilic syndrome, adrenal insufficiency
Eosinopenia: Acute and chronic inflammation, stress, drugs, glucocorticoid therapy
Basophils
1. Role mostly unknown, likely in allergic response —* N values: 0.0.— 0.3 x 1 0
/L
9
2. Basophilia: allergic reactions, drugs, myeloproliferative disorders, myelofibrosis, chronic inflammatory disorders
Platelet Count
Actual number of PLT per volume of blood —* N values: 150-400 x 1 0
/L
9
Thrombocytosis:
• Primary: Essential thrombocytàsis
Hemorrhage, Fe deficiency, surgery, splenectomy/hyposplenism, malignancy, acute or chronic
• Seconda 13’.
Inflammatory dz, Bi 2 deficiency, drugs
Thrombocytopenia:
. Folate/ Bi 2 deficiency, infection, cancer treatment, inherited dz, marrow injury/invasion, aplastic anemia,
• Decreased PLT production
malignancy
•Increased PLTdestruction ITP, DIC, TTP/HUS, HIV, SLE
‘Sequestration Splenomegaly, hemodilution
References
1. Fauci AS, Braunwald E, Kasper DL, Hauser SL, Longo DL, Jameson JL, Loscalzo J. editors. Harrison’s manual of medicine. 17” ed. New York: McGraw Hill;
2009.

INTERPRETATION OF CREATININE
2011 EdAuthors: Kimberley Krueger, Jason KiserMO, Mark JoffeMD FRCP
— OriginalAuthors: Kimberley Krueger, Carrie Ye MO, Mark Jaffe MO FRCPC
U,,
Station Objective
To have an organized approach in determining whether a rise in Cr is due to an acute, chronic or acute superimposed on chronic problem; tc
be able to identify and interpret appropriate laboratory findings in these settings.
1. SerumCrfin:
• ARF: Pre-renal (decreased ECFV, renal artery vasoconstriction); Renal (ATN, acute interstitial nephritis, GN, small vessel disease);
Post-renal (BPH, neurogenic bladder, ariticholinergic medications, malignancy, bilateral nephrolithiasis)
• CRF: DM, HTN, PCKD, GN, drug-induced, multiple myeloma, prolonged ARF
• Falsely t in: drug interference with assay (cefoxitin, flucytosine)
2. Serum Cr ‘I’ in:
• ‘i- muscle mass, pregnancy
Basics of Interpretation
1. N values for serum Cr: 50-1 10 pmol/L; N.B. N value depends on individual Pt (e.g., body mass, age) and previous creatinine values are
needed to interpret value
2. Cr produced in the body via breakdown of muscle creatine phosphate, concentration proportional to body mass
3. 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
4. Limitations in ability to estimate GFR exist because:
• Cr values influenced by age and muscle mass
• Contribution of tubular Cr secretion t with increasing renal impairment
• GFR must fall considerably before serum Cr has a notable t(50% fall in GFR —* doubling of serum Cr)
• Pt must be in steady state for Cr values to be used
Calculations to Estimate GFR

1. Cr Clearance (CrCL)
• Cr/CL (mi/mm) = (urine Cr x urine volume over 24 hrs)/(serum Cr x 140)
• Has the potential to overestimate GFR in Pts with advancing kidney impairment
2. Cockcroft-Gault
• CrCL (mI/mm) = (140— age)(wt in kg)(1 .2)(serum Cr (imol/L)) (NB in x 0.85 because of 4- muscle mass)
• Accounts for age, body wt and gender influences on GFR
3. MDRD (Modification of Diet in Renal Dz)
• Complex formula to estimate GFR (reported as GFR in mI/mm/i .73m2 body surface area)
• Uses the following indices: age, gender, serum Cr, African descent
Investigations
1. Volume status (pre-renal failure)
2. Blood work
• Electrolytes, osmolality, CBC, urea (to differentiate between causes of ARF)
3. Radiology/imaging
• Renal US (ARF vs. CRF, assess post-renal and vessel obstruction)
4. Special tests
• UA (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)
5. Surgical/diagnostic interventions
• Renal biopsy
Treatment
1. Treat underlying cause accordingly (see ARF and CRF stations)

2 Emergent:
• Follow Cr and watch for development of uremic Sx or other indications for urgent dialysis (academia, hyperkalemia, volume
overload) in those Pts with renal failure
• Uremic Sx tend to develop once serum Cr >530-71 Ommol/L or CrCL <10 mI/mm
References
1 Fauci AS, BraunWald E, Kasper DL, Hauser SL, Longo DL, Jameson JL, Loscaizo J. editors. Harrison’s manual of medicine. 1 7” ed. New York: McGraw Hill;
2009.

INTERPRETATION OF C-SPINE IMAGING
2011 Ed. Authors: Brendon Diederichs, Kotherine Leung MD, Tom Yeo MO FRCPC
OriginalAuthors: Christopher Fung, Winston Ying MO, Ed Wiebe MO FRCPC
Station Objective
Proper interpretation of a C-Spine series.
Basics
1. Name the study and orientation (eg. lateral, AP, open mouth)
2. Identify the patient and date
3. Comment on technical quality
4. Ask if previous studies are available for comparison
Lateral
• Mnemonic: All Able-Bodied Premeds Do Anatomy
• If collar present image with collar on
• Assess adequacy by counting the vertebral bodies.
• If you cannot see the top of Ti, order a swimmer’s view
• Alignment should then be commented on in the lateral view:
• (1) Anterior vertebral line
• (2) Posterior vertebral line
a
• (3) Spinolaminar line
• (4) Spinous process line
• Disruption of the normal contour of these lines may indicate fracture/
dislocation
Each vertebra should be examined for fracture (bones)
• Look for wedge shaped defects indicating compression fracture
• Also carefully examine each spinous process for # line
Next, examine the prevertebral space.
• The “7 at 3,27 at 7” rule gives the normal width of the prevertebral line at C3
[a] (7mm) and C7 [bI (21mm), widening may suggest pathology
b
Now check the intervertebral disc spaces
• Any narrowing may be suggestive of degenerative disc disease.
• Finally, examine the atlanto-axial joint
• Look at the space between the atlas (Cl) and the odontoid process of C2 to ensure there is no ligamentous damage resulting
in instability
• This space (the atlantodental distance) should be 3mm in width for adults
AP (Frontal)
1. Focus on the vertebral bodies
• Look for fractures of the pedicles and facets, any asymmetry may be pathologic and should be noted
• Examine the spinous processes for alignment and spacing
2. Examine the soft tissue for any masses
Open Mouth
This view provides an AP view of the odontoid
1. Alignment
• Look for the lateral sides of the atlas to align with the edges of the axis
• Also look for equal spacing bilaterally between the axis and the atlas
2. Fracture lines through the dens
• 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

oblique View
Oblique views may or may not be available depending on local imaging protocols (not typically performed in acute trauma setting)
1 Examine the foraminae
Each vertebral body should have an patent foramina, otherwise suspect fracture, poor positioning or degenerative uncovertebral
joint and/or facet joint changes
2 Examine the spinolaminar line
• This line is commonly described as “shingles on a roof’ in this view
• Disruption of this line suggests dislocation of the facet joint
Common Eponymous Fract res

1. Jefferson’s Fracture (unstable)
• Classically seen in the open mouth view as the lateral edges of the atlas extend beyond the lateral
edges of the axis (Cl ring has broken open)
2. Hangman’s Fracture (unstable)
• Originally occurred with hangings, now mainly seen in motor vehicle collisions.
• Mechanism is rapid extension of the neck, resulting in bilateral C2pedicle fracture
3. Clay-Shoveler’s Fracture (stable)
• This fracture of the lower C-spine spinous processes was once commonly seen among persons
shoveling clay, the shovel became stuck in the heavy material, and the resulting forced neck
flexion would cause an avulsion fracture of C6 or C7
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,NEJM 2003)
1. High risk? (if yes —+ radiographic imaging indicated)

• Age 65
• Dangerous mechanism
• Fall 3 feet/5 stairs, axial load to head, high speed MVC (lOOkm/hr), motorized recreational vehicle, bicycle collision
• Paresthesia in extremities
2. Factors allowing ROM assessment? (if no —* radiographic imaging indicated)
• Simple rear-end MVC
• Exceptions: pushed into traffic, rollover, hit by bus/large truck/high speed vehicle
• Sitting in emergency department
• Ambulatory at any time
ing • Delayed onset of neck pain
• Absence of midline C-spine tenderness
3. Able to actively rotate neck 450 left and right? (if no —* radiographic imaging is indicated)
References
1. 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.
2. Steill IG, Clement CM, et al. The Canadian C-Spine Rule versus the NEXUS Low-Risk Criteria in Patients with Trauam. NEJM 2003 Dec 349(26): 2510-2518.
3. Stobbe K. The Occasional C-spine X-ray. CJRM 2004 9(1): 38-42.
4. Ouellette H and Tetreault P. Clinical Radiology Made Ridiculously Simple. Miami: Medmaster; 2000.

;rn
INTERPRETATION OF CT
201 I Ed. Authors: Brendan Oiederichs, Katherine Leung MD, Ed Wiebe MD FRCPC
Or/gina/Authors: Christopher Fung, Winston Y1ngMD, Ed W1ebeMDFRCPC
V.’
Station Objective
To systematically interpret a CT scan of the head, chest, or abdomen.
Basics
1. Name the study and orientation (eg. Axial images from non-contrast CT head, etc.)
2. Identify the patient and date
3. Ask if previous studies are available for comparison
CT Orientation
CT scans are generally viewed in axial sections as viewed from the feet (see figures below)
Anterior
Right Left
Posterior
• Coronal reformats are common, and are similar in orientation to a PA CXR

• Contrast studies have vessels appearing white (approaching the attenuation of bone)
• Non-contrast studies have darker vessels (approaching the attenuation of soft tissue)
• CT images should be windowed properly according to what you are examining
• These are often preset and described as “Lung’ “Bone’ “Abdo’ etc
• Beam attenuation is measured in Hounsfield Units (HU)
• Air (-1000 HU) < Fat (-100 HU) <Water (0 RU) < Muscle (40 HU) <Bone (1000 HU)
CT Abdomen
CT Abdomen studies typically include slices from the diaphragm to the iliac crests
• Be systematic or be prepared to miss something! Review medical history to attune focus.
• Write down every system from the top to the bottom of the scan.
Enhanced Vs. Non-Enhanced +1 Oral Contrast
Lung Bases Pleural Spaces Lower mediastinum
Liver and Billiary Tract Pancreas Spleen
Kidneys Adrenals
Small/Large bowel Lymphadenopathy Vasculature
Free fluid/air Bones/ribs Peritoneum
Other
all I
• Look for masses, inappropriate air/fluid, changes in attenuation, and comment on general anatomy and variants, visualizing
systems will require several scroll-throug hs of the images
• On your written list comment on any findings beside each point, including normal findings

CT Chest
The CT chest series will include images from the lower neck to the diaphragm
A systematic approach is again the key to successful interpretation:
Contrast vs Non-contrast
Vessels Lungs
• Aorta • Masses
• Dissection • Consolidation
• Aneurysm • Atalectasis
• Vena cava/carotids • Nodules (examine periphe
• Pulmonary arteries • Bullae
Heart Pleura
• Chambers/valves • Masses
• Pericardium • Plaques
Thyroid/Thymus Free air
• Masses Effusion
Lymph nodes Spine/ribs
• Cervical • Fracture
• Mediastinal • Metastases
• Hilar Soft tissues
Airway • Masses
• Obstruction? Masses?
• Each point above has some possible findings listed, your list should be modified as required
CT Head
• The CT head consists of axial views from the vertex to the skull base
• First consider the medical history to attune your focus (trauma, new neurological deficits, etc.)
• Start from the bottom and work your way up to the top (or vice versa)
• Examine the CSF spaces first
• 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 cisterns patent? Is there blood (bright if recent) in the cisterns?
• Next focus on the brain parenchyma
• Move from central structures outward, ensuring each major section of the brain is without lesions and symmetrical (any
soft tissue asymmetry may indicate mass effect)
• Examineformidlineshift
• Examine the grey-white differentiation, look for changes suggesting edema
• Now look around the contours of the calvarium
• Are there any attenuation defects in keeping with a subdural (lens shaped, crosses sutures) or an epidural (crescentic,
within sutures) hematoma?
Normal Subdural Epidural
• Finally, examine the bone windows for any fractures

• Also look at the sinuses (air/fluid levels, fractures), the orbits, ocular muscles, and mastoid air cells
References
Hofer M. CT teaching manual: a systematic approach to CT reading. 2
nd
Ed. New York: Thieme; 2007

—•‘j
V. INTERPRETATION OF ECG
2017 Ed. Authors: Charles Lim, Craig Domke MD, Lucille Lalonde MD FRCPC
OriginalAuthors: Sabira Suleman, Kris Chan MD, Michael T]andrawidjaja MD, Evan Lockwood MD FRCPC
Station Objective
Interpret an ECG using a systematic approach. Combine ECG findings with clinical context to suggest possible diagnoses.
Rate
• Each thick line (5mm box) represents 0.2 s. Find a QRS that lands on a thick line and use the count off method for successive thick
lines. (300-1 50-1 00-75-60-50)
• If there is an irregular rate, count the number of QRS complexes in the entire strip and multiple by 5 (each strip is 12 s)
Bradycardia Normal Tachycardia

<60 beats per minute 60-100 beats per minute >100 beats per minute
Rhythm
Regularity
• Sinus rhythm: P wave before every QRS, QRS after every P wave, P waves upright in leads II and aVF
• Regular or irregular?
• If irregular, is it regularly irregular, or irregularly irregular?
• Regularly irregular rhythms include 2fl’ degree heart block and ventricular bi/trigeminy
• Irregularly irregular rhythms include atrial fibrillation, multifocal atrial tachycardia, or wandering atrial pacemaker
2. Important Differentiating Questions
• P-waves (PQRS pneumonic)
• P: Are P-waves Present? (eg. atrial fibrillation?)
• Q: What is the relationship between the P-waves and the RS? (eg. sinus rhythm?)
• R: Is the PR interval constant or different? Does the PR interval get progressively prolonged? (eg. Mobitz I?)
• 5: Are the p-waves the same shape? (eg. multifocal atrial tachycardia or wandering pacemaker?)
Axis
1. Vectors Method
• Lead aVF for vertical vector
• If QRS is positive, axis points down towards +90°, if QRS is negative, axis points up towards -90°
• The more positive the QRS, the more the overall vector points towards +90°
• Lead I for horizontal vector
• If QRS is positive, axis points right towards 0°, if QRS is negative, axis points left tow
• The more positive the QRS, the more the overall vector points towards 00 Left Axis
• Combine the vertical and horizontal elements to estimate the axis l(+)avF(-)
2. Isoelectric Lead Method
• Determine the quadrant for the axis (see fig 1) 180°
• Determine is QRS in lead I and lead aVF is positive or negative
• Look at the 6 limb leads and decide which one is closest to being the Right Axis Normal I(+)
isoelectric lead (positive and negative components of the QRS are equal) I (-) avF (+) avF(+)
• Draw a line perpendicular to the isoelectric lead vector towards the
appropriate quadrant. This estimates the axis to the nearest 30°.
3. Interpretation
• Normal axis is between -30° and + 90° +90°
• Note: if QRS is positive in lead I AND lead II, then axis is within normal range axis
Figure 1. Determining
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

Intervals
Normal: 0.12-0.205
PR Interval
—
• Shortened PR interval
• Fast conduction along an accessory pathway (pre-excitation, Wolf-Parkinson-White)
• Junctional rhythms with retrograde p-waves (p-waves occur within the QRS complex)
• Lengthened PR interval indicated delayed AVconduction
—
• 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 VTach
• Consider LBBB, RBBB, hyperkalemia, interventricular conduction delay
3. QT Interval — Normal approximation: QT should be <1/2 of preceding R-R interval
• Calculate QTc as the QTNRR interval (0.38-O.42s)
Shortened QT interval
• Hypercalcemia, digitalis
Lengthened QT interval (pnemonic: DIE, because the most serious complication is torsades de points)
• Drugs: amiodarone, quinidine, procainamide, sotalol, TCA antidepressants, antihistamines, macrolides, cocaine
• Injury: myocardial infarction, myocarditis, head injury, hypothermia, HIV, anorexia nervosa
• Electrolytes: 4’ K, 4’ Mg, 4.’ Ca
2
• A lengthened QT interval may also be congenital (very common)
HypertrOPhY
Atrial Enlargement
• Left atrial enlargement
• P-mitrale is a °m-shaped” p-wave O.i 2s wide with 0.O4s between peaks (most common in leads I and II)
• Negative component of p-wave in Vi is greater than or equal to lxi small boxes
Right atrial enlargement
• P-pulmonale are peaked p-waves 2.5mm tall (most common in leads II and Ill)
2. Ventricular Enlargement
Left ventricular hypertrophy
• Deepest S wave of V 2 + tallest R wave of V
1 or V 5 or V
6 35mm (Sokolow Lyon criteria)
• Or if any precordial lead is45mm
Right ventricular hypertrophy
• R:S ratio is >1 mV1 orV2
Pathological Features
T-waves
° T-waves should be positive in leads I, II, and 6
-V and negative in aVR.
3
V
,
° Abnormal T-waves: inverted, symmetrical, peaked, or tall (>2/3 of R-wave)
2. ST-segment
Elevation> 1mm in 2 contiguous leads from baseline (defined as the T-P 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
3. Q-waves
Signify necrosis: significant Q waves are 0.04s (1 small square) wide or> 1/3 amplitude of QRS
Location of Infarct Leads Showing lschemic Changes Coronary Arteries

AnteriorWall andV
3
V
4 LAD
Inferior Wall II, Ill, aVE RCA, LCx
Lateral Wall I, aVL, V
,V
5 6 LAD, LCx
Septal 1 and V
V 2 LAD
N.B. for Examples of ECG wave forms see final page of the Essential Clinical Skills section
References
1. Garcia, TB, Holtz, NE. 12-Lead ECG: The art of interpretation. Sudbury: Jones and Bartlett Publishers; 2001.

-m
—.v
INTERPRETATION OF ELECTROLYTES: CALCIUM

Station Objective
Perform proper calculations to determine corrected serum calcium. Interpret calcium levels and outline features and management of
hypercalcemia and hypocalcemia.
Corrected Calcium
• Measured serum calcium must be corrected because serum albumin influences ionized calcium to bound calcium ratio
• Corrected calcium (mmolIL) = 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 roughly 50% of serum calcium
Hypercalcemia diagnostic approach

—
Hypercalcemia (>2.6 mmol
Yes Elevated urinary calcium? Yes No Yes

4
PHPTH Elevated PTH? Elevated PTHrP?
No
No!
Yes Consider
FHH
Elevated Vitamin D? lymphoma,
sarcoidosis
No
PTHrP = parathyroid hormone related peptide
PHTPH = primary hyperparathyroidism
FHH familial hypocalciuric hypercalcemia Consider other causes
*
denotes common causes (eg. thiazides*, milk-alkali syndrome, TPN, endocrine
disorders, etc.)
Hypercalcemia history, symptoms, investigations and treatment

—
1. Focused History
HPI: diet (milk and antacids), drugs (thiazides, lithium, vitamin D), bone pain, abdo pain
MHx: endocrine disorders, malignancies
FHx: hypercalcemia or MEN syndromes, cancers
2. Signs and 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, arrhythmias
• GI: abdo pain, nausea, vomiting, anorexia, constipation, PUD
• GU: renal calculi, polyuria, polydipsia, renal failure
• MSK: weakness, bone pain, arthritis, osteoporosis, fractures
3. Investigations
• Routine labs
• Electrolytes, magnesium, calcium, albumin, phosphate, vitamin D, PTH, ALP, creatinine, urea
• Special tests
• 24 hour urine calcium for distinguishing PHTPH from FHH
—
• Protein electrophoresis for suspected multiple myeloma

—
• Parathyroid sestamibi scan —for hyperparathyroid lesions

4. Treatment
• Emergent (calcium > 3.0 mmol/L, acutely symptomatic)

• IV fluids, bisphosphonates, calcitonin, correct other electrolyte abnormalities
• Loop diuretics to promote excretion of calcium should only be used after dehydration is corrected
Chronic
• Treat underlying disease, stop offending meds, diet and lifestyle modification, consider surgery if applicable
Hypocalcemia diagnostc approach

—
Hypocalcemia (<2.2 mmol/L)
Yes No Yes
VitaminD Yes Elevated PTH? —+ OW
Hypomagnesemia
Deflciency* Low 25-OHD?
— i—
Magnesium?
No!
No!
Low 1 ,25(OH)
D?
2 Hypoparathyroidism*
No
25-OHD = 25-hydroxy-vitamiri D (inactive)
D = 1,25-dihydroxy-vitamin D (active)
2
1,25(OH)
Pseudohypoparathyroidism *
denotes common causes
(PTH resistance)
Hypocalcemia — history, symptoms, investigations and treatment

Focused History
• HPI: diet and meds (calcium and vitamin D)
• MHx: renal disease, autoimmune disorders, GI absorption disorders
• SHx: head and neck surgeries (parathyroid injury)
• FHx: familial hypocalcemia, polyglandular autoimmune syndromes
2. Signs and Symptoms
• CNS: confusion, depression, psychosis, seizures
• CVS: hypotension, prolonged QT, arrhythmias, CHF
• MSK/NEURO: tetany, spasms, myopathies, parasthesias
• SpecialTests
• 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
—
3. Investigations
• Routine labs
• Electrolytes, magnesium, calcium, albumin, phosphate, vitamin D, PTH, ALP, creatinine, urea
• Special tests
• 24 hour urine calcium decreased in hypoparathyroidism and vitamin D deficiency
—
4. Treatment
• Emergent (calcium < 1.0 mmol/L, acutely symptomatic)
• IV calcium gluconate, correct other electrolyte abnormalities
• Chronic
• Treat underlying disease, diet and lifestyle modification
• Oral calcium and/or vitamin D supplementation as appropriate
• Note: Normal reference ranges for serum calcium may vary by laboratory
• Note: Diagnostic approach figures present a simplified DD
References
Fauci AS, Braunwald E, Kasper DL, Hauser SL, Longo DL, Jameson JL, Loscalzo J. editors. Harrison’s principles of internal medicine. New York: McGraw-Hill;
2008.
2. Longrnore, M, Wilkinson, IB, Davidson EH, Foulkes A, Mafi AR. Oxford handbook of clinical medicine. 8” ed. New York: Oxford University Press; 2010
3. Fern FF, Cooper E, McClure M. Practical guide to the care of the medical patient. 7
th
ed. Philadelphia: Elsevier Mosby; 2007
4. Carroll MF, Schade DS. A practical approach to hypercalcemia. Am Fam Physician. 2003 May 1 ;67(9):1 959-66
5. Cooper MS, Gittoes NJ. Diagnosis and management of hypocalcemia. BMJ. 2008 Jun 7;336(7656):1 298-302

INTERPRETATION OF ELECTROLYTES: POTASSIUM
) 2011 EdAuthors: Kimberley Krueger; Jason KiserMO, Mark JoffeMD FRCPC
— OriginalAuthors: Kimberley Krueger, Carrie Ye MD, Mark Joffe MD FRCPC
Station Objective
To determine the main process for the electrolyte abnormality, identify key laboratory findings to aid in Dx, assess severity and design
management plan. (N values: K: 3.5-5.0 mmol/L)
Hypokalemia - Differential Diagnosis and Investigations

1. intake (uncommon): starvation, clay ingestion
2. Redistribution into cells: acid-base (alkalosis), hormonal (insulin, 132 adrenergic action), anabolic (B12 orfolate administration, TPN,
granulocyte-macrophage colony-stimulating factor), other (hypokalemic periodic paralysis)
3. Extrarenal losses (urine K <2Ommol/d): 61 losses (vomiting, diarrhea, tube drainage, laxative abuse), skin losses
4. Renal losses (urine K >2Ommol/d): hypertensive primary or secondary hyperaldosteronism, cushings, CAH, if non-HTN:
• Acidemic: DKA/RTA (Type 1 & 2)
• Alkalemic: diuretics/Bartter’s/Gitelman’s
• Variable: vomiting/hypoMg/drugs (amphotericin)
Hypokalemia Signs, Symptoms and Treatment

-
1. Recognize S/Sx of hypokalemia (see box) SISx of HyDokalemia:

2. Calculate transtubular K gradient = [(Kunne)(Osmser,,m)l/[(Ksem)(Osmurjne)]: >4 = renal N/V
loss, <2 = 61/non-renal loss Muscle weakness, (if severe:
3. Treat underlying cause and/or remove offending medication, replace K slowly (oral ascending paralysis, ileus, respiratory
KCI preferred over IV KCI, max dose 20-40 mEq oral, max infusion 20 mmol/h IV, NEVER failure, rhabdomyolysis, arrhythmias)
bolus K), check serum K frequently to avoid over-correcting, consider role of K-sparing ECG changes (flattened T wave, ST
diuretics in Tx plan; 1 meq/L reflects ‘‘200 meq total body loss segment depression, high U wave)
Hyperkalemia Differential Diagnosis and Investigations

—
Hyperkalemia (>5mmolfL)
Resdistribution +—before collection— K shift Out of cells? —after collection p Pseudohyperkalemia

(acidosis, B blocker,
cellular necrosis, no
I (hemolysis, leukocytosis,
thrombocytosis)
insulin deficiency, 4,
digitalis overdose, high Urine K excretion low TTKG
rhabdomyoly sis, burns)
4,
Increased intake >10
I
<6
(diet, KCI tabs/TV) 4’
Reduced Tubular Flow Decreased Aldosterone
(kidney failure, reduced ECV) Activity
Normal aldosterone/ Low aldosterone, low renin

1
Low aldosterone, normal renin
tubular resistance: (diabetes mellitus, NSAIDs, (ACEI, ARBs, aldosterone
(K-sparing diuretics, tubulointerstitial disease) deficiency, heparin)
pentamidine,
trimethoprim)
TTKG (transtubular potassium gradient) = [(Ku,ne)(Osmse,um)]/[(Kwm)(Osmrine)]

HyPerkatemia Signs/Symptoms and Treatment
-
5/Sx:
• NN
• Palpitations
• Muscle weakness
• Ascending paralysis
• HypoventilatiOn
• ECG changes: peaked T waves —* diminished R wave —* wide QRS —* prolonged PR —* loss of P wave —* Sine Wave —* v. fib
2. Tx: N.B. BeforeTx need to R/O pseudohyperkalemia via repeat serum K level
K <6.0 and N EKG 1. Tx underlying cause
2. Stop K intake and meds that t K
3. Promote K J (step 3 below)
and/oKGcigeS 1. Antagonize effects of K on myocardium (1 OmIs of 10% calcium gluconate LV. over 2-3 mins)
2. Shift K into cells:
• Insulin + glucose (eg. 10 units of rapid acting insulin+ 50 mL of 50% glucose solution l.V. as a
bolus followed by an infusion of glucose-containing solution, if Pt is significantly hyperglycemic,
A MEDICAL EMERGENCY: TX
URGENTLY insulin alone can be provided)
• 13 agonist (ventolin)
• Bicarbonate
3. Remove K
• Loop diuretics (furosemide)
• Cation exchange resin (eg. Na or calcium polystyrene sulfonate = Kayexylate); give with lactulose
to promote osmotic diarrhea and prevent sticking
• Hemodialysis
References
1. Fauci AS, Braunwald E, Kasper DL, Hauser SL, Longo DL, Jameson JL, Loscaizo J. editors. Harrison’s manual of medicine. 1 7
th
ed. New York: McGraw Hill,
2009.

INTERPRETATION OF ELECTROLYTES: SODIUM
20?? EdAuthors: Kimberley Krueger, Jason KiserMD, Mark Joffe MD FRCPC
OriginalAuthors: Kimberley Krueger, Carrie Ye MD, Mark Joffe MD FRCPC
Station Objective
To determine the main process for the electrolyte abnormality, identify key laboratory findings to aid in Dx, assess severity and design
management plan. (N values: Na: 133-146 mmol/L)
Hyponatremia - Differential Diagnosis and Investigations
1-lyponatremia (<l35mmol/L)
Iso-OmoIar s
5 molar
Hypo-t Hyper-csmo1ar
4, 4,
Pseudohyponatremia (usually Hyperglycemia
due to hyperlipidemalprotememia) Hypertonic infusion
Isotonic infusion
Hypovolemic Euvolemic Hypervolemic
Urine <lOmEq/L Urine Na !2OmEqfL Urine Na ‘2OmEq/L Urine Na 2OmeqfL

4, 4, 4,
Extrarenal losses Renal losses Water intoxication? E,rtrarenal Renal
(01, skin, lung, (diuretics, salt- polydipsia (CHF, cirrhosis, (ARF, CRF)
3rd spacing) wasting nephropathy, SIADH nephrosis)
adrenal insufficiency, Glucocorticoid deficiency
bicarbonaturia, Hypothyroidism
ketonuria) Stress
Hyponatremia Signs, Symptoms and Treatment

- SISx of hyponatremia:
a: box) • Headache
1. Recognize S/Sx of hyponatremi (see
• NN
• Signs of hypervolemia: 1’ JVD, 53 heart sound, inspiratory crackles, edema, 1’ body wt
• Anorexia
• Signs of hypovolemia: JVD, orthostatic BP tachycardia, skin turgor, .1’ body wt, L U/O, dry
,
• Lethargy
membranes, depressed fontanelle
• Seizures
2. Order plasma osmolality, urine electrolytes/osmolality/creatinine
• LOC
3. Tx guidelines
• Coma
• Treat underlying cause
• Fluid restrict [Tx of choice for hypervolemic states, SIADH, primary polydipsia, renal failure]
• Administer hypertonic saline and monitor serum Na and U/O to ensure appropriate correction rate:
Correction Rate
• Acute hyponatremia (<24 hours) More likely to be symptomatic and should be corrected quickly
Less likely to be symptomatic and should be corrected slowly to AVOID OSMOTIC
• Chronic hyponatremia (>24 hours)
DEMYELINATION SYNDROME (<1= 8mM/d correction)
Considerations for Choice of Saline (in hypoosmolar hyponatremia)
• Asymptomatic Normal saline
• Symptomatic /seizing Hypertonic 3% saline, may want to use demeclocyline

Hypernatremia — Differentia[Diagnosis and Investigations
Hypernatremia (>l45mmolIL)
Na Lain (rare) 4 yes 9

Hypervolemic no —+ Small volume of >800mOsmIkg urine?
(latrogenic, Cushings,
hyperaldosteronism) <25OmOsm/kg urine? .— no
yes
no yes
4 + E.vtrarenal losses offree waler!
Dng induced Response to ADH? volume contracted
Osmotic diuresis yes no (Insensible, respiratory, Gland
4, skin losses)
Central Diabetes Insipidus Nephrogenic Diabetes Insipidus
Hypernatremia — Signs, Symptoms and Treatments

1. Recognize symptoms of hypernatremia (see box) SISx of HyDernatremia:
2. Treat underlying cause, salt restrict, give water (oral preferred) to correct for water deficit: • Thrist
0 deficit = [total body water (TBW) x (serum Na 140)]/140;TBW,,,.ie= 0.6(wt);
2
H —
• Weakness
=O.5(Wt)
1
TBW Altered mental status
Replace water slowly (Serum Na should be I- no more than O.5mmol/LJhr); monitor serum Na
•
3. • Convulsions
frequently to avoid cerebral edema • Coma
References
1. Fauci AS, Braunwald E, Kasper DL, Hauser SL, Longo DL, Jameson JL, Loscaizo J. editors. Harrison’s manual of medicine. 17” ed. New York: McGraw Hill;
2009.

INTERPRETATION OF LFTS & ENZYMES
20 I I Ed. Authors: Mockenzie Lees, Simon Turner MD, Gordon Lees MD FRCSC
OriginolAuthors:Juhet Emomaullee PhD, Michael McCall MD, AM Jomes Shapiro MD PhD FRCSC FRCS (Eng)
Station Objective
In this station you will be expected to understand the use of and interpret abnormalities in liver function tests.
Basics
1. General Concepts
• 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 dz
2. Types of liver functions tests (* = first line)

Hepatocyte damage/inflammation (increased transaminases = cell death)
• *ALT: sensitive and specific marker of liver injury/inflammation
• Normal range: 5-45 U/L, levels 2x normal range are ABNORMAL
• Nonhepatic increases: severe rhabdomyolysis, systemic myopathies
• Can remain elevated weeks to months following liver injury ( if usually related to liver necrosis = severe)
• Can be NORMAL in presence of liver dz (EtCH, chronic HCV, or inactive cirrhosis)
• *AST: less sensitive and specific marker, useful as a screening test to determine AST/ALT ratio
• Normal range: 5-45 U/L; levels 2x
•
normal range are ABNORMAL
Nonhepatic increases:
I
AsT,ALT>1000H lschemic injury*, toxic injury*, acute viral hepatitis, acute
biliary obstruction, autoimmune hepatitis (less common)
Ml, extensive surgery, PE, AST . Unlikely to be EtCH-related liverdz 1
rhabdomyolysis
• Levels can be increased up to 20x normal range ( tt usually related to liver necrosis = severe)
• AST/ALT <1: viral hepatitis, autoimmune liver dz
• AST/ALT >2: EtCH liver dz, 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 jimol/L
• Test for indirect (RBC lysis) vs direct (biliary), determine cause of high total Bili
• An increased bili due to hepatic cause usually indicates advanced liver dz
• *ALp: Elevated in all forms of cholestatic liverdz, mild elevation in cirrhosis
• Normal range: 25-1 10 U/L
• Can also be high in pregnancy (placental ALP), bone dz, renal dz, and IBD
• GGT: useful to confirm that high ALP reflects hepatobiliary dz (order GGT when elevated ALP)
• Normal range: <65 U/L
• Specific, with poor sensitivity: can be high following recent EtOH ingestion, secondary to antiseizure meds, renal dz,
pancreatitis, DM, CAD, prostate Ca
Liver synthetic function QUICK LFT REFERENCE FOR JAUNDICE
• Coagulation factors (INR): PT-INR, measures extrinsic
pathway, Factor VII dependent (synthesized by the liver)
Pre hepatic (i.e.
hemolysis)
II
Hepatic
Post-hepatic
(i.e biliar
• Normal range: 0.8-1.2 I Normal/unchanged I i’ Large tSmalI
•
• Can be high with vitamin K deficiency
Albumin: major plasma protein (synthesized by the liver)
I Normal/unchanged I i’ Small t Large
• Normal range: 33-49 g/L
i t Small t Small or Large 1’ Large
• Can be low in liver dz, malnutrition, diarrhea, FE deficiency, infection
3. When to use LFTs:
Routine annual evaluation of patients in all age groups, esp. patients with risk factors for liver dz
• Risk factors: obesity, DM, dyslipidemia, high risk behaviours (IV drug use, EtCH, sexual promiscuity, tattoos, non-sterile ear or
body piercing, residence or travel to developing countries, occupational exposures, history of autoimmune dz, family history
of liver dz)
• History of unexplained RUQ pain, dark urine, acholic stools, jaundice
• Findings on physical exam: unintentional weight loss, stigmata of liver dz, impaired cognitive function
4. Approach to ordering LFT5:
Initial screening tests: ALT, AST, ALP

All patients with at least one abnormal liver screening test should have the following additional testing: GGT, Bill (including direct),
Albumin, INR
5 Patterns of LFT abnormalities
HepatOCellular cause:
• Very high ALT, e.g. 200-2000+ U/L
• Slight high ALP, unlikely >2x normal
• Elevated AST and ALT >2x in ft ALP —* likely hepatocellular cause
• Variable Bili, 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. 4x normal) —* likely cholestatic cause
Test Result Possible Cause Initial Action Management

Liver damage:
Perform additional blood tests (rd line
2
• Viral,
tAST/ALT • LFTs, HCV/HBV serology, autoimmune • Treat underlying cause
EtOH,
<1.0 panels, ferritin ceruloplasmin, al-anti • Specialist referral
Autoimmune
trypsin), abdominal U/S, liver biopsy
Heritable disorders
• Reduce EtCH ingestion
• EtCH, • Change hepatotoxic meds
AST/ALT . Recheck LETs q3-6 months
• Obesity • Lose weight if BMI>25
> 2.0
Hepatotoxic drugs • Specialist referral if:
• LFT >l.5x normal 2x, 6 months apart
Cholestatic:
t ALP and • Biliary obstruction • Additional testing: autoimmune panels,
GGT, +1- t • PBC viral serology, abdominal U/S, liver
• Specialist referral
Bilirubin • PSC biopsy
• Autoimmune hepatitis
Indirect:
• Look for cause of hemolysis
Bilirubin • Hemolysis
• Check direct/indirect Bill Direct:
only • Biliary obstruction
Likely Gilbert’s Syndrome
• No furtherTx necessary
• EtCH ingestion
• Anti-seizure meds
• Renal disease
• Review Patient’s PMHx
t GGT only • Pancreatitis
• Identify risk factors
• DM
• CAD
• Prostate CA
References
Minuk GY. Canadian Association of Gastroenterology Practice Guidelines: Evaluation of abnormal liver enzymes tests. Can J Gastroenterol 12:6 1999 Sept,
41 7-42 1.
ir or
tory

INTERPRETATION OF LIPIDS
201 I Ed. Authors:Adarsh Rao, Carol Chung MD, Arnold Voth MD FRCP
OriginalAuthors:Janna Tram, James Yeung MD, Matthew Wang MD CCFP
Station Objective
for developing coronary heart disease. Risk factors for
This station requires you to interpret a lipid profile in order to assess the patient’s risk
should be determined.
coronary heart disease should be identified and appropriate management for patients
Basics
The lipid profile includes the TC, HDL, LDL and TG
TC is the sum of LDL, HDL, and VLDL
with an increased risk.
Increased HDL correlates with a decreased risk of CAD, while increased LDL correlates
Therapy
Targets of 4
Risk Level Primary Target: LDL-C Class, level
Risk Factors for CAD
High <2 mmol/L
Male >45 or woman >55 years of • CVA, PVD, atherosclerosis
age or Class I, level A
• Most patients with diabetes 50% LDL-C
• Cigarette smoking FRS20%
• apoB <0.80 gIL
• Diabetes mellitus • RRS20%
• Cholesterol (TC, LDL-C or apoB)
• HDL-C Moderate
• Blood pressure • FRS1O%tol9%
• Family history of premature CAD • LDL-C> 3.5 mmol/L <2 mmol/L
(younger than 60 years of age) • TC/HDL-C>5.0 or
hs-CRP >2 mg/L in men Class la, level A
• Inflammatory biomarkers • 50% LDL-C
(especially hs-CRP) • >50 years and women apoB <0.80 gIL
• Overweight and obesity • >60 years of age
• Family history and hs-CRP
• modulate risk
Low 50% I- LDL-C Class Ila, level A
• FRS<10%
Investigations
1. Blood work
include familial hypercholesterolemia and
• Fasting lipid profile measuring TC, LDL, HDL, and TG. Primary causes of dyslipidemias
familial hypertriglyceridemia
for secondary causes such as hypothyroidism
• Hs-CRP,TSH, fasting glucose, Cr, electrolytes, urea, GGT(if EtOH suspected). Screen
syndrome, lifestyle (obesity, sedentary
chronic kidney disease, DM, drugs (tamoxifen, glucocorticoids, 1.-blockers), nephrotic
lifestyle, EtOH, smoking), diabetes specifically Type 2, and liver disease
-
corneal arcus
2. Signs of hyperlipidemia include atheromata, xanthoma, tendinous xanthoma and
3. Framingham Risk Score (FRS) calculation
BP (both sBP and dBP), presence of
• Sum of scores for multiple risk factors: age, gender, total cholesterol, tobacco use, HDL,
diabetes
• Used to estimate 1 0-year risk of CAD
Interpretation of Lipid Panel

The target lipid values for the primary prevention of CAD are as follows:
High Risk
• LDL <2.0 mmol/L, ..2 Risk Factors
• Total Cholesterol: HDL ratio <4 mmol/L
• 10 year risk of CAD >20%, or hx of CAD, PVD, atherosclerosis, or DM
• if TC >6 mM or LDL> 5 mM, suspect familial hypercholesterolemia
• If TG >5 mM, suspect familial hypertriglyceridemia
2. Moderate Risk
• LDL <3.5 mmolIL, 2 Risk Factors
• Total Cholesterol: HDL ratio <5 mmolIL
• loyearriskofCADll-19%

LoW Risk
LDL <5.0 mmol/L 0-1 Risk Factors
Total Cholesterol: HDL ratio < 6 mmol/L
Treatment
•or i Lifestyle changes: diet (I- saturated fats, tomega-3 fatty acid rich foods(.IJG), increase soluble fibre), exercise, wt.i, smoking cessation
2 Factors to I’ CAD risk: treat HTN, smoking cessation, stress management, moderation of EtOH intake
3 pharmacologic therapies
• HMG-C0A reductase inhibitors (statins) —* 1 line after unsuccessful lifestyle changes
• Slow cholesterol formation by inhibiting rate-limiting enzyme (ULDL, f HDL, 1TG)
• Ex. atorvastatin (Lipitor) 10-80 mg PC daily
• Monitor muscle enzymes and LFT’s (q6months due to risk of myopathy and hepatoxicity
• Check LFT before starting, then at 8-12 weeks, then if normal, q6months
• Niacin
• .I,LDL,ttHDL,.N.TG
• Ex. full dose niacin 3g PC daily
• Initiate at small dose to ttolerability
• Bile acid-binding resins
• Increases synthesis of bile acids utilizing hepatic cholesterol (.LLDL, TG, HDL)
• Ex. cholestyramine 12g PC divided TID mixed with water or juice
• Safe in pregnancy, may cause slight in t TG
• Fibric acid derivatives
• .I4TG,tHDLJLDL
• Ex. gemfibrozil 600mg PC BID
• Ezetimibe
• Blocks absorption of dietary and biliary cholesterol through intestinal walls (.1-LDL, .1-TG)
• 10mg P0 daily
• Combination drug therapy if monotherapy not sufficient
• Lipids should be measured after 6 weeks, and at 3 months after initiating drug therapy. ALT, AST, CK must be measured at baseline
and then 6 weeks later for signs of transaminitis or myositis
References
A 1. The College of Family Physicians of Canada [Internet]. Mississauga; c2009 [updated 2007 Jun 07; cited 2009 Sep 12]. Cholesterol What you can do to
—
lower your level; [about 4 screens]. Available from: http:ffwww.cfpc.ca/encilish/cfoc/orograms/patient%2oeducation/cholesterol/default.aso?s=1

2. Wilson PW, D’Agostino RB, Levy D, Belanger AM, Silbershatz H, Kannel WB. Prediction of coronary heart disease using risk factor categories. Circulation.
1998 May 12;97(18):1837-47.
nd Genest J, Frohlich J, Fodor G. Recommendations for the management of dyslipidemia and the prevention of cardiovascular disease: summary of the 2003
update. CMAJ 2003:1 69(9):921 -924.
4. McPherson Ret al. Canadian Cardiovascular Society position statement — Recommendations for the diagnosis and treatment of dyslipidemia and
ism, prevention of cardiovascular disease. Can J Cardiol 2009; 25(1 0):567-579.
5. Recommendations for the management of dyslipidemia and the prevention of cardiovascular disease: Summary of the 2003 update. Reprinted from
CMAJ 28 October 2003;1 69(1 ):921 -924.

INTERPRETATION OF PFT
201? Ed. Authors: Maleko Ramji, Mohit BhutaniMD FRCPC
OriginalAuthors: Charles Lim, Edward James PLJ:Janjeevan DeolMD, Dilini Vethanoyagam MD FRCPC
Station Objective
In this station you may be expected to use a systematic approach to interpreting pulmonary function tests to suggest pathophysiology of
underlying lung disease and generate associated differential diagnoses.
Basics
1. Patient ID and demographics (reference values are calculated based on patient demographics):
• Age, Height, Sex, Ethnicity, BMI
2. Test information
• Date of test
L
• Pre test data
• Pre-test medications taken
• Smoking and health history if available
3. Compare with previous patient PFT5 if available
• Don’t miss diagnoses in this list
A Simplified Differential Diagnosis
3.
Approach to Abnormal PFTs 4.
Obstructive Pattern Restrictive Pattern
/\ L DLCO D
N DECO
Not responsive to Responsive to I
Bronchodilator Bronchodilator
Normal Spirometry and Lung
4
Neuromuscular, Pleural ILD, 0*
2.
4 + Voluma with Abnormal DLCO dz sity
COPD Asthma
I DECO 0
C
1 0
N0 co j DECO
4 4
Polycythemia, mild CHF PE Anemia, Pulmonary HTN
Chronic bronchitis Emphysema Early ltD. Increased COHb
Spirometry 2.
1. Quality
• Acceptability: requires 3 artifact-free maneuvers (eg. no cough within is, no glottis closure, etc.)
2 4
• Note: a minimum of 6s of sustained expiration on each maneuver is required
• Repeatability: requires 3 maneuvers where the two largest values of FEy 1 are within 0.1 50L of each other and the two largest
values of FVC are within 0.1 50L of each other
2 6.
2. Flow-Volume Loop
• R 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
fixed and either an intra or extra thoracic in origin (eq. Tumor, thyroid goiter)
3. Diagnostic criteria for airflow obstruction and significant reversibility
• COPD:
• Post-bronchodilator FEV /FVC < 0.7 indicates that there is airflow obstruction that is not fully reversible
1
• Severity is based on the post bronchodilator percent FEy 6
1
• Mild: FEV 1 >80%
• Moderate: FEy 1 50-80%
• Severe: FEy 1 30-50%

• Very Severe: FEy
1 <30%
• Asthma:
• t 12% AND t 200 mL improvement in FEV1 post-bronchodilator indicates a significant reversible airflow obstruction3
• A normal FEV1/FVC ratio with significant reversibility is in keeping with Asthma
fjgielec
A) normal
Examples of Flow-Volume LooDs
flow-volume loop
::
B) typical obstructive defect with FEy
1 <lower limit of 2
normal
e.z:
C) typical restrictive defect with TLC < lower limit of
normal
D) typical mixed obstructive and restrictive defect
0 2 4
Valum (I.) VoIum (L Vhm (L VaIrn,, (L)
Lung Volumes
i. Quality
• VC 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 > than VA measured by diffusion capacity
2. 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 volume); using Body Plethysmography
(body box) is the best method as it measures total lung volume
• IfTLC measured by body plethysmography is greater than N 2 dilution, it suggests the presence of bullous lung disease
3. Residual Volume (RV)
• > 120% predicted suggests gas trapping due to poor patient effort or obstruction
4. Expiratory Reserve Volume (ERV) and Functional Residual Capacity (FRC)
In obese patients, both ERV and FRC are decreased
Diffusion Capacity
1. Check for DLCO correction for hemoglobin (Hb) or alveolar volume (VA)
2. .i 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
Airway Resistance
1. t airway resistance (Raw) suggests turbulent airflow (airway constriction, edema, etc.)
References
1. ATS Documents: Statements, Guidelines & Reports [Internet]. New York: American Thoracic Society; c2009 (cited 2009 Nov 23]. Available from http://
www.thoracic.org/sections/publications/statements/index.html.
2. Miller MR, Hankinson J, Brusasco V, Burgos F, Casaburi R, Coates A, et al. Standardisation of spirometry. Eur Respiri. 2005 Aug;26(2):319-38.
3. Pellegrino R,Viegi G, Brusasco V, Crapo RO, Burgos F, Casaburi R, et al. Interpretative strategies for lung function tests. Eur RespirJ. 2005 Nov;26(5):94
8-68.ATS-CQpD
4. CeIli BR, MacNee W, ATS/ER5 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):932-45.
5. WestJB. Pulmonary Pathophysiology: The Essentials. 6 a’ ed. Philadelphia: Lippincott Williams & Wilkins; 2003.
6. EO’Donnell D, Aaron 5, Bourbeau J, Hernandez P, Marciniuk DD, BaIter M. Canadian thoracic society recommendations for management of chronic
obstructive pulmonary disease—2007 update. Canadian Respiratory Journal: Journal of the Canadian Thoracic Society. 2007;1 4(Suppl B):5B.
ble

_________
INTERPRETATION OF URINALYSIS
2011 Ed. Authors:Aamir Eharmal, Cathy Lu MD, Valerie LuyckxMBBS
— OriginalAuthors: Brian Buchanan, Carrie Ye MD, Valerie Luyckx M8BS
Station Objective
To provide a systematic approach to assessment of various urinalysis parameters
Basics
1. Indications:
• UTI and suspected pyelonephritis, flank pain
• Renal calculi, hematuria
• DM: acute or chronic illness
• Renal failure: ARF or CRF
• Pregnancy
Appearance
Clear, light to dark yellow N variation with different physiological states of hydration
Colorless Diabetes insipidus, diuretics, excess fluid intake
Dark Acute intermittent porphyria, advanced malignant melanoma, cholestasis
Cloudy UTI, amorphous phosphate salts, blood, mucus, bile
Blood, Hgb, sepsis, dialysis, myoglobin, food coloring, beets, sulfa drugs, nitrofurantoin, salicylates,
Pink/red
laxatives (phenolphthalein)
Orange/yellow Dehydration, phenazopyridine (pyridium), bile pigments, drugs (rifampin)
Brown/black Myoglobin, bile pigments, melanin, cascara, Fe, nitrofurantoin, alkaptonuria, metronidazole
Green/blue Urinary bile pigments, indigo carmine, methylene blue
Foamy Proteinuria, bile salts
Hematuria (blood)
Type 1’ Free Hgb, myoglobin I 1’ Whole cell (erythrocyte)
Neoplasm, coagulopathy, menses
Differentiate free Hgb from RBCs Transfusion reaction, intravascular
(contamination), glomerulonephritis, foreign
by centrifuging urine (supernatant hemolysis, burns, crush injury, tissue I body (esp. Foley catheter), stones, renal infarct
is colored if pigment is free) ischemia
*to further delineate the nature of hematuria, analyze the nature of the sediment microscopically
Glucosuria (glucose)
Endocrine DM, pheochromocytoma, Cushing’s dz, hyperthyroidism, pancreatitis
Medications, Burns Steroids
latrogenic False (+) with large doses of aspirin, ascorbic acid, or cephalosporins
Ketonuria (ketones)
Endocrine DKA, hyperthyroidism
Metabolic NN, diarrhea, starvation
Medications Parkinsonian medications, stimulant laxatives
*Used primarily to detect acetone and acetoacetic acid, does not detect 3-hydroxybutyric acid
Leukocyte esterase
• Depends 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 —ye, (therefore, seen as surrogate markers for bacteria)

Nitrite
• Coagulase5Pli9 bacteria convert nitrates to nitrite, urine must be in the bladder for >4 hrs prior to voiding for conversion,
nitrates must be present
• Some bacteria do not produce nitrite (E. faecalis)
• Morning sample is preferred (stasis)
• False —yes —* dilute urine, non-nitrate reducing bacteria, insufficient bacterial counts
often limited to select clinical situations)

pH Range 4.6-8.0 (Utility is
Acidic Basic
High-protein (meat) diet UTI

Metabolic alkalosis
cidosis(secondaryt0 ketoacidosis in starvation, DM) Renal tubular acidosis
Diet (high vegetable diet, milk, immediately after meals)
Uric acid stones
3 therapy, vomiting
NaHCO
Protein
N protein excretion is < 150 mg/24 h (10 mg/i 00 mL in a spot specimen), proteinuria on dipstick requires quantification with 24 hr
urine studies
• Dipstick protein detection is limited to albumin primarily and will not detect immunoglobulins. Urine protein electrophoresis
must be utilized to detect immunoglobulins
• Differential Dx includes benign and pathological causes, See “Proteinuria’ for further discussion
Specific Gravity (Interpret in light of relative fluid status)

1.016—1.022 Value>1.O22ort
Diabetes insipidus (central or Average with N fluid intake
Volume depletion, CHF, adrenal insufficiency, DM, SIADH, t
nephrogenic), pyelonephritis, isosthenuria: specific gravity fixed at
proteins (nephrosis), newborn state, if markedly t (1.040—
glomerulonephritis, water load 1.010, regardless of intake, suggests
1.050), artifact or recent administration of plasma expanders/
with N renal function renal tubular dysfunction
radiographic contrast media
Urobilinogen and Bilirubin:

• Limited utility (dipstick analysis), bacteria in gut utilize conjugated bile to form urobilinogen —* cleared by the liver
• N, low level of urobilinogen excreted in the urine daily, but hemolytic processes or hepatocellular dz can lead to t urinary levels
• Complete biliary obstruction —* absence of urobilinogen in the urine.
• 1% of conjugated bile is filtered and usually undetectable, t levels associated with states of conjugated hyperbilirubinemia
Microscopic Examination of the Urinary Sediment (further analysis)

Bacteria or
>5 WBCs/ HPF indicates significant pyuria (DDx infection, neoplasm, calculous disease, etc)
Leukocytes
>5 RBCs/hpf on one occasion or >3/hpf on multiple warrants further investigation (DDx glomerular disease, neoplasm,
Erythrocytes
trauma)
N pts and stone-formers both will form uric acid, phosphate, and oxalate crystals, preferential formation of stones based
Crystals
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)
References
1. Stoller Marshall L, Kane Christopher J, Meng Maxwell V, “Chapter 23. Urologic Disorders” (Chapter). McPhee SJ, Papadakis MA, Tierney LM,
Jr.: CURRENT Medical Diagnosis & Treatment 2009.
both

INTUBATION AND LUMBAR PUNCTURE
D 2071 Ed. Authors: Moleka Ramji, Keir Peterson MD, CCFP (EM)
Staton Objective
Outline the indications and contraindications for performing an intubation or lumbar puncture. Highlight important aspects of the
procedure and possible complications
Intubation Precautions:
Indications • Wear protective equipment when
• Unable to adequately ventilate or oxygenate intubating (gloves, mask, eyewear)
• Need for airway protection
• Excessive work required for breathing
2. Procedure
• Prepare Equipment (including various EU tube sizes; usually 8.0-8.5mm for adult male, 7.5-8mm for adult female)
• Preoxygenate the patient
• Position the patient:
• Ensure the patient’s head is level to the waist to the intubator
• Take appropriate precautions to minimize neck movement when intubating a patient with a potential cervical spine
injury
• Elevate the head to sniffing position, aligning the patient’s laryngeal structures to the level of the anterior chest wall. This will
improve visualization of the glottic 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
• If visualization of the glottis is not clear, the BURP maneuver (backward, upward, rightward pressure on the external larynx)
can be used
• Hold the endotracheal tube with the right hand and pass the tip through the abducted vocal cords
• Ensure that the endotracheal tube cuff is pushed into the upper trachea and past the point of the larynx (from the corner of
the mouth, this is approximately 23cm in men and 21cm in women)
• Withdraw the laryngoscope and inflate the cuff.
• Secure the endotracheal tube
3. Post intubation
• Appropriate tube placement is best determined by visualization of the tube passing through the vocal cords
• Assess chest wall expansion and auscultate for presence of bilateral breath sounds, but be aware that these are not infallible signs
of adequate tube placement
• If lung sounds are absent and epigastric sounds are present, this may indicate esophageal placement of the tube
• If breath sounds on the right side are louder than the left, this could indicate right mainstem bronchial intubation
• An end-tidal CO2 detector is a valuable adjunct to confirm tube placement
• Chest x-ray should be performed after emergency intubation
4. Complications
• Pneumothorax
• Recurrent laryngeal nerve injury
• Hemorrhage
• Tracheal stenosis
• Lip Lacerations
• Dental fractures
• Dislocation of arytenoid cartilage
• Vocal cord injury
Lumbar Pucnture
Indications
• Suspected CNS infection (ex. meningitis)
• Suspected subarachnoid hemorrhage
• Suspected CNS disease (ex. Guillian Barre Syndrome, carcinomatous meningitis)
• Therapeutic relief of pseudotumor cerebri
2. Contraindications
• Absolute:
• Infected skin at intended site of needle entry
• Unequal pressures between the supratentorial and infratentorial compartments (identified through characteristic findings or
CT Head)

• Relative:
• Symptoms and signs of increased cranial pressure
• coagulopathy (anticoagulation therapy or disorder, severe 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-L5 interspace for your needle insertion site (L3-4 interspace may also be used if this is
unsuccessful)
• PreparatiOn
• Put on mask, gown, sterile gloves
• Cleanse the skin with cholorhexidine
• Drape the area with a sterile cloth
• Ensure that the needle insertion site is blotted dry with a gauze pad
ne • Anesthesia:
• Local anesthesia with injection of 3-5mL of 1% lidocaine
• LP Needle Size
• 22 gauge is typically used in adults, although smaller gauge may decrease risk of post LP headache
d • Length: Infants (3.8 cm), children (6.3 cm), adults (8.9 cm)
• 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
• Use a manometer to measure opening pressure
of • Collect 4-10 mL of CSF (certain studies may require up to 20-30 mL of CSF fluid)
• Send tubes for: tube 1 (cell count and duff), tube 2 (protein and glucose), tube 3 (culture and gram stain), tube 4 (cell count
and duff), plus special studies if indicated (viral PCR, fungal culture, etc.)
o Removal of needle
• Reinsert the stylet to avoid entrapment of a nerve root in the dura as the needle is removed
4. €omplications
igns o Post procedure headache Post LP headache:
• Infection (meningitis, discitis, vertebral osteomyelitis) • Most common complication
• Bleeding • Occurs in 10-30% of patients
• Cerebral herniation (most serious complication) • More common in women of younger age
o Radicular symptoms and lower back pain (not uncommon) • Usually begins within 48 hrs of the
• Epidermoid tumor (occurs years after the procedure is performed) procedure
• Abducens palsy • Headache is often positional: worse when
• Trauma to nerve roots or conus medullaris upright, better when supine
References
Bowers RC, Weaver JD. Chapter 8. Compromised Airway. In: Stone CK, Humphries RL: CURRENT Diagnosis &Treatment: Emergency Medicine, 6e: http.1L
wwwaccessmedicine.com.login.ezproxy.library.ualberta.ca/content.aspx?aID=31 18968.
2. White Si, Levitan RM, Stack LB. Chapter 22. Airway Procedures. Knoop KJ, Stack LB, Storrow AB, Thurman Ri: The Atlas of Emergency Medicine, 3e:
l2ttPLLwww.accessmedicine.com.Iopin.ezproxy.library.ualberta.ca/content.asox?aID=6007352.
3. Gomella LG, Haist SA. Chapter 20. Critical Care. Gomella LG, Haist SA: Clinician’s Pocket Reference:The Scut Monkey, lie: http://www.accessmedicine.com.
i2i!iezDroxv.library.uaIberta.ca/contentaspx?aID=26g5577
4. Johnson KS, Sexton DJ. Lumbar puncture: Technique; indications; contraindications; and complications in adults [Internet]. Aminoof Mi,
Wilterdink JL UpToDate; [updated 2010 June 02; cited 2010 October 01]. Available from htto://www.uotodate.com/patients/content/topic.
do?topicKey....osiLljywvqRve5.
5. Robbins E, Hauser SL. Chapter e32. Technique of Lumbar Puncture. Fauci AS, Braunwald E, Kasper DL Hauser SL, Longo DL, iameson JL, Loscalzo J:
Harrison’s Principles of Internal Medicine, 1 7e: htto://www.accessmedicine.com/content.asox?aID=2886062.
6. Gomella LG, Haist SA. Chapter 13. Bedside Procedures. Gomella LG, Haist SA: Clinician’s Pocket Reference:The Scut Monkey, lie: htt://www.
7. Tintn JE, Kelen GD, Stapczynski JS, Ma Ci, Cline DM:Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 6e: htto//www.accessmedicine.
flhiQ.giry.library.ualberta.ca/content.aspx?alD=6i 5534.

•v1
DtD
—3
LI. FAMILY HISTORY AND PEDIGREE
2071 Ed. Authors: Christina Beach, Norma Leonard MD FRCPC
Station Objective
Elicit a family history to establish if a condition is genetically determined and construct a three-generation pedigree including the proband
and first-degree relatives.
J. Mendelian Inheritance
• Autosomal Recessive (M=F; trait manifests with inheritance of two mutated copies of gene)
• Cystic fibrosis, sickle cell anemia, Tay Sachs disease
• Autosomal Dominant (M=F; on average, half the offspring of an affected parent may also be affected; may”skip”a generationff
incomplete penetrance)
• Familial hypercholesterolemia, hereditary colon cancer, polycystic kidney disease, Huntington disease, neurofibromatosis
• X-linked (M>F; 1) son of carrier female has 50% probability of being affected, 2) daughters of affected males are obligate carriers,
3) daughters of carrier females have 50% chance of being a carrier, 4) carriers usually do not manifest affected phenotype or have
a mild form of disease)
• Duchenne muscular dystrophy, hemophilia A
2. Multifactorial
Most common form of inheritance: arises from interaction between multiple genes +1- environment
• Neural tube defects, diabetes mellitus, hypertension
3. Chromosomal disorders
History SCREEN
1
• Number of chromosomes
• SC Is there Some Concern of a familial disease?
• Down Syndrome (trisomy 21), Klinefelter Syndrome (XXY)
• R Are there Reproductive issues (i.e. miscarriages,
• Rearrangements (e.g. translocations, inversions)
infertility) in the family?
• CML
• E Early deaths/disease onset in family members
• E Ethnicity (e.g. Ashkenazi Jews, French Canadians)
History • N Non-genetic risk factors
I • Age, gender, and ethnicity
I • As per concern prompting clinic visit

I I • Age of onset of condition, details of diagnosis, genetic and medical tests previously performed
RED FLAGS • Physically or socially isolated populations, congenital anomalies, family history of early onset cancer or disease,
presence of disease in an unlikely individual (e.g. male family member with breast cancer), unexplained MR or
developmental delay, advanced parental age (mother >35, father> 50)
PMHx • History of mother’s pregnancy (e.g. teratogen exposures) birth and development history, past illnesses
PO&GHx • Multiple spontaneous abortions or stillbirths, infertility, maternal age, triple test results (AFP, B-hCG, estriol),
abnormalities detected on US
Sibling/offspring with known chromosomal abnormality, consanguinity (i.e. are 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
:
2 ‘El
2
LI
3
0 4
1. Mark the proband (index case) and consultands (individuals seeking
genetic counseling)
2. Organize family by generations—each generation on a separate line
and designated by Roman numerals from top to bottom
n•
1 2 3
m 4
. 6
3. Label individuals with Arabic numerals from left to right in a

generation line Ill .
.. QQ
4. In a sibline, arrange individuals from eldest to youngest 2P 3 4 5 6
5. In unions, the male is on the left wherever possible
6. Establish relationships with lines: horizontal for relationships and vertical for descent
7. Notes may be made beneath individuals (e.g. karyotype, age when deceased) but not within the symbols
8. Provide a legend

Investigations
1. Blood work
• Newborn screening panel (in AB: endocrine, amino acid, organic acid, fatty acid oxidation disorders + biotinidase deficiency, CF)
• Prenatal: US (18-20 weeks)
• Postnatal: US, x-ray
3. Special Tests
• DNA sequencing, PCR, karyotyping, fluorescent in situ hybridization (FISH)
4. Diagnostic Interventions
• Prenatal: MSS, amniocentesis, chorionic villus sampling, preimplantation genetic diagnosis (during in vitro fertilization), fetal
blood sampling by cordocentesis
Treatment
1. 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)
• Medical: Enzyme replacement, pharmacological (e.g. imatinib for CML)
• Surgical: Plastic surgery (e.g. cleft palate), tumor resection, organ/bone marrow transplant
3. Follow-up with genetic counselor and multidisciplinary team as needed
4. Referrals
• Genetic counselor, dietician, neurodevelopmental clinic, support groups, psychologist, specialist physician (e.g. endocrinologist)
References
1. Hinton, RB. The family history: re-emergence of an established tool. Crit Care Nurs Clin N Am. 2008;20:1 49-1 58.
2. Bennett RL Steinhaus French K, Resta RG, Doyle L. Standardized human pedigree nomenclature: update and assessment of the recommendations of the
National Society of Genetic Counselors. J Genet Counsel. 2008;1 7:424-433.

PRESCRIPTIONS & PROGRESS NOTES
2071 Ed. Authors: Shawna Pandya, Brian Yang MD, Darren Nichols MD CCFP(EM)
OriginalAuthors: Sara Houlihan, Sarah Fargie MD FRCPC
Station Objective
To properly complete prescriptions and progress notes.
General
To minimize medical error, avoid using abbreviations that can be misinterpreted. Specifically:
• Use “daily”instead of”qd”
• Use “alternate daily” instead of”qod”
• Write”2”instead of”2.0’and”0.1”instead of”.l”
• Use “mcg” instead of”ig”
Prescriptions
The following information should be on a prescription:
1. Date of issue:
• Time must be included if in hospital
2. Name and address of the patient
• Consider writing Out to prevent pt. removing stickers to sell Rx
3. Medication information:
• Name of drug or ingredient(s)
• Generic name unless using combination product
• Spell the drug name correctly and write legibly -
• Strength
• Include pt. weight for wt-based dosages 3dt________
za3(,
-
• Dosage form
• Caps, tabs, gtt (drops) etc.
• Consider putting parentheses around dosages, and -
writing out numbers so they cannot be easily altered (e.g.

- ... -
consider “(30) (thirty) tabs” rather than “30 tabs”) Po 10

• When writing dosages in mg/kg (especially in pediatriacs),
also write total dosage (e.g. gentamycin 82.5g (1.5mg/kg)
lVq8hx7d,ptwt5skg
• Quantity (especially for pm dosing) L’S . / JV t w 7
• Route of administration
• P0 (by mouth), IV, IM, SC, PR (per rectum) 4
P14
• Directions for use
Daily, BID (twice daily), TID (three times daily), QID (four
•
times daily)
• PC (after meals), AC (before meals), HS (at bedtime), QAM
(every morning)
• PRN (as needed) LiDcr Yji
• Q_H (every _hours)
4. Number of refills authorized (write out and circle) and interval
I
between each refill
5. Prescriber’s name and phone number
6. Prescriber’s signature
• Orders written by medical students must be approved/co-signed by a physician before implementation
• Print out name under the signature
7. Draw a line under last Rx to prevent others from adding additional drugs
8. Outside of hospitals, controlled drugs (eg. narcotics) require triplicate prescriptions
Progress (soap) notes

1. Date, time, PtID Age, sex, Hx of (significant comorbidities), admitted with, if surgery — post-operative day (include any surgical
complications),
2. S Subjective
-
• Symptomatic information: how the patient feels, how are they coping?

• Historical information: changes since last note, new symptoms (SOB, CP)?
• Caregiver information: events in the past 24 hrs.
• General review: behavior, activity, sleep, appetite (N/V), bowel/bladder routine, pain control
0 0bjçCti
a 2 (on RA or on 0
Vitals (HR, BP, RR, Sp0 ),Tmax, daily wt
2
o General appearance (acutely ill, conversing readily, etc)
o PE findings (FOCUSED: usually include CVS, RESP, ABDO)
If applicable: incision/wound (clean/dry/intact), dressings
o Ins & Outs including drains (# of/ output/ character)
• NEW laboratory results, microbiology (culture report), XR’s, pathology reports
o Allied health updates / consult reports
• (Review medications —* don’t rewrite, assess whether any need to be added or discontinued)
4. A Assessment
• t status (improving, worsening, same)
• Summary of known medical problems and plan for each one (sometimes assessment & plan are combined)
• Short DDX
5. P-Plan
• Evaluation: additional laboratory studies and procedure
• Therapy: Tx, education etc.
• NB that Assessment & Plan are often combined into one section.
6. Signature
• Sign & print name, include level of training (e.g. 51-3 for third year intern, PGY-4 for fourth-year resident) & pager number
Mcd!cine SI Progress Note Sep 232010, 1400
Patient ID: 70 yo male admitted for delirium secondary to infection (urosepis vs perirectal abscess) +/- opioid toxicity. PMHx — rectal
tumour (currently actively being investigated, followed by Dr. Smith), rectal fistulas/abscesses, HTN, GERD, PVD. Lives independently.
5: 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).
OlE: Vitals — BP 137/62, Sp0 2 96% 2L, HR = 110, RR = 20, T 36 /General — Alert. Oriented to person (not time or place) /CV — N 51/52.
No 53/54/murmurs. / Resp — GAEB. No adventitious sounds. / GI — BS +. Abdo soft, non-tender. No organomegaly.
Labs/investigations: Blood culture pending / Urine culture — no growth (post antibiotics) / Urine culture (Sep 1 7 th pre-antibiotics) — E.
coli, CFU1 08/ CT abdo/pelvis (Sep rd)

22
— no intraabdominal hemorrhage. Invasion of rectal tumour into right Ievator ani muscle. R
inguinal LN spread of tumour. R ischiorectal fluid representing possible ischiorectal abscess. Abnormal labs: C1: 109/HCO
: 22/ALT: 53/
3
AST: 86/Hb: 98/PIt: 521/WBC: 23.9/Ca
:2.02
2
A/P
Active Issues
1. Delirium — Improving. Secondary to urosepsis/rectal abscess/opioid toxicity. Infections being treated with meropenem (see below).
Dilaudid decreased to hydromorph contin 3mg po bid and hydromophone 2-4mg po q4h pm.
2. Urosepsis — ESBL positive. Has had ESBL positive urine for months. Being actively treated and followed by Dr. Johnson in
community. ID consulted, being treated with meropenem 500mg IV q6h.
3. Rectal abscess — Elevated white count and CT suggests current active rectal abscess. ID consulted, being treated with meropenem
500mg IV q6h. Multiple rectal fistulas, abscesses and surgeries since 2005. Followed by Dr. Smith.
4. I tumour — diagnosed Jul 2010. 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.
5. Anrn1a —2 units pRBCs transfusion on admission. Cause unknown.
6. e Status — Full code.
7. jposition — home once delirium has cleared.
Inactive Issues
1. iIN — stable, on Adalat XL 60mg po daily.
2. — stable, on pantoprazole 40mg po daily.
3. Q — treated with femoral-femoral bypass graft in past.
Jane Doe, SI- 3

969-gggg
References
1 Blackbourne LH. Surgical recall. 5
th
ed. Baltimore: Wolter Kluwer; 2009.
2. Writing an Effective Daily Progress Note:’http://www.medicine.ufl.edu/3rd year clerkshio/documentsiWriting an Effective Daily Progress Note.pdf
3. Meier KR. “How to Write a Good Prescription’ University ofAlberta Pediatrics Clerkship Notes. (nd]
PROCEDURE & WARD CALL NOTES
2011 Ed Authors: Ryan Gallagher; Carrie Ye MD
Station Objective
on.
To outline a standardized approach to notes for call and procedures to help better facilitate chart based communicati
Procedure Note:
• Date + Time
• Who: who was present for this procedure, be sure to include supervising staff if applicable, on pelvic/other sensitive exams make
sure to document other staff who was present in the room
• Consent: make sure to comment on if consent was obtained (also be sure to comment on if patient was alert enough to give
appropriate consent + explanation of procedure)
• Why: make sure to include the purpose of the procedure
• Preparation: materials used
• E.g. aseptic technique, how freezing was applied, positioning of the patient
• Description of procedure
Findings
Complications
Outcome
Specimens taken (e.g. Bx for pathology)
Instructions given to patient
Example: Lumbar Puncture
Nov 5, 2010, 1315: Lumbar Puncture procedure note

• This proceedure was supervised by house staff Dr.
• Patient written consent obtained and potential complications explained
• Indication for LP: fever and headache
• INR/PTT and platelets normal
• Patient was positioned in usual seated position and prepped using sterile technique. Landmarking for L4/5 interspace done using
iliac crest palpation
• 3cc of 1% Lidocaine was used for anesthetic
20 guage spinal needle was introduced successfully into the arachnoid space.
CSF fluid was light yellow and clear. 5 cc CSF collected in 4 tubes.
Tubes were sent for: cell count and differential, gram stain and culture, glucose, protein, HSV PCR
Patient tolerated procedure well. No complications.
Ward Call Note:

Common Calls: Chest pain, shortness of breath, urinary incontinence/retention, pain medications, drug reaction
• When and why you were called and responded: What to ask for on the phone:
• ID: one line summary of: patient age, gender, reason for admission • ID: name, ID #, age, location
• Medical Hx:quick list of active medical issues + relevant PMHx • vitals
• 5: event Details: HPI from patient/family/staff • Progression of problem
• 0: physical Exam: Vitals and Relevant PE • Patient information (e.g. SAMPLE HIJ
• A: impression (include differential Dx) • What has been initiated
• P: • Who else has been called
• Actions taken
• Investigations ordered (make sure to note any outstanding that day time staff will need to address)
• Medications given
• Follow up necessary for day staff
• N.B. every good note is followed by a turnover to corresponding staff in AM While you’re walking there:
• Remember to write a follow-up note once the results of the investigations that you’ve • Think of differential for concern
ordered come back and you’ve re-evaluated the patient • Review management of probleiP

Chest Pain
GIM Student Intern on-call:

pV 5. 2010 21 15h.
Called at 21 OOh by patient’s nurse re: acute onset chest pain

Pt ID: 57yo M admitted Nov 2 with confusion and found to have bilateral pneumonia, currently treated by IV levofloxacin
PMHx: DM2, HTN, BPH, smoker
5:
• Onset CP around 2040h, gradually worsening-left anterior chest, 5/10, no radiation. Was lying in bed at onset of pain.
Not worsened with deep inspiration/cough/position. Has had same pain before-has not sought medical attention. No leg
swelling/SOB/palpitations. No metallic taste in mouth.
ke 0:
• Vitals: HR 101, BP 135/82, spO2 94% on 2L 02 (unchanged), T 37.2, RR 18, GCS 15/15
• CVS: pulses strong/regular at radial bilaterally, JVP 3 cm ASA, normal 5152, no murmur/S354, pain not reproduced on
palpation
• Chest: AE equal bilaterally. Breath sounds normal
• Abdo; soft, not tender to palpation
• Investigations:
• This AM: Hb 140, platelets 210, WBC 13, neutrophils 10.9. Lytes normal (K=4.1)
• CXR (Nov 2): bilateral airspace disease, no pleural effusion/pneumothorax
• ECG (Nov 2): NSR
• A:
• 57 yo 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, trop/CK, Nitro spray, CXR, repeat CBCd, lytes
2010; 2145h Follow-up Note:
• 5:
• Patient’s pain decreased with Nitrospray. Now 1/10
• 0:
• Repeat Vitals: unchanged except HR now 85
• CXR: unchanged, ECG: NSR, no T wave or ST changes compared with previous, l trop (-)
• Rest of bloodwork pending
• A/P:
• Patient’s pain resolving. No evidence of ACS on first ECG/trop.
• Repeat ECG and trop in 8 hours
• Nitrospray PRN for pain
• Consider Cardiology consult in AM for risk stratification (MIBI or EST)
em
blem

UNDERSTANDING ANTIBIOTICS
2011 Ed. Authors: Maleka Ramji
j
= — Original authors: Sara Houlihan
Station Objective
Understanding antibiotic principles and uses
Choice of Agent: Principles

• Antibiotics only effective versus bacteria
• Need effective concentration at the site of infection
• Need appropriate duration of therapy
• Inappropriate use contributes to the development of resistance
defense inadequat
• For most infections, the goal of Tx is concentration > minimum inhibitory concentration (MIC) except where host
then concentration must be> minimum bactericidal concentration (MBC)
Important considerations for antibiotic selection:

inactivate aminoglycosid
1. Site (ie. eye/brain/prostate = non-fenestrated capillary which impedes drug diffusion, low pH in abscesses
endocarditis creates huge vegetative growths
and erythromycin) & ability to reach site (ie. aminoglycosides not absorbed orally,
therefore longer duration of therapy is required, foreign objects such as catheters and joint replacements are prone to biofllm
production which provides a mechanism of resistance for the organism)
l agent and dose ie.’b
2. Immune status (may determine the organism ie. pneumocystitis carinhi in HIV pts, may determine antimicrobia
guns’ in immune suppressed patients)
3. Hepatic and renal function (dosage adjustments may be required, certain antibiotics contraindicat
ed ie. Tetracycline in renal failur.
chloramphen icol in babies due to inability to glucuronidat e)
Pregnancy and breastfeeding (teratogenicity of certain antibiotics, altered pharmacokinetics because oft
maternal volume of
4.
distribution, cardiac output and clearance)
5. Medication history (allergies, interactions)
Setting of acquisition of infection (country/region, community vs. hospital acquired, ward vs. ICU, contact
with animals)
6.

of Anti MOA Examples Spectrum of Activity Therapeutic Indications
pniC1llfl5 Interfere with the
synthesis of cell wall Streptococci,
peptidoglycan, some enterococci,
N. Menigitidis,
Results in formation of Many anerobes (excluding B.
defective cell walls that fragilis),
lyse and result in death Spirochetes (Treponema),
of the organism. Corynebactium diphtheriae
Bactericidal Most active vs. non beta-

Acute Pharyngitis (Grp A
Pen G(IM/IV) Iactamase producing Gram
Strep), Grp B Strep,
Pen VK (P0) + organisms, anaerobes and
Syphilis, Listeria, Actinomyces
selected Gram cocci
—
Bulky side chain provides

Cloxacillin (P0/IV/IM) increased activity against Staphylococci skin infections
beta-lactamase producing (excluding MRSA)
staphylococci
es
Amoxici I lin (P0) Streptococcus pneumoniae
Ampicillin (IV/lM) infections (Sinusitis, otitis,
More activity vs. enterococcus, CAP, AECOPD) (but beware
Covers the same Listeria monocytogenes, that resistance to penicillins
organisms as Penicillin, increased Gram- (E.coli, is increasing), H. pylon
but also covers H.influenzae, P.mirabilis, eradication in triple therapy,
additional gram-negative Salmomella, Shigella) Prevention of infective
organisms endocarditis in susceptible
patients
Increased spectrum to include

pseudomonas aeruginosa, P.
mirabilis, Enterobacter, some
Ticarcillin-clavulanate serratia, some B. fragilis
Similar to Pip-tazo
(IV)
Activity vs, non-beta Iactamase
producing E.coli, H.influenzae,
N. gonorrhea
Excellent activity vs. Nisseria,

H. influenza, enterobacteraciae,
Piperacillin Severe intraabdominal
dose related activity vs.
infections,
pseudomonas
Pip-tazo (Piperacillin + Severe nosocomial infections,
Tazobactam) E mpiric therapy in high risk
Used in combination with
febrile neutropenic patients
tazobactam for activity against
Gives broad coverage + aminoglycoside
beta-Iactamase producing
Gram— and Gram + organisms
Most Gram+ & Gram- bacteria
Broadest spectrum Severe intraabdominal

Most Gram+ (excluding infections,
MRSA, enterococci), Gram Severe polymicrobial skin
Imipenem-cilastin (IV)
(includingPseudomonas), most and soft tissue infection,
Meropenem (IV)
anerobes (except C.difficile) Fournier’s gangrene,
Resistent to most beat Severe ventilator-associated
Iactamases pneumonia where
Pseudomonas and S. aureus
coverage is needed.

Cephalosporins Bind transpeptidases, Increased stability to beta- Lin
disrupt cell wall lactamases produced by Staph
synthesis, activate (not active vs. MRSA) Surgical prophylaxis, soft
autolytic enzymes and First Generation Moderate activity vs. Strep tissue and skin infections
cause bacterial cell lysis. More activity vs. Gram— (E.coli, (impetigo, cellulitis erysipelas
Cefazolin (IM/lV) P.mirabilis, K. pneumonia, caused by MSSA) and bony
Bactericidal Cephalexin (PC) Moraxella sp.) infections like osteomyelitis Me
NOT active vs enterococci, and septic arthritis
Chlamydia and Mycoplasma, or
Haemophilus species
Slightly decreased activity vs.

Gram+ cocci, Increased vs.
Second Generation CAP, Ctitis, Sinusitis
Gram-rods, 2 subgroups:
Cefuroxime (PC/lV) Sul
Respiratory: increased activity Tn
Cefprozil (P0) Ab/pelvic infections, surgical
vs. H.influenzae & M. catarrhalis
Cefoxitin (IM/lV) prophylaxis
Cefotetan (IM/lV)
GI/GU: increased activity vs.
B.fragIlls
Enhanced activity against Niti
aerobic gram-negative Sepsis, meningitis (penetrate
organisms such as the blood brain barrier),
Third Generation Enterobacteriaceae; while hospital acquired pneumonia
retaining good activity Qul
Cefotaxime (IM/IV) against streptococci (except Ceftriaxone DCC for Lyme
Ceftriaxone (IM/lV) enterococci), it is less active disease
Ceftazidime (IM/IV) against staphylococci.
Cefixime (P0) Cefixime DCC for
Cefazidime active vs. uncomplicated gonorrhea
Pseudomonas but not good for
Strep pneumoniae
Good Gram+ & Gram- coverage
Fourth Generation Increased resistance to beta Similar to 3
cd
gen.
Van
lactamases (md of Staph and MonoRx for nonlocalizing
Cefepime (IV/IM) Enterobacter) febrile neutropenia
Lacks coverage of B. fragIlls
Aminoglycosides Inhibit protein
Gentamicin (IV/IM/OTIC/ Gram- UTI
biosynthesis by binding
OPTH) Pseudomonas Synergistic with wall active
to 30S ribosome;
Tobramycin (lV/IM/OPTH) No activity vs. anaerobes agents
Bactericidal
Macrolides Inhibits protein synthesis Alternative to Penicillin in
by binding reversibly acute pharyngitis,
to the 505 ribosomal rd line for otitis media,
3
subunits of susceptible AECCPD, sinusitis, Re
Erythromycin (P0/IV/
microorganisms. Staph, Strep, anaerobes Alternative to cloxacillin for
TOP/C PTH)
(excluding B.fragilis), superficial S.aureus infection,
N.gonorrhea, atypical Acne vulgaris,CAP, whooping 2.
Clarithromycin (PC)
(legionella, mycoplasma, cough, Chiamydia
chlamydia), Bordetella pertussis trachomatis & pro phylaxis
Azithromycin (IV/P0)
of ophthalmia neonatorum
due to N. gonorrhoeae or C
trachomatis s.
Tetracycline Inhibits bacterial protein 6.

synthesis by binding
Tetracycline (PC, CPTH) Gram+, Gram-, anerobes, CAP, AECCPD, Acne,
to 305 and to some
extent the 505 ribosomal
Doxycycline (PC)
Chlamydia, Mycoplasma,
Nocardia, Rickettsiae,
Chlamydia trachomatis, Rocky!
mountain spotted fever,
:
subunits.
Plasmodium, Vibrio Cholera, Brucellosis, Lyme disease,
Alters the cytoplasmic
Minocycline (PC) Brucella Malaria prophylaxis
membrane causing
leakage.

-
Binds to 505 ribosomal
Lincosam Mixed skin infections,
subunit of susceptible rd
3
Gram+, anaerobes including B. line acute pharyngitis,
bacteria, reducing the Clindamycin (PO/IV/IM/
fragilis, clostridium (excluding Group A Strep Necrotizing
rate of nucleic acid TOP)
C.difficiie), Gardnerella vaginalis faciitis (in combo with
as synthesis and ceases
penicillin), Bacterial vaginosis
protein synthesis.
MetrOnidazole Reduced substrate,
Anaerobic infections,
activated by Anaerobes including B. fragilis,
Mixed infections,
nitroreductase, affects C.difficile
C.difficile diarrhea or
anoxic or hypoxic cells Metronidazole (PO/IV/ Some H.pylori, amoeba
pseudomembranous colitis,
causing loss of the DNA TOP) and parasites (Trichomonas
Bacterial vaginosis,
helix and form and vaginalis, Entamoeba histolytica,
Trichomonas,
impairment of cellular Giardia lambia)
PUD triple therapy
function.
naide5/ Inhibits folic Gram+, Gram-, plasmodia,
TrimethoPrim acid synthesis by Chlamydia, toxoplasma,
competitively inhibiting actinomyces, mycoplasma, UTI, Prostatitis, Traveller’s
dihydrofolate reductase TMP/SMX (PO/IV)
Pneumocystic jiroveci (carinii) diarrhea, PJP prophylaxis
and other steps in the pneumonia (PJP)
pathway. No enterococci or anerobes
Nitrofurantoifl Reactive intermediates
ite alter bacterial Nitrofurantoin (P0)
Enterococci and E.coli UTI
ribosomal proteins and
nia macromolecules.
Quinolones Inhibits bacterial Ciprofloxacin (IV/PO/
DNA synthesis, by OTIC/OPTH)
UTI, refractory prostatitis,
targeting types II and IV Norfioxacin (P0) Enteric Gram- and atypical
Bacterial diarrhea
topoisomerases; Causes Ofloxacin (PO/OPTH) (Cipro has activity vs.
arrest of DNA replication Levofloxacin (IV/PO) pseudomonas)
Respiratory tract infection
and subsequent cell Moxifloxacin (IV/PO/
rd
3 with penicillin/macrolide
death. OPTH) and 4th
gen have increased
resistant 5. pneumonia,
Gatifloxacin (OPTH) activity vs. Gram+
AECOPD
Gemifloxacin (PC) D/C
2009
Vancomycin Inhibit peptidoglycan Severe or life-threatening
wall synthesis by binding staphylococcal infections
to precursor ONLY Gram+ when MRSA is suspected
(cloxacillin is the dru of choice
MRSA, penicillin highly for Staph aureus.)
Vancomycin (PO/IV) resistant S. pyogenes/S.
pneumonia, E.faecalis, E. Vancomycin PC ONLY
faecium, anerobes (excluding for the treatment of
B. fragilis) antibiotic associated
pseudomembranous colitis
produced by C. difficile.
References
1. Management of community acquired pneumonia in adults. [Internet). Alberta:Toward Optimized Practice. c2009 [updated 2008 Jan;cited 2009 Oct 29].
Available from: http://www.topalbertadoctors.org
pIng 2. Summary of the Alberta clinical practice guideline for acute otitis media. [Internet]. Alberta: Toward Optimized Practice. c2009 [updated 2008 Jan;cited
2009 Oct 29]. Available from: http://www.topalbertadoctors.org.
3. Guideline for the diagnosis and prevention of acute pharyngitis. [Internet). Alberta: Toward Optimized Practice. c2009 [updated 2008 Jan;cited 2009 Oct
im 29]. Available from: http://www.topalbertadoctors.org.
C.
‘• Summary of the Alberta clinical practice guideline for acute bacterial sinusitis. [Internet]. Alberta: Toward Optimized Practice. c2009 [updated 2008
Jan;cited 2009 Oct 29]. Available from: http://www.topalbertadoctors.org
5. Guideline for the management of acute exacerbation of chronic obstructive pulmonary disease [Internet]. Alberta: Toward Optimized Practice. c2009
(updated 2008 Jan;cited 2009 Oct 29]. Available from: http://www.topalbertadoctors.org.
6. Meyers BR et al. Antimicrobial therapy guide. 17” ed. Pennsylvania: Antimicrobial prescribing Inc. 2006.
7. BIon E, Fryters S. Bugs & Drugs. 1 “ed. Edmonton: Capital Health;2006.
ocky 8. Sabatine MS. Pocket Medicine: the Massachusetts General Hospital Handbook of Internal Medicine. 3 rd ed.Philadelphia: Wlter Kluwer. 2008.
9. Canadia,, Pharmacists Association [Internet] Ottawa (ON): e-Compendium of Pharmaceuticals and Specialities.; c2009 [updated 2009 Oct 29; cited 2009
Oct 29]. Available from: http.//www.etherapeutics.ca

PRE- AND POST-OPERATIVE ORDERS n FathimaniMDFRCSC
2011 Ed Aurhar5: Patricia Lee, Sarah LaiMO, Kamra
Station Objective
erative orders
To outline a template for writing pre- and post-op
Pre-Operative Orders: ABCD Mnemonic

Date, time, planned procedure, diagnosis
Ciprofloxacin (on call to OR vs. STAT)
1. Antibiotics: Ancef +1- Flagyl, Clindamycin +1-
Cr, INR, PU, type and screen/cross match
2. Blood work: CBCD, lytes, BUN,
• Bowel prep: laxativ es, enema s, suppos itories
• Booking the case: call OR
3. Consent: discuss potential benefits, risks,
and alternatives of surgery with patient and family
ary
• Consults: IM, ICU, Anesthesia, Cardiology as necess gulation (hold Coumadin, AS
previo us meds, cardiac meds (contin ue beta blockers and statins; hold diuretics and ACEi), anticoa
4. Drugs:
Plavix, therapeutic IV Heparin / SC LMWH)
5. Eating: NPO by midnight
6. Fluids: IV NS or RL maintenance
s give stress dose steroids
7. Glucocorticoids: if patient on long term steroid
in 5000 units sc 2h before OR)
8. Heparin: DVT prophylaxis (Hepar
9. Imaging:
CXR: if lung disorder or age >50 years
ECG: if cardiac disorder or age >50 years
Post-Operative Orders: DAVID Mnemonic

Date, time, admit to surgery, diagnosis diet
FF, DAT, tube feeds, diabetic diet, cardiac diet, renal
1. Diet: NPO, ice chips/popsicles,TPN, PPN, (F,
tions, ROB> 30°
2. Activity: AAT, NWB, bed rest, full spine precau
3. Vitals: q2h, q4h, routine
4. IV: NS, RL etc.
• Ins and Outs: q2h, q4h, qshift
• Investigations: (depending on surgery type)
PTH
• CBC, lytes, BUN, Cr, Mg, Phos, ionized calcium,
• LFTs: AST, ALT, Alk Phos, Bili, lipase
• INR,PTT
• CXR or necessary imaging
5. Drugs:
CNS . Anti-emetics, analgesics
CVS . Anti-hypertension, cardiac meds
Resp • Inhalers, 0,, incentive spirometry
GI Bowel routine, PPI
ID . Antibiotics
gs
DVT Prophylaxis: heparin or LMWH, pneumatic stockin
• Dressings:
• Closed wound: dry dressing PRN
• Open wound: saline soaked gauze BID/TID
, Foley to urometer, chest tube -20 cm H,O suction
• Drains: JP to bulb suction, NG to low intermittent suction
References
The Scut Monkey. limed.
1. 1. Gomella LG, Haist SA. Clinician’s Pocket Reference: th ed. Toronto: Type and Graphics mc; 2010.
26
2. 2. Baxter, SD arid McShe ffrey GG. The Toront o Notes 2010.
hip.
and Anesthesiology Clerks
3. 3. White, Jonathan. Medical Student’s Guide for Surgery
,f C,-,mmrrn Clinical Scenarios I Essential Clinical Skills

ECG (EXAMPLES)
Sabira Suleman, and James Huang
-
p-Pulmoflale P-Mitrale
(Left atrial enlargement)
(Right atrial enlargement)
First Degree AV Block Mobitz I Second-Degree Heart Block (Wenckebach)
Lengthening PR interval until dropped beat (R-R interval drops with each beat)
.. Mobitz II Second-Degree Heart Block Third-Degree (Complete) Heart Block
. Missed beat
Atria and ventricles are firing separately

Grouped beats with dropped beat between groups
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
ature Ventri
Corn plex
Ischemia and Infarction
Pathological
Qwaves
A -Jv ST Elevation
>1/3
QRS -k%J
Flipped, symmetrical T-waves ST Depression
>O.04s

EDMONTON MANUAL
Section #
-D
m3-
PHYSICAL EXA
— Section Editor: Lisa J. Steblecki MD MPH CCFP

Associate Professor
Abdominal Exam .65 Jugular Venous Pressure (JVP) Exam 75

Back and Hip Exam .66 KneeExam 76
Blood Pressure Measurement. .67 Lymphadenopathy and Spleen Exam 77
Cranial Nerve Exam .68 Male Genitourinary Exam 78
Diabetic Foot Exam .70 Precordial Exam 79
Examination for Liver Disease. .71 Neurological Exam 80
Female Genitourinary Exam.... .72 Respiratory Exam 82
Hand Exam .73 Thyroid Exam 83
HEENT Exam .74
64 Edmonton Manual of Common Clinical Scenarios I Physical Exam

ABDOMINAL EXAM Patricia Lee, VUayselvarajah MD, Clarence Wang MD FRCPCABGABIM
2011 Ed. Authors:
#2 StatiOn Objective
to the abdominal exam, a key component to investigating problems with the gastrointestinal, genitourinary,
Have a general approach
gynecologic and vascular systems.
Basics
1. Introduce yourself and ask for permission to perform physical examination, wash hands
2. ABC, vitals, IV, 02, monitors
Physical
1. General Approach
Vitals: HR, BP, RR, is the patient hemodynamically stable, febrile, tachycardic, dyspnic
‘5 General appearance: is the patient pale, in discomfort, diaphoretic, agitated, motionless
‘6 2. Exposure
77 . Examine the patient from the right side of the bed
• Bed should be flat, knees flexed, hands at sides
79 . Proper draping cover the patient’s legs up to the pubic bone and to lower part of chest
—
3. Inspection
30 From the foot of the bed note any asymmetry of the abdomen and thorax
32 • Obvious organomegaly? masses? bulging flanks/ascites?
33 • Distension, scars, erythema, shape, rash, hernias, engorged veins, Grey-Turner’s sign, Cullen’s sign
4. Auscultation
• Listen over 4 quadrants, listen for 1 minute prior to commenting on absence of bowel sounds
• Comment on pitch and frequency
• Aortic, renal, splenic or femoral bruits
5. Percussion
• Percussion tenderness: evaluate for acute abdomen/peritonitis
• Percussion of liver: percuss at mid-clavicular line from third intercostal space downwards 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)
6. Palpation
• All four quadrants, light (1 cm depth) and deep (4-5 cm depth) palpation
Palpation for hepatomegaly: palpate upwards from RLQ to RUQ in mid-clavicular line, move fingers up 2cm with expiration to
determine inferior border of liver comment on liver span given superior border identified by percussion
—
• Note that palpable liver edge present in number of normal patients

• If liver edge 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
7. Special Tests
Signs McBurney’s, Rovsing’s, obturator, psoas (appendicitis), Murphy’s (cholecystitis)
DRE Blood, masses, pain, anal sphincter tone
Pelvic exam Discharge, cervical tenderness, blood
Pyelonephritjs Percussion tenderness of CV angles
Pancreatjtis GreyTurner (flanks) and Cullen’s sign (umbilical area)
MSK Pain does not decrease in intensity when palpating over area on abdomen that was strained
References
1. Tintinalli JE et al.Tintinalli’s Emergency Medicine: A Comprehensive Study Guide .6” ed. USA: McGraw-Hill; 2004.
Leblond RF, Brown DD and DeGowin RL. DeGowin’s Diagnostic Examination. gth 3d. USA: McGraw-Hill; 2009.
Physical Exam Edmonton Manual of Common Clinical Scenarios 65

BACK AND HIP EXAM
2011 Ed. Authors: Maleka Romfi, Christopher Gee, MD, ShenyKhero MD CFPC, MPH
Station Objective
In this station, you will be asked to examine the patient’s back and hip
-v
x’< HipExam
3 1. Physical Exam
• Inspection
• With the patient standing, examine the alignment of the lower extremity
• Inspect from front and from behind for pelvic tilting and rotational deformity
• Examine gait looking for antalgic and Trendelenburg gait
• Perform the Trendelenburg test
• Measure leg length, both true and apparent
• Palpation
• Palpate anterior structures: iliac crest, greater trochanter, trochanteric bursa, 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
• Range of Motion Testing
• Observe the patient’s passive external and internal rotation of the hip
• Conduct the FABER test to assess for intra-articular pathology
• Have the patient lie in the supine position and flex, adduct and externally rotate the leg
• If the patient experiences pain in the anterior or posterior positions, this renders the test positive and suggests hip an
sacroiliac joint involvement
• Hip Strength Testing
• With the Pt in supine position, test resisted hip flexion, extension, adduction and abduction
• Observe for movements that cause pain or demonstrate weakness
Back Exam
2. Physical Exam
• Inspection
• Inspect for signs of swelling and deformity including hyperlordosis, kyphosis and scoliosis
• Inspect for skin markings, dimples and scars and inspect gait
• Palpation
• Landmark and palpate important structures: spinous process, facet joints, paravertebral muscles, sacroiliac joints and sacru
• On palpation note tenderness, muscle spasms, altered temperature
• Range of Motion Testing
• Evaluate passive and active range of motion particularly flexion and extension of the spine
• Neurologic Exam
• Examine for motor strength, reflexes and sensation in the lower extremities
• Other: occiput-wall distance test and Schober’s test to assess kyphosis and/or scoliosis
References
1. McPhee Si, Papadakis MA. Current Medical Diagnosis and Treatment 2010.
gth
4
ed. McGraw-Hill; 2009.
Lincoln M, McSheffrey G,Tran C, Wong D, editors. Essentials of Clinical Examination Handbook. ed.Toronto:The Medical Society, Faculty of Medicin(
th
6
2.
University of Toronto; 2010
3. Margo K, Drezner J, Motzkin D. Evaluation and management of hip pain: An algorithmic approach. i Fam Pract. 2003;52(8):6
3. 07-1 9.
66 Edmonton Manual of Common Clinical Scenarios Physical Exam

BLOOD PRESSURE MEASUREMENT
Authors: Nathan Hay, Yang Li Brian Sonnenberg MD FRC
MD,
-
Oil Ed.
c+atIon Objective Physical exam video resource:

accurate blood pressure measurement Videos in clinical medicine
To obtain an
Blood-Pressure Measurement
Williams JS, Brown SM, Conlin PR.
physical N EngI J Med 2009; 360:e6 January 29,2009
1 Basics
• Introduce self, wash hands, as for permission to do PE
• ABC’s, °2’ IV, monitors, vitals
2 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
3. EQUIPMENT accurate syphgmomanometer 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.
5. PERFORMANCE:
• While palpating radial artery of same arm, inflate cuff until radial pulse is no longer palpable. the pressure approximately 2mm
Hg/sec until the radial pulse is palpable again, note this pressure then deflate cuff Allow Pt 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 30 mm Hg above the pressure at which the radial pulse disappeared on palpation.
• Slowly ‘i pressure by 2mm Hg/sec and listen for the first time consecutive tapping sounds are heard (Korotkoff sounds). This is the
systolic BP (round to the nearest 2 mm Hg on the manometer). If Korotkoff sounds disappear during inhalation, go up 30mm Hg
and 1’ cuff pressure even slower, allowing at least 1 respiratory cycle / 2mm Hg 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 mm Hg).

• Continue to .1’ pressure and Korotkoff sounds will diminish in audibility, muffle and disappear. Pressure at which sounds disappear
is the diastolic BR If sounds are heard all the way down to 0 mm Hg, point at which sounds muffle should be taken as diastolic BR
Slowly .J pressure at same rate for 10 mm Hg to ensure no further sounds are heard, then rapidly deflate the cuff and remove. After
1 minute, repeat procedure in same arm.
5. RECORDING: Average the two readings and report the final averaged BP as systolic BP over diastolic BR Repeat procedure with opposite
arm.
1. Orthostatic Hypotension: in systolic BP by >20 mm Hg or diastolic BP >10 mm Hg within 3 mm of changing from recumbent to
standing position, indicates blood volume, vascular tone or venous return or abnormal BP reflexes (autonomic neuropathy / BP
drugs)
2. Widened Pulse Pressure: Pulse pressure (Systolic BP- Diastolic BP) 65 mm Hg, indicates t systolic pressure and/or diastolic .
pressure ie. Aortic regurgitation or vasodilatory state

3. Narrowed Pulse Pressure: Pulse pressure 30 mm Hg, indicates L stroke volume or 1. ventricular contraction rate ie. Cardiac
tamponade or other low output
4. Pulsus Paradoxus: Systolic BP disappears on inhalation till much lower BP reached. Pressure when Korotkoff l’ audible on
xhaIation Pressure when Korotkoff audible throughout respiration> 10mm Hg ie. Increased work of breathing (classic for cardiac
-
mponade> pericardial constriction)
1. LeBlorid RF, Brown DD, DeGowin RL,”Chapter 4. Vital Signs, Anthropometric Data, and Pain” (Chapter). LeBlond RF, Brown DD, DeGowin RL: DeGowin’s
Diagnostic Examination, 9e: http://www.accessmedicine.com.login.ezoroxy.Iibrary.ualberta.ca/content.asox?alD=3658971 .google
2. Canadian Hypertension Education Program Recommended technique for measuring blood pressure [Internet] Blood Pressure Canada. [updated 2010,
accessed 2010 Sept. 5]. Available from: htto://hvoertension.ca/chep/recommendation-tables/#tablel

CRANIAL NERVE EXAM
20!! Ed. Authors: Michael Driedger, Usho Ramanthan MD, George EllekerMO FRCP
OriginalAuthors: Victoria Lam, Jason WeatheraldMD, RahitMougdilMD PhD
Station Objective
To demonstrate abnormal cranial nerve findings in order to localize possible lesions
Basics
1. Introduce yourself
2. Wash hands
6.
3. ABC, IV, °2’ monitors, vitals
4. Ask for permission to PE
Table 1: Cranial
I II Ill IV V VI VII VIII IX X XI XII
Olfactory Optic Oculomotor Trochlear Trigeminal Abducens Facial Vestibulococh. 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
7,
Physical
CN I(Olfactory, sensory only smell)
-
• Smell test with one nostril closed (use cloves, peppermint oil or coffee beans). Get Pt 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
2. CNII (Optic, sensory only 4 vision)
• Visual acuity (use best corrected, Snellen eye chart)
• Visual Fields (4 quadrants, arms length away) tested by confrontation. If patient cannot do that then finger movement and if not 8.
that, then light stimulus
• Lesion anterior to optic chiasm 4 ipsilateral monocular visual loss
• Lesion at optic chiasm 4 bitemporal hemianopsia
• Lesion posterior to chiasm 4 homonymous hemianopsia (contralateral)
• Fundoscopy
• Colour test (optic neuritis can have red desaturation)
• Pupillary light reflex (afferent is CNII): Marcus Gunn pupil (relative afferent papillary defect (can be due to optic neuritis)
3. CN lll/IV/Vl (Oculomotor/Trochlear/Abducens, motor only 4 eye movements):
• “LR6SO4” rule, other movements are CN Ill
• Inspection:
• Pupil size/shape/symmetry, ptosis, alignment, pupillary light reflex (efferent is CNIII)
• accommodation(near response or constriction on attempted convergence), swinging flashlight
• Argyll Robertson pupil (accommodates but does not react to light): sign of syphilis
• Motor:
• Pursuit: follow “H” pattern (the 6 cardinal eye movements), saccadic movement: quick eye movements
• Monocular diplopia in local problem. Binocular diplopia in neuropathy, eye muscle disease. 2.
4. CN V (Trigeminal, sensory V1/2/3, motor only 4 mastication) 3.
• Inspection: 4.
• Atrophy (masseters or temporalis muscles), lateral deviation ofjaw to side of lesion
• Sensory (touch, temperature, pinprick tests)
• Vi forehead
• V2 upper lip/cheek
• V3 lower lip/chin (touch, temperature, pinprick tests)
• Motor:
• Clench teeth (palpate masseter/temporalis)
• Move jaw side to side (pterygoids)
• Open mouth 4 jaw deviates TOWARDS weak side, repeat against resistance
• Reflexes:
• Corneal (afferentVl, efferent VII), N = bilateral blink
• Jaw jerk (afferent V2, efferentV3), pseudobulbar palsy = t response

CN VII (Facial, sensory EAC & anterior 2/3 tongue taste, motor facial expression)
• 5 branches:
• “To Zanzibar By Motor Car” (temporal, zygomatic, buccal, mandibular, cervical)
• Inspection:
• Assymmetry, flat riasolabial fold, mouth droop, involuntary facial movements, retracted eyelid
• SensOry
• Taste on anterior 2/3 of tongue
• Motor ( LMN lesion (Bell’s palsy) affects entire face, UMN is forehead sparing):
• Raise eyebrows (fron tails)
• Close eyes tight (orbicuiaris ocuI,
• Show teeth (buccinator)
• Puff cheeks out forcefully(orbicuiaris oris)
• Tense neck muscles (piatysma)
6. CN VIII (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 Pt flO longer hears sound, place fork close to ear)
• N=AC>BC
• CHL=BC>AC
• SNHL = AC>BC, both conduction 4-
• Weber test (tuning fork on forehead midline)
• N=L&Rhearequally
• Sound localized to one ear (ipsilateral = CHL or contralateral = SNHL)
7. CN lX/X (Glossopharyngeal: sensory posterior 1/3 taste, motor palate elevation /Vagus: motor and sensory swallowing!
- - -
phonation, PS innervation to viscera)

• Motor:
• Pt says “AH” uvula deviates AWAY from lesion, palate falls TOWARDS lesion
-
• Pt drink water to assess swallowing

• Pt says “KA” and “GO” sounds to assess palatal speech
• Sensory:
• Taste to post 1/3 of tongue
• Reflexes:
• Gag absence can be N
-
8. CN Xl (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)
9. CN XII (Hypoglossal: motor only tongue mm)
-
• Inspect:
• Tongue fasciculations, atrophy, midline shift
-
• Motor:
• Stick out tongue (keep stationary) tongue deviates TOWARDS side of lesion (if facial weakness, watch tongue protrusion in
-
relation to front teeth)

• Pt push tongue to cheek
• If speech problems, have pt say”Ma, Ma, Ma”(CNVII),”Ka, Ka, Ka”(CNIX/X),”La, La, La”(CNXII)
References
DeMeyerw. Technique of the Neurological Examination (5th edition) McGraw Hill, 2003
2. Daniel D. Federman, M.D, Elizabeth G. Nabel, MD. ACP MEDICINE: Neurology (VI. Neoplastic Disorders). New York, 2009
3. Hohol Mi. The Neurological Exam: Cranial Nerves., University of Toronto. http://neuroexam.med.utoronto.ca/
4. Bickley LS, Szilagyi PG. Bates’ Guide to Physical Examination and HistoryTaking 9th ed. Philadelphia: Lippincott Williams & Wilkins, 2007.
Physical Exam I Edmonton Manual of Common Clinical Scenarios 69

_______________________________
DIABETIC FOOT EXAM

20?! Ed. Authors:Arabesque Parker, Stephanie Mullin MD, Laure Mereu MD FRCPC
Shoes
1. Is the patient wearing proper footwear? Ir
• Is there ample room for the toes?
• Are there arch supports and a cushioned sole?
2. Inspect inside for stones and sharps
Arterial Ulcer Venous Ulcer Neuropathic Ulcer
Usual Location Along the shins and feet Medial malleolus Pressure points on the bottom of the feet
2
Appearance Red, punched out Hyperpigmented, ragged border Red, often associated with breakdown of a callus
History Very painful Due to venous stasis Tingling, numbness, usually painless
-
F
Inspection
1. Skin
• Be sure to look between toes and along the sole
• Texture dry and atrophic?
—
• Colour 2
• Hair growth
• Calluses, fissures, or cracks
• Necrobiosis lipoidica diabeticorum central reddish brown pigmented plaque with central atrophy (associated with diabetes but
—
not related to diabetic control)

• Diabetic dermopathy thin, atrophic skin with shiny brown spots
—
Screen for Diabetic Neuropathy with 10 g Monofilament
2. Amputations 1. Test the monofilament on the patient’s foot, apply
3. Ulcers enough pressure for the monofilament to bend, 3
• Type: neuropathic, arterial, venous stasis indicating log has been applied
• Any gangrene? 2. Have the patient close her eyes and say yes every time
5. Bony deformity they feel the filament
• Hammer toes 3. Check 10 areas on each foot (one on top and 9 on the
• FIat feet sole of the foot)
• Charcot foot — grossly formed disorganized joint 4. A score of 6/10 indicates loss of the protective
sensation of the foot
Circulation
Screen for Diabetic Neuropathy with 128 Hz vibration
1. Colour tuning fork
2. Temperature 1. Strike the tuning fork and apply it to the patients 5
• Check temperature of each foot, compare to each other sternum to ensure they understand the vibration
3. Pulses present vs. absent, strong vs. weak
—
sensation
• Dorsalis pedis 2. Have the patient close her eyes and indicate both when
• Posterior tibia I they feel the vibration and when the vibration has
5. Capillary Refill stopped
6. Ankle/Brachial Index 3. Begin on the bony prominence on the dorsum of the
first toe, proceed to larger joints if vibration is not
Neurologic sensed
4. After the patient no longer senses vibration, apply
1. Pressure sensation: 10 g monofilament screen for diabetic neuropathy the tuning fork to your own thumb and measure how
2. Vibration sensation: 128 Hz vibration tuning fork screen for neuropathy long it takes for you to no longer sense the vibration.
3. Proprioception: start at peripheral joints, move proximally if A normal response is being able to feel the vibration
proprioception not intact in the hand for up to 10 seconds longer than in the
4. Power: dorsiflexion and plantar flexion patient’s foot, beyond this implies loss of vibration
5. Reflexes sense
References
1. Canadian Diabetes Association. Canadian Diabetes Association 2008 Clinical Practice Guidelines for the prevention and management of Diabetes in
Canada. Canadian Journal of Diabetes. 2008;32.

EXAMINATION FOR LIVER DISEASE
Patricia Lee, VaySelvarajah MD, Clarence Wong MD FRCPCABG ABIM
2011 Ed Authors:
Station Objective
will identify the extrahepatic stigmata of liver disease with physical exam. These physical manifestations present in
In this station you
hepat0cear cholestatic and mixed liver disease.
Basics
1. Etiquette: Introduce yourself and ask for permission to perform physical examination, wash hands
2. ABC, vitals, IV, 02 and monitors
Physical
1. General Approach
• Vitals: is the patient hemodynamically stable, ABCs, febrile?
• Patient’s general appearance: any evidence of weight loss or cachexia, muscle atrophy
• Encephalopathy: orientation to time, person, place, affect
• any L0C, delerium, coma
2. Inspection
Derm: jaundice, spider nevi (especially on chest, back and neck), petechiae, ecchymoses, excoriations from pruritis
HEENT: scleral icterus, check tongue/frenulum for jaundice, parotid hypertrophy (mostly EtOH), fetor hepaticus
Ut
• Hands: palmar erythema, clubbing, Dupuytren’s contractures, Terry’s nails (leukonychia), asterixis
• MSK/Extremities: peripheral edema, proximal muscle atrophy/weakness
• Abdomen: ascites (bulging flanks, everted umbilicus), caput medusa, splenomegaly, external hemorrhoids
• Males: gynecomastia, testicular atrophy, loss of facial/body hair in sex hormone dependant areas
3. Percussion
• Identify liver in RUQ then determine size:
• Percuss upwards from the RLQ along the midclavicular line for liver dullness
• Percuss downwards from chest along the midclavicular line for liver dullness
• Describe liver span and size (normal <12cm)
• Castell’s sign: last rib space on anterior axillary line
• Dullness any time during respiration abnormal or on inspiration (usually should be resonant at all times) indicates
splenomegaly
4. 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
5. Auscultation over liver and spleen
• Bruits, venous hums
6. Special Tests
ien Shifting dullness:
• 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:
• 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
reenburger J. Current Diagnosis and Treatment: Gastroenterology, hepatology and endoscopy. rd

3
ed. New York: McGraw Hill; 2009.

FEMALE GENITOURINARY EXAM
2011 Ed. Authors: Cassandra Hirt, Amanda Aiken MD, Jonathan anke MBB h FR
Station Objective
Perform and talk through the mechanism of the female genital urinal exam.
Common Conditions
Vaginal bleeding/discharge, abd pain, Hx dysmenorrhea/amenorrhea, urinary complaints
History
ID. Age
Periodic health exam
• Amenorrhea, excessive bleeding, dysmenorrhea, abd. pain, vaginal discharge, bacteria/cytological
HPI Discuss specific medical or psychosocial concerns in more detail
RED FLAGS Masses, recent Wt loss, signs or disclosure of sexual assault
PMHx Chronic medical conditions, other concerns
Meds/Allergies OCP, other contraception, HRT
Menstrual cycle: age of menarche, oligo/amenorrhea, cycle/menses length, moliminal Sx
PO&GHx
• LMP/LNMP, Obstetrical Hx, STI testing
PSHx Pelvic surgery, procedures
FHx • Chronic conditions, Ca
Physical Exam
1. General Approach: explain process (especially if nervous or first exam), offer
chaperone, check-in with Pt throughout
• Position Pt: drape mid abd. to knee, table elevated 30 degrees, feet in foot-rest, ov,y
slide down till buttocks at edge of exam table (ensure eye contact with pt and
have Pt position self)
2. General Exam: looks for hirsutism, acanthosis nigricans, anorexia signs
3. Abdominal Exam: masses, hernia, ascites, pain
4. External Exam:
• Assess sexual maturity, tanners staging
• Inspect: mons pubis, labia majora/minora, urethral meatus, clitoris (>1.5 cm), Uflflry Introit
vaginal introitus, and perianal region P,ianaIRon VinaI IfltrO,to,
• Note: inflammation, lesions (including nevi, ulcers, pustules, warts),

swelling, tenderness, signs of trauma (bruising, lacerations,...), atrophic
skin change or discolouration
5. Internal Exam:
• Warm and insert speculum (can use lubricant, ensure proper size to not cause discomfort)
• Check cervix location, colour, surface mucosa, cervical os and fix speculum in place
• Inspect for ulceration, lesions, masses, dysplasia, bleeding or discharge
• Pap Smear (see section 112) and collection of swabs (if appropriate)
• Remove speculum: assess the support of the vaginal wall (note any cystocele or prolapse) and avoid pinching
6. Bimanual exam:
• Lubricate index and middle finger and gently insert fingers (only insert index if have pain or never had vaginal delivery)
• Note any cervical motion tenderness or masses of vaginal wall
• Palpate cervix: shape, mobility, tenderness, regularity
• Palpate the uterus: using other hand palpate umbilicus and move down to pubis, press into abd and elevate cervix ant. pushing
the uterus between both hands.
• Note masses, nodules, shape, size and mobility, identify any tenderness. Assess retroversion/anteversion.
• Palpate ovaries/adnexa: place abd hand on the lower quadrant and the corresponding lateral fornix
• Feel for size, shape consistency mobility and tenderness, repeat for both ovaries
7. Pelvirectal Exam
• Withdraw middle finger, tell patient, verify consent
• Introduce middle finger into rectueel for masses and assess post vaginal wall
References
1. New England Journal of Clinical Medicine: Pelvic Exam, June 2007

HAND EXAM Hollie Power, Regan Guilfoyle MD, Michael MorhartMD FRCSC
2011 Ed. Authors:
Station Objective
perform a focused physical examination of the hand. COMMON HAND DEFORMITIES
• Bouchard and Heberden’s nodes: bony
enlargement of PIP & DIP joints in OA
General approach • Boutonniere deformity: PIP in flexion, DIP
• ABC’S, vitals, general appearance of the patient hyperextended
• Expose hands, forearms adequately (remove splints, casts, dressings etc.) • Claw hand: hyperextension of MCPs and
• Shoulder relaxed, elbow flexed at 900 flexion of the PIPs and DIPs
• Dupuytren’s contracture: flexion deformity
at MCPs, IPs with nodular thickening of
Inspection palmar fascia; palmar pits, knuckle pads
• Posture / resting cascade of the hand; compare with opposite hand • Mallet finger: DIP held in flexion; inability
• Skin: bruising, erythema, hair, pallor, rashes, lacerations, scars to actively extend
• Nails: clubbing, infection, leukonychia, onycholysis, pitting, splinter hemorrhages • Swan neck deformity: PIP hyperextended,
• Joints: swelling, dislocation, subluxation DIP in flexion (many causes)
• Deformities: see box • Uinar deviation of MCPs (RA)
• Other: muscle atrophy, masses (eg. ganglion cyst)
a
I
Palpation — Median
nerve 4.
i. Vascular
• Palpate radial and ulnar pulses
• Assess temperature of the skin, capillary refill (should be ‘-2-3 sec)
2.
•
Joints
•
Perform Allen’s test
Palpate individual MCP joints for pain, swelling, deformity, instability (2 Ulnar
rerve
I ..
Radial
nerve
Ulnar
nerve
finger method)
• Palpate IP joints using the 4 finger method to check for ballottement
3. Motor function Figure 1: Dermatomes in the hand
• Assess strength of intrinsic and extrinsic muscle groups (see Table 1) SPECIAL TESTS
• Assess grip strength • Allen’s test: to assess collateral blood
4. Sensation (see Table 1 and Figure 1) supply to the hand
• Assess sensation of median, ulnar and radial innervated territories • Finkeistein test: to assess for DeQuervain’s
• Assess 2-pt discrimination on pads of fingertips (normal —2-3mm) tenosynovitis
5. Soft tissue • Phalen’s /Tinel’s sign: to assess for
• Palpate soft tissues for any masses denervation
6. Tendons
Palpate for fibrosis, nodules, tenderness
Range of motion
• 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 out your 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
Table 1: Screening exam for peripheral nerve function in the hand
NERVE SENSATION EXTRINSIC MOTOR FUNCTION INTRINSIC MOTOR FUNCTION
Finger tip of index finger With palm facing up, point thumb to ceiling
Median Flexion of DIP on index finger (FDP)
(D2) (APB)
Ulnar Finger tip of little finger Abduction of index finger (FDI)

Flexion of DIP on little finger (FDP)
(D5)
Radial Dorsal first webspace (Dl) With palm facing down on table, extend None
thumb toward ceiling (EPL)
1.
References
Janis JE. Essentials of Plastic Surgery. St. Louis: Quality Medical Publishing; 2007.
2. Bickley LS. Bates’guide to physical examination and history taking. 1 edition. Philadelphia: Lippincott Williams & Wilkins; 2009.

HEENT EXAM J
201? Ed. Authors: Michael Driedger, Usha Ramanthan MD, George EllekerMD FRCP 20
Station 0 jective
To identify the signs and symptoms associated with HEENT lesions
To
Physical
1. Basics: Introduce yourself, ask permission to do PE exam and wash hands. ABC, °2’ monitors, vitals p
1. Head
Inspection
• Examine head for symmetry, size, shape, contour, masses, involuntary movements and proportion to neck and rest of body
• Hair: quantity, texture (fine-hyperthyroidism, coarse-hypothyroidism), distribution and pattern of hair loss
• Scalp: redness and scaling (seborrheic dermatitis, psoriasis, pilar cysts) lumps, lesions, scars and nits
• Facial appearance and expression at rest/during conversation. Assess colour, condition, lesions, scars, pigmentation, or hair
• Palpation
• Palpate scalp and skull for masses or tenderness (e.g. traumatic deformities of skull or muscular tenderness from tension HA)
• Examine temporal arteries for thickening, tenderness, or absent pulse in temporal arteritis
2. Eyes
• Visual Acuity: test at 20 feet with Snellen eye chart. Check need for vision correction (screen for myopia, presbyopia, or blindness)
• Visual Fields 2.
• Test by confrontation (begin screening in temporal lobes because most defects involve these areas)
• 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 ¼ field bilaterally)
• Inspection
• Observe eyes for position/alignment. Inspect eyebrows, eyelids, lacrimal apparatus, conjunctiva, sclera, cornea, lens and iris.
• Inspect the size, shape and symmetry of pupils. Examine the pupillary reaction to light. Assess EOM (CN5 Ill, IV, VI)
• Ophthalmoscopic Examination (examine opti disc, physiologic cup, arterioles, veins, macula and fovea)
• From 15 inches away and 15 lateral to patients line of vision, shine light beam on pupil and locate the red reflex, absence
suggests opacity of the lens (cataract) or the vitreous, or detached retina, retinoblastoma (in children)
3. Ears (examine auricle for size, position and symmetry. Note tissue deformities, lumps, inflammation, discharge or any skin lesions)
Otitis media • Red bulging tympanic membrane, lose landmarks. May have pain at mastoid bone
Otitis externa • Swollen, moist, pale/reddened and tender canal (if chronic, canal is often thickened, red, itchy)
• The tug test (movement of auricle and tragus) is painful in acute otitis externa
Serous effusion • Amber color behind TM, may visualize air bubbles
Retraced eardrum • Drum pulled medially, sharply outlined malleolar folds, protruding short process, short/horizontal malleus
handle
4. Nose
• Inspect anterior/inferior surfaces for asymmetry/deformities. Examine patency of nostrils by pressing ala nasi while pt sniffs
• Examine mucosa for swelling, bleeding, exudate, ulcers or polyps (note: nasal mucosa is somewhat redder than oral mucosa)
Reddened and swollen mucosa indicates viral rhinitis. May be pale, blue or red in allergic rhinitis
• Nasal septum deviation, inflammation, or perforation. Lower anterior portion common source of epistaxis
—
• Frontal and maxillary sinus palpation and transillumination tenderness (with pain, fever, nasal discharge) suggests acute
—
sinusitis. Absence of glow on one or both sides suggests thickened mucosa or absence of the sinus
5. Throat (for inspection, remove any dentures or lipstick)
• Lips: symmetry, colour and moisture. Note any ulcers, cracking, scaling or masses
• Oral mucosa (employ use of light and tongue blade): examine for colour, ulcers, nodules or white patches
• Gums/teeth: Examine gums for inflammation and the gingival margins/interdental papillae for ulceration/swelling. Inspect teeth
noting abnormalities, missing teeth or discolouration. Inspect hard palate for color and form
• Tongue and soft palate (palpation of tongue may be indicated if male and over age 50 with Hx of smoking and alcohol)
• Ask patient to stick out tongue (test for CN XII) and inspect for symmetry
• Examine all sides of tongue and floor of mouth where most cancer develops. Note any ulcerations, redness or white areas
-
• Pharynx R
• Examine uvula when Pt saying “ah”or yawning. Soft palate should rise symmetrically (test of CN X) and uvula stay mid-line
• Examine the anterior/posterior pillars, tonsils and pharynx. Note the colour, symmetry, swelling, exudates, or ulcerations
Refe ences
Bickley LS, Szilagyi PG. Bates’guide to physical exam and history taking. 10 ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams and Wilkins; 2009
University of Virginia, school of medicine [Internet]. HEENT exam; 1998-2005. [cited Sept 10,2010). Available from: http/fwww.med-ed.virginia.edu/.
ourses/poml /pexams/HEENT/

JUGULAR VENOUS PRESSURE (JVP) EXAM
Debra] Das, Olga Toleva MD, Michael Tjandrawidjaja MD, Paul W Armstrong MD FRCP
201 Ed- Authors:
-
Station Objective
a-systematic approach to the Jugular Venous Pressure (JVP) physical exam
To develop
physical
General Approach
• Check vitals BP, HR, RR, Temperature, Sa02 and overall appearance of patient
—
• Introduce yourself, ask patient for consent, drape patient appropriately, and wash hands thoroughly
Use of tangential lighting will ensure the best results for the JVP exam
• Normal jugular venous pulse contains 5 important components;
• “a wave” represents atrial contraction
• “x descent” represents atrial relaxation and descent of the base of the heart
• “c wave” represents closing of the tricuspid valve
• “v wave” represents atrial filling
• “y descent” represents opening of the tricuspid valve
Inspection
• Begin by lying the patient down at a 45-degree angle and turning the patient’s head slightly to the left
You will be looking for the Right Internal Jugular Vein (IJV), which usually provides the best and most direct access to right atrial
pressure. The IJV runs between the two heads (clavicular and sternal) of the sternocleidomastoid muscle
• The carotid artery lies adjacent and medial to the IJV and it is important to distinguish the carotid pulse from the JVR It may be
useful to palpate the left carotid pulse using your thumb while observing the right neck allowing you to time the JVP pulsations
with respect to that of the carotid. With this technique in patients with sinus rhythm, you should expect to see the JVP a-wave
followed by the palpable carotid pulse followed finally by the JVP v-wave
• Key features of the JVP include:
• JVP is usually not palpable
• JVP is usually occludable with pressure at the base of the neck
• JVP has multiple waves as opposed to the single outward wave of the carotid pulse
• JVP varies with respiration (decreases with inspiration) and varies with body position/incline
• JVP varies with the hepatojugular reflux (see below)
• Using a ruler vertically placed above the Angle of Louis, estimate how high in centimeters the JVP pulsation rises. The Angle of
Louis is also referred to as the Sternal Angle and is continuous with the second rib and below the manubrium. If you cannot find
the top of the JVP, it could be either too low or too high. Depending on whether the JVP is low or high you may need to reduce
(lay down) or increase (sit up) the patient incline respectively to be able to observe the height of the JVP.
• Add 5 cm to the height in cm for the JVP pulsation since it is estimated that the right atrium lies 5 cm below the Angle of Louis.
• Example: If the top of the JVP was 2cm above the Angle of Louis then the JVP for this patient would be 7cm (2 cm ÷ 5 cm). A
JVP between 7-9 cm is considered normal
• An elevated JVP is a direct reflection of elevated right atrial pressure and an indirect measurement of left ventricular end diastolic
pressure (correlates approximately 80% of time). Common causes of an elevated JVP include heart failure (both right and left
ventricular failure), constrictive pericarditis, and cardiac tamponade
3. Special Tests/Observations
• Hepatojugular Reflux also known as the abdominojugular test is often completed in conjunction with the JVP exam. Apply
- -
pressure of approximately 20-30 mmHg over the abdomen (usually right upper quadrant) for 10 seconds while observing the JVP.
A normal response is a transient rise of the JVP followed by a decrease back to baseline. An abnormal response is a sustained rise
in the jvP over the entire 10 second period. An abnormal hepatojugular reflux suggests reduced compliance of the right ventricle
and correlates with an elevated left ventricular end diastolic pressure
• In normal patients in sinus rhythm, the a wave is usually larger than the v wave. An absent a-wave is seen in patients with atrial
fibrillation. A prominent v wave is seen in patients with tricuspid regurgitation
• If you cannot detect the right IJV it is possible that it is occluded from prior intervention. Before reporting it as not seen be sure to
inspect the left IJV using the strategy above
References
Applefeld MM. The Jugular Venous Pressure and Pulse Contour. Clinical Methods: The History, Physical, and Laboratory Examinations htto://www.ncbi.
-
t1i!flhiib,oy,cgi?bookcm&DartA622

_________________________________________________________________________________________
________
_________
__________ _____
______ _____ ______ _____ _____ _____
KNEE EXAM MD, PhD, FRCS(C)

2011 Ed. Authors: BabokMoghdoori, KhaledAI-MonsooriMD, NodrMiomho
Station Objective
To conduct an examination of the knee including inspection, palpation, range of motion, joint stability, and special tests.
Physical
1. General Approach as above (compare bilaterally and examine hip, ankle and back):
2. Inspection:
• Gait: a normal gait is smooth and rhythmic; inspect upon Pt entry
• Carefully observe for any compensatory moves-pain/instability
• Swelling: 4- in med/lat hollow around patella
• Erythema
• Atrophy: quadriceps, measured 10 cm above patella
• Deformity: alignment (valgus/varus/recurvatum), symmetry
• Skin: warmth, scars, lesions, wounds, and discoloration 2
3. Palpation: tenderness, effusion wipe, ballotment, swelling, temperature, crepitation, popliteal fossa Van,,
4. Joint stability (Grade I laxity = 3-5mm translation, Grade II = 5-10mm, Grade Ill = >10mm):
Test Performance Results/Evaluation
Integrity of MCL • Hold pt’s ankle with one hand, other hand on lateral • Asymmetrical opening medially-laxity
Medial stability in aspect of the knee. A force is applied from the ankle with . Laxity often due to ligament injury on
extension (Valgus stress). the hand at the knee as a fulcrum (valgus stress) -test in medial side and/or femoral-tibial wear
full extension and 30° flexion (pseudolaxity). 3
Integrity of LCL Hold Pt’s heel with one hand, other hand hold medial Asymmetrical opening Iaterally->laxity
Lateral stability in side of the knee and acts as a fulcrum (varus stress) • Laxity often due to lateral hg injury and/or
extension (Varus stress) - test in full extension and 30° flexion femoral-tibial wear (pseudolaxity)
Integrity of ACL Pt supine, knee flexed 30°, heel resting on stretcher
.-. • Soft endpoint or t anterior translation
Anterior stability (Lachman Secure thigh with one hand and apply anteriorly indicative of tear
test) directed force to proximal calf from posterior 1.
Integrity of PCL Pt supine, knee 70-90° flexion. Palpate medial tibial step . Loss of medial tibial step-off or 4” posterior
Posterior stability off Apply posteriorly directed force on proximal tibia translation indicates injury to PCL 2.
(posterior drawer test)
3.
5. Active and passive range of motion tests:
Test Performance Normal Results/Evaluation
Active flexion Pt supine with legs extended. Request knee flexion, measure Evaluates hamstring muscle control around
angle with goniometer and distance of heel from buttocks knees as well as structural integrity
Passive flexion Apply gentle pressure to max flex without pain Evaluates structural integrity N—i 35°
—
Active extension Pt sits on the edge of examination table with knee flexed. Evaluates quadriceps muscular control and 4.
Request knee extension and measure structural integrity
Passive extension Apply gentle pressure to max extend without pain Evaluates structural integrity N ‘0-5°
—
6. Special Tests:
Test I Clinical Association Performance Results/Evaluation
McMurray Meniscal pathology Pt supine, knee fully passively flexed then +ve test includes palpable or
passive rotatory pressure while flexing/ auditory click with tenderness along
extending knee and palpating medial/lateral joint line
joint lines
Patellofemoral grind Chondromalacia Pt. supine, push patella into trochlear groove, Pt Irregular movement/crepitation
patella, osteoarthritis to tighten guads • atellofemoral articular • atholo’
Apley’s grind Meniscus pathology Pt. prone with knee flexed to 90° followed by +ve test indicated by pain
axial loading and rotation
Apprehension test Dislocating patella Pt supine with knee flexed 20-30°. Apply lateral +ve if Pt becomes apprehensive
force to medial_edge of patella (and vice versa) with feelin’ im.endin. dislocatiOfl
R
References
1. Hoppenfeld 5, Physical Examination of the Spine and Extremities. 1 ed. Prentice-Hall; 1976. 2
2. McRae R, Clinical Orthopaedic Examination. 6
th
ed. Churchill Livingston Elsevier; 2010.
3.
4.

LYMPHADENOPATHY AND SPLEEN EXAM
Todd Penney MSc, Henry Conter MD, Ryan Cooper MD MPH FRCPC
2011 Ed. Authors:
inaIAuth0r5ma Tram, James Yeung MD, Matthew Wang MD CCFP
Station Objective
may be asked to obtain a relevant history and physical exam in a patient with swollen lymph nodes (often benign) or
In this station, yO
p5 lenOmegalY (often pathologic) and to differentiate benign from pathologic causes.
1. Diagnostic Criteria
• LymphadenOpathy: generalized or localized palpable lymph nodes> 1 cm in size, fixed, firm/rubbery
• Splenomegaly (spleen is not normally palpable): palpable spleen, + Castell’s sign/Traube’s space tests, abdominal U/S or CT
shows large spleen
• Associated with regional or localized lymphadenopathy differential diagnosis is broad and includes infection in tissues drained
-
by that lymph node group, lymphoma, TB, metastatic cancer/neoplasia, EBV

• Associated with generalized lymphadenopathy systemic infections (typhoid fever, HIV, EBV, syphilis, etc.), medications, SLE,
-
sarcoidosis, 2° to liver disease, etc. There are many other causes.

• Associated with splenomegaly alone: hematologic disorders (ITP, AIHA), infective endocarditis, chronic inflammation, etc.
• Note: there are many other causes (the Ddx, especially for mild splenomegaly, is very broad)
• Massive splenomegaly has a shorter differential Dx: visceral leishmaniasis, CML, tropical splenomegaly syndrome, shistosomiasis.
• Malignancies such as lymphoma or metastatic cancer, infections causing systemic organ failure, advanced liver disease/portal
hypertension
Physical
1. General Approach
or • Ask about substantial unintentional weight loss, look for signs of wasting (temples, thenar area of hands)
2. Inspection
• Diaphoresis, bruises, mucosal bleeds, lymphedema, pallor, jaundice, visibly enlarged spleen/lymph nodes
3. Percussion
• Spleen (in addition to below, percussion for Nixon’s sign can also be done)
• Castell’s sign: percuss the 1 Qth intercostals space on patient’s left side continuously while patient breathes deeply. If percussion is
dull, test is positive for splenomegaly (dull sound usually found on inspiration)
• Traube’s space: landmark the triangle bordered by 6 th
rib, left costal margin and AAL. Percuss space while patient breathes
deeply. If any dullness is found, splenomegaly should be suspected
4. Palpation
• Spleen: +ve for splenomegaly if splen is palpated at any time
• Stand to the right of supine patient, place left hand underneath patient’s left thoracic rib cage, 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
• 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
• When left costal margin is reached, dig deep under the costal margin gently with right hand and ask patient to inspire to feel
the spleen tip (notch) move against fingers
• Lymph nodes (locations: axillary, epitrochlear, supraclavicular, scalene, inguinal, popliteal) Palpate lymph nodes by moving pads
-
of fingers in a circular motion. At first, palpation should be light and then progress to deep. When palpating the nodes, note
location, number, size C> 1-2 cm = abnormal), shape (irregular border = abnormal), mobility (immobile = abnormal), consistency
(non-soft = abnormal), tenderness (tender = abnormal). Virchow’s node: important node in L supraclavicular space that, when
palpable, suggests metastases from upper abdomen
5. Auscultation
• Spleen: place stethoscope on L costal margin at the AAL and listen for friction rubs on inspiration
References
1. Grover SA, Barkun AN, Sackett DL. The rational clinical examination. Does this patient have splenomegaly? JAMAl 993 Nov 10; 270(18): 2218-21
2. LeBlond RF, Brown DD, DeGowin RL, “Chapter 5. Non-Regional Systems and Diseases” (Chapter). LeBlond RF, Brown DD, DeGowin RL: DeGowin’s
Diagnostic Examination, 9e: http://www.accessmedicine.com.loain.ezoroxv.librarv.ualberta.ca/content.asox?aID=365931 0.
3. Hui D, Padwal R, editors. Approach to Internal Medicine: a Practical Guide to Clinical Problem Solving. 2
nd
Edition.
Filate W, Leung R, Ng D, Sinyor M. Essentials of Clinical Examination Handbook, sth ed. University of Toronto Medical Society, 2005.
• Armitage, j. Goldman: Cecil Medicine, 23 rd ed. Elsevier, 2007.

MALE GENITOURINARY EXAM
201? Ed. Author5: Babak Maghdoori, Phil Bach MD, Darcie Kiddoo MD FRCSC
Station Objective
To examine, assess, and manage the male genitourinary system in an organized, systematic, and coordinated manner.
Physical
1. General Approach
• Genitalia inspection, palpation for genital, inguinal and testicular pathology, and digital rectal exam
2. Genital inspection (ensure that gloves are being worn at all times)
• Inspect the penis;
• Tanner staging (pubic hair pattern, testicular size)
• Prepuce (foreskin): phimosis, paraphimosis
• Glans and the urethral meatus
• Presence of chancres, sores, warts, ulcerative/exophytic lesions, and growths)
• Hypospadias, epispadias, or meatal stenosis
• Discharge (usually due to gonorrhea)
• Inspect the scrotum for any swelling: hydrocele, tumour, varicocele
• Evaluation/classification of some commonly seen 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
3. Genital 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
torsecl
• Palpate the testicles and epididymis for any swelling (hydrocele,spermatocele, tumour) and tenderness (testicular torsion,
appendix testis, epididymitis, or orchitis)
• 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 tumour)

-
• 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
4. 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)
5. DRE
• Have patient standing and bent over the examining table or with the patient in the knee-chest position
• Place single gloved, lubricated, finger towards the anterior aspect of the patient palpate for the enlargement, tenderness,
-
texture, and softness/hard ness of the gland

6. Special tests:
the
• Prehn’s sign: Traditionally used to distinguish between testicular torsion (a surgical emergency) and epididymitis. Lifting
in
affected testicle results pain relief in epididymitis , but not in torsion.
torsion.
• Cremasteric reflex: Swipe the medial thigh to see if the ipsilateral testicle elevates. Can be absent in testicular
References
1. Orietn JM., Sapira’s Art and Science of Beside Diagnosis,
th
4 Edition, Wolters Kluwer/Lippincott Williams and Wilkins; 2010.

PRECORDIAL EXAM Olga Toleva MD, Michael Tjandrawidjaja MD, Paul W Armstrong MD FRCP
Ed. Authors: Oebraj Das,
.
Station Objective
standardized approach to the precordial physical examination
To develop a
physical
General Approach
o Check vitals BP, HR, RR, Temperature, 5a02 and overall appearance of patient
—
o Introduce yourself, ask patient for consent, drape patient appropriately and wash hands thoroughly
2. Inspection
• Check for any chest wall deformities (e.g. asymmetry) or surgical scars (e.g. sternotomy)
• check patient for any visible heaves or lifts and inspect apex visually
3. Palpation
• Note: Often unrewarding supine and must be undertaken in left lateral position for maximal information
• Palpate for apical impulse normally located at 4
—
sth
intercostal space at midclavicular line. Comment on size of apex (should be
no larger than a quarter), location (lateral displacement usually indicates enlarged left ventricle), quality (double, heaving, quiet)
and duration (sustained apex suggests left ventricular hypertrophy).
• Palpate for abnormal impulses or thrills at each valve location
-
o Palpate for left parasternat heave with heel of hand (suggests of RV overload or hypertrophy)
o Palpate for epigastric/subxiphoid impulse of either RV origin (impulse is directed caudally U C
-
and hits the side of your fingers) or aortic origin (impulse hits your fingers from beneath)
• Valve locations are as follows (refer to diagram): -Trispid
• AV located at 2
—
nd intercostal space right of the sternum
• PV— located at 2 nd intercostal space left of the sternum
—• TV located at the
— intercostal space left of the sternum
• MV located at the 5
—
th
intercostal space at the mid-clavicular line
4. Ausèultation
o Appropriate use of diaphragm for high pitched sounds and bell for low pitched sounds is key
• Diaphragm: Assess the presence, volume, timing, and character of Si and S2. Si is produced from the closure of the mitral and
tricuspid valves while 52 is produced from the closure of the aortic and pulmonary valves. Normally Si is louder than S2 in the
mitral and tricuspid regions whereas the S2 is louder than Si in the aortic and pulmonary regions. The S2 normally splits on
• inspiration with the softer pulmonary valve closure sound (P2) occurring after the louder aortic valve closure (A2).
• Diaphragm: Loud Si (associated with mitral stenosis as long as not severe), soft Si (severe mitral stenosis), loud P2 (pulmonary
hypertension), wide splitting of 52 (pulmonary hypertension, RBBB), fixed splitting of 52 (associated with ASD), paradoxical
splitting of S2 (LBBB, severe aortic stenosis).
• Bell: 53 (ventricular gallop) occurs at the beginning of diastole and is abnormal in most adults indicating left ventricular failure
and/or volume overload. RV S3 at lower left sternal border evident and augmented by inspiration. 53 can be normal in children,
‘adolescents, and pregnant women.
o Bell: S4 is a pre-systolic sound that is always pathological and is associated with atrial contraction into a hypertrophied ventricle at
the end of diastole.
o For murmurs note the location, timing (systole vs. diastole), character, intensity, and radiation
• Murmur intensity:
• Grade 1: barely audible (softer than S1/S2)
• Grade 2: audible and constant (same intensity as S1/S2)
• Grade 3: loud with no palpable thrill (louder than 51/52)
• Grade 4: loud with thrill (louder than S1/S2)
• Grade 5: heard with the stethoscope just touching the chest
• Grade 6: heard with the stethoscope off the chest
• Auscultate carotids for bruits and for radiation of the murmurs of aortic stenosis and mitral regurgitation
References
Felner JM. An Overview of the Cardiovascular System. Clinical Methods:The History, Physical, and Laboratory Examinations http://www.ncbi.nlm.nih.
-
2. Sorrentino A. & S. Baldwin. Heart Murmurs. Harwood-Nuss’ Clinical Practice of Emergency Medicine 4
th
edition http://www.msdlatinamerica.com/
-
ebooks/HarwoodNu5sClinical%2oracticeomergencyMedicifle,5id1 11621 2.html

1.
NEUROLOGICAL EXAM
Ta
2011 Ed. Authors: Michael Driedger, Usha Ramanthan MD, George EllekerMD FRCP
OriginalAuthors:Aaron Knox
Station Objective
To identify an abnormality in the nervous system and to differentiate CNS from PNS lesions
Physical
1. Motor System (as you assess motor system focus on pts body position, involuntary movements, muscle bulk/tone) 2.
Table 1: Motor System Ta
Action I Muscles I Nerves I Roots
Upper Extremity
Arm abduction Deltoids Axillary C5/C6
Elbow flexion Biceps Musculocutaneous C5/C6
Elbow flexion BR Radial C5/C6
Elbow extension Triceps Radial C6/7/8 —
Wrist flexion FCR Median C6/7 —
Wrist extension ECRB Radial C5/C6

Wrist ulnar deviation FCU Ulnar C7/8iTl
Wrist radial deviation ECRL Radial C5/C6
Flex PIPJ D2/3/4/5 FDS Median C7/C811
Flex PIPJ D2/3 FDP D2/3 Median C7/C8
3.
Flex PIPJ D4/5 FDP D4/5 Ulnar C7/C8
Ta
Ext D2J3/4/5 ED, El, EDM Radial (PlO) C7/C8
D2/3/4/5 adduction Palmar 10 Ulnar C8/T1
D2/3/4/5 abduction Dorsal IC, ADM Ulnar CS/Ti
Dl opposition OP Median C81fl
Dl adduction/flexion MCPJ AdP tJlnar C8,Tl
Dl abduction/extension MCPJ AbPL Radial (PlO) C7/C8
Dl abduction (palmar) AbPB Median C8/Tl
Lower Extremity
Hipflexion IP Femoral, Ll/2/3 roots Li/2/3/4 —
Knee flexion Hamstrings(ST, SM, BF) Sciatic L5/S1/2

Knee extension Quads Femoral L2/3/4
Led adduction OE, AdL, AdM, AdB, Gracilis Obturator L2/3/4 Ta
Leg abduction Gmed, Gmin, TFL Superior gluteal L4/5/Sl
Foot dorsiflex TA Deep peroneal L4/5
Foot plantarfiex Gastrocs, Soleus Tibial Si/2__.
Foot inversion TP Tibia I nerve L4/5_..
Foot eversion PL, PB Superficial peroneal L5/S1__.
Toe dorsiflex EHL, EDL Deep peroneal L5/S1_
Toe plantarfiex FHL, FDL, FDB Tibial (m plantar nn) 51/52 p
Table 3: UMN vs LMN

Table 2: Grading Power
UMN ULN
Grade
Power UE flex> ext and LE ext > flex 7absent
0 No contraction
Tone Spastic Flaccid
1 Fasciculations 3.
2 Horizontal only DTR f
4.
3 Against Gravity Plantars ft 41
Fasciculation Absent ±
4 Against resistance
Atrophy Late Early
5 Normal strength

1. Reflexes
Table Deep Tendon Reflexes
4
Root TableS: Grading Reflexes
jicestendoEE C5/6 Grade
C516 0 Nil
jptendo C6/Z/8 1 Low normal
jteIlartend0!L L2/314 2 Normal
Achilles tendon Si /2 3 High normal
ans sin Corticospinal 4 Clonus (>3 beats)
nski’s sin CorticosDinal (L5/Si)
2. Sensory
Table 6: Dermatome Landmarks
Root Anatomical landmark Root Anatomical landmark
€2 Occiput Ti0 Umbilicus
€3 Neck T12 Pubic bone
€4 Lower neck / Supraclavicular Li Inguinal ligament
€5 Lateral upper arm L2/L3 Thigh
€6 Thumb L4 Knee, medial foreleg
€7 Index/long finger L5 Big toe, dorsum of foot
€8 Little finger Si Heel, lateral foot
T4 Nipples S2/3 Genitals
T5 Inframammary fold S4/5 Perineum
16/’7 Xyphoid process S5 Anus
3. Localizing the lesion

Table 7: Localizing a CNS Lesion
Lesion location Motor Sensory DTR
Chronic contralateral UMN weakness
Cerebral Cortex UE: arm flex > ext Contralateral sensory loss in limb/trunk t
LE:_pflex>_dflex,_leg_externally rotated
Weakness/spasticity as cerebral cortex + CN deficits
Brainstem
+/-“crossed”cranial_nerve_signs
Variable t
Weakness/spasticityas cerebral cortex
Spinal Cord
Bilateral w bilater damage —÷ paraplegia/guadriplegia
Bilateral deficit at lesion, .L sensation below t
Gray Matter
Bradykinesia, rigidity, tremor Sensation not affected N/
(Basal_Ganglia)
Table 8: Localizing a PNS Lesion

Anterior horn Focal weakness, atrophy, fasciculations Sensation not affected
Spinal roots Root innervated pattern weakness, atrophy, +I fasciculations Corresponding dermatome deficit
Peripheral nerve dist’n-pattern atrophy, weakness . if nerve
Mononeuropathy Sensory deficit in nerve dist’n
fasciculations involved
distal>
Polyneuropathy Symmetrical distal weakness stocking glove distribution
proximal
References
1. Blumenfeld, H. Neuroexam.com. [Online]. 2001 [cited January 14, 2010]; Available from: URL:http://www.neuroexam.com/index.php
2. GeIb, D. The detailed neurological examination in adults. [Online]. October 1St 2009 [cited January 14, 2010]; Available from :http://
WWw.uptodate.com/online/content/topic.do?topicKeygenneuro/2959&selectedTftle=i 1 50&source
3. Brain. Aids to the Examination of the Peripheral Nervous System. 4th ed. Edinburgh: W.B. Saunders; 2000.
4. Bickley LS, Szilagyi PG. Bates’ guide to physical exam and history taking. 10th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams
and Wilkins; 2009.

RESPIRATORY EXAM
2071 Ed. Authors: Darwin Wan BSc, Dr. a n 500 MD, Dr. Dilini Vethanayagam MD FRCP
Station Objective
Perform and demonstrate proficiency with a respiratory physical examination.
General Approach
1. Introduction
• Introduce yourself, ask permission to perform exam, verbalize procedures to ensure understanding
• Tell patient at the beginning you will perform the posterior chest exam, followed by anterior
• Wash hands and disinfect stethoscope
• Ask patients to wear a gown with the back open (females bra off), then cover appropriately during the exam
• Examine peripheral to central (or vice versa), compare side-to-side, do posterior first then anterior
2. General Inspection
• Check ABCs and vitals, note rate, rhythm, depth, pattern (Kussmaul’s, ataxic, apneustic, paradoxical) and work of breathing (pursed
lip breathing, nasal flaring, tripoding), pulsus paradoxus as a sign of diaphragmatic fatigue
• Observe patient without direct eye contact to lessen anxiety
• Check for clubbing, height of proximal nail bed compared with DIP height, Shamroth’s sign, nicotine stains
• Examine hands, lips and mouth for cyanosis (central and peripheral)
• Check the position of the trachea for deviation, cricosternal distance and Hoover’s sign for hyperinflation
• Inspect for accessory muscle use (sternocleidomastoid, platysma, scalene, intercostal indrawing) during inspiration
• Observe at bedside for additional sounds (cough, wheeze, stridor)
• Inspect for barrel chest, traumatic flail chest, pectus excavatum, pectus carinatum, kyphoscoliosis
Posterior Chest Examination

1. Inspection
• Observe the shape and movement of the chest, noticing deformities, asymmetry, impairment, position, retraction
2. Palpation
• Palpate for deformities, lumps, masses, tenderness, pain suggests rib fractures
• Confirm expansion/symmetry during inspiration by placing hands on 10th rib and watching divergence of at least 5 cm
• Feel for tactile vocal fremitus by palpating with ulnar edge of palms, and asking patient to repeat “boy oh boy”
3. Percussion
• Use the middle finger of your dominant hand to strike the middle phalanx of the middle finger on your other hand
• Have patient cross arms in front of chest, then percuss over lung fields, noting flatness, stony dullness (fluid), dullness
(consolidation), resonance (normal lung), hyperresonance (increased air as in COPD or pneumothorax)
• Estimate diaphragmatic excursion by percussing lower lung border in expiration then inspiration (normal is 3-5 cm)
4. Auscultation
• Listen for at least one whole breath in each location, inspiration should be 1/3 of expiration, characterize if prolonged
• Are breath sounds present or equal in all zones? Quantify vesicular, bronchovesicular, or bronchial breath sounds
• Are adventitious sounds present (wheezes, coarse/fine/velrco crackles, pleural friction rub, mediastinal crunch)
• Broncophony(say”ninety-nine”), egophony (say”ee”) and whispering pectoriloquy (whisper”1-2-3”) may be useful if consolidation
is suspected
5. Special Maneuvers
• Forced expiratory time (normal <4 seconds, listen over trachea with patient seated, looking straight ahead)
• Auscultate for wheeze and cough, forced expiration may help”bring out”a wheeze
Anterior Chest Examination

1. Inspection, Palpation, Percussion, Auscultation
• As above, disrobing only as appropriate for females; do not percuss over the breast in females
References
1. Bickley LS, Hoekelman RA. Bates’Guide to Physical Examination and HistoryTaking. 7th ed. Philadelphia: Lippincott Williams &Wilkins; 1999.
2. Jarvis C. Physical Examination & Health Assessment. 4th ed. St. Louis: Saunders; 2004.
3. Munro J, Edwards CRW. Macleod’s Clinical Examination. 9th ed. Edingurgh: Churchill Livingstone; 1995.

THYROID EXAM Mz,e Lees, Simon Turner MD, Gordon Lees MD FRCSC
ii Ed. Authors:
Station Objective
any pathology. To determine whether a neck mass originates from the thyroid gland. To determine the status of thyroid
To determe
the individual.
funCtiOfl of
Examination of the Thyrod Gland

1 Basics
• Wash hands, introduce yourself to the patient, ask permission to do a physical exam
• Patient should be seated or supine with their neck so the area of the thyroid can be seen completely
Inspection of the thyroid region
From the front and side (tangential lighting useful)
• Tip patient’s head back and inspect region below cricoid cartilage for the thyroid
• Inspect with and without swallowing (thyroid cartilage, cricoid cartilage and thyroid gland rise with swallowing then return
to 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)
Common Systemic Signs of Thyroid Disease
1
Hypothyroidism Hyperthyroidism
• Dry, cool, coarse skin • Warm, smooth, moist skin
• Modest weight gain Weight loss
. Myxedema Excessive sweating and heat intolerance
• Cold intolerance • Tachycardia
• Bradycardia • Palpitations
. Periorbital puffiness • Eye signs: lid lag, stare, exopthalamos
• Swelling of face, hands, and legs • Onycholysis
• Dulled expression • Acropachy
• Loss of lateral one-third of eyebrow • Nervousness
Look for:
• Masses, scars, lesions (trauma)
• Atrophy/hypertrophy
• Discolouration
• Swelling
• Deviation from midline
• Muscle bulk/symmetry
• Exopthalamos
• Goiter
3. Palpation
• Note the size, shape, consistency of the gland
• Check for any nodules or tenderness
• Anterior approach: ask patient to turn their head upwards and towards the side being palpated
• With the finger pads of one hand, find the thyroid cartilage & the cricoid cartilage, move inferiorly to find the isthmus (usually
overlies the 4
n
2
r
3
t d/
h
d/
tracheal rings)
• Work laterally into the gutter between the trachea and the sternocleidomastoid muscle to feel one thyroid lobe for masses
• Get the patient to swallow and feel for masses (thyroid should move up). Repeat for other lobe.
• Posterior approach: ask patient to turn their head upwards and towards the side being palpated
• Reach around from behind the patient, with the finger pads of one hand, find the thyroid cartilage & the cricoid cartilage,
move inferiorly to find the isthmus
• Using one hand per lobe, work laterally into the gutters between the trachea & sternocleidomastoid muscles to feel both
lobes for masses. Get the patient to swallow and feel for masses (thyroid should move up). Repeat for other lobe.
4. Auscultation
• Auscultate for bruits using diaphragm of stethoscope (localized or continuous bruit may be heard in hyperthyroidism)
References
Bickley LS, Szilagyi PG. Bates’Guide to Physical Examination and HistoryTaking. 1 Or” ed. Philadelphia: Wolters Kluwer/Lippincott Williams &Wilkins; 2009.
Physical Exam I Edmonton Manual of Common Clirl Scenarios 83

I
EDMONTON MANUAL
In
Section #3 B
INTERNAL MEDICINE S
Section Editor: Vijay Daniels, MD, FRCPC
Assistant Professor
Division of General Internal Medicine S
S
lo
S
d
a
INTRODUCTION 85 Lower Back Pain .140 a
Abdominal Distention, Ascites, Liver Disease 86 Nausea and Vomiting .142
Abnormal Heart Sounds 88 Obstructive Lung Disease .144
Acute Confusion 90 Palpitations and Arrhythmias .146
Allergic Reactions 92 Parkinsons and Movement Disorders... .148 0
Altered Level of Consciousness 94 Peripheral Vascular Disease .150 q
Altered Sensation (Numbness and Tingling) 96 Pleural Effusion .152 U
Anemia 98 Polyarticular Arthritis and Joint Pain .154
Arthritis and Joint (Monoarticular) .100 Protein uria .156
Bleeding Disorders .102 Pruritus .158 di
Chest Pain, Angina and Cardiac Arrest. .104 flCl 101 IQIIUIC .160 (I
Congestive Heart Failure & Edema .106 Respiratory Tract Infection .162 m
Cough .108 Restrictive Lung Disease .164 if
Dehydration .110 Seizure .166 q
rkt .112 Sexual and High Risk Infections .168 0
.114 Shock .170
.116 Skin, Hair and Nails .172
flucnno .118 Sleep Apnea and Insomnia .174 C
.120 Sore Throat (Pharyngitis) .176
.122 Syncope .178 hi
Fatiaue.. 124 Thyroid Disease .180 q
Fever. 126 Unilaterally Swollen Leg .182 b
Gait Disturbance 128 Urinary Incontinence .184
Headache ....130 Vision Loss.... .186 S
Hearing Loss and Deafness ....132 Weakness .188
Herniplegia/Hemisensory Loss. ....134 Weight Gain. .190
y
....136 Weight Loss. .192
Hypertension 138
S
N.B. Not all stations in this section were reviewed by Dr. Daniels S
b
If
all
of
rel
A
a
1.
84 Edmonton Manual of Common Clinical Scenarios j Internal Medicine

INTRODUCTI
paniels, MD, FRCPC
jagn0Si5 Versus Management

that diagnosis is the trickier part to patient care. Once I know someone has heart failure, it’s generally easy to treat.
Internal Medicine, I feel
that this dyspneic patient in front of me has heart failure and not a COPD exacerbation or a pulmonary embolus? That is
3 aut how do I
know
the tricky part.
step 1 - Diagnose the problem

Recognition versus Clinical Data lnterretation
a nostiC Paft1
in rmat0l0gy clinic one day as a resident and I saw a patient with a skin lesion that I thought was either Basal Cell Carcinoma or
i was
squamous Cell Carcinoma. When the Dermatologist entered the room, he took one look at the patient and told me, “This patient has a
g features that led to this diagnosis, his response was, “because it
squamous cell carcinoma:’ When I asked him what were the discriminatin
carcinoma7 This is a classic example of diagnostic pattern recognition and much of dermatology is this way. But
looks like a squamous cell
is more often used by seasoned 1
physicians, comes with time. Those who are reading this have still a long way to go to
such a skill, which
diagnostic pattern recognition and thus you will fall back on what is called Clinical Data Interpretation where you collect the data
develop
in medical school (pre-renal, renal, post-renal for example). To do this, you need either an
and interpret it using the approaches you learned
approach or a differential diagnosis. This may be a bit different than what you learned in your preclinical years.
Iow to Take the History

I with little rhyme or reason. And then
When I was a medical student learning to take histories, I had this large inventory of questions asked
Family History? It dawned on me that not every
one day I came upon a silly realization: why am I asking a 90 year-old patient about his/her
question had to be asked every time. I only needed to ask questions to help me figure out what was wrong with this patient. But if I did not
use my inventory, what was Ito use? The differential diagnosis!
pain; I have a differential
I now approach every patient in real clinical practice with a differential in my head. Patient comes in with chest
diagnosis for that. Dyspnea, got one for that too. And yes, when I did my medical school OSCEs, I once had a differential for amenorrhea
of it now I think pregnancy was on the differential... I think:). The same approach should be taken for the O5CE:
(I remember some —
memorize a differential for each presenting symptom and when you get to the door and read that stem, quickly refresh your memory or
If you can, write it down on a scrap piece paper. Then enter the room and start the detective work. You do not need to have
a list of fifty
questions you ask for dyspnea, you just need to know the common causes and once you think of heart failure, you will know to ask about
orthopnea, PND, etc...
So do need to ask Family History if I do not think it is important?” The one major drawback with an OSCE is that it is scored with a
checklist. Although in an ideal world the focused history or physical examination should get you all of the checklist points, I concede that
the examination is not always written in the ideal fashion. Thus, even if you think they are not important, you should ask the past medical
history, medications, allergies, family history and social history. Whether you do a review of systems is up to you, but I usually feel if a
question is worth asking, ask it in the history of present illness. By taking a focused history, you look organized (which is often worth marks),
but then by always asking the rest of the history, you reduce the change you will miss anything.
Step 2— Find out why the patient has the diagnosis

When you do diagnose heart failure or pulmonary embolus, ask yourself (as you should in real life) “Why does this patient have this?” Then
you might find out the heart failure patient is a heavy drinker and has alcoholic cardiomyopathy or you may find out the pulmonary embolus
patient has B-symptoms and the ensuing work-up reveals cancer.
Step 3— Manage the life-threatening complications

Sometimes this is done before step 2. For example, if a patient were in renal failure with a Cr of 700, I would rather know the potassium level
before you tell me the underlying problem is pre-renal, renal or post-renal because the patient may need emergent interventions.
If you do these three things on the diagnostic stations, which are the tougher stations in my opinion, you will do well on your OSCE. So now
all you need is an approach to the common symptom presentations to reach a diagnosis, and then you will need to know the management
of the common diagnoses encountered. Hopefully this book will help with those.
One final warning: be careful with using diagnostic pattern recognition as it can mislead you. When I did my LMCC Part II, there was a
station that somehow led all of us to think the patient was in diabetic ketoacjdosis (the stem was Type I diabetic, confused, with a rapid
respiratory rate). We all went in ordering insulin boluses and IV fluids and at some point in the station asked for the glucose level. It was 1.5.
And then we all slammed on the breaks and started pushing D5OW and began to figure out why this patient was hypoglycemic. Sometimes
a past experience can mislead you so always fall back on your standard approaches / differential diagnoses.
Good luck!
1. Williams RG, Kiamen DL, Hoffman RM. Medical student acquisition of clinical working knowledge. Teach Learn Med. 2008 Jan-Mar;20(1):5-1o.
Internal Medicine I Edmonton Manual of Common Clinical Scenarios 85

ABD DISTENTION, ASCITES, LIVER DISEASE
2011 Ed. Authors: Charles Lim, Craig DomkeMD, Lucille LalondeMD FRCPC
OriginalAurhors:Juliet Emamaullee PhD, Michael McCall MD, AM James Shapiro MD PhD FRCSCFRCS (Eng)
Station ObJ’-tive
In this station you will be expected to understand and differentiate the causes of ascites and the different presentations of liver disease, and
also have a comprehensive approach to physical exam and appropriate investigation.
Features suggestive of • Abnormal LFTs, positive viral hepatitis serology, history of EtOH abuse, associated PMHx/FHx history of liver
liver dz dz, immigrant from hepatitis endemic region, stigmata of liver dz
Features suggestive of Hx/PE findings consistent with CHF
extrahepatic dz
Features suggestive of • >50 yrs old, unintentional weight loss, no underlying liver dz, rectal bleeding, abdominal mass, pelvic mass,
malignancy confirmatory imaging/biopsy studies
• Cirrhosis: EtCH, hepatitis B or C, NAFLD, cryptogenic
• Extrahepatic cause of ascites: CHF, malignancy
• Autoimmune liver dz: PBC/PSC/autoimmune hepatitis
• Hypoalbuminemia: nephrotic syndrome, poor nutrition
• Cirrhosis + hepatocellular Ca, spontaneous bacterial peritonitis
• End stage liver dz with intractable ascites and/or neurologic impairment (Child-Pugh Class C)
• Malignant ascites of any source
History
ID • Age, gender, ethnicity
CC • Variable: fatigue, bloating, weight gain, peripheral edema,jaundice, abdominal pain
HPI • Timing on onset (acute vs. chronic), increased girth (LR+ 4.2, LR- 0.17 for ascites), recent weight gain (LR+ 3.2 for
, ankle swelling (absence is good at ruling out ascites LR- 0.1 0)
1
ascites) — ’diet and appetite
1
11E FLAGS • Painless jaundice, febrile jaundice, massive UGIB, encephalopathy
PMHx • Liver dz, hepatitis (LR+ 3.2)1, autoimmune dz, CHF, blood transfusions, GI and GU cancers, drug OD
PSHx • Cholecystectomy, surgical intervention for GI bleeding, TIPS, CABG, CA resection
Meds • Diuretics, antivirals, hepatotoxic drugs (eg. acetaminophen, amiodarone, methotrexate, etc.)
FHx • Liver dz, hepatitis, autoimmune dz, GI and GU cancers
Social • EtCH abuse, smoking, IV drugs, tattoos, travel to hepatitis endemic areas
ROS • HEENT: altered mood, irregular sleep, drowsiness, confusion
• CV/RESP: SOB, orthopnea, PND
• GI/GU: unintentional weight gain or loss, acholic stools, dark urine, oliguria, painless rectal bleeding, nausea,
vomiting, bloating, anorexia 2
• MSK / DERM: jaundice, rashes, pruritis, increased bleeding, easy bruising 3
Risk Factors • IV drug use, EtCH, tattoos, blood transfusion, Asian ethnicity 4
5.
Physical
General Approach
• Vitals: is the patient stable? Any fever or tachycardia?
• Appearance: does the patient appear uncomfortable? Dehydrated? Cachetic? Conscious and oriented?
2. Inspection
• Stigmata of liver disease
• HEENT: Scleral icterus, fetor hepaticus, conjunctival pallor
• Trunk: spider angiomas, caput medusa, purpura, muscle wasting
• Hands: Terry’s nails, leukonychia, Dupuytren’s contracture, palmar erythema, clubbing
86 Edmonton Manual of Common Clinical Scenarios I Internal Medicine

• GU: gynecomaStia, testicular atrophy
Standard CV and RESP exam to look for signs of CHF
4 Abdominal exam
• Pt must be supine, lying flat, hands at sides, feet uncrossed, ABD should be exposed from xyphoid process to pubic
symphysis, maintain patient dignity, observe patient from foot of bed first
• çtion: contour of abdomen, obvious masses, scars, ABD stigmata of liver disease (caput medusa, spider nevi, bulging flanks)
g,jltation: listen for bowel sounds and bruits in 4 quadrants
• itioni ask the pt to identify any painful location, start in quadrant farthest from that location, begin with soft palpation,
observe pt reaction and ask them to indicate where they feel pain, move to area of indicated tenderness last, continue with deep
palpation
• pertinent findings:
• Signs of acute abdomen (rigidity, guarding, rebound) are unlikely in this setting
• Note any masses, HSM (percuss liver span and Traube’s space, Castell’s sign)
• Edema (absence is best test for ruling out ascites, presence is pretty good for ruling in): LR+ 3.8, LR- 0.21
• Bulging flanks (okay for ruling out ascites, not great for ruling in): LR+2.0, LR- 0.31
• Shifting dullness (bit better than bulging flanks for ruling in ascites, okay for ruling out) — LR+2.7, LR- 0.3’
• Fluid wave (best test for ruling in ascites): LR+ 6.0, LR- 0.4’
• Courvoisier’S sign: palpable gall bladder + painless jaundice —* associated with pancreatic Ca
• DRE: look for masses, occult bleeding, rectal varices
Investigations
i. Blood work (*routine tests; use remaining tests judiciously depending on HPI/PMHx)
• CBC-D: anemia, thrombocytopenia (liver dz)
o Iriver enzymes: ALT, AST —* t in liver disease, AST 2x>ALT in alcoholic liver dz
o Biliary markers: bili, ALP —* t in biliary obstruction and end stage liver dz
o Albumin and coagulation markers (INR, PU) —* indicators of liver function (1. albumin, t INR in failure)
o Cr/urea/electrolytes —+ indicators of renal function, dehydration, hepatorenal syndrome
• If t. ALT:
• Hep B and C serology, iron saturation (hemochromatosis)
• If indicationed by history: ANA, antiSMA, antiLKM (autoimmune hepatitis); ceruloplasmin and urine copper (Wilson’s); al-anti
trypsin
• If t Alk Phos & Bili: U/S; if indicated: Antimitochondrial antibodies (PBC), ANA (PSC)
o Cancer markers: AFP (hepatocellular carcinoma), CA-i 25 (ovarian), CEA (colon/GI), CA-i 9-9 (pancreatic)
o Abdominal U/S: look for signs of cirrhosis, portal HTN, biliary obstruction, ascites (gold standard), fatty liver
o Abdominal/pelvic CT + contrast: look for evidence of cirrhosis, abdominal/pelvic masses
3. SpecialTests
o Liver bx: to confirm histologic diagnosis of underlying liver dz
o Diagnostic paracentesis: test fluid albumin, cell count, gram stain and culture, measure serum albumin at same time, determine
serum-to-ascites-albumin gradient (SAAG = [alb(serum)]-[alb(ascites)])
• SAAG> ii g/L and t WBC cirrhosis + peritonitis
• SAAG> ii g/L and WBC = high gradient, likely cirrhosis or could be CHF or nephrotic syndome
• Serum albumin >25 —* likely CHF
• Serum albumin <25 —÷ likely cirrhosis
• SAAG < ii g/L = low gradient, malignant ascites, TB
Treatment
1. General Measures — sodium restriction, fluid restriction, diuretics, nutritional support, EtCH abstinence
2. Treat underlying cause if possible — hepatitis, CHF, malignancy, etc.
3. Treat symptoms — repeated therapeutic paracentesis, albumin infusion, TIPS
4. Treat spontaneous bacterial peritonitis — give prophylaxis in high risk patients or those with prior episode
5. Liver transplantation
References
1. Williams, Jr JW, Simel DL. Original article: does this patient have ascites? In: Simel DL, Rennie D, eds. The Rational Clinical Examination: Evidence-Based
Clinical Diagnosis, New York, NY: McGraw-Hill; 2009.
2. Longmore M, Wilkinson, IB, Davidson EH, Foulkes A, Mafl AR. Oxford handbook of clinical medicine. 8 th
ed. New York: Oxford University Press; 2010.
Internal Medicine I Edmonton Manual of C,mmon Clinical Scenarios 87

ABNORMAL HEART SOUNDS
2011 Ed. Authors:Alim NagjiB. Hsc,, Jam!! Kanji MD FRCPC, Ammara Sad!q MD
OriginalAuthors:Alyzee Sibtain, Carrie Ye MD, Taha TaherMD FRCPC
Station Objective
Recognize abnormal heart sounds, determine if heart dz is present, select pts requiring further care.
• Valvular dz, CHF, cardiomyopatriy, pericarditis
• CAD, CHF, Ml, FHx of CHD, prolonged Q-T, endocarditis, pericardial tamponade
History
ID • Age, sex
CC • Could be asymptomatic
HPI • SOB, angina, palpitations, syncope
• OPQRSTUV
RED FLAGS • FHx heart dz, Ml, sudden onset of murmur/abnormal heart sound, sx of endocarditis
PMHx • HTN (LVH, HTN cardiomyopathy), Ml, Streptococcus Beta-hemolytic infections, hyperthyroidism, chronic or past CVD,
recent dental surgery/past endocarditis,T2DM, vasculitis, ankylosing spondylitis, reactive arthritis, syphilis
PSHx • Past cardiothoracic, defibrillator/pacemaker implantation
Meds • Antihypertensives, DM medication, herbais, supplements, drug abuse (endocarditis, Ml)
FHx • HTN, Ml, CAD, CVA, sudden death, Marfan’s, cardiomyopathy, CHD
Social • Smoking/ETOH, lifestyle factors (diet, exercise, occupation, etc.)
ROS • RESP: hemoptysis, peripheral edema, orthopnea, PND, pulmonary disorders, cough, wheeze
• GI: abdominal distention (ascites), weight loss (endocarditis)
. MSK/DERM:sxofDVT
Risk Factors • CAD, untx strep pharyngitis, FHx, cardiac risk factors, atherosclerosis, poor social hx
Physical
1. General Approach
• CADJCLE (Cyanosis, Anemia, Dehydration, Jaundice, Cervical Lymphadenopathy, Edema), fever (endocarditis), distress
2. Inspection
• Clubbing (lung/heart/gi dz), cyanosis, typical facies
• Precordial exam: excavatum/carinatum/barrel shaped, scars, parasternal heaves, thrills, visible palpations
• PACES: Pyrexia, Anemia, Cardiac murmurs, Erythema nodosum/Emboli, Splenomegaly (endocarditis)
3. Palpation
• ), peripheral (coarctation of aorta)
Pulse: bilateral carotid (pulsus parvus et tardus —* slow upstroke LR+ 9.2 for AS
5
• PMI: laterally displaced, enlarged (LVD, old Ml), sustained (LVH); palpable P2 (pulmonary HTN)
4. Ausculation: see Table
5. Special Tests
• JVP: Prominent a wave (RVH, TS), v (TR), y (constrictive pericarditis); elevated (pleural effusion, ascites)
• Maneuvering: valsalva, squatting, L lateral, leaning forward, inspiration/expiration, apical/carotid delay (AOS), brachial/radial delay
(AOS)
Investigations
1. Blood work
• CBC-D (anemia, endocarditis), CK/troponins (Ml), BNP >500 (CHF)
• Serum creatinine (CHF), lipid profile (CAD), electrolytes (CHF ‘K,LNa), LFT (ascites, R CHF),TSH, ABG
-
• Blood culture (endocarditis)

• Genetic tests (Marfans, hypertrophic cardiomyopathy)
2. Radiology/Imaging (COPD, heart size)
3. Special Tests
• l2leadECG
• ECHO (Structural heart dz, CHF)
• Stress test (CAD)

5
g ical/Diagn05tic Interventions (cardiac catheterization)
4
Treatmt
merg based on level of distress. ABC, IV access, °2
2 Treatment Options: tX underlying etiology.
Surgical (consultation)
• Valvoplasty (valvular dz), CABG (CAD), transplant (CHF)
. Ejection click (AS, PS or dilation) • Organized by anatomical location of
jüiUSB
• Crescendo-Decrescendo (AS,PS) abnormal sound
• Radiation to R carotid (LR+ 8.1 for AS)5 • Best heard with diaphragm (high pitch)
• Radiation to R clavicle (LR- 0.1, i.e. absence of radiation good at ruling out)
5 unless labeled
= best heard with bell (low pitched
*
• Leaflet disease (RE, degeneration, bicuspid valve)
• Hypertrophic cardiomyopathy sounds)
• Aortic narrowing, coarctation • italics = systolic
• 52: • bold =diastolic
• Split (physiological: A2,P2), • Systolic murmurs are quite common
• Wide split (RBBB, PS, HTN, PE, L-R Shunt) and can be physiological (with absence
• Fixed split (ASD) of other cardiac findings)
• Paradoxical split (LBBB, severe AS, RV pacemaker) • Diastolic murmur = pathology
• Early aortic closure (MR, VSD) • A = Aortic area
23 R ICS)
(
rd
• No split: (Eisenmenger, severe PE, PS) 23
• Loud (l-ITN, aortic sclerosis) • P = Pulmonic area rd(
L ICS)
• Soft (AS (LR+ 75)5, hypotension, L sided CHF,) • T=Tricuspid area
Early decrescendo (PR Pt sitting forward, exhaling)
—
(L sternal border)
• Continous murmur (PDA) • M = Mitral area (apex, 4-5”' ICS mid
• Pericardial knock (constrictive pericarditis) axillary line)
• LLD = left lateral decubitus. used to
• Pansystolic (TR: radiates right sternum, 1w inspiration, VSD)
• Dilation of RV, tricuspid annulus (MI, dilated cardiomyopathy) accentuate left sided sounds
• Pulmonary HTN (L CHF, MS, MR, pulmonary disease, L-R shunt/Eisenmenger,
pulmonic stenosis)
• Valve abnormality (RF, endocarditis, Ebstein, carcinoid)
• Early decrescendo @ L Sternal Border (AR Pt sitting forward, exhaling. PR)
—
• Leaflet abnormality (RF, endocarditis, bicuspid valve, RA, AS, trauma

• Aortic root/ascending aorta (HTN, AS, Reiter Syndrome, Disecting aneurysm,
aortitis/syphilis)
• Mid to late murmur (TS, ASD)
LLSB or Apex • S3: LLD for left sided
• Normal in youth; elderly: volume overload, CHE, MR, TR, AR, CHF
• 54: LLD for left sided
• VH, myocardial ischemia, AS, PS, hypertrophic and ischemic cardiomyopathy,
HTN
• Opening snap diaphragm (MS, TS)
• Pansystolic (VSD no radiation, no w inspiration)
—
Apex 51:
• Split (RBBB)
• Loud (PR interval, mild MS, CO or tachycardia i.e. anemia, hyperthyroidism,
—
etc.)
• Soft (IPR interval, AV block, MR, severe MS, stiff LV, COPD)
• Pansystolic murmur (MR radiates left axilla, rio t w respiration)
—
• Leaflet disease (RF, SLE, Marfan’s, MVP, endocarditis, hypertrophic

cardiomyopathy)
• Chordae tendinea (Ml, MVP, RF, endocarditis, trauma)
• Papillary muscle (ischemia, infarct, aneurysm, dilated cardiomyopathy, trauma)
• Mitral annulus (calcification from RF, CRF; dilated cardiomyopathy)
• Late systolic murmur (MVP -
w valsalva)
• Mid to late murmur* (MS: LLD position)
• RF, SLE, RA, carcinoid
References
Lilly IS. Pathophysiology of Heart Disease. 4” ed. New York; 2007.
2. Lipincort Williams, Wilcott. Auscultation Skills: Breath and Heart Sounds. 4th
ed. New York: Soringhouse; 2009.
3. Braunv,,j E. Chapter 219: Approach to the Patient with Possible Cardiovascular Disease. I : Fauci AS, Braunwald E, Kasper DL Hauser SL, Longo DL,
Jameson JL, Loscalzo J, editors. Harrison’s Principles of Internal Medicine. New York: McGrjw-Hill; 2008.
4. Otto, CM. Valvular Aortic Stenosis: Disease Severity and Timing of Intervention. JACC. 20 .16;47(1 1 ):21 41-2151.
Cescon D, Etchells E. Update: Murmur Systolic In: Simel DL, Rennie D, eds. The Rationaftlinjcal Examination: Evidence-Based Clinical Diagnosis, Newyork,
NY: McGraw-Hill; 2009.
Internal Medicine Edmonton Manual of Common Clinical Scenarios 89

ACUTE CONFUSION
20!! Ed. Authors:JoffreMunro, Yang L1MD, Darren Nichols MDFFCP(EM)
Station Objective
To recognize, diagnose the underlying etiology, and man ge a patient presenting in an acute confusional state or delirium.
1. Diagnostic Criteria p
DSM IV Criteria for Delirium are as follows:
• Disturbance of consciousness with reduced ability to focus, sustain, or shift attention 1.
• A change in cognition or the development of a perceptual disturbance that is not due to dementia
• Disturbance develops over a short period of time (hours to days) and fluctuates during the course of the day 2.
• Due to a medical condition, substance intoxication/withdrawal, or medication side effect
• +/- Psychomotor behavioural disturbances, sleep disturbances, or emotional disturbances
2. Common Conditions: (Note: Many of the following have the potential to cause High Mortality / Morbidity)
DrugslToxins Infections Metabolic Causes structural Lesions 3
Intoxication: CNS: Substrate Deficiency: Traumatic:
Street Drugs (narcotics, viral/bacterial meningitis, hypoxia, hypovolemia, concussion, subdural or epidural 4
sedative-hypnotics, alcohol, encephalitis, abscess, hypoglycemia bleed
cocaine, ecstasy, crystal meth, neurosyphillis Electrolyte Imbalance: Atraumatic:
hallucinogens, GHB) Systemic: t/LNa, t4Ca, .IMg bleed (CVA, SAH, into tumor), mass
Poisons (CO. pesticides, etc) any systemic infection can cause Organ Dysfunction: lesion (primary/metastatic tumors),
Withdrawal: confusion primarily (eg UTI t4thyroidism, tparathyroidism, seizures
benzodiazepines, alcohol in elderly) or secondarily (eg adrenal insufficiency, CHF, MI,
(Wernicke’s encephalopathy) hypoxia from pneumonia), sepsis hypertensive encephalopathy,
Prescription: hepatic encephalopathy, uremia,
psychiatric drugs, narcotics, anemia
sedative-hypnotics, meds with Other: Miscellaneous
anticholinergic side effects hyper/hypothermia, CU psychosis, sundowning,
malnutrition, Wilson’s dz, hospitalization
cerebral lupus, CNS vasculitis,
TIP
History
ID Patient name, age, sex
CC • Acute disturbance in consciousness, cognition, and/or perception
HPI In addition to speaking with patient, obtain Hx from relatives, caregivers, other healthcare staff
• Determine patient’s baseline cognitive status
• OPQRST particularly onset, time course, fluctuation, worse in AM or PM
• Determine if patient is having delusions, illusions, hallucinations (visual and auditory)
• Distractible, inattentive, disoriented, cognitive impairment, amnesia
• Hx of recent infections or risks of infection (ie. use of catheters)
• Screen for symptoms of organ failure particularly hepatic, renal, and respiratory failure
• Hx of medication/drug overdose, toxin exposure, poisoning
RED FLAGS Extreme sudden onset, Hx of trauma, neck stiffness, fever/chills, weight loss, night sweats
PMHx General inquiry (see Common Conditions as guide)
• Previous episodes of delirium or confusion, dementia or other neurological illnesses
PSHx # of days post-op if recent surgery
Meds New/change in meds, Rx and OTC meds, herbals, anticoagulants, psychoactive drugs
Allergies General inquiry
Social Alcohol use, illicit drug use, dietary habits, malnutrition
90 Edmonton Manual of Common Clinical Scenarios Internal Medicine

• HEENT: headache, neck stiffness, photophobia, phonophobia, rhinorrhea, cough, fever
• CV / RESP: palpitations, chest pain, SOB
• GI: abdo pain, nausea, vomiting, diarrhea, ascites
• GU: dysuria, change in urinary frequency
• CNS: memory loss, language/speech difficulties, psychomotor agitation
• MSK / DERM: rash
• Other: lethargic, sleep/wake reversal, diaphoresis
Factors • Baseline cognitive dysfunction, old age, sensory deprivation, poor overall health, hospitalization
-
physical
1 General Approach
• ABCDE5; vitals (autonomic instability, decreased Sp02, fever); GCS; ensure patient safety +/- restraints/sedation
2 InspectiOn
• HEENT: scieral icterus, dry mucous membranes, cyanosis, malodorous breath (ie alcohol), elevated JVP
• CNS: papilledema, pupil constriction/dilation, cranial nerve exam, tremors, asterixis
• MSK / DERM: needle tracks, nail clubbing, Terry’s nails, Dupuytren’s contracture, gynecomastia, caput medusae, spider angiomas,
jaundice, rash, diaphoresis, gait for ataxia
3 Percussion
• ABDO: hepatomegaly, ascites
4. Palpation
• CNS: full neurological examination (sensation and motor function), stiff neck, Kernig’s and Brudzinski’s sign
• MSI< / DERM: enlarged lymph nodes, skin turgor, peripheral edema
5. AuscUltatiofl
• CVS / RESP: heart murmurs, extra heart sounds; decreased air entry, crackles (pulmonary consolidation)
6. Special Tests
• Mini Mental Status Exam (less useful in acute confusion)
Investigations
1. Blood work
• CBC-D, electrolytes, Ca, Mg, creatinine, urea, INR, PTT, LFTs, glucose, TSH, cortisol, vitamin B12, thiamine
• Venous blood gas, blood cultures, serum toxicology screen (consider ASA, acetaminophen, EtOH)
• Antinuclear antibodies, complement levels, p-ANCA, c-ANCA; HIV, RPR, viral serology (as indicated)
• Chest radiograph; consider MRI or CT head (as indicated)
3. Special Tests
• UA, urine C&S, LP, ECG, EEG (as indicated)
Treatment Low Risk Emergent Tx

Dextrose (D5OW) 1 amp IV (if glucose)
1. Emergent Oxygen administration (to everyone)
• Secure staff and patient safety; IV access and oxygen Naloxone 2 mg IV (if tiny pupils, slow/shallow breathing)
• Treat shock, respiratory failure, hyper/hypothermia, HTN (if present); Thiamine 100 mg IV (if Hx of EtOH abuse)
consider activated charcoal (if indicated)
• Medical
• If known, treat underlying cause of delirium (ex. antibiotics for infection, correct electrolyte imbalance)
• Supportive care. Clocks, calendars, and windows reduce confusion. Decrease any sensory impairment (ie glasses, hearing
aids). Attempt to correct sleep cycle. Maintain adequate nutrition and fluids
• Low dose chemical restraints, atypical antipsychotics, and sedatives if necessary
3. Referrals
• Consider referral to Psychiatry if indicated
References
1. Fauci AS et al. Harrison’s Principles of Internal Medicine. 17th ed. USA:The McGraw-Hill Companies, mc; 2008.
2. lifltinalli JE et al.]intinalli’s Emergency Medicine, A Comprehensive Study Guide. 6th ed. USA: The McGraw-Hill Companies, nc; 2004.
InternJ Medicine Edmonton Manual of Common Clinical Scenarios 91

ALLERGIC REACTIONS
2011 Ed. Authors: Mohammed Osman PhD, Michael Chu MD, Vay Daniels MD FRCPC
OriginalAuthors: Shaheed Merani PhD, Mohammed Osmon PhD, Lisa SrebleckiMD, MPH, CCFP
Station Objective
Develop an approach to allergic hypersensitivity I reactions (IgE-mediated), which includes localized (skin, respiratory, gastrointestinal 2.
reactions) and generalized reactions.
Differential Diagnosis 3
• Skin: atopic dermatitis, contact dermatitis (type IV hypersensitivity), allergic conjunctivitis, urticaria, angioedema
• Airways: allergic rhiriitis, seasonal allergies, angioedema, asthma 4.
• Gastrointestinal: food allergies (most common eggs, wheat, milk, shellfish, peanuts, tree nuts). Celiac disease is not IgE mediat
but is a gluten sensitive enteropathy. 5.
• Generalized: Drug allergy (any medication but more commonly penicillin, ASA, sulpha, NSAID), contrast, anaphylactic reactions,
blood transfusions.
High Mortality I Morbidity: 6.
• Anaphylaxis
• Diagnostic Criteria: any one of the following three criteria:
• Regardless of allergen exposure: Acute onset (minutes to hours) involving the skin and/or mucosa AND respiratory
compromise and/or symptomatic hypotension
• Exposure to likely allergens with at least 2 of: respiratory compromise, symptomatic hypotension, persistent GI symptorn
skin/mucosal involvement
• Exposure to known allergen with drop in BP after exposure to known allergen (<90 mm Hg or >30% decrease from 1.
baseline sBP)
Angioedema
History
ID • Age, gender
CC • One or combination of any of skin, airway, or GI symptoms
HPI • Onset quality, severity, timing, and progression of symptoms
• Determine which organ systems are involved 4.
• Obtain a chronological order to account for the potential cause. Can have reaction 7-1 4d post-exposure
• Triggers: foods, insect bites/stings, drugs (antibiotics, ACEi, NSAID), skin contact, inhaled agents, blood products,
latex, detergents, dust mites, mold pollen, pet exposure, animal dander, cockroaches, rodents, seasonal T
involvement, relationship to furnace lighting, exercise, cold air 1.
• Differentiate between food intolerance and food allergy
RED FLAGS • Anaphylac-tic shock, airway involvement, altered LOC, Medi-Alert bracelet, patient carrying epi-pen, PMHx of
anaphylactic reaction, strong atopic FHx, €@PD and L €HF (poor reserve)
PMHx • Asthma, hospitalization for asthma, eczema, allergic rhinitis, anaphylaxis
Meds • New or recent meds, epi-pen, beta blockers (reduce epi-pen efficacy), inhalers/anti-histamine use frequency.
Allergies • Known allergens (meds, non-meds) and reaction. Samter’s triad (asthma, nasal polyps and ASA/NSAID reactive 2.
allergies)
FHx • Food allergies, allergic rhinitis, asthma, hay fever, environmental/seasonal allergies, angioedema
Social • Smoking/smoke exposure, pets at home, exposures to fumes/animals at work
ROS • HEENT: facial/tongue swelling, allergic rhinitis (age of onset, duration, timing, seasonal), sneezing, itching, tearing
• CV: tachycardia, dizziness, syncope/pre-syncope R
• RESP: coughing, wheezing, SOB, night time symptoms, WOB
I.
• GI: diarrhea, crampy abdominal wall, NN
• MSK / DERM: rashes, itching, generalized or localized, fever, arthralgia, malaise 2.
Risk Factors • FHx of atopic disease, allergic rhinitis, asthma, atopic dermatitis, prior Hx of anaphylaxis 3.
92 Edmonton Manual of Common Clinical Scenarios j Internal Medicine

physical
General Approach: Focus exam based on likely etiology.
• ABCS, GCS, vitals including sBP (note variation with inspiratory and expiratory cycle and if sBP < 90 mmHg or > 30% baseline),
RR, Sp0
2
Note patency/involvement of airway talk to patient assessing for stridor, I WOB, quality of voice, cough, sneeze
—
o Children “allergic faces”- dark discoloration underneath both eyes.

2 Inspection
• HEENT: rhinoscopy (polyps, cobble stoning), visualization of oropharyrix (lip, tongue, uvular color and edema), conjunctival
irritation/swelling, periorbital edema, tearing, flushed face
o DERM: distribution of rashes involved.
3 Percussion
o Percuss all lung fields and abdominal quadrants.
4. Palpation
• Peripheral pulses, cervical lymphadenopathy, palpable rashes, and localized edema.
5. Au5cU1tat”
All lung fields, with close attention to length of inspiratory phase and expiratory phases and listening for stridor, wheeze, dyspnea,
and pleural rubs.
6. Special Tests
• Darier’s sign (simple stroke) / Dermatographism (specific pattern) both suggestive of mastocytosis. Stroking of skin results in
—
compression of mast cells with subsequent degranulation leading to erythema, pruritis and appearance of wheals in the area site
minutes later.
Investigations
1. Blood work: not routinely required, plasma histamine/tryptase can be elevated but non-specific. Consider blood cultures as anaphylaxis
and sepsis can look alike
2. Radiology/Imaging: CXR to rule out other pulmonary disease, suggest obstructive pulmonary disease.
3. Special Tests
PFT (if history suggest asthma/obstructive lung disease)
• Allergy skin testing (3-4 weeks after anaphylaxis episode)
• The Rational Clinical Examination, JAMA (2009)— Between 80-90% of patients reporting a penicillin allergy have a negative
skin test for penicillin hypersensitivity. At least 98% of patients with negative skin test to penicillin can tolerate it despite a
reported allergy to penicillin
• Food challenge
• Symptom/trigger diaries useful for identifying causative agent. S Seek help with recurrence
4. Surgical/Diagnostic Interventions: Rhinoscopy A Allergen avoidance
F F/U with MD/allergist
E Epi for emergencies
Treatment
1. Emergent (anaphylaxis)
• ABC, remove inciting agent, call for help, IM epinephrine (STAT (0.5 mg (1:1000) adult, or 0.01 mg/kg peds), place in supine
position and elevate LE bilaterally (venous return), 02, 2 large bore IV open NS, continuous monitoring HR, BP, RR, 02 saturation
and observe x 8h.
• Intubate GCS <8. If airway compromise, call for help anesthesia/ENT
• Corticosteroids (Solumedrol 125 mg IV), antihistamines (Hi RA and H2RA), inhaled salbutamol, and gIucaion (if on beta-blockers).
Once Stable x 8h, D/C home SAFEly
2. Treatment Options (outpatient).
Allergen avoidance, anaphylaxis education, smoking cessation, Medi-Alert Bracelet, Epi-pen
• Antihistamines.
• Corticosteroids (topic, nasal, oral).
3. Referrals: ENT (sinusitis, polyps), respirology (severe asthma), dermatology (eczema), allergy (skin testing)
References
1. Salkind AR, Cuddy PG, Foxworth JW.ls this patient allergic to penicillin? In: Simel DL, Rennie D, eds. The Rational Clinical Examination: Evidence-Based
New York, NY: McGraw-Hill; 2009.
2 UptoDate: Anaphylaxis: rapid recognition and treatment [Online] (2010). Available from: htto://www.uotodate.com
Simoris FE. Anaphylaxis. J Allergy Clin Immunol. 2010 Feb;1 25(2 Suppl 2):S1 61-81.

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ALTERED LEVEL OF CONSCIOUSNESS

20!! Ed. Authors:Ashraf Kharrat, James Keay MD CCFP 1.
OriginalAuthors: Victoria Lam, Michael Chu MD, RohitMoudgilMD PhD
2.
St tion Objecti e
Determine the etiology of altered LOC, which can be due to coma, delirium, confusion, dementia. Identify treatable versus irreversible causes
to establish initial treatment plan.
• Coma: if GCS <9
• Dementia: Lmemory, 1 cognitive problem, executive
function,1-cognition —
Delirium: acute onset, fluctuating course, inattention, Table i:Differentiating Delirium & Dementia
5
•
cognitive decline not due to dementia Delirium Dementia. 2
2. Common Conditions: Onset Over days Insidious
• Vascular: stroke, subarachnoid hemorrhage, subdural
hemorrhage, CNS vasculitis
Course in 24 h Fluctuating Stable 3
• Infectious: meningitis, encephalitis, bacteremia, urinary Consciousness Reduced Alert
tract infection, pneumonia, neurosyphilis 4
Attention Disordered . Normal
• Drugs: opioids, alcohol, sedatives, antipsychotics, drug
withdrawal
Cognition Disordered Impaired
• Psych: schizophrenia, depression, dementia Orientatio, Impaired ±impaired
• Metabolic: hypo/hyper-glycemia, hypo/hyper-Na,
Hallucinations Visual/auditory -ye
hypo/hyper-thyroidism, hyper-Ca, uremia, hepatic
encephalopath vit Bi 2 deficiency
Delusions Transient Usually-ye
• Structural: brai tumor, hydrocephalus Movements Asterixis ± tremor -ye
• Other:”sundow ing’ hypothermia, heat stroke
3. High Mortality / Mor Jity:
• Subarachnoid emorrhage, neurosyphilis, encephalitis, meningitis
History
ID • Age, gender, BMI, occupation
CC • Altered LOC
HPI • Fluctuating course, signs of inattention, disorientation, change in behaviour, slowed thinking, altered perception
and mood, impaired memory V
RED FLAGS • NN, papilledema, sudden collapse, pregnanc.y ± ec.Iarnpsia, extremes of age, “thunder c.Iap” headaohe
• cushing’s triad (fIP): (1) systolic FIflN (widening pulse pressure) (2) bradycardia (3) respiratory depression 2
3
• Hemodynamic instability
4
PMHx • Psychiatric illnesses, seizures, neoplasms, endocrinopathies 5
6
PO&GHx • OCP, eclampsia, pregnancy/partuition V
7
Meds • Sedatives, opiates, antidepressants, anticholinergics, antipsychotics, others a
FHx • Stroke, schizophrenia, depression, drug addiction
Social • Smoking, EtOH, recreational drug use
ROS • HEENT: headaches, neuro symptoms
• RESP: respiratory irregularities, SOB, difficulty breathing, hypoxia
• GI: constipation, hepatic encephalopathy, SBP, acute abdomen
• GU: urinary incontinence, UTI
• MSK/DERM: rash, cellulitis, necrotizing fasciitis
Risk Factors • Age, cognition, tcomorbidities, M>>F, depression, EtOH abuse

physical
1 General Approach
• ABC’S, vitals, GCS, then AMPLE Hx
2 Inspection
Trauma signs, needle marks (IVDU, DM), odors/breath, cyanosis, cherry-red color (tCO), bruises, bleeding, CSF leak, hyperemia,
dry skin (DKA, uremia), sweating (hypoglycemia/shock), facial asymmetry, jaundice, petechiae/purpura (UP, coagulopathy),
involuntary movements, edema
Special Tests
Neuro exam: MMSE, DTRs, pupil, EOMs, gait, respiration, oculocephalic (doll’s eyes) + oculovestibular reflexes (caloric stimulation),
muscle tone (hemiplegia, decorticated vs. decerebrated rigidity)
veStigat10n5
1 BloOd work
• /ABG, CBC-D, glucose/GTT, electrolytes, Ca
2
Sp0 , Mg, thiamine, vit B12, folate, PTH, LFTs,TSH, urea, Cr, INR, serum drug levels
2
(digoxin, theophylline, phenobarbital), blood cultures
2. adiOlogy/Imagfhg
• CT: GCS< 15, seizure, penetrating injury, TIA/stroke, focal neuro deficits, immunocompromised, anticoagulant/coagulopathy,
• MRI: brain infarct, carotid/cerebral dissection, mass lesion, demyelinating lesions, dementia
3. Special Tests
• U/A, blood/urine toxicology (aritipsychotics, EtOH, barbituates, opiates, heavy metals), EEG, ECG
LP: if suspect meningitis/encephalitis/bleed, peritoneal tap if SBP suspected
Treatment
i. Emergent
• GCS 8: indication to intubate
• IV access (fluids, pressors, glucose, blood), treat underlying cause
• Dementia: acetylcholinesterase inhibitors
Delirium: determine cause (DIMS: drug, infection, metabolic, structural), initially empiric treatment for underlying causes
(electrolyte correction, antibiotics, supportive management)
• Substitute decisions-making, power of attorney/wills, counseling, community support
3. Referrals
• Surgery: neurosurgery, vascular surgery
• Medicine: neurology, geriatrics, psychiatry
• Allied health practitioners
References
1. Stone KC, Humphrjes R. Current Diagnosis &Treatment Emergency Medicine 6th Ed. (2008).The McGraw-Hill Companies, Inc., 2008
-
2. Ropper AH, Samuels MA. Adams and Victor’s Principles of Neurology 9th Ed. New York., 2009.
-
3. ACP PIER & AHFS Dl Essentials: Delirium. http://onIine.statref.com/document.aspx?fdd=92&docid=1 146. Posted: 10/8/2009;
4. Moore EE, Feliciano DV, Mattox KL.TRAUMA 6th Ed. (2008): Diagnostic and Interventional Radiology. McGraw-Hill, Inc. USA, 2008.
-
5. lintinalli JE, Kelen GD, and Stapczynski iS. Emergency Medicine: A Comprehensive Study Guide 6th Ed. New York: McGraw-Hill, 2004
-
6. Fauci AS, Kasper DL, et al. Harrison’s Principles of Internal Medicine. 17th Ed. USA: McGraw-Hill, 2008
7. Bickley LS, Szilagyi PG. Bates’guide to physical examination and history taking. 9th ed. Philadelphia: Lippincott Williams & Wilkins, 2007.
8. Hoffman, LH et al. First Exposure Emergency Medicine. McGraw-Hill, Inc. USA, 2008.

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_______ ______
_______
________ _______
________
ALTERED SENSATION (NUMBNESS &TINGLING)

2011 Ed. Authors: Victoria Lam, Anu ParhorMD, RohitMoudgil MD PhD
Station Objective
Determine the origin (a. peripheral vs. central, b. neural axis, c. cause of lesion) of the abnormal sensation through a thorough physical exar
and appropriate clinical/laboratory tests in order to provide proficient initial management.
• Cerebral (hemiplegia, aphasia, apraxia): stroke [MRIICT brain lesion), demyelination (electrodiagnostic studies/biopsy/imaging),
l, encephalitis
tumors [MRI/CT & bx, -ye MRI/CT —* RIO tumor
2
• Brainstem (diplopia, dizziness, dysarthria, dysphagia): [PE + MRI/MRA posterior fossa & cerebellar strokes]
• 12 deficiency, tumor, syringomyelia,
Spinal cord: MS [McDonald’s criteria], disc lesion, spinal cord/ radiculopathy (± back pain), B
cord infarction [imaging], infections (epidural)
• PNS: mononeuropathy (carpel tunnel/ulnar neuropathy [U/S, electrodiagnosis]), stocking-glove/polyneuropathy (DM, uremia,
vasculitis, HIV, Lyme [serology], EtCH, paraneoplastic, amyloid)
2. High Mortality: Stroke + intracerberal hemorrhage
History
• Stroke risk: >50 yb, MS onset: 20-50 yb, BMI
• Numbness/tingling/altered sensation
HPI • OPQRST
• +ve sensory complaint: paraesthesia/dysesthesia or hypersensitivity
• -ye sensory complaint: hypoesthesia/anesthesia, detectable only by PE
• Hx of trauma, infection, recent Rx change, systemic symptoms, Hx of such presentation
RED FLAGS • Bowel/bladder dysfunction, saddle anesthesia, Ca, chronic disease, paraesthesia, night time pain, pain >1 month,
constitutional Sx, amaurosis fugax, Hx of lVlJ, vertebral tenderness
• Stroke: sudden onset, ± severe headache, ± focal Sx/aura/signs of SAH
1
• M5: 20-50 yb, associating fever/infection, Lhermitte’s sign 2
PMHx CAD, CVD, PVD, hyperlipidemia, DM2, HTN, ‘auto-immune disease, MS
FHx • As with PMHx, especially if early onset (<60 yb)
Mds • Recent vaccinations may provoke auto-immune demyelination, new med 3
Soci,l • Diurnal fatigue, smoking, EtCH, IV drugs

ROS • HEENT: Headache, vision problems, vertigo, facial nerve dysfunction, dysarthria, dysphagia, cognitive Sx, optic
neuritis (-Ivisual acuity, dimness, ‘1 color perception)
• CV: angina, rheumatic heart disease / valve replacement (embolic shower to brain), AF
• RESP: chest pain, difficulty breathing (pancoast tumor radiculopathy, Homer’s syndrome)
—
• GI: bowel dysfunction

• GU: bladder dysfunction
• MSK/DERM: sensory complaint, neglect, back pain, weakness, imbalance/ataxia
Risk Factors • Stroke: >50 yb, +ve FHx/PMHx, smoking, carotid bruit, TIA, AF, valvular dz
1
4
• MS: F>>M, age 20-50 ybo, FHx, caucasians living in higher latitudes
Table 1: Motor S stem Ph sical Exam
Physical Hipflexion:Li,2,3
• Elbowextension:C6-8 Ankle dorsiflexion:
1. General Approach (femoral)
(radial) L4,5 (deep peroneal)
• MMSE, CV exam, stroke assessment Hip adduction: L2,3,4
• Thumb flexion: C6,7 • Ankle plantar flexiOfl
2. Inspection (obturator)
(median) 51 52 (tibial)
• Tone, lesions, asymmetry, Hip abduction: L4,5, Si 2
• Wrist extensors: C7,8 Foot inversion: L4,5
atrophy, body position, color, ± (superior gluteal)
(radial) (posterior tibia I)
sweating, involuntary movements Knee extension: L2,3,4 3
• Hand interossei-flriger Foot eversion: L5, Si
fasciculations (femoral)
abduction/ adduction: C8, • (superficial peroneal)
3. Palpation Knee flexion-L5, 51,2
Ti (ulnar) I
• Peripheral pulses, edema, (sciatic)
deformities, palpate nerve trunk for
Tinel’s phenomenon, beading, enlargement
3
4. SpecialTests
• Contrast peripheral neuropathies, spinal cord/brain stem dysesthesia from cortical sensory dysfunction
• Neuro exam: define neural axis, PE based on Hx, a) sensory, b) CN, c) reflexes, d) motor system, L vs R
96 Edmonton Manual of Common Clinkal Scenarios Internal Medicine

Sensory facets: a) pain/temperature Table 2: Deep Tendon Reflex Physical Exam and Grade
[spinothalamic tracts], b) joint position & • Biceps tendon (C5-6)
vibration (128 Hz tuning fork) [posterior nil
=
• Brachioradialis tendon • Achilles tendon (51 -2)
columns], C) light touch (pathways a & b), 1 low normal
=
(C5-6) • Babinski’s reflex (L5-S1)
2 = normal
d) discriminative sensations (stereognosis, • Triceps tendon (C6-8) —p big toe dorsiflexion
graphesthesia), 2-point discrimination, point + 3 = high normal
• Knee jerk (L2-4) fanning other toes (UMN
localization) [cortex], Dermatome(s) vs. = clonus (>3
• Hoffman sign lesion)
control area, L vs R beats)
(corticospmnal)
mhle 3: Localizifla the Lesion
Central Nerve Disorders
—
Chronic contralateral UMN (weakness, spasticity), arm
Cerebral Cortex flexion>>extension, plantar flexion>>dorsiflexion, leg Contralateral sensory loss in limb & trunk
externally rotated
—-
Brainstem Weakness/spasticity as cerebral cortex + CN deficits Variable t

—
Weakness/spasticity as cerebral cortex, bilateral with Dermatomal dependent deficits, bilateral deficit at lesion
Spinal Cord bilateral cord damage—> paraplegia/quadriplegia level + .1. sensory below lesion
—
Gray Matter: Basal Ganglia Bradykinesia, rigidity, tremor Sensation not affected N/4.
Perhipheral Nerve Disorders
—-
Anterior Horn Focal weakness, atrophy, fasiculations Sensation not affected 4.

Root-innervated pattern weakness, atrophy ±
Spinal roots/nerves Corresponding dermatome sensory deficit .1.
fasiculations
peripheral nerve- Peripheral nerve-pattern atrophy, weakness ±
fasiculation
Sensory deficit, stocking-glove distribution 4.
mononeuropathy
Investigations Table 4: Upper VS Lower Motor Nerve Problems Differentiation

Blood work Reflexes Tone Power Fasciculation Atrophy
CBC-D, tox screen, vit , Upperlimbflexor>>extensor,
• 12 urea, Cr, clotting
B UMN 1 Spastic
lower limb flexor << extensor
No Latefinding
study, glucose/HbA1 c, electrolytes, ESR,
lipids, TSR
.1. power in specific
LMN 4. Rigid motor neuron/nerve root ± Common
2. Radiology/Imaging distribution
• MRI and CT specific to suspected
lesion location ± contrast, MRA
Table 5: Revised McDonald Criteria for Diagnosis of MS
3
’
1
for ischemia/infarction
Clinical Objective
3. Special Tests Additional requirements to Dx
Attacks Lesions
• ECG/Holter for AF, HE for
vegetation on valves and if—ye, 2 or more 2 or more None, additional evidence must be consistent with MS
do TEE Dissemination in space by MRI or +ve CSF and 2 or more MRI, MS
2ormore 1
• MS: Evoked potential, CSF consistent lesions or further clinical attack involving different site
(tmononuclear cell pleocytosis, 1 2 or more Dissemination in time by MRI or 2 ,,d
clinical attack
+ve lgG, -ye in serum, 1’ lgG Dissemination in space by MRI or +ve CSF and 2 or more MRI MS
index), MRI 1 (mono-
1 consistent lesions AND dissemination in time by MRI or 2 ,d
clinical
symptomatic)
Electrodiagnosis (EMG, nerve attack
conduction studies, evoked 1 yr progression + 2 of following: a) +ve brain MRI (9T2 or 4T2 lesions
1 (progress
potential), UA, U/S, XR 1 & +ve evoked potentials) b) +ve spinal cord MRI (2 focal T2 lesions) c)
from onset)
4. Surgical/Diagnostic Interventions +ve CSF
• LP, Bx, gram stain and culture for
epidural abscess
Treatment
1. Emergent
• Brain CT/MRI 30 mm of ER arrival +urgent neuro consult [stroke, SAH]
2. Follow-up
• Stroke: holter, carotid Doppler, vascular studies, ASA ± Plavix
3. Referrals
• Neurologist
References
American College
of Physicians. ACP PIER & AHFS DI Essentials: Stroke and Transient Ischemic Attack. http://online.statref.com.login.ezproxy.library.
ualbea ca/document aspx?fxid-..92&docid3539
2. Daniel D. Federman, M.D, Elizabeth G. Nabel, MD. ACP MEDICINE: Neurology (VI. Neoplastic Disorders). New York, 2009
Ropper AH, Samuels MA. Adams and Victor’s Principles of Neurology 9th Ed. New York., 2009.
-

ANEMIA
20?? Ed. Author5: Todd Penney MSc, Henry ConterMD, Ryan CooperMDMPHFRCPC
OriginalAuthors: Carrie Ye MD, Nancy Zhu MDFRCPC
Station Objective
To understand how to recognize anemia and its causes, understand the differences between normocytic, macrocytic and microcytic anemia,
learn to order the appropriate work-up and treat the problem.
1. Diagnostic Criteria: Hgb < 130 gIL of blood (adult males), Hgb < 120 gIL in adult females plus the criteria in Table 1
• Note: Anemia is not a diagnosis, but rather a condition that needs investigation
• Note: Often several causes of anemia exist simultaneously in a patient
TABLE 1
DIAGNOSTIC CRITERIA INVESTIGATIONS
TYPE OF ANEMIA COMMON CONDITIONS
(RBC volume in fL)
Acute blood loss, anemia of
chronic dz (e.g. HIV, malignancy, unconj bilirubin/haptoglobin/LDH (hemolysis),
autoimmune dz, chronic retic count, INR, PT1 fibrinogen (DIC), DAT
infection, etc.), Fe deficiency, (hemolysis), SPEP/UPEP (multiple myeloma),
Normocytic 80 MCV 100
hypothyroid, myelodysplasia, creatinine (renal failure causing j,erythropoietin),
alcoholism/chronic liver dz, TSH, AST/ALT/ALP/bilirubin/INR/PTT/albumin
sickle cell anemia, chronic renal (liver dz)
dz
Fe deficiency, anemia of
Ferritin, Fe,TIBC, Fe saturation (Fe deficiency,
chronic dz, a- or 13-Thalassemia,
Microcytic MCV < 80 anemia of chronic dz), anti-TrG/lgA (Celiac), Hb
lead ingestion/poisoning,
electrophoresis (thalassemia)
sideroblastic anemia
Vit Bi 2 and/or folate deficiency,
alcoholism/chronic liver
dz, AIHA, myelodysplasia, RBC folate, vit B1 2, TSH (hypothyroid), AST/ALT/
Macrocytic MCV> 100 ALP/bilirubin/INR/PTT/albumin (liver dz)
pernicious anemia, cytotoxic
chemotherapy, antiviral meds,
hypothyroidism

• High volume blood loss from any site- common situations include trauma, GI tract bleeds, menorrhagia
History
CC • Fatigue, generalized weakness, cold sensation in fingers/toes, dyspnea, pre-syncope/syncope, pallor, heavy menses,
black stools or blood in stools, changes in bowel habit, abdominal pain, weight gain (usually central i.e. ascites) or
weight loss, red/tea-colored urine, petechiae/purpura/easy_bruising
HPI • Patients usually present with a longstanding history of symptoms listed in CC
RED FLAGS • Active bleeding, melena and age> 50, change in bowel habit, evidence of pancytopenia
PMHx • Malignancy, chronic liver disease, hypothyroidism, myelodysplasia, multiple myeloma, chronic renal disease, sickle
cell anemia, GI diseases (Celiac, Crohn’s, colitis), rheumatologic disorders, mechanical heart valve
PSHx • Any recent surgeries as bleeding is a post-operative complication
PO&GHx • Menorrhagia, unusual increase in menstrual flow, recent pregnancies
Meds • Antiviral medications, chemotherapeutic medications, hydroxyurea, methotrexate, azathioprine, phenytoin,
Phenobarbital, TMP-SMX, zidovudine, warfarin, heparin
FHx • Familial anemias (thalassemias, sickle cell, etc.), colon cancer, autoimmune diseases
Social • EtCH intake
Risk Factors • Family Hx of anemias, cancer and/or autoimmune dz; alcoholism

physical
General Approach
o introduce yourself with title, wash your hands, check ABCs and add iv and monitors if necessary, ask for permission to do PE, check
vital signs (HR 1’ BP in general or from supine to seated/standing position, RR I are some changes in vitals you may expect)
2 Inspection
• In general: pale conjunctivae, pale skin
Signs of hypothyroidism: cool & dry skin, periorbital edema, thinning hair, apathetic look
o Signs of cytopenias other than anemia: petechiae, purpura
o Signs of liver disease: jaundice, sclera icterus, palmar erythemia, spider angiomas, caput medusae, asterixis, ascites, nail changes
percussion
If splenomegaly is suspected: percuss for Castell’s sign, percuss Traube’s space
If hepatomegaly and/or ascites are suspected: percuss the liver edges to gauge liver size, percuss for shifting dullness
4• Palpation
a Centrai/peripheral pulses, abdomen, thyroid, spleen and iiver
Auscultation
a Listen for increased heart rate, murmurs, extra heart sounds
5. Special Tests
a DRE: look for blood, mass, melena
Investigation
i. Blood work
• CBC-D, retic count (1= destruction/bleed, =decreased production), peripheral smear
• See INVESTIGATIONS column in Table 1
2. Radiology/imaging
U/S and/or CT: identify and characterize hepatospienomegaly, ascites, thyroid, abdominal masses
XR: identify unusual mass infiltrations in bones
3. Special Tests
• Bone marrow aspirate/biopsy if patient is pancytopenic/has abnormal smear and cause is not apparent
• Melena —* Gastoscopy; Fe deficiency anemia + age> 50 —* colonoscopy
Treatment
1. Emergent
ABCs, GCS < 8 then intubate, 02 lyE, transfuse PRBCs (0- at first then crossmatched cells once available), correct coagulopathy if
present (FFP, vitamin K, cryoprecipitate, octaplex), urgent plasmapheresis ifTTP/HUS
• Medical treat the underlying disorder
—
• Replenish deficient entities (Fe, folate, vit B1 2, erythropoietin, L-thyroxine), treat chronic dz (steroids, EtOH cessation, etc.)
• Surgical
• Bone marrow transplant (leukemia), splenectomy (AIHA, sequestration), colon resection (cancer)
3. Follow-up
• Repeat CBC-D, nutrient levels in blood, peripheral smear
4. Referrals
Hematology, oncology, endocrinology, gastroenterology
REFERENCES
Craver SA, Barkun AN, Sackett DL. The Rational Clinciai Examination: Does This Patient Have Splenomegaiy? JAMA 1993 Nov: 270(18): 2218-2221.
Sabatine MS (editor). Pocket Medicine: 3
rd
edition. Woiters, Kluwer/Lippincott, Williams &Wilkins. 2008:5.1-5.6.
Hoffman Ret ai. Hematology: Basic Principles & Practice, 5th
ed. Churchill Livingstone. 2008.
Internal Medicine Edmonton Manuai of Common Ciinicai Scenarios 99

ARTHRITIS AND JOINT (MONOARTICULAR)
201 I Ed Authors: Mohammed Osman PhD, Michelle Teo MD FRCPC, Elaine Yacyshy MD FRCPC
Station Obective
Approach to the diagnosis and management of patients presenting with monoarticular arthritis with emphasis on septic and crystal arthritis
Infectious
• Septic Arthritis (gonococcal, S. aureus, H. influenza, S. pneumo, gram negative bacilli, enterococcus, anaerobic).
• Mycobacterial (tuberculosis, and atypical mycobacterial)
• Fungal (candidal, coccidiomycosis)
• Lyme disease
• Osteomyelitis/Osteonecrosis
• Cellulitis
• Crystal induced arthropathy
• Gout (uric acid crystals)
• Pseudogout (calcium pyrophosphate arthropathy)
• Reactive arthritis, Psoriatic arthritis, IBD associated arthritis, rheumatoid arthritis)
• Inflammatory osteoarthritis
• Miscellaneous (sarcoid, hemarthrosis, trauma)
• Septic Arthritis
• Osteomyelitis/Osteonecrosis
History
ID • Age, gender
CC • Joint swelling, joint pain, can’t weight bear, restricted range of motion
HPI • morning stiffness, severity of pain, relapsing, pain with movement, fever, rigors, joint swelling, lower back pain,
duration of symptoms, recurrence, and progression. Other joints affected distribution, symmetry, additive or
—
migratory. Fatigue, skin changes over joints. Triggers.

RED FLAGS • Immunocompromised,, fever> 38.5, non-weight bearing, rapid onset/progression of symptoms, STI, IVDU,
myeloproliferative disease, SOB, high ESR/CRP, leukocytosis
PMHx • Diabetes, immunosuppression, hemophilia, trauma/surgery, hypertension, renal disease, nephrolithiasis, EtOH,
obesity, hypertriglyceridemia, IBD, recent GI infection/STI, myeloproliferative disease, receiving TB treatment —
PSHx • Joint prosthesis, open wound/joint debridement,

Meds • Steroids, cyclosporine, diuretics, low dose ASA, chemotherapy, allopurinol.
Allergies • General inquiry
FHx • Gout, Inflammatory arthritis, hemophilia,
Social • Ethanol, IVDU, camping in tick infested areas,
ROS • General: constitutional symptoms
• HEENT: eye pain/photosensitivity
• RESP: tachypnea, SOB/OE
• GI: abdominal pain, change in bowel movements
• GU: dysuria, discharge, dyspareunia
• DERM: new/old rash, new lumps/nodules
Risk Factors • Septic arthritis: IVDU, diabetes, immunosuppressed/compromised, trauma, prosthesis
• Gout: renal disease, chemotherapy, excess ethanol use, obesity, meds (diuretics, ASA, cyclosporine, ethambutol,
pyrazinamide)
Physical S
General Approach: ABC, vitals, temp, diaphoresis, increased work of breathing. E Erythen.a
2.
Inspection: SEADD AA0PIW
• Rashes: erythema migrans, eythema nodosum, psoriasis, tophi 0 Dktibuon(MCP/PIP0
• Range of motion: active then passive D Deformity
100 Edmonton Manual of Common Clinical Scenarios (Internal Medicine

• Palpation tenderness, warmth, effusion, synovial thickening
—
• Subcutaneous nodules, lymphadenopathy, hepatosplenomegaly

• Special tests wipe bulge test (small effusion), ballotment/patellar tap
-
estigat10ns
1 BloOd work CBC + differential, electrolytes, Creatinine, BUN, ESR, CRP, blood cultures, UA, urine culture, urine PCR for STI, serum urate.
—
diology/lmaging Xray of joint and contralateral limb of affected joint, bone scan, MRI
—
2
5urgical/Diagnostic Interventions Arthrocentesis for the 3C’s (cells, culture, crystals)
3
—
• Very cloudy, > 50, 000 WBC/cc, > 90% PMN, glucose (low), Gram stain/culture, gonococcal PCR highly suggestive of septic
—
arthritis
• JAMA 2007— WBC synovial counts >50,000 have a LR, 7.7 (95% Cl, 5.7-11.0) and for counts >100,000 LR, 28.0 (95% Cl, 12.0-
66.0). On the same synovial fluid sample, a PMN count of> 90% suggests septic arthritis with an LR of 3.4 (95% Cl, 2.8-4.2).
• Needle shaped, strong negative birefringence yellow crystals intra-cellular in acute attacks, extracellular in chronic gout, PMN
2000-50,000 gout JAMA (2003).
—
Treatment
1. Emergent ABC. Determine if septic arthritis or gout via history, exam, and arthrocentesis.
—
• Septic arthritis
• Percutaneous arthrocentesis (daily) and saline irrigation. Analgesia (codeine no NSAID), IV antibiotics x 2 weeks, then po
—
antibiotics x 3-4 weeks as per clinical response and gram stain/sensitivities. Limit weight bearing, encourage passive motion.
• Surgery arthrosopic lavage and debridement for axial and larger joints (e.g. hips).
-
• Gout
• Acute rest and elevate joint, hydration, reduce alcohol ingestion, NSAID, colchicine (0.6mg P0 bid), steroid (intra-articular
—
for mono/oligoarticular, systemic for polyarticular).

• Chronic weight loss, minimize alcohol, hydration, vitamin C 500 mg po daily, start allopurinol (2 weeks after acute attack) to
—
reduce urate level <360 mmol with prophylactic NSAID/colchicine 0.6 mg p0 bid until therapeutic levels reached.
References
1. Rott KTand Agudelo CA. Gout. JAMA (2003) 289:2857-2860.
2. 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.
3. Margaretten ME, Kohlwes J, Moore D, Bent 5. Does this adult patient have septic arthritis? JAMA (2007) 297(1 3):1 478-1488.
4. Mathews Ci, Weston VC, Jones A, Field M and Coakley 6. Bacterial Septic Arthritis in adults. Lancet (2010) 375(97 1 7) :846-855.

BLEEDING DISORDERS
2011 Ed. Authors:Janna Tram, James Yeung MD, Matthew Wang MD CCFP
Station Objective
In this station, you may be asked to obtain a history and physical from a patient who presents with excessive, delayed, or spontaneous
bleeding. You should be able to differentiate primary from secondary causes of hemostasis disorders and have an approach to correcting the
underlying pathology.
Differenti I iagnosis
1
• Primary hemostasis disorders are characterized by excessive, prolonged, superficial bleeding that occurs immediately postinjury
(PLT dysfunction —* PLT plug cannot form)
• ITP: isolated thrombocytopenia, N PT/PT1 dx of exclusion
• vWD: Factor VIII, 1’ bleeding time/PTT, PLTs usually N
• UP: thrombocytopenia, schistocytes and PLTs, N PT/PTT/fibrinogen, t markers of hemolysis
• Secondary hemostasis disorders are characterized by normal to only slightly prolonged bleeding, delayed bleeding deep in joints,
muscles, and Gl/GU tract (coagulation cascade disruption —* clot cannot form)
• Hemophilia A: positive FHx, t PU, N PT, I’ Factor VIII
• Hemophilia B: positive FHx, t PU, N PT, 4 Factor IX
• Liver dz: target cells on peripheral smear, abnormal coagulation studies and thrombocytopenia in setting of liver dz
• Vitamin K deficiency: t in PT out of proportion to t in PU, in vitamin K dependent factors (Factors II, VII, Xl, X)
• Disorders of primary hemostasis: vWD, ITP,TTP
• Disorders of secondary hemostasis: hemophilia A/B, liver dz, vitamin K deficiency
3. High Mortality:
• If hemodynamically unstable
• Untreated UP has mortality of >95%2
History
ID • Age
• Gender
CC • Bleeding tendency
HPI • Onset
• Bleeding tendency: immediately post-injury or delayed
• Site of bleeding: superficial mucocutaneous vs. deep joints or soft tissue
• Anticoagulation therapy
• Pregnancy, trauma, surgery, dental procedures
• Previous Hx: acquired vs. congenital
RED FLAGS Syncope, LOC, thunderclap headache, sepsis
PMHx • Liverdz,HIV
PSHx • Postoperative bleeding
PO&GHx • Postpartum hemorrhage, abnormal uterine bleeding
FHx • vWD, hemophilia or other heritable bleeding disorders
Meds • ASA, NSAIDS, warfarin, heparin, Plavix
Social • EtCH
ROS • HEENT: gingival bleeding, epistaxis, meningismus, thunderclap headache
• RESP: hemoptysis
• GI: hematochezia, melena, hematemesis
• GU: hematuria, excessive or prolonged menses
• MSK/ DERM: petechiae, ecchymoses, superficial bleeding, hemarthroses, hematomas
Risk Factors • FHx

physical
1 General Approach
• Focus on inspection for type and degree of bleeding
• Vitals:HR,BP,RR,T
2 Inspection
a petechiae (<2mm), purpura (<1cm), ecchymoses (>1cm)
• Bleeding from mucous membranes
o HemarthroSeS/hematOmaS
3 Percussion
a SplenomegallY: Castell’s sign, Traube’s space
4 Palpation
a Splenomegaly
• HepatOmegaly
5. AU5CUltti0
o Friction rub over spleen
nvestigations
1. Blood work
o PLT count, peripheral smear
a Bleeding time (or PFA-1 00 if available), PT/PU
o vWD: vWF antigen/activity, ristocetin cofactor/activity, Factor VIlI/IX
a If PT or PU abnormal —* mixing study
• If normalizes —* factor screen (I-Vlll = Hemophilia A, IX = Hemophilia B)
• If does not normalize —* inhibitor screen
a Hemolysis indicators: unconjugated bili, LDH, haptoglobin
a T&C if transfusion may be required
a Uncrossmatched Type 0 negative if hemodynamically unstable
2. Special Tests
• Bone marrow Bx (if ITP suspected)
Treatment
1, Emergent
If hemodynamically unstable, ABC’s, urgent consult to hematology as Tx dependent on etiology
1
a Transfuse with pRBC if Hgb low
o vWD: desmopressin (DDAVP)
a ITP: prednisone ± IVIG
• UP: plasmapheresis ± steroids (PLT transfusion is contraindicated)
a -Hemophilia A: Factor VIII concentrate
a Hemophilia B: Factor IX concentrate
o Liver dz: FFP, PLTs, treat underlying pathology
o Vitamin K deficiency: hold warfarin, Vitamin K IV/PO ± FFP
3. Follow-up
• Screen children of individuals affected by vWD, hemophilia
4. Referrals
• Hematology for continued management
References
1. Fogarty PF. Disorders of Hemostasis & Antithrombotic Therapy. In: McPhee Si, Papadakis MA, editors. Current Medical Diagnosis and Treatment 2009. New
York: McGraw Hill; 2009. p. 467-486.
2. Marques MB. Thrombotic thrombocytopenic purpura and heparin-induced thrombocytopenia: Two unique causes of life-threatening thrombocytopenia.
Clinics in Laboratory Medicine. 2009 Jun;29(2):321 -38.

CHEST PAIN, ANGINA & CARDIAC ARREST
201? Ed. Authors: Charles Lim, Craig Damke MD, Lucille Lalande MD FRCPC
OriginalAuthars: Sabira Suleman, Kris Chan MD, Michael Tjandrawidjaja MD, Evan LockwaadMD FRCPC
Station Objective
Differentiate causes of chest pain based on risk factors and typical presentations. Know the emergency treatment of life-threatening causes
such as Ml, aortic dissection, PE and tension pneumothorax.
• Ml defined as rise or fall of biomarkers (troponin) with at least one value 1h
99 %ile + at least one of the following:
> 1
• Symptoms of myocardial ischemia
• ECG changes indicative of new ischemia (ST segment elevation, new LBBB) or pathological Q waves
• Imaging evidence of new loss of viable myocardium
• Type 1: Ml from pathology in coronary artery wall (plaque erosion/rupture, fissuring, or dissection)
• Type 2: Mi from increased oxygen demand or decreased supply (coronary artery spasm, coronary artery embolus, anemia,
arrhythmias, hypertension or hypotension)
• CV: stable angina, unstable angina, valvular heart disease, pericarditis
• RESP: pneumonia, pleuritis, malignancy, pleural effusion
• Gl: esophageal spasm, GERD, Mallory-Weiss tear, biliary disease
• MSK: chest wall pain (costochondritis, herpes zoster, rib fracture)
• PSYCH: panic attackJanxiety disorder
• CV: acute Ml, aortic dissection, cardiac arrest
• RESP: PE, tension pneumothorax
• GI: esophageal rupture
History
ID • Age and gender
CC • Chestpain
HPI • OPQRST for chest pain features
• Previous episodes: Increasing frequency? Increasing severity?
• Association with meals, exercise, stress
• Associated symptoms: diaphoresis, pallor, nausea, dyspnea, cough, palpitations, pre-syncope
• What the Pt does when pain occurs: stop/rests (suggests angina), walks it off (unlikely angina)
RED FLAGS • Tearing, severe chest pain radiating to back (aortic dissection)
• Angina-like pain not relieved by nitroglycerin (unstable angina or MI)
• Syncope or pre-syncope indicating hypotension
• Pre-syncope with angina indicating large area of ischemia or critical AS
• .yspnea at rest (PE or tension pneumothorax)
• Pleuritic chest pain or hemopysis (PE)
PMHx • Cardiac risk factors (HTN, DM, dyslipidemia, obesity, smoking)
• Cardiac dz (prior Ml, angina, valvular dz, cardiomyopathy)
• Pulmonary: Asthma, COPD, pulmonary fibrosis
• GI: GERD, PUD, esophageal spasm
• Psych: anxiety or panic disorder, depression, stress
• Recent trauma to thoracic cavity (pneumothorax, aortic dissection), immobilization (PE), infection or flu-like illness
(pericarditis, myocarditis) or ‘I- in physical activity (costochondritis)
• CoagulopathiesorHxofCA(PE)
PSHx • Cardiac interventions: PCI, CABG, pacemaker, artificial valves
• Thoracic interventions: chest tube, positive pressure ventilation, esophageal instrumentation
Meds • Non-compliance: very common cause of recurrent or unstable angina
• Anticoagulants (warfarin, heparin) and antiplatelets (aspirin, clopidigrel)
FHx • Ischemic heart dz/atherosclerosis, Hx of cardiac risk factors (HTN, DM, dyslipidemia, obesity)
Social • Smoking, EtCH, drug use (esp. cocaine)

ROS Dysphagia, heartburn, immunosuppressed states (herpes zoster)
Risk Factors Cardiac risk factors (HTN, DM, dyslipidemia, obesity, smoking, sex, age, FHx)
physical
1. General Approach
• Assess risk: ensure vitals are stable, rio high mortality conditions (Ml, aortic dissection, PE, tension pneumothorax)
• Any female presenting with CP should be managed as aggressively as a male counterpart
• Approach by systems: CVS, RESP, GI, MSK, Psych
2 Patient Sitting
• Equal BP in both arms?
• Inspection
• Respiratory distress: tripoding, nasal flaring, cyanosis, indrawing, paroxysmal abdominal movement
• Tracheal deviation, distended neck veins, peripheral edema, cyanosis, circulation (capillary refill)
• Palpation
• Peripheral pulses: rate, rhythm, contour
• Palpate chest wall for deformity and isolated areas of pain, tactile fremitus, chest expansion
• Percussion of chest for areas of dullness/resonance, vertical asymmetry of percussion note (pneumothorax)
• Auscultate breath sounds to determine if AE is equal bilaterally and if there are adventitious sounds
3. Patient Lying
• Inspection
• JvP
• Palpation
• Heaves (parasternal) or thrills
• Apex: enlarged, sustained, or displaced
• Epigastric pain, Murphy’s sign (GI causes)
• Auscultation for heart sounds, extra sounds (S4 for MI, loud P2 in PE, friction rub, snap), murmurs, carotid bruits
Investigation
1. Blood work
• CBC-D, electrolytes, glucose, troponin I orT, CK/CK-MB, electrolytes, PTT, INR, D-Dimer
• CXR, Spiral CT if PE suspected, CT chest or TEE if aortic dissection suspected
3. Special Tests
• Urgent ECG —* in 20% of Ml, ECG may initially be normal
3
• Echocardiogram
• Thallium/MIBI scan
• Coronary angiography +/- stent
Treatment
1. Emergent
• Cardiac arrest: activate emergency response system and begin ACLS (Airway, Breathing, Circulation)
• STEMI: O2 morphine, aspirin, anti-emetic, beta-blocker, nitroglycerin, reperfusion therapy (PCI or thrombolytics)
Tension pneumothorax: needle decompression ( nd
2
intercostal space, midcIavicular line) followed by chest tube
• PE: start heparin or low molecular weight heparin and confirm with spiral CT
• Aortic dissection/Esophageal rupture: maintain hemodynamic stability, urgent surgical treatment
• Thrombolysis or angioplasty for STEMI, depending on timing and contraindications
3. Follow-up
• Risk stratification using stress test, coronary angiography and stenting if needed
• Management of risk factors: HTN, DM, dyslipidemia, smoking cessation
4. Referrals
• Admission to coronary care unit if STEMI or NSTEMI
References
Thygesen K, Alpert iS, White HD, Joint ESC/ACCF/AHA/WHF Task Force for the Redefinition of Myocardial infarction. Universal definition of myocardial
Infarction J Am Coil Cardiol. 2007 Nov 27;50(22):21 73-95.
2. LeeTH, Goldman L Evaluation of the patient with acute chest pain. N EngI J Med. 2000 Apr 20;342(16):1 187-95.
Longmore, M, Wilkinson IB, Davidson EH, Foulkes A, Mafi AR. Oxford handbook of clinical medicine. 8” ed. New York: Oxford University Press; 2010.

CONGESTIVE HEART FAILURE & EDEMA
20 I I Ed. Authors:Alim Nagji B. Hsc, Ammara Sadiq MD, Jamil Kanji MD FRCPC
OriginalAuthors: Sabira Suleman, Kris Chan MD, Michael Tjandrawidjaja MD, Evan Lockwood MD FRCPC
Station Objective
Determine the cause of the heart failure; suggest causes for peripheral edema and initiate management.
• New York Heart Association Heart Failure Classification
• I Heart disease present, no dyspnea with normal activity
—
• II Comfortable at rest, dyspnea with normal activity

—
• Ill Normal activities limited by dyspnea

—
• IV Dyspnea at rest
—
• Systolic CHF (CAD, HTN, Dilated CM, Ml, Viral, Toxins, Valvular dz, Coarctation)
• Can affect primarily LV or RV. LVF often leads to RVF
• Diastolic CHF (Hypertrophic CM, Restrictive CM, Aortic Stenosis, Pericardial dz)
• Diastolic CHF now known as’heart failure with preserved ejection fraction’
• High Output Failure (Anemia, Beriberi, Thyrotoxicosis, Pregnancy, Paget’s disease, AVfistula)
• Hepatic/Renal Failure
• Arrhythmia/Conduction: 5V1 a fib, AV block 3 n
2
(
r d)
d,
3. High Mortality! Morbidity:

• Tamponade, acute PE, high grade AV block, acute Ml
History
ID Age,sex
CC • SOB(OE)
• Weight gain (peripheral edema)
• Fatigue
HPI • Possible cardiac pathology (i.e. Ml)
• LVF: Orthopnea, PND, nocturnal cough (+pink frothy sputum), wheeze (pulmonary edema), nocturia, weight loss
• RVF:in abdominal girth (ascites), peripheral edema, anorexia, neck pulsations
RED FLAGS • SOB at rest
• Sudden onset of symptoms (tamponade or ACS)
• Fever (bacterial endocarditis)
PMHx • Cardiac risk factors (HTN, DM, dislipidemia, obesity, smoking, lifestyle, diet)
• Cardiac dz (heart failure (LR+5.8), Ml (LR+ 3.1), angina, valvular dz, arrhythmia)
• Pulmonary dz (COPD, HTN)
• Hepatic/renal failure
PSHx • Valve replacement
Meds • Rate slowing drugs: 13-blockers, CCB, most antiarrhythmics
• Fluid overload: NSAID, VI
• Cardiotoxic drugs: Anthracyclines, Chemotherapy (i.e. Doxorubicin), TCA
FHx • lschemic heart dz
• Atherosclerosis
• Cardiomyopathies
Social • Smoking, EtOH
• Diet/exercise (CAD, HTN)
• Recreational drug use (e.g. cocaine, methamphetamine, hepatitis)
ROS • HEENT: Sx of hyperthyrodismflhyrotoxicosis
• RESP: Cheyenne-Strokes breathing
• GU: Pregnancy
• MSK/DERM:Splinterhemorrhages

physical
General Approach
• Determine L vs RHF. Start with seated exam then proceed to supine. Note changes in distress.
2 Patient Sitting
• Inspection
expansion, position
• General: vitals, diaphoresis, pallor, cyanosis (central vs. peripheral), resp. distress, chest
• Pulsus paradoxus (pericardial effusion, tamponade)
• Edema (pitting vs. non-pitting, height)
• Percussion
• Dullness (pleural effusion)
• Palpation
• Peripheral pulses, rhythm, volume, contour, pulsus alternans (L sided (HF)
• Apical impulse (<2-3cm, 1 ICS), thrills, heaves (LSB —* LVH, subxiphoid RVH)
—
• Auscultation
• determine AE, breath sounds, crackles (LR+ 2.8)
3. Patient Lying
• Inspection
• JVP (LR+ 5.1), abdomiriojugular reflex (LR+ 6.4) (L sided (HF)
• Precordium scars (previous sx), heaves
• Palpation
• Apex: enlarged, sustained or displaced with L sided CHF
• Auscultation
• Specifically for S3 (volume overload), S4 (stiff ventricle), murmurs
4 Special Tests
• JVP — measure height, check for Kussmaul’s, AJR reflex
• Abdomen exam — palpate for tenderness, hepatosplenomegaly, fluid wave (ascites), caput medusa (portal HTN)
Investigation
Blood work
• CBC-D, BNP (1 50 pg/mL —* LR 3.1, < 50 pg/mL —* LR 0.06), Cr, BUN, Lytes, Ca, Mg, PC , glucose, albumin, LFT, TSH (if a-fib, old,
4
suspected on hx)
Radiology/Imaging
• Chest X-Ray
• Alveolar Edema (Bat’s wings) (LR+ 6)
• Kerley B lines, periBronchial cuffing and increased vascular markings (Interstitial edema — LR+ 12)
• Cardiomegaly (LR+ 3.3, LR- 0.33)
• Dilated prominent upper lobe vessels (Pulmonary venous congestion — LR+ 12)
• Pleural Effusion (LR+ 3.2)
3. Special Tests
• ECG (atrial fibrillation (LR+ 3.8), acute ischemia/infarct, hypertrophy, conduction abnormalities)
• Echo (ejection fraction, valvular dz, cardiomyopathy)
• Urinalysis (proteinuria)
Treatment
Emergent
• Lasix Morphine Nitrates 02 Position (upright with feet dependent) / Positive pressure (NIMV)
c Sx relief: nitrates, digoxin
o Improved survival: diet/lifestyle changes, ACEi/ARB, 13-blocker, (hydralazine/nitrates if can’t tolerate ACEi or black pt, NYHA lll/IV),
Spironolactone (NYHA III/IV & EF <35% after full dose ACEi/ARB, 13-blocker).
° No effective drugs for diastolic heart failure.
3. Referrals
• Cardiology: possible biventricular pacing/defibrillator if sx refractory and present at rest, multidisciplinary (HF clinic
References
Longmore M, Wikinson I, Turmezej T, Cheung CK. Oxford handbook of clinical medicine. 7’ ed. New York: Oxford University Press; 2008.
Arnold JMO, editor. Heart Failure. Merck Manual Professional. 18” ed. New Jersey: Merck Publishing; 2006.
Fans RE, Flather M, Purcell H, Poole-Wilson PA, Coats AJS. Diuretics for Heart Failure. Cochrane Library. 2009: 1-33.
4. Wang CS et al. Does This Dyspneic Patient in the Emergency Department Have Congestive Heart Failure? In: Simel DL, Rennie D, eds.The Rational Clinical
Examination: Evidence-Based Clinical Diagnosis, New York, NY: McGraw-Hill; 2009

COUGH
201 I Ed. Authors: KamalAbdulwahob, Abraam Isaac MD, Kourosh DinyariMD
Or/gina/Authors: Zoe Wo1i Ashley Gil/son MD, Mohit ShutaniMD FRCPCFACP
Station Objective
In this station you may be expected to differentiate acute from chronic cough, outline an approach to determining the underlying cause, and
describe a management plan.
• The diagnosis of the etiology of cough is largely dependent on history and physical exam. Pulmonary function testing, upper Gl
studies, esophageal pH studies, sinus radiography, and/or chest radiography may be used to augment the etiology of cough.
• Acute Cough
• Upper respiratory infection (including acute bronchitis); postnasal drip; COPD exacerbation; asthma*; pneumonia; sinusitis*
• Chronic Cough
• Chronic bronchitis, postnasal drip; postinfection cough (airway hyperresponsiveness after resolution of a viral or bacterial
respiratory infection); gastroesophageal reflux; foreign body; primary/secondary tumors; smoker’s cough
*may also present subacutely/chronically
• Conditions presenting with cough (±associated symptoms)
• Pulmonary embolism, congestive heart failure, cancer, pneumonia
History
ID • Ageandgender
CC • Cough
HPI • Duration: acute (< 3wks), subacute (3-8 wks), chronic (>8 wks)
• Timing and frequency: time of day (associated with meals, night symptoms, etc.), severity
• Character of cough: paroxysmal, dry or productive, sputum (purulent or clear), hemoptysis
• Precipitating factors: chemical irritants, smoke, allergies, pets, foods (e.g. milk)
• Ask about alleviating factors
• Associated symptoms: constitutional symptoms, wheezing, shortness of breath, nasal symptoms, sore throat, chest
pain, heartburn, sour taste, facial or dental pain, headache
RED FLAGS • Dyspnea, hemoptysis, weight loss, TB or HIV risk factors
PMHx • Respiratory: infection (viral, pneumonia, TB, pertussis), postnasal drip, COPD, asthma, bronchitis, CF/bronchiectasis,
sinusitis, interstitial lung disease, allergies
• Cardio: CHF, mitral stenosis, risk factors for pulmonary HTN; GI: GERD
• Other: Ca, DVT, sarcoidosis
Meds • ACEi, 3-bIockers, inhalers; ask about meds that improve cough
Allergies • Environmental allergies
FHx • Asthma, allergy, atopy
Social • Smoking, alcohol, pets, home environment, travel (to areas/regions with endemic fungal illness)
ROS • Complete general ROS with focus on RESP
Risk Factors • COPD, asthma, allergies, compromised immune system (e.g. HIV), environmental triggers (e.g. smoke, chemical
irritants) —
Physical
1. General Approach
• Vitals: BP, HR, RR, Temp, SpO2
2. Inspection
• Stable or in distress, on °2’ use of accessory muscles for breathing
• RESP: hands, chest wall structure and movement, nasal exam
• CV: mouth (central cyanosis), JVP
• Ears should be examined (signs of reflex cough); discoloration of lower eyelids; clubbing of the fingers

percu55i0
• RESP: consolidation, effusion
Palpation
• RESP: trachea midline, posterior chest wall expansion, tactile fremitus
• CV: apex, heaves, thrills, edema
• Palpate for cervical and clavicular lymph nodes
• Tenderness over sinuses
5 AuScU
t
1 i
• CV: heart sounds, murmurs, friction rub
• RESP: breath sounds and air entry, crackles/wheezes, egophony, whispered pectoriloquy
veStigati0n s
1 BloOd work
• As indicated by differential
2. adiology/lmagIg
• CXR: to help with identifying etiology but may not be necessary in young non-smoking patients
3. Special Tests
• Based on clinical suspicion of underlying cause
• Consider for pulmonary causes: full PFTs, methacholine challenge, sputum studies (cytology, gram stain, culture), chest CT, sinus
CT, bronchoscopy, ABG
• Consider for GERD: modified barium esophagography, 24 hour pH probe
Consider for cardiac causes: ECG, echo
Treatment
1. Emergent
• For PE, pneumonia, CHF please see appropriate sections in Edmonton Manual
• Cough Suppression
• Consider: narcotics (e.g. codeine), non-narcotics (e.g. dextromethorphan, diphenhydramine), inhaled corticosteroids, inhaled
-agonists, OTC decongestants (e.g. pseudoephedrine)
2
Treatment of underlying cause. See Table 1
Table 1. Treatment of common underlying causes of cough.
Common Causes of Cough Suggested Treatment of Underlying Cause
Common cold Symptom control (e.g. fluids, analgesics)
Influenza Symptom control, antivirals (e.g. oseltamivir)
Allergy Antihistamine*, avoidance of triggers
*avoid antihistamines for treatment of chronic cough in children
Bacterial sinusitis Symptom control, antibiotics (e.g. amoxicillin)
Asthma Refer to obstructive pulmonary disease section
Post-nasal drip Decongestants, nasal steroids, nasal saline rinses, cough suppressants, treat underlying cause of post
nasal drip (e.g. allergy, vasomotor, bacterial)
GERD Lifestyle changes, PPIs, H
RAs (insufficient evidence to show if treating GERD for chronic cough is any
2
better than placebo)
Medication induced Discontinue meds
3. Follow-up and referrals

Arrange for follow-up or set up referral based on etiology; smoking cessation counseling
References
1. http://www.merckandcoinc.neUmmpe/jndex.html [Internet]. New Jersey: Merck Sharp & Dohme Corp, © 2004-2010. Available from: htt://www.
2. Chang AB, Peake J, McElrea MS. Anti-histamines for prolonged non-specific cough in children. Cochrane Database ofSystematic Reviews 2008, Issue Art.
No.: C0005604 001: 10.1002/14651 858.C0005604.pub3.
3. Chang AR, Lasserson TJ, Gaffney J, Connor FL, Garske LA. Gastro-oesophageal refiux treatment for prolonged non-specific cough in children and adults.
Cochrane Database ofSystematic Reviews 2006, Issue 4. Art. No.: CD004823. DOI: 10.1002/14651 858.CD004823.pub3.
Irwin RS and Madison JM. The diagnosis and treatment of cough. N EngI J Med. 2000;343:1 712-1721.
Pratter MR, Brightling CE, Boulet, LP and Irwin RS. An empiric integrative approach to the management of cough: ACCP evidence-based clinical practice
guidelines Chest. 2006; 129:2225-231 S.

DEHYDRATION
20 I I Ed. Authors:Joffre Munro, Yang Li MD, Darren Nichols MD CCFP(EM)
Station Objective
To assess the hydration status of an adult patient presenting with a medical illness or injury that has the potential to result in dehydration.
• The following criteria have been adapted from the AMDA2 dehydration and fluid maintenance guidelines:
• Suspicion of increased output and/or decreased intake AND
• Physiological or functional signs or symptoms suggesting dehydration AND
• Elevated urea/creatinine ratio OR orthostatic hypotension OR tachycardia
• Note: Dehydration can be due to a fluid deficit, a sodium deficit, both fluid and sodium deficit, or blood loss
• Fluid Deficit
• Decreased Intake: secondary to dysphagia, cognitive dysfunction, or restricted access to fluids
• Increased Insensible Losses: fever, tachypnea, diaphoresis (including heat stroke)
• Increased Disease Losses: vomiting, diarrhea, ostomy, burns, DKA, diabetes insipidus
• Hypoalbuminemia: malnutrition, malabsorption syndrome, cirrhosis, nephrotic syndrome
• Sodium Deficit
• adrenal insufficiency, chronic nephritis, SIADH, diuretics, lithium, some fluid deficit conditions also
• Blood Loss
• Chronic: GI bleed, anemia (ie. aplastic, hemolytic)
• Acute: Please refer toStation 85: Shock” for details on hypovolemic shock
• Complications: falls, renal failure, delirium, myocardial infarction, death
History
ID • Patient name, age, sex
CC . Many presentations including cause of dehydration and/or symptoms of dehydration
HPI • Attempt to determine etiology and contributing factors
• OPQRST if presenting with a symptom (ie. weakness, light-headed, altered mental status)
• Signs of delirium (anxious, agitated, inattentive, hallucinations/delusions, somnolence, psychosis)
• Diet, feeding regimen (tube feeds, require assistance, etc)
• Change in fluid intake/output
• Change in body weight
• Increased falls, decreased ability to carry out ADLs
RED FLAGS Chest pain, altered mental status/loss of consciousness, tachypnea
PMHx • Chronic illnesses, previous hospital admissions
PSHx • Recent surgeries (potential for ongoing bleed)
PO&GHx • Currently pregnant
Meds • Diuretics, phenytoin, lithium, laxatives, anticoagulants
Allergies . General inquiry (medications, foods, environmental)
Social • Social supports (family and friends); living arrangements (ie assisted living, long term care, etc)
• Language barriers, isolation, restraints (impaired access to fluids)
• Alcohol, caffeine use
ROS • HEENT: dry mouth, dry eyes
• CV / RESP: palpitations, SOB, URTI/LRTI Sx (ie rhinorrhea, cough, SOB)
• GI: rapid weight loss, vomiting, diarrhea, constipation, blood in stool/melena
• GU: UTI Sx (ie dysuria), excessive/decreased urine output, dark coloured urine
• MSK / DERM: diaphoresis
• CNS: change in mental status, confusion, incoherent speech, irritability, seizures
• Other: fever, dizziness, fatigue, lethargy, weakness

msk Factors I• Cognitive impairment (dementia/delerium), depression
Dependence on feeding assistance, dysphagia/odynophagia, NPO/fluid restriction orders
• Chronic illnesses (ie stroke, diabetes, CHF), infection (ie respiratory or urinary tract), fever
• Previous episodes of dehydration
physical
1 General Approach
• ABCDES; vitals: orthostatic BP and pulse, fHR, tRR, 5p02, temperature, weights, LOC, urine output
2 Inspection
• Head to toe inspection for signs of bleeding (including DRE)
• HEENT: dry and sunken eyes, dry mucous membranes, longitudinal furrows on tongue, JVP
• MSK / DERM: dry axilla, decreased skin turgor, wet/clammy skin, draining wounds/ulcers
3. Palpation
CV: peripheral pulses, decreased capillary refill
MSK / DERM: decreased skin turgor (forearm or subclavian), wet/clammy skin, decreased capillary refill, decreased strength in
extremities
4. Auscultation
• CV: murmurs, extra heart sounds
• ABDO: decreased bowel sounds Simple Screen for Dehyration
Drugs (eg. diuretics)
End of life
Investigations High fever
.
Blood work Yellow urine turns dark
• CBC (hemoglobin, hematocrit), electrolytes, Ca, creatinine, urea, glucose Dizzy (orthostatic hypotension)
• Serum osmolality (mmol/L) = 2 x Na + urea + glucose Reduced oral intake
• Water deficit = [0.45 x basal body weight (kg)] -[140 mmol/L x basal body weight (kg) x 0.451 Axilla dry
2. SpecialTests serum Na (mmol/L) Tachycardia
Consider urinalysis, urine Na, urine osmolality Incontinence (fear of)
Swallowing assessment (if indicated) Oral problems/sippers
Neurological impairment
Sunken eyes
Treatment
Please refer to “Station 20: Fluid Resuscitation” for additional details on treatment.
1. Emergent
If severe dehydration or significant blood loss: establish vascular access with 2 large-bore peripheral IV lines and initiate isotonic
..crystalloid intravenous infusion; consider blood transfusion if necessary
o Treat cause of the dehydration if identifiable; treat any risk factors of dehydration if possible
• Replenish deficits and ongoing losses using oral, intravenous, or subcutaneous rehydration therapy
o Address and correct any electrolyte imbalances
o Closely monitor and reassess volume status throughout rehydration period
3. Referrals
o Consider referral to Emergency Department and onto Internal Medicine if admission is required
References
1. Thomas DR et al. Understanding clinical dehydration and its treatment. JAm Med DirAssoc 2008;9:292-301.
2. American Medical Directors Association (AMDA). Clinical Practice Guideline: Dehydration and fluid maintenance. Columbia (MD): AMDA; 2001. 28p.

Cognitive impairment (dementia/delerium), depression
Dependence on feeding assistance, dysphagia/odynophagia, NPO/fluid restriction orders
Chronic illnesses (ie stroke, diabetes, CHF), infection (ie respiratory or urinary tract), fever
Previous episodes of dehydration
physical
1 General Approach
• ABCDE5; vitals: orthostatic BP and pulse, tHR, 1’RR, Sp02, temperature, weights, LOC, urine output
2. Inspection
• Head to toe inspection for signs of bleeding (including DRE)
• HEENT: dry and sunken eyes, dry mucous membranes, longitudinal furrows on tongue, JVP
• MSK / DERM: dry axilla, decreased skin turgor, wet/clammy skin, draining wounds/ulcers
3• Palpation
CV: peripheral pulses, decreased capillary refill
MSK/ DERM: decreased skin turgor (forearm or subclavian), wet/clammy skin, decreased capillary refill, decreased strength in
extremities
4. Auscultation
• CV: murmurs, extra heart sounds
• ABDO: decreased bowel sounds Simple Screen for Dehyration
Drugs (eg. diuretics)
End of life
Investigations High fever
1. Blood work Yellow urine turns dark
• CBC (hemoglobin, hematocrit), electrolytes, Ca, creatinine, urea, glucose Dizzy (orthostatic hypotension)
• Serum osmolality (mmol/L) = 2 x Na + urea + glucose Reduced oral intake
• Water deficit = [0.45 x basal body weight (kg)] 1140 mmol/L x basal body weight (kg) x 0.451 Axilla dry
-
2. Special Tests Tachycardia

serum Na (mmol/L)
Consider urinalysis, urine Na, urine osmolality Incontinence (fear of)
Swallowing assessment (if indicated) Oral problems/sippers
Neurological impairment
Sunken eyes
Treatment
Please refer to “Station 20: Fluid Resuscitation” for additional details on treatment.
Emergent
• If severe dehydration or significant blood loss: establish vascular access with 2 large-bore peripheral IV lines and initiate isotonic
crystalloid intravenous infusion; consider blood transfusion if necessary
• Treat cause of the dehydration if identifiable; treat any risk factors of dehydration if possible
• Replenish deficits and ongoing losses using oral, intravenous, or subcutaneous rehydration therapy
Address and correct any electrolyte imbalances
• Closely monitor and reassess volume status throughout rehydration period
3. Referrals
Consider referral to Emergency Department and onto Internal Medicine if admission is required
References
1. Thomas DR et al. Understanding clinical dehydration and its treatment. JAm Med DirAssoc 2008;9:292-301.
2. American Medical Directors Association (AMDA). Clinical Practice Guideline: Dehydration and fluid maintenance. Columbia (MD): AMDA; 2001. 28p.

DIABETES
20!! Ed. Authors:Arabesque Parker, Stephanie Mu//in MD, Laurie Mereu MD FRCPC
OriginalAuthors:Arabesque Parker, Stephanie Mu//in MD, Laurie Mereu MD FRCPC
Station Objective
Diagnose diabetes, diabetic ketoacidosis, and hyperglycemic hyperosmolar state. Manage diabetes and its complications.
Diabetes Mellitus (any 1 of the following with confirmation on another day) Prediabetes
2. Classic symptoms of DM (polyuria, polydipsia, polyphagia, weight loss,
1 Impaired fasting glucose: FPG 6.1-6.9 mmol/L
blurry vision, nocturia, ketonuria) + random plasma glucose 1 1.1 mmol/L
2: Impaired glucose tolerance: 2hPG in a 75g OGTT
3. FPG 7.Ommol!L
7.8-1 1 mmol/L
4. 2hPG in a 75g OGTT 11.1 mmol/L
• Ti DM (13-cell destruction, insulin deficiency)
• T2DM (insulin resistance and relative insulin deficiency)
• Others: genetic defects, pancreatic dz, endocrinopathies, drugs, chemicals, infections
• Gestational DM
• Hyperglycemic comatose states: DKA and HHS
• Hypoglycemia
History
ID Ageandsex
CC DM
HPI • Typelortype2
• Age of onset and manner of diagnosis (symptoms, lab)
• Glucose monitoring (method, frequency, typical glucose and Al C results)
• Management (diet, oral hypoglycemic agents, insulin) and compliance (hospitalizations)
• Acute complications: thirst, urination, blurred vision
• Chronic complications: microvascular (retinopathy, nephropathy, autonomic neuropathy), macrovascular (CAD,
stroke, PVD)
• Foot care (regular foot exams, shoes, podiatry) and eye care (regular eye appointments)
RED FLAGS • DKA: polyuria, polydipsia, polyphagia, fatigue, NN, dehydration, abdominal pain, Kussmaul’s breathing, fruity
breath, and LGC
•
HHS: gradual onset, polyuria, polydipsia, weakness, dehydration, LØC
• Hypoglycemic reaction: autonomic symptoms first (tremor, palpitations, sweating, anxiety, hunger, NN) then
neuroglycopenic (difficulty concentrating, confusion, weakness, drowsiness, vision changes, difficulty speaking,
headache, dizziness)
PMHx Other CV risk factors: HTN, dyslipidemia, smoking, FHx of early heart dz
Meds Antihyperglycemic agents: biguanide, sulfonylurea, meglitinide, alpha glucosidase inhibitor, thiazolidinedione,
DPP4 inhibitor, GLP-i analog, insulin
FHx DM
ROS General: wt fatigue, dehydration, infections, peripheral sensory changes
,
• HEENT: blurred vision, fruity breath, cataracts

• CV: angina, orthostatic hypotension, claudication, foot ulcers, amputation
• GI: polydipsia, polyphagia, NN, abdominal pain, gastroparesis (bloating, early satiety)
• GU: polyuria, nocturia, urinary retention, ED
• MSK / DERM: Dupuytren’s contracture, bone demineralization, frozen shoulder
Risk Factors T2DM: Age >40 yrs, FHx, member of high risk ethnic population, Hx of IGT of IFG, vascular dz, Hx of gestational DM
Hx of macrosomic infant, HTN, dyslipidemia, obesity, PCOS, acanthosis nigrans, schizophrenia

physical
General Approach
Vitals: BP, HR, RR,Temp, Sp02, BMI
• HEENT, CV GI, RESP, NEURO, MSK, and DERM exams to follow complications
• Inspect insulin injection sites
• GCS when concerned about DKA, HSS, and hypoglycemia
• Diabetic Foot exam (See Chapter 35)
e5t1gatb0ns
1
work
BloOd
• Random glucose, fasting plasma glucose (FPG), or oral glucose tolerance test (OGTT)
• HbA1C to evaluate glycemic control over last 3 months
Treatment
Emergent DKA and HHS Treatment
• Hypoglycemia: 1. General Approach
• Oral ingestion of 15g of carbohydrate • Best managed in ICU or step-down setting with
• Unconscious or NPO and 5 years old: 1 mg glucagon SC or IM, specialist care
or 10-25 g glucose IV (1 amp D5OW) • Close monitoring (ql h) of volume status (ins
• After hypoglycemia reversed, prevent recurrence with meal or and outs), vital signs, neurologic status, lytes,
snack anion gap, osmolality and serum glucose
5. Treatment Options • Treat precipitating factors
• Lifestyle: healthy wt, regular exercise, and smoking cessation 2. IV Fluids
• Antihyperglycemic agents: for T2DM • Normal saline 1 L/hour initially to correct
• lnsulin:forTlDM, sometimesT2DM volume deficit, then 250-500mL/hour
• Annual influenza vaccine, pneumococcal re-vaccination if > 65 years • If Pt IS in shock, then continue normal saline
old 1 -2L/hour to correct shock
6. Treatment Targets • Once euvolemic, switch to half normal saline
• Glycemic targets: AIC 7, premeal and FPG 4-7 mmol/L, 2h • Once plasma glucose reaches 14 mmol/L, add
postprandial 5-10 mmol/L, 5-8 if Al C targets not being met D5W or Dl OW to maintain plasma glucose of
BP targets: <130/80 (<125/75 if microalbuminuria) 12-14 mmol/L
• Lipid targets: LDL <2.0 mmol/L (primary goal); total cholesterol to 3. Acidosis and Hyperglycemia
HDL ratio <4.0 mmol/L (secondary goal) • IV short acting insulin 0.1 units/Kg bolus, then
7. Follow-up 0.1 units/Kg/h, titrate against anion gap
• Self monitored blood glucose >3x/day if on insulin • pH <7: may consider giving 1 amp of sodium
• Ketone testing (blood or urine) during periods of acute illness (T1DM) bicarbonate
• AlCq3mo 4. Potassium Deficit
• Annual at dx forT2DM, 5 years after dx forTl DM K>5.5 mmol/L: no KCI replacement
• Spot urine albumin to Cr ratio plus urine dipstick • K 4-5.5 mmol/L: add 20 mmol KCI to IV, less
• Diabetic foot exam aggressive if renal failure
8. Referrals • K 3.3-4 mmol/L: add 40 mmol KCI to IV, less
• Ophthalmologist for annual eye exam at dx for T2DM, 5 years after dx aggressive if renal failure
for Ti DM • K <3.3 mmol/L: hold insulin and give 40
• Registered dietitian for nutrition counseling mmol/L KCI (max 40 mmol/h)
References
Canadian Diabetes Association. Canadian Diabetes Association 2008 Clinical Practice Guidelines for the prevention and management of Diabetes in
Canada. Canadian Journal of Diabetes. 2008;32.

DIARRHEA
201! Ed. Authors:Adarsh Rao, Carol Chung MD, Arnold Vorh MD FRCPC
OriginalAuthors: Carrie Ye MD, Vince 8am MD FRCPC
Station Objective
Diarrhea, both acute and chronic is a common disease worldwide causing significant morbidity and mortality. It is important to distinguish
between the causes of diarrhea, to determine when it is appropriate to investigate and initiate treatment.
Diagnostic Criteria: Acute diarrhea is defined as> 3 stools/day or >200 g of stool/day for> 2 days or less than 2 weeks. Stools are looser and
more frequent than usual. Chronic diarrhea lasts for >4 weeks.
1. ACUTE:
• Infectious —* Parasitic (Giardia, Crptosporidia, Cyclospora, Isospora, Amoebiasis), Bacteria (Camplyobacter, Salmonella, Shigella,
Listeria, ETEC, EHEC, C.difficile, Staph aureus, Bacillus cereus, Clostridium perfringens), Viral (Hep A, Rotavirus, Norovirus), Traveller
(ETEC, Norovirus, Shigella, Salmonella, Campylobacter, Giardia), Day care (Camplyobacter, Cryptosporidium parvum), Hospital
(C.difficile, Norovirus, Rotavirus —* children)
2. CHRONIC:
• Functional —* lBS (10-20% of pop.) constipation with overflow diarrhea, incontinence.
• Osmotic agents —* lactose, sugars —> sorbitol, mannitol, laxative abuse.
• Inflammatory —+ IBD (UC, CD), microscopic or collagenous colitis
• Metabolic —* Addison’s disease, hyperthyroidism, uremia, cystic fibrosis
• Maldigestion/malabsorption —+ Pancreatitis, celiac disease, short bowel syndrome, small intestinal bacterial overgrowth
• Neoplastic—* Colorectal cancer, carcinoid tumors, gastrinoma, medullary thyroid carcinoma
• latrogenic —> Drugs, alcohol, caffeine, surgery, radiation, laxative abuse
History
ID • Age, Gender, Demographics, Geography
CC • Diarrhea
HPI • Characterize Diarrhea:
• Onset: Abrupt onset is likely an infection or due to meds while diarrhea with insidious onset of longer duration is
likely early chronic illness.
. Urgency: Urgent defecation usually indicates rectal involvement.
• Frequency: Watery diarrhea that continues despite fasting —* Secretory; stops with fasting —* osmotic.
Alternating constipation and diarrhea — lBS. Nocturnal diarrhea is pathological.
• Quantity: Large bowel: small volume BM, frequent, mixed with blood, mucous or pus.
• Small bowel: large and infrequent BM.
• Quality of BM (bright red blood — large bowel; watery — small bowel; melena (black, tarry stool) —+ upper GI
bleed; mucous, foul smell, floating/oil drop —* steatorrhea)
• Risk Factors:Travel history, immunosuppression, homosexual contacts, food outbreaks (undercooked poultry
or eggs, Campylobacter, Salmonella), beef products CE. coli 01 57:H7), seafood (Vibrio parahaemolyticus,
cholera), extra-intestinal signs of IBD, family hx, antibiotics hx (clostridium difficile), diet, steatorrhea, weight loss,
malignancy, immunosuppressed (sepsis), laxative use, tumour history, healthcare exposure, childcare facilities.
• Associated Sx: Fever, abdominal pain, tenesmus, vomiting, cough, arthalgia, myalgia, sore throat
RED FLAGS • Fever, drenching night sweats, weight loss, age >50, hematochezia —* c!oloreotal Cancer CRC
• Vomiting, fever, arthritis, skin rash, anorexia
• Consider hospitalization: high unrelenting fever, bloody diarrhea, severe volume depletion, severe abdominal
pain, immunocompromised patients, pregnant patients
• Chronic diarrhea, noc.turnal symptoms, ciramping, weight loss, ±hematoc.hezia —* Inflammatory Bowel Eisease
IBD
PMHx • Hyperthyroidism, Addison’s disease, AIDS, Celiac disease, IBD, lBS. colorectal cancer, lactose intolerance, DM,
pancreatic disease, cystic fibrosis, incontinence
PSHx • Bowel resection (short gut), cholecystectomy (bile acid wasting)
Meds • Prior antibiotic use (C. difficile); laxative, chemotherapy, colchicine
FHx • Colon cancer, Celiac disease, IBD

Drugs, alcohol, caffeine, sexual history, exposures
• HEENT: uveitis (IBD), proptosis (hyperthyroidism), oral ulcers (Crohn’s Disease), postural lightheadedness
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
1 General Approach:
• Assess the vitals: dehydration—HR Ct, postural change), BP (N or or orthostatic hypotension), lnfectious:T (t)
2. Inspection:
• Assess the patient’s extracellular volume by examining mucous membranes, capillary refill, skin turgour and JVP evaluation
3. AuscultatiOn ABD:
• Bowel sounds increased (diarrhea), high pitched peristalsis in waves not related to pain (gastroenteritis, dysentery, active UC)
4. Percussion ABD:
• Dullness, tenderness, liver size (N=9-1 1cm at the MCL) and Castell’s sign (10th CS at the L anterior-axillary line) for completeness
5. Palpation ABD:
• Peritonitis (guarding and rebound tenderness). Both light and deep palpation looking for masses, and areas of tenderness
6. Special Tests DRE:
• mass (tumour, abscess), blood, irregular mucosa (UC, pseudomembranous colitis)
Investigation
Most episodes of diarrhea are self-limited, Investigate for patients with red flags (see above list):
1. Blood work
• CBC-D, WBC increase (infectious), Hgb with bloody diarrhea
• Fluid status: electrolytes, Cr, urea
• Anti-transglutaminase and IgA level (for Celiac disease), TSH (hyperthyroidism)
2. Microbiology
• Stools: C&S, O&P, C. difficile toxin, Giardia toxin, fat, WBC (inflammatory), phenothalin (laxative abuse), stool osmolality (secretory
vs. osmotic diarrhea)
• PCR (for noroviruses), Electron microscopy (noroviruses, and rotaviruses)
3. SpecialTests
• Barium enema + sigmoidoscopy (Crohn’s, CRC), Abdominal CT. Abdominal X-ray to rule out obstruction
• Colonoscopy if chronic (Crohn’s, UC, CRC)
• Gastroscopy (duodenal biopsy for Celiac disease)
• Check for occult blood (FOBT). Also check for fissues, hemorrhoids, fecal impaction or masses/ polyps
Treatment
1. Emergency
• IV fluids and electrolytes (depending on volume status). Moderate to severe febrility —* treat empirically or with quinolone. Most
common electrolyte/acid-base problem is metabolic acidosis or hypokalemia.
• Dependent on underlying condition-do NOT empirically prescribe anti-diarrheal agent
• Specific Tx: Gluten-free diet (celiac), flagyl or vancomycin (C. difficile), ciprofloxacin (Shigella, Salmonella, Campylobacter, E.coli
not EHEC because of increased progression to HUS and UP), pancreatic enzyme replacement/fat soluble vitamin (ADEK) for
pancreatic insufficiency.
• Referrals: GI when etiology of diarrhea is unclear despite multiple investigations; need to scope for malabsorption or IBD.
Oncology! Gen surgery if suspect CRC
Reference
1. Aranda-Michel, J. Giannella, R. Acute Diarrhea: A Practical Review. American Journal of Medicine. 10(6): 670:676, 1999.
2. Donowitz M., Kokke FT., Saidi R. Evaluation of Patients with Chronic Diarrhea. NEJM. 332 (11): 725:729, 1995.
3. Lam E., Leung ii. The Essentials of General Surgery. Essentials of Clinical Exam. 6
th
Edition, 4S7:463, 2010.
4. Eskander A., Kandel C. The Abdominal Exam. Essentials of Clinical Exam. 6
th
Edition, 42:47,2010.

DYSPEPSIA
201 I Ed. Authors: Mohammed Osman PhD, Vay5eIvarajah MD, Connie SwitzerMD FRCPC
Station Objective
Approach to the diagnosis and management of patients with symptoms of dyspepsia.
Organic GI causes(40% of patients)
• PUD — gastric or duodenal ulcer. Often associated with H. pylon infection or ASAINSAID use
• GERD/NERD
• Esophagitis — reflux, alcohol-induced, infectious (Candidal, HSV, CMV), or eosiniphilic esophagitis
• Gastritis — drugs (NSAID, ASA, iron), inflammatory, atrophic, stress-induced, H. pylon infection
• Motility disorder esophageal dysmotility, achalasia, diabetic gastroparesis, intestinal dysmotility
—
• Celiac’s disease, Upper Gl Crohn’s disease

• Neuroendocrine tumors of GI origin — e.g. Zollinger-Ellison Syndrome
• Infection: giardia lamblia and strongyloides stercoralis
• Functional Dyspepsia no organic etiology found for dyspepsia
-
• Cardiac angina pectoris, myocardial infarction, congestive heart failure, pericarditis

—
• Metabolic disorders diabetic ketoacidosis, uremia, hypothyroidism, hyperparathyroidism, hypercalcemia

—
• Connective tissue disease scleroderma, SLE

—
• Miscellaneous pleurisy, sarcoidosis, sepsis, TB, post-immobilization, post-vagotomy, dumping syndrome

—
• Psych — Mood disorders, anxiety disorders, conversion disorders, hypochondriasis

2. High Mortality/Morbidity:
• Neoplastic esophageal cancer, gastric cancer
—
• Myocardial infarction, dissecting aortic aneurysm

• Penetrating peptic ulcer
• Pancreatitis
History
CC • Constellation of symptoms including epigastric pain aching or discomfort +/- early satiety, nausea, vomiting,
abdominal bloating, belching, indigestion or hiccups
HPI • Onset, quality of pain, location, radiation, frequency, association with position, meals or dietary factors, night time
symptoms (cough, pain, acid taste), associated symptoms (odynophagia, heartburn or regurgitation) Rule out
cardiac features such as retrosternal chest pressure, radiation to shoulders, neck, diaphoresis,shortness of breath,
and exacerbation with meals, cold, and exertion.
• Symptomatic improvement with antacids, H2RA or PPI
RED FLAGS • Persistent vomiting, dysphagia, bleeding, unintentional weight loss (>3 kg in 3 mo, onset age >50, rapid onset
with progressive symptoms, fevers, chills, persistent NSAID use, palpable mass.
PMHx • Previous peptic ulcer disease, ischemic heart disease, dyslipidemia, chronic pain syndromes, ulcers, diabetes,
immunosuppression, recent antibiotic use
PSHx • Appendectomy, cholecystectomy, hysterectomy
• Gastroscopies, barium swallow
Meds • NSAID/ASA, steroids
FHx • Irritable bowel syndrome, esophageal or gastric CA
Social • Smoking, alcohol, marijuana, caffeine, Travel Hx/country of origin
ROS • General: fatigue, weight gain/loss, headache, vertigo, light headed
• CV: dependent edema, orthopnea, paroxysmal nocturnal dyspnea, palpitations,
• RESP: dyspnea, sputum, cough, hemoptysis, history of TB/pneumonia
• GI: abdominal pain post-parandial, diarrhea, bowel habits
• GU: decreased urine output
• MSK / DERM: arthralgia, myalgia, morning stiffness, cyanosis, pallor, jaundice, flushing

physical
ABCs, Vitals, orthostatic vitals (may suggest significant blood loss or dehydration). Focus exam based on likely etiology
2 Inspection: skin tightening, calcinosis, telangactesias and digital ulcers (scleroderma), clubbing,, pallor, ashen appearance, jaundice,
dental erosions, halitosis, oral ulcers/candidiasis
3 Percussion: chest tenderness to palpation, abdominal fields for obstruction
Palpation: cervical or supraclavicular lymphadenopathy (Virchow’s node), abdominal tenderness, rebound, guarding, palpable
gallbladder or masses, hepatosplenomegaly
5. Auscultati0 complete cardiac and respiratory exam, abdomen for bowel sounds, succession splash (gastroparesis)
6. Special Tests: evaluate for ascites, digital rectal examination
7. Evidence based examination:
• JAMA 2006- Clinical impression based on history and exam do not distinguish between organic and functional dyspepsia
• American JGastroenterology200l history and physical exam in patients with no red flags (see above) not good predictors of
—
endoscopic findings
investigations
1. Blood work: CBC-D, electrolytes, chemstrip, Ca, albumin, lipase, troponin, CK
2. Imaging: upper GI series oresophagogastroduodenoscopy (EGD) with or without biopsy
• Indications for endoscopy:
• Red flags (see above)
• Odynophagia, jaundice, epigastric mass, PMHx PUD
• Failure of several PPI treatments, FHx of gastric/esophageal cancer, NSAID
3. SpecialTests
• Urea breath test: no alarm symptoms, age <45 treat if H. pylon positive
—
• Esophageal manometry: normal EGD and symptoms suggestive of motility disorder

Ambulatory 24-hour esophageal pH monitoring- normal gastroscopy and suggestion of GERD
Fasting serum gastnin levels, or serum secretin test (ZES)
Treatment
1. Emergent: suspect UGI bleed if hemodynamically unstable
• ABC, monitors, 2 large bore IV CBC-D, lytes, BUN, Creat, INR, crossmatch/transfuse blood, pantoprazole 80 mg IV bolus then 8 mg/h
and volume resuscitate
• Proceed to therapeutic EGD
2. Treatment Options (Stable, outpatient)
• Lifestyle
• Discontinue NSAIDs and new medications that may be triggering
• Smoking/alcohol cessation,(good evidence for smoking cessation and weight loss) manage anxiety/depression, avoid foods
that trigger symptoms
• Weight loss, and reduction of fatty food ingestion, smaller meals, no eating 4 h presleep riple Therapy For H.Pylori Irradiation
(no evidence for except for elevating Head of bed decreases nocturnal pH exposure, not 1.)Omeprazole 20 mg po bid
symptoms) .)Ciarithromycin 500mg po bid
• .)Amoxiciilin 1 g p0 bid xlO-14 d
• Medical
• Non-ulcer dyspepsia: omeprazole 20 mg P0 CD or lansoprazole 15 mg p0 OD to omeprazole 20 mg po pm
• Functional dyspepsia: omeprazole 20 mg OD or itopride 50— 100 mg p0 tid +/- amitryptilline 50 mg qhs
• H. pylon: eradication of infection is controversial
• Treatment = triple therapy then treat as non-ulcer dyspepsia
• PUD: omeprazole 40 mg P0 OD x 8 weeks, then 20 mg CD after healing
• H. pylon: use triple therapy x 2 weeks, then treat as PUD
• Surgical: distal subtotal gastrectomy, (reserved for complicated GIB unresponsive to endoscopic therapy)
References
1. Malfertheiner P, Chan FK and McCoII KE. Peptic Ulcer Disease. Lancet. (2009) 374(9699): 1449-14461.
2. Moayeddi P, Talley NJ, Fannerty MB and Vakil N. Can the clinical history distinguish between organic and functional dyspepsia?JAMA (2006) 295(1 3):1 566.
3. TaIley NJ, Vakil NB and Moayyedi R American Gastroenterological Association Technical Review on the evaluation of dyspepsia. Gastroenterology
(2005)129:1756_ 1780
4. Danish Dyspepsia Study Group. Value of the unaided clinical diagnosis in dyspeptic patients in primary care. The American Journal of Gastroenterology
(2001) 96, 141 7—1421.
.
ABR Thomson. The Dyspepsia Alphabet: DLJ, GU, GERD, NERD, NUD/FD, and UD. Can J Gastroenterology (2000)15(1 ):49-55.

DYSPNEA
201 I Ed. Authors: KamalAbdulwahab, Abraam Isaac MD, Kourosh DinyariMD
OriginalAuthors: Ryan Gallagher, Lisa StebleckiMD MPH CCFP
Station Objective
To demonstrate an understanding of the etiologies and approach to, and the potentially life-threatening signs and symptoms of, dyspnea.
Useful to divide cause of dyspnea anatomically and in accordance to onset (seeTable 1)
Table 1. Conditions that can cause dyspnea (common ones are bolded but note this is not an exhaustive list)
Respiratory Cardiac Other
• Asthma
• Anaphylaxis
• PE CHF
• Panic attack
Acute • FB aspiration Ml
• Hyperventilation syndrome
(minutes) • Hemo/pneumothorax Rupture or dysfxn of papillary
• Myasthenia gravis
• Toxic airway damage (e.g. chlorine muscle
• Diaphragmatic paralysis
inhalation)
Subacute • Pneumonia • CHF pericardial effusion, .
. • Anemia
(hours-days) • AECOPD tamponade, stable angina,
• COPD
Chronic • Pleural Effusion • CHF • Anemia
(hours-years) • Restrictive lung disease • Stable angina • Deconditioning
• Interstitial lung diseases

PE, hemo/pneumothorax, Ml, Tamponade, anaphylaxis, lung/metastatic cancer, airway/chest trauma, recurrent pneumonia,
pericardial effusion, CHF, CAD
History
N.B. If the patient is unstable, proceed with ABC’S first and then proceed with an emergency SAMPLE hx: (symptoms (related),
Allergies, Medications, PMHx (relevant), Last meal, vents prior to presentation)
CC. SOB
HPI • Acute or chronic, previous events, previous hospitalization, chest pain or pressure, radiating pain
• Exertional (e.g. distance pt can walk w/out SOB, number of flights of stairs)
• Orthopnea, PND (tip: how many pillows do you need at night?), leg swelling
• Previous URTI (OPQRST), sick contacts, cough ± sputum, nasal congestion, rhinorrhea, cold/flu symptoms
• Recent travel, extended flight or periods of prolonged sitting (a common presentation of PE)
• Environmental exposures: asbestos, allergens, chemicals, cold
• Trauma: blood loss, chest crush injuries, penetrating chest trauma, rapid velocity changes
RED FLAGS • Fever, night sweats, change in weight, syncope, LOC, chest/shoulder pain, hemoptysis, crackles
PMHx • Asthma, COPD, CHF, asthma, previous episodes of DYSPNEA, Malignancy, previous PE
PSHx • Thoracotomy, heart surgery (possible phrenic nerve paralysis secondary to surgery)
PO&GHx • Pregnancy: DVT/PE, pressure of fetus
Meds ILD risk: Amiodarone, Bleomycin (cancer tx), Methotrexate, Nitrofurantoin;
OCP (DVT), immunosuppressive drugs (for pneumonias), coumadin, heparin, medication overdose, immunizations
(influenza), injection drug use (talc lung)
Allergies Environmental, food
FHx • a-i antitrypsin deficiency, CF, cancers, Ml, hypercoaguability, HTN, Ichol., asthma, allergies
Social • Smoking, anxiety disorders, injection drug use (talc lung), alcohol, medication overdose

• HEENT: neck masses
• CV: angina, CHF (pulmonary HTN)
• RESP: orthopnea
• GI/GU: bleeds (e.g. dark stools, coffee ground emesis, tea colored urine)
• MSK / DERM: scoliosis, ankylosing spondylitis, calf pain, leg swelling
Risk Factors Obesity, smoking, occupational exposure, aspiration (often secondary to swallowing dysfunction), decreased
mobilization (DVT/PE), DM
physical
1 General Approach
), U/C (watch for pulsus paradoxus)
ABC’s, GCS (<8 —* INTUBATE!), Vitals (BP, HR, RR,Temp, SpO
2
2. Inspection
General: appear septic, airway protection (e.g. tripod position), speech, exertional breathing, diaphoresis
HEENT: nasal flaring, pursed lip breathing, suprclavicular indrawing, central cyanosis, airway swelling, accessory mm use (e.g.
scalenes), tracheal deviation, JVP (Kussmauls’ sign)
0 RESP/CV: increased AP diameter, chest wall deformities, scars, intercostal indrawing, asymmetry, neck veins
ABDO: subcostal indrawing, accessory mm use (paradoxical abdominal breathing), HJR
Periphery: acrocyanosis, clubbing, cap refill, edema (CHF), cold/clammy skin, nicotine stains
DERM: angioedema, urticaria
3. Percussion
• RESP: lung fields (do not forget UL’s on ant chest wall), hypo- or hyper-resonance, diaphragmatic excursion
4. Palpation
a CV: palpable thrills/heaves, apex beat (position, amplitude, duration)
• RESP: tactile fremitus, chest wall expansion (place hands on back (thumbs at 1 0 th
rib) and have Pt inhale)
• Other: edema, pulses in all four limbs, lymphadenopathy (including inguinals, supraclavicular, and cervical)
5. Auscultation
• RESP: (all lobes, R vs L) crackles, wheeze, stridor, AE, prolonged expiration, egophony (consolidation)
• CV: 53/54, murmur, rhythm (AF)
6. Special Tests
• Laryngeal ht: distance from thyroid cartilage (top) to sternal notch (<4cm is abnormal), PFT/PEFR
Investigation
1. Blood work
• ), electrolytes, urea, Cr, (fluid status), glucose
CBC-D(infection/inflammation, anemia), ABGs (calc A-aDO
2
ECG, ECHO (cause of CHF ± pulmonary HTN), CXR, CT (if indicated),VQ scan (if indicated)
3. Special Tests
• 2 improves w/ admin of 02), oximetry, D-Dimer, troponin, BNP, sleep
PEFRJPFT, methacholine challenge test, 02 test (see if Sp0
study
• Thoracocentesis (pleural effusion), needle decompression + chest tube (notably for tension pneumothorax)
Treatment
1. 2 monitors, consider needle decompression if acute tension pneumothorax,
Emergent: O2 2x large bore IV’s, cardiac and SpO
bronchodilators or diuretics for symptom control, airway management equipment @ bedside
2. Treatment Options: medical and surgical Tx dependent on etiology, (see Hemoptysis, etc...)
3. Further workup: e.g. CHF —* elucidate original cause
4. Follow-up: especially with disease like asthma where frequent exacerbations affect long-term outcome
• Mid level evidence suggesting that psychosocial support, breathing control, and use of coping strategies (e.g. relaxation
techniques and coping strategies) may reduce dyspnea
5. Referrals: pulmonologist, other specialties dependent on etiology
References
1. Bickley LS and Szilagyi PG. Bates’Guide to Physical Examination and HistoryTaking 9th ed. Philadelphia: Lippincott Williams & Wilkins, 2007.
2. http://www.merckandcoinc.net/mmpe/index.html [internet]. New Jersey: Merck Sharp & Dohme Corp, © 2004-2010. Available from: httpi/www.
merckandcojncnet/mmpe,secO5/ch5/ch5dhtml#secO5ch5ch5d57
.
Bredin M. et al. Multicentre RCT of Nursing Intervention for Breathless in Patients with Lung Cancer.1 999. BMJ Apr 3;31 8(71 88):901 -4.

DYSPNEA
20?? Ed. Authors: KamalAbdulwahab, Abraam Isaac MD, Kourosh Dinyari MD
OriginalAuthors: Ryan Gallagher, Lisa Stebiecki MD MPH CCFP
Station Objective
To demonstrate an understanding of the etiologies and approach to, and the potentially life-threatening signs and symptoms of, dyspnea.
Useful to divide cause of dyspnea anatomically and in accordance to onset (seeTable 1)
Table 1. Conditions that can cause dyspnea (common ones are bolded but note this is not an exhaustive list)
Respiratory Cardiac Other
• Asthma
Anaphylaxis
• PE • CHF
Panic attack
Acute • FB aspiration • Ml
Hyperventilation syndrome
(minutes) • Hemo/pneumothorax • Rupture or dysfxn of papillary
Myasthenia gravis
• Toxic airway damage (e.g. chlorine muscle
Diaphragmatic paralysis
inhalation)
Subacute • Pneumonia • CIIF, pericardial effusion,
Anemia
(hours-days) • AECOPD tamponade, stable angina,
• COPD
Chronic • Pleural Effusion • CHF • Anemia
(hours-years) • Restrictive lung disease • Stable angina • Deconditioning
• Interstitial lung diseases
PE, hemo/pneumothorax, Ml,Tamponade, anaphylaxis, lung/metastatic cancer, airway/chest trauma, recurrent pneumonia,
pericardial effusion, CHF, CAD
History
N.B. If the patient is unstable, proceed with ABC’S first and then proceed with an emergency SAMPLE hx: (ymptoms (related),
IIergies, Medications, PMHx (relevant), Last meal, Events prior to presentation)
ID • Ageandgender
CC • SOB
HPI • Acute or chronic, previous events, previous hospitalization, chest pain or pressure, radiating pain
• Exertional (e.g. distance Pt can walk w/out SOB, number of flights of stairs)
• Orthopnea, PND (tip: how many pillows do you need at night?), leg swelling
• Previous URTI (OPQRST), sick contacts, cough ± sputum, nasal congestion, rhinorrhea, cold/flu symptoms
• Recent travel, extended flight or periods of prolonged sitting (a common presentation of PE)
• Environmental exposures: asbestos, allergens, chemicals, cold
• Trauma: blood loss, chest crush injuries, penetrating chest trauma, rapid velocity changes
RED FLAGS • Fever, night sweats, change in weight, syncope, LOC, chest/shoulder pain, hemoptysis, crackles
PMHx • Asthma, COPD, CHF, asthma, previous episodes of DYSPNEA, Malignancy, previous PE
PSHx • Thoracotomy, heart surgery (possible phrenic nerve paralysis secondary to surgery)
PO&GHx • Pregnancy: DVT/PE, pressure of fetus
Meds • ILD risk: Arniodarone, Bleomycin (cancertx), Methotrexate, Nitrofurantoin;
00’ (DVT), immunosuppressive drugs (for pneumonias), coumadin, heparin, medication overdose, immunizationS
(influenza), injection drug use (talc lung)
Allergies • Environmental, food
FHx • a-i antitrypsin deficiency, CF, cancers, Ml, hypercoaguability, HTN, tchol., asthma, allergies
Social • Smoking, anxiety disorders, injection drug use (talc lung), alcohol, medication overdose

HEENT: neck masses
CV: angina, CHF (pulmonary HTN)
RESP: orthopnea
GI/GU: bleeds (e.g. dark stools, coffee ground emesis, tea colored urine)
MSK / DERM: scoliosis, ankylosing spondylitis, calf pain, leg swelling
jFactOrS Obesity, smoking, occupational exposure, aspiration (often secondary to swallowing dysfunction), decreased
mobilization (DVT/PE), DM
physical
1 General Approach
ABC’s, GCS (<8 —* INTUBATE!), Vitals (BP, HR, RR, Temp, Sp0 ), U/O (watch for pulsus paradoxus)
2
2. Inspection
• General: appear septic, airway protection (e.g. tripod position), speech, exertional breathing, diaphoresis
• HEENT: nasal flaring, pursed lip breathing, suprclavicular indrawing, central cyanosis, airway swelling, accessory mm use (e.g.
scalenes), tracheal deviation, JVP (Kussmauls’ sign)
• RESP/CV: increased AP diameter, chest wall deformities, scars, intercostal indrawing, asymmetry, neck veins
• ABDO: subcostal indrawing, accessory mm use (paradoxical abdominal breathing), HJR
• Periphery: acrocyanosis, clubbing, cap refill, edema (CHF), cold/clammy skin, nicotine stains
• DERM: angioedema, urticaria
3. Percussion
• RESP: lung fields (do not forget UL’s on ant chest wall), hypo- or hyper-resonance, diaphragmatic excursion
4. Palpation
• CV: palpable thrills/heaves, apex beat (position, amplitude, duration)
• RESP: tactile fremitus, chest wall expansion (place hands on back (thumbs at 1 0 tF,
rib) and have Pt inhale)
• Other: edema, pulses in all four limbs, lymphadenopathy (including inguinals, supraclavicular, and cervical)
5. Auscultation
• RESP: (all lobes, R vs L) crackles, wheeze, stridor, .1 AE, prolonged expiration, egophony (consolidation)
• CV: S3/54, murmur, rhythm (AF)
6. Special Tests
• Laryngeal ht: distance from thyroid cartilage (top) to sternal notch (<4cm is abnormal), PFT/PEFR
Investigation
1, Blood work
• ), electrolytes, urea, Cr, (fluid status), glucose
CBC-D(infection/inflammation, anemia), ABGs (calc A-aDO
2
• ECG, ECHO (cause of CHF ± pulmonary HTN), CXR, CT (if indicated), VQ scan (if indicated)
3. Special Tests
• 2 improves w/ admin of 02), oximetry, D-Dimer, troponin, BNP, sleep
PEFR/PFT, methacholine challenge test, 02 test (see if Sp0
study
• Thoracocentesis (pleural effusion), needle decompression + chest tube (notably for tension pneumothorax)
Treatment
1. 2 monitors, consider needle decompression if acute tension pneumothorax,
Emergent: 02, 2x large bore IV’s, cardiac and SpO
bronchodilators or diuretics for symptom control, airway management equipment @ bedside
2. Treatment Options: medical and surgical Tx dependent on etiology, (see Hemoptysis, etc...)
3. Further workup: e.g. CHF —+ elucidate original cause
4. Follow-up: especially with disease like asthma where frequent exacerbations affect long-term outcome
• Mid level evidence suggesting that psychosocial support, breathing control, and use of coping strategies (e.g. relaxation
techniques and coping strategies) may reduce dyspnea
5. Referrals: pulmonologist, other specialties dependent on etiology
References
1. Bickley LS and Szilagyi PG. Bates’Guide to Physical Examination and HistoryTaking 9th ed. Philadelphia: Lippincott Williams & Wilkins, 2007.
2. http://www.merckandcoinc.net/mmpe/index.html [Internet]. New Jersey: Merck Sharp & Dohme Corp, © 2004-2010. Available from: http://www.
merckandco,ncnet/mmpe/seco5/ch045/chO45dhtml#5ec05ch045.ch045d.57
3. Brej M. et al. Multicentre RCT of Nursing Intervention for Breathless in Patients with Lung Cancer.1 BMJ Apr 3;31 8(71 88):901 -4.

DYSU RIA
20! I Ed. Authors: Todd Penney MSc, Henry ConterMD, Ryan Cooper MD MPH FRCPC
OriginalAuthars:Janna Tram, James Yeung MD, Matthew Wang MD CCFP
Station Objective
To learn how to recognize dysuria and to obtain a history from a patient presenting with pain on urination and/or difficulty urinating.
Recognizing and treating urinary tact infections can significantly reduce morbidity and complications.
• UTI
• Urine specimen contains> 1 0 /L CFU of a single organism in a symptomatic patient
8
• Positive leukocyte esterase or nitrite on urine dipstick with irritative voiding symptoms highly suggestive in young women
but less reliable in the elderly
• UTI Dx is often clinical, so a —ye urinalysis despite presence of UTI Sx still warrants UTI Dx
• Cystitis: Remember the KEEPS acronym for the most common bacteria causing UTIs
• (Kiebsiella, Escherischia coil, Enterococcus faecalis/Enterococcus cloacae, Proteus mirabilis/Pseudomonas, Staphylococcus
saprophyticus/Serratia marcescens; Note: E. coil is the cause in 95% of uncomplicated cystitis in young women
• Urethritis (Gonorrhea, Chiamydia, Trichomonas Vaginalis, Herpes simplex)
• Prostatitis, Epididymitis, testicular pain/orchitis
• Pyelonephritis systemic Sx or back pain can predominate over dysuria Sx here
—

• Urosepsis associated with renal stones
History
ID • Age, gender
CC • Difficulty voiding frequency, urgency, nocturia, pain on urination, hematuria, discharge, hesitancy, straining,
—
incomplete_emptying, incontinence, intermittency,_poor stream, in the elderly delirium and falls

—
HPI • Onset, provoking/relieving factors, pain quality, radiation, severity, timing of pain, region of pain (flank, scrotum,
back, perineum, rectum), unusual changes in frequency of urination, abdominal fullness, red vs. tea-colored urine,
type/color/odor/timing/texture of discharge
RED FLAGS • Fever/chills, N/VID, gross hematuria
PMHx • Frequent UTls, DM, immunosuppression, kidney stones, BPH, incontinence
PSHx • Recent instrumentation or GU tract (cystoscope, catheter), surgeries for incontinence (pessaries, sling, etc.)
PO&GHx • Current pregnancy, post-menopausal, prolapsed pelvic structures
Meds • Anticholinergics
FHx • Immunosuppressive disorders, GU cancer
Social • Sexual Hx including: # & genders of partners, types of sexual contact (oral, vaginal, anal), sex with sex trade workers,
contraceptives, age of sexual debut, foreign bodies, previous STIs
ROS • HEENT: uveitis, pharyngitis, grouped lesions on face
• GI: abdominal pain
• GU: gross hematuria, stone passage, genital ulcers, presence of discharge
• MSK/ DERM: arthritis, skin lesions/swelling/pain/rash in groin area
Risk Factors • Sexually active females, high risk sexual activity, congenital anatomical GU aberrancies
Physical
1. General Approach
• Introduce yourself, wash your hands, check ABCs + add IV and monitors if necessary, ask for permission to do PE, check vital signs
including temperature, note BMI, check mental status with MMSE/MOCA
2. Inspection
• In both genders: examine for systemically well vs. unwell patient, examine groin for skin abnormalities, examine lower abdomen
for hernias
• In men: examine testicles, epididymis, glans penis and prepuce for redness, swelling

• In women: examine pelvic area for prolapsed pelvic structures, foul discharge
3 Percussion
• Costovertebral angle for tenderness
4. Palpation
• Suprapubic area, testicles and scrotum for tenderness, DRE (+ prostate exam for males)
• Inguinal, iliac and supraclavicular lymph node exam (for evidence of possible prostate/testicular tumour)
• Kidneys for colicky pain (evidence of stones)
Special Tests
• In women: pelvic exam if Hx suggests possibility of new STI/PID as cause of dysuria
• Prehn’s sign: relief of pain with elevation of testicle suggests epididymitis
vestigatiOflS
1. Blood work
• CBC-D, urea, Cr, lytes, blood cultures if pyelonephritis or urosepsis is suspected
• Renal/pelvic U/S, spiral CT/KUB (stones), IVP
3, Special Tests
• U/A, midstream/initial stream urine C+S+ Gram stain, urine PCR for Gonorrhea/Chlamydia if sexually active
4. surgical/Diagnostic Interventions
• Cystoscopy if gross hematuria
Treatment
1. Emergent If septic, resuscitation with IV fluids, admission to hospital for IV Abx
-
• Treatment Options
Diagnosis Female Male
Cystitis TMP/SMX 1 DS tab PC BID 3 days
or TMP/SMX 1 DS tab P0 BID 1 week (For 1 St infection)
Nitrofurantoin_100mg_P0 BID 3_days
Gonorrhea Cefixime 400mg P0 single dose
Chlamydia Azithromycin 1 g P0 single dose
Recurrent cystitis Low dose or post-coital Abx TMP/SMX 1 DS tab P0 BID 6 weeks (for cystitis and
Ex.TMP/SMX 1 tab P0 daily or post-coital presumptive prostatitis)
Rule out cystocoele or bladder diverticulae in Referral to urology for investigation of BPH, anatomical
sexually inactive or post-menopausal aberrancies
Asymptomatic Treat if pregnant or prior to urological/gynecological surgery
bacteriuria TMP/SMX 1 DS tab P0 single dose
Prostatitis Typically a fluoroquinolone like Ciprofloxacin 500 mg PC ql 2h or TMP-SMX 1 tab PC bid
Pyelonephritis Ciprofloxacin 500 mg P0 qi 2h is often chosen
Epididymitis/ Special sling to elevate testicles and relieve pain; NSAIDs or acetaminophen for analgesia;
Orchitis In older men Ciprofloxacin 500 mg P0 BID for 10 days;
In sexually active men with suspected or confirmed STI: Ceftriaxone 250mg IM x 1 dose + Doxycycline 100 mg P0
BIDx 10-14 days
2. Follow-up if no resolution of symptoms after treatment

3. Referrals
Urology if BPH refractory to medical management, anatomical GU aberrancies suspected, kidney stones; nephrology
References
1. Bent 5, Nallamothu BK, Simel DL, Fihn SD, Saint S. Does this woman have an acute uncomplicated urinary tract infection? JAMA 2002 May 22-
29;287(20):2701 -10.
2. Nicolle LE, AMMI Canada Guidelines Committee. Complicated urinary tract infection in adults. Can infect Dis Med Microbiol. 2005 Nov;1 6(6):349-360.
3. Blondel-HilI E, Fryters 5, editors. Bugs and Drugs. 3
,d
ed. Edmonton: Capital Health; 2006.
4. Filate W, Leung R, Ng D, Sinyor M. Essentials of Clinical Examination Handbook, 5 th
ed. University ofToronto Medical Society, 2005.
5. Fort, GG, Mikolich Di. Fern: Fern’s Clinical Advisor 2011, vt ed. Mosby (Elsevier), 2010.
6. Ramakrishnan K, Scheid, DC. Diagnosis and Management of Acute Pyelonephritis in Adults. American Family Physician. 2005. 71(5):933-942.
Barry MJ, McNaughton-Collins, M. Benign Prostate Disease and Prostatis. Goldman. Cecil Medicine, 23 rd
ed. Saunders(Elsevier). 2007.

FALLS
201 I Ed. Authors:Aamir Bharmal, Cathy Lu MD, Marjan Abbasi MD CCFF Dip. CQE
OriginalAuthars:Aamir Bharma( Cathy Lu MD, Marjan AbbasiMD CCF Dip. CQE
Unexpected event in which the participant comes to rest on the ground, floor, or lower level
• Neuro: neurocardiogenic (vasovagal/situational), orthostatic, seizures, stroke, dementia/delirium, depression, narcolepsy
• HEENT: vertigo, visual disturbance, proprioceptive abnormality
• MSK: arthritis, muscle weakness
• Metabolic: electrolyte abnormality, hypoglycemia, adrenal insufficiency (postural hypotension)
• Medication: See meds in Hx
• Environmental, psychogenic
• Cardiac: see below under’High Mortality’
• Neurocardiogenic
• Generally multifactorial
• Cardiac
• Structural: AS, hypertrophic cardiomyopathy, PE, pulmonary HTN, Ml, tamponade, aortic dissection
• Bradycardia: sick sinus, AV block
• Tachycardia: V-tach, V-fib, Torsades de Pointes, SVT, Afib, Aflutter
History
ID • Age, gender
CC • Fall(s)
HPI • Characterize event(s): onset, prior falls, location of falls, events and activity preceding (especially change in position!
reaching), time spent on ground
• Nausea/warmth/diaphoresis (pre-syncope), faintness vs. vertigo, imbalance, weakness
• Palpitations, SOB, CP
• If elderly: cane, walker or wheelchair use
• Associated injuries: characterize (onset, palliating/aggravating factors, quality of pain, radiation, severity/associated
symptoms, timeline)
1IFLAGS • LOC
• Dysarthria, difficulty swallowing
• Bowel and/or bladder incontinence, tongue biting
PMHx • Seizures, dysrhythmias, CAD, DM, vertigo, narcolepsy, stroke, fractures, Parkinson disease, dementia,
hyperthyroidism, depression
PSHx . Fracture repair, cardiac valve repair, pacemaker
Meds • Sedatives and anxiolytics, antidepressants, antihypertensives, antiarrhythmics, corticosteroids, NSAIDs,
antichollnergics, hypoglycemic agents
FHx • Osteoporosis
Social • EtOH, street drugs
• Living situation, environmental hazards (home layout, lighting, stairs, footwear), possible abuse
• Nutrition: B12 deficiency, calcium (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), oxygen requirements
• GI: nausea/vomiting, diarrhea, hematemesis, hematochezia
• GU:dysuria, nocturia (assess for UTI/incontinence)
• MSK / DERM: muscle weakness, joint stiffness, gait disturbance

physical
1 General Approach
• Vital signs: tachycardia/bradycardia/arrhythmias, postural vitals
• Assess patient’s stability and cognitive status
• Deal with potentially distracting injuries first
2. Inspection
• Mucus membranes (dehydration), areas of active bleeding/bruising, continence
3.
• Cardiac: murmurs and arrhythmias
Neurologic Exam: Cranial nerves, extremity strength/tone/sensation/reflexes, finger-nose test (cerebellar), proprioception (Romberg,
vibration/position sense), cognitive assessment (MMSE)
5. Special Tests (based on Hx)
• Head-up tilt test (neurocardiogenic), Timed Up & Go test (mobility)
• MSK: joint exam, ROM, rule out bony tenderness
• Gait exam: stance, circumduction, tandem gait
Investigations
1. Blood work
• CBC-D, BUN, electrolytes, Cr, glucose, troponin, Bi 2, TSH
• X-ray for suspected fracture, head CT
3. SpecialTests
• EKG, stress test, ambulatory monitoring, toxicology screen, bone density
Treatment
1. Emergent
• Ensure patient is stable
• If prolonged time spent on ground, consider hypovolemia risk, ARF, and rhabdomyolysis —* start IV fluids immediately
• Medical: stop/taper potentially offending meds; determine triggers and counsel regarding exposure reduction; ensure good fluid
loading to decrease hypoglycemia/dehydration risk; balance retraining/group exercise programs
• Disease specific:
• Visual: optimize lighting, corrective lenses
• Seizures: anticonvulsant
• Footwear: optimize
• Cardiac: bradyarrhythmia (pacemaker), tachyarrhythmia (intracardiac device), address specific structural issues
• Surgical: depends on injuries
3. Follow-up
• Depends on injuries sustained, cause of fall
4. Referrals
• PT, OT, home care, home hazard assessment
References
1. Fuller GF. Falls in the elderly. Am Fam Physician 2000; 61(7): 2159-68, 73-4.

FATIGUE
2071 Ed. Authors: Daisy Hartmann, Anu ParharMD, Lisa Steblecki MD MPH CCFP
Station Objective
Differentiate from somnolence and musculoskeletal weakness. Investigate patients that have other positive symptoms or abnormal signs to
suggest a non-psychological cause of fatigue.
• Chronic Fatigue Syndrome (CFS): clinically evaluated, unexplained, fatigue >6 mo, not alleviated by rest and causes impact
on lifestyle + 4 or more associated symptoms: impairment of short-term memory or concentration causing a in function,
sore throat, tender cervical or axillary lymph nodes, muscle pain, multi-joint pain with no swelling or redness, new headache,
unrefreshing sleep, post-exertional malaise lasting >24hrs
• Psychogenic (depression, sleep disorder, life stresses, idiopathic chronic fatigue, chronic fatigue syndrome)
• Infectious (viral —+ hepatitis/mononucleosis/HIV/bacterial —* TB)
• Endocrine (DM, hypothyroidism)
• Substance abuse and drugs
• Anemia
• Obstructive Sleep Apnea
3. High Mortality:
• Malignancy
History
ID • Age, gender
CC • Fatigue
HPI • Distinguish between inability to initiate activity (due to perceived weakness / loss of interest), inability to maintain
activity (easy fatiguability), & mental fatigue or impaired concentration
• Onset, duration, course (worse, better, related to other) & timing of fatigue (morning, evening..)
• Fatigue unrelated to exertion/not improved with rest/”tired all the time”versus fatigue due to specific Sx (e.g.
dyspnea, MSK weakness, pain)
• Sleep (amount, timing, disruption, sleep apnea), sexual/eating/bowel habits, exercise
• Recent changes in meds, recent illness or lifestyle changes/stress
• Other symptoms: fever, nightsweats, weight loss/gain, chills, pain, palpitations, syncope, dizziness/vertigo, SOB,
bleeding, fever, N/V, MSK weakness, menorrhagia, LMP, cold intolerance, pallor, syncope
• Mood, sleep, appetite, feelings of guilt, energy, concentration, anhedonia
• Affect this has had on pt’s life and accommodations that family/pt has made to their lifestyle
RED FLAGS • Fever, weight loss, night sweats, neurological deficits, ill-appearing
PMHx • Psychologic, endocrine, CV/RESP, sleep disorder, Ca, severe obesity, hepatitis
• Thyroidectomy, heart surgery, Ca

PSHx
FHx • Psychologic, endocrine (DM, thyroid), Ca
Meds • Hypnotics, antihypertensives, antidepressants, drug abuse/withdrawal
Allergies • Medications and environmental
Social • EtOH, illicit drug use, smoking
ROS • HEENT: difficulty swallowing, voice changes,”globus sensation:’ goiter or other mass, vision changes, dizziness!
vertigo/lightheadedness, headache, diaphoresis
• CV: palpitations, angina
• RESP: SOB, tachypnea/bradypnea, cough, hemoptysis
• Gl: hematochezia/melena, hematemesis, any obvious mass, jaundice
• GU: hematuria, LUTS (prostate Ca vs. UTI)
• MSK / DERM: fatigue, weakness, any numbness/tingling (brain metastases), rash, painful joints (inflammatory
arthropathy)
Risk Factors • Associated psychological complaints/problems, especially if <6mo duration

physical
1 General Approach
• Complete a full physical exam, starting with vital signs
2 Inspection
• General appearance, mood, affect, pupil size, conjunctiva (pallor), thyroid, liver failure stigmata (ascites, caput medusae)
3 Palpation
• Organomegaly (heart, liver, spleen, thyroid), cardiomegaly(enlarged/shifted PMI)
• Thyroid and lymphadenopathy
• Breast exam, DRE if suspicious for malignancy
4. AuscuItatiO
• CV/RESP: murmurs, extra heart sounds, pulmonary edema, COPD, consolidation/mass
5• Special Tests
• Asterixis: bilateral asynchronous flapping of dorsiflexed hands with the arms outstretched, possible causes include portal-systemic
encephalopathy, uremia and severe heart failure
1
investigations
i. Select investigations with care (absence of other Sx and N PE usually indicates tests will be of minimal value)
2. Blood work
• CBC-D, electrolytes, urea, Cr, ESR, glucose, TSH, ferritin, Bi 2, total protein, albumin, AST, ALT, ALP, bill, calcium, phosphate, ANA,
13-HCG
• CXR (infection, heart failure, COPD), mammogram if Sx suspicious for Ca
4. SpecialTests
• U/A, ECG, sleep study
• Serologies and PPD skin tests to rule out infections (hepatities, lyme disease, HIV, TB)
• Colonoscopy/gastroscopy in age over 50 and weight loss or anemia
• If mass is found then further diagnostic and/or surgical intervention may be needed to rule out neoplasm
Treatment
• Treat the underlying cause
• Review all medications, looking for drug-drug interactions and side effects
• Encourage patient to stay physically active, return to work, maintain relationships
• Support, reassurance and follow-up important
• CFS: cognitive behaviour therapy and exercise
2. Referrals
• Supportive counseling and education, behavioral or group therapy
• Psychiatry
References
1. Merck Manual Professional [Internet]. Whitehouse Station: Merck and Co., Inc. ci 995-2009 [updated 2009 July; cited 2009 Nov 1] Introduction: Approach
to the Patient with Liver Disease; Available fro m: htw//www.merck.com/mmoe/seco3/ch022/chO22a.html#seco3-ch022-chO22a-1 1.
2. Fosnocht K, Ende J. Approach to the adult patient with fatigue. June 1 2009. UpToDate desktop version 17.3.
3. Gluckman S. Clinical features and diagnosis of chronic fatigue syndrome. UpToDate desktop version 17.3.

FEVER
2011 EdAuthor:Jamie Mcintyre, Craig DomkeMD, Matthew InwaodMBBChBAO
OriginalAuthor:Jamie Mcintyre, Tara Lynn Stewart MD, Lyle Thomas MD CCFP(EM)
Station Objective
Approach to diagnosis and treatment of acute and chronic fever as well as fever of unknown origin.
Diagnostic Criteria
• T> 38.5°C or FUO: T> 38.5°C,> 3 weeks duration, no known cause after a 1 wk of investigation
• Sepsis: SIRS critera:
• Any two of: T >38°C or <36°C; RR > 20 breaths/mm or paCO2 < 32mmHg; HR >9obpm; WBC >1 2X1 3 ceIIs/mm or <
O
ceIIs/mm or> 10% band cells
4X1 3
O
• AND an infectious source
2. Common Conditions
• Infection:
• Viral, bacteria, fungi, parasitic
• External & localized (ie. cellulitis)
• Internal & localized (ie. intra-abdominal abscess)
• Systemic (ie. bacteremia) Post Surgical (5 W’s)
• Malignancy POD Cause
• Leukemia, Iymphoma, myelodysplastic syndromes, metastatic Ca Atelectasis, pneumonia
Wind 1-2
• Autoimmune and Inflammatory Disorders
Water 3-5 UTI
• Vasculitis, RA
• IBD, sarcoidosis Walking 4-6 DVTand PE
• Endocrine: thyroid disease Wound 5-6 Surgical wound infection
• Post-surgical (5 W’s) Wonder drug 7+ Anesthetic, transfusion rxn
• Miscellaneous
• Allergic reaction, idiopathic/familial, EtOH withdrawal, transfusion reaction
• Drug induced: overdose or side effect
• Central causes: brain hemorrhage
• Environmental: heat stroke
History
ID Age, gender
CC Feeling warm or cold, sweating, shivering, change LOC
HPI Timing: onset in relation to medical condition, duration, recorded variations throughout the day
• Other related symptoms: general malaise, NN, diarrhea, pain
• Recent travel to areas of high risk infection, exposure to animals (sheep), blood transfusion, IV drug use
(amphetamines), trauma, time in sun or hot environment, sick contacts, sexual hx
RED FLAGS Change in LOC, neutropenic/immunosuppressed patient, B symptoms, constitutional symptoms
PMHx Recent acute or chronic infections, Hx RA, Hx of Ca, vaccination history, recent Abx use
PSHx • Recent surgery (see table)
PO&GHx Immobilization, recent delivery, recent instrumentation (le. D&C)
FHx • Malignancies, fever disorders
Social Hx • Occupation (ie. nurse working in an ID clinic)
Meds Chemotherapy, steroids, immune suppressing agents, drug induced fever, medication misuse, recent medication
change / discontinuation
Allergies Relevant allergies
ROS HEENT: Iymphadenopathy, sweating, goiter
• CV: palpitations, tachycardia, CP, BP
• RESP: increased work of breathing, sputum production, coryza, cough
• GI: constipation or diarrhea, abdominal distention or pain, ascites, jaundice
• GU: dysuria, discharge
• MSI< / DERM: muscle cramps or weakness, joint pain or swelling, rash, masses
• Neuro: headache, nuchal rigidity

physical
1 General Approach
• ABCDE, Vitals including C/S, localize cause of fever (head to toe exam), GCS
2. Inspection
• Does the patient look toxic?
• Signs of infection: erythema, pus, rash, tender, swollen
• Head to toe exam to locate source of infection
PercuSSiOfl
• Lungs: signs of consolidation
• Abdomen: peritonitis, hepatomegaly, splenomegaly (Traubes space)
4• Palpation
• Abdomen: tenderness, hepatomegaly, splenomegaly, peritonitis, Murphy’s/Rovsing’s sign, peritonitis
• Neck: thyroid nodules, lymphadenopathy
• Pulse: tachycardia
• Any lesions/wounds: redness, swelling, pain, tenderness, t local T
5. AuscultatiOn
• Heart: new or changed murmurs, friction rubs
• Lungs: crackles, wheezes, whispering pectoriloquy, egophony
• Abdomen: lack of bowel sounds
Investigations
i. Blood work
• CBC-D, electrolytes, urea, Cr, LFT’s, ALP, lipase,TSH/T31r4, ESR, CRP, ANA/antiCCP, blood culture, serum lactate, venous gas (acidosis
from sepsis)
• CXR: pneumonia, TB, metastasis
• U/S: possible infective sites, abscesses, visualization of abdominal organs and Echo for endocarditis
• CT: head, chest, abdomen, pelvis if needed
• Bone scan: metastasis
3. SpecialTests
• UA, urine C&S, urine catecholamine, throat swab, monospot, Sputum C&S
• Excision of mass or lymph node, bone marrow biopsy, percutaneous fluid aspiration, LP
Treatment
1. Emergent
• ABCDE’s and GCS, IV fluids, °2’ treat underlying cause of fever
• Broad spectrum IV antibiotics if sepsis is suspected
• Cooling if T 40°C by antipyretics and cooling blankets
• Source control: such as surgical excision of intra-abdominal abscess
• Fever should not necessarily be treated and most people recover without medical attention
• Antipyretics to lower the set point: acetaminophen, ASA, NSAIDs
• Treat underlying cause with the appropriate medical management: antibiotics, steroids, anticoagulation
3. Surgical
• May be both diagnostic and therapeutic
• Specific conditions where surgical treatment is curative (ie. necrotizing fasciitis, abscess drainage)
References
1. Bor D. Etiologies of fever of unknown origin in adults (Internet]. Ed. Weller R,Thorner A.: Up to Date; updated 2008 Aug 18; cited 2009 Dec 15. Available at:
http://www.uptodate.com/online/content/topic.do?topicKey=othr_inf/20191 &selectedTitle=8%7E 1 50&source=search_result.
2. Harvey 5. “Hyperthermia, Fever and Fever of Undetermined origin’lnfectious Disease:The Clinician’s Guide to Diagnosis, Treatment, and Prevention
[Internet]. Ed. Dale D. WebMD; Stat Ref Online: 2003 (updated 2009 Nov 25; cited 2009 Dec 15. Available from: http://online.statref.com.login.ezproxy.
Iibrary.ualberta.ca/ document.aspx?fxid=65&docid=3.
3. Porat R., Dinarello A. C., Pathophysiology and treatment of fever in adults [Interneti. Ed. Weller R, Thorner A.: Up to Date; updated 2009 Sept 30, cited 2009
Dec 15. Available from: http//www.uptodate.com/onhine/contentltopic.do? topicKey=othr_inf/16086&selectedTitle=1 0%7E1 50&source=search_result.
4. Tintinalli JE, Kelen GD, Stapczynski iS, editors. Emergency Medicine: A Comprehensive Study Guide, 6th ed. McGraw-Hill, Medical Publishing Division;
2004. Chapter 115.

GAIT DISTURBANCE
2011 Ed. Authors: Carrie Ye MD, Richard CamiciohMD FRCPC
Station Objective
LMN, cerebellar,
Differentiate neurogenic from non-neurogenic causes of gait disturbance and identify the neurogenic deficit (UMN,
parkinsonian, sensory, higher order)
1. Neurological:
Extra-pyramidal: Parkinson’s disease
• Frontal lobe: any frontal lobe lesion including normal pressure hydrocephalus and cerebrovascular dz
• Weakness: UMN(MS, stroke) vs. LMN(cauda equina, mononeuritis)
• Spasticity: UMN(post-stroke, CP, spinal cord lesion)
• Sensory deficit(proprioception): DM, syphilis, 812 deficiency, posterior column spinal cord lesion
• Cerebellar: hypothyroid, EtOH, stroke, mass lesion
• Vestibular dysfunction
2. Non-neurological:
• Orthopedic issues
• Visual disturbance
• Muscle dz
Pain
Psychogenic
History
ID • Age, gender
CC • “Trouble walking”
to
HPI • Ask Pt or pt’s family to describe the gait disturbance (higher order gait disorder exhibits: freezing —* feet sticking
the ground)
• Duration/onset/precipitant (stroke, EtOH, head trauma)
• Exacerbating factors (darkness, uneven surfaces, going through doorways)
• Weakness (difficulty getting out of the chair or reaching for items)/Sensory deficits (numbness, tingling, not
knowing where their feet are)Nertigo
• Tremor (Parkinsonism)
• Falls: frequency, major injuries, pre-syncope
• Previous episodes of sensory/motor deficits (MS, Cerebrovascular)
• Cognition
RED FLAGS . Urinary retention/overflow incontinence/bilateral leg weakness/stool incontinence (cauda equina syndrome)
• Urgency incontinence (normal pressure hydrocephalus or vascular)
• Acute onset lateralizing weakness/dysarthria/confusion/headache (stroke)
PMHx • Strokes (risk factors), MS, Ca (CNS metastasis, including spinal), DM, dementia
PSHx • Back surgery
FHx • Parkinson’s disease, Huntington’s disease
Meds • Anti-psychotics (can cause Parkinsonism)
Social • Living situation/safety
• EtOH
Physical
1. General Approach Table 1: Strenath
• Ask permission to perform exam; wash hands; proper draping 0/5 No muscie activity
• Vitals and GCS 1/5 Muscle twitch
• Focus PE according to the Hx 2/5 Movement in absence of gravity
2. Detailed NEURO exam, including: 3/5 Against gravity
• CN’s (impaired EOM’s (myasthenia) vertical gaze palsy (PSP), nystagmus (MSA),
,
4/5 Some resistance
dysarthria (vascular), tongue fasculations (ALS) 5/5 N strength

• Muscle bulk, fasciculation (LMN lesion)
• Tone: rigidity (lead-pipe, cog-wheel), spasticity (UMN)
• Strength (note pattern: proximal —* myopathy vs. distal — neuropathy)
• DTR (t=UMN, L=LMN), Babinski’s (UMN lesion)
• Romberg (vibration sense/proprioception)
• Finger-nose/heel-shin dysmetria and finger-tapping dysrhythmia (cerebellar)
• Tandem walking (neuropathy or midline cerebellar)
• Trendelenburg test (wt bearing on one leg, pelvis tilts down on contralateral side) —4 weakness of gluteus medius
•
Gait: observe ability to get up from a chair: station, initiation, base width, stride length, symmetry and turning
• Specific gait syndromes:
• Shuffling, short strides, stooped, no/little arm swing, festinating-Parkinsonism
• Antalgic pain
• Spastic/UMN/hemiplegic —÷ stroke, CP,
• Bilateral lower extremity —* spinal cord (myelopathy)
• High-stepping-foot drop (LMN) or proprioception deficit (worsens in diminished light)
• Circumduction —* weak hip fiexors (UMN)
• Waddling —* weak gluteus medius (myopathy—*Trendelenburg in motion)
• Scissoring —* bilateral UMN (CP)
• Narrow-based, toes turned in —* spastic
• Ataxic cerebellar (EtOH)
—
• Deviation to one side —* unilateral vestibular dysfunction

• Magnetic —* frontal lobe dysfunction (higher order gait dysfunction)
Investigations
Blood work
• CBC-D, electrolytes, urea, Cr
• Bi 2, fasting glucose, syphilis serology
• ESR, CRP, TSH, EtOH level
• Bladder scan-retention
• X-ray of affected joint
• CT/MRI head and spine is the most important test to obtain
Treatment
Emergent
• Fall precautions: treat injuries of fall
• Stroke: consult neurology, thrombolysis if acute ischemic
• Cauda equina: image, consult neurosurgery, surgical decompression
• Think myelopathy for bilateral UMN findings with no cranial findings, image appropriate level (e.g, cervical spine)
• Most patients will need long term multidisciplinary team for rehab, homecare can provide if subacute.
• Parkinson’s: levodopa/carbidopa
• MS: multidisciplinary approach with neurorehab, steroids for acute episodes, drugs to prevent relapses
• Foot drop: brace
• B12 deficiency: B12 replacement
3. Surgical: surgical fixation of fractures, tumor resection
4. Referrals: Neurology, Orthopedic surgery

HEADACHE
20?? Edition Authors: Scott McLeod, Francois Jacob MD, D.B. Sinclair MD FRCPC
OriginalAuthors: Daisy Hartmann, Anu ParharMD, Lisa Steblecki MD MPH CCFP
Station Objective
In this station you may be expected to differentiate and manage headaches ranging from life-threatening conditions to everyday headache
disorders. Identify patients that require referral/imaging (red flags).
Di erential Diagnosis
1. Diagnostic Criteria’
Number .
Headache type Timing Quality Associated symptoms Aggravating factors
of attaclcs
. Pressing/tightening
. 30 mins to 7 . Stress, muscle tension,
Tension-type 10 quality, mild-moderate None usually
days physical injury, poor posture
intensity, bilateral
Mostly unilateral, NA’, Photophobia,
Physical activity, ights,
Migraine > 5 4-72 hours pulsating, interfere with phonophobia,
. . . . sounds, motion sickness
daily activity osmophobia
Conjunctival infection,
Occur in series lasting lacrimation, nasal Smells, exercise, smoking
Cluster 5 15-180 minutes weeks to months, severe congestion, rhinorrhea, (these are not well
pain, hyperesthesia sweating, ptosis, eyelid understood)
edema
. Primary headaches
• Tension-type, migraine (with or without aura)
• Secondary headaches
• Medication overuse headaches
• Infectious causes (meningitis, sinusitis, mastoiditis, dental infections)
• Intracranial
• Vascular: SAH, stroke, temporal arteritis, venous sinus thrombosis, intracranial hematoma
• Non-vascular: T ICP from mass lesion, hydrocephalus, abscess
• Extracranial
• Glaucoma, optic neuritis, neuralgia, TMJ, cervical spine cause, CO poisoning
• SAH, stroke, temporal arteritis, meningitis, abcess, tumour
History
ID Age,sex
CC • Headache
HPI Onset (ask about rapid onset), location (unilateral/bilateral), progression
. Provoking/palliating factors (known triggers: lights, sounds, motion sickness)
. Quality of the pain (throbbing, dull, hyperesthesia)
• Radiation (to cervical musculature)
• Severity (especially in comparison to previous headaches)
• Timing (events leading up to the headache, and the headaches progression)
• Associated symptoms, NA’, aura, visual problems, vertigo, dizziness, focal neurological Sx, LOC, Trauma
RED FLAGS • “First or Worst” (think about SAH), Meningismus, Worse in morning (think high I€P), change in pattern of existing
headaches, scalp tenderness, jaw claudic-ation, Hx of HIV or €a, focal neurological deficits, fever
PMHx • Migraine/tension/culster headaches, HTN, HIV, cancer, recent trauma, seizure, glaucoma, polymyalgia rheumatic,
vasculitis or other rheumatological conditions
PSHx • Previous Ca surgery or intracranial surgery
FHx Migraines, SAH, aneurysms, stroke, seizures, motion sickness

Meds Nitroglycerin, analgesics (try to determine frequency of use), OCP
Allergies Medical or environmental
Social • Illicit drug use, smoking, and EtOH
ROS • HEENT: jaw claudication, scalp/temporal tenderness, photophobia/photophonia, aura, scintillating scotomas,
neurovisual disturbances, phonophobia
• CV: palpitations
• GI: NN, diarrhea
• MSK / DERM: weakness/paresthesia, myalgias, stiffness
Risk Factors HTN, DM, smoking, low physical activity, age, obesity, hypercholesterolemia, MI, OCP and previous thrombosis
(venous sinus thrombosis)
Physical
1. General Approach
• Vital signs, head circumference, GCS, CN examination, motor and sensory exam, reflexes
2. Inspection
• Fundoscopy (papilledema), visibly swollen temporal arteries, neurological deficits (facial droop, dysarthria, abnormal gait,
anisocoria
3. Palpation
• Temporal artery (beaded, prominent, enlarged, or absent pulse)
4. Auscultation
• Listen to the heart (atrial fibrillation), listen for bruits over the temporal artery if suspicious
5. Special Tests
• Kernig’s sign: pain with passive extension of flexed knee
• Brudzinski’s sign: flexion of the neck causing involuntary flexion of the knee and hip
Investigation
1. Blood work
• If suspicious of infectious causes then order CBC-D, if suspicious of vascular causes add INR, PU
• Non-contrast CT (SAH, epidural or subdural bleed, mass lesion and ICR unexplained focal deficits)
3. Special Tests
• Lumbar puncture, if suspecting meningitis (ensure there is not high ICP)
• Temporal artery biopsy if appropriate
Treatment
1. Emergent
• ABC’s, GCS, empiric therapy for meningitis if suspected
2
• Medical:
• Tension-type: NSAIDs, heat/ice on affected cervical musculature, massage
• Migraine: Acetaminophen, NSAIDs, serotonin receptor agonists (triptans), rest in a quiet dark room
• Cluster: 6-8L/min oxygen, Triptans, Ergot alkaloids, prophylactic agents (calcium channel blockers, lithium)
• Surgical: referral for SAH, increased ICP, and mass lesions, refractory cluster headaches
3. Follow-up
• As required based on symptom relief
4. Referrals
• Neurology (if intractable), Neurosurgery (SAH, mass lesions, refractory cluster headaches)
References
1. International Headache Society. International Classification of Headache Disorders 2 ed. (Cephalgia 2004; 24 suppl 1:1-160).
2. Fenichel, Gerald. Clinical Pediatric Neurology: A Signs and Symptoms Approach. Chapter 3.Philadelphia: Saunders Elsevier. 2009.
Internal Medicine j Edmonton Manual of Common Clinical Scenarios 131

HEARING LOSS & DEAFNESS
2011 Ed. Authors: Somapti Somapr Tom Nowacki MD
OriginolAuthors: Victoria Lam, MohommadAlmutawa MD, RohitMoudgilMo PhD
Station Objective
Assess conductive vs. sensory-neural hearing loss, and treat or prevent hearing loss accordingly.
Conductive hearing loss
• External ear: obstructed canal (cerumen impaction, foreign body), otitis externa, tumor (exostosis, osteoma, polyps), trauma,
congenital (microtia, atresia, stenosis)
• Middle ear: congenital (atresia of ossicular chain), otitis media, eustachian tube dysfunction, tumors (cholesteatoma),
otosclerosis, tympanic membrane perforation
Sensorineural hearing loss (sudden, chronic): almost always Inner ear
• Congenital or hereditary: teratogens (quinine, retinoid acid), infections (TORCH, mumps, measles), meningitis, Alport
syndrome
• Adults: presbycusis, noise exposure, ototoxic drugs (aminoglycosides, furosemide, erythromycin, tetracycline, chemo,
chloroquine), Meniere’s disease, MS, acoustic neuroma, CVA, syphilis, diabetic vasculopathy, autoimmune (relapsing
polychondritis, SLE, RA, PAN, Sjorgen’s), barotrauma, trauma (temporal bone #, perilymph fistula)
CVA
History
ID Age
CC Hearing loss
HPI • OPQRST
• Unilateral vs bilateral, sudden vs progressive
• Otalgia or otorrhea, association with tinnitus, vertigo or disequilibrium
• Trouble with background noise, misunderstanding conversations, asking people to repeat, turning up the volume
onTV
• Hx of trauma head trauma, barotrauma, foreign body or noise exposure
-
• Hx of recent illness otitis externa, otitis media, sinusitis

—
RED FLAGS Recurrent ear infections, temporal bone trauma, sudden hearing loss
PMHx • Unusual ingestions, DM, stroke, heart dz, autoimmune dz,TORCH infection, ear/craniofacial abnormalities,
recurrent otitis media, psychiatric illness
• Ear surgery
FHx • Hearing loss <50 yb, hearing loss
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 , drugs, congenital, complications at birth
Familial, excessive noise (85 dB for 8 hrs/day)
2
• Regular screening (pure-tone audiometry, speech discrimination, tympanometry) for excessive noise exposure, FHx
< 50 yb, elderly (>65 yb), smoking, DM
Physical
1. General Approach
• Vitals
2. Inspection
• Signs of illness, rashes, scars, facial asymmetry, nystagmus, cleft palate, unilateral weakness, craniofacial anomalies & pigmentarY
anomalies

3• Examination of the ear
• Otoscopy: distorted anatomy, membrane Hearing Test Interpretation
discoloration, FB, mobility of TM Type Rinne test Weber test Pure tone audiometry
SpecialTests +ve: AC> BC,
• Whisper test: cover one ear and whisper into the Normal -ye — bilateral Normal
bilateral
other (Sn 90-100%, Sp 70-87%)
• Rinne test: 512 Hz tuning fork on mastoid process BC normal; AC outside
(BC), Pt hears no sound, move fork to pinna (AC) and Sounds louder normal range; AC-BC
Conductive -ye: BC > AC
patient should normally be able to hear sound on the bad side threshold gap> 10db
• Weber test: 512 Hz tuning fork on forehead in (air-bone gap)
midline (NB louder in ear with conductive hearing AC + BC below
loss) +ve: AC> normal; AC-BC
S e n so r y - Sounds softer
• Formal audiologic assessment, Speech audiometry, BC, usually threshold gap < 10db
neural on the bad side
Impedance audiometry can be considered unilateral
(no air-bone gap)
BC = bone conduction; AC = air conduction
Investigation
1. Blood work
• CBC-D, TSR, blood glucose, serum aminoglycosides (if indicated), autoimmune work-up: ESR, RF, ANA (if progressive & bilateral
sensorineural hearing loss), RPR (if indicated)
• CT of posterior fossa & internal auditory canal: indication for progressive asymmetric sensorineural hearing loss (for acoustic
neuroma)
• CT of temporal bone: indication for head trauma (especially to temporal area)
• MRI + gadolinium (gold standard for internal auditory canal imaging and retrocochlear pathology)
3. Special Tests
• Consider auditory brainstem response test if persistent and undiagnosed hearing loss
Treatment
1. Emergent
• Trauma & hearing loss: hospitalization with full trauma work-up and continual neurological observation
• Hearing loss, tinnitus with episodic vertigo (Meniere’s dz): IV fluids, antiemetics, anti-vertigo medications
• Medical
• OM: refer to Chapter 128
• Cerumen obstruction: cerumen-softening drops to physically remove cerumen
• Sudden sensorineural hearing loss: idiopathic and often resolves spontaneously, however 10 d prednisone (60-80mg) could
be used (Grade 28 evidence), If no improvement on audiogram after 10 d, a trial of intratympanic steroids can be considered
(Grade 2B evidence).
• Meniere’s disease: low Na& calorie diet, diuretic. Destructive rx: intratympanic gentamicin & labyrinthectomy.
Nondestructive rx: Meniett & intratympanic steroid (monitor regularly)
• Hearing aid is not recommended until underlying pathology is treated
• Surgical: acoustic neuroma or otosclerosis
3. Follow-up
• Acute conditions (infection, Meniere’s, trauma, sudden onset): 1-4 wks serial audiograms & otoscopic exam until hearing loss
resolves
• Primary prevention: ear plugs, monitor drug levels & take baseline audiogram with ototoxic drugs, screen high-risk individuals, Pt
with otorrhea should keep water out of ears while draining
4. Referrals
• Audiologist for audiogram followed by an Otolaryngologist if etiology uncle
References
1. ACP PIER & AHFS D1 Essentials: Hearing Loss Delirium. http://online.statref.com Posted: 10/8/2009; accessed: 10/27/2009
2. HayWW, Levin Mi, Sondheimer JM, Deterding RR. Current Diagnosis &Treatment in Pediatrics, 19th Ed. USA: Lange Medical Books/McGraw-Hill, 2009.
3. Rauch, Steven D. Idiopathic sudden sensorineural hearing loss. NEJM 2008:359:833-840.
4. UptoDate: Etiology of Hearing Loss in Adults. (2010). Available from: htto://www.uotodate.com
5. UptoDate: Evaluation of Hearing Loss in Adults. (2010). Available from: http://www.uptodate.com

______
HEMIPLEGIA/HEMISENSORY LOSS
20!! Ed Authors: Scott McLeod, Francois Jacob MD, D.B. Sinclair MD FRCPC
OriginalAuthors: Victoria Lam, MohammadAlmutawa MD, RohitMoudgilMo PhD
Station Objective
Ensure medical stability and be able to recognize acute stroke. Elicit underlying causes of stroke and understand and treat reversible causes.
Identify risk factors for hemorrhage and thrombosis/embolism.
Table 1: Grading Power
Differential Diagnosis Grade
1. Common Conditions 0 No movement
• Transient brain ischemia (<24 hours of neurological deficit, reversible) Fasciculations
• lschemic stroke 80% of strokes
—
2 Horizontal only
• Thrombosis (atherosclerosis, dissection, fibromuscular dysplasia, vasoconstriction) 3 Against gravity
• Embolism (atrial thrombus, atrial fibrillation, endocarditis) 4 Against resistance
• Hypoperfusion (cardiac arrest, pulmonary embolism, pericardial tamponade)
5 Full strength
• Hemorrhagic stroke 20% of all strokes
—
• Intracerebral hemorrhage (hypertension, trauma, amphetamines, cocaine)

• Subarachnoid hemorrhage (arterial aneurysm, vascular malformation)
• Other causes
• Subdural hematoma, MS, brain abscess, tumours, cerebral venous thrombosis, hypoglycemia (transient hemiparesis)
History
CC • Acute hemiparesis, acute loss of sensation
HPI • Onset: what was happening when this started, sequence of events, any trauma
• Progression: improving or worsening over time
• Distribution: location of paralysis or sensory loss, unilateral or bilateral, proximal or distal
• Character: true paralysis or weakness, complete vs. partial loss of sensation
• Associated symptoms: decreased LOC, visual impairment, speech impairment, hearing loss, tremors, seizure,
aura, headache, dizziness
RED FLAGS • 4 LOC, quick onset, worsening Sx, worst headache of life, meningismus, nuchal rigidity, trauma
PMHx • StrokeslrlA, CVD, DM, dyslipidemia, HTN, atrial fibrillation, hypercoaguable states, bleeding tendency, seizure,
aneurysm, tumors, valvular disease, MS, immunocompromised, migraine
PSHx • Brain surgery, cardiac surgery, endovascular procedures
FHx • Cerebrovascular disease, aneurysms, 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), fundi
• CV: atrial fibrillation, palpitations, pericarditis
• RESP: SOB
• Gl:NN
• MSK/ DERM: petechiae, purpura, pain
Risk Factors • 2 Score to assess risk (in non-rheumatic, non-valvular A-fib): Congestive heart failure, HTN
Use the CHADS
consistently above 140/90 mmHg, age >75yrs, DM, prior stroke orTIA. The annual stroke risk increases with
these risk factors. Others include smoking, dyslipidemia, A-fib
Physical
General Approach
Assess ABC’s & Vital Signs & GCS
• Keep Sa0>92%
2
• Monitor BP rigourously
• BP is only initially treated if the systolic BP >220 mmHg,unless considering tPA
• If tPA administered or if a hemorrhagic stroke, then treat systolic BP>1 80 mmHg
• If febrile consider an infectious diagnosis

2. CN Examination (include visual fields to examine for neglect)
3. Language examination (aphasia, dysarthria) Table 2: Grading Reflexes
4. Motor examination Grade
• Muscle tone (t on affected side), Muscle power ( on affected side, table 1)
• Observe muscle bulk, and look for fasciculations 0 Nil
• DTRs & plantar reflexes (hyperreflexia & up-going toes on affected side, table 2) 1 Low normal
• Pronator drift (pronation & downward drift of the affected arm) 2 Normal
5. Sensory tests 3 High Normal
• Pain/temperature (spinothalamic tracts) 4 Clonus (>3 beats)
• Joint position and vibration sense with tuning fork (posterior columns)
• Light touch (spinothalamic tract and posterior columns)
• Stereognosis, graphesthesia, 2-point discrimination, localization (cortex)
• Compare dermatomes L to R (table 3) detail is not always necessary
—
Table 3: Important Dermatomes

6. Cerebellar/Coordination
Root Anatomical landmark
• Finger-nose test, heel-shin test, tandem gait
C2 Occiput
• Gait & balance : stroke patient may circumduct affected leg and not swing arm
C3 Neck
C4 Supraclavicular
Investigations C5 Lateral arm
C6 Thumb
1. Blood work C7 Index / long finger
• CBC-D, electrolytes, glucose (r/o hypoglycemia), Cr, Urea, INRIPTT
C8 Little finger
T4 Nipples
• CT head: r/o hemorrhage and CNS lesions. lschemic findings on CT scan may take 24-48
T5 Inframammary fold
hours to appear.
T6/7 Xiphoid process
• MRI: ischemic strokes
Tb Umbilicus
• Carotid Doppler and TTE/TEE (source of embolism)
T12 Pubic bone
3. Special Tests
ECG (atrial fibrillation), LP (if concerned about infection, but after CT is done to rule out Li Inguinal ligament
•
increased ICP) L2/3 Thighs
L314 Knees
Si Heels
Treatment S2/3 Genitals
S4/5 Perineum
1. Emergent
1
55 Anus
• ABCs, GCS, Vital signs, CT head to rule out hemorrhage and assess
• Supportive treatment
• IV fluids to prevent dehydration and maintain blood pressure
• Oxygen to maintain oxygenation to the brain tissues: keep SaO >92%
2
• BP is only initially treated if the systolic BP >220 mmHg, unless using tPA
• lftPA administered or if a hemorrhagic stroke, then treat systolic BP>180 mmHg (labetalol 10-20mg IV)
• Surgical
• If a hemorrhagic stroke consult with neurosurgery
2 Table 4: UMN vs LMN
• Medical UMN LMN
• Tissue plasminogen activator (t-PA): must be given within 4.5 hours of the
onset of symptoms, there must be no indication of hemorrhage, ASA OR Plavix UEflex>
OR Aggrenox for thrombotic; Coumadin if due to A. fib Power ext a-/absent
• Surgical
LE ext > flex
• Carotid endarterectomy (carotid stenosis), endovascular stenting (aneurysms) Tone Spastic Rigid
3. Follow-up
• Re-infarction risk greatest 3-6 months after initial event DTR 1/clonus
• Lifestyle modification to decrease RE’s (HTN-lower BP, DM, dyslipidemia-cholesterol Plantars 1 .14
lowering drugs, stop smoking)
4. Referrals Fasciculation Absent ±
• Neurology, Stroke Rehabilitatio n Program, SLP (for swallowing assessment),
Atrophy Late Early
Physiotherapy
References
1. Benavente 0, Hart RG. Stroke: Part II. Management of acute ischemic stroke. AAFP. 1999 May 1 5;59(1 0):2828-34
2. American College of Physicians. ACP PIER & AHFS DI Essentials: Stroke and Transient Ischemic Attack
3. NIH Stroke Scale. www.ninds.nih.gov/docrors/NJHSirokeScalepdf

HEMOPTYSIS
20!? Ed Authors: Zoe Wolt Ashley Gillson MD, Mohit BhutaniMD FRCPC FACP
Station Objective
In this station you may be required to differentiate acute from massive hemoptysis, investigate and identify the source of bleeding, and
develop a management plan.
Differential Diag osis

1. Anatomical DDx
1
• Pseudohemoptysis: epistaxis, hematemesis
• Pulmonary: infectious (bronchitis, TB, pneumonia: S.pneumoniae/S.aureus, abscess, parasitic, fungal), Ca, bronchiectasis, alveolar
(Wegener’s, Goodpasture’s, or other vasculidities), PE, pulmonary AVM
• Cardiac: CHF, mitral stenosis
• Pharmacologic (anticoagulant or other non Rx supplements), trauma or iatrogenic
2
• Acute or chronic bronchitis, bronchiectasis, lung Ca
History
CC • Coughing up blood
HPI • Onset, progression, provoking/palliative, timing, previous episodes
• Colour: rust-tinged sputum, clots, coffee grounds, purulent, frothy, pink, bright/dark red
• Quantify blood: massive (>200 mLI24 hrs), non-massive (200 mL/hrs)3
• Recent or past respiratory infections, travel Hx, infectious contacts, tuberculosis
• Previous or chronic cough
• Smoking, inhalation of chemicals, asbestos exposure
• Immunosuppression
• Joint inflammation, rash, bruising or other signs of bleeding diathesis
• Hematuria (gross or tea coloured)
• Congenital disorders: CF, ciliary dyskinesias
• Epistaxis, GI symptoms: NN, abdominal pain, hematemesis, change in stool colour
• Chest pain, irregular heartbeats
RED FLAGS • Unilateral calf tenderness, unilateral leg edema, pleuritic CP —* PE
• Smoking, other malignancy risk factors —* Ca
• Constitutional symptoms + travel Hx —* TB, fungal
PMHx • Ca: lung/breast/colon/renal/thyroid, CHF, mitral valve stenosis, Aflb, HIV,TB, CF, emphysema, chronic bronchitis, liver
failure, peptic ulcer, Wegener’s granulomatosis, Goodpasture’s sydrome, sarcoidosis, SLE
• Recent procedures to upper or lower respiratory tract
PSHx • Recent surgery (PE)
FHx. Ca
Meds • Anticoagulants and coagulants (PE), CAM
Social • Smoking, crack cocaine, EtOH
ROS • General ROS with a focus on RESP
Risk Factors • For lung Ca: male, >40 yrs, >40 pack yrs of smoking, hemoptysis for >1 week
4
Physical
1. General Approach: Vitals (HR, BP, RR, SpO
, T)
2
2. Inspection
• Stable vs. distressed, on O2 use of accessory muscles, nutrition status, SVC syndrome, trauma
• RESP: hands (clubbing, capillary refill), chest wall structure and movement, nasopharyngeal bleeding, mouth (central cyanosis)
• CV: hands (peripheral cyanosis), JVP
• ABD: signs of liver failure, peptic ulcer
• MSK/DERM: rash, joint inflammation

3 Percussion: RESP/ABD
4. Palpation
• Lymph nodes: cervical, supraclavicular, axillary
• RESP: trachea midline, posterior chest wall expansion, tactile fremitus
• CV: apex, heaves, thrills, edema
• VASC: calf tenderness, leg edema, bilateral leg circumference, general pedal edema
• ABD: hepatosplenomegaly, tenderness
• MSK/DERM: rash, joint inflammation
5. Auscultation
• CV: murmur, S3/S4
• RESP: crackles, wheezes, pleural friction rub
• ABD
Investigations
1. Lab Tests
3
• CBC-D, LFTs, liver enzymes, Cr, consider D-dimer (suspected PE), ABG, consider ANCA and anti-GBM, ESR, type/screen and cross
match if indicated
• Sputum for suspected infection: gram stain, acid-fast stain, cultures, sputum cytology if risk factors for Ca
• Purified protein derivative (PPD) for TB
• U/A
• ECG
• If bleeding suspected to be pulmonary in origin: CXR (PA and Lat)
3. Special Tests
3
• CT: used after CXR, good for diagnosing bronchiectasis and evaluating mass/nodule found on CXR, helpful if CXR normal but Pt
has risk factors for Ca
• Doppler U/S, ventilation-perfusion (VQ) scan, CT angiography (work-up of PE)
• Bronchoscopy should be done in most cases, including consideration of vasculitis to r/o occult infections and to confirm the
presence of bleeding on bronchoalveolar lavage
• Pulmonary atertiography: if considering bronchial artery embolization (BAE) for Tx of hemoptysis in the setting of a mass or
bronchiectasis
• Thoracic Surgery consult: if arteriography unsuccessful or if contraindications to arteriography
Treatment
1. Emergent (massive hemoptysis)
3
• ABC’s: 02, suction, intubate, 2 large bore IV’s, fluid resuscitation, obtain necessary blood work, continuous monitoring including
u/o
• Consult: Pulmonology, Thoracic Surgery, ICU, Interventional Radiology
• Massive: BAE or thoracic surgery
• Nonmassive: Tx of the underlying cause and if not resolving consider consultation with a Pulmonologist to help guide
management
3. Referrals
• Nonmassive, unresolving hemoptysis: to Pulmonologist for investigation and Tx direction
References
1. Corder R. Hemoptysis. Emerg Med Clin N Am. 2003:21:421-435.
2. Bidwell JL and Pachner RW. Hemoptysis: diagnosis and management. Am Fam Phys. 2005;72(7):1 253-1260.
3. KnotCraig Ci, Oostuizen JG, Rossouw 6, Joubert JR, Barnard PM. Management and prognosis of massive hemoptysis. Recent experience with 120
patients. I Thorac Cardiovasc Surg. 1 993;1 05:395-7.
4. O’Neil KM and Lazarus AA. Hemoptysis. Indications for bronchoscopy. Arch Intern Med. 1991 ;1 51:171-4.

HYPERTENSION
2011 Ed. Authors: Debra] Das, Olga Toleva MD, Michael T]andrawidjaja MD, Paul W Armstrang MD FRCP
OriginalAuthars:Alyzee Sibtain, Carrie Ye MD, Taha TaherMD FRCPC
Station Objective
Develop a systematic approach to Hypertension (HTN): define HTN, accurately measure and diagnose HTN, determine which patients need to
be investigated for secondary causes, and appreciate appropriate HTN management.
Differential Dagnosis
Diagnostic Criteria
• BP normally should be <120/80.
• Hypertension is diagnosed when individual presents with blood pressures consistently NIH HTN: classification for adults
>140/90 or >130/80 in diabetics and proteinuric/chronic kidney disease
Beware of white-coat hypertension (normal BP at home, high BP in office) and masked Normal <120k80
hypertension (high BP at home, normal BP in office) use 24 hour ambulatory BP
- Prehypertension 120-139/80-89
monitoring or regularly recorded home BP to rule in or out. Stage 1 HTN 140-159/90-99
Patient should be comfortable for 5 minutes, sitting with back supported and legs
uncrossed before taking the BP reading. Stage2HTN >160/>100
Both arms if BP elevated or disparity in radial pulses that should be felt simultaneously.
2. Etiology:
• Essential HTN majority of cases of HTN the cause is unknown.
—
• Secondary HTN demonstrable secondary cause such as kidney disease, renovascular disease, endocrine disorders
—
(hyperaldosteronism, thyroid disease, Cushing’s), pheochromocytoma, obstructive sleep apnea, and coarctation of aorta.
• HTN is a risk factor for cardiovascular morbidity and mortality.
• The risk of stroke in particular is reduced with appropriate BP control.
History
ID • Age, gender
CC • Headache, dizziness, nausea, vomiting, blurred vision, chest pain, dyspnea, no complaints
HPI • Symptom description (onset, aggravating and alleviating factors, etc.), previous HTN history and adequacy of
control, evidence’of symptoms related to target organ damage (heart failure symptoms, angina, TIA/stroke,
peripheral vascular disease, eye disease)
RED FLAGS • Headache, neurologic deficits, angina, visual disturbance, delirium, altered LØC
PMHx • Complications (CAD/strokes/PVD/CHF/ A. fib) and CAD risk factors (dyslipidemia, diabetes, smoking, family history),
secondary causes (kidney disease, renovascular disease)
PSHx • Cardiac, renal, vascular surgery
PO&GHx • Pre-eclampsia, aortic coarctation
Meds • Prior use of anti-hypertensive medications (diuretics, beta-blocks, ACE inhibitors, ARB5). OTC meds (contraceptives,
decongestants, NSAIDs), Recreational drug use (cocaine, amphetamines).
FHx • Cardiovascular disease in family
Social • Sodium consumption, smoking, alcohol consumption, physical activity, drug use, lifestyle changes
Risk Factors • Physical inactivity, age (>55 years ., >65 years ), microalbuminuria or GFR <6OmL/min, FHx of CVD (<55 years
., <65 ), excess intake of dietary sodium and/or alcohol, dyslipidemia, obesity (BMI >30 kg/mi, DM, metabolic
syndrome,_previous CV event, smoking and insufficient intake of K
Physical
1. Initial Approach
• Check vitals BP, HR, RR, Temperature, Sa02 and overall appearance of patient.
—
• Check radial pulse note rhythm and rate. Check both arms lying and standing (orthostatic hypotension).
— —
• Describe Korotkoff sounds and record measurement. Check for any signs of brady or tachycardia (HR <60 or >100).
2. Evidence of Target Organ Damage
• Fundoscopy for evidence of retinopathy
• Neurological exam for signs of stroke

• Evidence of heart failure (rales, 53 heart sound) or LVH (presence of S4 heart sound)
• Signs of aortic dissection check BP in both arms, pulse deficit, and neurological signs
—
• Check for presence of carotid bruits (better indicator of coronary disease than carotid disease)
.
Evidence of Secondary Causes of Hypertension
• Cushingoid appearance
• Abdominal bruits to check for renal artery stenosis
• Obesity, short neck, crowded oropharynx for evidence of obstructive sleep apnea
• Sweaty, flushed, and anxious for evidence of pheochromocytoma
• If coarctation suspected, simultaneous palpation of radial and femoral pulses for delay
Investigations
i. Blood work
• CBC-D, electrolytes check for Nat/K abnormalities, ferritin (anemia)
—
• Fasting blood sugar (diabetes control)

• Lipid profile (dyslipidemia)
• Serum Creatinine/GFR kidney dysfunction (e.g. renal artery disease, chronic kidney failure))
—
• Urinalysis (proteinuria, hematuria)

• ECG
2. Special Tests
• Home BP Monitoring (avoid white-coat HTN)
• 24 hour ambulatory BP monitoring
• ECHO (evaluated for left ventricular dysfunction and hypertrophy)
• Sleep study (obstructive sleep apnea)
• MR angiogram, Ultrasound rule out renal artery stenosis
—
• Tests to rule out endocrine abnormalities 24 hr urinary cortisol and dexamethasone suppression (Cushing’s), aldosterone/renin
—
ratio (hyperaldosteronism),TSH +T3/4 (thyroid disease)

• 24 urine metanephrines (rule out pheochromocytoma)
Treatment
1. a) Hypertensive emergency (excludes ischemic strokes see “Hemiplegia/hemisensory loss” station)
—
• Use IV antihypertensives e.g. labetalol, nitroprusside, hydralazine to reduce diastolic BP to 100-105 mm Hg in 2-6 hours
without dropping the MAP by more than 25%.
b) Hypertensive urgency
• Determine cause underlying disease-causing HTN or not. Treat underlying condition accordingly (medical/surgical
—
therapies).
• Move patient to a quiet room to rest (can drop BP 10-20 mm Hg)
• Use oral medications to target BP 160/100 in hours to days (or longer in elderly)
• Medical 1)—
• Lifestyle: DASH diet fruits, vegetables, low-fat dairy, reduced sodium (<2 g/day) and fat. Quit smoking, increase physical
—
activity, decrease alcohol consumption, counseling for stress reduction, weight reduction. 2)
• Rx: thiazide diuretics, ACE inhibitors, ARBs, BB, or CCBs. Combination therapy is often used for comprehensive HTN treatment.
Check patient Hx for contraindications for therapy chosen.
• Surgical: conditions requiring surgical removal of tumor (pheochromocytoma), coarctation
3. Follow-up
• BP goal <140/90 except diabetic patients or those suffering from proteinuric/chronic kidney disease (<130/80)
4. Referrals
• General Internal Medicine, Cardiology, nephrology, endocrinology
References
1. MCC Objectives Online. htto://www.mcc.ca/obiectives online/obiectives.pl?lang=enolish&role=expert&id=9-1
2. Flanigan iS and vitberg D. Hypertensive Emergency and Severe Hypertension: What to Treat, Who to Treat, and How to Treat. The Medical Clinics of North
America. (2006) 90:pp.439-451.
3. DynaMed. “Hypertensive Emergency”— Updated July 7, 2010.
4. 4. DynaMed.”Hypertension”— Updated August 18,2010.

LOWER BACK PAIN
2011 Ed Authors:Adarsh Rao, Carol Chung MD, Arnold Voth MD FRCP
OuiginalAuthors: Shaheed Merani PhD, Mohammed Osman PhD, Barbara Zhaa MD, Lisa StebleckiMD MPH CCFP
Station Objective
This station requires you to assess the common complaint of lower back pain, both acute and chronic, distinguish between malignant and
benign causes of back pain, and determine the appropriate management.
Basics
Introduce yourself, wash hands, and ask for permission to do PE. Ensure spinal precautions for acute back injury, and document your
observations carefully.
• Mechanical (90% of back pain) —* degenerative (osteoarthritis), muscle sprain/spasm, spinal stenosis (congenital, osteophytes,
central disc)
• Neurological —*peripheral nerve compression (disc herniation, radiculopathy), Sciatica: Pain caused by sciatic nerve entrapment,
Pain, burning and aching in buttocks radiating down to posterior thigh to posterolateral aspect of calf. Variable nerve
involvement: L4 (anterior thigh), L5 (lateral thigh, dorsal foot), Si (soles). Straight Leg Raising Test used in diagnosis. Cauda
Equina Syndrome: Most frequent cause is large central disc herniation. A progressive neurological deficit that presents with
saddle anaesthesia, decreased anal tone and reflex, fecal incontinence, urinary retention (can result in overflow), bilateral lower
leg weakness. Surgical emergency
• Neoplastic (primary or metastatic)
• Trauma (fractures involving compression, distraction, translation, or rotation)
• Spondyloarthropathies (ankylosing spondylitis)
• Referred pain (PID, pyelonephritis, ectopic pregnancy, ovarian mass, endometriosis, peptic ulcers, pancreatitis)
• High Mortality/Emergent: Leaking aortic aneurysm, malignancy, epidural hematoma or abscess, vertebral osteomyelitis
(infection), cauda equina syndrome
History
ID • Age, Gender, Demographics, Geography. Special consideration for pediatric populations
CC • Distinguish between acute and subacute (within 12 weeks) and chronic (more than 12 weeks)
HPI • Characterize lower back pain:
• Pain Hx: onset (trauma/injury), position, quality, radiation (hip/buttocks/legs/feet: unilateral vs. bilateral), severity,
timing, previous episodes, alleviating or aggravating factors
• Associated symptoms including bowel, bladder, and sexual function
• Impact of pain on function and sleep -
RED FLAGS • Cauda Equina Syndrome: sudden loss of bladder/bowel control, saddle anaesthesia (emergency)
• Severe worsening pain at night or when lying down. Pain >2-6 weeks
• Weight loss, history of cancer, fever
• Use of steroids or intravenous drugs
• Patient with first episode over 50 years (malignancy risk)
a Widespread neurological signs or significant trauma
PMHx • OA, Osteoporosis, Ank Spond, Vertebral Prolapse, Spina Bifida, DM, Cancers
PSHx • Spine, Hip, Lower Extremity. Trauma or fractures. Epidural catheters or spinal anaesthesia
Meds • Steroid use. Pain medications including route/frequency/dose
Social • Substance abuse including IV drugs. Look at mood, social withdrawal, occupation and working conditions,
problems with claim/compensation. Determine Hx of back pain/time-oft heavy work, and lack of family support
ROS • Fever, night sweats, significant weight loss

• CV/RESP: previous Hx of Aortic Aneurysm
• GI/GU: frequency and urgency of urination, bladder and bowel problems, dysuria
• MSK / DERM: rash, morning stiffness, response of pain to activity
Risk Factors • Previous infections (IVDU, immunocompromised such as DM and steroid use), fractures, or malignancy. Vocation or
lifestyle

physical
General Approach
Make sure the patient is comfortable and assess the general appearance of the patient and any signs of distress
2. Inspection
• Check for deformities or swelling. Inspect the spine for scoliosis, lordosis, kyphosis. Check body type, gait, and total spinal
posture. Skin markings: faun’s beard —* may indicate spina bifida occulta or diastematomyelia. Café-au-lait spots —* may indicate
neuroflbromatosis or collagen disease. Check dimples or scars
3. Palpation/Percussion
• Palpate for tenderness, altered temperature and muscle spasms. Palpate paravertebral muscles
• Anterior: supine patient —* palpate umbilicus, inguinal areas, iliac crests, symphysis pubis. Posterior: prone patient —* palpate
spinous processes (spondylisthesis), sacrum, sacroiliac joints, coccyx, iliac crests, ischial tuberosities
• MSK —* ROM: forward flexion, extension, side flexion, rotation, chest expansion
• Neuro —* sensation, reflexes (patellar L3-L4, medial hamstring L5-S1, lateral hamstring Si -S2, posterior tibial (L4-L5), Achilles reflex
S1-S2), motor in lower extremities
SpecialTests
• Schober’s test (lumbar flexion): mark 10cm above and 5 cm below dimples of Venus should increase to 20cm during flexion
• Straight leg test: raise leg until radicular pain felt. +ve: pain in sciatic L4-S3 at 30-70° of passive flexion
• Cross straight leg: raise asymptomatic extremity in similar fashion to straight leg test and positive result is pain on contralateral
(i.e. the affected) side
• straight leg test is better for ruling out disc herniation, cross straight leg raise is better for ruling in
• Lasegue Sign: hip and knee flexed to 90°; knee is extended until pain produced down back of leg
• Bragard’s test: if pain is generated with straight leg —* lower symptomatic extremity until pain disappears, dorsiflex foot at point
when pain disappears —* recreate pain: test is +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/L3
• Patrick test (SI Joint pain): Flexion, ABduction, External Rotation (FABER)
Investigations
Blood work
• CBC —D, ESR, urinalysis, Ca, P04, albumin (infection, malignancy, bone, muscle and soft tissue changes)
2. Radiology/Imaging/Special Tests
• Lumbar spine XR (pain >6 weeks or red flags), CT or MRI (soft tissue changes), Bone Scan (infection, malignancy),
Electromyography (skeletal muscle activity)
Treatment
1. Emergent
Cauda Equina Syndrome requires urgent investigation and decompression to preserve bowel and bladder function and prevent
paraplegia (Neurosurgery consult)
Mechanical back pain
• Early mobilization with strengthening exercises including gentle flexion/extension
• Acetaminophen or NSAID (eg. ibuprofen or diclofenac)
• Short course of muscle relaxants (eg. cyclobenzaprine)
• Short acting opioids are rarely necessary
3. Surgical
• May benefit those with a radiculopathy due to herniated disc or spinal defect including stenosis
4. Follow-up
• Mechanical lower back pain should resolve, pain lasting > 6 wks requires further investigation
5. Referrals
• Chronic non-specific/non-malignant pain: consider community-based rehabilitation/chronic pain program
• Radiculopathy (severe sciatica refractory to meds), cauda equina, cord compression, severe spinal stenosis, epidural abscess,
persistent nerve root compression, tumor, or systemic illness require orthopedics or neurosurgery
References
1. Low Back Pain. Towards Optimized Practice. 2009 (http: www.tonalbertadoctors.orgll
2. Lam E., Leung ii.The Musculoskeletal Exam. Essentials of Clinical Exam. 6
th
Edition, 163:166,2010.
3. Ochiai DH.The orthopaedic intern pocket survival guide. McLean (VA); International Medical Publishing, 2007.
4. Skinner HB. Current diagnosis and treatment in orthopedics. 4th
ed. New York (NY); McGraw-Hill, 2006.
5. FP Notebook (htto://www.fonotebook.com/Ortho/Sx/LwBckPnRdFlg.htm
6. Stern B, Deya RA, Rainville J. Update: Low Back Pain. In: Simel DL, Rennie D, eds.The Rational Clinical Examination: Evidence-Based Clinical Diagnosis, New
York, NY: McGraw-Hill; 2009
7. Fam AG, Lawry GV, Kreder Hi. Musculoskeletal Examination and Joint Injection Techniques. Philadelphia, (PA); Mosby Inc. 2006.

NAUSEA AND VOMITING
20?? Ed. Authors: Mohammed Osman PhD, Michael Chu MD, V4iay Daniels MD FRCPC
OriginalAuthors: Carrie Ye MD, Vince Bain MD FRCPC
Station Objective
Approach to determining the underlying cause of nausea and vomiting, with subsequent management.
• Drugs/Toxins: chemo/radiotherapy, opioids, antibiotics, alcohol, anticonvulsants, arsenic, organophosphates
• Infections: gastroenteritis (viral/bacterial), meningitis/encephalitis, systemic
• GI (non-infectious): bowel obstruction, ileus, pancreatitis, appendicitis, constipation, gastroparesis, GERD, PUD, dyspepsia, IBD,
volvulus, varices, hepatobiliary disease, food intolerance, gastric outlet obstruction/pyloric stenosis
• Neuro
• Central: higher intracranial pressure (mass lesion, hemorrhage), brainstem lesions, MS, encephalitis, neurosyphilis, complex
migraine, advanced parkinson’s disease
• Peripheral: otitis media, Meniere’s disease, labrynthitis, vestibulitis, acoustic neuroma, acute glaucoma
• Endocrine/metabolic: hyperthyroidism, DKA, adrenal insufficiency, hypercalcemia, pregnancy, uremia.
• Psych: bulimia, anorexia nervosa, anxiety, depression, conversion d/o.
• Misc: emotional response to unpleasant smells/tastes, acute myocardial infarction, nephrolithiasis, excess pain, HTN emergency,
pneumonia, connective tissue (e.g. SLE, scleroderma), testicular torsion.
High Morbidity/Mortality:
• Small/large bowel obstruction
• GI bleed
• Appendicitis
• Pancreatitis
• Meningitis/Encephalitis
• Adrenal crisis
History
ID • Age, gender
CC • Nausea and vomiting. Focus history based on likely etiology.
HPI • Onset, duration, number of vomiting, vomitus content (blood, fecal, undigested food, bilious), amount, projectile
vomiting.
• Triggers: postprandial (immediately vs >lh), certain foods, time of day, position of head, lying down vs supine
(exacerbating)
• Associated symptoms: H/A, epigastric/abd pain, obstipation, constipation, diarrhea, anorexia, early satiety, last meal,
last bm, diarrhea, fever, chills, weight loss, belching, hiccups, dry coughing, acid taste in am, retrosternal pain, chest
pain, SOB, focal neurological symptoms, vertigo, photophobia, polyuria, polydipsia
• Volume status: tachycardia while supine, postural lightheaded, decreased u/o, fluid intake
RED FLAGS • Worse with supine position (t ICP), focal neurological symptoms, pain that migrates to LLQ (appendicitis),
abdominal distention/feculent or bilious emesis (obstruction), severe epigastric pain (pancreatitis), 1 LOC, severe
dehydration (adrenal insufficiency).
PMHx • Diabetes, cancer, systemic sclerosis, pancreatitis, adrenal insufficiency, IBD, hernia, Parkinson’s
PSHx • Any abdominal surgery
PO&GHx • Last normal menstrual cycle, regularity
Meds • Steroids, chemotherapy, NSAID, SSRI, anti-convulsants, opioids
Allergies • General Inquiry
FHx • Autoimmune disorders
Social • Ethanol
ROS • HEENT: vertigo, acute changes in vision, red color, or visual change (MS)
• CV: chest pain
• GU: testicular pain, urination
• MSK / DERM: rash, arthralgia

physical
1. General Approach: ABCs, vitals, orthostatic vitals (HR, BP), temperature. Focus exam based on likely etiology.
2. Inspection: diaphoresis, I WOB
• HEENT: CN exam, nystagmus, papillary edema, signs of jaundice, dental enamel erosion, dry mucous membranes, tongue
furrows, oral ulcers, JVP
• Abdomen: scar, bulging flanks, distention, hernias
• MSK/Derm: grouped popular vesicles, joint swelling, telangiectasia, purpuric skin rash, skin tightening, dorsal hand surface
calluses, gait
• GU: chancres, genital ulcers, anal ulcers
3. Percussion: percussion tenderness (peritoneal sign)
4. Palpation:
• HEENT: Lymphadenopathy, dry axilla
• Abdomen: rebound tenderness, guarding/rigidity, ascites, liver edges, hernias, palpable abdominal mass
• DRE: mass, tone, blood
5. AuscultatiOn:
• CVS: tachycardia, S4, pericardial rub
• Lungs: pleural rubs, focal consolidation
• Abdomen: bowel sounds, sucussion splash (gastric outlet obstruction or gastroparesis).
6. Special Tests
• Murphy’s sign, McBurney’s sign, Kernig’s/Brudzinski’s signs, asterixus
Investigations
1, Blood work: CBD D, electrolytes (Na, Cl, K, Mg, PC
- ), urea, Creatinine, Ca, am cortisol, 3-hCG, lipase, glc
4
• If indicated: ANA, LFT, AST, ALT, ALP, bilirubin (direct and indirect), serial troponin T and CK-MB, ketoacids
2. Radiology/Imaging:
• AXR (3 views): free air, volvulus, air fluid levels
• CXR (PA and lateral)
• Abd U/S
• CT (if indicated) abdomen, head (mass lesion)
3. Surgical/Diagnostic Interventions: esophageogastroduonoscopy (EGD)
Treatment
1. Emergent: IV fluids to correct dehydration (NS bolus), IV NS + 20-40 mEq KCI/L + correct electrolyte abnormalities.
2. Medical:
• Analgesia (as needed)
• Symptom control:
• NPO
• Metoclopramide 5-10mg PO/IV qoh (contraindicated in complete bowel obstruction)
• Dimenhydrinate 25-50 mg PO/IV/IM q6h (best for vestibular causes of NN)
• Ondansentron 8 mg PO/IV q8h (very expensive, use only when others do not work)
• Bowel obstruction: NG tube
3. Surgical:
• Air enema (volvulus)
• Therapeutic EGD: PUD, UGI bleed
• OR for bowel obstruction, appendicitis, cholecystitis
References
1. Uptodate: Approach to the Adult with Nausea and Vomiting [Online] (2010). Available from: http://www.uptodate.com.
2. Quinlan JD and Hill A. Nausea and Vomiting of Pregnancy. Am Fam Physician (2003) 68(1 ):1 21-128.
3. Ye C and Bain V. Nausea and Vomiting. Edmonton Manual (2009) 1’, ed.
4. Powell DW. Approach to the Patient with Gastrointestinal Disease Nausea and Vomiting. In Goldman L, Ausiello D (editors). Cecil Textbook of Medicine
—
22 edition. 2004 Saunders. Philadelphia. pp 782-3.

OBSTRUCTIVE LUNG DISEASE
2011 Ed. Authors: KamalAbdulwahab, Abraam Isaac MD, Kourosh DinyariMD
OriginalAuthors: Charles Lim, Edward James PLlianjeevan Deol MD, 01/mi Vethanayagam MD FRCPC
Station Objective
In this station you may be expected to assess a patient with obstructive airways disease. A thorough assessment and appropriate laboratory
investigations should lead to a management plan for maintaining adequate symptom control. The approach presented is an introduction
designed to act as a basic framework.
Disease . . .
Diagnostic Modality Diagnostic Criteria
State
COPD History and physical exam Highly suggestive (see below)
• CXR May show increased bronchial markings (chronic bronchitis), chronic
• Spirometry (definitive) hyperinflation (emphysema), abnormal heart shadow
• Post bronchodilator ratio FEV
/FVC < 0.70
1
Asthma History and physical exam Highly suggestive (see below)
• Spirometry (definitive) (a) 12% and 200 mL improvement in FEy
1 from baseline 15 mm post-usage of
inhaled 3
-agonistn4
2
• /FVC < lower limit of normal for age, gender, height, and ethnicity)
(b) FEV
1
• Asthma (chronic disease characterized by reversible hyper-responsive, inflammation and broncho-constriction)
• COPD (chronic disease characterized by irreversible, progressively worsening airway obstruction, with episodes of partially
reversible acute exacerbations)
• Bronchiectasis, cystic fibrosis, interstitial lung disease
• Acute exacerbations (e.g. COPD), if severe enough, can lead to respiratory compromise/failure and ICU admission
• Recurrent infections (especially with COPD and cystic fibrosis)
• PE (occurs in about 25% of COPD exacerbations of unknown origin), CHF
History
ID • Age, gender, height, ethnicity
CC Dyspnea, wheeze, cough ± sputum, chest tightness (ask which is most problematic)
HPI Onset of symptoms, triggers (e.g. activity, smoke, pollen, cold air, etc.), sputum description
• Frequency of symptoms, nocturnal symptoms, use of rescue meds (e.g. short-acting 3 -agonist)
2
• Function: limitation to daily and physical activities (e.g. dyspnea while walking/climbing stairs/rest), absenteeism
from work/school
RED FLAGS Rescue inhaler 3/wk, nocturnal symptoms, symptoms of cor pulmonale, indicators of severe/worsening COPD
(home 02, steroids, mobility assistance, obesity, 4 episodes/yr)
PMHx • COPD (self-reported diagnosis: LR 4473)6
• Atopy (allergies, eczema, etc.)
• Samter’s triad (asthma, nasal polyps, and ASA sensitivity)
• Previous hospitalizations, ICU admission, intubations
• Pulmonary or cardiovascular co-morbidities (notably upper airway obstructions)
• Vaccination history
PSHx • Lung resection or lung transplant
Meds ASA/NSAIDs (ASA/NSAID induced worsening of OPD), vaccinations (pneumonia, influenza)
Allergies • Medications and environmental triggers
FHx Atopy (asthma,eczema, etc.); CF and other respiratory diseases
Social Smoking (pack years, cessation, etc.) ( >40 pk yrs has a LR = 12 for OPD)
6
• Occupational exposure (e.g. chemical, mining, welding, etc.)
ROS • HEENT: rhinitis, sinusitis, oral thrush (chronic inhaled corticosteroid use)
• CV: pleuritic chest pain, peripheral edema
• RESP: as indicated in HPI
• MSK / DERM: eczema, rashes

IE.iFactors .
Smoking, family history of asthma and atopy, al -antitrypsin deficiency I
physical
1. General Approach
• Vital signs: pulsus paradoxus, 02 saturation, HR, BP, RR
• Signs of respiratory distress: fragmented speech, pursed lip breathing, nasal flaring, tracheal tug, accessory muscle use, indrawing,
paradoxical abdominal movements, posture (tripoding)
2. Inspection
• Signs of peripheral or central cyanosis, AP diameter (barrel chest), chest wall deformities, clubbing, smoker’s fingers, accessory
muscle involvement
3. Percussion
• Hyperresonance due to emphysema or loss of cardiac dullness due to acute asthma
• Inferior diaphragm displacement due to hyperinflation
4. Palpation
• Chest expansion, laryngeal height, tracheal deviation, decreased tactile fremitus due to hyperinflation
5. Auscultation
• Breath sounds: bronchial, vesicular, length of inspiratory/expiratory phase
• Adventitious sounds: crackles, wheezes, stridor, rhonci (can indicate retained secretions)
• Auscultated wheezing or laryngeal height 4cm has a LR 4 for OPD 6
• Forced Expiratory time> 9 seconds: (LR 4.66.7)6
Investigations
1. Blood work
• CBC-D: HCT (compensation for decreased Pa0), eosinophils (allergy component)
2
• ABG (PaO
for 02 treatment assessment, PaCO2 to assess for C02 retention/need for NIPPV)
2
• CXR (may appear normal or show increased bronchial markings and/or hyperinflation, pneumothorax, pulmonary edema, or
pneumonia)
• ECHO (in the context of symptoms and signs of right ventricular dysfunction and pulmonary HTN), ECG
3. Special Tests
• PFT/Spirometry (see Diagnostic Criteria above), allergy testing, BMD, sputum induction, metacholine challenge
Treatment
1. Emergent
• ABCs; consider 02 supplementation
• Inhaled medications (e.g. salbutamol, ipratropium, corticosteroids), systemic corticosteroids (e.g. prednisone)
• NIPPV with respiratory failure (i.e. BiPAP)
• It is important that the patient receive education regarding environmental control and proper medication usage. Counseling for
smoking cessation is also critical!
• Medical
• Step up or step down medical therapy as needed to achieve adequate symptom control in stable patients
• Short-acting 3 —agonist, long acting bronchodilators, inhaled corticosteroids, systemic corticosteroids, home 02 etc.
2
• Surgical: lung resection, lung transplant
3. Follow-up
• Allergy skin testing (id triggers), specific inhalation challenge (occupational triggers), cardiopulmonary exercise test (sensitivity to
exercise)
• Strongly advice on vaccinations (pneumococcal and influenza)
4. Referrals
• Occupational health and social work if applicable;
• Counseling for smoking cessation (e.g. AADAC), pulmonary rehabilitation programs
References
1. Lougheed M.D. et al. CTS Asthma Management Continuum —2010 Consensus Summary for children six years of age and over, and adults. Can Respir J
2010;1 7(1 ):1 5-24
2. O’Donnell, D.E. et al. CTS recommendations for management of COPD —2008 update highlights for primary care. Can Respir J 2008;1 5 Suppl A;
—
3. ATS Documents: Statements, Guidelines & Reports [Internet]. New York: American Thoracic Society; c2009 [cited 2009 Nov 23]. Available from http://
www.thoracic.org/sections/publications/statements/index.html.
4. Pellegrino R. et al. Interpretative strategies for lung function tests. Eur Respir J. 2005 Nov;26(5):948-68.
5. Celli 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):932-46.
6. Simel DL. Update: Chronic Obstructive Airways Disease. In: Simel DL, Rennie D, eds.The Rational Clinical Examination: Evidence-Based Clinical Diagnosis,
New York, NY: McGraw-Hill; 2009

PALPITATIONS & ARRHYTHMIAS
2011 Ed. Authors: Michaeli Kopusta, Christopher Fung MD, AshrafKhon MBChB CCFP
OriginalAuthors: Sabira Sulemon, Kris Chan MD, Michael Tjandrowidjaja MD, Evan Lockwood MD FRCPC
Station Objective
Approach to the diagnosis and treatment of benign palpitations and those indicative of serious disease
• Benign vs more serious causes of palpitations
• Cardiac origin
• Arrhythmia: SV1 VT, premature contractions (atrial or ventricular)
• Non-arrhythmia: structural or ischemic heart disease
• Anxiety disorder
• Medications (particularly cardiac/thyroid) or drugs
• lschemic heart disease
• Life-threatening arrhythmia: AF, long QT, hypertrophic cardiomyopathy
• Thyrotoxicosis
istory
ID • 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
• Precipitating (pain, exercise, alcohol withdrawal) and palliating (Valsalva) factors
• Heart rate and rhythm (regular/irregular) during episode and at rest
• Associated chest pain, SOB, syncope/presyncope, dizziness, diaphoresis, NN, tingling
• History of palpitations
RED FLAGS • Associated chest pain, syncope/presyncope (hypotension), dyspnea
• History of cardiac disease
• Duration of episode >5mm
• Significant FHx
PMHx • Cardiac risk factors (smoking, DM, HTN, dyslipidemia, FHx)
• History 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)
• Weight loss (hyperthyroidism)
• Recent surgery or immobilization (PE)
• Episodic pallor, tremor, headache, diaphoresis (pheochromocytoma)
PSHx • Cardiac surgery
Meds • 3-agonists, stopping a 3-blocker, vasodilators, anti-cholinergics, Synthroid, insulin, theophylline, digitalis,
antiarrhythmics, pseudoephedrine, tricyclics, herbals
FHx • Syncope
• Sudden death, especially cardiac in 10 relatives (male<65 years, female<55 years)
• Serious arrhythmias
Social • Caffeine, smoking, EtOH
• Recreational drugs: cocaine, amphetamines, opiate withdrawal, alcohol withdrawal
ROS • RESP: asthma, lung disease
• GU: pregnancy (t cardiac output)

Physical
1. General Approach
• General Inspection: diaphoresis, pallor, LOC, conjunctival pallor (anemia), obvious discomfort/pain
2. Inspection
• HEENT
• Thyroid enlargement, tremor, exophthalmos (Graves)
• Cv
• JVP: t JVP indicates t intracardiac pressure (risk for AF)
• Visible impulses: apical (LV), parasternal (RV), upper sternal borders (aortic and pulmonary artery)
3. Palpation
• HEENT
• Thyroid nodules or enlargement
• CV
• Pulse deficit (difference in beat count between radial pulse and apical heart beats) suggestive of AF
• Parasternal heave: RV hypertrophy/hypertrophic cardiomyopathy
• Thrills: may be felt over the aortic, pulmonic, tricuspid, and mitral area
• Apical impulse: comment on amplitude, diameter, duration (sustained in AS, displaced and enlarged in CHF)
4. Auscultation
• CV
• Si & 52, extra heart sounds
• Murmurs: timing, shape, location, radiation, pitch, quality
Investigations
1. Blood work
• CBC-D, troponin, CPK, glucose, electrolytes, TSH, Cr, urea, INR
2. Special Tests
• ECG for any patient with suspicion of cardiac disease
• Holter monitor (patients with paroxysmal palpitations, syncope/presyncope, suspected mild ischemia)
• Urine metanephrines if pheochromocytoma suspected
• Electrophysiologic study if ECG or Holter reveal serious arrhythmia
Treatment
1. Emergent
• Asynchronous defibrillation forVF or pulselessVT
• Synchronized DC cardioversion for all other arrhythmias (stable or unstable)
• SVT: carotid sinus massage (after verifying no carotid bruits), Valsalva, adenosine IV push (avoid in suspected WPW)
• VT: amiodarone, lidocaine or procainamide IV
• AF: rate (13-blocker) control first or rate-limiting calcium channel blocker, consider anticoagulation with warfarin (CHADS
2 score >2)
3. Referrals
• Cardiology
• Electrophysiologic studies or ablation
References
1. Hurley, KF. OSCE and clinical skills handbook. Toronto: Elsevier; 2005.
2. Gonzales R, Nadler PL. Chapter 2. Common symptoms. In: McPhee Si. Papadakis MA, Tierney LM ir. CURRENT Medical diagnosis & treatment 2009: http.I/
www.accessmedicine.com.login.ezproxy.library.ualberta.ca/content.aspx?aID’79.
3. Bollinger BC, Heidenreich, I. Chapter 33. Cardiac Arrhythmias. In: Stone CK, Humphries RL, editors. CURRENT Diagnosis & treatment: Emergency medicine,
6e: http://www.accessmedicine.com.Iogin.ezproxy.library.ualberta.ca/content.aspx?aID=31 07067.

PARKINSONS & MOVEMENT DISORDERS
2071 Ed. Authors:Samapti Samapti, Tam NowackiMD
OriginalAuthors: Victoria Lam, RahitMaudgiIMD PhD
Station Objectives
Characterize abnormal movement(s) and describe specific features of Parkinsonism/Parkinson’s Disease (PD)
Approach to Abnormal Movements

1. Recognize classic motor syndromes
• “Pyramidal” (corticospinal tract) syndrome loss of volitional movement with spasticity
-
• Cerebellar syndrome incoordination (ataxia), dysmetria, dysdiadochokinesis

-
• “Extrapyramidal” (ie. basal ganglion) syndromes

• Hypokinetic BG syndrome akinesia, rigidity, and tremor without loss of voluntary movement e.g. PD
- -
• Hyperkinetic BG syndrome involuntary movements such as choreoathetosis e.g. Huntington’s disease

- -
2. Classify tremor
• Rest tremor tremor in a body part that is at rest and supported by gravity
-
• Action tremor occurs with movement

-
• Postural tremor occurs while maintaining a position against gravity

-
• Kinetic tremor occurs during a voluntary movement (e.g. intention tremor in finger-to-nose testing)
-
3. Recognize classic types of tremor

• Cerebellar tremor (postural, action or kinetic) 3-4 Hz, associated with ataxia or dysmetria
—
• Parkinsonian tremor slow frequency (4-6 Hz) resting tremor. “Pill-rolling” hand movements, often asymmetric. Inhibited during
-
sleep and voluntary movement. Increased by emotional distress.

• Classic Essential tremor bilateral action tremor (postural or kinetic). Often positive FmHx. Inhibited by EtCH
-
• Physiological tremor high-frequency (8-12 Hz) mainly postural tremor. Present in normal patients. Often enhanced by stimulants,
-
e.g. caffeine.
History
ID • Age, gender
CC • Tremor/movement abnormality (common CC is falls in the elderly)
HPI . Onset: acute (CVA event, cervical compression) vs chronic (degenerative disease, PD)
. Provoking/palliating factors: EtOH, caffeine, meds, toxin, uneven surfaces, dim light
• Functional hx: review basic and instrumental ADLs, use of assisted devices, rigidity and bradykinesia (LR+4.5, LR
0.12), trouble turning over in bed (LR+ 13), trouble opening jars (LR+ 6.1, LR- 0.26) or doing up buttons (LR+ 3, LR
0.33), difficulty rising from chair, falls
• Hx of recent infection or travel
PMHx • Hyperthyroidism, DM, stroke, head trauma, CV risk factors, encephalitis
PSHx • Intracranial surgery
FHx • Tremor, dementia, Parkinson’s Disease, Huntington’s Disease
Meds • Recent med changes, anti-dopaminergics? (anti-psychotics, certain anti-emetics)
Social • Smoking, EtOH, living situation, work, toxin exposure (Mn, CS
, MPTP, Hg, Pb, As)
2
ROS . Constitutional: general malaise, easy fatiguability
• CNS: memory, visual disturbances, tremor
• CV: pre-syncope/syncope
• GI: dysphagia, constipation, sialorrhea
• GU: sexual difficulties, urinary incontinence/urgency
• Psych: personality changes, disordered sleep, hallucinations, depression
Physical Examination in Parkinson’s Disease

1. General Examination
• Vital Signs: measure BP in lying/sitting and standing positions to look for orthostatic hypotension
• General Appearance: general poverty of movement (hypokinesia)
• HEENT: expression-less, “masked”facies (hypomimia), decreased blinking rate, soft and quiet voice (hypophonia), drooling
(sialorrhea caused by decreased swallowing frequency)
—
• GI: enlarged liver, gastric dysmotility, constipation

• Skin: facial seborrhea, excessive sweating
• Psych: high rate of depression in PD, consider screening (e.g. Geriatric Depression Scale)
2. Neurologic Examination
• Mental status
• LOC, orientation, consider cognitive screening test (MMSE or MOCA)
• Cranial Nerves
• EOM: impairment of eye convergence and upward gaze, delayed initiation of gaze movements, slowing of conjugate
movements
• Motor Examination
• Tremor: frequency, amplitude, body parts involved, resting or action tremor?
• PD: pill-rolling, slow frequency (4-6Hz) resting tremor
• Tone : test elbow flexion/extension, rapid forearm supination, slow wrist circumduction
• If increased, is it 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 (LR+ 4.5, LR- 0.12),
• Power: should not be altered in an extrapyramidal (BG) lesion
• Reflexes
• Deep tendon reflexes, plantar responses should not be altered in an extrampyramidal (BG) lesion
• PD: inability to suppress blinking on tapping glabella (positive glabellar tap/Myerson sign LR+ 4.5, LR- 0.13)
—
• Coordination/Cerebellar Function
• Coordination is intact, i.e. there is no dysmetria on finger-to-nose or heel-shin testing
• 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.
• Contrast to failure to perform rapid alternating movements, a sign of a cerebellar lesion
3. 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, decreased arm swing,”en bloc” turn, festination (involuntary acceleration of gait, may lead to a fall)
• Romberg test: not expected to be positive (as there is no sensory deficit)
• Pull test: ensure patient safety do not drop your patient!
—
• Normal is to regain balance with perhaps one backwards step. Multiple backwards steps (retropulsion) or uncontrolled fall,
indicates postural instability
Investigations
PD is a clinical diagnosis!
2. Blood work: generally not indicated, but may rule out other causes of tremor/abnormal movements
• TSH (r/o hyperthyroidism), serum ceruloplasmin/24 hr urine Cu 2 (r/o Wilson’s disease very rare)
—
3. Neuroimaging
• CT/MRI brain: not indicated for PD, order if suspected infarct/structural lesion
• [18F]-fluorodopa PET scan: research use only, decreased uptake of F-dopa at dopaminergic terminals in caudate and putamen
correlates with severity of neurodegeneration in substantia nigra
Treatment
1. PD: trial of levodopa, response to treatment is highly suggestive of diagnosis, refer to neurologist for follow-up
2. Enhanced physiological tremor: remove precipitating cause
3. Intention tremor: depends on underlying cause (e.g. focal lesion)
4. Indications for Hospitalization: neuropsychiatric disturbance, delirium, frequent falls, failure to cope at home
5. Referrals: refer to neurology if there is diagnostic uncertainty, for help with initiating/adjusting treatment, for f/u
References
1. Adams and Victor’s Principles of Neurology, 9th Ed. (2009)
2. Bradley: Neurology in Clinical Practice, 5th ed. (2008)
3. Rao G, Fisch L etaL Does this patient have Parkinson disease? JAMA 2003;289:347-353
4. ACP PIER & AHFS Dl Essentials: Parkinson’s Disease. http://online.statref.com.login.ezproxy.Iibrary.ualberta.ca/document.aspx? fxid=92&docid=2721.
Posted: 11/10/2009.

PERIPHERAL VASCULAR DISEASE
OriginalAuthars: Christopher Fung, Richdeep Gill MD, Gerrit WinkelaarMD FRCSC
Station Objective
Examine the peripheral arterial system of a patient. Outline the presentation and management of claudication.
Arterial insufficiency
• Classic Hx: exercise induced, reproducible walking distance, rapid relief with rest, cramping or aching in specific area of leg
(buttock, hip, thigh, calf, foot) corresponding to occluded vessel
• Atherosclerotic risk factors
• Fontaine’s stages: asymptomatic (I), mild claudication (Ila), moderate-severe claudication (lIb), ischemic rest pain (Ill),
ulceration or gangrene (IV)
• 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
• Acute limb ischemia
• Sudden onset
• 6 P’s (in temporal order): pain, pallor, pulselessness, poikilothermia, paresthesia, paralysis
• DVT
History
ID • Ageandgender
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 mm)
• Rest pain with recumbent position (burning or aching at toes or ball of foot)
• Cold extremities and difficult to warm
RED FLAGS • Rest pain, non-healing ulcers, gangrene
• Hair loss, thin shiny skin, pallor on elevation/rubor with dependency
PMHx • Atherosclerosis, DM, dyslipidemia, HTN, trauma, vasculitis, rheumatoid arthritis, Raynaud’s, clotting disorder, stroke,
CHF, renal failure, radiotherapy
PSHx • Bypass graft or stent placement
FHx • Atherosclerosis and associated sequelae, non-cerebral aneurysm, clotting disorders
Social • Smoking, drugs
ROS • HEENT: headache (rio temporal arteritis), vision change
• CV: angina, chest pain
• MSK / NEURO: focal weakness, focal paresthesias
Risk Factors • Advanced age, smoking, DM, dyslipidemia, HTN, hyperhomocysteinemia
Physical
1. General Approach
• Vitals: bilateral BP (comment on asymmetry)
2. Inspection
• Signs of insufficiency: pallor on elevation, dependant rubor, prolonged capillary refill (N <2s), loss of hair
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 discolouration of skin Malleolar, sites of venous stasis
Neurogenic Painless Deep, repeated trauma Plantar surface of metatarsal heads, lateral 5 th metatarsal head

Palpation
(comment
• Examine radial, ulnar, brachial, axillary, carotid, femoral, popliteal, posterior tibial, and dorsalis pedis pulses bilaterally
on differences, amplitude, contour and upstroke)
1
abnormal
• Dorsalis pedis pulse may be absent in up to 12% of normal population, but absent posterior tibial pulse is always
• Palpate abdominal aorta
Ankle Brachial Index
4. Auscultation
• Listen for carotid, abdominal, renal and femoral bruits bilaterally >0.90 Normal
.
SpecialTests 071 090 • I 0 b struc t ion
Mid
• Role of posture and pain on standing (to distinguish from spinal stenosis) . -
0.41-0.70 Moderate obstruction

• Ankle-brachial index (ABI)
• Use Doppler to find lower limb vessels <0.40 Severe obstruction
(waveforms tri/bi-phasic: normal, monophasic: prox arterial obstruction)
—
• Ankle BP (highest value of posterior tibial, dorsalis pedis, and peroneal arteries) / Brachial BP
luminal
• As compared to angiography, ABI is 89% sensitive, 99% specific, accuracy of 98%, threshold of 0.9 at detecting
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
—
Investigations
1. Blood work
• CBC-D, glucose, Cr, electrolytes, clotting profile, CRP (if suspicious of inflammatory cause)
• Duplex U/S
• CT or MR angiography ± digital subtraction angiography (arranged by vascular surgery)
3. Special Tests
• Treadmill exercise test and ABI pre/post exercise (differentiate neurogenic pseudoclaudication vs. true vascular claudication)
Treatment
1. Emergent
(Doppler) and
• Acute limb ischemia: immediate neurovascular assessment, refer to vascular surgery for assessment of limb viability
revascularization
• Consider local thrombolysis or surgical embolectomy, ensure anticoagulation post-op
2. Conservative Treatment
• Control atherosclerotic risk factors: HTN, DM, dyslipidemia, encourage smoking cessation
• Exercise: supervised program for patients with intermittent claudication (30-45 mm, 3x/wk for 12 wks)
• Generally, 1/3 improve with exercise, 1/3 stay the same, 1/3 deteriorate
• ASA 81 325mg daily or clopidogrel 75mg daily for prevention
—
• Pentoxifylline or cilostazol for claudication symptom relief

3. Surgical Treatment
macotherapy, or
• Indicated in patients with severe limb ischemia, significant functional disability, unresponsive to exercise/phar
have a reasonable likelihood of symptomatic improvement with surgery
• Type of intervention dependant on extent of dz: balloon dilation, stent placement, grafting, or bypass
tion not
• Sympathectomy or amputation considered with risk of sepsis from gangrene, intractable pain at rest, or revasculariza
possible
4. Follow-up
• Annual follow-up for patients with claudication, assess progression and risk reduction compliance
5. Referrals
• Vascular surgery
References
1. Hiatt WR. Medical treatment of peripheral arterial disease and claudication. N EngI J Med. 2001 May 24;344(21 ):1 608-21.
Proc. 2010 Jul;85(7):678-92.
2. Olin JW, Sealove BA. Peripheral artery disease: Current insight into the disease and its diagnosis and management. Mayo Cliii
of clinical medicine. 8” ed. New York: Oxford University Press; 2010
3. Longmor, M, Wilkinson, IB, Davidson EH, Foulkes A, Mafi AR. Oxford handbook

PLEURAL EFFUSION
20? I Ed. Authors: Zoe Wo1 A5hIey Gilison MD, Mohit Bhutoni MD FRCPCFACP
Station Objective
In this station you may be expected to perform a physical exam of the thorax, diagnose a pleural effusion, and interpret the results of pleural
fluid collection.
1. Diagnostic Criteria ( based on pleural fluid analysis
)
4
Transudate vs. exudate: Light’s criteria (table 2)
Empyema: pus, microorganisms on gram stain or culture, pH <7.2
Hemothorax: pleural/serum HCT 0.5
Chylothorax: triglycerides >1.2 mmol/L, chylomicrons
Table 1: Light’s criteria

2
Fluid classification Pleural/serum protein ratio Pleural/serum LDH ratio Serum LDH (lU/L)
Transudate 0.5 0.6 2/3 of upper limit of normal
Exudate >0.5 >0.6 >2/3 of upper limit of normal
34
• Most common
• Transudate: CHF, liver cirrhosis, peritoneal dialysis, hypoalbuminemia
• Exudate: infection, malignancy, connective tissue dz
• Less common
• Transudate: nephrotic syndrome, hypothyroidism, PE, mitral stenosis
• Exudate: TB, RA, pulmonary infarction, autoimmune, pancreatitis, asbestos exposure, DressIer’s Syndrome
History
CC • Most common: dyspnea
• CP /cough/asymptomatic
HPI Symptoms: OPQRST, previous episodes
• TB Hx, occupational Hx, connective tissue dz Hx, Hx of CHE, renal dz and liver cirrhosis, thyroid dz
• Constitutional symptoms and risk factors for malignancy
• Recent infections, exposure to infectious contacts, travel Hx
RED FLAGS Always consider PE (75% of patients with a PE pleural effusion have pleuritic CR PE cannot be diagnosed by pleural
fluid aspiration.
1
PMHx Ca: lung, metastatic
• Pneumonia, other lung infections/conditions
• Organ failure: heart, liver, kidneys
• Collagen vascular dz (SLE, RA)
• Pancreatitis
PSHx Cardiac
FHx • Ca
Meds Amiodarone, nitrofurantoin, phenytoin, methotrexate
3
Allergies Rx, Environmental
Social Smoking, EtOH
ROS General ROS with a focus on RESP system
Physical
1. General Approach
• Vitals: HR, BP, RR, Sp0
,T
2
2. Inspection
• Large effusion: tracheal deviation away from affected side

__________ ____________________________
3 Signs of effusion
Table 2: Physical findings to differentiate effusion from consolidation
Pathology Percussion Palpation Auscultation Over Affected Area Special Tests
• L tactile fremitus • or absent breath sounds
+ Bronchophony
Effusion Dull • lpsilateral L chest wall • Bronchial breathing at top
+ Whispered pectoriloquy
expansion of effusion
• t tactile fremitus • air entry - + Bronchophony
Consolidation Dull • Ipsilateral -I- chest wall • Bronchial breathing + Whispered pectoriloquy
expansion • Crackles + Egophony
Investigations
i. Blood work
• CBC-D, electrolytes, serum LDH, total protein, glucose, LFTs, liver enzymes
• CXR: PA and Lat —+ blunting of costophrenic angles would be initial sign of small effusion, lateral decubitus —* determine if
effusion is loculated and to assess for safety of thoracentesis (must be >10mm in height)
• U/S: to landmark or perform U/S guided thoracentesis (safer than blind)
• CT: to help with identifying etiology
3. Special Tests
• Thoracentesis for pleural fluid analysis
• Do not perform if <10mm or clinically a transudate that improves with treatment (CHF, post-surgical)
• Fluid analysis: LDH, protein, cholesterol, glucose, pH, cell count and differential, gram stain and culture (including TB and
fungal cultures)
4
’
3
Treatment
• Thoracentesis —* symptomatic effusions should be drained independent of the cause (NB Absolute contraindication: infection at
drainage site)
• Tube thoracostomy —* if associated pneumothorax, empyema, hemothorax, chylothorax, or complicated parapneumonic effusion
2. Further workup
• Manage underlying cause of effusion
3. Surgical
• Pleurodesis for recurrent malignant effusions
• lntrapleural fibrinolysis for loculated effusions
• Thorascopic surgery for certain cases of complicated empyemas and parapneumonic effusions
References
1. Light RW. Pleural effusion due to pulmonary emboli. Curr Opin PuIm Med. 2001 ;7:1 98-201.
2. Light RW, MacGregor Ml, Luchsinger PC, and Ball, WC. Pleural effusions: the diagnostic separation of transudates and exudates. Ann Intern Med.
1 972;77:507-1 3.
3. Maskell NA, and Butland RJA. BTS guidelines for the investigation of a unilateral pleural effusion in adults.Thorax. 2003;58(Suppl ll):ii8-iil 7.
4. Yataco, JC and Dweik RA. Pleural effusions: evaluation and management. Clev Clin J Med. 2005;72(1 0): 854-872.

POLYARTICULAR ARTHRITIS AND JOINT PAIN
20!! Ed. Authors: Mohammed Osman PhD, Michelle Teo MD, FRCPC, Elaine Yacyshyn MD, FRCPC, FRCPC (Rheumatology)
Station Objective
Approach to the diagnosis and management of patients presenting with oligoarthritis (2-4) or polyarthritis (5+) with emphasis on the
management of rheumatoid arthritis and osteoarthritis.
• Infectious:
• Septic Arthritis (gonococcal, S. aureus, H. influenza, S. pneumo, gram negative bacilli, enterococcus, anaerobic).
• Mycobacterial (tuberculosis, and atypical mycobacterial)
• Viral (HBV, HCV), HIV, EBV, parvovirus, rubella
• Lyme disease
• Rheumatoid arthritis
• Seronegative arthritis (ankylosing spondylitis, reactive, IBD, psoriatic)
• Crystal induced arthropathy
• Gout (uric acid crystals)
• Pseudogout (calcium pyrophosphate arthropathy)
• Osteoarthritis
• Connective Tissue Disease (SLE, Sjogren’s, Scleroderma, relapsing polychondritis)
• Myopathy (dermatomyositis, polymyositis)
• Vasculitis (Giant cell, Wegener’s, polyarteritis nodosa, Churg-Strauss, Behcet’s, cryoglobulinemia, HSP)
• Endocrine: hypothyroidism, acromegaly, hyperparathyroidism, hypomagnesemia, hemochromatosis, Wilson’s disease (osteomalacia
this is more fractures rather than arthritis)
• Misc: Polymyalgia rheumatica, sickle cell disease, multiple myeloma, sarcoidosis, amyloidosis
• Functional arthralgia: fibromyalgia, chronic fatigue syndrome
High Mortality
• Autoimmune: vasculitides, SLE, systemic scleroderma
• Neoplasia: multiple myeloma, paraneoplastic disease
• Infectious: Septic arthritis
History
ID • Age, gender
CC • Joint swelling, joint pain, limping, restricted range of motion
HPI • Onset (night vs daytime symptoms, > 6 weeks), morning stiffness> 30 mm, pain or relief with activity, fever, rigors,
weight loss, duration of symptoms, back pain, palindromic recurrence, fatigue. Other joints affected distribution
—
(proximal vs distal), symmetry, number, migratory vs additive. Back pain. Improvement with NSAIDs. Proximal
muscle pain/stiffness. Dactylitis/tenosynovitis
RED FLAGS • Symptoms> 6 weeks, immunocompromised, diabetic, open fracture/wound, rapid onset/progression of symptoms,
STI, IVDU, Family Hx of autoimmunity, fever> 38.5, tachycardia, tachypnea, hypotension, non-weight bearing, tophi,
elevated ESR/CRP, anti-CCP positive, rheumatoid factor +, anemia, leukocytosis
PMHx • Recent gastroenteritis, STI, IBD, psoriasis, hemochromatosis, thyroid disease, Wilson’s disease, immunocompromised,
sickle cell disease, trauma, renal disease, hypothyroidism, HSV, HIV, HBV/HCV, depression, lBS. cardiovascular
disease
PSHx • Joint prosthesis, open wound/joint debridement, joint replacement
PO&GHx • Gonococcal/chlamydial infection, PID, GP status
Meds • Steroids, NSAIDs, allopurinol, DMARD, cyclosporine, diuretics, low dose ASA, chemotherapy
Allergies • General inquiry
FHx • Gout, RA, seronegative spondyloarthopathy, IBD, psoriasis, CTD, sickle cell disease, Ehlers-Danlos, Marfan’s
syndrome
Social • Ethanol, smoking, IVDU, camping, THx (most of Canada), occupation, working/disability, drug insurance coverage

ROS HEENT: sicca symptoms, photophobia, facial swelling, scalp tenderness, jaw claudication, tinnitus, oral/nasal ulcers
• CV: tachycardia, palpitation, pre-syncope
• RESP: tachypnea, SOB/OE
• GI: diarrhea +1- bloody, abdominal pain
• GU: hematuria, dysuria, discharge, dyspareunia, genital ulcers
. DERM/Neuro/MSK: change in mental status, neck stiffness, rashes, foot drop, proximal muscle weakness/stiffness,
arthalgia, Raynaud’s phenomenon, claudication.
Risk Factors • RA: female gender, age (30-50), smoking, family history
• Poor prognostic factors: functional limitation, extra-articular disease (Sjogren’s, Felty’s, lung disease), positive anti
CCP, bone erosions on Xray
• OA: age, obesity, previous trauma, family history
Physical
i. General Approach: ABC, vitals (BP on both arms), temp, diaphoresis, increased work of breathing
• Inspection: hand: SEADD 5
• Deformities: swan neck, Boutonnierre, wrist radial/ MCP ulnar deviation, MCP subluxation, E Ehema
• Nodules: rheumatoid nodules, Bouchard/Heberden nodes A Atrophy
• Nails: pitting/transverse rigiding/onycholysis, nail fold dilated capillaries and drop out areas D Oistriboton (MCPIPIP vs DIP)
• Mucocutaneous: malar/discoid rash, alopecia, oral/nasal ulcers, genital ulcers, telangiectasia
D Deorntty
• Other: injected conjunctiva
• Range of motion: active first, then passive if needed
• Palpation: warmth, tenderness, effusion, subcutaneous nodules, lymphadenopathy, hepatosplenomegaly, crepitus (esp knee)
Peripheral neurological exam. Distal pulses. Pitting edema
• Auscultation: pericardial rub, S3/S4, aortic valve insufficiency, pleural rub
• Special tests: Wipe bulge sign (small effusion), ballotment/patellar tap (mod-large effusion). Phalen and linel’s test
Investigations
1. Blood work: CBC-D, electrolytes, Creatinine, BUN, ESR, CRP, AST, ALT, INR, bilirubin, blood cultures, urinalysis, urine culture, glucose,
serum urate, anti-rheumatoid factor, anti-CCP, ANCA, ANA, HLA-B27 (if suspect seronegative spondyloarthropathy)
2. Radiology/Imaging: Xray, ultrasound, MRI
3. Arthrocentesis with synovial fluid complete cell count + differential, Gram stain, culture, crystals
• Inflammatory arthritis: WBC 2,000—25,000
Treatment
1. Emergent: if septic arthritis, treat with empiric IV antibiotics. If pericardial/pleural effusion, then consider systemic high dose steroids
(e.g. prednisone 1mg/kg P0)
2. Treatment Options (out patient)
• Rheumatoid arthritis:
• Non-pharmacologic: Exercise, education, consult PT/OT
• Symptom control: NSAID (topical or oral), low dose oral steroids (<15 mg/day) once diagnosed, or intrarticular steroid
• DMARD: Methotrexate (first Iine)+/- hydroxychloroquine, sulfasalazine, or azathioprine
• Biologic (DMARD failures): anti-TNF (infliximab, adalimumab, etanercept, golimumab), anti-CTLA-4 (abatacept), anti-B cell
(rituximab)
Osteoarthritis:
• Non-pharmacologic: weight loss, exercise, education, physiotherapy, walking aid
• Symptomatic relief using analgesia: Tylenol, Tylenol around the clock, NSAID, intraarticular steroid injection
• Orthopedic surgery referral
References
I. Grassi W, De Angelis R, Lamanna G and Cervini C. The clinical feature ofrheumatoid arthritis. Eur. J Radiol (1998) 27(1): SI 8-24.
2. O’Dell JR. Therapeutic strategies for rheumatoid arthritis. N. Engi. J Med (2004) 350(25): 2591-2562.
3. Felson DT. Clinical Practice. Osteoarthritis of the knee. N. EngI J Med (2006) 354(8):841 -848.
4. Klareskog L, Catrina Al and Paget S. Rheumatoid arthritis. Lancet (2009) 373(9664):659-672.

_______________________________
PROTEINURIA
20?? Edition Authors: Cossandro Hirt, Stephanie Thompson MD, Valerie LuyckxMBBCH
OriginalAuthors: Brain Buchanan, Carrie Ye MD, Valerie Luyckx MBBCH
Station Objective
Proteinuria is often identified by dipstick on routine urinalysis and on admission to hospital in acutely ill patients. Differentiate benign
proteinuria (i.e. orthostatic proteinuria) from pathological causes proteinuria.
False +vel-ve DiDstick

Differential Diagnosis False +POS
Very concentrated or
Protelnurla Gold Standard >lSOmg/24 hr Urine ( UrPr:UrCr >l3mg/mmol random sample) alkaline urine
False —NEG
Dipstick Positive Dipstick Negative, Positive PCR Dipstick Negative, Very dilute, Light-chain
immunoglobulin’s
Positive ACR Diabetic
Measurements
Transient/Physiological Persistent (>2x) -* Pathological
Dipstick NOT sensitive
Any Acute Illness Microalbuminurla enough to pick up
• (retest when well) (>20mg) Microalbuminuria
QuantIfy (24 Ur) or Spot Proteln:Cre
Fever, exercise, CHIC, UT? DIabetes
Orthostatlc. resolve
overnight
ldiopathic <3 g/day (24 Ur) Common Conditions:
>3 g/day (24 Ui) UrPrUrCr ‘c300mg/mmoi
UrPr:UrCr >300mg/mmol
• Transient proteinuria
SPEP/UPEP to determine (entertain only if <3oyrs
Glomerular: content and normal renal
Inc. glon,erular permeability (>3.5g/24 hrs) function)
÷/ Nephrotlc Syndrome, Edema, >70% Albumin • DM Nephropathy
hypoalbuminela, hyperilpidemla Many Peaks Monoclonal • Hypertension
• Peds- Minimal Change
Tubular: Overflow: disease
Primary GlomeruIar
Impaired Tubular 1’low MW
IRenal disease)
reabsorption Protein
c1-2g/day production
High Mortality! Risk of
Neohrotlc: Adverse Outcomes:
(i.e. Fanconi (le Multiple
Membranous GN (elderly) • Presence of active
Syndrome, ATN, Myeloma,
Minimal change disease
AIN) amyloidosis, urine sediment (active
(‘ciSyr, >90% peds)
FSGS rhabdomyolysis) inflammation) with
uncontrolled HTN
Neohrltlc: may suggest nephritic
IgA Nephropathy (<10% syndrome
PCR= Protein Creatinine Ratio
pure nephrotic) • frisk of thrombosis!
ACR=Albumin Creatinine Ratio
Anti GBM Ab, ANCA, Lu pus
infection! malnutrition!
hyperlipidemia with
severe proteinuria and
Hstory Sr Albumin <20
ID. Age
CC • Edema, abdominal swelling, foaming urine
HPI • Dysuria, urinary frequency, fever, unwell, peripheral! generalized edema, B symptoms, vasculitis (rash,’joint pain),
new diagnosis of DM, connective tissue disease (Raynaud’s, photosensitivity, oral ulcers), PE or DVT, infection
(complications)
RED FLAGS • HTN, active urine sediment, ARF, 1’ albumin, t cholesterol
PMHx • DM, HTN, lupus, collagen vascular dz, malignancy, glomerulonephritis, illnesses associated with t 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 exam
• Cardiovascular disease (proteinuria is a risk factor)

physical
1. General Approach
• Vitals: BP, presence of HTN (typically with nephritic syndrome)
2. Inspection
• Facial and generalized edema (anasarca) in nephrotic syndrome, volume status —* asses JVP (low in nephrotic, and high in
nephritic)
• Skin: rash, pallor if anemic (secondary to chronic renal dz)
3. Percussion
• ABD: ascites, attempt kidney palpation (may be enlarged, rare to find ie Amyloidosis, DM, HIV, PKD)
4. Palpation
• Sacral, pretibial, ankle area edema (Nephrotic syndrome)
5. AuscultatiOn
• CV: pericardial rub (uremic pericarditis) —* found in renal failure, murmur (endocarditis)
• RESP: dependent rales with volume overload
Investigations
Blood work Nephrtic Vs. Nephrotic Fndngs
• CBC-D (anemia of chronic disease)
• SrCr (Kidney function, use to determine GFR) Nephritic Nephrotic
• Urea Hematuria (microscopic) Edema
• Electrolytes (K, Na, acid/base) Red blood cell casts and Lipid casts, hyperlipidemia
Dysmorphic red blood cells Hypoalbuminemia
• Glucose, HbA1 c, (Diabetic Control)
Minimal-to-moderate proteinuria Massive proteinuria (3g/24h or
• Albumin (Nephrotic), fasting lipid profile, higher)
• SPEP (Overflow, tubular, or glomerular)
2. Urine:
Urinalysis: UA dipsticks exclusively detect albumin (1 + to 4+ tAlbumin Conc.)
• Spot urine protein! Cr ratio (PCR): ..-g/d of proteinuria (also detects light chains)
• Screen pts with DM for microalbuminuria: spot urine analysis for albumin/Cr ratio
• 24 hr urine collection for protein and Cr (gold standard)
• UPEP
• Examine urine sediment, RBC casts! fatty casts and lipiduria (renal injury)
• Consider ABD! pelvic! renal U/S (polycystic kidney disease)
4. Special Tests
• Split 24 hour urine collection —* benign positional proteinuria)
• Urine and serum protein electrophoresis (SPEP!UPEP) (Overflow proteinuria to determine type)
• Serology: ANA, RF, p-ANCA, c-ANCA, cryoglobulins, complements (C3 + C4), Rep B, Hep C, HIV, ASOT (Systemic causes of GN),
blood culture, peripheral smear
• Consult nephrology and discuss with patient regarding renal biopsy; consider renal biopsy when persistent proteinuria of
unknown origin with or without abnormal renal function (for example if suspect a GN results can help determine treatment
course)
Treatment
• If asymptomatic (no evidence of UTI) and proteinuria discovered incidentally then repeat test within 1-2 weeks, asymptomatic
proteinuria without associated dz should be followed closely
• Treat underlying systemic disease and/or look for offending agents
• If DM with proteinuria, initiation of ACEi or ARB, follow K and Cr after initiation.
• Screen annually for glomerular dysfunction and subsequent microalbuminuria with spot urine albumin/Cr ratio (>30 mgI
mmol —* early sign of diabetic nephropathy)
2. Follow-up: the urine dipstick, PCR and ACR should be repeated at each visit until persistently -ye
3. Referrals: Nephrology: if proteinuria persists, signs of fcn, or symptoms —* refer to a Nephrologists
References
1. Naderi AS, Reilly RE. Primary care approach to proteinuria. JAm Board Fam Med. 2008 Nov-Dec;21 (6):569-74.

PRURITUS
201? Ed. Authors: Michael Samycia, Parbeer Grewal MD
OriginalAuthors: Summit Sawhney, Lisa Steblecki MD MPH CCFP
Station Objective
To provide an organized approach to interviewing and examining a patient with pruritus and differentiating between systemic and
dermatological pruritus.
Common Conditions
Drug related • Clonidine, cefotaxime, calcitriol, OCR opiates, ASA, any drug allergy ZZI
Skin Diseases Dry skin (xerosis), atopic dermatitis (eczema), contact dermatitis, fungal skin infections, psoriasis, scabies, lic_J
Systemic Diseases • Allergy/atopy, cholestasis, thyroid dysfunction, DM, Fe deficiency anemia, renal failure, psychiatric illness, HI]
2. High Mortality
• Malignancy
• Multiple Sclerosis
History
ID Age, gender
CC • Itching
HPI . Onset, duration, location of symptoms, migration
• Pattern of itch (nocturnal, diurnal, seasonal variation)
• Precipitating and palliating factors
• Progression and response to antihistamines
• Associated symptoms: inflammation, excoriation/infection at itch site, ABD pain/jaundice
• RashHx
RED FLAGS • Weight loss/fatigue/night sweats (Ca) and extremity weakness/numbness/tingling (MS)
PMHx • Eczema, dry skin, recurrent skin infections, renal/liver dz and any Ca being treated with chemotherapy
FHx Atopy, food allergy, asthma
Meds • Use of any oral (opioids, cocaine, aspirin) and topical (hydrocortisone, benadryl, moisturizers) medications
Allergies • To 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 tingling (MS)
• HEENT: visual disturbances (MS)
• CV: palpitations, diaphoresis (hyperthyroidism)
• GI: RUQ steatorrhea (cholestasis)
• GU: Urinary frequency with excessive thirst and wt loss (DM)
• MSK / DERM: pica with hair thinning, headaches (Fe deficiency anemia)
• Fever, wt loss, and night sweats (malignancy)
Physical
1. General Approach
• Vital signs
2. Inspection
• Obvious skin lesions/excoriations/infections, observe for jaundice, scleral icterus, wt change and fatigue
• Skin examination noting the presence, morphology, extent, and distribution of lesions
• Cutaneous examination noting any erythema, swelling, warmth, and yellow/honey crusting
3. Percussion
• Liver and spleen size for organomegaly
4. Palpation
Lymphadenopathy (cervical, axillary, clavicular and inguinal)
Liver and spleen for any obvious masses and tenderness

5 Auscultatlon
• 51/52 and screen for any palpitations (hyperthyroidism)
6. SpecialTests
• Screening for MS: assess strength, tone and sensation in the upper and lower limbs
nvestigat10n5
1. Blood work
• Cr, bili, albumin, AST, ALT, ALP (cholestasis)
• TSH (hypo and hyperthyroid)
• Fasting glucose (DM)
• Hemoglobin, Fe, ferritin,TIBC (Fe deficiency anemia)
• MRI of the brain and/or spinal cord (if presence of neurological symptoms to rule out multiple sclerosis)
• U/S of liver to further determine cause of cholestasis
3. SpecialTests
• Skin testing for certain allergens
• Biopsy skin lesions
Treatment
1. Emergent
• Antihistamines and supportive treatment
2. Non Emergent
• Skin care with cool or lukewarm water, limit use of soap
• Use of moisturizers and emollients, and avoidance of irritating or tight clothing, avoidance of contact irritants (i.e. wool clothing)
may also be helpful
• Topical medications (corticosteroids) are effective in relieving itch caused by inflammation
• Systemic medications are indicated for generalized itching or local itching resistant to topical agents, and antihistamines, most
notably hydroxyzine, are effective, especially for nocturnal itch
3. Further workup
• To determine the underlying cause of the pruritus (i.e. blood work, imaging, biopsy etc.)
4. Referrals
• Dermatologist if symptoms progress despite topical and systemic interventions
References
1. BergerTG. Dermatological Disorders. In: McPhee SJ, Papadakis MA, editors. Current Medical Diagnosis &Treatment. New York: McGraw-I-f iii; 2009.

RENAL FAILURE
201! Edtion Authors: Cossondro I-fin, Stephonie Thompson MO, Volerie Luyckx MBBCI-I
Or/gino/Author: Br/on Buchonon, Carrie YeMO, VolerieLuyckxMBBO-/
Station Objective
Determine whether the decreased renal function is primarily an acute, chronic, or an acute problem superimposed on a chronic one.
Differentiate prerenal from intrarenal and postrenal causes of acute renal failure.
Investigations! Differential Diagnosis/Treatment

• Base line Kidney Function
• Common Conditions:
• PreRenal: Volume Loss, renal perfusion
• Renal: ATN, ChronIc: DM Nephropathy,
• Post Renal: Obstruction uropathy (enlarged prostate)
• PreRenal: ARF with multisystem organ failure, acute GN, UP
Acute Renal Failure Chronic Renal Failure

Assess renal function via
Cockcroft-Gault Formula: Ho PE, Inc 5rCR, Inc BUN, urine ouut • Baseline Crc (if have)
GFR=U140-age) x (wt in • lIx: Inc 5rCl, often anemic, sex ecirogenic kidney on u/s
kg) x (0.85 if female)] / (72 • Investigations: COW, srcr (est. GFRI, OuN, lytes, U/A
x Cr[pmol/l]) (emacroscopic), urine volume, U/5, EMS (Hyperkalemla), URINE
to calculate estimated ouTpuT
CrCI, estimates GFR
Fractional excretion of Oinirt Ortliosraeic thurges in BP/HB. low BP, High ISO •urhar2onsescrvL urNa <20 mn,eI/L Low Output
ur. 2.5 rrm,ol/t orCEN. <lIt • U, O,mel cSOO mOire/k
4 u, QuasI ctOO mOsm/kg
Na (FENA) =[(LJNa/PNa) ÷ BUNSrCr v20:t PEN. >1% RraM 5,rgery. anuria (pmt odd resLdu.I <tODEntI
Bland UrIne Dipstick • Praitire Far grarss,lar casts
(UCr/PCr)] (interpret with Irswsrigationt peotflr to ttialoey
pilothle bladder, U/S drows l*oLrsnephroso
caution in diuretic use),

estimates what proportion
Pre Renal —flfl— Post Renal
of filtered Na is reabsorbed
via tubules Nypowolemla
Ureter Clot, tumor, fibrosIs
Tubular Bladder Outlet obstruction, mallgnaocy
Recent Blood Lost, Third SpacIng. vomltlesJblarrhea, MN iscir.mLsis.pos wlaa, Urethra stricture, cervical Ca, enlarged
DKA. Excessive DELiresis Intratubular obstruction Prostate Misplaced Foley
4 Effective Graslalleg Volume • Myeloma. uric acid. MIX. Acyclovir
Drugs To Stop in Acute Cardlogenlc shock. CHF SepsIs, 3° spacIng Glomendar
Renal Failure Pharm • Neprloc-RPGN (MICA-A. Immune Compleo,
NSAIDs, ARBsj’ACEIs, calclnerln Inhibitors, Tar, Ann-CAM! and gA deposition
• NSAIDs Cydosporln cxc tags, U/A nrot.b, bluod, oodnaen,orrokraIma*e,s
ACEi/ARBs Woctdarstenosls
• • Nepirrotic- P565 LOst It, 0 Ab,,nwr
RAS, PMD, RVT Ieastldal
• Contrast MN
• Other Nephrotoxic • Mcdi
• Infection Poo,wph,ns, woc
substances • Inftltrattre tarsost, 5)rn<h
*Adjust dose for Vaxculoa’
* Malnant HTN
Antibiotics and DM • EmbolI lrruomb,trl cholag.rolI
Meds •‘T’TP/HUs
Treatment* Iheatnsent frealinent:’ treatment: Resolve Obstruction’

Discontinue nepirrotoxins. restore profusion Treat underlying cause, prevent hypoperfuslon tower Trod: Poley/suprapubic catheter
Admit to ICU fluId resuscItation, address volume loss and dehydration, treat lr,fectlons upper trod: Consult urology for stent or
Critically ill Radiology for Nepbrostomy
Umitations of SrCr Estimation of GFR

Indications for Urgent dialysis (refractory to medical
• Need steady state- dependant on muscle percent and
body mass
treatment): Metabolic acidosis, electrolytes (hyperkalemia),
intoxication (i.e. ethylene glycol), volume overload, uremia,
• GFR must fall before see t SrCr
pericarditis, reduced level of conciseness, bleedinci
• Hyperfiltration: GFR is preserved but not representative
oft structural damage
• Tubular component of secretion

History
ID • Age
• Often asymptomatic, weakness, fatigue, N/V, L appetite, metallic taste in mouth, pruritis, confusion, restless legs/
nocturnal leg cramps, SOB, chest pain (pericarditis)
• Pre-renal: dehydration, diarrhea, diuretic medication, liver failure, sepsis, CHF, vomiting, drugs (ACEi/ARB, NSAID5),
contrast dye
• Renal: flank pain, edema, HTN, Hx of dialysis/transplant, Meds (AIN, ATN), trauma, vasculitis (rash, joint pain, gross
HPI
hematuria)
• Post-renal: dribbling, stream, hesitation, frequency, nocturia, retention, stones, dysuria
• Generic: 1- u/o, edema
• Intoxication (e.g. ethylene glycol), volume overload, signs and Sx of uremia including
RED FLAGS
• Neurological manifestations such as asterixis, confusion, liver dysfunction, acid-base misbalance
• DM, CHF, HTN, pregnancy, CAD, vascular dz, liver dz, solitary kidney, Hx of recurrent UTIs, BPH, scleroderma, SLE,
PMHx
vasculitis, Goodpasture’s, streptococcal infections (throat, impetigo), HIV, hepatitis
PSHx • Genitourinary tract procedures, nephrectomy, donation/ transplant
FHx • Polycystic Kidney dz, Alport syndrome, deafness, end stage renal dz
Meds • Nephrotoxic substances (aminoglycosides, other antibiotics, furosemide, contrast, NSAIDs, ACEi, ARB), start date
Social • Smoking, EtOH, IVDU
• General: infectious Sx, wt t, fatigue, poor sleep, difficult concentration
ROS Gl:NN
• MSK / DERM: rash, pruritis, petechiae, leg cramps
Physical
1. General Approach: Differentiate ARF, CRF and acute-on-chronic exacerbation
• Vitals: hypo or HTN, orthostatic hypotension, fever
2. Inspection
• 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: diffuse rash, livido reticularis, stigmata of liver dz, needle/track marks, crush injuries/ # (ATN, or hypopertusion)
3. Percussion
• CVA tenderness
4. Palpation
• ABD: ascites, hepatomegaly, ballotable kidneys, distended bladder (Obstructive, Post Renal)
• Pelvic exam: (cervical Ca) and/or DRE (prostatic enlargement)
5. Auscultation
• CV: 53, pericardial rub (Uremia)
• RESP: crackles (Volume overloaded)
Treatment
1. Further management: Renal biopsy when indicated, avoid further nephrotoxins, hypotension. Goal to achieve euvolemia and
normotension. Ensure renal dosing of medications, treat complications including fluid overload with NaCI restriction and loop diuretics.
Manage hyperkalemia medically according to severity including kayexalate, loop diuretics, agents to shift potassium, and IV calcium if
indicated; consult nephrology for dialysis if hyperkalemia refractory to therapy. Follow-up: ensure resolution of acute process, follow up
with family physician
2. Referrals: Nephrology, Urology
References
1. Patricia KhaliI MD, Preethi Murty MD & Paul M. Palevsky MD.The Patient with Acute Kidney Injury. Prim Care. 2008 Jun;35(2):239-64, vi.
Internal Medicine ( Edmonton Manual of Common Clinical Scenarios 161

RESPIRATORY TRACT INFECTION
201 I Ed. Authors: Sara Houllhan, MohammadAlmutawa MD, a Steb eckMDMPH CCFP
Station Objective
In this station you may be expected to differentiate common cold from pharyngitis, acute bronchitis, acute bacterial sinusitis, allergic rhinitis,
influenza and pneumonia.
“Sore Throat Score”
7
6
5
’
4
Pharyngeal or tonsillar exudates
Tender anterior cervical adenopathy
1. Diagnostic Criteria Hx of fever >38 o
• Difficult to differentiate bacterial from viral infections based on clinical Absence of cough
evaluation Pediatrics Age i Syo
• Pneumonia: infiltrate on plain CXR
3 *(Age 45 is-i point)
• GAS pharyngitis: must be confirmed by throat culture (see “Sore Throat Score” above) *1 Pt for each of the above
• Sinusitis: persistent Sx of URTI, no improvement after 10-14 d or worsening after 5 d with
both nasal congestion/purulent nasal d/c and facial pain ± fever/maxillary toothache/facial swelling.
9
’
8
• Common cold (Rhinovirus 30-50%, Coronavirus 10-15%, Influenza viruses 5-15%, Unknown 20%)2
• Pneumonia (S. pneumonia, H. influenzae, S. aureus, Enterobacteriacea C. pneumoniae, Legionella sp.)
• Acute pharyngitis (Viral 90%, GAS, f3-haemolytic streptococci (Group C and G), N. gonorrhoeae)
7
• Sinusitis (Viral, S. pneumoniae, H. influenza, M. catarrhalis anaerobes if chronic)
8
History
ID • Age, sex
CC • Nasal discharge, stuffiness, cough, sore throat (common cold), facial pain, headache
HPI • Clear nasal discharge, itchy watery eyes, exacerbated seasonally or after exposure to allergens e.g, pollens, dust
mites, cats/dogs dandruff (allergic rhinitis)
• Cough, fever, pleuritic CP, dyspnea/SOB and sputum production (pneumonia, bronchitis)
• Sudden onset sore throat, tender anterior cervical adenopathy, Hx of fever (>38C), headache, absence of cough!
rhinorrhea/hoarseness (bacterial pharyngitis)
V - • Ear-pressure/fullness, facial pain (aggravated by postural changes or by valsalva maneuver), nasal congestion, poor
response to decongestant, tooth pain, facial swelling (sinusitis)
• Other associated Sx: vomiting, malaise, anorexia
• Duration of Sx 7-1 0 days, fever 3 days, preceding viral infection (pneumonia)
• Recent exposure to sick contact (daycare/school/work & home)
• Travel Hx (fungal or tuberculosis)
RED FLAGS • Stridor, respiratory distress, toxic appearance, cyanosis, drooling (epiglottis) MUST R/ epiglottitis or peritonsillar/
retropharyngeal abscess and airway compromise
PMHx • Chronic illness (CHF, COPD, asthma, CF, CRF, liver dz), lung Ca, immunocompromised (HIV, DM), recurrent strep
pharyngitis, vaccinations, hospitalization (last 3 mo)
PO&GHx • Current pregnancy
Meds • Recent Abx use, chronic corticosteroid use
Allergies • Rx (especially Abx), environmental
Social • Smoker, EtOH, dentition, occupation, home environment, nursing home
ROS • HEENT: problems hearing, sinus problems, allergies (seasonal), hoarseness, anosmia
V • RESP: dyspnea, SOB, wheeze
• GI: NN, diarrhea, ABD pain, anorexia
• MSK / DERM: myalgia, rashes (mycoplasma)
Physical
1. General Approach
• If signs of severe distress: ABCs, call for help (epiglottitis —* experienced person to intubate), vital signs
• R/o 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. Inspection
• HEENT: cyanosis, periorbital edema, facial swelling, nasal erythema/swelling,TM (bulging or opacification), oropharynx/tonsils
(erythema, exudate, displaced uvula)
• RESP: AP diameter, kyphosis, scoliosis
3 Percussion
• HEENT: tenderness on paranasal sinuses or maxillary teeth
• RESP: lung fields, diaphragmatic excursion
4• Palpation
• HEENT: cervical lymph nodes
• RESP: chest wall tenderness, tactile fremitus
5. AuscultatiOn
• RESP: i’ AE, bronchial breath sounds, whispering pectoriloquy, localized crackles, pleural rub (consolidation)
Investigations
i. Blood work: if pneumonia suspected: CBC-D, glucose, electrolytes, Cr, ALT, blood cultures (Hx of chills/rigors
)
3
2. Radiology/imaging: CXR PA & lateral (if pneumonia or bronchitis suspected)
3. SpecialTests
• GAS throat culture if 2 on “Sore Throat Score”
• ABG: °2 sat <90%, COPD, chronic °2 use
• Sputum gram stain and culture (productive cough and suspected 3 pneumonia/bronchitis)
Treatment
1. Emergent
• Assess for need of hospitalization: CURB-65 or Pneumonia Severity Index (PSI)
3
• Ensure adequate hydration, analgesics/an tipyretics for pain and fever
• Common cold: OTC for Sx control (not approved for children 2 y/o)
• Pneumonia: Abx choice is based on comorbidities and recent Abx use 3
• Doxycycline or macrolides used for community acquired pneumonia in patient without risk factors
• GAS Pharyngitis: delay Abx therapy of acute pharyngitis until culture confirms GAS
7
• Pen VK or macrolides 10 days to prevent acute RF; 3-lactam allergic: clindamycin
• 9 or macrolide
Sinusitis: Amoxicillin 10 days, 13-lactam allergic —* TMP-SMX
3. Follow-up
• Persistence of high fever and severe Sx 2-3 days
• Routine FU in asymptomatic patients is not required for acute pharyngitis or bacterial sinusitis
• Post therapy CXR (at 6 weeks) for patients with extensive/necrotizing pneumonia, smoker, EtOH, COPD, >5% wt in past mo and
>50y/o
4. Prevention
• Hand-washing
• Vaccinations: influenza, pneumococcal, H. influenzae (if < 4y/o)
References
1. Bickley LS, Szilagyi (ed.) Bates’guide to the Physical Examination and HistoryTaking. gth edition. Philadelphia: Lippincott Williams &Wilkins, 2007.
2. Heikkinen,T, Jarvinen, A.The common cold. Lancet 2003; 361:51.
3. Mandell LA, Wunderink RG, et aL Infectious Diseases Society of America / American Thoracic Society consensus guidelines on the management of
community acquired pneumonia in adults Clin Infect Dis. 2007 Mar 1:44 suppl 2:527-72
4. Mclsaac Wi, White D, et al. A clinical score to reduce unnecessary antibiotic use in patients with sore throat. CMAJ. 1 998;1 58:75-83.
5. Mclsaac Wi, Goel V, et al. The validity of a sore throat score in family practice. CMAJ. 2000;1 63(7):81 1-5.
6. Mclsaac Wi, KellnerJD, et al. Empirical validation of guidelines for the management of pharyngitis in children and adults. JAMA. 2004:291(1 3):1 587-95.
7. Gerber MA, Baltimore R5, et al. Prevention of rheumatic fever and diagnosis and treatment of acute streptococcal Pharyngitis. Circulation. 2009;
119:1541-1551.
8. Low DE, Desrosiers M, et al. A practical guide for the diagnosis and treatment of acute sinusitis. CMAJ. 1997 Mar 1 5;1 56 Suppl 6:51-14.
9. Rosenfeld RM, Andes D, et al. Clinical practice guideline: adult sinusitis. Otolaryngol Head Neck Surg. 2007 Sep;1 37(3 Suppl):S1-31 1.

RESTRICTIVE LUNG DISEASE
20? I Ed. Authors: limothy Chon, Mohit Bhutani MD FRCPC
Station Objective
Understand the differences between obstructive and restrictive lung disease. Identify symptoms and different etiologies of restrictive lung
disease.
• Characterized by reduced lung volume: decreased total lung capacity (TLC), decreased forced vital capacity (FVC), decreased
Forced expiratory volume in 1 second (FEV1).
• Preserved air flow and normal airway resistance: normal functional residual capacity (FRC) & FEV1 :FVC ratio
• Pathophysiology: caused by disease in lung parenchyma or chest wall, pleura and respiratory muscles leading to reduced lung
compliance
Intrinsic Lung Diseases Extrinsic Lung Disease
Intersitial lung disease Chest wall deformities
• Idiopathic pulmonary fibrosis • Kyphosis
• Sarcoidosis . Ankylosing spondylitis
• Pneumoconiosis • Morbid obesity
• Silicosis Neuromuscular diseases:
• Asbestos • Muscular dystrophy
• Radiation fibrosis • Myasthenia gravis
• Pneumonia • Guillain-barre, Polio
• ARDS • Diaphragm dysfunction
• SLE • Phrenic nerve damage
• Connective tissue diseases

• IPF median survival time is <3 years
• Poor outcome predictors / Risk Factors: old age, male, severe dyspnea, cigarette smoking history, severity of fibrosis on imaging
History
ID • Ageand gender
CC • Shortness of breath, dry cough, decreased exercise tolerance
HPI • Duration (acute, subacute, chronic)
• Hemoptysis, wheezing, chest pain (uncommon)
• Recurrent respiratory infections, sleep disordered breathing, pulmonary HTN, cor pulmonale
• Smoking history strong association
RED FLAGS • Severe dyspnea, hemoptysis,
PMHx COPD, active TB, connective tissue diseases
Meds • Drug induced lung disease (nitrofurantoin, amiodarone, gold, chemotherapeutic agents, procainamide, and
hydralazine)
Allergies • Hypersensitivity to dust, pollen
FHx • IPF, Sarcoidosis, Lymphangioleiomyomatosis (LAM)
Social • Occupational history —job duties, exposure to environmental substances (asbestos, silica, cobalt)
ROS • CV: cyanosis, pulses, cardiac function
• Gl:GERD
• MSK / DERM: skeletal deformities, trauma, fractures

physical
1. General Approach
• Is the patient in respiratory distress? Vital signs stable, airway, 02 sats?
2. Inspection
• Obesity, asymmetrical/deformed chest wall, observe muscle usage
• Clubbing: common in IPF
• Erythema nodosum: sarcoidosis
• Spinal column and rib symmetry: kyphosis
• Cobb Angle >1 00 indicates severe deformity, respiratory failure
• Shallow breathing
3. Percussion
• Dullness: neuromuscular
4. Palpation
• Decreased tactile fremitus: neuromuscular
5. AuscultatiOn
• Crackles: end expiratory basilar, “dry” and “velcro” in quality
• Inspiratory squeaks, late high-pitched rhonchi
• Cor Pulmonale: loud P2, right sided gallop, right sided heave
Investigation
1. Blood work
• Elevated CK: may indicate myositis
• Antibodies: collagen vascular disorders, vasculitis, Goodpasture syndrome
• Chest Xray: common abnormality is reticular pattern, air space opacities
• Honey combing! ground glass: indicates advanced fibrosis
• Bilateral hilar lymphadenopathy: sarcoidosis
• Air space opacities
• CTScan
• Lower zone and peripheral infiltration, bilateral cysts and nodules, recticular fibrosis, air spaces
3. SpecialTests
• Pulmonary Function Test
• Reduced TLC, FRC and Residual Volume (RV)
• Decreased FEy 1 and FVC, Normal or increased FEV /FVC ratio
1
• (See Pulmonary Function Test Section)
• Bronchoalveolar lavage (BAL)
• Lung Biopsy
• Surgical Lung Biopsy
Treatment
1. Emergent
• Airway management, oxygen, 02 sats, stabilization
• Corticosteroids (first line therapy), cytotoxic agents (azathioprine), colchicines
• Correct ventilation problems in chest wall deformities: positive pressure mask, tracheotomy, weight loss
3. Referrals
• IM: pulmonology, RT
References
1. http://emedicine.medscape.com/article/301 760-overview

SEIZURE
20? I Ed. Authors:AshrafKharrat, James KeayMD CCFP
OriginalAuthars: Carrie Ye MD, Shila Lefresne, Penny Smyth MD FRCPC
Station Objective
Determine etiology of seizure in order to best plan treatment course.
• Seizure mimickers: migraine, syncope, stroke/TIA, psychogenic, movement disorders, night terrors, panic attacks
• Types of seizures:
• Simple partial: no altered LOC, aura, originates in a certain part of cortex
• Complex partial: altered LOC, automatism
• Generalized: bilateral cortex, altered LOC, tonic clonic, absence
• Tonic = muscle stiffness; clonic = jerky repetitive contractions
• Epilepsy = >1 unprovoked seizure
• Drugs: EtOH/benzo withdrawal, cocaine, LSD, methanol, ethylene glycol,TCA5, insulin, prescription drugs
• Infections: febrile seizure (kids), meningitis, encephalitis
• Metabolic: hypoglycemia, hyponatremia, hypocalcemia, NKHHC, hyperthyroid
• Structural: mass (tumour, abscess, blood), stroke, trauma, congenital malformations
• Complications of seizures: aspiration, hypoxia —* brain injury, lactic acidosis, rhabdomyolysis—* ARE
• Status epilepticus is >30mm of continuous seizure activity (or recurrent seizures without full recovecy)
History
ID • Age, gender
CC • Seizure
HPI • Characterize seizure: duration, loss of awareness, head or eye deviation, tongue biting, abnormal motor activity,
incontinence, aura (gestural or oroalimentary)
• Any injuries, especially head
• Postictal symptoms: disorientation, lack of awareness, hemiparesis and hemiplegia (Todd’s paralysis —+ suggests
focal onset)
• Sensations prior to LOC that may help differentiate seizure from other mimickers: aura (simple partial seizure),
epigastric fullness (seizure), intense emotion/light headedness/diaphoresis (syncope), no prodrome (cardiogenic)
• Triggering factors: sleep deprivation, flickering lights, menses, hyperventilation
• Events prior to incident: infection, trauma, medication/drug use
RED FLAGS • Sudden/worst headache, focal neurological signs, repeated seizure with no intervening period of normal neurologic
function, status epilepticus
PMHx • Previous seizures, CNS infections, head injuries, brain tumor, cerebrovascular disease, DM
PO&GHx • If pregnant: eclampsia
Meds • Meperidmne, buproprion, psychotropics, theophylline, benzodiazepines
Allergies • Medications, environmental
FHx • Epilepsy, neurologic or developmental disorders
Social Smoking, EtOH (withdrawal), drug use, employment, drivers license
ROS • HEENT: fever (febrile seizures in kids), headache, neck stiffness (meningitis)
• CV: CR palpitations (AF — stroke)
• RESP: SOB (hypoxia)
Physical
1. General Approach
• Vitals: HR (irregular —* arrhythmia), BP 2 (‘1- —* hypoxia)
(t—* stroke, L —*cardiogenic),T (1’—* febrile), Sp0
2. Neurological Exam
• CN: asymmetry

• Strength: grade from 1-5, look for lateralizing weakness (Todd’s paralysis vs. stroke)
• DTR: grade from 1-4, t (UMN, hyperthyroid), (LMN), symmetric vs asymmetric
• Tone: spastic (CP, post-CVA)
Investigations
1. Blood work
• 2 (, glucose (t, 4-), troponin, Cr, urea (renal failure-uremia)
CBC-D, electrolytes: Na (i), Ca
• CK (rhabdomyolysis), TSH (hyperthyroidism), INR, AST, ALT, bili, ALP (liver failure), 3-hCG, toxicology
• PRL —* measure 10-20 mm after event and if twice the baseline, supports Dx of seizure
1
• CT head if -ye and suspicious of stroke —* repeat CT in 48h
3. Special Tests
• LP: immunocompromised or symptoms/signs of infection (contraindicated in patients with tlCP)
• EEG: recommended for all patients with new onset seizure (may be done at follow up)
Treatment
i. Emergent
• ABCs, vitals. Prevent injury and aspiration.
• Treatment of acute seizing patient
• i) Ensure patient is in a safe environment. Place patient in recovery position
• ii) Anti-epileptics (phenytoin, phenobarbital, vaiproic acid)
• Treat underlying cause if identified
3. Education
• Seizure precautions —* no swimming/bathing along, no heights, no fire
• No driving until sees a neurologist, normal CT head and normal EEG
4. Referrals
• Neurology follow-up as an outpatient for assessment of possible epilepsy
References
1. 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):668-75.
2. Hoffman, LH etal. First Exposure Emergency Medicine. McGraw-Hill, Inc. USA, 2008.
Internal Medicine (Edmonton Manual of Common Clinical Scenarios 167

SEXUAL AND HIGH RISK INFECTIONS
20 I I Ed, Authors: Cassandra Hirt, Catherine Burton MD
OriginalAuthors: Sara Houlihan, Barabra Romanowski MD FRCPC
Station Objective
In this station you are expected to assess for risk of and screen for STI. Management of STI is necessary to mitigate sequelae and to prevent
further transmission.
• N. gonorrhoeae
• Chiamydia trachomatis
• Human Papilloma Wrus
• Syphilis
2. High Mortality/ Morbidity
• HIV
History
ID • Age, sex
CC • Genital Sx associated with STI (discharge, dysuria, ABD pain, testicular pain, rashes, lesions)
. Systemic Sx associated with STI (fever, wt, lymphadenopathy)
HPI • Onset&durationofSx
• Previous STl/HIV testing (when?)
• Previous episodes of STI’s
• Date of last sexual contact, methods of protection
RED FLAGS . HIV, hepatitis co-infection
• STI in pre-pubertal child: evaluate for Sexual Assault
PSHx • Blood transfusions
PO&GHx • LNMP
• Last pap test
• GPTAL
Meds • OCP(other methods of birth control), previous STI treatments
• Vaccinations: Hep A/B, HPV
Allergies • Especially to antibiotics including penicillin/cephalosporin
Social & Sexual • Intercourse with men, women, both? Regular sexual partner? # of different sexual partners in the past 2 mo? Past
Hx yr?
• Sexual acts: perform/receive: oral/vaginal/anal sex
• Risk assessment: sexual encounters with people from a country other than Canada, trade sex for money/drugs/
shelter, paid for sex or been paid for sex, use condoms
• Do you use EtOH/drugs/IVDU (shared injection equipment), tattoos or piercings, sterile equipment
• Do you have a home (if no —+ where does Pt sleep), do you live with anyone
ROS • HEENT: throat lesions, conjunctivitis, LN
• CV/RESP: signs of tertiary syphilis
• GI: RUQ pain, ABD pain, bowel Sx (dyschezia, diarrhea)
• GU: dysuria, frequency, urgency, change in vaginal discharge, urethral discharge, genital sores
• MSK / DERM: rashes, joint inflammation (Reiter’s)
Physical
1. General Approach
,T
2
• Systemic signs STI: wt k fever, enlarged lymph nodes
Inspection
• Mucocutaneous regions including pharynx
• External genitalia: cutaneous lesions, inflammation, genital discharge, anatomical irregularities

Components of PE specific to MALES
• Palpate scrotal contents with attention to the epididymis (tenderness)
• When foreskin is present, retract it to inspect glans (inflammation, lesions/chancer, d/c)
• “Milk” urethra to make any discharge more apparent
•
Components of PE specific to FEMALES
• Separate labia to adequately visualize vaginal orifice (swelling, inflammation, d/c)
• Perform an illuminated speculum exam (visualize cervix/vaginal walls/evaluate endocervical/vaginal d/c and obtain specimens-
Note: inflammation, lesions/chancer)
• Perform bimanual pelvic exam to detect uterine or adnexal masses or tenderness
Investigations
Blood work
• CBC-D (Elevated white count)
• 13-HCG (Pregnancy)
• EIA (Syphilis),
• HB5Ag anti-HBc (Hep B infection), anti-HCV (Hep C infection)
• EIA for anti-HIV ab (HIV infection)
2. Swabs
• Endocervical swabs (diagnosis of Chlamydia trachomatis and N. gonorrhoeae (NAAT or PCR))
• May culture N. gonorrhoeaeto determine antimicrobial susceptibility in cases of treatment failure (must collect in charcoal
transport medium)
• pallidum swab ulcer base for examination by dark-field
If lesion present: swab the lesion bed for HSV culture, for the detection ofT
microscopy or DFA testing
3. Urinalysis
• NAAT for Chiamydia trachomatis and N. gonorrhoeae (First catch urine >60 post last void)
• R&M, C&S if urinary Sx
,: IIITTTr.i,
Chlamydia azithromycin lg P0 Single Dose

Treatment
doxycycline 100mg P0 BID 7 day course
Treatment options (see table) P0 Single Dose
Gonorrhea cefixime 400mg
2. Further workup
counseling:
ceftriaxone 125mg IM Single Dose
Post-test
• Safer sex practices Syphilis penicillin 2.4mu IM Single Dose

• Tx information, issues pertaining to whether the doxycycline 100mg P0 BID 14 day course
infection is bacterial Herpes 1’s: acyclovir 200mg P0 5x daily 5-10 days
• (curable) versus viral (manageable) Simplex valacyclovir ig PC BID 10 day course
• Case reporting requirements to local public health unit
• In Canada, nationally reportable STIs: chiamydia, Recurrent: acyclovir 200mg P0 5x daily 5 days
gonorrhea and syphilis valacyclovir 500mg P0 BID 3 day course
• Partner notification either via the index case, the HPV Podofilox 0.5% scm Dermal BID 3 days ON, 4 days
physician or a public health official. OFF repeat 4 wks
• Immunization against Hep B and HPV if not already 3x/ week (max l6wks)
imiquimod (Aldara) 5% Dermal
administered, in MSM, consider Hep A vaccine cream
3. Follow-up
Cryotherapy,
• Test of cure at 3-4 wks only recommended if: Tri-chloroacetic acid,
• Sx do not resolve Surgical removal / laser
• compliance is sub-optimal
• pt is an adolescent or pregnant woman
• If immune compromised, HIV (+)
• Refer to Infectious Disease
References
Canadian Guidelines on SexuallyTransmitted Infections Expert Working Group on the Canadian Guidelines on SexuallyTransmitted Infections http://
www.phac.aspc.gc.ca/std_mts/sti_its/pdf/sti..its_eng.pdf

SEXUAL AND HIGH RISK INFECTIONS
20 I I Ed. Authors; Cassandra Hirt, Catherine Burton MD
OriginalAuthors: Sara Houlihan, Bara bra RomanowskiMD FRCPC
Station Objective
In this station you are expected to assess for risk of and screen for STI. Management of STI is necessary to mitigate sequelae and to prevent
further transmission.
• N. gonorrhoeae
• Chlamydia trachomatis
• Human Papilloma Virus
• Syphilis
2. High Mortality! Morbidity
• HIV
History
ID • Age, sex
CC • Genital Sx associated with STI (discharge, dysuria, ABD pain, testicular pain, rashes, lesions)
• Systemic Sx associated with STI (fever, L wt, lymphadenopathy)
HPI • Onset&duration of Sx
• Previous STI!HIV testing (when?)
• Previous episodes of STI’s
• Date of last sexual contact, methods of protection
RED FLAGS • HIV, hepatitis co-infection
• STI in pre-pubertal child: evaluate for Sexual Assault
PSHx Blood transfusions
PO&GHx • LNMP
• Last pap test
• GPTAL
Meds • OCP(other methods of birth control), previous STI treatments
• Vaccinations: Hep A/B, HPV
Allergies • Especially to antibiotics including penicillin!cephalosporin
Social & Sexual • Intercourse with men, women, both? Regular sexual partner? # of different sexual partners in the past 2 mo? Past
Hx yr?
• Sexual acts: perform/receive: oral/vaginal/anal sex
• Risk assessment: sexual encounters with people from a country other than Canada, trade sex for money/drugs!
shelter, paid for sex or been paid for sex, use condoms
• Do you use EtOH/drugs!IVDU (shared injection equipment), tattoos or piercings, sterile equipment
• Do you have a home (if no —* where does Pt sleep), do you live with anyone
ROS • HEENT: throat lesions, conjunctivitis, LN
• CV/RESP: signs of tertiary syphilis
• GI: RUQ pain, ABD pain, bowel Sx (dyschezia, diarrhea)
• GU: dysuria, frequency, urgency, change in vaginal discharge, urethral discharge, genital sores
• MSK/ DERM: rashes, joint inflammation (Reiter’s)
Physical
1. General Approach
• Vitals: HR, BR RR, Sp0
,T
2
• Systemic signs STI: wt fever, enlarged lymph nodes
,
2. Inspection
• Mucocutaneous regions including pharynx
• External genitalia: cutaneous lesions, inflammation, genital discharge, anatomical irregularities

3. Components of PE specific to MALES
• Palpate scrotal contents with attention to the epididymis (tenderness)
• When foreskin is present, retract it to inspect glans (inflammation, lesions/chancer, d/c)
• “Milk” urethra to make any discharge more apparent
4. Components of PE specific to FEMALES
• Separate labia to adequately visualize vaginal orifice (swelling, inflammation, d/c)
• Perform an illuminated speculum exam (visualize cervix/vaginal walls/evaluate endocervical/vaginal d/c and obtain specimens-
Note: inflammation, lesions/chancer)
• Perform bimanual pelvic exam to detect uterine or adnexal masses or tenderness
Investigations
Blood work
• CBC-D (Elevated white count)
• 13-HCG (Pregnancy)
• EIA (Syphilis),
• HBsAg anti-HBc (Hep B infection), anti-HCV (Hep C infection)
• EIA for anti-HIV ab (HIV infection)
2. Swabs
Endocervical swabs (diagnosis of Chiamydia trachomatis and N. gonorrhoeae (NAAT or PCR))
• May culture N. gonorrhoeaeto determine antimicrobial susceptibility in cases of treatment failure (must collect in charcoal
transport medium)
If lesion present: swab the lesion bed for HSV culture, for the detection ofT pallidum swab ulcer base for examination by dark-field
microscopy or DFA testing
3. Urinalysis
• NAAT for Chiamydia trachomatis and N. gonorrhoeae (First catch urine >60 post last void)
• R&M, C&S if urinary Sx
,: I]TTIr.j.
Treatment Chlamydia azithromycin lg P0 Single Dose

doxycycline 100mg P0 BID 7 day course
Treatment options (see table)
Gonorrhea cefixime 400mg P0 Single Dose
2. Further workup
Post-test counseling: ceftriaxone 125mg lM Single Dose
• Safer sex practices Syphilis penicillin 2.4mu IM Single Dose
• Tx information, issues pertaining to whether the doxycycline 100mg P0 BID 14 day course
infection is bacterial Vt: acyclovir 200mg
Herpes P0 5x daily 5-10 days
• (curable) versus viral (manageable) Simplex valacyclovir lg P0 BID 10 day course
• Case reporting requirements to local public health unit
• In Canada, nationally reportable STIs: chiamydia, Recurrent: acyclovir 200ma PC 5x daily 5 days
gonorrhea and syphilis valacyclovir 500mg P0 BID 3 day course
• Partner notification either via the index case, the Dermal
HPV Podofilox 0.5% saln BID 3 days ON, 4 days
physician or a public health official. OFF repeat 4 wks
• Immunization against Hep B and HPV if not already
imiquimod (Aldara) 5% Dermal 3x/ week (max l6wks)
administered, in MSM, consider Hep A vaccine
cream
3. Follow-up
cryotherapy,
• Test of cure at 3-4 wks only recommended if:
Tri-chloroacetic acid,
• Sx do not resolve Surgical removal / laser
• compliance is sub-optimal
• Pt San adolescent or pregnant woman
• If immune compromised, HIV (+)
• Refer to Infectious Disease
References
1. Canadian Guidelines on SexuallyTransmitted Infections Expert Working Group on the Canadian Guidelines on Sexually Transmitted Infections http://
Www.phac_aspc.gc.ca/std_mtsfsti_its/pdf/stiitseng.pdf

SHOCK
2011 EdAuthor:Jamie Mcintyre, Craig OomkeMD, Matthew InwoodMBBChBAO
OriginalAuthor:Jamie Mcintyre, Mike Saba MD CCF Lyle Thomas MD CCFP (EM)
Station Objective
Determine the type of shock a patient is experiencing whether it be:
• Distributive (D): insufficient intravascular volume due to redistribution
• Obstructive (0): circulation impeded due to obstruction of heart or great vessels
• Hypovolemic (H): insufficient circulating volume due to fluid loss
• Cardiogenic (C): circulation impeded due to failure of the heart to pump effectively
• Combined: ie. a trauma patient may have both hypovolemic shock and distributive shock
• perfusion of tissues, with possible end organ failure or dysfunction (most important)
• Hypotension (SBP <90 mm Hg)
• Tachycardia (HR >lOObpm)
• Bradycardia (neurogenic or decompensating)
Shock Examples
Hypovolemic Trauma, hemorrhage, NN, diarrhea, burns, addisonian crisis
Obstructive Tension pneumothorax, cardiac tamponade, PE, AS,
Distributive Sepsis, anaphylaxis, neurogenic shock, 3 spacing
Cardiogenic Ml, CHF, arrhythmias, blunt cardiac injury, pulmonary embolism
3. High Mortality / Morbidity
• If untreated any of these could lead to death
• Most common cause is hypovolemic
• Shock in a trauma patient is considered hemorrhagic/hypovolemic until proven otherwise
History
N.B. If patient is unstable: manage ABCDE’s first and then proceed with emergency SAMPLE history
(Symptoms (related), Allergies, Medications, Past medical history (relevant), Last meal, Events prior to presentation)
ID • Age, gender
CC . Hypotension, oliguria, altered LOC
HPI • Obtain collateral history if necessary
• SAMPLE Hx once patient is stable
• Trauma (H, 0, D or mixed)
RED FLAGS • Severely hypotensive, shifting from tachycardia to bradycardia, altered LOC or unconscious, arrhythmia,
CP, difficulty breathing, weakness, SOB on exertion or minimal_physical_activity,_rapid deterioration
PMHx • Ml (past 24 hrs) (C), coagulopathy (0), infection, pancreatitis, addisonian crisis (H), myxedema coma (D),
bleeding (H)
PSHx • Recent surgeries in abdomen - rd
3
spacing or bleed (H or 0), vascular surgeries (H)
PO&GHx • Recent pregnancy with bleeding (H)
Meds • 13-Blockers, steroids, chemotherapy, drug intoxication (D)
Allergies • Anaphylaxis (D)
ROS • HEENT: light headed, altered LOC, vision problems, throat closing, eyes swollen shut
• CV: palpitations, cold extremities, CP
• RESP: SOB
• GI: distension, bleeding (H), pain
• GU: bleeding, pain
• MSK/DERM: rashes (D), unable to feel/move limbs (D), obvious pain/trauma, sacral sensation

physical
1. General Approach
• ABCDE, vitals (including orthostatic vitals, GCS, C/S), head to toe exam
2. Inspection
• Signs of distress, signs of trauma, central or peripheral cyanosis, apnea, tracheal deviation, angloedema, bleeding, hives, rashes
(i.e. purpuritic rash/bruising, urticaria), asymmetrical chest movement
• Expose entire body: chest, abdomen, back, extremities elevated JVP, flat JVP
3. Percussion
• Lungs: hyperresonance (pneumothorax), dullness (consolidation/hemothorax)
• Abdomen: pain or distention
4. Palpation
• Rigid abdomen, masses, broken bones, peripheral pulses, capillary refill, cool extremities, tenderness during exposure step, DRE
(tone, blood and high riding prostate), swollen calf
5. Auscultation
• Heart: friction rub
• Chest: present or absent breath sounds, crackles or other adventitious breath sounds,
• Abdomen: absent BS
6. Special Tests
• Hyperreflexia, .i strength of limbs, lack of sensation (D)
Investigations
1. Blood work
• ABG 0 perfusion measured by f lactate and 1’ base excess), CBC-D, electrolytes, urea, Cr, AST, ALP, C/S, lipase, amylase, PTt INR,
fibrinogen, D-dimer, T&C, troponins (C, 0), culture (D), cortisol (D), CK, EtOH/tox screen, 3-hCG, urinalysis
• CXR, AXR, C/T/L spine XR (N), CT (head, thorax, abd), XR limbs, Abd U/S, Echo (C,O), EKG (C, 0)
3. SpecialTests
• FAST, Pulmonary artery catheterization for pressures, culture of potential infection sites including LP
• Diagnostic laparotomy (H), thoracotomy (H), decompression (0)
• Shock in trauma is considered hemorrhagic until proven otherwise
Treatment Resuscitation Fluid Examples

1. Emergent Crystalloid Normal Saline, Ringers Lactate
• ABC, 2 large bore for IV RESUSCITATION(careful with (C)) Blood
02, Monitors, foley (not if urethral trauma), C-Spine Colloid Albumin, Fresh frozen plasma, Dextran
• All cases of shock, regardless of etiology: IV lines, 02, place on monitor, identify underlying cause
• Anaphylactic: epinephrine, benadryl, H2 blocker, steroids, supportive care, find causative agent
• Distributive: locate and treat underlying cause, vasopressors, supportive care
• Cardiogenic: cath lab or thrombolysis, be careful of fluid overload, IABP, ionotropes
• Hypovolemic: fluid resuscitation/blood products, monitor O2 locate and treat underlying cause
• Obstructive: remove obstruction (pericardiocenesis/embolectomy), supportive care
3. Follow-Up
• Continue reassessing ABCDEs and perfusion
4. Surgical
• Source control (ie. stop bleeding, excise necrotic bowel).
5. Referrals
• ICU if unstable, ID if unknown infection, Cardiology if cardiogenic (C), Neurosurgery if neurogenic (D)
References
1. Gaieski D. Shock in adults:Types, presentation, and diagnostic approach [Internet]. Ed. Parsons P, Wilson K.: Up to Date; updated 2008 Aug 6, cited 2009
Dec 15. Available from: http://www.uptodate.com/online/ content/topic.do? topicKey=cc_medi/1 1 364&selectedTitle=1 %7E1 50&source=search_result.
2. Harbrecht B., Forsythe R., Peitzman A. Management of Shock In: Feliciano D., Moore E., Mattox K., editors.Trauma 6 th
ed. USA: McGraw Hill; 2008. Section 2,
Chapter 13.
3. Peitzman A., Harbrecht B., BilliarT. Shock In: Brunicardi F., editor. Schwartz Principles of Surgery 8
th
ed. New York: McGraw Hill; 2005. Part 1, Chap 4.
4. Tintinalli JE, Kelen GD, Stapczynski iS, editors. Emergency Medicine: A Comprehensive Study Guide, 6t1 ed. McGraw-Hill, Medical Publishing Division;
2004. Section 4.

_____________________________
SKIN, HAIR AND NAILS

20!? Ed. Authors: Michael Samycia, Parbeer Grewal MD
OriginalAuthors: Summit Sawhney, Jaggi Rao MD FRCPC
Station Objective
To provide an organized approach to examining the skin, hair and nails.
1. Primary skin diseases
• Melanoma and non-melanoma skin cancers (i.e. basal cell carcinoma, squamous cell carcinoma)
• Acne, folliculitis
• Eczematous conditions: atopic or contact
• Papulosquamous conditions (i.e. lichen planus, psoriasis)
• Infection or infestation
• Nails = Infection, Tumors, Inflammatory skin conditions, Genetic disorders, Systemic disease
• Hair = Infection, Inflammatory skin conditions, Genetic disorders, Systemic disease
2. Cutaneous manifestations of systemic disease Worrisome skin lesion (ABCDE)
• Endo: Addison’s, Cushing’s, Thyroid dysfunction, Diabetes Asymmetrical
• CV: peripheral vascular disease, congenital cyanotic heart disease Border irregular
• ID: HIV, sepsis, viral exanthema Color varied
• GU: Renal dysfunction, PCOS Diameter increasing or >6mm
• GI: liver dysfunction, ulcerative colitis, Crohn’s disease Elevation
• MSK: Connective tissue disorders (SLE, dermatomyositis, scleroderma), rheumatism
• Malignancy
3. Drug reaction
History
ID • Age and sex of patient
HPI • Size, color, shape, onset, duration, and location of lesion(s)
• Changes in lesion overtime (color, size, scaling, bleeding, pain)
• Change in sweating or dryness of skin or red, scaly areas that do not heal
• Associated symptoms (pain, pruritus, fevers, chills, anorexia, nausea/vomiting, malaise, weight loss)
• Aggravating and alleviating factors (sunlight, temperature, herbals, medication)
• Recent illnesses or stressors (hospitalization, pregnancy), exposure to toxins or chemicals, chemotherapy
• Cracking, ridging and brittleness of nails
RED FLAGS • Fevers, arthralgias, weight loss, malaise
PMHx • Allergies, skin cancer, measles, chicken pox, other skin conditions
• Chronic disease (DM, rheumatologic, thyroid, collagen vascular)
FHx • Atopy, skin cancer, psoriasis, connective tissue disorders, systemic conditions (DM, thyroid)
Meds • E.g. tetracycline photosensitizing, sulfonamides Steven Johnson’s syndrome
— —
• Herbals
Allergies • Drugs and food
Social • Smoking, EtOH, pets, travel, sexual Hx, skin/hair care habits
ROS • HEENT: thyroid dysfunction, hirsutism
• CV: SOB, palpitions, diaphoresis
• RESP: dyspnea
• GI: RUQ pain/enlargement (liver dysfunction), inflammatory bowel disease
• GU: urinary frequency (diabetes), menses (amenorrhea)
• MSK: arthralgias, myalgias, muscle wasting
• Fever, wt loss and night sweats (malignancy)
Physical
Skin
• Color: hypo or hyperpigmentation, erythema, pallor, cyanosis (check conjunctiva, nails), jaundice (check sclera)
• Texture: rough or smooth

• Moisture: dry, sweaty or oily
• Temperature: warm, cool, or clammy
• Mobility and turgor: lift a fold of skin and note the speed with which it returns to its place
Skin lesion descriptions

• Location / Distribution • Blanching/non-blanching
• Number (single/multiple) . Primary (macule, papule, ulceration)
• Consistency (soft, firm) . Secondary (scale, crust, excoriation)
• Size (measure) • Border
• Color • Arrangement (symmetrical or unilateral)
2. Hair
Texture: fine/smooth vs. coarse/brittle
Distribution: localized or generalized hair loss (or hair gain), symmetrical or asymmetrical
Scarring or non-scarring areas of hair loss
Examine scalp for dryness, infestations, masses, pigmentation, infection and inflammation
3. Nails
• Color and opacity: pink, yellow, white, dark, redness and swelling, pigmented deposits or bands
• Shape and contour: smooth, ridging, grooves, clubbing, spooning, pitting
• Consistency: brittle, hard, thick, thin, bogginess, adherence to nail bed
• Dilation or irregularity of nail fold capillaries suggestive of connective tissue disease
• Periungual skin: erythema, dystrophy, swelling, discharge
Investigations
1. Bloodwork
• CBC-D, Fe, ferritin, TIBC
• Bili, ALB, ALT, ALP (Liver Dysfunction)
• TSH (hypo and hyperthyroid)
• Fasting glucose (DM)
• Testosterone, androstenedione, DHEAS, fasting lipid profile (PCOS)
• Appropriate imaging for malignancy, connective tissue diseases and their complications
• Biopsy all suspicious skin/nail/scalp lesions
• Nail clipping or scalp scraping for fungal culture
—
• Hair pull test can be used to determine if the hair loss process is still active
• Dermoscopy to further examine skin/nail/hair lesions
Management
1. Highly dependent upon suspected diagnosis
2. Lesions concerning for malignancy should be referred to dermatology for biopsy/excision
References
1. Brown DD, LeBlond RF, DeGowin RL, editors. DeGowin’s Diagnostic Examination. gth ed. New York: McGraw-Hill; 2009.
2. Filate W, Leung R, Ng D, Sinyor M, editors. Essentials of Clinical Examination 5th ed. 2005
3. Epstein 0, Perkin G, de Bono D, Cookson J. Clinical Examination 2 ed. Mosby; 1997

SLEEP APNEA & INSOMNIA
2011 Ed. Authors: KamolAbdulwahab, Abroam Isaac MD, Kourosh Dinyari MD
OriginalAurhors:Zoe WoI Ashley Gillson MD, Mohit Bhutani MD FRCPC
Station Objective
In this station you may be expected to take a sleep history, perform a physical examination to identify conditions that affect sleep, and
develop a management plan for insomnia. You may also be expected to differentiate between central, obstructive, and mixed sleep apnea.
2. History and physical exam alone is insufficient to diagnose obstructive and central sleep apnea. Polysomnography results can be used
to diagnose and differentiate between the two types of sleep apnea or suggest mixed sleep apnea:
Disease State Diagnostic Criteria

Obstructive Sleep Apnea Excessive daytime sleepiness not explained by other factors
(airway is blocked leading • 2 of the following not explained by other factors: choking or gasping during sleep, recurrent
to apnea; typically an awakenings from sleep, unrefreshing sleep, daytime fatigue, and/or impaired concentration, jici.
anatomical problem) Sleep monitoring (polysomnography) demonstrates 5 obstructive apneas or hypopneas/hr of sleep
• One of the following not explained by other factors: excessive daytime sleepiness or fatigue, frequent
Central Sleep Apnea
nocturnal awakenings
(airway is patent and apnea
Polysomnography shows 5 central apneas (or hypopneas)/hr of sleep
due to higher respiratory
Normocapnia while awake (PaCO
2 of 35-45 mmHg)
centre problem/failure)
Not explained by presence medical disorder, meds, or substance abuse
• Obstructive sleep apnea (OSA), central sleep apnea, mixed apnea, obesity hypoventilation syndrome (often includes OSA but
characterized by obesity, dy and night hypoventilation, and hypercapnia while awake (PaCO
2 > 45mmHg))
• Others: shift work, meds, poor sleep environment, snoring, restless leg syndrome, sleep apnea 2to an airway tumor
• Untreated obstructive sleep apnea is associated with increased mortality, increased risk of CV disease, and increased
neurocognitive difficulties
• Recurrent central sleep apnea is commonly found in conjunction with neurologic disease and cardiac failure
• Increased risk of motor vehicle accident and falls
History
CC • Insomnia, daytime somnolence, fatigue
HPI • Onset, duration, and progression of symptoms
. Sleep routine: preceding activity, bedtime, ability to fall asleep, wake times (morning and nocturnal), sleep duration,
snoring, abnormal movement, daytime somnolence, sleep diary
• Nighttime: restless sleep, loud snoring, observed apnea/choking/ and/or gasping episodes, nocturnal sweating,
nocturnal enuresis, sleep paralysis
. Daytime: morning fatigue or irritability, excessive daytime sleepiness (EDS), need for daytime naps, difficulty with
driving, cataplexy
. Cognitive: memory loss, decreased cognitive function
• Psychiatric: depression, personality or mood changes, decreased libido
• Other: morning or nocturnal headaches, life stressors, shift work, travel (e.g. time zone) hypnogogic hallucinations,
caffeine, EtOH, medications
• Epworth Sleepiness Scale (assessment of daytime sleepiness)
PMHx • OSA, other sleep disorders, endocrine (DM, thyroid, PCOS, acromegaly)
• CV/RESP: HTN, GERD
• Restless leg syndrome, neurological problems, head trauma (including face and nose)
PSHx • Head and neck (e.g. adenoids, tonsils)
Meds • Stimulants (including caffeine) and sedatives
. Benzodiazepines, SSRIs, corticosteroids, theophylline, diuretics (nocturia), 3-agnoists

Allergies Medication allergies, environmental allergies
—
FHx • Effect on day-to-day activity (e.g. driving, work, school)
—
Social • Smoking, ETCH, substance abuse
ROS • General ROS focusing on RESP
Risk Factors For sleep apnea: male, middle-aged, African-American, central obesity, large neck, structural abnormalities in face/
hypothyroidism.
skull/soft palate, smoking, EtOH, DM, GERD, PCOS, chronic URTI, 1
Physical
1. General Approach
• Vitals: HR, BP, RR, Sp02,T
• Look for underlying cause: OSA vs. secondary to underlying medical conditions
2. Inspection
• Obesity, chest wall deformities,
,
• HEENT: neck size (collar size >17.5’), structural abnormalities (brachycephaly, narrow maxilla, long face, overbite, macroglossia
micrognathia, retrognathia), soft palate, tonsillar or uvular hypertrophy, redundant cervical adipose tissue
rhinorrhea
• Nasal cavity: deviated septum, nasal polyps, turbinate hypertrophy, nasal valve collapse, other obstructions, purulence,
3. Palpation: Thyroid, CV (apical impulse), ABD (observe for signs of congestive heart failure)
4. Auscultation: CV/RESP (observe for signs of pulmonary HTN)
Investigations
1. Blood work
• Not routine, but consider CBC-D,TSH, or other diagnostic markers of underlying primary conditions, ABG
• Specific to suspected underlying primary condition (e.g. CXR for CHF, COPD)
3. SpecialTests
• Polysomnography and/or multiple sleep latency test
monitoring
• Optional home diagnostic devices: home oximetry, nasal pressure recording, peripheral arterial tonometry, auto-CPAP
4. Comorbidity-specific
• ECG, ECHO (CHF, R heart strain), PFTs (airway obstruction), barium swallow, 24 hr pH probe (GERD)
Treatment
• Lifestyle modifications
• Reduce apnea by sleeping on side, use of nasal strips, weight loss, smoking cessation, avoidance of ETCH/caffeine/heavy
meals before bedtime, regular exercise, and good diet
• Medical
• Diagnose and manage underlying conditions
• CPAP,BIPAP
• Surgical
• Severe obstructive apnea uvulopalatopharyngoplasty
—
• Correction of nasal structural abnormalities

device,
• Other surgical options; laser assisted UPPP, pillar palatal implant, radio frequency ablation, mandibular advancement
adenotonsillectomy (first line for children with sleep apnea)
2. Referrals
• Sleep specialist for polysomnography or if diagnosis is unclear; ENT for surgical intervention
References
1. Fleetham J. et al. CTS guidelines: Diagnosis and treatment of sleep disordered breathing in adults. 2006. Can Respir J Vol 13 No 7.
surgery, 5
th
ed.
2. Ishman SL, Wakefield TL, Collop NA. Sleep Apnea and Sleep Disorders. In: Flint PW et al. editors. Cummings otolaryngology head & neck
—
2005.
3. Simon H. SLEEP APNEA. Sleep Apnea (A.D.A.M.) [serial on the Internet). (2007, July 18), [cited October 22,20091; 1-12. Available from: Health Source
-
Consumer Edition.
4. In the clinic Insomnia. Annals of Internal Medicine [serial on the Internet]. (2008, Jan), [cited October 22,2009]; 148(1): 131-1146. Available from: Academic
Search Complete

SORE THROAT (PHARYNGITIS)
20!! Ed. Authors: Mackenzie Lees, NamdarManouchehri MD, Gordon Lees MD FRCSC
On gina/Authors: Brian Buchanan, Carrie Ye MD, Linda Smith MD CCFP
Station Objective
To differentiate whether or not the patient has ‘strep throat’and whether to pursue treatment. Various causes for sore throat include viral and
bacterial, which are virtually indistinguishable on clinical exam.
Mclsaac Modification of the

Differential Diagnosis Mclsaac Classification
Centor Strep Score
3
1. Diagnostic Criteria 1. Hx of fever ( 38.3°C) (+1) Total Points Likelihood ratio
Streptococcal pharyngitis
• High degree of clinical suspicion based on relevant 2.Tonsillar exudate (+1) -1 toO 0.05
diagnostic characteristics 3. Cervical lymphadenopathy (+1) 1 0.52
• One point each for numbers 1-5 and minus one 2 0.95
4. Absence of cough (+1)
point for number 6 as shown in the table to the
right 5.Age<lSyo(+1) 3 2.5
• Rapid antigen testing can assist in Dx strep throat 6. Age >45 yo (-1) 4 or 5 4.9 —
• 60% of sore throats are secondary to the viral URTI from the following pathogens: adenovirus, coronavirus, coxsackie virus, HSV,
and parainfluena virus
• Allergic rhinitis with post-nasal drip, GERD
• EBV (rule out with heterophilic antibodies, EBV serology, and CBC and differential)
• Also: epiglottitis, RSV
• Streptococcal pharyngitis does not necessarily have a high mortality and typically resolves in 5 days, but can be followed by
significant complications if untreated including RF, peritonsillar/tonsillar abscess, and post-streptococcal glomerulnephritis* (*no
evidence thatTx reduces this particular complication)
• Epiglottitis
History
ID • Age
CC • Sore throat, difficulty swallowing/painful swallowing (dysphagia/odynophagia), difficulty speaking
HPI • Onset, duration, presence of fever/cough/runny nose, conjunctivitis, sinus headache, exposure to sick contacts,
travel history
RED FLAGS • Unimmunized, drooling, stiff neck, difficulty swallowing secretions, dysphonia (“hot potato&voice), palpable neck
swelling, splenectomized patients
PMHx • Hx of recurrent strep throat/tonsillitis
PSHx • Tonsillectomy
Meds • Recent antibiotic use
Social • Sexual Hx: recent, unprotected oral-genital contact
ROS • HEENT: headache
• RESP: SOB, dyspnea, productive cough
• GI: diarrhea
• MSK / DERM: associated rash, scarlatiniform highly indicative of strep (for scarlet fever, uncommon)
Risk Factors • Streptococcal pharyngitis more likely if autumn, <1 1 yrs, crowded living spaces, exposure to sick contacts, smoking,
allergies, poor hygiene, lowered immunity
Physical
1. General Approach
• Introduce yourself, wash hands, ask permission to do a PE
• General appearance of patient uncomfortable, in distress, toxic appearance
—

• Vitals: HR, BP, RR, temperature
2. Inspection
• HEENT: inspecting oral and nasal mucus membranes for erythema/petechiae and erythema/swelling, TM’s
• Examine oral cavity and pharynx for tonsillar enlargement, exudates, and airway patency
3. Percussion
• Splenomeglay (50% of patients with infectious mononucleosis)
4. Palpation
• Palpate anterior/posterior cervical and submandibular Iymphnodes
5. Auscultation
• CV exam
• Resp exam
Investigations
1. Blood work
• CBC-D
• Lateral C-spine film is suspected suppurative complication of strep throat
3. Special Tests
• Rapid streptococcal antigen test (sens 50-90%, spec 93%)
• Throat culture: gold standard of diagnosis of GAS pharyngitis
• Monospot test for heterophil antibodies
Treatment
1. Emergent
• Send patient to emerg or for a critical care consult for definitive airway management
• If compromised airway, severe sore throat, or toxic presentation, consider immediate ENT consult
• Medical: Streptococcal: Penicillin therapy 10 day course (oral or IM, Pen V 300 mg tid for adults, amoxicillin 40 mg/kg/day divided
q8h), erythromycin if penicillin allergic
• SupportiveTx includes salt-water gurgle, increased fluid intake, throat lozenges and analgesics/antipyretics
• Surgical: if >7 episodes of strep tonsillitis per yr, consider tonsillectomy
3. Follow-up
• If inadequate clinical response to therapy in expected time frame consider alternative Dx
4. Referrals
• ENT consult if concerns for retropharyngeal/peritonsillar abscess, epiglottitis
References
1. EbeIl MH; Smith MA; Barry HC;Ives K; Carey M. Does This Patient Have Strep Throat? JAMA, Dec 2000; 284:2912-2918.
2. Bisno AL Acute Pharyngitis. N EngI J Med. 2001 Jan 18; (3): 205-211.
3. Mclsaac WJ, Goel V, ToT, Low DE. The validity of a sore throat score in family practice. CMAJ. 2000; 163:811-815.

SYNCOPE
2071 Ed. Authors: IlmothyChan, Gabor Gyenes MD FRCPC
OriginalAuthors:AlyzEe Sibtain, Carrie Ye MD, Taha TaherMD FRCPC
Station Objective
Identify common causes of syncope. Distinguish the difference between syncope vs seizures. Understand important history, physical
examination findings and investigations for the evaluation of syncope.
• Sudden, transient, self-limited loss of consciousness from global cerebral hypoperfusion, with spontaneous recovery
• Differentiate syncope from hypoglycemia, seizures, vertigo, coma, falls, vasovagal,TIA, strokes
• Cardiogenic causes
• Arrhythmia (VT/yE, AV block)
• Decreased cardiac output (L-side: valvular disease AS/HOCM, myxoma; R-side: PE)
• Low flow states (CHF, cardiomyopathy)
• Non-cardiogenic causes
• Orthostatic (hypovolemia, autonomic dysfunction, medications)
• Vasovagal syncope (WS) most common in young adults precipitated by fear, emotion, stress, pain
—
• Situational syncope: precipitated by swallowing, coughing, urinating, defecating

Acute coronary syndrome, Arrhythmias, PE, Aortic dissection, Valvular Heart Disease, CHF, Hypoglycemia
Syncope Grand mal seizures

0
Warning symptoms Lightheadedness, dizzy, visual blurring May have aura
U’
i
Provocative factors Change of posture, dehydration Alcohol, meds, CNS infection, trauma
. Onset ±LOC, graying outvision Sudden onset if grand mal
a
0
U
‘ Duration Seconds Seconds to minutes
C
Movements Brief jerks Tonic/clonic movements
Autonomic features Low BP, dilated pupils, diaphoresis Increased BP, tachycardia
Confusion/Cognition Return to baseline immediately Post-ictal state

0
Speech Normal May be garbled, automatisms
& Focal Neurological defects None May be present
History
ID • Ageandgender
CC • Sudden LOC or postural tone, or preceded by presyncope
HPI • Important questions to ask: positive answers have high likelihood of being syncope
• If witnessed: Was LOC complete, rapid onset and short duration?
• Was recovery spontaneous, complete, without sequelae?
• Was postural tone lost? Previous of recurrence of syncopal episodes?
• Preceding event: emotional stimulus, postural change, exertion (AS/HOCM), lightheadedness, diaphoresis, nausea
and vomiting, palpitations, micturition, carotid sinus pressure
• During event: duration, tonic-clonic movements, automatisms, incontinence, tongue biting
• Post event: recovery time, head injuries, weakness/confusion, recall of event
RED FLAGS • Chest pain, palpitations, dyspnea, headac•he, syncope without warning (concerning for arrhythmia)
PMHx • Underlying structural disease (congenital heart disease, valvular disease), arrhythmias, IHD, left ventricular
dysfunction,_psychological_disorders, DM (autonomic_neuropathy),_epilepsy,_HTN

PO&GHx Eclampsia
Meds Cardiac meds (alpha blockers, antihypertensives, B-blockers, CCB diuretics, antirhythmics), antiepileptics,
phenothiazines, nitrates. Supplements, herbals, diet pills.
FHx CVD, neurologic disorders
Social EtCH use, cocaine use, diet. Function: occupation, driving.
Physical
i. General Approach
• Vital Signs including glucometer reading, ABCs, close monitoring of BP and HR
• Resuscitation orders: 2 large bore lVs, fluid resuscitation, oxygen, glucose administration
2. Inspection
• Pallor, diaphoresis, JVP, cyanosis, edema
3. Palpation
Systolic thrill in the sternal 2nd R ICS, sustained cardiac impulse, parvus et tardus carotid pulse (AS)
—
•
• Apical impulse with a sustained systolic thrust, spike & dome carotid pulse (hyptertrophic cardiomyopathy) m
4. Auscultation
• Mid-systolic ejection click, harsh crescendo-decrescendo medium! harsh-pitched murmur in R sternal 2nd ICS, 53, S4, paradoxical
—.
or single 52 (AS)
Mid-systolic, harsh, crescendo-decrescendo, mid-pitch murmur, L sternal 2nd/3rd ICS, wide 52 split, S4 (PS)
—
•
• Diastolic decrescendo low-pitched rumble at the apex (MS)
• Crescendo—decrescendo murmur at the L sternal 3rd and 4th ICS (hypertrophic cardiomyopathy)
Investigations
1. Blood work
• CBC-D, electrolytes, Mg, Ca, BUN, creatinine
2. SpecialTests
• ECG: should be performed on all patients who present with syncope
• Continuous ECG or outpatient portable Holter monitoring (though low yield)
• EEG: for detection of seizures
• Exercise stress test (if concerned re: exercise-induced arrhythmia)
• CT imaging head: only indicated if new focal neurological deficits; chest: as indicated by select cases
• Echocardiogram: looking for structural abnormalities
Treatment
1. Emergent
• Emergent: stroke (urgent thrombolysis, monitor and stabilize vitals)
• Medical
• Vasovagal/situational syncope avoidance of triggers, support stockings, discontinue offending meds
—
• Orthostatic hypotension support stockings, correction of fluid expansion, monitor BP

—
• Surgical
• Valve replacement (AS, M5, PS) tissue or mechanical
• lmplantable cardioverter defibrillator (ventricular tachyarrhythmia)
• Permanent pacemaker (bradyarrhythmias, sick sinus syndrome)
• Catheter ablation (supraventricular tachycardia, atrial flutter/tachycardia)
3. Referrals
• Cardiology
References
1. MCC Objectives Online. http://www.mcc.ca/Objecties/Online/objectives.pl?Iang=english&Ioc=obj&id=1 06-E
2. Carlson Mark D, Grubb Blair P, “Chapter 48. Diagnosis and Management of Syncope” (Chapter 48). Fuster V. O’Rourke RA, Walsh RA, Poole-Wilson P. Eds.
King SB, Roberts R, Nash IS, Prystowsky EN, Assoc. Eds.: Hurst’s The Heart, 12e
3. Carlson Mark D, “Chapter 21. Syncope’ Fauci AS, Braunwald E, Kasper DL, Hauser SL, Longo DL, Jameson JL, Loscalzo J: Harrison’s Principles of Internal
Medicine, 17e
4. 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. Nov 2009;30(21 ):2631 -71. [Medlinel

THYROID DISEASE
2071 Ed Authars:ioffre Munra, Carrie Ye MD, Laurie Mereu MD F PC
Station Objective
To recognize the clinical manifestations and interpret the investigations required for Dx and Tx of thyroid disease.
1. Diagnostic Criteria:
• Hypothyroidism:
• Primary: elevated TSH
• Secondary: normal or low TSH, low freeT4
• Hyperthyroidism:
• Primary: low TSH, elevated free T4 & free T3
• Secondary: elevated TSH, elevated free T4 & free T3
• Thyroid Nodules/Goiter/Cancer: Please refer to “Station 172: Neck Mass”
Primary: Hashimoto’s thyroiditis; subacute thyroiditis; post-

Primary (Thyrotoxicosis): Grave’s disease; subacute thyroiditis; post
partum thyroiditis; drugs (lithium, amiodarone); iodine deficiency;
partum thyroiditis; toxic multinodular goiter; toxic adenoma; drugs
iatrogenic (iodine ablation, thyroidectomy, radiation); absent!
(amiodarone, levothyroxine); iodine excess (seaweed, supplements)
ectopic thyroid gland
Secondary: hypopituitarism (pituitary adenoma, pituitary surgery! Secondary:TSH-secreting pituitary adenoma, gestational
radiation/destruction); hypothalamic disorders thyrotoxicosis

• Myxedema coma (hypothyroid)
• Thyroid storm (hyperthyroid)
• Thyroid cancer and/or metastases (euthyroid)
History
CC • Symptoms associated with either hypothyroidism or hyperthyroidism; neck mass/nodules
HPI • Fatigue, weight gain or loss, heat or cold intolerance, constipation or diarrhea, dry skin or sweaty palms,
palpitations, tremor, increased anxiety
• If neck mass/nodules: painful, growing, pressure symptoms (ie. dysphagia, dyspnea, hoarseness)
Hypothyroidism
Hyperthyroidism
• HEENT: impaired hearing, hoarseness
• HEENT: eye irritation, diplopia
• CV/RESP: dyspnea
• CV/RESP: palpitations
• GI: constipation, wt gain, decreased appetite
• GI: diarrhea, weight loss, increased appetite
• GU: menorrhagia
• GU: polyuria, oligomenorrhea, loss of libido
• MSK!DERM: weakness, arthralgia, myalgia,
• MSK/DERM: weakness
paresthesia, dry/itchy skin
• CNS: dysphoria, tremor
• CNS: depression, poor concentration/memory
• Other: hyperactivity, irritability, heat intolerance
• Other: fatigue, cold intolerance
RED FLAGS Fever and/of altered mental status (rule out thyroid storm or myxedema coma; see tables)
PMHx • Previous neck masses/nodules, thyroid disease, psychiatric illnesses, malignancies
PSHx • Neck surgery, thyroidectomy, parathyroidectomy
PO&GHx • Pre/Post menopause, previous pregnancies, potential for current pregnancy
Meds • Levothyroxine (Synthroid), liothyronine (Cytomel), amiodarone, lithium, herbals (check(iodine])
Allergies General inquiry
FHx • Thyroid disease, thyroid cancer

Social Diet (excess kelp, ingestion of animal thyroid tissue), caffeine intake, smoking, alcohol
Risk Factors Previous radioactive iodine or anti-thyroid drug therapy, radiation of neck, thyroid/neck surgery
physical
i. General Approach
ABCs, vitals, and aeneral aDrjearance, Drare Pt aooroDriatelv and ensure Dt is comfortable / aclreeable to the exam.
coarse hair, Queen Anne’s sign, myxedema (facial hair loss, exophthalamos, rapid speech, diaphoretic,
1. Inspection swelling), dull/blank affect, slowed speech, goiter, tremors, difficulty sitting still, muscle wasting
pallor, thin/brittle nails, shallow/slow respirations
bradycardia, dry/cool skin, peripheral edema, joint tachycardia, moist/warm skin, pretibial myxedema,
2. Palpation effusions, L muscle strength, delayed relaxation of decreased proximal muscle weakness
deep tendon reflexes, positive Tinnels/Phalens test
3. Special Tests lid lag, measure degree of exophthalamos
(Goiter/Thyroid Exam: Please refer to PE Thyroid)
Investigations
• Screen for thyroid disease: TSH
• Hypothyroidism: TSH, anti-TPO antibodies (may be helpful)
• Hyperthyroidism:
• TSH, free T4, free T3, TSH receptor antibodies, anti-TPO antibodies
• Thyroid scan or 24 hour radioactive iodine
• Thyroid Nodules: ultrasound plus FNA for nodules greater than 1.0cm (Please refer to “Station 172: Neck Mass”)
Treatment
Thyroid Storm
Emergent Signs Lab Findings
• Thyroid Storm:
• PTU1 gPOSTAT,then300mgPOq6h t HR; t BP; widened pulse tT4; t FT4; t glucose;
• Iodine drops 2-3 P0 q6h after each dose of PTU pressure; fever; LOC; shock
t WBC; .1. Hgb; f Ca; K
• Dexamethasone 2 mg IV q6h (severe cases)
• IVF, cooling blanket, Tylenol, correct electrolytes
• Tx precipitating event (sepsis, DKA, PE, bowel infarction) Mvxedema Coma
• Myxedema Coma: Signs Iab Findings
• L-thyroxine 500 mcg IV, then 100-300 mcg IV daily PRN
T4; L FT4; glucose;
• Hydrocortisone 100 mg IV q6h LHR;4BP;IRR; tWBC; 4’ Hgb;
• Dextrose-containing IVF, warm blanket, correct electrolytes hypothermia; 4’ LOC;
• Tx precipitating event (infection, GI bleed, overdose, CHF)
4’ Na; t CK
• Hypothyroidism: levothyroxineT4 (Synthroid, Eltroxin)
• Hyperthyroidism: antithyroid medications (ie Propylthiouracil or Methimazole)
• Once hyperthyroidism is stabilized, patients may consider iodine ablation or thyroidectomy.
3. Follow-up: RegularTSH levels to evaluate thyroid status
4. Referrals
• All cases of hyperthyroidism and thyroid disease during pregnancy warrants referral to an Endocrinologist
• Severe cases of hypothyroidism should also be referred to Endocrinology
• Thyroid masses may be referred to either Endocrinology or General Surgery
• Complicated or medication-refractory thyroid disease warrants referral to an Endocrinologist or General Surgeon
References
1. Fauci AS et al. Harrison’s Principles of Internal Medicine. 17th ed. USA: The McGraw-Hill Companies, mc; 2008.
2. McPhee Si, Papadakis MA. Current Medical Diagnosis & Treatment. USA: The McGraw-Hill Companies mc; 2011.

UNILATERALLY SWOLLEN LEG
2011 Ed. Authors: Timothy Chan, Mohit Bhutani MD FRCPC
Station Objective
Create a differential diagnosis for unilateral leg swelling. Identify symptoms of DVT and know appropriate management steps. Have an
approach to determining etiology of leg swelling and treatment options.
• 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 (heart failure, kidney disease). Generalized edema (arms and legs) is always caused by a
systemic disease
• DVT presents as acutely swollen, discolored, painful leg
—
• Venous insufficiency
• Cellulitis, myositis, fasciltis or infection
• Trauma / muscle injury ruptured gastrocnemius
—
Ruptured baker’s cyst, obstruction of poplilteal vein

Compartment syndrome
Venous obstruction (extrinsic pressure) from tumor, hematoma or lymphoma
Lymphatic obstruction
• Reflex sympathetic dystrophy

• DVT leading to PE, necrotizing fasciitis, compartment syndrome
History
CC • Unilateral swollen leg
HPI • Duration of swelling (acute <72 hours vs chronic)
• Any associated pain? PQRST
• Compartment syndrome has pain out of proportion, DVT and reflex sympathetic dystrophy are painful, CVI is low-
grade ache, lymphedema is painless
• Is the swelling warm?
• Does the edema improve overnight (venous more likely to improve than lymphedema)
• Recent trauma or extremes of activity eg. popping sensation after physical activity
-
• Recent immobilization surgery, paralysis, cast

-
• History of systemic disease (heart, liver, kidney)

RED FLAGS • Sudden onset (<72 hours) of leg swelling, painful, discolored rule out DVT
—
• Pain out of proportion necrotizing fasciitis, compartment syndrome

—
PMHx • History of malignancy, hypercoaguability, blood clots

PSHx • History of immobilization after surgery
PO&GHx • Pregnancy, Prolonged bedrest
Meds • CCB, prednisone and anti-inflammatory drugs are common causes of leg edema
• OCP
FHx • Hypercoaguability disorders (Factor V Leiden, Protein C, Protein 5, ATIII deficiency)
Social • Prolonged periods of immobilization — airplane travel
ROS • General: Fevers, chills cellulitis infection
—
• RESP: Dyspnea, hemoptysis, pleuritic chest pain

• MSK/DERM:Trauma,muscleinjury
Risk Factors • Virchow’s triad, major surgery/trauma, malignancy, immobilization, prior venous thromboembolism

physical
1. General Approach
• Vitals. (SOB, t HR, tRR, LO2 sat PE), fever (cellulitis)
-
Well’s Score for DVT

• History with DVT likely Dx (Well’s Score)
3 = high probability of DVT (75%)
• Paralysis or immobilization of lower extremity (+1)
1-2 = moderate (17%)
• Recent immobilization > 3 days / major surgery (+1)
0 = low risk (3%)
• Active cancer (+1), history of clots/DVT(+1)
• Likelihood of alternative diagnosis (-2)
• Compartment syndrome
• 6 P’s pain, pressure (pain with palpation), paraesthesia, paresis (late), pallor (late) and pulseless (last sign)
—
2. Inspection
• Skin changes, brown hemosiderin deposits venous insufficiency
—
• Erythema with demarcated border cellulitis —
• Swelling of entire leg (+1)

• 3 cm in calf circumference vs other leg (+1)
• Collateral superficial veins (+1)
3. Palpation
• Pain on palpation, warmth
• Distal pulses, capillary refill indications of arterial disease
—
• Increased pain with passive range of motion compartment syndrome

—
• Tenderness along deep veins (+1)

• Unilateral pitting edema (+1)
4. Auscultation
• Heart failure findings (arrhythmias, lung crackles, pleural rub)
Investigations
1. Blood work
• CBC, urinalysis, electrolytes, creatinine, blood sugar, TSH, albumin
• Serum albumin <2g/dL leads to edema from liver disease, nephrotic syndrome
• Doppler U/S
• Spiral CT angiogram for suspected PE, V/Q scan useful if CT angio not available
• CXR: useful to look for other causes
3. SpecialTests
• D-dimer: high sensitivity makes it useful in ruling out DVT in low risk patients. Elevated D-dimer should be followed up with
Doppler U/S
Treatment
1. Acute Management
• Immediate stabilization, IV access 2 large bore IVs, oxygen
—
• DVT/PE LMWH (1mg/kg SC qi 2h) with simultaneous warfarin therapy for two days until oral anticoagulation target INR 2.0-3.0
-
established, discontinue LMWH afterwards

• IVC filter, surgical thrombectomy if anticoagulatlon is contraindicated, Thrombolytic agents for massive PE’s
• Chronic venous insufficiency leg elevation and knee-high compression stockings that provide 30-40 mm HG pressure at ankle
—
• ABI if arterial insufficiency is a concern, compression stockings are contraindicated

• Compartment Syndrome remove constrictive dressings, elevate limb, fasciotomy to release compartments
—
3. Refer for further evaluation if findings indicate tumor
References
1. Approach to Leg Edema of Unclear Etiology Journal of the American Board of Family Medicine, JABFM. 2006 March; 19(2).
—

URINARY INCONTINENCE
2071 Ed. Authors: Todd Penney MSc, Henry ConterMD, Ryan Cooper MD MPH FRCPC
OriginalAuthors: Holly Kamitakahara, Juliette Sacks MD, Catherine Flood MD FRCSC
Station Objective
To learn how to approach a patient with urinary incontinence, focusing on the three most common types stress, urge and overflow; to learn
—
how to address acute transient incontinence in the geriatric population.
1. Diagnostic Criteria: See Table 1.
TABLE 1. DIAGNOSTIC CRITERIA OF COMMON TYPES OF INCONTINENCE

TYPE OF INCONTINENCE DESCRIPTION DIAGNOSTIC CRITERIA
Involuntary urine leakage due to rapid in Havepatientwithfullbladdergetintolithotomyposition,
STRESS abdominal pressure and insufficient closure thenhavepatientcoughordoValsalvamaneuver;ifurine
of sphincter leaks from urethra, test is +
. Test urodynamics uroflowmetry, cystometrogram
Involuntary urine leakage due to need to —
URGE
. video fluoroscopy; urodynamics are used to measure
void immediately; caused by overactivity of
simultaneous urethral, vesicular and intra-abdominal
bladder detrusor muscle
pressures (for more complicated or pre-operative cases)
Involuntary urine leakage that occurs when
bladder pressure exceeds urethral pressure
OVERFLOW . . — Test urodynamics with a full bladder
due to urinary retention and subsequent
bladder contraction
2. Common Conditions: See Table 2.
TABLE 2. CAUSES OF ACUTE VS. CHRONIC INCONTINENCE
Remember diapers acronym
Delirium/dementia
Infection/
Atrophic vaginitis
CAUSES OF ACUTE ONSET INCONTINENCE
Pharmaceuticals/Parkinson s dz/polyuria/psych issues
Endocrine issues/electrolyte imbalance/excess urine prod’n
Restricted mobility
Stroke/stool impaction/stone/spinal cord dz
Bladder tumour, stones, BPH, surgery, DM, hypercalcemia, neurological
CAUSES OF CHRONIC INCONTINENCE
disorder
• Cauda Equina Syndrome
History
ID Age, gender, race, GPTAL
CC • Involuntary voiding
HPI . Acute vs. chronic onset of Sx, intermittent vs. constant Sx, progressively worsening Sx, change in frequency of
urination, # of incontinent episodes vs. normal voids during day, worsening of Sx with physical activity or in
intra-abdominal pressure via sneezing, coughing, laughing, etc., feeling of sudden urge, incontinent of small
or large volume of urine, need to wear pads and how many times/day they are changed, fluid intake: amount,
time of day, type(caffeine, EtOH), associated Sx: nocturia, nocturnal enuresis, feeling of fullness in pelvic area,
dyspareunia; impact on daily function, symptoms of UTI (frequency, urgency, nocturia, dysuria, straining, hesitancy,
intermittency, poor stream, pelvic pain, etc.)
RED FLAGS . Associated fecal incontinence with back pain and neurologic Sx (Cauda Equina Syndrome); urinary incontinence +
sepsis (urosepsis, which is common in elderly)
PMHx UTls, kidney dysfunction, enlarged prostate, urinary tract stones, diabetes, spinal cord injury
PSHx . Pelvic surgery (e.g. hysterectomy, bladder tumour removal, prostate surgery)

PO&GHx Vaginal deliveries, operative deliveries, menopause status, Hx of prolapsed structures
Meds Diuretics, cholinergics/anti-cholinergics
FHx Incontinence, prostate Ca
Social Smoking, EtOH, mobility, occupation (e.g. heavy lifting), caffeine consumption
ROS • RESP: chronic cough
• GU: UTI Sx (dysuria, urgency, nocturia, fever, flank pain, weak flow, hematuria), vaginal dryness, vaginal/penile
discharge
• MSK / DERM: back pain, spinal cord/column abnormalities (e.g. spina bifida)
Risk Factors Current pregnancy, past baby deliveries
Physica
i. General Approach
• Introduce yourself, wash your hands, check ABCs + add IV and monitors if necessary, ask for permission to do PE, check vital signs,
note BMI, check mental status with MMSE/MOCA for dementia or CAM for delirium
2. Inspection
• Perform speculum exam for atrophic vaginitis or prolapse
3. Palpation
• Abdomen for ascites/masses/tenderness, bimanual exam for masses/prolapsed, DRE for stool impaction/rectal tone/prostate
abnormalities
4. SpecialTests
• Neurological exam for lower extremities + back: sensation to touch + pain + temp, reflexes, motor function; MMSE/MOCA, CAM
Investigations
1. Blood work
• CBC-D, fasting blood glucose, HbA1 c, Cr, BUN, lytes, PSA (if necessary)
• Urethrocystoscopy = examines urethra, urethrovesical junction, bladder walls and ureteral orifices (for patients with irritative
bladder Sx to rule out tumors or inflammation); U/S may be necessary; VCUG;
3. Special Tests
• U/A, urine C+S+Gram stain, patient voiding diary, PVR with bladder scan (normal <50 cc)
Treatment
1. Emergent
• Urgent spinal decompression if Cauda Equina Syndrome
2. Treatment Options: See Table 3
3. Referrals urology, geriatrics, gynecology if necessary
—
TYPE OF TREATMENT
INCONTINENCE MEDICAL SURGICAL
Pads, timed voiding (voiding at a specific time
of day), double voiding, 4 fluid intake, smoking
ALL cessation, cessation of fluids at a certain hour before
bed, Abx if UTI, stop provoking meds, bowel routine
if stool impaction
Kegel exercises to pelvic floor muscle tone, topical Cystourethropexy or sling to reinforce bladder neck?
STRESS
estrogen cream, proximal urethral injections urethra; pessary
URGE Antispasmodics (Oxybutynin), anticholinergics, TCAs
OVERFLOW Catheterization
References
1. Robert et al. Conservative management of urinary incontinence. JOCG (internet]. 2006 December [cited 2009 Nov 1 4];1 86:1113-1118. Available from:
ht.tLLwww.sogc.orp/ouideIines/documents/1 86E-CPG-Decembre2OO6.df

VISION LOSS
2011 Ed. Authors:Ashraf Kharrat, James KeayMD CCFP
OriginalAuthors: Nawaaz Nathoo, Chris Hanson MD, Christopheri RudniskyMO MPH FRCSC
Station Objective
Determine whether vision loss is chronic or acute, total or partial, and evaluate etiologies. Create an effective management plan, which may
involve ophthalmology referral (often urgently).
- Determine acuity of vision loss, location of pathology (corneal/anterior segment, vitreous, retinal, ON, central)
Acute vision loss: Chronic visual loss:
• Angle-closure glaucoma: painful, n/v • Pre-retinal conditions
• Vitreous Hemorrhage: seen on fundoscopy • Corneal disorders: cornea may appear cloudy
• Nervous system/vascular: • Lens disorders (age related, traumatic, or steroid-
• Retinal artery/vein occlusion: on fundoscopy induced cataracts)
• Migraine: characteristic Hx, transient • Open-angle glaucoma (primary, secondary): high
• Occipital infarct/hemorrhage: central neurological signs! intraocular pressure measurement
symptoms • Retinal dysfunction
• Retinal/macular/optic disc: • Diabetic (retinal edema, retinopathy): Hxofpoor
• Optic neuritis: painless, pupil/color vision dysfunction diabetic control or long duration of DM
• Retinal detachment: curtain of vision loss • Vascular insufficiency
• Anterior ischemic optic neuropathy/temporal arteritis: painful, • Tumors
scalp tenderness • Macular degeneration or dystrophy: often have +ve
• Infectious / inflammatory FHx
• Trauma (blunt, penetrating, foreign body, chemical) • Central lesions: central neurological signs
• Drug toxicity • Toxic/nutritional (nutritional deficiencies, tobacco-alcohol
• Functional loss: no organic cause found, often past psych Hx and/or amblyopia, methanol)
significant stress • Hereditary optic neuropathies

• Life-threatening: central lesions, temporal arteritis
• Sight-threatening: acute angle-closure glaucoma, retinal detachment, CRAO, intraocular FB
History
ID • Age, gender, occupation
CC • Loss of vision
HPI . Sudden or gradual; one eye or both; painful or painless
• Central or peripheral vision loss
• Total or partial (blacked out versus looking through a haze), and degree of loss
• Other visual disturbances (flashing lights, floaters, zig-zag lines)
• Associated headache or other neurological symptoms
• Trauma (blunt/penetrating, foreign body, chemical exposure)
• Infectious/inflammatory symptoms (redness, itchiness, discharge)
RED FLAGS • Sudden, painful vision loss (TA, angle-closure glaucoma, endophthalmitis)
• Sudden, painless vision loss (retinal detachment, vitreous hemorrhage)
PMHx • Vascular risk factors: HTN, DM
• Migraines and other neurological conditions: CVA, MS
• Glaucoma, high myopia (>6.OOD)
PSHx • Ocular surgery
Meds • Eye drops, CV disease medications
Allergies • To topical and oral medications
FHx • Ocular hx, CVD hx, DM, migraines
Social • Recreational drug use (especially IVDU), smoking hx

ROS • HEENT: symptoms of temporal arteritis (scalp tenderness, temporal pain, jaw, claudication, wt loss, fever, chills,
I nights), migraines
I CV: CV disease, stroke
DM, HTN, previous ocular hx
jFactors •
physical
1. General Approach
• Blood pressure, visual acuity, EOM’s, complete CN exam, visual fields by confrontation
• Colour vision testing: markedly decreased in optic neuropathies
2. Inspection
• Ptosis (measure interpalpebral fissures with eyes open), exopthalmos, enopthalmos, proptosis
• Fundoscopy (papilledema, hemorrhage, vascular occlusion)
3. Palpation
• Temporal arteritis: prominent temporal artery (± pulse) pain on temporal/scalp palpation, TMJ palpation with jaw mobility for
claudication
4. Special Tests
• Examine pupils: reactivity to light, swinging flashlight test
• Ophthalmoscopy:
• Examine optic disc for any abnormalities (eg: papilledema, pale optic disc, etc.)
• Examine retinal vasculature for any visible clots/bleeds (lack of view may point to retinal detachment, endophthalmitis, or
vitreous hemorrhage)
• Amsler grid (each eye separately) to identify any abnormalities that may suggest retinal pathology
• Screening neuro exam
• Slit-lamp examination: ensure there is no corneal or lenticular opacity contributing to vision loss
Investigations
1. Blood work
• Temporal arteritis: STAT ESR, CRP
• CBC-D, syphilis EIA (0rVDRL RPR, FTA-ABS),TSH,T4,T3, lipid profile, fasting glucose
2. Special Tests
• Intraocular pressure
Treatment
1. Emergent
• Acute vision loss for which a cause is not found requires emergent ophthalmology referral
• Most causes of vision loss, acute or chronic, will require referral to an ophthalmologist
References
1. Corbett JJ. (2009). Approach to the patient with visual loss. In Biller J, Practical Neurology (117-130). Philadelphia: Lippincott.
2. Hoffman, LH eta!. First Exposure Emergency Medicine. McGraw-Hill, Inc. USA, 2008.

WEAKN ESS
20?? Ed. Authors: Michaeli Kapusta, Carrie Ye MD, Ashraf Khan MBChB CCFP
Or/gina/Authors: Carrie Ye MD, Shilo Lefresn Penny Smyth MDFRCPC
Station Objective
Differentiate fatigue from true muscle weakness
• UMN (corticospinal tract lesions) vs. LMN (peripheral mono or polyneuropathies) vs. NMJ vs. muscle (myopathies)
• 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)
• Infectious: influenza, EBV, CMV, lyme, HIV
• Inflammatory: polymyositis, dermatomyositis, inclusion body myositic, lupus
• Neurologic: cerebrovascular disease (stroke, TIA), demyelinating disorders (MS, Guillain-Barre), spinal cord injury, neuromuscular
(myasthenia gravis, Eaton Lambert, botulism), ALS
• Metabolic: fCa, t/.LNa, B1 2 deficiency
• Endocrine: hypothyroidism, Cushing’s, acromegaly
• Drugs: steroids, statins, EtOH, cocaine, interferon
3. High Early Mortality / Morbidity:
• Stroke, GBS, rabies
History
ID • Age, gender
CC • Weakness
HPI • Onset: sudden, progressive, duration, intensity, fluctuations (cyclic/episodic), preceding illness/trauma/bite/toxic
ingestion, immobility
• Precipitating/palliating factors: AM/PM, exercise (worsens myasthenia gravis, improves Eaton-Lambert)
• Distribution of weakness: diffuse, focal, unilateral/bilateral, proximal/distal, hemiparesis vs para/quadriplegia
• Severity: trouble rising from chair/brushing hair, difficulties with other ADLs
• Speech becomes unintelligible after prolonged speaking, drooling, chewing swallowing difficulties (+LR 4.5, -LR
0.61 for myasthenia gravis)
• Associated symptoms: myalgia (viral), stiffness, numbness, tingling, fever, weight (malignancy), skin rash (SLE,
lyme, dermatomyositis), cold intolerance (hypothyroid), worsening with heat (MS), visual loss (MS/stroke)
RED FLAGS • Sudden onset, one sided weakness (CVA), ascending paralysis (rabies, GBS)
• Weakness that becomes severe within a few days
• Dyspnea
• Bulbar symptoms (dysarthria, dysphagia, facial weakness, ocular impairment)
PMHx • Recent or chronic 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 immunizations
FHx • Myasthenia gravis, muscular dystrophy, autoimmune disease, collagen vascular disease, ALS
Social • Occupation: possible occupational injury or exposures (organophosphates used in farming)
• EtCH, smoking, recreational drugs (cocaine), exposure to lead
ROS • Constitutional symptoms: fatigue, weight loss, fever, night sweats
• HEENT: headache, diplopia, dysarthria, dysphagia
• CV/RESP: palpitations, chest pain, claudication, SOB
• MSK / DERM: joint pain, muscle pain, neck pain, rash

Physical
1. General Approach
• Vitals, GCS, posture, fades
2. Motor Exam (see Table 1 and 2)
• CN: bulbar involvement
• Inspection: muscle bulk/atrophy, fasciculation, tremor, myoclonus, nystagmus, cerebellar ataxia
• Tone: rigidity (lead-pipe, cog-wheel), spasticity (UMN), decreased (LMN)
• Strength (note pattern): proximal weakness (myopathy/Guillain-Barre) vs distal weakness (neuropathy)
• Pronator drift: outward drift (muscle weakenss), pronation and downward drift (UMN lesion)
• Deep tendon and plantar reflexes (Babinski reflex highly specific for corticospinal tract lesion)
3. Systemic exam (if above exam is not suggestive of a lesion)
• CV, RESP, GI, DERM looking for signs of systemic disease
• Further neurological testing including sensory exam, coordination, gait
4. SpecialTests (for myasthenia gravis)
• Ice pack test: place ice on eyelid for 2 mm, improvement in ptosis suggests myasthenia gravis (+LR 24, -LR 0.16)
• Peek sign: within 30s of complete apposition of lid margins, patient involuntarily starts to separate the lids and clear starts to show
(+LR 30, -LR 0.88)
Investigations
1. Blood work
• CBC-D (tWBC: infectious/inflammatory, I-Hgb: malignancy/inflammatory)
Table 1. UMN vs LMN lesions
• , magnesium, phosphate, TSH
Electrolytes, glucose, corrected Ca
2
• CK (myopathy, rhabdomyolysis), ESR, ANA (SLE), HBV/HCV serology, UMN LMN
cryoglobulin
Power UE flex > extend
2. Radiology/Imaging I4absent
LE extend > flex
• CXR (paraneoplastic syndrome from lung CA), CT/MRI
3. LP for Guillain-Barre syndrome Tone Spastic Rigid
4. SpecialTests DTR t 4iabsent
• Electromyography (differentiate neuropathy and myopathy)
• Erdrophonium test: anticholinesterase inhibitor injection results in Sx
Plantars if
improvement within 30s in myasthenia gravis (+LR 15) Fasciculation Absent ±
• Acetylcholine receptor antibody testing Atrophy Late Early
• Muscle Bx (necessary for diagnosis for polymyositis)
Table 2. Muscle Strength
Treatment 0 No visible muscle activity
1. Emergent 1 Visible muscle twitch
CVA: thrombolysis (consult stroke neurology) 2 Movement but not against gravity
Respiratory failure: appropriate respiratory support 3 Movement against gravity, not resistance
• Medical: treat underlying disorder 4 Movement against some resistance
• Polymyositis: prednisone 5 Full Strength
• Myasthenia gravis: pyridostigmine/Mestinon, thymectomy if thymoma
• Eaton Lambert: treat underlying malignancy (associated with small cell lung cancer)
• ALS: antiglutamate
• GBS:IVIG
• Swallowing difficulties: OT/PT for swallowing assessment
3. Referrals
To appropriate specialty: neurology, rheumatology, endocrinology, oncology
References
1. Schere K, Bedlack RS and Simel DL. Does this patient have myasthenia gravis? JAMA 2005;293(1 5):1 906-14.

WEIGHT GAIN
2071 Ed. Authors: FirstArabesque Parker, Stephanie Mullin MD, Laurie Mereu MD FRCPC
OriginalAuthors:Arabesque Parker, Stephanie Mullin MD, Laurie Mereu MD FRCPC
Station Objective
Diagnose and classify obesity, determine if there is an endogenous cause, and manage the obese patient
Class BMI (kg/rn

)
2
Underweight < 18.5 Obese waist circumference (cm)
Healthy weight 18.5 — 24.9 Ethnicity Men Women t Waist to Hip Ratio
Europid > 94 > 80 Men > 0.9
Overweight 25 — 29.9
South Asian, Chinese > 90 > 80 Women > 0.85
Obese Class 1 30— 34.9
Obese Class 2 35 — 39.9 Japanese >85 >90
Obese Class 3 > 40
Exogenous
• t energy intake, L energy expenditure
• latrogenic (antidepressants, antiepileptics, antipsychotics, glucocorticoids, ext.)
Endogenous
• Endocrine (Hypothalamic syndrome, Cushing syndrome, Hypothyroidism, PCOS, T2DM)
• Genetic (ex. Prader-Willi)
History
ID • Age and sex
CC Obesity
HPI • Onset, duration, and amount of wt gain
• Location of wtt: generalized, central
• Eating and exercise behavior
• Assess for eating disorder or depression
• Assess readiness to change wt
• Fatigue, cold intolerance, constipation (hypothyroid)
• Easy bruising, myopathy (Cushing syndrome)
• Menstrual changes, infertility, hirsuitism (PCOS)
• Congenital dz
PSHx Bariatric surgery
• Hypothalamic surgery
Meds • Lookforcausesofwtt
FHx • Obesity
• Endocrine disorders
Social Support network for healthy eating and exercise
• Alcohol or illegal drug use
ROS CV: HTN, CAD, CHF, varicose veins, stroke
• RESP: dyspnea, sleep apnea, PE
• GI: GERD, hepatic steatosis, NAFLD, cholelithiasis, hernias
• ENDO: DM, hyperlipidemia, hyperuricemia
• MSK/DERM:OA
• CNS: idiopathic intracranial I-ITN (headache, NN, tinnitus, visual changes)
Risk Factors • Insulin resistant states, PCOS, FHx of obesity

Physical
1. Vital Signs (including BP with appropriate sized cuff —* width of cuff’s bladder 40% of arm circumference, length of cuff’s bladder
80% of arm circumference)
2. Obesity Evaluation
• ) (kg/m
BMI (wt/ht
2 )
2
• Waist circumference (measured at top of iliac crest)
• Waist-to-hip ratio (hip measured at widest diameter around the buttocks)
• General fat distribution (including moon face and dorsal fat pad —* Cushing syndrome)
3. Systemic Examination
• HEENT: thyroid and fundoscopy
• RESP:signsofCHF
• CVS: cardiomegaly, arrhythmias, and vascular bruits
• ABD: hepatomegaly and abdominal pannus
• Joints: edema, deformities, .1’ ROM associated with OA
• Skin: acanthosis nigricans, xanthomas, hirsuitism, venous stasis changes, intertrigo, purple striae
Investigations
1. Blood work
• Assess comorbidities:
• Fasting glucose
• Lipid profile (total cholesterol,TG, LDL, HDL cholesterol, total cholesterol! HDL)
• Look for endogenous causes when clinically appropriate:
• TSH
• 24 hr urinary free cortisol
• Free testosterone
Treatment
• Lifestyle modification (all BMls): nutrition therapy, physical activity, cognitive-behaviour therapy
• Pharmacotherapy (BMI 27 ÷ risk factors or 30)
• Bariatric surgery (BMI 35 + risk factors or 40)
2. Follow-up
• Regular assessment of obesity comorbidities
• Wt maintenance and prevention of wt regain
3. Referrals
• Registered dietitian
• Exercise health professional
• Psychologist or psychiatrist, if clinically indicated
• Endocrinologist for endogenous causes
References
1. Obesity Canada clinical practice guidelines expert panel. 2006 Canadian clinical practice guidelines on obesity. CMAJ 2007;1 76(8 suppl):online 1-1 17.

WEIGHT LOSS
207? Ed. Authors:Arabesque Parker, Stephanie Mu//in MD, Laurie Mereu MD FRCPC
OriginalAuthors:Arabesque Parker, Stephanie Mull/n MD, Lisa StebleckiMD MPH CCFP
Station Objective
Determine if weight loss is voluntary or involuntary, narrow the differential based on appetite change, and develop a management plan.
• >5% baseline body wt or 5 kg in <6-12 mo should always be investigated
2. Common Conditions (* indicates association with normal or increased appetite)
• Involuntary weight loss
• Decreased energy intake
• Malignancy
• HIV
• Endocrine disorder (adrenal insufficiency, hypercalcemia, DM*)
• Chronic illness (CHF, COPD)
• GI dz (dysphagia, abdominal pain, distension, nausea, malabsorption*)
• Psychiatric dz (bereavement, depression, bipolar disorder, paranoia/delusion)
• Drugs (EtOH, nicotine, opiates, cocaine, amphetamines, antiCa)
• Increased energy expenditure
• Hyperthyroidism*
• Pheochromocytoma*
• Chronic illness
• Malignancy
• Infection
• Increased nutrient loss
• Uncontrolled diabetes
• Diarrhea
• Vomiting
• Fistula tract drainage
• Voluntary weight loss
• Malignancy
History
ID • Age and sex
CC • Weight loss
HPI • Amount of weight loss (documented), onset, duration, previous weight fluctuation
• Appetite
• Voluntary wt loss (assess body image, fear of wt t, binging, purging, fasting, tphysical activity)
• Fatigue, heat intolerance, tremor, irritability (hyperthyroidism)
. Hyperpigmentation, salt cravings, abdominal pain (adrenal insufficiency)
• Polyuria, polydipsia, polyphagia (DM)
• Muscle weakness, depression, memory problems, polyuria, kidney stones (hypercalcemia)
RED FLAGS • Involuntary weight loss and constitutional symptoms (fever, chills, night sweats)
• Severe voluntary weight loss
PMHx • Malignancy
• Chronic disease
• Psychiatric disease
Meds • Review for potential causes of weight loss (antibiotics, NSAIDs, digitalis, synthroid, etc)
FHx • Chronic illness and cancer
Social • Substance use (EtOH, cigarettes, illegal drugs)
• Travel history

ROS • General: fever, night sweats, pain, masses
• RESP: dyspnea, cough, hemoptysis
• GI: NN, difficulty eating, dysphagia, anorexia, BM changes
• GU: urinary symptoms, menstrual history
• MSK I DERM: joint pain, hair loss, nail changes
• PSYCH: depression screen
Physical
i. General Approach
• Vital signs
• Measure weight and compare to previous records
• Mental status exam
2. Skin
• Pallor, jaundice, hyperpigmentation, scars from prior surgery, cancerous lesions
3. HEENT
• Oral thrush, dental disease, adenopathy, thyroid exam, parotid gland enlargement
4. Cancer screening
• DRE
• Breast/Pelvic exam
• Lymphadenopathy
5. Full CV, RESP, GI, and MSK exam
Investigations
1. Blood work
• CBC-D, electrolytes, calcium, glucose, LFTs, Cr, urea, TSH
• CXR
3. Special Tests
• Cancer screening appropriate for patient age (FOBT or colonoscopy, mammogram, pap smear, PSA)
4. Possible additional tests
• HIV serology
• ESR,CRP
• CTchest and abdomen
Treatment
• Dependent on underlying condition
• Refer patients in need of specialized care
References
1. Fauci AS, Braunwald E, Kasper DL, Hauser SL, Longo DL, Jameson L, Loscalzo J. Harrison’s principles of internal medicine. 17th ed. 2008.
Internal Medicine Edmonton Manual of Common clinical Scenarios 193

EDMONTON MANUAL
Section #4
OBSTETRICS & GYNECOLOGY
Section Editor: Sujata Chandra MD FRCSC
Residency Program Director
Department of Obstetrics & Gynecology
INTRODUCTION.. .195 lntrapartum Care. 214

• .1 II ,I II 196 Menopause 216
Antepartum Care 198 Pap Smear 218
Contraception 200 Pelvic Mass 220
Dysmenorrhea & PMS 202 Pelvic Organ Prolapse 222
Fetal Distress .204 Pelvic Pain 224
Hirsutism .206 Postpartum Complications 226
Hypertension in Pregnancy .208 Pregnancy Loss 228
Infertility .210 Vaginal Bleeding 230
Interpretation of Fetal Heart Rate .212 Vaginal Discharge 232
N.B. Not all stations in this section were reviewed by Dr. Chandra
194 Edmonton Manual of Common Clinical Scenarios Obstetrics & Gynecology

INTRODUCTION
Sujata Chandra MD FRCSC
Obstetrics and gynecology isa unique combination of medical and surgical issues that span the entire spectrum of a female’s life. This 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. 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
and whether this agrees with the menstrual dates is important. Accurate knowledge of gestational age impacts many things in Obstetrics
including timing of prenatal screening and ultrasound. It also impacts management in situations where delivery is a possibility such as in the
patient with severe preeclampsia or in the patient with preterm labour. 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 appreciate oral contraception as a “medicine” so you
must ask about this particular medication specifically. For adolescents who come in with their parents, please be sensitive to the fact that
matters related to sexual activity and contraception may not easily come out in the interview so it is important that your adolescent patient
has the opportunity to discuss obstetrical and gynecological matters with a private setting.
Most OSCE examinations will focus on history taking skills and talking through the mechanisms of a pelvic examination with a simulated
patient rather than having an actual patient. When faced with having to demonstrate a pelvic examination on a pelvic model, it is important
to mention about appropriately draping the patient and communicating with the patient on the examination.
There are several ethical and advocacy issues unique to obstetrics and gynecology that may appear on examinations. Specific areas to have
a working knowledge of 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, for most situations you encounter in obstetrics and gynecology as a medical student, you are able to manage to look after both the
mother and also assess fetal well-being.
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.
Obstetrics & Gynecology Edmonton Manual of Common Clinical Scenarios 195

AMENORRHEA
201 I Ed. Authors: Sarah Wozney, Juliette Socks MD, Jonathan Tankel MBBCh FRCSC
OriginalAuthors:Jennifer Coppens, Jonathan TankeIMBBCh FRCSC
Station Objective
Determine whether a woman presenting with an absence of regular menstruation during reproductive age is pregnant. 1• versus 2
amenorrhea must be determined to help identify a cause and manage associated complications.
• Primary: Absence of menses at age 16 with secondary sexual characteristics or no menses at age 14 with absent secondary sexual
characteristics.
• Secondary: Absence of menses in a woman who previously was menstruating for >6 months or 3 cycles; pregnant until proven
otherwise!
Pregnancy/Gestational 13-HCG, ultrasound

trophoblastic disease
Hypothalamus Anorexia/stress/systemic illness/excessive exercise
Tumor, injury, drugs, infection
Kailman’s syndrome (congenital absence of GnRH)
Pituitary Tumor (prolactinoma, acromegaly)
Hypopituitarism (Sheehan’s syndrome, empty sella syndrome, pituitary irradiation or infection)
Ovaries, Gonadal Dysgenesis Premature ovarian failure (idiopathic, infection, radiation, chemotherapy, Turner’s syndrome)
Menopause
PCOS, HAIR-AN
Other Thyroid dz, Cushing’s dz, non-classical CAH, 17 hydroxylase deficiency, androgen insensitivity
Androgen secreting tumor (adrenal or ovarian)
History
ID • Age
CC • Primary or secondary amenorrhea
HPI • Signs of pregnancy: weight gain, nausea, mood changes, etc.
• Diet, exercise, recent weight gain or loss, change in body habitus, psychological stress
• Menopausal symptoms ie. hot flashes, night sweats, mood changes, vaginal dryness
• Hyperandrogenism symptoms: hirsuitism, androgenic alopecia, acne
• Acanthosis nigricans, galactorrhea, headaches, visual changes, sx of thyroid/ Cushing’s dz
• Sexual development, pubertal milestones, tanner staging
• Menstrual hx: age at menarche, length of cycle, length of menses, LMP, dysmemorrhea, menorrhagia, PMS/moliminal
symptoms, regularity
• Sexual hx (vaginal intercourse and otherwise), contraception, dyspareunia, STI hx, possibility of pregnancy, sexual
abuse
• Reproductive hx: problems with infertility, obstetrical hx, breast feeding, failure to lactate
RED FLAGS • Virilization, visual field changes
PMHx • Radiation, chemotherapy
PSHx • Pelvic surgery: hysterectomy, oophorectomy, D & C, therapeutic abortion
PO&GHx • GTPAL, pap hx, menstrual hx, obstetrical hx, STI hx
Meds Hormonal contraception, steroid use, IUD, antidepressants, antipsychotics, chemo
FHx • Delayed menarche/ puberty, PCOS, endocrine disorders
Social • Smoking, alcohol use, recreational drug use, occupation, stressors, exercise, anabolic steroid use, relationships
196 Edmonton Manual of Common Clinical Scenarios I Obstetrics & Gynecology

physical
1. General Approach
• BR Nt, Wt, BMI, waist circumference
• Degree of sexual maturity (tanner staging)
2. Inspection
• Hyperandrogenism signs: hirsuitism, acne, androgenic alopecia
• Acanthosis nigricans, Cushing’s signs, turner’s syndrome, anorexia
3. Abdominal exam
• Masses, tenderness
4. Pelvic exam (speculum and bimanual)
• External genitalia, clitoromegaly, imperforate hymen, patent vagina, transverse vaginal septum, vaginal atrophy, cervical stenosis,
adnexal pathology, masses, presence of uterus
5. Thyroid exam
6. Breast exam
• Tanner staging, galactorrhea
7. Visual field testing
Investigations
1. Blood work
• B-HCG, estradiol, testosterone, androstenedione, DHEA-S, FSH, LH
• TSH, PRL, 17-OH-progesterone
• Transvaginal US, MRI Pelvis and! or Head
• Hysterosalpingogram, sonohysterogram, hysteroscopy if suspect uterine malformation or adhesions
3. Special Tests
• Progesterone challenge test: withdrawal bleed= anovulation, no withdrawal bleed= uterine! vaginal defect
• Karyotype
• 24 hour urine cortisol or dexamethasone suppression test
Treatment
1. Treat according to the underlying cause of the amenorrhea
2. Treatment options
• General: wt increase! decrease, exercise control, adequate diet and nutrition, stop causative medications
• Medical: combined OCP or HRT- induces thelarche with estrogen before combined OCP in px with absent breast development;
bromocriptine
• Surgical: correct anatomical abnormalities
• Intravenous pyelogram for px with mullerian dysgenesis
3. Follow-up regarding associated complaints and risk factors
• Infertility, hirsutism, endometrial hyperplasia, wt decrease, osteoporosis, DM, heart dz, HTN, hyperlipidemia, metabolic syndrome,
smoking cessation, mental illness
4. Referrals as needed to endocrinology, gynecology, obstetrics, neurosurgery, psychiatry
References
1. Alexander CJ, Mathur R, Laufer LR, Azziz R. Amenorrhea, Oligomenorrhea, and Hyperandrogenic Disorders. In: Hacker NF, Gambone JC, Hobel CJ, editors.
th Edition. Philadelphia: Saunders Elsevier Inc; 2010.
Hacker and Moore’s Essentials of Obstetrics and Gynecology. 5
2. Seminara SB, Hall JE. Amenorrhea. In: ACP PIER & AHFS D1 EssentiaIs’. Philadelphia: American College of Physicians; 2009
3. Hall JE. Normal and Abnormal Menstruation. In: Federman DD, Nabel EG, editors. ACP Medicine. New York: BC Decker mc; 2009
Obstetrics & Gynecology I Edmonton Manual of Common Clinical Scenarios 197

ANTEPARTUM CARE
20!! Ed. Authors: SomoptiSomopti
OriginalAuthors:Jackie Clayton, Jason WeatheraldMD, Roger W Turnell PhD MDCM MCEd FRCSC
Station Objective
In this station you will be responsible to discuss prenatal care in order to achieve optimal pregnancy outcome.
History
ID Age, GTPAL, ethnicity, GA
CC Possible pregnancy, first prenatal visit or ongoing prenatal care
HPI • Initial prenatal visit (6-10 wks GA):
• Establish EDC based on first day of LMP, determine nature of menstrual cycles (regularity & duration)
• Naegle’s rule: 1 ‘ day of LMP + 7days 3mo ± days above/below 28 day cycle, send for early U/S if date unsure
—
• Planned or unplanned pregnancy, tactfully assess desire to continue with pregnancy, assisted conception,
contraceptive use, breastfeeding or interval since last pregnancy,
• Sx of pregnancy: amenorrhea, breast tenderness, N/V, fatigue, urinary frequency
• discuss pregnancy blood work (see investigations below)
• Subsequent prenatal visits:
• Inquire about pt’s well being
• Assign GA
• 4 cardinal symptoms: fetal movement (at 18-20 wks), abdominal pain, gush of fluid, bleeding
RED FLAGS • Absence of fetal movement, bleeding, pain with cramping
PMHx HTN, DM, HIV, SLE, bleeding disorders, measles, chicken pox, spina bifida
PSHx • C-sections, anesthetic problems, abdominal, pelvic or cervical surgery
PO&GHx • Previous pregnancies: date of delivery, GA reached, delivery type, gender, birth wt., complications during
pregnancy, delivery or postpartum for mother or infant, child’s health, abortions (spontaneous or therapeutic)
• Date of last pap smear, abnormal pap smears & outcome
• Previous or currently at high risk of STI
Meds Folic acid, prenatal vitamins
• Teratogens: ACEi, warfarin, tegretol, isoretinoin (N.B. not complete list)
Allergies Medication/environment and nature of reaction, especially analgesics
FHx • HTN, DM, multiple gestation, still birth, chromosomal or genetic abnormalities
Social Occupation (mother, father, and those at home)
• EtOH, smoking, drug abuse
• Partner information, current living situation, safety at home (domestic violence)
• Diet, caffeine, exercise
ROS CV: varicose veins, edema
• GI: NN, heartburn, hemorrhoids, constipation
• GU: dysuria, nocturia, frequency
Risk Factors Age <17 or >35, HTN, DM, multifetal gestation, placenta previa, poor or lack of prenatal care
Expected Weigth Gain by starting BMI

Physical BMI <20: 12.5 18kg
—
General Approach BMI 20-27: 11.5-16kg

• Initial visit require a complete physical exam: BMI>27:7-11.Skg
• Measure baseline BMI
• BP, HR, HEENT, breast, RESP, CV, abdo, reflexes, varicosities/extremities, perineal/pelvic exam
• Measure wt & BP: expected wt gain varies based on starting BMI
2. Palpation
• SFH: pubic symphysis to uterine fundus (±2cm of GA at 20-37 wks), plot SFH on prenatal growth curve
• Fetal position (starting at 28-32 wks): systematic palpation of abdomen to determine lie/presentation of fetus, confirm
presentation of fetus at 36 wks
3. SpecialTests
• Determine FHR (starting at 12-14 wks) using doppler U/S

Note: DO NOT do a pelvic speculum exam in a pregnant woman with vaginal bleeding without an U/S to confirm the position of
the placenta (and r/o placenta previa)
Investigations
i. Blood work
• Confirmation of pregnancy: serum 13-hCG
• Initial visit (6-10 weeks):
• Routine: CBC, ABO/Rh, blood antibodies, HB5Ag, syphilis serology, HIV serology, rubella titre, varicella immune status
• Optional: explain maternal aneuploidy screening (FTCS-NT at 11-1 3wks and QUAD screen at 1 5-20wks), maternal serum
screen: AFP, unconjugated estriol, 3-hCG ± inhibin A, U/S for NT
• 24-28 wks: CBC, gestational DM screen, syphilis serology, ABC/Rh & antibodies (if Rh negative)
• U/S:
• 8-12 wks: dating U/S if unsure of dates
• 11-13 wks: FTCS-NT if appropriate
• 18-20 wks: routine for fetal anatomy and growth, placental position, multiple gestations
3. Special Tests:
• Initial visit: urine R&M, C&S, pap smear, vaginal/cervical cultures including GC/Chlamydia
• Subsequent visits: urine dipstick for protein/glucose
• 36 wks: GBS vaginal anal swab
Treatment
1. Identify Pt at high risk of pregnancy complication (see Risk Factors on previous page)
• Nutrition: prenatal vitamin, folic acid 0.4 mg/day, Ca 1500 mg/day
• constipation: dietary modification (increase fiber/water), bulk-forming agent (Metamucil °), stool softeners
• heartburn: avoid lying down after meals, elevate head of bed, calcium carbonate antacids
• NN: small frequent meals, avoid triggering foods, Diclectin (Vitamin B6/doxylamine)
• Rh (-): Rh IgG 300 mcg routinely at 28 wks and with episodes of antepartum hemorrhage
• 3. Follow-up (using provincial prenatal visit guidelines):
• <28 wks GA: visits every 4 wks
• 28-36 wks GA: visits every 2 wks
• >36 wks GA visits every 1 wk
3. Referrals:
• Obstetricians: high risk pregnancy (multiple gestation, complex maternal and fetal conditions)
• Emergent: fetal distress, hemorrhage
References
1. Publichealth.gc.ca (Internet]. Ottawa: Public Health Agency of Canada; [updated 2009 Oct 08; cited 2009 Oct 201. Available from: http://www.phac-aspc.
gc.ca
2. Hacker NF, Moore JG, Gamborne JC. Essentials of Obstetrics and Gynecology. 5th ed. Philadelphia: Elsevier Saunders; 2010.
3. Alberta Prenatal Record [Online] Accessed on Jan 6,2010. URL:http://www.aphp.ca/pdf/HS0001-125%2oFinal(200909)%20(3).pdf

CONTRACEPTION
Victoria Cook BSc MSc, Juliette Sacks BA BSc MD, Peggy Sage MSc MD FRCSC
Station Objective
Describe available contraceptive measures, discussing risks and benefits of each, and determine any relative or absolute contraindications
to the use of hormonal contraceptives. If the patient desires permanent contraception (sterilization) establish level of commitment and
understanding of options. Outline surgical and medical risks.
Histo y
ID Age and gender
CC • Patient wants to learn about contraceptive options
Sexual Hx Previous and present use of contraception
• Sexual orientation and practices
• Present and past number of partners, concurrent partners
• Relationship monogamous, healthy, age of partner (consider for very young patients and note the
—
legal age of consent in province of practice)

• STIs present and past
• Vaginal discharge
• Labial sores/lesions
• Pelvic pain, previous PID
• Possibility of current pregnancy
PO&GHx • Menarche
• Menstrual cycle length of period, regularity, amount of bleeding
—
• Premenstrual syndrome
• Dysmenorrhea, pelvic pain
• Previous gynecological procedures
• Previous pap results, date of last pap and pelvic exam
• Past pregnancies (including abortions) and deliveries, any abnormalities or complications
• 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 (Table 1)
PMHx HTN
• Liver disease
• Thromboembolic disease
• Cancer: breast, uterine, ovarian, liver
• Migraines (especially with neurological findings, aura)
Meds Note antibiotics, anticonvulsants and antacids (interfere with OCP efficacy)
FHx Cancer: breast, uterine, ovarian, liver
Social • Smoker
• EtCH
• Drugs
ROS HEENT: headaches (as mentioned above)
• CV, RESP, GI, GU, MSKJDERM
Risk Factors Smoking, other contraindications (Table 1)
Physical
General Approach
• Vitals: HR, BR BMI
• Competence
Special Tests
• Exclude presence of pregnancy
• Pelvic examination (speculum and bimanual) if suspicion of STI or PID (may defer if not sexually active)
• Pap test if indicated (patient meets screening criteria, see’Pap Test’ section)

nveStigatiOflS
i. Radiology/Imaging
• Order U/S if patient pregnant or if pelvic anatomical abnormalities are suspected
2. Special Tests
• STI testing chlamydia, gonorrhea, syphilis
—
ii. Absolute and Relative Contraindications to contraceptive measures1

Method Absolute contraindication Relative contraindication
jj5 Pregnancy Previous ectopic pregnancy
Abnormal vaginal bleeding Diagnosed STI in 3 months prior to IUD insertion
Cervical, uterine or salpingeal infection Anatomical abnormality of the uterus and/or presence of
Copper allergy or Wilson disease (copper IUD) fibroids
Current breast cancer (IUD with progesterone only) Current dysmenorrhea or menorrhagia (IUD with
progesterone only)
Combined Previous PE, CVA, DVT Fibroids
estrogen-progestin CAD Lactation
contraceptives Smoker >35 years Diabetes mellitus
Breast or endometrial cancer Controlled HTN
Abnormal vaginal bleeding Asymptomatic hepatic disease (i.e. early Hep C with no
Abnormal liver function changes in LFTs)
Pregnancy Migraines (without aura)
Severe hypercholesterolemia Seizure disorder
Severe hypertriglyceridemia Elective surgery (or long periods of bed rest)
Uncontrolled HTN Difficulty taking medications consistently
Migraine headaches with aura
p
p
Inherited thrombophilia
Complicated valvular heart disease
Progesterone-only Pregnancy Depression
contraceptives Severe hypercholesterolemia
Severe hypertriglyceridemia
Treatment
Emergent Table 2. Methods of Contraception
• Treat STI or PID if tests positive or high clinical index of Non-permanent Hormonal
suspicion Oral (combined estrogen and progestin),
2. Treatment Options progestin only)
• Outline methods of contraception (Table 2), risks of failure, Injectable (Depoprovera)
complications and drug interactions Transdermal
• Discuss efficacy, convenience, duration of action, reversibility Post-coital
and time to return of fertility, risk of adverse events, effect on Vaginal ring
uterine bleeding, STI protection and cost Barrier
• Counsel regarding adjustment ofOCP if missed pill, and state Diaphragm
that OCP + barrier method leads to reduced risk of HIV and STI Caps
transmission Condom (male and female)
• Consider progestin only pills (Micronor) as an alternative OCP IUD (Mirena or copper)
option in patients who are either diabetic or breastfeeding, or Abstinence
who smokers >35 who desire OCP option; stress necessity of Natural
taking progestin only pills at set time each day Rhythm
• Offer alternative forms of hormonal contraception (patch, Withdrawal
vaginal ring) if compliance is an issue Breast feeding
• Discuss correct usage of selected form of contraception
Permanent • Male Sterilization
• If interest in surgical sterilization, discuss failure rates and
• Female Sterilization
potential complications of both male and female procedures;
review awareness of permanency of procedures (regret rate is 30%) and make appropriate referral if desired
3. Follow-up
• For IUD, provide prescription and book appointment for insertion, ideally during the next menstrual cycle
• If new OCP prescription, book follow-up in 3 months
• For IUD insertions, book follow-up 4-6 weeks after procedure to check strings
References
1 Callahan T, Caughey AB. Blueprints obstetrics and gynecology, 5” ed. Baltimore: Lippincot Williams & Wilkins; 2009.
2. Hacker NF, Hobel Ci. Hacker and Moore’s essentials of obstetrics and gynecology, 5
th
ed. Gambone JC, editor. Philadelphia: Saunders; 2010.

DYSMENORRHEA & PMS
20? I Ed. Authors: Sarah Wozney, Juliette Sacks MD, Jonathan TankelMBBCh FRCSC
OriginalAuthors: Jennifer Cappens, Jonathan TankeIMBSCh FRCSC
Station Objective
In dysmenorrhea, or painful menstruation, it is important to differentiate primary (within the first 2 to 3 years of menarche, with regular
ovulatory menstruation) from secondary dysmenorrhea (caused by pelvic pathology).
PMS Affective and somatic Sx during the luteal phase for 3 consecutive cycles.
• Sx do not occur at other times of the cycle
• Sx interfere with daily life and/or relationships
PMDD Severe form of PMS with specific DSM-IV diagnostic criteria
1° dysmenorrhea- Onset generally within first 2-3 yrs of menarche
idiopathic- no pelvic Crampy pain strongest over lower abdomen with radiation to inner thighs/ back
pathology • Begins within a few hrs of onset of menstruation, lasting 48-72 hrs
• Ddx: Uterine contractions, ovarian cyst torsion, endometritis, PID, pregnancy complication, cystitis,
ureteral stone, gastrointestinal (appendicitis, etc)
20 dysmenorrhea Pain is less related to the first few days of menses, more likely premenstrual or postmenstrual symptoms
• Onset is usually in 30-40 year old age group
• DDx: Endometriosis (up to 70% of women who present with chronic pelvic pain), Adenomyosis, fibroids,
ovarian cyst, pelvic congestion syndrome, lactose intolerance, IBS, non-communicating horn of a
bicornuate uterus, cervical occlusion! stenosis, foreign body, infection, PID, transverse vaginal septum,
pregnancy_complication (need to rule out an ectopic)
2. Common Lonaitions:
PMS, 1 Dysmenorrhea, Endometriosis
History
ID Age
CC Pain with menses, mood changes, physical sx prior to menses
HPI Menstrual hx: LMP, menarche, length of cycle, length of menstruation, amount of bleeding, clots, regularity
• Affect on function: occupation, interpersonal relationships, socially
• Sexual hx: # of partners, practices, STI hx, pregnancy risk
• DYSMENORRHEA:
• Onset and timing of pain in relation to menses
• 1° dysmenorrhea: onset is in first few hrs of menstruation, frequently associated with prostaglandin Sx (change in
BM, nausea), is pain related to ovulation and does it recur prior to menstruation
• 2° dysmenorrheal: pain (not limited to menses), Sx vary by etiology
• OPQRST, therapy tried
• Menstrual Hx: menarche, length of cycle/menses, amount of bleeding, moliminal Sx, premenstrual spotting,
diarrhea premenstrually
• Associated Sx: discharge, pruritis, dysuria, dyspareunia, AUB, infertility, changes in bowel movements, nausea,
fatigue, dizziness, headache
. Reproductive history: PO&GHx, infertility, contraceptive use, sexual Hx, STI Hx
• PREMENSTRUAL SYNDROME:
• Affective Sx: depression, irritability, mood lability, anxiety, confusion, social withdrawal, difficulty concentrating,
feeling overwhelmed, sleep disturbance, change in appetite
• Somatic Sx: breast swelling/tenderness, bloating, headache, edema, wt f
• Onset, timing and severity of Sx, do they occur unrelated to menses
• Menstrual Hx: menarche, length of cycle/menses, amount of bleeding, dysmenorrheal
• Dyspareunia, contraceptive use
RED FLAGS . DYSMENORRHEA: if does not appear to be 1 °dysmenorrheal by clinical presentation or if treatment for 1° not
resolve pain, further investigation is warranted
• PMS: Sx 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 Ca, infertiligy, depression/ neuropsychiatric disorders
Social Smoking, EtCH, recreational drug use
• Occupation, family life, stressors, Hx of abuse, piercings
Risk Factors Major Depression, 1 Dysmenorrhea: age (adolescent), early menarche, menorrhagia
Physical
1. General Approach
• Vitals, Ht, Wt, BMI, waist circumference
2. Abdominal Exam
• Masses
3. Pelvic Exam
• External genitalia, speculum, bimanual (check for masses)
• Not required for mild 10 dysmenorrheal in adolescent who has never engaged in sexual activity
Investigations
1. Charting PMS Sx
• Transvaginal US if suspect 20 dysmenorrhea
3. SpecialTests
• Pap smear, vaginal and cervical swabs, urine NAAT for C. trachomatis and N. gonorrhoeae
• Laparoscopy if suspect endometriosis if px wants dx and pain is not controlled
Treatment
PMS/PMDD • Reassurance, diet, exercise, stress ..L, sleep hygiene, stop tobacco/ETCH/drugs
• Continuous use of combined OCP, 24-4 dosing of combined OCP
• SSRI: fluoxetine, sertraline, paroxetine taken during the luteal phase, CBT
• Sx specific —buspirone, calcium carbonate, spironolactone
1° dysmenorrhea • General reassurance that the condition is common

• NSAIDs to decrease inflammation and pain, hormonal contraception: atrophy of endometrium- decrease
prostaglandins, reduce menstrual flow (OCP, mirena, depo-provera)
• High frequency TENS, acupuncture, psychotherapy, heat for symptomatic tx
2° dysmenorrhea • Treat the underlying cause as indicated, GnRH analogues
• Can try treatments for 10 dysmenorrhea for symptomatic relief
2. Follow-up
• If px 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.)
3. Referrals: Gynecology, Psychiatry, Pain Management Clinic, Pelvic Floor Physiotherapy +I Acupuncture
References
1. Laufer LR, Gambone JC. Menstrual Cycle-Influenced Disorders. In: Hacker NF, Gambone JC, Hobel Ci, editors. Hacker and Moore’s Essentials of Obstetrics
and Gynecology. th
5
Edition. Philadelphia: Saunders Elsevier mc; 2010.
2. Rapkin AJ, Gambone JC. Pelvic Pain. In: Hacker NF, Gambone JC, Hobel CJ, editors. Hacker and Moore’s Essentials of Obstetrics and Gynecology. 5
th
Edition.
Philadelphia: Saunders Elsevier mc; 2010.
3. Berga SL, McCord JR, Spencer JB. Premenstrual Syndrome. In: Feclerman DD, Nabel EG, editors. ACP Medicine. New York: BC Decker mc; 2009.
4. Hall JE. Normal and Abnormal Menstruation. In: Federman DD, Nabel EG, editors. ACP Medicine. New York: BC Decker mc; 2009
5. Pearlstein T. Premenstrual Syndrome. In: ACP PIER & AHFS D1 Essentials’°. Philadelphia: American College of Physicians; 2009
6. Lefebvre G, Pinsonneault 0, Antao V, Black A, Burnett M, Feldman K, Lea R, Robert M; SOGC. Primary dysmenorrhea consensus guideline. J Obstet
Gynaecol Can. 2005 27(1 2):1 117-46.

FETAL DISTRESS
201 I Ed. Authors:Jessica Nicoll, Jeff Campbell MD,
OriginalAuthors:JenniferCoppens, Jonathan TankelMBBCh FRC
Station Objective
Fetal distress is of inadequate fetal oxygenation ranging from hypoxemia to acidosis. Identification and management of fetal distress is an
essential part of pregnancy care. The assessment of fetal status must take the entire clinical picture into account. It is important to determine
the cause of fetal distress, treat underlying or reversible conditions, and determine whether delivery is appropriate.
Fetal Heart rate> 160 bpm, lack of FHR variability, late decelerations, prolonged decelerations, fetal pH < 7.10, BPP = 4 high
probability of fetal asphyxia and BPP =2 fetal asphyxia
Placental insufficiency DM, maternal BP abnormalities, anti-phospholipid antibody, abruption, previa, postterm gestation —
Maternal factors • Maternal Age (very young/old)

• Maternal Systemic Illness
• Uncontrolled HTN, hypotension, DM, severe anemia, infection, seizures, autoimmune disease anti
phospholipid antibody, pulmonary, cardiac, renal, thromboembolic, thyroid disease,
• Uterine tetanic contractions or hyperstimulation
• Extremes ofBMI
• Assisted reproductive technologies
• Premature rupture of membranes
• Trauma
Fetal factors TORCH infection, acidosis, embryonic anomaly, IUGR, Premature labor, Postterm pregnancy, Twin-twin
transfusion,_multiple_gestation_oligohydraminos,_polyhydramnios
Cord compression • Cord problems: true knot, nuchal cord prolapse, vasa previa, short cord, hematoma
3. High mortality:
• Maternal:
• DM, HTN, infections, antiphospholipid Abs, Thrombophilias, Fetomaternal hemorrhage
• Fetal:
• TORCH infections, congenital anomaly, cord compression, erythroblastosis fetalis
History
CC fetal movements, non-reassuring fetal heart rate (NST) or BPP, decreased SFH or IUGR
HPI • GA, vaginal bleeding, contractions/cramping, leak of fluid, meconium, GBS status, Rh status, multiple
gestation
• Fetal Movements: how is mother doing the fetal movement count (quiet room, lying on side)
• Maternal Symptoms of infection, systemic disease
RED FLAGS • Fetal Movements: Less than 6 movements in 2 hrs, non-reassuring fetal heart rate, smaller than
expected SFH
PMHx • DM, HTN, HIV, HTN, DM, thyroid disease, GI disease, infections during the pregnancy and history of
STIs, thrombophilias, other chronic disease
PSHx • C-section, pelvic or abdominal surgery, need for any blood transfusions post op
PO&GHx • GTPAL. GA at delivery, type/complications of delivery, wt of baby, complications with the pregnancy:
IUGRIHTN/pre-eclampsia/placental_insufficiency!_umbilical cord_complications.
Meds • Insulin, metformin, antihypertensive medications, anti-coagulants
FHx • Of fetal or maternal RFs listed
Social • Smoking, EtOH, recreational drugs, stress

ROS HEENT: Diabetic Retinopathy
• CV: Dizziness, decreased exercise tolerance, fatigue and decrease energy
• RESP: Cough, wheezing, pharyngitis, shortness of breath
• GI: Diarrhea, vomiting, constipation,
• CU: Diabetic nephropathy, vaginal discharge, vaginal irritation
• MSK / DERM: Arthritis, butterfly rash, petechaie
Risk Factors Previous pregnancy: HTN, placental abruption, IUGR or stillbirth
• Current pregnancy: post term, HTN, DM, preterm prelabour rupture of membranes, preterm labour,
chronic abruption, iso-immunization, morbid obesity, advanced maternal age, vaginal bleeding, IUGR,
‘ fetal movements, abnormal maternal serum screen, assisted reproductive technologies, multiple
pregnancy, suspected_oligo/polyhydramnios,_smoking
Physical
1. General Approach
• Ask permission to do the exam, wash hands
• Maternal vitals BP, HR, RR, Sp0
— ,T
2
• Weight and weight gain
2. Inspection
• Cervical dilation, effacement, fetal position
3. Palpation
• Leopold’s maneuver, SFH
I
Investigations
1. Blood work
• CBC-D, blood culture, type and screen, electrolytes, urea, Cr, blood glucose and protein
• Depends on maternal clinical presentation (pre-eclampsia workup if pt is hypertensive, symptomatic)
2. Urinalysis
• Blood glucose and protein
• Doppler ultrasound
4. Special Tests
• Non stress test, BPP, Contraction stress test, fetal pH, vaginal fluid test for amniotic fluid, amniotic fluid test for pulmonary
maturation
Treatment
1. Emergent
• Lying mother in the left lateral position, urgent delivery if term or post term
• Medical-Treat underlying medical conditions, consider betamethasone if preterm
• Surgical- Cesarean section
3. Follow-up
• Fetal movement counting
• High risk pts require referral to specialist with t monitoring of pregnancy
4. Referrals
• Obstetrics and gynecology, maternal fetal medicine
References
1 Hacker NF, Gambone JC, Hobel CJ, editors. Hacker and Moore’s Essentials of Obstetrics and Gynecology. 5’’ Edition. Philadelphia: Saunders Elsevier lnc;
2010.
2. Liston R, Sawchuck D,Young D, Society of Obstetrics and Gynaecologists of Canada. British Columbia Perinatal Health Program. Fetal Health Surveillance:
Antepartum and Intrapartum Consensus Guideline. J Obstet Gynaecol Can. 2007 29(9 Suppl 4):S3-56.fs;G
3. Decherney A.H, Nathan L, Goodwin T.M, Laufer, N. Current Diagnosis and Treatment: Obstetrics and Gynecology, 1 0 t1 Edition.
United States: McGraw-Hill
Companies, nc; 2007.
4 Coppens, J, Tankel, J. Fetal Distress. In: Approach to the OSCE: The Edmonton Manual of Common Clinical Scenarios. 1st Edition. Edmonton: University of
Alberta Medical Student’s Association; 2010

HIRSUTISM
201? EdAuthors: Cassandra 1-lirt, Amanda Aiken MD, Janathan TankeIMBBCh FRCSC
OriginalAuthors:JenniferCappens, Cathy Lu MD, Janathan TankelMBBCh FRCSC
Station Objective
Hirsutism is excessive terminal hair growth in a male distribution pattern. It may be accompanied by other signs of virilization/
hyperandrogenism, work-up is required.
Differential Diagnosis Area of Hair Growth
Terminal Hair In Male Pattern Terminal Hair: Non Sexual Pattern
• Terminal hair in android
pattern Hirsutism Hypertrlchosls
2. Common Cause:
• PCOS
Drag Ideopatlilc/ SystemIc Illness:
• Idiopathic PCOS (83%) IdIopathic Familial Rarer
Familial Hypothrold,
• Familial Regular menses anorexia/
2/3 Rotterdam
and iQ. inc in malnutrition
• Drugs criteria:
orc androgens
A.) Polycystic ovaries
3. High Mortality/ Morbidity: on U/S
• Adrenal or Ovarian e,l OIigo/amenorrhea
Drug: Other:
C.) Signs ot .Thyrold condition
neoplasm hyperandrogenism Anabolic Steroids •llyperprolactinemla
• Anorexia Adrenal Danazol
.
• Terminal Hair: coarse, curly, Cushing Syndrome- CAH Androgen-secreting
pigmented increased ACTH production, 17-OH-progesteronase def. Adrenal/Ovarian
(+) Dexamethasone HAIR-AN: adenoma
Suppression Test Hypendrogenism, Insulin Rare, rapid onset,
Resistant, and Acanthosis severe symptoms,
Nigricans
incresed DHEA-S
Non ClassIcal CAH
History
ID • Age, sex
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 t/.J, change in fat distribution (android vs gynoid)
• Moderate to severe Acne, andrenarche, puberty
RED FLAGS . Acute onset, rapid progression with other signs of virilization or cushingoid dz:
. Androgenic alopecia, deepened voice, 1’ muscle bulk, clitoromegaly
PMHx • T2DM/Glucose intolerance, HTN, dyslipidemia, CVD
• CAH, Cushing or thyroid dz, Adrenal/ovarian tumor
PO&GHx • Menstrual/obstetrical/infertility Hx
• Menstrual cycle: age of menarche, oligo/amenorrhea, cycle/menses length, molimial Sx
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, etoclopramide, methyldopa, reserpine
Social • Anabolic steroid use, smoking, EtOH, recreational drugs
Risk Factors • FHx of excessive hair growth, obesity

physical
1. General Approach
• Vital signs, BP, BMI, waist circumference
• Establish presence of hirsutism (vs hypertrichosis- excessive hair growth) and look for other signs of hyperandrogenism
• Temporal hair recession, oily skin, deepened voice, well dev. muscles, clioroal enlargment, irregular periods
• Hair growth: location (abdomen, lip, chin, chest, back), quality of hair, degree of hirsutism, male pattern
• Dermatological changes: acne, acanthosis nigricans, striae, bruises Hyperandrog.....
• Signs of endocrine dz: thyroid, Cushingoid, hyperprolactinemia (galactorrhea) Temporal hair recession
GU Exam Oily skin
2.
• Speculum and bimanual pelvic exam Deepened voice
• Look for clitoromegaly and adrenal pathology. Well developed
ABD exam palpate for masses muscles
3. —
Thyroid exam Clitoroal enlargement

4.
Ferriman Gallwey Scoring system for hirsutism (rarely used clinically) Irregular periods
5.
Investigation
1. 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)
• Pelvic U/S for suspected polycystic ovaries or ovarian tumor
• CT/MRI for suspected adrenal neoplasm or pituitary adenoma
3. SpecialTests
• 24 hour urine cortisol or dexamethasone suppression test if suspect Cushing syndrome
Treatment
• General: treat underlying disorder (ie surgical removal of tumor)
• Wt J, exercise, proper nutrition
• Mechanical: hair removal treatments such as shaving, electrolysis, laser hair removal (consider cost)
• Pharmacological: Tx dependent on etiology
Combined OCP Spironolactone Flutamide Metformin
GnRH agonists Cyproterone acetate Finasteride Glucocorticoids
2. Follow-up
• Regarding associated risk factors or complaints: infertility, AUB, endometrial hyperplasia, wt , DM, CVD, HTN, hyperlipidemia,
metabolic syndrome, and smoking cessation
3. Referrals
• Endocrinology or Gynecology if signs of virilism, Cushing’s dz, or hyperandrogenism
References
1. SQGC Clinical Pracice Guidelines: Hirsutism: Evaluation & Treatment, 2002.

HYPERTENSION IN PREGNANCY
201 I Ed. Authors: Gabriela Pelinsko, Christina Kerr MD, Roger W Turnell PhD MDCM MCEd FRCS
Station Objective
Ten (10%) of pregnancies are complicated by hypertension. In this station you will classify hypertensive disorders of pregnancy (HDP) and
use a focused history and physical exam to diagnose and treat HPD.
• Diastolic BP of 90 mmHg, based on the average minimum 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 weeks gestation
A. Essential • Primary HTN
B. Secondary • Renovascular HTN, renal parenchymal dz, pheochromocytoma, Cushing’s syndrome
Pre-existing HTN & • After 2Owks gestation
preeclampsia Resistant HTN OR new or worsening proteinuria OR one or more adverse conditions
Gestational HTN • Develops after 20 weeks
A. Without preeclampsia • 24hr urine protein excretion <0.3g/d. No adverse conditions.
B. With preeclampsia With proteinuria (24hr urine protein excretion >3gId) OR one or more adverse conditions.
Severe preeclampsia • Onset <34 weeks & proteinuria (3-5g/d in 24hr urine OR one or more adverse conditions.
HELLP • H Hemolysis, EL elevated liver enzymes, LP low platelet count
— — —
•. . .
- Adverse Eonditio,s -
• SBP>l6Omm Hg • Severe nausea/vomiting • HELLP

• DBP>llOmgHg • EpigastricorRUQ pain/tenderness Placental abruption
• Proteinuria >5g/24hr • Elevated AST, ALT or LDH • IUGR
• Convulsions Serum albumin <20g/L • Oligohydramnios
• New/unusual headaches Thrombocytopenia (platelets <100,000 • Absent or reversed umbilical artery
• Visual disturbances /L)
x 10
9 end diastolic flow
• Pulmonary Edema • Elevated serum creatinine • Intrauterine fetal death
• Chest pain/SOB • Oliguria (<500 ml/24hr)
2. Etiology:
• Cause unknown, but several theories: Abnormal trophoblast invasion leading to endothelial dysfunction (imbalance of
vasodilatory and vasoconstrictor prostaglandins causing vasospasm), placental ischemia, abnormal hemostasis.
3. Prevalence:
• Approximately 1% of pregnancies are complicated by pre-existing hypertension, 5% to 6% by gestational hypertension without
proteinuria, and 1% to 2% by preeclampsia.
History
ID • Age, GTPAL, GA, blood type and Rh status, GBS status, EDD (whether established by LMP or U/S), LMP if known, HIV/
Hep B status
CC • Hypertension (HTN)
HPI Onset of HTN (whether> 20wks gestation)
• Prenatal care received, pregnancy complications, U/S findings
• Cardinal obstetric sx’s: contractions, leaking of fluid, vaginal bleeding, fetal movement
• Pain: OPQRST
RED FLAGS • Irritability, somnolence, visual disturbances (scotomata), frontal H/A, dyspnea &Ior chest pain, n/v, epigastric./RUQ
pain, seizures, urine output, edema, weight g, bleeding
PMHx • Medical dz (HTN, DM, cardiac, renal, thyroid, asthma, thrombophilias, connective tissue dz)
PSHx • C-Sections, abdominal or pelvic surgeries
PObsHx • Previous pregnancies: date, GA reached, delivery type (SVD, C/S, use of vacuum/forceps), complications (in
pregnancy, delivery or postpartum), gender, 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
208 Edmonton Manual of Common Clinical Scenarios Obstetrics&Gynecology

Meds Prescription, OTC, prenatal vitamin
Allergies Medication/environmental, note specific reaction
FHx HTN, DM, history of gestational HTN/preeclampsia
Social • Occupation, current living situation, information about partner, domestic abuse
• Recreational drugs/alcohol/smoking during pregnancy
Risk Factors • Demographics: maternal age 4oyrs, lower socioeconomic status, ethnicity: Black, South Asian
• Previous preeclampsia, anti-phospholipid antibodies, heritable thrombophilias, pre-existing medical dz (HTN, renal
& DM), BMI>35, multiple pregnancy, primigravida, inter-pregnancy interval> 1 Oyrs, family hx of preeclampsia, new
partner
Complications
• Maternal: stroke (high risk if sBP 1 60 mmHg), seizure, DIC, HELLP, pulmonary edema secondary to left ventricular failure, acute
kidney failure and hepatic dysfunction.
• Fetal: abruption, oligohydramnios, IUGR, prematurity, stillbirth.
Physical
1. General appearance & vitals (maternal: HR, BP, RR, Sp02, temperature & fetal heart rate)
2. HEENT: cranial nerve exam, fundoscopy (papilledema)
3. CV: assess heart sounds, 53/54
4. Respiratory: air entry, crackles (pulmonary edema)
5. Abdominal: epigastric/RUQ pain, SFH, Leopold’s maneuvers
6. Neurologic: reflexes (hyperreflexia, clonus)
7. Dermatologic: petechiae, pitting peripheral edema
Investigation
1. Blood work
• Hemoglobin, WBC, platelet count ( in HELLP), INR & PT1 fibrinogen (-.1- in DIC), creatinine & uric acid (for renal insufficiency),
glucose, liver enzymes: AST, ALT (t in HELLP), blood film & LDH (t in hemolysis), albumin, bilirubin, urinalysis, proteinuria (0.3g/d
in a 24-hr collection or 30 mg/mmol urinary creatinine in a spot sample.
2. Imaging
• Fetal monitoring: Non-Stress Test (baseline, variability, accels, number and description of decels).
• BPP with deepest amniotic fluid pocket, estimated fetal weight & umbilical artery doppler for increased resistance, absent or
reversed end-diastolic flow.
Treatment
1. Gestational HTN without preeclampsia: bed rest in left lateral decubitus, fetal surveillance, monitor for progression.
2. Severe HTN or preeclampsia: stabilize and deliver, maternal monitoring: neurovitals qi h, U/O qi h, U/A qi 2h, type & screen, repeat blood
work q6-8h, continuous fetal monitoring.
• Treatment for HELLP: consider ordering blood products, including platelets, when platelet count is < 50x 1 0A9/L.
3. Antihypertensive therapy: for sBP>1 60mm Hg and dBP>1 10mm Hg. GOAL: For women with no comorbidities, therapy should be used
to keep sBP within 130—155 mmHg and dBP from 80—105 mmHg.
• Labetolol: Start with 20 mg IV; repeat 20—80 mg IV q 30mm, or 1—2 mg/mm, max 300 mg (then switch to oral)
• Nifedipine: 5—10 mg capsule every 30 mm OR 10 mg PA tablet every 45 mm (max: 80 mg/day)
• Hydralazine: Start with 5 mg IV; repeat 5—i 0 mg IV every 30 mm, or 0.5—10mg/hr IV, (max: 20mg IV)
4. Anticonvulsant therapy: increases seizure threshold.
• MgSO4 4g IV bolus over 20 mm, then IV 2g/hr
• Monitor for Mg toxicity (DTR’s, RR, CNS depression). Antidote:Calcium gluconate 1 OmL of 10% sol’n over 2 mm
5. Antenatal corticosteroid treatment: for all women who present with preeclampsia before 34 weeks GA.
• Betamethasone 12mg IM every 24 hrs for 2 doses
6. Follow-up
• BP should be measured during the time of peak postpartum BP, at three to six days after delivery.
• Gestational HTN usually resolves by 6 weeks postpartum, but women with severe preeclampsia may remain hypertensive for up
three to six months.
References
1. SOGC. Diagnosis, Evaluation and Management of the Hypertensive Disorders of Pregnancy. Journal of Obstetrics and Gynecology of Canada. March 2008
(Vol 30, no 3).

IN FERTILITY
20!? Ed. Authors: Samopti Samapti

OriginalAuthors: Holly Kamitakahora, Juliette Sacks MD, Catherine Flood MD FRCSC
Station Objective
Elicit a history from both partners, and outline the investigations and therapeutic options for a couple who are unable to conceive after one
year of regular, unprotected intercourse.
Diagnostic Criteria
• No conception after 12 months of unprotected and frequent intercourse
• Primary: without any previous pregnancy
• Secondary: after previous conception
• Female factors:
• Ovulatory dysfunction: PCOS, POF, prolactinoma, thyroid dz, Cushing’s syndrome
• Uterine/tubal factors: PID, adhesions, previous ectopic pregnancy, uterine anomaly, IUD
• Cervical factors: structural imperfection, hostile mucous
• Peritoneal factors: endometriosis
Male factors:
• Testicular: varicocele, post-infectious (STD, mumps,TB), Klinefelter’s
• latrogenic: radiation, drugs (marijuana)
V.
• Structural: vasectomy, hernia repair

Male-female factors: frequency or timing of intercourse
History
P.
ID /c5age
CC • Infertility
HPI .
• Length & type of infertility • Length & type of infertility V
• Fertility in current or previous relationships • Fertility in current or previous relationships

• Coital frequency, intercourse timed around • Number & outcome of prior pregnancies (including ectopic &
ovulation, use of lubricants (which may be toxic miscarriages)
to sperm) • Coital frequency, intercourse timed around ovulation, use of
• Boxers or briefs (1’ testicular temperature), lubricants (which may be toxic to sperm)
erections, ejaculations, libido • Menstrual Hx: LNMP, cycle length and regularity, moliminal
V symptoms, cyclical pelvic pain,
• Sx of PCOS: hirsutism, acne, alopecia, t wt
• Sx of POF: hot flashes, vaginal dryness
• Sx of prolactinoma: headache, vision change, galactorrhea
• Sx of endometriosis: dysmenorrhea, dyspareuniä, dyschezia —
PMHx • DM (thinking ED), hx of chemo/radiation, • Thyroid dz, Cushing’s, Turner syndrome, hx of chemotherapy/
infections (STIs, mumps, TB), testicular trauma radiation
PSHx • Testicular torsion not repaired within 6 hrs, • Abdominal or pelvic surgery, especially for ruptured
hernia repair, vasectoy with reversal appendicitis (t chance of adhesions) or surgery for
endometriosis
PO&GHx • Pap Hx (cervical dysplasia)
• Hx of cone biopsy, LEER cervicitis (alters cervical structure or
mucous)
• Previous IUD use, past Hx of STls/PID, previous ectopic, (1’ risk of
tubal dz)
• Hx of fibroids, previous D&C
• Hxofabnormalanatomy
FHx • Infertility, congenital/chromosomal anomalies • Infertility, congenital/chromosomal anomalies
Meds • Pre-conception folic acid to decrease neural tube defects

Allergies List any allergies & their reactions • List any allergies & their reactions
Social Smoking, EtOH, drugs (especially marijuana) Smoking, EtOH, drugs
Excessive exercise or emotional stress
Physical
1. General Approach
• /3’ vitals, general appearance, BMI (overweight/underweight)
2. Inspection
• hirsutism, acne, alopecia (PCOS)
• abdominal scars from previous surgery
• ‘ gynecomastia, lack of body hair, hypospadias
• c tall, thin, gynecoid appearance (Klinefelter’s)

3. Palpation
enlarged thyroid
abdominal masses or tenderness
bimanual exam for masses, irregularly shaped uterus, or fixation of the uterus/adnexa (could suggest adhesions or
endometriosis)
• rectovaginal exam for nodularity of uterosacral ligaments (endometriosis)
• varicocoele, testicular size, presence of hernias, presence of masses
4. Special Tests
• speculum exam: PAP, vaginal/cervical swabs for STIs
Investigations
1. Blood work
• assess ovulation: day 3 LH/FSH/PRLJTSH/estradiol/DHEA, day 21 progesterone
• rubella and varicella status (if not immune, vaccinate before pregnancy)
• pelvic U/S: assess for uterine myomas & ovarian cysts
• HSG: assess tubal patency & uterine cavity, can also be therapeutic as it can clear the fallopian tubes
• hysteroscopy: directly visualize uterine cavity if a HSG is abnormal
3. 3. Special Tests
• semen analysis’: liquiflcation, count, motility, volume, morphology, pH, WBC count
• basal body temperature monitoring (to assess ovulation)
• cervical mucous analysis: assess post-intercourse for presence of motile sperm
4. 4. Surgical/Diagnostic Interventions
• c3’ diagnostic laparoscopy: allows for direct view of pelvis when looking for endometriosis or other pelvic pathology
Treatment
• education: time intercourse to 6 days prior to presumed ovulation day, sperm live 48-72 hrs a should have intercourse every
2-3 days
• ovulation induction: clomiphene citrate/gonadotropins/metformin (PCOS)/bromocriptine (IPRL)
• wtj.ifPCOS
• tubaldz:lVF
• c therapeutic donor insemination (azoospermia), IVF w/ lCSl (oligospermia), lUl (sperm motility problem)
• /c3’ counsel about adoption options
2. Surgical: tuboplasty for tubal disease, lysis of adhesions
References
1. Kumar et al. Infertility. In: DeCherney A, Nathan L, Goodwin T, Laufer N, editors. Current Diagnosis &Treatmer,t Obstetrics & Gynecology, 2 ed. New York:
Lange Medical Books/McGraw-Hill; 2007.Table 55-4.
2. UptoDate: Approach to Infertility. (2010). Available from: http://www.uotodate.com

____________________________
INTERPRETATION OF FETAL HEART RATE

20?? Ed. Authors:Jessica Nicoll, Jeff Compbe MD
OriginolAuthors: Christopher Fung, Michelle ocosse MD, Torek Moton MB ChB CCFP FRCSC
Station Objective
Assessing FHR is one way to help determine fetal status. Fetal heart tones are monitored during routine prenatal visits using a handheld
Doppler ultrasound probe. Electronic FHR monitoring (NST) is used in when adverse fetal outcomes are suspected.
History
CC Signs of fetal distress or risk factors for adverse outcomes
HPI GA, vaginal bleeding, contractions/cramping, leak of fluid, meconium, GBS status, Rh status
• Fetal Movement, chronic abruption, placenta previa/low lying placenta, cord abnormalities
• Maternal Sx: Infection, systemic, chronic disease
RED FLAGS o FEITAL LiNSTRESS: Eec.reased/Absent fetal movement, vaginal bleeding, severe uterine
PMHx DM, HTN, HIV, HTN, DM, thyroid or GI disease, infections, STIs, thrombophilias, anemia
PSHx C-section, pelvic or abdominal surgery, need for blood transfusions
PO&GHx GTPAL. GA at delivery, type/complications of delivery, wt of baby, complications with the previous pregnancies
Meds • Insulin, metformin, antihypertensive medications, anti-coagulants, contraindicated meds
Allergies
FHx • Of Fetal or Maternal RFs listed
Social Smoking, EtOH, recreational drugs, stress
ROS • HEENT: Diabetic Retinopathy, goitre
• CV: Dizziness, decreased exercise tolerance, fatigue and decrease energy,
• GU: Diabetic nephropathy, vaginal discharge, vaginal irritation,
Risk Factors • Maternal conditions, umbilical cord abnormalities, low lying placenta, abruption or placental infarction, fetal
anemia or infection, uterine hyperstimulation
Physical
1. General Approach FI?4.l,eb
I : IUdW
• Maternal Vitals and weight gain
2. Inspection
• Cervical effacement, dilation and fetal station Th•._
3. Palpation hihndnu nIup.;anitin
• Leopold’s maneuvers, SHF =
Electronic FHR monitoring (NST)
• External or Internal lead
• A normal NST is reassuring and suggests fetal viability for the next week, should the maternal-fetal condition remain stable, unless
post gestational dates or maternal DM, in which case the NST should be preformed twice weekly
1. Interpretation of NST must take into account the overall clinical picture
• GA, Hx of current pregnancy, risk factors and stages of labor Potential causes of inadequate tracings:
2. Approach High maternal BMI
• Quality of tracing and paper speed Poly/oligohydramnios
• Strip must be 20 mm long Detection of maternal pulse
• Scale: small squares are 0.5 cm, Paper speed: if 1 cm/mm, 2 squares = 1 mm Maternal movement
• Uterine Activity Very active fetus
• The tracing recorded bellow FHR Intrauterine Death
• Must not be in labor or is not an NST Fetal cardiac dysrhythmia
• Measures contraction duration and frequency NOT strength Fetal Position
212 Edmonton Manual of Common Clinical Scenarios Obstetrics&Gynecology

• Frequency: number of contractions in a 10 mm strip: >5 is tachysystole
• Duration: count the number of squares under the curve of the contraction 11
• Pattern: note coupling/tripling of contractions I 0net I I •ecovry
Baseline Heart Rate
Msec :
III
?30 II
• Definition: approximate mean FHR during a 10 minute segment of tracing I
• Normal: 110-160 bpm at term, Tachycardia:> 160 bpm, Bradycardia: < 110 bpm
Baseline Variability
• Definition: Beat to beat fluctuations in the baseline FHR as seen in a section without
accelerations or decelerations
IIhIiiii[;
__J__L._... I I
Nadir i
• Normal variability 5-25 bpm is a good indicator of a healthy fetus

• Flat baseline ddx: acidosis, sleeping, maternal sedative use
Accelerations Contraction .4.
• Definition: 15 bpm increase over baseline for 15 seconds
• <32 weeks GA: 10 bpm above baseline 15 seconds
Decelerations
• Definition: decrease in FHR relative to baseline
• Classification: early, variable, late mixed
i,pe Cause Pattern observed Pathologic?
Early Head compression when head Mirror image of uterine No- still has good beat to beat variability and returns to
is engaged contraction baseline
Variable Umbilical cord compression No relation to uterine Severity proportional to duration
and subsequent decrease in contractions, length depends on Mild <305, Moderate 30-60s
fetal BP duration of cord compression Severe> 60s
Late Inadequate fetal 02 due to Shifted to the right relative to YES! The severity of fetal hypoxemia and acidosis are
uteroplacental insufficiency the uterine contraction, later proportional to the amplitude of HR drop
onset, minimum and recovery Mild>l5bpm, Moderate 15-45 bpm Severe >45 bpm
Classification and Treatment

Parameter Normal Indeterminate Abnormal
Baseline In normal range 100-llObpm, >l6Obpm <30 <lOObpm or
mm >l6Obpm>3omin
Variability In normal range 5bpm for 40-80 mm >25 bpm for >10 minutes or <5 bpm for 80 mm
Accelerations > 2 normal accelerations 2 in 40-80 mm 2 in > 80 mm
Decelerations None, few uncomplicated variable Variable < 1 mm Complicated variable, late
Management Continue to monitor as the clinical Non predictive of fetal BPP or U/S, alter maternal position, 100% 02 by
situation dictates acid base status, continue face mask, D/C induction agents, further testing
., monitoring, perform a BPP
1. Referrals: Obstetrics and Gynecology or Maternal Fetal Medicine specialist if increased fetal surveillance during labor/NST required
References
1. Bashore RA, Koos BJ. Fetal Surveillance during Labor. In: Hacker NF, Gambone JC, Hobel Ci, editors. Hacker and Moore: Essentials of Obstetrics and
Gynecology. 5th Edition. Philadelphia: Saunders Elsevier mc; 2010.
2. Liston R, Sawchuck D, Young D. Fetal Health Surveillance: Antepartum and Intrapartum Consensus Guideline. J Obstet Gynaecol Can. 2007 29(9 Suppl
4):53-56.
3. Macones GA, Hankins GVD, Spong CY, Hauth J, Moore T. The 2008 National Institute of Child Health and Human Development Workshop Report on
Electronic Fetal Monitoring. Obstet Gynecol. 2008 Sep; 11 2(3):662-666.
4. 4. Fung C, Lacasse, M, Motan, T. Pregnancy Loss. In: Approach to the OSCE: The Edmonton Manual of Common Clinical Scenarios. 1st Edition.
Edmonton: University of Alberta Medical Student’s Association; 2010

INTRAPARTUM CARE
201 I Ed. Authors: Gabriela Pelinska, Nicole HubnerMD, Sujata Chandra MD FRCSC
OriginalAuthors:Jackie Clayton, Jason Weatherald MD, Charlotte Ballerman MD, Sujata Chandra MD FRC
Station Objective
In this station you will need to determine whether a term patient is in labour and appropriately manage a patient in labour. (Note: this topic
does not cover PROM or PPROM). Also see Interpretation of Fetal Heart Rate Monitoring.
Labour: regular, frequent, painful uterine contractions (CTX’s) AND cervical change (dilatation & effacement)
• 1 St stage:
• A. Latent Phase: uterine contractions irregular, and cervical dilatation < 3-4cm
• B. Active Phase: rapid cervical dilatation (4-10 cm) with regular contractions
• 2nd Stage: from full dilatation to delivery
• 3rd Stage: separation and expulsion of the placenta
• 4th Stage: first-hour post-partum (carries high risk of post-partum hemorrhage)
• Braxton Hicks contractions: irregular, less painful, no A frequency/intensity, no cervical change (not labour)
3. Abnormal Conditions:
• Abruption (ABD pain, vaginal bleeding), placenta previa (painless, vaginal bleeding), chorioamnionitis (ABD pain, fever,
leukocytosis), preterm labor, preterm ROM, ROM >24hrs at term
History
ID • Age, GTPAL, GA, GBS swab results, blood type & Rh status
CC • Suspected labour: 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, hypertension
• HIV, HepB, syphilis, rubella, varicella status
• ABCD: Activity, Bleeding, Contractions, Drench/Discharge
• (A) Fetal movement: decreased?
• (B) Bleeding: onset, quantity, color, prior bleeding
• (C) Contractions: onset, regularity, duration, interval between contractions, severity
• (D) Fluid leakage/rupture of membranes: onset, color, consistency, quantity, odor, meconium
• Pain: OPQRST
RED FLAGS Preterm, or post-term (<37 or >42 weeks GA, ROM >24hrs at term
• HTN, saotomata or blurred vision, headache, nausea/vomiting, RUQ/epigastric pain, seizures, 4 urine output, non-
dependent edema
a Vaginal bleeding in labour, 1. fetal movement, multiples, breech, vaginal birth after €/S
PMHx • Medical dz (HTN, DM, cardiac, renal, thyroid, asthma, connective tissue/SLE), trauma or MVA
PSHx • C-Sections, anesthetic problems, abdominal or pelvic Sx, procedures to cervix (LEEP, cone Bx)
PObsHx • Previous pregnancies: date, hospital/city, GA reached, del’y type (SVD, C/S, vacuum/forceps), complications (in
pregnancy, delivery or postpartum), gender, birth wt., child’s present health
PGyneHx • Date of last pap smear, abnormal pap smears + outcome /
• Menstrual cycle regular before pregnancy, contraception use + stop date

• Previous STI’s, whether at risk for STI’s currently?
Meds • Rx, OTC, CAM, known teratogens (e.g. coumadin, antiepileptics, ARB) & vitamins (folic acid)
Allergies • Drugs, latex — reaction to each
FHx • HTN, DM, multiples, congenital malformations
Social • EtOH, smoking, recreational drugs
• Occupation, partner information, current living situation, safety at home (domestic violence)
• Pts desires and expectations for intrapartum care and analgesia
ROS • Focus ROS on areas where Hx suggests relevant findings (ex. visual changes, SOB, RUQ pain, n/v, edema for pre
eclampsia)

physical
1. General Approach
• ), Non-stress test (NST), and contraction pattern
Maternal vital signs (BP, HR, RR, temperature, 5p0
2
2. Inspection & Palpation
• Abdomen: assess uterine tone, tenderness, palpate contractions
• Symphysis Fundal Height (SFH): uterine fundus to pubic symphisis (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: Internal examination of cervix, comment on each of the following:
External genitalia • examine for edema, skin lesions, bleeding
Dilatation • use fingers to assess the diameter of the internal os • 10cm — fully dilated
Effacement • length of the cervix 4cm —* 0cm or 0% - 100% respectively
Position • posterior, mid, anterior cervix moves from posterior to anterior
Consistency • soft, medium, firm
Station level of presenting part in relation to ischial spines • -22cm above, 0=spine, 2+= 2cm below
FetalPresentation position of head related to maternal pelvis • ex: Left Occiput anterior (OA)
• Active first stage of labour (dilated 3cm if nulliparous or 4cm if primiparous/multiparous, regular contractions). Use a Friedman
curve to follow labour progress and identify labour vs. dystocia (dilatation of <0.5cm/hr x 4 hrs during active 1st stage or 1 hr with
no decent during the 2nd stage).
3. Special Tests: Continuous vs. Intermittent Fetal Heart Rate monitoring (see Interpretation of Fetal Heart Rate)
Investigations
• U/S: as needed to confirm fetal presentation, position of placenta or amniotic fluid index
2. Special Tests
• Sterile speculum exam: to verify ROM
• Pooling of clear fluid in posterior fornix, (+) riitrazine, (+) ferning
• Urine R&M: proteinuria, UTI; swab for GBS if unknown
Treatmen
1. Emergent (see Fetal Distress)
• GBS prophylaxis (Indications: GBS +, GBS bacteriuria any time in current pregnancy, unknown, or previous infant with invasive
GBS), prolonged ROM> l8hrs
• Penicillin G 5 million units IV x 1 dose then 2.5 million units q4h until delivery
• If penicillin allergic: no penicillin anaphylaxis (cefazolin 2g IV then 1 g IV q8h), if anaphylaxis and positive test for sensitivity to
both Clinda/Erythro, then option of either Clindamycin 900mg IV q8h or Erythromycin 500mg IV q6h, if no sensitivity results
Vancomycin (ig lVql2h)
• Pain management:
• Non-pharmacological: continuous labour support, baths, maternal movement/positioning
• Nitrous oxide: self administered, inhale deeply at the onset of contraction
• Narcotics: morphine, fentanyl, avoid merperidine which has a longer ½ life
• Pudendal nerve block: local anesthetic for the perineum useful during 2 nd
stage or forceps
• Epidural block: relief throughout all stages of labour, may prolong l and 2 nd
stage
• Labour dystocia: Assess 4Ps power (CTX’s), passenger (fetal position), passage (pelvis), psychologic (effort)
—
• Consider interventions: amiriotomy, oxytocin augmentation, C-section

• Cardinal movements of delivery: engagement, descent, flexion, internal rotation, extension (delivery of head), external rotation
(restitution), expulsion (delivery of the shoulders (anterior,then posterior) and body)
• 3rd stage management (separation and expulsion of placenta, < 30mm):
• Oxytocin 10 units IM or 5 units IV with delivery of anterior shoulder
• Gentle umbilical cord traction and counter traction on uterine fundus
• Signs of placental separation(4):gush of blood, cord lengthens, fundus rises in ABDO and uterus becomes globular
• Laceration repair: Absorbable sutures, continuous locking above hymenal ring, interrupted sutures for perineal fascia
References
1 Hacker NF, Moore JG, Gamborne JC. Essentials of Obstetrics and Gynecology. 4th ed. Philadelphia: Elsevier Saunders; 2004.
2. DeCherney AH, Nathan L Current Obstetric & Gynecologic Diagnosis & Treatment. 9 th
Ed. New York: McGraw-Hill Companies, nc; 2003.

MENOPAUSE
Wctoria Cook BSc MSC, Juliette Sacks BA BSc MD, Peggy Sagle MSc MD FRCP
Station Objective
Counsel menopausal women about the inevitable cessation of ovarian function and explain the physiology behind the transition. Address
patient concerns and offer support and counseling to reduce symptoms including anxiety, depression and sleep disturbance. Discuss
osteoporosis as the most significant health risk of menopause and cardiovascular disease as the leading cause of death, and discuss
medications and preventative measures that can be used to reduce patient risks and symptoms.
• Physiologic (patient may be perimenopausal 2-8 years prior and up to 1 year after last menstrual period)
• Premature ovarian failure (<40 years) (radiation or chemotherapy)
• Induced (hysterectomy, oophorectomy, radiation therapy)
• Rule out other causes of amenorrhea
• Pregnancy
• Hypothalamic (anorexia, nutritional deprivation, extreme stress or systemic illness, tumours)
• Pituitary tumor
• Ovarian (PCOS, ovarian/adrenal hormone secreting tumours)
• Normal physiologic menopause most common
History
ID • Age
CC Cessation of menses
HPI • Decrease in amount and duration of menstrual flow
• Onset of amenorrhea (6-12 months is diagnostic)
• Symptoms associated with vaginal changes including discharge, bleeding with coitus, vaginal pruritis, excessive
dryness, vaginal burning
• UTI symptoms including 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
RED FLAGS • History of low or no-impact fractures
PMHx • Contraindications to HRT
• CVD
• Current or past breast cancer
• Gallbladder disease
• Past thromboembolitic events
• Osteopenia or osteoporosis
• HTN
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
• Dietary interventions such as soy
FHx Age of menopause and associated symptoms in direct female relatives
• Breast cancer
• CVD
Social • Married? Partners? Explore impact on sexual relationships
ROS • HEENT, CV, RESP, GI, GU, MSKJDERM

Factors Smoking (reduces age of menopausal onset)
I
physical
1. General Approach
• BMI,BP
2. Inspection
• Current hot flushing, signs of anxiety, changes in hair and skin (increased dryness)
3. Special Tests
• Pelvic examination
• Note pale vaginal mucosa, evidence of vaginal atrophy, reduced vaginal secretions, urinary incontinence, pain with speculum
insertion
• Breast examination
Investigations
i. Blood work
• Hormone levels: estradiol, LH, FSH (high FSH is
pathognomonic), testosterone if indicated Major Risk Factors Minor Risk Factors
Radiology/Imaging • Age 65 years • Past Hx of
2.
• Bone density study if osteoporosis suspected (65 years • Low trauma vertebral hyperparathyroidism
OR post-menopausal with 1 major OR 2 minor risk compression fracture or • Chronic anticonvulsant
factors, see box) any low trauma fracture> therapy
• Mammogram screening if patient meets guidelines 40 years • Low dietary Ca
2 intake
(women 50-69 should have a mammogram every 2 • FHx of osteoporotic fracture • Smoking
1
years) • Glucocorticoid Tx >3 mo • Excessive EtOH intake
SpecialTests • Malabsorption syndrome • Excessive caffeine
3.
• Pap smear if guidelines indicate
2 • Primary • Low weight (<57 kg)
hyperparathyroidism • Short term weight loss
• Hypogonadism >10% body weight
Treatment • Early menopause (<45 • Chronic heparin use
years) • RA
1. Emergent
• Symptom control (sleep disturbance, hot flushes)
• Counsel regarding osteoporosis prevention
• The only indication for HRT is symptom control (hot flushes, etc.) and HRT should only be used in women with no
contraindications; HRT is NOT indicated for prevention of CVD
• In menopausal women with contraindications to HRT, alternative pharmacologic therapy is available for osteoporosis prevention
• Discuss advantages and disadvantages of HRT
• Risks include endometrial cancer, breast cancer, hepatic function, HTN, thromboembolic disease, lipid metabolism changes
• Benefits include reduced risk of osteoporosis and reduction of menopausal symptoms including sleep disturbance,
incontinence, hot flushes and vaginal dryness and atrophy
• Outline guidelines for estrogen replacement therapy: it is indicated only in women with no contraindications presenting with
menopausal symptoms that significantly affect patient quality of life for periods of up to five years
• Discuss Ca
2 (1500mg OD) and Vitamin D (800-2000 IU OD) supplementation along with exercise for prevention of osteoporosis if
4
applicable
Discuss risk factors for CVD and preventative measures to reduce risk (including smoking, diet, activity levels)
3. Follow-up
• If patient decides to initiate HRT, schedule follow-up in 3-6 months to determine efficacy (symptom management)
4. Referrals
• Menopause clinic if available
References
Toward optimized practice. Guideline for the early detection of breast cancer. 2007.
2. Toward optimized practice. Guideline for screening for cervical cancer. 2009.
3. Brown and Josse. Clinical Practice Guidelines for the Diagnosis and Management of Osteoporosis in Canada. Revised 2002. CMAJ. 2002 Nov 12; 167 (10
Suppl): 51-34.
4. Hanly DA et aL Vitamin Din adult health and disease: a review and guideline statement from Osteoporosis Canada. CMAJ. 2010 Sept 7; 182(12):
E610-E518.

PAP SMEAR
Victoria Cook &Sc MSc, Juliette Sacks BA BSc MD, Peggy Sogle MSc MD FRCSC
Station Objective
Screen patients using a focused history to determine risk of cervical cancer and eligibility for screening tests. Verbalize the process of
performing a pap smear and discuss possible results. Based on these, identify patients requiring additional investigations.
History
ID. Age
CC What is cervical cancer risk and is patient eligible for screening
HPI Determine date of most recent pap test and any past abnormal results
• Current sexual activity, age at sexual debut
• Sex with men, women or both
• Number of sexual partners (present and past), multiple concurrent partners
• Sexual practices (oral, vaginal, anal)
• Safe practices and contraception (frequency of use and types)
• Previous or present STIs, PID, and presence of vaginal discharge
RED FLAGS Vaginal bleeding (especially post-coital)
• Persistent vaginal pruritis +1- discharge
PMHx • Immunosuppressed state (HIV positive, transplant recipient)
• Previous cancer
PSHx • Hysterectomy, if so what were the indications, and was the cervix removed
PO&GHx • Menarche
• Menstrual cycle length of period, regularity, amount of bleeding
—
. Any irregular bleeding post coital, intermenstrual, postmenopausal

—
• Previous gynecological procedures or instrumentation (cone bx, leep)

• Past abortions, pregnancies and deliveries, any complications
Meds Inquire about contraception
Social Smoking
• Drugs/EtCH
ROS • HEENT, Cv, RESP, GI, GU, MSKJDERM
Risk Factors HPV exposure
• Smoking
• Number of partners
• Vaginal and anal intercourse
Physical
General Approach
• Is the patient a candidate for pap screening?
• Refer to Alberta T.O.R (2009) and recent American College of Obstetricians and Gynecologists guidelines for cervical cancer
screening:
• Screening should begin age 21 or 3 years after sexual debut, whichever occurs later
• Cervical cytology screening is recommended every 2 years for women ages 21-29
• Women 30 years with 3 consecutive negative tests, no history of abnormal cervical cytology, not HIV infected or
immunocompromised and no prior exposure to diethylstilbestrol in utero may be screened every 3 years
• Women who have had a hysterectomy for benign reasons and who have no history of high-grade cervical lesions, routine
cytology testing should be discontinued, however if the hysterectomy was not for benign reasons or the woman has a history
of abnormal cytology, screening of the vaginal vault should continued
• Screening should be discontinued in women >69 years with 3 consecutive negative cervical cytology results
2. Special Tests
• Pap smear verbalize the method of obtaining a pap (Table 1)
—
• Describe sensitivity and specificity and incidence of false positive and false negative results

Table_1. Method for obtaining a pap smear
iiiuinmeflt Patient Preparation Sample Collection
Ensure patient comfort Inspect external genitalia and identify normal anatomy
Labeled slides or bottle of Appropriate draping Instruct patient to relax pelvic floor muscles
collection media Good light source Insert speculum and open to visualize the cervix, fix in place
Correctly-sized speculum Use ayres spatula to rotate around cervix and endocervical brush to sample the
Gown and drape endocervical canal
Gloves Sweep (spatula) and roll (brush) collected sample onto separate areas of the
slide to ensure single cell layer
Spray with alcohol fixative
pap smear
Resu It Interpretation
1. Sample Quality ASC-US Atypical squamous cells of
• Ensure sufficient cells and high quality sample undetermined significance
• Ensure effective endocervical sampling from the canal (especially important in ASC-H Atypical sguamous cells
older women) V cannot exclude high-grade
2. Pathology squamous intraepithelial
• Were analyzed cells normal or abnormal lesion
3. Final result (normal, ASC-US, ASC-H, AGC, LSIL, HSIL, cancer) AGC Atypical glandular cells
. Doresultswarrantfollow-up V
V LSIL Low-gradesquamous
. Refer to Table 2 for a list of abnormal pap smear results intraepithelial lesion
HSIL High-grade squamous
. intraepithelial lesion
Recommendations AIS Adenocarcinoma in Situ
1. Follow-up on abnormal results SCC Squamous cell carcinoma
• Refer to Towards Optimized Practice guidelines (2009) for cervical cancer screening:
Result Management in absence of HPV testing Management with available HPV testing
ASC-US, LSIL \ Additional screening q 6mo x 12 mo ASC-US >30y and LSIL >SOy should undergo HPV screening
,/ Subsequent abnormal results merit referral to Positive HPV results require referral to colposcopy
colposcopy, normal results allow return to normal Negative results allow return to normal screening
screening
ASC-H, HSIL, AGC or AIS Immediate referral to colposcopy
5CC, adenocarcinoma Refer immediately to specialist care
2. Preventative measures for cervical dysplásia and cervical cancer

Primary prevention involves any action that reduces exposure to HPV
• Abstinence, reduced number of sexual partners, avoidance of concurrent sexual partners, condom usage, reduction of
concurrent STls, HPV vaccination (<26 years)
Table 3. Treatment modalities for cervical lesions
1
• HPV vaccination choice between Gardasil and
Level Treatment
—
Cervarix
Pre-invasive Loop excision (if entire lesion is
• Secondary prevention involves any action that
visualized on colposcopy), cold-knife
reduces complications of HPV infection
conization (if pre-invasive but the
• Smoking cessation
entire lesion cannot be visualized) or
• Cervical cancer screening with pap test to identify
simple hysterectomy
precancerous lesions requiring follow-up
Intra-epithelial neoplasia Radical hysterectomy or radiation
Invasive cancer Chemoradiatjon
Treatment
1. Emergent
If cervical cancer is suspected on history or if a cervical lesion is visible on speculum examination, patient is not a candidate for
pap smear screening and should be urgently referred for colposcopy
2. Treatment options for pre-invasive, intra-epithelial neoplasia, and invasive cancer (Table 3)
3. Further workup, follow-up and referral to colposcopy or cancer clinic
References
1. Towards Optimized Practice. Guidelines for screening for cervical cancer, 2009.
2. Obstetrics and Gynecology. ACOG Practice Bulletin No.99: management of abnormal cervical cytology and histology, 2008.

PELVIC MASS
2017 Ed. Authors: Sarah Wozney, Julierte Sacks MD, Jonathan TankelMBBCh FRCSC
Station Objective
Determine if a patient is pregnant. From there, determine the anatomical origin of the mass; if it is gynecological or not.
1. Diagnostic Criteria: Palpable mass arising from the pelvis on vaginal! abdominal examination.
Ovary Adnexa Uterus Cervix Non-gyne

• Functional cysts (follicular, corpus luteum, • Ectopic • Pregnancy • Polyp • Appendiceal
theca lutein, hemorrhagic) pregnancy • Fibroids • Ca abscess
• Malignancy (epithelial, germ cell, stromal, • Tubal cyst • Adenomyosis Hematoma • Bowel abscess
metastatic) • Tubal • Endometrial Ca • Colorectal Ca
• Benign neoplasm (dermoid cyst) abscess • Leiomyosarcoma • Diverticulum
• Tubo-ovarian abscess • Fallopian • Hematometra • Bladder distension
• Endometrioma tube • Pyometra • Bladder Ca
• Polycystic ovary neoplasm • Pelvic kidney
.
History
ID- Age
CC • Pelvic mass, Pelvic! abdominal discomfort or pain
HPI • Pain description: OPQRST
• Menstrual hx: LMP, length of cycle, length of menstruation, amount of bleeding, clots, menopause, dysmenorrheal
• Obstetrical hx: GTPAL, vaginal or C-section, complications, previous abortions! miscarriages
• Sexual hx: sexually active, # of partners, STI hx, sexual practices, contraception, IUD
• Vaginal sx: dyspareunia, abnormal bleeding (menorrhagia, inter-menstrual bleeding, post-menopausal bleeding,
post-coital bleeding), discharge, odor
• Urinary sx: dysuria, frequency, hematuria, incontinence
• Bowel sx: constipation, diarrhea, melena, bowel habit changes, bright red blood per rectum
• Sx consistent with ovarian malignancy: persistent pelvic! abdominal pain, urinary urge! frequency, increased
abdominal size! bloating, early satiety, constitutional sx
• Sx consistent with pregnancy: NN, fatigue, breast tenderness, weight gain
RED FLAGS o €onstitutional sx: unexplained wt loss, fevers/c-hills, night sweats
• Abnormal vaginal bleeding, shoulder tip pain, hemodynamic instability
PMHx • Ca hx, previous pelvic mass
PSHx • Abdominal or pelvic surgeries (adhesions)
PO&GHx • STIs, PID, abnormal paps, endometriosis, PCOS
Meds • Contraception
FHx • Breast Ca, endometrial Ca, ovarian Ca, colorectal Ca, fibroids, BRCA gene
Social • Smoker
Risk Factors • Ovarian Ca: Early menarche! late menopause, increased age, Thx, nulliparity, OCP naïve, never breastfed
Physical
1. General Approach
• Vitals, general appearance (constitutional symptoms)
2. Inspection
• Abdominal: Distension, Obvious masses visible
• Pelvic: abnormal discharge or bleeding

3. PercusSion
• Abdominal: abnormal area of dullness, shifting dullness for ascites
4. Palpation
• Lymph node chains especially inguinal nodes
• Breast exam to determine if there is a primary source
• Abdominal Mass, Fluid Wave
• Pelvic: mass on uterus or adnexa, symmetry, tenderness, look specifically for cervical polyps or other abnormalities
• DRE: mass, tenderness, blood
Investi ations
i. Blood work
• CBC-D, 13-HCG (need to rule out ectopic!)
• Urinalysis
• Type and screen (need to know Rh status if mass is ectopic pregnancy)
• Blood tumor markers: CA125 (elevated in 50% of women with stage I ovarian Ca), serum alpha-fetoprotein and hCG (elevated in
extragonadal germ cell tumors), CEA (often elevated in colorectal cancers)
• Transvaginal or transabdominal US: determine size of mass, solid vs. cystic
• For unilateral masses that are suspected to be of functional origin, repeat imaging following next menses (approx 6 weeks)
• Further investigation required if mass continues to grow or take on a troubling appearance or causes increased symptoms
especially if constitutional symptoms
• CT or MRI if US is indeterminate
• CXR, mammogram
3. Special Tests
• Pap smear, vaginal! cervical swabs
• Endometrial biopsy
• FOBT, Colonoscopy especially if there is gastrointestinal symptoms, refer to Gastroenterology
4. Surgical/Diagnostic Interventions (determine anesthetic history, allergies, etc. prior to surgery)
• Diagnostic laparoscopy
• Depends on grade and staging, other prognostic factors
Treatment
1. Emergent
• STAT surgery if ectopic pregnancy
2. Treatment Options:
• Functional cysts: can watch and wait (typically regressed with the next menstrual cycle), OCP can help prevent further cysts, if the
mass continues to persist and become complex can undergo surgical exploration
• Chemotherapy, radiation if cancerous- discuss with Gynecology Oncology if suspected to be malignant
• Staging laparoscopy or laparotomy
:TAH/BSO, infra-colic omentectomy, peritoneal fluid sampling! pelvic sampling! pelvic
1
washing, biopsy of pelvic and periaortic lymph nodes, bilateral diaphragmatic scrapings! biopsy
• Surgical resection as indicated if such has not been done during investigations
• Gynecological surgical resections may include: total abdominal hysterectomy, bilateral salpingo-oophorectomy, infracolic
omentectomy, thorough staging, to preserve fertility can undergo unilateral salpingo-ooporectomy, may require masectomy
3. Follow- Up: dependent on specific condition and treatment
4. Referrals
• Gynecological Oncology, Radiation Oncology, Gastroenterology
References
1. Le et al. Initial evaluation and referral guidelines for management of pelvic/ovarian masses. JOCG [internet]. 2009 July [cited 2009 Nov 1 ];230:668-673.
Available from: http://www.sogc.org/guidelines/documents/gui230CPG0907.pdf
2. Rapkin AJ, Gambone JC. Pelvic Pain. In: Hacker NF, Gambone JC, Hobel Ci, editors. Hacker and Moore’s Essentials of Obstetrics and Gynecology. 5t1 Edition.
Philadelphia: Saunders Elsevier mc; 2010.

_________
PELVIC ORGAN PROLAPSE

2011 Ed. Authors: 7imothy Chan, Kate Collins MD, Catherine Flood MD FRCSC
OriginalAuthors:Jackie Clayton, Ariadne Daniel MD, Darren LazarMD FRCSC
Station Objective
Identify and determine pelvic organ prolapsed based on symptoms and physical examination. Know the risk factors for pelvic organ
prolapse.
Differential Diagnosis Table 1: Degree of Prolapse

1. Diagnostic Criteria: Grade 0 No prolapse
• Differentiate hernia of pelvic organ (uterus, vaginal apex, bladder, bowel, rectum)
Grade 1 Descent to 1cm above hymenal
and vaginal segment from its normal location ring
• Symptoms of prolapse (pressure, bulge, heaviness) Grade 2 Descent to hymenal ring
• Cystocele (bladder) +1- urethrocele: urinary frequency, urgency, nocturia, Grade 3 Descent to 1cm below hymenal
incontinence, pressure, urinary retention ring
• Rectocele (rectum): constipation, digital evacuation of stool Grade 4 Complete eversion, total
• Enterocele (small bowel): palpated on posterior vaginal wall during bimanual prolapsed (aka pocidentia) —
vaginal/rectal exam
• Uterine prolapse: groin or back pain, pelvic pressure worse with prolonged standing, better lying down
• Vaginal vault prolapse: descent of vaginal apex into lower vagina following hysterectomy
• 3. Other causes of pelvic pressure / bulge / heaviness
•
• Rectal Prolapse
• Vulvar or vaginal cyst/mass: urethral diverticulum, gartner’s duct, skene’s gland, bartholin’s gland, endometrial polyp
•
• Cervical Carcinoma, vaginal tumors, other pelvic tumors (urethra, bladder, colorectal, sarcoma)
History
CC • Vaginal fullness/pressure, vaginal protrusion/bulge, urinary and GI symptoms, dyspareunia
HPI • Prolapse: onset, pain, progression, provoking / palliating factors, severity, changes in activities
• Bleeding / discharge: onset, quantity, color, amount, odor
• Stress incontinence loss of urine witht pressure (sneeze, laugh, cough, heavy lifting)
—
• Urge incontinence involuntary urination, urgency, frequency, nocturia, multiple triggers

—
• Bowel Symptoms: incontinence of flatus, incomplete emptying, straining, urgency, digital evacuation, manual
splinting of vagina or perineum to start or complete defecation, sensation of blockage or obstruction, chronic
constipation
• Impact on quality of life
• Previous treatment (e.g. pessary)
RED FLAGS • Postmenopausal bleeding suggests vaginal erosion or endometrial Ca
PMHx • Pelvic or abdominal tumors, chronic cough (including asthma and COPD), ascites, connective tissue disease,
recurrent UTI, hernias, chronic constipation
PSHx • Pelvic surgeries, previous prolapse or bladder repair
PO&GHx • GTPAL, mode of delivery, complications: tears, episiotomy, forceps, C/S
• STI, PAP smears: dates, abnormalities
• Menstrual cycles: LNMP, regular, irregular, menopausal Sx (hot flashes, night sweats, vaginal dryness), dyspareunia
Meds • Laxatives, enemas, HRT
FHx • Connective tissues disease, bladder repairs, cancers (ovarian, breast, GI)
Social • Smoking, EtOH, recreational drugs, occupation, partner
ROS • RESP: chronic coughing
• GU: general review including above
• MSK / DERM: lower back pain or groin pain, joint hypersensitivity

Fik Factors Vaginal delivery, operative delivery (forceps), previous pelvic surgery, older age, high BMI, elevated intra-abdominal
I pressure (heavy lifting, chronic cough, chronic constipation), connective tissue disorders, atrophic changes,
,
[ genetics, ethnicity (caucasian higher risk)
Physical
i. General Approach
• Vitals, height, weight, BMI
• Evaluate vaginal prolapse in both upright and lying position, voiding diary
2. Inspection
• Erosions, ulcers, or skin lesions, vaginal atrophy. Separate labia to visualize obvious prolapse
• Examine the anterior and posterior vaginal walls separately using the posterior blade of speculum, ask Pt to strain or cough to
assess point of maximal prolapse (cystocele, rectocele, uterus, vaginal vault)
3. Palpation
• Pelvic exam for masses, assess ability to contract levator ani muscles (kegel strength)
• Rectovaginal exam: enterocele (examiner’s fingers separate during valsalva maneuver) and rectocele (palpate for septal defect)
4. Other Tests
• Q tip Test: insert Q tip into urethra and Pt strains, upward rotation > 30 degrees, associated with urethral hypermobility
• Cough stress test: observe for involuntary urine loss when patient forcefully coughs
• Post-void residual, latent incontinence (reduce prolapse and do cough stress test)
Investigations
1. General
• No specific tests beyond a complete gynecological exam
2. Other Tests
• Urinalysis, swabs and pap smear
• Postvoid residual urine (PVR volume): cathether or U/S
• Urodynamics: distinguish between stress incontinence, urge incontinence or overactive bladder
• (If preoperative, failed previous bladder repair, uncertain of diagnosis, or research protocol)
Treatment
1. Treatment Options: treat only if symptomatic
• Asymptomatic: observation + pelvic floor muscle rehab
• Kegel exercises ± biofeedback
• Physiotherapy, diet changes (fiber), weight loss, bowel routine, smoking cessation
• Vaginal estrogen if pen/post menopause
2. Pessary: restores prolapsed organs to normal positions, improves symptoms
• Fit largest pessary that does not cause discomfort, get patient to move around to ensure pessary is retained
• Follow up 1 week after for symptoms, every 3-6 months afterwards
3. Surgical Options
• Procedure depends on the type of prolapse:
• Uterine prolapse: abdominal hysterectomy & colposacropexy or vaginal hysterectomy & sacrospinous vault fixation
• Cystocele: anterior colporrhaphy, paravaginal repair
• Rectocele: posterior colporrhaphy, +1- perineorrhaphy
• Vault Prolapse: abdominal sacracolpopexy or sacrospinous vault suspension
• Oblilterative procedures: partial or complete colpocleisis (primarily for elderly and chronically ill patients with severe prolapse who
no longer desire coital function)
4. Referrals
• Failure of conservative therapy refer to urogyne specialists
References
1. Hacker NF, Moore JG, Gamborne JC. Essentials of Obstetrics and Gynecology. 4th ed. Philadelphia: Elsevier Saunders; 2004.
2. Decherney AH, Nathan L, Goodwin TM, Laufer N. Current Diagnosis & Treatment Obstetrics & Gynecology 10th ed. New York: McGraw Hill: 2006.
3. Farrell SA, Epp A, Flood C, Lajoie F, MacMillian B, Mainpnize T et al. The Evaluation of Stress Incontinence Prior to Primary Surgery. J Obstet gynaecol Can.
2003; 25(4):31 3-8.
4. Step-by-step approach to managing pelvic organ prolapse: Information for physicians Can Fam Physician. 2007 March; 53(3): 485—487.
5. Schorge, JO et al. Williams’ Gynecology. 1st ed. McGraw-Hill; 2008.
Obstetrics&GynecoIogy Edmonton Manual of Common ClinicalScenarios 223

PELVIC PAIN
201 I Ed. Authors: limothyChan, Kate Collins MD, Catherine Flood MD FRCSC
Station Objective
Distinguish between acute and chronic pain, determine if pregnancy is likely, rule out life-threatening gynecological causes, and know how
to stabilize a patient with acute and life-threatening pain.
Acute vs Chronic — chronic pelvic pain is intermittent or constant pain below umbilicus for at least 6 months duration
Acute Chronic
Gyne Non-Gyne Gyne Non-Gyne
• Ectopic pregnancy* • GI • Endometriosis IBD
• Miscarriage (SA) • Appendicitis Dysmenorrhea • lBS
• PID Diverticulitis Dyspareunia • Colon Ca*
• Hemorrhage/rupture! IBD PlD • Constipation
torsion of ovarian cyst or Bowell Obstruction Adenomyosis Hernia
neoplasm* • Urologic • Fibroids Celiacs
• Tubo-ovarian abscess Renal stone Uterine prolapsed • Chronic, Interstitial,
• Fibroid torsion • Pyelonephritis Neoplasms Radiation cystitis
• Endometritis • UTI Psychogenic
• Dysmenorrhea MSK • MSK
• Obstetrical Complications Vascular • Arthritis
• Ruptured AAA* • Strains/sprains
• Mesenteric lschemia* Shingles
*
High mortality! morbidity
History
ID Ageandgender
CC • Pelvic Pain
HPI • Qualify Pain: onset (acute vs chronic) location, onset, PQRST
—
• Timing: cyclical, intermittent, with menses, with intercourse, with BM, with voiding
• Associated symptoms: vaginal discharge, bleeding, dysmenorrheal, dyspareunia, NN
• Menstrual cycle: length/regularity, flow, menstrual symptoms (breast, cramp, bloating, mood)
RED FLAGS • Constitutional Symptoms (fever, chills, weight loss)
• Rule out Pregnancy:: LNMP, Sexual Hx, Contraceptives
• Ectopic Pregnancy: amenorrhea, vaginal bleeding, abdominal pain
PMHx • Fibromylagia, IBD, diverticular disease, IBS, depression, nephrolitithiasis, known AAA / hernia
PSHx • Abdominal or pelvic surgery
PO&GHx • LMP, last pap and results, STIs (last time checked), PID
• Sexually active? Number of partners? Condom use? Contraceptive method?
• Previous pregnancies (dates, type, complications)
Meds Contraception (OCP, IUD)
FHx CA (breast, ovarian, colon, endometrial), fibroids, ovarian cysts, endometriosis, gyne neoplasm
Social • Smoking, EtOH, drugs
ROS • General:fever,chills
• GI: constipation/diarrhea, changes in bowel movement
• GU: frequency, dysuria, urge, hematuria, hesistency

Risk Factors • PID: previous STIs, multiple partners, IUD use, young age, irregular checkups
• Ectopic: previous ectopic, tubal damage, endometriosis, smoking, >35 yo, STIs, IVF
physical
1. General Approach
• Vitals: overall appearance, vitals, tachycardia, fever, hypotensive?
• All reproductive aged women are pregnant until proven otherwise
2. Abdominal
• Inspection: Distension, visible masses, scars, skin changes, swelling
• Auscultate: decreased bowel sounds (obstruction), bruits
• Palpate/Percuss: masses, tenderness, guarding, rebound tenderness, McBurney’s Point, Rovsing’s, CVA
3. Pelvic
• External Genitilia: Bartholin’s glands, skene’s gland, urethra, labia
• Speculum Exam: discharge, bleeding, trauma, foreign body, cervicitis, cervical os open or closed, tissue in Os
• Swab or Urine for G&C, vaginal fluid culture and microscopy
• Bimanual Exam:
• Cervical motion tenderness, adnexal tenderness (PID)
• Uterine enlargement (fibroids), painful adnexa (endometrioma), adnexal masses (ovarian cyst, ectopic)
• Rectovaginal: Uterosacral ligament nodularity or tenderness, mass in rectovaginal pouch
Investigations
1. Lab work
• 3 -hCG (may need serial testing), CBC-D, syphilis screen
• If unstable INR/PTT, fibrinogen, type and screen, crossmatch
• Urinalysis, urine R&M, NAATforG&C
• -i-I- lytes, Cr, liver enzymes
• Pelvic U/S structural abnormalities (neoplasms, torsions, fibroids, pregnancies)
—
• CT/MRI appendicitis, non Gyne causes

—
3. Special Tests
• Swabs or urine for N. gonorrheae and C. trachomatis
• Swabs for BV/Trich /Yeast
• Laparascopy / Laparotomy
Treatment
1. Emergent
• 2 large-bore IVs, 02, attach to monitors
2. Non Surgical Treatment Options
• 2 single IM dose if ectopic meets criteria for medical management (Pt is stable, no fetal heart
Ectopic: Methotrexate 50 mg/m
activity, ectopic is <3.5cm and unruptured, ft can f/u)
• Dysmenorrhea, endometriosis, fibroids, adenomyosis: NSAIDS, OCPs
3. : if appropriate for outpatients Rx: Ceftriaxone 250 mg IM once + Doxycycline 100 mg P0 BID x 14 days
1
PID
• Inpatient Rx: Cefoxitin 2 g IV q6h + doxycycline 100 mg IV/P0 qi 2h or Clindamycin 900 mg IV q8h + gentamicin loading dose IV!
IM (2mg/kg), followed by 1.5mg/kg q8h (once clinically improved, stepdown to doxycycline 100 mg p0 BID x 14 days)
• Counseling on prevention of STIs
• If no changes in 3 months, consider laparoscopy
4. Surgical: D&C (spontaneous abortion), laparoscopic salpingostomy or salpingectomy (ectopic), laparascopic ablation (endometriosis),
hysterectomy (definitiveTx of fibroids and adenomyosis)
5. Follow-up: serial 13-hCG until <5 if ectopic pregnancy
6. Referrals
• Surgery, Obstetrics
Reference
1. Canadian Guidelines on SexuallyTransmitted Infections. Ottawa, ON: Public Health Agency of Canada. IRevised 2006]
Obstetrics &GynecoIogyEdmonton Manual of Common ClinicalScenarios 225

POSTPARTUM COMPLICATIONS
2011 Ed Authors: SamaptiSamapti
OriginalAuthors:Jackie Clayton, Jason WeatheraidMO, Charlotte Ballerman MD, Sujata Chandra MD FR
Station Objective
Assess and provide care for complications of a patient immediately following delivery to the six-week period after delivery.
• PPH: any blood loss threatening a women’s hemodynamic stability (>500cc vaginal, >1000cc cesarean)
• Postpartum fever: T> 38°C for 2 consecutive days during days 2-10 post partum
• PPH:4Ts(Tone,Tissue,Trauma,Thrombin)
• Tone: atonic uterus is the most common cause
• Tissue: vigorous cord traction, placenta accreta, retained placental lobe or blood clot
• Trauma: laceration of cervix, vagina, perineum, uterus if c-section, uterine rupture, uterine inversion
• Thrombin (coagulopathy): vWD, hemophillia, therapeutic heparin, acquired DIC/ITP/TTP
• Postpartum Fever: 5 Ws (Wind, Water, Wound, Walking, Wonder drug)
• Wind (24-48 hrs): atelectasis
• Water (Day 3): UTI
• Wound & infection (Days 5-10): Endometritis (most common cause) low grade temperature (T> 38°C for 2 consecutive days)
-
& tender uterus, Mastitis

• Walking (Days 7-10): DVT, PE
• Wonder drug (anytime): including blood transfusion & isoimmunisation
3. High Mortality:
• Puerperal sepsis, severe PPH
‘ History
ID • Age, GTPAL, delivery date & time, method of delivery, blood type, GBS status
CC PPH or post-pa rtum fever
HPI • Hemorrhage: see Treatment section below for emergent management
• Bleeding: onset, quantity, progressing/resolving, color, tissue
• Pain: OPQRST
• Hypovolemia symptoms: diaphoresis, pre-syncope, weakness, anxiety, agitation, confusion
. Pregnancy Hx: date, GA, delivery method, hours in labor, complications, wt
RED FLAGS • Fever, bleeding, pain, hypovolemia symptoms
PMHx • HTN, DM, bleeding diathesis
PSHx • C-sections, pelvic surgeries
PO&GHx • Complications during current pregnancy, delivery or postpartum for mother & infant
• Previous pregnancies: date, GA, delivery type, gender, child’s birth wt
Meds • Anticoagulants/antiplatelets
Allergies • Nature of reaction
Social • EtCH, smoking, recreational drugs
• Social support, partner information
ROS • HEENT: dizziness (PPH)
• CV: palpitations (PPH)
• RESP: SOB (PPH)
• GI: constipation, hemorrhoids, flatus/fecal incontinence, perianal tenderness
• GU: purulent vaginal discharge (Endometritis), dysuria, frequency, urgency (UTI), incontinence, dyspareunia, u/o
• MSK / DERM: bruising/petechiae
• Breast: breast tenderness (Mastitis)

Risk Factors PPH: muscle exhaustion (prolonged labor), over distended uterus (twins), operative delivery, uterine abnormalities
(fibroids), personal Hx of PPH
Endometritis: PROM, prolonged labor, cesarean, operative delivery, lacerations
Physical
1. General Approach (tailor to severity of situation)
• Vital signs and LOC
• Postural vital changes that predict significant blood loss: HR increase 3obpm, inability to stand due to severe postural dizziness,
postural BP drop of 2OmmHg, supine tachycardia or hypotension
2. Inspection
• General: pallor, cyanosis (peripheral & central)
• Pelvis: vaginal or perineal lacerations (discharge/erythema may indicate infection or active bleeding)
• Uterus: fundal height (indication of retained tissue)
3. Palpation
• Breast: palpate for tenderness, engorgement, heat (Mastitis)
• Pelvis: uterine tenderness (Endometritis), exclude pelvic hematoma/uterine inversion,
• Abdo: firm or boggy uterus (indication of uterine aTony)
Investigations
1. Blood work
• CBC-D, type and screen ± crossmatch (PPH)
• PTT/PT-INR, fibrinogen, bleeding time (if suspect Thrombin)
• Blood antibodies if Rh (-)
• Blood cultures (if suspect Endometritis)
2. Special Tests
• Culture endocervix and uterine cavity (suspect Endometritis)
• Urine R&M/C&S (all febrile postpartum patients)
• Manual exploration of the uterus under general anesthesia: retained Tissue, uterine wall laceration
Treatment
1. Emergent (For PPH):
• 2 large bore lv’s, crystalloid fluids, crossmatch 4 units pRBCs, catheter, uterine massage
• PPH
• ATony: drain bladder, uterine massage, oxytocin 40 units in 1000cc crystalloid, hemabate 250mcg IM, misoprostol PO/PV/PR
• Trauma: suture lacerations
• Retained Tissue: express uterine contents with fundal pressure, manual removal of placenta
• Post-pa rtum Fever
• Endometritis: broad spectrum coverage with cefoxitin+doxycycline (< 2 d postpartum), doxycycline (>2 d postpartum)
• Wind: encourage coughing, incentive spirometry, ambulation
• Walking: DVT prophylaxis, compression device, early ambulation
3. Surgical:
• Uterine aTony: uterine packing, intrauterine foley catheter, Bakri balloon, intrauterine Foley catheter
• Retained Tissue: manual removal in OR (curettage)
• Severe hemorrhage: compressive sutures, arterial ligation, uterine aa embolization, hysterectomy (last resort)
References
1 Hacker NF, Moore JG, Gamborne JC. Essentials of Obstetrics and Gynecology. 4th ed. Philadelphia: Elsevier Saunders; 2004.
2. McGee 5, Abernethy III WB, Simel DL. Is this Patient Hypovolemic? JAMA 1999; 281:1022-1029.

PREGNANCY LOSS
20?? Ed. Authors:Jessico Nicoll, Jeff Campbell MD

OriginalAuthors: Christopher Fung, Michelle Lacasse MD, Tarek Moton MB ChB CCFP FRCSC
Station Objective
Identify a nonviable pregnancy and counsel the patient regarding management.
1. Diagnostic Criteria for Spontaneous Abortion
• Definition: spontaneous termination of the pregnancy before the 20
th
gestational week
Type Vaginal Pain Cervix Notes
bleeding
Threatened Yes Maybe, dull ache in abdomen Closed I3hCG noting normally, 25-50% result in abortion
Inevitable Yes Crampy, lower abdomen Partially dilated 3hCG noting normally, Pain from uterine
contractions
Incomplete Yes Crampy Dilated 3hCG noting normally, Passage of products of
conception
Missed No No-have decreased uterine contractility Closed I3hCG ing or —ye, no heart beat, all products of
conception still in uterus
Complete Stopped Stopped Closed I3hCG -ye, all products of conception passed
• Recurrent abortion: 3 successive spontaneous abortions

2. Common Conditions: Vaginal Bleeding
• Physiologic bleeding due to placental development (implantation bleed)
• Post-coital / exam trauma
• Vaginal lesion (polyp, neoplasm)
• Dysfunctional uterine bleeding
• Fibroids
3. High Mortality: Vaginal Bleeding
• Ectopic pregnancy
• Molar pregnancy
History
CC • Vaginal bleeding, cramping
HPI GA, Fetal movement, Onset, amount and description of bleeding, Abdominal pain (often crampy lower abdominal,
may radiate to back)! Uterine contractions, Recent trauma, cotius or visible/palable polyps, IUD inserted (think
ectopic!), Trauma and other RFs listed
RED FLAGS Assess haemodynamic stability, fever/chills, signs of renal failure or DIC from sepsis
PMHx • Known coagulopathy, RecentTORCH, syphilis or mycoplasma infection systemic disease Eg: DM, Hypothyroidism,
SLE, severe HTN, pulmonary embolism or DVT
PSHx • Previous therapeutic abortions, D&C, any other abdominal or gyne surgeries
PO&GHx GxPx, previous spontaneous abortions or still births, uterine abnormalities, still birth or previous child with
morphologic or genetic abnormalities
Meds • Chemotherapy/Radiation, isotretinoin (accutane), heparin, anesthetics, toluene, methotrexate, thalidomide
FHx Genetic disorders, birth defects or developmental delay, still birth/neonatal death, spontaneous abortions,
thromboembolism, PE, consanguinity
Social • Smoking, EtOH intake, recreational drugs (especially cocaine), occupation, malnutrition
ROS HEENT: Diabetic Retinopathy
• CV: Dizziness, decreased exercise tolerance, fatigue and decrease energy
• GU: Diabetic nephropathy, vaginal discharge, vaginal irritation, renal failure

[iik Factors fi: significant genetic abnormality, TORCH infection
I Maternal: infection, systemic disease Eg: HTN, DM, thrombosis, autoimmune disease, epilepsy, severe anemia,
extremes of age and BMIs, smoking, previous abortions, uterine abnormalities and cervical incompetence
physical
1. General Approach
• Vitals: HR, BP, RR,T, SpO
2
2. Inspection
• Amount of cervical dilation, intensity of bleeding, visible products of conception, signs of polyps, neoplasia or trauma
3. Palpation
• Vaginal Exam: check for cervical motion tenderness, uterine size/tenderness, adnexal masses, Cervical swab for gonorrhoea!
chiamydia
Investigations
1. Blood work
• 13-hCG, maternal antibody screen, type and screen, TORCH and parvo B19 serology
• U/S : fetal viability, placental or cord complications
3. Special Tests:
• Karyotype, immunologic assays, thrombophilia assessment
Treatment of a spontaneous abortion

It is important to remove residual products of conception without delay to prevent sepsis
1. Emergent: Stabilize Pt if required, antibiotic therapy if septic abortion suspected
• Medical: Pain control, misoprostol to clear products of conception, RhoGam if indicated
• Surgical- D&C
3. Follow-up
• Reassure Pt and educate about risks of future spontaneous abortions
• Pt must return to hospital if: profuse vaginal bleeding, severe pelvic pain, or fever
• Monitor I3hCG weekly until <5 mlU/ml if products of conception not evacuated surgically
4. Referrals
• Genetic counselling: Karyotype evaluation may be required for recurrent abortions
References
1. Hacker NF, Moore JG, Gambone JC, editors. Essentials of Obstetrics and Gynecology.4t Ed. Philadelphia: Elsevier Saunders; 2004. P. 85-91
2. Puscheck EE, Pradhan A. First-Trimester Pregnancy Loss. eMedicine (internet]. Last updated Jun 25,2006. Available from: http://emedicine.medscaoe.
com/article/26631 7-overview
3. Fung C, Lacasse, M, Motan,T. Pregnancy Loss. In: Approach to the OSCE: The Edmonton Manual of Common Clinical Scenarios. 1st Edition. Edmonton:
University of Alberta Medical Student’s Association; 2010
4. Leduc, Land Maternal Fetal Medicine Committee. Stillbirth bereavment: Guidelines for Stillbirth Investigation. SOGC Clinical Practice Guidelines; 2006
Obstetrics&GynecoIogy Edmonton Manual of Common Clinical Scenarios 229

VAGINAL BLEEDING
20?? Ed. Authors: Malgorzota Ejsmont, Christine Bentz MD, Torek Moton MB ChB CCFP FRCSC
OriginalAuthors: Christopher Fung, Michelle Locosse MD, Tarek Motan MB ChB CCFP FRCSC
Station Objective
To differentiate causes of abnormal vaginal bleeding, including pregnancy versus non-pregnancy related bleeding and assessing
hemodynamic stability.
Differential Diagnosis Abnormal Vaginal Bleed
• Menorrhagia: regular cycle, prolonged bleed >7d, >8OmL blood Ovulatory Non-uterine Anovulatory
• Metrorrhagia: irregular bleeding, typically between cycles
• Menometrorrhagia: metrorrhagia that is prolonged
• Polymenorrhea: bleeding cycles 21d
• Oligomenorrhea: bleeding cycle 35 d
• Dysfunctional uterine bleeding: abnormal bleeding due to anovulation (unopposed estrogen)
2. Common Conditions: (decreasing order)
• Adolescent: anovulation, pregnancy, exogenous hormone, coagulopathy (von Willebrand’s)
• Reproductive: pregnancy, anovulation, exogenous hormone, fibroids, polyps, thyroid dysfunction
• Investigate if suspect fibroids/polyps/hyperplasia/Ca, in normal variations reassure
• Perimenopausal*: anovulation, fibroids, polyps, thyroid dysfunction
• Postmenopausal*: atrophic vaginitis, endometrial hypertrophy/polyps/Ca, exogenous hormone, other tumor
• *always investigate
• Endometrial Ca or hypertrophy with atypia: pen/post-menopausal women
• Ectopic pregnancy: pregnant patients with first trimester bleeding
• Cervical/vaginal/vulvar/ovarian neoplasm
History
ID • Age, GTPAL status, LNMP
• ABO/Rh status
CC • Vaginal bleeding
HPI • Onset/temporal pattern (cyclical vs. non-cyclical, trauma?)
• Amount (heavy vs. light/spotting, how often D pad/tampon, passage of tissue/clots)
• Precipitating factors (intercourse, etc.)
• Fatigue, nausea, breast tenderness, urinary frequency (pregnancy)
• Pelvic pain, discharge, fever (PID)
• Abdominal or associated pain/discomfort
RED FLAGS • Assess hemodynamic stability (if urgent transfusion/surgery is required)
• All premenopausal women: pregnant until proven otherwise, ectopic until proven otherwise
PMHx • Wt D, PCOS, bleeding disorder, DM, HTN, thyroid dysfunction, liver Dz
PSHx • Any GU surgery performed (hysterectomy, ectopic pregnancy, etc)
PO&GHx • Regularity of cycles, onset of menarche, onset of menopause (if applicable)
• Abnormal pap smear, Ca/precancer lesions, fibroids, STI Hx, prior post-partum hemorrhage
Meds • IUD (t risk of ectopic pregnancy), anticoagulant therapy (ASA, coumadin, heparin, LMWH)
Allergies • Medications
FHx • Ovarian/uterine/breast/colon Ca, HNPCC
Social • Smoking, EtOH use
ROS • CV: menopausal symptoms (palpitations, hot flashes, etc)
• MSK / DERM: hyper/hypothyroid symptoms

r Risk Factors Endometrial Ca: Age, relative t estrogen exposure (anovulatory cycles, nulliparity, obesity), FHx endometrial/colon
Ca. Highest Risk: 45yo and 90kg
Physical
1. General Approach
• Vitals: HR, BP, RR,T, 5p0
2
• If unstable • emergent treatment before continuing exam
• Offer chaperone for pelvic exam
2. Inspection
• General/ABD Exam: signs of thyroid dysfunction, liver disease, coagulopathy, PCOS
• Pelvic Exam (Note: if >20 gestation • check last U/S before exam to rio placenta previa)
• Speculum: cervical os, cervical lesions, vaginal wall (identify source/intensity of bleed)
3. Palpation
• ABD Exam: As usual + signs of peritonitis (hemoperitoneum), fundus
• Pelvic Exam
• Bimanual: check for cervical motion tenderness, uterine size/tenderness, adnexal masses, investigations
• i-i- DRE if unsure of source of bleed, rectovaginal exam if suspect mass
Investigations
1. Blood work
• Acute: 13-hCG, CBC-D, type and screen, INR/PTT
• Further workup: TSR, hormones (ovulatory status)
• Pelvic U/S to evaluate the uterus, endometrial thickness, adenexa
• If 4mm in postmenopausal, warrants further investigation
• If pregnant: r/o ectopic (see Pregnancy Loss)
3. SpecialTests
• Pap smear, vaginal swabs, urine for GC/Chlamydia
• Endometrial Bx (peri/postmenopausal + high risk premenopausal)
• Hysteroscopy, sonohysterogram, D&C
Treatment
1. Emergent: ABCs, IV access, crystalloids, ins/outs, type/crossmatch to stabilize
• Hemodynamically unstable • consider Premarin 25 mg IV, repeat pm until bleeding stops (1-5 hrs)
• Hemodynamically stable • low dose progestin-dominant OCP: 2-4 pills x 7d, then 1 pill x 1 4d
• Medical Premenopausal
—
• Ovulatory menorrhagia: NSAIDS (onset, q 6-8 h pm), tranexamic acid (500-1000 mg q 6-8 h pm), +/- hormonal Tx (see
Contraception)
• Anovulatory menorrhagia: as above + endometrial protection (combined OCP or progestins)
• t trimester bleed, Rh(-): Rhogam
V
• Fibroids: tranexamic acid, low dose combined OCP, androgens or GnRH agonists (none if asymptomatic)
• Medical — Postmenopausal
• Atrophic Vaginitis: estrogen cream (Premarin), tablets (Vagifem), ring (Estring) or lubricants/moisturizers
• Surgical: D&C, endometrial ablation, hysterectomy
3. Follow-up
• Close follow-up by Family doctor or Gynecologist
4. Referrals: if persistent, high risk or oncological
References
1. Cranmer H, Foran M. Vaginal Bleeding. In: Marx JA, editor-in-chief. Rosen’s Emergency Medicine. 4’’ ed. Philadelphia: Mosby Elsevier; 2009. Chapter 27.
2. Hacker NF, Moore JG, Gambone JC, editors. Essentials of Obstetrics and Gynecology. 4 th
Ed. Philadelphia: Elsevier Saunders; 2004. p.409-412, 478-480.
3. Millie AB, Price TM. Dysfunctional Uterine Bleeding. eMedicine (internet]. Last updated Jun 11,2009. Available from: http://emedicine.medscape.com/
article/257007-overview
4. Telner DE, Jakubovicz D. Approach to diagnosis and management of abnormal uterine bleeding. Canadian Family Physician [Internet]. 2007 Jan [cited
2010 Sept 151; 53 (1): 58-64. Available from: http://www.cfp.ca/cgi/reprint/53/1 /58

VAGINAL DISCHARGE
2011 Ed. Authors: Malgorzato Ejsmont, Christine BentzMD, Tarek Motan MB ChB CCFP FRCSC
OriginalAuthors: Christopher Fung, Michelle Lacasse MD, Tarek Motan MB ChB CCFP FRCSC
Station Objective
Discern the cause of vaginal discharge based on clinical and laboratory assessment while recognizing the likelihood of co-infections and
differentiate between UTI and vaginal infections.
Cause Discharge pH Whiff test Wet mount Other
Bacterial profuse, milky, fishy > 4.5 + “clue” cells, PMN

Vaginosis odour
Vulvovaginal white, thick/curdy < 4.5 - pseudohyphae, vulvar erythema, dysuria, itch, superficial
candidiasis budding yeast dyspareunia
Trichomoniasis green-yellow, frothy > 4.5 - motile trichomonads vulvar erythema,”strawberry” cervix,
dysuria, itch
Atrophic scant, clear-yellow, > 5.5 - immature basal!
Vaginitis blood-tinged parabasal cells
2. Common Con itions:
• Non-physiologic discharge (may be asymptomatic)
• Bacterial vaginosis (most common): genital tract organism overgrowth (Gardenerella, Prevotella, Mobiluncus spp.), RF: t if
sexually active, new sexual partner
• Vulvovaginal candidiasis: 90% Candida albicans
• RF: weakened immunity (diabetes, immunocompromise, corticosteroids, Abx), pregnancy, t if sexually active
• Trichomoniasis: protozoa, sexually transmitted
• Physiologic discharge
• Post-menopausal: Atrophic vaginitis
• C trachomatis/N. gonorrhoeae cervicitis (P ID)
History
ID • Age, GP status, LNMP
CC • Vaginal discharge
HPI • Colour, consistency, odour, quantity, duration, frequency
• Relationship to menses, sexual activity, contraception
• Associated symptoms: pruritis, pain, dyspareunia, dysmenorrhoea, bleeding
RED FLAGS • PID: bleeding, lower abd pain, dyspareunia, sexual Hx
PMHx • Past Hx same, DM, HIV
PSHx • Previous gynecological Shx
PO&GHx • Pap smear results, douching!foreign body, infertility
• Sexual Hx: sexually active, partners, condom use, STI Hx &Tx, partners with STI
Meds • OCP, HRT, recent antibiotics, immune suppressants
Allergies • Antibiotics
FHx
Social • Occupation (sex-trade), drug use
ROS • HEENT: conjunctivitis
• GU: dysuria (common CC in vaginitis ® distinguish from UTI by +1- discharge), hematuria, urgency, frequency
• MSK/ DERM: sores, rash, swelling, genital warts, arthritis
Risk Factors • Change in vaginal pH, Sexual Hx as above, immunocompromised

physical
1. General Approach
• ,T
Vitals: KR, BP, RR, Sp0
2
• Offer chaperone for pelvic exam
2. Inspection
• Pelvic Exam (Speculum): vulvar erythema/atrophy/irritation, skin lesions, discharge appearance, cervix friability/mucopurulent
discharge
Palpation
• Pelvic Exam (Bimanual): cervical motion tenderness, uterine size/tenderness, adnexal masses
• +/- Rectovaginal: if an indication exists (endometriosis)
.
Special Tests: vaginal swabs (see below)
Investigations
i. Special Tests
• pH paper: normal pH <4.7 in ovulating women
• Whiff test:”fishy”odourwith addition of 10% KOH to spoon of speculum after removal
• Pap smear/wet mount of discharge (may add 10-20% KOH to visualize spores/hyphae of Candida)
• Gram stain/culture
• If + Trichomoniasis/STI risk® consider first catch urine: Chlamydia/Gonorrhea, serology: Syphilis, HIV, Hep B (see Sexual and High
Risk Infections)
Treatment
• Bacterial vaginosis: treatment efficacy 75-85%
• Symptomatic: Metronidazole 500mg P0 bid x 7d or Clindamycin cream 2% 5g intravaginally qhs x 7d (other: oral
Clindamycin and vaginal Metronidazole). If pregnant Ct risk PROM, preterm labour): use oral treatments
• Recurrent infection: reconfirm Dx® Metronidazole 500mg P0 bid x 10-14d
• Asymptomatic: only if high risk pregnancy, prior to IUD insertion or gynecological surgery
• Vulvovaginal candidiasis: treatment efficacy 80-90%
• Fluconazole 150mg P0 xl dose (contraindicated in pregnancy) or OTC intravaginal creams
• Recurrent infections (4x in 12 mo.): vaginal culture/full species identification • 6 mo therapy, evaluate RF: cause for
immunocompromise
• Trichomoniasis: treatment efficacy 82-88%, t if partner treated
• Metronidazole 2g P0 single dose or 500 mg P0 BID x 7d
• Not reportable STI but treat current partner regardless of +/- symptoms
Atrophic vaginitis: topical estrogen (cream, ring, tablet, gel)
C trachomatis: Doxycycline 100mg P0 bid x 7d or Azithromycin 19 P0 single dose if poor compliance
• N. gonorrhoeae: Cefixime 400mg P0 single dose or Ceftriaxone 125 mg IM single dose
2. Prevention
• Discuss risk factors, HPV vaccine
3. Follow-up
• Not needed unless reportable STI, pregnant or sexual assault
4. Referrals
• Patient pregnant or recurrent symptoms.
References
5. Hacker NF, MooreJG, GamboneJC, editors. Essentials of Obstetrics and Gynecology. 4th Ed. Philadelphia: Elsevier Saunders; 2004. p.296—306
6. Canadian Guidelines of Sexually Transmitted Infections [Internet]. Ottawa (ON): Public Health Agency of Canada; 2008 ed. (cited 2010 Sep 15]. Available
from: http/Iwww.phac-aspc.gc.ca/std-mts/sti-its/guide-lignesdir-eng.php

EDMONTON MANUAL
Section #5
PSYCHIATRY
Section Editor: Jorge Perez-Parada BSc MD MSc FRCPC
Assistant Professor
Department of Psychiatry
INTRODUCTION 235 Personality Disorders 244

Abuse 236 Psychosis
Gender Identity Disorder 238 Substance Abuse 248
Mood Disorders 240 Suicidal Behaviour 250
Panic and Anxiety 242
234 Edmonton Manual of Common Clinical Scenarios Psychiatry

INTRODUCTION
orgePerezftrada BSc MD MSc 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. Psychiatric
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 often initiate 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 does not only include descriptions of behaviour, mood/affect, and thought, but may require a
MMSE or other such cognitive screening tool. The mental status may be required in stations that initially appear to be surgery or medicine
specific. SafetY is important to cover 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 to also remind you of the
ubiquitous nature of psychiatric disorders in medicine.
Psychiatry I Edmonton Manual of Common Clinical Scenarios 235

ABUSE
20 I I Ed. Authors: Gabriela Pelinska, Jorge Perez-Parada MD FRCPC
OriginalAuthors: Gabriela Pelinska, Jorge Perez-Parada MD FRCPC
Station Objective
Diagnose abuse and assess the role of abuse as an underlying factor in other health concerns and assess risk to the victim.
Basics
1. Screen for abuse: “Do you feel safe with your partner? Does your partner hit, insult, threaten or scream at you?”
2. Consent: the role of the physician is to provide care for the patient’s physical and psychological well-being. If the patient consents,
forensic evidence may be collected for future prosecution
3. Documentation: record details of history and physical exam, be precise, and use patient’s own words
4. Safety: evaluate patient safety, formulate a safety plan, and offer advice about services available
1. Definition: physical harm causing pain or injury, sexual assault, and psychological abuse including intimidation, isolation, manipulation,
financial abuse, coercion, or threat
• Depression, anxiety, PTSD, somatization disorder, substance abuse
• Determine whether acute injury is accidental, deliberately inflicted or self-inflicted
History
ID • Ageandgender
CC • May directly indicate”abuse”or present with non-specific complaints
HPI Document presence of physical harm, sexual assault, or psychological abuse
• Frequency, severity, recent change in severity/frequency, use of weapon
• Sexual assault: identity of assailant, description of event (physical assault: use of weapon or fist, sexual abuse:
vaginal, anal, or oral penetration), physical injuries, time and place, evidence of drug facilitated sexual assault
(memory loss, intoxication inconsistent with EtOH consumption), bath/shower or change of clothing since the time
of event, timing of last consensual intercourse
• Suicidal ideation (thoughts or documented plans), previous attempts/homicidal ideation
RED FLAGS • Partner refuses to leave the room during interview, partner answers questions for patient
• Eelayed presentation, description of injy inconsistent with mechanism
PMHx • Chronic medical conditions, previous abuse, injuries related to the abuse
• Fibromyalgia, IBS, migraines, chronic fatigue and chronic pain syndromes, multiple unexplained physical symptoms
P’PHx • Depression, anxiety, PTSD, substance abuse
• Violence or sexual abuse as a child, previous sexual assault
PSHx • Recurrent injuries requiring surgical intervention
PO&GHx • LNMP
• Gynecologic: chronic pelvic pain, dyspareunia
• Pregnancy: previous therapeutic abortion, miscarriage, vaginal bleeding, PROM, preterm labor
Meds • Drug (illegal or Rx) abuse or EtOH abuse
• Contraception
Social • Financial stressors, employment status
• Children witnessing event in the household (may need to report to Children Services)
• Support available for Pt (family, friends)
ROS • Psychiatric: depression (hopelessness, energy, irritability, changes to appetite or sleep), somatization (multiple
unexplained physical symptoms), anxiety (panic attacks), PTSD (tstartle response, hyperarousal: disordered sleep,
concentration), pattern of avoidant behaviour
• NEURO: headaches, weakness, dizziness, chronic pain syndromes
• CV: palpitations, tachycardia, CP
• RESP: hyperventilation syndromes
• GI: abdominal pain, IBS, GERD
Risk Factors • Cognitive impairment or mental illness, isolation (newly immigrated or recently relocated), pregnancy, previous Hx
of abuse, adolescence, poverty

Mental Status Exam
Appearance (general description, behavior and psychomotor activity, signs of anxiety), speech (volume, quantity, rate, rhythm), mood
(depressed, irritable, angry, anxious, guilty), affect (normal, blunted, flat, exaggerated), thought process (logical, tangential, evasive, rambling,
distractibility), thought content (delusions, obsessions, preoccupations, phobias), perception (hallucinations, illusions), cognition, memory,
insight, judgment
Physica
RED FLAGS Recurrent injuries, different stages of healing, patterned injuries, injuries sustained in self-defense
1. General Considerations
• Examination in a private setting (consider chaperone), attention to sensitive and compassionate care, careful draping of the Pt
2. Approach
• Examine head to toe (particular attention to the head, oral cavity, neck, arms, breasts, abdomen, thighs, buttocks), document
bruises, lacerations, or specific injuries (Table 1)
Table 1: Injuries resulting from physical abuse
Head Facial #s, loose or recently lost teeth, TM perforation
Traumatic brain injury with permanent neurological deficits
Neck Asphyxiation causing laryngeal swelling and changes in voice or trouble swallowing
Finger_marks, bruises, abrasions from attempted_asphyxiation
Breast, abdomen Difficult to visualize as covered by clothing but should be inspected carefully
Potential internal bleeding with abdominal injury
Extremities Injuries with characteristic features (cigarette burns, belt or whip marks, burns)
Sprains, dislocations and #‘s_(especially_if consistent with attempted_defense)
Perineum Lacerations and abrasions
Vagina/cervix Perform a speculum exam, document any vaginal! cervical secretions, and lacerations
Investigation
1. Blood work
• CBC-D, electrolytes, urea, Cr, LETs (if suspecting internal bleed), 3-hCG
• CT (head injury with neurological deficits, internal bleed), XR (suspected dislocation, #)
3. Refrain from performing extensive investigations for nonspecific symptoms, address underlying cause
Treatment
1. Emergent
• Sexual assault: notification of sexual assault response team, emergency contraception, STI prophylaxis
• Wound care: cleaning site, sutures if necessary, applying dressing
• Determine level of Pt safety: evaluate severity of abuse (lack of permanent injuries or pain, head injury with permanent sequelae,
asphyxiation, internal injury, or severe #), sexual assault, psychological abuse (threats, intimidation, manipulation), use of weapon,
increasing severity of abuse, partner characteristics (employment status, substance abuse)
• Create a safety plan: routes of escape in high-risk situation, individuals who can offer assistance, safe location for escape
3. Referrals
• Sexual assault: social worker/counselor, give information about the sexual assault centre and hotline number
• Family violence program: provides information about emergency shelters, legal services, financial support, assistance with
attaining employment, further education, group counseling, mental health services
References
1. Gallahue FE, Melville LD, editors. Emergency care of the abused. New York: Cambridge University Press; 2008.
2. “HITS Scale’ Sherin KM, Sinacore JM, Li XQ Zitter RE, Shakil A. HITS: a short domestic violence screening tool for use in a family practice setting. Family
Medicine. 1998; 30(7): 508-5 12.
3. Tintinalli JE, Kelen GD, Stapczynski is, editors. Emergency Medicine: A Comprehensive Study Guide. 6th ed. New York: McGraw-Hill; 2004.
Psychiatry I Edmonton Manual of Common Clinical Scenarios 237

GENDER IDENTITY DISORDER
20!! Ed. Authors: Sarah Wozney, AviAulakh MD, John DewartMD FRCPC
QiriginalAuthars: Daisy /-lartmann, Justin Petryk MD, Jarge Perez-Parada MDFRCPC
Station Objective
Elicit factors precipitating and maintaining the sexual concern(s), up to date effort to deal with the concern, and relevant medical history to
rule out reversible organic conditions. Determine the patient’s social and physical sexual development and behavior as well as the patient’s
3 GID is also referred to as Transgenderism.
sexual orientation and comfort with it.
• Strong and persistent cross-gender identification. Children must display four characteristics listed in HPI
• Persistent discomfort in and an overwhelming sense of inappropriateness in the gender role of an individual’s sex
• Is not concurrent with a physical intersex condition (CAH, androgen insensitivity syndrome)
• Disturbance in gender causes significant impairment or distress in social, occupational or other areas of important functioning
2. Conditions in the Differential:
• Transvestite fetishism
• Schizophrenia (delusion of belonging to the opposite sex)
• Body dysmorphic disorder (excessive preoccupation with imaginary/minor defect in appearance)
• Simple nonconformity to stereotypical sex-role behavior
• OCD
• As many as 1 in 30000 adult males and 1 in 100000 females seek sex-reassignment surgery
History
ID • Name, age, sex/gender, race, occupation, source of income, living arrangements
CC • Persistent preoccupation with acquiring sex characteristics of the opposite gender and assuming that gender role,
often apparent by cross dressing
HPI • Child (majority of cases begin in childhood):
• Repeated stated desire or insistence that one is of the opposite sex
• Boys show a preference for cross-dressing or simulating female attire while girls insist on wearing stereotypical
masculine clothing
• Cross-gender roles in make-believe play with a persistent preference to play that role or persistent fantasies of
being the opposite sex
• Strong preference for playmates of the opposite sex
• Desire to participate in games and pastimes of the opposite sex
• Adult:
• Persistence of childhood characteristics as listed above
• Preoccupation with getting rid of primary and secondary sexual characteristics
• Sexual attraction and/ or arousal- gynephilic (attracted to females) vs. androphilic (attracted to males)
• Exploration of opposite sex role playing and/ or attempted passing as the opposite sex
• Take a thorough sexual history!
PIPHx • Comorbid depression, personality disorders, substance abuse
• Self-mutilation (including genital damage), mood lability, identity difficulties
• Enquire about hx of sexual abuse or assault, and incest
PSHx • Sexual reassignment surgery
Meds • Hormones, steroid use
FHx • Psychiatric illness
Social • Fear of occupational, social and interpersonal reactions
• Religious affiliation
• Positive/ negative support systems (has the patient confided in anyone)

Mental Status Exam
1. Appearance: dress, self-care, general behavior, facial expression, eye contact, gender role
2. Mood (subjective) & Affect (objective)
.
Speech: rate, rhythm, volume, tone
Thought Form & Content: how are they thinking, what are they thinking
5• Perception: hallucinations, delusions, illusions
6. cognition & Memory
7. Insight: recognize need for tx
8. Judgment: impulsivity risk, reasonable
Physical
i. General approach
• Neurologic exam, peripheral neuropathy (ability to achieve erection following a stimulation/desire) and examination of genitalia
2. Inspection & Palpation
• Examine genitalia (undescended testicles, ambiguous genitalia, signs of surgery or self-mutilation/autocastration)
• Examine secondary sexual characteristics
Investigations
1. Blood work
• Hormone assays (testosterone, estradiol, progesterone, 1 7-hydroxyprogesterone)
• Karyotyping
Treatment
1. Non-Surgical Treatment Options
• Psychotherapy: adjustment and further exploration of preferred gender role, handling day-to-day problems
• Referral to community resources (lesbian, gay, bisexual and transgender support groups)
• Treating co-morbid psychiatric disorders (schizophrenia, depression, anxiety disorders, substance use, personality disorders)
• Hormone therapy (individuals typically spend 6 months in preferred gender role before initiation of hormones):
• Male-to-Female: spironolactone or cyproterone (block effects of endogenous testosterone), estrogen and progesterone po or
patch; changes are reversible
• Female-to-male: testosterone; changes are irreversible
2. Surgical (sexual reassignment surgery)
• Male-to-female: laser/electrolysis to remove hair, removal of testes, penis and vaginoplasty
• Female-to-male: breast reduction and male chest contouring, hysterectomy, oophorectomy, phallopalsty
3. Follow-up
4. Referrals
• Psychiatry (requires 1 year of psychiatric follow-up prior to sexual reassignment surgery)
• Endocrinology
References
1. American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition,Text Revision. Washington, DC, American
Psychiatric Association, 2000.
2. Andreasen N, Black D. Sexual Dysfunction, Paraphilias, and Gender Identity Disorders. lntroductoryTextbook of Psychiatry, Fourth Edition. Washington,
DC, 2006. p 322-325.
3. Sexually Concerned Patient/Gender Identity Disorder. Medical Council of Canada: Objectives for the Qualifying Examination. 2010; 332-333.
Psychiatry Edmonton Manual of Common Clinical Scenarios 239

MOOD DISORDERS
201 I Ed, Authors: Sarah Wozney, AviAluokh MD, John DewartMD FRCPC
OriginalAuthors: Madhav Sarda, Jorge Perez-Parada MD FRCPC
Station Objective
Distinguish between normal sadness and the presence of a clinical syndrome.
Disorder Abbreviated DSM IV symptoms Timeline and other criteria
Major 5 of the following symptoms (must include depressed mood or 2 weeks, change from previous level of
Depressive anhedonia): hypersomnia or insomnia, significant weight or appetite function
Disorder increase or decrease, psychomotor retardation or agitation, fatigue No hx of mania or psychotic disorder; not due
or loss of energy, feelings of worthlessness or inappropriate guilt, to GMC, substances, or bereavement
inability to concentrate & recurrent suicidal ideation Social/occupational dysfunction
Grief/ Similar to depression, but all symptoms related to loss, Pt does 2 months
Bereavement not experience psychomotor retardation, prolonged and marked Normal bereavement varies by cultural norms
functional impairment, morbid feelings of worthlessness, or
hallucinations aside from brief voices or images of loved one
Disorder Abbreviated DSM IV symptoms Timeline and other criteria
Dysthymia Depressed mood most of day, more days than not and 2 years (children & adolescents 1 year)
2 of: change in appetite, insomnia or hypersomnia, low energy and never symptom free for more than 2
or fatigue, low self-esteem, poor concentration or difficulty making months at a time, does not meet depression
decisions and hopelessness criteria
No mania or psychosis
Not due to GMC/ substance
Bipolar Type I: 1 episode of mania: elevated, expansive or irritable 7 days or hospitalization (Type 1)
Disorder mood at least 1 week plus 3 (4 if irritable) of grandiosity, I- need for Affects function, not due to substances
sleep, talkative, flight of ideas, distractible, 1’ goal directed activity, t (need to rule out cocaine & amphetamines),
pleasurable activity medications, or GMC (damage to the frontal
Type II: 1 Major Depressive Episode and 1 hypomanic episode (like lobes can present like mania)
mania but only lasts 4 days and does not cause marked functional
impairment)

• Suicidal ideation
History
ID Name, age, sex, race, occupation, source of income, living arrangements
CC Depressed mood, anhedonia or depressive equivalents (see below)
HPI Depression: MSIGECAPS= Mood, Sleep, Interest, Guilt, Energy, Concentration, Appetite, Psychomotor Retardation,
Suicidal
• Mania: DIG FAST= Distractible, Impulsivity/ Irritability, Grandiosity, Flight of Ideas, Activity, Sleep (1- need), Talkative
• Duration, time during the day
• Suicidal ideation: Is there a plan? Have they acted upon it? Previous attempts?
• Impairment in function: occupational, social, and interpersonal relationships
• Last time they felt well (euthymia >1 week)
• Specific triggers to depressed mood (e.g. premenstrual, post-partum, seasonal)
• Stressors that bring on symptoms (relationships, occupation)
• Hallucinations: auditory, visual, tactile, gustatory, olfactory
• Delusions or illusions
• Loss of a loved one <2 months (bereavement)
• Substance abuse
RED FLAGS . SUICIDAL IDEATION (plan! timeframe! access to means)

PMHx • Psychiatric illness including previous suicide attempts and treatments
• Previous manic or depressive episodes
PSHx • Hyper or hypothyroid, Cushing’s, DM, malignancy, autoimmune disorders, CVA, Parkinson’s, dementia, CAD
Meds • Steroids, interferon, beta blockers, OCP, levadopa, psych meds
FHx • Psychiatric history, suicide, substance abuse
Social • Substance use, stressors in any functional domain, past hx of abuse
Risk Factors • Other psychiatric illness, chronic medical condition, FHx of psychiatric illness
Mental Status Exam

1. Appearance: dress, grooming, self-care, general behavior, facial expression, eye contact
2. Mood (subjective): how the px reports feeling vs. Affect (objective): how does the px look
.
Speech: rate, rhythm, volume, tone
4. Thought Form &Thought Content: what are they saying and how are they saying it
5. Perception: hallucinations, delusions
6. Cognition, Memory, Insight & Judgment
Physical
. General PE to r/o other medical conditions
Investigation
1. Blood work
• CBC-D, TSH, electrolytes, glucose, urea, Cr, ALT, AST, B1 2, folate, EtOH, urine analysis, drug screen
• May consider CT depending on presentation- focal neurological deficits
Treatment
G
Emergent
• Admit to hospital if high danger to self or others, may require certification
Unipolar Depression Bipolar Depression
Bio Antidepressant (SSRIs, SNRIs, Bupropion, Mirtazepine Lithium, Antidepressant (in bipolar depression, if given alone, can
> TCAs, MAOI5) precipitate rapid cycling) + mood stabilizer, Carbamazepine, Divalproex
ECT sodium, Lamotrigine
Atypical antipsychotics (Quetiapine) to augment ECT, Atypical antipsychotics (Quetiapine)
Psycho Psychotherapy (interpersonal, cognitive behavioral, Proactively address interpersonal conflict, expressed -ye emotions and
supportive, psychodynamic) loss
Social Education re: illness Education of pt and family
Promote regular exercise Decrease substance use
Establish a therapeutic alliance
3. Follow-up
Close follow-up for response to tx and safety assessment
4. Referrals
Psychiatry: if tx resistant, severe, thought disorder/ psychosis, unsure of dx
References
1. Medical Council of Canada [Internet]. Ottawa: Medical Council of Canada.; c2008-09. Objectives for the Qualifying Examination [3rd Edition); 2008. [cited
2009 Oct 26]. Available from: http://www.mcc.ca/Objectives_oriline/
3. Sydney, E. and Hahn, S. ACP PIER & AHFS DI’ EssentialstM. 2009 [updated 2009 Sep21; cited 2009 Oct 26]. In: STAT!Ref Online Electronic Medical Library
[Internet]. Philadelphia (PA): American College of Physicians. C2009 Available from: http//www.statref.com
- .
4. Canadian Network for Mood and AnxietyTreatment [Internet]. CANMAT.; c2005 [cited 2009 Oct 26). Available from: httpi/www.canmat.org.
-.

PANIC AND ANXIETY
2011 Ed. Authors; Madhov Sardo MD, Mansfield Me/c MD FRCP
OriginalAuthors; Madhav Sordo, Jorge Perez-Parodo MD FRCP
Station Objective
Differentiate situational stress from true anxiety disorder and from drug and physical causes of anxiety.
• Panic Disorder:
• Recurrent panic attacks causing concern & change in behaviour, with or without agoraphobia (fear & avoidance of places
where escape is difficult if panic attack occurred); 1 mo, not due to substances or other GMC
• Generalized Anxiety Disorder:
• Excessive anxiety & worry, difficult to control, 3 of restlessness, easily fatigued, poor concentration, irritability, muscle
tension, poor sleep; 6 mo, impairs function, not due to other Axis I or GMC
• Specific Phobia
• Social Phobia
• Post-Traumatic Stress Disorder
• Obsessive Compulsive Disorder
—
• Major Depressive Disorder

• Other Medical Causes: asthma, hyperthyroid, intoxication, hyper/hypoglycemia, pheochromocytoma
• MI,PE
History
ID • Age, sex
HPI (& CC) . Panic (fear/discomfort, SOB):
• Speed of onset, time to peak, total duration
• Duration and intensity (how many attacks over how long)
• Palpitations, diaphoresis, tremor, SOB, sensation of choking, CP, nausea, dizziness, feeing of unreality, fear of
losing control, fear of dying, numbness / tingling, chills
• Triggers for panic attacks
• Agoraphobia (fear & avoidance of places where escape may be difficult)
• Concern about the panic attacks & resultant change in behaviour (avoidance, etc.)
. Anxiety (multiple somatic complaints, excessive worry, fear):
• Duration & intensity (out of proportion to events, ability to control)
• Restlessness, easily fatigued, concentration, irritability, muscle tension, sleep disturbance
• Triggers
• Impaired function: social, occupational, relationship! interpersonal
• Recent life stresses
• Intrusive ego-dystonic thoughts / impulses or repetitive behaviours (handwashing, etc.) (OCD)
• Excessive, unreasonable or irrational fear due to a specific object! situation (Specific Phobia)
• Excessive fear of embarrassment in social or performance situations (Social Phobia)
• Experienced actual or threatened death I serious injury
• Re-experiencing trauma, avoidance of triggering stimuli, hyper-arousal (PTSD)
• Mood symptoms and anhedonia
• Concurrent, pre-existing, or developed after anxiety / panic
RED FLAGS • Pain with exertion, Si, Sp0
, crushing CP
2
PMHx • CAD, CHF, Asthma, DM, Hypo or Hyperthyroid, COPD
PWHx • Any psych illness, particularly other anxiety disorders
Meds • Levothyroxine, SSRIs, steroids, sympathomimetics, anticholinergics, EtOH, benzodiazepines
Social • Hx of abuse / neglect, substance abuse, caffeine intake, EtOH, gambling
FHx • Any psych history, particularly anxiety or depression
ROS • Include headache, CP, radiation of pain
Risk Factors • FHx of anxiety disorder, Hx of mood & other anxiety disorders, female, early adulthood onset

Mental Status Exam
1. Appearance / Behaviour: agitated, psychomotor restlessness, diaphoretic, tremulous, may be unremarkable
2. Speech: may be more rapid rate
3. Affect / Mood: may be depressed or irritable, may be euthymic
4. Thought process: generally appropriate
5. Thought content: variable, no delusions though may have some cognitive distortions
6. Safety: suicide/ideations, plan, timeframe (anxiety is independent risk factor for suicide)
7. Hallucinations / Perceptual disturbances: generally none
8. Orientation: should be oriented to person, place, & time
9. Insight/Judgment: insight may or may not be intact, especially for GAD and OCD
Physical Exam
i. General Physical Exam to r/o other causes
Investigations
1. Blood work
• CBC-D (infection, anemia), TSH (hypo or hyperthyroid), EtOH, ASA (intoxication), Troponin (if associated with CP), Electrolytes
(hyponatremia), U/A, toxicology (intoxication), BNP (if suspect CHF), D-Dimer (if suspect PE), Blood glucose (hypoglycemia)
• CXR (if c/o SoB)
3. Special Tests
• ECG (if c/o CP or new onset panic >40 y/o)
Treatment
1. Emergent
• Low dose Lorazepam (or other rapid onset benzodiazepine) 0.5 —2 mg sub-lingual
• Biological
• SSRIs, SNRIs (start at lower doses than anti-depressants)
• Short-acting benzodiazepines (may use short-term 2-4 weeks until SSRIs / SNRIs take effect)
• Buspirone (for GAD only)
• Clomipramine (for OCD)
• Psychological
• Cognitive Behavioural Therapy (most commonly used and studied for most anxiety disorders)
• Group Cognitive Behavioural Therapy (particularly for Social Anxiety)
• Exposure / desensitization (particularly for Specific Phobia, Social Anxiety)
• Insight oriented therapy (particularly for Panic)
• Relaxation and mindfulness training (particularly for Panic)
• Social
• Re-assurance and education regarding nature of disorder
• Group therapy
3. Follow-up
• Follow-up in two weeks if starting new SSRI / SNRI to assess for suicidality
4. Referrals
• Refer to Psychiatry if Tx-resistant or unsure of Dx
References
rd Edition 3.3.0]; [cited 2010
3
[
1. Medical Council of Canada [Internet]. Ottawa: Medical Council of Canada.; c201 0. Objectives for the Qualifying Examination
Sep 12]. Available from: htto://www.mcc.ca/Obiectives online!
3. Nicholas, LM, Maloney AE, and Siegfried SL. Panic Disorder. ln:Tintinalli, JE, Kelen GD, and Stapczynski, JS, editors. Emergency Medicine: A Comprehensive
Study Guide. 6th
Ed. New York: McGraw-Hill; 2004. p. 1826-1829.
4. Canadian Network for Mood and AnxietyTreatment (Internet]. CANMAT.; c2005 [cited 2010 Sep 3rdl. Available from: http://www.canmat.org.
-.
5. Sadock, BJ, Sadock,VA. Synopsis of Psychiatry. lath ed. Philadelphia: Lippincott Williams & Wilkins; 2007.
6. Allgulander, C. Novel approaches to treatment of generalized anxiety disorder. Curr Opin Psychiatry. 2010.23:37-42.

PERSONALITY DISORDERS
201! Ed. Authors: MadhavSarda MD, Mansfield Mela MD FRCP
OriginalAuthors: Madhav Sarda, Jorge Perez-Parada MD FRCP
Station Objective
Differentiate personality disorders from patients with repetitive but short-lived episodes of disturbed behaviour.
Diagnostic Criteria Cluster”A” Cluster”B” Cluster”C”
• Personality Disorder (PD)
• Paranoid Antisocial Avoidant
• Pattern of behaviour involving cognition, affectivity,
Schizoid Borderline Dependent
interpersonal functioning and/or impulse control causing
. Schizotypal Histrionic Obsessive-Compulsive
significant distress, consistent since adolescence / early
Narcissistic
adulthood
Borderline PD Instability of relationships / self-image / affect, impulsivity, poor sense of identity, frantic avoiding of real or
imagined abandonment, recurrent suicidal / parasuicidal behaviour
Antisocial PD Disregard for and violation of others’ rights since age 15, deceitfulness, trouble with law, lack of remorse, Hx of
Conduct Disorder
Schizotypal PD Difficulty with social relationships, cognitive or perceptual distortions, eccentricities of behaviour, no Axis I
psychotic disorder or Pervasive Developmental Disorder
Obsessive-Compulsive Preoccupation with orderliness! perfection / control at expense of flexibility / openness / efficiency, displays
PD rigidity / stubbornness / indecisiveness
Bipolar Disorder NOT a PD, but common misdiagnosis; must have TRUE manic episode ( 7 days or hospitalization) forType I,
symptoms not pervasive outside of manic or depressive episodes
Substance Abuse NOT a PD, but must determine whether substances are cause of behaviour or if substance use is due to
underlying PD or if co-existent
Personality Change Examples of etiological causes include: head trauma (most common), cerebral neoplasms, cerebrovascular
due to a GMC bleeds and strokes
No PD has high mortality, but some presentations (e.g. suicidal / homicidal ideation in Borderline and Antisocial PD) can carry
significant mortality/morbidity
History
ID Age, sex
CC Suicidal ideation, social problems
HPI Onset of current symptoms, time course
• Mood: 1’ or .J,, how long, last time felt euthymic, stability / fluctuation, angry outbursts
• Hx of true manic episode at any time
• Suicidal ideation: plan, timeframe, events and thought process leading up to ideation / attempt
• Para-suicidal attempts (i.e. self-mutilation)
RED FLAGS High suicidal intent, access to means, organized plan and established timeframe
PWHx Past suicide and para-suicidal attempts: how many, how they were intervened on, triggers
• Any psychiatric illness, particularly depression, anxiety, schizophrenia, bipolar
Social! • Relationships: nature of and for how long, stable or unstable relationship Hx, friends
Personal Hx Occupation: how long, stable or unstable work Hx
• Family relationship Hx: loss of parent, abuse, family dynamic
• Education: how far, level of success, interaction with others, frequency of disciplinary actions
• Criminal Hx: nature of, age of first offense, number of criminal events
• Substance abuse: EtOH, marijuana, cocaine, Rx, effect of abuse on function
• Hx of impulsivity in any self-damaging area: sex, spending, reckless driving
PMHx • Head injury, seizure disorder, chronic pain
Meds • Anti-psychotics, anti-depressants (and response), mood stabilizers
FHx • Any psychiatric Hx

actorS FHx of PD (especially Anti-social & Borderline), unstable childhood, child abuse I
Mental Status Exam

1. Appearance / Behaviour: posture, attire, eccentric dress
2. speech: dramatic, aggressive
.
Affect / Mood: fluctuation, unstable, inappropriately extreme given context
.
Thought process: generally organized
5. Thought content: overvalued ideas, grandiosity, black & white thinking, rigid, paranoia / suspicion, magical thinking
6. safety: suicidal / homicidal ideation (plan, timeframe, intent, access to means)
7. Hallucinations: generally none, schizotypal may have “perceptual distortions’ not true hallucinations
8. Orientation: should be oriented to person, place, and time
9. Insight / Judgment: may be impaired
Physical Exam
i. General Physical Exam to r/o other causes
Investigation
i. Blood work
• EtOH, U/A for Cocaine, Amphetamines, Cannabis (substance use affecting presentation)
• CT head (if suspect head injury or change in personality to r/o bleed or mass)
3. Special Tests
• Neuro-psychological referral / testing if unsure of diagnosis
Treatment
1. Emergent
• Admit to hospital if significant risk to self or others, may require certification
• Biological
• No medication is approved to treat personality disorders directly
• Some medications can be used to treat specific symptoms
• SSRIs irritability, depressive symptoms, anger dyscontrol
—
• Lithium, Carbamazepine mood instability, irritability

—
• Anti-psychotics impulsivity, mood instability

—
• Anxiolytics anxiety
-
• Psychological
• Dialectical Behaviour Therapy (particularly for Borderline Personality Disorder)
• Cognitive Behavioural Therapy, Psychodynamic Therapy, & forms group therapy among other modalities of psychotherapy
have all been used, specific type of therapy must be tailored to the individual
• Psycho-education and strong doctor/patient relationship while maintaining appropriate boundaries
• Social
• Life skills training (may be part of psychological treatment)
• Encourage maintaining connections with family / friends
• Encouraging pro-social activities
• NOTE: Remember to treat any co-morbid Axis I disorder
3. Follow-up
• May require repeat visits at different points in patient’s life to be sure of diagnosis
• Acknowledging need for follow-up, be wary of developing dependence (particularly in Dependent PD)
4. Referrals
• Refer to Psychiatry if severe effect on functioning, unsure of diagnosis, unsure of appropriate treatment
References
1. Medical Council of Canada [Internet]. Ottawa: Medical Council of Canada.; c201 0. Objectives for the Qualifying Examination [3rd Edition 3.3.0]; (cited 2010
Sep 12]. Available from: htto://www.mcc.ca/Objectives online/
2. American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision. Washington, DC, American
3. Pfohl, B. Personality Disorders. May 282008. In: UpToDate [DVDI Waltham (MA): UpToDate, Inc. Ver. 16.2.2008.
4. Sadock, BJ, Sadock, VA. Synopsis of Psychiatry. 10th ed. Philadelphia: Lippincott Williams &Wilkins; 2007.

PSYCHOSIS
2071 Ed. Authors: Madhav Sardo MD, Monsfield Mela MD FRCP
OriginolAuthors: MadhavSarda, Jorge Perez-Parodo MD FRCP
Station Objective
Determine the possibility of the psychotic disorder being caused by a medical condition or substance induced episode. Differentiate a
psychotic patient from one with delirium
Schizophrenia
• 1 mo Hx of at least 2: delusions, hallucinations, disorganized speech, disorganized / catatonic behaviour, or negative
symptoms (affective flattening, alogia, avolition)
• 6 mo Hx of disturbance in function
• Subtypes: Disorganized, Paranoid, Catatonic (decreased movement or purposeless movement), Undifferentiated (mix of
above), Residual (less +ve symptoms, -ye symptoms remain)
• Substance Induced Psychotic Disorder
• Delirium
• Schizophreniform (criteria same as Schizophrenia but disturbance in function> 1 mo, < 6 mo)
• Brief Psychotic Disorder (disturbance in function> 1 day, < 1 mo)
• Schizo-affective Disorder (mood disorder & psychosis, 1 instance of psychosis with no mood symptoms)
• Delusional Disorder (nonbizarre delusions >1 mo, doesn’t meet criteria for schizophrenia, function otherwise normal)
• EtOH or benzodiazepine withdrawal, any severe medical condition causing delirium, intracranial mass / lesion
History
SAFETY • Assess environment / access to weapons, consider security personnel, be aware of all safe exits
ID • Age, sex
CC • Bizarre behaviour, aggression, agitation, social withdrawl
HPI • Get collateral Hx if possible (may need it to answer some of the questions below)
• Extent, duration, onset of delusions / hallucinations
• Course of symptoms (fluctuation vs. consistent)
• Delusions (bizarre vs. non-bizarre), paranoia
• Hallucinations: auditory (including running commentary, two voices conversing, command), visual, tactile,
gustatory, olfactory
• Insight vs. no insight
• Associated mood (depression or mania, egosyntonic or egodystonic)
• Negative symptoms (avolition, alogia, affective flattening, anhedonia)
• Safety (assess suicidal & homicidal ideation; Hx of violence / aggression)
Recent Hx • Premorbid functioning, memory impairment / orientation
(prior to HPI) • Potential prodromal symptoms of schizophrenia: irritability, social isolation, anxiety, depression
• Recent trauma, fall
RED FLAGS • Focal neurological signs, febrile, meningismus, hypoxia
PMHx • Any recent significant illness, malignancy, HIV, CVA, dementia, seizures, hypo or hyperthyroid, parathyroid
dysfunction, hepatic or renal disorders, lupus
PSHx • Recent surgery
PWHx • Any psychiatric illness
Meds • Any recent change in medication, anti-psychotics, Levothyroxine, steroids
Social • Impact of behaviour on social, occupational, and daily living function
• Substance use: EtCH intoxication or withdrawal, cocaine, amphetamines, benzodiazepines, hallucinogens
(mushrooms, LSD, ecstacy), PCP, marijuana, opiates
FHx • Hx of psychiatric illness
Risk Factors • FHx of psychotic disorder, age 16—30, Hx of marijuana use
246 Edmonton Manual of Common Clinical Scenarios I Psychiatry

Mental Status Exam
1. Appearance / Behaviour: may be catatonic or highly agitated, disheveled, avolition, stereotypic mannerisms (e.g. saluting), tics, may be
unremarkable
2. Speech: rate, rhythm, volume, alogia
•
Affect / Mood: may be blunted / flat, inappropriate, incongruent, perplexed, anhedonic
•
Thought process: may be tangential, circumstantial, word salad, disorganized, loose associations
5. Thought content: perseveration, bizarre or nonbizarre delusions, persecution, grandiose
6. Safety: suicidal and homicidal ideations (plan, timeframe, access to means, intended target, command hallucinations)
7. Hallucinations: most commonly auditory for schizophrenia, visual more likely to be delirium
8. Orientation: poor orientation / memory more likely in psychosis due to GMC or delirium
9. Insight /judgment: may be impaired or intact, depending on severity & underlying cause
10. Mini-mental exam: more likely to be abnormal in dementia / delirium, but can be in schizophrenia as well
Physical Exam
General Physical Exam to r/o other medical causes; weight and waist circumference (if on chronic anti-psychotics)
lnvestgations
1. Blood work
• CBC-D (infection), electrolytes, Ca
, Mg, Cr, Urea (metabolic disturbance), ALT, AST (hepatic failure), TSH (hypo or hyperthyroid),
2
EtOH (intoxication or withdrawal), ASA, Acetaminophen, Anticholinergics (toxic ingestion), U/A for Amphetamines / Cocaine /
Barbituates / Opiates / Benzodiazepines / Cannabis
• CT head if new onset symptoms at older age, Hx of trauma, malignancy or concurrent neuro symptoms
3. SpecialTests
• LP if suspect meningitis
• EEG if suspect temporal lobe epilepsy
• Neuro-psychological referral / testing
Treatment
1. Emergent
• Admit to hospital if danger to self or others, may require certification
• Ethically required to report to police if patient reports specific threat to specific target
• Security and physical restraint may be necessary
• Anti-psychotics (e.g. Haloperidol 5 mg IM, Olanzapine 10 mg P0, may repeat q3omin until settled / sedated)
• Benzodiazepines (e.g. Lorazepam 2 mg PO/IM/IV, may repeat q3omiri until settled / sedated)
• Biological
• Anti-psychotics: atypical > typical (e.g. Olanzapine 5 10 mg initially, titrate upwards)
—
• Long-acting depot injections (e.g. Fluphenazine 12.5 37.5 mg q2weeks)

—
• Clozapine (if Tx-resistant)

• Benztropine (if extrapyramidal side effects of anti-psychotics)
• Psychological
• Psycho-education regarding illness
• CBT can be used in patients with some level of insight
• Social
• Educate family members of diagnosis & symptoms
• Social skills and vocational training may be necessary
3. Referrals
• Most patients should be referred to and follow-up with a Psychiatrist
References
1. Medical Council of Canada [Internet]. Ottawa: Medical Council of Canada.; c201 0. Objectives for the Qualifying Examination [3rd Edition 3.3.01; [cited 2010
Sep 121. Available from: http://www.mcc.ca/Objectives online/.
2. American Psychiatric Association: Diagnostic and Statistical Manual ofMental Disorders, Fourth Edition,Text Revision. Washington, DC, American Psychiatric
Association, 2000.
3. Jibson, MD. Overview of Psychosis. August 14, 2007. In: UpToDate [DVD] Waltham (MA): UpToDate, Inc. Ver. 16.2. 2008.
4. Jibson, MD. Overview of Antipsychotic Medications. June 17,2008. In: UpToDate [DVD] Waltham (MA): UpToDate, Inc. Ver. 16.2.2008.
5. Sadock, BJ, Sadock, VA. Synopsis of Psychiatry. 10th ed. Philadelphia: Lippincott Williams & Wilkins; 2007.

SUBSTANCE ABUSE
2071 Ed. Authors: Christina Beach and Dr. Jorge Perez-Parada MD FRCPC
OriginalAuthors: Daisy Hartman, Justin Petryk MD, Jorge Perez-Parada MD FRCPC
Station Objective
The goals of this station are to: DSM-IV Alcohol Abuse
1. Determine if the patient is in need of emergency care (1 or more criteria for over 1 year)
2. Differentiate social from problem drinking/dependence • Role Impairment (e.g. failed work or home obligations)
3. Conduct an initial plan of management for a patient with substance • Hazardous use (e.g. Driving, swimming or operating
abuse machinery while intoxicated)
• Legal problems related to Alcohol use
Differential Diagnosis • Social or interpersonal problems due to Alcohol
• Stimulants (amphetamines, cocaine, MDMA, phencyclidine);
Depressants (EtCH, benzodiazepines, barbiturates, rohypnol), DSM-IV Alcohol Dependence
Hallucinogens (marijuana, LSD, mushrooms), Volatile inhalants (3 criteria for over 1 year)
(glue, NO, amyl nitrate), Nicotine, Other (e.g. ketamine) • Tolerance (increased drinking to achieve same effect)
2. Diagnostic Criteria • Alcohol Withdrawal signs or symptoms
• CAGE-AID questionnaire for EtCH and drug dependence (positive • Drinking more than intended
screen is 2/4 for men, 1/4 for women) • Unsuccessful attempts to cut down on use
3. High Mortality/Morbidity: • Excessive time related to Alcohol (obtaining, hangover)
• EtOH withdrawal has a 20% mortality rate if left untreated but a • Impaired social or work activities due to Alcohol
1-5% mortality rate if recognized
1 • Use despite physical or psychological consequences
History
CC • Substance abuse/withdrawal, bizarre behavior
HPI • Past and recent quantity/frequency of abuse (review all substances and routes—e.g. isopropyl EtOH, cough syrup,
IVDU)
• Severity of abuse and dependence (blackouts, withdrawal symptoms ranging from mild to severe, DTs, withdrawal
seizures, admissions to hospital for intoxication/withdrawal) V
• Adverse consequences/social problems with use such as assault, impaired driving, incarceration, frequent injuries;
Compulsive use, loss of control
• Social versus problem drinking (7 drinks/week for females, 14 drinks/week for males), CAGE-AID orTWEAK
(recommended for white females, score >3 indicates problem)
3 questionnaires
• Readiness to change versus denial
RED FLAGS • Autonomic instability, decreased LC, agitated behavior, active psychosis, Wernicke encephalopy, Ts
PMHx • Withdrawal seizures, DTs
• Liver disease (including HépB and HepC)
• Infectious endocarditis, talc lung, HIV
• Past attendance at substance abuse rehab programs (outpatient or inpatient/residential)
PWHx • Mood and anxiety disorders
PO&GHx • Drinking during pregnancy
Meds • Prescription meds with the potential for abuse (narcotics, stimulants, sedatives), increases in meds, early refill
requests, visits to multiple health care providers
FHx • Substance abuse, psychiatric illness
Social • Support network (Do close contacts also have substance abuse problems?)
• Legal and occupational Hx, financial situation
ROS HEENT: auditory or visual disturbances, headache, clouding of the sensorium, agitation, seizures, amnesia,
insomnia, sneezing, yawning, lacrimation, miosis/mydriasis
• CV and RESP: palpitations, brady/tachycardia, HTN, bradypnea
• GI: NN, cramping, anorexia, PUD, gastritis, pancreatitis, diarrhea
• MSK / DERM: paroxysmal sweats, flushing, tremor, skin infections, piloerection
Risk Factors • Contaminated needles: increased risk of HepB, HepC, HIV, and bacterial endocarditis
248 Edmonton Manual of Common Clinical Scenarios I Psychiatry

physical
1. General Approach
• Vitals: pulse, BR T, RR, Sp0
, GCS, blood sugar
2
2. Inspection
• Pupils (dilated versus pinpoint), stigmata of liver failure (caput medusae, jaundice), presence of track marks, tongue lacerations
(from seizures), head and facial trauma, signs of infection
3• Percussion/Palpation
• Hepatomegaly, ascities, lymph nodes, pulse rate and rhythm (atrial fibrillation)
4. Auscultation
• Wheeze (asthma), pericardial rub (infectious endocarditis in IV drug users), consolidation/crackles (aspiration pneumonia), scratch
test (hepatomegaly)
5. Special Tests
• Reflexes, motor/sensory exam, orientation
Investigations
1. Blood work (including special tests)
• CBC-D (anemia), electrolytes, ALT, AST, ALP, GGT, total protein, albumin, bilirubin, Cr, urea, lipase, serum EtOH; urine for cannabis,
amphetamines, cocaine, barbiturates, benzodiazepines, opioids, MDMA
• CXR
Treatment
1. Emergent
• ABCs, intubation and mechanical ventilation if GCS <8 or falling
• For patients with altered mental status and suspected poisoning: °2’ glucose as D5OW 25-50 ml, thiamine 100mg and naloxone
2mg (Universal antidotes)
• Supportive care (hydration, glucose, and electrolytes)
• Thiamine 1 00mg/day plus multivitamin while being treated for withdrawal (give thiamine before glucose when
EtOH withdrawal
4 practical to prevent Wernicke encephalopathy)
G
• Clinical Institute Withdrawal Assessment for Alcohol, Revised (CIWA-Ar) for monitoring: if score >8, treat with
medication—benzodiazepines are recommended therapy
• Medications such as opioid agonists (methadone), opioid partial agonists (buprenorphine), alpha 2-agonists
Opioid withdrawal
5 (clonidine)
• Naloxone for acute overdose
• Gradual taper and carbamazepine as adjunct
Benzodiazepine • Flumenazil (benzodiazepine antagonist) 0.4-1mg reverses effects of overdose (typically only used in ER/ICU
6
withdrawal settings)
• IV glucose if possible concurrent EtOH ingestion
Non-
pharmacological • Behavioral modification, psychotherapy, mutual/self-help, residential or outpatient treatment programs
options
Supportive
. • Detox centres, half-way houses, Alcoholics Anonymous, Narcotics Anonymous
services
3. Referrals
ICU, medicine, psychiatry, FASD clinic
References
1. McKeown NJ, West PL. Withdrawal syndromes: treatment and medication. eMedicine [Internet]. 2010 Mar [cited 2010 Sep 15]. Available from: hLL
rridicine.medscape.com/article/81 9502-overview
2. Stephens E.Toxicity, opioids: treatment and medication. eMedicine [Internet]. 2010 Apr [cited 2010 Sep 15]. Available from: http://emedicine.medscape.
Com/article/81 5784-treatment
3. Cohagan A, Worthington R, Krause RS. Alcohol and substance abuse evaluation. eMedicine [Internet]. 2009 Dec [cited 2010 Sep 15]. Available from: httpLL
!fljcine.medscaoe.com/article/8O5O84-overview
4. DynaMed [Internet]. lpswich (MA): EBSCO Publishing. 1993-2010. Record No. 114807, Alcohol withdrawal; [updated 2010 Aug 11; cited 2010 Oct 12];
[about 74 screens]. Available from: http://ebscohost.com/dynamed. Registration and login required
5. DynaMed [Internet]. lpswich (MA): EBSCO Publishing. 1993-2010. Record No. 115893, Opiate withdrawal; [updated 2010 Jul 20; cited 2010 Oct 12]; [about
51 screens]. Available from: htto://ebscohost.com/dvnamed. Registration and login required
6. DynaMed [Internet]. lpswich (MA): EBSCO Publishing. 1993-2010. Record No. 114858, Sedative-hypnotic overdose; [updated 2010 Jun 16; cited 2010 Oct
12]; [about 18 screens]. Available from: htto://ebscohost.com/dvnamed. Registration and login required.
7. (1994) DSM-IV, APA, p.181-3

SUICIDAL BEHAVIOUR
2077 Ed. Authors: Christina Beach, Jorge Perez-Parada MD FRCPC
OriginalAuthors: Daisy Hortmann, Justin Petryk MD, Jorge Perez-Parodo MD FRCPC
Station Objective
As suicidal behavior is a psychiatric emergency, physicians are expected to determine the likelihood of a suicide attempt by assessing risk
factors and manage the suicidal patient.
Differential Diagnoss
• Psychiatric disorders: mood disorders, anxiety disorders, schizophrenia, substance abuse, eating disorders, adjustment disorder,
conduct disorder, personality disorders (borderline, antisocial)
• Psychosis (delusions, paranoia, command hallucinations)
• Delirium (DSM-lV-TR criteria as part of the DDx for suicidal behavior):
• Disturbance of consciousness with decreased ability to focus, sustain, or shift attention
• A change in cognition or the development of a perceptual disturbance that is not better accounted for by a pre-existing,
established, or evolving dementia
• The disturbance develops over a short period of time and fluctuates during the course of the day
• Evidence from Hx, PE or lab findings that the disturbance is caused by the direct physiological consequences of a GMC
• Hypo/Hyperglycemia and other metabolic causes of delirium (e.g. TSH, electrolyte imbalance, infection)
History
CC • Suicidal behavior (e.g. suicide note, social isolation, preparing a will, giving away possessions, purchasing a burial
plot, feelings of hopelessness, suicide attempt)
HPI • History of risk factors (see below)
• Hopelessness, anhedonia, insomnia, anxiety, decreased cognition, psychomotor agitation, panic attacks
• Suicidal thoughts: content, duration, frequency
• Plan: lethality, rehearsal, access to means (e.g. firearm at home), intent, presence of suicide note
• Recent stresses and life events (e.g. sexual orientation, job loss, dissolution of relationship)
• Is the patient psychotic, depressed, or intoxicated?
• Are command hallucinations present?
• What protective factors are present (e.g. religious beliefs, children in the home, spouse/partner)?
RED FLAGS • History of attempted suicide, major depression, substance abuse, agitation, violence toward others, impulsiveness,
hopelessness, detailed plan
PYHx • Prior suicide attempt(s), depression or other psychiatric illness
• Severity and outcome of previous suicide attempts
• Childhood physical/sexual abuse
• Personality disorder
PMHx • Chronic illnesses or diseases
Meds • Medications that may be used in a suicide attempt (e.g. TCAs)
Allergies • Medications, environmental
FHx • Suicide attempts, psychiatric illness (mood disorders, anxiety disorders, schizophrenia, substance abuse, and family
dysfunction)
Social • Support systems available
• Legal history
• Domestic partner violence
• Substance abuse
Risk Factors • SADPERSONS (see box)
• Race/ethnic background (Aboriginal Canadians on reserves)
• Age (1 5-24 and >60 years old)

physical
General Approach
• Vitals: HR, RR, BP,T, Sp02
2. Inspection
• Signs of suicide attempts: scars on flexor surface of wrists (cutting), bruising/scars around neck (hanging), old blunt trauma (fall,
car crash)
.
Mental Status exam Sex (male)
• Appearance/behavior (e.g. general appearance, psychomotor agitation, restlessness) Age (> 60y/o)
• Speech: rate, rhythm, volume depression
• Affect (objective)/mood (subjective): flat, depressed revious attempts
• Thought process EtOH abuse
• Thought content (future orientation) Rational thinking loss
• Safety: suicidal/homicidal ideation uicide in the family
• Hallucinations/delusions Qrganized plan
• Orientation No spouse/support systems
• Insight/judgment serious illness/intractable pain
Investigations
i. Blood work
• EtOH, salicylate, and acetaminophen levels
• CBC-D, electrolytes, Cr, ammonia, ALT, ALP, albumin, TSH, glucose (rule out medical causes of altered behavior)
• U/A (infection is a common cause of delirium in the elderly population)
Treatment
1. Emergent
• Certification (Alberta-specific legislation)
• Involuntary detention in a hospital for up to 24 hours for assessment
• Requires all three of the following:
• “The person is suffering from a mental disorder”
• “The person is likely to cause harm to self or others or to suffer substantial mental or physical deterioration or serious
physical impairment”
• “The person is unsuitable for admission to a facility other than as a formal patient (in the case of an admission
certificate); or the formal patient is unsuitable to continue at a facility other than as a formal patient (in the case of a
renewal certificate)”
.
3
• Within 24 hours, another certificate may be completed and allows involuntary admission for up to one month from the date
of the 2” certificate
• Treat underlying psychiatric disorder (medications, psychotherapy, ECT)
• Inform and counsel family and friends
• Advise about support groups and other community resources
3. Follow-up
• Contracts are often used in clinical practice but may not influence outcome
4
4. Referrals
• Psychiatry, social worker, psychologist
References
1. American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision. Washington, DC, American
2. Andreasen N, Black D. Psychiatric Emergencies. lntroductoryTextbook of Psychiatry, Fourth Edition. Washington, DC, 2006. p 369-378.
3 Government of Alberta Health and Weliness [Internet]. Edmonton: Government of Alberta; ci 995-2010. [updated 2009 Dec; cited 2010 Sep 12]. Available
from: http://www.health.alberta.ca/newsroom/mental-health-act-oatients.html.
4. Work Group on Suicidal Behaviors. Practice guideline for the assessment and treatment of patients with suicidal behaviors. Am J Psychiatry. 2003
Nov; 160(11 Suppl): 1-60. doi: 10.11 76/appi.books.9780890423363.56008. PubMed PMID: 14649920.

EDMONTON MANUAL
Section #6
PEDIATRICS
Section Editor: Melanie Lewis BN MD MEd FRCPC
Associate Professor
Department of Pediatrics
INTRODUCTION mmunizauons 278

Abnormal Sexual Maturity .254 Limoino Child 280
Abnormal Stature .256 Neonatal ‘
Jata’ ‘ti’c 282
ADHD/Learning Disorder .258 Newborn Respiratory Distress/Cy nOsi5 .284
Anemia (Pediatric) .260 Pediatric Emergency .286
Childhood Communicable Diseases .262 Pediatric First Presentation .288
Depressed Newborn .264 Pediatric Whe°° .290
Developmental Delay .266 Periodic Health Exam of a Newborn .292
Down Syndrome .268 Periodic Health Exam in a Toddler/Child .294
Ear Pain .270 Periodic Health Exam in an Adolescent .296
Failure to Thrive .272 Speech and Language Abnormalities .298
Fever Without a Source in a Child < 3 .274 Stridor nn
Genetic Concerns & Pedigree .276
252 Edmonton Manual of Common Clinical Scenarios I Pediatrics

INTRODUCTION
MeIOn,eLew15BNMD MEd FRCPC
Pediatric OSCE preparation entails considering unique scenarios related to the fact most children are dependent on their caregivers to
provide the necessities of life. The history is usually relayed by a parent who will in turn carry out the plan within the context of the family
unit. When extracting a history, it is crucial to not only consider how the diagnosis and management plan will affect the patient, but how it
will affect the entire family. This often requires flexibility and ingenuity while ensuring patient safety.
A competent student will extract a history from the parent or guardian while involving the child or adolescent as much as possible to
gather key information and build rapport. Adolescent patients need to be afforded the opportunity to speak with the pediatrician alone to
enable exploration of challenging adolescent issues such as: sex, drugs, and relationships. Physical examination of a child requires a flexible
approach, but luckily it is rare that a small child will actually appear in an OSCE as standardization is impossible. Adolescent patients are
commonly used in examinations.
Development will often play a starring role in examinations. While painful to learn...it is a must know. The developmental stage of the child
will influence the approach to the patient and the management. Development also will play a role in OSCE stations where anticipatory
guidance is required; such scenarios include: safety, nutrition, and behaviour (sleep, toilet training, discipline).
Unique ethical and advocacy issues are common place in pediatric examinations. The parent who on behalf of their child: refuses
immunizations, declines conventional chemotherapy for a cancer diagnosis, or provides inadequate nutrition are examples of issues that
—
can appear in a pediatric OSCE. Similarly, recognizing and responding appropriately to child abuse (calling Children Services if you believe a
child is need of protective services) is a common scenario faced by clinicians in practice, and hence commonly appears in examinations.
Above all when approaching any OSCE station read and re-read your task. While outside the door write down key points you do not want to
forget in the stress of the moment. Take a deep breath and get into your assigned role. Be professional, honest (if you don’t know something
DON’T FAKE IT), and appropriately conclude the encounter.
Enclosed in this section, you will find a clinical based approach to many common pediatric problems that you may encounter in OSCEs and
in real life. I hope you find this document useful in your studies, but more importantly, it may be useful beyond your academic years and into
your clinical practice of medicine, regardless of the career path you may choose. Good luck.
Pediatrics Edmonton Manual of Common Clinical Scenarios 253

ABNORMAL SEXUAL MATURITY
2011 Ed. Authors: Chris Gerdung, Gary Ga/ante MD, Melanie Lewis SN MEd MD FRCPC
Origina/Authors: Chris Gerdung, Gory Ga/ante MD, Melanie Lewis SN MEd MD FRCPC
Station Objective
Evaluate abnormal sexual maturity in children by history, physical exam and select laboratory tests, as well as consider a broad differential
diagnosis for primary and secondary causes.
Diagnostic Criteria
• Delayed Puberty
• Lackoftesticularenlargement(>2.5cm)in males byl4years
• Lack of breast development in females by 12 years, or a lack of menarche 5 years after breast budding
• Constitutionally delayed or advanced (idiopathic)
• Premature thelarche: transient isolated breast development usually apparent in 1st year of life
• Premature adrenarche: sexual hair development <8 years in females, <9 years in males
• Precocious puberty
• Incomplete/premature pubarche (#1 cause of premature adrenarche) or premature thelarche
• Considered idiopathic. Bone age normal, pre-pubertal LH/FSH and gonadal steroid levels
• Central “true” puberty (pubertal levels of FSH, LH, T/E2, advanced bone age and linear growth, F>>M)
• Idiopathic or constitutional: 80-90% cases, F>>M
• CNS: tumor, irradiation, trauma, infection, inflammatory, congenital, etc.
• Endocrine: excessive androgens, 10 hypothyroidism
• Peripheral “pseudo” (FSH/LH levels suppressed; 2° to androgen/estrogen from adrenal or gonadal tissue)
• Ovarian cysts/tumors, testicular/germ cell tumors, testitoxicosis, adrenal tumors, CAH, McCune-Albright
• Malignancy
History
ID • Name, age, gender, ethnicity
CC • Delayed/Precocious puberty
HPI • Signs/symptoms of puberty and age at onset, presence of secondary sexual characteristics
• Menstrual history (age of menarche, cycle regularity, duration/volume of menses)
• Has the child maintained, increased or decreased their growth pattern
• Exercise, nutrition, stress, fatigue, anosmia
• Diarrhea, wt decrease, abdominal pain
RED FLAGS • Wt decrease, neuro signs/symptoms, contrasexual pubertal development before 8 years in girls, and 9 years in boys,
or no secondary sexual characteristics after the age of 14 years
PMHx • Asthma, CNS disease, endocrine disorder, IBD, liver disease, Cancer/chemotherapy/radiation, chronic infection,
malnutrition, renal failure
PSHx • Previous surgeries
PO&GHx • Gestation, GPTAL, route of delivery, birth wt, PROM, gestational infection, gestational DM, GBS screen
Meds • Any medications, whether OTC, vitamins, CAM or otherwise
Allergies • Allergies to medications, food or environment
FHx • Age of puberty onset in the child’s mother/father/siblings, ñnal height of family
• History of precocious puberty (CAH, testitoxicosis, McCune Albright)
• PCOS, DM, neoplasm, genetic syndromes
Social • HEADS (see PHE adolescent), stressors, body image, drugs/EtOH/smoking, mood, abuse
ROS • HEENT: craniofacial abnormalities, midline defects
• GI: diarrhea, abdominal pain, melena
• MSK / DERM: short stature, erythema nodosum, clubbing
Risk Factors • Genetic conditions
254 Edmonton Manual of Common Clinical Scenarios Pediatrics

physical
1. General Approach
• 2 T, growth parameters (Ht/Wt/HC), growth charts, assess for cognition
Vitals: HR, BP, RR, 5p0
• DetermineTanner staging, body proportions/habitus, facial abnormalities, shield chest, gynecomastia in males, stigmata of IBD
(erythema nodosum, perianal tags, clubbing)
Proportions: arms span>ht, upper/lower body ratio (suggests eunochoidal habitus and hypogonadism)
2. Exam
Full exam: evidence of chronic disease, dysmorphic features, abdominal masses
Full neuro exam: including fundoscopy (papilledema), visual fields, CNs (anosmia), strength
Size of testes(>2.Scm = pubertal), penis size, clitoris (clitoromegaly), palpate breasts (glandular tissue vs. adipose tissue)
Tanner Pubic Hair Development Female Breast Development Male Genital Development
1 Pre-pubertal hair pattern Pre-pubertal — only papilla elevated Pre-pubertal size (as in early childhood)
(vellus)
2 Long, sparse pigmented Breast bud (elevation of breast and Testes/scrotum enlarge, scrotal skin reddens
downy hair at base of penis! papilla) and areolar enlargement with change in texture
labia
3 Darker, coarser, curlier hair — Breasts and areola continue to enlarge Enlargement of penis (length 1 st), continued
extends to pubis growth of scrotum and testes
4 Hair is adult type but covers Areola and papillae form secondary Continued growth of penis, development of the
smaller area (no spread to mound, above level of breast glans, darkening of scrotal skin
medial thigh)
5 Adult hair distribution and Mature female breasts Adult genitalia (size/appearance)
density
Investigations
1. Blood work
• CBC-D, electrolytes, glucose, cortisol, PRL,TSH, LH, FSH, GnRH, Cr, urea, AST, ALT, ALP, CRP, ESR, testosterone, estrogen, estradiol,
DHEA, 1 7-OHP (for CAH), 3-hCG
• Bone age, MRI if suspecting neurologic lesion, abdominal US if hormone secreting tumor is suspected
3. SpecialTests
• Karyotype if considering Turner’s or Klinefelter’s syndrome, GnRH!ACTH stimulation test
Treatment
• Medical: treat underlying pathology
• Endocrine abnormalities: inhibit or replace abnormal hormones as needed
• Surgical
• Remove tumor, if present. Radiation may or may not be needed as adjunct therapy
2. Follow-up
• Follow up with a pediatrician for constitutionally delayed or advanced
3. Referrals
• Endocrinology, Oncology, Genetics, Psychiatry/Psychology
References
1. Bramswig J, Dubbers, A. Disorders of Pubertal Development. Continuing Medical Education. 2009; 106(1 7):295-304
2. Traggiai C, Stanhope R. Delayed Puberty. Best Practice & Research Clinical Endocrinology and Metabolism. 2002;1 6(1 ):1 39-151
Pediatrics I Edmonton Manual of Common Clinical Scenarios 255

ABNORMAL STATURE
201! Ed. Authors: Chris Gerdung, Gaiy Galante MD, Melanie Lewis 8N MEd MD FRCPC
OriginalAuthors: Chris Gerdung, Gory Galante MD, Melanie Lewis BN MEd MD FRCPC
Station Objective
To thoroughly evaluate abnormal stature in children by means of history and examination, while considering a broad DDx for primary and
secondary causes of this abnormal stature.
• Short Stature
• Ht less than the 3
rd percentile
• Growth velocity < 5 cm/yr

• Tall Stature
• Ht greater than the 97
th
percentile
Short Stature Tall Stature
• Normal variants (GV> 5 cm/yr) • Normal variants
• Familial short stature • Familial tall stature
• Constitutional short stature (late bloomer) • Constitutional tall stature
• Abnormal variants (GV <5cm/yr) • Abnormal variants
• Genetic syndromes (Turner/Down syndrome) • Genetic syndromes (Klinefelter’s, Marfan’s
• Hormonal deficiency (GH,Thyroid) • Hormonal excess (adrenal, GH)
• Chronic dz (poorly controlled asthma, IBD, celiac) • Other (obesity)
• latrogenic_(steroids)

• Marfan’s syndrome, malignancy
History
CC • Abnormal Stature (short or tall)
HPI • Growth pattern (height and weight percentiles)
• Increased or decreased growth velocity
• Abnormal body proportions
• Precocious puberty
-Q • Sexual maturity
i’D
0. RED FLAGS • Dysmorphic features, growth velocity <5 cm per year, precocious puberty
PMHx • Nutritional status
-ç • Genetic abnormalities
• CVD, renal disease, IBD, hypo/hyper growth hormone, hypo/hyper-thyroid, asthma, cancer (radio/chemo therapy)
• Immunodeficiency, frequent infections
• PSHx • Neuro/CV surgery
PO&GHx • Gestational age, GTPAL, route of delivery, birth weight, PROM, oligohydramnios, GDM
• Infections (TORCH)
• Nutrition, smoking, EtOH or recreational drug use
Meds • Any medications, especially corticosteroids, or chemotherapy
• OTC meds, vitamins, CAM or otherwise
Allergies • Atopy and allergy (food, medication, environmental)
FHx • Mother and father’s height and age
• Height of siblings, grandparents and other relatives
• Genetic syndromes
• Cancer, celiac disease, Cushing disease, GH deficiency, hypothyroidism

Social EtOH, smoking, recreational drug use, exercise
• Effect of stature on psyche
—.
• ROS HEENT: visual changes, headaches, energy level
• CV: shield chest, wide-spaced nipples (Turner’s), heart sounds, murmurs, femoral pulses
• RESP: SOB, wheeze, cough, stridor
• Gl: vomiting, abdominal pain, diarrhea/constipation
• GU: appropriate sexual maturation for age
Risk Factors • Familial (short/tall parents), genetic syndromes (Down’s/Turner’s), radiotherapy
physical
1. General Approach
• , Temp. growth parameters (height/weight/HC, growth charts)
Vitals: HR, BP, RR, Sp0
2
• Full exam: evidence of chronic disease, dysmorphic features, systemic disease
2. Inspection
• Dysmorphic features
• Upper/lower body ratio
• Body proportions (ie. head, trunk, legs, arms all appear proportionate)
• Sexual maturity (Tanner staging)
• Obesity
3. SpecialTests
• Full neuro exam to rule out CNS lesion
• Include fundoscopy (papilledema), visual fields, CNs (anosmia), strength, reflexes
• Calculation of the mid-parental ht
• For girls = ((father’s ht 13) + mother’s ht)/2
—
• For boys = ((mother’s ht + 13) + father’s ht)/2

• Measure arm span (t in Marfan’s syndrome)
• Stigmata of Turner’s (neck webbing, hyperconvex fingernails, small mandible, broad chest, prominent ears)
Investigation
1. No investigations warranted in short stature if growth velocity is normal (>5cm/year)
2. Blood work (as guided by history and physical)
• CBC-D, ESR, LETs, UA, serum cortisol, IGF-1, IGFBP-3, GH,TSH, ferritin, glucose, LH, FSH testosterone, estradiol, homoscysteine, 17
OHP (CAH)
• Bone age (anterior radiograph of left wrist)
4. SpecialTests
• Karyotype if genetic syndrome suspected
• Further workup as needed, guided by history and physical (ie. stool for occult blood if suspecting IBD)
Treatment
1. No treatment needed for normal variants
• Medical
• Treat underlying hormone deficiency/excess (GH therapy, thyroxine replacement)
• Surgical
• Tumor resection if present
3. Referrals
• Pediatrics, Endocrine, Geneticist
References
1. Nwosu BU, Lee MM. Evaluation of short and tall stature in children. American Family Physician 2008; 78(5):597-604

ADHD/LEARNING DISORDER
2011 Ed. Authors: Peter Gill, Gary Galante MD, Melanie Lewis EN MEd MO FRCPC
OriginalAuthors: Peter Gill, Gory Galante MO, Melanie Lewis BN MEdMD FRCPC
Station Objective
Evaluate a child with a suspected learning disorder (LD) and overview diagnostic criteria for attention deficit hyperactivity disorder, while
excluding cognitive, psychosocial, or behavioral issues as confounders or co-morbidities
• LD: intrinsic cognitive difficulty, results in under-achievement for one’s intellectual potential
• Scores on achievement tests in reading, mathematics or written expression below (> 2 SD) expected
• Interferes with academic achievement or ADLs that require reading, mathematics or writing skills
• ADHD: developmentally inappropriate levels of inattention, impulsivity and hyperactivity (see Table 1)
• Classified by predominant symptom: Table 1. DSM-IV Criteria for ADHD
• Inattentive 6 signs of inattention OR hyperactivity/impulsivity
• Hyperactive/Impulsive • Present for at least 6 mo and is disruptive/inappropriate for
• Combined (6/9 for both) development level
• MUST RIO other causes of inattention (see below) • Some symptoms present before age 7
• Co-morbidities: LD, ODD, CD, depression, anxiety, Present in 2 settings
tic disorder, substance abuse • Significant impairment in social setting, school
2. Common Conditions • R/o other causes
• Organic:
• Neuro: CNS injury/infection, epilepsy, FASD, genetic disease like T21 /Fragile X
• Sensory: hearing/visual impairment, recurrent AOM
• Medical concerns leading to chronic fatigue/pain: thyroid disease Fe deficiency anemia, undernourished, DM, sleep disorders
such as obstructive sleep apnea
• Cognitive: LD, speech/language disorder, developmental delay/MR, PDD/ASD, ADHD
• Behavioral/emotional: mood disorder (depression, anxiety, PTSD, OCD), ODD, CD
• Environment: poverty, stress, social isolation, child abuse, poor learning/language model, family dysfunction
• Medication/Drugs: anticonvulsants, marijuana, EtOH, cranial radiation
History
ID • Age, sex, ethnicity, name, home
CC • Identify parental/caregiver concern: school failure, poor performance, academic challenges
HPI • Timeline: onset/course of symptoms, recent event (divorce/domestic violence/death), regression
• School: have teachers noticed learning problems, grade retention, special education resources
• Performance: grades, best/worst subjects, homework, impairments, mood, absenteeism
• Multiple settings (home, school, playground) and behaviors: annoying/disruptive, avoidance (school/work),
aggression/violence, authority (oppositional), attention, activity
• Attention: disorganized, forgetful, easily distracted, loses things, careless/poor attn to detail, doesn’t listen when
spoken to directly, no follow-through, avoids or difficulty sustaining attn
• Hyperactive-impulsive: fidgets, excess running/climbing/talking, leaves seat, can’t play quiet, “on the go”or restless,
blurts Out answers, interrupts/intrudes, difficulty waiting turn
• Current developmental level, ask parent/child to identify strengths/abilities
• Collateral Hx from other sources: teacher, babysitter, siblings
RED FLAGS • Regression, neonatal complications, FHx, child abuse/neglect, new/recent onset
PMHx • Prenatal: prenatal care, U/S frequency, maternal illness (GDM, HTN, infections, rash, fever, bleeding), maternal
exposures to toxins/teratogens, smoking/EtOH/drugs, IUGR
• Perinatal: asphyxia, APGAR scores, prematurity, low birth wt, abnormal presentation
• Postnatal: neonatal complications (TORCH infection, meningitis, encephalitis, seizure d/o,jaundice, CNS trauma),
NICU admission, length of stay, neonatal metabolic screen
• Head trauma/irradiation, chronic illness, seizures, recurrent/chronic OM, Fe deficiency, Ca
PSHx • CNS surgeries (shunt, tumour)
PO&GHx • Gestation, GTPAL, route of delivery

FHx ADHD, LD/school failure, autism, deafness, blindness, MR, mental health
3 generation pedigree: consanguinity, pertinent familial dz
Meds Rx (particularly neuroleptics, bronchodilators, corticosteroids), CAM, vitamins, OTC
Allergies Medications, food, environmental
-
Social • Marital status/family unit, finances, school/peer relations, health plan, effect of illness on family
• Psychosocial situation: adoption, parental neglect, abuse
—
Dev. Age of developmental milestones, GM skills compared to peers, ability to perform daily tasks
—
lmmun Routine, special
ROS Vision/hearing problem, nutrition/diet, sleep habits/snoring/fatigue (screen for OSA)
Risk Factors Prematurity, perinatal asphyxia, genetic abnormality, chronic disease, +ve Family Hx
Physical
i. General Approach
• Vitals (especially BP/HR before stimulants), Growth measurements: HC (micro/macrocephaly), wt, ht
• Well-being and behavior, alertness, attention span, impulsivity, energy/activity, cooperation
• Developmental level, communication, parent-child interaction
2. Inspection
• Dysmorphic features (see Genetic Concerns and Pedigree), neurocutaneous findings (e.g. café au lait)
3. Neurologic examination + hearing/vision screen
• CN, strength, muscle tone (hypo/hypertonia), reflexes, coordination, gait and limb movements
Investigations
1. Adjunctive clinical assessments:
• Audiology and vision assessment: 1st line investigations to r/o sensory abnormality
• Rating scales (completed by parents and teachers):
• Narrow-band (Conners’ short form): focus specifically on core ADHD sx, used for Dx
• Broad-band (Conners’ long form/Vanderbilt): assess behavioral sx, narrow DDx, identify comorbidities (ODD, depression etc)
• Neuro/psychoeducational tests: identify strengths/weaknesses in intellectual potential (WISC, WIAT)
2. Blood work: only indicated if suspect organic pathology
• Karyotype, fragile X testing (FMR1 triplet repeat)
• If clinically indicated: CPK, thyroid function studies, lead, Fe, metabolic workup
• Neuroimaging indicated if micro/macrocephaly, neurological symptoms (MRI preferable over CT)
4. SpecialTests
• EEG if seizures are suspected
Treatment
1. Treatment options: largely depends on identified problem
• Appropriate communication and management plan tailored to family needs, resources, etc.
• Multidisciplinary services: specialized educational support and recreational activities
• Behavioral management strategies and psychological counseling (if required)
• Pharmacologic: stimulant medication e.g. Methyiphenidate (Ritalin) - DA/NE in frontal lobes
2. Follow-up
• Regular appointments to monitor developmental progress, growth and behavior
3. Referrals
• Developmental Pediatrician, child Psychiatrist/Psychologist, speech language pathologist, OT
References
1. Zorc JJ, Alpern ER, Brown LW, Loomes KM, Marino BS, Mollen CJ, Raffini U, editors. Schwartz’s clinical handbook of pediatrics. 4
th
ed.
Philadelphia. Elsevier Inc.; 2009
2. Cheung A, Williams BA, Sivarajan By, editors. The HSC handbook of pediatrics. 1 Ot ed. Elsevier Inc.; 2003.
3. MialI L, Rudolf M, Levene M. Paediatrics at a glance. 2
r,d
ed. Oxford. Blackwell Publishing Ltd.; 2007.

ANEMIA (PEDIATRIC)
201 I Ed. Authors: Lauren Kitney BSc MD, Gary Galante BSc MD, Melanie Lewis SN MEd MD FRCPC
OriginalAuthors: Lauren Kitney BSc, Gary Galante BScMD, Melanie Lewis BNMEdMD FRCPC
Station Objective
To develop a thorough, efficient approach to anemia in the pediatric age group
Table 1: Anemia alaorithm
1. Common Conditions Reticulocytosis T
• Iron deficiency anemia Microcytic Normocytic Macrocytic
increased MCV)
2. High Mortality • Iron deficiency • Chronic kidney disease • Hypothyroidism Blood loss
• Bleeding, malignancy, • Lead • Malignancy/infiltration • Chronic liver disease Hemolytic Disorders
Aplastic anemia, poisoning • Chronic Disease (e.g. • B12 deficiency (rare- ileal Sickle cell disease
kernicterus • Chronic infection, IBD, CTD) resection, vegan) Enzymopathy
disease • Aplastic anemia • Folate def (drugs, Membranopathy
(inflammation) (idiopathic, infxn, toxin, malabsorption, malnutn) DIC/HUSIrTP
• Thalassemia immune, NYD) • Congenital causes of BM Immune Hemolysis
• Sideroblastic • Transient failure/ inherited aplastic Auto/isoimmune
anemia erythroblastopenia of anemias Drug-Induced
childhood (TEC)
History
ID . Age, sex, ethnicity
CC • Fatigue, pallor, incidental finding
HPI . Nutrition: iron sources, amount and duration of breast milk/cow’s milk/formula (iron-enriched?)/juice, restricted diet
(strict veganism Bi 2 def), mother’s diet (if breastfeeding)
—
• Sx of anemia: fatigue, lethargy, irritable, pallor, SOBOE, feel cold, presyncope/palpitations

• Sources of blood loss: stool, urine, emesis, hemoptysis, epistaxis, bruises, iatrogenic, trauma
• Malabsorption: steatorrhea, diarrhea, abdominal pain/cramping, abdominal distention (ascites)
• Signs of chronic disease/malignancy: fevers, weight loss, lack of growth, fatigue, anorexia
• Other: jaundice/dark urine (hemolysis), rashes, recurrent infections, pica (non-food appetite), pagophagia (appetite
for ice suggest Fe deficiency)
—
RED FLAGS • Weight loss, fatigue, failure to thrive, splenomegaly, lymphadenopathy, abnormality in other cell lines
PMHx • Perinatal: gestation, birth weight, IUGR, APGARS, mode of delivery, neonatal jaundice, complications, birth
anomalies (particularly extremities assocd with congenital BM failure)
—
• Medical: chronic condition (liver/kidney/bowel/thyroid, autoimmune, pancreas), prior hospitalizations/emergency

department visits, blood transfusions/episodic anemia
• Growth or developmental (FM, GM, social, language) concerns, behavior/school performance
• Menstrual (if applicable): amount of blood loss, LMP, cycle length
PSHx • Recent surgery (blood loss), bowel resection, splenectomy
PO&GHx • Maternal illness/infections (HIV), blood type, Rh incompatibilities, transfusions
(D FHx Ethnicity, consanguinity, anemia, jaundice, neonatal jaundice, inflammatory bowel disease, cow’s milk protein
0 allergy, celiac disease, splenectomy or cholecsytectomy, thalassemia/sickle cell disease, G6PD deficiency,
autoimmune disease
. Meds Prescription (ASA/NSAID5, or phenobarbital/phenytoinfrMP-SMX assoc with folate deficiency), any recently started
meds, CAM (known ingredients)
Allergies • Drugs, environmental, foods
Social • # of school days missed, exposures, safety concerns, neglect, health plan, psychosocial concerns, old house/recent
renovation/ neigbourhood risk (lead), recent immigrant
Immun • Routine, other (travel history; if positive immunizations or chemoprophylaxis)
—
ROS Sleep, appetite, activity level

• HEENT: cough, lumps (lymphadenopathy), neck pain, headache, yellow sclera
• CV/RESP: chest pain, palpitations, shortness of breath, increased work of breathing
• GI/GU: abdominal pain, diarrhea, vomiting, dysuria, dark/tea-colored urine
• MSK / DERM: limp, arm/leg pain (night), finger pain (dactylitis in SCD), rash, jaundice
Risk Factors • >24 oz of milk/day or + juice (nutritional deficielicies), FHx anemia, chronic disease, ethnicity (African,
Mediterranean, Southeast Asian, Hispanic), prematurity

physical
1. General Approach
• ABCs, vitals, general appearance, growth measurements: head circumference, weight, height, BMI (wt/ht )
2
2. Inspection
• HEENT: dysmorphic features [congenital disease], frontal bossing/maxillary hyperplasia [f3thal], lethargy, hydration status, focal
infection, thyroid, scleral icterus, pallor of conjunctiva/oral mucus membranes
• SKIN: pallor (palmar creases/nail beds), jaundice, petechiae, purpura, cool temperature, brittle hair/nails [Fe deficient], angular
stomatitis fissure at corners of mouth/glossitis [Fe/B12 deficient], rash [inheritedAA]
-
• RESP: signs of respiratory distress

• CVS: tachycardia, SBP < [70 +(2 x age in yrs)] mm Hg, orthostatic change, delayed cap refill (>2 sec)
• MSK/NEURO: confusion, altered vibration/position sense, spastic weakness, hyperreflexia (cord damage in B1 2 deficiency),
peripheral neuropathy (lead toxicity, Bi 2 deficiency), hypotonia
3. Palpation
• GI: hepatomegaly, splenomegaly, abdominal pain/tenderness, FOBT positive
• LYMPH: focal or generalized lymphadenopathy
4. AuscultatiOn
• RESP: decreased breath sounds, crackles, wheezes
• CVS: heart sounds, systolic ejection murmur (innocent, flow)
iTable 2: Iron deficiency anemia
p4emiology Most common cause
, Etiology Nutritional deficiency (Term infants deplete iron stores by 6 months, pre-terms by 2-3 months need iron fortified
—
formula or cereal thereafter), excessive/early cow’s milk (poorly absorbed iron source, satiating, calcium impairs iron
absorption),_GI_malabsorption,_chronic_blood_loss_(e.g._occult GIB_in_CMPI)
Presentation Asymptomatic, pallor, fatigue, irritability
Iperipheral smear Hypochromic, microcytic
Iron studie -.-ferritin, serum iron, tTIBC, -i,-transferrin saturation
Treatment Oral elemental iron 6mg/kg/d in three divided daily doses x 3 months (take with juice/vitamin C)
Follow for response (treticulocytes by 2-3d, tHgb 4-30 d)
Investigations
1. Blood work
• Initial Work-up:
• CBC with differential, reticulocyte count
• Peripheral smear [may suggest hemolytic cause, megaloblastic orsideroblastic anemia, infiltration, Fe deficiency]
• Ferritin,TIBC, serum iron, transferrin saturation [iron deficiency],TSH, Cr, BUN [chronic disease], serum lead level (if risk)
• Oral iron trial, If fails: gA, ATTG[celiac disease], FOBTx 3, +1- Hgb electrophoresis[hemoglobinopathies]
• Direct antiglobulin testing, total bilirubin, haptoglobin, LDH [hemolytic anemia], vitamin B1 2 & folate
• Bone marrow aspirate if unexplained anemia, leukopenia, thrombocytopenia or pancytopenia [malignancy]
• If indicated
Treatment
1. Emergent
• ABCs, fluid resuscitation, possible transfusion
• Vary with etiology
3. Surgical
• May need splenectomy for spherocytosis (If so, vaccine for encapsulated organisms pneumococcal/meningococcal/H.influenzae
-
type B vaccination)
4. Follow-up
• Pediatrics, dietician (if secondary to nutritional deficiency)
5. Referrals
• Hematology, oncology, gastroenterology (may require endoscopy), genetics, nutrition
References
1. Heng M, Greenwald JA. Toronto notes (2007). 23rd ed. Toronto: Toronto Notes for Medical Students, Inc.; 2007
2. Hayw, Levin M, SondheimerJ, Deterding R. Lange Current Diagnosis &Treatment in Pediatrics. 18 th ed. United States: McGraw-Hill
Companies, Inc.; 2007.

3. Pearson H, Dallman P. Anemia: Diagnosis and Classification. In: Rudolph C, Rudolph A, Hostetter M, Lister G, Siegel N, editors. Rudolph’s
Pediatrics 21’
ed. United States: McGraw-Hill Companies, Inc.; 2003.
t
4. Bomgaars, L. Approach to the child with anemia In: Up to Date desktop 17.2, 2009.

CHILDHOOD COMMUNICABLE DISEASES
201 I Ed. Authors: Peter Gill, Gary Ga/ante MO, Melanie Lewis SN MEd MO FRCPC
Or/gina/Authors; Peter Gill, Gary Ga/ante MD, Melanie Lewis BNMEdMD FRCPC
Station Objective
Describe the principles of immunization procedures, determine the incubation period and possible route of communication and outline
measures of prevention to contain the spread of communicable disease
Di erential Diagnosis
Table 1. Pediatric Exanthems
—
Etiology Rash Incubation Communicability Therapy Isolation
—
Measles Erythematous maculopapular - fades 4 d before (PEP) Post

Morbillivirus (brown color/desquamates) 8-1 3d symptoms to 4d exposure Resp
Head to trunk/extremities after rash prophylaxis
Scarlet fever Erythematous maculopapular, 1-4 days
Penicillin x 10- Barrier until
S. pyogenes blanches, sandpaper like, diffuse (<48 h of During infx
14d ABx
Fades with desquamation fever)
Rubella Erythematous maculopapular, face to 7d before rash to 5d
14-21d None Resp
Rubivirus trunk, discrete after rash
Erythema infectiosum Slapped cheek appearance -
(“Fifth Disease”) Maculopapular trunklextremity- Unknown (mostly

4-14d None Resp
Parvovirus 819 Lacelike (reticulate) rash mostly on during incubation)
extremities_(central_clearing)
Roseola infantum Erythematous maculopapular, on neck,
HHV-6 arms,trunk 5-15d Unknown None None
Rash_with/after_defervescence
Varicella Red papules -* clear vesicles on 1 -2d before rash
None ± acyclovir, Airborne
VZV erythematous base lysis
- 10-21d until all lesions
PEP and contact
Pruritis, lesions in different stages crusted over
History
CC • Fever, rash, sore throat
HPI Onset/time course of rash, associated pain/pruritis, discharge, honey crust, location/distribution, aggravating/
alleviating (exercise, rubbing, bathing may cause rash recurrence in
— disease)
• Has the rash evolved (location, color, type), peeling/fading, is there> 1 rash
• Associated symptoms: fever, seizure, H/A, malaise/lethargy, confusion, gait disturbances, sore throat, otalgia,
cough, SOB, NN/D, anorexia, sore/red eyes, sore/swollen joints, decreased U/O
• Determine if associated Sx preceded or followed onset of rash
. AnyTx attempted: topical steroids, creams, etc.
• Suspected precipitants, Hx of similar rash
. Hx of sick contacts, travel, pets, bug bites, daycare, farm visits, ingestion of unpasteurized milk or uncooked meat,
source of water supply, plants
RED FLAGS Petechiae (non-blanching rash), altered LOC/lethargy, seizures, stiff neck, high fever, hypotension, rapidly
progressing (Rio necrotizing fasciitis), short of breath, immunosuppressed
PMHx Prenatal: prenatal care, U/S frequency, IUGR, maternal illness (GDM, HTN, bleeding), GBS/HIV/lmmune status (HBV/
RubellaNZV), maternal exposures to teratogens, smoking/ EtOH/drugs, Hx of fever, rash, flu-like illness, genital
lesions, cleaning cat litter, deli meats, etc.
• Perinatal: asphyxia (APGAR scores), prematurity, low birth wt, abnormal presentation
• Postnatal: neonatal complications (TORCH infection, meningitis, encephalitis, seizure d/o, jaundice, CNS trauma),
• Immunodeficiency, chronic illness
PSHx • Splenectomy, solid organ transplant, stem cell transplant
PO&GHx Gestation, GTPAL, route of delivery, presentation,
FHx Eczema, RA/Kawasaki, immunocompromised, unimmunized

-
Meds New medications, list all medications, CAM, vitamins, OTC

—
Allergies Medications, food, environmental, specify reaction if exposed
-
Social Marital status/family unit, home crowding, finances, school/peer relations, daycare, health plan
-
Dev. • GM, FM, language, personal-social

Immun Routine IUTD (ask to see immunization record), Influenza (6+ months)
• Other (Hep A, RSVIg, Pneumo polysaccharide 23-valent, Meningoccocal conjugate 4-valent)
ROS • Stiff neck, H/A, VA problems, otalgia, mastoid tenderness, pharyngitis, rhinorrhea, urine freq.
Risk Factors • Immunocompromised, environmental (daycare, sick contacts)
Physica
i. General Approach
• ABC and vitals, growth measurements: HC (micro/macrocephaly) wt, ht
2. Inspection
• GENERAL (toxic?): activity level, lethargy, color, tone, weakness, vigor, irritability, hydration status
• SKIN/MSK
• Exanthem Distribution (don’t forget hairline, nails, umbilicus, palms/soles, groin)
—
• Appearance: color, shape, size, scaling, morphology (macule, papule, vesicle, pustule)
• Pattern: dermatomal (zoster), linear, confluent/diffuse, discrete
• Enanthem (mucus membranes conjunctiva, lips/buccal, nasal, anogenital)
—
• Koplik spots (grey-blue dots on buccal mucosa measles), strawberry tongue (scarlet fever, Kawasaki), vesicles (VZV/
-
HSV), Forschheimer spots (rose spots on soft palate rubella)

—
• Signs of local/superimposed infection: purulent discharge, honey crust, bullae, lymphangitis

• Check skin/mucous membranes esp. ear, umbilical stump, genitalia, joints/extremities
—
• Jaundice, mottling, cyanosis, pallor, petechiae/purpura (congenital infxn, DIC, meningococcemia)

• HEENT: conjunctivitis, rhinitis, rhinorrhea, middle ear effusion/inflammation
• RESP: signs of respiratory distress, tachypnea (>60/mm), grunting, nasal flaring, retractions, apnea
• CV: tachy/bradycardia, hypotension (SBP < 60 mm Hg), delayed cap refill (>2 sec)
• NEURO: bulging fontanelle, nystagmus, ataxia, tremor, CN palsy or focal deficits, ascending paralysis (GBS)
3. Palpation
• HEENT: lymphadenopathy, parotitis, GI/GU: hepatosplenomegaly, epididymo-orchitis
4. Auscultatiori
• RESP: I. AE, bronchial breath sounds, crackles, wheezes
Investigation
1. Blood work: diagnosis is often clinical (specific serology may be available, looking at 1gM antibody titres)
• Suspect scarlet fever throat swab
-
• If clinically indicated: CBC-D, blood C&S, urine R&M, C&S, LP (CSF for HSV), LFT’s, ASOT, CXR
Treatment
1. Management: See Table 1
• Conservative management for most conditions
• Appropriate isolation and precautions (VZV: avoid contact with immunocompromised hosts)
• Routine immunization schedule
3. Follow-up
• Ensure resolution of rash, complete immunization schedule
References
1. Kleigman RM, Marcdante KJ, Jenson HB, Behrman RE. Nelson essentials of pediatrics. 5 th
ed. Philadelphia. Elsevier Inc.; 2006.
2. Zorc JJ, Alpern ER, Brown LW, Loomes KM, Marino BS, Mollen Ci, Raffini U, editors. Schwartz’s clinical handbook of pediatrics. 4 th
ed.
Philadelphia. Elsevier Inc.; 2009
3. Cheung A, Williams BA, Sivarajan By, editors. The HSC handbook of pediatrics. 1 0tt ed. Elsevier Inc.; 2003.

DEPRESSED NEWBORN
2011 Ed Authors: Peter Gilt Gary Ga/ante MD, Melanie Lewis 8NMEdMDFRCPC
OriginalAuthors: Peter Gill, Gary Galante MD, Melanie Lewis BN MEdMD FRCPC
Station Objective
Elicit selective maternal history, determine vital signs, rapidly assess for possible causes of a depressed neonate
• Largely clinical based on Hx and PE findings: respiratory distress, cyanosis, shock, etc.
• RDS: premature, respiratory distress
• Hypoglycemia: glucose < 2.8 mmol/L (< 2.5 mmol/L in premature)
• Anemia: Hb <140 g/L
• Respiratory distress: (see Respiratory Distress in a Child) RDS, meconium aspiration
• Sepsis: GBS
• Anemia: erythroblastosis fetalis, secondary hydrops fetalis
• Maternal: drugs, DM, pregnancy induced HTN, narcotics during labor
• Congenital: malformation, birth asphyxia, genetic
• Metabolic: hypothermia, hypoglycemia, inborn errors of metabolism
• Other: shock, cyanosis, congenital heart dz
3. High Mortality:
• Asphyxia, infections, congenital abnormalities, prematurity, erythroblastosis fetalis
History
ID . GA, sex, ethnicity
CC • Depressed newborn, respiratory distress
HPI • Complete a focused and selective maternal Hx
• OPQRSTU of event and reason for assessment
• Prenatal Hx: prenatal care, U/S frequency, estimated date of delivery
• Rh status, maternal blood type, GBS status
• Maternal illness: GDM, HTN, infections, rash, fever, bleeding
• Maternal exposures: medications, toxins, teratogens, smoking, EtOH, drugs
• Prenatal complications: Poly/oligohydramnios, fetal movements
• Labor: length, spontaneous/induced, membrane rupture (time, spontaneous/induced), antibiotics
• Narcotics during labour
• Delivery: route of delivery, birth wt, presentation, forceps/vacuum, trauma
• APGAR scores, meconium present
RED FLAGS • Meconium, low APGARS, prematurity, low birth wt
PMHx . IUGR, GA, prematurity (steroids), newborn screen if available
PO&GHx • GTPAL, previous high-risk pregnancies
FHx • Hematological disorder, congenital abnormalities
Meds • Rx, vitamins, OTC
Social • Marital status/family unit, finances, health plan, psychosocial situation
ROS • Nutrition, choking with feeding, voiding and stool pattern,V/D, urine color/amount
Risk Factors Prematurity, perinatal asphyxia, genetic abnormality, maternal risk factors
•
Table 1. APGAR Score

Sign 0 1 2
Physical 1.HR Absent <100 >100
2. Resp effort Absent Slow, irregular Good. crvincl
—
1. General Approach 3. Irritability No response Grimace Coucih/cry

• ABCs and VITALS Limp Some flexion Active Motion
4.Tone
• APGAR score at 1 mm, 5 mm Cometelyp
5. Colour Blue, pale Body pink, extremities blue
2. Inspection
• GENERAL: lethargy, weakness, vigor, irritability, dysmorphic feat.
264 Edmonton Manual of Common Clinical Scenariosj Pediatrics

• DERM: jaundice, mottled, cyanosis, petechia
• RESP: signs of respiratory distress
• Tachypnea (>60/mm), grunting, nasal flaring, retractions, apnea
• CV: tachy/bradycardia, hypotension (sBP < 60 mm Hg), delayed cap refill (>2 sec)
• GI/GU: testis/clitoris, ambiguous genitalia
• NEURO: cephalohematoma, micro/macrocephaly, seizures, response to stimuli
3• Palpation
• GIIGU: hepatomegaly, palpable testis
• NEURO: bulging fontanelle, weak suck, hypo/hypertonia
4. AuscultatiOfl
• RESP: ,J AE, crackles
.
SpecialTests
• Transilliuminate chest wall if suspect pneumothorax
Investigations
i. Blood work
• CBC-D, electrolytes, glucose, T&C, Ca
, Mg, + CRP, PT/PT1 LETs, ABG
2
• Septic w/u: blood C&S, urine C&S and CSF cultures (LP if pt stable)
• Hemolytic w/u: peripheral blood smear, Coombs test, bill (conjugated/unconjugated)
• CXR + abdominal x-ray
• Consider head U/S or CT head
Treatment
1. Emergent
• Before ABC’S, resuscitate ALL infants: warmth, position/clear airway (“sniffing” position), stimulate/dry
• Airway: gentle suction of mouth then nose suction trachea if meconium AND baby not vigorous
-
• Breathing: PPV with 100% 02 at 40-60 breaths/mm with visible chest rise
• Circulation: If HR <60, apply chest compressions (“60 or less, compress”) compress 1/3 of AP diameter
-
• 90 compressions coordinated with 30 breaths/mm (3:1 compressions/breath, breath q2 sec)

• Drugs: epinephrine (HR<60), naloxone/narcan (maternal narcotic use, respiratory depression)
• Identify newborn in need of prompt respiratory support
• Assess need for circulatory support: consider umbilical vein for quick venous access
• Identify pts that require ongoing specialized care and initiate respiratory and blood pressure support
• Ventilatory support, volume expanders, inotropes
• Tx underlying cause: antibiotics, steroids, glucose, anticonvulsants,
• Counsel and provide explanation and support to family
3. Further workup
• Guided by clinical suspicion: chromosome analysis, sweat chloride, metabolic workup, abdo U/S, MRI
4. Referrals
• NICU if patients clinical status deteriorates
References
2. Zort ii, Alpern ER, Brown LW, Loomes KM, Marino BS, Mollen Ci, Raffini U, editors. Schwartz’s clinical handbook of pediatrics. 4th
ed. Philadelphia. Elsevier
Inc.; 2009
3. Cheung A, Williams BA, Sivarajan By, editors. The HSC handbook of pediatrics. 10
th
ed. Elsevier Inc.; 2003.
Pediatricsj Edmonton Manual of Common Clinical Scenarios 265

DEVELOPMENTAL DELAY
201 I Ed, Authors: Peter Gill, Gary Ga/ante MD, Melanie Lewis BN MEd MD FRCPC
OriginalAuthors: Peter Gill, Gary Ga/ante MD, Melanie Lewis BN MEd MD FRCPC
Station Objective
Evaluate a child with suspected developmental delay and determine the etiology.
skills
Developmental delay: below average intelligence existing with limitations in adaptive
• Gross motor concern
• CP: neuroimaging (MRI > CT), classified as spastic/extrapyramidal/mixed
bx
• Muscular dystrophy: + Gower sign, t CPK, PCR detect absent dystrophin gene, muscle
• Language delay (see Speech and Language Abnormality )
• Social concern (see Speech and LanguageAbnormality)
• LD (see ADHD/Learning Disorder)
• GDD: a significant delay (> 2 SD below mean) in > 2 developmental domains
• Fragile X: PCR excessive triplet repeats (FMR1), normal chromosome analysis
• Trisomy2l:abnormal karyotype
dysfunction; and d) evidence of maternal
• FASD: Dx requires: a) growth deficiency; b) abnormal craniofacial features; c) CNS
drinking during pregnancy
• Prenatal/postnatal factors: fetal hypoxia, FASD, TORCH, meningitis, DM, malnutrition, prematurity
• Genetic: Trisomy 21, Fragile X
• Psychosocial factors: under stimulation, low SES, parental neglect, family instability
idiopathic
• Other: inborn errors of metabolism, congenital hypothyroidism, anemia, lead poisoning,
3. High Mortality:
• Muscular dystrophy, CP, metabolic disorders
History
ID • Age (correct for prematurity), sex, ethnicity, name, home
CC • Delay in development, speech delay, language delay
HPI • Identify parental/care-giver concern for child development
• Timeline: when was it noticed, how, who noticed it, any loss of function, etc
• Current level of developmental function in all four spheres (GM, FM, speech, social)
• Ask if any formal vision and hearing testing
RED FLAGS • New onset, regression, neonatal complications, FHx, child abuse/neglect
bleeding), maternal
PMHx • Prenatal: prenatal care, U/S frequency, maternal illness (GDM, HTN, infections, rash, fever,
exposures to toxins/teratogens, smoking/EtOH/drugs, IUGR
• Perinatal: asphyxia, APGAR scores, prematurity, birth wt, abnormal presentation
CNS trauma),
• Postnatal: neonatal complications (TORCH infection, meningitis, encephalitis, seizure d/o,jaundice,
• Head trauma, chronic illness, child abuse/neglect
PSHx • CNS surgeries (shunt, tumour)
PO&GHx • Gestation, GTPAL, route of delivery
FHx • Deafness, blindness, MR, neurologic d/o
• Three generation pedigree: consanguinity, learning difficulties, pertinent familial dz
Meds • Rx, CAM, vitamins, OTC
Allergies Medications, food, environmental
Social • Marital status/family unit, finances, school/peer relations, health plan, effect of illness on family
Dev. • See Table 1.
Immun • Routine, special
ROS • Vision, hearing problems, nutrition and diet

J
a
5 ctors Prematurity, perinatal asphyxia, genetic abnormality
Table 1. Developmental milestones

phvslca I Gross motor:
General Approach Sit (6 mo), crawl (10 mo), walk (15 mo), stairs (24
1.
• Growth measurements: HC (micro/macrocephaly), wt, ht mo), tricycle (3 yr), bicycle (5 yr)
• Wellbeing and behavior, alertness, attention span, impulsiveness, Fine motor:
attentiveness • Grasps (3 mo), pincer (10 mo), scribble (15 mo),
• Observe developmental abilities and developmental milestones tower of 2 cubes (18 mo)
2. Inspection Language:
• Dysmorphic features (see Genetic Concerns and Pedigree) • Coos (3 mo), babbles (6 mo), words (12 mo),
• SKIN: multiple café au lait spots, adenoma sebaceum, ash-leaf spots, port 2-word phrases (18 mo)
wine nevus Personal-social:
• HEENT: examine TM for evidence of recurrent/chronic OM • Stranger anxiety (6 mo), peek-a-boo (12 mo),
• MSK: calf hypertrophy parallel play (24 mo)
3. Palpation
• NEURO: fontanelle and sutures
• GI:HSM
• MSK: joint contractures
4. Neurologic examination
• CNs, strength, muscle tone (hypo/hypertonia), reflexes, coordination
• GAIT: observe for spasticity, toe-walking, asymmetry, etc.
5. Special Tests
• Gower sign: patient stands up by using hands to walk up their thighs from sitting position
Investigations
1. Adjunctive clinical assessments:
• Audiology and vision assessment: 1st line investigations to r/o sensory abnormality
• Formal developmental assessment or developmental screening test (ASQ or PEDS)
2. Blood work:
• Only indicated if clinical suspicion, consider watching approach
• Karyotype, Fragile X testing (FMR1 triplet repeat)
• Further testing if clinically indicated e.g CPK,TSH, metabolic workup
• Neuroimaging indicated if micro/macrocephaly, seizures, loss of psychomotor skills, neurologic signs
• MRI preferable to CT scan except when intracranial calcifications (TORCH, tuberous sclerosis)
Treatment
• Largely depends on identified problem: speech, language, GM, FM, etc.
• Appropriate communication and management plan tailored to family needs, resources, etc.
• Multidisciplinary services: OT, PT, speech-language pathologist, specialized educational support
2. Follow-up
• Regular appointments to monitor progress and growth is essential
3. Referrals
• Consider allied health care professionals, developmental pediatrician, child psychiatrist
References
1. Zorc JJ, Alpern ER, Brown LW, Loomes KM, Marino BS, Mollen Ci, Raffini U, editors. Schwartz’s clinical handbook of pediatrics. 4
th
Inc.; 2009
2. Shevelle M. Global Developmental Delay and Mental Retardation or Intellectual Disability: Conceptualization, Evaluation and etiology. Pediatr Clin N Am
55 (2008) 1071—1084

DOWN SYNDROME
201 I Ed. Authors: Taryn Brown, Gory Galante MD, Melanie Lewis BN, MD, MMedEd, FRCPC
Station Objective
To develop an organized approach to the diagnosis and management of Down Syndrome/Trisomy 21 (T21) and its associated conditions
Diagnosis
Etiology: Table 1: Classic Dysmorphic Features of T21
• Most common chromosomal condition (-.1/800 live births)
Craniofacial:
and #1 genetic cause of mental retardation
• Due to 1 of 3: Trisomy 21(94%), Robertsonian translocation © Nirupanvipulananthan 2010
(3.3%), or mosaicism (2.4%, milder phenotype) Large Poste
Fontanelle
• Translocation-typeT2l may be inheritable; others are due to
nondysjunction events and are not inherited!
2. Screening and Diagnosis:
• All patients should be counseled on the screening options
• Prenatal screening: in the context of maternal age (pre-test), Brushfletd Spots
screening generates a (post-test) probability for giving birth
to an infant with T21 if substantial (>1/385) offer invasive
—
EcanINcFoIs
diagnostic tests
• Nuchal Translucency (11 13 wks): U/S measure of
— Overfotded Helix end
nuchal thickness or fluid behind neck (t NT associated Smail lowered Eers
with T21)
• First Trimester Screen (11-14 wks) = NT + serum markers Shon Neck and Excess Skbi
13-HCG (1’ in T21) and PAPP-A (I, in T21) +/- U/S screen for
absence of nasal bone (which makes T21 more likely)
• Maternal Serum Screen (MSS) (15 —20 wks): Quadruple
Extremities:
test, DS associated with t !3-HCG and inhibin —A, I’
maternal serum AFP and unconjugated estriol (uE3) • Hands: single transverse palmar crease, short/broad
• Gold Standard for Diagnosis: Chromosomal karyotype fingers, clinodactyly + small 5
1h
middle phalanx,
• Prenatal Dx: chorionic villus sampling (10-l4wks) or brachydactyly
amniocentesis (>15 wks) • Feet f distance between 1 ‘ and 2 d
toes (“sandal” sign)
• Postnatal Dx: get karyotype if infant demonstrates 2 or • General: hypotonia, hyperfiexive ligaments
more dysmorphic features
History

CC • Review patient and parental concerns
HPI • Obtain HPI for each concern
RED FLAGS • obstruction: delayed passage of meconium, abdominal pain/irritable, bilious vomiting
• Heart failure: dyspnea, edema, increased RR/HR,fatigue, diaphoresis, poor feeding, FTT
• Leukemia: fever, anorexia, weight loss, night sweats, fatigue, bone pain, xs bruising/infec-tions
• Spinal cord compression (2° to Cl (2 instability): neck pain/wry, weakness and spasticity, difficulty walking/loss of
ambulatory skills, altered bowel or bladder function
PMHx • Birth parameters, Apgars, need for NICU/resuscitation, associated conditions and complications, including
newborn/infant period (hypotonia, hip dysplasia, jaundice, transient leukemia, hypothyroid, heart disease,
hearing loss, etc.)
DvtI Hx • Past and present, including intellectual impairment, self-care skills, behavior/emotions, pubertal development
PSHx • Inquire about corrective cardiac or abdominal surgery
PO&GHx • Maternal age, prenatal care, screening, U/S, infections/illness (GDM, HTN), meds/toxins, previous pregnancies
and outcomes, complications, GA and birth wt, resus
Meds/AllergfImm • Review, ensure immunizations are UTD, inquire about special immunizations
FHx • History of genetic syndromes in family or previous pregnancies
Social • Living conditions and arrangement, stressors, financial and health insurance status

ROS General: growth (weight relative to height), fatigue, weight gain, cold intolerance
• HEENT: ear pain, fever, and irritability (AOM), vision or hearing concerns, tooth pain
• CV: cyanosis, fatigue, diaphoresis, poor feeding, FT1 edema, syncope, palpitations
• RESP: cough, rhinorrhea, URTI, snoring, restless sleep, excessive daytime somnolence, apnea
• GI: dysphagia, dyspepsia, bloating, abdominal pain, diarrhea, constipation, vomiting
• MSK: gait problems and clumsiness, neck pain, weakness, joint pain
• DERM: easy bruising, dry, thick skin, infections/pustules
• Nutrition: feeding history (ensure adequate intake and growth), feeding difficulties
Risk Factors Maternal age >35 at delivery (1/214 at age 35, 1/19 at age 45)
• Previous pregnancy with chromosomal abnormality
• Abnormalities on prenatal screening (tNTS, AbN biochemical markers, absent nasal bone)
Table 2: Complications and Associated Conditions

physical Exam HEENT Ocular and visual abnormalities (cataracts and
*NOTE: findings depend on age use list as a general outline
—
refractive errors), hearing loss, recurrent URTIs and
• General: FTT, short stature, obesity (plot on T21 curve) AOM, conjunctivitis, periodontal disease
• HEENT: narrow palate, strabismus, cataracts (loss of red reflex), CV 50% have cardiac anomaly (AVSD most common,
nystagmus, narrow ear canals, hearing loss, OME/AOM also VSD, ASD, TOF), later risk MVP/Aortic regurg
• CV: murmur, t HR/RR, prolonged CRT, cyanosis, abN pulses
RESP Obstructive sleep apnea, pulmonary HTN
• GI: abdominal distension, hepatosplenomegaly, adenopathy
• MSK: arthritis, joint laxity, Cl-C2 hypermobility/instability, pelvic GI Constipation, Hirschprung disease, GI tract
hypoplasia anomalies (eg. duodenal atresia), celiac dz, IBD
• DERM: petechiae (thrombocytopenia), dry/hyperkeratotic skin, GU Cryptoorchidism, nearly all males are sterile
pustules, rashes, skin infections, alopecia
MSK Atlantoaxial instability +1- dislocation,
• GU: cryptorchidism, hypogonadism, L penis/testes volume
arthropathy (OA, gout, RA), pelvic dysplasia
• CNS: signs of spinal cord compression (hyperreflexia, babinski
sign, AbN gait, clonus), hypotonia and Moro reflex in ENDO Hypothyroidism, short stature, obesity
newborn CNS Developmental delay, behavioral disorders, early
Alzheimer’s, emotional dysregulation
Surveillance/Investigations/Management HEME- f risk of leukemia (especially AML-M7, also ALL and
ONC transient leukemia)
1. Gold Standard for Diagnosis: Chromosomal karyotype
No curative treatment, therefore need to have regular follow-up/review with high index suspicion for associations
2. Surveillance
HEENT:
• Newborn hearing screen/ABR by 3 mo, then behavioral auditory testing q6mo until 3 years, then annually. ENT specialist for
recurrent otitis media, or conductive hearing loss
• Ophthalmologic assessment by 6 months, then annually by pediatric ophthalmologist
• Dental visit at 2 yrs, then q6months; referral for orthodontic problems
• CV: Newborn echocardiogram and pediatric cardiologist consult, even if asymptomatic; routine clinical evals
• Resp: Monitor for obstructive sleep apnea at every visit
G
• GI: Screen for Celiac at 2 years, then PRN, manage constipation
• MSK: C-spine radiographs: screening controversial get flexion/extension views for special Olympics or if symptomatic (watch for
—
spinal cord compression with prompt surgical consult and MRI if present)
• ENDO:TSH/T4 @ birth, 6 months, 12 months, then annually
• CNS: Assess for and treat behavioral and psychiatric conditions
• HEME: CBC-D as newborn, then yearly between 13 and 21 years. If patient had transient myeloproliferative disorder, follow them
more frequently. Exercise vigilance when looking for signs of leukemia
3. Multidisciplinary Care:
• Referral to early intervention program (PT, OT, SLP) by 3 years
• Individualized Educational Plan (IPP), screen routinely for autistic features
4. Family Resources:
• Genetic counseling, Down Syndrome parent group, informative publications, advocacy groups
• Discuss financial support: child tax credit and FSCD (Family Support for Children with Disabilities)
References
1 Harrison A. Down Syndrome (Pediatrics), ACP PIER & AHFS DI° Essentials” [Interneti. American College of Physicians: STAT!Ref Online Electronic Medical
Library (US); c201 0. Available from: htto://online.statref.com.loain.ezoroxv.librarv.ualberta.ca/document.asox?fxid=92&docid=1 305
2. Edmonton Down Syndrome Society. Clinical Guidelines for the Down syndrome Population. httø://www.edss.ca/?a=node/50

EAR PAIN
201 I Ed. Authors: Chris Gerdung, Gary Galante MD, Melanie Lewis BNMEd MD FRCPC
OriginalAuthors: Chris Gerdung, Gary Galante MD. Melanie Lewis BN MEdMD FRCPC
Station Objective
To thoroughly evaluate earache in children by means of history and examination while considering a broad differential diagnosis for primai.,
and secondary causes of ear pain. Rule out life/hearing-threatening conditions. Diagnose & manage actue otitis media and otitis externa.
1. Diagnostic Criteria of ACM, OME, CE
Required Signs for Dx of ACM: Signs of CME:
1. Acute otalgia (irritability if preverbal) 1. Otalgia, ear fullness, hearing loss
2. Effusion: immobile TM mobility, air fluid level, opacity, L- bony landmarks, 2. Limited TM mobility (± retraction)
ruptured TM with otorrhea 3. Variable color (NCT red)
3. Inflammation: bulging TM with discoloration (hemorrhagic, gray, or yellow) 4. +/-airfluid Levels
Signs of CE: Bacteria Involved in ACM

1. Pain/tenderness of tragus/auditory meatus 1. Streptococcus pneumonia
2. Fullness, itching of canal 2. Moraxella catarrhalis
3. Red/swollen canal, ± discharge, ± erythematousTM 3. Nontypeable Haemophilus influenzae
• Auricle: traumatic abrasion/laceration, cellulitis, sunburn, local allergic reaction or contact dermatitis
• Ear canal: CE, cerumeri impaction, foreign bodies, atopic dermatitis (eczema)
• Middle/inner Ear: AOM, OME ± perforation or tympanostomy tubes
• Secondary otalgia (referred pain): dental infection, sinusitis, TMJ
3. High Mortality / Morbidity (primarily hearing loss):
• Malignant CE, mastoiditis, labyrinthitis, abscess/meningitis/sinus venous thrombosis
History
CC • Earpain
HPI • Fever/viral prodrome (cough, sneeze, rhinorrhea, sore throat/mouth), preverbal children may exhibit irritability,
poor sleeping and feeding
• Environment: sick contacts, recent swimming, sunburn, foreign body, hot tub use
• Trauma: baro (slap, air travel), penetrating (pencil, Q-tip), minor (bug bite, scratch, piercing)
• Ctorrhea: blood, serosanguinous (straw), purulent, CSF like (thin/watery)
• Neuro symptoms: altered mental status, new HA, vomiting, seizure, stiff neck, Bell’s palsy
(D
RED FLAGS • Speech delay, hearing loss, Bell’s palsy
0) PMHx • Craniofacial abnormality (e.g. cleft palate, Trisomy 21)
• ACM (# episodes), history of antibiotic use
• Immunodeficiency
PSHx • ENT surgery (tympanostomy tubes)
• Dental surgery, craniofacial surgery (cleft palate)
PO&GHx • Gestation, GPTAL, route of delivery, birth wt, PRCM, breast feeding
Meds • Recent/current: especially antibiotics, topical analgesics/antibiotics to auditory canal
Allergies • Allergies (ie. food, medication, environmental etc.), atopy (eczema, allergic rhinitis)
Immun • Immunization status (especially conjugate pneumococcal vaccine)
Social • First Nations, exposure to 2nd hand smoke, low SES, house crowding, daycare, oral hygiene
• Breast feeding, bottle-feeding practices
Risk Factors • Major: young age, daycare
• Cthers: bottle feeding, craniofacial abnormalities, male, Inuit/First Nations, immunocompromised, extreme
premature, crowding,_passive smoking, recurrent ACM, FHx ACM, Down syndrome

physical
1. General Approach
, T, growth parameters: ht/wt/HC
2
• Assess for irritability and toxic appearance, mental status
2. Inspection
• Auricle/mastoid: laceration, hematoma, erythema/swelling/induration, ear protrusion, battle sign
• Auditory canal: mass, foreign body, cerumeri, erythema/swelling, flaking, otorrhea/discharge, bullae, eczema
• TM: redness, air fluid levels, bulging, discharge, perforations, masses, effusion, inflammation
• Inflammation: bulging TM with marked discoloration
• Effusion: limit TM mobility, ruptured TM with otorrhea, air fluid level, opacity, loss bony landmarks
• Oral cavity/oropharynx: caries, dental abscess, anterior or post-nasal discharge
3. Palpation
• Tenderness: mastoid bone, TMJ (also feel for pain/crepitus with motion), on tragus motion
4. Auscultation
• Lungs: AE, wheeze, or adventitious lung sounds (crackles, etc) — r/o LRTI
5. Special Tests
• Assessment of hearing, Weber and Rinne test, pneumatic-otoscopy to check for ear drum mobility
Investigation
1. Blood work
• CBC-D, blood culture if suspect serious infection (mastoiditis, malignant OE)
• CT if strong suspicion for intracranial injury, mastoiditis, malignant OE
3. Special Tests
• Audiometry, culture discharge/otorrhea if suspect severe otitis externa or perforated TM
• Full septic work-up with LP if meningitis is suspected
Treatment
1. Emergent
• If suspect trauma/emergent condition —+ urgent evaluation/referral ± surgical drainage, IV access
• Analgesia: acetominophen 15mg/Kg P0 q4h (max 5 doses/day) or ibuprofen 10mg/kg q6-8h PRN
• AOM: watchful waiting if> 6 mo, non-severe, EU ensured, and previously healthy’
• If worsening status or no improvement in 48-72 hrs —* failure
• 1” line antibiotic —* amoxicillin 75-90 mg/kg/d, div BID x 5 or 10 days (length depends on age, etc.)
• OE: aural toilet, topical antibiotics ± topical steroids (ciprodex
2
)
TM
• OME: watchful waiting if not at risk for speech/language/learning problems, mild hearing loss, <3 mo (bilateral) or < 6 mo
(unilateral), with close F/U q 3 mo with serial hearing tests
3. Referrals
• Referral to ENT if suspected mastoiditis and for tympanostomy tubes if recurrent AOM or complicated/prolonged OME
References
1. Forgie 5, Zhanel G, Robinson J. Management of acute otitis media. Paediatr Child Health 2009; 1 4(7):457-60
2. Leung AKC, Fong JHS, Leong AG. Otalgia in children. Journal of the National Medical Association 2000 May;92:254-260
3. Majumdar 5, 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
MD FRCPC
201 I Ed. Authors: Lauren Kitney BSc MD, Gary Galante BSc MD, Melanie Lewis SN MEd
Gary Galante BSc MD, Melanie Lewis BN MEd MD FRCPC
OriginalAuthors: Lauren Kitney BSc,
Station Objective
To develop an approach to growth failure in an infant, child or adolescent
Table 1: Caloric Intake Requirements
Differential Diagnosis Newborn 180— 1 4Okcal/kg_day(Avg= 1O0kcaldav)
Child 140 9okcal/kg/day
Diagnostic Criteria
—
• CDC: weight-for-age < rd

3
%ile, crosses two major percentiles, <80% I Adolescent 130—50 kcal/kq/day
oe percentile, BMI-for-age
1
<
ideal body weight, weight/length
<5%ile on appropriate growth chart (key = serial measurements required) Table 2: Average rates of weight gain
• CPS (2010) promotes new WHO growth charts percentile lines now represent Weight Gain
—
Age
z-scores
used
• “Underweight”: <3%ile wt-for-age for <10 yb (wt-for-age should NOT be 25-30 g/d
0-3 mos
past then)
<3%ile BMI
• “Wasted”: <3%iIe wt/length or <89% IBW (ideal body wt) @0-2 yb, 3-6 mos 1 5-20 g/d
for-age @2-19 yb 6-9mos 12-13g/d
regular
• Newborn caloric requirements translated into breast milk/formula amounts:
9-l2mos 9-13g/d
strength formula/breast milk contains 20kcal/30mls (2okcals/ounce) = 0.67kcal/ml
=
120—21 Oml/kg/day (or 4-7 oz/kg/day) 1-3 yrs 0.25 kg/month

2. Common Conditions: 4 yr puberty 2 kg/yr
—1/2”non-organic” (difficulty breastfeeding, improperly mixing formula), GI disease
-
•
common organic cause
Table 3: Etiology of failure to thrive
Increased Metabolic Demands/Ineffective Inadequate Gl absorption/Increase loss
Decreased Intake .. .
Utilization
Neurological: Cerebral palsy, • Vomiting: ANY infection, increased
• Nutrient deficiency: problems •
neurodegenerative disease intracranial pressure, drug5, adrenal

breastfeeding, mixing formula,
Chronic inflammatory : IBD, Lupus, JIA disease
excessive juice, restrictive diet •
Chronic/recu rrent infections, • Obstruction: Pyloric stenosis,

• Parental: neglect, dysfunction, • j
immunodeficiency intussuscepti on, hernia, etc.
disturbed relationship, poverty, lack of
knowledge, etc. • Endocrine: Diabetes mellitus, •
hyperthyroidism, hypopituitarism, • Malabsoprtion: Biliary atresia, cirrhosis,

• Mechanical: TEF, cleft palate/lip,
adrenal insufficiency pancreatic insufficiency, CF, infectious
micrognathia, tonsillar enlargement,
Malignancy diarrhea, cow’s milk protein allergy,
nasal obstruction •
IBD, celiac disease
Metabolic: hypercalcem ia, storage lactose intolerance,
• Swallow/suck dysfunction: CNS, •
disease, galactosemia , etc • Decreased length: Short bowel

neuromuscular
Head + Neck: Obstructive sleep apnea syndrome, Necrotizing enterocolitis
• Poor appetite/inadequate intake: •
syndromes, chronic disease/infection, • Respiratory: Cystic Fibrosis, Chronic

medications, pain/discomfort with lung disease
eating (GERD, caries) • Cardiac: Acquired or congenital heart
• Psycho-beha vioral: Eating disorder, disease
ADHD, infantile anorexia, rumination, nj: Chronic renal impairment, Renal
aversion tubular acidosis
3. High Mortality:
• Malignancy, infectious etiology, chronic disease, abuse
History
ID • Age, sex, ethnicity
CC • Weight loss or growth failure
HPI • Onset, duration, severity
per day?
• Nutritional intake (detailed 1-3 day recall): what, amount, frequency, >6 wet diapers
strong suck/latch, choking, audible swallow, nipple/breast problems
• Breast feeding let down,
—
• Formula —type, how is it mixed, volumes

• Restrictions/aversion to food
• Parent-child interaction! bonding, child’s temperament, feeding behaviour/environment
• Abdominal pain, bowel movements (frequency, amount, consistency, blood, steatorrhea)
feeds
• Vomiting, regurgitation, heartburn, dysphagia, back arching, apneas or cyanosis with
• Frequent URTI! AOMbpneumonia! sinusitis, HIV risk, daycare, travel

iD FLAGS Signs of abuse/neglect, signs of chronic disease, multiple hospitalizations/emergency visits, weight loss/rapid
decrease in percentiles, developmental delay, growth velocity < 5cm/yr
• Prenatal: Prenatal care, U/S (frequency/abnormality/IUGR) Maternal illness (GDM, HTN, infections, rash, fever,
bleeding), toxins/teratogens (including smoking/EtCH/drugs)
• Perinatal: gestation, fevers, antibiotics, APGARS/resuscitation, birth weight, mode
• Postnatal: Neonatal complications: fever, shock, hypotonia, seizures, NICU admission, neonatal metabolic screen,
congenital anomaly (e.g. cleft lip/palate)
• Medical: hospitalizations/emergency visits, chronic illnesses/infections, frequent injuries
• Development (FM, GM, social, language), psychological (depression/ADHD)
—....
PSHx Prior surgeries and complications

FHX • Consanguinity, metabolic or genetic conditions, chronic disease, stillbirths, SIDS, developmental delay, eating
disorders, parental/sibling height, weight and growth patterns
Meds • Stimulants, corticosteroids, diuretics, ipecac, CAM
Allergies • Medications, environment, food
Immun Routine, seasonal influenza vaccines, additional, are they up to date?
Social • Stressors: body image, poverty, parental abuse/neglect/depression, substance use
ROS • Shortness of breath on exertion, tiring/diaphoresis with feeds, wheeze/stridor/snoring, floppy, polyuria/polydipsia,
sleep history, pubertal development (menarche, LMP), rashes (e.g. erythema nodosum), canker sores, lanugo, heat
or cold intolerance, fevers
Risk Factors • Prematurity, developmental delay, chronic medical condition, psychosocial stressors
Physical
1. General Approach
• Growth: plot all three on appropriate chart for gender, ethnicity and syndrome. Wt/length, BMI
• Vitals, general appearance (well vs. unwell), parent-child interaction, feeding session
• Signs of malnutrition pallor, fat stores (back of neck, buttocks, thighs), alopecia, temporal wasting
-
2. HEENT: dysmorphic, cataracts, retinal hemorrhage, nasal obstruction, oropharynx (aphthous stomatitis, tonsillar enlargement, caries,
cleft lip/palate, ankyloglossia, micrognathia), thyroid enlargement
3. CV: perfusion x 4 extremities, BP, cyanosis, murmur, hyperactive precordium
4. RESP: distress, clubbing, hyperinflation, poor air entry, wheezes, crackles, prolonged expiratory phase
5. ABDO: distention, hyperactive bowel sounds, pain, masses, stool, hepatosplenomegaly
6. GU + Rectal: ambiguous genitalia, hernia, perianal disease (fissures, abscess, fistula), Tanner stage
7. MSK: abnormally located/shaped bruises or injuries, edema, lanugo, rashes (erythema nodosum, candidiasis, etc)
8. NEURO: cranial nerves, tone (abnormal, spastic), weakness, deep tendon reflexes, primitive reflexes
Investigations
1. Blood work (only if indicated and etiology unclear)
• Initial: CBC, lytes, Cr, BUN, ESR/CRP, urinalysis
• Based on clinical suspicion: liver enzymes, lipase, albumin/total protein, glucose, ferritin, TIBC, % saturation, immunoglobulins,
sweat chloride, stool (fat, reducing substances, C&S, O&P), ATTG, IgA
• CXR, GI studies (UGIS/SBFT,VFSS, abdo U/S, endoscopy), MRI head if indicated
Tre tment
1. Emergent
• ABCs, maintain hydration, admit if severely malnourished or dehydrated, serious intercurrent illness, etc.
• Support breast feeding/formula, high calorie/protein diet and multivitamin supplementation
• Feeding regimen ideally ad lib, frequent meals, enteral nutrition, positive feeding environment
• Investigation/treatment of organic etiologies and psychosocial stressors, parental education/support
3. Follow-up
• Frequent follow up with pediatrician (every 1-2 weeks initially) +/- interdisciplinary team
4. Referrals
• Dietitian, lactation consultant, subspecialists if indicated, children’s services, social work, SLP/OT, etc.
References
1. Heng M, Greenwald JA.Toronto notes (2007). 23
rd
ed. Toronto: Toronto Notes for Medical Students, Inc.; 2007
2. HayW, Levin M, Sondheimeri, Deterding R. Lange Current Diagnosis & Treatment in Pediatrics. 18th ed. United States: McGraw-Hill Companies, Inc.; 2007.

FEVER WITHOUT A SOURCE IN A CHILD <3 MO
201! Ed. Authors: Peter Gill, Gary Galante MD, Melanie Lewis BN MEd MD FRCPC
OriginalAuthors: Peter Gill, Gary Galante MD, Melanie Lewis BN MEdMD FRCPC
Station Objective
Determine whether the fever without a source is of short duration or is prolonged, differentiate between acute viral and serious bacterial
infections and identify a child with septic shock or meningitis and initiate immediate therapy
Diagnostic criteria
Hx/PE often suggest etiology
• Otherwise fever without souce
-
Table 1. CSF Findings
WBC <5 or >15, bands >1.5 x 109/L suggest Etioloav
infection t WBC in fluids)
(also
Normal Bacterial Viral TB
• Blood, urine and CSF C&S
Glucose (mmol/L) >2.8 <2.8 <3.3 <-2.8
• CXR±jointaspiration Glucose(%ofserum <50
>50 <40 <40
2. Common Conditions: >90% of fevers in <3 month alucose)
suspected viral etiology Protein (alL)
.
<0.3 >0.6 0.3-0.8 0.5.0.8
• Bacteremia:
E. coil, GBS, Listeria WBCIuL 0-30 >1000 1 00-5 00 1oi.ooo
• Meningitis: GBS, E. coil, Listeria %PMN 0 50-5000 20-2000 1 Ôö
• Encephalitis: HSV(and other TORCH)
• Pneumonia: GBS, E. coil (÷ other enteric GNB), S.pneumoniae, H. influenzae, Chiamydia trachomatis, S. aureus, Listeria, viraiinfeatjon
• UTI: E. coil, Proteus mirabills, Kiebsiella pneumoniae, Pseudomonas, enterococci, staphylococci, GBS
• Omphalitis/cellulitis: S. aureus,GAS, E.coli, Klebsiella, Proteus, GBS (most are polymicrobial)
3. High Mortality:
Meningitis, sepsis
History
ID • GA, sex, ethnicity
CC • Fever
HPI • Onset of fever, elicit parental concerns (fever OR child’s behavior)
• Tmax, how fever was measured: ear/rectal (vs. tactile report)
• Constant or fluctuating, AM or PM, any relief with Tylenol/Advil
• Appetite, fluid intake, u/o
• Source?: lethargy, inconsolability, irritability, cough, NN, diarrhea, rhinorrhea, conjunctivitis, lesions/rashes, joint
swelling, jaundice, apnea, cyanosis, voiding (foul smell, # of wet diapers)
• Exposure to sick contacts in household, daycare, pets or animals, travel Hx
RED FLAGS • Lethargy, poor feeding, inconsolable, poor tone, activity, irritability, seizure
PMHx • Prenatal compilcations: poly/oligohydramnios, 4. fetal movements, bleeding, NRFS
• Labor length, spontaneous/induced, membrane rupture (duration >1 8hrs, spontaneous/induced/ premature), Abx
and # of doses, fever or signs of chorioamnionitis (foul D/C, tender uterus)
• Delivery: route of delivery, GA, birth wt, forceps/vacuum, trauma
• Perinatai: APGAR scores, meconium present, IUGR, prematurity (steroids), NICU admission, length of stay, neonatal
metabolic screen, hypoglycemia, resp distress, hypotonic, jaundice
• Chronic medical conditions, immunodeficiency
PSHx • Splenectomy
Antenatal Hx • Prenatal History: prenatal care (STI testing), abnormal U/5, estimated date of delivery
• Maternai heaith: GDM, HTN, infections, rash, fever, UTI, STI, GBS/immune status
• Maternai exposures: medications, toxins, teratogens, smoking, EtOH, drugs, deli meat or unpasteurized cheese
(Listeria), cat litter box (Toxoplasmosis)
• PO&GHx: GTPAL, previous high-risk pregnancies, stillbirths, GBS sepsis
FHx • Maternal fetal loss, congenital anomalies, immunodeficiencies, sickle cell dz
Meds • Rx (recent Abx), CAM, vitamins, OTC
Social • Marital status/family unit, finances, health plan, psychosocial situation

Immun 1 Vaccination status of household members
ROS • Nutrition (breast/formula), poor/choking with feeding, Hearing/vision concerns (TORCH)
Risk Factors • Prematurity, perinatal complication, immunocompromised, recent antibiotics, steroids, surgery
Physical
1. General Approach
• ABCs and VITALS
• Growth measurements: HC, wt, ht
2. Inspection
• GENERAL: toxic, activity level, lethargy, color, tone, weakness, vigor, irritability, hydration status
• SKIN/MSK:
• Signs of localized infection: skin, mucous membrane, ears, umbilical stump, genitalia, joints/extremities
• Jaundice, mottling, cyanosis, petechiae, purpura, vesicles (HSV)
• RESP: signs of respiratory distress, tachypnea (>60/mm), grunting, nasal flaring, retractions, apnea
• CV:Tachy/bradycardia, hypotension (5BP <60mm Hg), delayed cap refill (> 2 sec)
• NEURO: cephalohematoma, micro/macrocephaly, bulging fontanelle (late finding), central tone
3. Palpation
• GI/GU: hepatomegaly
• NEURO: weak suck, hypo/hypertonia on passive ROM, paradoxical irritability (more irritable when held)
4. Auscultation
• a’
RESP: AE, crackles, wheezes
Investigations
1. FULL SEPTIC WORKUP IF CHILD < 1 MONTH OR <3 MONTHS AND ANY RISK FACTOR!!
• CBC-D, blood C&S, urine R&M, C&S, blood glucose, electrolytes Table 2. ABx Choice in FUO < 1 month
• LP: CSF analysis, send 4 tubes: Ampicillin + Gentamicin (suspected SBI)
• 1) Gram stain/culture
--OR--
• 2) Chemistry (glucose/protein)
Amipicillin + Cefotaxime or Ceftriaxone (for suspected
• 3) Cell count and differential
meningitis, better CSF pen)
• ± 4) HSV +1- Enterovirus PCR ‘Consider Acyclovir for HSV meningitis (If ill!
• LP contraindications: papilledema, focal neurological signs, Pt
lethargic + either: CSF pleocytosis with —ye cultures,
unstable, bleeding diathesis
seizures, coagulopathy, mucocutaneous vesicles, or
• Stool C&S if diarrhea
transaminitis)
1f child aged 1-3 months old, consider adding
2
• CXR in anyone with respiratory S/Sx
Vancomycin to cover penicillin resistant pneumoniae
Treatment
1. Emergent
• ABC’s and identify newborn in need of prompt support
• Treat with empiric antibiotics pending culture results
• Ampicillin 200 mg/kg/d divided q6h
• Cefotaxime 200 mg/kg/d divided q6h
• If focus identified, antimicrobial therapy as appropriate
• Counsel and provide explanation and support to family
3. Follow-up
• Pediatrician post discharge to monitor for complications
• If meningitis urgent audiology referral (short time period in which could receive cochlear implants PRN)
-
4. Referrals
• NICU/PICU
References
2. Cheung A, Williams BA, Sivarajan By, editors. The HSC handbook of pediatrics. 1 0
th ed. Elsevier Inc.; 2003.

GENETIC CONCERNS & PEDIGREE
20?! Ed. Authors: Lauren Kitney BSc, Gary Galante BScMD, Melanie Lewis SN MEd MD FRCPC
OriginalAuthars: Lauren Kitney SSc, Gary Galante BSc MD, Melanie Lewis SN MEd MD FRCPC
Station Objective
Elicit a history from a family presenting with genetic concerns and formulate a three generation pedigree
• Down syndrome (Trisomy 21), Turner Syndrome, Kleinfelter Syndrome, Fragile X, Noonan Syndrome
2. High Mortality:
• Patau syndrome (Trisomy 13), Edwards syndrome (Trisomy 18)
History
CC • Genetic concern
HPI • Who raised the concern, why
RED FLAGS Failure to meet developmental milestones, dysmorphic features, abnormal prenatal or newborn screen
PMHx • Prenatal: prenatal care/testing, U/S frequency, maternal illness (GDM, HTN, infections, rash, fever, bleeding),
maternal exposures to toxins/teratogens, smoking/EtOH/drugs, IUGR
• Perinatal: gestation, APGARS, birth weight, mode of delivery
• Postnatal: neonatal complications, NICU admission, neonatal metabolic screen
• Medical: course since birth
• Development: is child meeting milestones in GM, FM, language, social
PSHx • Prior surgeries and any complications
PO&GHx • Mother’s age at delivery, G,T,PAL,
FHx • Consanguinity, genetic/metabolic concerns, miscarriages/stillbirths/neonatal deaths, mental retardation, neural
tube defects
Meds • Prescription, CAM
Allergies • Drugs, environmental, foods
Immun • Routine, seasonal influenza vaccines, up to date?
Social • Primary caregiver, financial situation, drug plan
ROS • Sleep, nutrition, bowel movements, urination, vision, hearing, seizures, behaviour, vomiting, tremor, sweating,
pallor
Risk Factors • Family history of genetic syndromes or metabolic disease
Physical
1. General Approach
• ) (plot on appropriate growth chart)
Growth measurements: wt, ht, HC, BMI (wt/ht
2
• Vitals, general appearance (skin colour & odour), social, language, GM and FM skills
2. System-based Physical Exam (*note: be sure to compare the child’s features to the parents)
• HEENT: skull contour/symmetry; hair: texture, whorls; ears: placement, symmetry, rotation, size, structure; eyes: shape, placement,
inner canthal distance, epicanthal folds, palpebral fissure length, coloboma, fundoscopy; nose: nasal bridge, nostrils; philtrum:
length, shape; mouth: vermillion border, palate, tongue; chin: micrognathia; neck: webbing, length
• CVS: chest shape, nipple spacing, heart sounds, murmurs, pulses, capillary refill
• RESP: breath sounds, adventitious sounds
• ABDO: shape, bowel sounds, masses, hepatosplenomegaly
• GU: ambiguous genitalia
• MSK: scoliosis/kyphosis, limb length/symmetry, transverse palmar crease, syndactyly, clinodactyly, etc
• NEURO: cranial nerves, tone, reflexes, sensation, gait
• DERM: dimple or skin changes at base of spine, abnormal skin findings
Investigations
1. Blood work
• Prenatal Screening: surveying the population to identify individuals at higher risk for a genetic disorder; should be offered to all
pregnant women in Canada

• If positive the individual falls above the risk cut-off range for a particular disorder and diagnostic testing and counseling
should be offered
• 151 trimester: nuchal translucency (11-14 wk U/S) + biochemical markers (PAPP-A, free 13-hCG) OR biochemical markers
(PAPP-A, free B-hCG) + second trimester AFP if nuchal translucency unavailable
• 2 trimester: quadruple screen (MSuE3, MShCG, MSAFP, DIA), 18-20 wk screening U/S
• Prenatal Diagnosis: diagnostic testing for individuals identified as high risk
• Indicated if screening test result falls above risk cut-off range or maternal age >40 years old
• Newborn/child
• Newborn metabolic screen (Table 2)
• Karyotype by FISH as guided by history and physical
• CK, lactate dehydrogenase [muscular dystrophy]
• CBC, extended lytes, ABG, glucose, lactate, ammonium, urine for organic acids, serum amino acids
• If indicated
Muscle biopsy, EMG [muscular dystrophy]
Table 1: Prenatal Diaanosis
Amniocentesis Chorionic Villus Sampling
J’rocedure U/S guided amniotic fluid removal Transcervical or transabdominal U/S guided chorion sampling
Common tests Cytogenetic diagnosis; AFAFP detects NTD Cytogenetic diagnosis
Gestational Age After 15 weeks 10-13+6 weeks
Sensitivity 99.6% 99.6%
Specificity 99.93% 99.90%
Advantages Screens for neural tube defects Earlier GA, rapid karyotyping
Disadvantages Results not available until 1 7-20 wks GA Confined placental mosaicism; further testing required for NTD
Risks Fetal injury/loss, infection, AF leakage, bleeding Maternal contamination, fetal injury/ loss, infection
Table 2: Alberta Newborn Metabolic Screening Program

Metabolic Disorder Endocrine Disorders Other
Amino Acid Organic Acid Disorders Fatty Acid Oxidation Disorders Other
Disorders
• Citrullinemia • Glutaric aciduria • Carnitine uptake defect • Biotinidase • Congenital adrenal • Cystic fibrosis
(CIT) type 1 (GAl) (CUD) deficiency hyperplasia (CAH)
• Maple syrup • 3-Hydroxy-3-methyl • Long chain hydoxyacyl-CoA (BlOT) • Congenital
urine disease glutaric aciduria dehydrogenase deficiency hypothyroidism
(MSUD) (HMG) (LCHAD) (CH)
Phenylketonuria • Isovaleric acidemia • Medium chain acyl-C0A
(PKU) (IVA) dehydrogenase deficiency
• Methymalonic (MCAD)
acidemia (MMA) • Trifunctional protein
• Propionic acidemia deficiency (TPF)
(PA) • Very long chain acyl-C0A
dehydrogenase deficiency
G
(VLCAD)
Treatment
1. Medical treatment will vary depending on genetic or metabolic condition
2. Counseling
• Children with disabilities, support groups, breaking bad news, options, end of life issues
3. Referrals
• General pediatrics, genetics, developmental pediatrics, palliative care, social work
References
1. Alberta’s Newborn Metabolic Screening Program: Information for Healthcare Providers. 2007 ww.health.aiberta.ca/documents/NMS-Professional-Brochure.
pdf
2. Ghidini A. Amniocentesis: Techniques and complications. In: Up to Date desktop 17.2, 2009
3. Heng M, Greenwald JA.Toronto notes (2007). 23 ,d
4. Summers A, Langlois 5, Wyatt, P, Wilson R; Society of Obstetricians and Gynaecologists of Canada. Prenatal Screening for Fetal Aneuploidy. JOGC. February
2007; 187: 146-1 61.
5. Wilson R; Society of Obstetricians and Gynaecologists of Canada. Amended Canadian Guideline for Prenatal Diagnosis (2005) Change to 2005- Techniques
for Prenatal Diagnosis. JOGC. November 2005; 168; 1048-1054.

IMMUNIZATIONS
20? I Ed. Authors: Taryn Brown, Gary Galante MD, Melanie Lewis SN, MD, MMedEd, FRCPC
Station Objective Routine Immunization Schejj

1. Obtain a complete immunization history AB
2. Counsel a patient on vaccine benefits and risks of vaccinations Age Immunization
3. Organize an effective plan of management for patients with special considerations
DTaP-IPV-Hib
2m Pneumococcal conjugate
Vaccine-Preventable Illnesses Meningococcal conjuga
4. Viralconditions DTaP-IPV-Hib
• Polio (Inactivated polio vaccine/IPV) 4m Pneumococcal Conjugate
• Measles-Mumps-Rubella (MMR) live vaccine
— Meningococcal Conjugate
• Chickenpox (Varicella zoster virusNZV) live vaccine
—
6m DTaP-IPV-Hib
• Hepatitis B Pneumococcal conjugate
• 3 doses over 6 mo must be given in infancy if mom’s serology is HBsAg+ or
—
unknown, otherwise in grade 5 6 m —2 yr Influenza (annual)

• Human papillomavirus (HPV) MMR, VZV
• Protects against HPV 16 and 18 (Gardisal and Cervarix; these cause 70% of cervical 12 m Meningo conjugate
cancer) and types 6 and ii (Gardisal only; these cause 90% of anogenital warts) 18m DTaP-IPV-Hib
• 3 doses given over 6 mo, approved for use in 9-26 yb females Pneumo conjugate
• Influenza (annual e.g. trivalent inactivated, Hi Ni strain included)
—
5. Bacterial conditions 4-6yrs DTaP-IPV, MMR

• Diphtheria-Tetanus-[acellularl Pertussis (DTaP, Tdap and Td boosters) Grade 5 HepB,HPV
• Strep pneumoniae (pneumococcus conjugate)
14-l6yrs Tdap
• Haemophilus influenza serotype B (Hib)
• Neisseria meningitidis (meni ngococcal conjugate) Adults Td (qlO years)
NOTE: Schedules may differ in each
province
History
ID • Age and gender, country of birth
CC/HPI • Inquire about and discuss patient and parental concerns regarding immunizations
RED FLAGS • Previous anaphylactic reaction to vaccine (urticaria, angiodema, respiratory distress, shock), recent steroids or
blood product transfusions
PMHx • Current state of health, primary immunodefiency, Hx of immunoglobin or blood product transfusion, chronic
disease, functional hyposplenia, HIV, Guillain-Barré syndrome, seizures
PSHx • Splenectomy, organ transplant, hematopoietic stem cell transplant
Birth Hx • Maternal serology (e.g. anti-HBsAg), requirement for IVIg/vaccinations at birth, prematurity
Meds • Immunosuppressive drugs (chemotherapy, azathioprine, cyclosporine, cyclophosphamide, infliximab), systemic
steroids, recent administration of IVIg
Allergies • Drugs and food, specifically to eggs, antibiotics, latex, or gelatin
Immunizations • Ensure they are up to date (UTD) including seasonal influenza shots, date of last immunization, adverse reactions
or anaphylaxis to previous vaccinations
FHx • Seizure disorders, severe reactions to a vaccine
Social • Ethnicity, recent immigration, travel history, sexual history (adolescents), community outbreaks
Patient and Parent Counseling

Be familiar with the types of vaccines available and the kinds additives found within them
• 3 types: live-attenuated, whole inactivated, or subunit (organism parts, protein/toxoid, polysaccharide +/- conjugate)
• Live vaccines include MMR, varicella, oral typhoid, yellow fever, and BCG
• Most are intramuscular injections (live vaccines are subcutaneous), and some shots contain multiple vaccines
• +1- adjuvant to enhance immune response (eg. Aluminum Salt)
• -i-b- preservative (eg. thimerosal) and/or other additives (eg. egg and animal proteins) to support growth
2. Educate parents and guardians about immunizations the common misconceptions surrounding them
• Acknowledge and respect parental concerns always provide current information and let them make the decision
—
• It is not harmful or unsafe for an and infant to receive multiple vaccines early in life all vaccines are tested prior to use and early
—

vaccination ensures children are protected against vaccine-preventable illnesses as soon as possible
• There is no evidence showing a link between autism and the MMR or thimerosal-containing vaccines
• The 1998 study making this claim was very flawed and involved very small number of children. Numerous studies since have
refuted this link
• There is no legitimate safety reason to avoid the use of vaccines that contain thimerosal (a mercury-based preservative that
prevents contamination of multi-dose vials of some influenza and Hep B vaccines)
Counsel patients on the benefits of immunizations
• Prevents serious childhood infections that may result in serious illness or death (eg. epiglottitis, measles encephalitis, whooping
cough, poliomyelitis, meningitis, pneumonia, tetanus, hepatitis/cirrhosis, cervical cancer)
• I- the chance of transmission and infection by causal organisms in those unable to be immunized (herd immunity)
• Unvaccinated children have a much greater chance of getting a vaccine-preventable illness
• Stopping immunization (eg UK) has lead to disease outbreaks with morbidity + mortality in previously-well kids
4, Counsel patients about the risks and side effects of immunizations
• It is most effective to compare the risks of vaccines with the risks associated with the vaccine-preventable illnesses —* not
vaccinating a child is not a risk-free decision
• Common, mild: pain, erythema, and swelling at injection site, irritability, rash, fever
• 10-15 mg/kg acetaminophen q4H pm (max 5 doses per day) for fever or pain, prophylactic use controversial
• Less common, moderate: seizure, hypotonic unresponsive state, inconsolable crying (DTaP-IPV), fever, arthralgias, parotitis (MMR)
—* history of these adverse events are NOT a contraindication for future immunizations
• Life threatening:anaphylaxis (-1-2 out of 1 million), Guillain-Barré rate following influenza vaccination may be higher than
background rate (already low) of 1 additional case per million vaccinated
Special consderations
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 (influenza, yellow fever)
• Streptomycin (IPV)
• Immunodeficiency or active immunosuppressive therapy — generally all live vaccines are contraindicated
• Following solid organ transplant: generally resume non-live vaccinations in 6— 12 mos, consider live in 2+ yrs
• HIV: vaccinate early in disease when CD4 counts are still high
• High dose systemic steroids taken for> 2 weeks - defer all vaccines until off steroids for 1 month
• Pregnancy: defer live vaccines until immediate postpartum (however, breastfeeding is not a contraindication!)
• Take precaution with vaccine administration under these circumstances:
• All vaccines: moderate - severe illness, severe bleeding disorder
• Live vaccines: recent administration of IVIg or blood products: wait 3 — ii months (generally 6 months)
2. Missed immunizations: no need to restart immunizations if one is missed — patients can pick up where they had left off
• If there are inadequate immunization records (eg. immigrants), restart on 10 immunization protocol based on age
3. Hyposplenia and Asplenia (congenital, surgical, or functional): no contraindications to any vaccines
• They are at an increased risk for encapsulated bacterial infections (S. pneumoniae, Hib, N. meningitides)
• Ensure immunizations are UTD, children > 2 should receive additional vaccines against encapsulated bacteria:
• Pneumococcus and meningococcus polysaccharide vaccines offer additional serovar protection, however boosters are
required q2-5 yrs and q3-5 yrs, respectively
• Consider reimmunization with Hib booster for all asplenic patients > yrs
4. Additional immunizations:
• Influenza: 2010-2011 seasonal trivalent inactivated vaccine will contain 2009 pandemic Hi Ni strain, recommend:
• Children 6-48 ma, chronic health condition, Aboriginals, pregnant, 65+ yo (and associated contacts & caregivers)
• 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 individual with a negative Mantoux test)
• RSVIg (palivizumab): monthly IM injection recommended for all entering RSV season (Nov — April) who are:
• 2 yrs of age with chronic lung disease or hemodynamically significant congenital heart disease OR premature infant 6
mos of age (ex-32 wks OR ex-36 wk and living in a remote community)
References
1. National Advisory Committee on Immunization. Canadian Immunization Guide. 7’ ed. Ontario: Public Health Agency of Canada; 2006. 389 p.

LIMPING CHILD
2071 Ed. Authors: Peter Gill, Gary Galante MD, Melanie Lewis BN MEdMD FRCPC
OriginalAuthors: Peter Gill, Gary Galante MD, Melanie Lewis SN MEd MD FRCPC
Station Objective
Determine whether the pain originates in joints or soft tissue and determine whether the worsening knee pain is unilateral
Diagnostic Criteria
Determined by of Hx, PE, investigations and clinical impression: MUST rio SEPTIC JOINT
• Septic arthritis: acute, febrile, warm/swollen/painful joint, t ESR/CRP, 1’ WBC, >75% PM synovial fluid
• Osteomyelitis: febrile, bone pain, t ESR/CRP, t WBC, ± blood C&S, normal x-ray, bone scan/MRI
• Transient synovitis: recent URTI, afebrile, well, onset 1-2 days, minimal exam findings (clinical dx)
• LCPD: limited hip internal rotation, normal labs, x-ray diagnostic
• SCFE: limited hip internal rotation, x-ray diagnostic (need frog leg views)
• JIA: gradual, AM stiffness, polyarthritis, tESR/CRP, Rf, i-ANA (50%)
-
• Malignancy: systemic symptoms, night pain, abnormal bruising/pallor, -Hg,I-WBC, IPlt, X-ray (poor-defined margins, onion
skin/sun burst appearance w/o sclerosis)
Table 1. Cause of Limp in Various Aae GrouDs
Cause <3yo 4—lOyo iiiio
• Trauma
Trauma X X
• Infections: septic arthritis, osteomyelitis
Septic arthritis X X
• Inflammatory: JIA, transient synovitis, toxic synovitis of hip,
Osteomyelitis X X
Kawasaki, HSP
• Neoplasm: leukemia, bone tumours, Mets Transient synovitis X
• Other JIA X X X
• LCPD, SCFE, DDH HSP X
• Osgood-Schlatter disease LCPD X
• Discitis, spinal abscess, bursitis, cellulitis SCFE X X
Growing pains Neoplasm X X X
Hematologic X X X
Growing pains X X
History
CC • Limp - any alteration in child’s normal gait (due to pain, weakness, or deformity)
HPI • Onset: acute/chronic, recent trauma, recent URTI/illness, is it getting worse
• Palliating/precipitating: pain effect of activity/rest, prolonged sitting/kneeling, NSAIDS
-
• Quality: painful or painless, continuous or intermittent, sharp or dull/vague

. Radiation/region: focal/hip/groin/knee/foot, unilateral vs. bilateral, migratory
• Severity: can child wt bear, activities sacrificed, subjective description
• Timing: AM stiffness or limping, pain at night or wakes from sleep
• Unique symptoms: fever, night sweats, I- appetite, wt I-, fatigue
• 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 WB, back pain/incontinence
PMHx • JIA, Chronic illness, sickle cell, endocrinopathy
PSHx • Joint repair, fractures, splenectomy
PO&GHx • Prenatal, perinatal or neonatal complications, gestation, GTPAL, delivery, presentation, birth wt
FHx • RA, SLE, psoriasis, IBD, hematological disorder, sickle cell, leukemia
• 3 generation pedigree: consanguinity, pertinent familial dz
Meds • Rx, CAM, vitamins, OTC
Allergies • Medications, food, environmental
Social • Marital status/family unit, psychosocial situation (parental neglect, abuse, sexually active)
Dev. • GM, FM, language, personal-social
ROS • Diet/nutrition, level of activity

physical
1. General
• General: ill or toxic in appearance, vitals/T appropriate and stable, mental statu
• HEENT: conjunctivitis, pallor, tonsillar exudates, mucosal lesions, LAD
• CV: new onset murmur (ARE), tachycardia/CHF (myocarditis)
• GI: HSM, signs of peritonism
• DERM: rashes, subcutaneous nodules, swollen hands/feet ± desquamation
2. MSK/NEURO: (spine, lower extremity including joints from hip down)
• Inspection
• Observe gait: smooth versus antalgic, Trendelenburg, toe-walking
• 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, check feet for callus, ingrown toenail, poorly fit shoes
• Palpation
• Landmarks/anatomy, effusion, swelling, temperature, crepitus
• Pain/tenderness over tendon insertion (apophysitis), bony points (osteomyelitis, tumor), muscle
-
• ROM (active/passive)
• Back, knee, hip, spine + ankle: look for limitation, guarding, discomfort
• NEURO: muscle strength, bulk, tone, DTR, sensation (dermatomes/peripheral nn distributions)
3. SpecialTests
• FABER test for SI joint pathology: hip flexion, abduction and external rotation + if pain
-
• Galeazzi test: + if knees different ht when Pt supine with ankles to buttocks and hips/knees flexed
Investigations
1. Blood work: indicated if uncertain of etiology from Hx and PE
• IF SUSPICIOUS, MUST rio SEPTIC JOINT WITH JOINT ASPIRATION
• Send fluid for WBC, dif, gram stain, cultures, protein, glucose
• CBC-D, ESR/CRP, blood C& S if worrisome joint swelling
• If suspect infectious etiology: ASOT, DNAse B, throat swab, urine C&S, R&M, FOBT, stool C&S/O&P
• Joint X-ray: AP, lateral, frog leg views of pelvis (beware, initial XR —ye in some fractures, AVN, OM, septic joint)
• Technetium bone scan, MRI if suspicion despite N XR (for spine pathology, OM, stress fracture, early AVN)
3. SpecialTests
• ANA, HLA-B27, sickle cell, viral serologies, complement, immunoglobulins
Treatment
1. Treatment Options: largely depends on etiology
• Trauma: symptomatic Tx, RICE, NSAIDS
• Infection: IV antibiotics + irrigation and debridement
• JIA: biologics
2. Follow-up
• Ensure mobility, resolution of infection
3. Referrals
• Pediatric rheumatologist, orthopedic surgeon, pediatric oncologists as needed
References
2. Rudolf M, Levene M. Paediatrics at a glance. 2” ed. Oxford. Blackwell Publishing Ltd.; 2007.
Miall L,
Pediatricsj Edmonton Manual of Common Clinical Scenarios 281

NEONATAL JAUNDICE
20!! Ed. Authors: Lauren Kitney BSc MD, Gory Ga/ante BSc MD, Melanie Lewis BN MEd MD FRCPC
OriginalAuthars: Lauren Kitney BSC, Gary Ga/ante BSc MD, Melanie Lewis BN MEdMD FRCPC
Station Objective
To develop an approach to neonatal jaundice and differentiate between physiologic and pathologic etiologies
1. Diagnostic Criteria (Table 1 &2)
Table 1: Etiology of Unconjugated Hyperbilirubinemia
Patholoaic
Physiologic Hemolvtic Non-Hemolytic
Intrinsic Extrinsic
• Breast feeding • Red cell membrane defects • Drugs • Hemorrhage/Hm
jaundice • Spherocytosis • Vitamin K (e.g. cephalohematoma)
• Breast milk • Elliptocytosis • Sepsis • Polycythemia
jaundice • Erythrocyte enzyme defects • Splenomegaly • GI obstruction/ileus
• Jaundice of • G6PD deficiency • lsoimmune mediated • Crigler-Najjar Syndrome
prematurity • Pyruvate kinase deficiency • ABO, Rh(D) or other minor • Gilbert Syndrome
• Congenital erythropoietic antigen incompatibilities • Congenital hypothyroidism
porphyria
• Hemoglobinopathies
• aThalassemia
Table 2: Etiology of Conjugated Hyperbilirubinemia

Hepatic Post-hepatic
• Infection: TORCH, hepatitis, E.coli UTI • Biliaryatresia
. Genetic/Metabolic/Endocrine: galactosemia, fructose intolerance, • Choledochal cyst
tyrosinemia, a-antitrypsin deficiency, hypopituitarism, hypothyroid, neonatal
1 • Inspissated bile/mucus: cystic fibrosis
hemochromatosis, Alagille syndrome • Spontaneous perforation of extra-hepatic bile
• Drugs: carbamazepine, rifampin, anti-retrovirals, antibiotics (ceftriaxone, sulfa) ducts
• Total parenteral nutrition • Tumour/mass
• Idiopathic neonatal hepatitis
• Inspissated bile/mucus: cystic fibrosis
• Unconjugated hyperbilirubinemia: breast feeding jaundice, breast milk jaundice
3. High Mortality:
. Biliary atresia, acute bilirubin encephalopathy, sepsis
History
ID Age, sex, ethnicity
CC Jaundice
HPI Gestational age, onset, who noticed, duration, evolution/progression
• Nutrition: breastfed vs. formula, amount, frequency, difficulties, vomiting, weight loss >10%
• Sleep (duration, frequency) high pitched cry, inconsolable/temperament change, lethargy, fever
• Voids (dark urine, # wet diapers per day) & bowel movements (frequency, consistency, pale)
RED FLAGS ønset <24 hours, pged (‘>1-2 weeks), pale stools, dark urine, hper/hpotonia, dehydration
PMHx Prenatal: Prenatal care, abnormal U/S, maternal illness (GDM, HTN, infections, rash, fever, bleeding), GBS status,
exposures to toxins/teratogens (smoking/EtCH/drugs), IUGR, RhoGAM
• Perinatal: gestation, intrapartum fever, APGARS/resuscitation, birth weight, mode (forceps/vacuum), injury, PROM,
delayed cord clamping
• Postnatal: complications (fever, shock, hypotonia, seizures) NICU, neonatal metabolic screen
• Medical: course since birth, infections
PSHx Prior surgeries & any complications
PO&GHx GTPAL, previous pregnancies with hyperbilirubinemia, maternal fever/illness, result of mother’s ABO and Rh (Dl
blood type and red cell antibody screen during pregnancy
FHx Consanguinity, anemia, jaundice (newborn/other age), hepatobiliary disease, G6PD deficiency, splenectomy,
miscarriages, hemoglobinopathies, autoimmune disease, cystic fibrosis

—..
Meds Prescription, OTC, CAM
-
Allergies Medications, environmental, food
—
Social • Primary caregiver, family’s financial situation, drug plan
—
ROS Hypo/hypertonia, seizures, coma [acute bilirubin encephalopathy], cough/wheeze, apnea/apparent life threatening
event (ALTE), respiratory distress, abdominal distention, bleeding, rash/lesions
Risk Factors ABO incompatibility (mother type 0, infant type A or B), onset within 24 hours, jaundice before discharge,
prematurity, sibling with severe hyperbilirubinemia, birth trauma, male, mother >25, Asian/European ethnicity,
infection, breastfeeding, macrosomic infant of diabetic mother, poor feeding, prolonged TPN, sepsis RE (GBS+,
PROM/PPROM, chorioamnionitis)
Physical
i. General Approach
• ABCs and vitals (HR, BR RR, 02 saturation, temperature), appearance (toxic), growth (HC, ht, wt)
2. Inspection
• LOC/vigor, jaundice (sclera, mucus membranes, palmar creases, tip of nose) cataracts, abnormal facies [triangular in Alagille],
,
dehydration (decreased turgor, dry mucus membranes, delayed capillary refill), cephalohematoma/birth trauma, bruising/
petechiae, abdominal distention, retrocollis, opisthotonos
3. Percussion/Palpation
• Bulging/sunken fontanelle, hypo/hypertonic, primitive reflexes, hepatosplenomegaly, abdominal mass
4. Auscultation
• Heart sounds, murmurs, breath sounds
Investigations
1. Blood work
• Total serum/conjugated/unconjugated bilirubin (fractionate if jaundice > 2wks, or markedly elevated TSB)
• Cord blood for blood group and DAT (Coombs test) if early jaundice or mother’s type & screen unknown
• Blood smear, reticulocyte count
• Septic workup: CBC duff, blood/urine culture, +/-CXR, +/- LP if indicated, TORCH screen, Hep serology
• Screening for G6PD deficiency if severe hyperbilirubinemia or high risk based on ethnicity, TSH screen
• If conjugated hyperbilirubinemia AST, ALT, ALP, PT/INR, PT1 albumin, ammonia, sweat chloride test as well as metabolic and
-
genetic screens (serum a-i AT, RBC GALT assay for galactosemia, etc.)
• Abdominal U/S, HIDA scan ]normal clearance excludes atresia and stasis] if conjugated hyperbilirubinemia
• Liver biopsy [undiagnosed conjugated hyperbilirubinemia], intra-operative cholangiogram [biliary atresia]
Treatment
1. Emergent
• ABCs, rehydration, antibiotics if septic
• Exchange transfusion immediately if signs of acute bilirubin encephalopathy
• 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
3. Surgical
• Kasai procedure (hepatoportoenterostomy) +/- liver transplant for biliary atresia, resect choledochal cysts
4. Follow-up
• Re-assessment in 24-48 hrs; close monitoring of wt gain & serum bilirubin; repeat hemoglobin at 2 & 4 wks for infants with
isoimmu n ization
• After exchange transfusion, close follow-up and hearing test with brainstem evoked auditory potentials
5. Referrals
• Lactation consultant, general pediatrics, NICU, surgery, hematology, genetics
References
1. Heng M, Greenwald JA. Toronto notes (2007). 23
,d
2. HayW, Leviri M, Sondheimeri, Deterding R. Lange Current Diagnosis &Treatment in Pediatrics. 18
th
ed. United States: McGraw-Hill Companies, Inc.; 2007.
3. Candian Paediatric Society. Guidelines for detection, management and prevention of hyperbilirubinemia in term and late preterm newborn infants (35 or
more weeks’ gestation). Paediatric Child Health May/June 2007;1 2(5): 401-7.
4. Wong R, Bhutani V. Pathogenesis and etiology of unconjugated hyperbilirubinemia in the newborn. In: Up to Date desktop 17.2, 2009.
5. Abrams 5, Shulman R. Causes of neonatal cholestasis. In: Up to Date desktop 17.2,2009.

NEWBORN RESPIRATORY DISTRESS/CYANOSIS
201 I Ed. Authors: Chri5 Gerdung. Gary Galante MD, Melanie Lewis SN MEd MD FRCP
OriginalAuthars: Chris Gerdung, Melanie Lewis SN Med MD FRCPC
Station Objective
Evaluate respiratory distress/cyanosis in a newborn while considering a broad DDx. Rule out life-threatening conditions.
1. Diagnostic Criteria — classic criteria on P/E (Increased HR/RR, grunting, nasal flaring, subcostal/suprasternal retractions)
• Cardiac: PPHN, cyanotic heart disease, acyanotic obstructive/regurgitant lesions (Not L-R shunts)
• Pulmonary: TTN, RDS, MAS, pneumotx, pneumonia, congenital UAWOIlung malformation/diaphragmatic hernia
• Systemic/Metabolic: Sepsis (especially GBS), hypoglycemia, inborn errors of metabolism
• Neurologic: CNS damage (hypoxic-ischemic encephalopathy, intraventricular hemorrhage), drug withdrawal
2. Common Conditions and Treatment:
Table 1: Pulmonary causes of respiratory distress/cyanosis
Causes XR Findings Tx
UN Streaky interstitial infiltrates (mostly perihilar), hyperinflation, Supportive Tx (02, nCPAP, careful fluids +/- nutrition usually
fluid in interlobar spaces sufficient)
RDS Reticulonodular, air bronchograms, decreased lung volume Surfactant, supportive (often intubated)
MAS Patchy atelectasis/infiltrates, air trapping, often hyperinflation, Supportive +1- surfactant +1- inhaled nitric oxide (iNO) +1-
RIO pneumothorax (up to 20%) . antibiotics
Pneumonia* Hazy/distinct infiltrates, may see plural effusion Oxygen, antibiotics, ± vasopressors (sepsis)
PPHN Normal, may see increase in hilar markings Tx cause, 02, correct acid-base, iNO, HFV -
CCAM Air trapping, cysts Supportive, Surgery (resection)

*
Pneumonia can be differentiated based on when the infection started: intrauterine (TORCH), at birth (GBS, E. coil, Klebsieiia sp, C.
trachomatis), after birth (viral, Group A, B and C Strep, S. aureus, Kiebsieiia sp, Proteus sp, P. aeruginosa, E. coii) . .
Table 2: Congenital cardiac causes of cyanosis (unresponsive to 02, which can promote ductus closure)
Causes Age of symptom onset Exam findings Tx -
TOE 25% at birth (cyanosis), 75% by 1 yr Exertional dyspnea, S2 single, harsh , Surgery (RVOTO repair, VSD closure)
1
PGE
(Tet spells/squatting, EU) SEM @ LSB (RVOTO)
TGA Cyanosis in hrs-days (as foramen Distress, other findings variable PGE septostomy if no VSD, definitive surgery
,
1
ovale and ductus arteriosus close), (sternal heave, single S2, +/- (arterial switch)
or CHF in few wks if VSD present murmur if VSD/PDA)
Pulmonary Cyanosis in neonatal period after Distress, loud single S2 +/-VSD/ , surgery (syst-PA shunt, complete repair)
1
PGE
Atresia ductus arteriosus closes PDA murmurs
Tricuspid Birth-infancy (85% before 2 Single 52, +/-VSD/PDAJ syst-pulm PGE,, surgery (depends on PBF)
Atresia mo) — cyanosis(dec. PBF), CHEf collateral murmurs
FTT(increase PBF)
Truncus Cyanosis in NB, but more commonly SEM (truncal flow) ± diastolic Surgery (close VSD, commit LV to trunk,
Arteriosus CHF (worsen as pulm. vascular murmur (regurg), L precordial reconstruct RVOT)
resistance decreases.) bulge, hyperactive precordium
Ebstein Newborn to teenage/adult years Eatigue, holosystolic murmur over , surgery
1
PGE
Anomaly depending on severity left precordium (TR)

Cyanotic heart disease, acyanotic heart disease, sepsis, congenital diaphragmatic hernia, IVH/HIE
History (following initial assessment + cardiorespiratory management)

HPI • Onset of respiratory distress or cyanosis (rapidity, day of life), course/progression, duration
• Cyanosis worse with crying, activity or position
RED FLAGS • Poor perfusion, cyanosis, poor resp efforts or apnea, gasp/choke/stridor, worsening condition
PMHx • Previous episodes of cyanosis, resp. distress, stridor, intubations, APGAR scores, immune status
PSHx Any previous surgeries, especially surgeries of the heart or lung

PO&GHx GTPAL, prenatal care, BPP, genetic screens, serology/immune status/infections (GBS, STI, TORCH), drugs/cigs/EtOH/
meds (Li, antiepileptic), disease (GDM/HTN/asthma/SLE)
• Prenatal U/S oligohydramnios (PRS, lung hypoplasia), polyhdramnios (EA/TEF), defects
—
• Labor: gestation,PROM/maternal fever/chorio (inflcn), meconium, bleed, fetal HR abN, opioids/ anesthesia(central
depression), C/S + short labor (UN), birth trauma, nuchal cord/asphyxia
• BW, Apgars/perinatal depression, resuscitation (PPV, intubation, suction for mec)
Allergies Allergies to medications, food or environment
FHx Lung/congenital heart disease, genetic-metabolic syndromes, SIDS/early death, imm deficiency
Social Second hand smoke, SES
ROS • HEENT: cough, rhinorrhea, red/purulent eye, blue trunk/face/lips, choking
• CARDIO/RESP: diaphoresis/tachypnea with feeds, wheeze, cough, SOB, stridor, gasping, apnea
• GI: feeding changes, regurgitation/vomiting (esp bilious), diarrhea, failure to pass meconium
Risk Factors • Intubation, immunodeflciency, craniofacial malformation (or FHX of same), preterm delivery
Physical
1. General Approach
• Vitals: HR, BP (in all 4 limbs), RR, Sp0
3 (on and off of oxygen), temp, capillary refill
• Signs of impending collapse: obstructive airway(gasp/stridor), poor/no resp effort, dusky/bradycardic = get help!
• Growth characteristics: Birth weight, current weight, growth curves
2. Inspection
• Nasal flaring, grunting, chest retractions (supraclavicular suggests UAWO), symmetry of chest movement, head bobbing
(accessory muscle use), see-saw breathing (chest in and abdo out during inspiration, may be seen in healthy newborns as well),
tracheal tug chest shape, audible stridor, wheeze or cough,
• Cyanosis, scaphoid abdomen (CDH or prox Gl obstruction)
• Dysmorphisms/craniofacial abnormalities (Pierre-Robin- PRS— micrognathia, cleft palate, glossoptosis)
3. Palpation
• Chest expansion, precordial heaves, point of maximal impulse, thrills, peritonitis, tone + primitive reflexes
4. Auscultation
• Air entry, crepitations, wheeze, stridor, murmurs, extra heart sounds (53, S4 pericardial rubs etc), BS in chest
5. Special Tests
• 2 in R hand and foot to assess for flow through ductus arteriosus
Sp0
Investigations
1. Blood work
• CBC-D, electrolytes, blood glucose, blood C&S +1- LP, ABG
• CXR (inspiratory and expiratory), Echo, ECG, CT chest (if indicated)
3. Special Tests
• Tracheal secretions, Hyperoxia test (Pa02 < 150 mm Hg on 100% FiO2 suggests cyanotic lesion/severe PPHN)
• Intubation/cricothyrotomy if needed •
Treatment
1. Emergent
• Intubate if necessary, ensure airway is patent, and maintain patency of ducus arteriosus if suspecting a duct dependent lesion, 02
(unless remains cyanotic), bronchodilators, nebulized epinephrine
• Monitor BP and HR to ensure adequate tissue perfusion
2. Treatment_SeeTables 1 and 2
3. Follow-up
• Follow up with Cardiology, Respirology as needed
4. Referrals
• Peds Cardiology, Respirology, ICU
References
1. Bernstein, D. Cyanotic Congenital Heart Lesions: Lesions associated with Decreased Pulmonary Blood Flow. Kliegman: Nelson Textbook of Pediatrics.
Philadelphia. Saunders Elsevier; 2007. Chapter 430.
Bernstein, D. Cyanotic Congenital Heart Lesions: Lesions associated with Increased Pulmonary Blood Flow. Kliegman: Nelson Textbook of Pediatrics.
Philadelphia. Saunders Elsevier; 2007. Chapter 431.
3 Steinhorn RH. Evaluation and Management of the Cyanotic Neonate. Clinical Pediatric Emergency Medicine. 2008;9-1 69-1 75
FlidelRimon 0, Shinwell ES. Respiratory Distress in the Term and Near-Term Infant. NeoReviews. 2005 June;6(6):289-297
Pediatrics j Edmonton Manual of Common Clinical Scenarios 285

PEDIATRIC EMERGENCY
201? Ed. Authors: Lauren Kitney BSc MD, Gary Ga/ante BSc MD, Melanie Lewis BNMEdMD FRCPC
OriginalAuthors: Lauren Kitney BSc, Gary Ga/ante BSc MD, Melanie Lewis BNMEd MD FRCPC
S atio Objective
Develop an approach to the acutely ill infant or child
• Suspected physical abuse
• Abusive head trauma (shaken baby syndrome): subdural hemorrhages, retinal hemorrhages, posterior rib fractures,
metaphyseal fractures; burns: glove and stocking distribution; bruises: inaccessible locations, not cruising, patterned; any
presentation inconsistent with developmental capabilities or history!
• 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
• Status epilepticus, status asthmaticus, croup, bronchiolitis, DKA, adrenal crisis, trauma, foreign body aspiration, sepsis/systemic
inflammatory response syndrome, meningitis, hypovolemia
3. High Mortality:
• Trauma, bacteremia, respiratory distress, burns, head injuries, submersion, poisoning, anaphylaxis
Check: ABC, IV, 02. Monitors. Vitals
History
ID. Age
CC • Trauma, altered level of consciousness, respiratory distress
• SAMPLE • Signs and symptoms, Allergies, Medications, Past medical history, Last meal, Immunizations, Family Hx (pertinent!
sick contacts), Interventions en-route, Events related to injury, Drug use
RED FLAGS • Patient brought in by EMS, unresponsive, altered mental status, unstable vitals
Table 1: Normal vitals in children
Physical Systolic
General Approach Respiratory Urine
Age Heart rate blood
• Assess ABCs —* PROCEED TO EMERGENT TREATMENT rate output
pressure
SECTION BELOW Om— 3m 85-160 60-90 40-50 2.0 n’kg/h
2. Secondary Survey (head-to-toe exam) 3m — 2y 100-160 75-105 24-40 1.5 mI/kg/h
• HEENT: fontanelles (bulging/sunken), suture lines, 2y—lOy 60-120 85-112 12-30 1.Oml/kg/h
scalp (lacerations, hematomas), pupils (size, symmetry, >lOy 60-100 97-112 12-20 O.5ml/ki
reactivity), fundoscopy (papilledema, hemorrhages)
extra-ocular movements, nystagmus, tympanic membranes, discharge from ears, nose (position, discharge) mouth (tongue biting,
oropharynx, lips, tongue swelling, blood), facial bones (symmetry, bony deformities, pain), lymphaden.opathy, clavicles
• RESP: stridor, increased WOB (nasal flaring, retractions), tracheal position, flail segments, subcutaneous emphysema, symmetry of
breath sounds, adventitious sounds. Beware of bradypnea w/o improvement
• CVS: 51 & S2, murmurs,extra sounds, capillary refill, peripheral pulses
• ABDO: 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, cranial nerves, reflexes,strength, tone, sensation
DERM: rashes, urticaria/angioedema, purpura, petechiae, abnormal skin findings
Treatment Table 2: Pediatric Airway Management Considerations

EMERGENTTREATMENT/PRIMARY SURVEY Estimation of ETT size
Anatomic differences (from adult airway)
• Vitals, general appearance (1-lOy)
• C- Spine precautions Uncuffed = age/4 + 4 Narrow nasal passages
• Airway — observe for signs of respiratory distress, Cuffed = age/3 + 4 Large occiput
skin colour, UAWO (abnormal or no sounds) Emergency drugs that can Large tongue
• Approach to airway management: suction, be given via ETT Superior larynx @ level C3 (C4/5 in adults)
reposition, NPA/OPA, FB relief (<ly/o — back Lidocaine, epinephrine, Narrowest at subglottic area (cords in adults)
slaps/chest thrusts, >1 y/o — abdo thrusts), atropine, naloxone, Anteriorly slanted cords (perpendicular to
intubation with laryngeal mask airway (LMA) salbutamol trachea in adults)

or endotracheal tube (EU)
• Breathing — assess rate, rhythm, oxygen saturation, effort, skin colour
• Approach to breathing management: oxygen, ventilation
• Circulation assess pulses, blood pressure, skin colour/temperature, capillary refill, mental status
—
• Follow pediatric advanced life support algorithms for septic shock, tachycardia, bradycardia or pulseless arrest (may involve
chest compression, defibrillation, resuscitation drugs)
• Establish vascular access (peripheral, central, intraosseous)
• Draw blood for CBC, electrolytes, calcium, blood glucose, ABG/VBG (lactate, mixed venous 02 sats)
• Volume resuscitation: 20 mI/kg 0.9%NaCI or RL (no maximum vol), consider PRBCs if not responding
• Continue post-resuscitation monitoring: cardiac monitor, vitals q5-1 5 mm, volume status, urine output
• Disability assess level of consciousness (GCS/AVPU), pupil size/reactivity, movement of extremities
—
• Exposure undress patient, log roll, palpate spine/extremities for deformities/pain, DRE, warming measures
—
• Empiric antibiotics broad-spectrum (<1 hr ideal, sooner is better) if suspect shock

—
• Note: ifpossible allow parental presence during resuscitation

• Proceed with secondary survey portion of physical examination (see above)
Investigations
1. Blood work
• Further blood work depending on presentation may include full septic workup (blood & urine cultures, do not LP unless stable),
liver and kidney function, lactate, INR, PU, type & screen, crossmatch
• Dependent on presentation
3. SpecialTests
• Possibly lumbar puncture as part of septic workup, ECG, EEG
• If indicated
Treatment
Table 3: Approach to emergency presentations
Croup/Bacterial tracheitis Epiglottitis Meningitis Sickle Cell Disease
Dexamethasone 0.1 5-0.6 mg/ Call PICU, anaesthesia, ENT to Antibiotics chosen depend on age of Pain management for vaso-occiusive crisis
kg x 1 secure airway child * per kg doses vary with age (morphine)
Nebulized L-epinephrine 5mL Do not agitate or attempt to Neonatal: ampicillin ÷ gentamycin or Fluid bolus followed by 1 .5x maintenance
1:1000 (5mg) q20-30 mm PRN secure an airway on your own, ampicillin + cefotaxime +1- acyclovir If febrile, start IV antibiotics empirically
Intubation as last resort (smaller 02 by mask if tolerated 1-3 months: ampicillin + cefotaxime +1- (ceftriaxone 1 00mg/kg/dose +/- vancomycin
tube than estimated based on Cefuroxime 150 mg/kg/d IV vancomycin if severely ill)
size) div q8h for 10 days (2nd/3rd >3 months: ceftriaxone or cefotaxime, Use Hx/PE to evaluate for acute chest
If bacterial tracheitis: 3rd generation cephalosprins, GAS ÷/- vancomycin syndrome, aplastic/splenic sequestration
generation cephalosporin + and S. aureus are now more Viral meningitis supportive, acyclovir
— crisis, shock, meningitis, sepsis, etc.; tailor
vancomycin common than Hib) for HSV work-up /treatment accordingly
Adrenal Crisis Status epilepticus Anaphylaxis Status asthmaticus
Hydrocortisone 100 mg/m2 Maintain patent UAW (suction! 0.01 mg/kg of 1:1000 epinephrine IM Inhaled B agonist: nebulized salbutamol 0.1
IV bolus then 100 mg/m2/d position), 02, Lorazepam 0.1 qsmin PRN mg/kg x 3
divided 4-6 h mg/kg IV/SLJPR q 5 mm Bronchodilators: salbutamol if Nebulized ipratropium bromide 250 mcg x 3
Phenytoin 2Omg.kg IV over 20 bronchospasm Systemic corticosteroids: methyiprednisolone
mm OR Antihistamines: diphenhydramine 1-2 1-2 mg/kg IV divided q 6h or hydrocortisone
Phenobarbitol 20 mg/kg IV/IM mg/kg IV 4-6 mg/kg IV q4-6h
over 20 mm (preferred 2nd line Ranitidine 2-6 mg/kg/d IV q6-1 2 h Magnesium sulphate 20-50 mg/kg IV over
in neonates) Corticosteroids: hydrocortisone 5-10 20 mm
If refractory rapid sequence mg/kg IV q4-6h Salbutamol start at 1-2 mcg/kg/min IV
intubation, PICU Observe vs. admit depending on
severity
1. Further workup
• If indicated (toxicology, anticonvulsant levels, metabolic workup)
2. Follow-up
• May require further monitoring in PICU
3. Referrals
• Pediatrics, other subspecialties if indicated, child protection services if abuse suspected
References
1. Rubin M, Sadovnikoff N. Pediatric Airway Management. In: Tintinalli J, Kelen G, Stapczynski 5, Editors. Emergency Medicine: A Comprehensive Study
Guide — 6t Ed. New York: McGraw-Hill; 2004.
2. Heng M, Greenwald JA.Toronto notes 2007. 23 rd
3. Dipchand A, Friedman J.The Hospital for Sick Children Handbook of Pediatrics 1 1” Ed. Toronto: Elsevier Canada; 2009.

PEDIATRIC FIRST PRESENTATION OF SEIZURE
OriginalAuthors: Christina Yang. Mark Enarson MD FRCPC
Station Objective
In this station, you need to recognize a neurological emergency in a child. You may be asked to differentiate between the different types of
pediatric seizures and appropriately manage a child during a seizure.
• Seizure: abnormal electrical activity in the brain, which may cause a change in motor activity and/or behaviour
• Epilepsy: two or more unprovoked seizures
• Status epilepticus: classically defined as a seizure lasting over 30 minutes or without recovery to baseline in between ictal events;
in practice, treatment is initiated at 5 minutes of continued seizure activity because, after this point, they become increasingly
unlikely to cease without treatment
• Breath-holding spells
• Syncope (e.g. cardiac causes, vasovagal)
• Migraine
• Benign paroxysmal vertigo
• Gastroesophageal reflux (Sandifer’s sign)
3. High Mortality / Morbidity
• Non-accidental injury
• Cerebrovascular accident
• Hypoglycemia, hyponatremia, poisoning
• Brain tumor
• Encephalitis, meningitis
History
CC • Suspected ictal event
HPI • Note duration of each stage, symmetry/spread, time of day (e.g. upon waking, nocturnal)
• Pre-ictal symptoms: also known as aura, usually associated with focal / partial seizures
• Younger child: irritability, behavioral changes, somnolence, dinginess
• Older child: epigastric sensation, déjà-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, loss of continence, 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
• Post-ictal symptoms: note level of consciousness and degree of recollection of event
• Headache, Todd’s paralysis, somnolence, weakness, behavioral changes (e.g. aggressiveness, persistent
crying)
• Length of time to return to baseline (e.g. seconds —* breath-holding spell, hours —* seizure)
• Provoked seizure: head trauma, infection, intoxication, dehydration, hypoglycemia, stroke (e.g. sinus venous
thrombosis), brain tumor, minor trauma, behavioral event, hyper/hyponatremia
• Febrile seizure: associated with fever, occurs in children of 6 months to 6 years old
RED FLAGS • Significant head trauma • Suspicious mechanism, inconsistent histor,y, delayed
• Persistent focal defic•its presentation —* suspect inflicted head trauma
• Unwell child (e.g. significant intercurrent illness, a Persistently altered level of consciousness
signs of meningjjs) • Eevelopmental regression
PO&GHx • GTPAL, method of conception, pregnancy follow-up, blood work, U/S, complications, toxin use
• GBS and STI status, ROM, induction vs spontaneous labour, length of labour, instrumentation
• Birth weight, head circumference, APGARS, resuscitation required
• Complications in first month of life: jaundice, kernicterus

IoI,rnent Milestones, regression, developmental delay
PMHx • Acquired brain injury, neurological problems, metabolic disease
PSHx Cranial surgeries
• Recent antibiotic use (rule out infection), use of and recent changes in anticonvulsant meds
Allergies • Adverse reactions to drugs
FHx • Seizures, epilepsy, stroke, thrombotic events, bleeding / clotting disorders
• Spontaneous abortions, 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
initial Management
i. Emergent
• ABCDFG (Don’t Forget Glucose), LOC,
• Vitals: HR, BP, RR,Temp, 5p02
• Identify and treat life-threatening conditions
• Aspiration, head injury, metabolic derangements (e.g. lactic acidosis, hypoxia, hyperthermia, hypoglycemia)
2. Stop the seizure
• First line AED5 (anti-epileptic drugs)
• Benzodiazepines: diazepam acts fast, can be given PR, lorazepam lasts longer, midazolam given IM or IN
— — —
• Second line AEDs

• Give phenytoin first, then consider phenobarbital if ongoing seizure activity
• NB: phenobarbital plus benzo = respiratory depression (be prepared to intubate)
Physical Exam
1. Inspection: symmetry, dysmorphism, microcephaly, tongue-biting, signs of trauma, infection, sepsis or meningitis
2. MSKIDerm: café au lait spots or port wine stains indicating neurocutaneous disorders, rash (viral exanthems, purpura)
3. Cardio-respiratory exam: murmur or arrhythmia, decreased breath sounds
4. Full neurological exam: meningismus, symmetry and focal neurological signs
Inve tigations
1. Bloodwork should be ordered based on individual clinical circumstances that include suggestive historical or clinical findings (e.g.
vomiting, diarrhea, dehydration or failure to return to baseline alertness):
• CBC-D, glucose, electrolytes, calcium, magnesium, BUN, creatinine, LETs, consider metabolic workup
2. Imaging is recommended for afebrile, first-time seizures, although urgency depends on various factors:
• Urgent (CT if MRI unavailable) for, but not limited to:
• 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 hours, underlying medical condition predisposing to adverse
intracranial events (e.g. tuberous sclerosis, neurofibromatosis)
• Remember that abusive head trauma rarely has any visible injuries
3. EEG to classify seizure type and predict recurrence risk
4. Lumbar puncture if CNS infection is suspected and child is in stable condition
Long Term Management

1. Counseling
• First unprovoked seizure with a normal MRI: 30% chance of second
• First-time seizure is rarely treated with Iongterm AEDs
2. Referrals
• Neurology if status epilepticus is refractory to treatment and to later follow-up as an outpatient
References
1. Chu-Shore Ci and Tseng BS. First seizure, pediatric perspective. eMedicine; 2010.
2. Marshall R5 and Mayer SA. On call neurology, 3d
Ed. 2007. Philadelphia: Saunders Elsevier: pp.45-56.

PEDIATRIC WHEEZE
OriginalAuthors: Christina Yang, Mark Enarsan MD FRCPC
Station Objectve
In this station, you need to recognize the clinical picture of wheeze, generate a differential diagnosis and appropriately manage a wheezy
child.
• Wheeze: continuous high or low-pitched sound during inspiration or expiration due to intra-thoracic airway narrowing
• Versus stridor: harsh, high-pitched sound during inspiration due to extra-thoracic airway narrowing (please refer to Stridor station)
• Acute wheeze:
• Infection (e.g. viral bronchiolitis common in infants)
-
• Mechanical obstruction (e.g. foreign body 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 • Age, genderand ethnicity
CC • Wheeze
HPI • Onset: age and course (acute versus gradual)
• Acute:
• SOB, cough, anxiety, history of choking
• Persistent:
• Rule out congenital or structural abnormalities, bronchial compression by mass, interstitial lung disease
• Intermittent:
• Likely asthma
• Associations:
• Seasonal variation and common triggers including URTI, exercise, allergens (suggest asthma)
e
• Association with feeding or vomiting (suggests GERD)
• Urticarial rash (rule out anaphylaxis)
• Other:
• Poor weight gain and recurrent ear or sinus infections (suggest cystic fibrosis, immunodeficiency)
• Progressive dyspnea, exercise intolerance, failure to thrive (suggest interstitial lung disease)
RED FLAGS • History of choking and wheezing with minimal cough (suggests foreign body aspiration)
• Decreased LOC
• Toxic appearance
• Significant respiratory distress
• Cyanosis
• Silent chest
PO&GHx • Pregnancy follow-up, blood work, U/S, complications, toxin use
• Neonatal or perinatal respiratory problems / wheezing since birth (suggests congenital abnormality)
• Birth weight and gestational age, APGARS, resuscitation required
PMHx • Asthma, eczema, infections, cystic fibrosis, congenital heart disease, previous admissions or ED visits for asthma,
previous Rx of oral or inhaled steroids/salbutamol, history of”pneumonia”or protracted course of viral URTIs
PSIIx Upper respiratory tract or lung surgery
Meds • Response to asthma medications
Allergies • Seasonal, environmental, foods
• Adverse reactions to drugs
FHx • Asthma, atopy, cystic fibrosis
Social • Environment (e.g. type of heating, rugs), daycare, smoking, pets

Initial Management
1. Emergent
• ABCs
• Provide oxygen as needed to keep Sp02 > 92%
• Vitals: HR, BR RR,Temp, SpO2 —* continuous monitoring
2. identify’ and treat life-threatening conditions
• E.g. foreign body aspiration, anaphylaxis
Physical Exam
1. General: height, weight, vitals (pulse, BR RR, temperature, oxygen saturation)
2. Respiratory exam:
• 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, pectus excavatum, scoliosis)
• Palpation: cervical adenopathy, subcutaneous emphysema
• Percussion: diaphragm position, differences in resonance among lung regions
• Auscultation: define characteristics and location of wheeze, prolonged expiration, crackles
3. Cardiac exam: murmurs, extra heart sounds, signs of heart failure
4. Derm: eczema, urticarial rash
Investigations
1. Imaging:
• Chest x-rays are recommended for the first presentation of wheeze, but are not always necessary for every incidence afterward,
especially for a typical presentation of asthma or bronchiolitis
• Barium swallowNFSS (video fluoroscopic swallowing study) will be helpful when conditions like vascular rings, swallowing
dysfunction and GERD are suspected
2. Lab investigations are ordered rarely and only when relevant:
• E.g. CBC-D, sputum cultures, immunoglobulin levels, sweat chloride test
3. Pulmonary Function Test:
• Assesses presence, degree, and location of airway obstruction in cooperative, older children as well as response to bronchodilators
• Methacholine challenge and exercise testing can confirm hyperreactive airways
4. Bronchoscopy:
• For patients with suspected foreign body aspiration, persistent symptoms, or who are unresponsive to therapy
Long Term Managemen

1. Supportive (e.g. for viral bronchiolitis): maintain oxygenation and hydration
2. Confirm diagnosis and set goals
3. Asthma: inhaled corticosteroids for maintenance therapy and bronchodilators for acute exacerbations
References
1. Majaesic C. 2009. Approach to the wheezy child. Powerpoint presentation. a
2. Fakhoury K, Redding G, TePas E. Approach to wheezing in children. UpToDate online versionl 8.2: May 2010.

PERIODIC HEALTH EXAM OF A NEWBORN
2071 Ed. Authors: Chris Gerdung, Gary Ga/ante MD, Melanie Lewis SN MEd MD FRCPC
OriginalAuthars: Chris Gerdung, Gary Ga/ante MD, Melanie Lewis BN MEd MD FRCPC
Station Objective
To thoroughly examine a newborn child and review the maternal history, as well as elicit any parental concerns regarding the nutritional
status and development of the child.
Common Conditions
1. Inadequate nutrition (breastfeeding difficulty)
2. Failure to thrive
3. Congenital anomalies
History
ID Name, age, gender, ethnicity of mother, father and child
CC • Periodic health exam of a newborn
• Nutritional status of newborn
HPI Elicit concerns of parents regarding newborn development and attachment to parent
• Is baby breast or bottle-fed, # of wet diapers/day, BM frequency, waking to feed at night?
. If breastfed: breast problems (latching, cracked/sore nipples, mastitis, thrush, etc.), milk supply (feeds both breasts,
let-down, change in congestion), frequency/duration of feedings, Vit D use
• If bottle-fed: formula used (how much/how often/how is it mixed), 61 symptoms of cow’s milk protein intolerance
RED FLAGS Lack of maternal-infant bonding, distress, <6 wet diapers/d, wt loss >10% of birth wt, failure to regain BW or
jaundice by 2wks, fever, no social smile by 6 wks, neglect
PMHx Prenatal: prenatal care, maternal age and PMHx, GTPAL, U/S testing, CBS screen, gestational DM/HTN screen,
prenatal infection, smoking/EtCH/drug use, antepartum bleeding
• Perinatal: gestation, route of delivery, APGAR, birth wt/ht/HC, NICU intervention/resuscitation
• Antinatal: hospitalized following delivery, meconium passage
PSHx • Surgeries at the time of delivery or prenatally for mother or child (including circumcision)
Meds Maternal: prescribed medications, OTC, vitamins, CAM or otherwise
• Newborn: vitamin D, any other medications whether OTC, vitamins, CAM or otherwise
Allergies • Foods, medications, environmental
. IgE and non-IgE”allergies”(Ie. Cow’s milk protein intolerance)
FHx • Congenital heart disease, auto-Immune disorders, bleeding/clotting disorder, congenital anomalies, genetic
syndromes, learning disabilities, perinatal deaths, SIDS, chronic disease
Social • Infant-parental attachment, parental stress/mood, parental support, second hand smoke, SES
ROS Fevers, weight decr. or poor weight incr., jaundice, irritability, fatigue/lethargy, floppy, jittery
. Development: startles to sound, EOM full range, cries, social smile, moves all 4 extremities
• CV: cyanotic spells/squatting, puffy eyelids, diaphoresis/dyspnea with feeds
• RESP: distress, tachypnea, stridor, wheeze, cough/coryza
• GI: reflux(arches backJirritable)/aspirationfchoking with feeds, vomiting (projectile/bilious), bowel habit/
consistency/blood/mucus, age at first meconium
• GU: ambiguous genitalia, abnormal stream, descended testicles, inguinal masses, asymmetry
. MSI< / DERM: extremity swelling/asymmetry/deformity, hip instability, rash Hx
Risk Factors • Low SES, 2nd
hand smoke, poor prenatal care, perinatal complications, domestic violence, parental mental health,
lack of support
Physical
1. General Approach
• Birth measurements: weight, length, HC
• General appearance: dysmorphic features, distress, grunting, lethargy, tone
• Vitals: HR (N= 90-1 80), RR (N= 30-60), sBP (N= 60-90),T(N= 36.5-37.5CC), SaC
2

2. InspectiOn
Head Size/shape of skull, size/fullness of fontanels, dysmorphic facial features, symmetry in head and face, caput/
cephalohematoma, rule out cleft palate
Eyes Spontaneous eye opening, EOM, spacing, shape, epicanthal folds, red reflex, pupil size/shape/light reflexes,
subconjunctival hemorrhage, discharge
Ears Skin tags/pits, shape, proper positioning, TM abnormalities
Mouth Dentition, hard and soft palate abnormalities, tongue and chin size/shape
Neck Goiter, cysts, full ROM, neck webbing
CV Murmurs, extra heart sounds, PMI, heaves, BP equal in all limbs, pulses regular and equal, femoral pulses (r/o
coarctation), brachial-femoral pulse_delay,_capillary refill
RESP RR, symmetry, pectus deformity, cyanosis, gasping/grunting/wheeze, crackles, paradoxical abdominal
movement, accessory muscle use, equal breath sounds bilaterally
GI Distension/indentation, masses, hepatosplenomegaly, kidney position, bowel sounds, umbilical cord
appearance (granulation tissue, bowel tissue?)
GU Presence of normal genitalia, descended testes, penis size, clitoromegaly, urethral opening, symmetry,
masses, passage of urine and stool
MSK/DERM • Equal and spontaneous limb movements, Barlow, Ortolani, and Galeazzi test for hip dislocation, additional
limbs/digits, palmar/plantar creases and nail abnormality, presence of lesions/rash on skin, birthmarks
(hemangiomas,_Mongolian_spots,_nevi), spine curvature, dimpling, hair patches
NEURO (N’s, tone, primitive (suck, root, Moro, palmar/plantar grasp, Galant, tonic neck, Babinski), deep tendon, and
superficial (abdominal, anal wink) reflexes
Investigation
1. Blood work
• No routine blood work is needed unless abnormalities are found on physical exam or if child is at high risk
• No routine imaging is needed
Treatment
1. Treatment options are related to chief complaint and physical exam findings
2. Dietary Considerations
• Encourage breastfeeding for 1 6 mo of life
• Infants generally feed 6-9x/day and consume roughly 60-9OmL/feeding
• Infants up to 6 mo of age have energy requirements of roughly 110 kcal/kg/day and roughly 1 OOkcal/kg/day between 6 and 12
mo (breast milk and commercial formulas mixed appropriately provide the adequate amount of calories, as well as protein, fat and
carbohydrate required)
• Diet should be high in Fe and vitamin D (supplemented with 400-8001U/day)
• Solid food must be initiated at 6 mo of age due to depletion of Fe stores
• Honey should be avoided in the 1 yr of life due to the risk of botulism
• By 1 yr of age diet should contain foods from all food groups, solid foods should initially be initiated weekly to assess for allergies
3. Follow-up
• With family physician or pediatrician at 7-14 days of age, then at 6 wks, 3 mo, 6 mo and at 1 yr
References
1. Heird WC. The Feeding of Infants and Children. Kliegman: Nelson Textbook of Pediatrics. Philadelphia. Saunders Elsevier; 2007. Chapter 42.
2. Lowe MC, Woolridge DP. The Normal Newborn Exam, or Is It?. Emergency Medicine Clinics of North America 2007;25:921 -946
3. StoIl BJ. The Newborn Infant. Kliegman: Nelson Textbook of Pediatrics. Philadelphia. Saunders Elsevier; 2007. Chapter 94.
4. Rourke, L, Leduc D, Rourke J. Rourke Baby Record: Evidence-Based Infant/Child Health Maintenance Guide (Interneti. Canadian Family Physician; 2006.
Available from: http://www.rourkebabyrecord.ca/documents/RBR_National_EN.pdf

PERIODIC HEALTH EXAM IN A TODDLER/CHILD
2011 Ed Authors: Lauren Kitney BSc MD, Gary Galante BSc MD, Melanie Lewis BN MEd MD FRCPC
OriginalAuthors: Lauren Kitney BSc, Gary Galante BSc MD, Melanie Lewis BNMEdMD FRCPC
Station Objective
To complete a periodic health exam in a child/toddler
Common Conditions:
• Developmental delay (see developmental delay)
• Learning disorder/ADHD (see ADHD/learning disorder)
• Asthma
• Eczema
• Sleep issues
• Nutritional issues (most commonly picky eaters)
History
CC • Periodic health exam; other chief complaints
HPI • Discuss specific medical or psychosocial concerns in more detail
RED FLAGS • Failure to thrive, developmental delay, regression, signs of abuse/neglect
PMHx • Prenatal: Prenatal care, U/S frequency, maternal illness (GDM, HTN, infections, rash, fever, bleeding), maternal
exposures to toxins/teratogens (including smoking/EtOH/drugs) IUGR
• Perinatal: gestation, APGARS/resuscitation, birth weight, mode of delivery
• Postnatal: Neonatal complications (TORCH infection, meningitis, encephalitis, seizure disorder, jaundice, CNS
trauma), NICU admission, length of stay, neonatal metabolic screen
• Medical: chronic medical conditions, prior hospitalizations/emergency visits, other concerns
• Nutrition: what is the child eating, how much, following Canada Food Guide, how much milk, how much juice, how
long was the child breastfed for
• Exercise: is the child engaging in physical activity? What type? How often?
• Sleep: where, how long, quality, naps, snoring, apneas
• Development: is child meeting developmental milestones for FM, GM, social and language (see Rourke Baby
Record), any concerns, regression, abilities compared to peers (see developmental delay)
PSHx • Prior surgeries & any complications
FHx • Obesity, asthma, eczema, atopy, chronic medical conditions, psychiatric disorders
• Meds • Prescription, CAM, OTC
-D
tD Allergies • Medications, food, environmental, previous reactions, prior skin testing
0.
Social • Who is the primary caregiver, discipline, attending school/daycare, marks in school, extra-curricular activities,
: interests, mood, socialization (school, home, etc), bullying at school, personal safety (home/school/community),
safety equipment (bicycle safety, sporting equipment), smoking in the home or car, childcare after school, family’s
financial situation, drug plan
lmmun • Routine, seasonal influenza vaccines, special, up to date
ROS • HEENT: vision, hearing, dental problems, frequent infections (pharyngitis, AOM, sinusitis)
• CVS: hydration status, cyanosis
• RESP: cough, wheeze, stridor, exercise tolerance, secretions, snoring, apneas
• GI: vomiting, regurgitation, reflux, abdominal pain, bowel movements, encopresis
• GU: toilet training, enuresis, precocious puberty
• MSK/DERM: eczema, diaper rash, handedness, limp
Risk Factors • Smoking in the home, low SES, domestic violence, complicated perinatal course

physical
1. General Approach
• Vitals
• Growth measurements: weight, height, head circumference, BMI (wt/ht) (plot on growth chart)
2
• General appearance, social, language, GM and FM skills (observe during history and physical)
• Child-caregiver interaction (observe during history and physical)
2. Systems Based Physical Exam
-
• HEENT: eyes, ears, nose, throat, dentition, lymphadenopathy, thyroid

• CVS: heart sounds, murmurs, pulses, skin colour & temperature
• RESP: breath sounds bilaterally
• ABDO: appearance, bowel sounds, tenderness, masses, organomegaly
• GU: normal female/male genitalia, descended testicles in males, circumcised?
• MSK: bony abnormalities, focal deficits, strengths, coordination, gait
• NEURO: tone, cranial nerves, deep tendon reflexes, sensory or motor deficits
• DERM: rashes, birthmarks, abnormal skin findings
Investigations
. Blood work
• If warranted
• If warranted
Treatment
• Treatment related to chief complaint
• Counseling/anticipatory guidance: immunizations, nutrition, dental care, growth, exercise, sleep, toilet training, injury prevention,
personal safety
• Parental support if needed
2. Further workup
• If applicable
3. Follow-up
• In one year for periodic health exam or sooner if warranted
4. Referrals
• Pediatrics, developmental pediatrics, psychiatry, other subspecialties, social work if applicable
References
1. Ffeng M, Greenwald JA. Toronto notes (2007). 23
,d
2. Rourke L, Leduc D, Rourke J. Rourke Baby Record: Evidence-Based Infant/Child Health Maintenance Guide. Canadian Family Physician, 2006.

PERIODIC HEALTH EXAM IN AN ADOLESCENT
2011 Ed Authors: Lauren KitneyBScMo, Gary Ga/ante BSc MD, Melanie Lewis SN MEd MD FRCPC
OriginalAuthors: Lauren Kitney BSc, Gary Ga/ante BSc MD, Melanie Lewis BN MEd MD FRCPC
Station Objective
To complete a periodic health exam in an adolescent patient with emphasis on obtaining a psychosocial history
• Obesity: BMI = weight 2 m
(kg)/he
(
) - ight overweight (25-30), obese (>30)
• Eating Disorders: anorexia nervosa, bulimia nervosa
Table 1: DSM-IV Diaanostic Criteria for Anorexia Nervosa and Bulimia Nervosa
Criteria Anorexia nervosa Bulimia nervosa
I Body weight <85% of expected Recurrent episodes of binge eating
Recurrent inappropriate compensatory behaviour to prevent weight gai
II Intense fear of gaining weight (laxatives, vomiting, diuretics, excessive exercise)
Disturbance in way body weight or shape is Binge eating and inappropriate compensatory behaviours occur at least
Ill experienced, undue influence on self-evaluation, 2x/week for 3 months
denial of seriousness of low body weight
Amenorrhea defined as absence of at least 3 Self evaluation unduly influenced by body shape and weight
Iv
consecutive menstrual cycles
Disturbance does not occur exclusively during episodes of anorexia
nervosa
Subtypes Restricting or binge/purging Purging or non-purging
• Pregnancy, sexually transmitted infections (chlamydia, gonorrhea, syphilis, etc.)
• Substance abuse (tobacco, alcohol, marijuana, illicit drugs), mood disorders (anxiety, depression, etc.)
• Eating disorders, obesity
History
Confidentiality statement: everything discussed will be kept between you and the adolescent except suicidality, homicidality and abuse
CC • Periodic health exam; other chief complaints (medical or psychosocial concerns)
HPI Discuss specific medical or psychosocial concerns in more detail
RED FLAGS • Homelessness, absence or failure from school, abnormal eating behaviours and/or distorted body image,
depression, substance abuse, risky sexual behaviour, self harm, suicidality, abuse
PMHx • Medical: chronic medical conditions, other medical concerns
. Prenatal/Perinatal/Postnatal: prenatal care, maternal illness/exposures, gestation, birth weight, complications
Development: any concerns
PSHx • Prior surgeries and any complications
PO&GHx • LMP, prior pregnancies, deliveries, miscarriages, therapeutic abortions, children at home, social services
involvement, supports (family, father, government, other), prior STIs, last pap smear
FHx • Obesity, eating disorders, substance abuse, suicide, depression, abuse, pertinent familial diseases, delayed puberty
Meds Prescription, oral contraceptive pill, CAM, OTC
Social • Psychosocial (HEEADSSS history)
• H-Home situation: where living, who with, getting along, discipline
. E-Education/Employment: attending school, grades, stress/balance, financial stressors
• E-Eating: eating behaviours, body image, nutrition, dietary restrictions
• A-Activities: interests, physical activity, interactions with family and peers, social network
. D-Drugs: alcohol, tobacco, marijuana & other recreational drugs, friends using, are they using, how much,
how often, when, why, driving under the influence
. S-Sexuality: sexual preference, sexual activity oral, vaginal, anal, age of partner, consensual, contraceptiofl
—
STI5
• S-Suicide & Depression: mood, self harm, suicidality
• S-Safety: home! school! work/community, bullying, bicycle & automobile safety

I Routine, additional (Hepatitis B, Gardasil, Influenza, Menactra)
ROS Vision, hearing problems, sleep concerns, other
Factors Prior abuse, lower socioeconomic status, lack of social and familial supports
mmun
physica I
General Approach Table 2: Tanner Staging
. Growth Female Male/Female Male
measurements: Stage
Breast Pubic Hair Genitalia
weight, height, BMI
1 Pre-pubertal Pre-pubertal Pre-pubertal
(plot on growth chart)
. General appearance 2 Breast Bud Sparse hair along base of penis/labia Scrotal/testes enlargement
& vitals
Systems Based Physical
3 Bud enlarges Hair over pubis t in length of penis
2. -
Exam Areola + papilla Further t in length and

Coarse adult hair
. HEENT: eyes, Secondary mound breadth of penis
ears, nose, throat, Areola recedes
5 Extends to medial thigh Adult size and shape
lymphadenopathy, Adult size and shape
thyroid
. CVS: heart sounds, murmurs, pulses, skin colour & temperature
• Breasts: Tanner staging in female (Table 1)
. RESP: breath sounds bilaterally
• ABDO: appearance, bowel sounds, tenderness, masses, organomegaly
• GU: Tanner staging male and female (Table 1)
• MSK: focal deficits, strengths, coordination, gait
• NEURO: cranial nerves, deep tendon reflexes, sensory or motor deficits
• DERM: rashes, birthmarks, abnormal skin findings
Investigations
Blood work
• If warranted
• If warranted
3. Special test
• CRAFFT screen if indicated:
Table 3: CRAFFT Substance Abuse Screening Test
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
4
Treatment
1. Treatment
• Treatment related to chief complaint
• Counseling re: sexuality and sexual health, healthy eating behaviours, personal safety and mental health, adjustment and coping
skills for adolescents with chronic illness
2. Further workup
• If applicable
3. Follow-up
• In one year for periodic health exam or sooner if warranted
4. Referrals
• Pediatrics, Obstetrics & Gynecology, Psychiatry, Adolescent Medicine if applicable
References
1. Goldenring JM, Rosen, DS. Getting into adolescent heads: An essential update. Contemporary Pediatrics, 2004 Jan; 21(1): 64-90.
2. Heng M, Greenwald JA.Toronto notes (2007). 23 rd
3. Diagnostic and Statistical Manual of Mental Disorders. Fourth Edition.Text Revision. Washington: American Psychiatric Association; 2000.
4. Knight JR, Sherritt L, Shrier LA, Harris 5K, Chang G. Validity of the CRAFFT substance abuse screening test among adolescent clinic patients. Achives of
Pediatrics & Adolescent, 2002; 156(6)607-614.

SPEECH AND LANGUAGE ABNORMALITIES
20?? Ed. Authors: Peter Gill, Gary Ga/ante MD, Melanie Lewis BN MEd MD FRCPC
Origina/Authors: Peter Gill, Gary Ga/ante MD, Melanie Lewis BNMEdMD FRCPC
Station Objective
disorder
Evaluate a child with speech and language abnormalities and identify appropriate management of
Diagnostic Criteria Table 1. DSM-IV-TR Criteria for ASD
• Language disorder: child’s language skills are significantly
a) Need a total of> 6 items from 1,2,3
< nonverbal/overall cognitive skills
1. 2 impairment in social interaction:
• Identify etiology after appropriate investigations and • Impairment in non verbal social behaviors
neurodevelopmental assessment Failure to develop peer relationships
• Classify (relative to what is appropriate for age and Lack of seeking to share enjoyment/interests
child’s nonverbal cognitive skills): Lack of social/emotional reciprocity
• Mixed expressive-receptive: difficulty
2. 1 impairment in communication:
formulating ideas into words and Delay in spoken language
understanding language Problem initiating/sustaining conversation
• Expressive: difficulty formulating ideas into . Repetitive/stereotyped use of language
words Lack of social imitative play
• May be specific language impairment or secondary repetitive/stereotyped behavior/interests:
3. 1
to other developmentally-related causes Preoccupation w stereotyped/restricted interest
•
• Stuttering: disturbed fluency/time patterning of speech Inflexible nonfunctional routines/rituals
• Phonological: fail to use age-appropriate speech sounds Motor mannerisms
2. Common confounding/contributory conditions: . Preoccupation w parts of objects
. Pervasive developmental disorder
• Includes Autism, Rett & Asperger’s syndrome
b) Delay or abnormal functioning in 1 of: social interaction,
• Severe and pervasive impairments in social communication, play (onset <3 yb)
interaction and communication skills
• Neuromotor-Cognitive disability c) Not better accounted for by Rett’s disorder or childhood
• Developmental delay (see Developmental Delay) disintegrative disorder
• Learning disorder: (see ADHD/Learn ing Disorder)
• Brain injury, neuromotor disorder (dysarthria)
. Hearing impairment: conductive, sensorineural
. Mechanical: cleft lip/palate, VC lesion (polyp/nodule/paralysis), adenotonsillar hypertrophy, ankyloglossia
. Selective mutism (social anxiety), developmental dysfluency (brief stutters, resolve by school age)
3. High Mortality:
. Rett syndrome, neuromotor, metabolic, neurodegenerative disorder
History
ID . Age, sex, ethnicity, name, home
CC Teacher/caregiver concern: speech delay, poor social skills
HPI . Speech (articulation, stuttering, phonation) and/or language (receptive ± expressive delay)
. Timeline: when was it noticed, how, who noticed it, any loss of function, settings
• School Hx: performance, hyperactive-impulsive, homework, any formalized/standardized tests
• Social: brings/shares objects, point to needs, shy/withdrawn, aggressive, anxious
emotional/
. Autistic features: poor eye contact, repetitive play, inappropriate social actions, hand flapping, lack of
social reciprocity, resistance to change/restricted activity
RED FLAGS Loss of language/social milestones, combined language/social delays, caregiver/teacher concern
. Neonatal complications, FHx, child abuse/neglect, dysphagia
. Language: no babble at 9-12 mo / words at 15 mo / simple commands at 18 mo / combos at 2yr
. Speech: unintelligible to parents at 2yr/strangers at 3yr, excessive stuttering, teased by peers
PMHx Prenatal: prenatal care, U/S freq., maternal illness/exposure to toxins (smoking/EtOH/drugs)
. Perinatal: asphyxia, APGAR scores, prematurity, birth wt, abnormal presentation
• Postnatal: neonatal complications, NICU admission, length of stay, neonatal metabolic screen
• Head trauma, chronic illness, AOM/OME, cleft palate, ankyloglossia, child abuse/neglect
PSHx CNS surgeries (shunt, tumour), LP
PO&GHx Gestation, GTPAL, route of delivery

FHx Autism, Rett, deafness, blindness, mental retardation, neurologic disorder, stutter, anxiety
• 3 generation pedigree: consanguinity, pertinent familial dz
Meds Rx, CAM, vitamins, OTC
Social Marital status/family unit, finances, school/peer relations, health plan, linguistic background
• Psychosocial situation: adoption, parental neglect, abuse, effect of illness on family
Dev. GM: roll (4 mo), sit (6 mo), walk (15 mo), climb (18 mo), stairs (24 mo), tricycle (3 yr)
• FM: grasps (3 mo), pincer (10 mo), scribble (15 mo), tower of 2 cubes (18 mo)
• Language: coos (3 mo), babbles (6 mo), 1 other word! simple requests (12 mo), phrases/2-step requests (2yr), 3-5
word phrase (3yr), follows adult conversation/adult-like sentences (4-5yr)
• Personal-social: stranger anxiety (6 mo), peek-a-boo (9-12 mo), parallel play (24 mo)
ROS Vision/hearing problems, snoring, mouth breathing, nasal/congested voice, seizures
• Nutrition/diet, dysphagia (cough, choke, nasal regurgitation w/ feeds)
Risk Factors Prematurity, perinatal asphyxia, genetic abnormality, male, FHx, low parental education/SES
Physical
1. General Approach
• Growth measurements: HC (micro/macrocephaly), wt, ht
• Well-being and behavior, alertness, attention span, impulsiveness, attentiveness
• Observe for specific behaviors such as hand-wringing, hyperventilation, aversion of eye contact
• Observation/qualitative analysis of verbal/social interactions (syntax, semantics, vocalization)
2. Inspection
• Dysmorphic features (see Genetic Concerns), signs of abuse/neglect
• HEENT:TM (evidence of recurrent/chronic OM), oropharynx (ankyloglossia, cleft lip/palate, tonsils)
3. Neurologic examination
• CN, strength, muscle tone (hypo/hypertonia), reflexes, coordination, gait and limb movements
Investigations
1. Adjunctive clinical assessments
• 1St line, to r/o sensory abnormality or developmental language impairment
• Audiology, formal developmental assessment or screening test (ASQ or PEDS), broad cognitive assessment
• Previous evaluations (vision, hearing, cognition, emotional), standardized tests for speech/language
• Autism spectrum disorder and other questionnaires for care-giver/teacher
2. Blood work:
• Only indicated if Hx/PE suggest its importance
• Karyotype, Fragile X testing (FMR1 triplet repeat)
• Further testing if clinically indicated (CPK, TSH, metabolic workup, etc)
• Neuroimaging/EEG: if micro/macrocephaly, seizures, loss of psychomotor skills, neurologic signs
• MRI preferable to CT scan except when intracranial calcifications (TORCH, tuberous sclerosis)
Treatment
1. Treatment options: appropriate communication and management plan tailored to pt/family needs, resources
• Plan should address identified problems, create short and long-term outcomes, EARLY INTERVENTION
• Multidisciplinary services: specialized educational support, audiology, speech therapy, amplification devices
• Psychopharmacologic therapies to maladaptive and repetitive behaviors, treat comorbid anxiety, etc.
2. Follow-up
• Regular appointments to monitor progress and growth is essential
3. Referrals
• Developmental Pediatrician, child Psychiatrist, speech-language pathologist (individual/group Rx)
References
1. Zorc JJ, Alpern ER, Brown LW, Loomes KM, Marino BS, Mollen Cl, Raffini U, editors. Schwartz’s clinical handbook of pediatrics. 4
th
Inc.; 2009.
2. Cheung A, Williams BA, Sivarajan By, editors. The HSC handbook of pediatrics. 1 0
th
ed. Elsevier Inc.; 2003.

STRI DOR
2017 Ed. Authors: Chris Gerdung, Gary Galante MD, Melanie Lewis 8N MEdMD FRCPC
OriginalAuthars: Chris Gerdung, Gary Galante MD, Melanie Lewis BN MEdMD FRCPC
Station Objective
intervention is needed.
To recognize different pathologies causing acute and chronic stridor, and when immediate
area’
• Stridor is a harsh, medium pitched, inspiratory sound associated with obstruction of the laryngeal
• Laryngomalacia: #1 cause chronic stridor, infants (1 wk to 3 mo onset), constant/intermittent, worse supine
• Croup: #1 cause of acute stridor, barky cough, hoarse voice, 1-3 day viral prodrome, usually clinical Dx
• Foreign body: Hx often +ve, XR may show radio-opaque foreign body or be unremarkable
y
• Laryngotracheal FB: often severe/acute Sx w/drooling, dysphagia, require removal w/rigid bronchoscop
• Epiglottitis: acutely toxic, high fever, drooling, dysphagia, muffled voice, tripod position
• Bacterial tracheitis: like severe croup, but higher fever, look sick, deteriorate despite Rx for presumed croup
• Anaphylaxis: usually systemic symptoms (urticaria and itching), along with appropriate history
History
ID • Name, age, sex, ethnicity. Get vitals if patient stridorous.
CC • Stridor (coarse high-pitched inspiratory/biphasic sound, secondary to upper airway narrowing)
HPI . Onset: age (e.g. 1st wks suggests congenital, 6mos-3yrs foreign body), progression: sudden onset (FBA,
anaphylaxis), insidious/slow progression (croup), recurrent/chronic (vocal cord dysfunction, compression with
rings, tumors, stenosis, etc.)
• Provoking: sleep (pharyngeal obstruction), exercise/wakefulness (LTB), feeding (reflux/aspiration)
• Quality: describe sound (high pitched, musical, wheeze, inspiratory/expiratory/biphasic)
• Severity: cyanosis, respiratory distress, gasping, ill/toxic, lethargic, altered mental status
. Timing: recent allergic exposures, foreign bodies in mouth/choking episodes, URTI prodrome
• Assoc. Sx: fever, URTI sx (cough, coryza, red eyes), voice change, drooling, dysphagia, nasal regurgitation/cough
with feed, allergic Sx (urticaria, itching, NN, flushing, facial swelling)
RED FLAGS • Drooling, tripod posture, cyanosis
PMHx • Antenatal: prenatal care, U/S, teratogens, HPV/HSV infection, complications, illness
• Perinatal: gestation/complications, APGARs, resuscitation (intubation/ventilation), birth weight, 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 or burns
PSHx • Previous neck, thorax or cardiac surgeries
Allergies • Medication, food, environmental
FHx • Pediatric cancer, allergy, asthma, hereditary angioedema
Social • 2nd hand smoke, home & environmental allergen exposures, sick contacts
Immun • Immunization status (especially H. influenzae type B)
ROS • HEENT: cough, rhinorrhea, pharyngitis, drooling, hoarsness
• RESP: wheeze, cough (productive or dry), SOB
• GI: reflux, regurgitation
• MSK/DERM:hemangiomas
Risk Factors • Intubation, allergies, immune compromised state, craniofacial malformation

Physical
1. General Approach
• If Pt iS unstable!resp failure/severe obstruction —* ABC, call ENT/anesthesia STAT!
• ,T, pt comfort and general appearance/position (eg.tripoding)
Vitals: HR, BP, RR, Sp0
2
• Growth measurements: ht and wt (plotted on growth curve), BMI (FTT)
2. Inspection
• Upper airway patency: audible speech/cough, drooling, gasp, choke, ability to speak full sentences
• RESP distress: nasal flaring, retractions, tracheal tug, accessory muscle use
• RESP failure: cyanosis, obtunded, decreased chest wall movement, bradypnea or extreme tachypnea
• HEENT: surgical scars, neck brusing/edema, hemangioma/neurofibroma, tongue/mandible size/position, refuse to move neck
(RPA), tonsillar hypertrophy, peritonsillar mass/trismus (PTA), blood/secretions visible
3. Percussion
• Lung fields for dullness, asymmetry, respiratory excursion
4. Palpation
• Chest expansion bilaterally, tactile fremitus, SC emphysema, cervical lymphadenopathy, tracheal tenderness
5. Auscultation
• Inspiratory, expiratory or biphasic stridor, audible crackles or wheezes, AE bilaterally
• Listen over mouth/neck for snoring/low-pitched sounds, barky cough
Investigations
1. Blood work
• CBC-D, blood/throat cultures if bacterial source (epiglottitis, retropharyngeal/peritonsillar abscess), VBG
• Do NOT attempt throat exam/throat swab with a tenuous airway
• Inspiratory/expiratory CXR if suspect foreign body (hyperinflation, contralateral mediastinal shift, atelectasis, post-obstructive
pneumonia)
• AP and lateral neck XR (RPA — widened retropharyngeal space, croup —* steeple sign with narrowed upper trachea on AP or
subglottic haziness on lateral, epiglottitis —÷ thumb sign with epiglottic edema)
3. Special Tests
• Culture of tracheal secretions
• Lateral decubitis simulates expiratory film if young/uncooperative
• Intubation if unstable/impending respiratory failure, rigid bronchoscopy/laryngoscopy may be Dx & Rx
Treatment
1. Emergent
• Airway: comfortable position (head tilt-chin lift/jaw thrust), remove visible FB, intubate if resp failure
• Breathing: assist ventilation, high-flow 02, monitor pulse oximetry
• Circulation: monitor HR/rhythm, vascular access as needed (avoid agitation if possible)
• Medical
• Croup: supportive 0 /cool mist, P0 dexamethasone/nebulized pulmicort, nebulized epinephrine
2
• Bacterial tracheitis/epiglottitis/retropharyngeal/peritonsillar abscess: antibiotics IV, support, drain abscess
• Monitor child with laryngomalacia, condition usually improves without intervention
• Surgical
• Tracheotomy or laryngoplasty for severe laryngomalacia, cricothyroidotomy for severe airway compromise
3. Referrals
• PICU, Anesthesia, ENT, Respirology may all be necessary
References
I. Babin et al. How we do it: Management of tracheobronchial foreign bodies in children. Clin Otolaryngol Allied Sci. 2004; 29:750-753.
2. BoatTF, Green TR Chronic or Recurrent Respiratory Symptoms. Kliegman: Nelson Textbook of Pediatrics. Philadelphia. Saunders Elsevier; 2007. Chapter
381.
3. Genie E. Roosevelt. Acute Inflammatory Upper Airway Obstruction (Croup Epiglottitis, Laryngitis, and Bacterial Tracheitis). Kliegman: Nelson Textbook of
Pediatrics. Philadelphia. Saunders Elsevier; 2007. Chapter 382.

EDMONTON MANUAL
Section #7
SURGERY
Section Editor: Jonathan White MB BCh BAO BMedSci(Hons) MSc(MedEd) PhD FRCS(Gen Surg)
Director of Undergraduate Surgical Education
Department of Surgery
INTRODUCTION 303 Gastrointestinal Bleed 338

Abdominal Mass, CRC Screening Guidelines 304 Gynecomastia 340
Abdominal Pain 306 I-land (Pain, Fractures, Dislocations) 342
Anal Pain 308 HeadTrauma 344
Ankle and Foot (Pain, Fractures, Dislocations) 310 Hematemesis 346
Arm and Shoulder (Pain, Fractures, Dislocations) 312 Hematuria 348
Biliary Disease: Cholelithiasis 314 Hernia 350
Bites and Dirty Wounds 316 Hip (Pain, Fractures, Dislocations) 352
Bladder Obstruction and Prostate Cancer 318 Jaundice 354
Breast Lump and Cancer Screening 320 Knee (Pain, Fractures, Dislocations) 356
Bright Red Blood Per Rectum and Melena 322 Neck Mass/Goiter 358
Burns 324 Pediatric Strabismus 360
Constipation 326 Pupil Abnormalities 362
Diplopia 328 Red Eye 364
DizzinessNertigo 330 Scrotal Mass and Scrotal Pain 366
Dysphagia 332 Tinnitus 368
Epistaxis 334 Trauma 370
Erectile Dysfunction 336
302 Edmonton Manual of Common Clinical Scenarios I Surgery

INTRODUCTION
onathan White MB BCh BAD BMed5ci(Hons) MSc(MedEd) PhD FRCS(Gen Surg)
OK, so, you’re about to walk into a Surgery station in the OSCE. What are you likely to encounter and what is the best way to approach the
station? How can you show what you know?
First things first it sounds simple, but the easiest way to ace the OSCE is to figure out what you’re supposed to learn and then learn it.
-
Get your list of learning objectives, take it apart and make sure you’ve covered everything. Make sure you know how to perform the skills
required, and how to handle patients with the various clinical presentations, because these are the things you will need to pass the OSCE.
Second, prepare for the exam. Get the exam blueprint to figure out how many stations of each type there are and how long each is. Think
about what’s likely to be in each station. If it’s a skills station, it could be suturing, or maybe Foley placement, intubation or IV access. If it’s an
X-ray station, think free air or bowel obstruction. If it’s a station with a patient in it, consider those common surgical presentations: abdominal
pain, rectal bleeding, jaundice, breast mass or maybe a neck lump. Don’t forget cold limb or abdominal swelling. It could even be a surgical
counselling station in that case, get ready for the patient to ask you some questions!
-
Third tip try to forget this is an examination, just approach everything like you would in a real clinical setting. “Oh, the station is just another
-
patient with abdominal pain, that’s great, I’ve seen a million of those, and I saw one in Emerg yesterday let’s go!” If you have prepared well
-
for the OSCE, it can be a lot of fun applying what you know!
OK, you’re in the room, what’s next? Here are some more tips:
i.Carefullv read the information you are given and stick to it

Figure out what skill you are supposed to demonstrate, or what part of the body you need to examine. Don’t get distracted.
2. Be organized and have a alan

Figure out the presenting complaint. Get the timeline (how long has this been going on?) If it’s about pain, ask the pain questions. Don’t be
random ask about things that are likely to be associated with the main complaint. Don’t forget to take the previous history: operations,
-
major illnesses, drugs and allergies. Ask about problems with the chest and the heart. Don’t forget diabetes, asthma and epilepsy. Ask about
smoking and drinking. If you forget about these, it may trip you up later.
3. Be prepared to demonstrate what you know

Don’t just talk about it, do it. Time is limited, so don’t waste it by taking 2 minutes to slowly wash your hands in each station. Use a quick
squirt of alcohol and start working. In a skills station, you should be able to describe the set-up for the skill (informed consent, local
anesthesia, etc) while you are getting ready to demonstrate the skill. Add value to your performance by talking about what you are doing
while you are doing it. This will also make it look like you are confident in what you are doing.
4. Know your stuff

You shouldn’t be examining an axilla for the first time in the OSCE. You are being tested on skills you have practiced again and again and
again. Develop an efficient system that works for you and use it. Inspect, palpate, percuss, auscultate. You should know how to demonstrate
all of the physical signs in the textbook even if you don’t use them every day (whispering pectoriloquy, anyone?). Don’t forget the JVP, and
get good at finding it. Expose the abdomen from the xiphisternum to the pubis before you examine it. Don’t forget that the abdomen
contains kidneys too. Check for groin hernias. At the end of your abdominal exam, say you would like to do a DRE (you won’t have to do
it). Treat your simulated patient with respect, just as you would a real patient, and cover them up once you have finished examining them.
Practice, practice practice.
£jntljeatient stations, take notes as you go and once you are finished, take a moment to collect your thoughts
What is the most likely diagnosis? What do you think is going on? What is in your differential? What tests would you order to confirm or refute
your impression? What would you tell the patient? Be logical and precise. Think about how you have seen similar patients managed on the
ward, Imagine you are a physician in practice what would you actually do?
-
&ii,yqjj have to Dresent your findings, get to the point quickly

Practice summarizing the key features of the case using just 2 sentences. “This is an A year old man who presents with a B-day history of
C, associated with D He also reports E, F and G’ Make a diagnosis and keep a few differentials up your sleeve. Be prepared to explain your
reasoning, and have the rest of the history at your fingertips the examiner will ask for it. Be ready for examiner to push you a little: “OK, let’s
-
say that you’re wrong, and it’s not appendicitis what else could it be?”or”OK, so tell me how that operation is done have you seen any?
- -
What are the key steps?”
And that’s it. Do the work to prepare, be logical, precise and professional, keep it simple and show that you know your stuff. Good luck!
Surgery I Edmonton Manual of Common Clinical Scenarios 303

ABDOMINAL MASS, CRC SCREENING GUIDELINES
2011 Ed Authors:AamirBharmal Marta Broniewska MD, Daniel SchillerMD FRCSC
OriginalAuthors:Aamir Bharmal, Marta Broniewska MD, Daniel SchillerMD FRCSC
Station Objective
Provide a systematic approach to abdominal mass, as well as a framework for CRC screening
1. By anatomic region
• RUQ: gallbladder (cholecystitis, Ca), biliary tract (Ca), liver (hepatomegaly, hepatitis, abscess, Ca)
• Epigastric: pancreas (Ca, pseudocyst), abdominal aorta (AAA), stomach (Ca)
• LUQ: spleen (splenomegaly, Ca, abscess), stomach (Ca)
• RLQ/LLQ: intestine (stool, Ca, abscess), ovary (ectopic pregnancy, cyst, Ca), fallopian tube (ectopic pregnancy), abdominal abscess,
appendiceal tumor, diverticular abscess
• Suprapubic: uterus (pregnancy, fibroid), bladder distension, bladder/prostate tumor
• Anatomic: hernias (umbilical, inguinal and epigastric)
• Infectious: EBV (hepatomegaly and splenomegaly)
• Ca, AAA, bowel perforation
History
ID • Age, gender
CC • Abdominal mass, abdominal pain, early satiety, fatigue, jaundice
HPI • Characterize mass: size, location, onset, growth rate, associated pain, pulsatile (AAA), reducible
• Nausea, vomiting, bloating
• 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, weight loss, night sweats
• Blood in stools: characterize color, where/when noticed
• Change in bowel or bladder habit
PMHx • Ca, liver disease, cysts, cardiac events, Crohn’s or ulcerative colitis
PSHx • GI/GU surgeries, other Ca surgeries
PO&GHx • LNMP, ovarian pathology
Allergies • Gluten/wheat (Celiac’s), lactose intolerance
FHx • Ca (especially CRC), cysts, polyps, Crohn’s, ulcerative colitis
Social • Smoking, EtOH, recent travel (hepatic pathology)
ROS • HEENT: sore throat/difficulty swallowing (esophageal or EBV), aphthous ulcers (Crohn’s)
• CV: dependent edema (CHF)
• 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 (Ca), jaundice, shoulder pain (spleen/gallbladder/liver pathology)
Physical
1. General Approach
• Ask permission to perform exam, wash hands, proper draping
• Vital signs
Inspection
• Overall appearance: comfortable vs. distressed, still (peritonitic) vs. moving, cachectic
• HEENT: mucus membranes yellow, sclera icterus (hepatic), oral ulcers (Crohn’s), enlarged tonsils (EBV), lymphadenopathy
(lymphomaNirchow’s node)
• CV: dependent edema, elevated JVP
• GI: abdomen distended, surgical scars, discrete mass visible, caput medusae, ascites, hernias

• MSK/DERM: gynecomastia, petechiae, jaundice, spider nevi (hepatic)
3. Auscultation
• GI: bowel sounds/high pitched peristalsis not related to pain episodes (gastroenteritis, dysentery, active UC)
4. Percussion
• 61: tenderness, dullness, liver size (normal=9-1 1cm at the MCL), Castell’s sign (1 0
th ICS at L anterior-axillary line), Traube’s space
(splenomegaly)
Palpation
• 61: start with light palpation then deep palpation, palpate all 4 quadrants, rigidity, tenderness, palpable masses, reducible vs.
incarcerated hernias, pulsatile mass, liver and spleen
6. Special Tests
• DRE, bimanual examination (ovarian cyst, fibroid)
Investigations
i. Blood work
• CBC+D, BUN, electrolytes, Cr, ALT, AST, TBili, albumin, PT, PT1 ALP, lipase, 13-hCG, urinalysis
• Abdominal/pelvic U/S, AXR, +/- CT scan or ERCP/MRCP if warranted
3. Special Tests
• Gastroscopy (gastric tumor), colonoscopy (CRC, polyp), barium enema (CRC)
4. Further workup
• Thrombocytosis (splenomegaly), amylase/lipase (pancreas), prostate biopsy, CEA (CRC screening baseline)
5. CRC Screening
• If FHx:
• 10 relative diagnosed at <60 y/o OR two 10 relatives - colonoscopy q5 yr starting at age 40
• 10 relative diagnosed at > 60 y/o OR two 2° degree relatives - qi yr FOBT ± q5 yr sigmoidoscopy OR ql 0 yr colonoscopy
starting at age 40
• One 2° or 30 relative - ql yr FOBT ± q5 yr sigmoidoscopy OR ql 0 yr colonoscopy starting at age 50
• HNPCC/FAP - genetic testing
• HNPCC qi -2 yrs colonoscopy starting at age 20
—
• FAP— ql yrsigmoidoscopystartingatagelO
• NoFHx:
• Age < 50 - no screening
• Age> 50 - qi yr FOBT ± q5 yr sigmoidoscopy or ql 0 yr colonoscopy
Treatment
1. Emergent
• Depend on underlying condition
3. Referrals
• General surgery for causes requiring surgical repair
• Urology for prostatic/renal causes
• GI for hepatic/biliary disease
• Obs/gyn for ovarian/uterine causes
References
1. Desch CE, Benson AB 3rd, Somerfield MR, Flynn Pi, Krause C, Loprinzi CL, eta!. Colorectal cancer surrveillance: 2005 update of an American Society of
Clinical Oncology practice guideline. J Clin Oncol. 2005; 23(33): 8512-9.

2. Leddin D, Hunt R, Champion M, Cockeram A, Flook N, Gould M, eta!. Canadian Association of Gastroenterology and the Canadian Digestive Health
Foundation: Guidelines on colon cancer screening. Can J Gastroenterol. 2004; 18(2): 93-9.
Surgery) Edmonton Manual of Common Clinical Scenarios 305

ABDOMINAL PAIN
2011 Ed. Authors:Armin Badre, Sayf Gaza/a MD, Adriana Lazarescu MD FRCPC
Or/gina/Authors: Tamara Kuzma
Station Objective
Approach to patients with acute and chronic abdominal pain including differentiation, diagnosis and effective management plan
• RUQ: biliary disease, pancreatitis, hepatitis, pyelonephritis, subdiaphragmatic abscess, RLL pneumonia, right sided PE, Ml
• LUQ: pancreatitis, splenic enlargement, splenic abscess, splenic infarct, gastritis, gastric ulcer, pyelonephritis, LLL pneumonia,1J
• RLQ:appendicitis, inguinal hernia, nephrolithiasis, IBD, mesenteric adenitis, salpingitis, ovarian torsion, ectopic pregnancy
• LLQ:diverticulitis, inguinal hernia, nephrolithiasis, sigmoid volvulus, IBD, IBS, salpingitis, ectopic pregnancy
• Epigastric: PUD, GERD, gastritis, dyspepsia, pancreatitis, pericarditis, esophagitis, ruptured AAA, Ml
• Periumbilical: early appendicitis, gasteroenteritis, bowel obstruction, peritonitis, ruptured AAA
• D/ffuse: gasteroenteritis, metabolic (DKA, porphyria, lead poisoning), bowel obstruction, IBS, IBD, peritonitis, mesenteric
ischemia
*Bold: conditions with high mortality
History
ID • Age, sex
CC • Abdominal pain
HPI • Onset: sudden (e.g. organ perforation or ischemia, obstruction of small tubular structure [e.g. biliary tract or ureter],
vascular emergencies), gradual (inflammatory or infectious process, obstruction of a larger tubular structure [e.g.
bowel])
• Aggravating and alleviating palliating factors: change with eating, bowel movements, urination, position, deep
breaths, going over bumps
• Quality: burning (ulcer), tearing (aortic dissection), colicky (distention of a hollow tube)
• Radiation/referred pain: shoulder pain (duodenal ulcer, pancreatitis), R subscapular area (gallbladder dz)
• Site: refer to Common Conditions above
• Timing: duration (hours vs. weeks), 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, signs of peritonitis, abdominal distention, blood in stool or urine, anorexia and wt loss,
abdominal mass or organomegaly, fever, jaundice, awakening pain
PMHx • GI/GU conditions, CV risk factors
PSHx • Abdominal surgery, gyne surgery
PO&GHx • LNMP, GPTAL, ? sexually active, method of birth control
Meds • Steroids and immunosuppressants (inhibit inflammatory response to perforation/peritonitis), anticoagulants
(increased risk of bleeding), EtCH (hepatitis, pancreatitis)
FHx • IBD,Gl/GUCa
Social • Smoking and EtCH use
ROS • CV: CV risk factors, CAD, PVD, atrial fibrillation
• RESP: shortness of breath, cough
• GI: constipation, diarrhea, vomiting, mucus or blood in stool, GERD, jaundice, anorexia/wt loss
• GU: hematuria, dysuria, vaginal discharge
Physical
1. General Approach
• Ask permission to perform physical exam, wash hands, proper draping
• Vital signs (T, HR, RR, BP, °2 sat)
2. Inspection
• Appearance (pale, motionless vs. restless)
• ABD: abdominal distention, surgical scars, hernias, obvious masses, Cullen’s sign, Grey Turner’s sign

3. Auscultation
• ABD: presence or absence of bowel sounds, aortic or renal bruits
• CV: heart sounds, murmurs, atrial fibrillation (increases suspicion for mesenteric ischemia)
• RESP: breath sounds, adventitious lung sounds, evidence of consolidation
4• Percussion
• Abdominal tenderness, costovertebral angle tenderness, flank dullness, shifting dullness
5• Palpation
• Peritoneal signs (involuntary guarding, rigidity, rebound tenderness), masses, hernias, pulsative mass (AAA)
6. Special Tests
• DRE
• Testicular exam in men and pelvic exam in women with lower abdominal pain
• Carnett’s sign, Murphy’s sign, Obturator sign, Psoas sign, Rovsing’s sign
Investigations
i. Blood work
• CBC+D, electrolytes, urea, Cr, glucose, 3-HCG (all women of childbearing age)
• Upper or mid abdominal pain: AST, ALT, ALP, bilirubin, lipase
• U/A
• Blood and urine culture (in the presence of fever and unstable vital signs)
• INR, PT1 crossmatch (if OR imminent)
• CXR: it’s 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
• Angiography: mesenteric ischemia
Treatment
1. Emergent
• IV fluids, Foley catheter (monitoring ins/outs), IV antibiotics (perforation or on call to OR)
• All physiological conditions should be treated with appropriate medical and/or surgical approach
• Functional abdominal pain is mainly a diagnosis of exclusion and requires a multidisciplinary approach to treatment
3. Referrals
• General surgery, Vascular surgery, Gynecology, Gastroenterology, Medicine
References
1. Kendall JL, Moreira ME. Evaluation of the adult with abdominal pain in the emergency department. In: Hockberger RS, editor. UpToDate, Waltham, MA;
2009
2. Fishman MB, Aronson MD. Differential diagnosis of abdominal pain in adults. In: Fletcher RH, editor. UpToDate, Waltham, MA: 2009
3. Beers MH, Porter RS, Jones TV, Kaplan JL, Berkwits M, editors. Chronic and Recurrent Abdominal Pain. In: The Merck Manual. 1 8’ ed. Whitehouse Station
(NJ): Merck Research Laboratories; 2006
• Beers MH, Porter RS, Jones TV, Kaplan JL, Berkwits M, editors. Acute Abdominal Pain. In: The Merck Manual. 18 th
ed.
Whitehouse Station (NJ): Merck Research Laboratories; 2006
Surgery j Edmonton Manual of Common Clinical Scenarios 307

ANAL PAIN
201! Ed. Authors:Aamir Sharmal, Marta Broniewska MD, Daniel SchillerMD FRCSC
OriginalAuthors: Aamir Bharmal, Marta Broniewska MD, Daniel SchillerMD FRCSC
Station Objective
Provide a systematic approach to the patient who presents with anal pain or pain on defecation.
1. Organic:
• Infectious: proctitis, anorectal abscess, STI, HIV
• Non-infectious: Crohn’s, anal fissure, hemorrhoid, foreign body, rectal prolapse, CRC, proctalgia fugax, UC
2. Medication induced: radiation therapy, antibiotics, enema use
History
ID • Age, gender
CC • Anal pain
HPI • Characterize pain: onset, precipitating/aggravating factors, quality, radiation, associated symptoms and timeline,
pain with defecation, how long pain lasts after defecation
• Has Pt ever had this problem before?
• Associated rectal bleeding and/or mucoid discharge? If so, characterize episodes
• Recent constipation or diarrhea
• Visible sores on anus present
• Fevers, fluctuant masses, purulent discharge (abscesses)
• Excoriated and itchy skin
RED FLAGS • Constitutional’B’symptoms: fever, weight loss, night sweats
• Change in bowel/bladder habit, incontinence
PMHx • IBD,Ca,STIs
PSHx • GI/GU surgeries
PO&GHx • GTPAL, episiotomy/tearing with delivery
Meds • Antibiotics, radiation therapy, enemas, immunosuppressants
Allergies • Gluten intolerance
FHx • IBD,Ca
Social • 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)
Risk Factors • Prior history of radiation treatment
Physical
1. General Approach
• Ask permission to perform exam; wash hands; proper draping
• Focus PE according to the Hx
2. Inspection
• HEENT: oral ulcers, pharyngitis
• GI/anal: distended, external hemorrhoid, anal fissures, fluctuant masses, purulent discharge, erythematous skin, rectal prolapsed
(reducible/non-reducible)
• GU: genital/anal ulcers/lesions, active discharge being expressed
• DERM: ulcers/lesions
3. Auscultation
• GI: bowel sounds
4. Percussion
• GI: tenderness

5• Palpation
• 61: tenderness (especially in LLQ)
• If pt too tender to permit examination, may need to be examined under anesthesia
• DERM: characterize if lesions raised/painful to palpation/fluctuant mass
6. Special Tests
• Digital rectal exam: check for blood, impacted stool, assess rectal tone, prostatic contour, palpable mass, abnormal amounts of
pain elicited
Investigations
1. Blood work
• CBC+D, BUN, electrolytes
• If abscess not clinically evident -) CT, MRI, trans-rectal U/S
• Colonoscopy
3. Special Tests
• Stool culture and sensitivity, ova and parasites, C duff, toxin, culture from lesions (gonorrhea and chlamydia), VDRL (syphilis)
Treatment
i. Emergent
• Ensure patient is stable
• Rule out emergent (thrombosed external hemorrhoids, Fournier’s gangrene) and high mortality (Ca) cases
• Depend on etiology:
• Functional/fissure: Sitz bath, antispasmodic medication, stool softener, low residue diet
• Infectious enteric: antibiotic; if rare infection consider possibility of patient being immunocompromised
• Ulcerative colitis: steroid enema, suppository
• Abscess: incision, drainage, packing with antibiotics
• STIs
• Gonorrhea: ceftriaxone or doxycycline
• Chlamydia: azithromycin or doxycycline
• Herpes: antiviral
• Surgical: thrombosed external hemorrhoid, Fournier’s gangrene, Ca, fistula, abscess, lateral superficial internal sphincterotomy
(anal fissure refractory to meds)
3. Follow-up
• Dependent on condition
4. Referrals
• Colorectal surgeon if proximal lesion/symptomatology suspected
References
1. Lacy BE, Weiser K. Common anorectal disorders: diagnosis and treatment. Curr Gastroenterol Rep. 2009; 11(5): 413-9.
2. 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 Parameters Committee. Am J Gastroenterol. 2004; 99(7): 1371-85.

ANKLE & FOOT (PAIN, FRACTURES, DISLOCATIONS)
20 I I Ed. Authors: Joifre Munro, Yang Li MD, Darren Nichols MD CCFP(EM)
OriginalAuthors:Joffre Munro, Yang LIMD, Darren Nichols MD CCFP(EM)
Station Objective
To assess and manage a patient presenting with ankle or foot pain caused by acute injury or of insidious onset.
• Traumatic/Acute Injury:
• Ankle: ligament sprain (ant/post. talofibular, calcaneofibular); fibular fracture; tibial avulsion fracture
• Foot: metatarsal or calcaneal stress fractures; fracture of the base of the 5th metatarsal
• Atraumatic/Insidious Onset:
• Ankle: arthritis (gout, rheumatoid, osteo); tendonitis (posterior tibial, peroneal); arterial insufficiency ulcer; osteomyelitis;
Charcot joint; avascular necrosis
• Foot: plantar fasciitis; arthritis (gout, rheumatoid, osteo); Achilles tendonitis; bursitis (pre-Achilles, retrocalcaneal);
neuropathy; arterial insufficiency ulcer; osteomyelitis; tarsal tunnel syndrome; bony heel spur; Morton’s neuroma; cellulitis;
miscellaneous (ingrown nail, bunions, calluses, corns, warts)
• Pathological fracture with underlying etiology md. metastatic lytic lesion, bone tumor, or osteopenia/osteoporosis
• Compartment syndrome (Pain out of proportion, Paraesthesia, Pallor, Pulseless, Poikilothermia)
History
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
• History of redness, swelling, or stiffness
• Changes in sensation, strength, ROM, ability to weight bear
RED FLAGS Fever/chills, night sweats, weight loss, high energy mechanism (look for further injuries)
PMHx • Bleeding disorders, arthritis, heart disease, IBD, diabetes
• Falls: why did they fall (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, analgesic use, anticoagulation meds, antibiotics
Allergies • Specifically to antibiotics and pain medications (NSAID5, acetaminophen, codeine, opioids, etc)
FHx • Arthritis, IBD, Cancer
Social • EtOH use, IV drug use, physical abuse, falls (baseline gait, ambulating aids)
ROS • HEENT: headaches, vertigo, visual disturbances, fever, mental status changes, conjunctivitis
• CV / RESP: palpitations, chest pain, SOB
• GI: change in bowel habits, diarrhea, blood in stool, abdominal pain, cramping, anorexia
• MSK / DERM: rash, psoriasis, sensation and motor function in ankle and foot
Risk Factors • Fractures: osteopenia, osteoporosis, cancer (bone mets or tumors)
Physical Fiii1
1. General Approach I Erythema
Atrophy I
Note: Examine both the ankle and foot together as well as joints above and below area of concern)
• ABCDE, 10 and 20 surveys if necessary, vitals, general appearance of the patient
I I
• Remove clothing/splints/casts/dressings/etc, from site of pain and drape properly
2. Inspection
• MSK: SEADS (comparison to opposite joint), open fracture, laceration, bleeding, observe gait, and alignment
310 Edmonton Manual of Common Clinical Scenarios Surgery

3• Palpation
• MSK: palpate for localized tenderness, deformities, warmth, or joint effusion (include palpation over tibia and fibula); check active
and passive ROM at ankle, foot, and metatarsals; reflexes (ankle jerk, plantar)
• NEURO: sensation and muscle strength supplied by saphenous, peroneal, and tibial peripheral nerves
• VASC: pulses (posterior tibial, dorsalis pedis, popliteal), capillary refill, temperature difference
investigation Ottawa Ankle & Foot Rules

Blood work Ankle Xrays required if pain in malleolar zone + one of:
1.
• CBC-D, electrolytes, glucose, creatinine, urea • Tender along distal 6cm of posterior edge of tibia or tip of medial malleolus
• INR, PT1 Mg, Ca, P04, ESR, CRP (if indicated) • Tender along distal 6cm of posterior edge of fibula or tip of lateral malleolus
Radiology/Imaging • Inability to weight bear for 4 steps both at time of injury and in ED
2.
• Ottawa Ankle & Foot Rules Foot Xrays required if pain in midfoot zone + one of:
• At minimum AP + lateral views Tender at base of 5th metatarsal
• Consider knee and tibia/fibula x-rays Tender at the navicular bone
SpecialTests Inability to weight bear for 4 steps both at time of injury and in ED
3.
• Bone scan (osteomyelitis, bone mets, tumors)
• Arthrocentesis (investigate joint effusion)
Treatment
1. Emergent
• ABCDE, life before limb, once stable tend to injuries that are not life threatening
• Medical
• Reduce fracture/dislocation (ASAP to prevent neurovasc. injury then x-ray and re-check neurovasc. status)
• Irrigation, debridement, and antibiotics (open fracture)
• Manage pain: analgesic medications
• Reduce swelling (RICE): Restricted Activity, Ice, Compression, Elevation
• Immobilization; Ambulation aids and instruction (if required)
• Tetanus prophylaxis if not up to date (open fracture)
• Further workup (may be required for insidious onset etiologies)
• Surgical
• Fixation, manipulation, arthroscopy (if indicated)
3. Follow-up
• Instructions to return if increased swelling, cyanosis, significant increase in pain, decreased sensation
• Possible complications: nonunion, malunion, joint stiffness, AVN, osteomyelitis
4. 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)
References
1. Tintinalli JE et aI.Tintinalli’s Emergency Medicine, A Comprehensive Study Guide. 6th ed. USA:The McGraw-Hill Companies, mc; 2004.
2. Bickley LS et al. Bates’Guide to Physical Examination and HistoryTaking. 10th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2009.
I
Surgery Edmonton Manual of Common Clinical Scenarios 311
ARM & SHOU LDER (PAIN, FRACTURES, DISLOCATIONS)
201 I Ed. Authors:Joffre Munro, Yang Li MD, Darren Nichols MD CCFP(EM)
OriginalAuthars:Joffre Munro, Yang Li MD, Darren Nichols MD CCFP(EM)
Station Objective
To assess and manage a patient presenting with arm or shoulder pain caused by acute injury or of insidious onset.
Differe tial Diagnosis

• Traumatic/Acute Injury:
• Shoulder: rotator cuff tear; acromioclavicular separation; dislocation; fracture (clavicle, scapula, humeral head and neck);
biceps tendon rupture
• Arm: fracture (radial head, midshaft or distal radius/ulna, scaphoid); dislocation (radius, ulna, lunate); sprain
• Atraumatic/Insidious Onset:
• Shoulder: tendonitis (rotator cuff, bicipital, calciflc); subacromial bursitis; adhesive capsulitis; arthritis (rheumatoid, osteo,
septic); PMR; flbromyalgia; thoracic outlet syndrome; brachial plexus neuropathy; referred pain (neck, gallbladder, heart,
diaphragm, Pancoast tumor)
• Arm: epicondylitis (lateral = tennis elbow, medial = golfer’s elbow); olecranon bursitis; arthritis (gout, rheumatoid, osteo,
septic, reactive, psoriatic); tendonitis (distal insertion of biceps); rheumatoid nodule; ulnar nerve entrapment at elbow; carpal
tunnel syndrome; DeQuervain’s tenosynovitis; pronator teres syndrome; triangular flbrocartilage complex injury; dorsal root
ganglion; neuropathy; cellulitis
• Pathological fracture with underlying etiology md. metastatic lytic lesion, bone tumor, or osteopenia/osteoporosis
• Compartment syndrome (Pain out of proportion, Paraesthesia, Pallor, Pulseless, Poikilothermia)
History
CC • Arm (wrist, elbow) or shoulder pain
HPI • OPQRST
• Mechanism of injury (low energy think underlying pathological process)
-
• Previous problems with this site/joint or similar problems with other joints
• History of redness, swelling, stiffness, locking, catching, grinding, crepitus
• Response to activity and rest
• Changes in sensation, strength, ROM
RED FLAGS • Fever/chills, night sweats, weight loss, high energy mechanism (look for further injuries)
PMHx • Bleeding disorders, arthritis, heart disease, IBD
• Previous injuries to the area
• Falls: why did they fall (syncope/presyncope/focal weakness/seizure)
• Osteopenia, osteoporosis, malignancy (pathological fractures)
PSHx • Previous surgeries (specifically to joint in question)
Meds Rx, analgesic use, anticoagulation meds, antibiotics
Allergies • Specifically to antibiotics and pain medications (NSAID5, acetaminophen, codeine, opioids, etc)
FHx • Arthritis, IBD, Cancer
Social • EtOH use, IV drug use, physical abuse, falls (baseline gait, ambulating aids, etc), sexual/STI Hx
• Occupation and handedness
ROS • HEENT: earaches, vertigo, visual disturbances, fever, mental status change, conjunctivitis
L0 • CV/RESP: palpitations, chest pain, SOB
(D • GI: change in bowel habits, diarrhea, blood in stool, abdominal pain, cramping, anorexia
1
• GU: urinary frequency, dysuria
• MSK/DERM: rash, psoriasis, sensation/motor function of arm
Risk Factors • Fractures: osteopenia, osteoporosis, cancer (bone mets or tumors)

physical
1. General Approach (Examine the joints above/below the area of concern. le. shoulder = neck/elbow) Swelling
• ABCDE, 10 and 20 surveys if necessary, vitals, general appearance of the patient Erythema
• Remove clothing/splints/casts/dressings/etc from site of pain and drape properly Atrophy
2. Inspection Deformity
• MSK: SEADS with comparison to opposite joint, open fracture, laceration, bleeding Skin Changes
3• Palpation
• MSK: palpate for localized tenderness, deformities, warmth, joint effusion; check active and passive ROM
• NEURO: know the distribution and sensory/motor function of C5 Ti, radial, median, ulnar, and musculocutaneous nerves;
—
reflexes (C5,C6 = biceps, brachioradialis; C7,C8 = triceps)

• VASC: pulses (brachial, radial), capillary refill, Temp difference Key Points on Shoulder Exam
4. Special Tests Inspection
• Carpal tunnel: Tinel’s sign, Phalen’s sign • Atrophy: supraspinatus/infraspinatus fossas, deltoid
• AC joint: cross-body adduction test, O’Brion’s test • Scapular winging
• Instability (shoulder): sulcus sign, load and shift test, apprehension Palpation
test, relocation test AC joint, clavicle, bicipital tendon, subacromial bursa
• Impingement (rotator cuff tendonitis): Neer and Hawkin’s
impingement signs, impingement test
Investigations Rotator cuff muscles & function (SITS)

Supraspinatus = abduction (Jobe’s test)
1. Blood work Infraspinatus = external rotation
• CBC-D, electrolytes, glucose, creatinine, urea
Teres minor = external rotation
• INR, PT] Mg, Ca, P04, ESR, CRP (if indicated)
Subscapularis = internal rotation (lift off test)
• Plain x-ray of the site including proximal and distal joints
• Often require 3 views (wrist: PA/lateral/oblique; shoulder: AP in neutral, internal + external rotation)
• Ultrasound, Arthrogram/CT arthrogram (for rotator cuff tears), MRI (as indicated)
3. Special Tests
• Bone scan (osteomyelitis, bone mets, tumors)
• EMG, nerve conduction studies (as indicated)
• Arthroscopy
Treatment
1. Emergent
• ABCDE, life before limb, once stable tend to injuries that are no life threatening
• Medical
• Reduce fracture/dislocation (ASAP to prevent neurovasc. injury then x-ray and re-check neurovasc. status)
• Irrigation, debridement, and antibiotics (open fracture)
• Manage pain: analgesic medications
• Reduce swelling (RICE): Restricted Activity, Ice, Compression, Elevation
• Immobilization
• Tetanus prophylaxis if not up to date (open fracture)
• Further workup (may be required for insidious onset etiologies)
• Surgical
• Fixation, manipulation, arthroscopy (if indicated)
3. Follow-up
• Instructions to return if swelling increases, cyanosis, significant increase in pain, decreased sensation
• Possible complications: nonunion, malunion, joint stiffness, osteomyelitis
4. Referrals
• Urgent Orthopedic Surgery (compartment syndrome, neurovascular compromise, irreducible, open fracture, Salter-Harris fracture
grade 3, consider dislocations). Rheumatology, Infectious Diseases, Oncology (if indicated)
References
1. Tintinalli JE et aI.Tintinalli’s Emergency Medicine, A Comprehensive Study Guide. 6th ed. USA: The McGraw-Hill Companies, nc; 2004.
2. Bickley L5 et al. Bates’Guide to Physical Examination and HistoryTaking. lath ed. Philadelphia, PA: Lippincott Williams &Wilkins; 2009.

BILIARY DISEASE: CHOLELITHIASIS
201 I Ed. Authors: Shawna Pandya,Jonathan White MB BCh BAD BMedSci(Hons) MSc(MedEd) PhD FRCS(Gen Surg)
OriginalAuthors:Juliet Emamaullee PhD, MichaeIMcCall MD, AM James Shapiro MD PhD FRCSC FRCS (Eng)
Station Objective
To diagnose and manage common and severe acute biliary conditions.
Biliary colic: intermittent obstruction of the cystic duct by gall stones
• Intermittent RUQ pain/tenderness, worse post-greasy/spicy meals, wakes Pt up, ± Murphy’s sign, cholelithiasis on U/S
• Cholecystitis: gallstone has obstructed the cystic duct —* inflammation of the gall bladder
• Constant epigastric pain migrating to RUQ ± radiating to tip of right scapula, ± progresses post-greasy/spicy meal, RUQ
tenderness, Hx biliary colic, Murphy’s sign, U/S findings
• Biliary colic
• Cholecystitis
• Cholangitis
• Cholangitis: high mortality, emergency
• Gall stones rarely cause mortality
• Gall bladder cancer is rare
istory
ID Age, gender, ethnicity are important (females: more likely to have gallstones)
CC • RUQ or epigastric pain/tenderness
HPI • Hx pain: OPQRST/AAA pain assessment, woken from sleep by pain
• Food: onset post-meal, specific types of food (fatty/greasy/spicy)
• Change in stool, urine color (pale stools, dark urine —* biliary obstruction)
• Fever/chills, NN or diaphoresis, jaundice, itchiness
RED FLAGS • Fever is usually only present in cholangitis -medicaI emergency!
PMHx • Prior bout of biliary colic
PSHx • Abdominal surgeries (cholecystectomy)
FHx • Gallstones, cholecystectomy, IBD
Social • EtOH
ROS • Energy: fever, malaise, lethargy
• Sleep: awoken at night by pain
• HEENT: signs of jaundice
• RESP: tachypnea, distress
• CV:tachycardia
• GI: last meal, last normal bowel movement, NN, diarrhea, pale stools
• GU: darkening of urine
• MSK/Derm: pruritis, jaundice
Risk Factors • Biliary colic more common in the 4”F”s: Female, Fertile, Fat and over Forty
Physical
1. General Approach (introduction, wash hands, vitals, permission)
2. Inspection
• General: discomfort, pain, dehydration, jaundice
• Abdomen: contour of abdomen, masses, scars, stigmata of liver disease
3. Auscultation
• Listen for bowel sounds in 4 quadrants: L./absent in biliary colic/cholecystitis/cholangitis

•
Palpation
• Soft palpation: Start farthest from most painful area —+ most tender. Deep palpation if tolerated
• Murphy’s sign: RUQ pain and inspiratory arrest when RUQ palpated on inspiration
5 Percussion
• Use to detect for rebound tenderness or for presence of ascites (both unlikely w/ cholelithiasis)
6. Special Tests
• DRE to check for masses, bleeding, tenderness, rectal tone
.
Special Associations
• Charcot’s triad: fever, RUQ pain, and jaundice associated with cholangitis
• Reynaud’s pentad: Charcot’s triad + septic shock and mental confusion
Investigations
1. Blood work
• CBC-D: Normal in biliary colic, ± tWBC in cholecystitis, tWBC in cholangitis,
• Cr/urea/electrolytes: renal function/hydration status
• Bili, LFTs/Iiver enzymes: normal in biliary colic; mild Bili, ALP, ttransaminases in cholecystitis, marked t in LFTs in cholangitis
• Abdominal U/S: biliary dilatation, wall thickening, gallstones, pericholecystic fluid
3. SpecialTests
• ERCP for Dx 4Tx intervention, MRCP to image biliary tree, endoscopic U/S, CT abdomen
• Laparoscopic cholecystectomy: elective for biliary colic, necessary for cholecystitis: laparoscopic
Treatment
1. Emergent
• Cholecystitis, cholangitis: ABCs, NPO, IV fluids, analgesia, broad-spectrum antibiotics
• Medical
• Bowel rest, narcotic analgesia, IV hydration/ABx (cholangitis: parenteral), anti-emetics
• Surgical
• Laparoscopic cholecystectomy for symptomatic biliary colic and cholecystitis
• Cholangitis: drainage (ERCP or PTC), IV antibiotics, ICU care if pt is unstable
3. Follow-up
• Watch medically treated biliary pts for recurrence; surgical pts for complications (e.g. infection)
4. Referrals
• General surgery, gasteroenterology
REFERENCES
1. Blumgart, L.H, Ed. Surgery of the Liver, BiliaryTract, and Pancreas. 4
th
Edition. Saunders: Philadelphia, PA, 2006.
2. Gilroy RK, Mukherjee 5, Botha iF. Biliary Colic. E-Medicine. 2009 Dec 11. [cited September 12,2010]. Available from http://emedicine.medscape.com/
article/i 71256-overview.
3. Gladden D, Migala AF, Beverly CS, Wolff J. Cholecystitis. E-Medicine. 2010 May 19. [cited September 16, 20101. Available from: http://emedicine.medscaoe.
cornLarticle/1 71886-overview.
4. Rosh AJ, Manko J, Sally, S. Cholangitis. E-Medicine. 2010 Jun 11. [cited September 16,2010]. Available from http://emedicine.medscaoe.com/
article/774245-followup.

BITES & DIRTY WOUNDS
201 I Ed. Authors: Ho/lie Power, JayZhu MD, James Wo/fli MD FRCSC
Or/gina/Author: Tamara Kuzma
Station Objective
Assess the patient presenting with a bite or dirty wound, look for evidence of infection or joint penetration, and determine which
investigations and treatments are required.
1. Human bites
• Streptococcus spp, Staphylococcus aureus, Elkenella spp, and oral anaerobes
2. Animal bites
• Cat: Pasteurella multocida, Staphylococcus spp, Streptococcus spp and oral anaerobes (Bartonella henselae may cause “cat scratch
disease” 1-2 weeks following bite)
• Dog: S. aureus, S. viridans, P. multocida, and oral anaerobes
History
CC • Bite or cut
HPI • Location, depth of wound
• Mechanism of wound (scratch, laceration, crush, puncture)
• Agent involved (human, dog, cat, insect, snake, foreign object)
RED FLAGS • Symptoms and signs suggesting:
• Septic arthritis (pain with passive range of motion & axial loading of joint, swelling, erythema, warmth over affected
bone or joint)
• Sepsis (tachycardia, tachypnea, fever, chills)
PMHx • Immunization status
• Immunocompromised states (eg. immunosuppression post-transplant, asplenism, DM)
Allergies • Antibiotics, local anesthetics
Risk Factors • Cat bites: more likely to cause abscess due to deep penetration; heavily contaminated (up to 80% infection rate)
• 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)
• Rabies: fatal if untreated; important to know treatment algorithm
• If animal unknown and possible carrier, must observe animal or start rabies prophylaxis
Physica
1. General Approach
• Vitals (BP, HR, RR, T, Sa0
)
2
2. Inspection
• Wound: location, size, obvious contaminants, foreign bodies, surrounding erythema, discharge, exposed vital structures (eg.
tendon, bone)
3. Palpation
• Vascular integrity: palpate peripheral pulses, check capillary refill, skin color and temperature
• Joints: examine ROM, ask about pain associated with active and passive movement
• Motor function: examine strength Kanavel’s Cardinal Signs:
• Sensory function: check sensation in superficial nerve distributions • Fusiform swelling
• Tendons: check integrity of tendons near injury site (especially important in the hand), • Pain on passive extension of the
rule out suppurative flexor tenosynovitis (Kanavel’s signs see box)
—
digit
• Partially flexed posture of the digit
• Tenderness over flexor tendon
sheath

Table 1:Recommendations for tetanus prophylaxis Tetanus-prone wound:
previous doses Clean and minor wound Tetanus-prone wound • >6 hrs since injury, >1cm deep
of adsorbed • Stellate, avulsion or abrasion
tetanus toxin Tetanus toxoid TIGA Tetanus toxoid TIGA
configuration
• Injury mechanism of missile, crush, burn or
<3 or unknown Yes No Yes Yes
frostbite
Only if last dose Only if last dose • Infected, devitalized, denervated or
>3 No No
given 10 yrs ago given 5 yrs ago ischemic tissue
*Tetanus toxoid: 0.5 ml IM A Tetanus immune globulin (TIG): 250 units IM • Presence of dirt, feces, soil, saliva
Investigations
i. 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 antibiotics)
• X-rays of the affected body part to look for retained foreign body (eg. tooth fragment) or fractures
• Bone scan or MRI if osteomyelitis suspected
3. Diagnostic Interventions
• Aspirate of synovial fluid if septic arthritis suspected
Treatment
1. 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 (see Table 1)
• Determine if antibiotics are indicated
• Determine if rabies IG, HBIG, HBV 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)
2. Treatment options for cat, dog, and human bites
• Prophylaxis: amoxicillin-clavulanate 500mg P0 tid or 875mg P0 bid x 3-Sd
• Infection: amoxicillin-clavulanate as above x 7-1 Od
• f3-Iactam allergy: doxcycline 100mg P0 bid (durations as above)
• Longer treatment durations in osteomyelitis (4-6wks) and septic arthritis (3-4wks)
• Severe infections warrant broad spectrum antibiotics (i.e. ertapenem, piperacillin-tazobactam) and consultation with Infectious
Disease specialists
3. 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
4. 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)
References
1. Blondel-Hill E, Fryters S. Bugs & drugs. Edmonton: Capital Health; 2006.
2. Chao JJ, Morrison BA. Infections of the upper limb. In:Thorne CH, editor. Grabb and smith’s plastic surgery. 6tI ed. Philadelphia: Lippincott, Williams &
Wilkins; 2007. p.817-825.
3. Endom E. Initial management of animal and human bites. In: Danzl DF, Wiley iF, editors. Up to Date. Waltham: Up to Date; 2010.

BLADDER OBSTRUCTION & PROSTATE CANCER
2071 Ed. Authors: Todd PenneyMSc, Henry ConterMo, Ryan CooperMDMPHFRCPC
OriginalAuthors: MichoelMetcalfe, Conrad MaciejewskiMD, James Metcalfe MD FRCSC
Station Objective
To determine if a male patient has urinary retention and to classify the type of urinary retention (acute, chronic, complete, partial, etc.); to
demonstrate the ability to screen for and diagnose prostate cancer; to understand how to manage bladder outlet obstruction
PSA 4.0 (very controversial and age dependent ranges have been considered in past) + abnormal DRE combination is a common
positive screen. If PSA and DRE both suggest Ca, a transrectal ultrasound guided biopsy (TRUS) to obtain tissue samples is done
and a diagnosis can be made from the tissue. Since PSA is so controversial, other factors can be used to raise clinical suspicion
about prostate Ca and do a Bx such as: PSA velocity, % free PSA, Fam Hx of prostate Ca
2. Common Conditions: See Table 1
Table 1: Common Causes Of Bladder Obstruction

Child Male adult (bladder abnormality) Male adult (outflow obstruction)
• Posterior Urethral • Neuropathic Bladder: spinal cord injury, spina Prostatic: BPH (most common), Ca, Prostatitis
Valves bifida, MS, tumor, iatrogenic, medication induced Anatomical abnormalities: high bladder neck,
• Stricture urinary retention compression from adjacent organ (rectum)
• Phimosis • Bladder stone, blood clot, fungi or sloughed Urethral stricture/contracture: post instrumentation
papillae of urinary tract

• Prostate cancer; spinal cord compression; acute urinary retention from any cause can lead to renal failure
History
ID • Gender, age, race
CC • Difficulty voiding; sometimes with prostate Ca, patient may be asymptomatic
HPI • Obstructive vs. irritative voiding Sx (seeTable 2); pain/dysuria, hematuria, hemospermia, incontinence. Remember
acronym FUND (irritative) SHIP (obstructive) Sx: Frequency, Urgency, Nocturia, Dysuria, Straining, Hesitancy,
Intermittency, Poor stream
RED FLAGS • Anuria, prostate Ca (bony pain, fever, night sweats, wt SI’); Cauda Equina Syndrome/spinal cord compression (leg
weakness, absent perineal sensation), autonomic dysreflexia (in pts with complete spinal lesion lower than T6 —*
HTN, bradycardia, vasodilation above lesion, vasoconstriction below)
PMHx • HTN, congenital abnormalities of GU tract, neurological dz, prior urologic w/u for BPH, prostatitis, retention,
recurrent UTI5, trauma, stricture
PSHx • Instrumentation to the GU tract
PO&GHx • # of vaginal deliveries, prolapsed pelvic structures
Meds Anticholinergics, antihistamines, antidepressants, antiarrhythmics, anti HTN meds, sympathomimetics, a- blockers,
5-a reductase inhibitors, antibiotics
FHx • Prostate Ca
Social • Diet, EtOH, previous STIs, voiding habits, smoking
ROS • MSK/DERM: signs of spina bifida: dimple/tuft of hair midline on the back
Risk Factors • Advancing age, race (African American/Jamaican > Caucasian > Orientals), Fam Hx of prostate Ca
Physical
1. General Approach
Introduce yourself, wash your hands, check ABCs + add IV and monitors if necessary, ask for permission to do PE, check vital signs
(Note: urinary retention can lead to high BP)

2. Inspection
• Abdominal distension
• Males: check the phallus commenting on blood at the meatus, urinary incontinence, curvature to the penis
• Females: pelvic exam is indicated
3. Percussion
• GU: suprapubic/flank tenderness
4. Palpation
• Palpable bladder, abdominal masses, supraclavicular/inguinal lymphadenopathy, bony metastasis assessment
5. Special tests
• DRE: ensure pt is covered + comfortable (position is important), recommend Pt to be lying on their 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 3600 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 Ca), symmetry and tenderness
• Check for blood on glove after exam
Investigations
1. Blood work
• PSA (note: can be falsely elevated after DRE, after sex/masturbation, during/shortly after bout of prostatitis) and there are often
high false +ves with PSA
• CBC-D, lytes, urea, Cr
• Bladder scan to assess post void residual/bladder capacity; renal and/or abdominal U/S looking for hydronephrosis/bladder
pathology
3. Special Tests
• U/A, urine C & S; uroflowmetry, urodynamics, cystoscopy can be done for complex cases
• TRUS (trans rectal ultrasound guided biopsy) for all men with +ve prostate screen
Treatment
1. 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

• BPH
• Lifestyle: fluid/caffeine/EtOH intake prior to bed to frequency & nocturia
• Medical: 5-a reductase inhibitors (tamsulosin) or 5-dihydrotestosterone inhibitors (finasteride)
• Surgical: symptomatic men failing lifestyle + med mgmt who have chronic/recurrent infections or renal sequelae 2° to
obstruction/hematuria/bladder stones —* TURP
• If not a candidate for surgical intervention —* indwelling catheter or clean intermittent catheterization (careful of UTls)
• Prostate Ca
• Depending on PSA, Bx Gleason grade, clinical stage as determined by DRE and considering the pt’s life expectancy, the Pt
should be counseled by an urologist regarding: watchful waiting, active surveillance, radical prostatectomy, brachytherapy,
external beam radiation therapy or hormonal therapy.
3. Referrals
• Urology, nephrology
References
1 Barry Mi, Fowler FJ Jr.,O’Leary MI’, et al. (1992). The American Urological Association symptom index for benign prostatic hyperplasia. J Urol 148: 1549-57.
2. Reynard J, Brewster S, Biers S. Oxford Handbook of Urology. 2nd Edition. New York: Oxford Universit’ Press Inc.; 2009.
3. Prostate Cancer Screening Group. Use of PSA and the Early Diagnosis of Prostate Cancer. 2009 Toward Optimized Practice. Available from ww
Qaibertadoctors.org/cosa/orostate cancer.html.
4. Carroll P, Albertsen PC, Greene K, Babian RJ, Carter HB, Gann PH et al; Prostate-Specific Antigen Best Practice Statement Update Panel Members. Prostate-
Specific Antigen Best Practice Statement: 2009 Update. American Urological Association Clinical Practice Guideline 2009. Available from: http://www.
iAaflet./content/puidelines-and-puality-care/clinical-guidelines.cfm.
.
Carter HB, Mohamad EA, Partin AW. Diagnosis and Staging of Prostate Cancer. Wein: Campbell-Walsh Urology, 9th ed. Saunders (Elsevier). 2007.
I
BREAST LUMP AND CANCER SCREENING
2011 Ed. Authors: David Lesniak, Tamara Kuzma MD, Gordon Lees MD FRCSC
OriginalAuthors: Saleem Al-Nuaimi, BushrMrad MD, Michael ChatenayMO FRCSC
Station Objective
Identify risk factors for developing breast cancer. Outline a primary prevention strategy. Perform a breast exam.
Distinguishing Features
Differential Onset Age (yrs) Number! Shape! Mobility Consistency! Tenderness Retract
Cysts Majority >35/ Pen- Single or multiple/round! Soft or firm, elastic /usually tender Absent
menopausal mobile
Fibroadenoma Most common benign
Usually single/round/very
mass <30/uncommon . Usually firm, rubbery/non-tender Absent
mobile
>45
BREAST CA . Usually single/irregular Very hard, skin changes present/ Maybe
Incidence increases> 50 Usually non-tender present
shape/may be fixed
Fibrocystic Common 40-50/ Usually firm, non elastic/usually very
Nodular, ropelike/ mobile
.
Absent
ilanges
CI-
.
fluctuates with menses tender (pain common)

Infections Erythema, swelling, pain, tenderness, must r/o inflammatory breast Ca (mammography, breast U/S, Bx of 2-3 areas,
including_skin)! Note:_—50% of inflammatory breast Ca_is_undetected_on_imaging
Table adapted from
1
2. High Mortality / Morbidity: BREAST CA
History
ID Age (fibroadenoma —* mostly women < 30y/o, breast Ca —* mostly women >50 y/o), gender (incidence 10:1
female to male)
CC Palpable breast mass, nipple discharge (nipple or skin changes, mastalgia) —* uncommon with cancer, except
nipple- Paget’s dz
HPI Onset (when and how did you notice it)
• Change in size (fluctuates with menses —+ usually benign cystic changes)
• Nipple discharge (bloody <10% Ca, majority -Ibenign intraductal papilloma), unilateral vs. bilateral,
spontaneous vs. induced, frequency & duration
• Presence of pain or skin changes
RED FLAGS Bony pain, anorexia, wt, dyspnea, CP, hemoptysis, signs of metastasis
PMHx Previous mammograms
• Breast Ca, benign breast dz, prior Ca radiation to breast or axilla, preivous breast Bx (atypical hyperplasia, DCIS,
LCIS), ovarian! endometrial Ca
PSHx Cyst drainage, lumpectomy, mastectomy, hysterectomy ± oopherectomy
PO&GHx • LMP/LNMP, normal menstrual cycle, menstrual irregularities
• Time of menarche (early < 1 2y/o) & age of menopause (late > 55y/o)
• Nullipanity or 1’ pregnancy> 30y/o (breast feeding hx)
• OCP, HRT (estrogen ± progesterone) (aggravates breast cancer, doesn’t casue breast cancer)
• Cancer during pregnacy is very bad
Meds Rx, OTC, CAM
FHx 1 degree relative with breast or ovarian Ca (age of onset, details of Ca type)
Social Smoking, EtOH, sedentary lifestyle, high fat diet, SBE (?)
ROS CV:CP
• RESP: dyspnea, hemoptysis
• Gl: wt, change in bowel habit, abdominal distension, BRBPR, melena
• GU: pap smears
• MSK / DERM: bony pains
Risk Factors FHx, BRCA gene mutation, personal Hx of breast Ca, older age, female gender, significant radiation to the chest,
late menopause (>55), early menarche (<12), late first gestation (>30), nulliparous, postmenopausal HRT/OCP
(estrogen only), moderate alcohol intake (> 2-3 drinks/day), smoking, sedentary
320 Edmonton Manual of Common Ciinicai Scenarios I Surgery

Physical
General Approach
• Effective clinical breast exam depends upon thorough examination of both breasts and all regional lymph nodes
• Gown Pt and expose waist, presence of chaperone is recommended, provide feedback to comfort Pt
2. Inspection
Pt sitting —* bilaterally inspect breast, areola, nipple and 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, inverstion, excoriation (Paget’s)), and
variation in symmetry and contour
3. Palpation
• Pt sitting —* lymph nodes: axillary (5 groups), supraclavicular, infraclavicular and cervical
• Pt supine, arms behind head-bilaterally palpate breast areola, nipple and axillae
• Note: location/size/shape/consistency/tenderness/mobility
Investigations
• Bilateral diagnostic mammography
• Breast U/S (useful for identifying benign cysts/ monitor and guide core Bx)
• MRI for “difficult to characterize” lesions
2. Special Tests
• BRCA1 and BRCA2 genetic testing (FHx, male breast Ca, known gene mutation)
• HER-2 and hormone receptor testing if mass is Ca
3.SLirgical/Diagnostic Interventions
Test Indication Information
• If fluid is non-bloody and lump completely disappears —* consistent with benign
FNA cystic dz (discard fluid)
All lesions likely to be cysts
(not diagnostic) • If bloody, or if lump remains/ solid lump -send fluid for cytology and re-aspirate the
residual_lump
Clinically suspicious lesion —÷ not
Core Bx (diagnostic) Distinguish in-situ from invasive lesions
cyst by U/S or FNA
Treatmen
• Radiation, chemotherapy, or combined modalities
M e dica
• Hormone and biological therapy (for sensitive Ca)
• Modified radical mastectomy (>5cm, multiple nodes +ve, contraindication to radiation) (possible skin sparing: immediate reconstruction)
Surgical • Lumpectomy with radiation (in women with small breasts, a lumpectomy can sometimesbe more disfiguring than a masectomy)
• Sentinel lymph node Bx followed by axillary node dissection if sentinel node is +ve (axillary node dissection only if nodes are clinically +ve)
2. Follow-up! Referrals
• Immediate follow-up if any change in size, consistence or appearance
• Clinical breast exam; 4-6 wks if cystic
• Referral to general surgeon/surgical oncologist
Screening
Screening Modality Age (yr) Recommendation (for women)
Clinical Breast Exam >40 Every two years (complimentary to mammographic screening)
<40 Routine screening not recommended

40-49 Assess risks and benefits on case by case basis
Screening recommended every two years
Mammography 50-69
>70 Continue screening considering co-morbidities and life expectancy
Screening mammograms every year starting age 40, or 5-10 yrs prior to the age of onset in 1” degree
Stron g FHx
relative
Breast self-exam Not generally recommended
Breast MRI and u,s Generally non-effective screening tools
References
1. Bickley L, editor. Bates’guide to physical examination and history taking. 10th ed. Philadelphia: Lippincott Williams & Wilkins; 2009.
2. Alberta Medical Association Towards Optimized Practice [Internet]. c2009 [updated 2007 Mar; cited 2009 Oct 30]. Early detection of breast cancer.
Available from: http://www.topalbertadoctors.org/cpgs/breast_cancer.html
3. Pruthi S. Detection and evaluation of a palpable breast mass. Mayo Clin Proc. 2001 Jun 76(6);641-648. PMID: 11393504
4. Screening for breast cancer: U.S. Preventive Services Task Force recommendation statement. Ann Intern Med. Nov 17 2009;1 51(1 0):71 6-726, W-236.
Surgery j Edmonton Manual of Common Clinical Scenarios 321

BRIGHT RED BLOOD PER RECTUM & MELENA
201 I Ed. Authors:Aamir Bharmal, Marta Broniewska MD, Daniel SchillerMD FRCSC
OriginalAuthors:Aamir Sharmal, Marta Broniewska MD, Daniel SchillerMD FRCSC
Station Objective
Determine if bleeding is from an upper GI or lower GI source and provide a systematic approach to bleeding based on that distinction. Rule
out malignant causes for a lower GI bleed.
Upper GI (bleeding proximal to ligament of Treitz)
• Esophageal: epistaxis, esophageal varices, Mallory-Weiss tear, esophageal Ca, esophagitis
• Gastric: gastric ulcer, gastritis, gastic Ca, Dieulafoy lesion (abnormal gastric submucosal vessel)
• Dueodenal/small bowel: ulcer, vascular malformation, aorto-enteric flstula (especially if previous aneurysm repair), iatrogenic
post-procedure bleed (after ERCP and papillotomy)
• Biliary: hemobilia (bleeding from liver/biliary tree)
• Coagulopathy: liver diseae, medication-induced, renal disease, bone marrow disord
Lower GI (bleeding distal to ligament of Treitz)
• Inflammatory: colitis, infectious, diverticulitis
• Neoplastic: polyp, CRC
• Vascular: angiodysplasia, hemorrhoids
• Other: Meckel’s diverticulum, ischemia
• latrogenic: post-polypectomy
• Anal fissure
• Upper GI: esophageal varices, Mallory-Weiss tear, gastric ulcer, duodenal ulcer
• Lower GI: diverticulosis/diverticulitis, hemorrhoids, Ca, polyps, angiodysplasia
• Esophageal varices, aorto-enteric fistula, Ca
History
ID • Age, gender
CC • ‘Blood in stools change in stool color, fatigue, change in stool caliber
HPI • Characterize bleeding: onset, duration, severity, where observed (on wiping, mixed in stools, coating stool, toilet
bowl), color/consistency of stools (black and tarry = melena, more indicative of UGIB), with every bowel movement
or episodic
• Constipation
• Abdominal pain or mass
• Vomiting (especially hematemesis, UGIB) and/or fevers
RED FLAGS • Constitutional ‘B’ symptoms: fever, weight loss, night sweats, decrease in appetite
• Change in bowel habit or tenesmus (feeling of incomplete emptying or spasms)
PMHx • CVD, DM, Ca, liver dz, Hx of past GI bleeding, hemorrhoids, fissures, bleeding disorders
PSHx • GI surgeries, previous colonoscopies or gastroscopies
PO&GHx • LNMP
Meds • Anticoagulant therapy, NSAIDs, Tylenol, steroids; iron and bismuth (may darken stool, but no bleed present)
V., FHx • Gl dz: especially polyps, Ca (especially CRC), bleeding disorders, UC
C
- Social • EtOH, sick contacts/recent travel (infectious)
LD
tD ROS • HEENT: vertigo, lightheadedness/dizziness (anemia)
‘<
• RESP: SOB(OE)
• GU: hematuria/dysuria, menorrhagia
• MSK / DERM: bruising
Risk Factors • Chronic NSAID use, chronic EtOH, IBD, hepatic disease, ulcers, CRC (personal/FHx)

Physical
1. General Approach
• Focus exam according to Hx
2. Inspection
• DERM: petechiae, bruising, pallor, stigmata of hepatic disease, pyoderma gangrenosum (IBD), uveitis (IBD)
• HEENT: sclera pallor, sclera icterus (hepatic disease)
• ABD: distended, surgical scars, masses, ascites (bulging flanks)
3. Auscultation
• ABD: bowel sounds
4. Percussion
• ABD: percuss for dullness/shifting dullness (tumor/ascites),Traube’s space, hepatomegaly
5. Palpation
• ABD: hepatosplenomegaly, palpable mass, rigidity/guarding (peritonitis), tenderness
6. SpecialTests
• DRE: feel for rectal mass, stool in rectum, prostate/cervix, blood on glove, uncomfortable NOT painful
Investigations
1. Blood work
• CBC-D, urea, electrolytes, Cr, AST, ALT, PTT, PT/INR, type & screen, blood gases
• NG aspirate to rule out UGIB
• Endoscopy (flexible sigmoidoscopy/colonoscopy) or gastroscopy (for upper GI bleed)
• Bleeding/esophageal varices endoscopic banding; bleeding ulcers epinephrine, clipping/coagulating vessel
— —
Treatment
1. Emergent
• ABC’s, ensure airway stable (especially UGIB)
• Pt stabilization (2 large bore IV’s, IV fluids, cross and type, monitoring)
• Determine if bleeding is from an upper GI or lower GI source (if unsure, differentiate via NG aspirate)
• Rule out esophageal varices
• If non-variceal upper Gl - keep NPO, give a high dose of PPI (bolus 40mg IV than run infusion at 8mg/hr), monitor Hgb for
hemodynamic instability, gastroscopy for source of bleeding with possible cautery/clipping
• For variceal bleed - give 50 Jg octreotride IV followed by drip of 5Opg/hr IV, gastroscopy for banding/sclerosis
• 80% of upper GI bleeds remit spontaneously/with supportive therapy
3. Further workup
• If lower GI bleed - sigmoidoscopy to determine source of bleed
• If continued bleeding at <0.5mL/h -* radionuclide-labelled red cell scan
• If continued bleeding at >0.5mL’h -* angiogram
• If bleeding stops colonic lavage followed by colonoscopy, CRC work up
-
4. Surgical depends on bleeding source

—
References
1. Barnert J, Messmann H. Mangement of lower gastrointestinal tract bleeding. Best Pract Res Clin Gastroenterol. 2008; 22(2): 295-312.
2. Lame L, Peterson WL Bleeding peptic ulcer. N EngI J Med. 1994; 331(11): 717-27.
3. Zuckerman GR, Prakash C. Acute lower intestinal bleeding. Part II: etiology, therapy, and outcomes. Gastrointest Endosc. 1999; 49(2):228-38.

BURNS
2011 Ed Authors: Hollie Power, JayZhu MD, James Wolfli MD FRCSC
OriginalAuthors: Cara Boblitz, Jay Zhu MD
Station Objective
Identify the mechanism of the burn, assess the extent and depth of the burn and outline the initial
management
Types of Burns: Estimated size of the burn (%TBSA):
• Chemical: acid, alkali • Adults (rule of 9’s): Arm (9%), Leg (18%), Head (9%), Anterior
• Electrical: low/high voltage, trunk (18%), Posterior trunk (18%), Genitalia (1%)
lightning • Pediatrics (<9yrs): different body proportions depending on
• Thermal: flame, contact, age
scald *Only count 2° and 3° burns, 10 burns do not count toward the
• Radiation: medical, TBSA
therapeutic, UV
Table 1: Classification of Burns

Depth Appearance Blanches Blisters Damage Surface Sensation Healing/Treatment
Superficial (1°) Pink, red Yes No Epidermis Dry Painful 3-5 days
Superficial Epidermis, papillary Very
partial thickness Pink, red Yes Yes Moist 7-1 4d
dermis Painful
(2°)
>21 d, t incidence of
Epidermis, hypertrophic scar, excision
Deep partial Yes entire dermis & Moist None
Red or white No & grafting gives best
thickness (2°) appendages aesthetic result
White/ Epidermis, dermis,
Full thickness No ± underlying Dry, leathery None Early excision and grafting
brown, No
(3°) structures
charred
History
ID • 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 (i.e. explosion, fall)
• Treatment received from time of incident to presentation
RED FLAGS • Indications for transfer to a burn centre:
• 2° and 3° burns to >20% total body surface area (TBSA)
• 2° and 3° burns >1 0%TBSA burns if <1 Oyrs or >5oyrs
• 3° burns to >5% TBSA
• 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
PMHx • AMPLE trauma history (allergies, meds, PMHx, last meal, events)
Immunizations • Tetanus

Social • Occupation, place of residence, social support network
EtOH, smoking, illicit drugs
Physical
i. Primary survey (ABCDE), secondary survey
2. General Approach: remove clothing and jewelry as needed; initial dressing with saran wrap appropriate (protects wound but allows for
examination by burn team)
• Classify burn depth (see table 1) and fill out burn diagram
• Estimate size of burn: rule of 9’s or use area of patient’s palm as -1%TBSA Compartment Syndrome
• Inspection: obvious deformity, singed hairs, pharyngeal swelling, tongue edema Pain (out of proportion)
• Listen for stridor, hoarseness Paraesthesia
3. Consult burn surgeon for potential transfer if any red flags present Pallor
4. CV: rhythm (electrical burns may cause arrhythmias) Paralysis
5. Resp: carbonaceous (black) sputum, air entry Pulselessness
6. GI: bowel sounds, abdominal distension
7. GU: accurate urine output, color of urine (dark brown consider myoglobinuria)
—
8. Extremities: rule out compartment syndrome for electrical injuries (see box). Assess need for escharotomies
Investigations
1. Laboratory investigations:
• CBC-D, electrolytes, urea, Cr, CK, Ca
2
• ABG: pH and COHb (>10% suggests inhalation injury)
2. CXR,ECG
3. Bronchoscopy (if you suspect inhalation injury)
4. Compartment pressure (if you suspect compartment syndrome)
Indications for Early Intubation:
• Deep facial/neck burns
Treatment • GCS<8
1. Primary Survey: ABCDE • Inhalation injury
Airway: intubation if significant inhalation injury • Oxygenation /ventilation
Breathing: provide humidified 02 via face mask <40,
compromise (Pa0
2
Circulation: >50, RR>40)
2
PCO
• Obtain vascular access
• Fluid resuscitation is required for adults with burns to >10% TBSA
• Resuscitate with RL using Parkiand formula (4m1 x weight (kg) x %TBSA); with half given over the first 8 hrs, and the remaining
half given over the following 16 hrs
• Titrate fluid infusion to u/o (0.5m1/kg/hr in adults; 1 mI/kg/hr in children) and BP (MAP>70)
• 3 zones of injury: necrosis (not viable), stasis (viable with aggressive resuscitation), inflammation (viable)
• Escharotomy for circumferential full thickness burns
Disability: assess neurologic status (GCS), orientation to person, place, time
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
2. Secondary Survey
• CVS: electrical injuries require continuous cardiac monitoring at least 6 hrs post-injury
• GI: high protein, high calorie nutrition (via NG tube if necessary), watch for abdominal compartment with massive fluid resus
• GU: accurate u/o via Foley catheter (if rhabdomyolysis u/o goal to 1 5Occ/hr, consider adding NaHCO
)
3
• ID: swab wounds, start antibiotics only if evidence of infection (no role for prophylactic antibiotics)
• MSK: monitor for compartment syndrome
• Resp: if CO poisoning, provide 100% 02 and nebulized bronchodilators
3. Wound Care
• Small burns: polysporin + adaptic usually sufficient
• If TBSA >20%: topical antimicrobial dressings (eg. silver nitrate, Acticoat, Sulfamylon)
• Superficial burns will heal with daily dressing changes
• Deep burns will require debridement and skin grafts
Chemical burns require copious irrigation
References
Janis JE. Essentials of plastic surgery. St. Louis: Quality Medical Publishing; 2007.
2. Kao CC, Garner WL. Acute burns. Plastic and Reconstructive Surgery. 2000; 105:2482-2493.
3. Sood R, Achauer BM. Achauer and Sood’s burn surgery: reconstruction and rehabilitation. Philadelphia: Elsevier; 2006.

CONSTIPATION
201 I Ed. Authors:Aamir Bharmal, Marta Broniewska MD, Daniel SchillerMD FRCSC
OriginalAuthors:Aamir Bharmal, Marta Broniewska MD, Daniel SchillerMD FRCSC
Station Objective
1. To determine if constipation is the result of a functional or organic cause
2. To differentiate between constipation and obstipation (no flatus and no bowel movement)
• Passage of infrequent or hard stools with straining (stool water <5OmL/day)
• Bowel frequency <3x/week
• In absence of secondary causes, is functional and due to lack of liber/change in diet
• Obstipation = no flatus AND no bowel movement
• Medications, hypothyroidism, diabetes mellitus, electrolyte abnormalities
• Electrolyte abnormalities, neoplasm, intestinal obstruction
History
ID • Age, gender
CC • Constipation, pain with defecation
HPI • Characterize: onset, palliating/aggravating factors, associated symptoms, timeline; frequency of bowel movement
(concerning if <3x/week)
. Bleeding with bowel movements; if so, where/when noticed (toilet paper, toilet bowl, coated on stool?), characterize
bleeding (dark/tarry [upper GI] vs. bright red [lower GIl)
• Diet: recent changes, dietary fibre intake
• Pain: relieved by defecation, hard stools, straining, manual maneuvers used, hemorrhoids
• Overflow diarrhea
• Sense of incomplete emptying (tenesmus), difficulty emptying bladder (weak stream, nocturia)
• Abdominal pain/bloating, nausea and/or vomiting
RED FLAGS • Sudden change in bowel habit especially with bleeding, change in stool shape/caliber
PMHx • Neuro: Parkinson disease, MS, intestinal pseudo-obstruction
• Metabolic: Diabetes, hypothyroidism, electrolyte abnormalities
. Collagen/vascular disease: scleroderma, amyloid
• Neoplastic: CRC, anal cancer, prostate cancer/BPH
• Anatomic abnormality: prolapse, rectocele
• GI: IBS, diverticular disease, Hirschsprung’s disease
• Psychiatric: depression
PSHx • Recent surgeries (GI and others)
PO&GHx • Current pregnancy
Meds • Opioids, antidepressants, anticonvulsants, iron supplements
FHx • Malignancy(especiallyCRC),diabetes
ROS • HEENT: vision changes (DM, MS)
• CV: palpitations/bradycardia (hypothyroid)
• General: constitutional symptoms
Physical
1. General Approach
• Vital signs
• Focus physical exam to history
2. Inspection
• GI: abdominal distension, visible masses, assess prolapse

3 Percussion
• GI: abdominal tenderness, tympany (may indicate bloating)
•
Palpation
• GI: masses, hernias
5 AuscultatiOn
• GI: bowel sounds
6. specialTests
• DRE: assess for hemorrhoids, fissures, obstructing rectal mass, rectal prolapse, prostatic contours
• Pelvic exam: focus on posterior vaginal wall for internal prolapse or rectocele
nvestigatiOflS
1. Blood work
• , Cr,TSH, +1- FOBT
CBC+D, electrolytes, glucose, Ca
2
• AXR—3 views
• Possible air contrast barium enema (if chronic constipation in setting of any obstruction)
• Possible abdominal CT scan (if intra-abdominal process suspected)
3. SpecialTests
• Colonoscopy, colonic transit studies, defecography, motility studies
• Dependent on underlying etiology
Treatment
1. Emergent
• IV fluids (if dehydrated)
• If obstruction suspected, NPO with bowel rest/NG tube to decompress stomach
• If obstruction ruled out, consider enema or suppository
• Medical
• Medication —induced stop offending agent and observe if any change
—
• Functional bulk-forming laxative or osmotic agent (Lactulose)

—
• Secondary to general medical condition treat underlying condition

—
• Surgical
• Correction of volvulus, obstruction
3. Referrals
• General surgery if malignancy or surgical intervention required
References
1. Lennard-Jones JE. Clinical management of constipation. Pharmacology. 1993; 47 Suppl 1:216-23.
2. Stark ME. Challenging problems presenting as consipation. Am J Gastroenterol. 1999; 94(3):567-74.

DIPLOPIA
2011 Edition Authors:ScottMcLeod, FrancoisiacobMD, 0.8. S1ncIa1rMDFRCPC
Nawaaz Nathoo, Chris Hanson MD, Christopheri Rudnisky MD MPH FRCSC
Station Objective
Determine whether the patient’s double vision is monocular or binocular. Understand the muscles that move the eye in each direction
and the nerves that supply them, and determine in which direction of gaze the diplopia is worst, thereby suggesting a root cause of the
pathology. Differentiate muscle fatigue, paralysis, entrapment, and inflammation.
• Monocular diplopia:
• Refractive error, keratoconus, cataract, decompensated congenital eso/exo-tropia, functional, dislocated lens
• Binocular diplopia:
• Oculomotor nerves (CN 3/4/6): ischemia, DM, aneurysm, hemorrhage, trauma, tumour
• Neuromuscular junction (myasthenia gravis)
• EOM restriction/entrapment: thyroid related, inflammation/infection, tumour, orbital fracture
• Strabismus
• Aneurysm in Circle of Willis —* CN palsy, unilateral pupil dilation (typically aneurysm of PCom)
• Pupil constriction fibres run on top of 3 rd
CN —* compressive lesion (aneurysm or neoplasm) will involve the pupil, whereas
rd
3 pupil unaffected
ischemia of the CN leaves the
• Association of CN6 and CN7 —* lower pontine lesion
History
ID • Age
CC • Double vision
HPI • Gradual vs. sudden onset
• Monocular (diplopic with only one eye open) vs binocular (diplopia resolves if one eye closed)
• When does the Pt notice it most: certain directions of gaze vs. head tilted to one side
• Constant or intermittent
• Pain: headaches, temple, eyebrows, scalp tenderness
• Focal neurological symptoms
• Control: is Pt able to fuse images for a set amount of time, make image single with a certain posture or head tilt
RED FLAGS • Sudden onset is suggestive of ischemia/infarct and involvement of multiple CNs suggests tICP, gradually worsening
could suggest tumor or inflammation
• Pupillary involvement of any degree suggests a compressive lesion (rather than nerve ischemia)
• Any other neurological symptoms
• Proptosis (rule out a cavernous sinus fistula or thrombosis)
• Pain, headache, scalp tenderness, weight 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, #‘s
PSHx • Any ocular surgery, especially past strabismus surgery
Li, FHx • Family ocular history, autoimmune conditions, thyroid disease, DM, CVA, Ml, aneurysms, polycystic kidney disease
C Social • Smoking
-
ROS • HEENT: any other CN symptoms
tb
-‘ • CV: risk factors for CAD
• RESP: SOB
• GI: difficulty swallowing
• MSK / DERM: mm weakness, fatigue

physical
1. General Approach
• Visual acuity, pupillary reactivity (light/dark) to look for anisocoria and RAPD, visual fields by confrontation
• Determine whether diplopia is present in one eye or both: cover one eye at a time and see if diplopia resolves (binocular diplopia
is only present with both eyes open)
• Determine whether diplopia is worse in certain gaze positions: ask patient to look through all cardinal positions of gaze and
determine if diplopia is better/worse in any direction, check for diplopia on Rand L head tilts
• Check EOM’s: observe for limitation of movements, comparing movement of L vs. R to determine if there is asymmetry (see figure
1)
• Assess which CN are involved (LR-CN6, SO-CN4, All the Rest- CN3)
2. lnspection• . Figure 1: Table of EOM and which muscles are being isolated
• Ptosis: measure interpalpebral fissure height with
patient looking comfortably in the distance
• Exophthalmos, enophthalmos
SR 10 SR
3. Palpation
• Temporal arteritis: palpable, beady temporal artery,
temporal pain, scalp tenderness, TMJ pain
4. SpecialTests U?.
• Determine if eye (or other muscles fatigue) with
L.R
repeated use, suggesting myasthenia gravis or have
patient gaze upwards for 60 sec looking for signs of
fatigability w so
• Screening thyroid exam including lid lag
Investigations
1. Blood work
• Thyroid testing if signs/symptoms of thyroid disease
• Acetylcholine receptor antibody if considering myasthenia gravis
• Glucose and Hgb A1C
2. 2. Radiology/Imaging
• Older pts 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 mo should be further evaluated with CT/MRI)
• All other pts —* CT/MRI for orbital, CN, or other neurological abnormalities
• Clinical picture worrisome for infection, aneurysm, or acute CVA (< 3 h) —* urgent imaging, angiography
3. Special Tests
• Tensilon test (for myasthenia gravis): tensilon (edrophonium, an acetyicholinesterase 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
Treatment
1. Emergent
• lschemia/infarct should be emergently treated with a full stroke work-up, control of appropriate risk factors
• Aneurysms, bleeds, and tumors should be emergently referred to neurosurgery for surgical consult
• Varies depending on underlying causative factor of the diplopia
3. Referrals
• Monocular diplopia —* Ophthalmology
• Myasthenia gravis, or any patient with suspected ischemia/infarct —+ Neurology
• Binocular diplopia due to any other cause — Ophthalmology
• Fracutures/tumors/thyroid eye disease —* Ophthalmology
NB: be sure to inform Pt’s that driving is not permitted until the diplopia resolves
References
1. Bradford C. (2005). Basic Ophthalmology. San Francisco: American Academy of Ophthalmology.

DIZZINESS/VERTIGO
20! I Ed. Authors: Scott McLeod, Francois Jacob MD, 0.8. SinclarMO FRCPC
HNS)
OriginalAuthors:Abdullah Saleh, Peter DziegielewskiMo. Hamdy El-Hakim MD FRCS(Ed) FRCS(QRL-
Station Objective
or strokes. To differentiate between central and
To develop an approach to distinguish true vertigo from dizziness, pre-syncope, seizures
peripheral vertigo using approach to investigate and manage these conditions.
Dizziness is described in many different ways:
maintaining posture
• Presyncope = an impending sense of LOC, lightheaded, sweating, panic, anxious, difficulty
or arising, not present lying or sitting
• Disequilibrium= a sensation of imbalance when standing, walking,
difficult to describe, localize, underlying psychiatric disease likely
• Psychogenic dizziness=constant complaints,
perception of self or an unpleasant distortion of orientation that is the result of a mismatch between
• Vertigo= an erroneous
(described as dizziness, spinning, lightheaded,
the 3 sensory systems: the vestibular, visual and somatosensory systems
unsteady)
• True vertigo
Meniere’s disease
• Peripheral : benign paroxysmal positional vertigo (BPPV), labrynthitis, vestibular neuronitis,
with severe nausea & vomiting, and commonly has auditory symptoms
• Peripheral vertigo tends to present
cerebrovascu lar disorders, migrainous vertigo, multiple sclerosis, tumours, acoustic neuroma
• Central:
• Central vertigo tends to present with severe problems with balance, neurological symptoms
• Non-vertiginous dizziness
aortic stenosis, vasovagal
• Organic or physiologic causes (loss of global brain perfusion-presyncope): cardiac arrhythmias,
, medication side effects, caffeine,
response, orthostatic hypotension, hyperventilation, metabolic causes (hypotension
nicotine)
• Functional causes (psychogenic): depression, anxiety, panic disorders, phobic dizziness
3. High Mortality/Morbidity
• Cerebrovascular accident, aortic stenosis, arrhythmias, high ICP
History
ID • Age, gender
CC • “Dizziness,””Spinning7”Lightheaded7”Unsteadiness”
HPI • Onset, palliative when sitting, severity, timing, direction of spinning
permanent
• Associated otologic symptoms: tinnitus/aural fullness/hearing loss, occur with vertigo episode or
• Associated neurological symptoms: dysarthria/dy sphagia, LOC, headaches, ataxia, falls
• Recent URTI, OM, trauma, NN
• Travel, sick contacts, rashes, tick bites
• Pre-syncope, palpitations, SOB
• Changes in vision, hearing eyes moving (superior semi-circular canal dehiscence)
RED FLAGS • Syncope, angina, focal neurologic deficits, headache, diplopia
stroke, epilepsy,
PMHx • Recent URTI, AOM, hearing loss, previous labyrinthitis, cholesteatoma, syphilis, MS, Parkinson’s, TIA,
anxiety, depression, Afib, carotid stenosis, valvular pathology (aortic
Ca (possible metastases to brain), migraines,
HTN, CHF, renal insufficiency , anemia, visual impairment, recent antibiotic use, psychiatric
stenosis), head trauma,
history
PSHx • Anyearsurgery
PO&GHx • LNMP, pregnant currently
FHx • CVA, brain Ca, vertigo, Meniere’s
Meds • ASA, aminoglycosides, loop diuretics, anticonvulsants, hypnotics, EtOK, caffeine, others
Social • Smoking, EtOH, IVDU, STDs, workplace noise levels

• HEENT: ear pain/fullness, effusion, vertigo/dizziness, tinnitus, diplopia, facial droop, dysphagia, anxiety/depression
CV: palpitation, signs of valve disease (low and slow pulse)
• RESP: difficulty breathing (anxiety vs. SOB)
• Gl: pain (IBS), melena, BRBPR
• GU: hematuria
• MSK / DERM: numbness/weakness, uncoordinated, bull’s eye/target rash (lyme)
Physical
General Approach
ABCs/vitals, orthostatic BP, GCS
2. Neuro-otologic exam (for vertigo)
. General appearance • Smooth pursuit (observe during CN Ill, IV, VI exam)
. Ears (out to in) • Vestibulo-ocular reflex
. Nose (signs of URTI) • Cerebellar exam: finger to nose, heel shin, dysdiadochokinesis,
. Oral cavity/oralpharanx (signs of pharyngitis) Romberg, tandem gait
. Neck (masses/lymphadenopathy) • Fundoscopy to look for high ICP
• CN: ll-Xll • Cardiovascular examination
• Head shaking nystagmus
3. Special Tests:
• Dix-Hailpike position test (diagnostic of BPPV): rapidly move the patient from a sitting position to a supine position with the head
hanging over the table turned to one side at 45° holding that postion for 2Osec
Investigations
1. Blood work (as indicated by H&P)
• CBC-D, electrolytes, Cr, urea, troponin
2. Radiology/Imaging (if suspicious of brain lesions, infection)
• CXR, carotid doppler, CT (labrythitis), MRI (acoustic neuroma), MRA head
3. Special Tests
• Orthostatic BP, EKG, 24 hr holter monitor (arrhythmias), BNP (CHF), EEG (seizures), pure-tone audiometry, Weber and Renne tests
(conductive hearing loss)
• Peripheral vertigo: tuning forks, audiogram, VNG (calorics, ENG, posturography)
• Central vertigo: CT head
Treatment
1. Emergent
• Assess ABC’s, bed rest, antiemetics if needed, vestibular sedatives (Gravol), benzos, antibiotics if suspect infectious cause
• High ICP (burr hole + catheter)
• Treatment of high ICP in the context of idiopathic raised intracranial pressure is LP
2. Treatment Options (depends on etiology)
• Orthostatic hypotension: increase water and salt intake (<1 gm added salt/day)
• Supportive: antihistamines (Meniere’s), benzodiazepines, antiemetics, barbituates
• Chronic vertigo/benign positional paroxysmal vertigo: Epley’s maneuver
3. Surgical (only used for tumours/refractory cases)
• Labyrinthectomy and vestibular nerve section for Meniere’s, translabyrinthine resection of acoustic neuroma, obliteration of
superior semicircular canal
4. Follow-up:
• If symptoms persist or are chronic in nature
5. Referrals:
• Possibly Otolaryngology, Neurosurgery, Neurology, Cardiology
i’D
References
1. Tintinalli JE, Kelen GD, Stapczynski JS: Tintinalli’s Emergency Medicine:A Comprehensive Study Guide, 6
th
Edition: http://acessemergencymedicine.com.

DYSPHAG IA
2011 Ed. Authors: Showna Pandya, KalArisari MD FRCSC, Diplomate (ABO), Diplomate (ABFPRS)
OriginalAuthor: Tamara Kuzma
Station Objective
To list the appropriate Hx, physical exam maneuvers, investigations and initial management in a patient with dysphagia.
• Oral preparation/oropharyngeal: difficulty initiating swallowing, drooling/spilling, nasal regurg, tracheal aspiration followed by
coughing. Usually in patients with neurological/muscular disorders or tumors of upper aerodigestive tract
• Esophageal: sensation of food sticking in chest or throat due to either a motility disorder or mechanical obstruction. Dysphagia
with solids alone suggests mechanical obstruction
• Pharyngeal diverticulum: regurgitation of food following lateral compression of neck is virtually diagnostic.
• Dysphagia with both solid AND liquid foods is non-specific
• Oral prep/oropharyngeal: neuro (e.g. Parkinson’s, stroke), muscular (e.g. myasthenia gravis) disorder, CN dysfunction
• Esophageal: achalasia, spastic motor disorder, obstruction (e.g. peptic stricture, web/ring, diverticulum), scleroderma
3. High Mortality:
• Esophageal carcinoma
• Resulting aspiration pneumonia
History
ID • Age
CC • “Food gets stuck after I swallow”
HPI • Onset, pain (PQRST/AAA)
• Upper aerodigestive Sx: cough, drool, nasal regurg, snort/sputter/sneeze with swallow, throat pain, odynophagia,
voice change, difficulty breathing, hemoptysis, hematemesis, weight loss
• Swallowing: food stuck in throat upon swallowing —+ esophageal, ask patient to point to location — intermittent =
motility disturbance, constant = mechanical obstruction, occurrence with liquids = motility disturbance, solids only
= mechanical, both = non-specific, pain after cold drinks —* esophageal spasm; reflux Sx —* peptic stricture
• Progression: Slow = achalasia; gradual solids —* liquids = mechanical; rapid suggests Ca
• Gurgling or regurgitation of undigested food (Zenker’s diverticulum)
RED FLAGS • Inability to swallow anything, drooling, wt emesis, hematemesis, change in voice, drastic change in reflux
,
symptoms, new focal neurological deficit (especially new weakness)

PMHx • GERD, DM, scieroderma, Sjorgen’s syndrome, AIDS, syphilis, poliomyelitis, stroke, achalasia, peripheral neuropathy,
myasthenia gravis, muscular dystrophy, MS, Parkinson’s, Ca
• Previous endoscopies: indications, findings
PSHx • Laryngeal, esophageal, gastric or spine surgery
Meds • NSAIDs (mucosal injury), new medications (pill esophagitis)
FHx • Cancer of the upper aerodigestive tract
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:CP
• RESP: cough, SOB
• GI: ABD pain, heartburn, reflux
• MSK: atrophy, muscle/joint pain,
• Derm: Scleroderma, rash, swelling, thickening, Raynaud’s

Physical
1. General Approach (introduction, hand-wash, ABC, IV, 02, monitors, vitals, permission)
2. Inspection
• Well vs unwell patient
• Nutritionally replete, deplete or emaciated
• Oral cavity: poor dentition, xerostomia, peritonsillar abscess, pharyngitis, tumor
• Skin: cutaneous lesions suggestive of CTD, Raynaud’s phenomenon (collagen vascular dz), rashes, sclerosis
• Muscles for wasting, fasciculations
•
Palpation
• Head, neck and supraclavicular lymph nodes (infectious pharyngitis, carcinoma) & muscle tenderness
• Neck masses: Thyroid (goiter, nodule(s) —* external esophageal compression), other masses (external compression)
4. Auscultation
• Respiratory: bronchial breath sounds, tactile fremitus (focal consolidation, pulmonary aspiration)
.
SpecialTests
• Neuro Exam
• Gross Neuro: proximal skeletal weakness: tremor, polymyositis, cogwheeling, rigidity, shuffling gate —* Parkinson’s
• CN: deficits of sensory br of V, IX, X and motor br of V, X, Xl, XII involved in swallowing suggest oropharyngeal
• Check for easy fatiguability by asking Pt to perform repetitive motion (e.g. eye blink, counting aloud)
• Balance/Gait
Investigations
1. Blood work
• CBC-D (anemia: red flag in men >50/post-menopausal women), electrolytes, urea, Cr, albumin for nutrition assessment
• Videofluoroscopic swallowing study or modified barium swallow (for obstruction or aspiration)
• CT & MRI esp useful for evaluating suspected CNS etiologies and neck/chest tumors
• CXR (if suspecting aspiration or mediastinal mass)
3. SpecialTests
• Reflex cough test —* done bedside to assess aspiration risk
• Esophageal pH monitoring (GERD)
• Esophageal manometry (for diagnosing achalasia)
• Endoscopy (esp if barium swallow positive) —* ENT for upper aerodigestive tract, GI/gen surg/thoracics if esophageal
Treatment
1. Emergent
• Food impaction/foreign body obstruction: push or pull the food bolus with forceps or endoscopy to relieve symptoms
• Medical
• Dietary modification: different food consistencies, enteral feeding, G tube feeds if unable to tolerate swallowing
• Lifestyle modification: head tilt while swallowing (consult speech pathologist) elevate head of bed, weight loss
• Surgical
• Endoscopy with dilatation for webs and strictures
• Heller myotomy, endoscopic dilatation or botulinum toxin injection for achalasia
• Surgical resection, chemotherapy and radiotherapy for Ca, laryngetcomy for intractable aspiration
3. Follow-up
• Ensure resolution of malnutrition, aspiration pneumonia, dehydration, if initially present
• Rehabilitation specialist following stroke, head or neck trauma or degenerative neuro dz
4. Referrals
• Otolaryngology, Neurology, Gastroenterology, Medicine, General Surgery, Oncology
References
1. Paik NJ. Dysphagia. Emedicine. 2008 Jun [cited 2010 Sep 24]. Available from: htto://emedicine.medscape.com/article/324096-overview
2. DiMarino MC. Dysphagia. Merck Manual Online. 2009 Jun (cited 2010 Sep 24]. Available from: http://www.merck.com/mmoe/sec02/ch012/ch012b.html.

EPISTAXIS
OriginalAuthors: MichaelJ Kapusta, Christopher Fung MO, AshrafKhan MBChB CCFP
Station 0 jective
Approach to the diagnosis and treatment of epistaxis
• Anterior epistaxis (Kiesselbach’s area, 90%) vs. posterior epistaxis (100
• Nasal trauma
• Dry nasal mucosa
• Rhinosinusitis
• Hypertension
• Posterior epistaxis
History
ID . Age, gender
CC • Nose bleed
HPI • Onset (sudden/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 (colour/consistency of blood): bright, dark, clots, mucous
• Region: unilateral/bilateral discharge (anterior epistaxis is most often unilateral)
RED FLAGS • Signs of hypovolemia
• Epistaxis that does not stop with 15 minutes of direct pressure
• Recurrent epistaxis
• Use of anticoagulants
• Signs of bleeding disorder (bruising, excessive bleeding from minor injuries or brushing teeth)
PMHx • Previous epistaxis
• Bleeding disorders or conditions associated with coagulopathy (i.e. hemophilia, pregnancy, liver disease)
• Hypertension
PSHx • ENT
Meds • Medications that may promote bleeding (i.e. ASA, NSAIDs, clopidogrel, heparin, warfarin)
FHx • Epistaxis or bleeding disorders
Social • Smoking, EtOH
• Exposure to low humidity environment
ROS • HEENT: headache, fever, sinus congestion, allergies
• MSK / DERM: bruising, petechiae

Physical
1. General Approach
• Vitals (assessing for potential hypovolemia)
2. Inspection Anterior ethm old artery
• Have patient in sitting position (reduces venous pressure)
• Signs of nasal fracture (swelling, ecchymosis, nasal Posterior ethmoid artery
deformity)
• Nasal speculum and headlamp (and possibly suction) to
visualize source of bleed
• Phenylephrine, two sprays of 0.5-1% solution, acts as a Kiesselbach’s
vasoconstrictor and can assist visualization plexus
• Fiberoptic endoscopy may be required for severe bleeding
or to visual a posterior bleed
• Examine for other signs of infectious cause
Investigations
1. Blood work
• Not routinely required unless there is a t suspicion of
anemia from recurrent or prolonged episodes of epistaxis
• INR/PTT if coagulopathy is suspected
Treatment
1. Emergent
• Direct pressure (pinching soft area of nose) maintained continuously for 10-15 minutes
• Significant blood loss: IV normal saline, 2 units PRBCs if necessary
• Cautery (anterior bleeds only): silver nitrate sticks can be applied when bleeding site is easily visualized
• Nasal packing: when direct pressure, vasoconstrictors and cautery have been unsuccessful
• Embolization or surgical ligation: when all conservative measures have failed
3. Referrals
• ENT
References
1. Schlosser, Ri. Epistaxis. NEngliMed. 2009 Feb 19;360(8):784-9.
2. WatersTA, Peacock IVWF. Chapter 241. Nasal Emergencies and Sinusitis. ln:Tintinalli JE, Kelen GD, Stapczynski J5, Ma OJ, Cline DM.Tintinalli’s Emergency
Medicine: A Comprehensive Study Guide, 6e: http://www.accessmedicine.comiogin.ezproxy.library.ualberta.ca/content.aspx?alD=609033.
3. Kaplan JL Beers MH, Berkwits M, Porter RS, Jones TV, eds. Nose and Paranasal Sinus Disorders. In: The Merck Manual of Diagnosis and Therapy 1 gth Ed.
—
(2006). http://online.statref.com.login.ezproxy.library.ualberta.ca/document.aspx?fxid=21 &docid=372.
Surgeryf Edmonton Manual of Common Clinical Scenarios 335

ERECTILE DYSFUNCTION
201? Ed. Authors: Brendan Diederichs, Tray Schultz MO, Eric EsteyMO FRCSC
OriginalAuthors: Michael Metcalfe, Conrad Maciejewski MO, James Metcalfe MO FRCSC
Station Objective
Determine contributing factors, order and interpret pertinent laboratory studies, and conduct an effective management plan for a patient
with ED. The student must recognize that ED is an early indicator of vascular disease.
Di erential Diagnosis:
Two broad categories of ED: organic (more common) vs inorganic/psychogenic
Causes of Impotence
I Inflammatory • Prostatitis
M Mechanical • Peyronie’s dz
P Psychological Depression, anxiety, relationship difficulties, libido, stress, L Sleep
0 Occlusive Vascular Factors HTN, smoking, hyperlipidemia, DM, PVD
T Trauma Pelvic fracture, penile injury, prior surgery (prostatectomy)
Extra Factors
E . . Age, CRF, cirrhosis
(comorbidities)
• CNS: MS, Parkinsons, tumor
N Neurogenic Spinal cord: spina bifida, Sd, MS. syringomyelia, tumor
• PNS: peripheral neuropathy (DM, EtOH)
C Chemical Anti-HTN, anti-arrythmics, antidepressants, anti-androgens, anti-parkinsonian, anxiolytics, EtOH,
E Endocrine • DM
History
ID Age
CC • Difficulty achieving or maintaining an erection
•
,interest in or enjoyment of sex
HPI . Onset: sudden (likely psychogenic) vs. gradual (typically sporadic initially)
• When was the last time pt. consistently had a normal erection?
• Characterize erection hardness (erection hardness scale)
• Validated questionnaire: International Index of Erectile Function (IIEF)
. Ability to maintain an erection to ejaculation
• Nocturnal erections/morning erections (“morning wood”)
. Psychological factors: desire, libido, anxiety, fatigue, depressive symptoms, partner satisfaction
RED FLAGS Complete lack of nocturnal erections suggests a vascular or neurogenic etiology
PMHx Metabolic syndrome, CVD, PVD, DM, obesity, neuro/psych/endocrine Hx
PSHx Pelvic surgery/radiation, retroperitoneal surgery, back surgery
Meds Anti-HTN, anti-arrythmic, anti-convulsant, anti-depressant, anti-androgen, statin
FHx CAD, PVD, DM, obesity, ED
Social • EtOH, smoking, drug abuse, sedentary lifestyle
• Relationship issues
ROS Psych: depression, anxiety
• HEENT: headache
• CV: angina, claudication, HTN
• GU: any voiding symptoms (dysuria, incomplete voiding, double voiding, decrease flow)
Risk Factors ED is an early marker for vascular dz and is a predictor of CAD and cardiac events
Physical
1. General Approach
• Full PE including CVS, CNS, and PVD is recommended to look into the long DDx of ED
2. Inspection
• Assess secondary sexual characteristics (presence and pattern of hair growth, gynecomastia, size of testicles)

• External genitalia: meatus (hypospadias), foreskin phimosis, Peyronie’s plaques Erection hardness scale
3, Palpation
• Confirm presence, size and location of testicles 0 No change in tumescence of penis
• Palpate the shaft for any plaques or signs of trauma Mild change in tumescence of penis
• Palpate the testicles, epididymis, spermatic cord and inguinal region for masses, An erection not suitable for penetration
2
tenderness asymmetry, or atrophy
• Palpate femoral and peripheral pulses 3 An erection suitable for penetration but
4. SpecialTests not as potent as desired by patient or
• Test the bulbocavernosus reflex: squeezing the glans causes anal sphincter and partner
bulbocavernosal muscle contraction (1. suggests neuropathic ED) 4 An erection of maximal potency enjoyed
• Test cremaster reflex: stroking inner thigh causes elevation of ipsilateral scrotum by patient and partner
(ensures integrity of thoracolumbar erection center)
Investigations
1. Blood work: fasting glucose/lipid profile, serum (free) testosterone (AM),
• Extra tests if abnormal testosterone or abnormal physical exam: LH/FSH, PRL, TSH
2. U/A (if presence of LUTS lower urinary tract symptoms)
Treatment
1. Conservative Management:
• Lifestyle modification: improve cardiovascular risk factors (eg. heart healthy diet, exercise, etc.)
• Alleviate aggravation factors: change medications (eg. beta blockers, cimetidine, HCTZ, etc.)
• Psychosexual therapy: addresses underlying psychological issues, provides information and treatment in the form of sex
education, improvement on communication, and CBT (cognitive behavioral therapy)
• Vacuum erection device (pumps blood into penis, then constricting band placed at base to keep blood in)
2. Medical Management
• Phosphodiesterase type-5 (PDE-5) inhibitors: sildenafil (Viagra), tadalafil (Cialis), vardenafil (Levitra)
• Meds must be taken on full stomach 30 mm. prior to sex, often takes several tries (2-5)
• All 3 are equally efficacious, their difference mostly depending on ½ life
• Often pts need to try all 3 of them before they find out which ones work
• NB: do not give if on nitroglycerin therapy (Absolute contraindication)
• Intra-cavernosal injection therapy (prostaglandins, alpha agonists)
• lntraurethral medications (prostaglandins)
• Androgen replacement therapy (for libido secondary to hypogonadism)
3. Surgical Management
• Penile prosthesis (sensation intact, purely a mechanical”fix”)
• Microvascular arterial bypass and venous ligation surgery (rarely indicated surgeries)
References
1. MulhallJP, Goldstein I, Bushmaken AG, cappelleri JC, Hvidsten K. “Validation of the erection hardness scale” J sex med 2007, November 4: (6); 1626-1 634.
2. Schwartz BG, Kloner RA. How to save a life during a clinic visit for erectile dysfunction by modifying cardiovascular risk factors. International Journal of
Impotence Research 2009, August 20:1-9.
3. Reynard J, Brewster 5, Biers S. Oxford Handbook of Urology. 2nd
Edition. New York: Oxford University Press Inc.; 2009.

GASTROINTESTINAL BLEED
2011 Ed. Authors: MichaelfKapusta, Christopher Fung MD, AshrafKhan MBChB CCFP
OriginolAuthors: Tamoro Kuzmo
Station Objective
Approach to the patient with complaints of hematemesis, hematochezia, or melena. Differentiate upper from lower gastrointestinal bleeding.
1. Diagnostic Criteria/Common Conditions
UGIB vs. LGIB (proximal or distal to the ligament of Treitz, respectively)
Table 1: Upper vs Lower GI Bleeding
UGIB LGIB
Classification AboveligamentofTreitz BelowligamentofTreitz
Signs Hematemesis, hematochezia (rapid bleed), melena Hematochezia, melena

• Peptic ulcer Diverticular hemorrhage
. Esophageal varices • IBD (UC and Crohn’s)
• Gastritis Polyps
. Erosive esophagitis • Neoplasm
Common etiology Angiodysplasia
• Mallory-Weiss tear •
• Vascular malformation Hemorrhoids

• Fissures
• Infections (dysentery)

Hypovolemic shock
• Persistent and/or rebleeding
• Sepsis/DIC
History
ID Age, gender
CC Vomiting blood
• Blood on toilet paper
• Blood in toilet bowl and/or mixed with stool
• Black, tarry stool
HPI Onset
• Precipitant: vomiting, trauma, straining with bowel movement
• Quality: bright red, dark, clots, coffee grounds
• Severity: volume of blood in the stool (streaks on outside of stool, mixed in with stool) and toilet
• Change in bowel habits (shape, frequency (waking up at night), consistency)
• Painless (varices, diverticulosis, angiodysplagia, carcinoma)
• Painful: sudden severe (perforation), out of proportion with physical findings (ischemic bowel), epigastric (PUD),
rectal (fissure, abscess)
• Associated symptoms: fever, chills (infection, inflammatory); weight loss, fatigue, anorexia (malignancy);
presyncope, dizziness (significant blood loss), diaphoresis
RED FLAGS Hypotension
• Syncope
• Tachycardia
• Diaphoresis
• Weight loss over months/years (may suggest cancer)
PMHx GI bleeds
• Bleeding diatheses, liver dysfunction, portal hypertension
• PUD, hemorrhoids, IBD
• Cancer
• Radiation exposure
PSHx Gl,vascular
Meds NSAIDs, ASA, Plavix, steroids, anticoagulants, Fe supplements, Pepto Bismol

FHx • GI Cancer, IBD
Social • Smoking, EtCH, travel history
• Diet (Fe, beets, licorice)
ROS HEENT: scleral jaundice
• MSK/ DERM: jaundice, purpura, ecchymoses
Risk Factors Long term NSAID use, multiple comorbidities, Hx of GI bleeds
physical
1. General Approach
• ABCs (resuscitation with IV fluids or PRBCs if indicated), vitals
• General appearance: anxious, pale, diaphoretic, active bleeding, signs of shock
2. Inspection
• ABD: distension, surgical scars, caput medusa
• DERM: signs of liver disease including jaundice, petechiae, ecchymoses, spider nevi
3. Auscultation
• Presence or absence of bowel sounds
4. Percussion
• ABD: ascites, hepatomegaly, tenderness, gaseous distension
5. Palpation
• ABD: guarding (peritonitis: intraperitoneal bleed, perforation, ischemic bowel), hepatosplenomegaly, masses, perianal inspection
and DRE (fissures, hemorrhoids, rectal mass, melena)
Investigation
1. Blood work
• CBC-D
• INR,PTT
• Type and cross match
• Electrolytes, BUN, Cr, liver enzymes
• 3 views abdominal X-ray
• Esophagogastroduodenoscopy, colonoscopy
4. Special Tests
• Angiography
• RBCscan
Treatment
1. Resuscitation
• ABCs, 2 large bore IVs, RL or NS bolus 20cc/kg, PRBCs at 10cc/kg
• NG tube and suction (determine UGIB vs LGIB)
• Foley to urometer (monitor fluid status)
• UGIB (also see Hematemesis)
• ER Management
• Non-variceal bleeding: Pantoprazole 80mg IV bolus, then 8mg IV per hour
• Variceal bleeding: octreotide Somcg IV bolus, then 5omcg IV per hour
• Endoscopy or colonoscopy: locate bleeding site and coagulate lesion
• Balloon tamponade
• Surgical
• Laparotomy: unstable patient, failed medical management, failed endoscopy therapy twice, requiring transfusion of 6
units PRBCs/24 hours
• LGIB
• ER Management:
• Consider colonoscopy/sigmoidoscopy
• Symptomatic management until etiology is confirmed
3. Referrals: Gastroenterology, General Surgery
References
1. Subramanian R, McCashland T. Gastrointestinal Hemorrhage. In: Hall JB, Schmidt GA, Wood LDH. Principles of Critical Care. New York: McGraw-Hill
Companies; 2005.
2. Kaplan JL, Beers MH, Berkwits M, Porter RS, Jones TV, eds. GI Bleeding. In: The Merck Manual of Diagnosis and Therapy 1 8
—
th
Ed. (2006). http://online.
statref.com.login.ezproxy.library.ualberta.ca/document.aspx?fxid=21&docid=41.

GYN ECOMASTIA
2011 Ed. Authors: Mackenzie Lees, Simon Turner MD, Gordon Lees MD FRCSC
OriginalAuthors: Saleem Al-Nuaimi, BushrMrad MD, Michael ChatenayMD FRCSC
Station Objective
To differentiate gynecomastia from pseudo-gynecomastia and breast cancer and to differentiate the etiology of gynecomastia.
1. Common Conditions: Differential Diagnosis for Gynecomastia
• Physiologic gynecomastia: pubescent and elderly pts, asymptomatic, may
Klinefelter’s syndrome
complain of pain/tenderness (due to proliferation), generally lasts less than 6 mo
Obesity
and then regresses
Cancer
• Lipomastia (pseudo-çivnecomastia): sub-areolar fat without enlargement of the
Puberty
breast glandular tissue, lacks concentric/rubbery/firm tissue with nipple-areolar
Drugs
complex Chronic liver disease
•
• Pharmacologic gynecomastia: drugs that mimic estrogen or increase estrogen
• Hyperthyroidism
synthesis, drugs that block testosterone synthesis/action, etc. Adrenal disease
•
• Qfl smooth and mobile mass
• Idiopathic
• j skin dimpling, nipple retraction, nipple discharge, hard, immobile mass
• Ca
History
ID • Age (pubertal, older age)
CC • “I have nipple swelling”
HPI • Onset
• Change in size, fluctuations
• Nipple discharge (bloody)
• Presence of pain
• Presence of skin changes
RED FLAGS • Wt ‘, hemoptysis, dyspnea, bony pain, CP
PMHx • Hyperthyroidism, liver dz, renal dz, tumors (testicular), hypogonadism
PSHx • Previous breast/chest surgery
PO&GHx • Infertility
Meds • Estrogens, estrogen synthesis enhancers (exogenous testosterone), anti-androgens (spironolactone,
chemotherapeutics), OTC and herbals, digoxin
FHx • Gynecomastia
Social • Anabolic steroids, marijuana, EtOH, oploids, malnutrition
ROS • HEENT: headache, visual changes, diaphoresis
• CV: palpitations, DP
• RESP: dyspnea, hemoptysis
• GI: abdominal pain, change in bowel habit
• GU: testicular pain/trauma/or enlargement, libido, ED
-
• MSK/ DERM: bony pain/back pain, jaundice

• Other: heat intolerance, nervousness, tremors
Risk Factors • Adolescence, older age, Klinefelter’s Syndrome, liver dz, renal dz, hyperthyroidism, anabolic steroids, recreational
drugs, majority are idiopathic
Physical
1. General Approach
• Introduce yourself, wash hands, ask permission to do a PE
• Assess Pt’s LOC, vitals, proper draping

2. InspectiOn
• HEENT: goiter, diaphoresis, exopthalamos, jaundice, scleral icterus
• Breasts: obvious mass/lump, asymmetry, skin changes, nipple inversion/retraction/discharge
• ABD: enlargement (ascites, hepatomegaly)
• GU: testicular enlargement/atrophy, ambiguity
• Other: signs of feminization (spider nevi, palmar erythema, sparse hair, loss of eustacheon hair)
• Consider degree of virilization (voice, facial and body hair, muscular development) and secondary sexual development)
3. Percussion
• ABD: shifting dullness (ascites), liver size (cirrhosis), hepatosplenomegaly
4. Palpation
• HEENT: thyroid
• Lymph nodes: axillary, supraclavicular, infraclavicular, and cervical lymphadenopathy
• Breasts: palpate breast (start with normal) with Pt supine with hands clasped beneath head, note Iocation/size/shape/consistency/
tenderness/skin dimpling/mobility
• ***True gynecomastia characterized by rubbery/firm tissue concentric with nipple-areolar complex, pseudo-gynecomastia
lacks this finding
• Hardness is a major factor in predicting the presence of male breast cancer
• ABD: tenderness, hepatosplenomegaly, mass
• GU: testicular size, testicular masses
5. Auscultation
• Goiter: bruit
• CV/RESP: heart and respiratory sounds
Investigations
1. Blood work
• If pt has uni/bilateral gynecomastia that is tender/painful with no etiology determined on Hx or PE: 3-hCG, LH, free testosterone,
estradiol
• If stigmata of liver dz: AST, ALT, total bili, ALP, INR, albumin
• If stigmata of thyroid dz:TSH
• If stigmata of renal dz: Cr, urea
• CXR
• Diagnostic mammography
• FNA, core Bx if Ca suspected
Treatment
• Medical: discontinuation of offending drug(s)
• Androgens (testosterone), anti-estrogen (clomiphere), estrogen anatagonist (tamoxifen)
• Surgical: consider for cosmetics and gynecomastia >lyr (fibrosis) —* subcutaneous mastectomy, U/A assisted liposuction, suction
assisted lipectomy
• Further work-up: testicular U/S if 3-hCGt or testicular ca suspected, serum PRL if testosterone with normaI/ LH, adrenal CT
or MRI if festradiol and normal/.I. LH with normal testicular U/S
2. Follow-up
• Asymptomatic and pubertal gynecomastia require reassurance and reevaluate in 6 mo (HX/PE)
• If pt on medical therapy, reevaluate and assess response to therapy (e.g. F/U in 3 mo with tamoxifen)
3. Referrals
• Surgeon, Endocrinologist
References
1. Narula HS, Carlson HE. Gynecomastia. Endocrinol Metab Clin North Am. 2007 Jun;36(2):497-51 9.
2. Federman DD, Nabel EG, eds. 2010. ACP Medicine. NewYork, NY. BC Decker Inc. ISBN 0-9703902-9-7. STAT!Ref Online Electronic Medical Library.hitpfL
onhine.statref.com.login.ezproxv.library.ualberta.ca/document.aspxThad=48&docid=597.
3. Allee MR, Baker MZ. Gynecomastia. Last updated 2009 Sep 23. Available from: http://emedicine.medscape.com/article/l 20858-overview
4. Braunstein GD. Gynecomastia. N EngIJ Med. 2007 Sept 20;357:1 229-37.

HAND (PAIN, FRACTURES, AND DISLOCATIONS)
Authors: Ho/lie Power, Regan Guilfoyle MD, MichoelMorhort MD, FR
Station Objective
Assess the patient presenting with hand pain, fracture or dislocation and outline the initial investigations and management. Identify patients
in need of specialized care.
Common hand pathologies:
1. 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, eg. RA)
2. Non-trauma
• Joints: osteoarthritis, Rheumatoid arthritis
• Nerves: carpal tunnel syndrome
• Tendons: DeQuervain’s tenosynovitis, trigger finger
• Other: ganglion cyst, Dupuytren’s contracture
History
ID • Age, gender, occupation, hand dominance
CC TRAUMA NON-TRAUMA
HPI • When, where, how did the injury occur? • Pain history (onset, provoking/palliating factors,
• Any unusual sounds or sensations? quality, region/radiation, severity, time of day,
• Dominant or non-dominant hand injured? treatments)
• Other injuries or open wounds? • Progression of symptoms? In what order?
• What treatment has been administered? • Are any other joints affected?
• Tetanus status • How is your function affected?
RED FLAGS • Signs of neurovascular compromise
PMHx • Previous trauma to hand/wrist • Arthritis, bleeding diatheses, 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, EtCH
Physical
1. General Approach
• ABC’S, vitals, general appearance of the patient Important things to rule out:
• Expose hands, forearms adequately (remove splints, casts, dressings etc.) • Skeletal instability/joint
2. Inspection dislocation
• Posture / resting cascade of the hand • Compartment syndrome
• Swelling, erythema, atrophy, deformities, skin changes (SEADS) • Actual or threatened skin loss
• Bony alignment, lacerations, surgical scars • Neurovascular injury
3. Palpation • Tendon injury or infection
Vascular: radial and ulnar pulses, capillary refill, temperature, color of the skin *If present, seek specialized care (i.e.
Motor: check strength of muscles supplied by median, ulnar, and radial nerves plastic surgeon)
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
4. ROM:
Check active ROM for all joints in the hand
• Quick screen: ask patient to “make a fist” then “straighten out your fingers”; visualize dorsal and volar surfaces looking for
rotation, scissoring, decreased or abnormal flexion/extension, assess for pain against resisted flexion/extension
• Passive ROM for any abnormal movement on active ROM
• Isolate FDP/FDS tendons in each finger and test function

Table 1: Clinical and diagnostic features of common hand pathologies
Condition Common Findings on Examination Confirmation of Diagnosis
• PIP/DIP/MCP: dorsal dislocation most common (hyperextension injury) Hand x-ray (3 views)
Dislocations
. May have subluxation with mvmt —* implies severe ligamentous injury
• Most commonly affect border digits (thumb & little finger)
• Distal phalanx: often accompanied by soft tissue injury, subungual hematoma
Fractures Middle/proximal phalanx: rotation, scissoring (overlap of fingers while making a • Hand x-ray (3 views)
fist), shortening
Bone Metacarpal: loss of prominence of metacarpal head, scissoring
Bony enlargement of PIP/DIP joints (Bouchard/Heberden nodes), stiffness, .1. ROM; • Hand x-ray (3 views)
Osteoarthritis
pain/stiffness exacerbated by activity, relieved by rest
Clinical diagnosis, ESR,
Rheumatoid Swelling of PIP and MCP joints, usually >1 joint, symmetric, morning stiffness, serologies (RF etc.), hand
Arthritis ROM x-rays
Carpal tunnel Sensory changes + weakness in median nerve distribution; positive Phalen’s or Nerve conduction studies,
Nerve Tinel’s signs EMG
syndrome
Boutonniere Clinical diagnosis
• PIP in flexion, DIP hyperextended
deformity
• Local anesthetic block at
DeQuervain’s Positive Finkelstein test: knifelike pain just proximal to the radial styloid when radial styloid should .1.
—
tenosynovitis thumb is clasped in palm and wrist forced into ulnar deviation pain
Mallet finger DIP held in fiexion; inability to actively extend Clinical diagnosis
Tendon
Stenosing • Local anesthetic block at
tenosynovitis Loss of smooth motion of PIP joint; catching, snapping or locking; palpable nodule flexor tenosynovium —
(“trigger proximal to MCP joint should pain
finger”)
Swan Neck Clinical diagnosis
. PIP hyperextended, DIP in fiexion
deformity
Dupuytren’s Nodular thickening of palmar fascia, flexion contracture, palmar pits, knuckle pads • Clinical diagnosis
contracture (commonly D5>D4>D3)
Other • Trans-illumination or cyst
Ganglion cyst Cystic swelling usually on dorsal aspect of hand/wrist aspiration
Investigations
1. Blood work: CBC-D, ESR, rheumatoid factor
• Hand x-ray with AP, lateral, oblique views
• CT/MRI wrist for complex carpal fractures and dislocations
3. Special Tests: nerve conduction studies, electromyography (EMG)
Treatment
1. Emergent: ABC’s, life before limb
2. Medical Treatment
• Reduce #s or dislocations ASAP to prevent neurovascular injury
• Irrigation, debridement, ± antibiotics for lacerations and open #s
• Tetanus prophylaxis if indicated Position of safety:
• Analgesia, anti-inflammatories • MCP joints in 70-90° of flexion
• Reduce swelling: Rest, Ice, Compression, Elevation • lPjoints in extension
• Splinting: depends on type of injury; when possible: use position of safety (see box) • Wrist in 20-30° extension
• Early motion is often crucial to rehabilitation, so physiotherapy recommended
3. Surgical Treatment
• Complex dislocations and fractures may require CRPP (closed reduction and percutaneous pinning) or ORIF
• Repair of associated injuries to digital nerves, ligaments, tendons
4. Referrals
• Plastic surgery, physical medicine & rehabilitation, rheumatology
• Occupational therapy, physiotherapy
References
1. Anderson BC. Evaluation of the patient with hand pain. In: Shmerling RH, Romain PL, editors. Up to Date. Waltham: Up to Date; 2010.
2. Green, DP, Hotchkiss, RN, Pederson WC, Wolfe SW. Green’s Operative Hand Surgery. Fifth Edition. Philadelphia: Elsevier Churchill Livingstone; 2005.
3. Janis JE. Essentials of Plastic Surgery. St. Louis: Quality Medical Publishing; 2007.

HEAD TRAUMA
201 I Ed.Authors:AshrafKharrat,JamesKeayMDCCFP
OriginalAuthors: Nawaaz Nathoo, Chris Hanson MD, Patrick San Agustin MD FRCPC
Station Objective
Identify features of head trauma that warrant further investigation including depressed or changing mental status, focal neurological deficits
depressed skull fracture, or penetrating head injury.
• Primary survey (ABCDE), vitals, C-spine evaluation (collar and board if any major trauma)
• Establish IV access, 02 as necessary, monitors
• Order necessary stat labs and imaging (chemstrip, ABG/venous gases, ECG)
• Secondary survey including head to toe inspection, pupils and CN’s, corneal and gag reflex, doll’s eyes, CV/RESP/ABD exam, long
bone exam, log roll to perform spinal evaluation, DRE
• Fracture: orbital, facial (Le Fort I, II, Ill), basal skull
• Hemorrhage: epidural, subdural, subarachnoid
• Concussion
• Any patient with decreased or change in LOC, focal neurological defects, depressed skull fracture, or penetrating head injury
requires an emergent CT or MRI (refer to CT head 2 and C-spine rules’)
History
ID • Age, sex, handedness, occupation
CC • Head trauma
HPI • Mechanism of injury (seatbelt, speed traveling, airbag, location in car, location of impact, status of car, status of
others involved in accident)
• Timing of injury (if >6 hrs and asymptomatic, serious complications much less likely)
• Other systemic injuries sustained
• Altered sensation, weakness, lethargy, walking since the injury, seizures
• Confusion, altered LOC (temporary or sustained), amnesia, seizures, vomiting since the event, diplopia, fecal or
urinary incontinence
• Falls: height, position of landing, surface of landing
• Last meal
RED FLAGS • Depressed or changing mental status, focal neurological deficits, depressed skull fracture, penetrating head injury,
seizures
• Abnormal vital signs including hypo/hyper-tension
• Cushing’s triad: (1) systolic HTN (2) bradycardia (3) respiratory depression
PMHx • Past seizure or other neurological/psychiatric disorders
• Hypercoagulable state
PO&GHx • Pregnancy status
Meds • Anticoagulants, tetanus vaccination status
FHx • Neurological disorders, clotting disorders
Social • Drugs/EtOH (especially at time of injury), suicide hx to r/o toxidromes, assaults
ROS • HEENT: neck pain, deficits in facial/ENT functions
• GU: incontinence, saddle anesthesia
• NEURO: altered sensation, motor weakness, abnormal reflexes, numbness and tingling
Physical
1. General Approach
• Primary and secondary surveys (ATLS protocol)
2. Inspection

• HEENT: fractures, lacerations, fluid drainage from facial orifices, visible bleeds (including mastoid ecchymosis [Battle’s sign], blood
behind TM or from EAC, blood from nares, periorbital ecchymosis [raccoon eyes], hyphema, subconjunctival hemorrhage)
• Extremities: fractures, bleeding, arms for IV track marks
3. Percussion
• Deep tendon reflexes (triceps, biceps, brachioradialis, finger flexion, knee, ankle)
4. Palpation
• Sensation along dermatomal distributions (pin prick, vibration sense, temperature, proprioception, two-point discrimination),
gross/fine motor evaluation (power, tone, rigidity)
5. SpecialTests
• CN exam, Babinski reflex
• Cerebellar exam: random alternating movement, dysdiadochokinesis, finger-to-nose test, toe-to-shin test, gait (including standing
from seated, walk, turn, heel-to-toe, heel walk, tiptoe)
Investigations
1. Blood work
• CBC-D, electrolytes, PT-INR, PU, urea, Cr, glucose, 3-HCG
• C-spine XR: refer to Canadian C-Spine Rules for clinical decision making protocol
1
• Head CT: refer to Canadian CT Head Rules
, plain films of the skull are generally not helpful
2
• NB: unstable patients cannot go to CT scanner
• Epidural hematoma from middle meningeal artery will be visible on CT immediately after injury while epidural or subdural
hematoma from venous injury will generally take longer to appear on CT
• Repeat CT in 4-8 hrs if any intracranial hemorrhages, coagulopathies or if Pt fails to improve, or sooner if pt deteriorates
further
3. SpecialTests
• EtOH/tox screen, Mg, Ca, PC, trops, CK-MB, lactate, digoxin levels, dilantin levels
Treatment
4. Emergent
• ABCDE (Airway, Breathing, Circulation, Disability (GCS), Environment plus C-spine)
• 2 large bore IVs, cardiac monitoring, °2’ vitals (T, BP, RR, HR, Sp0
)
2
• Control bleeding
• Specific therapy as needed:
• Pain control, sedation • If signs of ICP, consider mannitol 1 g/kg IV
• Tetanus toxin for all lacerations if not immune • Dilantin for seizures
(no vaccine in past 10 yrs) or if unsure • If Pt 5 on warfarin, consider vitamin K, FFP,
• Antibiotics (cefazolin) for open skull #s and octaplex
Burr hole for subdural hematoma
5. Referrals
• Neurosurgery (head and spinal trauma), orthopedics (spinal and long bone trauma), neurology (neurological non-surgical deficits,
seizure), internal medicine, general surgery (abdominal or chest pathology), psychiatry (substance abuse, suicide), trauma team/
ICU pm
• In the case where brain death has occurred but the heart is still beating, communicate this to transplant team
• If pt has no indicated wishes regarding organ donation, counsel the family regarding this possibility
• Determine Pt DNR status and wishes when stable or if preexisting documentation exists
• If such documents do not exist, determine capacity or attain consent from the appropriate source
References
1. Stiell IG, Wells GA, Vandemheen KL, Clement CM, Lesiuk H, De Maio Vi, et al. The Canadian Cervical Spine Radiography Rule for alert and stable trauma
patients. Journal of the American Medical Association 2001; 286:1841-1 848.
2. Stiell 1G. Wells GA, Vandemheen K, Clement C, Lesiuk H, Laupacis A, McKnight RD, Verbeek R, Brison R, Cass D, Eisenhauer ME, Greenberg G, Worthington J.
The Canadian CT Head Rule for patients with minor head injury. Lancet 2001 ;357;1 391-6.
3. Hoffman, LH eta!. First Exposure Emergency Medicine. McGraw-Hill, Inc. USA, 2008.

HEMATEMESIS
OriginalAuthors: Michoeli Kapusta, Christopher Fung MD, Ashraf Khan MBChB CCFP
Station Objective
Approach to the diagnosis and treatment of various causes of hematemesis.
• Causes of hematemesis (UGI bleed proximal to ligament of Treitz)
• Peptic-ulcer disease (55%)
• Helicobacterpylori (common)
• Systemic and psychological stress
• Zollinger-Ellison syndrome (rare)
• Portal hypertension (gastroesophageal varices) (15%)
• Other
• Upper GI tumors (begin and malignant)
• Mallory-Weiss (M-W) tear
• Erosive esophagitis/gastritis
• Clotting disorder
• M-Wtear
• Esophageal varices
• Perforated organ
History
ID • Age, gender
CC • Vomiting blood
HPI • Precipitant: food (spicy/fatty, coffee), alcohol, vomiting followed by pain then blood (M-W tear), trauma
• Palliating factors: food, antacids
• Quality: bright red blood, dark blood, clots,”coffee grounds”
• Quantity of bloody vomitus
• Painless: varices, carcinoma
• Painful: sudden escalating (perforation), epigastric (PUD)
• Nausea
RED FLAGS • Recent frequent vomiting and/or retching followed by pain then blood (M-W tear)
• Signs of hypovolemic shock (tachycardia, hypotension, syncope, diaphoresis)
PMHx • Previous GI bleeds, PUD
• Liver or renal disease
• Bleeding disorders
• Previous hospitalization (a significant source of stress)
Meds • PPI, NSAIDs, steroids, ASA, thrombolytics, anticoagulants, oral Fe, OTC antacids
FHx • Bleeding disorders, PUD (H. pylon “runs” in families)
Social • EtOH, smoking, recreational drug use
Lft ROS • l-IEENT: epistaxis as source of blood
C • CV: presyncope, dizziness
• GI: hematochezia (from major upper GI bleed), melena
(D • Mental state: encephalopathy (chronic liver disease)

Physical
i. General Approach
• Vitals
• Assess for hypovolemia: BP supine and standing, JVP, HR
2. Inspection
• Stigmata of chronic liver disease (palmar erythema, jaundice, caput medusa, spider nevi, gynecomastia)
• Ascites
• Volume of blood emesis
3. Percussion/Palpation
• Hepatosplenomegaly
• Ascites
• Rebound tenderness from a perforation
• DRE
Investigations
1. Blood work
• CBC-D
• INR/PTT
• Type and cross-match if appropriate
• Electrolytes, BUN, Cr, glucose
• Liver function tests
• 3 view abdominal X-ray
• Endoscopy (also a therapeutic intervention)
Treatment
1. Emergent
• ABCs, 2 large bore lVs, RL or NS
• Consider blood transfusion if Hb <70g/L
• Foley to urometer (monitor fluid status)
• Medical
• NPOfor24hours
• NG tube and suction to determine active (bright red blood) from recent (coffee grounds) bleed
• Non-variceal bleeding: Pantoprazole 80mg IV bolus, then 8mg IV per hour
• Variceal bleeding: octreotide 5omcg IV bolus, then 5omcg IV per hour
• Endoscopy (cauterize or clip acute bleeds)
• Balloon tamponade
• Surgical
• Laparotomy: unstable patient, failed medical management, failed endoscopy therapy twice, requiring transfusion of 6 units
PRBCs/24 hours.
• TIPPS for resistant varices
3. Follow-up
• Urease breath test in 4 weeks (for H. pylon) and possible triple therapy (PPI, clarithromycin, metronidazole)
4. Referrals
• Gastroenterologist
• General surgery: when endoscopic hemostasis therapy unsuccessful, severe bleeding
References
1. Longmore M, Wilkinson IB, Davidson EH, Foulkes A, Mafi AR. Upper gastrointestinal bleeding. In: Oxford Handbook of Clinical Medicine 8th Ed. Oxford:
-
Oxford University Press; 2010. p. 252-255.

HEMATU RIA
201! Ed. Authors:Armin Badre, Leyla Asadi MD, Alan McMahon MD FRCPC
OriginalAuthors: MichaelMetcalfe, ConradMaciejewski MD, James Metcalfe MD FRCSC
Station Objective
hematuria and effective management
Approach to patients with true hematuria including differentiation, diagnosis of gross/microscopic
plan.
with supernatant being clear
• Gross hematuria: after centrifugation, the red to brown colour is seen only in the urine sediment
hematuria: >2 RBCs per high power field on two microscopic urinalysis without recent history of exercise, menses,
• Microscopic
sexual activity or instrumentation
RBCs, red cell casts, brown cola-
• Signs of Glomerular hematuria: proteinuria (>500mg of protein/day in urine), 80% dysmorphic
colored urine with gross hematuria
• Presence of blood clots highly suggestive of a non-glomerular cause of hematuria
Glomerular Upper urinary tract Lower urinary tract
Pre-renal
IgA nephropathy (most • Renal cell Ca • Bladder Ca
• Exercise hematuria •
common) Nephrolithiasis • Prostate Ca

• Anti-coagulation •
Thin basement membrane Pyelonephritis • BPH

. Neoplasm • •
Hereditary nephritis Polycystic kidney • Cysitis, prostatis, urethritis

• Thromboembolism • •
Focal glomerular nephritis Ureteral stricture • Polyps

• Coagulopathies • •
• Post-infectious • Renal trauma • Schistosomiasis

glomerulonephritis • Sickle cell, papillary • Urethral strictures
• Anti-GBM disease necrosis, TB • Trauma
• Systemic (vasculitis, SLE..) • Trauma
History
ID • Age, sex
CC • Gross hematuria, microscopic hematuria
HPI • Onset: how long it has been going on
.
• Provocative and palliating factors

• Pain: flank pain C? pyelonephritis), suprapubic pain (? cystitis), perineal pain, dysuria
of
RED FLAGS • Smoking history or occupational exposure to chemicals/dyes, history of gross hematuria, age >40, history
of chronic
urologic disorders, histoiy of persistent irritative voiding symptoms, history of pelvic irradiation, history
or recurrent UTI, analgesic abuse, previous exposure to cyclophosphamide (bladder Ca)
PMHx • Urological disorders, nephrologic conditions, urinary retention, recurrent UTI, malignancy, HTN
PSHx • Instrumentation of GU tract
PO&GHx • Menstruation (psuedohematuria)
Meds • Anticoagulants, medications that might cause nephritis
FHx • Hereditary nephritis, polycystic kidney disease, sickle cell disease, renal stones, malignancy
Social • African American patients should be screened for sickle cell trait
• Smoking history and industrial exposure to tetraethylchloride, benzene and aromatic amines
ROS • HEENT: headache (HTN)
• CV: HTN, signs of anemia
• RESP: SOB, cough, hemoptysis, recent URTI (2-3 days: lgA nephropathy, 2-3 weeks: post streptococcal
glomerulonephritis)
or
• GU: pyuria and dysuria (UTI, bladder malignancy), cyclic hematuria in women that is most prominent during
shortly after menstruation (endometriosis of urinary tract), trauma
rashes,
• MSK / DERM: recent impetigo (post streptococcal glomerulonephritis), edema, bone pain (metastasis),
bruising, evidence of trauma
• Other: constitutional Sx of fatigue, wt loss and night sweats (tumor)

physical
1. General Approach
2. Inspection
• Look for signs of anemia (pale skin, pallor conjunctiva), signs of infectious/inflammatory conditions, rashes, bruising, evidence of
trauma
3. Percussion
• Costovertebral angle tenderness
• Pain along the spine or major bones (? metastasis)
4. Palpation
• Flank tenderness, suprapubic tenderness
• Lymphadenopathy: enlargement of supraclavicular and deep inguinal nodes (node of cloquet)
• Palpation of kidneys (e.g. for polycystic kidney disease)
5. Auscultation
• Renal bruits
6. SpecialTests
• Men: DRE and examination of external genitalia
• Women: pelvic exam
Investigations
1. Blood work
• CBC-D, electrolytes, urea, Cr, PT1 INR
2. Urine:
• Urine dipstick: to diagnose microscopic hematuria, pyuria, proteinuria
• Urine microscopy: to confirm presence of intact RBCs and RBC casts
• Quantitation of proteinuria (24hr urine protein or spot urine protein:creatinine ratio)
• Culture: 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
• Multidetector CT urography: preferred imaging technique of the upper tracts for patients >40 years or those <40 years 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
4. 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)
Treatment
1. Follow-up
• Patients with asymptomatic microscopic hematuria and negative radiology, cytology, cystoscopy, should be followed up with
urine cytology and urinalysis at 6, 12, 24,36 months. Some centers recommend repeat U/S and cystoscopy at one year in high-risk
patients with persistent hematuria
2. Referrals
• Glomerular disease: Nephrology
• Other causes of hematuria: Urology
References
1. Rose BD, Fletcher RH. Evaluation of hematuria in adults. In: Glassock Ri, O’Leary, MB Editors. UpToDate, Waltham, MA; 2009.
2. Assymptomatic Microscopic Hematuria in Adults: Summary of AUA best practice policy recommendation” Am Earn Physician. 2001; 63:1145-1154
3. Wollin T, Laroche B, Psooy K. Canadian Guidelines for the management of assymptomatic hematuria in adults. Canadian Urology Association Journal.
2009.
4. Cohen and Brown,” Microscopic Hematuria. The New England Journal of Medicine 2003; 348:2330-8.
5. Wein AJ, Kavoussi LR, Novick AC, et al. Campbell-Walsh Urology. gth ed. 2009; 3 (1): 77-80.

HERNIA
OriginalAuthors:Armin Badre, Sayf Gazala MD, Chris de Gara FRCS FACS
Station Objective
Approach to patients with the most common types of hernias including differentiation, diagnosis and effective management plan.
Differential Diagnosis Common Types of Hernia

Common conditions:
• Enlarged lymph nodes
• Pseudoaneurysms
• Saphena-varix
• Tumor
• Hydrocele
• Groin abscess
• Hematoma
2. Definitions Indstoeal Hernia
• Hernia: abnormal protrusion of an organ through the wail of the
cavity that normally contains it LJmblcaI Hernia
• Abdominal hernia: protrusion of a peritoneal sac through a
musculoaponeurotic barrier (e.g. abdominal wall) due to a fascial
defect
Classifications of hernia DIrect Ingulnal Hernia
3.
• Reducible hernia: ability to return the hernia contents to their usual Indirect Ingulnal Hernia
anatomic site either spontaneously or manually
• Irreducible (incarcerated) hernia: divided into 3 categories Fernoral Hernia
• Incarcerated and strangulated: vascular supply of the bowel
is compromised due to incarceration of hernia contents; look (
for signs and symptoms of ischemia and necrosis (fever, sick
appearance, pain out of proportion to findings)
• incarcerated and obstructed: look for signs and symptoms of bowel obstruction
• Incarcerated but not strangulated nor obstructed: contents are fixed within the hernia sac without any signs of strangulation
or obstruction
• inguinal hernia: two types (it is not important to differential between these clinically)
• Direct hernia is a protrusion through Hesselbach’s triangle and it’s due to weakness of anterior abdominal wail
• Indirect hernia is a protrusion through inguinal canal and is the result of persistent patency of the processus vaginalis
(congenital abnormality)
• Femoral hernia: through femorai canal
• Umbilicai hernia: through umbilicus
• Epigastric hernia: protrusion in the abdominal midline between the umbilicus and the xiphoid process
• Incisional hernia: through previous incision site
History
ID • Age, sex
CC • Swelling, fullness, or aching at the hernia site
HPI . Duration and site of hernia
• Pain: location, radiation, severity, duration, effect on daily activity
. Timing: post-op, extraneous exercise
RED FLAGS . Severe abdominal pain, fever, vomiting, constipation
PMHx • History of chronic illness
PSHx • Abdominal surgery, gyne surgery, inguinal surgery
Meds • Immunosuppressive medications, steroids
FHx • Hernias, connective tissue disorders
Social • Smoking, EtOH, occupation

ROS GI: abdominal pain, swelling
• GU: groin pain, swelling
• MSK/DERM: thigh pain
Risk Factors Increased intra-abdominal pressure (chronic cough, straining), obesity, ascites, congenital abnormalities (e.g. patent
processus vaginalis), heavy lifting, any condition that inhibit natural wound healing (e.g. smoking), smaller hernia
(increased risk of incarceration and strangulation)
Physical
1. General Approach
2. Inspection
• Look at the abdomen, previous surgical sites and groin for any swelling (ask the patient to cough or strain for better visualization;
it is important to note that hernia is not the only cause of cough impulse)
3. Palpation
• Surface anatomy: it is important to palpate ASIS and pubic tubercle (NOT pubic symphysis) as inguinal ligament is stretched from
ASlS to the pubic tubercle
• Palpate the hernia sac with finger pads and ask the patient to cough or strain
• A bulge felt below the inguinal ligament is most likely a femoral hernia
• A bulge in the inguinal canal is most likely an inguinal hernia
• Assess whether hernia is reducible or not
4. Auscultation
• Auscultate for bowel sounds (not a very reliable test)
5. Special tests:
• DRE: to help rule out other pathologies
Investigations
1. Blood work (is not necessary in most cases)
• CBC-D: leukocytosis with left shift may occur in strangulation
2. Radiology/Imaging (is not necessary in most cases especially if patients require urgent surgery)
• 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 perform PIE due to body habitus
Treatment
1. Emergent
• Emergency surgery is indicated for strangulated hernia, bowel perforation and peritonitis and should be performed within 6 hours
2. Elective surgery
• Goal: to prevent strangulation, symptom relief or cosmosis depending on risk-benefit assessment
• Note: femoral hernias should eventually be repaired in patients who are fit for surgery
3. Referrals
• General Surgery
References
1. Lawrence PF, editor. Abdominal Wall, including Hernia. In: Essentials of General Surgery. 4
th
ed. Baltimore: Lippincott Williams &Wilkins; 2006.
2. Brooks DC. Abdominal wall hernias. ln:Turnage R, editor. UpToDate, Waltham, MA; 2009.
3. Nicks BA, Askew K. Hernias. MedGenMed. 2010. hrtpi/emedicine.medscape.com/article/775630-overview. Accessed September 06,2010.
4. Beers MH, Porter RS, Jones TV, Kaplan JL, Berkwits M, editors. Abdominal Wall Hernias. In: The Merck Manual. 1 8th
ed. Whitehouse Station (NJ): Merck
Research Laboratories; 2006.

HIP (PAIN, FRACTURES, AND DISLOCATIONS)
20 I I Ed. Authors:Armin Badre, Colleen Weeks MD, Carlo Panaro MD FRCSC
Station Objective
management plan
Approach to patients with hip pain, fractures & dislocations including differentiation, diagnosis, and effective
fracture, acute
• Groin/anterior thigh pain: osteoarthritis, osteonecrosis, hip fracture, hip dislocation, pelvic fracture, femoral
, muscle strain, inflammatory arthritis, femoroacetab ular impingemen t, labral pathology
synovitis, septic arthritis, osteomyelitis
hip pain: trochanteric bursitis, hip abductor weakness (esp. gluteus medius), Meralgia paresthetica, iliotibial band
• Lateral
syndrome
hip extensor/rotator
• Posterior hip pain: lumbar degenerative disc disease, facet arthropathy, spinal stenosis, SI joint pathology,
muscle strain
, s,
• Anterior thigh pain not aggravated by palpation or repetitive flexion: inguinal hernia, GI pathology (appendicitis diverticuliso
IBD), GU pathology (UTI, nephrolithiasis, prostatitis), referred pain from lumbar spine
• Pediatric cases: SCFE, hip dysplasia, Perthes disease
History
ID • Age, sex, occupation

CC • Groin pain, anterior thigh pain, lateral hip pain, buttock pain, inability to weightbear
HPI • Onset/duration of pain: acute, chronic, progressive
• Provocative and palliating factors
• Radiation: can radiate distally down the femur or up to the pelvis
• Severity
• Site: refer to Common Conditions above
• Timing: morning stiffness of less than 30-60 minutes (osteoarthritis), pain exacerbated by activity and relieved by
rest (osteoarthritis), constant pain esp. at night (infection/ inflammation/ neoplasm),”start up pain”: pain that occurs
only with the first few steps after prolonged sitting/lying down (trochanteric bursitis/loosening of the cup or stem
from previous THR)
• Associated symptoms: fever, chills, sweats, fatigue, weight loss, involvements of other joints
RED FLAGS • Systemic symptoms, history of Ca, history of significant trauma
PMHx • Developmental dysplasia of the hip, osteoarthritis, inflammatory arthritis, previous femoral /pelvic fractures,
previous hip dislocations, trauma, pelvic irradiation, thrombophlebitis, syncope
PSHx • Previous THR, hip surgery, spinal surgery
Meds • Steroids (associated with osteonecrosis), antihypertensives (associated with hypotension and fall), Vitamin D, Ca,
bisphosphonates (? Association with fractures of proximal femur)
Social • EtOH (associated with osteonecrosis), smoking (associated with osteonecrosis), ambulatory status before the injury,
living situation
Physical
1. General Approach
• Vital signs (T, HR, RR, BP, 02 sat)
2. Inspection
• Gait: antalgic,Trendelenburg, short leg limp, non-weight bearing
• Note any leg length discrepancy, obvious deformity, shortening, rotational deformity, pelvic tilting, degree of lumbar lordosis,
spinal scoliosis, muscle atrophy
• Note any swelling, ecchymosis, skin changes, old incisions
• Inability to change position (e.g. climbing the examination table) suggest severe hip arthritis, osteonecrosis, metastatic disease,
dramatic muscle weakness, dramatic radiculopathy and infection
3. Palpation
• Palpate the iliac crest, greater trochanter, trochanteric bursa, ASIS, P515, ischial tuberosity, symphysis pubis, SI joint, lumbosacral

joint, sacrococcygeal joint, inguinal ligament
• Palpate hip flexors, abductor muscles for sign of pathology
• Point tenderness over the trochanteric bursa (-.1 inch posterior and superior to the greater trochanter) indicates trochanteric
bursitis
4. ROM
• Perform/measure full ROM of the hip noting patient’s tolerance of the maneuver and any endpoint stiffness (flexion: —1 200,
extension: —1 50, abduction: —40°, adduction: -30°, internal rotation: 300400, external rotation: _300400)
• 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 (<1 50) is the most sensitive sign of early osteoarthritis
• Patient with nondisplaced fracture have a positive log-roll test (pain on internal and external rotation of the limb)
5. Motor
• Examine lower extremity myotomes
• Muscle atrophy/weakness (radiculopathy/myelopathy/myopathy)
6. Sensory
• Examine lower extremity dermatomes
• Paresthesia/hypoesthesia of the anterolateral thigh without impaired reflexes or muscle weakness (meralgia paresthetica)
7. Reflexes
• Examine lower extremity reflexes
• Impaired reflexes (radiculopathy)
8. Special Tests
• Assess neurovascular status of the affected limb
• Trendelenburg test: positive test indicates hip abductor weakness, hip joint pathology
• Patrick’s Test (FABERE): positive test indicates hip joint pathology, SI joint pathology or ileopsoas spasm
• Impingement test for anterior and posterior impingement are highly sensitive for this syndrome
• Always examine the joint above and below and in case of fracture, always examine other extremities, pelvis and the spine looking
for other fractures/injuries
Investigations
1. Blood work
• In the presence of systemic symptoms: CBC-D, ESR, CRP
• In trauma: follow ATLS protocol
• 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
• In trauma follow ATLS protocol
• Hip aspiration: recommended with acute and severe hip pain or other evidence suggestive of infection
Treatment
1. Emergent
• Fluid resuscitation, continually reassess hemodynamic status
• Septic joint: surgical irrigation and debridement, empiric antibiotic therapy if patient is systemically unwell otherwise wait for
culture sensitivity
• Treat underlying condition with appropriate medical and/or surgical approach
• Investigate precipitating factors
3. Referrals
• Orthopedic surgery, rheumatology, sports medicine, general internal medicine (e.g. fall in elderly)
References
1. Anderson BC. Evaluation of the adult with hip pain. In: Fields KB, editor. UpToDate, Waltham, MA; 2009
2. Greene WB, editor.The Pelvis, Hip and Thigh. In: Netter’s Orthopedics. 1 g ed. Philadelphia: Elsevier mc; 2006
3. Ortiguera Ci, Raposo JM. Groin pain. Epocrates online [internet]. San Mateo (CA): Epocrates, mc; 2009. Accessed Sep. 10,2010
4. Burroughs KE, Walker KM. Hip fractures in adults. In: Eiff B editor. UpToDate, Waltham, MA; 2009
5. Petrisor BA, Bhandari M. Hip fractures. Epocrates online [internet]. San Mateo (CA): Epocrates, nc; 2009. Accessed Sep. 10, 2010

JAUNDICE
2017 Ed. Authors:Armin Badre, Leyla Asadi MD, Adriana Lozarescu MD FRCPC
OriginalAuthors:Juliet Emamaullee PhD, Michael McCall MD, AM James Shapiro MD PhD FRCSC FRCS (Eng)
Staton Objective
Approach to patients with jaundice including differentiation, diagnosis and effective management plan
• Careful clinical examination cannot detect jaundice until the serum bilirubin is >40l.lmol/L (twice normal upper limit)
• Unconjugated hyperbilirubinemia is caused by:
• Overproduction of bilirubin: e.g. extravascular and intravascular hemolysis, extravasation of blood in tissues,
dyserythropoiesis (e.g. megaloblastic and sideroblastic anemias, severe iron deficiency anemia, lead poisoning)
• Reduced bilirubin uptake: e.g. liver disease, CHF, Gilbert’s syndrome, drugs
• Impaired bilirubin conjugation: e.g. Gilbert’s syndrome, Crigler-Najjar syndrome, neonatal jaundice, hyperthyroidism, chronic
hepatitis, cirrhosis, Wilson’s dz
• Conjugated hyperbilirubinemia is caused by:
• Biliary obstruction: e.g. gallstones/Mirizzi’s syndrome, biliary stricture, PSC, neoplasm, pancreatitis, parasites (Ascaris
lumbricoides)
• Intrahepatic cholestasis: e.g. viral hepatitis, alcoholic hepatitis, NASH, PBC, PSC, cirrhosis, TPN, drugs, etc.
• Hepatocellular injury: e.g. neoplasm, metabolic liver dz, hereditary liver dz, infection, drugs, etc.
Hstory
ID • Age, sex
CC • Yellow discoloration of skin, sciera or mucus membranes
HPI . Timing (acute vs. subacute), pain (e.g. back, abdomen), pruritis
RED FLAGS • Painless jaundice in elderly with constitutional Sx (cancer), febrile jaundice, altered mental status, GI bleeding
(gross/occult), severe abdominal pain
PMHx • Hepatitis, cirrhosis, gallstones, hemoglobinopahty, G6PD deficiency, IBD, infiltrative disorders, HIV, travel hx
PSHx • Abdominal surgery (esp. gallbladder surgery)
Meds • Drugs and toxins that affect the liver including herbal medications
FHx • Liver disease, hemolytic disorders
Social • EtOH, exposure to toxic substances, IV drug use, sexual Hx
ROS • GI: abdominal pain, hepatitis risk factors, recent history of pale stools (obstructive jaundice)
• GU: dark urine
• MSK / DERM: joint pain and swelling, ecchymoses, petechiae, purpura
• Other: wt loss, HIV status, Charcot’s triad (ascending cholangitis)
Physical
1. General Approach
• Vital signs (T, HR, RR, BP, 02 sat)
• Mental status assessment
2. Inspection
• Scleral icterus, yellowing of oral mucosa membranes (under the tongue, hard palate)
• ABD: ascites, surgical scars, caput medusa
• MSK/DERM: Dupuytren’s contractures, asterixis, palmar erythema, spider nevi, xanthomas, clubbing, leukonychia,
hyperpigmentation, ecchymoses, petechiae, purpura
• In men, check for testicular atrophy and gynecomastia
3. Auscultation
• Presence or absence of bowel sounds

4. Percussion
• Percuss for the edge and span of the live, Castell’s sign, flank dullness, shifting dullness
5. Palpation
• Palpate for hepatosplenomegaly, masses, liver nodularity, abdominal tenderness
• Courvoisier sign (obstruction of biliary tree), Murphy’s sign (cholecystitis)
• Lymphadenopathy: Virchow’s node (L supraclavicular node) and Sister Mary Joseph’s node (periumbilical node) associated with GI
malignancy
6. Special Tests
• DRE: to look for gross or occult blood
Investigation
1. Blood work
• Serum total bilirubin, serum unconjugated bilirubin
• ALP, ALT, AST, PT, albumin
• If normal: jaundice associated with hemolysis or inherited disorders of bilirubin metabolism
• Predominant elevation of ALP compared to AST and ALT: biliary obstruction or intrahepatic cholestasis
• Predominant elevation of AST and ALT: intrinsic hepatocellular disease
• AST/ALT>2: strongly suggests the diagnosis of alcoholic hepatitis
• Prolonged PT that corrects with vitamin K administration: impaired intestinal absorption of fat-soluble vitamins (obstructive
jaundice)
• Abdominal U/S: screening of choice for diagnosis of obstructive jaundice of unknown etiology
• EUS or MRCP: indicated for diagnosis in patients with high expectation of extrahepatic obstruction
3. Special Tests
• Viral hepatitis serology
• Antimitochondrial antibody (primary biliary cirrhosis)
• Antinuclear, anti-smooth muscle and liver-kidney microsomal antibodies (autoimmune hepatitis)
• Ferritin, serum iron markers (iron, transferrin saturation, and total iron binding capacity) (hemochromatosis)
• Serum levels of ceruloplasmin, 24-hour urine copper (Wilson’s disease)
• Alpha-i antitrypsin activity (alpha-i antitrypsin deficiency)
Treatment
• The underlying disease and any complications of it should be treated appropriately
2. Referrals
• Gastroenterology, Medicine, General Surgery
References
1. Chowdhury NR, Chowdhury JR. Diagnostic approach to the patient with jaundice or asymptomatic hyperbilirubinemia. In: Chopra 5, editor. UpToDate,
Waltham, MA; 2009.
2. Chowdhury NR, Chowdhury JR. Classification and causes of jaundice or asymptomatic hyperbilirubinemia. In: Chopra 5, Rand EB, editors. UpToDate,
Waltham, MA; 2009.
3. Beers MN, Porter RS, Jones TV, Kaplan JL, Berkwits M, editors. Jaundice. In: The Merck Manual. 1 8” ed. Whitehouse Station (NJ): Merck Research
Laboratories; 2006.
4. Weisiger RA. Hyperbilirubinemia, conjugated. www.emedicine.com, Accessed 1 November 2009.

KNEE (PAIN, FRACTURES, AND DISLOCATIONS)
201 I Ed. Authors: Bobak Maghdoori, KhaIedAI-Monsoori MD, NadrM Jomho MD, PhD, FRCS(C)
Station Objectives
pain, fracture, and dislocation.
To systematically examine, evaluate, and manage a patient presenting with acute or chronic knee
• Traumatic Injury:
fractures
• Knee: cruciate or collateral ligament sprains/tears, meniscus tears, patellar dislocations, and
• Atraumatic Onset:
band syndrome, medial plica
• Knee: arthritis, tendonitis, bursitis, septic joint, Baker’s cyst, patellofemoral syndrome, iliotibial
syndrome, bone tumor, Charcot joint, Osgood-Schl atter disease, osteochondri tis dissecans, and referred pain (lumbar nerve
root “sciatica’: hip pathology)
2. Pathological (underlying etiology):
metabolic
• Tumours (primary or secondary, osseous vs. soft tissue), osteoporosis, inflammatory, infectious, endocrine,
3. High mortality/mo rbidity:
• Metastatic cancers, bone or soft tissue tumors, fractures resulting in reduce mobility (esp in the elderly)
History
ID • Patient’s name, age, and sex

CC • Knee pain
HPI • OPQRST (Onset, Provocation/Palliation, Quality, Region/Radiation, Severity, Time (history))
• Mechanism of injury (note: low energy levels may indicate an underlying pathological process)
• History of any joint pathologies or previous trauma
• History of swelling, stiffness, locking or catching (meniscal pathology), crepitus, instability or giving way (ligament
pathology), audible “pop’: stiffness (duration and timing) and night pain
• Changes in sensation, strength, ROM, and ability to weight bear
RED FLAGS • Fever, chills, night sweats, wt 4, night pain —* must rule out cancer and infection
PMHx • Relevant medical conditions including arthritis, diabetes mellitus, bleeding disorders, neurologic disorders, cardiac
or respiratory diseases, metabolic/inflammatory/endocrine disorders, heart disease, pulmonary disease, prior
malignancy among others
• Falls: Underlying etiology important for prevention (syncope/pre-syncope/focal weakness/seizure)
PSHx • Previous surgeries (specifically to the joint in question and in general)
FHx • Arthritis, bone cancer, other relevant diseases
Meds • Include prescription, OTC, and herbal medications
Allergies • Specifically to antibiotics and analgesics
Social • EtOH use, smoking, physical abuse, sexual history (STI risk factors)
ROS • HEENT: headaches, vertigo, visual disturbances, fever, mental status change, conjunctivitis
• CV: palpitations, chest pain
• RESP: SOB, cough
• GI: 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
1. General Approach (Note: Always examine the joint above and below the area of concern)
• ABCDE, 10 and 20 surveys if necessary, vitals, general appearance of the pt
• Remove clothing/splints/casts/dressings/etc. from the affected area and drape the patient appropriately
2. Inspection
• MSK: SEADS (comparison to opposite joint), open fractures, laceration, bleeding, observe gait, alignment
3. Palpation

________________________
• MSK: palpate for any localized tenderness/deformities/warmth/joint effusion, all bony prominences, specific tendons, joint line
• VASC: colour, regional pulses (popliteal, post tibial and dorsalis pedis), capillary refill, and temperature difference
• NEURO: sensation (central dermatomes and peripheral nerves including saphenous, sural, superficial and deep peroneal and
tibial) and muscle strength/function, reflexes (patellar, Achilles, Babinski)
4, Function
• Joint ROM active first and then passive
—
Ottawa Knee Rules
• Muscle function knee (quads, hamstrings)
—
Knee Xray required if knee injury + 1 of the following:
5. Special Tests • >55y/o
• Ligament stability (knee): Lachman test, anterior/posterior drawer test, • Isolated tenderness of the patella
valgus/varus stress test • Tenderness at the head of the fibula
• Meniscal tests: McMurray test, Apley grind test • Inability to flex to 90 degrees
• Patellar subluxation apprehension test • Inability to wt bear for 4 steps both at time of injury
• Thompson test Achilles tendon integrity
—
and in ED
Investigations
1. Blood work (if indicated)
• CBC-D, electrolytes, glucose, Cr, urea
• PT INR, PT1 Mg, PO, Ca, Alk phos, serum protein electrophoresis, PSA, ESR, CRP
2
2. Radiology/Imaging Compartment Syndrome
• Ottawa Knee Rules (see box) Pain (out of proportion)
• XR of site including proximal and distal joints Paraesthesia
• CT or bone scan if occult fracture suspected Pallor
• MRI if ligamentous or meniscal pathology suspected Paralysis
3. SpecialTests Pulselessnescs
• Bone mineral density (osteoporosis)
• Bone scan (osteomyelitis, bone mets, bone tumors)
• Arthrocentesis (investigate joint effusion, 4Cs: Cell count, Culture, Cell stain, Crystals; note that hemarthrosis does not necessarily
require aspiration)
Treatment
1. Emergent
• ABCDE, life before limb; once stable, tend to injuries that are not life threatening
• Reduce open fracture or dislocation (ASAP to prevent neurological deficit or vascular /skin compromise and cartilage injury)
• Irrigation, debridement, sterile covering, tetanus prophylaxis and antibiotics (open fractures)
• Pain control and immobilize (splint, half cast, full cast)
• Reduce swelling: rest, ice, compression, and elevation
• Ambulation aids and instruction (if required)
3. Further workup (may be required for insidious onset etiologies)
4. Surgical
• Can include fracture fixation, arthroscopy, arthrotomy, ligament r/c, etc
5. Follow-up
• Instructions to return if swelling, cyanosis, significant in pain, ,t. sensation, redness
6. Referrals to consider
• Emergent Orthopedic surgery for compartment syndrome, circulatory or neurologic compromise, displaced fractures, open
fractures, and joint dislocations, septic arthritis, necrotizing fasciitis
• Rheumatology, Infectious Diseases, Physiatry, Neurology, Oncology (if indicated)
7. Complications:
• DVT, pulmonary embolus, fat embolus, ischemic contracture, nonunion, malunion, joint stiffness, traumatic arthritis, AVN,
osteomyelitis, septic arthritis, compartment syndrome, amputation
References
1. Tintinalli JE et aI.Tintinalli’s Emergency Medicine, A Comprehensive Study Guide. 6th ed. USA: The McGraw-Hill companies, Inc; 2004.
2. Bickley IS et al. Bates’Guide to Physical Examination and HistoryTaking. 10th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2009.

NECK MASS/GOITER
2011 Ed. Authors: Shawna Pandya, KalAnsari MD FRCSC, Diplomate (ABO), Diplomate (ABFPRS)
OriginalAuthors:Abdullah Saleh, Peter Dziegielewski MD, Hamdy El-Hakim MD FRCS(Ed) FRCS(ORL-HNS)
Station Objective
To list the relevant history, exam, initial investigations and management for a patient with a neck mass.
• Thyroid: Autoimmune (Graves Hashimoto’s), inflammatory (subacute/radiation thyroiditis), neoplastic (papillary, follicular,
medullary, Hurthle cell, anaplastic), parathyroid, post-partum, 12
• Congenital: Cysts (thyroglossal duct, dermoid, branchial cleft), cystic hygroma, hemangioma, laryngocoele, sternocleidomastoid
tumor of infancy, teratoma
• Cystic: thymic, epidermal & sebaceous gland cysts; plunging ranula
• Inflammatory/infectious: lymphadenopathy (reactive, primary, autoimmune), abscess, TB, cat scratch (Bartonella), Kawasaki,
infectious mononucleosis, sialolithiasis+/-infection
• Neoplastic: malignant (lymphoma/leukemia, skin Ca, salivary gland tumor (benign too), neuroblastoma, metastases), Benign:
(schwannoma, neuroma, paraganglioma, carotid body, lipoma)
• Also: trauma (hematoma, post-operative seroma, vascular aneurysm), autoimmune
• <40y.o: inflammatory> congenital > neoplastic
• > 40y.o: neoplastic> inflammatory> congenital
• Thyroid: multinodular goiter, thyroid nodules (5% of population), Graves, Hashimoto
3. High Mortality
• Anaplastic carcinoma, metastatic 5CC, lymphoma
History
ID • <30 and > 60 y/o — new mass more concerning
CC • “I have noticed a lump in my neck”
HPI • Location/onset/inciting event (e.g. trauma, URTI, HIV/TB)/prior Hx
• Growth: slow/fast (<2 wks suggests malignancy), up/down, fluctuant/constant, pain/tenderness, lumps/bumps
on other parts of body, uni/bi-lateral
• Hx dysphagia, odynophagia, hoarseness, SOB, stridor/wheezing, hemoptysis, halitosis = upper airway
malignancy/recurrent laryngeal nerve invasion
• Hx 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, wt
loss, palpitations
PMHx • Radiation, Ca Hx: breast, lung, kidney, melanoma, head & neck, lymphoma
PSHx • Thyroidectomy or any neck surgery
PO&GHx • Pregnant or post-partum
Meds • Thyroxin, propylthiouracil, Li, 13-blockers, allopurinol, penicillins, phenytoin
FHx • Thyroid Ca, MEN-Il, head and neck Ca, paraganglioma, neurofibromatosis
Social • Smoking, EtOH, travel (lyme disease risk, TB, fungal infection, typhoid), sex (HIV), saw dust, chemical fumes,
beryllium, silicone, radiation, cat scratch
ROS • HEENT: diplopia, sensory changes, difficulty speaking, focal weakness
• RESP: SOB/stridor, hemoptysis
• GU: nodal swelling in groin
• MSK / DERM: skin lesion/melanoma (sun exposed areas), tremors
Risk Factors • FHx, Ca, radiation Hx, smoking/EtOH, chemical fume exposure,tage

P ysical
4. General Approach (Introduction, wash hands, vitals, permission, stability)
5. Inspection
• Location (midline/lateral/distal), skin (radiation exposure, breakdown, infection, inflammation)
• Check externally & internally (ears, head/neck skin, oral cavity, etc.) for lesions, symmetry, deformations via rhinoscopy, otoscopy
and oral cavity exam, signs of cachexia, SOB
6. Palpation
• Size, mobility (fixed/mobile), nodularity/consistency (rubbery/hard), pulsatile, involvement (local/distal), single/confluent, tender,
bimanual palpation of floor of mouth & tongue
7. Auscultation (only if mass is pulsatile, then auscultate the mass and do a CV exam)
• Heart sounds, murmurs, thyroid/carotid bruits (r/o these causes)
8. Special Tests
• Tongue protrusion —* elevation of thyroglossal duct; swallow —* elevation of thyroid mass; valsalva —* expansion of laryngocoele
Investigations
1. Blood work & infectious disease investigations
• , HIV/EBV serology, Monospot/throat swab, peripheral blood smear, Mantoux skin test
CBC-D, TSH/freeT3/T4, PTH/Ca
2
• Autoimmune work-up: ANA, ACE level, ESR, CRP, RF, c & p-ANCA
• U/S, contrast CT (head/neck/chest), CXR, MRI, MRA (carotid body tumor), PET, mammogram
3. SpecialTests
• 1231 scintiscan, urine catecholamines
• FNAB/open Bx if necessary, aerodigestive tract laryngoscopy, bronchoscopy, esophagoscopy + Bx
Treatment
1. Emergent
• Airway obstruction due to mass effect requires emergent intubation or tracheosotomy
• Medical : Lifestyle (4 EtOH & smoking to prevent recurrence), ABx, Ca chemotherapeutics
• Surgical: l&D abscess, FNAB (preferable to excisional biopsy), regional excision/dissection
• Radiation
• Combination of the above
3. Follow-up
• Endoscopy, post-op 131j scan (DxJTx)
4. Referrals
• Otolaryngology, General Surgery, Infectious Diseases
References
1. Schwetschenau E, Kelley DJ. The adult neck mass. Am Fam Physician. 2002 Sep 1 ;66(5):831 -8.
2. Fried MR Neck Mass. Merck Manual Online. 2008 Oct. [cited October 7,20101. Available from: htto:/Iwww.merck.com/mmpe/sec08/ch089/chO89d.html.

PEDIATRIC STRABISMUS
2071 Ed. Authors: Terence Kwan-Wong, Chris Hanson MD, Christopheri. RudniskyMo MPH FRCSC
OriginalAuthors: Nawaaz Nathoo, Chris Hanson MD, Christopheri. RudniskyMD MPH FRCSC
Station Objective
Students are expected to determine the type of strabismus present in a child, and to determine the timing of any interventions needed.
Students should also be able to counsel parents about the need for timely management in order to prevent the development of
amblyopia.
• Categories of ocular misalignment
• Tropia (manifest) —* apparent during binocular vision
• Phoria (latent) —* only apparent during monocular vision (i.e. when binocularity is interrupted)
• Types of ocular misalignment
• Esodeviation —* inward, nasal turning of the eye (esotropia, esophoria)
• Types: congenital, accommodative, non-accomodative, VI nerve palsy
• Exodeviation —* outward, temporal turning of the eye (exotropia, exophoria)
• Types: basic exotorpia, Ill nerve palsy
• Hyperdeviation —* upward, superior turning of the eye (hypertropia, hyperphoria)
• Pseudostrabismus —* not a true strabismus but mimics esodeviation because of wide nasal bridge
History
ID • Ageandgender
CC • Parents notice that child’s eyes are not straight
HPI • Onset: age
• Duration: gradual/sudden/intermittent (if intermittent, timing is important —* e.g. only when fatigued, happens
later in the day)
• Nature of deviation: direction of misalignment/diplopia/which eye seems to deviate
• Provoking factors: gaze position/focus distance (near vs. far)/fatigue
• Visual function: watching TV/reading/ADL’s/clumsiness/walking into objects/school activities/attentiveness
RED FLAGS • Sudden onset (especially after head trauma)
• Associated neurological symptoms
PMHx • Prior strabismus
• Cerebral palsy
• Previous trauma
PSHx • Ocular
• Intracranial
PO&GHx • Prematurity/small for gestational age
• Complicated delivery: vacuum or forceps delivery, stat cesarean
• Genetic disorders
FHx • Strabismus
• Glasses at a very young age; especially relevant if hyperopic
• Genetic disorders
• Neurological disorders
Social • Functioning at level appropriate for age
• School performance
• Self-esteem / peer considerations
Physical
1. General Approach
Vision testing for each eye independently
• General testing principles: acuity, visual field, diplopia, pupil reactivity, EOM in six cardinal positions of gaze
• Depending on the age of the child, may perform different tests such as letter naming (Snellen, ETDRS), picture visual acuity

(Allen, Lea), Sheridan Gardner letter matching visual acuity, illiterate E visual acuity game; in very young children, may simply
note if child is fixing and following objects
• Screening neurological & cranial nerve exams
2. Inspection
• Obvious ocular misalignment
• Also consider features that suggest pseudostrabismus (e.g. wide nasal bridge, epicanthal folds, etc.)
• Abnormal head position: rotation/tilt may suggest compensation for misalignment
3. Special Tests
• Corneal light reflex: with the child looking at a light, the reflection should be in the same location on each pupil
• Cover/uncover test: perform for distance and near in primary position. To perform cover/uncover test:
• Ask patient to fixate on object in distance (or near)
• Cover one eye with occluder, and observe uncovered eye for movement (tests for tropia)
• Remove occluder and observe if covered eye refixates or not
• Repeat with other eye
• Alternate cover test: perform in distance and near in primary gaze position, and if necessary, in different gaze positions, and with
head tilted left/right to help observe variations in strabismus and to help delineate cause. To perform alternate cover test:
• Ask patient to fixate on object in distance (or near), and cover one eye
• As occluder is moved to opposite eye, observe previously covered eye (tests for combined tropia plus phoria)
• Repeat multiple times to fully dissociate eyes and assess amount of strabismus present
• Repeat in other gaze positions as necessary to determine if deviation is comitant (equal in all gaze positions)
• Ophthalmoscopy and slit lamp exam: assessing health of each eye
• Check pupils for reactivity and relative afferent papillary defect (RAPD)
• Check for equal red light reflex
• Key findings to suggest underlying cause of strabismus and amblyopia are diseases which disrupt the anterior visual pathway
from the eyelids and cornea to the optic nerve head, including:
• Ptosis • Lens opacity / cataract • Retinal disease
• Corneal opacity • Vitreous opacity • Optic nerve disease
• Unequal or
bilaterally high
refractive error
Investigations
Radiology/Imaging
• MRI head/orbits if trauma is suspected or onset is acute
Treatment
Treatment Options: depends on underlying cause of strabismus. Requires involvement of opthalmologist.
• Medical
• Occlusion therapy: patching stronger eye for 4-1 2h per day will improve acuity in weaker eye, but will not correct
misalignment
• Optical devices (glasses, prisms): improves symptoms while wearing glasses but does not correct underlying misalignment
• Pharmacological: cycloplegic drops such as atropine treat accommodative strabismus, botox injections into extraocular
muscles can be used as temporary solution (long term effects unknown)
• Orthoptics: eye exercises have been shown to be effective in certain types of strabismus
• Surgical
• Recession/resection of extraocular muscles
• Correction of orbital defects
• Conservative
• Occasionally used for traumatic misalignments —+ observe for 6 mo for improvement
2. Referrals
• Ophthalmologist for detailed assessment and treatment plan
References
West CE, AsburyT. Strabismus. In: Riordan-Eva P. Whitcher J. Vaughan & Asbury’s General Ophthalmology. New York: McGraw-Hill; 2007.

PUPIL ABNORMALITIES
2011 Ed. Authors: Terence Kwan-Wong, Chris Hanson MD, Christopheri. RudniskyMD MPH FRCSC
OriginalAuthors: Nawaaz Nathoo, Chris Hanson MD, Christopheri. RudniskyMD MPH FRCSC
Station Objective
Students are expected to be able to differentiate the different types of pupil abnormalities, and to determine whether there has been
previous ocular inflammation, trauma, loss of vision, or eye pain in order to begin ruling out local disorders.
• Unilateral or bilateral pupillary abnormality
• Anisocoria — unequal pupil size
• Corectopia — displacement of pupil from its normal, central position
• Asymmetrical pupillary reaction
• Physiologic anisocoria
• Traumatic mydriasis
• Pharmacological (e.g. mydriatics, mioptics, opioids)
• Adie’s tonic pupil
• CN Ill palsy with pupil dilation
• Extrinsic compression — often due to intracranial aneurysm
• Brainstem stroke
• Closed angle glaucoma
• Homer’s syndrome
History
ID • Age, gender
CC • Photophobia
• Visual changes
• Asymmetrical pupils
• Pain
HPI • Problems with vision — acuity, near vision, 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 Ill palsy with pupil dilation and diplopia —* aneurysm ± rupture
• Symptoms consistent with closed angle glaucoma (NN, pain)
PMHx • Neurological symptoms
• Stroke / CV disease
• Ocular —* ntis, glaucoma, central retinal vein occulsion
• Recent illness —* Adie syndrome
• Vasculitis — temporal arteritis, polymyalgia rheumatica
PSHx • Ocular —* e.g. cataract extraction, glaucoma
Meds • Attempt to elicit full list of meds to r/o pharmacologic anisoconia
FHx • Ocular disease, CVA, Ml, DM, glaucoma
Social • Recreational drug use, smoking

Physical
1. General Approach
• 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
• Vision testing for each eye
• Acuity, visual fields, diplopia, pupil reactivity, range of motion
• Screening neurological & cranial nerve exams
2. Inspection
• Assess pupil size, shape and reactivity in room light, to a bright stimulus, in dim light and to an accommodative target
3. Special Tests
• Swinging flashlight test — assesses for relative afferent pupillary defect (RAPD)
• Shine focused light source on one eye for 1-2 seconds, 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, which is 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 opthalmologist)
• Cocaine —* failure of eye to dilate = Homer 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
• Gonioscopy —* assess ocular (cornea-iris) angle to help determine presence of glaucoma
nvestigation
1. Blood work
• Usually indicated if features suspicious for systemic disease are present on exam
• MRI —+ suspected intracranial tumour
• MR / CT angiogram —* suspected intracranial aneurysm
• CT head / orbits —* trauma
3. SpecialTests
• Refer to physical section
Treatment
1. Emergent
• Cerebral aneurysm / intracranial tumour —+ neurosurgery referral
• Dependent on etiology of pupillary abnormality
3. Referrals
• Neurology
• Ophthalmology
• Neurosurgery
Refere ces
1. Friedman Dl, Trobe J, Pupillary Abnormalities. In: MedLink Neurology; 2010.
2. Riordan-Eva P, Hoyt W R Neuro-Opthalmology. In: Riordan-Eva P, Whitcher J. Vaughan & Asbury’s General Ophthalmology. NewYork: McGraw-Hill; 2007.

RED EYE
OriginalAuthors: Darwin Wan, Dr. Christopher Hanson MD, Dr. Christopher RudniskyMD FRCS
Sta ion Objective

Create a differential diagnosis for red eye and determine urgency of referral to Ophthalmology.
• Eyelid: dry eye (environmental, blepharitis), bacterial (hordeolum, preseptal cellulitis), inflammatory (contact dermatitis, atopic
dermatitis)
• Conjunctiva: bacterial (acute bacterial conjunctivitis, chlamydia), viral (viral conjunctivitis, epidemic keratoconjunctivitis),
inflammatory (pinguecula, pterygium), injury (chemical toxicity/burn, blunt/penetrating trauma), allergic conjunctivitis, neonatal
conjunctivitis, subconjunctival hemorrhage
• Lacrimal System: infectious (dacryoadenitis, dacryocystitis), naso-lacrimal duct obstruction
• Cornea: bacterial (bacterial keratitis ie. streptococcus, staphylococcus, pseudomonas), viral (HSV, HZV), fungal/parasitic
(fungal keratitis, acanthamoeba keratitis), inflammatory (peripheral ulcerative keratitis, contact lens overwear syndrome), injury
(chemical toxicity, flash burn, abrasion, foreign body, recurrent cornea) erosion)
• Sclera: inflammatory (scleritis, episcleritis)
• Uveitis: idiopathic, inflammatory (ankylosing spondylitis, IBD, psoriatic arthritis, Reiter’s syndrome), bacterial (syphilis, TB), viral
(HSV, HZV), fungal/parasitic (fungal, toxoplasmosis), injury (trauma)
• Orbit: bacterial (orbital cellulitis), injury (retrobulbar hemorrhage), inflammatory (thyroid orbitopathy)
• Globe: injury (globe rupture, retrobulbar hemorrhage)
• Acute angle closure glaucoma
• Endophthalmitis
• Bolded diagnoses are emergent and have a high morbidity and mortality
History
ID • Age, gender, occupation
CC • Red eye
HPI • Characterize onset, duration, symptoms of red eye, deep or superficial
• Trauma: foreign body, 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, NN
• Contact lens use
RED FLAGS • Severe ocular pain, acute visual loss, traumatic etiology, chemical burn
PMHx • Ankylosing spondylitis, psoriasis, IBD, Reiter syndrome, sarcoidosis,TB, syphilis, Behcet’s, HZV
PSHx • Eye surgery
PO&GHx • Chlamydia, herpes simplex, gonorrhea, syphilis
Meds • Any medications, including eye drops
Allergies • Hayfever, giant papillary and contact conjunctivitis, allergies to eye drops
FHx • Inflammatory conditions, glaucoma esp angle closure glaucoma, recent ill contacts
Social • Contact lens Hx: hard or soft lens, disposable, weekly or monthly, length of actual wear, sleep in contacts, swim or
hot tub in contacts, method of lens cleaning
ROS • HEENT: recent URTI
• CV: hypertension, bleeding disorder
• RESP: URTI
• GI: IBD, lBS symptoms
• GU: urethritis, STIs
• MSK / DERM: psoriasis, skin rash, arthritis, lower back pain
Risk Factors • Contact lens wear, chemical/allergen exposure, injury, infection/conditions above, surgery

Physical
1. General Approach
• Ask permission to perform exam, wash hands, position patient
• Focus physical exam according to the history as red eye has a large differential, watching for red flags (severe mucopurulent
discharge, distorted or unreactive mid-dilated pupil, corneal opaciflcation or ulcer, hyphema, hypopyon, Seidel sign (aqueous
humour leak from cornea), proptosis
2. Inspection
• Lookfor signs of:
• Trauma (conjunctival laceration, foreign body, distorted pupil, Seidel sign)
• Infection (discharge, corneal opacity, ulceration, uveitis)
• Irritation (abrasion, fluorescein exam, localized conjunctival injection)
• Angle closure glaucoma (measure intraocular pressure, corneal edema)
3. Tests
• Measure visual acuity
• Perform tests of optic nerve function: visual fields, pupil reactivity & shape, extraocular motility, photophobia, signs of proptosis
• Examine from inside out: the skin and periorbita, slit-lamp exam to look at lids and lashes, conjunctiva, cornea, iris, anterior
chamber for cells and flare, fundoscopy
• Special tests: fluorescein staining, tonometry if available
Investigations
1. Blood work and lab testing, radiology/imaging
• Depends on Hx and DDx
• Conjunctivitis: C&S
• Infectious keratitis: refer to ophthalmology for corneal scraping
• Uveitis, scleritis, episcleritis: refer to ophthalmology for appropriate workup
• Orbital cellulitis, thyroid-related orbitopathy and retrobulbar hemorrhage: CT orbits
• Trauma: orbital XR, CT orbits
• Endophthalmitis: refer to ophthalmology for vitreous tap and injection of antimicrobials
Treatment
1. Emergent
• Globe rupture: refer to Ophthalmology
• Acute angle closure glaucoma: refer to Ophthalmology
• Infectious keratitis esp in contact lens wearers: refer to Ophthalmology
• Chemical burn: flush eye with Morgan lens and normal saline or Ringer’s lactate to normal pH 7
• Endophthalmitis: refer to Ophthalmology
• Orbital cellulitis: refer to Ophthalmology
2. Non-emergent
• Dry eye: warm compresses, tear drops QID
• Conjunctivitis: viral (cold compresses, hand hygiene), bacterial (Polysporin drops QID x 5/7), allergic (cold compresses,
antihistamines), chemical (withdraw aggravating agent, tears)
• Foreign body on cornea: remove with burr or needle tip, Polysporin drops QID x 5/7, refer to Ophthalmology if unable to remove)
• Preseptal cellulitis: appropriate antibiotics depending on likely offending bacteria
• Marginal keratitis: refer to Ophthalmology
• Uveitis, scleritis, episcleritis: refer to Ophthalmology
References
1. Cronau H, Kankanala RR, MaugerT. Diagnosis and Management of Red Eye in Primary Care. Am Family Physician. 2010 Jan 15:81(2): 137-44.
2. Mahmood AR, Narang AT. Diagnosis and Management of the Acute Red Eye. Emerg Med Clin N Am. 2008 Feb:26(1): 35-55.
3. Sethuraman Li, Kamat D.The Red Eye: Evaluation and Management. Clin Pediatr. 2009 Apr 8:48(6): 588-600.
4. Wirbelauer C. Management of the Red Eye for the Primary Care Physician. Am I of Med. 2006 Apr:1 19(4): 302-6.

SCROTAL MASS & SCROTAL PAIN
2071 Ed. Authors: Brendan Diederichs, Winston Teo MD
OriginalAuthars: Michael Metcalfe, Conrad Maciejewski MD, James Metcalfe MD FRCSC
Station Objective
Recognize the importance of early diagnosis and treatment of scrotal pain. Differentiate between scrotal masses and recognize features of a
testicular cancer. A student must recognize that a possible testicular torsion is a surgical emergency.
1. Differential Diagnosis:
• Intratesticular mass: testicular malignancy, germ cell tumor, sex cord tumor, lymphoma, hydrocele
• Extratesticular mass: varicocele (bag of worms), inguinal hernia, spermatocele, scrotal edema
• Pain: testicular torsion, epididymitis, orchitis, abscess or Fournier’s gangrene, referred (STI, ureteric colic...)
• Testicular torsion
• Must be ruled out in the setting of scrotal pain
• Testicular malignancy
• Fournier’s gangrene
• Strangulated inguinal her
History
ID • Age
CC • Painless scrotal mass/heaviness vs. scrotal pain
HPI • Onset (suddenly over hrs vs. days vs. chronic), delay in presentation is a common issue (NB: 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: NN,
RED FLAGS • Acute onset, diffusely tender scrotum, history of minor trauma, pain woke from sleep (torsion)
• Fever, wt J, night sweats (malignancy)
PMHx • Undescended testicle at birth
PSHx • Hernia, orchidectomy, orchiopexy
FHx • Ca
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 dz may cause cough/SOB/hemoptysis
• GI: change in BM (herniated bowel), NN, 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
Risk Factors • Malignancy: cryptorchid testis (undescended testis), exogenous estrogen to mother during pregnancy, previous
testicular cancer
• Torsion: bell-clapper deformity (congenital absence of posterior anchoring of the gubernaculum)
Physical
1. General Approach
• Prior to focusing on the genitalia, state that a full PE will be performed, look for systemic signs of testicular Ca/infection/other
trauma

• Examination of the genitalia should be performed in a warm room with the Pt relaxed and fully exposed, Pt needs to be examined
while lying down and standing
2. Inspection
• Systemic signs of testicular Ca: wt J, gynecomastia, supraclavicular lymphadenopathy
• Leg edema: retroperitoneal mass may cause peripheral leg edema
• Signs of trauma or infection to the testicle (erythema, discharge, ulcer, chancre, laceration, hematoma)
• Swelling: general scrotal vs. gential and unilateral vs. bilateral testicular
• Horizontal lying testicle may indicate torsion
3. Palpation (4 key points): intra vs. extratesticular, tenderness, transillumination, and change in size during valsalva
• Supraclavicular lymph nodes (note: testicular tumors drain to retroperitoneum)
• Inguinal region: masses, nodes, pulses
• Glans penis & urethral meatus: for discharge, sores, chancre
• Bimanual exam of each testicle: hold testicle between finger and thumb with each hand, pinch the epididymis at the posterior
aspect of the testicle, start inspection with the testicle, examine for any palpable masses
4. Auscultation
• Bowel sounds may be auscultated in the scrotum in the setting of indirect inguinal hernia
5. Special Tests
• Transillumination: masses must be transilluminated (hydrocele/spermatocele will transilluminate, tumors/varicoceles/blood will
not transilluminate). To transilluminate, dim the lights (do not make the room completelydark while Pt has genitalia exposed) and
hold a flash light to the mass, observe whether or not the mass transilluminates
• Valsalva, cough, or standing: will enlarge hernia or varicocele if present with subsequent resolution in supine position. Check for
cremasteric reflex (usually absent in testicular torsion)
Investigations
1. Blood work
• AFP, 3-hCG and LDH
• 90% of testicular tumors will have either t AFP or 13-hCG
• CBC-D, electrolytes, urea, Cr
• U/A R&M C&S, urethral swab/genprobe if indicated
• Scrotal U/S: include as a part of the testicular PE, hypoechoic intratesticular lesions ± demonstrable hypervascularity suggests
testicular cancer, doppler scrotal ultrasound for torsion or epididymitis/orchitis
• If scrotal U/S positive for possible cancer, obtain CXR, CT abdomen and pelvis
• If torsion suspected on Hx alone, pt must go for surgical exploration within 6 hrs of onset
• Any primary intratesticular mass is a cancer until proven otherwise, and necessitates radical orchiectomy
• Transscrotal biopsy is contraindicated as lymphatic drainage of scrotum differs from testicles
Treatment
1. Emergent
• IV fluids to correct dehydration if NN (bolus: NS, maintenance: NS+2OmEq KCI/Iitre or RL)
• Surgical exploration if torsion suspected clinically
• Definitive treatment depends upon etiology
• Symptom control:
• Morphine 5-10mg P0 q4-6h pm
• Dimenhydrinate 25-50mg PO/IV/IM q6h
• Metoclopramide 5-10mg PO/IV/IM q4h
• Ondansetron 8mg PO/lV daily/BID
• Torsion: emergent surgical detorsion and bilateral fixation of testes. Manual detorsion (rotate medial to lateral) may be attempted
if surgery delayed
• Malignancy: orchiectomy with active surveillance, chemotherapy, or radiotherapy depending on stage and type
3. Referrals
• Urologist, Oncologist
References
1. Reynard J, Brewster 5, Biers S. Oxford Handbook of Urology. 2nd Edition. New York: Oxford University Press Inc.; 2009.
2. Wein AJ, Kavoussi LR, Novick AC, et al. Neoplasms of the Testis. In: Campbell-Walsh Urology. 9th ed. 2009:2411-52.
I
TINNITUS
2011 Ed. Authors: Shawna Pandya, KalAnsari MD FRCSC, Dip/ornate (ABO), Dip/ornate (ABFPRS)
OriginolAuthors:Abdullah Saleh, Peter Dziegielewski MD, Harndy El-I-/ak/rn MD FRCS(Ed) FRCS(ORL-HNS)
Station Objective
To list the appropriate Hx, physical exam, investigations and initial Mx in a patient with tinnitus.
• Subjective
• Unilateral: otoscopy normal (no impacted wax/perforation/otitis media); vertigo, deafness, neurological deficits (eg Meniere’s,
acoustic neuroma, MS, brainstem lesion) may be seen
• Bilateral: wi hearing loss (noise-induced, drug-induced, otosclerosis, presbycusis), w/o hearing loss (thyroid, hyperlipidemia,
Bi 2 deficiency, HTN, anxiety/depression, fibromyalgia)
• Objective
• Pulsatile: vascular (AVMs, acquired shunts, aneurysms, glomus tumour, carotid stenosis)
• Intermittent (TMJ crepitus with eating) vs Continuous (patulous eustachian tube, palatal myoclonus, stapedial muscle spasm)
• Environmental: living next to power cables
• Presbyacusis, noise-induced hearing loss, Meniere’s, drug induced ototoxicity, trauma, aging
• Meningitis, increased ICR aneurysms, malignancy
History
ID • Most prevalent between 40-70 y/o (men=women), sometimes seen in children
CC • “Ringing” in the ear(s)/tinnitus
HPI • Onset, location, uni vs bilateral, duration, pattern, character (pulsatile, intermittent, constant) pitch,
‘whoosh: aggravated/alleviated by, 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, Hx of syphilis
PSHx • Chiari malformation surgery, any 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, exopthalmos
• CV:CP,HTN
• RESP:SOB
• GI: constipation, diarrhea
• MSK/ DERM: numbness/weakness/asymmetry, rash on body
Risk Factors • Noise exposure, sudden air pressure change, Hx CNS & ear infections/trauma, radiation to head, recent
weight loss (patulous Eustachian tube), meds above
Physical
1. General Approach (introduction, hand-wash, ABC, IV, 02, monitors, vitals, permission)
2. Inspection
• Inspect behind ear, pinna, canal. Anterior rhinoscopy of nose. Oropharynx for pulsatile mass
• Otoscopy: wax, foreign bodies, perforation, retracted/bulging TM/OM/OE, reddish hue on TM -Shwartze’s sign, pulsatile mass
behind TM, blue mass behind TM (paraganglioma)

• Pneumatic otoscopy: movement of TM, does red mass/blue mass blanch (paraganglioma)
3. Palpation
• Check neck for masses; TMJ for crepitus
4. Auscultation
• Ear canal: listen for objective tinnitus, pulsation, clicking w/ stethoscope tubing (remove bell)
• Ascultate around the external ear and over neck and carotid artery & jugular vein for masses
5. Special Tests
• CN ll-Xll, peripheral strength, sensation, reflexes, tuning forks (Weber & Rinne Tests), pressure on ipsilateral carotid (pulsations
behind TM stop —* carotid body tumor)
Investigations
1. Blood work
• CBC-D, electrolytes, Cr, urea, TSH, lipid profile, glucose, blood test for syphilis
• MRA head, carotid doppler for pulsatile tinnitus
• Gd-enhanced MRI of posterior cranial fossa to RIO retrocochlear lesions/acoustic neuroma
Special Tests
1. Audiogram = first test of choice; ENG for vertigo; Pre-op angiogram w/ embolization, urine catecholamines for carotid body tumor/
paraganglioma
Treatment
1. Emergent
• Antibiotics (meningitis), burr hole + catheter (t ICP), neurosurgery (aneurysms/malignancy)
• Lifestyle: noise exposure, salt intake (Meniere’s), BP, glucose, thyroid control, stop ototoxic factors,Tx anxiety/depression, Tx
allergic rhinitis, hearing aids/tinnitus maskers, wax removal
3. Surgical
• Resection of tumor, repair of malformation/shunt, myringotomy + tube insertion, tympanoplasty
4. Follow-up
• If symptoms persist, or if chronic problem
5. Referrals
• Otolaryngology, Neurosurgery
References
1. Crummer, RW, Hassan, GA. Diagnostic approach to tinnitus. Am Earn Physician. 2004 Jan 1 ;69(1 ):1 20-6.
2. Tucci DL. Tinnitus. Merck Manual Online. 2009 Jan. [cited October 7,2010]. Available from: http//www.merck.com/mmoe/secO8/chOS4/ch084d.html.

TRAU MA
20?? Ed.Authors:Ashraf Kharrat,James KeayMDCCFP
OriginalAuthor: Saleem Al-Nualmi, SushrMrad MD, Alan SobeyMD FRCSC
Station Objective
To evaluate a patient in accordance with the Advanced Trauma Life Support protocol. To assess and stabilize the patient’s airway, breathing,
hemodynamic and neurologic statuses, and to conduct a complete physical examination.
History and Physical

RED FLAGS Life-threatening bleed (intracranial, pelvic, chest), shock, loss of consciousness, papilledema, focal neurologicai
signs, cardiac tamponade
Primary survey: ABDCE

Airway Ensure airway protection; protected if patient is talking or • Intubate if airway compromised or in
making noises imminent danger of obstruction (GCS <8,
• Assess for direct airway injury, head/neck burns, respiratory failure, severe facial injury, burns,
inhalational injury, significant edema, foreign body inhalation injury)
. Surgical airway (cricothyroidotomy,
tracheostomy)
Breathing • Ensure patient is able to ventilate and oxygenate Treatment with tube thoracostomy
• Assess vitals (RR, Sp02) (needle decompression followed by tube
• Look (for chest movement), Listen (for breathe sounds), thoracostomy if tension pneumothorax), may
and Feel (exhaled air) require mechanical ventilation (bag-valve
• Assess for pneumothorax (hyperresonance), hemothorax mask, intubation and ventilator)
(dullness to percussion), tension pneumo, flail chest, chest
asymmetry, tracheal deviation, dyspnea or absent breath
sounds
Circulation Assess BP and pulse (rate, rhythm and quality) Active bleeds: apply direct pressure and tx
• Assess life threatening bleeding sites: scalp/chest/pelvis! appropriately
abdomen/limb injury Chest/abdomen —4 OR
• R/o cardiac tamponade: hypotension, elevated JVP, muffled Pelvis —+ bind with bed sheet
heart sounds (interventional radiology for
embolization, or OR)
• Long bone —* reduce, urgent OR
Deformity! • GCS, pupils (PERLA) • May require IV mannitol/IV steroids/hypertonic
Disability Gross motor exam to determine any weakness saline/sedatives/paralytics
. Urgent neurosurgical consult if intracranial HTN suspected
(head trauma, pupillary asymmetry/dilatation, absent/
impaired_light_reflex, focal weakness)
Exposure • Remove all clothing Treat for hypothermia (warm blankets, warm
. Log roll and assess patient for any spinal tenderness or IV fluids, heat lamps, warmed air-circulating
bony deformity, conduct DRE assessing for blood/tone! blankets)
high_riding_prostate
2. Secondary survey
• Review vitals and repeat primary survey (ABCDE)
• If patient stable, obtain AMPLE hx: Allergies, Meds, PMHx, Last meal, Event details
• May be obtained from family or emergency medical services
• Complete head-to-toe examination
• HEENT: evaluate ears, nose and eyes, signs of basilar skull fracture (raccoon eyes, battle sign), facial fracture, evaluate mouth
(foreign body, loose teeth or mobile maxilla/foreface), inspect neck for vessel injury (hematoma, crepitus), palpate C-spine for
bony abnormality or tenderness
• CV/RESP: inspect for asymmetry, entry and exit wounds, other injury, palpate chest wall for tenderness/crepitations, percuss
lung fields, auscultate heart and lungs
• Cl: inspect for distention, Grey-Turner’s or Cullen’s sign, other injury, auscultate bowel sounds, palpate for tenderness!
peritoneal signs, look for signs of seatbelt injury
• GU: inspection of perineum bleed, gross vaginal bleeding, penile injury
• MSK: pelvic stability and extremities for tenderness and swelling, neurovascular status, ROM

• NEURO: CN exam, assessment of LOC, focal neurological findings (weakness, reflexes, sensory changes, cerebellar function)
3. Tertiary survey
• Repeat primary survey and secondary survey within 24 hrs of admission and prior to discharge
• Review all laboratory results and diagnostic imaging reports
• Continue to monitor Pt’s overall status
Investigations
1. Blood work
• CBC-D, Electrolytes, Cr, urea, random glucose, INR, PTT, type and screen, cross match, AST, ALT, total bili, ALP, CK, lipase, ABG,
toxicology screen, U/A R&M C&S
• ECG, lateral Cspine XR, CXR, pelvic XR —* all pts. Limb XR if any # suspected
• CT head -4 any significant head injury, neurological deficits, signs of intracranial HTN
• CT chest —* significant penetrating/blunt trauma (pneumothorax, hemothorax, pulmonary parenchymal injury, aortic injury,
tracheobronchial injury, #‘s diaphragm injury)
• CT abdo/pelvis —. significant penetrating/blunt trauma, peritoneal signs, gross hematuria
• CT spine —* significant mechanism, bony tenderness, neurological deficits
3. Special Tests
• FAST —* assess for peritoneal fluid
4. Surgical Interventions
• Emergency laparotomy
Treatment
1. Emergent
• Start IV, stabilize vitals, replace fluids, start antibiotics as needed
• Urgent consult to general surgery, orthopedic surgery, neurosurgery, as required
• Shock is hypovolemic until proven otherwise
• Insert 2 large bore IV: 14-18G in antecubital fossa, give 2L crystalloid fluid challenge)
• Send blood work including type and screen and cross match (may require 0- blood transfusion)
• Insert foley to measure urine output (contraindication = urethral injury)
References
1. Dries Di, Perry iF. Initial evaluation of the trauma patient. Last updated 2008 Aug 19. Available from: httpj/emedicine.medscape.comfarticlef4347O7-
overview.
2. Hoffman, LH etal. First Exposure Emergency Medicine. McGraw-Hill, Inc. USA, 2008.

EDMONTON MANUAL
Section #8
PH EL®
(PHELO) Population Health, and the Ethical, Legal, and Organizational Aspects of Medicine
Section Editor: Lisa J. Steblecki MD MPH CCFP

Associate Professor
WI
INTRODUCTION 373 Personal and Professional Conduct
Approach to Medical Literature 374 Research Ethics
Clinical Epidemiology 376 Resource Allocation
Confidentiality 377 Sexual Health History
QC
Doctor-Patient Relationship 378 Truth Telling
Dying Patient/Bereavement 379
Informed Consent 380
I 372 Edmonton Manual of Common Clinical Scenarios I PHELO

INTRODUCTION
a J. StebleckiMO 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
address other knowledge which is essential for the 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 which 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’s relatively easy
to look up treatment for a given disease, or the appropriate work-up 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’s important to remember that you can’t know everything, but you should have an idea of what resources are
out there for the times when you need help. If you’re unsure if you really should be giving out confidential information, or if a certain action
could be considered unprofessional, it’s 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 to find out’ is better than guessing and risking a critical error.
PHELO Edmonton Manual of Common Clinical Scenarios 373

APPROACH TO MEDICAL LITERATURE
2071 Ed. Authors: AIim Nagji B. Hsc., Nowaoz Nathoo MD, Ashnoor Nogj1MD CCFP
Station Objective
Comprehend basic study design and evaluate literature for internal and external validity.
Hierarchy of Study Designs

1. N of 1 Trials: Single pt alternates between periods of placebo and tx, with both Pt & MD blinded
• Pt offers quantitative ratings of sx. Allows for tailored tx plan based on which intervention offers greatest relief of sx
2. Systematic Review of RCT: compilation of results from multiple RCTs.
• Meta-analysis, creates single estimation of tx effect. Not always applicable (i.e. if interventions are already very heterogeneous)
3. Randomized Control Trial (RCT): pts randomly grouped to receive tx or placebo. Minimizes bias
4. Observational Studies (non-randomized)
• Cohort: can be prospective/retrospective. Analyzes risk factor to outcome and suggests but does not prove causation. (e.g.
smokers do they get CA?)
-
• Case-Control: analyzes from outcome to risk factor. Retrospective. Useful for rare conditions (eg. baby with limb deformities -
exposed to thalidomide?)
• Cross Sectional: data collected at defined time period (snapshot). Include entire population. (e.g. surveys)
5. Physiologic studies (e.g. in vitro studies)
6. Unsystematic clinical observations (e.g. case reports, expert opinion)
Validity
1. Internal Validity: ability of study to support a cause-effect relationship between the treatment and outcome
• Allocation sequence design
• Adequately ensure participants are being assigned to groups in a random manner. (e.g. computer generated sequence)
• Allocation sequence concealment
• Sequence hidden from investigators before group assignment to minimize potential bias. Does not affect randomization
• E.g. use independent sources to allocate participants
• Inadequate concealment can lead to a 30-40% overestimation of tx
• Blinding
• Sequence hidden from investigators after allocation
• Cannot always be done because investigators may directly interact with participants or their data
• Can lead to an overestimation of tx effect up to 17%
• Balance of prognostic factors
• Intervention and treatment group should be as similar as possible in terms of demographics, diseases, etc.
• Intention-to-Treat analysis
• Pt analyzed in allocated group, whether or not they complete regiment
• Minimizes Type I error
• Preserves the the unbiased comparison afforded by randomization
• Completeness of follow up
• How do the authors deal with missing data?
2. External Validity: generalizability to pts outside the study
Bias
Leads to systematic errors in measurement and affects validity of results
• Selection: differences between who is selected to participate and who is not
• Confounding: differences may be caused by another, unaccounted causal factor (confounder)
• Interviewer: subconscious or conscious differences in data obtained. Minimized through blinding of interviewer
• Placebo Effect: differences are caused by Pt expectation that tx will cause an effect. Minimized by blinding of pt
Error
1. Type I Error (a error): claiming there is an effect when there actually is not
• p-value: indicates probability of committing a error. Probability that findings are due to chance. Usually set to p=0.05
2. Type II Error (b error): claiming there is no effect when there actually is
• Power: probability of finding a statistically significant difference. Increases with increased sample size. Power = 1 -I
374 Edmonton Manual of Common Clinical Scenarios I PHELO

Reliability
1. Ability of instrument to yield same results in repeated attempts with different observers in constant population
• Definition: true score/ (true score + error)
• Inter-rater (two different raters, same subject) vs. Intra-rater (same rater, different time, same subject)
• e.g. Mean difference, Standard Error of Measurement (0 = perfect agreement), Intraclass correlation coefficient, kappa (1 =
perfect agreement)
2. Sensitivity to change: ability of instrument to detect and measure change vs. responsiveness: ability to detect and measure clinically
meaningful change
3. Accuracy: single best estimate of treatment effect vs. Precision: range of values which contain actual measurement (Confidence
intervals. Should not cross line of no effect, otherwise results are inconclusive)
Asking the Research Question

1. Components of the Question
• Timeframe
• Outcome
• Patients
• Intervention
• Control
• Study Design
2. Efficacy (explanatory): can intervention achieve results under ideal circumstances?
Effectiveness (pragmatic): can the intervention work under usual circumstances?
3. A priori hypothesis: was there a hypothesis before the trial?
Endpoints
1. Surrogate: outcome measure that is not of direct clinical importance but reflects a clinically relevant result
• Requires causal relationship between surrogate and pt outcomes
• E.g. reduction in cholesterol as surrogate for reduction in mortality
2. Composite: endpoint comprised of several other endpoints
• Used to t’ number of events (%J,-sample size)
• E.g. CVA+MI = vascular events
Systematic Reviews
1. Distinct methodology to minimize bias and synthesize results from multiple trials. Always desirable
• Improves generalizability, provides subgroup analysis,t sample size
• Assess search strategy for completeness, bias:
• Positive trials are more likely to be published (publication bias)
• Released more rapidly (timelag bias)
• In English (language bias)
• In multiple journals (duplication bias)
• Cited more frequently by others (citation bias)
• Leads to overestimation of tx effect
• Can be countered with use of funnel plot (symmetrical plot = bias less likely, studies included from broad range)
• Determine thoroughness of quality assessment: examining internal validity of each trial
2. Meta-Analysis: statistical analysis of individual trials, attempts to create single measure of effect
• Results displayed on forest plot. Individual studies shown with summary measurement
• Should not be done with trials of vastly heterogeneous methodology
• Clinical heterogeneity (external validity): differences in pt/diseases factors
• Methodological heterogeneity (internal validity): differences in study design/execution
• Statistical tests for heterogeneity
• Cochrane chi-square test: tests for similarity/association. Cannot conclusively indicate homogeneity (low power)
• 12 value: indicates percent variability due to actual heterogeneity vs. chance
• ANOVA: compares 3+ groups on one or two factors
References
1. Schulz K. Assessing allocation concealment and blinding in randomized control trials: why bother? Evid Based Nurs. 2001 ;4:4-6.
2. Guyatt G, Rennie D. User’s guides to the medical literature: A manual for evidence-based clinical practice. 1 ‘ ed. Chicago: JAMA; 2005.
3. Evans D. Hierarchy of evidence: a framework for ranking and evaluating healthcare interventions. J Clin Nursing. 2003; 12:77-84.

CLINICAL EPIDEMIOLOGY
2017 Ed. Authors:Alim Nagji B. Hsc., Nawoaz Nathoo MD, AshnoorNagji MD CCFP
Station Objective
Evaluate and understand public health programming, as well as define and calculate key terminology.
Key Definitions
1. Incidence: new cases of dz in time interval! population at risk Disease
2. Prevalence: number of existing cases of dz in time interval! total population AbWflt
3. Attack Rates: #cases of dz/population at risk; used in epidemics Exposui/ Present A B
4. Case Fatality Rates: Pt who die as a result from contracting specific dz; lmeFl’Ltlon
differentiate from death rate Ab$n C
5. 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)
6. Odds Ratio (OR): ratio of odds that event will occur in exposed vs. unexposed groups. When prevalence of dz is low, OR approximates RR
• OR=A/B÷C!D
7. Attributable Risk (AR): amount of risk that is due to exposure
• AR=A!(A+B)-C!(C+D)
8. Number Needed to Treat (NNT): # of Pt who needed to be tx to avoid one adverse outcome
• NNT = 1/Absolute Risk Reduction (where ARR=Control event rate Experimental event rate)
-
9. Specificity: proportion of Pt without the dz who test negative. Positive test rules IN (SpIN)
• Specificity = TN!(TN+FP)
10. Sensitivity: proportion of Pt with the dz who test positive. Negative test rules OUT (SnOUT)
• Sensitivity= TP!(TP+FN)
11. 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)
• -ye LR= (1-Sensitivity)!Specificity
12. Positive Predictive Value = proportion of pt with positive test who have the disorder = TP!(TP+FP)
13. Negative Predictive Value = proportion of Pt with negative test who do not have disorder = TN!(TN+FN)
14. Standardization: adjusting raw measurements to a ‘standard population’ to minimize bias due to varying demographics
Assessing Causation
1. Strength: size of effect Dusee
2. Consistency: repeated in different studies in different populations PrecerIt Absen
3. Specificity: agent associated with specific outcome
Test Resu[t PosItive Thie False
4. Temporality: exposure precedes outcome
5. Biological gradient: exposure/response P05 ye
6. Plausibility: biological mechanism Negdtive False
7. Coherence: follows currently understood principles N Live Live
8. Experiment: if exposure removed, dz rate should decline
9. Analogy: similar effects with similar agents
Screening Tests
1. Must detect dz before clinical dx, where test is acceptable to population, facilities for dx exist and tx is acceptable and effective
2. Pre-Test Probability: based on clinician’s experience and interpretation of patient’s s/sx
3. Post-Test Odds: pre-test odds x likelihood ratio. Calculate with nomogram
4. Bias
• Lead-time: earlier detection, longer apparent survival
• Length-time: preferentially detect dz with slower progression
• Volunteer: volunteers are usually healthier people
• Sampling: non-representative sample chosen (e.g. characteristics of larger population not reflected)
References
1. Guyatt G, Rennie D. User’s guides to the medical literature: A manual for evidence-based clinical practice. 1st ed. Chicago: JAMA; 2005.
2. Goodman KJ, Phillips CV: The Hill criteria of causation. In Encyclopedia of Statistics in Behavioral Sciences. London: Wiley; 2005.
.
CONFIDENTIALITY
201 I Ed. Authors: Patricia Lee, Lisa Steblecki MD CCFP MPH, Brendan Leier PhD
Station Objective
To discuss professional confidentiality of the physician-patient relationship and identify situations where confidential information must be
disclosed.
Ethical Basis of Confidentiality

1. Patient autonomy
Patients have the right to control their personal information
• Confidentiality is a fiduciary duty (legal)
2. Confidentiality is not absolute, ensure to communicate to patients the limits of maintaining confidentiality
3. When interacting with families, maintain patient wishes as the priority, recognizing there may be exceptions
Legal Aspects of Confidentiality

1. 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 or 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
1. May be broken in certain situations, examples include:
• A child in need of intervention (e.g. child abuse/neglect) to social services
• Fitness to drive to provincial Ministry of Transportation
—
• Certain communicable disease (e.g. AIDS, STIs) to medical officer of health

—
• Inappropriate behavior by other health care professionals to professional regulatory body

—
• If clear risk of harm to identifiable person(s), serious bodily harm or death and imminent danger to that person
2. Resources for physicians
• Hospital ethics boards
• Local health authority
CMPA
Privacy commissioner
3. Appropriate pre-test counseling
• Remember to inform your patients about situations in which their confidentiality may be broken
• Ex: Before testing for STIs such as gonorrhea and chlamydia, counsel your 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.
References
1. Baxter, SD and McSheffrey GG.TheToronto Notes 2010. 26
th
edToronto:Type and Graphics mc; 2010.
2. CMA Code of Ethics 2004.
PHELO I Edmonton Manual of Common Clinical Scenarios 377

DOCTOR-PATIENT RELATIONSHIP
2011 Ed. Authors: Maleko Romji, Lisa Steblecki MD CCFP MPH
Station Objective
Recognize and describe the elements of the doctor-patient relationship as highlighted by the current national codes
Physician obligations
1. The physician must place the best interests of the patient first
2. The physician must follow through on undertakings made to the patient, in good faith
3. 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 render
Conflicts of interest
1. The physician must always act in the patient’s best interest
2. 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
3. The physician should not act for personal advantage financial, academic or other
—
4. It is a physician’s duty therefore, 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
1. The physician should respect and maintain professional boundaries with the patient
2. This applies to physical, social, emotional and sexual boundaries
Physician and patient rights

1. 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
• Except in emergency situations, in which case care must be rendered
2. Once having accepted a patient into care, the physician may terminate the relationship, but must ensure the following:
• That care has been transferred to another physician, OR:
• That adequate notice has been offered to the patient to make alternate arrangements
• AND: without consideration of race, age, gender, sexual orientation, financial means, religion or nationality
Care of family
1. Physicians should not diagnose or treat family members except for minor conditions or emergencies, where they are the only available
physician
References
1. Medical Council of Canada [Internet). CLEO: Objectives of the Considerations of the Legal, Ethical and Organizational Aspects of the Practice of Medicine;
c201 0 [cited 2010 Sep 121.4.8. Doctor Patient Relationship; Available from: htto://www.mcc.ca/objectives online/obiectives.ol?lang=english&loc=cieo#
.
4
2. Ethical Legal and Organization Aspects of Medicine: Doctor Patient Relationship. In: Baxter SD, McSheffrey GG, editors.Toronto Notes: Comprehensive
Medical Reference and Review for MCCQE I and USMLE II. 26 th
Edition. Toronto, Canada; 2010. P ELOAM 12-13.
378 Edmonton Manual of Common Clinical Scenarios PHELO

DYING PATIENT/BEREAVEMENT
20!! Ed. Authors: Michael Driedger, Chris Gee MD, Sheny Khera MD, CCF MPH
Station Objective
To understand the stages of grief a dying patient may experience and to develop an approach to end of life care.
General Approach
It is extremely important to always convey empathy and support toward a dying patient and their family. Patients want to know that they
will not be abandoned; the physician will be there to provide support and focus on quality of life throughout the duration of their illness.
This will maintain a sense of confidence in the physician allowing the patient to begin to deal with their emotions and cope with their
situation.
Kubler Ross 5 Stages of Grief

1. Denial and Isolation
2. Anger
3. Bargaining
4. Depression or sadness
5. Acceptance Diagnostic Criteria
• 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 towards the patients feelings about death
• Watch for cues that the patient is willing to speak/share
• Allow time for the patient to ask questions
• Explore concerns and provide information that may be requested
• Demonstrate a commitment of support for the duration of the illness
End of Life Care

1. Control of pain and other symptoms
• It is difficult to address the social, psychological and spiritual issues without adequate pain and symptom management
• Focus on quality of life
2. Advance directive/Advance care planning
• The creation of an advance directive or advanced care planning, as well as an enduring power of attorney, ensures that clinical
care is shaped by the patient’s preferences and ideals 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 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
3. Support patients and their families
• Ask the patient and family what support they may need 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 and bereavement; pay attention to risk factors regarding poor adjustment to bereavement
References
1. Bickley LS, Szilagyi PG. Bates’guide to physical exam and history taking. th
10
ed. Philadelphia: Wolters Kiuwer Flealth/Lippincott Williams and Wilkins;
2009.
2. Singer PA, MacDonald N. Bioethics for clinicians: quality end of life care. CMAJ. 1998; 159-162.
3. Canadian hospice palliative care association [Internet]. Ottawa; c201 0. [cited Oct. 1,20101. Available from: http://www.chpca.net.

IN FORMED CONSENT
2011 Ed. Authors: Mackenzie Lees, Simon Turner MD, Gordon Lees MDFRCSC
Station Objective
To explain what informed consent is, its purpose/importance, and how to properly obtain it.
Basics
1. What is Informed Consent?
• Voluntary agreement given by a patient or their responsible proxy (e.g. their 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 autonomy and beneficence
• A necessary part of a physician’s duty to care for their patient
• Legal consequences if not properly obtained
2. When to obtain consent?
• 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)
• Made in advance
• Well documented
3. Consent from whom?
• Competent patients or substitute decision makers
• Patient has appropriate capacity (e.g. the ability to communicate/understand information/reason and deliberate/choose/etc.)
• Patient cannot give consent and their consent should not be accepted if they are incompetent
• If incapable, use substitute decision maker
4. Who should obtain the consent?
• The treating physician or the resident
5. What should be disclosed?
• Exact nature of the procedure and any alternatives (including ‘zero option’= do nothing)
• Prognosis (with/without treatment)
• Associated risks and benefits (of treatment and alternatives) and serious risks (even if rare)
• 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
6. How to obtain informed consent?
help
• Explain simply, clarify when/if necessary, word the information appropriately and use translators and/or pictures /diagrams to
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 you 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
important
• Keep in mind that obtaining consent does not mean getting the patient to sign a consent form, but is rather a complex,
process as outlined above.
7. Exceptions to consent:
• Patient waver or patient incapacity (consent must come from a properly informed proxy decision maker)
evidence
• Emergencies: immediate treatment required to preserve life or health, patient’s or proxy’s consent can’t be obtained, no
of prior competent refusal and/or treatment prescribed under legislation (i.e. The Mental Health Act, The Public Health Act, The
Child, Youth and Family Enhancement Act, etc.)
• Exceptions to this exception: suicide notes and if the patient previously refused the same treatment
References
nd ed. Don Mills, ON: Oxford University Press; 2009
2
1. Hebert PC. Doing Right: A Practical Guide to Ethics for Medical Trainees and Physicians.

PERSONAL AND PROFESSIONAL CONDUCT
201! Ed. Authors: Bobok Moghdoori, Michel DonoffMD FRCPC
Station Objective
To provide a concise overview of the fundamentals required for personal and professional conducts in a clinical setting, outlined by the
Medical Council of Canada (MCC) and the College of Physician and Surgeons of Alberta (CPSA).
General Principles
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 general principles:
1. Accountability to self:
• Maintenance of competence:
• Evaluation of personal and professional competence, recognition of personal limitations, as well as ongoing education to
maintain and enhance competence
• Personal health:
• Evaluation and maintenance of the necessary balance between personal and professional conduct
• Establishment of the significance of practicing without impairment from any substances/medications, ill health, or other
forms of incapacity (such as incapacitating mental or emotional conditions)
2. Accountability to others:
• Conduct oneself in a manner that promotes safety, high standards of personal and professional honesty, high quality of patient
care, and adequate collaboration with the other members of the health care team
• Take responsibility for one’s actions and behaviors.
• Maintain clarity, honesty, passion, and integrity in all forms of communication.
• Diagnose, record, report, and follow-up patients’ histories, diagnoses, physical findings, and test results in an organized, consistent,
and timely manner
• Ensure fair attribution of the ideas, thoughts, and credit for the works conducted
• Recognize real/perceived conflicts of interests and deal with them in an honest, open, and consistent manner.
• Participate in learning in a perpetual and consistent manner
3. Maintaining confidentiality:
• Recognize and maintain the confidentiality of the patients, research participants, and colleagues as a primary obligation
• Limit access to patient health records, patient health issues, and other related concerns to appropriate and private settings
• Ensure patient consents are obtained prior to disclosing any patient information, as outlined by personal/professional/ethical
conduct codes as well as legal guidelines
• Actively follow, understand, and comply with the relevant legislations regarding confidentiality
4. Maintaining utmost respect for others:
• Maintain the highest levels of respect, politeness, and dignity in dealing with patients/families, visitors, employees, colleagues,
volunteers, and other healthcare providers
• Do not engage in any verbal or physical behaviors that may be considered remotely offensive or disruptive of the workplace and
the patient care
• Ensure respect and maintenance for the patient’s autonomy at all times
• Allocate sufficient time and resources for discussion of courses of action, medical diagnoses, investigational approaches, and
any other relevant health issues
• Ensure the patient is mentally competent and fully appreciates the consequence of her/his decisions
• Ensure appropriate consultation of a legally-appropriate surrogate decision maker for a mentally incompetent Pt
• Refrain from any physical contact not indicated by the physician’s role
• Avoid sexual and romantic involvements with patients
• Avoid any forms of discrimination based on age, gender, race, origin, beliefs, sexual orientation, or any other protected grounds, as
defined by human rights legislations
References
1. CPSA code of conduct: Expectations of Professionalism for Alberta Physicians. College of physician and surgeons of Alberta. 2010 April.

RESEARCH ETHICS
2011 Ed. Authors: Darwin Won, Dilini Vethanayagam MD FRCP
Station Objective
To gain an understanding of common and emerging ethical issues in medical research.
Broad General Principles

1. Respect: autonomous decision-making respected
2. Beneficence: act in the patient’s best interests
3. Justice: fair distribution of benefit/potential harm, should not exploit the vulnerable (disabled, children, cognitively impaired)
Study Design and Purpose

1. Ensure study is clinically relevant, scientifically/ethically sound (prior statistical analysis, RCT, gold standard)
2. Studies must address a question of sufficient value for justification of the risks involved
3. Studies must be conducted with honesty, maintain the approved protocol
Patient Interaction
1. Full disclosure of risks and benefits, obtain informed consent in quiet room, free from coercion, ensure comprehension
2. Inform patients of the right of non-participation or withdrawal without prejudice
3. Refuse to enroll patients in research which has not been scientifically and ethically approved
Clinical Registries
1. Use of data, location of storage, purpose of storage needs to be considered, who’s accessing data, what trails in place
Industry research
1. Industry-funded research can impact multi-centre clinical trials, investigator-initiated trials or basic research
2. Investigator’s industry relationships, financial interest, funding and conflict of interest must be disclosed
Biobanking
1. Benefit
• Type of specimen, invasive or noninvasive
• Subjects often participate in this type of research out of altruism, but are there financial gains or commercial interest?
• Balancing conflicting interests involved in biobanking, society may be served by access to new products
2. Consent
• An emerging issue, growing acceptance of broad consent justified on basis of public good; legal/ethical validity of broad consent
to future unspecified research debated
• Modification of consent requirements can’t be justified on expediency, should be on a principled approach
Dissemination of Research Findings

1. Ask why you are involved in a study, what is the ultimate goal, what is out there already, is publication the only means of dissemination,
how will this translate into clinical use now or in the future
2. Determine if statistical analysis should be done a priori to minimize statistical bias
3. Publication should not favour positive results, time lag bias causes null result studies to lose influence, citation bias lessens their impact,
multiple publication bias overestimates treatment effects
References
1. Kay J, Stranger M. Principles and Practice in Biobank Governance. Burlington: Ashgate; 2009.
2. Lexchin K. Implications of Pharmaceutical Industry Funding on Clinical Research. Annals Pharmacotherapy. 2004 Nov 23; 39(1): 194-7.
3. Thompson A, Temple NJ. Ethics, Medical Research, and Medicine. Dordrecht: Kluwer Academic Publishers; 2001.
4. Weijer C, Dickens B, Meslin EM. Research ethics. Can Med Assoc J. 1997 Apr 1 5;1 56(8): 1153-7.
5. MCC Objectives for the Qualifying Examination [Internet]. Ottawa: Medical Council of Canada; c2010 [cited 2010 Oct 15]. Available from: http//www.mcc.
ca/Objectives_Online/objectives.pl?loc=home&Iang=english

RESOURCE ALLOCATION
20 liEd. Authors: Debra] Dos, Olga Toleva MD, Michael Tjandrawid]aja MD, Paul W Armstrong MD FRCP
Station Objective
To appreciate the ethical issues surrounding Resource Allocation in the Canadian healthcare system.
Overview
There is no doubt that with an aging population, new medical therapies, and increasing financial strain on the healthcare system, the issue
of resource allocation is a relevant topic in today’s society. Maximal benefit with minimal cost is the mentality surrounding scarce resource
allocation and healthcare providers are expected to abide by their patients and ensure the best care possible regardless of costs. However, at
times this philosophy is difficult to maintain by and as a result, many ethical dilemmas and conflicts can arise.
What is Resource Allocation?

In the context of healthcare, resource allocation can be divided into three major concepts: macro, meso, and micro allocation
• Macroallocation refers to the resources provided by all levels of government federal, provincial, and municipal
—
• Mesoallocation refers to an individual hospital’s allocation of finances and services

• Microallocation refers to deliverance of resources to every individual patient
Resource allocation is a broad term but includes things such as finances, services offered (cancer therapy, dialysis etc.), and even organ
availability. With rising costs, an aging population, and increasing standards of care, resource allocation has become an issue in the day-to
day lives of clinicians.
Ethics, Law, and Pohcy

From the ethical standpoint of resource allocation, 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 such as,”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, it is established that discrimination based upon age, sex, religion etc. is strictly prohibited breaching -
this fundamental law will naturally lead to major legal consequences. Physicians juggle these patient characteristics with medical therapy
and prognosis. Each individual case is unique and courts are cautious in interfering with day-to-day practices of clinicians. In the end
however, 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 my local hospitals or institutions in an attempt to standardize each clinicians 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 3 major concepts of ethics, economics, and quality. In
addition, the CMA’S Code of Ethics clearly states every physician has the responsibility to”promote fair access to healthcare resources” as well
as use healthcare resources”prudently.”
Approach To Resource Allocation in Practice

1. Select therapies, tests, and exams with proven cost effectiveness
2. Decrease use of’marginally’ beneficial and unnecessarily repeated tests/exams
3. Advocate and meet your patient’s needs first but also be open with them particularly if it will not alter your management plan
-
4. Unacceptable shortages in medical resources need to be brought up with individuals and administration responsible for macro and
mesoallocation
References
1. Bioethics for Clinicians: Resource Allocation. CMAJ. July 15, 1997; 157.

SEXUAL HEALTH HISTORY FRCSC
201 I Ed. Authors: Cassandra Hirt, Amanda Aiken MD, Jonathan Tankel MBBCh
Station Objective
Take a focused sexual health history Special Groups
Cognitive Impairment
Basics Physically Disabled
Introduce yourself Sexual Orientations
2. Consent and confidentiality Assault Survivors —
History
ID Age, sex, gender
orgasmia
. Pregnancy/contraception, STIs, sexual function: desire, decreased libido,
• Discuss specific medical or psychosocial concer ns in more detail
• Onset, duration, dissipating/aggravating factors

HPI Males: erection and ejaculation
• Female: dyspareunia, vaginismus, vaginal dryness
RED FLAGS Signs or disclosure of sexual assault
• Chronic conditions: DM, HTN, CVD, Ca
PMHx
• STlpastHx
• Menstrual/obstetrical/infertility Hx
PO&GHx • , moliminal Sx
Menstrual cycle: age of menarche, oligo/amenorrhea, cycle/menses length
PSHx Any past surgeries
Meds OTC, Rx, CAM
Social • Smoking, EtCH, recreational drugs, disclosure of sexual assault
Sexual Health History

1. Pt. can be very uncomfortable, be mindful of why each question is asked
2. ENSURE convey non-judgment and non-assumption
3. Past Sexual Hx Sexual Cycle
Orgasm
• No. of partners/gender
• Partner faithfulness
• Sexual practices: oral, vaginal, anal
• Does this include intercourse or penetration (be specific)
• Date of last sexual contact Arousal/Excitement
• Important for pregnancy, contraception, STI and HIV testing
• Protection use
4. Sexual Function/Sexual Cycle
• Desire: interest, aversion, who initiates? Desire
• Arousal/Excitement: foreplay, sufficient duration and nature
• Orgasm: is sex satisfying? Resolution
• Men: premature or delayed ejaculation?
• Resolution: does relaxation occur, if not what interferes?
5. Sexual Assault/Domestic Violence Screen
a persons health and well being, I now ask all my
• “Because sexual violence is an enormous problem in our society and can affect
patients about sexual assault:’
, some tension, no tension
• In general how would you describe your relationship? A lot of tension
Some difficulty?
• Do you and your partner work out arguments with: great difficulty?
es that made you uncom fortabl e?
• Has anyone forced you to have sexual activat
6. Use of protection/contracep tion
• Frequency, consistency, correct use (investigate what Pt means by this)
References
SOGC Clinical Practical Guidelines: Intimate Partner Violence Consensus Statement,
2005
1.
2. Tools and Techniques for taking a Sexual History: Sheila Hughes, 2010
3. The Sexual Cycle, W Masters, V Johnson, and HS Kalpan, 1996

TRUTH TELLING
2011 Ed. Authors: Nathan Hay, Brendon Leler PhD.
Station Objective
To understand physician’s duty to their patients to be truthful, which may conflict with the physician’s obligation of non-maleficence
Ethical Basis ABCDE of Breaking Bad News

Advance preparation
1.The autonomy of the patient must be respected
(Ask what they already know, arrange
2.Truth telling establishes trust between the physician and patient and avoids paternalism
time and place for meeting, prepare
3.Patients need to make realistic life decisions
emotionally)
4.Patients may find comfort in the fact that their physician can name their condition
5.If a patient is unaware of their condition, they may not seek the medical attention they need
Build a therapeutic environment!
6.A patient’s information is the property of the patient, not the physician
relationship (quiet place without
disturbances, sit close enough to touch if
Legal Basis necessary, reassure about suffering/pain)
1. Standard for disclosure is what would a reasonable person in the patient’s circumstances Communicate (be direct, no jargon,
want to know (ie. purpose and implications of investigation, Dx and prognosis, risks and acronyms or euphemisms, allow silence,
benefits, health risks of test), consult CMA Code of Ethics or CMPA if unclear use’death’and ‘cancer’ and ask them to
2. Obtaining informed consent is a legal obligation: failure to do so may result in legal action, repeat their understanding of news
obtaining consent with incomplete or false information can be considered negligence
3. Disclosure is a vital component of obtaining full consent from a Pt Deal (with patient and family reactions,
assess patient reaction ie. withdrawal,
Difficulties encountered in practice disbelief, anger, listen actively, empathize,
and support the patient
1. Concern bad news may harm the patient thus conflicting with the obligation of non-
maleficence, refer to ABCDE of breaking bad news Encourage- correct distortions, address
2. Uncertainty about the diagnosis further needs, offer to tell others on
3. When medical error occurs: Disclose error without suggesting it resulted from negligence; patient behalf, develop a plan for near
negligence is a finding made in court not by the physician and long term, assess suicide risk, arrange
4. Patient’s family is opposed to truth telling- counsel them about truth telling as you would referrals and follow up, be aware of own
any medical problem feelings
MinichielloTA, Ling D, Ucci DK (2007)

Exceptions to truth telling
1. Patient waives right to information, must be capable of making decision
2. 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)
3. Common reasons for refusal: disclosure would cause harm to the patient, cultural values, incapacitation, emergency
4. If the request is authentic and contrasts with the family’s wishes, the physician must respect patient’s wishes above family’s
5. “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
References
1. Heber PC, Hoffmaster B, Glass KC, Singer PA. 1997. Bioethics for clinicians 7. Truth telling. Can Med Assoc J 1 56;225-8.
2. MinichielloTA, D Ling, DK Ucci. 2007. Breaking bad news: a practical approach for the hospitalist. Journal of Hospital Medicine 2:415-21.

APPENDIX A: ABBREVIATIONS
A ARMD age related macular degeneration
aa artery AS aortic stenosis
AAA abdominal aortic aneurysm AS ankylosing spondylitis
2 alveolar-arterial oxygen gradient
A-aDO ASAP as soon as possible
MD antibiotic-associated diarrhea ASC-H atypical squamous cells cannot exclude high grade
AAO alert, awake, and oriented intraepithelial lesion
MT activity as tolerated ASC-US atypical squamous cells of undetermined significance
A&O alert & oriented ASD atrial septal defect
ABCDE airway breathing circulation disability exposure ASIS anterior superior iliac spine
aBd abduction ASOT anti-streptolysin o titres
ABD abdomen ASQ ages & stages questionnaire
ABG arterial blood gas AST aspartate transaminase
ABI ankle brachial index ATLS advanced trauma life support
AbPB abductor pollicis brevis mm ATN acute tubular necrosis
AbPL abductor pollicis longus mm ATTG anti-transglutaminase
Abx antibiotics AUA american urology association
AC air conduction AUB abnormal uterine bleeding
ACEI angiotensin converting enzyme inhibitors AV atrioventricular
ACLS advanced cardiac life support A-V arteriovenous
ACTH adrenocorticotropic hormone AVM arteriovenous malformation
AD alzheimer’s disease, autosomal dominant AVN avascular necrosis
AdB adductor brevis mm A-V02 arteriovenous oxygen
aDd adduction AXR abdominal Xray
ADH anti-diuretic hormone
ADHD attention deficit hyperactivity disorder B
ADL activity of daily living BADL basic activity of daily living
AdDM adductor digiti minimi mm BAE bronchial artery embolism
AdL adductor longus mm BBB bundle branch block
AdM adductor magnus mm BC bone conduction
AdP adductor pollicis mm BCC basal cell carcinoma
ADR adverse drug reaction BE barium enema
ad lib as much as needed BF biceps femoris mm
AF atrial fibrillation B-hCG beta human chorionic gonadotropin
AF afeb rile bid twice a day
AF amniotic fluid BKA below the knee amputation
AFB acid-fast bacilli BM bone marrow, bowel movement
AFP alpha-fetoprotein BMI body mass index
AGC atypical glandular cells BP blood pressure
Al aortic insufficiency BPH benign prostatic hypertrophy
AlO anterior interosseous BPM beats per minute
AIS adenocarcinoma in situ BPP biophysical profile
AKA above the knee amputation BPPV benign positional paroxysmal vertigo
AID alcoholic liver disease BR brachioradialis mm
ALL acute lymphocytic leukemia BR bed rest
ALP alkaline phosphatase Br branches
ALS advanced life support BRBPR bright red blood per rectum
ALS amyotrophic lateral sclerosis BRCA breast cancer (gene)
ALT alanine transaminase BRP bed rest with bathroom privileges
ALTE apparent life threatening event BS bowel
amb ambulate BS breath sounds
AML acute myelogenous leukemia BSA body surface area
ANA antinuclear antibody BSO bilateral salpingo-oophorectomy
ANS autonomic nervous system BUN blood urea nitrogen
anti-GBM anti-glomerular basement membrane BW body weight
AODM adult onset diabetes mellitus Bxbiopsy
AOM acute otitis media
AP anteroposterior C
AR autosomal recessive Clq complement subcomponent lq
ARB angiotensin II receptor blockers C3 complement component 3
ARDS acute respiratory distress syndrome C4 complement component 4
ARF acute renal failure Ca cancer
386 Edmonton Manual of Common Clinical Scenarios I Appendix

Ca calcium
2 D2 index finger
CA-125 cancer antigen 125 D3 long finger
CABG coronary artery bypass graft D4 ring finger
CAD coronary artery disease D5 little finger
CAH congenital adrenal hyperplasia D5W 5% dextrose in water
c-ANCA circulating anti-neutrophil cytoplasmic antibody DAT diet as tolerated
CAM complementary and alternative medicine DAT direct antiglobulin test
CAT computerized axial tomography dBP diastolic blood pressure
CABG coronary artery bypass graft DBT dialectical behavioural therapy
CBC complete blood count DC discontinue
CBC-D CBC with differential DC discharge
CBD common bile duct D&C dilation and curettage
CBE clinical breast examination DCIS ductal carcinoma insitu
CBG capillary blood gas DDH developmental dysplasia of the hip
CBT cognitive behavioural therapy DDx differential diagnosis
CBT carotid body tumor dflex dorsiflexion
CC chief complaint DHEA dehydroepiandrosterone
CCAM congenitial cystic adenomatoid malformation DI diabetes insipidus
CCU cardiac care unit DIA dimeric inhibin-a
CD conduct disorder DIC disseminated intravascular coagulopathy
CEA carcinogenic embryonic antigen DIP distal interphalangeal joint
CEA carotid endarterectomy DJD degenerative joint disease
CF cystic fibrosis DKA diabetic ketoacidosis
CF clear fluids DLCO diffusing capacity of the lung for carbon monoxide
CGL chronic granulocytic leukemia DM diabetes mellitus
CHF congestive heart failure DMARD disease modifying anti-rheumatic drug
CHL conductive hearing loss DMT1 diabetes mellitus type I
CI cardiac index DMT2 diabetes mellitus type II
CML chronic myelogenous leukemia DNR do not resuscitate
CMPI cows milk protein intolerance D/O disorder DOE dyspnea on exertion
CMV cytomegalovirus DPT diphtheria, pertussis, tetanus
CN cranial nerves DRE digital rectal exam
CNS central nervous system DSM-IV Diagnostic and Statistical Manual of Mental Disorders IV
CO cardiac output DT’s delirium tremens
dO complaining of DTR deep tendon reflexes
COPD chronic obstructive pulmonary disease DVT deep venous thrombosis
CP chest pain DX diagnosis
CP cerebral palsy Dz disease
CPA costopherenic angle
CPAP continuous positive airway pressure E
CPK creatine phosphokinase EAC external auditory canal
CPR cardiopulmonary resuscitation EBL estimated blood loss
Cr creatinine EBV epstein-barr virus
CrCL creatinine clearance ECF extracellular fluid
CRC colorectal cancer ECFV extracellular fluid volume
CREST calcinosis, Raynaud’s phenomena, esophageal dysmotility, ECG electrocardiogram
sclerodactyly, telangectasia ECRB extensor carpi radialis brevis mm
CRF chronic renal failure ECRL extensor carpi radialis longus mm
CRP C-reactive protein ECT electroconvulsive therapy
CRTx chemoradiation therapy ED erectile dysfunction
C&S culture and sensitivity ED extensor digitorum mm (arm)
CSF cerebrospinal fluid EDC estimated day of confinement
CT computerized tomography EDL extensor digitorum longus mm (leg)
CTx chemotherapy EDM extensor digiti minimi mm
CV cardiovascular EHB extensor hallicus brevis mm
CVD cardiovascular disease EHL extensor hallicus longus mm
CVA cerebrovascular accident El extensor indicis mm
CVA costovertebral angle EIA enzyme immunoassay
CVP central venous pressure EMG Electromyogram
CXR chest X-ray EMV eyes, motor, verbal response (Glasgow coma scale)
ENG electronystagmogram
D ENT ears, nose, and throat
Id per day EOM extraocular muscles, extraocular movements
Di thumb EPS extrapyramidal symptoms
Appendix I Edmonton Manual of Common Clinical Scenarios 387

GSW gun shot wound
ESR erythrocyte sedimentation rate
gtorgttdrops
ET endotracheal
GTT glucose tolerance test
ETT endotracheal tube
ERCP endoscopic retrograde cholangio —pancreatography GU genitourinary
GV growth velocity
EtOH ethanol
EUA examination under anesthesia
ext extension H
H
R
2 A histamine 2 receptor antagonist
F HA headache
FAP familial adenomatous polyposis HepA hepatitis A virus
FASD fetal alcohol spectrum disorder HepB hepatitis B virus
FAST focused assessment with sonography for trauma HepC hepatitis C virus
HBP high blood pressure
FBA foreign body aspiration
FBS fasting blood sugar HC head circumference
FCR flexor carpi radialis mm hCG human chorionic gonadotropin
FCU flexor carpi ulnaris mm HCT hematocrit
FDB flexor digitorum brevis mm HDL high density lipoprotein
HEENT head, eyes, ears, nose, throat
FDL flexor digitorum longus mm
FDP flexor digitorum profundus mm Hgb hemoglobin
FDS flexor digitorum superficialis mm HgbAlc hemoglobin Aic
FVC forced vital capacity HHS hyperosmolar hyperglycemic state
HI homicidal ideation
FEV forced expiratory volume
FESS functional endoscopic sinus surgery HIE hypoxic ischemic encephalopathy
FF full fulids HIV human immunodeficiency virus
FFP fresh frozen plasma HJR hepatojugular reflex
FHR fetal heart rate HLA histocompatibility locus antigen
FISH fluorescence in situ hybridization HNPCC hereditary nonpolyposis colorectal cancer
flex flexion HOB head of bed
HPF high powered field
FM fine motor
FNA fine needle aspirate HPI history of present illness
FOBT fecal occult blood test HR heart rate
FPG fasting plasma glucose HRT hormone replacement therapy
Fr french size HS at bedtime
FRC functional residual capacity hs-CRP high sensitivity C reactive peptide
FSGS focal segmental glomerulosclerosis HSG hysterosalpingogram
FSH follicle stimulating hormone HSIL high grade squamous intraepithelial lesion
FSWU full septic work up HSM hepatosplenomegaly
FTA-ABS fluorescent treponemal antibody absorbed test HSP henoch-scholein purpura
FTT failure to thrive HSV herpes simplex virus
FL) follow-up Ht height
FUO fever of unknown origin HTLV-III human lymphotropic virus, type Ill
FVC forced vital capacity HTN hypertension
Hx history
G
GA gestational age
GAD generalized anxiety disorder IABP intra-aortic balloon pump
GAS group A strep IAC internal auditory canal
GBS group B strep IADL instrumental activity of daily living
GC gonorrhea IBD inflammatory bowel disease
GCS glascow coma scale lBS irritable bowel syndrome
GDD global developmental delay ICF intracellular fluid
GDM gestational diabetes mellitus ICH intracerebral hemorrhage
GERD gastroesophageal reflux disease ICS intercostal space
GFR glomerular filtration rate ICS inhaled corticosteroid
GH growth hormone ICSI intracytoplasmic sperm injection
GI gastrointestinal ICP intracranial pressure
GM gross motor ICU intensive care unit
Gmax gluteus maximus mm ID infectious disease, identification
GMC generalized medical condition I&D incision and drainage
Gmed gluteus minimus mm IDDM insulin dependent diabetes mellitus
Gmin gluteus maximus mm IFG impaired fasting glucose
GN glomerulonephritis IFN interferon
GnRH gonadotropin releasing hormone Ig immunoglobulin
GPTAL gravida, para, term, abortion, living IGF insulin like growth factor
388 Edmonton Manual of Common Clinical Scenarios Appendix

IGFBP insulin like growth factor binding protein LOC level of consciousness
IGT impaired glucose tolerance LP lumbar puncture
IM intramuscular LRTI lower respiratory tract infection
Immun immunizations LSB lower sternal border
INF intravenous nutritional fluid LSIL low grade squamous intraepithelial lesion
INR international normalized ratio LTB laryrngotracheal broncitis
0 interosseous LTRA leukotriene receptor antagonist
I&0 intake and output LUL left upper lobe
lop inter ocular pressure LUQ left upper quadrant
IP illopsoas mm, interphalyngeal LV left ventricle
IPJ interphalyngeal joint LVD left ventricular dilation
IT interthecal LVEDP left ventricular end diastolic pressure
ITP idiopathic thrombocytopenic purpura LVH left ventricular hypertrophy
IV intravenous
IVC intravenous cholangiogram M
IVC inferior vena cava MAL mid axillary line
IVH intra-ventricular hemorrhage MAS meconium aspiration syndrome
IVP intravenous pyelogram MCI mid-clavicular line
IVDU iv drug user MAO monoamine oxidase
ILJD intrauterine device MAP mean arterial pressure
IUGR intrauterine growth restriction MAST medical antishock trousers
IUI intrauterine insemination MCH mean cell hemoglobin
IUTD immunizations up to date MCHC mean cell hemoglobin concentration
IVF in vitro fertilization MCV mean cell volume
WIG intravenous immunoglobulin MD muscular dystrophy
lx investigations MEN multiple endocrine neoplasia
MG myasthenia gravis
J Ml myocardial infarction
JIA juvenile idiopathic arthritis MI mitral insufficiency
JODM juvenile onset diabetes mellitus ml milliliter
JVD jugular venous distention mm muscle
JVP jugular venous pressure
MM multiple myeloma
K MMA middle meningeal artery
K potassium mmol millimole
KUB kidneys, ureters, bladder mmol/L millimoles/litre
KVO keep vein open MMR measles, mumps, rubella
MMSE mini-mental state examination
L MR mitral regurgitation
LIeft MR mental retardation
LABD long acting bronchodilator MRA magnetic resonance angiogram
LAD left axis deviation, left anterior descending MRCP magnetic resonance cholangiopancreatography
LAE left atrial enlargement MRI magnetic resonance imaging
LAHB left anterior hemiblock MRSA methicillin resistant staph aureus
LAP left atrial pressure MS multiple sclerosis
LAP leukocyte alkaline phosphatase MS mitral stenosis
LBBB left bundle branch block MS morphine sulfate
LCIS lobular carcinoma insitu MSA multi system atrophy
LCPDz legg-calve perthes disease MSAFP maternal serum alpha feto-protein
LD learning disorder MShCG maternal serum chorionic gonadotropin
LDH lactate dehydrogenase MSuE3 maternal serum unconjugated estriol
LDL low-density lipoproteins MSL mid-sternal line
LE lupus erythematosus, lower extremity MSS maternal serum screen
LEEP loop electrosurgical excision procedure MSSA methicillin-sensitive staph aureus
LFT liver function tests MVA motor vehicle accident
LGIB lower gastrointestinal bleed MVP mitral valve prolapse
LH luteinizing hormone
ILL left lower lobe N
LLQ left lower quadrant N nausea
LMA laryngeal mask airway N normal
LMN lower motor neuron Na sodium
LMP last menstrual period NAAT nucleic acid amplification test
LNMP last normal menstrual period NAFLD nonalcoholic fatty liver disease
LOC loss of consciousness NB Newborn

NG nasogastric PCWP pulmonary capillary wedge
NICU neonatal intensive care unit PD parkinsons disease
NIDDM non-insulin dependent diabetes mellitus PDA patent ductus arteriosus
NKA no known allergies PDD pervasive developmental delay
NKDA no known drug allergies PDE-5 phosphodiesterase type 5
NKHHC non ketotic hyperglycemic hyperosmolar coma PE pulmonary embolus
NMR nuclear magnetic resonance PE physical exam
nn nerve PE pleural effusion
NPO nothing by mouth PEDS pediatrics
NPV negative predictive value PEDS parental evaluation of developmental status questionnaire
NRFS non reassuring fetal status PEEP positive end expiratory pressure
NS normal saline PEFR peak expiratory flow rate
NSAID non-steroidal anti- inflammatory drugs pflex plantar flexion
NSR normal sinus rhythm PFT pulmonary function tests
NST non-stress test PGE1 prostaglandin El
NT nasotracheal, nuchal translucency pH potential of hydrogen
NTD neural tube defect PHTN pulmonary hypertension
NN nausea/vomiting PICA posterior inferior cerebellar artery
NWB non weight bearing PICU pediatric intensive care unit
PID pelvic inflammatory disease
PlO posterior interosseous
OB obstetrics PKU phenylketonuria
OC oral cavity PL peroneous brevis mm
OCP oral contraceptive pill PL palmaris longus mm
OD overdose PLT platelet
OD right eye PMDD post menstral dysphoric disorder
ODD opositional defiant disorder PMH previous medical history
OE otitis externa PMI point of maximal impulse
OE obturator externus mm PMN polymorphonuclear leukocyte (neutrophil)
OGTT oral glucose tolerance test PMR polymyalgia rheumatica
01 obturator intern us mm PMS premenstrual syndrome
OM otitis media, osteomyelitis PND paroxysmal nocturnal dyspnea
OP opponens pollicis mm PND post nasal drip
OP oropharynx PNS peripheral nervous system
OPQRST onset, provoking/palliating factors, quality, region/radiation, P0 by mouth
severity, time/treatments POD post-op day
O&P ova and parasites PP postprandial
OPV oral polio vaccine PP pulsus paradoxus
OR operating room PPD purified protein derivative
OS left eye PPH post partum hemorrhage
OSA obstructive sleep apnoea PPHN persistent pulmonary hypertension of the newborn
OT occupational therapist PPROM preterm premature rupture of membranes
OTC over the counter PPV positive pressure ventilation
OU both eyes PPV positive predictive value
OME otitis media with effusion PR by rectum
PRBC packed red blood cells
PRL prolactin
PA posteroanterior PRN as needed
PAC premature atrial contraction PROM premature rupture of the membranes
PAD peripheral artery disease PRS Pierre Robin syndrome
pANCA perinuclear anti-neutrophil cytoplasmic antibody PS pulmonic stenosis
PAO2 partial pressure of alveolar oxygen PSA prostate specific antigen
PaO2 partial pressure of arterial oxygen PSC primary sclerosing cholangitis
PAP pulmonary artery pressure PSGN post streptococcal glomerulonephritis
PAPP-A pregnancy associated plasma protein a P515 posterior superior iliac spine
PAT paroxysymal atrial tachycardia PSP progressive supranuclear palsy
PB peroneous brevis mm, palmaris brevis mm PT prothrombin time
PBC primary biliary cirrhosis PT physical therap
PBF pulmonary blood flow PT peroneous tertious mm
PCA posterior communicating artery Pt patient
PCI percutaneous coronary intervention PTA peritonsillar abscess
PCKD polycystic kidney disease PTA pure tone audiometery
PCOS polycystic ovarian syndrome PTC percutaneous transhepatic cholangiography
PCR polymerase chain reaction PTCA percutaneous transluminal coronary angioplasty

PTH parathyroid hormone SABD short acting bronchodilator
PTHC percutanous transhepatic cholangiogram SBE subacute bacterial endocarditis
PTSD post traumatic stress disorder SBE self breast examination
PTT partial thromboplastin time SBFT small bowel follow through
PUD peptic ulcer disease SBI serious bacterial infection
PV pulmonary valve sBP systolic blood pressure
PVC premature ventricular contraction SBP spontaneous bacterial peritonitis
PVD peripheral vascular disease SC spinal cord
PVR post void residual 5CC squamous cell carcinoma
SCFE slipped capital femoral epiphysis
Q SCM sternocleidomastoid mm
q every 5Cr serum creatinine
q4h, q6h every 4 hours, every 6 hours etc SD standard deviation
qdeveryday SEM systolic ejection murmur
qh every hour Sens sensitivity
qid four times a day SES socioeconomic status
qod every other day SFH symphysis fundal height
SGA small for gestational age
R SGGT serum gamma glutamyl transpeptidase
R&M urinalysis routine and microscopic SGOT serum glutamic oxaloacetic transaminase
R right SGPT serum glutamic pyruvic transaminase
RA rheumatoid arthritis SI sacroiliac
RA right atrium SI suicidal ideation
RAD right atrial axis deviation SIADH syndrome of inappropriate antidiuretic hormone
RAE right atrial enlargement SIDS sudden infant death syndrome
RAM rapid alternating movements SL sublingual
RAP right atrial pressure 511 systemic lupus erythematosus
RAPD relative afferent pupillary defect SLP speech language pathologist
RBBB right bundle branch block SM semimembranosis mm
RBC red blood cell SNHL sensineural hearing loss
RDS respiratory distress syndrome SNRI serotonin-norepinephrine reuptake inhibitor
RDW red cell distribution width SOAP subjective, objective, assessment, plan
RF risk factor, SOB shortness of breath
RF rectus femoris mm SOBOE shortness of breath on exertion
Rh rhesus factor Spec specificity
RhoGAM anti rhesus factor D immune globulin SPEP serum protein electrophoresis
RICE rest ice compress elevate 2 saturation of hemoglobin with oxygen as measured by pulse
SpO
RL ringer’s lactate oximetry
RLL right lower lobe SQ subcutaneous
RLQ right lower quadrant SISx signs and symptoms
RML right middle lobe SSRI selective serotonin reuptake inhibitor
RNA ribonucleic acid 555 sick sinus syndrome
RIO rule out ST semitendonosis mm
ROM range of motion STAT immediately
ROS review of systems STI sexually transmitted infection
RPA retropharngeal abscess SVD spontaneous vaginal deliver
RPR rapid plasma regain SVT supraventricular tachycardia
RSD reflex sympathetic dystrophy Sx symptoms
RT respiratory, radiation therapy
RTA renal tubular acidosis T
RTx radiation therapy T temperature
RUG retrograde urethogram TA tibialis anterior mm
RUL right upper lobe T&C type and crossmatch
RUQ right upper quadrant TAH total abdominal hysterectomy
RV residual volume TAPVR total anomalous pulmonary venous return
RVH right ventricular hyperthrophy TB tuberculosis
RVOT right ventricular outflow tract TBW total body water
RVOTO right ventricular outflow tract obstruction TCA tricyclic antidepressant
Rx prescription Td tetanus-diphtheria toxoid
TEE transesophageal echocardiogram
S TEF tracheoesophageal flstula
SA sinoatrial TENS transcutaneous electrical nerve stimulation
SAAG serum-ascites albumin gradient TENS toxic epidermal necrolysis
SAH subarachnoid hemorrhage TFL tensorfascialata mm

TG triglycerides VSD ventricular septal defect
TGA transposition of the great arteries VSR vital signs routine
THR total hip replacement VSS vital signs stable
TIA transient ischemic attack VT ventricular tachycardia
TIBC total iron binding capacity vv vein
tid three times a day Vvv varicose veins
TIG tetanus immune globulin vWD von Willebrand’s disease
TIPS transjugular intrahepatic portosystemic shunt VZV varicella zoster virus
TKO to keep open
TLC total lung capacity w
TM tympanic membrane WB weight bear
TMJ temporomandibular joint WBC white blood cell (count)
TOF tetralogy of fallot WC waist circumference
TORCH toxoplasmosis, other (syphilis), rubella, CMV, HIV WIAT Wechsler individual achievement test
TP tibialis posterior mm WISC Wechsler intelligence scale for children
TPN total parenteral nutrition WPW Wolff-Parkinson-White
TPPAT pallidum particle agglutination Wt weight
TR tricuspid regurgitation WIU workup
TS tricuspid stenosis
TSB total serum bilirubin X
TSH thyroid stimulating hormone x2d times 2 day
TTE transthoracic echocardiogram XL extended release
TTN transient tachypnea of the newborn XM crossmatch
TTP thrombotic thrombocytopenic purpura XOM extraocular movements
TURBT transurethral resection of bladder tumors XRT X-ray therapy (radiation therapy)
TURP transurethral resection of prostate xULN times upper limit of normal
TV tidal volume
TVH total vaginal hysterectomy Y
Tx treatment YF yellow fever
Tx transplant yo years old
yr year
U ytd year to dat
UA urinalysis
UAC umbilical artery catheter z
UAO upper airway obstruction ZE Zollinger-Ellison
UC ulcerative colitis
UC umbilical cord NUMERIC
UE upper extremity # fracture
UFH unfractionated heparin —ye negative
UGI upper gastrointestinal +ve positive
UG(B upper gastrointestinal bleed 1 7-OHP 17 hydroxyprogesterone
UMN upper motor neuron
U/O urine output
UPEP urine protein electrophoresis
URTI upper respiratory infection
URQ upper right quadrant
US ultrasound
UTI urinary tract infection
V
V vomiting
Vi first division of trigeminal nerve
V2 second division of trigeminal nerve
V3 third division of trigeminal nerve
VAcTERr vertebral, anal, cardiac, te fitula,
renal ,radial
VC vital capacity, vocal chord
VCUG voiding cysourethrogram
VDRL venereal disease research laboratory (test for syphilis)
VLDL very low-density lipoproteins
VMA vanillymadelic acid
VNG Videonystagmography
V/Q ventilation perfusion
—
VRE vancomycin resistant enterococcus

APPENDIX B: TRIADS, TETRADS, AND PENTADS .
Adrenomedullary excess (catecholamines) Biotin deficiency CD

• tachycardia • glossitis 0.
• vasoconstriction • alopecia
• sweating • dermatitis
x
Albinism Bochdaleck’s triad (hernia)
• black locks • respiratory distress
• occulo-cutaneous albinism • apparent dextrocardia
• deafness (sensorineural) • scaphoid abdomen
Alkaptonuria Carney’s triad

• ochronotic arthritis • functioning paraganglioma
• ochronotic pigmentation • gastric leiomyosarcoma
• urine darkens on standing • pulmonary chondroma
Alports syndrome Charcot’s triad (billiary colic/cholangitis)

• sensorineural deafness pain
• progressive renal failure • fever
• ocular anomalies • jaundice
Anderson triad Charcots triad (multiple sclerosis)

• bronchiectasis scanning speech
• cystic fibrosis intentional tremors
• vitamin A deficiency nystagmus
Aspergillosis (bronchopulmonary) Currarino’s triad (congenital anomalies in the anococcygeal region)

• bronchospasm • scimitar sacrum
• hemoptysis • presacral anterior meningocele, teratoma, or cyst
• bronchiectesis • rectal malformations
Bartters syndrome Dieulafoy’s triad

metabolic alkalosis • hypersensitiveness of the skin
hypokalemia • reflex muscular contraction
normal or decreased bp • tenderness at McBurney’s point in appendicitis.
Beck’s triad (cardiac compression/cardiac tamponade) Donoghue triad (rotational force in a weight bearing knee)
• muffled heart sound • medial collateral ligament injury
• distended neck veins (high venous pressure) • anterior cruiciate ligament injury
• hypotension (low arterial pressure) • medial meniscus injury
Becks triad (renal cell Ca) Fanconi syndrome

• hematuria • aminoaciduria
• flankpain • proteinuria
• palpable flank mass • phosphaturia
Behcet’s syndrome Gradenigos triad

• recurrent oral ulcers • sixth cranial n. palsy
• genital ulcers • mastioditis (persistent ear discharge)
• iridocyclitis • deep seated retro orbital & temporal pain
Bergmanns triad (fat embolism) Grancher’s triad (early pulmonary tuberculosis)

• petechial hemorhages over chest • lessened vesicular quality of breathing
• moderate rise in temperature • skodaic resonance
• fall of hematocrit • increased vocal fremitus
Bezold’s triad (otosclerosis) Grawitz tumour (hypernephroma)

• prolonged bone conduction (negative rinne test) hematuria
• lessened perception of low tones pain
• negative rinne’s test palpable renal tumor

Heerfordt syndrome Rubella
• uveitis • patent ductus arteriosis
• fever • deafness
• parotid enlargement • cataract
Hemobilia Osler’s triad (hereditary hemorrhagic telangiectasia)

• melena • telangiectasia
• obstructive jaundice • capillary fragility
• biliary colic • hereditary hemorrhagic diathesis
Hemolytic uremic syndrome Paroxysmal nocturnal hemoglobinuria

• anemia • hemolytic anaemia
• thrombocytopenia • venous thrombosis
• renal failure • deficient hemopoesis
Hypernephroma Reiter’s syndrome

• pain • arthritis
• hematuria • urethritis
• renal mass • conjunctivitis
Hutchinson’s triad (congenital syphilis) Rokytansky Kuster Hauser syndrome

• mulberry molars • absent vagina
• interstitial keratitis • non functional uterus
• labyrinthine disease (nerve deafness) • normal xx female
Kartagener s syndrome Saint’s triad

• bronchiectasis • gall stones
• recurrent sinusitis • diverticulosi5
• situs inversus • hiatus hernia
Kwashiorkar Sampter’s triad

• growth retardation • aspirin allergy
• mental changes • bronchial asthma
• edema • nasal polyp
Triad of Luciani (cerebellar disease) Triad of Schultz

• asthenia • jaundice
• atonia • gangrenous stomatitis
astasia • leukopenia
Miniere’s disease Tetany in children

• vertigo stridor
• tinnitus • carpopedal spasm
sensorineural hearing loss • convulsions
Melkerson-Rosenthal syndrome Trotter’s triad

• recurrent facial palsy • conductive deafness
• plication of tongue • immobility of homolateral soft palate
• facial edema • trigeminal neuralgia
Multiple myeloma Urethral diverticulum

• plasmacytosis >10% • dribbling of urine after voiding
• hypergammaglobulinemia • dysuria
• lytic bone lesions • dyspareunia
Murphy’s triad (acute appendicitis) Vanderhove syndrome

• pain • blue sclera
• fever • multiple fractures
vomitting • otosclerosis
Normal pressure hydrocephalus Virchows triad (predisposing to vascular thrombosis)

• dementia • stasis
• urinary incontinence • hypercoagulabilty
• ataxia/gait apraxia • 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 weeks
Whipples triad (insulin-producing tumors)

• hypoglycaemia during attacks
• serum glucose <40 mg%
• prompt relief on glucose administration
Youngs syndrome
• sinusitis
• bronchiectasis
• azoospermia
Hemoplytic uremic syndrome pentad

• microangiopathic hemolytic anemia
• acute renal failure
• thrombocytopenia
• fever
• hypertension
Tetrology of Fallot
• atrial septal defect
• overarching aorta
• pulmonary stenosis
• right ventricular hypertrophy
Penta logy of Fallot

• Fallot’s Tetralogy
• + patent foramen ovale or atrial septal defect
Raynaud’s pentad
• Charcot’s triad
• + sepsis
• + mental status changes
Pentad of TTP
• microangiopathic haemolytic anaemia
• fever
• disturbed neurological function
• renal failure
• thrombocytopenia

Canadian Federation of Medical Students
Your federation. Your voice.
Servces I’ crg
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CFMS FEMC
Canadian Federation Fddération den étudiants et den
of MedcaE Studentn etudiantes en médectne du Canada
.4
Rprsn1afion Communkafion
• The Canadian Federation of Medical Students (CFMS) is the national representative voice of medical
students in Canada.
• Our membership includes over 7000 medical students pursuing their medical careers in 14 member
schools from coast to coast.
• Your membership to your Medical Student Society or Association automatically grants you full CFMS
membership benefits.
Visit www.cfms.org to learn more about our student resources and your member benefits:
from travel and textbook discounts to residency matching advice, and so much more.
CFMS . 324 Somerset Street West, Suite 300• Ottawa, ON, K2P 0J9• (613) 565-7740 offlce@cfms.org www.cfms.org

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Approach to the OSCE:

The Edmonton Manual of

Common Clinical Scenarios

Edmonton Manual Features:

New to the 2011 Edition:

The Edmonton Manual will strengthen your”Approach to the OSCE”!

APPROACH TO THE OSCE:

Edmonton Manual of Common Clinical Scenarios 1

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

Copyright © 2011 University of Alberta Medical Students’ Association

explicit permission from the copyright owner.

errors or omissions to us by postal mail or e-mail.

information on this publication.

2 Edmonton Manual of Common Clinical Scenarios

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

Edmonton Manual of Common Clinical Scenarios 3

Senior Editor Jasmine Pawa

Junior Editor David Lesniak

Internal Medicine Section Editor: Vijay Daniels, MD, FRCPC

Obstetrics & Gynecology Section Editor Sujata Chandra MD FRCSC

Pediatrics Section Editor Melanie Lewis BN MD MEd FRCPC

Psychiatry Section Editor Jorge Perez-Parada BSc MD MS FRCPC

Physical Exam and PHLEO Lisa J. Steblecki MD MPH CCFP

Design and Production

4 Edmonton Manual of Common Clinical Scenarios

Resident Contributing Authors

Staff Physician Contributing Authors

Edmonton Manual of Common Clinical Scenarios 5

Section #1: Essential Clinical Skills

Section #2: Physical Exam 64

Section #3: Internal Medicine 84

100 Parkinsons and Movement Disorders 148

6 Edmonton Manual of Common Clinical Scenarios

Section #4: Obstetrics and Gynecology 194

Section #5: Psychiatry 234

Section #6: Pediatrics 252

Section #7: Surgery 302

Edmonton Manual of Common Clinical Scenarios 7

8 Edmonton Manual of Common Clinical Scenarios

This book is divided into eight sections:

1. Essential Clinical Skills (ECS)

Edmonton Manual of Common Clinical Scenarios 9

How to excel at the OSCE

10 Edmonton Manual of Common Clinical Scenarios

APPROACH TO THE OSCE:

2ND EDITION 2011

Edmonton Manual of Common Clinical Scenarios 11

ESSENTIAL CLINICAL SKILLS

Admission and Daily Orders .14 Interpretation of Electrolytes: Sodium 40

Interpretation of a Abdominal Radiograph .20 Interpretation of PFT 46

Interpretation of C-Spine Imaging 30 Procedure and Ward Call Notes.

12 Edmonton Manual of Common Clinical Scenarios I Essential Clinical Skills

The Edmonton Manual EditorialTeam

Essential Clinical Skills Edmonton Manual of Common Clinical Scenarios 13

14 Edmonton Manual of Common Clinical Scenarios Essential Clinical Skills

• Imaging X-ray, MRI, CT, bone scan

• Other ABG, EKG, echo

• 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

Essential Clinical Skills Edmonton Manual of Common Clinical Scenarios 15

BOX 1: Assessing malignancy in lesions:

16 Edmonton Manual of Common Clinical Scenarios I Essential Clinical Skills

Nails: Pitting, separation from nail bed (onycholysis), Yellow