Toronto Notes 2023 - Rheumatology & Orthopedics

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COMPREHENSIVE MEDICAL REFERENCE

AND A REVIEW FOR MCCQE +
Editors-in-Chief • Anders Erickson & Jennifer Parker
https://medical-amboss.com
Associate Editors, Primary •Dorrin Zarrin Khat & Ming Li
Associate Editors, Medicine • Karolina Gaebe & Alyssa Li
Associate Editors, Surgery • Vrati Mehra & Chunyi Christie Tan
TORONTO NOTES
2023
Comprehensive Medical Reference

and a Review for the Medical Council of Canada Qualifying Exam
(MCCQE)
39th Edition
Editors-in -Chief:
Anders W. Erickson & Jennifer Parker
Toronto Notes for Medical Students, Inc.

Toronto, Ontario, Canada +
2 Editorial Toronto Xotcs 2023
Thirty-ninth Edition
Copyright © 2023 - Toronto Notes for Medical Students, Inc. Toronto, Ontario, Canada
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Preface - From the Editors
Dear reader . and the Climate Crisis are also fully addressed. In addition to
content updates, the Toronto Notes 2023 Clinical Handbook has
We are grateful to present Toronto Notes 2023 to you. This been restructured to prioritize high - yield content to guide your
edition is the product of an exceptional effort from the learning during clerkship rotations. Toronto Notes prioritizes
hundreds of editors and contributors who worked tirelessly with cultural sensitivity, health equity, and strives for accurate
us as we navigated through the year. Together, we have created representation of our vibrant and diverse communities. To
the thirty- ninth edition of Toronto Notes, thus continuing enhance our team’s editorial lens on these concepts while editing
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our organization's rich tradition of providing an up to- date, the chapters, training was provided by the Anti - Racism and
comprehensive, and concisely written medical resource to our Cultural Diversity Office and Office of Inclusion & Diversity at
readers. the University of Toronto.
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Thirty nine years ago, Toronto Notes began as a humble We sincerely thank each of our 170 student editors and
initiative, with medical students from the University of Toronto 103 faculty editors, whose meticulous revisions and shared
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Notes has become one of the most trusted medical review texts; team , and are especially grateful to everyone for contributions
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Li, Dorrin Zarrin Khat, Christie Ian, Yrati Mehra, Alyssa Li,
The Toronto Notes for Medical Students Inc. is a nonprofit and Karolina Gaebe - for their tireless leadership, exceptional
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The 2023 edition features substantial content revisions to
the text, figures, and graphics of all 32 chapters, following a
comprehensive review by our student and faculty editorial
team . Up- to-date, evidence - based medicine studies are also Sincerely,
summarized in highlighted boxes throughout the text. In rn
LJ
particular, the Ethical Legal, and Organizational Medicine Anders W. Erickson, MD/ PhD student
chapter has been thoroughly revised and expanded, and all Jennifer Parker, MD/ PhD student
chapters reflect the most- updated COV1D-19 guidelines. The - -
Editors in Chief, Toronto Sotes 2023
new MCCQE objectives on Clinical Informatics and Health +
Acknowledgements
We would like to acknowledge the exceptional work of all previous Toronto Notes ( formerly MCCQE Notes)
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Editors in-Chief and their editorial teams, lhe 39th edition of this text was made possible with their contributions.
2022 ( 38th ed.): Yuliya Lytvyn and Maleeha A. Qazi
2021 ( 37 th ed.) : Megan Urupals and Matthacus Ware
2020 ( 36th ed.): Sara Mirali and Ayesh Seneviratne
2019 ( 35th ed.): Taraneh (Tara ) Tofighi and Mark Shafarenko
2018 ( 34 th ed.): Tina Binesh Marvasti and Sydney McQueen
.
2017 ( 33rd ed ): Jieun Kim and Ilya Mukovozov
2016 (32 nd ed.): Zamir Merali and Justin D. Woodfine
2015 (31th ed.): Justin Hall and Azra Premji
2014 (30th ed.): Miliana Vojvodic and Ann Young
.
2013 (29th ed ): Curtis Woodford and Christopher Yao
2012 (28 th ed.): Jesse M. Klostranec and David L. Kolin
2011 (27th ed.): Yingming Amy Chen and Christopher Tran
2010 (26th ed.): Simon Baxter and Gordon McSheffrey
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2009 ( 25th ed ): Sagar Dugani and Danica Lam
2008 ( 24th ed.): Rebecca Colrnan and Ron Somogyi
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2007 ( 23rd ed ): Marilyn Heng and Joseph Ari Greenwald
2006 ( 22 nd ed.): Carolyn Jane Shiau and Andrew Jonathan Ibren

.
2005 ( 21st ed ): Blair John Normand Leonard and Jonathan Chi Wai Yeung-
.
2004 ( 20 th ed ): Andrea Molckovsky and KashifS. Pirzada
2003 ( 19th ed.): Prateek Lala and Andrea Waddell
2002 ( 18th ed.): Neety Paint and Sunny Wong
2001 ( 17th ed.): Jason Yue and Gagan Ahuja
.
2000 ( 16th ed ): Marcus Law and Brian Kotcnberg
.
1999 ( 15th ed ): Sofia Ahmed and Matthew Cheung
1998 ( 14 th ed.): Marilyn Abraham and M Appleby
1997 (13th ed.): William Harris and Paul Kurdyak
1996 (12th ed.): Michael B. Chang and Laura J. Macnow
1995 (11th ed.): Ann L. Mai and Brian J. Murray

1994 (10th ed.): Kenneth Pace and Peter Ferguson n
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1993 ( 9th ed.): Joan Cheng and Russell Goldman
1992 (8th ed.): Gideon Cohen - Nehemia and Shanthi Vasudevan

+
All former Chief Editors from 1991 ( 7th ed.) to 1985 ( 1st ed.)
Student Contributors
Editors- in -Chief Clinical Handbook Editors Copyright Managers
Anders Erickson Justin Lu Mercy Danquah
Jennifer Parker Rayoun Ramendra Marta Karpinski
BMC Production Editors Online Content Managers

Jennifer Xin Ran Shao Jeffrey Lam Shin Cheung
Aimy Meng Yu Wang Sandra Lee
Amanda Mac
Muhammad Shahid
BMC ILLUSTRATORS
Viktoriva Khymych Viola Yu Amy Ke Er Zhang
PRIMARY
Associate Editors EBM Editor
Ming Li Yijithan Sugumar
Dorrin Zarrin Khat
CHAPTER EDITORS
Ethical, Legal, and Dermatology Family Medicine Paediatrics Psychiatry
Organizational Medicine Natalie Kozlowski Neda Pirouzmand Onyinyechukwu Esenwa Tania Da Silva
Kenya Costa-Dookhan Yuliya Lytvyn Bree Sharma Anna Jiang Rawaan Elsawi
Zuhal Mohmand Sara Mirali Maryam Thrava Raima Rasouli Rachel Goud
Mary Xie
Anestlicsia Emergency Medicine Medical Genetics Tinting Yang Public Health and
Evan Tang V'inyas 1 Iarish Andrew Mazzanti Preventive Medicine
Kathak Vachhani Danny Ma Palliative Medicine Jenny Cho
Kwasi Nkansah Medical Imaging Manu Sharma Muhammad Maaz
Clinical Pharmacology Tsz Ying So Grace Grafham Christine Wu
Max Solish Jeffrey Lam Shin Cheung
COPY EDITORS
Ethical, Legal, and Dermatology' Family Medicine Paediatrics Psychiatry'
Organizational Medicine Chidalu Edechi Jaskaran Gill Tania Da Silva David Kim
Noroh Dakim Jaycie Dalson Shiyu Sunny Zheng Priscilla Kim
Alex German Ajantha Xadarajah Public Health and
Emergency Medicine Medical Genetics Yasmeen Razvi Preventive Medicine
Anesthesia Graham Colby Ryan Karim i Caitlin Monaghan
Max Solish Sanch Gupta Palliative Medicine HunsterYang
Janet Tang Lara Murphy Medical Imaging Samuel Wier
rT
Daniel Shane Victoria Anthes c. J
Clinical Pharmacology Hayley McKee
Fatimah Roble
+
Student Contributors
MEDICINE
Associate Editors EBM Editors
Karolina Gaebe Wei Fang Dai
Alyssa Li Camilla Giovino
CHAPTER EDITORS
Cardiology and Cardiac Gastroenterology Hematology Nephrology Respirology
Surgery Sahibjot Grewal Reid Gallant David Buchan Brian Bursic
I lardil Bhatt Anna Lee Syed Sluhan I laider I Juaqi Li Emma Price
Akachukwu Nwakoby Andrew Rogalsky Nathan Kuelmc Rajiv Tanwani
Jeremy Roslt Neurology
Emily Tam Geriatric Medicine Infectious Diseases Thomas Milazzo Rheumatology
Imnan Khcrani Christopher Knox Maleeha Qazi Rachel Goldlarh
Endocrinology Saba Manzoor Erika Nakajima Eden Meisels
Maria Samy Rachel Tran
Claire Sethuram
COPY EDITORS
Cardiology and Cardiac Endocrinology Hematology Nephrology Respirology
Surgery Winston Li Pedro Boasquevisque Anders Erickson Andrew Rogalsky
Shamara Nadarajah Kathryn Wiens Daniel Lindsay Jennifer Parker Raza Syed
Julianah Oguntala Brandon Tse
Calurn Slapnicar Gastroenterology Neurology Rheumatology
Vivian Tam Oliver Chow Infectious Diseases Lauren Kanee Serena Dienes
Parker McNabb Nicholas Chiang Kristiana Xhima Tsz Ying So
TediIloxha
Geriatric Medicine
Pooja Sankar
SURGERY
Associate Editors EBM Editor
Vrati Mehra Arjan Dhoot
Chunyi Christie Tan
CHAPTER EDITORS
General and Thoracic Neurosurgery Ophthalmology Otolaryngology Urology
Surgery Dan Budiansky Michael Balas Alyssa Li Adree Khondker
Ryan Daniel Jack Su Josh I Ierman Jessica Trac Shamir Malik
Jacqueline Lim Raza Syed Michelle Lim Sheila Yu
Smruthi Ramesh Vascular Surgery
Obstetrics Orthopaedic Surgery Plastic Surgery George Elzawy
Gynaecology I Iarsukh Benipal John - Petcr Bonello Shaishav Datta Raumil Patel
Eliot Winkler Emma Sparks Kalter 1 Iali Tiffany Ni
Sarah Zachariah Jane Zhu Robert Koucheki
Rehona Zamani Marc Manzo
COPY EDITORS
General and Hioracic Neurosurgery Ophthalmology Otolaryngology Urology
Surgery Bhadra Pandya Kevin Chen Ryan Daniel Kellie Kim rT
LJ
Tasnim Abdalla Jacob Peller Matthew Veitch Siddhartha Sood Gabriela Leon
Audrey Jong
Lisa Vi Obstetrics Orthopaedic Surgery Plastic Surgery Vascular Surgery
Julia Avolio 1 lannah Drkulec Thomas Milazzo Serena I lope
Gynaecology I layley Good Anders Erickson Jenn Parker +
Laura Diamond Erin Pucrsten
Katherine Kim
I Iolsa Zia https://medical-amboss.com
S Editorial Toronto Notes 2023
Faculty Contributors, University of Toronto

All of the following contributors have been appointed at the University of Toronto.
PRIMARY
ETHICAL, LEGAL. AND
ORGANIZATIONAL MEDICINE
Kaif Pardhan, BSc MD MMEd FRCPC
Emergency Physician
.
Tyler Groves, MSc MBBS, FRCPC
Department of Paediatrics, Michael Garron Hospital
Andria Bianchi, PhD Sunnybrook Health Sciences Centre & McMaster
Bioethicist, University Health Network Children’s Hospital .
Giuseppe ( Joey ) Latino MD, FRCPC
Assistant Professor, Delia Lana School of Public Department ot Paediatrics
Health, University of Toronto FAMILY MEDICINE Division of Genetics, Department of Medicine
Affiliate Scientist, KITE Research Institute, Ruby Alvi, MD, CCFP, MHSc FCFP North York General Hospital
Toronto Rehab Department of Family and Community Medicine
Education Investigator 2, TIER ( The Institute for University of Toronto .
Laila Premji, MD FRCPC
Education Research ) Division ol Paediatric Medicine,
Chung Kit ( Jacks ) Lai. MD, CCFP Department of Paediatrics
Nadia Incardona, MD, MHSc. BSc, CCFP ( EM ) Department of Family and Community Medicine The Hospital for Sick Children
Assistant Professor Royal Victoria Regional Health Centre
Department of Family and Community Medicine University' of Toronto Shazeen Suleman MSc, MD, MPH ( FRCPC !
Michael Garron Hospital Women and Childrens Health
Chase Everett McMurren, BA, BEd, MD, CCFP SL Michael s HospitaL Unity Health Toronto
Chase Everett McMurren , BA, BEd, MD, CCFP Department of Family and Community Medicine
Department of Family and Community Medicine University of Toronto Janaki Vallipuram, MD. FRCPC
University of Toronto Division of Paediatric Medicine,
Rachel Walsh , MD, MSc, CCFP Department of Paediatrics
ANESTHESIA Department of Family and Community Medicine The Hospital for Sick Children,
Ahtsham Niazi, MBBS, FCARCSI, FRCPC Sunnybrook Health Sciences Centre Markham Stouffville Hospital
Department of Anesthesia and University' of Toronto
Pain Management, University Health Network PALLIATIVE MEDICINE
MEDICAL GENETICS Risa Bordman, MD, CCFP( PC ), FCFP
CLINICAL PHARMACOLOGY Vanda McNiven, MD, MSc, FRCPC Associate Professor
Das id Juurlink, BPhm, MD, PhD, FRCPC Division of Clinical Genetics and Metabolics & Faculty Development Program Lead,
Division of Clinical Pharmacology and Division of Hematology and Oncology Office of Education Scholarship
Toxicology, Departments of Medicine and Departments of Paediatrics and Medicine Department of Family & Community Medicine
Paediatrics, Sunnybrook Health Sciences Centre The Hospital for Sick Children, The University Health
Network, and Mount Sinai Hospital Adam Rapoport, MD, FRCPC, MHSc
Cindy Woodland, PhD Departments of Paediatrics and Family &
Associate Professor, Teaching Stream Graeme AM Nimmo, MBBS, MSc, FRCPC, FCCMG Community Medicine, University of Toronto
. .
Director, Collaborative Speci tli 7 uion in The Fred A Litwin Family Centre in Genetic Paediatric Advanced Care Team, SickKids
Biomedical Toxicology Medicine, Department of Medicine Emily’s House Childrens Hospice
Director, Applied Clinical Pharmacology Program Mount Sinai Hospital and University Health Network
Donna Spaner, MD, CCFP( PC), FCFP, MScCH
DERMATOLOGY MEDICAL IMAGING Division of Palliative Care, Department of Family and
Patrick Fleming, Sc ( Nutrition !. MSc (Community Andrew Brown, MD, MBA, FRCPC Community Medicine
Health ), MD, FRCPC, FCDA Assistant Professor Toronto Grace Health Centre
Assistant Professor of Medicine, Vascular and Interventional Radiology
Department of Medicine, University of Toronto Department of Medical Imaging PSYCHIATRY
Dermatologist, York Dermatology & Research Centre Unity Health Toronto - SL Michaels Hospital Saulo Castel, MD, PhD, FRCPC
Consultant Dermatologist, Director, Inpatient Services
University Health Network .
Beniamin Fine, SM MD, FRCPC Sunnybrook Health Sciences Centre
Clinician Scientist, Medical Imaging Assisiant Professor Department of Psychiatry
Marissa Joseph , MD, MScCH. FRCPC, FRCPC Trillium Health Partners, University of Toronto
Division of Dermatology, Department of Medicine Tamara Milovic, MD, MBA, FRCPC
Women's College Hospital and The Hospital for Sick Kieran Murphy, MB, FRCPC, FSIR Psychiatrist, Centre for Addiction and Mental Health
Children Interventional Neuroradiology, Lecturer, Department ot Psychiatry,
'
Professor of Medical Imaging University ot Toronto

Jensen Yeung, MD, FRCPC
Division of Dermaiology, Department of Medicine Ciara O’Brien , MB BCh BAO (MD ), FFR RCSI Jerome Perera, MD, FRCPC
Women's College Hospital Staff Radiologist, Abdominal Division Psychiatrist, North York General I Iospital
Joint Department of Medical Imaging .
Clinician Teacher Department of Psychiatry,
EMERGENCY MEDICINE University I Iealth Network, Ml Sinai 1 Iospital, University of Toronto
Mark Freedman , BSc, MD, FRCPC Womens College Hospital
Department of Emergency Medicine Assistant Professor, Department of Medical Imaging, liana Shawn, MD FRCPC
Sunnybrook Health Sciences Centre University' of Toronto ‘ ' "
Department of Psychiatry, Sc Michael's 1Iospital
Assistant Professor Department of Psychiatry
Laura Hans, MD, CCFP ( EM ) Anastasia Oikonomou, MD, PhD, FRCPC
Department of Emergency Medicine Associate Professor, University of Toronto PUBLIC HEALTH AND
SL Michael's Hospital Division of Cardiothoradc Imaging, PREVENTIVE MEDICINE
Department of Medical Imaging, ~ Jason J Pennington. MD, MSc, FRCSC
Adam Kaufman, MD CCFPiEM ) Sunnybrook Health Sciences Centre Division of General Surgery, Department of Surgery,
Emergency Physician, Michael Garron Hospital, Scarborough Health Network
Toronto East Health Network PAEDIATRICS Assistant Professor, Department of Surgery', rT
.Assistant Professor, Department of Family and Tanvi Agarwal, MD, FRCPC MScCH (c) University' of Toronto LJ
Community Medicine, University of Toronto Division of Paediatric Medicine
Department of Paediatrics Andrew Pinto, BSc, MD, CCFP, FRCPC, MSc
Jo Jo Leung, MD, CCFPIEM ), MScCH( HPTE) The Hospital for Sick Children Department of Family and Community Medicine,
Emergence Physician , University Health Network and SL Michaels Hospital
Trillium Health Partners Jillian Baker, MD, MSc, FRCPC Department of Family and Community Medicine +
Assistant Professor, Department of Family and Assistant Professor of Pediatrics, University of Toronto University of Toronto
Community Medicine, University of Toronto Divisions of Pediatrics and Hematology/Oncologv Dalla Lana School of Public 1 Iealth ,
Department of Pediatrics, Unity Health Toronto (St University'of Toronto
Michaels Hospital ) & The Hospital for Sick Children
MEDICINE
CARDIOLOGY AND CARDIAC SURGERY Thiru Yogaparan, MD, FRCP Alireza Zahirieh, MD, FRCPC
Paul Dorian, MD, MSc, FRCPC Division of Geriatric Medicine, Department of Division of Nephrology, Department of Medicine
Division of Cardiology Medicine, Baycrest I lealth Sciences Sunnybrook I lealth Sciences Centre
St. Michael 's Hospital
HEMATOLOGY NEUROLOGY
Douglas 1. Ing, MD, FRCPC, FACC .
Matthew Cheung, MD FRCPC Charles D. Kassardjian, MD, MSc, FRCPC
Division of Cardiology Division of Medical Oncology and 1lematology . Division of Neurology, Department of Medicine
Toronto General Hospital Department of Medicine St. Michael's Hospital
Sunnybrook Health Sciences Centre
Bobby Yanagawa, MD, PhD, FRCSC Alexandra MucciUi, MD, MEd, FRCPC
Division of Cardiac Surgery Lisa Chodirker, MD, FRCPC Division of Neurology, Department of Medicine
St Michael 's Hospital Division of Medical Oncology and Hematology, SL Michaels Hospital
Department of Medicine
ENDOCRINOLOGY Sunnybrook Health Sciences Centre Liza Pulcine, MD, MSc, FRCPC
Angela Assal, MD, MHSc, FRCPC Assistant Prolessor, Fellowship Director
Division of Endocrinology and Metabolism, Depart- Helena Dhamko. MD, FRCPC MScCH Children's Stroke Program
ment of Medicine Division of Hematology. E>epartment of Medicine Division of Neurology, Department of Paediatrics,
Sunnybrook Health Sciences Centre University Health Network The Hospital for Sick Children
University of Toronto
Zachary Liederman, MD, FRCPC MScCH RESPIROLOGY
Jeremy Gilbert, MD, FRCPC Division of Hematology, Department of Medicine Samir Gupta, MD, FRCPC
Division of Endocrinology and Metabolism Universitv Health Network Division ofRespirology Department of Medicine
Sunnybrook Health Sciences Centre Unity Health Toronto
Michael Scott, MD, FRCPC
Adrian Lau, MD, MScCH, FRCPC Clinical Hematologist; Adjunct Lecturer, Ambrose Lau, MD, MEd, FRCPC
Division of Endocrinology and Metabolism Division of Medical Oncology and Hematology- Division ofRespirology, Department of Medicine
Department of Medicine Department of Medicine, Unity Health Toronto, University Health Network and
Women’s College Hospital SL Michael's Hospital Unity Health Toronto
University of Toronto Assistant Professor, University of Toronto
Martina Trinkaus, MD, FRCPC
Maria Wolfs, MD MHSc FRCPC Division of Hematology, E>epartment of Medicine Christopher Li, MD, FRCPC, DABSM
Division of Endocrinology and Metabolism SL Michael's Hospital Division ofRespirology; Department of Medicine
St. Michael 's Hospital Unity Health Toronto - SL Michael’s
INFECTIOUS DISEASES
GASTROENTEROLOGY Andrea K. Boggild, BSc, MSc, MD, DTMH, RHEUMATOLOGY
Maria Cino, BSc( Hon ), Hon BSc, MSc, MD, FRCPC Ahmed Omar, MBBCh, MRCP, MSc
FRCPC CAGF Tropical Disease Unit, Toronto General Hospital Assistant Professor, University of Toronto
Division of Gastroenterology, Division of Infectious Diseases, Division of Rheumatology, Department of Medicine
University Health Network - Toronto Western Site
-
University Health Network
Department of Medicine, University of Toronto
Mount Sinai Hospital, University Health Network
Associate Professor, University of Toronto Institute of Medical Science, University of Toronto Arthur Bookman, MD, FRCPC
Division of Rheumatology, Department of Medicine
Flavio Habal, MD,PhD,FRCP,FAGA . .
Paul L Bunce, BSc MA. MD FRCPC University 1 lealth Network
Division of Gastroenterology Division of Infectious Diseases
University Health Network, Department of Medicine
.
SahilKoppikar MD FRCPC
Assistant Professor, Division of Rheumatology
Toronto Western Division
Associate Professor, University of Toronto Department of Medicine,
Susan M. Poutancn, MD. MPH, FRCPC Women's College I lospital
Piero Tartaro, MD, MScCl I , FRCPC Department of Microbiology,
Division of Gastroenterology, University Health Network & Sinai Health Dharini Mahendira, MD, FRCPC, MScCH
Department of Medicine Division of Infectious Diseases, Assistant Professor, Division of Rheumatology-
Sunnybrook Health Sciences Centre Department of Medicine Department of Medicine, St. Michael 's Hospital
University Health Network & Mount Sinai Hospital
GERIATRIC MEDICINE Medha L. Soowamber, MD, MSc, FRCPC
Jillian .Alston, MD, FRCPC, MScCH NEPHROLOGY Division of Rheumatology, Department of Medicine
Division of Geriatrics .
Damien Noone MB BCh BAO, MSc Mount Sinai Hospital ri
Department of Medicine Division of Paediatric Nephrology, LJ
St. Michael's Hospital Department of Paediatrics
The Hospital tor Sick Children
Vicky Chau, MD, MScCH, FRCPC
Division of Geriatric Medicine,
Gemini Tanna, MD, FRCPC
Division of Nephrology, Department of Medicine
+
Sinai Health System & University Health Network Sunnybrook Health Sciences Centre
SURGERY
GENERAL AND THORACIC SURGERY Melissa Walker, MD, MSc, ERCSC PLASTIC SURGERY
Abdollah Behzadi, MD, MBA, ERCSC FACS Staff Obstetrician Gynecologist, Department of Joel Fish, MD, MSC, FRCS
Division of Thoracic Surgery, Department of Surgery Obstetrics & Gynecology, Mount Sinai Hospital Professor, Plastic and Reconstructive Surgery
Trillium Health Partners, University of Toronto Assistant Professor, Department of Obstetrics & Department of Surgery
Gynecology; University of Toronto The Hospital for Sick Children
Sayf Gazala, MD. MSc, FRCSC
Assistant Professor, Thoracic Surgery Department of OPHTHALMOLOGY Siba Haykal, MD, PhD, FRCSC, FACS
Surgery; Michael Garron Hospital Asiin Ali, MD, FRCSC Division of Plastic and Reconstructive Surgery,
Professor of Ophthalmology, University of Toronto Department of Surgery
Jesse Pasternak, MD, MPH, FRCSC Ophthalmologist-in-Chief, The Hospital for Sick University' Health Network
Section of Endocrine Surgery- Children
Division of General Surgery, Department of Surgery UROLOGY
University Health Network Wai-Ching Lam, MD, FRCSC Monica Farcas, BEng, MEng, MD, FRCSC
Department of Ophthalmology and Vision Science Assistant Professor, Division of Urology
Fayez Quereshy, MD, MBA, FRCSC University Health Network, Department of Surgery, Unity I Iealth Toronto
Department of General Surgery Toronto Western Hospital
University Health Network . The Hospital for Sick Children Yonah Krakowsky, MD, FRCSC
Toronto Western Division of Urology
Hospital Jonathan Micicli, MD, FRCSC Womens College & Mount Sinai Hospital
Department of Ophthalmology and Vision Sciences;
GYNAECOLOGY Division of Neurology; Department of Medicine; .
Jason Lee, MD MHPE, FRCSC
.
Michael Chaikof MD, FRCSC, MS-HPEd Kensington Vision and Research Centre, Division of Urology; Department of Surgery
Division of Urogynecology St. Michaels Hospital, University of Toronto .
University Health Network Toronto General
Department of OBGYN Hospital
Sunnybrook Health Sciences Centre ORTHOPAEDIC SURGERY
Jeremy Hall, MD, FRCSC Michael Ordon, MD, MSc, FRCSC
Sari Kives, MD, FRCSC Division of Orthopaedic Surgery, Department of Division of Urology; Department of Surgery
Associate Professor Surgery; St. Michaels Hospital SL Michael’s Hospital
Division of Obstetrics and Gynecology
Department of Obstetrics and Gynecology
- Paul Kuzyk, MD, MASc, FRCSC VASCULAR SURGERY
St Michaels hospital Assistant Professor Elisa Greco, BSc, MEd, MD, RPYI, FRCSC
Lower Extremity' Reconstruction Surgery- Vascular Surgeon, St Michaels Hospital
NEUROSURGERY Division of Orthopaedic Surgery
Sunit Das, MD, PhD George Oreopoulos, MD, MSc, FRCSC
Division of Neurosurgery Jesse Wolfstadt, MD, MSc, FRCSC Division of Vascular Surgery,
St. Michaels Hospital Granovsky Gluskin Division of Orthopaedic Surgery, Department of Surgery
Department of Surgery, Sinai 1 Iealth Sy stem University Health Network
.
Michael G. Fehlings, MD PhD, FRCSC, FACS
Professor of Neurosurgery; Department of Surgery; OTOLARYNGOLOGY
University ofToronto Yvonne Chan , MD, MSc, FRCSC
Vice Chair Research, Department of Surgery; --
Otolaryngologist in chief,
University of Toronto St. Michael’s Hospital, Unity Health
Senior Scientist, Krembil Brain Institute, Associate Professor and Continuing Professional
University Health Network Development Director
-
Staff Neurosurgeon, University Health Network
Co-Director, University of Toronto Spine Program
Department of Otolaryngology -
Head & Neck Surgery
Eric M. Massicotte MIX MSc, MBA, FRCSC Antoine Eskandcr, MD, ScM, FRCSC
Associate Professor University of Toronto Assistant Professor
Staff Neurosurgeon, University Health Network Department of Otolaryngology -
Medical Director, Back & Neck Program Altum I lead & Neck Surgery
Health Sunnybrook Health Sciences Centre,
Odette Cancer Centre
OBSTETRICS Michael Garron Hospital
.
Richard Pittini, MD, MEd FRCSC, FAC.OG
Department of Obstetrics and Gynecology; Jonathan Irish, MD, MSc, FRCSC
University of Toronto Department of Otolaryngology,
Sunnybrook I Iealth Sciences Centre l lead and Neck Surgery,
Mara Sobel, MD, MSc. FRCSC
Department of Obstetrics and Gynecology;
University- of Toronto
+
Mount Sinai Hospital University Health Network,
Toronto General Hospital, Womens College Hospital
Table of Contents
Index Abbreviations
Common Acronyms and Abbreviations Used in Medicine

Common Unit Conversions
Commonly Measured Laboratory Values
Ethical, Legal, and Organizational Medicine ELOM

Anesthesia A
Cardiology and Cardiac Surgery . C
Clinical Pharmacology CP
Dermatology D
Emergency Medicine ER
Endocrinology E
Family Medicine FM
Gastroenterology G
General and Thoracic Surgery .. GS
Geriatric Medicine GM
Gynaecology GY
Hematology H
Infectious Diseases ID
Medical Genetics MG
Medical Imaging Ml
Nephrology NP
Neurology N
Neurosurgery ... NS
Obstetrics OB
Ophthalmology OP
Orthopaedic Surgery OR
Otolaryngology OT
Paediatrics P
Palliative Medicine PM
Plastic Surgery PL
Psychiatry PS
Public Health and Preventive Medicine PH
Respirology R ri
Rheumatology . . RH
LJ
Urology U
Vascular Surgery VS +
How To Use This Book

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S Key Objectives
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Chapter Divisions
To aid in studying and finding relevant material quickly, many chapters incorporate the following general framework:
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
Diagnoses
• the bulk of the book
r “i
• etiology, epidemiology, pathophysiology, clinical features , investigations , management, complications, and prognosis LJ
Common Medications
• a quick reference section for review of medications commonly prescribed
+
Common Acronyms and Abbreviations Used in

Medicine
The following are common medical acronyms/abbreviations that may be used without definition throughout the Toronto
Notes text. These are typically not included in the acronym list at the beginning of each chapter. Please refer back to this
list for definitions.
U concentration ECC, electrocardiogram

p - hCG beta human chorionic gonadotropin ED emergency department
ABx
ACE
antibiotics
angiotensin -converting enzyme
EEC
EMC
ENT
. electroencephalography
electromyography
cars, nose, and throat
ACTH Adrenocorticotropic hormone ESR erythrocyte sedimentation rate
AIDS acquired immune deficiency syndrome EtOH cthanol/alcohol
ALP alkaline phosphatase
ALT alanine aminotransferase FMHx family medical history
AR absolute risk FSH follicle stimulating hormone
ASA acetylsalicylic acid
glucosc -6- phosphate dehydrogenase
AST
aSx
AXR
aspartate transaminase
asymptomatic
abdominal x - ray GH
.
G 6PD
GG T gamma - glutamyl transferase
growth hormone
GHB gamma hydroxybutyrate
BID twice a day ( bis in die ) GI gastrointestinal
BMI body mass index GU genitourinary
BP blood pressure
BPM/ bpm beats per minute Hb hemoglobin
HIV human immunodeficiency disease
C/I contraindication HR heart rate
C&S culture and sensitivity HTN hypertension
CAD coronary artery disease Hx history
CBC complete blood count
CC chief complaint I& D incision and drainage
CHF congestive heart failure ICP intracranial pressure
COPD chronic obstructive pulmonary disease ICU intensive care unit
CPR cardiopulmonary resuscitation IM intramuscular
Cr creatinine IV intravenous
CRH corticotropin - releasing hormone
CSF cerebrospinal fluid JVP jugular venous pressure
CT computed tomography
CXR chest x- ray LDH lactate dehydrogenase
LFT liver function test
D&C dilatation and curettage LH luteinizing hormone r
dBP diastolic blood pressure LR likelihood ratio
DDx differential diagnosis
DM diabetes mcllitus
DNR do not resuscitate
+
Dx diagnosis
H Editorial Toronto Notes 2023
Common Acronyms and Abbreviations Used in

Medicine
MAO monoamine oxidase sBP systolic blood pressure
MAOI monoamine oxidase inhibitor SC subcutaneous
MDI metered -dose inhaler SL sublingual
MI myocardial infarction SLE systemic lupus erythematosus
MRI magnetic resonance imaging SOB shortness of breath
MSK musculoskeletal STAT urgent or immediately ( statum )
STI sexually transmitted infection
N/ V nausea/vomiting Sx symptom (s)
NG nasogastric
NMDA N - Mcthyl - D -aspartate TlDM type 1 diabetes mellitus
NPO nothing by mouth ( nil per os ) T2 DM type 2 diabetes mellitus
NSAID non -steroidal anti - inflammatory drug TB tuberculosis
TID three times a day ( ter in die)
OR operating room TNM tumour, nodes, and metastases
OTC over-die-counter TRH thyroid releasing hormone
TSH thyroid stimulating hormone
PCR polymerase chain reaction Tx treatment
PE pulmonary embolism
PMHx past medical history U/A urinalysis
PO oral administration ( per os ) U/S ultrasound
POCUS point -of -care ultrasound UTI urinary tract infection
PPI proton pump inhibitor UTox urine toxicology screen
PRN as needed ( pro re nata )
VDRL Venereal Disease Research Laboratory test
QID four times a day (quatcr in die)
WBC white blood cell
RBC red blood cell wt weight
RCT randomized controlled trial
ROS review of symptoms
Rx medical prescription
pi
Common Unit Conversions

To convert from the conventional unit to the SI unit, multiply by conversion factor
To convert from the SI unit to the conventional unit, divide by conversion factor
Conventional Unit Conversion Factor SI Unit
ACTH pg/mL 0.22 pmol/L

Albumin g/dL 10 g/L
Bilirubin mg /dL 17.1 pmol/ L
Calcium mg /dL 0.25 mmol/L
Cholesterol mg/dL 0.0259 mmol/L
Cortisol pg /dL 27.59 nmol/L
Creatinine mg /dL 88.4 pmol/ L
Creatinine clearance mL/min 0.0167 mL/s
Ethanol mg/dL 0.217 mmol/L
Ferritin ng/mL 2.247 pmol/L
Glucose mg /dL 0.0555 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 pg /dL 0.179 pmol/L

Lactate (lactic acid) mg /dL 0.111 mmol/L
LDL cholesterol mg/dL 0.0259 mmol/L
3
Leukocytes
^
x lO ells/mm 1 x 109cells/L
Magnesium mg /dL 0.411 mmol/L
MCV pm3 1 fL
x lO ells/mm 3 x 109cells/L
Platelets
^ 1
Reticulocytes % of RBCs 0.01 proportion of 1.0
Salicylate mg /L 0.00724 mmol/L
Testosterone ng /dL 0.0347 nmol/ L
Thyroxine (T 4) ng/dL 12.87 pmol/L
Total Iron Binding Capacity pg /dL 0.179 pmol/L
Triiodothyronine (T3) pg/dL 0.0154 pmol/L
Triglycerides mg /dL 0.0113 mmol/L
Urea nitrogen mg/dL 0.357 mmol/L
Uric acid mg/dL 59.48 pmol/L
Celsius •* Fahrenheit F = (C x 1.8) + 32 r

LJ
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
Commonly Measured Laboratory Values

Test Conventional Units SI Units
Arterial Blood Gases

pH 7.35 -7.45 7.35 -7.45
PC02 35 -45 mmHg -
4.7 6.0 kPa
PO 2 80-105 mmHg 10.6 -14 kPa
Serum Electrolytes
Bicarbonate -
22 28 mEq/L -
22 28 mmol/L
Calcium 8.4-10.2 mg/dL 2.1- 2.5 mmol/L
Chloride 95 -106 mEq/ L 95 -106 mmol/ L
Magnesium 1.3 -2.1 mEq/L 0.65-1.05 mmol/L
Phosphate 27-4.5 mg /dL 0.87-1.45 mmol/L
Potassium 3.5 - 5.0 mEq /L 3.5- 5.0 mmol/L
Sodium 136 -145 mEq /L 136-145 mmol/ L
Serum Nonelectrolytes
Albumin 3.5 - 5.0 g/dL 35- 50 g / L
ALP 35 -100 U/ L 35-100 U/L
ALT 8 - 20 U/L 8 -20 U /L
Amylase -
25 125 U /L -
25 125 U/ L
AST 8 - 20 U/L 8 -20 U /L
Bilirubin (direct) 0-0.3 mg /dL 0- 5 pmol/L
Bilirubin (total) 0.1-1.0 mg/dL 2-17 pmol/L
BUN 7-18 mg/dL 2.5 -7.1 mmol/L
Cholesterol <200 mg/dL < 5.2 mmol/L
Creatinine ( female) 10 -70 U/L 10-70 U/L
Creatinine (male) 25 - 90 U /L 25 - 90 U/L
Creatine Kinase - MB fraction 0-12 U/L 0-12 U/L
Ferritin (female) 12-150 ng/mL 12-150 pg/L
Ferritin (male) 15 - 200 ng/mL 15 -200 pg /L
Glucose ( fasting) 70-110 mg/dL 3.8- 6.1 mmol/L
HbA1c < 6% < 0.06
LDH 100-250 U/L 100 - 250 U/ L
Osmolality 275-300 mOsm/kg 275-300 mOsm/kg
Serum Hormones
ACTH (0800h) <60 pg/mL <13.2 pmol/L
Cortisol (0800h) -
5 23 pg /dL 138- 635 nmol/L
Prolactin <20 ng/ mL <20 ng/mL
Testosterone (male, free) 9-30 ng /dL 0.31-1 pmol/ L
Thyroxine (T4) 5-12 ng/dL 64-155 nmol / L
Triiodothyronine (T 3) 115 -190 ng/ dL 1.8 - 2.9 nmol/L
TSH 0.5- 5 pU/mL -
0.5 5 pU/mL
Hematologic Values
ESR (female) 0-20 mm / h 0-20 mm /h
ESR (male) 0-15 mm / h 0-15 mm /h
Hemoglobin (female) -
12.3 15.7 g/dL -
123 157 g/ L
Hemoglobin (male) 13.5-17.5 g /dL 140-174 g/ L
Hematocrit (female) 36-46% 36 - 46%
Hematocrit (male) 41- 53% 41-53% r "> \
INR 1.0-1.1 10-1.1
1 <- J J
Leukocytes 4.5-11 x 103cells/mm 3 4.5-11 x 109cells/L
MCV 88 -100 pm 3 88 -100 fL
Platelets 150 - 400 x 103/mm 3 150-400 X 109/L +
PTT 25- 35 s 25 -35 s
Reticulocytes 0.5-15% of RBC 20- 84 x 109/L
Rheumatology
Rachel Goldfarb and Eden Meisels, chapter editors
Karolina Gaebe and Alyssa Li , associate editors
Wei Fang Dai and Camilla Giovino, EBM editors
Dr. Arthur Bookman , Dr. Sahil Koppikar, Dr. Dharini Mahendira , Dr. Ahmed Omar, and
'
Dr. Medha Soowamber , staff editors
Acronyms ... RH2

Anatomy of Joint Pathology , RH2
Basics of Immunology. .RH2
Immune Mechanisms of Disease
Immunogenetics and Disease
Differential Diagnoses of Common Presentations , RH3
Synovial Fluid Analysis RH4
Septic Arthritis RH5
Degenerative Arthritis: Osteoarthritis RH5
Seropositive Rheumatic Disease RH7
Connective Tissue Disorders RH8
Rheumatoid Arthritis
Systemic Lupus Erythematosus
Antiphospholipid Antibody Syndrome
.
Scleroderma (i.e Systemic Sclerosis)
Inflammatory Myopathy
Sjogren's Syndrome
Mixed Connective Tissue Disease
Overlap Syndrome
Vasculitides RH18
Small Vessel Non-ANCA-Associated Vasculitis
Small Vessel ANCA-Associated Vasculitis
Medium Vessel Vasculitis
Large Vessel Vasculitis
Seronegative Rheumatic Disease RH23
Ankylosing Spondylitis
Enteropathic Arthritis
Psoriatic Arthritis
Reactive Arthritis
Crystal-Induced Arthropathies ..RH27
Pseudogout (Calcium Pyrophosphate Dihydrate Disease)
Non-Articular Rheumatism . ... RH28
Polymyalgia Rheumatica
Fibromyalgia
Common Medications ....RH31
,„
Landmark Rheumatology Trials . .. RH32

References RH35
+
RHl Rheumatology https://medical-amboss.com Toronto Notes 2023
R1I2 Rheumatology Toronto Notes 2023
Acronyms
AAV antineutcophil cytoplasmic CMC carpometacarpal joint GPA granulomatosis with polyangiitis PMN polymorphonuclear leukocyte
antibody-associated vasculitis CNS central nervous system H/ A headache PMR polymyalgia rheumatica
Ab antibody CTD connective tissue disease HLA human leukocyte antigen PR3 proteinase 3
ACPA anti- citrullinated protein CPPD calcium pyrophosphate IA intra - articular PsA psoriatic arthritis
antibodies deposition disease IBB inflammatory bowel disease PIT partial thromboplastin time
Ag antigen CRP C- rcactivc protein IE infective endocarditis PUO peptic ulcer disease
ANA antinuclear antibody CVA cerebrovascular accident IgA immunoglobulin A RA rheumatoid arthritis
ANCA antineutrophil cytoplasmic CVS cardiovascular system Iqk immunoglobulin E ReA reactive arthritis
antibody OAT direct antiglobulin test IqG immunoglobulin G RF rheumatoid factor
Anti - RNP antiribonudear protein dual energy x - ray
DEXA ILD interstitial lung disease ROM range of motion
Anti-Sm anti- Smith antibodies absorptiometry IP interphalangeal joint SI sacroiliac
Anti -SRP anti-signal recognition particle DIP distal interphalangeal joint UP idiopathic thrombocytopenic SNRI serotonin - norepinephrine
Anti-SSA anti -Sjogren's syndrome antigen DMARD disease- modifying anti- purpura reuptake inhibitors
A rheumatic drug MCP metacarpophalangeal joint SpA spondyloarthritis
APIA antiphospholipid antibodies DMM dermatomyositis MCTD mixed connective tissue disease SS Sjogren's syndrome
APS antiphospholipid antibody dsDNA double stranded DNA MHC major histocompatibility SSA Sjogren's syndrome antigen A
syndrome EA cnteropathic arthritis complex SSB Sjogren's syndrome antigen B
aPTT activated partial thromboplastin ECASA enteric -coated acctylsalicylic MPA microangiopathic polyangiitis SSc systemic sclerosis
time acid MPO myeloperoxidase SS2 sulfasalazin
AS ankylosing spondylitis EGPA eosinophilic granulomatosis and MTP metatarsophalangeal joint tumour necrosis factor
AVN avascular necrosis polyangiitis .
t‘ I X methotrexate
INF
TIP thrombotic thrombocytopenic
BlyS B lymphocyte stimulator FVC forced vital capacity OA osteoarthritis purpura
CCB calcium channel blocker GC Neisseria gonorrhoeae PAN polyarteritis nodosa ULN upper limit of normal
CCP cyclic dtrullinated peptide gonococcus PIP proximal interphalangeal joint U-SpA undifferentiated
CK creatine kinase GCA giant cell arteritis PM polymyositis spondyloarthropathy
Anatomy of Joint Pathology

Muscl
Bursa
one Erosion § Terminology in Rheumatology
Synovial Cartilage £ Arthritis: inflammation in the joint(s)

'' membrane destruction 1
• Joint swelling: effusion/synovial

thickening
-Synovitis £
Tendon _ _ Synovial
fluid
-Cartilage . Effusion
S
5
• Pain
• Warmth
Cartilage j
Osteophyte - particle • Erythema
Joint \ Cartilage loss ol ' Arthralgia: joint pain without
capsule destruction joint space oint space Z
< swelling, redness, or warmth
narrowing JJ
-
Normal Joint Degenerative Joint Inflammatory Joint «9
Figure 1. Structure of normal, degenerative, and inflammatory joint
Innate Immune Cells
Neutrophil ( PMN): circulates in
blood and responds to inflammatory
Basics of Immunology stimuli, kills invading organisms by
phagocytosis, degranulation and .
neutrophil extracellular traps
Natural Killer Cell: innate immunity
Immune Mechanisms of Disease against intracellular infections
(especially viruses), killing function, and
produces cytokines
Macrophage: arrives after PMNs,
Table 1. Mechanisms of Immune- Mediated Disorders suppresses PMN efflux and
Type Pathophysiology Examples phagocytoses PMN debris, secretes
pro-inflammatory cytokines in response
IgE - Mcdiated / lmmcdiate Hypersensitivity Allergens bind to IgE antibodies on mast cells, Asthma, allergic rhinitis, anaphylaxis to microbial debris
fiypcD inducing their degranulation Dendritic Cell: actively phagocytic
Antibody Medinted / Cylotoxic ( TypeII) IqG or IgM antibodies deposit and bind lo cell Autoimmune hemolytic anemia, anti - when immature, activated by signals
.
-
membrane or matrix - associated antigen glomerular bascmonl membrane disease from toll like receptor (ILR) releases
leading to lysis ol the target cell .
(Goodpasture syndrome) Graves' disease, pro- inflammatory cytokines, presents
.
pemphigus vulgaris, rheumalic lever IIP antigens to T cells in lymph nodes
Eosinophil: responds to inflammatory
Immune Complex (Type III) Ag - Ab complexes deposit in tissues,
which activates complement and cecruits
SLE, PAN. post-streplococcal
glomerulonephritis, serum sickness,viral
.
cytokines and degranulates releasing
reactive oxygen species and cytokines,
inflammatory mediators,resulting in tissue hepatitis associated with allergy, asthma, and
injury parasitic infection rt
Cell -Mediated/ Delayed Hypersensitivity Release of cytokines by sensitized 1 cells and 1 Contact dermatitis, insect venom, Mast Cell: presents in connective tissue iJ
( Type IV ) cell- media led cytotoxicity mycobacterial proteins ( e.g. tuberculin skin and mucosa, allergen cross -linking
lest ) of IgE bound to mast cell triggers
degranulation and the release of
inflammatory mediators
+
RH3 Rheumatology Toronto Notes 2023
Immunogenetics and Disease

Key Cytokine Targets of Biologic Drugs
• the short arm of chromosome 6 contains the genes that encode H LA molecules
• in humans, HLAs act as MHCs which present antigens to be recognized by T cell receptors and TNF
identify the self to the immune system such that they must be matched for in organ transplantation • Source of cytokine: T cells,
• certain HLA haplotypes are associated with increased susceptibility to autoimmune diseases macrophages/monocytes
• Major functions: apoptotic cel
Table 2. Classes of MHCs death, cachexia, induces other
MHC Class Types Location Function

.
cytokines T cell stimulation,
induces metalloproteinases and
I HUS- A.B. C All nucleated cells -
Recognized by CD8 (cytotoxic) prostaglandins, increases expression
of adhesion molecules;increases
T lymphocytes
vascular permeability, leading to
II HU- DP. DO. DR Ag presenting cells (mononuclear Recognized by CD 4- ( helper) increased entry of IgG. complement
.
phagocytes B cells, etc.) Ilymphocytes and cells into tissues
III Some components of the In plasma Chemotaxis. opsonization,lysis of
complement cascade bacteria and cells lnterleukin- 6 (IL-6)
• Source of cytokine:many
cells including monocytes and
Table 3. HLA- Associated Rheumatic Diseases macrophages
HLA Type Associated Conditions Comments • Major functions: anemia of
inflammation (hepcidin production),
B 27 AS Relative risk - 20x for developing AS and ReA proliferation of B and T cells, acute
ReA phase reactant induces natural
EA (axial) protease inhibitor, promotes
PsA (axial) erosions, induces elevated CRP
DR4 DR1. RA -
In RA.relative risk 2-10x: found in 933s of patients
DR 3 ss DR 3 is associated with the producbon of anli -Ro/ SSA and
SLE anti- laSSB antibodies
Adaptive Immune Cells
• B cell: produces antibodies after
activation by specific antigen and B
Differential Diagnoses of Common cell co-receptor, additional signals
provided by CD4+ T helper cells
Presentations -
• Cytotoxic T cell: CD8 ceil,directs
cytotoxicity of target cells at sites
of infection, kills via lytic granules
and FasL-Fas interaction, recognizes
Joint Pain specific antigen and MHC I
I • Helper T cell: subset of CD4- cells,
activates and helps other types of
Articular Non- Articular cells carry out immune defense
(activates macrophages, helps B
cells, releases cytokines)
Inflammatory
1
T
Degenerative
1
• Regulatory T cell: subset of CD4 -
cells, suppresses activation of name
autoreactive T cells
Seropositive
T
Seronegative *
Crystal Infectious/Septic
I I
Primary Secondary Localized *
Generalized
RA Gout Gonococcal 0A Metabolic Bursitis PMR
Scleroderma
SLE Pseudogout
Hydroxyapatite
-
Non gonococcal
Lyme disease
Hemophilic
Neuropathic
Tendinitis
Capsulitis
Fibromyalgia
Myofascial pain
Causes of Joint Pain
DMM/PM Viral Trauma Muscle sprain syndrome
SS Mycobacterial
SOFTER TISSUE
Fungal
Sepsis
OA
Symmetrical Asymmetrical Fracture
AS ReA Tendon /musde
EA PsA Epiphyseal
Figure 2. Clinical approach to joint pain Referred
Tumour
Ischemia
Table 4. Differential Diagnosis of Acute Monoarthritis Seropositive arthritides
Non- lnflammatory Inflammatory Seronegative arthritides
Urate (gout)Zother crystal
-
Crystal Induced Infectious Extra - articular rheumatism (PMR/
Hemarthrosis.internal derangement (e,g. Monosodium urate (MSU - gout), CPPO.1 Gonococcal non-gonococcal,mycobacterial, fibromyalgia)
loose body, tom meniscus) pseudogout, hydroxyapatite and fungal
Table 5. Differential Diagnosis of Oligoarthritis /Polyarthritis

Patterns of Joint Involvement
Acute ( 6 wk) Chronic (>6 wk)
‘ • Symmetrical vs. asymmetrical
Post - viral infection (parvovirus Seropositive inflammatory Seronegative inflammatory Degenerative .
• Small vs large
B19. HIV) arthritis arthritis OA .
• Mono vs oligo (2-4 joints) vs.
Post -bacterial infection (GC and RA AS polyarticular ( >5 joints)
.
non- GC rheumatic fever) SLE EA .
• Axial vs peripheral
Crystal-induced Scleroderma PsA
.
Other (sarcoidoss Lyme disease) DMM ’PM ReA
+
Very early rheumatoid arthritis Crystal (polyarticular gout)
( VERA)
Ril l Rheumatology Toronto Notes 2023
Table 6 . Symptoms of Inflammatory Arthritis vs. Degenerative Arthritis

Inflammatory Degenerative
The presence of synovitis often indicates
Pain attest, relieved with activity Pain with motion, relieved by rest
articular as opposed to non-articular
Morning stiffness >1h Morning stiffness <1h
joint pain: synovitis presents with:soft
Cardinal signs of inflammation (warmth, swelling, erythema, Joint instability, buckling, gelling
tissue swelling, effusion, warmth, and
tenderness, loss offunction) Bony enlargement, malalignment/ deformity (late finding)
stress pain (passive movement of the
Malalignmenl /delormity (late finding) Eveningfendof day pain
joint through its range , plus a little bit
-
Extra articular manifestations
further)
Nighttime awakening due to pain
Table 7. Seropositive vs. Seronegative Rheumatic Diseases

Seropositive Seronegative
G .
Monitoring CRP vs ESR
Demographics F»M -
M F • CRP is more sensitive for
inflammation than ESR
Peripheral Arthritis Symmetrical Usually asymmetrical • CRP responds more quickly to
Small ( PIP, MCP ) and medium joints ( wrist, Usually larger joints, lower extremities changes in the clinical situation
knee, ankle, elbow ) common (exception:PsA) than ESR
DIP less often involved DIP in PsA • False negative and false positive
Dactylitis I'sausage digit') results are more common with ESR
• ESR is increased by renal disease,
Pelvk / Axial Disease -
No (except for C spine) Ves
female sex, older age, pregnancy,
fnthesitis No Ves and other chronic diseases such
-
Extra Articular Nodules Iritis (anterior uveitis) as DM, multiple myeloma, and
congestive heart failure
Vasculitis Oral ulcers
Sicca Gastrointestinal • ESR can be useful at detecting low -
Raynaud's phenomenon Dermatological (psoriasis, nail pitting, grade bone and joint infections and
Rashes, internal organ involvement (lung, onycholysis, or keratoderma) monitoring disease activity in CTDs
such as SLE. PMR, and GCA
cardiac) Genitourinary inflammation
Entrapment neuropathies |i.e.carpal tunnel • Do not order ESR for acute
syndrome) inflammation
Synovial Fluid Analysis

m
Enthesitis: inflammation of tendon or
ligament at site of attachment to bone
•synovial fluid is an ultrafiltrate of plasma plus hyaluronic acid ; it lubricates joint surfaces and
nourishes articular cartilage
Indications
• diagnostic: to clarify cause of inflammation; to analyze fluid for culture , crystal, and cell count to
differentiate inflammatory vs. degenerative; septic vs. crystal-induced vs . hemarthrosis
• therapeutic: drainage of blood , purulent or tense effusions; corticosteroid injection in the absence of
sepsis
Contraindications to Joint Aspiration or Injection

• absolute : open lesion or suspected infection of overlying skin or soft tissue
• relative: bleeding diathesis , thrombocytopenia , prosthetic joint
Synovial Fluid Analysis

• most important to assess the 3 Cs: cell count ( WBC) and differential , culture and Ciram stain , and
crystal analysis
• other parameters to consider are listed in Table 8
Table 8. Synovial Fluid Analysis
Parameter Normal Non * Inflammatory Septic Hemorrhagic
Inflammatory
Colour Pate yellow Pale yellow Pale yellow Vellow to while Red/ brown
Clarity Clear Cleat Opaguc Opaque /purulcnt Sangurnous
WBC /mm
’ ‘200 -> 2000 » 2000 »50000 Variable Most Important Tests of Synovial Fluid
-
(crystal induced
arthritis - often much 3 Cs
higher than 2000) Culture and Gram stain
% PMN
‘25% ‘25% »50% »75% Variable Cell count and differential
Crystal examination
Culture /Gram Slain Usually positive
Examples Trauma Seropositive S. auieus Irauma rm
0A Seronegative Gram negative Hemophilia L
Neuropathy Crystal arthropathies GC » dilficult to
Hypertrophic
arthropathy
- culture (may have
low WBC )
RH 5 Rheumatology Toronto Notes 2023
Septic Arthritis
Choosing Wisely Canada
Definition Recommendations
• invasion of the joint by an infectious agent 1. Do not order ANA as a screening test
• septic arthritis is a medical emergency; it can lead to rapid joint destruction and has a 10-15% risk of in patients without specific signs or
mortality symptoms of SIE or another CTD
-
2. Do not order an HLA B27 unless
.
• knee and hip are most commonly affected joints, with knee accounting for approximately 50% of cases
poor prognostic factors: older age, immunocompromised, delay in treatment, previously damaged
joint , and joint prosthesis
spondyloarthritis is suspected based
on specific signs or symptoms
3. Do not repeat DEXA scans more
often than every 2 yr
Clinical Presentation 4. Do not prescribe bispliosphonates
for patients at low risk of fracture
• acute onset of: joint pain , swelling, erythema, immobility, and heat .
5 Do not perform whole body bone
scans (e.g. scintigraphy ) for
Pathophysiology diagnostic screening for peripheral
• most commonly caused by hematogenous spread of bacterial infection (Gram - positive cocci > Gram - and axial arthritis in the adult
negative bacilli ) population
6. Do not prescribe opioids for
management of chronic rheumatic
Risk Factors diseases before optimizing the use
• very young or very old age ( >80 yr), portal of entry (IV drug use, hemodialysis), recent infection with
STIs, RA (related to prior joint damage and immunosuppressed state of host ), type 2 DM
-
of non opioid approaches in pain
management
7. Do not delay or avoid palliative
Investigations symptom management and advance
• synovial fluid analysis: VVBC count with differential, crystal analysis, Gram stain , and culture (see
care planning for a patient with life
limiting rheumatic diseases because
-
Table 8, RH4 ) -
they arc pursuing disease directed
• blood work: GBG and C&S treatment
• ± endocervical, urethral, rectal , and oropharyngeal swabs ( if gonococcal septic arthritis is suspected )
• ± plain x- ray to establish joint baseline and to monitor treatment
Treatment Septic arthritis is a medical emergency:
«consider empiric IV antibiotic therapy until septic arthritis is excluded or until cultures come back to it leads to rapid joint destruction and
narrow antibiotic choice -
there is a 10 15% risk of mortality
• source control and joint decompression
• see Infectious Diseases. 1D13 and Orthopaedic Surgery. Septic Joint OR 11
Degenerative Arthritis: Osteoarthritis

--
• see Family Medicine. l - M l l
Definition
• progressive deterioration of articular cartilage and surrounding joint structures caused by genetic,
metabolic, biochemical, and biomechanical factors with secondary components of inflammation
Classification (Based on Etiology)

•primary ( idiopathic)
most common, unknown etiology OA of MCPs can be seen in
• secondary -
hemochromatosis or CPPD related
post- traumatic or mechanical disease (chondrocalcinosis)
post - inflammatory (e.g. RA ) or post - infectious
heritable skeletal disorders (e.g. scoliosis)
• endocrine disorders (e.g. acromegaly, hyperparathyroidism , hypothyroidism )
• metabolic disorders ( e.g. gout, pseudogout , hemochromatosis, Wilsons disease, ochronosis)
neuropathic (e.g. Charcot joints ), atypical joint trauma due to peripheral neuropathy (e.g. DM,
svphilis )
• AVN
other (e.g. congenital malformation )
Pathophysiology
•the process appears to be initiated by abnormalities in biomechanical forces and /or, less often, in
cartilage
•elevated production of local pro- inflammatory cytokines is important in OA progression
• tissue catabolism > repair
- -
• contributing factors ( mechanisms unknown ): genetics, alignment ( bow legged varus, knock - • Hand ( DIP, PIP. 1st CMC )
-
kneed valgus), joint deformity ( hip dysplasia ), joint injury ( meniscal or ligament tears), obesity,
environmental, mechanical loading, age, and gender • Hip
r
L
• considered to be a systemic musculoskeletal disorder rather than a focal disorder of synovial joints • Knee
• IstMTP -
• L-spine ( L4- L5. L5-S1 )
Epidemiology
-
• C spine a
-
• most common arthropathy (accounts for 75% of all arthritides) •Uncommon: ankle, shoulder, I +
•increased prevalence with increasing age ( 35% of 30 y/o, 85% of 80 y/o) .
elbow MCP rest of wrist
Risk Factors Figure 3. Common sites of joint

involvement in OA
• genetic predisposition , advanced age, obesityhttps://medical-amboss.com
(for knee and hand OA), female, and trauma
RII6 Rhcunialologv Toronto Notes 2023
Table 9. Signs and Symptoms of OA

Signs Symptoms
Joint line tenderness; stress pain t joint effusion Joint pain with motion ; relieved with rest
Bony enlargement at affected joints Short delation of stiffness|<1/ 2 h ) after immobility, called gelling
Malalignmonl / deformily (angulation ) Joint inslabilityfbuckling lotion due to liqdmcntous instability )
Limited ROM Joint locking due to " joint mouse" ( boneot cartilage fragment )
Crepitus on passive ROM loss ol function (e .g. meniscal tear or other internal derangements)
Inflammation ( mild if present! Insidious onset ol pain , localised to affected joints
Periarticular muscle atrophy Fatigue, poor sleep, impact on mood
Table 10. Radiographic Features of Specific Arthritides 1. Thumb squaring

2. Heberden's nodes
Radiographic Hallmarks of Osteoarthritis Radiographic Hallmarks of Inflammatory Arthritis
j. Bouchard's nodes
Subchondrial sclerosis
- -
Joint space narrowing typically non uniform -
Joint space narrowing typically uniform
Soft tissue swelling Figure 4. Hand findings in OA
Subchondrral cyst formation Erosions
Osteophytes Periarticular osteopenia
.
Knee , hip OIP joints - . .
Rheumatoid: C spine carpus , MCP joints MIP joint
Older, overused joint Often younger
Nevr bone formation|i.e. psoriatic arthritis)
Joint Involvement
• generalized OA:3+ joint groups
• asymmetric (knees usually affected bilaterally)
• hand
• DIF (Heberden's nodes = osteophytes > enlargement of joints)
• FIF ( Bouchards nodes)
CMC ( usually thumb squaring ) Differential Diagnosis of Elevated ESR
I st MCF (other MCFs are usually spared )
• Systemic inflammatory diseases
• hip • Localized inflammatory diseases
usually presents as groin pain ± dull or sharp pain in the trochanteric area, internal rotation and • Malignancy
abduction are lost first • Trauma
pain can radiate to the anterior thigh but generally does not go below the knee • Infection
• knee • Tissue injury/ ischemia
-
initial narrowing of one compartment , medial > lateral:seen on standing x rays, often patellar- femoral
joint involved
• foot
common in 1st M I F and midfoot
• lumbar spine
E
The Radiographic Hallmarks of OA
• Joint space narrowing
very common, especially L4-L5, L5-S1 • Subchondral sclerosis
degeneration of intervertebral discs and facet joints • Subchondral cysts
• reactive bone growth can contribute to neurological impingement (e.g. sciatica, neurogenic claudication ) • Osteophytes
or spondylolisthesis (forward or backward movement of one vertebra over another)
• cervical spine ’
-
commonly presents with neck pain that radiates to scapula , especially in mid lower cervical area (C5 C6) -
Emcise for Osteoarthritis of the Knee:
Investigations A Cochrane Systematic Review
• Woodwork B r J Sports Med 2015:49:1554 1557
• normal CBC KSR, and CRF
• negative Rl- and AN A
. Purpose: 1o determine if land -based therapeutic
exercise s beneficial for people with knee OS in
• radiology: 4 hallmark findings, see sidebar reducing pain, improving physical function, and
improving quality of life.
• synovial fluid: non -inflammatory (see Table 8, RH4 ) Methods: five databases searchedforiandumiied
cl nical trials comparing therapeut < eieitrse with a
Treatment noaeiercisc control .
• presently, no treatment alters the natural history of OA Results lid studies identified . Results from 44
,
• prevention: prevent injury, weight management, physical activity ( maintenance of muscle strength ) trials indicate thatexercise significantly reduced
non -pharmacological therapy pam (12 poirtshOO: 95% Cl 10 lo 15) and improved
• weight loss ( minimum 5-10 lb loss) if overweight physical function (10 pointsHOO: 95% Cl S to 13)
exercise: more effective if supervised, often by physiotherapists or in a class setting; Tai chi is strongly after treatment . Additionally, 13 studies showed
recommended for hip/knee OA hpioved quality of life with exercise.12 studies
showed reduced knee pern (6 pointed®):95% Cl 3 to
self-efficacy and self-management programs ( goal-setting, positive thinking, education on the disease) 19 ) end 10 studies showed i mproved physical function
thermal intervention: heat or cold .
(3 po nts 'lOO ; 95 % Cl 1 to 5) with eiercse 2 6 mo
• occupational therapy: aids, splints, cane, walker, bracing after treatment.
• pharmacological therapy (see Table :35, R H M ) Conclusion In people w < tli knee 0A. lend based
• stepped approach to therapy (local > systemic therapy) therapeutic exercise provides short term benefit that
• local therapy: a susta rned a lew m o after treatrre nt.
topical NSAlDs, topical capsaicin ( knee, hand OA)
injections: 1A glucocorticoids ( knee, hip OA) rn
systemic therapy: LJ
acetaminophen, oral NSAlDs
centrally acting agents (e.g. duloxetine )
• the following are not recommended based on lack of high -qualilv evidence: opioids and medical
glucosamine
-
cannabinoids ( for pain ), hyaluronatcs, platelet rich plasma , stem cell injections, chondroitin, and
+
• surgical treatment
total and /or partial joint replacement, joint debridement ( not shown to be effective ), osteotomy, fusion
Seropositive Rheumatic Disease

• diagnosis vs. classification in rheumatology
• diagnostic criteria are selected for sensitivity as opposed to specificity and thus may misdiagnose
some cases
• classification criteria are developed for specificity so well - defined cases can be studied in clinical
trials
modern classification criteria are more sensitive and specific for diagnostic use in studies of
earlier disease
• seropositive arthropathies are characterized by the presence of a serologic marker such as positive Rl
or ANA
• a small subset of the vasculitides ( i . e. the small vessel ANCA-associated vasculitides) has a measurable
serological component, but they are often considered a separate entity from seropositive disease by
experts
Table 11. Autoantibodies and Their Prevalence in Rheumatic Diseases

Autoantibody Disease Healthy Controls Comments
RF BA 8 (To S 25%- Serologic hallmark ol RA
SS 50% Autoantibodies directed against Fc domain ol IgG
Sit 20% Sensitive In RA (can be negative early in disease course)
-
RF is associated with more aggressive joint disease and extra articular features (e g ..
nodules)
May be presentin AHA - positive diseases often in lower litre
,
.
Nonspecific: may be present in IE IB. hepatitis C , silicosis, sarcoidosis
Anti CCP - R A 80 '
J
-
Specific for RA ( 94 98%)
May be useful in early disease and to predict persistent and erosive disease: can occur
before clinical disease becomes apparent
Associated with increased extra -articular RA manifestations
ANA SLE 98% High litres 1:640 <5% .
Ab against nudearcomponents ( DNA. RNA histones , centromere)
MOD 100% low litres1:40 Sensitive but not specific foi SLE
-
SS 40 70%
CRESI syndrome 60 - 80%
Op to 30% .
-
Prevalenceol non disease -
Given high false positive rate - only measure when high pre test probability o( CIO
(Often seen in other CIDs) related AHA rises with age
-
Anti dsDHA SLE 50 -70 % 0% Specific for SLE (95%)
levels correlate with disease activity (i.e. SLE flare)
Anti Sm - SLE « 30% |J Specific but not sensitive lor SIE
Does not correlate with SLE disease activity
It positive, will remain positive through disease course
Anti - Ro (SSA) SS 40 95% - 0.5% Seen in SS
SSc 21% Also seen in subacute cutaneous SIE (74%)
SLE 32% May be the only Ab present in ANA negative SIE
HA 15% Presence in piegnancy increases risk of having a child with neonatal lupus syndrome and
congenital heart block
-
Anti La (SSB) SS 40% M Usually occurs with anti Ro -
SLE 10 % Specific for SS and SLE when anti - Ro is also positive
Increases risk of having a child with neonatal lupus syndrome
. .
Antiphospholipid Ab ( LAC oCLA
aB 2 GP )
APS 100%
SLE 31- 40 %
« 5% By definition , present in APS
Only small subset of SLE patients develop clinical syndrome ol APS
It positive, will often get a false positive VDRL test
-
Anti Histone Drug - induced SLE 95% 0% -
Highly specific lor drug induced SIE
SLE 30 80% 0%
Anti RNP MCI 0 20% High titles present in MCIO: present in many other CIOs ( especially SLE )
SLE
Anti -Centromere Limited SSc (CREST ) >80 % 0% Specific for CRESI. limited cutaneous varianlof systemic sclerosis
-
Anti Topoisomerasc I (formerly Diffuse SSc 26 76%- 0 Specific for SSc
-
Scl 70 ) Increased risk lor pulmonary fibrosis in SSc
Anti Jol - PM 0 MM 0% less frequent for 0MM
-
Associated with interstitial pulmonary fibrosis and anti synthetase syndrome
c-AHCA Active GPA 90% 0% -
Specific 80 95% for GPA
MPA 25% Sensitivity can vary between moderate to high depending on technique and timing of
EGPA < 5% . -
sample ELISA method|anti PR 3) is more specific than IF
p - ANCA 6 PA 10 0% . .
Nonspecific and poor sensitivity (lound in ulcerative colitis PAN microscopic polyangiitis .
MPA 50 60% - -
E 6 PA, rapidly progressive glomerulonephritis). ELISA method (anti MPO) is more specific
EGPA 50 -70 % than IF
rm
LJ
Anti Mi 2- - 0 MM 15 - 20 % Specific but not sensitive ( not available in all centres)

Ab Against RBCs , WBCs , or Platelets SLE . .
Perform DAI test Hb reticulocyte, leukocyte, platelet count, and antiplatelel Abs
-
Anti Mitochondria Primary biliary cholangitis 0% Sensitive and specific +
Note: some individuals in the normal population test positive for RF ardor ANA, but do not have the conditions listed above
RH8 Rheumatology Toronto Xotcs 2023
Connective Tissue Disorders

Table 12 . Features of Seropositive Arthropathies
RA SLE Scleroderma Dermatomyositis
CLINICAL FEATURES
History Symmetrica! polyarthritis (small joint Multisystem disease: rash, Skin lightness, stillness ol fingers. .
Heliotrope rash (periorbital) Goltron's papules
involvement ) mouth ulcers, photosensitivity, Raynaud 's , heartburn, dysphagia. SOB (violaceous papules over knuckles and IPs)i
Morning stillness|>1 h) Raynaud 's, alopecia, cardiac on exertion due to pulmonary Hill or poikiloderma
Dyspnea on exertion |IL 0) in '30 % and pulmonary serosilis CHS . .
ILO lenal crisis with new onset Hill or Shawl sign: photosensitivity , macular erythema
symptoms, glomerulonephiilis hypertensive urgency /emergency over chcsl and shoulder
Proximal muscle weakness » pain, dyspnea on
exertion
Physical Examination Early: clluscd joints, tenosynovitis, Check BP. rash, mouth ulcers. Skin tightness on dorsum ol hand. .
Heliotrope rash Goltron's papules, shawl sign ,
subcutaneous nodules, alopecia . Raynaud 's phenomenon , facial skin lightening , telangiectasia . proximal muscle weakness ( usually painless) ,
other extra articular manifestations serositis, s cflused (typically calcinosis , non effused joint, inspiratory crackles
Late: join! deformities, small) joints (can bemimmal. look inspiratory crackles, features ol right-
bone - on - bone crepitus in advanced for soil tissue swelling) side hear! failure
disease , inspiratory crackles
LABORATORY
Nonspecific t ESRin 50 -60 % « ESR a Hb t CRP
tCRP Platelets (autoimmune) Normal WBC + Hb
•Platelets • Hb (autoimmune) .
Possibly t Cr proteinuria Normal Y/ BC
» Hb (chronic disease) YYBC (leukopenia, lymphopenia) tCK
« V/ BC (neutropenia rare) *
t Cr. proteinuria. RBC casts
Specific Rf -positive in "80% AHA- posilive in 98%. AIIA - posilivein >90% CK elevated in 80%
Anli- CCP - posilivein "80% Anli - dsDNA - posilive in 50-70%, Anti - topoisomerase T (diffuse) AHA - positivein 33 %
Anti - Sm - positive In 30%, Anti- centromere (usually in CRESI. see Anti Jo - 1. anti Ml 2
.
C 3 C4. tola! Sidebar, CRISI Syndrome RHI4). Muscle biopsy
hemolytic complement, EMG
false positive VORL (in SLE MRI
subtypes)
APIA
Radiographs Very early: normal Hon - erosive * Pulmonary fibrosis,' ILD l Esophageal dysmotility
Early: periarticular osteopenia - Osteopenia t Esophageal dysmotility ± ILD
Later: join! space narrowing t Soft tissue swelling ' Calcinosis 1 Calcifications
Erosions
Symmelricfconcentric
•110/lung nodules
Rheumatoid Arthritis
Definition
• chronic, symmetric, erosive synovitis of peripheral joints ( c.g. wrists, MCPs, Ml Hs)
'
RA is art independent risk factor for
• characterized by inflammatory joint disease ± a number of extra- articular features atherosclerosis and CV disease. RA
• 1 joint with definite clinical synovitis ( swelling ) not explained by another disease is associated with increased overall
mortality/morbidity from all causes:
Table 13. 2010 ACR /EULAR Classification Criteria for RA CV disease, neoplasm (especially
( score based algorithm: add score ol categories A 0 ; n score ol 6110 for dcfinilc RA) lymphoma). Infection
Criteria Score Comments

A. Joint involvement { swollen or lender)
1 large joint ( shoulders, elbows, hips, knees, and ankles ) 0
Common Presentation
2 -10 large joints 1
• Morning stiffness >1 h. improves
1-3 small joints (MCPs, PIPs. wrists, 2nd- Sth MIPs) 2 with use
4-10 small joints 3
>10 joints (at least 1 small joint ) S • Symmetric joint involvement
• Initially involves small joints of hands
6 . Serology Total score of e6: definite RA
and feet
Negative RE and negative Anli CCP 0 Musi have rf joint with definite clinical swelling, nol belter
explained by another disease • Constitutional symptoms
Low - positive RF or low -positive Anti- CCP (< 3 x ULN ) 2
High -positive RF or high - positive Anli - CCP (>3x ULH) 3
C. Acute phase reactants
Normal CRP and normal ESR 0
Abnormal CRP and abnormal ESR 1
0. Duration of symptoms
«6 wk 0 rn
LJ
iSwk 1
Arthritis Rheum 2010:62:2569-2581
Pathophysiology
• autoimmune disorder, unknown etiology; may have genetic and environmental component
• complex genetic and environment interactions lead to disruption of immune tolerance, ultimately
resulting in synovial inflammation
• genetic predisposition: HLA - DR4/ DR 1 association ( 93% of patients have either HLA type),
cytokine promoters, T cell signaling
• environmental predisposition: induction of enzymes that convert arginine to citrulline caused
by environmental stress (cigarette smoking), propensity for immune reactivity to neoepitopes
created by protein citrullination
• inflammatory process causes transformation of synovium into an invasive pannus tissue that
degrades cartilage and bone with absence of repair
elevated TNF level increases osteoclasts and decreases osteoblasts at the site of inflammation
(results in periarticular osteopenia )
upregulation of RANK ligand increases osteoclast -mediated destruction
• Wrist, not 1st CMC
Epidemiology • Elbow
• Shoulder
• most common inflammatory arthritis: prevalent in 1% of population • Knee *
• F:M=3:1 • Ankle o
-
• age of onset 20- 40 yr • MTP
• C- spine
Clinical Presentation
• variable course of exacerbations and remissions Figure 5. Common sites of joint
• morning stiffness > 1 h, improves with use, worsens with rest involvement in RA
• polyarthritis: symmetric joint involvement (tender, swollen ), small joints affected , most commonly in
hands and feet ( MCF, PIP, MTP)
• constitutional symptoms: profound fatigue , depression, myalgia , weight loss
• extra -articular features
• limitation of function and decrease in global functional status
• complications of chronic synovitis
signs of mechanical joint damage: loss of motion, instability, deformity, crepitus , joint deformities Boutonniere Deformity
swan neck deformity, boutonniere deformity
ulnar deviation and subluxation of MCP, radial deviation of wrist joint
hammer toe, mallet toe, claw toe
flexion contractures
• atlanto-axial and subaxial subluxation Swan Neck Deformity
C-spine instability
- neurological impingement ( long tract signs )
- difficult /dangerous intubation: risk of worsening subluxation and damage to spinal cord
• limited shoulder mobility, spontaneous tears of the rotator cuff leading to chronic spasm
• tenosynovitis -> may cause rupture of tendons
• carpal tunnel syndrome Claw Toe
• ruptured Baker’s cyst ( outpouching of synovium behind the knee ); presentation similar to acute deep
vein thrombosis ( DVT)
• poor prognostic factors include: young age of onset, high RF litre, elevated ESR, activity of >20 joints,
and presence of extra-articular features
Table 14. Extra - Articular Features of RA Classified by Underlying Pathophysiology

System Vasculitic Lymphocytic Infiltrate
Hammer Toe
Skin Periungual infarction, cutaneous ulcers, Rheumatoid nodules ( may have vasculitic
palpable purpura component)
i
Ocular Episcleritis, sderitis Keratoconjunctivitis sicca
Head and Heck .
Xerostomia Haslilmoto's thyroiditis (see
Mallet Toe
.
Endocrinology E31)
Cardiac -
Peri /myocarditis. valvular disease, conduction Figure 6. Joint deformities
defects
Pulmonary Pulmonary fibrosis, pleural effusion, pleuritis,
pulmonary nodules
Neurologic Peripheral neuropathy:sensory stocking -
glove, mononeuritis multiplex Syndromes in RA
Hematologic Splenomegaly, neutropenia ( Felty's syndrome) • SS (common): keratoconjunctivitis
sicca and xerostomia (dry eyes and
Renal -
Amyloidosis caused by accumulation of mouth)
abnormal proteins • Caplan's syndrome (very rare): j
combination of RA + pneumoconiosis
Classification of Global Functional Status in RA that manifests as multiple
• Class I : able to perform usual activities of daily living ( self-care, vocational , avocational ) intrapulmonary nodules
• Class II : able to perform self - care and vocational activities, restriction of avocational activities • Felly's syndrome (rare): arthritis,
splenomegaly, neutropenia
-
• Class III : able to perform self care, restriction of vocational and avocational activities +
• Class IV: limited ability to perform self-care, vocational , and avocational activities
Investigations
• Woodwork
-
RF: 80% sensitivity but non specific; may not be present at onset of symptoms; levels do not Poor prognostic features of RA include:
correlate with disease activity young age of onset, high RF litre,
« -
can be associated with more erosions, more extra articular manifestations, and worse elevated ESR, activity of >20 joints, and
presence of e xtra -articular features
function
- -
anti CCP: 80% sensitivity but more specific (94 98%); may precede onset of symptoms
• increased disease activity is associated with decreased Hb ( anemia of chronic disease) and increased
platelets, HSR, and CRP
• imaging Side Effects of Steroids
bilateral hands/wrists, ankles/feet x-ray • Weight gain
-
first change is periarticular osteopenia, followed by erosions
- -
(1 spine x ray ( may be normal at onset, required for preoperative assessment in long standing
.
• Osteoporosis
AVN
disease)
U/S (with power Doppler) - often changes of synovitis/erosion noted in advance of those seen on
.
• Cataracts, glaucoma
PUD
• Susceptibility to infection
-
plain x ray
.. HTN
• Easy bruising
MR 1 may fee used to image hands to detect early synovitis and erosions Acne
MR 1 T’l inflamed synovium is hypointense and hyperintense on T2; bone marrow edema can be
seen as well as areas of increased uptake gadolinium contrast
..Hyperlipidemia
Hypokalemia, hyperglycemia
• Mood swings
Treatment
• goals of therapy: remission or lowest possible disease activity
key is early diagnosis and early intervention with DMARDs
“window of opportunity”
remission
= early treatment within first 3 mo of disease may allow better control/ .
DMARDs prednisone, and biologies
( bOMARDs) but not analgesics or
- -
assess poor prognostic factors at baseline ( Rl ' positive, functional limitations, and extra articular
features)
NS AIDs. alter the course of RA
• behavioural
exercise program : active, gentle ROM and isometric exercise during flares; aquatic /aerobic/
strengthening exercise between flares
job modification , assistive devices as necessary
interventions to reduce cardiovascular disease, smoking cessation, lipid control
• pharmacologic: alter disease progression
DMARDs and biologies ( not analgesics or NSAlDs ) can alter the course of RA
• DMARDs
treatment with DMARDs should be started as soon as RA diagnosis is made and should be
aimed at reaching sustained remission
MIX is the gold standard and is first -line unless contraindicated
- prior to M I X therapy: CBC profile, liver enzymes ( ALT ), Cr (Cr clearance), hepatitis B
and C serology, and a CXR should be done
- monitor and if inadequate response (3-6 mo) -> combine or switch
- consider combination therapy to MTX if patients have poor prognostic features or high
disease activity
- therapy includes: hydroxychloroquine, SSZ, leflunomide, biologies
- contraindications include liver disease, significant alcohol intake, pregnancy, and
lactation
- if contraindication to MTX , then hydroxychloroquine, SSZ, and /or leflunomide should
be considered with the former being considered as a weaker agent and the latter as more
potent
• biologies (bDMARDs)
should be used if inadequate response to DMARDs
should be combined with DMARD therapy ( initiating with combination therapy is associated
with faster response rates and longer duration of effect )
first-line (anti-TNF) options: infliximab, etanercept , adalimumab, golimumab, and
certolizumab
- -
non anti TNl agents include anakinra ( almost never used for RA ), abatacept , rituximab, and
tocilizumab
reassess every 3-6 mo and monitor disease activity ( predominantly via assessing swollen joint
count)
JAR inhibitors ( including tofacitinih and upacitinib) are oral small molecule synthetic
DMARDs; used if other DMARDs and biologies fail
• pharmacologic: supportive to reduce inflammation and pain
NSAlDs
individualize according to efficacy, tolerability, and comorbidities
r
LJ
- )
contraindicated /cautioned in some patients (e.g. PUD, ischemic cardiac disease, pregnancy,
CKD, anticoagulant use)
add acetaminophen for synergistic pain control
corticosteroids +
local: injections to control symptoms in a specific joint
systemic ( oral prednisone) or 1 M

- low dose (5-10 mg/d ) useful for short-term to improve symptoms if NSAlDs are
ineffective and to bridge gap until DM ARDs take effect
-do baseline DEXA bone density scan and consider bone supportive pharmacologic
therapy ( e.g. bisphosphonates ) if using corticosteroids 7.5 mg /d >3 mo, particularly in
those with other risk factors
- cautions/ contraindications: active infection, TB, osteoporosis, H l N, gastric ulcer, DM ' '
•surgical
• indicated for structural joint damage
surgical options include: synovectomy, joint replacement, joint fusion , reconstruction / tendon
repair
Follow -Up Management and Clinical Outcomes

-
• clinical reassessment every mo initially, then 3 6 mo if still ongoing activity, then 6 12 mo after -
inflammation has been suppressed
• examine joints for active inflammation - if active, consider adjusting medications, physical therapy/
occupational therapy ( PT/OT)
• RA patients should be screened and managed for cardiovascular disease given increased risk
-
• if assessment reveals joint damage consider analgesia, referral to PT/OT, surgical options
• outcome depends on disease activity, joint damage, physical functional status, psychological health,
and comorbidities
• functional capacity is a useful tool for determining therapeutic effectiveness; many tools for
evaluation have been validated
• patients with RA have an increased prevalence of other serious illnesses: infection (e.g. pulmonary,
skin, joint ), osteoporosis, mental health disorders, renal impairment, lymphoproliferative disorders,
cardiovascular disease (correlates with disease activity and duration )
• risk of premature mortality, decreased life expectancy ( most mortality not directly caused by RA )
Systemic Lupus Erythematosus

• see Nephrology, NP26 Diagnostic Criteria of SLE
Definition MD SOAP BRAIN

• chronic autoimmune disease of unknown etiology resulting in multi-system inflammation Malar rash
Discoid rash
• characterized by production of autoantibodies and diverse clinical manifestations Scrositis
Oral ulcers
Table 15 . Classification Criteria of SLE * ANA
Entry criterion: ANA at a titre of >1:80 and Additive Criteria Photosensitivity
1. Do not count criterion il there is a more likely explanation than SLE Blood
2 . Occurrence ol a criterion on at least one occasion is sufficient Renal
3 . Within each domain, only the highest weighted criterion is counted towards the total score Arthritis
Immune
Clinical Domains and Criteria Score Neurologic
Constitutional Fever 2
Hematologic leukopenia 3
thrombocytopenia 4
A Systematic Review of Guidelines lor Managing
Autoimmune hemolysis 4 Rheumatoid Arthritis
Neuropsychiatric Delirium 2 EMC Rheumatol 2019:3:42
Five general principles formanagement:
Psychosis 3 • Start OMAROs as soon as possible following the
Seiture S diagnosis.
• The best ir tie’ treatment is MIX.
Mucocutaneous Non- scarring alopecia 2 • Monitor disease activity regularly.
Oral ulcers 2 • Bio 'og cs should be initiated in patients with
pertstently active disease despite MIX treatment.
Subacute cutaneous or discoid lupus 4
• Goals ol treatment should be aimed at low disease
Acute cutaneous lupus 6 activity or remission.
Serosal Pleural or pericardial effusion 5
Acute pericarditis 6 Environment
Stress, viruses, sun
Musculoskeletal Joint involvement 6
Genetic Hormonal
Renal Proteinuria (»0.5 g!24 h) 4 HLA
Renal biopsy Class II or V lupus nephritis 8 T cells i rugs
Renal biopsy Class III or IV lupus nephritis 10 rT

LJ
Immunology Domains and Criteria Score
Antiphospholipid antibodies Anti- cardiolipin antibodies or Anti-|!2PG1 antibodies or lupus anticoagulant 2 —,
I— Formation of
Complement proteins Low C 3 or low C4 3 Auto- Ab
lowC3 andlswC4 4 Cytotoxic Ah Immune complexes +
SLE specific antibodies Anh- dsDHA or Anti Srn antibodies 6 i
Cell damaye/dealh Inflammation
’Classification of SLE requires total score of >10 with >1clinical criterion
. . . . .
Sindhu R. Johnson Thomas Dorner Ray Naden et aL Arthritis & Rheumatology ( 71, 9), p.1400 copyright 2020 Modilied by Permission of John
Figure 7. Multi-factorial etiology of
Wiley and Sons https://medical-amboss.com SLE
Etiology and Pathophysiology

• production of cytotoxic autoantibodies and immune complex formation
-
• multi factorial etiology
• genetics
-
common association with HLA- B8/ DR 3; 10% have positive family history
• strong association with defects in apoptotic clearance > fragments of nuclear particles captured
by antigen - presenting cells > develop ANAs
cytokines involved in inflammatory process and tissue injur)': BlyS, 1 L -6, 1L - 17, IL-18, TNl '-a -
• environment
UV radiation , cigarette smoking, infection , vitamin D deficiency, silica dust
• estrogen
• increased incidence after puberty, decreased incidence after menopause
• men with SLE have higher concentration of estrogenic metabolites
increased risk of SEE associated with use of combined oral contraceptive pills and hormone
replacement therapy
• infection
viral ( non -specific stimulant of immune response )
• drug- induced
• antihypertensives ( hydralazine), anticonvulsants ( phenytoin ), antiarrhythmics ( procainamide), Drug-Induced SLE
isoniazid, biologies Often presents atypically with systemic
anti-histone Abs are commonly seen in drug- induced SLE features and serositis; usually associated
symptoms resolve with discontinuation of offending drug -
with anti histone Ab
Epidemiology
• prevalence: 0.05% overall
=
• E:M I 0: I
• age of onset in reproductive yr ( 15 45 ) -
• more common and severe in Hispanic and Asian individuals, and individuals of African descent
• bimodal mortality pattern
• early ( within 2 yr)
active SLE, active nephritis, infection secondary to steroid use
late
inactive SLE , inactive nephritis, atherosclerosis likely due to chronic inflammation
• characterized by periods of flares and remission
Table 16 . Signs and Symptoms of SLE

System Symptoms
Systemic fatigue, malaise , weight loss, fever, lymphadenopathy
Raynaud's Phenomenon
Hematologic Anemia ol chronic disease , hemolytic anemia , leukopenia , neutropenia , thrombocytopenia , pancytopenia , Vasospastic disorder characteristically
thrombosis, splenomegaly causing discolouration of fingers and
Hematuria , proteinuria (glomerulonephritis). HTN. peripheral edema , renal failure toes ( white blue » red)
Renal *
Classic triggers: cold and emotional
Dermatologic Photosensitivity, malar rash , discoid rash , oral ulcers , alopecia ( hair loss) , purpura , panniculitis (inflammation of stress
subcutaneous lat and muscle tissue) , urticaria
Musculoskeletal Polyarthralgias, polyarthritis , myalgias. AVN. reducible deformities of hand ( Jaccoud 's arthritis )
Ophthalmic Keratoconjunctivitis sicca , episcleritis, sderitis, cytoid bodies (cotton wool exudates on fundoscopy - infarction
ol nerve cell layer of retina)
Cardiac Pericarditis. CAD. nonbacterial endocarditis ( Libman -Sacks). myocarditis
Vascular Note: SLEis an independent risk factor for atherosclerosis and CAD
Respiratory Raynaud 's phenomenon , livedo reticularis (mottled discolouration of skin due to narrowing of blood vessels,
-
characteristic lacy or net like appearance) , vasculitis
Gastrointestinal . .
Pleutilis, ILD pulmonary HIN. PE alveolar hemorrhage
Neurologic/ Psychiatric Pancreatitis. SLE enteropathy hepatitis, hepatomegaly, dysphagia , esophagitis, intestinal pseudo- obstruction ,
,
peritonitis, mesenteric vasculitis
-
lifo/ Organ Ihrcalcning Cardiac: coronaiy vasculitis, malignant HIN. tamponade
Hematologic: hemolytic anemia , neutropenia, thrombocytopenia. TIP, thrombosis
Neurologic:seizures. CVA. stroke
Respiratory: pulmonary HIN . pulmonary hemorrhage , emboli
Investigations
ri
-
• ANA (98% sensitivity, but poor specificity > used as a screening test; ANA titres are not useful to LJ
follow disease course, see ( ./ loosing Wisely Recommendations , RH 5 )
'
- -
• anti dsDNA and anti Sm are specific ( 95 99% )
-
-
• anti dsDNA titre and serum complement (C3, C 4) are useful to monitor treatment response in patients Consider SLE in a patient who has
who are clinically and serologically concordant (anti-dsDNA increases, C3 and C4 decrease with
disease activity)
involvement of 2 or more organ systems
+
- - -
• AFI.A (anti cardiolipin Ab, SLE anticoagulant , anti |52 glycoprotein 1 Ab), may cause increased risk of
clotting and increased aPT'T
Treatment
• goals of therapy
aim for remission , prevention of flares
• hydroxychloroquine ± glucocorticoid
treat early and avoid long - term steroid use, if unavoidable see Endocrinology, E 4 b for
The arthritis of SLE can be deforming
osteoporosis management but it is non-erosive (in contrast to RA) -
if high doses of steroids are necessary for long-term control, taper when possible and add called Jaccoud 's arthritis
immunosuppressive therapies (MTX, azathioprine, mycophenolate )
• treatment is tailored to organ system involved and severity of disease
• moderate refractory disease can be treated with belimumab
all medications used to treat SLH require periodic monitoring for potential toxicity
• dermatologic
• sunscreen , avoid UV light and estrogens
• topical steroids, hydroxychloroquine
• musculoskeletal
NSAlDs ± gastroprotective agent for arthritis (also beneficial for pleuritis and pericarditis)
-
• hydroxychloroquine improves long term control and prevents flares
bisphosphonates, calcium , vitamin D to combat osteoporosis
• other considerations
smoking cessation
• immunizations ( influenza ); live vaccines are generally not recommended
• for women with APLA , avoid estrogen -containing contraceptives because of increased risk of
thrombosis
• organ -threatening disease
high - dose oral prednisone or IV methylprednisolone in severe disease
-
• steroid sparing agents: azathioprine, MTX, mycophenolate (can use mofetil or sodium )
• IV cyclophosphamide for serious organ involvement (e.g. cerebritis or lupus nephritis ) for clinical
features of lupus nephritis
refractory disease can be treated with rituximab
Antiphospholipid Antibody Syndrome

Definition
-
• multi system vasculopathy manifested by recurrent thromboembolic events, spontaneous abortions,
and thrombocytopenia
Manifestations of APLA
• Thromboembolic events
• circulating antiphospholipid autoantibodies interfere with coagulation • Spontaneous abortions
• primary APS: occurs in the absence of other disease • Thrombocytopenia
• secondary APS: occurs in the setting of a connective tissue disease ( including SLH ), malignancy, drugs • Associated with livedo reticularis,
( hydralazine, procainamide, phenyloin, interferon, quinidinc ), and infections ( HIV, TB, hepatitis C‘.
infectious mononucleosis)
. migraine headaches
• catastrophic APS: development within 1 wk of small vessel thrombotic occlusion in >3 organ systems
with positive APLA ( high mortality)
Table 17. Classification Criteria of APS * Arterial and venous thrombosis are
usually mutually exclusive
Criteria Description
CLINICAL
Vascularthrombosis One or more clinical episodes of arterial, venous, or small vessel thrombosis in any tissue or organ
Must be conlrrmcd by imaging or histopalliology
Pregnancy morbidity 1. >1 death ol morphologically normal fetus (confirmed by U /S or fetal exam ) at >10 wk gestation: OB
2. >1 premature birth ol morphologically normal neonate belore 34 wit gestation doe to eclampsia ,
preedampsia. or placental insufficiency; OR
. -
3 >3 consecutive spontaneous abortions 10 wk gestation (excluding maternal anatomic and hormonal
'
abnormalitres or palernal /mateinal chromosomal causes)

LABORATORY Labs must be positive on 2 occasions, at least 12 wk apart
Lupus anticoagulant Present in plasma, detected according to the guidelines of the International Society on Ihrombosisand See Landmark Rheumatology Trials .
Haemostasis RH32lor more information on the
TULIP- 2 trial. It examined the efficacy of
Anti cnrdiolipin Ab .
IgG and / or IgM plasma or serum , present in medium high Hire (i.e. > 40 CPI or MPl, or *99 lh percentile), anifrolumab for the treatment of SLE.
measured by ELISA
-
Anti p2 glycoprotein ! Ab IgG and/or IgM. plasma or serum , present in high litre (i.e. >99 th percentile), measured by ELISA
must be present
* 1clinic ill and 1 laboratory criteria
J Thromb Haemost 200G;4: 29 D - 30 G
• see clinical criteria ( Table 17 )
• hematologic
• thrombocytopenia, hemolytic anemia , neutropenia
• dermatologic +
» livedo reticularis, Raynaud ’s phenomenon, purpura , leg ulcers, gangrene
RHl I Rheumatology Toronto Notes 2023
Treatment
• thrombosis
• lifelong anticoagulation with warfarin
target 1NR 2.0 -3.0 for first venous event, >3.0 for recurrent event, target 1NR > 3.0 for arterial
event, or target 1 NR 2.0 - 3.0 + ASA
• recurrent fetal loss
• heparin / low molecular weight heparin ± ASA during pregnancy
• catastrophic APS
• high - dose steroids , anticoagulation, cyclophosphamide, plasmapheresis
Scleroderma (i.e. Systemic Sclerosis)

Definition
• a non - inilammatory autoimmune disorder characterized by widespread small vessel vasculopathy,
production of autoantibodies, and fibroblast dysfunction causing fibrosis CREST Syndrome
Cal cinosis
Sclorodortna Raynaud ' s phenomenon
Esophageal dysmotility
li e. systemic sclerosis )
Sderodactyly
I Telangiectasia
*
Localized Generalized
( no involvement ol internal organs )
•Mostly children and young adults
I I
T
Morphea
•Hard oval patches
*
Linear
•Line of thickened skin
Limited systemic sclerosis
•Skin sclerosis restricted to
hands, face, neck
Diffuse systemic sclerosis
•Widespread skin disease
( proximal to wrist, can
Scleroderma is the most common cause
of secondary Raynaud 's phenomenon
on the skin •3rd to 4th decade involve trunk ), tendons
• Pulmonary HTN common • Early visceral involvement
•CREST ( renal, pulmonary fibrosis )
Figure 8. Forms of scleroderma
Etiology and Pathophysiology Cyclophosphamide vs. Mycophcoolitc Mofctil in

•idiopathic vasculopathy (not vasculitis) leading to atrophy and fibrosis of tissues Scleroderma lung Disease
L arret Respir Wed 2016;4:708-719
characterized by several hallmark pathogenic features: small vessel vasculopathy resulting in .
Study Double ; 'd randomized , parallel group
tissue hypoxia , production of autoantibodies, and fibroblast dysfunction leading to increased MI
deposition of extracellular matrix Purpose: locompare the toxicity and efficacy of
• resembles malignant HTN cyclophosphamide vs. mycoptierrolate mofetil on
lung function.
• lung disease is the most common cause of morbidity and mortality Results: In both treatment groups, ( be adjusted
percent predctedfVC Improved from baseline In 24
Table 18. The American College of Rheumatology (ACR ) / European League Against Rheumatism no. Mycophenotate mofetil was associated with less
(EULAR ) Criteria for the Classification of Scleroderma * tonicity and was better tolerated.
Conclusion : Treatment of SSc -ltD with
Item Sub item - Score
mycophenolatemofetil for 2 yr oe cyclophosphamide
1. Skin thickening of fingers of both hands 9 lor 1 yr both result in improved long function .
extending proximal to the MCP (sufficient However, mycophenolatemofetil is the current
criterion) preference for treatment of SSc-tlO due to its better
2. Skin thickening of the lingers Fully lingers 2 Mtnbllity .
Sderodactyly
3. fingertip lesions Oigital tip ulcers 4
fingertip pilling scats
4. Telangiectasia 2 Raynaud 's Phenomenon DDx
5.Abnormal nailfold capillaries 3 COLD HAND
6. Pulmonary arterial HTNiILD (max score 2) Pulmonary arterial HTN 2 Cr yoglobulins/Cryofibrinogens
ILD Obstruction /Occupational
Lupus erythematosus, other connective
7. Raynaud’s phenomenon 2
tissue disease
8. Scleroderma - related Ab Anti- centromere 2 DM / Drugs
-
Anti toporsomcrase I Hematologic problems ( polycythemia ,
Anti RNA polymerase III leukemia , etc.)
.
' Score ol > 9 is sufficient to classify a patient as having definite scleroderma (sensitivity 0.95 spedlicity 0.93) Arterial problems (atherosclerosis) /
Anorexia nervosa
Epidemiology Neurologic problems ( vascular tone)
-
• I : M =3 4: I , peaking in 5 th decade
• associated with HLA - DR 1 and environmental exposures ( silica, epoxy resins, toxic oil, aromatic
Orscasc of unknown origin ( idiopathic )
rm
LJ
hydrocarbons, polyvinyl chloride)
• limited systemic sclerosis has a higher survival prognosis ( >70 % at 10 yr ) than diffuse systemic
sclerosis (40-60% at 10 yr )
+
RHl 5 Rheumatology Toronto Notes 2023
Table 19. Clinical Manifestations of Scleroderma Features of Pathologic Raynaud ’s

System Features Syndrome
• New onset
Dermatologic Painless non pitting edema » skin tightening
• Asymmetric
.
Ulcerations, calcinosis, periungual erythema , hypo / hyperpigmenlation pruritus, telangiectasias • Precipitated by stimuli other than
-
Characteristic lace: mask like (acies with light lips, beak nose, radial perioral furrows cold or emotion
Vascular Raynaud 's phenomenon •» digital pits, gangrene • Associated with distal pulp pitting or
Thrombosis tissue reabsorption
-
Gastrointestinal ( 90 %) Distal esophageal hypomolilily » dysphagia
Loss ollower esophageal sphincter lunction * gastroesophageal reflux disease (GERD), ulcerations, strictures
• Digit ischemia
• Capillary dilatation by capillaroscopy
Renal
-
Small bowel hypomotility * bacterial overgrowth, diarrhea, bloating , cramps, malabsorption , weight loss
Large bowel hypomolilily wide mouth diverticula are pathognomonic radiographic finding on barium study
Mild proteinuria, Cr elevation , KIN
-
"Scleroderma renal crisis" (10 15%) may lead to malignant arterial HIN , oliguria , and microangiopathic hemolytic
anemia
-
Pulmonary ( SOS )
Cardiac
. .
Interstitial librosis pulmonary HTN pleurisy , pleural effusions
lelt ventricular dysfunction , pericarditis, pericardial effusion , arrhythmias
Musculoskeletal Polyarthralgias
"Resorption of distal tufts ” (radiological finding )
Proximal weakness 2° to disuse, atrophy, low grade myopathy, tendon friction rubs
Endocrine Hypothyroidism
Investigations
• blood work
CBC Cr ANA ..
anti-topoisomerase l / anti-Scl-70 antibody: specific but not sensitive for diffuse systemic sclerosis
anti-centromere antibody: favours diagnosis of CREST ( limited systemic sclerosis)
-
• anti RNA polymerase 111 antibody: associated with severe skin involvement , increased risk of
renal crisis
-
• P1'T
assess and monitor for 1LD
• echocardiogram
• rule out pulmonary HTN
• imaging
baseline CXR to rule out ILL)
Treatment
• dermatologic
• good skin hygiene
-
• low dose prednisone ( > 20 mg may provoke renal crisis if susceptible ) M I X ( limited evidence ) .
• vascular
Raynaud’s: keep hands and body warm, smoking cessation
vasodilators (CCBs, local nitroglycerine cream , systemic PGE 2 inhibitors, PDE 5 inhibitors ),
fluoxetine
• gastrointestinal
GERD: PPls are first-line, then H 2 - receptor antagonists
• small bowel bacterial overgrowth: broad spectrum antibiotics ( tetracycline, metronidazole)
motllltydisturbanccs: prokinetics
• renal disease
ACE inhibitor for hypertensive crisis
see
• pulmonary
early interstitial disease: mycophenolate mofetil ( less toxicity ) or cyclophosphamide
pulmonary HTN: vasodilators (e.g. bosentan, epoprostenol, and PDE5 inhibitors)
rapidly progressive disease at risk of organ failure: consider hematopoietic stem cell
transplantation
• cardiac
pericarditis: systemic steroids
• musculoskeletal
arthritis: NSAIDs
• myositis: systemic steroids r1
Inflammatory Myopathy 0
Definition
• autoimmune diseases characterized by proximal muscle weakness ± pain
• muscle becomes damaged by a non -suppuralive lymphocytic inflammatory process
• associated with malignancy
increased risk of malignancy: age >50, DMM > PM , elevated CK , peak incidence of malignancy
at onset of myositis or within 1st yr, dysphagia , ulcerative skin lesions, cutaneous vasculitis,
-
anti P155/ 140 antibody
• associated with other CTDs, Raynaud 's phenomenon , autoimmune disorders
Classification
• PM / DMM
• adult and juvenile forms
• newly characterized entities:
focal necrotizing myopathy (secondary to statin )
amyopathic myopathy (anti-synthetase syndrome, MDA-5 syndrome)
Inclusion Body Myositis
-
• age >50, M >1', slowly progressive, vacuoles in cells on biopsy
• patient unresponsive to treatment
• distal and proximal muscle weakness
• muscle biopsy positive for inclusion bodies
POLYMYOSITIS /DERM ATOM YOSITIS
Definition
• PM and DMM arc idiopathic inflammatory myopathies characterized by inflammation and proximal
skeletal muscle weakness
• notably, DMM often presents with characteristic skin manifestations Signs of DMM
Cottron's papules and Gottron's sign ate
pathognomonic of DMM (occur In 70%
Etiology and Pathophysiology of patients)
• PM is a T cell- mediated process with myocytes being the primary target, characterized by focal
endomysial infiltrates (CD8+ T cells ) surrounding muscle fibres, found in adults
• DMM is a complement mediated process with perivascular inflammatory infiltrates (CD4 + T cells >
CD8+ T cells) leading to perifascicular atrophy of muscle fibres
• progressive symmetrical proximal muscle weakness (shoulder and hip) developing over wk to mo;
Malignancies Associated with DMM
difficulty lifting head off pillow, arising from chair, climbing stairs
• dermatological
DMM has characteristic dermatological features (1'> M, children and adults)
-
..
Breast
Lung
Colon
Gottron’s papules • Ovarian
- pink-violaceous, flat-topped papules overlying the dorsal surface of the MCP and IP
Gottron’s sign
- erythematous, smooth or scaly patches over the extensor surface of elbows, knees, or
medial malleoli
heliotrope rash: violaceous rash over the eyelids; usually with edema
shawl sign : poikilodermatous, erythematous rash over neck, upper chest , and shoulders
mechanic's hands: dry, crackled lesions on palmar and lateral surfaces of digits, especially
-
over the pulp space, also seen in a subtype of myositis called anti synthetase syndrome
periungual erythema
• cardiac
• arrhythmias, congestive heart failure, conduction defect, ventricular hypertrophy, pericarditis
• oropharyngeal and lower esophageal dysphagia, reflux
• pulmonary
• weakness of respiratory muscles, ILD, aspiration pneumonia
Investigations
• general lab tests: CK, CBC, ESR and /or CRP, TSH
- -
• serologic tests: ANA , anti ) o- l ( DMM ), anti-Mi 2, anti-SRP ( usually not available at commercial labs)
• imaging: MR 1 may be used to localize biopsy site
• EMG: characteristic findings of muscle inflammation and damage
-
r >
LJ
• muscle biopsy can aid in diagnosis, however not needed in those with classic skin findings and muscle
weakness
Treatment
• non -pharmacological treatment
P I and OT, speech-language therapy for esophageal dysfunction
• pharmacological treatment
high - dose glucocorticoid (e.g. prednisone 1 mg/ kg/d ) usually not exceeding 80 mg daily and slow
taper after patient improvement ( 6 wk )
• add immunosuppressive agents (azathioprine, MIX )
-
• 1V1G if severe or refractory
hydroxychloroquine for DMM rash
• malignancy surveillance
• detailed history and physical ( breast, pelvic, and rectal exams )
• CXR, abdominal and pelvic VIS , fecal occult blood, Fap test , mammogram ± CT scan ( thoracic,
abdominal , pelvic)
Sjogren’s Syndrome
Definition
• autoimmune condition characterized by dry eyes ( keratoconjunctivitis sicca/xerophthalmia ) and dry
mouth ( xerostomia ), caused by lymphocytic infiltration of salivary and lacrimal glands
• exists on a spectrum and may evolve into a systemic disorder ( 20% ) with diminished exocrine gland
activity and extraglandular features
• primary and secondary forms (associated with RA , SLH . DMM, and HIV )
• prevalence 0.5%, F»M at 10:1, 40-60 yr
• increased risk of non-Hodgkin’s lymphoma (lifetime incidence 6-7%)
Table 20. The American College of Rheumatology ( ACR )ZEuropean League Against Rheumatism
(EULAR ) Classification Criteria for Primary Sjogren’s Syndrome (at least 1 inclusion criteria, no
condition in exclusion criteria , score >4)
Criteria Score Comments
Labial salivairy gland biopsy with focal lymphocytic 3 Focus scores are histopathologic grading systems
.
sialadenitis with focusscorea1foois '4mmi Strongly associated with phenotypic ocularand serological
components of Sjogren 's
-
Anti SSA - or Ro- positive 3
Ocular staining score > 5 (or van Gi jsterfeld score >4 1 Ocular staining score based on fluorescein dye examination of
on at least one eye) conjunctiva and cornea to determine clinical changes
Schirmer 's test <5 mm /5 min on at least one eye 1
Unstimulated whole saliva flowrate <03 mL/min 1
Inclusion criteria ( positive response to at least one question ):1) Have you had daily persistent troublesome dry eyes for more than 3 mo? 2) Do
, ,
you have a recurrent sensation of sand or gravel in the eyes? 3) Do you use tear substitutes more than 3 bmes a d ? 4 ) Have you had a daily feeling
of dry mouth for more than 3 mo ? 5) Do you frequently drink liquids to aid in swallowing dry food?
.
Exclusion criteria include prior diagnosis of any of the foi:owing conditions:1) History of head and neck radiabon treatment 2) Active hepatitis C
. -
infection (with confirmation by polymerase chain react on.3) AIDS. 4) Sarco.dosis. 5) Amyloidosis 6 ) Graftversus- host disease, 7) lgG 4 related
disease
-
Arthritis Rheumatol. 2017:69:35 45
• “sicca complex": dry eyes ( keratoconjunctivitis sicca/ xerophthalmia ), dry mouth ( xerostomia ),
complicated by staphylococcal blepharitis
• dental caries, oral candidiasis, angular cheilitis ( inflammation and Assuring at the labial commissures
of the mouth )
• extra -glandular manifestations
fatigue, low-grade fever
Classic Triad (identifies 93% of
• autoimmune thyroid dysfunction Sjogren's patients)
• arthralgias, arthritis • Dry eyes
• subclinical diffuse ILD. xerotrachea leading to chronic dry cough • Dry mouth ( xerostomia ) » dysphagia
• renal disease, glomerulonephritis .
• Arthritis (small joint , asymmetrical
palpable purpura, vasculitis non erosive) but may be associated
with rheumatoid arthritis, in which
• peripheral neuropathy case, the arthritis is erosive and
• lymphoma risk greatly increased symmetric
Treatment
• ocular
artificial tears/ tear gel if severe, moisture retaining eyewear, humidifiers, or surgical punctal LJ
occlusion for dry ev es
• oral
• good dental hygiene, hydration
• avoid alcohol and tobacco
• parasympathomimetic agents that stimulate salivary flow ( e.g. pilocarpine) +
topical nystatin or clotrimazole x4-6 wk for oral candidiasis
• systemic treatments (e.g. hydroxychloroquine, corticosteroids) are ineffective, rituximab can be used
in severe organ -threatening disease (e.g. vasculitis )
Activate Windows
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Mixed Connective Tissue Disease

Definition
• syndrome with features of 3 different ( I Ds (e.g. SLE, scleroderma , myositis)
"
• common symptoms: Raynaud ’s phenomenon, swollen fingers
Investigations
• blood work: anti- RNP ( see Table 12 , RHS )
Treatment
• treatment is generally guided by the severity of symptoms and organ system involvement
Prognosis
• prognosis is variable: some individuals go into remission, others develop a distinct connective tissue
disease (e.g. SLE, SSc ), and others develop a severe disease course
• pulmonary arterial HTN is a major cause of death
Overlap Syndrome
Definition
• syndrome with sufficient diagnostic features of 2 + different CT' Ds
Vasculitides
• inflammation and subsequent necrosis of blood vessels leading to tissue ischemia or infarction of any
organ system
• diagnosis
clinical suspicion: suspect in cases of unexplained multiple organ ischemia or systemic illness
with no evidence of malignancy or infection; constitutional symptoms such as fever, weight loss,
anorexia, fatigue
• labs non-specific: anemia, increased WBC and CRP, abnormal U /A
..
Features of Small Vessel Vasculitis
» investigations: biopsy if tissue accessible; angiography if tissue inaccessible
Palpable purpura
• treatment generally involves corticosteroids and /or immunosuppressive agents Vesicles
• Chronic urticaria
Table 21. Classification of Vasculitis and Characteristic Features • Superficial ulcers (erosions)
m
Classification Characteristic Features
SMAUVESSEL
Non- ANCA -assooated
Anh CBM (Goodpaslure's disease)
Immune complex- mediated ( most common mechanism)
Autoantibodies targeting type IV collagen in both glomerular basement
. c - ANCA (e.g. pR3-ANCA):
cytoplasmic anti-neubophil
membrane and alveoli causing glomerulonephntisandor pulmonary findings cytoplasmic Ab associated with
Anti- Clg vasculitis (hypocomplemenlemic urticarial vasculitis
syndrome)
Specific autoimmune disorder with at least 6 mo of urticaria with Clg
complement deficiency with various systemic findings
. anti-PR3
p - ANCA (eg.MPO-ANCA):
perinuclear anti-neutrophil
Predominantly cutaneous vasculitis Also known as hypersensitivily/leukocytKlasbc vasculitis cytoplasmic Ab associated
IgA vasculitis (formerly Henoch-Schonlein purpura (BSP)) ..
Vascular deposition of IgA causing systemic vasculitis (skin 61 renal), usually with multiple antigens, e.g.
(see Paediatrics. P98) self -limiting: most common in childhood myeloperoxidase, lactoferrin (IBD).
Cryoglobuinemic vasculitis (CV) Systemic vasculitis caused by circulating cryoproteins forming immune
.
cathepsin etastase. etc. Of these,
only antibodies to myeloperoxidase
.
complexes; 60 - 80% of cases are due to hepatitis C 5 -10 % are due to a CID
. . .
(SLE DA SS) 5 -10 % are due to a lymphoprotiferative disorder, and the
remaining 5 -10% are idiopathic or 'essential.' CV may be associated with
have been associated with the
development of vasculitis
..
underlying infection (e g hepatitis C) or CTO
ANCA -associated (i.e. PR 3 - ANCA) Granulomatous inflammation of vessels of respiratory bad and kidneys
.
Granuiomatosis with polyangiitis (GPA formerly Wegener's) leading to pulmonary hemorrhage and glomerulonephritis: initially may have
PR3 (c-ANCA) > MP0 |p - ANCA) upper respiratory trad infection (URTI) symptoms (sinusitis): most common
EGPA Triad
in middle age
• Allergic rhinitis and asthma (often
EGPA.formerly Churg-Strauss syndrome (50% AHCA positive) Granulomatous inflammation of vessels with hypereosinophilia and quiescent at time of vasculitis)
eosinophilic tissue infiltration, frequentlung involvement (asthma, allergic • Eosinophilic infiltrative disease
rhinitis), associated with MPO- ANCAin 40 -50% of cases.Other manifestations
.
include peripheral neuropathy (70%) Gl involvement myocarditis, and rarely . resembling pneumonia
Systemic vasculitis often
mononeuritis multiplex'peripheral
coronary arteritis; average age 40s
neuropathy and peripheral
Microangiopathic polyangiitis ( MPA) Fauci -immune necrotizing vasculitis, affects kidneys (necrotizing
eosinophilia
(70% ANCA positive, usually MPO ) glomerulonephritis), lungs (capillaritis and alveolar hemorrhage), and skin;
most common in older age
<- J
ME 0IUM VESSEL
PAN Segmental, non granulomatous necrotizing inflammation
Features of Medium Vessel Vasculitis
.
Unknown etiology in most cases, any age (average 40-50s) M*F
• Livedo reticularis
.
Kawasaki disease (see Paediatrics P98) Arteritis and mucocutaneous lymph node syndrome • Erythema nodosum
+
• Raynaud's phenomenon
• Nodules
• Digital infarcts
• Ulcers
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Table 21. Classification of Vasculitis and Characteristic Features

Classification Characteristic Features
LARGE VESSEL
GCA Temporal arteritis Inflammation predominantly of Ihe aorta and its branches
Ages »50.F*M
Temporal headache, jaw claudication,scalp tenderness,rision loss
lakayasu's '
.
Pulseless disease " unequal peripheral pulses,chronic inflammation,most
often the aorta and its branches
.
Host common in young adults of Asian descent,ages 10 - 40 f - M.risk of aortic
aneurysm
OTHER VASCUllTIDES
Buerger 's disease Inflammation and clotting of small and medium - sued arteries and veinsof
("Thromboangiitis Obliterans") .
distal entremities may lead to distal daudicabon and gangrene, the most
important etiologic factor is cigareltesmoking. Host commonin young Asian
.
males M >F
Behcet's disease Multi system disorder presenting with ocular involvement (uveitis),recurrent
oral and genital ulceration, venous thrombosis, skin and joint involvement
Most common in Mediterranean and Asian populations,average age 30 y/o .
M >f
Vasculitis mimicry (i.e. pseudovasculitis) Cholesterol emboli, atrial myxoma, subacute bacterial endocardibs |SBE). APS
Takayasu'sateiitis
Kawasaki disease
Small Vessel Vasculitis -

ANCA Associatcd Vasculitis
-
Non ANCA - Associated Vasculitis
Cryoglobulinemic vascuCbs
IgA vasulitisllgAV)
Hypocomplementennc urtcanal vasculibs
Figure 9. Classification of vasculitides by vessel sire

-
CWIIOM Tjr B 2031
J . C. Jcrrelte. R. J. Falk. P. A. Bacon, et al. Arthritic & Rheuno totogy (65. t). p. 1. copyright 2020. Modified by Permaiion of John Wiley and Sons
Small Vessel Non- ANCA- Associated Vasculitis

CUTANEOUS VASCULITIS
•subdivided into:
drug-induced vasculitis
serum sickness reaction
vasculitis associated with other underlying primary diseases (CTD, infections, malignancies -
hematologic > solid tumours)

• cutaneous vasculitis following:
• drug exposure (allopurinol, gold , sulfonamides, penicillin , phenytoin )
• viral or bacterial infection
• idiopathic causes
• small vessels involved ( post -capillary venules most frequently )
• usually causes a leukocytoclastic vasculitis: debris from neutrophils around vessels
• sometimes due to cryoglobulins which precipitate in cold temperatures
Clinical Presentation ri
• palpable purpura (usually on lower extremities) ± vesicles and ulceration, urticaria, macules, papules, -
L I
bullae, subcutaneous nodules

renal or joint involvement may occur, especially in children
Investigations +
• vascular involvement ( both arteriole and venule ) established by skin biopsy
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RH 20 Rheumatology Toronto Xotes 2023
Treatment
• stop possible offending drug; treat underlying primary disease
• NSAIDs, low- dose corticosteroids
• immunosuppressive agents in resistant cases
-
• usually self limiting
Small Vessel ANCA- Associated Vasculitis

GRANULOMATOSIS WITH POLYANGIITIS
(GPA , formerly known as Wegener’s Granulomatosis)
Definition
• granulomatous inflammation of vessels that may affect the upper airways (rhinitis, sinusitis ), lungs
Classic Features of GPA
( pulmonary nodules, infiltrates caused by pulmonary hemorrhage), and kidneys (glomerulonephritis,
• Necrotizing granulomatous vasculitis
renal failure) of lower and upper respiratory tract
• highly associated with c-ANCA by indirect immunofluorescence ( 11 F ) and PR3-AXCA by HL1SA; • Focal segmental glomerulonephritis
however, changes in A NLA levels do not predict remission or relapse
• incidence: 2-3 in 100000; more common in Northern latitudes
Table 22. Classification Criteria for GPA*

See Landmark Rheumatology Trials
Clinical Criteria Score
RH34 for more information on the
Criteria Description RAVE trial. It examined the efficacy
Nasal involvement
perforation
.
Crusting, ulcers, epistaxis congestion, blockage,or septal defect' *3
of rituximab for the induction and
maintenance of remission in patients
with ANCA-associated Vasculitides.
Cartilaginous mvohrtment Ear /nose cartilage inflammation, hoarseness or stridor, endobronchial *2
involvement, or saddle nose deformity
Nearing loss
.
Laboratory Imaging, and Biopsy Criteria
c- ANCA or anti-FR3-positive
Conductive or sensorineural * r
5
o
See Landmark Rheumatology Trials
RH34 for more information on the
Pulmonary nodules,mass, or cavitation on chest imaging 2
<
MAINRITSAN3 trial. It examined the
Granuloma, extravascu'ar granulomatous inflammation,or giantcells on biopsy »2 efficacy of extended maintenance
rituximab in patients with ANCA-
Inflammation,consolidation, or effusion of nasal/paranasal sinuses, or mastoiditis on imaging A associated Vasculitides
Pauci- immune glomerulonephritis on biopsy »1
- - -
p ANCA or anti MPO positive 1
•
Blood eosinophil comt >1x10 l

‘Diagnosed if a5
/
* • 4
.
American College of Rheumatology 2022

• pathogenesis depends on genetic susceptibility and environmental triggers ( e.g. infection )
• dysregulated immune response due to loss of B and T cell tolerance
• acute vascular injury mediated by neutrophils and monocytes
• systemic
malaise, fever, weakness, weight loss
• head, eyes, ears, nose, and throat ( HHENT )
• sinusitis or rhinitis, nasal crusting and bloody nasal discharge, nasoseptal perforation, saddle
nose deformity
• proptosis due to: inflammation / vasculitis involving extraocular muscles, granulomatous
retrobulbar space-occupying lesions or direct extension of masses from the upper respiratory
tract
hearing loss due to involvement of cranial nerve ( CN ) VIII
• pulmonary
cough, hemoptysis, granulomatous upper respiratory tract masses, tracheal and bronchial
stenosis
• renal
hematuria, proteinuria, elevated Lr, glomerulonephritis
• other
• -
joint, skin, eye complaints iritis, vasculitic neuropathy
Investigations
• blood work: anemia ( normal mean corpuscular volume ( MCV )), increased WBC, increased Lr,
increased CRP, elevated platelet count , ANCA ( HR 3 > MPO)
• urinalysis: proteinuria, hematuria, RBL casts
• CXR /CT: pneumonitis, lung nodules, infiltrations, cavitary lesions +
• biopsy for confirmation of disease: skin, renal (segmental necrotizing glomerulonephritis), lung
( vasculitis, necrosis)
• LRP may be used to monitor response to treatment in some patients
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Treatment
• severe, life or organ -threatening disease
• induction therapy: IV glucocorticoids + either IV or oral cyclophosphamide OR rituximab
- -
glucocorticoid : methylprednisolone 0.5 l .0 g/d IV xI 3 d followed by prednisone 1 mg / kg /d PO
x 2 - 4 wk and then gradual taper
• cyclophosphamide: 2 mg / kg /d ( max 200 mg /d ) PO for maximum of 3 6 mo OK 15 mg/ kg IV ( max
-
1200 mg ) every 2 wk for 3 doses, then every 3 wk for 3 6 doses (dose adjust for older age and renal
-
failure)
rituximab: 375 mg / m 2 x4 weekly infusions
» maintenance therapy: initiated once remission is achieved, consider corticosteroid -sparing agents
such as rituximab for maintenance, azathioprine, M I X , and mycophenolate are reasonable
alternatives
• plasma exchange can be an adjunct treatment for patients with severe organ involvement ( renal
failure, pulmonary hemorrhage) not responding to conventional induction treatment
• non -organ - threatening disease
prednisone 0.5-1 mg/ kg/d PO and MTX 15-25 mg PO/SC weekly OR azathioprine 2 mg/ kg/d
• screening and prophylaxis
all patients should receive screening and prophylaxis for corticosteroid-induced osteoporosis,
PUD prevention, and Pneumocystis jirowci prophylaxis (trimethoprim /sulfamethoxazole 160/800
mg PO 3x /wk )
Medium Vessel Vasculitis

POLYARTERITIS NODOSA
Definition
• systemic, necrotizing vasculitis of medium -sized vessels, defined as visceral arteries and their
branches
- - -
• ANCA negative, classically lung sparing
• 5 10% associated with hepatitis B positivity
• incidence: 0.7 in 100000; affects individuals between 40 60 yr; M:l;» 2:l -
Table 23. Classification Criteria for PAN '
Criteria Description
1. Weight loss >4 kg.not due to dieting or other factors
2. Myalgias, weakness, or leg tenderness Oilfuse myalgias or muscle weakness
3. livedo reticularis Mottled, reticular pattern over skin
4. Neuropathy .
Mononeuropalhy mononeuropathy multiplex , or polyneuropathy
5. Testicular pain or tenderness Not due to infection, trauma, or other causes
6. dBP >90 mmHg Development of BIN with dBP »90 mmHg
7. Elevated Cr or BUN Cr >130 pmot / L (1.5 mg/dL), DUN >14.3 mmol/ L (40 mg/dL)
8. Hepatitis B positive Presence of hepatitis B surface antigen or Ab
9. Arteriographic abnormality Commonly aneurysms
10. Biopsy of artery Presence of granulocytes and /or mononuclear leukocytes in the artery wall
'Diagnosed if 3 or more of the above to criteria present
American College of Rheumatology, 1990

• focal pan - mural necrotizing vasculitis in small and medium -sized arteries
• thrombosis, aneurysm, or dilatation at lesion site may occur
• healed lesions show proliferation of fibrous tissue and endothelial cells that may lead to luminal
occlusion
• systemic: fatigue, weight loss, weakness, fever, arthralgias
• dermatologic: livedo reticularis, nodules, purpura , eruptions
• renal: renal insufficiency leading to HTN
• neurologic: mononeuropathy multiplex in both motor and sensory nerves
• abdominal: abdominal pain , mesenteric arteritis
Investigations n
• blood work: CBC, CRP, Cr, BUN, urinalysis, liver enzymes, p-ANCA , hepatitis B and C serology
LJ
• imaging: CT or MR1 angiography shows beading appearance of blood vessels seen

• biopsy of affected organ (e.g. skin, nerve); biopsy of highly vascular tissues (e.g. liver) not
recommended due to risk of aneurysm rupture
Treatment
+
• PAN with no major organ manifestations
glucocorticoids ± azathioprine
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• PAN with major organ manifestations (CNS, cardiac, GI, renal )

induction therapy with high -dose glucocorticoids + cyclophosphamide for 3-6 mo followed by
-
maintenance therapy with low dose prednisone and either azathioprinc, M I X , or leflunomide
treatment should be a minimum of 18 mo
• hepatitis B virus -associated vasculitis
prednisone 1 mg/ kg /d PO x 7 d ( then taper and withdraw by 14 d ) ± methylprednisolone 15 mg/
kg/d IV xl -3 d
after corticosteroid therapy, treat with plasma exchange + antiviral therapy
Large Vessel Vasculitis

GIANT CELL ARTERITIS/TEMPORAL ARTERITIS
s
Table 24. Classification Criteria for GCA *
Criteria Description GCA Criteria
Presence of 3 or more criteria yields
1. A9eatonsel >50 sensitivity of 94%, specificity of 9t%
2.New H/A Oflen temporal
3. Temporal artery abnormality Temporal artery lender ness or decreased pulsations, not due lo arteriosclerosis
4.Elevated ESN ESR >50 mm/ h
5. Abnormal arlery biopsy Mononuclear cell infiltration or granulomatous inflammation,usually with mullinudeated giant cells
'Diagnosed if 3 or more of the above S criteria present
.
American College ol Rheumatology 1990
Epidemiology
• most common vasculitis in North America
• patients > 50 yr; peak incidence 70 80 yr -
• F:M=2:1
• north -south gradient ( predominance in Northern Europe and US)
• affects extracranial arteries
• new onset temporal H /A ± scalp tenderness overlying temporal artery
• sudden, painless loss of vision and/or diplopia due to narrowing of the ophthalmic or posterior ciliary
arteries ( PCA more common ); can affect both eyes
• tongue and jaw claudication ( pain in muscles of mastication on prolonged chewing )
<§
Medical Emergency
If untreated. GCA can lead to permanent
• PMR ( proximal pain and stiffness, constitutional symptoms, elevated HSR ) occurs in 30% of patients
• aortic arch syndrome ( involvement of subclavian and brachial branches of aorta resulting in pulseless
-
blindness in 20 25% of patients
Treat on clinical suspicion
disease), aortic aneurysm ± rupture are late complications
• constitutional symptoms (e.g. fever of unknown origin in patients £ 65 yr) and shoulder/ pelvic girdle
pain and stiffness
Investigations
• diagnosis made by clinical suspicion, increased HSR, increased CRP, colour Doppler U /S of temporal ±
axillary arteries ( + halo sign ), MR1, consider temporal artery biopsy
Treatment
• if suspect GCA, immediately start high-dose prednisone 1 mg/ kg PO in divided doses for 2 4 wk, and
-
then taper prednisone by 10 mg per 1 2 wk as symptoms resolve; highly effective in treatment and
-
prevention of blindness and other vascular complications
• consider low-dose ASA to help decrease visual loss
• if presenting with vision loss at diagnosis, methylprednisolone 1000 mg /d IV for 3 d followed by high -
dose prednisone 1 mg / kg /d PO in divided doses for 4 wk
-
• tocilizumab, an 1L 6 receptor monoclonal antibody, has also been used in combination with
glucocorticoids to treat GCA ( new or relapsing )
Prognosis
• increased risk of thoracic aortic aneurysm and aortic dissection
• yearly CXR ± abdominal U /S as screening
c:
+
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R H 23 Rheumatology Toronto Notes 2023
Seronegative Rheumatic Disease

Table 25 . A Comparison of the Spondyloarthropathies
Feature AS PsA ReA EA
M:F 3:1 1:1 8:1 1:1
AgeolOnset 20 s 35 45 20s Any
Peripheral Arthritis 25% 96% 90% Common
Distribution Axial, large joints Any If If
Sacroiliitis 100% 40% 80% 20%
Dactylitis Uncommon Common Occasional Uncommon
Enthesitis Common Common Common Less Common Figure 10. Spondyloarthropathy
subsets
Skin Lesions Rare 100 % Occasional Occasional
Eventually psoriasis. Keratoderma Pyoderma, erythema
70% al onset ol arthritis blcnnorihaqicd nodosum
Uveitis Common Occasional 20% Rare
Urethritis Rare Uncommon Common Rare AS shares some features with the
HLA 827 90 95% 40% 80% 30% other three types of seronegative
spondyloarthropathies such as feA. EA.
'LE = lower extremities
.
PsA and U-sPA
Ankylosing Spondylitis
Definition
• chronic Inflammatory arthritis involving the sacroiliac joints and vertebrae
• enthesitis is a major feature (e.g. Achilles tendinitis, plantar fasciitis )
• prototypical spondyloarthropathy Consider AS in the differential for causes
of aortic regurgitation
Table 26 . ASAS Classification Criteria for Axial Spondyloarthritis*
.
1 Back pain of any type for at least 3 mo and age of onset < 45 yr
.
2 Sacroiliitis on imaging plus >1 AS feature or HLA - B27 positive plus >2 AS features
AS Features Sacroiliitis on Imaging Rule of 2s
AS occurs in
HLA - B 27 positive Active ( acute) inflammation on MRI highly suggestive of sacroiliitis associated wilh AS
0.2% of the general population
Inflammatory back pain OR -
2% of HLA B27 positive individuals
20% of HLA B27 positive individuals with
Arthritis Oclinite radiographic sacroiliitis ( grade 2 bilaterally or grade 3 - 4 unilaterally
affected family member
Enthesitis (heel )
Uveitis
Dactylitis
Psoriasis
Crohn'sdisease /colitis
Good response toNSAIDs
EMHx ofSpA
Elevated CRP
'SpondylorUnapjIhy: inflammatory joint disease ol the vertebral column

> osteopenia > erosion -) ossification > osteoproliferation (syndesmophytes)
• inflammation
Epidemiology
I
• Spondylitis
• M:T =3:1; females have milder disease ( may be under- diagnosed ), more peripheral arthritis, and upper
• Hip
spine spondylitis • Shoulder
- -
• 90 95% of patients are HI.A B27 positive (9% of the general population is HLA B27 positive ) - Figure 11. Common sites of
involvement of AS
The Bath Ankylosing Spondylitis r t

Disease Activity Index (BASDAI) LJ
Self-reported scoring system that
focuses on fatigue, axial pain, peripheral
.
pain, enthesitis and morning stiffness
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Table 27. Types of Back Pain NORMAL POSTURE

Parameter Mechanical Inflammatory Cervical lordosis
Past History
Family History
Onset
Age
t
Acute
-
15 90 yr
Insidious
<45 yr
! Thoracic kyphosis
Lumbar lordosis
Sacral kyphosis
ANKYLOSING SPONDYLITIS
Sleep Disturbance t ++ (worse during 2nd half of night)
Morning Stiffness <30 min >1 h Increased occiput
to wall distance
Involvement of Other Systems
Increased cervical
Exercise Worse 8elter flexion
Rest Better Worse Increased
NSAIO Responsiveness - thoracic kyphosis
Radiation of Pain Anatomic (L5 - S1) Olfluse ( thoracic, buttock) Decreased lumbar
Sensory Symptoms lordosis
Motor Symptoms ® Cassandra Collin
Clinical Presentation .
Figure 12 AS postural change
• axial
mid and lower back stiffness, morning stiffness > 1 h, night pain , alternating buttock pain, painful
SI joint ( + l-ABER test )
spinal restriction (decreased ROM ): lumbar (decreased Schbber), thoracic (decreased chest wall
expansion, normal >5 cm at T4), cervical ( global decrease, often extension first ) .
FABER ( Flexion , ABduction and
postural changes: decreased lumbar lordosis + increased thoracic kyphosis + increased cervical External Rotation ) Test
flexion = increased occiput to wall distance (> 5 cm) fessively flex, abduct, then gently
• peripheral externally rotate the leg. If pain is
asymmetrical large joint arthritis, most often involving lower limb elicited during this movement, the
location of the pain may help determine
• enthesitis: tenderness over tibial tuberosity, or Achilles tendon and plantar fascia insertions into the location of the patient's pathology
the calcaneus .. . .
(e g hip joint SI joint) However, it is
• dactylitis: toes or fingers poorly reproducible and inaccurate in
• extra - articular manifestations .
discerning inflammatory vs mechanical
•
• renal: amyloidosis ( late and rare), IgA nephropathy
-
ophthalmic: acute anterior uveitis is common ( 25 30% patients ) back pain
• gastrointestinal : IBD
• cardiac: aortitis, aortic regurgitation, pericarditis, conduction disturbances, heart failure ( rare ) ft
respiratory: apical fibrosis ( rare)
neurologic: cauda equina syndrome (rare) Modified Schober Test
• Patient must be standing erect with
• skin: psoriasis normal posture
• Mark an imaginary horizontal line
Investigations connecting both posterior superior
• x- ray of SI joint: “ pseudowidening" of joint due to erosion with joint sclerosis -> bony fusion ( late ), iliac spines (close to the dimples of
symmetric sacroiliitis Venus)
-
• x ray of spine: “squaring of edges” from erosion and sclerosis on corners of vertebral bodies ( shiny • A mark is placed 10 cm above this
horizontal line, and another 5 cm
corner sign ) leading to ossification of outer fibres of annulus fibrosis ( bridging syndesmophytes) -> below
“ bamboo spine” radiographically • The patient bends forward
• MRI of spine: assess activity in early disease; detection of cartilage changes, bone marrow edema, maximally: measure the difference
bone erosions, and subchondral bone changes. Best seen on T 2 short tau inversion recovery (STIR )
images (suppress fat and see bone edema )
.
• labs: CBC, elevated ESR /CRP, ALP, Ca 2 * serum protein electrophoresis (SPEP ), BMD, HLA B27 -
- between these two points
Report the Increase (in cm to the
nearest 0.1 cm)
• The better of two tries is recorded
Treatment
• non - pharmacological therapy
prevent fusion from poor posture and disability through: exercise (e.g. swimming), postural and
deep breathing exercises, outpatient PT, and smoking cessation
• pharmacological therapy
-
Extra Articular Manifestations of AS
» NSAlDs (first line of treatment for peripheral and axial disease) 5 As
glucocorticoids (topical eye drops, local injections, occasionally require systemic steroids prior to Anterior uveitis
other effective Rx) Apical lung fibrosis
Aortic incompetence
DMARDs only for peripheral arthritis (SSZ, M I X ) Amyloidosis ( kidneys)
if inadequate response to two NSAlDs (or DMARD for peripheral arthritis only), consider anti- Autoimmune bowel disease ( ulcerative
- -
TNF agents or anti IL 17 for axial and peripheral involvement colitis)
-
• manage extra articular manifestations -
t J
• surgical therapy
• hip replacement and vertebral osteotomy for marked deformity ( latter rarely performed )
Prognosis
• spontaneous remissions and relapses are common and can occur at any age
+
• function may be excellent despite spinal deformity
• favourable prognosis if female and age of onset > 40 yr
• early onset with hip disease may lead to severehttps://medical-amboss.com
disability; may require arthroplasty
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Enteropathic Arthritis
Definition
• see Gastroenterology. Inflammatory Bowel Disease G 22 ,
• MSK manifestations in the setting of either ulcerative colitis ( UC ) or Crohn's disease (CD ) include Both AS and BA feature symmetric
peripheral arthritis ( large joint, asymmetrical ), spondylitis , and hypertrophic osteoarthropathy sacroiliitis
• non - arthritic MSK manifestations can occur secondary to steroid treatment of bowel inflammation
(arthralgia, myalgia, osteoporosis, AVN )
Table 28. Comparing Features of Spondylitis vs. Peripheral Arthritis in EA

Parameter Spondylitis Peripheral Arthritis
HLA- B27 Association Yes No
Gender M *F M- F
Onset Before IBD Yes No
Parallels I8 D Course No Yes
Type of IBD UC'CO CD
Treatment NSAIDs (use cautiously, may exacerbate bowel .
NSAIDs DMARDs: INF inhibitors if resistant
disease): TNF inhibitors if resistant
Psoriatic Arthritis
Definition
• arthritic inflammation associated with psoriasis

Check “ hidden" areas (or psoriatic
• unclear but many genetic, immunologic, and some environmental factors involved (e.g. bacterial, lesions (eats, hairline, umbilicus, gluteal
viral, and trauma) cleft nails)
TNF inhibitors are effective treatments
Epidemiology for PsA with no important added risks
• psoriasis affects 1% of the population -
associated with their short term use
• arthropathy in 15% of patients with psoriasis
-
• 15 20% of patients will develop joint disease before skin lesions appear
• dermatologic
• psoriasis: well - demarcated erythematous plaques with silvery scale
• psoriatic nail changes ( potential predictor for PsA ): pitting, transverse or longitudinal ridging,
discolouration , subungual hyperkeratosis, onycholysis, and oil drops
• musculoskeletal
• 5 general patterns
•
asymmetric oligoarthritis (< 5 small and /or large joints affected in asymmetric distribution;
-
most common 70%)
•
arthritis of DIPs with nail changes
* symmetric polyarthritis (similar to RA )
sacroiliitis and spondylitis (usually older , male patients)
» arthritis mutilans (destructive and deforming small joint polyarthritis)
• other findings: dactylitis, enthesopathy, morning stiffness >30 min ( 50% )
• ophthalmic
conjunctivitis, iritis ( anterior uveitis)
• cardiac and respiratory ( late findings)
aortic insufficiency
• apical lung fibrosis
• neurologic
• cauda equina syndrome
• radiologic
floating syndesmophytes
pencil-in - cup appearance at IPs
osteolysis, periostitis r ->
LJ
Treatment
• treat skin lesions (e.g. steroid cream , salicylic and /or retinoic acid, tar, UV light )
• NSAIDs and /or 1A steroids (as an adjuvant), benefit should be seen within a few wk, should not be the
sole therapy >3 mo
• DMARDs to minimize erosive disease (use earlv in peripheral joint involvement)
+
non -biologic DMARDs ( MTX, SSZ, or leflunomide )
-
biologic therapies include anti-TNl' agents, anti-lL-17 (secukinumab), and anti- lL-12/23
( ustekinumab) https://medical-amboss.com
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RH 26 Rheumatology Toronto Notes 202.
'
Table 29. CASPAR Criteria for PsA*
Criterion Description
.
1 Evidence of psoriasis Current, past, or lamily history
.
2 Psoriatic nail dystrophy Onycholysis, pitting, hypetheralosis
3. Negative results for RE Preferably by ELISA, ncphclometry
.
4 Dactylitis Current or past history
5. Radiological evidence Juxta -articular bone formation on hand or foot x -rays
" To meet the CASPAR (ClASsrfication criteria for Psoriatic ARthritis) criteria, a patient must have inflammatory articular disease (joint, spine, or
en theseal) with > 3 poi nts from the above 5 categorries.
-
Arthritis Rheum 2006 Aug54(8): 2665 2673. Classification criterialor PsA development
Reactive Arthritis
Definition
• one of the seronegative spondyloarthropathies in which patients have a peripheral arthritis ( >1 mo
Clinical Triad of Reactive Arthritis
duration ) accompanied by one or more extra -articular manifestations that appears shortly after
certain infections of the Cil or (ill tract • Arthritis
• Conjunctivitis/uveitis
• this term should not be confused with rheumatic fever or viral arthritidcs • Urethritis/cervicitis
Etiology
• onset following an infectious episode either involving the G1 or CiU tract
• Gl: Shigella, Salmonella , Campylobacter, Yersinia, C . difficile species
GU: Chlamydia ( isolated in 16-44% of ReA cases), Mycoplasma species
• acute clinical course “Can't See, Can’t Pee, Can't Climb a
• onset 1-4 wk post - infection Tree”
• lasts wk to mo T riad of conjunctivitis, urethritis, and
• often recurring arthritis is 99% specific (but 51%
sensitive) for ReA
• spinal involvement persists
Epidemiology
• in HLA-B27 patients, axial > peripheral involvement
• M >1 -
• musculoskeletal
• asymmetric peripheral arthritis, spondylitis/ sacroiliitis, enthesitis ( Achilles tendinitis , plantar
fasciitis), dactylitis
• ophthalmic
iritis (anterior uveitis), conjunctivitis
• dermatologic
keratoderma blennorrhagicum ( hvperkeratotic skin lesions on palms and soles) and balanitis
drdnata (small , shallow, painless ulcers of glans penis and urethral meatus) are diagnostic
• oral ulcers, diarrhea
• genitourinary
• urethritis, prostatitis, cervicitis, cystitis, sterile pyuria; presence not related to site of initiating
infection
Investigations
• diagnosis is clinical plus laboratory
• evidence of antecedent or concomitant infection ( stool culture, urine , and genital swab testing )
• blood work : norntocytic , normochromic anemia , and leukocytosis
• sterile cultures
• serology: HLA - B 27 positive , elevated ESR /CRP
Treatment
• antibiotics for non -articular infections
• NSAIDs ( naproxen 500 mg BID/ TID, diclofenac 50 mg HD, indomethadn 50 mgTTD/ QlD), PT,
exercise
• local therapy rt
IA steroid injection ( triamcinolone acetonide) LJ
• topical steroid for ocular involvement
• systemic therapy
corticosteroids (starting dose 20 mg /d )
DMARDs (for refractory reactive arthritis with peripheral joint involvement only ) (SSZ , MT' X )
TNP - ct inhibitors for spinal inflammation ( for disease refractory to NSAIDs, DMARDs )
+
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Prognosis
- -
• self limited, typically 3 5 mo, varies based on pathogen and patient's genetic background
-
• chronic in 15 20% of cases
Crystal-Induced Arthropathies
Table 30. Gout vs. Pseudogout
Parameter Gout Pseudogout
Gender M »F M- f
Age Middle - aged males Usually elderly
Post menopausal females
Onset of Disease Acule Acute
Can become chronic if high uric acid untreated, Chondrocalcinosis is asymptomatic but the S
people with renal failure, kidney transplant clinical feature is generally acute 2
Crystal Type Monosodium urate CPPD %
Negative birefringence (yellow when parallel
to compensator filter ), needle - shaped
Positive birefringence (bluewhen parallel),
rhomboid - shaped 1
S
Distribution First MIP classically:also midfoot, ankle, Knee, wrist: monoarticular, or polyarticular • 1st MTP - podagra 3
knee, or polyarticular il chronic • Ankle -
Radiology ( notefindings are nonspecific) Erosions Chondrocalcinosis • Knee
OA (knee, wrist,2nd and 3rd MCP)
Figure 13. Common sites of
Treatment Acute: NSAIOs.corticosteroids, colchicine NSAIDs, corticosteroids
involvement of gout (asymmetric
.
Chronic: tallopurinol febuxostat
joint involvement)
Gout
Definition
• derangement in purine metabolism resulting in hyperuricemia; monosodium urate crystal deposits in
tissues (tophi ) and synovium ( microtophi )
An acute gout attack may mimic
Etiology and Pathophysiology cellulitis; however, joint mobility is
• uric acid can be obtained from the diet or made endogenously by xanthine oxidase, which converts usually preserved in cellulitis unless it
overlaps a joint
xanthine to uric acid
• an excess of uric acid results in hyperuricemia
• uric acid can deposit in the skin /subcutaneous tissues ( tophi ), synovium ( microtophi), and kidney,
where it can crystalize to form monosodium urate crystals that lead to gout
Precipitants of Gout
• non - modifiable risk factors include: genetic mutations, male gender, and advanced age
• modifiable risk factors include: diet (alcohol, purine rich foods such as meats and seafoods, fructose/ Drugs are FACT
sugar sweetened foods; see list of precipitants below ) Furosemide
• other risk factors: renal failure, metabolic syndrome, dehydration (e.g. diuretics) Aspirin 1 (low-dose)/Alcohol
Cyclosporine
Thiazide diuretics
• single episode progressing to recurrent episodes of acute inflammatory arthritis Foods are SALT
• acute gouty arthritis Seafood
severe pain , erythema , joint swelling, usually involving lower extremities Alcohol ( beer and spirits)
Liver and kidney
• joint mobility may he limited
-
• attack will subside spontaneously within d to wk ( 5 10 d ); may recur
• tophi
Turkey ( meat )
• urate deposits on cartilage, tendons, bursae, soft tissues, and synovial membranes
• common sites: first MTP, ear helix, olecranon bursae, tendon insertions (common in Achilles 2020 American College ol Rheumatology
tendon ) Guideline for the Managementol Goul
• kidney Arthritis Rheumatol 2020:72:879-95
• gouty nephropathy • Inflate urate awering therapy (IW) lor patents
» uric acid nephrolithiasis viitli :
• >1SC tophi
• Radiographic damage attributable to gout
Investigations • Freguentgoutflares (»2/yr)
• joint aspirate: >90% of joint aspirates show crystals of monosodium urate ( negatively birefringent, • Allopurino! is preferred over at other ULTsas a first -
needle-shaped ) if done early in course of presentation line agent for all patients Rnctjdi -g CKO stage » 3|
• x- rays may show tophi as soft tissue swelling, bone/ joints - punched -out lesions, erosion with “over - • Initiate concomitant anti-indamnratory prophylaxis
hanging" edge . .
(e.g.colchicine NSAIDs predn sore prednisolone)
lor 3 - 6 mo
-
• U /S shows double contour sign -
• Conl .nue 01! to target and maintain strum urate
• correlated with hyperuricemia in the blood 0 mgfdl j
• In patients with frequent gout Daiesor
Treatment nomesolvingSC tophi who have failed loach eve
• acute gout .
serum urate < 0 mgfdl on uticosutlcs ualhine
oxidase inhibitors, and other interventions,
• NSAIDs: high - dose, then taper as symptoms improve
• corticosteroids: 1 A, oral, or IM ( if renal, cardiovascular, or (il disease and /or if NSAIDs
peglotitase should be initiated and the current ULI
should be discontinued +
contraindicated or failed ). IV for patients with multiple joints flaring, unable to take oral • tout flares should he managedwith NSAIOs.
medication, and already have IV line low - dose colchicine, nr glucocorticoids as trst -lloe
colchicine 1.2 mg at the first signs of an attack followed by 0.6 mg 1 h later and 0.6 mg BID on agents
subsequent days until the attack has resolved
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• chronic gout
• conservative
avoid foods with high purine content (e.g. visceral meats, sardines, shellfish , beans, peas)
avoid drugs with hyperuricemic effects (e.g. pyrazinamide, ethambutol, thiazide, alcohol )
additional management of lifestyle factors: limiting alcohol intake, limiting high -fructose
corn syrup, for overweight/obese patients weight loss is recommended ( regardless of activity
level)
medical
antihyperuricemic drugs (first line: allopurinol (not nephrotoxic) second line: febuxostat ):
decrease uric acid production by inhibiting xanthine oxidase. Start low and titrate up. Do not
use febuxostat if history of cardiovascular disease
uricosuric drugs ( probenecid, sulfinpyrazone ): very rarely used in combination with
allopurinol or febuxostat in patients in whom hyperuricemia is not controlled with the latter
- -
• prophylaxis with low dose NSAlD/colchicine should be started with urate lowering therapy
-
• in renal disease secondary to hyperuricemia , use low dose allopurinol nnd monitor Cr
• indications for treatment with antihyperuricemic medications include
• attacks (>2/yr), tophi, bone erosions/arthritis
Pseudogout (Calcium Pyrophosphate Dihydrate Disease)
Definition
• joint inflammation caused by calcium pyrophosphate (CCP) crystal deposition in connective tissue
• acute inflammatory arthritis due to phagocytosis of IgG -coated CPPD crystals by neutrophils and
subsequent release of inflammatory mediators within joint space
• usually monoarticular but can be polyarticular
- -
• slower onset in comparison to gout, lasts up to 2 3 wk but is self limited
Risk Factors
• old age, advanced OA , neuropathic joints -
• other associated conditions: hyperparathyroidism , hypothyroidism , hypomagnesemia , • Polyarticular wrist r;
hypophosphatasia ( low ALP), DM , hemochromatosis • Hand (MCPI
• Foot (1st MTPI
• Hip
I
• affects knees, wrists, MCPs, hips, shoulders; less likely elbows, ankles, big toe, spine Figure 14. Common sites of
• asymptomatic crystal deposition (seen on radiograph only ) involvement of CPPD
• acute crystal arthritis (self-limited flares of acute inflammatory arthritis resembling gout )
• pseudo- OA ( progressive joint degeneration, sometimes with episodes of acute inflammatory arthritis)
• pseudo-RA ( symmetrical polyarticular pattern with morning stiffness and constitutional symptoms)
• frequently triggered by dehydration, acute illness, surgery, trauma EULAR Rccornmendations for the Management
of CPPD
Investigations Ann RheumOis 2011;10:511 5 -
• must aspirate joint to rule out septic arthritis and gout -
1. Pharmacological and non pharmacologicai
treatment mould troth be used to manage CPP0.
• CPPD crystals: present in 60% of patients, often only a few crystals, positive birefringence ( blue ) and .
2 treating acute CPP crystal arthritis with ice or cool
rhomboid shaped .
packs, rest , jointaspmation and Uiojecbon of
-
• x rays show chondrocaldnosis in 75%: radiodensities in fibrocartilaginous structures (e.g. knee -
long acting glucocoitrcoids ( CC$) may be sufficient
for many patients.
menisci ) or linear radiodensities in hyaline articular cartilage
.
3 Acute CPP crystal arthritis can be treated
systemically with HSAIDs and low-dose oral
Treatment colchicine , although their use may be Imited in
• acute CPP: joint aspiration, steroid injection, cool packs, temporary rest, and protection older patients by tonicity and comorbidity.
• chronic CPP: NSAlDs with gastroprotection and /or low-dose prophylactic colchicine 0.6 -1.2 mg /d PO 4.A brief tapering course of oral or parenteral CCS
(controversial ) or MTU may be effective for acute CPP crystal
arthritis that is not amenable to IA 6CS injection.
5. Low -dose oral colchicine ixNSAIO can be used as
prophylaxis against frequent recurrent acute CPP
Non-Articular Rheumatism crystal arthritis.
.
6. For patients with OA and CPPD management goals
and options are the same as those for 0A alone.
Definition 7. Ibe order of pharmacological preference (or
• disorders that primarily affect soft tissues or periarticular structures chronic CPP ciyslal inflammatory art hubs is USAID
• includes bursitis, tendinitis, tenosynovitis, fibromyalgia, and PMR - .
andlor colchicine, low dose corticosteroid MIX
and hydroxychloroquine .
I. Associated conditions should be treated d
Polymyalgia Rheumatica detected.
9. Ihere are no disease- modrfyieg treatments lor CTP
crystal arthritisand no treatment is MruMfor
Definition asymptomatic cboodrocaldnosis.
• characterized by pain and stiffness of the proximal extremities (girdle area)
• closely related to GCA (15% of patients with PMR develop GCA )
• no muscle weakness +
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Table 31. PMR Classification Criteria Scoring Algorithm *

.
Required criteria: age > 50 yr bilateral shoulder aching, and abnormal ESR.CHP
Points without U/ S (0 - 6) Points with Abnorma I
U/S" ( 0- 8)
Morning stillness duration '45 min 2 2
Hip pain or limited ROM 1 1
Absence of RForACPA 2 2
Absence ol other joint involvement 1 1
At least one shoulder with subdeltoid and/ or biceps tenosynovitis and / or N:A 1
glenohumeral synovitis (either posterior or axillary) and at least one hip with
synovitis and/or trochanteric bursitis on U/S
Both shoulders with subdeltoid bursitis,biceps tenosynovitis, or gleno- M/ A 1
humeral synovitison U/S
'A score oi 4 or more is categorized as PMR in the algorithm without U/ S and a score ot 5 or more is categorized as PMR in the algorithm with U/S
"Optional U/S criteria
-
Ann Rlieum Ols 2012:71:484 492
Epidemiology
• incidence: 50 in 100000 per yr in those > 50 yr
• age of onset typically > 50 yr , T: M = 2: I
• constitutional symptoms prominent ( fever, weight loss, malaise)
• pain and stilTness of symmetrical proximal muscles ( neck, shoulder and hip girdles, thighs )
• gel phenomenon (stiffness after prolonged inactivity)
• physical exam reveals tender muscles, but no true weakness or atrophy
Investigations
• blood work: often shows anemia of chronic disease, elevated platelets, elevated HSR and CRP, and
normal CK; up to 5% of PMR reported with normal inflammatory markers
Treatment
• goal of therapy: symptom relief
• start with prednisone 12.5- 25 mg PO once daily, reconsider diagnosis if no response within several
days
• taper slowly with improvement over 1 yr period with close monitoring, if in remission taper until
discontinued
• relapses should be diagnosed and treated on clinical basis; do not treat a rise in HSR as a relapse
• treat relapses aggressively ( 50% relapse rate )
• monitor for steroid side effects, glucocorticoid- induced osteoporosis prevention, and follow for
symptoms of GC /\
Fibromyalgia
Definition
• chronic (>3 mo ), widespread (axial , left - and right -sided , upper and lower segment ), non -articular
pain with characteristic tender points
Diagnosis
Table 32. 2010 ACR Preliminary Diagnostic Criteria for Fibromyalgia

Criteria Comments
Y/idespread Pam Index - number ol areas in which the palienl had pain
A paticnl satisfies diagnostic critena lor fibromyalgia II the following 3
over the last wk (max score 19): conditions are met:
. . . .
L and R: shoulder girdle, upper arm lower arm hip upper leg lower
.
leg jaw
1. Widespread Pain Index (WPI) >7 and SS score >5 or WPI 3 6 and
SS score >9
One Area: chest, abdomen, upper back , lower back, neck .
2 Symptoms have been present at a similar level lor at least 3 mo
Symptom Severity (SS) Score * sum of: 3. Ihe patient does not have a disorder that would otherwise explain
a) severity of fatigue the pain
b) waking unrefreshed
c) cognitive symptoms over the past wk
.
d) extent ol somatic symptoms (IBS, N/ A abdominal pain/cramps,
dry mouth, fever,hives, ringing in ears, vomiting,heartburn, dry ri
. . .
eyes SOB loss of appetite, rash, hair loss, easy bruising, etc ) LJ
. .
All (a d) rated on 0 3 scale: 0 * no problem 1 * mild 2 •moderate
3 > severe
.
-
Arthrit Care amt Res 2010:62(5):600 610
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.Epidemiology
I-:M=3: 1
'
• primarily ages 25-45, some adolescents

• prevalence of 2-5% in general population
• overlaps with chronic fatigue syndrome and myofascial pain syndrome
• strong association with psychiatric illness
• widespread aching, stiffness
• easy fatigability
• sleep disturbance: non - restorative sleep, difficulty falling asleep, and frequent wakening
• symptoms aggravated by physical activity, poor sleep, emotional stress
• patient feels that joints are diffusely swollen although joint examination is normal
• neurologic symptoms of hyperalgesia, paresthesias, allodynia
• associated with irritable bowel or bladder syndrome, migraines, tension H /As, restless leg syndrome,
obesity, depression, and anxiety
• physical exam should reveal only tenderness with palpation of soft tissues, with no specificity for
trigger / tender points
Investigations
• blood work: includes TSH; all typically normal unless unrelated , underlying illness present
-
• serology: do not order ANA or Rl unless there is clinical suspicion for a CTD or inflammatory
arthritis
• laboratory sleep assessment
Treatment
• non - pharmacological therapy
graded exercise programs including aerobic ( >2() min /d, 2 -3 d / wk ) and resistance training ( >8
repetitions per exercise, 2-3 d/ wk )
other therapies with some evidence: acupuncture, CBT, hydrotherapy, meditative movement
(yoga, Tai chi )
there is no evidence for biofeedback , chiropractics, hypnotherapy, meditation
• pharmacological therapy ( to help with symptoms, not curative)
low dose tricyclic antidepressant (e.g. amitriptyline )
-
for sleep restoration
select those with lower anticholinergic side effects
SNR1: duloxetine, milnacipran
.
anticonvulsant: pregabalin gabapentin
analgesics may he beneficial for pain that interferes with sleep ( NSAIDs, not narcotics )
Prognosis
• variable; usually chronic, waxes and wanes, svith some pain and fatigue that usually persists
Table 33. Clinical Features of Inflammatory Myopathy vs. Polymyalgia Rheumatica vs.
Fibromyalgia
Polymyositis PMR Fibromyalgia
Epidemiology -
F> M. 40 50 yr .
F> M >50 yr -
F»M , 25 45 yr
Muscle Involvement Proximal muscle Proximal muscle Diffuse
Weakness Yes No No
Pain Painless Painful Painful
Stiffness Present Significant morning and gelling May have morning stiffness
stiffness (shoulders, neck , hips)
Investigations . .
Muscle biopsy CK , EMC ruleout
malignancy
.
ISR /CRP rule out CCA .
Sleep assessment ISH
ESRCRP Usually normal Markedly elevated Normal

Treatment -
High dose steroids,
immunosuppressants
-
Low dose steroids Exercise, sleep restoration
n
LJ
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RH3I Rheumatology Toronto Notes 2023
Common Medications
Table 34 . Common Medications for Osteoarthritis
Class Generic Drug Trade Name Dosing ( PO ) Indications Contraindications Adverse
Name Effects
Analgesics acetaminophen Tylenol: 1000 mg 110 q4 h 1st line Severe liver disease / Hepatoloiicity .
(3 g daily mail impairment overdose .
potentiates
warfarin
NSAIDs ibuprofen Advil -
200 - 600 mg TID 2nd line Gl bleed, renal Nausea, tinnitus,
diclofenac Voltaren -
25 SOmg TID impairment, allergy vertigo, rash,
diclofenac /
misoprostol
Arlhrotec :
Naprosyn 1
50 - 75/ 200 mg TI0
125- 500 mg BID
.
to ASA NSAIDs
pregnancy ( T3)
.
.
dyspepsia. Gl
bleed. PUD.
Aleve: 7.5-15 mg once anticoagulants hepatitis,
naproien
meloucam Mobicoi daily renal failure
.
HIN nephrotic
.
syndrome
COX -2 Inhibitors celecoiib Celebrex : 200 mg once daily Dyspepsia /GERD Renal impairment, SameasNSAIOs
cardiovascular above
.
disease Gl Bleed
Other Treatments Comments
Combination analgesics (acetaminophen codeine, -
Enhanced short term effect compared to acetaminophen alone
acetaminophen NSAIDs) .
More adverse effects: sedation constipation, nausea Gl upset .
IA corticosteroid injection Short - term ( wk -mo). joint specific treatment
Decrease in pain and improvement in function
Used for managcmenl of an IA inflammatory process when infection has been ruled out
IA hyaluronic acid q6 mo Used for mild-moderate OAof the knees; however, little supporting evidence and not
considered to be effective
Precaution with chicken/egg allergy
Topical NSAIDs .
Topical diclofenac (Pennsaid ' Voltaren Emulgcl ' )
May use for patients who fail acetaminophen treatment and who wish to avoid
systemic therapy, better on small joints
Capsaicin cream Mild decrease in pain
Glucosamine sulfate * chondroitin Limited evidence of benefitin 0A knee. No regulation by Health Canada
Table 35. DMARDs

Generic Drug Name Trade Name Dosing Contraindications Adverse Effects
COMMONLY USED
hydroxychloroquine
$
Plaqueml ' 400 mg P0 once daily
initially
Retinal disease GGPD
deficiency
. Gl symptoms, skin rash, macular
damage, neuromyopathy
200 - 400 mg POonce Requires annual ophthalmological
daily maintenance screening to monitor for retinopathy
(5 mg/ kg ideal body
weight per day to a
maximum of 400 mg/d)
sulfasalazine
S
Salaaopyrim
Arullidme ' ( US)
1000 mg P 0 BID - TID Sulfa /ASA allergy, kidney
.
disease GGP0 deficiency
.
Gl symptoms, rash, H /A leukopenia
methotrexate
S
Rheumatrex :
Folexj Mexate 3
7.5- 25 mg PO /SC Bone marrow .
Oral ulcers Gl symptoms, cirrhosis,
.
' weekly suppression, liver disease, myelosuppression pneumonitis,
significant lung disease
immunodeficiency,
. tubular necrosis
.
pregnancy EtOHuse
leflunomide Arava ’ 10 - 20 mg P 0 once daily Liver disease, lung disease . .
Alopecia Gl symptoms, liver
ss pregnancy dysfunction, interstitial pulmonary
fibrosis HIN.
NOT COMMONLY USED
cyclosporine Neoral ' 2.5 -3 mg /kg /d divided Kidney/liver disease, HTN. decreased renal function, hair
Si and given in 2 doses P 0 infection HIN . growth, tremors, bleeding
gold (injectable) Solganal 3 50 mg IM weekly after IBD.kidney/ liver disease Rash, mouth soreness /ulcets,
s Myochrysine ® gradual introduction proteinuria, marrow suppress! on
aialhiopiine Imuran ' 2 mg /kg /d P0 once Kidney/liver disease Rash, pancytopenia ( especially
S daily thiopurine . .
WBC t AS! ALT ), biliary stasis, *
.
S - methyItransferase ( TPMI) vomiting diarrhea r T
LJ
deficiency
Cytoxan ' Kidney/liver disease, Cardioloxicity, Gl symptoms,
cyclophosphamide
s '
1q /m /mo IV as per
protocol neutropenia hemorrhagic cystitis, nephrotoxicity,
bone marrow suppression,sterility,
bladder cancer +
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Table 35 . DMARDs
Generic Drug Name Trade Name Dosing Controindicotions Adverse Effects
NEWER DMARDs (Biologies)
etanercept Enbrel: 25 mg biweekly or 50 Fusion protein of INF receptor and Fc portion of IgG
sss mg weekly SC
infliximab
SSS
Remicade -
3 5 mg /kg IV q8 wk Chimeric mouse/human monoclonal anti INF
adalimumab Humira ' 40 mg SCq2 wk Monoclonal anti -INF

SSS
golimumab Simponi' 50 mg SC q1mo or 2 Monoclonal anti-INF
SSS mg/kg q8 wk
certolizumab Cimna '
400 mg SC q2 wk «3 PEGylated monoclonal anti INF-
SSS then 200 mg SC q 4 wk
apremilast Oterla Day 1:10 mg (AM ) P0, PDE4 inhibitor which reduces production of INFo
SSS titrate up to 30 mg BID
by day 6
abataccpt Orencia ' 500 -1000 mg IV Coslimulalion modulator of Icell activation
SSS infusion ql mo or 125
mgSCqlwk
rituximab Rituxan ' 1g x 2 IV infusions, 2 wk Causes 8 cell depletion, binds to CD 20
SSS apart q 6 mo
tocilizumab Actemra; 4 -8 mg /kg IV q4 wk or IL- 6 receptor antagonist

SSS 162 mg SCq1- 2 wk
tofacitmib Xcl|anr ' 5 mg 8ID Selective JAK 1/ 3 inhibitor and thus interferes with JAK - SIAT
S$ signaling pathway
upadacitinib Rinvoq: 15 mg once daily Selective JAK1 inhibitor and thus interferes with JAK -STAT signaling
ss pathway
secukmumab Coscnlyx 150 mg monthly Blocks IL-17 A
SSS
Landmark Rheumatology Trials

Trial Name Reference Clinical Trial Details
RHEUMATOID ARTHRITIS
COMET Lancet 2008:372:375 82 Title: Comparison of Methotrexate Monotherapy with a Combination of Methotrexate and Etanercept in Active. Early. Moderate to
Severe Rheumatoid Arthritis (COME!): A Randomised, Double Blind, Parallel Treatment Trial
Purpose: To compare the efficacy ol MIX monotherapy or MIX plus etaneiccpt for remission and radiographic non - progression in RA
patients.
Methods: 542 RA MTX-naive outpatients with moderale - to - severe disease for 3 - 24 mo were randomly assigned to MIX alone (titrated
from 7.5- 20 mgfwk) or MIX (same titration) plus etanercept 50 mg /wk.
. .
Results : Clinical remission was achieved in 50 % ol patients on combined treatment vs 28% taking MIX alone (difference 22.05%:
.
P'0.0001). 80% and 59%, respectively, achieved radiographic non- progression (difference 20.98%: P'0.0001). Both groups
experienced similar adverse events.
Discussiond yr of Ireatment with etanercept plus MIX can achieve clinical remission and radiographic non- progression in early severe
RA ,
ERA NEJM 2000:343:1586 - 93 Title: A Comparison of Etanercept and Methotiexate in Patients with Early Rheumatoid Arthritis
Purpose: To investigate the efficacy of etanercept in reducing disease activity and joint damage in patients with early and active RA.
Methods: 632 patients received either SC etanercept (10 or 25 mg /wk) twice weekly or oral MIX (19 mg/wk) for 12 mo. Clinical response
was defined by criteria of the American College ol Rheumatology .
Results: Patients on 25 mg etanercept improved quicker than those on MIX, with significantly mote improvements in disease activity
within 6 mo (P'0.05). During the first 6 and 12 mo, there vrere significantly greater increases in mean erosion scores in the MIX group
(P‘0.007). Fewer adverse events (P‘0.02) and infections ( P‘0.006) vrere seen in 25 mg etanercept.
.
Conclusion: In patients with early active RA etanercept more rapidly reduced symptoms and slowed joint damage as compared to MIX.
BeSt Arthritis Rheum Title: Clinical and Radiographic Outcomes ol Four Different Treatment Strategies in Patients with Early Rheumatoid Arthritis (the 8 eSl
2005:52:3381- 90 .
Study): A Randomized Controlled Trial
Purpose: To identify the optimal therapeutic strategy for preventing long term joint damage and functional decline in RA.
Methods: 508 patients were randomly assigned to 1 of 4 therapeutic strategies: (1) sequential disease - modifying antirheumatic
. . -
diug monotherapy ( 2) step up combination therapy (3) initial combination therapy with tapered high dose prednisone, or ( 4) initial
combination therapy with infliximab .
Results: At 3 mo. groups 3 and 4 showed significantly greater functional improvement (as defined by the Dutch version of the Health
.
Assessment Questionnaire (D - HA 0)) with mean scores of 0.6 as compared lo mean scores of 1.0 in groups 1 and 2 (P'0.001). At 1 yr .
mean D - HA0 scores in groups 3 and 4 were 0.5, as compared to 0.7 in groups 1and 2 (P‘0.009).
Conclusion: As compared to sequential monotherapy or step-up combination therapy, initial combination therapy with piednisone or ri
infliximab led lo earlier functional improvements and less radiographic damage in patients with early RA. LJ
Infliximab and MIX NEJM 2000:343:1594 - 602 Title: Infliximab and Methotrexate in the Treatment of Rheumatoid Arthritis. Anti- Tumor Necrosis Factor Trial in Rheumatoid Arthritis
with Concomitant Therapy Study Group
Purpose: lo assess infliximab for potential sustained benefits and effects on|Oint damage in RA.
Methods: 428 patients who had active RA despite MIX therapy were treated with IV infliximab (3 or 10 mg /kg every 4 or 8 wk plus oral
MIX for 54 wk) or placebo. +
.
Results: As compared lo MIX alone, infliximab plus MIX significantly reduced signs and symptoms of RA (clinical response 51.8 %
.
vs. 17.0%: P'0.001) Ihere was grealer evidence of joint damage on MIX alone but not on infliximab plus MIX (mean change in
radiographic score, 7.0 vs. 0.6. P'0.001).
Conclusion : Repeated doses of infliximab plus MTX in persistently active RA was clinically effective and slowed the progression of joint
damage .
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Irealment o> Active Rheumatoid Arch Intern Med Title : Treatment of Active Rheumatoid Arlhrilis with lellunomidc Compared with Placebo and Metholrcialc . leflunomide Rheumatoid
Arthritis with leflunomide 1999:159:2542 50 Arthritis Investigators Group
Compared with Placebo and Purpose: lo compare the safely and efficacy of leflunomide vs. MIX in patients with active RA .
Melhotr exale. Leflunomide Methods: 482 patients with active RA were randomly assigned to receive leflunomide (20 mg/d ). MIX ( 7.5 -15 mgi'wk ). or placebo.
Rheumatoid Arthritis Results: Clinical response and success rales on leflunomide |S 2% and 41% ) and MIX ( 46 % and 35 %) were significantly greater than
Investigators Group. Strand et those on placebo (26% and 19 %) (P' 0.001). On leflunomide. common adverse events included gastrointestinal complaints, shin rash,
al. 1999 and reversible alopecia.
Conclusion: In patients with active RA. leflunomide was associated with better clinical responses than placebo and had similar
efficacies as MIX.
PREMIER Arthritis Rheum . .
Title : Ihc PRiMIER Study: a Multic enter Randomiied Double Blind Clinical Trial of Combination Therapy with Adalimumab plus
2006:54:26 37 Melhotreiale versus Methotrexate Alone or Adalimumab Alone in Patients with Early. Aggiessive Rheumatoid Arthritis Who Had Not Had
Previous Methotrexate Treatment
Purpose: To compare the efficacy and safety of adalimumab plus MIX versus MIX alone or adalimumab alone in patients with early,
aggressive RA who were MTX- naive.
-
Methods: 799 patients with active disease 3 yr were randomly assigned lo adalimumab 40 mg SC every other wk plus oral MIX
adalimumab 40 mg SC every other wk, or oral MTXweekly.
.
Results: American College of Rheumatology 50 % improvement was achieved in significantly more patients on combination therapy
(62%) than MIX or adalimumab ( 46 % and 41%, respectively; both P'0.001). Patients on combination therapy had significantly less
radiographic progression (P'0.002 ) than those on cither monotherapy. 49 % of patients on combination therapy achieved remission at
2 yr.
Conclusion: Adalimumab plus MIX was significantly superior to either MlX or adalimumab alone in early , aggressive RA .
OSTEOARTHRITIS
Hyaluronan Ann Rheum Dis Title : Intra Articular Hyaluronan is without Clinical Ellecl in Knee Osteoarthritis: a Multicenlre , Randomised. Placebo Controlled.
2010:69:1097-1102 Double Blind Study of 337 Patients Followed for 1 Year
Purpose: To assess the long- term safety and efficacy of 5 hyaluronan 1A injections in knee osteoarthritis.
Methods: 337 patients with knee osteoarthritis and a lequesne algofunctional index score (LFI) »10 received IA hyaluronan product
( sodium hyaluronate; Hyalgan * ) or saline weekly for 5 wk .
Results: Treatment had no significant effed on time lo recurrence or baseline change in LFI or walking pain . There were also no
significant differences in paracetamol consumption, patients' global assessment, responder rales, or adverse events.
Conclusion: Hyaluronan injections were not clinically effective in patients with osteoarthritis of the knee with moderate- severe
disease (LFI >10).
SYSTEMIC LUPUS ERYTHEMATOSUS
8 e !imumab Lancet 2011:377:721 31 Title: Efficacy and Safely of 8elimumab in Patients with Active Systemic Lupus Erythematosus:a Randomised . Placebo - Conlroiled.
Phase 3 Trial
Purpose: To assess the efficacy and safely of belimumab in patients with active SLE .
Methods: 867 patients (aged >18 yr ) who were seropositive with scores of > 6 on SELENA SIEDAI were randomly assigned lo belimumab
1 mg / kg or 10 mglkg. or placebo plus standard of care ( based on disease manifestation and local guidelines ).
Results: Significantly higher SRI (SLE Responder Index ) rates occurred with belimumab 1 mg/kg (51%. OR 1.55; P'0.0129) and 10 mg/ kg
( 58% , 1.83; P 0.0006) than placebo ( 44%). There was a greater frequency of SELEHA - SLEDAI reduction by >4 points with belimumab 1
‘
.
mg/kg [ 53%, 1.51; P‘0.0189 ) and 10 mg / kg ( 58 % 1.71: P‘0.0024 ) than placebo (46%).
Conclusion: Belimumab may be the lirst targeted biologic that is specifically approved for SLE.
Mycophenolate Mofetil or NEJM 2005:353:2219 - 28 Title: Mycophenolate Mofetrl or IntravenousCydophosphamide for Lupus Nephritis
Intravenous Cyclophosphamide Purpose: To investigate if mycophenolate mofelil is effective for treating lupus nephritis.
for lupus Nephritis. Gimlet et Methods: 140 patients with active lupus nephritis were randomly assigned to oral mycophenolate moletil (1000 mgld increased to
.
at 2005 3000 mgfd) or monthly IV cyclophosphamide ( 0.5 g /m 2 increased to 1.0 g/m ),
'
Results: 22.5% of patients on mycophenolate mofelil and 5.8% of those on cyclophosphamide experienced complete remission
(absolute difference. 16.7%:95% Cl. 5.6 - 27.9%:P'0.005) , thus demonstrating that mycophenolate mofetil is more efficacious than
cyclophosphamide.
Conclusion: In active lupus nephritis, mycophenolate mofetil wasmorc effective than IVcyclophosphamide in inducing remission and
had a belter safely profile.
CONNECTIVE TISSUE DISORDERS
Aialhioprine or Methotrexate NEJM 2008:359:2790 - 803 Title: Arathioprine or Methotrexate Mainlenancefor ANCA - Associated Vasculitis
Maintenance for ANCA - Purpose: To compare malhioprine ( A 2 A ) and MIX lor safely and efficacy in Wegener 's granulomatosis and microscopic polyangiitis.
Associated Vasculitis. Pagnoux Methods: 159 patients who achieved remission with IV cydophosphamtde and corticosteroids were randomly assigned to receive oral
et al. 2008 AZA orMIXfor 12 mo.
Results: The rates of adverse events (requiring discontinuation of the study drug or causing death) were not significantly different
between groups. Event - free survival was also not significantly different between groups.
Conclusion: In patients wilh Wegener ' s granulomatosis and microscopic polyangiitis. AZA and MIX are similar alternatives lor
maintenance therapy after initial remission.
CYCLOPS Ann Intern Med Title: Pulse versus Daily Oral Cydophosphamidefor Induction of Remission in Antineutrophil Cytoplasmic Antibody- Associated
2009:150:670 80 Vasculitis: a Randomiied Trial
Purpose: Tocompare Ihc efficacy of pulse cyclophosphamide vs . daily oral cyclophosphamide for inducing remission in ANCA
associated vasculitis.
Methods: 149 patients with newly diagnosed generalized ANCA- assodated vasculitis with renal involvement received
cyclophosphamide 15 mg/kg every 2- 3 wk (pulse), or daily cyclophosphamide 2 mg/kg orally , plus prednisolone.
Results: Ihere was no significant difference in lime lo remission |P‘0.59 ) or percentage of patients who went into remission at 9 mo
.
( 88.1% in pulse vs. 87.7% in oral ) The oral group had higher cumulative cyclophosphamide doses |P' 0.001). Lower rates ol leukopenia
were seen in the pulse group (hazard ratio. 0.41; 95% Cl. 0.23 to 0.71).
Conclusion: In ANCA- associated vasculitis, pulse cyclophosphamide induced remission as effectively as the daily oral regimen, r ->
required less cumulative cyclophosphamide, and caused lewer cases of leukopenia. LJ
Cyclophosphamide vs. Placebo NEJM 2006:354:2655 66 Title : Cyclophosphamide versus Placeboin Scleroderma lung Disease
in Scleroderma Lung Disease. Purpose: Todetermine the efficacy of oral cyclophosphamide in patients with active alveolitis and scleroderma - related ILD.
Tashkin et al. 2006 Methods:158 patients with scleroderma , restrictive lung physiology, dyspnea, and evidence of inflammatory ILD received oral
cyclophosphamide|s 2 mg/kg/d ) or placebo for 1 yr.
Results: Ihe mean absolute difference in 12 mo adjusted FVC between cyclophosphamide and placebo was 2.53 % (95 % Cl. 0.28 lo +
4.79%), indicating great efficacy ol cyclophosphamide (P'0.03). The dillerence in FVC belwcen groups was sustained at 24 mo.
Conclusion: In patients with symptomatic scleroderma -related ILD. oral cyclophosphamide had significant clinical benefit.
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HEJM 2005;352:351- 361 Title: Etanercept plus Standard Therapy lor Wegener 's Granulomatosis
WGEI Purpose: to investigate the solely and etficocy of etanercept for remission maintenance In GPA
Methods: 180 patients with GPA were randomly assigned to receive either etanercept or placebo, in addition to standaid treatment
(glucocorticoids plus cyclophosphamide or MIX ).
Results: Ho significant differences were observed between the etanercept and control groups in the rates of stable periods of low -level
. .
disease activity|86.5% vs. 90.6”», p-0.32). sustained remission (69.7% vs. 75.3% P‘0.39) or the time necessary to reach those
outcomes. Oisease flares and adverse events were common in both groups but not significantly different.
Conclusion: Etanercept is not effective for remission maintenance in GPA.
IMPROVE JAMA 2010;304:2381- 88 Title: Mycophenolate Mofetil versus Acathiopnne for Remission Maintenance in Anti neutrophil Cytoplasmic Antibody -Associated
Vasculitis (AAV): a Randomized Controlled Trial
Purpose: To compare the efficacy of mycophenolate mofetil vs. arathioprine ( A 2 A ) preventing relapses in patients with AAV.
.
Methods: following remission induction with cyclophosphamide and prednisotone 156 patients with newly diagnosed AAV were
.
randomly assigned to A 2 A (initiated at 2 mg kg / d ) or mycophenolate mofetil (initialed at 2000 mg/d|
'
Results: The mycophenolate mofetil group experienced significantly more relapses ( 55%) as compared to A 2 A (37.5%) (hazard ratio
. .
for mycophenolate mofetil 1.69. 95% Cl 1.06-2.70; P 0.03). There was no significant difference in the rates of severe adverse events
-
between groups.
Conclusion: Mycophenolate moletil was less effective than A 2 A lor maintaining disease remission in AAV.
RAVE MEJM 2010:363:221- 32 Title: Rituximab versus Cyclophosphamide for ANCA -Associated Vasculitis
Purpose: To investigate if rituximab is more effective and/or safer than a cyclophosphamide for treating AAV.
Methods: 197 ANCA -positive patients randomly assigned to receive rituximab (375 mg /m1 for 4 wk) or cyclophosphamide (2 mg/kg /d) .
Results: 64% of Ihe rituximab group reached the primary endpoint (remission of disease without the use ol prednisone at 6 mo), as
. .
compared with 53% of controls (nonInferiority P< 0.001) Rituximab was more effective than cyclophosphamide for inducing remission
of relapsing disease; 67% vs. 42% reached the primary endpoint (P-0.01).
.
Conclusion: In severe AAV rituximab was noninferior to cyclophosphamide for remission induction and may be superior in relapsing
disease.
MAINRITSAN3 Ann Intern Med Title: long - term Rituximab Use to Maintain Remission ol Antmcutrophil Cytoplasmic Antibody Associated Vasculitis: A Randomized Inal
-
2020:173:179 187 Purpose: To assess Ihe efficacy ol prolonged rituximab therapy in reducing AAV relapses in patients in complete remission following an
initial phase of maintenance therapy.
Methods: 68 patients were randomized to receive an infusion of rituximab or placebo every 6 mo for 18 mo.
. -
Results: At 28 mo estimates of relapse free survival were 96% and 74% in the rituximab and placebo groups, respectively,
. .
representing an absolute difference of 22% (Cl 9 - 36%) and a hazard ratio of 7.5 (Cl 1.67- 33.7) |P'0.003 )
Conclusion: Prolonged rituximab therapy resulted in lower rates of AAV relapse than standard maintenance therapy
.
.
GOUT
Febuxostat Compared with -
HEJM 2005;353:2450 61 Title: Febuxostat Compared with Altopurinol in Patients with Hyperuricemia and Gout
Altopurinol in Patients with Purpose: lo investigate the use of febuxostat as a potential alternative to altopurinol foi patients wilh hyperuricemia and gout.
Hyperuricemia and Gout . Becker Methods: 762 patients with gout and with serum urate :8.0 mg/dl were randomly assigned to receive either daily febuxostat (80 or 120
etal. 2005 mg) or daily altopurinol ( 300 mg) for 52 wk.
Results: Primary endpoint (serum urate <6.0 mg/dl at the last 3 monthly measurements) occurred in 53 % of patients on febuxostat 80
. . -
mg 62% on febuxostat 120 mg and 21% on altopurinol (P 0.001 for both febuxostat groups vs.altopurinol). The overall incidence of
gout flares during wk 9 -52 was similar in all groups and decreased with continued treatment.
Conclusion: In patients with hyperuricemia and gout, febuxostat was more effective than altopurinol at towering serum urate .
ANKYLOSING SPONDYLITIS
ATLAS Arthritis Rheum Title: Efficacy and Safety of Adalimumab in Patients with Ankylosing Spondylitis: Results of a Multicenter, Randomized, Double -Blind,
2006:54:2136 46 Placebo- Controlled Trial
Purpose: lo assess the safety and efficacy ol adalimumab in patients with active AS.
Methods: 208 AS patients were randomly assigned lo SC injection of adalimumab (40 mg every other wk) or placebo loi 24 wk. Primary
outcome was a 20 % response according to the Assessment in AS International Working Group ( ASA20).
Results: 58.2% of adalimumab - treated patients reached an ASAS20 response at wk 12 vs. 20.6% of placebo - treated patients
(P«0.001). Adalimumab also demonstrated significantly greater ASAS40 and ASAS 5 / 6 responses at wk 12 and 24 (P'0.001). Significantly
more adverse events were seen wilh adalimumab.
Conclusion: Adalimumab was well- tolerated and clinically effective in treating active AS.
ASSERT Arthritis Rheum .
Title: Efficacy and Safety of Infliximab in Patients with Ankylosing Spondylitis:Results of a Randomized Placebo -Controlled Trial
2005:52:582- 91 ( ASSERT )
Purpose: lo evaluate the efficacy and safety of infliximab in AS.
. . . .
Methods: 279 patients were randomly assigned lo receive 5 mg /kg infliximab infusions at wk 0.2 6.12 and 18 or placebo Primary
outcome was a 20 % response according to the Assessment in AS International Working Group ( ASA 20).
Results: As compared with placebo, significantly more patients on infliximab achieved the primary outcome (61.2% vs. 19.2%)
IP'0.001). Infliximab produced clinical benefits beginning at wk 2 that were sustained over the 24 wk. Adverse events were common in
-
both groups but generally mid moderate in severity.
.
Conclusion: In patients with AS infliximab was clinically effective and well tolerated over 24 wk.
SPINE Ann Rheum Dis Title: Efficacy of Etanercept on Rheumatic Signs and Pulmonary Function Tests in Advanced Ankylosing Spondylitis: Results of a
2011:70:799 -804 Randomized Double - Blind Placebo- Controlled Study (SPINE)
Purpose: To assess the efficacy of etanercept ( ETN ) in advanced AS.
Methods: 82 patients wilh severe, active AS that were refractory lo NSAIOs and anti -INF naive were treated wilh ETN 50 mg once per
wk or placebo.
Results: Over 12 wk. there were significantly greater improvements in the Bath AS Oisease Activity Index IBASDAI) in the E1H group
vs. placebo group ( -19.8:16.5 vs. -11.0:16.4. P'0.019). ETH also improved CRP levels (P'0.001). total back pain (P'0.010), and FVC
(P-0.006). pt
. . .
Conclusion: In advanced AS ETN has short - term efficacy for improving pain CRP spinal mobility and pulmonary function. LJ
Sulfasalazine Arthritis Rheum
1995:38:618 27 Purpose: To evaluate the safety and efficacy of SS2 in treating spondylarthropathy.
.
Title: Sulfasalazine in the Treatment of Spondylaithropathy. A Randomized. Multicenter, Double - Blind Placebo Controlled Study
Methods: 351 patients with active disease despite treatment with NSAIOs received SS 2 (3 g/ d) or placebo. Primary efficacy outcomes
.
included the patient 's and physician 's overall assessments, pain, and morning stiffness
Results: 60% ol patients taking SS 2 improved by at least 1/ 5 points on patient assess me nl of disease activity, in conlias! to 44% +
.
taking placebo (only significant difference among 4 primary outcomes) SS 2 had greater clinical efficacy in a subgroup of patients with
psoriatic arthritis, as measured by primary efficacy variables and joint inflammation.
.
Conclusion: SS2 was more effective than placebo in treating active spondylarthropathy particularly in patients with psoriatic arthritis.
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RH35 Rheumatology Toronto Xotes 2023
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Wolfe F.Qauw DJ Filzcharles MA.etal.The American College of Rheumatology preliminary diagnostic criteria for fibromyalgia and measurement of symptom severity. Athritis Care Res (Hoboken) 2010:62:600-
c:
WolfeF. Smythe HA, Yunus MB. etal.The American College of Rheumatology 1990 criteria for the classificationof fibromyalgia:report of the multicenter criteria committee. Arthritis Rheum 1990:33:160-172.
. .
Yates M Warrs RA, Bajema IM et al.EUULR. ERA - EDTA recommendations for the management of ANCA - associated vascuhts.Ann Rheum Dis 2016:75:1583-1594.
. .
Zhang W Doherty M, Pascual E etal.EUIAR recommendations for calcium pyrophosphate deposition. Part It management Ann Rheum Dis 2011;70(4):571-575.
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Orthopaedic Surgery
John- Peter Bonello, Kalter Hali , Robert Koucheki, and Marc Manzo, chapter editors
Chunyi Christie Tan and Vrati Mehra , associate editors
Arjan S. Dhoot, HBM editor
Dr. Jeremy Hall, Dr. Paul Kuzyk, and Dr. ) esse Wolfstadt, start editors
'
Acronyms OR 2 Knee OR 34
Basic Anatomy Review OR 2 Evaluation of Knee
Cruciate Ligament Tears
Fractures - General Principles . OR 5 Collateral Ligament Tears
Fracture Description Meniscal Tears
Approach to Fractures Popliteal Cysts
Fracture Healing Quadriceps/Patellar Tendon Rupture
General Fracture Complications Dislocated Knee
Articular Cartilage , OR 7 Patella OR 38
Orthopaedic X -Ray Imaging OR 8 Patellar Fracture
Patellar Dislocation
Orthopaedic Emergencies OR9 Patellofemoral Syndrome
Trauma Patient Workup
Tibia OR 40
Open Fractures
Cauda Equina Syndrome Tibial Plateau Fracture
Compartment Syndrome Tibial Shaft Fracture
Osteomyelitis Ankle OR 41
Septic Arthritis Evaluation of Ankle and Foot Complaints
Shoulder OR12 Ankle Fracture
Shoulder Dislocation Ankle Ligamentous Injuries
Rotator Curt Disease Foot OR 42
Acromioclavicular Joint Pathology Talar Fracture
Clavicle Fracture Calcaneal Fracture
Frozen Shoulder (Adhesive Capsulitis) Achilles Tendonitis
Humerus OR17 Achilles Tendon Rupture
Proximal Humeral Fracture Plantar Fasciitis
Humeral Shaft Fracture Bunions (Hallux Valgus)
Distal Humeral Fracture Metatarsal Fracture
Elbow. OR19
Paediatric Orthopaedics OR 45
Supracondylar Fracture Fractures in Children
Stress Fractures
Radial Head Fracture
Olecranon Fracture Physeal Injury
Slipped Capital Femoral Epiphysis
Elbow Dislocation
Developmental Dysplasia of the Hip
Epicondylitis
Forearm OR 21
-
Legg- Calve Perthes Disease (Coxa Plana)
Osgood-Schlatter Disease
Radius and Ulna Shaft Fractures Congenital Talipes Equinovarus (Club Foot)
Monteggia Fracture Scoliosis
Nightstick Fracture
Bone Tumours OR 50
Galeazzi Fracture
Benign Active Bone Tumours
Wrist OR 23 Benign Aggressive Bone Tumours
Colles' Fracture Malignant Bone Tumours
Smith's Fracture
Complications of Wrist Fractures Common Medications OR 53
Scaphoid Fracture Landmark Orthopaedic Trials OR 54
Hand OR 25 References , OR 54
Spine OR 25
Fractures of the Spine
Cervical Spine
Thoracolumbar Spine
Pelvis OR 29
Pelvic Fracture
Hip., OR 30
Hip Dislocation
Hip Fracture r T
Arthritis of the Hip LJ
Hip Dislocation Post-Total Hip Arthroplasty
Femur OR 33
Femoral Diaphysis Fracture
Distal Femoral Fracture +
OR I Orthopaedic Surgery Toronto Notes 202 J
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0R2 Orthopaedic Surgery Toronto Notes 2023
Acronyms
ABI ankle brachial index DDH developmental dysplasia of the MCL medial collateral ligament RA rheumatoid arthritis
AC acromioclavicular r 3 M metatarsal RCD rotator cuff disease
.
ACL
All
anterior cruciate ligament
anterior interosseous nerve
DRUJ
DVT
distal radioulnar joint
deep vein thrombosis
MTP
MVC
metatarsophalangeal
motor vehicle collision
ROM
RSD
range of motion
reflex sympathetic dystrophy
AP anteroposterior EtOH ethanol/alcohol NVS neurovascular status SCFE slipped capital femoral epiphysis
ARDS acute respiratory distress FAI femoroacetabular impingement NWB non - weight bearing SLAP superior labrum, anterior
syndrome FOOSH fall on outstretched hand OA osteoarthritis posterior
AVN avascular necrosis GA general anesthetic ORIF open reduction internal fixation SN sensitivity
CA coracoacromial HO heterotopic ossification PCI posterior cruciate ligament THA total hip arthroplasty
CC coracoclavicular l&D incision and drainage PE pulmonary embolism TSA total shoulder arthroplasty
CRPS complex regional pain syndrome IM intramedullary PIN posterior interosseous nerve WB weight -bearing
C&S culture and sensitivity LCL lateral collateral ligament PIC posterolateral corner t fracture
Basic Anatomy Review

C5 ,oC7
C6 28
C7
C8
' T1
iT1
Coracobrachialis
Musculocutaneous
nerve
Bleeps brachii
Median -Ulnar
nerve nerve
-Medial cutaneous
Brachialis nerve of the arm
Lateral cutaneous
nerve of forearm ( sensory)
( sensory)
Pronator teres
Pronator teres
Flexor carpi radiaiis

Rexor digitorum — Rexor
ulnaris
carpi
profundus
Palmaris longus Medial cutaneous
Imedial 4.5 digits )
Rexor pollicis nerve ot the forearm
( sensory)
longus Flexor digitorum
superficialis
Dorsal cutaneous
Flexor digitorum branch ( sensory)
Pronator profundus
quadrates {lateral 2,3 digits)
Palmar cutaneous
'/I branch ( sensory)
Adductor
Thenar pollicis , Palmar interossei
muscles
'almaris brevis
2.3 lumbricals lypothenar muscles
Dorsal /
interossei 4,5
lumbricals r “i
Palmar sensory r
.
i J
branches of median
CM
nerve
Superficial terminal i
s
branches (sensory) 3
i
@
+
ANTERIOR VIEW
Figure 1. Median, musculocutaneous, and ulnar nerves: innervation of upper limb muscles
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0 R3 Orthopaedic Surgery Toronto Notes 2023
15
LC
C7
Axillary C8
Subclavian
Deltoids , Subscapularis
Posterior
Circumflex
humeral [ Anterior
Thoracoacromial
.Teres major
Axillary norvo
lateral thoracic
Subscapular \ 'latissimus
\ dorsl
Brachial Upper cutaneous , Radial nerve
Profundi artery norvo of the arm
brachii
S Superior ulnar
( sensory! 'Triceps brachii Hong head!
collateral Triceps brachii (medial head)
Inferior ulnar Brachioradialh
collateral Extensor carpi J.
radialis longus (I
Radial -
recurrent
Extensor carpi
radialis brevis/ /
Anterior and posterior iSupinator
ulnar recurrent
Radial , Posterior-^
Ulnar interosseous
nerve f AExtensor carpi ulnaris
Anterior interosseous Abductor,^'"' [ 'Extensor digit! minimi
pollicis longus Extensor digitorum
Abductor
^ , ^ 'Extensor indicis
pollicis brevis
Superficial-
Deep palmar arch radial nerve
( sensory )
Superficial palmar arch
I
5
J
*
ANTERIOR VIEW POSTERIOR VIEW
Figure 2. (Left ) Blood supply to the upper limb, ( Right ) Axillary and radial nerves: innervation of the upper
limb
Table 1Sensory and Motor Innervation of the Nerves in the Upper and Lower Extremities
Nerve Motor Sensory Nerve Roots
Axillary Dcltoidlferes Minor /Tiiceps (long Lateral upper arm (Sergeant 's .
C5 C 6
head) Pilch)
Musculocutaneous Biceps/ Grachialis Lateral lorcarm .
C 5 C6
Radial Triceps (medial andlateral heads)
Wrist/ thumb / finger Extensors
Lateral dorsum of the hand
Medial upper lorcarm
...
C5 C6 CJ C8
Wrist abductors
Median Wrist flexors Palmar thumb lo radial hall ol 4 th C6, C 7
Flexion of 1st - 3rd digits digit, and the dorsal lips of digits t
to radial hall ol digit 4
Ulnar Wrist flexors and adductors Medial palm and dorsum ol hand .
C8 T1
flexion of 4th -5lh digits 5th digit and medial half ol 4th
digit
Tibial Ankle plantar flexion
Knee flexion
Sole of foot .
LS St
Great toe flexion

Superficial Peroneal Ankle eversion Dorsum of foot .
L5 S1
Deep Peroneal Ankle dorsiflexion and Inversion 1st web space .
L5 S1 ( n\
Great toe extension
Sural Lateral foot S1, S 2
Saphenous Anteromedial ankle L3, L4
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OR l Orthopaedic Surgery Toronto Notes 2023
ANTERIOR VIEW POSTERIOR VIEW

Common iliac artery
Lateral cutaneous nerve of
the thigh
Femoral nerve
.
Superior gluteal nerve
External iliac artery
Internal iliac artery
Deep circumflex iliac artery -Inferior gluteal nerve
Superficial circumflex iliac
artery •Sciatic nerve
Medial cutaneous -Posterior cutaneous
nerve of the thigh nerve of the thigh
Lateral circumflex femoral Lateral circumflex
artery femoral artery
Obturator nerve -Medial circumflex
femoral artery
Profunda femoris artery Prolunda lemoris artery
Femoral artery
Descending branch
Femoral artery
Intermediate cutaneous
nerve of the thigh
Hiatus in adductor magnus
-Tibial nerve
-(Common fibular
peroneal) nerve
Saphenous nerve - Popliteal artery
Common fibular
(peroneal) nerve
Deep fibular (peroneal)
nerve -Posterior tibial artery
Superficial libular
(peroneal) nerve
-Anterior tibial artery
Anterior tibial artery Sural nerve
Calcaneal branch 2
Dorsalis pedis artery m
IS Medial plantar nerve
Medial plantar artery -
Lateral plantar nerve
Lateral plantar artery I
UJ
Plantar artery
a©
Figure 3. Nerves and arteries of lower limbs
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Table 2. Muscle and Compartment Review of the Limbs

Arm Forearm Thigh Leg
Anterior Compartment Biceps Bractrii PronatorIeres Sartorius Tibialis Anterior
Brachialis fleior Carpi Babralis Ouadriceps Eitensor Hallucis Longus
Co racobra cilialis Palmarrs Loogus Bectus Femoris Eitensor Drgitorum Longus
Fleior Carpi Ulnaris Vastus Lateralis Peroneus tertius
Fleior Drgitorum Vastus Intermedius
Superficialis Vastus Medralis
Fleior Drgitorum Profundus
Fleior Pollers longus
Pronator Ouadratus
Posterior Compartment Triceps Brachioradialis Hamstrings Superficial
Aconeus Eitensor Carpi Badialis Semitendinosus Gastrocnemius
longus Semimembranosus Soleus
Eitensor Carpi Radiahs Biceps Femoris Plantaris
Brens
Eitensor Carpi Ulnarrs Deep
Eitensor Digrtorum Popliteus
Eitensor Digiti Minimi Flexor Hallucis Longus
Abductor Pollicis Longus Flexor Digitorum longus
Eitensor Pollicis longus Tibialis Posterior
Eitensor Pollicis Brevis
Eitensor Indrcis
Supinator
Medial Compartment Adductor Longus
Adductor Brevis
Adductor Magnus
Sracilis
Pectineus
Lateral Compartment Peroneuslongus
Fibularis Brevis
Fractures - General Principles

Fracture Description
Displacement
1. Name of Injured Bone
Refers to position of the distal fragment
relative to the proximal fragment
2. Integrity of Skin/Soft Tissue
• closed: skin /soft tissue over and near fracture is intact
• open: skin /soft tissue over and near fracture is lacerated or abraded, such that fracture site can
communicate with contaminants ( Le. outside environment or bowel )
Varus/Valgus Angulation
• signs: continuous bleeding from puncture site, or fat droplets in blood are suggestive of an open Refers to the distal segment of the bone
fracture compared to the proximal segment
Varus ~ Apex away from midline
3. Location Valgus - Apex toward midline
• epiphyseal: end of bone, forming part of the adjacent joint
• metaphyseal: the tlared portion of the bone at the ends of the shaft
• diaphyseal: the shaft of a long bone ( proximal, middle, distal )
• physis: growth plate Quick Upper Extremity Motor Nerve
Exam
4 . Orientation / Fracture Pattern (see figure t , OK6) - “Thumbs Up ”: PIN (Radial Nerve)
“OK Sign": AIN (Median Nerve)
• transverse: fracture line perpendicular (< 30° of angulation ) to long axis of bone; result of direct high “Spread Fingers": Ulnar Nerve
energy force
-
• oblique: angular fracture line ( 30° 60° of angulation ); result of angulation and compressive force, high
energy
• butterfly: triangular or wedge -shaped fragment resembling a butterfly; commonly between the two X -Ray Rule of 2s
main fracture fragments in comminuted long bone fractures 2 sides - bilateral
• segmental: a separate segment of bone bordered by fracture lines; often the result of high -energy force 2 views AP lateral
-
• spiral: complex, multi planar fracture line; result of rotational force, low energy 2 joints - joint above below
2 times - before * after reduction
• comminuted / multi -fragmentary: >2 fracture fragments
• intra-articular: fracture line crosses articular cartilage and enters joint
• compression: impaction of bone: typical sites are vertebrae or proximal tibia ri
LJ
• torus: compression of bony cortex on one side while the other remains intact, often seen in children
(see figure 50, UR45 ) Sample Fracture Description
• screens tick: compression of one side with fracture of the opposite cortex, often seen in children (see Closed (overlying skin integrity) spiral
figure 50, OR45 ) fracture (fracture pattern) of the distal
third (location) of the left tibia (injured
• pathologic: fracture through abnormal bone weakened by disease (e.g. tumour ) bone), with mild varus angulation, lateral +
translation and angulation (alignment of
fracture fragments). The fracture does
not extend to the joint surface
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5 . Alignment of Fracture Fragments (see Figure 5)

• non -displaced: fracture fragments are in anatomic alignment
• displaced: fracture fragments are not in anatomic alignment
• distracted: fracture fragments are separated by a gap ( opposite of compression )
• translated: percentage of overlapping bone at fracture site
• angulated: direction of fracture apex ( e.g. varus / valgus )
• rotated: fracture fragment rotated about long axis of bone
• shortened: fracture fragments are compressed , resulting in shortened bone
• avulsion: tendon or ligament tears/ pulls off bone fragment
ir
“t A \U V F
Spongy
/ bone
B. Oblique .
C Butterfly D. Segmental .
E Spiral F. Comminuted Proximal -
, V
t N
A. Transverse .
© Lisa Qiu 2019 alter 3 Carly Vanderlee 2011
epiphysis
- vj
^
_ Articular
cartilage
""Epiphyseal line
v Periosteum
Figure 4. Orientation/ fracture pattern
Compact bone
-- Medullary
haphysrs
A. Translated C. Rotated D. Sliorlened E. Avulsion

B. Angulated
.
Si Lisa Qiu 2019 altar © Carly Vanderlaa 2011
Orstal
epiphysis—
Figure 5. Alignment of fracture fragments Figure 6. Schematic diagram of the
long bone
Approach to Fractures
I . Clinical Assessment Reasons for Closed Reduction and
ABCs, primary survey, and secondary survey ( Advanced Trauma Life Support ( AT'LS) protocol ) Splinting
assess for life threatening Injury • Pain control
assess for open and other fractures • Reduces further damage to vessels,
-
• AMPLE E history ( minimum ): Allergies , Medications, Past medical history Last meal, Events
( mechanism of injury ), function pre- injury
. nerves, and skin and may improve
neurovascular status
• Reduces point loading on articular
previous significant injury or surgery to affected area surfaces
consider pathologic fracture with history of only minor trauma • Decreases risk of inadvertently
converting closed to open fracture
• physical exam: inspect (deformity, soft tissue integrity); palpate ( maximal tenderness, N VS- • Facilitates patient transport
document best possible neurovascular exam, avoid ROM / moving injured area to prevent
exacerbation )
2. Analgesia
• oral, IV, or local (e.g. hematoma block ) Indications for Open Reduction
3. Imaging ( see Orthopaedic X - Ray Imaging , ORR )
I. Reduction: closed vs. open NO CAST
Nonunion
• closed reduction (with IV sedation and muscle relaxation if necessary ) Open fracture
apply traction in the long axis of the limb Neurovascular Compromise
reverse the mechanism that produced the fracture Displaced intra-Articular fracture
open reduction -
Salter Harris 3,4,5 rT
“ NO CAST" (see sidebar) PolyTrauma LJ
other indications include
-
failed closed reduction
-- pathologic fractures
unable to cast or apply traction due to site
+
-
potential for improved function and /or outcomes with OR 1E
• ALWAYS re- check and document N VS after reduction and obtain post - reduction x- ray
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5. Immobilization
external stabilization: splints, casts, traction, external fixator
internal stabilization: percutaneous pinning, extramedullary fixation (screws, plates, wires), IM Buck's Skin Traction
fixation ( rods) A system of weights, pulleys, and
6. Follow- up ropes that are attached to the end of
evaluate stages of bone healing (see Fracture Healing ) a patient' s bed exerting a longitudinal
7. Rehabilitation force on the distal end of a fracture,
improving its length, alignment and
recommend rehabilitation when appropriate to regain function and avoid joint stiffness rotation temporarily while awaiting
fixation (typically used for lower
extremity fractures)
Fracture Healing
Normal Healing
Weeks 0-3 Hematoma, macrophages surround fracture site
Wolffs Law
Weeks 3-6 Osteoclasts remove sharp edges, callus forms within hematoma Bone adapts to the amount of force
applied by increasing or decreasing its
Weeks 6-12 Bone forms within the callus, bridging fragments mass to resist the applied stress
Months 6-12 Cortical gap is bridged by bone
Years 1- 2 Normal architecture is achieved through remodelling
Figure 7. Stages of bone healing
Evaluation of Healing: Tests of Union

• clinical: no longer tender to palpation, no mobility, minimal or no deformity on physical exam
• x- ray: trabeculae cross fracture site, visible callus bridging site on at least 3 of 4 cortices
General Fracture Complications Fracture Blister

Formation of vesides or buBae that
occur on edematous skin overlying a
Table 3. General Fracture Complications fractured bone
Early Late
Local Compartment syndrome Mai-,'non-union
Neurological injury AVN
Vascular injury Osteomyelitis Heterotopic Ossification
Infecbon Heterotopic ossification The formation of bone in abnormal
Implant failure Post- traumatic OA locations (e.g. in musde). secondary to
fracture blisters Joint stiffness/adhesive capsulitis pathology
CUPS type l/ RSD
Systemic Sepsis
DVT
PE
AS OS secondary to fat embolism CRPSRSD
Hemorrhagic shock Sustained sympathetic activity
characterized by pain out of proportion
to physical exam findings: symptoms of
hyperalgesia and alodynia. and signs
of autonomic dysfunction (temperature
Articular Cartilage asymmetry, mottling, hair or nai
changes)
Properties
• hyaline cartilage
-
• 2 4 mm layer covering ends of articulating bones, provides nearly frictionless surface
• avascular ( nutrition from synovial fluid ), aneural, alymphatic Avascular Necrosis
Ischemia of bone due to disrupted
ARTICULAR CARTILAGE DEFECTS blood supply, most commonly affecting
the femoral head, talus, or proximal
scaphoid
Etiology
• overt trauma, repetitive minor trauma (such as repetitive ankle sprains or patellar maltracking )
• degenerative conditions such as early stage OA or osteochondritis dissecans
Osteochondritis Dissecans
Clinical Features Avascular necrosis of subchondral
• part of OA presentation: pain with movement, decreased range of motion, joint line pain with possible bone most often occurraig in children ri
effusion and adolescents and causing pain and LJ
• have predisposing factors such as: ligament injury; malalignment of the joint (e.g. varus or valgus ); potentially hindering joint motion
obesity; AVN; and inflammatory arthropathy
• may have mechanical symptoms of locking or catching related to the torn /displaced cartilage
Investigations
+
• x- ray (to rule out bony defects and check alignment )
• MR 1 ( if x- ray is normal; MR1 is not needed to assess cartilage loss associated with osteoarthritis)
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Table 4 . Outerbridge Classification of Chondral Defects

Grade Chondral Damage
I Softening and swelling of cartilage
II Fragmentation and fissuring <l/2" in diameter
III Fragmentation and fissuring >112* in diameter
IV Frosion of cartilage down to bone
Treatment
• individualized
• patient factors (age, skeletal maturity, activity level, etc.)
• defect factors ( Outerbridge Classification, subchondral bone involvement, etc.)
-
• non operative
• rest, COX2 inhibitors, NSAIDs, bracing, physiotherapy, intra -articular corticosteroids
• operative
• microfracture, osteochondral grafting ( autograft or allograft ), autologous chondrocyte
implantation
Orthopaedic X-Ray Imaging

General Principles - “Rule of 2s”
• x- ray 1 joint above and 1 below
• obtain at least 2 orthogonal views ± specialized views
• 2 sides, as needed for comparison
When reading a radiograph consider

• open or closed fracture ( air/gas seen in the soft tissue) Sample radiograph description:
“There is a simple transverse fracture of
• the view the proximal right humerus diaphysis.
• anatomical location There is 1cm of shortening. The distal
• laterality ( right vs. left ) fragment is medially angulated 70
• skeletally mature vs. immature degrees"
• intra-articular vs. extra-articular
• joint congruent, subluxed or dislocated
• rotation
• angulation
• displacement
• shortening
Table 5. Orthopaedic X- Ray Imaging

Site Injury X- Ray Views
Shoulder Anterior dislocation AP
Posterior dislocation Axillary t stress mew with 10 lb in hand
AC separation Trans-scapular
Tanca view (10-15 cephalic tilt)
Arm Humerus A AP
Lateral
Elbow/Forearm Supracondylar A AP
Radial head A Lalecal
Monteggia A
Nightstick A
Galeazzi A
Wrist Colies' A AP
Smith A lateral
Scaphoid A Clenched Fist (foe scaphotunate dissociation)
Pelvis Pelvic A AP pelvis
Inlet and outlet views
Judet mews (obturator and iliac oblique for acetabular A )
Hip Femoral head 'neck A AP
Intertrochanteric A lateral
Arthritis Frog-leg lateral
SCFE Ounr
FAI False profile
Developmental dysplasia of the hip ( DDH|
Knee Knee dislocation AP standing,lateral ri
Femur /tibia A Skyline (tangenbal new with knees flexed at 45° to see patellofemoral joint) -
< J
Patella A
Patella dislocation
Patella femoral syndrome
Leg Tibia shaft A
Fibula shaft A
AP
lateral
+
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Table 5. Orthopaedic X- Ray Imaging

Site Injury -
X Ray Views
Ankle Ankle S AP
Lateral
Mortise view (ankle at 15° of internal rotation)
Foot Talar t AP
Calcaneal t lateral
MTI Oblique
lisftanc injuries lateral. Karris, anal
Spine Compression i AP spine
Burst t AP odontoid
Cervical spine A lateral
Oblique
Swnmmec'jnew (lateral view with arm abducted 180' to evalua te C7- I1
junction if lateral view is inadequate )
lateral Reuorv’eilension new: evaluate subluxation of cervical vertebrae
Orthopaedic Emergencies
Trauma Patient Workup
Etiology Orthopaedic Emergencies
• high energy trauma (e.g. MVC, fall from height )
• may be associated with spinal injuries or life-threatening visceral injuries VON CHOP
Vascular compromise
Clinical Features Open fracture
Neurological compromise/cauda
• comminuted, open fractures with significant soft tissue injury equina syndrome
• local swelling, tenderness, deformity of the limbs, and instability of the pelvis or spine Compartment syndrome
• decreased level of consciousness, hypotension, hypovolemia Hip dislocation
• consider involvement of EtOH or other psychoactive substances Osteomyelitis/septic arthritis
Unstable Pelvic fracture
Investigations
• trauma survey ( see Emergency Medicine. ER2 )
• x- rays: lateral cervical spine, AP chest, AP pelvis, AP and lateral of all bones suspected to be injured
CT is also utilized to inspect for musculoskeletal injuries in the trauma setting Controversies in Initial Management of Open
Fractures
• other views of pelvis: AP, inlet, and outlet; )udet views for acetabular fracture ( see Table 19, OR30 ) Scar,dJSurg 2014;103( 2):132-137
Study: Literaturereview exam icing the initial
Treatment management of open fractures. 40 studies ir.duded.
• ABCDEs: initiate resuscitation for life- threatening injuries ( ATLS protocol ) Findings:
• assess genitourinary injury ( rectal exam / vaginal exam mandatory ) • A first -generation cephalosporin ( or clindavlyda}
should be administered upon arnvaL In general. 24
• external or internal fixation of all fractures h of antibiotics after each debridement is sufficient
• if patient unstable then Damage Control Orthopaedics - use of external fixation for fractures initially to reduce infection rates.
and then bring patient back to OR for definitive fixation (1M nail or OR1E ) once hemodynamically •Although cultures ate taken from delayed (»24 h|
stable or infected injuries, it may not be necessary to
• DVT prophylaxis once stable routinely take post -debridenent cultures open
fractures.
• Open fractures should be debrided as soon as
Complications possible , although the '6 h rule' is not generally
-
• hemorrhage - life threatening ( may produce signs and symptoms of hypovolemic shock ) valid.
• fat embolism syndrome - SOB, hypoxemia, petechial rash, thrombocytopenia, and neurological • Wo undo should be closed w.thi.n 7 d once soft tissue
symptoms has stood red and all non - nob e tissue removed .
• Negative pressure wound therapy ( HPWT) has
• venous thromboembolism - DVT and PE been shown to decrease infectkm totes in open
• bladder/ urethral/ bovvel injury froctores.
• neurological and vascular damage
• persistent pain /stiffness/ limp/ vveakness in affected extremities
-
• post traumatic OA of joints with intra -articular fractures
• sepsis and /or tetanus infection especially if missed open fracture
LJ
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ORIO Orthopaedic Surgery Toronto Notes 2023
Open Fractures
• fractured bone and hematoma in communication with the external or contaminated environment
33% of patients with open fractures have
Emergency Measures multiple injuries
• ABCs, primary survey, and resuscitate as needed
• remove obvious foreign material once in a controlled hospital environment
• irrigate with normal saline if grossly contaminated
• cover wound with sterile dressings Antibiotic Prophylaxis in the Management of
• immediate IV antibiotics Open Fractures
• tetanus toxoid or immunoglobulin as needed (see Plastic Surgery. PL28) J8JS Reviews: 2019 Feb:7(2|:e1
Purpose: Provide current practice recommendations
• N PO and prepare for OR ( blood work, consent, ECC>, CXR)
-
operative irrigation and debridement within 6 8 h to decrease risk of infection on prophylaxis for patients with open fractures of
the extremities .
OKI I Methods: Systematic survey of plications from
traumatic wound may be left open to drain with vacuum assisted closure if necessary - January 200) to June 201),andsearch of WohdCat for
-
re examine with repeat irrigation and debridement in 18 h if necessary - textbooks and websites for institutional guidelines.
Results: Most recommendationssuggested
Table 6. Gustilo Classification of Open Fractures Cram - positive antibiotics up to 3 d postxnjury
for less severe injuries. For more severe injr es.
Gustilo Grade Length of Description Prophylactic Antibiotic Regimen most recommendations included broad spectrum
Open Wound anti biotics for 2-3 d. A s well,most sources
recommend immediately administration of
I «1 cm Minimal contamination and soft tissue injury First generation cephalosporin (cefa zolin) 2 g IV q8
Simple or minimaly comminuted fracture h for 2 d antibiotics.
If allergy use clindamycin 300 mg IV q8 h Conclusions: Current practice recommendations
If MRSA positive use vancomycin 15 mgi'kg IV q12 h supportear lysystemx prophylaxis for patents
with open fractures of the extremities. However,
II 1-10 cm Moderate contamination As per Grade I differences are seen across antibiotic regimens,
Moderate soft tissue injury doses, and duration of administration.
III* >10 cm IIIA:Extensive soft tissue mjury with adequate First generation cephalosporin (cefazolin) for 2
ability of soft tissue to cover wound d plus Gram - negative coverage Igentamidn or
IIIB:Extensive soft tissue injury with periosteal ceftriaxone) for at least 3 d
stripping and bone exposure: inadequate soft For soil or fecal contamination, metronidazoleis
tissue to cover wound added for anaerobic coverage r penicillin G
NIC: Vascular injury- compromise If MRSA positive use vancomycin 16 mgi'kg IV q12 h
. .
'Any high energy,comminuted fracture,shot gun tarmysnt soil water contemirstjor exposure to oral flora,or fracture >8 hold is immediately
classified as Grade III
Cauda Equina Syndrome

• see Neurosurgery NS32 .
Compartment Syndrome
• increased interstitial pressure in an anatomical compartment (forearm , calf ) where muscle and tissue
are bounded by fascia and bone ( fibro-osseous compartment), with little room for expansion
• interstitial pressure exceeds capillary perfusion pressure, leading to irreversible muscle necrosis ( in
4-6 h ) and eventually nerve necrosis
Etiology
• intracompartmental Most important sign is increased pain
• fracture ( particularly tibial shaft or paediatric supracondylar and forearm fractures) with passive stretch. Most important
• reperfusion injury, crush injury, or ischemia symptom is pain out of proportion to
• extracompartmental: constrictive dressing (circumferential cast ), poor position during surgery, injury
circumferential burn
Increased pressure from blood
and intracompartmental swelling"
*
1
5 Ps of Compartment Syndrome
Pa in: out of proportion for injury and
*
Decreased venous drainage Transudation into tissue
not relieved by analgesics
Decreased lymphatic drainage surrounding compartment • Increased pain with passive stretch
of compartment muscles
Pallor: late finding
Intracompartmental pressure Leaky basement Paresthesia
greater than perfusion pressure membranes Paralysis: late finding
Pulselessness: late finding
Acidosis 4-
Figure 8. Pathogenesis of compartment syndrome

Muscle and
nerve anoxia ^
"
Musc and
^
nerve necrosis
LJ
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Clinical Features
• pain out of proportion to injury ( typically first and most significant symptom )
• pain with active contraction of compartment
• pain with passive stretch ( most sensitive sign ) Plain Film Findings of Osteomyelitis
• swollen, tense compartment • Soft tissue swelling
• suspicious history • Lytic bone destruction"
• Periosteal reaction (formation of new
bone, especially in response to •)"
• 5 Ps: late sign - do not wait for these to develop to make the diagnosis! -
'Generally not seen on plain films unU 10 12 d after
onset olinlection
Investigations
• compartment syndrome is a clinical diagnosis; investigations usually not necessary
• in children, unconscious patients, or associated peripheral nerve injury where clinical exam is
unreliable, compartment pressure monitoring with catheter ( normal = 0 mmHg; elevated >30 mmHg Rapid progression of signs and
or [dBP - measured pressurej <30 mmHg) symptoms (over hours) necessitates
need for serial examinations
Treatment
• non -operative
remove constrictive dressings (casts, splints), elevate limb to the level of the heart
• operative
urgent fasciotomv
• 48 -72 h postoperative: necrotic tissue debridement + wound closure Acute osteomyelitis is a medical
• may require delayed closure and/ or skin grafting emergency which requires an early
diagnosis and appropriate antimicrobial
Complications and surgical treatment
• Volkmann’s ischemic contracture: ischemic necrosis of muscle; followed by secondary fibrosis; and
finally calcification - especially following supracondylar fracture of humerus
• rhabdomyolysis, renal failure secondary to myoglobinuria
Joints most commonly affected by septic
arthritis in descending order
Osteomyelitis -
knee hip » elbow ankle *
sternoclavicular joint
-
• bone infection with progressive inflammatory destruction
Etiology
Plain Film Findings in a Septic Joint
• most commonly caused by S. aureus
• Early (0- 3 d): usually normal:may
• mechanism of spread: hematogenous ( most common ) vs. direct-inoculation vs. contiguous focus show soft-tissue swelling or joint
• risk factors: recent trauma / surgery, immunocompromised patients, DM, IV drug use, poor vascular space widening from localized
supply, peripheral neuropathy edema
• Late ( 4- 6 d): joint space narrowing
Clinical Features and destruction of cartilage
•symptoms: pain and fever

• on exam: erythema, tenderness, edema common ± abscess/ draining sinus tract; impaired function /
VVB
Serial C reactive protein (CRP) can be
Diagnosis used to monitor response to therapy
•see Medical Imaging, MI 24 and M 127
• workup may include: WBC and differential , ESR, CRP, blood culture, aspirate culture / bone biopsy
Table 7. Treatment of Osteomyelitis Docs This Adult Patient Have Septic Arthritis?
JAMA 2007:297(13|:1478 -t488
Acute Osteomyelitis Chronic Osteomyelitis Purpose: To review the accuracy and pretss:- of : e *
IV antibiotics 4 -6 wk:started empirically and adjusted alter obtaining Surgical debridement clinical evaluatin'! for the diagnosis of nongrscocca
blood and aspirate cultures bacterial arthritis.
Methods: Devew of t4 studies me hiling 6242
± surgery (liD) for abscess or significant involvement Antibiotics:both local (e.g.antibiotic beads) and systemic (IV ) patients of which 653 had positive srnov a: cu tire
* hardware removal (if present) (gold standard diagnostic tnol forseptx afnts).
Results: Age, diabetes nelStos. rbearztod
arthritis, joint surgery , hip or knee prosthesis, sc r
infection , and human immunodeficiency eras type
Septic Arthritis t infection significantly increase the proPati ity of
septic arthritisJoint pain, history of joct swtfrg.
and fever are found m >50 of cases. The presence
• joint infection with progressive destruction if left untreated *
ol inoeased WBC increases the Iiielzood rano for
.
counts <2SOOO/pL: W, 0.32; 95 a 0.23 0.43
Etiology . ** -
for counts >25000/pL LR 2.9:95 0.2J 3.4: foe
• most commonly caused by S. aureus in adults counts elOOOOOipL: IR. 2 B.0: 95 0, C.0-66.C|. A
*
polymorphonuclear cell count of ?90 mueases oe
*
•consider coagulase - negative Staphylococcus in patients with prior joint replacement IR of septic arthritis hy 3.4.* !e a PMI cel coat of
•consider ,V. gonorrhocac in sexually active adults, and newborns <90% reduces theLR by 0.34.
• most common route of infection is hematogenous Conclusions Clinical findings may pe used a idem ’
• risk factors: young /elderly (age >80 yr), prosthetic joint, recent joint surgery, skin infection / ulcer, patients with monoarticular arthritis who may
-
IV drug use, recent intra articular corticosteroid injection, immunocompromised ( cancer, DM , have septic arthritis, laboratory findings from as
alcoholism , RA ) arthrocentesis are also required and helpful poor a
Oram stain and culture.
+
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Clinical Features
• inability/ refusal to hear weight, localized joint pain , erythema , warmth , swelling , pain on active and
passive ROM , ± fever Posterior Shoulder Dislocation
Up to 60-80% are missed on initial
Investigations presentation due to poor physical exam
• x- ray ( to rule out fracture , tumour, metabolic bone disease), ESR , CRP, WBC , blood cultures and radiographs
• joint aspirate: cloudy yellow fluid , WBC > 50000 with > 90% neutrophils, protein level >4.4 rng /dL,
joint glucose level <60% blood glucose level , no crystals, positive Gram stain results
• listen for heart murmur ( if concern for infective endocarditis, use Duke Criteria )
There are 4 Joints in the Shoulder
Treatment . .
Glenohumeral AC sternoclavicular (SC),
scapulothoradc
• IV antibiotics, empiric therapy ( based on age and risk factors), adjust following joint aspirate C&S
results
• non - operative
• therapeutic joint aspiration, serially if necessary
Shoulder passive ROM: abduction -
• operative
• arthroscopic or open irrigation and drainage
.
180°, adduction - 45° flexion - 180° .
extension - 45°.int rotation - level of
T4, ext. rotation -‘90° likely more...
Shoulder
Factors Causing Shoulder Instability
Shoulder Dislocation , Shallow glenoid
• Loose capsule
•complete loss of continuity between the two articular surfaces of the glenohumeral joint; may be • Ligamentous laxity
anterior or posterior .
Frequency of Dislocations
Anterior shoulder > Posterior
shoulder
Investigations • Posterior hip > Anterior hip
-anterior dislocation x-rays: AP, trans-scapular, and axillary views of the shoulder
•posterior dislocation x - rays: AP, trans-scapular, and axillary views of the shoulder; or CT scan
• The glenohumeral joint is the most
commonly dislocated joint in the
body since stability is sacrificed for
motion
Table 8. Anterior and Posterior Shoulder Dislocation
Anterior Shoulder Dislocation (>90%) Posterior Shoulder Dislocation (5 %)
MECHANISM
Abducted externally rotated/hyperextended arm Adducted, internally rotated, flexed arm
Blow to posterior shoulder FOOSK
Involuntary, usually Iraumalic; voluntary, atraumatic 3 Es (epilepticseizure. EtOH. electrocution)
Blow to anterior shoulder
CLINICAL FEATURES
Symptoms Pain, arm slightly abducted and externally rotated with Pain,arm is held in adduction and internal rotation;
inability to internally rotate external rotation is blocked
Shoulder Exam " Squared off shoulder Anterior shoulder flattening, prominent coracoid,
Positiveapprehension test : palientlooks apprehensive palpable mass posterior to shoulder
with gentle shoulder abduction and external rotation to 90” Positive posterior apprehension (“ jerk ") test: with
as humeral head is pushed anteriorly and recreates feeling .
patientsupine flex elbow 90° and adduct,internally .
1 Manubrium
of anterior dis' ocation rotate the arm while applying a posterior force to the
.
2 Sternoclavicular joint
Positive relocation test: a posteriorly directed force shoulder;patient will “jerk* back with the sensation of
.
3 Clavicle
applied durmgthe apprehension test relieves apprehension subluxaton
4. Coracoid process
since anterior subluxation is prevented Note: the posterior apprehension test is used to test for
.
5 AC joint :
Positive sulcus sign: presence of subacromial indentation .
recurrent posterior instability NOT lor acute injury
6. Acromion er
with distal traction on humerus indicates inferior shoulder 7. Humerus §

instability 8. Glenohumeral joint
,9. Scapula e
These tests are more commonly used for chronic recurrent Figure 9. Shoulder joints
instability
Neurovascular Exam Axillary nerve: sensory patch over deltoid and deltoid Full Renovascular exam as per anterior shoulder
Including contraction dislocation
Musculocutaneous nerve: sensory patch on lateral Coracoid
forearm and biceps contraction process
V
RADIOGRAPHIC FINDINGS
Acromion
Axillary View Humeral head is anterior Humeral head is posterior /
Trans scapular 'Y° View Humeral head is anterior to the center of the "Mercedes- Humeral head is posterior to center of "Mercedes- Bent *
Bent "sign sign
2
AP View Sub- coracoid lie of the humeral head is most common Partial vacancy of glenoid fossa (vacant glenoid sign) and r -t
>6 mm space between anterior glenoid rim and humeral I
_ LJ
head (positive rim sign), humeral head may resemble a
lightbulb due to internal rotation (lightbulb sign) 1_
Humcru
Hill -Sachs and Bony ? Hill - Sachs lesion: compression fracture of posterior t Reverse Hill -Sachs lesion (75% of cases): divot in -
Bankart Lesions humeral head due to forceful impaction of an anteriorly anterior humeral head 1
dislocated humeral head against the glenoid rim * Reverse bony Bankart lesion: avulsion of the posterior
I
+
- Bony Bankart lesion: avulsion of the anterior glenoid
labrum (with attached bone fragments) from the glenoid
glenoid labrum from the bony glenoid rim
e
rim
Figure 10. Mercedes-Benz
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OR 13 Orthopaedic Surgery Toronto Notes 2023
Table 8 . Anterior and Posterior Shoulder Dislocation Bankart

Anterior Shoulder Dislocation (>90%) Posterior Shoulder Dislocation (5%)
TREATMENT
Closed reduction with IV sedation and muscle relaxation Closed reduction with IV sedation and muscle relaxation
Traction - countertraction : assistant stabilizes torso with Interior traction on a Hexed elbow with pressure on the
a folded sheet wrapped across the chest while the surgeon back of the humeral head
applies gentle steady traction Obtain post -reduction x - rays
Stimson: while patient lies prone with arm hanging over Check post - reduction NVS Hill- Sachs
table edge, hang a 5 lb weight on wrist lor 15 - 20 min Sling in abduction and external rotation x 3 wk.
Hippocratic method: place heel into patient’s axilla and followed by shoulder rehabilitation [dynamic stabilizer
Figure 11. Posterior view of anterior
apply traction to arm strengthening)
Cunningham 'smethod: gentle longitudinal support dislocation causing Hill-Sachs and
and traction of the arm at the patient's side, massage/ Bankart lesions
relaxation of deltoid, trapezius, and biceps to allow
atraumatic shoulder reduction, low -risk, low pain;if not
successful try above methods
Obtain post -reduction x- rays
Check post - reduction MVS
Sling x 3 wk (avoid abduction and external rotation),
followed by shoulder rehabilitation (dynamic stabilizer
strengthening)
Prognosis
• recurrence rate depends on age of first dislocation
• < 20 yr 65 - 95%; 20 - 40 yr = 60- 70%; > 40 yr 2- 4%
Specific Complications
• recurrent dislocation ( most common complication )
• unreduced dislocation
• shoulder stiffness
• rotator cuff or capsular or labral tear ( Bankart / SLAP lesion )
• injury to axillary nerve / artery, brachial plexus
-
u>
§ I
-
-5s a
I
.
Antorior apprehension sign
—
O
«
Sulcus sign
r
s
I S
sa i
s >-
5 4
e
Posterior apprehension sign Traction- countertraction
Figure 12. Shoulder maneuvers
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Rotator Cuff Disease

• rotator cuff consists of 4 muscles that act to stabilize the humeral head within the glenoid fossa
Table 9. Rotator Cuff Muscles (SITS )

Muscle Muscle Attachments Nerve Supply Muscle Function
Supraspinatus
Acromion L
\
—
4k
ligament
Coracoid
process
Proximal Distal
Supraspinatus Scapula Greater tuberosity ol Suprascapular nerve Abduction
humerus
Infraspinatus Scapula Greater tuberosity of Suprascapular nerve Eitemal rotation 1-
humerus -
Teres Minor Scapula Greater tuberosity ol Axillary nerve filer nalrotation ASubscapularis I
-
humerus
Subscapularis Scapula lesser tuberosity of Subscapular nerve Internal rotation and Joint capsule
Infraspinatus
humerus adduction capular body j
Teres minor 5
SPECTRUM OF DISEASE: IMPINGEMENT. TENDONITIS, MICRO OR MACRO TEARS
Etiology Figure 13. Lateral view of the

muscles of the rotator cuff
• narrowing of subacromial space
• most commonly due to a relative imbalance of rotator cuff and larger shoulder muscles, allowing for
superior translation and subsequent wear of the rotator cuff muscle tendons
• glenohumeral ( rotator cuff ) muscle weakness leading to abnormal motion of humeral head
scapular muscle weakness leading to abnormal motion of acromion - poor posture Bigliani Classification of Acromion
Morphology
• acromial abnormalities, such as congenital narrow space or osteophyte formation or Type Ill • Type I - flat
acromion morphology • Type II - curved
1. outlet / subacromial impingement: “ painful arc syndrome,” compression of rotator cuff • Type III - hooked
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
Screening Out Rotator Cuff Tears
• No night pain (SN 87.7%)
Clinical Features • No painful arc (SN 97.5%)
• insidious onset, but may present as an acute exacerbation of chronic disease, night pain, and difficulty • No impingement signs (SN 97.2%)
sleeping on affected side • No weakness
Returning to the bedside; Using the
• pain worsens with active motion (especially overhead ); passive movement generally permitted
history and physical examination to
• weakness and loss of ROM , especially between 90-130° (e.g. trouble with overhead activities ) identify rotator cuff tears
• tenderness to palpation over greater tuberosity « -
J Am eeriatr Sac 2m :K33 K37
• rule out bicep tendinosis ( Speed ’s test ) and SLAP lesions ( O' Brien’s test )
Investigations
-
• x ray: AP view may show sclerosis of the undersurface of the acromion or greater tuberosity, high Ruling in Rotator Cuff Tears 98% -
riding humerus relative to glenoid, indicating large tear, evidence of chronic tendonitis probability of rotator cuff tear if all 3 of
• MR1: coronal / sagittal, oblique, and axial orientations are useful for assessing full / partial tears and the following are present:
tendinopathy ± arthrogram : geyser sign ( injected dye leaks out of joint through rotator cuff tear) • Supraspinatus weakness
• arthrogram: not commonly used but can assess full thickness tears, difficult to assess partial tears • External rotation weakness
• Positive impingement sign(s)
• ultrasound: may be a useful adjunct but limited ability to evaluate other intra-articular pathology Diagnosis of rotator cuff tears.
Uriel 2001:357:765-770
Treatment
• non-operative
first line treatment, rotator cuff injury treatment begins with physiotherapy ( regardless of severity
on MR 1 findings ) Does this Patient with Shoulder Faia have Rotator
• physiotherapy, activity modification, non- narcotic analgesia ± steroid injection Cull Disease’ The Rational Clinical Euniaation
• mild or moderate cases frequently improve Systematic Review
• progression to surgery if necessary JAMA 2013:310:837 847-
Study: 5 studies of suficien:gcalty netd ‘ 3
• operative 30-203 shoulders and a peeve e te of ICO ranging
*
severe tear or impingement that is refractory to 2 -3 mo physiotherapy and 1 -2 corticosteroid -

from 33 81%.
injections Results / Condosions: Jmong pan prpvocatio-
arthroscopic or open surgical repair ( i.e. acromioplasty, rotator cuff repair ) tesis, a positive pairfal ait test fad the gaetes:
specificity aid sensitnrty (SP 81%.SI 21%). Amrg
strength tests, a positveeftrael rotetion lag as:
and internal rotation lag as!were the nnstamiraa
fnr fidl-thickness tears $P 47%.SI 94%:SP 92%. rT
SH 83% respectively ). The Menal rotation legtesJ LJ
-
was therefore also the mast accs aa far Meutdywg
patients without a ful-tticksess aar.
A positive drop arm test is helpful to ; dertify patients
with RCD (SN 24%. SP 93 %L
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Table 10. Rotator Cuff Special Tests

Test Examination Positive Test
Jobe's Test (i e.. Empty Can Test) Supraspinatus: place the shoulder in 90’of Weakness with actnre resistance suggests a
adduction and 30’of horizontal flexion (from supraspinatustear
the scapular plane) and internally rotate the
arm so that the thumb is pointing toward
the floor
lift- off Test Subscapularis: internally rotate arm so dorsal Inability to actively lift hand away from back
surface of hand rests on lower back;patient suggests a subscapularis tear
instructed to actively lift hand away from back
against examiner resistance (use Belly Press
Test if too painful)
Posterior-Cuff Test Infraspinatus and teres minor; arm positioned Weakness with active resistance suggests
at patient's side in 90 " of flexion:patient posterior cuff tear
instructed to externally rotate arm against the
resistance of the examiner
fleer's Test Rotator cuff impingement;passive shoulder Pam elicited between 130-170" suggests
flexion impingement
Hawkins -Kennedy Test Rotator cuff impingement: shoulder flexion to Pain with internal rotation suggests
90’and passive internal rotation impingement
Painful Arc Test Rotator cuff tendinopathy: patient instructed Pain with abduction >90’suggests
to actively abduct the shoulder tendinopathy
Speed's Test Apply resistance to the forearm when the arm Pam in the bicipital groove
is in forward flexion with the elbows fully
extended
O'Brien's Test SLAP lesion: forward flexion of the arm to Pain or clicking in the glenohumeral joint in
90’while keeping the arm extended. Arm is internalrotation but not external rotation
adducted 10-15"
Internally rotate the arm so thumb is facing
down and apply a downward force. Repeat the
test with arm externally rotated
\
/
)
Jobe s test Lift- off test Posterior cuff test
2
Neer's test s
r
-
Ur
£
130-170" i
0
Hawkins- Kennedy test I CM
1
Z.
I©
Figure 14. Rotator cuff tests
n
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0R 16 Orthopaedic Surgery Toronto Notes 2023
Acromioclavicular Joint Pathology

•subluxation or dislocation of AC joint
• 2 main ligament groups attach clavicle to scapula: AC and CC ligaments
Pneumothorax or pulmonary contusion
Mechanism are potential complications of severe
clavicle fracture and rarely severe AC
• fall onto shoulder with adducted arm or direct trauma to point of shoulder ( usually fall onto the joint dislocation
posterosuperior aspect of the lateral shoulder )
Clinical Features
• pain with adduction of shoulder and /or palpation over AC joint
• palpable step deformity between distal clavicle and acromion (with dislocation ) i.e. piano key sign
• limited ROM
Investigations
• x - rays: bilateral AP, Zanca view ( 10-15° cephalic tilt ), axillary
Treatment
• non - operative
sling 1 -3 wk, ice, analgesia, early ROM, and rehabilitation
•operative
» indication: Rockwood Class IV-VI ( 111 if labourer or high level athlete)
• number of different approaches involving AC/ CC ligament reconstruction or screw /hook plate
insertion
Table 11. Rockwood Classification of Acromioclavicular Joint Separation

Grade Features Treatment
I Joint sprain, absence of complete tear of either ligament Non - operative
II Complete tear of AC ligament,incomplete tear of CC Non - operative
ligament, without marked elevation of lateral clavicular
head
Complete tear of AC and CC ligaments, >5 mm elevation Most non-operative, operative if labourer or high level
at AC joint, superior aspect of acromion is below the athlete
inferior aspect of the clavicle Will heal with step deformity, although most fully
funcbonalin 4-6 mo
IV -VI Based on the anatomical structure the displaced clavicle Operative in most cases
is in proximity to (posterior,very superior, inferior)
Grade AC Ligament CC Ligament Reducible Treatment
I Sprained Normal N, A -
Non operative
II lorn Sprained Yes Non- operative
III lorn Torn Yes Most non-operative,
operative if labourer or
high-level athlete
Will heal with step
deformity. alLhough most
fully functional in 4- 6 mo
IV - VI lorn Torn No Operative in most cases
Rockwood separations IV- VI are determined based on direction ot displacement
IV: Distal clavicle displaced posteriorly into trapezius (seen on axillary XR)
V: Distal clavicle herniated through dellotrapezial fascia into subcutaneous tissue
VI: Distal davide displaced interior to acromion or coracoid under conjoined tendon (rare)
Opea iedictioi aid litenalFiiati:a vs.

iMsirgical Treataeitii Displaced Midshaft
Clavicle Fracture Qavide Fra dares:A Meta -dialysis
J (top Irac=a 203J2(7)a2)5 -e2!3
Purpose: Compare c.icotes frpn DBF ard »-
• incidence: proximal (5%), middle ( 80% ), or distal ( 15%) third of clavicle eperane treaheeats a ispacednd-shaft dander
• common in children ( unites rapidly without complications) fradires.
Methods Keta aa'ysis ittSKIs reportag
Mechanism .
xpuini toctxuai outcomes, and ssbsegoei:
surgeres pateds older thas K yr.

• fall on shoulder (87% ), direct trauma to clavicle ( 7%), 100SH (6%) Destlts: 9 ia:dp= zed dital trialsniI02) ata
patents iere ".ded. OJLF lasassocated a •
Clinical Features sgahcadly loaer toe ® rate of LTV compared
• pain and tenting of skin
* -
to H 5'« ‘or ae Mt -ope-avre teat ect gtozps (M
• arm is clasped to chest to splint shoulder and prevent movement . .
0.8 95% CL 0.0S-0-31).Fatctozal ooica ces rated
.
by ether DASH or Coestad set res mere s 3 cScact y
better it Olf gp to 6 wo.lies eidodeg elect re
Investigations pate reoovaL de rate ot szbsegsett szrger es«s
• evaluate N VS of entire upper limb sgaScaatly lower i«ie ODD cohort (Aft is. W% .
-
• x ray: AF, 45" cephalic tilt (superior/ inferior displacement ), 45° caudal tilt ( AP displacement ) M 0-36.95% C10.2A-0.5SL
Coidisiots OBf isassocatediisgtocao:
+
• C l : useful for medial physeal fractures and sternoclavicular injury
redochoos « ootswes aadeerier fsscboual
- -
octtoses n dspaced dstaftdatdi fradres.
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Treatment
-
• medial and middle third clavicle fractures
• for nondisplaced fractures, simple sling for I -2 wk pm Associated Injuries with Clavicle
early ROM and strengthening once pain subsides Fractures
» if fracture is shortened >2 cm , consider ORIF • Up to 9% ol clavicle fractures are
-
• distal third clavicle fractures
• undisplaced ( with ligaments intact ): sling for 1-2 wk
associated with other fractures (most
commonly rib fractures)
• Majority of brachial plexus injuries
• displaced (CC ligament injury): ORIF are associated with proximal third
fractures
Specific Complications ( see General Fracture Complications, OR7 )
• cosmetic bump ( most common complication )
• shoulder stiffness, weakness with repetitive activity
• pneumothorax, brachial plexus injuries, and subclavian vessel (all very rare )
Frozen Shoulder (Adhesive Capsulitis)

•disorder characterized by progressive pain and stiffness of the shoulder, usually resolving
spontaneously within 18 mo
Stages of Adhesive Capsulitis
Mechanism 1. Freezing phase: gradual onset, diffuse
pain (lasts 6-9 mo)
•primary adhesive capsulitis 2. Frozen phase: decreased ROM
idiopathic, often associated with DM impacts function (lasts 4-9 mo)
usually resolves spontaneously in 9-18 mo 3. Thawing phase: gradual return of
•secondary adhesive capsulitis motion (lasts 5- 26 mo)
• due to prolonged immobilization
• shoulder- hand syndrome: CRPS/ RSD characterized by arm and shoulder pain, decreased motion ,
and diffuse swelling
• following Ml, stroke, shoulder trauma
• poorer outcomes
Clinical Features ft
• gradual onset ( weeks to months) of diffuse shoulder pain with:
Conditions Associated with an
• decreased active AND passive ROM Increased Incidence of Adhesive
• pain worse at night and often prevents sleeping on affected side Capsulitis
increased stiffness as pain subsides: continues for 6-12 mo after pain has disappeared • Prolonged immobilization (most
significant)
Investigations • Female gender
•x- ray: AP ( neutral, internal/external rotation ), scapular Y, and axillary views of the shoulder • Age >49
• DM (Sx)
may be normal, or may show demineralization from disease • Cervical disc disease
• Hyperthyroidism
Treatment . Stroke
•freezing phase - Ml
maintenance of active and passive ROM (physiotherapy) • Trauma and surgery
• Autoimmune disease
NSAlDs and steroid injections if limited by pain
• thawing phase
aggressive physiotherapy, possible manipulation under anesthesia and early physiotherapy
• arthroscopy for debridement/decompression
Humerus
Proximal Humeral Fracture
Mechanism
• young: high energy trauma (MVC) Necr Classification
• elderly: l 'OOSH from standing height in osteoporotic individuals Based on 4 parts of humerus
• Greater tuberosity
Clinical Features • Lesser tuberosity
• Humeral head
• proximal humeral tenderness, deformity with severe fracture, swelling, painful ROM, bruising - Shaft
extends down arm and chest One- part fracture: any of the 4 parts
• physical exam usually reveals diminished forward elevation, with or without disuse atrophy of deltoid with none displaced n
and periscapular musculature Two-part fracture: any of the 4 parts LJ
with 1displaced
Three-part fracture: displaced fracture
Investigations of surgical neck + displaced greater
• test axillary nerve function (deltoid contraction and skin over deltoid )
-
• x-rays: AP, trans-scapular, and axillary views of the shoulder are essential
• CT’ scan: to evaluate for tuberosity or articular involvement and fracture displacement, and if the
tuberosity or lesser tuberosity
Four-part fracture: displaced fracture
of surgical neck + both tuberosities
+
diagnosis of non - union is unclear
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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 displaced fractures, not the fracture line, in determining
classification
• ± dislocated /subluxed: humeral head dislocated /subluxcd from glenoid
Treatment
• assess for and treat osteoporosis if needed
• non - operative
nondisplaced and minimally displaced (85% of patients): broad arm sling immobilization , begin
ROM within 14 d to prevent stiffness
• most displaced fractures in low-demand elderly patients
• operative
• OR1F (anatomic neck fractures, displaced, associated irreducible glenohumeral joint dislocation )
or 1M nail (surgical neck)
hemiarthroplasty or reverse TSA may be necessary, especially in elderly
minimally invasive percutaneous pinning and intramedullary nail fixation are indicated in rare
instances
Specific Complications ( see General Fracture Complications, OR7 )

• AVN, nerve palsy ( 45%; typically axillary nerve ), malunion , post-traumatic arthritis, persistent pain
and weakness, frozen shoulder 'Greater tuberosity
Lesser tuberosity
Humeral Shaft Fracture v
Mechanism
• young: high energy trauma (direct blows/ M VC ) 11 ' Anatomical neck
• elderly: FOOSH , twisting injuries, mctastascs Surgical neck
Clinical Features t 1
• pain , swelling, weakness ± shortening, motion /crepitus at fracture site .
• must test radial nerve function before and after treatment: look for drop wrist , sensory impairment in ;
dorsum of hand
Investigations
• x- ray: AP and lateral views of the humerus, including the shoulder and elbow joints
Figure 15. Fractures of the proximal
Treatment humerus
• in general, humeral shaft fractures are treated non-operatively
• non -operative
± reduction; can accept deformity due to compensatory ROM of shoulder
hanging cast ( weight of arm in cast provides traction across fracture site) with collar and cuff Acceptable Humeral Shaft Deformities
sling immobilization until swelling subsides, then Sarmiento functional brace, followed by ROM -
for Non Operative Treatment
• <20° anterior angulation
• operative
• <30° varus an gulation
indications: see NO CAST sidebar, OR6 , pathological fracture, “floating elbow” ( simultaneous
unstable humeral and forearm fractures) • <3 cm of shortening
ORIF: plating ( most common ), IM rod insertion, external fixation ( rare )
Specific Complications ( seeGeneral Iracture Complications, OR7)

(§ >
Risk of radial nerve and brachial artery
• failure of functional bracing ( seen in up to 30% of patients)
-
• radial nerve palsy: expect spontaneous recovery in 3 4 mo, otherwise send for EMli Injury
-
• non union: most frequently seen in middle 1 /3
• decreased ROM
• compartment syndrome
Distal Humeral Fracture

The anterior humeral line refers to an
Mechanism imaginary line drawn along the anterior
• young: high energy trauma ( MVC) surface of the humeral cortex that
passes through the middle third of the
• elderly: lower energy falls in patients with osteoporotic bone capitellum when extended interiorly.
In subtle supracondylar fractures, the rT
Clinical Features LJ
anterior humeral line is disrupted,
• elbow pain and swelling typically passing through the anterior
• assess brachial artery (ecchymosis over anteromedial forearm is suggestive of brachial artery injury) third of the capitellum
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Investigations
• x- ray: AP and lateral views of the humerus and elbow
• Cl scan: helpful when suspecting shear fracture of capitulum or trochlea, and for preoperative
planning
• assess NVS: radial, ulnar, and median nerve
Classification
• supracondylar, distal single column, distal bicolumnar, and coronal shear fractures
Treatment
• goal is to restore a functional ROM of at least 30-130° flexion (unsatisfactory outcomes in 25%)
• non-operative ( paediatric patients and elderly patients with medical comorbidities)
cast immobilization ( in supination for lateral condyle fracture; pronation for medial condyle
fractures): short immobilization and early range of motion
• operative
• indications: displaced , supracondylar, bicolumnar
• closed reduction and percutaneous pinning (children ); OKU '; total elbow arthroplasty (complex
bicolumnar in elderly)
adult fractures are almost always treated operatively due to risk of elbow stiffness with non-
operative management
Elbow
Supracondylar Fracture
• subclass of distal humerus fracture: extra-articular, fracture proximal to capitulum and trochlea,
Three Joints at the Elbow
usually transverse Humeroradial joint
• most common in paediatric population ( peak age ~7 yr), rarely seen in adults Humeroulnar joint
• AIN ( median nerve) injury commonly associated with extension type Radioulnar joint
Mechanism
• >96% are extension injuries via 1'OOSH (e.g. fall off monkey bars); <4% are flexion injuries
Normal carrying angle of elbow is ~10°
Clinical Features of valgus
• pain, swelling, point tenderness
• neurovascular injury: median and radial nerves, radial artery Humera
Investigations
-
• x ray: AR and lateral views of the elbow
disruption of anterior humeral line suggests supracondylar fracture
• fat pad sign: a sign of effusion and can be indicative of occult fracture
assess NVS: median and radial nerves, radial artery
Treatment
• non - operative Figure 16. X-ray of transverse
• nondisplaced ( paediatric): closed reduction with long arm plaster slab in 90° flexion x 3 wk displaced supracondylar fracture of
• operative humerus with elbow dislocation
• indications: see NO CAST sidebar , OR6; displaced >50%, vascular injury, open fracture
requires closed reduction plus percutaneous pinning followed by limb cast with elbow flexed <90°
in adults, OK 1F is necessary • i [/Anterior Humeral Line
uv apitellum
m
Specific Complications (see General Fracture Complications, OR7 ) Radio- Capitellar Line
•stiffness is most common
• brachial artery injury ( kinking can occur if displaced fracture), median or ulnar nerve injury, -
*
compartment syndrome ( leads to Volkmann's ischemic contracture ), malalignment cubitus varus
(distal fragment tilted into varus) j
Radial Head
© Oasmond Ballance 2006
Figure 17. Lateral view of elbow

ri
LJ
Capitellum moves posteriorly to the

anterior humeral line in extension type
fractures and anteriorly in fhxion type
+
fractures
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Radial Head Fracture

• a common fracture of the upper limb in young adults (85% occur between 30 60 yr ) -
Mechanism
• FOOSH with elbow extended and forearm pronated Terrible Triad
Radial head fracture
Coronoid fracture
Clinical Features Elbow dislocation
• marked local tenderness on palpation over radial head (lateral elbow)
• decreased ROM at elbow, ± mechanical block to forearm pronation and supination
• pain on pronation /supination
Investigations
• x- ray: AF and lateral views of the elbow
• enlarged anterior fat pad ("sail sign ”) or the presence of a posterior fat pad on lateral view
indicates effusion , which could occur with occult radial head fractures
Table 12. Classification and Treatment of Radial Head Fractures
Mason Class Radiographic Description Treatment
1 Nondisplaced fracture (< 2 mm) -
Elbow slab or sling x 3 5 d with early ROM
Figure 18. Lateral x-ray of elbow with
2 Displaced fracture|>2 mm ) ORIf if: angulation >30", involves >1/3 of Ihe radial head, or if
>3 nun of joint incongruity exists, block to forearm rotation effusion (“sail sign”)
3 Comminuted fracture Radial head excision t prosthesis (if ORIF not feasible)
4 Comminuted fracture with posterior elbow dislocation Radial head ORIF or radial head excision with prosthesis
Treatment To avoid stiffness, do not immobilize

• ORIF remains the gold standard in management -
elbow joint >2 3 wk
• arthroscopic repair can be considered: offers improved visualization and enhances soft tissue
preservation of the joint
Specific Complications (see Genera/ Fracture Complications OR7 ) ,

-
• myositis ossificans calcification of muscle
• recurrent instability ( if MCL injured and radial head excised )
Olecranon Fracture
Mechanism
• direct blow: fall onto point of elbow ( posterior aspect )
• indirect blow: FOOSH (typically transverse/oblique fracture)
Clinical Features
• localized pain, palpable defect
• ± loss of active extension due to avulsion of triceps tendon
Investigations
-
• x ray: AF and lateral ( require true lateral to determine fracture pattern )
Treatment
-
• non operative
• non - displaced (< 2 mm , stable): cast x 2-3 wk (elbow in 90° flexion , often in full elbow extension ),
then gentle ROM
• operative
displaced ± non-intact extensor mechanism
Elbow Dislocation
• third most common joint dislocation after shoulder and patella
• simple: dislocation with no associated features
• complex: dislocation with associate features ( fracture along with anterior capsule and /or collateral
ligaments disrupted )
Mechanism
• elbow hyperextension via FOOSH or valgus/supinalion stress during elbow flexion
• usually the radius and ulna are dislocated together, alternatively the radial head dislocates in isolation
and the ulna is fractured (see Monteggia Fracture, OR 22 )
• 80% are posterior / posterolateral, anterior are rare and usually devastating +
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Clinical Features
• elbow pain, swelling, deformity
• flexion contracture
• ± absent radial or ulnar pulses
Elbow Dislocation
Investigations The radio-capitellar line refers to an
• x- ray: AP and lateral views of the elbow imaginary line along the longitudinal axis
of the radial neck that passes through
• assess N VS: brachial artery, median and ulnar nerves the centre of the capitellum, regardless
of the degree of elbow florion. If the
Treatment -
radio capitellar line does not pass
-
• non operative through Ihe centre of the capitellum a
• closed reduction under conscious sedation ( post - reduction x - rays required ) dislocation should be suspected
• Parvin’s method: patient lies prone with arm hanging down; apply gentle traction downwards on
wrist ; as olecranon slips distallv, gently lift up the arm at elbow to reduce joint
• long-arm splint with forearm in neutral rotation and elbow in 90° flexion
• early ROM (< 2 wk )
• operative
• indications: complex fracture dislocation or persistent instabilitv after closed reduction
• OR1 P
Specific Complications ( see General Fracture Complications UK 7 ) .
• stiffness ( loss of extension ), intra -articular loose body, neurovascular injury ( ulnar nerve, median
nerve, brachial artery), radial head fracture
• recurrent instability uncommon
Epicondylitis
• lateral epicondylitis= “tennis elbow,” inflammation of the common extensor tendon as it inserts into
the lateral epicondyle
• medial epicondylitis = “ golfer’s elbow," inflammation of the common flexor tendon as it inserts into
#
Tennis Elbow = laTeral epicondylitis; pain
associated with extension of wrist
the medial epicondyle
Mechanism
•repeated or sustained contraction of the forearm musdes/chronic overuse
Clinical Features
• point tenderness over humeral epicondyle and /or distal to it over forearm musculature
• pain upon resisted wrist extension (lateral epicondylitis ) or wrist flexion ( medial epicondylitis )
• generally a self-limited condition, but may take 6- 18 mo to resolve
Treatment
• non -operative (vert' good outcomes)
rest, ice, NSAlDs
Elbow Joint Injection
use brace/strap Inject at the centre of the triangle
physiotherapy, stretching, and strengthening formed by the lateral epicondyle, radial
activity modification /ergonomics head , and olecranon
• corticosteroid injection
• operative
-
• indication: failed 6 12 mo conservative therapy
• percutaneous or open release of common tendon from epicondyle
Forearm
Radius and Ulna Shaft Fractures
Mechanism
• high - energy direct or indirect ( MVA, fall from height, sports) trauma
• fractures usually accompanied by displacement due to high energy mechanism
Clinical Features
rT
• deformity, pain, swelling LJ
• loss of function in hand and forearm
Investigations
• x- ray: AP and lateral of forearm ± oblique of elbow and wrist
• CT if fracture is close to joint +
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Treatment
• goal is anatomic reduction since imperfect alignment significantly limits forearm pronation and
supination
• OR IT with plates and screws; closed reduction with immobilization usually yields poor results for
displaced forearm fractures (except in children )
Specific Complications ( seeGeneral Fracture Complications, OR7 )

- compartment syndrome
• soft tissue contracture resulting in limited forearm rotation - surgical release of tissue may be
warranted
Monteggia Fracture
• fracture of the proximal ulna with radial head dislocation and proximal radioulnar joint injury
- more common and better prognosis in the paediatric age group when compared to adults
Mechanism
• direct blow to the posterior aspect of the forearm
• hvperpronation
• fall on the hyperextended elbow Figure 19. Monteggia fracture
Clinical Features
• pain, swelling, decreased rotation of forearm ± palpable lump at the radial head
• ulna angled apex anterior and radial head dislocated anteriorly ( rarely the reverse deformity occurs) In all isolated ulna fractures, assess
proximal radius to rule out a Monteggia
Investigations fracture
• x-ray: AT and lateral views of the elbow, wrist, and forearm
Treatment
• adults ( if stable ): splint and early postoperative ROM if elbow completely stable, otherwise Bado Type Classification of Monteggia
-
immobilization in plaster with elbow flexed for 2 3 wk Fractures
Based on the direction of displacement
• adults ( if unstable ): OR1F of ulna with indirect reduction of radiocapitellar joint in 90% of patients of the dislocated radial head, generally
(open reduction of radiocapitellar joint if unsuccessful ) the same direction astheapexofthe
• paediatrics: attempt closed reduction and immobilization in plaster with elbow flexed for Bado Type ulnar fracture
1-111, surgery for Type IV Type b anterior dislocation of radial
head and proximal/middle third ukiar
fracture (60%)
Specific Complications ( seeGeneral Fracture Complications, OR7 ) Type II: posterior dislocation of radial
• PIN injury: most common nerve injury; observe for 3 mo as most resolve spontaneously head and proximal/middle third ulnar
• radial head instabilitv/ redislocation fracture (15%)
• radioulnar synostosis Type III: lateral dislocation of radial
head and metaphyseal ulnar fracture
(20%)
Nightstick Fracture -
Type IV combined: proximal fracture
of the ulna and radius, dislocation of the
radial head in any direction (<5%)
•isolated fracture of ulna without dislocation of radial head
Mechanism
•direct downward blow to upward block forearm (e.g. holding arm up to protect face)
Treatment
•non-operative
indication: non -displaced
below elbow cast (x 10 d ), followed by forearm brace ( ~8 wk)
•operative
• indication: significantly displaced
ORIT if >50% shaft displacement or >10° angulation
Galeazzi Fracture Figure 20. Nightstick fracture
•fracture of the distal radial shaft with disruption of the DRU|

• most commonly in the distal 1 /3 of radius near junction of metaphysis/diaphysis
For all isolated radius fractures assess
Mechanism DRUJ to rule out a Galeazzi fracture rh
LJ
•FOOSH with axial loading of pronated forearm or direct wrist trauma
•forceful axial loading of radial shaft (e.g. direct trauma to distal 1 /3 of radius ) (§)
Monteggia vs. Galeazzi Fractures
Clinical Features Remember the mnemonic 'MUGGER':
•pain, swelling, deformity, and point tenderness at fracture site Monteggia +
Ulnar fracture
Galeazz
Radial fracture
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Investigations Fracluro ol distal radius

-
• x ray: AP, and lateral views of the elbow, wrist, and forearm
shortening of distal radius > 5 mm relative to the distal ulna
• widening of the OKU ) space on AP
• dislocation of radius with respect to ulna on true lateral
Treatment
• all cases are operative ( “ fracture of necessity")
OR1P of radius; afterwards, assess DRU|stability by balloting distal ulna relative to distal radius
if DRU ) is stable and reduced, splint for 10-14 d with early ROM encouraged
if DRU ) is unstable, OR1P or percutaneous pinning with long arm cast in supination x 2-3 wk
Wrist Dislocation of ulna

Figure 21. Galeazzi fracture
Colles’ Fracture
Indications for Direct Surgical
• extra -articular transverse distal radius fracture ( ~2 cm proximal to the radiocarpal joint ) with dorsal Management of Codes' Fracture
displacement ± ulnar styloid fracture • Displaced intra - articular fracture
• most common fracture in those > 40 yr, especially in women and those with osteoporotic bone • Comminuted
• Severe osteoporosis
• Dorsal angulation >5‘ or volar tilt
Mechanism >20"
. KOOSH • >5 mm radlal shortening
Clinical Features
• “dinner fork " deformity
• swelling, ecchymosis, tenderness Features of Inadequate Closed
Reduction that Require ORIF
Investigations -- Radial shortening >3 mm or
Dorsal tilt >10“ or
• x- ray: AP and lateral ± oblique views of wrist - Intra- articular displacement/step-off
>2 mm
Treatment
• goal is to restore radial height (13 mm), radial inclination (22°), volar tilt (11°), as well as DRU )
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: traction with extension (exaggerate injury ); traction with ulnar deviation ,
-
pronation , flexion ( of distal fragment not at wrist )
• dorsal
- -
slab/ below elbow cast for 5 6 wk
obtain post reduction Aims immediately; repeat reduction if necessary Lateral View
-
• x ray at 1 wk, 3 wk, and at cessation of immobilization to ensure reduction is maintained
operative
•
indication: failed closed reduction, or loss of reduction
percutaneous pinning, external fixation, or ORIF
Smith’s Fracture
• volar displacement of the distal radius (i.e. reverse Colies’ fracture)
AP View
Mechanism 1. Dorsal tilt
2. Dorsal displacement
• fall onto the back of the flexed hand 3. Radial shortening
4. Ulnar stylold fracture
Investigations 5 Radial tilt
• x- ray: AP and lateral ± oblique views of wrist 6. Radial displacement
Treatment Figure 22. Colles’ fracture and

associated bony deformity
• if non - displaced / stable: closed reduction and splinting in wrist extension with hematoma or regional
nerve block; long arm cast in supination x6 wk
• if displaced / unstable: ORIF
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Complications of Wrist Fractures

• most common complications are poor grip strength, stiffness, and radial shortening
• distal radius fractures in individuals < 40 yr of age are frequently high energy/comminuted and are
more likely to require ORU' -
• % have normal function in 6-12 mo
80
.
Table 13 Early and Late Complications of Wrist Fractures
Early Late
Difficult reduction t loss ol reduction Malunion, radial shortening
Compartment syndrome Painful wrist secondary to ulnar prominence
Extensor pollicis longus tendon rupture -
Froren shoulder (“shoulder hand syndrome")
Acute carpal tunnel syndrome -
Post traumatic arthritis AP view
Finger swelling with venous block Carpal tunnel syndrome
Complications ot a tight cast/ splinl CRPS/ RSD A. Radial inclination
B. Radial length
Scaphoid Fracture
Epidemiology
• most common carpal bone injured
• common in young men; not common in children or in patients beyond middle age
.
• may be associated with other carpal or wrist injuries (e g. Colies’ fracture)
Mechanism
• FOOSH : impaction of scaphoid on distal radius, most commonly resulting in a transverse fracture
through the waist (65%), distal (10%), or proximal ( 25%) scaphoid Lateral view
Clinical Features .
C Volar tilt
• pain with resisted pronation Effect ol Colics’ Iracturo 1
• tenderness in the anatomical “snuffbox”, over scaphoid tubercle, and pain with long axis compression on distal radius o
into scaphoid
• usually nondisplaced .
Figure 23 Normal wrist angles *
wrist angles in Codes’ fracture
Investigations Note the relative shortening of the
-
• x ray: AP, lateral, and scaphoid views with wrist extension and ulnar deviation
• ± Q’ or MRI: detect occult fracture and prevent AVN
radius relative to the ulna on AP
view in Codes’ fracture
• bone scan rarely used
• note: a fracture may not be radiologically evident up to 2 wk after acute injury, so if a patient
complains of wrist pain and has anatomical snuffbox tenderness but a negative x ray, treat as
-
- -
if positive for a scaphoid fracture and repeat x ray 2 wk later to rule out a fracture: if x ray still
Scaphoid Fracture Special Tests
Tender snuff box: 100% sensitivity, but
negative, order CT or M R1 29% specific, as it is also positive with
many other injuries of radial aspect of
Treatment wrist with FOOSH
• early treatment critical for improving outcomes
• non -operative
• non - displaced (< 1 mm displacement / 5° angulation ): long-arm thumb spica cast x 4 wk, then
^
short arm cast until radiographic evidence of healing is seen ( 2 3 mo) - The proximal pole of the scaphoid
• operative receives as much as 100% of its arterial
blood supply from the radial artery that
• displaced: OR It with headless/countersink compression screw is the mainstay treatment enters at the distal pole. A fracture
through the proximal third disrupts
Specific Complications (seeGeneral Fracture Complications, OR7 ) this blood supply and results In a high
• most common: nonunion /malunion ( use bone graft from iliac crest or distal radius with fixation to incidence of AVN/nonunion
heal )
• AVN of the proximal fragment
• delayed union ( recommend surgical fixation )
• scaphoid nonunion advanced collapse (SNAC) - chronic nonunion leading to advanced collapse and
arthritis of wrist
Prognosis
• proximal pole: proximal fifth fracture, AVN rate 100%; proximal third fracture: AVN rate 33%
• waist: middle of the scaphoid fractures have healing rates of 80 -90%
• distal pole: distal third fractures have healing rates close to 100% n
LJ
.
Figure 24 ORIF left scaphoid
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Hand Ulna Radius
• sec Plastic Surperv. PL 24 Lunate 'Scaphoid

Trapezium
Triquetrum •Trapezoid
Spine Pisiform ^ ** Capitate

Hamate ^ 3
Spinous
; n
process Metacarpal
Lamina -
. 1
-
bones ( 1 5)
Transverse
process
Pedicle Neural arch
u- Superior u © Hisheva Merci
articular
process
Figure 25. Carpal bones
1/
V- •
V- iVertebral '
y
/ Order of Carpal Bones
body Pedicli Transverse .
So Long To Pinky Here Comes The
-1M
•
- - - r i: Thumb
ir Proximal Row: Scaphoid . Lunate .
Triquetrum. Pisiform ( Lateral to Medial)
Vertebral
foramen Distal Row: Hamate. Capitate.
8 .
Trapezoid Trapezium ( Medial to Lateral )
Inferior Spinous Vertebral
articular process body
s
' .
process *
J
1
a.
Left Lateral View Superior View
Figure 27. Schematic diagram of vertebral anatomy
Adapted fron: Moore KL Agi.r AMR. Essential Clinical Anatomy, 3rd ed . Philadelphia: Lippincott Williams and Wilkins. 2007. p274
Fractures of the Spine

• see Neurosurgery. NS 39
Compression
Cervical Spine
General Principles
• Cl (atlas): no vertebral body, no spinous process
• C2 (axis): odontoid = dens
• 7 cervical vertebrae; 8 cervical nerve roots
• nerve root exits above vertebra ( i .e. C4 nerve root exits above C 4 vertebra ), C8 nerve root exits below
C7 vertebra
• radiculopathy = impingement of nerve root Burst
• myelopathy = impingement of spinal cord
Special Testing
• compression test: pressure on head worsens radicular pain
• distraction test: traction on head relieves radicular symptoms
• Valsalva test: Valsalva maneuver increases intrathecal pressure and causes radicular pain
• Lhermitte Sign: electric shock sensation radiating to back upon forward flexion of the neck, some
etiologies include multiple sclerosis, cervical myelopathy, and B 12 deficiency
• occiput-wall distance ( OW' D ): patient stands against a wall with erect posture and distance between
the occiput and the wall is measured, value greater than 2 cm is abnormal, indicative of thoracic Fracture- dislocation
hyper-kvphosis Figure 26. Compression, burst, and
dislocation fractures of the spine
Table 14 . Cervical Radiculopathy/Neuropathy
Root C5 C6 a C8
Motor Deltoid Biceps triceps Interossei
Biceps Brachioradialis Wrist flexion Digital flexors
Wrist extension Finger extension
Sensory Axillary nerve (patch over thumb Index and middle finger Bing and little finger
lateral deltoid )
Reflex Biceps Biceps triceps Finger jerk
Brachioradialis
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X- Rays for C-Spine

• AP spine: alignment
• AP odontoid: atlantoaxial articulation
• lateral
vertebral alignment: posterior vertebral bodies should be aligned ( translation >3.5 mm is
abnormal )
• angulation: between adjacent vertebral bodies (> 11° is abnormal )
disc or facet joint widening
anterior soft tissue space (at C3 should be S3 mm: at C4 should be <8 10 mm ) -
• oblique: evaluate pedicles and intervertebral foramen
• ± swimmer’s view: lateral view with arm abducted 180“ to evaluate C7-T1 junction if lateral view is
inadequate
• ± lateral flexion /extension view: evaluate subluxation of cervical vertebrae
Differential Diagnosis of C- Spine Pain

• neck muscle strain, cervical spondylosis, cervical stenosis, RA (spondylitis), traumatic injury,
whiplash , myofascial pain syndrome, acute discogenic nerve root entrapment, infection , fracture,
neoplasm , pain from soft tissue structure
C- SPINE INJURY
.
• see Neurosurgery NS38
Thoracolumbar Spine
General Principles
• spinal cord terminates at conus medullaris ( Ll /2)
..
• individual nerve roots exit below pedicle of vertebra ( i e L 4 nerve root exits below L4 pedicle)
Special Tests
-
• straight leg raise: passive lifting of leg ( 30 70“ ) reproduces radicular symptoms of pain radiating down
posterior/ lateral leg to knee ± into foot
• Lasegue maneuver: dorsillexion of foot during straight leg raise makes symptoms worse, or if leg is
less elevated , dorsillexion will bring on symptoms
.
• femoral stretch test: with patient prone Hexing the knee of the affected side and passively extending
the hip results in radicular symptoms of unilateral pain in anterior thigh
Table 15. Lumbar Radiculopathy/Neuropathy

Root L4 L5 S1
Motor Ouadnceps ( knee extension hip Extensor hallucis longus Peroneus longus brevis (ankle eversion )
adduction) Gluteus medlus (hip abduction) Gastrocnemius soleus ( plantar (lesion )
Tibialis anterior (ankle Inversion •
dorsillexion )
Sensory Medial malleolus 1st dorsal webspace and lateral leg lateral foot
Screening Test Squat and rise Heel walking Walking on toes
Reflex Knee (patellar ) Medial hamstring* Ankle (Achilles)
Test Femoral stretch Straight leg raise Straight leg raise
Differential Diagnosis of Back Pain

1. mechanical or nerve compression (>90%)
• degenerative (disc, facet, ligament )
• nerve root compression (e.g. disc herniation )
spinal stenosis (congenital, osteophyte, central disc)
2. others (<10%)
• neoplastic (primary, metastatic, multiple myeloma)
• infectious (osteomyelitis, TB)
• metabolic (osteoporosis)
traumatic fracture (compression, distraction, translation, rotation )
• spondyloarthropathies (ankylosing spondylitis)
referred (aorta, renal, ureter, pancreas)
DEGENERATIVE DISC DISEASE

• loss of vertebral disc height with age resulting in:
n
bulging and tears of annulus fibrosus c j
change in alignment of facet joints
osteophyte formation
Mechanism
• compression and dehydration of disc material over time with age
+
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Clinical Features
• axial back pain
• pain worse with axial loading and flexion
• negative straight leg raise
Investigations
• x-ray, MRI, provocative discography
• imaging only indicated if symptoms persist greater than 6 wk or if red flag symptoms are present
Treatment
• non-operative
• staying active with modified activity
back strengthening
• NSAlDs
do NOT treat with opioids; no proven efficacy of spinal traction or manipulation
• operative - rarely indicated
decompression ± fusion ( in cases of severe or progressive neurological deficit; refractory cases
with impaired quality of life)
SPINAL STENOSIS
• narrowing of spinal canal
• congenital (idiopathic, osteopetrosis, achondroplasia) or acquired (degenerative, iatrogenic - post
spinal surgery, ankylosing spondylosis, Paget's disease, trauma )
Clinical Features
• ± bilateral back and leg pain
• neurogenic claudication
• ± motor weakness
Investigations
• CT/MR1 reveals narrowing of spinal canal
Treatment
• non -operative
physiotherapy ( flexion exercises, stretch /strength exercises), NSAlDs, lumbar epidural steroids
* operative
indication: non-operative failure > 6 mo
decompressive surgery
Table 16. Differentiating Claudication
Neurogenic Vascular
Aggravation With slandinglwalking Walking/exercise (reproducible)
Walking distance variable
Alleviation .
Change in position (usually flexion sitting. Stop walkingleaercise
lying down)
Time Relief in "10 min -
Relief in 2 min
MECHANICAL BACK PAIN

• back dominant pain that does not involve nerve impingement i
Clinical Features Cauda equina syndrome and ruptured

• dull backache aggravated by activity and prolonged standing (or sitting, depending on cause and aortic aneurysms are causes of low
pathology') back pain that are considered surgical
emergencies
• morning stiffness (e.g. if facet OA)
• no neurological signs
Treatment Disc Prolapse

Annulus librusjs
• symptomatic (analgesics, physiotherapy, weight loss, and exercise program )
-
• prognosis: symptoms may resolve in 4 6 wk, others become chronic \ Nucleus
NYpulposus
LUMBAR DISC HERNIATION

• tear in annulus fibrosus allows protrusion of nucleus pulposus, causing either a central, posterolateral,
'// //1 root
Nerve
or lateral disc herniation, most commonly at L5-S1 > L4-5 > L3-4
• M:F=3:1 ,1£ ri
LJ
• only 5% become symptomatic
• usually a history of flexion -type injury |
Vertebra
Clinical Features +
• back dominant pain (central herniation ) or leg dominant pain (lateral herniation )
• tenderness between spinous processes at affected level Figure 28. Disc herniation causing
• muscle spasm i loss of normal lumbar lordosis nerve root compression
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OR2 H Orthopaedic Surgery Toronto Notes 2023
• neurological disturbance is segmental and varies with level of central herniation

• motor weakness ( L 4, L5, SI )
• diminished rellexes ( 1.4 , SI ) Neurogenic claudication Is position
• diminished sensation ( 1.4 , L5, SI ) dependent; vascular claudication is
• positive straight leg raise exercise dependent
• positive contralateral SLU
• positive Lasegue and Bowstring sign
• cauda equina syndrome ( present in l - 10%): surgical emergency
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
Treatment
MRI abnormalities (e.g. spinal stenosis,
• non - operative
disc herniation) are quite common in
symptomatic both asymptomatic and symptomatic
extension protocol physiotherapy program individuals and are not necessarily
NSAlDs an indication for intervention without
• operative clinical correlation
• 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
Table 17. Types of Low Back Pain

Mechanical Back Pain Direct Nerve Root Compression Red Flags for
Disc Origin Facet Origin Spinal Stenosis Root Compression
BACK PAIN
Pain Dominance Back Back Leg Leg Bowel or bladder dysfunction
Aggravation Flexion Extension, standing, Exercise, extension, flexion Anesthesia (saddle)
walking v/ al king, standing Constitutional symptoms/malignancy
Khronic disease
Onset Gradual More sudden Congenital or acquired Acute leg t back pain
Paresthesias
Duration Long ( weeks, months) Shorter (days, v/ eeks) Acute or chronichistory Constant and severe pain, Age >50 yr
( weeks to months) lasting weeks) IV drug use
Neuromotor deficits
Treatment Relief of strain, Relief of strain, Belief of strain, Relief of strain,
physiotherapy and physiotherapy and physiotherapy ( flexion physiotherapy ( extension
exercise, weighlloss. exercise, weighlloss. back program), surgical back program for disc
NSAlDs, acetaminophen .
NSAlDs acetaminophen decompression if herniation), surgical
progressive or severe decompression il
.
deficit NSAlDs. progressive or severe Sciatica
acetaminophen .
delieit NSAlDs. • Most common symptom of
acetaminophen radiculopathy ( L4 - S3)
• Log dominant , constant , burning pain
• Pain radiates down leg i foot
Back Pain • Most common cause - disc herniation
*
Back Dominant Ley Dominant
Constant
Inflammatory
Mechanical
*
Intermittent
T
T
Constant
Disc Herniation ( lateral)
Intermittent
Spinal Stenosis
Disc Herniation ( central) Facet Joint
Figure 29. Approach to back pain

.-
f K
i
SPONDYLOLYSIS
[Spondylolysis
Definition
• defect in the pars interarticularis with no movement of the vertebral bodies ,
Mechanism h
• trauma; gymnasts, weightlifters, backpackers, loggers, labourers t

Spondylolisthesis
( anterioi displacement )
Clinical Features .
f*
-
• activity related back pain , pain with unilateral extension ( Michelis " test ) 8
:
V) a
Investigations
• oblique x- ray; “collar ” break in the “Scottie dog’s" neck V 1
y
+
• bone scan
Figure 30. Spondylolysis,
• CTscan Spondylolisthesis
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Treatment
• non -operative Superior articular
activity restriction, brace, stretching exercise process (ear) Fracture
> I
ADULT ISTHMIC SPONDYLOLISTHESIS
Definition 1 * v
A
f
' ^
• defect in pars interarticularis causing a forward translation or slippage of one vertebra on another,
-
usually at L5 S1, less commonly at L4 5 - Transverse Inferior articular
Mechanism process (nose ) process
Eg
• degenerative (adults), traumatic, pathological, teratogenic
Figure 31. “Scottie dog ” fracture
Clinical Features
• lower back pain radiating to buttocks relieved with sitting
• neurogenic claudication
• L5 radiculopathy
• Meyerding Classification ( percentage of slip)
Investigations
- -
• x ray ( AP, lateral, oblique flexion extension views), MRI
Treatment
• non -operative
activity restriction , bracing, NSAIDs
• operative
Table 18. Classification and Treatment of Spondylolisthesis
Class Percentage of Slip Treatment
1 0- 25\ Symptomatic operative lesion only lor intractable pain
2 2S SO Same ns above
3 sore Decompression lor spondylolisthesis end spinal fusion
4 re -ioo Same as above
s 100
» Same as above
• may present as cauda equina syndrome due to roots being stretched over the edge of L5 or sacrum
Pelvis
Pelvic Fracture
Mechanism
• young: high energy trauma, either direct or by force transmitted longitudinally through the femur
• elderly: low energy trauma, fall from standing height
• lateral compression , vertical shear, or anteroposterior compression fractures
Clinical Features -Anterior
column
• pain, inability to bear weight
• local swelling, tenderness -
Posterior pr. i
• abnormal lower extremity positioning: external rotation of one or both extremities, limb-length column S
discrepancy 3.
• pelvic instability
A
V
Investigations ©
• x-ray: AP pelvis, inlet and outlet views, ) udet views (visualizes obturator and iliac oblique when Figure 32. Pelvic columns
acetabular fracture suspected )
6 cardinal radiographic landmarks of the acetabulum: ilioischial line, iliopectineal line, teardrop,
weight bearing roof, posterior rim, anterior rim
CT scan useful for evaluating posterior pelvic injury and acetabular fracture (if stable) n
i j
may see contrast blush (indicating active bleeding )
• assess genitourinary injury (rectal exam, vaginal exam, hematuria, blood at urethral meatus)
if involved, the fracture is considered an open fracture
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Classification
Table 19. Tile Classification of Pelvic Fractures Possible Radiological Findings

Type Stability Description • Pubic rami fractures: superior/inferior
A Rotationally stable A1: fracture not involving pelvic ring|i.e. avulsion or iliac wing fracture) • Pubic symphysis diastasis_ : common
in AP compression (N 5 mm)
Vertically stable A 2: minimally displaced fracture of pelvic ring je.g. ramus fracture)
A3: transverse sacral or coccygeal fracture • Sacral fractures: common in lateral
compression
6 Rotationally unstable B1: open book (external rotation ) • SI joint diastasis: common in AP
Vertically stable -
62: lateral compression ipsilateral
62 1: with anterior ring rolation/displacemenl through ipsilateral rami
compression (N M mm)
*
• Disrupted anterior column

- -
62 2: with anterior ring rolation/ displacemenl through non ipsilateral rami (bucket handle ) (iliopectineal line) or posterior
63: bilateral column (ilioischial line)
C Rotationally unstable Cl: unilateral • “Teardrop" displacement: acetabular
fracture
Vertically unstable -
C1 1: iliac fracture
-- -
C1 2: sacroiliac fracture dislocation
C1 3: sacral fracture
• Iliac, ischial avulsion fractures
• Displacement of the major fragment
C2: bilateral with 1 side type 8 and 1 side type C superior (VS), open book (APC).
C3: bilateral both sides type C bucket handle (LC)
Treatment
• ABCDEs
• emergency management
IV fluids/ blood
pelvic binder/sheet
± pre- peritoneal packing
externa ] fixation vs. emergent angiography/embolization
± laparotomy ( if EAST/ DHL positive)
• non - operative treatment: protected \VB
indication: stable fracture (e.g. elderly patient with fracture sustained in fall from standing ) Stable avulsion fracture
• operative treatment: OKIE
• indications
unstable pelvic ring injury
symphysis diastasis > 2.5 cm
open fracture
Specific Complications ( see General Fracture Complications, 0 R7 )

• hemorrhage ( life - threatening)
• injury to rectum or urogenital structures
• obstetrical difficulties, sexual and voiding dysfunctions Open book fracture
• persistent SI joint pain
-
• post traumatic arthritis of the hip with acetabular fractures
• high - risk of DVT/ PE
Hip
Hip Dislocation Typo C
Unstable vertical fracture
-
• full trauma survey (see Emergency Medicine. Patient Asscssmcnt/ Managemcnt, FR 2 ) Figure 33. Tile classification of pelvic
•examine for neurovascular injury prior to open or closed reduction fractures
• high index of suspicion for associated injuries
• 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 post-
reduction
-
•see Hip Dislocation Post Total Hip Arthroplasty, OR32 Up to 50% of patients with hip
dislocations suffer fractures elsewhere
ANTERIOR HIP DISLOCATION at the time of injury
• mechanism : posteriorly directed axial loading of the femur with hip widely abducted and externally
rotated 3. External rotation
•classified into inferior ( flexion , abduction, external rotation ) and superior (extension and external 2. Internal rotation
rotation )
•clinical features: shortened, abducted , externally rotated limb
• treatment
!raction
t ri
LJ
closed reduction under conscious sedation /GA , v
post- reduction Cl to assess joint congruity
© Janet SM Chan 2009
Figure 34. Rochester method

+
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POSTERIOR HIP DISLOCATION

• most frequent type of hip dislocation (90%)
• mechanism: severe axial load to knee with hip flexed and adducted
• e.g. knee into dashboard in MVC
• clinical features: shortened, adducted, internally rotated limb
• x- ray: affected femoral head will appear smaller than unaffected femoral head
-
• Thompson and Hpstein classification posterior dislocation:
I - with no or minor posterior acetabular wall fracture
II - with large posterior acetabular wall fracture
III - with comminuted acetabular fracture
IV - with acetabular floor fracture
V - with fracture of femoral head
• treatment
• closed reduction under conscious sedation / GA only if no associated femoral neck fracture or
ipsilateral displacement
• GRIT if unstable, intra-articular fragments, or significant displacement
post- reduct ion CT to assess joint congruity and fractures
COMPLICATIONS FOR ALL HIP DISLOCATIONS

• post-traumatic OA
• AVN of femoral head
• associated fractures (e.g. femoral head , neck, or shaft )
• sciatic nerve palsy in 25% (10% permanent )
• HO
• thromboembolism - DVT / PH
Hip Fracture
General Features
• acute onset of hip pain after a fall
• unable to weight-bear
• shortened and externally- rotated leg X- Ray Features of Subcapital Hip
Fractures
• painful ROM • 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
-
120 130")
IF DVT Prophylaxis in Hip Fractures

- LMWH (i.e. enoxaparin 40 mg SC once
-
-
daily ), fondaparinux, low dose heparin
Cl
Normal joint Subcapital fracture Intertrochanteric Subtrochanteric m on admission, do not give <12 h before
fracture 0 surgery
fracture
Source: UptoDat •Prevention ol venous
*
Ihrcmbcefnbcfam in adult orthopedic surgical pitienb.
Figure 35. Subcapital, intertrochanteric , and subtrochanteric hip fractures tnouparin (IOYHMM) US FIX approved product
information https. vswrv.jccesvdatj rdi.gcrdrwgvatldj
.
1
,
Table 20. Overview of Hip Fractures do(vilat>ei/20 T7D 20164s110IM.pdl
Fracture Type Definition Mechanism Investigations Treatment Complications

Femoral Neck Intracapsulat Young: MVC, fall from X- Ray: AP hip , AP .
See table 21 OH 32 DV1. non - union. AVN.
( Subcapital) height pelvis, cross fable dislocation
Elderly: fall from lateral hip AVN of Femoral Head
standing , rotational
• Distal to proximal blood supply along
force femoral neck to head (medial and
Intertrochanteric Exlracapsular fracture Same as femoral neck X - Ray: AP hip , AP Closed reduction OVT. varus lateral femoral circumflex arteries)
Stable: intact between the greater fracture pelvis, cross table under lluoroscopy displacement ol • Susceptible to AVN If blood supply
posteromedial cortex and lesser trochanters Oirect or indirect lateral hip then dynamic Inp proximal fragment , disrupted
Unstable: non - inlacl and transitional bone force transmitted to screw or IM nail malrotation , non - • Etiology: femoral neck fracture,
posteromedial cortex between the neck the intertrochanteric union, failure of chronic systemic steroid use, SCFE.
and shall area fixation device Legg-Calvd- Perthes. SLE, RA
Subtrochanteric Fracture begins at Young: high energy X- Ray: AP pelvis. API Closed/ open Malalignment,
or below the lesser trauma lateral hip and lemur reduction under nonunion, wound
trochanter and Elderly : osleopenic fluoroscopy, then infection
involves the proximal bone * fall, IM nail
femoral shaft pathological fracture
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Table 21. Garden Classification of Femoral Neck Fractures

Type Displacement Extent Alignment Trabeculae Treatment
Comparative Effectiveness of Pain Management
I None "Incomplete" Valgus or neutral Disrupted Internal fixation to prevent displacement Interventions for Hip Fracture:A Systematic
(valgus impacted fracture) He view
II None Complete Neutral Aligned Internal fixation to prevent displacement -
Ann Intern Med 20l1;155( 4): 234 245
Study: Randoniied contro-ed trials|BCIs|:
III Partial Complete Varus Disrupted Young: ORIF
.
Elderly: hemi ‘ total hip arthroplasty
-
nonrandoniied controlled trials|non tCIs|: and
cohort studies of pain management techniques in
IV Complete Young:ORIF older adults afteracute hip fracture.
Complete Varus Disrupted
.
Elderly: hemi- 'total hip arthroplasty Conclusions: Nerve blockade seems to be effective
i reducing acute pam after hip fracture. Low - level
evidence suggests that preoperabve traction does not
reduce acute pain. Evidence was insufTicent on the
benefits and harms of many other interventions.
Figure 36. Garden classification of femoral neck fractures
Arthritis of the Hip

Etiology
-
• OA, inflammatory arthritis, post traumatic arthritis, late effects of congenital hip disorders, or septic
arthritis
Clinical Features
• OA: pain ( groin , medial thigh ) and stiffness aggravated by activity, relieved with rest
• inflammatory RA: joint pain, morning stiffness >1 h , multiple joint swelling, hand nodules
• decreased ROM ( internal rotation is usually lost first )
• crepitus
• leg length discrepancy (secondary to loss of cartilage and /or bone in affected joint)
• ± fixed flexion contracture leading to apparent limb shortening ( Thomas test )
• ± Trendelenburg sign and /or gait ( limp)
Investigations
• x- ray: W B views of affected joint
.
OA findings - LOSS: Loss of joint space Osteophytes, Subchondral sclerosis, Subchondral cysts
inflammatory (e.g. RA ): osteopenia, periarticular erosions, concentric joint space narrowing
• blood work: ANA, RF
Treatment
• non -operative
-
• weight loss, activity modification, physiotherapy, analgesics, anti inflammatory medications,
walking aids
• operative
• indication : advanced disease with symptoms significantly affecting quality of life
realign = osteotomy; replace = arthroplasty", fuse = arthrodesis
• complications with arthroplasty: component loosening, dislocation . HO, thromboembolism,
infection, neurovascular injury, limb length discrepancy, persistent limp, periprosthetic fracture
• arthroplastv is standard of care in most patients with hip arthritis
Hip Dislocation Post-Total Hip Arthroplasty

-
• occurs in 1-4% of primary1HA and 10 16% of revision THAs
• common indication for early revision
rn
• risk factors: post- traumatic arthritis, revision surgery, substance use, cognitive impairment LJ
(dementia ), spastic or neuromuscular disease, posterior surgical approach , spinal fusion
Mechanism
• flexion , adduction, and internal rotation ( posterior dislocation ), or extension and external rotation
(anterior dislocation ) +
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Investigations
-
• x ray: AP pelvis, AP and lateral views of the hip
DVT Prophylaxis in Elective THA
Treatment -
(continue 10 35 d postoperative)
-
• non operative OOACs (e.g. rlvaroxaban ), ASA,
(ondaparinux, low molecular weight
• closed reduction and immobilization heparin, or warfarin
• operative
indication : recurrent dislocations, associated polyethylene wear, malalignment, hardware failure,
or infection
revision THA
infected hip (infection can cause hip instability)
Complications
• sciatic nerve palsy in 25% (10% permanent)
• HO
• infection
Femur
Femoral Diaphysis Fracture
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 trauma (spiral fracture )
-
always consider the possibility of non accidental trauma (child abuse )
Clinical Features
• shortened, externally rotated leg ( if fracture displaced )
• inability to weight-bear
• often open injury, always a Gustilo Ill (see Table 6 , OR 10 )
• Winquist and Hansen classification
Investigations
It is important to rule out ipsilateral
• x-ray: AP pelvis, AP, and lateral views of the hip, femur, knee femoral neck fracture, as they occur in
Treatment -
2 6% of femoral diaphysis fractures and
-
are reportedly missed in 19 31% of cases
• non -operative ( paediatric, uncommon in adults)
possible indication: non -displaced femoral shaft fractures in patients with significant
-
comorbidities who are non ambulatory
-
most femoral shaft fractures require fixation as this is a life threatening injury
• operative
OKI!' with anterograde IM nail ( most common ) or retrograde IM nail or with plate and screw
fixation
• external fixation may be used initially (e.g. unstable patients or polytrauma patients )
early mobilization and strengthening
Complications
• blood loss
• infection
• fat embolism leading to ARDS
• VTE
• malrotation, leg length discrepancy
• malunion/ nonunion
Associated Injuries
• extensive soft tissue damage
-
.
• ipsilateral hip dislocation / fracture ( 2 6%)
nerve injury
ri
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Distal Femoral Fracture

• fractures from articular surface to 5 cm above metaphyseal flare
Mechanism
• direct high energy force or axial loading ( may occur due to fall from standing in osteoporotic patients )
• three types: extra articular, partial articular, complete articular
Clinical Features Supracondylar Condylar
• extreme pain worse with knee motion
• knee effusion ( hemarthrosis)
• neurovascular deficits can occur with displaced fracture
Investigations
-
• x ray: AP and lateral views
• AB1 if diminished pulses or concern for vascular injury, angiography ( AB1 <0.9)
12'
• CT: to evaluate the articular surface and degree of comminution

Treatment Intercondylar
• non -operative (uncommon ) Figure 37. Distal femoral fractures
indication: non -displaced extra-articular fracture, poor surgical candidate
hinged knee brace
• operative
indication: displaced fracture, intra-articular fracture
« ORIT with plate or retrograde 1M nail fixation
• knee arthroplasty with distal femoral replacement prosthesis (elderly, low demand patient with
comminuted fracture)
•early mobilization
Specific Complications (see General Fracture Complications, OR7)
1. Posterior horn of lateral meniscus
• vascular injury 2. Anterior horn of lateral meniscus i
• nerve injury 3. PCL
• angular deformities/ malunion 4. ACL
• post-traumatic arthritis 5. Posterior horn of medial meniscusijL
6. Anterior horn of medial meniscus 0
^
Figure 38. Diagram of the right tibial
Knee plateau
Evaluation of Knee
Patellar
tendon . mtv Proximal patellar
Patella .
<
Common Complaints
• locking, instability, and swelling ACL 'CL
• -
suggests intra articular pathology such as a torn meniscus or cruciate ligament injury
-
• pseudo locking: limited ROM without mechanical block lateral
meniscus
N
hal
lomscus
• muscle spasm after injury, arthritis
• painful , audible clicking
LCL
• torn meniscus, cartilage injury, or floating body
U sta
patellar
Special Tests of the Knee iDMment ICl
• anterior and posterior drawer tests ( Figure 40, OR 35 ) 'c .- ul
C lrrm Stamshavikaya 2012 j
• demonstrates torn ACL and PCL, respectively Figure 39. Knee ligament and
• knee flexed at 90°, foot immobilized, hamstrings relaxed anatomy
anterior subluxation of the tibia (anterior drawer test ), suggests ACL injury
posterior subluxation of the tibia ( posterior drawer test ), suggests PCL injury
anterior drawer test for ACL: 3.8 positive likelihood ratio, 0.30 negative likelihood ratio
posterior drawer test for PCL: 16.2 positive likelihood ratio, 0.2 negative likelihood ratio
6 Degrees of Freedom of the Knee
• Lachman test
• Flexion and extension
• demonstrates tom ACL • External and internal rotation
hold knee in 20-30° flexion, stabilizing the distal femur with one hand • Varus and valgus angulation
• with contralateral hand, attempt to sublux tibia anteriorly on femur
similar to anterior drawer test, more reliable due to less muscular stabilization ..
• Anterior and posterior glide
Medial and lateral shift
Compression and distraction
n
for ACL: 25.0 positive likelihood ratio, 0.1 negative likelihood ratio LJ
• pivot shift sign
• demonstrates tom ACL
start with the knee in extension
• requires relaxed patient, best performed in patient under spinal or general anesthesia
internally rotate foot, slowly flex knee while palpating and applying a valgus force
On physical exam of the knee, do not
forget to evaluate the hip
+
• 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”)
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reverse pivot shift (start in flexion, externally rotate, apply valgus, and extend knee ) suggests
posterolateral corner injury
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
suggests torn PCL
• posterior tibial subluxation may lead to false positive anterior drawer sign Anterior drawer test
• flex knees and hips to 90°, hold ankles and knees
view from the lateral aspect
visible posterior tibial sag when compared to uninjured knee suggests PCL injury
• collateral ligament stress test ( varus/ valgus instability)
• 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 suggests MCL injury ( valgus force), LCL injury ( varus force) Posterior drawer test
opening in 20° of flexion and full extension suggests MCL, cruciate, and joint capsule damage
( valgus force) .
Figure 40 Anterior and posterior
• tests for meniscal tear drawer test
• joint line tenderness
joint line pain when palpated
palpate medial and lateral joint line and observe patient for signs of pain
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 Examination for medial
with knee in flexion, palpate joint line for painful pop or click meniscal tear
lateral meniscus tear exam: internally rotate foot, apply varus stress, and extend knee
medial meniscus tear exam: externally rotate foot, apply valgus stress, and extend knee
for meniscal tear: 1.3 positive likelihood ratio, 0.S negative likelihood ratio
-
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
Examination for lateral
• Ottawa Knee Rules (see hmergencv Medicine. LR 16) meniscal tear
Cruciate Ligament Tears Figure 41. McMurraytest
• ACL tear much more common than PCL tear
Table 22. Comparison of ACL and PCL Injuries

Anterior Cruciate Ligament Posterior Cruciate Ligament
Anatomy Originates from medial wall of lateral femoral condyle, Originates at the lateral wall of medial femoral condyle, inserts
inserts at the anteromedial and posterolateral at the posterior intercondyloid eminence of the tibial plateau
intercondyloid eminence of the tibial plateau
Mechanism Non contact (more commoa): sudden deceleration with Non contact (less common):hyperflexion or hyperextension
change of direction or landing maneuver (anterior tibial Contact: sudden posterior displacement ol tibia when knee is
translation with valgus knee stress) fleied or hyper extended|e.g. dashboard MVC injury)
Contact: direct blow to lateral aspect of knee
History Audible "pop" Audible 'pop - .
Figure 42 T1 MRI of torn ACL and
Immediate swelling immediate swelling PCL
Knee "giving way" Pain with push off
Inability to continue activity Cannot descend stairs
Physical Effusion (bemarthrosis) Effusion (hemarthrosis)
Posterolateral joint line tenderness Anteromedial jointline tenderness
Positive anterior drawer Positive posterior drawer
Positive lachmann Reverse pivot shift
Pivot shift Other ligamentous,bony injuries
lest for collateral ligament and meniscal injuries
look for second fracture on stay (commonly associated
with ACL injuries)
Treatment Stable knee with minimal functional impairment: Unstable knee or young person/highdemand lifestyle: ligament
immobilization 2-4 wk with early ROM and strengthen ng reconstruction
Nigh demand lifestyle: ligament reconstruction
iJ
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Collateral Ligament Tears

Mechanism
• valgus force to knee = MCL tear
• varus force to knee = LCL tear
O’Donoghue'5 Unhappy Triad
• ACL rupture
Clinical Features • MCL rupture
• stvelling/effusion • Meniscal damage (medial and or
• tenderness above and below joint line medially (MCL) or laterally ( LCL) lateral)
• joint laxity with varus ( LCL) or valgus ( MCL) stress tests
• 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
Investigations
• x- ray: AP and lateral views of the knee; MR1
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
Meniscal Tears
• medial tear much more common than lateral tear
Mechanism
• twisting force on knee when it is partially flexed (e.g. stepping down and turning) Meniscal repair may be performed in
select patients if tear is peripheral with
• requires moderate trauma in young person, but only mild trauma in elderly due to degeneration good vascular supply is a longitudinal
Clinical Features
-
tear, and 1 4 cm in length
Partial meniscectomy may be performed
•immediate pain, difficulty WB, instability, and clicking when tears are not amenable to repair
•increased pain with squatting and/or twisting (complex, degenerative, radial)
•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 )
Investigations
• MR1, arthroscopy Tissue Sources for ACL Reconstruction
• Hamstring autograft
Treatment • Middle 1/3 patellar tendon (bone-
patellar-bone autograft)
• non-operative
• Allograft (e.g. cadaver)
indication: not locked, degenerative tear in the presence of osteoarthritis
ROM and strengthening ( NSAIDs)
•operative
indication: locked knee is a surgical emergency ( i.e. patient cannot fully extend knee, due to
mechanical block) or failed non-operative treatment
arthroscopic repair/partial meniscectomy generally indicated for younger patients with
traumatic/ non -degenerative meniscus pathology
Popliteal Cysts
•synovial fluid - filled mass located in the popliteal fossa ( i.e. Baker’s cyst )
Etiology
•classified as primary (distension of the bursa with no communication to joint) or secondary
(communication between bursa and joint, bursa fills with articular fluid)
• primary cysts are usually congenital in children, while secondary are acquired from traumatic injury
or degenerative/inflammatory joint disease in adults ri
L J
Clinical Features
• usually asymptomatic bulge on the posterior aspect of the knee
• usually located between the semimembranosus and medial head of gastrocnemius
• may cause local tightness, restricted range of motion, or posterior knee pain +
•symptoms may worsen with physical activity
-
•for secondary popliteal cysts, symptoms are more associated with the underlying condition of the
knee
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Investigations
• clinical diagnosis is often sufficient
• ultrasonography can be used to identify' cyst and its relation to adjacent soft tissue structures
• knee x- ray to assess for joint abnormalities that may be associated with the cyst
• MRI allows for clearest visualization but this is only indicated to plan for surgery, when an underlying
knee pathology such as a meniscal tear is suspected, or when the diagnosis is uncertain after
ultrasonography
Treatment
• asymptomatic cysts do not require treatment
• non -operative
indication: initial treatment for symptomatic secondary popliteal cysts
identify and treat underlying cause
• rest, NSAlDs, cold packs for symptomatic treatment
image guided aspiration and intra -articular steroid injection may offer temporary relief
Quadriceps/Patellar Tendon Rupture

Mechanism
• sudden forceful contraction of quadriceps during an attempt to decelerate
• eccentric loading of the extensor mechanism, usually with the foot planted and the knee slightly bent
• DM, SLK, RA, steroid use, renal failure on dialysis
• more common in obese patients with pre- existing degenerative changes in tendon
Clinical Features
• inability to extend knee or weight-bear
• tenderness and /or palpable gap at rupture site
• possible audible “ pop"
• patella in lower or higher position with palpable gap above or below patella , respectively Patella alta - high riding patella
Patella baja - low riding patella
• may have an effusion
investigations
• ask patient to perform straight leg raise ( unable to with complete rupture, although may be inhibited
by pain, if unclear, can reassess in 10 d )
• knee x- ray to rule out patellar fracture, MRI to distinguish between complete and partial tears
• lateral view: patella alta with patellar tendon rupture, patella baja with quadriceps tendon rupture
Treatment
• non -operative
indication: incomplete tears with preserved extension of knee
immobilization in brace, followed by progressive physiotherapy
• operative
indication: complete ruptures with loss of extensor mechanism function
• early surgical repair: better outcomes compared with delayed repair ( >6 wk post- injury)
• delayed repair complicated by quadriceps contracture, patella migration, and adhesions
Dislocated Knee
Mechanism
• high energy trauma more common ( i.e. MVC), low energy ( sport- related ), or ultra -low velocity
(obesity )
• by definition , caused by tears of multiple ligaments Schenck Classification
Typel
Clinical Features Singe cruciate (ACl or PCL) and single
• knee instability collateral (MCLorPLC)
• effusion Type 2
Injury to ACL and PCL
• pain Type 3-M
• ischemic limb, neurological deficit , or compartment syndrome . .
Injury to ACL PCL and MCL
Type 3- L
Classification .
Injury to ACL, PCL and PLC
• Kennedy classification ( based on direction of tibial displacement ) classified by relation of tibia with Type 4
respect to femur . .
Injury to ACL PCL MCL LCL
Type 5
• anterior, posterior, lateral, medial, rotary Multiliqamcnlous injury associated with
j
• Schenck classification ( based on pattern of ligamentous injury) fracture /dislocation of knee
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Investigations
-
• x ray: AP and lateral
associated radiographic findings may include extensor mechanism injury, tibial plateau fracture
dislocations, proximal fibular fractures, and/or avulsion of fibular head
• assessment of NVS:
AB1 (abnormal if <0.9)
arteriogram or CT angiogram if abnormal vascular exam (such as abnormal pedal pulses or
abnormal AB1)
detailed neurologic assessment, paying close attention to the peroneal nerve ( foot drop is
common )
Treatment
• urgent closed reduction and immobilization
can be complicated by interposed soft tissue ( posterolateral variant )
• assessment and management of neurovascular injuries and compartment syndrome
• emergent operative repair if vascular injury, open injury, irreducible or grossly unstable dislocation,
or compartment syndrome
• ligament reconstruction to restore knee stability is typically performed in a delayed fashion
• early, comprehensive physiotherapy
• high incidence of associated injuries (tibia / fibula fracture, extensor mechanism injury)
• popliteal artery injury
• peroneal nerve injury
• chronic: instability, stiffness, post - traumatic arthritis
Patella
Patellar Fracture Undisplaced
Mechanism
• direct impact injury: fall, MVC (e.g. dashboard )
• indirect trauma: rapid knee flexion against contracted quadriceps ( rare )
© ‘Qi-
Lowor/upper pole Comminuted
Clinical Features displaced
• marked tenderness
• inability to extend knee or straight leg raise
• proximal displacement of patella
• patellar deformity Transverse Osteochondral
• ± effusion/hemarthrosis Figure 43. Types of patellar fractures
Investigations
-
• x rays: AP, lateral, skyline
• do not confuse with bipartite patella: congenitally unfused ossification centers with smooth margins
-
on x ray at superolateral corner ( most often ) Complications
• Symptomatic hardware
• Loss of reduction
Treatment • Osteonecrosis
• non - operative • Hardware failure
• indication: • Knee stiffness
• Nonunion
non or minimally displaced (step-off < 2-3 mm and fracture gap < 1-4 mm )
• Infection
intact extensor mechanism
• straight leg immobilization 1 -4 wk with removable brace/splint, WB as tolerated
• -
Post traumatic arthritis
• progress in flexion after 2-3 wk

• physiotherapy: quadriceps strengthening when pain has subsided
• operative
indication:
-
>2 mm articular step off, >3 mm fragment separation , comminuted , disrupted extensor
mechanism, open fracture
GRIP, if comminuted may require partial /complete patellectomy
- goal: restore extensor mechanism with maximal articular congruency ri
LJ
Patellar Dislocation
Mechanism
• usually a non - contact twisting injury with knee extended , externally rotated tibia and fixed foot -
J sign: Associated with patella alta;
Increased lateral translation in extension
+
• lateral displacement of patella after contraction of quadriceps at the start of knee flexion in an almost which pops into the patcllofcmoral
straight knee joint groove as the patella engages the
• direct blow (e.g. knee/ helmet to knee collision ) trochlea early in flexion
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Risk Factors
• 2nd -3rd decade of life, female
• Q-angle (quadriceps angle) S15° (males), > 20° ( females)
• miserable malalignment syndrome: femoral anteversion, genu valgum, external tibia ) torsion /
pronated feet ASIS
-
• high riding patella ( patella alta )
• weak vastus medialis
• ligamentous laxity (eg. Ehlers Danlos, Marfan Syndrome)
-
Clinical Features
Q-angle
• knee catches or gives way with walking
• severe pain, tenderness anteromedially from rupture of capsule
• weak knee extension or inability to extend leg unless patella reduced
• positive patellar apprehension test
• passive lateral translation results in guarding and patient apprehension
• often recurrent , self- reducing
• concomitant MCL injury
• J -sign
Central
Investigations patella I /
-
3
• x- rays: AP, lateral, and skyline views of the knee
<
• check for fracture of medial patella ( most common ) and lateral femoral condyle
• consider M It I in young patient if concerned for osteochondral injury/loose body 'tuberosity
Tibial I®
Treatment Figure 44.0- angle
• non -operative first The angle between a vertical line
closed reduction through the patella and tibial
NSAlDs, activity modification, and physical therapy tuberosity and a line from the ASIS
short-term immobilization for comfort, then 6 wk controlled motion to the middle patella; the larger the
progressive WB and isometric quadriceps strengthening angle, the greater the amount of
• operative lateral force on the knee (normal
indication: if recurrent or loose bodies present < 20')
• chronic instability: surgical tightening of medial capsule and release of lateral retinaculum,
possible medial patcllofemoral ligament ( MPl ' L ) reconstruction
patellar dislocation associated with congenital deformity: tibial tuberosity transfer
Patellofemoral Syndrome
•syndrome of anterior knee pain associated with idiopathic articular changes of patella
Risk Factors
• malalignment causing patellar maltracking ( Q-angle S20 , genu valgus)
g
• female > male, physically active, < 40 y/o

• excessive knee strain (athletes, especially running and weight training )
• recurrent patellar dislocation, ligamentous laxity, post- trauma
• deformity of patella or femoral groove
Mechanism
• softening, erosion , and fragmentation of articular cartilage, predominantly medial aspect of patella
Clinical Features
• diffuse pain in peri - or retropatellar area of knee ( major symptom ) Pain with firm compression of
exacerbated by prolonged sitting (theatre sign), strenuous athletic activities, stair climbing, patella into medial femoral groove
squatting, or kneeling is pathognomonic of patellofemoral
• insidious onset and vague in nature syndrome
• sensation of instability, pseudolocking
• pain with compression of patella with knee ROM or with resisted knee extension
• swelling rare, minimal if present
• palpable crepitus
Investigations
• x- ray: AP, lateral, and skyline views of the knee - may find chondrosis, lateral patellar tilt, patella alta /
baja, or shallow sulcus rn
LJ
• CT: patellofemoral alignment, rule out fracture
• MR1: best to assess articular cartilage
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Treatment
-
• non operative
• continue non - impact activities; rest and rehabilitation
NSAlDs
• physiotherapy: vastus medialis, core, and hip strengthening
• operative
indication: failed non-operative treatment
« arthroscopic debridement
lateral release of retinaculum
patellar realignment (e.g. anterior tubercle elevation )
Tibia
Tibial Plateau Fracture
Mechanism
• varus/ valgus load ± axial loading (e.g. fall from height )
• femoral condyles driven into proximal tibia
Schatzker Classification
• can result from minor trauma in those with osteoporosis
Type Description
Clinical Features
• frequency: lateral > bicondylar > medial I lateral plateau split fracture
• medial fractures require higher energy - often have concomitant vascular injuries II lateral split-depressed fracture
• knee effusion , swelling III Lateral pure depression fracture
• inability to bear weight IV Medial plateau fracture
• risk of compartment syndrome, meniscal tears, and neurovascular injuries V Bicondylar plateau fracture
• Schatzker classification
VI Bicondylar with metaphincaVdidpljseal
disassociate
Investigations
-
• x ray: AH, lateral, and oblique views
• CT: preoperative planning, identify articular depression and comminution
• ABI if any differences in pulses between extremities
Treatment
• non-operative
indication: # depression is <3 mm
protected WB with immobilization in a splint for 6-12 wk with early progressive ROM
• operative
indication: articular step-off >3 mm, condylar widening > 5 mm, open #s, neurovascular injury,
significant varus/valgus instability ( >15°)
-
• OR11' often requiring bone grafting to elevate depressed fragment
-
Specific Complications (see General l ' nactiire Complications, OR7 )
-
• post traumatic OA
meniscal lesions
•
Tibial Shaft Fracture
• most common long bone fracture and open fracture
Mechanism
•low energy' pattern: torsional injury
• high energy: including MVC, falls, sporting injuries
Clinical Features
-
•pain, inability to weight bear, deformity
•open vs. closed
• neurovascular compromise
•compartment syndrome
n
L
Investigations Flgure 45. Tibial shaft fracture
-
•x ray: full length AH and lateral views treated with IM nail and screws
AF, lateral , and oblique views of ipsilateral knee and ankle
consider dedicated ankle x-rays or CT scan to rule out intra-articular extension of middle third or
distal tibia shaft fractures $
Tibial shaft fractures have high incidence
+
of compartment syndrome and are often
associated with soft tissue injuries
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Treatment
• non -operative
indication : closed and minimally displaced or adequate closed reduction -
Danis Weber Classification
Based on level of fibular fracture
• long leg cast x 6 -8 wk, convert to functional ( patellar tendon hearing ) brace for another 6 wk with •
relative to syndesmosis
progressive W B -
• Type A (infra syndesmotic)
• operative • Pure inversion injury, tibiofibular
• indication : displaced or open syndesmosis remains intact
if displaced and closed: ORIF with IM nail, plate and screws, or external fixator • Avulsion of lateral malleolus below
plafond or torn calcaneofibular
if open: antibiotics, 18, D, external fixation or IM nail, and vascularized coverage of massive soft ligament
tissue defects
• ± shear fracture of medial malleolus
-
• Type B (trans syndesmotic)
Specific Complications ( see General Fracture Complications, OR7) • External rotation and eversion ( most
• significant incidence of compartment syndrome common )
• knee pain associated with infrapatellar IM nailing (>50% anterior knee pain ) • ± avulsion of medial malleolus or
rupture of deltoid ligament
• malunion, nonunion • Spiral fracture of lateral malleolus
• lack of soft tissue coverage secondary to open fracture may require further surgery for muscle flap starting at plafond
coverage -
• Type C (supra syndesmotk )
• Pure external rotation
• Avulsion of medial malleolus or torn
Ankle deltoid ligament
• t posterior malleolus avulsion with
posterior tibio fibular ligament
• Fibular fracture is above plafond
• Frequently tears syndesmosis
Evaluation of Ankle and Foot Complaints
Special Tests
• anterior drawer: examiner stabilizes the tibia with one hand and attempts to displace the foot
anteriorly with the contralateral hand with the ankle held in neutral or plantar flexion Ottawa Ankle and Foot Rules
• talar tilt: foot is stressed in inversion and angle of talar rotation is evaluated (see Emergency Medicine. ER16 )
-
X rays are only required if:
X-Ray Pain in the malleolar zone AND any of:
bony tenderness over posterior or tip of
• AP, mortise, and lateral views lateral malleolus; OR bony tenderness
• mortise view: ankle at 15° of internal rotation over posterior or tip of medial malleolus;
gives true view of ankle joint OR inability to weight bear both
joint space should be symmetric with no talar tilt immediately after injury and in the ER
• Ottawa Ankle and Foot Rules should guide x - ray use (see Emergency Medicine, ER 16); nearly 100%
sensitivity
• ± CT to better characterize fractures
Ankle Fracture
Mechanism
• pattern of fracture depends on the position of the foot when trauma occurs
• classification systems
-
• Danis Weber: based on location of main fibular fracture line relative to the syndesmosis
Lauge-Hansen: based on foot position and direction of applied stress/ force
Treatment Norma ank e

• non -operative
indication: non -displaced, Danis -Weber Type A, and some isolated undisplaced Danis- Weber
Type B
early protected WB in walking boot
• operative
• indications
-
fracture dislocation
-
most Danis Weber Type B, and all T ype C
any talar displacement
displaced isolated medial or lateral malleolar fracture
trimalleolar ( medial , posterior, lateral ) fractures
displaced and large posterior malleolar fractures
« persistent medial clear space widening despite attempt at closed reduction and
immobilization .
1 Posterior malleolus
2. Medial malleolus
open fracture /open joint injury 3. Deltoid ligament ri
ORIF with plates and screws LJ
4. Syndesmosis
.
5 Lateral malleolus
Complications 6. Calcaneofibular
• risk of poor wound healing and deep infections ( up to 20 % ) in patients with DM, particularly if Type C ligament
concomitant peripheral neuropathy +
• postoperative stiffness Figure 46. Ring principle of the ankle
• malunion, nonunion and Danis-Weber classification
• post- traumatic arthritis
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Ankle Ligamentous Injuries

Medial Ligament Complex ( deltoid ligament )
• eversion injury
• usually avulses medial or posterior malleolus and strains syndesmosis
Lateral Ligament Complex
(anterior talofibular, calcaneofibular, posterior talofibular)
• inversion injury, > 90% of all ankle sprains
-
• anterior talofibular ( ATT ) 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
Treatment
-microscopic tear (tirade I )
• non operative Legend
PTF: Posterior talofibular
rest , ice, compression, elevation CF: Calcaneotibular
macroscopic tear (Grade 11) ATF: Anterior talofibular
strap ankle /aircast for up to a few weeks, should not interfere with early rehabilitation; PTT: Posterior tibiotalar
TC: Tibiocalcaneal
NSAlDs ATT: Anterior tibiotalar
physiotherapy: strengthening and proprioceptive retraining TN: Tibionavicular
complete tear (Grade 111)
Figure 47. Ankle ligament complexes
-
below knee walking boot x 4 6 wk ( controversial and variable); NSAlDs
physiotherapy: strengthening and proprioceptive retraining
surgical intervention may be required if chronic symptomatic instability develops
With a history of significant trauma
from axial loading of lower limb, always
Foot consider spinal injuries and talar/
calcaneal fractures
Talar Fracture
Mechanism
• forced dorsiflexion with axial load, commonly from M VC or fall from height
-
• 60% of talus covered by articular cartilage; fractures often intra articular
• talar neck is most common fracture of talus (50%)
- -
• non neck talus fractures are rare, and can include talar body ( 15 25%), process ( 10%), or head
fractures
• tenuous blood supply runs distal to proximal along talar neck
high-risk of AV N with displaced fractures
Investigations
• x- ray: AP, lateral, and Canale views ( maximum equinus, 15° pronated ) of the foot
• CT to better characterize fracture and assess for ipsilateral foot injuries ( up to 88% incidence)
• MRI not helpful acutely, but can clearly define extent of AVN during follow up
Treatment
• non -operative
indication: non -displaced
-
emergent reduction in ER, below- knee cast 8 12 wk ( NWB first 6 wk )
• operative
indication: displaced
• OR1F
—
Complications
• AVN ( 30% risk of osteonecrosis)
• malunion/ nonunion
-
• post traumatic arthritis ( subtalar most common )
Calcaneal Fracture LJ
• most common tarsal fracture Calcaneal Fracture Treatment

Principles
Mechanism • Restore articular congruity
-
• Avoid wound complications (10 25%)
+
• high energy axial loading: fall from height onto heels, MVA • Restore normal calcaneal width and
• 75% are intra -articular and 10% are bilateral height
• 10% of fractures associated with compression fractures of thoracic or lumbar spine ( rule out spine • Maximum functional recovery may
https://medical-amboss.com take longer than 12 mo
injury)
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Clinical Features
• marked swelling, pain, inability to weight bear, bruising on heel /sole
• wider, shorter, flatter heel when viewed from behind Haglund Deformity: an enlargement of
may have apparent varus deformity -
the posterior superior tuberosity of the
calcaneus
Investigations
• x-rays: AP, lateral, and oblique foot ( mandator)' views); Broden view, Harris view, or AP ankle
(optional)
loss of Bohler’s angle, double-density sign
• CT: gold-standard, assess intra-articular extension
Treatment
• dosed vs. open reduction is controversial
• N \VB cast x 6- 12 wk with early ROM and strengthening
Complications
• wound complications
• subtalar arthritis
• compartment syndrome
• malunion The most common site of Achilles tendon
-
rupture is 2 6 cm from its insertion
where the blood supply is the poorest
Achilles Tendonitis
• Achilles: largest tendon in the body
• formed by confluence of soleus and gastrocnemius tendons
Mechanism
-
•chronic inflammation from activity or poor fitting footwear
• may develop painful heel bumps ( i.e. retrocalcaneal bursitis or Haglund deformity)
Clinical Features
•posterior heel pain, swelling, burning, stiffness
• thickened tendon, palpable bump
Investigations
• x-rav: lateral, evaluate bone spur and calcification
• U /S, MRI can assess degenerative change
Treatment
-
• non operative
• rest, NSAlDs, activity and 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
avoid steroid injections (risk of Achilles tendon rupture )
•operative
open or arthroscopic debridement of Hagelung lesion
Achilles Tendon Rupture

Mechanism
• sudden forced plantar flexion, violent dorsiflexion when plantar flexed
- -
• loading activity, stop and go sports ( e.g. squash , tennis, basketball )
Complications of Achilles Tendon
Rupture
• secondary to chronic tendonitis, steroid injection, fluoroquinolone antibiotics . Infection/wound healing
complications (operative
Clinical Features management)
• audible “pop," sudden pain with push -off movement • Sural nerve injury (operative
management)
• pain or weakness/inability to plantarfiex
• palpable gap
• apprehensive toe off when walking
• Thompson test: with patient prone, squeeze calf, normal response is plantar flexion n
no passive plantarflexion is positive test = ruptured tendon LJ
Investigations
-
• x rav: rule out other pathology
• U /S or MRI: differentiate between partial vs. complete ruptures +
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OR'I I Orthopaedic Surgery Toronto Notes 2023
Treatment
-indication: low functional demand (level I evidence suggests no difference in re rupture rates
• non operative
• -
between operative and non -operative management with functional rehabilitation )
• functional bracing /casting in resting equinus ( plantar flexion ), with functional rehabilitation x
12 wk
• operative
indication: high functional demand (e.g. professional athlete)
surgical repair, followed by functional rehabilitation x 12 wk
Plantar Fasciitis
Definition
• inflammation of plantar aponeurosis at calcaneal origin
• common in athletes ( especially runners, dancers )
• also associated with obesity, DM , inflammatory arthropathies
Mechanism
• repetitive strain injury causing microtears and inflammation of plantar fascia
Clinical Features Bone spur Calcaneus
• insidious onset of heel pain, often when getting out of bed , and stiffness
• intense pain when walking from rest that subsides with ambulation; worse at end of day after Figure 48. X- ray of bony heel spur
prolonged standing
• tenderness to palpation at medial tuberosity of calcaneus
• pain with toe dorsiflexion (stretches fascia) and palpation of fascia from heel to forefoot Surgical vs. Nonsurgical Methods for Acute
Investigations
-
Achilles Tendon Rupture: AMeta Ana lysis of
R andomited Controlled Trials
• x- ray to rule out fractures, may shosv plantar heel spur J Foot Ankle Surg Am 2018 Nov • Dec; 57(6):1I9M1M
• spur is secondary to inflammation, not the cause of pain Purpose: To compare surgical treatment and
conservative treatment olacuteAchiles lendoo
Treatment
rupture.
-
Methods: A meta analysis was performed looking
-
• non operative at randomned trials comparing surgical with
• rest , ice, NSAlDs, steroid injection

-
• pain control and stretching programs are first line nonsurgical treatment or comparing different surgical
Irealments ol Achilles lendoo rupture.
physiotherapy: Achilles tendon and plantar fascia stretching, extracorporeal shockwave therapy Results: 10 randomiied cinical trials w <th a total of
934 randomited patients were included. Fatients
• orthotics with heel cup - to counteract pronation and disperse heel strike forces in the non -surgical group had a higher re-rupture
• operative rate than patients in the surgical group.Howeier.
very rarely indicated re-rupture rates were equiralentfP *.08) if an early
when performed, includes endoscopic release of fascia range of motion eie rcises protocol was performed ,
lower incidence of complications (eicbdtng re-

-
rupture) was fou nd in non surgical patients.
Bunions (Hallux Valgus) Conclusions: Non -surgical treatment for acute
Achiles tendon rupture is preferred if a functional
rehabilitation protocol with early range of motion
Definition is possible. If not, surgical treatment should he
• bony deformity characterized by medial displacement of first metatarsal and lateral deviation of -
considered because of the lower rate of re rupture.
hallux
Mechanism Normal angle <15“

• valgus alignment of 1 st MTP ( hallux valgus), loose medial and tight lateral joint capsule, adductor Hallux Valgus angle >15 “
hallucis becomes a deforming force
• formation of a reactive exostosis and thickening of the skin creates a bunion
• associated with poor-fitting footwear ( high heel and narrow toe box )
• can be hereditary (70% have family history)
• more frequent in women
Clinical Features
• painful bursa over medial eminence of 1st MT head
• pronation ( rotation inward ) of great toe
• numbness over medial aspect of great toe
Investigations
-
• x ray: standing AP, lateral, and oblique views; sesamoid can be helpful
.
Figure 49 Hallux valgus
Treatment
• indications: painful corn or bunion , overriding 2nd toe
• non -operative ( first -line )
properly fitted shoes ( low heel ) and toe spacer +
• operative: persistent symptoms, goal is to restore normal anatomy, not cosmetic reasons alone
osteotomy with realignment of 1st MTP joint
arthrodesis
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Metatarsal Fracture
• use Ottawa l - oot Rules to determine need for x - ray
'
Ottawa Ankle and Foot Rules

(see Emergency Medicine. ERIE)
Table 23. Types of Metatarsal Fractures
X- rays only required if;
Fracture Type Mechanism Clinical Features Treatment Pain in the midfoot zone AND any of:
Avulsion of Base of 5th MT Sudden inversion followed by lender base of 5 th MT Conservative management bony tenderness over the navicular or
contraction of peroneus brevis base of the fifth metatarsal; OR inability
to weight bear both immediately after
Proximal Shaft of 5th MT ( Jones Stress injury Painful over base of 5 th MT -
•NWBBK cast x 6 8 wk
injury and in the ER
Fracture )
Fracture )
.
Shaft 2 nd 3rd MT ( March ORIF if athlete, displacement , or
skin tenting
Painful shaft ol 2nd or 3rd MI Symptomatic ( protected weight
bearing , pain management )
1st MT Trauma Painful 1st Ml ORIF if displaced otherwise * NW 6
BK caslx 3 wk then walking cast
x 2 vrk
-
Tarso - MT Fracture Dislocation Forceful axial load on a plantar Pain over base of 2 nd MT ORIF or arthrodesis if displaced
( Lisfranc Fracture) flexed footor direct crush injury Swelling over midfoot Cast immobilization if undisplaced
Inability to bear weight x 8-12 wk
Bruising on plantar aspect of
midfoot
’NWB BK = Non weight beating , below knee
Paediatric Orthopaedics
Fractures in Children
• type of fracture
thicker, more active periosteum results in paediatric-specific fractures; greenstick (one cortex ), I
torus ( i.e. ‘buckle’, impacted cortex ) and plastic ( bossing ) i
<
distal radius fracture most common in children ( phalanges second ), the majority are treated ssith
closed reduction and casting I
• epiphyseal growth plate *
weaker part of bone, susceptible to injuries froximal Radius Proximal Radius ,
-
growth plate often mistaken for fracture on x ray and vice versa ( x ray opposite limb for
comparison ), especially in elbow
- Figure 50. Greenstick (left) and torus
(right) fractures
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 ha\re worse consequences in children because they usually involve the
growth plate, and may affect future bone growth Greenstick fractures are easy to reduce
• anatomic reduction but can redisplace while in cast due to
gold standard with adults intact periosteum
may accept greater angular deformity in children as remodeling minimizes deformity at skeletal
maturity
• time to heal
shorter in children
-
• always he aware of the possibility of child abuse ( non accidental injury, NAI )
ensure stated mechanism is compatible with injury presentation
-
• high index of suspicion with fractures in non ambulating children ( < l yr ); look for other signs,
-
including x ray evidence of healing fractures at different sites and different stages of healing
common suspicious fractures in children: metaphyseal corner fracture ( hallmark of non -
accidental trauma ), femur fracture < 1 y/o, humeral shaft <3 y/o, sternal fractures, posterior rib
fractures, spinous process fractures
if concerned for NAI, admit child to hospital, contact appropriate authorities, engage allied health
such as social work, and treat injuries as normal
Stress Fractures
Mechanism
• insufficiency fracture rT
LJ
normal or physiologic stress applied to a weak or structurally deficient bone
• fatigue fracture
repetitive, excessive force applied to normal hone
• most common in adolescent athletes
• common in tibia, calcaneus, and metatarsals +
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Diagnosis
• localized pain and tenderness over the involved bone
• plain films may not show fracture initially
• bone scan positive in 12-15 d, MR1 demonstrates abnormal edema
Treatment
• rest from strenuous activities to allow remodeling ( can take several months )
• protected weight bearing
• splinting /Aircast optional
Physeal Injury ^Typo I
Table 24. Salter - Harris Classification of Epiphyseal Injury

-
SALT(E) R Harris Type Description Treatment
I (Straight through; Stable) Transverse through growth plate Closed reduction and cast immobilization; heals well
95% do nol affect growth
.
It (Above) through metaphysis and along growth plate Closed reduction and cast if anatomic ; otherwise closed t
open reduction , internal fixation
III ( Below)’ Through epiphysis to plate and along growth
plate
Anatomic reduebon by ORIF to preventgrowth arrest
avoid fixation across growth plate
.
IV (Through and through )’ Through epiphysis and metaphysis Closed reduction and cast if anatomic; otherwise ORIF
Typo III
V (Ram )’ Crush injury of growth plate Cast immobilization (operative management is rarely
indicated ): high Incidence ol growth arrest
-
’ Types III V are more likely to cause growth arrest and progressive delormity
Slipped Capital Femoral Epiphysis Typo IV
• most common adolescent hip disorder, peak incidence at pubertal growth spurt
Definition
• type 1 Salter- Harris epiphyseal injury at proximal hip with anterosuperior displacement of the
metaphysis relative to the epiphysis ( remains in the acetabulum )
Etiology 5
• multifactorial
• genetic: autosomal dominant, Black children at highest risk =
|
cartilaginous physis hypertrophies too rapidly under growth hormone effects
overweight: mechanical stress
• trauma: causes acute slip .
Figure 51 Salter-Harris classification
of epiphyseal injury
• risk factors: obesity ( No. l factor ), male, hypothyroid, growth hormone deficiency, previous radiation
to hip region, renal osteodystrophy, Down Syndrome
Clinical Features
•acute: sudden, severe pain with limp, less than 3 wk duration
•chronic: typically groin and anterior thigh pain , may present with knee pain Bilateral involvement occurs In about
25%
• positive T rendelenburg sign on affected side, due to weakened gluteal muscles
•can be associated with knee pain due to activation of the medial obturator nerve
• restricted internal rotation, abduction, flexion
Drehmann sign: obligator)' external rotation during passive flexion of hip
.
• Loder classification: stable vs unstable ( provides prognostic information ) Klein's Line
On AP view, line drawn along supero-
• stable = able to bear weight, with or without crutches ( risk of osteonecrosis < 10%) lateral border of femoral neck should
• unstable = unable to ambulate even with crutches ( high - risk of osteonecrosis, between 24-47% ) cross at least a portion of the femora!
.
epiphysis. If it does not suspect SCFE
Investigations
- -
• x ray: AP, frog leg lateral radiographs both hips
• posterior and medial slip of epiphysis
disruption of Klein 's line
AP view may be normal or show widened/lucent growth plate compared with opposite side
ri
Treatment LJ
•operative: percutaneous in-situ fixation without reduction ( reduction is highly controversial )
•consider prophylactic fixation of contralateral hip in high risk patients -
Complications
•z\VN, chondrolysis (loss of articular cartilage, resulting in narrowing of joint space), pin penetration,
+
premature OA, loss of ROM, contralateral SCFE
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Developmental Dysplasia of the Hip

Definition
• abnormal development of hip, resulting in shallow acetabulum (dysplasia ), displacement with some
remaining contact between the articular surfaces (subluxation ), or complete displacement of the joint
(dislocation )
• most common orthopaedic disorder in newborns
• all newborns require screening with physical exam
Etiology
• due to ligamentous laxity, muscular underdevelopment, and abnormal shallow slope of acetabular
roof
• spectrum of conditions
• dysplastic acetabulum , more shallow, and more vertical than normal
head subluxates out of joint when provoked
• dislocatable head in socket Barlow's test
dislocated femoral head completely out of acetabulum
Physical Exam
• diagnosis is clinical lv
\
limited abduction of the flexed hip ( <60°)
affected leg shortening results in asymmetry in skin folds and gluteal muscles, wide perineum
Barlow’s test demonstrates whether hips are dislocatable
flex hips and knees to 90° and grasp thigh
fully adduct hips, push posteriorly to try to dislocate hips, feeling for a distinct clunk
Ortolani’s test demonstrates whether hips are reducible
i®
initial position as above but try to reduce hip with fingertips during abduction
positive test: palpable clunk is felt ( not heard ) if hip is reduced
T rendelenburg test and gait useful if older ( >2 yr )
Cialeazzi 's sign Ortolani's tost
knees at unequal heights when hips and knees flexed Figure 52. Barlow ’s test and
appearance of a shorter femur ( lower knee ) on affected side Ortolani's test
difficult test if child < 1 yr
Investigations
• perform screening U /S at 4 -6 weeks in patients with risk factors and positive physical findings to view
cartilage ( bone is not calcified in newborns until 4-6 mo)
• follow- up radiograph after 3 mo
(*3
5 Fs that Predispose to Developmental
• x-ray signs (at 4-6 mo): false acetabulum , acetabular index >25°, broken Shenton’s line, femoral neck Dysplasia of the Hip
above Hilgenreiner’s line (horizontal line through right and left triradiate cartilage), ossification Fanily history
centre outside of inner lower quadrant (quadrants formed by intersection of Hilgenreiner’s and Female
Perkin’s lines) Frank breech
First born
LeFt hip
Treatment
• 0-6 mo: reduce hip using Pavlik harness to maintain abduction and flexion
• 6-18 mo: reduction under GA, hip spica cast x 2-3 mo (if Pavlik harness fails)
• 18 nio- 2 yr: open reduction with spica casting
• >2 yr: pelvic and /or femoral osteotomy
Complications
• redislocation, inadequate reduction , stiffness
• AVN of femoral head may be seen at any point in treatment; due to impingement of medial circumflex
femoral artery with severe abduction and flexion secondary to prolonged Pavlik harness or spica cast
treatment
Legg- Calve- Perthes Disease (Coxa Plana)

Definition Most common in adolescent athletes,
especially jumping/sprinting sports
• idiopathic AVN of femoral head, presents at 4 -8 yr of age
. 12% bilateral, M:P =5:1, 1 /1200 children
• associations
low birth weight
- -
family history of Legg Calve Perthes Disease r »
LJ
Children diagnosed with coxa plana
abnormal pregnancy /delivery < 6 yr of age have improved prognosis
• ADHD in 33% of cases, delayed bone age in 89%
-
second hand smoke exposure
• key features
» AVN of proximal femoral epiphysis, abnormal growth of the physis , and eventual remodeling of
+
regenerated bone
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Clinical Features
• child tvith antalgic or T rendelenburg gait ± pain
• intermittent knee, hip, groin, or thigh pain
• flexion contracture (stiff hip )
• decreased internal rotation and abduction of hip
• limb length discrepancy ( late)
Investigations
• x- ray: AP pelvis, frog leg lateral
• initially, may be negative; if high index of suspicion, obtain bone scan or MR1 .
Figure 53 Pelvic x- ray and reference
• eventually, collapse of femoral head will be seen (diagnostic) lines and angles for assessment of
DDH
Treatment Triradiate Cartilage
• goal is to keep femoral head contained in acetabulum and maintain ROM (contain and maintain ) y-shaped epiphyseal plate at junction
• non -operative of ilium, ischium, and pubis
physiotherapy: ROM exercises Hilgenreiner’sLine
restricted weightbearing Line running between triradiate
• operative cartilages
«femoral or pelvic osteotomy (>8 yr of age or severe) Perkin's Line
Line through lateral margin of
prognosis better in males, <6 yr, <50% of femoral head involved, abduction >30° acetabulum, perpendicular to
• 60% of involved hips do not require operative intervention Hilgenreiner's Line
• natural history is early onset OA and decreased ROM Shenton’s Line
Arced line along Inferior border of
Osgood- Schlatter Disease femoral neck and superior margin of
obturator foramen
Acetabular Index
Definition Angle between Hilgenreiner 's Line
.
• inflammation of patellar ligament at insertion point on tibial tuberosity
M > F; boys 12 - 15 yr; girls 8 - 12 yr
and line from triradiate cartilage to
point on lateral margin of acetabulum
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)
Clinical Features
• tender lump over tibial tuberosity
• pain on resisted leg extension
• anterior knee pain exacerbated by jumping or kneeling, relieved by rest
Investigations
• x-ray lateral knee: fragmentation of the tibial tubercle, ± ossicles in patellar tendon
Treatment
• benign, self-limited condition, does not resolve until growth halts
• non -operative ( majority)
• avoid aggravating activities such as basketball or cycling
NSAJDs, 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 )
Congenital Talipes Equinovarus (Club Foot)

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
Etiology
• intrinsic causes ( neurologic, muscular, or connective tissue diseases) vs. extrinsic (intrauterine
growth restriction); maybe idiopathic, neurogenic, or syndrome-associated
• fixed deformity
Physical Exam
-
• 1-2 in 1000 newborns, 50% bilateral, M > F 2:1, severity 1;>M <§>
CAVE deformity
Midfoot Cavu (tight intrinsics, FHL, FDL)
n
LJ
Forefoot Adductus (tight tibialis

• examine for CAVE deformity posterior)
• examine hips for associated DDH Hindfoot Varus tight Achilles tendon,
• examine knees for deformity tibialis posterior, tibialis anterior) +
• examine back for dysraphism ( unfused vertebral bodies) Hindfoot Equinus (Hindfoot Equinus
• diagnosis is often from physical exam findings alone, radiographs unnecessary (tight Achilles tendon)
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-
Treatment ' Plantar flexion

• largely non -operative via Ponseti Technique (serial manipulation and casting) of ankle joint
• correct deformities in CAVE order
change strapping /cast ql -2 wk Talus in equinus I
typically requires percutaneous Achilles tendon release after ~ 2 months of casting with and varus - v, I
another 3 weeks of casting in maximal dorsiflexion
surgical release in refractory case ( rare ) 0
• delayed until age 3-4 mo [0
-
• 3 yr recurrence rate = 5 10% / -j
• mild recurrence common; affected foot is permanently smaller/stiffer than normal foot with calf
muscle atrophy I1
Forefoot
bones in
varus ,
Inversion of
calcaneus
i
Scoliosis
-
Figure 54. Club foot depicting the
gross and bony deformity
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
Clinical Features
• cosmetic concern ± back pain
• primary curve where several vertebrae affected
• secondary compensatory curves above and below fixed primary curve to try to maintain normal
position of head and pelvis
• asymmetric shoulder height when bent forward
• Adam’s test: thoracic or lumbar prominence on affected side with forward bend at the waist
• prominent scapulae, creased flank, asymmetric pelvis
• associated posterior midline skin lesions in neuromuscular scoliosis
- -
• cafe au lait spots, dimples, neurofibromas
• axillary freckling, hemangiomas, hair patches .
Figure 55 Cobb angle -
• associated pes cavus or leg atrophy used to monitor the progression of
• apparent leg length discrepancy the scoliotic curve
• Scoliosis Lenke Classification: guide to select curves to be included within the fusion construct
Investigations
• x- ray: 3-foot standing, AP, lateral Scoliosis screening is not recommended
measure curvature: Cobb angle in Canada (Grieg A, et al. 2010; Health
• may have associated kyphosis Canada.1994)
Treatment
• based on Cobb angle
• < 25°: observe for changes with serial radiographs In structural or fixed scoliosis, bending
• >25° or progressive: bracing ( many types, controversial ) that halt /slow curve progression but do forwards makes the curve more obvious
not reverse deformity
• > 45°, cosmetically unacceptable, or respiratory problems: surgical correction (spinal fusion )
Postural scoliosis can be corrected by
correcting the underlying etiology
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Bone Tumours
• primary bone tumours are rare after 3rd decade
• metastases to bone are relatively common after 3rd decade
Red Flags
Clinical Features • Persistent skeletal pain
• malignant ( primary' or metastasic ): local pain and swelling ( weeks to months), worse on exertion and • Localized tenderness
at night, ± soft tissue mass • Spontaneous fracture
• minor trauma can be the initiating event that calls attention to lesion -
• Enlarging mass soft tissue swelling
Table 25. Distinguishing Benign from Malignant Bone Lesions on X - Ray

Benign
..
No periosteal reaction or benign appearing reaction (e g uniform
smooth periosteal thickening as seen in a healing fracture)
Malignant
Acute periosteal reaction
•Codman’s triangle
©
Describing Bone Tumours on X rays -
•"Onion skin" 1 Location (which bone and whether
•"Sunburst ” it is in the diaphysis. metaphysis. or
Sharp,well-demarcated borders,narrow zone of transition (between Poorly defined borders, with a wide zone of transition,or infiltrative epiphysis)
lesion andnormal bone,suggesting slow - growing lesion) (suggesting fast - growing lesion) 2 Size
3 Solitary vs. multifocal
Well-developed bone formation Varied bone formation 4 Morphology: geographic, permeative,
Intraosseous and even calcification Eitraosseousand irregular calcification or moth-eaten margins
5 Presence of periosteal reaction
No soft tissue mass Soft tissue mass present 6 Presence of bony remodeling
No cortical destruction or uniform cortical destruction in some low Aggressive cortical destruction or tumour infiltration without cortical 7 Cortical involvement
grade and locally aggressive benign lesions destruction 8 Matrix: osteoid (cumulus cloud),
Adapted from Bucktioltz RW . Heckman JD. Rockwood and Green's Fractures in Adults. Volume 1. Philadelphia: Uppincotl Williams & Wilkins. 2001. chondroid (punctate or popcorn
p558 calcification ), or fibrous (ground glass
appearance)
Diagnosis 9 Presence of soft - tissue mass
10 Associated pathological fracture
• malignancy is suggested by rapid growth, warmth , tenderness, aggressive features on imaging
• may be associated with constitutional symptoms such as fevers, night sweats, weight loss, or loss of
appetite
• staging should include:
• local
full length radiographs of the affected bone
± CT and/or MR1 of affected bone
biopsy
should be referred to specialized centre for biopsy
• systemic
blood work (CBC, electrolytes, liver function assays, inflammatory markers, bone profile,
extended electrolytes including calcium )
serum electrophoresis for older patients ± Bence ) ones protein Neoplasi
CT chest /abdo/ pelvis
Bone scan or bone marrow biopsy depending on preliminary diagnosis Periosteum
Benign Active Bone Tumours

Codman's
triangle
BONE-FORMING TUMOURS 1
.
Osteoid Osteoma Figure 56. Codman’s triangle

• benign bone tumour arising from osteoblasts; not known to metastasize A radiographic finding in
• peak incidence in 2 nd and 3rd decades, M:F=2-3:1 malignancy, where the partially
ossified periosteum is lifted off the
• proximal femur> tibia diaphysis most common locations; spine ( can cause painful scoliosis)
cortex by neoplastic tissue
• radiographic findings: small, round radiolucent nidus (<1.5 cm ) surrounded by dense sclerotic bone
-
("bulf's eye ” )
• symptoms: constant and progressive pain from prostaglandin secretion and COXI /2 expression
• pain worse at night (diurnal prostaglandin production ); characteristically relieved by NSAIDs
-
• treatment: NSAIDs are first line; percutaneous radiofrequenev ablation or surgical resection for
refractory lesions
FIBROUS LESIONS
Fibrous Cortical Defect (i.e . non- ossifying fibroma , fibrous bone lesion)
• developmental defect in which areas that normally ossify are filled with fibrous connective tissue _
r1
t j
• 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
• distal femur > distal tibia > proximal tibia most common locations
• radiographic findings: diagnostic, metaphyseal eccentric ‘bubbly’ lytic lesion near physis; thin ,
-
smooth / lobulated , well defined sclerotic margin +
• multiple lesions can be present; large lesions may be associated with pathologic fractures
• treatment: most lesions resolve spontaneously; curettage and hone grafting for symptomatic lesions or
to prevent pathologic fractures in larger lesions
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Osteochondroma
• cartilage capped bony lesion arising on the external surface of a bone
• 2 nd and 3rd decades, M >1:
• most common benign bone tumour ( ~30% ); true incidence unknown as many asymptomatic
• 2 types: sessile ( broad based and increased risk of malignant degeneration ) vs. pedunculated ( narrow
stalk )
• metaphysis of long bone near tendon attachment sites (distal femur, proximal tibia, or proximal
humerus)
- -
• radiographic findings: cartilage capped bony spur on surface of bone ( “ mushroom" on x ray)
-
• may be multiple ( hereditary, autosomal dominant form ) higher risk of malignant change
• generally very slow growing and asymptomatic unless impinging on neurovascular structure
(‘painless mass’)
growth usually ceases when skeletal maturity is reached
• malignant degeneration occurs in 1-2% (becomes painful or rapidly grows)
• treatment: observation; surgical excision if symptomatic or concern for malignant transformation
Enchondroma
• benign hyaline cartilage growth ; abnormality of chondroblasts, develops in medullary cavity
single / multiple enlarged rarefied areas in tubular bones
lytic lesion with sharp margination and irregular central calcification (stippled / punctate/ popcorn Figure 57. T1 MRI of femoral
appearance) enchondroma
• majority asymptomatic, presenting as incidental finding or pathological fracture
• 2 nd and 3rd decades
-
• 60% occur in the small tubular bones of the hand and foot; others in femur ( 20% Figure 57 ),
humerus, ribs
• radiographic findings: well -defined, lucent, central medullary lesions that calcify over time
• malignant degeneration to chondrosarcoma occurs in 1-2% (rest/nocturnal pain in absence of
pathologic fracture is an important clue)
• treatment: observation with serial x-rays; surgical curettage if symptomatic or lesion grows
CYSTIC LESIONS
Unicameral/Solitary Bone Cyst

• most common cystic lesion; serous fluid-filled lesion with fibrous lining
• children and young adults, peak incidence during first 2 decades
• proximal humerus and femur most common
• symptoms: asymptomatic, or localized pain ; complete pathological fracture ( 50% of presentations ) or
incidental detection
• radiographic findings: lytic translucent area on metaphyseal side of growth plate, cortex thinned /
expanded ; well-defined lesion
• treatment: observation with serial radiography 4 -6 mo; if needed, aspiration followed by steroid
injection; curettage ± bone graft indicated if structural integrity of bone is compromised
Benign Aggressive Bone Tumours

Giant Cell Tumours/Aneurysmal Bone Cyst/Osteoblastoma
• affects patients of skeletal maturity, peak 3rd decade
• osteoblastoma: most commonly found in posterior elements of spine Figure 58. X-ray of aneurysmal bone
• giant cell tumour: pulmonary metastases in 3% cyst
-
• aneurysmal bone cysts: either solid with fibrous /granular tissue, or blood filled Note the aggressive destruction of
• radiographic findings bone
• giant cell tumour: eccentric lytic lesions in epiphyses adjacent to subchondral bone; may break
through cortex; T2 MRI enhances fluid within lesion ( hvper-intense signal )
aneurysmal bone cyst: expansile, eccentric, and lytic lesion with bony septae ( “ bubbly
appearance"); will have fluid -fluid levels on MRI
osteoblastoma: often nonspecific; calcified central 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 )
Treatment
• intralesional curettage + bone graft or cement
• wide local excision of expendable bones
• recurrence rates of up to 20%
Figure 59. X-ray of osteosarcoma of
distal femur
+
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OR52 Orthopaedic Surgery
Age
«1
-
110
10 30
30 40
>
Malignant Bone Tumours
Table 26 . Most Common Malignant Tumour Types for Age
-
40
Osteosarcoma
Tumour
Neuroblastoma
Ewing’s ol tubular bones
Osteosarcoma . Ewing's ol Hat bones
Reticulum cell sarcoma, fibrosarcoma , periosteal osteosarcoma, malignant giant cell tumour, lymphoma
Metastatic carcinoma , multiple myeloma , chondrosarcoma
• malignant bone tumour

• 2 nd most common primary malignancy in adults after myeloma
• majority occur in 2 nd decade of life, second peak in elderly patients with history of Paget’s disease
osteochondroma
-
-
-
• predilection for sites of rapid growth: distal femur (45% Figure 59, OR51 ), 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 blastic and destructive lesion ( “sunburst" pattern ),
periosteal reaction ( Codman's triangle ), soft tissue mass with maintenance of bone cortices;
destructive lesion in metaphysis may cross epiphyseal plate
• bone scan - rule out skeletal metastases; CT chest - rule out pulmonary metastases
• treatment: staging, neo -adjuvant chemotherapy, re-staging, limb salvage resection /reconstruction
(rarely amputation ), post-surgical neo-adjuvant chemotherapy
• prognosis: 90% survival for low-grade; 70% survival for high -grade
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
• age range 25 45 yr, better, prognosis than primary chondrosarcoma

• symptoms: progressive pain uncommonly palpable mass or pathologic fracture
• radiographic findings: in medullary cavity, irregular "popcorn" calcification
• treatment: no role for neo-adjuvant chemotherapy or radiation; treat with wide surgical resection +
reconstruction; regular follow-up x-rays of resection site and chest
• prognosis: 90% ten- year survival for low-grade; 29-55% survival for high -grade
Ewing's Sarcoma
• malignant, small round cell sarcoma; metastases frequent without treatment
• most occur between ages 5-25 yr
• tlorid periosteal reaction in metaphysis oflong bone with diaphyseal extension
• signs/symptoms: presents with pain , fever, erythema , and swelling; anemia, increased WBC, HSR ,
LDH ( mimics an infection )
pattern (“onion -skinning")
-
• radiographic findings: destructive lesion with moth eaten appearance and periosteal lamellated
treatment: resection + chemotherapy ± radiation (can be treated solely with radiation in younger
patients in select anatomic locations)
• prognosis: 70% survival; distant metastases significantly lower survival (<30%)
n"
Toronto Notes 2023
Figure 60. X- ray of femur

chondrosarcoma
Signs ol Hypercalcemia
.
Bones. Stones Moans, Groans
Psychiatric overtones"
Most Common Tumours

Metastatic to Bone
Breast
Lung
Kidney ^ ^
. Thyroid ,
Melanotna )
.
CNS: headache, confusion , irritability,
blurred vision
Gl: N19, abdominal pain, constipation,
weight loss
MSK: fatigue, weakness, unsteady gait,
bone and joint pain
GU: nocturia, polydipsia , polyuria, UTIs
Breast
Lung
Kidney
Multiple Myeloma
• proliferation of neoplastic plasma cells Prostate
• most common primary bone malignancy
• 90% occur in people > 40 yr; M :l- = 2:1; twice as common in individuals of African descent
'
BLT with a Kosher Pickle
• signs/symptoms: localized bone pain (cardinal early symptom ), compression / pathological fractures, Breast
renal failure, nephritis, high incidence of infections (e.g. pyelonephritis / pneumonia ), systemic Lung
(weakness, weight loss, anorexia ) Thyroid
• labs: anemia , thrombocytopenia, increased HSR, hypercalcemia, increased Cr Kidney
• radiographic findings: multiple, “ punched-out” well-demarcated lesions, no surrounding sclerosis, Prostate
marked bone expansion n
• diagnosis LJ
• serum /urine immunoelectrophoresis ( monoclonal gammopathy )
-
• CT guided biopsy of lytic lesions at multiple bony sites
• treatment
• multiagent chemotherapy ± stem cell transplantation ± bisphosphonates +
• surgery for impending fractures: debulking, internal fixation
• prognosis: 5 yr survival 52%, prognosis increases with decreasing age
• see Hematology, H 5 I
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Bone Metastases
• most common cause of bone lesions in adults; typically age >40
• majority arise from breast or prostate; some arise from lung, thyroid, and kidney
• usually osteolytic lesions; prostate occasionally osteoblastic
• may present with mechanical pain and/or night pain, pathological fracture, hypercalcemia
• bone scan for MSK involvement; MR1 if suspected spinal involvement
• treatment: pain control, bisphosphonates, surgical stabilization of impending fractures if Mirel’s
Critera >8
Table 27. Mirel’s Criteria for Impending Fracture Risk and Prophylactic Internal Fixation
Variable Number Assigned
1 2 3
Site Upper arm Lower extremity Peritrochanleric
Pain Mild Moderate Severe
Lesion Elastic Mixed lytic
Siie <1/ 3 bone diameter -
1/3 2Z3 diameter > 2/ 3 dtamcler
Common Medications
Table 28 . Common Medications
Drug Name Dosing Schedule Indications Comments
ccfazolin ( Anccl ) 12 g IV qS h Preoperativcanlibiolic First generation cephalosporin; can
prophylaxis be used with penicillin allergy |< t0 %
cross - reactivity; significantly higher
rales ol SSI /PTI with alternative ABx )
IMWH S000 IU SC once daily 0VI prophylaxis Fixed dose, no monitoring, improved
dalteparin (Fragmin ' ) 30 - 40 mg SC once daily to BIO bioavailability, increased bleeding
enoxaparin ( Lovenox :) 2.5 mg SC once daily rates
oral anticoagulants 110 mg P 0 x1 then 220 m g P0 DVT prophylaxis Predictable, no monitoring,oral
dabigatran |Pradaxa!) once daily administration
rivaroxaban fXarelto 10 mg P0 once daily Reversal agents:
apixaban ( Eliquis 5 ) 2.5 mg P0 BID idarucirumab (dabigatran)
andexanet alia|rivaroxaban,
apixaban)
Aspirin ( ASA ) gtmgPOBIO 0VI prophylaxis Recent evidence suggests similar
efficacy to IMWH and Rlvaroxaban
with belter side effect profile ( lower
hematoma /sliffness in TJA)
tranexamicacid (TXA ) 10 - 20 mg/ kg IV Reduce perioperative blood loss No evidence for increase in
Topical application to wound and transfusion thromboembolic events
acetaminophen (Tylenol - ) 1000 mg POqGh or q8 h Analgesia for pain control Max dose up to 4000 mg every 24 h
Higher doses can be hepatotoxic in
susceptible individuals
.
ibuprofen ( Advil Motrin ) 200 - 800 mg P0 q6 - 8 Ir
(max 3200 mg / d|
Analgesia for inflammatory pain
(arthritis)
.
NSAID maycause gastric erosion
and bleeding;avoid il concurrent
advancedrenal disease
triamcinolone ( Aristocort ' )
an injectable steroid
- 0.5 -1 ml ol 25 mg/ml Suspension (Injected inlo
inflamed joint or bursa); amount
Potent anti inflammatory died;
increased pain for 24 h. rarely
varies by joint sire causes falnetrosis and skin
depigmentalion
naproxen ( Aleve - , Naprosyns) 250- 500 mg BID Analgesia for pain due to .
NSAID maycause gastric erosion
inflammation, arthritis,soft and bleeding;avoid if concurrent
tissue injury advanced renal disease
celecoxib (Celebrex - ) 200 mg P0 BID Component of multimodal pain NSAID ( COX -2 inhibitor ), cardiotoxic
control and prophylaxis of HO
after THA
indomethacin (Indocid ) 2SmgP0 IID Prophylaxis of HO alter 1HA Use with misoprostol
ri
LJ
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Landmark Orthopaedic Trials

HEALTH NEJM 2019: 381:2199 - 2208 Title: Total Hip Arthroplasty or Hemiarthroplasty for Hip Fracture
Purpose: Despite being amongst the top 10 causes of disability in adults, there is still ambiguity in the treatmentof displaced
femoral neck fractures.
-
Methods: 1495 patients who were 50 years old and had a displaced femoral neck fracture were randomly assigned to have a total
hip arthroplasty or hemiarthroplasty.
Results: A secondary hip procedure within 24 months of follow up occurred in 7.9% of the total hip arthroplasty and 8.3% of the
hemiarthroplasty group. Hip Instability occurred in 4.7% ol the total hip arthroplasty, and 2.4% of the hemiarthroplasty group .
Function was modestly better in total hip arthroplasty over hemiarthroplasty .
Conclusions: The incidence ol secondary procedures, and function over 24 months between the total hip arthroplasty and
hemiarthroplasty group did not have a significant difference.
PR 0FHER JAMA 2015 Mar 10:313(10):1037- 47 Title: Surgical vs.Honsurgical Treatment of Adults with Displaced Fractures of the Proximal Humerus:the PROFHER Randomized
Clinical Trial
Purpose: To evaluate the efficacy of surgical management in adults with displaced fractures of the proximal humerus involving the
surgical neck.
.
Methods: A randomized clinical trial where 260 palienls who presented to 32 UK hospitals alter sustaining a displaced fracture of
the proximal humerus involving the surgical neck were randomized into surgical and nonsurgical lioatmcnt groups, then followed
for 2 years.
Results: No significant mean treatment group differences in Oxford Shoulder Score averaged over 2 years ( 39.07 points for the
surgical group vs.38.32 points for the nonsurgical group: difference of 0.75 points (95% Cl, -1.33 to 2.84 points); P * .48).
Conclusions: No significant differences between surgical treatmentvs. non -surgrcal treatment.These results do notsupport the
use of surgery for patients with displaced proximal humerus fractures involving the surgical neck.
FLOW N Engl J Med 2015:373:2629 2641 Title: A Trial of Wound Irrigation in the Initial Management of Open Fracture Wounds
Purpose: to investigate the effects of castile soap versus normal saline irrigation delivered by means of high, low, or very low
Irrigation pressures .
Methods: 2551 palienls from 41 clinical centers, who had an open fracture ol an extremity undergoing irrigation were randomly
assigned to one of three irrigation pressures (high, low, and very low) and one of two irrigation solutions (castile soap versus normal
saline). The primary outcome in this study was reoperation within 12 months after the initial surgery.
Results: Hazardratio showed no significant difference between the rates of reoperation within 12 months between the different
. .
irrigation pressures. Reoperation occurred in 14.8% in the soap group and in 11.6% in the saline group (hazard ratio 1.32 95% Cl,
1.06 to 1.66; P-0.01).
Conclusions: Rates of reoperation were similar regardless of irrigation pressure. The reoperation rate was higher in the soap group
than in the saline group. These findings indicate low pressure saline irrigation is an acceptable form ol wound irrigation.
References
AA 0 S. The treatment of distal radius fractures: summary of recommendations. 2009. Available from:httpJi'www.aaos.ocg /research/guidelines /DRFguideline.asp.
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COMPREHENSIVE MEDICAL REFERENCE

Comprehensive Medical Reference

Toronto Notes for Medical Students, Inc.

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Preface - From the Editors

2019 ( 35th ed.): Taraneh (Tara ) Tofighi and Mark Shafarenko

2018 ( 34 th ed.): Tina Binesh Marvasti and Sydney McQueen

2016 (32 nd ed.): Zamir Merali and Justin D. Woodfine

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

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

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

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

2010 (26th ed.): Simon Baxter and Gordon McSheffrey

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

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

2001 ( 17th ed.): Jason Yue and Gagan Ahuja

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

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

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

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

1993 ( 9th ed.): Joan Cheng and Russell Goldman

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

BMC Production Editors Online Content Managers

Faculty Contributors, University of Toronto

Professor of Medical Imaging University ot Toronto

Faculty Contributors, University of Toronto

Faculty Contributors, University of Toronto

Common Acronyms and Abbreviations Used in Medicine

Ethical, Legal, and Organizational Medicine ELOM

How To Use This Book

The layout of Toronto Notes allows easy identification of important information.

Icon Icon Name Significance

Basic Anatomy/ Physiology Review

Common Differential Diagnoses

Common Acronyms and Abbreviations Used in

U concentration ECC, electrocardiogram

Common Acronyms and Abbreviations Used in

Common Unit Conversions

Conventional Unit Conversion Factor SI Unit

ACTH pg/mL 0.22 pmol/L

Iron, total pg /dL 0.179 pmol/L

Celsius •* Fahrenheit F = (C x 1.8) + 32 r

Commonly Measured Laboratory Values

Arterial Blood Gases

Acronyms ... RH2

Landmark Rheumatology Trials . .. RH32

Anatomy of Joint Pathology

Synovial Cartilage £ Arthritis: inflammation in the joint(s)

• Joint swelling: effusion/synovial

Immunogenetics and Disease

MHC Class Types Location Function

Table 5. Differential Diagnosis of Oligoarthritis /Polyarthritis

Table 6 . Symptoms of Inflammatory Arthritis vs. Degenerative Arthritis

Table 7. Seropositive vs. Seronegative Rheumatic Diseases

Synovial Fluid Analysis

Contraindications to Joint Aspiration or Injection

Synovial Fluid Analysis

Degenerative Arthritis: Osteoarthritis

Classification (Based on Etiology)