Toronto Notes 2018 [34 ed.] 9781927363409

Table of contents :
Cover
Title
Copyright
Dedication
Preface – From the Editors
Acknowledgements
Student Contributors
Faculty Contributors, University of Toronto
Table of Contents
1. Common Unit Conversions
2. Commonly Measured Laboratory Values
3. Ethical, Legal, and Organizational Medicine
4. Anesthesia and Perioperative Medicine
5. Cardiology and Cardiac Surgery
6. Clinical Pharmacology
7. Dermatology
8. Emergency Medicine
9. Endocrinology
10. Family Medicine
11. Gastroenterology
12. General Surgery and Thoracic Surgery
13. Geriatric Medicine
14. Gynecology
15. Hematology
16. Infectious Diseases
17. Medical Genetics
18. Medical Imaging
19. Nephrology
20. Neurology
21. Neurosurgery
22. Obstetrics
23. Ophthalmology
24. Orthopedics
25. Otolaryngology
26. Pediatrics
27. Plastic Surgery
28. Population Health and Epidemiology
29. Psychiatry
30. Respirology
31. Rheumatology
32. Urology
33. Vascular Surgery
34. Index
A
B
C
D
E
F
G
H
I
J
K
L
M
N
O
P
Q
R
S
T
U
V
W
X
Y
Z

Citation preview

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COMPREHENSIVE MEDICAL REFERENCE & REVIEW FOR MCCQE AND USMLE II

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Editors-in-Chief: Tina Binesh Marvasti & Sydney McQueen

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Production Managers: Ilya Mukovozov & Kirill Zaslavsky

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TORONTO NOTES

2018

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Toronto Notes fr

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Comprehensive medical reference and review for the Medical Council of Canada Qualifying Exam (MCCQE) Part I and the United States Medical Licensing Exam (USMLE) Step 2

34th Edition.

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Editors-in-Chief: Tina Binesh Marvasti and Sydney McQueen

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Wherever the art of medicine is loved, there is also a love of humanity. – Hippocrates

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Toronto, Ontario, Canada

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Toronto Notes for Medical Students, Inc

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Thirty-fourth Edition

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Copyright © 2018 – Toronto Notes for Medical Students, Inc. Toronto, Ontario, Canada. Typeset and production by Type & Graphics Inc. ISBN 978-1-927363-40-9 (34th ed.)

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All rights reserved. Printed in Toronto, Ontario, Canada. Toronto Notes 2018 is provided for the sole use of the purchaser. It is made available on the condition that the information contained herein will not be sold or photocopied. No part of this publication may be used or reproduced in any form or by any means without prior written permission from the publisher. Every effort has been made to obtain permission for all copyrighted material contained herein. Previous editions copyright © 1985 to 2018.

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Cover illustration: Matan Berson and Natividad Chen Illustrations: Biomedical Communications, University of Toronto

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Notice: THIS PUBLICATION HAS NOT BEEN AUTHORED, REVIEWED, OR OTHERWISE SUPPORTED BY THE MEDICAL COUNCIL OF CANADA NOR DOES IT RECEIVE ENDORSEMENT BY THE MEDICAL COUNCIL AS REVIEW MATERIAL FOR THE MCCQE PART I. THIS PUBLICATION HAS NOT BEEN AUTHORED, REVIEWED, OR OTHERWISE SUPPORTED BY THE NATIONAL BOARD OF MEDICAL EXAMINERS U.S.A NOR DOES IT RECEIVE ENDORSEMENT BY THE NATIONAL BOARD AS REVIEW MATERIAL FOR THE USMLE.

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The editors of this edition have taken every effort to ensure that the information contained herein is accurate and conforms to the standards accepted at the time of publication. However, due to the constantly changing nature of the medical sciences and the possibility of human error, the reader is encouraged to exercise individual clinical judgement and consult with other sources of information that may become available with continuing research. The authors, editors, and publisher are not responsible for errors or omissions or for any consequences from application of the information in this textbook, atlas, or software and make no warranty, expressed or implied, with respect to the currency, completeness, or accuracy of the contents of the publication. In particular, the reader is advised to check the manufacturer’s insert of all pharmacologic products before administration.

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FEEDBACK AND ERRATA We are constantly trying to improve the Toronto Notes and welcome your feedback. If you have found an error in this edition please do not hesitate to contact us. As well, we look forward to receiving any comments regarding any component of the Toronto Notes package and website.

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Please send your feedback to: [email protected]

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Alternatively, send mail to: Toronto Notes for Medical Students Editors-in-Chief c/o The Medical Society 1 King’s College Circle, Room 2260 Toronto, Ontario M5S 1A8 Canada email: [email protected] Tel: 1-416-946-3047 Fax: 1-416-978-8730

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Library of Congress Cataloging-in-Publication Data is available upon request

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Toronto Notes 2018

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Dedicated to all

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past and present contributors and

supporters of Toronto Notes

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who have made the production of the 2018 edition possible!

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The Toronto Notes for Medical Students is dedicated to helping fund many charitable endeavours and medical student initiatives at the University of Toronto’s Faculty of Medicine and beyond. Programs that have received Toronto Notes for Medical Students funding include: Medical School Clubs • Books with Wings • Women in Medicine • University of Toronto International Health Program • Complementary and Alternative Medicine • Peer Support for Students • History of Medicine Society • Faculty of Medicine Yearbook

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Community Affairs Projects • Saturday Program for Inner City High School and Grade 8 students • St. Felix Mentorship Program for Inner City children • Parkdale Mentorship Program for Grade 10-12 students • WoodGreen Community Centre Let’s Talk Science • Growing Up Healthy

Other Events • Save a Child’s Heart • Australian Medical School Association Conference • Medical Student Research Day • Ontario Medical Students Weekend (OMSW) • OMSA’s Medical Student Education Research Grant (MSERG)

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Annual Faculty Showcase Events • Daffydil, in support of the Canadian Cancer Society • Earthtones Benefit Concert • Convocation and Ceremonies

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Scholarships and Bursaries • Nishant Fozdar Memorial Award • Graduating Medical Class Scholarships and Bursaries

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Note: Many of you have wondered about the Toronto Notes logo, which is based on the rod of Asclepius, the Greek god of medicine. The rod of Asclepius consists of a single serpent entwined around a staff. This icon symbolizes both rebirth, by way of a snake shedding its skin, and also authority, by way of the staff. In ancient Greek mythology, Asclepius was the son of Apollo and a skilled practitioner of medicine who learned the medical arts from the centaur Chiron. Asclepius’ healing abilities were so great that he was said to be able to bring back people from the dead. These powers displeased the gods, who punished Asclepius by placing him in the sky as the constellation Orphiuchus. The rod of Asclepius is at times confused with the caduceus, or wand, of Hermes, a staff entwined with two serpents and often depicted with wings. The caduceus is often used as a symbol of medicine or medical professionals, but there is little historical basis for this symbolism. As you may have guessed, our logo uses the rod of Asclepius that is modified to also resemble the CN Tower – our way of recognizing the university and community in which we have been privileged to learn the art and science of medicine.

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Thomas O’Brien, MD Class of 2009, M.D. Program, University of Toronto

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Preface – From the Editors Australian Medical School Association, among others. We would like to thank you for supporting these initiatives through your purchase of Toronto Notes 2018

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Dear Readers,

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As the Editors-in-Chief of Toronto Notes 2018, we are proud to present the 34th Edition!

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We would like to continue to encourage feedback – this year’s edition saw many improvements thanks to suggestions from our readers. We hope that Toronto Notes 2018 enhances your medical knowledge and allows you to perform better on both your clinical rotations and licensing exams. On behalf of the Toronto Notes 2018 team, we wish you success in your studies and academic endeavours.

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Tina Binesh Marvasti, MSc, MD/PhD Candidate and Sydney McQueen, MSc, MD/PhD Candidate Editors-in-Chief, Toronto Notes 2018 MD Program, University of Toronto

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Sincerely,

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Toronto Notes 2018 is produced by Toronto Notes for Medical Students Inc., which is a non-for-profit organization supporting various charity organizations and medical student initiatives in the city of Toronto and across the globe. This year, sponsored organizations included Community Affairs, the Ontario Medical Student Weekend (OMSW), the University of Toronto Class Councils, Save A Child’s Heart, Earth Tones, Medical Student Research Day (MRSD) The Medical Student Education Research Grant (MSERG), Daffydil, the Conference of the

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For the past 33 years we have remained committed to our original vision. The 2018 edition of Toronto Notes contains significant improvements and new editions including: 1. A brand new Medical Genetics chapter with evidence based medicine highlights. 2. Updated versions of the Clinical Handbook and STAT Notes that are more concise, with new figures and additions. 3. An updated website featuring a colour atlas, ECG and heart sound tutorials, essentials of medical imaging, and over 50 OSCE practice questions and scenarios. 4. A significantly improved interactive eBook with many new high-quality colour images. 5. An updated Toronto Notes Quiz App, which is available for free on iTunes and Google Play. This app contains hundreds of questions allowing users to test themselves on the content contained within Toronto Notes.

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We would like to highlight the exceptional work of our team, composed of over 150 medical students, medical illustrators, and faculty members at the University of Toronto Faculty of Medicine. Without the tireless effort expended by these individuals, the production of Toronto Notes 2018 would not have been possible. In particular, we would like to highlight the work of the executive team, all of whom made personal sacrifices in balancing their clinical and academic duties with the responsibilities asked of them: our production managers, Ilya Mukovozov and Kirill Zaslavsky, our associate editors, Graham Mazereeuw, Samik Doshi, Mark Shafarenko, Sangwoo Leem, Tara Tofighi, Sheliza Halani, and our EBM editors, Alexander Sapa, Keeth Krishnan, Shubham Shan, Jin Kyu Kim, Sukhmani Sodhi, Arnav Agarwal. We also want to highlight the work of Rajkumari Chatterjee from University of Toronto Bookstore, who has contributed to the production of Toronto Notes for the past ten years, and has been instrumental in the annual launch of the Toronto Notes Ebook. Lastly, we would like to thank our partners at Type & Graphics Inc., particularly Enrica Aguilera, for their assistance during the production of Toronto Notes 2018.

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Toronto Notes began humbly in 1985 from a set of student notes circulated among medical students at the University of Toronto. Over time, Toronto Notes has grown into one of the premier study resources for generations of medical trainees in Canada and abroad. This rich history solidified our commitment to publish a comprehensive study resource for medical students engaged in clinical rotations and studying for both the Canadian MCCQE Part 1 and USMLE Step 2.

Toronto Notes 2018

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Acknowledgements

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We would like to acknowledge the exceptional work of all previous Toronto Notes (formerly MCCQE Notes) Editors-in-Chief and their editorial teams The 34th edition of this text was made possible with their contributions.

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2017 (33rd ed.): Jieun Kim and Ilya Mukovozov 2016 (32nd ed.): Zamir Merali and Justin D. Woodfine

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2015 (31th ed.): Justin Hall and Azra Premji

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2014 (30th ed.): Miliana Vojvodic and Ann Young

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2013 (29th ed.): Curtis Woodford and Christopher Yao

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2012 (28th ed.): Jesse M. Klostranec and David L. Kolin

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2011 (27th ed.): Yingming Amy Chen and Christopher Tran

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2010 (26th ed.): Simon Baxter and Gordon McSheffrey 2009 (25th ed.): Sagar Dugani and Danica Lam

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2008 (24th ed.): Rebecca Colman and Ron Somogyi

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2007 (23rd ed.): Marilyn Heng and Joseph Ari Greenwald

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2006 (22nd ed.): Carolyn Jane Shiau and Andrew Jonathan Toren

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2005 (21st ed.): Blair John Normand Leonard and Jonathan Chi-Wai Yeung

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2004 (20th ed.): Andrea Molckovsky and Kashif S. Pirzada

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2003 (19th ed.): Prateek Lala and Andrea Waddell 2002 (18th ed ): Neety Panu and Sunny Wong 2001 (17th ed.): Jason Yue and Gagan Ahuja

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2000 (16th ed.): Marcus Law and Brian Rotenberg

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1999 (15th ed.): Sofia Ahmed and Matthew Cheung

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1998 (14th ed.): Marilyn Abraham and M Appleby

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1997 (13th ed.): William Harris and Paul Kurdyak

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1996 (12th ed.): Michael B. Chang and Laura J. Macnow

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1995 (11th ed.): Ann L. Mai and Brian J. Murray

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1994 (10th ed.): Kenneth Pace and Peter Ferguson 1993 (9th ed.): Joan Cheng and Russell Goldman

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1992 (8th ed.): Gideon Cohen-Nehemia and Shanthi Vasudevan

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All former Chief Editors from 1991 (7th ed.) to 1985 (1st ed.)

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Student Contributors

Clinical Handbook Editors STAT Notes Editor Waleed S. Ahmed Mina Faheim Claudia Frankfurter Kimia Sorouri

MEDICINE Associate Editors Samik Doshi Graham Mazereeuw

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EBM Editors Arnav Agarwal Sukhmani Sodhi

Associate Editors Sangwoo Leem Mark Shafarenko

Population Health and Epidemiology Arjun Sithamparapillai Vishalini Sivarajah

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Emergency Medicine Cecilia Alvarez-Veronesi Omri Arbiv Matt Piaseczny

Psychiatry Ayan Dey Jonah Himelfarb Yasmin Nasirzadeh

Hematology Lianne Rotin Xin (Kevin) Wang

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Orthopedics Michael Dzingala Tyler Hauer

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Respirology Sameer Kushwaha Albert Lee

Plastic Surgery Josephine D’Abbondanza Maya Deeb Matthew Lee Talha Maqbool

Neurosurgery Ann Mansur Cel na Nahanni Nardin Samuel

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Neurology Ikreet Cheema Dhruv Kumar Jain Tal Milman

Gynecology Maria Daniel Tammy Ryan Michal Sheinis Evelyn Waugh

Otolaryngology Ragavan Ganeshathasan Armin Rahmani Stephen Szeto Siraj Zahr

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Geriatric Medicine Victoria Chuen Jessica Mak

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Pediatrics Jessie Peng Shirley Poon

Dermatology Arvin Ighani Sarah Park Stephanie Zhou

Gastroenterology Raghad Al-Saqqar James Bao Roseanna Presutti

General Surgery and Thoracic Surgery Amanpreet Brar Zacharie Cloutier Jeff Metz Alexander Tigert

Urology Viranda H. Jayalath Anand Lakhani Ahmad Mousa

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Clinical Pharmacology Rushi Gandhi Pamela Leung

Nephrology Tamoor Afzaal Sarah Cao Tianyang (Day) Dai

Rheumatology Patrina Cheung Stephanie Wan

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Medical Imaging Mark Barszczyk Tian Yang (Darren) Liu Zafir Syed Jinhui (Bill) Yan

Endocrinology Jesse Creamer Ahmed Shah Corita Vincent

EBM Editors Jin Kyu Kim Shubham Shan

Chapter Editors Infectious Diseases Zane Brickman Robyn Elphinstone Rochelle Melvin

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Medical Genetics Spencer van Mil

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Anesthesia and Perioperative Medicine Lior Krimus Abdulkarim Muhaseen Pauline Sawicki

Cardiology and Cardiac Surgery Manpreet Basuita Yehia Fanous Jason Gencher

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Family Medicine Mohammed Firdouse Simran Mundi Gary Tran

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Ethical, Legal, and Organizational Medicine Sabrina Agnihotri Arash Khairandish

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Chapter Editors

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Chapter Editors

SURGERY EBM Editors Keeth Krishnan Alexander Sapa

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PRIMARY AND OTHER SPECIALTIES

BMC Production Editors Matan Berson Natividad Chen

Obstetrics Emily Bartsch Stephanie Searle Curtis Sobchak Ophthalmology Daniel Q. Li Fady Sedarous Tarek Bin Yameen

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Vascular Surgery Asha Behdinan Joshua Mehta

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Sydney McQueen

Associate Editors Sheliza Halani Taraneh (Tara) Tofighi

Atlas Editor Ali Helmi

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Tina Binesh Marvasti

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Production Managers Ilya Mukovozov Kirill Zaslavsky

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Editors-in-Chief

Copy Editors

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Leedan Cohen Mammon Mirriam Mikhail Sara Mirali Jason (Jaewoo) Park Austin Pereira Casey Rosen Leigha Rowbottom Shihab Sarwar

Arunima Sivanand Sivisan Suntheralingam Jaya Tanwani Fang Zhou (Faith) Xu Eric (Yu Hang) Zheng

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Jethro Kwong Kimberley Lam Min Joon Lee Chantal Li Emily (Yujin) Li Helen Liu Marissa Lu Alexandra Majerski

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Helen Genis Salwa Hasan Kizanee Jegatheeswaran Danielle Jeong Jason Jia Shicheng (Tony) Jin Eshita Kapoor Brij Karmur

Armin Abadeh Melissa Allwood Amira Balbaa Chloe Cadieux Alon Coret Ari Cuperfain Taylor Dear Megan Drupals

Lucas Lin Ryan Park

Dani Sayeau

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Jerry Gu Andrea Lam

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BMC ILLUSTRATORS

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Faculty Contributors, University of Toronto

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Vicky Chau, MD, MScCH, FRCPC Division of Geriatric Medicine Department of Medicine University Health Network

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Wai-Ching Lam, MD, FRCSC Department of Ophthalmology and Vision Science University Health Network Toronto Western Hospital

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Chloe Leon, MD, FRCPC Division of Brain and Therapeutics Department of Psychiatry Centre for Addiction and Mental Health Armando Lorenzo, MD, FRCSC Division of Urology Department of Surgery The Hospital for Sick Children

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Sari L. Kives, MD, FRCSC Department of Obstetrics and Gynecology St. Michael’s Hospital and The Hospital for Sick Children

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Sender Herschorn, MDCM, FRCSC Division of Urology Department of Surgery Sunnybrook Health Sciences Centre and Women’s College Hospital

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Philip C. Hébert, MA, PhD, MD, FCFPC Department of Family and Community Medicine Joint Centre for Bioethics Sunnybrook Health Sciences Centre

Gabor Kandel, MD, FRCPC Division of Gastroenterology Department of Medicine St. Michael’s Hospital

Todd Mainprize, MD, FRCSC Department of Neurosurgery Sunnybrook Health Sciences Centre Eric Massicotte, MD, MSc, FRCSC Department of Neurosurgery University Health Network Toronto Western Hospital

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Simon Carette, MD, FRCPC Division of Rheumatology Department of Medicine Mount Sinai Hospital

Jeremy Hall, MD, FRCSC Division of Orthopedic Surgery Department of Surgery St Michael’s Hospital

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John Byrne, MD, MB, BCh, BAO Division of Vascular Surgery Department of Surgery University of Toronto

Tanna Gemini, MD, FRCPC Division of Nephrology Department of Medicine Sunnybrook Health Sciences Centre

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Arthur Bookman, MD, FRCPC Division of Rheumatology Department of Medicine University Health Network Toronto Western Hospital

Mark Freedman, MD, FRCPC Department of Emergency Medicine Sunnybrook Health Sciences Centre

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Andrea Boggild, MSc, MD, FRCPC Tropical Disease Unit and Division of Infectious Diseases University Health Network Toronto General Hospital

Alfonso Fasano, MD, PhD, FRCPC Division of Neurology University Health Network Toronto Western Hospital

David Juurlink, BPhm, MD, PhD, FRCPC Division of Clinical Pharmacology and Toxicology Departments of Medicine and Pediatrics Sunnybrook Health Sciences Centre

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Ari Bitnun, MD, MSc, FRCPC Division of Infectious Diseases The Hospital for Sick Children

Michelle Farrugia, M.D., MEd., FRSCS Department of Obstetrics and Gynecology Mount Sinai Hospital Department of Obstetrics and Gynecology University of Toronto

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Matthew Binnie, MD Division of Respirology University Health Network St. Michael’s Hospital

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Katherine Bingham, MD, MPH, CCFP-EM Faculty of Medicine University of Toronto

Hanna Faghfoury, MDCM, FRCPC, FCCMG The Fred A Litwin Family Centre in Genetic Medicine Department of Medicine Mount Sinai Hospital and University Health Network

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Abdollah Behzadi, MD, MBA, FRCSC, FACS Division of Thoracic Surgery Department of Surgery University of Toronto

Maria Cino, HonBSc, MSc, MD, FRCPC Division of Gastroenterology University Health Network Toronto Western Hospital

Julie Johnston, MD (FRCPC), MScCH Department of Pediatrics The Hosp tal for Sick Children Division of Pediatric Medicine University of Toronto

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Allison Chris, MD, MSc, FRCPC Division of Clinical Public Health Dalla Lana School of Public Health

Nasir Jaffer, MD, FRCPC Division of Abdominal Imaging Department of Medical Imaging Joint Department of Medical Imaging University of Toronto

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Jillian Baker, MD, MSc, FRCPC Pediatrician and Pediatric Hematologist St. Michael’s Hospital and The Hospital for Sick Children Faculty of Medicine, University of Toronto

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Chi-Ming Chow, MDCM, MSc, FRCPC Division of Cardiology Department of Medicine St. Michael’s Hospital

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Ruby Alvi, MD, CCFP, MHSc Department of Family and Community Medicine University of Toronto

Jonathan C. Irish, MD, MSc, FRCSC Department of Otolaryngology Head and Neck Surgery University Health Network

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Alice Cheung, MD, FRCPC Division of Endocrinology and Metabolism Department of Medicine St. Michael’s Hospital

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David Adam, MD, FRCPC Division of Dermatology Department of Medicine St. Michael’s Hospital

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All contributing professors have been appointed at the University of Toronto.

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Fernando Teixeira, MD, FRCPC Department of Emergency Medicine St. Michael’s Hospital

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Ramesh Prasad, MBBS,MSc,MA,PhD, FRCPC Faculty of Medicine, University of Toronto Division of Nephrology Department of Medicine St. Michael’s Hospital

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Joshua C. Teichman, MD, MPH, FRCSC Ophthalmology and Vision Sciences Trillium Health Partners Univers ty of Toronto

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Piero Tartaro, MD, FRCPC Division of Gastroenterology Department of Medicine Sunnybrook Health Sciences Centre

Mary Preisman, MD, FRCPC Department of Psychiatry Mount Sinai Hospital

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Jensen Yeung, MD, FRCPC Division of Dermatology Department of Medicine Women’s College Hospital Eugene Yu, MD, FRCPC Division of Neuroradiology Department of Medical Imaging University Health Network

Martina Trinkaus, MD, FRCPC Division of Hematology Department of Medicine St. Michael’s Hospital

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Laila Premji, MD, FRCPC Division of Paediatric Medicine Department of Paediatrics The Hospital for Sick Children

Anna Woo, MD CM, SM, DABIM, FRCPC Division of Cardiology Department of Medicine University Health Network Toronto General Hospital

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Susan M. Poutanen, MD, MPH, FRCPC Department of Microbiology University Health Network and Mount Sinai Hospital Departments of Laboratory Medicine & Pathobiology and Medicine University of To onto

Fay Weisberg, MD, FRCSC Division of Reproductive Endocrinology and Infertility Department of Obstetrics and Gynecology University of Toronto

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Diana Tamir, MD, FRCPC Department of Anesthesia and Pain Management University Health Network

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Richard Pittini, MD, MEd, FRCSC, FACOG Department of Obstetrics and Gynaecology University of Toronto Sunnybrook Health Sciences Centre

Alice Wei, MD CM, MSc, FRCSC Division of General Surgery Department of Surgery University Health Network

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George Oreopoulos, MD, MSc, FRCSC Division of Vascular Surgery Department of Surgery University Health Network

Joyce So, MD, PhD, FRCPC, FCCMG The Fred A. Litwin Family Centre in Genetic Medi ine Department of Medicine Mount Sinai Hospital and University Health Network

Jeffrey Wassermann, MD, FRCPC Department of Anesthesia St. Michael’s Hospital

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Elizabeth Slow, MD, PhD, FRCP Division of Neurology University Health Network

Melinda Musgrave, MD, PhD, FRCSC Division of Plastic and Reconstructive Surgery Department of Surgery St. Michael’s Hospital

Kyle R. Wanzel, MD, MEd, FRCSC Division of Plastic Surgery St. Joseph’s Health Centre

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Kevin Skarratt, MD, FRCPC Department of Emergency Medicine Sunnybrook Health Sciences Centre

Ally Murji, MD, MPH, FRCS(C) Department of Obstetrics and Gynecology Mount Sinai Hospital

Oshrit Wanono, MD, FRCPC Division of Child and Adolescent Psychiatry Department of Psychiatry Centre for Addiction and Mental Health

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Marisa Sit, MD, FRCSC Department of Ophthalmology University Health Network Toronto Western Hospital

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Istvan Mucsi, MD PhD, FRCPC, FASN Department of Medicine (Nephrology) University of Toronto Kidney Transplant Program Toronto General Hospital University Health Network

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Michelle Sholzberg, MDCM, MSc, FRCPC Division of Hematology Department of Medicine St. Michael’s Hospital

Danielle Vicus, MD, MSc Gynecologic Oncologist Sunnybrook Health Sciences Centre Department of Obstetrics and Gynecology University of Toronto

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Azadeh Moaveni, MD, CCFP Department of Family and Community Medicine University Health Network Toronto Western Hospital

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Amanda Selk, MD, FRCSC Department of Obstetrics and Gynecology Mount Sinai Hospital

Herbert P. von Schroeder, MD, MSc, FRCSC Divisions of Orthopedic Surgery and Plastic Surgery Department of Surgery University Health Network

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Evan Propst, MD, MSc, FRCSC Division of Head and Neck Surgery Department of Otolaryngology The Hospital for Sick Children

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Michael McDonald, MD, FRCPC Division of Cardiology and The Multi-Organ Transplant Program Department of Medicine University Health Network Toronto General Hospital

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Faculty Contributors, University of Toronto

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Table of Contents Index Abbreviations Common Unit Conversions

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Commonly Measured Laboratory Values

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Ethical, Legal, and Organizational Medicine . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ELOM

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Anesthesia and Perioperative Medicine . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . A

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Cardiology and Cardiac Surgery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . C

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Clinical Pharmacology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . CP

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7. Dermatology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . D Emergency Medicine . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ER

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9. Endocrinology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . E

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10. Family Medicine . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . FM 11. Gastroenterology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . G 12. General Surgery and Thoracic Surgery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . GS 13. Geriatric Medicine . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . GM 14. Gynecology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . GY

.

.

15. Hematology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . H

re

16. Infectious Diseases . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ID

s

17. Medical Genetics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . MG

o

18. Medical Imaging . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . MI

b

19 Nephrology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . NP 20. Neurology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . N 21. Neurosurgery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . NS 22. Obstetrics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . OB 23. Ophthalmology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . OP

re

24. Orthopedics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . OR

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25. Otolaryngology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . OT

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26. Pediatrics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . P 27. Plastic Surgery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . PL

e

28. Population Health and Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . PH 29. Psychiatry . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . PS 30. Respirology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . R 31. Rheumatology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . RH 32. Urology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . U

e

33. Vascular Surgery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . VS 34. Index

9

Toronto Notes 2018

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How to Use This Book

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This book has been designed to remain as one book or to be taken apart into smaller booklets. Identify the beginning and end of a particular section, then carefully bend the pages along the perforated line next to the spine of the book. Then tear the pages out along the perforation.

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The layout of Toronto Notes allows easy identification of important information. These items are indicated by icons interspersed throughout the text:

Icon Icon Name

Significance

Clinical Pearl

This icon is found in sidebars of the text. It identifies concise, important information which will aid in the diagnosis or management of conditions discussed in the accompanying text.

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Key Objectives

This icon is found next to headings in the text. It identifies key objectives and conditions as determined by the Medical Council of Canada or the National Board of Medical Examiners in the USA. If it appears beside a dark title bar, all subsequent subheadings should be considered key topics.

b

This icon is found in sidebars of the text. It identifies helpful mnemonic devices and other memory aids.

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Memory Aid

This icon is found in sidebars of the text. It indicates information or findings that require urgent management or specialist referral.

Cross-Reference

This icon is found in sidebars of the text. It indicates a cross-reference for information that is discussed in a separate chapter.

Evidence Based Medicine

This icon is found in sidebars of the text. It identifies key research studies for evidence-based clinical decision making related to topics discussed in the accompanying text.

Colour Photo Atlas

This icon is found next to headings in the text. It indicates topics that correspond with images found in the Colour Photo Atlas available online (www torontonotes.ca).

Radiology Atlas

This icon is found next to headings in the text It indicates topics that correspond to images found in the Radiology Atlas available online (www.torontonotes.ca).

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This icon is found next to headings in the text. It indicates topics that correspond with electronic resources such as Functional Neuroanatomy or ECGs Made Simple, available online (www.torontonotes.ca).

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Online Resources

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Clinical Flag

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Chapter Divisions

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To aid in studying and finding relevant material quickly, each chapter is organized in the following general framework:

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Basic Anatomy/Physiology Review • features the high-yield, salient background information students are often assumed to have remembered from their early medical school education Common Differential Diagnoses • aims to outline a clinically useful framework to tackle the common presentations and problems faced in the area of expertise

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Diagnoses • the bulk of the book • etiology, epidemiology, pathophysiology, clinical features, investigations, management, complications, and prognosis

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Common Medications • a quick reference section for review of medications commonly prescribed 10

Toronto Notes 2018

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Common Unit Conversions

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To convert from the conventional unit to the SI unit, multiply by conversion factor

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Conventional Unit

Conversion Factor

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To convert from the SI unit to the conventional unit, divide by conversion factor SI Unit g/L

Bilirubin

mg/dL

17.1

µmol/L

Calcium

mg/dL

0.25

mmol/L

Cholesterol

mg/dL

0.0259

mmol/L

Cortisol

µg/dL

27.59

nmol/L

Creatinine

mg/dL

88.4

µmol/L

Creatinine clearance

mL/min

0.0167

Ethanol

mg/dL

0.217

eb

pmol/L

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0.22 10

e.

pg/mL g/dL

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ACTH Albumin

mL/s

mmol/L pmol/L mmol/L

HbA1c

%

0.01

proportion of 1.0

Hemaglobin

g/dL

10

g/L

HDL cholesterol

mg/dL

0.0259

mmol/L

Iron, total

µg/dL

0 179

µmol/L

Lactate (lactic acid)

mg/dL

0.111

mmol/L

LDL cholesterol

mg/dL

0.0259

mmol/L

1

x 109 cells/L

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103

cells/mm3

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2.247 0.0555

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ng/mL mg/dL

e

Ferritin

Glucose

mg/dL

0.411

µm3

1

fL

1

x 109 cells/L

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MCV

103

cells/mm3

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Magnesium

m

x

oo

Leukocytes

mmol/L

x

Reticulocytes

% of RBCs

0.01

proportion of 1.0

Salicylate

mg/L

0.00724

mmol/L

Testosterone

ng/dL

0.0347

nmol/L

Thyroxine (T4)

ng/dL

12.87

pmol/L

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Platelets

0.179

µmol/L

0.0154

pmol/L

Triglycerides

mg/dL

0.0113

mmol/L

Urea nitrogen

mg/dL

0.357

Uric acid

mg/dL

59.48

Celsius  Fahrenheit

F = (C x 1.8) + 32

Fahrenheit  Celsius

C = (F – 32) x 0.5555

Kilograms  Pounds

1 kg = 2.2 lbs

Pounds  Ounces

1 lb = 16 oz

Ounces  Grams

1 oz = 28.3 g

Inches  Centimetres

1 in = 2.54 cm

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11

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µg/dL pg/dL

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Total Iron Binding Capacity Triiodothyronine (T3)

mmol/L µmol/L

Toronto Notes 2018

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Commonly Measured Laboratory Values SI Units

Arterial Blood Gases pH PCO2 PO2

7 35-7.45 35-45 mmHg 80-105 mmHg

7.35-7.45 4.7-6.0 kPa 10.6-14 kPa

Serum Electrolytes Bicarbonate Calcium Chloride Magnesium Phosphate Potassium Sodium

22-28 mEq/L 8.4-10.2 mg/dL 95-106 mEq/L 1.3-2.1 mEq/L 2.7-4.5 mg/dL 3.5-5.0 mEq/L 136-145 mEq/L

22-28 mmol/L 2.1-2.5 mmol/L 95-106 mmol/L 0.65-1.05 mmol/L 0.87-1.45 mmol/L 3.5-5.0 mmol/L 136-145 mmol/L

Serum Nonelectrolytes Albumin ALP ALT Amylase AST Bilirubin (direct) Bilirubin (total) BUN Cholesterol Creatinine (female) Creatinine (male) Creatine Kinase – MB fraction Ferritin (female) Ferritin (male) Glucose (fasting) HbA1c LDH Osmolality

3 5 5.0 g/dL 35-100 U/L 8-20 U/L 25-125 U/L 8-20 U/L 0-0.3 mg/dL 0.1-1.0 mg/dL 7-18 mg/dL stomach>esophagus>colon>breast); lymphoma Sarcoidosis, amyloidosis, hemochromatosis

Vascular

Bilateral adrenal hemorrhage (risk increased by heparin and warfarin) Sepsis (meningococcal Pseudomonas) Coagulopathy in adults or Waterhouse-Friderichsen syndrome in children Thrombosis, embolism, adrenal infarction

Drugs

Inhibit cortisol: ketoconazole, etomidate, megestrol acetate Increase cortisol metabolism: rifampin, phenytoin, barbiturates

Others

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TB (7-20%) (most common in developing world) Fungal: histoplasmosis, paracoccidioidomycosis HIV, CMV Syphilis African trypanosomiasis

b

Infection

Adrenoleukodystrophy Congenital adrenal hypoplasia (impaired steroidogenesis) Familial glucocorticoid deficiency or resistance

E34 Endocrinology

Toronto Notes 2018

c

Adrenal Medulla

s

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SECONDARY ADRENOCORTICAL INSUFFICIENCY • inadequate pituitary ACTH secretion • multiple etiologies (see Hypopituitarism, E19), including withdrawal of exogenous steroids Clinical Features

b

b

Table 25. Clinical Features of Primary and Secondary Adrenal Insufficiency (AI) Secondary AI

Dark (palmar crease, extensor surface)

Pale

Potassium

High

Normal

Sodium

Low

Normal or Low

Metabolic Acidosis

Present

Absent

Associated Diseases

Primary hypothyroidism, type 1 DM, vitiligo, neurological deficits

Central hypogonadism or hypothyroidism, growth hormone deficiency, DI, headaches, visual abnormalities

Associated Symptoms

Weakness, fatigue, weight loss, hypotension, salt craving, postural dizziness, myalg a, arthralgia GI: N/V, abdominal pain, diarrhea

Diagnostic Test

Insulin tolerance test Cosyntropin Stimulation Test High morning plasma ACTH

c

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Adapted from: Salvatori R. JAMA 2005;294:2481-2488

Same except: No salt craving GI less common Insulin tolerance test Cosyntropin Stimulation Test Low morning plasma ACTH

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Primary AI (Addison’s or Acute AI) Skin and Mucosa

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Treatment • acute condition – can be life hreatening ■■ IV NS in large volumes (2-3 L); add D5W if hypoglycemic from adrenal insufficiency ■■ hydrocortisone 50 100 mg IV q6-8h for 24h, then gradual tapering ■■ identify and correct precipitating factors • maintenance ■■ hydrocortisone 15-20 mg total daily dose, in 2-3 divided doses, highest dose in the AM ■■ Florinef® (fludrocortisone, synthetic mineralocorticoid) 0 05-0.2 mg PO daily if mineralocorticoid deficient increase dose of steroids 2-3 fold for a few days during moderate-severe illness (e.g. with vomiting, fever) ■■ major stress (e.g. surgery, trauma) requires 150 300 hydrocortisone IV daily divided into 3 doses ■■ medical alert bracelet and instructions for emergency hydrocortisone/dexamethasone IM/SC injection

Adrenal Medulla

m

Catecholamine Metabolism

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s

Pheochromocytoma

bo

bo

Definition • rare catecholamine secreting tumour derived from chromaffin cells of the sympathetic system Epidemiology • most commonly a single tumour of adrenal medulla • rare cause of HTN (200 ng/mL) after IV injection of secretin ◆◆ nsulinoma: reduced fasting blood glucose (hypoglycemia) with elevated insulin and C-peptide levels ◆◆ glucagonoma: elevated blood glucose and glucagon levels ◆◆ pituitary tumours: assess GH, IGF-1, and prolactin levels (for over-production), TSH, free T4, 8 AM cortisol, LH, FSH, bioavailable testosterone or estradiol (for underproduction due to mass effect of tumour) ◆◆ hyperparathyroidism: serum Ca2 and albumin, PTH levels; bone density scan (DEXA) ■■ imaging ◆◆ MRI for pituitary tumours, gastrinoma, insulinoma ■■ MEN II ■■ laboratory ◆◆ genetic screening for RET mutations in all index patients – if a mutation is identified, screen family members who are at risk ◆◆ calcitonin levels (MTC); urine catecholamines and metanephrines (pheochromocytoma); serum Ca2+, albumin, and PTH levels (hyperparathyroidism) ◆◆ pentagastrin ± calcium stimulation test if calcitonin level is within reference range ◆◆ FNA for thyroid nodules-cytology ■■ imaging ◆◆ CT or MRI of adrenal glands, metaiodobenzylguanidine (MIBG) scan for pheochromocytoma ◆◆ octreoscan and/or radionuclide scanning for determining the extent of metastasis

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Treatment • MEN I ■■ medical ◆◆ proton pump inhibitor (PPI) for acid hypersecretion in gastrinoma ◆◆ cabergoline or other dopamine agonists to suppress prolactin secretion ◆◆ somatostatin for symptomatic carcinoid tumours ■■ surgery for hyperparathyroidism, insulinoma, glucagonoma, pituitary tumours (if medical treatment fails for the latter) ◆◆ trans-sphenoidal approach with prn external radiation • MEN II ■■ surgery for MEN IIa with pre-operative medical therapy ◆◆ prostaglandin inhibitors to alleviate diarrhea associated with thyroid cancer ◆◆ α blocker for at least 10-21 d for pheochromocytoma pre-operatively ◆◆ hydration, calcitonin, IV bisphosphonates for hypercalcemia

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Calcium Homeostasis

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• normal total serum Ca2+: 2.2-2.6 mmol/L • ionic/free Ca2+ levels: 1.15-1.31 mmol/L • serum Ca2+ is about 40% protein bound (mostly albumin), 50% ionized, and 10% complexed with PO43and citrate • regulated mainly by two factors: parathyroid hormone (PTH) and vitam n D • actions mainly on three organs: GI tract, bone, and kidney

E37 Endocrinology

Toronto Notes 2018

c

Calcium Homeostasis

Net Effect

Stimulated by low serum Ca and high serum PO43-; inhibited by chronic low serum Mg2+, high serum Ca2+, and calcitriol

h Ca2+ h Cacitriol i PO43-

Dietary intake Synthesized from cholesterol: UV on skin makes cholecalciferol (vitD3) liver makes calcidiol (25-(OH)D3) kidneys make calcitriol

Renal calcitriol production is stimulated by low serum PO43and PTH; inhibited by high serum PO43- and calcitriol in negative feedback

h Ca2+ h PO43-

Thyroid C cells

Stimulated by pentagastrin (GI hormone) and high se um Ca2+; inhibited by low serum Ca2+

i Ca2+ (in pharmacologic doses) i PO43-

c

Major intracellular divalent cation

See Magnesium, NP15

Cofactor for PTH secretion

PO43-

Intracellular anion found in all tissues

See Phosphate, NP14

i Ca2+

UV light

Diet

k

Mg2+

 ECF Mg2+ (acute)

Primary Hyperparathyroidism Increased PTH secretion commonly due to parathyroid adenoma lithium therapy; less often parathyroid carcinoma or parathyroid h perplasia Secondary Hyperparathyroidism Partial resistance to PTH action leads to parathyroid gland hyperplasia and increased PTH secretion, often in patients with renal failure and osteomalacia (due to low or low normal serum calcium levels)

 ECF Ca2+

Cholecalciferol

PARATHYROID GLAND

LIVER

 PTH

Tertiary Hyperparathyroidism Irreversible clonal outgrowth of parathyroid glands, usually in long-standing inadequately treated chronic renal failure on dialysis

KIDNEY Primary Hyperparathyroidism is the most comm n cause of hypercalcemia in healthy outpatients. Most commonly related to a solitary adenoma or less commonly multiple gland hyperplasia. Surgical excision acts as definitive treatment and is recommended for patients who are symptomatic. For mild asymptomatic disease medical surveillance may be appropriate with annual serum calcium, creatinine, and bone mineral density (BMD) For asymptomatic patients surgery is recommended for those who meet ≥1 of the following criteria: • Serum calcium concentration more than 0.25 mmol/L (1.0 mg/dL) above the upper limit of normal • Creatinine clearance 3 mmol/L (12 mg/dL) Increased alertness Anxiety Depression Cognitive dysfunction Organic brain syndromes >4 mmol/L (16 mg/dL) Psychosis (moans)

Hypoton a Hyporeflexia Myopathy Paresis

** Hypercalcemic crisis (usually >4 mmol/L or 16 mg/dL): primary symptoms include oliguria/anuria and mental status changes including somnolence and eventually coma g this is a medical emergency and should be treated immediately!

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Treatment • treatment depends on the Ca2+ level and the symptoms • treat the underlying cause of the hypercalcemia • treat acute, symptomatic hypercalcemia aggressively • mild asymptomatic hypercalcemia; monitor, avoid: thiazide, volume depletion, high Ca2+ diet, lithium, bed rest

The most common cause of hypercalcemia in hospital is malignancy-associated hypercalcemia • Usually occurs in the later stages of disease • Most commonly seen in lung, renal, breast, ovarian, and squamous tumours, as well as lymphoma and multiple myeloma

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Renal

k

GI

ks

Cardiovascular

The symptoms and signs of hypercalcemia include: “Bones, stones, groans, and psychiatric overtones”

Mechanisms: • Secretion of parathyroid hormone-related protein (PTHrP) which mimics PTH action by preventing renal calcium excretion and activating osteoclast-induced bone resorption • Cytokines in multiple myeloma • Calcitriol production by lymphoma • Osteolytic bone metastases direct effect • Excess PTH in parathyroid cancer

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Table 28. Symptoms of Hypercalcemia

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Clinical Features • symptoms depend on the absolute Ca2+ value and the rate of its rise (may be asymptomatic)

E39 Endocrinology

Toronto Notes 2018

c

Calcium Homeostasis

Isotonic saline (4-5 L) over 24 h ± loop diuretic (e.g. furosemide) but only if hypervolemic (urine output >200mL/h) Calcitonin: 4 IU/kg IM/SC q12h 8 IU/kg IM/SC q6h Only works for 48 h Rapid onset within 4 6 h

Differential Diagnosis of Hypercalcemia • Primary hyperparathyroidism • Malignancy: hematologic, humoral, skeletal metastases (>90% from 1 or 2) • Renal disease: tertiary hyperparathyroidism • Drugs: calcium carbonate, milk alkali syndrome, thiazide, lithium, theophylline, vitamin A/D intoxication • Familial hypocalciuric hypercalcemia • Granulomatous disease: sarcoidosis, TB, Hodgkin’s lymphoma • Thyroid disease: thyrotoxicosis • Adrenal disease: adrenal insufficiency, pheochromocytoma • Immobilization

m

e

sf

Increase Urinary Ca2+ Excretion

s

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Table 29. Treatment of Acute Hypercalcemia/Hypercalcemic Crisis

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Bisphosphonates (treatment of choice) Inhibits osteoclastic bone resorption and promotes renal excretion of calcium Acts rapidly but often transient response (decreased by 0.3-0.5 mmol/L beginning within 4-6 h) max effect usually in 7 d Combination of calcitonin and steroids may prolong reduction in calcium Tachyphylaxis may occur Indicated in malignancy-related hypercalcemia (IV pamidronate or zoledronic acid used) Mithramycin (rarely used) – effective when patient cannot tolerate large fluid load Dangerous – hematotoxic and hepatotoxic

Diminish Bone Resorption

Corticosteroids in hypervitaminosis D and hematologic malignancies Anti-tumour effects g decreased calcitriol production by the activated mononuclear cells in lung and lymph node Slow to act (5-10 d); need high dose

fre

re

Decrease GI Ca2+ Absorption

k

Watch Out for: • Volume depletion via diuresis • Arrhythmias

o

b

b

Treatment of last resort Indication: severe malignancy-associated hypercalcemia and renal insufficiency or heart failure

Dialysis

Hypocalcemia

Acute Management of Hypercalcemia/ Hypercalcemic Crisis • Volume expansion (e.g. NS IV 300-500 cc/h): initial therapy • Calcitonin: transient, partial response • Bisphosphonate: trea ment of choice • Corticosteroid: most useful in vitamin D toxicity granulomatous disease, some maligna cies • Saline diuresis + loop diuretic (for volume overload): temporary measure

co

m

m

Definition • total corrected serum Ca2+ 0.8 mmol/L) ■■ treat by increasing dietary Ca2+ by 1000 mg/d ■■ calcitriol 0.25 µg/d (especially in renal failure) acute or symptomatic hypocalcemia (ionized Ca2+ 5 mg bid Max: 20 mg/d

gliclazide

ks

r Useful in obese type 2 DM Improves both fasting and postprandial hyperglycemia Also i TG

Comments

co m

Micronase® Glynase PreTab®

500 mg OD titrated to 2000 mg/d maximum

c

ks

Diabeta® Euglucon®

Side Effects

s

sulfonylureas: glyburide

Contraindications

sf

Stimulates insulin release from β cells by causing K+ channel closure g depolarization g Ca2+ mediated insulin release Use in nonobese type 2 DM

m

Insulin Secretagogue

Indications

ok

Glucophage® Glumetza®

Dosing

ok

metformin

US Name (if different)

bo

Sensitizes peripheral tissues to insulin g increases glucose uptake Decreases hepatic glucose production by simulation of hepatic AMP-activated protein kinase (AMPK)

m

Biguanide

re

Canada Name

sf

co

Generic Drug Name

e

Mechanism of Action

E49 Endocrinology

Drug Class

Common Medications

Diabetes Medications

Toronto Notes 2018

.c

Enhances urinary glucose excretion by inhibiting glucose reabsorption in the proximal renal tubule

Canagliflozin

Invokana®

100 mg OD before first meal of the day

Dapagliflozin

Forxiga®

5 mg OD in the morning with or without food

Empagliflozin

Jardiance

Dosing

Byetta®

5-10 µg SC bid 1 h before meals

Victoza®

0.6-1.8 mg OD SC

Indications

Contraindications ABSOLUTE: Type 1 DM DKA Acute pancreatitis Hx RELATIVE: Gastroparesis ESRD Personal or family history of medually thyroid cancer (MTC)

S de Effects

Comments

N/V diarrhea Dizziness, headache Muscle weakness Anti-exentide antibodies Pancreatitis

i HbA1c 1.0%

UTI, genital infections Hypotension caution with concomitant loop diuretic use Caution with renal dysfunction Hyperlipidemia (raises LDL and HDL) Dapagliflozin not to be us d in patients with active or history of bladder cancer Rare diabetic ketoacidosis (may occur with no hyperglycemi )

i HbA1c 0.7-1.0%

m

Liraglutide

US Name (if different)

re

Canada Name

sf

Exenatide

fr

Generic Drug Name

Binds to GLP-1 receptor to promote insulin release Insulinotropic effect suppressed as plasma glucose 3.5 mmol/L GI mo ility disorder

Constipation Nausea Flatulence Bloating Rise in TG

Hypersensitivity Hepatic dysfunction Do not combine with fibrates or bile acid resins

Fatigue Pharyngitis Sinusitis Abdominal pain Diarrhea Arthralgia

Used for h LDL, apo B

om

Inhibits cholesterol absorption at the small intestine brush border

bo

Inhibits secretion of hepatic VLDL via lipoprotein lipase (LPL) pathway g decreased VLDL and LDL; decreased clearance of HDL

Hepatic disease Renal disease



Toronto Notes 2018

Cholesterol Absorption Inhibitors

GI symptoms Rash, pruritus h liver enzymes Myositis (h risk if combined with fibrates) Rhabdomyolysis

bo

re

bo

Bile Acid Sequestrants

Niacor®

Side Effects

om

Bezalip® Lipidil® Lopid®

Contraind cations Active liver disease Persistent h in AST, ALT unexplained

e

bezafibrate fenofibrate gemfibrozil

Indications 1st line monotherapy Used for h LDL, h TG

eb o

Upregulate lipoprotein lipase + apo A1, i VLDL, i TG, modest i LDL, modest h HDL

Dosing

10-80 mg/d 20-80 mg/d 20-80 mg/d 10-40 mg/d 5-40 mg/d 10-80 mg/d

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Fibrates

US Name (if different)

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Lipitor® Lescol® Mevacor® Pravachol® Crestor® Zocor®

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Canada Name

atorvastatin fluvastatin lovastatin pravastatin rosuvastatin simvastatin

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Generic Drug Name

Inhibits cholesterol biosynthesis, i LDL synthesis, h LDL clearance, modest h HDL, limited i VLDL

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Mechanism of Action

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Drug Class HMG-CoA Reductase Inhibitor (statins)

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Dyslipidemia Medications

Common Medications

For insulin formulations see Table 9, E9

Niacin

E50 Endocrinology

Diabetes Medications (continued)

Generic Drug Name

Decreases thyroid hormone production by inhibiting iodine and peroxidase from interacting with thyroglobulin to form T4 and T3 PTU also interferes with conversion of T4 to T3

propylthiouracil (PTU)

Propyl-Thyracil®

Start 100 mg PO tid, then adjust accordingly Thyroid storm: start 200 300 PO qid then adjust accordingly

methimazole (MMI)

Start 5-20 mg PO OD, then adjust accordingly Up to 60 mg OD may be required

Radioactive isotope of iodine that is incorporated into the thyroid gland irradiating the area and destroying local glandular tissue

sodium iodide I-131

Iodotope®

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Levoxyl®

0.05-2.0 mg/d, usually 1.6x weight (kg) is dose in micrograms In elderly patients start at 0.025 mg/d

Hypothyroidism

Recent MI, thyrotoxicosis

If wrong dosing: symptoms of hypothyroidism or hyperthyroidism Skin rash from dye in pill

Dose corrected for 24 h radioactive iodine uptake Hyperthyroidism 4-12 mCi Thyroid Ca 50-150 mCi

Hyperthyro dism Thyroid malignancy

Hypersensitivity Concurrent antithyroid medication Pregnancy, lactation

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Antithyroid Agent Radiopharmaceutical

N/V Rash Drug-induced hepatitis Agranulocytosis Hepatitis with PTU Cholestasis with MMI

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Synthroid® Eltroxin®

Side Effects

Hypersensitivity Relative: renal failure, liver disease PTU recommended in 1st trimester, MMI during 2nd and 3rd trimester Lactation: safe with PTU 50): Assess for risk factors for: osteoporosis and fracture (A), Counsel on osteoporosis, Counsel on risks/benefits of hormone replacement therapy (B)

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TB High Risk Groups: Mantoux skin testing (A)

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STI High Risk Groups: Voluntary HIV antibody screening (A), Gonorrhea screening (A) Chlamydia screening in women (B), Syphillis screen (A)

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Pediatrics: Routine immunizations (A), Hepatitis B, HPV and Meningococcal immunizations are offered in schools in most Canadian provinces Influenza High Risk Groups: Outreach strategies for vaccination (A), Annual immunization (B), now recommended for all

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TB High Risk Groups INH prophylaxis for household contacts or skin test converters (B), INH prophylaxis for high risk sub-groups (B) Immunocompromised/Age≥65/COPD/Asthma/CHF/ Asplenia/Liver Disease/Renal Failure/DM: Pneumococcalvaccine (Pneumovax®) (A)

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Folic acid supplementation to women of child-bearing age (A) Pharmacologic treatment of HTN (Refer to CHEP Guidelines) (A) Varicella vaccine for children age 1-12 and susceptible adolescents/adults (A) Rubella vaccine for all non-pregnant women of child-bearing age unless there is proof of immunity via immunization records or serology (B) Tetanus vaccine: routine booster q10yr if had 1° series (A) Pertussis vaccine: adults 65: Visual acuity (Snellen sight chart) (B), Hearing impairment (inquiry, whispered voice test, audioscope) (B)

Folic Acid Supplementation in Pregnancy (Joint SOGC-Motherisk Clinical Guideline) • To prevent neural tube defects in all women capable of becoming pregnant • Low risk women (no personal health risks, planned pregnancy): 0.4-1.0 mg daily folic acid supplementation for at least 2-3 mo before conception and throughout pregnancy and postpartum period • High risk women (health risks including epilepsy, insulin dependent diabetes, BMI >35, family history of NTD, high risk ethnic group): at least 3 mo prior to conception until 10-12 wk post conception: daily supplementation with multivitamins with 5 mg folic acid • From wk 12 post-conception until postpartum period (4-6 wks or as long as breastfeeding continues): 0.4-1.0 mg of folic acid supplementation is sufficient • Women with additional lifestyle issues (poor compliance with medications, no consistent birth control, taking possible teratogenic substances): higher folic acid dose of 5 mg and counselling about prevention of birth defects

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Adults >65: Follow-up on caregiver concern of cognitive impairment (A), Multidisciplinary post-fall assessment (A)

First-Degree Relative with Melanoma: Full body skin exam (B) Tests

Choosing Wisely Canada http://www.choosingwiselycanada.org/ A campaign to help clinicians and patients engage in conversations about unnecessary tests and treatments and make smart and effective choices to ensure high quality ca e

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Physical

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Discussion

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General Population

FM4 Family Medicine

Toronto Notes 2018

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Periodic Health Examination

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Mammography • age 40-49: routine screening with mammography not recommended (weak recommendation moderate quality evidence) • age 50-74: routine screening q2-3yr (age 50-69: weak re ommendation; moderate quality evidence, age 70-74: weak recommendation; low quality evidence) • age 75+: screen if benefits outweigh harm, must take overall health into account

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Magnetic Resonance Imaging • no routine screening with MRI scans (weak recommendation - low quality evidence)

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Clinical Breast Examination • no routine CBE alone or in conjunction with mammography to screen for breast cancer (weak recommendation - low quality evidence)

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Breast Self-Examination • recommend not advising women to routinely practice breast self-examination • for more information on benign breast lesions and breast cancer, see General Surgery, GS55

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Lung Cancer Screening Guidelines

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2016 Canadian Task Force on Preventative Health Care • apply to adults aged 18 and older who are not suspected of having lung cancer • annual screening with low dose CT for adults aged 55-74 with at least a 30 pack-year smoking history who currently smoke or quit less than 15 years ago, up to three consecutive times

Colorectal Cancer Screening Guidelines

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• recommendations for average risk individuals (asymptomatic, no family history of UC, polyps, or CRC) • average risk testing should begin at age 50, but assessment for risk factors should begin earlier to identify high-risk individuals ■■ Canadian Task Force on Preventative Health Care (2016) ◆◆ FOBT (either high sensitivity FOBT or FIT - fecal immunochemical testing) q2yr OR flexible sigmoidoscopy q10yr ◆◆ no colonoscopy as a screening test ◆◆ no screening after age 75 is recommended for average risk patients, but it may be assessed on an individual basis for ages 76-85 • for more information on colorectal neoplasms, see General Surgery, GS33 Men and Women

Symptomatic

Diagnostic Workup

Asymptomatic regardless of age but positive family history

FAP Sigmoidoscopy annually Begin at age 10-12 AAPC Colonoscopy annually Begin at age 16-18

Begin at age 40 or 10 yr younger than the earliest case of polyp or cancer in the family, whichever comes first

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Begin at age 50

Average risk screening

Begin at age 40

Figure 1. Approach to higher risk screening

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1-2 tubular adenomas 2 adenomas: colonoscopy in 3 y Incomplete examination, numerous polyps advanced adenoma, malignant or large sessile adenoma: colonoscopy after a short interval based on clinical judgment

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Colonoscopy every 5 years

Average risk screening

Polyps found at colonoscopy

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HNPCC Colonoscopy every 1-2 yr Begin at age 20 or 10 yr younger than the earliest case in the family, whichever comes first

One second-degree relative or third degree relative affected

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Genetic counselling and special screening

One first-degree relative with cancer or adenomatous polyp affected at age >60 or Two or more second-degree relatives with polyps or colon cancer

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One first-degree relative with cancer or adenomatous polyp at age 88 cm (35 in)

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Men ≤102 cm (40 in) Women ≤88 cm (35 in)

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Underweight

Obesity Class

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Table 5. Classification of Weight by BMI, Waist Circumference, and Associated Disease Risks in Adults

Losing Weight • Aim for caloric intake 500-1000 kcal/d less than total daily energy expenditure (TDEE) • 3500 kcal energy expended/lb of fat burned, results in 1-2 lb (0.5-1 kg) weight loss per week • Achieved by combination of increased activity and/or decreased caloric intake

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• see Canadian Task force on Preventive Health Care recommendations (CMAJ February 2015) at: canadiantaskforce.ca/ctfphc-guidelines/2015 obesity-adults/ • body mass index (BMI) = weight (kg)/height (m)2 = weight (lbs)/height (in)2 x 703; BMI is a poor predictor of obesity • waist circumference (WC) = flexible tape placed on horizontal plane at iliac crest, normal depends on ethnic background • increased WC for BMI 25-35 increases the risk of cardiovascular disease and type 2 diabetes BMI (kg/m2)

Effectiveness of Behavioural and Pharmacologic Treatment for Overweight and Obesity in Adults CMAJ Open 2014;2:E306-17 Purpose: To evaluate the effectiveness of behavioural and pharmacological treatments for overweight and obese adults. Methods: Review of RCTs of primary-carerelevant behavioural (diet, exercise, lifestyle) and pharmacological (orlistat, metformin) treatments with or without behavioural interventions in overweight or obese adults with 12 month follow-up from baseline for weight outcomes or harms. Secondary health outcomes (total cholesterol, LDL, fasting blood glucose, incidence of type 2 DM, systolic and diastolic BP) were also studied. Results: 68 RCTs were included, and showed that intervention participants had greater weight loss (-3.02 kg, 95% CI -3 52 to -2.52), waist circumference reduction (-2.78, -3.34 to -2.22) and body mass index reduction (-1.11, -1.39 to -0.84). Relative risk for weight loss of 5% or greater body weight was 1 77 (1.58 to 1.99, NNT 5, 95% CI 4-7) Incidence of type 2 DM was lower among pre-diabetic intervention participants. Conclusion: Behavioural and pharmacological treatments for overweight and obese adults may lead to clinically important reductions in weight and type 2 DM incidence in pre-diabetics.

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Decreased risk of hypertriglyceridemia, HTN, osteoporosis, certain cancers

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Recommendations Fat, Carbohydrates, Protein

Low BMI Associations • Osteoporosis • Eating disorders • Under-nutrition • Pregnancy complications

From: Classification of Overweight and Obesity by BMI, Waist Circumference, and Associated Disease Risks, National Institute of Health, National Heart Lung and Blood Institute, Obesity Education Initiative, http://www.nhlbi.nih.gov/health/public/heart/obesity/lose_wt/bmi_dis.htm

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Adverse Medical Consequences of Obesity • Type 2 DM • Dyslipidemia • CAD Osteoarthritis • Stroke • Sleep apnea • HTN • Certain cancers • Gallbladder • CHF disease • Low back pain • Non-alcoholic • Increased total steatohepatitis mortality • pregnancy complications

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Epidemiology • 25.1% of Canadian adults over 18 (excluding pregnant females) were obese in 2008 and 36.8% were overweight (StatsCan, 2008) • obesity rate in people of Aboriginal origin was 1.6 times higher than the national average • proportion of children aged 6-11 who are overweight has more than doubled in the last 25 yr; percentage of overweight adolescents has tripled • overweight and obesity rates in children are directly proportional to screen time (see Exercise, FM10) • only 10-15% of population consume 60 min on most days. Add endurance exercise training. (Medical evaluation is advised before starting activity program) Cognitive behavioural therapy

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Assess and screen for depression, eating and mood disorders

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Treat comorbidities and other health risks, if present

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Assess readiness to change behaviours and barriers to weight loss

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Satisfactory progress or goal achieved? Yes

No

No

Regular monitoring Assist with weight maintenance Reinforce healthy eating and physical activity advice

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Bariatric surgery BMI ≥35 kg/m2 + risk factors or BMI ≥40 kg/m2

Adjunct to lifestyle modifications: consider if patient has not lost 0.5-1 kg (1-2 lb) per wk by 3-6 mo after lifestyle changes

Consider if other weight loss attempts have failed. Requires lifelong medical monitoring

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Address other risk factors: periodic monitoring of weight, BMI and waist circumference q1-2yr

Pharmacotherapy BMI ≥27 kg/m2 + risk factors or BMI ≥30 kg/m2

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Weight maintenance and prevention of weight regain Nutrition therapy Physical activity Cognitive behavioural therapy

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Figure 4. 2006 Canadian clinical practice guidelines on the management and prevention of obesity in adults and children Adapted

from: CMAJ 2007;176:S1-S13

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Conduct linical and laboratory investigations to assess comorbidities: Blood pressure, heart rate, fasting glucose, lipid profile (total cholesterol, triglycerides, LDL and HDL cholesterol, and ratio of total cholesterol to HDL cholesterol)

Hyperlipidemia Signs Atheromata: plaques in blood vessel walls • Xanthelasmata: a sharply demarcated yellowish deposit of cholesterol underneath the skin, usually on or around the eyelid • Tendinous xanthoma: lipid deposit in tendon (especially Achilles) • Eruptive xanthoma: hypertriglyceridemia induced reddish yellow, pruritic, and painful papular or nodular rash • Lipemia retinalis: thin atheromata seen in the retinal blood vessels • Corneal arcus (arcus senilis): lipid deposit in cornea

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Devise goals and lifestyle modification program for weight loss and reduction of risk factors Weight loss goal: 5-10% of body weight, or 0.5 1 kg (1-2 lb) per wk for 6 mo

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If BMI >25 kg/m2 or waist circumference is above cutoff point

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IMPORTANT MESSAGE A modest weight loss of 5-10% of body weight is beneficial Weight maintenance and prevention of weight regain should be considered as long-term goals

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Overweight or obese adult Measure BMI Measure waist circumference if BMI is >25 and ≤35 kg/m2

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Pharmacologic • the task force recommends against pharmacologic intervention to manage patients who are overweight and obese, although some patients may prefer medications and be good candidates for pharmacologic treatment • high benefit of behavioural modification alone, NNH (number needed to harm) 10 (mostly GI side effects) for pharmacotherapy

“The Latest Evidence on Fad Diets…” Comparison of the Atkins, Ornish, Weight Watchers, and Zone Diets for Weight Loss and Heart Disease Risk Reduction JAMA 2005;293:43-53 Purpose: To assess the effectiveness and adherence rates of four popular diets for weight loss and reduction of cardiac risk factors. Methods: Single centre RCT at academic medical centre in Boston, MA. Participants were randomized to either Atkins (carbohydrate restriction), Zone (macronutrient balanced and low glycemic load), Weight Watchers (low calorie/portion size), or Ornish (fat restriction) diet groups for a period of 18 mo. Participants were adults aged 22-72 years with known HTN, dyslipidemia, or fasting hyperglycemia. Results: 160 participants were randomized. Assuming that participants who discontinued the study remained at baseline, the mean weight loss at 1 yr (and self selected dietary adherence rates per self report) were 2 1 kg for Atkins (53% of participants completed, p=0.009), 3.2 kg for the Zone (65% of participants completed, p=0.002), 3.0 kg for Weight Watchers (65% completed, p35 and risk factors or BMI >40 are candidates for bariatric surgery failing behavioural modification

Pharmacotherapy for Obesity • Orlistat: gastrointestinal lipase inhibitor, reduces fat absorption by 30% by inhibition of pancreatic lipase • Orlistat is associated with several adverse effects and not approved for clinical use longer than 2 yr • Orlistat should be avoided in people with inflammatory or chronic bowel disease

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Screening Recommendations • the CANRISK or FINRISC scores can be used to assess the risk for type 2 DM in overweight and obese patients • BMI risk assessment should be done every 3-5 yr in people at high risk of developing diabetes within 10 yr

Family Medicine FM9

Toronto Notes 2018

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Health Promotion and Counselling

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Dyslipidemia

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• see Endocrinology, E2 • defined as abnormal elevation of plasma cholesterol or triglyceride levels

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RISK ASSESSMENT, STRATIFICATION AND TREATMENT CONSIDERATION

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To calculate Framingham Risk Score, go to http://www.framinghamheartstudy.org/ risk-functions/cardiovascular-disease/10-yearrisk.php#

Calculate risk (unless statin-indicated condition) using the Framingham Risk Score (FRS) or Cardiovascular Life Expectancy Model (CLEM) Repeat screening every 5 years for FRS 27)

LDL-C ≥5 mmol/L genetic dyslipidemia

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Low Risk FRS 50 yr or who are menopausal, or at any age for adults with additional dyslipidemia risk factors (see sidebar) • screen for secondary causes: hypothyroidism, chronic kidney disease, DM, nephrotic syndrome, liver disease • risk category ■■ estimate using the model for 10 yr CAD risk developed from the Framingham data (Framingham Risk Score – FRS) ◆◆ FRS calculated based on the following factors: gender, age, HDL-C, total cholesterol, sBP, smoking, DM ◆◆ family history of CVD 65 yr

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Hearing Impairment

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Acupuncture for Migraine Prophylaxis Co hrane DB Syst Rev 2016:6:CD001218 Purpose: To investigate whether acupuncture is more e fective than no prophylactic treatment, routine care only or than sham acupuncture, and whether t is as effective as prophylactic pharmacological treatment, in terms of reducing headache frequency in adults with episodic migraine. Methods: Meta-analysis of RCTs with a minimum of an 8 wk dur tion, comparing acupuncture intervention with a no-acupuncture control (no prophylaxis, routine care, sham, or pharmacological prophylaxis). Results: 22 trials with 4,985 participants were included. Acupuncture was associated with moderate headache frequency reduction compared to no acupuncture (standardized mean difference (SMD) -0.56, 95% CI -0.65 to -0.48), and a reduction of >50% in headache frequency for 41% and 17% of participants receiving acupuncture and no acupuncture, respectively (pooled risk ratio (RR) 2.40, 2.08 to 2.76; number needed o treat (NNT) 4, 3 to 6). Acupuncture showed a small but statisticaly significant reduction over sham both post-treatment (SMD 0.18, -0.28 to -0.08) and post-folow-up (SMD -0.19, -0.30 to -0 09), w th 50%+ headache frequency reduction being achieved in 50% versus 41% of those receiving acupuncture and sham, respectively (pooled RR 1.23, 1.11 to 1.36; NNT 11, 7 to 20) these numbers were 53% and 42%, respectively, post-follow-up (pooled RR 1.25, 1.13 to 1.39; NNT 10, 6 to 18). Number of participants dropping out and reporting adverse effects did not d ffer significantly between acupuncture and sham groups. Compared to pharmacological prophylaxis, a significant reduction in migraine frequency was noted w th drugs (SMD -0.25, -0.39 to -0.10), but the significance was not maintained at follow-up. After 6 months, headache frequency was halved in 59% of patients receiving acupuncture and 54% receiving prophylactic drugs (pooled RR 1.11, 0.97 to 1.26). Those receiving acupuncture were less l kely to drop out due to adverse effects or to report adverse events than those receiving drugs. Conclusion: Adding acupuncture to symptomatic treatment of attacks reduces frequency of headaches. Acupuncture is more effective than sham, and is similarly effective to pharmacological interventions for migraine prophylaxis.

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Etiology • aneurysm • medication overuse headache • space-oc upying lesion • systemic infection (meningitis, encephalitis) • stroke • subarachnoid hemorrhage • systemic disorders (thyroid disease, HTN, pheochromocytoma, etc.) • temporal arteritis • traumatic head injuries • TMJ or C-spine pathology • serious ophthalmological and otolaryngological causes of headache

FM34 Family Medicine

Toronto Notes 2018

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Common Presenting Problems

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Hypertension

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Hypertension Guidelines are reviewed and updated annually, for up-to-date recommendations, please see www.hypertension.ca/chep

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Renovascular HTN Suspected if Patient Presenting with 2 or more of: • Sudden onset or worsening of HTN and age >55 or 90%) ■■ undetermined cause • secondary HTN (10%)

Suspect Hyperaldosteronism when • HTN refractory to treatment with ≥3 drugs • Spontaneous hypokalemia • Profound diuretic-induced hypokalemia (120 with minimal or no target organ damage • hypertensive emergency ■■ severe HTN (dBP > 120) + acute target-organ damage ■■ accelerated HTN ◆◆ significant recent increase in BP over previous hypertensive levels associated with evidence of vascular damage on fundoscopy, but without papilledema ■■ malignant HTN ◆◆ sufficient elevation in BP to cause papilledema and other manifestations of vascular damage (retinal hemorrhages, bulging discs, mental status changes, increasing creatinine) • white coat hypertension ■■ high clinic BP with normal home BP and 24 ambulatory BP, caused by anxiety in clinic • masked hypertension ■■ normal clinic BP with high BP in home and/or ambulatory setting, often provoked by anxiety, job stress, exercise

Symptoms of HTN are usually NOT PRESENT (this is why it is called the “silent killer”) May have occipital headache upon awakening or organ-specific complaints if advanced disease

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Epidemiology • 22% of Canadian adults suffer from HTN (prevalence is 52% in the 60-70 age group) • lifetime risk of developing hypertension is approximately 90% • 64% of Canadians who have HTN are treated and controlled, while 17% are unaware that they have HTN • 3rd leading risk factor associated with death ■■ risk factor for CAD, CHF, cerebrovascular disease, renal failure, peripheral vascular disease

• male • age >30 • excessive salt intake/fatty diet • African American ancestry • dyslipidemia

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Hypertensive Emergencies • Malignant HTN • Cerebrovascular Hypertensive encephalopathy Stroke Intracerebral hemorrhage SAH • Cardiac Acute aortic dissection Acute refractory LV failure Myocardial infarction/ischemia Acute pulmonary edema • Renal failure

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Predisposing Factors • family history • obesity (especially abdominal) • alcohol consumption • stress • sedentary lifestyle • smoking

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Table 21. Causes of Secondary HTN

Endocrine

1º hyperaldosteronism Pheochromocytoma Cushing’s syndrome Hyperthyroidism/hyperparathyroidism Hypercalcemia of any cause

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Renovascular HTN Renal parenchymal disease, glomerulonephritis, pyelonephritis, polycystic kidney

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Common Cause

Renal

Coarctation of the aorta Renal artery stenosis

Drug-Induced

Estrogens/OCP MAOIs Coca ne

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Vascular

Steroids Lithium Amphetamines

NSAIDs Decongestants Alcohol

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Investigations • for all patients with HTN ■■ electrolytes, Cr, fasting glucose and/or HbA1c, lipid profile, 12-lead ECG, urinalysis ■■ self-measurement of BP at home is encouraged (recommended devices listed at www.hypertension.ca) • for specific patient subgroups ■■ DM or chronic kidney disease: urinary protein excretion ■■ if suspected renovascular HTN: renal ultrasound, captopril renal scan (if GFR >60 mL/min), MRA/ CTA (if normal renal function)

Family Medicine FM35

Toronto Notes 2018

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Common Presenting Problems

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■■ if suspected endocrine cause: plasma aldosterone, plasma renin (aldosterone-to-renin ratio) ◆◆ measured from morning samples taken from patients in sitting position after resting 15 min ◆◆ discontinue aldosterone antagonists, ARBs, β-blockers and clonidine prior to testing ■■ if suspected pheochromocytoma: 24 h urine for metanephrines and creatinine ■■ echocardiography for left ventricular dysfunction assessment if indicated

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Diagnosis • all Canadian adults should have BP assessed at all appropriate clinical visits, oscillometric preferred to manual Elevated BP Reading(s) - office, home or pharmacy

Hypertension Visit 1

BP ≥180/110

Hypertension

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History, Phys cal Examination and Diagnostic Tests

No Hypertension

AOBP ≥135/85 OBPM ≥140/90

No

(Annual BP Measurement Recommended)

Yes Out of Office Assessment - ABPM (preferred) - HBPM Diagnostic Series

OBPM: Hypertension Visit 2

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Alternate Method (If ABPM or HBPM is not available)

≥140 sBP or ≥90 dBP

Hypertension Visit 3

Hypertension Visit 2

≥160 sBP or ≥100 dBP

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(within 1 month)

Daytime ABPM or HBPM ≥135/85 24 h ABPM ≥130/80

White Coat Hypertension If the average HBPM 60 yr)

As for uncomplicated isolated diasto ic HTN, except for use of β-blocker

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Labetolol Nifedipine

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If >3 Cardiovascular Risk Factors or Established Atherosclerotic Disease

Statin (age >40), low-dose ASA (age >50)

Caution with use of ASA in patients with uncontrolled BP

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Adapted from: McAlister FA, Zarnke KB, Campbell NRC, et al. The 2001 Canadian recommendations for the management of hypertension: Part two – Therapy. Can J Cardiol 2002;18:625-641 and The 2012 Canadian Hypertension Education Progr m Re ommendations

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Diuretic

Thiazides as First-Line Antihypertensive Therapy – ALLHAT JAMA 2002;288:2981-2997 Purpose: To evaluate whether calcium channel blocker or angiotensin-converting enzyme inhibitors lower incidence of coronary heart disease (CHD) or other cardiovascular disease (CVD) relative to treatment with a d uretic. Methods: Randomized, double-blind, activecontrolled clinical trial with mean follow-up of 4.9 yrs. Part cipa ts with stage 1 or 2 hypertension (HTN) and at least 1 other CHD risk factor were included, and randomized to receive chlorthalidone (12.5-25 mg/d), amlodipine (2.5-10mg/d), or lisinopril (10-40 mg/d). Target BP was 65 and those with T-score ≤-2.5 • Lumbar spine T-score 5 cm ◆◆ assess fall risk by ability to get up from chair without support with arms, and walking several steps and return

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Vitamin D Content in Food • Milk fortified with vitamin D3 contains 100 IUs per 250 mL glass • Foods such as margarine, eggs, chicken livers, salmon, sardines, herring, mackerel, swordfish, and fish oils (halibut and cod liver oils) all contain small amounts; supplementation is necessary to obtain adequate levels as dietary intake has minimal impact • Most multivitamins provide 400 IUs of vitamin D3

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Epidemiology • for current guidelines and tools see www.osteoporosis.ca • age-related disease characterized by decreased bone mass and increased susceptibility to fractures • affects 1 in 4 Canadian women and 1 in 8 Canadian men

FM42 Family Medicine

Toronto Notes 2018

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Common Presenting Problems

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Investigations • CBC, Cr, corrected Ca2+, ALP, TSH, 25-OH-D (after 3-4 mo of adequate supplementation), and serum protein electrophoresis if there are vertebral fractures

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Indications for Bone Mineral Density Testing and Management • see Endocrinology, E41

• see Geriatric Medicine, GM13

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Palliative and End-of-Life Care Rash • see Dermatology, D13

When an STI is detected in a child, evaluation for sexual abuse is mandatory

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Epidemiology • high incidence rates worldwide • Canadian prevalence in clinical practice ■■ common: chlamydia (most common), gonorrhea (2nd most common), HPV, genital herpes (increasing incidence of chlamydia and gonorrhea) ■■ less common: hepatitis B, HIV, and syphilis (increasing in incidence), trichomoniasis ■■ rare: chancroid, granuloma inguinale, lymphogranuloma venereum • non-sexually transmitted genital tract infections: vulvovaginal candidiasis (VVC), bacterial vaginosis (BV) • three most ommon infections associated with vaginal discharge in adult women are BV, VVC, and trichomoniasis

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Management • primary prevention is vastly more effective than treating STIs and their sequelae • offer hepatitis B vaccine if not immune • offer Gardasil® to women over 9 years of age (can be offered to men as well but not covered by OHIP) • discuss STI risk factors (e.g. decreasing the number of sexual partners) • direct advice to ALWAYS use condoms or to abstain from intercourse • condoms are not 100% effective against HPV or HSV • an STI patient is not considered treated until the management of his/her partner(s) is ensured (contact tracing by Public Health) • patients diagnosed with bacterial STI or trichomonal infection should abstain from sexual activity until treatment completion and for 7 d after treatment for both partners, or until test of cure completed • mandatory reporting: chlamydia, gonorrhea, hepatitis B, HIV, syphilis

Efficacy of Human Papillomavirus Vaccines – A Systematic Quantitative Review Int J Gynecol Cancer 2009;19:1166-1176 Purpose: To evaluate two vaccines for human papillomavirus (HPV) in terms of efficacy, safety and immunogenicity. Methods: Systematic review of RCTs involving women between the ages of 9 and 26 years, randomly assigned to receive vaccination with HPV L1 virus-like particle in either quadrivalent (HPV 6, 11, 16, 18), bivalent (HPV 16, 18), or univalent (HPV 16) form or placebo. Main outcomes were prevention of cytologica ly and/or histologically proven lesions (including LSIL, HSIL, VIN, VAIN, AIN, adenocarcinoma in situ of the cervix, or cancer of the cervix associated with HPV infection). Results: Six studies involving 47,236 women were included. Bivalent and quadrivalent vaccines reduced the rate of lesions in the cervix, vulva, vagina, and anogenital region with efficacy of 93% (95% CI 87-96%) and 62% (95% CI 27-70), respectively. More symptoms were found in he bivalent vaccine group (35%, 5-73%) compared to control groups. Conclusion: Prophylactic vaccination can prevent HPV infection in women aged 9 to 26 years not previously infected with HPV subtypes covered by the vaccines.

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Investigations/Screening • individuals at increased risk, even those who are asymptomatic, should be screened for chlamydia, gonorrhea, hepatitis B, HIV, and syphilis • Pap test if none performed in the preceding 12 mo

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Sexual History 5 P’s Partners (numbers, gender) Practices (vaginal, oral, anal insertive/ receptive) Protection Past history of STIs Pregnancy prevention

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b

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History • sexual history ■■ age of first intercourse, sexual orientation, sexual activity (oral, anal, and/or vaginal intercourse), sexual activity during travel ■■ total number of partners in the past year/month/week and duration of involvement with each • STI history ■■ STI awareness, contraception, previous STIs and testing (including Pap tests), partner communication regarding STIs ■■ local symptoms such as burning, itching, discharge, sores, vesicles, testicular pain, dysuria, abdominal pain ■■ systemic symptoms such as fever, lymphadenopathy, arthralgia

STI Risk Factors • Sexually active males and females 2 sexual partners in the past 12 mo • Street involved, homeless, and/or substance abuse

om

b

bo

Definition • diverse group of infections caused by multiple microbial pathogens • transmitted by either secretions or fluids from mucosal surfaces

.c

• see Gynecology, GY27

ee

ok sf re

fre

Sexually Transmitted Infections

Family Medicine FM43

Toronto Notes 2018

c

Common Presenting Problems

e

Table 25. Diagnosis and Treatment of Common STIs M: urethral strictures, epididymitis, infertility

~70% asymptomatic If symptoms appear (usually 2-6 wk after infection) then similar to gonococcal symptoms (see above)

Same as above

ok sf r

For condylomata: cryotherapy, electrocautery, laser excision, topical therapy (patient-applied or office-based) For cervical dysplasia: colposcopy and possible excision, dependent on grade of lesion

F: screening for cervical dysplasia through regular Pap smears

1° episode: painful vesicoulcerative genital lesions ± fever, tender lymphadenopathy, protracted course Recurrent episodes: less extensive lesions shorter course may have “trigger factors”

Swab of vesicular content for culture, type-specific serologic testing for HSV-1 vs. HSV-2 antibodies and to determine 1° vs. recurrent episode

1° Episode Acyclovir 200 mg PO 5x/d x 5-10 d or Famciclovir 250 mg PO tid x 5 d or Valacyclovir 1,000 mg PO bid x 10 d

1°: chancre (painless sore), regional lymphadenopathy 2°: rash and flu-like symptoms, meningitis, headache, uveitis, retinitis, condyloma lata, mucus lesions, alopecia Latent Phase: asymptomatic 3°: neurologic, cardiovascular, and tissue complications

Specimen collection from 1° and 2° lesions, screen high risk individuals with serologic syphilis testing (VDRL), universal screening of pregnant women

Benzathine penicillin G IM (dose depends on stage and patient population. Check Public Health Canada guidelines ) Notify partners (last 3 12 mo) Continuous follow-up and testing until patients are seronegative

ok sf

F: cauliflower lesions and/or pre-neoplastic/neoplastic lesions on cervix/vagina/vulva

M and F: anal cancer MSM and F who have receptive anal sex: rectal cancer F: cervical/vaginal/vulvar cancer Genital pain, urethritis, cervicitis, aseptic meningitis, increased risk of acquiring and transmitting HIV

m

m

M and F: Arthritis, increased risk of acquiring and transmitting HIV

Same as above

None needed if simple condylomata Potential biopsy of suspicious lesions

m

m

oo

eb

Azithromycin 1 g PO single dose + gonococcal urethritis/cervicitis Rx* Same follow-up as above

Most are asymptomatic M: cauliflower lesions (condylomata acuminata) on skin/mucosa of penile or anal area

Recurrent Episode Acyclovir 200 mg PO 5x/d x 5d or 800 mg PO tid x 2 d or Famciclovir 125 mg PO bid x 5 d or Valacyclovir 500 mg PO bid x 3 d or 1,000 mg PO OD x 3 d

eb

m

Chronic neurologic and cardiovascular sequelae, increased risk of acquiring and transmitting HIV

m

m

oo

oo

Infectious Syphilis (Treponema pallidum)

oo

r

co

F: PID, infertility, ectopic pregnancy, perinatal infection, chronic pelvic pain

co m

m

M and F: urine PCR, rectal/ pharyngeal swabs if indicated

k

Ceftriaxone 250 mg IM single dose* If risk factors for treatment failure (e.g. pregnancy, pharyngeal/rectal infection, potentially reduced susceptibility) Test of cure: culture 4 d post-treatment (preferred) or urine PCR 2 wk post treatment (alternative) If no risk factors, rescreen 6-12 months post treatment

M and F: often asymptomatic, can involve rectal symptoms in cases of unprotected anal sex

.c om

ks f

Genital Herpes (HSV-1 and -2)

M: u ethral swab for Gram stain and culture

bo

k

oo

Human Papillomavirus (genital warts, cervical dysplasia)

Complications

F: urine PCR, endocervical swab for Gram stain and culture, vaginal swab for wet mount (to rule out trichomonas)

F: mucopurulent endocervical discharge, vaginal bleeding dysuria, pelvic pain, dyspaurenia

Non-Gonococcal Urethritis/Cervicitis (Usually Chlamydia trachomatis**)

Treatment

m

M: urethral discharge, unexplained pyuria, dysuria, irritation, testicular swelling, Sx of epididymitis

Gonococcal Urethritis/ Cervicitis (Neisseria gonorrhoeae)

Investigations

ok sf

Signs and Symptoms

F = females; M = males *N.B. if urethritis/cervicitis is suspected, always trea for both gonococcal and non-gonococcal types (i.e. ceftriaxone AND azithromy in) **Most common reportable STI in Canada

e

Sinusitis

s

• see Otolaryngology, OT24

m

co

co

e.

fre

ks

ks

fre

e.

co

m

Management of Acute Sinusitis • may provide symptom relief: oral analgesics (acetaminophen, NSAIDs), nasal saline rinse, short-term use of topical or oral decongestants • do not prescribe antihistamines • intra-nasal corticosteroids if diagnosed with mild to moderate acute bacterial sinusitis • antibiotics and intra-nasal corticosteroids if diagnosed with severe acute bacterial sinusitis ■■ first-line antibiotic is amoxicillin, and second line is amoxicillin-clavulanic acid or a fluoroquinolone ■■ ENT referral if: anatomic defect (e.g. deviated septum, polyp, adenoid hypertrophy), failure of second-line therapy, or ≥4 episodes/yr, refer urgently when there is development of complications (e.g. orbital extension, meningitis, intra-cranial abscess, venous sinus thrombosis), altered mental status, headache, systemic toxicity, or neurological findings

Red Flags for Urgent Referral • Altered mental status • Headache • Systemic toxicity • Swelling of the orbit or change in visual acuity or EOM • Hard neurological findings • Signs of meningeal irritation • Suspected intra- ranial complications (meningitis, intra-cranial abscess, cavernous sinus thrombosis) • Involvement of associated structures (periorbital cellulitis, Pott’s puffy tumour)

ee

e

eb

oo

Etiology • viral etiology is more common • viral: rhinovirus, influenza, parainfluenza • bacterial: S. pneumoniae, H. influenzae, M. catarrhalis

FM44 Family Medicine

Toronto Notes 2018

c

Common Presenting Problems

Symptoms of Sinusitis >7 d

7 d

Yes

No

Continue course

Use second-line agent or change antibiotic class

s

e

No

s

Yes

Clinical response in 72 h? Yes

No

om

For symptoms lasting more than 4 wk, consider chronic rhinosinusitis (CRS). Persistent severe symptoms require prompt urgent referral.

c

Figure 16. Diagnosis and management of sinusitis

ee

ABRS = acute bacterial rhinosinusitis Adapted from: Desrosiers M, et al. Allergy Asthma Clin Immunol 2011;7:doi:10.1186/1710-1492-7-2

ok

s

Sleep Disorders

bo

• see Respirology, R32 and Neurology, N46

om

co m

m

e

Definition • most often characterized by one of three complaints ■■ insomnia ◆◆ difficulty falling asleep, difficulty maintaining sleep, early-morning wakening, non-refreshing sleep ■■ parasomnias ◆◆ night terrors, nightmares, restless leg syndrome, somnambulism (performing complex behaviour during sleep with eyes open but without memory of event) ■■ excessive daytime sleepiness

fr

fr

Epidemiology • 1/3 of patients in primary care setting have occasional sleep problems, 10% have chronic sleep problems

Family Medicine FM45

Toronto Notes 2018

c

Common Presenting Problems

eb

m

m

eb

oo

s

ks fr

Etiology • primary sleep disorders ■■ primary insomnia, narcolepsy, obstructive sleep apnea, restless leg syndrome, periodic limb movements of sleep • secondary causes ■■ medical: COPD, asthma, CHF, hyperthyroidism, chronic pain, BPH, menopause, GERD, PUD, pregnancy, neurological disorders ■■ drugs: alcohol, caffeine, nicotine, nicotine replacement therapy, β-agonists, antidepressants, steroids ■■ psychiatric: mood and anxiety disorders ■■ lifestyle factors: shift work, jet-lag

ee

e.

o

.c om

Investigations • complete sleep diary every morning for 1-2 wk ■■ record bedtime, sleep latency, total sleep time, awakenings, quality of sleep • rule out specific medical problems (e.g. CBC and differential, TSH) • refer for sleep study nocturnal polysomnogram, or daytime multiple sleep latency test if suspicion of sleep apnea or periodic leg movements of sleep

b

om

m

Risk Factors for Obstructive Sleep Apnea • 2% of women, 4% of men between ages 30-60 • Obesity (due to upper airway narrowing). BMI >28 kg/m2 present in 60-90% of cases • Children (commonly due to large tonsils and adenoids) • Aging (due to decreased muscle tone) • Persistent URTIs, allergies, nasal tumours, hypothyroidism (due to macroglossia), neuromuscular disease • Family history

ee .

m

fr

ok

ok

sf

re

e.

co

m

eb

oo

ks

ks

f

fr

c

c

m

m

m

eb

bo

oo

k

ok

sf

fre

re

e

co

co

m

m

eb

o

ok s

Treatment of Specific Problems • Primary insomnia ■■ majority of cases ■■ person reacts to insomnia with fear or anxiety around bedtime or with a change in sleep hygiene, which can progress to a chronic disorder (psychophysiological insomnia) ■■ treat any suspected medical or psychiatric cause ■■ exercise regularly, avoid heavy exercise within 3 h of bedtime ■■ first-line treatment (CBT) ◆◆ sleep hygiene: avoid alcohol, caffeine, nicotine; comfortable sleep environment; regular sleep schedule; no napping ◆◆ relaxation therapy: deep breathing, meditation, biofeedback ◆◆ stimulus control therapy: re-association of bed/bedroom with sleep, re establishment of a consistent sleep-wake schedule, reduce activities that cue staying awake ◆◆ sleep restriction therapy: total time in bed should closely match the total sleep time of the patient (improves sleep efficacy) ◆◆ address inappropriate beliefs and attitudes that perpetuate dysfunctional sleep ■■ pharmacologic treatment (used to supplement CBT; short-term prescription of 38ºC?

1

Tonsillar exudate?

1

Swollen, tender anterior nodes?

1

Age 3-14

1

Age 15-44

0

Age >45

–1

eb

Cough absent?

oo

POINTS

1-2.5%

1

2

3

5-10%

11-17%

28-35%

Suggested action

NO culture or antibiotic

4 or more

c

0

e

Score Chance patient has strep

51-53%

Culture all, treat with antibiotics only if culture is positive

Culture all, treat with antibiotics on clinical grounds1, discontinue antibiotics if culture comes back negative

ks fr

o

In communities with moderate levels of strep infection (10-20% of sore throats):

o

eb

eb

o

Clinical grounds include a high fever or other indicators that the patient is clinically unw ll and is presenting early in the course of the illness Limitations: *This score is not applicable to patients 27 kg) amoxicillin 40 mg/kg/d PO div bid-tid x 10 d 2nd line: erythromycin estolate 40 mg/kg/d PO div bid-tid x 10 d 3rd line: cephalexin 25 50 mg/kg/d PO div qid x 10 d cefprozil 15 mg/kg/d PO div bid x 10 d Adults: 1st line: penic llin V 300 mg PO tid or 600 mg bid x 10 d 2nd line: erythromycin 250 mg PO qid x 10 d 3 d line: cephalexin 250 mg PO qid x 10 d cefadroxil 500 mg PO bid x 10 d

Sinusitis

S. pneumoniae H. influenzae M. catarrhalis S. aureus

Children: 1st line: amoxicillin 80 mg/kg/d PO div bid-tid x 5-10 d (max 3 g/d) x 10-14 d 2nd line: amoxicillin/clavulanate 40-80 mg/kg/d div bid (max 3 g/d) x 10-14 d cefprozil 30 mg/kg/d PO div bid x 10-14 d 3rd line: cefuroxime-AX 30-40 mg/kg/d PO div bid x 10-14 d clarithromycin 15 mg/kg/d PO div bid x 10-14 d Adults: 1st line: amoxicillin 500 mg PO tid x 5-10 d 2nd line: amoxicillin/clavulanate 500 or 875 mg PO bid x 5-10 d cefuroxime-AX 250-500 mg PO bid x 5-10 d 3rd line: levofloxacin 500 mg PO OD x 5-10 d moxifloxacin 400 mg PO OD x 5-10 d

S pneumoniae H. influenzae M. catarrhalis Group A Strep S. aureus

Children: Treat if under age 6 mo If age 6 24 mo, watchful waiting appropriate if parents can observe child for 48-72 h with appropriate medical follow-up If age >24 mo, treat if worsens after 48-72 h 10 d course if age 24 mo 1st line: amoxicillin 80 mg/kg/d PO div bid-tid (max 3 g/d) 2nd line: amoxicillin/clavulanate 40-80 mg/kg/d PO div bid (max 3 g/d) cefprozil 30 mg/kg/d PO div bid 3rd line: cefuroxime-AX 30-40 mg/kg/d PO div bid clarithromycin 15 mg/kg/d PO div bid Chronic TM perforation or ventilation tubes: Ciprodex® otic suspension 4 drops bid x 5 d Adults: 1st line: amoxicillin 500 mg PO tid x 7-10 d 2nd line: amoxicillin/clavulanate 500 mg PO tid or 875 mg PO bid x 7-10 d cefprozil 250-500 mg PO bid x 7-10 d Chronic TM perforation or ventilation tubes: Ciprodex® otic suspension 4 drops bid x 5 d

None

om

m

eb

o

fre

e

co m

m

Acute Rhinitis (common cold)

e

re

re

P aeruginosa Coliforms S. aureus

Cortisporin® otic solution 4 drops tid or qid (3 drops tid or qid for children) TM defect: Ciprodex® otic suspension 4 drops bid x 5 d Necrotizing (i.e. bone involvement): ciprofloxacin 750 mg PO bid x 4-8 wk

Bronchitis

H. influenzae, parainfluenza, coronavirus, rhinovirus, RSV

None

Community A quired Pneumonia: Outpatient without Comorbidity

S. pneumoniae M. pneumoniae C. pneumoniae

1st line: amoxicillin 1,000 mg PO tid x 7-14 d (for patients over age 50 where mycoplasma infection is less likely) erythromycin 500 mg PO qid x 7-14 d clarithromycin 500 mg PO bid or 1,000 mg (ER) PO OD x 7-14 d azithromycin 500 mg PO on 1st d then 250 mg PO OD x 4 d or 500 mg PO OD x 3 d 2nd line: doxycycline 100 mg PO on 1st d then 100 mg PO OD x 7-14 d

Community Acquired Pneumonia: Outpatient with Comorbidity

S. pneumoniae M. pneumoniae C. pneumoniae H. influenzae

ANYONE of the β-lactam agents below: amoxicillin 1,000 mg PO tid x 7-14 d amoxicillin/clavulanate 500 mg PO tid or 875 mg PO bid x 7-14 d cefuroxime-AX 500 mg PO bid x 7-14 d cefprozil 500 mg PO bid x 7-14 d PLUS ONE of the following: clarithromycin 500 mg PO bid or 1,000 mg (ER) PO OD x 7-14 d azithromycin 500 mg PO OD on 1st d then 250 mg PO OD x 4 d doxycycline 100 mg PO bid on 1st d then 100 mg PO OD x 7-14 d OR ANY ONE of the following: levofloxacin 750 mg PO OD x 7-14 d moxifloxacin 400 mg PO OD x 7-14 d

Dental Infections/Periapical and Periodontal Abscesses

Oral Flora

oo

e

e.

oo

f

m

co m

sf re e.

m

eb

oo

k

.c

Otitis Externa

co

o

m

m

bo

o

sf

Acute Otitis Media

.

RESPIRATORY/ENT

penicillin V potassium 500 mg PO qid x 7-10 d clindamycin 300 mg PO qid or 600 mg bid x 7-10 d

FM50 Family Medicine

Toronto Notes 2018

c

Antimicrobial Quick Reference

k

Mild to moderate (i.e. 3 BM/d, blood, fever): olfloxacin 400 mg PO single dose or 300 mg PO bid x 3 d (prevention: 300 mg PO OD) norfloxacin 800 mg PO single dose or 400 mg PO bid x 1-3 d (prevention: 400 mg PO OD) ciprofloxacin 750 mg PO single dose or 500 mg PO bid x 1-3 d (prevention: 500 mg PO OD) levofloxacin 500 mg PO OD x 1-3 d (prevention: 500 mg PO OD) azithromycin 1,000 mg PO single dose or 500 mg PO OD x 1-3 d (children: 10 mg/kg/d x 3 d)

m

m

m

Enterotoxigenic E. coli (ETEC) Campylobacter Salmonella Shigella Viruses Protozoa

oo

ks fr

Diarrhea – Enteritis

Antimicrobial

eb

Microorganisms

GASTROENTEROLOGY

re

Condition

o

Severe (WBC ≥15 x 109/L and Cr ≥1.5 x baseline): vancomycin 125 mg PO qid x 10-14 d (children: 40 mg/kg/d PO div tid-qid x 10-14 d max 2 g/d)

b

1st line: (PPI PO bid + amoxicillin 1,000 mg PO bid + clarithromycin 500 mg PO bid x 7 d [e.g. HP-PAC: lansoprazole 30 mg PO bid + amoxicillin 1,000 mg PO bid + clarithromycin 500 mg PO bid x 7 d]) (PPI PO bid + metronidazole 500 mg PO bid + clarithromycin 500 mg or 250 mg PO bid x 7 d) 2nd line: (PPI PO bid + metronidazole 500 mg PO bid + amoxicillin 1,000 mg PO bid x 7 d) (PPI PO bid + bismuth subsalicylate 2 tabs or 30 mL qid + metronidazole 250 mg PO qid + tetracycline 500 mg PO qid x 7-14 d)

m

bo

re e

H. pylori

e

Peptic Ulcer Disease (non-NSAID related)

Mild to moderate (WBC 50, Caucasians, smokers, overweight, hiatus hernia, and long history of reflux symptoms

G8 Gastroenterology

Toronto Notes 2018

c

Esophagus

fre

Dysphagia

ok

Definition • difficulty swallowing Remember: Dysphagia = Difficulty in swallowing Odynophagia = Pain on swallowing

b

Dysphagia Esophageal (inability to move food down esophagus)

Solid foods and liquids

Mechanical obstruction

Neuromuscular disorder

Heartburn

bo

m

Carcinoma*

*Most common

Intermittent

Intermittent

Lower esophageal ring*

Diffuse esophageal spasm (DES) (chest pain)

Peptic stricture*

Progressive

Reflux symptoms Scleroderma Achalasia*

m

Age >50 (wt loss)

o

Progressive

co m

Solid food only

f

ee

c

Muscular Neurological* Structural Muscular dystrophy Zenker’s diverticulum Cortical Polymyositis Bulbar Thyromegaly Myasthenia gravis Peripheral Cervical spur Cricopharyngeal

Key Questions in Dysphagia • Difficulty in starting swallowing? • Associated symptoms? (regurgitation, change in voice pitch, weight loss) • Solids, liqu ds, or both? • Intermittent or progressive? • History of heartburn? • Change in eating habits/diet?

ee

Oropharyngeal (difficulty initiating swallowing  choking, coughing, nasal regurgitation)

Figure 4. Approach to dysphagia (eosinophilic esophagitis omitted)

m

Esophageal Motor Disorders

ee

Clinical Features • dysphagia with solids and liquids • chest pain (in some disorders)

ok

Diagnosis • motility study (esophageal manometry) • barium swallow sometimes helpful

b

Causes • idiopathic • achalasia (painless) • scleroderma (painless) • DM • DES: rare and can be difficult to diagnose due to intermittent presentation

Normal peristalsis interspersed with frequent, repetitive, spontaneous, high pressure, non-peristaltic waves (tertiary peristalsis) Idiopathic

Potential mechanisms include impaired inhibitory innervation to esophageal body, malfunction in endogenous nitric oxide synthesis Barium x-ray: “Corkscrew pattern” Manometry: >30% (but 12 mm, provided peristalsis is normal • dysphagia with large food boluses • Schatzki ring ■■ mucosal ring at squamo-columnar junction above a hiatus hernia ■■ causes intermittent dysphagia with solids ■■ treatment involves disrupting ring with endoscopic bougie

Plummer-Vinson Syndrome Triad • Iron deficiency anemia • Dysphagia • Esophageal webs * rare (prevalence 7%

m

om

bo

oo

ok

k

sf

fr

re

Treatment • dietary counselling ■■ gluten free diet; avoid barley, rye, wheat (as these grains are related and also have toxic factor, similar to gliadin) ■■ oats allowed if not contaminated by other grains (grown in soil without cross-contamination) ■■ rice and corn flour are acceptable ■■ iron, folate supplementation (with supplementation of other vitamins as needed) • if poor response to diet change, consider ■■ alternate diagnosis ■■ non-adherence to gluten-free diet ■■ concurrent disease (e.g. microscopic colitis, pancreatic insufficiency) ■■ development of intestinal (enteropathy-associated T-cell) lymphoma (abdominal pain, weight loss, palpable mass) ■■ development of diffuse intestinal ulceration, characterized by aberrant intraepithelial T-cell population (precursor to lymphoma)

ee

sf

sf re e

Prognosis • associated with increased risk of lymphoma, carcinoma (e.g. small bowel and colon; slight increase compared with general population), autoimmune diseases • risk of lymphoma may be lowered by dietary gluten restriction

Gluten Found in BROW Barley Rye Oats (controversial) Wheat

G19 Gastroenterology

Toronto Notes 2018

c

Small and Large Bowel

f

fre

Inflammatory Bowel Disease

o

ok

Definition • Crohn’s disease (CD), ulcerative colitis (UC), indeterminate colitis or IBD-unclassified (IBDU)

m

b

Pathophysiology • poorly understood • most likely a sustained response of the immune system, perhaps to enteric flora • lack of appropriate down-regulation of immune responsiveness after an infection in a genetically predisposed individual

oo

ok sf r

ks fre

e

o

co m

Genetics • increased risk of both UC and CD in relatives of patients with either disease, especially siblings, early onset disease ■■ familial risk greater if proband has CD rather than UC • likely polygenomic pattern: 9 gene loci are associated • CARD15/NOD2 gene mutation associated with CD (relative risk in heterozygote is 3, in homozygote is 40), especially Ashkenazi Jews, early onset disease, ileal involvement, fistulizing and stenotic disease ■■ CARD15 gene product modulates NFκβ, which is required for the innate immune response to microbial pathogens, best expressed in monocytes-macrophages

eb

Clinical Features

Ulcerative Colitis

Any part of GI tract Small bowel + colon: 50% Small bowel only: 30% Colon only: 20%

Isolated to large bowel Always involves rectum, may progress proximally

Uncommon; possible if colonic disease

Very common (90%)

Diarrhea

Less prevalent, large volume, watery Usually non-bloody (may be bloody, particularly if distal colonic involvement)

e

Crohn’s Disease

m

e

Table 10. Clinical Differentiation of Ulcerative Colitis from Crohn’s Disease

Frequent, mucous, bloody, small volume stools

Abdominal Pain

Post-prandial/colicky

Uncommon; predefecation

c

Uncommon

Urgency/Tenesmus

Uncommon (unless rectum involved)

Common

Palpable Mass

Frequent (25%), RLQ

Rare (if present, often related to cecum full of stool)

Recurrence After Surgery

Common

None post-colectomy

Endoscopic Features

Segmental inflammation, ulcers (aphthous, stellate, linear), patchy lesions, pseudopolyps, cobblestoning

Continuous diffuse inflammation, erythema, friability, loss of no mal vascular pattern, pseudopolyps

e

m

co

Mucosal distribution, continuous disease (no skip lesions) Architectural distortion, gland disruption, crypt abscess Granulomas absent

e

Transmural distribution with skip lesions Focal inflammation ± noncaseating granulomas, deep fissuring + aphthous ulcerations, strictures Glands intact

re

Histologic Features

co

m

eb

Fever

b

Common

o

k

Rectal Bleeding

co

m

Location

Complications

Strictures, fistulae, perianal disease

Toxic megacolon

Colon Cancer Risk

Increased if >30% of colon involved

Increased except in proctitis

eb

b

o

Cobblestone mucosa Frequent strictures and fistulae AXR: bowel wall thickening “string sign”

ks

Radiologic Features

Lack of haustra Strictures rare; need to rule out complicating cancer

G20 Gastroenterology

Toronto Notes 2018

c

Small and Large Bowel

Ulcerative Colitis

fr

Crohn’s Disease

oo

15% 10% 10% Less common 75-80% Rare Common Rare Statistically associated in 5-10% of those with IBD but not an EIM

15-20% of those with IBD (CD>UC) 10% of those with IBD (CD>UC) Occurs equally in CD and UC

3-4% of IBD patients (CD>UC)

ks

15-35% of patients with ileal Crohn s 1-5% of IBD cases involving colon

m

e

Most common in CD, especially following ileal resection Characteristic of Crohn’s

e

c

bo

o

e

bo

ok

System Dermatologic Erythema nodosum Pyoderma gangrenosum Perianal skin tags Oral mucosal lesions Psoriasis Stomatitis Rheumatologic Peripheral arthritis Ankylosing spondylitis Sacroiliitis Ocular (~10% of IBD) Uveitis (vision threatening) Episcleritis (benign) Hepatobiliary Cholelithiasis PSC Fatty liver Gallstones Urologic Calculi Ureteric obstruction Fistulae Others Thromboembolism Vasculitis Osteoporosis Vitamin deficiencies (B12, Vit ADEK) Cardiopulmonary disorders Pancreatitis (rare) Phlebitis

m

e

Table 11. Extraintestinal Manifestations (EIM) of IBD

ok

Crohn’s Disease

e

e

b

Definition • chronic transmural inflammatory disorder potentially affecting the entire gut from mouth to perianal region (“gum to bum”)

e

e

o

co

m

Epidemiology • incidence 1-6/100,000; prevalence 10-100/100,000 • bimodal: onset before 30 yr, second smaller peak age 60; M=F • incidence of Crohn’s increasing (relative to UC) especially in young females • more common in Caucasians, Ashkenazi Jews ■■ risk in Asians increases with move to Western countries • smoking incidence in Crohn’s patients is higher than general population

bo

oo

k

ok

s

Pathology • most common location: ileum + ascending colon • linear ulcers leading to mucosal islands and “cobblestone” appearance • granulomas are found in 50% of surgical specimens 15% of mucosal biopsies

e

m

co

co

m

m

e

Clinical Features • natural history unpredictable; young age, perianal disease, and need for corticosteroids have been associated with poor prognosis, but associations are not strong enough to guide clinical decisions • most often presents as recurrent episodes of abdominal cramps, non-bloody diarrhea, and weight loss • ileitis may present with post-prandial pain, vomiting, RLQ mass; mimics acute appendicitis • extra-intestinal manifestations are more common with colonic involvement • fistulae, fissures, abscesses are common • deep fissures with risk of perforation into contiguous viscera (leads to fistulae and abscesses) • enteric fistulae may communicate with skin, bladder, vagina, and other parts of bowel

f

ok

ok

sf

re

Investigations • colonoscopy with biopsy to visualize (less often gastroscopy) • CT/MR enterography to visualize small bowel • CRP elevated in most new cases, useful to monitor treatment response (especially acutely in UC) • bacterial cultures, O&P, C. difficile toxin to exclude other causes of inflammatory diarrhea

G21 Gastroenterology

Toronto Notes 2018

c

Small and Large Bowel

e

Management (see Figure 7)

s

Table 12. Management of Crohn’s Disease Notes

Lifestyle/Diet

Smoking cessation Fluids only during acute exacerbation Enteral diets may aid in remission only for Crohn’s ileitis, not colitis No evidence for any non-enteral diet changing the natural history of Crohn’s disease, but may affect symptoms Those with extensive small bowel involvement or extensive resection require electrolyte, mineral, and vitamin supplements (vit D, Ca2+, Mg2+, zinc, Fe, B12)

Traditional Medical Management of Crohn’s Induction of Remission 5-ASA* ? Steroids + Immunosuppressive + Antibiotics + MTX + Infliximab +

m

m

e

Loperamide (Imodium®) > diphenoxylate (Lomotil®) > codeine (cheap but addictive) All work by decreasing small bowel motility, used only for symptom relief CAUTION if colitis is severe (risk of precipitating toxic megacolon), therefore avoid during flare-ups

5-ASA**

Efficacy controversial: Is currently used for mild ileitis Sulfasalazine (Salazopyrin®): 5-ASA bound to sulfapyridine Hydrolysis by intestinal bacteria releases 5-ASA (active component) Dose-dependent efficacy Mesalamine (Pentasa®): coated 5-ASA releases 5-ASA in the ileum and colon when inflammation is mild

m

.c om

Antidiarrheal Agents*

o

oo

m

eb

m

m

om

e

e

c

*Cholestyramine: a bile-salt binding resin; for watery diarrhea with 1 attack in almost all patients • more colonic involvement in the 1st yr correlates with increased severity of attacks and increased colectomy rate ■■ colectomy rate = 1% for all patients after the 1st yr; 20-25% eventually undergo colectomy • normal life expectancy • if proctitis only, usually benign course • stool calprotectin increasingly recognized as a marker of bowel mucosal inflammation, reported especially to be useful in monitoring the activity of inflammatory bowel disease, but accuracy is still controversial

co

Irritable Bowel Syndrome

fre

re

Definition • a form of functional bowel disease; more than just a label for GI symptoms unexplained after normal investigations

bo

ok

Epidemiology • 20% of North Americans • onset of symptoms usually in young adulthood • F>M

om

om

Pathophysiology • associated with either abnormal perception of intestinal activity or abnormal intestinal motility • abnormal motility: multiple abnormalities described; unclear if associations or if causative • psychological: stress may increase IBS symptoms but probably does not cause IBS • types of IBS: IBS with diarrhea, IBS with constipation, IBS-mixed type (both diarrhea and constipation), and IBS untyped (insufficient abnormality in stool consistency to meet other types) Diagnosis

f

e

Table 13. Rome IV Criteria for Diagnosing Irritable Bowel Syndrome

s

IBS Rome IV Crite ia

bo

o

o

Recurrent abdominal pain, on average, at least 1 day per week in the last 3 months, associated with 2 or more of the following: 1. Related to defecation 2 Associated with a change in frequency of stool 3. Associated with a change in form (appearance) of stool

m

Symptom onset at least 6 months before diagnosis and criteria present during the last 3 months

om

The following are supportive, but not essential to the diagnosis: Abnormal stool frequency (>3/d or 1/4 of defecations Abnormal stool passage (straining, urgency, feeling of incomplete evacuation) >1/4 of defecations Passage of mucus >1/4 of defecations Bloating Diagnosis of IBS Less Likely in Presence of “Red Flag” Features Weight loss Fever Nocturnal defecation

s

s

Anemia Blood or pus in stool Abnormal gross findings on flexible sigmoidoscopy

bo

o

Normal Physical Exam

om

m

e

Investigations • if history consistent with Rome IV criteria, no alarm symptoms, and no family history of IBD or colorectal cancer, limited investigations required • aim is to rule out diseases which mimic IBS, particularly celiac disease and IBD • investigations can be limited to CBC, inflammatory markers (ESR, CRP) and celiac serology • if available, fecal calprotectin is likely more reliable test to rule out IBD • consider TSH, stool cultures depending on clinical circumstances • consider colonoscopy (e.g. if alarming features present, family history of IBD or age >50)

fre

ks

ks

fre

e

Treatment • reassurance, explanation, support, aim for realistic goals • relaxation therapy, biofeedback, hypnosis, stress reduction, probably exercise • low FODMAP diet for pain, bloating gas, irregular bowel movements • no therapeutic agent consistently effective, pain most difficult to control, no drug changes natural history so the drug should be “wanted, since it is not needed”

IBS Mimickers • Enteric infections e.g. Giardia • Lactose intolerance/other disaccharidase deficiency • Crohn’s disease • Celiac sprue • Drug-induced diarrhea • Diet-induced (excess tea, coffee, colas)

G24 Gastroenterology

Toronto Notes 2018

c

Small and Large Bowel

oo

k

Prognosis • 80% improve over time • most have intermittent episodes • normal life expectancy

e

co m

m

Rifaximin Therapy for Patients with Irritable Bowel Syndrome Without Constipation NEJM 2011;364:22-32 Purpose: Previous evidence suggests that gut flora may play an important role in the pathophysiology of IBS. This study evaluated rifaximin, a minimally absorbed antibiotic, in treating IBS without constipation. Methods: Two phase 3, double-blind, placebo-controlled trials (TARGET 1 and TARGET 2). 1,260 patients who had IBS without constipation were randomly assigned to rifaximin (550 mg dose) or placebo, 3 times daily for 2 wk, with a follow-up of 10 wk The primary endpoint was adequate self-reported relie of global IBS symptoms. Results: Significantly more patients in the rifaximin group had adequate self-reported relief of global IBS symptoms compared to the placebo group during the first 4 wk after treatmen (40.8% vs. 31.2% respectively). Also, more patients in the rifaximin group had adequate relief of bloating compared to the placebo group (39.5% vs. 28.7% respectively). Conclusions: Rifaximin therapy for 2 wk provided significant relief of symptoms, bloating, abdominal pain, and stool consistency associated with IBS without constipation.

fre

e

re e

ee

co

e

o

s

ks fre

• symptom-guided treatment ■■ pain predominant ◆◆ antispasmodic medication before meals (e.g. hyoscine, pinaverium, trimebutine - low level evidence) ◆◆ tricyclic antidepressants (TCA), selective serotonin reuptake inhibitors (SSRI - moderate level of evidence) ■■ IBS with diarrhea (IBS-D) ◆◆ increase dietary fibre (bran or psyllium) to increase stool consistency but may worsen abdominal gas ◆◆ loperamide (Imodium®) ◆◆ diphenoxylate (Lomotil®) ◆◆ cholestyramine ◆◆ eluxadoline ■■ IBS with constipation (IBS-C) ◆◆ increase fibre in diet ◆◆ linaclotide ◆◆ osmotic or other laxatives (help more with the constipation than the pain) ■■ mixed (alternating constipation and diarrhea) (IBS-M)

Constipation Definition • passage of infrequent or hard stools with straining (stool water coffee ground emesis > melena > occult blood in stool

bo

Transfusion Strategies for Acute Upper Gastrointestinal Bleeding NEJM 2013;368:11-21 Study: Prospective, unblinded, RCT, follow-up up to 45 d. Populations: 921 patients with hematemesis, bloody nasogastric aspirate, melena, or both. Exclusion criteria included massive bleed, ACS, stroke/TIA or transfusion within previous 90 d; recent trauma/surgery; lower GI bleed. Intervention: Patients randomized to restrictive ( ALT = alcoholic liver disease or other causes of hepatitis (i.e. non-alcoholic liver disease) that have progressed to advanced cirrhosis

m

m

eb

oo

o

ks

ks

fr

fre

e.

c

o

B. Tests of Liver Injury • disproportionately increased AST or ALT = hepatocellular damage ■■ ALT more specific to liver; AST from multiple sources (especially muscle) ■■ elevation of both highly suggestive of liver injury ■■ most common cause of elevated ALT is fatty liver • disproportionately increased ALP (and GGT) = cholestasis (stasis of bile flow) ■■ if ALP is elevated alone, rule out bone disease by fractionating ALP and/or checking GGT ■■ if ALP elevation out of proportion to ALT/AST elevation, consider 1. obstruction of common bile duct (e.g. extraluminal = pancreatic Ca, lymphoma; intraluminal = stones, cholangiocarcinoma, sclerosing cholangitis, helminths) 2. destruction of microscopic ducts (e.g. PBC) 3. bile acid transporter defects (e.g. drugs, intrahepatic cholestasis of pregnancy) 4. infiltration of the liver (e.g. liver metastases, lymphoma, granulomas, amyloid)

Definition • viral hepatitis lasting 10-20x normal in hepatocellular necrosis) • ALP minimally elevated • viral serology, particularly the IgM antibody directed to the virus

ee

ks

Major Sources of ALP • Hepatobiliary tree • Bone • Placenta

c

c

co

ee

Prognosis • poor prognostic indicators: comorbidities, persistently high bilirubin (>340 mmol; 20 mg/dL), increased INR, decreased albumin, hypoglycemia

s

re

Alcoholic hepatitis: history of recent alcohol, RUQ abdominal pain, AST/ALT>2, AST usually 1000 due to • Viral hepatitis • Drugs/toxins • Autoimmune hepatitis • Hepatic ischemia • Less often, common bile duct stone

ee

oo

ks

sf

fre

Clinical Features • most are subclinical • flu-like prodrome may precede jaundice by 1-2 wk ■■ nausea/vomiting, anorexia, headaches, fatigue, myalgia, low-grade fever, arthralgia and urticaria (especially HBV) • only some progress to icteric (clinical jaundice) phase, lasting days to weeks ■■ pale stools and dark urine 1-5 d prior to icteric phase ■■ hepatomegaly and RUQ pain ■■ splenomegaly and cervical lymphadenopathy (10-20% of cases)

G29 Gastroenterology

Toronto Notes 2018

Liver

s

ks fr

Complications • cholestasis (most commonly associated with HAV infection) • hepatocellular necrosis: AST, ALT >10-20x normal, ALP and bilirubin minimally increased, increased cholestas s

bo

Hepatitis A Virus

• RNA virus • fecal-oral transmission; incubation period 4-6 wk • diagnosed by elevated transaminases, positive anti-HAV IgM • in children: characteristically asymptomatic • in adults: fatigue, nausea, arthralgia, fever, jaundice • can cause acute liver failure and subsequent death (20,000 IU/mL), HBeAg positive, but normal ALT/ AST; due to little immune control and minimal immune-mediated liver damage; characteristic of perinatal infection (or ‘incubation period’ in adult with newly-acquired HBV) 2. immune clearance (or immunoactive): HBV-DNA levels (>20,000 IU/mL), HBeAg positive; due to immune attack on the virus and immune-mediated liver damage; characterized by progressive disease without treatment and increasing liver fibrosis (sometimes progressing to cirrhosis and/or hepatocellular carcinoma); likely to benefit from treatment 3. immune control: lower HBV-DNA (2,000 IU/mL), HBeAg negative because of pre-core or core promoter gene mutation, anti-HBe positive, ALT/AST high; characterized by progressive disease without treatment and increasing liver fibrosis (sometimes progressing to cirrhosis and/or hepatocellular carcinoma); likely to benefit from treatment

ok

Without treatment, 8-20% of those with ongoing immunoactive chronic hepatitis can develop cirrhosis within 5 yr. In contrast, those in the immune tolerant phase (with extremely high HBV-DNA levels) are at minimal risk for liver fibrosis as they do not have immune-mediated liver injury

e.

2

re

1

Anti-HBc IgM

m

eb

o

HBsAg

Acute HBV

HCV (and HBV) treatment lowers the risk of hepatocell lar carcinoma

ee

s

Table 15. Hepatitis B Serology

G30 Gastroenterology

Toronto Notes 2018

Liver

re

Hepatitis D

m

om

m

m

co

e

m

fre

m

e

m

om

fr

ks

e

m

co

om

.

e. co

re

sf

ok

b

Prognosis • 80% of acute hepatitis C become chronic (of these 20% evolve to cirrhosis) • risk of hepatocellular carcinoma increases if cirrhotic • can cause cryoglobulinemia; associated with membranoproliferative glomerulonephritis, lymphoma

e.

m

eb

m

m

Treatment • blood-borne precautions; vaccinate for hepatitis A and B if serology negative; avoid alcohol • clearest indication for treatment is in subgroup likely to develop clinically significant liver disease, i.e., persistently elevated transaminases, liver biopsy showing fibrosis/cirrhosis, and at least moderately severe necrosis/inflammation • treatment depends partly on genotype; length of treatment depends on degree of fibrosis, level of serum HCV-RNA, comorbidities, and previous treatment • oral interferon-free regimens (for all genotypes) (e.g. sofosbuvir/ledipasvir, ombitasvir/paritaprevir/ ritonavir+dasabuvir, or elbasvir/grazoprevir and sofosbuvir/velpatasvir ) are now the standard of care with >90% success rate without significant side-effects including those who failed previous interferonbased reatment

Treatment of Hepatitis C: A Systematic Review JAMA 2014;312(6):631-40 Purpose: To evaluate the evidence for the safety, efficacy and tolerability of interferon and noninterferon based, oral therapies in the treatment of Hepatitis C virus (HCV) Study: Literature review of phase 2, 3, and 4 studies published from January 1, 2009 – May 30, 2014, with data graded according to Oxford Centre for Evidence Based Medicine criteria. Population: 19, 063 adult patients infected with HCV genotype 1, 2, or 3 with or without HIV coinfection. Outcome: Sustained virologic response (SVR) of undetectable plasma HCV RNA at 12 or 24 weeks post-therapy. Results: Achievement of SVR was more difficult in HCV genotype 1 patients. Treatment of HCV genotype 1 patients with sofosvubir with pegylated interferon and ribavirin yielded high rates of SVR (89-90%) and shorter duration of therapy. HCV genotype 2 or 3 patients treated with sofosbuvir and ribavirin alone achieved SVR of 82-93% and 8095% for genotype 2 at 12 weeks and genotype 3 at 24 weeks, respectively Patients with HCV and HIV coinfection with compensated cirrhosis should be treated in the same manner as HCV-monoinfected patients. Conclusions: High SVR rates can be achieved for HCV patients with or without HIV coinfection using shorter durations of non-interferon therapies. HCV genotype 1 patients are likely to benefit from co-treatment with interferon and non-interferon therapies.

e. c

oo

ok

Diagnosis • suspected on basis of elevated ALT/AST and positive serum anti-HCV • diagnosis established by detectable HCV-RNA in serum • virus genotype correlates with response to treatment but not prognosis ■■ serum HCV-RNA inversely correlates with response to treatment • normal transaminases can have underlying cirrhosis on biopsy, but otherwise excellent prognosis

re

fre

re

e

co

co

m

• RNA virus (7 genotypes; genotype 1 is most common in North America) • blood-borne transmission; sexual transmission is “inefficient” • major risk factor: injection drug use • other risk factors: blood transfusion received before 1992 (or received in developing world), tattoos, intranasal cocaine use • clinical manifestation develops 6-8 wk after exposure ■■ symptoms mild and vague (fatigue, malaise, nausea) therefore not commonly diagnosed in acute stage

bo

From Description to Cure in One Generation Ledipasvir and Sofosbuvir for Untreated HCV Genotype 1 Infection NEJM 2014;370;1889-1898 If you ever need an example to demonstrate the miraculous advances of modern medicine, consider using chronic hepatitis C. It inflicts about 6 per 1000 of Canadians and is the commonest reason for liver transplant in most studies. Yet until 1989, when the virus was first cloned, this condi ion was so poorly understood that it was labelled as what it wasn’t - it was called hepatitis non-A, non-B because there was insufficient evidence to even appreciate that it was one disease, let alone an infection. Today it can be cured by taking a safe drug regimen for 6 o 24 weeks, depending on the virus strain, previous treatments, and the degree of liver damage. This recent study showed that sofosbu ir (nucleoside polymerase inhibitor) and led spavir (NS5A inhibitor) led to a 99% cure rate in genotype 1 (the most common) infection with only minimal side-effects. These antiviral drugs are designer drugs: specifically tailored in the laboratory to combat pathogenic features of the hepatitis C virus.

re

Hepatitis C Virus

eb

bo

oo

ks

ok s

• defective RNA virus requiring HBsAg for entry into hepatocyte, therefore infects only patients with HBV; causes more aggressive disease than hepatitis B virus alone • coinfection: acquire HDV and HBV at the same time • HDV can present as ALF and/or accelerate progression to cirrhosis • treatment: low-dose interferon (20% response) and liver transplant for end-stage disease

DDx for Hepatomegaly • Congestive (right heart failure, Budd-Chiari syndrome) • Infiltrative • Malignant (primary, secondary, lymphoproliferative, leukemia) • Benign (fatty liver, cysts, hemochromatosis, extramedu lary hematopoiesis, amyloid) • Proliferative • Infectious (viral, tuberculosis, abscess, echinococcus) • Inflammatory (granulomas [sarcoid], histiocytosis X)

fr

m

o

co m

m

e

o

oo

oo

k

ks

fr

r

Treatment • counselling: 40% of men and 10% of women with perinatal infection without treatment will die from HBV-related complications • prolonged immune-mediated damage leads to higher risk of liver fibrosis • hepatocellular carcinoma screening with ultrasound q6mo, especially if high serum HBV-DNA levels, cirrhosis, men, (age >40 in Asian men, >50 in Asian women, and >20 in African descent) • consider pharmacological therapy if: 1. HBeAg positive + HBV-DNA >20,000 IU/mL + elevated ALT ; or 2. HBeAg negative + HBV-DNA >2,000 IU/mL + elevated ALT ± stage ≥2 fibrosis on liver biopsy 3. treat to prevent flare when placed on immunosuppressive therapy such as prednisone, chemotherapy, biologics, etc. • treatment goal: reduce serum HBV-DNA to undetectable level • treatment options: interferon, tenofovir, entacavir, lamivudine • vaccinate against HAV if serology negative (to prevent further liver damage) • follow blood and sexual precautions

G31 Gastroenterology

Toronto Notes 2018

Liver

HCV

HDV

HEV

CMV

EBV

Virus Family

Picornaviridae

Hepadnaviridae

Flaviviridae

Deltaviridae

Caliciviridae

Herpesviridae

Herpesviridae

Flavivirus

Genome

RNA

DNA

RNA

RNA

RNA

DNA

RNA

RNA

Envelope

No

Yes

Yes

Yes

Transmission

Fecal-oral

Parenteral/sexual or equivalent Vertical

Incubation

4-6 wk

6 wk 6 mo

Onset

Usually abrupt

Communicability

2-3 wk in late incubation to early clinical phase Ac te hepatitis in most adults, 10% of children

Chronicity

Saliva-oral

Vector (mosquito)

2-26 wk

3-13 wk

2-8 wk

20-60 d

30-50 d

3-6 d

Usually insidious

Insidious

Usually abrupt

Usually abrupt

Variable

Variable

Usually abrupt

HBsAg+ state highly communicable Increased during third trimester or early post-partum

Communicable prior to overt symptoms and throughout chronic illness

Infectious only in presence of HBV (HBsAg required for replication)

Unknown

Variable – dormant or persistent

Communicable highest during year after primary infection but never zero

Variable, vectordependent

None, although can relapse

5% adults, 90% infants

80%, 20% of which develop cirrhosis

5%

None

Common; latent

Common; latent

Infection confers lifelong immunity

Serology

Anti-HAV (IgM)

See Table 15

HCV-RNA Anti-HCV (IgG/IgM)

HBsAg Anti-HDV (IgG/IgM)

Anti-HEV (IgG/IgM)

Anti- CMV (IgM/IgG)

Monospot; anti-EBV IgM/IgG, EBV DNA quantitation

Anti-YF (IgM/IgG)

Immunity

Yes

Yes

?

Yes

?

?

?

Yes

Vaccine

Havrix, 2 doses q6mo, combined with Twinrix at 0, 7, and 21 d

Recombivax HBTM, age 11-15, 2 doses q6mo

No

No

No

No

No

YF-VAX, 1 dose booster q10yr

Management

General hygiene Treat close contacts (antiHAV Ig) Prophylaxis for high-risk groups (HAV vaccine ± HAV Ig) unless immune

Prevention: HBV vaccine and/or hepatitis B Ig (HBIG) for needlestick, sexual contact, infants of infected mothers unless already immune Rx: oral antivirals vs. interferon if indications met

Prevention: no vaccine Rx: IFN + ribavirin ± protease inhibitor; although all oral anti-viral (IFN-free) therapy now available is highly efficacious

Prevention: HBV vaccine

Prevention: general hygiene, no vaccine

In high risk transplant patients: CMV IG and anti-virals (ganciclovir, valganciclovir)

Supportive treatment post infection

.c

Prevention Supportive treatment post infection

Acute Mortality

0.1-0.3%

0.5-2%

1%

2-20% coinfection with HBV, 30% superinfection Predisposes HBV carriers to more severe hepatitis and faster progression to cirrhosis

1-2% overall, 1020% in pregnancy

Rare in immunocompetent adults

Rare

20-60% in developing countries

Oncogenicity

No

Yes

Yes

?

No

No

Yes

No

Complications

Can cause acute liver failure and subsequent death (48 h: continued hepatic necrosis possibly complicated with ALF or resolution ◆◆ note: potential delay in presentation in sustained-release products ■■ blood levels of acetaminophen correlate with the severity of hepatic injury, particularly if time of ingestion known ■■ therapy ◆◆ gastric lavage/emesis (if 1000 ■■ considered if compound heterozygote and potential other cause of liver injury (e.g. fatty liver, etc.) ■■ if C282Y/C282Y and no markers of advanced fibrosis, then biopsy generally not needed • HCC screening if cirrhosis

Gene mutation not 100% penetrant, so not all with homozygous gene defect have clinically significant iron overload

G34 Gastroenterology

Toronto Notes 2018

Liver

fre

Alcoholic Liver Disease

eb

o

oo

k

Definition • spectrum of diseases, ranging from: ■■ fatty liver (all alcoholics): always reversible if alcohol stopped ■■ alcoholic hepatitis (35% of alcoholics): usually reversible if alcohol stopped ■■ cirrhosis (10-15% of alcoholics): potent ally irreversible

o

bo

ok

ok

sf

m

m

Investigations • blood tests are non-specific, but in general ■■ AST:ALT >2:1 (both usually 2-3 standard drinks/d in females and >3-6 standard drinks/d in men for >10 yr leads to cirrhosis, but only in about 10-20% of those who consume this amount daily on a continuous basis; cirrhosis risk increases with amount of alcohol consumed above threshold • clinical findings do not accurately predict type of liver involvement • fatty liver ■■ mildly tender hepatomegaly; jaundice rare ■■ mildly increased transaminases zone I (around portal tracts, where oxygenated blood enters) ■■ necrosis and hepatic vein sclerosis • histology of alcoholic hepatitis ■■ ballooned (swollen) hepatocytes often containing Mallory bodies, characteristically surrounded by neutrophils ■■ large fat globules ■■ fibrosis: space of Disse and perivenular

Standard Drink Equivalent 1 standard drink= 14 g EtOH = 12 oz beer (5% alcohol) = 5 oz wine (12-17%) = 3 oz fortified wine (17-22%) = 1.5 oz liquor (40%) Tip: percentage alcohol multiplied by oz in 1 standard drink roughly equals 60

G35 Gastroenterology

Toronto Notes 2018

Liver

fre

fre

Non-Alcoholic Fatty Liver Disease

b

o

oo

k

Definition • spectrum of disorders characterized by macrovesicular hepatic steatosis, sometimes with inflammation and/or fibrosis • most common cause of liver disease in North America Etiology • pathogenesis not well elucidated; insulin resistance implicated as key mechanism, leading to hepatic steatosis • histological changes indistinguishable from those of alcoholic hepatitis despite negligible history of alcohol consumption

e.

c

c

Risk Factors • likely a component of the metabolic syndrome along with type 2 DM, HTN, hypertriglyceridemia • rapid weight loss or weight gain

oo

oo

k

ks fr

Clinical Features • often asymptomatic • may present with fatigue, malaise, and vague RUQ discomfort • elevated serum triglyceride/cholesterol levels and insulin resistance

m

eb

Investigations elevated serum AST, ALT ± ALP; AST/ALT 300 µmol/L, INR >3.5, creatinine >200 µmol/L

G36 Gastroenterology

Toronto Notes 2018

Liver

fre

Cirrhosis Pla

te

let

s

R

IN

Al

bu

m

in

bin

liru

Bi

Figure 12. Progression of liver dysfunction based on liver function tests – the “W”

m

eb

m

m

eb

bo

o

ok

Definition • liver damage characterized by diffuse distortion of the basic architecture and replacement with scar tissue and formation of regenerative nodules • Stage 1 cirrhosis is compensated and asymptomatic, can last for 10-20 yr with almost normal life expectancy • Stage 2 cirrhosis is decompensation, typically development of ascites (most common), variceal bleeding, encephalopathy, characteristically presents abruptly even though histologically the liver fibrosis is gradually progressive

o

oo

k

fr

ks fre

e

om

Etiology • fatty liver (alcoholic or non-alcoholic fatty liver disease) • chronic viral hepatitis (B, B+D, C; not A or E) • autoimmune hepatitis • hemochromatosis • primary biliary cirrhosis • chronic hepatic congestion ■■ cardiac cirrhosis (chronic right heart failure, constrictive pericarditis) ■■ hepatic vein thrombosis (Budd-Chiari) • cryptogenic (i.e. no identifiable cause, although many of these patients may represent “burnt-out NASH”) • rare Wilson’s disease, Gaucher’s disease, α1-antitrypsin deficiency

o

o

fe

fre

e.

e.

c

c

m

m

m

Investigations • definitive diagnosis is histologic (liver biopsy) • other tests may be suggestive ■■ blood work: fall in platelet count 6 mo; use MELD score

Classification

m

Table 18. Child-Pugh Score and Interpretation 1

2

3

Serum bilirubin (µmol/L)

51

Serum albumin (g/L)

>35

28-35

2.3

Controllable

Refractory

Encephalopathy

Absent

Minimal

Severe

ok

ok

bo

s

1.7-2.3

Absent

s

5 mmHg

r

sf

o

fre

Pathophysiology • 3 sites of increased resistance (remember pressure = flow x resistance) ■■ pre-sinusoidal (e.g. portal vein thrombosis, schistosomiasis, sarcoidosis) ■■ sinusoidal (e.g. cirrhosis, alcoholic hepatitis) ■■ post-sinusoidal (e.g. right-sided heart failure, hepatic vein thrombosis, veno-occlusive disease, constrictive pericarditis)

Fibrosis may regress and disappear if cause of liver injury is treated or resolves

ee

.c

bo

ok

Effects of Portal Hypertension Esophageal varices Gastric varix  melena Splenomegaly Caput medusa, umbilical hernia Ascites Hemorrhoids

Loss of sexual hair, testicular atrophy Ankle edema Palmar erythema, Dupuytren's contracture, asterixis anemia Leuckonychia, Terry's nails, clubbing

ks

Hepatopulmonary Syndrome Clinical Triad • Liver disease • Increased alveolar-arterial gradient while breathing room air • Evidence for intrapulmonary vascular abnormalities

o

m

co

e.

re

sf

Effects of Liver Failure Encephalopathy (coma) Xanthelasma Scleral icterus, jaundice Fetor hepaticus Spider angioma Gynecomastia Muscle wasting Bleeding tendency (bruising)

oo

Usual causes of death in cirrhosis: renal failure (hepatorenal syndrome), sepsis, GI bleed, or HCC

o

oo

fre

sf re

co m

m

b

oo

oo

s

e

ok sf re

■■ half of patients with cirrhosis have gastroesophageal varices and one-third of these develop hemorrhage with an overall mortality of >30% ■■ hepatic venous pressure gradient (HVPG) ≥10 mmHg is the strongest predictor of variceal development ■■ treatment: resuscitation, antibiotic prophylaxis, vasoactive drugs (e.g. octreotide IV) combined with endoscopic band ligation or sclerotherapy, Transjugular Intrahepatic Portosystemic Shunt (TIPS) • renal failure in cirrhosis ■■ classifications ◆◆ pre-renal (usually due to over-diuresis) ◆◆ acute tubular necrosis ◆◆ Hepatorenal Syndrome (HRS) – Type I: sudden and acute renal failure (rapid doubling of creatinine over 2 wk) – Type II: gradual increase in creatinine with worsening liver function (creatinine doubling over years) ◆◆ HRS can occur at any time in severe liver disease, especially after – overdiuresis or dehydration, such as diarrhea, vomiting, etc. – GI bleed – sepsis ◆◆ treatment for hepatorenal syndrome (generally unsuccessful at improving long-term survival) – for type I HRS: octreotide + midodrine + albumin (increases renal blood flow by increasing systemic vascular resistance) – definitive treatment is liver transplant • hepatopulmonary syndrome ■■ majority of cases due to cirrhosis, though can be due to other chronic liver diseases, such as noncirrhotic portal HTN ■■ thought to arise from ventilation-perfusion mismatch, intrapulmonary shunting and limitation of oxygen diffusion, failure of damaged liver to clear circulating pulmonary vasodilators vs. production of a vasodilating substance by the liver ■■ clinical features ◆◆ hyperdynamic circulation with cardiac output >7 L/min at rest and decreased pulmonary + systemic resistance (int apulmonary shunting) ◆◆ dyspnea, platypnea (increase in dyspnea in upright position, improved by recumbency), and orthodeoxia (desaturation in the upright position, improved by recumbency) ◆◆ diagnosis via contrast-enhanced echocardiography: inject air bubbles into peripheral vein; air bubbles appear in left ventricle after third heartbeat (normal = no air bubbles; in ventricular septal defect, air bubbles seen 11 g/L (1.1 g/dL) Portal Hypertension Related

m

Table 19. Serum-Ascites Albumin Gradient as an Indicator of the Causes of Ascites Serum [Alb] – Ascitic [Alb] 500 mL) ■■ bulging flanks, shifting dullness, fluid-wave tes positive ■■ most sensitive symptom: ankle swelling

co

m

m

Investigations • diagnostic paracentesis ■■ 1st aliquot: cell count and differential ■■ 2nd aliquot: chemistry (especially albumin, but also total protein; amylase if pancreatitis; TG and chylomicrons if turbid and suspect chylous ascites) ■■ 3rd aliquot: C&S, Gram stain ■■ 4th aliquot: cytology (usually positive in peritoneal carcinomatosis)

m

om

m

eb

bo

oo

oo

ks

fr

Treatment • non-refractory ascites ■■ Na+ restriction (daily sodium intake 11 g/L portal HTN • ascitic fluid total protein >25 g/L, suggests cardiac portal hypertension • ascitic fluid total protein 1000 mg/dL), Hypercalcemia, Hypothermia Emboli or ischemia Drugs/toxins ■■ azathioprine, mercaptopurine, furosemide, estrogens, methyldopa, H2-blockers, valproic acid antibiotics, acetaminophen, salicylates, methanol, organophosphates, steroids (controversial)

Gallstones only cause acute pancreatitis (not chronic pancreatitis)

e.

e.

co

co

m

Pathophysiology • activation of proteolytic enzymes within pancreatic cells, starting with trypsin, leading to local and systemic inflammatory response • in gallstone pancreatitis, this is due to mechanical obstruction of the pancreatic duct by stones • in ethanol-related pancreatitis, pathogenesis is unknown • in rare genetic diseases, mutations prevent the physiological breakdown of trypsin required normally to stop proteolysis (e.g mutant trypsin in hereditary pancreatitis or mutation in SPINK 1 gene which normally inhibits activated trypsin); may be model for ethanol-related pancreatitis

m

co

co

m

m

eb

oo

ks

f

Pathology • mild (interstitial) ■■ per -pancreatic fat necrosis ■■ interstitial edema • severe (necrotic) ■■ extensive peri-pancreatic and intra-pancreatic fat necrosis ■■ parenchymal necrosis and hemorrhage → infection in 60% ■■ release of toxic factors into systemic circulation and peritoneal space (causes multi-organ failure) • severity of clinical features may not always correlate with pathology • 3 phases ■■ local inflammation + necrosis → hypovolemia ■■ systemic inflammation in multiple organs, especially in lungs, usually after IV fluids given → pulmonary edema ■■ local complications two weeks after presentation → pancreatic sepsis/abscess

e

o

fre

o

ok

sf

re

e

f

Grey-Turner’s Sign Flank ecchymosis

Increased Amylase • Sensitive, not specific Increased Lipase • Higher sensitivity and specificity • Stays elevated longer

c

c

co

m

Investigations • increased serum pancreatic enzymes: amylase, lipase (more specific) • ALT >150 specific for biliary cause • increased WBC, glucose, low calcium • imaging: CT most useful for diagnosis and prognosis ■■ x-ray: “sentinel loop” (dilated proximal jejunem), calcification, and “colon cut-off sign” (colonic spasm) ■■ U/S: useful for evaluating biliary tree (67% sensitivity, 100% specificity) ■■ CT scan with IV contrast: useful for diagnosis and prognosis because contrast seen only in viable pancreatic tissue, non-viable areas can be biopsied percutaneously to differentiate sterile from infected necrosis ■■ ERCP or MRCP if cause uncertain, assess for duct stone, pancreatic or ampullary tumour, pancreas divisum

Cullen’s Sign Periumbilical ecchymosis

e

bo

ok

ks

sf

fr

re

e

Signs and Symptoms • pain: epigastric, noncolicky, constant • jaundice: compression or obstruction of bile duct • can radiate to back • Cullen’s/Grey-Turner’s signs • may improve when leaning forward (Inglefinger’s sign) • tetany: transient hypocalcemia • tender rigid abdomen; guarding hypovolemic shock: can lead to renal failure • N/V • acute respiratory distress syndrome • abdominal distention from paralytic ileus • coma • fever: chemical, not due to infection

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Pancreas

Acute necrotic collection (ANC)

Pancreatic pseudocyst

All of these collections are classified as infected or not infected

m

co m

e.

m

co

e.

bo

k

ok

fre

fre

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e

c

co

Late Complications • pseudocysts: follow if asymptomatic, drain if symptomatic or growing ■■ drain: choice of endoscopic, percutaneous under radiological guidance, or surgical • infected necrosis/abscesses: antibiotics + percutaneous drainage, endoscopic vs. surgical • bleeding: (1) gastric varices if splenic vein thrombosis, (2) pseudoaneurysm of vessels in areas of necrosis, especially splenic artery, (3) duodenal ulcer related to compression of duodenum by enlarged pancreas • splenic and portal vein thrombosis: no effective therapy described, anticoagulation not proven, hazardous • rare: DM, pancreatic duct damage

Prophylactic Antibiotics Cannot Reduce Infected Pancreatic Necrosis and Mortality in Acute Necrotizing Pancreatitis: Evidence from a MetaAnalysis of Randomized Controlled Trials Am J Gastroenterol 2008;103:104-110 Purpose: To review the effectiveness of IV antibiotics on pancreatic necrosis. Study Selection: RCTs comparing antibiotics with placebo or no treatment. Results: Seven trials (n=467) were included. Antibiotics were not statistically superior to controls in reduction of infected necrosis and mortality. Conclusion: Prophylactic a tibiotics cannot reduce infected pancreatic necrosis and mortality in patients with acute necrotizing pancreatitis. Note: In pra tice the temptation to give antibiotics for pancreatitis is mainly in the setting of a sick patient with fever and suggestive pancreatic necrosis on CT scan. It is difficult to determine whether pancreatic necrosis has become infected without aspiration biopsy (see Curr Gastroenterol Rep 2009;11:104-110).

re

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ks

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Treatment • goals (only supportive therapy available) 1. hemodynamic stability 2. analgesia 3. oxygen 4. stop progression of damage (difficult) 5. treat local and systemic complications • antibiotics controversial except in documented infection (use cephalosporins, imipenem) • aspirate necrotic areas of pancreas to diagnose infection; drain if infected • IV fluids (crystalloid or colloid) ■■ beware third spacing of fluid, monitor urine output carefully • NG suction (lets pancreas rest) if vomiting, stomach very dilated • endoscopic sphincterotomy if severe gallstone pancreatitis (i.e. cholangitis or ongoing obstruction) • nutritional support: nasojejunal feeding tube or TPN if cannot tolerate enteric feeds ■■ recent evidence supports nasogastric enteral (or oral if feasible) feeds • no benefit: glucagon, atropine, aprotinin, H2-blockers, peritoneal lavage • follow clinically and CT/ultrasound to exclude complications • chief role of invasive intervention is to excise necrotic tissue (necrosectomy) in the case of infected pancreatic necrosis (try to delay for > two weeks to allow demarcation between viable and necrotic tissue), better done endoscopically or radiologically than surgically if technically possible

sf

bo

Walled-off necrosis (WON)

m

Acute peripancreatic fluid collection (APFC)

Chronic

m

Solid

co

Liquid

e.

sf re

ks fre

Table 21. Collections in pancreatitis (Revised 2012 Atlanta Classification)

sf re

co m

co m

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o

o

Prognosis • usually a benign, self-limiting course, single or recurrent • occasionally severe leading to ■■ shock ■■ pulmonary edema ■■ multi-organ dysfunction syndrome ■■ GI ulceration due to stress ■■ death ■■ numerous scales to describe severity: probably most useful is proportion of pancreas not taking up contrast on CT done 48 h after presentation (necrotic pancreas does not take up the contrast dye) ■■ presence of organ failure, particularly organ failure that persists > 48 h, is associated with worse outcomes

Acute

When to Call the Surgeon in Acute Pancreatitis? Endoscopic Transgastric vs. Surgical Necrosectomy for Infected Necrotizing Pancreatitis: A Randomized Trial JAMA 2012; 307:1053-61 Once it was recognized that severe acute (necrotizing) pancreatitis had a terrible prognosis because of an exuberant inflammatory response leading to multiorgan failure, pancreatectomy was attempted. However, contrary to the expected favourable results, clinical experience has shown that surgical pancreatectomy is usually not helpful, perhaps because once the inflammatory cascade starts, it pers sts as a self-perpetuating cycle. The problems caused by acute pancreatitis can be thought of a widespread burn initiated by inflammation in he pancreas, but having little do with o going problems within the pancreas itself. Studies suggest that the only compelling indication for surgery is infected necrotizing pancreatitis not responding to antibiotics. As predicted, without removal of such infected pancreatic tissue, death is likely from sepsis. In this recent randomized trial, transgastric necrosectomy, an endoscopic technique that also removes infected necrotic pancreatic tissue, reduced both a composite end-point of major pancreatitis complications (especially new onset organ failure) and the pro-inflammatory response (as measured by serum IL-6 levels) to a greater extent than surgical necrosectomy. Of course, not all necrotic collections are in areas amenable to endoscopic intervention, and the advice of an experienced surgeon should always be welcomed in severe acute pancreatitis, but the role of surgery in this previously considered surgical disease is rapidly diminishing.

s

sf r

Classification • interstitial edematous vs. necrotizing • mild, moderate, severe

m

Chronic Pancreatitis

f

ks

ks

fre

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Etiology/Pathophysiology • alcohol (most common) ■■ causes a larger proportion (>90%) of chronic pancreatitis than acute pancreatitis ■■ changes composition of pancreatic juice (e.g. increases viscosity)

Symptoms of Chronic Pancreatitis • Abdominal pain • Diabetes • Steatorrhea Etiology = Almost Always Alcohol

fre

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Definition • irreversible damage to pancreas characterized by 1. pancreatic cell loss (from necrosis) 2. inflammation 3. fibrosis

Treatment • Alcohol abstinence • Pancreatic enzyme replacement • Analgesics • Pancreatic resection if ductular blockage

G46 Gastroenterology

Toronto Notes 2018

c

Pancreas

eb

o

ok s

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■■ decreases pancreatic secretion of pancreatic stone protein (lithostathine) which normally solubilizes calcium salts ◆◆ precipitation of calcium within pancreatic duct results in duct and gland destruction ■■ toxi effect on acinar and duct cells – directly or via increasing free radicals ■■ acinar cell injury leads to cytokine release, which stimulates pancreatic stellate cells to form collagen (leading to fibrosis) ■■ varying degrees of ductular dilatation, strictures, protein plugs, calcification ■■ no satisfactory theory to explain why only a minority of alcoholics develop pancreatitis ■■ unusual causes • cystic fibrosis ■■ severe protein-calorie malnutrition ■■ hereditary ■■ idiopathic

ok

ok sf re

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c

Signs and Symptoms • early stages ■■ recurrent attacks of severe abdominal pain (upper abdomen and back) ■■ chronic painless pancreatitis: 10% • late stages: occurs in 15% of patients ■■ malabsorption syndrome when >90% of function is lost, steatorrhea ■■ diabetes, calcification, jaundice, weight loss, pseudocyst, ascites, GI bleed

s

s

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co

m

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Investigations • laboratory ■■ increase in serum glucose ■■ increase in serum ALP, less commonly bilirubin (jaundice) ■■ serum amylase and lipase usually normal ■■ stool elastase is low in steatorrhea • AXR: pancreatic calcifications • U/S or CT: calcification, dilated pancreatic ducts, pseudocyst • MRCP or ERCP: abnormalities of pancreatic ducts-narrowing and dilatation • EUS: abnormalities of pancreatic parenchyma and pancreatic ducts, most sensitive test • 72 h fecal fat test: measures exocrine function • secretin test: gold standard, measures exocrine function but difficult to perform, unpleasant for patient, expensive • fecal pancreatic enzyme measurement (elastase-1, chymotrypsin): available only in selected centres

fre

fre

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m

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Treatment • most common problem is pain, difficult to control general management ■■ total abstinence from alcohol ■■ enzyme replacement may help pain by resting pancreas via negative feedback ■■ analgesics ■■ celiac ganglion blocks ■■ time: pain decreases with time as pancreas “burns out” • endoscopy: sphincterotomy, stent if duct dilated, remove stones from pancreatic duct • surgery: drain pancreatic duct (pancreaticojejunostomy) if duct dilated (more effective than endoscopy); resect pancreas if duct contracted • steatorrhea ■■ pancreatic enzyme replacement ■■ restrict fat, increase carbohydrate and protein (may also decrease pain) ■■ neither endoscopy nor surgery can improve pancreatic function

o

o

Autoimmune Pancreatitis

b

b

• most commonly presents as a mimicker of pancreatic cancer (pancreatic mass detected because of jaundice ± abdominal pain)

re

Treatment • responds to prednisone

c

o

Investigations • histology: lymphocyte and plasma cell infiltration of pancreas • imaging: focal or diffuse enlargement of pancreas on CT or MRI, sausage shaped, low density rim around pancreas • serology: increased serum IgG4 • other organ involvement: sialadenitis, retroperitoneal fibrosis, biliary duct narrowing, nephritis

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Clinical Nutrition

fr

Clinical Nutrition

o

o

Determination of Nutritional Status

eb

m

m

eb

b

• corrected weight loss (expressed as body mass index [kg/m2]) is most important parameter in assessing need for nutritional support • Subjective Global Assessment: simple bedside tool to assess nutritional status, to help identify those who will benefit from nutritional support

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Investigations • plasma proteins: albumin, pre-albumin (shorter half life than albumin), transferrin • decrease may indicate decreased nutritional status or disease state • thyroid-binding globulin, retinol-binding protein (may be too sensitive) • anthropometry (e.g triceps skinfold thickness), grip strength less often used Table 22. Areas of Absorption of Nutrients

+++

+++

Proteins, Lipids Na+, H2O

Bile Acids

+++

+

ok s

CHO

Vit B12

bo

Duodenum

Fe

Jejunum

+

+

++

+

+

Ileum

+

+

++

+++

+++

Enteral Nutrition

ok

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b

Feeds • polymeric feeds contain whole protein, carbohydrate, fat as a liquid, with or without fibre • elemental feeds contain protein as amino acids, carbohydrate as simple sugars, fat content low (therefore high osmolarity) • specific diets: low carbohydrate/high fat solution for ventilated patients (carbohydrate has a high respiratory quotient so minimizes carbon dioxide production), high energy, low electrolyte solutions for dialysis patients

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c

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Relative Contraindications • non-functioning gut (e.g intestinal obstruction, enteroenteral or enterocutaneous fistulae) • uncontrolled diarrhea • GI bleeding

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Complications • aspiration • diarrhea • refeeding syndrome (rare): carbohydrate can stimulate excessive insulin release, leading to cellular uptake and low serum levels of phosphate, magnesium, potassium • overfeeding syndrome (rare): hypertonic dehydration, hyperglycemia, hypercapnea, azotemia (from excess protein)

bo

Most Common Indications for Artificial Nutrition Support • Preexisting nutritional deprivation • Anticipated or actual inadequate energy intake by mouth • Significant multiorgan system disease

Whenever possible, enteral nutrition is ALWAYS preferable over parenteral nutrition

e.

Indications • oral feeding inadequate or contraindicated

s

fre

fre

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o

o

Definition • enteral nutrition (tube feeding) is a way of providing food through a tube placed in the stomach or the small intestine • choice of tubes: nasogastric (NG), nasojejunal (NJ), percutaneous endoscopic gastrostomy (“G-tube” or “PEG tube”), percutaneous endoscopic jejunostomy (J-tube) • tubes can also be placed endoscopically, radiologically or surgically

G48 Gastroenterology

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Clinical Nutrition

fre

Parenteral Nutrition

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Relative Contraindications • functional GI tract for enteral nutrition • active infection; at least until appropriate antibiotic coverage • inadequate venous access; triple-lumen central venous lines usually prevent this problem • unreliable patient or clinical setting

b

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Complications of PN • sepsis: most serious of the common complications • mechanical pneumothorax from insertion of central line, catheter migration and thrombosis, air embolus metabolic: CHF, hyperglycemia, gallstones, cholestasis

om

m

Enteral Nutrition vs. Parenteral Nutrition • fewer serious complications (especially sepsis) • nutritional requirements for enterally administered nutrition better understood • can supply gut-specific fuels such as glutamine and short chain fatty acids • nutrients in the intestinal lumen prevent atrophy of the gut and pancreas • prevents gallstones by stimulating gallbladder motility • much less expensive

m

Enteral vs. Parenteral Nutrition for Acute Pancreatitis Cochrane DB of Syst Rev 2010;1:CD002837 Purpose: Compare EN vs TPN on mortality, morbidity, and hospital stay in patients with pancreatitis. Study Selection: RCTs of TPN vs. EN in pancreatitis Results: Eigh trials (n=348) were included. Enteral nutrition decreases RR of death (0.50), multiple organ failure (0.55), infection (0.39), and other local complications (0.70). It also decreased hospital stay by 2.37 d. Conclusion: EN reduces mortality, organ failure, infections, and length of hospital stay in patients with pancreatitis.

c

co m

co m

Indications • short-term (15% of pre-morbid weight, serum albumin 70% of small bowel (e.g. small bowel infarction) ■■ severe motility diseases (e.g. scleroderma affecting bowel)

Hypomagnesemia may be an initial sign of short bowel syndrome in patients who have undergone surgical bowel resection

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Definition • parenteral nutrition (PN) is the practice of feeding a person intravenously, bypassing the usual process of eating and digestion

G49 Gastroenterology

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Common Medications

fr

Common Medications Mechanism of Action

Indications

Contraindications

Side Effects

Proton Pump Inhibitors (H+/K+-ATPase inhibitors)

omeprazole

Losec®/ Prilosec®

20 mg PO OD

Inhibits gastric enzymes H+/K+-ATPase (proton pump)

Duodenal ulcer, gastric ulcer, NSAID-associated gastr c and duodenal ulcers, reflux esophagitis, symptomatic GERD, dyspepsia, Zollinger-Ellison syndrome, eradication of H. pylori (combined with antibiotics)

Hypersensitivity to drug

Dizziness, headache, flatulence abdominal pain, nausea, rash increased risk of osteoporotic fracture (secondary to impaired calcium absorption)

lansoprazole or dexlansoprazole

Prevacid® Dexilant®

Oral therapy: lansoprazole 15 30 mg OD (before breakfast), dexlansoprazole 30-60mg OD (does not need to be taken before breakfast)

Same as above

Same as above

Same as above

S me as above

pantoprazole

Pantoloc® Protonix®

40 mg PO ODfor UGIB: 80 mg IV bolus then 8 mg/h infusion

Same as above

fr

Same as above and UGIB

Same as above

rabeprazole

Pariet®/ Aciphex®

40 mg PO OD

Same as above

Same as above

Same as above

Same as above

esomeprazole

Nexium®

20-40 mg PO OD

Same as above

Same as above

Same as above

Same as above

ranitidine

Zantac®

300 mg PO OD or 150 mg bid IV therapy: 50 mg q8h (but tachyphylaxis aproblem)

Inhibits gastric histamine H2-receptors

Duodenal ulcer, gastric ulcer, NSAID associated gastric and duodenal ulcers, ulcer prophylaxis, reflux esophagitis, symptomatic GERD; not useful for acute GI bleeds

Hypersensitivity to drug

Confusion, dizziness, headache, arrhythmias, constipation, nausea, agranulocytosis, pancytopenia, depression

famotidine

Pepcid®

Oral therapy: duodenal/gastric ulcers: 40 mg qhs GERD: 20 mg bid IV therapy: 20 mg bid

Same as above

Same as above

Same as above

Same as above

Stool Softener

docusate sodium

Colace®

100-400 mg PO OD, divided in 1-4 doses

Promotes incorporation of water into stool

Relief of constipation

Presence of abdominal pain, fever, N/V

Throat irritation, abdominal cramps, rashes

Osmotic Laxatives

lactulose

Lactulose/ Constulose®

Constipation: 15 30 mL PO OD to bid Encephalopathy: 15 30 mL bid to qid

Poorly absorbed in GI tract and is broken down by colonic bacteria into lactic acid in the colon, increases osmotic colonic contents, increases stool volume

Chronic constipation, prevention, and treatment of portal-systemic encephalopathy

Patients who require a low galactose diet

Flatulence, intestinal cramps, nausea, diarrhea if excessive dosage

PEG3350

Lax-a-day®/ Golytely®

Constipation: 17 g powder dissolved in 4 8 oz liquid PO OD

Osmotic agent causes water retention in stool and promotes frequency of stool

Relief of constipation Colonoscopy prep

Hypersensitivity to drug

Abdominal distension, pain, anal pain, thirst, nausea, rigor, tonic clonic seizures (rare)

magnesium hydroxide

Milk of Magnesia/ Pedia-Lax®

Constipation (adult): 400 mg/5 mL: 30-60 mL PO qhs

Osmotic retention of fluid which distends the colon and increases peristaltic activity

Relief of constipation

Patients with myasthenia gravis or other neuromuscular disease Renal impairment

Abdominal pain, vomiting, diarrhea

Senokot®

Tablets: 1-4 PO qhs Syrup: 10-15 mL PO qhs

Induce peristalsis in lower colon

Constipation

Patients with acute abdomen

Abdominal cramps, discolouration of breast milk, urine, feces, melanosis coli and atonic colon from prolonged use (controversial)

bisacodyl

Bisacodyl®

5-30 mg PO OD (start at 10 mg for bowel preparation)

Enteric nerve stimulation and local contact-induced secretory effects Colonic movements

Constipation Preparation of bowel for procedure

GI obstruction Gastroenteritis

Abdominal colic, abdominal discomfort, proctitis (with suppository use), diarrhea

Bulk Laxatives

psyllium

Metamucil®

2-6 tabs (1 tab = 0.52 g) PO od-tid prn

Increases stool bulk → water retention in stool

Constipation

Hypersensitivity to drug GI obstruction

GI obstruction, diarrhea, constipation, abdominal cramps

Antidiarrheal Agents

loperamide

Imodium®

Acute diarrhea 4 mg PO initially, followed by 2 mg after each unformed stool

Acts as antidiarrheal viacholinergic, noncholingeric, opiate, and nonopiate receptormedicated mechanisms; decreases activity of myenteric plexus

Adjunctive therapy for acute non-specific diarrhea, chronic diarrhea associated with IBD and for reducing the volume of discharge for ileostomies, colostomies, and other intestinal resections

Children 5 mg/kg

Reported cases of reactivated TB, PCP, lymphoma, other infections Other TNFα share similar serious side-effects

adalimumab

Humira®

CD induction: four 40 mg SC on day 1, then 80 mg 2 wks later (day 15) CD maintenance: 40 mg every other wk beginning day 29

Monoclonal antibody to TNFα

Medically refractory CD or poor response to infliximab

Hypersensitivity to adalimumab Severe infection Moderate-to-severe heart failure

Headaches, skin rashes, upper respiratory tract infection

Simponi®

RA: 2 mg/kg at wks 0, 4 and then every 8 wks thereafter (use with methotrexate) UC induction: 200 mg SC at wk 0, then 100 mg at wk 2 UC maintenance: 50 mg every 4 wk

Monoclonal antibody to TNFα

Active ankylosing spondylitis Psoriatic arthritis Moderate-to-severe active RA (combined with methotrexate) UC: medically refractory UC

Hypersensitivity to golimumab or latex Severe infection Moderate-to-severe hea t failure

Entyvio®

CD/UC: 300 mg at 0, 2, 6 wks and then every 8 wks thereafter

Monoclonal antibody to α4β7 integrin

Medically refractory CD/UC, including other TNFα inhibitors and corticosteroids

Hypersens ivity to vedolizumab



m

e

ks

ks

vedolizumab

s

golimumab

m

o

Biologics

om

fre

e.

IBD: active inflammation and to maintain remission

Complications of steroid therapy

m

Pu inethol®

m

ok

sf

re

e

Abdominal pain, constipation, arthralgia, headache

om

c

m

sf re

m

Anti-inflammatory

6-mercaptopurine (6-MP)

o

Immunosuppressive Agents

20-40 mg PO OD for acute exacerbation

m

prednisone

ee

IBD Agents

m

r

e.

co m

o m

m

dimenhydrinate

fr

Dosing

k

Trade Name

o

Anti-Emetics

Generic Drug Name

fr

Class

re

Table 23. Common Drugs Prescribed in Gastroenterology (continued)

Infections, liver injury, and progressive multifocal leukoencephalopathy

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Landmark Gastroenterology Trials

fr

MELD score as a predictor of death in chronic liver disease

Gastroenterology 2003;124:91-6

MELD score can be applied for allocation of donor livers as it accurately predicts 3 mo mortality in patients with chronic liver failure

Infliximab, azathioprine, or combination for Crohn’s disease

NEJM 2010;362:1383-95

In moderate-severe Crohn’s disease, infliximab + azathioprine was more likely to result in corticosteroid-free remission than infliximab monotherapy. Infliximab monotherapy was more effective than azathioprine monotherapy. Similar results have been reported for ulcerative colitis (Gastroenterology 2014; 146:392-400)

Enteral versus parenteral nutrition for acute pancreatitis

Cochrane DB Syst Rev 2010;1:CD002837

For acute pancreatitis, no trial was convincing alone, but in aggregate, enteral feeds via nasogastric tube is preferable to either no feeding or parenteral nutrition

NEJM 2010;362:1071-81

The most convincing of several articles establishing this non-absorbable antibiotic as the treatment of choice for hepatic encephalopathy for maintaining remission from hepatic encephalopathy and reducing hospitalization associated with the disease

Adenoma detection rate and risk of colorectal cancer and death

NEJM 2014;370:12981306

A high miss rate for colorectal cancers has been suggested, chiefly in the right colon. This study demonstrates a method of assessing the competence of endoscopists in detecting cancers using adenoma detection rate (the proportion of colonoscopic exams in which a physician detects one or more adenomas) as a surrogate marker. Adenoma detection rate was associated with lower risk of interval colorectal cancer and has launched quality assurance programs for screening colonoscopies

Prednisolone or pentoxifylline for alcoholic hepatitis

NEJM 2015;372:1619-28

bo

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For alcoholic hepatitis, prednisolone improved survival when the Maddrey’s discriminant function > 32, but the benefit did not reach statistical significance and pentoxifylline was of no advantage at all. Other studies had shown some benefit with pentoxifylline, but this study was the most definitive

.c

m

m

eb

eb

bo

o

fr

Rifaximin treatment in hepatic encephalopathy

o

Results

co

Reference

eb

Trial

o

fr

Landmark Gastroenterology Trials

G52 Gastroenterology

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References

fr

References

b

bo

o

Atlas Kandel G. Division of Gastroenterology, St. Michael’s Hospital, Toronto. Olscamp G Division of Gastroenterology, St. Michael’s Hospital, Toronto. Saibil F. Division of Gastroenterology, Sunnybrook and Women’s College Health Sciences Centre, Toronto. Haber G. Division of Gastroenterology, Lennox Hall Hospital, New York.

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Esophageal and Gastric Disease Devault KR, Castell DO. Guidelines for the diagnoses and treatment of gastroesophageal reflux disease. Arch Intern Med 1995;115:2165-2173. DiPalma JA. Management of severe gastroesophageal reflux disease. J Clin Gastroenterol 2001;32:19-26. Sharma P, Sarin SK. Improved survival with the patients with variceal bleed. Int J Hepatol 2011: Epub 2011Jul 7. Verbeek RE, van Oijen MG, ten Kate FJ, et al. Surveillance and follow-up strategies in patients with high-grade dysplasia in Barrett’s esophagus: a Dutch population-based study. Am J Gastroenterol 2012;107:534-542. Wang KK, Sampliner RE. Updated guidelines 2008 for the diagnosis, surveillance and therapy of Barrett’s esophagus. Am J Gastroenterol 2008;103:788-797. Wilcox CM, Karowe MW. Esophageal infections: etiology, diagnosis, and management. Gastroenterol 1994;2:188-206.

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e.

Stomach and Duodenum American Gastroenterological Association position statement: evaluation of dyspepsia. Gastroenterol 1998;114:579-581. Howden CW, Hunt RH. Guidelines for the management of helicobacter pylori infection. Am J Gastroenterol 1998;93:2330-2338. Hunt RH, Fallone CA, Thom on ABR. Canadian helicobacter pylori consensus conference update: infection in adults. J Gastroenterol 1999;13:213-216. Laine L, Peterson WL Bleeding peptic ulcer. NEJM 1994;331:717-727. Lanza FL. A guideline for the treatment and prevention of NSAID-induced ulcer. Am J Gastroenterol 1998;93:2037-2046. McColl KE. Clinical practice helicobacter pylori infection. NEJM 2010;362:1597-601. Peek RM, Blaser MJ. Pathophysiology of helicobacter pylori-induced gastritis and peptic ulcer disease. Am J Med 1997;102:200-207. Salcedo JA, A Kawas F. Treatment of helicobacter pylori infection. Arch Intern Med 1998;158:842-851. Schmid CH, Whitling G, Cory D, et al. Omeprazole plus antibiotics in the eradication of Helicobacter pylori infection: a meta-regression analysis of randomized, contro led trials. Am J Ther 1999;6:25-36. Soll AH. Practice parameters: committee of the American College of Gastroenterology: medical treatment of peptic ulcer disease. JAMA 1996;275:622-629 Thijs JC, van Zwet AA, Thijs WJ, et al. Diagnostic tests for helicobacter pylo i: a prospective evaluation of their accuracy, without selecting a single test as the gold standard. Am J Gastroenterol 1996;91:2125-2129.

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Small and Large Bowel Aranda-Michel J, Giannella R. Acute diarrhea: a practical review. Am J Med 1999;670-676. Colorectal cancer screening: recommendation statement from the Canadian task force on preventative health care. CMAJ 2001;165:206-208. Donowitz M, Kokke FT, Saidi R. Evaluation of patients with chronic diarrhea. NEJM 1995;332:725-729. Drossma DA. The functional gastrointestinal disorders and the Rome III process. Gastroenterol 2006;130:1377-1390. Forrest JA, Finlayson ND, Shearman DJ. Endoscopy in gastrointestinal bleeding. Lancet 1974;2:394-397. Ghosh S, Shand A. Ulcerative colitis. BMJ 2000;320:1119-1123. Hanauer SB. Drug therapy: inflammatory bowel disease. NEJM 1996;334:841-848. Hatchette TF, Farina D. Infectious diarrhea: when to test and when to treat. CMAJ 2011;183:339-344. Horwitz BJ, Fisher RS. Current concepts: the irritable bowel syndrome. NEJM 2001;344:1846-1850. Jennings JSR, Howdle PD. Celiac disease. Curr Opin Gastroen 2001;17:118-126. Laine L, Sahota A, Shah A Does capsule endoscopy improve outcomes in obscure gastrointestinal bleed ng? Randomized trial vs. dedicated small bowel radiography. Gastroenterol 2010;138:1673-1680. Pimentel M, Lembo A, Chey WD, et al. Rifaximin therapy for patients with irritable bowel syndrome without constipation. NEJM 2011;364:22-32. Rubio-Tapia A, Hill ID, Kelly CP, et al. ACG clinical guidelines: Diagnosis and management of celiac disease. Am J Gastroenterol 2013; 108: 656-676.

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Liver and Biliary Tract Angulo P Primary biliary cirrhosis and primary sclerosing cholangitis. Clin Liv Dis 1999;3:529-570. Andr oli T Carpenter C, Griggs R, et al. (editors). Cecil essentials of medicine, 5th ed. P iladephia: WB Saunders Company, 2001. Custis K. Common biliary tract disorders. Clin Fam Pract 2000;2:141-154. Diehl AM. Alcoholic liver disease. Clin Liv Dis 1998;2:103-118. Feldman M, Friedman LS, Sleisenger MH (editors). Gastrointestinal and liver disease: pathophysiology, diagnosis, management, 7th ed., vol. 2. Philadelphia: WB Saunders Company, 2004. Haubrich WS, Schaffner F, Berk JE (editors). Bockus gastroenterology, 5th ed., vol 4. Chapter 74: Pregnancy-related hepatic and gastrointestinal disorders. Philadelphia: WB Saunders Company, 1995. 1448-1458. Haubrich WS, Schaffner F, Berk JE (editors). Bockus gastroenterology, 5th ed., vol 4. Chapter 184: Pregnancy and the gastrointestinal tract. Philadelphia: WB Saunders Company, 1995. 3446-3452. Kohli A, Shaffer A, Sherman A, and Kottilil S. Treatment of hepatitis C: a systematic review. JAMA 2014; 312: 631-640. Malik AH. Acute and chronic viral hepatitis. Clin Fam Pract 2000;2:35-57. Reynolds T. Ascites. Clin Liv Dis 2000;4:151-168. Sandowski SA. Cirrhosis. Clin Fam Pract 2000;2:59 77. Sherman M. Chronic viral hepatitis and chronic liver disease. Can J Diag 2001;18:81-90. Sternlieb I. Wilson’s disease. Clin Liv Dis 2000;4:229-239. Williams JW, Simel DL. Does this patient have ascites? JAMA 1992;267:2645-2648. Yapp TR. Hemochromatosis. Clin Liv Dis 2000;4:211-228. Yu AS, Hu KQ. Management of as ites. Clin Liv Dis 2001;5:541-568.

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Rational Clinical Examination Grover SA, Barkun AN, Sackett DL. Does this patient have splenomegaly? JAMA 1993;270:2218-2221. Kitchens JM. Does this patient have an alcohol problem? JAMA 1994;272:1782-1787. Naylor CD. Physical exam of the liver. JAMA 1994;271:1859-1865. Williams JW, Simel DL. Does this patient have ascites? How to divine fluid in the abdomen. JAMA 1992;267:2645-2648.

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Pancreas Beckingham IJ, Bornman PC. ABC of diseases of liver, pancreas, and biliary system. Acute pancreatitis. BMJ 2001;322:595-598. Beckingham IJ, Bornman PC. ABC of diseases of liver, pancreas, and biliary system. Chronic pancreatitis. BMJ 2001;322:660-663. Steer ML. Chronic pancreatitis. NEJM 1995;332:1482-1490. Sternby B, O’Brien JF, Zinsmeister AR, et al. What is the best biochemical test to diagnose acute pancreatitis? A prospective clinical study. Mayo Clin Proc 1996;71 1138-1144. Whytcomb DC. Acute pancreatitis. NEJM 2006;354:2142-2150.

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General Surgery and Thoracic Surgery

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Amanpreet Brar, Zacharie Cloutier, Jeff Metz, and Alexander Tigert, chapter editors Sangwoo Leem and Mark Shafarenko, associate editors Jin Kyu Kim and Shubham Shan, EBM editors Abdollah Behzadi and Alice Wei, staff editors

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Surgical Complications. . . . . . . . . . . . . . . . . . . 7 Post-Operative Fever Wound/Incisional Complications Urinary and Renal Complications Post-Operative Dyspnea Respiratory Complications Cardiac Complications Intra-Abdominal Abscess Paralytic Ileus Delirium

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Thoracic Surgery. . . . . . . . . . . . . . . . . . . . . . . . . 13 Hiatus Hernia Esophageal Perforation Esophageal Carcinoma Thymoma Pleura, Lung, and Mediastinum Tube Thoracostomy Lung Transplantation Chronic Obstructive Pulmonary Disease

Stomach and Duodenum . . . . . . . . . . . . . . . . . . 18 Peptic Ulcer Disease Gastric Carcinoma Gastrointestinal Stromal Tumour Bariatric Surgery Complications of Gastric Surgery

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SMALL INTESTINE

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Small Bowel Obstruction . . . . . . . . . . . . . . . . . . 21 Mechanical Small Bowel Obstruction Paralytic Ileus Intestinal Ischemia Tumours of Small Intestine Short Gut Syndrome

Abdominal Hernia . . . . . . . . . . . . . . . . . . . . . . . . . 25 Groin Hernias

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Other Conditions of the Large Intestine . . . . . . . 36 Angiodysplasia Volvulus Toxic Megacolon Fistula Stomas Anorectum. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38 Hemorrhoids Anal Fissures Anorectal Abscess Fistula-In-Ano Pilonidal Disease Rectal Prolapse Anal Neoplasms

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Pre-Operative Preparations . . . . . . . . . . . . . . . . 7

Colorectal Neoplasms. . . . . . . . . . Colorectal Polyps Familial Colon Cancer Syndromes Colorectal Carcinoma

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Differential Diagnoses of Common Presentations. . . . . . . . . . . . . . . . . . . . . . . . . . . 4 Acute Abdominal Pain Abdominal Mass Gastrointestinal Bleeding Jaundice

Liver . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 42 Liver Cysts Liver Abscesses Neoplasms Liver Transplantation Biliary Tract . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 46 Cholelithiasis Biliary Colic Acute Cholecystitis Acalculous Cholecystitis Choledocholithiasis Acute Cholangitis Gallstone Ileus Carcinoma of the Gallbladder Cholangiocarcinoma

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Basic Anatomy Review. . . . . . . . . . . . . . . . . . . . . . 2

Diverticular Disease. . . . . . . . . . . . . . . . . . . . . . . . 31 Diverticulosis Diverticulitis

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Acronyms. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2

Pancreas. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 51 Acute Pancreatitis Chronic Pancreatitis Pancreatic Cancer Spleen. . . . . . . . . . . . . Splenic Trauma Splenectomy Splenic Infarct

. . . . . . . . . . . . . . . . . . . 54

Inflammatory Bowel Disease. . . . . . . . . . . . . . . . 28 Crohn’s Disease Ulcerative Colitis

Surgical Endocrinology. . . . . . . . . . . . . . . . . . . . . 60 Thyroid and Parathyroid Adrenal Gland Pancreas

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Appendix . . . . . . . . . . . Appendicitis

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. . . . . . . . . . . . . . . . . . 27

Breast. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 55 Benign Breast Lesions Breast Cancer

Pediatric Surgery. . . . . . . . . . . . . . . . . . . . . . . . 62

LARGE INTESTINE Large Bowel Obstruction . . . . . . . . . . . . . . . . . 29 Mechanical Large Bowel Obstruction Functional LBO: Colonic Pseudo-Obstruction (Ogilvie’s Syndrome)

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Skin Lesions. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 65 Common Medications. . .

. . . . . . . . . . . . . . . . 65

References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 65

General Surgery and Thoracic Surgery GS1

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Toronto Notes 2018

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GS2 General Surgery and Thoracic Surgery

Toronto Notes 2018

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Acronyms

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Acronyms

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Access to RUQ or LUQ contents i.e. gallbladder, spleen

Upper Midline Access to stomach, duodenum, gallbladder, liver, transverse colon Paramedian

Paramedian Lateral Paramedian

McBurney’s Lower midline

Pfannenstiel

Lower Midline Access to pelvic organs, sigmoid colon, and rectum

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Arcuate line

Incision made at outer 1/3 medial 2/3 border of rectus Modification of paramedian but with lower risk of dehiscence or ventral hernia Not commonly used

Pfannenstiel

Suprapubic incision for access to pelvic cavity

McBurney’s

Access to appendix

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Upper midline

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Lateral paramedial

Can make similar incision in each quadrant for access to each quadrant’s contents Not c mmonly used Post operative ventral hernias common

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Kocher’s (subcostal)

© Cassandra Cetlin 2014, after Agnes Chan 2012

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Kosher’s (subcostal)

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Basic Anatomy Review

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Figure 1. Abdominal incisions

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Lateral Abdominal Wall Layers and their Continuous Spermatic and Scrotal Structures (superficial to deep) 1. skin (epidermis, dermis, subcutaneous fat) 2. superficial fascia ■■ Camper’s fascia (fatty) → Dartos muscle/fascia ■■ Scarpa’s fascia (membranous) → Colles’ superficial perineal fascia 3. muscle (see Figure 2 and Figure 3) ■■ external oblique → inguinal ligament → external spermatic fascia and fascia lata ■■ internal oblique → cremasteric muscle/fascia ■■ transversus abdominis → posterior inguinal wall 4. transversalis fascia → internal spermatic fascia 5. preperitoneal fat 6. peritoneum → tunica vaginalis

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Midline Abdominal Wall Layers (superficial to deep) 1. skin 2. superficial fascia 3. rectus abdominis muscle: in rectus sheath, divided by linea alba (see Figure 3) ■■ above arcuate line (midway between symphysis pubis and umbilicus) ◆◆ anterior rectus sheath = external oblique aponeurosis and anterior leaf of internal oblique aponeurosis ◆◆ posterior rectus sheath = posterior leaf of internal oblique aponeurosis and transversus abdominis aponeurosis ■■ below arcuate line ◆◆ aponeuroses of external oblique, internal oblique, transversus abdominis all pass in front of rectus abdominis 4. arteries: superior epigastric (branch of internal thoracic), inferior epigastric (branch of external iliac); both arteries anastomose and lie behind the rectus muscle (superficial to posterior rectus sheath above arcuate line) 5. transversalis fascia 6. peritoneum

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proton pump inhibitor PPI PTC percutaneous transhepatic cholangiography PUD peptic ulcer disease SBO small bowel obstruction SCC squamous cell carcinoma SIADH syndrome of inappropriate anti-diuretic hormone SMA superior mesenteric artery SMV superior mesenteric vein SNLB sentinel lymph node biopsy TED thromboembolic deterrent TEE transesophageal echocardiogram TTE tran thoracic echocardiogram UGIB upper gastrointestinal bleed VATS video-assisted thorascopic surgery VIP vasoactive intestinal peptide

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IPAH idiopathic pulmonary arterial hypertension IPF idiopathic pulmonary fibrosis LAR low anterior resection LBO large bowel obstruction LCIS lobular carcinoma in situ LES lower esophageal sphincter LGIB lower gastrointestinal bleed LVRS lung volume reduction surgery MALT mucosa-associated lymphoid tissue MBP mechanical bowel preparation MEN multiple endocrine neoplasia MIBG metaiodobenzylguanidine MIS minimally invasive surgery MRCP magnetic resonance cholangiopancreatography NGT nasogastric tube OGD oesophagogastroduodenoscopy POD post-operative day

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DRE digital rectal exam EBL estimated blood loss ERCP endoscopic retrograde cholangiopancreatography EUA examinati n under anesthesia EUS endoscopic ultrasound FAP familial adenomatous polyposis FAST focused abdominal sonography for trauma FNA fine needle aspiration FOBT fecal occult blood test GERD gastroesophageal reflux disease GI gastrointestinal GIST gastrointestinal stromal tumour GU genitourinary HDGC hereditary diffuse gastric carcinoma HIDA hepatobiliary imino-diacetic acid HNPCC hereditary nonpolyposis co orectal cancer I&D incision and drainage

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5-FU 5-fluorouracil AAA abdominal aortic aneurysm ABG arterial blood gas ABI ankle brachial index ALND axillary lymph node dissection APR abdominoperineal resection ARDS acute respiratory distress syndrome ATN acute tubular necrosis BRBPR bright red blood per rectum BCS breast conserving surgery CBD common bile duct CF cystic fibrosis CHF congestive heart failure CRC colorectal cancer CVA costovertebral angle CVP central venous pressure DCIS ductal carcinoma in situ DIC disseminated intravascular coagulation DPL diagnostic peritoneal lavage

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GS3 General Surgery and Thoracic Surgery

Toronto Notes 2018

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Basic Anatomy Review

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© Leanne Chan 2011

Transversus abdominis muscle Internal oblique muscle External oblique aponeurosis Peritoneum Preperitoneal fat Inferior epigastric artery Inferior epigastric vein Transversalis fascia Deep inguinal ring Membranous layer of superficial fascia (Scarpa’s fascia)

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External ob ique muscle Internal oblique muscle Aponeurosis of internal oblique muscle Aponeurosis of external oblique muscle (cut edge) Cremaster muscle Spermatic cord

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Fatty layer of superficial fascia (Camper s fascia) Superficial inguinal ring Tun ca vaginalis Testis Internal spermatic fascia Cremaster muscle External spermatic fascia Colle’s superficial perineal fascia Dartos muscle Skin of scrotum

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Figure 2. Continuity of the abdominal wall with layers of the scrotum and spermatic cord Skin Superficial fascia (Camper’s + Scarpa’s fascia) External oblique Internal oblique Transversus abdominis Transversalis fascia Preperitoneal fat Peritoneum

Rectus abdominis

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Above arcuate line

Inferior epigastric artery

Transversalis fascia Preperitoneal fat Peritoneum

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Skin Superficial fascia External oblique Internal oblique Transversus abdominis

© Bryce Hough

Below arcuate line

Figure 3. Midline cross-section of abdominal wall

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Figure 4. Arterial blood supply to the GI tract

Superior mesenteric artery (10) i) Right colic artery (12) ii) Middle colic artery (11) iii) Ileocolic artery (13) iv) Ileal and jejunal branches (14) Inferior mesenteric artery (15) i) Left colic artery (16) ii) Sigmoid arteries (17) ii) Superior rectal artery (18)

© Frances Yeung 2005

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Celiac trunk (1) i) Common hepatic artery (2) • Hepatic proper (3) – Left hepatic artery (4) – Right hepatic artery (5) • Right gastric artery (7) • Gastroduodenal artery (8) ii) Left gastric artery (6) iii) Splenic artery (9)

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Toronto Notes 2018

Differential Diagnoses of Common Presentations

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GS4 General Surgery and Thoracic Surgery

Venous Flow

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Portal vein (1)

Organ Liver

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Superior mesenteric vein (7) i) Ileal and jejunal veins (13) ii) Ileocolic vein (14) iii) Right colic vein (12) iv) Middle colic vein (11) v) Pancreaticoduodenal vein (8) vi) Right gastroepiploic vein (9)

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Left gastric (coronary) vein (2)

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Right gastric vein (3)

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Splenic vein (5) i) Inferior mesenteric vein (10) (superior rectal vein until crossing common iliac vessels) • Left colic veins (15) • Sigmoid veins (16) • Superior rectal veins (17) ii) Pancreatic veins iii) Left gastroepiploic vein iv) Short gastric veins (6)

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© Carly Vanderlee 2011

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Cystic vein (4)

Arterial Blood Supply Left and right hepatic (branches of hepatic proper) Splenic Spleen Cystic (branch of right hepatic Gallbladder artery) 1. Lesser curvature: right and Stomach left gastric 2. Greater curvature: right (branch of gastroduodenal) and left (branch of splenic) gastroepiploic 3. Fundus: short gastrics (branch of splenic) 1 Gastroduodenal Duodenum 2. Pancreaticoduodenals (superior branch of gastroduodenal, inferior branch of superior mesenteric) 1. Pancreatic branches of splenic Pancreas 2. Pancreaticoduodenals Small intestine Superior mesenteric branches: jejunal, ileal, ileocolic Large intestine 1. Superior mesenteric branches: right colic, middle colic 2. Inferior mesenteric branches: left colic, sigmoid, superi r rectal

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Paraumbilical vein – (within round ligament, not shown

Figure 5. Venous drainage of the GI tract

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Differential Diagnoses of Common Presentations

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Types of Peritonitis • Primary peritonitis: spontaneous without clear etiology • Secondary peritonitis: due to a perforated viscus • Tertiary peritonitis: recurrent secondary peritonitis more often with resistant organisms

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Gastrointestinal Appendicitis Crohn’s disease Tuberculosis of the ileocecal junction Cecal tumour Intussusception Mesenteric lymphadenitis (Yersinia) Cecal diverticulitis Cecal volvulus Hernia: femoral, inguinal obstruction, Amyand’s (and resulting cecal distention) Gynecological See ‘suprapubic’ Genitourinary See suprapubic’ Extraperitoneal Abdominal wall hematoma/abscess Psoas abscess

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Localization of Pain Most digestive tract pain is perceived in the midline because of bilaterally symmetric innervation; kidney, ureter, ovary, or somatically innervated structures are more likely to cause lateralized pain

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Referred Pain • Biliary colic to right shoulder or scapula • Renal colic: to groin • Appendicitis: periumbilical to right lower quadrant (RLQ) • Pancreatitis: to back • Ruptured aortic aneurysm: to back or flank • Perforated ulcer: to RLQ (right paracolic gutter) • Hip pain: to groin

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Hepatobiliary Biliary colic Cholecystitis Cholangitis CBD obstruction (stone, tumour) Hepatitis (includes perihepatitis/Fitz-Hugh-Curtis syndrome) Portal vein thrombosis Budd-Chiari syndrome Hepatic abscess/mass Right subphrenic abscess Gastrointestinal Pancreatitis Presentation of gastric, duodenal, or pancreatic pathology Hepatic flexure pathology (CRC, subcostal incisional hernia) Genitourinary Nephrolithiasis Pyelonephritis Renal: mass, ischemia, trauma Cardiopulmonary RLL pneumonia Effusion/empyema CHF (causing hepatic congestion and R pleural effusion) MI Pericarditis Pleuritis Miscellaneous Herpes zoster Trauma Costochondritis

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Table 1. Differential Diagnosis of Acute Abdominal Pain

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• acute abdomen = severe abdominal pain of acute onset and requir s urgent medical attention • in patients with acute abdominal pain, the first diagnoses that you should consider are those requiring potential urgent surgical intervention • two main patterns constituting urgent general surgery referrals are peritonitis and obstruction

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Acute Abdominal Pain

In all patients presenting with an acute abdomen, order the following: KEY TESTS FOR SPECIFIC DIAGNOSIS • ALP, ALT, AST, bilirubin • Lipase/ amylase • Urinalysis • β-hCG (in women of childbearing age) • Troponins • Lactate KEY TESTS FOR OR PREPARATION • CBC, electrolytes, creatinine, glucose • INR/PTT • CXR (if history of cardiac or pulmonary disease) • ECG if clinically indicated by history or if >69 yr and no risk factors

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GS5 General Surgery and Thoracic Surgery

Toronto Notes 2018

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Differential Diagnoses of Common Presentations

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Table 1. Differential Diagnosis of Acute Abdominal Pain (continued) Pancreatic Pancreatitis (acute vs. chronic) Pancreatic pseudocyst Pancreatic tumours Gastrointestinal Gastritis PUD Splenic flexure pathology (e.g. CRC, ischemia) Splenic Splenic infarct/abscess Splenomegaly Splenic rupture Splenic artery aneurysm Cardiopulmonary (see RUQ and Epigastric) Genitourinary (see RUQ)

Gast ointestinal Diverticulitis Diverticulosis Colon/sigmoid/rectal cancer Fecal impaction Proctitis (ulcerative colitis, infectious; i.e. gonococcus or Chlamydia) Sigmoid volvulus Hernia Gynecological See ‘suprapubic’ Genitourinary See ‘suprapubic’ Extraperitoneal Abdominal wall hematoma/abscess Psoas abscess

Most Common Presentations of Surgical Pain • Sudden onset with rigid abdomen = perforated viscus • Pain out of proportion to physical findings = ischemic bowel • Vague pain that subsequently localizes = appendicitis or other intra-abdominal process that irritates the parietal peritoneum • Waves of colicky pain = bowel obstruction

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See Gynecology, Urology, Respirology, and Cardiology and Cardiac Surgery for further details regarding respective etiologies of acute abdominal pain DIFFUSE

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Gastrointestinal Peritonitis Early appendicitis, perforated appendicitis Mesenteric ischemia Gastroenteritis/colitis Constipation Bowel obstruction Pancreatitis Inflammatory bowel disease Irritable bowel syndrome Ogilvie’s syndrome Cardiovascula /Hematological Aortic d ssection/ruptured AAA Sickle cell crisis Genitourinary/Gynecological Perforated ectopic pregnancy PID Acute urinary retention Endocrinological Carcinoid syndrome Diabetic ketoacidosis Addisonian crisis Hypercalcemia Other Lead poisoning Tertiary syphilis

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Gastrointestinal (see RLQ/LLQ) Acute appendicitis IBD Gynecological Ectopic pregnancy PID End metriosis Threatened/incomplete abortion Hydrosalpinx/salpingitis Ovarian torsion Hemorrhagic fibroid Tubo-ovarian abscess Gynecological tumours Genitourinary Cystitis (infectious, hemorrhagic) Hydroureter/urinary colic Epididymitis Testicular torsion Acute urinary retention Extraperitoneal Rectus sheath hematoma

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Cardiac Aortic dissection/ruptured AAA MI Pericarditis Gastrointestinal Gastritis GERD/esophagitis PUD Pancreatitis Mallory-Weiss tear

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SUPRAPUBIC

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EPIGASTRIC

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Abdominal Mass

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Table 2. Differential Diagnosis of Abdominal Mass Spleen: splenomegaly, tumour, abscess subcapsular splenic hemorrhage, can also present as RLQ mass if extreme splenomegaly Stomach: tumour

Right Lower Quadrant (RLQ)

Lower Midline

Left Lower Quadrant (LLQ)

Intestine: stool, tumour (CRC), mesenteric adenitis, appendicitis, appendiceal phlegmon or other abscess, typhlitis, intussusception, Crohn’s inflammation Ovary: ectopic pregnancy, cyst (physiological vs. pathological), tumour (serous, mucinous, s ruma ovarii, germ cell, Krukenberg) Fallopian tube: ectopic pregnancy, tubo-ovarian abscess, hydrosalpinx, tumour

Uterus: pregnancy, leiomyoma (fibroid), uterine cancer, pyometra, hematometra GU: bladder distention, tumour

Intestine: stool, tumour, abscess (see RLQ) Ovary: see RLQ Fallopian tube: see RLQ

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Left Upper Quadrant (LUQ)

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Upper Midline Pancreas: pancreatic adenocarcinoma, other pancreatic neoplasm, pseudocyst Abdominal aorta: AAA (pulsatile) GI: gastric tumour (adenocarcinoma, gastrointestinal stromal tumour, carcinoid tumour), MALT lymphoma

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Right Upper Quadrant (RUQ) Gallbladder: cholecystitis, cholangiocarcinoma, peri-ampullary malignancy, cholelithiasis Biliary tract: Klatskin tumour Liver: hepatomegaly, hepatitis, abscess, tumour (hepatocellular carcinoma, metastatic tumour, etc.)

Pancreatitis can look like a surgical abdomen, but is rarely an indication for immediate surgical intervention

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GS6 General Surgery and Thoracic Surgery

Toronto Notes 2018

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Differential Diagnoses of Common Presentations

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Gastrointestinal Bleeding

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Indications for Surgery failure of medical management • exsanguinating hemorrhage: hemodynamic instability despite vigorous resuscitation • recurrent hemorrhage with up to two attempts of endoscopic hemostasis • prolonged bleeding with transfusion requirement >3 units • bleeding at rate >1 unit/8 h

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Etiology

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Transfusion Strategies for Acute Upper Gastrointestinal Bleeding NEJM 2013;368:11-21 Recent study by Villanueva et al., demonstrates that a restrictive transfu ion strategy (transfusion with hemoglobin below 70 g/L) significantly improves outcomes in patients with acute UGIB, compared to a liber l transfusion strategy (transfusion with hemoglobin below 90 g/L). Refer to study for details.

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Table 3. Differential Diagnosis of GI Bleeding Anatomical Source

Overt bleeding: obvious hematemesis, hematochezia or melena per rectum (i.e. visi le to naked eye) Occult bleeding: bleeding per rectum is not obvious to naked eye (e.g. positive guaiac FOBT) Obscure bleeding: bleeding with no identifiable source after colonoscopy and endoscopy (source usually in small bowel). Can be either overt or occult

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Surgical Management of GI Bleeding • UGIB ■■ bleeding from a source proximal to the ligament of Treitz ■■ often presents with hematemesis and melena unless very brisk (then can present with hematochezia) ■■ initial management with endoscopy; if fails, then consider surgical management appropriate to etiology ■■ PUD accounts for approximately 55% of severe UGIB • LGIB ■■ bleeding from a source distal to the ligament of Trei z ■■ often presents with BRBPR unless proximal to transverse colon ◆◆ may occasionally present with melena ■■ initial management with colonoscopy to detect and potentially stop source of bleeding ■■ 75% of patients will spontaneously stop bleeding, however if bleeding continues barium enema should NOT be performed ■■ angiography or RBC scan to determine source as indicated ■■ surgery indicated if bleeding is persistent - aimed at resection of area containing source of bleeding ■■ obscure bleed may require blind total colectomy if the source is not found

IHOP Ischemia Hemorrhage Obstruction Perforation

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Indications for Urgent Operation

Hematological

Excess anticoagulation (coumadin, heparin, etc.) Excess antiplatelet (clopidogrel, ASA)

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Epistaxis

Esophagus

Esophageal varices Mallory-Weiss tear Esophagitis

Aorto-esophageal fistula (generally post endovascular aortic repair)* Esophageal cancer

Stomach

Gastritis Gastric varices Dieulafoy’s lesion

Gastric ulcer Gastric cancer*

Duodenum

Duodenal ulcer Perforated duodenal ulcer*

Duodenal cancer*

Jejunum

Tumours* Polyps Ulcers

Ileum and Ileocecal Junction

Meckel’s diverticulum (rare surgical management) Small bowel obstruction

Crohn’s disease* Tuberculosis of ileocecal junction

Large Intestine

Colorectal cancer* Mesenteric thrombosis/ischemic bowel* Ulcerative colitis* (subtotal colectomy if failure of medical management) Angiodysplasia Diverticulosis (*if bleeding is persistent)

Crohn’s disease (less frequently presents with bleeding)* Pancolitis (infectious, chemotherapy, o radiation induced) Bleeding post-gastrointestinal anastomosis

Sigmoid

Diverticulosis (*if bleeding is persistent) Sigmoid cancer* Bleeding post-polypectomy

Polyps (*if not amenable to colonoscopic polypectomy) Inflammatory bowel disease (IBD)

Rectum and Anus

Hemorrhoids Fissures Rectal cancer* Anal varices

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Biochemical Signs for Differentiating Jaundice Hepatocellular: Elevated bilirubin + elevated ALT/AST Cholestatic Elevated bilirubin + elevated ALP/GGT ± duct dilatation upon biliary U/S Hemolysis:  haptoglobin  LDH

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Jaundice

Polyps (*if not amenable to colonoscopic polypectomy) Crohn’s or ulcerative colitis* Solitary rectal ulcer syndrome

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*Managed surgically in most cases

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DIC Congenital bleeding disorders

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Note: cholestatic jaundice is often surgical

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GS7 General Surgery and Thoracic Surgery

Toronto Notes 2018

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Pre-Operative Preparations

Bilirubin Levels

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Pre-Operative Preparations  

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In patients with liver disease and an acute abdomen spontaneous bacterial peritonitis must be ruled out

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Prehepatic Intrahepatic Posthepatic Serum Bilirubin Indirect Direct Urine Urobilinogen Bilirubin Fecal Urobilinogen

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Considerations • informed consent (see Ethical, Legal, and Organizational Medicine, ELOM7) • screening questionnaire to determine risk factors e g. age, exercise capacity, medication use, allergies • consider pre-operative anesthesia, medicine consult as indicated to optimize patient status • NPO according to guidelines (see Anesthesia and Perioperative Medicine, A4) • IV – balanced crystalloid at maintenance rate (4:2:1 rule → roughly 100-125 cc/h): normal saline or Ringer’s lactate; bolus to catch up on estimated losses including losses from bowel prep ■■ appropriate use of fluids perioperatively decreases risk of cardiorespiratory complications • patient’s regular medications included with the exception of hypoglycemic agents, diuretics and ACEI • patients on steroids may require stress dose coverage, anticoagulation/antiplatelet medication must be managed to decrease surgical bleeding but not put patient at risk for increased thrombotic events (e.g. switching from warfarin to LMWH) • prophylactic antibiotics depending on wound class (within 1 h prior to incision): usually cefazolin (Ancef®) ± metronidazole (Flagyl®) • consider MBP: cleans out bowel ■■ oral cathartic (e.g. fleet Phosphosoda®) starting previous day ■■ in selected cases, current evidence does not support routine use • consider VTE prophylaxis for all inpatient surgery (LMWH or heparin) • do not hold anticoagulation prior to surgery unless epidural is expected • smoking cessation and weight loss pre-operative can significantly decrease post-operative complications • infection: delay elective surgery until infection controlled, including respiratory infection (particularly in asthma patients)

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• general principles in preventing complications during the post-operative period include ■■ frequent examination of the patient (daily or more) and their wound ■■ removal of surgical tubes as soon as possible (e.g Foley catheters and surgical drains) ■■ early ambulation ■■ monitor fluid balance and electrolytes ■■ analgesia - enough to adequately address pain, but not excessive ■■ skillful nursing care

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Surgical Complications

Mechanical Bowel Preparation Strategies: A Clinical Practice Guideline developed by the University of Toronto s Best Practice in Surgery Informed by: Can J Surg 2010;53:385–395. 14 RCTs (5,071 participants), 8 meta-analyses 1. All open/laparoscopic colorectal procedures (excluding LARs ± diverting stoma) • No MBP • No dietary restrictions before NPO • Fleet enema for left colon anastomoses with transrectal stapling 2. Open/laparoscopic LAR ± diverting stoma • MBP • No dietary restrictions before MBP; clear fluids after MBP complete

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Drains • NGT ■■ indications: gastric decompression, analysis of gastric contents, irrigation/dilution of gastric contents, feeding, if necessary ■■ contraindications: suspected basal skull fracture, obstruction of nasal passages, esophageal stricture, esophageal varices • Foley catheter with urometer ■■ indications: to accurately monitor urine output, decompression of bladder, relieve obstruction, rapidly expanding suprapubic mass ■■ contraindications: suspected urethral injury, and difficult insertion of catheter

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Best Practice in General Surgery (BPIGS) http://www.bpigs.ca/ BPIGS is a University of Toronto initiative with the goal of standardizing care in general surgery. This link contains EBM based guidelines which have been implemented by consensus within all Toronto teaching hospitals. This is a highly recommended source for the most up-to-date pre-operative and general treatment guidelines

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Investigations • see Anesthesia and Perioperative Medicine, A4 • routine pre-operative laboratory investigations for elective procedures should be selective ■■ only ASA class and surgical risk have been found to independently predict post-operative adverse effects • blood components: group and screen or cross and type depending on procedure • CBC, electrolytes, creatinine • INR/PT, PTT • CXR (PA and lateral) for patients with history of cardiac or pulmonary disease • ECG as indicated by history or if >69 yr and no risk factors • β-hCG testing in all women of reproductive age

Surgical Emergencies: Take an AMPLE History Allergies Medications Past medical/surgical history (including anesthesia and bleeding disorders) Last meal Events (HPI)

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s

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• fever does not necessarily imply infection particularly in the first 24-48 h post-operative • fever may not be present or is blunted if patient is receiving chemotherapy, glucocorticoids, or immunosuppression • timing of fever may help identify cause ■■ hours after surgery – POD #1 (immediate) ◆◆ inflammatory reaction in response to trauma from surgery; unlikely to be infectious ◆◆ reaction to blood products received during surgery ◆◆ malignant hyperthermia

Drain Size Measured by the unit French: French = diameter (mm) x 3

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Post-Operative Fever

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GS8 General Surgery and Thoracic Surgery

Toronto Notes 2018

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Surgical Complications

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■■ POD #1-2 (acute) ◆◆ atelectasis (most common cause of fever on POD #1) ◆◆ early wound infection (especially Clostridium, Group A Streptococcus – feel for crepitus and ook for “dishwater” drainage) ◆◆ aspiration pneumonitis ◆◆ other: Addisonian crisis, thyroid storm, and transfusion reaction ■■ POD #3-7 (subacute): likely infectious ◆◆ UTI, surgical site infection, IV site/line infection, septic thrombophlebitis, and leakage at bowel anastomosis (tachycardia, hypotension, oliguria, and abdominal pain) ■■ POD #8+ (delayed) ◆◆ intra-abdominal abscess, DVT/PE (can be anytime post-operative, most commonly POD #810), and drug fever ◆◆ other: cholecystitis, peri-rectal abscess, URTI, infected seroma/biloma/hematoma, parotitis, C. difficile colitis, and endocarditis

Pre- and Post-Operative Orders

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ADDAVIDS Admit to ward X under Dr. Y Diagnosis Diet Activity Vitals (q4h from ED and post-operative is standard) IV, Investigations, Ins and Outs Drugs, Dressings, Drains Special procedures

5 Ws o Post-Operative Fever Wind POD #1-2 (pulmonary – atelectasis, pneumonia) Water POD #3-5 (urine – UTI) Wound POD #5-8 (wound infection - if earlier think streptococcal or clostridial infection) Walk POD #8+ (thrombosis – DVT/PE) Wonder drugs POD #1+ (drug)

fre

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Treatment • treat primary cause • antipyrexia (e.g. acetaminophen)

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Wound/Incisional Complications

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SURGICAL SITE INFECTION

ok

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Etiology • S. aureus, E coli, Enterococcus, Streptococcus spp., Clostridium spp.

bo

Risk Factors

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Table 4. Procedures and Their Impact on Surgical Site Infection Incision under sterile conditions; MAJOR contamination of wound during procedure (i.e. gross spillage of stool, infection in biliary, respiratory, or GU systems)

Hernia repair

Routine cholecystectomy; colon resection

Bowel obstruction with enterotomy and spillage of contents; necrotic bowel resection; fresh traumatic wounds

Appendiceal abscess; traumatic wound with contaminated devitalized tissue; perforated viscus

Infection Rate

100 mL

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Treatment • Foley catheter to rest bladder, then trial of voiding OLIGURIA/ANURIA (see Nephrology, NP18)

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fr

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Etiology • prerenal vs. renal vs. postrenal • most common post-operative cause is prerenal ± ischemic ATN ■■ external fluid loss: hemorrhage, dehydration, and diarrhea ■■ internal fluid loss: third-spacing due to bowel obstruction, and pancreatitis

b

o

Clinical Presentation • urine output 8 wk pre-operative) • post-operative prophylaxis ■■ incentive spirometry, deep breathing exercise, chest physiotherapy, and intermittent positivepressure breathing ■■ selective NGT decompression after abdominal surgery ■■ short-acting neuromuscular blocking agents ■■ minimize use of respiratory depressive drugs, appropriate pain control, and early ambulation PNEUMONIA/PNEUMONITIS • may be secondary to aspiration of gastric contents during anesthetic induction or extubation, causing a chemical pneumonitis

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Risk Factors • aspiration: general anesthetic, decreased LOC, GERD, full stomach, bowel/gastric outlet obstruction + non-functioning NGT, pregnancy, and seizure disorder • non-aspiration: atelectasis, immobility, and pre-existing resp ratory disease

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Clinical Features • productive cough, and fever • tachycardia, cyanosis, respiratory failure, and decreased LOC • CXR: pulmonary infiltrate

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Treatment • prophylaxis: see atelectasis prophylaxis, pre-operative NPO/NGT, and rapid sequence anesthetic induction • immediate removal of debris and fluid from airway • consider endotracheal intubation and flexible bronchoscopic aspiration • empiric IV antibiotics to cover oral nosocomial aerobes and anaerobes (e.g.piperacillin-tazobactam, cefepimemetronidazole)

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PULMONARY EMBOLUS (see Respirology, R18)

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Clinical Features • unilateral leg swelling and pain (DVT as a source of PE), sudden onset dyspnea, pleuritic chest pain, tachycardia, and fever • most commonly POD #8-10, but can occur anytime post-operatively, even after discharge • diagnosis made by Chest CT scan usually

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Treatment • initial treatment: IV heparin or subcutaneous LMWH, bridging to therapeutic anticoagulation is required for a minimum of 3 mo; for patients with cancer, or other risk factors for hypercoagulability, the duration of anticoagulation may be longer • Greenfield (IVC) filter if contraindications to anticoagulation • prophylaxis: subcutaneous heparin (5,000 U bid) or LMWH, compression stockings (TED™ Hose), and sequential compression devices PULMONARY EDEMA

bo

Clinical Features • shortness of breath, crackles at lung bases, and CXR abnormal

o

o

Treatment (LMNOP) • Lasix • Morphine (decreases symptoms of dyspnea, venodilator, and afterload reduction) • Nitrates (venodilator) • Oxygen + non-invasive ventilation • Position (sit patient up)

ee .

N w onset “asthma” and wheezing in the elderly is cardiogenic until proven otherwise

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Etiology • cardiogenic vs. noncardiogenic • circulatory overload: excess volume replacement, LV failure, shift of fluid from peripheral to pulmonary vascular bed, negative airway pressure, and alveolar injury due to toxins (e.g. ARDS) ■■ more common with pre-existing cardiac disease • negative pressure pulmonary edema due to inspiratory efforts against a closed glottis upon awakening from general anesthesia

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GS12 General Surgery and Thoracic Surgery

Toronto Notes 2018

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Surgical Complications

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RESPIRATORY FAILURE

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Clinical Features • dyspne , cyanosis, and evidence of obstructive lung disease • earliest manifestations – tachypnea and hypoxemia (RR >25, pO2 60, consider ARDS (see Respirology, R27)

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Cardiac Complications

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• abnormal ECGs common in post-operative period (compare to pre-operative ECG) • common arrhythmias: supraventricular tachycardia, atrial fibrillation (secondary to fluid overload, PE, and MI)

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MYOCARDIAL INFARCTION • see Cardiology and Cardiac Surgery, C27 • surgery increases risk of MI • incidence ■■ 0.5% in previously asymptomatic men >50 yr old ■■ 40-fold increase in men >50 yr old with previous MI

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Risk Factors • pre-operative HTN, CHF • previous MI (highest risk ≤6 mo, but risk never returns to baseline) • increased age • intra-operative hypotension • operations >3 h • angina

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Clinical Features • majority of cases on day of operation or POD #3-4 (shifting of third space fluid back into intravascular compartment) • often silent without chest pain, may only present with new-onset CHF (dyspnea), arrhythmias, and hypotension

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Intra-Abdominal Abscess

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Etiology • usually polymicrobial: Gram-negative bacteria, and anaerobes ■■ consider Gram-positives if coexisting cellulitis

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Definition • collection of pus walled-off from rest of peritoneal cavity by inflammatory adhesions and viscera

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Risk Factors • emergency surgery, and contaminated OR • GI surgery with anastomoses • poor healing risk factors (DM, poor nutrition, etc.) • may occur POD #3 after laparotomy when third space fluid re-distribution occurs

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Investigations • CBC, blood cultures x2 • CT ± IV and water-soluble contrast • DRE (pelvic abscess)

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Clinical Features • persistent spiking fever, dull pain, and weight loss • mass difficult to palpate • peritoneal signs if abscess perforation and secondary peritonitis • leukocytosis or leukopenia (immunocompromised, and elderly) • co-existing effusion (pleural effusion with subphrenic abscess) • common sites: pelvis, Morrison’s pouch (space between kidney and liver), subphrenic, paracolic gutters, lesser sac, peri-appendiceal, post-surgical anastomosis, diverticular, and psoas

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GS13 General Surgery and Thoracic Surgery

Toronto Notes 2018

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Thoracic Surgery

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Treatment • drain placement by interventional radiology (preferred), laparoscopy, and open drainage • subsequent antibiotic coverage; ceftriaxone + metronidazole or piperacilin-tazobactam (Pip-Tazo)

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Paralytic Ileus

• see Bowel Obstruction, GS23

Delirium

m

• see Psychiatry, PS19 and Neurology, N20

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Thoracic Surgery

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Hiatus Hernia Esophagus

Esophagus

Differential Diagnosis of Hiatus Hernia

GE junction

Diaphragm Stomach

Stomach

GE junction

Diaphragm

Normal Anatomy

Sliding Hiatus Hernia Esophagus

Esophagus

Stomach

Stomach

GE junction © Jerusha Ellis 2012

Diaphragm

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Diaphragm GE junction

Mixed Hiatus Hernia

Paraesophageal Hiatus Hernia Figure 6. Types of hiatus hernia

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SLIDING HIATUS HERNIA (TYPE I) • see Figure 6 • herniation of both the stomach and the gastroesophageal (GE) junction into thorax • 90% of esophageal hernias

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Risk Factors • age • increased intra-abdominal pressure (e.g. obesity, pregnancy, coughing, and heavy lifting) • smoking

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bo

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Clinical Features • majority are asymptomatic • hernias frequently associated with GERD due to decreased competence of LES

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Complications • most common complication is GERD • other complications are rare and are related to reflux • esophagitis (dysphagia, and heartburn) • consequences of esophagitis (peptic stricture, Barrett’s esophagus, and esophageal carcinoma) • extra-esophageal complications (aspiration pneumonitis/pneumonia, asthma type bronchospasm, cough, and laryngitis)

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Investigations • barium swallow, endoscopy (esophago-gastroscopy), or esophageal manometry (technique for measuring LES pressure) • 24 h esophageal pH monitoring to quantify reflux • endoscopy with biopsy to document type and extent of tissue damage and rule out esophagitis, Barrett’s esophagus, and cancer

GI Causes

Non-GI Causes

Cholelithiasis Diverticulitis Peptic ulcer Achalasia Pancreatitis GERD Gastritis

MI Angina Pericarditis

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GS14 General Surgery and Thoracic Surgery

Toronto Notes 2018

c

Thoracic Surgery

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Treatment • lifestyle modification ■■ stop smoking, weight loss, elevate head of bed, no meals IPF > IPAH • 10 yr survival: CF, α-1 antitrypsin deficiency > IPAH > COPD IPF

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Chronic Obstructive Pulmonary Disease

• see Respirology, R9

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Long-Term Survival Analysis of the Canadian Lung Volume Reduction Surgery Trial Ann Thorac Surg 2013;96:1217-1222 Study: Retrospective observational study assessing the long-term surv val f patients enrolled in the CLVRS at 8-10 yr follow-up. Results/Conclusions: Compared with the best medical care group, patients in the LVRS group showed a 16-mo survival advantage and a 20% reduction in mortality. Although not statistically significant, LVRS may provide long-term benefits in the treatment of end-stage emphysema.

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Treatment • indications for surgical management ■■ dyspnea despite maximal medical therapy and pulmonary rehabilitation ■■ CT showing hyperinflation and heterogeneously distributed emphysema predominant in the upper lung zone ■■ may be used as a bridging procedure to lung transplantation • contraindications ■■ age >75, cigarette smoking within the prior 6 mo, higher risk of surgical mortality ■■ homogeneously distributed emphysematous changes without areas of preserved lung tissue ■■ diffusing capacity of lung for carbon monoxide 60 mmHg, PaO2 10 yr post-gastrectomy) • host-related factors ■■ blood type A ■■ hereditary nonpolyposis colorectal cancer (HNPCC), hereditary diffuse gastric carcinoma (HDGC) ■■ gastric adenomatous polyps ■■ hypertrophic gastropathy ■■ genetic syndromes: hereditary diffuse gastric cancer E-cahedrin (CDH-1) gene • environmental factors: smoking, alcohol, smoked food, and nitrosamines

fre

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Epidemiology • 5th most common cancer in the world • M:F = 3:2 • most common age group = 50-59 yr • incidence has decreased by 2/3 in past 50 yr • incidence of adenocarcinoma 10 cm) ■■ mitotic activity (worse if >5 mitotic figures or 50/hpf) ■■ degree of nuclear pleomorphism ■■ location: with identical sizes, extra-gastric location has a higher risk of progression than GISTs in the stomach • metastases to liver, omentum, peritoneum; nodal metastases rare

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Treatment • surgical resection if >2 cm; follow with serial endoscopy if 4 cm with significant mitotic activity) • advanced disease (i.e. metastases to liver and/or peritoneal cavity) ■■ palliative intent chemotherapy with imatinib ■■ metastectomy may be considered for liver limited disease

Bariatric Surgery

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• weight reduction surgery for morbid obesity • indications: BMI ≥40 without illness or BMI ≥35 with 1+ serious comorbidity (e.g. DM, CAD, sleep apnea, or severe joint disease)

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Complications • perioperative mortality ~1% (anastomotic leak with peritoneal signs, PE) • obstruction at enteroenterostomy (see Complications of Gastric Surgery) • staple line dehiscence • dumping syndrome • cholelithiasis due to rapid weight loss (20-30%) • band abscess (if long-term)

Bariatric (Weight Loss) Surgery for Obesity is Considered when Other Treatments have Failed Cochrane DB Syst Rev 2009;2:CD003641 Benefits • Greater weight loss in patients with BMI >30 at 2 yr. • Reduction in comorbidities (type 2 DM, HTN, and medication use). • Improvement in quality of life at 2 yr (physical function, physical role, general health, vitality, and emotional role). Risks • Complications: leaks, hernias, infection, pulmonary embolism and post-operative mortality. • Side effects specific to type of procedure (i.e. vomiting dumping syndrome, and food intolerance). • Cholecystitis occurs as a result of rapid weight loss

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Surgical Options • malabsorptive/restrictive ■■ laparoscopic Roux-en-Y gastric bypass (most common) • staple off small gastric pouch (restrictive) with Roux-en Y limb to pouch (malabsorptive) with dumping syndrome physiology most effective, higher complication rates • restrictive ■■ laparoscopic adjustable gastric banding ◆◆ silicone band around fundus creates pouch, adjustable through port under skin ■■ laparoscopic vertical sleeve gastrectomy ◆◆ vertical stapled small gastric pouch • malabsorptive ■■ biliopancreatic diversion with duodenal switch ■■ gastrectomy, enteroenterostomy, duodenal division closure, and duodenoenterostomy

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GS21 General Surgery and Thoracic Surgery

Toronto Notes 2018

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SMALL INTESTINE

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Complications of Gastric Surgery

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Liver Stomach

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• most resolve within 1 yr

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Alkaline Reflux Gastritis • duodenal contents (bilious) reflux into stomach causing gastritis ± esophagitis • treatment ■■ medical: H2-blocker, metoclopramide, cholestyramine (bile acid sequestrant) ■■ surgical: conversion of Billroth I or II to Roux-en-Y

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Bile juice

A. Alkaline Reflux Gastritis Liver Stomach

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Gallbladder Pancreas

Obstruction

B. Afferent Loop Syndrome Liver Stomach Food Flow

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Dumping Syndrome • early: 15 min post-prandial ■■ etiology ◆◆ hyperosmotic chyme released into small bowel (fluid accumulation and jejunal distention) ■■ clinical features ◆◆ post-prandial symptoms ◆◆ epigastric fullness or pain, emesis, nausea, diarrhea, palpitations, dizziness, tachycardia, diaphoresis ■■ treatment ◆◆ small multiple low carbohydrate, low fat, and high protein meals and avoidance of liquids with meals ◆◆ last resort is interposition of antiperistaltic jejunal loop between stomach and small bowel to delay gastric emptying • late: 3 h post-prandial ■■ etiology: large glucose load leads to large insulin release and hypoglycemia ■■ treatment: small snack 2 h after meals

Gallbladder Pancreas

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Afferent Loop Syndrome • accumulation of bile and pancreatic secretions causes intermittent mechanical obstruction and distention of afferent limb • clinical features ■■ early postprandial distention, RUQ pain, nausea, bilious vomiting, anemia • treatment: surgery (conversion to Roux-en-Y increases afferent loop drainage)

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Gallbladder Pancreas Small Intestine

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Blind-Loop Syndrome • bacterial overgrowth of colonic Gram-negative bacteria in afferent limb • clinical features ■■ anemia/weakness, diarrhea, malnutrition, abdominal pain, and hypocalcemia • treatment: broad-spectrum antibiotics, and surgery (conversion to Billroth I)

C. Dumping Syndrome

Postvagotomy Diarrhea • up to 25% • bile salts in colon inhibit water resorption • treatment: medical (cholestyramine), and surgical (reversed interposition jejunal segment)

Liver Food Flow Stomach

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SMALL INTESTINE

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Gallbladder Pancreas Chyme Bacteria

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D. Blind Loop Syndrome

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Mechanical Small Bowel Obstruction

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Liver Cut CN X Stomach

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Pathophysiology • obstruction → gas and fluid (swallowed or GI secretions) accumulate proximal to site of obstruction and distal decompression → intestinal activity increases to overcome obstruction → colicky pain and diarrhea (initially) • bowel wall edema and disruption of normal bowel absorptive function can lead to increased intraluminal fluid and transudative fluid loss into peritoneal cavity, electrolyte disturbances • increase intramural pressure can lead to impaired microvascular perfusion leading to intestinal ischemia and necrosis (strangulated bowel obstruction)

H2O

Gallblader Pancreas

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Small Bowel Obstruction

Colon

E. Postvagotomy Diarrhea © Wensi Sheng 2010

Figure 10. Complications of gastric surgery

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GS22 General Surgery and Thoracic Surgery

Toronto Notes 2018

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Small Bowel Obstruction

Etiology

s

Table 7. Common Causes of SBO Extramural

Intussusception Gal stones Bezoars

Crohn’s Radiation stricture Adenocarcinoma

Adhesions from previous surgeries (75% SBO) Incarcerated hernia Peritoneal carcinomatosis

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Investigations • radiological ■■ abdominal x-ray (3 views): triad of dilated small bowel (>3 cm in diameter), air-fluid levels on upright film, paucity of air in colon (high sensitivity, low specificity as ileus and LBO can present similarly) ■■ CT: discrete transition zone with proximal bowel dilation, distal bowel decompression, and intraluminal contrast does not pass the transition zone ◆◆ most importantly to rule out ischemic bowel/strangulation: pneumatosis intestinalis (free air in bowel wall) and thickened bowel wall, air in portal vein, free intraperitoneal fluids, and differential wall enhancements (poor uptake of IV contrast into the wall of the affected bowel) ■■ other ◆◆ less used: upper GI series/small bowel series (if no cause apparent, i.e. no hernias, and no previous surgeries) ◆◆ may consider U/S or MRI in pregnant patients • laboratory ■■ may be normal early in disease course ■■ creatinine, and hematocrit to assess degree of dehydration ■■ fluid, and electrolyte abnormalities; metabolic alkalosis due to frequent emesis; amylase elevated ■■ if strangulation: leukocytosis with left shift, elevated lactate (late signs)

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Treatment • IV isotonic fluid resuscitation + urine output monitoring with catheter ■■ SBO related vomiting and decrease PO intake leads to volume depletion • NG tube in the stomach for gastric decompression; decrease nausea, distention, and risk of aspiration from vomiting • Partial SBO/Crohn’s/Carcinomatosis: conservative management with fluid resuscitation and NG tube decompression ■■ 48 h of watchful waiting; if no improvement or develops complications, surgery • Complete SBO, if no clinical features of strangulation, short course of conservative management with fluid resuscitation and NG tube decompression with frequent re-examination by surgical team ■■ duration of observation varies from hours to a few days ■■ if SBO fails to resolve, or if symptoms of strangulation develop, then surgery

re e

Patients presenting with a SBO in setting of “virgin” abdomen should have surgery ASAP – EXCEPTION: malignant obstruction from history and imaging

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Clinical Features • 1) distinguish mechanical obstruction from ileus; 2) determine etiology of obstruction; 3) recognize partial from complete SBO; 4) differentiate simple from complicated (e.g. strangulated) obstruction • symptoms: colicky abdominal pain, nausea/vomiting, obstipation ■■ vomiting is more prominent with proximal than distal ■■ more feculent vomitus suggests more established obstruction because of bacterial overgrowth ■■ continue passage of gas and/or stool 6-12 h after onset of symptoms suggest partial than complete obstruction • signs: abdominal distention (most prominent if obstruction at distal ileum), hyperactive proceeding to minimal bowel sound • strangulated obstruction: abdominal pain disproportionate to physical exam findings suggest intestinal ischemia ■■ may have tachycardia, localized abdominal tenderness fever, marked leukocytosis, and lactate acidosis

Increased Risk of Perforation with Distention as seen on Abdomen Imaging • Small bowel ≥3 cm • Distal colon ≥6 cm • Proximal colon ≥9 cm • Cecum ≥12 cm

In a non-virgin abdomen – adhesional SBOs resolve spontaneously with NGT decompression 70% of time

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Risk Factors • prior abdominal or pelvic surgery ■■ abdominal wall or groin hernia ■■ history of malignancy ■■ prior radiation

MUST DO Rule out CRC in constipated patient Send for TURP in patient with BPH (treat intraabdominal HTN)

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• three types ■■ partial SBO: only a portion of intestinal lumen is occluded, allows passage of some gas & fluid, low risk of strangulation ■■ complete SBO: the lumen of the intestine is occluded, no passage of gas or stool, at higher risk of strangulation ■■ closed-loop obstruction: segment of intestine is obstructed both proximally and distally (e.g. volvulus), leading to rapid rise in intraluminal pressure from gas and fluid that cannot escape, high risk of strangulation due to bowel wall ischemia

Top 3 Causes of SBO (in order) ABC Adhesions Bulge (hernias) Cancer (neoplasms)

Causes of SBO SHAVING Stricture Hernia Adhesions Volvulus Intussusception/IBD Neoplasm Gallstones

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Intramural

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Intraluminal

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GS23 General Surgery and Thoracic Surgery

Toronto Notes 2018

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Small Bowel Obstruction

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• High risk for strangulation based on clinical symptoms: urgent surgery to prevent irreversible ischemia ■■ early post operative SBO: if bowel function does not return within 3-5 d after surgery; usually partial, extended conservative therapy (2-3 wk) with bowel rest, fluids, and TPN is appropriate ◆ surgery if presence of peritonitis or complete SBO demonstrated

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Prognosis • related to etiology; mortality: non-strangulating 36 h), ischemic = up to 50% Prevention • open surgery has four fold increase in risk of SBO in 5 yr compared to laparoscopic surgery

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Paralytic Ileus

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Pathogenesis • temporary, reversible impairment of intestinal motility; mostly frequently caused by: ■■ abdominal operations, infections and inflammation, medications (opiates, anesthetics, psychotropics), and electrolyte abnormalities ■■ passing gas is the most useful indicator • NOT the same as intestinal pseudo-obstruction ■■ chronic pseudo-obstruction refers to specific disorders that affect the smooth muscle and myenteric plexus, leading to irreversible intestinal dysmotility Clinical Features • symptoms and signs of intestinal obstruction without mechanical obstruction ■■ bowel sounds are diminished or absent (in contrast to initial hyperactive bowel sounds in SBO)

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Investigations • routine post-operative ileus: expected, no investigation needed • if ileus persists or occurs without abdominal surgery ■■ review patient medications (especially opiates) ■■ measure serum electrolyte to monitor for electrolyte abnormalities (including extendedelectrolytes like Mg, Calabour, PO4) ■■ CT scan to rule out abscess or peritoneal sepsis, or to exclude complete mechanical obstruction

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Treatment • most important: NPO + fluid resuscitation • NGT decompression, correct causative abnormalities (e.g. sepsis, medications, electrolytes), consider TPN for prolonged ileus • post-operative: gastric and small bowel motility returns by 24-48 h, colonic motility by 3-5 d • current interest in novel therapies such as gum chewing and pharmacologic therapy (e.g. alvimopan, an opioid antagonists)

m

Intestinal Ischemia

Ileal/sub-ileal (F Usually non-Hodgkin’s lymphoma

Most common site of GI metastases in patients with metastatic melanoma

Crohn’s, celiac disease, autoimmune disease, immunosuppression, radiation therapy, and nodular lymphoid hyperplasia

Melanoma, breast, lung, ovary, colon, and cervical cancer

eb

b

Classified based on embryological origin (foregut, midgut, and hindgut) Originate from gut enterochromaffin cell Appendix 46%, distal ileum 28%, rectum 17%

Usually distal ileum Proximal jejunum in patients with celiac disease

Hematogenous spread from breast, lung, and kidney Direct extension from cervix, ovaries, and colon

Clinical Features

Early metastasis to lymph n des 80% metastatic at time of operation Abdominal pain (common)

N/V, anemia, GI bleeding, jaundice, and weight loss (less common) Often slow-growing Usually asymptomatic, incide tal finding Obstruction, bleeding, crampy abdominal pain, and intussusception Carcinoid syndrome (F

sf

Epidemiology

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Table 8. Malignant Tumours of the Small Intestine

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GS25 General Surgery and Thoracic Surgery

Toronto Notes 2018

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Abdominal Hernia

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Table 8. Malignant Tumours of the Small Intestine (continued) Carcinoid

Lymphoma

Metastatic

r

Adenocarcinoma Surgical resection ± chemotherapy

Surgical resection ± chemotherapy Carcinoid syndrome treated with steroids, histamine, and octreotide Metastatic risk 2% if size 2 cm

Low grade: chemotherapy with cyclophosphamide High grade: surgical resection, and radiation Palliative: somatostatin, doxorubicin

Palliation

Prognosis

5 yr survival 25% (if node positive)

5 yr survival 70%; 20% with liver metastases

5 yr survival 40%

Poor

b

o

Treatment

TNM

TNM

Ann Arbor

c

Staging System

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Short Gut Syndrome

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Definition • reduced surface area (length) of small bowel causing insufficient intestinal absorption leading to diarrhea, malnutrition, and dehydration

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Etiology • acute mesenteric ischemia: resection of large amount of bowel at once • Crohn’s disease: cumulative resections • malignancies

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Prognostic Factors • residual small bowel length, residual colon length (reabsorption of water and electrolytes and some reabsorption of nutrients), condition of the remnant small bowel (healthier bowel facilitate better reabsorption), presence of ileocecal valve (delay transition into colon leading to more reabsorption) • resection of ileum is less tolerated than resection of jejunum (ileum reabsorbs bile salt and vitamin B12)

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• see Hiatus Hernia, GS13

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Definition • defect in abdominal wall causing abnormal protrusion of intra-abdominal contents

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Risk Factors • activities which increase intra-abdominal pressure ■■ obesity, chronic cough, asthma, COPD, pregnancy, constipation, bladder outlet obstruction, ascites, and heavy lifting • congenital abnormality (e.g. patent processus vaginalis, and indirect inguinal hernia) • previous hernia repair, especially if complicated by wound infection • loss of tissue strength and elasticity (e.g. hiatus hernia, aging, and repetitive stress)

Inguinal Canal Walls = MALT x 2 2M Roof 2 muscles (internal oblique, transversus abdominis) 2A Ant. wall 2 aponeuroses (external and internal oblique) 2L Floor 2 ligaments (inguinal and lacunar) 2 Ts Post. wall 2T (transversalis fascia, conjoint tendon)

Borders of Hesselbach’s Triangle • Lateral: inferior epigastric artery • Inferior: inguinal ligament • Medial: lateral margin of rectus sheath

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Epidemiology • M:F = 9:1 • lifetime risk of developing a hernia: males 20-25%, females 2% • frequency of occurrence: 50% indirect inguinal, 25% direct inguinal, 8-10% incisional (ventral), 5% femoral, and 3-8% umbilical • most common surgical disease of males

oo

Inguinal Hernias – MD’s don’t LIe MD: Medial to the inferior epigastric a. = Direct inguinal hernia LI: Lateral to the inferior epigastric a. = Indirect inguinal hernia

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Abdominal Hernia

Indirect Inguinal Hernias: Rule of 5s 5% lifetime incidence in males 5x more common than direct inguinal hernias 5-10x more common in males than females Generally occur by 5th decade of life

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Therapy • medical ■■ TPN: replenish lost fluid and electrolytes in diarrhea ■■ HT2R antagonist or PPI to prevent gastric acid secretion ■■ antimotility agent to prolong transit time in the small intestine ■■ consider octreotide to decrease GI secretion and cholestyramine for bile acid absorption • surgical: non-transplant ■■ to slow transit time: small bowel segmental reversal, intestinal valve construction, or electrical pacing of small bowel ■■ to increase intestinal length: ◆◆ LILT (longitudinal intestinal lengthening and tailoring) procedure ◆◆ STEP (serial transverse enteroplasty procedure) in dilated small bowels • surgical: transplant ■■ indication: life-threatening complication from intestinal failure or long-term TPN ◆◆ liver failure, thrombosis of major central veins, recurrent catheter-related sepsis, recurrent severe dehydration

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GS26 General Surgery and Thoracic Surgery

Toronto Notes 2018

c

Abdominal Hernia

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Post-Operative Complications • recurrence (15-20%) ■■ risk factors: recurrent hernia, age >50, smoking, BMI >25, poor pre-operative functional status (ASA ≥3 – see Anesthesia and Perioperative Medicine, A4), associated medical conditions: type 2 DM, hyperlipidemia, immunosuppression, and any comorbid conditions increasing intraabdominal pressure ■■ less common with mesh/”tension-free” repair • scrotal hematoma (3%) ■■ painful scrotal swelling from compromised venous return of testes ■■ deep bleeding: may enter retroperitoneal space and not be initially apparent ■■ difficulty voiding • nerve entrapment ■■ ilioinguinal (causes numbness of inner thigh or lateral scrotum) ■■ genital branch of genitofemoral (in spermatic cord) • stenosis/occlusion of femoral vein ■■ acute leg swelling • ischem c colitis

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Outcomes of Laparoscopic vs. Open Repair of Primary Ventral Hernias JAMA Surg 2013;148:1043-1048 Purpose: To compare outcomes (surgical site infection (SSI), hernia recurrence and bulging) of patients undergoing laparoscopic ventral hernia repair (LVHR) versus open ventral hernia repair (OVHR). Results/Conclusions: 79 patients with LVHR matched to 79 patients with OVHR with mesh with a median follow-up of 56 mo LVHR was associated with fewer SSIs (7.6% vs. 34.1%) but more cases of bulging (21.5% vs 1 3%) and port-site hernia (2.5% vs. 0.0%). No differences in recurrence were observed.

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Treatment • surgical treatment (herniorrhaphy) is only to prevent strangulation and evisceration, for symptomatic relief, for cosmesis; if asymptomatic can delay surgery • repair may be done open or laparoscopic and may use mesh for tension-free closure • most repairs are now done using tension free techniques – a plug in the hernial defect and a patch over it or patch alone • observation is acceptable for small asymptomatic inguinal hernias

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Complications • incarceration • strangulation ■■ small, new hernias more likely to strangulate ■■ femoral >> indirect inguinal > direct inguinal ■■ intense pain followed by tenderness ■■ intestinal obstruction, gangrenous bowel, sepsis ■■ surgical emergency ■■ DO NOT attempt to manually reduce hernia if septic or if contents of hernial sac gangrenous ■■ will cause closed loop SBO – and EMERGENCY

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Anatomical Types • groin ■■ indirect and direct inguinal, femoral ■■ pantaloon: combined direct and indirect hernias, peritoneum draped over inferior epigastric vessels • epigastric: defect in linea alba above umbilicus • incisional: ventral hernia at site of wound closure, may be secondary to wound infection • other: Littre’s (involving Meckel’s), Amyand’s (containing appendix), lumbar, obturator, peristomal, umbilical, Spigelian (ventral hernia through linea semilunaris)

Watchful Waiting vs. Repair of Inguinal Hernia in Minimally Symptomatic Men: A Randomized Clinical Trial JAMA 2006;295:285-292 Purpose: To compare pain and the physical component score (PCS) of the Short Form 36 Version 2 survey at 2 yr in men with minimally symptomatic inguinal hernias treated with watchful waiting or surgical repair. Methods: RCT of 720 men (n=364 watchful waiting, n=356 surgical repair) followed up for 2-4.5 yr. Watchfulwaiting patients were followed up at 6 mo and annually and watched for hernia symptoms; repair patients received standard open tension-free repair and were followed up at 3 and 6 mo and annually The main outcome was pain and discomfort interfering with usual activities at 2 yr and change in PCS from baseline to 2 yr. Secondary outcomes were complications, patient-reported pain, functional status, ac ivity levels, and satisfaction with care. Results: Primary intention-to-treat outcomes were similar a 2 yr for watchful waiting vs. surgical repair: pain limiting activities (5.1% vs. 2.2%, respectively; p=0.06 [corrected]); PCS (improvement over baseline, 0.29 points vs. 0.13 points; p=0.79). Twenty-three percent of patients assigned to watchful waiting crossed over to receive surgical repair (increase in hernia-related pain was the most common reason offered); 17% assigned to receive repair crossed over to watchful waiting. Self-reported pain in watchful-waiting patients crossing over improved after repair. Occurrence of post-operative hernia-related complications was similar in patients who received repair as assigned and in watchful-waiting patients who crossed over. One watchful-waiting patient (0.3%) experienced acute hernia incarceration without strangulation within 2 yr; a second had acute incarceration with bowel obstruction at 4 yr, with a frequency of 1.8/1,000 patient/yr inclusive of patients fo lowed up for as long as 4.5 yr. Conclusion: Watchful waiting is an acceptable option for men with minimally symptomatic inguinal hernias. Delaying surgical repair until symptoms increase is safe because acute hernia incarcerations occur rarely.

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Classification • complete: hernia sac and contents protrude through defect • incomplete: partial protrusion through the defect • internal hernia: sac herniating into or involving intra-abdominal structure • external hernia: sac protrudes completely through abdominal wall • strangulated hernia: vascular supply of protruded viscus is compromised (ischemia) ■■ requires emergency repair • incarcerated hernia: irreducible hernia, not necessarily strangulated • Richter’s hernia: only part of bowel circumference (usually anti-mesenteric border) is incarcerated or strangulated so may not be obstructed ■■ a strangulated Richter’s hernia may self-reduce and thus be overlooked, leaving a gangrenous segment at risk of perforation in the absence of obstructive symptoms • sliding hernia: part of wall of hernia sac formed by retroperitoneal structure (usually colon)

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Investigations physical examination usually sufficient • U/S ± CT (CT required for obturator hernias, internal abdominal hernias, and Spigelian and/or femoral hernias in obese patients)

Shouldice Technique vs. Other Open Techniques for Inguinal Hernia Repair Cochrane DB Syst Rev 2012;4:CD001543 Purpose: To evaluate the efficacy and safety of the Shouldice technique to other non-laparoscopic techniques. Results/Conclusions: 16 RCTs or quasi-randomized RCTs with 2,566 hernias (1,121 mesh; 1,608 non-mesh). The recurrence rate with Shouldice was higher than mesh (OR 3.80, 95% CI 1.99-7.26) but lower than non-mesh (OR 0.62, 95% CI 0.450.85). There was no difference in chronic pain or complications. In conclusion, with respect to recurrence rates, Shouldice herniorrhaphy is the best non-mesh technique, although inferior to mesh. However it is also more time consuming and results in slightly longer post-operative hospital stays.

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Clinical Features • mass of variable size • tenderness worse at end of day, relieved with supine position or with reduction • abdominal fullness, vomiting, constipation • transmits palpable impulse with coughing or straining

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GS27 General Surgery and Thoracic Surgery

Toronto Notes 2018

Appendix

Groin Hernias

sf r Indirect Inguinal

Femoral

1% of all men

Most common hernia in men and women M>F

Affects mostly females

Acquired weakness of transversalis fascia “Wear and tear” Increased intra-abdominal pressure

Congenital persistence of processus vaginalis in 20% of adults

Pregnancy – weakness of pelvic floor musculature Increased intra-abdominal pressure

Through Hesselbach s triangle Medial to infe ior epigastric artery Usually does not descend into scrotal sac

Originates in deep inguinal ring Lateral to inferior epigastric artery Often descends into scrotal sac (or labia majora)

Into femoral canal, below inguinal ligament but may override it Medial to femoral vein within femoral canal

Surgical repair

Surgical repair

Surgical repair

3-4% risk of recurrence

F • 80% between 5-35 yr of age

.

Direct Hernia

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Pathogenesis • luminal obstruction → bacterial overgrowth → inflammation/swelling → increased pressure → localized ischemia → gangrene/perforation → localized abscess (walled off by omentum) or peritonitis • etiology ■■ children or young adult: hyperplasia of lymphoid follicles, initiated by infection ■■ adult: fibrosis/stricture, fecolith, or obstructing neoplasm ■■ other causes: parasites, or foreign body

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Femoral Hernia

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Figure 12. Schematic of inguinal (direct and indirect) and femoral hernias

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Femoral ring

© Laura E. Smith 2013

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Clinical Features • most reliable feature is progression of signs and symptoms • low grade fever (38ºC), rises if perforation • abdominal pain then anorexia, N/V • classic pattern: pain initially periumbilical; constant, dull, poorly localized, then well localized pain over McBurney’s point ■■ due to progression of disease from visceral irritation (causing referred pain from structures of the embryonic midgut, including the appendix) to irritation of parietal structures ■■ McBurney’s sign • signs ■■ inferior appendix: McBurney’s sign (see sidebar), Rovsing’s sign (palpation pressure to left abdomen causes McBurney’s point tenderness). McBurney’s sign is present whenever the opening of the appendix at the cecum is directly under McBurney’s point; therefore McBurney’s sign is present even when the append x is in different locations ■■ retrocecal appendix: psoas sign (pain on flexion of hip against resistance or passive hyperextension of hip) ■■ pelvic appendix: obturator sign (flexion then external or internal rotation about right hip causes pain) • complications ■■ perforation (especially if >24 h duration) ■■ abscess, phlegmon ■■ sepsis

McBurney’s Sign Tenderness 1/3 the distance from the ASIS to the umbilicus on the right side

o

GS28 General Surgery and Thoracic Surgery

Toronto Notes 2018

c

Inflammatory Bowel Disease

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• see Gastroenterology, G19

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Principles of Surgical Management • can alleviate symptoms, address complications, and improve quality of life • conserve bowel: resect as little as possible to avoid short gut syndrome • perioperative management ■■ optimize medical status: may require TPN (especially if >7 d NPO) and bowel rest ■■ hold immunosuppressive therapy pre operative, provide pre-operative stress dose of corticosteroid; if patient had recent steroid therapy, taper steroids post-operative ■■ VTE prophylaxis: LMWH or heparin (IBD patients at increased risk of thromboembolic events)

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Inflammatory Bowel Disease

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Prognosis • mortality rate: 0.08% (non-perforated), 0.5% (perforated appendicitis)

Effect of Delay to Operation on Outcomes in Adults with Acute Appendicitis Arch Surg 2010;145:886-892 Purpose: To examine the effect of delay to appendectomy on morbidity and mortality among adults with appendicitis. Method: Retrospective cohort study with he main exposure being time to operation, and main outcomes being 30 d overall morbidity and serious morbidity/mortality. Results: Of 32,782 patients in the study, 75.2%, 15.1%, and 9.8% underwent surgeries within 6 h, 6-12 h, and >12 h of admission, respectively. Differences in operative duration and length of post-operative stay were statistically significant but not clini ally meaningful. No significant differences we e observed in adjusted overall morbidity or serious morbidity/mortality. Duration from surgical admission to anesthesia induction was not predictive in regression models for either outcomes. Conclusions: Delay of appendectomy for acute appendicitis among adults does not adversely affect outcomes.

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Treatment • surgery is for symptom management, it is NOT curative, but over lifetime ~70% of Crohn’s patients will have surgery • indications for surgical management ■■ failure of medical management ■■ SBO (due to stricture/inflammation): indication in 50% of surgical cases ■■ abscess, fistula (enterocolic, vesicular, vaginal, cutaneous abscess), quality of life, perforation, hemorrhage, chronic disability, failure to thrive (children), and perianal disease • surgical procedures ■■ resection and anastomosis/stoma if active or subacute inflammation, perforation, or fistula ◆◆ resection margin only has to be free of gross disease (microscopic disease irrelevant to prognosis) ■■ stricturoplasty – widens lumen in chronically scarred bowel: relieves obstruction without resecting bowel (contraindicated in acute inflammation)

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• see Gastroenterology, G20

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Crohn’s Disease

Antibiotics vs. Placebo for Prevention of PostOperative Infection After Appendectomy Cochrane DB Syst Rev 2005;3:CD001439 Purpose: To determine the effectiveness of antibiotics against post operative infections after appendectomy Method: Meta-analysis of randomized controlled trials (RCTs) and controlled clinical trials (CCTs), on both adults and children, in which any antibiotic regime was compared to placebo in patients undergoing appendectomy for suspected appendicitis. The main outcomes of interest were wound infection, intra-abdominal abscess, length of hospital stay, and mortality. Results: 45 studies (n=9,576) were included. Treatment with antibiotics decreased wound infection and abscess rates. Conclusion: Various prophylactic antibiotic regimens are effective in preventing post- perative complications after appendectomy.

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Treatment • hydrate, correct electrolyte abnormalities • appendectomy (gold standard) ■■ laparoscopic vs. open (see sidebar) ■■ complications: intra-abdominal abscess, appendiceal stump leak ■■ perioperative antibiotics: ◆◆ cefazolin + metronidazole if uncomplicated peri-operative dose is adequate ◆◆ consider treatment with post-operative antibiotics for perforated appendicitis • for patients who present with an abscess (palpable mass or phlegmon on imaging and often delayed diagnosis with symptoms for >4-5 d), consider radiologic drainage + antibiotics x 14 d ± interval appendectomy once inflammation has resolved = (controversial) • recent research supports antibiotic only treatment as reasonable for uncomplicated appendicitis, with 10-20% recurrence rates • colonoscopy in the elderly to rule out other etiology (neoplasm)

Laparoscopic vs. Open Appendectomy Cochrane DB Syst Rev 2010;10:CD001546 Laparoscopic Surgery • Wound infection less likely • Intra-abdominal abscesses 2x more likely • Reduced pain on POD #1 • Reduced hospital stay by 1.1 d • Sooner return to normal activity, work, and sport • Costs outside hospital are reduced Open Surgery • Shorter duration of surgery • Lower operation costs Overview Diagnostic laparos opy and laparoscopic appendectomy appear to be advantageous over open appendectomy, particularly for young female patients and obese patients.

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Investigations • laboratory ■■ mild leukocytosis with left shift (may have normal WBC counts) ■■ higher leukocyte count with perforation ■■ β-hCG to rule out ectopic pregnancy ■■ urinalysis • imaging ■■ U/S: may visualize appendix, but also helps rule out gynecological causes – overall accuracy 90-94%, can rule in but CANNOT rule out appendicitis (if >6 mm, SENS/SPEC/NPV/PPV 98%) ■■ CT scan: thick wall, enlarged(>6 mm), wall enhancement, appendicolith, and inflammatory changes – overall accuracy 94-100%, optimal investigation

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Crohn’s 3 Major Patterns • leocecal 40% (RLQ pain, fever, weight loss) • Small intestine 30% (especially terminal ileum) • Colon 25% (diarrhea)

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Complications of Treatment • short gut syndrome (diarrhea, steatorrhea, malnutrition) • fistulas • gallstones (if terminal ileum resected, decreased bile salt resorption → increased cholesterol precipitation) • kidney tones (loss of calcium in diarrhea → increased oxalate absorption and hyperoxaluria → stones)

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GS29 General Surgery and Thoracic Surgery

Toronto Notes 2018

LARGE INTESTINE

Findings in Crohn’s • “Cobblestoning” on mucosal surface due to edema and linear ulcerations • “Skip lesions”: normal mucosa in between • “Creeping fat”: mesentery infiltrated by fat • Granulomas: 25-30%

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Prognosis • recurrence rate at 10 yr: ileocolic (25-50%), small bowel (50%), colonic (40-50%) • re-operation at 5 yr: primary resection (20%), bypass (50%), s ricturoplasty (10% at 1 yr) • 80-85% of patients who need surgery lead normal lives • mortality: 15% at 30 yr

b

Ulcerative Colitis

re e

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Complications of Treatment • early: bowel obstruction, transient urinary dysfunction, dehydration (high stoma output), anastomotic leak • late: stricture, anal fistula/abscess, pouchitis, poor anorectal function, reduced fertility

Findings in Ulcerative Colitis • Patients usually present with diarrhea (± blood in their stool) • Associated symptoms include colicky abdominal pain, urgency, tenesmus, and incontinence • Presence of extra-intestinal manifestations • Endoscopically, there is loss of vascular markings, erythema, granularity of mucosa, petechiae, exudates, edema, erosions, and spontaneous bleeding • Biopsy features included crypt abscesses, crypt branching, shortening and disarray, and crypt atrophy • Inflammation is continuous and usually involves rectum

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Treatment • indications for surgical management ■■ failure of medical management (including inability to taper steroids) ■■ complications: hemorrhage, obstruction, perforation, toxic megacolon (emergency), failure to thrive (children) ■■ reduce cancer risk (1-2% risk per yr after 10 yr of disease) • surgical procedures ■■ proctocolectomy and ileal pouch-anal anastomosis (IPAA) ± rectal mucosectomy (operation of choice) ■■ proctocolectomy with permanent end ileostomy (if not a candidate for ileoanal procedures) ■■ colectomy and IPAA ± rectal mucosectomy ■■ in emergency: total colectomy and ileostomy with Hartmann closure of the rectum, rectal preservation

.c

• see Gastroenterology, G21

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Prognosis • mortality: 5% over 10 yr • total proctocolectomy will eliminate risk of cancer • perforation of the colon is the leading cause of death from ulcerative colitis

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LARGE INTESTINE

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Large Bowel Obstruction

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Mechanical Large Bowel Obstruction Etiology

Intramural

Extramural

Adenocarcinoma Diverticulitis IBD stricture Radiation stricture

Volvulus Adhesions Hernias (sigmoid colon in a large groin hernia)

b

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Clinical Features (unique to LBO) • open loop (10-20%) ■■ incompetent ileocecal valve allows relief of colonic pressure as contents reflux into ileum, therefore clinical presentation similar to SBO • closed loop (80-90%) (dangerous) ■■ competent ileocecal valve, resulting in proximal and distal occlusions ■■ massive colonic distention → increased pressure in cecum → bowel wall ischemia → necrosis → perforation

Top 3 Causes of LBO (in order) • Cancer • Diverticulitis Volvulus

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Constipation Foreign bodies

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Intraluminal

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Table 11. Common Causes of LBO

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Treatment • surgical correction of obstruction (usually requires resection + temporary diverting colostomy) • volvulus requires sigmoidoscopic or endoscopic decompression followed by operative reduction if unsuccessful ■■ if successful, consider interval sigmoid resection on same admission • cecal volvulus can be a true volvulus or a cecal ‘bascule’ (cecum folds anteriorly to the ascending colon producing a flap valve occlusion to cecal emptying) – both need surgical treatment

In a patient with clinical LBO consider impending perforation when: • Cecum ≥12 cm in diameter • Tenderness present over cecum

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GS30 General Surgery and Thoracic Surgery

Toronto Notes 2018

c

Large Bowel Obstruction

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Prognosis • overall mortality: 10% • cecal perforation + feculent peritonitis: 20% mortality

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Table 12. Bowel Obstruction vs. Paralytic Ileus LBO

Paralytic Ileus

Early, may be bilious

Late, may be feculent

Present

Abdominal Pain

Colicky

Colicky

Minimal or absent

Abdominal Distention

+ (prox SBO), ++ (distal SBO)

++

+

Constipation

+

+

+

Bowel Sounds

Normal, increased Absent if secondary ileus (delayed presentation)

Normal, increased (borborygmi) Absent if secondary ileus (delayed presentation)

Decreased, absent

Air-fluid levels “Ladder” pattern (plicae circularis) Proximal distention (>3 cm) + no colonic gas

Air-fluid levels “Picture frame” appearance Proximal distention + distal decompression No small bowel air if competent ileocecal valve Coffee bean sign (sigmoid volvulus)

Air throughout small bowel and colon

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AXR Findings

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N/V

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SBO

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Functional LBO: Colonic Pseudo-Obstruction (Ogilvie’s Syndrome)

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Definition • acute pseudo-obstruction • distention of colon without mechanical obstruction in distal colon • exact mechanism unknown, likely autonomic motor dysregulation → possibly sympathetic deprivation to colon, unopposed parasympathetic tone, and interruption of sacral parasympathetic tone to distal bowel

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Associations • most common: trauma, infection, and cardiac (MI, CHF) • disability (long-term debilitation, chronic disease bed-bound nursing home patients, and paraplegia), drugs (narcotic use, laxative abuse, and polypharmacy), other (recent orthopedic or neurosurgery, post-partum, electrolyte abnormalities including hypokalemia, retroperitoneal hematoma, and diffuse carcinomatosis)

om

Clinical Features • most prominent is abdominal distention (acute or graduate over 3-7 days) • abdominal pain, nausea and vomiting, constipation/diarrhea • watch out for fever, leukocytosis, and presence of peritoneal signs

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Investigations • AXR: cecal dilatation – if diameter ≥12 cm, increased risk of perforation

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Treatment • treat underlying cause • NPO, NGT • decompression: rectal tube, colonoscopy, neostigmine (cholinergic drug), surgical decompression (ostomy/resection) uncommon • surgery (extremely rare): if perforation, ischemia, or failure of conservative management Prognosis • most resolve with conservative management

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GS31 General Surgery and Thoracic Surgery

Toronto Notes 2018

Diverticular Disease

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Diverticular Disease

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Definitions • diverticulum: abnormal sac-like protrusion from the wall of a hollow organ • diverticulosis: presence of multiple diverticula • diverticulitis: inflammation of diverticula • true (congenital) diverticuli: contain all layers of colonic wall, often right-sided • false (acquired) diverticuli: contain mucosa and submucosa, often left-sided FALSE DIVERTICULUM (mucosal herniations)

Antimesenteric tenia

Mucosa

© Sonya Amin 2003

Circular muscle Mesocolon

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Mesenteric tenia

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Figure 13. Diverticular disease – cross-sections of true and false diverticuli

Diverticulosis

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Epidemiology • 5-50% of Western population, lower incidence in non-Western countries, M=F • prevalence is age dependent: tubular

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Table 14. Characteristics of Tubular vs. Villous Polyps Villous

Incidence

Common (60-80%)

Less common (10%)

Size

Small (2 cm)

Attachment

Pedunculated

Sessile

Malignant Potential

Lower

Higher

Distribution

Even

Left-sided predominance

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Tubular

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Investigations • colonoscopy is the gold standard for diagnosis and treatment of colonic polyps • CT colonography: increasing in availability; patients still require bowel prep and will require colonoscopy if polyps are identified • other: flexible sigmoidoscopy if polyps are detected, proceed to colonoscopy for examination of entire bowel and biopsy

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Treatment • indications: symptoms, malignancy or risk of malignancy (i.e adenomatous polyps) • endoscopic removal of entire growth • indications for segmental resection for malignant polyps: 1) lymphovascular invasion; 2) tumour budding; 3) positive resection margin; 4) poorly differentiated cells; 5) evidence of regional or distant metastases on staging. Most of these cases are usually discussed at multi-disciplinary tumour boards • follow-up endoscopy 1 yr later, then every 3 5 yr

Familial Colon Cancer Syndromes

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FAMILIAL ADENOMATOUS POLYPOSIS

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Pathogenesis • autosomal dominant inheritance, mutation in adenomatous polyposis coli (APC) gene on chromosome 5q21

Figure 15. Sessile and pedunculated polyps

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GS34 General Surgery and Thoracic Surgery

Toronto Notes 2018

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Colorectal Neoplasms

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Clinical Features • hundreds to thousands of colorectal adenomas usually by age 20 (by 40s in attenuated FAP) • extracolonic manifestations ■■ carcinoma of large bowel (i.e. polyps in colon), bile duct, pancreas, stomach, thyroid, adrenal, and small bowel ■■ congenital hypertrophy of retinal pigment epithelium presents early in life in 2/3 of patients; 97% sensitivity ■■ virtually 100% lifetime risk of colon can er (because of number of polyps) • variants ■■ Gardner’s syndrome: FAP + extra-intestinal lesions (sebaceous cysts, osteomas, desmoid tumours) ■■ Turcot syndrome: FAP + CNS tumours (childhood cerebellar medulloblastoma)

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Treatment • surgery indicated by age 17-20 • total proctocolectomy with ileostomy or total colectomy with ileorectal anastomosis • doxorubicin-based chemotherapy • NSAIDs for intra-abdominal desmoids

Referral Criteria for Genetic Screening for APC • To confirm the diagnosis of FAP (in patients with ≥100 colorectal adenomas) • To provide pre-symptomatic testing for indiv duals at risk for FAP (1st degree elatives who are ≥10 yr old) • To confirm the diagnosis of attenuated FAP (in patients with ≥20 colorectal adenomas)

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Investigations • genetic testing (80-95% sensitive, 99-100% specific) • if no polyposis found: annual flexible sigmoidoscopy from puberty to age 50, then routine screening • if polyposis or APC gene mutation found: annual colonoscopy and consider surgery (see Figure 15); consider upper endoscopy to evaluate for periampullary tumours

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HEREDITARY NON-POLYPOSIS COLORECTAL CANCER – LYNCH SYNDROME

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Pathogenesis • autosomal dominant inheritance, mutation in a DNA mismatch repair gene (MSH2, MSH6, MLH1) resulting in microsatellite genomic instability and subsequent mutations • microsatellite instability account for approximately 15% of all colorectal cancers

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Diagnosis • Amsterdam Criteria ■■ 3 or more relatives with verified Lynch syndrome associated cancers, and 1 must be 1st degree relative of the other 2 ■■ 2 or more generations involved ■■ 1 case must be diagnosed before 50 yr old ■■ FAP is excluded • genetic testing (80% sensitive) – colonoscopy mandatory even if negative ■■ refer for genetic screening individuals who fulfill EITHER the Amsterdam Criteria OR the revised Bethesda Criteria • colonoscopy (starting age 20) annually • surveillance for extracolonic lesions

Revised Bethesda Criteria for HNPCC and Microsatellite Instability (MSI) Tumours from individuals should be tested for MSI in the following situations: • Colorectal cancer diagnosed in a patient who is 50 (dominant risk factor in sporadic cases), mean age is 70 • genetic: FAP, HNPCC, or family history of CRC • colonic conditions ■■ adenomatous polyps (especially if >1 cm, villous, multiple) ■■ IBD (especially UC: risk is 1-2%/yr if UC >10 yr) ■■ previous colorectal cancer (also gonadal or breast) • diet (increased fat, red meat, and decreased fibre) and smoking • DM and acromegaly (insulin and IGF-1 are growth factors for colonic mucosal cells)

APR removes distal sigmoid colon, rectum, and anus; permanent end colostomy required LAR removes distal sigmoid and rectum with anastomosis of distal colon to anus

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GS35 General Surgery and Thoracic Surgery

Toronto Notes 2018

c

Colorectal Neoplasms

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Pathogenesis • adenoma-carcinoma sequence; rarely arise de novo

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Clinical Features • often asymptomatic • hematochezia/melena, abdominal pain, and change in bowel habits • others: weakness, anemia, weight loss, palpable mass, and obstruction • 20% patients have distant metastatic disease at time of presentation • spread ■■ direct extension, lymphatic, and hematogenous (liver most common, lung, bone, and brain; tumour of distal rectum → IVC → lungs) ■■ peritoneal seeding: ovary, and Blumer’s shelf (pelvic cul-de-sac)

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LAR

Rectum

25%

35%

30%

Pathology

Ulcerating

Constipation ± overflow (alternating bowel patterns), abdominal pain, decreased stool calibre, rectal bleeding

Obstruction, tenesmus, rectal bleeding

Signs

Fe-deficiency anemia, RLQ mass (10%)

Palpable mass on DRE BRBPR

Invasion into submucosa

N2

Metastasis in 4 or more regional nodes

T2

Invasion into muscularis propria

T3

Invasion through muscularis propria and into serosa

T4

Invasion into adjacent structures or organs

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e

e

Treatment • colon cancer ■■ wide surgical resection of lesion and regional lymphatic drainage; usually colectomy with primary anastomosis ◆◆ curative: wide resection of lesion (5 cm margins) with nodes (>12) and mesentery ◆◆ metastatic lesions confined to the liver can be resected with curative intent ◆◆ palliative: if distant spread, local control for hemorrhage or obstruction ◆◆ care is taken to not spread tumour by unnecessary palpation ◆◆ cancer-bearing portion of colon is removed according to vascular distribution of segment ■■ adjuvant chemotherapy (5-FU or oral capecitabine with oxaliplatin) for stage III and is considered in select stage II patients • rectal cancer ■■ choice of operation depends on individual case; types of operations ◆◆ low anterior resection of rectum (LAR): curative procedure of choice if adequate distal margins (~2 cm); uses technique of total mesorectal excision ◆◆ abdominoperineal resection of rectum (APR): if adequate distal margins cannot be obtained; involves the removal of distal sigmoid colon, rectum, and anus – permanent end colostomy required ◆◆ transanal m nimally invasive surgery (TAMIS)- local excision for select T1 lesions only ◆◆ palliative procedures involve proximal diversion with an ostomy for obstruction and radiation for bleeding or pain ■■ adjuvant therapy ◆◆ combined neoadjuvant chemoradiation therapy followed by post-operative adjuvant chemotherapy for stages II and III

c

e.

Pre-Operative vs. Post-Operative Chemoradiotherapy for Locally Advanced Rectal Cancer: Results of the German CAO/ARO/AIO-94 Randomized Phase III Trial after a Median Follow-Up of 11 Yr J Clin Oncol 2012;30:1926-1933 Background: The CAO/ARO/AIO-94 trial (published 2004) recommended pre-operative chemoradiotherapy (CRT) as standard treatment for locally advanced rectal cancer. However, no survival benefit was shown after median follow-up of 46 mo, and this study reports long-term effects Methods: Patients with stage II to III rectal cancer (n=799) were randomly assigned to pre-operative (n=404) or postoperative CRT (n=395) with fluorouracil (FU), radiation, and adjuvant FU chemotherapy, in addition to total mesorectal excision surgery. Follow-up was designed to assess long-term overall survival as the primary end point; and cumulative incidence of local and distant relapses and disease-free survival as secondary end points. Results: 10 yr incidence of local relapse was significantly lower in the pre-operative CRT group than in the postoperative group (7.1% vs. 10.1%, p=0.048). Overall survival at 10 yr was similar at ~60% for patients treated with pre-operative or post-operative CRT (p=0.85). Disease-free survival rates at 10 yr was similar at ~68% for patients treated with pre-operative or post-operative CRT (p=0.54). No significant difference was detected for 10-yr incidence of distant metastases (pre-operative CRT 29.8% vs. postoperative CRT 29 6%, p=0.9). Conclusion: There is long-term reduction in local currence of stage II to III rectal cancer with pre-operative chemotherapy, but no improvement in overall survival or distant recurrence of disease.

m

T1

o

Distant metastasis

e. c

No distant metastasis

M1

co m

M0

Metastasis in 1-3 regional nodes

sf

No regional node involvement

N1

re

N0

Carcinoma in situ

sf

No primary tumour found

5-yr Survival Rates for CRC Stage Colon Rectum I 74% 74% IIA 67% 64% IB 59% 52% IIC 37% 32% IIIA 73% 74% IIIB 46% 45% IIIC 28% 33% IV 6% 6%

sf re e.

co

re

T0

ok

Distant Metastasis (M)

ok

Regional Lymph Nodes (N)

sf

Primary Tumour (T)

ok

Figure 16. APR vs. LAR

m

m

co

e

Table 16. TNM Classification System for Staging of Colorectal Carcinoma (AJCC/IUCC 2010)

b

e

BRBPR, LBO

Investigations • colonoscopy (best), look for synchronous lesions (3-5% of patients); alternative: air contrast barium enema (“apple core” lesion) + sigmoidoscopy • if a patient is FOBT +ve, or has microcytic anemia or has a change in bowel habits, do colonoscopy • laboratory: CBC, urinalysis, liver enzymes, liver function tests, carcinogenic embryonic antigen (CEA) (pre-operative for baseline, >5 ng/mL have worse prognosis) • staging: CT chest/abdomen/pelvis; bone scan, CT head only if lesions suspected • rectal cancer: pelvic MRI or endorectal U/S to determine T and N stage

Tis

APR

bo

ok sf

sf r

Annular, invasive les ons

Weight loss, weakness, rarely obstruction

b

Exophytic lesions with occult bleeding

Symptoms

© Laura Greenlee 2013, after Cheung & Chen

Left Colon

Frequency

bo

Right Colon

o

Table 15. Clinical Presentation of CRC

o

GS36 General Surgery and Thoracic Surgery

Toronto Notes 2018

c

Other Conditions of the Large Intestine

ks

ks fr

Follow-Up • currently there are no data suggesting optimal follow-up • combination of periodic CT chest/abdomen/pelvis, CEA, and colonoscopy is recommended • CEA to monitor for initial response to treatment, and for surveillance (q6mo)

eb

b

bo

Other Conditions of the Large Intestine Angiodysplasia

m

Definition • vascular malformation: focal submucosal venous dilatation and tortuosity

ok sf re

ee

e.

Clinical Features • most frequently in right colon of patients >60 yr old • bleeding typically intermittent, rarely massive, and not usually hypotensive (melena, anemia, and occult blood positive stools)

eb

bo

oo

Investigations • colonoscopy: cherry red spots, branching pattern from central vessel • angiography: early-filling vein, vascular tuft, and delayed emptying vein; rarely active bleeding • RBC technetium-99 scan • barium enema is contraindicated (obscures other x-rays, i.e. angiogram)

Volvulus

m

Treatment • none if asymptomatic • cautery, right hemicolectomy, embolization, vasopressin infusion, sclerotherapy, band ligation, laser, octreotide, and rarely segmental resection if other treatments fail

ok

ks

f

sf

r

Definition • rotation of segment of bowel about its mesenteric axis • sigmoid (65%), cecum (30%), transverse colon (3%), and splenic flexure (2%) • 5-10% of large bowel obstruction; 25% of intestinal obstruction during pregnancy

m

k

ks

fre

ee

e

Investigations • AXR (classic findings): “omega”, “bent inner-tube”, “coffee-bean” signs • barium/Gastrografin® enema: “ace of spades” (or “bird’s beak”) appearance due to funnel-like luminal tapering of lower segment towards volvulus • sigmoidoscopy or colonoscopy as appropriate • CT: “whirl pattern” of mesenteric vessels twisting about the volvulus axis

b

e.

fe

ks

ks

fre

e

m

b

o

Treatment • initial supportive management (same as initial management for bowel obstruction (see Large Bowel Obstruction, GS29) • cecum ■■ nonsurgical ◆◆ may attempt colonoscopic detorsion and decompression; successful 15-20% of cases ■■ surgical ◆◆ right colectomy + ileotransverse colonic anastomosis • sigmoid ■■ nonsurgical ◆◆ decompression by flexible sigmoidoscopy and insertion of rectal tube past obstruction ◆◆ subsequent elective surgery recommended (50-70% recurrence) ■■ surgical ◆◆ surgical resection with or without primary anastomosis ◆◆ ndications: strangulation, perforation, or unsuccessful endoscopic decompression

Cecal Volvulus AXR: Central cleft of “coffee bean” sign points to RLQ

o

om

om

Clinical Features • symptoms due to bowel obstruction (see Large Bowel Obstruction, GS29) or intestinal ischemia (see Intestinal Ischemia, GS23) • colicky abdominal pain, persistence of pain between spasms, abdominal distention, and vomiting

Sigmoid Volvulus AXR: Central cleft of “coffee bean” sign points to LLQ Barium enema: “ace of spades” or “bird’s beak” sign

r

m

eb

bo

Risk Factors • age (50% of patients >70 yr: stretching/elongation of bowel with age is a predisposing factor) • high fibre diet (can cause elongated/redundant colon), chronic constipation, laxative abuse, pregnancy, bedridden, and institutionalization (less frequent evacuation of bowels)

o

GS37 General Surgery and Thoracic Surgery

Toronto Notes 2018

c

Other Conditions of the Large Intestine

fre

Toxic Megacolon

oo

oo

k

Pathogenesis • extension of inflammation into smooth muscle layer causing paralysis • damage to myenteric plexus and electrolyte abnormalities are not consistently found

m

e

Etiology • inflammatory bowel disease (ulcerative colitis > Crohn’s disease) • infectious colitis: bacterial (C. difficile, Salmonella, Shigella, and Campylobacter), viral (cytomegalovirus), and parasitic (E. histolytica)

e

ee

co

co

Clinical Features • infectious colitis usually presents for >1 wk before colonic dilatation • diarrhea ± blood (sudden improvement of diarrhea may signify onset of megacolon) • abdominal distention, tenderness, ± local/general peritoneal signs (suggest perforation) • triggers: hypokalemia, constipating agents (opioids, antidepressants, loperamide, and anticholinergics), barium enema, and colonoscopy

eb

bo

ok

ok s

Diagnostic C iteria • must have both colitis and systemic manifestations for diagnosis • radiologic evidence of dilated colon • three of: fever, HR >120, WBC >10.5, and anemia • one of: fluid and electrolyte disturbances, hypotension, or altered LOC

m

om

Investigations • CBC (leukocytosis with left shift, and anemia from bloody diarrhea), electrolytes, elevated CRP, and ESR • metabolic alkalosis (volume contraction and hypokalemia) and hypoalbuminemia are late findings • AXR: dilated colon >6 cm (right > transverse > left), loss of haustra • CT: useful to assess underlying disease

ee

Use caution when giving antidiarrheal agents, espec ally with bloody diarrhea

m

m

e

oo

ok

ks

s

fe

ee

Treatment • NPO, NGT, stop constipating agents, correct fluid and electrolyte abnormalities, and transfusion • serial AXRs • broad-spectrum antibiotics (reduce sepsis, and anticipate perforation) • aggressive treatment of underlying disease (e.g. steroids in IBD, and metronidazole for C. difficile) • indications for surgery (50% improve on medical management) ■■ worsening or persisting toxicity or dilation after 48-72 h ■■ severe hemorrhage, perforation ■■ high lactate and WBC, especially for C. d fficile • procedure: subtotal colectomy + end ileostomy (may be temporary, with second operation for re-anastomosis later) Prognosis • average 25-30% mortality

Fistula

e

bo

o

Etiology • foreign object erosion (e.g. gallstone, graft) • inflammatory states (e.g. infection, IBD [Crohn’s > UC], and diverticular disease) • iatrogenic/surgery (e.g. post-operative anastomotic leak, and radiation) • congenital, trauma • neoplastic

om

Investigations • U/S, CT scan, fistulogram • measure amount of drainage from fistula

re

re

e

Treatment • decrease secretion: octreotide/somatostatin/omeprazole • surgical intervention: dependent upon etiology (for non-closing fistulas); uncertainty of diagnosis

Why Fistulae Stay Open

s

sf

fr

r

Definition • abnormal communication between two epithelialized surfaces (e.g. enterocutaneous, colovesical, aortoenteric, and entero-enteric)

FRIENDO Foreign body Radiation Infection Epithelialization Neoplasm Distal obstruction (most common) Others: increased flow; steroids (may inhibit closure, usually will not maintain fistula)

o

GS38 General Surgery and Thoracic Surgery

Toronto Notes 2018

c

Anorectum

fr

Stomas

eb

eb

o

o

ok

Definition • an opening of the GI tract onto the surface of the abdomen wall ■■ stomas can be constructed as either end stomas: the proximal end of the GI tract forms the stoma and the distal end of the GI tract is not part of the stoma, or loop stomas: a loop of the GI tract is brought up to the skin and the anti-mesenteric surface of the bowel is matured as a stoma. The proximal and distal GI tract remain in continuity

.c

Colostomy/Ileostomy • Connection of proximal limb of colon or ileum to abdominal wall skin Mucous Fistula • Connection of distal limb of colon to abdominal wall skin Ileal Conduit • Connection of bowel to ureter proximally and abdominal wall distally to drain urine

re e

fre

e

ee

co m

co m

Ileostomy • usually positioned in RLQ; ileum is brought through rectus abdominus muscles • indications: after protocolectomy for ulcerative colitis, in some cases of Crohn’s disease or familial polyposis • conventional ileostomy: discharges small quantities of liquid material continuously, appliance (plastic bag attached to a sheet of protective material) required at all times • continent ileostomy: reservoir is constructed from distal ileum, emptied by inserting catheter into stoma several times a day; rarely used, has mostly been replaced by ileal pouch anal anastomosis

o

eb

m

eb

bo

oo

k

ok s

Colostomy • indications: to decompress an obstructed colon, to protect a distal anastomosis after resection, or to evacuate stool after distal colon or rectum is removed • colostomies can be done by making an opening in a loop of colon (loop colostomy) or by dividing the colon and bringing out one end (end colostomy) • most common permanent colostomy is a sigmoid colostomy – expels stool once per day, no appliance required • chronic paracolostomy hernia is a common complication

o

Loop Colostomy

fe

e

e

om

m

Complications (10%) • obstruction: herniation, stenosis (skin and abdominal wall), adhesive bands, volvulus • peri-ileostomy abscess and fistula • skin irritation • prolapse or retraction • diarrhea (excessive output), which may lead to fluid, electrolyte and nutritional imbalances Removed

End Colostomy

(Distal)

Mucous Fistual

© Geoffrey Cheung 2010

Colostomy

e

Ileostomy

(Proximal)

End Colostomy

Figure 18. Ostomies

© Jean Yi-Chun Lin 2014

fr

fr

Figure 17. End vs. loop colostomy

o

Anorectum

b

Hemorrhoids

Etiology • vascular and connective tissue complexes form a plexus of dilated veins (cushion) • internal: superior hemorrhoidal veins, above dentate line, portal circulation • external: inferior hemorrhoidal veins, below dentate line, systemic circulation

Internal hemorrhoid

nferior rectal vein

Dentate line External hemorrhoid

Figure 19. Hemorrhoids

s

.

Risk Factors • increased intra-abdominal pressure: chronic constipation, pregnancy, obesity, portal HTN, heavy lifting

© Shelley Wall 2003

m

Middle rectal vein

o

GS39 General Surgery and Thoracic Surgery

Toronto Notes 2018

eb

m

Band ligation can be done as outpatient

m

om

fre

o

oo

e

m

External Hemorrhoids

Painless BRBPR

Sudden severe perianal pain

Rectal fullness or discomfort

Perianal mass

Mucus discharge

e

Anal Fissures

m

e

bo

oo

k

ok

Definition • tear of anal canal below dentate line (very sensitive squamous epithelium) • 90% posterior midline, 10% anterior midline • if off midline: consider other possible causes such as IBD, STIs, TB, leukemia, or anal carcinoma • repetitive injury cycle after first tear ■■ sphincter spasm occurs preventing edges from healing and leads to further tearing ■■ ischemia may ensue and contribute to chronicity

m

Etiology • forceful dilation of anal canal: large, hard stools and irritant diarrheal stools • tightening of anal canal secondary to nervousness/pain leads to further tearing • others: habitual use of stool bulking agents, and childbirth

m

m

eb

o

k

ok

sf

fre

re

Clinical Features • acute fissure ■■ very painful bright red bleeding especially after bowel movement, sphincter spasm on limited DRE ■■ treatment is conservative: stool softeners, bulking agents, and sitz baths (heals 90%) • chronic fissure (anal ulcer) ■■ triad: fissure, sentinel skin tags, and hypertrophied papillae ■■ treatment ◆◆ stool softeners, increased fibre intake, and sitz baths ◆◆ topical nitroglycerin or calcium channel blocker (nifedipine): increases local blood flow, promotes healing, and relieves sphincter spasm ◆◆ lateral internal anal sphincterotomy (most effective): objective is to relieve sphincter spasm → increases blood flow and promotes healing; but 5% chance of fecal incontinence therefore not commonly done ◆◆ alternative treatment: botulinum toxin: inhibits release of acetylcholine (ACh), reducing sphincter spasm

External hemorrhoids will often recur

c

e.

ok sf re

Table 17. Signs and Symptoms of Internal vs. External Hemorrhoids Internal Hemorrhoids

Always rule out more serious causes (e.g. colon CA or anal canal cancer) in a person with hemorrhoids and rectal bleeding

b

o

oo

ks

ks fre

Clinical Features and Treatment • internal hemorrhoids ■■ engorged vascular cushions usually at 3, 7, 11 o’clock positions (patient in lithotomy position) ■■ PAINLESS rectal bleeding, anemia, prolapse, mucus discharge, pruritus, burning pain, and rectal fullness ◆◆ 1st degree: bleed but do not prolapse through the anus – treatment: high fibre/bulk diet, sitz baths, steroid cream, parmoxine (Anusol®), rubber band ligation, sclerotherapy, and photocoagulation ◆◆ 2nd degree: bleed, prolapse with straining, and spontaneous reduction – treatment: rubber band ligation, and photocoagulation ◆◆ 3rd degree: bleed, prolapse, and requires manual reduction – treatment: same as 2nd degree, but may require closed hemorrhoidectomy ◆◆ 4th degree: bleed, permanently prolapsed, and cannot be manually reduced – treatment: closed hemorrhoidectomy • external hemorrhoids ■■ dilated venules usually mildly symptomatic ◆◆ PAIN after bowel movement, associated with poor hygiene ◆◆ medical treatment: dietary fibre, stool softeners, steroid cream (short course), parmoxine (Anusol®), and avoid prolonged straining ■■ thrombosed hemorrhoids are very painful ◆◆ resolve within 2 wk, may leave excess skin = perianal skin tag ◆◆ treatment: consider surgical decompression within first 48 h of thrombosis, otherwise medical treatment

s

c

Anorectum

o

GS40 General Surgery and Thoracic Surgery

Toronto Notes 2018

c

Anorectum

re

Anorectal Abscess

oo

ok

Definition • infection typically originating within an obstructed anal crypt which forms an abscess • common bacterial: E. coli, Proteus, Streptococci, Staphylococci, Bacteroides, and anaerobes

Supralevator space Supralevator abscess Levator muscle Column of Morgagni Internal sphincter Deep external sphincter

o

Intersphincteric abscess (origin)

External sphincter Perianal abscess Normal

Inflammed

© Cynthia Yoon 2003

e

Ischiorectal abscess

c

Figure 20. Different types of perianal abscesses

ok

sf

sf

r

re

Clinical Features • throbbing pain that may worsen with straining and ambulation • abscess can spread vertically downward (perianal), vertically upward (supralevator), or horizontally (ischiorectal) • tender perianal/rectal mass on exam

b

Treatment • I&D ■■ curative in 50% of cases ■■ 50% develop anorectal fistulas • may require antibiotics if diabetic, heart murmur, or cellulitis

Recurrent perianal abscesses is associated with Crohn’s disease

Antibiotics are not typically helpful in the treatment of perianal abscesses

om

Fistula-In-Ano

re

ee

Definition • fistula from anal canal to perianal skin • an inflammatory tract with internal os at dentate line, external os on skin

bo

o

oo

k

Etiology • see Fistula, GS37 • same processes that lead to the formation of an anal abscess • other causes: post-operative, trauma, anal fissure, malignancy, and radiation proctitis

m

Clinical Features • intermittent or constant purulent discharge from perianal opening • pain • palpable cord-like tract

ks

re

fre

Anterior Secondary opening Primary opening n crypt

e. c

e

Treatment • identification ■■ internal opening ◆◆ Goodsall’s rule – fistulas originating anterior to a transverse line through the anus will have a straight course and exit anteriorly, whereas those originating posterior to the transverse line will begin in the midline and have a curved tract ■■ fistulous tract ◆◆ probing or fistulography under anesthesia

Transverse anal line

Posterior

Figure 21. Goodsall’s rule

o

GS41 General Surgery and Thoracic Surgery

Toronto Notes 2018

c

Anorectum

Rectum

e

oo

ok

ks f

fr

• surgery ■■ fistulotomy: unroof tract from external to internal opening, allow drainage, heals by secondary intention ■■ low lying fistula (does not involve external sphincter) → primary fistulotomy ■■ high lying fistula (involves external sphincter) → staged fistulotomy with Seton suture placed through tract ◆◆ promotes drainage ◆◆ promotes fibrosis and decreases incidence of incontinence ◆◆ delineates anatomy ◆◆ usually done to spare muscle ■■ alternative for high lying fistula → LIFT (ligation of Intersphicteric fistula tract) procedure ◆◆ access fistula between sphincter muscles, sparring them Post-Operative • sitz baths, irrigation, and packing to ensure healing proceeds from inside to outside

Internal sphincter Fistula tract

External sphincter

Seton

Anus

Drainage © Agnes Chan 2013

c

c

Figure 22. Fistulotomy

Complications • recurrence • rarely fecal incontinence

o

Pilonidal Disease

m

e

e

eb

Definition • pilo = hair, nidal = nest; cyst or abscess near or on the intergluteal cleft of the sacrococcygeal area containing hair and skin debris Epidemiology • occurs most frequently in young men age 15-35 yr; rare in >50 yr

e.

e.

c

c

Etiology • obstruction of the hair follicles in this area → formation of cysts, sinuses, or abscesses • associated with occupations that require prolonged sitting, obesity, and high amounts of body hair

ks

sf

fr

Clinical Features • asymptomatic or chronically itchy until acutely infected, then pain/tenderness, purulent discharge, and increased moisture near the tailbone

m

m

e

bo

Treatment • acute abscess ■■ I&D (often performed by primary care doctors) ■■ wound packed open ■■ 40% develop chronic pilonidal sinuses • surgery ■■ indication: failure of healing after I&D, recurrent disease, or complex disease ■■ pilonidal cystotomy: excision of sinus tract and cyst; wound closed by secondary intention, primary closure with tissue flap, or marsupialization (cyst edge sewn to surrounding tissue to leave sinus tract open)

ee

Rectal Prolapse

k

k

Definition • protrusion of some or all of rectal mucosa through external anal sphincter

True rectal prolapse

o

ok

s

Risk Factors • gynecological surgery • chronic neurologic/psychiatric disorders affecting motility

External hemorrhoids

Figure 23 Rectal prolapse (true vs. false)

e.

om

ee

re

e

co

m

Etiology • lengthened attachment of rectum secondary to constant straining • 2 types 1. false/partial/mucosal: protrusion of mucosa only, radial furrows at junction with anal skin; most common type of rectal prolapse in childhood 2. true/complete (most common): full thickness extrusion of rectal wall, concentric folds in: ◆◆ first degree: prolapse includes mucocutaneous junction ◆◆ second degree: without involvement of mucocutaneous junction ◆◆ third degree (internal intussusception): prolapse is internal, concealed, or occult

© Katie McCormack

bo

Epidemiology • extremes of ages: 5th decade • 85% women

o

GS42 General Surgery and Thoracic Surgery

Toronto Notes 2018

Liver

oo

oo

ks fre

Clinical Features • extrusion of mass with increased intra-abdominal pressure • difficulty in bowel regulation ■■ tenesmus, constipation, fecal incontinence • permanently extruded rectum with excoriation, ulceration, and constant soiling • may be associated with urinary incontinence or uterine prolapse

om

Treatment • Type I ■■ conservative: gentle manual reduction of prolapsed area, especially in children ■■ mucosectomy with excision of redundant mucosa, mostly in adults • Type II ■■ conservative: reduce if possible ■■ surgery: abdominal, perineal, and transsacral approaches

e.

Anal Neoplasms

fr

ANAL CANAL

m

e

eb

bo

oo

o

Squamous Cell Carcinoma of Anal Canal (Above Dentate Line) • most common tumour of anal canal (75%) • anus prone to human papillomavirus (HPV) infection, therefore at risk for anal squamous intraepithelial lesions (ASIL) ■■ high grade squamous intra-epithelial lesion (HSIL) and low grade squamous intra-epithelial lesion (LSIL) terminology used • clinical features: anal bleeding, pain, mass, ulceration, and pruritus; 25% asymptomatic • treatment: chemotherapy ± radiation ± surgery • prognosis: 80% 5-yr survival

c

re

e.

c

Malignant Melanoma of Anal Canal • 3rd most common site for primary malignant melanoma after skin, eyes • aggressive, distant metastases common at time of diagnosis • treatment: wide excision or APR ± chemoradiation • prognosis: 4 cm

Only if symptomatic partial liver resection drainage

Complete excision of cysts liver transplant if cyst involves intrahepatic bile ducts (Caroli’s disease)

Albendazole (anti-helminthic) cure up to 30% Surgical (risk of spillage into abdomen): Conservative: open endocystectomy or PAIR (Percutaneous Aspiration, Injection of protoscolicidal agent, Re-aspiration) Radical: partial hepatectomy or total pericystectomy

All complex, multiloculated cysts (except echinococcal) should be excised because of malignancy risk

Complications

Intracystic hemorrhage

Biliary cirrhosis, portal HTN, rupture, cholangiocarcinoma Abnormal pancreaticobiliary junction is associated with increased risk of malignancy

Inferior vena cava compression rupture can cause biliary colic, jaundice, cholangitis, pancreatitis, or anaphylactic reaction

Cystadenocarcinoma can invade adjacent tissues and metastasize

oo

co m

e

m

c

fre

Liver Abscesses

o

m

e

o

o

Etiology • types ■■ pyogenic (bacterial): most common etiology; most often polymicrobial – E. coli, Klebsiella, Proteus, Strep. milleri ■■ parasitic (amoebic): Entamoeba histolytica, Echinococcal cyst ■■ fungal: Candida ■■ sources: direct spread from biliary tract infection, portal spread from GI infection, systemicinfection (e.g. endocarditis)

co

Clinical Features • fever, malaise, chills, anorexia weight loss, abdominal pain, and nausea • RUQ tenderness, hepatomegaly, and jaundice

sf

fre

re

Investigations • leukocytosis anemia, elevated liver enzymes, and echinocco al serology • U/S, CXR (right basilar atelectasis/effusion), CT, cyst aspiration with C&S, and MRI

eb

m

b

bo

o

Treatment • treat underlying cause • bacterial abscesses generally will treat initially with antibiotics, and add surgical or percutaneous drainage and IV antibiotics for larger abscesses (initially ceftriaxone + metronidazole or piperacillin/ tazobactam) • consider potential source of sepsis (e.g. biliary source, infected tumour)

m

Prognosis • overall mortality 15% – higher rate if delay in diagnosis, multiple abscesses, and malnutrition

m

m

eb

m

ks

re

m

bo

Treatment

m

Cystadenoma (Premalignant)/ Cystadenocarcinoma

oo

Hydatid (Cystic Echinococcosis)

e

Choledochal Cysts

om

Polycystic Liver Disease

e

Simple Cysts

o

k

Table 18. Characteristics of Liver Cysts

o

GS44 General Surgery and Thoracic Surgery

Toronto Notes 2018

Liver

fre

Neoplasms

k

BENIGN LIVER NEOPLASMS

m

b

Differential Diagnosis of Metastatic Liver Mass Some GU Cancers Produce Bumpy Lumps Stomach GenitoUrinary cancers (kidney, ovary, uterus) Colon Pancreas Breast Lung

e

co

co

b

bo

Hemangioma (cavernous) pathogenesis: most common benign hepatic tumour; results from malformation of angioblastic fetal tissue • risk factors: F:M = 3:1 • clinical features ■■ usually small and asymptomatic ■■ consumptive coagulopathy if giant (in children) • investigations ■■ contrast CT (well-demarcated hypodense mass with peripheral enhancement on arterial phase with centripetal filling on delayed phases), U/S (homogenous hyperechoic mass), MRI ■■ avoid biopsy: may result in hemorrhage • treatment ■■ usually none

m

m

eb

bo

ok

ok s

Focal Nodular Hyperplasia • pathogenesis: unclear, may be regenerative response to hyperperfusion from anomalous arteries at centre of nodule • risk factors: female, age 20-50 • clinical features: asymptomatic, rarely grows or bleeds, and no malignant potential • investigations: central stellate scar on CT scan; MRI, biopsy may be required • treatment: may be difficult to distinguish from adenoma/fibrolamellar HCC (malignant potential) ■■ if confirmed to be FNH → no treatment required

ok

k

s

c

e

Staging Criteria for Hepatocellular Carcinoma

re

re

ee

e.

.c

co

m

Adenoma • definition: benign glandular epithelial tumour • risk factors: female, age 20-50, estrogen (OCP, pregnancy), and obesity • clinical features: asymptomatic, 25% present with RUQ pain or mass, may present with bleeding • investigations: CT (well-demarcated masses, often heterogeneous enhancement on arterial phase, isodense on venous phase without washout of contrast), U/S, MRI, biopsy often needed • treatment ■■ stop anabolic steroids or OCP ■■ excise especially if large (>5 cm), due to risk of transformation to hepatocellular carcinoma and spontaneous rupture/hemorrhage

Milan Criteria*

1 tumour ≤5 cm Up to 3 tumours each ≤3 cm

UCSF Criteria*

1 tumour ≤6.5 cm Up to 3 tumours each ≤4.5 cm, total diameter ≤8 cm

Toronto Criteria*

No tumour size of number restrictions No systemic symptoms Not poorly differentiated

*Each criteria assumes no extrahepatic and no macrovascular invasion

e.

Child-Turcotte-Pugh Score (Prognosis of Chronic Liver Disease/Cirrhosis, Including Post-Operatively) 1 Point

2 Points

3 Points

Albumin (g/L)

>35

28-35

80%, at 5 yr: 60-70%

ee .

ee

co

m

Post-Operative Complications • primary non-function (graft failure): urgent re-transplantation is indicated • acute and chronic rejection, ischemia-reperfusion injury • vascular: hepatic artery or portal vein thrombosis, IVC obstruction • biliary complications: fever, increasing bilirubin and ALP • complications related to immunosuppression: HTN, renal disease, DM, obesity, hyperlipidemia, osteoporosis, malignancy, neurologic complications, infection (leading cause of mortality following transplant)

m

co

e

Living Donor Liver Transplantation vs. Deceased Donor Liver Transplantation for Hepatocellular Carcinoma: Comparable Survival and Recurrence Liver Transplant 2012;18:315-322 Purpose: To compare the overall survival and hepatocellular carcinoma (HCC) recurrence rates after living donor liver transplantation (LDLT) versus deceased donor liver transplantation (DDLT) in a series of patients with HCC Methods: Study conducted between 1996 and 2009 at a single centre 345 patients with HCC undergoing liver transp antation included. Results: The overall survival rates at 1, 3, and 5 yr did not significantly differ between the LDLT and DDLT groups (p=0.62). Disease free survival at 1, 3 and 5 yr did not differ between the groups (p=0.82). The recurrence rates at 1, 3, and 5 yr also did not differ between the two group (p=0.54). Conclusion: LDLT and DDLT lead to similar survival and recurrence rates.

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Contraindications • active alcohol/substance abuse • extrahepatic malignancy within 5 yr advanced cardiopulmonary disease • active uncontrolled infection

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Criteria for Transplantation • Model for End-Stage Liver Disease (MELD): prognostic model to estimate 3 mo survival and disease severity if patient does not receive transplant; based on creatinine, bilirubin, INR; MELD scores from 6-40 used to prioritize liver allocation • Child-Turcotte-Pugh Score: classification system to assess the prognosis and mortality of liver disease; patient must have ≥7 points (Class B)

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Clinical Indications • early referral for transplant should be considered for all patients with progressive liver disease not responsive to medical therapy, especially: ■■ decompensated cirrhosis (ascites, esophageal variceal hemorrhage, spontaneous hepatic encephalopathy, coagulopathy, progressive jaundice, severe fatigue) ■■ unresectable primary liver cancers ■■ fulminant hepatic failure • end-stage liver disease with life expectancy 16 x 109/L 3. Glucose >11 mmol/L 4. LDH ≥350 IU/L 5. AST >250 IU/L B. During initial 48 h 1. Hct drop >10% 2. BUN rise >1.8 mmol/L 3 Arterial PO2 4 mmol/L 5 Calcium 6 L C. Interpretation ≥2 = difficult course ≥3 = high mortality (≥15%)

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Investigations LFTs show obstructive picture • U/S, CT: bile ducts usually dilated, but not necessarily • ERCP or PTC: to determine resectability, for biopsies • CXR, bone scan: for metastatic workup

Obstructive jaundice is the most common presenting symptom for cholangiocarcinoma

o

GS51 General Surgery and Thoracic Surgery

Toronto Notes 2018

c

Pancreas

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Pancreas

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Acute Pancreatitis

b

• see Gastroenterology, G44

m

GALLSTONE PANCREATITIS (45% of Acute Pancreatitis)

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Pathogenesis • obstruction of pancreatic duct by large or small gallstones and biliary sludge • backup of pancreatic enzymes can cause autodigestion of the pancreas

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Clinical Features (Pancreatitis of Any Etiology) • pain (epigastric pain radiating to back), N/V, ileus, peritoneal signs, jaundice, and fever • Inglefinger’s sign: pain worse when supine, and better when sitting forward • may have coexistent cholangitis or pancreatic necrosis • Ranson’s criteria for determining prognosis of acute pancreatitis (see sidebar) • physical exam may show: tachypnea, tachycardia, hypotension, abdominal distention and tenderness, Cullen’s sign, and Grey Turner’s sign

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Investigations • lipase (most Sn and Sp), elevated amylase (higher than alcoholic pancreatitis), and leukocytosis • elevated ALT (>150 IU/L), AST strongly suggest gallstone etiology of pancreatitis • U/S may show multiple stones (may have passed spontaneously), and edematous pancreas • CXR, AXR, and CT (if severe to evaluate for complications)

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Treatment • supportive: e.g. NPO, hydration, analgesia, and early enteric nutrition • antibiotics for severe cases of necrotizing pancreatitis or signs of sepsis • stone often passes spontaneously (~90%); usually no surgical management in uncomplicated acute pancreatitis • cholecystectomy during same admission (25-60% recurrence if no surgery) • may need urgent ERCP + sphincterotomy if CBD stone impacted or cholangitis • surgical indications in acute pancreatitis (rare): ■■ drain placement and debridement for necrotizing pancreatitis if refractory to medical management, if septic or in ICU without other sources of sepsis

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Complications • Local complications ■■ acute fluid collections ■■ walled-off pancreatic fluid collection/pseudocyst (>4 wk old) ■■ abscess/infection, necrosis • Systemic complications ■■ splenic/mesenteric/portal vessel thrombosis ■■ pancreatic ascites/pancreatic pleural effusion ■■ DM (b/c pancreatic & insulin insufficiency) ■■ ARDS/sepsis/multiorgan failure ■■ coagulopathy/DIC ■■ severe hypocalcemia

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Chronic Pancreatitis

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• see Gastroenterology, G45

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Surgical Treatment • treatment is generally medical • indications for surgery ■■ failure of medical treatment ■■ debilitating abdominal pain ■■ pseudocyst complications: persistence, hemorrhage, infection, and rupture ■■ CBD obstruction (e.g. stric ures), and duodenal obstruction ■■ pancreatic fistula, variceal hemorrhage secondary to splenic vein obstruction ■■ rule out pancreatic cancer (present in 15% of chronic pancreatitis treated surgically) ■■ anatomical abnormality causing recurrent pancreatitis • pre-operative CT and/or ERCP are mandatory to delineate anatomy • minimally invasive options ■■ endoscopic pancreatic duct decompression: less effective than surgery ■■ extracorporeal shockwave lithotripsy: if pancreatic duct stones ■■ celiac plexus block: lasting benefit in 30% patients, less effective in those 3 d) or major surgery within past 4 wk (1) • Localized tenderness in deep vein system (1) • Swelling of entire leg (1) • Calf swelling >3 cm than other leg (measured 10 cm below the tibial tuberosity) (1) • Pitting edema greater in the symptomatic leg (1) • Collateral non-varicose superficial veins (1) • Active cancer or cancer treated within 6 mo (1) • Alternative diagnosis more likely than DVT (e.g. Baker's cyst, cellulitis, muscle damage, superficial venous thrombosis) (-2)

m

m

Investigations for DVT • D-dimer test only useful to rule out DVT if negative with low clinical suspicion of disease and no other acute medical issues • doppler ultrasound is most useful diagnostic test for DVT ■■ sensitivity and specificity for proximal DVT ~95% ■■ sensitivity for calf DVT ~70% • other non invasive tests include MRI and impedence plethysmography • venography is the gold standard, but is expensive, invasive, and higher risk • CTPA or V/Q scan if PE suspected

P-value 0.007

Total Score Interpretation 3-8: High probability 1-2 Moderate probability, -2-0: Low probability

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Differential Diagnosis of DVT • muscle strain or tear, lymphangitis or lymph obstruction, venous valvular insufficiency, ruptured popliteal cysts, cellulitis, arterial occlusive disease

RR (95% CI) 1.79 (1.18-2.71) 1.58 (1.01-2.51) 1.67 (1.01-2.77) 0.94 (0.59-1.51) 0.51 (0.08-3.38)

Low Molecular-Weight Heparin vs. Coumarin for the Prevention of Recurrent Venous Thromboembolism in Patients with Cancer NEJM 2003;349:146-153 Study: RCT comparing the efficacy of LMWH (dalteparin) with an oral anti-coagulant agent (coumarin) in preventing recurrent thrombosis in patients with cancer. Methods: Patients with cancer who had acute symptomatic proximal DVT, PE, or both were randomly assigned to either dalteparin or coumarin treatment for 6 mo. Results: 27 of 336 patients in the dalteparin group had recurrent VTE versus 53 of 336 patients in the coumarin group (hazard ratio, 0.48; p=0.002). The probability of recurrent thromboembolism at 6 mo was 9% and 17% in dalteparin and coumarin groups respectively. There was no significant difference in bleeding rates. The mortality rate was 39% in the dalteparin group and 41% in the coumarin group. Conclusions: In patients with cancer and acute VTE, dalteparin was more effective than coumarin in decreasing the risk of recurrent thromboembolism without increasing the risk of bleeding.

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Clinical Features of DVT • absence of physical findings does not rule out disease • unilateral leg edema, erythema, warmth, and tenderness; purple-blue colour • palpable cord (thrombosed vein) • phlegmasia alba dolens (white appearance) and phlegmasia cerula dolens (acute pain and edema) with massive thrombosis • Homan’s sign (pain with foot dorsiflexion) is unreliable

Risk Factor Age >75 yr Cancer Previous VTE Obesity Hormone therapy

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Etiology (Virchow’s Triad) • endothelial damage ■■ exposes endothelium to prompt hemostasis ■■ leads to decreased inhibition of coagulation and local fibrinolysis • venous stasis ■■ immobilization (post-MI, CHF, stroke, post-operative) inhibits clearance and dilution of coagulation factors • hypercoagulability ■■ inherited (see Hypercoagulable Disorders, H33) ■■ acquired ◆◆ age (risk increases with age) ◆◆ surgery (especially orthopedic, thoracic, GI, and GU) ◆◆ trauma (especially fractures of spine, pelvis, femur or tibia, spinal cord injury) ◆◆ neoplasms (especially lung, pancreas, colon, rectum, kidney, and prostate) ◆◆ blood dyscrasias (myeloproliferative neoplasms, especially PV, ET), PNH, hyperviscosity (multiple myeloma, polycythemia, leukemia, sickle cell disease) ◆◆ prolonged immobilization (CHF, stroke, MI, leg injury) ◆◆ hormone related (pregnancy, OCP, HRT, SERMs) ◆◆ APS ◆◆ heart failure (risk of DVT greatest with right heart failure and peripheral edema) • idiopathic (10-20% are later found to have cancer)

Risk of VTE in Hospitalized Patients Receiving Ineffective Antithrombotic Therapy

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Definition • thrombus formation and subsequent inflammatory response in a superficial or deep vein • superficial thrombophlebitis, deep vein thrombosis (DVT), and pulmonary embolism (PE) • thrombi propagate in the direction of blood flow (commonly originating in calf veins) • more common in lower extremity than upper extremity • incidence ~1% if age >60 yr • most important sequelae are pulmonary embolism (~50% chance with proximal DVT) and chronic venous insufficiency

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Venous Thromboembolism

H36 Hematology

Toronto Notes 2018

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Venous Thromboembolism

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Approach to Treatment of Venous Thromboembolism

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Initiation of Warfarin Therapy Requires Bridging with Heparin Therapy for 4-5 Days • 10 mg loading dose (for example) of warfarin causes a precipitous decline in protein C levels in first 36 h resulting in a transient hypercoagulable state • Warfarin decreases Factor VII levels in first 48 h, INR is prolonged (most sensi ive to Factor VII levels), however full antithrombotic effect is not achieved until Factor IX, X, and II are sufficiently reduced (occurs after ~4 d)

Low Risk Surgical Patients 1 risk factor for VTE, GA >30 min

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High Risk Surgical Patients >40 yr, surgery for malignancy or lower extremity orthopedic surgery lasting >30 min, inhibitor deficiency or other risk factor High Risk Medical Patients Hea t failure, severe respiratory disease, ischemic stroke and lower limb paralysis, confined to bed and have >1 additional risk factor (e.g. active cancer, previous VTE, sepsis, acute neurologic disease, IBD)

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Common Medications that Interact with Warfarin • Acetaminophen (interference with vitamin K metabolism) • Allopurinol • NSAIDs (GI injury) • Fluconazole • Metronidazole • Sulfamethoxazole • Tamoxifen

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Long-Term Treatment • anticoagulation therapy ■■ warfarin ■■ standard treatment; should be initiated with heparin overlap: dual therapy for at least 48 hours with INR >2, due to initial prothrombotic state secondary to warfarin’s inhibition of natural anticoagulants protein C/S, half-life of vitamin K factors and risk of warfarin-induced skin necrosis ■■ INR: warfarin dosed to maintain INR at 2-3, monitor twice weekly for 1-2 wk. Discontinue heparin after INR>2.0 for 2 consecutive days ■■ direct oral anticoagulants (DOACs) ◆◆ apixaban or rivaroxaban; with no laboratory monitoring required, patients with CrCl > 50 ml/ min ◆◆ dabigatran (factor IIa inhibitor): LMWH or IV heparin for at least 5-10 days before initiating dabigatran, patients with CrCl >30 mL/min ◆◆ important drug interactions to consider for DOACs (no relevant food interactions however) ■■ cancer patients: LMWH more effective than warfarin at preventing recurrence of venous thrombosis in cancer patients • duration of anticoagulant treatment ■■ provoked VTE with transient risk factor: 3 mo ■■ provoked VTE with ongoing risk factor: consider indefinite therapy with annual reassessment ■■ first unprovoked VTE: at least 3 mo, subsequent reassessment ■■ unprovoked proximal DVT or PE: consider indefinite therapy with annual reassessment ■■ second unprovoked VTE: consider indefinite therapy ■■ cancer-associated DVT: at least 3 mo, longer if continued evidence of cancer • IVC filtres ■■ temporary filter indicated only if acute DVT (35% (41.9% vs. 0.7%) and this was sustained in 67% at 48 wk. Ruxo itinib also led to greater symptom improvement (45% vs. 5.3%) and less mortality (13 vs 24) There was no difference in rate of discontinuation due to adverse events (11.0% vs. 10.6%) but anemia and thrombocytopenia were more common with ruxolitinib. Conclusions: Ruxolitinib reduced spleen size, improved symptoms and improved survival, compared with placebo.

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Treatment • allogeneic stem cell transplant is potentially curative • JAK2 inhibitors (Ruxolitinib) • symptomatic treatment ■■ transfusion for anemia ■■ erythropoietin: 30-50% of patients respond ■■ androgens for anemia (e.g. danazol has shown transient response with response rates of 65; hemoglobin 25,000/ mm3; circulating blast cells ≥1% ■■ based on the calculated score, a patient’s IMF is categorized as “low”, “intermediate 1”, “intermediate 2”, or “high” with a mean survival of 185, 78, 35, and 16 mo, respectively • risk of transformation to AML (8-10%)

Essential Thrombocythemia

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Definition • overproduction of platelets in the absence of recognizable stimulus • must rule out secondary thrombocythemia

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Epidemiology • increases with age; F:M = 2:1, but F=M at older age

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Treatment • low dose ASA if previous history of thrombotic event, ≥1 cardiovascular risk factors, older, or symptomatic • cytoreductive therapy if thrombosis or thrombotic symptoms: hydroxyurea (HU) (1st line therapy), anagrelide, interferon-α, or 32P (age >80 or lifespan 1,000 x 10⁹/L) • constitutional symptoms, splenomegaly • pregnancy complications; increased risk of spontaneous abortion • risk of transformation to AML (0.6-5%), myelofibrosis

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Anagrelide vs. Hydroxyurea for Essential Thrombocythemia: ANAHYDRET Study, A Randomized Controlled Trial Blood 2013;121:1720-8 Study: Prospective, non-inferiority, RCT. Majority of patients followed beyond 1 yr. Population: 259 previously untreated, high-risk patients with essential thrombosis as per the WHO guidelines. Intervention: Patients were randomized to receive either non-immediate release formulation of anagrelide or hydroxyurea. Outcome: Examined platelet counts, hemoglobin levels, leukocyte coun s, and occurrence of ETrelated events. Results: The hazard ratio (HR) of developing thrombocythem a was 1.19 (95% CI 0.61-2.30). The HR for a reduction of hemoglobin was 1.03 (95% CI 0.57-1.81), and 0.92 (95% CI 0.57-1.46) for leukocytosis. There was no statistical difference in occurrence of major or minor arterial or venous thrombosis, severe or minor bleeding events, or rate of discontinuation between the two arms. Conclusions: In patients with ET, anagrelide is non-inferior to hydroxyurea in the prevention of thrombotic complications.

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Diagnosis (2008 WHO Criteria) requires meeting all four criteria: 1. sustained platelet count >450 x 10⁹/L 2. bone marrow biopsy specimen showing proliferation mainly of the megakaryocytic lineage with increased number of enlarged, mature megakaryocytes; no significant increase or left shift of neutrophil granulopoiesis or erythropoiesis 3 not meeting WHO criteria for PV, primary myelofibrosis, bcr-abl CML, or myelodysplastic syndrome or other myeloid neoplasms 4. demonstration of JAK2 V617F or calreticulin (or in its absence another clonal marker), no evidence for reactive thrombocytosis

H44 Hematology

Toronto Notes 2018

c

Lymphoid Malignancies

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Lymphoid Malignancies

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Acute Lymphoblastic Leukemia

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Definition • malignant disease of the bone marrow in which early lymphoid precursors proliferate and replace the normal hematopoietic cells of the marrow • WHO subdivides ALL into two types depending on cell of origin ■■ 1. B-cell: precursor B lymphoblastic leukemia ■■ 2. T-cell: precursor T lymphoblastic leukemia • the French-American-British (FAB) classification (L1, L2, L3) is no longer encouraged, as morphology is not prognostic

75% of ALL occurs in children 10 x 10⁹/L (occurs in 50% of patients); neutropenia, anemia, or thrombocytopenia • may have increased uric acid, K+, PO43-, Ca2+, LDH • PT, aPTT, fibrinogen, D-dimers for DIC • leukemic lymphoblasts lack specific morphological (no granules) or cytochemical features, therefore diagnosis depends on immunophenotyping • cytogenetics: Philadelphia (Ph) chromosome in ~25% of adult ALL cases • CXR: patients with ALL may have a mediastinal mass • LP prior to systemic chemotherapy to assess for CNS involvement (ensure adequate platelet count and PT/PTT)

m

Treatment of ALL vs. AML • No proven benefit of maintenance chemotherapy in AML • No routine CNS prophylaxis in AML

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Treatment • eliminate abnormal clonal cells 1. induction chemotherapy: to induce complete remission (undetectable leukemic blasts, restore normal hematopoiesis) 2. consolidation and/or intensification of chemotherapy ◆◆ consolidation: continuing same chemotherapy to eliminate subclinical leukemic cells ◆◆ intensification: high doses of different (non-cross-reactive) chemotherapy drugs to eliminate cells with resistance to primary treatment 3. maintenance chemotherapy: low dose intermittent chemotherapy over prolonged period (2-3 yr) to prevent relapse 4. prophylaxis: CNS radiation therapy or methotrexate (intrathecal or systemic) • hematopoietic stem cell transplantation: potentially curative (due to pre-implant myeloablative chemoradiation and post-implant graft-versus-leukemia effect) but relapse rates and non-relapse mortality high

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Prognosis • depends on response to initial induction or if remission is achieved following relapse • good prognostic factors: young, WBC 5 yr) ■■ higher cure rates in children because of better chemotherapy tolerance, lower prevalence of BCRAbl fusion gene (associated with chemotherapeutic resistance) • adult ALL: 30-40% 5 yr survival Table 32. Differentiating AML From ALL

Small blasts

Big mortality rate

Small mortality rate (kids)

Lots of cytoplasm

Less cytoplasm

Lots of nucleoli (3-5)

Few nucleoli (1-3)

Lots of granules and Auer rods

No granules

Myeloperoxidase, Sudan black stain

PAS (periodic acid-Schiff)

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Maturation defect beyond myeloblast or promyelocyte

Maturation defect beyond lymphoblast

To Differentiate AML From ALL: Remember Big and SmALL

.c

Small people (kids)

Big blasts

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ALL

Big people (adults)

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AML

H45 Hematology

Toronto Notes 2018

c

Lymphomas

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Lymphomas

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Definition • collection of lymphoid malignancies in which malignant lymphocytes accumulate at lymph nodes and lymphoid tissues ■■ leading to lymphadenopathy, extranodal disease, and constitutional symptoms

American Society of Hematology Choosing Wisely Recommendation Limit surveillance CT scans in asymptomatic patients after curative-intent treatment for aggressive lymphoma

Table 33. Ann Arbor System for Staging Lymphomas

II

Involvement of two or mo e lymph node regions or an extralymphatic site and one or more lymph node regions on same side of diaphragm

III

Involvement of lymph node regions on both sides of the diaphragm; may or may not be accompanied by single extra lymphatic site or splenic involvement

IV

Diffuse involvement of one or more extralymphatic organs including bone marrow

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• subtypes ■■ A = absence of B-symptoms (see Approach to Lymphadenopathy, H12) ■■ B = presence of B-symptoms

• Ann Arbor staging can be used for both Hodgkin and non-Hodgkin lymphoma, but grade/histology is more important for nonHodgkin lymphoma because the outcome differs significantly depending on type of lymphoma • Prognostic scores are different for indolent versus aggressive lymphomas • Highly aggressive lymphomas act like acute leukemias

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Involvement of a single lymph node region OR extralymphatic organ/site (Stage IE)

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Description

I

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Stage

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Table 34. Chromosome Translocations Translocation

Gene Activation

Associated Neoplasm

t(2;5)

ALK1 mutation

Anaplastic large cell lymphoma

t(8;14)

c-myc activation

Burkitt’s lymphoma

bcl-2 activation

Follicular lymphoma

Overexpression of cyclin D1 protein

Mantle cell lymphoma

t(11;18)

MALT1 activation

Mucosa-associated lymphoid tissue (MALT)

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t(14;18) t(11;14)

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Hodgkin Lymphoma

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Clinical Features • asymptomatic lymphadenopathy (70%) ■■ non-tender, rubbery consistency ■■ cervical/supraclavicular (60-80%), axillary (10-20%), inguinal (6-12%) • splenomegaly (50%) ± hepatomegaly • mediastinal mass ■■ found on routine CXR, may be symptomatic (cough) ■■ rarely may present with SVC syndrome, pleural effusion • systemic symptoms ■■ B symptoms (especially in widespread disease; fever in 30%), pruritus • non-specific/paraneoplastic ■■ alcohol-induced pain in nodes, nephrotic syndrome • starts at a single site in lymphatic system (node), spreads first to adjacent nodes ■■ disease progresses in contiguity with lymphatic system

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Investigations • CBC ■■ anemia (chronic disease, rarely hemolytic), eosinophilia, lymphopenia, platelets normal or increased early, decreased in advanced disease • biochemistry ■■ HIV serology ■■ liver enzymes and/or LFTs (liver involvement) ■■ renal function tests (prior to initiating chemotherapy) ■■ ALP, Ca2+ (bone involvement) ■■ ESR, LDH (monitor disease progression) • imaging ■■ CXR, CT chest (lymph nodes, mediastinal mass), CT abdomen/pelvis (liver or spleen involvement), PET scans have replaced gallium scans

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Hodgkin lymphoma classically presents as a painless, non-tender, firm, rubbery enlargement of superficial lymph nodes, most often in the ce vical region

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Epidemiology • bimodal distribution with peaks at 20 yr and >50 yr • association with Epstein-Barr virus in up to 50% of cases, causal role not determined

Hodgkin is distinguished from non-Hodgkin lymphoma by the presence of Reed-Sternberg cells

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Definition • malignant proliferation of lymphoid cells with Reed-Sternberg cells (thought to arise from germinal centre B-cells)

H46 Hematology

Toronto Notes 2018

c

Lymphomas

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■■ cardiac function assessment (MUGA scan or echocardiography): for patients at high risk of pretreatment cardiac disease (age >60, history of HTN, CHF, PUD, CAD, MI, CVA, malnourished), treatment can be cardiotoxic ■■ PFTs: if history of lung disease (COPD, smoking, previous radiation to lung) • excisional lymph node or core biopsy confirms diagnosis • bone marrow biopsy to assess marrow infiltration (only necessary if B-symptoms, stage III or IV, bu ky disease or cytopenia)

Treatment of HL depends on stage; treatment of NHL depends on histologic subtype

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Treatment • stage I-II: chemotherapy (ABVD) followed by involved field or involved site radiotherapy (XRT) • stage III-IV: chemotherapy (ABVD) with XRT for bulky disease • relapse, resistant to therapy: high dose chemotherapy, autologous stem cell transplant ■■ PET scan results essential in clarifying disease response

e

International Prognostic Factors Project 1998 Prognostic Factors FFP 0 84% 1 77% 2 67% 3 60% 4 51% 5-7 42% FFP = freedom from progression at 5 yr

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Prognosis • Hasenclever adverse prognostic factors: 1. serum albumin 4 nodal areas; elevated LDH; Lugano stage III-IV; hemoglobin 60; Ann Arbor stage (III-IV); performance status (ECOG/Zubrand 2-4); elevated LDH; >1 extranodal site ■■ based on calculated risk, mean 5 yr survival ranges from 26-73% ■■ ~40% rate of cure Burkitt Lymphoma

Mantle Cell Lymphoma

Percentage of NHLs

22-30%

33%

F

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Pathophysiology • accumulation of neoplastic lymphocytes in blood, bone marrow, lymph nodes, and spleen

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Investigations • CBC: clonal population of B lymphocytes >5 x 10⁹/L • peripheral blood film ■■ lymphocytes are small and mature ■■ smudge cells • flow cytometry (CD5, CD20dim, CD23) • cytogenetics: FISH (dictates response therapy and prognosis) • bone marrow aspirate ■■ lymphocytes >30% of all nucleated cells ■■ infiltration of marrow by lymphocytes in 4 patterns: nodular (10%), interstitial (30%), diffuse (35% worse prognosis), or mixed (25%)

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Natural History and Treatment • natural history: indolent and incurable; most cases show slow progression • small minority present with aggressive disease; usually associated with chromosomal abnormalities (e.g. p53 deletion) • first line therapy is dictated by cytogenetic status and patient co-morbidities ■■ observation if early, stable, asymptomatic ■■ treatment options vary by region; ideal first line therapy should include a monoclonal CD20 agent (e.g. rituximab, obinutuzumab) ◆◆ commonly fludarabine + cyclophosphamide + rituximab (FCR) in fit patients with normal CrCl; bendamustine + rituximab (BR) in less fit ◆◆ chlorambucil + anti-CD20 obinutuzumab in the elderly ■■ corticosteroids, IVIg: especially for autoimmune phenomenaradiotherapy • molecular therapies ■■ Idelalisib – PI3K inhibitor ■■ Ibr tinib – BTK (Bruton’s tyrosine kinase) inhibitor

Smudge cells are artifacts of damaged lymphocytes from slide preparation

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Clinical Features • 25% asymptomatic (incidental finding) • 5-10% present with B-symptoms (≥1 of: unintentional weight loss ≥10% of body weight within previous 6 mo temperature >38ºC or night sweats for ≥2 wk without evidence of infection, extreme fatigue) • lymphadenopathy (50-90%), splenomegaly (25-55%), hepatomegaly (15-25%) • immune dysregulation: autoimmune hemolytic anemia (DAT positive), ITP, hypogammaglobulinemia ± neutropenia • bone marrow failure: late, secondary to marrow involvement by CLL cells

H49 Hematology

Toronto Notes 2018

c

Malignant Clonal Proliferations of Mature B-Cells

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Prognosis • 9 yr median survival, but varies greatly • prognosis predicted by Rai staging and cytogenetic status • low risk: ymphocytosis in blood and bone marrow only • intermediate risk: lymphocytosis with enlarged nodes in any site or splenomegaly, hepatomegaly • high risk: lymphocytosis with disease-related anemia ( 0.5 cm Calcium > 2.80 mmol/L Renal failure (Cr > 176 mmol/L) Anemia Bony lesions (lytic lesions or osteoporosis felt to be caused by myeloma)

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Definition • neoplastic clonal proliferation of plasma cells producing a monoclonal immunoglobulin resulting in end organ dysfunction • usually single clone of plasma cells, although biclonal myeloma also occurs; rarely non-secretory

H50 Hematology

Toronto Notes 2018

c

Malignant Clonal Proliferations of Mature B-Cells

m

Routine urinalysis will not detect light chains as dipstick detects albumin. Need sulfosalicylic acid or 24 h urine protein for immunofixation or electrophoresis

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Light Chain Disease 15% of MM produce only light chains Renal failure is a major problem Kappa > lambda light chain has better prognosis

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Investigations • CBC ■■ normocytic anemia, thrombocytopenia, leukopenia ■■ rouleaux formation on peripheral film • biochemistry ■■ increased Ca2+, increased ESR, decreased anion gap, increased Cr, albumin, β2-microglobulin (as part of staging), proteinuria (24 h urine collection) monoclonal proteins ■■ serum protein electrophoresis (SPEP): demonstrates monoclonal protein spike in serum in 80% (i.e. M protein) ■■ urine protein electrophoresis (UPEP): demonstrates light chains in urine = Bence-Jones protein (15% secrete only light chains) ■■ immunofixation: demonstrates M protein and identifies Ig type; also identifies light chains ■■ serum free light chain quantification: kappa and lambda light chains, calculated ratio • bone marrow aspirate and biopsy ■■ often focal abnormality, greater than 10% plasma cells, abnormal morphology, clonal plasma cells; send for FISH or cytogenetics (prognostic implications) • skeletal series (X rays), MRI if symptoms of cord compression ■■ presence of lytic lesions and areas at risk of pathologic fracture ■■ bone scans are not useful since they detect osteoblast activity • β2-microglobulin, LDH, and CRP are poor prognosticators

m

m

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b

Diagnosis • International Myeloma Working Group Criteria 1. serum or urinary monoclonal protein 2. presence of clonal plasma cells in bone marrow (>60% without “CRAB”) or a plasmacytoma 3. presence of end-organ damage related to plasma cell dyscrasia, such as: ◆◆ increased serum Ca2+ ◆◆ lytic bone lesions ◆◆ anemia ◆◆ renal failure

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Prognosis • ISS - International Staging System (β2-microglobulin and albumin) used to stage and estimate prognosis • revised ISS for risk stratification: combination of original ISS, cytogenetic profile (i.e. p53 mutation associated with poor survival and resistance to chemotherapy) and LDH • median survival based on stage, usually 3-7 yr

Serum Free Light Chain Ratio is an Independent Risk Factor for Progression in MGUS Blood 2005;106:812-817 Purpose: To determ ne whether the presence of monoclonal free kappa or lambda immunoglobulin light chains in MGUS increases the risk of progression to malignancy. Methods Retrospective study with median follow-up of 15 yr. Baseline serum samples obtained from 1,383 MGUS patients seen at the Mayo clinic between 1960-1994. 1,148 baseline samples were obtained within 30 d of diagnosis. Results: Malignant progression had occurred in 87 (7.6%) patients. In 379 (33%) patients, an abnormal serum free light chain (FLC) ratio was detected. There was a significantly higher risk of progression in patients with an abnormal FLC atio relative to patients with a normal ratio (hazard ratio, 3.5; 95% Cl 2.3-5.5; p70 yr of age ■■ asymptomatic

fr

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Diagnosis • presence of a serum monoclonal protein (M protein) at a concentration 1 h apart ■■ persistent bacteremia is the hallmark of endovascular infection (such as IE) • repeat blood cultures (at least 2 sets) after 48-72 h of appropriate antibiotics to confirm clearance • blood work: CBC and differential (normochromic, normocytic anemia), ESR (increased), RF (+), BUN/ Cr • urinalysis (proteinuria, hematuria, red cell casts) and urine C&S • ECG: prolonged PR interval may indicate perivalvular abscess • echo findings: vegetations, regurgitation, abscess ■■ TTE (poor sens tivity) inadequate in 20% (obesity, COPD, chest wall deformities) ■■ TEE indicated if TTE is non-diagnostic in patients with at least possible endocarditis or if suspect prosthetic valve endocarditis or complicated endocarditis (e.g. paravalvular abscess/perforation) (~90% sensitivity)

ID18 Infectious Diseases

Toronto Notes 2018

c

CNS Infections

fr

CNS Infections

o

Meningitis

• see Pediatrics, P54 Definition • inflammation of the meninges Etiology

Age >3 mo

GBS E. coli S. pneumoniae N. meningitidis H. influenzae

S. pneumoniae N. meningitidis L. monocytogenes (age >50 and comorbidities)

Cryptococcus Coccidioides

Lyme disease Neurosyphilis TB

c

HSV-1, 2 VZV Enteroviruses Parechoviruses West Nile

m

co

co

m

m

Risk Factors • lack of immunization against H. influenzae type b, S. pneumoniae, and N. meningitidis in children • most cases of bacterial meningitis are due to hematogenous spread from a mucosal surface (nasopharynx) • direct extension from a parameningeal focus (otitis media, sinusitis) less common • penetrating head trauma • anatomical meningeal defects – CSF leaks • previous neurosurgical procedures, shunts • immunodeficiency (corticosteroids, HIV, asplenia, hypogammaglobulinemia, complement deficiency) • contact with colonized or infected persons

Markedly Increased

Increased

WBC

500-10,000/µL

10-500/µL

Neutrophils

Lymphocytes

k

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Predominant WBC

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Treatment • bacterial meningitis is a medical emergency: do not delay antibiotics for CT or LP • empiric antibiotic therapy ■■ age ≤28 days: ampicillin + cefotaxime ■■ age 29 days-3 mo: cefotaxime + vancomycin ■■ age >3 mo: ceftriaxone + vancomycin
 ◆◆ add ampicillin IV if risk factors for infection with L. monocytogenes present: age >50, alcoholism, immunocompromised • steroids in acute bacterial meningitis: dexamethasone IV within 20 min prior to or with first dose of antibiotics ■■ continue in those patients with proven pneumococcal meningitis ■■ not recommended for patients with suspected bacterial meningitis in some resource-limited countries ■■ not recommended for neonatal meningitis

e

m

co

e

Protein (g/L)

m

Normal

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Viral

Decreased

Does this Adult Patient Have Acute Meningitis? From The Rational Clinical Examination JAMA 2009; http://www.jamaevidence.com/ content/3482857 Study: Systematic review of articles assessing the sensitivity and specificity of clinical exam maneuvers for the diagnosis of adult meningitis. Results: In retrospective studies, sensitivity for headache was 68%, and 52% for nausea and vomiting. Sensitivity for physical exam findings is similarly low (fever: 87%, neck stiffness: 80%, altered mental status: 69%). Sensitivity for the combination of the classic triad of fever, neck stiffness, and altered mental status was 46%. In prospective studies, sensitivity of H/A was 92% while sensitivity of N/V could not be pooled, and ranged from 32-70%. Brudzinski’s and Kernig’s signs had a sensitivity of 5% and Kernig’s sign only 5-9%. Jolt accentuation had a sensitivity of 97%. Conclusions: Data were heterogeneous, and lacked standardization of c inical exams. No single item on clinical history or physical exam was sufficient to rule out meningitis, including Kernig’s and Brudzinski’s signs, or the absence of the classic triad of fever, neck stiffness, and altered mental status meningitis. Jolt accentuation has high sensitivity, but further research is needed. LP may be performed safely without CT head in patients without altered LOC, no recent seizure, no history of CNS disease, not immunocompromised, and 5 mm if immunocompromised, close contact with active TB >10 mm all others; positive PPD → CXR; decision to treat depends on individual risk factors False(–): poor technique, anergy, immunosuppression, infection 2 large i.e. segmental mismatched perfusion defects), intermediate, low, very low, or normal according to modified PIOPED II criteria although now are increasingly reported as PE present, indeterminate or normal ■■ useful in finding clinically important emboli ■■ decreased detection of incidentalomas commonly found on CT • not valid for assessment of PE when patients have consolidation and the test can be limited by ventilatory problems (e.g. COPD), much like CT • modified V/Q scan (perfusion only, lower dose contrast) may be used for pregnant patients if CXR is normal or if there are ventilatory problems

V/Q Scan For PE investigation: normal scan makes PE unlikely Probability of PE: high 80-100%, intermediate 20-80%, low 38% is normal) can be measured after a fatty meal or CCK to assess for biliary dyskinesia

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RBC Scan • IV injection of radiotracer with sequential images of the abdomen (99mTc RBCs) • GI bleed ■■ if bleeding acutely at 0.5 mL/min, use angiography (more specific) • liver lesion evaluation ■■ hemangioma has characteristic appearance: cold early (limited blood flow to lesion), fills n later (accumulation of tagged cells greater than surrounding liver parenchyma)

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m

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Other Important Nuclear Medicine Abdominal Tests • Meckel’s Scan: uses 99mm pertechnetate; give patient ranitidine premedication; Meckel’s diverticulum contains gastric mucosa which will light up at the same time as the stomach and get brighter with time like stomach • 111In octreoscan: a somatostatin analog used for evaluation and staging of neuroendocrine tumours including carcinoid; gastrinoma and carcinoid tend to be more octreotide avid than insulinoma. • iodinated MIBG: a norepinephrine analogue, used for pheochromocytoma, neuroblastoma and medullary thyroid cancer most commonly; limited cardiac applications as above • solid and liquid gastric emptying: a standardized solid or liquid meal is labelled, usually with 99m Tc sulfur colloid and gastric emptying studied over time. There are normal ranges for solids and liquids

eb

b

o

bo

o

Urea Breath Test • indication: diagnosis of gastric Helicobacter pylori infection • patient administered 14C-labelled urea orally, urea metabolized by H. pylori to ammonia and 14CO2, 14 C-labled CO2 is measured via plastic filament detectors or liquid scintillation

.c om

e. c

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Functional Renal Imaging • evaluation of renal function and anatomy using 99mTc DTPA or 99m Tc MAG3 • frequently used to provide index of relative function between two kidneys • frequently used in adults to assess for UPJ obstruction (by assessing the clearance half time with lasix), and assess renal transplants or as a nuclear GFR study in patients wanting to donate kidneys • in children, imaging with 99m Tc DMSA is used to assess for pyelonephritis • in children, the injection of tracer into the bladder via foley catheter is often used to assess for reflux

MI28 Medical Imaging

Toronto Notes 2018

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Interventional Radiology

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Bone

eb

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m

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Bone Scan • isotopes, usually 99mTc-diphosphonate • radioactive tracer binds to hydroxyapatite of bone matrix increased binding when increased blood supply to bone and/or high bone turnover (active osteoblasts) • indications: bone pain of unknown origin, staging or restaging of cancer with boney mets (or primary bone cancer), imaging of arthroplasty complications like loosening or infection, osteomyelitis imaging • when used to assess for osteomyelitis, usually done in combination with gallium or white blood cell scan • differential diagnosis of positive bone scan: bone metastases (breast, prostate, lung, thyroid), primary bone tumour, arthritis, fracture, infection, anemia, Paget’s disease • lytic lesions like multiple myeloma, renal cell cancer, eosinophilic granuloma: typically normal or cold (false negative); need a skeletal survey • “superscan”: increased bone uptake and poor renal uptake due to diffuse metastases (breast, prostate) or metabolic causes (e.g renal osteodystrophy)

ks

s

Interventional Radiology

o

Vascular Procedures

m

m

Advanced ischemia patients should receive surgery rather than thrombolysis

ok

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co

m

m

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Angiography • injection of contrast material through a catheter placed directly into an artery or vein to delineate vascular anatomy • catheter can be placed into a large vessel (e.g. aorta, vena cava) for a “flush” or selectively placed into a branch vessel for more detailed examination of smaller vessels and specific organs • indications: diagnosis of primary occlusive or stenotic vascular disease, aneurysms, coronary, carotid and cerebral vascular disease, PE, trauma, bleeding (GI, hemoptysis, hematuria), vascular malformations, as part of endovascular procedures (endovascular aneurysm repair, thrombolysis, stenting, and angioplasties) • complications (70 yr, but may continue screening if in good general health ■■ if 9-11 mmol/L leads to filtration that exceeds tubular resorption capacity 2. increased GFR (e.g. pregnancy) 3. proximal tubule dysfunction (e.g. Fanconi’s syndrome)

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24 h Urine Collection • Discard first morning specimen • Collect all subsequent urine for the next 24 h • Refrigerate between voids • Collect second morning specimen and take to lab immediately

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2. pH • urine pH is normally between 4.5-7.0; if persistently alkaline, consider ■■ RTA ■■ UTI with urease-producing bacteria (e.g. Proteus)

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1. Specific Gravity ratio of the mass of equal volumes of urine/H2O • range is 1.001-1.030 • values 1.020 reflect concentrated urine • value usually 1.010 in ESRD (isosthenuria: same specific gravity as plasma)

m

Positive dipstick for leukocyte esterase and nitrites is highly specific for diagnosing a UTI

e.

e.

c

5. Leukocyte Esterase • enzyme found in WBC and detected by dipstick • presence of WBCs indicates infection (e.g. UTI) or inflammation (e g. AIN)

co

m

m

e

4 Protein • dipstick only detects albumin; other proteins (e.g. Bence-Jones, Ig, Tamm-Horsfall) may be missed • microalbuminuria (morning ACR of 2.0 - 20 mg/mmol) is not detected by standard dipstick, greater than these ranges would be macroalbuminuria (see Diabetes, NP31) • sulfosalicylic acid detects all protein in urine by precipitation • gold standard: 24 h timed urine collection for total protein

r

6. Nitrites • nitrates in urine are converted by some bacteria to nitrites • high specificity but low sensitivity for UTI

ks

Nitrite Negative Bacteria • Enterococci • Staphylococci

b

o

7. Ketones positive in alcoholic/diabetic ketoacidosis, prolonged starvation, fasting 8. Hemoglobin • positive in hemoglobinuria (hemolysis), myoglobinuria (rhabdomyolysis), and true hematuria (RBCs seen on microscopy)

m

Urine Microscopy

c

Table 2. Comparison of Urinary Sediment Findings

ok

sf

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Any one or more of the following seen on microscopy

Active Sediment = Suggestive of Parenchymal Kidney Disease Red cell casts White cell casts Muddy-brown granular or epithelial cell casts >2 red cells per HPF >4 white cells per HPF

Bland Sediment = Less Likely Parenchymal Kidney Disease Only hyaline casts Small quantities of crystals Small amount of bacteria 20 mmol/L suggests a renal problem or the action of a diuretic ■■ urine [Na+] 20-30 rads

OB12 Obstetrics

Toronto Notes 2018

c

Antenatal Fetal Surveillance

fr

fr

Antenatal Fetal Surveillance

o

Fetal Movements

c

DDx of Decreased Fetal Movements DASH Death of fetus Amniotic fluid decreased Sleep cycle of fetus Hunger/Thirst

om

co m

m

m

eb

eb

b

• patients will generally first notice fetal movement (“quickening”) at 18-20 wk in primigravidas; can occur 1-2 wk earlier in multigravidas; can occur 1-2 wk later if placenta is implanted on the anterior wall of uterus • if the patient is concerned about decreased fetal movement, she is counselled to choose a time when the fetus is normally active to count movements (usually recommended after 26 wk) • all high risk women should be told to do FM counts ■■ if there is a subjective decrease in fetal movement, try drinking juice, eating, changing position, or moving to a quiet room and count for 2 h; ≥6 movements in 2 h expected ■■ if there are 160 bpm for 30 min Erratic baseline

Variability

6-25 bpm (moderate) ≤5 (absent or minimal) for 10 min

Decelerations

None or occasional variable 60 s Late deceleration(s)

Accelerations in Term Fetus

2 accelerations with acme of ≥15 bpm, lasting 15 s over 10 bpm, lasting 10 s in 80 min

FURTHER ASSESSMENT OPTIONAL, based on total clinical picture

FURTHER ASSESSMENT REQUIRED

URGENT ACTION REQUIRED An overall assessment of the situation and further investigation with U/S or BPP is required; some situations will require delivery

eb

80 min

om

2 accelerations with acme of ≥15 bpm, lasting 15 s in 40-80 min

m

ok

b

Abnormal NST (Previously “Non-Reactive”)

om

Normal NST (Previously “Reactive”)

om

Parameter

e

e

Adapted from: SOGC, Fetal Health Surveillance: Antepartum and Intrapartum Consensus Guideline, Septemb r 2007

k

ks

Operating Characteristics • false positive rate depends on duration; false negative rate = 0.2-0.3%

BIOPHYSICAL PROFILE

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Definition • U/S assessment of the fetus ± NST

oo

oo

ks

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Indications • post-term pregnancy • decreased fetal movement • IUGR • any other suggestion of fetal distress or uteroplacental insufficiency

m

m

eb

o

Interpretation • normal: at least 2 accelerations of FHR >15 bpm from the baseline lasting >15 s in 20 min • abnormal: 15 bpm from baseline, lasting >15 s in 20 min

OB13 Obstetrics

Toronto Notes 2018

c

Obstetrical Hemorrhage

re

Operating Characteristics • false positive rate ≤30%, false negative rate = 0.1%

oo

oo

k

Table 9. Sco ing of the BPP Parameter

Reassuring (2 points) Reassuring BPP (8/8)

eb

Tone (limb extension then flexion) At least one episode of limb extension followed by flexion Movement

Three discrete movements

Breathing

At least one episode of breathing lasting at least 30 s

AFV*

Fluid pocket of 2 cm in 2 axes

LAMB Limb extension + flexion AFV 2 cm x 2 cm Movement (3 discrete) Breathing (one episode x 30 s)

*AFV is a marker of chronic hypoxia, all other parameters indicate acute hypoxia

fr

fre

e.

Interpretation • 8: perinatal mortality rate 1:1,000; repeat BPP as clinically indicated • 6: perinatal mortality 31:1,000; repeat BPP in 24 h • 0-4: perinatal mortality rate 200:1,000; deliver fetus if benefits of delivery outweigh risks

o

o

Obstetrical Hemorrhage

eb

Definition vaginal bleeding from 20 wk to term

e

m

Differential Diagnosis • bloody show (shedding of cervical mucous plug) – most common etiology in T3 • placenta previa • abruptio placentae – most common pathological etiology in T3 • vasa previa • cervical lesion (cervicitis, polyp, ectropion, cervical cancer) • uterine rupture • other: bleeding from bowel or bladder, abnormal coagulation

s

Table 10. Comparison of Placenta Previa and Abruptio Placentae Abruptio Placentae Premature separation of a normally implanted placenta after 20 wk GA

Etiology

Idiopathic

Idiopathic

Epidemiology

0.5-0.8% of all pregnancies

1-2% of all pregnancies

Risk Factors

History of placenta previa (4-8% recurrence risk) Multiparity Increased maternal age Multiple gestation Uterine tumour (e g fibroids) or other uterine anomalies Uterine scar due to previous abortion, C/S, D&C, myomectomy

Previous abruption (recurrence rate 5-16%) Maternal HTN (chronic or gestational HTN in 50% of abruptions) or vascular disease Cigarette smoking (>1 pack/d), excessive alcohol consumption, cocaine Multiparity and/or maternal age >35 yr PPROM Rapid decompression of a distended uterus (polyhydramnios, multiple gestation) Uterine anomaly, fibroids Trauma (e.g motor vehicle collision, maternal battery)

Bleeding

PAINLESS

Usually PAINFUL

om

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o

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o

Abnormal location of the placenta near, partially or completely over the internal cervical os

e

o

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Placenta Previa

Definition

o

Placenta Previa

Greater than 20 mm of overlap over the internal os in the third trimester of pregnancy is highly predictive of the need for a C/S. Any degree of overlap after 35 wk is an indication for a C/S

e. c

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c

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Clinical Features • PAINLESS bright red vaginal bleeding (recurrent), may be minimized and cease spontaneously but can become catastrophic • mean onset of bleeding is 30 wk GA, but onset depends on degree of previa • physical exam ■■ do not perform pelvic exam until ruling out placenta previa ■■ uterus soft and non-tender ■■ presenting fetal part high or displaced ■■ FHR usually normal ■■ shock/anemia correspond to degree of apparent blood loss

om

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m

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Definition • placenta implanted in the lower segment of the uterus, presenting ahead of the leading pole of the fetus • placental position is described in relation to the internal os as “mm away” or “mm of overlap”

OB14 Obstetrics

Toronto Notes 2018

c

Obstetrical Hemorrhage

m

m

e

s

ks

• complications ■■ fetal ◆◆ perinatal mortality low but still higher than with a normal pregnancy ◆◆ prematurity (bleeding often dictates early C/S) ◆◆ intrauterine hypoxia (acute or IUGR) ◆◆ fetal malpresentation ◆◆ PPROM ◆◆ risk of fetal blood loss from placenta especially if incised during C/S ■■ maternal ◆◆ 20 wk gestation

eb

eb

oo

oo k

ks

om

om

Complications • fetal complications: perinatal mortality 25-60%, prematurity, intrauterine hypoxia • maternal complications: 40yo): consideration should be given to IOL due to increased risk of stillbirth • GA 40-41 wk: expectant management ■■ no evidence to support IOL or C/S unless other risk factors for morbidity are present (see prognosis) • GA >41 wk: offer IOL if vaginal delivery is not contraindicated ■■ IOL shown to decrease C/S, fetal heart rate changes, meconium staining, macrosomia, and death when compared with expectant management • GA >41 wk and expectant management elected: serial fetal surveillance ■■ fetal movement count by the mother ■■ BPP q3-4d • if AFI is decreased, labour should be induced

oo

oo

k

Prognosis • if >42 wk, perinatal mortality 2-3x higher (due to progressive uteroplacental insufficiency) • morbidity increased with HTN in pregnancy, DM, abruption, IUGR, and multiple gestation

m

e

Intrauterine Fetal Death (Demise)

e

bo

o

Clinical Features • decreased perception of fetal movement by mother SFH and maternal weight not increasing • absent fetal heart tones on Doppler (not diagnostic) • high MSAFP • on U/S: no fetal heart rate. Depending on timing of death, may see skull collapse, brain tissue retraction, empty fetal bladder, non-filled aorta, poor visualization of midline flax

ok

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Management • diagnosis: absent cardiac activity and fetal movement on U/S required for diagnosis • determine secondary cause ■■ maternal: HbA1c, fasting glucose, TSH, Kleihauer-Betke, VDRL, ANA, CBC, anticardiolipins, antibody screens INR/PTT, serum/urine toxicology screens, cervical and vaginal cultures, TORCH screen ■■ fetal: karyotype, cord blood, skin biopsy, genetics evaluation, autopsy, amniotic fluid culture for CMV, parvovirus B19, herpes ■■ placenta: pathology, bacterial cultures

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re

Obstetrical Causes • Abruption • Gestational HTN • Fetal demise • PPH DIC-specific Blood Work • Platelets • aPTT and PT • FDP • Fibrinogen Treatment • Treat underlying cause • Supportive • Fluids • Blood products • FFP, platelets, cryoprecipitate • Consider anti-coagulation as VTE prophylaxis

c

sf

fr

r

Etiology • 50% idiopathic • 50% secondary to HTN, DM, erythroblastosis fetalis, congenital anomalies, umbilical cord or placental complications, intrauterine infection, APS

DIC: Generalized Coagulation and Fibrinolysis Leading to Depletion of Coagulation Factors

ee .

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Epidemiology • occurring in 1% of pregnancies

co

Definition • fetal death in utero after 20 wk GA (before 20 wk GA called spontaneous abortion)

OB19 Obstetrics

Toronto Notes 2018

c

Obstetrical Complications

b

bo

bo

ok sf r

Treatment • 20 wk: induction of labour • monitor for maternal coagulopathy (10% risk of DIC) • parental psychological care/bereavement support as per hospital protocol • comprehensive discussion within 3 mo about final investigation and post-mortem results, help make plans for future pregnancies

Intrauterine Growth Restriction

o

Definition • infant weight 34 wk • liberal use of C/S since IUGR fetus withstands labour poorly

bo

Macrosomia

o

Definition • infant weight >90th percentile for a particular GA or >4,000 g

e

e

Etiology/Risk Factors • maternal obesity, GDM, past history of macrosomic infant, prolonged gestation, multiparity

o

sf

r

Clinical Features • increased risk of perinatal mortality • CPD and birth injuries (shoulder dystocia, fetal bone fracture) more common • complications of DM in labour (see Table 15, OB27)

ok

TORCH Toxoplasmosis Others: e.g. syphilis Rubella CMV HSV • See Table 12, OB20

m

m

bo

oo

sf r

ks fr

Etiology/Risk Factors • 50% unknown • maternal causes ■■ malnutrition, smoking, drug abuse, alcoholism, cyanotic heart disease, type 1 DM, SLE, pulmonary insufficiency, previous IUGR (25% risk, most important risk factor), chronic HTN • maternal fetal ■■ any disease causing placental insufficiency ■■ includes gestational HTN, chronic renal insufficiency, gross placental morphological abnormalities (infarction, hemangiomas, placenta previa, abnormal cord insertion), prolonged gestation fetal causes ■■ TORCH infections, multiple gestation, congenital anomalies/chromosomal abnormalities (10%)

OB20 Obstetrics

Toronto Notes 2018

c

Obstetrical Complications

oo

ks

s

Investigations • serial SFH • further investigations if mother at high risk or SFH >2 cm ahead of GA • U/S predictors ■■ polyhydramnios ■■ third trimester AC >1.5 cm/wk ■■ HC/AC ratio 4,500 g in diabetic woman ■■ no evidence that prophylactic C/S improves outcomes • risks and benefits of early induction (risk of C/S vs. risk of dystocia) must be weighed in diabetic mothers, as current research is unclear

ks

re

re

Polyhydramnios/Oligohydramnios Table 12. Polyhydramnios and Oligohydramnios AFI 25 cm U/S: single deepest pocket >8 cm

e

Polyhydramnios

Definition

OB21 Obstetrics

Toronto Notes 2018

c

Multi-Fetal Gestation and Malpresentation

fr

re

Multi-Fetal Gestation and Malpresentation

eb

eb

bo

oo

o

Epidemiology • incidence of twins is 1/80 and triplets 1/6,400 in North America • 2/3 of twins are dizygotic (fraternal) ■■ risk factors for dizygotic twins: IVF, increased maternal age, newly discontinued OCP, ethnicity (e.g. certain African regions) • monozygous twinning occurs at a constant rate worldwide (1/250) • determine zygosity by number of placentas, thickness of membranes, sex, blood type Clinical Features

o

Table 13. Complications Associated with Multiple Gestation

e

The Ps of Multiple Gestation Complications

s

Monoamnionic Monochorionic (one cord)

Diamnionic Dichorionic (fused) *0-72 h

Diamnionic Dichorionic (separated)

Diamnionic Monochorionic *4-8 d

fre

e

Monoamnionic Monochorionic *9-12 d

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Figure 4. Classification of twin pregnancies

*Indicates time of cleavage

© Qing Huang 2004

ok

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Management • U/S determination of chorionicity must be done within first trimester (ideally 8-12 wk GA) • increased antenatal surveillance ■■ serial U/S q 2-3wk from 24 wk GA to assess growth (uncomplicated diamniotic dichorionitic) ■■ increased frequency of ultrasounds in monochorionic diamniotic and monochorionic monoamniotic twins ■■ Doppler flow studies weekly if discordant fetal growth (>30%) ■■ BPP as needed • may attempt vaginal delivery if twin A presents as vertex, otherwise C/S (40-50% of all twin deliveries, 15% of cases have twin A delivered vaginally and twin B delivered by C/S) • mode of delivery depends on fetal weights, GA, presentation

Monoamnionic Monochorionic (forked cord)

ncreased rates of Puking Pallor (anemia) Preeclampsia/PIH Pressure (compressive symptoms) PTL/PROM/PPROM Polyhydramnios Placenta previa/abruptio PPH/APH Prolonged labour Cord prolapse Prematurity Malpresentation Perinatal morbidity and mortality Parental distress Postpartum depression

sf r

Prematurity* IUGR Malpresentation Congenital anomalies Twin-twin transfusion Increased perinatal morbidity and mortality Twin interlocking (twin A breech twin B vertex) Single fetal demise

eb

o

eb

o

bo

Fetal

m

Increased PROM/PTL Polyhydramnios Placenta previa Placental abruption PPH (uterine atony) Umbilical cord prolapse Cord anomalies (velamentous insertion, 2 vessel cord)

.

Uteroplacental

Hyperemesis gravidarum GDM Gestational HTN Anemia Increased physiological stress on all systems Increased compressive symptoms C/S

e

Maternal

OB22 Obstetrics

Toronto Notes 2018

c

Multi-Fetal Gestation and Malpresentation

fre

fre

Twin-Twin Transfusion Syndrome

oo

o

k

Definition • formation of placental intertwin vascular anastomoses causes arterial blood from donor twin to pass into veins of the recipient twin Epidemiology • 10% of monochorionic twins • concern if >30% discordance in estimated fetal weight

o

om

Clinical Features • donor twin: IUGR, hypovolemia, hypotension, anemia, oligohydramnios • recipient twin: hypervolemia, HTN, CHF, polycythemia, edema, polyhydramnios, kernicterus in neonatal period

re

Investigations • detected by U/S screening, Doppler flow analysis

m

eb

bo

oo

o

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ok s

Management • therapeutic serial amniocentesis to decompress polyhydramnios of recipient twin and decrease pressure in cavity and on placenta • intrauterine blood transfusion to donor twin if necessary • laparoscopic occlusion of placental vessels • fetoscopic laser ablation of placental vascular anastomoses when indicated and if available

Breech Presentation

A. Complete Breech

sf

fr

re

e.

o

co

Definition • fetal buttocks or lower extremity is the presenting part as determined on U/S • complete (10%): hips and knees both flexed • frank (60%): hips flexed, knees extended, buttocks present at cervix ■■ most common type of breech presentation ■■ most common breech presentation to be delivered vaginally • incomplete (30%): both or one hip flexed and both or one knee present below the buttocks, feet or knees present first (footling breech, kneeling breech)

bo

oo

Epidemiology • occurs in 3-4% of pregnancies at term (25% 36 wk • EFW 2,500-3,800 g based on clinical and U/S assessment (5.5–8.5 lb) • Fetal head flexed • Continuous fetal monitoring • 2 experienced obstetricians, assistant, and anesthetist present • Ability to perform emergency C/S within 30 min if required

ee .

m

om

e. c

ee

co

m

eb

o

ok

ok

s

sf

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re

Management • ECV: repositioning of singleton fetus within uterus under U/S guidance ■■ overall success rate of 65% ■■ criteria: >36 wk GA, singleton, unengaged presenting part, reactive NST, not in labour ■■ contraindications: previous T3 bleed, prior classical C/S, previous myomectomy, oligohydramnios, PROM, placenta previa, abnormal U/S, suspected IUGR, HTN, uteroplacental insufficiency, nuchal cord ■■ risks: abruption, cord compression, cord accident, ROM, labour, fetal bradycardia requiring C/S (140/90 prior to 20 wk GA, persisting >7 wk postpartum • essential HTN is associated with an increased risk of gestational HTN, abruptio placentae, IUGR, and IUFD GESTATIONAL HTN

k

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Definition • sBP >140 or dBP >90 developing after 20th wk GA in the absence of proteinuria in a woman known to be normotensive before pregnancy

Ominous Symptoms of HTN in Pregnancy RUQ pain, headache, and visual disturbances

f

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Adverse Maternal Conditions • sBP >160 mmHg • dBP >100 mmHg • HELLP • Cerebral hemorrhage • Renal dysfunction: oliguria 40 yr or 4,500 g (9.9 lbs) (controversial) • monitoring ■■ during labour, monitor blood glucose q1h with patient on insulin and dextrose drip ■■ aim for blood glucose between 3.5-6.5 mmol/L to reduce the risk of neonatal hypoglycemia

Monitoring Glucose Levels • Frequent measurements of blood glucose during pregnancy are advised for women with type 1 or 2 DM to help prevent or treat both hypoglycemia and hyperglycemia, and also improves neonatal outcome • Aim for: • FPG ≤5.3 mmol/L (95 mg/dL) • 1 h post prandial PG ≤7.8 mmol/L (140 mg/ dL), 2 h post prandial PG ≤6.7 mmol/L (120 mg/dL) • Most women can be followed with monthly HbA1c determinations

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Pregnancy • if already on oral medication, generally switch to insulin therapy ■■ continuing glyburide or metformin controversial ■■ teratogenicity unknown for other oral anti-hyperglycemics • tight glycemic control ■■ insulin dosage may need o be adjusted in T2 due to increased demand and increased insulin resistance • monitor as for normal pregnancy, plus initial 24 h urine protein and creatinine clearance, retinal exam, HbA1c ■■ HbA1c: >140% of pre-pregnancy value associated with increased risk of spontaneous abortion and congenital malformations • increased fetal surveillance (BPP, NST), consider fetal ECHO (if high Hgb A1c in first trimester or just prior to pregnancy) to look for cardiac abnormalities

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Postpartum • insulin requirements dramatically drop with expulsion of placenta (source of insulin antagonists) • no insulin is required for 48-72 h postpartum in most type 1 DM • monitor glucose q6h, restart insulin at two-thirds of pre-pregnancy dosage when glucose >8 mmol/L

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Post-prandial blood glucose values seem to be the most effective at determining the likelihood of macrosomia or other adverse pregnancy outcomes

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Risk Factors for GDM • Age >25 yr • Obesity • Ethnicity (Aboriginal, Hispanic, Asian, African) • FHx of DM • Previous history of GDM • Previous child with birthweight >4.0 kg • Polycystic ovarian syndrome • Current use of glucocorticoids • Essential HTN or pregnancy-related HTN

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Screening and Diagnosis • all pregnant women between 24-28 wk GA (or at any stage if high risk) • 2 screening options ■■ 1-step screening with fasting 75 g OGTT; GDM if ≥1 of: ◆◆ FPG ≥ 5.1 mmol/L ◆◆ 1h PG ≥ 10.0 mmol/L ◆◆ 2h PG ≥ 8.5 mmol/L ■■ 2-step screening (recommended by the Canadian Diabetes Association) ◆◆ Step 1: Perform a random non-fasting 50 g OGCT – 1h PG < 7.8 mmol/L is normal – 1h PG ≥ 11.1 mmol/L is GDM – if 1h PG 7.8-11.0 mmol/L, proceed to Step 2 ◆◆ Step 2: Perform a fasting 75 g OGTT, GDM if ≥1 of: – FPG ≥ 5.3 mmol/L 1h PG ≥ 10.6 mmol/L – 2h PG ≥ 9.0 mmol/L

OB27 Obstetrics

Toronto Notes 2018

Medical Complications of Pregnancy

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Management • first line is management through diet modification and increased physical activity • initiate insulin therapy if glycemic targets not achieved within 2 wk of lifestyle modification alone • glycemic targets: FPG 20 to 42 wk GA) • false labour (Braxton-Hicks contractions): irregular contractions, with unchanged intensity and long intervals, occur throughout pregnancy and not associated with any cervical dilatation, effacement, or descent ■■ often relieved by rest or sedation

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Virchow’s Tr ad for VTE • Hypercoagulable state • Stasis • Endothelial damage

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Management • before initiating treatment, obtain a baseline CBC including platelets and aPTT • warfarin is contraindicated during pregnancy due to its potential teratogenic effects • unfractionated heparin ■■ bolus of 5,000 IU followed by an infusion of ~30 000 IU/24h ■■ measure aPTT 6 h after the bolus ■■ maintain aPTT at a therapeutic level (1.5 2x normal) ■■ repeat q24h once therapeutic ■■ heparin-induced thrombocytopenia (HIT) uncommon (3%), but serious complication ■■ LMWH can also be used in pregnancy • compression stockings • poor evidence to support a recommendation for or against avoidance of prolonged sitting • VTE prophylaxis ■■ women on long-term anticoagulation: full therapeutic anticoagulation throughout pregnancy and for 6-12 wk postpartum ■■ women with a non-active PMHx of VTE: unfractionated heparin regimens suggested ■■ insufficient evidence in pregnancy to recommend routine use of LMWH for all patients ■■ current prophylaxis regimens for acquired thrombophilias (e.g. APS syndrome) include low dose Aspirin® in conjunction with prophylactic heparin

OB31 Obstetrics

Toronto Notes 2018

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Normal Labour and Delivery

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Frontal Fontanelle or Anterior Fontanelle

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Biparietal Diameter 9 5 cm

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Sagittal Fontanelle

Occiput Posterior

Left Occiput Anterior

Right Occiput Posterior

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Occiput Anterior

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Figure 6. Fetal positions

Right Occiput Transverse

© Simon Ip 2009

Occipital Fontanelle or Posterior Fontanelle

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Reference Point for Describing Fetal Position • Occiput for cephalic presentation • Sacrum for breech presentation Mentum for face presentation

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• fetal lie: orientation of the long axis of the fetus with respect to the long axis of the uterus (longitudinal, transverse, oblique) • fetal presentation: fetal body part closest to the birth canal ■■ breech (complete, frank, incomplete) (see Figure 5, OB22) ■■ cephalic (vertex/occiput, face, asynclitic, brow) ■■ transverse (shoulder) ■■ compound (fetal extremity prolapses along with presenting part) ■■ all ex ept vertex are considered malpresentations (see Obstetrical Complications, OB15) • fetal position: position of presenting part of the fetus relative to the maternal pelvis ■■ OA: most common presentation (“normal”) – left OA most common ■■ OP: most rotate spontaneously to OA; may cause prolonged second stage of labour ■■ OT: leads to arrest of dilatation ◆◆ normally, fetal head enters maternal pelvis and engages in OT position ◆◆ subsequently rotates to OA position (or OP in a small percentage of cases) • attitude: flexion/extension of fetal head relative to shoulders ■■ brow presentation: head partially extended (requires C/S) ■■ face presentation: head fully extended ◆◆ mentum posterior always requires C/S, mentum anterior can deliver vaginally • station: position of presenting bony part relative to ischial spines – determined by vaginal exam ■■ at ischial spines = station 0 = engaged ■■ -5 to -1 cm above ischial spines or ■■ +1 to +5 cm below ischial spines

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The Fetus

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• dilatation latent phase (0-4 cm, variable time); active phase (4-10 cm) • effacement: thinning of the cervix by percentage or length of cervix (cm) • consistency: firm vs. soft • position: posterior, mid, or anterior • application: contact between the cervix and presenting part (i.e. well or poorly applied) • see Bishop Score (Table 22, OB36)

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Maternal Triage Assessment ID: Age, GPA, EDC, GA, GBS, Rh, Ser CC HPI: 4 key questions: • Contractions: Since when, how close (q x min), how long (x s), how painful • Bleeding: Since when, how much (pads), colour (pinky mucous=show vs. brownish vs. bright red ± clots), pain?, last U/S, trauma/intercourse? • Fluid (ROM): Since when, large gush vs. trickle, soaked pants? clear vs. green vs. red?, continuous? • FM: As much as usual?, When last movement?, Kick counts (lie still for 1-2 h, cold juice, feel FM – should have 6 movements in 2 h) PregHx: Any complications (HTN, GDM, nfections), IPS/FTS screening, last U/S (BPP score, growth/estimated fetal weight, position), last vaginal exam POBHx: Every previous pregnancy and outcome: Year, SVD/CS/miscarriage/abortion, baby size, length of labour, use of vacuum or forceps, complications PMHx, Meds, Allergies, SHx O/E: Maternal vitals, fetal heart tracing (baseline, variability, presence of accelerations/decelerations), Leopold’s, vaginal exam, U/S

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The Cervix

OB32 Obstetrics

Toronto Notes 2018

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Normal Labour and Delivery

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Four Stages of Labour Course of Normal Labour* Stage Nulliparous Multiparous First 6-18 h 2-10 h Second 30 min-3 h 5-30 min Third 5-30 min 5-30 min *without epidural

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Fourth Stage of Labour • first postpartum hour • monitor vital signs and bleeding, repair lacerations • ensure uterus is contracted (palpate uterus and monitor uterine bleeding) • inspect placenta for completeness and umbilical cord for presence of 2 arteries and 1 vein • 3rd and 4th stages of labour most dangerous to the mother (i.e. hemorrhage)

Continuous Support for Women During Childbirth Cochrane DB Syst Rev 2011;16:CD003766 Study: Systematic review of 21 RCTs from 11 countries, 15,061 women in labour. Intervention: Continuous support during labour vs. usual care. Outcome: Effects on mothers and their babies. Results: Continuous intrapartum support increased likelihood of shorter labour, spontaneous vaginal birth, decrease in analgesia use, and a decrease in dissatisfaction with childbirth experience. Greatest benefit when provider is not a health care pro essional. Continuous support was also associated with decreased likelihood to have a Cesarean or instrumental vaginal birth, regional analgesia, or a baby with a low 5 min APGAR score.

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Third Stage of Labour (delivery of the baby – delivery of the placenta) • from baby’s birth to separation and expulsion of the placenta • can last up to 30 min before intervention is indicated • demonstrated by gush of fresh blood, umbilical cord lengthening, uterine fundus changing shape (firm and globular) and rising upward • active management: start oxytocin IV drip, or give 10 U IM or 5 mg IV push after delivery of anterior shoulder in anticipation of placental delivery, otherwise give after delivery of placenta • routine oxytocin administration in third stage of labour can reduce the risk of PPH by >40%

Signs of Placental Separation • Gush of blood • Lengthening of cord • Uterus becomes globular Fundus rises

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Second Stage of Labour (10 cm dilation – delivery of the baby) • from full dilatation to delivery of the baby; duration varies based on parity, contraction quality, and type of analgesia • mother feels a desire to bear down and push with each contraction • women may choose a comfortable position that enhances pushing efforts and delivery ■■ upright (semi-sitting, squatting) and LLDP are supported in the literature • progress measured by descent

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First Stage of Labour (0 – 10 cm cervical dilation) • latent phase ■■ uterine contractions typically infrequent and irregular ■■ slow cervical dilatation (usually to 4 cm) and effacement • active phase ■■ rapid cervical dilatation to full dilatation (nulliparous ≥1.0 cm/h, multiparous ≥1.2 cm/h) ■■ phase of maximum slope on cervical dilatation curve ■■ painful, regular contractions q2-3min, lasting 45-60 s ■■ contractions strongest at fundus

2. Engagement, descent, flexion

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4. Complete rotation, beginning extension

8. Delivery of posterior shoulder

© Danielle Bader

7. Delivery of anterior shoulder

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6. Restitution (external rotation)

Figure 7. Cardinal movements of fetus during delivery Adapted from illustration in Williams Obstetrics, 19th ed

3. Further descent, internal rotation

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1. Head floating, before engagement

5. Complete extension

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The Cardinal Movements of the Fetus During Delivery

OB33 Obstetrics

Toronto Notes 2018

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Normal Labour and Delivery

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Analgesic and Anesthetic Techniques in Labour and Birth

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• pain or anxiety leads to high endogenous catecholamines, which produce a direct inhibitory effect on uterine contractility

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Non-Pharmacologic Pain Relief Techniques • reduction of painful stimuli ■■ maternal movement, position change, counter-pressure, abdominal compression • activation of peripheral sensory receptors ■■ superficial heat and cold ■■ immersion in water during labour ■■ touch and massage, acupuncture, and acupressure ■■ TENS ■■ intradermal injection of sterile water ■■ aromatherapy • enhancement of descending inhibitory pathways ■■ attention focusing and distraction ■■ hypnosis ■■ music and audio analgesia ■■ biofeedback

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Pharmacologic Methods (see Anesthesia and Perioperative Medicine, A26) • nitrous oxide (e.g. self-administered Entonox®) • narcotics (usually combined with anti-emetic) • pudendal nerve block • perineal infiltration with local anesthetic • regional anesthesia (epidural block, combined spinal-epidural, spinal)

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Fetal Monitoring in Labour

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• see online Fetal Heart Rate Tutorial

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Vaginal Exam • membrane status, as indicated by amniotic fluid (clear, pink, bloody, meconium) • cervical effacement (thinning), dilatation, consistency position, application • fetal presenting part, position, station • bony pelvis size and shape • monitor progress of labour at regular intervals and document in a partogram

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Approach to the Management of Abnormal FHR POISON – ER Position (left lateral decubitus position) O2 (100% by mask) IV fluids (corrects maternal hypotension) Fetal scalp stimulation Fetal scalp electrode Fetal scalp pH Stop oxytocin Notify MD Vaginal exam to rule out cord prolapse Rule out fever, dehydration, drug effects, prematurity • If above fails, consider C/S

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Electronic FHR Monitoring • FHR measured by Doppler; contractions measured by tocometer • described in terms of baseline FHR, variability (short-term, long-term), and periodicity (accelerations, decelerations) • Baseline FHR ■■ normal range is 110-160 bpm ■■ parameter of fetal well-being vs. distress • Variability ■■ physiologic variability is a normal characteristic of FHR ■■ variability is measured over a 15 min period and is described as: absent, minimal (25 bpm) ■■ normal variability indicates fetal acid-base status is acceptable ■■ can only be assessed by electronic fetal monitoring (CTG) ■■ variability decreases intermittently even in healthy fetus ■■ see Table 19, OB34

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Intrapartum Fetal Monitoring • intermittent fetal auscultation with Doppler device q15-30min for 1 min in first stage active phase following a contraction, q5min during second stage when pushing has begun • continuous electronic FHR monitoring reserved for abnormal auscultation, prolonged labour, labour which is induced or augmented, meconium present, multiple gestation/fetal complication ■■ use of continuous electronic monitoring shown to lead to higher intervention rates and no improvement in outcome for the neonate when used routinely in all patients (i.e. no risk factors) ■■ techniques for continuous monitoring include external (Doppler) vs. internal (fetal scalp electrode) monitoring • fetal scalp sampling should be used in conjunction with electronic FHR monitoring and contraction monitoring (CTG) to resolve the interpretation of abnormal or atypical patterns

OB34 Obstetrics

Toronto Notes 2018

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Normal Labour and Delivery

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• Periodicity ■■ accelerations: increase of ≥15 bpm for ≥15 s, in response to fetal movement or uterine contraction (or ≥10 bpm for ≥10 s if 60 s in duration with slow return to baseline

Variable in duration, intensity, and timing

120 100

Complicated Variable Decelerations

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Late Decelerations

Late Decelera ion

Onset of deceleration

160

Nadir of deceleration

140

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BPM

FHR

120 100

30 seconds of lag time

Recovery time

Acme of contraction

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• Uniform shape with onset, nadir, and recovery occurring after peak of contraction, slow return to baseline • May cause decreased variability and change in baseline FHR • Due to fetal hypoxia and acidemia, maternal hypotension, or uterine hypertonus • Usually a sign of uteroplacental insufficiency (an ominous sign)

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• FHR drop 60 s • Loss of variability or decrease in baseline after deceleration • Biphasic deceleration • Slow return to baseline • Baseline tachycardia or bradycardia • May be associated with fetal acidemia

Onset of contraction

Uterine contraction End of contraction

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• Variable in shape, onset, and duration • Most common type of periodicity seen during labour • Often with abrupt drop in FHR >15 bpm below baseline (>15 s, 160 for 30-80 min Rising baseline

Bradycardia 160 bpm for >80 min Erratic baseline

≤5 bpm for 40-80 min

80 min ≥25 bpm for >10 min Repetitive (≥3) complicated variable decelerations Repetitive late decelerations Any prolonged deceleration (≥3 min)

Variability

6-25 bpm ≤5 bpm for 2 h • management: if CPD ruled out, IV oxytocin augmentation ± amniotomy

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Risks of Dystocia • inadequate progression of labour is associated with an increased incidence of: ■■ maternal stress ■■ maternal infection ■■ postpartum hemorrhage ■■ need for neonatal resuscitation ■■ fetal compromise (from uterine hyperstimulation) ■■ uterine rupture ■■ hypotension

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Shoulder Dystocia

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Etiology/Epidemiology • incidence 0.15-1.4% of deliveries • occurs when breadth of shoulders is greater than biparietal diameter of the head

Approach to the Management of Shoulder Dystocia

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*Note that suprapubic pressure and McRobert’s maneuver together will resolve 90% of cases

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Presentation • “turtle sign”: head delivered but retracts against inferior portion of pubic symphysis • complications ■■ fetal ◆◆ hypoxic ischemic encephalopathy (chest compression by vagina or cord compression by pelvis can lead to hypoxia) ◆◆ brachial plexus injury (Erb’s palsy C5-C7; Klumpke’s palsy: C8-T1), 90% resolve within 6 mo ◆◆ fracture (clavicle, humerus, cervical spine) ◆◆ death ■■ maternal ◆◆ perineal injury ◆◆ PPH (uterine atony lacerations) ◆◆ uterine rupture

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ALARMER Apply suprapubic pressure and ask for help Legs in full flexion (McRobert’s maneuver) Anterior shoulder disimpaction (suprapubic pressure) Release posterior shoulder by rotating it anteriorly wi h hand in the vagina under adequate anesthesia Manual corkscrew i.e. rotate the fetus by the posterior shoulder until the anterior shoulder emerges from behind the maternal symphysis Episiotomy Rollover (on hands and knees)

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Risk Factors • maternal: obesity, DM, multiparity, previous shoulder dystocia • fetal: prolonged gestation, macrosomia (especially if associated with GDM) • labour ■■ prolonged 2nd stage ■■ instrumental midpelvic delivery

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Definition • fetal anterior shoulder impacted above symphysis pubis after fetal head has been delivered • life threatening emergency

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Treatment • goal: to displace anterior shoulder from behind symphysis pubis; follow a stepwise approach of maneuvers until goal achieved • other options ■■ cleidotomy (deliberate fracture of neonatal clavicle) ■■ Zavanelli maneuver: replacement of fetus into uterine cavity and emergent C/S ■■ symphysiotomy Prognosis • 1% risk of long-term disability for infant

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Etiology/Epidemiology • increased incidence with prematurity/PROM, fetal malpresentation (~50% of cases), low-lying placenta, polyhydramnios, multiple gestation, CPD • incidence: 1/200-1/400 deliveries

Umbilical Cord Accident Causes • Nuchal cord • Type A (looped) • Type B (hitched) • Body loop • Single artery • True knot • Torsion • Velamentous • Short cord 80 cm

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Definition • descent of the cord to a level adjacent to or below the presenting part, causing cord compression between presenting part and pelvis

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Umbilical Cord Prolapse

OB39 Obstetrics

Toronto Notes 2018

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Abnormalities and Complications of Labour and Delivery

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Presentation • visible or palpable cord • FHR changes (variable decelerations, bradycardia, or both)

• 1/3 of protraction disorders develop into 2º arrest of dilatation due to CPD • 2/3 of protraction disorders progress through labour to vaginal delivery

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Treatment • emergency C/S • O2 to mother, monitor fetal heart • alleviate pressure of the presenting part on the cord by elevating fetal head with a pelvic exam (maintain this position until C/S) • keep cord warm and moist by replacing it into the vagina ± applying warm saline soaks • roll mom onto all fours • position mother in Trendelenburg or knee-to-chest position • if fetal demise or too premature (2 fetuses, lower segment adhesions, obstructing fibroid, morbidly obese patients

7 Layers to Dissect Skin, fatty layer, fascia, muscle separation (rectus abdominis), peritoneum, bladder flap, uterus

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Indications • maternal: obstruction, active herpetic lesion on vulva, invasive cervical cancer, previous uterine surgery (past C/S is most common), underlying maternal illness (eclampsia, HELLP syndrome, heart disease) maternal-fetal: failure to progress, placental abruption or previa, vasa previa • fetal: abnormal fetal heart tracing, malpresentation, cord prolapse, certain congenital anomalies

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Risks/Complications • complications related to general anesthesia* (e.g. aspiration) • hemorrhage (average blood loss ~1,000 cc) • infection (UTI, wound, endometritis) ■■ single dose prophylactic antibiotic should be used (e.g. cefazolin 1-2 g) • injury to surrounding structures (bowel, bladder, ureter, uterus) • thromboembolism (DVT, PE) • increased recovery time/hospital stay • maternal mortality (600 µg) • tranexamic acid (Cyklokapron®), an antifibrinolytic, 1 g IV

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Local Control • bimanual massage: elevate the uterus and massage through patient’s abdomen • uterine packing (mesh with antibiotic treatment) • Bakri Balloon for tamponade: may slow hemorrhage enough to allow time for correction of coagulopathy or for preparation of an OR

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Surgical Therapy (Intractable PPH) • D&C (beware of vigorous scraping which can lead to Asherman’s syndrome) • embolization of uterine artery or internal iliac artery by interventional radiologist • laparotomy with bilateral ligation of uterine artery (may be effective), internal iliac artery (not proven), ovarian artery, or hypogastric artery, compression sutures (B-Lynch or Cho sutures) • hysterectomy last option, with angiographic embolization if post-hysterectomy bleeding

Retained Placenta Definition • placenta undelivered after 30 min postpartum

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Etiology • placenta separated but not delivered • abnormal placental implantation (placenta accreta, placenta increta, placenta percreta)

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Risk Facto s • placenta previa, prior C/S, post-pregnancy curettage, prior manual placental removal, uterine infection

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Clinical Features • risk of postpartum hemorrhage and infection Investigations • explore uterus • assess degree of blood loss

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Management • 2 large bore IVs, type and screen • Brant maneuver (firm traction on umbilical cord with one hand applying suprapubic pressure cephalad to avoid uterine inversion by holding uterus in place) • oxytocin 10 IU in 20 mL NS into umbilical vein • manual removal if above fails • D&C if required • Ancef 2 g IV if manual removal or D&C

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Uterine Inversion

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Definition • inversion of the uterus through cervix ± vaginal introitus

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Etiology/Epidemiology • often iatrogenic (excess cord traction with fundal placenta) • excessive use of uterine tocolytics • more common in grand multiparous (lax uterine ligaments) • 1/1,500-1/2,000 deliveries

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Management • urgent management essential, call anesthesia • ABCs: initiate IV crystalloids

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Clinical Features • can cause profound vasovagal response with bradycardia, vasodilation, and hypovolemic shock • shock may be disproportionate to maternal blood loss

OB45 Obstetrics

Toronto Notes 2018

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Puerperal Complications

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• can use tocolytic drug (see Management of Preterm Labour, OB16) or nitroglycerin IV to relax uterus and aid repla ement • replace uterus without removing placenta • remove placenta manually and withdraw slowly • IV oxytocin infusion (only after uterus replaced) • re-explore uterus • may require general anesthetic ± laparotomy

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Postpartum Pyrexia

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Definition • fever >38°C on any 2 of the first 10 d postpartum, except the first day Etiology • endometritis • wound infection (check C/S and episiotomy sites) • mastitis/engorgement • UTI • atelectasis • pneumonia • DVT, pelvic thombophlebitis

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Etiology of Pos partum Pyrexia

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B-5W Breast: engorgement, mastitis Wind: atelectasis, pneumonia Water: UTI Wound: episiotomy, C/S site infection Walking: DVT, thrombophlebitis Womb: endometritis

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Investigations • detailed history and physical exam, relevant cultures • for endometritis: blood and genital cultures

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Treatment • depends on etiology ■■ infection: empiric antibiotics, adjust when sensitivities available ◆◆ endometritis: clindamycin + gentamycin IV ◆◆ mastitis: cloxacillin or cephalexin ◆◆ wound infection: cephalexin, frequent sitz baths for episiotomy site infection ■■ DVT: anticoagulants • prophylaxis against post-C/S endometritis: administer 2g of Cephazolin IV 30 minutes prior to skin incision

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ENDOMETRITIS • definition: infection of uterine myometrium and parametrium • clinical features: fever, chills, abdominal pain, uterine tenderness, foul-smelling discharge, or lochia • treatment: depends on infection severity; oral antibiotics if well, IV with hospitalization in moderate to severe cases

Risk Factors for Endometritis C/S, intrapartum chorioamnionitis, prolonged labour, prolonged ROM, multiple vaginal examinations

VENOUS THROMBOEMBOLISM • see Venous Thromboembolism, OB30

Mastitis

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• definition: inflammation of mammary glands • must rule out inflammatory carcinoma, as indicated • differentiate from mammary duct ectasia: mammary duct(s) beneath nipple clogged and dilated ± ductal inflammation ± nipple discharge (thick, grey to green), often postmenopausal women

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Table 24 Lactational vs. Non-Lactational Mastitis

Unilateral localized pain Tenderness Erythema

Treatment

Heat or ice packs Continued nurs ng/pumping Antibiotics (cloxacillin/cephalexin) (erythromycin if pen-allergic) Fluctuant mass Purulent nipple discharge Fever, leukocytosis Discontinue nursing, IV antibiotics (nafcillin/oxacillin), I&D usually required

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If mass does not resolve, FNA to exclude cancer and U/S to assess presence of abscess Treatment includes antibiotics, aspiration, or I&D (tends to recur) May develop mammary duct fistula A minority of non-lactational abscesses may occur peripherally in breast with no associated periductal mastitis (usually S. aureus)

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Symptoms

Abscess

Non-Lactational Periductal mastitis most common Mean age 32 yr May be sterile May be infected with S. aureus or other anaerobes Smoking is risk factor May be associated with mammary duct ectasia Subareolar pain May have subareolar mass Discharge (variable colour) Nipple inversion Broad-spectrum antibiotics and I&D Total duct excision (definitive)

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Lactational Epidemiology More common than non-lactational Often 2-3 wk postpartum S. aureus Etiology

OB46 Obstetrics

Toronto Notes 2018

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Postpartum Care

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Postpartum Mood Alterations

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POSTPARTUM BLUES • 40-80% of new mothers, onset day 3-10; extension of the “normal” hormonal changes and adjustment to a new baby self-limited, should resolve by 2 wk • manifested by mood lability, depressed affect, increased sensitivity to criticism, tearfulness, fatigue, irritability, poor concentration/despondency, anxiety, insomnia

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POSTPARTUM DEPRESSION • definition: major depression occurring in a woman within 6 mo of childbirth (see Psychiatry, PS12) • epidemiology: 10-15%, risk of recurrence 50% • risk factors ■■ personal or family history of depression (including PPD) ■■ prenatal depression or anxiety ■■ stressful life situation ■■ poor support system ■■ unwanted pregnancy ■■ colicky or sick infant • clinical features: suspect if the “blues” last beyond 2 wk, or if the symptoms in the first 2 wk are severe (e g extreme disinterest in the baby, suicidal or homicidal/infanticidal ideation) • assessment: Edinburgh Postnatal Depression Scale or other • treatment: antidepressants, psychotherapy, supportive care, ECT if refractory • prognosis: interferes with bonding and attachment between mother and baby, so it can have long-term effects

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POSTPARTUM PSYCHOSIS • definition: onset of psychotic symptoms over 24-72 h within first month postpartum, can present in the context of depression • epidemiology: rare (0.2%)

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Postpartum Care

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Postpartum Office Visit at 6 Weeks

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Breastfeeding Problems • inadequate milk: consider domperidone • breast engorgement: cool compress, manual expression/pumping • nipple pain: clean milk off nipple after feeds, moisture cream, topical steroid if needed • mastitis: treat promptly (see Postpartum Pyrexia, OB45) • inverted nipples: makes feeding difficult • maternal medications: may require pediatric consultation (see Breastfeeding and Drugs)

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Baby care and breastfeeding (latch, amount) Uterus – firm or boggy? Bladder function – Voiding well? Dysuria? Bowel function – Passing gas or stool? Constipated? Lochia or discharge – Any blood? Episiotomy/laceration/incision – Pain controlled? Symptoms of VTE – Dyspnea? Calf pain?

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Physiological Changes Postpartum • uterus weight rapidly diminishes through catabolism, cervix loses its elasticity and regains firmness ■■ should involute ~1 cm below umbilicus per day in first 4-5 d, reaches non-pregnant state in 4-6 wk postpartum • ovulation resumes in ~45 d for non-lactating women and within 3-6 mo for lactating women and sometimes later • lochia: normal vaginal discharge postpartum, uterine decidual tissue sloughing ■■ decreases and changes in colour from red (lochia rubra; presence of erythrocytes, 3-4 d) → pale (lochia serosa) → white/yellow (lochia alba; residual leukorrhea) over 3-6 wk ■■ foul-smelling lochia suggests endometritis

The acronym “BUBBLES” for what to ask about when rounding on postpartum care. Modify this for C/S or vaginal delivery

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Care of Mother (The 10 Bs) • Be careful: do not use douches or tampons for 4-6 wk post-delivery • Be fit: encourage gradual increases in walking, Kegel exercises • Birth control: assess for use of contraceptives; breastfeeding is NOT an effective method of bir h control (see Gynecology, GY17, for more detail about different contraceptive options postpartum) • Bladder: assess for urinary incontinence, maintain high fluid intake • Blood pressure: especially if gestational HTN • Blood tests: CBC (for anemia if had PPH) • Blues: (see Postpartum Mood Alterations) • Bowel: fluids and high-fibre foods, bulk laxatives; for hemorrhoids/perineal tenderness: pain meds, doughnut cushion, Sitz baths, ice compresses • Breast and pelvic exam: watch for Staphylococcal or Streptococcal mastitis/abscess, ± Pap smear at 6 wk

OB47 Obstetrics

Toronto Notes 2018

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Common Medications

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Bladder Dysfunction • pelvic floor prolapse can occur after vaginal delivery • stress or urge urinary incontinence common • increased risk with instrumental delivery or prolonged second stage • conservative management: pelvic floor retraining with Kegel exercises/pelvic physiotherapy, vaginal cone or pessaries, lifestyle modifications (e.g. limit fluid, caffeine intake) • surgical management: minimally invasive procedures (tension-free vaginal tape, transobturator tape, midurethral sling)

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Puerperal Pain • “after pains” common in first 3 d due to uterine contractions; encourage simple analgesia • ice packs can be used on perineum if painful • encourage regular analgesia and stool softener

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Breastfeeding and Drugs Contraindicated When Breastfeeding

Analgesics (e g. acetaminophen, NSAIDs) Anticoagulants (e.g. heparin) Antidepressants (e.g. sertraline, fluoxetine, TCAs) Antiepileptics (e.g. phenytoin, carbamazepine, valproic acid) Antihistamines Antimicrobials (e.g. penicillins, aminoglycosides, cephalosporins) β-adrenergics (e.g. propanolol, labetalol) Insulin Steroids OCP (low dose) – although may decrease breast milk production

Chloramphenicol (bone marrow suppression) Cyclophosphamide (immune system suppression) Sulphonamides (in G6PD deficiency, can lead to hemolysis) Nitrofurantoin (in G6PD deficiency, can lead to hemolysis) Tetracycline Lithium Phenindione Bromocriptine Anti-neoplastics and immunosuppresants Psychotropic drugs (relative contraindication)

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Breastfeeding: Contraindicated Drugs

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BREAST Bromocriptine/Benzodiazepines Radioactive isotopes/Rizatriptan Ergotamine/Ethosuximide Amiodarone/Amphetamines Stimulant laxatives/Sex hormones Tetracycline/Tretinoin

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Safe During Breastfeeding

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Table 25. Drug Safety During Breastfeeding

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Common Medications

Indications/Comments Enhancement of fetal pulmonary maturity for PTL

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Dosing Schedule 12 mg IM q24h x 2 doses

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For ectopic pregnancy or medical abortion Treatment of uterine atony

0.5-2.0 mU/min IV or 10 U/L NS increase by 1 2 mU/min q20-60min Max 36-48 mU/min 10 U IM at delivery of anterior shoulder and of placenta 20 U/L NS or RL IV continuous infusion 5 million U IV, then 2.5 million U IV q4h until delivery GBS prophylaxis 0.5 mg PV q6-12h; max 3 doses Induction of labour 300 µg IM x 1 dose Given to Rh negative women Routinely at 28 wk GA Within 72 h of birth of Rh+ fetus Positive Kleihauer-Betke test With any invasive procedure in pregnancy Ectopic pregnancy A tepartum hemorrhage Miscarriage or therapeutic abortion (dose: 50 µg IM only)

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Penicillin G PGE2 gel (Prostin® gel) Rh IgG (Rhogam®)

Misoprostol (Cytotec®) is also indicated to protect against NSAID-induced gastric ulcers in non-pregnant individuals. The use of misoprostol for cytoprotection is contraindicated in pregnancy; warn female patients of this contraindication

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For treatment of PPH For medical abortion/retained products of conception Also used for NSAID-induced ulcers (warn patients of contraindications) Augmentation of labour (also induction of labour) Prevention of uterine atony Treatment of uterine atony

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oxytocin (Pitocin®)

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methotrexate methylergonavine maleate (Ergotamine®) misoprostol (Cytotec®)

Treatment of uterine atony GBS prophylaxis (penicillin allergic and not at risk for anaphylaxis) Used in endometritis Enhancement of fetal pulmonary maturity for PTL Induction of labour Advantage: can remove if uterine hyperstimulation Each tablet contains 10 mg doxylamine succinate with vitamin B6 Used for hyperemesis gravidarum GBS prophylaxis (penicillin allergic and at risk for anaphylaxis) Prevention of ONTD

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0.25 mg IM/IMM q15min; max 2 mg 2 g IV then 1 g q8h 900 mg IV q8h 6 mg IM q12h x 4 doses 10 mg PV (remove after 12 h) Max 3 doses 2 tabs qhs + 1 tab qAM + 1 tab qPM Max 8 tabs/d 500 mg IV q6h 0.4-1 mg PO OD x 1-3 mo preconception and T1 5 mg PO OD with past Hx of NTD/risks for NTD 50 mg/m2 IM or 50 mg PO x 1 dose .25 mg IM/IMM q15min up to 1.25 mg or IV bolus 0.125 mg 600-1000 µg PR x 1 dose 400 µg PO/SL x 1 dose or 800 µg PV x 1 dose 3-7 d after methotrexate

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Drug Name (Brand Name) betamethasone valerate (Celestone®) carboprost (Hemabate®) cefazolin clindamycin dexamethasone dinoprostone (Cervidil®: PGE2 impregnated thread) doxylamine succinate (Diclectin®) erythromycin folic acid

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Table 26. Common Medications

OB48 Obstetrics

Toronto Notes 2018

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References

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References

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American College of Obstetricians and Gynecologists. Available from: www.acog.org. The Society of Obstetricians and Gynaecologists of Canada. Available from: www.sogc.org Alfirevic Z Devane D, Gyte GM. Continuous cardiotocography (CTG) as a form of e ectronic fetal monitoring (EFM) for fetal assessment during labour. Cochrane DB Syst Rev 2013;5:CD006066. Antenatal Corticosteroid Therapy for Fetal Maturation. SOGC clinical practice guidelines policy statement. December 1995:53. Arsenault M, Lane CA. Guidelines for the management of nausea and vomiting in pregnancy. SOGC Clinical Practice Guidelines Committee Opinion 2002;120:1 7. Banti S, Mauri M, Oppo A, et al. From the third month of pregnancy to 1 year postpartum. Prevalence, incidence, recurrence, and new onset of depression. Results from the perinatal depression-research & screening unit study. Compr Psychiatry 2011;52:343-51. Baskett T. Essential management of obstetric emergencies, 3rd ed. Bristol: Clinical Press, 1999. Bastian LA, Piscitelli JT. Is this patient pregnant? Can you reliably rule in or rule out early pregnancy by clinical examination? JAMA 1997;278:586-591. Berghella V, Odibo AO, Tolosa JE. Cerclage for prevention of preterm birth in women with a short cervix found on transvaginal examination: a randomized trial. Am J Obstet Gynecol 2004;191:1311-1317. Berghella V, Rafael TJ, Szychowski JM, et al. Cerclage for short cervix on ultrasonography in women with singleton gestations and previous preterm birth: a meta-analysis. Obstet Gynecol 2011;117:663-671. Blenning CE, Paladine H. An approach to the postpartum office visit. Am Fam Physician 2005;72:2491-2496. Boucher M. Mode of delivery for pregnant women infected by the human immunodeficiency virus. Clinical Practice Guidelines Policy Statement 2001:101. Boucher M, Gruslin A. The reproductive care of women living with hepatitis C infection. Clinical Practice Guidelines Policy Statement 2000:96. Bricker L, Luckas M. Amniotomy alone for induction of labour. Cochrane DB Syst Rev 2000;(4):CD002862. Carroli G, Mignini L. Episitotomy for vaginal birth. Cochrane DB Syst Rev 2009;1:CD000081. Chamberlain G, Zander L. Induction BMJ 1999;318:995-998. Chamberlain G, Steer P. Labour in special circumstances. BMJ 1999;318:1124-1127. Chamberlain G, Steer P Obstetric emergencies. BMJ 1999;318:1342-1345. Chamberlain G, Steer P Operative delivery. BMJ 1999;318:1260-1264. Chamberlain G Steer P. Unusual presentations and positions and multiple pregnancy. BMJ 1999;318:1192-1194. Chodirker BN, Cadrin C, Davies GAL, et al. Canadian guidelines for prenatal diagnosis. Techniques of prenatal diagnosis. SOGC Clinical Practice Guidelines 2001:105. Chyu JK, Strassner HT. Prostaglandin E2 for cervical ripening: a randomized comparison of cervidil vs. prepidil. Am J Obstet Gynecol 1997;177:606-611. Cohen-Kerem R, Nulman I, Abramow-Newerly M, et al. Diagnostic radiation in pregnancy: perception versus true risks. JOGC 2005;28:43-48. Crane J. Induction of labour at term. SOGC Clinical Practice Guidelines 2001;107:1-12. Farrell S, Chan MC, Schulz JA. Midurethral minimally invasive sling procedures for stress urinary incontinence. SOGC Clinical Practice Guidelines 2008;213:728-733. Findley I, Chamberlain G. Relief of pain. BMJ 1999;318:927-930. Ford HB, Schust DJ. Recurrent pregnancy loss: etiology, diagnosis, and therapy. Rev Obstet Gynecol 2009;2:76-83. Gagnon A, Wilson R. Obstetrical complications associated with abnormal maternal serum markers analytes. SOGC Clinical Practice Guidelines 2008;216:918-932. Gavin NI et al. Perinatal depression: a systematic review of prevalence and incidence. Obstet Gynecol. 2005;106:1071-83. Goldenberg RL, Culhane JF, Iams JD, et al. Epidemiology and causes of preterm birth. Lancet 2008;371;75-84. Guise JM, Berlin M, McDonagh M, et al. Safety of vaginal birth after cesarean: a systematic review. Obstet Gynec 2004;103:420 429. Hajenius PJ, Mol F, Mol BW, et al. Interventions for tubal ectopic pregnancy. Cochrane DB Syst Rev 2007;1:CD000324. Hamilton P. Care of the newborn in the delivery room. BMJ 1999;318:1403-1406. Hennessey MH, Rayburn WF, Stewart JD, et al Preeclampsia and induction of labour: a randomized comparison of prostaglandin E2 as an intracervical gel, with oxytocin immediately, or as a sustained release vaginal insert. Am J Obstet Gynecol 1998;179:1204-1209. Hod M, Bar J, Peled Y, et al. Antepartum management protocol. Timing and mode of delivery in gestational diabetes. Obstet Gynecol 2009;113:206-217. Hodnett ED, Gates S, Hofmeyr GJ, et al. Continuous support for women during childbirth. Cochrane DB Syst Rev 2011;2:CD003766. Howarth GR, Botha DJ. Amniotomy plus intravenous oxytocin for induction of labour. Cochrane DB Syst Rev 2001;3:CD003250. Kelly AJ, Tan B. Intravenous oxytocin alone for cervical ripening and induction of labour. Cochrane DB Syst Rev 2001;3;CD003246. Kent N. Prevention and treatment of venous thromboembolism (VTE) in obstetrics. SOGC Clinical Practice Guidelines 2000;95:2-8. Koren G. Mothe isk update: Caffeine during pregnancy? Can Fam Physician 2000;46:801-803 Kotaska A, Menticoglou S, Gagnon R, et. al. Vaginal delivery of breech presentation. SOGC Clinical Practice Guidelines 2009;226:557-566. Langlois S, Ford J, Chitayat D. Carrier screening for thalassemia and hemoglobinopathies in Canada. J Obstet Gynaecol Can 2008;217:950-959. Langlois S, Wilson R. Carrier screening for genetic disorders in individuals of Ashkenazi Jewish descent. SOGC Clinical Practice Guidelines 2006;177:324-332 L ng F Duff P. Obstetrics and Gynecology, Principles for practice. USA: McGraw-Hill Companies, 2002. Liston R, Sawchuck D, Young D. Fetal health surveillance: antepartum and intrapartum consensus guideline. SOGC Clinical Practice Guidelines 2007;197:S1-60. Lowder JL, Burrows LJ, Krohn MA, et al. Risk factors for primary and subsequent anal sphincter lacerations: a comparison of cohorts by parity and prior mode of delivery. Am J Obstet Gynecol 2007;196:344.e1-5. Luckas M, Bricker L. Intravenous prostaglandin for induction of labour. Cochrane DB Syst Rev 2000;4:CD002864. Mackeen AD, Seibel-Seamon J, Muhammad J, et al. Tocolytics for preterm premature rupture of membranes. Cochrane DB Syst Rev 2014;2:CD007062. Magee LA, Helewa M, Moutquin J-M, et al. Diagnosis, evaluation, and management of the hypertensive disorders of pregnancy. J Obstet Gynaecol Can 2008;30:S1-48. Menezes EV, Yakoob MY, Soomro T, et al. Reducing stillbirths: prevention and management of medical disorders and infections during pregnancy. BMC Pregnancy Childbirth 2009;9(Suppl 1):S4. Menticoglou S, Gagnon R, Kotaska A. Vaginal delivery of breech presentation. SOGC Clinical Practice Guidelines 2009;226:557-566. Ministry of Health and Long Term Care and Canadian Medical Association. Antenatal record 1. Ontario. Ministry of Health and Long Term Care and Canadian Medical Association. Antenatal record 2. Ontario. Money D, Dobson S. The prevention of early-onset group B streptococcal disease. SOGC Clinical Practice Guidelines 2004;149:826-832. Morgan S, Koren G. Is caffeine consumption safe during pregnancy? Can Fam Physician 2013;59(4):361-362. Mottola MF, Wolfe LA, MacKinnon K, et al. Exercise in pregnancy and the postpartum period. SOGC Clinical Practice Guidelines 2003;129:1-7. Mount Sinai Hospital. First trimester combined screening program. 2001. Nicolaides KH, Syngelaki A, Ashoor G, et al. Noninvasive prenatal testing for fetal trisomies in a routinely screened first-trimester population. Am J Obstet Gynecol 2012;207(5):374 North York General Hospital Genetics Program. Integrated prenatal screening. 1999. Ottinyer WS, Menara MK, Brost BC. A randomized control trial of prostaglandin E2 intracervical gel and a slow release vaginal pessary for preinduction cervical ripening. Am J Obstet Gynecol 1998;179:349-353. Ross S, Robert M Conservative management of urinary incontinence. SOGC Practice Guidelines 2006;186:1113-1118. Schrag SJ, Zell ER, Lynfield R, et al. A population-based comparison of strategies to prevent early-onset group B streptococcal disease in neonates. NEJM 2002;347 233 239. Schuurmans N, Gagne G, Ezzat A, et al. Healthy beginnings: guidelines for care during pregnancy and childbirth. Clinical Practice Guidelines Policy Statement 1998;71:1 65. Steer P Flint C. Physiology and management of normal labour. BMJ 1999;318:793-796 Steer P, Flint C. Preterm labour and premature rupture of membranes. BMJ 1999;318:1059-1062. Stewart D. A broader context for maternal mortality. CMAJ 2006;74:302-303. Stewart JD, Rayburn WF, Farmer KC, et al. Effectiveness of prostaglandin E2 intracervical gel (prepidil) with immediate oxytocin vs. vaginal insert (cervidil) for induction of labour. Am J Obstet Gynecol 1998;179:1175-1180. Summers A, Langlois S, Wyatt P, et al. Prenatal screening for fetal aneuploidy. SOGC Clinical Practice Guidelines 2007;187:146-161. Thompson D, Berger H, Feig D, et al. Diabetes and Pregnancy. Can J Diabetes 2013;37:S168-S183. Van den Hof M, Crane J. Ultrasound cervical assessment in predicting preterm birth. SOGC Clinical Practice Guidelines 2001;102:1-4. Verani JR, McGee L, Schrag SJ. Prevention of perinatal group B streptococcal disease. MMWR 2010;59(No.RR-10):1-32. Zander L, Chamberlain G. Place of birth. BMJ 1999;318:721-723. Zhang J, Bowes WA Jr, Fortney JA. Efficacy of external cephalic version: a review. Obstet Gynecol 1993;82(2):306-312.

Ophthalmology

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Daniel Q. Li, and Fady Sedarous, and Tarek A. Bin Yameen, chapter editors Sangwoo Leem and Mark Shafarenko, associate editors Jin Kyu Kim and Shubham Shan, EBM editors Dr. Wai-Ching Lam, Dr. Marisa Sit, and Dr. Joshua Teichman, staff editors

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7 9

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The Orbit . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Globe Displacement Orbital Cellulitis Preseptal Cellulitis

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Lacrimal Apparatus. . . . . . . . . . . . . . . . . . . . . . . 10 Dry Eye Syndrome (Keratoconjunctivitis Sicca) Epiphora (Excessive Tearing) Dacryocystitis Dacryoadenitis Lids and Lashes. . . . . . . . . . . . . . . . . . . . . . . . . . . 11 Entropion Lid Swelling Ectropion Ptosis Trichiasis

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Malignancies . . . . . . . . . . . . . . . . . . . . . . . . . . 31 Lid Carcinoma Metastases Uveal Melanoma

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Optics. .

Ocular Manifestations of Systemic Disease . . . . 32 HIV/AIDS Other Systemic Infections Diabetes Mellitus Hypertension Multiple Sclerosis TIA/Amaurosis Fugax Graves’ Disease Connective Tissue Disorders Giant Cell Arteritis/Temporal Arteritis Sarcoidosis

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The Ocular Examination. . . . . . . . . . . . . . . . . . . . . 5

Pupils . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 28 Pupillary Light Reflex Pupil Abnormalities Dilated Pupil (Mydriasis) Constricted Pupil (Miosis) Relative Afferent Pupillary Defect

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Ocular Emergencies. . . . . . . . . . . . . . . . . . . . . . . . . 5

Glaucoma. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25 Primary Open-Angle Glaucoma Normal Tension Glaucoma Secondary Open Angle Glaucoma Primary Angle-Closure Glaucoma Secondary Angle Closure Glaucoma

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Differential Diagnoses of Common Presentations. . . . . . . . . . . . . . . . . . . . 3 Loss of Vision Red Eye Ocular Pain Floaters Flashes of Light (Photopsia) Photophobia (Severe Light Sensitivity) Diplopia (Double Vision) Ocular Problems in the Contact Lens Wearer Acute Painless Vision Loss

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Basic Anatomy Review. . . . . . . . . . . . . . . . . . . . . . 2

Retina. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22 Central/Branch Retinal Artery Occlusion Central/Branch Retinal Vein Occlusion Retinal Detachment Retinitis Pigmentosa Age-Related Macular Degeneration

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Acronyms. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2

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Pediatric Ophthalmology . . . . . . . . . . . . . . . . . 36 Conjunctiva . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13 Pinguecula Subconjunctival Hemorrhage Strabismus Amblyopia PterygiumTrichiasis Conjunctivitis Leukocoria Retinoblastoma Sclera . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15 Retinopathy of Prematurity Episcleritis Scleritis Nasolacrimal System Defects Ophthalmia Neonatorum Cornea . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16 Congenital Glaucoma Herpes Zoster Foreign Body Ophthalmicus Corneal Abrasion Ocular Trauma. . . . . . . . . . . . . . . . . . . . . . . . . . . . 39 Keratoconus Recurrent Erosions Blunt Trauma Arcus Senilis Corneal Ulcer Penetrating Trauma Herpes Simplex Keratitis Kayser-Fleischer Ring Hyphema Blow-Out Fracture The Uveal Tract . . . . . . . . . . . . . . . . . . . . . . . . . . . 19 Chemical Burns Uveitis

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Vitreous . . . . . . . . . . . . . . . . . . . . . . . . . Posterior Vitreous Detachment Vitreous Hemorrhage Endophthalmitis and Vitritis

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Lens. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20 Cataracts Dislocated Lens (Ectopia Lentis) . . . . 21

Ocular Drug Toxicity . . . . . . . . . . . . . . . . . . . . . 41 Common Medications. . . . . References . . . . . . . . .

Ophthalmology OP1

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Toronto Notes 2018

OP2 Ophthalmology

Toronto Notes 2018

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Acronyms

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Acronyms RAPD RD ROP RPE SLE SPK TIA VEGF YAG

optical coherence tomography ocular hypertension primary angle-closure glaucoma proliferative diabetic retinopathy photodynamic therapy pupils equal, round, and reactive to light and accommodation primary open-angle glaucoma photorefractive keratectomy posterior vitreous detachment rheumatoid arthritis

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OCT OHT PACG PDR PDT PERRLA POAG PRK PVD RA

relative afferent pupillary defect retinal detachment retinopathy of prematurity retinal pigment epithelium systemic lupus erythematosus superficial punctate keratitis transient ischemic attack vascular endothelial growth factor yttrium aluminium garnet

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EOM extraocular movement FML fluoromethalone GAT Goldmann applanation tonometry GCA giant cell arteritis GPC giant papillary conjunctivitis HRT Heidelberg retinal tomography INO internuclear ophthalmoplegia IOL intraocular lens IOP intraocular pressure LASIK laser-assisted in situ keratomileusis MS multiple sclerosis

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AION anterior ischemic optic neuropathy AMD age-related macular degeneration BCVA best corrected visual acuity BRAO branch retinal artery occlusion BRVO branch retinal vein occlusion C:D cup to disc ratio CMV cytomegalovirus CRAO central retinal artery occlusion D diopter DM diabetes mellitus DR diabetic retinopathy

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Basic Anatomy Review Lateral View

Superior View

Tendon of superior rectus muscle

Cornea Ciliary muscle and body

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Retina

Choroid

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Meibomian gland

Ciliary muscle and body

Tendon of lateral rectus muscle

Sclera

Eyelash

Tendon of medial rectus muscle

Retina

Lens

Cornea

Lens

Anterior chamber Iris Bulbar conjunctiva

Optic nerve

Choroid

Optic nerve Retinal blood vessels

Tendon of inferior rectus muscle

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Conjunctival fornix

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Figure 1. Anatomy of the eye RETINAL LAYERS (10) 1. Inner limiting membrane 2. Nerve fibre layer

CELL TYPES

LIGHT RAYS

Vitreous humour Optic nerve fibres

3. Ganglion cell layer

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Ganglion cells

4. Inner plexiform layer Amacrine cells Bipolar cells

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5. Inner nuclear layer

Horizontal cells 6. Outer plexiform layer

7. Outer nuclear layer

Rod nuclei Cone nuclei

8. Outer limiting membrane

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Rod cells Cone cells

9. Photoreceptor layer

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Pigmented cells

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10. Retinal pigmented epithelium

Bruch’s membrane Choroid

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© Melissa Phachanhla 2016 after Sarah A. Kim 2005

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Figure 2. Layers of the retina

© Jenn Tse 2006

Fovea

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Retinal blood vessels

Bulbar conjunctiva

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Sclera

Palpebral conjunctiva

OP3 Ophthalmology

Toronto Notes 2018

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Differential Diagnoses of Common Presentations

Lacrimal gland

Lacrimal canaliculus

Meibomian gland

Fundus of lacrimal sac Nasolacrimal duct

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© Jenn Tse 2006

Inferior concha

Figure 3. Tear drainage from the eye (lacrimal apparatus)

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Loss of Vision

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Differential Diagnoses of Common Presentations

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Red Eye

Table 1. Common Causes of Red Eye

Conjunctiva/sclera Subconjunctival hemorrhage Conjunctivitis Dry eyes Pterygium Episcleritis/scleritis Preseptal/orbital cellulitis

Anterior chamber Anterior uveitis (iritis, iridocyclitis) Acute glaucoma Hyphema (blood in anterior chamber) Hypopyon (pus in anterior chamber)

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Other Trauma Post-operative endophthalmitis Pharmacologic (e g. prostaglandin analogs)

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Cornea Foreign body (including contact lens) Keratitis Abrasion, laceration Ulcer

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Lids/orbit/lacrimal system Hordeolum/chalazion B epharitis Entropion/ectropion Foreign body/laceration Dacryocystitis/dacryoadenitis

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Note: Anti-VEGF treatm nt for exudative AMD and diabetic macular edema may reverse some vision loss

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Figure 4. Loss of vision

Top 3 Differential Diagnosis of Chronic Loss of Vision Reversible • Cataract • Refractive error • Corneal dystrophy • Glaucoma Irreversible • AMD • DR

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Vitreous/Retina/ Cortical/Other Optic Nerve • Pituitary adenoma • AMD • DR • Medicationinduced • Retinal vascular insufficiency (sildenafil, • Compressive amiodarone) optic neuropathy • Nutritional (intracranial mass, deficiency • Papilledema orbital mass) • Int aocular neoplasm • Retinitis pigmentosa

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Cornea/Anterior Segment • Corneal dystrophy/ scarring/edema • Refractive error • Cataract • Glaucoma

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Vitreous/Retina/ Cortical/Other Optic Nerve • Occipital infarction/ • Vitreous hemorrhage hemorrhage • RD • Cortical blindness • Retinal artery/ vein occlusion • Functional (non-organic, • Acute macular diagnosis of lesion • Optic neuritis exclusion) • Temporal arteritis • Anterior ischemic optic neuropathy (AION)

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Cornea/Anterior Segment • Corneal edema • Hyphema (blood in anterior chamber) • Acute angleclosure glaucoma • Trauma/foreign body

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Top 3 Differential Diagnosis of Acute Loss of Vision • Vitreous hemorrhage Retinal artery/vein occlusion • Retinal detachment

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Chronic (weeks to months)

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• Transient ischemic attack (TIA) • Migraine with aura

Acute (seconds to days)

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Transient (seconds to hours)

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Loss of Vision

OP4 Ophthalmology

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Differential Diagnoses of Common Presentations

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Ocular Pain • differentiate from eye fatigue (asthenopia) • ocular surface disease • herpes zoster prodrome • trauma/foreign body • blepharitis • keratitis

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• corneal abrasion/ulcer • acute glaucoma • acute uveitis • scleritis • episcleritis • optic neuritis

Floaters

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• PVD (often secondary to age-related vitreous syneresis) • vitreous hemorrhage • retinal tear/detachment • intermediate uveitis (pars planitis) • posterior uveitis (chorioretinitis)

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Flashes of Light (Photopsia)

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• PVD (often secondary to age-related vitreous syneresis) retinal tear/detachment • migraine with aura

Photophobia (Severe Light Sensitivity) • corneal abrasion, corneal ulcer • keratitis • acute angle-closure glaucoma • iritis

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• meningitis/encephalitis • migraine • subarachnoid hemorrhage (SAH)

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Diplopia (Double Vision)

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Table 2 Common Causes of Diplopia Occurs with both eyes open, eliminated with occlusion of either eye

Occurs with one eye open, remains with occlusion of unaffected eye

Causes

Causes

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Monocular Diplopia

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Binocular Diplopia

Occular motor nerve dysfunction: III IV, VI Nerve Palsy

Mechanical process: dislocated lens, postoperative sequelae (cataract surgery, peripheral laser iridotomy)

Neuromuscular junction disease: myasthenia gravis, botulism

Other: strands of mucus in tear film (keratoconus)

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Optical factors: refractive error/astigmatism

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Disease of eye muscle: congenital strabismus syndromes

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Mechanical process: muscle restriction/entrapment, thyroid ophthalmopathy

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f

Supranuclear Causes INO (multiple sclerosis, brainstem infarct)

• SPK from dry eyes • limbal stem cell deficiency • corneal neovascularization • sterile corneal infiltrates (immunologic) • infected ulcers (Pseudomonas, Acanthamoeba)

fre

• vitreous hemorrhage • retinal artery/vein occlusion • RD

• AION • optic neuritis • amaurosis fugax/TIA/stroke

sf r

e. c

Acute Painless Vision Loss

om

• solution hypersensitivity • tight lens syndrome • corneal abrasion • giant papillary conjunctivitis/contact lens allergy

b

b

bo

Ocular Problems in the Contact Lens Wearer

Toronto Notes 2018

OP5 Ophthalmology

Toronto Notes 2018

c

Ocular Emergencies

re

Table 3. Common Differential Diagnoses of Red Eye Conjunctivitis

Acute Iritis

Acute Glaucoma

No

Profuse tearing

Keratitis (Corneal Abrasion/Ulcer)

Bacterial: purulent

bo

o

Discharge

Viral: serous/mucoid ±

++ (dull/achy)

+++ (nausea)

++ (sharp)

Photophobia

No

+++

+

++

Blurred Vision

No

++

+++

Varies

Pupil

Normal

Smaller

Fixed in mid dilation

Same or smaller

Injection

Diffuse conjunctival injection involving the bulbar conjunctiva for 360 + palpebral or tarsal conjunctiva

Ciliary flush (peri-limbal)

Conjunctival injection

±

Limbal Pallo

Ciliary flush

Diffuse

Diffuse

No

Cornea

Normal

Keratic precipitates

Cloudy

Infiltrate, edema, and may have keratic precipitates

Varies

Increased markedly

Normal or slightly decreased

+++ Cells and flare

Shallow

Cells and flare or normal

Posterior synechiae

Coloured halos

Not every red eye has conjunctivitis

Other

Large, tender pre auricular node(s) if viral

Example 1 SC 20/40 –1 20/80 +2 g 20/25 PH

V

Example 2 CC CF 3' HM

V

re

e

Ocular Emergencies

Note: RIGHT EYE visual acuity always listed on top.

s

s

These require urgent ophthalmology consultation for management

fe

Nausea and vomiting

V Vision SC Without correction CC With correction All except one letter of 20/40 -1 20/40 20/80+2 All of 20/80 plus two letters of 20/70 PH Visual acuity with pinhole correction CF Counting fingers HM Hand motion

bo

o

Sight Threatening • lid/globe lacerations • chemical burn corneal ulcer • gonococcal conjunctivitis • acute iritis • acute glaucoma • CRAO • intraocular foreign body • RD (especially when macula threatened) • endophthalmitis • GCA

fr

ok

ks

OD = oculus dexter = right eye OS = oculus sinister = left eye OU = oculus uterque = both eyes

b

s

o

co

Figure 5. Ophthalmology nomenclature for visual acuity

Life-Threatening • proptosis (rule out cavernous sinus fistula or thrombosis) • CN III palsy with dilated pupil (intracranial aneurysm or externally compressive neoplastic lesion) • papilledema (elevated increased intracranial pressure workup) • orbital cellulitis • leukocoria: white reflex (absent red reflex, must rule out retinoblastoma)

oo

m

Normal

c

Anterior Chamber

e

Normal

m

IOP

m

o

e

k

ee

.c

m

Pain

co

No

e

Allergic: mucoid

m

The Ocular Examination

Snellen visual acuity of 20/20 equates to “normal” vision

ok

e. c

Normal Infant and Child Visual Acuity • 6-12 mo: 20/120 • 1-2 yr 20/80 • 2-4 yr: 20/20

re

c

sf re e

sf

ee

c

Visual Acuity – Distance • Snellen Acuity (Figure 5) = testing distance (usually 20 ft or 6 m) smallest line patient can read on the chart ■■ e.g. 20/40 = what the patient can see at 20 feet (numerator), what a “normal” person can see at 40 feet (denominator) • distance visual acuity should be tested with distance glasses on in order to obtain best corrected visual acuity • testing hierarchy for low vision: Snellen acuity (20/x) → counting fingers at a given distance (CF) → hand motion (HM) → light perception with projection (LP with projection) → light perception (LP) → no light perception (NLP)

OP6 Ophthalmology

Toronto Notes 2018

c

The Ocular Examination

sf r

ks fre

• legal blindness is BCVA that is ≤20/200 in best eye • minimum visual requirements to operate a non-commercial automobile in Ontario are: 20/50 BCVA with both eyes open and examined together, 120° continuous horizontal visual field, and 15° continuous visual field above and below fixation

For patients with dark irides, test pupils using an ophthalmoscope focused on the red reflex; this will provide a better view than using a penlight

m

m

eb

o

Visual Acuity – Near • use pocket vision chart (Rosenbaum Pocket Vision Screener) • record Jaeger (J) or Point number and testing distance (usually 30 cm) e.g. J2 @ 30 cm • conversion to distance visual acuity possible (e.g. immobile patient, no distance chart available)

4 Ps of Inspection Pupil: shape, size, symmetry Position: esotropia, exotropia, central Ptosis Primary nystagmus

fre

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Visual Acuity for Infants, Children, Non-English Speakers, and Dysphasics • newborns ■■ VA cannot be tested conventionally • 3 mo-3 yr (can only assess visual function, not acuity) ■■ test each eye for fixation symmetry using an interesting object ■■ normal function noted as “CSM” = central, steady, and maintained • 3 yr until alphabet known ■■ pictures or letter cards/charts such as HOTV or Sheridan-Gardner test (children point to optotypes on a provided matching card) ■■ tumbling “E” chart Colour Vision • test with Ishihara pseudoisochromatic plates • record number of correctly identified plates presented to each eye, specify incorrect plates • important for testing optic nerve function (e.g. optic neuritis, chloroquine use, thyroid ophthalmopathy) • note: red-green colour blindness is sex-linked and occurs in 7-10% of males

RIGHT EYE fields drawn on right side; LEFT EYE fields drawn on left side (as if seen through patient’s eyes).

m

CF Able to count fingers in specified quadrant with peripheral vision

e

Gross visual field deficit in specified quadrant using peripheral vision

e

fre

c

c

m

VISUAL FIELDS • test “visual fields by confrontation” (4 quadrants, each eye tested separately) for estimation of visual field loss • accurate, quantifiable assessment with automated visual field testing (Humphrey or Goldmann) or Tangent Screen • use Amsler grid (each eye tested separately) to check for central or paracentral scotomas (blindspots) in patients with AMD

CF CF

co

m

e

bo

CF CF CF CF

f

Figure 6. Ophthalmology nomenclature for visual fields by confrontation

o

Deep

m

eb

bo

oo

o

PUPILS • use reduced room illumination with patient focusing on distant, fixed object to prevent near reflex • examine pupils for shape, size, symmetry, and reactivity to light (both direct and consensual response) test for RAPD with swinging flashlight test, check by reverse RAPD if one pupil non-reactive • test pupillary constriction portion of near reflex by bringing object close to patient’s nose • “normal” pupil testing often noted as PERRLA (pupils equal, round, reactive to light and accommodation)

Light source

co

m

ANTERIOR CHAMBER DEPTH • shine light tangentially from emporal side • if >2/3 of nasal side of iris in shadow → shallow anterior chamber

© Doris Leung

e

sf r

Figure 7. Estimation of anterior chamber depth

fre

m

sf

re

e.

Movement • examine movement of eyeball through six cardinal positions of gaze • ask patient if diplopia or pain is present in any position of gaze • observe for horizontal, vertical, or rotatory nystagmus (rhythmic, oscillating movements of the eye) • resolving horizontal nystagmus at end-gaze is usually normal

oo

Light source

m

Alignment • Hirschberg corneal reflex test ■■ examine in primary position of gaze (i.e. straight ahead) with patient focusing on distant object ■■ shine light into patient’s eyes from ~30 cm away ■■ corneal light reflex should be at the same position on each cornea • strabismus testing as indicated (cover test, cover-uncover test, prism testing) (see Strabismus, OP50)

Diplopia • see Neurology – Neuro-ophthalmology Diplopia

Shallow

o

EXTRAOCULAR MUSCLES

ok

oo

s

s

re

e

ee

The van Herick Method (Slit Lamp technique) • shine thin-angled slit beam onto the peripheral cornea of each eye, view at a 60° angle from the beam • estimate depth between the posterior surface of the cornea and the iris as a proportion of corneal thickness • ratios ≤1/4 implies risk of occludable angle; however, if >1/4, this does not rule out risk • gonioscopy, as performed by an ophthalmologist, is gold-standard for assessing anterior chamber depth

OP7 Ophthalmology

Toronto Notes 2018

Optics

re

SLIT-LAMP EXAMINATION

IO

IO

SR

r

SR

Ocular Adnexa • lids, lashes, lacrimal system

MR MR

s

ks

LR SO

SO

IR

© Sherry H. Lai 2006

Figure 8. Diagnostic positions of gaze for isolated primary actions of extraocular muscles

m

Extraocular Muscle Innervations

c

LR6 SO4 AE3 Lateral Rectus via CN VI Superior Oblique via CN IV All Else via CN III (superior, medial, and infe ior rectus, inferior oblique)

m

om

Note: RIGHT EYE drawn on the left, LEFT EYE drawn on the right (as if looking at patient’s face) ok injected 1+ edema 2+ cells ok 2+ NS

e

LLL SC K AC d+q NS

om

x

fre

fe

Lids, lashes, lacrimal Sclera, conjunctiva Cornea Anterior chamber Deep (not shallow) and quiet (no cells in AC) Nuclear sclerosis (cataract)

N D/M/V (normal disc macula, vessels)

e. co

e

oo

ok

Optics

x

m

Any abnormality or pathology is drawn on the sketch in the appropriate location, and is labelled (e.g. trichiasis, conjunctivitis/episcleritis/scleritis corneal abrasion/ulcer, foreign body, etc.) © Tobi Lam 2012

Figure 9. Slit-lamp examination note

T

m

m

co m

Cup : Disc ratio Fovea

16 14

16

14

e. c

sf re e

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m

b

C:D x

C:D 0.4

Note: RIGHT EYE lOP always listed on top. Always include time.

re

ok

C:D 0.3

REFRACTION • two techniques used ■■ flash/streak retinoscopy: refractive error determined objectively by the examiner using lenses and retinoscope ■■ manifest: subjective trial using loose lenses or a phoropter (device the patient looks through that is equipped with lenses) ■■ cycloplegic: manifest refraction with accommodation temporarily paralyzed with cycloplegics • a typical lens prescription would contain ■■ sphere power in dioptre (measurement of refractive power of lens, equal to reciprocal of focal length in metres) ■■ cylinder power in dioptre to correct astigmatism ■■ axis of cylinder in degrees ■■ “add” (bifocal/progressive reading lens) for presbyopes ■■ e.g. -1.50 + 1.00 x 120 degrees, add +2.00

ok ok clear d+q ok ok

Eyelids/eyelashes Conjunctiva/sclera/episclera Cornea/Iris/anterior surface of lens

s

sf

r

DIRECT OPHTHALMOSCOPY • best performed with pupils dilated (for list of mydriatics and cycloplegics see Table 13, OP58) 1. asse s red reflex ◆ light reflected off the retina produces a “red reflex” when viewed from ~1 foot away ◆◆ anything that interferes with the passage of light will diminish the red reflex (e.g. large vitreous hemorrhage, cataract, retinoblastoma) 2. examine the posterior segment of the eye ◆◆ vitreous ◆◆ optic disc (colour, C:D ratio, sharpness of disc margin) ◆◆ macula (~1.5-2 disc diameters temporal to disc), fovea (foveal light reflex) ◆◆ retinal vessels ◆◆ retinal background • contraindications to pupillary dilatation ■■ shallow anterior chamber – can precipitate acute angle-closure glaucoma ■■ iris-supported anterior chamber lens implant ■■ potential neurologic abnormality requiring pupil evaluation ■■ use caution with cardiovascular disease – mydriatics may cause tachycardia and hypertension

LLL SC K AC Iris Lens

(After Bader)

e

co

m

m

m

TONOMETRY • measurement of IOP • normal range is 9-21 mmHg (average 15 mmHg) • IOP has diurnal variation, so always record the time of day at which the measurement was taken • commonly measured by ■■ GAT: clinical gold standard, performed using the slit-lamp with special tip (prism) ■■ Tono-Pen®: benefit is portability and use of disposable probe tips; use when cornea is scarred/ asymmetric (GAT inaccurate) ■■ air puff (non-contact and least reliable) • use topical anesthetic for GAT and Tono-Pen®; apply fluorescein dye when using GAT

Aqueous Flare • Resembles dust particles in a beam of light • Results from protein leaking from blood vessels • Distinguish from aqueous cells (individual cells in anterior chamber)

.c

bo

ks

fre

e

Posterior Segment (requires 78D or 90D lens) • vitreous • optic disc (colour, C:D ratio, sharpness of disc margin) • macula (~1.5 2 disc diameters temporal to disc), fovea (foveal light reflex) • retinal vessels • retinal background

ok sf

IR

e.

m

m

bo

Anterior Segment • conjunctiva / sclera • cornea ■■ fluorescein dye: stains de-epithelialized cornea; dye appears fluorescent green with cobalt blue filtered light ■■ Rose Bengal dye: stains devitalized corneal epithelium • anterior chamber/angle (Van Herick) • iris/pupil • lens (assess for cataract) • anterior vitreous

LR

Note method used to measure lOP (GAT, Tono-Pen®, airpuff).

Figure 10. Tonometry

OP8 Ophthalmology

Toronto Notes 2018

c

Optics

bo

bo

o

oo

sf r

ks fre

REFRACTIVE EYE SURGERY • permanently alters corneal refractive properties by ablating tissue to change curvature of the cornea • used for correction of myopia, hyperopia, and astigmatism • common types include PRK and LASIK • potential risks/side-effects: infection, under/overcorrection, increased glare/halo perception at night, corneal haze (PRK only), dry eyes (more common in LASIK than PRK), regression, and flap complications such as free cap (loss of flap), traumatic flap dislocations, buttonhole flap, and epithelial in growth (LASIK only)

Central Corneal Thickness (CCT) Average CCT = 550 µm By GAT, IOP is over-estimated with thick corneas and under-estimated with thin corneas

Table 4. Optics No refractive error

Myopia

Globe too long relative to refractive mechanisms, or refractive mechanisms too strong Light rays from distant object focus in front of retina → blurring of (distance) vision

“Nearsightedness” Usually presents in 1st or 2nd decade, stabilizes in 2nd and 3rd decade; rarely begins after age 25 except in patients with DM or cataracts Blurring of distance v sion; near vision usually unaffected Prevalence: 30 40% in U.S. population

Correct with negative diopter/ concave/”negative” lenses to diverge light rays Refractive eye surgery

Retinal tear/ detachment, macular hole, open angle glaucoma Other complications that are not prevented with refractive correction

Globe too short relative to refractive mechanisms, or refractive mechanisms too weak Light rays from distant object focus behind retina → blurring of near ± distant vision May be developmental or due to any etiology that shortens globe

“Farsightedness” Youth: usually do not require glasses (still have sufficient accommodative ability to focus image on retina), but may develop accommodative esotropia (see Strabismus, OP36) 30s-40s: blurring of near vision due to decreased accommodation, may need reading glasses >50s: blurring of distance vision due to severely decreased accommodation

When symptomatic, correct with positive diopter/convex/”plus” lenses to converge light rays Refractive eye surgery

Angle-closure glaucoma, particularly later in life as lens enlarges

Light rays not refracted uniformly in all meridians due to non-spherical surface of cornea or non-spherical lens (e.g. football-shaped) Two types Regular – curvature uniformly different in meridians at right angles to each other Irregular – distorted cornea caused by injury, keratoconus (cone-shaped cornea), corneal scar, or severe dry eye

Affects ~30% of population, with prevalence increasing with age Mild astigmatism unnoticeable Higher amounts of astigmatism may cause blurry vision, squinting, asthenopia, or headaches

Correct with cylindrical lens (if regular Try contact lens (if irregular) Refractive eye surgery

Normal aging process (>40 yr) Hardening/reduced deformability of lens results in decreased accommodative ability Accommodative power is 14D at age 10, diminishes to 3.5D by age 40 yr Near images cannot be focused onto the retina (focus is behind the retina as in hyperopia)

If initially emmetropic, person begins to hold reading material farther away, but distance vision remains unaffected If initially myopic, person removes distance glasses to read If initially hyperopic, symptoms of presbyopia occur earlier

s

oo

LMN Long globe Myopic Negative correction/Nearsighted

F

Emmetropia

o

F

Myopia F

f

re

e.

om

m

eb

re e Hyperopia

Myopia

c

Image of distant objects focus exactly on the retina

m

Emmetropia

fre

Complications

c

Treatment

ee

Clinical Features

.c om

Pathophysiology

eb

Figure 11. Emmetropia and refractive errors

Structures Responsible for Refractive Power • Cornea (2/3) • Lens (1/3)

ee

co

m

m

b

Astigmatism

oo

k

Hyperopia

Myopia corrected with negative diverging lens

eb

oo

Correct with positive diopter/convex/”plus” lenses for reading

F

co

ee .

Anisometropia Difference in refractive errors between eyes

Hyperopia corrected with positive converging lens

Figure 12. Correction of refractive errors

m

m

m

Presbyopia

F

Second most common cause of amblyopia in children

OP9 Ophthalmology

Toronto Notes 2018

The Orbit

fre

The Orbit

o

Globe Displacement

e

b

Table 5. Exophthalmos (Proptosis) and Enophthalmos Enophthalmos

co m

Investigations CT/MRI head/orbits ultrasound orbits, thyroid function tests

CT/MRI orbits

Note: rule out pseudoexophthalmos (e.g. lid retraction) Graves’ disease (unilateral or bilateral, most common causein adults) Orbital cellulitis (unilateral, most common cause in children) 1° or 2° orbital tumours Orbital/retrobulbar hemorrhage Cavernous sinus thrombosis or fistula

“Blow-out” fracture (see Ocular Trauma, OP39) Orbital fat atrophy Congenital abnormality Metastatic disease

sf re

e

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Etiology

Posterior displacement (retraction) of the globe

co

Exophthalmos (Proptosis)

Anterior displacement (protrusion) of the globe Exophthalmos generally refers to an endocrine etiology or protrusion of >18 mm (as measured by a Hertel exophthalmometer) Proptosis generally refers to other etiologies (e.g. cellulitis) or protrusion of >18 mm

Definition

o

Preseptal Cellulitis

m

e

infection of soft tissue anterior to orbital septum Etiology • usually follows periorbital trauma or dermal infection Clinical Features

Present

Chemosis

Absent or mild

Marked

Proptosis

Absent

Present

Pain on eye movement

Absent

Present

Ocular mobility

Normal

Decreased

Vision

Normal

Diminished ± diplopia

RAPD

Absent

May be seen if severe

Leukocytosis

Moderate

Marked

ESR

Normal or elevated

Elevated

Additional findings

Skin infection

Sinusitis, dental abscess

eb

ks

re

fre

Treatment • systemic antibiotics (suspect H. influenzae in children; S. aureus or Streptococcus in adults) ■■ e.g. amoxicillin-clavulanic acid • if severe or child 0.2, or cup approaches disc margin

Arcuate defect

Superior expansion 10

20

5

4

3

2

Figure 19. Aqueous flow and sites of potential resistance

© Janice Wong

co

e

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Figure 18. Glaucomatous damage

1. Ciliary body processes 2. Pupillary block 3. Pretrabecular 4. Trabecular and Canal of Schlemm 5. Post-trabecular

re

c

Advanced/total cupping

© Diana Dai 2005

1 Temporal central island

OP26 Ophthalmology

Toronto Notes 2018

c

Glaucoma

fre

fre

Primary Open-Angle Glaucoma

oo

Major Risk Factors • ocular hypertension (IOP >21 mmHg) • age: prevalence at 40 yr is 1-2% and at 80 yr is 10% • ethnicity: African descent • familial (2-3x increased risk); polygenic • thin central cornea (OHTS trial)

m

Risk Factors for POAG A FIAT Age Family history IOP African descent Thin cornea

bo

oo

s

ks fr

Minor Risk Factors • myopia • HTN • DM • hyperthyroidism (Graves’ disease) • chronic topical ophthalmic steroid use in steroid responders – yearly eye exams recommended if >4 wk of steroid use • previous ocular trauma • anemia/hemodynamic crisis (ask about blood transfusions in past)

om

m

Clinical Features • asymptomatic initially • insidious, painless, gradual rise in IOP due to restriction of aqueous outflow • bilateral, but usually asymmetric • earliest signs are optic disc changes ■■ increased C:D ratio (vertical C:D >0.6) ■■ significant C:D asymmetry between eyes (>0.2 difference) ■■ thinning, notching of the neuroretinal rim ■■ flame shaped disc hemorrhage ■■ 360° of peripapillary atrophy ■■ nerve fibre layer defect ■■ large vessels become nasally displaced • visual field loss • slow, progressive, irreversible loss of peripheral vision • paracentral defects, arcuate scotoma, and nasal step are characteristics (Figure 19) late loss of central vision if untreated

Open- and Closed-Angle Glaucoma POAG PACG • Common (95%) • Rare (5%) • Chronic course •Acute onset • Painless eye •Painful red eye without redness •Extremely  IOP • Moderately  IOP •Hazy cornea • Normal cornea •Mid-dilated pupil and pupil unreactive to light • No N/V •± N/V, abdominal • No halos around pain light •Halos around light

fr

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• most common form, >95% of all glaucoma cases • within the trabecular meshwork and the Canal of Schlemm • insidious and asymptomatic, screening is critical for early detection

bo

o

ok

sf

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e.

e.

Elevated IOP is the only modifiable risk factor that has been proven to prevent progression of glaucoma. Treatment of patients with ocular hypertension but no signs of glaucoma also benefit from a reduction in risk of development of glaucoma

m

Normal Tension Glaucoma

ok

s

Treatment • treat reversible causes

e

ee

c

• POAG with IOP in normal range • often found in women >60 yr, but may occur earlier • associated with migraines, peripheral vasospasm, systemic nocturnal hypotension, sleep apnea • damage to optic nerve may be due to vascular insufficiency

e

fre

e

co

m

The Ocular Hypertension Treatment Study Arch Ophthalmol-Chic 2002;120:701-713 Study: Randomized clinical trial Patients: 1,636 patients with no evidence of glaucomatous damage, aged 40-80 yr, and with IOP between 24-32 mmHg in one eye and between 21-32 mmHg in the other eye. Intervention: Randomized to observation or treatment with commercially available topical ocular hypotensive medication. Main Outcome: Development of visual field abnormality or optic disc deterioration attributed to POAG. Results: Mean reduction in IOP in the medication group was 22.5% ± 9.9% vs. 4.0% ± 11.6% in the observation group. At 5 yr, the probability of developing POAG was 4.4% in the medication group and 9.5% in the observation group (p40 mmHg) • shallow anterior chamber ± cells in anterior chamber

3

B Closed angle with abnormal aqueous flow

c

m

bo

o

fr

Risk Factors • hyperopia: small eye, big lens – large lens crowds the angle • age >70 yr • female • family history • more common in people of Asian and Inuit descent • mature cataracts • shallow anterior chamber • pupil dilation (topical and systemic anticholinergics, stress, darkness)

A. Open angle with normal aqueous flow

e

co m

co m

• 5% of all glaucoma cases • peripheral iris bows forward obstructing aqueous access to the trabecular meshwork • sudden forward shift of the lens-iris diaphragm causes pupillary block and results in impaired drainage, leading to a sudden rise in IOP

m

Primary Angle-Closure Glaucoma

co

m

m

Treatment • OCULAR EMERGENCY: refer to ophthalmologist for acute angle closure glaucoma ■■ aqueous suppressants and hyperosmotic agents • medical treatment (see Glaucoma Medications, Table 14, OP42) ■■ miotic drops (pilocarpine) to reverse pupillary block ■■ multiple topical IOP-lowering agents ■■ hypserosmotic agents such as oral glycerine, or IV mannitol • laser iridotomy is definitive

o

Uveitis • inflamed iris adheres to lens (posterior synechiae)

fre

re

Secondary Angle-Closure Glaucoma

m

e

b

Neovascular Glaucoma • abnormal blood vessels develop on surface of iris (rubeosis iridis), in the angle, and within the trabecular meshwork • due to retinal ischemia associated with PDR or CRVO • treatment with laser therapy to retina reduces neovascular stimulus to iris and angle vessels

Collaborative Normal Tension Glaucoma Study Curr Opin Ophthalmol 2003;14:86-90 Treatment aimed at lowering IOP by 30% in patients with normal tension glaucoma tends to reduce the rate of visual field loss. Due to variability in disease progression and a significant group that shows no visual field loss at 5 yr despite no treatment, urther studies are needed to delineate which subgroups may benefit most from treatment.

m

eb

bo

o

oo

k

Complications • irreversible loss of vision within hours to days if untreated • permanent peripheral anterior synechiae, resulting in permanent angle closure

OP28 Ophthalmology

Toronto Notes 2018

c

Pupils

fr

Pupils

m

om

e

Pupillary Light Reflex

oo

bo

bo

o

ok sf

fr

• light shone directly into eye travels along optic nerve (CN II, afferent limb) → optic tracts → bilateral midbra n • impulses enter bilaterally in midbrain via pretectal area and Edinger-Westphal nuclei • nerve impulses then travel down CN III (efferent limb) bilaterally to reach the ciliary ganglia, and finally to the iris sphincter muscle, which results in the direct and consensual light reflexes

m

α1 – Pupillary dilator muscle contraction (Mydriasis) β2 – Ciliary muscle relaxation (Non-accommodation); increased aqueous humour production M3 – Pupillary sphincter contraction (Miosis); increased ciliary muscle contraction (Accommodation)

m

Pupil Abnormalities

o

oo

ks

ks

fre

ee

.

e.

c

Denervation Hypersensitivity • when post-ganglionic fibres are damaged, the understimulated end-organ attempts to compensate by developing an excess of neuroreceptors and becomes hypersensitive • postganglionic parasympathetic lesions (i.e. Adie’s pupil) ■■ pupil will constrict with 0.125% pilocarpine (cholinergic agonist), normal pupil will not • postganglionic sympathetic lesions (this test is used to differentiate between pre- and post-ganglionic lesions in Horner’s syndrome) ■■ pupil will dilate with 0.125% epinephrine, normal pupil will not

m

oo

ks

fre

e

Anisocoria • unequal pupil size • idiopathic/physiologic anisocoria ■■ 20% of population ■■ round, regular, 2mm F – Subretinal Fluid S – Symptoms – Vision changes O – Orange pigment M – Margin within 3 mm of optic disc

OP33 Ophthalmology

Toronto Notes 2018

Ocular Manifestations of Systemic Disease

eb

b

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k

fr

ok sf r

• toxoplasmosis ■■ focal, grey-yellow-white, chorioretinal lesions with surrounding vasculitis and vitreous infiltration (vitreous cells) ■■ can be congenital (transplacental) or acquired (caused by Toxoplasma gondii protozoa transmitted through raw meat and cat feces) ■■ congenital form more often causes visual impairment (more likely to involve the macula) ■■ treatment: pyrimethamine, sulfonamide, folinic acid, or clindamycin. Consider adding steroids if severe inflammation (vitritis, macular or optic nerve involvement)

Macular edema is the most common cause of visual loss in patients with background DR

e

ee

c

co m

• most common cause of blindness in young people in North America • loss of vision due to: ■■ progressive microangiopathy leading to macular edema ■■ progressive DR → neovascularization → traction → RD and vitreous hemorrhage ■■ rubeosis iridis (neovascularization of the iris) leading to neovascular glaucoma (poor prognosis) ■■ macular ischemia

om

Diabetes Mellitus

s

DIABETIC RETINOPATHY

eb

o

bo

o

Background • altered vascular permeability (loss of pericytes, breakdown of blood-retinal barrier, thickening of basement membrane) • predisposition to retinal vessel obstruction (CRAO, CRVO, and BRVO)

fre

e.

co

m

Expanded 2 Year Follow-Up of Ranizumab Plus Prompt or Deferred Laser or Triamcinuclone Plus Prompt Laser for Diabetic Macular Edema Ophthalmology 2011;118:609-614 Ranibizumab (Lucentis®) with prompt or deferred laser is more effective than intravitreal corticosteroid injections + laser or laser alone with sustained efficacy up to 24 mo

.c

om

m

om

ee

e.

k

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ks

Lens Changes • earlier onset of senile nuclear sclerotic and cortical cataracts • may get hyperglycemic cataract due to sorbitol accumulation (rare) • changes in blood glucose levels (poor control) can suddenly cause refractive changes by 3-4 diopters

m

e

Intravitreal Aflibercept for Diabetic Macular Edema Ophthalmology 2014;121:2247-54 At 52 weeks, intravitreal aflibercept demonstrated significant superiority in functional and anatomic endpoints over laser with similar efficacy in the 2mg q4wks and 2mg q8wks gr up.

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Treatment • Diabetic Control and Complications Trial (DCCT) ■■ tight control of blood sugar decreases frequency and severity of microvascular complications • blood pressure control • focal laser for clinically significant macular edema • intravitreal injection of corticosteroid or anti-VEGF for fovea-involved diabetic macular edema • pan-retinal laser photocoagulation for PDR: reduces neovascularization, hence reducing the angiogenic stimulus from ischemic retina by decreasing retinal metabolic demand → reduces risk of blindness • vitrectomy for non-clearing vitreous hemorrhage and tractional RD in PDR • vitrectomy before vitreous hemorrhage does not improve the visual prognosis

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Presence of DR in Type 1 DM • 25% after 5 yr • 60% af er 10 yr • >80% after 15 yr Type 2 DM • 20% at time of diagnosis • 60% after 20 yr

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Screening Guidelines for Diabetic Retinopathy • type 1 DM ■■ screen for retinopathy beginning annually 5 yr after disease onset ■■ annual screening indicated for all patients over 12 yr and/or entering puberty • type 2 DM ■■ initial examination at time of diagnosis, then annually • pregnancy ■■ ocular exam in 1st trimester, close follow-up throughout as pregnancy can exacerbate DR ■■ gestational diabetics are not at risk for DR

Clinically significant macular edema is defined as thickening of the retina at or within 500 µm of the centre of the macula

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Classification • non-proliferative: increased vascular permeability and retinal ischemia ■■ microaneurysms ■■ dot and blot hemorrhages ■■ hard exudates (lipid deposits), non-specific for DR ■■ macular edema • advanced non-proliferative (or pre-proliferative) ■■ non-proliferative findings plus: ◆◆ venous beading (in ≥2 of 4 retinal quadrants) ◆◆ intraretinal microvascular anomalies (IRMA) in 1 of 4 retinal quadrants – IRMA: dilated, leaky vessels within the retina ◆◆ cotton wool spots (nerve fibre layer infarcts) • proliferative ■■ 5% of patients with DM will reach this stage ■■ neovascularization of iris, disc, retina ◆◆ neovascularization of iris (rubeosis iridis) can lead to neovascular glaucoma ◆◆ vitreous hemorrhage, bleeding from fragile new vessels, fibrous tissue can contract causing tractional RD ■■ may remain asymptomatic well beyond stage of optimal treatment ■■ high risk of severe vision loss secondary to vitreous hemorrhage, RD

OP34 Ophthalmology

Toronto Notes 2018

Ocular Manifestations of Systemic Disease

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Extraocular Muscle Palsy • usually CN III infarct • pupil usually spared in diabetic CN III palsy, but ptosis is observed • may involve CN IV and VI • usually recover within few months

Aflibercept, Bevacizumab, or Ranibizumab for Diabetic Macular Edema: 2 Year Result from a Comparative Effectiveness Randomized Clinical Trial Ophthalmology 2016; 123:1351-1359 All 3 anti-VEGF groups showed improvement of VA and deceased number of injections in year 2. Among eyes with worse baseline VA, aflibercept had superior 2 yr VA compared with bevacizumab, but superiority over ranibizumab in year 1 was no longer identified.

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Optic Neuropathy visual acuity loss due to infarction of optic disc/nerve Inner limiting membrane Nerve fibre layer

Flame shaped hemorrhage

Ganglion cell layer

.

Effects of Medical Therapies on Retinopathy Progression in Type 2 DM NEJM 2010;363:233-244 Purpose: To determine whether or not intensive glycemic control, combination therapy for dyslipidemia, and intensive blood-pressure control may limit the progression of DR in persons with type 2 DM. Methods: RCT with 10,251 participants with type 2 DM at high risk of cardiovascular disease. Intensive or standard treatment for glycemia (glycated hemoglobin level 4.4 mg/dL, joint glucose level 80 yr), RA, prosthetic joint, recent joint surgery, skin infection/ulcer, IV drug use, previous intra-articular corticosteroid injection, immune compromise (cancer, DM, alcoholism)

There are 4 Joints in the Shoulder glenohumeral, AC, sternoclavicular (SC), scapulothoracic

OR11 Orthopedics

Toronto Notes 2018

Shoulder

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Table 7. Anterior and Posterior Shoulder Dislocation Posterior Shoulder Dislocation (5%)

Abducted arm is externally rotated/hyperextended, or blow to posterior shoulder Involuntary, usually traumatic; voluntary, atraumatic

Adducted, internally rotated, flexed arm FOOSH 3 Es (epileptic seizure, EtOH, electrocution) Blow to anterior shoulder

Shoulder passive ROM: abduction – 180°, adduction – 45°, flexion – 180°, extension – 45°, int. rotation – level of T4, ext. rotation – 40-45°

s

Anterior Shoulder Dislocation (>90%)

Shoulder Exam

“Squared off” shoulder Positive apprehension test: patient looks apprehensive with gentle shoulder abduction and external rotation to 90º as humeral head is pushed anterio ly and recreates feeling of anterior dislocation (see Figure 11) Positive relocation test: a posteriorly directed force applied during the apprehension test relieves apprehension since anterior subluxation is prevented Positive sulcus sign: presence of subacromial indentation with distal traction on humerus indicates inferior shoulder instability (see Figure 11)

Anterior shoulder flattening, prominent coracoid, palpable mass posterior to shoulder Positive posterior apprehension (“jerk”) test: with patient supine flex elbow 90° and adduct, internally rotate the arm while applying a posterior force to the shoulder; patient will “jerk” back with the sensation of subluxation (see Figure 11) Note: the posterior apprehension test is used to test for recurrent posterior instability, NOT for acute injury

Axillary nerve: sensory patch over deltoid and deltoid contraction Musculocutaneous nerve: sensory patch on lateral forearm and biceps contraction

Full neurovascular exam as per anterior shoulder dislocation

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Humeral head is anterior to the centre of the “Mercedes-Benz”sign

Humeral head is posterior to centre of “Mercedes-Benz” sign

AP View

Sub coracoid lie of the humeral head is most common

Partial vacancy of glenoid fossa (vacant glenoid sign) and >6 mm space between anterior glenoid rim and humeral head (positive rim sign), humeral head may resemble a lightbulb due to internal rotation (lightbulb sign)

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sf Closed reduction with IV sedation and muscle relaxation Traction-countertraction: assistant stabilizes torso with a folded sheet wrapped across the chest while the surgeon applies gentle steady traction Stimson: while patient lies prone with arm hanging over table edge, hang a 5 lb weight on wrist for 15-20 min Hippocratic method: place heel into patient’s axilla and apply traction to arm Cunningham’s method: low risk, low pain; if not successful try above methods Obtain post-reduction x-rays Check post-reduction NVS Sling x 3 wk (avoid abduction and external rotation), followed by shoulder rehabilitation (dynamic stabilizer strengthening)

Closed reduction with sedation and muscle relaxation Inferior traction on a flexed elbow with pressure on the back of the humeral head Obtain post-reduction x-rays Check post reduction NVS Sling in abduction and external rotation x 3 wk, followed by shoulder rehabilitation (dynamic stabilizer strengthening)

Figure 8. Shoulder joints

Coracoid process Acromion

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Humerus

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© Mary Sims 2003

Bankart

Specific Complications • rotator cuff or capsular or labral tear (Bankart/SLAP lesion), shoulder stiffness • injury to axillary nerve/artery, brachial plexus • recurrent/unreduced dislocation (most common complication)

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Scapula

Figure 9. Mercedes-Benz

Prognosis • recurrence rate depends on age of first dislocation • 40 yr = 2-4%

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© Kajeandra Ravichandiran 2012

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TREATMENT

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± reverse Hill-Sachs lesion (75% of cases): divot in anterior humeral head ± reverse bony Bankart lesion: avulsion of the posterior glenoid labrum from the bony glenoid rim

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± Hill-Sachs lesion: compression fracture of posterior humeral head due to forceful impaction of an anteriorly dislocated humeral head against the glenoid rim (see Figure 10) ± bony Bankart lesion: avulsion of the anterior glenoid labrum (with attached bone fragments) from the glenoid rim (see Figure 10)

8 7 1. Manubrium 2. Sternoclavicular joint 3. Clavicle 4. Coracoid process 5. AC joint 6. Acromion 7. Humerus 8 Glenohumeral joint 9. Scapula

© Jason Raine

Humeral head is posterior

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Trans-scapular ‘Y’ View

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Humeral head is anterior

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Axillary View

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RADIOGRAPHIC FINDINGS

Hill-Sachs and Bony Bankart Lesions

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re e Neurovascular Exam Including

Factors Causing Shoulder Instability • Shallow glenoid • Loose capsule • Ligamentous laxity Frequency of Dislocations • Anterior shoulder > Posterior shoulder • Posterior hip > Anterior hip The glenohumeral joint is the most commonly dislocated joint in the body since stability is sacrificed for motion

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Pain, arm is held in adduction and internal rotation; external rotation is blocked

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Pain, arm slightly abducted and externally rotated with inability to internally rotate

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Symptoms

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CLINICAL FEATURES

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MECHANISM

Hill-Sachs

Figure 10. Posterior view of anterior dislocation causing Hill-Sachs and Bankart lesions

OR12 Orthopedics

Toronto Notes 2018

© Lori Waters 2005

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Shoulder

© Lori Waters 2005

Sulcus sign

© Lori Waters 2005

© Tabby Lulham 2010

Anterior apprehension sign

Traction-Countertraction

Posterior apprehension sign Figure 11. Shoulder maneuvers

Rotator Cuff Disease

Nerve Supply

Muscle Function

Supraspinatus

Scapula

Greater tuberosity of humerus

Suprascapular nerve

Abduction

Infraspina us

Scapula

Greater tuberosity of humerus

Suprascapular nerve

External rotation

Teres Minor

Scapula

Greater tuberosity of humerus

Axillary nerve

External rotation

Subscapularis

Scapula

Lesser tuberosity of humerus

Subscapular nerve

Internal rotation and adduction

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SPECTRUM OF DISEASE: IMPINGEMENT, TENDONITIS, MICRO OR MACRO TEARS

Scapular body Teres minor

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Bigliani Classification of Acromion Morphology • Type I – flat • Type II – curved • Type III – hooked

Screening Out Rotator Cuff Tears* • No night pa n (SN 87.7%) • No painful arc (SN 97.5%) • No impingement signs (SN 97.2%) • No weakness *Returning to the bedside: Using the history and physical examination to identify rotator cuff tears

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Figure 12 Muscles of the rotator cuff

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Investigations • X-ray: AP view may show high riding humerus relative to glenoid, indicating large tear, evidence of chronic tendonitis • MRI: coronal/sagittal, oblique and axial orientations are useful for assessing full/partial tears and tendinopathy ± arthrogram: geyser sign (injected dye leaks out of joint through rotator cuff tear) • arthrogram: can assess full thickness tears, difficult to assess partial tears

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Infraspinatus

Joint capsule

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Clinical Features • insidious onset, but may present as an acute exacerbation of chronic disease, night pain, and difficulty sleeping on affected side • pain worse with active motion (especially overhead); passive movement generally permitted • weakness and loss of ROM, especially between 90°-130° (e.g. trouble with overhead activities) • tenderness to palpation over greater tuberosity • rule out bicep tendinosis: Speed test; SLAP lesion: O’Brien’s test

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Subscapularis

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Etiology • anything that leads to a narrow subacromial space • most commonly, a relative imbalance of rotator cuff and larger shoulder muscles, allowing for superior translation and subsequent wear of the rotator cuff muscle tendons ■■ glenohumeral muscle weakness leading to abnormal motion of humeral head ■■ scapular muscle weakness leading to abnormal motion of acromion • acromial abnormalities, such as congenital narrow space or osteophyte formation or Type III acromion morphology 1. outlet/subacromial impingement: “painful arc syndrome”, compression of rotator cuff tendons (primarily supraspinatus) and subacromial bursa between the head of the humerus and the undersurface of acromion, AC joint, and CA ligament 2 bursitis and tendonitis 3. rotator cuff thinning and tear if left untreated

JAM Geri Soc 2000;48:1633-1637

© Andreea Margineanu 2012

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Distal

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Proximal

Supraspinatus AC ligament Acromion Coracoid process

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Muscle Attachments

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Muscle

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Table 8. Rotator Cuff Muscles (SITS)

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• rotator cuff consists of 4 muscles that act to stabilize the humeral head within the glenoid fossa

OR13 Orthopedics

Toronto Notes 2018

Shoulder

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Treatment • non-operative ■■ for mild (“wear”) or moderate (“tear”) cases ■■ physiotherapy, NSAIDs ± steroid injection • operative ■■ indication: severe (“repair”) ■■ impingement that is refractory to 2-3 mo physiotherapy and 1-2 corticosteroid injections ■■ arthroscopic or open surgical repair (i.e acromioplasty, rotator cuff repair)

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Ruling in Rotator Cuff Tears – 98% probability of rotator cuff tear if all 3 of the following are present: • Supraspinatus weakness • External rotation weakness • Positive impingement sign(s) Diagnosis of rotator cuff tears. Lancet 2001; 357:769-770

Positive Test

Jobe’s Test

Supraspinatus: place the shoulder in 90° of abduction and 30° of forward flexion and internally rotate the arm so that the thumb is pointing toward the floor

Weakness with active resistance suggests a supraspinatus tear

Lift-off Test

Subscapularis: internally rotate arm so dorsal surface of hand rests on lower back; patient instructed to actively lift hand away from back against examiner resistance (use Belly Press Test if too painful)

Inability to actively lift hand away from back suggests a subscapularis tear

Posterior-Cu f Test

Infraspinatus and teres minor: arm positioned at patient’s side in 90° of flexion; patient instructed to externally rotate arm against the resistance of the examiner

Weakness with active resistance suggests posterior cuff tear

Neer s Test

Rotator cuff impingement: passive shoulder flexion

Pain elicited between 130-170° suggests impingement

Hawkins-Kennedy Test

Rotator cuff impingement: shoulder flexion to 90° and passive internal rotation

Pain with internal rotation suggests impingement

Painful Arc Test

Rotator cuff tendinopathy: patient instructed to actively abduct the shoulder

Pain with abduction >90° suggests tendinopathy

Speed’s Test

Apply resistance to the forearm when the arm is in forwa d flexion with the elbows fully extended.

Pain in the bicipital groove

O’Brien’s Test

SLAP lesion: forward flexion of the arm to 90 degrees while keeping the arm extended. Arm is adducted 10-15 degrees. Internally rotate the arm so thumb is facing down and apply a downward force. Repeat the test with arm externally rotated

Pain or clicking in the glenohumoral joint in internal rotation but not external rotation

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© Tabby Lulham 2010

Lift-off test

Posterior cuff test

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130-170º

Hawkins-Kennedy test

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Figure 13. Ro ator cuff tests

© Erin Duff 2009

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Neer’s test

© Tabby Lulham 2010

Jobe’s test

Does this Patient with Shoulder Pain have Rotator Cuff Disease? The Rational Clinical Examination Systematic Review JAMA 2013;310:837-847 Study: 5 studies of sufficient quality including 30-203 shoulders and a prevalence of RCD ranging from 33-81%. Results/Conclusions: Among pain provocation tests, a positive painful arc test had the greatest specificity and sensitivity (SP 81%, SN 71%) Among strength tests, a positive external rotation lag test and internal rotation lag test were the most accurate for full-thickness tears (SP 47%, SN 94%; SP 97%, SN 83% respectively). The internal rotation lag test was therefore also the most accurate for identifying patients without a full-thickness tear A positive drop arm test is helpful to identify patients with RCD (SN 24%, SP 93%).

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Examination

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Test

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Table 9. Rotator Cuff Special Tests

OR14 Orthopedics

Toronto Notes 2018

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Shoulder

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Acromioclavicular Joint Pathology

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• subluxation or dislocation of AC joint • 2 main ligaments attach clavicle to scapula: AC and CC ligaments

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Mechanism • fall onto shoulder with adducted arm or direct trauma to point of shoulder Clinical Features • pain with adduction of shoulder and/or palpation over AC joint • palpate step deformity between distal clavicle and acromion (with dislocation) • limited ROM

Pneumothorax or pulmonary contusion are potential complications of severe AC joint dislocation

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Investigations • X-rays: bilateral AP, Zanca view (10-15° cephalic tilt), axillary

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Treatment • non-operative ■■ sling 1-3 wk, ice, analgesia, early ROM and rehabilitation • operative ■■ indication: Rockwood Class IV-VI (III if labourer or high level athlete) ■■ number of different approaches involving AC/CC ligament reconstruction or screw/hook plate insertion

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Table 10. Rockwood Classification of Acromioclavicular Joint Separation Treatment

I

Joint sprain, absence of complete tear of either ligament

Non-operative

II

Complete tear of AC ligament, incomplete tear of CC ligament, without marked elevation of lateral clavicular head

Non-operative

III

Complete tear of AC and CC ligaments, >5 mm elevation at AC joint, superior aspect of acromion is below the inferior aspect of the clavicle

Most non-operative, operative if labourer or high level athlete Will heal with step deformity, although most fully functional in 4-6 mo

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Based on the anatomical structure the displaced clavicle is in proximity to

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IV-VI

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Features

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Grade

Operative in most cases

Clavicle Fracture • incidence: proximal (5%), middle (80%), or distal (15%) third of clavicle • common in children (unites rapidly without complications)

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Mechanism • fall on shoulder (87%), direct trauma to clavicle (7%), FOOSH (6%)

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Investigations • evalua e NVS of entire upper limb • X-ray: AP, 45° cephalic tilt (superior/inferior displacement), 45° caudal tilt (AP displacement) CT: useful for medial physeal fractures and sternoclavicular injury

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Treatment • medial and middle-third clavicle fractures ■■ simple sling x 1-2 wk ■■ early ROM and strengthening once pain subsides ■■ if fracture is shortened >2 cm, consider ORIF • distal-third clavicle fractures ■■ undisplaced (with ligaments intact): sling x 1-2 wk ■■ displaced (CC ligament injury): ORIF

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Specific Complications (see General Fracture Complications, OR6) • cosmetic bump usually only complication • shoulder stiffness, weakness with repetitive activity • pneumothorax, brachial plexus injuries, and subclavian vessel (all very rare)

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Associated Injuries with Clavicle Fractures • Up to 9% of clavicle fractures are associated with other fractures (most commonly rib fractures) • Majority of brachial plexus injuries are associated with proximal third fractures

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Clinical Features • pain and tenting of skin • arm is clasped to chest to splint shoulder and prevent movement

OR15 Orthopedics

Toronto Notes 2018

Humerus

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Frozen Shoulder (Adhesive Capsulitis)

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• disorder characterized by progressive pain and stiffness of the shoulder, usually resolving spontaneously after 18 mo

Clinical Features • gradual onset (weeks to months) of diffuse shoulder pain with: ■■ decreased active AND passive ROM ■■ pain worse at night and often prevents sleeping on affected side ■■ increased stiffness as pain subsides: continues for 6-12 mo after pain has disappeared

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Conditions Associated with an Increased Incidence of Adhesive Capsulitis • Prolonged immobilization (most significant) • Female gender • Age >49 yr • DM (5x) • Cervical disc disease • Hyperthyroidism • Stroke • MI • Trauma and surgery • Autoimmune disease

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Mechanism • primary adhesive capsulitis ■■ idiopathic, usually associated with DM ■■ usually resolves spontaneously in 9-18 mo • secondary adhesive capsulitis ■■ due to prolonged immobilization ■■ shoulder-hand syndrome: CRPS/RSD characterized by arm and shoulder pain, decreased motion, and diffuse swelling ■■ following MI, stroke, shoulder trauma ■■ poorer outcomes

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Investigations X-ray: AP (neutral, internal/external rotation), scapular Y, axillary ■■ may be normal, or may show demineralization from disease

Treatment • freezing phase ■■ active and passive ROM (physiotherapy) ◆◆ NSAIDs and steroid injections if limited by pain • thawing phase ■■ manipulation under anesthesia and early physiotherapy ◆◆ arthroscopy for debridement/decompression

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Stages of Adhesive Capsulitis 1. Freezing phase: gradual onset, diffuse pain (lasts 6-9 mo) 2. Frozen phase: decreased ROM impacting functioning (lasts 4 9 mo) 3. Thawing phase: gradual return of motion (lasts 5 26 mo)

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Humerus

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Proximal Humeral Fracture

Mechanism • young: high energy trauma (MVC) • elderly: FOOSH from standing height in osteoporotic individuals

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Classification • Neer classification is based on 4 fracture locations or ‘parts’ • displaced: displacement >1 cm and/or angulation >45° • the Neer system regards the number of displa ed fractures, not the fracture line, in determining classification • ± dislocated/subluxed: humeral head dislocated/subluxed from glenoid

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Treatment • treat osteoporosis if needed • non-operative ■■ nondisplaced: broad arm sling immobilization, begin ROM within 14 d to prevent stiffness ■■ minimally displaced (85% of patients) - closed reduction with sling immobilization x 2 wk, gentle ROM • operative ■■ ORIF (anatomic neck fractures, displaced, associated dislocated glenohumeral joint) ■■ hemiarthroplasty or reverse TSA may be necessary, especially in elderly

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Specific Complications (see General Fracture Complications, OR6) • AVN, nerve palsy (45%; typically axillary nerve), malunion, post-traumatic arthritis

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Neer Classification Based on 4 parts of humerus • Greater Tuberosity • Lesser Tuberosity • Humeral Head • Shaft One-part fracture: any of the 4 parts with none displaced Two-part fracture: any of the 4 parts with 1 displaced Three-part fracture: displaced fracture of surgical neck + displaced greater tuberosity or lesser tuberosity Four-part fracture: displaced fracture of surgical neck + both tuberosities

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Investigations • test axillary nerve function (deltoid contraction and skin over deltoid) • X-rays: AP, trans-scapular, axillary are essential • CT scan: to evaluate for articular involvement and fracture displacement

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Clinical Features • proximal humeral tenderness, deformity with severe fracture, swelling, painful ROM, bruising extends down arm and chest

Anatomic neck fractures disrupt blood supply to the humeral head and AVN of the humeral head may ensue

OR16 Orthopedics

Toronto Notes 2018

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Humerus

Humeral Shaft Fracture

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Greater tuberosity Lesser tuberosity

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Mechanism • high energy: direct blows/MVC (especially young); low energy: FOOSH, twisting injuries, metastases ( n elderly)

Anatomical neck

Clinical Features • pain, swelling, weakness ± shortening, motion/crepitus at fracture site • must test radial nerve function before and after treatment: look for drop wrist, sensory impairment dorsum of hand

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Surgical neck

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Investigations • X-ray: AP and lateral radiographs of the humerus, including the shoulder and elbow joints

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Figure 14. Fractures of the proximal humerus

Acceptable Humeral Shaft Deformities for Non-Operative Treatment • 5° or volar tilt >20° • >5 mm radial shortening

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• extra-articular transverse distal radius fracture (~2 cm proximal to the radiocarpal joint) with dorsal displacement ± ulnar styloid fracture • most common fracture in those >40 yr, especially in women and those with osteoporotic bone

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Mechanism • FOOSH

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Clinical Features • “dinner fork” deformity • swelling, ecchymosis, tenderness Investigations • X-ray: AP and lateral wrist

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Treatment • goal is to restore radial height (13 mm), radial inclination (22°), volar tilt (11°), as well as DRUJ stability and useful forearm rotation • non-operative ■■ closed reduction (think opposite of the deformity) ◆◆ hematoma block (sterile prep and drape, local anesthetic injection directly into fracture site) or conscious sedation ◆◆ closed reduction: 1) traction with extension (exaggerate injury), 2) traction with ulnar deviation, pronation, flexion (of distal fragment – not at wrist) ◆◆ dorsal slab/below elbow cast for 5-6 wk ◆◆ x-ray at 1 wk, 3 wk, and at cessation of immobilization to ensure reduction is maintained ■■ obtain post-reduction films immediately; repeat reduction if necessary

ORIF Colles’ Fracture if Post-Reduction Demonstrates • Radial shortening >3 mm or, • Dorsal tilt >10° or, • Intra-articular displacement/step-off >2 mm

© Desmond Ballance 2006

Clinical Features • pain, swelling, deformity, and point tenderness at fracture site

OR21 Orthopedics

Toronto Notes 2018

Wrist

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• operative ■■ indicatio : failed closed reduction, or loss of reduction ■■ percutaneous pinning, external fixation, or ORIF

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Smith’s Fracture 2

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• volar displacement of the distal radius (i.e. reverse Colles’ fracture)

3

Mechanism • fall onto the back of the flexed hand

Lateral View 4

5

Investigations • X-ray: AP and lateral wrist

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AP View

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• most common complications are poor grip strength, stiffness, and radial shortening • distal radius fractures in individuals 90%) ■■ degenerative (disc, facet, ligament) ■■ peripheral nerve compression (disc herniation) ■■ spinal stenosis (congenital, osteophyte, central disc) ■■ cauda equina syndrome 2. others ( L4-5 > L3-4 • 3:1 male o female • only 5% become symptomatic • usually a history of flexion-type injury

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Nucleus pulposus

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Clinical Features • back dominant pain (central herniation) or leg dominant pain (lateral herniation) • tenderness between spinous processes at affected level • muscle spasm ± loss of normal lumbar lordosis • neurological disturbance is segmental and varies with level of central herniation ■■ motor weakness (L4, L5, S1) ■■ diminished reflexes (L4, S1) ■■ diminished sensation (L4, L5, S1) • positive straight leg raise • positive contralateral SLR • positive Lasegue and Bowstring sign • cauda equina syndrome (present in 1-10%): surgical emergency

Nerve root

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Vertebra

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Figure 27. Disc herniation causing nerve root compression

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MRI abnormalities (e.g. spinal stenosis, disc herniation) are quite common in both asymptomatic and symptomatic individuals and a e not necessarily an indication for ntervention without clinical correlation

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Treatment • non-operative ■■ symptomatic ◆◆ extension protocol ◆◆ NSAIDS • operative ■■ indication: progressive neurological deficit, failure of symptoms to resolve within 3 mo, or cauda equina syndrome due to central disc herniation ■■ surgical discectomy • prognosis ■■ 90% of patients improve in 3 mo with non-operative treatment

Neurogenic claudication is position dependent; vascular claudication is exercise dependent

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Investigations • X-ray MRI, consider a post-void residual volume to check for urinary retention; post-void >100 mL should heighten suspicion for cauda equina syndrome

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Table 16. Types of Low Back Pain Mechanical Back Pain

Direct Nerve Root Compression Spinal Stenosis

Root Compression

Pain Dominance

Back

Back

Leg

Leg

Aggravation

Flexion

Extension, standing, walking

Exercise, extension, walking, standing

Flexion

Onset

Gradual

More sudden

Congenital or acquired

Acute leg ± back pain

Duration

Long (weeks, months)

Shorter (days, weeks)

Acute or chronic history (weeks to months)

Short episodes Attacks (minutes)

Treatment

Relief of strain, exercise

Relief of strain, exercise

Relief of strain, exercise + surgical decomp ession if progressive or severe deficit

Relief of strain, exercise + surgical decompression if progressive or severe deficit

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Red Flags for Leg Dominant

Intermittent

Disc Herniation (central)

Constant Disc Herniation (lateral)

Facet Joint

Intermittent Spinal Stenosis

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Back Dominant Constant Inflammatory Mechanical

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Facet Origin

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Disc Origin

Back Pain

BACK PAIN Bowel or bladder dysfunction Anesthesia (saddle) Constitutional symptoms/malignancy Khronic disease Paresthesias Age >50 yr IV drug use Neuromotor deficits

Figure 28. Approach to back pain

SPONDYLOLYSIS

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Mechanism • trauma: gymnasts, weightlifters, backpackers, loggers, labourers

Sciatica Most common symptom of radiculopathy (L4-S3) • Leg dominant, constant, burning pain • Pain radiates down leg ± foot • Most common cause = disc herniation

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Definition • defect in the pars interarticularis with no movement of the vertebral bodies

© Kataryna Nemethy 2007

OR25 Orthopedics

OR26 Orthopedics

Toronto Notes 2018

Pelvis

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Clinical Features • activity-related back pain, pain with unilateral extension (Michelis’ test)

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Investigations • oblique X-ray: “collar” break in the “Scottie dog’s” neck • bone scan • CT scan

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Spondylolysis

Treatment • non-operative ■■ activity restriction, brace, stretching exercise

Spondylolisthesis (anterior displacement) © Ryo Sakai 2007

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ADULT ISTHMIC SPONDYLOLISTHESIS

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Definition • defect in pars interarticularis causing a forward translation or slippage of one vertebra on another, usually at L5-S1, less commonly at L4-5 Figure 29. Spondylolysis, spondylolisthesis

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Mechanism • congenital (children), degenerative (adults), traumatic pathological, teratogenic

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Clinical Features • lower back pain radiating to buttocks relieved with sitting • neurogenic claudication • L5 radiculopathy • Meyerding Classification (percentage of slip)

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Investigations • X-ray (AP, lateral, oblique flexion-extension views), MRI

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Treatment • non-operative ■■ activity restriction, bracing, NSAIDS • operative Figure 30. “Scottie dog” fracture

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Table 17. Classification and Treatment of Spondylolisthesis Percentage of Slip

Treatment

0-25%

Symptomatic operative fusion only for intractable pain

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Class 1

25-50

Same as above

50-75

Decompression for spondylolisthesis and spinal fusion

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2 3 4

75-100

Same as above

5

>100

Same as above

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Specific Complications • may present as cauda equina syndrome due to roots being stretched over the edge of L5 or sacrum

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Pelvis

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Pelvic Fracture

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Figure 31. Pelvic columns

© Emilie McMahon 2005

Posterior column

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Clinical Features • pain, inability to bear weight • local swelling, tenderness • deformity of lower extremity • pelvic instability

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Anterior column

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Mechanism • young: high energy trauma, either direct or by force transmitted longitudinally through the femur • elderly: fall from standing height, low energy trauma • lateral compression, vertical shear, or anteroposterior compression fractures

OR27 Orthopedics

Toronto Notes 2018

Hip

Classification Table 18. Tile Classification of Pelvic Fractures Stability

A

Rotationally stable Vertically stable

Description

B

Rotationally unstable Vertically stable

B1: open book (external rotation) B2: lateral compression – ipsilateral B2-1: with anterior ring rotation/displacement through ipsilateral rami B2-2: with anterior ring rotation/displacement through non-ipsilateral rami (bucket-handle) B3: bilateral

C

Rotationally unstable Vertically unstable

C1: unilateral C1-1: iliac fracture, C1-2: sacroiliac fracture-dislocation C1-3: sacral fracture C2: bilateral with 1 side type B and 1 side type C C3: bilateral both sides type C

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Type

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A1: fracture not involving pelvic ring (i.e. avulsion or iliac wing fracture) A2: minimally displaced fracture of pelvic ring (e.g. ramus fracture) A3: transverse sacral fracture

Possible Radiological Findings • Pubic rami fractures: superior/inferior • Pubic symphysis diastasis: common in AP compression (N=5 mm) • Sacral fractures: common in lateral compression • SI joint diastasis: common in AP compression (N=1-4 mm) • Disrupted anterior column (iliopectineal line) or posterior column (ilioischial line) • “Teardrop” displacement: acetabular fracture • Iliac, ischial avulsion fractures • Displacement of he major fragment: superior (VS), open book (APC), bucket handle (LC)

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Investigations • X-ray: AP pelvis, inlet and outlet views, Judet views (obturator and iliac oblique for acetabular fracture) ■■ 6 cardinal radiographic lines of the acetabulum: ilioischial line, iliopectineal line, teardrop, roof, poste ior rim, anterior rim • CT scan useful for evaluating posterior pelvic injury and acetabular fracture • assess genitourinary injury (rectal exam, vaginal exam, hematuria, blood at urethral meatus) ■■ if involved, the fracture is considered an open fracture

Type A Stable Avulsion Fracture

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Treatment • ABCDEs • non-operative treatment: protected weight bearing ■■ indication: stable fracture • emergency management ■■ IV fluids/blood ■■ pelvic binder/sheeting ■■ external fixation vs. emergent angiography/embolization ■■ ± laparotomy (if FAST/DPL positive) • operative treatment: ORIF ■■ indications ◆◆ unstable pelvic ring injury ◆◆ disruption of anterior and posterior SI ligament ◆◆ symphysis diastasis >2.5 cm ◆◆ vertical instability of the posterior pelvis ◆◆ open fracture

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Type C Unstable Vertical Fracture

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Specific Complications (see General Fracture Complications, OR6) • hemorrhage (life-threatening) • injury to rectum or urogenital structures • obstetrical difficulties, sexual and voiding dysfunction • persistent SI joint pain • post-traumatic arthritis of the hip with acetabular fractures • high risk of DVT/PE

© Seline McNamee

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Type B Open Book

Figure 32. Tile classification of pelvic fractures

Hip

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Hip Dislocation

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ANTERIOR HIP DISLOCATION • mechanism: posteriorly directed blow to knee with hip widely abducted • clinical features: shortened, abducted, externally rotated limb • treatment ■■ closed reduction under conscious sedation/GA ■■ post- eduction CT to assess joint congruity

Up to 50% of patients with hip dislocations suffer fractures elsewhere at the time of injury

3. External rotation 2. Internal rotation

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full trauma survey (see Emergency Medicine Patient Assessment/Management, ER2) • examine for neurovascular injury PRIOR to open or closed reduction • reduce hip dislocations within 6 h to decrease risk of AVN of the femoral head • hip precautions (no extreme hip flexion, adduction, internal or external rotation) for 6 wk postreduction • see Hip Dislocation Post-Total Hip Arthroplasty, OR29

1. Traction

© Janet SM Chan 2009

Figure 33. Rochester method

OR28 Orthopedics

Toronto Notes 2018

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Rochester Method to Reduce Posterior Dislocations • Patient lying supine with hip and knee flexed on injured side • Surgeon stands on patient’s injured side • Surgeon passes one arm under patient’s flexed knee, reaching to place that hand on patient’s other knee (thus supporting patient’s injured leg) • With other hand, surgeon grasps patient’s ankle on injured side, applying traction, while assistant stabilizes pelvis • Reduction via traction, internal rotation, then external otation once femoral head clears acetabular rim

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POSTERIOR HIP DISLOCATION • most frequent type of hip dislocation • mechanism: severe force to knee with hip flexed and adducted ■■ e.g. knee into dashboard in MVC • clinical features: shortened, adducted, internally rotated limb • treatment ■■ closed reduction under conscious sedation/GA only if no associated femoral neck fracture or ipsilateral displacement ■■ ORIF if unstable, intra-articular fragments, or posterior wall fracture ■■ post-reduction CT to assess joint congruity and fractures ■■ if reduction is unstable, put in traction x 4-6 wk

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COMPLICATIONS FOR ALL HIP DISLOCATIONS • post-traumatic OA • AVN of femoral head • fracture of femoral head, neck, or shaft • sciatic nerve palsy in 25% (10% permanent) • HO • thromboembolism – DVT/PE

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Hip Fracture

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General Features • acute onset of hip pain • unable to weight-bear • shortened and externally-rotated leg • painful ROM

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X-Ray Features of Subcapital Hip Fractures • Disruption of Shenton’s line (a radiographic line drawn along the upper margin of the obturator foramen, extending along the inferomedial side of the femoral neck) • Altered neck-shaft angle (normal is 120130°)

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© Sean Wang 2007

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DVT Prophylaxis in Hip Fractures LMWH (i.e. enoxaparin 40 mg SC bid), fondaparinux, low dose heparin on admission, do not give 1 h, multiple joint swelling, hand nodules • decreased ROM (internal rotation is lost first) • crepitus • effusion • ± fixed flexion contracture leading to apparent limb shortening (Thomas test) • ± Trendelenburg sign

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Investigations • X-ray: weight-bearing views of affected joint ■■ OA: joint space narrowing, subchondral sclerosis, subchondral cysts, osteophytes • RA: osteopenia, erosion, joint space narrowing, subchondral cysts • blood work: ANA, RF

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Treatment • non-operative ■■ weight reduction, activity modification, physiotherapy, analgesics, walking aids • operative ■■ indication advanced disease ■■ realign = osteotomy; replace = arthroplasty; fuse = ar hrodesis • complications with arthroplasty: component loosening dislocation, HO, thromboembolism, infection, neurovascular injury, limb length discrepancy • arthroplasty is standard of care in most patients with hip arthritis

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Hip Dislocation Post-Total Hip Arthroplasty

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• occurs in 1-4% of primary THA and 10-16% of revision THAs • risk factors: neurological impairment, post-traumatic arthritis, revision surgery, substance abuse

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Investigations • X-ray: AP pelvis, AP and lateral hip

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Mechanism • THA that is unstable when hip is flexed, adducted, and internally rotated, or extended and externally rotated (avoid flexing hip >90° or crossing legs for ~6 wk after surgery)

OR30 Orthopedics

Toronto Notes 2018

Femur

DVT Prophylaxis in Elective THA (continue 10-35 d post-operative) Fondaparinux, low molecular weight heparin, or warfarin

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Treatment • non-operative ■■ closed reduction: external abduction splint to prevent hip adduction (most often) • operative ■■ indication: 2 or more dislocations with evidence of polyethylene wear, malalignment, hardware failure ■■ revision THA ■■ conversion to hemiarthroplasty with a larger femoral head ■■ resection arthroplasty is a last resort Complications • sciatic nerve palsy in 25% (10% permanent) • HO • infection

Femur

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Femoral Diaphysis Fracture

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Mechanism • high energy trauma (MVC, fall from height, gunshot wound) ■■ pathologic as a result of malignancy, osteoporosis, bisphosphonate use • in children, can result from low energy t auma (spiral fracture)

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Clinical Features • shortened, externally rotated leg (if fracture displaced) • inability to weight-bear • often open injury, always a Gustilo III (Table 5) • Winquist and Hansen classification It is important to rule out ipsilateral femoral neck fr cture, as they occur in 2-6% of femoral diaphysis fractures and are reportedly missed in 19-31% of cases

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Treatment • non-operative (uncommon) ■■ indication: non-displaced femoral shaft fractures in co-morbid patients ■■ long leg cast • operative ■■ ORIF with anterograde IM nail (most common) or retrograde IM nail; external fixator for unstable patients, open fractures, or highly vascular areas; or plate and screws for open growth plates within 24 h ■■ early mobilization and strengthening

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Investigations • X-ray: AP pelv s, AP/lateral hip, femur, knee

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Complications • blood loss • fat embolism leading to ARDS • extensive soft tissue damage • ipsilateral hip dislocation/fracture (2-6%) • nerve injury

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Distal Femoral Fracture

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• fractures from articular surface to 5 cm above metaphyseal flare

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Mechanism • direct high energy force or axial loading • three types: extra articular, partial articular, complete articular

Condylar

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Investigations • X-ray: AP, lateral • CT, angiography if diminished pulses

Intercondylar Figure 36. Distal femoral fractures

© Paul Belletrutti 2003

Supracondylar

Clinical Features • extreme pain • knee effusion (hemarthrosis) • neurovascular deficits can occur with displaced fracture

OR31 Orthopedics

Toronto Notes 2018

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Knee

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Specific Complications (see General Fracture Complications, OR6) • femoral artery tear • popliteal artery injury • nerve injury • extensive soft tissue injury • angulation deformities

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Posterior horn of lateral meniscus Anterior horn of lateral meniscus PCL ACL Posterior horn of medial meniscus Anterior horn of medial meniscus

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1. 2. 3. 4. 5. 6.

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Knee

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Figure 37. Diagram of the right tibial plateau

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Evaluation of Knee

Patellar tendon Patella

Proximal patellar ligament (cut)

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Common Complaints • locking, instability, and swelling ■■ torn meniscus/loose body in joint • pseudo-locking: limited ROM without mechanical block ■■ effusion, muscle spasm after injury, arthritis • painful clicking (audible) ■■ torn meniscus • giving way: instability ■■ cruciate ligament or meniscal tear, patellar dislocation

Medial meniscus

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Lateral meniscus

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LCL Distal patellar l gament (cut)

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PCL

ACL

Special Tests of the Knee • anterior and posterior drawer tests (Figure 39) ■■ demonstrate ACL and PCL, respectively ◆◆ knee flexed at 90°, foot immobilized, hamstrings released ◆◆ if able to sublux tibia anteriorly (anterior drawer test), then ACL may be torn ◆ if able to sublux tibia posteriorly (posterior drawer test), then PCL may be torn ◆◆ anterior drawer test for ACL: 3.8 positive likelihood ratio, 0.30 negative likelihood ratio • Lachman test ■■ demonstrates torn ACL ■■ hold knee in 10-20° flexion, stabilizing the femur ■■ try to sublux tibia anteriorly on femur ■■ similar to anterior drawer test, more reliable due to less muscular stabilization ■■ for ACL: 25.0 positive likelihood ratio, 0.1 negative likelihood ratio • pivot shift sign ■■ demonstrates torn ACL ■■ start with the knee in extension ■■ internally rotate foot, slowly flex knee while palpating and applying a valgus force ■■ if incompetent ACL, tibia will sublux anteriorly on femur at start of maneuver. During flexion, the tibia will reduce and externally rotate about the femur (the “pivot”) ■■ reverse pivot shift (start in flexion, externally rotate, apply valgus and extend knee) suggests torn PCL ■■ composite assessment for ACL: 25.0 positive likelihood ratio, 0.04 negative likelihood ratio ■■ composite assessment for PCL: 21.0 positive likelihood ratio, 0.05 negative likelihood ratio • posterior sag sign ■■ demonstrates torn PCL ■■ may give a false positive anterior draw sign ■■ flex knees and hips to 90°, hold ankles and knees ■■ view from the lateral aspect ■■ if one tibia sags posteriorly compared to the other, its PCL is torn • collateral ligament stress test ■■ palpate ligament for “opening” of joint space while testing ■■ with knee in full extension, apply valgus force to test MCL, apply varus force to test LCL ■■ repeat tests with knee in 20° flexion to relax joint capsule ■■ opening in 20° flexion due to MCL damage only ■■ opening in 20° of flexion and full extension is due to MCL, cruciate, and joint capsule damage • Thessaly test ■■ demonstrates meniscal tear ■■ patient stands flat footed on one leg while the examiner provides his or her hands for balance. The patient then flexes the knee to 20° and rotates the femur on the tibia medially and laterally three times while maintaining the 20° flexion

MCL © Inessa Stanishevskaya 2012

Figure 38. Knee ligament and anatomy

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© Tabby Lulham 2010

Posterior Drawer Test

Figure 39. Anterior and posterior drawer test

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6 Degrees of Freedom of the Knee • Flexion and extension • External and internal rotation • Varus and valgus angulation • Anterior and posterior glide • Medial and lateral shift • Compression and distraction

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On physical exam of the knee, do not forget to evaluate the hip

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Anterior Drawer Test

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© Jenn Platt 2004

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Treatment • non-operative (uncommon) ■■ indication non-displaced extra-articular fracture ◆◆ hinged knee brace • operative ■■ indication: displaced fracture, intra-articular fracture, non-union ◆◆ ORIF or retrograde IM nail if supracondylar and non-comminuted ◆◆ early mobilization and strengthening

OR32 Orthopedics

Toronto Notes 2018

Knee

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Figure 40. McMurray test

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X-Rays • AP standing, lateral • skyline: tangential view with knees flexed at 45° to see patellofemoral joint • 3-foot standing view: useful in evaluating leg length and varus/valgus alignment • Ottawa Knee Rules (see Emergency Medicine, ER16)

Examination for Lateral Meniscal Tear

© Tabby Lulham 2010

Examination for Medial Meniscal Tear

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■■ positive for a meniscal tear if the patient experiences medial or lateral joint line discomfort ■■ for medial meniscus: 29.67 positive likelihood ratio, 0.11 negative likelihood ratio ■■ for lateral meniscus: 23.0 positive likelihood ratio, 0.083 negative likelihood ratio • tests fo meniscal tear ■■ joint line tenderness ◆◆ joint line pain when palpated ◆◆ palpate one side at a time and watch patient’s eyes ◆◆ for meniscal tear: 0.9 positive likelihood ratio, 1.1 negative likelihood ratio ■■ crouch compression test ◆◆ joint line pain when squatting (anterior pain suggests patellofemoral pathology) ■■ McMurray’s test (Figure 40) ◆◆ with knee in flexion, palpate joint line for painful “pop/click” ◆◆ lateral meniscus tear exam: internally rotate foot, varus stress, and extend knee ◆◆ medial meniscus tear exam: externally rotate foot, valgus stress, and extend knee ◆◆ for meniscal tear: 1.3 positive likelihood ratio, 0.8 negative likelihood ratio ■■ composite assessment for meniscal tears: 2.7 positive likelihood ratio, 0.4 negative likelihood ratio

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Cruciate Ligament Tears • ACL tear much more common than PCL tear

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Table 21. Comparison of ACL and PCL Injuries Posterior Cruciate Ligament

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Anterior Cruciate Ligament From medial wall of lateral femoral condyle to the anteromedial and posterolateral intercondyloid eminence of the tibial plateau

Lateral wall of medial femoral condyle to posterior intercondyloid eminence of the tibial plateau

Mechanism

Sudden deceleration Hyperextension and internal rotation of tibia on femur (i.e. “plant and turn”)

Sudden posterior displacement of tibia when knee is flexed or hyperextended (e.g. dashboard MVC injury)

History

Audible “pop” Immediate swelling Knee “giving way” Inability to continue activity

Audible “pop” Immediate swelling Pain with push off Cannot descend stairs

Physical

Effusion (hemarthrosis) Posterolateral joint line tenderness Positive anterior drawer Positive Lachmann Pivot shift Test for MCL, meniscal injuries

Effusion (hemarthrosis) Anteromedial joint line tenderness Positive posterior drawer Reverse pivot shift Other ligamentous, bony injuries

Treatment

Stable knee w th minimal functional impairment: immobilization 2-4 wk with early ROM and strengthening High demand lifestyle: ligament reconstruction

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PCL

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Figure 41. T1 MRI of torn ACL and PCL

Collateral Ligament Tears

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ACL

Unstable knee or young person/high-demand lifestyle: ligament reconstruction

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Anatomy

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Mechanism valgus force to knee = MCL tear • varus force to knee = LCL tear

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Investigations • x-ray: AP and lateral; MRI

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O’Donoghue’s Unhappy Triad • ACL rupture • MCL rupture • Meniscal damage (medial and/or lateral)

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Clinical Features • swelling/effusion • tenderness above and below joint line medially (MCL) or laterally (LCL) • joint laxity with varus or valgus force to knee ■■ laxity with endpoint suggests partial tear ■■ laxity with no endpoint suggests a complete tear • test for other injuries (e.g. O’Donoghue’s unhappy triad), common peroneal nerve injury

OR33 Orthopedics

Toronto Notes 2018

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Treatment • non-operative ■■ partial tear: immobilization x 2-4 wk with early ROM and strengthening ■■ complete tear: immobilization at 30° flexion • operative ■■ indication: multiple ligamentous injuries ■■ surgical repair of ligaments

Partial ligamentous tears are much more painful than complete ligamentous tears

Meniscal Tears • medial tear much more common than lateral tear

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Clinical Features • immediate pain, difficulty weight-bearing, instability, and clicking • increased pain with squatting and/or twisting • effusion (hemarthrosis) with insidious onset (24-48 h after injury) • joint line tenderness medially or laterally • locking of knee (if portion of meniscus mechanically obstructing extension)

Meniscal repair is done if tear is peripheral with good vascular supply, is a longitudinal tear and 1-4 cm in length Partial meniscectomy is done with tears not amenable to repair (complex, degenerative, adial)

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Mechanism • twisting force on knee when it is partially flexed (e.g. stepping down and turning) • requires moderate trauma in young person, but only mild trauma in elderly due to degeneration

Investigations • MRI, arthroscopy

Tissue Sources for ACL Reconstruction • Hamstring • Middle 1/3 patellar tendon (bone-patellar bone) • Allograft (e.g. cadaver)

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Treatment • non-operative ■■ indication: not locked ■■ ROM and strengthening (NSAIDs) • operative ■■ indication: locked or failed non-operative treatment ■■ arthroscopic repair/partial meniscectomy

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Quadriceps/Patellar Tendon Rupture

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Mechanism • sudden forceful contraction of quadriceps during an attempt to stop • more common in obese patients and those with pre-existing degenerative changes in tendon ■■ DM, SLE, RA, steroid use, renal failure on dialysis

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Investigations • ask patient to straight leg raise (unable with complete rupture) • knee X-ray to rule out patellar fracture, MRI to distinguish between complete and partial tears • lateral view: patella alta with patella tendon rupture, patella baja (infera) with quadriceps tendon rupture

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Treatment • non-operative ■■ indication: incomplete tears with preserved extension of knee ■■ immobilization in brace • operative ■■ indication: complete ruptures with loss of extensor mechanism • early surgical repair: better outcomes compared with delayed repair (>6 wk post-injury) • delayed repair complicated by quadriceps contracture, patella migration, and adhesions

Patella alta = high riding patella Patella baja (infera) = low riding patella

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Clinical Features • inability to extend knee or weight-bear • possible audible “pop” • patella in lower or higher position with palpable gap above or below patella, respectively • may have an effusion

OR34 Orthopedics

Toronto Notes 2018

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Patella

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Dislocated Knee

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Mechanism • high energy trauma • by definition, caused by tears of multiple ligaments

Clinical Features • classified by relation of tibia with respect to femur ■■ anterior, posterior, lateral, medial, rotary • knee instability • effusion • pain • ischemic limb • Schenck classification

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Schenck Classification Type 1: single ligament injury (ACL or PCL) Type 2: Injury to ACL and PCL Type 3: Injury to ACL, PCL and either MCL or LCL Type 4: Injury to ACL PCL, MCL, LCL Type 5: Multiligamentous injury with periarticular fracture

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Investigations • X-ray: AP, lateral, skyline • associated radiographic findings include tibial plateau fracture dislocations, proximal fibular fractures, and avulsion of fibular head • ABI (abnormal if 10° ◆◆ medial clear space on X-ray greater than superior clear space ◆◆ open fracture/open joint injury ■■ ORIF

1 2

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Mechanism • pattern of fracture depends on the position of the ankle when trauma occurs • generally involves ■■ ipsilateral ligamentous tears or transverse bony avulsion ■■ contralateral shear fractures (oblique or spiral) • classification systems ■■ Danis-Weber ■■ Lauge-Hansen: based on foot’s position and motion relative to leg

Type A

Type B

Type C

Legend 1. Posterior malleolus 2. Medial malleolus 3. Deltoid ligament 4 Syndesmosis 5 Lateral malleolus 6. Calcaneofibular ligament

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Complications • high incidence of post-traumatic arthritis

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Figure 45 Ring principle of the ankle and Danis-Weber classification

OR38 Orthopedics

Toronto Notes 2018

Foot

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Lateral Ligament Complex (Anterior Talofibular, Calcaneofibular, Posterior Talofibular) • inversion injury, >90% of all ankle sprains • ATF most commonly and severely injured if ankle is plantarflexed • swelling and tenderness anterior to lateral malleolus • ++ ecchymosis • positive ankle anterior drawer • may have significant medial talar tilt on inversion stress X-ray

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Treatment • non-operative ■■ microscopic tear (Grade I) ◆◆ rest, ice, compression, elevation ■■ macroscopic tear (Grade II) ◆◆ strap ankle in dorsiflexion and eversion x 4-6 wk ◆◆ physiotherapy: strengthening and proprioceptive retraining ■■ complete tear (Grade III) ◆◆ below knee walking cast x 4-6 wk ◆◆ physiotherapy: strengthening and proprioceptive retraining ◆◆ surgical intervention may be required if chronic symptomatic instability develops

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Medial Ligament Complex (deltoid ligament) eversion injury • usually avulses medial or posterior malleolus and strains syndesmosis

Danis-Weber Classification • based on level of fibular fracture relative to syndesmosis Type A (infra-syndesmotic) • pure inversion injury • avulsion of lateral malleolus below plafond or torn calcaneofibular ligament • ± shear fracture of medial malleolus Type B (trans-syndesmotic) • external rotation and eversion (most common) • ± avulsion of medial malleolus or rupture of deltoid ligament • spiral fracture of lateral malleolus starting at plafond Type C (supra-syndesmotic) • pure exte nal rotation • vulsion of medial malleolus or torn deltoid ligament • ± posterior malleolus avulsion with posterior tibio-fibular ligament • fibular fracture is above plafond (called Maisonneuve fracture if at proximal fibula) • frequently tears syndesmosis

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• see Figure 46 for ankle ligaments

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Ankle Ligamentous Injuries

Foot

With a history of significant trauma from axial loading of lower limb, always consider spinal injuries, femoral neck, tibial plateau, and talar/ calcaneal fractures PTF CF ATF

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Talar Fracture

PTT

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Mechanism • axial loading or hyperdorsiflexion (MVC, fall from height) • 60% of talus covered by articular cartilage talar neck is most common fracture of talus (50%) • tenuous blood supply runs distal to proximal along talar neck ■■ high risk of AVN with displaced fractures

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TC ATT

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Investigations • X-ray: AP, lateral, Canale view • CT to better characterize fracture • MRI can clearly define extent of AVN

TN Legend PTF: Posterior talofibular CF: Calcaneofibular ATF: Anterior talofibular PTT: Posterior tibiotalar TC: Tibiocalcaneal ATT: Anterior tibiotalar TN: Tibionavicular

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Treatment • non-operative ■■ indication: non-displaced ■■ NWB, below-knee cast x 6 wk • operative ■■ indication: displaced ■■ ORIF (high rate of nonunion, AVN) ■■ neck fracture: ORIF

Figure 46. Ankle ligament complexes

Calcaneal Fracture • most common tarsal fracture

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Mechanism • high energy, axial loading: fall from height onto heels • 10% of fractures associated with compression fractures of thoracic or lumbar spine (rule out spine injury) • 75% are intra-articular and 10% are bilateral

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Clinical Features • marked swelling, bruising on heel/sole • wider, shortened, flatter heel when viewed from behind • varus heel

OR39 Orthopedics

Toronto Notes 2018

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Foot

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Investigations • X-rays: AP, lateral, oblique foot (mandatory views); can also assess with Broden view, Harris view, or AP ankle. • loss of Bohler’s angle • CT: gold standard, assess intra-articular extension

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Treatment • closed vs. open reduction is controversial • NWB cast x 3 mo with early ROM and strengthening

Calcaneal Fracture Treatment Principles • Avoid wound complications (10-25%) • Restore articular congruity • Restore normal calcaneal width and height • Maximum functional recovery may take longer than 12 mo

Achilles Tendonitis

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Haglund Deformity: an enlargement of the posterior superior tuberosity of the calcaneus

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Mechanism • chronic inflammation from activity or poor-fitting footwear • may also develop heel bumps (retrocalcaneobursitis or Haglund deformity)

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Clinical Features • pain, stiffness, and crepitus with ROM • thickened tendon, palpable bump

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Investigations • X-ray: lateral, evaluate bone spur and calcification; U/S, MRI (to assess degenerative change)

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Treatment • non-operative ■■ rest, NSAIDs, shoe wear modification (orthotics, open back shoes) ■■ heel sleeves and pads are mainstay of non-operative treatment ■■ gentle gastrocnemius-soleus stretching, eccentric training with physical therapy, deep tissue calf massage ■■ shockwave therapy in chronic tendonitis ■■ DO NOT inject steroids (risk of tendon rupture)

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Achilles Tendon Rupture

The most common site of Achilles tendon rupture is 2-6 cm from its insertion where the blood supply is the poorest

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Clinical Features audible pop, sudden pain with push-off movement • pain or inability to plantarflex • palpable gap • apprehensive toe off when walking • weak plantarflexion strength • Thompson test: with patient prone, squeeze calf, normal response is plantar flexion ■■ no passive plantarflexion s positive test = ruptured tendon

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Mechanism • loading activity, stop-and-go sports (e.g. squash, tennis, basketball) • secondary to chronic tendonitis, steroid injection

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Investigations • X-ray (to rule out other pathology), U/S or MRI (for partial vs. complete ruptures) Treatment • non-operative ■■ indication: low athletic demand or elderly ■■ cast foot in plantar flexion (to relax tendon) x 8-12 wk • operative ■■ indication: high athletic demand ■■ surgical repair, then cast as above x 6-8 wk

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Complications of Achilles Tendon Rupture • Infection • Sural nerve injury • Re-rupture: surgical repair decreases likelihood of re-rupture compared to nonoperative management

Plantar Fasciitis (Heel Spur Syndrome)

Cuneiform

Talus

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Mechanism • repetitive strain injury causing microtears and inflammation of plantar fascia

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Definition • inflammation of plantar aponeurosis at calcaneal origin • common in athletes (especially runners, dancers) • also associated with obesity, DM, seronegative and seropositive arthritis Navicular Bone spur

Calcaneus

Figure 47. X-ray of bony heel spur

OR40 Orthopedics

Toronto Notes 2018

Foot

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Clinical Features • insidious onset of heel pain, pain when getting out of bed, and stiffness • intense pain when walking from rest that subsides as patient continues to walk, worse at end of day with prolonged standing • swelling, tenderness over sole • greatest at medial calcaneal tubercle and 1-2 cm distal along plantar fascia pain with toe dorsiflexion (stretches fascia) Investigations • plain radiographs to rule out fractures • often see bony exostoses (heel spurs) at insertion of fascia into medial calcaneal tubercle • spur is secondary to inflammation, not the cause of pain

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Treatment • non-operative ■■ pain control and stretching programs are first-line ■■ rest, ice, NSAIDs, steroid injection ■■ physiotherapy: Achilles tendon and plantar fascia stretching, extracorporeal shockwave therapy ■■ orthotics with heel cup – to counteract pronation and disperse heel strike forces • operative ■■ indication: failed non-operative treatment ■■ endoscopic surgical release of fascia ■■ spur removal is not required

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Bunions (Hallux Valgus)

Normal angle 15º

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Mechanism • valgus alignment on 1st MTP (hallux valgus) causes eccentric pull of extensor and intrinsic muscles • many associated deformities in foot from altered mechanics • reactive exostosis forms with thickening of the skin, creating a bunion • most often associated with poor-fitting footwear (high heel and narrow toe box) • can be hereditary (70% have family history) • 10x more frequent in women

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Definition • bony deformity characterized by medial displacement of first metatarsal and lateral deviation of hallux

© Michelle Lui 2004

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Clinical Features • painful bursa over medial eminence of 1st MT head • pronation (rotation inward) of great toe • numbness over medial aspect of great toe

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Investigations • X-ray: standing AP/lateral/sesamoid view, NWB oblique Treatment • indications: painful corn or bunion, overriding 2nd toe • non-operative (first-line) ■■ properly fitted shoes (low heel) and toe spacer • operative: goal is to restore normal anatomy, not cosmetic reasons alone ■■ osteotomy with realignment of 1st MTP joint (Chevron Procedure) ■■ arthrodesis

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Figure 48. Hallux valgus

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Metatarsal Fracture

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Table 22. Types of Metatarsal Fractures

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*NWB BK = Non weight bearing, below knee

Treatment Requires ORIF if displaced

Painful shaft of 5th MT

*NWB BK cast x 6 wk ORIF if athlete Symptomatic

Painful shaft of 2nd or 3rd MT

Trauma

Painful 1st MT

Fall onto plantar flexed foot or direct crush injury

Shortened forefoot prominent base

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Stress injury

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Tarso-MT Fracture – Dislocation (Lisfranc Fracture)

Clinical Tender base of 5th MT

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Midshaft 5th MT (Jones Fracture) Shaft 2nd, 3rd MT (March Fracture) 1st MT

Mechanism Sudden inversion followed by contraction of peroneus brevis Stress injury

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Fracture Type Avulsion of Base of 5th MT

ORIF if displaced otherwise *NWB BK cast x 3 wk then walking cast x 2 wk ORIF

Ottawa Ankle and Foot Rules (see Emergency Medicine, ER17) X-rays only required if: Pain in the midfoot zone AND bony tenderness over the navicular or base of the fifth metatarsal OR inability to weight bear both immediately after injury and in the ER

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• as with the hand, 1st, 4th, 5th MT are relatively mobile while the 2nd and 3rd are fixed • use Ottawa Foot Rules to determine need for x-ray

OR41 Orthopedics

Toronto Notes 2018

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Pediatric Orthopedics

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Pediatric Orthopedics

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Fractures in Children

© Sarah A. Kim 2005

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Proximal Radius

Proximal Radius

Figure 49. Greenstick (left) and torus (right) fractures

Greenstick fractures are easy to reduce but can redisplace while in cast due to intact periosteum

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• type of fracture ■■ thicker, more active periosteum results in pediatric-specific fractures: greenstick (one cortex), torus (i.e. ‘buckle’, impacted cortex) and plastic (bowing) ■■ distal radius fracture most common in children (phalanges second), the majority are treated with closed reduction and casting ■■ adults fracture through both cortices • epiphyseal growth plate ■■ weaker part of bone, susceptible to fractures ■■ plate often mistaken for fracture on x-ray and vice versa (X-ray opposite limb for comparison), especially in elbow ■■ tensile strength of bone < ligaments in children, therefore clinician must be confident that fracture and/or growth plate injury have been ruled out before diagnosing a sprain ■■ intra-articular fractures have worse consequences in children because they usually involve the growth plate • anatomic reduction ■■ gold standard with adults ■■ may cause limb length discrepancy in children (overgrowth) ■■ accept greater angular deformity in children (remodelling minimizes deformity) • time to heal ■■ shorter in children • always be aware of the possibility of child abuse ■■ make sure stated mechanism compatible with injury ■■ high index of suspicion with fractures in non-ambulating children (18 mo: open reduction; pelvic and/or femoral osteotomy

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Complications • redislocation, inadequate reduction, stiffness • AVN of femoral head

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Legg-Calvé-Perthes Disease (Coxa Plana) P

A

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Triradiate Cartilage y-shaped epiphyseal plate at junction of ilium, ischium and pubis Hilgenreiner’s Line Line running between triradiate cartilages Perkin’s Line Line through lateral margin of acetabulum, perpendicular to Hilgenreiner’s Line Shenton’s Line Arced line along inferior border of femoral neck and superior margin of obturator foramen Acetabular Index Angle between Hilgenreiner’s Line and line from triradiate cartilage to point on lateral margin of acetabulum

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Investigations • X-ray: AP pelvis, frog leg laterals • may be negative early (if high index of suspicion, move to bone scan or MRI) • eventually, characteristic collapse of femoral head (diagnostic)

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Most common in adolescent athletes, especially jumping/sprinting sports

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Osgood-Schlatter Disease

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Definition • inflammation of patellar ligament at insertion point on tibial tuberosity • M>F • age of onset: boys 12-15 yr; girls 8-12 yr

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Mechanism • repetitive tensile stress on insertion of patellar tendon over the tibial tuberosity causes minor avulsion at the site and subsequent inflammatory reaction (tibial tubercle apophysitis)

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Invest gations • X-ray lateral knee: fragmentation of the tibial tubercle, ± ossicles in patellar tendon

Children diagnosed with coxa plana 8 yr of age or severe) ◆◆ prognosis better in males, F = 5:1, 1/1,200 • associations ■■ family history ■■ low birth weight ■■ abnormal pregnancy/delivery ■■ ADHD in 33% of cases, delayed bone age in 89% ■■ second-hand smoke exposure ■■ Asian, Inuit, Central European • key features ■■ AVN of proximal femoral epiphysis, abnormal growth of the physis, and eventual remodelling of regenerated bone

OR44 Orthopedics

Toronto Notes 2018

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Pediatric Orthopedics

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Treatment • benign, self limited condition, does not resolve until growth halts • non-operative (majority) ■■ may restrict activities such as basketball or cycling ■■ NSAIDs, rest, flexibility, isometric strengthening exercises ■■ casting if symptoms do not resolve with conservative management • operative: ossicle excision in refractory cases (patient is skeletally mature with persistent symptoms)

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Plantar flexion of ankle joint Talus in equinus and varus

Physical Exam • examine hips for associated DDH • examine knees for deformity • examine back for dysraphism (unfused vertebral bodies)

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Figure 53. Club Foot - depicting the gross and bony deformity

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CAVE deformity • midfoot Cavus • forefoot Adductus • hindfoot Varus • hindfoot Equinus

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Treatment • largely non-operative via Ponseti Technique (serial manipulation and casting) ■■ correct deformities in CAVE order ◆◆ change strapping/cast q1-2wk ◆◆ surgical release in refractory case (rare) – delayed until 3-4 mo of age • 3 yr recurrence rate = 5-10% • mild recurrence common; affected foot is permanently smaller/stiffer than normal foot with calf muscle atrophy

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Inversion of calcaneus

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Forefoot bones in varus

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Etiology • intrinsic causes (neurologic, muscular, or connective tissue diseases) vs. extrinsic (intrauterine growth restriction); may be idiopathic, neurogenic, or syndrome-associated • fixed deformity

© Emilie McMahon 2005

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Definition • congenital foot deformity • muscle contractures resulting in CAVE deformity • bony deformity: talar neck medial and plantar deviated; varus calcaneus and rotated medially around talus; navicular and cuboid medially displaced • 1-2/1,000 newborns, 50% bilateral, occurrence M>F, severity F>M

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Congenital Talipes Equinovarus (Club Foot)

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Scoliosis

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Definition • lateral curvature of spine with vertebral rotation • age: 10-14 yr • more frequent and more severe in females Etiology • idiopathic: most common (90%) • congenital: vertebrae fail to form or segment • neuromuscular: UMN or LMN lesion, myopathy • postural: leg length discrepancy, muscle spasm • other: osteochondrodystrophies, neoplastic, traumatic

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Investigations • X-ray: 3-foot standing, AP, lateral ■■ measure curvature: Cobb angle ■■ may have associated kyphosis

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Figure 54. Cobb angle – used to monitor the progression of the scoliotic curve

Scoliosis screening is not recommended in Canada (Grieg A, et al. 2010; Health Canada, 1994)

In structural or fixed scoliosis, bending orwards makes the curve more obvious

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Clinical Features • ± back pain • primary curve where several vertebrae affected secondary curves above and below fixed 1° curve to try and maintain normal position of head and pelvis • asymmetric shoulder height when bent forward • Adam’s test: rib hump when bent forward • prominent scapulae, creased flank, asymmetric pelvis • associated posterior midline skin lesions in neuromuscular scolioses ■■ café-au-lait spots, dimples, neurofibromas ■■ axillary freckling, hemangiomas, hair patches • associated pes cavus or leg atrophy • apparent leg length discrepancy

© Crista Mason 2005

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Cobb angle

OR45 Orthopedics

Toronto Notes 2018

Bone Tumours

Postural scoliosis can be corrected by correcting the underlying problem

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Treatment • based on Cobb angle ■■ 25° or progressive: bracing (many types) that halt/slow curve progression but do NOT reverse deformity ■■ >45°, cosmetically unacceptable, or respiratory problems: surgical correction (spinal fusion)

Bone Tumours

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• primary bone tumours are rare after 3rd decade • metastases to bone are relatively common after 3rd decade

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Red Flags • Persistent skeletal pain • Localized tenderness • Spontaneous fracture Enlarging mass/soft tissue swelling

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Clinical Features • malignant (primary or metastasis): local pain and swelling (wk – mo), worse on exertion and at night, ± soft tissue mass • benign: usually asymptomatic • minor trauma often initiating event that calls attention to lesion

Malignant

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Benign No periosteal reaction

Acute periosteal reaction • Codman’s triangle (Figure 55) • “Onion skin” • “Sunburst”

Thick endosteal reaction Well developed bone formation Intraosseous and even calcification

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Broad border between lesion and normal bone Varied bone formation Extraosseous and irregular calcification

X-ray Findings • lytic, lucent, sclerotic bone • involvement of cortex, medulla, soft tissue • radiolucent, radiopaque, or calcified matrix • periosteal reaction • permeative margins • pathological fracture • soft tissue swelling

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Table 24. Distinguishing Benign from Malignant Bone Lesions on X-Ray

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Adapted from: Buckholtz RW, Heckman JD. Rockwo d and Green’s Fractures in Adults. Volume 1. Philadephia: Lippincott Williams & Wilkins, 2001. p558

Neoplasm

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Benign Active Bone Tumours

Periosteum

Codman’s triangle

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FIBROUS LESIONS

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Fibrous Cortical Defect • or non-ossifying fibroma; fibrous bone lesion • most common benign bone tumour in children, typically asymptomatic and an incidental finding • occur in as many as 35% of children, peak incidence between 2-25 yr old higher prevalence in males • femur and proximal tibia most common locations, 50% of patients have multiple defects that are usually bilateral, symmetrical • radiographic findings: diagnostic, metaphyseal eccentric ‘bubbly’ lytic lesion near physis; thin, smooth/ lobulated, well-defined sclerotic margin • treatment: most lesions resolve spontaneously

Figure 55. Codman’s triangle – a radiographic finding in malignancy, where the partially ossified periosteum is lifted off the cortex by neoplastic tissue

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Osteoid Osteoma • bone tumour arising from osteoblasts • peak incidence in 2nd and 3rd decades, M:F = 2:1 • proximal femur and tibia diaphysis most common locations • not known to metastasize • radiographic findings: small, round radiolucent nidus (2 cm) with radiolucent halo and sclerosis • symptoms: local tenderness and swelling, pain may be progressive (giant cell tumours), ± symptoms of nerve root compression (osteoblastoma) • 15% recur within 2 yr of surgery

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Treatment • intralesional curettage + bone graft or cement • wide local excision of expendable bones

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Figure 57. X-ray of aneurysmal bone cyst Note the aggressive destruction of bone

OR47 Orthopedics

Toronto Notes 2018

Bone Tumours

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Malignant Bone Tumours

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Table 25. Most Common Malignant Tumour Types for Age Malignant

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Benign

No periosteal reaction

Acute periosteal reaction • Codman’s triangle • “Onion skin” • “Sunburst”

Thick endosteal reaction Well developed bone formation Intraosseous and even calcification

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Broad border between lesion and normal bone Varied bone formation Extraosseous and irregular calcification

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Adapted from: Buckholtz RW, Heckman JD. Rockwood and Green’s Fractures in Adults. Volume 1. Philadephia: Lippincott Williams & Wilkins, 2001. p558

Figure 58. X-ray of osteosarcoma of distal femur

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Osteosarcoma • malignant bone tumour • most frequently diagnosed in 2nd decade of life (60%), 2nd most common primary malignancy in adults • history of Paget’s disease (elderly patients), previous radiation treatment • predilection for sites of rapid growth: distal femur (45% - Figure 58), proximal tibia (20%), and proximal humerus (15%) ■■ invasive, variable histology; frequent metastases without treatment (lung most common) • painful symptoms: progressive pain, night pain, poorly defined swelling, decreased ROM • radiographic findings ■■ characteristic periosteal reaction: Codman’s triangle (Figure 55) or “sunburst” spicule formation (tumour extension into periosteum) ■■ destructive lesion in metaphysis may cross epiphyseal plate • management: complete resection (limb salvage, rarely amputation), neo-adjuvant chemo; bone scan – rule out skeletal metastases, CT chest – rule out pulmonary metastases • prognosis: 70% survival (high-grade); 90% survival (low-grade)

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Chondrosarcoma • malignant chondrogenic tumour • primary (2/3 cases) ■■ previous normal bone, patient >40 yr; expands into cortex to cause pain, pathological fracture • secondary (1/3 cases) ■■ malignant degeneration of pre-existing cartilage tumour such as enchondroma or osteochondroma ■■ age range 25-45 yr, better prognosis than primary chondrosarcoma • symptoms: progressive pain, uncommonly palpable mass • radiographic findings: in medullary cavity, irregular “popcorn” calcification (Figure 59) • treatment: unresponsive to chemotherapy, treat with aggressive surgical resection + reconstruction; regular follow-up X-rays of resection site and chest • prognosis: 10 yr survival 90% for low-grade, 20-40% for high-grade

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Signs of Hypercalcemia “Bones, Stones, Moans, Groans, Psychiatric overtones” CNS: headache, confusion irritability, blurred vision GI: N/V, abdominal pain constipation, weight loss MSK: fatigue, weakness, unsteady gait, bone and joint pain GU: nocturia, polydipsia, polyuria, UTIs

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Multiple Myeloma proliferation of neoplastic plasma cells • most common primary malignant tumour of bone in adults (~43%) • 90% occur in people >40 yr old, M:F = 2:1; twice as common in African-Americans • signs/symptoms: localized bone pain (cardinal early symptom), compression/pathological fractures, renal failure, nephritis, high incidence of infections (e.g. pyelonephritis/pneumonia), systemic (weakness, weight loss, anorexia) • labs: anemia, thrombocytopenia, increased ESR, hypercalcemia, increased Cr • radiographic findings: multiple, “punched-out” well-demarcated lesions, no surrounding sclerosis, marked bone expansion • diagnosis ■■ serum/urine immunoelectrophoresis (monoclonal gammopathy) ■■ CT-guided biopsy of lytic lesions at multiple bony sites

Figure 59. X-ray of femur chondrosarcoma

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Ewing’s Sarcoma • malignant, small round cell sarcoma • most occur between 5-25 yr old • florid periosteal reaction in metaphyses of long bone with diaphyseal extension • metastases frequent without treatment • signs/symptoms: presents with pain, mild fever, erythema, and swelling; anemia, increased WBC, ESR, LDH (mimics an infection) • radiographic findings: moth-eaten appearance with periosteal lamellated pattern (“onion-skinning”) • treatment: resection, chemotherapy, radiation • prognosis – 70% survival, worst prognostic factor is distant metastases

OR48 Orthopedics

Toronto Notes 2018

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Common Medications

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• treatment: chemotherapy, bisphosphonates, radiation, surgery for symptomatic lesions or impending fractures – debulking, internal fixation • prognosis: 5 yr survival 30%; 10 yr survival 11% • see Hematology, H49

Thyroid

Kidney

Upper arm

Lower extremity

Peritrochanteric

Pain

Mild

Moderate

Severe

Lesion

Blastic

Size

2/3 diameter

Common Medications Indications

Comments

cefazolin (Ancef )

1-2 g IV q8h

Prophylactically before orthopedic surgery

First generation cephalosporin; do not use with penicillin allergy

heparin

5000 IU SC q12h

To prevent venous thombosis and pulmonary emboli

Monitor platelets, follow PTT which should rise 1.5-2x

LMWH dalteparin (Fragmin®) enoxaparin (Lovenox®) fondaparinux (Arixtra®)

5000 IU SC OD 30-40 mg SC bid 2.5 mg SC OD

DVT p ophylaxis especially in hip and knee surgery

Fixed dose, no monitoring, improved bioavailability, increased bleeding rates

oral anticoagulants dabigatran (Pradaxa®) rivaroxaban (Xarelto®) apixaban

110 mg PO x1 then 220 mg PO OD 10 mg PO OD 2.5 mg PO bid

DVT prophylaxis especially TKA and THA

Predictable, no monitoring, oral administration; no antidote

midazolam (Versed®)

0.02-0 04 mg/kg IV

Conscious sedation for short procedures

Medication used during fracture reduction – monitor for respiratory depression

fentanyl (Sublimaze®)

0.5-3 µg/kg IV

Conscious sedation for short procedures

Short acting anesthetic used in conjunction with midazolam (Versed®)

triamcinolone (Aristocort®) – an injectable steroid

0.5-1 mL of 25 mg/mL

Suspension (injected into inflamed joint or bursa); amount varies by joint size

Potent anti-inflammatory effect;increased pain for 24 h, rarely causes fat necrosis and skin depigmentation

naproxen (Aleve®, Naprosyn®)

250-500 mg bid

Pain due to inflammation, arthritis, soft tissue injury

NSAID, may cause gastric erosion and bleeding

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Dosing Schedule

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Table 27. Common Medications

Prophylaxis of HO after THA

Use with indomethacin

25 mg PO tid

Prophylaxis of HO after THA

Use with misoprostol

ibuprofen (Advil®, Motrin®)

200-400 mg tid

Pain (including post-operative), inflammation (including arthritis)

NSAID, may cause gastric erosion and bleeding

propofol (Diprivan®)

1-2 mg/kg IV maintenance 0.5 mg/kg

Conscious sedation for short procedures

Short acting anesthetic often used in conjunction with fentanyl (Sublimaze®)

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200 µg qid

indomethacin (Indocid®)

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misoprostol (Cytotec®)

BLT with a Kosher Pickle B east Lung Thyroid Kidney Prostate

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Number Assigned 2

Drug Name

Kidney Prostate

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Melanoma

Table 26. Mirel’s Criteria for Impending Fracture Risk and Prophylactic Internal Fixation Variable

Breast Lung

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Breast Lung

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Bone Metastases • most common cause of bone lesions in adults; typically age >40 • 2/3 from breast or prostate; also consider thyroid, lung, kidney • usually osteolytic; prostate occasionally osteoblastic • may present with mechanical pain and/or night pain, pathological fracture, hypercalcemia • bone scan for MSK involvement, MRI for spinal involvement may be helpful • treatment: pain control, bisphosphonates, stabilization of impending fractures if Mirel’s Critera >8 (ORIF, IM rod, bone cement)

Most Common Tumours Metastatic to Bone

OR49 Orthopedics

Toronto Notes 2018

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References

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References

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AAOS. The treatm nt of distal radius fractures: summary of recommendations. 2009. Available from: http://www.aaos.org/research/guidelines/DRFguideline.asp. Adams JC, Hamb en DL. Outline of fractures: including joint injuries, 11th ed. Toronto: Churchill Livingstone, 1999. Adkins SB. H p pain in athletes. Am Fam Phys 2000;61:2109-2118. Armagan OE, Shereff MJ. Injuries of the toes and metatarsals. Orthop Clin North Am 2001;32:1-10. Barei DP, Bellabarba C, Sangeorzan BJ, et al. Fractures of the calcaneus. Orthop Clin North Am 2001;33:263-285. Barrett SL. Plantar fasciitis and other causes of heel pain. Am Fam Phys 1999 59:2200-2206. Blackbourne LH (editor). Surgical recall, 3rd ed. Philadelphia: Lippincott Williams & Wilkins, 2002. Brand DA, Frazier WH, Kohlhepp WC, et al. A protocol for selecting patients with injured extremities who need x-rays. NEJM 1982;306:833-839. Brinker MR. Review of orthopedic trauma. Toronto: WB Saunders, 2001. Brinker M, Miller M. Fundamentals of orthopedics. Philadelphia: WB Saunders, 1999. Canadian CT Head and C-Spine (CCC) Study Group. Canadian c-spine rule study for alert and stable trauma patients: background and rationale. CJEM 2002;4:84-90. Canale ST, Beaty JH. Campbell’s operative orthopaedics, 12th ed. Philadelphia: Elsevier Mosby, 2013. Carek PJ. Diagnosis and management of osteomyelitis. Am Fam Phys 2001;63:2413-2420. Dee R, Hurst LC, Gruber MA, et al. (editors) Princip es of orthopedic practice, 2nd ed. Toronto: McGraw-Hill, 1997. Donatto KC. Ankle fractures and syndesmosis injuries. Orthop Clin North Am 2001;32:79-90. Duane TM, Wilson SP, Mayglothling J, et al Canadian cervical spine rule compared with computed tomography: a prospective analysis. J Trauma 2011;71:352-355. Fernandez M. Discitis and vertebral osteomyelitis in children: an 18-year review. Pediatrics 2000;105:1299-1304 Flyn JM. Orthopaedic Knowledge Update 10. Rosemont IL: American Academy of Orthopaedic Surgeons, 2011. Fortin PT. 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Clinical assessment of scaphoid injuries and the detection of fractures. J Hand Surg Br 1996;21:341-343. Gustilo RB, Mendoza RM, Williams DN. Problems in the management of type III (severe) open fractures: a new classification of type III open fractures J Trauma 1984;24:742-746. Hamilton H, McIntosh G, Boyle C. Effectiveness of a low back classification system. Spine J 2009;9:648-657. Harty MP. Imaging of pediatric foot disorders. Radiol Clin North Am 2001;39:733-748. Hermans J, Luime JL, Meuffels DE, et al. Does this patient with shoulder pain have rotator cuff disease? The rational clinical examination systematic review. JAMA 2013;310:837-847. Irrgang JJ. Rehabilitation of multiple ligament injured knee. Clin Sports Med 2000;19:545-571. Kao LD. Pre-test surgery. Toronto: McGraw-Hill, 2002. Karachalios T, Hantes M, Zibis AH, et al. Diagnostic accuracy of a new clinical test (the Thessaly test) for early detection of meniscal tears. J Bone Joint Surg Am 2005;87:955-962. Lawrence LL. The limping child. Emerg Med Clin North Am 1998;169:911-929. Litaker D, Pioro M, El Bilbeisi H, et al. Returning to the bedside: using the history and physical examination to identify rotator cuff tears. J Am Geriat Soc 2000;48:1633-1637. Lo IK, Nonweiler B, Woolfrey M, et al. An evaluation of the apprehension, relocation, and surprise tests for anterior shoulder nstability. Am J Sports Med 2004;32:301-7. Magee DJ. Orthopedic physical assessment, 5th ed. St. Louis: WB Saunders Elsevier, 2008. Margaretten ME, Kohlwes J, Moore D et al. Does this adult patient have septic arthritis? JAMA 2007;297:1478 1488. Mathews CJ, Coakley G Septi arthritis: current diagnostic and therapeutic algorithm. Curr Opin Rheumatol 2008;20:457-462. Mazzone MF. Common c nditions of the Achilles tendon. Am Fam Phys 2000;65:1805-1810. Miller MD, Thompson SR, Hart J. Review of Orthopaedics, 6th ed. Philadelphia: Elsevier, 2012. Miller SL. Maligna t and benign bone tumours. Radiol Clin North Am 2000;39:673-699. Murrell GA, Walton JR. Diagnosis of rotator cuff tears. Lancet 2001;357:769-770. Ochiai DH The orthopedic intern pocket survival guide. McLean: International Medical Publishing, 2007. Okike K, Bhattacharyya T. Trends in the management of open fractures: a critical analysis. J Bone Joint Surg Am 2006;88:2739-2748. Oudjhane K. Imaging of osteomyelitis in children. Radiol Clin North Am 2001;39:251-266. Patel DR. Sports injuries in adolescents. Med Clin North Am 2000;84:983-1007 Roberts DM, Stallard TC. Emergency department evaluation and treatment of knee and leg injuries. Emerg Med Clin North Am 2000;18:67-84. Rockwood CA, Williams GR, Young DC. Disorders of the acromioclavicular joint. Rockwood CA, Masten FA II (editors). The shoulder. Philadelphia: Saunders, 1998. 483-553. Rockwood CA Jr, Greene DP, Bucholz RU, et al. (editors). Rockwood and Green’s fractures in adults, 4th ed. Philadelphia: Lippincott Raven, 1996. Russell GV Jr. Complicated femoral shaft fractures. Orthop Clin North Am 2002;33:127-142. Ryan SP, Pugliano V. Controversies in initial management of open fractures. Scan J Surg 2014;103(2):132-7. Skinner HB. Current diagnosis and treatment in orthopedics, 4th ed. New York: McGraw-Hill, 2006. Solomon DH, Simel DL, Bates DW, et al. The rational clinical examination: does this patient have a torn meniscus or ligament of the knee? Value of the physical examination. JAMA 2001;286:1610-1620. Solomon L, Warwick DJ, Nayagam S. Apley’s system of orthopedics and fractures, 8th ed. New York: Hodder Arnold, 2001 St Pierre P. Posterior cruciate ligament injuries. Clin Sports Med 1999;18:199-221. Steele PM, Bush-Joseph C, Bach Jr B. Management of acute fractures around the knee, ankle, and foot. Clin Fam Pract 2000;2:661-705. Stewart DG Jr, Kay RM, Skaggs DL Open fractures in children. Principles of evaluation and management. J Bone Joint Surg Am 2005;87:2784-2798. Swenson TM. The dislocated knee physical diagnosis of the multiple-ligament-injured knee. Clin Sports Med 2000;19:415-423. Testroote M, Stigter WA, Janssen L, et al. Low molecular weight heparin for prevention of venous thromboembol sm in patients with lower-leg immobilization. Cochrane DB Syst Rev 2014;4:CD006681. Thompson JC. Netter’s concise atlas of orthopedic Anatomy. USA: Elsevier, 2001. Wong M. Pocket orthopedics: evidence-based survival guide. Sudbury: Jones and Bartlett Publishers 2010. Zhang Y. Clinical Epidemiology of Orthopedic Trauma. New York: Thieme Medical Publishers, 2012 Zollinger PE, Tuinebreijer WE, Kreis RW, et al. Effect of vitamin C on frequency of reflex sympathetic dystrophy in wrist fractures: a randomized trial. Lancet 1999;354:2025 2058.

OR50 Orthopedics

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Toronto Notes 2018

Common Medications

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Otolaryngology – Head & Neck Surgery

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Ragavan Ganeshathasan, Armin Rahmani, Stephen Szeto, and Siraj Zahr, chapter editors Sangwoo Leem and Mark Shafarenko, associate editors Jin Kyu Kim and Shubham Shan, EBM editors Dr. Jonathan C. Irish and Dr Evan J. Propst, staff editors

Facial Nerve (CN VII) Paralysis. . . . . . . . . . . . . . . 22

Basic Anatomy Review. . . . . . . . . . . . . . . . . . . . . . 2 Ear Nose Throat Head and Neck Anatomical Triangles of the Neck

Rhinitis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23 Allergic Rhinitis (i.e. Hay Fever) Vasomotor Rhinitis

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Diseases of the Middle Ear. . . . . . . . . . . . . . . . . . 17 Acute Otitis Media and Otitis Media with Effusion Chronic Otitis Media Cholesteatoma Mastoiditis Otosclerosis

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Diseases of the Inner Ear. . . . . . . . . . . . . . . . . . . 19 Congenital Sensorineural Hearing Loss Presbycusis Sudden Sensorineural Hearing Loss Autoimmune Inner Ear Disease Drug Ototoxicity Noise-Induced Sensorineural Hearing Loss Temporal Bone Fractures

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Neck Masses . . . . . . . . . . . . . . . . . . . . . . . . . . 31 Approach to a Neck Mass Evaluation Congenital Neck Masses. . . . . . . . . . . . . . . . . . . . 32 Brachial Cleft Cysts/Sinuses/Fistulae Thyroglossal Duct Cysts Lymphatic, Venous, or Mixed Venolymphatic Malformations Neoplasms of the Head and Neck . . . . . . . . . . . . 34 Thyroid Carcinoma

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Pediatric Otolaryngology . . . . . . . . . . . . . . . . . . 38 Acute Otitis Media Otitis Media with Effusion Adenoid Hypertrophy Adenoidectomy Sleep-Disordered Breathing in Children Acute Tonsillitis Peritonsillar Abscess (Quinsy) Tonsillectomy Airway Problems in Children Signs of Airway Obstruction Acute Laryngotracheobronchitis (Croup) Acute Epiglottitis Subglottic Stenosis Laryngomalacia Foreign Body Deep Neck Space Infection

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Diseases of the External Ear. . . . . . . . . . . . . . . . 15 Cerumen Impaction Exostoses Otitis Externa Malignant (Necrotizing) Otitis Externa (Skull Base Osteomyelitis)

Salivary Glands . . . . . . . . . . . . . . . . . . . . . . . . . . 30 Sialadenitis Sialolithiasis Salivary Gland Neoplasms Parotid Gland Neoplasms

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Tinnitus. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15

Hoarseness. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 28 Acute Laryngitis Chronic Laryngitis Vocal Cord Polyps Vocal Cord Nodules Benign Laryngeal Papillomas Laryngeal Carcinoma

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Vertigo . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12 Evaluation of the Dizzy Patient Benign Paroxysmal Positional Vertigo Ménière’s Disease (Endolymphatic Hydrops) Vestibular Neuronitis (Labyrinthitis) Acoustic Neuroma (Vestibular Schwannoma)

. . . . . . . . . . . . . . . . . . . . . . 26

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Hearing. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9 Normal Hearing Physiology Types of Hearing Loss Pure Tone Audiometry Speech Audiometry Impedance Audiometry Auditory Brainstem Response Otoacoustic Emissions Aural Rehabilitation

Epistaxis. . . . . . . .

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Differential Diagnoses of Common Presentations. . . . . . . . . . . . . . . . . . . . . . . . . . 6 Dizziness Otalgia Hearing Loss Tinnitus Nasal Obstruction Hoarseness Neck Mass

Rhinosinusitis. . . . . . . . . . . . . . . . . . . . . . . . . . . . 24 Acute Bacterial Rhinosinusitis Chronic Rhinosinusitis

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Acronyms. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2

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OT

Common Medications. . . References . . . . . . . .

Otolaryngology OT1

. . . . . . . . . . . . . . . . . 46

. . . . . . . . . . . . . . . . . . . . 48 Toronto Notes 2018

OT2 Otolaryngology

Toronto Notes 2018

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Acronyms

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Acronyms SCC squamous cell carcinoma SCM sternocleidomastoid SNHL sensorineural hearing loss SRT speech reception threshold TEF tracheoesophageal fistula TM tympanic membrane TNM tumour, node, metastases URTI upper respiratory tract infection

human papillomavirus intranasal corticosteroids middle ear effusion middle ear inflammation otitis externa otitis media with effusion obstructive sleep apnea rheumatoid arthritis

b

HPV INCS MEE MEI OE OME OSA RA

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Epstein-Barr virus familial adenomatous polyposis functional endoscopic sinus surgery fine needle aspiration gastroesophageal reflux disease granulomatosis with polyangiitis head and neck hearing loss

eb

b

EBV FAP FESS FNA GERD GPA H&N HL

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auditory brainstem response air conduction acute otitis media bone anchored hearing aid bone conduction conductive hearing loss cerebellopontine angle external auditory canal

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ABR AC AOM BAHA BC CHL CPA EAC

m

Basic Anatomy Review Ear Middle

Temporalis fascia and muscle

Antihelix Scapha

Auditory ossicles

Malleus

Helix

Incus

Semicircular canals

Stapes

o

Triangular fossa

Inner

f

External

Vestibular nerve

Helical crus

Cochlear nerve

Vestibulocochlear nerve (CN VIII)

Tragus

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o

Facial nerve (CN VII) Cochlea

Antitragus Lobule

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External acoustic Tympanic meatus membrane

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© Aarti Inamdar

b

Figure 1. Surface anatomy of the external ear; anatomy of ear View into tympanic cavity after removal of tympanic membrane

Fossa of round (cochlear) window Cone of light

e

Pars tensa

Figure 2. Normal appearance of right tympanic membrane on otoscopy

Tympanic plexus (branch of CN IX)

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Tendon of stapedius muscle Long process of malleus Umbo (Flat portion)

Tensor tympani tendon Tensor tympani muscle

Hypotympanum

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Pars flaccida Neck of malleus Lateral process of malleus Incus long process Stapes

Annulus

m

Tympanic membrane viewed through speculum

© Diana Dai 2006

Eustachian tube © Susan Park 2009

OT3 Otolaryngology

Toronto Notes 2018

c

Basic Anatomy Review

Nose Adenoid Sphenoid sinus Superior turbinate Middle turbinate Middle meatus Inferior turbinate © Jason Raine 2003

m

Inferior meatus

Speculum View of Right Nostril

Palatine process of maxilla Soft palate Opening for Eustachian tube

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Figure 3. Nasal anatomy

o

Anterior ethmoid a. Frontal sinus

Posterior ethmoid a.

Sphenoid sinus

Septal branch of sphenopalatine a.

Branch of superior labial a.

Internal carotid a. Greater palatine a.

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External carotid a. Common carotid a.

© Barbara Brehovsky 2012

Kiesselbach’s plexus

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Figure 4. Nasal septum and its arterial supply (see Epistaxis, OT26 for detailed blood supply)

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Frontal sinus Orbit Ethmoid sinus Lamina papyracea Osteomeatal complex Maxillary sinus Nasal cavity Teeth

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Figure 5. Anatomy of the four paranasal sinuses: maxillary, ethmoid, sphenoid and frontal

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Reprinted from: Dhillon RS East CA. Ear, Nose and Throat and Head and Neck Surgery, 2nd ed. Copyright 1999, with permission from Elsevier

o

Throat

Coronal Section

Mid-Saggital View

Superior View Valeculla

Anterior

Vestibule

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Thyroid cartilage Vestibular folds (false cords) Vocal folds (true cords) Trachea © Glen Oomen 2002

Arytenoid cartilage

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Poster or View

Pyriform fossa

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Figure 6. Anatomy of a normal larynx; superior view of larynx on indirect laryngoscopy

Posterior

Epiglottis

Hyoid bone

Vestibular ligaments (false cords)

Thyrohyoid membrane

Arytenoid cartilage

Thyroid cartilage

Vocal ligaments (true cords)

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Epiglottis

Median cricothyroid ligament Cricoid cartilage © Natalie Cormier 2015

OT4 Otolaryngology

Toronto Notes 2018

c

Basic Anatomy Review

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Head and Neck Temporal branch Zygomatic branch

Buccal branch

Superficial temporal a.

Styloid process Mastoid process Stylomastoid foramen

Maxillary a.

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Angular a.

Occipital a.

Lateral nasal a.

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Facial n. (CN VII) Posterior belly of digastric m. Parotid gland Mandibular branch Marginal mandibular branch Cer ical branch

Posterior auricular a.

Ascending pharyngeal a.

External carotid a. Facial a. Lingual a.

Common carotid a.

b

b

Superior thyroid a.

Figure 8. Blood supply to the face

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Figure 7. Extratemporal segment of facial nerve

© Sean Wang 2007

Internal carotid a.

Inferior labial a.

© M. Romanova 2010

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Superior labial a.

Branches of facial nerve (in order from superior to inferior) To Zanzibar By Motor Car

Branches of the external carotid artery (in order from inferior to superior) Some Angry Lady Figured Out PMS

Hyoid bone Thyrohyoid membrane

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External carotid a.

Post. belly digastric m.

Thyroid cartilage

Common carotid a. bifurcation Common arotid a. bifurcation Sternocleidomastoid m.

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Sternohyoid m.

Sternocleidomastoid m.

Ant. belly omohyoid m.

Posterior triangle

Omohyoid m.

Median cricothyroid ligament

Internal jugular v.

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Ant. belly digastric m. Hyoid bone

Trapezius m.

Anterior triangle

Cricoid cartilage

Post. belly omohyoid m

Thyroid gland

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Sternohyoid m. Trachea

Clavicle

e.

© Inessa Stanishevskaya 2012 after

Sternocleidomastoid m. Greater auricular n. Lesser occipital n. Ventral ramus (C2) Ventral ramus (C3) Accessory n. (CN XI)

Digastric m. Hypoglossal n. (CN XII) Superior root ansa cervicalis

Ventral ramus (C5) Anterior scalene m. Phrenic n.

Inferior root ansa cervicalis Vagus n.

e

Brachial plexus

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Figure 9. Anatomy of the neck

© Kateryna Procunier 2014, after

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Subclavian a. and v.

OT5 Otolaryngology

Toronto Notes 2018

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Basic Anatomy Review

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Anatomical Triangles of the Neck

Drainage

Base of skull, posterior

Posterior scalp

2. Retroauricular (R)

Superficial to mastoid process

Scalp, temporal region, external auditory meatus, posterior pinna

3. Parotid-preauricular (P)

Anterior to ear

External auditory meatus, anterior pinna, soft tissue of frontal and temporal regions, root of nose, eyelids palpebral conjunctiva

4. Submental (Level IA)

Anterior bellies (midline) of digastric muscles, tip of mandible, and hyoid bone

Floor of mouth, anterior tongue, anterior mandibular alveolar ridge, lower lip

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co

e.

Oral cavity, anterior nasal cavity, soft tissues of the mid-face, submandibular gland

Skull base to inferior border of hyoid bone along SCM muscle

Oral cavity, nasal cavity, naso/oro/hypopharynx, larynx, parotid glands

7. M ddle jugular (Level III)

Inferior border of hyoid bone to inferior border of cricoid cartilage along SCM muscle

Oral cavity, naso/oro/hypopharynx, larynx

8. Lower jugular* (Level IV)

Inferior border of cricoid ca tilage to clavicle along SCM muscle

Hypopharynx, thyroid, cervical esophagus, larynx

9. Posterior triangle** (Levels VA and VB)

Posterior border of SCM, anterior border of trapezius, from skull base to clavicle

Nasopharynx and oropharynx, cutaneous structures of the posterior scalp and neck

10. Anterior compartment*** (Level VI)

Hyoid b ne (midline) to suprasternal notch between the common carotid arteries

Thyroid gland, glottic and subglottic larynx, apex of piriform sinus cervical esophagus

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TC CC SPG TG IPG

* ITA RRLN

© Erin Kenzie 2104 after Marisa Bonofiglio 2003

STA CCA IJV

VN (CN X) LRLN

STA CCA IJV ITA RRLN TC CC SPG TG IPG VN (CN X) LRLN

– – – – – – – – – – – –

Superior thyroid artery Common carotid artery Internal jugular vein Inferior thyroid artery Right recurrent laryngeal nerve Thyroid cartilage Cricoid cartilage Superior parathyroid gland Thyroid gland Inferior parathyroid gland Vagus nerve (CN X) Left recurrent laryngeal nerve

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4 Strap Muscles of the Neck • Thyrohyoid • Omohyoid • Sternohyoid • Sternothyroid

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*Virchow node: left lower jugular (level IV) supraclavicular node **Includes some supraclavicular nodes ***Includes pretracheal, prec icoid paratracheal, and perithyroidal nodes

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6. Upper jugular (Levels IIA and IIB)

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Anterior belly of digastric muscle, stylohyoid muscle, body of mandible

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5. Submandibular (Level IB)

• Left-sided enlargement of a supraclavicular node (Virchow’s node) may indicate an abdominal malignancy • Right-sided enlargement may indicate malignancy of the mediastinum, lungs, or esophagus • Occipital and/or posterior auricular node enlargement may indicate rubella

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1. Suboccipital (S)

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“Ears Tears, Face, Taste” Ears: stapedius muscle Tears: lacrimation (lacrimal gland) and salivation (parotid) Face: muscles of facial expression Taste: sensory anterior 2/3 of tongue (via chorda tympani)

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Location

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Nodal Group/Level

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Function of Facial Nerve

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Table 1. Lymphatic Drainage of Nodal Groups and Anatomical Triangles of Neck

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Paired Parasympathetic Ganglia of the Head and Neck • Ciliary: pupillary constriction • Pterygopalatine: lacrimal gland, nasal mucosa • Submandibular: submandibular, sublingual glands • Otic: parotid gland

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Anterior triangle • bounded by anterior border of SCM, midline of neck, and lower border of mandible • divided into: ■■ submental triangle: bounded by both anterior belly of digastric and hyoid bone ■■ digastric triangle: bounded by anterior and posterior bellies of digastric and inferior border of mandible ■■ carotid triangle: bounded by sternocleidomastoid, anterior belly of omohyoid, and posterior belly of digastric ◆◆ contains: tail of parotid, submandibular gland, hypoglossal nerve, carotid bifurcation, and lymph nodes Posterior triangle • bounded by posterior border of sternocleidomastoid, anterior border of trapezius, and middle third of clavicle • divided into: ■■ occipital triangle: superior to posterior belly of the omohyoid ■■ subclavian triangle: inferior to posterior belly of omohyoid • contains: spinal accessory nerve and lymph nodes

*Thyroidea ima artery: present in 3% of population, arises from aortic arch or innominate artery

Figure 10. Anatomy of the thyroid gland

OT6 Otolaryngology

Toronto Notes 2018

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Differential Diagnoses of Common Presentations

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Differential Diagnoses of Common Presentations

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Dizziness

Dizziness

Non-Vertiginous

Common causes in bold

Functional

Cerebrovascular disorders Vertebrobasiliar insufficiency Transient ischemic attacks Wallenberg’s syndrome Cerebellar infarction Migrainous vertigo Multiple sclerosis Inflammation Meningitis Cerebellar abscess Trauma: cerebellar contusion Toxic: alcohol, hypnotics, drugs Tumours CPA tumours Posterior fossa tumours Glomus tumours

Cardiac Arrhythmias Aortic stenosis Vasovagal Orthostatic hypotension Anemia Peripheral neuropathy Visual impairment

Depression Anxiety Panic disorder (hyperventilation) Personality disorder Phobic dizziness

fe

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Organic Diseases

e

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Benign paroxysmal positional vertigo (BPPV) Labyrinthitis Menière’s disease Vestibular neuronitis Autoimmune inner ear disease Cholesteatoma Ototoxic drug exposure Perilymph fistula Recurrent vestibulopathy Superior semicircular canal dehiscence Temporal bone fracture

Central

m

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Peripheral (Vestibular)

Figure 11. Differential diagnosis of dizziness

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Otalgia

Otalgia

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Figure 12. Differential diagnosis of otalgia

Referred Pain Infection Ramsay Hunt syndrome Tonsillitis Tracheitis Trauma Cervical arthritis Thyroiditis Other Glossopharyngeal neuralgia Neoplasm of oral cavity, larynx, pharynx Teeth TMJ syndrome Trismus

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Infection AOM Mastoiditis Myringitis Otitis media with effusion Skull base infections Trauma Barotrauma Traumatic perforation Other Cholesteatoma Neoplasm Wegener's granulomatosis

s

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Infection Auricular cellulitis External canal abscess Herpes simplex/zoster Otitis externa Trauma Burns Frostbite Hematoma Lacerations Other Cerumen impaction Foreign body Ne plasm of external canal

Middle Inner Ear

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External Ear

True nystagmus and vertigo caused by a peripheral lesion will never last longer than a few weeks, due to compensation from the cerebellum (unless here is a history of cerebellar ischemia/stroke). Central lesions do not compensate, therefore nystagmus and vertigo will persist

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True Vertigo

5 “D”s of Vertebrobasilar Insufficiency Drop attacks Diplopia Dysarthria Dizziness Dysphagia

OT7 Otolaryngology

Toronto Notes 2018

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Differential Diagnoses of Common Presentations

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Hearing Loss Hearing Loss

Conductive

Sensorineural

Congenital

Acquired

Impacted cerumen Otitis externa Foreign body Keratosis obturans Exostoses, osteomas Tumour of canal Congenital stenosis/microtia

AOM Otitis media with effusion TM perforation Otosclerosis Tympanosclerosis Eustachian tube dysfunction Cholesteatoma Ossicular malformations Ossicular discontinuity Hemotympanum Middle ear tumour

Genetic Non-syndrome associated Syndrome associated Intrauterine infections (i.e. TORCH) Teratogens Perinatal hypoxia Prematurity/low birth weight Hyperbilirub nemia

Presbycusis Noise-induced Menière’s disease Labyrinthitis Sudden SNHL Autoimmune inner ear disease Ototoxic drug exposure Temporal bone trauma Infectious Postmeningitis Syphilis Viral: mumps, CMV, HSV Neoplastic Acoustic neuroma CPA tumours Vascular occlusi n/emboli Auditory neuropathy

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Middle Ear

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External Ear

Common causes in bold

Figure 13. Differential diagnosis of hearing loss

Tinnitus Tinnitus

Vascular Benign intracranial hypertension Arteriovenous malformation Glomus tympanicum Glomus jugulare Arterial bruits: High-riding carotid artery Vascular loop Persistent stapedial artery Carotid stenosis Venous hum: High jugular bulb Hypertension Hyper/hypothyroidism Mechanical Patulous eustachian tube Palatal myoclonus Stapedius muscle spasm

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Figure 14. Differential diagnosis of tinnitus

Common causes in bold

Glomus Tympanicum/Jugulare Tumour Signs and Symptoms • Pulsatile tinnitus • Hearing loss • Blue mass behind TM • Brown’s sign (blanching of the TM with pneumatic otoscopy)

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Otologic Presbycusis Noise-induced hearing loss Otitis media with effusion Menière’s disease Otosclerosis Cerumen Foreign body against TM Drugs ASA NSAIDs Aminoglycosides Ant hypertensives Heavy metals Metabolic Hyper/hypothyroidism Hyperlipidemia Vitamin A, B, Zinc deficiency Neurologic Head trauma Multiple sclerosis CPA tumours Psychiatric Anxiety Depression

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Objective Can be heard by others (rare)

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Subjective Only heard by patient (common)

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Tinnitus is most commonly associated with SNHL

OT8 Otolaryngology

Toronto Notes 2018

c

Differential Diagnoses of Common Presentations

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Nasal Obstruction

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Table 2. Differential Diagnosis of Nasal Obstruction Congenital

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Acquired

Nasal Cavity Nasal dermoid cyst Encephalocele Glioma Choanal atresia

Nasal Septum Septal deviation Septal hematoma/abscess Dislocated septum

Nasal Septum Septal deviation Septal hematoma/abscess Dislocated septum

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Nasal Cavity Rhinitis Acute/chronic Vasomotor Allergic Rhinosinusitis Foreign bodies Enlarged turbinates Tumour Benign: polyps, inverting papilloma Malignant SCC Esthesioneuroblastoma (olfactory neuroblastoma) Adenocarcinoma

Nasopharynx Adenoid hypertrophy Tumour Benign: juvenile nasopharyngeal angiofibroma (JNA), polyps Malignant: nasopharyngeal carcinoma Systemic

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Granulomatous diseases, diabetes vasculitis

e.

Hoarseness

fr

Table 3. Differential Diagnosis of Hoarseness Acute/chronic laryngitis Laryngotracheobronchitis (croup)

Inflammatory

GERD Vocal cord polyps/nodules Lifestyle: smoking, chronic EtOH use

Trauma

External laryngeal trauma Endoscopy and endotracheal tube (e.g. intubation granuloma)

Neoplasia

Benign tumour Papillomas (HPV infection) Minor salivary gland tumours Other

Cysts

Retention cysts

Systemic

Endocrine Hypothyroidism Virilization

Connective tissue disease RA SLE

Neurologic vocal cord paralysis due to superior ± recurrent laryngeal nerve injury)

Central lesions Cerebrovascular accident (CVA) Head injury Multiple sclerosis (MS) Skull base tumours Arnold-Chiari malformation Peripheral lesions Unilateral Lung malignancy

Iatrogenic injury: thyroid, parathyroid surgery, carotid endarterectomy, patent ductus arteriosus (PDA) ligation Bilateral Iatrogenic injury: bilateral thyroid surgery, forceps delivery Neuromuscular Myasthenia gravis

Functional

Psychogenic aphonia (hysterical aphonia)

Congenital

Laryngomalacia Laryngeal web Laryngeal atresia

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Lung malignancy is the most common cause of extralaryngeal vocal cord paralysis

Malignant tumours (e.g. thyroid) SCC Other

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Infectious

OT9 Otolaryngology

Toronto Notes 2018

Hearing

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Neck Mass Neck Mass

Congenital

Neoplastic

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Inflammatory/Infections

Midline Reactive lymphadenopathy TB or atypical mycobacteria Infectious mononucleosis Abscesses Cat scratch fever Sarcoidosis Kawasaki disease HIV

Lateral

Thyroglossal duct cyst Thyroid tumour/goitre Pyramidal lobe of thyroid gland Ranula

Malignant

Branchial cleft cyst Cystic hygroma

Salivary gland neoplasm Lipoma Fibroma Vascular

Lymphoma Thyro d Sarcoma Salivary gland neoplasm Rhabdomyosarcoma Neuroblastoma

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Benign

Head and neck primary Infraclavicular primary Leukemia

Figure 15. Differential diagnosis of a neck mass

Hearing

e.

Order of the Neural Pathway (with corresponding waves on ABR) E COLI Eighth cranial nerve (I – II) Cochlear nucleus (III) Superior Olivary nucleus Lateral leminiscus (IV – V) Inferior colliculus

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• conductive pathway (EAC to cochlea): air conduction of sound down the EAC → vibration of TM → sequential vibration of middle ear ossicles (malleus, incus stapes) → transmission of amplified vibrations from stapes footplate to the oval window of the cochlea → transmitted vibrations via cochlear fluid create movement along the basilar membrane within the cochlea • neural pathway (nerve to brain): basilar membrane vibration stimulates overlying hair cells in the organ of Corti → stimulation of bipolar neurons in the spiral ganglion of the cochlear division of CN VIII → cochlear nucleus → superior olivary nucleus → lateral lemniscus → inferior colliculus → Sylvian fissure of temporal lobe

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Normal Hearing Physiology

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Types of Hearing Loss

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1. Conductive Hearing Loss • conduction of sound to the cochlea is impaired • can be caused by external and middle ear disease

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e

e

2. Sensorineural Hearing Loss • defect in the conversion of sound into neural signals or in the transmission of those signals to the cortex • can be caused by disease of the inner ear (cochlea), acoustic nerve (CN VIII), brainstem, or cortex

o

ok

s

3. Mixed Hearing Loss • combination of conductive and sensorineural hearing loss

o

e. c

Weber Test lateralization = ipsilateral conductive hearing loss or contralateral sensorineural hearing loss The Webe test is more sensitive in detecting conductive hearing loss than the Rinne test

fre

o

e. c

fr

fre

e. c

om

m

eb

bo

Auditory Acuity • whispered-voice test: mask one ear and whisper into the other tuning fork tests (see Table 4; audiogram is of greater utility) ■■ Rinne test ◆◆ 512 Hz tuning fork is struck and held firmly on mastoid process to test bone conduction (BC); the tuning fork is then placed beside the pinna to test air conduction (AC) ◆◆ If AC >BC → positive Rinne (normal) ■■ Weber test ◆◆ 512 Hz tuning fork is held on vertex of head and patient states whether it is heard centrally (Weber negative) or is lateralized to one side (Weber right, Weber left) ◆◆ can place vibrating fork on patient’s chin while they clench their teeth, or directly on teeth to elicit more reliable response ◆◆ will only lateralize if difference in hearing loss between ears is >6 dB

OT10 Otolaryngology

Toronto Notes 2018

c

Hearing

r

e

Table 4. The Interpretation of Tuning Fork Tests Examples

Weber

Rinne AC>BC (+) bilaterally BC>AC (–) right

Frequency of Tuning Fork (Hz)

Minimum Hearing Loss for Rinne to Reverse (BC>AC, NEGATIVE Rinne) (dB)

Right-sided sensorineural hearing loss, normal left ear

Lateralizes to left

AC>BC (+) bilaterally

256

15

Lateralizes to left

BC>AC (–) right*

512

30

1024

45

e

bo

m

Right-sided severe sensorineural hearing loss or dead right ear, normal left ear

eb

Central Lateralizes to right

ok

Normal or bilateral sensorineural hearing loss Right-sided conductive hearing loss, normal left ear

*A vibrating tuning fork on the mastoid stimulates the cochlea bilaterally, therefore in this case the left cochlea is stimulated by the Rinne test on the right (e.g. a false negative test). These tests are not valid if the ear canals are obstructed with cerumen (e.g. will create conductive loss)

.

Range of Frequencies Audible to Human Ear • 20 to 20000 Hz • Most sensitive frequencies: 1000 to 4000 Hz • Range of human speech: 500 to 2000 Hz

s

ok sf re

re e

e

c

• a threshold is the lowest intensity level at which a patient can hear the tone 50% of the time • thresholds are obtained for each ear at frequencies of 250, 500, 1000, 2000, 4000, and 8000 Hz • air conduction thresholds are obtained with headphones and measure outer, middle, inner ear, and auditory nerve function • bone conduction thresholds are obtained with bone conduction oscillators which bypass the outer and middle ear

ee

co m

Pure Tone Audiometry

A. Normal Audiogram 500

1000 2000 4000 8000 -10 0 10 20 30 40 50 60 70 80 90 100 110 120

ee

C. Conductive Hearing Loss (Otosclerosis)

250

500

1000 2000 4000 8000 -10 0 10 20 30 40 50 60 70 80 90 100 110 120

D. Sensorineural Hearing Loss (Noise Induced)

s

Figure 16 Types of hearing loss and associated audiograms of a left ear

o

PURE TONE PATTERNS 1 Conductive Hearing Loss (Figure 16B and 16C) • BC in normal range • AC outside of normal range • gap between AC and BC thresholds >10 dB (an air-bone gap)

eb

b

om

2. Sensorineural Hearing Loss (Figure 16D and 16E) • both air and bone conduction thresholds below normal • gap between AC and BC 10 dB (an air-bone gap)

fre

1000 2000 4000 8000 -10 0 10 20 30 40 50 60 70 80 90 100 110 120

B. Conductive Hearing Loss (Otitis Media)

o

250

500

250

500

1000 2000 4000 8000 -10 0 10 20 30 40 50 60 70 80 90 100 110 120

E. Sensorineural Hearing Loss (Presbycusis)

Hearing loss most often occurs at higher frequencies. Noise-induced (occupational) HL is classically seen at 4000 Hz. HL associated with otosclerosis is seen at 2000 Hz (Carhart’s notch)

m

250

m

FREQUENCY (Hz) 500 1000 2000 4000 8000 -10 0 10 20 30 40 50 60 70 80 90 100 110 120

o

250

HEARING LEVEL (dB)

Audiogram Legend for a Left Ear x = AC Unmasked > = BC Unmasked  = AC Masked ] = BC Masked

m

eb

bo

Degree of Hearing Loss • determined on basis of the pure tone average (PTA) at 500, 1000, and 2000 Hz

OT11 Otolaryngology

Toronto Notes 2018

Hearing

fre

Speech Audiometry

b

m

eb

bo

o

ok

Speech Reception Threshold • lowest hearing level at which patient is able to repeat 50% of two syllable words which have equal emphasis on each syllable (spondee words) • SRT and best pure tone threshold in the 500 to 2000 Hz range (frequency range of human speech) usually agree within 5 dB; if not, suspect a retrocochlear lesion or functional hearing loss • used to assess the reliability of the pure tone audiometry

o

oo

Impedance Audiometry

ks fr

ks fre

e

e

co m

om

Speech Discrimination Test • percentage of words the patient correctly repeats from a list of 50 monosyllabic words • tested at 40 dB above the patient’s SRT, therefore degree of hearing loss is taken into account • patients with normal hearing or conductive hearing loss score >90% • rollover effect: a decrease in discrimination as sound intensity increases; typical of a retrocochlear lesion (e.g. acoustic neuroma) • investigate further if scores differ more than 20% between ears, as asymmetry may indicate a retrocochlear lesion • best predictor of hearing aid response: a poor discrimination score indicates significant neural degeneration and hearing aids may not be the best option for the patient

om

m

e

Tympanogram • the Eustachian tube equalizes the pressure between the external and middle ear • tympanograms graph the compliance of the middle ear system against a pressure gradient ranging from to –400 to +200 mmH2O • tympanogram peak occurs at the point of maximum compliance: where the pressure in the external canal is equivalent to the pressure in the middle ear • normal range: –100 to +50 mmH2O High

Type B

Type C

Compliance

e

Type A

O Air Pressure

+

–

O Air Pressure

+

–

O Air Pressure

b

–

• Normal pressure peak at 0 • Note: with otosclerosis, peak is still at 0 mmH2O but has a lower amplitude • Note: with ossicular chain discontinuity, peak is still at 0 mmH2O but has a higher amplitude

• No pressure peak • Poor TM mobility indicative of middle ear effusion (OME) or perforated TM

+

• Negative pressure peak • Indicative of Eustachian tube dysfunction or early stage otitis media without effusion

m

Low

Figure 17. Tympanograms

ok

ks

sf

fe

re

e

e

Static Compliance • volume measurement reflecting overall stiffness of the middle ear system • normal range: 0 3-1.6 cc • negative middle ear pressure and abnormal compliance indicate middle ear pathology • in a type B curve, ear canal volumes of >2 cc in children and >2.5 cc in adults indicate TM perforation or presence of a patent ventilation tube

m

om

e

e

co

m

m

e

b

Acoustic Stapedial Reflexes • stapedius muscle contracts in response to loud sound • acoustic reflex threshold = 70-100 dB greater than hearing threshold; if hearing threshold >85 dB, reflex likely absent ■■ stimulating either ear causes bilateral and symmetrical reflexes ■■ for reflex to be present, CN VII must be intact with no conductive hearing loss in monitored ear ■■ if reflex is absent without conductive or severe sensorineural loss, suspect CN VII lesion • acoustic reflex decay test = ability of stapedius muscle to sustain contraction for 10 s at 10 dB ■■ normally, little reflex decay occurs at 500 and 1000 Hz • with cochlear hearing loss, acoustic reflex thresholds are 25-60 dB • with retrocochlear hearing loss (acoustic neuroma), absent acoustic reflexes or marked reflex decay (>50%) within 5 s

OT12 Otolaryngology

Toronto Notes 2018

c

Vertigo

fre

fre

Auditory Brainstem Response

b

bo

bo

ok

ok

• measures neuroelectric potentials (waves) in response to a stimulus in five different anatomic sites (see Order of Neural Pathway sidebar on OT9; this test can be used to determine the site of lesion) • delay in brainstem response suggests cochlear or retrocochlear abnormalities does not require volition or co-operation of patient (therefore, of value in children and malingerers)

m

Otoacoustic Emissions Pre-lingually deaf infants are the best candidates for aural rehabilitation because they have maximal benefit from ongoing developmental plasticity

co m

c

co m

• objective test of hearing where a series of clicks is presented to the ear and the cochlea generates an echo which can be measured • often used in newborn screening • can be used to uncover normal hearing in malingering patients • absence of emissions can be due to hearing loss or fluid in the middle ear

fre

Aural Rehabilitation

o

m

eb

eb

om

Evaluation of the Dizzy Patient

e.

re

sf

re

e.

• vertigo: illusion of rotational, linear, or tilting movement of self or environment • vertigo is produced by peripheral (inner ear) or central (brainstem cerebellum) stimulation • it is important to distinguish vertigo from other potential causes of “dizziness” (see Figure 11, OT6)

ok

Table 5. Peripheral vs. Central Vertigo

Nausea and Vomiting

Severe

Variable

Auditory Symptoms

Common

Rare

Neurologic Symptoms

Rare

Common

Compensation

Rapid

Slow

Nystagmus

Unidirectional Horizontal or rotatory

Bidirectional Horizontal or vertical

co

Mild-moderate

b

Central

Moderate-severe

bo

Peripheral

Imbalance

m

m

Pre-lingual deafness: deafness occurring before speech and language are acquired Post-lingual deafness: deafness occurring after speech and language are acquired

re

e

fre

ks

oo

Vertigo

Symptoms

Bone Anchored Hearing Aids (BAHA) BAHAs function based on bone conduction and are indicated primarily for patients with conductive hearing loss, unilateral hearing loss, and mixed hearing loss who cannot wear conventional hearing aids. BAHAs consist of a titanium implant, an external abutment, and a sound processor. The sound processor transmits vibrations through the external abutment to the titanium implant and then directly to the cochlea

c

co

m

oo

k

k

• dependent on degree of hearing loss, communicative requirements, motivation, expectations, and physical and mental abilities • negative prognostic factors ■■ poor speech discrimination ■■ narrow dynamic range (recruitment) ■■ unrealistic expectations • types of hearing aids ■■ BTE: behind-the-ear (with occlusive mould or open fit which allows natural sound to pass – for milder hearing losses) ■■ ITE: in-the-ear, placed in concha ■■ ITC: in-the-canal, placed entirely in ear canal ■■ CIC: contained-in-canal, placed deeply in ear canal ■■ bone conduction – bone-anchored hearing aid (BAHA): attached to the skull ■■ contralateral routing of signals (CROS) • assistive listening devices ■■ direct/indirect audio output ■■ infrared, FM radio, or induction loop systems ■■ telephone, television, or alerting devices • cochlear implants ■■ electrode is inserted into the cochlea to allow direct stimulation of the auditory nerve ■■ for profound bilateral sensorineural hearing loss not rehabilitated with conventional hearing aids ■■ established indication: post-lingually deafened adults, pre-and post-lingually deaf children

OT13 Otolaryngology

Toronto Notes 2018

Vertigo

e

Table 6. Differential Diagnosis of Vertigo Based on History Benign Paro ysmal Positional Vertigo (BPPV)

Seconds

–

Minutes to hours Precedes attack

Labyrinthitis/Vestibular Neuronitis

Hours to days

Acoustic Neuroma

Chronic

Aural Fullness

–

Uni/bilateral, fluctuating

Pressure/warmth

±Whistling

m

Unilateral

Progressive

Other Features

–

+

eb

bo

Ménière’s Disease

Tinnitus

–

+

–

May have recent AOM

m

Hearing Loss

s

Duration

ok

Condition

Ataxia CN VII palsy

o

Table 7. Differential Diagnosis of Vertigo Based on Time Course Time Course

Condition BPPV

Single episode, lasting minutes to hours

Migraine, transient ischemia of the labyrinth or brainstem

Recurrent to hours

Ménière s

ok

fr

ks fr

Recurrent, lasting

Prolonged

Vestibular neuritis, MS, brainstem/cerebellum infarct Chronic

o

Acoustic neuroma

om

om

Definition • acute attacks of transient rotatory vertigo lasting seconds to minutes, initiated by certain head positions, accompanied by torsional (i.e rotatory) nystagmus (geotropic = fast phase towards the floor) • most common form of positional vertigo (50% of patients with peripheral vestibular dysfunction)

BPPV is the most common cause of episodic vertigo; patients are often symptomatic when rolling over in bed or moving their head to a position of extreme posterior extension (such as looking up at a tall building or getting their hair washed at the hairdresser)

om

m

e

Benign Paroxysmal Positional Vertigo

o

oo

ok

ks

sf

re

fre

e

e

Etiology • due to canalithiasis (migration of free floating otoliths within the endolymph of the semicircular canal) or cupulolithiasis (otolith attached to the cupula of the semicircular canal) ■■ can affect each of the 3 semicircular canals, although the posterior canal is affected in >90% of cases ■■ causes: head injury, viral infection (URTI), degenerative d sease, idiopathic ■■ results in slightly different signals being received by the brain from the two balance organs, resulting in sensation of movement

m

e

eb

Diagnosis history (time course, provoking factors, associative symptoms) • positive Dix-Hallpike maneuver (sensitivity 82%, specificity 71%)

co

m

e

bo

ok

ks

sf

r

Treatment • reassure patient that process resolves spontaneously • particle repositioning maneuvers ■■ Epley maneuver (performed by MD or by patient with the help of devices such as the DizzyFIX™) ■■ Brandt-Daroff exercises (performed by patient) • surgery for refractory cases • an i-emetics for N/V • drugs to suppress the vestibular system delay eventual recovery and are therefore not used

Signs of BPPV seen with Dix-Hallpike Maneuver • Latency of ~20 s • Crescendo/decrescendo vertigo lasting 20 s • Geotropic rotatory nystagmus (nystagmus MUST be present for a positive test) • Reversal of nystagmus upon sitting up • Fatigability with repeated stimulation

ee .

co

om

m

Dix-Hallpike Positional Testing (see website for video and illustrations) • the patient is rapidly moved from a sitting position to a supine position with the head hanging over the end of the table, turned to one side at 45°, and neck extended 20° holding the position for 20 s • onset of vertigo and rotary nystagmus indicate a positive test for the dependent side • other diagnostic testing is not indicated in posterior canal BPPV

Ménière’s Disease (Endolymphatic Hydrops)

ok

s

Epidemiology • peak incidence 40-60 yr • bilateral in 35% of cases

c

Diagnostic Criteria for Ménière’s Disease (must have all three) • Two spontaneous episodes of rotational ver igo ≥20 minutes • Audiometric confirmation of SNHL (often low frequency) • Tinnitus and/or aural fullness

e

e.

ee

.

Proposed Etiology • inadequate absorption of endolymph leads to endolymphatic hydrops (over accumulation) that distorts the membranous labyrinth

fre

m

m

Definition • episodic attacks of tinnitus, hearing loss, aural fullness, and vertigo lasting minutes to hours

OT14 Otolaryngology

Toronto Notes 2018

c

Vertigo

eb

o

bo

k

fr

ok sf re

Clinical Features • episodic vertigo, fluctuating low frequency SNHL, tinnitus, and aural fullness • ± drop attacks (Tumarkin crisis), ± N/V • vertigo disappears with time (min to h), but hearing loss remains • early in the disease: fluctuating SNHL • later stages: persistent tinnitus and progressive hearing loss • attacks come in clusters and can be debilitating to the patient triggers: high salt intake, caffeine, stress, nicotine, and alcohol

oo

oo

k

fre

ks fre

e

e.

c

c

m

Treatment • acute management may consist of bed rest, antiemetics, antivertiginous drugs (e.g. betahistine [Serc®], meclizine, dimenhydramine), and anticholinergics (e.g. scopolamine) • long-term management may include ■■ medical ◆◆ low salt diet, diuretics (e.g. hydrochlorothiazide, triamterene, amiloride) ◆◆ Serc® prophylactically to decrease intensity of attacks ◆◆ intratympanic gentamicin to destroy vestibular end-organ, results in complete SNHL ◆◆ intratympanic glucocorticoids (e.g. dexamethasone) may improve vertigo symptoms ■■ surgical ◆◆ selective vestibular neurectomy or labyrinthectomy ◆◆ potential benefit for endolymphatic sac decompression or sacculotomy • must monitor opposite ear, as bilaterality occurs in 35% of cases

e

Vestibular Neuronitis (Labyrinthitis)

om

Definition • acute onset of disabling vertigo often accompanied by N/V and imbalance without hearing loss that resolves over days, leaving a residual imbalance that lasts days to weeks • vestibular neuronitis: inflammation of the vestibular portion of CNVIII • labyrinthitis: inflammation of both vestibular and cochlear portions

sf

fe

re

e

e

Etiology • thought to be due to a viral infection (e.g. measles, mumps, herpes zoster) or post-viral syndrome • only ~30% of cases have associated URTI symptoms • labyrinthitis may occur as a complication of acute and chronic otitis media, bacterial meningitis, cholesteatoma, and temporal bone fractures

oo

Clinical Features • acute phase ■■ severe vertigo with N/V and imbalance lasting 1-5 d ■■ irritative nystagmus (fast phase towards the offending ear) ■■ ataxia: patient tends to veer towards affected side ■■ tinnitus and hearing loss in labyrinthitis • convalescent phase ■■ imbalance and motion sickness lasting days to weeks ■■ spontaneous nystagmus away from affected side ■■ gradual vestibular adaptation requires weeks to months

m

om

m

eb

Drop Attacks (Tumarkin’s Otolithic Crisis) are sudden falls occurring without warning and without LOC, where patient experiences feeling of being pushed down into the ground

re

Before proceeding with gentamicin treatment, perform a gadolinium enhanced MRI to rule out CPA tumour as the cause of symptoms

o

oo

s

ks

fre

Treatment • acute phase ■■ bed rest, antivertiginous drugs ■■ corticosteroids (methylprednisolone) ± antivirals ■■ bacterial infection: treat with IV antibiotics, drainage of middle ear, ± mastoidectomy • convalescent phase ■■ progressive ambulation, especially in the elderly ■■ vestibular exercises: involve eye and head movements, sitting, standing, and walking

e

Definition • schwannoma of the vestibular portion of CN VIII

ks

ok

sf

r

Clinical Features • usually presents with unilateral SNHL (chronic) or tinnitus • dizzine s and unsteadiness may be present, but true ver igo is rare as tumour growth occurs slowly, and thus compensation occurs

e

In the elderly, unilateral tinnitus or SNHL is acoustic neuroma until proven otherwise

re

e.

co

co

Pathogenesis • starts in the internal auditory canal and expands into cerebellopontine angle (CPA), compressing cerebellum and brainstem • when associated with type 2 neurofibromatosis (NF2): bilateral acoustic neuromas, juvenile cataracts, meningiomas, and ependymomas

Acoustic neuroma is the most common intracranial tumour causing SNHL and the most common cerebell pontine angle tumour

m

e

Acoustic Neuroma (Vestibular Schwannoma)

OT15 Otolaryngology

Toronto Notes 2018

Tinnitus

fre

fre

• facial nerve palsy and trigeminal (V1) sensory deficit (corneal reflex) are late complications • risk factors: exposure to loud noise, childhood exposure to low-dose radiation, history of parathyroid adenoma

m

e

bo

o

Diagnosis • MRI with gadolinium contrast (gold standard) • audiogram (to assess SNHL) • poor speech discrimination relative to the hearing loss • stapedial reflex absent or significant reflex decay • ABR: increase in latency of the 5th wave • vestibular tests: normal or asymmetric caloric weakness (an early sign)

e.

co

Treatment • expectant management if tumour is very small, or in elderly • definitive management is surgical excision • other options: gamma knife, radiation

sf r

Tinnitus

b

o

bo

o

Definition • an auditory perception in the absence of an acoustic stimuli, likely related to loss of input to neurons in central auditory pathways and resulting in abnormal firing

m

History • subjective vs. objective (see Figure 14, OT7) • continuous vs. pulsatile (vascular in origin) • unilateral vs. bilateral • associated symptoms: hearing loss, vertigo, aural fullness, otalgia, otorrhea

ok

ok

sf

re

re

Investigations • audiology • if unilateral ■■ ABR, gadolinium-enhanced MRI to exclude a retrocochlear lesion ■■ CT to diagnose glomus tympanicum (rare) ■■ MRI or angiogram to diagnose AVM • if suspect metabolic abnormality: lipid profile, TSH, zinc levels

Cerumen impaction is the most common cause of conductive hearing loss for those aged 15-50 yr

co

m

m

e

eb

bo

Treatment • if a cause is found, treat the cause (e.g. drainage of middle ear effusion, embolization or excision of AVM) • with no treatable cause: 50% will improve, 25% worsen, 25% remain the same • avoid loud noise, ototoxic meds, caffeine, smoking • tinnitus clinics • identify situations where tinnitus is most bothersome (e.g. quiet times), mask tinnitus with soft music or “white noise” • hearing aid if coexistent hearing loss • tinnitus instrument: combines hearing aid with white noise masker • trial of tocainamide

fre

Syringing

Diseases of the External Ear

oo

Cerumen Impaction

m

m

e

Etiology • ear wax: a mixture of secretions from ceruminous and pilosebaceous glands, squames of epithelium, dust, and debris

m

Risk Factors • hairy or narrow ear canals, in-the-ear hearing aids, cotton swab usage, osteomata

e.

Clinical Features • hearing loss (conductive) • ± tinnitus, vertigo, otalgia, aural fullness

s

ks

Treatment • water or ceruminolytic drops (bicarbonate solution, olive oil, glycerine, Cerumenol®, Cerumenex®) • manual debridement (by MD)

Contraindications • Active infection • Previous ear surgery • Only hearing ear • TM perforation Complications • Otitis externa • TM perforation • Trauma • Pain • Vertigo • Tinnitus • Otitis media Method • Establish that TM is intact Gently pull the pinna superiorly and posteriorly • Using lukewarm water, aim the syringe nozzle upwards and posteriorly to irrigate the ear canal

fre

sf

sf

r

Indications • Totally occlusive cerumen with pain, decreased hearing, or tinnitus

OT16 Otolaryngology

Toronto Notes 2018

c

Diseases of the External Ear

fre

Exostoses

o

ok

Definition • bony protuberances in the external auditory canal composed of lamellar bone

e

b

Etiology • possible association with swimming in cold water Clinical Features • usually an incidental finding • if large, they can cause cerumen impaction or otitis externa

o

Treatment • no treatment required unless symptomatic

e.

Otitis Externa

s

Definition • inflammation of external auditory canal or auricle

bo

bo

o

Etiology • bacterial (90% of OE): Pseudomonas aeruginosa, Pseudomonas vulgaris, E. coli, S. aureus • fungal: Candida albicans, Aspergillus niger

m

m

Risk Factors • associated with swimming (“swimmer’s ear”) • mechanical cleaning (Q-tips®), skin dermatitis, aggressive scratching • devices that occlude the ear canal: hearing aids, headphones, etc. • allergic contact dermatitis, dermatologic conditions (psoriasis, atopic dermatitis)

oo

m

eb

oo

oo

ks

fre

e

e

Clinical Features • acute ■■ pain aggravated by movement of auricle (traction of pinna or pressure over tragus) ■■ otorrhea (sticky, yellow purulent discharge) ■■ conductive hearing loss ± aural fullness 2° to obstruction of external canal by swelling and purulent debris ■■ posterior auricular lymphadenopathy ■■ complicated OE exists if the pinna and/or the periauricular soft tissues are erythematous and swollen • chronic ■■ pruritus of external ear ± excoriation of ear canal ■■ atrophic and scaly epidermal lining, ± otorrhea, ± hearing loss ■■ wide meatus but no pain with movement of auricle ■■ tympanic membrane appears normal

Malignant (Necrotizing) Otitis Externa

m

(Skull Base Osteomyelitis)

c

Definition • osteomyelitis of the temporal bone

oo

k

Etiology • rare complication of otitis externa • Pseudomonas infection in 99% of cases

fr

fr

Epidemiology • occurs in elderly diabetics and immunocompromised patients

m

m

o

oo

ks

ks

fr

fr

e.

e.

om

om

Treatment • clean ear under magnification with irrigation, suction, dry swabbing, and C&S • bacterial etiology ■■ antipseudomonal otic drops (e.g. ciprofloxacin) or a combination of antibiotic and steroid (e.g. Cipro HC®) ■■ do not use aminoglycoside if the tympanic membrane (TM) is perforated, because of the risk of ototoxicity ■■ introduction of fine gauze wick (pope wick) if external canal edematous ■■ ± 3% acetic acid solution to acidify ear canal (low pH is bacteriostatic) ■■ systemic antibiotics if either cervical lymphadenopathy or cellulitis is present • fungal etiology ■■ repeated debridement and topical antifungals (gentian violet, Mycostatin® powder, boric acid, Locacorten®, Vioform® drops) • ± analgesics • chronic otitis externa (pruritus without obvious infection) → corticosteroid alone (e.g. diprosalic acid)

Pulling on the pinna is extremely painful in otitis externa, but is usually well tolerated in otitis media

OT17 Otolaryngology

Toronto Notes 2018

c

Diseases of the Middle Ear

sf r

fr

Clinical Features • otalgia and purulent otorrhea that is refractory to medical therapy • granulation tissue on the floor of the auditory canal

Gallium and Technetium Scans Gallium scans are used to show sites of active infection. Gallium is taken up by PMNs, and therefore only lights up when active infection is present. It will not show the extent of osteomyelitis. Technetium scans provide information about osteoblastic activity and as a result, are used to demonstrate sites of osteomyelitis. Technetium scans help with diagnosis, whereas gallium scans are useful in follow-up

bo

o

o

Complications • cranial nerve palsy (most commonly CN VII>CN X>CN XI) • systemic infection, death

m

Management • imaging: high resolution temporal bone CT scan, gadolinium-enhanced MRI, technetium scan • requires hospital admission, debridement, IV antibiotics, hyperbaric O2 • may require OR for debridement of necrotic tissue/bone

co

Diseases of the Middle Ear

re

re

Acute Otitis Media and Otitis Media with Effusion

k

• see Pediatric Otolaryngology, OT38

o

Chronic Otitis Media

m

e

Definition • an ear with TM perforation in the setting of recurrent or chronic ear infections

m

Benign • dry TM perforation without active infection

co

Chronic Serous Otitis Media • continuous serous drainage (straw-coloured)

fre

e

Chronic Suppurative Otitis Media • persistent purulent drainage through a perforated TM

k

Cholesteatoma

eb

eb

bo

Definition • a cyst composed of keratinized desquamated epithelial cells occurring in the middle ear, mastoid, and temporal bone • two types: congenital and acquired

o

co

m

Congenital • presents as a “small white pearl” behind an intact tympanic membrane (anterior and medial to the malleus) or as a conductive hearing loss • believed to be due to aberrant migration of external canal ectoderm during development • not associated with otitis media/Eustachian tube dysfunction

ks

r

e

co

co

m

Clinical Features • history of otitis media (especially if unilateral), ventilation tubes, ear surgery • symptoms ■■ progressive hearing loss (predominantly conductive, although may get sensorineural hearing loss in late stage) ■■ otalgia, aural fullness, fever • signs ■■ retraction pocket in TM, may contain keratin debris ■■ TM perforation ■■ granulation tissue, polyp visible on otoscopy ■■ malodourous, unilateral otorrhea

oo

Mechanisms of Cholesteatoma Formation • Epithelial migration through TM perforation (2° acquired) • Invagination of TM (1° acquired) • Metaplasia of middle ear epithelium or basal cell hyperplasia (congenital)

s

m

m

eb

o

ok

s

sf

re

Acquired (more common) • primary cholesteatoma ■■ frequently associated with retraction pockets in the pars flaccida (may lead to attic cholesteatomas, which are difficult to visualize) ■■ often has crusting or desquamated debris on lateral surface • secondary cholesteatoma ■■ pearly mass evident behind TM, frequently associated with marginal perforation ■■ may appear as skin that have replaced the mucosa of the middle ear • the associated chronic inflammatory process causes progressive destruction of surrounding bony structures

OT18 Otolaryngology

Toronto Notes 2018

c

Diseases of the Middle Ear

Complications

s

Table 8. Complications of Cholesteatoma Intracranial

oo

Local

Meningitis

bo

Ossicu ar erosion: conductive hearing loss

Sigmoid sinus thrombosis

Temporal bone infection: mastoiditis, petrositis

Intracranial abscess (subdural, epidural, cerebellar)

m

Inner ear erosion: SNHL, dizziness, and/or labyrinthitis Facial paralysis

Investigations • audiogram and CT scan

e

ee

Treatment • there is no conservative therapy for cholesteatoma • surgical: mastoidectomy ± tympanoplasty ± ossicular reconstruction

ks

Mastoiditis

b

eb

bo

Definition infection (usually subperiosteal) of mastoid air cells, most commonly seen approximately two weeks after onset of untreated or inadequately treated acute suppurative otitis media • more common in children than adults

m

Etiology • acute mastoiditis caused by the same organisms as AOM: S. pneumoniae, H. influenzae, M. catarrhalis, S. pyogenes, S. aureus, P. aeruginosa

ok

s

sf

m

m

eb

bo

Treatment • IV antibiotics with myringotomy and ventilation tubes – usually all that is required acutely • cortical mastoidectomy ■■ debridement of infected tissue allowing aeration and drainage • indications for surgery ■■ failure of medical treatment after 48 h ■■ symptoms of intracranial complications ■■ aural discharge persisting for 4 wk and resistant to antibiotics

Classic Triad Otorrhea Tenderness to pressure over the mastoid • Retroauricular swelling with protruding ear

re

re

e

Clinical Features • otorrhea • tenderness to pressure over the mastoid • retroauricular swelling with protruding ear • fever, hearing loss, ± TM perforation (late) • CT radiologic findings: opacification of mastoid air cells by fluid and interruption of normal trabeculations of cells (coalescence)

Complications of AOM are rare due to rapid and effective treatment of AOM with antibiotics

c

Otosclerosis

f

fr

Definition • fusion of stapes footplate to oval window so that it cannot vibrate

bo

o

oo

Etiology • autosomal dominant, variable penetrance approximately 40% • F>M, progresses during pregnancy (hormone responsive)

m

m

om

m

Clinical Features • progressive conductive hearing loss first noticed in teens and 20s (may progress to sensorineural hearing loss if cochlea involved) • ± pulsatile tinnitus • tympanic membrane normal ± pink blush (Schwartz’s sign) associated with the neovascularization of otosclerotic bone • characteristic dip at 2000 Hz (Carhart’s notch) on audiogram (see Figure 16C, OT10)

sf

sf re

Treatment • monitor with serial audiograms if coping with loss • hearing aid (air conduction, bone conduction, BAHA) • stapedectomy or stapedotomy (with laser or drill) with prosthesis is definitive treatment

Otosclerosis is the 2nd most common cause of conductive hearing loss in 15-50 yr old (after cerumen impaction)

OT19 Otolaryngology

Toronto Notes 2018

c

Diseases of the Inner Ear

fr

fr

Diseases of the Inner Ear

o

o

Congenital Sensorineural Hearing Loss

ok sf e

e.

om

om

b

Hereditary Defects non-syndrome associated (70%) ■■ often idiopathic, autosomal recessive ■■ connexin 26 (GJB2) most common • syndrome associated (30%) ■■ Waardenburg: white forelock, heterochromia iridis (each eye different colour), wide nasal bridge, and increased distance between medial canthi ■■ Pendred: deafness associated with thyroid gland disorders, SLC26A4 gene enlarged vestibular aqueducts ■■ Treacher-Collins: first and second branchial cleft anomalies ■■ Alport: hereditary nephritis

ks

Prenatal TORCH Infections • toxoplasmosis, others (e.g. HIV, syphilis), rubella, CMV, HSV

bo

Perinatal • Rh incompatibility • anoxia • hyperbilirubinemia • birth trauma (hemorrhage into inner ear) Postnatal • meningitis, mumps, measles

m

m

b

bo

ok

sf

re

e.

co

High Risk Factors (for hearing loss in newborns) • low birth weight/prematurity • perinatal anoxia (low APGARs) • kernicterus: bilirubin >25 mg/dL • craniofacial abnormality • family history of deafness in childhood • 1st trimester illness: TORCH infections • neonatal sepsis • ototoxic drugs • perinatal infection, including post-natal meningitis • consanguinity • 50-75% of newborns with SNHL have at least one of the above risk factors and 90% of these have spent time in the NICU

m

m

Treatment • presence of any risk factor: ABR study performed before leaving NICU and at 3 mo adjusted age • early rehabilitation improves speech and school performance

e.

Presbycusis

s

Presbycusis is the most common cause of SNHL

s

s

Definition • SNHL associated with aging (starting in 5th and 6th decades)

eb

bo

o

Etiology • hair cell degeneration • age related degeneration of basilar membrane, possibly genetic etiology cochlear neuron damage • ischemia of inner ear

m

m

Clinical Features • progressive, bilateral hearing loss initially at high frequencies, then middle frequencies • loss of discrimination of speech, especially with background noise present – patients describe people as mumbling • recruitment phenomenon: inability to tolerate loud sounds • tinnitus

f

ks

ks

f

Treatment • hearing aid if patient has difficulty functioning, hearing loss >30-35 dB, and good speech discrimination • ± lip reading, auditory training, auditory aids (doorbell and phone lights)

OT20 Otolaryngology

Toronto Notes 2018

c

Diseases of the Inner Ear

fre

fre

Sudden Sensorineural Hearing Loss Sudden SNHL may easily be confused with ischemic brain events. It is important to keep a high index of suspicion especially with elderly patients presenting with sudden SNHL as well as vertigo

Treatment • intratympanic or oral corticosteroids within 3 d of onset: prednisone 1 mg/kg/d for 10-14 d

Treatment of Sudden SNHL Arch Otolaryngol Head Neck Surg 2007;133(6):582-6 Summary 1. Although standard of practice in North America for treating sudden SNHL is systemic steroids, metaanalysis shows no significant benefit of steroids over placebo. 2. There s no difference in addition of antiviral therapy to ystemic steroids vs. systemic steroids alone. 3 There was no difference between systemic steroids vs. any other active treatment.

.c om

m

m

e

eb

o

oo

k

Clinical Features • presents as a sudden onset of significant SNHL (usually unilateral) ± tinnitus, aural fullness • usually idiopathic, rule out other causes ■■ autoimmune causes (e.g. ESR, rheumatoid factor, ANA) ■■ MRI to rule out tumour and/or CT to rule out ischemic/hemorrhagic stroke if associated with any other focal neurological signs (e.g. vertigo, ataxia, abnormality of CN V or VII, weakness)

re e

ee

c

Prognosis • depends on degree of hearing loss • 70% resolve within 10-14 d • 20% experience partial resolution • 10% experience permanent hearing loss

ks

ks

Autoimmune Inner Ear Disease

m

e

e

bo

Etiology • idiopathic • may be associated with systemic autoimmune diseases (e.g. rheumatoid arthritis, SLE), vasculitides (e.g. GPA, polyarteritis nodosa), and allergies Epidemiology • most common between ages 20-50

.

.c

Clinical Features • rapidly progressive or fluctuating bilateral SNHL • ± tinnitus, aural fullness, vestibular symptoms (e.g. ataxia, disequilibrium, vertigo)

fr

Investigations • autoimmune workup: CBC, ESR, ANA, rheumatoid factor

Drug Ototoxicity

bo

oo

Treatment • high dose corticosteroids: treat early for at least 30 d • consider cytotoxic medication for steroid non-responders

bo

oo

ks

ks

fe

fe

e

o

e. co

m

Aminoglycosides • streptomycin and gentamicin (vestibulotoxic), kanamycin, and tobramycin (cochleotoxic) • toxic to hair cells by any route: oral, IV, and topical (if the TM is perforated) • destroys sensory hair cells: outer first, inner second (therefore, otoacoustic emissions are lost first) • high frequency hearing loss develops earliest • ototoxicity occurs days to weeks post-treatment • must monitor with peak and trough levels when prescribed, especially if patient has neutropenia and/or history of ear or renal problems • q24h dosing recommended (with amount determined by creatinine clearance) • aminoglycoside toxicity displays saturable kinetics, therefore, once daily dosing presents less risk than divided daily doses • duration of treatment is the most important predictor of ototoxicity ■■ treatment: immediately stop aminoglycosides

m

Salicylates • hearing loss with tinnitus, reversible if discontinued Antimalarials (Quinines) • hearing loss with tinnitus • reversible if discontinued but can lead to permanent loss

e

Others • many antineoplastic agents are ototoxic (weigh risks vs. benefits) • loop diuretics

OT21 Otolaryngology

Toronto Notes 2018

c

Diseases of the Inner Ear

fe

fre

Noise-Induced Sensorineural Hearing Loss

m

m

bo

bo

o

ok

Pathogenesis • 85-90 dB over months or years or single sound impulses >135 dB can cause cochlear damage • bilateral SNHL initially and most prominently at 4000 Hz (resonant frequency of the temporal bone), known as “boilermaker’s notch” on audiogram, extends to higher and lower frequencies with time (see Figure 16D, OT10) • speech reception not altered until hearing loss >30 dB at speech frequency, therefore considerable damage may occur before patient complains of hearing loss • difficulty with speech discrimination, especially in situations with competing noise

sf re

e

c

co m

Phases of Hearing Loss • dependent on: intensity of sound and duration of exposure ■■ temporary threshold shift ◆◆ when exposed to loud sound, decreased sensitivity or increased threshold for sound ◆◆ may have associated aural fullness and tinnitus ◆◆ with removal of noise, hearing returns to normal ■■ permanent threshold shift ◆◆ hearing does not return to previous state

bo

o

Treatment • hearing aid • prevention ■■ ear protectors: muffs, plugs ■■ limit exposure to noise with frequent rest periods ■■ regular audiologic follow-up

co

m

Temporal Bone Fractures Table 9. Features of Temporal Bone Fractures Longitudinal (2) Into middle ear

Incidence

10-20%

70-90%

Etiology

Frontal/occipital trauma

Lateral skull trauma

CN Pathology

CN VII palsy (50%)

CN VII palsy (10-20%)

Hearing Loss

SNHL due to direct cochlear injury

CHL secondary to ossicular injury

Vestibular Symptoms

Sudden onset vestibular symptoms due to direct semicircular canal injury (vertigo, spontaneous nystagmus)

Rare

Other Features

Intact external auditory meatus, TM ± hemotympanum Spontaneous nystagmus CSF leak in Eustachian tube to nasopharynx ± rhinorrhea (risk of meningitis)

Torn TM or hemotympanum Bleeding from external auditory canal Step format on in external auditory canal CSF otorrhea Battle s sign = mastoid ecchymoses Raccoon eyes = periorbital ecchymoses

1

e

2

© Teddy Cameron 2002

m

b

Figure 18. Types of temporal bone fractures

co

om

m

e

Into bony labyrinth and internal auditory meatus

om

e

.

Transverse (1)

Extension

ok

Diagnosis • otoscopy • do not syringe or manipulate external auditory meatus due to risk of inducing meningitis via TM perforation • CT head • audiology, facial nerve tests (for transverse fractures), Schirmer’s test (of lacrimation), stapedial reflexes if CN VII palsy • if suspecting CSF leak: look for halo sign, send fluid for β-2 transferrin or β trace protein (prostaglandin D synthase)

ok

sf

re

Signs of Basilar Skull Fracture Battle’s Sign Racoon Eyes CSF Rhinorrhea/Otorrhea

o

Cranial Nerve Involvement: facial palsy g CN V I, ystagmus g CN VI, facial numbness g CN V

e. c

e.

c

Treatment • ABCs • medical: expectant, prevent otogenic meningitis • surgical: explore temporal bone; indications: ■■ CN VII palsy (immediate and complete) ■■ gunshot wound ■■ depressed fracture of external auditory meatus ■■ early men ngitis (mastoidectomy) ■■ bleeding intracranially from sinus ■■ CSF otorrhea (may resolve spontaneously)

m

m

o

bo

Hemotympanum can be indicative of temporal bone trauma

s

fre

fre

• characterized as longitudinal or transverse relative to the long axis of the petrous temporal bone • temporal bone fractures are rarely purely transverse or longitudinal (often a mixed picture)

OT22 Otolaryngology

Toronto Notes 2018

c

Facial Nerve (CN VII) Paralysis

ks fre

Complications • AOM ± labyrinthitis ± mastoiditis • meningitis/epidural abscess/brain abscess • post-traumatic cholesteatoma

bo

bo

Facial Nerve (CN VII) Paralysis

m

m

Peripheral Facial Paralysis (PFP) • mononeuropathy of the facial nerve where there is weakening in the facial muscles, which alters facial symmetry and functions • can have a detectable cause (secondary facial nerve palsy) or may be idiopathic (primary)

c

Etiology • supranuclear and nuclear (MS, poliomyelitis, cerebral tumours) • infranuclear

oo

o

ks

s

Treatment • treat according to etiology, plus provide corneal protection with artificial tears, nocturnal lid taping, tarsorrhaphy, gold weighting of upper lid • facial paralysis that does not resolve with time or with medical treatment will often be referred for possible reanimation techniques to restore function ■■ common reanimation techniques include ◆◆ direct facial nerve anastomosis ◆◆ interpositional grafts ◆◆ anastomosis to other motor nerves ◆◆ muscle transpositions Table 10. Differential Diagnosis of Peripheral Facial Paralysis (PFP)

.c

ee

F/U Spontaneous remission should begin within 3 wk of onset Delayed (3-6 mo) recovery portends at least some functional loss Px ENoG testing between day 3-14 of onset: 90% + no voluntary EMG motor unit potentials= surgical decompression Poorer if hyperacusis, >60 yr, DM, HTN, severe pain

m

F/U: 2-4 wk

ok

s

Px Poorer prognosis than Bell’s palsy; 22% recover completely, 66% incomplete paralysis, 10% complete paralysis

Skull X-rays CT head

P/E Trauma to side of head Neuro findings consistent with epidural/subdural bleed Hx Blow to frontal or occipital area P/E Trauma to front or back of head Iatrogenic

Variable (depending on level of injury)

Skull X-rays CT head

Px Nerve transection more likely

Wait for lidocaine to wear off EMG

Rx Exploration if complete nerve paralysis No exploration if any movement present Source: Paul Warrick, MD

c

40% have PFP

o

Transverse (10%)

Px Injury usually due to stretch or impingement; may recover with time

m

Hx Blow to side of head

m

20% have PFP

m

Longitudinal (90%)

bo

o

TEMPORAL BONE FRACTURE *rarely a patient has a single type of fracture

s

P/E Vesicles on pinna, external canal (errupt 3-7 d after onset of pain) Associated herpes zoster ophthalmicus (uveitis, keratoconjunctivitis, optic neuritis, or glaucoma)

Rx Avoid touching lesions to prevent spread of infection Systemic steroids can relieve pain, vertigo avoid postherpetic neuralgia Acyclovir may lessen pain, aid healing of vesicles

e. co

m

Stapedial reflex absent Audiology SNHL Viral ELISA studies to confirm MRI with gadolinium (86% of facial nerves enhance)

e. co

co

e.

Varicella zoster infection of CN VII/VIII

Risk Factors: >60 yr Impaired immunity Cancer Radiotherapy Chemotherapy

Hx Hyperacusis SNHL Severe pain of pinna, mouth, or face

ks

4.5-9% of PFP

Ramsay Hunt Syndrome (Herpes Zoster Oticus)

Rx Protect the eye to prevent exposure keratitis with patching or tarsorraphy Systemic steroids may lessen degeneration and hasten recovery Consider antiviral (acyclovir)

m

m

eb

P/E Paralysis or paresis of all muscle groups on one side of the face Absence of signs of CNS disease Absence of signs of ear or CPA diseases

co

Stapedial reflex absent Audiology normal (or baseline) EMG – best measure for prognosis Topognostic testing MRI with gadolinium – enhancement of CN VII and VIII High resolution CT

e

Hx Acute onset Numbness of ear Schirmer’s test Recurrence (12%) + FHx (14%) Hyperacusis (30%)

Risk Factors: DM Pregnancy Viral prodrome (50%)

ok

ks

r

Idiopathic, (HSV) infection of the facial nerve Diagnosis of exclusion

fre

80-90% of PFP

e.

Bell’s Palsy

Treatment, Follow-up, and Prognosis (Px)

oo

Investigations

e

Findings

o

Incidence

co

Etiology

OT23 Otolaryngology

Toronto Notes 2018

c

Rhinitis

fr

Rhinitis

eb

o

oo

Definition • inflammation of the lining (mucosa) of the nasal cavity Table 11. Classification of Rhinitis Rhinitis medicamentosa Topical decongestants Hormonal Pregnancy Estrogens Thyroid Idiopathic vasomotor

Rhinitis medicamentosa: rebound congestion due to the ove use of intranasal vasoconstrictors; for prevention, use of these medications for only 5-7 d is recommended

bo

ok s

e

om

Non-Inflammatory

Perennial non-allergic Asthma, ASA sensitivity Allergic Seasonal Perennial Atrophic Primary: Klebsiella ozena (especially in elderly) Acquired: post-surgery if too much mucosa or turbinate has been resected Infectious Viral: e.g. rhinovirus, influenza, parainfluenza, etc. Bacterial: e g S. aureus Fungal Granulomatous: TB, syphilis, leprosy Non infectious Sarcoidosis GPA Irritant Dust Chemicals Pollution

c

Inflammatory

o

Table 12. Nasal Discharge: Character and Associated Conditions Associated Conditions

.c

Character Watery/mucoid

Allergic, viral, vasomotor, CSF leak (halo sign) Bacterial, foreign body

Serosanguinous

Neoplasia

Bloody

Trauma, neoplasia, bleeding disorder, hype tension/vascular disease

k

Mucopurulent

bo

bo

Allergic Rhinitis (i.e. Hay Fever)

Definition • rhinitis characterized by an IgE-mediated hypersensitivity to foreign allergens • acute-and-seasonal or chronic-and-perennial • perennial allergic rhinitis often confused with recurrent colds

s

sf

r

ok

sf

Complications • chronic s nusitis/polyps • serous otitis media

ee

ee

.

m

b

bo

o

Clinical Features • nasal: obstruction with pruritus, sneezing • clear rhinorrhea (containing increased eosinophils) • itching of eyes with tearing • frontal headache and pressure • mucosa: swollen, pale, “boggy” • seasonal (summer, spring, early autumn) ■■ pollens from trees ■■ lasts several weeks, disappears, and recurs the following year at same time • perennial ■■ inhaled: house dust, wool, feathers, foods, tobacco, hair, mould ■■ ingested: wheat, eggs, milk, nuts ■■ occurs intermittently for years with no pattern or may be constantly present

co

e.

Epidemiology • age at onset usually 5 d) of nasal drops and sprays (Dristan®, Otrivin®)

sf

re

e.

Clinical Features • chronic intermittent nasal obstruction, varies from side to side • rhinorrhea: thin, watery • mucosa and turbinates: swollen • nasal allergy must be ruled out

m

m

b

oo

Treatment • elimination of irritant factors • parasympathetic blocker (Atrovent® nasal spray) • steroids (e.g. beclomethasone, fluticasone) • surgery (often of limited lasting benefit): electrocautery, cryosurgery, laser treatment, or emoval of inferior or middle turbinates • vidian neurectomy (rarely done) • symptomatic relief with exercise (increased sympathetic tone)

co

Rhinosinusitis

sf

e

fre

Definition • inflammation of the mucosal lining of the sinuses and nasal passages

o

Classification • acute: 8-12 wk

oo

bo

ok

Pathogenesis of Rhinosinusitis • ostial obstruction or dysfunctional cilia permit stagnant mucous and, consequently, infection • all sinuses drain to a common prechamber under the middle meatus called the osteomeatal complex

OT25 Otolaryngology

Toronto Notes 2018

c

Rhinosinusitis

e

Table 13. Etiologies of Rhinosinusitis Inflammation

URTI Allergy

Mechanical

Septal deviation Turbinate hypertrophy Polyps Tumours Adenoid hypertrophy Foreign body Congenital abnormalities (e.g. cleft palate)

m

e

o

Ostial Obstruction

PA Lymphoma, leukemia Immunosuppressed patients (e.g. neutropenics, diabetics, HIV)

m

Immune

Cystic fibrosis Immotile cilia (e.g. Kartagener’s

Systemic Dental

Infection

Trauma

Facial fractures

e

Direct Extension

ks

ok sf

Acute Bacterial Rhinosinusitis

o

bo

o

ok

s

ks

Etiology • bacteria: S. pneumoniae (35%), H. influenzae (35%), M. catarrhalis, S. aureus, anaerobes (dental) • children are more prone to a bacterial etiology, but viral i still more common • maxillary sinus most commonly affected • must rule out fungal causes (mucormycosis) in immunocompromised hosts (especially if painless, black or pale mucosa on examination)

o

e

e

e

co

co

m

m

Clinical Features • sudden onset of: ■■ nasal blockage/congestion and/or purulent nasal discharge/posterior nasal drip ■■ ± facial pain or pressure, hyposmia, sore throat • persistent/worsening symptoms >5-7 d or presence of purulence for 3-4 d with high fever • speculum exam: erythematous mucosa, mucopurulent discharge, pus originating from the middle meatus • predisposing factors: viral URTI, allergy, dental disease, anatomical defects • differentiate from acute viral rhinosinusitis (course: 7 d • clinical diagnosis requiring ≥2 major symptoms, and at least one of the symptoms is either nasal obstruction or purulent/discoloured nasal discharge Major Symptoms (at least 2 of PODS, 1 must be O or D) Minor Symptoms P Facial Pain/Pressure/fullness Headache O Nasal Obstruction Halitosis D Purulent/discoloured nasal Discharge Fatigue S Hyposmia/anosmia (Smell) Dental pain Cough Ear pain/fullness

ee .

m

m

Use of Single Dose Azithromycin as Treatment of Acute Bacterial Rhinosinusitis Otolaryngol Head Neck Surg 2005;133(2):194-200 Summary: Single-dose azithromycin microspheres were comparable to 10 days of levofloxacin and may be a safe and effective treatment for acute bacterial rhinosinusitis. Results: An international, multicentre, doubleblind, double-dummy RCT omparing single dose azithromycin vs. 10-day levofloxacin group for treatment of acute bacterial rhinosinusitis. Clinical success were 94.5% (242/256) in the azithromycin group and 92.8% (233/251) in the levofloxacin group.

co

c

om

m

eb

bo

Management • depends on symptom severity (i.e. intensity/duration of symptoms, impact on quality of life) mild-moderate: INCS ■■ if no response within 72 h, add antibiotics • severe: INCS + antibiotics • antibiotics ■■ 1st line: amoxicillin x 10 d (TMP-SMX or macrolide if penicillin allergy) • if no response to 1st line antibiotics within 72 h, switch to 2nd line ■■ 2nd line: fluoroquinolones or amoxicillin-clavulanic acid • adjuvant therapy (saline or HOCL (pediatric sinusitis) irrigation, analgesics, oral/topical decongestant) may provide symptomatic relief • CT indicated only if complications are suspected

e

ok

ks

s

Diagnosis • along with clinical criteria, can confirm radiographically and/or endoscopically using antral puncture for bacterial cultures

OT26 Otolaryngology

Toronto Notes 2018

c

Epistaxis

fr

Chronic Rhinosinusitis

o

oo

oo

k

Definition • inflammation of the mucosa of paranasal sinuses and nasal passages >8-12 wk • diagnosis requires ≥2 major symptoms for >8-12 wk and ≥1 objective finding of inflammation of the paranasal sinuses (CT/endoscopy)

m

o

bo

Clinical Features (similar to acute, but less severe) - at least 2 of CPODS for >8-12 wk • facial Congestion/fullness • facial Pain/Pressure • chronic nasal Obstruction • purulent anterior/posterior nasal Discharge • hyposmia/anosmia (Smell) • others: halitosis, chronic cough, maxillary dental pain

e

fre

e.

fr

FESS = Functional Endoscopic Sinus Surgery Opening of the entire osteomeatal complex in order to facilitate drainage while sparing the sinus mucosa

oo

oo

k

ks

fr

e.

o

Management • identify and address contributing or predisposing factors • obtain CT or perform endoscopy • if polyps present: INCS, oral steroids ± antibiotics (if signs of infection), refer to otolaryngologist/H&N surgeon • if polyps absent: INCS, antibiotics, saline irrigation, oral steroids (severe cases) • antibiotics for 3-6 wk ■■ amoxillin-clavulanic acid, fluoroquinolone (moxifloxacin), macrolide (clarithromycin), clindamycin, Flagyl® (metronidazole) • surgery if medical therapy fails or fungal sinusitis FESS, balloon sinoplasty

Allergic fungal rhinosinusitis is a chronic sinusitis affecting mostly young, immunocompetent, atopic individuals Treatment options include FESS ± intranasal topical steroids, antifungals, and immunotherapy

m

ok sf re

c

m

co m

Etiology • unclear etiology but the following may contribute or predispose ■■ inadequate treatment of acute rhinosinusitis ■■ bacterial colonization/biofilms ◆◆ S. aureus, enterobacteriaceae, Pseudomonas, S. pneumoniae, H. influenzae, β-hemolytic Streptococci ■■ fungal infection (e g. Aspergillus, Zygomycetes, Candida) ■■ anatomic abnormality (e.g. lost ostia patency, deviated septum – predisposing factors) ■■ allergy/allergic rhinitis ■■ ciliary disorder (e.g. cystic fibrosis, Kartagener syndrome) ■■ chronic inflammatory disorder (e.g. GPA) ■■ untreated dental disease

Complications • same as acute sinusitis, mucocele

Epistaxis

fre

oo ks

e

bo

ok

sf

re

.c o

Blood Supply to the Nasal Septum (see Figure 4, OT3) 1. Superior posterior septum ■■ internal carotid → ophthalmic → anterior/posterior ethmoidal 2. Posterior septum ■■ external carotid → internal maxillary → sphenopalatine artery → nasopalatine 3. Lower anterior septum ■■ external carotid → facial artery → superior labial artery → nasal branch ■■ external carotid → internal maxillary → descending palatine → greater palatine • these arteries all anastomose to form Kiesselbach’s plexus, located at Little’s area (anterior-inferior portion of the cartilaginous septum) • bleeding from above middle turbinate is internal carotid, from below is external carotid

90% of nose bleeds occur in Little’s area

OT27 Otolaryngology

Toronto Notes 2018

Epistaxis

Trauma (most common) Fractures: facial, nasal Self-induced: digital, foreign body

Tumours Benign: polyps, inverting papilloma, angiofibroma Malignant: SCC, esthesioneuroblastoma (olfactory neuroblas oma)

o

o

Iatrogenic: nasal, sinus, orbit surgery

Inflammation Rhinitis: allergic, non-allergic Infections: bacterial, viral, fungal

Barometric changes Nasal dryness: dry air ± septal deformities

Special Cases • Adolescent male with unilateral recurrent epistaxis - consider juvenile nasopharyngeal angiofibroma (JNA); this is the most common benign tumour of the nasopharynx • Thrombocytopenic patients: use resorbable packs to avoid risk of re-bleeding caused by pulling out the removable pack

Idiopathic

m

Septal perforation

om

Local

Causes

bo

Type

ks fe

Table 14. Etiology of Epistaxis

Chemical: cocaine, nasal sprays, ammonia, etc. Coagulopathies Meds: anticoagulants, NSAIDs Hemophilias, von Willebrand’s Hemato ogical malignancies Liver failure, uremia

ks fre

e

ee

.

c

Systemic

ks

Vascular: HTN, atherosclerosis, Osler-Weber-Rendu (hereditary hemorrhagic telangectasia) Others: GPA, SLE

b

Investigations • CBC, PT/PTT (if indicated) • X-ray, CT as needed Treatment • locate bleeding and achieve hemostasis

e

e

co

co

1. ABCs • lean patient forward to minimize swallowing blood and avoid airway obstruction • apply constant firm pressure for 20 min on cartilaginous part of nose (not bony pyramid) • if significant bleeding, assess vitals for signs of hemorrhagic shock ± IV NS, cross-match blood

o

e

eb

bo

oo

ok

ks

s

r

2. Determine Site of Bleeding • anterior/posterior hemorrhage defined by location in relationship to bony septum • visualize nasal cavity with speculum • use cotton pledget with topical lidocaine ± topical decongestant (i.e. Otrivin®) to help identify area of bleeding (often anterior septum) • if suspicious bleeding disorder, coagulation workup (platelet number and platelet function assay)

om

om

m

eb

oo

ks

ks

fre

ee

.

e.

co

m

3. Control the Bleeding • first-line: topical vasoconstrictors (Otrivin®) • if first-line fails and bleeding adequately visualized, cauterize with silver nitrate • do not cauterize both sides of the septum at one time due to risk of septal perforation from loss of septal blood supply A. Anterior hemorrhage treatment ■■ if failure to achieve hemostasis with cauterization ◆◆ place anterior pack* with half inch Vaseline®-soaked ribbon gauze strips layered from nasal floor toward nasal roof and extending to posterior choanae, or lubricated absorbable packing (i.e. Gelfoam wrapped in Surgicel®) for 2-3 d ◆◆ can also attempt packing with Merocel® or nasal tampons of different shapes ◆◆ can also apply Floseal® (hemostatic matrix consist ng of topical human thrombin and crosslinked gelatin) if other methods fail B. Posterior hemorrhage treatment ■■ if unable to visualize bleeding source, then usually posterior source ◆◆ place posterior pack* using a Foley catheter, gauze pack, or Epistat® balloon ◆◆ subsequently, layer anterior packing bilaterally ◆◆ admit to hospital with packs in for 3-5 d ◆◆ watch for complications: hypoxemia (naso-pulmonic reflex), toxic shock syndrome (Rx: remove packs immediately), pharyngeal fibrosis/stenosis, alar/septal necrosis, aspiration C. If anterior/posterior packs fail to control epistaxis ■■ ligation or embolization of culprit arterial supply by interventional radiology ■■ ± septoplasty

e.

*antibiotics for any posterior pack or any pack left for >48 h because of risk of toxic shock syndrome

ok

s

sf

4. Prevention • prevent drying of nasal mucosa with humidifiers, saline spray, or topical ointments • avoidance of irritants • medical management of HTN and coagulopathies

OT28 Otolaryngology

Toronto Notes 2018

c

Hoarseness

fr

Hoarseness If hoarseness present for >2 wk in a smoker, laryngoscopy must be done to rule out malignancy

m

eb

bo

oo

o

Definitions • hoarseness: change in voice quality, ranging from voice harshness to voice weakness; reflects abnormalities anywhere along the vocal tract from oral cavity to lungs • dysphonia: a general alteration in voice quality • aphonia: no sound emanates from vocal folds

Acute Laryngitis

eb

bo

Clinical Features • URTI symptoms, hoarseness, aphonia, cough attacks, ± dyspnea • true vocal cords erythematous/edematous with vascular injection and normal mobility

c

co

Treatment • usually self-limited, resolves within ~1 wk • voice rest • humidification • hydration • avoid irritants (e.g. smoking) • treat with antibiotics if there is evidence of coexistent bacterial pharyngitis

fre

Chronic Laryngitis

ok

Definition • >2 wk inflammatory changes in laryngeal mucosa

om

m

b

Etiology • repeated attacks of acute laryngitis • chronic irritants (dust, smoke, chemical fumes) • chronic voice strain • chronic rhinosinusitis with postnasal drip • chronic EtOH use • esophageal disorders: GERD, Zenker’s diverticulum, hiatus hernia • systemic: allergy, hypothyroidism, Addison’s disease

ok

fr

fre

e.

Clinical Features • chronic dysphonia: rule out malignancy • cough, globus sensation, frequent throat clearing 2° to GERD • laryngoscopy: cords erythematous, thickened with ulceration/granuloma formation, and normal mobility

m

eb

bo

Treatment • remove offending irritants • treat related disorders (e.g. antisecretory therapy for GERD) • speech therapy with voice rest • ± antibiotics ± steroids to decrease inflammation • laryngoscopy to rule out malignancy

m

Vocal Cord Polyps

oo

ks

Etiology • most common benign tumour of vocal cords • voice strain (muscle tension dysphonia) • laryngeal irritants (GERD, allergies, tobacco)

e

e

Definition • structural manifestation of vocal cord irritation • acutely, polyp forms 2° to capillary damage in the subepithelial space during extreme voice exertion

.c om

Bilateral: cords rest in midline, therefore voice remains good but respiratory function is compromised and may present as stridor. If no respiratory issues, may monitor closely and wait for improvement. If respiratory issues, intubate and will likely require vocal cord lateralization, arytenoidectomy, posterior costal cartilage graft, or tracheotomy

m

ks fre

e

Etiology • viral: influenza, adenovirus, HSV • bacterial: Group A Streptococcus • mechanical acute voice strain → submucosal hemorrhage → vocal cord edema → hoarseness • environmental: toxic fume inhalation

Vocal Cord Paralysis Unilateral: affected cord lies in the paramedian position, inadequate glottic closure during phonation  weak, breathy voice. Usually medializes with time, whereby phonation and aspiration improve. Treatment options include voice therapy, injection laryngoplasty (Radiesse), medialization using silastic block

re e

o

Definition • F

Vocal Cords: Polyps vs. Nodules Polyps

Nodule

Unilateral, asymmetric

Bilateral

Treatment • avoid irritants • endoscopic laryngeal microsurgical removal if persistent or if high risk of malignancy

Subepithelial capillary breakage

Acute: submucosal hemorrhage or edema Chronic: hyalinization within submucosal lesion

Etiology • early nodules occur 2° to submucosal hemorrhage mature nodules result from hyalinization, which occurs with long-term voice abuse • chronic voice strain • frequent URTI, smoke, EtOH

eb

m

m

Epidemiology • frequently in singers, children, bartenders, and school teachers • F>M

ok

k

sf

re

e

Clinical Features • hoarseness worst at end of day • on laryngoscopy ■■ often bilateral ■■ at the junction of the anterior 1/3 and posterior 2/3 of the vocal cords – point of maximal cord vibration • chronic nodules may become fibrotic, hard, and white

b

Treatment • voice rest • hydration • speech therapy • avoid irritants • surgery rarely indicated for refractory nodules

o

Benign Laryngeal Papillomas

f

fr

Etiology • HPV types 6, 11 • possible hormonal influence, possibly acquired during delivery

ok

ok

Epidemiology • biphasic distribution: 1) birth to puberty (most common laryngeal tumour) and 2) adulthood

bo

Clinical Features • hoarseness and airway obstruction can seed into tracheobronchial tree • highly resistant to complete removal • some juvenile papillomas resolve spontaneously at puberty • may undergo malignant transformation • laryngoscopy shows wart-like lesions in supraglottic larynx and trachea

sf

Laryngeal Carcinoma • see Neoplasms of the Head and Neck, OT34

e

e.

co

Treatment • microdebridement or CO2 laser • adjuvants under investigation: interferon, cidofovir, acyclovir • HPV vaccine may prevent/decrease the incidence, but more research is needed

om

Often follow a chronic course

Soft, smooth fusiform pedunculated mass

Acute: small, discrete nodules Chronic: hard, white, thickened fibrosed nodules

Proton pump inhibitor

Voice rest but no whispering, hydration, speech therapy if refractory to therapy

fre

ok s

Definition • vocal cord callus • i.e. “screamer’s or singer’s nodules”

o

Gradual onset

May resolve spontaneously

e

e.

Vocal Cord Nodules

bo

Acute onset

o

o

m

e

bo

o

Clinical Features • hoarseness, aphonia, cough attacks ± dyspnea • pedicled or sessile polyp on free edge of vocal cord • typically, polyp asymmetrical, soft, and smooth • more common on the anterior 1/3 of the vocal cord • intermittent respiratory distress with large polyps

Surgical excision Surgical excision as last if persistent or resort in presence of risk factors for laryngeal cancer

OT30 Otolaryngology

Toronto Notes 2018

c

Salivary Glands

fr

Salivary Glands

o

Sialadenitis

b

Definition • inflammation of salivary glands

o

m

Etiology • viral most common (mumps) • bacterial causes: S. aureus, S. pneumoniae, H. influenzae • obstructive vs. non-obstructive ■■ obstructive infection involves salivary stasis and bacterial retrograde flow

.

Predisposing Factors • HIV • anorexia/bulimia • Sjögren’s syndrome • Cushing’s, hypothyroidism, DM • hepatic/renal failure • meds that increase stasis: diuretics, TCAs, β-blockers, anticholinergics, antibiotics • sialolithiasis (can cause chronic sialadenitis)

fr

o

bo

ok sf r

Bilateral enlargement of the parotid glands may be a manifestation of a systemic disease, such as Mumps, HIV, Sjögren’s or an eating disorder (i.e. anorexia, bulimia)

m

m

m

Clinical Features • acute onset of pain and edema of parotid or submandibular gland that may lead to marked swelling • ± fever • ± leukocytosis • ± suppurative drainage from punctum of the gland

c

c

Investigations • U/S imaging to differentiate obstructive vs. non-obstructive sialadenitis

f

sf

r

Treatment • bacterial: treat with cloxacillin ± abscess drainage, sialogogues • viral: no treatment

oo

Sialolithiasis

m

m

Definition • ductal stone (mainly hydroxyapatite) in adults, sand/sludge in children, leading to chronic sialadenitis • 80% in submandibular gland, F): 10% ■■ cysts lymph nodes, and adenomas: 10% ■■ oncocytoma: 40

1. Neoplastic

2. Inflammatory

3. Congenital

eb

o

1. Congenital

20-40

b

1.5 cm in diameter, or a retropharyngeal node >1 cm in diameter • A node of any size which contains central necrosis

m

m

m

eb

b

oo

ok

s

sf

re

c

Treatment • treatment depends on ■■ histologic grade of tumour ■■ stage ■■ physical and psychological health of patient ■■ facilities available ■■ expertise and experience of the medical and surgical oncology team • in general ■■ 1° surgery for malignant oral cavity tumours with radiotherapy reserved for salvage or poor prognostic indicators ■■ 1° radiotherapy for nasopharynx, oropharynx, hypopharynx, larynx malignancies with surgery reserved for salvage ■■ palliative chemotherapy for metastatic or incurable disease ■■ concomitant chemotherapy increases survival in advanced disease ■■ chemotherapy has a role as induction therapy prior to surgery and radiation ■■ panendoscopy to detect primary disease when lymph node metastasis is identified ■■ anti-EGFR treatment (cetuximab, panitumumab) has a role as concurrent therapy with radiation for SCC of the head and neck (for advanced local and regional disease)

Detection of cervical lymph nodes on physical exam False negative rate: 15-30% False positive rate: 30-40%

m

m

m

b

Investigations • initial metastatic screen includes CXR • scans of liver, brain, and bone only if clinically indicated • CT scan is superior to MRI for the detection of pathologic nodal disease and bone cortex invasion • MRI is superior to discriminate tumour from mucus and to detect bone marrow invasion • ± PET scans

fre

fre

e

Prognosis • synchronous tumours occur in 9-15% of patients • late development of 2nd primary is most common cause of post treatment failure after 36 mo

Common sites of distant metastases for head and neck neoplasms lungs > liver > bones

OT35 Otolaryngology

Toronto Notes 2018

c

Neoplasms of the Head and Neck

e

e

Table 16. Quick Look-Up Summary of Head and Neck Malignancies – Etiology and Epidemiology Epidemiology

Risk Factors

Mean age: 50-60 yr M>F Most common site of H&N cancers 50% on anterior 2/3 of tongue

Smoking/EtOH Poor oral hygiene Leukoplakia, erythroplakia Lichen planus, chronic inflammation Sun exposure – lip HPV infection

Risk Factors for Head and Neck Cancer • Smoking • EtOH (synergistic with smoking) • Radiation • Occupational/environmental exposures • Oral HPV infection (independent of smoking and EtOH exposure)

s

Etiology

m

m

eb

bo

95% SCC others: sarcoma, melanoma, minor salivary gland tumour

e

Oral Cavity

f

Epstein-Barr virus (EBV) Salted fish Nickel exposure Poor oral hygiene Genetic – Southern Chinese

Mean age: 50-70 yr Patients with HPV+ OPC are approximately 10 yrs younger Prevalence of HPV+ OPC has increased by 225% from 1988 to 2004. M:F = 4:1

Smoking/EtOH HPV 16 infection: increased sexual encounters, specifically oral sex

Mean age: 50-70 yr M>F 8-10% of all H&N cancer

Smoking/EtOH

Mean age: 45-75 yr M:F = 10:1 45% of all H&N cancer

Smoking/EtOH HPV 16 infection strongly associated with the risk of laryngeal squamous cell cancers

eb

o

Mean age: 50-59 yr M:F= 2.4:1 Incidence 0.8 per 100,000 100x increased incidence in Southern Chinese

co

bo

o

sf

re

Hypopharynx 95% SCC 3 sites 1. pyriform sinus (60%) 2. post-cricoid (30%) 3 post pharyngeal wall (10%)

m

m

Larynx

SCC most common 3 sites 1. supraglottic (30-35%) 2. glottic (60-65%) 3. subglottic (1%) Salivary Gland

Mean age: 55-65 yr M=F 3-6% of all H&N cancer Percentage of malignant tumours n each gland: Parotid 15-25% Submandibular 37-43% Minor salivary >80%

sf

r

The smaller the salivary gland, the greater the likelihood that a mass in the gland is malignant

fr

f

40% mucoepidermoid 30% adenoid cystic 5% acinic cell 5% malignant mixed 5% lymphoma

Thyroid (90% benign – 10% malignant) Children Adults 60 yr Nodules more common in females Malignancy more common in males

Parathyroid

Mean age: 44-55 yr Rare tumour

Radiation exposure Family history – papillary CA or multiple endocrine neoplasia – MEN II Older age Male Papillary – Gardner’s, Cowden’s, familial adenomatous polyposis (FAP)

m

m

>80% papillary 5-15% follicular 5% medullary 20 PY): 64% group III (T4 or N3, age ≤70): 57% group IVA (T4 or N3, age >70): 40%

Pharyngoscopy Biopsy CT

1o radiation 2o surgery

5 yr survival T1: 53% T2/T3: 36-39% T4: 24%

Laryngoscopy CT/MRI

1o radiation 2o surgery 1o surgery for bulky T4 disease

5 yr survival T4: >40% (surgery with radiation) Control rate early lesions >90% (radiation) 10 to 12% of small lesions fail radiotherapy

FNA MRI/CT/U/S

1o surgery ± neck dissection Post-operative radiotherapy Chemotherapy if unresectable

Parotid 10 yr surv val: 85, 69, 43, and 14% for stages T1 to T4 Submandibular 2 yr survival: 82%, 5 yr: 69% Minor salivary gland 10 yr survival: 83, 52, 25, 23% for stages T1 to T4

FNA U/S

1o surgery I131 for intermediate and high risk well differentiated thyroid cancer

Recurrences occur within 5 yr Need long-term follow-up: clinical exam, thyroglobulin

Sestamibi

Wide surgical excision Post operative monitoring of serum Ca2+

Recurrence rates 1 yr: 27% 5 yr: 82% 10 yr: 91% Mean survival: 6-7 yr

5 yr survival T1/T2: 75% T3/T4: 30-35% Poor prognostic indicators Depth of invasion, close surgical margins location (tongue worse than floor of mouth) Cervical nodes, extra-capsular spread

m

bo

Asymptomatic neck mass (30%) Non-healing ulcer ± bleeding Dysphagia, sialorrhea, dysphonia Oral fetor, otalgia, leukoplakia, or erythroplakia (pre-malignant changes or CIS)

oo

o

Oral Cavity

co

Early Symptoms Unilateral nasal obstruction Epistaxis, rhinorrhea

co m

Nose and Paranasal Sinus

sf re

Late Symptoms 2º to invasion of nose, orbit, nerves, oral cavity, skin, skull base, cribriform plate

bo

bo

Cervical nodes (60-90%) Nasal obstruction, epistaxis Unilateral otitis media ± hearing loss CN III to VI, IX to XII (25%) Proptosis, voice change, dysphagia

o

o

Nasopharynx

co

fre

e.

e.

o

ks

fre

e.

Odynophagia, otalgia Ulcerated/enlarged tonsil Fixed tongue/trismus/dysarthria Oral fetor, bloody sputum HPV+ OPC predominantly arises at base of tongue or tonsillar region Cervical lymphadenopathy (60%) Distant mets: lung/bone/liver (7%)

co

Oropharynx

Dysphagia, odynophagia Otalgia, hoarseness Cervical lymphadenopathy

b

bo

Hypopharynx

co

bo

bo

ok

s

Painless mass (occ. pain is possible) CN VII palsy Cervical lymphadenopathy Rapid growth Invasion of skin Constitutional signs/symptoms

ok

Salivary Gland

s

e.

Dysphagia, odynophagia, globus Otalgia, hoarseness Dyspnea/stridor Cough/hemoptysis Cervical nodes (rare with glottic CA)

o

Larynx

Thyroid Thyroid mass, cervical nodes Vocal cord paralysis Hyper/hypothyroidism Dysphagia

e

Increased serum Ca2+ Neck mass Bone disease, renal disease Pancreatitis

e. c

Parathyroid

OT37 Otolaryngology

Toronto Notes 2018

c

Neoplasms of the Head and Neck

fre

Thyroid Carcinoma

k

Table 18. Bethesda Classification of Thyroid Cytology Risk of Malignancy

o

oo

Category

Unknown

eb

Non-diagnostic or unsatisfactory Benign

0-3%

Follicular lesion of undetermined significance/ Atypia of undetermined significance

5-15%

Follicular/hürthle cell neoplasms

15-30%

Suspicious for malignancy

60-75%

Malignant

97-99%

Follicular

70-80%

10-15%

Route of Spread

Lymphatic

Hematogenous

Histology

Orphan Annie nuclei Psammoma bodies Papillary architecture

Capsular/vascular invasion Invasion influences prognosis

Amyloid May secrete calcitonin, prostaglandins, ACTH, serotonin, kallikrein, or bradykinin

Other

Ps – Papillary cancer Popular (most common) Palpable lymph nodes Positive I131 uptake Positive prognosis Post-operative I131 scan to guide treatments

Fs – Follicular cancer Far away mets Female (3:1) NOT FNA (cannot be diagnosed by FNA) Favourable prognosis

Ms – Medullary cancer Multiple endocrine neoplasia (MEN IIa or IIb) aMyloid Median node dissection

More common in elderly 70% in women 20-30% have Hx of differentiated thyroid Ca (mostly papillary) or nodular goitre mass Rapidly enlarging neck Rule out lymphoma

Usually non-Hodgkin’s lymphoma Rapidly enlarging thyroid mass Hx of Hashimoto’s thyroiditis increases risk 60x 4:1 female predominance dysphagia, dyspnea, stridor, hoarseness, neck pain, facial edema, accompanied by “B” symptoms*

98% at 10 yr

92% at 10 yr

50% at 10 yr 20% at 10 yr if detected when clinically palpable

20-35% at 1 yr 13% at 10 yr

5 yr survival Stage IE 55%-80% Stage IIE 20%-50% Stage IIE/IV 15%-35%

Small tumours: Near total thyroidectomy or lobectomy Diffuse/bilateral: Total thyroidectomy ± neck dissection ± postoperative I131 treatment

Small tumours: Near total thyroidectomy/lobectomy/ isthmectomy Large/diffuse tumours: Total thyroidectomy

Total thyroidectomy Median and/or lateral compartment node neck dissection (based on serum calcitonin) Modified neck dissection Post-ope ative thyroxine, radiotherapy Tracheostomy Screen relatives

Subtotal thryoidectomy, radiation, chemotherapy, palliative care Small tumours: Total thyroidectomy ± external beam

Non-surgical Combined radiation Chemotherapy (CHOP**)

Lymphoma 1 cm and low suspicion nodule >1.5 cm should undergo FNA • nodules 1 episode by 3 yr old • seasonal variability: peaks in winter

oo

ks fre

sf re

Etiology • primary defect causing AOM: Eustachian tube dysfunction/obstruction → stasis/colonization by pathogens • bacterial: S pneumoniae, non-typable H. influenzae, M. catarrhalis, Group A Streptococcus, S. aureus • viral: RSV, influenza, parainfluenza, adenovirus • commonly due to bacterial/viral co-infection

m

m

e

ok

s

sf

e

re

e

c

co

m

Predisposing Factors • Eustachian tube dysfunction/obstruction ■■ swelling of tubal mucosa ◆◆ upper respiratory tract infection (URTI) ◆◆ allergic rhinitis ◆◆ chronic rhinosinusitis ■■ obstruction/infiltration of Eustachian tube ostium ◆◆ tumour: nasopharyngeal carcinoma (adults) ◆◆ adenoid hypertrophy (by maintaining a source of infection rather than obstruction) ◆◆ barotrauma (sudden changes in air pressure) ■■ inadequate tensor palati function: cleft palate (even after repair) ■■ abnormal Eustachian tube ◆◆ Down syndrome (horizontal position of Eustachian tube), Crouzon syndrome, cleft palate, and Apert syndrome • disrup ion of action of: ■■ cilia of Eustachian tube: Kartagener’s syndrome ■■ mucus secreting cells ■■ capillary network that provides humoral factors, PMNs, phagocytic cells • immunosuppression/deficiency due to chemotherapy, steroids, DM, hypogammaglobulinemia, cystic fibrosis

c

e. co

m

m

Risk Factors • non-modifiable: young age, family history of OM, prematurity, orofacial abnormalities, immunodeficiencies, Down syndrome, race, and ethnicity • modifiable: lack of breastfeeding, day care attendance, household crowding, exposure to cigarette smoke and air pollution, pacifier use

s

sf r

om

m

eb

bo

Clinical Features • triad of otalgia, fever (especially in younger children), and conductive hearing loss • rarely tinnitus, vertigo, and/or facial nerve paralysis • otorrhea if tympanic membrane perforated • infants/toddlers ■■ ear-tugging (this alone is not a good indicator of pathology) ■■ hearing loss, balance disturbances (rare) ■■ irritable, poor sleeping ■■ vomiting and diarrhea ■■ anorexia • otoscopy of TM ■■ hyperemia ■■ bulging, pus may be seen behind TM ■■ loss of landmarks: handle and long process of malleus not visible

Clinical Assessment of AOM in Pediatrics JAMA 2010;304:2161-69 In assessment of AOM in pediatrics, ear pain is the most useful symptom with a likelihood ratio (LR) between 3.0-7.3. Useful otoscopic signs include erythematous (LR 8.4, 95% CI 7 11), cloudy (LR 34, 95% CI 28-42), bulging (LR 51, 95% CI 36-73), and immobile tympanic membrane (LR 31, 95% CI 26-37) on pneumatic otoscopy.

co m

ok

s

sf

r

Pathogenesis • obstruction of Eustachian tube → air absorbed in middle ear → negative pressure (an irritant to middle ear mucosa) → edema of mucosa with exudate/effusion → infection of exudate from nasopharyngeal secretions

OT39 Otolaryngology

Toronto Notes 2018

c

Pediatric Otolaryngology

m

e

e

oo

ks

ks

Diagnosis • history ■■ acute onset of otalgia or ear tugging in a preverbal child otorrhea, decreased hearing ■■ unexplained irritability, fever, upper respiratory symptoms, poor sleeping, anorexia, N/V, and diarrhea • physical ■■ febrile ■■ MEE on otoscopy: immobile tympanic membrane, acute otorrhea, loss of bony landmarks, opacification of TM, air-fluid level behind TM ■■ MEI on otoscopy: bulging TM with marked discolouration (hemorrhagic, red, grey, or yellow)

co m

e.

m

m

co

e.

re sf

m

m

eb

o

ok

s

sf

re

ee

e

c

Treatment • antimicrobial agents for AOM ■■ 5 d course of appropriate dose antimicrobial recommended for most ≥ 2 yr old with uncomplicated AOM. 10 d course for 6-24 mo, and perforated TM or recurrent AOM ■■ 1st line treatment (no penicillin allergy) ◆◆ amoxicillin: 5 d course of 45-60 mg/kg/d divided 3x/d, or 75-90 mg/kg/d divided 2x/d ■■ 2nd l ne treatment ◆◆ cefprozil: 30 mg/kg/d divided 2x/d ◆◆ cefuroxime axetil: 30 mg/kg/d divided 2-3x/d (1st line for penicillin allergy) ◆◆ ceftriaxone: 50 mg/kg IM (or IV) x 3 doses (1st line for penicillin allergy) ◆◆ azithromycin: 10 mg/kg OD x 1 dose, then 5 mg/kg OD x 4 doses ◆◆ clarithromycin: 15 mg/kg/d divided 2x/d ■■ if initial therapy fails (i.e. no symptomatic improvement after 2-3 d) ◆◆ amoxicillin-clavulanate: 45-60 mg/kg/d (7:1 formulation, 400 mg/5 mL suspension) for 10 d for child weighing ≤35 kg, or 500 mg tablets TID for 10 d for child weighing >35kg ◆◆ if AOM-related symptoms do not resolve with amoxicillin/clavulanate, a course of ceftriaxone 50 mg/kg/d IM (or IV) OD x 3 doses could be considered

o

m

e

b

o

ok

sf

fre

re

e

e

Complications • extracranial ■■ hearing loss and speech delay (secondary to persistent MEE), TM perforation, extension of suppurative process to adjacent structures (mastoiditis, petrositis, labyrinthitis), cholesteatoma, facial nerve palsy, middle ear atelectasis, ossicular necrosis, vestibular dysfunction, persistent effusion (often leading to hearing loss) • intracran al ■■ meningitis, epidural and brain abscess, subdural empyema, lateral and cavernous sinus thrombosis, carotid artery thrombosis, facial nerve paralysis • other ■■ mastoiditis, labyrinthitis, sigmoid sinus thrombophlebitis

Otitis Media with Effusion

m

Definition • presence of fluid in the middle ear without signs or symptoms of ear infection

ks

ok

sf

re

e.

Epidemiology • most common cause of pediatric hearing loss • not exclusively a pediatric disease • frequently follows AOM in children • middle ear effusions have been shown to persist following an episode of AOM for 1 mo in 40% of children, 2 mo in 20%, and >3 mo in 10% (i.e. 90% of children clear the fluid within 3 mo – observe for 3 mo before considering myringotomy and tubes)

Antibiotics for Acute Otitis Media in Children Cochrane DB Syst Rev 2013;1:CDOOO219 Study: Meta-analysis of Randomized Controlled Trials (RCTs) on children (1 15 mo) with acute otitis media comparing any ntibiotic regime to placebo and expectant observation. Data Sources: Cochrane Central Register of Controll d Trials (2012 issue 10), MEDLINE (1966 to October 2012), OLDMEDLINE (1958 to 1965), EMBASE (January 1990 to November 2012), Current Contents (1966 to November 2012), CINAHL (2008 to November 2012) and LILACS (2008 to November 2012) without language restrictions. Main Outcomes: 1) Pain at 24 h, 2-3 d, and 4-7 d; 2) Abnormal tympanometry findings; 3) TM perforation; 4) Contralateral otitis; 5) AOM recurrences; 6) Serious complications from AOM; 7) Adverse effects from antibiotics. Results: Treatment with antibiotics had no significant impact on pain at 24 h. However, pain at 2-3 d and 4-7 d was lower in the antibiotic groups with a NNT of 20. Antibiotics had no significant effect on tympanometry findings, number of AOM recurrences, or severity of complications. Antibiotic treatment led to a significant reduction in TM perforations (NNT 33) and halved contralateral AOM (NNT 11). Adverse events (vomiting, diarrhea, or rash) occurred more often in children taking antibiotics. Conclusion: The role of antibiotics is largely restricted to pain control at 2-7 d, but most (82%) settle without antibiotics. This can also be achieved by analgesics. However, antibiotic treatment can reduce risk of TM perforation and contralateral AOM episodes. These benefits must be weighed against risks of adverse events from antibiotics.

sf re

m

eb

bo

oo

ok

ks fre

re e

e.

co m

co m

Management • supportive care and symptom management: maintain hydration, analgesic, and antipyretic (acetaminophen, ibuprofen) • watchful waiting: in a generally healthy child >6 mo of age with unilateral non-severe suspected AOM ■■ without MEE, OR with MEE but non-bulging or mildly erythematous TM ◆◆ consider viral etiology ◆◆ reassess in 24-48 h if not clinically improved (or earlier if worsening) ■■ mildly ill (alert, responsive, no rigors, mild otalgia, fever 3 mo and symptoms likely attributable to OME (e.g. balance problems, poor school performance, ear discomfort, etc.) • At-risk children (permanent hearing loss, speech/language delay, autism-spectrum disorder, syndromes/craniofacial disorders, blindness, cleft palate, developmental delay) with unilateral or bilateral OME with type B tympanogram or persistent effusion >3 mo • RAOM (>3 episodes in 6 mo or >4 in 12 mo) with unilateral or bilateral middle ear effusion *Clinical practice guidelines: Tympanostomy tubes in children. Otolaryng Head Neck 2013;149:S1-S35

re e

om

o

oo

k

Clinical Features • conductive hearing loss ± tinnitus ■■ confirm with audiogram and tympanogram (flat) (see Figure 16B, OT10 and Figure 17B, OT11) • fullness – blocked ear ± pain, low grade fever • otoscopy of tympanic membrane ■■ discolouration – amber or dull grey with “glue” ear ■■ meniscus fluid level behind TM ■■ air bubbles ■■ retraction pockets/TM atelectasis ■■ most reliable finding with pneumatic otoscopy is immobility

Upper midline in nasopharynx

sf

re

Adenoid Hypertrophy • size peaks at age 5 and resolves by age 12 • increase in size with repeated URTI and allergies

ok

Tubal tonsil (x2)

Around openings of Eustachian tubes

s

m

eb

o

Complications • Eustachian tube obstruction leading to serous otitis media interference with nasal breathing, necessitating mouth-breathing • malocclusion • sleep apnea/respiratory disturbance • orofacial developmental abnormalities

co

m

Adenoidectomy

o

oo

ks

fr

fre

e

e.

Indications for Adenoidectomy • chronic upper airway obstruction with sleep disturbance/apnea ± cor pulmonale • chronic nasopharyngitis resistant to medical treatment • chronic serous otitis media and chronic suppurative otitis media (with 2nd set of tubes) • recurrent acute otitis media resistant to antibiotics • suspicion of nasopharyngeal malignancy • persistent rhinorrhea secondary to nasal obstruction

e

Lingual tonsil

Under mucosa of posterior 1/3 of tongue

Figure 20. Waldeyer’s ring An interrupted circle of protective lymphoid tissue at the upper ends of the respiratory and alimentary tracts

co m

m

m

co

e

ks

Diagnosis • enlarged adenoids on nasopharyngeal exam (usually with flexible nasopharyngoscope) • enlarged adenoid shadow on lateral soft tissue x-ray

Either side of oropharynx

© June Li 2010

Palatine tonsil (x2)

b

Clinical Features • nasal obstruction ■■ adenoid facies (open mouth, high arched palate, narrow midface, malocclusion) ■■ history of hypernasal voice and snoring ■■ long-term mouth breather; minimal air escape through nose • choanal obstruction ■■ chronic rhinosinusitis/rhinitis ■■ obstructive sleep apnea • chronic inflammation ■■ nasal discharge, post nasal drip, and cough ■■ cervical lymphadenopathy

OT41 Otolaryngology

Toronto Notes 2018

c

Pediatric Otolaryngology

oo

k

ks fr

Contraindications • uncontrollable coagulopathy • recent pharyngeal infection • conditions that predispose to velopharyngeal insufficiency (cleft palate, impaired palatal function, or enlarged pharynx)

m

eb

Complications • bleeding, infection • velopharyngeal insufficiency (hypernasal voice or nasal regurgitation) • scarring of Eustachian tube orifice

m

m

Sleep-Disordered Breathing in Children

c

c

Definition • spectrum of sleep-related breathing abnormalities ranging from snoring to OSA

r

fr

Epidemiology • peak incidence between 2-8 yr when tonsils and adenoids are the largest relative to the pharyngeal airway

m

o

bo

o

Etiology • due to a combination of anatomic and neuromuscular factors ■■ adenotonsillar hypertrophy ■■ craniofacial abnormalities ■■ neuromuscular hypotonia (i.e. cerebral palsy, Down syndrome) ■■ obesity

om

om

Clinical Features • heavy snoring, mouth breathing pauses or apnea, enuresis, excessive daytime sleepiness, behavioural/ learning problems, diagnosis of ADHD, morning headache, failure to thrive, sleeping with neck hyperextended, cyanosis

ks

ks

fre

fre

Investigations • flexible nasopharyngoscopy for assessment of nasopharynx and adenoids • polysomnography (apnea-hypopnea index >1/h considered abnormal) ■■ children: Mild OSA ≥1 to 38.3 °C, cervical adenopathy, tonsillar exudate, or positive test for Group A β-hemolytic Streptococcus (Paradise Criteria) • chronic tonsillitis with halitosis (bad breath) or sore throat ± tonsilloliths (clusters of material that form in the crevices of the tonsils) • complications of tonsillitis: quinsy/peritonsillar abscess, parapharyngeal abscess, retropharyngeal abscess • failure to thrive

o

ok

sf

fre

re

Relative Contraindications • velopharyngeal insufficiency: overt or submucous/covert cleft of palate, impaired palatal function due to neurological or neuro-muscular abnormalities • hematologic: coagulopathy, anemia • infectious: active local infection without urgent obstructive symptoms

eb

bo

Complications • hemorrhage: primary (within 24 h); secondary (within first 7-10 d) • odynophagia and/or otalgia; dehydration 2 to odynophagia • infection • atlantoaxial subluxation (Grisel’s syndrome) - rare

m

Airway Problems in Children

co

DIFFERENTIAL DIAGNOSIS BY AGE GROUP

o

ok

sf

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Neonates (Obligate Nose Breathers) • extralaryngeal ■■ choanal atresia (e.g. CHARGE syndrome) ■■ nasopharyngeal dermoid, glioma, encephalocele ■■ glossoptosis: Pierre-Robin sequence, Down syndrome, lymphatic malformation, hemangioma

OT43 Otolaryngology

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Pediatric Otolaryngology

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• laryngeal ■■ laryngomalacia: most common cause of stridor in children ■■ vocal cord palsy (due to trauma or Arnold-Chiari malformation) ■■ glotti web ■■ subglottic stenosis ■■ laryngeal cleft ■■ laryngocele • tracheal ■■ tracheoesophageal fistula ■■ tracheomalacia ■■ vascular rings ■■ complete tracheal rings

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2-3 Months • congenital ■■ laryngomalacia ■■ vascular: subglottic hemangioma (more common), innominate artery compression, double aortic arch ■■ laryngeal papilloma • acquired ■■ subglottic stenosis: post-intubation ■■ tracheal granulation: post-intubation ■■ tracheomalacia: post-tracheotomy and TEF repair

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Infants – Sudden Onset • foreign body aspiration • croup • bacterial tracheitis • caustic ingestion • epiglottitis

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Children and Adults • infection ■■ Ludwig’s angina ■■ peritonsillar/parapharyngeal abscess ■■ retropharyngeal abscess • neoplastic ■■ squamous cell carcinoma (SCC) (adults): larynx, hypopharynx ■■ retropharyngeal: lymphoma, neuroblastoma ■■ nasopharyngeal: carcinoma, rhabdomyosarcoma • allergic ■■ angioneurotic edema ■■ polyps (suspect cystic fibrosis in children) • trauma ■■ laryngeal fracture, facial fracture ■■ burns and lacerations ■■ post-intubation ■■ caustic ingestion • congenital ■■ lingual thyroglossal duct cyst ■■ lingual tonsil hypertrophy ■■ lingual thyro d

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Signs of Airway Obstruction

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Stridor • note quality, timing (inspiratory or expiratory) • body position important ■■ lying prone: double aortic arch ■■ lying supine: laryngomalacia, glossoptosis • site of stenosis ■■ vocal cords or above: inspiratory stridor ■■ subglottis and extrathoracic trachea: biphasic stridor ■■ distal tracheobronchial tree: expiratory stridor

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Respiratory Distress • nasal flaring • supraclavicular and intercostal indrawing • sternal retractions • use of accessory muscles of respiration • tachypnea • cyanosis • altered LOC

Toronto Notes 2018

OT44 Otolaryngology

Toronto Notes 2018

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Pediatric Otolaryngology

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Feeding Difficulty and Aspiration • supraglottic lesion • laryngomalacia • vocal cord paralysis • laryngeal cleft → aspiration pneumonia • TEF

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Acute Laryngotracheobronchitis (Croup)

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Definition • inflammation of tissues in subglottic space ± tracheobronchial tree • swelling of mucosal lining and associated with thick, viscous, mucopurulent exudate which compromises upper airway (subglottic space is narrowest portion of upper airway) • normal function of ciliated mucous membrane impaired

Signs of Croup The 3 Ss Stridor Subglottic swelling Seal bark cough

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Clinical Features • age: 4 mo-5 yr • preceded by URTI symptoms • generally occurs at night • biphasic stridor and croupy cough (loud, sea lion bark) • appear less toxic than epiglottitis • supraglottic area normal • rule out foreign body and subglottic stenosis • “steeple-sign” on AP X-ray of neck • if recurrent croup, think subglottic stenosis

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Etiology • viral: parainfluenzae I (most common), II, III, influenza A and B, RSV

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Treatment • racemic epinephrine via MDI q1-2h prn (only if in respiratory distress) • systemic corticosteroids (e.g. dexamethasone 0.5 mg/kg, prednisone) • adequate hydration • close observation for 3-4 h • intubation if severe (use smaller endotracheal tube than expected for age) • hospitalize if poor response to steroids after 4 h and persistent stridor at rest • consider alternate diagnosis if poor response to therapy (e.g. bacterial tracheitis) • if recurrent episodes of croup-like symptoms, perform high kV croup series X-ray (AP and lat) when well to rule out underlying subglottic stenosis and consider bronchoscopy for definitive diagnosis

Acute Epiglottitis Acute epiglottitis is a medical emergency

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Definition • acute inflammation causing swelling of supraglottic structures of the larynx without involvement of vocal cords

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Etiology • H. influenzae type b • relatively uncommon condition due to Hib vaccine

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Investigations and Management • investigations and physical exam may lead to complete obstruction, thus preparations for intubation or tracheotomy must be made prior to any manipulation • stat ENT/anesthesia consult(s) • WBC (elevated), blood and pharyngeal cultures after intubation • lateral neck radiograph (only done if patient stable)

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Treatment • secure airway • IV access with hydration • antibiotics: IV cefuroxime, cefotaxime, or ceftriaxone • moist air • extubate when leak around tube occurs and afebrile • watch for meningitis

When managing epiglottitis, it is important not to agitate the child, as this may precipitate complete obstruction

Thumb sign: cherry-shaped epiglottic swelling seen on lateral neck radiograph

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Clinical Features • any age most commonly 1-4 yr • rapid onset • toxic-looking, fever, anorexia, restlessness • cyanotic/pale, inspiratory stridor, slow breathing, lungs clear with decreased air entry • prefers sitting up (“tripod” posture), open mouth, drooling, tongue protruding, sore throat, dysphagia

OT45 Otolaryngology

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Pediatric Otolaryngology

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Subglottic Stenosis

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Congenital • diameter of subglottis 90% of cases • if severe, division of the aryepiglottic folds (supraglottoplasty) provides relief

Foreign Body

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Ingested • usually stuck at cricopharyngeus muscle • coins, toys, batteries (emergency) • presents with drooling, dysphagia, stridor if very large

Foreign body inhalation is the most common cause of accidental death in children

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Aspirated • usually stuck at right main bronchus • peanuts, carrot, apple core, popcorn, balloons • presentation ■■ stridor if lodged in trachea ■■ unilateral “asthma” if bronchial, therefore often misdiagnosed as asthma ■■ if totally occludes airway: cough, lobar pneumonia, atelectasis, mediastinal shift, pneumothorax, death

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Batteries MUST be ruled out as a foreign body (vs. coins) as they are lethal and can erode through the esophagus. Batteries have a halo sign around the rim on AP x-ray and a step deformity on lateral x-ray

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Diagnosis and Treatment • sudden onset, not necessarily febrile or elevated WBC • any patient with suspected foreign body should be kept NPO immediately • older patient: inspiratory-expiratory chest X-ray (if patient is stable) • younger patient: right and left decubitus chest X-rays. Lack of lung deflation while resting on dependent side suggests foreign body blocking bronchus • bronchoscopy or esophagoscopy with removal

OT46 Otolaryngology

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Common Medications

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Deep Neck Space Infection

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• most commonly arise from an infection of the mandibular teeth, tonsils, parotid gland, deep cervical lymph nodes, middle ear, or the sinuses • often a rapid onset and may progress to fatal complications

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Etiology • usually mixed aerobes and anaerobes that represent the flora of the oral cavity, upper respiratory tract, and certain parts of the ears and eyes Clinical Features • sore throat or pain and trismus • dysphagia and odynophagia • stridor and dyspnea • late findings may include dysphonia and hoarseness • swelling of the face and neck, erythema • asymmetry of the oropharynx with purulent oral discharge • lymphadenopathy

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These investigations should be obtained carefully and the surgeon should consider accompanying the patient, as the worst place to lose an airway is during imaging

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Ludwig’s angina is the prototypical infection of the submandibular and sublingual space

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Diagnosis • lateral cervical view plain radiograph • CT • MRI Treatment • secure the airway • surgical drainage • maximum doses of IV systemic antimicrobials regimens according to the site of infection

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Common Medications

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Table 21. Antibiotics

Notes

Streptococcus, Pneumococcus, H. influenzae, Proteus coverage

May cause rash in patients with infectious mononucleosis

piperacillin with tazobactam (Zosyn®)

3 g PO q6h

Gram-positive and negative aerobes and anaerobes plus Pseudomonas coverage

May cause pseudomembranous colitis

ciprofloxacin (Cipro®, Ciloxan®)

500 mg PO bid

Pseudomonas, Streptococci, MRSA, and most Gramnegative; no anaerobic coverage

Animal studies suggest that systemic quinolones may cause cartilage necrosis in children

erythromycin (Erythrocin®, EryPed®, Staticin®, T-Stat®, Erybid®, Novorythro Encap®)

500 mg PO qid

Alternative to penicillin

Ototoxic

Dose

Indications

Notes

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Indications

Adult: 500 mg PO tid Children: 75-90 mg/kg/d in 2 divided doses

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Dose

amoxicillin (Amoxil®, Amoxi®, Amox®)

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Generic Name (Brand Name)

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Generic Name (B and Name)

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Table 22. Otic Drops ciprofloxacin (Ciprodex )

4 gtt in affected ear bid

neomycin, polymyxin B sulfate, and hydrocortisone (Cortisporin Otic®)

5 gtt in affected ear tid

For otitis externa Used for inflammatory conditions which are currently infected or at risk of bacterial infections

May cause hearing loss if placed in inner ear

hydrocortisone and acetic acid (VoSol HC®)

5-10 gtt in affected ear tid

For otitis media

Bactericidal by lowering pH

tobramycin and dexamethasone (TobraDex®)

5-10 gtt in affected ear bid

For chronic suppurative otitis media

Risk of vestibular or cochlear toxicity

For otitis externa and complications of otitis media Pseudomonas, Streptococci, MRSA, and most Gram-negative; no anaerobic coverage

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®

OT47 Otolaryngology

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Common Medications

Indications

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Steroid Allergic rhinitis Chronic sinusitis

Requires up to 4 wk of consistent use to have effect Long-term use Dries nasal mucosa; may cause minor bleeding Patient should stop if epistaxis May sting Flonase® and Nasonex® not absorbed systemically

Allergic rhinitis

Immediate effect If no effect by 3 d then discontinue Use during allergy season

Acute sinusitis Rhinitis

Careful if patient has hypertension Short-term use (7 yr, considered second line therapy, may be used for sleepovers/camp): DDAVP oral tablets (similar success rate as “wet” alarm therapy but higher relapse rate), imipramine (Tofranil®) (rarely used, lethal if overdose, SE: cardiac toxicity, anticholinergic effects)

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General Approach • should be evaluated if dysuria, change in colour, odour, stream, secondary or diurnal, change in gait, stool incontinence

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Definition • involuntary urinary incontinence by day and/or night in child >5 yr

P10 Pediatrics

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Common Complaints

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Encopresis

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• definition fecal incontinence in a child >4 yr old, at least once per mo for 3 mo • prevalence: 1-1.5% of school-aged children (rare in adolescence); M:F = 6:1 in school-aged children • causes: chronic constipation (retentive encopresis), Hirschsprung disease, hypothyroidism, hypercalcemia, spinal cord lesions, anorectal malformations, bowel obstruction

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Retentive Encopresis • definition: child holds bowel movement develops constipation, leading to fecal impaction and seepage of soft or liquid stool (overflow incontinence) • etiology ■■ physical: painful stooling often secondary to constipation ■■ emotional: disturbed parent-child relationship, coercive toilet training social stressors • clinical presentation ■■ history ◆◆ crosses legs or stands on toes to resist urge to defecate ◆◆ distressed by symptoms, soiling of clothes ◆◆ toilet training coercive or lacking in motivation ◆◆ may show oppositional behaviour ◆◆ abdominal pain ■■ physical exam ◆◆ digital rectal exam or abdo x-ray: large fecal mass in rectal vault ◆◆ anal fissures (result from passage of hard stools) ■■ palpable stool in LLQ • management ■■ complete clean-out of bowel: PEG 3350 given orally is most effective, enemas and suppositories may be second line therapies, but these are invasive and often less effective ■■ maintenance of regular bowel movements (see Constipation Treatment, P36) ■■ assessment and guidance regarding psychosocial stressors ■■ behavioural modification • complications: recurrence, toxic megacolon (requires >3-12 mo to treat) bowel perforation

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Toilet Training

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• 90% of children attain bladder control before bowel control • generally, females train earlier than males • 25% by 2 yr (in North America), 98% by 3 yr have daytime bladder control • signs of toilet readiness ■■ ambulating independently, stable on potty, desire to be independent or to please caregivers (i.e. motivation), sufficient expressive and receptive language skills (2-step command level), can stay dry for several h (large enough bladder), can recognize need to go, able to remove clothing

Failure to Thrive

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Mid-Parental Height • Boys target height = (father ht + mother ht + 13) / 2 • Girls target height = (father ht + mother ht – 13) / 2 Note: height should be taken in cm

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Clinical Signs of FTT

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SMALL KID Subcutaneous fat loss Muscle atrophy Alopecia Lethargy Lagging behind normal Kwashiorkor Infection (recurrent) Dermat tis

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• definition ■■ weight 500 µg/d divided bid

Asthma

ibuprofen

5-10 mg/kg/dose PO q6-8h

Analgesic, antipyretic

iron

6 mg/kg/d elemental iron OD or divided tid

omeprazole

0.7-3.3 mg/kg/d (max dose 20 mg/d) OD or divided bid/tid

GERD

SE: headache, diarrhea, nausea, abdominal pain

ondansetron

0.15 mg/kg/dose (max dose 16 mg) q4-8h up to 3x

Post-operative N/V Gastroenteritis Cyclic vomiting

SE: QTc prolongation, orally disintegrating tablets contain phenylalanine (caution in PKU patients)

phenobarbital

3-5 mg/kg/d PO OD or bid

Seizures

SE: CNS depression

polyethylene glycol 3350 (PEG)

Disimpaction: 1-1.5 g/kg/d x 3 d Maintenance: starting dose at 0.4-1 g/kg

prednisone/ prednisilone

1-2 mg/kg/d PO x 5 d 3-4 mg/kg/d PO then taper to 1-2 mg/kg/d PO once platelet count >30 x 109/L 60 mg/m2/d PO

Asthma ITP Nephrotic syndrome

Oral prednisone is bitter tasting, consider using prednisilone

Acute asthma

Can cause tachycardia, hypokalemia, restlessness

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amoxicillin dexamethasone

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Drug Name

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Table 44 Commonly Used Medications in Pediatrics

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Source: Lau E (2009) The 2010-2011 Formulary – The Hospital for Sick Children

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SE: dark stoo constipation, dark urine

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Anemia

Maintenance treatment for asthma

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0.01-0.03 mL/kg/dose in 3 mL NS via nebulizer q0.5-4h prn 100-200 µg/dose prn, max 4-8 puffs frequency q4h

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salbutamol (Ventolin®)

Cautious use in patients with liver impairment, history of GI bleeding or ulcers

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fluticasone (Flovent®)

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References

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References

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Cardiology Bhandar A Bhandari V. Pitfalls, problems, and progress in bronchopulmonary dysplasia. Ped atrics 2009;123;1562-1573. Ganz . Sinus tachycardia. Rose BD (editor). Waltham: UpToDate. 2012. National Heart, Lung, and Blood Institute (Bethesda, Maryland). Task force on blood pressure control in children: report of the second task force on blood pressure control in children. Pediatrics 1987;79:1-2. Silversides CK, Kiess M, Beauchesne L, et al. Canadian Cardiovascular Society 2009 Consensus Conference on the management of adults with congenital heart disease: outflow tract obstruction, coarctation of the aorta, tetralogy of Fallot, Ebstein anomaly and Marfan’s syndrome. Can J Cardiol 2010; 26:e80 Singh RK, Singh TP. Etiology and diagnosis of heart failure in infants and children. Rose BD (editor). Waltham: UpToDate. 2013. Vick GW, Bezold LI. Classification of atrial septal defects (ASDs), and clinical features and diagnosis of isolated ASDs in children. Rose BD (editor). Waltham: UpToDate. 2014.

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Endocrinology Lenhard MJ, Reeves GD. Continuous subcutaneous insulin infusion: a comprehensive review of insulin pump therapy. Arch Int Med 2001;161:2293-3000. Muir A. Precocious puberty. Pediatr Rev 2006;27:373-380. Panagiotopoulos C, Riddell MC, Sellers EAC Canadian Diabetes Association 2013 Clinical Practice Guidelines for the Prevention and Management of Diabetes in Canada: Type 2 diabetes in children and adolescents. Can J Diabetes 2013;37(suppl 1):S163-S167. Silverstein J, Kilgensmith G, Copeland K, et l. Care of children and adolescents with type 1 diabetes: a statement of the American Diabetes Association. Diabetes Care 2005;28:186-208. Styne DM, Glaser NS. Nelson’s essentials of pediatrics, 4th ed. Philadelphia: WB Saunders, 2002. Endocrinology. 711 766. Wherrett D, Huot C, Mitchell B, et al Canadian Diabetes Association 2013 Clinical Practice Guidelines for the P evention and Management of Diabetes in Canada: Type 1 diabetes in children and adolescents. Can J Diabetes 2013;37(suppl 1):S153-S162

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Gastroenterology American Acad my of Pediatrics Subcommittee on Chronic Abdominal Pain. Chronic abdominal pain in children. Pediatrics 2005;115:812. Foisy M, Ali S Geist R, et al. The Cochrane Library and the treatment of chronic abdominal pain in children and adolescents: an overview of reviews. Evid-Based Child Health 2011;6:1027-1043. Friedman JN Risk of acute hyponatremia in hospitalized children and youth receiving maintenance intravenous fluids. Canadian Pediatric Society, 2013. Kirshner BS, Black DD. Nelson’s essentials of pediatrics, 3rd ed. Philadelphia: WB Saunders, 1998. The gastrointestinal tract. 419-458. Rowan-Legg A. Oral health care for children: a call for action. Canadian Pediatr c Society, 2013. Rowan-Legg A. Canadian Pediatric Society, Community Pediatrics Committee. Managing functional constipation in children. Pediatr Child Health 2011;16(10):661-665. Scott RB. Recurent abdominal pain during childhood. Can Fam Phys 1994;40:539-547.

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General Topics Albright EK. Pediatric history and physical examination, 4th ed. Current Clinical Strategies Publishing, 2003. American Academy of Pediatrics Task Force on Circumcision. Circumcision policy statement. Pediatrics 2012;130(3):585-86. Blank S, Brady M, Buerk E, et al. Male circumcision. Pediatrics 2012;130(3):e756-85. Canadian Task Force on Preventive Health Care Recommendations for growth monitoring, and prevention and management of overweight and obesity in children and youth in primary care. CMAJ 2015;187(6):411-21. Chan ES, Cummings C. Dietary exposures and allergy prevention in high-risk infants. Paediatr Child Health 2013:18(10):545-49. Critch JN. Nutrition for healthy term infants, birth to six months: an overview. Canadian Pediatric Society, 2013. D’Augustine S, Flosi T. Tarascon pediatric outpatient pocketbook, 1st ed. Tarascon Publishing, 2008. Dipchand A, Friedman J, Bismilla Z, et al.The Hospital for Sick Children handbook of pediatrics, 11th ed. Toronto: Elsevier Canada, 2009. Greer FR, Sicherer SH, Burks AW, et al. Effects of nutritional interventions on the development of atopic disease in infants and children: the role of maternal dietary restriction, breastfeeding, timing of introduction of complementary foods, and hydrolyzed formulas. Pediatrics 2008;129:183-191. Hospital for Sick Children. Clinical Practice Guidelines: fluid and electrolyte administration in children, 2011. Hospital for Sick Children handbook of pediatric emergency medicine. Sudbury: Jones and Bartlett, 2008. Klemola T, Vanto T Juntunen-Backman K, et al. Allergy to soy formula and to extensively hyd olyzed whey formula in infants with cows’ milk allergy: a prospective, randomized study with a follow-up to the age of 2 years. J Pediatr 2002;140:219 224. Lau E 2010-2011 Drug handbook and formulary. Toronto: Hospital for Sick Children Department of Pharmacy, 2009. McGahren ED, Wilson WG. Pediatrics recall, 3rd ed. Baltimore: Lippincott Williams & Wilkins, 2008. Nelson essentials of pediatrics, 5th ed. Philadelphia: Elsevier Saunders, 2006. Pediatric Emergency Medicine. Apparent life-threatening events. Saunders Elsevier, 2008. 269-272. Publicly funded immunization schedules for Ontario. August 2011. Scruggs K, Johnson MT. Pediatrics 5-minute reviews. Current Clinical Strategies Publishing, 2001-2002. Shields M. Measured obesity: overweight Canadian children and adolescents. Nutrition findings from the Canadian Community Health Survey. Statistics Canada, 2005.

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Genetic Disorders and Developmental Disorders Amato RSS. Nelson’s essentials of pediatrics, 4th ed. Philadelphia: WB Saunders, 2002. Human genetics and dysmorphology. 129-146. Blake KD, Prasad C. CHARGE syndrome, orphanet. J Rare Diseases 2006;1. Biggar W. Duchenne muscular dystrophy. Pediatr Rev 2006;27:83-88. Chudley AE, Conry J, Cook JL, et al. Fetal alcohol spectrum disorder: Canadian guidelines for diagnosis. CMAJ 2005;172(5 Suppl):S1-21. Moeschler JB, Shevell M. Committee on Genetics. Comprehensive evaluation of the child with intellectual disability or global developmental delays. Pediatrics 2014;134(3):e903-18. doi:10.1542/peds.2014-1839. Nicholson JF. Nelson’s essentials of pediatrics, 4th ed. Philadelphia: WB Saunders, 2002. Inborn errors of metabolism. 153-178. Vissers LE, van Ravenswaaij CM, Admiraal R, et al. Mutations in a new member of the chromodomain gene family cause CHARGE syndrome. Nat Genet 2004;36:955-957.

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Hematology Baker RD, Greer FR Committee on Nutrition American Academy of Pediatrics. Diagnosis and prevention of iron deficiency and iron-deficiency anemia in infants and young children (0-3 yr of age). Pediatrics 2010;126:1040-1050. Corrigan J, Boineau F. Hemolytic-uremic syndrome. Pediatr Rev 2001;22:365-369. Pearce JM, Sills RH. Childhood leukemia. Pediatr Rev 2005;26:96-102. Provan D, Stasi R, Newland AC, et al. International consensus report on the investigation and management of primary immune thrombocytopenia. Blood 2010;115:168 186. Segel GB Anemia. Pediatr in Rev 1988;10:77-88.

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Infectious Disease and Immunizations Advisory Committee Statement National Advisory Committee on Immunization. Volume 28. ACS-2. American Academy of Pediatrics. Committee on quality improvement: subcommittee on urinary tract infection. Practice parameter: the diagnosis, treatment, and evaluation of the initial urinary tract infection in febrile infan s and young children. Pediatrics 1999;103(4pt1):843. American Academy of Pediatrics. Red Book, 28th ed. 2009. Haemophilus influenzae infections: 2009 report of the committee on infectious diseases. 324. American Academy of Pediatrics. Red Book, 28th ed. 2009. Pertussis (whooping cough) 2009 report of the committee on infectious diseases. 504. Baraff LJ, Lee SI, Schriger DL. Outcomes of bacterial meningitis in children: a meta-analysis. Pediatr Infect Dis J 1993;12:389. Forgie S, Zhanel G, Robinson J. Canadian Paedia ric Society Infectious Diseases and Immunization Committee, 2009. Position statement on management of acute otitis media. Available from: http://www cps.ca/documents/position/ acute-otitis-media. National Advisory Committee on Immunization. Canadian Immunization Guide (CIG), 7th edition. Public Health Agency of Canada, 2006. Last modified 2014. Available at: http://www.phac-aspc.gc.ca/publicat/cig-gci/ Special Writing Group of the Committee. Rheumatic fever, endocarditis, and Kawasaki disease of the council on cardiovascular disease in the young of the American Heart Association. Guidelines for the diagnosis of rheumatic fever – Jones criteria, 1992 update. JAMA 1992;268:2069. Tiwari T, Murphy TV, Moran J, et al. National Immunization Program, CDC. Recommended antimicrobial agents for the treatment and postexposure prophylaxis of pertussis: 2005 CDC guidelines. MMWR Recomm Rep 2005;54(RR14):1. Wubbel L, McCracken D McCracken GH. Management of bacterial meningitis. Pediatr Rev 1998;19(3):78 84. Zorc JJ, Kiddoo DA Shaw KN. Diagnosis and management of pediatric urinary tract infections. Clin Microbiol Rev 2005;18:417.

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References

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Neonatology Barrington KJ, Sankaran K. Guidelines for detection, management and prevention of hyperbilirubinemia in term and late preterm newborn infants. Pediatr Child Health 2007;12:1B- 2B. Gomella TL, Cunningham MD, Eyal FG, et al. Neonatology: management, procedures, on-call problems, diseases and drugs, 5th ed. New York: McGraw-Hill, 2004. Assessment of gestational age. 21-28, 491-6, 559-62. Jain L, Douglas E. Physiology of fetal lung fluid clearance and the effect of Labor. Seminars in Perinatology, 2006. Joseph J, Zorc ZK. A cyanotic infant: true blue or otherwise? Pediatr Ann 2001;30(10):597-601. Meinzen-Der J, Poindexter B, Wrage L, et al. Role of human milk in extremely low birth weight infants’ risk of necrotizing enterocolitis or death. J Perinatol 2009;29:57-62. Niermeyer S, Kattwinkel J, Van Reempts P, et al. International guidelines for neonatal esuscitation: an excerpt from the guidelines 2000 for cardiopulmonary resus itation and emergency cardiovascular care: international consensus on science. Pediatrics 2000;106:E29.

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Nephrology Diven SC, Luther BT. A practical primary care approach to hematuria in children. Pediatr Nephrol 2000;14:65-72. Hogg RJ, Portman RJ, Milliner D, et al. Evaluation and management of proteinuria and nephrotic syndrome in children: recommendations from a pediatric nephrology panel established at the National Kidney Foundation Conference on proteinuria, albuminuria, risk assessment, detection and elimination (PARADE). Pediatrics 2000;105:1242-1249. Michael RS. Toilet training. Pediatr Rev 1999;20(7):240-245.

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Neurology Bergman I, Painter MJ. Nelson’s essentials of pediatrics, 4th ed. Philadelphia: WB Saunders, 2002. Neurology. 767-820. Hirtz D, Ashwal S, Berg A, et al. Practice parameter evaluation of a first nonfebrile seizure in children. Report of the quality s andards subcommittee of the American Epilepsy Academy of Neurology. The Child Neurology Society and The American Epilepsy Society. Neurology 2000;55:616-623. Levy RG, Cooper PN, Giri P. Ketogenic diet and other dietary treatments for epilepsy. Cochrane DB Syst Rev 2012;3:CD001903. Lewis DW, Ashawal S, Dahl G, et a Report of the Quality Standards Subcommittee of the American Academy of Neu ology and the Practice Committee of the Child Neurology Society. Practice parameter: evaluation of children and adolescents with recurrent headaches. Neurology 2002;59:490-498. Lewis D, Ashwal S, Hershey A, et al. American Academy of Neurology. Practice parameter: pharmac logical treatment of migraine headache in children and adolescents. Neurolo y 2004;63:2215-24. Tenembaum S. Clinical neurology and neurosurgery. Elsevier, November 2007. Disseminated encephalomyelitis in children.

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Oncology SEER Cancer Stat stics Review, National Cancer Institute. Bethesda, MD. Available at: http://seer.cancer.gov/faststats/selections.php?#Output (Accessed on April 04, 016 . Strahm B, Malkin D. Hereditary cancer predisposition In children: Genetic basis and cl nical implications. International Jounral of Cancer 2006;119,2001-2006.

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Respirology Canadian cystic fibrosis patient data registry report. Canadian Cystic Fibrosis Foundation, 2008. Ducharme FM, Dell SD, Radhakrishnan D, et al, Diagnosis and management of asthma in preschoolers: A Canadian Thoracic Society and Canadian PaediatricSociety position paper. Paediatr Child Health. 2015 Oct;20(7):353-71. Gadomski AM, Brower M. Bronchodilators for bronchiolitis. Cochrane DB Syst Rev 2010;12:CD001266. Garrison MM, Christakis DA, Harvey E, et al. Systemic corticosteroids in infant bronchiolitis: a meta-analysis. Pediatrics 2000;105:e44. Lougheed MD, Lemiere C, Dell SD, et al. Canadian Thoracic Society Asthma Management Continuum: 2010 consensus symmary for children six yr of age and over, and adults. Can Respir J 2010;17:15-24. Ortiz-Alvarez O, Mikrogianakis A. Canadian Pediatric Society Acute Care Committee. Managing the pediatric patient with an acute asthma exacerbation. Pediatr Child Health 2012;17(5):251-255. Summary of recommedations from the Canadian Asthma Consensus Guidelines, 2003 and Canadian Pediatric Asthma Consensus Guidelines, 2003 (updated December 2004) CMAJ 2005;173(suppl):S1-56.

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oo

Web-Based Resources http://www.medscape.com/home/topics/pediatrics. http://www.icondata.com/health/pedbase. http://www.cda-adc.ca. http://www.aboutkidshealth.ca. http://www.healthychildren.org. http://www.publichealth.gc.ca. http://www.cps.ca. www.uptodate.com.

.

c

fr

e.

fre

fre

e

c

Rheumatology Minich LL, Sleeper LA, Atz AM, et al, Pediatric Heart Network Investigators. Delayed diagnosis of Kawasaki disease: what are the risk factors? Pediatrics 2007;120(6):e1434. Newburger JW, Takahashi M, Gerber MA, et al. Diagnosis, treatment, and long-term management of Kawasaki disease: a statement for health professionals from the Committee on Rheumatic Fever Endocarditis and Kawasaki Disease, Council on Cardiovascular Disease in the Young, American Heart Association. Circulation 2004;110:2747 71 Olson JC. Nelson’s essentials of pediatrics, 3rd ed. Philadelphia: WB Saunders, 1998. Rheumatic diseases o childhood. 299-314. Wormser GP, Dattwyler RJ, Shapiro ED, et al. The clinical assessment, treatment, and prevention of Lyme disease, human granulocytic anaplasmosis, and babesiosis: clinical practi e guidelines by the Infectious Diseases Society of America. Clin Infect Dis 2006;43:1089.

P90 Pediatrics

Notes sf

Toronto Notes 2018



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c

Plastic Surgery

bo

ok s

s

Josephine D’Abbondanza, Maya Deeb, Matthew Lee, and Talha Maqbool, chapter editors Sangwoo Leem and Mark Shafarenko, associate editors Jin Kyu Kim and Shubham Shan, EBM editors Dr. Melinda A. Musgrave and Dr. Kyle R. Wanzel, staff editors

m

e

Basic Surgical Techniques. . . . . . . . . . . . . . . . . . . . 6 Sutures and Suturing Excision Skin Biopsy Types and Techniques

ee

Pediatric Plastic Surgery. . . . . . . . . . . . . . . . . . . . 39 Craniofacial Anomalies Congenital Hand Anomalies References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 41

o

Wounds. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8 Types of Wounds Infected Wounds Dressings Reconstruction

Aesthetic Surgery . . . . . . . . . . . . . . . . . . . . . . . 39 Aesthetic Procedures

k

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Skin Lesions and Masses . . . . . . . . . . . . . . . . . . 5 Differential Diagnosis of Skin Lesions/Masses Surgical Management of Malignant Skin Lesions

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Basic Anatomy Review. . . . . . . . . . . . . . . . . . . . . . 2 Skin Hand Brachial Plexus Face

Breast. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 34 Anatomy Breast Reduction Mastopexy (Breast Lift) Breast Augmentation Gynecomastia Breast Reconstruction Nipple Areolar Complex Reconstruction

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Acronyms. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2

ee

.

Soft Tissue Infections . . . . . . . . . . . . . . . . . Erysipelas Cellulitis Necrotizing Fasciitis

. . . 15

Ulcers. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16 Lower Limb Ulcers Pressure Ulcers

co

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Burns. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18 Burn Injuries Pathophysiology of Burn Wounds Diagnosis and Prognosis Indications for Transfer to Burn Centre Acute Care of Burn Patients Special Considerations . . 23

m

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Hand. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Traumatic Hand General Management of Hand Injuries Hand Infections Amputations Tendons Fractures and Dislocations Dupuytren’s Disease Carpal Tunnel Syndrome

Brachial Plexus. . . . . . . . . . . . . . . . . . . . . . . . . . . . 30

co

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Craniofacial Injuries. . . . . . . . . . . . . . . . . . . . . . . . 31 Approach to Facial Injuries Mandibular Fractures Maxillary Fractures Nasal Fractures Zygomatic Fractures Orbital Floor Fractures

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PL

Plastic Surgery PL1

Toronto Notes 2018

PL2 Plastic Surgery

Toronto Notes 2018

c

Acronyms

fr

Acronyms

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eb

m

e.

c

m

o

o

b

RL Ringer’s lactate ROM range of motion SGAP superior gluteal artery perforator SIADH syndrome of inappropriate antidiuretic hormone SIEA superficial inferior epigastric artery SLP speech language pathology SOF superior orbital fissure STSG split thickness skin graft TBSA total body surface area TMJ temporomandibula joint TRAM transverse rectus abdominus myocutaneous UCL ulnar collateral ligament UV ultraviolet

IP interphalangeal IVIg intravenous immunoglobulin MC metacarpal MCP metacarpal phalangeal joint NCV nerve conduction velocity NS normal saline NSAIDs nonsteroidal anti-inflammatory drugs OM otitis media OR operating room ORIF open reduction internal fixation PIP proximal interphalangeal joint PMN polymorphonuclear PVD peripheral vascular disease RA rheumatoid arthritis

om

diabetes mellitus DM EMG electromyography ENT ear, nose, throat EOM extraocular movement EPB extensor pollicis brevis FDP flexor digitorum profundus FDS flexor digitorum superficialis FTSG full thickness skin graft GBS group B Streptococcus HTN hypertension I&D incision and drainage ICP intracranial pressure ICU intensive care unit IGAP inferior gluteal artery perforator

ABI ankle brachial index ABG arterial blood gas APL abductor pollicis longus ARDS acute respiratory distress syndrome ATLS advanced trauma life support BMR basal metabolic rate CHF congestive heart failure CMC carpo-metacarpal CO carbon monoxide CSF cerebrospinal fluid CVD cerebrovascular disease CXR chest x-ray D5W 5% dextrose in water DIEP deep inferior epigastric perforator DIP distal interphalangeal joint

fe

Basic Anatomy Review

m

o

Skin

Thin

Medium

Upper (papillary) Dermis

Lower (reticular)

o

Subcutaneous tissue

Supplied mainly by D

© Karen Petruccelli

sf

Full thickness skin graft

Supplied mainly by C

e

Thick

re

Split thickness skin graft

Epidermis

Figure 1. Split and full thickness skin grafts

Hand

A

m

5

Figure 3. Carpal bones

© Jackie Robers

C A: B: C: D:

D

Superficial palmar arch Deep palmar arch Ulnar artery Radial artery

Figure 2. Arterial supply in the hand

Radial

m

4

8 9 10 11

Ulnar

Dorsal View

Figure 4. Sensory distribution in the hand

e.

3

Median

e

2

6 7

Radius Scaphoid Trapezium Trapezoid Capitate Ulna Lunate Pisiform Triquetrum Hamate Metacarpal bones

© Teresa McLaren 2003

1

1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11.

Ulnar

Volar View

© Karyn Ho 2014

B

BONES AND NERVES

PL3 Plastic Surgery

Toronto Notes 2018

2

o

DIP Central slip

Flexor digitorum profundus

1

sf

s

Lateral bands

Distal interphalangeal joint

© Ashley Hui 2016

c

Basic Anatomy Review

5 6 7

3 4

PIP

Proximal interphalangeal joint

Extensor hood

8

Oblique fibres

c

Sagittal fibres Camper’s chiasm Flexor digitorum superficialis

© Crista Mason 2005

1. Hyponychium 2. Sterile matrix 3. Germinal matrix 4. Ventral floor 5. Lunula

Extensor digitorum communis

6. Eponychium 7. Dorsal root 8. Distal phalanx 9. Extensor tendon 10. Flexor tendon

m

Interosseous muscles © Qing Huang 2005

Figure 7. Nail anatomy

Figure 6. Extensor mechanism of digits

o

Flexor Tendons All require OR repair

c

o

10

s

Metacarpal phalangeal joint

Figure 5. Flexor tendon insertion at PIP and DIP

9

MCP

Lumbrical

e

Palmar

Extensor Tendons ER repair unless proximal/multiple tendons

Flexor carpi radialis tendon Flexor pollicis longus tendon Trapezium

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Flexor digitorum superficialis tendons Flexor digitorum profundus tendons Hamate

Trapezoid

Capitate

Dorsal

Carpal Bone Mnemonic © Diego Accorsi 2011

Median nerve

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Palmaris longus tendon Ulnar artery Ulnar nerve

Flexor retinaculum

Figure 8. Carpal tunnel

9 7

10

1. Extensor retinaculum Compartment 1 2. Abductor pollicis longus 3. Extensor pollicis brevis Compartment 2 4. Extensor carpi radialis brevis 5. Extensor carpi radialis longus Compartment 3 6 Extensor pollicis longus (EPL tendon passes around Lister’s tubercle) Compartment 4 7. Extensor digitorum 8. Extensor indicis Compartment 5 9. Extensor digiti minimi Compartment 6 10. Extensor carpi ulnaris

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Figure 9. Extensor compartment of the wrist (dorsal view and cross-sectional view)

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3 2

2 3

8

1 6 4 5

s

9

7

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10

8

f

1 6 4 5

So Long to Pinky. Here Comes The Thumb. Scaphoid Lunate Triquetrum Pisiform Hamate Capitate Trapezoid Trapezium

PL4 Plastic Surgery

Toronto Notes 2018

c

Basic Anatomy Review

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Brachial Plexus Brachial Plexus Rob Thomas Drinks Cold Beers Roots Trunks Divisions Cords Branches

o

C4

Dorsal scapular

C5

Suprascapular ior

r nte

m

r

Pos

o

Anterior

ral

Late

C6

Nerve to subclavius

teri o

A

Lateral pectoral Musculocutaneous

r

erio

Sup

C7

Middle

rior

ste

Po

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Axillary

Po

ste

erior

Radial

Post

C8

rio

r

r

rio

Infe

T1

Lower subscapular

ter

An

T2

Medial pectoral

Ulnar

Long thoracic nerve

CORDS

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BRANCHES

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Medial cutaneous nerves of arm and forearm

DIVISIONS

Figure 10. Brachial plexus anatomy

TRUNKS

ROOTS

© Julian Kirk-Elleker 2006

Median

m

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Upper subscapular Thoracodorsal ial Med

ior

o

Face 10

10

8

1

5 6

7 2

6 2

3

Figure 11. Skull and facial bones

6. 7. 8. 9. 10.

Sphenoid bone Temporal bone Parietal bone Occipital bone Frontal bone

© Julian Kirk-Elleker 2006

m

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1. Lacrimal bone 2. Zygomatic bone 3. Maxilla 4. Mandible 5. Nasal bone

o

9 4

4

3

PL5 Plastic Surgery

Toronto Notes 2018

c

Skin Lesions and Masses

Frontal bar Lateral maxillary (+ lateral orbital wall) Upper transverse maxillary (+ orbital floor) Medial maxillary (+ medial orbital wall)

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Lower transverse maxillary (+ palate) Posterior vertical Upper transverse mandibula Lower transverse mandibular

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Figure 12 Craniofacial horizontal and vertical buttresses

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b

Skin Lesions and Masses Differential Diagnosis of Skin Lesions/Masses

m

• for background information and medical management (see Dermatology, D5) • for biopsy techniques, see Skin Biopsy Types and Techniques, PL7

c

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Surgical Management of Malignant Skin Lesions

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• surgical treatment for all malignant skin lesions involve total excision of the primary lesion • excision margin of lesion depends on the type of lesion, the lesion diameter, and (for melanoma) the lesion depth • for decisions regarding reconstruction using flaps or skin grafts, see Reconstruction, PL11

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Precursors of Malignant Lesions

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Table 1. Precursors Squamous Cell Carcinoma

Malignant Melanoma

Nevus sebaceous of Jadassohn

Actinic keratosis Bowen’s disease Bowenoid papulosis Leukoplakia Erythroplasia

Lentigo maligna Giant congenital nevus Dysplastic nevus



m

Basal Cell Carcinoma



Surgical Margins

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Table 2. Surgical Margins for Basal Cell Carcinoma Surgical Margins 3 mm 3-5 mm

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Type of Lesi n Low Risk High Risk*

b

m

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*High risk features include: diameter and location (>20 mm trunk, >6 mm face hands, and feet), poorly defined borders, recurrent lesion, poor differentiation, and type of lesion (e.g. morpheoform)

Table 3. Surgical Margins for Squamous Cell Carcinoma Type of Lesion Low Risk High Risk*

Surgical Margins 4 mm 5-10 mm

o

o

*High risk features include: depth >2 mm, facial lesions, poorly defined borders, recurrent lesion, perineural invasion, po r differentiation, and type of lesion (e.g. morpheoform)

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Surgical Margins 0.5 cm 1 cm 1-2 cm 2 cm

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Depth of Lesion In situ 24 h, including ulcers) • tetanus prophylaxis (see Table 8 and Figure 16) • irrigation and debridement ■■ traumatic tattooing can occur if foreign materials left in wound • systemic antibiotics • topical antimicrobials: beneficial for minor wounds, but no additional benefit for wounds requiring systemic antibiotics. May aid in healing of chronic wounds • closure: final closure via secondary intention (most common), delayed wound closure (3° closure), skin graft, or flap; successful closure depends on bacterial count of ≤105/cm3 prior to closure and frequent dressing changes

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Tetanus Prophylaxis in Routine Wound Management ASSESS WOUND

A clean, minor wound

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All other wounds (contaminated with dirt, feces, saliva, soil; puncture wounds; avulsions; wounds resulting from flying or crushing objects, animal bites, burns, frostbite)

Has patient completed a primary tetanus diphtheria series?1,7 NO/ UNKNOWN

YES

Administer vaccine today Instruct patient to complete series per age-appropriate vaccine schedule

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2,3,4

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Vaccine not needed today Patient should receive next dose at 10 year interval after last dose

Tdap* is preferred for persons 10-64 years of age if using Adacel™‡ or ≥10 years of age if using Boostrix™‡ who have never received Tdap Td is preferred to tetanus toxoid (TT) for persons 7-9 years f age, or ≥65 years of age if only Adacel™‡ is available, or those who have received a Tdap previously. If TT is administered, an adsorbed TT product is preferred to fluid TT (all DTaP/DTP/Tdap/DT/Td products contain adsorbed tetanus toxoid) Give TIG 250 U IM for all ages. It can and should be given simultaneously with the tetanus-containing vaccine For infants Bacteroides • mechanism: most commonly over dorsal MCP from a punch in mouth; “fight-bite” • serious, as mouth has 109 microorganisms/mL, which get trapped in joint space when fist unclenches and overlying skin forms an air-tight covering ideal for anaerobic growth – can lead to septic arthritis • investigations ■■ radiographs prior to therapy to rule out foreign body e.g. tooth) or fracture ■■ culture for aerobic and anaerobic organisms, Gram stain • treatment ■■ urgent surgical exploration of joint, drainage, and debridement of infected tissue ■■ wound must be copiously irrigated ■■ Clavulin® 500 mg PO q8h or (if penicillin allergy) clindamycin 300 mg PO q6h + ciprofloxacin 500 mg PO q12h + secondary closure ■■ splint

Dressings

m

m

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Negative-pressure wound therapy or vacuumassisted closure (VAC) uses sealed vacuum dressings that suction wound fluid and promote increased blood flow to enhance the healing process. VACs may be placed under deep wounds or to enhance skin graft take

sf

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• dressing selection depends on the wound characteristics and surgeon preference ■■ as the wound progresses through healing, it will require different types of dressings; therefore, routine inspection is recommended ◆◆ principles of dressing clean vs. infected wounds – clean wounds can be dressed with non-adherent dressing (which is non-adhering to epithelializing tissue); requires secondary dressing – infected wounds may need debridement and antibiotics and can be dressed with iodine gauze, silver-containing dressings, or antimicrobial dressings ◆◆ moist vs. dry wounds – purpose of dressings should be to promote moist wound healing i.e. moistening dry wounds or drying (removing excess exudate/blood) wet wounds ◆◆ wide-based vs. cavitary/tunnelling wounds – cavitary or tunnelling wounds (i.e. through a fascial layer) can be packed with saline-soaked ribbon gauze (non-infected) or Betadine®-soaked ribbon gauze (infected)

PL12 Plastic Surgery

Toronto Notes 2018

c

Wounds

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Table 9. Recommended Dressings for Wound Type Dressing Material

Superficia

Lightly exuding

Films (Opsite®), hydrogels (Intrasite®, Nu-gel®, Duoderm®) Contact layers

Light to moderately exuding wounds

Deep

Amorphous gels, hydrogels, hydrocolloids (Duoderm®, Tegaderm®), collagen, hypertonic saline gauze (Mesalt®)

e

Any exudate level

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Exudate Level

k

Wound Depth

Foams (Mepilex®, Allevyn®), alginates (Sorbsan®, Kalto-stat®), hypertonic saline gauze, hydrofibre (Aquacel®)

m

m

Moderately to heavily exuding wounds Adapted from Grabb & Smith’s Plastic Surgery, 6th ed. Chapter 3, Table 3.3

o

Reconstruction Reconstruction Ladder Free flap

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Definition • an approach to wound management with successively more complex methods of treatment • surgeons should start with the least complex method and progressively increase in complexity as appropriate

e

e.

RECONSTRUCTION LADDER

Tissue expansion

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Pedicle flap

SKIN GRAFTS

Random pattern flap

Definition • tissue composed of epidermis and varying degrees of dermis, that does not carry its own blood supply. Survival requires the generation of new blood vessels from the recipient site bed

m

Full thickness graft Split thickness graft Delayed closure

m

s

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b

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Classification of Skin Grafts 1. by species ■■ autograft: from same individual ■■ allograft (homograft): from same species, different individual ■■ xenograft (heterograft): from different species (e.g. por ine) 2. by thickness: see Table 10

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Primary closure

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Healing by secondary intention ©Andrea Lam 2017

Figure 17. Reconstructive ladder - in order of increasing complexity

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Partial Thickness Skin Graft Survival • 3 phases of skin graft “take” 1. plasmatic imbibition: diffusion of nutrition from recipient site (first 48 h) 2. inosculation: vessels in graft connect with those in recipient bed (d 2-3) 3 neovascular ingrowth: graft revascularized (d 3-5) • requirements for graft survival ■■ well-vascularized bed (recipient site). Unsuitable beds include: bone, tendon, heavily irradiated, infected wounds, etc. ■■ good contact between graft and recipient bed. Staples, sutures, splinting, and pressure dressings are used to prevent movement/ shearing of graft and hematoma or seroma formation ■■ low bacterial count at recipient site (95% • types: muscle and skin (common), bone, jejunum, omentum, fascia • e.g. radial forearm, scapular, latissimus dorsi

Characteristic

Normal

Arterial Insufficiency

Colour

Pink

Pale

.c

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Table 12. Characteristics of Healthy Free Flap

Warm

Cool

Arterial Pulse (Doppler)

+

–

±

Turgor

Soft, but with some firmness

Decreased tissue firmness

Increased (tissue firmness with tissue stiffness)

2-5 s

>5 s

45 yr Slow progression

ABI in diabetics can be falsely normal due to incompressible arteries secondary to plaques/ calcification

c

Dependent edema, trauma Rapid onset ± thrombophlebitis, varicosities

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History

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Arterial

o

Cause

Venous (70% of vascular ulcers)

e

Characteristic

PL17 Plastic Surgery

Toronto Notes 2018

Ulcers

e

Table 14. Venous vs. Arterial vs. Diabetic Ulcers (continued) Diabetic

Pulses

Normal distal pulses

Decreased or no distal pulses

Decreased pulses likely (take caution in calcified vessels)

Vascular Exam

ABI >0.9 Doppler; abnormal venous system

ABI 6 h of pressure 4. ulcer: necrotic area breaks down – N.B. skin is like tip of an iceberg

m

m

e

Classification (National Pressure Ulcer Advisory Panel 2014) • Stage I: non-blanchable erythema present >1 h after pressure relief, skin intact • Stage II: partial-thickness skin loss • Stage III: full-thickness skin loss into subcutaneous tissue • Stage IV: full-thickness skin loss into muscle, bone, tendon, or joint ■■ if an eschar is present, must fully debride before staging possible • Stage X: unstageable ulcer

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Prevention • good nursing care (clean dry skin, frequent repositioning), special beds or pressure relief surface, proper nutrition, activity early identification of individuals at risk (e g. immobility, incontinence, paraplegia, immunocompromised, DM, etc.)

m

o

Complications • cellulitis, osteomyelitis, sepsis, gangrene

b

eb

bo

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Treatment • depends on individual patient and condition • treat underlying medical issues including nutrition • continue with preventative measures (pressure relief, assess for pressure points e.g. wheelchairs; manage continence issues, divert contaminants e.g. urine and feces) • wound debridement, moisture retentive or antimicrobial dressing, regular reassessment • systemic antibiotics for infections • assess for possible reconstruction

PL18 Plastic Surgery

Toronto Notes 2018

c

Burns

fr

Burns

o

Burn Injuries

b

Causal Conditions • thermal (flame contact, scald) • chemical • radiation (UV, medical/therapeutic) • electrical Most Common Etiology • children: scald burns • adults: flame burns

Consequence of Burn Injury

Intervention Required

Thermoregulation

Prone to lose body heat

Must keep patient covered and warm

Control of fluid loss

Loss of large amounts of water and protein from the skin and other body tissues

Adequate fluid resuscitation is imperative

High risk of infection

Antimicrobial dressings (systemic antibiotics if signs of specific infection present)

eb

m

Mechanical barrier to bacterial invasion and immunological organ

e

b

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Skin Function

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Table 15. Skin Function and Burn Injury

Tetanus prophylaxis if not already administered

m

Pathophysiology of Burn Wounds

Skin surface

c

Epidermis

e

Dermis: Nerves Vessels

sf

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co

Circumferential burns can restrict respiratory excursion and/or blood flow to extremities and require escharotomy

b

k

TBSA does not include areas with 1° burns

m

b

Prognosis best determined by burn size (TBSA), age of patient, presence/absence of inhalation injury

e.

om

om

e

fre

Zone of coagulation

Blood vessels and nerves are found in the dermis Figure 19. Zones of thermal injury

• burn size ■■ % of TBSA burned: rule of 9s for 2° and 3° burns only (children 0.5 cc/kg h (adults) and 1.0 cc/kg/h in children 10% TBSA, or deeper than superficial-partial thickness, need 0.5 cc tetanus toxoid ■■ also give 250 U of tetanus Ig if prior immunization is absent/unclear, or the last booster >10 yr ago • baseline laboratory studies (Hb, U/A, BUN, CXR, electrolytes, Cr, glucose, CK, ECG, cross-match if traumatic injury, ABG, carboxyhemoglobin) • cleanse, debride, and treat the burn injury (antimicrobial dressings) • early excision and grafting important for outcome

PL21 Plastic Surgery

Toronto Notes 2018

Burns

e

Burn Wound Healing

s

Table 17. Burn Shock Resuscitation (Parkland Formula) Hour 24 30

0.35-0.5 cc plasma/kg/%TBSA

>Hour 30

D5W at rate to maintain normal serum sodium

e

o

4 cc RL/kg/% TBSA with 1/2 of total in first 8 h from time of injury and 1/2 of total in next 16 h from time of injury

bo

Hour 0-24

*Do not forget to add maintenance fluid to resuscitation

Table 18. Burn Wound Healing Healing

m

Depth

No scarring; complete healing

First degree

e.

Second degree (Superficial partial)

Spontaneously re-epithelialize in 7-14 d from retained epidermal structures ± residual skin discolouration

fr

Hypertrophic scarring uncommon; grafting rarely required Re-epithelialize in 14-35 d from retained epidermal structures

k

k

Deep secon degree (Deep partial)

oo

Hypertrophic scarring frequent

eb

Grafting recommended to expedite healing Re-epithelialize from the wound edge

m

Third degree (Full thickness)

Grafting/flap necessary to replace dermal integrity, limit hypertrophic scarring Often results in amputations

Fourth degree

m

If not requiring amputation, needs flap for coverage after debridement (do not reepithelialize, cannot graft)

None or transient

Adverse Effects

Minimal

May cause methemoglobinemia, stains (black), leaches sodium from wounds

Medium, does not penetrate eschar

May stain, producing a pseudoeschar or facial discolouration (argyria-like symptoms); raised liver enzymes

eb

Nanocrystalline silvercoated dressing (Acticoat®)

Penetration

c

m

Silver nitrate (0.5% solution)

None

m

Pain with Application

bo

Antibiotic

oo

ks

Table 19. Antimicrobial Dressings for Burns

Minimal

Medium, penetrates eschar poorly Most commonly used

Slowed healing, leukopenia, mild inhibition of epithelialization

(Sulfamylon®)

Moderate

Well, penetrates eschar

Mild inhibition of epithelialization, may cause metabolic acidosis with wide application

sf

e

Silver sulfadiazine (cream) (Flamazine®, Silvadene®)

re

Risk Factors for Infection of Burn Wounds

s

Patient Related • Extent >30% TBSA • Depth: full-thickness and deep partialthickness • Patient age (higher risk with very young and very old) • Comorbidities • Wound dryness • Wound temperature • Secondary impairment of blood flow to wound • Acidosis

e.

co

Microbial Factors • Density >105 organisms per gram of tissue • Motility • Virulence and metabolic products (endotoxin, exotoxin, permeability factors, other factors) • Antimicrobial resistance

re

m

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fre

e.

e. co

m

m

m

bo

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ks

fr

fre

Treatment • 3 stages 1. assessment: depth determined 2. management: specific to depth of burn and associated injuries 3. rehabilitation • first degree ■■ treatment aimed at comfort ■■ topical creams (pain control, keep skin moist) ± aloe ■■ oral NSAIDs (pain control) superficial second degree/partial thickness ■■ daily dressing changes with topical antimicrobials (such as polysporin); leave blisters intact unless circulation impaired or over joint and inhibiting motion • deep second degree/deep partial thickness and third degree/full thickness ■■ prevent infection and sepsis (significant complication and cause of death in patients with burns) ◆◆ most common organisms: S. aureus, P. aeruginosa, and C. albicans – day 1-3 (rare): Gram-positive – day 3-5: Gram-negative (Proteus, Klebsiella) ◆◆ topical antimicrobials: treat colonized wounds (from skin flora, gut flora, or caregiver) ■■ remove dead tissue ◆◆ surgically debride necrotic tissue, excise to viable (bleeding) tissue

PL22 Plastic Surgery

Toronto Notes 2018

c

Burns

s

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• early excision and grafting is the mainstay of treatment for deep/full thickness burns • initial dressing should decrease bacterial proliferation • prevention of wound contractures: pressure dressings, joint splints, early physiotherapy

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Other Considerations in Burn Management

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Altered Hemodynamics ( CO  SVR) Vascular Permeability and Edema Hypermetabolism

SEVERE BURN

Progressive Pulmonary Insufficiency

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Immunosuppression

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Renal Failure (2º to  Renal Blood Flow)

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Increased Gut Mucosal Permeability (GI Bleed Risk)

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Figure 22. Systemic effects of severe burns

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• nutrition ■■ hypermetabolism: TBSA >40% have BMR 2-2.5x predicted ■■ consider nutritional supplementation e.g. calories, vitamin C, vitamin A, Ca2+, Zn2+, Fe2+ • immunosuppression and sepsis ■■ must keep bacterial count 48 h post-burn, mental status changes, azotemia, thrombocytopenia, hypofibrinogenemia, hyper/hypoglycemia (especially if burn >40% TBSA) • GI bleed may occur with burns >40% TBSA (usually subclinical) ■■ treatment: tube feeding or NPO if there is a GI bleed, antacids, H2 blockers (preventative) • renal failure secondary to under resuscitation, drugs, myoglobin, etc. • progressive pulmonary insufficiency ■■ can occur after: smoke inhalation, pneumonia, cardiac decompensation, sepsis • wound contracture and hypertrophic scarring (outcomes optimized with timely wound closure, splinting, pressure garments) and physiotherapy

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Special Considerations

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CHEMICAL • major categories: acid burns, alkaline burns, phosphorous burns, chemical injection injuries • common agents: cement, hydrofluoric acid, phenol, tar • mechanism of injury: chemical solutions coagulate tissue protein leading to necrosis ■■ acids → coagulation necrosis ■■ alkalines → saponification followed by liquefactive necrosis • severity related to: type of chemical (alkali worse than acid), temperature, volume, concentration, contact time, site affected, mechanism of chemical action, degree of tissue penetration • burns are deeper than they initially appear and may progress with time

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Treatment (General) • ABCs, monitoring • remove contaminated clothing and brush off any dry powders before irrigation • irrigation with water for 1-2 h under low pressure (contraindicated in heavy metal burns, such as sodium, potassium, magnesium, and lithium; in these cases, soak in mineral oil instead) • inspect eyes, if affected: wash with saline and refer to ophthalmology • inspect nails, hair, and webspaces • correct metabolic abnormalities and tetanus prophylaxis if necessary • contact poison control line if necessary • local wound care 12 h after initial dilution (debridement) • wound closure same as for thermal burn • beware of underestimated fluid resuscitation, renal, liver, and pulmonary damage Special Burns and Treatments Water irrigation, followed by dilute solution of sodium bicarbonate

Hydrofluoric Acid

Water irrigation; clip fingernails to avoid acid trapping; topical calcium gel ± subcutaneous injection of calcium gluconate ± 10% calcium gluconate IV depending on amount of exposure and pain

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T eat with soap/lime prior to irrigation, as direct water exposure produces extreme heat

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Tar

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Sulfuric Acid

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Acid Burn

Remove with repeated application of petroleum-based an ibiotic ointments (e.g. Polysporin®)

PL23 Plastic Surgery

Toronto Notes 2018

Hand

s

Tissue Resistance to Electrical Current nerve < vessel/blood < muscle < skin < tendon < fat < bone

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ELECTRICAL BURNS • depth of burn depends on voltage and resistance of the tissue (injury more severe in tissues with high resistance) • often presents as small punctate burns on skin, with extensive deep tissue damage which requires debridement • electrical burns require ongoing monitoring, as latent injuries can occur • watch for system-specific damages and abnormalities ■■ abdominal: intraperitoneal damage ■■ bone: fractures and dislocations especially of the spine and shoulder ■■ cardiopulmonary: anoxia, ventricular fibrillation, arrhythmias ■■ muscle: myoglobinuria indicates significant muscle damage → compartment syndrome ■■ neurological: seizures and spinal cord damage ■■ ophthalmology: cataract formation (late complication) ■■ renal: ATN resulting from toxic levels of myoglobin and hemoglobin ■■ vascular: vessel thrombosis → tissue necrosis (increased Cr, K+, and acidity), decrease in RBC (beware of hemorrhages/delayed vessel rupture)

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Treatment • ABCs, primary and secondary survey, treat associated injuries • beware of cardiac arrhythmias (continue cardiac monitoring) • monitor: hemochromogenuria, compartment syndrome, urine output • wound management: topical agent with good penetrating ability (silver sulfadiazine or mafenide acetate) • debride nonviable tissue early and repeat prn (every 48 h) to prevent sepsis • amputations frequently required FROSTBITE • see Emergency Medicine, ER46

Hand

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Traumatic Hand

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Table 20. Key Features of the History and Physical Exam of the Inju ed Hand HISTORY Diabetes

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Smoking status

Time and place of accident

Last oral intake

Mechanism of injury

Abnormal cascade (fingers normally slightly flexed and point towards scaphoid), scissoring

Deformity

Bony protrusions or specific deformities (e.g. mallet, boutonnière, and swan neck deformity)

Bruising or swelling

May indicate underlying skeletal injury

Sweating pattern (usually felt more so than from observation)

May indicate denervation

Anatomical structures beneath

If open laceration, need to explore within wound (under sterile conditions)

Structure

Examination

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c

Position of finger

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TIN AX Tetanus prophylaxis Irrigate with NS (copious irrigation and debridement in a timely manner) NPO (NPO if you are considering replanting or an urgent OR, otherwise most operations are done as elective procedures) Antibiotic prophylaxis (controversial – most require no ABx, mainly needed for animal bites and dirty wounds) X-rays

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Digital arteries

Assess capillary refill (50% of the nail surface area need to be drained (trephination), done under a digital block by puncturing nail plate • if suspecting greater severity of injury (e.g. distal phalanx displaced fracture, laceration of nail bed), remove nail plate to examine underlying nailbed under digital block anesthesia • irrigate wound and nail thoroughly • suture repair of nailbed with chromic suture • replace cleaned nail, which acts as a splint for any underlying distal phalangeal fracture and prevents adhesion formation between nail fold and nailbed

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Hand Exam • Never blindly clamp a bleeding vessel as nerves are often found in close association with vessels • Never explore any volar hand wound in the ER • Arterial bleeding from a volar digital laceration is likely associated with a nerve laceration (nerves in digits are superficial to arteries)

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Vessels • often associated with nerve injury (anatomical proximity) • control bleeding with direct pressure and hand elevation • if digit devascularized, optimal repair within 6 h • close skin, then dress, immobilize, and splint hand with fingertips visible • monitor colour, capillary refill, skin turgor, fingertip temperature post-revascularization

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Nerves • test the nerve function BEFORE putting in local anesthesia • primary repair for a clean injury within 7 d and without concurrent major injuries; secondary repair if >7 d (may require nerve graft) • epineurial repair of all digital nerves with minimal tension • post-operative: dress wound, elevate hand, and immobilize • Tinel’s sign (cutaneous percussion over the repaired nerve) produces paresthesias and defines level of nerve regeneration ■■ Wallerian degeneration occurs in the first 2 wk, which is why there is no Tinel’s sign until after this time period ■■ a peripheral nerve regenerates at 1 mm/d ■■ paresthesias felt at area of percussion because regrowth of myelin (Schwann cells) is slower than axonal regrowth → percussion on exposed free-end of axon generates paresthesia

PL25 Plastic Surgery

Toronto Notes 2018

Hand

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Hand Infections

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Principles • trauma is most common cause • 5 cardinal signs: rubor (red), calor (hot), tumour (swollen), dolor (painful), and functio laesa (loss of function) • 90% caused by Gram-positive organisms • most common organisms (in order) – S. aureus, S. viridans, Group A Streptococcus, S. epidermidis, and Bacteroides melaninogenicus (MRSA is becoming more common)

TYPES OF INFECTIONS

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Deep Space Infections • abscess formation in deep spaces of the hand, most commonly thenar or mid-palm space • uncommon, there are 9 spaces in the hand

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Felon • definition: abscess in the pulp of a fingertip or thumb that occurs following a puncture wound into the pad of the digit; may be associated with osteomyelitis (akin to compartment syndrome and can lead to skin necrosis) • treatment: elevation, warm soaks, cloxacillin 500 mg PO q6h (if in early stage); if obvious abscess or pressure on the overlying skin or failure to resolve with conservative measures, then needs I&D, take cultures/gram stain and adjust antibiotics to culture results

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Flexor Tendon Sheath Infection • Staphylococcus > Streptococcus > Gram-negative rods • definition: abscess within the flexor tendon sheath (flexor tenosynovitis), commonly caused by a penetrating injury and can lead to tendon necrosis and rupture if not treated; it is often suppurative; however, there can be very little pus early on • clinical features: Kanavel’s 4 cardinal signs 1. point tenderness along flexor tendon sheath 2. severe pain on pas ive extension of digit 3. fusiform swelling of entire digit 4. flexed posture (increased comfort) • treatment ■■ OR I&D, copious irrigation and debridement, IV antibiotics, resting hand splint until infection resolves, aggressive hand therapy after

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Herpetic Whitlow • HSV-1, HSV-2 • definition: painful vesicle(s) around fingertip or thumb ■■ often found in medical/dental personnel and children • clinical features: can be associated with fever, malaise and lymphadenopathy, prodromal phase ■■ patient is infectious until lesion has completely healed • treatment: diagnosed clinically, if in doubt confirm with viral culture/PCR or Tzanck smear, usually self-limited, consider oral acyclovir in severe cases; I&D is contraindicated

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Paronychia • acute = Staphylococcus; chronic = Candida • definition: infection (granulation tissue) of soft tissue around fingernail (within the paronychium and/ or beneath eponychial fold) • etiololgy ■■ acute paronychia: a “hangnail”, artificial nails, and nail biting ■■ chronic paronychia: prolonged exposure to moisture • treatment ■■ acute paronychia: warm compresses and oral antibiotics if caught early; if abscess present, drainage with blade (avoid hitting nail bed) and oral/IV antibiotics; if abscess extends to below nail plate, nail plate removal may be required ■■ chronic paronychia: anti-fungals, eponychial marsupialization, nail plate removal may be required

PL26 Plastic Surgery

Toronto Notes 2018

Hand

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Amputations

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Hand or Finger • emergency management: injured patient and ampu ated part require attention ■■ patient: x-rays (stump and amputated part), NPO, clean wound and irrigate with NS, dress stump with nonadherent dressing, cover with dry sterile dressing, tetanus and antibiotic prophylaxis (cephalosporin/erythromycin) ■■ amputated part: x-rays, gently irrigate with RL, wrap amputated part in a NS/RL soaked sterile gauze and place inside waterproof plastic bag, place in a container, then place container on ice • indications for replantation ■■ age: children often better results than adults ■■ level of injury: thumb and multiple digit amputations are higher priority; multiple level amputation is a contraindication to replant ■■ nature of injury: clean cut injuries have greater success; avulsion and crush injuries are relative contraindications to replant • if replant contraindicated, manage stump with revision amputation ■■ involves debriding stump of wound, trimming back the bone and nerve endings, and gently closing the skin ■■ commonly done in the ER under digital block

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Tendons

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Common Extensor Tendon Deformities Table 21. Extensor Tendon Deformities Zone (see Figure 23)

Etiology/Clinical Features

Treatment

Mallet Finger

DIP flexed with loss of active extension

1

There are bony and non-bony mallets Bony: Fracture of distal phalanx distal to tendon insertion Non-bony: Forced flexion of the extended DIP leading to extensor tendon rupture at DIP (e.g. sudden blow to tip of the finger)

Splint DIP in extension for 6 wk, followed by 2 wk of night splinting; if inadequate improvement after 6 wk, check splinting routine and recommend 4 more wk of continuous splinting

Boutonnière Deformity

PIP flexed, DIP hyperextended

3

Injury or disease affecting the extensor tendon insertion into the dorsal base of the middle phalanx Associated with RA or trauma laceration, volar dislocation, acute forceful flexion of PIP)

Splint PIP in extension and allow active DIP motion

Swan Neck Deformity

PIP hyperextended, DIP flexed

1,3

Trauma (PIP volar plate injury) Associated with RA and old, untreated mallet deformity Splint to prevent PIP hyperextension or DIP flexion

Corrective procedures involve tendon rebalancing or arthrodesis/arthroplasty

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Definition

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Injury

A

B

C

DIP flexion

PIP

DIP

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PIP hyperextension © Jackie Robers

Zone 1

Zone 3 Zone 4 Zone 5

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De Quervain’s Tenosynovitis • definition: tenosynovitis is inflammation of the tendon and/or its sheath. Most common is De Quervain’s tenosynovitis (inflammation of the extensor tendons in the 1st dorsal compartment [APL and EPB]) • clinical features ■■ +ve Finkelstein’s test (pain over the radial styloid induced by making fist, with thumb in palm, and ulnar deviation of wrist) ■■ pain localized to the 1st extensor compartment ■■ tenderness and crepitation over radial styloid may be present ■■ differentiate from CMC joint arthritis (CMC joint arthritis will have a positive grind test, whereby crepitus and pain are elicited by axial pressure to the thumb)

Zone 2

Zone 6 Zone 7 Zone 8

© Jackie Robers | Erina He 2016

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Figure 23. (A) Mallet finger deformity (B) Boutonnière deformity (C) Swan neck deformity

Figure 24. Zone of extensor tendon injury (odd numbered zones fall over a joint)

PL27 Plastic Surgery

Toronto Notes 2018

Hand

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• treatment ■■ mild: NSAIDs, splinting and steroid injection into the tendon sheath (successful in over 60% of cases) ■■ severe surgery to open 1st dorsal compartment and release stenotic tendon sheaths of APL and EPB

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IV V

Figure 25. Zones of the flexor tendons

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Fractures and Dislocations

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• for fracture principles, see Orthopedics, OR4

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FRACTURES • about 90% of hand fractures are stable in flexion (splint to prevent extension) • position of safety ■■ wrist extension 0-30° ■■ MCP flexion 70-90° ■■ IP full extension ■■ this is done if you want to immobilize a fracture but are not sure whether there are other injuries • stiffness secondary to immobilization is the most important complication; Tx = early motion

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Distal Phalanx Fractures • most commonly fractured bone in the hand • usual mechanism is crush injury, and thus accompanied by soft tissue injury • subungual hematoma is common and must be decompressed, especially if there is involvement of >50% of the nail surface area

A-2 and A-4 pulleys are most important for function; prevent bowstringing of tendons

© Shelley Wall 2003

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Flexor pollicis longus

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III

Stenosing Tenosynovitis (trigger finger/thumb) • definition: inflammation and thickening of tendon or tendon sheath/pulley (most commonly at A-1 pulley near MCP), preventing smooth gliding of tendon through the sheath/pulley and resulting in locking of thumb or finger in flexion/extension • etiology: idiopathic or associated with RA, DM, hypothyroidism, gout, and pregnancy • clinical features ■■ ring finger is most commonly affected, then long finger and thumb ■■ patient complains of catching, snapping, or locking of affected finger ■■ tenderness to palpation/nodule at palmar aspect of MCP over A-1 pulley ■■ women are 4 times more likely to be affected than men • non-surgical treatment ■■ NSAIDs ■■ steroid injection; injections less likely to be successful in patients >60 yr, or symptoms greater than 6 mo ■■ splint • surgical treatment ■■ indicated if no relief of symptoms or minimal relief with steroids ■■ incise A-1 flexor pulley to permit unrestricted, full active finger motion

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Flexor digitorum superficialis

II

Common Flexor Tendon Deformities • flexor tendon zones (important for prognosis of tendon lacerations) • “no-man’s land” (zone 2) (see Figure 24) ■■ between distal palmar crease and mid-middle phalanx ■■ zone where superficialis and profundus lie ensheathed together ■■ recovery of glide very difficult after injury

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Flexor digitorum profundus

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Ganglion Cyst • definition ■■ fluid-filled synovial lining that protrudes between carpal bones or from a tendon sheath; most commonly carpal in origin ■■ most common soft tissue tumour of hand and wrist (60% of masses) • clinical features ■■ most commonly on the dorsal wrist overlying the scapholunate ligament, followed by the volar surface of the wrist overlying the radioscaphoid or scaphotrapezial joints ■■ 3 times more common in women than in men ■■ more common in younger individuals (2nd to 4th decades) ■■ can be large or small – may drain internally so size may wax and wane ■■ often non-tender although tenderness increased when cyst is smaller (from increased pressure within smaller cyst sac) • treatment ■■ conservative treatment: do nothing ■■ aspiration (recurrence rate 30-60%) ■■ steroid injection if painful (done in combination with aspiration, as results alone are no better than aspiration) ■■ consider operative excision of cyst and stalk (recurrence rate 5.9% for dorsal wrist ganglion, 30% for volar)

PL28 Plastic Surgery

Toronto Notes 2018

Hand

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• injury involving >50% of the nail surface area often suggests a nail bed laceration, in which the patient would benefit from nail plate removal and nailbed repair surgery • treatment consists of 3 wk of digital splinting (immobilize the DIP with a STAX splint); if intra-articular fracture displaced >30%, then percutaneous pinning (K-wires) and splint

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Proximal and Middle Phalanx Fractures • check for: rotation, scissoring (overlap of fingers on making a fist), shortening of digit • non-displaced or minimally displaced: closed reduction (if extra-articular), buddy tape to neighbouring stable digit, elevate hand, motion in guarded fashion early, splinted for 2-3 wk • displaced, non-reducible, not stable with closed reduction, or rotational or scissoring deformity: percutaneous pinning (K-wires) or ORIF, and splint

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Metacarpal Fractures • generally accept varying degrees of deviation before reduction required: up to 10° (D2), 20° (D3), 30° (D4), or 40° (D5) • Boxer’s fracture: acute angulation of the neck of the 5th metacarpal into palm ■■ mechanism: blow on the distal-dorsal aspect of closed fist ■■ loss of prominence of metacarpal head, volar displacement of head ■■ up to 30-40° angulation may be acceptable ■■ if greater angulation, closed reduction should be considered to decrease the angle ■■ if stable, ulnar gutter splint for 4-6 wk • Bennett’s fracture: two-piece fracture/dislocation of the base of the thumb metacarpal, usually intra articular ■■ unstable fracture ■■ APL pulls MC shaft proximally and radially, causing adduction of thumb ■■ treat with percutaneous pinning or ORIF, followed by thumb spica x 6 wk • Rolando fracture: T- or Y-shaped fracture of the base of the thumb metacarpal ■■ treated like a Bennett’s fracture

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DISLOCATIONS • must be reduced as soon as possible • dislocation vs. subluxation ■■ dislocation: severe injury where articular surfaces of a joint are no longer in contact with one another ■■ subluxation: articular surfaces of a joint are partially out of place (i.e. “partial dislocation” – often unstable and requires reduction)

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PIP and DIP Dislocations (PIP more common than DIP) • usually dorsal dislocation (commonly from hyperextension) if closed dislocation: closed reduction and splinting in position of function for 1 wk or buddy taping, and early mobilization (prolonged immobilization causes stiffness) • open injuries are treated with wound care, irrigation, and debridement, followed by closed or open reduction and antibiotics

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MCP Dislocations (relatively rare) • dorsal dislocations much more common than volar dislocations • dorsal dislocation of proximal phalanx on metacarpal head; most commonly index finger (hyperextension) • two types of dorsal dislocation ■■ simple (reducible with manipulation): treat with closed reduction and splinting for 2-4 wk at 60-70° MCP flexion ■■ complex (irreducible - most commonly due to volar plate blocking the reduction): treat with open reduction

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Ulnar Collateral Ligament (UCL) Injury • forced abduction of thumb (e.g. ski pole injury) • Skier’s thumb: acute UCL injury – if stable, treated with splint x 6-8 wk; if unstable, patient may have Stener lesion • Gamekeeper’s thumb: chronic UCL injury, often requires open repair and tendon graft for stabilization • Stener Lesion: the distal portion of the UCL can detach and flip superficial to the adductor aponeurosis and will not appropriately heal – requires open repair • evaluation: radially deviate thumb MCP joint in full extension and at 30° flexion and compare with non-injured hand. UCL rupture is presumed if injured side deviates more than 30° in full extension or more than 15° in flexion

PL29 Plastic Surgery

Toronto Notes 2018

Hand

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Dupuytren’s Disease

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Definition • proliferative disorder of the palmar fascia, forming nodules (usually painless), fibrous cords, and flexion contractures at the MCP and interphalangeal joints • flexor tendons not involved • Dupuytren’s diathesis: male sex, early age of onset, strong family history (autosomal dominant inheritance), involvement of multiple digits, bilateral involvement, and involvement of sites other than palmar aspect of hand, including the plantar fascia (Ledderhose’s) and the penis (Peyronie’s) – (see Urology, U30)

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Epidemiology • unusual in patients from African and Asian countries, high incidence in northern Europeans, men > women, often presents in 5th-7th decade of life; associated with but not caused by alcohol use, smoking, and DM

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Clinical Features • nodules, cords and contractures of MCP, PIP, DIP • order of digit nvolvement (most common to least common) ring > little > long > thumb > index • risk of recurrence

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Carpal Tunnel Syndrome

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Definition • median nerve compression at the level of the flexor retinaculum/transverse carpal ligament

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Etiology • median nerve entrapment at wrist • primary cause is idiopathic • secondary causes: space occupying lesions (tumours, hypertrophic synovial tissue, fracture callus, and osteophytes), metabolic and physiological (pregnancy, hypothyroidism, acromegaly, and RA); job/ hobby related repetitive trauma, especially forced wrist flexion

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Epidemiology • female:male = 4:1, most common entrapment neuropathy

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Clinical Features • classically, patient awakened at night with numb/painful hand, relieved by shaking/dangling/rubbing • on exam, sensory loss in median nerve distribution (see Figure 4), but thenar eminence sensory loss is spared (palmar cutaneous branch given off prior to carpal tunnel) • decreased light touch and 2-point discrimination at DIP adial and ulnar creases; discriminative touch often lost first • advanced cases: thenar wasting/weakness due to involvement of the motor branch of the nerve • ± Tinel’s sign (tingling sensation on percussion of nerve) • ± Phalen’s sign (wrist flexion induces symptoms)

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Investigations • clinical diagnosis • NCV and EMG studies may be used to objectively confirm the diagnosis

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Treatment • avoid repetitive wrist and hand motion, wrist splints at night and when repetitive wrist motion required • conservative: night-time splinting to keep wrist in neutral position • medical: NSAIDs local corticosteroids injection (relief from local corticosteroid injections is also diagnostic) • surgical decompression: transverse carpal ligament incision to decompress median nerve • indications for surgery: persistent signs and symptoms of median nerve compression not relieved by conservative management

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Nodule

© Monika Musial

Cord

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Palmar aponeurosis

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Figure 26. Dupuytren’s disease

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Treatment • palmar pit or nodule: no surgery (steroid injections for pain) palpable band/cord with no limitation of extension (i.e. no contracture) of either MCP or PIP: no surgery • MCP contracture >30 degrees or PIP contracture of any degree: needle aponeurotomy, collagenase injection, or surgical fasciectomy • contractures impeding function and/or hygiene: needle aponeurotomy, collagenase injection, or surgical fasciectomy • MCP joints have better outcomes than PIP joints post-treatment (achievement of near full extension, lower risk of recurrence)

PL30 Plastic Surgery

Toronto Notes 2018

c

Brachia Plexus

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Brachial Plexus

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Etiology • common causes of brachial plexus injury: complication of childbirth and trauma • other causes of injury: compression from tumours, ectopic ribs Common Palsies Table 22. Named Neonatal Palsies of the Brachial Plexus Location of Injury

Mechanism of Injury

Features

Upper brachial plexus (C5-C6)

Head/shoulder distraction (e g. motorcycle)

“Waiter’s tip deformity” (shoulder internal rotation, elbow extension and pronation, wrist flexion)

Lower brachial plexus (C7-T1)

Traction on abducted arm

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Palsy

Klumpke’s Palsy

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Duchenne-Erb Palsy

“Claw hand” May include Horner’s syndrome

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Differential Diagnosis of Adult-Acquired Brachial Plexus Palsies • trauma (blunt, penetrating) • thoracic outlet syndrome ■■ associated with large cervical rib, anomalous first rib, strenuous arm work, neck muscle hypertrophy ■■ neurogenic: compression of brachial plexus, resulting in upper limb paresthesia, pain, and weakness ■■ vascular: compression/thrombosis of subclavian artery/vein, resulting in pain; pallor and Raynaud’s if arterial; swelling and cyanosis if venous • tumour ■■ schwannoma: well-defined margins enable total resection ■■ neurofibromas: associated with neurofibromatosis type I ■■ other: e.g. Pancoast syndrome (apical lung tumour) • neuropathy (compressive, post-irradiation, viral, diabetic, idiopathic)

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Investigations • EMG • MRI: gold standard for identifying soft tissue masses and nerve roots • CT myelogram: controversial, although some people think that it is better than MRI for identification of nerve root avulsion • closed injuries: if avulsion suspected, then CT myelogram or MRI initially; otherwise, EMG/NCS 6-12 weeks post-injury to assess healing progress • open injuries: OR for exploration within a few days post-injury (once patient stable) Management

ee

Usually improves (unless expanding mass, e.g. hematoma) If no continued insult, follow for 3 4 mo for improvement

Obstetric palsy

Surgery if no significant improvement and/or residual paresis at 6 mo of age

Sharp or vascular injury

Explore immediately in OR

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Traction/stretch

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Open Injuries

Treatment

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Concussive/compressive

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Type Closed Injuries

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Table 23. Management of Brachial Plexus Injuries

PL31 Plastic Surgery

Toronto Notes 2018

c

Craniofacial Injuries

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Craniofacial Injuries

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• low velocity vs. high velocity injuries determine degree of damage • fractures cause bruising, swelling, and tenderness → loss of function • management: most can wait ~5 d for swelling to decrease before ORIF required

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Approach to Facial Injuries

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Investigations • CT (gold standard) ■■ axial and coronal (specifically request 1.5 mm cuts): for fractures of upper and middle face, as well as mandible ■■ indicated for significant head trauma, suspected facial fractures, pre-operative assessment • panorex radiograph: shows entire upper and lower jaw; best for isolated mandible fracture, but patient must be able to sit; however, if high clinical suspicion and negative panorex, CT should be done

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Patients with major facial injuries are at risk of developing upper airway obstruction (displaced blood clots, teeth, or fracture fragments; swelling of pharynx and larynx; loss of support of hyomandibular complex → retroposition of tongue); also at risk of ocular injury

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• ATLS protocol • inspect, palpate, clinical assessment for injury to underlying structures (e.g. facial nerve, bony injuries, septal hematoma, ocular involvement, etc.) • tetanus prophylaxis • radiological evaluation: CT scan with fine cuts through the orbit • wound irrigation with NS/RL and remove foreign materials • conservative debridement of detached or nonviable tissue • repair at the time of presentation with 4-0 nylon sutures when the patient’s general condition allows • consider intracranial trauma; rule out skull fracture

Signs of Basal Skull Fracture • Battle’s sign (bruised mastoid process) • Hemotympanum • Raccoon eyes (periorbital bruising) • CSF otorrhea/rhinorrhea

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Treatment Goals • consultation when indicated (dentistry, ophthalmology) • re-establish normal occlusion if occlusion is an issue • normal eye function (extraocular eye movements and vision) • restore stability of face and appearance

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Mandibular Fractures

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• two points of injury since it is a ring structure (includes fractures and dislocations) • commonly at sites of weakness (condylar neck, angle of mandible)

e

Etiology • anterior force: bilateral fractures • lateral force: ipsilateral subcondylar and contralateral angle or body fracture • note: classified as open if fracture into tooth bearing area (alveolus) Clinical Features • pain, swelling, difficulty opening mouth (“trismus”) • malocclusion, asymmetry of dental arch • damaged, loose, or lost teeth • palpable “step” along mandible • numbness in V3 distribution • intra-oral lacerations or hematoma (sublingual) • chin deviating toward side of a fractured condyle

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Body

From the symphysis to the distal alveolar border of the third molar

Angle

Triangular region between the anterior border of the masseter and the posterosuperior insertion of the masseter distal to the third molar

Ramus

Pa t of the mandible that extends posteriosuperiorly into the condylar and coronoid processes

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Midline of the mandible; between the central incisors from the alveolar process through the inferior border of the mandible

Area of the coronoid process of mandible

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Area below the condylar neck (i.e. sigmoid notch) of the mandible

Coronoid Process

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Subcondylar

*Most common mandibular fracture type

Symphysis

Angle

Parasymphysis

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Symphysis

Area of condylar process of mandible

Ramus

© Susan Park 2009

Figure 27. Mandibular fracture

Table 24. Mandibular Fracture Classifications by Anatomic Region

Condylar*

Subcondyle

Body

Classification

Areas/Boundaries

Condyle

PL32 Plastic Surgery

Toronto Notes 2018

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Craniofac al Injuries

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Treatment • maxillary and mandibular arch bars wired together (intramaxillary fixation) or ORIF ideally managed within 48 h as indicated by best current evidence • antibiotics from initial presentation until at least 3 doses post-operatively; if late presentation, may consider treatment with antibiotics for an extended course

b

Maxillary Fractures

Table 25. Le Fort Classification Le Fort II

Le Fort III

Alternative Name

Guérin fracture

Pyramidal fracture

Craniofacial dysjunction

Type of Fracture

Horizon al

Pyramidal

Transverse

Piriform aperture

Nasofrontal suture

Medial orbital wall

Zygomatofrontal suture

Pterygoid plates

Maxilla

Zygomatic arch

Pterygoid pla es

Pterygoid plates Detach entire midfacial skeleton from cranial base

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Maxillary teeth and midsection of the maxi la separated from upper face

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Maxilla divided into 2 segments

Anatomical Result

Le Fort I Fractures

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Nasal bones

Maxillary sinus

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Structures Involved

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Le Fort I

Nasal Fractures

Le Fort II Fractures

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Etiology • lateral force → more common, good prognosis • anterior force → can produce more serious injuries • most common facial fracture

©Rio Sakay 2007

Figure 28. Le Fort fractures

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Treatment • treated for airway or cosmetic issues • always inspect for and drain septal hematoma as this is a cause of septal necrosis and perforation – completed in the ER with small incision in the septal mucosa followed by packing • closed reduction with Asch or Walsham forceps under anesthesia, pack nostrils with petroleum or nonadhesive gauze packing, nasal splint for 7 d • best reduction immediately (10 d) • reconstruction of orbital floor with bone graft or alloplastic material • after repair, assess for diplopia: may require additional surgery for strabismus

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Complications • persistent diplopia • enophthalmos

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Superior Orbital Fissure Syndrome • fracture of SOF causing ptosis, proptosis, anesthesia in V1 distribution, and painful ophthalmoplegia (paralysis of CN III, IV, VI) • uncommon complication seen in Le Fort II and III fractures (1/130) • recovery time reported as 4.8-23 wk following operative reduction of fractures

e

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Orbital Apex Syndrome • fracture through optic canal with involvement of CN II at apex of orbit • symptoms are the same as SOF syndrome plus vision loss • treatment is urgent decompression of fracture in optic canal (posterior craniotomy for decompression) or steroids

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© Aimée Worrell

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Clinical Features • check visual fields and visual acuity for injury to globe • periorbital edema and bruising, subconjunctival hemorrhage • ptosis, exophthalmos, exorbitism, enophthalmos, or hypoglobus • orbital rim step-offs with possible infraorbital nerve anesthesia • vertical dystopia (abnormal displacement of the entire orbital cone in the vertical plane) – assessed by comparing the symmetry of the two pupils by a horizontal line running through the pupil of the unaffected eye • orbital entrapment ■■ clinical diagnosis that is a surgical emergency ■■ diplopia with straight gaze: unable to look up or down (entrapment of inferior rectus), limited EOM ■■ severe pain or nausea and vomiting with upward globe movement ■■ requires urgent ophthalmology evaluation if there are associated visual acuity changes

Figure 30. Blow-out fracture

PL34 Plastic Surgery

Toronto Notes 2018

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Breast

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Breast

o

Anatomy

b

Vascular Supply Subclavian artery Thoracoacromial artery Axillary artery Lateral thoracic artery

o

nternal thoracic artery

Thoracodorsal artery Internal thoracic perforating branches

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Medial intercostal perforators Anterolateral intercostal perforators

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©Midori Nediger 2016

Figure 31. Breast vasculature

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Innervation • innervated in a dermatomal pattern from branches of the thoracic intercostal nerves (T3-6) ■■ medially innervated from anterior cutaneous branches of I-VI intercostal nerves ■■ lateral innervated from lateral cutaneous nerve branches of II-VII intercostal nerves • lateral and upper portions of the breast innervated by lower fibres of the cervical plexus (C3, C4) • nipple areolar complex (NAC) ■■ supplied by anterior and lateral cutaneous branches of intercostal nerve IV ■■ additional innervation by cutaneous branches of intercostal nerves III and VI Intercostobrachial nerve

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Cervical plexus

Antero ateral intercostal nerves

3 4 5

3 4 5 6

Anteromedial intercosal nerves

© Ruth Chang 2016

Figure 32. Innervation of the breast

Breast Reduction

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Indications • symptomatic (general symptoms) ■■ musculoskeletal pain (back, strap, neck), chronic headache, paresthesia in upper limb, rashes under the breast, breast discomfort and physical impairment • breast reduction methods can be classified based on pedicle (i.e. blood supply to the nipple/areolar complex) and skin resection pattern (i.e. the resultant scar)

PL35 Plastic Surgery

Toronto Notes 2018

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©Midori Nediger 2016

Breast

Inferior pedicle technique

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Superior pedicle technique

Superomedial pedicle technique

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Figure 33. Types of pedicles

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Table 26. Common Types of Pedicles

©Ursula Florjanczyk 2016

Pedicle Description

Figure 34. Inverted T shape

Most commonly used technique; versatile use in small-large breast reduction

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Inferior Pedicle

Critiqued for boxy shape breast along with more extensive scarring (wise pattern skin resection)

m

m

Recommended pedicle width 6-8 cm, 8-10 cm in large breasts Pedicle derived from the internal mammary perforator of the second intercostal space

Superior Pedicle

c

Ped cle must be thinned to permit inset Modified from horizontal bi-pedicle (Strombeck) techniques

e.

Medial Pedicle

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Blood supplied from internal mammary perforator from third intercostal and potentially fourth intercostal space Incorporate the descending artery from second intercostal space as medial pedicle base extended superolaterally to breast meridian

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Superomedial Pedicle

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Table 27. Type of Skin Resections/Scar Options Indications

Inverted T Pattern

Description

Large breasts Breasts with poor quality skin that are challenging to remodel

Commonly used in association with inferior pedicle

m

Large portion of skin removed in horizontal and vertical direction

sf

Parenchyma needed to shape skin No horizontal scar Small to moderate reductions

m

b

Complications • NAC necrosis • sensory alteration of nipple (may vary with type of reduction pattern) • unsatisfactory scarring, including hypertrophic or keloid scar • wound healing complications (1-5% in healthy patients, higher in patients with elevated BMI) • difficulty breastfeeding (potential issue in women of childbearing age) • asymmetry • hematoma • wound infection

©Ursula Florjanczyk 2016

Figure 35. Vertical T shape

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Used in association with superior or medial pedicle

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Skin must be healthy and easy to remodel

e

Vertical Pattern

e

c

Skin integrity important to shape and hold breast parenchyma

PL36 Plastic Surgery

Toronto Notes 2018

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Breast

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Mastopexy (Breast Lift)

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Definition • aesthetic procedure of the breast used to correct for breast ptosis by modifying the contour and size of the breast along with elevating the position of the nipple

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Clinical Grading of Ptosis (Regnault Ptosis Grade Scale) 1. minor ptosis (1st degree) ■■ nipple at inframammary fold 2. moderate ptosis (2nd degree) ■■ nipple below inframammary fold, but above lower breast contour 3. severe ptosis (3rd degree) ■■ nipple below inframammary fold and at lower breast contour 4. glandular ptosis ■■ nipple above inframammary fold, but breast hangs below fold 5. pseudoptosis ■■ nipple above inframammary fold, but breast is hypoplastic and hangs below the fold Table 28 Type of Skin Resection/Scar Options

o

Circumareolar Mastopexy

Indications

Description

Nipple located 1-2.5 cm too low

Originally described as “donut mastopexy”

e

Reduce areolar diameter while simultaneously raising nipple (1 cm

Figure 36. Skate flap A-C, skate flap with primary closure of donor site. D-F, with skin graft

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Disadvantages

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Advantages

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Description

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Skate flap

© Kara Lukasiewicz 2016

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Nipple Areolar Complex Reconstruction

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Height of nipple

Circumference of nipple

m

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Donor site morbidity Decreased contralateral nipple sensation

C

©Ursula Florjanczyk 2016

Figure 37. CV flap

c

Nipple graft

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Diameter of nipple

CV flap

PL39 Plastic Surgery

Toronto Notes 2018

c

Aesthetic Surgery

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Table 32. Types of Areolar Reconstruction Advantages

Full thickness skin grafts, commonly from inner aspect of thigh or opposite areola

m

May require touch-ups due to pigment fading over time with skin sloughing

Provides texture and pigment resembling a natural areola

Donor site morbidity

o

Skin graft

Can provide more accurate colour matching

e

Conducted 3-4 months after nipple reconstruction when most of the projection has stabilized

e

Tattoo

Disadvantages

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Description

* Tattoo and skin grafting can be used in conjunction

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Aesthetic Surgery

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Aesthetic Procedures Description Aesthetic improvement of hair growth patterns using hair follicle grafts or flaps

Otoplasty

Surgical correction of protruding ears Surgical procedure to lift the forehead and eyebrows

Rhytidectomy

Surgical procedure to reduce wrinkling and sagging of the face and neck; “face lift”

Blepharoplasty

Surgical procedure to shape or modify the appearance of eyelids by removing excess eyelid skin ± fat pads

Rhinoplasty

Surgical reconstruction of the nose± nasal airway

m

Forehead/Brow lift

Chin augmentation via osteotomy or synthetic implant to improve contour

o

Genioplasty

Application of one or more exfoliating agents to the skin resulting in destruction of portions of the epidermis and/or dermis with subsequent tissue regeneration

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Chemical peel

Skin resurfacing with a rapidly rotating abrasive tool; often used to reduce scars, irregular skin surfaces, and fine lines

Laser resurfacing

Application of laser to the skin which ultimately results in collagen reconfiguration and subsequent skin shrinking and t ghtening; often used to reduce scars and wrinkles

Injectable fillers

An injectable substance is used to decrease facial rhytids; can augment lips to create fuller appearance; substances include: collagen, fat, hyaluronic acid, and calcium hydroxyapatite (most common substances include hyaluronic acid and fat)

Abdominoplasty

Removal of excess skin and repair of rectus muscle laxity (rectus diastasis); tummy tuck”

Calf augmentation

Augmentation of calf muscle with implants

Liposuction

Surgical removal of adipose tissue for body contouring (not a weight loss procedure)

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k

Dermabrasion

m

m

Other

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Skin

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Hair transplants

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Head/Neck

Procedure

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Location

s

Table 33. Aesthetic Procedures

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Pediatric Plastic Surgery

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Craniofacial Anomalies Table 34. Pediatric Craniofacial Anomalies Cleft Lip

Failure of fusion of maxillary and medial nasal processes

1 in 1000 live births (1 in 800 Caucasians, increased in Asians, decreased in Blacks) M:F=2:1

Classified as incomplete/complete and uni/bilateral; 2/3 cases: unilateral, left-sided, male

Surgery (3 mo): Millard Tennison-Randall, or Fisher (additional corrective surgeries usually required later on - especially for nasal deformity)

Cleft Palate

Failure of fusion of lateral palatine/median palatine processes and nasal septum

Isolated cleft palate: 0.5 per 1000 (no racial variation) F>M

Classified as incomplete/complete and uni/bilateral Isolated (common in females) or in conjunction with cleft lip (common in males)

Special bottles for feeding Speech pathologist Surgery (6-9 mo): Von Langenbeck or Furlow Z-Plasty ENT consult – often recurrent otitis media, requiring myringotomy tubes

Craniosynostosis

Premature fusion of ≥1 c anial sutures

1 in 2000 live newborns; M:F=52:48 Syndromes include: Crouzo s, Apert’s, Saethre-Chotzen Carpenter’s, Pfeiffer s JacksonWeiss, and Boston-type syndromes

Primary (no known cause), or secondary (associated with a known cause or syndrome)

Multidisciplinary team (including neurosurgery, ENT, genetics, dentistry, pediatrics, SLP) The type, timing, and procedure are dependent on which sutures (lambdoid, sagittal, etc.) are involved Early surge y prevents secondary deformities h ICP is an indication for emergent surgery

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Treatment

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Clinical Features

ee

Epidemiology

b

Definition

PL40 Plastic Surgery

Toronto Notes 2018

Pediatric Plastic Surgery

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Congenital Hand Anomalies

k

Features

Transverse absence (congenital amputation)

At any level (often below elbow/wrist)

Longitudinal absence (phocomelia)

Treatment

o

Early prosthesis

Absent humerus Thalidomide association

Radial deficiency (radial club hand)

Radial deviation Thumb hypoplasia M>F

Thumb hypoplasia

Degree ranges from small thumb with all components to complete absence

Depends on degree – may involve no treatment, webspace deepening, tendon transfer, or pollicization of index finger

Ulnar club hand

Rare, compa ed to radial club hand Stable wrist

Splinting and soft tissue stretching therapies Soft tissue release (if above fails) Correction of angulation ( lizarov distraction)

Cleft hand

Autosomal dominant Often functionally normal (depending on degree)

First web space syndactyly release Osteotomy/tendon transfer of thumb (if hypoplastic)

Syndactyly

Fusion of ≥2 digits 1/3,000 live births M:F=2:1 Classified as partial/complete Simple (skin only) vs. complex (osseous or cartilaginous bridges)

Surgical separation before 6-12 mo of age May require a skin graft to cover the fingers Usually good result

Symbrachydactyly

Short fingers with short nails at fingertips

Digital separation Webspace deepening

Camptodactyly

Congenital flexion contracture (usually at PIP, especially 5th digit)

Early splinting Volar release Arthroplasty (rarely)

Clinodactyly

Radial or ulnar deviation Often middle phalanx

None (usually); if severe, osteotomy with grafting

Polydactyly

Congenital duplication of digits May be radial (increased in Aboriginals and Asians) or central or ulnar (increased in Blacks)

Amputation of least functional digit Usually >1 yr of age (when functional status can be assessed)

Physiotherapy + splinting Soft tissue release if splinting fails Distraction osteogenesis (Ilizarov) ± wedge osteotomy Tendon transfer Pollicization

Overgrowth

e

Duplication

Undergrowth

om

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b Failure of Differentiation/ Separation

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Failure of Formation

Example

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Classification

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Table 35. American Society for Surgery of the Hand (ASSH) Classification of Congenital Hand Anomalies

Macrodactyly

Rare

None (if mild) Soft tissue/bony reduction

Brachydactyly

Short phalanges

Removal of nonfunctional stumps Osteotomies/tendon transfers Distraction osteogenesis

Symbrachydactyly

Short webbed fingers

As above + syndactyly release

Urgent release for acute, progressive edema distal to band in newborn Other reconstruction is case specific

i.e. amniotic (annular) band syndrome

Variety of presentations

Generalized Skeletal Abnormality

Achondroplasia, Marfan’s, Madelung’s

Variety of presentations



co

Constriction Band Syndrome

e

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Brachysyndactyly

e

Phalangeal/free toe transfer

Treatment depends on etiology

PL41 Plastic Surgery

Toronto Notes 2018

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References

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References

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American Society for Surgery of the Hand. The hand: examination and diagnosis, 3rd ed. Philadelphia: Churchill Livingston, 1990. Beredjiklian PK, Bozenika DJ. Review of hand surgery. Philadelphia: WB Saunders, 2004. Britt LD, Trunkey DD, Feliciano DV. Acute care surgery: principles and practice. New York: Springer, 2007. Borges AF. The rhombic flap. Plast Reconstr Surg 1981;67:458-466. Bray DA. Clinical applications of the rhomboid flap. Arch Otolaryngol 1983;109:37-42. Brodland DG, Zitelli JA. Surgical margins for excision of primary cutaneous squamous cell carcinoma. J Am Acad Dermatol 1992;27:241-8. Brown DL, Borschel GH. Michigan manual of plastic surgery. Philadelphia: WB Saunders, 2004. Centers, B. Guidelines for the operation of burn centers. Resources for Optimal Care of the Injured Patient, 2006. Daver BM, Antia NH, Furnas DW. Handbook of plastic surgery for the general surgeon, 2nd ed. New Delhi: Oxford University Press, 1995. Department of Health, Western Australia. Guidelines for use of nanocrystalline silver dressing – Acticoat™. Perth: Health Networks Branch, Department of Health, Western Australia, 2011. Diehr S, Hamp A, Jamieson B. Clinical inquiries: do topical antibiotics improve wound healing? J Fam Pract 2007;56:140-144. Fee WE Jr, Gunter JP, Carder HM. Rhomboid flap prin iples and common variations. Laryngoscope 1976;86:1706-1711. Georgiade GS, Riefkohl R, Levin LS. Georgiade plastic maxillofacial and reconstructive surgery, 3rd ed. Baltimore: Williams & Wilkins, 1997. Gourgiotis S, Villias C, Germanos S, et al. Acute limb compartment syndrome: a review. J Surg Educ 2007;64:178-186. Graham B, Regehr G, Naglie G, et al. Development and validation of diagnostic criteria for carpal tunnel syndrome. J Hand Surg 2006;31:919.e1-919.e7. Greene FL, Page DL, Fleming ID, et al AJCC cancer staging handbook: from the AJCC cancer staging manual, 6th ed Springer, 2002. Gulleth Y, Goldberg N, Silverman R et al What is the best surgical margin for a basal cell carcinoma: a meta-analysis of the literature. Plast Reconstr Surg 2010;126:1222-1231. Huang CC, Boyce SM. Surgical margins of excision for basal cell carcinoma and squamous cell carcinoma Seminars In Cutaneous Med and Surg 2004;23:167-173. Hunt TK, Doherty GM, Way LW (editors). Current surgical diagnosis and treatment, 12th ed. Norwalk: McGraw-Hill, 2006. Chapter: wound healing. Janis JE. Essentials of plastic surgery: a UT Southwestern Medical Center handbook. St. Louis: Quality Medical, 2007. Johnson RE, M rad MH Gynecomastia: pathophysiology, evaluation, and management. Mayo Clin Proc 2009;84(11):1010-15. Khalifian S, Brazio PS, Mohan R, et al. Facial transplantation: the first 9 years. Lancet 2014; S0140-6736(13)62632-X. Kraft R, Herndon DN, Al-Mousawi AM, et al. Burn Size And Survival Probability In Paediatric Patients In Modern Burn Care: A Prospective Observational Cohort Study Lancet 2012; 379:1013-21. Larrabee WF Jr, Trachy R, Sutton D, et al. Rhomboid flap dynamics. Arch Otolaryngol 1981;107:755-757. Lavigne E, Holowaty EJ, Pan SY, et al. Breast cancer detection and survival among women with cosmetic breast implants: systematic review and meta-analysis of observational studies. BMJ 2013;346:f2399 Mackinnon SE, Novak C. Thoracic outlet syndrome. Curr Probl Surg 2002;39 1070-145. Muangman P, Chuntrasakul C, Silthram S, et al. Comparison of efficacy of 1% silver sulfadiazine and acticoat for treatment of partial thickness burn wounds J Med Assoc Thailand 2006;89:953-958. Noble J. Textbook of primary care medicine, 3rd ed. St. Louis: Mosby 2001. Ong YS, Samuel M, Song C. Meta-analysis of early excision of burns. B rns 2006;32:145-150. Plastic Surgery Educational Foundation. Plastic and reconstructive surgery essentials for students. Arlington Heights: Plastic Surgery Educational Foundation, 2007. Available from: http://www.plasticsurgery.org/medical_professionals/publications/Essentials-for-Students.cfm. Richards AM. Key notes in plastic surgery. Great Britain: Blackwell Science, 2002. Salzberg CA, Ashikari AY, Koch RM, et al. An 8-year experience of direct-to-implant immediate breast reconstruction using human acellular dermal matrix (Allo Derm). Plast Reconstr Surg 2011;127:514-524 Sermer NB. Practical plastic surgery for nonsurgeons Philadelphia: Hanley & Belfus, 2001. Sibbald RG, Williamson D, Orsted HL, et al Preparing the wound bed – debridement, bacterial balance, and moisture balance Ost Wound Manag 2000;46:14-35. Singer AJ, Hollander JE, Subramanian S, et al. Pressure dynamics of various irrigation techniques commonly used in the emergency department. Ann Emerg Med 1994;24:36-40. Smith DJ, Brown AS, Cruse CW, et al. Plastic and reconstructive surgery. Chicago: Plastic Surgery Educational Foundation, 1987. Stone C. Plastic surgery: facts. London: Greenwich Medical Media, 2001. Thorne CH. Grabb & Smith’s plastic surgery, 6th ed. Lippincott Williams & Wilkins, 2007. Townsend CM. Sabiston textbook of surgery – the biological basis of modern surgical practice, 16th ed Philadelphia: WB Saunders, 2001. Chapter: plastic and reconstructive surg ry. Wolff K, Johnson RA Fitzpatrick’s colour atlas and synopsis of clinical dermatology, 6th ed. McGraw-Hill, 2009. Weinzweig J. Plas ic surgery secrets. Philadelphia: Hanley and Belfus, 1999.

PL42 Plastic Surgery

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PH

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Population Health and Epidemiology

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Arjun Sithamparapillai and Vishalini Sivarajah, chapter editors Sheliza Halani and Taraneh Tofighi, associate editors Arnav Agarwal and Sukhmani Sodhi, EBM editors Dr. Katherine Bingham and Dr. Allison Chris, staff editors

o

Measurements of Health and Disease in a Population. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7

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Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8 Interpreting Test Results Effectiveness of Interventions

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Types of Study Design. . . . . . . . . . . . . . . . . . . . . . 11 Qualitative vs Quantitative Observational Study Designs Experimental Study Designs Summary Study Designs

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Methods of Analysis . . . . . . . . . . . . . . . . Distributions Data Analysis Common Statistical Tests Causation Assessing Evidence

. . . . . 14

Environmental Health. . . . . . . . . . . . . . . . . . . . 20 Risk Assessment Air Water Soil Food

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Determinants of Health. . . . . . . . . . . . . . . . . . . . . 3 Concepts of Health Vulnerable Populations Disease Prevention

Occupational Health . . . . . . . . . . . . . . . . . . . . . . . 23 Taking an Occupational Health History Occupational Hazards Workplace Legislation Workplace Health Promotion and Protection Workplace Disease Prevention and Identification Workplace Treatment and Rehabilitation

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Public Health Context. . . . . . . . . . . . . . . . . . . . . . . 2 Public Health Services in Canada Legislation and Public Health in Canada

Outbreak of Infectious Diseases. . . . . . . . . . . . . . 18 Definitions Steps to Control an Outbreak Infection Control Targets

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Acronyms. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2

Appendix – Mandatory Reporting . . . . . . . . . . . 24 Reportable Diseases Other Reportable Conditions References . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . 26

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Health Services Research. . . . . . . . . . . . . . . . . . . 17 Continuous Quality Improvement Cost Analysis

e

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For more detail on topics covered in this chapter, use website http://phprimer.afmc.ca/ as a resource

o

Population Health and Epidemiology PH1

Toronto Notes 2018

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PH2 Population Health and Epidemiology

Toronto Notes 2018

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Acronyms

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Acronyms number needed to treat negative predictive value odds ratio Public Health Agency of Canada per protocol analysis positive predictive value potential years of life lost quality adjusted life years quality improvement randomized controlled trial

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NNT NPV OR PHAC PP PPV PYLL QALY QI RCT

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false negatives infant mortality atio intention to reat analysis low income cut-off likelihood ratio Medical Health Officer Medical Officer of Health maternal mortality ratio Material Safety Data Sheets number needed to harm

RR relative risk SMR standardized mortality ratio SN sensitivity SP specificity TP true positives TN true negatives WHMIS Workplace Hazardous Materials Information System WHO World Health Organization WSIB Workplace Safety and Insurance Board

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FN IMR ITT LICO LR MHO MOH MMR MSDS NNH

m

attributable risk Chi dren’s Aid Society cost benefit analysis cost effectiveness analysis case fatality rate Chief Public Health Officer disability adjusted life years evidence based medicine Health Canada false positives

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AR CAS CBA CEA CFR CPHO DALY EBM HC FP

Public Health Context

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• see Ethical, Legal, and Organizational Medicine, ELOM2 Overview of Canadian Healthcare System for the organization of health care in Canada including the legal foundation and historical context

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Sources: Shah, CP. Chapter 15 Community Health Services. Public Health and Preventive Medicine in Canada 5e. Toronto: Elsevier, 2003. The Association of Faculties of Medicine of Canada Public Health Educators’ Network. The Organization of Health Services in Canada. AFMC Primer on Population Health.

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1 health protection: measures taken to address potential risks to health at the population level, including through regulation and advising government (e.g. safe water and food supply) 2. health surveillance: monitoring and predicting health outcomes and determinants with systematic, longitudinal data collection 3. disease and injury prevention: address infectious disease through preventive (e.g. vaccination, droplet protection) and control (e.g. quarantine) measures; reduce morbidity through lifestyle improvement 4. population health assessment: studying and engaging with a community to understand their needs and produce better policies and services 5. health promotion: advocate for improved health through broad community and government measures (e.g. policy, interventions, community organizing) 6. emergency preparedness and response: developing protocols and infrastructure for natural (e.g. hurricane) and man-made (e.g. toxic waste spill) disasters

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Primer on P pulation Health, Accessed: March 25 2016)

CPHO of Canada • Responsible for the PHAC and reports to the Minister of Health • As the federal government’s lead public health professional, provides advice to the Minister of Health and Government of Canada on health issues • Collaborates with other governments, jurisdictions, agencies, organizations, and countries on health matters • Communicates public health information to health professionals, stakeholders, and the public • In an emergency, such as an outbreak or natural disaster, provides direction to PHAC staff, including medical professionals, scientists, and epidemiologists, as they plan and respond to the emergency

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Mission: to promote and protect the health of Canadians through leadership, partnership, innovation, and action in public health” (Public Health Agency of Canada) • local public health units and services within regional health authorities (in most provinces except Ontario, where local public health units are either autonomous or within local government) provide programs and activities for health protection, promotion, and disease prevention at local and regional levels • catchment-area populations range widely (100s–1,000,000s), covering areas of 15 km2 to 1.5 million km2 • the “core functions” of public health include six essential activities (The Organization of Health Services in Canada. AFMC

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Public Health Services in Canada

Historical Perspective Over the last century, Public Health has evolved through three main epidemiological phases: • Infectious diseases: controlled in the more developed world but an issue in less developed countries (e.g. polio, malaria) • Chronic diseases: chronic diseases and other noncommunicable conditions have increased morbidity and mortality (e.g. heart disease and cancer due to risk factors and/or exposures) • Re-emerging infectious diseases: new or re-emergent infections emerge due to unfamiliar or new pathogens, inefficient or inappropriate antibiotic use, travel, and global warming (e.g. HIV, drug resistant TB and malaria)

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Sources: Shah, CP. Chapter 2 Measurement and Investigation. Public Health and Preventive Medicine in Canada, 5e. Toronto: Elsevier, 2003. Shah CP. Chapter 15 Community Health Services. Public Health and Preventive Medic ne in Canada, 5e. Toronto: Elsevier, 2003.

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Preparing for the LMCC The AFMC Primer on Population Health is the core text for the LMCC and is available as an online resource on the AFMC website (http:// phprimer.afmc.ca) For the LMCC exam, it is recommended that you also read Chapter 15 in Shah CP. Public health and preventive medicine in Canada, 5th ed. Toronto: Elsevier, 2003

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Definitions • population health ■■ refers to the health of defined groups of people, their health determinants, trends in health, and health inequalities ■■ influenced by: physical, biological, social, environmental, and economic factors; personal health behaviours; health care services ■■ broader scope vs. public health, accounts for socio-economic, policy, historical issues • public health ■■ “efforts organized by society to protect, promote, and restore the peoples’ health” and prevent morbidity and mortality ■■ refers to the practices, programs, policies, institutions, and disciplines required to achieve the desired state of population health • epidemiology ■■ “study of the distribution […] of determinants of disease, health-related states, and events in populations” • public hea th and preventive medicine (formerly called community medicine) ■■ the postgraduate study of health and disease in the population or a specified community ■■ 5 year Royal College specialty training ■■ goal: to identify and address health problems and evaluate the extent to which health services and others address these issues

Source: Public H alth Agency of Canada. http://www. phac-aspc.gc.ca/cpho-acsp/cpho-acsp-role-eng.php

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PH3 Population Health and Epidemiology

Toronto Notes 2018

Determinants of Health

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Legislation and Public Health in Canada

Local boards of health deliver programs mandated by provincial and municipal or regional legislation Boards of health are responsible for the delivery of most public health services, such as: • Infectious disease control, including the follow up of reported diseases and management of outbreaks • Inspection of food premises including those in hospitals, nursing homes, and restaurants • Family health services including preconception, preschool, school-aged, and adult health programs • Tobacco control legislation enforcement • Assessment and management of local environmental health risks • Collection and dissemination of local health status reports • Public dental health services to children • By-laws may be approved by municipal governments to facilitate public health issues



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Medical Officer of Health (MOH) (Ontario) • May be called “Medical Health Officer” (MHO) in other provinces • Appointed to each public health unit by the board of health • Held by a licensed physician with public health training • Responsibilities include: • Collection and analysis of epidemiological data • Occupational and environmental health surveillance • Implementation of health programs, including: Counselling • Family planning services • Parenting programs, prenatal courses • Preschool and school health services • Disease screening programs • Tobacco use prevention programs • Nutrition services to schools and seniors’ centres • The Medical Officer of Health can require an individual/premise/agency to take or refrain from any action due to a public health hazard

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Legislation is in the form of Acts and Regulations Each province has its own Public Health Act or equivalent (e.g. the Health Protection and Promotion Act in Ontario) • Designates the creation of geographic areas for the provision of public health services • Gives powers to the Chief Medical Officer of Health to control public health hazards • Specifies infectious diseases to be reported to public health units by physicians, laboratories, and hospitals (see Appendix, PH24) • Has the ability to mandate programs that address public health issues, environmental health, and chronic disease prevention

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Municipal (Ontario)

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Health Canada • Provides health services to First Nations, Aboriginal peoples, the Canadian military, and veterans • Approves new drugs and medical devices Canadian Food Inspection Agency • Monitors food products • Deals with animal-related infections • Regulates food labeling Public Health Agency of Canada (main Government of Canada agency responsible for public health) • An independent body created to strengthen public health capacity • Focuses on preventing chronic diseases preventing injuries, and responding to public health emergencies and infectious disease outbreaks • Oversees immigration screening, protects Canadian borders (e.g. airport health inspection) • Liaises with the World Health Organization (WHO) on global health issues

Provincial

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Federal

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Table 1. Leg slation and Public Health in Canada

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Determinants of Health

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Concepts of Health

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Determinants of Health • Income and social status • Social support networks • Education and literacy • Employment and working conditions • Social and work environments • Physical environment • Personal health practices and coping skills • Healthy child development • Biology, genetics, and epigenetics • Health serv ces • Gender • Culture

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Sources: Shah, CP. Concepts, Determinants, and Promotion of Health. Public Health and Preventive Medicine in Canada, 5e. Toronto: Elsevier, 2003. The Association of Faculties of Medicine of Canada Public Health Educators’ Network. Concepts of Health and Illness. AFMC Primer on Population Health.

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Determinants of Health • 1974: the Honourable Marc Lalonde, federal Minister of Health, publishes A New Perspective on the Health of Canadians which outlines four factors that determine health: “human biology, environment, lifestyle, and health care organizations.” The idea of determinants of health has since been expanded and refined to include many additional factors

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Definitions of Health • First multidimensional definition of health, as defined by the WHO in 1948: “state of complete physical, mental and social well-being and not merely the absence of disease or infirmity” • WHO updated the definition (socioecological definition) of health in 1986: “The ability to identify and to realize aspirations, to satisfy needs, and to change or cope with the environment. Health is therefore a resource for everyday life, not the objective of living Health is a positive concept emphasizing social and personal resources, as well as physical capacities” (Ottawa Charter for Health Promotion) • Other definitions of health have since been proposed that incorporate other dimensions f health (e.g. “Health is a social, economic, and political issue and above all a fundamental human right“ – The People’s Charter for Health)

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• wellness: “state of dynamic physical, mental, social, and spiritual well-being that enables a person to achieve full potential and have an enjoyable life” • disease: “abnormal, medically-defined changes in the structure or function of the human body” • illness: “an individual’s experience or subjective perception of a lack of physical or mental well-being and consequent inability to function normally in social roles” • illness behaviour: an individual’s actions resulting from and responding to their illness, including their interactions or avoidance of the health care system • sickness: views the individual and their society hold towards a health condition, affecting their thoughts and actions • impairment: “any loss or abnormality of psychological, physiological, or anatomical structure or function” • disability: “any restriction or lack of ability to perform an activity within the range considered normal for a human being” • handicap: a disadvantage for an individual arising due to impairment or disability ■■ “limits or prevents the fulfillment of an individual’s normal role as determined by society and depends on age, sex, social, and cultural factors” • health equity: when all people have “the opportunity to attain their full health potential” and no one is “disadvantaged from achieving this potential because of their social position or other socially determined circumstance.” Health inequities are systematic differences in the health of individuals/ groups which are considered unjust • health equality: defined as where populations have equal or similar health status. Health inequalities are systematic differences in the health of groups that do not necessarily carry a moral judgement

Source: Public Health Agency of Canada www.phacaspc.gc.ca/ph-sp/determinants/determinants-eng.php

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PH4 Population Health and Epidemiology

Toronto Notes 2018

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Determinants of Health

Hea th care services

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Unemployment

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Housing

Living and working conditions

Education

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Individual lifestyle factors Age, sex, and hereditary factors

Agricu ture and food production

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© Cassandra Cetlin 2014

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Adapted from Dahlgreen G, Whitehead M. European strategies for tackling social inequities in health: Leveling up Part 2. World Health Organization, 2006.

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• cultural safety: “interactions with people from different cultures that treat them respectfully in a manner that acknowledges relevant differences but does not create a sense of discrimination” • cultural sensitivity: “being aware of (and understanding) the characteristic values and perceptions of your own culture and the way in which this may shape your approach to patients from other cultures”

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Vulnerable Populations

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Sources: The Association of Faculties of Medicine of Canada Public Health Educators’ Network. Glossary. AFMC Primer on Population Health.

Mental health awareness Aboriginal-specific DM initiatives Substance abuse treatment programs

Elder abuse Lack of emotional support Isolation

Low hazard tolerance Institutionalization Mobility issues

Inactivity Polypharmacy Medical comorbidities

Aging in place of choice Falls and injury prevention Mental health promotion Preventing abuse and neglect

Low income Family dysfunction Lack of educational opportunities

Housing availability Unsafe housing Lack of recreational space

Poor supervision Food insecurity High risk behaviours

Improvements in family income most significant Early childhood education

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Based on Low Income Cut Offs (LICO) LICO is an income threshold below which a family will likely devote a larger share of its income on the necessities of food, shelter and clothing than the average family

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New Immigrants to Canada • Mandatory medical exams on entry to Canada by a designated medical practitioner: • Complete medical examination for all persons of all ages • Chest x-ray and repo t for persons 11 yr of age and over • Urinalysis for persons 5 yr of age and over • Syphilis serology for persons 15 yr of age and over • HIV testing for applicants 15 yr of age and over as well as for those children who have received blood or blood products, have a known HIV-positive mother, or have an identified risk. An ELISA HIV screening test should be done for HIV 1 and HIV 2 • Serum creatinine if the applicant has hypertension (resting blood pressure greater than 140/90 mmHg), a history of treated hypertension, DM, autoimmune disorder, persistent proteinuria, or kidney disorder

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Children in Poverty

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Individuals >65 yr

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Smoking Substance misuse Excessive gambling Poor nutrition Sedentary lifestyle High BMI Higher risk of suicide

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Isolated Seniors

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Crowded housing Inefficient ventilation Environmental toxins (botulism) TB declining but prevalence higher than rest of population

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Low income Family violence Low education status Unemployment Homelessness Longer length of disability

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Four specific groups: First Nations Status Indians (registered under the Indian Act), non-Status Indians, Métis, and Inuit

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Population-Specific Interventions

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Environment

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Physical

Aboriginal Peoples

Individual Behaviour

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Psychosocial/ Socioeconomic

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Definition

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Table 2. Health Determinants of Vulnerable Populations

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Figure 1. Population health model

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Social and community networks

Work environment

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General socio-economic, cultural and environmental conditions

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Water and sanitation

Social Determinants: Indigenous People’s Health in Canada • Colonization: subjugation of Indigenous peoples by the Europeans, leading to the loss of lands, cultural practices, and selfgovernment • Residential schools: placement of children from Indigenous groups in church run, government-funded schools for the purpose of assimilation, resulting in loss of identity, alienation, and abuse, with long-lasting consequences of higher rates of addictions, abusive relationships, and suicide • Treaties and land claims: inadequate services fo those living on reserves leading to poverty and poor quality infrastructure, reflected in disproportionate burden of infectious diseases (e.g. pertussis, Chlamydia, hepatitis, shigellosis) Traditional approach to healing: restoring balance in the four realms of spiritual, emotional, mental and physical health of a person acting as an individual, as well as a member of a family, community and nation • Ideas represented by medicine wheel of First Nations peoples, the Learning Blanket of Inuit peoples, and the Metis tree model of Holistic Lifelong Learning • Contrast to Western medicine focus of treating illness, leading to challenges for practitioners of Western medicine to meet Aboriginal patients’ needs • National Aboriginal Health Organization (NAHO) offers 8 guidelines on practicing culturally safe health care for Aboriginal patients including need to allow Aboriginal patients access to ceremony, song, and prayer; the need for information and for family support; guidelines for the appropriate disposal of body parts and for handling death

Citizenship and Immigration Canada Handbook http:// www.cic.gc.ca/english/resources/publications/ dmp-handbook/

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PH5 Population Health and Epidemiology

Toronto Notes 2018

Determinants of Health

Individual Behaviour

Population-Specific Interventions

People with Disabilities

Includes impairments, activity limitations, and participation restrictions

Low income Low education status Discrimination Stigma

Institutionalization Barriers to access Transportation challenges

Substance misuse Poor nutrition Inactivity Dependency for ADLs

Transportation support Multidisciplinary care Unique support for individuals with specific disabilities (e.g Trisomy 21)

New Immigrants

Person born outside of Canada who has been granted the right to live in Canada permanently by immigration authorities

Access to community services Cultural perspectives (including reliance on alternative health practices)

Exposure to diseases and conditions in country of origin (e.g. smoke from wood fires, incidence of TB, etc.)

Employment, ESL Healthy Newcomer Effect (health worsens over time to match that of the general population) Cultural or religious expectations

Women’s health Mental health Infectious diseases (syphilis blood test, CXR, HIV) Dental and vision screening Vaccinations Cancer screening

Homeless Persons

An individual who lacks permanent housing

Low income Food insecurity Mental illness

Exposure to temperature extremes Infections such as West Nile Virus

Substance misuse Violence

Safe housing Addictions support Mental health

Refugee Health

Forced to flee country of origin because of a well-founded fear of persecution and given protection by the Government of Canada

Post-traumatic stress disorders Depression Adjustment problems

Diseases and conditions in country of origin (e.g. malaria, TB, onchocerciasis, etc.) Direct and indirect effects of war

Employment ESL Longstanding prior lack of access to health care (chronically neglected problems) Cultural or religious expectations

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Partial health coverage via Interim Federal Health Program

Vaccinations Women’s health Mental health Infectious diseases Dental and vision screening Political advocacy

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Refugee claimant: Arrive in Canada and ask to be considered refugee

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Environment

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Physical

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Psychosocial/ Socioeconomic

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Definition

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Table 2. Health Determinants of Vulnerable Populations (continued)

Primary

Protect health and prevent disease onset

Immunization programs (e.g. measles, diphtheria, pertussis, tetanus, polio, see Pediatrics, P4) Smoking Cessation Seatbelt use

Secondary

Early detection of disease to minimize morbidity and mortality

Mammography Routine Pap smears

Tertiary

Treatment and rehabilitation of disease to prevent progression, permanent disability, and future disease

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Sample Strategies

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Goal

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Level of Prevention

DM monitoring with HbA1c eye exams, foot exams Medication

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Basic Concepts in Prevention, Sur eillance, and Health Promotion. AFMC Primer on Population Health (http://phprimer.afmc.ca/Part1-TheoryThinkingAboutHealth Chapter4BasicConceptsInPreventionSurveillanceAndHealthPromotion/Thestagesofprevention)

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Ottawa Charter for Health Promotion (1986) • Health promotion: the process of enabling people to increase co trol over and improve their health • The charter states that governments and health care providers should be involved in a hea th promotion process that includes: 1. Building healthy public policy 2. Creating supportive environments 3. Strengthening community action 4. Developing personal skills 5. Re-orienting health services

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Table 3. Levels of Disease Prevention

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Disease Prevention Strategies • measures aimed at preventing the occurrence, interrupting through early detection and treatment, or slowing the progression of disease/mitigating the sequelae

Example of Primary Prevention Gardasil Vaccine and Its Efficacy in the Prevention of Cervical Cancer Gardasil® is a quadrivalent HPV vaccine covering strains 6,11,16,18. The efficacy ol Gardasil® was studied in 4 randomized, double-blind, placebo controlled trials on females between 16 and 26 yr of age and was found to prevent nearly 100% of precancerous cervical changes for up to 4 yr after vaccination

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Natural History of Disease • course of a disease from onset to resolution 1. pathological onset 2. presymptomatic stage: from onset to first appearance of symptoms/signs 3. clinical manifestation of disease: may regress spontaneously, be subject to remissions and relapses, or progress to death

Passive prevention, measures that operate without the person’s active involvement (e.g. airbags in cars) are more effective than active prevention, measures that a person must do on their own (e.g. wearing a seatbelt)

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Disease Prevention

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Note: this chart delineate the major challenges faced by each group, but the issues listed are not unique to each population Sources: Shah, C . The Health of Vulnerable Groups. Public Health and Preventive Medicine in Ca ada, 5e. Toronto: Elsevier, 2003.

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PH6 Population Health and Epidemiology

Toronto Notes 2018

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Determinants of Health

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Screening (Secondary Prevention) • “presumptive identification of unrecognized disease or defect by the application of tests, examinations, or other procedures which can be applied rapidly” • types of screening ■■ mass screening: screening all members of a population for a disease (e.g. phenylketonuria (PKU) and hypothyroidism in all newborns) ■■ selective screening: screening of targeted subgroups of the population at risk for a disease (e g mammography in women >50 yr old) ■■ multiphasic screening: the use of many measurements and investigations to look for many disease entities (e.g. periodic health exam) • bias in screening ■■ lead-time: false improvement in survival time caused by changing the starting point of measurement, as opposed to real improvements measured from the original starting point (e.g. due to better therapy) ■■ lead-time bias: overestimation of survival time ‘from diagnosis’ when the estimate is made from the time of screening, instead of the later time when the disease would have been diagnosed without screening ■■ length time bias: overestimation of the survival time due to screening at one time point including more stable cases than aggressive cases of disease, who may have shorter survival times Overt Disease

Occult Disease

Onset of Disease

Death from Disease

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Lead Time

Screen Detected

Clinically Detected

Figure 2. Lead-time bias

Health Care System

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Test High specificity and sensitivity Safe, rapid, easy, relatively inexpensive Acceptable to providers and to population

Adequate capacity for reporting, follow-up, and treatment of positive screens Cost effective Sustainable program Clear policy guidelines

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Causes significant suffering and/or death Natural history must be understood Must have an asymptomatic stage that can be detected by a test Early detection and intervention must result in improved outcomes Incidence is not too high or too low

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Disease

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Table 4. Ideal Criteria for Screening Tests

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Health Promotion Strategies

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Adapted from: Shah CP. Public Health and Preventive Medicine in Canada, 5th ed. Toronto: Elsevier, 2003 Sou ces: Shah, CP. Concepts, Determinants, and Promotion of Health. Public Heal h and Preventive Medicine in Canada, 5e. Toronto: Elsevier, 2003 Shah, CP. Measurement and Investigation. Public Health and Preventive Med cine in Canada, 5e. Toronto: Elsevier, 2003 The Association of Faculties of Medicine of Canada Public Health Educators’ Network. Concepts of Health and Illness. AFMC Primer on Populati n Health

Medical model (passive ole)

Participatory model of health

Aimed mainly at high risk groups in the population

Aimed at the population in its total environment

One-shot strategy, aimed at a specific pathology

Diverse and complementary strategies aimed at a network of issues/determinants

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Source: International Conference on Health Promotion, Adelaide, South Australia (1998)

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Healthy Public Policy • characterized by an explicit concern for health and equity in all areas of policy and by an accountability for health impact • main aim: to create a supportive environment to enable people to lead healthy lives, thereby making healthy choices easier for citizens • government sectors must take into account health as an essential factor when formulating policy and should be accountable for the health consequences of their policy decisions • methods ■■ fiscal: imposing additional costs (e.g. taxes on tobacco and alcohol) ■■ legislative: implementing legal deterrents (e.g. smok ng bans, legal alcohol drinking age) ■■ social: improving health beyond providing universally funded health care (e.g. providing affordable housing)

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Source: Shah CP. Public Health and Preventive Medicine in Canada, 5th ed. Toronto: Elsevier, 2003

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Led by non-professional organizations, civic groups, local, municipal, regional, and national governments

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Focused on a person’s health status and environment

Led by professional groups from health disciplines

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Focused mostly on individuals and groups of subjects

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Facilitating and enabling approaches by incentives offered to the population

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Health = positive and multidimensional concept

Directive and persuasive strategies enforced in target groups

Example of Harm Reduction Strategies: Tobacco Harm Reduction and The Case for the Electronic Cigarette Harm Reduct J 2013 Oct 4;10:19. Con entional smoking cessation strategies such as nicotine replacement therapy, buproprion or varenicline pharmacotherapy have demonstrated low uptake and poor overall efficacy despite garnering some increase in quit rates. Alternative sources of nicotine, such as the electronic cigarette, deliver nicotine vapor without combustion products responsible for most of the damaging effects experienced by traditional smoking methods, and without the emission of traditional cigarette toxins. Therefore, the electronic cigarette represents a harm reduction strategy with health risks similar to smokeless tobacco, with approximately 1% of the mortality risk associated with traditional cigarette smoking. Electronic cigarettes have also been associated with other benefits, such as improved exercise tolerance, decreased cough symptoms, decreased odourous breath, relief from withdrawal and craving symptoms of traditional cigarettes, relatively lower expenses and increased likelihood o smoking abstinence.

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Health Promotion

Health = absence of disease

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Disease Prevention

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Table 5. Disease Prevention vs. Health Promotion Approach

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PH7 Population Health and Epidemiology

Toronto Notes 2018

c

Measurements of Health and Disease

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1. Precontemplation: the individual is not seriously considering change (for various reasons) and is not interested in any kind of intervention

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Relapse: possible at any stage

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3. Preparation the individual begins experimenting, making small changes; he or she resolves to make a serious attempt in the future (usually defined as 30 days)

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2. Contemplation: the individual begins to seriously consider making the change within the foreseeable future (often defined as six months)

Example of Harm Reduction Strategy – Evaluation of a Pilot Medically Supervised Safer Injecting Facility CMAJ 2006;175:1399-1404 Purposes: To evaluate the outcomes of a supervised safer injecting facility facilitating pre-obtaining illicit drugs under supervision of medical staff, conducted over a 3 year period. Methods: Illicit drug users (IDUs) of the Vancouver area were allowed to inject previously obtained illicit drugs under the supervision of nurses and physicians. IDUs were offered addiction counselling and supports for appropriate community resources. Results: A random sample of 670 IDUs was recruited and monitored from Dec 2003-July 2004. Characteristics of IDUs who used the safe injecting facility included age 1 yr of age reported during a given time period divided by the number of live births reported during the same time period and expressed per 1000 live births per year

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Maternal Mortality Rate (MMR) • “number of deaths of women during pregnancy and due to puerperal causes […] per 1000 live births in the same year” MEASURES OF DISEASE BURDEN

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Potential Years of Life Lost (PYLL) • calculated for a population using the difference between the actual age at death and a standard/expected age at death • increased weighting of mortality at a younger age

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Disability Adjusted Life Year (DALY) • life expectancy weighted by amount of disability experienced • both premature death and time spent with disability accounted for; these disabilities can be physical or mental

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Qual ty Adjusted Life Year (QALY) • years of life weighted by utility (similar to quality of life), ranging from 0-1 assigned to a year of life based on perceived quality of life; a yr in “perfect” health is considered equal to 1 QALY, the value of a year in ill health would be lowered based on the burden of disease • it is possible to have “states worse than death” for example QALY 4 and risk of developing Trisomy 21) • randomization, stratification, matching, and regression modelling can help minimize confounder effects Figure 4. Understanding sensitivity and specificity

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Interpreting Test Results

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Source: The Association of Faculties of Medicine of Canada Public Health Educators’ Network. Assessing Evidence and Information. AFMC Primer on Population Health.

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TP = True positive TN = True negative FP = False positive FN = False negative Disease Present Test Result

Negative

Positive

TP

FP

Negative

FN

TN

Sensitivity = TP/(TP+FN) Specificity = TN/(TN+FP)

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— well person — person with disease

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Figure 4a. Hypothetical population

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LR+ = Sensitivity = [TP/TP+FN)] 1 - Specificity [FP/(TN+FP)]

LR– = 1 - Sensitivity = [FN/(TP+FN)] Specificity [TN/(TN+FP)]

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Likelihood Ratio (LR) • Likelihood that a given test result would be expected in a patient with disease compared with the likelihood that the same result would be expected in a patient without disease • LR+ indicates how much the probability of disease increases if the test is positive • LR- indicates how much the probability of disease decreases if the test is negative

PPV =

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Positive Predictive Value (PPV) • Proportion of people with a positive test who have the disease TP TP + FP

Dark grey — positive test result Light grey — negative test result

Negative Predictive Value (NPV) • Proportion of people with a negative test who are free of disease NPV= TN TN + FN

Negative

68

147

PPV =

68 = 31.6% (68+147)

NPV =

2234 = 91.2% (2234+216)

216

2234

284

2381

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Sensitivity = 68/284 = 23.9% Specificity = 2234/2381 = 93.8%

Figure 4c. Sensitivity of test (e.g. 24/30 = 80% sensitive)

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Negative Total

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Positive

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Present

LR+ = 0.239 = 3.85 1 - 0.938 1 - 0 239 LR– = = 0.81 0.938

Advanced Neoplasia Test Result

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Figure 4b. Results of diagnostic test on hypothetical population

Figure 5. Interpreting test results: Practical example using FOBT testing in advanced colon cancer

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Sensitivity • proportion of people with disease who have a positive test

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Specificity • proportion of people without disease who have a negative test

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Pre-Test Probability • the probability a particular patient has a given disease before a test/assessment results are known

Figure 4d. Specificity of test (e.g. 56/70 = 80% specific)

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Source: Numbers from Collins J, Lieberman D, Durbin T, et al. Accuracy of screening for fecal occult blood on a single stool sample obtained by digital rectal examination: a comparison with recommended sampling practice. Ann Intern Med 2005;142:81-85

Source: Loong TW. Understanding sensitivity and specificity with the right side o the brain. BMJ 2003;327:716-719

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PH10 Population Health and Epidemiology

Toronto Notes 2018

c

Epidemiology

Effectiveness of Interventions

0.002 0.003 0.005 0.007 0.01

0.3 0.4 0.5 0.6 0.7

B

A+B

0.8

Absent

C

D

C+D

A+C

B+D

A+B+C+D

0.9 0.93 0.95 0.97 0 98

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A

c

Present

0.99 0.993 0.995

A×D B×C

Cohort Study C = incidence rate of health outcome in non-exposed C+D A attributable risk = A+B (AR)***

C C+D

e

A ÷ C relative risk = A+B C+D (RR)**

e

A = incidence rate of health outcome in exposed A+B

0.2 0.1 0.07 0.05

PSA =3

0.03 0.02 0.01 0.007 0.005

PSA =0.5

0.997 0.998

0.003 0.002

0.999

0 001

©N

D

2016

Figure 6. Fagan’s likelihood ratio nomogram: Practical example using PSA levels to calculate post-test probability of prostate cancer

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*Ratio of the odds in favour of the health outcome among the exposed to the odds in favour among the unexposed **Ratio of the risk of a health outcome among exposed to the risk among the unexposed ***Rate of health outcome in exposed individuals that can be attributed to the exposure

Source: Modified from Holmstrom B, Johansson M, Bergh A, et al. Prostate specific antigen for early detection of prostate cancer: longitudinal study. BMJ 2009;339:b3537

Figure 7. Measures of effect by study type

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Number Needed to Treat (NNT) • number of patients who need to be treated to achieve one additional favourable outcome • only one of many factors that should be taken into account in clinical or health system decision making (e.g. must take into account cost, ease, feasibility of intervention) ■■ a condition with death as a potential outcome can have a higher NNT (and be acceptable), as compared to an intervention to prevent an outcome with low morbidity, in which a low NNT would be necessary

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Number Needed to Harm (NNH) • number of patients who, if they received the experimental treatment, would lead to one additional patient being harmed, compared with patients who received the control treatment

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Adherence (formerly compliance) • degree to which a patient follows a treatment plan

e.

Coverage • extent to which the services rendered cover the potential need for these services in a community

e.

PSA =4

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=

07 0.6 0.5 0.4 0.3

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A B ÷ C D

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=20

Equations to Assess Effectiveness CER = control group event rate EER = experimental group event rate RR = EER/CER ARR = CER – EER NNT = 1/ARR

Beware Do not be swayed by a large RR or odds ratio, as it may appear to be large if event rate is small to begin with. In these cases AR is more important (e.g. a drug which lowers an event which occurs in 0.1% of a population to 0.05% can boast a RR of 50%, and yet the AR is only 0.05%, which is not nearly as impressive)

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Case-Control Study

0.98 0.97 0.95 0.93 0.9

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0.05 0.07 0.1

Absent

odds ratio (OR)*=

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Present

0.998 0.997 0.995 0.993 0.99

LIKELIHOOD RATIO

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Disease (e.g. lung CA)

Total

POST - TEST PROBABILITY 0.999

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PRE - TEST PROBABILITY 0.001

Effectiveness, Efficacy, Efficiency • three measurements indicating the relative value (beneficial effects vs. harmful effects) of an intervention ■■ efficacy: the extent to which a specific intervention produces a beneficial result under ideal conditions (e.g RCT) ◆◆ ideal conditions include adherence, close monitoring, access to health resources, etc. ■■ effectiveness: measures the benefit of an intervention under usual conditions of clinical care ◆◆ considers both the efficacy of an intervention and its actual impact on the real world, taking into account access to the intervention, whether it is offered to those who can benefit from it its proper administration, acceptance of intervention, and degree of adherence to intervention ■■ efficiency: a measure of economy of an intervention with known effectiveness ◆◆ considers the optimal use of resources (e g. money, time, personnel, equipment, etc.)

Exposure (e.g. smoking)

Sensitivity and specificity are characteristics of the test LR depends on the test characteristics, not the prevalence PPV and NPV depend on the prevalence of the disease in the population

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Post-Test Probability • a revision of the probability of disease after a patient has been interviewed/examined/tested • calculation process can be explicit using results from epidemiologic studies, knowledge of the accuracy of tests, and a nomogram/Bayes’ theorem • the post-test probability from clinical examination is the basis of consideration when ordering diagnostic tests or imaging studies ■■ after each iteration the resultant post-test probability becomes the pre-test probability when considering new investigations

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Sources: Shah, CP. Health Indicators and Data Sources. Public Health and Preventive Medicine in Canada 5e. Toronto: Elsevier, 2003 The Association of Facult es of Medicine of Canada Public Health Educators’ Network. Assessing Evidence and Information. AFMC Primer on Population Health. NNT Consult http://www.thennt.com for quick summaries of evidence-based medicine (includes NNT, LR, and risk assessments)

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PH11 Population Health and Epidemiology

Toronto Notes 2018

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Types of Study Design

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Types of Study Design

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Qualitative vs. Quantitative

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Table 6. Qualitative vs. Quantitative Study Designs Qualitative

Quantitative “Top down” approach Theory → hypothesis → observation → confirmation

Sampling approach to obtain representative coverage of ideas , concepts, or experiences

Sampling approach to obtain representative coverage of people in the population

Narrative: rich, contextual, and detailed information from a small number of participants

Numeric: frequency severity, and associations from a large number of participants

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Often tests hypothesis (What? How much/many?)

“Bottom up” approach Observation → pattern → tentative hypothesis → theory

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Often used to generate hypothesis (Why? What does it mean?)

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Source: Adapted from http://phprimer.afmc.ca Source: The Association of Faculties of Medicine of Canada Public Health Educators’ Network. Assessing Evidence and Information. AFMC Primer on Population Health.

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Quant tative Research Methods Were exposures assigned by the investigator? Formulating a Research Question PICO Population/Patient Characteristics Intervention/Exposure of Interest Comparison Group or Control Group Outcome that you are trying to prevent or achieve

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No

Yes

Observational Study

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Experimental Study

Testing a hypothesis?

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Random allocation to groups?

No

Yes

No

Randomized Controlled Trial

NonRandomized Designs

Analytical Study

Descriptive Study

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Sampling based on

Exposure

Outcome

Neither

Cohort Study

Case-Control Study

Cross-Sectional Study

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Figure 8. Quantitative study designs Source: Adapted from h tp://phprimer.afmc.ca

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• observational studies involve neither the manipulation of the exposure of interest nor randomization of the study subjects • there are two main subtypes of observational studies: descriptive and analytic studies

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Descriptive Studies • describe the events and rates of disease with respect to person, place and time; estimates disease frequency and time trends • can be used to generate an etiologic hypothesis and for policy planning

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Analytic Studies • observational studies used to test a specific hypothesis • includes ecological studies, cohort studies, case-control studies, and cross-sectional studies

An example of an ecological fallacy would be concluding that red wine drinking leads to lower risk of death from CVS disease after an ecological study shows that countries with a higher rate of red wine consumption have a lower rate of death from CVS causes

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Observational Study Designs

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PH12 Population Health and Epidemiology

Toronto Notes 2018

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Types of Study Design

Cohort

Definition

Units of analysis are populations or groups of people, rather than individuals

Use individual data on exposures and outcomes gathered at the same time

Samples a group of people who already have a particular outcome (cases) and compares them to a similar sample group without that outcome (controls)

Subjects are sampled and, as a group, classified on the bas s of presence or absence of exposure to a particular risk factor

Subjects

Aggregated groups (e g. cities)

Sample of a population

Two or more samples of individuals with and without the outcome(s) of interest (i.e. cases and controls)

One or more cohorts Cohort: group of people with common characteristics (e.g. year of birth, region of residence) Divided into measured exposed vs. non-exposed groups

Methods

Descriptions of the average exposure or risk of disease for a population Can use regression models to test associations between area-level predictors and aggregate outcomes

Collect information from each person at one particular time Tabulate the numbers in groups (e.g by presence or absence of disease/factor of interest) Make tables and compare groups Estimate prevalence Use regression models to test associations between predictors and outcomes of interest

Select sample of cases of a specific disease during a specific time frame Representative of spectrum of clinical disease Select control(s) Represent the general population To minimize risk of bias, may select more than one control group and/ or match controls to cases (e.g. age, gender) Assess past exposures (e.g. EMR, quest onnaire) Association can be concluded between the risk factor and the disease (odds ratio)

Collect information on factors from all persons at the beginning of the study Subjects are followed for a specific period of time to determine development of disease in each exposure group Prospective: measuring from the exposure at present to the future outcomes Retrospective: measuring forward in time from exposures in the past to later outcomes Use statistical models to test associations between exposures and disease or other measured outcomes Provides estimates of incidence, relative risk, attributable risk

Advantages

Quick, easy to do Uses readily available data Generates hypothesis

Determines association between variables Quick and uses fewer resources Surveys with validated questions allows comparison between studies

Often used when disease in population is rare (less than 10% of population) due to increased efficiency or when time to develop disease is long Less costly and time consuming

Shows an association between risk factor(s) and outcome(s) Stronger evidence for causation Can consider a variety of exposures and outcomes

Disadvantages

Poor generalizability to individual level (not direct assessment of causal relationship) Ecological fallacy: an incorrect inference from groups to individuals Confounding

Does not allow for assessment of temporal relationship or offer strong evidence for causation between variables Confounding Selection bias Recall bias (see Bias, PH9)

Recall bias (see Bias, PH9) Confounding Selection bias for cases and controls Only one outcome can be measured

Confounding may occur due to individuals self-selecting the exposure, or unknown/ unmeasured factors are associated with the measured exposure and outcome Cost and duration of time needed to follow cohort Selection bias

A study looking at the association between smoking rates and lung cancer rates in different countries at the population level without individual data on both factors

A study that examines the distribution of BMI by age in Ontario at a particular point in time

A famous case control study published by Sir Richard Doll demonstrated the link between tobacco smoking exposure and lung cancer cases at the individual level

A famous cohort study is the Framingham Heart Study, which assessed the long-term cardiovascular risks of diet, exercise, medications such as ASA, etc.

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Examples

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Cross-Sectional

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Type of Study

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Case Control

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Table 7. Observational Study Designs

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Sources: Shah, CP. Measurement and Investigation. Public Health and Preventive Medicine in Canada, 5e. Toronto: Elsevier, 2003. The Association of Faculties of Medicine of Canada Public Health Educators’ Network. Assessing Evidence and Information. AFMC Primer on Population Health. Rothman KJ, Greenland SG, Lash TL. Modern Epidemiology, 3e. Philadelphia: Wolters Kluwer, 2012

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PH13 Population Health and Epidemiology

Toronto Notes 2018

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Types of Study Design

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Experimental Study Designs

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• not discu sed here are non-randomized control trials (e.g allocation by clinic or other non-random basis – performed when randomization is not possible)

Study begins by sampling subjects based on outcome

Exposed Unexposed

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Methods • random allocation of individuals into two or more treatment groups through a centralized concealed process • method of assessment to reduce bias ■■ single-blind: subject does not know group assignment (intervention or placebo) ■■ double-blind: subject and observer both unaware of group assignment ■■ triple-blind: subject, observer, and analyst unaware of group assignment • one group receives placebo or standard therapy one or more groups receive(s) the intervention(s) under study • baseline covariates and outcome(s) are measured and the groups are compared • all other conditions are kept the same between groups

Review records

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No Disease (controls)

Disease (cases)

Subjects • individuals are selected using explicit inclusion/exclusion criteria with recruitment targets guided by sample size calculations

Classify Exposure

Figure 9. Case-control study Adapted from http://phprimer.afmc.ca

Study begins Exposed group

Unexposed group

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Disadvantages • some exposures are not amenable to randomization (e.g. cannot randomize subjects to poverty/wealth or to harmful exposures such as smoking) due to ethical or feasibility concerns • can be difficult to randomly allocate groups (e.g communities, neighbourhoods) • difficult to study rare events, since RCTs would require extremely large sample sizes • contamination, co-intervention, and loss to follow-up can all limit causal inferences • can have poor generalizability • costly

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Advantages • “gold standard” of studies, upon which the practice of EBM is founded • provides the strongest evidence for effectiveness of intervention • threats to validity are minimized with sufficient sample size and appropriate randomization • randomization is one of few methods that can address selection bias and confounding (including unmeasured confounders) • allows prospective assessment of the effects of intervention

Exposed

Disease No disease

Disease No disease

Outcomes Figure 10. Cohort study

Adapted from http://phprimer.afmc.ca

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Sources: Shah, CP. Measurement and Investigation. Public Health and Preventive Medicine in Canada, 5e. Toronto: Elsevier, 2003. The Association of Faculties of Medicine of Canada Public Health Educators’ Network. Assessing Evidence and Information. AFMC Primer on Population Health.

Summary Study Designs

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Advantages • attempts to overcome the problem of reduced power due to small sample sizes of individual studies • ability to control for inter-study variation • can address questions (e.g. subgroup analyses) that the original studies were not powered to answer

An example of an RCT is the SPARCL trial, which demonstrated intense lipid-lowering with atorvastatin reduces the risk of cerebroand cardiovascular events in patients with and without carotid stenosis when compared to placebo

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Methods • selection of relevant studies from the published literature which meet quality criteria • statistical models used to combine the results of each independent study • provides a summary statistic of overall results as well as graphic representation of included studies (forest plot)

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Subjects • all the studies identified through the review (or all subjects used in original studies for individual level meta-analysis)

Intention-to-Treat Analysis (ITT) When groups are analyzed exactly as they existed upon randomization (i.e. using data from all patients, including those who did not complete the study)

An examp e of a meta-analysis is one that compares the effects of ACE inhibitors, CCBs, and other antihypertensive agents on mortality and major cardiovascular events by compiling and analyzing data from a full set of reported RCTs

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Definition • a form of statistical analysis that synthesizes the results of independent studies addressing a common research question, as identified through systematic review

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Analysis Per-Protocol Analysis (PP) Strategy of analysis in which only patients who complete the entire study are counted towards the results

META-ANALYSIS

© Emilie Wiens 2016 after Laura Greenlee 2014

Definition • subjects are assigned by random allocation to two or more groups, one of which is the control group, the other group(s) receive(s) an intervention

© Emilie Wiens 2016 after Laura Greenlee 2014

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RANDOMIZED CONTROLLED TRIAL (RCT)

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PH14 Population Health and Epidemiology

Toronto Notes 2018

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Methods of Analysis

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Methods of Analysis Distributions

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Mode Median Mean

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Negatively Skewed

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Type I Error (α Error) • the null hypothesis is falsely rejected (i.e. concluding an intervention X is effective when it is not, or declaring an observed difference to be real rather than by chance) • the probability of this error is denoted by the p-value • studies tend to be designed to minimize this type of error, since a type I error can have larger clinical significance than a type II error

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Type II Error (β Error) • the null hypothesis is falsely accepted (i.e. stating intervention X is not effective when it is, or declaring an observed difference/effect to have occurred by chance when it is present) • by convention a higher level of error is often accepted for most studies • can also be used to calculate statistical power

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Power • probability of correctly rejecting a null hypothesis when it is in fact false (i.e. the probability of finding a specified difference to be statistically significant at a given p-value) • power increases with an increase in sample size • power = 1 – β, and is therefore equal to the probability of a true positive result

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Statistical Significance • the probability that the statistical association found between variables is due to random chance alone (i.e. there is no association) • the preset probability is set sufficiently low that one would act on the result; frequently p Flat

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Cognitive Assessment Use MMSE to assess • Orientation (time and place) • Memory (immediate and delayed recall) • Attention and concentration • Language (comprehension, reading, writing, repetition, naming) • Spatial ability (intersecting pentagons) Gross screen for cognitive dysfunction: Total score is out of 30; 65 yr ■■ sex: male ■■ race/ethnic background: white or Native Canadians ■■ marital status: widowed/divorced ■■ living situation: alone; no children 1 mo

Delusional Disorder

Non-bizarre delusions, hallucinations

>1 mo

2º to Subs ance Intoxication/ Withdrawal

Delusions or hallucinations

During intoxication/withdrawal, not >1 mo without use

Mood symptoms dominant + delusions/ hallucinations (mood congruent)

Psychosis may be present for the du ation of the mood episode

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Disorganized Behaviours in Schizophrenia • Catatonic stupor: fully conscious, but immobile, mute, and unresponsive • Catatonic excitement: uncontrolled and aimless motor activity, maintaining bizarre positions for a long time • Stereotypy: repeated but non-goal-directed movement (e.g. rocking) • Mannerisms: goal-directed activities that are odd or out of context (e.g. grimacing) • Echopraxia: imitates movements and gestures of others • Automatic obedience: carries out simple commands in robot-like fashion • Negativism: refuses to cooperate with simple requests for no apparent reason • Inappropriate affect, neglect of self-care, other odd behaviours (random shouting)

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A. two (or more) of the following, each present for a significant portion of time during a 1 mo period (or less if successfully treated). At least one of these must be (1), (2), or (3) 1. delusions 2. hallucinations 3. disorganized speech (e.g. frequent derailment or incoherence) 4. grossly disorganized or catatonic behaviour 5. negative symptoms (i.e. diminished emotional expression or avolition) B. decreased level of function: for a significant portion of time since onset, one or more major areas affected (e.g. work, interpersonal relations, self-care) is markedly decreased (or if childhood/adolescent onset, failure to achieve expected level) C at least 6 mo of continuous signs of the disturbance Must include at least 1 mo of symptoms (or less if successfully treated) that meet Criterion A (i.e. active-phase symptoms) and may include periods of prodromal or residual symptoms, during which, disturbance may manifest by only negative symptoms or by two or more Criterion A symptoms present in an attenuated form (e.g. odd beliefs, unusual perceptual experiences) D. rule out schizoaffective disorder and depressive or bipolar disorder with psychotic features because either 1) no major depressive or manic episodes have occurred concurrently with the active-phase symptoms, or 2) if mood episodes have occurred during active-phase symptoms, they have been present for a minority of the total duration of the active and residual periods of the illness E. rule out other causes: GMC, substances (e.g. drug of abuse, medication) F. if history of autism spectrum disorder or communication disorder of childhood onset, the additional diagnosis of schizophrenia is made only if prominent delusions or hallucinations are also present for at least 1 mo (or less if successfully treated) • specifiers: type of episode (e.g. first episode, multiple episodes, continuous), with catatonia, current severity based on quantitative assessment of primary symptoms of psychosis (in acute episode, in partial remission, in full remission)

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Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, 5th ed. 2013. American Psychiatric Association

Management of Acute Psychosis and Mania • Ensure safety of self, patient, and other patients • Have an exit strategy • Decrease stimulation • Assume a non-threatening stance • IM medications (benzodiazepine + antipsychotic) often needed as patient may refuse oral medication • Physical restraints may be necessary • Do not use antidepressants or stimulants

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DSM-5 Diagnostic Criteria for Schizophrenia

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Ddx for psychosis • Primary psychotic disorders: schizophrenia, schizophreniform, brief psychotic, schizoaffective, delusional disorder • Mood disorders: depression with psychotic features, bipolar disorder (manic or depressive ep sode with psychotic features) • Personality disorders: schizotypal, schizoid, borderline, paranoid, obsessive-compulsive • General medical conditions: tumour, head rauma, dementia, delirium, metabolic, infection, stroke, temporal lobe epilepsy • Substance-induced psychosis: intoxication or withdrawal, prescribed medications, toxins

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Duration

Schizophrenia

Figure 1. Differentiating psychotic disorders with duration

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Psychotic Symptoms ≥1 positive symptoms of criterion A

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Disorder Brief Psychotic Disorder

2º to Mood Disorder

Brief Psychotic Schizophreniform Schizophrenia Disorder >6 months Disorder 1-6 months M, 2:1 • family history: depression, alcohol abuse, suicide attempt or completion • childhood experiences: loss of parent before age 11, negative home environment (abuse, neglect) • personality: neuroticism, insecure, dependent, obsessional • recent stressors: illness, financial, legal, relational, academic • lack of intimate, confiding relationships or social isolation • low socioeconomic status

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Etiology • biological ■■ genetic: 65-75% MZ twins; 14-19% DZ twins, 2-4 fold increased risk in first-degree relatives ■■ neurotransmitter dysfunction: decreased activity of 5-HT, NE, and DA at neuronal synapse; changes in GABA and glutamate; various changes detectable by fMRI ■■ neuroendocrine dysfunction: abnormal HPA axis activity ■■ neuroanatomy and neurophysiology: decreased hippocampal volume, increased size of ventricles; dec eased REM latency and slow-wave sleep; increased REM length ■■ immunologic: increased pro-inflammatory cytokines IL-6 and TNF ■■ secondary to medical condition, medication, substance use disorder psychosocial ■■ psychodynamic (e.g. low self-esteem, unconscious aggression towards self or loved ones, disordered attachment) ■■ cognitive (e.g. distorted schemata, Beck’s cognitive triad: negative views of the self, the world, and the future) ■■ environmental factors (e.g. job loss, bereavement, history of abuse or neglect, early life adversity) ■■ comorbid psychiatric diagnoses (e.g. anxiety, substance abuse, developmental disability, dementia, eating disorder)

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Epidemiology • lifetime prevalence: 12% • peak prevalence age 15-25 yr (M:F = 1:2)

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Antidepressants for Depression in Physical Medical Illness Cochrane Database Syst Rev 2000;(4):CD001312 Purpose: To evaluate whether antidepressants are clinically effective and acceptable for treatment of depression in patients who also have a physical illness. Methods: Systematic review of RCTs comparing any antidepressant drug as defined by the British National Formulary with placebo or no treatment, in patients aged 16 years and over who have been formally diagnosed with depression by any criterion, and have a specified physical disorder. Main outcome measures were number of individuals demonstrating mprovement or recovery by the end of the trial, and number completing treatment (as a proxy for trea ment acceptability). Results Eighteen studies with 838 patients having varied physical illnesses were included. Patients treated with antidepressants were significantly more likely to improve than those given placebo (13 studies, OR 0.37, 95% CI 0.27-0.51) or no treatment (1 study, OR 3.45, 11.1-1.10) (number needed to treat relative to placebo = 4.2, 3.2-6.4). Most antidepressants were associated with a small but significant increase in dropouts (OR 1.66, 1.14-2.40; NNH 9.8, 5.4-42.9). Among two s udies evaluating impact on function and quality of life, drug was found to be better than no treatment for HIV patients, and drug was not significantly different than placebo in lung disease patients. Tricyclics appeared to be more effec ive than SSRIs but also more likely to produce dropouts, based on nonrandomized comparisons between trials. Conclusion: Antidepressants cause improvements in depression in patients with various physical diseases ignificantly more frequently than placebo or no treatment. Antidepressants were reasonably acceptable to patients. Tricyclics may be more effective than SSRIs but may also produce more dropouts. As such, antidepressants should at least be considered in those with concomitant physical illness and depression.

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A. presence of a MDE B. the MDE is not better accounted for by schizoaffective disorder and is not superimposed on schizophrenia, schizophreniform disorder, delusional disorder, or psychotic disorder NOS C. there has never been a manic episode or a hypomanic episode Note: This exclusion does not apply if all of the manic-like, or hypomanic-like episodes are substance or treatment-induced or are due to the direct physiological effects of another medical condition • specifiers: with anxious distress, mixed features, melancholic features, atypical features, mood-congruent psychotic features, mood-incongruent psychotic features, catatonia, peripartum onset, seasonal pattern • single vs. recurrent is an episode descriptor that carries prognostic significance. Recurrent is classified as the patient having two or more distinct MDE episodes; to be considered separate the patient must have gone 2 consecutive months without meeting criteria

PS11 Psychiatry

Toronto Notes 2018

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Mood Disorders

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PERSISTENT DEPRESSIVE DISORDER

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Prognosis • one year after diagnosis of MDD without treatment: 40% of individuals still have symptoms that are sufficiently severe to meet criteria for MDD, 20% continue to have some symptoms that no longer meet criteria for MDD, 40% have no mood disorder

St. John’s Wort for Major Depression Cochrane Database Syst Rev 2008;(4):CD000448 Purpose: To evaluate whether extracts of hypericum are more effective than placebo, and as effective as standard anti depressants with fewer adverse effects for the treatment of major depression. Methods: Systematic review of double-blinded RCTs involving patient with major depression, comparing St John’s wort (hypericum extracts) with placebo or standard antidepressants. Main efficacy outcome was treatment response measured by a depression scale; mean safety outcome was the proportion of patients who dropped out due to adverse effects. Results: Twenty-nine trials involving 5,489 patients were included. St John’s wort was found to be more effective than placebo (response rate ratio (RRR) = 1.28, 95% CI 1.10-1.49), and similarly effective as tri- or tetracyclic antidepressants and selective serotonin reuptake inhibitors (RR = 1.02, 0.90-1.15; 1.00, 0.90-1.11, respectively) Less dropouts due to adverse effects were found with hypericum extracts relative to older antidepressants (odds ratio (OR) 0.24, 0.13-0.46) or SSRIs (OR 0.53, 0.34-0.83). Conclusion: St. John’s wort is superior to placebo in patients with major depression, similarly effective compared to antidepressants, and has fewer sideeffects than standard anti-depressants.

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Treatment • lifestyle: increased aerobic exercise, mindfulness-based stress reduction, zinc supplementation • biological: SSRIs, SNRIs, other antidepressants, somatic therapies (see Pharmacotherapy, PS42, and Somatic Therapies, PS49) ■■ 1st line pharmacotherapy: sertraline, escitalopram, venlafaxine, mirtazapine ■■ for partial or non-response, can change class or add augmenting agent (bupropion, quetiapine-XR, aripiprazole, lithium) ■■ typical response to antidepressant treatment: physical symptoms improve at 2 wk, mood/cognition by 4 wk; if no improvement after 4 wk at a therapeutic dosage, alter regimen ■■ ECT: currently fastest and most effective treatment for MDD. Consider in severe, psychotic or treatment resistant cases ■■ rTMS: early data support efficacy equivalent to ECT with good safety and tolerability ■■ phototherapy: especially if seasonal component, shift work, sleep dysregulation • psychological ■■ individual therapy (interpersonal, CBT), family therapy, group therapy • social: vocational rehabilitation, social skills training • experimental: magnetic seizure therapy, deep brain stimulation, vagal nerve stimulation, ketamine

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Depression in the Elderly • affects about 15% of community residents >65 yr old; up to 50% in nursing homes • high suicide risk due to social isolation, chronic medical illness, decreased independence • suicide peak: males aged 80-90; females aged 50-65 • dysphoria may not be a reliable indicator of depression in those >85 yr • often present with somatic complaints (e.g. changes in weight, sleep, energy) or anxiety symptoms • may have prominent cognitive changes after onset of mood symptoms (dementia syndrome of depression) • see Table 3, PS21, for a comparison of delirium and dementia

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DSM-5 Diagnostic Criteria for Persistent Depressive Disorder Note: in DSM-IV-TR this was referred to as Dysthymia

Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, 5th ed. 2013. American Psychiatric Association

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Treatment • psychological ■■ traditionally, psychotherapy was the principal treatment for persistent depressive disorder; recent evidence suggests some benefit, but generally inferior to pharmacological treatment. Combinations of the two may be most efficacious • biological ■■ antidepressant therapy: SSRIs (e.g. sertraline, paroxetine), TCAs (e.g. imipramine) as an outpatient

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Epidemiology • lifetime prevalence: 2-3%; M=F

Cognitive Therapy vs. Medications in the Treatment of Moderate to Severe Depression Arch Gen Psychiatry 2005;62:409-416 Purpose: To compare the efficacy of antidepressant medications with cognitive therapy versus placebo in moderate to severe depression. Methods: Outpatients with moderate to severe major depressive disorder (MDD), aged 18-70 years, were treated with 16 weeks of paroxetine with or without augmentation with lithium carbonate or desipramine hydrochloride versus cognitive behavioural therapy. Response up to 8 wk was controlled by pill placebo. The Hamilton Depression Rating scale was used to determine response to treatment. Results: 240 patients were included, 60 assigned to the intervention arm and 60 assigned to placebo. At 8 wks, 50% (95%CI 41-59%) of patients on medication and 43% (31-56%) of patients on CBT had responded, in comparison to 25% (16-38%) of patients on pill placebo. There was no significant difference between medication and CBT. At 16 wk, 46% of patients on medication and 40% of patients on CBT achieved remission. Conclusion: There is no difference in efficacy between CBT vs. paroxetine in the treatment of moderate to severe depression.

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A. depressed mood for most of the day, for more days than not, as indicated either by subjective account or observation by others, for ≥2 yr Note: in children and adolescents, mood can be irritable and duration must be at least 1 yr B presence, while depressed, of ≥2 of the following: ■■ poor appetite or overeating ■■ insomnia or hypersomnia ■■ low energy or fatigue ■■ low self-esteem ■■ poor concentration or difficulty making decisions ■■ feelings of hopelessness C. during the 2 yr period (1 yr for children or adolescents) of the disturbance, the person has never been without the symptoms in criteria A and B for more than 2 mo at a time D. criteria for a major depressive disorder may be continuously present for 2 yr E. there has never been a manic episode or a hypomanic episode, and criteria have never been met for cyclothymic disorder F. the disturbance is not better explained by a persistent schizoaffective disorder, schizophrenia, delusional disorder, or other specified or unspecified sch zophrenia spectrum and other psychotic disorder G. the symptoms are not due to the direct physiological effects of a substance or another medical condition H. the symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning

PS12 Psychiatry

Toronto Notes 2018

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Mood Disorders

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Postpartum Mood Disorders

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Postpartum “Blues” • transient period of mild depression, mood instability, anxiety, decreased concentration; considered to be normal changes in response to fluctuating hormonal levels, the stress of childbirth, and the increased responsibilities of motherhood • occurs in 50-80% of mothers; begins 2-4 d postpartum, usually lasts 48 h, can last up to 10 d • does not require psychotropic medication • usually mild or absent: feelings of inadequacy, anhedonia, thoughts of harming baby, suicidal thoughts

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MAJOR DEPRESSIVE DISORDER WITH PERIPARTUM ONSET (POSTPARTUM DEPRESSION)

Selective Serotonin Reuptake Inhibitors in Pregnancy and Infant Outcomes Paediatr Child Health 2011;16:562-563 Canadian Pediatric Society (CPS) clinical practice guideline recommendations: It is important to treat depression in pregnancy. There is no evidence that SSRIs increase the risk of major malformations. There is conflicting evidence concerning the association of paroxetine and cardiac malformations. SSRIs are not contraindicated while breast-feeding.

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Clinical Presentation • MDD with onset during pregnancy or within 4 wk following delivery • typically lasts 2-6 mo; residual symptoms can last up to 1 yr • may present with psychosis (rare, 0.2%), usually associated with mania, but also with MDE • severe symptoms include extreme disinterest in baby, suicidal and infanticidal ideation

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Epidem ology • occurs in 10% of mothers, risk of recurrence 50%

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Risk Factors • previous history of a mood disorder (postpartum or otherwise), family history of mood disorder • psychosocial factors: stressful life events, unemployment, marital conflict, lack of social support, unwanted pregnancy, colicky or sick infant

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Treatment • psychotherapy (CBT or IPT) • short-term safety of maternal SSRIs for breastfeeding infants established; long-term effects unknown • if depression severe or psychotic symptoms present, consider ECT

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Prognosis • impact on child development: increased risk of cognitive delay, insecure attachment, behavioural disorders • treatment of mother improves outcome for child at 8 mo through increased mother-child interaction

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Bipolar Disorders

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BIPOLAR I / BIPOLAR II DISORDER

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Definition • Bipolar I Disorder ■■ disorder in which at least one manic episode has occurred ■■ if manic symptoms lead to hospitalization, or if there are psychotic symptoms, the diagnosis is BP I ■■ commonly accompanied by at least 1 MDE but not required for diagnosis ■■ time spent in mood episodes: 53% asymptomatic, 32% depressed, 9% cycling/mixed, 6% hypo/manic • Bipolar II Disorder ■■ disorder in which there is at least 1 MDE, 1 hypomanic and no manic episodes ■■ while hypomania is less severe than mania, Bipolar II is not a “milder” form of Bipolar I ■■ time spent n mood episodes: 46% asymptomatic, 50% depressed, 1% cycling/mixed, 2% hypo/manic ■■ Bipolar II is often missed due to the severity and chronicity of depressive episodes and low rates of spontaneous reporting and recognition of hypomanic episodes

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Bipolar II is quite often missed and many patients are symptomatic for up to a decade before accurate diagnosis and treatment

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Classification • classification of bipolar disorder involves describing the disorder (I or II) and the current or most recent mood episode as either manic, hypomanic, or depressed • specifiers: with anxious distress, depressed with mixed features, hypo/manic with mixed features, melancholic features, atypical features, mood-congruent or -incongruent psychotic features, catatonia, peripartum onset, seasonal pattern, rapid cycling (4+ mood episodes in 1 yr)

Patients with bipolar disorder are at higher risk for suicide when they switch from mania to depression, especially as they become aware of consequences of their behaviour during the manic episode

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Risk Factors • genetic: 60-65% of bipolar patients have family history of major mood disorders, especially bipolar disorders • clinical features of MDE history favouring bipolar over unipolar diagnosis: early age of onset (2 mo • never have met criteria for MDE, manic or hypomanic episodes ■■ symptoms not better explained by any psychotic disorder (including schizoaffective, schizophrenia, schizophreniform, delusional disorder, or other specified/unspecified) • symptoms are not due to the direct physiological effects of a substance or GMC • symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning

A Randomized Controlled Trial of Cognitive Therapy for Bipolar Disorder: Focus on LongTerm Change J Clin Psychiatry 2006;67:277-286 Purpose: To evaluate long-term change with cognitive therapy plus emotive techniques for the treatment of bipolar disorder. Methods: Blinded RCT including patients with DSM-IV bipolar I or II disorder allocated to either a 6 mo trial of cognitive therapy (CT) with emotive techniques or treatment as usual. Both groups received mood stabilizers. Main outcomes were relapse rates, dysfunctional attitudes, psychosocial functioning, hopelessness, self-control, and medication adherence. Patients were assessed by independent raters blinded to treatment group. Results: At 6 mo, CT patients experienced fewer depressive symptoms and fewer dysfunctional attitudes. There was a non-significant (p=0.06) trend to greater time to depressive relapse. At 12 mo follow-up, CT patients had lower Young Mania Rating scores and improved behavioural self-control. At 18 mo, CT patients reported less severity of illness. Conclusions: CT appears to provide benefits in the 12 mo after completion of therapy.

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CYCLOTHYMIA

The 4 L’s or Bipolar Depression Lithium, Lamotrigine, Lurasidone, SeroqueL

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Course and Prognosis • high suicide rate (15% mortality from suicide), especially in mixed states • BP I and II are chronic conditions with a relapsing and remitting course featuring alternating manic and depressive episodes; depressive symptoms tend to occur more frequently and last longer than manic episodes • can achieve high level of functioning between episodes • may switch rapidly between depression and mania without any period of euthymia in between • high recurrence rate for mania – 90% will have a subsequent episode in the next 5 yr • long term follow-up of BP I – 15% well, 45% well with relapses, 30% partial remission, 10% chronically ill

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Monotherapy with antidepressants should be avoided in patients with bipolar depression as patients can switch from depression into mania

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Treatment • lifestyle: psychoeducation regarding cycling nature of illness, ensure regular check ins, develop early warning system, “emergency plan” for manic episodes, promote stable routine (sleep, meals, exercise) • biological: lithium, anticonvulsants, antipsychotics, ECT ( f refractory); monotherapy with antidepressants should be avoided ■■ mood stabilizers vary in their ability to “treat” (reduce symptoms acutely) or “stabilize” (prevent relapse and recurrence) manic and depressive symptoms; multi-agent therapy is common ■■ treating mania: lithium, valproate, carbamazepine (2nd line), SGA, ECT, benzodiazepines (for acute agitation) ■■ preventing mania: same as above but usually at lower dosages, minus benzodiazepines ■■ treating depression: lithium, lurasidone, quetiapine, lamotrigine, antidepressants (only with mood stabilizer), ECT ■■ preventing depression: same as above plus aripiprazole, valproate (note: quetiapine first line in treating bipolar II depression) ■■ mixed episode or rapid cycling: multi-agent therapy, lithium or valproate + SGA (lurasidone, aripiprazole, olanzapine) • psychological: supportive psychotherapy, CBT, IPT or interpersonal social rhythm therapy, family therapy • social: vocational rehabilitation, consider leave of absence from school/work, assess capacity to manage finances, drug and EtOH cessation, sleep hygiene, social skills training, education and recruitment of family members

PS14 Psychiatry

Toronto Notes 2018

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Anxiety Disorders

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Differential Diagnosis

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Table 2. Differential Diagnosis of Anxiety Disorders Post-MI, arrhythmia, congestive heart failure, pulmonary embolus, mitral valve prolapse

Respiratory

Asthma, COPD, pneumonia, hyperventilation

Endocrine

Hyperthyroidism, pheochromocytoma, hypoglycemia, hyperadrenalism, hyperparathyroidism

Metabolic

Vitamin B12 deficiency porphyria

Neurologic

Neoplasm, vestibular dysfunction, encephalitis

Substance-Induced

Intoxication (caffeine, amphetamines, cocaine, thyroid preparations, OTC for colds/decongestants), withdrawal (benzodiazepines, alcohol)

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Cardiovascular

Psychotic disorders, mood disorders, personality disorders (OCPD), somatoform disorders

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Other Psychiatric Disorders

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Medical Workup of Anxiety Disorder • routine screening: physical exam, CBC, thyroid function test, electrolytes, urinalysis, urine drug screening • additional screening: neurological consultation, chest X-ray ECG, CT head

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Panic Disorder

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DSM-5 Diagnostic Criteria for Panic Disorder

Panic attack

Increased anxiety and generalization to other situations

Mentally associated with situation

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Situational trigger

Figure 2. Pan c attack

Criteria for Panic Disorder (≥4) STUDENTS FEAR the 3 Cs Sweating Trembling Unsteadiness, dizziness Depersonalization, Derealization Excessive heart rate, palpitations Nausea Tingling Shortness of breath Fear of dying, losing control going crazy 3 Cs: Chest pain, Chil s, Choking

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A. recurrent unexpected panic attacks - a panic attack is an abrupt surge of intense fear or intense discomfort that reaches a peak within minutes, and during which time four (or more) of the following symptoms occur ■■ palpitations, pounding heart, or accelerated heart rate ■■ sweating ■■ trembling or shaking ■■ sensations of shortness of breath or smothering ■■ feelings of choking ■■ chest pain or discomfort ■■ nausea or abdominal distress ■■ feeling dizzy, unsteady, light-headed, or faint ■■ chills or heat sensations ■■ paresthesias (numbness or tingling sensations) ■■ derealization (feelings of unreality) or depersonalization (being detached from oneself) ■■ fear of losing control or “going crazy” ■■ fear of dying B. 1 mo (or more) of “anxiety about panic attacks” - at least one of the attacks has been followed by one or both of the following: ■■ persistent concern or worry about additional panic attacks or their consequences ■■ a significant maladaptive change in behaviour related to the attacks C. the disturbance is not attributable to the physiological effects of a substance or another medical condition D. the disturbance is not better explained by another mental disorder

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Reprinted with permission from the Diagnostic and Statistical Manual of Men al Disorders, 5th ed. 2013. American Psychiatric Association

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Epidemiology • prevalence: 2-5% (one of the top five most common reasons to see a family doctor); M:F = 1:2-3 • onset: average early-mid 20s, familial pattern Panic Attack vs. Panic Disorder Panic disorder consists of panic attacks + other criteria Panic attack is not a codable disorder and can occur in the context of many different disorders

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Prognosis • 6-10 yr post-treatment: 30% well, 40-50% improved, 20-30% no change or worse • clinical course: chronic, but episodic with psychosocial stressors

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Starting Medication for Anxiety Start low, go slow, aim high and explain symptoms to expect prior to initiation of therapy to prevent non-compliance due to physica side effects

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Treatment • psychological ■■ CBT: interoceptive exposure (eliciting symptoms of a panic attack and learning to tolerate the symptoms without coping strategies); cognitive restructuring (addressing underlying beliefs regarding the panic attacks), relaxation techniques (visualization, box-breathing) • pharmacological ■■ SSRIs: fluoxetine, citalopram, paroxetine, fluvoxamine, sertraline ■■ SNRI: venlafaxine ■■ with SSRI/SNRIs, start with low doses, titrate up slowly ■■ anxiety disorders often require treatment at higher doses for a longer period of time than depression (i.e. full response may take up to 12 wk) ■■ treat for up to 1 year after symptoms resolve to avoid relapse ■■ to prevent non-compliance due to physical side effects, explain symptoms to expect prior to initiation of therapy ■■ other antidepressants (mirtazapine, MAOIs) ■■ consider avoiding bupropion or TCAs due to stimulating effects (exacerbate anxious symptoms) ■■ benzodiazepines (short-term, low dose, regular schedule, long half-life, avoid prn usage)

PS15 Psychiatry

Toronto Notes 2018

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Anxiety Disorders

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Agoraphobia

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DSM-5 D agnostic Criteria for Agoraphobia

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Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, 5th ed. 2013. American Psychiatric Association

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A. marked fear or anxiety about two (or more) of the following five situations: ■■ using public transportation ■■ being in open spaces ■■ being in enclosed places ■■ standing in line or being in a crowd ■■ being outside of the home alone B. the individual fears or avoids these situations because of thoughts that escape might be difficult or help might not be available in the event of developing panic-like symptoms or other incapacitating or embarrassing symptoms C. the agoraphobic situations almost always provoke fear or anxiety D. the agoraphobic situations are actively avoided, require the presence of a companion, or are endured with intense fear or anxiety E. the fear or anxiety is out of proportion to the actual danger posed by the agoraphobic situations and to the sociocultural context F. the fear, anxiety, or avoidance is persistent, typically lasting ≥6 mo G. the fear, anxiety, or avoidance causes clinically significant distress or impairment in social, occupational, or other important areas of functioning H. if another medical condition is present, the fear, anxiety, or avoidance is clearly excessive I. the fear, anxiety, or avoidance is not better explained by the symptoms of another mental disorder and are not related exclusively to obsessions, perceived defects or flaws in physical appearance, reminders of traumatic events, or fear of separation Note: agoraphobia is diagnosed irrespective of the presence of panic disorder. If an individual’s presentation meets criteria for panic disorder and agoraphobia, both diagnoses should be assigned

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Treatment • as per panic disorder

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Generalized Anxiety Disorder

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Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, 5th ed. 2013. American Psychiatric Association

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A. excessive anxiety and worry (apprehensive expectation), occurring more days than not for at least 6 mo, about a number of events or activities (such as work or school performance) B. the individual finds it difficult to control the worry C the anxiety and worry are associated with three (or more) of the following six symptoms (with at least some symptoms having been present for more days than not for the past 6 mo) 1. restlessness or feeling keyed up or on edge 2. being easily fatigued 3. difficulty concentrating or mind going blank 4. irritability 5. muscle tension 6. sleep disturbance (difficulty falling or staying asleep, or restless, unsatisfying sleep) D. the anxiety, worry, or physical symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning E. the disturbance is not attributable to the physiological effects of a substance or another medical condition F. the disturba ce is not better explained by another mental disorder

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Epidemiology • 1 yr prevalence: 3-8%; M:F = 1:2 ■■ if considering only those receiving inpatient treatment, ratio is 1:1 • most commonly presents in early adulthood

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Treatment • lifestyle: caffeine and EtOH avoidance, sleep hygiene • psychological: CBT including relaxation techniques, mindfulness • biological ■■ SSRIs and SNRIs are 1st line (paroxetine, escitalopram, sertraline, venlafaxine XL) ■■ 2nd line: buspirone (tid dosing), bupropion (caution due to stimulating effects), ■■ add-on benzodiazepines (short-term, low dose, regular schedule, long half-life, avoid prn usage) ■■ β-blockers not recommended

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Prognosis • chronically anxious adults become less so with age • depends on pre-morbid personality functioning, stability of relationships, work, and severity of environmental stress • difficult to treat

Criteria for GAD (≥3)

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DSM-5 Diagnostic Criteria for Generalized Anxiety Disorder

C-FIRST Concentration issues Fatigue Irritability Restlessness Sleep disturbance Tension (muscle)

PS16 Psychiatry

Toronto Notes 2018

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Anxiety Disorders

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Phobic Disorders Adopted/summarized from the Diagnostic and Statistical Manual of Mental Disorders, 5th ed. 20 3 American Psychiatric Association

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Specific Phobia • definition: marked and persistent (>6 mo) fear that is excessive or unreasonable, cued by presence or anticipation of a specific object or situation • lifetime prevalence 12-16%; M:F ratio variable • types: animal/insect, environment (heights, storms), blood/injection/injury, situational (airplane, closed spaces), other (loud noise, clowns)

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Social Phobia (Social Anxiety Disorder) • definition: marked and persistent (>6 mo) fear of social or performance situations in which one is exposed to unfamiliar people or to possible scrutiny by others; fearing he/she will act in a way that may be humiliating or embarrassing (e.g. public speaking, initiating or maintain ng conversation, dating, eating in public) • 12 mo prevalence rate may be as high as 7%; M:F ratio approximately equal

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Diagnostic Criteria for Phobic Disorders • exposure to stimulus almost invariably provokes an immediate anxiety response; may present as a panic attack • person recognizes fear as excessive or unreasonable • s tuations are avoided or endured with anxiety/distress significant interference with daily routine, occupational/social functioning, and/or marked distress

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Treatment • psychological ■■ cognitive behaviour therapy (focusing on both in vivo and virtual exposure therapy, gradually facing feared situations) ■■ behavioural therapy is more efficacious than medication • biological ■■ SSRIs/SNRIs (e.g. fluoxetine, paroxetine, sertraline, venlafaxine), MAOIs ■■ β-blockers or benzodiazepines in acute situations (e.g. public speaking) Prognosis • chronic

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Obsessive-Compulsive Disorder

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DSM-5 Diagnostic Criteria for Obsessive-Compulsive Disorder

Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, 5th ed. 2013. American Psychiatric Association

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A. presence of obsessions, compulsions, or both ■■ obsessions are defined by (1) and (2) 1. recurrent and persistent thoughts, urges, or images that are experienced, at some time during the disturbance, as intrusive and unwanted, and cause marked anxiety or distress in most individuals 2. the individual attempts to ignore or suppress such thoughts, urges, or images, or to neutralize them with some other thought or action (i.e. by performing a compulsion; see below) ■■ compulsions are defined by (1) and (2) 1. repetitive behaviours (e.g. hand washing, ordering, checking) or mental acts (e.g. praying, counting, repeating words silently) that the individual feels driven to perform in response to an obsession or according to rules that must be applied rig dly 2. behaviours mental acts are aimed at preventing or reducing anxiety or distress, or preventing some dreaded event or situation; however, these behaviours or mental acts are not connected in a realistic way with what they are designed to neutralize or prevent, or are clearly excessive B. the obsessions or compulsions are time-consuming (e.g. take >1 h/d) or cause clinically significant distress or impairment in social, occupational, or other important areas of functioning C. the obsessive-compulsive symptoms are not attributable to the physiological effects of a substance or another medical condition D. the disturbance is not better explained by the symptoms of another mental disorder

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Epidemiology • 12 mo prevalence 1.1-1.8%; females affected at slightly higher rates than males • rate of OCD in first-degree relatives is higher than in the general population

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Prognosis • tends to be refractory and chronic

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Treatment • CBT: exposure with response prevention (ERP) – involves exposure to feared situations with the addition of preventing the compulsive behaviours; cognitive strategies include challenging underlying beliefs • pharmacotherapy: SSRIs/SNRIs (12-16 week trials, higher doses vs. depression), clomipramine; adjunctive antipsychotics (risperidone)

PS17 Psychiatry

Toronto Notes 2018

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Trauma- and Stressor-Related Disorders

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Trauma- and Stressor-Related Disorders

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Post-Traumatic Stress Disorder

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DSM-5 Diagnostic Criteria for Post-Traumatic Stress Disorder

Rep inted with permission from the Diagnostic and Statistical Manual of Mental Disorders, 5th ed. 2013. American Psychiatric Association.

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Criteria for Post-Traumatic Stress Disorder

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TRAUMA Traumatic event Re-experience the event Avoidance of stimuli associated with the trauma Unable to function More than a Month Arousal increased + negative alterations in cognition and mood

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Epidemiology • prevalence of 7% in general population • men’s trauma is most commonly combat experience/physical assault; women’s trauma is usually physical or sexual assault

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Treatment • psychotherapy, CBT ■■ ensure safety and stabilize: emotional regulation techniques (e g. breathing, relaxation) ■■ once coping mechanisms established, can explore/mourn trauma - challenge dysfunctional beliefs, etc. ■■ reconnect and integrate - exposure therapy, etc.

Acute Stress Disorder • May be a precursor to PTSD • Similar symptoms to PTSD • Symptoms persist 3 d after a trauma until 1 mo after the exposure

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A. exposure to actual or threatened death, serious injury, or sexual violence in one (or more) of the following ways: 1. directly experiencing the traumatic event(s) 2. witnessing, in person, the event(s) as it occurred to others 3. learning that the traumatic event(s) occurred to a close family member or close friend. In cases of actual or threatened death of a family member or friend, the event(s) must have been violent or accidental 4. experiencing repeated or extreme exposure to aversive details of the traumatic event(s) (e.g. first responders collecting human remains: police officers repeatedly exposed to details of child abuse) B. presence of one (or more) of the following intrusion symptoms associated with the traumatic event(s), beginning after the traumatic event(s) occurred 1. recurrent, involuntary, and intrusive distressing memories of the traumatic event(s) 2. recurrent distressing dreams in which the content and/or affect of the dream are related to the traumatic event(s) 3. dissociative reactions (e.g. flashbacks) in which the individual feels or acts as if the traumatic event(s) were recurring 4. intense or prolonged psychological distress at exposure to internal or external cues that symbolize or resemble an aspect of the traumatic event(s) 5. marked physiological reactions to internal or external cues that symbolize or resemble an aspect of the traumatic event(s) C. persistent avoidance of stimuli associated with the traumatic event(s), beginning after the traumatic event(s) occurred, as evidenced by one or both of the following 1. avoidance of or efforts to avoid distressing memories, thoughts, or feelings about or closely associated with the traumatic event(s) 2. avoidance of or efforts to avoid external reminders (people, places, conversations, activities, objects, situations) that arouse distressing memories, thoughts, or feelings about or closely associated with the traumatic event(s) D. negative alterations in cognitions and mood associated with the traumatic event(s), beginning or worsening after the traumatic event(s) occurred, as evidenced by two (or more) of the following 1. inability to remember an important aspect of the traumatic event(s) 2 persistent and exaggerated negative beliefs or expectations about oneself, others, or the world 3 persistent, distorted cognitions about the cause or consequences of the traumatic event(s) that lead the individual to blame himself/herself or others 4. persistent negative emotional state (e.g. fear, horror, anger, guilt, or shame) 5. markedly diminished interest or participation in significant activities 6. feelings of detachment or estrangement from others 7. persistent inability to experience positive emotions E. marked alterations in arousal and reactivity associated with the traumatic event(s), beginning or worsening after the traumatic event(s) occurred, as evidenced by two (or more) of the following 1. irritable behaviour and angry outbursts (with little or no provocation) typically expressed as verbal or physical aggression toward people or objects 2. reckless or self-destructive behaviour 3. hypervigilance 4. exaggerated startle response 5. problems with concentration 6. sleep disturbance (e.g. difficulty falling or staying asleep or restless sleep) F. duration of the disturbance (criteria B, C, D, and E) is more than 1 mo G. the disturbance causes clinically significant distress or impairment in social, occupational, or other important areas of functioning H. the disturbance is not attributable to the physiological effects of a substance or another medical condition

PS18 Psychiatry

Toronto Notes 2018

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Bereavement

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• biological ■■ SSRIs (e g. paroxetine, sertraline) ■■ prazosin (for treating disturbing dreams and nightmares) ■■ benzodiazepines (for acute anxiety) ■■ adjunctive atypical antipsychotics (risperidone, olanzapine) • eye movement desensitization and reprocessing (EMDR): an experimental method of reprocessing memories of distressing events by recounting them while using a form of dual attention stimulation such as eye movements, bilateral sound, or bilateral tactile stimulation (its use is controversial because of limited evidence)

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Complications • substance abuse, relationship difficulties, depression, impaired social and occupational functioning disorders, personality disorders

Adjustment Disorder

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Definition • a diagnosis encompassing patients who have difficulty coping with a stressful life event or situation and develop acute, often transient, emotional or behavioural symptoms that resemble less severe versions of other psychiatric conditions

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DSM 5 Diagnostic Criteria for Adjustment Disorder

Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, 5th ed. 2013. American Psychiatric Association

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A. the development of emotional or behavioural symptoms in response to an identifiable stressor(s) occurring within 3 mo of the onset of the stressor(s) B. these symptoms or behaviours are clinically significant as evidenced by either of the following: ■■ marked distress that is in excess of what would be expected from exposure to the stressor ■■ significant impairment in social or occupational (academic) functioning C. the stress-related disturbance does not meet criteria for another mental disorder and is not merely an exacerbation of a pre-existing mental disorder D. the symptoms do not represent normal bereavement E. once the stressor (or its consequences) has terminated, the symptoms do not persist for more than an additional 6 mo ■■ specifiers: with depressed mood, with anxiety, with mixed anxiety/depression, with conduct disturbance, with mixed disturbance of conduct/emotions unspecified

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Classification • types of stressors ■■ single (e.g. termination of romantic relationship) ■■ multiple (e.g. marked business difficulties and marital problems) ■■ recurrent (e.g. seasonal business crises) ■■ continuous (e.g. living in a crime-ridden neighbourhood) ■■ developmental events (e.g. going to school, leaving parental home, getting married, becoming a parent, failing to attain occupational goals, retirement)

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Epidemiology • F:M 2:1, prevalence 2-8% of the population

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Treatment • brief psychotherapy individual or group (particularly useful for patients dealing with unique and specific medical issues; e.g. colostomy or renal dialysis groups), crisis intervention • biological ■■ benzodiazepines may be used for those with significant anxiety symptoms (short-term, low-dose, regular schedule)

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Bereavement

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Risk Factors for Poor Bereavement Outcome • Poor social supports • Unanticipated death or lack of preparation for death • Highly dependent relationship with deceased • High initial distress • Other concurrent stresses and losses • Death of a child • Pre-existing psychiatric disorders, especially depression and separation anxiety

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Clinical Presentation • bereavement is a normal psychological and emotional reaction to a significant loss, also called grief or mourning • length and characteristics of “normal” bereavement are variable between individuals/cultures • normal response: protest → searching and acute anguish → despair and detachment → reorganization • presence of the following symptoms may indicate abnormal grief/presence of MDD ■■ guilt about things other than actions taken or not taken by the survivor at the time of death ■■ thoughts of death other than the survivor feeling that they would be better off dead or should have died with the deceased person; morbid preoccupation with worthlessness ■■ marked psychomotor retardation; prolonged and marked functional impairment ■■ hallucinatory experiences other than thinking that the survivor hears the voice of or transiently sees the image of the deceased person ■■ dysphoria that is pervasive and independent of thoughts or triggers of the deceased, absence of mood reactivity

PS19 Psychiatry

Toronto Notes 2018

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Neurocognitive Disorders

Bereavement is associated with a significant increase in morbidity and mortality acutely following the loss, with effects seen up to 1 yr after

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• after 12 mo, if patient continues to yearn/long for the deceased, experience intense sorrow/emotional pain in response to the death, remain preoccupied with the deceased or with their circumstance of death, then may start to consider a diagnosis of “persistent complex bereavement disorder” • if a patient meets criteria for MDD, even in the context of a loss or bereavement scenario, they are still diagnosed with MDD

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Treatment • support and watchful waiting should be first line, as well as education and normalization of the grief process • screen for increased alcohol, cigarette and drug use • normal grief should not be treated with antidepressant or antianxiety medication, as it is important to allow the person to experience the whole mourning process to achieve resolution • psychosocial: for those needing additional support, complex grief/bereavement, or significant MDD, grief therapy (individual or group) is indicated • pharmacotherapy: if MDD present, past history of mood disorders, severe or autonomous symptoms

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Neurocognitive Disorders

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Delirium

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• see Neurology, N20 and Geriatric Medicine, G4

Confusion Assessment Method (CAM) for Diagnosis of Delirium

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I WATCH DEATH • Infectious (encephalitis, meningitis, UTI, pneumonia) • Withdrawal (alcohol, barbiturates, benzodiazepines) • Acute metabolic disorder (electrolyte imbalance, hepatic or renal failure) • Trauma (head injury, post-operative) • CNS pathology (stroke, hemorrhage, tumour, seizure disorder, Parkinson’s) • Hypoxia (anemia, cardiac failure, pulmonary embolus) • Deficiencies (vitamin B12, folic acid, thiamine) • Endocrinopathies (thyroid, glucose, parathyroid, adrenal) • Acute vascular (shock, vasculitis, hypertensive encephalopathy) • Toxins: substance use sedatives, opioids (especially morphine), anesthetics, anticholinergics anticonvulsants, dopaminergic agents, steroids, insulin, glyburide, antibiotics (especially quinolones), NSAIDs • Heavy metals (arsenic, lead, mercury)

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Etiology of Delirium

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Investigations • standard: CBC and differential, electrolytes (including Ca, Mg and PO4), glucose, BUN, Cr, TSH/T4, LFTs, vit B12, folate, albumin; urinalysis, urine C+S • as indicated: ECG (to assess QT interval when considering treatment with an antipsychotic agent), CXR, CT head, toxicology/heavy metal screen, VDRL, HIV, LP blood cultures, EEG (typically abnormal generalized slowing [most common] or fast activity, can also be used to rule out underlying seizures or post-ictal states as etiology)

Visual hallucinations are organic until proven otherwise

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Risk Factors • most common precipitating factors include: polypharmacy (particularly involving psychoactive drugs such as anticholinergics), infection, dehydration, immobility, malnutrition, and use of bladder catheters • other factors include: ■■ hospitalization (incidence 10-56%), frail and surgical patients are at the greatest risk ■■ previous delirium ■■ nursing home residents (incidence 60%) ■■ old age (especially males) ■■ severe illness (e.g. cancer, AIDS) ■■ recent anesthesia or surgery ■■ brain vulnerability: substance abuse, past psychiatric illness, pre-existing neurologic or neurocognitive disorder

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Need (1) + (2) + (3 or 4) (1) Acute onset and fluctuating course (2) Inattention (3) Disorganized thinking 4) Altered level of consciousness hyperactive or hypoactive

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Clinical Presentation and Assessment • common symptoms ■■ distractibility, disorientation (time, place, rarely person) ■■ misinterpretations, illusions, hallucinations ■■ speech/language disturbances (dysarthria, dysnomia) ■■ affective symptoms (anxiety, fear, depression, irritability, anger, euphoria apathy) ■■ shifts in psychomotor activity (groping/picking at clothes, attempts to get out of bed when unsafe, sudden movements, sluggishness, lethargy) ■■ impairment in sleep duration and/or architecture (e.g. sleep-wake reversal) • Folstein Mini Mental Status Exam or Montreal Cognitive Assessment are helpful to assess baseline of altered mental state (i.e. score will improve as symptoms resolve)

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Highly sensitive and specific method to diagnosis delirium • Part 1: an assessment instrument that screens for overall cognitive impairment • Part 2: includes four features found best able to distinguish delirium from other cognitive impairments

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A. attention and awareness: disturbance in attention (i.e. reduced ability to direct, focus, sustain, and shift attention) and awareness (reduced orientation to the environment) B. acute and fluctuating: disturbance develops over short period of time (usually hours to days), represents a change from baseline attention and awareness, and tends to fluctuate in severity during the course of a day C. cognitive changes: an additional disturbance in cognition (e.g. memory deficit disorientation, language, visuospatial ability, or perception) D. not better explained: disturbances in criteria A and C are not better explained by another neurocognitive disorder (pre-existing, established, or evolving) and do not occur in the context of a severely reduced level of arousal (e.g. coma) E. direct physiological cause: evidence that disturbance is a direct physiological consequence of another medical condition, substance intoxication or withdrawal (i.e due to a drug of abuse or medication), toxin, or is due to multiple etiologies • Note: del rium can be described as HYPERactive, HYPOactive, or MIXED presentation. While patients with hyperactive delirium may demonstrate features of restlessness and agitation, as well as experience hallucinations and delusions, those with hypoactive delirium present with lethargy, sedation and respond slowly to questioning

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Rep inted with permission from the Diagnostic and Statistical Manual of Mental Disorders, 5th ed. 2013. American Psychiatric Association

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DSM-5 Diagnostic Criteria for Delirium

PS20 Psychiatry

Toronto Notes 2018

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Neurocognit ve Disorders

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• indications for CT head: focal neurological deficit, acute change in status, anticoagulant use, acute incontinence, gait abnormality, history of cancer • MRI may be useful to exclude acute or subacute stroke and multifocal inflammatory lesions in patients with de irium of unknown cause and negative head CT

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Management • identify and manage underlying cause ■■ identify and treat underlying cause immediately ■■ stop all non-essential medications ■■ maintain nutrition, hydration, electrolyte balance and monitor vitals • optimize the environment ■■ environment: quiet, well-lit, near window for cues regarding time of day ■■ optimize hearing and vision ■■ room near nursing station for closer observation; constant care if patient jumping out of bed, pulling out lines ■■ family member present for reassurance and re-orientation ■■ frequent orientation - calendar, clock, reminders • pharmacotherapy ■■ low dose, high potency antipsychotics: haloperidol has the most evidence; reasonable alternatives include risperidone, olanzapine (more sedating, less QT prolongation), quetiapine (if EPS), aripiprazole (may shorten QTc) ■■ benzodiazepines only to be used in alcohol/substance withdrawal delirium; otherwise, can worsen delirium (antipsychotics will not be useful in substance withdrawal delirium) ■■ try to minimize anticholinergic side effects • physical restraints to maintain safety only if necessary (last resort) Prognosis • up to 50% 1 yr mortality rate after episode of delirium

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Major Neurocognitive Disorder (Dementia) • see Neurology, N21

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DSM-5 Diagnostic Criteria for Major Neurocognitive Disorder

Reprinted with permissi n fr m the Diagnostic and Statistical Manual of Mental Disorders, 5th ed. 2013. American Psychiatric Association

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Alzheimer’s disease: predominantly memory and learning issues Frontotemporal degeneration: language type (early preservation), behavioural type (apathy/ disinhibition/self-neglect) Lewy body disease: recurrent, soft visual hallucinations (e.g. rabbits), autonomic impairment (falls, hypotension), EPS, does not respond well to pharmacotherapy, fluctuating degree of cognitive impairment Vascular disease: vascular risk factors, focal neurological signs abrupt onset, stepwise progression Normal pressure hydrocephalus: abnormal gai , early incontinence, rapidly progressive

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Subtypes • with or without behavioural disturbance (e.g. wandering, agitation) • early-onset: age of onset 65 yr

Flags for Differentiating Most Common Causes of Dementia

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Huntington’s disease Another medical condition Multiple etiologies Unspecified

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Normal pressure hydrocephalus Substance/medication use HIV infection Prion disease Parkinson’s disease

Epidemiology • prevalence increases with age: 5% in patients >65 yr of age; 35-50% in patients >85 yr of age • pre-test probability of dementia in an older person with reported memory loss is estimated to be 60% • prevalence is increased in people with Down’s syndrome and head trauma • Alzheimer’s disease comprises >50% of cases; vascular causes comprise approximately 15% of cases (other causes of dementia neurocognitive disorder – see Neurology, N23) • average duration of illness from onset of symptoms to death is 8 10 yr

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The “Mini Cog” Rapid Assessment • 3 word immediate recall • Clock drawn to “10 past 11” • 3 word delayed recall

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Specify whether due to: Alzheimer’s disease Frontotemporal lobar degeneration Lewy body disease Vascular disease Traumatic brain injury

The 4 As of Dementia Amnesia Aphasia Apraxia Agnosia

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A. evidence of significant cognitive decline from a previous level of performance in one or more cognitive domains (complex attention, executive function, learning and memory, language, perceptual-motor, or social cognition) based on: 1 concern of the individual, a knowledgeable informant, or the clinician that there has been a significant decline in cognitive function; and 2. substantial impairment in cognitive performance, preferably documented by standardized neuropsychological testing or, in its absence, another quantified clinical assessment B. cognitive deficits interfere with independence in everyday activities (i.e. at a minimum, requiring assistance with complex instrumental activities of daily living such as paying bills or managing medications) ■■ Note: if deficits do not interfere as in B, and impairments are mild-moderate as in A, this is considered “mild neurocognitive disorder”; see Neurology, N21 C. cognitive deficits do not occur exclusively in the context of a delirium D. cognitive deficits are not better explained by another mental disorder (e.g. major depressive disorder, schizophrenia) E. in the case of neurodegenerative dementias such as Alzheimers Disease, disturbances should be of insidious onset and progressive

PS21 Psychiatry

Toronto Notes 2018

c

Substance-Related and Addictive Disorders

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Investigations (rule out reversible causes) • standard: see Delirium, PS19 • as indicated: VDRL, HIV, SPECT, CT head in dementia • indications for CT head: same as for delirium, plus: age 60 mmol/L (non-tolerant drinkers) and 90-120 mmol/L (tolerant drinkers)

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Women: 2 or less/d (≤10/wk)

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Make sure to ask about other alcohols: mouthwash, rubbing alcohol, methanol, ethylene glycol, aftershave (may be used as a cheaper alternative)

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Table 4. Canada’s Low-Risk Alcohol Drinking Guidelines Men: 3 or less/d (≤15/wk)

Confabulations: the fabrication of imaginary experiences to compensate for memory loss

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History • CAGE: validated screening questionnaire C ever felt the need to Cut down on drinking? A ever felt Annoyed at criticism of your drinking? G ever feel Guilty about your drinking? E ever need a drink first thing in morning (Eye opener)? ■■ for men, a score of ≥2 is a positive screen; for women, a score of ≥1 is a positive screen ■■ if positive CAGE, then assess further to distinguish between problem drinking and alcohol use disorder

PS24 Psychiatry

Toronto Notes 2018

c

Substance-Related and Addictive Disorders

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Wernicke-Korsakoff Syndrome • alcohol-induced amnestic disorders due to thiamine deficiency • necrotic lesions: mammillary bodies, thalamus, brainstem • Wernicke’s encephalopathy (acute and reversible): triad of oculomotor dysfunction such as nystagmus (CN VI palsy), gait ataxia, and confusion • Korsakoff ’s syndrome (chronic and only 20% reversible with treatment): anterograde amnesia and confabulations; cannot occur during an acute delirium or dementia and must persist beyond usual duration of intoxication/withdrawal • management ■■ Wernicke’s: thiamine 100 mg PO OD x 1-2 wk ■■ Korsakoff ’s: thiamine 100 mg PO bid/tid x 3-12 mo

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Treatment of Alcohol Use Disorder • non-pharmacological ■■ see General Approach to Treatment, PS4 • pharmacological ■■ naltrexone (Revia®): opioid antagonist, shown to be successful in reducing the “high” associated with alcohol, moderately effective in reducing cravings, frequency or intensity of alcohol binges ■■ disulfiram (Antabuse®): prevents oxidation of alcohol (blocks acetaldehyde dehydrogenase); with alcohol consumption, acetaldehyde accumulates to cause a toxic reaction (vomiting, tachycardia, death); if patient relapses, must wait 48 h before restarting Antabuse®; prescribed only when treatment goal is abstinence. RCT evidence is generally poor or negative ■■ acamprosate (Campral®): NMDA glutamate receptor antagonist; useful in maintaining abstinence and decreasing cravings

Opioids

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Naltrexone (Revia®) • Can be used for EtOH dependence (although not routinely used) • Long half life (h)

Naloxone (Narcan®) • Used for life-threatening CNS/respiratory depression in opioid overdose • Short half life (48 h with long-acting opioids) • caution with longer half-life; may need to observe for toxic reaction for at least 24 h

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Acute Intoxication • direct effect on receptors in CNS resulting in decreased pain perception, sedation, decreased sex drive, nausea/vomiting, decreased GI motility (constipation and anorexia), and respiratory depression

Opioid Antagonists Naltrexone vs Naloxone

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• types of opioids: heroin, morphine, oxycodone, Tylenol #3® (codeine), hydromorphone, fentanyl • major risks associated with the use of contaminated needles: increased risk of hepatitis B and C, bacterial endocarditis, HIV/AIDS

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Treatment of Opioid Use Disorder • see General Approach to Treatment, PS4 • long term treatment may include withdrawal maintenance treatment with methadone (opioid agonist) or buprenorphine (mixed agonist-antagonist) • Suboxone® formulation includes naloxone in addition to buprenorphine, in an effort to prevent injection of the drug. When naloxone is injected, it will precipitate opiate withdrawal and block the opiate effect of buprenorphine; however it will not have this antagonist action when taken sublingually

Cocaine

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• street names: blow, C, coke, crack, flake, freebase, rock, snow • alkaloid extracted from leaves of the coca plant; blocks presynaptic uptake of serotonin (causing euphoria), dopamine (linked to its addictive effect), norepinephrine and epinephrine (causing vasospasm, HTN) • sodium channel blockade - cocaine slows or blocks nerve conduction and acts as a local anesthetic by altering recovery of neuronal Na+ channels. It has a similar effect on cardiac Na+ channels and in overdose can manifest on ECG as prolongation of the QRS complex • self-administered by inhalation (90% bioavailability), insufflation (e.g. intranasal; 80% bioavailability), or intravenous route

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Maintenance Medication for Opiate Addiction: The Foundation of Recovery J Addict Dis 2012;31:207-225 Maintenance treatment of opioid addiction with methadone or buprenorphine is associated with retention in treatment, reduction in illicit opiate use, dec eased craving, and improved social function. Recently, studies showing extended release naltrexone injections have showed some promise.

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Withdrawal • symptoms: depression, insomnia, drug-craving, myalgias, nausea, chills, autonomic instability (lacrimation, rhinorrhea, piloerection) • onset: 6-12 h; duration: 5-10 d • complications: loss of tolerance (overdose on relapse), miscarriage, premature labour • management: long-acting oral opioids (methadone, buprenorphine), α-adrenergic agonists (clonidine)

PS25 Psychiatry

Toronto Notes 2018

c

Substance-Related and Addictive Disorders

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Withdrawal • initial “crash” (1-48 h): increased sleep, increased appetite • withdrawal (1-10 wk): dysphoric mood plus fatigue, irritability, vivid unpleasant dreams, insomnia or hypersomnia, psychomotor agitation or retardation • complications relapse, suicide (significant increase in suicide during withdrawal period) • management: supportive management

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Treatment of Cocaine Use Disorder • see General Approach to Treatment, PS4 no pharmacologic agents have widespread evidence or acceptance of use

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Findings Weight loss (especially cocaine, heroin) Injected conjunctiva (cannabis) Pinpoint pupils (opioids) Track marks (injection drugs) Trauma MSK Viral hepatitis (injection GI drugs) Unexplained elevations in ALT (injection drugs) Behavioural Missed appointments Non-compliance Drug-seeking (especially benzodiazepines, opioids) Psychological Insomnia Fatigue Depression Flat affect (benzodiazepines, barbiturates) Paranoia (cocaine) Psychosis (cocaine, cannabis, hallucinogens) Marital discord Social Family violence Work/school Absenteeism and poor performance

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Complications • cardiovascular: arrhythmias, MI, CVA, ruptured AAA, chest pain (accounts for 40% of all cocainerelated ED visits) • neurologic: seizures • psychiatric: psychosis, paranoia, delirium, suicidal ideation • other: nasal septal deterioration, acute/chronic lung injury “crack lung”, possible increased risk of connective tissue disease

System General

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Overdose • medical emergency: HTN, tachycardia, tonic-clonic seizures, dyspnea, and ventricular arrhythmias • treatment with IV diazepam to control seizures • beta-blockers (incl. labetalol or propranolol) are not recommended because of risk from unopposed alpha-adrenergic stimulation

Common Presentations of Drug Use

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Intoxication • elation, euphoria, pressured speech, restlessness, sympathetic stimulation (e.g. tachycardia, mydriasis, sweating) • prolonged use may result in paranoia and psychosis

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• onset and duration of action: onset within seconds if inhaled, lasting 15-30 min; onset in 3-5 min if insufflated, blood levels peak at 10-20 min with effects begin ing to fade after 45-60 min. Cocaine has a biologic half life of 1 h, thus repeated self-administration is common among users to maintain an effect

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Amphetamines

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• includes prescription medications for ADHD such as Ritalin® and Adderall® • intoxication characterized by euphoria, improved concentration, sympathetic and behavioural hyperactivity and at high doses can mimic psychotic mania, can eventually cause coma • chronic use can produce a paranoid psychosis which can resemble schizophrenia with agitation, paranoia, delusions and hallucinations • withdrawal symptoms include dysphoria fatigue, and restlessness • treatment of amphetamine induced psychosis: antipsychotics for acute presentation, benzodiazepines for agitation, β-blockers for tachycardia, hypertension

Cannabis

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Cannabinoid Hyperemesis Syndrome An nteresting and relatively new clinical phenomenon associated with chronic cannabis use characterized by cyclical, recurrent severe nausea, vomiting, and colicky pain. Possibly due to increased potency of available THC products. Patients often present to ED in acute distress with no evidence of specific GI pathology. Many patients will successfully self-medicate with hot baths or showers

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Medical Uses of Marijuana • Anorexia-cachex a (AIDS, cancer) • Spasticity, muscle spasms (multiple sclerosis, spinal cord injury) • Levodopa-induced dyskinesia (Parkinson’s Disease) • Controlling tics and obsessive-compulsive behaviour (Tourette’s syndrome) • Reducing intra-ocular pressure (glaucoma)

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• cannabis (marijuana) is the most commonly used recreational drug • psychoactive substance: delta-9-tetrahydrocannabinol (Δ9-THC) • general clinical manifestations: intoxication characterized by tachycardia, conjunctival vascular engorgement, dry mouth, altered sensorium, increased appetite, and muscle relaxation • neuropsychiatric effects: ■■ altered mood, perception and thought content: increased sense of well-being, euphoria/laughter ■■ impaired cognitive and psychomotor performance: reduced reaction time, impaired attention, concentration and short-term memory. It may also impair motor coordination required to complete complex tasks requiring divided attention. Notably, psychomotor impairments may interfere with one’s ability to operate heavy machinery such as automobiles • inhaled marijuana: onset of psychoactive effects occurs rapidly with peak effects felt 15-30 min after intake and lasting up to 4 h ■■ acute exacerbation in patients with asthma may be a complication with inhalation • ingested marijuana: following oral ingestion, psychotrophic effects set in with a delay of 30-90 min, reach their maximum after 2-3 h and last for about 4-12 h, depending on dose (Grotenhermen, 2003, pharmacokinetics and pharmacodynamics of cannabinoids) • high doses can cause depersonalization, paranoia, anxiety and may trigger psychosis and schizophrenia if predisposed • chronic use is associated with tolerance and an apathetic, amotivational state, and increases risk of later manic episodes • assessment: standard urine drug screens • treatment of cannabis use disorder: see General Approach to Treatment, PS4 • cessation following heavy use produces a significant withdrawal syndrome: irritability, anxiety, insomnia, decreased food intake

PS26 Psychiatry

Toronto Notes 2018

c

Substance-Related and Addictive Disorders

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“Club Drugs”

Cannabis Use and Risk of Psychotic or Affective Mental Health Outcomes: A Systematic Review The Lancet 2007;370:319-328 Purpose: To review the evidence for cannabis use and occurrence of psychotic or affective mental health outcomes. Study Characteristics: A meta-analysis of 35 population-based longitudinal studies, or casecontrol studies nested within longitudinal designs. Results: There was an increased risk of any psychotic outcome in individuals who had ever used cannabis (pooled adjusted odds ratio =1.41, 95% CI 1.20-1.65). Findings were consistent with a doseresponse effect, w h greater risk in people who used cannabis more frequently (2.09, 95% CI, 1.542.84). Findings for depression, suicidal thoughts, and anxiety outcomes were less consistent. In both cases (psychotic and affective outcomes), a substantial confounding effect was present. Conclusions: The findings are consistent with the view that cannabis increases risk of psychotic outcomes independent of transient intoxication effects, although evidence is less strong for affective outcomes. Although cannabis use and the development of psychosis are strongly associated, it is difficult to determine causality and it is possible that the association results from confounding factors or bias. The authors did conclude that there is sufficient evidence to warn young people that using cannabis could increase their risk of developing a psychotic illness later in life.

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• types of hallucinogens by primary action ■■ 5-HT2A agonists: LSD, mescaline (peyote), psilocybin mushrooms, DMT (ayahuasca) ■■ NMDA antagonists: PCP, ketamine ■■ κ-opioid agonists: salvia divinorum, ibogaine • 5-HT2A agonists are most commonly used; intoxication characterized by tachycardia, HTN, mydriasis, tremor, hyperpyrexia, and a variety of perceptual, mood and cognitive changes (rarely, if ever, deadly; treat vitals symptomatically) • psychological effects of high doses: depersonalization, derealization, paranoia, and anxiety (panic with agoraphobia) • tolerance develops rapidly (hours-days) to most hallucinogens so physical dependency is virtually impossible, although psychological dependency and problematic usage patterns can still occur • no specific withdrawal syndrome characterized • management of acute intoxication • support, reassurance, diminished stimulation; benzodiazepines or high potency antipsychotics seldom required (if used, use small doses), minimize use of restraints • long term adverse effects: controversial role in triggering psychiatric disorders, particularly mood or psychosis, thought to be chiefly in individuals with genetic or other risk factors • Hallucinogen Persisting Perception Disorder: DSM-5 d agnosis characterized by long lasting, spontaneous, intermittent recurrences of visual perceptual changes reminiscent of those experienced with hallucinogen exposure

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Hallucinogens

Acts on serotonergic and dopaminergic pathways, properties of a hallucinogen and stimulant

Effect Enhanced sensorium; feelings of well-being, empathy

Sweating, tachycardia fatigue, muscle spasms (especially jaw clenching), ataxia, hyperthermia, arrhythmias, DIC, rhabdomyolysis, renal failure, seizures, death

Gamma Hydroxybutyrate (GHB, “G”, “Liquid Ecstasy”)

Biphasic dopamine response (inhibition then release) and releases opiate-like substance

Euphoric effects, increased aggression, impaired judgmen

Sweating, tachycardia, fatigue, muscle spasms (especially jaw clenching), ataxia, severe withdrawal from abrupt cessation of high doses: tremor, seizures, psychosis

Flunitrazepam (Rohypnol®, “Roofies”, “Rope”, “The Forget Pill”)

Potent benzodiazepine rapid oral absorption

Sedation, psychomotor impairment, amnestic effects, decreased sexual inhibition

CNS depression with EtOH

Ketamine (“Special K”, “Kit-Kat”)

NMDA receptor antagonist, rapid-acting general anesthetic used in pediatrics and by veterinarians

“Dissociative” state, profound amnesia/ analgesia; hallucinations and sympathomimetic effects

Psychological distress, accidents due to intensity of experience and lack of bodily control. In overdose: decreased LOC, respiratory depression, catatonia

Amphetamine stimulant, induces norepinephrine, dopamine, and serotonin release

Rush begins in min, effects last 6-8 h, increased activity, decreased appetite, general sense of well-being, tolerance occurs quickly, users often binge and crash

Short-term use: high agitation, rage, violent behaviour, occasionally hyperthermia and convulsions Long-term use: addiction, anxiety, confusion, insomnia, paranoia, auditory and tactile hallucinations (especially formication), delusions mood disturbance, suicidal and homicidal thoughts, stroke May be contaminated with lead, and IV users may present with acute lead poisoning

Emerging Medical Uses of Hallucinogens Many hallucinogens are currently under investigation for therapeutic benefit; LSD & Psilocybin for end of life anxiety, MDMA for PTSD, Ketamine for rapid treatment of depression, ibogaine derivatives for addiction

Amnestic, euphoric, hallucinatory state

Horizontal/vertical nystagmus, myoclonus, ataxia, autonomic instability (treat with diazepam IV), prolonged agitated psychosis (treat with haloperidol); high risk for suicide; violence towards others High dose can cause coma

Formication Tactile hallucination that insects or snakes are crawling over or under the skin (especially associated with crystal meth use)

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Not understood, used by veterinarians to immobilize large animals

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Phencyclidine (“PCP”, “angel dust”)

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Date Rape Drugs • GHB • Flunitrazepam (Rohypnol®) • Ketamine

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Methamphetamine (“speed”, “meth”, “chalk”, “ice”, “crystal”)

Adverse Effects

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Mechanism

MDMA (“Ecstasy”, “X”, “E”, “M”, “Molly”)

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Table 6. The Mechanism and Effects of Common “Club Drugs”

PS27 Psychiatry

Toronto Notes 2018

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Somatic Symptom and Related Disorders

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Somatic Symptom and Related Disorders

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Management of Somatic Symptom and Related Disorders • brief, regular scheduled visits with GP to facilitate therapeutic relationship and help patient feel cared for • limit number of physicians involved in care, minimize medical investigations; coordinate necessary investigations • emphasis on what the patient can change and control; the psychosocial coping skills, not their physical symptoms (functional recovery > explanation of symptoms) • do not tell patient it is “all in their head,” emphasize these disorders are real entities or functional in nature • psychotherapy: CBT, mindfulness interventions, biofeedback, conflict resolution • minimize psychotropic drugs: anxiolytics in short-term only, antidepressants for comorbid depression and anxiety

Somatic Symptom Disorder

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DSM-5 Diagnostic Criteria for Somatic Symptom Disorder

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Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, 5th ed. 2013. American Psychiatric Association

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A. one or more somatic symptoms that are distressing or result in significant disruption of daily life B. excessive thoughts, feelings, or behaviours related to the somatic symptoms or associated health concerns as manifested by at least one of the following 1. disproportionate and persistent thoughts about the seriousness of one’s symptoms 2. persistently high level of anxiety about health or symptoms 3. excessive time and energy devoted to these symptoms or health concerns C. although any one somatic symptom may not be continuously present, the state of being symptomatic is persistent (typically >6 mo) • somatic symptom disorder with predominant pain (previously pain disorder) for those whose somatic symptom is primarily pain • patients have physical symptoms and believe these symptoms represent the manifestation of a serious illness • persistent belief despite negative medical investigations and may develop different symptoms over time • lifetime prevalence may be around 5-7% in the general adult population • females tend to report more somatic symptoms than males do, cultural factors may influence sex ratio • complications: anxiety and depression commonly comorbid (up to 80%), unnecessary medications or surgery • often a misdiagnosis for an insidious illness so rule out all organic illnesses (e.g. multiple sclerosis)

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Illness Anxiety Disorder

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• preoccupation with fear of having, or the idea that one has, a serious disease, to the point of causing significant impairment • convictions persist despite negative investigations and medical reassurance • somatic symptoms are mild or not present • there is a high level of anxiety about health and the individual is easily alarmed about personal health status • person engages in maladaptive behaviour such as excessive physical checking or total healthcare avoidance • duration is ≥6 mo; onset in 3rd-4th decade of life • a new diagnostic entity so epidemiology is not well known; however, it is likely less common than SSD • possible role for SSRIs due to generally high level of anxiety

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Malingering: intentional production of false or grossly exaggerated physical or psychological symptoms, motivated by secondary gain / external reward (e.g. avoiding work, obtaining financial compensation, or obtaining drugs) Factitious Disorder: intentional production or feigning of physical or psychological signs or symptoms. Unlike malingering patients are not motivated by secondary gain but rather may seek sympathy, nurturance and attention

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General Characteristics • physical signs and symptoms lacking objective medical support in the presence of psychological factors that are judged to be important in the initiation, exacerbation, or maintenance of the disturbance • cause significant distress or impairment in functioning • symptoms are produced unconsciously and are not the result of malingering or factitious disorder, which are disorders of voluntary presentation of symptoms (or intentionally inducing, e.g injecting feces) for secondary gain • primary gain: somatic symptom represents a symbolic resolution of an unconscious psychological conflict; serves to reduce anxiety and conflict with no external incentive • secondary gain: the sick role; external benefits obtained or unpleasant duties avoided (e.g. work)

PS28 Psychiatry

Toronto Notes 2018

c

Dissociative Disorders

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Conversion Disorder (Functional Neurological Symptom Disorder)

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la belle indifférence An inappropriately cavalier patient attitude in the face of serious symptoms; classically associated with conversion disorder

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• one or more symptoms or deficits affecting voluntary motor or sensory function that mimic a neurological or GMC (e.g. impaired coordination local paralysis, double vision, seizures, or convulsions) • does not need to be preceded by a psychological event as per previous DSM criteria, however this is still worth exploring as many patients will present after such an event or related to a medical diagnosis in a first-degree relative • 2-5/100,000 in general population; 5% of referrals to neurology clinics • more common in rural populations and in individuals with little medical knowledge • spontaneous remission in 95% of acute cases, 50% of chronic cases (>6 mo) • incompatible findings detected from specific neurological testing can help differentiate between functional and neurological origin (e.g. Hoover’s sign, dermatome testing)

Conversion Disorder

Malingering

Somatic Symptoms

Present

Mild or absent

Neurologic, voluntary motor or sensory

Psychological or physical

Psychological or physical

Symptoms Produced

Unconsciously

Unconsciously

Unconsciously

Consciously

Consciously

Physical Findings

Absent

Absent

Incompatible

Possible, attempts to falsify

Possible, attempts to falsify

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Illness Anxiety Disorder

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Somatic Symptom Disorder

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Factitious Disorder

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Table 7. Differential of Somatic Symptom and Related Disorders

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Dissociative Disorders

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Definition • severe dissociation resulting in breakdown of integrated functions of consciousness and perception of self • differential diagnosis PTSD, acute stress disorder, borderline personality disorder, somatic symptom disorder, substance abuse, GMC (various neurologic disorders including complex/partial seizures, migraine, Cotard syndrome)

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Dissociative Identity Disorder

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disruption of identity characterized by two or more distinct personality states or an experience of possession • can manifest as sudden alterations in sense of self and agency (ego-dystonic emotions, behaviours, speech) • features recurrent episodes of amnesia (declarative or procedural)

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Dissociative Amnesia

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• inability to recall important autobiographical information, usually of a traumatic or stressful nature, that is inconsistent with normal forgetting and not attributable to a psychiatric disorder or medical illness • localized/selective amnesia: failure to recall all/some events during a prescribed period of time • generalized amnesia: (more rare) complete loss of memory for one’s life history, ± procedural knowledge, ± semantic knowledge. Usually sudden onset. Often presen s with perplexity, disorientation, aimless wandering

oo

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Depersonalization/Derealization Disorder

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Fugue Purposeful travel or bewildered wandering while in amnesic state

During depersonalization or derealization, patients usually have intact reality testing, which adds to their alarming nature

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• persistent or recurrent episodes of one or both of: ■■ depersonalization: experiences of detachment from oneself, feelings of unreality, or being an outside observer to one’s thoughts, feelings, speech, and actions (can feature distortions in perception including time, as well as emotional and physical numbing) ■■ derealization: experiences of unreality or detachment with respect to the surroundings (e.g. feeling as if in a dream, or that the world is not real, external visual world is foggy or distorted) • transient (seconds-hours) experiences of this nature are quite common in the general population • episodes can range from hours-years, patients are often quite distressed and verbalize concern of “going crazy”

PS29 Psychiatry

Toronto Notes 2018

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Sleep Disorders

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Sleep Disorders

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• for more information regarding normal sleep cycles and the illnesses described, see Neurology, Sleep Disorders, N46

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Overview • adequate sleep is essential to normal functioning; deprivation can lead to cognitive impairment and increased mortality • circadian rhythms help regulate mood and cognitive performance • neurotransmitters commonly implicated in psychiatric illnesses also regulate sleep ■■ acetylcholine activity and decreased activity of monoamine neurotransmitters is associated with greater REM sleep ■■ decreased adrenergic and cholinergic activity are associated with NREM sleep • depression is associated with decreased ∆ (deep, slow-wave) sleep, decreased REM latency, and increased REM density • criteria ■■ must cause significant distress or impairment in normal functioning ■■ not due to a GMC or medications/drugs (unless specified)

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Management • pharmacological treatments are illness-specific ■■ non-benzodiazepines preferable (e.g. trazodone, zoplicone, quetiapine), but benzodiazepines a short term option ■■ medication should not be prescribed without having first made a diagnosis and considering major psychiatric illnesses (major depression and alcohol use disorders are common etiologies) • sleep hygiene is a simple, effective, but often underutilized method for addressing sleep disturbances; recommendations include ■■ waking up and going to bed at same time every day, including on weekends ■■ avoiding long periods of wakefulness in bed ■■ not using bed for non-sleep activities (reading, TV, work) ■■ avoiding napping ■■ discontinuing or reducing consumption of alcohol, caffeine, drugs ■■ exercising at least 3-4x per week (but not in the evening, if this interferes with sleep) • Cognitive Behavioural Therapy for insomnia (CBTi)

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Table 8. Major DSM-5 Sleep-Wake Disorders

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Note: F r m re information regarding specific disorders, see: Neurology Sleep Disorders, N46; Family Medicine Sleep Disorders, FM44; and Respirology Sleep Apnea, R32

Category

Disorder

Description

(Uncategorized)

Insomnia disorder

Difficulty sleeping

Hypersomnolence disorder

Feeling sleepy throughout the day Recurrent attacks of irrepressible need to sleep

Circadian rhythm sleep-wake disorders

Insomnia or excessive sleepiness due to misalignment or alteration in endogenous circadian rhythm

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Narcolepsy

Disturbance in sleep (insomnia or daytime sleepiness) caused by substance/medication intoxication or withdrawal

Obstructive sleep apnea hypopnea

Breathing issues due to obstruction

Central sleep apnea

Breathing issues due to aberrant brain signaling

Sleep-related hypoventilation

Breathing issues due to decreased responsiveness to carbon dioxide levels

Non-rapid eye movement sleep arousal disorders

Incomplete awakening from sleep, complex motor behaviour without conscious awareness; amnesia regarding episodes; includes symptoms of: Sleepwalking: rising from bed and walking about, blank face, unresponsive, awakened with difficulty Sleep terrors: recurrent episodes of abrupt terror arousals from sleep, usually beginning with a panicky scream, intense fear and autonomic arousal, relative unresponsiveness to comfort during episodes Specifiers: sleep-related sexual behaviour (sexsomnia) and sleeprelated eating

Nightmare disorder

Repeated extended, extremely dysphoric, often very vivid, wellremembered dreams that usually involve significant threats; rapid orientation and alertness on awakening with autonomic arousal

Rapid eye movement sleep behaviour disorder

Arousal during sleep, associated with vocalization and/or complex motor behaviours; can cause violent injuries; rapid orientation and alertness on awakening

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Parasomnias

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Breathing-related sleep disorders

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Uncomfortable, frequent urge to move legs at night

Substance/medication-induced sleep disorder

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Restless legs syndrome

PS30 Psychiatry

Toronto Notes 2018

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Sexuality and Gender

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Sexuality and Gender

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Gender Dysphoria

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Definition • the distress that may coincide with conflict between one’s experienced/expressed gender and one’s assigned gender

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Typical Presentation • strong and persistent cross-gender identification • desire to be rid of primary/secondary sex characteristics and to gain the primary/secondary sex characteristics of their identified gender • repeated stated desire or insistence that one is of the opposite sex • preference for cross dressing, cross-gender roles in make-believe play • intense desire to participate in the stereotypical games and pastimes of the opposite sex • strong preference for playmates of the opposite sex • significant distress or impairment in functioning and persistent discomfort with his or her sex or gender role

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Treatment • psychotherapy • hormonal therapy • sexual reassignment surgery

Paraphilic Disorders

Treatment • anti-androgen drugs • behaviour modification • psychotherapy

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Definition • intense and persistent sexual interest that is not sexual interest in genital stimulation or preparatory fondling with phenotypically normal, physically mature, consenting human partners • paraphilic disorder: paraphilia that causes distress or functional impairment to the individual, or a paraphilia whose realization entails personal harm, or risk of harm to others • subtypes: voyeuristic, exhibitionistic, frotteuristic, sexual masochism, sexual sadism, pedophilic, fetishistic, ransvestic, other specified paraphilic disorder, unspecified paraphilic disorder • rarely self referred; come to medical attention through interpersonal or legal conflict • person usually has more than one paraphilia; 5% of paraphilias attributed to women • typical presentation: begins in childhood or early adolescence; increasing in complexity and stability with age • chronic, decreases with advancing age but may increase with stress

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SEXUAL DYSFUNCTION • see Gynecology, GY33 and Urology, U34

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Eating Disorders

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Definition • eating disorders are characterized by a persistent disturbance of eating that impairs psychosocial functioning or health • disorders include: anorexia nervosa, avoidant/restrictive food intake disorder, binge eating disorder bulimia nervosa, pica and rumination disorder. Epidemiology • anorexia nervosa (AN): 1% of adolescent and young adult females; onset 13-20 yr old • bulimia nervosa (BN): 2-4% of adolescent and young adult females; onset 16-18 yr old • F:M=10:1; mortality 5-10%

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Etiology • multifactorial: psychological, sociological, and biological associations • individual: perfectionism, lack of control in other life areas, history of sexual abuse • personality: obsessive-compulsive, histrionic, borderline • familial: maintenance of weight equilibrium and control in dysfunctional family

PS31 Psychiatry

Toronto Notes 2018

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Eating Disorders

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• cultural factors: prevalent in industrialized societies, idealization of thinness in the media • genetic factors ■■ AN: 6% prevalence in siblings, with one study of twin pairs finding concordance in 9 of 12 monozygotic pairs versus concordance in 1 of 14 dizygotic pairs ■■ BN: higher familial incidence of affective disorders than the general population

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Reprinted with permission from he Diagnostic and Statistical Manual of Mental Disorders, 5th ed. 2013. American Psychiatric Association

A. intake and weight: restriction of energy intake relative to requirements, leading to a significantly low body weight in the context of age, sex, developmental trajectory, and physical health. Significantly low weight is defined as a weight that is less than minimally normal or, for children and adolescents, less than that minimally expected B. fear or behaviour: intense fear of gaining weight or of becoming fat, or persistent behaviour that interferes with weight gain, even though at a significantly low weight C. perception: disturbance in the way in which one’s body weight or shape is experienced, undue influence of body weight or shape on self-evaluation or persistent lack of recognition of the seriousness of the current low body weight • specifiers: partial remission, full remission, severity based on BMI (mild = BMI >17 kg/m2, moderate = BMI 16-16.99 kg/m2, severe = BMI 15-15.99 kg/m2, extreme = BMI