General Principles of Orthopedics and Trauma [2nd ed.] 978-3-030-15088-4;978-3-030-15089-1

Table of contents :
Front Matter ....Pages i-xxi
Anatomy of Bone, Fracture, and Fracture Healing (K. Mohan Iyer)....Pages 1-17
Complications of Fractures (K. Mohan Iyer)....Pages 19-26
Fractures in Children (K. Mohan Iyer)....Pages 27-34
Infection (K. Mohan Iyer)....Pages 35-55
Osteoarthritis (K. Mohan Iyer)....Pages 57-62
Rheumatoid Arthritis (K. Mohan Iyer)....Pages 63-74
Tuberculosis (K. Mohan Iyer)....Pages 75-115
Peripheral Nerve Lesions (K. Mohan Iyer)....Pages 117-128
Congenital Anomalies (K. Mohan Iyer)....Pages 129-182
Metabolic and Endocrine Disorders (K. Mohan Iyer)....Pages 183-248
Developmental Disorders (K. Mohan Iyer)....Pages 249-258
Degenerative Disorders (K. Mohan Iyer)....Pages 259-296
Poliomyelitis and Spina Bifida (K. Mohan Iyer)....Pages 297-308
Cerebral Palsy (K. Mohan Iyer)....Pages 309-321
Bone Tumors (K. Mohan Iyer)....Pages 323-366
Low Back Pain (K. Mohan Iyer)....Pages 367-377
General Affections of the Soft Tissues (K. Mohan Iyer)....Pages 379-383
Amputations (K. Mohan Iyer)....Pages 385-406
Arthroscopy and Tissue Engineering (Pradeep Baskaran, David V. Rajan)....Pages 407-428
Total Joint Replacement (Sharad Goyal, Tarang Tandon, Dhrumin Sangoi, Edward J. C. Dawe)....Pages 429-489
Recent Advances in Imaging and Radiology in Orthopedics (E. McLoughlin, E. M. Parvin, S. L. James, R. Botchu)....Pages 491-525
Plaster of Paris (K. Mohan Iyer)....Pages 527-533
Emergencies in Orthopedics (K. Mohan Iyer)....Pages 535-551
Sports Injuries to the Hip Joint (Prakash Chandran, Rohit Singhal)....Pages 553-573
Stem Cells in Orthopedics (Raju Vaishya, Abhishek Vaish)....Pages 575-582
3D Printing in Orthopedics (Raju Vaishya, Abhishek Vaish)....Pages 583-590
External Fixation (K. Mohan Iyer)....Pages 591-606
The Principles of the Ilizarov Apparatus (K. Mohan Iyer)....Pages 607-617
The Direct Anterior Approach to the Hip (Hiran Amarasekera)....Pages 619-628
Use of Robotic-Assisted Surgery in Orthopedics (Jeeshan Rahman, Karam Al-Tawil, Wasim S. Khan)....Pages 629-637
The Interlocking Nailing System and Technique (Damien F. Gill, Fouzia Khatun, Wasim S. Khan)....Pages 639-659
Total Knee Replacement (Nadim Tarazi, Rui Zhou, Wasim S. Khan)....Pages 661-679
Endoscopic Surgery in Orthopedics (Rosamond J. Tansey, Michael J. Dunne, Wasim S. Khan)....Pages 681-691
Hip-Preserving Surgery (Jaison Patel, Wasim S. Khan)....Pages 693-704
Recent Advances in Minimally Invasive Surgery in Trauma and Elective Surgery (Mira Pecheva, Humza Tariq Osmani, Wasim S. Khan)....Pages 705-716
Short-Stem Total Hip Arthroplasty (Karl Philipp Kutzner)....Pages 717-737
Advances in Bearing Surfaces of Total Hip Arthroplasty (Alexander Durst, Kate Spacey, Wasim S. Khan)....Pages 739-746
Back Matter ....Pages 747-778

Citation preview

General Principles of Orthopedics and Trauma K. Mohan Iyer Wasim S. Khan  Editors Second Edition

123

General Principles of Orthopedics and Trauma

K. Mohan Iyer  •  Wasim S. Khan Editors

General Principles of Orthopedics and Trauma Second Edition

Editors K. Mohan Iyer Formerly Locum Consultant Orthopaedic Surgeon Royal Free Hampstead NHS trust Royal Free Hospital London UK

Wasim S. Khan Division of Trauma and Orthopaedic Surgery, Addenbrooke’s Hospital University of Cambridge Cambridge Cambridgeshire UK

ISBN 978-3-030-15088-4    ISBN 978-3-030-15089-1 (eBook) https://doi.org/10.1007/978-3-030-15089-1 © Springer Nature Switzerland AG 2019 This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed. The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use. The publisher, the authors, and the editors are safe to assume that the advice and information in this book are believed to be true and accurate at the date of publication. Neither the publisher nor the authors or the editors give a warranty, express or implied, with respect to the material contained herein or for any errors or omissions that may have been made. The publisher remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. This Springer imprint is published by the registered company Springer Nature Switzerland AG The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland

To the memory of my respected teacher (Late) Mr. Geoffrey V. Osborne and My wife, Mrs. Nalini K. Mohan My daughter, Deepa Iyer, MBBS, MRCP (UK) My son, Rohit Iyer, BE (IT) My grandsons, Vihaan and Kiaan

First Foreword to the Second Edition

Nicola Maffulli is Professor of Trauma and Orthopedic Surgery, Keele University School of Medicine and Consultant Trauma and Orthopedic Surgeon at the North Staffordshire Royal Infirmary and City General Hospital, Stoke on Trent in Staffordshire, UK. He is one of the most pre-eminent sports medicine and orthopedic consultants in the UK. He is currently editor in chief of Continuous Medical Education in Orthopaedics and is an editorial board member for the British Journal of Sports Medicine, Clinical Journal of Sport Medicine, and Arthroscopy. He is President of the British Orthopaedic Sports Trauma Association (BOSTA) and serves as an examiner for the Royal College of Surgeons, Edinburgh, and for the Intercollegiate Academic Board of Sports and Exercise Medicine. His areas of particular clinical interest include tendon problems, ACL injuries, and the management of osteoarthritis in young patients. It is always an honor to be asked to write a preface. Apprehensive: I am still wary of not being able to convey how good this whole endeavor is. A great many orthopods of their time—true innovators, forward thinkers, superb surgeons with impeccable technique—taught me the science and the art of trauma and orthopedic surgery. My two great mentors, Mr. John Fixsen, MChir, FRCS, and Prof. John B King, FRCS, FFSEM, both now sadly deceased,  had two things in common, in addition to their first names: they taught me that one should learn concepts, not techniques. Another one of my teachers, again not with us any longer, Prof. Richard Porter, MD FRCS, explained to me why techniques can, and do, become obsolete overnight, while concepts remain and allow us to progress. This is the essence of what I try and communicate to my trainees, though at times I feel that I am fighting a losing battle: indeed, the requirements of modern health care and the pressures we are subjected to seem to favor a purely technical approach to our specialty. Unfortunately, if we just act as technicians, we forget to be professionals and lose sight of the fact that our specialty, Trauma and Orthopedics, also embraces the

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First Foreword to the Second Edition

basic sciences of the musculoskeletal system and a great deal of nonoperative means of musculoskeletal conditions. This second edition is a progress but retains the essence of the first one. The title itself reflects how it should open the minds of readers. We should learn the general principles and use the book not as an end but as the first step of a one thousand miles journey in our specialty that has started with this text. And, in years to come, remember that it all started from here. The approach used to develop and embrace knowledge in this second edition is “traditional.” It does not mean that it is obsolete. It means instead that it is stimulating and an eye opener. It should open the reader’s mind to search for the physiopathology of the conditions described and identify through  the now ever present electronic databases the latest research in our field. The two editors have performed an Atlantean task, a never ending quest for better, deeper, more detailed knowledge, expressed in an easy-to-understand language, with figures to match. Have fun, and enjoy reading it Nicola Maffulli Specialty Surgery Department University of Salerno Medical School Salerno, Italy Queen Mary University of London Centre for Sport and Exercise Medicine London, England Keele University School of Medicine Institute of Science and Technology in Medicine Stoke on Trent, England

Second Foreword to the Second Edition

I was pleased and honored to receive a request from K.  Mohan Iyer to write a foreword for the second edition of this book entitled “General Principles of Orthopedics and Trauma.” Edited by Dr. Iyer himself and my colleague from Cambridge, Mr. Wasim S. Khan, this book is certainly one which not only addresses the basic principles in trauma and orthopedics but also handles the latest developments in the field. There are many textbooks on the topic, but there are not many that cover the breath of orthopedics and trauma and apply to different healthcare settings and at the same time are suitable to different level of practitioner expertise. This book achieves this by being internationally relevant to healthcare practitioners of all levels of experience. The senior author is a very experienced orthopedic and trauma surgeon who has worked, taught, and collaborated across the world. His experience allows a timeless dimension to the book that builds on basic principles and critically analyses the current trends. As anyone who has written a book of this magnitude would appreciate, selecting and coordinating international authors of different chapters, getting relevant permissions, and liaising with the publishers are a mammoth task. This does not become easier with the second edition where there is pressure to build on previous successes. I believe the editors have managed this task extremely well. They have built on the more traditional chapters in the first edition and supplemented them with chapters that cover stem cells and regenerative medicine, advanced trauma and arthroplasty techniques including robotics, and, a topic very close to my heart, hip preserving surgery.

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Second Foreword to the Second Edition

I do hope you enjoy reading the book. I believe it will help build strong foundations that will enable readers across the globe to deliver orthopedic and trauma care for years to come. Vikas Khanduja Addenbrooke’s Hospital Cambridge, UK University of Cambridge Cambridge, UK

Foreword to the First Edition

Several decades ago I was fortunate to hear Dr. K.  Mohan Iyer speak about a limited, posterior greater trochanteric osteotomy as an adjunct to a posterior approach to the hip. Since then I have used this method, as it allows easy access to the hip for joint replacement and then a secure posterior capsule and short external rotator muscle repair upon joint closure. Postoperative dislocations ceased to be an issue. As you might recognize, I have looked forward to additional contributions from Dr. Iyer, and here we have it—General Principles of Orthopedics and Trauma, Orthopedics of the Upper and Lower Limb, and Trauma Management in Orthopedics (Springer). What a huge task to organize such books: Deciding on the material to be included, writing multiple chapters, and asking for skilled contributors who will embrace the challenge and have the talents to write either a general or subspecialty chapter. The text is aimed at the newcomer to this field of medicine, and it will serve that purpose quite well. I have always felt the best approach to learning orthopedic surgery is to read, cover to cover, a text such as this, aggressively study anatomy, read about the problems in the patients under one’s care, read subspecialty texts, and read at least the abstracts in selected journals. By doing these things one can be an educated person in the field—but it starts with the basic text! In addition to the fundamentals, Dr. Iyer has added details about trauma and regional orthopedics. A cad has said only two types of doctors are necessary, and the others are optional. One of these is a physician who cares for broken bones. Details about fractures are essential to the field and to humanistic patient care. The regional chapters serve as a transition to the later reading about each anatomic region in detail, what will be required to become an orthopedic surgeon. So there you have it. An editor who is an energetic, dedicated scholar and teacher. Plus, the type of textbook most needed to jump into the field of musculoskeletal medicine and surgery. Learning is a joy. Lucky readers, enjoy the intellectual journey. Rochester, MN, USA

Robert H. Cofield xi

Preface

I have mainly written this preface in memory of late Mr. Geoffrey V. Osborne, who was like a father figure to me. After his retirement from the University of Liverpool, he was busy writing a thesis for his PhD in printing from the University of Liverpool, UK, which he managed to get in the end. During his later years just before his retirement, he was extremely keen to propagate his approach and nicknamed it the “Liverpool Approach,” along with late Professor Robert Owen, both of whom attended the Indian Orthopaedic Association and were patrons of the same. Late Mr. Osborne inspired me with his approach and knowledge of orthopedics, which is unforgettable, and I would not have followed in his footsteps had it not been for him. He patiently listened when I presented my original research on the hip joint done in Liverpool, with my teacher, late Dr. Rasik M. Bhansali, who was the chairman at the Conference of the Association of Surgeons of India in December 1982. Despite my original research work on the hip joint, he inspired me to do a follow-up of his cases of excision of the trapezium and arthrography of the pseudojoint to be presented as a thesis to the University of Liverpool, UK, for the MCh Orth. degree, along with Prof. Graham Whitehouse, the newly appointed professor of radiodiagnosis at the University of Liverpool, UK. I am extremely grateful to Magdi E.  Greiss, MD, MCh Orth., FRCS, Senior Consultant Orthopedic Surgeon, North Cumbria University Hospitals, UK, and Former President, BOFAS, UK, for his invaluable snaps, which he had preserved in his life during his training and early years after becoming a consultant in orthopedics. The first foreword has been written by Professor Nicolla Maffulli as there was considerable anxiety regarding the foreword being given by Vikas Khanduja which he had assured me of the same at a very early stage in the publication of this book. I have been extremely fortunate to get the second foreword from Vikas Khanduja who was in Coimbatore for IOACON 2018 to deliver the AK Saha Eponymous Lecture. Vikas Khanduja is a Consultant Orthopedic Surgeon specializing in both xiii

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the arthroplasty and sports surgery aspects of hip and knee surgery and has a particular interest in arthroscopic surgery (keyhole) of the hip and the knee. He holds a full time consultant position in trauma and orthopedic surgery based at Addenbrooke's at the Cambridge University Hospitals NHS Trust. He is also the co‐founder of the London Hip Arthroscopy Centre based at the Wellington Hospital in London. He also consults and operates at the Spire Cambridge Lea Hospital and the Nuffield Hospital in Cambridge. He qualified as a doctor in 1997. He then obtained his Basic Surgical Training in London. Following this he received his Higher Surgical Training in Trauma and Orthopedics on the North Thames circuit (Royal London Hospital Rotation) in London, gaining the FRCS (Orth) in 2005. Subsequently, he undertook his subspecialty training fellowships in knee and hip surgery with eminent surgeons in the field in London by my former colleague (late Mr. GSE Dowd) and Cambridge (Mr. RN Villar) and then went to Prof. Ganz in Zurich and Prof. Salvati at Hospital for Special Surgery in New York to further refine his surgical techniques in hip surgery. He writes and lectures extensively and is on the faculty for many national and international courses teaching arthroplasty and arthroscopic techniques in knee and hip surgery. He convenes the Basic Science Course in Cambridge and the Advances in Knee Arthroplasty meeting in London annually. He is also the associate editor of the Journal of Bone and Joint Surgery (Br). Following his appointment in Addenbrooke’s, he has been instrumental in establishing the tertiary Young Adult Hip Service in Cambridge. He has performed over 1000 hip arthroscopies and hip preservation procedures. Mr. Vikas Khanduja now offers robotic orthopedic surgery at Nuffield Health Cambridge Hospital with the state-of-the-art Mako™ robotic arm system. Robotic arm-assisted surgery provides patients with a personalized surgical plan for joint replacement surgery. The system works alongside the surgeon from the presurgery planning stage through to assisting in the surgery itself in order to improve the accuracy and precision of the procedure.

Acknowledgments I would like to thank Dr. David Rajan, M.S. Orth, MNAMS, FRCS(G), Consultant Orthopedic Surgeon, Director, Ortho One, Coimbatore, India, and Past President of the Indian Arthroscopy Society, India, for updating the chapter on “Arthroscopy of the Knee” in an up-to-date manner that it has developed into. I would also like to thank Sharad Goyal,Associate Specialist,D. Ortho (Gold Med), M.S. (Ortho), DNB(Ortho), M.Ch.Ortho (Liv) e-mail: [email protected],Tarang Tandon,MBBS, M.S, MRCS, Associate Specialist,email:tandon 2004@yahoo. co,uk,Dhrumin Sangoi, Registrar,email:[email protected] and Edward J.C.Dawe,Consultant Foot and Ankle Surgeon, email:[email protected]. uk for their chapter no.20 on Total Joint Replacement along with the Mr. Edward J.C.  Dawe, Consultant Orthopedic Surgeon at the above hospital for his help

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particularly in the addition of the Total Ankle and MTP joint section (big toe) in this difficult chapter. I would also like to thank Dr. E McLoughlin, Dr. E M Parvin, Dr. S L James, and Dr. R Botchu at the Radiology Department, Royal Orthopaedic Hospital, Birmingham, United Kingdom, and the Physics Department, The Open University, Milton Keynes, United Kingdom, for their chapter on “Recent Advances in Imaging and Radiology in Orthopedics.” I am also grateful to Dr. Prakash Chandran, Consultant Orthopedic Surgeon, Warrington and Halton Hospitals NHS Foundation Trust, for his excellent original chapter on “Sports Injuries to the Hip Joint.” I would extend my gratefulness to Prof. Raju Vaishya [MS, MCh Orth, FRCS Eng, President, Indian Cartilage Society and  Arthritis Care Foundation, Senior Consultant Orthopedic and Joint Replacement Surgeon, Indraprastha Apollo Hospitals, New Delhi, INDIA] and Dr. Abhishek Vaish for their evolving chapters on “Stem Cell Therapy in Orthopedics and  3D Printing.” Above all I am grateful to Dr. Hiran Amarasekera, Orthopedic Research Fellow/PhD and Consultant Orthopedic Surgeon, Warwick Medical School, University of Warwick, UK, who helped me out with his innovative chapter on “The Direct Anterior Approach to the Hip Joint” owing to the pulling out of a contributor at the last minute and in a short span of time. I am thankful for the chapter on “Advances in Short-Stem THA” by Dr. med. Karl Philipp Kutzner, St. Josefs Hospital, 65189 Wiesbaden, Germany, along with permissions for figures from Mathys Ltd Bettlach, which is an evolving concept on the continent and the world in total hip arthroplasty. I am extremely grateful and obliged to Mr. Wasim S. Khan, MBChB, MRCS, Dip Clin Ed, MSc, PhD, FRCS (Tr&Orth), University Lecturer, University of Cambridge, Honorary Consultant Trauma and Orthopedic Surgeon, Addenbrooke's Hospital, Cambridge, for his supervision and guidance of the junior residents, Jeeshan Rahman and Karam Al-Tawil, in their chapter on the “Use of RoboticAssisted Surgery in Orthopedics”; and also for his valuable guidance to Damien Gill and Fouzia Khatun for their excellent presentation of their chapter with drawings by Springer in the inter-locking nailing system and technique. He has helped immensely in the chapter on “Total Knee Replacement” written by Nadim Tarazi and Rui Zhou, though this has been covered partly in an excellent way in Chapter 20, “Total Joint Replacement,” written by Sharad Goyal, Tarang Tandon, Dhrumin Sangoi, and Edward J.C.  Dawe. His guidance especially in the chapter on “Endoscopic Surgery in Orthopedics” written by Rosey Tansey and Mike Dunne is acknowledged. He has provided valuable contribution to the chapter on “Hip Preserving Surgery” written by Jason Patel and Wasim S. Khan, though he has contributed to the chapter on “Digital Templating in Total Hip Arthroplasty,” in my book Hip Preservation Surgery along with Shalin Shaunak. He has provided guidance in the development of the chapter on “Recent Advances in Minimally Invasive Surgery in Orthopedics” written by Mira Pecheva and Humza Osmani, a concept which has gained considerable importance recently to avoid infection. Above all, his participation in the chapter on “Advances in Bearing Surfaces in Total Hip Arthroplasty” written by Kate Spacey and Al Durst is valuable.

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I would also like to express my thanks to Dakshini Egodawatte for her immense help and patience in helping out with the figures in Chapter 29. Above all, I am extremely thankful to Mr. Anand Shanmugam (Project Coordinator [Books] for Springer Nature, SPi  Global DLF  –  SEZ IT Park, Manapakkam, Chennai, India - 600 089) and Ruga Lincy ([Ms.], Project Manager, SPi Technologies India Private Ltd.) for their help, patience, and assistance during formatting and publishing the entire book. Also I would like to thank Mr. Mohan Kumar, Graphics Designer Bangalore, India for his immense help in line diagrams used in this book, which have been sketched by using an illustrative tool. Above all I highly appreciate the help of my son, Mr. Rohit Iyer, in the presentation and publication of this book. Bengaluru, Karnataka, India

K. Mohan Iyer

Preface

Trauma and orthopedics is an ever-evolving specialty, and the second edition of this established textbook was an obvious step. The book covers basic sciences and pathology as well as the breadth of trauma and orthopedic practice. It would be useful to medical students as well as trainees and specialists in orthopedics. The order of the chapters is logical and the layout is easy to follow. The recent additions include sections on stem cells, 3D printing, robotics, minimally invasive surgery, and advances in arthroplasty and ensure the book reflects the interesting times and challenges that the specialty faces.

Acknowledgments Dr. K. Mohan Iyer is an internationally renowned orthopedic surgeon, teacher, and mentor with whom it has been an honor to collaborate with on this venture. I am grateful to the many international authors and especially ORCA (Orthopaedic Research Collaborative east Anglia) for updating the previous chapters and adding in new chapters that reflect the evolving face of orthopedics. It is a pleasure to have one of my great mentors, Professor Maffulli, and a Cambridge colleague, Mr. Khanduja, write the forewords to this edition. Above all I would like to acknowledge all of our patients who I believe it is a great honor to treat. Hopefully in at least some small way our patients would be better served by this collection of knowledge. Cambridge, UK

Wasim S. Khan

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Contents

1 Anatomy of Bone, Fracture, and Fracture Healing��������������������������������   1 K. Mohan Iyer 2 Complications of Fractures ����������������������������������������������������������������������  19 K. Mohan Iyer 3 Fractures in Children��������������������������������������������������������������������������������  27 K. Mohan Iyer 4 Infection������������������������������������������������������������������������������������������������������  35 K. Mohan Iyer 5 Osteoarthritis����������������������������������������������������������������������������������������������  57 K. Mohan Iyer 6 Rheumatoid Arthritis��������������������������������������������������������������������������������  63 K. Mohan Iyer 7 Tuberculosis������������������������������������������������������������������������������������������������  75 K. Mohan Iyer 8 Peripheral Nerve Lesions�������������������������������������������������������������������������� 117 K. Mohan Iyer 9 Congenital Anomalies�������������������������������������������������������������������������������� 129 K. Mohan Iyer 10 Metabolic and Endocrine Disorders�������������������������������������������������������� 183 K. Mohan Iyer 11 Developmental Disorders�������������������������������������������������������������������������� 249 K. Mohan Iyer 12 Degenerative Disorders����������������������������������������������������������������������������� 259 K. Mohan Iyer 13 Poliomyelitis and Spina Bifida������������������������������������������������������������������ 297 K. Mohan Iyer

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14 Cerebral Palsy�������������������������������������������������������������������������������������������� 309 K. Mohan Iyer 15 Bone Tumors���������������������������������������������������������������������������������������������� 323 K. Mohan Iyer 16 Low Back Pain�������������������������������������������������������������������������������������������� 367 K. Mohan Iyer 17 General Affections of the Soft Tissues������������������������������������������������������ 379 K. Mohan Iyer 18 Amputations ���������������������������������������������������������������������������������������������� 385 K. Mohan Iyer 19 Arthroscopy and Tissue Engineering ������������������������������������������������������ 407 Pradeep Baskaran and David V. Rajan 20 Total Joint Replacement���������������������������������������������������������������������������� 429 Sharad Goyal, Tarang Tandon, Dhrumin Sangoi, and Edward J. C. Dawe 21 Recent Advances in Imaging and Radiology in Orthopedics���������������� 491 E. McLoughlin, E. M. Parvin, S. L. James, and R. Botchu 22 Plaster of Paris ������������������������������������������������������������������������������������������ 527 K. Mohan Iyer 23 Emergencies in Orthopedics �������������������������������������������������������������������� 535 K. Mohan Iyer 24 Sports Injuries to the Hip Joint���������������������������������������������������������������� 553 Prakash Chandran and Rohit Singhal 25 Stem Cells in Orthopedics ������������������������������������������������������������������������ 575 Raju Vaishya and Abhishek Vaish 26 3D Printing in Orthopedics ���������������������������������������������������������������������� 583 Raju Vaishya and Abhishek Vaish 27 External Fixation �������������������������������������������������������������������������������������� 591 K. Mohan Iyer 28 The Principles of the Ilizarov Apparatus ������������������������������������������������ 607 K. Mohan Iyer 29 The Direct Anterior Approach to the Hip������������������������������������������������ 619 Hiran Amarasekera 30 Use of Robotic-Assisted Surgery in Orthopedics������������������������������������ 629 Jeeshan Rahman, Karam Al-Tawil, and Wasim S. Khan

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31 The Interlocking Nailing System and Technique������������������������������������ 639 Damien F. Gill, Fouzia Khatun, and Wasim S. Khan 32 Total Knee Replacement���������������������������������������������������������������������������� 661 Nadim Tarazi, Rui Zhou, and Wasim S. Khan 33 Endoscopic Surgery in Orthopedics�������������������������������������������������������� 681 Rosamond J. Tansey, Michael J. Dunne, and Wasim S. Khan 34 Hip-Preserving Surgery���������������������������������������������������������������������������� 693 Jaison Patel and Wasim S. Khan 35 Recent Advances in Minimally Invasive Surgery in Trauma and Elective Surgery ������������������������������������������������������������������ 705 Mira Pecheva, Humza Tariq Osmani, and Wasim S. Khan 36 Short-Stem Total Hip Arthroplasty���������������������������������������������������������� 717 Karl Philipp Kutzner 37 Advances in Bearing Surfaces of Total Hip Arthroplasty���������������������� 739 Alexander Durst, Kate Spacey, and Wasim S. Khan Index�������������������������������������������������������������������������������������������������������������������� 747

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Anatomy of Bone, Fracture, and Fracture Healing K. Mohan Iyer

The osseous tissue (osteon) is a specialized form of dense connective tissue consisting of bone cells (osteocytes) which are embedded in a matrix of calcified intercellular substance which contains collagen fibers and the minerals calcium phosphate and calcium carbonate. The process of bone formation is called ossification. All bone is of mesodermal origin and there are two types of ossification, namely (1) intramembranous ossification and (2) endochondral ossification. 1. Intramembranous ossification is a mesenchymal condensation and highly ­vascular. It is a process of laying down of bundles of collagen fibers in the mesenchymal condensation with osteoblast formation called osteoid and involves calcium salts deposition to form the lamellus of bone. In the development of the ossification center, the osteoblasts secrete the organic extracellular matrix resulting in calcification whereby calcium and other mineral salts are deposited and the extracellular matrix calcifies or ossifies. The extracellular matrix then develops into trabeculae which fuse to form spongy bone. The mesenchyme at the periphery of the bone develops into the periosteum. 2. Endochondral ossification ossifies bones that originate as hyaline cartilage; most bones originate as hyaline cartilage, and growth and ossification of long bones occurs in six steps, namely: Step 1: when the chondrocytes in the center of hyaline cartilage first enlarge to form struts and then calcify and later die, leaving cavities in cartilage, Step 2: when the blood vessels grow around the edges of the cartilage and the cells in the perichondrium change to osteoblasts which produce a layer of superficial bone around the shaft which will continue to grow and become compact bone, a process called as appositional growth. Step 3: when blood vessels enter the cartilage bringing fibroblasts that become osteoblasts and the spongy develops as the primary ossification center. Step 4: when remodeling creates a marrow cavity and bone replaces cartilage at the metaphyses. K. M. Iyer (*) Royal Free Hampstead NHS Trust, Royal Free Hospital, London, UK © Springer Nature Switzerland AG 2019 K. M. Iyer, W. S. Khan (eds.), General Principles of Orthopedics and Trauma, https://doi.org/10.1007/978-3-030-15089-1_1

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Step 5: when capillaries and osteoblasts enter the epiphyses creating secondary ossification centers. Step 6: when the epiphyses are filled with spongy bone when (a) the cartilage within the joint cavity is the articulation cartilage and (b) the cartilage at the metaphysis is epiphyseal cartilage. It must be summarized here that (1) Steps 1–3 occur during the fetal week 9 through till the 9th month; (2) Stage 4 is just before birth; and (3) Stage 5 is the process of long bone growth during childhood and adolescence. Thus, in the skeletal organization, typically there are about 206 bones, and the actual number of bones in the human skeleton varies from person to person and for convenience the skeleton is divided into the: (1) axial skeleton and (2) appendicular skeleton, with the axial skeleton comprising of skull, spine, and rib cage, and the appendicular skeleton consisting of the upper limbs, lower limbs, shoulder girdle, and the pelvic girdle. Classification of bones by shape are as follows: (1) long bones (humerus), (2) short bones, (3) flat bones (sternum), (4) irregular bones (vertebrae), (5) pneumatized bones, and (6) sesamoid bones (short bones). 1. Long bones: They have a diaphysis or shaft, an epiphysis which are the expanded ends, a shaft with three surfaces and three borders, a medullary cavity, and a nutrient foramen directed away from the growing end, for example, humerus, radius, ulna, and femur. 2. Short bones: They are small and thick with their shape usually cuboid, cuneiform, trapezoid, or scaphoid, for example, carpal and tarsal bones. 3. Flat bones: They are thin with parallel surfaces, and are found in the skull, sternum, ribs, and scapula. They form boundaries of certain body cavities and resemble a sandwich of spongy bone as they are between two layers of compact bone. 4. Pneumatic bones: They are certain irregular bones containing large air spaces lined by epithelium. They make the skull light in weight, help in resonance of voice, and act as air conditioning chambers for inspired air, for example, maxilla, sphenoid, and ethmoid. 5. Sesamoid bones: They resemble a grain of sesame in size or shape as bony nodules found embedded in the tendons or joint capsules. They have no periosteum and ossify after birth and are related to an articular or nonarticular bony surface, for example, patella, pisiform, and fabella. 6. Irregular bones. They have complex shapes, for example, spinal vertebrae and pelvic bones.

Developmental Classification They occur in (1) membrane (dermal) bones, (2) cartilaginous bones, and (3) membrano-­cartilagenous bones. 1. Membrane (dermal) bones: They ossify in membrane (intramembranous of ­mesenchymal) and are derived from mesenchymal condensations, for example,

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the bones of the vault of skull and facial bones, and defect causes cleidocranial dysostosis. 2. Cartilaginous bones: They ossify in cartilage (intracartilaginous or endochondral) and are derived from preformed cartilaginous models, for example, bones of limbs, vertebral column, and thoracic cage, and any defect results in the common type of dwarfism called achondroplasia. 3. Membrano-cartilagenous bones: They ossify partly in cartilage and partly in membrane, for example, the clavicle, mandible, and occipital.

Structure of Bone Bone cells: They are elements comprising bone tissue. Bone tissue consists of bone cells or osteocytes separated by intercellular substance (mature bone cell that maintains the bone matrix) which consists of (1) osteoblasts which are bone producing cells (immature bone cells secreting the organic components of the matrix), (2) osteoclasts which are bone removing cells (multinucleate cell which secretes acids and enzymes to dissolve bone), and (3) osteoprogenitor cells from which are derived osteoblasts and osteoclasts (stem cell whose divisions produce osteoblasts). • Osteoprogenitor cells: They are mesenchymal stem cells that divide to produce osteoblasts and are located in inner, cellular layer of the periosteum (endosteum) which mainly assist in fracture repair. • Osteoblasts: They are immature bone cells that secrete matrix compounds (osteogenesis). The osteoid is the matrix produced by osteoblasts, but not yet calcified to form bone, and these osteoblasts which are surrounded by bone become osteocytes. • Osteocyte: These are mature bone cells that maintain the bone matrix. They live in lacunae and are located between layers (lamellae) of matrix which connect by cytoplasmic extensions through canaliculi in lamellae and do not divide. • Osteoclast: They are giant, multinucleate cells which secrete acids and protein-­ digesting enzymes which dissolve bone matrix and release stored minerals (osteolysis). They are derived from stem cells that produce macrophages.

Structural Classification Macroscopically they are divided into (1) compact bone and (2) cancellous bone. 1. Compact bone is strong and dense to make 80% of the skeleton. It consists of multiple osteons (haversian systems) with intervening interstitial lamellae which is best developed in the cortex of long bones. These osteons are made up of concentric bone lamellae with a central canal (haversian canal) containing o­ steoblasts and an arteriole supplying the osteon. These lamellae are connected by canaliculi which are cement lines which mark the outer limit of osteon (bone resorption

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Fig. 1.1  Line diagram showing the parts of a bone

Articular cartilage

Epiphysis

Epiphyseal line

Spongy bone Medullary cavity Nutrient foramen

Diaphysis

Endosteum Periosteum

Articular cartilage

Epiphysis ended). The Volkmann’s canals are radially oriented, having an arteriole, and connect adjacent osteons which is an adaptation to bending and twisting forces (compression, tension, and shear). 2. Osteon: This is the basic unit of mature compact bone (Fig. 1.1) which has osteocytes arranged in concentric lamellae, around a central canal containing blood vessels. 3. Cancellous bone (spongy or trabecular): This is open in texture containing a meshwork of trabeculae (rods and plates) with crossed lattice structure which makes up 20% of the skeleton. It has a high bone turnover rate as bone is resorbed by osteoclasts in Howship’s lacunae and formed on the opposite side of the trabeculae by osteoblasts. Here, osteoporosis is common in cancellous bone, making it susceptible to fractures which is commonly found in the metaphysis and epiphysis of long bones and caused by adaptation to compressive forces. It does not have osteons but the matrix forms an open network of trabeculae which have no blood vessels. Microscopically, it is made up of (a) lamellar bone and (b) woven bone. (a) The lamellar bone is made up of layers or lamellae which is a thin plate of bone consisting of collagen fibers and mineral salts, deposited in gelatinous ground substance, and between adjoining lamellae we see small flattened spaces called lacunae. These lacunae (1) contains one osteocyte, (2) have fine canals or canaliculi that communicate with those from other lacunae, and the fibers of one lamellus run parallel to each other, but those of adjoining lamellae run at varying angles to each other.

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(b) Woven bone is found in all newly formed bone and is later replaced by lamellar bone. They have collagen fibers that are present in bundles which run randomly and interlacing with each other. An abnormal persistence is found in Paget’s disease.

Gross Structure of an Adult Long Bone It consists of a shaft and two ends (Fig. 1.2). The shaft is composed of: (1) periosteum, (2) cortex, and (3) medullary cavity. Periosteum: The external surface of any bone covered by a membrane which has two layers, an outer fibrous membrane and an inner which is mainly cellular. In young bones the inner layer has numerous osteoblasts and forms the osteogenetic layer. In adults these osteoblasts are not conspicuous, but osteoprogenitor cells present here can form osteoblasts when the need arises. Its functions are as follows: (a) it is a medium through which muscles, tendons, and ligaments are attached, (b) it forms a nutritive function, (c) it can form bone when required, and (d) it also forms a limiting membrane that prevents bone tissue from “spilling out” into neighboring tissues. The cortex is made up of a compact bone which gives the desired strength and can withstand all possible mechanical strains. The endosteum is an incomplete cellular layer which lines the marrow cavity and covers trabeculae of spongy bone and also lines central canals. It contains osteoblasts, osteoprogenitor cells, and osteoclasts and is active in bone growth and repair. The medullary cavity is filled with red or yellow bone marrow; it is red at birth, indicating hemopoiesis, and yellow as age advances, which atrophies and becomes fatty, but red marrow persists in the cancellous ends of long bones. The parts of young bone: It ossifies in three parts, the two ends from the secondary centers with the intervening shaft from a primary center. The epiphysis is located at the ends of a bone which ossify from secondary centers and are of various types such as (1) pressure epiphysis, which are concerned with transmission of the weight, for example, the head of the femur, (2) traction epiphysis, which provides attachment to one or more tendons and which exerts a traction on the epiphysis, for Osteocyte cell body within lacuna Osteocyte cellular extensions within canaliculi (connect lamellae) Cement line (arks end of osteon. liis where osteoblastic bone resorption stopped and new bone formation began). Oldest bone in the osteon Newest bone in the osteon

Fig. 1.2  Line diagram showing the basic structure of a long bone

lnterstitial lamellae (not part of the osteon) Central (haversian) canal containing capillary, nerve fiber, and perivascular (progenitor) cells and lined with osteoblasts

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example, the trochanters of femur, (3) atavistic epiphysis, which phylogenetically is an independent bone that fuses to another bone, for example, the coracoids process of scapula, and (4) aberrant epiphysis, which is not always present, for example, the head of the first metacarpal and base of other metacarpal. The diaphysis is the elongated shaft of a long bone that ossifies from a primary center and is made of thick cortical bone which is filled with bone marrow. The metaphysis is at the epiphyseal ends of a diaphysis. It is a zone of active growth that is typically made of cancellous bone which has hairpin bends of end arteries. The epiphyseal plate of cartilage separates epiphysis from the metaphysis and its proliferation is responsible for the lengthwise growth of the long bone and can no longer grow when there is epiphyseal fusion. It is nourished by both epiphyseal and metaphyseal arteries.

Blood Supply of Bones In long bones the blood supply is derived from: (1) nutrient artery, (2) periosteal artery, (3) epiphyseal artery, and (4) metaphyseal artery (Fig. 1.3).

Articular cartilage

Epiphysis

Epiphyseal vein Epiphyseal artery Epiphyseal line

Metaphysis

Metaphyseal vein Metaphyseal artery Periosteum Periosteal artery Periosteal vein Medullary cavity

Diaphysis

Compact bone

Nutrient foramen Nutrient vein Nutrient artery

Fig. 1.3  Line diagram showing the blood supply of a long bone

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1. Blood supply from the nutrient artery: (a) enters through the nutrient foramen, (b) and then divides into ascending and descending branches. In the medullary cavity, (c) the branch divides into small parallel channels which terminate in adult metaphysis, (d) anastomosing with the epiphyseal, metaphysical, and periosteal arteries which (e) supply the medullary cavity, inner two-third of the cortex, and metaphysis and (f) a nutrient foramen which is directed away from the growing end of the bone. 2. Periosteal arteries: (a) They are numerous beneath the muscular and ligamentous attachments, (b) They ramify beneath the periosteum and enter the Volkmann’s canals to supply the outer one-third of the cortex. 3. Epiphyseal arteries: (a) They are derived from periarticular vascular arcades (circulus vasculosus), (b) They arise out of the numerous vascular foramina in this region and a few admit arteries and rest venous exits, (c) Their number and size give an idea of the relative vascularity of the two ends of long bone. 4. Metaphyseal arteries: (a) They are derived from the neighboring systemic vessels and (b) pass directly into the metaphysis and reinforce the metaphyseal branches from the primary nutrient artery.

Homeostasis of Bone Tissue (1) Bone resorption occurs by the action of osteoclasts and parathyroid hormone aka parathormone aka PTH, (2) bone deposition occurs by the action of osteoblasts and calcitonin and (3) by direction of the thyroid and parathyroid gland.

Factors Affecting Bone Tissue 1 . Deficiency of vitamin A retards bone development. 2. Deficiency of vitamin C results in fragile bones. 3. Deficiency of vitamin D results in rickets and osteomalacia. 4. Insufficient growth hormone results in dwarfism. 5. Excessive growth hormone results in gigantism and acromegaly. 6. Insufficient thyroid hormone delays bone growth. 7. Sex hormones: They promote bone formation and stimulate the ossification of epiphyseal plates. 8. Physical stress stimulates bone growth.

Chemical Analysis of Bone The bone consists of organic (Ca, phosphorus, sodium, magnesium, carbonate, and phosphate) and inorganic constituents (Fig. 1.4).

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K. M. Iyer Bone Contains...

Composition of Bone

Organic compounds (mostly collagen) 33%

Calcium 39% Potassium 0.2% Sodium 0.7% Magnesium 0.5% Carbonate 9.8%

99% of the body’s Calcium 4% of the body’s Potassium 35% of the body’s Sodium 50% of the body’s Magnesium 80% of the body’s Carbonate

Phosphate 17%

99% of the body’s Phosphate

Total inorganic 67% components

Fig. 1.4  Line diagram showing the constituents of bone

Applied Anatomy 1. The periosteum is particularly sensitive to tearing or tension as follows: (a) Drilling into the compact bone without anesthesia which causes only dull pain while (b) Drilling into spongy bone is much more painful and (c) Fractures, tumors, and infections of the bone are very painful 2. The blood supply of bone is so rich that it is very difficult to sufficiently kill the bone. 3. In rickets the calcification cartilage fails and ossification of the growth zone is disturbed. As a result: (a) The osteoid tissue is formed normally and the cartilage cells proliferate freely, while (b) Mineralization does not take place 4. In scurvy the formation of collagenous fibers and matrix is impaired. 5. In osteoporosis bone resorption proceeds faster than deposition.

Fracture Definition: A fracture is a break or disruption in the continuity of bone or it is a disruption of the normal architecture of the bone. Etiology: 1. Traumatic injuries. 2. Fractures occur when the bone is subjected to stress greater than it can absorb. 3. Fractures are caused by direct blows, crushing forces, sudden twisting motions, and even extreme muscle contractions. 4. Metabolic bone diseases like osteoporosis.

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Predisposing factors: 1. Neoplasm. 2. Postmenopausal estrogen loss. 3. Protein malnutrition. 4. High-risk recreation and employment-related activities (rock climbing). 5. Victims of domestic violence.

Classification of Fractures 1. Type 2. Communication or noncommunication with the external environment 3. Anatomic location of the fracture on the involved bone Types of fractures (Fig. 1.5): a

b

c

d

Avulsion Comminuted

Displaced

Greenstick

Fig. 1.5  Line diagram showing the different types of fractures. (a) Avulsion: Avulsion is a fracture of bone resulting from the strong pulling effect of tendons or ligaments at their bone attachment. (b) Comminuted fracture: It is a fracture with more than two fragments. The smaller fragments may appear to be floating. (c) Displaced (overriding) fracture: It involves a displaced fracture segment that is overriding the other bone fragment. The periosteum is disrupted on both sides. (d) Greenstick fracture: It is an incomplete fracture with one side splintered and the other side bent. (e) Impacted fracture: It is a comminuted fracture in which more than one fragments are driven into each other. (f) Interarticular fracture: It is a fracture extending to the articular surface of the bone. (g) Longitudinal fracture: It is an incomplete fracture in which the fracture line runs along the longitudinal axis of the bone and the periosteum is not torn away from the bone. (h) Oblique fracture: It is a fracture in which the line of the fracture extends in an oblique direction to the longitudinal axis of the bone. (k) Pathologic fracture: It is a spontaneous fracture at the site of bone disease whose causes are bone tumors, metastatic lesions, infection, metabolic disease, and an injury to old fracture site. (i) Spiral fracture: It is a fracture in which the line of the fracture extends in a spiral direction along the shaft of the bone where the bone is usually broken by twisting. (l) Stress fracture: It is a fracture that occurs in normal (Fig. 1.6) or abnormal bone that is subject to repeated (Figs. 1.7 and 1.8) stress, such as from jogging or running. They are considered as overuse injuries. (j) Transverse fracture: It is a fracture in which the line of the fracture extends across the bone shaft at a right angle to the longitudinal axis of the bone. (m) Depressed fracture of the skull: When the skull is fractured inward. (n) Hairline fracture: A very thin crack or break in the bone is a hairline fracture. An important point is does the fracture have any communication or noncommunication with the external environment to differentiate whether it is an open fracture when there is a communication or a closed fracture when there is no communication with the external environment

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e

f

Impacted

i

g

Interarticular

j

h

Longitudinal

k

Oblique

l

Stress Pathologic

m

Transverse

Spiral

n

Hairline fracture

Fig. 1.5 (continued)

Pathophysiology Initially following a fracture there is a disruption of muscles attached to the bone when the muscles undergo spasm and pull the fracture fragments out of position. The fracture fragments may be displaced sideways and may also be rotated with the periosteum and blood vessels in the cortex and marrow of the fractured bone being

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Fig. 1.6  Stress fracture classic sites (Courtesy: Magdi E. Greiss, Whitehaven, Cumbria, UK)

Figs. 1.7 and 1.8  Missed stress fracture fibula treated by lengthening, grafting, and fixation (Courtesy: re-used with the kind permission of Magdi E. Greiss, Whitehaven, Cumbria, UK)

disrupted when bleeding occurs from both the soft tissue and the damaged end of bone to result in a hematoma in the medullary canal. Thereafter the bone tissue surrounding the fracture site dies, creating an intense inflammatory response. Vasodilatation, edema, pain, loss of function, exudation of plasma, and leukocytosis result, which serve as the initial step in bone healing.

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Fracture Healing • First stage: Fracture hematoma: when a fracture occurs, bleeding creates a hematoma, which surrounds the ends of the fragments (within 72 h). • Second stage: Granulation tissue: active phagocytosis absorbs the products of local necrosis. The hematoma converts to granulation tissue. Granulation tissue produces the basis for new bone substance called osteoid (days 3–14). • Third stage: Callus formation: As minerals and new bone matrix are deposited in the osteoid, an unorganized network of bone is formed. It usually appears by the end of the second week after injury. Evidence of callus formation can be verified by X-ray. • Fourth stage: Ossification: Ossification of the callus occurs from 3  weeks to 6 months after the fracture and continues until the fracture has healed. During this stage of clinical union the patient may be allowed limited mobility or the cast may be removed. • Fifth stage: Consolidation: As callus continues to develop, the distance between bone fragments diminishes and eventually closes. This stage is called consolidation, and ossification continues. It can be equated with radiologic union. • Sixth stage: Remodeling: Excess bone tissue is reabsorbed in the final stage of bone healing, and union is completed. Gradual return of the injured bone to its pre-­injury structural strength and shape occurs. Radiologic union occurs when there is X-ray evidence of complete bony union. This phase can occur up to a year following injury.

Clinical Manifestations 1. Pain 2. Loss of function 3. Deformity 4. Shortening 5. Crepitus 6. Swelling and discoloration 7. Muscle spasm 8. Tenderness

Diagnostic Studies for Fracture 1 . X-ray examinations: Determines location and extent of the fracture. 2. Additional when needed are bone scans, tomograms, computed tomography (CT)/ magnetic resonance imaging (MRI) scans: Visualizes fractures, bleeding, and softtissue damage; differentiates between stress/trauma fractures and bone neoplasms. 3. Complete blood count (CBC): Hematocrit (Hct) may be increased (hemoconcentration) or decreased (hemorrhage). 4. Increased white blood cell (WBC) count is a normal stress response after trauma.

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5. Urine creatinine (Cr) clearance: Muscle trauma increases load of Cr for renal clearance. 6. Coagulation profile: Alterations may occur because of blood loss, multiple transfusions, or liver injury. 7. Arteriograms: May be done when occult vascular damage is suspected.

Treatment of Fracture Phase I Emergency care: It begins at the site of the accident and consists of “splint them where they lie.” (a) For a closed fracture: Before splinting remove any ring or bangles worn by the patient. Almost any available object (e.g., folded newspaper, magazine, rigid cardboard, stick, umbrella, pillow) can be used for splinting at the site of the accident. (b) For an open fracture: The bleeding from the wound is stopped by applying firm pressure using a clean piece of cloth and a circular bandage can be applied proximal to the wound in order to stop bleeding. If the wound is very dirty, it is washed with clean tap water and covered with a clean cloth and then the fracture is splinted. In the emergency department, the use of the basic life support and the bleeding is recognized and stopped by local pressure. A wooden plank, cramer-wire splint, Thomas’ splint, and inflatable splint are some of the splints used in emergency department. After emergency care is provided, suitable radiological and other investigations are then carried out. For open fracture: Wound care is given along with prophylactic antibiotics, such as Cephalexin which is a good broad-spectrum antibiotic for this purpose. In serious compound fractures, a combination of third generation cephalosporins and an amino-glycoside is preferred. Tetanus prophylaxis and analgesics should be given parentally to make the patient comfortable. Phase II Definitive care: The aim of treatment is rehabilitation of the limb to the pre-injury status such as anatomic realignment of bone fragments (reduction) with immobilization to maintain realignment and restoration of normal or near normal function of the injured part. Methods of treatment: Vary as not all fractures need all four of these treatments: (1) Treatment by functional use of the limb: Some fractures (e.g., fractured ribs, scapula) need no reduction or immobilization. These fractures unite despite functional use of the body part. Analgesics are needed for the initial few days. (2) Treatment by immobilization: Fractures without significant displacement or fractures where the displacement is of no concern are treated this way. (3) Treatment by reduction followed by immobilization: It is required for most displaced fractures. These, otherwise, result in deformity, shortening, etc. (4) Open reduction and internal fixation: Some fractures, such as intra-articular fractures, are best treated by open reduction and internal fixation. Fracture reduction: Reduction of a fracture can be carried out by following methods either (a) closed reduction or (b) open reduction or (c) continuous traction. (a) Closed reduction: It is a nonsurgical, manual realignment of bone fragments to their previous anatomic position by which traction and counter traction are

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manually applied to the bone fragments which is usually performed under local or general anesthesia. After reduction, traction, casting, external fixation, splints, or orthoses immobilize the injured part to maintain alignment until healing occurs. (b) Open reduction: Open reduction is the correction of bone alignment through a surgical incision. It usually includes internal fixation of the fracture with the use of wires, screws, pins, plates, intramedullary rods, or nails. These techniques allow anatomic reduction and the creation of highly stable constructs. Their indications are as follows: (1) fracture that cannot be reduced except by operation, (2) fracture that are inherently unstable and prone to displacement after reduction, (3) fracture that unite poorly and slowly, principally fracture of the femoral neck, (4) pathological fracture where the bone disease may prevent healing, (5) multiple fractures, where early fixation reduces the risk of general complications, and (6) fracture in patient who presents severe nursing difficulty. Types of internal fixation such as (1) screw—an interfragmentary screw (lag screw) is used for fixing small fragment onto the main bone, or (2) wires like a Kirschner wire often inserted percutaneously without exposing the fracture or used in situation where fracture healing is predictably quick. Pins and screws: They are the simplest implants which are often placed percutaneously. Kirschner wires may be used temporarily and frequently for the stabilization of small fragments. Screws can be used for inter fragmentary compression. Plates and screw are useful for treating metaphyseal fracture of long bones and diaphyseal fracture of radius and ulna. An intramedullary nail is suitable for long bones when the nail is inserted onto medullary canal to splint the fracture. A rotational fracture is resisted by introducing a locking screw which can transfix both the bone cortices and the nail proximal and distal to the fracture. Tension bands are mainly used to convert the displacing tensile forces on one side of a fracture into a compressive force across the entire contact area. Traditionally wires or cables are used to create tension bands. External fixation: The main principle is that the bone is transfixed above and below the fracture with screw or pins or tension wire and these are then clamped to a frame or connected to each other by rigid bars outside the skin. Continuous traction is the application of a pulling force to an injured or diseased part of the body or an extremity while counter traction pulls in the opposite direction. The purposes of traction are as follows: (1) to prevent or reduce muscle spasm, (2) to immobilize a joint or part of the body, (3) to reduce a fracture or dislocation, and (4) to treat a pathologic condition. The two most common types of traction are (1) skin traction and (2) skeletal traction. 1. Skin traction is generally used for short-term treatment (48–72 h) until skeletal traction or surgery is possible. It is mainly used as an adhesive strap is applied on the skin and traction applied. The traction weights are usually limited to 2.3– 4.5  kg. A pelvic or cervical skin traction may require heavier weights to be applied intermittently. The traction force is transmitted from the skin through the deep fascia and intermuscular septae to the bone.

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2. Skeletal traction: It provides long-term pull that keeps the injured bones and joints aligned. It is applied directly on the bone by inserting K-wire or Steinmann pin through the bone to align and immobilize the injured body part. It is used to align injured bones and joints or to treat joint contractures and congenital hip dysplasia. The weight for skeletal traction ranges from 2.3 to 20.4  kg. The use of too much weight can result in delayed union or nonunion. Fracture immobilization: It is mainly used to prevent displacement or angulation of the fracture and to prevent movement that might interfere with the union or to relieve pain. After the fracture has been reduced, the bone fragments must be immobilized, or held in correct position and alignment, until union occurs. Immobilization may be accomplished by external or internal fixation. Methods of external fixation include bandages, casts, splints, continuous traction, and external fixators. Metal implants used for internal fixation serve as internal splints to immobilize the fracture. Strapping: The fractured part is strapped to an adjacent part of the body. For example, a phalanx fracture, where one finger is strapped to the adjacent normal finger. Sling: A fracture of the upper extremity is immobilized with the help of a sling, mostly to relieve pain in cases where strict immobilization is not necessary. For example, a triangular sling used for a fracture of the clavicle. Casts immobilization: A cast is a temporary circumferential immobilization device. It allows the patient to perform many normal activities of daily living while providing sufficient immobilization to ensure stability. The cast materials are natural (plaster of Paris), synthetic acrylic, latex-free polymer, or a hybrid of materials. Plaster of Paris (gypsum salt) is CaSO4·1/2H2O in dry form, which becomes CaSO4·2H2O on wetting. This conversion is an exothermic reaction and is irreversible. The plaster sets in the given shape on drying. Plaster casts commonly used are (1) Minerva cast—cervical spine disease, (2) Colles’ cast-colles’ fracture, (3) hip spica for a pediatric fracture of the femur, and (4) a hanging cast for a fracture of the humerus. Splints: Splints are used for immobilizing fractures, either temporary during transportation or for definitive treatment. Commonly used splints and their uses: (1) Thomas splint: fracture femur, (2) crammer-wire splint: emergency immobilization, (3) Volkmann’s splint: for Volkmann’s ischemic contracture, (4) aluminum splint: immobilization of fingers, (5) Boston brace: Scoliosis, and (6) lumbar corset: back ache. Operative methods are mainly divided into external fixation and/or internal fixation. Drug therapy is mainly used for pain management, such as central and peripheral muscle relaxants, for example, carisoprodol, cyclobenzaprine, or methocarbamol may be prescribed for relief of pain.

 hase III: Rehabilitation of a Fractured Limb P Rehabilitation begins at the time of injury, and goes on till maximum possible functions have been regained. Exercises during immobilization: Parts of the limb

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out of plaster should be mobilized to prevent stiffness and weakness of these parts. The muscles within the plaster should be exercised in order to prevent wasting. After removal of immobilization: (1) the skin is cleaned, scales removed, and some oil applied to take care of the dryness and (2) the joints are moved, to regain the range of motion. It needs hot fomentation, active and active-assisted joint mobilizing exercises. Complications of fractures: (1) systemic or (2) local. 1. Systemic—the most important is Hypovolemic shock, venous thrombosis and pulmonary embolism, fat embolism, fracture fever, crush syndrome, ARDS, hypostatic pneumonia and tetanus in compound fracture. 2. Local—such as injury to major vessels, injury to muscles and tendons, injury to joints, or injury to viscera. (a) Shock (early): Hypovolemic or traumatic shock resulting from hemorrhage (both visible and nonvisible blood loss) and from loss of extracellular fluid into damaged tissues. It may occur in fractures of the extremities, thorax, pelvis, or spine, because the bone is very vascular, large quantities of blood may be lost as a result of trauma, especially in fractures of the femur and pelvis. The treatment of shock consists of restoring blood volume and circulation, relieving the patient’s pain, providing adequate splinting, and protecting the patient from further injury and other complications. (b) Volkmann’s contracture: It results from unrelieved compartment syndrome and is due to ischemia muscle which is gradually replaced by fibrous tissue. It leads to a permanently stiff, claw-like deformity of the hand and arm. Prevention by prompt recognition followed by limb splinting and compartment decompression. (c) Deep vein thrombosis (DVT), pulmonary embolus (PE): They are associated with reduced skeletal muscle contractions and bed rest. Patients with fractures of the lower extremities and pelvis are at high risk for thromboembolism. Pulmonary emboli may cause death several days to weeks after injury. (d) Disseminated intravascular coagulopathy (DIC): It includes a group of bleeding disorders with diverse causes, including massive tissue trauma. The manifestations of DIC include ecchymoses, unexpected bleeding after surgery, and bleeding from the mucous membranes, venipuncture sites, and gastrointestinal and urinary tracts. (e) Local are mainly infection, compartment syndrome, and fat embolism syndrome (early). • Infection: All open fractures are considered contaminated. Surgical internal fixation of fractures carries a risk for infection. The nurse must monitor for and teach the patient to monitor for signs of infection, including tenderness, pain, redness, swelling, local warmth, elevated temperature, and purulent drainage. All infections must be treated promptly and antibiotic therapy must be appropriate and adequate for prevention and treatment of infection.

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• Fat embolism syndrome (early): After fracture of long bones or pelvis, multiple fractures, or crush injuries, fat emboli may develop. They are seen most frequently in young adults (typically those 20–30 years of age) and elderly adults with fractures of the proximal femur. At the time of fracture, fat globules may move into the blood. These fat globules (emboli) may occlude the small blood vessels that supply the lungs, brain, kidneys, and other organs. The onset of symptoms is rapid, usually occurring within 24–72 h, but may occur up to a week after injury. • Compartment syndrome (early): It develops when tissue perfusion in the muscles is less than that required for tissue viability. The patient complains of deep, throbbing, unrelenting pain, which is not controlled by opioids. The forearm and leg muscle compartments are involved most frequently. The pressure within a muscle compartment may increase to such an extent as to decrease microcirculation, causing nerve and muscle anoxia and necrosis. Permanent function can be lost if the anoxic situation continues for longer than 6 h.

Late Complications 1. Delayed union 2. Malunion 3. Nonunion 4. Cross-union 5. Avascular necrosis 6. Shortening 7. Volkmann’s ischemic contracture 8. Myositis ossificans 9. Joint instability and stiffness

Nursing Management A nursing assessment is initially carried out as follows: Ask patient how the fracture occurred, mechanism of injury. Ask patient to describe location, character, and intensity of pain. To aid in evaluation of neurovascular status ask patient to describe sensations in injured extremity. To assess functional mobility observe patient’s ability to change position. Note patient’s emotional status and behavioral indicators of ability to cope with stress of injury. Assess patient’s support system; identify current and potential sources of support, assistance, and care giving.

2

Complications of Fractures K. Mohan Iyer

Classification Complications of fractures tend to be classified according to whether they are local or systemic and when they occur, such as (1) immediate, (2) early, or (3) late. 1. Immediate: It is the commonest cause of death following fractures; it is caused by external/internal hemorrhage; the treatment is IV crystalloids like ringer lactate, followed by colloids and blood. 2. Early complications: They occur at the time of the fracture (immediate) or soon after. They are again classified into (A) local complications which tend to affect mainly the soft tissues or (B) systemic. Among the early local complications are included (a) Vascular injury causing hemorrhage, such as internal or external (b) Visceral injury causing damage to the structures such as brain, lung, or bladder (c) Damage to surrounding tissue, nerves, or skin (d) Hemarthrosis (e) Compartment syndrome {Volkmann’s ischemia} (f) Wound infection, more common for open fractures (g) Tetanus (h) Gas gangrene (i) Injury to joints Vascular injury: Blood vessels lie in close proximity to bones and hence liable to injury; popliteal is the commonly injured one, with consequences of exercise ischemia leading to ischemic contracture and gangrene. Signs are 5 Ps—there is pain along with an absent pulse, pallor, parasthesia, and paralysis, as shown in Table 2.1: K. M. Iyer (*) Royal Free Hampstead NHS Trust, Royal Free Hospital, London, UK © Springer Nature Switzerland AG 2019 K. M. Iyer, W. S. Khan (eds.), General Principles of Orthopedics and Trauma, https://doi.org/10.1007/978-3-030-15089-1_2

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Table 2.1  Vascular injuries and skeletal trauma

Vessels injured 1. Femoral 2. Popliteal 3. Posterior tibial 4. Subclavian 5. Axillary 6. Brachial

Trauma Fracture of lower third of femur Supracondylar fracture of the femur Dislocation of the knee, fracture of tibia Fracture of the clavicle Fracture dislocation of the shoulder Supracondylar fracture of the humerus

Management of vascular injury to the limb: First contact—No pulse, then (a) Loosen tight bandages. (b) Correct gross displacement of the fracture under sedation. (c) Correct any acute flexion deformity of the nearby joints. (d) Watch for return of pulse within ½ to 1 h. If pulse does not return—then refer to a specialized center. If still no pulse, then consider one of the following alternatives: 1. If good peripheral circulation—splint the fracture in a loose splint and observe. If good circulation persists, then reduce the fracture after 48 h and then treat it as in similar cases. 2. If doubtful or poor peripheral circulation, then proceed with exploration of the vessel. (a) If vessel in continuity, it indicates spasm—then treat with xylocaine, papaverine, or sympathectomy. (b) If contusion with thrombosis, then treat with a thrombectomy using a Fogarty’s catheter or excision of the affected segment and anastomosis. (c) If lacerated or ruptured vessel, then repair end to end or use a vein graft or a synthetic graft. Visceral injuries are commonly seen in pelvic and rib fractures. Nerve and skin tissue damages: The radial nerve is commonly injured and its consequences lead to neurapraxia, axonotmesis, or neurotmesis, for example, radial nerve is commonly involved in a fracture shaft of humerus giving rise to a wrist drop, the axillary nerve is commonly injured in dislocation of shoulder resulting in deltoid paralysis, the median nerve is commonly involved in supracondylar fracture of humerus resulting in a pointing index, the ulnar nerve in fracture medial epicondyle humerus resulting in a claw hand, and the sciatic nerve in posterior dislocation of hip resulting in a foot drop. Hemarthrosis is bleeding in the joint because of fracture. Compartment syndrome: Fractures of the limbs can cause severe ischemia, even without damage to a major blood vessel resulting in bleeding or edema in an osteofascial compartment increases pressure within the compartment, reducing capillary

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flow and causing muscle ischemia. This leads to a vicious circle which develops into further edema and pressure build-up, leading swiftly to muscle and nerve necrosis and may eventually result in limb amputation if untreated. Compartment syndromes can also result from crush injuries caused by falling debris or from a patient’s unconscious compression of their own limb resulting in a swelling of a limb inside an over tight cast. Compartment syndrome can occur in any compartment, e.g., the hand, forearm, upper arm, abdomen, buttock, thigh, and leg. 40% occur following fracture of the shaft of the tibia (with an incidence of 1–10%) and about 14% following fracture of a forearm bone. The risk is highest in those under 35 years. Compartment syndrome may also lead to Volkmann’s ischemia when an arterial damage has been spotted which leads to ischemia and reduced blood flow which when untreated by fasciotomy leads to increased compartment pressure as seen in edema by direct injury leading to painful, pale, pulseless, paresthic, paralysis [1]. The presentation shows signs of ischemia (5 Ps: pain, paresthesia, pallor, paralysis, pulselessness) along with sign of raised intracompartmental pressure such as (1) swollen arm or leg, (2) tender muscle—calf or forearm pain on passive extension of digits, (3) pain out of proportion to injury, and (4) redness, mottling, and blisters. At this stage a watch is kept for signs of renal failure (low-output indicative of uremia with acidosis).

Management Remove/relieve external pressures (fasciotomy), prompt decompression of threatened compartments by open fasciotomy, debride any muscle necrosis, treat hypovolemic shock and oliguria urgently, and renal dialysis may be necessary. Complications: Acute renal failure secondary to rhabdomyolysis, DIC, and Volkmann’s contracture (where infarcted muscle is replaced by inelastic fibrous tissue). Gas gangrene: caused by Clostridium welchii (perfringens). Their clinical presentation is of subcutaneous crepitations leading to myonecrosis. Their treatment is debridement with penicillin. Tetanus: The causative agent is Clostridium tetani with presentation of trismus, dysphagia, risus sardonicus, and opisthotonus. Their treatment consists of bed rest and sedation, immunoglobulin, respiratory support, and penicillin. Systemic early complications are as follows: fat embolism, shock, ARDS, thromboembolism (pulmonary or venous), exacerbation of underlying diseases such as diabetes or CAD, pneumonia, aseptic traumatic fever, septicemia, and crush syndrome. Fat embolism: This is a relatively uncommon disorder that occurs in the first few days following trauma with a mortality rate of 10–20%. The fat drops are thought to be released mechanically from bone marrow following fracture, coalesce and form emboli in the pulmonary capillary beds and brain, with a secondary inflammatory cascade and platelet aggregation. An alternative theory suggests that free fatty acids

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are released as chylomicrons following hormonal changes due to trauma or sepsis. There are a number of risk factors such as closed fractures, multiple fractures, pulmonary contusion, or long bone/pelvis/rib fractures. It usually presents as sudden onset of dyspnea, hypoxia, fever, confusion, coma, convulsions, and transient red-brown petechial rash; it usually affects the upper body, especially axilla. Diagnosis is by retinal artery emboli—seen as exudates, sputum and urine for fat globules and an X-ray chest which shows a characteristic snow storm appearance. Treatment is mainly by (1) respiratory support, (2) heparinization, and (3) intravenous low molecular weight dextran (lomodex 20) and corticosteroids; IV 5% dextrose solution with 5% alcohol helps in emulsification of fat globules.

Deep Vein Thrombosis They are a common complication associated with lower limb injuries and with spinal injuries. A DVT proximal to the knee is a common cause of life-threatening complication of pulmonary embolism. They are mainly caused by immobilization following trauma or a fracture of leg. Their main symptoms are leg swelling with calf tenderness. Their consequences are pulmonary embolism, tachypnea, and dyspnea typically 4–5 days after trauma. Their treatment: elevation of the limb, anticoagulating therapy, respiratory support and heparin therapy {respiratory embolism}, early internal fixation of fractures, and active mobilization of the extremity.

Aseptic Trauma Fever This is supposed to be due to absorption of the fibrin ferment taking place or it may, however, be due to some irritation, as of a badly fitting splint, and disappears on removal of it. Septicemia It is mainly because of trauma when a large amount of bacteria can enter in the blood stream and may cause septicemia. Its symptoms are a rash, fever and vomiting, cold extremities, rapid breathing, stomach pain and joint pain, and feeling drowsy. The management is by initial resuscitation—ABC, secure airway, support breathing, restore circulation with fluid therapy and inotropic support, antimicrobial therapy and respiratory support.

Crush Syndrome It is a crushing injury to skeletal muscles because of the fracture due to crushing of muscles when myohemoglobin enters the circulation and forms a precipitate in renal tubules which accounts for renal failure resulting in shock and renal failure. Management: To avert disaster, a limb that is crushed severely and for several hours should be amputated. Late complications are those which occur after a substantial

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time has passed and are as a result of defective healing process or because of the treatment itself. They are again classified into two groups: (1) imperfect union of the fracture such as delayed union, nonunion, malunion, and cross-union and (2) others such as avascular necrosis, shortening, joint stiffness, Sudeck’s dystrophy, osteomyelitis, Volkmann’s ischemic contracture, myositis ossificans, and osteoarthritis. Delayed union is when a fracture takes more than the usual time to unite, it is said to have gone in delayed union due to (1) inadequate blood supply, (2) infection, or (3) incorrect splintage which may be caused by insufficient splintage or excessive traction. The clinical signs are: (a) the fractured site is usually tender, (b) the bone may appear to move in one piece; if, however, it is subjected to stress, pain is immediately felt and the bone may angulate, (c) the fracture is not consolidated, (d) X-ray: shows the fractured site is still clearly visible, and (e) the bone ends are not sclerosed. It is treated by (1) conservative: (a) plaster should be sufficiently extensive and must fit accurately, (b) replace traction by plaster splintage, and (c) use of functional bracing, or (2) operative: bone grafting with or without internal fixation. Nonunion is when the process of fracture healing comes to a stand before its completion, the fracture is said to have gone in nonunion. It is not before 6 months that a fracture can be so labeled and nonunion is one endpoint of delayed union. The causes are the injury such as (1) soft tissue loss, (2) bone loss, (3) intact fellow bone, and (4) soft tissue inter position or the bone such as (1) poor blood supply, (2) poor hematoma, (3) infection, or (4) pathological lesion. It usually presents as (1) pain at fracture site, (2) nonuse of extremity, (3) tenderness and swelling, (4) joint stiffness (prolonged >3  months), and (5) movement around the fracture site (pseudarthrosis). The investigations that may confirm this are: Absence of callus (remodeled bone) or lack of progressive change in the callus suggests delayed union, closed medullary cavities suggest nonunion, radiologically, bone can look inactive, suggesting the area is avascular (known as atrophic nonunion) or there can be excessive bone formation on either side of the gap (known as hypertrophic nonunion). The treatment is 1. Conservative: (a) Occasionally symptom less, needing no treatment, (b) Functional bracing may be sufficient to induce union, or (c) Electrical stimulation which promotes osteogene. 2. Operative: (a) Very rigid internal fixation with hypertrophic nonunion or (b) Fixation with bone graft is needed in case of atrophic nonunion. Malunion: It occurs when the bone fragments join in an unsatisfactory position, usually due to insufficient reduction. Its causes are either (1) primary—(a) the fracture was never reduced and has thus united in a deformed position and (b) shortening is, of course, one type of deformity or (2) secondary—(a) the fracture was

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reduced but the reduction was not held or (b) redisplacement may occur during the first week, and hence a check X-ray at 1 week is advisable. The signs: The deformity is usually obvious. There may be painful limitation of joint movements. At elbow, valgus deformity may present with delayed ulnar nerve palsy. The treatment is (1) conservative—(a) if shortening is the main feature a raised shoe is usually sufficient, (b) in child usually no treatment is required because it is expected to correct by remodeling or (2) operative—(a) osteotomy, (b) excision of protruding bone, (c) osteoclasis, and (d) redoing the fracture surgically. Avascular necrosis: Blood supply of some bones is such that the vascularity of a part of it is seriously jeopardized following fracture, resulting in necrosis of the part. The consequences are as follows: Avascular necrosis causes deformation of the bone. This leads, a few years later, to secondary osteoarthritis and causes painful limitation of joint movement. Diagnosis: 1. X-ray changes: (a) sclerosis of the necrotic area, (b) deformity of the bone, and (c) osteoarthritis. 2. Bone scan: Changes can be seen before X-ray changes: visible as cold area on the bone. Treatment: Avascular necrosis can be prevented by early, energetic reduction of susceptible fractures and dislocations. The treatment options. 1 . Delay weight bearing till revascularization to prevent collapse 2. Revascularization 3. Excision of the avascular segment 4. Total joint replacement Shortening: It is a common complication of fractures and results from: 1 . Malunion of the long bones 2. Crushing: actual bone loss 3. Growth defects: growth plate or epiphyseal injuries Treatment: Usually the shortening of upper limbs goes unnoticed. For lower limb treatment depends upon the amount of shortening: (1) shortening less than 2 cm: can be compensated by shoe raise, (2) shortening more than 2  cm: limb length-­ equalization procedures. Joint stiffness: It is a common complication of fracture treatment. The shoulder, elbow, and knee joints are particularly prone to stiffness following immobilization. Usual causes are intra-articular or para-articular adhesions which are secondary to immobilizations. Contracture of the muscles around a joint usually results because of prolonged immobilizations and tethering of muscles at fracture site and Myositis

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ossificans. The consequences are that it hampers the normal physical activity and results in late osteoarthritis. The treatment is usually heat therapy and exercise and manipulation of the joint under anesthesia. If no relief, then surgical interventions are considered: 1 . To excise an extra articular bone block 2. To lengthen contracted muscles or 3. Joint replacement, if there is pain due to secondary arthritis Algodystrophy (Sudeck’s dystrophy): It is also known as reflex sympathetic dystrophy. It involves a disturbance in the sympathetic nervous system. It results in pain, hyperesthesia, tenderness, and swelling. Here the skin become red, shiny, and warm in early stages and there is a progressive atrophy of the skin, muscles, and nails in later stages. Finally joint deformity and stiffness ensues and the X-ray shows a characteristic spotty rarefaction. The treatment is mainly occupational therapy and physiotherapy which constitutes the principle modality of treatment. The use of a β-blocker may be considered. In resistant cases, sympathetic blocks have been shown to aid in recovery. Osteomyelitis: Osteomyelitis is an infection of a bone. Many different types of bacteria can cause osteomyelitis. However, infection with a bacterium called Staph. aureus is the most common cause, and infection with a fungus is a rare cause. The treatment is antibiotics as after operative treatment of fracture bacteria may spread to the bone and may cause osteomyelitis. Surgery: (1) in case of abscess formation, (2) the infection presses on other important structures, (3) the infection has become “chronic” (persistent) and some bone has been destroyed, and lastly (4) hyperbaric oxygen. Volkmann’s ischemic contracture: This a sequel to Volkmann’s ischemia when the ischemic muscles are replaced by fibrous tissue and if the peripheral nerves are also affected, then sensory or motor paralysis may happen. The clinical features show marked atrophy, flexion deformity and the nails shows atrophic changes with the skin becoming dry and scaly. The treatment can be summarized as follows: Mild deformity can be corrected by passive stretching using a turn-buckle splint (Volkmann’s splint); for moderate deformities, a soft tissue sliding operation, where the flexor muscles are released from their origin, is performed; and for a severe deformity, bone shortening operations may be required. Myositis ossificans: Myositis ossificans is where calcifications and bony masses develop within muscle and can occur as a complication of fractures. It may also happen because of the ossification of the hematoma around a joint after compound fractures. The clinical features are pain, tenderness, focal swelling, and joint/muscle contractions. Treatment: Massage following injury is strictly prohibited. In early stages rest is advised and NSAIDS may help to reduce pain. In late stages occupational therapy and physiotherapy are prescribed to regain movements. Ultrasound and in some cases surgical excision of myositic mass is done. Osteoarthritis: Osteoarthritis is liable to follow malunion and traumatic injuries to the joints. The joint surfaces become incongruent and the direction of stress

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transmission is abnormal which increases the wear and tear at the joint. Treatment: Osteoarthritis cannot be cured, but it can be treated. The goal of every treatment for arthritis is to: (1) reduce pain and stiffness, (2) allow for greater movement, and (3) slow the progression of the disease. Anti-inflammatory medications are very helpful. The treatments are e.g. cortisone injections, occupational therapy and physiotherapy, weight loss, and activity modification; diet: obesity is a risk factor for developing osteoarthritis.

Iatrogenic Complications 1. Casts—(a) pressure ulcers, (b) thermal burns during plaster hardening and thrombophlebitis. 2. Traction—Traction prevents patients mobilizing causing additional muscle wasting and weakness. 3. Other complications include: (a) pressure ulcers, (b) pneumonia/urinary tract infections, (c) permanent footdrop contractures, (d) peroneal nerve palsy, (e) pin tract infection, and (f) thromboembolism. External fixation: Problems include: (a) pin tract infection, (b) pin loosening or breakage, (c) interference with movement of the joint, (d) neurovascular damage due to pin placement, and (e) misalignment due to poor placement of the fixator.

Reference 1. Holden CEA. The pathology and prevention of Volkmann’s ischaemic contracture. J Bone Joint Surg. 1979;61-B:296–300.

3

Fractures in Children K. Mohan Iyer

General Principles of Management Pediatric Fractures Children’s bones (Table 3.1) are different in many respects.

Remodeling of Bone in Children Children have the unique ability for healing their fractures and remodeling their deformities, which depends on the child’s age and the distance from the growth plate. This is an age-related fracture pattern: (1) infants: diaphyseal fractures, (2) ­children: metaphyseal fractures, and (3) adolescents: epiphyseal injuries. The statistics are as follows: 1 . ~50% of boys and 25% of girls expected to have a fracture during childhood. 2. Upper Limb fractures—more common with fracture in distal radius, elbow region fracture, viz. distal humeral and prox. radial being common. Most fractures in home/school, femur and pelvic fractures more with RSA. 3. Boys more than girls. Table 3.1  Management of pediatric fractures

Feature 1. Thick joint cartilage 2. Thick periosteum 3. More collagen 4. More cancellous bone 5. Growth plate 6. Ligaments are stronger

Management Not seen on X-rays Healing is rapid Fractures easily Simple fracture patterns Remodels deformity Bone fails first

K. M. Iyer (*) Royal Free Hampstead NHS Trust, Royal Free Hospital, London, UK © Springer Nature Switzerland AG 2019 K. M. Iyer, W. S. Khan (eds.), General Principles of Orthopedics and Trauma, https://doi.org/10.1007/978-3-030-15089-1_3

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4 . Rate increases with age. 5. Physeal injuries with age. General Principles are as follows: 1 . Failure of union is rare. 2. Few fractures require operative treatment. 3. Presence of growth plate presents a challenge to the surgeon. 4. Special considerations: These are given to pathological fractures and malignancies and child abuse (multiple fracture and injuries at different stages of healing, epiphysio-metaphysis corner injuries).

Centers of Ossification 1 . Ossification center is usually diaphyseal. 2. Ossification centers are usually epiphyseal which occur at different stages of development and usually occur earlier in girls than boys. The physis is the primary center for growth in most bones and known as the EPIPHYSIS. It has four functional zones, namely: 1 . Reserve zone or the germinal layer for cartilage cells. 2. Proliferation zone where the bone length is created by active growth of cartilage cells. 3. Hypertrophic zone consisting of terminally divided cells where there is no active growth, and which is gradually extending toward metaphysis and to the zone of degeneration. Physeal injuries: 1 . They account for ~25% of all children’s fractures. 2. They are more in boys. 3. More in upper limb. 4. Most heal well rapidly with good remodeling. 5. Growth may be affected. 6. Physis responds to compression as well as distraction (fracture implants ­infection, etc.). Salter–Harris classification (Salter–Harris remains universally accepted-first five types) (Fig. 3.1) • Type I: They are through the physis only. • Type II: They are usually through physis and metaphysis.

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II

III

IV

V

Fig. 3.1  Line diagram showing the Salter–Harris classification

• • • • • •

Type III: They are through the physis and epiphysis. Type IV: They are through metaphysis, physis, and epiphysis. Type V: It is usually a crush injury to entire physis. Type VI: Injury to the perichondral structures. Type VII: Isolated injury to the epiphyseal plate. Type VIII: Isolated injury to the metaphysis, with a potential injury related to endochondral ossification. • Type IX: Injury to the periosteum that may interfere with membranous growth.

Salter–Harris Classification General Treatment Principles [1] • Type I and II: Closed reduction and immobilization. • Type III and IV: Intra-articular and physeal step-off needs anatomic reduction and ORIF, if necessary. Physeal injuries: They are less than 1% cause of physeal bridging affecting growth with a specific mention regarding 1 . Small bridges (less than 10%) which may lyse spontaneously. 2. Central bridges more likely to lyse. 3. Peripheral bridges more likely to cause deformity. 4. Avoid injury to physis during fixation. 5. Monitor growth over a long period. 6. Image suspected physeal bar (CT, MRI). 7. Smooth pins should be used for fixation, not threaded ones if they are to cross physes. Epiphyseal injuries: Here the principle is to try not to cross the physis, but rather parallel it in the epiphysis or pin the fracture spike in the metaphysis.

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Growth Arrest Secondary to Physeal Injury 1. Complete cessation of longitudinal growth which leads to limb length discrepancy. 2. Partial cessation of longitudinal growth occurs in an angular deformity, if peripheral and in progressive shortening, if central. Hence it is much better to warn parents about early operative complications and late complications, such as bony bridge formation and angular deformity. Growth Arrest Lines—These are indicated by the following features: 1 . Transverse lines of Park-Harris Lines. 2. Occur after fracture/stress. 3. Result from temporary slowdown of normal longitudinal growth. 4. Thickened osseous plate in metaphysis. 5. These lines should parallel physis. 6. They appear 6–12 weeks after fracture. 7. Look for them in follow-up radiographs after fracture. 8. If parallel physis—no growth disruption. 9. If they are angled or point to physis, then suspect bar. A physeal bar—Imaging can be done by (a) tomograms/CT scans, (b) MRI, or (c) map bar to determine the location and extent. The various types of physeal bars: I—peripheral, which are an angular deformity, II—central, which are a tented physis, with shortening, and III—combined/ complete with shortening. The treatment of these physeal bars are first to address whether they result in an angular deformity or a limb length discrepancy. Then secondly to assess the Growth remaining, with the amount of physis involved, and the degree of angular deformity and finally the projected LLD (limb length discrepancy) at maturity. Physeal bar resection—Indications are if >2 years remaining growth, 15–20° deformity, completion epiphysiodesis (tethering physis with staple screw) and contralateral epiphysiodesis may be more reliable in older child and when the central bar > peripheral bar. Physeal bar resection—Techniques by direct visualization, by burr/curettes, and by interpositional material (fat, cranioplast) easiest to prevent reformation when the arrest is removed, leaving in its place a metaphyseal-epiphyseal cavity with an intact physis surrounding the area of resection.

Torus Fracture It is a greenstick fracture, a fracture in a young, soft bone in which the bone bends and partially breaks. This is owing in large part to the thick fibrous periosteum of immature bone; here are three basic forms of greenstick fracture [2]. In the first, a

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transverse fracture occurs in the cortex which extends into the midportion of the bone and becomes oriented along the longitudinal axis of the bone without disrupting the opposite cortex. The second form is a torus or buckling fracture which is caused by impaction; the word torus is derived from the Latin word “Tori,” meaning swelling or protuberance. The third is a bow fracture in which the bone becomes curved along its longitudinal axis. Usually pop splint is given.

Diaphyseal Fracture This is more common in infants when a watch is kept for neurovascular insufficiency during convalescence, and abuse should be considered a possible cause of injury in all young children with multiple long-bone fractures in association with head injury. The general principles of fixation essentially remain the same with most diaphyseal fractures being treated conservatively, displaced fractures and open fractures requiring internal/external fixation. Methods of fixation: (1) casting—still the commonest. (2) K-wires are most commonly used for metaphyseal fractures. (3) K-wires could be replaced by absorbable rods. (4) Intramedullary wires, elastic nails are very useful and reserved for diaphyseal fractures. (5) The last option is screws. (6) Plates—multiple trauma (more extensive operative exposure which is not load sharing and hence removal is needed); Best is the newer minimally invasive such as percutaneous submuscular plating. (7) IMN—adolescents only (injury to growth). (8) Ex-fix—usually in open fractures.

Titanium Elastic Nail The aim of this biological, minimally invasive fracture treatment is to achieve a level of reduction and stabilization that is appropriate to the age of the child. The biomechanical principle of the elastically stable intramedullary nailing (ESIN) is based on the symmetrical bracing action of two elastic nails [3] inserted into the metaphysis, each of which bears against the inner bone at three points. This produces the following four biomechanical properties: flexural stability, axial stability, translational stability, and rotational stability. All four are essential for achieving optimal results. Indications: 1 . Age lower limit is 3–4 years and the upper limit 13–15 years. 2. Type of fracture: transverse fractures, short oblique or spiral fractures with cortical support, long oblique fractures with cortical support. 3. Fracture site: femur: diaphyseal, distal femur: metaphyseal, femur: subtrochanteric, lower leg: diaphyseal, humerus: diaphyseal, subcapital even supracondylar, radius and ulna:shaft radial neck, radius: neck, prophylactic stabilization with juvenile bone cysts. 4. Contraindications: intra-articular fractures, complex femoral fractures, particularly overweight (50–60 kg) and/or age (15–16 years).

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Acceptable Reduction 1. Initial considerations: growth will not correct rotational deformity with age, distance from physis, and the amount of deformity. 2. Bayonet apposition: generally bayonet appposition will require operative reduction; historically, overriding of a both-bones forearm fracture was acceptable if there was no deviation of radius and ulna toward each other, or there was no encroachment of the interosseous space, or patient is less than 10 years of age. 3. In patients 10° is unlikely to correct after 10 years.

Indications for Operative Fixation 1. Open fractures. 2. Displaced intra-articular fractures (Salter–Harris III–IV). 3. Fractures with vascular injury. 4. Compartment syndrome. 5. Fractures not reduced by closed reduction (soft tissue interposition, button-­ holing of periosteum). 6. If reduction could be only maintained in an abnormal position.

Complications 1. Malunion is not usually a problem (except cubitus varus). 2. Nonunion is hardly seen (except in the lateral condyle). 3. Growth disturbance—epiphyseal damage. 4. Vascular—Volkmann’s ischemia. 5. Infection—rare. 6. Malunion. 7. Limb length discrepancy. 8. Physeal arrest. 9. Nonunion (rare). 10. Crossunion. 11. Osteonecrosis.

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3  Fractures in Children

Complications of fractures, mainly soft tissue: (a) Vascular injury, especially at the elbow/knee (b) Neurologic injury which is usually neuropraxia (c) Compartment syndrome especially in the leg/forearm (d) Cast sores/pressure ulcers (e) Cast burns (f) Use care with cast saw Complications of fractures—cast syndrome: Here the patient is in a spica/body cast; there is acute gastric distension, vomiting; it may possibly be mechanical such as obstruction of the duodenum by the superior mesenteric artery.

Location-Specific Pediatric Fractures (Table 3.2): Complications Closed Reduction of Forearm Fractures Open reduction and internal fixation with plates and screws may be appropriate in the management of fractures with delayed presentation or fractures that angulate late in the course of cast care, when significant fracture callus makes closed reduction and percutaneous passage of intramedullary nails difficult. Tens nail and im nail have improved results and are preferred in displaced angulated fractures.

Femoral Shaft Fractures In a baby under 6 months old, a brace (called a Pavlik Harness) may be able to hold the broken bone still enough for successful healing. Traction before spica casting is indicated when the fracture is unstable or if the shortening of the bones is too much (more than 3 cm). In children between 7 months and 5 years old, a spica cast is often applied. In general, a spica cast begins at the chest b/w umbilicus and nipple and extends all the way down the fractured leg, with flexion at 50–90° at knee and hip.

Table 3.2  Sites of complications in pediatric fractures Complication 1. Cubitus varus 2. Volkmann’s ischemic contracture 3. Refracture 4. Overgrowth 5. Nonunion 6. Osteonecrosis 7. Progressive valgus

Fracture Supracondylar humerus fracture Supracondylar humerus fracture Femur fracture, mid-diaphyseal radius/ulna fractures Femur fracture (especially 6 cm in length. The fibula, iliac crest, ribs, lat. scapula, metatarsal, and lat. portion of radius can be used for this. The fibula is used when based on one or more nutrient vascular perforators which include a flap of muscle [PB, PL, FHL] and it is most useful for defects >10 cm with a length 6–35 cm. The iliac crest can be used when based on multiple nutrient perforators from deep circumflex iliac vessels and it is useful for shorter defects 101 °F. Nodules: 30–40%, benign subcutaneous nodules and the common sites are forearm, sacral prominence, Achilles tendon, lung, pleura, pericardium, and Peritoneum. They are firm, non-tender, and adherent to periosteum, tendon, and bursae. Their presence is a sign of increased disease activity. They are invariably associated with infection, ulceration, and gangrene.

Complications 1. Sjogren’s syndrome: 10% of RA patients 2. Kerratoconjunctivitis sicca 3. Xerostomia 4. Pulmonary such as pleuritic chest pain, friction rub, effusion-exudative, and nodules 5. Interstitial lung disease • Symptoms: cough, SOB • Diagnosis: HRCT, restrictive pattern in PFT • Very poor prognosis with bronchiolitis and bronchiectasis 6. Cardiac such as pericarditis, cardiomyopathy, myocarditis, CAD, and amyloid infiltration 7. Vasculitis: Rare 10 Joints (at least one small joint) Negative RF and negative ACPA Low positive RF or low positive-CCP antibodies (3 times ULN) Normal CRP and normal ESR Abnormal CRP and abnormal ESR 6 weeks

Score 0 1 2 3 5 0 2 3 0 1 0 1

6 . Hyperplasia and increased cellularity. 7. Pannus: Consists of edema of synovium with overgrowth and villous projections protruding into joint cavity. 8. Cytokines: TNF-a from macrophages of synovium which triggers inflammation cascade. There is an imbalance between pro- and anti-inflammatory cytokines leading to chronic inflammatory synovitis. 9. RH synovitis: It has a variable number of B-cells. These polyclonal increase in immunoglobulins which results in autoantibodies production; lymphoid aggregates coupled with CD4+Th1, Th17 and t-helper, memory cells. Classification (Table 6.1) of RA.

Lab Investigations 1. ESR 2. CRP 3. Reversal of alb/globulin ratio 4. Raised serum alkaline phosphatase 5. Hepatic enzymes 6. RBS 7. Renal parameters 8. RA factor 9. Anti-CCP 10. Imaging 11. MRI: Periarticular osteopenia 12. Narrowing of joint space 13. Loss of cartilage of joint The American College of Rheumatology revised criteria for diagnosis as follows: To make a diagnosis of rheumatoid arthritis criteria 1–4 must have been present for at least 6 weeks [1]:

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1. Morning stiffness. 2. Arthritis of three or more joint areas. 3. Arthritis of hand joints. 4. Symmetric arthritis. 5. Rheumatoid nodules. 6. Serum rheumatoid factor. 7. Radiographic changes.

Treatment of RA • • • •

Damage, disability seen during first few months to 2 years Delay of 3–4 years is disastrous Plan for early and aggressive treatment program To combine medical, surgical, and rehabilitative procedures. Goals of treatment:

1 . To suppress joint inflammation 2. To maintain joint function 3. To prevent deformities 4. To repair damage 5. To relieve pain 6. To improve function/mobility of joint

Basic Principles (a) Early diagnosis for better outcome (b) Accurate objectified assessment of disease activity (c) Aggressive treatment with disease-modifying drugs (d) As monotherapy or in combination (e) Step-up, step-down, saw tooth strategy (f) Methotrexate is the anchor drug which prevents damage to joints or any other complications (g) Judicious use of corticosteroids is better. Methotrexate: It is the initial choice of DMARD and is indicated in RA with synovitis and myositis, also in Felty’s with leucopenia. There is an evidence of increased disease activity. It is a purine inhibitor and folic acid antagonist. The clinical response in 4–8  weeks. Start with 7.5–10  mg weekly once and increment of 2.5–5 mg every month to be followed. It is contraindicated in pregnancy, hepatic and renal impairment. Dose is 1–2 mg folic acid to reduce toxicity. Its side effects are GI intolerance, stomatitis/headache, rash/alopecia, BM suppression with higher doses, and cirrhosis of liver. Other drugs that may be useful (Table 6.2).

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Table 6.2  Showing the other drugs that may be used NSAIDS Nonselective Acetic acid derivative— Indomethacin, Etodolac Anthranilic acid, Mefenamic acid Aryl propionic acid, Ibuprofen, Naproxen or Ketoprofen Enolic acid-­ Piroxicam/ Meloxicam Leflunomide Pyrimidine inhibitor

Sulfasalazine Good in seronegative 500 mg orally, weekly increments by 500 mg up to 2–3 months. Response seen in 6–10 weeks.

HCQ Antimalarial used in RA, SLE 4–6 mg/kg/daily. Response seen in 4–8 weeks, i.e., 200–400 mg once daily

Avoid in sulfa allergy, G6PD deficiency High toxicity with nausea

Safe in pregnancy

Used in RA treatment; 10–20 mg daily; response seen in 4–8 weeks

Good in seronegative RA, may be used in those with poor response to DMARD’s, reduces joint damage, monoclonal antibodies with suffix MAB, fusion proteins with suffix CEPT Etanercept—50 mg/week SC, Infliximab—3 mg/kg initially at 2 month/6th or 8th weekly thereafter, IV infusion with methotrexate. Adalimumab—40 mg SC every other week, specific to TNF-a.

Contraindicated in pregnancy and hepatic dysfunction GI side effects common, diarrhea in 20% cases Loperamide or dose reduction

Frequent monitoring of CBP and LFT required TNF-a inhibitors Expensive

Golimumab—once a month Certolizumab—pegylated humanized FAB fragment of TNF-a, monthly once.

Contraindications 1. Serious infections/sepsis 2. In active/latent tuberculosis 3. CHF or LVEF ECU subsheath stretching > ECU subluxation > supination of the carpal bones away from the head of the ulna > volar subluxation of the carpus away from the ulna > increased pressure over the extensor compartments > tendon rupture. Treatment is early synovectomy of the radiocarpal and DRUJ can be done as an open procedure or, when extensor tendon synovitis is absent, as an arthroscopic procedure. Treatment of manifest caput ulnae syndrome: Resection of the ulnar head together with a dorsal wrist stabilization is indicated. Less often, arthrodesis of the DRUJ with segmental resection of the ulna or an arthroplasty are indicated (Sauvé-­ Kapandji). When choosing the procedure, the type and stage of wrist changes have to be considered. The DRUJ usually has to be treated together with the radiocarpal joint. Its isolated treatment is rarely indicated.

Radiocarpal Destruction Synovitis and capsular distension leads to supination, radial deviation, and ulnar and volar translocation of the carpus on the radius; this causes ulnar deviation of the fingers at the MP joints creating the classic zigzag deformity. Treatment is as follows: 1 . Synovectomy for early disease. 2. Transfer of ECRL to ECU to diminish deforming forces (Clayton’s procedure). 3. Radiolunate fusion (Chamay) for intermediate disease.

Rheumatoid Elbow • Synovitis—swelling and pain—may develop FFD due to holding in flexed position. • Annular ligament may rupture—anterior displacement of radial head due to pull of biceps. • Collateral ligaments may rupture ML instability. • Ulnar nerve neuropathy secondary to synovitis and rheumatoid nodule. • Cartilage and bone destruction—severe cartilage damage causing instability and bony destruction.

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Treatment options: 1 . Synovectomy ± radial head excision. 2. Arthrodesis/resection arthroplasty. 3. Arthroplasty = non-constrained, semiconstrained, and constrained; indications: pain, loss of motion, and instability; semiconstrained device has best results; reliable procedure for advanced RA of elbow. Shoulder conditions: RA is most prevalent form of inflammatory process affecting the shoulder, with >90% developing shoulder symptoms. Commonly associated with rotator cuff tears; classic radiographic findings include: 1 . Central glenoid wear 2. Periarticular osteopenia 3. Cysts Treatment: 1. Nonsurgical management is the primary treatment, including pharmacologic and physical therapy regimens for patients with mild symptoms and functional disability. 2. Surgical intervention is indicated in patients with significant pain and functional limitation when nonsurgical treatment fails to provide relief. 3. The procedure selected depends on careful assessment of the degree of articular cartilage injury and compromise of the periarticular soft tissues.

Knee RA Pathoanatomy as described above Surgical options: 1. Synovectomy of knee: It decreases pain and swelling but does not alter prevent radiographic progression and does not prevent the need for TKA in the future. Normal synovium reforms, but degenerates to rheumatoid synovium over time. Range of motion is not improved. 2. In advanced disease, TKA has proven to be the most successful intervention that reduces knee pain and improves physical function in rheumatoid arthritis patients. However, as rheumatoid arthritis patients carry additional potential for late complications, many important considerations regarding preoperative evaluation and surgical technique must be taken into account in order to improve the results of total knee arthroplasty in this subgroup of patients. 3. Resurfacing of the patella during total knee arthroplasty.

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The life span of RA patients with a knee replacement is not well known; h­ owever, assuming that RA patients have a normal life span, a TKA in this subgroup of patients on average needs to last longer, and accordingly the potential risk of late complications increases. Many authors also expressed concern that late failure of the PCL could lead to late posterior instability. Foot and Toe: Usually bilateral and symmetric. Forefoot joints are the first to be affected. Toe hyperextension deformity: The earliest manifestation of RA of the forefoot is synovitis of the MTP joints with eventual hyperextension deformity of the MTP joints including distal migration of the forefoot pad, painful plantar callosities, and skin ulcerations over bony prominences. Rx: Arthrodesis of the first MTP joint and lesser MTP joint resections. Talonavicular arthritis: Common to have degenerative changes; treatment—fusion.

Tendon Problems Extensor tenosynovitis is a common presenting upper extremity problem and, unless it resolves with medical management, preventative tenosynovectomy is indicated to prevent tendon rupture. When a rupture has occurred, tendon reconstruction with either a transfer or a graft has a reasonable chance of restoring function as long as the number of tendons involved is limited. Rupture of a single extensor tendon requires surgical treatment to eliminate the cause and prevent further damage, as well as repairing the injured tendon. Extensor Tendon Rupture: Frequency EDM > EDC (ring) > EDC (small) > EPL; treatment—tendon transfer, interposition graft, or Darrach’s procedure. Mannerfelt syndrome—rupture of FPL in carpal tunnel due to scaphoid osteophytes; treated by FDS to FPL tendon transfer. Vaughan-Jackson syndrome—describes the rupture of the hand digital extensor tendons which occur from the ulnar side of the wrist first, then moves radially; treated by EIP to EDC transfer and distal ulna resection.

References 1. Callegari PE, Williams MV.  Laboratory tests for rheumatic diseases. Postgrad Med. 1995;97(4):65–8, 71–4. 2. American College of Rheumatology Subcommittee on Rheumatoid Arthritis Guidelines. Guidelines for the management of rheumatoid arthritis: 2002 update. Arthritis Rheum. 2002;46:328–46.

7

Tuberculosis K. Mohan Iyer

Definition Tuberculosis (TB) is a potentially fatal contagious disease that can affect almost any part of the body but is mainly an infection of the lungs. It is derived from the Neo-­Latin word: “Tubercle” which means a round nodule/swelling and “Osis” which means condition. The causative organisms is Mycobacterium tuberculosis, which is of two types, namely: human and Mycobacterium bovis which is found in animals. The other causative organisms are (1) Mycobacterium africanum and (2) Mycobacterium microti. The Non-Mycobacterium Genus are (1) Mycobacterium leprae, (2) Mycobacterium avium, and (3) Mycobacterium asiaticum, all together constitute M. tuberculosis complex along with M. africanum, M. bovis, M. canetti, and M. microti. The characteristics of Mycobacterium tuberculosis is that it is a gram-positive organism, which is an obligatory aerobe, non-spore-forming and non-motile rod. It is a mesophile about 0.2–0.6  ×  2.4  μm3. It has a slow generation time of about 15–20 h when it may contribute to virulence. It has a lipid-rich cell wall which contains mycolic acid with 50% being its cell wall dry weight. It is acid fast which retains acid stains, and confers resistance to detergents and antibacterials.

Classification 1 . Pulmonary TB which may be a primary disease or a secondary disease. 2. Extrapulmonary such as (a) Lymph node TB (b) Pleural TB (c) TB of upper airways K. M. Iyer (*) Royal Free Hampstead NHS Trust, Royal Free Hospital, London, UK © Springer Nature Switzerland AG 2019 K. M. Iyer, W. S. Khan (eds.), General Principles of Orthopedics and Trauma, https://doi.org/10.1007/978-3-030-15089-1_7

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(d) Skeletal TB (e) Genitourinary TB (f) Miliary TB (g) Pericardial TB (h) Gastrointestinal TB (i) Tuberculous meningitis (j) Less common forms

Epidemiology In 2011, there were an estimated 8.7 million incidence cases of TB globally. It is equivalent to 125 cases in 1,00,000 population. • • • • •

Asian: 59% African: 26% Eastern Mediterranean Region: 7.7% The European Region: 4.3% Region of the America: 3%

India is the highest TB burden country accounting for more than one-fifth of the global incidence (global incidence is 9.4 million while India annual incidence is 1.96 million). Incidence of tuberculosis: Its annual incidence in different age groups shows a maximum in the age groups above 55 years and the annual deaths from infections due to tuberculosis than others such as HIV, measles, STD, malaria, and tropical diseases.

Spread of Tuberculosis Commonest form of spread is coughing without covering the mouth, crowded places with poor ventilation, and due to spitting everywhere.

Severe Symptoms 1. Persistent cough 2. Chest pain 3. Coughing with bloody sputum 4. Shortness of breath 5. Urine discoloration 6. Cloudy and reddish urine 7. Fever with chills 8. Fatigue

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Types Pulmonary TB 1. Primary tuberculosis: The infection of an individual who has not been previously infected or immunized is called primary tuberculosis or Ghon’s complex or childhood tuberculosis. Lesions forming after infection is peripheral and accompanied by hilar which may not be detectable on chest radiography. 2. Secondary tuberculosis: The infection of an individual who has been previously infected or sensitized is called secondary or post primary or reinfection or chronic tuberculosis.

Extrapulmonary TB These are found in 20% of patients of TB Patient. Affected sites in body are: 1. Lymph node TB (tuberculous lymphadenitis): Seen frequently in HIV-infected patients. Symptoms: Painless swelling of lymph nodes most commonly at cervical and supraclavicular (Scrofula) regions. Systemic systems are limited to HIV-­ infected patients. 2. Pleural TB: Involvement of pleura is common in primary TB and results from penetration of tubercle bacilli into pleural space. 3. TB of upper airways: Involvement of larynx, pharynx, and epiglottis. Symptoms: dysphagia, chronic productive cough. 4. Genitourinary TB: 15% of all Extrapulmonary cases. Any part of the genitourinary tract gets infected. Symptoms: urinary frequency, dysuria, hematuria. 5. Skeletal TB: Involvement of weight-bearing parts like spine, hip, knee. Symptoms: pain in hip joints and knees, swelling of knees, trauma. 6. Gastrointestinal TB: Involvement of any part of GI tract. Symptoms: abdominal pain, diarrhea, weight loss. 7. TB meningitis and tuberculoma: 5% of all extrapulmonary TB. Results from hematogenous spread of 10 and 20 TB. 8. TB pericarditis: 1–8% of all extrapulmonary TB cases. Spreads mainly in mediastinal or hilar nodes or from lungs. 9. Miliary or disseminated TB: Results from hematogenous spread of tubercle bacilli. Spread is due to entry of infection into pulmonary vein producing lesions in different extrapulmonary sites. 10. Less common extrapulmonary TB: It may manifest as uveitis, panophthalmitis, painful hypersensitivity, and related phlyctenular conjunctivitis.

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Table 7.1  Interpretation of the tuberculin test Diameter of induration Less than 6 mm

6 mm or greater, but less than 15 mm > − 15 mm

Interpretation Negative

Hypersensitive to tuberculin protein. May be due to previous TB infection, BCG or exposure to atypical mycobacteria. Strongly hypersensitive to tuberculin protein. Suggestive of TB infection or disease.

Action Previously vaccinated individuals may be given BCG, provided there are no contraindications. Should not be given BCG.

Should not be given BCG. Refer for further investigation and supervision which may include chemotherapy.

Diagnosis 1. Bacteriological test: (a) Ziehl-Neelsen stain, (b) Auramine stain (fluorescence microscopy). 2. Sputum culture test: (a) Lowenstein–Jensen (LJ) solid medium: 4–18 weeks, (b) liquid medium: 8–14 days, (c) agar medium: 7–14 days. 3. Radiography: Chest X-ray (CXR). 4. Nucleic acid amplification: Species identification; several hours; low sensitivity, high cost; most useful for the rapid confirmation of tuberculosis in persons with AFB-positive sputa; has utility value in AFB-negative pulmonary tuberculosis and extrapulmonary tuberculosis. 5. Tuberculin skin test (PPD): Injection of fluid into the skin of the lower arm. 48–72 h later checked for a reaction (Table 7.1). Diagnosis is based on the size of the wheal. 1 dose = 0.1 mL contains 0.04 μg tuberculin PPD. 6. Other biological examinations: Cell count (lymphocytes), protein (Pandy and Rivalta tests)—Ascites, pleural effusion, and meningitis.

Preventive Measures 1. Mask 2. BCG vaccine 3. Regular medical follow-up 4. Isolation of patient 5. Ventilation 6. Natural sunlight 7. UV germicidal irradiation

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7 Tuberculosis Table 7.2  Table showing the management with mechanism of action in tuberculosis

First-line drugs Isoniazid Rifampin Rifapentine Rifabutin Ethambutol Pyrazinamide

Drugs Isoniazid Rifampicin Pyrazinamide

Ethambutol Streptomycin

Second-line drugs Cycloserine Ethionamide Levofloxacin Moxifloxacin Gatifloxacin p-Aminosalicylic acid Streptomycin Amikacin/Kanamycin Capreomycin Mechanism of action Inhibits mycolic acid synthesis. Blocks RNA synthesis by blocking DNA-dependent RNA polymerase Bactericidal—slowly metabolizing organism within acidic environment of phagocyte orcaseous granuloma Bacteriostatic Inhibition of arabinosyl transferase Inhibition of protein synthesis by disruption of ribosomal function

BCG vaccine: Bacille Calmette Guerin (BCG), First used in 1921, is the only vaccine available today for protection against tuberculosis. It is most effective in protecting children from the disease, given 0.1 mL intradermally, duration of protection 15–20  years, efficacy 0–80%. It should be given to all healthy infants as soon as possible after birth unless the child presented with symptomatic HIV infection. Management (Table 7.2). Monitoring side effects of common antitubercular drugs (Table 7.3). Dosage regimen: 1 . Intensive phase + continuation phase. 2. HREZ (2 months) + HRE (4 months). Recommended dosage for the initial treatment of tuberculosis in adults (Table 7.4):

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Table 7.3  Table showing the side effects of drugs Drug Rifampin

Side effect Rash, liver dysfunction, flulike syndrome, red-orange urine, drug interactions, fever chills.

Isoniazid

Hepatitis, peripheral neuritis, optic neuritis, seizures.

Pyrazinamide

Hepatitis, hyperuricemia

Ethambutol

Optic neuritis

Streptomycin, amikacin, capreomycin

Ototoxicity, renal toxicity

Management Observe patient, stop drug if significant. Monitor AST/limit alcohol consumption/monitor hepatitis symptoms. Administer at least twice weekly/limit dose to 10 kg/adults. Reassure patients. Consider monitoring levels of other drugs affected by Rifampin, especially with contraceptives, anticoagulants, and digoxin/avoid use of protease inhibitors. Stop drug. Monitor AST/limit alcohol consumption/monitor for hepatitis syndrome/educate patient/stop drug at first symptoms of hepatitis (nausea, vomiting, anorexia, flulike syndrome); administer B6/stop drug Monitor AST/limit daily dosage to 15–30 mg/kg/ discontinue with signs and symptoms of hepatitis. Monitor uric acid levels only in cases of gout and renal failure. Use 25 mg/kg daily only for first 2 months (except in drug resistant tuberculosis), then lower daily dose to 15 mg/kg; when possible monitor/visible acuity (eye chart) and red and green color chart (Ishihara color book); stop drug at first change of vision. Limit dose and duration of drug as much as possible/avoid daily therapy in patients >50 years old/monitor BUN and serum creatine levels and possibly conduct audiometry before as treatment needed during therapy/question patients regarding tinnitus/stop drug if patients develop tinnitus.

Table 7.4  Table showing the dosage of antitubercular drugs used Drug Isoniazid Rifampicin Pyrazinamide Ethambutol

Daily dose 5 mg/kg, maximum 300 mg 10 mg/kg, maximum 600 mg 20–25 mg/kg, maximum 2 g 15–20 mg/kg

Thrice weekly dose 15 mg/kg, maximum 900 mg 10 mg/kg, maximum 600 mg 30–40 mg/kg, maximum 3 g 25–30 mg/kg

Dots Directly observed treatment, short-course. DOT means that a trained health care worker or other designated individual ­provides the prescribed TB drugs and watches the patient swallow every dose (sure  cure for TB).

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Multidrug Resistance TB TB is caused by strains of Mycobacterium tuberculosis that are resistant to at least isoniazid and rifampicin, the most effective anti-TB drug. Globally, 3.6% are estimated to have MDR-TB. Almost 50% of MDR-TB cases worldwide are estimated to occur in China and India.

Extensively Drug Resistance TB Extensively drug-resistant TB (XDR-TB) is a form of TB caused by bacteria that are resistant to isoniazid and rifampicin (i.e., MDR-TB) as well as any fluoroquinolone and any of the second-line anti-TB injectable drugs (amikacin, kanamycin, or capreomycin).

Tuberculosis and HIV Worldwide the number of people infected with both HIV and TB is rising. The HIV virus damages the body’s immune system and accelerates the speed at which TB progresses from a harmless infection to a life-threatening condition. The estimated 10% activation of dormant TB infection over the life span of an infected person is increased to 10% activation in 1  year, if HIV infection is superimposed. It is the opportunistic infection that most frequently kills HIVpositive people.

Epidemiological Impact Reactivation of latent infection: People who are infected with both HIV and TB are 25–30 times more likely to develop TB again than people only infected with TB.  Primary infection that is new tubercular infection in people with HIV can progress to active disease very quickly. Recurring infection—in people who were cured of TB.

Diagnosis of TB in People with HIV HIV-positive people with pulmonary TB may have a higher frequency of having sputum negative smears. The tuberculin test often fails to work, because the immune system has been damaged by HIV. It may not even show a response even though the person is infected with TB. Chest X-ray will show less cavitation. Cases of extrapulmonary TB are more common.

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Tuberculosis of Bones and Joints Tuberculosis of the Spine Spine is the most frequent site of osseous involvement by TB in about 50% of cases. The disease was first described by Sir Percival Pott in 1779, hence the name Pott’s disease. There has been a resurgence of the disease in the developed countries following the HIV pandemic. It is defined as an infection by Mycobacterium tuberculosis of one or more of the extradural components of the spine, namely the vertebra, intervertebral disks, paraspinal soft tissues, and epidural space.

Pathophysiology It is usually by hematogenous route. Perivertebral arterial or venous plexus is still in debate, but arterial route is considered more important. The primary focus in the lung or other extra-osseous foci such as lymph nodes, GIT, or any other viscera. The lower thoracic and lumbar vertebrae are most often affected followed by middle thoracic and cervical vertebrae. The C2–C7 region is reportedly involved in 3–5% of cases and the atlanto-axial articulation in 1.03 upper: lower segment ration less than 0.89, arachnodactyly (positive steinberg/wrists signs). 6. Abnormal skin striae, hyperextensibility, thin skin, papyraceous scarring. 7. Eye signs: drooping eyelids or myopia or antimongoloid slant. 8. Varicose veins or hernia or uterine/rectal prolapse. BJHS is diagnosed in the presence of two criteria or one major and two minor criteria, or four minor criteria. Two minor criteria will suffice where there is an unequivocally affected first-degree relative. Acute pain episodes are commonly managed using taping, bracing, or splinting or with NSAIDs as needed. Physical therapy is of the outmost importance, and encouraging an active lifestyle may improve function and enhance QOL. Strengthening exercises focused on muscles around hypermobile joints may help to enhance joint support throughout movement and reduce pain; closed chain exercises may enhance proprioceptive feedback and optimize muscle action. Proprioception may be improved by coordination and balance exercises. PT should also address cardiorespiratory, musculoskeletal, and neurological aspects of movement with the aim to reduce deconditioning.

Ehlers-Danlos Syndromes (EDSs) EDSs comprise a very heterogeneous group of heritable disorders of CT. The increased flexibility and fragility of the soft connective tissues result in a wide range of changes in the skin, ligaments, joints, blood vessels, and internal organs. Villefranche classification recognizes six subtypes, according to clinical features, inheritance pattern, and underlying molecular defects. In the last few years, rarer phenotypes that do not fit in the Villefranche classification have been described. Prevalence of EDS is estimated to be approximately 1 in 5000 births, with no racial predisposition.

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CT fragility follows abnormalities in the expression or structure of the fibrillar collagen types I, III, and V, as well as enzymatic abnormalities in the posttranslational modification and processing of these collagens. Mutations in the COL5A1 and COL5A2 genes, encoding the α1- and the α2-chains of type V collagen, respectively, are found in approximately 50% of individuals with the classic type of EDS. Mutations in TNX-B, encoding for Tenascin X, in approximately 5% of patients with the hypermobility type, while vascular EDS is caused by heterozygous mutations in the COL3A1 gene, encoding type III collagen. The clinical spectrum of EDSs varies from mild skin and joint hyperlaxity to severe physical disability and life-threatening vascular complications. The classic, hypermobility, and vascular subtype of EDS are the most common, whereas the kyphoscoliosis, arthrochalasis, and dermatosparaxis types are very rare conditions. The diagnosis of the autosomal dominant (AD) classic subtype of EDS requires the presence of skin hyperextensibility, widened atrophic scars, and joint hypermobility, three major diagnostic criteria, next to a series of “minor” diagnostic manifestations. Characteristic facial features include epicanthic folds, excess skin over the eyelids, presence of dilated scars on the forehead, and vaulted palate. Joint hypermobility is usually generalized and can vary in severity and with age. At birth, uni- or bilateral dislocation of the hip may be present. Even if the hypermobility is asymptomatic, this condition can result in childhood in congenital clubfoot, pes planus, and joint effusions. In young adulthood the classic subtype can be complicated by repetitive subluxations and dislocations either spontaneously or after minimal trauma. Patients usually report chronic and recurrent pain that is difficult to treat, and premature osteoarthritis is a major concern. One of the most typical features is the skin hyperextensibility, which means that the skin stretches easily but snaps back after release. The skin is often smooth and velvety to the touch. For pediatric rheumatologists, a real diagnostic challenge is represented by the hypermobility subtype of EDS (EDS-HT), which is by far the most common subtype. The genetic basis of EDS-Hybermobile is largely unknown and a reliable diagnostic test for this EDS subtype is lacking. According to the Villefranche classification, the major diagnostic criteria are generalized joint hypermobility and presence of typical skin manifestations. It is still a matter of debate if EDS-HT and BJHS really represents two different diseases or if they should be reviewed as a spectrum of a single entity, sharing common genetic bases and showing considerable variability in clinical presentation, between as well as within families. JH is typically limited to the small joints of the hands in the vascular subtype. This subtype has the worst prognosis because of a high rate of spontaneous arterial rupture usually in the third or the fourth decade of life. Unlike other EDS types, the skin is not hyperextensible, but rather thin and translucent, showing a visible venous pattern over the chest, abdomen, and extremities. Excessive bruising is the

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most common sign and is often the presenting complaint, especially in children. Other early manifestations include premature rupture of the membranes, congenital clubfoot or congenital hip dislocation, inguinal hernia, and severe varicosities. The facial and cutaneous features may be very subtle or even absent. If there is a strong clinical suspicion of vascular EDS, direct DNA analysis is mandatory, even in the absence of an abnormal biochemical abnormality. The management of children with Ehlers-Danlos syndromes requires a multidisciplinary approach: Children are advised to avoid contact sports and to wear protective gear. Cutaneous stitches should be left in place twice as long as usual, and additional fixation of adjacent skin with adhesive tape can help to prevent stretching of the scar. In children PT support is important. Acetaminophen should be preferred over NSAIDs for joint pain. Patients with mitral valve prolapse and regurgitation require antibiotic prophylaxis for bacterial endocarditis. A baseline echocardiogram before 10 years of age, with follow-up according to whether an abnormal measurement is found. For the vascular and vascular-like types of EDS, invasive vascular procedures such as arteriography and catheterization should be avoided because of the risk for life-threatening vascular rupture. Surgical interventions are generally avoided.

Marfan Syndrome (MS) MS is a hereditary autosomal dominant, multisystem disorder of connective tissue with extensive clinical variability. It is a relatively common condition, with approximately 1 in 5000 people affected. This disease demonstrates autosomal-dominant inheritance with high penetrance and marked inter- and intra-familial variability. It is caused by defects in FBN1, the gene that codes for the protein fibrillin, although patients with mutations in other genes, including TGFBR1 and TGFBR2, have also been rarely reported. Mutations in FBN1 are associated with a wide phenotypic spectrum ranging from classic features of Marfan syndrome presenting in childhood and early adulthood to severe neonatal presentation. Advanced paternal age is a risk factor. Cardinal features involve the ocular, musculoskeletal, and cardiovascular systems. Skeletal system involvement in MS is characterized by bony overgrowth. Frequent findings are pectus excavatum, pectus carinatum, scoliosis or spondylolisthesis, calcaneal displacement, “protrusio acetabuli,” arachnodactyly, and pes planus. Recently, Marfan patients have been reported to have reduced bone mass and muscle mass, compared to healthy controls. All this skeletal abnormalities may account for the very high incidence of severe daily pain that Marfan patients report. Joint laxity may be significant in young MS patients and can lead to ligament injury, dislocations, chronic joint pain, and degenerative arthritis.

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The facial features of Marfan syndrome include a long and narrow face with deeply set eyes (enophthalmos), downward slanting of the eyes, flat cheek bones (malar hypoplasia), and high arched palate. Ectopia lentis is a cardinal feature of Marfan syndrome and an ophthalmologic examination is mandatory in suspected cases. During early childhood, patients may occasionally present with isolated bilateral ectopia lentis. Cardiovascular involvement is particularly worrisome because the progressive aortic root dilatation can lead to acute dissection, aneurysms, and sudden death. Marfan syndrome continue to have high rates of cardiovascular disease and premature death. The diagnosis is clinical, according to the revised Ghent criteria. These criteria however perform well in patients showing the typical phenotypes. These criteria are not as useful in milder MS variants, when only isolated features are present. In young children Marfan syndrome is not always recognizable, especially in the absence of a family history, because many of the more specific clinical features are age dependent (e.g., ectopia lentis, aortic dilation, dural ectasia, protrusio acetabuli). For subjects suspected to have Marfan syndrome based on clinical grounds, FBN1 testing should be considered. A useful tool for risk stratification of suspected pediatric patients can be represented by the Kid-Short Marfan Score. Diagnosis and management require a multidisciplinary approach by geneticists, cardiologists, orthopedic surgeons, and ophthalmologists with experience in this field. Cardiovascular follow-up should include serial evaluation with electrocardiography and serial cardiac imaging, especially CT/MRI angiography. Exercise restriction is wise and elective aortic-root replacement is sometimes needed. Endocarditis prophylaxis is indicated in those with valvular defects. Medical therapy with betablockers seems to be able to decrease aortic root enlargement, especially when started relatively early in the disease course, while the role of ACE inhibitors is still debated.

Loeys-Dietz Syndrome (LDS) LDS is a recently described rare autosomal dominant connective tissue disorder characterized by a severe and widespread arterial involvement since childhood. Its exact incidence have not been established. The disorder is most often caused by heterozygous mutations in TGF-β receptors TGFBR1 and TGFBR2. The classification depends on the presence or absence of craniofacial features (hypertelorism, bifid uvula, and cleft palate). Affected individuals show generalized arterial abnormalities, ascending aneurysms, and rapidly progressive aortic aneurysm. Skeletal features in all types of LDS may show overlap with Marfan syndrome (i.e., pectus deformity, arachnodactyly, scoliosis, and pes planus) but height and proportions are typically within the normal range. Joint hypermobility is also common. A more specific finding is the association of arachnodactyly with advanced carpal bone ossification and joint hyperextension.

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LDS diagnostic criteria have not been defined and confirmatory genetic testing is required. Management of LDS involves regular cardiology follow-up to establish the extent of vascular involvement, early surgical intervention, genetic counseling, and monitoring in pregnancy. There is a higher risk of dissection compared to Marfan syndrome, and early surgical correction may be crucial. Aggressive medication regimens, with β-blockers and angiotensin receptor antagonists, are recommended as this treatment may halt disease progression and postpone surgical repair.

Stickler Syndrome (SS) SS is a multisystem connective tissue disorder that can affect the eye, craniofacies, inner ear, skeleton, and joints. Stickler syndrome has been associated with mutations of COL2A1, which encodes for the alpha-1 chain of type II collagen, COL11A1 gene, which encodes for the alpha-1 chain of type XI collagen, and COLL11A2 gene. Rarer autosomal recessive forms have been linked to mutation of the three genes encoding collagen IX: COL9A1-2-3. Variable phenotypic expression of Stickler syndrome occurs both within and among families. Based on the vitreous abnormalities Stickler syndrome is classified as Type 1 (“membranous,” characterized by a persistence of vestigial vitreous gel in the retrolental space) and the rare Type 2 (“beaded,” characterized by sparse and irregularly thickened bundles throughout the vitreous cavity). A nonprogressive myopia is common. Craniofacial findings may include a flat facial profile, telecanthus and epicanthal folds, micrognathia and cleft palate. Hearing impairment, especially sensorineural deafness for high tones, is common but the overall sensorineural hearing loss in type I Stickler syndrome is typically mild and not significantly progressive. The musculoskeletal features are early onset arthropathy, short stature, and mild spondyloepiphyseal dysplasia. In children and adolescents joint hypermobility is seen and usually becomes less prominent with age. The diagnosis of Stickler syndrome is clinically based. At present, clinical diagnostic criteria have been proposed only for type 1 Stickler syndrome. Type 1 individuals have the membranous type of vitreous abnormality. The diagnosis of Stickler syndrome requires genetic analysis of the involved genes. COL2A1 gene may be tested first in individuals with type 1 “membranous” vitreous abnormalities and milder hearing loss. COL1A1 mutations can be frequently found in patients with craniofacial and joint manifestations as well as hearing loss but without ocular findings.

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Torticollis Derived from the Latin word: tortus (twisted) + collis (neck or collar). Torticollis is a symptom related to turning or bending of the neck. Many different causes are possible: In newborns, Torticollis usually results from injury during labor and delivery or the infant’s position in the uterus. Less often, it is caused by birth defects. In older children, torticollis may result from injuries to the neck muscles, common infections, or other causes. Torticollis refers to a symptom rather than a distinct disease process. It can be caused by a wide variety of conditions (over 80 causes have been described) which range from relatively simple self-limited to life-threatening. May be congenital or acquired. Occurs more frequently in children than in adults. The right side is affected in 75% of patients. Abnormal twisting of the neck. Usually, child’s head is tipped toward one side, with the chin pointing in the other direction. Painful spasms of the neck muscles may occur. Other symptoms may be present, depending on the cause, for example, there may be a tender lymph node (gland) if the cause is infection. Causes of Torticollis: (1) Congenital muscular torticollis or (2) Acquired torticollis. 1. Congenital muscular torticollis (CMT): CMT refers to muscular disorders causing torticollis at birth or shortly after due to unilateral shortening of the sternocleidomastoid muscle. More common in males and on the right side. The affected muscle develops fibrotic changes which can be associated with a mass (fibromatosis colli) or without a mass. Presentation is usually during the first 4 weeks of life with torticollis and/or nontender neck mass. It is thought to be caused by intrauterine and perinatal events. Risk factors for CMT include overcrowding environments such as first-born, oligohydramnios, breech presentation, and difficult delivery. Ultrasound (US) is the imaging modality of choice for initial investigation. There is diffuse or focal enlargement of the sternocleidomastoid muscle. The focal mass is usually hypoechoic and homogenous. The mass usually resolve within the first year of life with conservative treatment. The condition is treated with physical therapies, such as stretching to release tightness, strengthening exercises to improve muscular balance, and handling to stimulate symmetry. A Collar is sometimes applied. About 5–10% of cases fail to respond to stretching and require surgical release of the muscle. 2. Acquired torticollis: The most common etiologies (Table 9.2) are: (a) self-limiting, (b) trauma, (c) infections, (d) inflammatory conditions, and (d) central nervous system tumors or lesions. (a) Self-limiting: A self-limiting spontaneously occurring form of torticollis with one or more painful neck muscles is by far the most common (“stiff neck”) and will pass spontaneously in 1–4 weeks. Usually the sternocleidomastoid muscle or the trapezius muscle is involved. Colds or unusual postures are implicated; however in many cases no clear cause is found.

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Table 9.2  Table showing the differential diagnosis of acquired torticollis Differential diagnosis list of acquired torticollis: Trauma: Occipital condyle fracture, dislocation, AARF, hematoma. Infection: Head and neck infections, spinal infections, meningitis, AARF (Grisel syndrome). Inflammation: Juvenile idiopathic arthritis, symptomatic intervertebral disc calcification. Neoplasm: CNS Tumors, Bone tumors, neck tumors. Miscellaneous: Vascular abnormalities, congenital etiologies, presenting later in life.

(b) Trauma: Occipital condyle fracture and facet dislocation may present with torticollis. Atlanto-axial rotatory fixation (AARF) of C2. Spontaneous spinal epidural hematoma is a rare disorder which might manifest with painful torticollis followed by weakness and sensory loss and is mostly common at the cervicothoracic level. Subarachnoid hemorrhage. CT is the modality of choice in most trauma cases. MRI is indicated in any case of concern for ligamentous injury or when there is a neurologic deficit. (c) Infection and inflammation: Head and neck and spinal column infections may cause torticollis either by muscular or ligamentous irritation or from direct spinal disease. Infectious and inflammatory causes of Torticollis: (1) CNS related such as meningitis, (2) head and neck related such as Upper respiratory infections, otitis media, Mastoiditis/Bezold’s abscess, cervical adenitis, or Retropharyngeal abscess, and (3) spine related such as vertebral osteomyelitis and/or discitis, epidural abscess or rheumatoid arthritis. Infection: A lateral neck X-ray radiograph will show increased soft tissue thickness anterior to the C spine in retropharyngeal abscess. An US may show superficial lymphadenitis and abscess. A CT is used to visualize the deep neck spaces and for presurgical planning. MRI is useful in spinal column infections due to its increased sensitivity and its ability to show soft tissue and epidural extension. (d) Tumors: Tumors of the CNS, spine and neck may cause torticollis. CNS tumors are usually in the posterior fossa or C spine. The common presentation of C spine tumor is pain due to dural irritation. Posterior fossa tumors (cerbellar tumor) may also have signs of increased intracranial pressure. In any case of insidious development of torticollis the possibility of a tumor should be considered. MRI is the imaging modality of choice. (e) Other causes: The use of certain drugs, such as antipsychotics, Antiemetics, Neuroleptic Class, and Phenothiazines, can cause torticollis. Treatment: Treatment for torticollis depends on the cause: For newborns with torticollis, gentle motion of the head and neck is recommended to stretch the muscles. Often, a physical therapist is involved. To avoid injury, this should be done only as recommended by a doctor. For older children with torticollis related to infection or inflammation, treatment may include: antibiotics for the specific infection, rest, anti-inflammatory medications (such as ibuprofen), passive motion to keep the muscles from getting stiff, and surgery if indicated. If the cause is related to trauma (even sleeping position) treatments may include: muscle relaxants—Valium (generic name: diazepam) and passive motion. A soft collar or brace to support the neck.

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Conclusion 1 . Torticollis is a clinical sign that might signify an underlying disorder. 2. In newborn infants with CMT, ultrasound is preferred and often diagnostic. 3. In older children CT is used to diagnose traumatic insult, neck infection, and vertebral anomalies. 4. MRI is used to diagnose inflammatory and infectious spinal disorders and in cases in which CNS or neck malignancy is suspected.

Cleidocranial Dysostosis It is also known as cleidocranial dysplasia or Marie and Sainton’s disease, Scheuthaner-Marie-Saniton syndrome, or Mutational dystosis. It is defined as a congenital disorder of bone formation manifested with clavicular hypoplasia (Fig. 9.2) or agenesis with a narrow thorax, which allows approximation of the shoulders in front of the chest. It is a congenital condition transmitted as autosomal dominant trait. It is manifested as retardation or partial failure of the development of the bones of the clavicle and of the skull but not of the mandible.

Etiology It is familial and appears as true dominant mendelian characteristic. Mutations in the core binding factor alpha 1 (CBFA) gene located on chromosome 6p21 is the cause of cleidocranial dysplasia.

Clinical Features 1. Characterized by abnormalities of skull, teeth, jaw, shoulder girdle as well as by occasional stunting of long bones. 2. Head is brachycephalic. Fig. 9.2 Cleidocranial dysostosis (Courtesy: reused with the kind permission of Magdi E. Greiss, Whitehaven, Cumbria, UK)

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3. Paranasal sinuses are underdeveloped and narrow. 4. Faulty development of foramen magnum. 5. Dysplasia of paranasal sinuses. 6. Defect of shoulder girdle ranges from absence of clavicle about in 10% of cases, to partial absence or even thinning of one or both clavicles. 7. Defects of vertebral column, pelvis, and long bones as well as of bones of disease are also relatively common. 8. Oral manifestations: (a) Maxilla and paranasal sinuses are underdeveloped resulting in maxillary macrognathia. (b) Maxilla underdeveloped in relation to the mandible. (c) Prolonged retention of deciduous teeth and subsequent delay in eruption of teeth. 9. Complete absence of cementum. 10. Disorganization of developing permanent dentition. 11. Presence of supernumerary teeth usually in anterior region. 12. High narrow arched palate and cleft palate is common. 13. Roots of teeth are often short and thinner than normal. 14. Crown may be pilled as a result of enamel hypoplasia.

Radiographic Examination 1. Clavicles are typically reduced to single or double fragments on each side with the middle part being deficient. 2. Changes are asymmetric. 3. Delay in ossification of pelvic bones, especially pubic and ischial bones. 4. Spina bifida occulta observed in cervical and upper thoracic levels.

Treatment 1 . No specific treatment. 2. Care of oral condition is important. 3. Retained deciduous tooth should be restored if they become carious.

Congenital Short Neck (Klippel-Feil Syndrome) Features 1 . Congenital fusion of cervical vertebrae. 2. Failure of normal segmentation of the cervical vertebrae/somite between 3rd and 8th week of fetal development (rather than a secondary fusion). 3. It was initially described by Maurice Klippel and Andre Feil—1912.

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4 . Incidence—1 in 42,000 births; more in females. 5. It is a autosomal dominant inheritance—C2–C3 fusion; autosomal recessive— C5–C6 fusion. 6. Feil’s triad of: (a) low posterior hair line, (b) short neck, and (c) limitation of head and neck movements/decreased range of motion in cervical spine.

Classification Feil’s Classification • Type I—massive fusion of many cervical and upper thoracic vertebrae with synostosis • Type II—fusion of only 1 or 2 vertebrae (with hemivertebrae, scoliosis, occipito atlantoid fusion) • Type III—presence of lower thoracic and upper lumbar spine anomalies with I/II • Type IV—sacral agenesis  amartzis’s Classification (2006) [2] S To clarify prognosis • Type I—single congenitally fused cervical segment • Type II—multiple noncontiguous fused segments • Type III—multiple contiguous fused segments

Clinical Features 1. Patients with upper cervical spine involvement tend to present at an earlier age than those with lower cervical spine involvement. 2. Rotational loss and lateral bending is usually more pronounced than loss of flexion and extension because latter movements take place mostly between occiput and atlas. 3. Scoliosis—some patients congenital due to involvement of thoracic spine, others scoliosis compensatory to cervical scoliosis. 4. Webbing of soft tissues on each side of the neck (extending from mastoid process to acromion of shoulders)—“pterygium colli.” 5. Assocd torticollis due to contracture of sternocleidomastoid muscle or bony abnormalities. 6. Facial asymmetry. 7. Sprengel deformity/high scapula. 8. Scoliosis and/or kyphosis. 9. Musculoskeletal sys-cervical rib, congenital fusion of ribs, abnormal costovertebral joints, syndactyly, hypoplastic thumb, supernumerary digits, hypoplasia of pectoralis major, hemiatrophy of upper or lower limbs, CTEV, sacral agenesis.

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10. Urinary tract abnormalities—agenesis of kidney, horseshoe kidney, hydronephrosis, tubular ectasia, renal ectopia, double collecting system. 11. Cardiovascular—VSD, PDA, coarctation of aorta, patent foramen ovale. 12. Deafness (absence of auditory canal and microtia). 13. Synkinesia—involuntary paired movements of the hand (mirror movements). 14. Neurologic deficit—facial nerve palsy, rectus muscle palsy, ptosis of eye, cleft palate, etc.

Radiological Findings 1. Cervical spine routine X-ray followed by flexion/extension lateral X-rays. These may show flattening and widening of vertebrae, hemivertebrae or block vertebrae, instability. 2. MRI with head flexed and extended will most accurately access subluxation and cord compression along with cord anomalies. 3. Wasp-waist sign-anterior concave indentation at the site of the absent or fused interspace between the fused vertebrae. 4. In the young child (  knees  > feet > hips > hands > shoulders. Workup needed: Many forms of AMC mapped to loci on chromosomes. Frequently presents as inherited disorder (family tree). Radiographs of affected joints. Head, abdominal US-rule out other anomalies. CT scan brain. MRI brain, spinal cord. EEG, EMG, muscle biopsy. Chromosomes. Management: Initial finding of AMC often overwhelming to parents. Differentiate between neurogenic and myopathic (neurogenic-worse prognosis). Birth is when baby is at its worst. Work with orthopedic surgical team, physiotherapist to improve movement and decrease stiffness. If no CNS or neurogenic component-normal IQ; early is the intervention key. 1 . Passive stretching with or without splints 2. Serial casting

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3. Surgical interventions 4. Physical therapy is a lifelong process 5. Care begins in NICU

Outcome Hall reported 1% mortality with limb involvement; 7% with limb and other organ, and 50% with limb and CNS involvement; ventilator dependent at birth-poor prognosis. Pena-Shokier syndrome: It is described as a syndrome of camptodactyly, multiple ankyloses, facial anomalies, and pulmonary hypoplasia. Usually a lethal condition. It is an autosomal recessive most common transmission pattern with a recurrence risk 0–25%; Incidence is unknown and 30% stillborn; The live births succumb from pulmonary complications. The muscle histology abnormal, predominantly neurogenic atrophy; the spinal cord and CNS often abnormal as well with lack of fetal movement often predicts the ultimate outcome for these children. The chromosomes helpful as phenotype overlaps with trisomy 18. Pena-Shokeir syndrome: Characteristic facies, short neck, mild contractures at the hip, moderate contractures at elbows and knees, severe contractures, and camptodactyly with ulnar deviation of the hands.

Congenital Absence of the Radius Congenital malformations of the hand encompass a myriad of deformities, all of which carry different functional and cosmetic implications for the patient and parents. Classification by Swanson, Barsky, and Enti for congenital deformity of hand [4]. Failure of formation-(arrest of development) are of two types: (1) Longitudinal deficiencies or (2) transverse deficiencies. Transverse deficiencies include those deformities in which there is complete absence of parts distal to some point on the upper extremity, producing amputation-like stumps that allow further classification by naming the level at which the remaining stump terminates. Longitudinal deficiencies: Longitudinal deficiencies include all failure-of-­ formation anomalies that are not considered transverse deficiencies, e.g., phocomelia, radial ray dysplasia, ulnar ray dysplasia, and central dysplasia. In the Iowa study these deformities constituted 9.3% of reported malformations, compared with the 7.1% incidence of transverse deficiencies. Radial club hand: radial ray deficiencies include all malformations with longitudinal failure of formation of parts along the preaxial or radial border of the upper extremity: deficient or absent thenar muscles,

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a shortened, unstable, or absent thumb, and a shortened or absent radius, commonly referred to as radial club hand. Epidemiology: The primary insult is to the apical ectodermal ridge during critical limb development period (between 4th and 7th weeks). It is mostly due to environmental factors such as: 1. Compression 2. Inflammatory processes 3. Nutritional deficiency 4. Irradiation 5. Infection (Figs. 9.10, 9.11 and 9.12) 6. Medications (especially thalidomide) Fig. 9.10 Sequelae following infection and trauma in the second decade (Courtesy: reused with the kind permission of Shibu P. Krishnan, London, UK)

Fig. 9.11 Sequelae following infection and trauma in the second decade (Courtesy: reused with the kind permission of Shibu P. Krishnan, London, UK)

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Fig. 9.12  X-rays of the above case (Courtesy: reused with the kind permission of Shibu P. Krishnan, London, UK)

It results from a radial ray deficiency during embryological development. The incidence ranges from 1  in 30,000 to 1  in 100,000. It also ranges from 4.7% to 6.1% of all congenital anomalies. It is slightly more common in males than females and in Caucasians. It is bilateral in 38–50% of cases. When unilateral, occurs twice as frequent on right side. The deformity is radial deviation of hand with a short forearm (50–75% the length of normal forearm). It is almost always present at birth. There is a prominent knob at distal end of ulna. No single definite implicating factors. Genetic studies have failed to show any genetic basis except when deformity is associated with a syndromal picture as in Holt-Oram, Fanconi’s, and TAR syndrome. Interestingly, one study found that twice as many affected patients born during summer months than winter months. The thumb may be absent or severely deficient. The hand typically small. The MCP joints with limited flexion and some hyperextensibility. There may be flexion contractures of PIP joints. Elbow extension contracture common as a result of weak or absent elbow flexors. The obvious deformity of a short forearm and radially deviated hand is almost invariably present at birth. These conditions may occur as isolated deficiencies, but more commonly they occur to some degree in association with each other. Radial club hand occurs in an estimated 1 per 100,000 live births. When the deformity is unilateral, the right side is more commonly affected. Both sexes are equally affected. Complete radial absence is more common than partial absence. In most cases of radial club hand the cause is unknown, and the deformities are believed to occur sporadically. In a study Wynne-Davies and Lamb found a higher proportion of a first-degree relative with minor congenital anomalies than would be expected from a random survey, which suggests a genetic contribution. The currently accepted and most useful classification of congenital radial dysplasias is a modification of that proposed by Heikel.

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Heikel Classification [5] In type I (short distal radius) the distal radial physis is present but is delayed in appearance, the proximal radial physis is normal, the radius is only slightly shortened, and the ulna is not bowed (Fig. 9.13). In type II (hypoplastic radius)—both distal and proximal radial physes are present but are delayed in appearance, which results in moderate shortening of the radius and thickening and bowing of the ulna (Fig. 9.14).

Fig. 9.13  Line diagram drawing of Type I absence of the radius

Fig. 9.14  Line diagram drawing showing Type II absence of the radius. Type III deformity: There is a partial absence of the radius which may be proximal, middle, or distal, with absence of the distal third being most common; the carpus usually is radially deviated and unsupported, and the ulna is thickened and bowed (Fig. 9.15)

Fig. 9.15  Line diagram showing Type III absence of the radius

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Fig. 9.16  Line diagram showing Type IV absence of the radius

The type IV pattern = There is a total absence of the radius which is the most common, with radial deviation of the carpus, palmar and proximal subluxation, frequent pseudoarticulation with the radial border of the distal ulna, and a shortened and bowed ulna (Fig. 9.16). A summary of Heikel’s classification of radial dysplasia is as follows: (a) Type I—short distal radius. (b) Type II—hypoplastic radius. (c) Type III—partial absence of radius. (d) Type IV—total absence of radius. Variable degrees of thumb deficiencies are frequent with all patterns OF radial club hand.

Associated Syndromes Associated cardiac, hemopoietic, gastrointestinal, and renal abnormalities occur in approximately 25% of patients with radial club hand and may pose significant morbidity and mortality risks. The most frequently associated syndromes are Holt-­ Oram syndrome, Fanconi anemia, thrombocytopenia—absent-radius TAR syndrome, VATER syndrome, which consists of vertebral segmentation deficiencies, anal atresia, tracheoesophageal fistula, esophageal atresia, renal abnormalities, and radial ray deficiencies. In the Holt-Oram syndrome the cardiac abnormality (most commonly an atrial septal defect) requires surgical correction before any upper limb reconstruction measure is taken. Cardiac defects most frequently seen are ASD, VSD, tetralogy

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of Fallot, mitral valve prolapse, PDA, total anomalous pulmonary venous return. Congenital heart defects required for diagnosis. Associated syndrome: Children with Fanconi anemia, a pancytopenia of early childhood, have a very poor prognosis, and death usually occurs 2–3  years after onset of the disease. It is an autosomal dominant with the thumb always present, a progressive pancytopenia and it may not progress until mid-childhood. The prognosis is poor. Associated syndrome: In TAR syndrome, thrombocytopenia usually resolves by the age of 4–5 years and, although it may delay reconstruction, but is not a contraindication to surgical treatment. The thumb is always present and radial deficiency is bilateral. Autosomal recessive mode of inheritance. Typically, prognosis is good and platelet count improves to normal by age 4–5. Always check platelet count in child with radial club hand and a thumb prior to entertaining surgery. Associated syndrome: Approximately half of these patients also have cardiac defects. Successful treatment of the associated abnormalities usually is possible, and upper extremity reconstruction may be appropriate in selected patients. Radial deficiency also is associated with trisomy 13 and trisomy 18; these children have multiple congenital defects and mental deficiency that may make reconstruction inappropriate despite significant deformity. Anatomical abnormalities of congenital absence of the radius: The scapula, clavicle, and humerus often are reduced in size, and the ulna is characteristically short, thick, and curved, with any radial remnant. Anatomical abnormalities = Total absence of the radius is most frequent, but in partial deficiencies, the proximal end of the radius is present most often. The scaphoid and trapezium are absent in more than half of these patients; the lunate, trapezoid, and pisiform are deficient in 10%; the thumb, including the metacarpal and its phalanges, is absent in more than 80%, although a rudimentary thumb is not uncommon. The capitate, hamate, triquetrum, and the ulnar four metacarpals and phalanges are the only bones of the upper extremity that are present and free from deficiencies in nearly all patients. The muscular anatomy always is deficient, although the deficiencies are highly variable. Muscles that frequently are normal are the triceps, extensor carpi ulnaris, extensor digiti quinti proprius, lumbricals, interossei (except for the first dorsal interossei), and hypothenar muscles. The long head of the biceps is almost always absent, and the short head is hypoplastic. The brachialis often is deficient or absent as well. The brachioradialis is absent in nearly 50% of patients. The extensors carpi radialis longus and brevis frequently are both absent or may be fused with the extensor digitorum communis. The pronator teres often is absent or rudimentary, inserting into the intermuscular septum, and the palmaris longus often is defective. The flexor digitorum superficialis usually is present and is abnormal more frequently than is the flexor digitorum profundus. The pronator quadratus, extensor pollicis longus, abductor pollicis longus, and flexor pollicis longus muscles usually are absent. In summary: Preaxial musculature from lateral epicondyle most severely affected. Radial wrist extensors ECRL, ECRB, and BR either absent or severely deficient. Finger extensors usually present. Long head of biceps almost always absent. Short head typically hypoplastic. Brachialis deficient or absent.

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Neurovascular abnormality: The peripheral nerves generally have an anomalous pattern, with the median nerve being the most clinically significant. The nerve is thicker than normal and runs along the preaxial border of the forearm just beneath the fascia. This nerve is at considerable risk during radial dissections because it is quite superficial. The ulnar nerve characteristically is normal according to most authors, and the musculocutaneous nerve usually is absent. The vascular anatomy usually is represented by a normal brachial artery, a normal ulnar artery, a well-­ developed common interosseous artery, and an absent radial artery. Median nerve thickened and runs just below fascia. At risk for injury during surgical dissection along concavity of deformity. Radial nerve typically ends at lateral epicondyle after innervating triceps. Ulnar nerve normal. MC nerve absent. The forearm is between 50% and 75% of the length of the contralateral forearm, a ratio that usually remains the same throughout periods of growth. The thumb characteristically is absent or severely deficient; flexion contractures often occur in the proximal interphalangeal joints. Stiffness of the elbow in extension, probably the result of weak elbow flexors, frequently is associated with a radial club hand. Most authors emphasize the elbow extension contracture as an extremely important consideration in evaluating these patients for reconstruction. Because of the radial deviation of the hand, the child usually can reach the mouth without elbow flexion. Lamb found that unilateral involvement did not significantly affect the activities of daily living, but bilateral involvement reduced activities by one third. Associated cardiac or hematological problems may worsen the overall prognosis. Management of radial club hand: It can be divided into (1) nonoperative treatment and (2) operative treatment.

 onoperative Management of Radial Club Hand N Immediately after birth the radial club hand often can be corrected passively, and early casting and splinting generally are recommended. A light, molded plastic, short arm splint (Fig. 9.17) is applied along the radial side of the forearm and is removed only for bathing until the infant begins to use the hands; then the splint is worn only during sleep. Riordan recommended applying a long arm corrective cast as soon after birth as possible. The cast is applied in three stages by means of a technique similar to that used for clubfoot casting (Ponseti casting). The hand and wrist are corrected first, and then the elbow is corrected as much as possible. Milford concluded that casting and splinting in a child younger than 3 months of age often is impractical. Fig. 9.17  Line diagram showing the light molded plastic short arm splint

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Lamb reported that elbow extension contracture can be improved by splinting the hand and wrist in neutral position; 20 of his 27 patients improved to 90°. He also cautioned that elbow flexion never improves after centralization procedures. There is no satisfactory conservative therapy for the significant thumb deformities associated with radial club hand.

 perative Treatment of Radial Club Hand O It consist of centralization of the carpus on the forearm, along with thumb reconstruction, and occasionally transfer of the triceps to restore elbow flexion. Although surgery may be postponed for 2–3 years with adequate splinting, there is general agreement favoring operative correction at 3–6 months of age in children with inadequate radial support of the carpus. Pollicization, when indicated, follows at 9–12 months of age if possible. PS: contraindications to operative treatment: (a) Severe associated anomalies not compatible with long life. (b) Inadequate elbow flexion. (c) Mild deformity with adequate radial support (type I and some type II deformities). (d) Older patients who have accepted the deformities and have adjusted accordingly. Centralization of hand: Centralization of the hand over the distal ulna was first reported in 1893 by Sayre, who suggested sharpening the distal end of the ulna to fit into a surgically created carpal notch. Techniques: Centralization arthroplasty technique, transverse ulnar approach. (a) Incision. (b) Exposure of muscle, tendon, and nerve. (c) Capsular incision (Fig. 9.18). (d) Exposure of carpoulnar junction and excision of segment of carpal bones. (e) Insertion of Kirschner wire. (f) Reattachment of extensor carpi ulnaris tendon. Techniques: Centralization of radial club hand. (a) Z-plasties on radial and ulnar sides of wrist. (b) Incisions allow lengthening on radial side. Ulnar incision takes up skin redundancy, transposing it to deficient radial side. Fig. 9.18  Line diagram showing the dorsal capsular incision.

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(c) Radial incision in wrist for identification of median nerve. (d) View from ulnar incision across wrist to radial incision after resection of all nonessential central structures. (e) Distal ulna seen through radial incision at wrist. (f) Kirschner wire passed through lunate, capitate, and long finger metacarpal. (g) After centralization, Kirschner wire passed into ulna to maintain position. Lidge modified this method by leaving the ulnar epiphysis intact, providing the forerunner of modern centralization techniques. Other procedures have been performed in an attempt to stabilize the hand on the forearm. Bardenheuer in 1894 suggested splitting the distal ulna longitudinally to allow the carpus to become wedged between the two halves. Albee in 1919 attempted to create a radius with a free tibial graft. Starr in 1945 and Riordan in 1955 used a nonvascularized fibular graft to support the carpus, but fibular growth did not continue and the deformity recurred. DeLorme in 1969 suggested intramedullary fixation of the carpus on the ulna. Centralization has been shown to improve function, particularly in bilateral involvement. Bora et al. reported total active digital motion of 54% of normal after surgery, compared with 27% in untreated patients. Forearm length was functionally doubled, and the metacarpal-ulnar angle averaged 35° after surgery, compared with 100° in untreated patients. Tsuyuguchi et al., however, reported that only 6 of their 12 patients were satisfied with the results despite obvious functional gains. Bayne and Klug reported that 52 of 53 patients believed that cosmesis and function had been improved by centralization. Good results had the following factors in common: 1 . All had adequate preoperative soft tissue stretching. 2. Surgical goals were obtained. 3. There were no problems with postoperative bracing. 4. Most had less severe soft tissue contractures. 5. Most were younger than 3 years of age at the time of centralization. Complications of centralization include: (a) Growth arrest of the distal ulna. (b) Ankylosis of the wrist. (c) Recurrent instability of the wrist. (d) Damage to neural structures (particularly the anomalous median nerve). (e) Vascular insufficiency of the hand. (f) Wound infection, necrosis of wound margins, fracture of the ulna, and pin migration and breakage. (g) Major neurovascular complications are rare.

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After treatment: The hand is elevated for 24–48  h. The dressing is changed and sutures are removed 2 weeks after surgery. A long arm cast is applied and worn for an additional 4  weeks. The Kirschner wire is removed at 6  weeks, and a short arm cast is applied to be worn for an additional 3 weeks. Night splinting is continued until physeal closure to avoid recurrence of radial deviation.

Centralization of Hand and Tendon Transfers Bora et al. suggested that treatment be started immediately after birth with corrective casts to stretch the radial side of the wrist. When the patient is between 6 and 12  months old, the hand is centralized surgically over the distal end of the ulna, and tendon transfers are carried out 6–12 months later. Three tendon transfers are performed 6–12  months after the centralization procedure. Before attempting to transfer the flexor digitorum sublimis tendons, test for function, because in some instances the sublimis tendon is nonfunctioning in one or more of the three ulnar digits. Passively maintain the metacarpophalangeal joints and the wrist joint in hyperextension and the interphalangeal joints in extension, and release one finger at a time. After treatment: A cast is applied after the procedure and is worn for 1 month; after this a night splint is worn for at least 3 months. Careful follow-up should be made to observe for possible recurrence of deformity. A night splint can be used for several years.

Pollicization for Reconstruction of Thumb with Radial Club Hand Although the thumb frequently is absent or severely deficient in radial dysplasia, children usually are able to adapt to the thumbless hand with ulnar-side-of-index to radial-side-of-middle finger prehension and finger-to-palm prehension after centralization. Despite this adaptability, overall function and self-care activities are impaired and can be improved with successful pollicization. Because normal as well as compensatory prehensile patterns are firmly established within the first year of life, it is desirable that surgical reconstruction be performed early. Pollicization is recommended for both unilateral and bilateral cases. If a “floating” thumb deformity is present, with inadequate musculotendinous and bony elements, the remnant should be amputated before pollicization to allow reconstruction of a stable thumb. Gosettin 1949 was the first to report replacement of the thumb with the index finger, and the index finger continues to be the preferred donor digit if it is not too deficient. Despite reports of successful single-stage toe-to-hand transfers, in the congenitally deficient thumb the index is preferred because the appearance is more acceptable and there is less donor site morbidity.

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Buck-Gramcko reported that results were better when pollicization was performed in the first year of life; his youngest patient was 11 weeks old. Side-to-side grip between index and middle fingers, particularly for smaller objects, persisted in children whose reconstruction was performed later in life. Buck-Gramcko reported that results were better when pollicization was performed in the first year of life; side-to-side grip between index and middle fingers, particularly for smaller objects, persisted in children whose reconstruction was performed later in life. The index finger must be rotated 160° and placed in 40° of palmar abduction for optimal function and appearance. Hyperextension instability at the index metacarpophalangeal joint is prevented by positioning the metacarpal head in 70–80° of hyperextension before fixation. The reattached intrinsic muscles are important in the function of the thumb and in the formation of a new thenar eminence for cosmesis. After treatment: The hand is immobilized for 3 weeks, and then careful active motion is begun. Opponensplasty: Abductor digiti minimi opponensplasty, as described by Huber, may be appropriate for the rare patient with only isolated thenar aplasia in association with the radial club hand or for patients with weakness in apposition after pollicization. Manske and McCarroll reported improvement in appearance, dexterity, strength, and usefulness of the thumb in 20 of 21 patients with an average age at operation of 4 years and 9 months. Triceps transfer to restore elbow flexion: An elbow stiff in extension is a contraindication to centralization; rarely, however, a child may have passive elbow flexion but minimal or no active flexion because of complete absence of elbow flexors. Menelaus reported that triceps transfer restored elbow flexion in two patients when performed 2–3 months after centralization; both patients improved from a preoperative passive range of motion of 0–45° to a postoperative active range of motion of 0–90°.

Summary 1. Always be mindful of associated syndromal patterns and concomitant medical problems when approaching radial club hand deformity. 2. Set reasonable treatment goals and counsel families on reasonable expectations. 3. Know that elbow flexion typically does not improve after surgery, so it is imperative to address this pre-op in order to maintain ADLs.

Congenital Absence of the Ulna Ulnar club hand is much less frequent than radial club hand and it ranges from mild deviation of hand on the ulnar side of forearm to complete absence of ulna. Ulnar club hand is usually isolated anomaly. Treatment: It ranges as follows: (1) exercise, (2) limb lengthening, (3) osteotomy, (4) radialization, (5) splint, and (6) wrist centralization.

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Congenital Subluxation of the Wrist The classifications of inferior radioulnar dislocations are as follows: 1. With fracture 2. Without fracture (a) Congenital (Madelung’s deformity) (b) Acquired: • Traumatic • Pathological

Madelung’s Deformity A growth disturbance in the volar-ulnar distal radial physis, volar and ulnar tilted distal radial articular surface, volar translation of the hand and wrist. It also has a dorsally prominent distal ulna [6].

Pathogenesis (Brailsford) 1. Stunted development of inner third of the growth cartilage at the lower end of the radius, due to still unknown cause. 2. Growth of the outer two-thirds continues and, as a result, the radial shaft is bowed backward, the interosseous space is increased, there is overgrowth of lower end of ulna and is subluxated backward.

Clinical Features • Often bilateral, hence disability may not be identified early and hence late presentation is common. • Often seen for the first time in adolescence. • Females > males. • Early cases: mild symptoms of ulnocarpal impaction with power grip activities, and distal radioulnar joint incongruity with forearm rotation. • Wrist appears enlarged; dorsiflexion of the hand is impaired. Flexion may be increased. • In severe cases pronation and supination are limited. • May be associated with dyschondrosteosis (Leri Weill syndrome), Turner’s syndrome, achondroplasia, Ollier’s disease.

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Vender and Watson Classification (a) Posttraumatic, (b) dysplastic, (c) genetic, (d) idiopathic.

X-Ray • Steep ulnar slope and deficient ulnar margin of radius. • Lunate uncovered. • The carpus subluxates ulnar and palmarward and appears wedge shaped (lunate lies at the apex of the wedge). • Increased width between the distal radius and ulna. • Relatively long ulna compared to radius (positive ulnar variance). • Decreased carpal angle. • Triangularization of the distal radial epiphysis. • Carpus migrates more proximal into the increasing diastasis between the radius and the ulna. • Treatment –– In recent or acute cases, dorsiflexion of the wrist-maintained by a full arm plaster for 4 weeks. –– Indications for surgery: Acute pain and deformity. • Early presentation: –– In early-detected cases distal radial epiphysiolysis is done (Vickers and Nielsen et al.) –– Epiphysiolysis involves resection of the abnormal volar, ulnar physeal region of the radius and fat interposition. At the same time, any aberrant, tethering anatomic structures are excised. –– Early presentation with marked deformity and complete lack of a lunate fossa for carpal support, needs combined radial and ulnar osteotomies. Alternatively ulnar and radial epiphysiodesis maybe done • Late presentation: –– Osteotomy of the lower end of the radius may be done. –– Options include dome osteotomy, dorsal radial closing-wedge osteotomy, or volar opening-wedge radial osteotomy and bone grafting. –– Ulnar shortening procedure like the Sauve-Kapandji maybe useful, though there may already be deterioration of the articular cartilage, wrist ligaments, or triangular fibrocartilage, resulting in continued pain and limitation of motion postoperatively. It is usually seen in adolescent females with pain, decreased range of motion, and deformity. It can be seen due to a genetic etiology and is associated with mesomelic dwarfism and a mutation on the X chromosome.

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Surgery addressing the deforming bony and ligamentous lesions, correcting the abnormal position of the radial articular surface, and equalizing the longitudinal levels of the distal radius and ulna.

Congenital Absence of the Fibula The term Fibular deficiency is congenital absence of all or a part of fibula and is the most common long bone deficiency (Fig. 9.19). The syndrome of fibular deficiency encompasses a spectrum of abnormalities affecting the femur, knee, tibia, ankle, and foot. Etiology: It is a rare disorder occurring in only 1 in 40,000 births. Bilateral fibular hemimelia is even rarer. The precise cause of fibular hemimelia is unknown in most of the cases and the deformity normally occurs sporadically. Although genetic abnormalities are linked to FH, the condition is not heritable. The gene mutations and abnormalities are occurring only in the forming limb and not anywhere else, and thus cannot be transmitted to the next generation. Graham 1993 suggested that vascular or mechanical interference with embryonic apical ectodermic ridge might lead to fibular hemimelia. Angiographic study has detected vasculature abnormalities including persistence embryonic vascular Fig. 9.19  Absent fibula absent lateral column of foot (Courtesy: figure reused with the kind permission of Magdi E. Greiss, Whitehaven, Cumbria, UK)

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pattern, failure of plantar arch formation, absence of anterior tibial artery or absence of normal trifurcation of the popliteal artery at the level of the knee, and presence of one large posterior artery in the leg.

Classification (Achtermann and Kalamchi Classification) Classifies fibular hemimelia [7] based on the degree of fibular deficiency present. Type 1—If any portion of fibula is present it is classified as type 1. In type 1A the epiphysis of the proximal fibula is distal to the level of tibial growth plate and physis of distal fibula is proximal to the dome of talus. In type 1B, the fibula is shorter by 30–50%, and distally the fibula does not provide any support at the ankle joint. The reported total limb length discrepancy at maturity was 12% in type 1A and 18% in type 1B. If the fibula is completely absent, the deformity is classified as type 2. Limb length discrepancy was 20% in type. Birch classification: A major short coming of other classifications is that they do not deal with shortening of the total limb which is one of the most important factor. A functional foot was defined as one that was or could be made plantigrade and had 3 or more rays. A direct correlation was found between the number of rays and chances of preserving the foot. It was possible to preserve all five rayed feet whereas no foot with two or fewer rays was salvageable.

Other Classifications • Stanitski classification • Frantz and O’Rahilly classification • Coventry and Johnson classification

Clinical Features Children with fibular hemimelia (Table 9.3) present with three major complaints: 1. Limb length discrepancy: Unilateral fibular hemimelia leads to length discrepancy due to inhibition of growth of the tibia and foot. In addition, many children with FH have some femoral growth inhibition (congenital femoral deficiency). The foot grows shorter in height, contributing to limb length discrepancy, but it is also shorter in length. This limb length discrepancy follows a Shapiro 1a curve, meaning its growth inhibition remains constant. This characteristic makes the leg length discrepancy of FH predictable using the Anderson and Green, Moseley straight line graph, Amstutz method or Paley Multiplier method. The limb length discrepancy with FH ranges from very mild to very severe inhibition, ranging at maturity of the patient from 2 to 25  cm in the absence of femoral deficiency

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Table 9.3  Table showing the types of fibular hemimelia Classification Type 1 functional foot  1A = 0–5% inequality  1B = 6–10% inequality  1C = 11–30% inequality  1D = >30% inequality Type 2 non functional foot  2A = Functional upper limb  2B = Non functional Upper limb

Treatment Orthosis, epiphysiodesis Epiphysiodesis ± limb lengthening One or 2 limb lengthening/Amputation More than 2 limb lengthening/Amputation Early amputation Consider limb salvage

discrepancy. With combined inhibition of the femur and tibia the magnitude of leg length discrepancy at maturity can be 30 cm. 2. Foot and ankle deformities. Foot and ankle deformities have been the most challenging and disabling problems with FH. FH foot deformity has many components. At the ankle there is a dysplasia of the distal tibia and of the talus, which ranges from mild valgus of the distal tibia to severe dysplasia with flat malformed, maloriented joint surfaces. The distal tibial physis is more affected then the proximal tibial physis, with the former being often wedge shaped. The talus too ranges in its articular shape from normal to ball shaped in the frontal plane and from round to nearly flat in the sagittal plane. The fibula normally contributes to the lateral stability of the ankle. If the fibula is absent or deficient, then the ankle will sublux or roll into valgus. The subtalar joint pathology ranges from a normal subtalar joint to a subtalar joint with subtalar coalition. (Three types of wedge-shaped distal tibial epiphyses were identified. A mildly wedged (type I) epiphysis was found in seven patients, a moderately wedged (type II) epiphysis was found in seven patients, and a severely wedged (type III) epiphysis, in six patients. We believe that after lengthening, one should anticipate varying degrees of mild growth retardation and minimal foot deformity in patients with type I epiphysis, worsened asymmetric growth retardation and progressive foot deformity in patients with type II epiphysis, and severe growth retardation and severe foot deformity in patients with type III epiphysis  =  Ref.: J Paediatr Orthop 2000;20(4):428–36); Tibial deformity—There is often a mild to severe diaphyseal tibial deformity of the valgus-procurvatum. A skin dimple is usually present over the apex of this angulation. The fibular anlage is located like the string of a bow in a straight line opposite the concavity of this deformity. This thick fibro-­ cartilaginous remnant may contribute to this angulation by tethering the growth of the tibia on its posterior-lateral side. 3. Knee deformity: The knee joint frequently has a valgus deformity. This valgus is related both to the distal femur and the proximal tibia. The lateral epiphysis of the proximal tibia may be delayed in its ossification compared to the normal opposite side. 4. Other deformities—ACL deficiency, absence of tibial spine and tarsal coalition. Knee instability—Many patients with FH have hypoplasia or aplasia of the anterior and or posterior cruciate ligaments. The tibia may be subluxed anteriorly

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relative to the femur. The ligament deficiency and subluxation are often not symptomatic at a young age, but these become a bigger problem when the child becomes taller and heavier. Treatment: The goals of managing fibular hemimelia cases include managing the limb deficiency, correcting bone angulations, and achieving a well, plantigrade, and a painless foot.

 artial Fibular Hemimelia P The decision to treat patients with partial fibular hemimelia by amputation or limb lengthening depends on the degree of predicted shortening at maturity and the condition of the affected limb foot and ankle. If the predicted discrepancy at maturity is 25 cm or more and there is severe valgus of the ankle with a deformed foot the patient should be treated with Syme or Boyd amputation and prosthetic management. If the patient has a predicted shortening of 8 cm or less, a functional plantigrade foot with four or more rays and a stable mobile ankle he is a good candidate for lengthening procedure with or without epiphysiodesis. Realignment of obliquity of distal tibial epiphysis may be needed in this group of patients. Ilizarov method for fibular hemimelia can be another alternative. The choice of amputation or lengthening for children the criteria identified must be made on an individual basis. For the patients who qualify, single or staged lengthening with repositioning of the foot may be successful and the short fibula may be differentially lengthened relative to the tibia to establish a more normal tibiofibular relation. Most of these patients however have a tarsal coalition and an abnormal talotibial articulation and its difficult to predict long term functional outcome of retained foot and ankle. Regardless of the treatment method used, some patients develop gradually progressive valgus of the knee. This condition is best treated 1–2 years before the patient reaches skeletal maturity at which time partial growth arrest may be done.  omplete Fibular Hemimelia C Amputation—In the past different procedures were done in an attempt to centralize the patients foot and lengthen the limb. Today, there is consensus that ankle disarticulation is the best treatment for complete fibular hemimelia. The procedure should be done in early childhood and the patient should be fitted with Syme prosthesis afterward. Some surgeons prefer the Boyds amputation, in which the retained calcaneus can be used to stabilize the heel pad, especially for older boys. The optimal time to perform the amputation is when the child is just starting to pull up to stand (9–10 months age). If the operation is done at this time the child will be able to ambulate in a prosthesis at approximately 1 year of age and will be able to function at near normal level in all sports. Mild tibial bowing is usually well tolerated and corrective osteotomy is not necessary. However if the bowing is marked and there is too great an anterior prominence tibial osteotomy can be done.

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Bilateral FH: Have a very little length discrepancy but major problem is disproportion between lengths of legs and rest of the body. Treated either by amputation or lengthening.

Conclusion 1 . FH is rare. 2. Etiology is unknown, and probably related to abnormalities in forming limb bud. 3. Encompasses a spectrum of deformities rather than absence of fibula alone. 4. Prognosis depends on expected LLD and number of rays and degree of deformity of foot. 5. Severe deformities with expected LLD >25 cm are managed best by Symes or Boyd amputation. 6. Mild deformities with a functional foot can be treated by foot reconstruction and lengthening procedures. 7. Treatment must be individualized and surgical options and prognosis must be explained to parents in detail and involve them in the decision making process.

Congenital Hand Anomalies Embryology: The upper limb bud Develops from lateral wall of embryo. On 4th week after fertilization. It consists of mesodermal cells covered by ectoderm. Under guidance of three signaling centers: (1) AER (apical ectodermal ridge)—proximodistal, (2) ZPA (zone of polarizing activity)—antero-posterior growth, and (3) NRE (non-ridge ectoderm) (wing less type)—dorsoventral growth. Swanson classification: Accepted by IFSSH and ASSH. Based on their embryologic origin and morphological appearance. It was expanded by Knight and Kay in 2000, and Upton in 2006. But recently, adequacy of this classification has been questioned. Swanson classification [4]: It is based on the failure of formation of parts, that is by failure of differentiation or separation of parts, duplication, overgrowth, undergrowth, congenital constriction ring syndrome, and generalized skeletal abnormalities and syndromes.

Failure of Formation of Parts It can be detected prenatally and is of two types: (1) transverse arrest and (2) longitudinal arrest: The details are (a) radial club hand (preaxial arrest), (b) ulnar club hand (post-axial arrest), (c) cleft hand (central arrest), and (d) phocomelia (intercalary arrest)—an intervening segment of limb is absent.

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1. Congenital transverse arrest: It is rare, always U/L.  Sporadic/environmental. Level defined by skeletal absence. Commonly at level of proximal forearm. Defect in AER signaling, Lt > Rt, two groups: namely—defect in limb formation and Intrauterine amputation after limb formation. Most will not require surgery, but benefited from prosthesis if referred early. 2. Longitudinal arrest (a) Phocomelia (seal limb): It is an intercalary arrest and the intervening segment of limb is absent (arm/forearm); usually due to thalidomide in first trimester = Type I (complete)—hand directly attached to trunk and Type II (proximal)—short forearm attached to trunk. Type III (distal)—short humerus attached to hand. Surgery—very little role. (b) Radial ray dysplasia (aka: radial club hand/preaxial deficiency/longitudinal radial deficiency): The hand is radially deviated, flexed hand with pronated and shortened forearm. Deficient thumb ray and carpal bones (scaphoid and trapezium), radial nerve and vessels Normal ulnar two digits, the median nerve subluxed toward concave side. It is commonly associated with syndromes (e.g., VATER, TAR, Holt Oram). It is usually in the U/L, M  >  F, Rt > Lt. Type I—Short radius, II—Hypoplastic radius, III—Partial absence of radius (replaced by anlage), IV—Complete absence of radius—most severe and common. (c) Ulnar ray dysplasia (Table 9.4) (aka: Ulnar club hand/Postaxial deficiency): It is the rarest of the longitudinal ray deficiency. Association with syndromes—uncommon. There is a disruption of ZPA signaling resulting in a short, bowed radius with a hypoplastic or absent ulna. The elbow is severely affected (with a relatively stable wrist). It is commonly seen in M  >  F, Lt > Rt, U/L > B/L. Bayne and Klug classification of ulnar longitudinal ray deficiency (Fig. 9.20). (d) Central ray deficiency/cleft hand (Table 9.5): It is the most common longitudinal deficiency. Defect in AER signaling. B/L (frequently). Structures proximal to wrist—normal. Little finger—always present. Associated syndactyly and narrow web space. Complex syndactyly (thumb and index)—in severe cases. Hand—“functionally good but aesthetically a disaster”. It is seen in association with cleft feet in 1/3rd cases (SHSF). Other syndromic associations: EEC syndrome (ectrodactyly, ectodermal dysplasia). Table 9.4  Table showing the varieties of Ulnar ray deficiency Bayne classification I—Ulnar hypoplasia II—Partial ulnar aplasia III—Total ulnar aplasia IV—Radiohumeral synostosis

Paley and Herzenberg classification I—Ulnar hypoplasia with intact distal epiphysis II—Partial ulnar aplasia (distal 1/3rd) III—Partial ulnar aplasia (distal 2/3rd) IV—Total ulnar aplasia V—Radiohumeral synostosis

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Fig. 9.20  Line diagram showing ulnar longitudinal ray deficiency

Table 9.5  Table showing the types of cleft hand

Typical cleft hand Deep V-shaped central defect Bilateral Inherited (AD) Cleft feet associated Hypoplasia of long ray Thumb involved Associated cleft lip/palate No chest wall involvement Little finger—only digit

Atypical cleft hand Shallow U-shaped defect Unilateral Sporadic Not Rays of central three digits Rarely No Seen in Poland syndrome Thumb—only digit

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Manske’s Classification of Cleft Hand • • • • •

Type I: Normal first web. Type II: A—mildly narrowed web and B—severely narrowed. Type III: Syndactylized web. Type IV: Merged web. Type V: Absent web: A—Partial suppression of radial ray and B—Complete suppression of radial ray.

Failure of Differentiation or Separation of Parts 1. Syndactyly: It is one of the most common congenital hand malformations. It usually affects the third web >fourth web >second web. It is often seen in association—Poland, Apert syndrome; A more complicated syndactyly—more than only distal bony fusion. Abnormal bone structure inside (fusion, missing bone, abnormal joints, rudimentary bones, cross bones). It is seen in Apert syndrome, Central synpolydactyly and Typical cleft hand. 2. Contracture: (a) Clinodactyly (inclined finger): There is a Radio ulnar deviation of digit (>10) distal to MCPJ. Most common—Radial deviation of little finger at DIP. (Middle phalanx of little finger—last bone to ossify); second most common—proximal phalanx of thumb; Due to Delta phalanx (a trapezoid-shaped middle phalanx). (b) Camptodactyly (arched finger): It is a painless, progressive flexion contracture of PIPJ (antero posteriorly). Due to imbalance in flexors and extensors; It affects the little finger (>70% cases); It is of three types: type I:newborn (M = F), type II: adolescent females and type III. Multiple digits/with syndromes. (c) Congenital trigger thumb: It is a stenosing tenosynovitis of FPL tendon at A1 pulley. It has a fixed flexion of IPJ (thumb locked in flexion). “Notta node”—palpable nodule over flexor aspect of MCPJ of thumb proximal to A1 pulley. Snapping/popping as the nodule passes beneath A1 pulley, There is compensatory hyperextension at MCPJ. It is frequently B/L. (d) Congenital clasped thumb: It is a deficient thumb extensor mechanism. It has three types as follows: Mild clasped (type I)—deficiency of EPB with an extension lag at MCPJ.  Severe clasped (type II)—deficiency of EPB and EPL with an extension lag at both MCPJ and IPJ and a Type III—clasped associated with arthrogryposis. (e) Kirner’s deformity: It is a progressive palmar radial curvature of the distal phalanx of little finger (deviation in two planes) along with distortion and widening of physeal plate along with curvature of the diaphysis of the distal phalanx. (f) Arthrogryposis: It is a non progressive multiple congenital joint contracture which commonly affects the elbow with lack of flexion.

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PS: Amyoplasia—classic type of symmetric limbs with shoulders-­ adducted, internally rotated and the elbow—extension forearm—pronation and the wrist—flexion hand—ulnar deviation with the thumb—flexed, adducted and the fingers held flexed. (g) Synostosis: Here there is a union of two or more adjacent bones. It is often associated with other conditions, such as Symphalangism in Apert syndrome. Metacarpal, carpal, radio ulnar synostosis are rare.

Duplication (a) Polydactyly: It is the most common congenital anomaly (Table  9.6) in upper extremity (Fig. 9.21).

Table 9.6  Table showing the types of congenital anomalies of the fingers Radial (preaxial) 1. Asians 2. Isolated 3. U/L 4. Wassel classification: type I—VII type IV—most common (50%)

Central/Ulnar (post axial) 1. Africans 2. Syndromic 3. B/L 4. Temtamy and McKusick: Type A—well formed and Type B—rudimentary

Fig. 9.21  Polydactyly (Courtesy: Figure reused with the kind permission of Magdi E.  Greiss, Whitehaven, Cumbria, UK)

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Overgrowth (a) Macrodactyly: It is rare. It is a misleading term while “Digital nerve oriented neurofibroma” is the correct term. The whole finger clinodactyly if one digital nerve involved and Syndactyly may coexist. Flatt’s classification: Type I—lipofibromatosis.

Undergrowth (a) Hypoplastic Thumb: Blauth Classification: Type I—mild hypoplasia (all structures present), Type II—moderate hypoplasia (thenar muscles absent), Type III—severe hypoplasia (skeletal hypoplasia) = A—stable CMC joint and B— unstable CMC joint; Type IV—floating thumb (pouce flottant) [only soft tissue bridge], Type V—aplasia. There are additional five categories: Type VI—central deficiency (cleft hand), Type VII—constriction ring syndrome, Type VIII—five fingered hand, Type IX—radial polydactyly and Type X—syndromic short skeletal thumb ray. (b) Madelung’s deformity: It is a radial and palmar angulation of distal radius. The Ulnar and palmar part of distal radial physis—growth disturbance point.

Constriction Band Syndrome (Streeter’s Dysplasia) It is quite common and its etiology is a constricting amniotic band and intrinsic causes have been proposed. Patterson classification: (a) simple constrictions (partial/circumferential)—intrauterine amputation, (b) constrictions with distal deformity (lymphedema ±), and (c) constrictions with acrosyndactyly-characteristic (fenestrated syndactyly).

Generalized Skeletal Abnormalities Most common is multiple exostoses. Others are (1) Poland syndrome (symbrachydactyly), (2) Apert syndrome (complex syndactyly), (3) Haas syndrome, (4) Freeman Sheldon syndrome (windblown hand), (5) Mohr Wriedt syndrome (radial clinodactyly of index finger) and (6) Pierre–Robin syndrome (clasped thumb). 1. Apert syndrome (acrocephalosyndactyly): It is characterized by (a) Craniosynostosis. (b) Acrosyndactyly. (c) Symphalangism (second, third, fourth finger). (d) Radial clinodactyly of thumb. (e) Simple syndactyly of fifth finger (fourth web).

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2. Haas syndrome: It is characterized by the presence of six metacarpals with >5 digits and all having three phalanges. 3. “Windblown hand” in Freeman Sheldon syndrome: It is characterized by severe hyperflexion of fingers at MCPJ with ulnar deviation. Due to metacarpal bone shortening. “Whistling face” syndrome.

 odified Classification of Congenital Anomalies M of Hand and Upper Limb 1. Malformation: (a) Failure in axis formation and differentiation—entire upper limb. (b) Failure in axis formation and differentiation—hand plate. (c) Failure in hand plate formation and differentiation—unspecified axis. 2. Deformations: (1) Constriction ring syndrome; 3. Dysplasias: (1) macrodactyly, (2) limb hypertrophy, and (3) tumorous conditions. (a) Failure in axis formation and differentiation—entire upper limb (Table 9.7). (b) Failure in axis formation and differentiation—hand plate (Table 9.8). (c) Failure in hand plate formation and differentiation—unspecified axis (Table 9.9).

Table 9.7  Table showing the congenital anomalies of the upper limb Proximo—distal axis 1. Symbrachydactyly 2. Transverse deficiency 3. Intersegmental deficiency

Table 9.8  Table showing congenital anomalies of the hand rays

Radio—ulnar axis 1. Radial longitudinal deficiency 2. Ulnar longitudinal deficiency 3. Ulnar dimelia 4. Radio—ulnar synostosis 5. Humero—radial synostosis

Radio-ulnar (AP) axis 1. Radial polydactyly 2. Ulnar polydactyly 3. Triphalangeal thumb

Dorso ventral axis 1. Nail patella syndrome

Dorsal ventral axis 1. Dorsal dimelia (palmar nail) 2. Hypoplastic/aplastic nail

Table 9.9  Showing the types of congnital hand anomalies Soft tissue 1. Syndactyly 2. Camptodactyly 3. Trigger digits

Skeletal 1. Brachydactyly 2. Clinodactyly 3. Kirner’s deformity 4. Metacarpal and carpal synostoses

Complex 1. Cleft hand 2. Synpolydactyly 3. Apert hand

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Symbrachydactyly • • • • • • •

Type 1—triphalangeal type Type 2—diphalangeal type Type 3—monophalangeal type Type 4—aphalangeal type Type 5—ametacarpia type Type 6—acarpia type Type 7—forearm amputation type

Dorsal Dimelia of Little Finger It is a failure in axis formation and differentiation in hand plate. It involves dorsoventral axis. Non-ridge ectoderm—signaling center. Palmar nail.

Triphalangeal Thumb It is an AD. The extra phalanx of variable size, variable shape (triangular/trapezoid/ rectangular) normal appearing thumb. When fully developed extra phalanx lying in the finger plane, it is considered as five fingered hand (Fig. 9.22).

Brachydactyly Bell’s classification: (a) Brachymesophalangy (b) Apical dystrophy

Fig. 9.22  Line diagram showing the various stages of a triphalangeal thumb

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(c) Drinkwater type (d) Brachymegalodactyly (stub thumb) (e) Brachymetacarpi Mohr—Wriedt syndrome—It is characterized by radial deviation (clinodactyly) of index finger due to brachydactyly (middle phalanx of index). Mirror hand/ulnar dimelia: It is extremely rare with symmetric duplication of the limb in midline. A central digit with three digits (long, ring, little) on either side with a total of seven digits, but the thumb is absent. There are two ulna, no radius (ulnar dimelia). It is mainly due to transplantation/replication of ZPA.

References 1. Grahame R, Bird HA, Child A. The revised (Brighton 1998) criteria for the diagnosis of benign joint hypermobility syndrome (BJHS). J Rheumatol. 2000;27(7):1777–9. 2. Samartzis DD, Herman J, Lubicky JP, Shen FH. Classification of congenitally fused cervical patterns in Klippel-Feil patients: epidemiology and role in the development of cervical spine-­ related symptoms. Spine (Phila Pa 1976). 2006;31(21):E798–804. 3. Hall JG.  Arthrogryposis multiplex congenita: etiology, genetics, classification, diagnostic approach, and general aspects. J Pediatr Orthop B. 1997;6(3):159–66. 4. Swanson AB.  A classification for congenital limb malformations. J Hand Surg Am. 1976;1(1):8–22. 5. Heikel HA. Aplasia and hypoplasia of the radius. Acta Orthop Scand Suppl. 1959;39:1. 6. Madelung OW. Die spontane Subluxation den Hand nach vorne. Archiv für/miscue Clzirurgie. 1879;23:395. 7. Achterman C, Kalamchi A.  Congenital deficiency of the fibula. J Bone Joint Surg Br. 1979;61-B(2):133–7.

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Rickets Causes of rickets: 1 . Vitamin D disorders 2. Calcium deficiency 3. Phosphorus deficiency 4. Renal losses 5. Distal RTA

Vitamin D Disorders • Nutritional vit D deficiency • Congenital vit D deficiency • Secondary vit D deficiency due to (a) malabsorption, (b) increased degradation and decreased liver 25-hydroxylase • Vit D-dependent rickets type 1 • Vit D-dependent rickets type 2 and chronic renal failure Low intake due to (a) diet or (b) premature infants (rickets of prematurity); malabsorption due to (a) primary disease or (b) dietary inhibitors of calcium absorption. Inadequate intake due to (a) premature infants [1] (rickets of prematurity) or (b) aluminum-containing antacids

K. M. Iyer (*) Royal Free Hampstead NHS Trust, Royal Free Hospital, London, UK © Springer Nature Switzerland AG 2019 K. M. Iyer, W. S. Khan (eds.), General Principles of Orthopedics and Trauma, https://doi.org/10.1007/978-3-030-15089-1_10

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• XL hypophosphatemic rickets • AD hypophosphatemic rickets • Hereditary hypophosphatemic rickets with hypercalciuria Overproduction of phosphatonin due to (a) tumor-induced rickets, (b) McCune-­ Albright syndrome [2], (c) epidermal nevus syndrome, or (d) neurofibromatosis. Fanconi syndrome and Dent disease.

Diagnosis of Rickets History Regarding 1. Diet intake of vit D, calcium. 2. Sun exposure. 3. Maternal risk factors for vit D deficiency. 4. Child’s medication history. 5. History of liver or intestinal disease—malabsorption of vit D. 6. History of renal disease. 7. Family history of bone disease, short stature, unexplained sibling death. 8. History of dental caries, poor growth, delayed walking, waddling gait, pneumonia, and hypocalcemic symptoms Clinical Features • General  =  such as failure to thrive, listlessness, protruding abdomen, muscle weakness (especially proximal), and fractures. • Head = such as craniotabes (softening of cranial bones. Detected by applying pressure at the occiput or parietal bones), frontal bossing, delayed fontanelle closure, delayed dentition, caries, and craniosynostosis. • Chest  =  such as rachitic rosary, Harrison groove, respiratory infections, and atelectasis. • Back = such as scoliosis, kyphosis, and/or lordosis. • Extremities = such as enlargement of wrists and ankles, valgus or varus deformities, anterior bowing of the tibia and femur, coxa vara (Fig. 10.1), leg pain, valgus or varus deformities such as windswept deformity (combination of valgus deformity of 1 leg with varus deformity of the other leg). • Hypocalcemic symptoms = such as tetany, seizures, or stridor due to laryngeal spasm. 1. Craniotabes: Softening of cranial bones. Detected by applying pressure at the occiput or parietal bones. Craniotabes may also be secondary to osteogenesis imperfecta, hydrocephalus, syphilis. It may be a normal finding in many newborns, especially near the suture lines, but disappears within a few months of birth. 2. Rachitic rosary: Widening of costochondral junctions which is called as rachitic rosary. It also feels like beads of a rosary as the examiner’s fingers move along the costochondral junctions from rib to rib.

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Fig. 10.1  Line diagram showing coxa vara

3. Growth plate widening: This is also responsible for the enlargement at wrists and ankles. 4. Harrison groove: It is a horizontal depression along lower anterior chest due to pulling of softened ribs by diaphragm during inspiration. The softening of ribs impairs air movement and predisposes to atelectasis. The risk of pneumonia is high in children with rickets. Radiology Decreased calcification due to thickening of growth plate (Fig. 10.2). Fraying: edge of metaphysis loses its sharp border. Cupping: edge of metaphysis changes from convex or flat to concave surface. Most easily seen at distal ends of radius, ulna, fibula. Widening of distal end of metaphysis which clinically causes thickened wrists and ankles, and rachitic rosary. Especially on PA view of wrist and also in other growth plates. Other radiologic features: coarse trabeculation of diaphysis leading to generalized rarefaction. Lab tests (Fig. 10.3). Initial laboratory blood tests should include: 1. Serum calcium 2. Phosphorus 3. Alkaline phosphatase 4. Parathyroid hormone (PTH) 5. 25-hydroxyvitamin D 6. 1,25-dihydroxyvitamin D3 7. Creatinine

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Fig. 10.2  Decreased calcification with growth plate fraying and widening (Courtesy: reused with the kind permission of Magdi E. Greiss, Whitehaven, Cumbria, UK)

DISORDER

Ca Pi PTH 25-OHD 1,25-(OH)2D ALK PHOS URINE Ca URINE Pi

Vitamin D deficiency

N, ↓ ↓ ↑

↓

↓, N, ↑

↑

↓

↑

VDDR, type 1

N, ↓ ↓ ↑

N

↓

↑

↓

↑

VDDR, type 2

N, ↓ ↓ ↑

N

↑↑

↑

↓

↑

Chronic renal failure

N, ↓ ↑ ↑

N

↓

↑

N, ↓

↓

Dietary Pi deficiency

N

↓ N, ↓ N

↑

↑

↓

↓

XLH

N

↓ N

N

RD

↑

↓

↑

ADHR

N

↓ N

N

RD

↑

↓

↑

HHRH

N

↓ N, ↓ N

RD

↑

↓

↑

Tumor-induced rickets N

↓ N

N

RD

↑

↓

↑

Fanconi syndrome

↓ N

N

RD or ↑

↑

↓ or ↑

↑

Dietary Ca deficiency N, ↓ ↓ ↑

N

↑

↑

↓

↑

N

Fig. 10.3  Line diagram table showing the laboratory findings in disorders causing rickets

8. Electrolytes Urinalysis: Useful for detecting glycosuria and aminoaciduria (positive dipstick for protein) in Fanconi syndrome. Evaluation of urinary excretion of calcium (24  h collection for calcium or calcium-­creatinine ratio): If hereditary hypophosphatemic rickets with hypercalciuria or Fanconi syndrome is suspected. Direct measurement of other fat-soluble vitamins (A, E, and K) or indirect assessment of deficiency (prothrombin time for vitamin K deficiency): if malabsorption is a consideration.

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PS: PTH results in increased calcium, decreased phosphate, while 1,25-D results in increased calcium and increased phosphate whereas calcitonin results in decreased calcium.

 utritional Vit D Deficiency N It is the most common cause of rickets globally, with its etiology: which is most common in infancy: due to poor intake + inadequate cutaneous synthesis. There is a transplacental transport of vitamin D, mostly 25-D, provides vitamin D for first 2 months of life unless there is severe maternal vitamin D deficiency. In breast-fed infants, because of low vitamin D content of breast milk, they rely on cutaneous synthesis or vitamin supplements. Infants who receive formula receive adequate vitamin D, even without cutaneous synthesis. Cutaneous synthesis is limited by ineffective winter sun and by increased skin pigmentation. Mothers may have same risk factors which leads to decreased maternal vitamin D [3] and reduced vitamin D in breast milk + less transplacental delivery of vitamin D. Unconventional dietary practices, such as vegan diets that use unfortified soy milk or rice milk. Laboratory Findings There is an elevated PTH hypophosphatemia which leads to hypophosphatemia. This variable hypocalcemia and hyperparathyroidism results in upregulation of renal 1α-hydroxylase with wide variation in 1,25-D levels (low, normal, or high). This 1,25-D is only low when there is severe vitamin D deficiency. Some have metabolic acidosis secondary to PTH-induced renal bicarbonate-wasting. There may be generalized aminoaciduria. Diagnosis There is a history of poor vitamin D intake and risk factors for decreased cutaneous synthesis. There are radiographic changes consistent with rickets and laboratory findings. The normal PTH level almost never occurs with vitamin D deficiency and suggests a primary phosphate disorder. Calcium deficiency may occur with or without vitamin D deficiency. A normal level of 25-D and a dietary history of poor calcium intake support a diagnosis of isolated calcium deficiency. Treatment: It is by vitamin D + calcium + phosphorus. There are two strategies for vitamin D administration: 1. Stoss therapy: 300,000–600,000 IU of vitamin D oral or IM as 2–4 doses over 1  day, because doses are observed, Stoss therapy is ideal where adherence to therapy is questionable. 2. Alternative: Daily, high-dose vitamin D, with doses ranging from 2000 to 5000 IU/day over 4–6 weeks. Most importantly either strategy should be followed by daily vitamin D intake of 400 IU/day, typically given as a multivitamin. Also ensure adequate dietary calcium and phosphorus (milk, formula, and other dairy products). Symptomatic hypocalcemia: IV calcium acutely, followed by oral calcium supplements, tapered over 2–6 weeks in children who receive adequate dietary calcium. There may be a place for the transient use of intravenous or oral 1,25-D (calcitriol)

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to reverse hypocalcemia in acute phase (by providing active vitamin D during the delay as supplemental vitamin D is converted to active vitamin D). Prognosis. In most cases there is an excellent response to treatment with radiologic healing within a few months. The laboratory tests normalize rapidly. Many of the bone malformations improve dramatically, but children with severe disease may have permanent deformities. The short stature does not resolve in some children. Their prevention is by the universal administration of daily multivitamin containing 200–400 IU of vitamin D to children who are breast-fed, and for other children, diet should have sources of vitamin D.

 ongenital Vit D Deficiency C It occurs if severe maternal vitamin D deficiency during pregnancy [4]. The maternal risk factors are: 1 . Poor dietary intake of vitamin D 2. Lack of adequate sun exposure 3. Closely spaced pregnancies The newborns may have: 1. Symptomatic hypocalcemia 2. Intrauterine growth retardation 3. Decreased bone ossification 4. Classic rachitic changes Subtler maternal vitamin D deficiency may have an adverse effect on neonatal bone density, an adverse effect on birthweight, a defect in dental enamel, and may predispose to neonatal hypocalcemic tetany. Treatment of congenital rickets: 1 . Vitamin D supplementation 2. Adequate intake of calcium and phosphorus Prevention: By the use of prenatal vitamins containing vitamin D.

 econdary Vit D Deficiency S Etiology is inadequate intake, inadequate absorption, decreased hydroxylation in liver, and increased degradation. Inadequate absorption is mainly liver and gastrointestinal diseases such as: 1 . Cholestatic liver disease 2. Defects in bile acid metabolism 3. Cystic fibrosis 4. Other causes of pancreatic dysfunction 5. Celiac disease

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6. Crohn disease 7. Intestinal lymphangiectasia 8. After intestinal resection Decreased hydroxylation in liver is usually due to severe liver disease as seen in insufficient enzyme axn (25 hydroxylase). Increased degradation usually caused by drugs by inducing P450 such as anticonvulsants like Phenobarb and Phenytoin; ATT like Isoniazid and Rifampin. Treatment 1. Malabsorption: It requires high doses of vitamin D. 25-D (25–50 μmg/day or 5–7 μmg/kg/day) for better absorption which is superior to vitamin D3 or alternatively: 1,25-D (also better absorbed in presence of fat malabsorption) or parenteral vitamin D. 2. In rickets due to increased degradation of vit D by P450 system: It require the same acute therapy as for nutritional deficiency, followed by long-term administration of high doses of vit D (e.g., 1000 IU/day), (With dosing titrated based on serum levels of 25-D). Some patients may require as much as 4000 IU/day.

 itamin D-Dependent Rickets, Type 1 V It is an autosomal recessive with mutations in gene encoding renal 1α-hydroxylase. It helps to prevent conversion of 25-D into 1,25-D. It is normally present during first 2 years of life and can have any features of rickets, including symptomatic hypocalcemia. The normal levels of 25-D, but low levels of 1,25-D. Occasionally, 1,25-D levels may be low normal with high PTH, low serum phosphorus levels with metabolic acidosis and generalized aminoaciduria. (Due to renal tubular dysfunction). Occasionally, 1,25-D levels may be at the lower limit of normal, but this is inappropriate, given the high PTH and low serum phosphorus levels, both of which should increase the activity of renal 1α-hydroxylase and cause elevated levels of 1,25-D. As in nutritional vitamin D deficiency, renal tubular dysfunction may cause a metabolic acidosis and generalized aminoaciduria. Treatment: long-term treatment with 1,25-D (calcitriol). Initial: 0.25–2 μmg/day, with lower doses used once the rickets has healed. During initial therapy, ensure adequate intake of calcium. Periodic monitoring of urinary calcium excretion, with target of 1 fractures.

T-score T > −1 T score between −1 and −2.5 T score 70 years. It is most beneficial in first 12–36 h of attack; 1 g initially and then 0.5 g every quarterly until either symptoms are relieved or GI side for nausea, vomiting and diarrhea or 7 mg given total. Renal dosing (1) If Cr clearance 10 mg/dL. 3. Nephrolithiasis. 4. Any history of symptoms of gout, especially w/ worsening renal function. 5. Presence of gouty tophi in bone or soft tissues. 6. Radiographic signs of gouty arthritis. 7. Impending chemotherapy or radiotherapy for leukemia or lymphoma.

Which Drug to Use? Base choice on above considerations and whether patient is an overproducer or underexcretor. Need to get a 24-h urine for urate excretion: If 700—overproducer (allopurinol). 90% of the patients are underexcretors.

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Prevention 1 . Maintain the concentration of uric acid level within the normal range. 2. Drinking plenty of water. 3. Balance your weight with proper diet and exercise. 4. Avoid purine-rich foods. 5. Reducing alcohol consumption. 6. Avoid diuretic drugs.

Newer Drugs Uricase enzymes: They catabolize urate to allantoin: More soluble, excretable form. They are currently approved for hyperuricemia in tumor lysis syndrome. There are some concerns: fatal immunogenicity and unknown long-term effects.

The Hemophilias Definition It is defined as “love of bleeding.” There are two types: A and B. Hemophilia A: X linked recessive hereditary disorder that is due to defective or deficient factor VIII.

History The first references are mentioned in Jewish texts in second century AD by Rabbi Ben Gamaliel who correctly deduced that sons of mother—that he did not know at that time—was an hemophilic carrier bled to death after circumcision. Hence, he made a ruling that excepted newborn Jewish boys of this ritual if two previous brothers had had bleeding problems with it. Then Rabbi and physician Maimonides in the XII century noted that the mothers were the carriers, hence the second ruling that if she married twice the newborns from the second marriage were also excepted. In 1800 John Otto a physician in Philadelphia wrote a description of the disease where he clearly appreciated the cardinal features: an inherited tendency of males to bleed. In 1928 the word Hemophilia was defined.

Incidence It is the second most common inherited clotting factor abnormality (after von Willebrand disease), 1 in 5000–10,000 live male births with no difference between racial groups.

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Pathophysiology There is a sequential activation of a series of proenzymes or inactive precursor proteins (zymogens) to active enzymes, resulting in significant stepwise response amplification. There are two pathways: intrinsic and extrinsic measured by two lab tests. F VIII is a cofactor for intrinsic Xa. FvW is its carrier which is activated by Xa and thrombin and inactivated by activated protein C in conjunction with protein S.

Genetics It is transmitted by females, suffered by males. The female carrier transmits the disorder to half their sons and the carrier state to half her dtrs. The affected male does not transmit the disease to his sons (Y is nl) but all his dtrs are all carriers (transmission of defected X). Hemophilia in females: If a carrier female mates with an affected male there’s the possibility that half their daughters are homozygous for the disease. The other possibility: Turner syndrome (45,X0) with a defective X. Factor VIII gene is Xq28, which is one of the largest genes known-186k base pairs with 26 exons. Its large size predisposes it to mutations. In hemophilia A there is no uniform abnormality. There are deletions, insertions, and mutations with 200 genes studied-7 dif mutations. 4—transposition of a single base-3 lead to stop codon, 1 changed an aa with 3—deletions. Approx 40% of severe hemophilia A is caused by a major inversion in the gene—the breakpoint is situated within intron 22. In 1/3 of hemophiliac patients, there is no family history of bleeding. This is consistent with the Haldane hypothesis that predicted that maintenance of a consistent frequency of a genetic disorder in the population would require that approx 1/3 cases are spontaneous mutations.

Clinical Manifestations Frequency and severity of bleeding are related to F VIII levels (Table 10.18):

Table 10.18  Table showing severity of bleeding with factor VIII levels Severity Severe

Factor VII activity 5%

Clinical manifestations Spontaneous hemorrhage from early infancy. Frequently sp hemarthrosis. Hemorrhage secondary to trauma or surgery. Occasional sp hemarthrosis. Hemorrhage secondary to trauma or surgery. Rare sp bleeding.

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Hemarthrosis It is the most common, painful, and most physically, economically, and psychologically debilitating manifestation. Clinically: 1 . Aura: tingling warm sensation 2. Excruciating pain 3. Generally affects one joint at the time 4. Most commonly: knee; but there are others as elbows, wrists, and ankles 5. Edema, erythema, warmth, and LOM 6. If treated early it can subside in 6–8 h and disappear in 12–24 h Complications: Chronic involvement with joint deformity complicated by muscle atrophy and soft tissue contractures. Pathophysiology: The bleeding probably starts from synovial vessels into the synovial space. Reabsorption of this blood is often incomplete leading to chronic proliferative synovitis, where the synovium is more thickened and vascular, creating a “target joint” with recurrence of bleeding. There is destruction of surrounding structures as well-bone necrosis and cyst formations, osteophytes. In the terminal stage: chronic hemophiliac arthropathy: fibrous or bony ankylosing of the joint. There is a radiological classification for the stages (Table 10.19).

Hematomas Subcutaneous and muscular hematomas spread within fascial spaces, dissecting deeper structures. Subcutaneous bleeding spreads in characteristic manner—in the site of origin the tissue is indurated purplish black, and when it extends the origin starts to fade, may compress vital structures: such as the airway if it is bleeding into the tongue, throat, or neck; it can compromise arteries causing gangrene and ischemic contractures are common sequelae, especially of calves and forearms.

Table 10.19  Table showing the radiological classification of stages Stage 0 1 2 3 4 5

Findings Normal joint. No skeletal abnormalities, but soft tissue swelling is present. Osteoporosis and overgrowth of epiphysis, no cysts and no narrowing of cartilage space. Early subchondral bone cysts, preservation of cartilage space but with irregularities. Finding of stage 3 but more advanced; cartilage space narrowed. Fibrous joint contracture, loss of cartilage space, extensive enlargement of the epiphysis and substantial disorganization of the joint.

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There are muscle hematomas: (1) calf, (2) thigh, (3) buttocks, (4) forearms. Psoas hematoma—if right sided may mimic acute appendicitis. The retroperitoneal hematoma: can dissect through the diaphragm into the chest compromising the airway. It can also compromise the renal function if it compresses the ureter.

Pseudotumors They are dangerous and a rare complication. The blood filled cysts (Fig. 10.7) that are gradually expanding occur in soft tissues or bones. Most commonly in the thigh as they increase in size they may erode contiguous structures. They may require radical surgeries or amputation, and surgery is often complicated with infection. A pseudotumor may deform the cortex of the femur. Other ossified masses in the soft tissues are probably soft-tissue pseudotumors. Fig. 10.7  Hemorrhagic haemophilic bone cysts (Courtesy: reused with the kind permission of Magdi E. Greiss, Whitehaven, Cumbria, UK)

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Intracranial Hemorrhage It is the leading cause of death of hemophiliacs which is either spontaneous or following trauma. It may be subdural, epidural, or intracerebral. The suspect always in hemophilic patient that presents with unusual headache. If suspected—FIRST TREAT, then pursue diagnostic workup. LP only when F VIII has been replaced to more than 50%.

Others 1. Gastrointestinal bleeding: PUD is five times more common in hemophiliac patients than regular males. Associated with ingestions of NSAIDs for hemarthrosis. Frequent cause of UGIB. 2. Mucous bleeding: Epistaxis, gum bleeding. 3. Genitourinary bleeding: Frequently severe hemophiliac can experience hematuria and a structural lesion should be ruled out.

Laboratory Diagnosis 1. Nomenclature: (a) F VIII—protein that is lacking or aberrant (b) F VIIIc—functional F VIII measured by clotting assays (c) F VIIIag—Antigenic protein that can be detected with immunoassays 2. Deficit can be quantitative or qualitative. 3. General Lab: prolonged aPTT, nl PT, and BT. 4. Mixing studies: aPTT corrects with normal plasma—if there are no factor VIII antibodies present. 5. Clotting assays: F VIII activity, expressed in % of normal—decreased— QUANTITATIVE. 6. Immunoassays: “Cross Reactive Material” Positive—there is an antigen similar to the F VIII protein—QUALITATIVE. It is clinically impossible to differentiate from Hemophilia B-FIX def-­Christmas’ disease. The type 2N vWD, transmitted as an autosomal recessive trait, is characterized by mutations in vWF within the factor VIII binding domain. Affected patients present with low levels of factor VIII (usually 5–15% of normal), because of unimpeded proteolytic cleavage of factor VIII, along with a clinical pattern of bleeding similar to that seen in hemophilia A, rather than that associated with classical vWD—should be suspected in families in which an autosomal recessive (rather than X-linked) inheritance pattern is seen.

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Carrier Detection and Antenatal diagnosis 1. Family history: if we follow the inheritance pattern a female is a carrier if she has an hemophilic father and has two hemophilic sons of which one son hemophilic son and has a family history and the other has a son but no family history, there is a 67% chance that she is. 2. Coagulation-based assays: Generally heterozygous females have 5 Bethesda units, low responders 90% by 60  years of age. So the

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prevalence of abnormal MRI of the cervical spine as related to age in asymptomatic individuals emphasizes the dangers of predicting operative decisions on diagnostic tests without precisely matching those findings with clinical signs and symptoms. The course of cervical spondylosis may be slow and prolonged. May either remain asymptomatic or have mild cervical pain. Long periods of nonprogressive disability are typical. Few cases—the patient’s condition progressively deteriorates. Both sexes affected equally. Cervical spondylosis usually starts earlier in men than in women. Most commonly in individuals aged 40–60 years. Symptoms may appear in persons as young as 30 years. Morbidity ranges from chronic neck pain to radicular pain; diminished cervical range of motion (ROM), headache, predominantly suboccipital; Myelopathy leading to weakness and impaired fine motor coordination to quadriparesis and/or sphincteric dysfunction in advanced cases. Pathophysiology: Intervertebral discs lose hydration and elasticity with age— leading to cracks and fissures. The surrounding ligaments also lose their elastic properties and develop traction spurs. The disk subsequently collapses as a result of biomechanical incompetence, causing the annulus to bulge outward. As the disk space narrows, the annulus bulges, and the facets override. This change, in turn, increases motion at that spinal segment and further hastens the damage to the disk. Annulus fissures and herniation may occur. Acute disk herniation may complicate chronic spondylotic changes. Due to annulus bulges—the cross-sectional area of the canal is narrowed. This effect may be accentuated by hypertrophy of the facet joints (posteriorly) and of the ligamentum flavum, which becomes thick with age. Neck extension causes the ligaments to fold inward, reducing the anteroposterior (AP) diameter of the spinal canal. As disk degeneration occurs, the uncinate process overrides and hypertrophies, compromising the ventrolateral portion of the foramen. Likewise, facet hypertrophy decreases the dorsolateral aspect of the foramen. This change contributes to the radiculopathy that is associated with cervical spondylosis. Marginal osteophytes begin to develop. Additional stresses, such as trauma or long-term heavy use, may exacerbate this process. These osteophytes stabilize the vertebral bodies adjacent to the level of the degenerating disk and increase the weight-bearing surface of the vertebral endplates. The result is decreased effective force on each of these structures. Degeneration of the joint surfaces and ligaments decreases motion and can act as a limiting mechanism against further deterioration. Thickening and ossification of the posterior longitudinal ligament (OPLL) also decreases the diameter of the canal. The blood supply of the spinal cord is an important anatomic factor in the pathophysiology. Radicular arteries in the dural sleeves tolerate compression and repetitive minor trauma poorly. The spinal cord and canal size also are factors. A congenitally narrow canal does not necessarily predispose a person to myelopathy, but symptomatic disease rarely develops in individuals with a canal that is larger than 13 mm. Flexion of the cervical spine may lead to compression of the spinal cord against osteophytic bars while extension may lead to compression against the hypertrophied ligamentum flavum. Clinical features: In the initial series reported by Brain et  al., the duration of symptoms ranged from 1 week to 26 years, and almost half of the patients presented

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symptoms for more than 1 year at the time of diagnosis. Common clinical syndromes associated with cervical spondylosis include the following: • Cervical pain: Chronic suboccipital headache may be present. Mechanisms include direct nerve compression; degenerative disk, joint, or ligamentous lesions; and segmental instability. Pain can be perceived locally, or it may radiate to the occiput, shoulder, scapula, or arm. The pain, worse when the patient is in certain positions, can interfere with sleep. • Cervical radiculopathy: Compression of the cervical roots leads to ischemic changes that cause sensory dysfunction (e.g., radicular pain) and/or motor dysfunction (e.g., weakness). Most commonly occurs in persons aged 40–50 years. An acute herniated disk or chronic spondylotic changes can cause cervical radiculopathy and/or myelopathy. The C6 root is the most commonly affected because of the predominant degeneration at the C5–C6 interspace; the next most common sites are at C7 and C5. Most cases of cervical radiculopathy resolve with conservative management; few require surgical intervention. • Cervical spondylotic myelopathy (CSM): The most serious consequence of cervical intervertebral disk degeneration, especially when it is associated with a narrow cervical vertebral canal. Insidious onset, which typically becomes apparent in persons aged 50–60 years. Complete reversal is rare once myelopathy occurs. Involvement of the sphincters is unusual at presentation. In a review of 1076 patients with CSM, gait disturbance was the most common presentation. In this series, spastic gait was one of the first symptoms, followed by upper extremity numbness and loss of fine motor control of the hands. Other common symptoms of CSM were neck pain, as well as referred pain in the shoulder or subscapular area. One-third of patients with cervicalgia due to CSM present with headache and >2/3 patients may present with unilateral or bilateral shoulder pain. A significant number of these patients also present with irradiated pain to the arm, forearm and/or hand pain with long periods of remission.

Causes 1. Age observed most commonly in elderly individuals. Among persons younger than 40 years, 25% have degenerative disk disease (DDD), and 4% have foraminal stenosis, as confirmed with MRI. In persons older than 40 years, almost 60% have DDD, and 20% have foraminal stenosis, as confirmed with MRI. 2. Trauma: Controversial role. Repetitive, subclinical trauma probably influences the onset and rate of progression of spondylosis. 3. Work activity significantly higher in patients who carry loads on their head than in those who don’t. 4. Genetics: Unclear role. However, a retrospective, population-based study by Patel et al. [2] shows that genetics may play a role in the development of cervical spondylotic myelopathy (CSM). Patients older than 50 years who have normal cervical spine radiographic findings are significantly more likely to have a sibling with normal or mildly abnormal radiographic results.

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Physical Examination 1. Decreased ROM in the cervical spine, especially with neck extension. 2. Hand clumsiness. 3. Sensory deficits. 4. Hyper-reflexia in the lower extremities and in the upper extremities below the level of the lesion. 5. A characteristically broad-based, stooped, and spastic gait. 6. Extensor plantar reflex in severe myelopathy. 7. Spurling sign—Radicular pain is exacerbated by extension and lateral bending of the neck toward the side of the lesion, causing additional foraminal compromise. 8. Lhermitte sign—This generalized electrical shock sensation is associated with neck extension. 9. Hoffman sign—Reflex contraction of the thumb and index finger occurs in response to nipping of the middle finger. This sign is evidence of an upper motor neuron lesion. Imaging 1. Plain cervical radiography: Routine in every patient with suspected cervical spondylosis. It is valuable in evaluating the uncovertebral and facet joints, the foramen, intervertebral disk spaces, and osteophyte formation. Flexion-extension views may be needed to detect instability. 2. Myelography, with computed tomography (CT) scanning, can also be used to assess spinal and foraminal stenosis. Since myelography method is invasive, most physicians depend on MRI in diagnosing cervical spondylosis. Myelography adds anatomic information in evaluating spondylosis. May be especially useful in visualizing the nerve root take off. CT scanning, with or without intrathecal dye, can be used to estimate the diameter of the canal. CT scans may demonstrate small, lateral osteophytes and calcific opacities in the middle of the vertebral body. 3. MRI is a considerable advance in the use of imaging to diagnose cervical spondylosis with following advantages: (a) direct imaging in multiple planes, (b) better definition of neural elements, (c) increased accuracy in evaluating intrinsic spinal cord diseases, and (d) non-invasiveness. False-positive and false-negative MRI results occur frequently in patients with cervical radiculopathy; therefore, MRI results and clinical findings should be used when interpreting root compression. T2-weighted hyperintensity at the level of spinal compression has also been shown to correlate with CSM severity and has been supposed to be an important prognostic factor. Such findings are thought to represent edema and inflammation. On the other hand T1-hypointensity has been shown to be a more severe sign, representing ischemia, myelomalacia, or gliosis as has been correlated with postoperative worst outcome.

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Histology: Thinning and fragmentation of the articular cartilage may be observed. The normal smooth, white articular surface becomes irregular and yellow. Continued loss of articular cartilage leads to exposure of areas of subchondral bone, which appear as shiny foci on the articular surface (eburnation). Fibrosis, increased bone formation, and cystic changes frequently occur in the underlying bone. Loss of articular cartilage stimulates new bone formation, usually in the form of nodules (osteophytes) at the bone edges.

Differential Diagnosis 1. Congenital—Arnold-Chiari malformation, tethered cord, syringomyelia 2. Acquired—trauma, herniated intervertebral disc, kyphosis, extramedullary hematopoiesis, epidural lipomatosis 3. Neoplastic—spinal cord tumors, carcinomatous meningitis, paraneoplastic syndrome 4. Vascular—hematoma, spinal cord infarction, spinal cord AVM 5. Autoimmune—multiple sclerosis, Devic syndrome 6. Infectious—paraspinal abscess, osteitis/osteomyelitis, pyogenic discitis, AIDS-­ related myelopathy, tuberculosis, spinal meningitis, viral and syphilitic involvement 7. Amytrophic lateral sclerosis Treatment 1. Physical therapy: Immobilization of the cervical spine is the mainstay of conservative treatment for patients with cervical spondylosis. Immobilization limits the motion of the neck, thereby reducing nerve irritation. Soft cervical collars are recommended for daytime use only, but they are unable to appreciably limit the motion of the cervical spine. More rigid orthoses (e.g., Philadelphia collar, Minerva body jacket) can significantly immobilize the cervical spine. The patient’s tolerance and compliance are considerations when any of the braces are used. A program of isometric cervical exercises may help to limit the loss of muscle tone that results from the use of more restrictive orthoses. Molded cervical pillows can better align the spine during sleep and provide symptomatic relief for some patients. The use of cervical exercises has been advocated in patients with cervical spondylosis. Isometric exercises are often beneficial to maintain the strength of the neck muscles. Neck and upper back stretching exercises, as well as light aerobic activities, are also recommended. The exercise programs are best initiated and monitored by a physical therapist. Passive modalities generally involve the application of heat to the tissues in the cervical region, either by means of superficial devices (e.g., moist-heat packs) or mechanisms for deep-­ heat transfer (e.g., ultrasound, diathermy). Mechanical traction is a widely used technique. May be useful because it promotes immobilization of the cervical region and widens the foraminal openings. However, traction in the treatment of cervical pain was not better than placebo in two randomized trials.

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Manual therapy, such as massage and mobilization may provide further relief for patients with cervical spondylosis. Mobilization is performed by a physical therapist and is characterized by the application of gentle pressure within or at the limits of normal motion, with the goal of increasing the ROM. Manual traction may be better tolerated than mechanical traction in some patients. 2. Occupational therapy: Patients with upper extremity weakness often lose their ability to perform activities of daily living (ADL), vocational activities, or recreational activities. Lifestyle modifications may involve an evaluation of workplace ergonomics, postural training, neck-school therapy (supervised, small-group therapy), stress management, and vocational assistance. Disability can be improved with specific strengthening exercises of the upper extremities, special splinting to compensate for weakness, and the use of assistive devices that allow the patient to perform previously impossible activities. 3. Drugs: NSAIDs, Steroids, Opioids, Drugs for radicular pain like Carbamazepine, Pregabalin. With nonoperative treatment, approximately 75% of patients have complete or partial, but significant, relief of symptoms. Nonoperative treatment of spondylosis with radiculopathy has not been compared with surgical therapy in randomized trials. Kadaňka et  al. compared in a randomized study conservative and surgical treatment of spondylotic cervical myelopathy to establish predictive factors for outcome after conservative treatment and surgery. The clinical, electrophysiological, and imaging parameters were examined to reveal how they characterized the clinical outcome. The patients with a good outcome in the conservatively treated group were of older age before treatment, had normal central motor conduction time (CMCT), and possessed a larger transverse area of the spinal cord. The patients with a good outcome in the surgically treated group had a more serious clinical picture. Conclusion was: (1) patients should preferably be treated conservatively if they have a spinal transverse area larger than 70 sq. mm, are of older age and have normal CMCT and (2) surgery is more suitable for patients with clinically worse status and a lesser transverse area of spinal cord.

Surgical Interventions Indications for surgery include the following: 1 . Progressive neurologic deficits 2. Documented compression of the cervical nerve root and/or spinal cord 3. Intractable pain The aims of surgery are to relieve pain and neuronal structure compression, as well as, in select cases, to achieve stabilization. Approaches for surgery—anterior or posterior or combined.

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Anterior approaches include the following: (1) diskectomy without bone graft, (2) diskectomy with bone graft, and (3) cervical instrumentation. Posterior approaches include the following: (1) decompressive laminectomy and foraminotomy, (2) hemilaminectomy, and (3) laminoplasty. The approach selected is determined by the type and location of pathology and by the surgeon’s preference. When anterior compression of the spinal cord is the most important component, anterior techniques are preferred. Some examples are disc protrusions or marked osteophytosis. Anterior approaches have the advantage of more readily restoring the cervical lordosis, which is useful for cases where the kyphosis exacerbates the spinal cord compression. While using this approach, the compressive factors should not exceed 2–3 disc levels. An anterior approach is: (1) technically more demanding, (2) carries a higher risk, and (3) often requires fusion. There are mainly two posterior approaches for the treatment of CSM: 1 . laminectomy (with or without fusion) 2. laminoplasty Posterior approaches may be considered when the pathology is located at the posterior portion of the spinal canal, for example, in cases of hypertrophied ligamentum flavum. Nevertheless, posterior decompression also addresses anterior compression because it indirectly decompresses the spinal cord by enlarging the spinal canal. When compared to anterior approaches, posterior procedures offer advantage for the treatment of CSM—enables direct visualization of the spinal canal and wide decompression of spinal cord and nerve roots. Procedures such as laminectomy without fusion and laminoplasty also present disadvantage: (1) development of instability or postlaminectomy kyphosis, (2) furthermore, none of the posterior approaches enable primary resection of anterior pathology. Laminoplasty: It preserves most of the bony posterior vertebral elements and, therefore, may decrease the risk of postlaminectomy kyphotic deformity in comparison with laminectomy. Besides that, in comparison with laminectomy with fusion, laminoplasty seems to present a decreased incidence of adjacent-level degeneration by preserving normal cervical range of motion. Laminectomy (with and without fusion): The oldest technique for posterior decompression of CSM is laminectomy without fusion. The major postoperative complication of such approach is post-laminectomy instability. The groups of patients in risk for such complication are those who present signs of preexisting instability and those in which aggressive facet resection is performed. In these cases instrument stabilization at the time of laminectomy is recommended. Instrumented fusion serves to both stabilize the cervical spine as well as secure the spine in an optimal lordotic configuration. For performing a decompressive cervical laminectomy/laminotomy (“posterior approach”), the compressive changes should be present in more than 2–3 disc

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levels. So-called “keyhole foraminotomies” are carried out at levels involved with radiculopathy. The posterior approach to cervical radiculopathy has similar results as the anterior approach when used for the proper indications. Surgical intervention for cervical myelopathy is controversial. Once moderate neurological signs and symptoms develop, surgical intervention is likely to be beneficial over further medical treatment. Predictive factors for the outcome of surgery for CSM are: 1. Age 2. Duration of symptoms 3. Preoperative clinical status 4. Anteroposterior diameter of the canal 5. Area of the spinal cord at the level of the maximal compression 6. Findings of hyperintense areas in the spinal cord 7. One level or multilevel compression 8. Congenital diameter of the spinal canal (expressed as Pavlov’s index) 9. Chosen method of decompression Prevention: 1 . Avoid high-impact exercise (e.g., running, jumping). 2. Maintain cervical ROM with daily ROM exercise. 3. Maintain neck muscle strength, especially neck extensor strength. 4. Avoid holding the head in one position for a long period (for example, while driving or watching TV). 5. Avoid prolonged neck extension. 6. Be careful when performing physical activities that are done infrequently; such activities can trigger a flare in symptoms.

Spinal Stenosis Historical perspective: • • • • •

1803: Portal of France postulated the cause of back and legs pain 1893: Lane of England performed first laminectomy 1911: Bailey and Casamajor on spinal pains and facet joint exostosis 1954: Verbiest described the syndrome of lumber stenosis 1978: Kirkaldy-Willis et  al. on pathology and pathogenesis (Three Joints Complex)

Diameters (Fig. 12.1): • AP Diameter: 15–27 mm, Lateral Recess: 3–4 mm. • AP diameter 4 mm translation 6. 10–12° angulation Normal AP diameters on lateral film Average Lower normal Severe stenosis

• • • •

22–25 mm 15 mm Grade 2. Scoliosis with Cobb angle ≥25° 3. Cauda equina syndrome 4. Spinous process fracture 5. Bilateral pars defects 6. Osteoporosis (hip T-score on Dexa < −2.5)

Outcome Poor outcome in: Females; those involved in litigation or compensation cases, those with previous failed surgeries, those with new sensory deficits postoperatively. Poor prognostic factors: Diabetes, prior hip surgery, osteoporosis, or preop spine fracture. Morbidity/mortality: (1) In-hospital mortality = 0.32%, (2) unintended durotomy (0.32–13%), (3) deep infection (5.9%), (4) superficial infection (2.3%), (5) DVT (2.8%), (6) damage to cauda equina. Nonunion (risk factors): (1) Smoking, (2) levels, and (3) NSAIDs use (Ketorolac). Success of operation: No RCT comparing conservative to surgical treatment exist, improvement in patients with a postural component (96% good outcome), more improvement in legs pain than back pain. Relapse of symptoms: 30% to restenosis at the operated level, 30% to stenosis at new level and 75% responds to redo surgery. Early failure of pain relief: Erroneous patient selection, technical failure (not decompressing the foramina in presence of stenosis), missed diagnoses.

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Long-term outcome: Good to excellent outcome after surgery with a mean of 64%, 37% much improved and 29% somewhat improved, 78–88% success rate at 6 weeks to 6 months and 70% at 1 year and 5 years; success rates slightly lower for lateral recess syndrome.

Conclusion 1 . Spinal stenosis is a predominantly surgical disorder. 2. Surgery has good to excellent outcome in those who have been properly selected. 3. Comorbids, psychiatric illness and redo surgeries carry risk of poor or no response in terms of pain relief. 4. Endoscopic facetectomy has been evaluated with documented good results.

Ankylosing Spondylitis Ankylosing spondylitis (AS)—is a chronic systemic inflammatory disease of the axial skeleton, with variable involvement of peripheral joints and nonarticular structures. AS is one of the seronegative spondyloarthropathies and has a strong genetic predisposition. It mainly affects joints in the spine and the sacroiliac joint in the pelvis. In severe cases, complete fusion and rigidity of the spine can occur. Synonyms  =  Bekhterev (Bechterew’s) disease, Marie-Strümpell disease, Bekhterev-Marie-Strümpell disease. Epidemiology: The prevalence ranges from 0.1% to 1% of the population; men are affected three times more than women; commonly develops between the ages of 15 and 40; predominant in Caucasians worldwide. Etiology: Etiology is unknown, but probable etiologic factors are: (1) genetic predisposition—% of people with AS share the genetic marker HLA-B27; (2) bacterias—Klebsiella pneumoniae and some other enterobacterias. Human leukocyte antigen (HLA) B27 is a surface antigen encoded by the B locus in the major histocompatibility complex (MHC) on chromosome 6 and presents antigenic peptides to T cells. It lies on the surface of WBC.  HLA-B27 is strongly associated with ankylosing spondylitis, and other associated inflammatory diseases referred to as “spondyloarthropathies.” More than 100 disease associations have been made, including many ocular diseases and systemic diseases with specific ocular manifestations.

Associated Pathologies 1. Ankylosing spondylitis 2. Juvenile rheumatoid arthritis (JRA) 3. Arthritis related to Crohn’s disease or ulcerative colitis 4. Psoriatic arthritis

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5 . Reactive arthritis (Reiter’s syndrome) 6. Uveitis HLA-B27 Typing is a laboratory immunogenetic PCR blood test that determines the presence or absence of the HLA B27 alleles. Venous blood is been tested. Patient shouldn’t smoke for 1 h before blood collecting. Indications: differential diagnostics of systemic diseases. Most valuable in case of validating ankylosing spondylitis and reactive arthritis, making out it’s prognosis. PS:HLA-B27: It’s an additional test which helps to validate Ds of AS; this test is negative in about 10% of patients with AS. The Enterobacteriaceae are a large family of Gram-negative bacteria that includes, along with many harmless symbionts, many of the more familiar pathogens, such as: 1. 2. 3. 4.

Salmonella Escherichia coli Yersinia pestis Klebsiella pneumonia

Pathogenesis: There are two theories: 1. Receptors theory—HLA B27 is a receptor for etiologic factor (bacteria, virus, etc.). The resulting complex provokes production of cytotoxic T-cells which cause damage to cells with HLA B27 molecule. So, urinary or bowel infection can be a trigger for AS. 2. Molecular mimicry theory—bacterial antigen (or other damaging factor) in complex with other HLA molecule gets similar to HLA B27 properties and is been recognized by cytotoxic T-cells as HLA B27 or decreases the immune reaction at pathologic peptide (immunological tolerance). In both cases autoimmune inflammatory process is a result. It has features: Usually starts with affection of sacroiliac joints, then intervertebral and costovertebral joints are involved (rarely—peripheral joints). Characterized by active fibrosis with further ossification and calcification, and ankylosis as result.

Pathomorphology 1. Enthesitis—the site of ligamentous attachment to bone is the primary site of pathology. The early lesions consist of subchondral granulation tissue, infiltrates of lymphocytes and macrophages in ligamentous and periosteal zones, and subchondral bone marrow edema. 2. Synovitis—may progress to pannus formation with islands of new bone formation.

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3 . Ostitis—with fibrosis and ossification. 4. Ankylosis. Sites of affection: (1) Sacroiliac joints, (2) intervertebral joints, (3) costovertebral joints, (4) brachial (shoulder) joints, (5) coxofemoral (hip) joints, (6) knee joints, (7) ankle joints, and (8) small joints of hands.

Symptoms (Early AS) 1. Pain in sacroiliac and lower back regions: permanent; dull, worsens in rest; in the morning; nocturnal, reliefs in motion; in the afternoon. 2. Buttock pain: it radiates into posterior surface of hip, migrates from left to right gluteus. 3. Lower back stiffness: in the morning, for ≥30 min, reliefs after activity, warm shower. 4. Chest pain: mimicries intercostal neuralgia and intercostal muscles myositis, worsens in coughing, sneezing, deep breathing. 5. Stiffness and tenderness of back muscles. 6. Flattening of lumbar lordosis. 7. Bilateral sacroiliitis. 8. Enthesopathies—pain in the site of ligamentous attachment to bone: iliac crests, trochanters, spinous processes of vertebrae, costovertebral joints. 9. Extra-articular manifestations—usually eyes affection (anterior uveitis); bilateral, acute onset, lasts for 2–3 months, registered in 30% of patients.

Symptoms (Advanced AS) 1. Pain in different segments of spine. 2. Question mark posture. 3. Atrophy of back muscles. 4. Decreased thorax excursion. 5. Decreased articulations in spine. 6. Ankylosis of sacroiliac and intervertebral joints. 7. Cutaneous lesions—that are identical to pustular psoriasis. 8. Cardiovascular system involvement: aortitis, aortic insufficiency, pericarditis, myocarditis. 9. Bronchopulmonary system involvement—fibrosis of apical lung segments. 10. Urinary system involvement = amyloidosis, IgA-nephropathy. 11. Gastrointestinal system involvement = ulcerative colitis, Crohn’s disease. Question mark posture, or suppliant posture—loss of lumbar lordosis, fixed kyphosis, compensated extension of cervical spine, protuberant abdomen.

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Extra-Articular Manifestations 1 . Ocular (anterior uveitis) 2. Cardiovascular (aortitis, myocarditis, AV-block) 3. Gastrointestinal (colitis, enteritis) 4. Cutaneous (pustular psoriasis) 5. Pulmonary (fibrosis) 6. Renal (amyloidosis) Ocular manifestations: Anterior uveitis (iritis, iridocyclitis)—is an inflammation of the front part of the eye, between the cornea and the lens. Appears in 20–30% of patients with AS.  Symptoms: eye pain, sensitivity to light, eye redness, blurred vision, spots in field of vision. Usually resolves within 2–3 months without residual visual impairment. Complications: hypopyon, synechia, cataract, and glaucoma. Treatment: steroid, antibiotic and mydriatic eye drops, usage of sunglasses. Cardiovascular manifestations: May include: (1) aortitis, (2) aortic insufficiency, (3) pericarditis, (4) myocarditis, (5) AV-blocks; registered in about 33% of patients with AS; Investigations: ECG, echocardiography, CT. All these conditions should be treated by cardiologist. Gastrointestinal manifestations: Inflammatory bowel diseases (IBD)—is a group of inflammatory conditions of the colon and small intestine, which include: (1) Crohn’s disease, (2) ulcerative colitis; diagnosed in 5–10% of patients with AS. Symptoms: abdominal pain, vomiting, diarrhea, rectal bleeding, severe internal cramps, weight loss, anemia. Complications: toxic megacolon, bowel perforation, colorectal cancer, intestinal obstruction, fistulas, abscesses, malabsorption and malnutrition. Investigations: stool analysis, colonoscopy with biopsy. Treatment: steroids, immunosuppressants, antibiotics, TNF inhibitors, surgery, fecal bacteriotherapy (PS: NSAIDs are prohibited in case of IBD). Cutaneous manifestations: Psoriasis is a chronic autoimmune disease characterized by patches of abnormal skin (typically red, itchy, and scaly) that may vary in severity from small and localized to complete body coverage. There are five main types: plaque, guttate, inverse, pustular, and erythrodermic; pustular psoriasis associates with AS. Occurs in 10–25% of patients with AS. Dermatologist’s assistance is needed. Pustular psoriasis usually exists as a large red area covered with green tender pustules (blisters) that are 1–2 mm diameter. Pulmonary manifestations: Apical (upper lobe) fibrosis—is a rather prevalent complication of a large number of pathologies. Symptoms: productive/nonproductive cough, dyspnea; develops in up to 50% of patients with AS (PS: Check for tuberculosis). Renal manifestations: Renal amyloidosis—renal deposits of amyloid, especially in glomerular capillary walls, which may cause albuminuria and the nephrotic syndrome. IgA nephropathy—deposition of the IgA antibody in the glomerulus, the most common variant of nephritic syndrome; Met in 10–35% of patients with AS. Complication: chronic renal failure, cooperation with nephrologist is needed.

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Complications 1 . Functional insufficiency (ankylosis). 2. Spinal fractures (osteoporosis). 3. Cauda equina syndrome—is a rare complication that occurs when nerves at the bottom of spine become compressed. Causes pain or numbness in lower back and buttocks, weakness in legs (can affect ability to walk), urinary incontinence or bowel incontinence. PS: A large number of different specialists may be needed for management of AS patients or sometimes one may be enough.

Forms of the Disease 1 . Central—affection of only spine and sacroiliac joints. 2. Rhizomelic—affection of spine, shoulder, and hip joints. 3. Peripheral—affection of both axial and peripheral joints (knee, ankle, etc.) 4. Scandinavic—affection of spine and hand joints (mimicries rheumatoid arthritis). 5. Visceral—affection of joints and internal organs.

Mobility Measurement 1. Lumbar mobility: Modified Schober test (lumbar flexion test), finger-to-floor distance (Tomayer test), and lumbar lateral flexion. 2. Thoracic mobility: Chest expansion. 3. Cervical mobility: Occiput-to-wall distance (Forestier test), tragus-to-wall distance, and cervical rotation. 4. Hip mobility: Intermalleolar distance. Schober test: Patient standing upright. Two marks are made on the patient’s back: one at the level of the sacral dimples (at the fifth lumbar spinous process) and the other 10 cm above. The patient then bends forward as far as possible (i.e., attempts to touch toes with knees extended), and the distance between the two marks is again measured. Normally the overlying skin will stretch to 15 cm. Values less than this can be indicative of reduced lumbar mobility. Modified Schober test: In this test marks are made 5 cm below and 10 cm above the sacral dimples. The distance between these marks should increase from 15 cm to at least 20 cm with lumbar flexion. The distance less than 5 cm is abnormal. Finger-to-floor distance: Expression of spinal column mobility when bending over forward. Measured distance is between the tips of the fingers and the floor when the patient is bent over forward with knees and arms fully extended.

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Lateral lumbar flexion: Patient stands with heels and buttocks touching the wall, knees straight, shoulders back, outer edges of feet 30 cm apart, feet parallel. The patient bends laterally as much as he can. Measure minimal fingertip-to-floor distance in full lateral flexion without flexion, extension or rotation of the trunk or bending the knees. The difference between start and endpoint is recorded. Normally >10 cm. Chest expansion: Measured as the difference between maximal inspiration and maximal forced expiration in the fourth intercostal space in males or just below the breasts in females. Normal chest expansion is ≥5 cm. Normal values depending on age and sex Age Sex cm

18–24 M/F 7/5.5

25–34 M/F 7.5/5.5

35–44 M/F 6.5/4.5

45–54 M/F 6/5

55–64 M/F 5.5/4

65–74 M/F 4/4

75+ M/F 3/2.5

Occiput to wall distance: Patient stands, with heels and buttocks against the wall; the head is placed back as far as possible, keeping the chin horizontal; patient extends his neck maximally in an attempt to touch the wall with the occiput. Normally = 0. Tragus to wall distance: Patient stands, with heels and buttocks against the wall. The head is placed back as far as possible, keeping the chin horizontal. Normally 100 cm. Tests for sacroiliitis: Pelvic compression test, Fabere test, and Gaenslen test. 1. Pelvic compression test: Test irritability by compressing the pelvis with the patient prone. Sacroiliac pain will be lateralized to the inflamed joint. 2. Fabere test: FABER test (Fabere test, Patrick test, Figure Four test) is performed by having the tested leg flexed, abducted, and externally rotated. If pain occurs anteriorly on the same side of the body → hip joint disorder. If pain occurs posteriorly on the opposite side of the body → sacroiliac joint disorder. 3. Gaenslen test: The non-tested leg is kept in extension, while the tested leg is placed in maximal flexion. The examiner places one hand on the anterior thigh of the non-tested leg and the other hand on the knee of the tested leg to apply a flexion overpressure. The extended leg may also be placed off the table to create a greater force. A positive test occurs if it produces low back pain.

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Laboratory tests 1 . CBC: increased ESR, sometimes—hypochromic anemia and leukocytosis. 2. Biochemistry: increased level of α-2-globulins and γ-globulins, seromucoid, sialic acid, CRP. 3. Rheumatoid factor in blood—negative. 4. HLA-B27 Typing—positive in about 90% of cases. Others—depending on extra-­ articular manifestations and complications. Instrumental tests: 1 . X-ray—main diagnostic method 2. Scintigraphy 3. CT-scan, MRI 4. Others—depending on extra-articular manifestations and complications

X-Ray Grading of SI Joints • • • •

Grade 0: normal Grade I: some blurring of the joint margins—suspicious (A) Grade II: minimal sclerosis with some erosion (B) Grade III: definite sclerosis on both sides of joint with severe erosions with widening of joint space with or without ankylosis (C) • Grade IV: complete ankylosis (D) Bamboo spine: Bamboo spine (Fig. 12.2) occurs as a result of vertebral body fusion by marginal syndesmophytes. It is often accompanied by fusion of the posterior vertebral elements as well. Typically involves the thoracolumbar and or lumbosacral junctions and predisposes to unstable vertebral fractures. The outer fibers of the annulus fibrosus of the intervertebral discs ossify, which results in the formation of marginal syndesmophytes between adjoining vertebral bodies. The resulting radiographic appearance therefore is that of thin, curved, radiopaque spicules that completely bridge adjoining vertebral bodies. There is also accompanying squaring of the anterior vertebral body margins with associated reactive sclerosis of the vertebral body margins (shiny corner sign). Modified New York Criteria (1984) Clinical criteria Low back pain, >3 months, improved by exercise, not relieved by rest Limitation of lumbar spine motion, sagittal and frontal planes Limitation of chest expansion relative to normal values for age and sex

Radiologic criteria Sacroiliitis grade 2 bilaterally Sacroiliitis grade 3–4 unilaterally

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Fig. 12.2  Ankylosing spondylitis = Bamboo spine (Courtesy: reused with the kind permission of Magdi E. Greiss, Whitehaven, Cumbria, UK)

Definite AS if radiologic criterion present plus at least one clinical criteria. Probable AS if: Three clinical criterion; radiologic criterion present, but no signs or symptoms satisfy clinical criteria. ASAS Criteria (2010) Sacroiliitis on imaging and >1SpA feature SpA features: inflammatory back pain, Arthritis, enthesitis (heel pain), uveitis, dactylitis, psoriasis, Crohn’s, colitis, good respond to NSAIDs, family history of SpA, HLA-B27, elevated CRP.

HLA B27 positive and two other SpA features Sacroiliitis on imaging (a) Active(acute) inflammation on MRI; highly suggestive of sacroiliitis associated with SpA (b) Definite radiographic sacroiliitis according to New York Modified Criteria

Treatment 1. Regime 2. Drug therapy: NSAIDs, Steroids, DMARDs, Anti-TNF drugs 3. Physiotherapy 4. Surgical treatment 1. Regime: Regular exercises—swimming, yoga. Contact sports are NOT recommended. Hard bed. Posture—sit/walk straight. Diet—rich with calcium, avoid overweight. 2. NSAIDs: Indomethacin (Indocin)—25  mg 3 times per day, up to 150  mg/day. Diclofenac (Cataflam, Voltaren-XR, Zorvolex)—25–50  mg 3 times per day. Ibuprofen (Motrin, Advil)—200 mg 3 times per day.

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3. Steroids: Used when NSAIDs noneffective. Prednisone—5–60 mg/day (1 mg/ kg/day). Hydrocortisone—20–240  mg/day. Pulse therapy—prednisone IV 1000 mg 1 time per day for 3 days. 4. DMARDs: Extremely effective in case of peripheral form of AS. Sulfasalazine—2–3 g/day. Methotrexate—7.5–20 mg 1 time per week. 5. TNF inhibitors: TNF inhibitors—are pharmaceutical drugs that suppresses the physiologic response to tumor necrosis factor (TNF), which is part of the inflammatory response. Advantages: high specificity, selectivity; decreased risk of immunosuppression. Disadvantages: high price, increased oncological risk. Indications: rheumatoid arthritis, ankylosing spondylitis, inflammatory bowel disease, psoriasis. Side effects: lymphomas, infections, congestive heart failure, demyelinating disease, a lupus-like syndrome, induction of auto-antibodies, injection site reactions. Golimumab (Simponi)—SC 50  mg every month. Adalimumab (Humira, Exemptia)—SC 40  mg 1 time per 2  weeks. Infliximab (Remicade, Remsima, Inflectra)—IV drop 5 mg/kg once, repeat in 2 weeks, then in 6 weeks and perform every 6–8 weeks. 6. Physiotherapy: Exercises, massage, heat procedures. 7. Surgical Treatment: Spine osteotomy is a surgical procedure in which a section of the spinal bone is cut and removed to allow for correction of spinal alignment. Usually needed for correction of severe deformed, rigid and fixed spinal deformity. The three main types of osteotomy are: 1 . Smith-Petersen osteotomy (SPO) 2. Pedicle subtraction osteotomy (PSO) 3. Vertebral column resection osteotomy (VCR) Smith-Petersen osteotomy (SPO)—is recommended in patients in whom a relatively small amount of correction (10–20° for each level) is required [3]. A section of bone with posterior ligament and facet joints are removed from the back of the spine causing the spine to lean more toward the back. SPO may be performed at one or multiple locations along the spine to restore lordosis. Pedicle subtraction osteotomy (PSO)—is recommended in patients in whom a correction of approximately 30° is required mainly at the lumbar level. PSO involves all three posterior, middle, and anterior columns of the spine. A posterior element and facet joints (similar to a SPO) and a portion of the vertebral body along with the pedicles are removed. PSO allows for more correction of the lordosis than SPO. Vertebral column resection osteotomy (VCR)—involves the complete removal of a single or multiple vertebral bodies. It allows for maximum correction that can be achieved with any spinal osteotomy. It introduces a large defect in the spine, so the spinal fusion is also performed over these levels for reconstruction (autograft, structural allograft or metal cage).

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Spondylolisthesis Historical aspects: In 1782, Herbiniaux, a Belgian obstetrician, noted a bone prominence in front of the sacrum that caused problems in delivery. In 1854, Kilian coined the term spondylolisthesis, derived from the Greek spondylos, meaning “vertebra,” and olisthenein, meaning “to slip.” Definition: Spondylolisthesis is defined as the forward slippage of one vertebra on its adjacent caudal segment. Spondylolysis is a defect in pars interarticularis (the part of neural arch just caudal to the confluence of the pedicle, the superior articular process and the most cephalad part of the lamina). Spondyloptosis: used to describe as fall of L5 vertebra into the pelvis and lie anterior to sacrum. Pars interarticularis: portion of bone between superior and inferior articulating processes and the thinnest part of the neural arch. Neural arch: bridge of bone formed by the posterior elements of a vertebra that surrounds the spinal cord. Facet joint: the contact junction between the inferior articular process of one vertebra and the superior articulating process of the vertebra below it. Motion segment: functional unit of the spine, consisting of two adjacent vertebrae and the intervening disc along with, facet joints, capsule and ligaments. Pedicles: thick bony struts that connect the vertebral body with the posterior elements Lamina: the portion of the neural arch between the articular processes and the spinous process. Spondylosis: degenerative changes of the spine (vertebral joints and disc).

Hook and Catch Concept Hook: Pedicle, pars interarticularis, and the inferior process of the cephalad level. Catch: Superior process of the caudal level. Classification: Wiltse et al. [4] (based on a mixture of etiological and topographical criteria), Meyerding classification (based on percentage of slip in lateral radiograph), Marchetti and Bartolozzi (emphasizes the developmental and dysplastic aspects), Spinal Deformity Study Group/SDSG classification. Wiltse et al., Clin Orthop (1976) Type I II

III IV V VI

Name Congenital Isthmic A B C Degenerative Traumatic Pathologic Iatrogenic

Description Dysplastic abnormalities Lytic (stress fracture) Healed fracture (elongated, intact) Acute high-energy fracture Segmental instability Fracture of hook other than pars Underlying pathology Surgical excision of posterior elements.

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Type I: Dysplastic (20%): Occurs only at L5–S1 level. Primary congenital dysplasia of L5–S1 facet joints. Typically the inferior facet of L5 is dysplastic and the sacral facet absent. No pars interarticularis defect. Frequent association with spina bifida occulta of L5 and sacrum. More common in females. Increased incidence in first-degree relatives of patients: genetic. Type II: Isthmic (50%): Defect in pars interarticularis that allows forward slippage of L5 over S1. Three types: (a) Lytic: stress fracture of pars interarticularis, (b) healed version of Lytic—pars interarticularis intact but elongated, (c) Acute fracture of pars interarticularis due to high-energy injury. Spondylosis most common at L5 (87%), L4 (10%), L3 (3%). The incidence tends to stabilize in adulthood. Type III: Degenerative (25%): Due to intersegmental instability of long duration and subsequent remodeling of the articular process. Often accompanied by spinal stenosis, older than 40 years. Most common at L4–5 (six times more), women (four to six times); two theories: sagittal facet theory and disc degeneration theory. Studies show progressive spondylolisthesis occurred in 34%, and further disc space narrowing continued in the patients without further slip. Low back pain improved in patients with continued disc space narrowing: autostabilization. Type IV: Traumatic: fracture in the area of the bony hook other than pars, i.e., pedicle, laminas, or facets. Type V: Pathological: Due to generalized or localized bone disease, osteogenic imperfecta, multiple myeloma, infection. Type VI: Post surgical: Due to loss of posterior elements secondary to surgery.

Meyerding Classification Based on the ratio of [overhanging part of the superior vertebral body] to [anteroposterior length of the adjacent inferior vertebral body]: • • • • •

Grade I: 0–25% Grade II: 26–50% Grade III: 51–75% Grade IV: 76–100% Grade V (spondyloptosis): >100%

Spinal Deformity Study Group (SDSG) classification Low Grade: 50% slip; Myerding 0–2 Type 1 = nutcracker; displacement 45° Type II = normal; displacement 45–60° Type III = shear; PL >60°

High Grade: >50% slip; Myerding 3 or > Type IV = Balanced pelvis Type V = Retroverted pelvis, balanced spine Type VI = Retroverted pelvis, unbalanced spine

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Epidemiology Incidence: 6% in general population male:female ratio: 2:1, slippage more in females. Incidence in children 40 years) more common in females. Genetic and familial association: 26% of patients with isthmic spondylolisthesis had first-degree relatives with same disease. Developmental spondylolisthesis with lysis: It is due to stress fracture in children with genetic predisposition for the defect. Wiltse et al.: normal flexon contracture of the hip in childhood causes increased lumbar lordosis leading to increased force at pars interarticularis. Lett et  al.: shear stress greater at pars when lumbar spine is extended. Cryon and Hutton: pars is thinner and vertebral disc is less resistant to shear in children and adolescents than in adults. Isthmic spondylolisthesis: Due to upright walking and wt. bearing. M = F: 2:1. Risk factors: gymnastics/football/wt. lifting, dancing, and others with excessive lordosis or hyperflexion of the lumbar spine. Etiology of degenerative spondylolisthesis.

Two Theories (a) Sagittal facet theory: Facet oriented in such a way that it doesn’t resist intratranslation forces over time leading to degeneration and spondylolisthesis. (b) Disc degeneration theory: Disc narrows first leading to overloading of facets, accelerated arthritic changes, secondary remodeling, anterolisthesis. Traumatic: Acute fracture other than pars. Post surgical: Laminectomy, intervertebral fusion. Pathophysiology: (1) Traumatic pathway, (2) dysplastic pathway, and (3) degenerative pathway. 1. Traumatic pathway: In erect posture—center of gravity is anterior to LS joint. Lumbar spine—forward force and rotate anteriorly into flexion about the sacral dome. Initiated by the repetitive cyclic loading. Sup. and inf. articular process impingement creates a bending moment that is resisted by the pars. Repetitive impingement—fatigue stress fracture of pars and post. Neural arc separates from body. Gap occupied by the fibrous tissue. Nonunion. Increased shear load to disc though axial load remains unchanged. Premature disc degeneration. Vertebral subluxation. 2. Dysplastic pathway: Initiated by the cong. defect (dysplasia) in the bony hook or its catch. Repeated loading unopposed by bony constraints. Plastic deformation of soft tissue restrains: IV Disc, Antr and Postr ligament complex. Subluxation of vertebra, with continuous growth, slippage and abnormal growth in the involved vertebral bodies or sacrum.

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Changes seen: Trapezoid shape of L5. Rounding of supero-anterior aspect of sacrum. Vertical orientation of the sacrum. Junctional kyphosis at involved segments—compensatory hyperlordosis at the adjacent levels. 3 . Degenerative spondylolisthesis: Sagittal facet degeneration. No resistance for anterior translation force. Predilection for slippage. Anterolisthesis. Boden et al.—sagittal facet angles of >45° at L4–L5—25 times greater likelihood of degenerative spondylolisthesis. Disc degeneration. Disc narrowing and subsequent overloading of facets. Accelerated arthritic changes. Secondary remodeling. Anterolisthesis. Pathological spondylolisthesis: Due to local or systemic pathological process causing a defect in the neural arch. Vertebral subluxation. Traumatic spondylolisthesis: High-energy trauma. Translational deformity. Fracture of bony hook other than pars, i.e.: pedicle, superior and inferior articular facets, associated multiple bony and STI subluxation.

Post Surgical 1. Laminectomy: Removal of >1/2 or entire articular process. Destabilize the spine which leads to subluxation. 2. Fusion of segments: Resection of capsular, supraspinous and interspinous ligaments. Increasing motion demand which leads to subluxation.

Natural History Risk factors for the progression: 1 . Young age at presentation. 2. Female gender. 3. A slip angle of >10°. 4. A high-grade slip. 5. Dome-shaped or significantly inclined sacrum. Natural history is predominantly determined by: 1 . Developmental or acquired spondylolisthesis. 2. Low or high dysplasia. 3. Quality of pedicle, pars, and facets. 4. Age when diagnosis is made. 5. Degree of lordosis and position of gravity line. 6. Degree of secondary or remodeled deformity. 7. Competency, hydration, and height of the disc.

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1. Dysplastic spondylolisthesis: Early age; usually asymptomatic. Severe slip (9–15, seldom after 20). Risk of neurological complications. Higher risk of slip progression—cauda equina syndrome as the neural arc is intact. Natural history of isthmic spondylolisthesis: No progression of slip 25% slip Symptomatic Risk of slip progression Backache in later life

Natural history of degenerative spondylolisthesis: Rare before 50. Matsunaga et al. 10 years prospective study—34% showed progression of the slippage-though no significant effect in the clinical outcome, further disc space narrowing continued in those without slip. However back pain improved (Autostabilization)—83% of the pts. with neurological signs and symptoms deteriorated.

Clinical Evaluation Usually asymptomatic—Incidental finding in X-ray. Symptoms depend on the severity of slip and is caused by: 1. Chronic muscle spasm: Body limits motion around a painful pseudoarthrosis of facet and its pars. 2. Tears in the annulus fibrosus of the degenerated discs. 3. Compression of the nerve roots. When symptomatic: In children and young adults: back fatigue and back pain-on movement (hyperextension) due to instability of the affected segment. Hamstring fatigue and pain due to irritation of L5 nerve root. Sciatica—may occur in one or both legs. In patients >50 years: Backache. Sciatica. Pseudoclaudication d/t spinal stenosis when subluxation is severe. Other signs of nerve root compression—motor weakness, reflex changes, and sensory deficits.

Compression of Central Canal Features: 1 . Bladder and bowel dysfunction 2. Bilateral leg symptoms 3. +ve SLRT B/L 4. +ve crossed SLRT

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On Inspection • Buttocks: Flat, Heart shaped in high-grade slip d/t sacral prominence. • Sacrum—more vertical, appears to extend to the waist. • Lumbar hyperlordosis above the level of the slip to compensate for the displacement. • Transverse loin crease. • With severity—absence of waist line. • Peculiar spastic gait—due to hamstring tightness and lumbosacral kyphosis. Scoliosis—esp in children—three types: (a) Sciatic: Lumbar curve caused by the muscle spasm resolve with symptoms. (b) Olisthetic: Due to asymmetrical slipping of vertebra. (c) Idiopathic: In olisthetic crisis with total canal occlusion—typical posture— decrease nerve root tension by supporting trunk with hands on knee. In spondyloptosis—shortening of lumbar spine. Palpation: Palpable step. Tenderness over pars defect. Hamstring tightness on leg raising. Movements: Usually normal in young pts. May be—hamstring + paraspinal muscle tightness limiting forward bending and hip flexon. Degenerative type: spine—often stiff. Positive nerve root tests if root compression. The pain generators: Leg pain: L5 compression/traction. Abnormal motion. Facet joint arthrosis. Pars scar. The disc above far-lateral.

Imaging Radiographs: • AP view. • Standing lateral view including the hips (15% of deformities spontaneously reduce on supine imaging.) • Oblique view: helps in viewing pars interarticularis defect (decapitated scotty dog). • Lateral flexion and extension views: determination of translational instability. • Flexion-extension lateral views may reveal instability, which is considered to be present when 4 mm of translation or 10 degrees of sagittal rotation greater than the adjacent level is identified. • Fegurson view depicts the L5 pedicles, transverse processes, and sacral ala more clearly. Fegurson view (20° Caudo cephalic AP view).

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Flexion extension X-rays: Demonstrates a bilateral break in the pars interarticularis or spondylolysis that allows the L5 vertebral body to slip forward on the S1 vertebral body. Inverted napoleon’s hat sign: indicates the presence of bilateral spondylosis and significant spondylolisthesis. The dome of the hat is formed by the overlying body of L5 vertebra and the brim is formed by downward rotation of the transverse processes.

Other Investigations 1. CT myelography and MRI are used as indicated for the evaluation of spinal stenosis and may show facet overgrowth, hypertrophy of the ligamentum flavum, and, rarely, disc herniation, tumors, etc. 2. SPECT: most sensitive for impending spondylolysis. Can determine the chronicity of lytic defect. 3. NCV, EMG: to rule out peripheral neuropathy. 4. Arterial Doppler/CT angiography: to rule out vascular causes of claudication. Role of SPECT: A Single-photon Emission Computed Tomography bone scan is necessary to show whether uptake is increased in the pars. A SPECT scan is helpful in determining whether the process is acute or chronic. If increased uptake is confirmed, a CT scan can be obtained to evaluate whether there are thickened cortices consistent with a stress reaction or whether there is an acute stress fracture. Magnetic resonance imaging: Allows for additional visualization of soft tissue and neural structures and is recommended in all cases associated with neurologic findings. In the early course of the disease, MRI helps in identifying the stress reaction at the pars interarticularis before the end-stage bony defect. MRI may show the degree of impingement of neural elements by fibrous scar tissue at the spondylolytic defect. Status of disc. Disc degeneration: MRI Grade I II

III IV

V

Structure Homogenous, bright white. Inhomogenous with or without horizontal bands. Inhomogenous gray. Inhomogenous gray to black. Inhomogenous black. Grade I

Distinction of nucleus and annulus Clear Clear

Signal intensity Hyperintense, isotense to CSF. Hyperintense, isotense to CSF.

Unclear

Intermediate

Lost

Intermediate to hypointense

Lost

Hypointense

Grade II

Grade III Grade IV

Height of intervertebral disc Normal Normal

Normal to slightly decreased. Normal to moderately decreased Collapsed disc space. Grade V

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Important Radiological Parameters 1. Slip angle (by Boxall et al.): The slip angle is measured from the superior border of L5 and a perpendicular line from the posterior edge of the sacrum. Angle greater than 45–50° associated with greater risk of slip progression, instability, and development of postoperative pseudarthrosis. It is the best predictor of progression of slip. A slip angle greater than 55° is associated with a high probability and increased rate of progression. 2. Pelvic incidence (PI): Pelvic incidence: A line perpendicular to the midpoint of the sacral end plate is drawn. A second line connecting the same sacral midpoint and the center of the femoral heads is drawn. The angle subtended by these lines is the pelvic incidence. Pelvic incidence: Pelvic tilt + sacral slope. Normal, ≈50°. Unaffected by posture. Increased PI may predispose to spondylolisthesis. 3. Pelvic tilt (PT): Pelvic tilt: A line from the midpoint of the sacral end plate is drawn to the center of the femoral heads. The angle subtended between this line and the vertical reference line is the pelvic tilt. Higher pelvic tilt predisposes to spondylolisthesis. 4. Sacral slope (SS): Sacral slope: A line parallel to the sacral end plate is drawn. The angle subtended between this line and the horizontal reference line is the sacral slope. Vertical sacrum (SS  boys Symptomatic Postural or gait abnormality

Radiographic Growth years (9–15) Vertical sacrum >50% slip Instability on flex/ext views

Management: (1) Nonoperative treatment and (2) operative treatment. 1. Nonoperative management or conservative management: Includes complete cessation of activity, rehabilitation with strengthening of the abdominal and paraspinal musculature, minimization of pelvic tilt, and antilordotic bracing. The brace is worn for 23 h/day for minimum of 3–6 months. If clinical symptoms improve, the brace can be gradually weaned through a period of part-time wear. Vigorous activities are restricted and back, abdominal and core strengthening exercises are prescribed. If the symptoms are more severe, a brief period of bed rest or brace immobilization may be required. Once the pain has improved and the hamstring tightness has lessened, the child is allowed progressive activities. Yearly examinations with standing spot lateral radiographs of the lumbosacral spine are advised to rule out the development of spondylolisthesis. If the patient remains asymptomatic, limitation of activities or contact sports is not necessary. If the SPECT scan reveals metabolic activity and a CT scan shows thickening of the pars, avoidance of aggravating activity and core strengthening exercises are recommended. If the SPECT scan is metabolically active and CT indicates an acute stress fracture, a 3-month trial of orthotic treatment is warranted. If the defect has not healed in 3 months, continued orthotic wear is not indicated. The CT scan is the most helpful radiographic technique to determine the presence or absence of healing. Have excellent relief of symptoms or only minimal discomfort at long-term follow-up. If a child does not respond to conservative measures, other causes of back pain should be ruled out. Special attention should be paid to children whose symptoms do not respond to bed rest

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or who have objective neurological findings. A very small percentage of children with spondylolysis who do not respond to conservative measures and in whom the other possible causes of back pain have been eliminated may require. 2. Operative treatment: indications: Persistent symptoms despite 9  months to 1  year of conservative treatment, Persistent tight hamstrings, abnormal gait, and pelvic-trunk deformity. Development of a neurological deficit. In a skeletally immature patient with slippage greater than 50% or a mature adolescent with a slip greater than 75%, even if the patient is asymptomatic.

Surgical Goals 1 . Address the pars defect and the rattler 2. Decompress the foraminal stenosis 3. Address the degenerate disc/s 4. Address the dynamic instability

Operative Options 1 . Direct repair of pars defect. 2. Decompression and fusion without fixation. 3. Decompression and fusion with pedicle screw fixation. 4. Posterolateral in situ fixation. 5. Partial reduction and fixation. 6. Complete reduction, fusion, and fixation. 7. Posterolateral interbody fusion and fixation/PLIF. 8. Trans foraminal interbody fusion/TLIF. 9. Anterior interbody fusion/ALIF. PS: repair preserves motion segment; fusion removes motion segment.

Decompression: Absolute Indications 1. Neurological deficit 2. Non-relieving leg pain 3. Sphincter dysfunction 4. Claudication The Gill procedure: Removal of the loose laminar arch; foraminotomy + facetectomy. Never in isolation. Associated with ↑ pseudarthrosis rate.

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Decompression and Interbody Fibular Graft Fixation I n Situ Posterolateral Fusion L5 S1 only adequate: (1) Burkus, JBJS Am (1992), (2) Frennerd, Spine (1991), (3) Ishikawa, Spine (1994). Improvement in leg pain even when not decompressed: deLobrresse, Clin Orthop (1996). Posterior Instrumentation Better fusion rate, better clinical outcomes: (1) Zdeblick, Spine (1993), (2) Yuan, Spine (1994), (3) Bjarke, Spine (2002), (4) Deguchi, J Spinal Dis (1998), (5) Ricciardi, Spine (1995). Un-instrumented better for osteoporotic bones: Moller, Spine (2000). Levels to instrument: Look at the changes at the levels above. Higher slip angle: retro-listhesis above the slip.

Repair of Spondylolytic Defect Principles Debridement, Grafting of the site with autogenous bone graft, and compression across the fracture. If a direct repair of the spondylolysis is considered, the disc status should be evaluated with MRI. If disc degeneration is significant, an arthrodesis at that level may be a better choice.

Procedures 1. Buck technique. 2. Scott wiring and modified Scott technique. 3. Kakiuchi procedure (repair with an ipsilateral pedicle screw and hook). 1. Buck Technique: Direct repair of pars interarticularis: Fibrous tissue at the pars defect is identified, thoroughly débrided, and stabilized with a 4.5-mm stainless steel cortical screw in compression [5]. This technique was indicated only in cases in which the gap was smaller than 3–4 mm. The narrowness of the lamina, a minimal displacement or malposition of the screw can lead to implant failure or complications Such as nerve root irritation, injury to the posterior arch or dura, or pseudarthrosis. Better clinical results have been obtained in patients younger than age 30 years, possibly because chronic instability leads to degenerative disc disease in older patients, which causes continued symptoms despite fusion of the defect. 2. Scott technique: A stainless steel wire is looped from the transverse processes to the spinous process of the level involved and tightened, in conjunction with local

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iliac crest bone graft. This wire creates a tension band construct, placing the pars defect under compression, and holds the bone graft in place. Bradford and Iza reported 80% good to excellent results and 90% radiographic healing of the defects. This technique requires greater surgical exposure, with extensive stripping of the muscles to expose the transverse process. Complications such as wire breakage are common with this technique. Modified Scott technique: Modified Scott technique in which a wire is passed around the cortical screws introduced into both pedicles and tightening it beneath the spinous process. Biomechanical tests show that fixation of the wire to the pedicle screw does not increase the stiffness of the system. This technique has defect healing rates of 86–100% [6]. 3. Kakiuchi technique: Kakiuchi reported successful union of pars defects with the use of a pedicle screw, laminar hook, and rod system. A pedicle screw is placed in the pedicle above the pars defect. The pars defect is bone grafted. A rod is placed in the pedicle screw and then into the caudal laminar hook, and compression is applied [7]. This gives a more stable construct than that afforded by wire techniques.

In Situ Pedicle Screw Fixation Grob’s technique: Direct pediculobody fixation: In situ fusion is a relatively safe and reliable procedure associated with a high rate of arthrodesis and at lower risk of neurologic injury. Fixation of the segment is achieved by two cancellous bone screws inserted bilaterally through the pedicles of the lower vertebra into the body of the upper slipped, vertebra. In advanced intervertebral disc degeneration. Inter-body fusions: theoretical considerations: Anterior column support. Bio-­ mechanically superior: large area for fusion; grafts under compressive loads; degenerate disc removed. Consider disc height. Build in the lordosis. Treatment of severe (high dysplastic) spondylolisthesis: Most authors agree that slippage of more than 50% requires fusion. The reduction of spondylolisthesis with instrumentation improves the chance of fusion, but these procedures have many risks and potential complications/neurological injury. Fusion in situ should be considered a method of choice in severe L5 isthmic spondylolisthesis. PS: in severe spondylolisthesis, the sacral roots are stretched over the back of the body of S1 and are sensitive to any movement of L5 on S1. Treatment of spondyloptosis L5 vertebrectomy [8].

References 1. Brain WR, Northfield D, Wilkinson M. The neurological manifestations of cervical spondylosis. Brain. 1952;75(2):187–225. 2. Patel AA, Spiker WR, Daubs M, et  al. Evidence of an inherited predisposition for cervical spondylotic myelopathy. Spine (Phila Pa 1976). 2012;37(1):26–9.

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3. Smith-Petersen MN, Larson EB, AuFranc OE. Osteotomy of the spine for correction of flexion deformity in rheumatoid arthritis. J Bone Joint Surg (Am). 1945;27-A:1–11. 4. Wiltse LL, Newman PH, Macnab I. Classification of spondylolysis and spondylolisthesis. Clin Orthop Relat Res. 1976;117:23–9. 5. Buck JE. Direct repair of the defect in spondylolisthesis. Preliminary report. J Bone Joint Surg. 1970;52-B:432–7. 6. Scott JHS. The Edinburgh repair of isthmic (Group II) spondylolysis. J Bone Joint Surg Br. 1987;69:491. 7. Kakiuchi M. Repair of the defect in spondylolysis. Durable fixation with pedicle screws and laminar hooks. J Bone Joint Surg Am. 1997;79:818–25. 8. Gaines RW, Nicholds WK. Treatment of spondyloptosis by two-stage L5 vertebrectomy and reduction of L4 onto S1. Spine. 1985;10:680–6.

Poliomyelitis and Spina Bifida

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Definition Poliomyelitis (polio) is a highly infectious viral disease caused by any of three serotypes of human enteric poliovirus, which mainly affects young children. The virus is transmitted through contaminated food and water, and multiplies in the intestine, from where it can invade the nervous system. Michael Underwood described poliomyelitis as a debility of the lower extremities in the second edition of his book Treatise on the Diseases of Children, 1789. In 1840, Jacob von Heine described anterior acute poliomyelitis and the differences with other types of paralysis. Lesions in the spinal medulla were demonstrated in 1870 by Jean-Martin Charcot and Alex Joffroy. Poliomyelitis was recorded in the late 1700s with the first epidemic in the late 1800s. The cases that were reported in 1979 where mild and self-limited and do not result in paralysis. The Bavarian neurologist Wilhelm Heinrich Erb coined the term “anterior acuta poliomielitis” for clinical adult cases. In Greek, polios means gray and myelos medulla. Of course, the ending –itis means inflammation of Polio = gray matter and Myelitis = inflammation of the spinal cord. Poliovirus, the causative agent of poliomyelitis, is a human enterovirus and a member of the family of Picornaviridae. It is composed of a RNA genome and a protein capsid. The genome is single-stranded positive-sense RNA. Serotypes: Specificity to receptor restricts mutation rate; slow genetic drift. Three serotypes with no cross immunity: Type 1 polio 90%, weakest, only 1% causes neuroparalysis; Type 2 polio 9% (eliminated); and Type 3 polio 1%.

K. M. Iyer (*) Royal Free Hampstead NHS Trust, Royal Free Hospital, London, UK © Springer Nature Switzerland AG 2019 K. M. Iyer, W. S. Khan (eds.), General Principles of Orthopedics and Trauma, https://doi.org/10.1007/978-3-030-15089-1_13

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It has greater temperature stability and requires trivalent polio vaccine. Polioviruses can also vary in phenotype of virulence, host cell lysis, and ability to raise host defense triggers. Polio infection: The incubation period is 3–21 days, on average 14 days. Predisposing factors: 1 . Severe muscular activity can lead to paralysis, as it increases the blood flow. 2. May produce paralysis in the limb or bulbar region. 3. Injecting vaccines with adjuvant can predispose to paralysis. 4. Patients who underwent tonsillectomy have higher incidence as IgG secretion is reduced. 5. Rarely oral polio vaccine produces poliomyelitis. Transmission: Poliovirus is transmitted through both oral and fecal routes. Implantation and replication occurring either in the oropharyngeal or in the intestinal mucosa. Most infected for 7–10 days before and after clinical symptoms begin.

Pathogenesis and Pathology The virus enters through mouth, and multiplies in oropharynx tonsils and intestines. It is excreted in stool. It enters the CNS from blood and spreads along the axons of peripheral nerves to CNS.  It then progresses along the fibers of the lower motor neurons spinal cord or brain. They destroy the anterior horn cells of the spinal cord and do not multiply in muscles; only muscles manifest with weakness and flaccid paralysis result is secondary. It occasionally produces myocarditis and lymphatic hyperplasia. Paralytic disease occurs in 0.1–1% of those who become infected with the polio virus. Paralysis of the respiratory muscles or from cardiac arrest if the neurons in the medulla oblongata are destroyed. Patients have some or full recovery from paralysis, usually apparent with proximally 6 months. Clinical features: Often child around the age of 9 months which gives history of mild pyrexia associated with diarrhea. There is inability to move a part or whole of the limb along with paralysis of varying severity and asymmetrical. Types of poliomyelitis: There are mainly two types, namely—spinal polio and bulbar polio. Spinal polio: Spinal polio is the most common form of paralytic poliomyelitis; it results from viral invasion of the motor neurons of the anterior horn cells, or the ventral (front) gray matter section in the spinal column (Fig. 13.1). The virus invasion causes inflammation of the nerve cells, leading to damage or destruction of motor neuron ganglia. Bulbar polio: Making up about 2% of cases of paralytic polio. Bulbar polio occurs when poliovirus invades and destroys nerves within the bulbar region of the brain stem (Fig. 13.2). Nerves weaken the muscles supplied by the cranial nerves, producing symptoms of encephalitis.

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Fig. 13.1  Line diagram of the spinal polio

Fig. 13.2  Line diagram of bulbar polio

Virus is mainly localized in anterior horn cells and certain brain stem motor nuclei.

Clinical Manifestations 1 . Asymptomatic infection (90–95%) 2. Abortive poliomyelitis 3. Non-paralytic polio myelitis 4. Paralytic polio myelitis (1%)

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Clinical Course Three stages, namely—acute stage, convalescent stage, and the chronic stage. 1. Acute stage: It lasts usually 7–10 days with all superficial reflexes absent and the deep tendon reflexes disappear when the muscle group is paralyzed. Treatment in this stage mainly consists of bed rest, analgesics, hot packs, anatomical positioning of limbs to prevent flexion contracture, and gentle passive ROM exercises. Distribution: Lower limbs 92%, trunk + LL 4%, LL + UL 1.33%, bilateral UL 0.67%, and trunk + UL + LL 2%. 2. Convalescent stage: This is the recovery phase with varying degree of spontaneous recovery in muscle power taking place. There is a  >80% return of strength—recovered muscles and  10–11 years 6. Ankle arthrodesis in >18 years

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Claw Toe It is caused by hyperextension of MTP and flexion of IP and seen when long toe extensors are used to substitute dorsiflexion of ankle. The treatment is as follows: (a) For lateral toes division of extensor tendon by z-plasty incision, dorsal capsulotomy of MTP and (b) For great toe, the FHL transferred to prox. phalanx, IP joint arthrodesis (or) division of EHL, proximal slip attached to the neck of first MT, distal slip to soft tissues+ IP arthrodesis. Dorsal bunion: It is seen when the shaft of first MT is dorsiflexed and great toe is plantar flexed and seen in muscle imbalance, between anterior tibial and peroneus longus muscle. Lapidus operation [4]: It is done to remove abnormal bone from MT head. If anterior tibial is overactive—detach its tendon and transfer it to second or third cuneiform bone or remove the inferior wedge of bone from first metatarso cuneiform joint to bring the end of the FHL through the tunnel in first MT and anchor to the capsule over dorsum of MTP joint.

Equinus Foot The anterior tibial muscle is affected and the deformity is caused by the peroneal and long toe extensor muscles. The treatment: is by serial stretching and cast, Achilles tendon lengthening along with posterior capsule release or a posterior bone block of Campbell with a Lambrinudi operation or Pantalar arthrodesis. Equinovarus deformity: It is caused by affection of the tibialis anterior and long toe extensors and peroneal muscle. Its treatment: (1) young children 4–8  years: stretching of plantar fascia and posterior ankle structure with wedging casting and TA lengthening with posterior capsulotomy and anterior transfer of tibialis posterior or split transfer of tibialis anterior to insertion of p. brevis (if tibialis posterior is weak) and (2) children >8 years: triple arthrodesis along with anterior transfer of tibialis posterior or a modified jones procedure. Equinovalgus deformity: This is caused by anterior and posterior muscle weakness with strong peroneals and gastrocnemius-soleus muscle. Treatment: (1) skeletally immature: repeated stretching and wedging cast with TA lengthening and anterior transfer of peroneals with subtalar arthrodesis and anterior transfer of peroneals (Grice and green arthrodesis) and (2) skeletally mature: TA lengthening with triple arthrodesis followed by anterior transfer of peroneals. Cavovarus deformity: It is seen due to imbalance of extrinsic muscles or by unopposed short toe flexors and other intrinsic muscles. It is treated by plantar fasciotomy, release of intrinsic muscles, and resecting motor branch of medial and lateral plantar nerves before tendon surgery. The peroneus longus is transferred to the base of the second MT and the extensor hallucis longus is transferred to the neck of first MT.

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Calcaneus deformity: It is caused by affection of the gastrocnemius-soleus muscles. Keeping in slight equinus position during acute stage of poliomyelitis. It is treated by plantar fasciotomy, intrinsic muscle release before tendon transfer. It depends on residual strength of GS muscle. Transfer of peroneus brevis and tibialis posterior to the heel. Both peroneals transferred for calcaneovalgus deformity. The posterior tibial and FHL can be transferred for cavovarus deformity and the anterior tibial tendon can be transferred posteriorly—DRENNAN TECHNIQUE. For mild deformity—braces used; tenodesis of Achilles tendon to fibula. There is progressive equinus deformity with subsequent growth in pt with Achilles tenodesis.

Flail Foot Here all muscles are paralyzed distal to the knee and an equinus deformity results because of passive plantar flexion and cavoequinus deformity because intrinsic muscles may retain some function. It is best treated by a radical plantar release with tenodesis. In older pt mid-foot wedge resection may be required or an ANKLE ARTHRODESIS.

Spina Bifida Definition Spina bifida (Latin: “split spine”) is a developmental congenital disorder caused by the incomplete closing of the embryonic neural tube. Some vertebrae overlying the spinal cord are not fully formed and remain unfused and open. If the opening is large enough, this allows a portion of the spinal cord to protrude through the opening in the bones. There may or may not be a fluid-filled sac surrounding the spinal cord. Incidence: Spina bifida is one of the most common birth defects, with an average worldwide incidence of one to two cases per 1000 births, but certain populations have a significantly greater risk. Myelomeningocele is the most significant and common form, and this leads to disability in most affected individuals. This condition is more likely to appear in females; the cause for this is unknown.

Causes 1. Maternal diabetes. 2. Family history. 3. Obesity.

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4. Increased body temperature from fever or external sources such as hot tubs and electric blankets may increase the chances of delivery of a baby with a spina bifida. 5. Medications such as some anticonvulsants. 6. Pregnant women taking valproic acid have an increased risk of having children with spina bifida. 7. Genetic basis. 8. Folic acid deficiency.

Embryology Spina bifida is caused by the failure of the neural tube to close during the first month of embryonic development (often before the mother knows she is pregnant). Under normal circumstances, the closure of the neural tube occurs around the 23rd (rostral closure) and 27th (caudal closure) day after fertilization. Types: Spina bifida malformations fall into three categories: 1 . Spina bifida occulta. 2. Spina bifida cystica with meningocele. 3. Spina bifida cystica with myelomeningocele (The most common location of the malformations is the lumbar and sacral areas). 1. Spina bifida occulta: Occulta is Latin for “hidden.” This is the mildest form of spina bifida. In occulta, the outer part of some of the vertebrae is not completely closed. The splits in the vertebrae are so small that the spinal cord does not protrude. The skin at the site of the lesion may be normal, or it may have some hair growing from it; there may be a dimple in the skin, or a birthmark. The incidence of spina bifida occulta is approximately 10% of the population, and most people are diagnosed incidentally from spinal X-rays. 2. Meningocele: The least common form of spina bifida is a posterior meningocele (or meningeal cyst) (Fig. 13.3). In this form, the vertebrae develop normally, but the meninges are forced into the gaps between the vertebrae. 3. Myelomeningocele: This type of spina bifida often results in the most severe complications (Fig. 13.4). In individuals with myelomeningocele, the unfused portion of the spinal column allows the spinal cord to protrude through an opening. The meningeal membranes that cover the spinal cord form a sac enclosing the spinal elements. Spina bifida with myeloschisis is the most severe form of myelomeningocele. In this type, the involved area is represented by a flattened, plate-like mass of nervous tissue with no overlying membrane. The exposure of these nerves and tissues makes the baby more prone to life-threatening infections such as meningitis. The protruded portion of the spinal cord and the nerves that originate at that level of the cord are damaged or not properly developed. As a result, there is usually some degree of paralysis and loss of sensation below the level of the spinal cord defect.

306 Fig. 13.3  Line diagram of myelocoele

Fig. 13.4  Line diagrams of meningomyelocele and meningocele

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Clinical Manifestations Physical Signs 1. Orthopedic abnormalities (i.e., club foot, hip dislocation). 2. Bladder and bowel control problems, including incontinence, urinary tract infections, and poor renal function. 3. Pressure sores and skin irritations. 4. Abnormal eye movement. 5. 68% of children with spina bifida have an allergy to latex. 6. Paralysis. 7. Scoliosis. 8. Back pain. 9. Partial or complete lack of sensation. 10. Weakness of the hips, legs, or feet of a newborn. 11. Other symptoms may include: hair at the back part of the pelvis called the sacral area, dimpling of the sacral area, difficulty swallowing, which can lead to choking, hoarseness, breath-holding and problems in breathing during sleep, and below-average intelligence. Neurological complications: Many individuals with spina bifida have an associated abnormality of the cerebellum, called the Arnold Chiari II malformation. In affected individuals, the back portion of the brain is displaced from the back of the skull down into the upper neck. Executive function: Specific areas of difficulty in some individuals include planning, organizing, initiating, and working memory. Problem-solving, abstraction, and visual planning may also be impaired. Children with spina bifida and shunted hydrocephalus have higher rates of ADHD. Academic skills: Individuals with spina bifida may struggle academically, especially in the subjects of mathematics and reading. In one study, 60% of children with spina bifida were diagnosed with a learning disability. Social complications: Compared to typically developing children, youths with spina bifida may have fewer friends and spend less time with peers.

Diagnostic Evaluation Pregnancy screening: Neural tube defects can usually be detected during pregnancy by testing the mother’s blood (AFP screening) or a detailed fetal ultrasound. Increased levels of maternal serum alpha-fetoprotein (MSAFP) should be followed up by two tests—an ultrasound of the fetal spine and amniocentesis of the mother’s amniotic fluid (to test for alpha-fetoprotein and acetylcholinesterase). Prevention: Dietary supplementation with folic acid has been shown to be helpful in reducing the incidence of spina bifida. Sources of folic acid include whole grains, fortified breakfast cereals, dried beans, leaf vegetables, and fruits. It is recommended that any woman considering becoming pregnant take 0.4  mg of folic acid a day. Pregnant women need 1 mg/day.

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Treatment There is no known cure for nerve damage caused by spina bifida. The spinal cord and its nerve roots are put back inside the spine and covered with meninges. In addition, a shunt may be surgically installed to provide a continuous drain for the excess cerebrospinal fluid produced in the brain, as happens with hydrocephalus. Shunts most commonly drain into the abdomen or chest wall. Monitor growth and development of bones, muscles, and joints. Treat and evaluate nervous system issues, such as seizure disorders. Physical therapy and speech therapy are useful. Immediate care: (1) Place the child in prone position, (2) cover the affected area with sterile gauze piece dipped in normal saline, (3) maintain hydration, and (4) monitor for associated defects. Lifelong treatment: (1) Catheters, (2) braces, (3) high-fiber diet, and (4) antibiotics may be used to treat or prevent infections such as meningitis or urinary tract infections.

Complications (1) Difficult delivery with problems resulting from a traumatic birth, including cerebral palsy and decreased oxygen to the brain, (2) frequent urinary tract infections, (3) hydrocephalus, (4) loss of bowel or bladder control, (5) meningitis, and (6) permanent weakness or paralysis of legs.

References 1. Peabody FW, Draper G, Dochez AR. A clinical study of acute poliomyelitis. Monograph 4. New York: Rockefeller Institute for Medical Research; 1912. p. 12–8. 2. Breusch SJ, Wenz W, Döderlein L. Function after correction of a clawed great toe by a modified Robert Jones transfer. J Bone Joint Surg (Br). 2000;82-B:250–4. 3. Reidy JA, Broderick TF, Barr JS. Tendon transplantations in the lower extremity: a review of end results in poliomyelitis. I. Tendon transplantations about the foot and ankle. J Bone Joint Surg Am. 1952;34:900–8. 4. Blitz NM, Lee T, Williams K, Barkan H, DiDimenico LA. Early weight bearing after modified lapidus arthodesis: a multicenter review of 80 cases. J Foot Ankle Surg. 2010;49(4):357–62.

Cerebral Palsy

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Brain development: Brain grossly differentiates into cerebrum and cerebellum during first trimester of embryonic life. The neurons begin to develop in second trimester, and by the end of second trimester all neurons are formed and any damage occurring now is irreversible. Synaptic connections occur in third trimester. It was first described in 1862 by William John Little, an orthopedic surgeon, who observed that children with tone and developmental abnormalities often had prolonged labor, prematurity, or breech delivery. Cerebral palsy was known as Little’s disease [1] for decades. The term cerebral palsy originated with William Osler and Sigmund Freud when static encephalopathy has been used interchangeably with cerebral palsy. Definition: It is a static, nonprogressive disorder of CNS secondary to an insult to immature brain, resulting in varying degrees of motor milestone delay and dysfunction. CP is a disorder of tone, posture, or movement, which results in paralysis, weakness, incoordination, or abnormal movement. Incidence: It is about 2.4–2.7 for every 1000 live births.

Etiology Prenatal 1. Infection: TORCH complex, HIV (TORCH complex or syndrome refers to infection of a developing fetus or newborn by any of a group of infectious agents. “TORCH” is an acronym meaning (T)oxoplasmosis, (O)ther agents, (R)ubella (also known as German measles), (C)ytomegalovirus, and (H)erpes simplex.

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Infection with any of these agents (i.e., Toxoplasma gondii, rubella virus, ­cytomegalovirus, herpes simplex viruses) may cause a constellation of similar symptoms in affected newborns.) Cerebral malformation Obstetrical complication: pre-eclampsia, eclampsia, abruptio placentae, placenta previa, placental infarction Maternal diseases Abuse of drugs

Perinatal 1. Prematurity 2. Low birth weight 3. Complicated delivery 4. Asphyxia 5. Cerebral trauma 6. Hyperbilirubinemia 7. Blood incompatibilities 8. Infections: herpes simplex, meningitis 9. Severe hypoglycemia

Post natal 1. Infections: meningitis, encephalitis 2. Head injury 3. Cerebral anoxia 4. Aspiration 5. Asphyxia 6. Seizures 7. Near drowning 8. Cardiac arrest 9. Cerebrovascular accidents 10. Sickle cell anemia 11. Vascular malformations Classification: Because of the wide variability in presentation and types of cerebral palsy, there is no universally accepted classification scheme. Classification based on geographical distribution: (1) Monoplegia, (2) hemiplegia, (3) paraplegia, (4) diplegia, (5) quadriplegia, (6) double hemiplegia, and (7) total body.

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Geographical classification of cerebral palsy [2] Type Monoplegia Hemiplegia Paraplegia Diplegia Quadriplegia Double hemiplegia Total body

Description Only one extremity involved, usually lower. Both extremities on one side involved, Usually upper extremity involved more than lower. Both lower extremities equally involved. Lower extremities more involved than upper extremities with fine motor/ sensory abnormalities in the upper extremity. All extremities equally involved with normal head/neck control. All extremities involved, the upper more than the lower. All extremities severely involved with no head/neck control.

Physiologic Classification [3] Types (Fig. 14.1) 1. 2. 3. 4. 5. 6. 7.

Spastic Athetoid Choreiform Rigid Ataxic Hypotonic Mixed

1. Spastic: It is the most common type and is associated with injury to pyramidal tracts in immature brain. 2. Athetoid: It is usually associated with injury to extrapyramidal tracts with dyskinetic purposeless movements. Dystonia or hypotonia can occur with athetoid cerebral palsy. Fig. 14.1  Line diagram of types of cerebral palsy

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3. Choreiform: It is characterized by continual purposeless movements of wrists, fingers, toes, and ankles. 4. Rigid: It is the most hypertonic form in the form of cogwheel or leadpipe rigidity. 5. Ataxic: It is very rare due to injury to the developing cerebellum resulting in a disturbance of coordinated movement, viz. walking. It is characterized by weakness, incoordination, a wide based gait, and trouble with fine and rapid movements. 6. Hypotonic: It is the passing stage in spastic or ataxic cerebral palsy. 7. Mixed: It shows signs of pyramidal and extrapyramidal deficits.

Spastic Diplegia Bilateral spasticity of legs, which is first noticed when infant begins to crawl, tends to drag the legs behind more (commando crawl). There is severe spasticity and the application of diaper is difficult due to excess adduction of hips. It has brisk reflexes with ankle clonus. There is a scissoring posture of lower extremity when suspended by axilla. Walking tiptoes, disuse atrophy, impaired growth of lower extremity. Intellectual development normal with minimal seizures. The CT/MRI shows a periventricular leukomalacia of white matter mainly lower limb fibers. All spastic types characterized by toe walking, a crouched gait, and flexed knee, with scissoring. Spastic hemiplegia: Arms often more involved than leg—difficulty in hand manipulation is obvious by 1 year. Delayed walking—18–24 months. Equinovarus deformity of foot, walks on tip toes because of increased tone. Affected upper limb has dystonic posture when child runs. The deep tendon reflexes are increased, ankle clonus, and the Babinski sign + 1/3rd have seizure disorder while 25% have MR. The CT/MRI shows atrophic cerebral hemisphere with dilated lateral ventricle contralateral to the affected side. Spastic quadriplegia: It is the most severe form and most common. All extremities severely impaired with the high association with MR and seizures. There are flexion contractures of knees and elbows. Athetoid cerebral palsy: After age 1 year—athetoid movements become evident and the speech is affected (slurred, voice modulation impaired) due to involvement of oropharyngeal muscles. The upper motor neuron signs are not present. Seizure uncommon. Intellect is preserved. Characterized by an exaggerated step, hip and knee hyperextension, a backward lean, and shoulder girdle and trunk extension.  ross Motor Function Classification G 1. Has nearly normal gross motor function. 2. Walks independently, but has limitations with running and jumping. 3. Uses assistive devices to walk and wheelchair for long distances. 4. Has ability to stand for transfers, but minimal walking ability; depends on wheelchair for mobility. 5. Lacks head control, can’t sit independently, is dependent for all aspects of care. Associated Problems: 1. Mental retardation 2. Communication disorders 3. Behavioral disorder

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4. Seizures 5. Vision disorders 6. Hearing loss 7. Somatosensation (skin sensation, body awareness) 8. Temperature instability 9. Nutrition 10. Drooling 11. Dentition problems 12. Neurogenic bladder 13. Neurogenic bowel 14. Gastroesophageal reflux 15. Dysphagia 16. Autonomic dysfunction Gait: Gait in cerebral palsy: (1) idiopathic toe walking, (2) spastic knee gait, and (3) crouch gait.

Clinical Assessment. Goals of Physical Examination 1 . Determine grades of muscle strength and selective control. 2. Evaluate muscle tone and determine type. 3. Evaluate degree of deformity/contracture at each joint. 4. Assess linear, angular, and torsional deformities of spine, long bones, hands, and feet. 5. Appraise balance, equilibrium, and standing/walking posture.

Diagnosis 1. History 2. Examination 3. X-ray skull-intracranial calcification 4. EEG 5. CT/MRI 6. Test of hearing, vision 7. IQ test Goals of management (treatment): Achievable goals should be set. The child with CP becomes the adult with CP. Goals based on needs of adults are as follows: 1. Communication: verbal/nonverbal 2. Mobility 3. Walking 4. Activity of daily living (ADL) feeding, dressing, toileting, bathing 5. Turn focus of parents from the disease to the goal-oriented approach Types of management (Treatment) include (1) control of spasticity, (2) physical therapy, (3) orthotics, and (4) orthopedic surgery.

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Control of spasticity: Spasticity is present in most patients with CP (65%). When it is reduced, patients may perform integrated muscle movement to develop muscle strength in order to function at a higher level. The Approaches: (1) Selective dorsal rhizotomy, (2) intrathecal baclofen, or (3) botulinum-A toxin. Other oral medicines used in cerebral palsy: (1) Dantrolene, (2) Flexeril, (3) Antiepileptic drugs such as Phenytoin, Sodium Valproate, and Carbamazepine. Physical therapy: Conventional PT: works on muscles, tendons, and ligaments by (1) active exercises, (2) passive ROM exercises, (3) passive stretching, and (4) bracing. Involve parents as much as possible (even if they resist). Do not raise false hopes which could increase frustration. Orthotics: Casting. Short leg casts are applied with extended toe plates, careful molding of the heel and metatarsal head control. For a period of time varies but usually a minimum of 6 weeks, and is followed by the use of orthoses. There is a limited role for casting in patients with cerebral palsy. Orthoses. These can be helpful in improving gait in ambulatory patient with cerebral palsy. Ankle-foot orthoses (AFO) are most commonly prescribed to assist the child with positioning of the ankle and foot during gait.

Orthopedic Procedures Orthopaedic procedures can be planned as follows: The primary deformity needs treatment as the compensatory treatment may improve without intervention. Surgery usually done to prevent structural changes—usually early and to improve function—usually later.

Prerequisites for Effective Surgery 1. Type: spastic. 2. Extent: hemiplegics/diplegics: good results; quadriplegics: minimal improvement. 3. Age: 3–12 years. 4. IQ: good. 5. Good upper limb function: for walking. 6. Underlying muscle power: not weak. 7. Walker/non-walker: surgery hardly changes state but improves gait.

Timing for Orthopedic Surgery 1. For structural changes: Early, e.g., hip subluxation, usually 30% uncoverage/broken Shenton’s line). Hip at risk: Because early intervention can be very effective in preventing or delaying the development of dislocation, considerable work has been done to identify hips at risk. Operative treatment: Varus derotational osteotomy, usually combined with soft-­ tissue releases, is indicated for patients with excessive anteversion and valgus deformity of the proximal femur and a hip that is either subluxated or dislocated. A combined One-Stage Correction of Spastic Dislocated Hip (San Diego Procedure) A medial approach (soft-tissue release) with anterior approach (open reduction) is carried out by a lateral approach (femoral osteotomy) along with anterior approach (pericapsular pelvic osteotomy), Proximal femoral resection is an alternative for painful dislocated hips. Hip arthrodesis: The ideal candidate is a patient with unilateral disease and no spinal involvement. Hip arthrodesis may be preferable in ambulatory patients because it allows weight bearing, in contrast to proximal femoral resections. Knee: Deformities of the knee rarely occur in isolation. The hip and the knee are tightly coupled because of the muscles that cross both joints, the “two-joint muscles.” Deformities of the knee are mainly of four types: flexion deformity, recurvatum of the knee, knee valgus or patella alta. Flexion deformity: Most common knee deformity in patients with cerebral palsy and frequently occurs in ambulatory children leading to a crouching gait. Knee assessment (knee flexion): Straight leg raising angle 11.5  mg/dL), renal insufficiency (creatinine >2 mg/dL), anemia (Hb 1 month and not responding to nonoperative management or red flags are present such as infection (IV drug user, h/o of fever and chills), tumor (h/o or cancer), trauma (h/o car accident or fall), cauda equina syndrome (bowel/bladder changes). MRI with gadolinium: useful for revision surgery as it allows to distinguish between post-surgical fibrosus (enhances with gadolinium) vs. recurrent herniated disc (does not enhance with gadolinium).

Treatment Rest and physical therapy, and anti-inflammatory medications—indications: First line of treatment for most patients with disc herniation—90% improve without surgery, technique: bed rest followed by progressive activity as tolerated;

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medications—NSAIDS, muscle relaxants (more effective than placebo but have side effects)—oral steroid taper. Physical therapy: extension exercises extremely beneficial; traction; chiropractic manipulation.

Indications Second line of treatment if therapy and medications fail, technique: epidural or selective nerve block, outcomes: leads to long lasting improvement in ~50% (compared to ~90% with surgery). The results are best in patients with extruded discs as opposed to contained discs and utilizes a paraspinal approach of Wiltse [2]. Laminotomy and discectomy (microdiscectomy): indications: persistent disabling pain lasting more than 6 weeks that have failed nonoperative options (and epidural injections); progressive and significant weakness; cauda equina syndrome, technique: can be done with small incision or through “tube” access, outcomes: positive predictors for good outcome with surgery such as (1) leg pain is chief complaint (as opposed to back pain), (2) positive straight leg raise and (3) weakness that correlates with nerve root impingement seen on MRI. Outcomes of surgery: improvement of pain and function, 70% improvement of back pain, neurologic recovery less predictable; 50% motor or sensory recovery, 25% reflex recovery, patients with worker’s compensation claims have less relief from symptoms and less. Improvement in quality of life with surgical treatment: Far lateral microdiscectomy-indications; for far-lateral disc herniations-technique. Dural tear (1%): If have tear at time of surgery then perform water-tight repair. Recurrent HNP: can treat nonoperatively initially; Discitis (1%), vascular catastrophe caused by breaking through anterior annulus and injuring vena cava/aorta.

Thoracic HD Relatively uncommon and makes up only 1% of all HNP. Epidemiology: demographics—most commonly seen between fourth and sixth decades of life, as the disc desiccates it is less likely to actually herniate; location— usually involves middle to lower levels; T11–T12 most common level; 75% of all thoracic disc herniations occur between T8 and T12; Risk factors—underlying Scheuermann’s disease may predispose to thoracic HNP. Pain: axial back or chest pain is most common symptom, thoracic radicular pain which is band-like chest or abdominal pain along course of intercostal nerve, arm pain (see with HNP at T2–T5). Neurologic: numbness, paresthesias, sensory changes, myelopathy, paraparesis, bowel or bladder changes (15–20% of patients), sexual dysfunction.

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Localized tenderness; root symptoms—dermatomal sensory changes (paresthesias and dysesthesia). Cord compression and findings of myelopathy—weakness. Weakness or mild paraparesis with abnormal rectal tone—upper motor neuron findings such as hyperreflexia, sustained clonus, positive Babinski sign, Gait changes with wide based spastic gait. Horner’s syndrome seen with HNP at T2–T5.

Investigations 1. Lateral radiographs—may show disc narrowing or may show calcification (osteophytes). 2. MRI: most useful and important imaging method to demonstrate thoracic disc herniation as it allows for identification of neoplastic pathology; can see intradural pathology; will show myelomalacia; may not fully demonstrate calcified component of herniated disc. Disadvantage is high false positive rate—in a study looking at asymptomatic individuals when 73% had thoracic disk abnormalities, 37% hand frank herniations and 29% of these had cord compression.

Treatment 1. Activity modification, physical therapy, and symptomatic treatment: indications-­ the majority of cases—modalities include immobilization and short term rest, with analgesic and progressive activity restoration with injections may be useful for symptoms of radiculopathy. Outcomes: majority improve with nonoperative treatment. 2. Operative: discectomy with possible hemicorpectomy or fusion, indica tions  =  surgery indicated in minority of patients; acute disc herniation with myelopathic findings attributable to the lesion, especially if there is progressive neurologic deterioration; persistent and intolerable pain. Technique: debate between discectomy with or without fusion is controversial as most studies do indicate that anterior or lateral (via costotransversectomy) is the best approach. (a) Transthoracic discectomy: indications—best approach from central disc herniations but complications being intercostal neuralgia; techniques—can be done with video assisted thoracic surgery (VATS). (b) Costotransversectomy: indications—lateral disc herniation being an extruded or sequestered disc.

Cervical Disc Herniation They are most frequent at C6–7 level but also occur at C5–6 and to a lesser extent at C4–5 and other levels. In relatively younger persons soft disk protrusion is more common than hard disk protrusion.

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Differential diagnosis: types of herniation: intraforaminal herniation: most common type: cause predominately sensory changes. Symptoms: neck pain from nerve root compression; pain radiating into ipsilateral upper extremity w/ paresthesias, numbness, or weakness; pain and paresthesias may be intensified by neck movement, especially by extension or by lateral flexion to side of herniation, and by coughing or straining; Cervical radiculopathy and myelopathy: limitation of neck extension; downward head compression increases pt’s radicular pain and paresthesias, especially if neck is flexed to side of involvement; shoulder abduction relief test: significant relief of arm pain with shoulder abduction; this sign is more likely to be present w/ soft disc herniation, whereas, the test is likely to be negative with radiculopathy caused by spondylosis (osteophyte compression). Spurling’s sign: mechanical stress, such as excessive vertebral motion, may exacerbate symptoms; the provocation of the patient’s arm pain with induced narrowing of the neuroforamen—gentle neck hyperextension with the head tilted toward the affected side will narrow the size of the neuroforamen and may exacerbate the symptoms or produce radiculopathy; ipsilateral rotation of the neck will also increase radiculopathy; downward head compression increases the patient’s radicular pain and paresthesias, especially if the neck is flexed to the side of involvement; provocation of pt’s arm pain w/ induced narrowing of neuroforamen; oblique cervical extension augments root compression and increases symptoms; lower motor neuron dysf(x) (muscle weakness and hypotonia, reduction of deep tendon reflexes) at level of cord compression; upper motor neuron dysfunction (spasticity, clonus, increased deep tendon reflexes, Babinski’s sign, reduction of sensation) below level; loss of erection, bladder, and bowel f(x) may occur; Treatment: surgery is usually performed by a posterior approach through a hemi-­ laminectomy or by an anterior approach to approach the intervertebral disc; anterior approach: anterior approach tends to be more popular with orthopedic surgeons and is especially indicated for central or peri-central disc herniation; decompression is usually followed by arthrodesis; posterior approach: posterior decompression is a smaller operation that takes less time and does not require a bone graft; posterior decompression is most indicated for far-lateral disc herniation.

References 1. Weiner BK, Fraser RD. Foraminal injection for lateral lumbar disc herniation. J Bone Joint Surg Br. 1997;79:804–7. 2. Wiltse LL. The paraspinal sacrospinalis-splitting approach to the lumbar spine. Clin Orthop Relat Res. 1973;91:48–57.

General Affections of the Soft Tissues

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It includes infections of skin, subcutaneous tissue, fascia, and muscle, encompass a wide spectrum of clinical presentations, ranging from simple cellulitis to rapidly progressive necrotizing fasciitis. Diagnosing the exact extent of the disease is critical for successful management of a patient of soft tissue infection.

Types 1. 2. 3. 4. 5. 6. 7. 8.

Impetigo Folliculitis Furuncles Carbuncles Erysipelas Cellulitis Necrotizing fasciitis Pyomyositis

Impetigo Impetigo is an acute, highly contagious gram-positive bacterial infection of the superficial layers of the epidermis. Skin lesions such as cuts, abrasions, and chickenpox can also become secondarily infected (impetiginized) with the same pathogens that produce classic impetigo. Impetigo occurs most commonly in children, especially those who live in hot, humid climates. Pathophysiology: Intact skin is usually resistant to colonization. Requires fibronectin for colonization which leads to infection. K. M. Iyer (*) Royal Free Hampstead NHS Trust, Royal Free Hospital, London, UK © Springer Nature Switzerland AG 2019 K. M. Iyer, W. S. Khan (eds.), General Principles of Orthopedics and Trauma, https://doi.org/10.1007/978-3-030-15089-1_17

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Presentation: Impetigo is characterized by blisters that rupture and coalesce to become covered with a honey-colored crust. Treatment: Treatment is directed at washing the affected areas and applying topical antistaphylococcal treatments, and broad-spectrum oral antibiotics if streptococcal infection is implicated. Mupirocin ointment (Bactroban) and oral Cephalexin are helpful.

Folliculitis Folliculitis is a primary inflammation of the hair follicle that occurs as a result of various infections, or it can be secondary to follicular trauma or occlusion. Management: Antibacterial soap. Antibiotics for Staphylococcus aureus—preferably dicloxacillin or a cephalosporin.

Furuncles and Carbuncles Furuncles and carbuncles are subcutaneous abscesses caused by S. aureus. The lesions are red, tender nodules that may have a surrounding cellulitis. They often drain spontaneously. If fluctuant, these lesions should be incised and drained in conjunction with antibiotics, especially if systemic symptoms or cellulitis is present.

Cellulitis Cellulitis usually follows a breach in the skin. In some cases, there is no obvious portal of entry and the breach may be due to microscopic changes in the skin or invasive qualities of certain bacteria. There is a widespread swelling and redness at the area of inflammation but without definite localization. Risk factors: Trauma, skin break, insect bite, animal bite dental infections, diabetes, and obesity. Clinical features: There is varying degree of fever and toxemia. The affected part is very much swollen and tender and hot. The affected part is warm, swollen, and tender. There is pitting edema and brawny induration. Regional lymph nodes will be enlarged and tender with acute lymphadenitis. Calf tenderness test R/O dvt. Diagnosis: Most often clinical. Blood culture. Ultrasound. Treatment: Rest and elevation of the part to reduce edema. Appropriate antibiotic preferably broad spectrum should be administered. Pain relief. Failure of inflammatory swelling to subside after 48–72 h suggests that an abscess has developed and hence I&D UGA.

Erysipelas It is an acute infection of the upper dermis and superficial lymphatics, usually caused by streptococcus bacteria. Erysipelas [1] is more superficial than cellulitis, and is typically more raised and demarcated.

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Pathophysiology: Bacterial inoculation into an area of skin trauma is the initial event in developing erysipelas. The infection rapidly invades and spreads through the lymphatic vessels. This can produce overlying skin “streaking” and regional lymph node swelling and tenderness. Clinical features: The area affected is erythematous and edematous. The patient may be febrile and have a leukocytosis. Typical rosy rash disappears on pressure and feels stiff. Raised rash of erysipelas has a sharply defined margin which is better felt than inspected. Treatment: Prompt administration of broad-spectrum antibiotics.

Necrotizing Fasciitis It is a severe and extensive necrosis [2] of the superficial fascia and subcutaneous fat with destruction of those tissues. Gram + and − bacteria involved. Pathophysiology: Organisms spread from subcutaneous tissues along superficial and deep planes, facilitated by bacterial enzymes and toxins. Infection causes vascular occlusion, ischemia, and necrosis. Superficial nerves damaged, producing anesthesia. Septicemia ensues. Pathophysiology: M1 and M3 surface proteins increase adherence of the bacteria to the tissues, protect from phagocytosis. Streptococcal pyrogenic exotoxins release cytokines and produce hypotension. Symptoms: pain or soreness of a muscle. The skin may be warm with red or purplish areas of swelling that spread rapidly. There may be ulcers, blisters, or black spots on the skin. Fever, chills, fatigue (tiredness), or vomiting may follow the initial wound or soreness. Diagnosis: History and physical examination of the patient! This is a simple diagnostic test that works every time. Microbiology: group A Streptococcus pyogenes, Coliforms, Staphylococcus Aureus, Bacteroides species, and rarely Clostridium septicum. Six Clinical Criteria: 1 . Necrosis of the superficial fascia with undermining of the surrounding tissues. 2. Systemic toxic reaction with altered mental status. 3. Absence of muscle involvement. 4. No Clostridia species isolated. 5. No arterial inflow occlusion. 6. Pathological exam of debrided tissue shows intense leukocytic infiltration, focal fascial and surrounding tissue necrosis and thrombosis of microvasculature. Diagnosis: The Laboratory Risk Indicator for Necrotizing Fasciitis (LRINEC) score. It uses six serologic measures: C-reactive protein, total white blood cell count, hemoglobin, sodium, creatinine, and glucose. A score greater than or equal to six indicates that necrotizing fasciitis should be seriously considered.

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LRINEC-Criteria The scoring criteria are as follows: CRP (mg/L) ≥150: 4 points, WBC count (×103/ mm3) 1 . 25: 2 points Hemoglobin (g/dL) 1 . >13.5: 0 points 2. 11–13.5: 1 point 3. 10: 1 point. Radiology: Standard X-rays of little use. CT more sensitive. MRI and CT can delineate and determine extent of surgical resection. Imaging: Radiology—Plain X-ray: shows gas in tissues only in 30% of cases. Ultrasound: not useful. Treatment: Regardless of the etiology, the primary therapy is emergent surgical debridement and treatment with antibiotics that are active against streptococci, clostridium species, and mixed aerobes and anaerobes. Clindamycin and pen G IV or Ceftriaxone 2 g q12h IV.

Pyomyositis Pyomyositis [3], also known as tropical pyomyositis or myositis tropicans, is a bacterial infection of the skeletal muscles which results in a pus-filled abscess. Deep infection of muscle usually caused by S. aureus and occasionally by group A streptococci or enteric bacilli. Patients present with fever and tender swelling of the muscle; following exercise or muscle injury, the skin is usually minimally involved. Treatment: Surgical debridement and appropriate antibiotics are curative (nafcillin-­oxacillin or vanco 1 g q12h IV).

Clostridial Myonecrosis Principally C. perfringens but C. novyi and C. septicum also seen. Predisposing event—deep trauma with gross contamination, surgical wound, hematogenous spread from colonic lesion. Incubation period 2–3 days; then explosive spread.

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Presentation = Severe pain out of proportion to clinical findings, erythema and cutaneous blisters, gangrene with crepitus and brown foul smelling discharge with loss of motor function. Pathophysiology: Clostridia spores tissues contamination, severe and open wounds germinate and grow rapidly. If normal tissue ox-red potential lowered, e.g., cell injury. Lesion involves coinfection with an alpha toxin and other exotoxins secreted. Enzymes break down ground substance facilitating spread resulting in fermentation of tissue carbohydrates. “Gas Gangrene” [4]. Treatment: Debridement and excision, with amputation necessary in many cases. Antibiotics alone are not effective because they do not penetrate ischemic muscles sufficiently to be effective. Penicillin is given as an adjuvant treatment to surgery. In addition to surgery and antibiotics, hyperbaric oxygen therapy (HBOT) is used and acts to inhibit the growth of and kill the anaerobic C. perfringens [5].

Compound Palmar Ganglion Introduction: Compound palmar ganglion of tuberculous origin is uncommon. The clinical picture is very typical and is always confirmed by histopathology. Compound palmar ganglion is considered a severe form of extrapulmonary musculoskeletal tuberculosis. Intraoperative finding of melon seed bodies or rice bodies as seen in our case is pathognomonic of tuberculous tenosynovitis [6]. According to literature, extensive debridement and full course chemotherapy brings about a better prognosis. Early diagnosis, complete debulking and appropriate anti-tubercular therapy is the recommended treatment. It can improve the patient functionally by preventing a subsequent arthrodesis which is a major concern for both the surgeon and the patient.

References 1. Bonnetblanc JM, Bedane C.  Erysipela: recognition and management. Am J Clin Dermatol. 2003;4:157–63. 2. Sarani B, Strong M, Pascual J, Schwab CW. Necrotizing fasciitis: current concepts and review of the literature. J Am Coll Surg. 2009;208(2):279–88. 3. Bickels J, Ben-Sira L, Kessler A, Wientroub S. Primary pyomyositis. J Bone Joint Surg Am. 2002;84-A:2277. 4. Altemeier WA, Fullen WD. Prevention and treatment of gas gangrene. JAMA. 1971;217:806. 5. Stevens DL, Bryant AE, Adams K, Mader JT. Evaluation of therapy with hyperbaric oxygen for experimental infection with Clostridium perfringens. Clin Infect Dis. 1993;17:231. 6. Al-Qattan MM, Bowen V, Manktelow RT.  Tuberculosis of the hand. J Hand Surg Br. 1994;19:234–7.

Amputations

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Amputation It is defined as loss of a limb or part of a limb. The word amputation is derived from the Latin word amputare, “to cut away.” It should not be viewed as a failure of treatment but as the first step in rehabilitation. It should be performed by the most experienced surgeon in team. History: The earliest amputation was done on unanesthetized patients and hemostasis attained by crushing or dipping the open stump in boiling oil. Hippocrates was the first to use ligatures. Morel introduced tourniquet in 1674 while Lister introduced antiseptic technique in reducing mortality.

Indications 1. Dead limb—Gangrene. 2. Deadly limb-wet gangrene, spreading cellulitis, arteriovenous fistula, and others (e.g., malignancy). 3. “Dead loss” limb—Severe rest pain, paralysis. 4. Others (e.g., contracture, trauma). The only absolute indication: irreversible ischemia in a diseased or traumatized limb, namely: 1 . Peripheral vascular disease 2. Trauma 3. Burns 4. Frostbite K. M. Iyer (*) Royal Free Hampstead NHS Trust, Royal Free Hospital, London, UK © Springer Nature Switzerland AG 2019 K. M. Iyer, W. S. Khan (eds.), General Principles of Orthopedics and Trauma, https://doi.org/10.1007/978-3-030-15089-1_18

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5. Infections 6. Tumors 1. Peripheral vascular disease: The most common age group is 50–75 years and most patients have concomitant disease processes in cerebral vasculature, coronary arteries, and kidney. Comorbid conditions—diabetes, smoking, prior stroke, prior major amputation, decreased transcutaneous oxygen levels, decreased ankle-brachial blood pressure index, and ulcers. Most significant predictor of amputation in diabetics is peripheral neuropathy as measured by insensitivity to the Semmes Weinstein 5.07 monofilament. Perioperative mortality rate—30% and 40% die within 2 years. 2. Trauma: Most common in young patients. Male > Female. Lange’s absolute indications for amputation in type III C tibial injuries include: (a) crush injury with warm ischemia time of >6 h, (b) relative indications, (c) serious associated injuries, and (d) severe ipsilateral foot injuries; decision as to a limb which can be saved, should be saved or not. Early amputation and prosthetic fitting: decreased morbidity, fewer operations, shorter hospital stay, decreased hospital costs, shorter rehabilitation, and earlier return to work. In acute trauma: The functional stump length of stump must be maintained whenever possible. Mangled extremity severity score (Table 18.1): Points × 2 if ischemic time exceeds 6 h [1] Table 18.1  Classification of Mangled extremity severity score Type 1

Characteristics Low energy

2

Medium energy High energy

3 4 Shock group 1 Shock group 2 Shock group 3

Massive crush Normotensive hemodynamics Transiently hypotensive Prolonged hypotension

Ischemia group 1 Ischemia group 2 Ischemia group 3

None Mild Moderate

Ischemia group 4

Advanced

Age group 1 Age group 2 Age group 3

50 years

Injuries Stab wounds, closed simple fractures, small caliber gunshot wounds. Open or multiple-level fractures, dislocations, moderate crush injuries. Shotgun blast (close range), high velocity gunshot wounds. Logging, railroad, oil rig accidents Stable blood pressure in field and in the operating room Unstable blood pressure in the field but responsive to IV fluids Systolic blood pressure 40–45° linked with increased risk of pseudotumor formation due to edge loading [16]. • Implant size—Head size 7  ppb or 119 nmol/L cobalt and 135 nmol/L chromium) with evidence of increasing levels at 3 months or abnormal imaging indicates revision surgery should be considered . • Asymptomatic patients with large head MoM THR should have annual clinical review and metal ion levels. • Any hip replacement with ASR bearing should have annual review with clinical and cross-sectional imaging for life of implant.

Surgical Approaches 1. Transgluteal (Hardinge) approach: This is the approach through the abductor muscles. Advantages: • Lower rate of dislocation. • Sciatica nerve injuries are less compared with the posterior approach. • Preservation of the posterior soft tissue envelope. • Avoids the technical difficulties of trochanteric osteotomy. Disadvantages: • Potential damage to superior gluteal nerve. • Damage to abductor muscles, leading to Trendelenburg limp. • Exposure of the proximal acetabulum is limited. • Inability to adjust trochanteric tension. • Some risk of heterotopic ossification. 2. Posterior Approach: In this approach the gluteus maximus is split bluntly in line with its fibers. Short external rotators are released at the insertion site to protect the sciatic nerve. Advantages: • Trendelenburg limp is avoided as the abductors are preserved. • Low incidence of heterotopic ossification. • A more consistent exposure can be expected. • Preferred approach for revision hip surgery. Disadvantages: • Increased risk of dislocation and infection.

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3. Charnley approach: Here the hip is approached via a trochanteric osteotomy (Fig. 20.9). Advantages: • Easy dislocation. • Good exposure. • Good femoral component alignment is achieved. • Favored by some surgeons in the revision surgery. Disadvantages: • Increased blood loss. • Increased operating time. • Difficulty reattaching the greater trochanter (sometimes). • Nonunion (30%). • Limp due to nonunion of greater trochanter. • Broken wires. 4. Minimally invasive technique (MIS): It allows the surgeon to do hip replacement through one or two smaller incisions. It may be indicated in slim and well-­ motivated patients. Advantages: • Smaller incision. • Earlier recovery less postoperative pain. Fig. 20.9  Right hip replacement using trochanteric wires

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Disadvantages: • Needs special instruments. • Fluoroscopy needed intraoperatively. • Evidence suggests that there is no advantage over a smaller scar. 5. Anterior supine intermuscular approach. The patient is laid supine on the operating table. This can be used for primary and revision hip arthroplasty and also for resurfacing. The incision starts two fingerbreadth below the anterior superior iliac spine (ASIS) and two fingerbreadth lateral to ASIS. It is centered over the greater trochanter. Care is taken of the lateral femoral cutaneous nerve. Incision is made over the muscle belly of the tensor fascia lata (TFL) and carried on distally. Muscle interval is developed between the TFL which is situated on the lateral side and the sartorius on the medial side. Advantages: • Less invasive muscle-sparing approach. • No limp. • Early recovery and discharge from hospital. Disadvantages: • Learning curve. • Higher intraoperative complication rate. Following chart (Fig. 20.10) shows the advantages and disadvantages of various approaches of the hip joint:

Approach

Advantages

Disadvantages

POSTERIOR

•

No Limp

• •

Dislocation Rate Sciatic Nerve Injury

HARDINGE

•

Dislocation Rate

•

Trendelenburg Gait

CHARNLEY

•

Good Exposure

•

Non-union trochanter

MIS (Min Invasive)

• • •

Less tissue injury Early Recovery Less blood loss

• • • •

Restricted view Learning curve Fluoroscopy +/– Special instrumentation

ASI approach

•

Intermuscular approach No limp No muscle damage Less hospital stay

• • • •

High learning curve Complication rate Fluoroscopy needed Special instrumentation

• • •

Fig. 20.10  Shows the advantages and disadvantages of various hip approaches

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Complex Primary Total Hip Arthroplasty (A) Adult development dysplasia of hip. 1. Crowe and Tonis classification. (a) Type I and II—Low hip dislocation—subluxed femoral head in the false acetabulum with the true acetabulum being shallow with increased ante version and posterosuperior wall deficiency. (b) Type III and IV—High hip dislocation—femoral head dislocated posterio-­ superiorly with narrow, shallow and triangular true acetabulum, the iliac wing is anteverted and the entire rim of acetabulum may be deficient. 2. Typical deformities in femur—short, valgus neck with increased ante version; narrow canal with thinner cortices with anterior bow of femur displaced distally with increasing dysplasia. The above deformities lead to shortened leg. 3. Acetabular reconstruction: (a) Challenges—anatomic landmarks difficult to identify with compromised bony anatomy. (b) Aim—to place acetabular component close to the tear drop with restoration of hip offset and biomechanics. CT scan is a useful imaging modality to plan the surgery. (c) Technique. • Small size uncemented acetabular component (38–44  mm) placed in native acetabulum in high hip dislocation. • In low hip dislocation socket uncoverage (>30%) requires use of bulky femoral head auto graft. • Anteversion of the component should be based on the combined orientation of the femoral and acetabular components to maximize stability and ROM. 4. Femoral reconstruction. (a) cemented and uncemented stems can be used, (b) Modular stems and narrow cemented stems are commonly used to allow correction of excessive femoral anteversion and to accommodate metaphyseal– diaphyseal size-mismatch seen in these cases. (c) Subtrochantric femoral osteotomy with shortening is commonly done in high hip dislocation to avoid over lengthening of leg and subsequent sciatic nerve injury when the hip is reduced in the anatomic hip center. (B) THA in post-traumatic situations. 1. Preoperative planning. (a) Possibility of latent infection to be considered: • ESR and CRP obtained. • If inflammatory markers raised, hip aspiration/ biopsy prior to replacement surgery.

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• If in any doubt frozen section cultures at time of surgery with consideration of two stage procedure with the use of antibiotic spacer. (b) X-rays: • Full lengths femur X-rays—concern for any additional deformity or limb length discrepancy. • Judet views of acetabulum—concern for wall/column deficiency. (c) CT scan/CT angiogram: • Femoral/acetabular anteversion and acetabular wall/column deficiency or pelvic discontinuity. • Pelvic hardware and its proximity to pelvic vessels. 2. Previous failed femoral fixations—THA after failed femoral neck or pertrochanteric fixation can be challenging. Challenges: (a) AVN of femoral head. (b) Nonunion of greater trochanter (free floating) with loss of calcar in IT fracture. (c) Retained hardware with contracture of soft tissues and scarring of nerves. (d) Poor bone quality. (e) Deformity and shortening of leg. Pearls and pitfalls in reconstruction • Exposure—an approach permitting extensile exposure is indicated. Posterior and lateral approach can be used. An extended trochanteric osteotomy may be indicated with versus remodeling of proximal femur. • Gentle dislocation of hip is done before removal of hardware to prevent propagation of fractures through areas of stress risers in the bone where hardware was removed. • Failed intertrochanteric fractures are more difficult to manage than failed femoral neck fractures. This is due to proximal femoral varus remodeling and retroversion with compromised greater trochanter and calcar. Longer femoral stems bypassing the most distal stress risers by at least two cortical diameters are indicated. • Calcar replacement stems and modular stems may be required along with use of GTR plates to stabilize the greater trochanter. In elderly, osteoporotic bone, proximal femoral replacement may be an option as well. 3. Previous acetabular fractures with post-traumatic arthritis. Challenges: (a) Bone loss—wall/column +/− pelvic discontinuity. (b) Scarring of sciatic nerve. (c) Protrusio/deformity due to malunion. (d) Retained hardware. Pearls and pitfalls • Posterior approach—helpful to provide access to acetabulum and hardware, permitting exposure and mobilization of sciatic nerve. • Only hardware protruding into acetabular cavity should be removed—metal cutting burrs are indispensable.

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• Cemented and uncemented cups can be used. Large rim fit cups for protrusio defects with morcellized bone from femoral head to fill cavitatory defects. Segmental defects may require revision implants using augments and cages. (C) Conversion of a hip arthrodesis to THR. Challenges: • Proximal femoral deformity with no reference for neck cut. • No reference for cup position (Transverse acetabular ligaments may be present). • Infection to be ruled out if it was an indication for arthrodesis. • Retained hardware. • Soft tissue contractures and poor bone stock. Pearls and pitfalls • Must have functioning abductors for a reasonable outcome. Assess with MRI scans and EMG studies. • Reference neck cut from retained hardware or visible trochanter • Retractor placed in obturator foramen/presence of TAL helps to position the cup. Intraoperative X-rays to assess cup position before reaming. • Use burrs/drills/osteotomy with proximal femoral sclerosis/deformity. (D) THR in Paget’s disease—principles of treatment. • Hypervascular bone and increased blood loss during surgery—potent bisphosphonates and intraoperative blood salvage are useful measures. • Proximal femoral deformity involves coxa vara of femoral neck with retroversion of proximal femur. • ETO may be necessary to access the femoral canal. • Cementless stems are preferred over cemented stems. Modular or tapered titanium Wagner type of stem provide good distal fixation with independent adjustment of femoral version with good results [17]. (E) THR in neuromuscular conditions. Two types of neuromuscular conditions are usually seen: 1. Intrinsic NM disorders such as cerebral palsy, myelomeningocele, and Charcot—Marie tooth disease are seen in children. Hips are at increased risk for subluxation/dislocation. 2. Extrinsic NM disorders are usually seen in adults in later life and include dyskinesis, athetosis, Parkinson’s, multiple sclerosis, and adult CVA. These lead to contractures about the hip and painful degenerative arthritis. (a)  Muscle contractures can be improved by adductor tenotomy and the iliopsoas release can reduce risk of dislocation of the hip replacement. (b)  Dual mobility cups and constrained liners can also reduce risk of hip instability. (c) Use of aggressive pharmacological treatment (e.g., antiparkinsonian drugs) has shown to improve outcomes in hip replacements in this difficult group of patients.

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Rapid Recovery Pathways in THA Rapid recovery programs have become a key element to the hip replacement care pathway in most high-volume orthopedic centers worldwide. These programs provide safe, high quality care to the patients while improving the efficiency and decreasing the costs associated with THA.  Standardized multidisciplinary, multimodal approach is at the heart of these programs and involves the following key elements: Preoperative phase—This stage involves proper patient selection and medical optimization. “Joint education classes” provided by some institutions cover the entire spectrum of patient education and rehabilitation protocols involved in joint replacement surgery. Preoperative optimization of patients medical comorbidities allows the patient to be treated under a “healthy patient model” rather than “traditional sick patient” model. Perioperative phase—Pre-emptive analgesia and anesthesia involves neuraxial anesthesia combined with local infiltrative anesthetic agents. Surgical considerations—efficient operation minimizing soft tissue trauma and blood loss with optimization of blood and fluid management perioperatively. Postoperative phase—Effective post op pain management pathways prevent nausea, dizziness, and sedation. This allows aggressive rehabilitation programs emphasizing mobility and independence which are the crux of any rapid recovery programs.

Outcomes Studies have shown that in rapid recovery programs, length of stay varies from 1 to 3 days in most patients [18].

Total Knee Replacement (TKR) The surgical procedure to replace the articular surfaces of the femoral condyles, tibial plateau, and patella (surgical preference) to provide sustainable pain relief and improve functional status of the patients (Fig. 20.11).

History • The pioneer of knee replacement surgery was Leslie Gordon Percival Shiers (FRCS) (McKeever 1957; MacIntosh 1958, 1964). • Early replacements were primitive spacers. In the 1960s, Frank Gunston from Sir John Charnley Hip Centre developed a metal on polyethylene knee replacement. • The 1970s saw the birth of current day “geometric” design and condylar knee design (Insall).

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Fig. 20.11  Shows left total knee replacement (AP view)

• Hinge constrained knee replacements were popularized by Guepar but had problems due to wear. Gradually metal backing of plastic components (modern) knee replacements were introduced. Biomechanics of native knee • Several studies have looked at kinematics of normal knee, using different methods such as cadaveric testing using knee simulators, in vivo RSA studies, noninvasive skin markers, invasive bone pins and fluoroscopic techniques. • These studies are in general agreement on how a knee moves. At full extension, the femur is internally rotated with respect to tibia and anterior to mid-point of tibial plateau. As the knee flexes, the average lateral femoral condylar roll back on lateral tibial plateau is 21 mm and that for medial femoral condyle being only 1.9 mm. This asymmetric rollback leads the femur to effectively externally rotate on tibia as the knee flexes, an average of 17.8° as observed in vivo studies [19]. • This differential roll back is attributed to asymmetrical geometry of medial and lateral femoral condyle with varying sagittal radii of curvatures. The convex lateral tibial plateau with a mobile lateral meniscus and a concave (dished) medical tibial plateau with a relatively fixed medial meniscus also play a role in this asymmetrical role back. • The biomechanical advantage of femoral roll back is to increase the lever arm of quadriceps and to allow clearance of femur from tibia in deep flexion. During knee extension, the femur rolls forward, increasing the lever arm of hamstrings to act as a brake on hyperextension.

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TKR

Unconstrained TKR

Semiconstrained TKR

Constrained TKR

Bicruciate TKR e.g. LCCK Post Cruciate retaining Post Cruciate stabilising

Rotating Hinge

e.g. TC III

Bicruciate stabilising

Fig. 20.12  Classification various types of knee replacements

Biomechanics/ kinematics and implant design considerations in total knee replacements • A large degree of variability exists in the kinematics of replaced knee, with no consensus on a knee design that best recreates the kinematics of the normal knee. • Modern knee replacements are condylar TKRs. (Resurfacing of distal femur and proximal tibia with implants whose shape resembles the normal knee). They were conceived by three groups (Insall, Freeman, and Walker) between 1969 and 1974. • TKR kinematics are dependent on the implant design and its interaction with soft tissue structures. The spectrum of these designs vary from unconstrained to semi-constrained to fully constrained rotating hinged knee replacements. Also TKR can be subclassified based on the implant geometry and its interaction with TKR kinematics. TKR kinematics in relation to implant designs. Chart below (Fig. 20.12) shows the various types of knee replacements and how they are categorized: (A) Unstrained designs are subclassified as: 1. Bicruciate retaining—both cruciates are retained. 2. Posterior cruciate remaining (PCR)—ACL sacrificed/PCL retained. 3. Posterior cruciate stabilizing (PS)—both cruciate sacrificed and implant provides for mechanical stabilization for PCL. 4. Bicruciate stabilizing (BS)—both cruciate sacrificed and implant provides for mechanical stabilization of ACL and PCL. 1. Bicruciate retaining (BCR). These implant designs are believed to better replicate normal knee kinematics due to retention of ACL, which provides better stability and proprioception.

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Mueller, in a multicenter analysis, found that 90% of patients with BCR knee have posterior motion of medial and lateral femoral condyle [19]. Concerns: • Limited scope of utilization of these variants—typically ACL is not fully functional in arthritic knees. • More challenging surgery with the studies showing higher revision rates [20]. 2. Cruciate retaining (CR). Commonly used implant designs. Theoretically it is believed that retention of PCL would replicate normal knee kinematics with posterior femoral rollback. However, studies have shown paradoxical anterior femoral slide of medial condyle with reverse axial rotational pattern during knee flexion [21].   Paradoxical anterior slide of femur reduces knee flexion due to impingement of posterior femoral condyle on the posterior tibial lip. Reverse axial rotational patterns lead to patellofemoral instability.   Also to facilitate femoral roll back, these implants have low conformity with round- on- flat design (flat polyethylene insert). This design facilitates in coronal plane femoral condyle lifts off, leading to slam down and edge loading of polyethylene, resulting in increased contact stress and polywear. To overcome these disadvantages, design changes were incorporated such as ultracongruent option for polyethylene insert to counter anterior femoral side, increased tibial slope and adequate posterior femoral condylar offset to improve knee flexion. 3. Posterior stabilized (PS) and Bicruciate stabilizing (BCS). PS knees are commonly used design and suitable for almost all knees. PS design would be favored over CR design in patients with patellectomy (weak quadriceps allows increased anteroposterior instability), inflammatory arthritis and previous PCL injury (incompetent PCL).   Advantages over CR design—higher conformity with dished polyethylene leading to less contact stress and polywear. Some degree of varus-valgus stability.   Disadvantages over CR design—more conformity leads to more constraint and stress transfer to implant bone interface leading to implant loosening. More bone resection to accommodate cam and post mechanisms. Cam/ post interaction leading to potential for fracture, wear and CAM jump in high flexion. Despite these perceived pros and cons of these designs, several studied have reported no difference in functional outcomes between CR and PS knees [22]. (B) Semiconstrained and constrained designs. Semiconstrained designs include LCCK and TC III prosthesis with a broader and more elevated CAM/POST design providing greater coronal plane stability than PS designs. They do not provide greater sagittal plane stability. Fixed and rotating hinge knee designs provide even greater constraint with coronal and sagittal plane stability. These designs are more suitable for complex primary knee replacements and revision scenarios with associated collateral ligament insufficiency and bone loss requiring augments.

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The greater constraint provided by these implants increases the forces transmitted to implant cement bone interface contributing to loosening. Use of intramedullary stems with these designs help to dissipate these forces. TKR kinematics based on implant geometry. Implant geometry variations in TKR can be broadly categorized based on bearing mobility (fixed versus mobile) and sagittal curvature of femoral component (single versus multi-radius) • Based on bearing mobility. • Mobile bearing knees were designed to reduce contact stress and wear in the PE insert by replicating more “normal like” knee kinematics by decoupling rotational and translational kinematics during knee flexion. • The mobile bearing allows rotational component to occur between the insert and tibial tray while translational motion occurs between femoral component and PE insert. • However, multiple studies have shown no difference between mobile and fixed bearings in terms of ROM, knee scores and survivorship [23]. • Based on femoral component geometry. • Some designs have a single sagittal radius while others have 3–4 different radii through the flexion arc, with reducing radii in deeper flexion. However, neither of these designs have shown improved survivorship in in-vivo studies. • Continuous innovation in design and techniques have improved functional outcomes of TKA, with no clear consensus been reached on the superiority of different designs. • Outcomes are also affected by surgical technique (mechanical or kinematic alignment, gap balancing or matched resection) as well as patient related factors (age, BMI, preexisting comorbidities, deformity, and individual anatomy).

Principles of TKR Surgery The biomechanical goals of condylar TKR are: • Restore the mechanical axis—passing through centers of hip, knee, and ankle joints. • The femoral and tibial bone cuts are made perpendicular to the mechanical axis. The thickness of the prosthesis aims to recreate the original thickness of bone and cartilage in flexion and extension of the knee joint with preservation of the height of the joint line. • Ligament balancing in both coronal and sagittal plane to create a stable knee to reduce wear and improve function. • Rigid durable fixation (cemented/uncemented) of the prosthesis. • The following steps are followed to achieve the above goals: Standard surgical approach—midline skin incision with a medial parapatellar approach to explore the knee joint. This was originally described by Von Langenbeck and popularized by Insall. Hoffman advocated a subvastus approach but is not

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commonly used due to difficulties in gaining exposure, risk of bleeding, and unclear benefits. Engh popularized the mid vastus approach, which spares the quadriceps tendon and has been embraced by enthusiasts of minimally invasive techniques of TKR and in UKR. Bone cuts—In routine TKA a series of bone cuts are usually made. In measured resection technique, these bone cuts aim to reproduce the joint lines with the thickness of the prosthesis. (A) Osteotomy of proximal tibia. (a) The natural tibial plateau is 3° versus to the mechanical axis. However, it is recommended that the tibia is cut perpendicular to the mechanical axis as it is easily reproducible surgically. This also allows even loading of medial and lateral compartments. (b) The depth of tibial cut should correspond to the thickness of the insert (in general, 10 mm combined thickness of tibial tray and insert is preferred). This can be achieved using intra/extra medullary alignment guides. (c) The correct tibial component rotation is a key element and this can be achieved by aligning the center of the tray with medial third of tibial tuberosity. Malrotation leads to maltracking of patella including its dislocation, anterior knee pain, and stiffness. (B) Osteotomy of distal femur. (a) This cut determines the extension gap. (b) The distal femur is cut at a valgus angle between 5 and 7° aiming to cut the femur perpendicular to the mechanical axis. The valgus cut angle is the angle between the femoral anatomical and mechanical axis and can be calculated with full length radiographs. (C) Anterior and posterior femoral condylar/chamfer cuts. (a) These cuts determine the size and rotation of the prosthesis—flexion gap. (b) Rotation can be judged as follows: • Measured degrees of external rotation—measured resection technique. Femoral component is placed in 3° of external rotation to create a rectangular flexion gap (remember native tibial plateau is in 3° of varus and was cut perpendicular to mechanical axis). • Trans-epicondylar axis—component parallel to this axis is in optimum position. Sometimes, the only parameter available to judge rotation in revision knees. • Whiteside’s line (a vertical line joining the roof of the notch with deepest point of the trochlea)—component perpendicular to this line is parallel to epicondylar axis. • Tension technique to obtain rectangular flexion gap. • Malrotation of femoral component can lead to patellar maltracking and its associated problems. (D) Intercondylar notch cut. (a) This is indicated only in PS knees to allow for cam/ post interaction in these designs.

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(E) Retropatellar osteotomy. (a) This is optional based on whether patella is resurfaced or not. Dome and anatomical designs of all polyethylene patellar buttons are available. Metal backed designs have been discontinued due to their poor outcomes.

Patellar Surfacing or Not? A recent meta-analysis of randomized controlled trials included 14 studies [24]. They found that the risk of reoperation was reduced by 4% in the patellar resurfacing arm, implying that one would have to resurface 25 patellae in order to prevent one reoperation. They also concluded that no difference between the two groups was noted in terms of anterior knee pain, knee pain score, KSS, and knee function score. Similar conclusions have been derived from other meta-analysis [25]. Also the higher incidence of reoperations in the non-resurfaced TKR might be attributed to the fact that secondary patellar resurfacing is an easier and less morbid procedure than revision TKR for persistent pain following TKR. Low percentage of success following this procedure also questions its validity. The 2009 annual report of Swedish Arthroplasty register commented that resurfacing is used in less than 10% of cases in Sweden, 70% of cases in Denmark, 5% in Norway, and 45% in Australia [26]. Based on current evidence, it is impossible to provide conclusive evidence for or against routine patella resurfacing. Selective resurfacing probably reflects the majority of arthroplasty surgeon’s practices. Rheumatoid arthritis, “bone on bone contact” (grade IV), and high BMI are some of the indications for “selective resurfacers.” To conclude, the final decision is operator dependent, and with optimal implant design and surgical technique, satisfactory outcomes can be achieved both with and without resurfacing.

Patellar Tracking in TKR This can be optimized by external rotation of tibial and femoral components, aligning the femoral component with lateral cortex of lateral femoral condyle and medialization of patellar button.

Patella Height and TKR Patella Baja is created by shortened/contracted patellar tendon. A functional Baja is created by elevating the joint line. This can lead to restricted knee flexion as inferior pole of patella impinges on the polyethylene insert. It is a difficult problem to rectify. Lowering the joint line can help by distalizing the femoral component or placing the patellar dome superiorly.

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Ligament balancing. Varus deformity—the following sequence of release of structures is usually done with increasing severity of deformity: • Sharp subperiosteal direction of deep and superficial MCL along with insertion of pes anserine tendons up to mid coronal plane and 3–4 cm distal to joint line on anteromedial tibia. • Excision of osteophytes. • Insertion of semimembranosus from posterior medial corner of upper third tibia. • In severe varus, medial subperiosteal dissection is continued posteriorly and distally, maintaining continuity of the sleeve. • Valgus deformity—the following sequence of release of contracted structures is usually followed. With knee in extension, joint distracted with laminar spreaders, posterolateral capsule and arcuate ligament are released at the joint line. • The iliotibial and lateral retinaculum are pierced with No 15 blade in “pie crust” fashion. • For severe deformities, LCL, popliteus, and posterolateral capsule are detached at their insertion with “a wafer thin bone” from lateral femoral condyle. Very rarely, lateral head of gastrocnemius is released. Fixed flexion deformity—can be graded as • I (30°). • • • •

Following algorithms can be used for correction of this deformity. Step 1—Posterior osteophyte removal and posterior capsular release. Step 2—Additional distal femur resection of 2 mm- CR trial. Step 3—Release of PCL with further 2 mm of distal femur resection—PS trial. Step 4—if contracture persists, further soft tissue releases from contracted side of coronal deformity is done until fill extension is achieved. This may necessitate conversion to semi-constrained/ constrained device. Polyethylene wear and periprosthetic osteolysis—failure of TKR

• Femoral component is made of cobalt chrome alloy while the tibial component is usually titanium alloy base plate with polyethylene insert or an all polyethylene tibial component. • Wear particle accumulation in TKA results from a combination of delamination, pitting, adhesion, abrasion, and burnishing backside wear. • Patient can remain asymptomatic for long periods until catastrophic failure of polyethylene occurs. • Factors influencing PE wear and osteolysis are.

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1. Implant design. • Bearing conformity, congruity, and constraint. • Locking mechanism of PE—backside wear in tibial tray. 2. Polyethylene insert. • PE thickness—thinner poly (8  mm- minimum acceptance) has low yield strength. • PE manufacturing—best is direct compression molded. • PE sterilization—irradiation in inert gas. Avoid highly cross-linked (HXLPE) and vitamin E infused poly—(vulnerable to fatigue wear). 3. Patient factors—BMI, age, and activity level. 4. Surgical technique—alignment, balance, and stability of knee.

Difficult Primary TKR 1. Severe varus/valgus deformities—We have discussed the soft tissue releases of the above deformities earlier. However, if we are unable to correct the flexionextension mismatch in the severe deformities, one has to consider using semi-­ constrained and hinged implants (Fig. 20.13). 2. The stiff knee (ankylosis). (a) “Stiff knee”—knees with less than 50° arc of motion are considered stiff (b) Causes—severe contractures, post-traumatic or septic arthritis, heterotopic ossification, and patella Baja. The most important predictor of range of motion (ROM) after TKR is preoperative ROM [27]. (c) Extensile surgical approaches—these approaches maybe indicated in “stiff knees” to facilitate knee flexion. • Quadriceps snip—This approach involves the proximal extension of the arthrotomy along the quadriceps tendon directed in the proximal lateral direction 30–40° in line with the fibers of the vastus lateralis muscle. One study compared with standard medial parapatellar approach and found no difference in functional outcomes and incidence of extensor lag [28]. • Tibial tubercle osteotomy (TTO)—this approach may be indicated if further exposure is necessary and “quadriceps snip” is not sufficient. TTO may also aid in difficult stem extraction in revision knees, tibial tuberosity malposition, and patellar ligament contracture. (patella baja) A 2016 study comparing TTO with standard medial parapatellar approach showed no difference in functional outcomes (knee flexion, WOMAC, and KSS scores) after 1 year [29]. • V-Y quadriceps turn down—this approach uses the medial parapatellar approach with a diverging incision through the quadriceps tendon distally and laterally at an angle of 45° over the lateral retinaculum towards the tibia. It gives an excellent exposure as the entire patella may be easily exerted. However, it should be used with caution as it leads to extensor leg and disruption of blood supply to the patella which may lead to necrosis of extensor mechanism.

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Fig. 20.13 Complex primary total knee replacement (AP view)

3. Extra-articular deformities in TKA. (a) Causes—fracture malunion (femur or tibia), congenital or metabolic bone disease, Blount disease, hereditary hyperparathyroidism), prior high tibial osteotomy or distal femoral osteotomy, tumor, and Paget’s disease of bone. (b) Evaluation—(a) History and physical examination, (b) imaging modalities—full length long leg weight-bearing AP and lateral radiographs. CT scans help identify rotational abnormalities. (c) Treatment principles. The importance of extra-articular deformity is determined by two criteria: the magnitude of the deformity and its distance from the knee joint. The magnitude of deformity can be calculated from full length weightbearing AP views. The product of proportional distance and the angula-

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tion (magnitude) of the deformity yields the contribution of the angulation to the knee deformity. (Proportional distance can be calculated via the division of femoral segment proximal to deformity by the length of femur). Furthermore, the closer the deformity to knee joint, translates to greater alterations in the joint space angle and mechanics compared with deformities further away. • Standard intra-articular corrections—Intra-articular resection can be used to manage extra-articular deformities and avoid the potential morbidities associated with an osteotomy, such as nonunion, arthrofibrosis, and greater risk of infection. Satisfactory outcomes have been noted in deformities up to 15° in coronal plane and 8° in sagittal planes with this technique [30]. • TKA with simultaneous or staged osteotomy—Concerns still exist in managing an extra-articular deformity at any level of 10° more in coronal plane and 20° or more sagittal plane with intra-articular resection [31]. Such deformities require extensive intra-articular reaction leading to compromise of collateral ligaments, necessitating use of constrained prosthesis or ligament reconstruction. Moreover, persistent femoral deformity may require hip adduction or abduction leading to gait abnormalities and accelerated degeneration of hip joint. Hence, TKA performed with simultaneous or staged osteotomy is advantageous to achieve mechanical joint balance, anatomical alignment and adequate ligament stabilization. Some studies used a lateral approach, enabling hardware removal, osteotomy, and internal fixation (pre contoured blade plate/ locked nail) to be performed through same incision with good outcomes. • Newer techniques using computer-assisted navigation (CAS) and patient specific instrumentation (PSI)—In PSI technique, CT or MRI scans are used to construct positioning guides and cutting blocks specific to patients altered anatomy. CAS and PSI techniques are able to overcome the reliance on medullary canal as guides (not available in EA deformities) in conducting knee replacement surgery. Various studies have shown excellent outcomes with these techniques. 4 . Inflammatory arthropathies. • Patients with rheumatoid arthritis and JRA are at risk of poor wound healing, weakened immune system (high risk of infection) and have poor bone quality due to underlying disease process and being on DMARDs and steroids. • Moreover, cervical spine is often affected (Atlanto-axial subluxation) and patients must have screening radiographs of C- spine preoperatively. Patients scheduled to have general anesthesia may need fiber-optic intubation or epidural /spinal anesthesia in substantial Atlanto-axial instability.

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• Poor bone quality, bone deficiency, and ligamentous instability (usually valgus deformity) may require bone graft, augments, and implants with greater constraint. 5. Special consideration in TKR. (a) TKR in young patients. • TKA  30 are considered obese whereas those with BMI > 40 are morbidly obese. Obesity is considered to be an independent risk factor for revision TKA. • Obese patients need to be counseled preoperatively regarding the risks of requiring revision secondary to infection, loosening, implant positioning, and wound complications. Enhanced Recovery Pathways in TKR (Outpatient TKA) • Enhanced recovery pathways in TKR follow the same principles as discussed earlier in THA. • The main aim is to provide patient with a durable, well-functioning joint while minimizing complications. • A multidisciplinary approach is required which involves thorough patient selection, patient education, protocols with medical and anesthesia team regarding perioperative pain management, blood and fluid management, and postoperative rehabilitation. • An efficient pathway not only makes the patient journey more pleasurable but also makes joint replacements more financially viable in institutions doing high volume surgery.

Patellofemoral Arthroplasty (PFA) Indications • Isolated patellofemoral osteoarthritis, post-traumatic arthritis, or advanced chondromalacia (Outerbridge grade IV) on either or both the trochlear and patellar surface. • Effective in the presence of patellar or trochlear dysplasia. • Slight patellar tilt or subluxation on preoperative radiographs or intraoperatively (with a normal Q angle) can be managed with lateral retinacular release, medialization of patellar component, and resection of lateral patellar facet.

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Contraindications • Any evidence of tibiofemoral arthritis or advanced chondromalacia. • Patients with inflammatory arthritis or those with chondrocalcinosis of menisci or weight-bearing surfaces of tibiofemoral compartments. • Avoid in the presence of severe coronal deformity unless corrected. • A high Q angle is also a relative contraindication unless a tibial tubercle antero-­ medialization is performed before or simultaneously with PFA. • It is unknown whether obesity or cruciate ligament insufficiency have deleterious effects on outcomes of PFA. Clinical Outcomes • Clinical results of PFA are affected by trochlear component design, as well as patient selection and surgical technique. • Currently, with the use of third-generation trochlear implant designs, outcomes of PFA have improved with decrease in the need for secondary soft tissue surgery to enhance patellofemoral tracking. Complications • Early failure was due to patellar snapping and instability which have reduced with newer designs. • Late failure is due to component subsidence, polyethylene wear or loosening. • Development of tibiofemoral arthritis is the most common failure mechanism in 20% knees at 15 years [33].

Unicompartmental Knee Arthroplasty Indications: (a) Both cruciate ligaments should be intact. However, with deficient ACL, Uni knee can be done if • Wear pattern is in anterior two-third of tibia. • No radiological evidence of tibiofemoral subluxation. • Little or no posterior slope applied to tibial resection. • No greater than grade I changes in opposite compartment. (b) Up to grade III in patellofemoral compartment. However, eburnated bone is probably a contraindication. (c) No inflammatory synovitis or crystalline disease (gout/pseudogout). Contraindications: •  10–15° fixed flexion deformity • Lax MCL in valgus knee (>2  mm laxity) with lateral compartment involvement. • Varus >10° or valgus deformity >15°. • Morbid obesity.

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Survival Analysis of UKA • Designer surgeons of Oxford Uni knee Arthroplasty (OUKA) have had excellent outcomes with 10-year survival analysis of phase 3 implants as 96% and 15-year survival analysis at 91% [34]. • Independent series by non-designer surgeons have less good outcomes of OUKA with survival of 82–85% at 10 years [35]. • Consistently, data from national joint registries show a significantly higher revision rate for UKA than for TKA [36]. Some experts feel that as UKA is easier to revise than TKA, thus there is a lower threshold for revising them. Hence, the registry data could be misleading and should be interpreted with caution. Conclusion • Epidemiological studies suggest that up to 50% of patients in UK undergoing knee arthroplasty are suitable for UKA, yet only 8–10% have the procedures (Fig. 20.14). • There is increasing evidence that supports appropriate use of UKA, with better outcomes in terms of function and satisfaction, lower morbidity and reduced health care costs. • Revision rates are higher for UKA compared to TKA, but can be reduced with appropriate indications and appropriate surgical experience.

Fig. 20.14  Left medial unicompartmental knee replacement (fixed bearing)

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Newer Technologies in Knee Arthroplasty (A) Patient specific instrumentation (PSI) AND Custom made knees. • PSI uses the premise that every patient’s knee is different and unique and thus “off the shelf” design does not fit everyone appropriately and is not the optimal treatment option. • The process involves creating a 3D image of the bony architecture of the knee using CT or MRI.  Patient specific tailored cutting blocks are then ­created taking into account bony morphology and mechanical alignment of the joint. • The presumed benefit of this process is that it should allow more accurate positioning of implants translating into better functional outcomes. The key question is, does the use of PSI meet these goals? • A systematic review by Sassoon et al. looked at 16 studies, investigating the effect of PSI on mechanical alignment and clinical outcomes [37]. The majority of studies did not show an improvement in limb alignment, surgical efficiency, or clinical outcomes when PSI was compared with standard instrumentation. • CONFORMIS knee system (CUSTOM made knees) uses the above principles. The prosthesis mimics the shape and contour of each patient’s knee using PSI cutting blocks. Early results in terms of patient’s outcome are encouraging for the TKR [38] and UKR [14] with the patients stating a more natural feel of replaced knee. Moreover, this technology is completely adaptable and malleable and can be used in any 3 compartments of the knee (iTtotal; iUni, or iDuo). Long-term results are awaited. (B) Computer navigation or computer-assisted surgery. • Broadly speaking, navigation systems are classified into open (applied to any prosthesis) or closed (applied to only a single specific prosthesis). Most systems do not require CT or MRI and are termed “imageless.” Instead, they use sensors on small pins implanted into bone around the knee and a hand held sensor to reference certain key anatomical bony landmarks. These are instantaneously recorded via an optical laser-tracking camera, which uses computer software to create an image model of the joint. • Does CAS improve accuracy of component position and functional outcomes? De Steiner analyzed data from Australian joint registry of all navigated primary knee replacements performed [39]. There was a significant difference in ­cumulative revision rates at 9 years overall and in patients younger than 65 years, when comparing non-navigated knee replacements with navigated knee replacements (7.8% versus 6.3% 5 PMN/5 HPF (×400). –– Single positive culture. ◦  Acute and chronic: Positive. It is important to note that PJI may exist even if these criteria are not met, especially with low virulent organisms, such as Propionibacterium acnes. Identifying the organism is critical not only for diagnosis, but also for indicating the most appropriate method of treatment and effectiveness of antibiotics. Gram-­ positive cocci appear to be involved in the majority of PJI affecting the knee and hip joint. Staphylococcus aureus and coagulase negative staphylococcus species are fairly similar in incidence constituting more than half of the cases. Risk factors and prevention: Hyperglycemia, found in patients with poorly controlled diabetes, impairs bacterial defense mechanisms and wound healing. As such, HbA1c level should be maintained at less than 7%. Extreme obesity (BMI > 40 kg/ m2), malnutrition, and vascular insufficiency all need to be addressed. Heavy smoking, alcohol consumption, and intravenous drug abuse should be stopped 4–6 weeks before surgery. Systemic or local infection at the surgical site or in a distant organ should be eradicated. Perioperative measures that need to be taken are intravenous antibiotics within 1 hour of incision, maintenance of a relatively particle-free environment by using laminar air-flow. Postoperatively, prophylactic antibiotics for more than 24 h should be avoided, as there is little evidence of benefit, and such practice may contribute to emergence of antibiotic resistant bacteria. Classification (Fig. 20.20) and likely sources of PJI [45]: Treatment of PJI: The goal in management of a PJI is to eradicate the infection and restore pain free function of the replaced joint while minimizing the PJI related morbidity and mortality. Whichever option is chosen, the intention is to remove all of the infected tissue and prosthetic hardware; in effect, removing the established biofilm. At the same time, intraoperative soft tissue samples can be collected and sent for microbial culture, thus establishing pathogenesis and guiding antimicrobial treatment. Debridement and implant retention (DAIR) involves the radical debridement of soft tissue envelope surrounding the prosthesis, exchange of any removable components, extensive tissue lavage, and appropriate antibiotic treatment based on tissue samples taken at the time of operation.

Single-Stage Revision The rationale behind this strategy is that all prosthetic material, including cement if used, is removed and a thorough soft tissue debridement and washout is performed.

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A new prosthesis is then inserted in the same sitting, which is usually associated with a period of antibiotic cover. The concern with this technique is the ability to completely eradicate the infection.

Two-Stage Revision This method is considered the current gold standard of revision surgery for an infected TKR.  The aim is to eliminate the underlying infection and in doing so restore function back to the affected joint the stages involved in this technique start with the extensive debridement of the soft tissues and removal of the prosthesis and any cement used. This is followed by a period of time (usually two to six weeks) of antibiotic therapy (ideally microbe specific) to treat the infection, followed by implantation of a new prosthesis. 3. Thromboembolism: One of the complications after TKA/THA is the development of deep venous thrombosis (DVT), possibly resulting in life-threatening pulmonary embolism (PE). The reported incidence of (symptomatic and asymptomatic) DVT after THR and TKR and fracture neck of femur is up to 40–70%. The incidence of fatal pulmonary embolism is 0.5% after THR and 1% after TKR. Risk factors: Obesity, smoking, estrogen use, prolonged immobility, previous thromboembolism, cancer, diabetes mellitus, age older than 40 years, hypertension, varicose veins. Venography is the classic radiographic method of detection of DVT and is still considered the gold standard. Duplex ultrasound has been reported as an alternative method of diagnosis with sensitivity of 67–86% compared to venography. Prevention of DVT should be the goal with using mechanical devices such as compression stockings or foot pumps and pharmaceutical agents such as low molecular weight heparin, fondaparinux (factor Xa inhibitor) or aspirin. 4. Neurovascular Complications: Knee—Arterial compromise after TKA is a rare but devastating complication that occurs in 0.03–0.2% of patients. The vascular status of the limb should be carefully examined before operation. Tourniquet should be avoided in those with significant vascular compromise. Peroneal nerve palsy can occur after TKA after correction of fixed valgus and flexion deformities. Hip—Sciatic nerve is susceptible to injury in THA with hip dysplasia, posterior approach, revision surgery, and significant lengthening of the limb. The sciatic, femoral, and superior gluteal nerves can be injured by direct surgical trauma, traction, pressure from retractors, and extremity positioning.

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The incidence of vascular injury is 0.04–0.2% after primary THA and increases to 5% after revision cases. The external iliac, femoral, and obturator vessels are most commonly injured [46]. 5. Instability: Hip—Dislocation is one of the most common complications (Fig. 20.21). Reports on the incidence of dislocation vary from 0.3% to 10% for primary THA and up to 28% after revision THA. Risk factors include patient specific—prior hip surgery, neuromuscular or cognitive disorders, noncompliance and THA for femoral neck fracture and surgeon specific factors—surgical approach, inadequate soft tissue balancing, component malpositioning, impingement and surgeon experience. Most early dislocations can be managed by closed reduction, but revision may be necessary for recurrent instability. Use of dual mobility components (Fig. 20.22) and constrained constructs have helped in better management of instability [47]. Knee—Instability after TKA can be due to ligamentous imbalance and incompetency, malalignment, deficient extensor mechanism, inadequate prosthetic design, and surgical error. Anteroposterior or flexion space instability can be treated with conversion to a posterior- stabilized implant. For varus-valgus instability a constrained condylar design can be used. 6. Loosening: Hip—Aseptic loosening of implants is caused by osteolysis. It is most significant factor limiting longevity of THA. Revision for loosening is 4× higher than next leading cause (dislocation at 13.6%), and it is particularly problematic in younger patients [43]. Osteolysis is bone resorption caused by the body’s response to particulate debris generated as the THA implant wears out. Motion between any two components of the prosthesis (i.e., the femoral head and the acetabular liner, the head-neck junction of the femoral stem, or the liner and shell of the acetabulum) generates debris that floats around the joint. This debris stimulates a host response. Particles of metal, poly, or cement can all cause osteolysis, albeit different types of reaction. Osteolysis is important because it leads to implant loosening and/or periprosthetic fractures. The femur and pelvis have been divided into zones called Gruen Zones, which help to identify areas of osteolysis. In general serial X-rays are performed, and changes in implant positioning, such as stem subsidence, provide the best evidence. The accepted diagnostic criteria for loosening is progressive radiolucency or implant migration. The decision to operate on a hip depends on a few variables: rate of progression, location of osteolysis, type of implant, activity level, and age of the patient. In general, lesions that progress over 3–6-month period should be revised.

20  Total Joint Replacement Fig. 20.21  Dislocation of right total hip replacement

Fig. 20.22  Dual mobility left total hip replacement in a patient prone to falls

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Knee—Aseptic loosening after TKA can be due to malalignment of the limb, ligamentous laxity, duration of implantation, polyethylene wear, and patients with high activity demands. Tibial component loosening is more common than femoral loosening. It appears on radiograph as a complete radiolucent line of 2  mm or more around the prosthesis at the bone-cement interface in cemented arthroplasty. Component loosening can also be manifested by implant migration shown on sequential radiographs. In the absence of clinical symptoms, stable osteolytic lesions less than 1 cm can be closely monitored with serial radiographs. Loosening in turn leads to instability and pain requiring revision surgery with metal augments, cones, sleeves, or structural allograft. Polyethylene wear and subsequent particle induced osteolysis remains an important cause of failure of TKA. Newer generation of polyethylene like highly cross-­ linked polyethylene (HXLPE) or vitamin-E infused polyethylene (VEPE) are being evaluated and studied to prove their beneficial effect. Complications Specific to THA: 1. Limb—Length Discrepancy: LLD is one of the most common complications and is also a major source of patient dissatisfaction. It can also result in functional disabilities including limp, scoliosis, trochanteric bursitis and low back pain [48]. Preoperatively limb length discrepancy must be identified and documented. Block testing, in which wedges of known widths are placed under the affected extremity until the patient perceives equal leg lengths, best quantifies the functional limb-length discrepancy. Correct soft tissue tension may occasionally have to take precedence over equal leg lengths to optimize abductor function and maintain dynamic hip stability. Patients should also be counseled preoperatively as to the types of limb-length discrepancies that can be reliably addressed at the time of surgery, those that will likely correct over time, and those that will persist and require treatment with a shoe lift or alternative treatment methods. Complications Specific to TKA: 1. Patellofemoral Complications: Common patellofemoral complications after total knee arthroplasty (TKA) include instability, patellar fracture, implant loosening, component breakage, osteonecrosis, and accelerated polyethylene wear. Nonsurgical management of these complications after TKA is almost always indicated initially but has been associated with mixed results. Because femoral or tibial component malposition is often the etiology of patellar complications, revision of the malpositioned TKA components is usually required. Proximal realignment for patellar maltracking in the setting of properly positioned and sized components is associated with good results.

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Surgical treatment is recommended for patellar fracture with disruption of the extensor mechanism, with or without loosening of the implant and those with an intact extensor mechanism but loosening of the implant. Internal fixation may be performed in cases with good bone stock vs. partial or total patellectomy in poor bone stock patients.

Total Shoulder Replacement (TSR) History It was in 1893 when the first recorded shoulder replacement was done by Pean. This was done for a tuberculous infection. Later, shoulder replacements started to become routine by 1950s. The first generation of TSR came into use in 1953; these were of monobloc design. Second-generation implants were modular prosthesis with a separate stem and head. Initially these implants were highly constrained but gradually evolved into less constrained and allowing more motion. The third generation has evolved into anatomic shoulder replacement reflecting the actual anatomy of shoulder. Modern shoulder implant resembles the ball and socket with a stem which can be cemented or cementless (for bone ingrowth). In patients with poor rotator cuff muscles, the reverse shoulder implant has been designed. Indications • • • • • •

Rheumatoid arthritis. Osteoarthritis. Posttraumatic (complex fractures). Rotator cuff tear arthropathy (reverse shoulder replacement). Instability. Tumors.

Types of Shoulder Replacements Shoulder replacements can be of the following types: • • • •

Hemiarthroplasty (Fig. 20.23). Total shoulder replacement. Surface replacement. Reverse shoulder replacement (Fig. 20.24).

Hemiarthroplasty is done if the glenoid is having no arthritis. It involves removal of the humerus head and its replacement only, whereas total shoulder replacement (TSR) replaces the glenoid and the humerus head. The prerequisite for total

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Fig. 20.23  Left shoulder hemiarthroplasty

Fig. 20.24  Reverse left total shoulder arthroplasty

shoulder replacement is to have good rotator cuff muscles and good bone stock in the glenoid. In the reverse shoulder arthroplasty, the ball and socket are reversed to improve muscle function and because center of rotation is moved medially (Fig. 20.24). The deltoid has longer moment arm and can generate more force in weakness of rotator

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cuff muscles. The biomechanics are changed so that the rotator cuff deficient shoulder works well with the help of deltoid muscle even with significant bone loss. In an arthritic shoulder, joint replacement of shoulder is indicated, but the main aim here is relief of pain and range of movement comes as a secondary achievement. If range of motion is improved, then it is taken as a bonus. Achieving normal anatomy is the aim here which can be achieved by thin stem (usually cemented) or press-fit uncemented stem. Surface replacement is another option. It has evolved over the years. The surface of the head of the humerus is replaced with hydroxyapatite-coated implant, and it ensures a more anatomical replacement as glenoid remains native without replacement. Survivorship is more than 90% at 10 years. The survivorship of total shoulder replacement TSR is over 90% at 10  years, whereas for reverse shoulder replacement, it varies from 84 to 91% (Guery JBJS 2006). Figure 20.25 shows advantages and disadvantages of various types of shoulder replacements.

Surgical Approach Deltopectoral approach: The interval is between deltoid and pectoralis major muscle. Cephalic vein is retracted laterally. The subscapularis muscle is then split preserving the most inferior fibers to protect the axillary nerve. Deltoid Splitting Approach: In this approach, deltoid splitting is done up to 5 cm below the acromion to protect the axillary nerve traversing in the substance of the muscle. Supraspinatus tendon is exposed and allows for repair of rotator cuff and further exposure of head for resurfacing or hemiarthroplasty.

Shoulder Pros Replacement Hemiarthroplasty • Humeral head OA • Replaces humeral head • Replaces the glenoid and humerus head Total shoulder • Needs intact rotator cuff to function • Good bone stock needed • Normal biomechanics is maintained Reverse shoulder • Can be done in rotator cuff deficient patients

Cons

• Not useful if glenoid is also osteoarthritic • Not useful if rotator cuff is torn or deficient

• Ball and socket are reversed • Relies on deltoid function • Biomechanics of shoulder changed

Fig. 20.25  Pros and cons of various types of shoulder replacements

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Total Ankle Replacement (TAR) History Total ankle replacement (TAR) has been in use for over 30 years but there have been numerous developments in prosthesis design and relatively high failure rates have persisted despite evolutions in surgical strategy. Particular challenges are the high forces acting through the ankle joint, the relative avascularity of the talus which limits bonding of an uncemented prosthesis, limited talar bonestock and the poor soft tissue envelope which makes infective complications particularly poorly tolerated. Modern TARs tend to use an uncemented design with either a fixed or mobile bearing. Some designs such as the Scandinavian Total Ankle Replacement (STAR) have been in use for over 20 years and have a low reported revision rate (94% at mean of 12  years, Coughlin [49]. More recently, systematic reviews have looked at the global survival of ankle replacement in the literature. In 2007 Haddad reported [50] a failure rate of a around 2.7% per year, while Gougoulias [51] questioned whether the rate of failure was potentially higher than this, and also cast doubt on whether ankle replacement really results in a meaningful increase in ankle motion when compared to a fusion. TAR (Fig.  20.26) is a highly technical procedure, and essential skills for the operating surgeon include the ability to reconstruct incompetent medial or lateral ankle ligaments, normalize the forces through the ankle by correcting cavus or

Fig. 20.26  Left total ankle replacement

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planus deformity in the foot, and ensuring that the prostheses are correctly aligned with respect to the mechanical axis of the lower limb. The long-term results of TAR remain relatively poorly understood with a number of high-profile design failures such as the Mobility™ (De Puy Synthes) which was withdrawn. This design was in widespread usage in the UK and formed over half of the joints recorded in the UK joint registry at the time it was withdrawn from use. As such total ankle replacement remains a relatively experimental technique, although in the setting of multi-joint hindfoot arthritis or inflammatory arthropathy there are strong arguments for superiority over ankle fusion.

Total Elbow Replacement History Total elbow arthroplasty (TEA) began in 1940, but increased interest developed in the 1970s. Hinged implants are more a stable version (Conrad Morrey), but less constrained designs are favored by many (Kudo). • • • •

Osteoarthritis (Fig. 20.27). Rheumatoid arthritis. Complex fractures. Tumors.

Fig. 20.27  Osteoarthritis of the right elbow joint

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Types of Elbow Replacement: Most commonly they may be: • Linked (Coonrad Morrey) (Fig. 20.28). • Unlinked (Kudo & Southern Strathclyde). Recent review of English literature shows that linked-type implants restore a better arc of movement and may have higher proportion of good results and less radiological loosening. Survivorship—initial survivorship was 56–84% at 3.5  years for unlinked and linked cohort of patients, respectively (Levy et al. JSES 2009). In this series, linked prosthesis worked better.

Surgical Approach Posterior approach: It is the usual approach through the triceps tongue or olecranon osteotomy. Protection of the ulnar nerve is utmost important.

 irst Metatarsophalangeal Joint Replacement F (MTP of the Big Toe) History Carpometacarpal joint replacement (CMC) of the thumb: Silicone implant arthroplasty used before showed improved function but in the long-term showed Fig. 20.28  Right total elbow replacement (hinged)

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subluxation, cold creep, and synovitis (Swanson JBJS Am 1972). Titanium arthroplasty used by Naidu et al. (JHS Am 2006) and recommended that it may be used for lower demand patients. Total joint replacement is in experimental stages and used for severe CMC joint OA. These are cementless, unconstrained HA-coated implants. Ulrich-Vinther et al. (JHS, Oct 2008) found that CMC replacement had better results than tendon interposition arthroplasty in prospective study after 1-year follow-up. Indications • Osteoarthritis. • Rheumatoid arthritis. • Patient demanding mobility of the joint. Types of MTP Replacements. Although metatarsophalangeal joint arthrodesis remains the gold standard for arthritis (hallux rigidus), these can be: • Flexible hinged silicone implants: This started failing due to high shear forces (Granberry et al. 1991). • Titanium grommets provide longer life for silicone implants, but problems of silicone debris remained (foreign body reaction, synovitis, and bone erosion). They were started by Yee and Lau (2008). • Titanium hemi-great toe implant: 2-component first MTPJ implant by Gerbert et al. (1995) and Moje press-fit ceramic implant by Malviya et al. (2004) came into use. Moje implant works very well at a mean follow-up of 35 months, and there was significant improvement in foot function. However, Gutteck and colleagues (2011) found that high loosening rate of Moje prosthesis caused disappointing median term results.

Wrist Joint Replacement History Wrist replacement was first developed by Mr. Gluck in 1980, and Dutch wrist implant developed in 2003. These were used mainly for rheumatoid patients. Joint replacement surgery in the wrist is not common. Indications • Rheumatoid arthritis. • Osteoarthritis.

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Fig. 20.29 Postoperative oblique X-ray of arthrodesis with plate and screws (X-rays reproduced with kind consent from Guus M.Verneulen, MD, PhD., Plastic Surgeon, Xpert Clinic, Amsterdam, Netherlands)

Symptoms • Pain. • Stiffness. • Swelling. • Weakness of grip/pinch.

Approach Wrist joint is approached dorsally between third (extensor pollicis longus EPL) and fourth extensor compartment (extensor digitorum ED and extensor indicis EI). The tendons are protected and retracted to approach the wrist joint for replacement. Proximal carpal row is removed before implanting the wrist replacement.

Aim of Surgery Joint replacement surgery of the wrist is to relieve the pain and to maintain the function in the hand and wrist. There are other options also available like synovectomy and arthrodesis of the joint. The benefit of joint replacement is that it preserves the movement of the wrist.

20  Total Joint Replacement Fig. 20.30 Postoperative X-rays of trapeziectomy (X-rays reproduced with kind consent from Guus M. Verneulen,MD, PhD., Plastic Surgeon, Xpert Clinic, Amsterdam, Netherlands)

Fig. 20.31 Postoperative X-rays of TJA (Guepar prosthesis) (X-rays reproduced with kind consent from Guus M.Verneulen,MD, PhD., Plastic Surgeon, Xpert Clinic, Amsterdam, Netherlands)

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Implant The wrist joint replacement normally has two metal components and one plastic insert which goes between the two metal components. The two metal components are called as radial component and carpal component which are fixed to the radius and carpal bone, respectively.

 arpometacarpal (CMC) Joint Replacement of the Thumb (CMC C Joint of Thumb) This is the most commonly affected joint in the hand. Indications • Osteoarthritis (usually seen after 40 years of age). • Rheumatoid arthritis. • Gout. Symptoms • Pain at the base of the thumb. • Commonly seen in women. • Can be isolated or part of generalized osteoarthritis in the body. Signs • Tenderness at the base of the first metacarpal (grinding test). • Adduction contracture of the metacarpal. • X-ray can show osteoarthritis at the carpometacarpal joint.

Treatment Options and types of Joint Replacement CMC joint osteoarthritis can be treated surgically by various means. This can include [49] arthrodesis of CMC joint (Fig. 20.29) or trapeziectomy (Fig. 20.30). There are various types of implants available though each of them has got their limitations. Implants can be: • Swanson silicone implant. • Steffee prosthesis, Guepar prosthesis (Fig. 20.31) [52].

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Metacarpophalangeal Joint Replacement (MCP of the Fingers) History 1910: Wolff introduced transplantation of the articular surface. 1940: Burman started Vitallium cup arthroplasty for degenerated metacarpal head. 1954: Resection arthroplasty was popularized. 1960: Swanson et al. introduced silicone rubber (Silastic). Subsequently, Reis-Calnan finger joint implants made of polypropylene came into use. Newer designs include hinge pins and other alumina ceramics and high-­ density polyethylene (HDPE) and pyrolytic carbons. Indications • Rheumatoid arthritis (affect mainly MCP joints of the fingers). • Osteoarthritis (affect mainly IP joint of the fingers).

Implant Neuflex MCP and PIPJ Replacement Systems. Unique design implants are made up of silicone and special hinge design incorporates the natural bend of the finger.

Rehabilitation The primary goal of total joint replacement is achievement of pain-free function of the joint to improve the patient’s quality of life. Rehabilitation is of utmost importance to optimize the recovery.

Total Hip Replacement Mobilization—New enhanced recovery programs get the patient out of bed on the first postoperative day, but most frequently mobilization begins on the first postoperative day. The patient is taught to walk by the physiotherapist using walking aids and is full weight-bearing. On discharge, physiotherapy is necessary in less than 50% of the patients, but hydrotherapy is often valuable especially in bilateral procedures. A Trendelenburg gait (sailors gait) can be seen and be permanent after the lateral approach to the hip.

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Instructions to patients (for 6 weeks): • Flexion to 90° (raised toilet seat, upright chair). Flexion beyond 90° can increase the risk of dislocation, especially with posterior approach. • No driving. • Sleep on back (if a patient cannot tolerate this, they may lay on their side with a pillow between their legs). Instructions to patients (for 6 weeks): • All restrictions lifted, but common sense must prevail. • Showering is preferable to bathing for first 6 weeks but in most patients can be undertaken between 6 and 12 weeks. • Walking aids can be discarded as confidence allows. • Long-haul air travel should be avoided for a minimum of 3 months. • Resumption of sporting activities usually begins from 3 months with avoidance of regular running advised. Tennis, golf, and even skiing are acceptable with caution in the early phases. Total Knee Replacement

Mobilization and Physiotherapy Perioperative—Mobilization is often commenced immediately after surgery using a continuous passive motion (CPM) machine. However, opinion is divided as to its value. Mobilization—New enhanced recovery programs begin a full weight-bearing regime on the day of surgery, but classical practices begin on day one. Mobilization is facilitated by walking aids (frame, crutches, or sticks), which are used up to 12 weeks. Physiotherapy is vital until free flexion to 90° is achieved. It however focuses on early full extension that can determine optimal full functional recovery. Between 5 and 10% of patients may require a manipulation under anesthetic; between 4 and 8 weeks in flexion does not reach 90°. Delay to manipulate can lead to long-term stiffness and limitation of function. Patient expectation—Occasional discomfort especially anterior knee pain is frequent. Night pain can be severe for up to 12 weeks and requires strong analgesia. As many as 1:4/5 patients are unhappy with the outcome of TKR.

Rehabilitation After Total Ankle Replacement Mobilization commences on the first postoperative day. The patient’s weight-­ bearing status can be partial to full dependent on the prosthesis implanted. A splint or brace is advised for 6–8 weeks.

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Rehabilitation After MTP Joint Replacement Mobilization is facilitated using rigid sole shoe. This is worn for 6 weeks before progression to normal footwear. Physiotherapy is advised to optimize flexibility.

Rehabilitation After Shoulder and Elbow Replacement Passive exercises begin on the first postoperative day. Passive exercises are followed by progression to active assisted, active movements, and finally active against resistance (Thera-Band elasticated bands) is the standard protocol. The postoperative rehabilitation regime is a minimum of 12 weeks. In addition, it is vitally important that the patient carries out their own daily exercise regime. It is important that taking weight through the elbow is avoided for 8 weeks. Complication: Hematoma formation after elbow arthroplasty is a well-­recognized complication. This is not only painful but can lead to troublesome stiffness.

Rehabilitation After Wrist and Finger Joint Replacements A specialist hand physiotherapist and occupational therapist to make appropriate, splints are crucial for minimizing stiffness and optimizing function.

References 1. Hirschmann MT, Konala P, Cobb JP. The position and orientation of total knee replacement components: a comparison of conventional radiographs, transverse 2D-CT slices and 3D-CT reconstruction. J Bone Joint Surg Br. 2011;93(5):629–33. 2. Kwon YM, Cabanela ME, Jacobs JJ. Risk stratification algorithm for management of patients with dual modular total hip arthroplasty. J Arthroplast. 2014;29(11):2060–4. 3. Abele JT, Flemming JP. The accuracy of SPECT/T arthrography in evaluating aseptic loosening of hip and knee prosthesis. J Arthroplast. 2015;30(9):1647–51. 4. Meding JB, Ritter MA. Cemented and uncemented total hip arthroplasty using the same femoral component. Hip Int. 2016;26(1):62–6. 5. Australian Orthopaedic Association. National joint Replacement Registry:2015 annual reports. https://aoanjrr.sahmri.com. 6. Long WJ, Lewallen DJ. Uncemented porous tantalum acetabular components: early follow-up and failures in 599 revisions total hip arthroplasties. Iowa Orthop J. 2015;35:108–13. 7. Berry DJ, Morrey BF. 25 Year survivorship of 2000 consecutive primary charnley total hip replacements: factors affecting survivorship of acetabular and femoral components. J Bone Joint Surg. 2002;84-A(2):171–7. 8. Swedish Hip Arthroplasty Register: Annual report 2014. http://www.shpr.se/en/. 9. Bichara DA, Malchau E.  Vitamin E diffused highly cross-linked UHMWPE particles induce less osteolysis compared to highly cross-linked virgin UHMWPE particles in-vivo. J Arthroplast. 2014;29(9 suppl):232–7. 10. Tan SC, Lanting BA. Effect of taper design on trunnionosis in metal on polyethylene total hip arthroplasty. J Arthroplast. 2015;30(7):1269–72. 11. Selvarajah E, Inglis G. The rates of wear of X3 highly cross-linked PE at 5 years when coupled with a 36mm diameter ceramic femoral in young patients. Bone Joint J. 2015;97-B(11):1470–4.

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12. Owen DH, Walter WL. An estimation of the incidence of squeaking and revision surgery for squeaking in ceramic-on-ceramic total hip replacement: a meta-analysis and report from AOA NJR. Bone Joint J. 2014;96-B(2):181–7. 13. Traina F, Faldini C. Fracture of ceramic bearing surfaces following total hip replacement: a systematic review. Biomed Res Int. 2013;2013:157247. 14. Jameson SS, Baker PN, Mason J, et al. Independent predictors of revision following metal-on-­ metal hip resurfacing: a retrospective cohort study using National Joint Registry data. J Bone Joint Surg. 2012;94:746–54. 15. National Joint Registry for England and Wales: 8th Annual Report. http://www.njrcentre.org. uk/njrcentre 16. Glyn-Jones S, Pandit H, Kwon Y-M, et al. Risk factors for inflammatory pseudo tumour formation following hip resurfacing. J Bone Joint Surg. 2009;91:1566–74. 17. Wegrzyn J, Guyen O. Cementless total hip arthroplasty in Paget’s disease of bone: a retrospective review. Int Orthop. 2010;34(8):1103–9. 18. Stambough JB, Clohisy JC. Rapid recovery protocols for primary total hip arthroplasty can safely reduce length of stay without increasing readmissions. J Arthroplast. 2015;30(4):521–6. 19. Dennis DA, Komistek RD, Mahfouz MR, Haas BD, Stiehl JB.  Coventry award paper: multicentre determination of in  vivo kinematics after total knee arthroplasty. Clin Orthop. 2003;416:37–57. 20. Dennis DA, Komistek RD, Mahfouz MR, Walker SA, Tucker A.  A multicentre analysis of axial femorotibial rotation after total knee arthroplasty. Clin Orthop. 2004;428:180–9. 21. Haas BD, Komistek RD, Stiehl JB, Anderson DT, Northcut EJ.  Kinematic comparison of posterior cruciate sacrifice versus substitution in a mobile bearing total knee arthroplasty. J Arthroplast. 2002;17:685–92. 22. Argenson JN, Parratte S, et al. Survival analysis of total knee arthroplasty at a minimum of 10 years follow up: a multicentre French nationwide study including 846 cases. Orthop Traumatol Surg Res. 2013;99(4):385–90. 23. Ranawat AS, Rossi R, Loreti I, Rasquinha VJ, Rodriguez JA, Ranawat CS. Comparison of the PFC Sigma fixed-bearing and rotating-platform total knee arthroplasty in the same patient: short-term results. J Arthroplast. 2004;19:35–9. 24. Chen K, Li G, Fu D, Yuan C, Zhang Q, Cai Z.  Patellar resurfacing versus non resurfacing in total knee arthroplasty: a meta-analysis of randomised controlled trials. Int Orthop. 2013;37:1075–83. 25. Pakos EE, Ntzani EE, Trikalinos TA. Patellar resurfacing in total knee arthroplasty. A meta-­ analysis. J Bone Joint Surg Am. 2005;87:1483–95. 26. Wallin A., and Dalholm A.B. The Swedish knee arthroplasty register—annual report. 2009. 27. Ritter MA, Berend ME. Predicting ROM after total knee arthroplasty: clustering, log linear regression and regression free analysis. J Bone Joint Surg Am. 2003;85-A:1278–85. 28. Barrack RL, Rorabeck C. Comparison of surgical approaches in total knee arthroplasty. Clin Orthop Relat Res. 1998;356:16–21. 29. Langen S, Berend H. Lateral subvastus approach with TTO for primary TKA: clinical outcome and complications compared to medial parapatellar approach. Eur J Orthop Surg Traumatol. 2016;26:215–22. 30. Wang JW, Wang CJ. Total knee arthroplasty for arthritis of knee with extra-articular deformity. J Bone Joint Surg Am. 2002;84-A(10):1769–74. 31. Lonner JH, Lotke PA. Simultaneous femoral osteotomy and TKA for treatment of osteoarthritis associated with severe extra-articular deformity. J Bone Joint Surg Am. 2000;82(3):342–8. 32. Workgroup of the AAHKS Evidence based committee. Obesity and total joint arthroplasty: a literature based review. J Arthroplast. 2013;28(5):714–21. 33. Cartier P, Khefacha A. Long term results with the first patellofemoral prosthesis. Clin Orthop Relat Res. 2005;436:47–54. 34. Pandit H, Hamilton TW, Jenkins C, Mellon SJ, Dodd CAF, Murray DW. The clinical outcome of minimally invasive Phase 3 Oxford unicompartmental knee arthroplasty: a 15-year follow­up of 1000 UKAs. Bone Joint J. 2015;97-B:1493–500.

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35. Vorlat P, Putzeys G, Cottenie D, et al. The Oxford unicompartmental knee prosthesis: an independent 10-year survival analysis. Knee Surg Sports Traumatol Arthrosc. 2006;14:40–5. 36. National Joint Registry. National joint registry: 11th annual report. 37. Sassoon A, Nam D, Nunley R, Barrack R. Systematic review of patient-specific instrumentation in total knee arthroplasty: new but not improved. Clin Orthop Relat Res. 2015;473:151–8. 38. Kurtz W., Sinha R., Martin G., and Kimball K. Early outcomes utilizing a first-generation customized patient-specific TKA implant. In (eds): Presentation at the proceedings of British Association for Surgery of the Knee. 39. de Steiger RN, Liu YL, Graves SE. Computer navigation for total knee arthroplasty reduces revision rate for patients less than sixty-five years of age. J Bone Joint Surg Am. 2015;97:635–42. 40. Roberts TD, Clatworthy MG, Frampton CM, Young SW.  Does computer assisted navigation improve functional outcomes and implant survivability after total knee arthroplasty? J Arthroplast. 2015;30:59–63. 41. Orthopaedic Knowledge update: Hip and Knee Reconstruction, AAOS, 20:240 2017. 42. Duncan CP, Masri BA.  Fracture of the femur after hip replacement. Instr Course Lect. 1995;44:293. 43. Meek RM, Norwood T, Smith R, et al. The risk of peri-prosthetic fracture after primary and revision total hip and knee replacement. J Bone Joint Surg Br. 2011;93(1):96–101. 44. Parvizi J, Zmistowski B, Berbari EF, et  al. New definition for periprosthetic joint infection: from the workgroup of the Musculoskeletal Infection Society. Clin Orthop Relat Res. 2011;469:2992–4. 45. Pastides P, Nathwani D. Update on the diagnosis and management of the periprosthetic knee joint infection. Orthop Trauma. 2017;31(1):53–6. 46. Shubert D, Madoff S, Milillo R, Nandi S.  Neurovascular structure proximity to acetabular retractors in total hip arthroplasty. J Arthroplast. 2015;30(1):145–8. 47. Soong M, Rubash HE, Macaulay W. Dislocation after total hip arthroplasty. J Am Acad Orthop Surg. 2004;12(5):314–21. 48. Whitehouse MR, Stefanowich-Lawbuary NS, et al. The impact of leg length discrepancy on patient satisfaction and functional outcome following total hip arthroplasty. J Arthroplast. 2013;28(8):1408–14. 49. Jastifer JR, Caughlin MJ. Long-term follow-up of mobile bearing total ankle arthroplasty in the United States. Foot Ankle Int. 2015;36(2):143–50. 50. Haddad SL, et al. Intermediate and long term outcomes of total ankle arthroplasty and ankle arthrodesis. A systemic review of the literature. J Bone Joint Surg Am. 2007;89:1899–905. 51. Gougoulias N, et al. How successful are current ankle replacements? A systematic review of the literature. Clin Orthop Relat Res. 2010;468(1):199–208. 52. Guus M. Vermeulen. Thesis submitted for the PhD on 29th January 2014, to the University of Erasmus MC, Netherlands on `Thumbs Up’ Surgical Management and outcome of Primary Osteoarthritis at the base of the Thumb by Guus M.Vermeulen, MD, PhD.

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Introduction In recent years, there has been a significant increase in the demand for imaging examinations across all specialties, including orthopedics, and imaging is now a vital component in the assessment and workup of the orthopedic patient. A variety of imaging modalities are available to evaluate musculoskeletal pathology and include radiography, ultrasound (US), computed tomography (CT), magnetic resonance imaging (MRI), and nuclear imaging. These imaging modalities are commonly categorized as those which use either ionizing or non-ionizing radiation.

Ionizing and Non-ionizing Radiation Ionizing radiation can ionize atoms or molecules by removing electrons. Imaging modalities that use ionizing radiation include the following: • X-ray techniques such as plain-film radiography, computed tomography (CT), and fluoroscopy: These use electromagnetic radiation of higher energy than ­non-ionizing radiation.

E. McLoughlin (*) · S. L. James · R. Botchu Radiology Department, Royal Orthopaedic Hospital, Birmingham, UK e-mail: [email protected] E. M. Parvin School of Physical Sciences, The Open University, Milton Keynes, UK

© Springer Nature Switzerland AG 2019 K. M. Iyer, W. S. Khan (eds.), General Principles of Orthopedics and Trauma, https://doi.org/10.1007/978-3-030-15089-1_21

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• Nuclear medicine examinations using radiopharmaceuticals: These use radioactive tracers that emit gamma rays, which are high-energy electromagnetic radiation. There are two main categories of imaging that use non-ionizing radiation: • Ultrasound (US) uses very-high-frequency sound waves. • Magnetic resonance imaging (MRI) uses a strong magnetic field and low-energy electromagnetic radiation in the form of radio waves. Although MRI and US are safer and extremely useful imaging modalities, there is still a need for the modalities that use ionizing radiation. Therefore, consideration must be given to the safety of both the patient and the operator when imaging modalities using potentially damaging ionizing radiation are utilized.

Radiation Safety Ionizing radiation can cause tissue damage by changing the chemical properties of molecules following radiation exposure. The adverse effects of radiation exposure can be grouped into deterministic or stochastic effects: Deterministic effects are those which occur above a threshold radiation dose and their severity increases with dose [1]. They are associated with radiationinduced cell malfunction or death. Deterministic effects are divided into local and whole-­ body effects and occur shortly after exposure. Tissue-specific effects include cataracts, skin erythema/necrosis, hair loss, gastrointestinal mucosa lining loss, central nervous system tissue damage, and infertility. Whole-body effects include bone marrow damage/reduction in blood cell production, radiation sickness, and death. Stochastic effects are probabilistic effects and occur years after exposure. The risk increases with radiation dose, but the severity is independent of dose [1]. Stochastic effects are associated with damage to the DNA of cells and include cancer induction and genetic changes/teratogenesis. Orthopedic patients are increasingly undergoing multiple X-ray-based diagnostic investigations and image-guided procedures in the investigation and management of musculoskeletal pathology. This has implications for the radiation protection of staff and patients. Procedures involving radiation exposure during which medical professionals need to maintain close physical contact with the patient (e.g., CT-guided intervention or orthopedic procedures using fluoroscopy) can result in significant occupational exposure to X-rays. In order to minimize the harmful effects of ionizing radiation, medical professionals using ionizing radiation need to ensure that: • Imaging is justified [2] and used appropriately in all cases. • Imaging departments have protocols in place to ensure image optimization while keeping radiation doses as low as reasonably practicable (ALARP).

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• Established working procedures are in place in the radiology department and operating theatres to ensure that staff using ionizing radiation receive adequate training on how to operate imaging equipment. • Radiation monitoring and personal protective equipment including lead aprons, thyroid collars, and eye shields are available to ensure that medical professionals are appropriately protected [3].

Contrast Agents Specific contrast agents have been developed for use in CT, MRI, and, more recently, US imaging (see US advances section) and help to differentiate between tissues by improving contrast resolution. CT uses an iodine-based contrast which can be administered intravenously (IV) although contrast-enhanced CT studies are performed much less frequently in musculoskeletal imaging than in abdominal/chest imaging. Intra-articular injection of contrast, known as arthrography, may be performed to detect chondral abnormalities. The risks associated with iodine-based contrast agents include anaphylaxis, renal dysfunction in patients with acute or chronic renal failure, and extravasation causing potential soft-tissue necrosis. The risk of severe anaphylaxis is estimated at 0.04% [4]. MRI uses a gadolinium-based contrast agent and is used in musculoskeletal imaging to characterize tumors and identify areas of inflammation/infection. Contrast can also be used in the postsurgical spine to differentiate between postoperative scarring and recurrent disc herniation [5]. Intra-articular contrast is used to assess for internal derangement of joints. The most serious complication associated with gadolinium contrast is nephrogenic systemic fibrosis (NSF), and is more likely to occur in patients with impaired renal function. This iatrogenic disorder has an incidence of between 0.02% and 0.04% [6] and causes irreversible fibrosis of the skin, joints, internal organs, and eyes. Recent studies have also found that gadolinium crosses the blood–brain barrier and accumulates in the brain following multiple contrast-enhanced studies which may result in neurotoxicity [7, 8]. Due consideration should be given to the risks associated with contrast administration, particularly in patients with a history of contrast allergy or renal impairment.

Imaging Modalities Radiography Radiography uses X-rays to visualize the internal structures of the body. X-rays are transmitted through the area of interest and are attenuated (i.e., absorbed or scattered) in varying degrees by the different tissues within the body to create an image. This differing attenuation allows for excellent contrast between low-attenuation soft tissues and high-attenuation bone within the image and gives a two-dimensional representation of the area of interest.

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Fig. 21.1  Anteroposterior (a) and lateral (b) radiographs of the right ankle demonstrating a mixed lytic/sclerotic lesion in the distal tibia with cortical breach and periosteal reaction in keeping with an osteosarcoma

Radiography is the most frequently used modality in the preliminary evaluation of bone and joint disorders and for the identification of fractures/traumatic injury and bone lesions (see Fig. 21.1). Two orthogonal projections of the body part should be obtained. This aids in the diagnosis of acute fractures and minimizes misinterpretation of overlapping structures. The standard projections taken are in the lateral and anteroposterior (AP) planes. Additional or alternative views may be required in complex anatomical areas or if a particular pathology is suspected. Although assessment of soft tissues is limited on radiographs, identification of a joint effusion, soft-tissue swelling, or lipohemarthrosis (see Fig. 21.2) in the trauma setting may point to an underlying ligamentous injury or an occult fracture. Radiography

Advantages: • Readily available • Rapid acquisition of images • Allows for initial soft-tissue assessment (soft-tissue swelling and joint effusion) • Dynamic real-time assessment (fluoroscopy)

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Fig. 21.2  Lateral view of the knee demonstrating a fat-fluid level in the suprapatellar pouch in keeping with lipohemarthrosis

Disadvantages: • Ionizing radiation • Limited soft-tissue detail • Difficult to interpret imaging at sites with overlapping anatomy (e.g., cervical spine, medial clavicle)

 adiography Advances and Applications in Musculoskeletal R Imaging  omputed Radiography (CR) and Digital Radiography (DR) C Traditionally, radiographs were viewed as hard-copy films; however, significant advances in technology now mean that the images are digitized and transferred to the picture archiving and communication system (PACS). There are two types of digital radiography systems—computed radiography (CR) and digital radiography (DR), the latter rapidly superseding the former. CR uses a cassette-based system which includes a phosphor imaging plate to create a digital image; DR uses a digital X-ray detector to acquire images. Although soft-tissue detail is limited on radiographs, the differing X-ray attenuation characteristics of skeletal muscle, fat, fluid, and air allow for some discrimination of these structures.  tress, Weight Bearing, Standing, and Flexion/Extension Views S Stress views allow for dynamic assessment of a particular body part by imaging the area at rest and under active or passive stress and may provide indirect assessment of ligamentous injury [9]. Weight-bearing views can be performed and compared to the equivalent non-weight-bearing views to assess for underlying ligamentous instability [10]. Standing flexion and extension views of the lumbar spine can be performed to assess for spinal instability in the setting of spondylolisthesis. Flexion and extension views of the cervical spine can be performed to assess for atlantoaxial instability in at-risk patients (see Fig. 21.3).

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Fig. 21.3  Lateral flexion (a) and extension (b) radiographs of the cervical spine in a patient with rheumatoid arthritis demonstrating cervical instability at the atlantoaxial joint on flexion, with widening of the predental space

Fluoroscopy Fluoroscopy is an imaging technique that uses a continuous or pulsed X-ray beam to obtain real-time, dynamic images. An X-ray beam is passed through the area of interest and real-time images are displayed on a monitor and can be stored on the PACS system as imaging loops or static images. This imaging technique is a useful diagnostic tool for radiologists and is used to guide interventional procedures such as needle placement in joint and spinal injections, vertebroplasty (see Fig. 21.4), and arthrography. Fluoroscopy is also used by orthopedic surgeons to guide intraoperative prosthetic placement and to assess fracture reduction. Arthrography Arthrography is the introduction of a contrast agent (iodine or gadolinium) into a joint space. This is performed under fluoroscopic guidance, which ensures correct needle placement and intra-articular injection of contrast (see Fig. 21.5). This technique can be used in combination with CT or MRI following injection of the appropriate contrast agent and allows for optimal visualization of the internal joint structures on cross-sectional imaging compared to conventional studies. Dynamic assessment of joints following injection of contrast can also be performed under fluoroscopic guidance.

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Fig. 21.4  AP fluoroscopic views of the lumbar spine during a vertebroplasty with needles in situ (a) and following introduction of cement (b)

Fig. 21.5  AP arthrogram of the glenohumeral joint with contrast in situ which was introduced via a 22G needle

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Fig. 21.6  Ultrasound probes used in musculoskeletal imaging: from left to right 14 Hz hockey stick, 14 Hz linear, 9 Hz linear, 6 Hz curvilinear, 18 Hz linear probes

Ultrasound (US) Ultrasound uses high-frequency sound waves to produce images of soft-tissue structures. Ultrasound waves are produced by the stimulation of piezoelectric crystals by electrical currents within the ultrasound probe. These ultrasound waves are transmitted from the ultrasound probe and propagate through soft tissues and some are reflected back to the probe at soft-tissue interfaces. The reflected echoes are converted into electric currents by the piezoelectric crystals and are processed to form an ultrasound image which is displayed on the monitor. High-frequency (9–18 Hz) linear array ultrasound transducers are typically used in musculoskeletal ultrasound and allow optimal spatial resolution of superficial soft-tissue structures. A lower frequency transducer may be used for assessment of deeper structures but gives a lower spatial resolution. A hockey stick transducer is useful in the assessment of the small joints of the hands and feet (see Fig. 21.6). Ultrasound is an invaluable tool in the high-resolution assessment of soft-tissue structures such as tendons (see Fig. 21.7), ligaments, and muscles. It is useful in the characterization of soft-tissue masses and can identify joint effusions and synovitis. Dynamic assessment can identify tendon subluxation, impingement, or ligamentous laxity. Although visualization of bone is severely limited, evaluation of the bone-­ soft tissue interface and periosteum is possible in some circumstances.

Artifact Musculoskeletal ultrasound is prone to artifact including anisotropy and beam edge artifact. Anisotropy is the artifactual loss of reflectivity when the ultrasound beam is oblique to the tissue fibers during scanning. Beam edge artifact causes loss of normal signal and posterior acoustic shadowing at the edge of larger tendons. These

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Fig. 21.7  US of the shoulder demonstrating a full-thickness tear of the supraspinatus tendon (a and b) with fluid (*) within the subacromial subdeltoid bursa (c)

artifacts may prompt an incorrect diagnosis of tendinopathy or tendon tear. A solid knowledge base and good ultrasound technique are required for accurate assessment and prevention of the misinterpretation of findings.

Ultrasound

Advantages: • Readily available • Non-ionizing radiation • No patient contraindications • Dynamic, real-time assessment allows for correlation of patient symptoms and US findings by the operator Disadvantages: • Operator dependent • Poor visualization of bone • Prone to artifact • Risk of thermal heating or mechanical injury to tissues due to the high frequencies used • Visualization of structures may be limited by large body habitus

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 ltrasound Advances and Applications in Musculoskeletal U Imaging The use of ultrasound in musculoskeletal imaging has significantly increased over the last 30 years and ultrasound technology has continued to improve and evolve to meet the demand. Rapidly advancing technology has led to better image quality with a reduction in artifact. Ultrasound machines have a greater range of transducers and are smaller and easier to use. Portable and handheld units are now widely available. Recent advances in ultrasound technology have led to a broader range of applications in musculoskeletal imaging.

US-Guided Intervention US is commonly used in the musculoskeletal setting to guide needle placement in minimally invasive procedures such as steroid, botulinum toxin and platelet-rich plasma (PRP) injections, dry needling, barbotage, and soft-tissue biopsies (see Fig. 21.8). Studies have found that ultrasound is also beneficial over open surgery in minimally invasive procedures such as trigger finger release with reduced days off work and better cosmetic results over open repair [11].

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Fig. 21.8  US image of a soft-tissue lesion with intralesional vascularity (a). An US-guided biopsy was performed (b) with the arrows outlining the biopsy needle passing through the lesion. Histology confirmed a soft-tissue sarcoma

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 xtended Field of View (EFOV) US E This is a useful tool in musculoskeletal imaging which allows for a panoramic, continuous image of a soft-tissue structure to be obtained. This is used when the structure being assessed extends beyond the field of view of the ultrasound probe. The image acquired highlights the pathology more clearly (see Fig. 21.9). Doppler Imaging The vascularity of tissues can be assessed using Doppler imaging. The Doppler effect depends on the fact that the frequency of sound reflected from a moving body is increased or decreased depending on whether the body is moving towards or away from the transducer. This allows blood flow to be detected and measured. Both color and power Doppler modes have important applications in musculoskeletal disease because many inflammatory and degenerative musculoskeletal disorders demonstrate changes in microcirculation [12, 13]. Color Doppler provides information on the strength of Doppler signal as well as the direction and speed of blood flow. Power Doppler demonstrates the strength of the Doppler signal in color only. Power Doppler is three times more sensitive than color Doppler in detecting low-­ velocity flow while maintaining maximal spatial resolution [14] and is more widely used for musculoskeletal applications. Doppler imaging can detect new blood vessel formation (neovascularity) and therefore can be used to characterize soft-tissue masses and assess for active inflammation in joints and tendons (see Fig. 21.9).  ontrast-Enhanced Ultrasound (CEUS) C CEUS is a promising diagnostic tool in the musculoskeletal setting [15, 16]. A contrast agent containing gas microbubbles is injected intravenously and enhances the a

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Fig. 21.9  EFOV image (a) of the Achilles tendon demonstrating thickening and hypo-­echogenicity of the midportion. US images (b) and (c) show increased vascularity on color Doppler in keeping with Achilles tendinitis

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Doppler signal. This allows for the detection of low-speed blood flow, which would otherwise be undetectable using traditional color or power Doppler. CEUS is more sensitive than conventional ultrasound in identifying active synovitis as a marker for disease activity in arthritis [17, 18]. It may also be used to characterize soft-tissue lesions [19] and assess the vascularity of repaired rotator cuff tendons [20]. Muscle perfusion may also be assessed using this technique and used as an adjuvant in the diagnosis of inflammatory myopathies and myositis [21, 22].

 uperb Microvascular Imaging S This technique has been developed by Toshiba and detects perfusion of tiny vessels with slow flow without the need for intravenous contrast. Studies have discussed its potential uses in detecting low-grade inflammation in joints and tendons which would otherwise be undetectable using Doppler techniques, and in monitoring response to treatment [23]. It may also be used to stage progression of tendinosis in sports medicine and can be used to monitor healing in chronic injuries such as tendinitis [24]. A recent study has also shown it to be a potentially useful diagnostic tool in carpal tunnel syndrome by detecting low-flow blood flow in the median nerve [25]. Sonoelastography Noninvasive, qualitative assessment of soft-tissue elasticity and stiffness (relative to a reference stiffness such as subcutaneous fat) can be performed using sonoelastography. This technique involves applying repeated manual compression to the area of interest using an ultrasound transducer and then measuring the tissue displacement. It is based on the principle that compression causes greater displacement of tissues that are soft and less displacement in tissues that are stiff. There is increasing evidence for the use of elastography in the assessment of tendon, muscle, and nerve pathology [16]. Normal tendons are stiffer than abnormal tendons and studies on the use of sonoelastography to identify Achilles, patellar, and common extensor tendinopathy of the elbow have been encouraging [26]. Studies have also shown that the diagnostic sensitivity of tendinopathy can be increased through the combined use of sonoelastography and conventional ultrasound techniques [27]. This technique may also be used to monitor healing and treatment outcomes in tendinopathy [28]. Limitations include its reliance on skilled, repetitive manual compression to obtain high-quality images.  hear Wave Elastography (SWE) S SWE provides a quantitative assessment of tissue elasticity. This technique is more objective and reliable than sonoelastography in that it does not rely on the ultrasound operator to apply manual compression to the target tissue [29]. This technique involves the transfer of an acoustic pulse from the ultrasound probe into the target tissue. This produces a shear wave which extends laterally in the insonated tissue [16]. The shear wave velocity is calculated which provides a measure of the stiffness of the insonated tissue with normal (stiffer) tissues demonstrating a higher shear wave velocity than abnormal (softer) tissues. This technique has shown promise in assessing tendon [30], muscle, and nerve disorders [16].

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 D Ultrasound Imaging 3 This imaging technique allows for three-dimensional image rendering of a region of interest by obtaining and reconstructing volumetric data in any plane. This is particularly beneficial in the assessment of soft-tissue masses and in the evaluation of muscle tears [31] as well as in planning US-guided interventional procedures [32].  ltrasound Tissue Characterization (UTC) U This three-dimensional technique allows for tendon characterization by identifying tiny changes in tendon structure not visible using traditional ultrasound [16]. Tendons can be characterized into different echo-type patterns according the structural integrity of the tendon, ranging from normal to amorphous tendon patterns [30]. UTC has shown promise beyond standard ultrasound in improving diagnostic accuracy of tendinopathy, in predicting tendons at risk, and in monitoring healing. This is particularly useful in sports medicine and could potentially increase the clinician’s ability to accurately diagnose the extent of tendon pathology as well as identify preclinical injury and monitor tendon healing [33]. Fusion Imaging Fusion imaging combines two imaging modalities by preloading cross-sectional images (CT or MRI) onto the ultrasound machine. This allows for real-time spatial registration of the ultrasound images with previously acquired cross-sectional images of the area of interest. The CT or MRI images act as a map and can improve the anatomic localization of lesions on ultrasound. This has been shown to improve outcomes over conventional ultrasound in certain musculoskeletal procedures including perineural injections, calcific tendinopathy barbotage, and certain soft-­ tissue biopsies [34, 35].

Computed Tomography (CT) CT uses X-rays to produce cross-sectional images of the body. The X-ray tube is positioned within a circular gantry surrounding the CT table. The patient lies on the CT table, which slowly moves through the gantry while the X-ray tube rotates around the patient, continuously emitting an X-ray beam. The X-rays are detected by multiple detectors, which are located opposite the X-ray tube in the gantry, and electrical signals are created. Data are acquired from multiple angles and the CT images are reconstructed through a complex, computerized process known as Fourier back projection. CT is widely used in orthopedics and is invaluable in the assessment of complex fractures in the trauma setting. Three-dimensional reconstructions of complex fractures are particularly useful to the orthopedic surgeon in preoperative planning (see Fig. 21.10). CT can also be used to assess fracture healing and to identify malunion and nonunion. Loose bodies can be readily identified on CT, in contrast to other imaging modalities where loose body detection is difficult. Characterization of the

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Fig. 21.10  Complex, comminuted, intra-articular fracture of the ankle joint demonstrated on AP radiograph (a), CT (b), and 3D CT reformat (c)

matrix mineralization pattern of benign and malignant bone lesions and the staging of malignant bone tumors can also be achieved using CT. Although CT provides excellent spatial resolution and demarcation of bony structures, its assessment of soft-tissue structures is limited. Despite this, CT should be considered in the assessment of soft tissues, particularly in patients where MRI is contraindicated (see MRI disadvantages).

CT

Advantages: • Readily available • Rapid image acquisition • Excellent bony detail • Surface-rendered 3D reformats can be used for operative planning Disadvantages: • Ionizing radiation (involving larger radiation doses than plain radiography) • Poor differentiation of soft-tissue structures • Limited assessment of bone marrow • Artifact from metallic orthopedic prostheses degrades image quality

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CT Advances and Applications in Musculoskeletal Imaging In recent years, there has been increased media attention and public focus [36, 37] on the potential risks involved in radiation exposure from CT, even when the benefits of imaging outweigh the potential risks. To address this, developments in CT imaging have predominately revolved around reducing the dose as much as possible while maintaining image quality. This is achieved using a number of different techniques including scanning parameter modification, iterative reconstruction, and multi-planar image reconstruction [38]. CT doses can be significantly reduced by modifying CT scanning parameters such as X-ray tube current, tube potential, pitch, and gantry rotation time. Iterative reconstruction techniques can then be applied to these reduced-dose CT examinations to improve the image quality. In multi-planar reformatting, images are acquired in a two-dimensional axial plane but can be reformatted into two-dimensional coronal and sagittal planes which are of equal resolution to axial images and three-dimensional surface-rendered images can also be created using post-processing techniques.

 ual-Energy CT (DECT) D DECT is an evolving imaging technique in the musculoskeletal setting. DECT allows for the contemporaneous acquisition of images using two different X-ray energies, and therefore showing different tissue contrasts. This can be achieved by a number of methods but most commonly by rapid kilovoltage switching of a single X-ray source or by dual-source DECT.  Rapid kilovoltage switching uses a single X-ray tube that rapidly switches between two energy levels to acquire two datasets. Dual-source DECT uses two X-ray tubes and detector plates positioned at right angles to each other in the gantry to acquire two datasets simultaneously. DECT has a number of advantages over conventional CT; DECT can reduce artifact, aid in image optimization, and provide additional information on tissue composition [39]. The clinical applications of DECT include the following: 1. Bone Marrow Edema Detection: On conventional CT, fine trabecular bone cannot be distinguished from bone marrow. DECT may be used to remove high-attenuation bone from marrow by using material decomposition protocols, which significantly improves the evaluation of bone marrow [40]. DECT has shown promise in clinical studies in the detection of traumatic bone bruising and undisplaced long-bone and vertebral body fractures [41–43]. 2. Metal Artifact Reduction Software (MARS): Image degradation due to beam artifact from metal prostheses causes significant difficulty in interpreting CT in the orthopedic setting. Using post-processing techniques, DECT can significantly reduce artifact from metal prostheses by

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combining datasets at the two different energies to create an image that has a lower susceptibility to beam hardening artifacts [44, 45]. This allows for more accurate assessment of the bone and adjacent soft tissue and may also be used in patients with external fixators in situ. 3. Analysis of Ligaments and Tendons: Although differentiation of soft-tissue structures on conventional CT is poor, DECT can be used to differentiate soft-tissue collagenous structures such as tendons and ligaments through the use of a tissue decomposition algorithm. Recent studies have reported on the ability of DECT to evaluate the integrity of the stabilizing ligaments of the knee [46, 47], and to diagnose tendinopathy and tendon tears [48]. 4 . Detection of Bone Metastases and Osseous Lesions: In the oncology setting, differentiation of bone metastases from incidental, benign bone lesions is a common dilemma for radiologists. This can have implications for the subsequent management of the patient. DECT has shown early promise in differentiating between benign and malignant bone lesions through a number of techniques including quantitative and qualitative tissue decomposition, virtual non-contrast-enhanced imaging, and iodine mapping [39]. A recent study differentiated vertebral body metastases from Schmorl’s nodes using quantitative tissue decomposition techniques to measure the water content and bone composition of both lesions [49]. DECT has also shown encouraging results in detecting diffuse bone marrow involvement in multiple myeloma using decomposition protocols [50]. 5 . Detection of Monosodium Urate Crystals (MSU) in Gout: Traditionally, the diagnosis of gout is made by identifying MSU crystals in ­aspirated synovial fluid. This procedure is invasive, and interpretation can be difficult in certain cases [51]. DECT can be used to identify MSU crystals, in a noninvasive way, using tissue decomposition techniques [39].

 one Beam CT (CBCT) C CBCT, also known as flat-panel CT, is an imaging technique consisting of a cone-­ shaped X-ray beam and a flat-panel detector, as opposed to conventional CT which consists of a fan-shaped beam and multiple linear detectors. In CBCT, the X-ray tube and detector rotate around the patient and single-projection images are acquired at certain intervals from which a volumetric dataset is generated. This dataset can be used to reconstruct images in three planes. CBCT allows for high spatial resolution assessment of bony architecture at a lower radiation dose than conventional CT. Limitations of CBCT include the small field of view and limited soft-tissue assessment. CBCT has a number of applications in orthopedics including identification of fractures which are occult on plain radiography, more accurate assessment of joint degeneration compared to plain radiography, and assessment of sequestrum in chronic osteomyelitis. CBCT can be combined with arthrography which allows for detailed assessment of the articular cartilage, identification of intra-articular loose bodies and synovial tumors/PVNS, and evaluation of osteochondral defects [52].

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Fig. 21.11  Prone CT of the sacrum demonstrating a lytic lesion in the left sacral body (a). CT-guided sacroplasty with sacroplasty needles in situ (b) which are used to take a biopsy as well as introduce cement (c)

CT Arthrography CT arthrography involves the intra-articular injection of iodine contrast under fluoroscopic guidance (see Arthrography section) followed by a CT of the region of interest. This allows better visualization of the internal joint structures. Although MR arthrography is more commonly performed due to the excellent soft-tissue detail, CT arthrography has an important role in orthopedics. It can be used to assess the meniscus for a tear following meniscal repair [53] and has been shown to be superior to MR arthrography in assessing the cartilage in the hip [54]. The potential for DECT arthrography to improve contrast resolution over conventional CT arthrography has shown potential benefits, but refinement of post-­ processing techniques and larger trials are required to further investigate this [55]. CT-Guided Intervention CT is commonly used in the musculoskeletal setting to guide needle placement in minimally invasive procedures such as steroid and botulinum toxin injections, vertebroplasty, sacroplasty (see Fig. 21.11), and bone biopsies.

Magnetic Resonance Imaging (MRI) MRI uses the interaction between hydrogen (H) nuclei (protons) in the body and a strong magnetic field to create high-contrast images of the soft tissues and organs of the body. It depends on the fact that many body components (most

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notably water and fat) contain large numbers of hydrogen atoms and the nuclei of these atoms (the protons) behave like small magnets. The MRI scanner applies a magnetic field which causes the protons in the region of interest to align with the main magnetic field. At the same time, their magnetic axis rotates around the field direction; this is known as precession. Electromagnetic radiofrequency pulses are then applied via radiofrequency coils and, if the frequency of the pulse is the same as the precessional frequency of the protons, a phenomenon called resonance occurs; they absorb energy and their alignment is changed. When the radiofrequency pulses are switched off, the protons realign with the main magnetic field. They do this at different rates depending on the body tissue in which the hydrogen atoms are located. There are two key relaxation processes with relaxation times known as T1 and T2. T1 and T2 are different for different tissues. The radiofrequency signals emitted during relaxation are detected by radiofrequency coils and form the basis of the MRI signal from which images are generated. There are many complex sequences used in MRI but a study of these is beyond the scope of this chapter. Conventional imaging sequences used in musculoskeletal investigations include T1-, T2-, and proton density-­weighted sequences (with or without fat suppression); short T1 inversion recovery (STIR); gradient echo (GRE); and gadolinium-enhanced T1 sequences (see Contrast Agents section). MRI has revolutionized orthopedic imaging since its introduction in the 1970s and allows for high spatial resolution and multi-planar imaging of the musculoskeletal system with unparalleled soft-tissue contrast. MRI technology continues to develop and evolve to meet the increasing demand for imaging in the musculoskeletal setting.

MRI

Advantages: • Non-ionizing radiation • Excellent spatial resolution • Multi-planar ability • Superb soft-tissue detail and contrast resolution Disadvantages: • Enclosed scanner may not be suitable for patients who are claustrophobic. • Contraindicated in patients with MRI-incompatible implanted devices such as cardiac pacemakers, metallic foreign bodies, and aneurysm coils. • Metallic prostheses can cause significant artifacts and limit interpretation of images. • Highly sensitive modality but not always specific.

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MRI Advances and Applications in Musculoskeletal Imaging  RI Magnet Strength M MRI magnetic field strength is measured in Tesla (T). Previously, MRI imaging was performed using low field strengths of 1.5 T or less; however, the use of 3 T MRI has become increasingly common in routine practice and more recently higher field MRI strengths of up to 7 T have become available for research. The use of stronger magnets has resulted in reduced scanning times and better image resolution with improved visualization of cartilage, menisci, ligaments, and tendons.  losed, Open, Upright, and Extremity MRI Scanners C Conventional, closed MRI scanners use a cylindrical bore magnet. The patient lies supine in a narrow, tubular tunnel which is enclosed by the magnet. Although this is the fastest and most accurate way of scanning as high-field-strength magnets can be used, it can be difficult to tolerate in patients with claustrophobia. In recent years, newer closed scanners with shorter tubes and more internal space have been designed to increase patient comfort. Open, upright, and extremity scanners have also been developed: Open MRI scanners consist of two horizontally orientated metal discs which are the poles of the magnet. The patient lies supine between the metal discs. Open scanners do not have sides and are more comfortable for obese or claustrophobic patients. Upright MRI scanners allow images of the spine to be acquired under true weight-bearing conditions using a vertically open scanner. The patient sits or stands between two vertically orientated metal discs which are the poles of the magnet and can adopt various positions (for example flexion, extension, neutral) for comparison of the anatomy at different points. Current open and upright MRI magnets are only available in low or medium field strengths of 0.2  T–0.6  T and image resolution is therefore reduced compared to conventional scanners. Extremity MRI scanners can be used to image peripheral body parts such as the knee and ankle and are currently available in magnetic field strengths of up to 1.5 T. Although these scanners can be useful in the musculoskeletal setting, not all patients are suitable due to the limitations in field of view from the closed-bore configuration.  adiofrequency (RF) Coils R All radiofrequency signals transmitted to, and received from, the patient are via one or more RF coils. There are fixed coils which transmit the RF signal. These coils can also act as receive coils; however better quality images can often be obtained by using a separate receive coil which is placed closer to the part of the body to be imaged. There have been significant improvements in the design of such receive coils in recent years with a wide variety of RF coils now available for use in the

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musculoskeletal setting including surface coils for imaging specific joints such as the ankle and knee.

Cartilage Imaging MRI is the imaging modality of choice in assessing the articular cartilage and the availability of high-field-strength magnets, joint-specific surface coils, and cartilage-­ specific sequences has significantly improved evaluation of the articular cartilage in recent years. Cartilage-specific MRI sequences such as proton density fast spin-­echo (FSE-PD), three-dimensional fat-suppressed T1 gradient-echo (3D-FS T1 GRE), and spoiled gradient-echo sequences (SPGR) allow for optimal imaging of the articular cartilage and are commonly used to detect for morphological change [56]. Biochemical changes such as variations in cartilage water content and cartilage composition occur earlier than morphological changes and can now also be identified using diffusion MRI techniques, T2 mapping, T1rho imaging, and delayed gadoliniumenhanced MR imaging of the cartilage (dGEMRIC) [56]. Studies assessing cartilage sodium content as a marker of early biochemical change are also showing promise [57].  iffusion-Weighted Imaging (DWI) D DWI is an advanced MRI technique that provides information on tissue cellularity and cell-membrane integrity by assessing the random movement (diffusion) of water molecules within the body. The degree of diffusion depends on the cellularity or viscosity of a particular tissue/fluid. In general, malignant tumors have greater cellularity than benign tumors. This causes greater impedance to diffusion, i.e., diffusion restriction. Infective processes such as osteomyelitis and spondylodiscitis also demonstrate diffusion restriction due to high-viscosity, protein-rich fluids. In order to evaluate the diffusion within a lesion, the diffusion-weighted sequence and apparent diffusion coefficient (ADC) map need to be assessed in tandem (see Fig. 21.12). A highly cellular lesion or abscess will demonstrate high signal intensity on DWI and corresponding low signal intensity on ADC. DWI is showing promise in a number of applications in musculoskeletal imaging including differentiation between benign and malignant vertebral body fractures [58, 59], assessment of post-treatment response of skeletal metastases [60, 61], whole-body staging for bone metastases as an alternative to bone scintigraphy [62] (see Nuclear Medicine section), and differentiation between sarcomas and chronic expanding hematomas [63]. The role of DWI in differentiating between benign and malignant musculoskeletal tumors and bone/soft-tissue infection is unclear due to the overlapping spectrum of findings and additional research is needed to establish its clinical value [64].  iffusion Tensor Imaging (DTI) D DTI is an emerging MR technique that allows noninvasive assessment of the microstructure of muscles and nerves by measuring the direction of water molecule diffusion (fractional anisotropy (FA)) within tissues which is then depicted on a three-dimensional map. The FA of muscles and nerves is altered in the presence of pathology such as median nerve compression in carpal tunnel syndrome, lumbar

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Fig. 21.12  Coronal T1 (a) and contrast-enhanced T1 fat-saturated (b) images of the right leg demonstrating a low signal lesion in the proximal tibia with some enhancement postcontrast. DWI showed low signal on the ADC map (c) with corresponding high signal on B1200 image (d), in keeping with diffusion restriction. Biopsy-confirmed osteosarcoma

nerve compression, peripheral nerve tumors, and muscle ischemia. DTI shows promise for the detection of early abnormalities in muscles and nerves before they become apparent on conventional MRI; however, further research in this area is needed to assess the clinical utility of this technique [65].

 R Elastography (MRE) M A number of musculoskeletal conditions can lead to changes in tissue stiffness; for example, tissue stiffness is increased in neuromuscular disease [66] and decreased in myositis [67]. MRE is a noninvasive technique to assess tissue stiffness quantitatively. It does this by applying a mechanical wave through tissue and imaging this wave using a modified phase-contrast sequence and then converting the image into an elastogram. MRE correlates with electromyography in the assessment of muscle activity [68]. MRE is showing promise in characterizing neuromuscular disease and evaluating response to treatment [69, 70].  hemical Shift Imaging (CSI) C CSI (also known as opposed-phase imaging) is an important tool in musculoskeletal imaging. It is used to differentiate between benign and malignant tumors based on the premise that a lesion containing fat is highly suggestive of a benign lesion [71]. Because of the small magnetic field produced by the electrons surrounding a proton, its resonant frequency will vary slightly depending on their chemical

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environment. As a result, the resonant frequencies of protons in different tissues are slightly different. This shift in resonant frequency is known as a chemical shift. In particular, there is a small difference between the resonant frequencies of protons in fat and water, and this is utilized in CSI. Because of the difference in frequencies, the signals from fat and water will sometimes be in phase and sometimes out of phase. These signals are additive at the point when the protons are cycling in phase, and subtractive when cycling out of phase. Therefore, lesions containing similar quantities of water and fat decrease in signal intensity on out of phase as the fat and water signals will cancel each other out. Areas containing water only (due to pathological replacement of fat) will not decrease in signal intensity as there is no fat to cancel out the signal from water. Signal dropout of >20% on out-of-phase images is suggestive of benign process (see Fig.  21.13), with signal dropout of 75 F (24 °C), use of more than eight layers, and use of a pillow (inadequate ventilation). Plaster residue in the dip water did not increase the exothermic reaction. Moisture on the outside of the cast decreased the temperature of the plaster [10]. According to Halanski et al., the surface of the cast was 2.7 ± 1.9 °C cooler than the internal temperature. A dip water temperature of 50 °C, a 24-ply cast thickness, use of a plastic pillow, overwrapping of a curing plaster cast with synthetic, and use of a splint folded on itself were associated with temperatures causing burns [11]. Plaster of Paris (POP) is a building material having gypsum as its main component. It is used for coating walls and ceilings and also for creating architectural designs. Plaster of Paris is manufactured as a dry powder and is mixed with water to form a paste when used. Below are some of its advantages and disadvantages to give you an idea whether you should use it in your dream home or not. Advantages of plaster of Paris: 1. It is light in weight and more durable. 2. It has low thermal conductivity. 3. It is a very good fire resistant and hence a very good heat-insulating material. 4. It does not shrink while setting. Therefore, it does not develop cracks on heating or setting. 5. It forms a thick surface to resist normal knocks after drying. 6. It mixes up easily with water and is easy to spread and level. 7. It has good adhesion on fibrous materials. 8. It gives a firm surface on which the colors can settle. 9. It has no appreciable chemical action on paint and does not cause alkali attack. 10. Plaster of Paris gives a decorative interior finish. Its gypsum content provides it a lot of shine and smoothness. 11. It can easily be molded into any shape. Disadvantages of plaster of Paris: 1 . Gypsum plaster is not suitable for exterior finish as it is slightly soluble in water. 2. It is more expensive than cement or cement lime plaster. 3. It cannot be used in moist situations.

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4. Skilled labor is required for precise application and thus labor cost for applying plaster of Paris is high. Orthopedic uses of cast: 1. To support fractured bones, controlling the movement of fragments, and resting the damaged tissues 2. To stabilize and rest the joints in ligamentous injury 3. To support and immobilze joints and limbs postoperatively until healing has occurred 4. To correct a deformity 5. To ensure rest of infected tissues 6. To make a negative mold of a part of the body Materials available for casting: 1 . Plaster of Paris 2. Plaster of Paris with melamine resins 3. Materials which undergo polymerization: (a) Water activated (b) Non-water activated 4. Low-temperature thermoplastics

Plaster of Paris The name POP is derived from an accident to a house built of gypsum, near Paris. The house burnt down. When rain fell on baked mud of the floors, it was observed that the footprints in the mud set rock hard. Plaster of Paris was first used by Matthysen, a Dutch military surgeon in 1952. The POP bandage consists of rolls of muslin stiffened by dextrose or starch and impregnated with the hemihydrate of calcium sulfate. When water is added, the calcium sulfate takes up its water of crystallization: 2(CaSo4 + ½H2O) + 3H2O = 2(CaSo4 + 2H2O) + Heat. The setting time is the time taken to change from the powder form to the crystalline form. The drying time is the time taken to change from the crystalline to the anhydrous form. The average setting time is around 3–9 min and the drying time is around 24–72 h. The factors which decrease the setting time are (1) hot water, (2) salt, (3) borax, and (4) resin. The factors which increase the setting time are (1) cold water and (2) sugar. The POP is of various forms such as (1) slab when only a part of the circumference of the limb is incorporated, (2) cast when encircles the entire circumference of the limb, (3) spica, and (4) brace.

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The advantages are as follows: (1) cost effective, (2) nonallergic, and (3) ease of molding into different forms. The disadvantages are as follows: (1) radio-opaque and hence may occlude fracture lines, (2) heavy, and (3) easily breaks when comes in contact with water. Rules for application of POP casts: The first is padding which is applied from distal to proximal with a 50% overlap, a minimum of two layers, along with extra padding over the fibular head, malleoli, patella, and olecranon. The plaster can then be applied by dipping it in cold water which will maximize the molding time, 8 in. width for the thigh, 6 in. width for the leg, and 4 in. width for the arm and the forearm. In a summary the rules for POP casts are as follows: 1 . 8 in. for the thigh, 6 in. for the leg, and 4 in. for the forearm. 2. Must include one joint above and one joint below. 3. It must be molded with palms and not the fingers to avoid indentation. 4. The joints should be immobilized in a functional position. 5. It should not be too tight or too loose, i.e., with adequate padding. 6. The pop is dipped vertically into the water till air bubbles cease to come. 7. The uniform thickness of plaster is preferred. Hence depending on the technique used, these plaster casts can be divided into three types namely (1) badly padded plaster, (2) unpadded plaster, and (3) padded plaster. Both fiberglass and plaster casts are applied to injured limbs to immobilize them and allow the bones, ligaments, tendons, or muscles to heal after an injury such as a break, sprain, or dislocation. They are also applied after surgical procedures including correction of clubfoot and other congenital limb deformities. Plaster cast material is made from a type of naturally occurring gypsum known as plaster of Paris that is used to coat fiber bandages. Fiberglass casting tape is made from woven fiberglass that is coated with polyurethane resin. This accounts for their differences in composition. Both fiberglass and plaster casts differ in appearances in that a plaster cast is smooth and always white as only white plaster of Paris bandages are available. A fiberglass cast is webbed in texture and appearance and it is often colored. Common fiberglass cast colors include blue, pink, and green. Both types of casts can be and often are signed and decorated with felt tip markers. Both fiberglass and plaster casts differ in weight, strength, and durability. Fiberglass casts are lighter and stronger than plaster casts. They also last longer as they are more resistant to water damage and wear. However, neither type of cast is waterproof, unless a specific waterproof lining is used with a fiberglass cast. Both also differ in porosity, drying time, and flexibility: Fiberglass is more porous than plaster, so that a fiberglass cast is often more comfortable to wear. In addition, a fiberglass cast takes 30 min to 2 h to dry as opposed to up to 48 h for a plaster cast. However, plaster is easier to mold than fiberglass. Both also differ in price as plaster is less expensive than fiberglass. Recent uses and alternatives.

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Plaster of Paris or calcium sulfate has found other uses as well. It has been used as bone graft substitute and to fill up bone defects [12]. It has been used in spinal surgery as a bone graft substitute. POP is also being investigated as an antibiotic delivery mechanism [13]. However POP usage has been declining in its use as casting material after the advent of fiberglass or polyurethane tapes and splints. Plaster has certain technical advantages over synthetics. Plaster can be tucked or pleated. Plaster requires less tension for application. Gloves are not required. Plaster absorbs fluids, including pus, blood, and sweat. If a cast saw is not available, the plaster cast may be removed by soaking and unrolling or using simple hand-cutting instruments. However, compared with fiberglass, plaster may be difficult to store in humidity and is more difficult to keep clean. Plaster casts are heavier than fiberglass, exhibit more breakdown for short-leg casts, and are judged to be more restrictive and less comfortable [14]. However in a country like India where the cost considerations come into play POP still remains the choice of material in casting. From the early days of orthopedics when fracture management was mostly conservative to the present era of technological advancement where every fracture is managed aggressively and immediately with internal fixation, POP has been our constant companion, and we can safely hazard a guess that it will remain so in the future. This places a responsibility on the orthopedic residents to learn proper plaster techniques and not look down upon this simple and effective method for the treatment of fractures. A consideration may also be given to more emphasis of closed management of fractures using POP as a part of orthopedic curriculum in a developing country like India where access to surgical facilities is limited especially in remote places. The liberty has been taken to state that the days of identifying orthopedicians in hospital corridors by looking at the white POP stains on trousers and shoes will not be history.

References 1. Sarmiento A, Kinman PB. Functional bracing of fractures of the shaft of the humerus. J Bone Joint Surg Am. 1977;59:596–601. 2. Ponseti IV, Smoley EN. Congenital clubfoot: the results of treatment. J Bone Joint Surg Am. 1963;45:2261–70. 3. Peltier LF. Orthopedics: a history and iconography. San Francisco: Norman Publishing; 1993. p. 195–222. 4. Risser JC, Norquist DM. A follow-up study of the treatment of scoliosis. J Bone Joint Surg Am. 1958;40:555–69. 5. Nawijn SE, van der Linde H, Emmelot CH, Hofstad CJ. Stump management after trans-tibial amputation: a systematic review. Prosthetics Orthot Int. 2005;29:13–26. 6. Nabuurs-Franssen MH, Sleegers R. Total contact casting of the diabetic foot in daily practice: a prospective follow-up study. Diabetes Care. 2005;28:243–7. 7. Connolly J. Non-operative fracture treatment. In: Bucholz RW, Heckman JD, Court-Brown C, Tornetta P, Koval KJ, Wirth MA, editors. Rockwood and green’s fractures in adults, vol. vol. 1. 6th ed. Philadelphia, PA: Lippincott Williams and Wilkins; 2006. p. 145–208. 8. Ma HJ, Yang Y. Acquired localized hypertrichosis induced by internal fixation and plaster cast application. Ann Dermatol. 2013;25:365–7.

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9. Malviya A, Tsintzas D, Mahawar K, Bache CE, Glithero PR. Gap index: a good predictor of failure of plaster cast in distal third radius fractures. J Pediatr Orthop B. 2007;16:48–52. 10. Lavalette R, Pope MH, Dickstein H. Setting temperatures of plaster casts. The influence of technical variables. J Bone Joint Surg Am. 1982;64:907–11. 11. Halanski MA, Halanski AD, Oza A, Vanderby R, Munoz A, Noonan KJ. Thermal injury with contemporary cast-application techniques and methods to circumvent morbidity. J Bone Joint Surg Am. 2007;89:2369–77. 12. Borrelli J Jr, Prickett WD. Treatment of nonunions and osseous defects with bone graft and calcium sulfate. Clin Orthop. 2003;411:245–54. 13. Cai X, Han K, Cong X. The use of calcium sulfate impregnated with vancomycin in the treatment of open fractures of long bones: a preliminary study. Orthopedics. 2010;33 14. Kowalski KL, Pitcher JD Jr, Bickley B.  Evaluation of fiberglass versus Plaster of Paris for immobilization of fractures of the arm and leg. Mil Med. 2002;167:657–61.

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Open Fractures An open (or compound) fracture occurs when the skin overlying a fracture is broken, allowing communication between the fracture and the external environment [1]. Open Fractures: Gustilo-Anderson Classification: • Grade I: wound 5 cm, or gross contamination, crush injury, or excessive soft-­ tissue loss. A—adequate soft-tissue coverage B—fracture cover not possible without local/distant flaps C—arterial injury that needs to be repaired Open Fractures: Management: 1 . Check neurovascular status, fluid resuscitation. 2. Remove large pieces of debris and cover with sterile wet dressing. 3. Immediate parenteral antimicrobials: first-generation cephalosporin and add aminoglycoside for types II and III. 4. Urgent orthopedic consultation and most require irrigation and debridement in OR. Open Fractures: Complications: Wound Infection—2% in Type I, >10% in Type III, Osteomyelitis—Staph aureus, Pseudomonas sp.,Gas Gangrene, Tetanus, Nonunion/Malunion. Acute Compartment Syndrome: Compartment syndrome (CS) is a serious lifeand limb-threatening complications of extremity trauma. K. M. Iyer (*) Royal Free Hampstead NHS Trust, Royal Free Hospital, London, UK © Springer Nature Switzerland AG 2019 K. M. Iyer, W. S. Khan (eds.), General Principles of Orthopedics and Trauma, https://doi.org/10.1007/978-3-030-15089-1_23

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History Richard von Volkmann in 1881 published an article [2] in which he attempted to describe the condition of irreversible contractures of the flexor muscles of the hand to ischemic processes occurring in the forearm due to the application of restrictive dressing to an injured limb. Hildebrand in 1906 first used [3] the term Volkmann ischemic contracture to describe the final result of any untreated compartment syndrome, and was the first to suggest that elevated tissue pressure may be related to ischemic contracture. Thomas in 1909 reviewed the 112 published cases of Volkmann ischemic contracture and found fractures to be the predominant cause [4]. He also noted that tight bandages, an arterial embolus, or arterial insufficiency could also lead to the problem. Murphy in 1914 was the first to suggest that fasciotomy [5] might prevent the contracture. He also suggested that tissue pressure and fasciotomy were related to the development of contracture. Ellis in 1958 reported a 2% incidence of compartment syndrome with tibia fractures [6], and increased attention was paid to contractures involving the lower extremities. Seddon, Kelly, and Whitesides in 1967 demonstrated the existence of four compartments in the leg and the need to decompress more than just the anterior compartment [7]. Since then, compartment syndrome has been shown to affect many areas of the body, including the hand, foot, thigh, and buttocks.

Compartment Syndrome: Etiology Compartment size: It is usually caused by a tight dressing; bandage/cast, or localized external pressure; lying on limb; and also closure of fascial defects. Compartment content: Bleeding; fractures, vascular injury, bleeding disorders, and capillary permeability; caused by ischemia/trauma/burns/exercise/snake bite/ drug injection/IVF. Fracture: It is the most common cause with an incidence of accompanying compartment syndrome of 9.1%. The incidence is directly proportional to the degree of injury to soft tissue and bone which occurs most often in association with a comminuted, grade III open injury to a pedestrian. Blunt trauma is the second most common cause and about 23% of compartment syndrome which is 25% due to direct blow.

ACS: Etiology 1. Crush injury 2. Circumferential burns 3. Snake bites 4. Fractures—75% 5. Tourniquets, constrictive dressings/plasters 6. Hematoma—patient with coagulopathy at increased risk Pathophysiology of Compartment Syndrome (Fig. 23.1).

23  Emergencies in Orthopedics Fig. 23.1  Line diagram of the pathophysiology of compartment syndrome

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Pathophysiology of Compartment Syndrome Arterial Damage

Direct injury

lschaemia

Reduced Blood Flow

Painful Pale Pulseless Paraesthetic Paralysed

Oedema

Increased Compartment Pressure

Fasciotomy

ACS: Findings 1 . Severe pain (out of proportion to injury) 2. Pain with passive stretch 3. Tense compartment 4. Tight, shiny skin 5. Along with (5 Ps) of ischemia, namely (A) pain, (B) paresthesias, (C) paralysis, (D) pulselessness, and (E) pallor. One can confirm diagnosis (Fig. 23.2) by measuring intracompartmental pressures (Stryker STIC).

ACS: Management 1. Early recognition 2. Muscle necrosis at delta pressure 24–48 h)

Fasciotomy Principles 1 . Make early diagnosis. 2. Long extensile incisions. 3. Release all fascial compartments. 4. Preserve neurovascular structures. 5. Debride necrotic tissues. 6. Coverage within 7–10 days.

Compartment Syndrome = Lower Leg Four compartments: (1) Lateral: Peroneus longus and brevis; (2) anterior: EHL, EDC, tibialis anterior, and peroneus tertius; (3) superficial posterior—gastrocnemius and soleus; (4) deep posterior—tibialis posterior, FHL, and FDL. Single Incision: Perifibular fasciotomy: Matsen et  al. [9]. Single incision just posterior to fibula; be careful of the common peroneal nerve. Double Incision: Mubarak et al. [10]. In most instances it affords better exposure of the four compartments (Fig. 23.4), namely two vertical incisions separated by

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anterior intermuscular septum superficial peroneal nerve/lateral

tibial nerve/ deep posterior compartment intermuscular septum

compartment fibula posterior intermuscular Septum

sural nerve/ superficial posterior compartment

Fig. 23.4  Line diagram showing that all the four compartments should be decompressed

minimum 8 cm: one incision over anterior and lateral compartments (take care to avoid the superficial peroneal nerve) and the other incision located 1–2 cm behind posteromedial aspect of tibia (take care to avoid the saphenous nerve and vein). PS: Look for superficial peroneal nerve: Superficial peroneal nerve exits from lateral compartment about 10 cm above lateral malleolus and courses into the anterior compartment (risk of injury). Perifibular: Posterior to fibular head to just above lateral malleolus—expose and protect common peroneal nerve proximally; more difficult to decompress deep compartment, anterior incision mobilized around fibula decompression of anterior/ lateral compartments. Two incisions: First incision placed halfway between tibia crest and fibula. Transverse fascia incision to identify the intermuscular septum. Watch out for superficial peroneal nerve close to the septum. Second incision posteromedial approach—2 cm posterior to posteromedial margin of tibia as it avoids saphenous nerve/vein. Use a generous incision: (1) Lengthening the skin incisions to an average of 16 cm decreases intracompartmental pressures significantly. (2) The skin envelope is a contributing factor in acute compartment syndromes of the leg and the use of generous skin incisions is supported.

Compartment Syndrome: Forearm Anatomy: three compartments: mobile wad-BR, ECRL, ECRB; volar-superficial and deep flexors; and dorsal-extensors; pronator quadrates are described as a separate compartment.

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Forearm Fasciotomy: Volar-Henry approach—Includes a carpal tunnel release; releases lacertus fibrosus and fascia. Protects median nerve, brachial artery, and tendons after release. Forearm Fasciotomy: (1) Protects median nerve, brachial artery, and tendons after release and (2) considers dorsal release. Hand Fasciotomy: Interosseous muscles surrounded by investing fascia—not a true compartment; dorsal incisions along second and fourth MC releasing on both sides and deep bluntly. Can reach the adductor compartment via second MC incision. Thenar radial side of thumb hypothenar ulnar side of fifth MC. Compartment Syndrome—Hand: There is a nonspecific aching of the hand which is a disproportionate pain. There is a loss of digital motion and continued swelling with MP extension and PIP flexion which makes it difficult to measure tissue pressure.

Fasciotomy of Hand There are ten separate osteofascial compartments—dorsal interossei (4), palmar interossei (3), thenar and hypothenar (2), and adductor pollicis (1). Finger fasciotomy: The investing fascia supported by tough volar skin; it compartmentalizes at flexion creases with ulnar side index, long, and ring fingers and radial side thumb and small. It spares dorsal digital nerve branches; it makes incision at neutral axis of motion—where flexor creases end over distal phalanx close to nail. Compartment Syndrome—Foot: There are nine compartments, namely medial, superficial, lateral, calcaneal—interossei (4), adductor. Careful exam with any swelling; clinical suspicion with certain mechanisms of injury such as Lisfranc fracture dislocation and calcaneus fracture. Foot Fasciotomy: Traditionally five compartments (lateral, medial, central, interosseous, and calcaneal); two dorsal incisions over second and fourth MT which release interossei and adductor; medial incision—3  cm from plantar surface and 4  cm from posterior heel—subsequent release of superior and inferior exposing plantar aponeurosis and gets abductor hallucis, calcaneal compartment, and digiti quinti. Compartment Syndrome—Foot: (1) Dorsal incision—to release the interosseous and adductor; (2) medial incision—to release the medial, superficial lateral, and calcaneal compartments. Compartment Syndrome—Thigh: (1) Lateral to release anterior and posterior compartments. (2) May require medial incision for adductor compartment. Delayed Fasciotomy: The infection rate of 46% and amputation rate of 21% after a delay of 12 h; 4.5% complications for early fasciotomies and 54% for delayed ones. Recommendations: If the CS has existed for more than 8–10 h, supportive treatment of acute renal failure should be considered. The skin is left intact and late reconstructions may be planned. In delayed cases, routine fasciotomy may not be successful.

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Wound Management 1 . After the fasciotomy, a bulky compression dressing and a splint are applied. 2. “VAC” (vacuum-assisted closure) can be used. 3. Foot should be placed in neutral to prevent equine contracture. 4. Incision for the fasciotomy usually can be closed after 3–5 days.

Interim Coverage Techniques (1) Simple absorbent dressing which is a semipermeable skin-like membrane or a vessel loop “bootlace” and (2) “VAC” (vacuum-assisted closure). Wound is not closed at initial surgery and a second-look debridement is done with consideration for coverage after 48–72 h. Limb should not be at risk for further swelling. Patient should be adequately stabilized and usually requires skin graft. DPC is possible if residual swelling is minimal. Flap coverage is needed if nerves, vessels, or bone are exposed. Goal is to obtain definitive coverage within 7–10 days. Wound Closure: STSG or a delayed primary closure with relaxing incisions.

Complications Related to Fasciotomies 1. Altered sensation within the margins of the wound (77%) 2. Dry, scaly skin (40%) 3. Pruritus (33%) 4. Discolored wounds (30%) 5. Swollen limbs (25%) 6. Tethered scars (26%) 7. Recurrent ulceration (13%) 8. Muscle herniation (13%) 9. Pain related to the wound (10%) 10. Tethered tendons (7%)

Complications Related to CS Late Sequelae: 1. Volkmann’s contracture 2. Weak dorsiflexors 3. Claw toes 4. Sensory loss 5. Chronic pain 6. Amputation

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Joints: Dislocations: 1 . Displacement of bones at a joint from their normal position. 2. Do X-rays before and after reduction to look for any associated fractures.

Dislocation: Shoulder 1. Most common major joint dislocation: Anterior (95%)—usually caused by fall on hand while posterior (2–4%) electrocution/seizure. 2. May be associated with fracture dislocation, rotator cuff tear, or a neurovascular injury.

Dislocation: Knee 1 . Injury to popliteal artery and vein is common. 2. Peroneal nerve injury in 20–40% of knee dislocations. 3. Associated with ligamentous injury. 4. Anterior (31%). 5. Posterior (25%). 6. Lateral (13%). 7. Medial (3%).

Dislocation: Hip 1 . Usually seen in high-energy trauma. 2. It is more frequent in young patients: (a) Posterior—hip in internal rotation, most common (b) Anterior—hip in external rotation (c) Central—acetabular fracture 3. It may result in avascular necrosis of femoral head, and there is sciatic nerve injury in 10–35%.

Neurovascular Injuries In fractures and dislocations it is better to check before and after reduction. Neurovascular Injuries—Etiology: 1 . Fracture for example humerus and femur 2. Dislocation for example elbow and knee 3. Direct/penetrating trauma 4. Thrombus

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5 . Direct compression/acute compartment syndrome 6. Cast, unconscious Common vascular injuries Injury First rib fracture Shoulder dislocation Humerus—supracondylar fracture Elbow dislocation Pelvic fracture Femoral supracondylar fracture Knee dislocation Proximal tibial

Vessel Subclavian vein Axillary artery Brachial artery Brachial artery Presacral and internal iliac Femoral artery Popliteal artery or vein Popliteal artery or vein

Clinical Features and Management 1. Paraesthesia/numbness 2. Injured limb cold, cyanosed, pulse weak/absent 3. Call for help!. At the same time (a) remove all bandages and splints and (b) reduce the fracture/dislocation and reassess the circulation. 4. If no improvement then vessels must be explored by operation. 5. If vascular injury is suspected angiogram should be performed immediately. Common nerve injuries Injury Shoulder dislocation Humeral shaft fracture Humeral supracondylar facture Elbow medial condyle Monteggia fracture—dislocation Hip dislocation Knee dislocation

Nerve Axillary nerve Radial nerve Radial or median nerve Ulnar nerve Posterior—interosseous Sciatic nerve Peroneal nerve

Clinical Features and Management 1 . Paraesthesia and weakness to supplied area. 2. Closed injuries: nerve seldom severed, 90% recovery in 4  months. If not do nerve conduction studies +/− repair.

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3. Open injuries: Nerve injury likely complete. Should be explored at the time of debridement/repair.

Indications for Early Exploration 1 . Nerve injury associated with open fracture. 2. Nerve injury in fracture that needs internal fixation. 3. Presence of concomitant vascular injury. 4. Nerve damage diagnosed after manipulation of fracture.

Septic Joints/Septic Arthritis It is defined as inflammation of a synovial membrane with purulent effusion into the joint capsule, followed by articular cartilage erosion by bacterial and cellular enzymes. It is usually monoarticular, and usually bacterial with Staph aureus, or Streptococcus or Neisseria gonorrhoeae. It is usually by direct invasion through penetrating wound, intra-articular injection, or arthroscopy. It may be by direct spread from adjacent bone abscess and in some cases may be by blood spread from distant site. Sites: (1) Knee—40–50%; (2) hip—20–25%* (hip is the most common in infants and very young children); (3) wrist—10%; and (4) shoulder, ankle, and elbow—10–15%.

Septic Joint: Risk Factors (1) Prosthetic joint; (2) joint surgery; (3) rheumatoid arthritis; (4) elderly; (5) diabetes mellitus; (6) IV drug use; (7) immunosuppression; and (8) AIDS. Septic Joint: Signs and Symptoms: 1. Rapid onset 2. Joint pain 3. Joint swelling 4. Joint warmth 5. Joint erythema 6. Decreased range of motion 7. Pain with active and passive ROM 8. Fever, raised WCC/CRP, positive blood cultures

Septic Joint: Diagnosis Diagnosis by aspiration which on gram stain, microscopy, and culture shows leucocytes >50,000/mL, highly suggestive of sepsis.

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Septic Joint: Treatment: (1) Joint washout in theatre, (2) IV Abx 4–7 days and then orally for another 3 weeks, (3) analgesia, and (4) splintage. Septic Joint: Complications: 1 . Rapid destruction of joint with delayed treatment (>24 h) 2. Growth retardation, deformity of joint (children) 3. Degenerative joint disease 4. Osteomyelitis 5. Joint fibrosis and ankylosing 6. Sepsis 7. Death

Conus Medullaris and Cauda Equina Syndromes Conus medullaris and cauda equine syndromes are clinical entities. Diagnosis based on clinical findings 1. History and physical examination: Diagnosis prompts emergent acquisition of appropriate radiographic workup. 2. Exclude psychogenic causes. 3. Identify the pathology to aid in the formulation of a treatment plan.

Introduction Patients with conus medullaris syndrome typically present with symptoms consistent with spinal cord compression, spinal cord dysfunction, and “intrinsic pathology” while patients with cauda equina syndrome typically present with symptoms consistent with lumbosacral radiculopathies and “extrinsic pathology.” Practically = There is much overlap in symptomatology and both require complete evaluation, including imaging, to manage appropriately.

Conus Medullaris Syndrome Historically (i.e., in the “pure, classic” syndrome) defined as signs consisting of: 1 . Paralytic bladder incontinence 2. Bowel incontinence 3. Impotence 4. Perineal sensory changes 5. Absence of lower extremity weakness Presently, a constellation of signs and symptoms including: 1. Bowel dysfunction 2. Bladder dysfunction

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3. Sexual dysfunction 4. Poor rectal tone 5. Perianal sensory changes 6. Sometimes, lower extremity weakness Etiologies: tumor, vascular lesion, diabetic neuropathy, trauma, and disc herniation. Symptoms/Conus Medullaris Syndrome: 1. Back pain 2. Unilateral or bilateral leg pain 3. Bladder dysfunction 4. Bowel dysfunction 5. Sexual dysfunction 6. Diminished rectal tone 7. Perianal sensory loss 8. Lower extremity weakness Conus medullaris syndrome: Trauma. Definition: Combination of upper and lower motor neuron deficits, with initial flaccid paralysis of the legs and anal sphincter (Fig. 23.5). Conus medullaris syndrome: Trauma. Symptoms 1. Acute Phase: • Flaccid paralysis of the legs • Paralysis of the anal sphincter 2. Chronic Phase: • Muscle atrophy of the legs • Lower extremity spasticity • Lower extremity hyperreflexia 3. Extensor plantar response may be present: • Development of a low-pressure, high-capacity neurogenic bladder 4. Sensory deficits are variable. Conus medullaris versus cauda equina syndromes

Vertebral level Spinal level Presentation Radicular pain Low back pain

Conus medullaris syndrome L1–L2 Sacral cord segment and roots Sudden and bilateral Less severe More

Cauda equina syndrome L2–sacrum Lumbosacral nerve roots Gradual and unilateral More severe Less

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Cauda equina

CAUDA EQUINA Spinal cord

Filum terminale

Cauda equina

Fig. 23.5  Line diagram showing the level of the conus medullaris syndrome

Motor strength

Reflexes Sensory Sphincter dysfunction Impotence

Conus medullaris syndrome Symmetrical, less marked, hyperreflexic distal paresis of LL, fasciculation Ankle jerks affected Localized numbness to perianal area, symmetrical and bilateral Early urinary and fecal incontinence

Cauda equina syndrome More marked asymmetric, areflexic paraplegia, atrophy more common

Frequent

Less frequent

Both knee and ankle jerks affected Localized numbness at saddle area, asymmetrical and unilateral Tend to present late

Cauda Equina Syndrome Historically: It is characterized by bilateral sciatica which is expanded to include unilateral sciatica. • What about a central disc herniation at L5–S1 sparing the motor and sensory roots of the lower extremities but affecting bowel and/or bladder function? • The frequency of daily urination is much greater than bowel evacuation. Presently: It is characterized by bladder dysfunction with a decrease in perianal sensation (Fig. 23.6).

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Cauda Equina Syndrome Upper Motor Neurons lie, within the spinal cord,

Conus medullaris Cauda equina

ConusMedullaris

Lower Motor Neurons are spinal nerves that branch off the spinal cord,

Filum terminale

Cauda Equina

Fig. 23.6  Line diagram showing the level of the cauda equina syndrome

Etiologies 1. Disc herniation 2. Disc fragment migration 3. Iatrogenic epidural hematoma due to post-LP or spinal anesthesia 4. Postoperatively due to infection, tumor, or trauma

Symptoms Back pain and radicular pain which may be bilateral or unilateral with motor loss, sensory loss, and urinary dysfunction: • Overflow incontinence • Inability to void • Inability to evacuate the bladder completely with decrease in perianal sensation

Clinical Features 1. Motor (LMN signs) such as • Weakness/paraparesis in multiple root distribution • Reduced deep tendon reflexes (knee and ankle)

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• Sphincter disturbance (urinary retention and fecal incontinence due to loss of anal sphincter tone) 2. Sensory such as • Saddle anesthesia (most common sensory deficit) • Pain in back radiating to legs, crossed straight leg test • Bilateral sensory loss or pain: involving multiple dermatome Management: It is a surgical emergency—requires urgent investigation and decompression (80, previous joint space larger than 2 mm, and labral repair rather than resection during the arthroscopy procedure.

Articular Cartilage Injuries Articular cartilage defects can occur on both the femoral head and the acetabular surface. Labral tears occurring at the watershed zone may destabilize the adjacent acetabular cartilage. Arthroscopic observations support the concept that labral disruption, acetabular chondral lesions, or both frequently are part of a continuum of degenerative joint disease. Chondral injuries may occur in association with a multitude of hip conditions including labral tears, loose bodies, osteonecrosis, slipped capital femoral epiphysis, dysplasia, and degenerative arthritis. MR arthrogram can help assess the presence and severity of articular cartilage injuries/loss [24, 25]. The articular cartilage in the hip is thin and due to the direct apposition of the femur and acetabulum it is difficult to differentiate femoral from acetabular cartilage with standard MR imaging. Sensitivity and specificity of MR arthrography in the detection of chondral lesions using T1-weighted spin-echo sequence are estimated to be about 62–79% and 77–94%. Cartilages are categorized into normal, signal heterogeneity, fissuring, thinning to 50% of the normal thickness, and full-thickness cartilage loss. Arthroscopically, (Fig.  24.5) the cartilage integrity is evaluated and various restoration techniques like fibrin glue for cartilage delamination, microfracture in cartilage loss, stem cell therapy for cartilage lesions, autologous chondrocyte implantation, mosaic plasty, osteochondral autograft, and osteochondral allograft

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Fig. 24.5 Articular cartilage tears

are described. Although good results have been reported, most studies lack a control group and the small number of patients limits the strength of these studies.

Injuries to the Ligamentum Teres Injuries to the ligamentum teres such as complete or partial tear can be reported. The injury usually follows traumatic dislocation or subluxation of the hip join, iatrogenic injury sustained during open surgical dislocation, and repetitive “microtrauma” often associated with hyperlaxity. Partial tears are commonly seen in hip arthroscopy and can be associated with the bony deformities seen with developmental dysplasia and femoroacetabular impingement. Degenerated ligamentum teres identified in young patients is often associated with avascular osteonecrosis of the femoral head or slipped capital femoral epiphysis. Recently studies have demonstrated that deficient ligamentum teres can lead to microinstability [26]. Clinically, ligamentum teres ruptures can lead to feeling of instability when crossing their involved leg behind their uninvolved leg when standing and when squatting. Clinical examination may show a reduced and painful range of movement of the hip joint, either in extension or in combined flexion and internal rotation. Tests indicative of intra-articular pathology may be positive in the presence of ligamentum teres tears, but are nonspecific. O’Donnell et al. [27, 28] have described a new clinical test known as the ligamentum teres test. The examined hip is flexed to approximately 70° and abducted 30°, and the knee flexed to 90°. Then the hip is rotated internally and externally to its full extent. Pain provocation represents a positive test. In this position there should be no bony impingement and the ligamentum teres will be selectively tightened. Recommended treatment for ligamentum teres tears has been simply debridement with either mechanical shavers or radiofrequency (RF) probes, along with addressing associated pathologies including FAI, capsular tightening in the presence of instability, or periacetabular osteotomy in the presence of hip dysplasia. Arthroscopic debridement alone of the isolated ligamentum teres rupture has a short-term beneficial result in more than 80% of cases. Various techniques of ligamentum teres

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reconstruction have been described but remain a rarely performed operation, with uncertain indications, minimal outcome data, and no agreement regarding technique [29, 30].

Intra-articular Loose Bodies Intra-articular loose bodies following trauma can be of bony or cartilaginous origin. It is often detected following relocation of a traumatic dislocated hip joint or following a significant sporting injury to the hip. Clinical presentation in subacute cases will be locking episodes of the hip and/or sharp catching pain felt in the groin and giving way episodes. CT and MR with contrast [arthrography] help differentiate intra-articular loose bodies from osteophytes, synovial folds, or hypertrophic synovitis. The intra-­ articular loose bodies are seen surrounded by contrast medium and only partially in the case of osteophytes and synovial folds or hypertrophy. Arthroscopically the loose bodies can be removed to relieve the symptoms.

Extra-Articular Injuries  uscle and Tendon Strain M Various musculotendinous injuries are not uncommon around hip. Most prominent among these are hamstring, quadriceps, and adductor strain. All these entities involve sudden burst of muscular activity such as sprinting, jumping, or side-to-side cutting as the inciting event. Clinically the presentation is following an acute injury with significant pain. Local tenderness at the origin of the muscle and discomfort with muscular contraction against resistance will clinch the diagnosis. Diagnosis is usually clinical while radiological investigations such as ultrasonographic or MRI could be performed to define and quantify the injury. Plain radiographs are adequate to identify avulsion fractures which commonly occur around the anterior superior iliac spine, anterior inferior iliac spine, and ischial tuberosity. The avulsion fractures represent injuries at the tendon bone or ligament bone interface with a significant bony component. Management of these injuries depends on the severity of injury, size of displacement fragment, and patient’s age. Conservative management forms the mainstay which includes, rest, activity modification/restriction, and pain relief. Surgical reattachment of avulsed bone fragment is indicated if the bony fragment is large and significantly displaced. Greater Trochanteric Bursitis Greater trochanteric bursitis is a relatively common condition causing lateral hip pain in adults. Most important risk factors are female gender, obesity, iliotibial band pain, low back pain, scoliosis, and hip and knee pain. Proposed underlying etiology is related to abductor tendinopathy or enthesiopathy. It may be associated with degenerative tears of gluteus medius or minimus. The main positive clinical sign is tenderness on greater

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trochanter palpation. It may cause antalgic or Trendelenburg gait. Radiological investigations can be carried out in cases with equivocal clinical findings. Treatment includes physiotherapy in the form of fascia lata stretching exercises, analgesia, and activity modification. For persistent symptoms local steroid injection may be considered. Surgery can be offered in very recalcitrant cases in the form of bursectomy, iliotibial band lengthening, or repair of abductor tendon tear [31, 32]. Bursitis over the iliopectineal eminence while iliopsoas muscles pass over the prominence and bursitis over ischial tuberosity have also been described as causes of anterior pelvic pain and buttock pain, respectively. Diagnostic local anesthetic injections under ultrasound guidance can aid in detecting the source of symptoms in doubtful cases.

Snapping Hip Snapping hip is an audible or a palpable snap during hip movement, associated with or without pain. The snapping can be largely differentiated into intra- and extra-­ articular etiology. Intra-articular pathology leading to snapping is commonly due to acetabular labral tears, cartilage defects, loose bodies, and intra-articular fracture fragments. These can also present as catching, locking, clicking, or popping sensation. Extra-articular snapping hip can be differentiated into external and internal snapping. Patients with external snapping often describe a sensation of the hip subluxing or dislocating. The external snapping occurs lateral to the hip joint, over the greater trochanter, and is due to the movement of the iliotibial band across the greater trochanter. Thickening of the posterior aspect of the ITB or the anterior aspect of the gluteus maximus further accentuates the snapping sound. Patients typically present with audible or palpable sound in the form of a “snap” when the hip goes through flexion, abduction, and external rotation. In the internal form of snapping hip, the snap occurs in the anterior region of the hip joint and is attributed to movement of the iliopsoas tendon or the iliacus muscle across the anterior aspect of the iliopectineal eminence or the lesser trochanter, femoral head, and associated joint capsule, as the hip moves from flexion to extension [33]. Higher incidence of snapping hip has also been reported in a number of competitive and recreational athletes, including soccer players, weight lifters, dancers, and runners. Post-surgery external snapping hip has been linked to knee reconstruction procedures wherein a portion of the iliotibial band is used. External snapping has been reported following total hip arthroplasty and has been linked to prominence of the greater trochanter. Reproduction of the audible or palpable snap and its concurrence with pain are among the key diagnostic indicators of the snapping hip. The movement to reproduce the symptom is dependent on the type of snapping hip. Provocation tests for external snapping hip typically include femoral rotation and/or flexion. Movement tests for snapping include internally and externally rotating the extended and adducted hip, flexing the extended hip, and extending the flexed hip. When snapping is present during walking, externally rotating the limb may eliminate the snapping [34]. Provocation tests for internal snapping hip generally require contraction of the iliopsoas. Interestingly, the movement that most often elicits the snap [extending the

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flexed hip] should not require contraction of the iliopsoas. One of the most commonly described tests uses a combination of all three movements. In this test, the leg is moved from flexion, abduction, and external rotation to extension, adduction, and internal rotation while the patient actively supports the leg. Snapping usually occurs between 30° and 45° of hip flexion and may be decreased when manual pressure is applied to the iliopsoas tendon over the pelvic brim [35]. The diagnosis of snapping hip is usually made from clinical examination; however, imaging has been used to rule out other pathologies, to confirm the involved structures, and to investigate tissue changes. In patients with extra-articular snapping hip, results from plain radiographs are most often normal but are helpful to rule out other pathologies. A small femoral neck angle (coxa vara) or developmental dysplasia may contribute to snapping hip [36]. Magnetic resonance imaging has been used to detect pathologic soft-tissue changes in the involved tendon and bursa. In patients with internal snapping hip, signal hyperintensity has been noted along the iliopsoas tendon and at the musculotendinous junction. Magnetic resonance imaging combined with arthrography is also beneficial in detecting labral pathology. Dynamic fluoroscopic examination with contrast of the iliopsoas bursa, or iliopsoas bursography, may help detect the internal snapping hip. The contrast-filled bursa outlines the iliopsoas, allowing visualization of the tendon during hip movements. Ultrasound has become one of the most commonly used tools for snapping hip. Ultrasound can detect bursitis, tendinitis, and synovitis. Dynamic ultrasound can detect abrupt movement of the involved tendon during hip movement. With external snapping hip, abrupt anterior movement of the ITB or gluteus maximus may occur as the hip is moved from extension to flexion or flexion to extension. With internal snapping hip, the iliopsoas tendon may move abnormally when the hip is extended from flexion, with or without abduction and external rotation. Management principally relies on rest, anti-inflammatory medications, activity modification, physical therapy, and patient rehabilitation. Therapy involves stretching of the ITB for external snapping hip and the iliopsoas for internal snapping of the hip. Physical therapeutic modalities in use are heat and ice, ultrasound with or without topical corticosteroid, iontophoresis, deep massage, myofascial release, and neuromuscular reeducation. Majority of cases with snapping hip resolve with conservative treatment. Injection of a local anesthetic with a corticosteroid into the involved bursa or around the tendon sheath has also been found to be useful in a large number of patients. Although it is difficult to precisely quantify the number of symptomatic snapping hips, the majority resolve without surgical intervention. Between 36% and 67% of patients diagnosed with snapping hip had reduction or resolution of symptoms with conservative measures. For external snapping hip, the aim is to achieve lengthening of the ITB by a Z-plasty. Although resolution of symptoms can be achieved, a mild-to-moderate Trendelenburg gait is reported as a complication. The persistence of hip abduction

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weakness or Trendelenburg gait would be a significant impairment for an athlete or a dancer [37]. The goal of surgical intervention for internal snapping hip is to decrease the tension in the iliopsoas tendon by fractional lengthening or by complete release. Complete release of the iliopsoas tendon is performed at the level of the iliopectineal eminence, pelvic brim, or femoral head or at the tendon’s insertion on the lesser trochanteric, leaving the muscular portion of the iliacus intact. This can be performed by open or by arthroscopic techniques. Complications reported with iliopsoas lengthening or release include persistent hip pain, anterior thigh paraesthesias, partial femoral nerve palsy, hip flexor weakness, bursa formation over the lesser trochanter, heterotopic ossification, and wound infection. Of these, hip flexor weakness is the most commonly reported complication. In recalcitrant cases, surgery to lengthen the ITB or the iliopsoas tendon has produced symptom relief but can result in muscle weakness [38].

Nerve Entrapments Common nerve entrapments described around the hip are lateral cutaneous nerve of the thigh often called as meralgia paresthetica, pudendal nerve, and ilioinguinal nerve entrapment. Other described nerve entrapments are that of obturator nerve, femoral nerve, and sciatic nerve (pyriformis syndrome). Meralgia paresthetica (MP) is a nerve entrapment which causes pain, paraesthesias, and sensory loss within the distribution of the lateral cutaneous nerve of the thigh. The spontaneous origin is usually due to compression of the lateral cutaneous nerve of the thigh along its course. Patients complain of pain, burning sensation, numbness, muscle aches, coldness, lightning pain, or stinging in their lateral or anterolateral aspect of the thigh. Meralgia paresthetica is commonly reported with long-distance walking or cycling. Other more common associations are with obesity, pregnancy, older age diabetes mellitus, alcoholism, and lead poisoning. Mechanical factors resulting in compression of the lateral cutaneous nerve of the thigh have been implicated with tight garments, military armor, police uniforms, seat belts, direct trauma, muscle spasm, scoliosis, iliacus hematoma as a postsurgical complication, and leg length changes. Increased incidence has been identified with sporting and physical activities such as gymnastics, baseball, soccer, bodybuilding, and strenuous exercise. Iatrogenic meralgia paresthetica has been found to occur after a number of orthopedic procedures, such as anterior iliac-crest bone-graft harvesting and anterior pelvic procedures. Prone positioning for spine surgery has also been identified as a risk factor [39–41]. History and clinical assessment helps in arriving at the diagnosis, mainly by excluding other causes. Specifically the pelvic compression test can be performed to establish the diagnosis. This is a negative provocative test; the patient lies on the side and the examiner applies a downward compression force to the pelvis and maintains pressure for 45 s. If the patient reports an alleviation of symptoms the test is considered positive. Nerve conduction studies and lately magnetic resonance neurography, a modification of magnetic resonance imaging, have been utilized to capture direct images of the nerve to confirm the site of compression.

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Relief of pain and paraesthesias after injection of a local anesthetic agent are helpful in establishing the diagnosis. Local infiltration with lidocaine is at the site where the lateral cutaneous nerve of the thigh exits the pelvis at the inguinal ligament [site of injection is 1 cm medial and inferior to the ASIS or at the point of maximum pain]. The test is considered positive if the patient has immediate symptom relief that lasts for 30–40 min. Idiopathic meralgia paresthetica is usually managed by nonoperative modalities, such as removal of compressive agents, nonsteroidal anti-inflammatory drugs, avoiding compression activities, and physical therapy. Local infiltration with a combination of local anesthetic and corticosteroid or recently pulsed radiofrequency ablation has been used in controlling the symptoms. If intractable pain persists despite such measures, surgery can be considered, although whether neurolysis or transection is the procedure of choice is still controversial [42]. Compression of ilioinguinal nerve or pudendal nerve can present with groin or perineal pain with numbness around the genitalia. Ilioinguinal nerve compression occurs over the iliac crest around the lower abdominal muscles. It is seen in bodybuilders or hockey players. Pudendal nerve involvement is seen in cyclists and may occasionally cause impotence. Activity modification may help to provide symptomatic relief.

Pyriformis Syndrome Pyriformis syndrome is a sciatic nerve entrapment syndrome. This can occur due to primary anatomical anomaly/variations or secondary to trauma, muscle hypertrophy, inflammation, or local ischemic effect. The symptoms are usually pain and discomfort in the buttock region radiating down the posterior aspect of the leg, made worse by prolonged sitting or sometimes by downhill running or sprinting which triggers the symptoms due to eccentric contraction of pyriformis muscle. Commonly patients present with some paraesthesia or numbness in the sciatic nerve distribution, and classical signs of radiculopathy are rare. The diagnosis usually relies on the clinical findings and by exclusion due to difficulties in finding objective evidence as the source of pain. Provocative tests such as Freiberg’s test and Pace’s sign have been described for clinical diagnosis. Freiberg’s test elicits pain by passive internal rotation of the extended hip, when the patient is in supine. The purpose of this test is to stretch the irritated pyriformis muscle and to provoke sciatic nerve compression. Pace’s sign consists of pain and weakness by resisted abduction and external rotation of the hip in a sitting position. Radiological imaging (Fig. 24.6) and neurophysiological studies can be carried out mainly to rule out other diagnostic possibilities [43, 44]. Primary management of pyriformis syndrome includes pharmacological agents [nonsteroidal anti-inflammatory agents, muscle relaxants, and neuropathic pain medication], physical therapy, lifestyle modifications, and psychotherapy. Injection of local anesthetics, steroids, and botulinum toxin into the pyriformis muscle can serve both diagnostic and therapeutic purposes. The practitioner should be familiar with variations in the anatomy and limitations of landmark-based techniques. An ultrasound-guided injection technique allows for visualization and

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Fig. 24.6 Pyriformis

accurate placement of the needle prior to injection. Injections can be of diagnostic and therapeutic value in the treatment of pyriformis syndrome [43, 45]. Surgical treatment in the form of pyriformis tenotomy can be considered when the nonsurgical treatment has failed in resistant cases causing significant debilitation. Classic indications for surgical treatment include abscess, neoplasms, hematoma, and painful vascular compression of the sciatic nerve caused by gluteal varicosities.

 thletic Pubalgia/Inguinal Disruption or Sports Hernia A This is a condition of chronic pain in an athlete’s groin, sometimes described as a sportsman’s groin (SG) or inguinal disruption (ID). Over the years it has been attributed to a possible or an incipient hernia, a groin disruption, or athletic pubalgia. Sports that involve increased pelvic and torso movements or kicking action are known to predispose to this painful condition. ID can therefore be defined as pain, either of an insidious or acute onset, which occurs predominantly in the groin area near the pubic tubercle where no obvious other pathology, such as a hernia, exists to explain the symptoms. Athletic pubalgia is prevalent in athletes at all levels of expertise [amateur and elite] and nonathletes can also suffer from this condition. The pathophysiology is attributed to the increase in tension in the groin area due to the high level of twisting, turning, sprinting, and kicking action the athletes undertake during their sporting activity. The pain is often experienced at the common point of attachment of the adductor longus tendon, rectus abdominis muscle, and inguinal ligament on the pubic bone. It is caused by either repetitive strain, microtrauma, or acute trauma to these structures. It is more common in men participating in intense sports such as ice hockey, rugby, or soccer. Detailed history and examination help in arriving at the diagnosis, usually by excluding other possible causes of chronic groin pain. British hernia society has provided criteria for clinical diagnosis of sports hernia. The diagnosis of ID can be made if at least three out of the five clinical signs below are detectable [46]: 1. Localized tenderness over the pubic tubercle at the point of insertion of the conjoint tendon 2. Palpable tenderness over the deep inguinal ring

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3 . Pain and/or dilation of the external ring with no obvious hernia evident 4. Pain at the origin of the adductor longus tendon 5. Dull, diffused pain in the groin, often radiating to the perineum and inner thigh or across the midline Radiological investigations in the form of MRI scan or ultrasonography can be requested to visualize signs of injury such as soft tissue or bone edema and muscle or tendon disruption and also to exclude other pathologies. Treatment includes physical therapy in the form of rest from activity, pelvic and abdominal musculature-strengthening exercises, and rehabilitation that is recommended for all athletes in the first instance. There are advocates for the use of injection treatment; various options like dry needling, local anesthetic, sclerosants, cortisone, platelet-enriched plasma, or autologous blood can be considered on their own or in combination. Uncontrolled studies have shown significant pain relief in symptomatic athletes; however there are no randomized studies for efficacy of injection treatment compared to rehabilitation and/or surgery. Patients who fail to respond to full physiotherapy rehabilitation regime may be considered for surgical treatment which may involve pelvic floor repair in the form of posterior abdominal wall reinforcement with mesh [47] or decompression of genital branch of genitofemoral nerve. Repair of the ID can be carried out by either open or laparoscopic technique with the surgeon advised to use his/her own preferred method. With both these repair techniques, the principal aim is to identify the anatomy and release any abnormal tension in the inguinal ligament. Any resultant defects or weaknesses created should be repaired or reinforced with a mesh. Laparoscopically, a formal release of the inguinal ligament can be performed with little risk of developing of a femoral hernia.

Osteitis Pubis Osteitis pubis is inflammation or stress injury to pubic symphysis area seen more often in men involved in high-demanding sporting activities such as soccer and ice hockey. Repetitive microtrauma caused by frequent acceleration and deceleration movements or repetitive kicking has been proposed to be main etiological factors. Clinical presentation is an ill-defined vague pain in the anterior pelvic region, groin perineum, and occasionally testicles. This may be associated with localized tenderness over pubic symphysis area. Radiographs may show cystic, sclerotic changes or sometimes diastasis of symphysis. MR scan or bone scan can be done to show inflammatory activity in cases where radiographs are negative for any abovementioned findings. Physical therapy focused on core strengthening with balance control and adductor stretching is the main component of the treatment. Local steroid injection can be tried in cases which don’t improve with physical therapy. Surgical treatment in the form of curettage, variable resection of the involved area, or arthrodesis of the pubic symphysis has also been described [48–51].

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Rectus Femoris Tendon injuries Injuries of the rectus femoris tendon origin are not so uncommon, particularly seen in the adolescent and young adults. The injury results from significant sporting impact; often there is a bony avulsion fragment from the attachment of the straight head of rectus femoris at the anterior inferior iliac spine. Recurrent less severe injuries could result in a chronic tendinopathy, leading to groin pain and loss of function. Diagnosis usually by imaging, radiographs, or magnetic resonance can be helpful. Conservative treatment with analgesics and physical therapy is the gold standard; large bony avulsion fragment may require surgical stabilization. In some cases excessive bone formation after avulsion injuries has been reported which can lead to a posttraumatic heterotopic ossification and may require consideration of surgical removal [52].

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Stem Cells in Orthopedics

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Raju Vaishya and Abhishek Vaish

Introduction The concept of “stem cell” was first described in 1868 by a German scientist Ernst Haeckel who worked with the concepts of “phylogeny and ontogeny.” The first definitive evidence for the existence of stem cells came in the early 1960s, after the Canadian scientists Ernest McCulloch and James Till performed experiments on the bone marrow of mice and observed that different blood cells come from a special class of cells [1]. Stem cell research has progressed rapidly since 1981 when the British scientist Martin Evans and the American scientist Gail Martin succeeded in isolating and culturing mice embryonic stem cells (ESCs). In the late 1990s, American scientist James Thomson first isolated human ESCs, revealing the potential for a pluripotent stem cell that would be a source of various germ layers and new organs. Recognition of the pluripotency of human stem cells triggered the exponential developments in stem cell research seen over the last two decades. Regenerative medicine is developing at a rapid pace in all the fields of medicine, including orthopedics [2]. Leland Kaiser introduced the term “stem cell” only recently, in 1992. Since then the attempts are being made to regenerate damaged tissues or even substitute whole organs. Belief in the technology and cost at present are concerns and confounding factors to its use in the healthcare system, all over the world.

Stem Cell Types Stem cells represent unspecialized cells, which can differentiate into different adult cell types. The stem cells are of two types: • Embryonic stem cells (prenatal) • Adult stem cells (postnatal) R. Vaishya (*) · A. Vaish Department of Orthopaedics and Joint Replacement Surgery, Indraprastha Apollo Hospitals, Sarita Vihar, New Delhi, India © Springer Nature Switzerland AG 2019 K. M. Iyer, W. S. Khan (eds.), General Principles of Orthopedics and Trauma, https://doi.org/10.1007/978-3-030-15089-1_25

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Embryonic stem cells (ESCs) are only found in early developmental stages of the organism. They represent the only cell type, which can renew itself indefinitely and is genuinely pluripotent. As a unique precursor cell, it can differentiate into cells of all three germ layers. Besides the ethical concerns, the use of embryonic stem cells is problematic, as the application of allogenic pluripotent cells inheres a distinct oncogenic potential that currently forbids the application in patients. Mesenchymal stem cells (MSCs) have been found to be the most promising cells, as these show good differentiation potential towards specialized cells like that of cartilage, tendon, and bone. These can be isolated from mesenchymal tissues like bone marrow, fat, synovial membrane, and periosteum. Induced pluripotent stem cells (iPS cells) provide the possibility of autologous therapy with pluripotent and easily accessible cells in the future. Besides the great potential this technique undoubtedly represents, it bears some essential safety problems which are currently far from being solved. Similar to ESCs, these cells inhere a high oncogenic potential which currently forbids application in patients. If these are injected in an undifferentiated state, they cause teratomas, and mice generated from iPS cells show high rates of tumors. This oncogenicity may be due to the transcription factors used for dedifferentiation which are known to be oncogenes, due to the insufficient epigenetic remodeling or due to the oncogenic retro viruses used for transfection. The use of adult stem cells raises less ethical concerns and has proved to be much safer than pluripotent stem cells. Also, these cells have further advantages compared to ESCs; for example, use for autologous cell therapies, using patients’ cells to reduce possible immune responses, is more comfortable to realize.

Sources of Stem Cells The two most common sources of adult stem cells for clinical application in orthopedics are (a) Bone marrow (b) Adipose tissue Both bone marrow aspirate (Fig. 25.1) and lipo-aspirate contain different cell fractions. When bone marrow aspirate is centrifuged (Fig. 25.2), bone marrow aspirate concentrate (BMAC) can be obtained (Fig. 25.3) from the buffy-coat layer which contains mononuclear cells including a very low percentage of mesenchymal stem cells (MSCs). When lipo-aspirate is treated by enzymes and undergoes differential centrifugation fat, mature adipocytes in the upper layer are separated. The bottom layer is a stromal vascular fraction (SVF) that contains a low percentage of MSCs. When BMAC and SVF are put into a monolayer culture on plastic dishes and passaged, cells that have characteristics of MSCs can be i­ solated. Stem cell offers exciting possibilities to not only treat but also cure diseases.

25  Stem Cells in Orthopedics Fig. 25.1  Bone marrow aspiration being done from the iliac crest

Fig. 25.2  A centrifuge machine for separating the stem cells

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Fig. 25.3  A bone marrow aspirate separation kit

Indications of Stem Cells in Orthopedics Stem cell treatments may provide an innovative therapy for various musculoskeletal problems like bone defects, nonunion of fractures, avascular necrosis, and cartilage defects of the joints (Table 25.1). While complete regeneration usually occurs after a bone injury, critical size defects of long bone require are challenging to manage. Conventionally, these require harvesting a large portion of bone either as an autograft (with significant morbidity) or as an allograft (implantation that is associated with several complications). Osteonecrosis of the femoral head (ONFH) causes the collapse of the femoral head and secondary osteoarthritis of the hip joint, leading to premature total hip arthroplasty (THA) in young patients. Nonunion of long bone often presents a challenge in achieving a bony union. Unlike bone, which is a self-regenerating tissue, articular cartilage has limited potential for self-regeneration, and damage to it eventually leads to premature and

25  Stem Cells in Orthopedics Table 25.1  Indications of stem cells in orthopedics

579 1. Fractures   (a) Nonunion   (b) Bone defects 2. Articular cartilage defects   (a) Posttraumatic (Fig. 25.5)   (b) Osteoarthritis   (c) Osteochondritis dissecans (OCD) 3. Avascular necrosis (AVN)   (a) Hip joint (Fig. 25.4) 4. Tendinopathy   (a) Degenerative tendon disorders   (b) Large rotator cuff tears   (c) Anterior cruciate ligament tears 5. Spinal fusion

Fig. 25.4 Avascular necrosis (AVN) of the femoral head of the hip is being decompressed and prepared for stem cell treatment

early onset of osteoarthritis (OA). As the defect of articular cartilage is not amenable to conventional procedures such as microfracture, it can be a good candidate for regenerative therapy with stem cell implantation (Fig. 25.6). More diffuse damage of articular cartilage is seen in OA, and this may also become a target of stem cell therapy because the current treatment modalities do not offer a regenerative option for patients. Other candidates for stem cell treatment are degenerative tendon disorders, including advanced rotator cuff tears, which are not successfully treated by repair techniques.

Acquisition, Processing, and Delivery of Stem Cells Sources The stem cells can be sourced from various tissues in the body including bone marrow, periosteum, adipose tissue, placenta, umbilical cord, blood, human amniotic fluid, dental pulp, synovial tissue, skin, and skeletal muscle.

580 Fig. 25.5  A large articular cartilage defect over the medial femoral condyle of the knee

Fig. 25.6  A large articular cartilage defect is being treated with stem cell injection

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Isolation The stem cells are isolated after centrifugation or “selected” and enhanced in culture utilizing their affinity to tissue plastics. Route of Administration The stem cells may be directly applied into a lesion either surgically or via local injection with a suitable scaffold/carrier.

 echanism of Healing with Stem Cells M Mesenchymal stem cells (MSCs) can migrate chemotactically to tissues showing inflammation and injury in the organism. Besides their unique ability to differentiate into different cell types, MSCs were found to secrete a variety of cytokines (TGF-B, VEGF, BMPs) showing anti-inflammatory activity and create an anabolic microenvironment. Also, direct cell-cell contact immunomodulation has been shown [6]. Thus, these cells participate in the regeneration of injured tissues in different ways: (a) Directly differentiate into tissue-specific cells and thus substitute damaged or lost cells. (b) Indirectly influence tissue regeneration by the secretion of soluble factors. (c) Modulate the inflammatory response. Thus, they can promote vascularization, cell proliferation, and differentiation and modulate an inflammatory process. MSCs release paracrine factors for example IGF-1, HGF, VEGF, IGF-2, bFGF, or pre-microRNAs which protect host cells, promote cell proliferation, and enhance angiogenesis. Also, MSCs enhance lung function by regulating endothelial and epithelial permeability, decreasing inflammation, enhancing tissue repair, and inhibiting bacterial growth in acute lung injury and acute respiratory distress syndrome. There is increasing evidence that the cells themselves are relatively nonimmunogenic and they can be readily transplanted between different individuals without initiating an immune response.

 hallenges with the Use of Stem Cells C 1. Cost: The technology of stem cell isolation, procurement, and delivery with the scaffold is a daunting process. The final product ready for implantation also needs to undergo many testings. The whole procedure is at present not very cost effective with variable results. 2. Purity: The cells need to be cleared of the unwanted nonspecific inflammatory and other cells and scaffold. The process is performed only at few centers at present. 3. Time to culture: The cells usually take around 5–6 weeks to culture in a laboratory. Hence, this technology is seldom beneficial in acute settings.

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4. Risk of infection: The cells have to be stored in vitro for processing and culture purposes. They are also scanned for a retrovirus, hepatitis, and other viruses. Still, there are remote chances of these cells getting infected if not handled with utmost care. 5. Loss of function, in vitro: The cells are known to lose its potency with time. 6. Belief: In general, the people at present are confused about the use of stem cells as it is a newer technology. Many people are injecting blood without isolating stem cells and using a scaffold as a vehicle. This does not work and hence further deteriorates the belief in stem cells.

Conclusion Stem cells seem to be a very promising gift for the future. These have proven its mantle in the field of bone marrow transplantation by the mechanism of homing. However, in other fields such as orthopedics, these are still in a very early stage and many discoveries are yet to follow. The use of stem cells may act as a double-edge sword and hence one needs to apply rationale and science before its usage. The implications of the successful use of these cells are tremendous and one needs to be patient and keep an open mind about its applications.

References 1. Mafi R, Hindocha S, Mafi P, Griffin M, Khan WS. Sources of adult mesenchymal stem cells applicable for musculoskeletal applications—a systematic review of the literature. Open Orthop J. 2011;5(Suppl 2):242–8. 2. Murrell WD, Anz AW, Badsha H, Bennett WF, Boykin RE, Caplan AI. Regenerative treatments to enhance orthopedic surgical outcome. PMR. 2015;7:S41–52. 3. Gobbi A, Karnatzikos G, Scotti C, Mahajan V, Mazzucco L, Grigolo B.  One-step cartilage repair with bone marrow aspirate concentrated cells and collagen matrix in full-thickness knee cartilage lesions results at 2-year follow-up. Cartilage. 2011;2:286–99. 4. Vaishya R.  Recent advances in the management of chondral injuries. Apollo Med J. 2005;2(2):101–6. 5. Vaishya R.  The journey of articular cartilage repair. (Editorial). J Clin Orthop Trauma. 2016;7(3):135–6. 6. Abumaree M, Al Jumah M, Pace RA, Kalionis B. Immunosuppressive properties of mesenchymal stem cells. Stem Cell Rev. 2012;8:375–92.

3D Printing in Orthopedics

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Raju Vaishya and Abhishek Vaish

Introduction Orthopedic surgery is moving ahead in leaps and bounds. Precision in performing procedures is of paramount importance. The scope of this has grown many folds with the introduction of 3D printing technology in the field of medicine. This technology has already proven its mantle in the fields of aerospace, jewelry making, dentistry, etc. However its inclusion to treat patients brings exciting possibilities and advantages. Chuck Hall is considered as the father of 3D printing and is the first one to develop stereolithography (STL) in 1984, which is a critical element of this technology. The 3D printing technology may provide a chance for the orthopedic surgeons and technicians to independently develop innovative medical devices [1]. Based on imaging techniques such as computed tomography (CT) and magnetic resonance imaging (MRI), raw data in DICOM format is processed into a 3D model (Fig. 26.1), which can be manipulated and used as a template for virtual planning [2]. The prototypes of the bones can be obtained using the layered manufacturing technique (LMT) for teaching, presentation, and surgical design. Metal 3D printing is of particular relevance to orthopedic practice, as it allows customized implants or devices to be made. These printers are still costly and are not readily available; however, these would also become an affordable reality in the future. 3D printed implants and devices will also open a new avenue of the research model. It needs to be established that the biomechanical proportions are acceptable before implanting the devices. We will also discuss the bioprinting which could be the ultimate game-changer in healthcare delivery [3]. This technology will not take away presurgical planning from the surgeon [4]. On the other hand, it will get surgeons even closer to the details of the problem to R. Vaishya (*) · A. Vaish Department of Orthopaedics and Joint Replacement Surgery, Indraprastha Apollo Hospitals, Sarita Vihar, New Delhi, India © Springer Nature Switzerland AG 2019 K. M. Iyer, W. S. Khan (eds.), General Principles of Orthopedics and Trauma, https://doi.org/10.1007/978-3-030-15089-1_26

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R. Vaishya and A. Vaish Image Acquisition

Image Processing

DICOM to STL conversion

Editing and Preoperative Planning on software

Three-Dimensional Printing (Additive/Subtractive)

Final 3D model

Fig. 26.2  A 3D printing machine

be addressed. This technological progress has merely provided us with more efficient means for going forward, and a “real-world” clinical translation would reveal the value and future of 3D printing in orthopedics.

Three-Dimensional Printing Three-dimensional printers use a variety of technologies to “additively manufacture” or construct objects layer by layer [5, 6]. Whereas the old manufacturing methods included the subtraction of layers from raw material, 3D printing works on the model of “additive manufacturing.” In additive manufacturing, layer by layer of the raw material is “added” in a predetermined manner (Fig. 26.2), hence achieving accurate and excellent three-dimensional framework. Industrial-grade printers use lasers to precisely sinter granular substrates (e.g., metal or plastic powders). After each layer of the structure is completed,

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the printer adds a new layer of unfused powder on top of the old one, and the subsequent round of sintering builds the next cross section fused to the previous one. The advantages of these printers are high print speeds, ability to recycle unfused powder easily, and capacity to use stronger materials with higher melting points (e.g., titanium, which had been challenging to sculpt by standard subtractive methods).

Uses in Orthopedics Preoperative Planning 3D printing technology can help manufacture bone models which can be used in complex orthopedic cases. The scenarios like compound fractures with bone loss, especially occurring after high-speed road traffic accidents and bomb blasts, can be easily managed by developing a prototype of the contralateral side and can be used as a guide during surgery (Fig. 26.3). In cases where there is no normal side to the template on, normal anatomy can be used to make models which in turn can help in fitting the missing pieces. Another scenario is complex joint replacements, wherein the surgeon can develop a 3D model, know of the possible intraoperative hurdles, and plan accordingly.

Fig. 26.3  CT images of the shoulder showing fracture and posterior dislocation of the right shoulder joint

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Overall, the innovation of using 3D printed replicas of bone fractures can help doctors, surgeons, and researchers thoroughly test methods before the surgery even begins. 1. Complex trauma: 3D printing is especially useful in complex trauma cases [7]. The 3D printed models provide a visual and tactile aid in conceptualizing complex fracture patterns (Fig. 26.4). The model can be sterilized and reviewed intraoperatively as required. Preoperative reviews of the 3D model can allow the surgeon to anticipate intraoperative difficulties, selection of optimal surgical approach, and need for specific equipment. Challenging pelvic fractures provide an example of these concepts. There are published examples where 3D technology has been utilized in complex cases of the upper limb and lower limb osteotomies. These articles support the notion that this technology simplifies complex surgery, providing confidence that goals of surgery are being achieved and reduce operative time. Trials comparing routine preoperative planning with the use of 3D printing are required. 2. Arthroplasty: Most implant companies have 3D printed guides available to assist in standard knee joint arthroplasty. A guide to assist with hip resurfacing has also been described. This process is commonly called patient-specific instrumentation [8]. Patients have either a CT scan or a MRI scan to produce DICOM images. 3D images are then created, and a preoperative surgical plan is constructed to achieve perfect implant placement. Disposable cutting blocks are then fabricated Fig. 26.4  A 3D printed model of the shoulder, showing posterior dislocation

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Fig. 26.5  A 3D printed customized knee block for total knee replacement

to match and conform to the patient’s anatomy using 3D printing technology (Fig. 26.5). The proposed benefits include improved reproducibility of component alignment, reduced surgical time, and optimized efficiency and cost-­ effectiveness. Despite these proposed benefits, it is yet to be proven to be better than the standard techniques. 3D printing has allowed the emergence of custom implants. Customized implants for joint arthroplasty are useful when the patient does not fit the standard range of implant size or their disease. 3. Spinal surgery: Preoperative computer-assisted planning and custom 3D printed guides have also been described in pedicle screw placement. 4 . Pediatric orthopedics: Pediatric orthopedic surgeons have utilized 3D printed models to assist in the management of complex spine scoliosis, coalition in the foot, and Perthes’ and Blount’s disease. The models were used to assist in preoperative planning, communication with the patient, reference during surgery with reported improvements in the safety of the procedure, and reducing operative time. Simple and complex osteotomies can be planned using models preoperatively. The surgeon can study the deformity and plan the surgery with a computer model. This includes the exact placement of implants and the ideal osteotomy site. 3D printing can produce jigs to allow for pre-drilling of holes for customized plates with built-in osteotomy guides.

Intraoperative Guides 3D printing can also help in manufacturing guides which can be used intraoperatively for taking precise bone cuts. These can dramatically decrease the surgical time and have widespread implications for the patient, surgeon, and hospital setup. The anesthesia time for the patient as well as the OR efficiency can be improved while ensuring superior outcomes.

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Cases like complex deformities and severe kyphoscoliosis can be dealt with in a more efficient and scientific manner by using specific 3D printed jigs.

Training 3D printing can also help develop models which can be used for training as well as presentation purposes. Moreover, using the 3D printed models can redefine patient education wherein the patients can themselves understand their problem and measures are being taken to rectify the problem. Research Improvements in implant design is an important area which can be effectively dealt with using 3D printing. Earlier, during the times of normal manufacturing, even a small change in the design used much time, but with the advent of rapid prototyping technology, the designer can improvise and develop a new implant. It can be easily available and much cheaper than the old implant designing protocols. The developer can check the prototype for accuracy and any fallacies and can rapidly order changes and reassess the resultant product. Certain metals like titanium have been approved to be used in these 3D printers and can help manufacture implants. The 3D printing technology holds much promise in all fields of medicine, but the field which has been revolutionized the most is the field of orthopedics. It has widespread implications for research, development, and improving surgical outcomes. Studies in the future can be performed to assess the following: • Study the usefulness and applicability of 3D printing for complex orthopedic problems • Evaluate the clinic-radiological outcomes of these cases, with the use of 3D printing • Determine the cost-effectiveness of 3D printing in these challenging cases • Assess the best indications for 3D printing in difficult orthopedic cases • Analyze the complexities associated with 3D printing and how to overcome these problems Indications: • Cases with complex orthopedic problems (severe deformities of the bones and joints), which usually are considered challenging and difficult surgically • Patients who are willing to give consent for the use of 3D printing and to undergo preoperative CT scan Contraindications: • Routine orthopedic surgical cases, which can be managed by conventional surgery • Those cases who are not willing to give consent for the use of 3D printing • Acute orthopedic condition and traumatic injuries, which require immediate treatment and cannot wait for the 3D printed model

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Advantages of 3D Printing There are various advantages of using this technology: 1. Reduction in the duration of surgery: With the planning and alterations of implants based on the pathology pre-hand the surgical time spent on table reduces, and the surgeon, as well as the team, exactly knows the accurate surgical steps. 2. Reduction in intraoperative bleeding: With pre-hand knowledge about surgical steps and reduction in overall surgical time there is a reduction in the overall per-­ operative bleeding. This fastens the return to normal faster than conventional. 3. Increased precision: With the availability of the exact model in hand the surgeons can plan the surgery better. The implants can be molded beforehand according to the bone shape and size. It increases the precision and reduces the intraoperative duration. 4. Patient education: In the recent times with increased patient awareness and knowledge, with the availability of a 3D print model in hand it is easier for the doctor to explain about the pathology and the surgical procedure to be done to the patients. It helps the patient to be well informed, and they exactly know what to expect from the surgical procedure. 5. Medicolegal litigations: With the help of models patients are better informed about what to expect. These improve the communication between the doctor and patients and thus reduce the chances of medical litigations. 6. Patient-specific instruments and jigs: Every human being is different, and so are the sizes of bones. Hence with this technology, it is possible to customize implants according to the exact patient dimensions and also prepare jigs.

Clinical Uses of 3D Printing in Various Medical Specialties 1. 2. 3. 4. 5. 6. 7.

Orthopedic surgery Craniofacial surgery Dental surgery Plastic surgery Urology Ophthalmology surgery General surgery

Medical models, surgical implants, surgical guides, external aids, and bio-­ manufacturing have been done in these fields. Some examples of the usage of 3D printing in medicine are as follows: 1. Bioprinting or tissue and organ fabrication: (a) Bones (b) Cartilage

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(c) Cornea (d) Organs like skin, kidney, liver, and heart 2. Creating anatomical models, implants, and prostheses: (a) Complex fractures and dislocations (b) Deformity correction (c) Patient-specific implants for joint replacement (d) Patient-specific orthosis (braces, foot wear, etc.) and prosthesis (artificial limb) 3. Pharmaceutical research (drug discoveries, delivery, and dosage forms): (a) Preoperative imaging: In order to procure a 3D printed model, an MRI or CT scan of the involved area is necessary. In cases where there is a defect in the bone (for instance complex acetabular fractures) then the scans of the opposite side are essential in order to replicate the same on the deficient side. (b) Complications: No complications have been reported in the literature yet with the usage of this technology. However, no technology can replace human judgment as no two patients are similar, and conditions intraoperatively seldom may change which may demand alteration of some steps in order to achieve optimal results. (c) Pearls and pitfalls: This is a relatively newer technology in the field of medicine. The learning curve is high. The software is better used by engineers at present; however the surgical planning is to be done by the operating surgeon himself/herself. Hence, in the future, it would be better if the doctor could learn to master the software in order to benefit the patients maximally.

References 1. Hoang D, Perrault D, Stevanovic M, Ghiassi A. Surgical applications of three-dimensional printing: a review of the current literature & how to get started. Ann Transl Med. 2016;4(23):1–19. 2. Dahake SW, Kuthe AM, Mawale MB, Bagde AD. Applications of medical rapid prototyping assisted customized surgical guides in complex surgeries. Rapid Prototyp J. 2016;22:934–46. 3. Vaish A, Vaish R. 3D printing and its applications in orthopedics. J Clin Orthop Trauma. 2018;9(Suppl 1):S74–5. 4. Maini L, Vaishya R, Lal H. Will 3D printing take away surgical planning from doctors? J Clin Orthop Trauma. 2018;9(3):194–201. 5. Wong KC. 3D-printed patient-specific applications in orthopaedics. Orthop Res Rev. 2016;8:57–66. 6. Thomas H, Anja T, Steffen N, Eckhard B. Recent developments in metal laminated tooling by multiple laser processing. Rapid Prototyp J. 2003;9:24–9. 7. Vaishya R, Vijay V, Vaish A, Agarwal AK. Three-dimensional printing for complex orthopedic cases and trauma: a blessing. Apollo Med. 2018;15:51–4. 8. Vaishya R, Vijay V, Birla V, Agarwal AK.  CT based ‘patient specific blocks’ improve postoperative mechanical alignment in primary total knee arthroplasty. World J Orthop. 2016;7(7):426–33.

External Fixation

27

K. Mohan Iyer

The History of External Fixators Currently, external fixation (EF) is a widely utilized method for the treatment of fractures, pseudoarthrosis, infections, correction of deformities, and osteotomy. The history of EF dates back to 400 B.C. when Hippocrates described a simple external fixator utilized for a fracture of the tibia. In 1853, French physician Malgaigne [1] described a clawlike device used percutaneously to compress and immobilize the major fragments of fractured patellae. In 1893, Keetley, noting the frequency of malunions in the femur, recommended that rigid pins be inserted percutaneously and held in a special external fixation device. In 1897, Parkhill described the use of two half-pins above and two half-pins below (Fig. 27.1). Thereafter Freeman [2] published a series of papers from 1909 to 1919 advocating the use of external pins (Fig. 27.2). Belgian physician Lambotte (Fig.  27.3) [3] in 1912 and Humphry in 1917 were the first to advocate the use of threaded pins, but they used only one above and one below the fracture site. In 1948, Charnley [4] popularized his compression device to facilitate arthrodesis of joints, and this technique rapidly grew in popularity (Fig. 27.4). In 1966 and 1974, Anderson et al. reported the use of transfixing pins incorporated into a plaster cast for the successful management of large series of tibial shaft fractures. Sladek and Kopta from 1968 to 1970 and Vidal [5] and Vidal et al. modified the original Hoffmann device from a single half-pin unit to a quadrilateral bicortical frame, greatly increasing its rigidity. K. M. Iyer (*) Royal Free Hampstead NHS Trust, Royal Free Hospital, London, UK

© Springer Nature Switzerland AG 2019 K. M. Iyer, W. S. Khan (eds.), General Principles of Orthopedics and Trauma, https://doi.org/10.1007/978-3-030-15089-1_27

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Fig. 27.1  Line diagram showing a Parkhill external fixator

The main landmarks were as follows: Malgaigne—nineteenth century: 1 . Lambotte: 1902—unilateral frame 2. Raul Hoffman: 1938—universal ball joints 3. Roger Anderson: USA—thru and thru pins 4. Otto Sader: 1937—veterinary surgeon distraction 5. Vidal: quadrilateral frame using Hoffman 6. A.O: 1977—tubular fixator, monoplanar, monolateral External fixation is a method of immobilizing fractures by means of pins passed through the skin and bone. (1) Pin pierces the limb completely or from one side and these pins are joined outside the limb by a rigid scaffolding and hence the name external fixator (Fig. 27.5). (2) Minimum metal exists inside the tissue. (3) Fracture elements are at will realigned, distracted, or compressed. (4) Wound area is well

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Fig. 27.2  Line diagram showing a Freeman fixator

exposed; local lavage, flushing, dressing, and surgical procedures are easy and convenient. (5) It provides efficient stabilization. (6) It also facilitates limb elevation and (7) allows early movements of the adjacent joint. Aim of application of an external fixator is to achieve an environment conducive to fracture and soft-tissue healing. Briefly there are two main types of pin fixators and ring fixators.

Pin Fixators They are applied quickly to stabilize most diaphyseal # with adequate wound access—management of soft tissue (Fig. 27.6). The components of a pin fixator are bone screws or pins, clamps, and connecting rods or tubes. The pin is a Schanz screw or half-pin, having threads at one end and a rounded tip at the other. They are 3–6 mm in diameter, have a stabilizing hold on bone segment, and do not pass much beyond far cortex. It is a modified cortical screw but the core diameter is slightly larger than the corresponding cortical screw (3.4  mm instead of 3  mm for a 4.5  mm screw) and has increased torsional and bending strength. The Steinmann pin is available in 3, 4, and 5 mm.

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Fig. 27.3  Line diagram showing a Lambotte’s external fixator

A pin is described under four headings as tip, thread, core, and shaft. A tip is of the following varieties: Triangular tip cuts its own threads in the bone and the pilot hole is drilled before inserting the pin and a variety of pin tips are in use. The threads take hold in the bone and provide a secure purchase. Cutting threads initiate bone thread formation; sizing threads bring this up to the required shape and size. Depending on the length of the threaded portion, a pin may have a hold in one or both cortices while a short thread engages the distal cortex only. A core diameter affects the strength of the pin. Its torsional strength is a cube of the core diameter and its tensile strength is the square of the core diameter shaft. The strongest part of the pin is more rigid than the threaded portion and is used to fasten pins to clamps. Clamps: They provide connection between pins and other components. They also permit a multiplanar adjustment of the pin. The tube interface is of two types, namely pin to rod and rod to rod. The clamps also provide connection between pins and other components and also permit multiplanar adjustment of the pin to the tube interface which are of two types namely pin to rod and rod to rod.

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Fig. 27.4  Charnley’s compression arthrodesis (courtesy: reused with the kind permission of Magdi E.Greiss, Whitehaven, Cumbria, UK)

Fig. 27.5  Line diagram showing an external fixator

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Fig. 27.6  Line diagram showing a pin fixator

They may be unilateral uniplanar, which are simple to construct, with stiffness in sagittal plane being higher with fewer skin entry holes with less chances of infection and less scars when the pins are applied in safe corridors when sufficient stability is achieved, and the reduction has to be done before the frame is complete. They may be unilateral biplanar which are most stable of unilateral frames and used for treatment of tibia # when a stable fixation is achieved. It is also useful in prolonged application of the fixator in cases of bone loss or open wounds. These clamps may be bilateral uniplanar when a Steinmann pin is used in (1) cases of transverse or short oblique # or in osteotomy when axial compression is achieved by preloading the Steinmann pin and (2) for long oblique or spiral # when a lag screw might be inserted along with the construct for stability. They are also useful in complete elimination of lateral movements and uniform distribution of stresses on the cortices when the skin is exposed to two possible sources of contamination and double-scar mark and used only for lesions of leg and supracondylar region of femur which is weaker than unilateral frame in sagittal plane. A bilateral biplanar clamp is indicated mainly in tibia, occasionally distal femur and rarely elbow, in large bony defects, for arthrodesis of knee and elbow. It also has great torsional stability. A modular frame has the following features: (1) It is a modification of unilateral uniplanar frame. (2) It has two pins of one segment that are connected to a short tube with a pin—tube clamp and another tube and a tube-to-tube clamps are used to connect short tubes in two bone segments. (3) All tubes can be rotated and fixed to reduce the fracture as used in humerus #, for stabilization of pelvis #, and open tibial #. The advantages of a modular frame (Fig.  27.7) are as follows: (1) total pin placement freedom, (2) increased possibility of fracture reduction, (3) secure fixation, (4) easy dynamization, (5) quick pin addition or removal, (6) applicable in segmental fracture or joint injuries, and (7) table for bone segment transportation. The important factors affecting stiffness are the following: 1. Number of pins used: (a) more number of pins—more stability, (b) two pins/ segment for tibia and three for femur, (c) pins closer to #—more rigid, (d) more

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Fig. 27.7  Line diagram showing a modular frame

pin-to-pin distance in a segment—more is the bending stiffness, pin angled at 90°—increases torsional stiffness. 2. Pin diameter: (a) 4.5–5.5 mm for tibia and femur, (b) 3.5 mm for radius ulna, and (c) 2.5 mm for metacarpals or metatarsals; in a nutshell, the more the diameter, the more is the stiffness. 3. Distance between the bone and the connecting rod: (a) the closer the pin clamps can be to the pin–bone interface—the more rigid fixation with an optimal distance—4 cm, (b) two rods increases the stiffness (instead of one), and (c) stiffness of the connecting rod. 4. Pin–clamp interface. 5. Slippage of clamp decreases stiffness. 6. Periodic tightening. There are certain stress-reducing factors at pin–bone interface, such as the following: (a) Pin: (1) Large diameter, (2) high modulus material, (3) multiple pin cluster, (4) reduced span, and (5) preloading.

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( b) Fixator: Two-plane fixation construct. (c) Patient: Reduced weight bearing. Preloading: It is a static force of sufficient magnitude applied to an implant to overcome all dynamic and muscular contracture forces and to maintain uninterrupted pin-bone contact. A lack of tension leads to micromotion and pin loosening when osteoclast initiates bone resorption at periosteal and endosteal surfaces. This radial preloading— best method of preloading—is achieved by inserting a pin which is larger in diameter than the predrilled hole—a designed misfit. The optimal misfit is 0.1 mm and not more than 0.3 mm. Their disadvantages are as follows: (a) # has to be reduced before construction of frame. (b) They have the presence of a fixed bar, remote from the axis of the bone, and limit adjustability of frame to control angulatory and rotator deformities. (c) Cantilevered system does not allow axial loading. (d) They have a high incidence of delayed union or nonunion unless fixator is modified or bone grafting is carried out. (e) Angular deformities may occur.

Ring Fixators They are used in the treatment of problems requiring complex reconstruction with their frames that have replicate structure of long tubular bone like exoskeleton (Fig. 27.8). Here bone is stabilized by tensioned wires acting like elastic band which provides sufficient stability for most complicated diaphyseal fractures. Here multiplane deformity correction can be achieved and it is excellent for progressive deformity correction, limb lengthening, and management of nonunion. However their disadvantages are as follows: (a) heavy and cumbersome, (b) time-consuming procedure to plan and construct, (c) poor access to soft tissues, and (d) risk of neurovascular damage.

Hybrid Fixator This is used in hybrid fixation for periarticular fractures by using thin wires near joint and also pins (Schanz screws) in shaft, the main aim being to reduce and fix the joint surface and to span the diaphyseal segment without disturbing the soft tissues. However, this external fixation can be combined with internal fixation. Advantages are as follows: 1. Provides rigid fixation of the bones by compression, neutralization, or fixed distraction of the fracture fragments. 2. Allows direct surveillance of the limb and wound status, including wound healing, and neurovascular status. 3. Immediate motion of the proximal and distal joints is allowed. 4. Insertion can be performed with the patient under local anesthesia.

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Fig. 27.8  Line diagram showing a ring fixator

5. It is very useful in polytrauma for temporary stabilization of long-bone injuries in an unstable patient as it is minimally invasive and decreases bleeding with pain control and nursing care and is on the lines of “damage control.” 6. It can also be used for pelvic fractures as it provides temporary stabilization for closed fractures, and also controls hemorrhage and decreases clot shear. It is extremely useful in open pelvic fractures or “the lethal injury.” In pelvic fractures its advantages are (a) quick application, (b) open or percutaneous pin insertion, and (c) ease of removal for definitive ORIF. 7. It has a definite place in children’s fractures particularly femoral fractures, which is an alternative to skeletal traction and used less with use of flexible nails. In children’s fractures one must be very careful when pin placement must avoid the growth plate and a watch must always be kept for pin tract infection and occasional joint stiffness. The disadvantages are as follows: 1. Meticulous pin insertion technique and skin and pin track care are required to prevent pin track infection.

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2. The pin and fixator frame can be mechanically difficult to assemble by the uninitiated surgeon. 3. The frame can be cumbersome, and the patient may reject it for esthetic reasons. 4. Fracture through pin tracks may occur. 5. Refracture after frame removal may occur, unless the limb is adequately protected until the underlying bone can become accustomed to stress again. 6. The equipment is expensive. 7. A noncompliant patient may disturb the appliance adjustments. The main accepted indications are as follows: 1 . Severe type II and III open fractures 2. Fractures associated with severe burns 3. Fractures requiring subsequent cross-leg flaps, free vascularized grafts, or other reconstructive procedures 4. Certain fractures requiring distraction (e.g., fractures associated with significant bone loss or fractures in paired bones of an extremity in which maintenance of equal length of the paired bones is important) 5. Limb lengthening 6. Arthrodesis 7. Infected fractures or nonunions 8. Correction of malunions The relative or possible indications are as follows: 1 . Certain pelvic fractures and dislocations 2. Open, infected pelvic nonunions 3. Reconstructive pelvic osteotomy (i.e., exstrophy of the bladder) 4. Fixation after radical tumor excision with autograft or allograft replacement 5. Femoral osteotomies in children (use of this method eliminates the necessity of subsequent removal of internal fixation appliances such as plates and screws) 6. Fractures associated with vascular or nerve repairs or reconstructions 7. Limb reimplantation Complications: 1 . Pin track infection 2. Neurovascular impalement 3. Muscle or tendon impalement 4. Delayed union 5. Compartment syndrome 6. Refracture 7. Limitation of future alternatives The frame biomechanics of the external fixator are:

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1 . Large pin fixators 2. Use of half-pins of diameter between 2 and 6 mm 3. Pins with thread in between 4. The large pins have an ability to neutralize deforming forces 5. They provide rigid fixation, and avoid collapse of fracture The pins may be: 1 . Large thread diameter cancellous bone 2. Small pitch angle and narrow thread diameter for dense cortical bones 3. Hydroxyapatite coated for bone apposition 4. Conic Schanz screw (trocar tip) 5. Nonconic Schanz screw (trocar tip) 6. Nonconic Schanz screw cancellous thread (trocar tip) 7. Conic Schanz screws (regular tip) 8. Nonconic Schanz screw (regular tip) They may be (1) a pin with screw hole >30% of bone diameter and has 45% reduction in torsional strength or (2) a pin with diameter more than 6 mm which increases the risk of stress fractures. The radial preload may be (A) implant–bone interface that has an effect on pin loading; when it is the concept of prestresses the bone–pin interface in a circumferential pattern or (B) fixator pins are placed with slight mismatch in the greater thread diameter versus core diameter of the pilot hole which reduces the chances of pin loosening. Hence a large mismatch results in a high degree of radial preload and chances of stress fractures, and microscopic structural damage to the bone surrounding the pin. The pin insertion depends on the type of the pin whether it is (A) predrilled or (B) to be drilled. The new AO Schanz-type screws for unilateral external fixation may be (1) combined deep- and shallow-thread Schanz-tip screw when the thread near the tip has a 4.5 mm outer and 3.2 mm core diameter, and the tip is self-cutting. The shaft is 46 mm in diameter and connects with a conical part. It is furthermore provided with a shallow thread to engage and drive the screw forwards when the thread near the tip HA is not yet engaged in the far cortex. This Schanz screw is designed for use in cortical bone providing automatic radial preload. It is preferred wherever the axial holding strength requires priority, or (2) shallow-thread Schanztype screw when this screw is provided with only a shallow thread and is especially designed for use in cancellous bone where transverse surfaces are present (good strength in relation to a force acting perpendicularly to the long axis). This screw has a disadvantage wherever the resistance to transverse forces has priority over the axial holding strength (e.g., in short metaphyseal fragments). The placement of the pin is important as the pin placed perpendicular to the long axis of bone can act as cantilever as they do not reduce the shear force vector. Half-­ pins placed parallel to fracture are in direct opposition to shear force, which gets converted to compression and in this way compression is dependant on shear load.

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The exact pin placement is as follows: An external fixator that allows pin offset angle of 60° can equalize the forces in sagittal and coronal plane which provides mechanical stimulation closer to normal. In oblique fractures there is inherent shear present and it is here that steerage pins should be placed. However if obliquity is more than 60°, these steerage pins are also ineffective so the frame should be a neutralizing device. Improved effectiveness of external fixation pins: In the past decade it has become clear that pin loosening and pin tract infections can be significantly reduced by 1 . Using larger pins 2. Generating radial preload with the inserted pins Based on early clinical experience the AO introduced, in 1984, short-threaded Schanz screws with a core diameter of 3.5 mm and a shaft diameter of 4.5 mm. These screws provided excellent purchase in cortical bone while making the smooth shaft of 4.5  mm the effective pin diameter in the near cortex. These Schanz screws were considerably stiffer than the 5 mm screws previously used, where the threaded portion (core diameter of 4.0  mm) engaged in both cortices. Clinical experience in the early 1980s indicated that using pins with short threads inserted in pin holes smaller than the shaft diameter lowered the empirical rate of pin tract infections and loosening. Hence with these systems, misfits between drill hole and pin shaft (radial preload) of somewhere between 0.5 mm and 1.0 mm were created. Thus: 1. An exact fit between pin and bone results in pin loosening without prior mechanical damage to the interfacing bone. 2. Oversize of 0.1  mm results in the best bone structure and avoidance of pin loosening due to adequate fit. 3. Oversize of 0.3 mm results in mechanical damage, instability, and consequent micromotion-induced bone resorption. 4. Oversize of 0.5  mm results in massive mechanical destruction of bone by overload. On closer examination of this issue, it was predicted on theoretical grounds that mismatches between core and shaft diameter of 0.1–0.2 mm would be highly effective, yet small enough to prevent mechanical disruption of the surrounding cortex. 5. It further established the effectiveness of radial preload using a pneumatically operated pin motion system in the sheep tibia. 6. Similar experiments carried out confirmed the theoretical prediction. Hence based on these insights, a new AO Schanz-type screw for unilateral external fixation has been developed. (a) It has a 3.4 mm core diameter and a 4.5 mm outer diameter of the thread near the trocar tip. (b) A very shallow thread with 4.7 mm core diameter and 5.0 mm outer diameter connects to the 5 mm drive shaft.

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(c) The portion of the screw with the shallow thread produces forward propulsion of the pin until the far cortex is engaged by the tip portion. (d) These special design features result in a 0.2 mm misfit for all parts of the new Schanz screw. It is, therefore, not a conical screw but a conically preloaded cylindrical screw, as this avoids the disadvantage of the conical threads, and they require a predetermined position along the long axis of the screw, i.e., a predetermined position in relation to the depth within the bone. (e) Hence a uniform design of the Schanz screw has been adopted, which exerts radial preload on both cortices and requires only drilling of both cortices to 4.5 mm. This simplifies Schanz screw application significantly. Biomaterials: 1 . Stainless steel—increases stress at bone–pin interface 2. Titanium—less elastic modulus 3. HA pins—better for cancellous-stainless steel—increases stress at bone–pin interface 4. Titanium—less elastic modulus 5. HA pins—better for cancellous Bones are painful while removing stainless steel which increases stress at bone– pin interface Factors affecting the stability are as follows: (1) pin number, (2) pin proximity, (3) pin separation, (4) bone bar distance, (5) pin to center of rotation, and (6) insufficient holding of clamp to bar/pin. Monolateral Frames: 1 . Known for flexibility. 2. They build up and down concept. 3. Their components can be removed for stress at fracture site. 4. Have angle variation. 5. Fracture reduction. Delta Frames: They are basically two monoplanar constructs at 90° and they help transfer more load, while a unilateral biplanar delta frame is more stable than bilateral transfixing devices. Monotube Fixators: They have a fixed pin placement with a telescopic tube for axial compression and distraction. They have no pin spread possible and are placed near the bone to increase stability. They have rigidity increased by large-diameter tube and high bending stiffness and torsional stiffness, and variable axial stiffness. They also have ball joints which require frequent tightening (chao) due to insufficient holding strength of pin which decreases rigidity.

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The pins placed at 60° and 10° of separation decreased torsional stress by 97%. The pins are placed divergent to each other with pin placed out of plane which increases the angular and torsional rigidity. The development of tube-to-tube clamps: A recent contribution to external fixation consists of the “tube-to-tube” fixation. This tube-to-tube fixation allows for very versatile assembly of the tubes which connect the pins. According to the philosophy of the AO group the fragments of the fracture are fixed subsequent to appropriate reduction. Therefore extensive secondary corrections are actually a less important indication for tube-to-tube fixation. More important is the possibility to apply pins in distinctly different planes. A good example for such application is the external fixation of the humerus, where damage to the radial nerve can best be avoided by applying the pins in Iwo planes, at right angles to each other. This tube-to-tube fixation is a typical example of AO ingenuity, where versatility is achieved without complicated additions to the system of instrumentation and implants. In spite of the extended possibilities offered, the system remains simple and can be taught and learned with little effort. The quality and simplicity are equally important and guidelines for the development of implants and instruments. Dynamization: It converts static fixator which neutralizes all forces, including the axial motion, and allows the passage of forces across the fracture site. It also helps to restore cortical contact. It produces a stable fracture pattern with inherent mechanical support. It is also known as secondary contact for healing. It decreases translation shear forces and produces fibrous union which occurs with weight bearing, with progressive closure of fracture gap. The theory of dynamization is as follows: Once there is evidence of biologic activity (early fracture callus), there should be a slow and progressive load transfer to the healing callus. As hypothesized and later explained in different terms (with interfragmentary strain theory), pure compression and hydrostatic pressure will stimulate the mesenchymal cells to differentiate toward chondrogenesis and subsequently endochondral ossification. A strain will result in the formation of collagenous tissue and subsequent intramembranous ossification. Combinations of these two temporally spaced events (compression then strain) can manifest themselves as callus healing or, as is the case with the use of the Ilizarov principle, regenerate formation (Figs. 27.9 and 27.10). All of this, however, depends on adequate blood flow because, in its absence, there will be no bone healing, regardless of the type of fracture fixation. Thus, as the initial construct with the stiff fixator begins to demonstrate some biologic activity, the fixator undergoes a “controlled destiffening” so that there is a slow but definitive transfer of load bearing from the fixator to the bone. This load sharing will gradually stimulate the developing callus until solid bone healing has occurred. Micromotion is a very important mechanical stimulus force in a construct, as these forces are imparted to the periosteal callus. The quantity, magnitude, and timing of micromotion are still under study.

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Figs. 27.9 and 27.10  Photographs of Ilizarov frame for correction of reconstruction osteotomy for neglected dislocation of the hip in young adults (figure by the courtesy of Osman A.E. Mohamed, Faculty of Medicine, Al-Azhar University, Damietta)

Dynamization in fixators is by adjusting pin bar clamps, and by releasing the body in monotube or by releasing tension of wires in Ilizarov. By dynamization, there is a race between the load-carrying capacity of healing bone and failure of pin–bone interface. This dynamization decreases these stresses, and prolongs the life of fixators. In unstable fractures there is a localized yielding failure due to pin– bone interface. Dynamization in fixators can be accomplished by adjusting pin bar clamps, or by releasing the body in monotube or by releasing tension of wires in Ilizarov. In dynamization, there is a race between the load-carrying capacity of healing bone and failure of pin–bone interface. Dynamization decreases these stresses, and prolongs the life of fixators. In unstable fractures localized yielding failure is due to pin–bone interface. Ligamentotaxis: The term ligamentotaxis, common in the European literature, suggests that certain intra-articular fractures can be treated by external fixation using traction by the fixator on the capsular and ligamentous structures around the joint. This concept works well in comminuted intra-articular fractures of the distal radius, for which pins and plaster have commonly been employed.

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References 1. Meccariello L, Bisaccia M, Caraffa A, et al. From the down to modern era: the history of the nailing. Can Open Orthop Traumatol J. 2016;3(2):10–7. 2. Freeman L. The application of extension to overlapping fractures, especially of the tibia by means of bone screws and a turnbuckle, without open operation. Ann Surg. 1919;70(2):231–5. 3. Lambotte A.  The operative treatment of fractures: report of fractures committee. Br Med J. 1912;2:1530. 4. Charnley J. Positive pressure in arthrodesis of the knee joint. J Bone Joint Surg. 1948;30-B:478. 5. Vidal J. External fixation. Clin Orthop Relat Res. 1983;180:7–14.

The Principles of the Ilizarov Apparatus

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K. Mohan Iyer

Professor Gavril Abramovich Ilizarov was born in the Caucasus, in the Soviet Union in 1921. He was involved, without much orthopedic training, in looking after injured Russian soldiers in Kurgan, Siberia, in the 1950s. Without any proper equipment, he was faced with crippling conditions of unhealed, infected, and malaligned fractures. With the help of a local cycle shop he devised ring external fixators tensioned like the spokes of a cycle. With the help of this equipment he achieved healing, realignment, and lengthening which considerably surprised him and used its principles for devising the modern apparatus, which is still used today as one of the distraction osteogenesis methods. In 1954 he published his first article on transosseous osteosynthesis. He headed the world’s largest orthopedic hospital which is known as the Kurgan All-Union Scientific Centre for Restorative Orthopaedics and Traumatology. Professor Ilizarov continued working in this field of orthopedics for 41 years until his death in 1992 at the age of 71. Professor Ilizarov’s methods were brought to the West in 1981 by an Italian doctor, Prof. A. Bianchi-Maiocchi. The main principles of Ilizarov can be summarized as follows: Law of tension-stress which can be elaborated as 1. Distraction osteogenesis 2. Mechanical induction of new bone formation 3. Neovascularization 4. Stimulation of biosynthetic activity 5. Activation and recruitment of osteoprogenitor cells 6. Intramembranous ossification

K. M. Iyer (*) Royal Free Hampstead NHS Trust, Royal Free Hospital, London, UK © Springer Nature Switzerland AG 2019 K. M. Iyer, W. S. Khan (eds.), General Principles of Orthopedics and Trauma, https://doi.org/10.1007/978-3-030-15089-1_28

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A

B C D

E

Fig. 28.1  Line diagram showing the stages of neovascularization

Ilizarov developed the law of tension-stress, which describes the gradual process of new bone and soft-tissue regeneration under the effect of tension-stress caused by slow and gradual distraction (Fig. 28.1). These biological principles can be summarized as follows: 1 . Minimal disturbance of bone and soft tissues 2. Delay before distraction 3. Rate and rhythm of distraction 4. Site of lengthening 5. Stable fixation (Fig. 28.2) of the external fixator 6. Functional use of the limb and intense physiotherapy Distraction osteogenesis, also called callus distraction, callotasis, and osteodistraction, is a surgical process used to reconstruct skeletal deformities and lengthen the long bones of the body. A corticotomy is initially used to fracture the bone into two segments, and the two bone ends of the bone are gradually moved apart during the distraction phase, to allow the new bone to form in the gap or tunnel thus created. When the desired or possible length has been reached, a consolidation phase follows in which the bone is allowed to keep healing. Thus distraction osteogenesis has the benefit of simultaneously increasing bone length and also the volume of surrounding soft tissues around it. This distraction osteogenesis is also called callus distraction, callotasis, and osteodistraction which is a surgical process used to reconstruct skeletal deformities and at the same time also lengthen the long bones of the body. A corticotomy is used to fracture the bone into two segments, whereby the two bone ends of the bone are gradually moved apart during the distraction phase, thus allowing new bone to form in the gap or tunnel thus developed. When the desired or possible length is achieved, a consolidation phase follows in which the bone is allowed to keep healing.

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Fig. 28.2  Stable fixation (photograph by the courtesy of Osman A.E. Mohamed, Faculty of Medicine, Al-Azhar University, Damietta)

POSTERIOR

Tibialis posterior muscle Anterior tibial artery and vein Deep peroneal nerve

Fig. 28.3  Line diagram showing the passage of wires subcutaneously

The Exact Procedure/Technique Firstly wires of 1.5 or 1.8  mm diameter are passed percutaneously (through the skin) through bones by means of a drill and the protruding ends of these wires are then fixed to rings with special “wire-fixation” bolts (Fig. 28.3). These rings then in

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Fig. 28.4  Line diagram showing the assembly of the Ilizarov frame

turn are connected and fixed to one another by threaded rods; when once it is fixed, the Ilizarov frame affords a stable support to the affected limb (Fig. 28.4). A corticotomy is then performed; it is an osteotomy (cutting the bone only) where the periosteum of the bone is preserved like a tunnel. Adjustments in the rods produce compression or distraction as desired between the bone ends, and simultaneously deformities are also corrected. The ring fixator is then removed at the end of the treatment.

Aftercare of the Apparatus The postoperative management of a patient requires the frequent contact and close monitoring by the surgeon: 1 . Deformities and contractures cannot be allowed to persist or progress. 2. The patient must be encouraged to bear weight on the lengthening limb.

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3. Pin- or wire-site sepsis must be treated aggressively; osteolysis around an implant suggests that additional transosseous fixation is needed. 4. Adequate physiotherapy is essential as follows: (a) The patient has to participate in a proper program of exercises, mobilization, and ambulation. (b) In fact following the Ilizarov’s original technique requires the patients to stay in hospital and participate in at least 2 h of therapy in various forms every day. (c) When the services of a physiotherapist are not always available, it is ideal and preferable for the surgeon himself/herself to supervise the therapy for the patient. (d) Achieving length or correcting a deformity at the cost of decreased motion, mobility, or function is not a worthwhile goal.

Removal of the Apparatus 1 . Broadly a month too late is far better than a day too early. 2. The follow-up X-rays must show at least three cortices; that is, out of four cortices (anterior, posterior, medial, and lateral) in AP and lateral projections, at least three should be fully ossified, with a sharp outline of the cortical bone. 3. Finally before actually removing the frame the patient must be administered a “stress test” and asked to use the limb in a functional manner (weight bearing for the lower limb and functional activities for the upper limb). 4. If the patient is able to do this the frame can then be removed with confidence along with actual removal of the fixator to be usually done under anesthesia.

Advantages No skin incision is made as in a conventional operation. Incidents of hemorrhage, tissue trauma, and infection are much fewer. 1. This is a minimally invasive procedure as only wires are used to fix the bones to the rings and hence there is very little soft-tissue damage. 2. The Ilizarov fixator is very versatile; the cylindrical shape of the fixator permits deformities to be corrected simultaneously in three dimensions. 3. The patient remains mobile throughout the course of the treatment. Intensive physiotherapy is started early; and hence, problems of joint stiffness and contractures are rare. Above all, the patient’s stay in the hospital is considerably reduced.

Disadvantages 1. Mechanical: (a) Distraction of fracture site

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(b) Inadequate immobilization (c) Pin-bone interface failure (d) Weight/bulk (e) Refracture (may be seen in a pediatric femur) 2. Biologic 3. Infection (pin track) 4. Neurovascular injury 5. Tethering of muscle 6. Soft-tissue contracture

Indications 1. Limb lengthening 2. Deformity correction (Figs. 28.5a, 28.5b, 28.5c, and 28.5d) 3. Infected nonunions 4. Congenital pseudarthrosis 5. Treatment of joint contractures, e.g., resistant congenital talipes equino varus, post-burn contractures, and posttraumatic stiffness (Fig. 28.6).

Fig. 28.5a  Line diagram showing the first step in deformity correction

28  The Principles of the Ilizarov Apparatus

Fig. 28.5b  Line diagram showing the deformity finally corrected Fig. 28.5c  Photograph of Ilizarov frame for correction of reconstruction osteotomy for neglected dislocation of the hip in young adults (figure by the courtesy of Osman A.E. Mohamed, Faculty of Medicine, Al-Azhar University, Damietta)

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Fig. 28.5d  Photograph of Ilizarov frame for correction of reconstruction osteotomy for neglected dislocation of the hip in young adults (figure by the courtesy of Osman A.E. Mohamed, Faculty of Medicine, Al-Azhar University, Damietta)

Anteir tibial artery and vein Deep peroneal nerve

Fig. 28.6  Line diagram showing the steps in the correction of joint contractures

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6 . Fixation of complex fractures (Fig. 28.7) 7. Bone transport and osteomyelitis (treatment of missing bone in the limb, due to various causes). 8. Arthrodesis (fusion or joining of two bones across a joint) (Fig. 28.8). 9. Peripheral vascular disease like thromboangiitis obliterans.

Fig. 28.7  Fixation of complex fracture. Photograph of Ilizarov frame (figure by the courtesy of Osman A.E. Mohamed, Faculty of Medicine, Al-Azhar University, Damietta)

Fig. 28.8  Arthrodesis (photograph by the courtesy of Osman A.E. Mohamed, Faculty of Medicine, Al-Azhar University, Damietta)

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Treatment of Nonunions 1. Ilizarov revolutionized the treatment of recalcitrant nonunions demonstrating that the affected area of the bone could be removed, the freshened ends “docked,” and the remaining bone lengthened using an external fixator device. 2. The time taken for healing after such treatment is much longer than normal bone healing. 3. Usually there are signs of union within 3  months, but the complete treatment may continue for many months beyond that.

Treatment of Infected Nonunion Ilizarov is the gold standard for the management of nonunion of osteomyelitis for both achieving union and eradication of infection, however generous, though careful sequential debridement and hardware/dead tissue removal and bone grafting are also options for some selected cases. Osteomyelitis burns in the fire of regeneration, thus activating a biosynthetic process, while increasing local resistant to infection. Hence there are three ways to correct INU: 1 . Controlled osteogenesis, filling of cavities by newly formed tissue 2. Resection of infected bone and subsequent intercalary bone lengthening 3. Gradual bone transport of one wall of the cavity

Limb Lengthening Limb-lengthening and reconstruction techniques can be used to replace missing bone and lengthen and/or straighten deformed bone segments as these procedures can be performed on both children and adults who have limb length discrepancies due to birth defects, diseases, or injuries. Here the regenerated bone is normal and does not wear out. The muscles, nerves, and blood vessels grow in response to the slow stretch like they do during a growth spurt or in pregnancy. The actual procedure is minimally invasive and requires only one or two nights in the hospital and literature says that successful limb lengthening is possible up to 18 cm (Fig. 28.9).

Buerger’s Disease Here in this condition, arterial reconstructive surgery is not feasible and sympathectomy has temporary limited role and progression of the disease invariably leads to amputation. Ilizarov’s method increases the vascularity of the ischemic limb and hence Ilizarov’s method is an excellent and affordable procedure in the treatment of Buerger’s disease.

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A B

C D

E

Fig. 28.9  Line diagram showing the stages of limb lengthening

Summary Ilizarov is a compression-distraction device that can do osteogenesis: 1. Infection nonunion and congenital deformity corrections are one of the golden indications. 2. You can be taller even after 18 years with this. 3. Wearing Ilizarov is not a fancy style. It returns painful discomfort. 4. Physiotherapy is essential.

The Direct Anterior Approach to the Hip

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Hiran Amarasekera

Introduction Background The hip joint, a ball-and-socket joint covered by strong muscles, is situated deeply in pelvis and can be approached almost in any direction (Fig. 29.1). However out of the many approaches described the commonest used approaches for arthroplasty have been posterior [1], anterolateral [2], and anterior approaches [3]. Different approaches have been popular during different times in the history of orthopedics depending on instrumentations, implants, surgeon’s preference and training, and patients’ active lifestyles, early return to working, and need to achieve high range of motion with minimal risk of dislocation.

History Hueter initially described the direct anterior approach in 1881 [4]. It was later popularized by Smith Peterson in 1917 [5]; in early 1950s direct anterior approach (DAA) was a popular mode for hip arthroplasty. In 1950 two French surgeons Judet and Judet reported this as a successful approach for hip replacement [6] and later O’Brien published a case series of total hip arthroplasty done via the anterior approach [7].

H. Amarasekera (*) Faculty Of Medicine, University of Kelaniya, Ragama, Sri Lanka University Hospitals of Coventry and Warwickshire, Coventry, UK Warwick Medical School, Coventry, UK © Springer Nature Switzerland AG 2019 K. M. Iyer, W. S. Khan (eds.), General Principles of Orthopedics and Trauma, https://doi.org/10.1007/978-3-030-15089-1_29

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H. Amarasekera Posterior approach (Southern) Postero-medial (Ferguson)

Postero-lateral

Direct Lateral (Hardinge)

Medial approach

Antero-lateral (Watson-Jones) Anterior Approach (Smith-Petersen)

Antero-medial and Ludloff approach

However with the introduction of Charnley’s low-friction arthroplasty in late 1950s this approach fell out of favor among the orthopedic surgeons giving way for the posterior approach to come into vogue [8–10]. Throughout this approach has been popular for other surgeries mainly for pediatric hip surgery such as developmental dysplasia, hip biopsy, and drainage of septic arthritis.

Resurgence of the Approach With increasing life expectancy, ageing population, increased demand for physical activity, and early return to work more and more surgeons have planned minimally invasive approaches to the hip. With a clear inter-nervous plane without any requirement for muscle detachment stability being maintained with minimal dislocation rates [11, 12] and new instrumentation and devices being developed minimally invasive direct anterior approach has gained popularity among the arthroplasty surgeons since the last few decades. Interests appear to be rapidly growing and gaining increasing popularity among arthroplasty surgeons with modern concepts of hip preservation, minimally invasive hip surgery, and hip resurfacing, in a population with a highly active lifestyle, demanding early return to work or sports activities.

Key Advantages and Disadvantages of the Approach The key advantages of the approach include the ability to directly access the hip through the true inter-nervous planes with minimal or no muscle dissection leading to early recovery and higher functional rates. The approach also preserves the blood flow to the hip joint as the posterior structures are not damaged, thus making this a popular approach in hip-preservation surgery and surface replacement of hip joint [13].

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However the steep learning curve, poor cosmetic scar, and lack of specialized instrumentation made the approach less preferred by orthopedic surgeons in last few decades. At present these issues have been addressed with specific training courses, cadaveric run in cadaveric skill labs, and development of specific instruments [14, 15].

The Approach Indications and Contraindications Given the proper training and after gaining experience with the use of the correct instrumentation and selecting the ideal patient most hip surgeries can be performed through most approaches. Key indications for the approach in modern-day practice still remain to be most pediatric surgeries, hip-preservation surgery, surgical dislocation of the hip, open osteochondroplasty, arthrotomy for drainage or biopsy, total hip replacement, and experienced centers’ revision hip arthroplasty [16]. However contraindications and caution when selecting the patients and surgeries remain. Obesity and BMI >40 are contra indications as they increase wound infection rates.

Anatomy The approach uses the Hueter interval (Figs. 29.2 and 29.3) between tensor fasciae latae and sartorius. Key anatomical landmark is the anterior superior iliac spine (ASIS) felt as a bony prominence at the anterior-most point of iliac crest. The sartorius and the inguinal ligament originate from here. Tensor fasciae latae (TFL) originates just below and lateral to ASIS along with the gluteus medius. The femoral vessels and nerve are medial to sartorius a key point to remember that too medial dissection will put these structures at risk. Lateral cutaneous nerve of the thigh (LCNT) begins from the lower end of lumbar plexus emerging laterally to the psoas major and crossing the iliacus. Then it runs near the ASIS running laterally through the muscular lacuna under the inguinal ligament crossing over the sartorius and Fig. 29.2  Table and supine position with sandbag under operatingside buttock

Table extension at hip

Pillow under buttocks

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Fig. 29.3  Skin incision: Note that the traditional incision runs from 2 cm inferior and posterior to ASIS

Anterior Superior IIiac spine

Skin incision

Femoral Head

Greater Trochanter

Fig. 29.4 Superficial dissection showing the Hueter interval

Tensor Fasciae Latae (Superior Gluteal Nerve)

Sartorius (Femoral Nerve)

Hueter Interval

enters the thigh. The nerve divides into anterior and posterior branches and supplies the skin over the anterolateral part of the thigh and the skin over the gluteal region. The rectus femoris muscle originates from two heads, the straight head from the anterior inferior iliac spine and the reflected head from the anterior lip of acetabular and the hip joint capsule. Gluteus medius originates from the gluteal surface of ilium, runs anteromedially, and inserts to the oblique ridge on the lateral surface of greater trochanter. This along with gluteus minimus forms the abductor complex. The approach uses inter-­nervous muscle plane between superior gluteal nerve and femoral nerve (Figs. 29.4 and 29.5).

29  The Direct Anterior Approach to the Hip Fig. 29.5  Deep dissection showing clear internervous plane

623 Lateral Cutaneous Nerve to Thigh

Femoral Nerve Femoral Artery Femoral Vein

Deep Inter Nervous Plane

Fectus Femoris

Gluteus Medius

Fig. 29.6 Transverse section of the thigh (dissection and tissue planes marked in blue)

Iliopsoas

Sartorius Rectus Femoris Tensor fasciae latae

Obturator Internus

Gluteus minimus Gluteus medius

Gluteus medius

Superior Gamellus

Gluteus maximus

The Traditional Approach Position The patient is placed in the supine position with a sandbag placed under the buttock of the operating side as it helps to identify the muscle planes easily (Fig. 29.6). Incision The incision lies along a line drawn along the anterior half of the iliac crest towards ASIS and curving downwards in a slight lateral direction heading towards the outer border of the patella (Fig. 29.7).

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Fig. 29.7 Capsulotomy and dislocation of head

Capsule

External Rotation

Vertical arm of the incision is limited to around 8–10 cm as it crosses the hip joint anteriorly.

Approach Initially the gap between the tensor fasciae latae and sartorius is identified facilitated by external rotation of the limb, which tenses the muscles. Care should be given to protect the LCNT that passes across sartorius. Once retractors are placed (Fig. 29.4) deep dissection is done medially to TFL identifying the rectus femoris in the deep layer. Lateral margin of the rectus femoris is identified and an interval between it and the gluteus medius is developed. Rectus femoris can be detached from the origin if needed. The retractors are gently placed between the muscles taking care not to damage the femoral neurovascular bundle. The joint capsule is seen through this interval.  uscle Inter-nervous Plane M Both in superficial and deep layers the inter-nervous plane lies between the femoral and the superior gluteal nerves. Superficially medially bound by the sartorius (femoral nerve) and laterally bound by TFL (superior gluteal nerve) and deep layer medially

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bound by rectus femoris (femoral nerve) and laterally gluteus medius (Superior gluteal nerve), this is considered a true inter-nervous plane (Figs. 29.4 and 29.5)

Capsule Arthrotomy Depending on the surgery the capsular arthrotomy can be done as a straight line, vertical, triangular, or any preferred way (Fig. 29.7). Dislocation The head is dislocated by gentle traction, external rotation and adduction, and external rotation. Surgical Procedures Once the hip is approached many surgical procedures can be carried out: arthrotomy, drainage, surgical dislocation, and preservation surgeries such as osteochondroplasty, biopsy, pediatric surgery such as DDH, osteotomies, combined pelvic and acetabular procedures, and total, partial, or surface hip replacements are few of the common and popular procedures done through this approach. Closure The tissue planes are closed in layers as there are no tendon or muscle reattachment needed.

 odifications, New Instrumentations, and Minimally M Access Approach [17] Incision Modern operating tables can be extended at the mid-trunk level to enhance the position created by a sandbag placed under the buttocks. Some surgeons prefer to use both as it gives better presentation of the capsule anteriorly. Approach The mini incision anterior approach or the minimally invasive approach utilizes small 6–7 cm incision starting 2 cm posterior and 2 cm inferior to ASIS running around 2 cm below the greater trochanter [18].  uscle Inter-nervous Plane M These are respected as per the traditional approach Capsule Arthrotomy This remains a surgeon’s preference decided based on the procedure itself. Closure Stepwise layers of closure are advocated with function and cosmesis kept in mind.

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Rehabilitation Protocol As in all approaches rehabilitation plays a key role in early recovery, early return to work, and early return to sport. Functional recovery is believed to be faster than in any approach [19, 20] and development of a standard protocol for rehab is mandatory. Even though these may change from institution to institution or surgeon to surgeon, and the surgical procedure, by and large the principles remain the same. Basic principle in rehabilitation following THR through anterior approach is outlined below. Once the general recovery following surgery is passed the patients are put on full-weight-bearing mobilization ideally from day 1. ROM (range of motion exercises), gait training, and day-to-day activities such as walking and climbing stairs are achieved within first 3 days and the patient is discharged. Within 0–2 weeks gait training, quadriceps and muscle strengthening, and core strengthening exercises are started. 3–6 weeks further ROM muscle strengthening including abductors, adductors, and core body workouts are developed. Patients can return to work within 2–4 weeks depending on the work. From 7–12 weeks further gait training is continued within specific concentration of muscle groups. Sport activities are started during this period and full return to sports can be achieved as early as 12 weeks.

Complications Apart from the general complications that are common to all surgical approaches around the hip such as damages to neurovascular structures, bleeding, deep vein thrombosis, and pulmonary embolism certain specific set of complications are unique to this approach. Higher rate of wound complications [21, 22] and superficial wound infection have been reported. One main reason is the anterior thigh area being covered by skin folds in obese patients. Poor scar is another complication as the approach cuts across the Langer’s lines. Dislocation rates are believed to be low capered to traditional approaches such as the posterior [11]. Damage to lateral cutaneous nerve of the thigh (LCNT) can lead to loss of sensation around anterior thigh sometimes leading to meralgia paresthetica [23]. Going too medially medial to sartorius runs the risk of damaging femoral vessels and nerve; this can be avoided by staying lateral to sartorius and keeping to the correct tissue plane (Fig. 29.4); sometimes the retractors itself can damage these structures rather than the dissection itself. Carefully placing retractors is key to avoid this; especially if a retractor comes out replacing it should be done by the surgeon himself/herself. These are high usually within the learning curve and with experience these can be avoided. In hip-preservation surgeries and resurfacing femoral neck fracture is a known complication that leads to failure of the procedure [24]. Cautiously dislocating the hip mastering the technique and using customized implants [25] will help to reduce this complication.

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Pearls and Pitfalls Steep learning curve is probably the single most reason many orthopedics surgeons have been hesitant to perform this approach over the years. However with present-­ day demand this may be an essential approach where all hip surgeons are expected to master. To avoid steep learning curves at present there are many cadaveric courses, other training materials, and many training programs available throughout the word. Special instruments including retractors, guide wires, broach handles [26], and reamers along with operating tables have been developed [27]. It is essential to avoid too much medial dissection and to stick to the correct tissue planes to avoid damaging the femoral vessels and nerve. Careful handling of instruments, training, or minimally invasive techniques, using special tables, will help to avoid all these complications. Even though the mini incision is shorter both traditional and mini incisions do not respect Langer’s lines and achieving a cosmetically acceptable scar has been a challenge. Some surgeons have developed a more cosmetically accepted bikini incision to overcome this [28].

Conclusions Direct anterior approach seems to have evolved over the years and has return to modern orthopedic practice gaining rapid popularity among orthopedic surgeons in this decade [29]. Many reasons such as modern patients’ demands, active lifestyles, development of modern instruments, demand for minimally invasive techniques, and more hip-preservation work carried out in young adult hips have all contributed for this resurgence. However it is worth noting that to achieve successful results, training in specific procedures reduces steep learning curve, and familiarizing with modern instrumentation is key to success. In modern day all hip surgeons should know this approach or need to learn the basic concepts as more and more open hip procedures are done through this approach. Acknowledgement  Figures and illustrations by: Dakshini Egodawatte MBBS (SAITM), Clinical demonstrator in Trauma and Orthopaedics Neville Fernando Teaching Hospital, Malabe, Sri Lanka.

References 1. Hunter SC. Southern hip exposure. Orthopedics. 1986;9:1425–8. 2. Jones W. Fractures of the neck of femur. Br J Surg. 1936;23:787–808. 3. Smith Petersen MN. Approach to and exposure of the hip joint for mold arthroplasty. J Bone Joint Surg Am. 1949;31A:40–6. 4. Rachbauer F, Kain MS, Leunig M. The history of the anterior approach to the hip. Orthop Clin North Am. 2009;40:311–20. 5. Smith Petersen MN. A new supra–articular subperiosteal approach to the hip joint. J Orthop Surg (Phila, Pa). 1917;s2–15:593.

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6. Judet J, Judet R. The use of an artificial femoral head for arthroplasty of the hip joint. J Bone Joint Surg. 1950;32(B):166–73. 7. O’Brien RM. The technic for insertion of femoral head prosthesis by the straight anterior or Hueter approach. Clin Orthop. 1955;6:22–6. 8. Charnley J. Arthroplasty of the hip. A new operation. Lancet. 1961;1:1129–32. 9. Charnley J.  Total hip replacement by low friction arthroplasty. Clin Orthop Relat Res. 1970;(72):7–21. 10. Charnley J, Cupic Z. The nine and ten year results of the low friction arthroplasty of the hip. Clin Orthop Relat Res. 1973:9–25. 11. Tsukada S, Wakui M. Lower dislocation rate following total hip arthroplasty via direct anterior approach than via posterior approach: five year average follow up results. Open Orthop J. 2015;9:157–62. 12. Sariali E, Leonard P, Mamoudy P. Dislocation after total hip arthroplasty using Hueter anterior approach. J Arthroplast. 2008;23:266–72. 13. Amarasekera HW. Surface replacement of the hip joint. In: Fokter SK, editor. Recent advances in hip and knee arthroplasty. 1st ed. Croatia: Intech; 2012. p. 181–90. 14. Paillard P.  Hip replacement by a minimal anterior approach. Int Orthop. 2007;31(Suppl 1):S13–5. 15. Oinuma K, Eingartner C, Saito Y, Shiratsuchi H. Total hip arthroplasty by a minimally invasive, direct anterior approach. Oper Orthop Traumatol. 2007;19:310–26. 16. Nogler M, Mayr E, Krismer M. The direct anterior approach to the hip revisionOper Orthop Traumatol. 2012;24:153–64. 17. Rachbauer F.  Minimally invasive total hip arthroplasty. Anterior approach. Orthopade. 2006;35:723-4–6-9. 18. Rachbauer F, Krismer M. Minimally invasive total hip arthroplasty via direct anterior approach. Oper Orthop Traumatol. 2008;20:239–51. 19. Rodriguez JA, Deshmukh AJ, Rathod PA, et al. Does the direct anterior approach in THA offer faster rehabilitation and comparable safety to the posterior approach? Clin Orthop Relat Res. 2014;472:455–63. 20. Zhang Z, Wang C, Yang P, Dang X, Wang K. Comparison of early rehabilitation effects of total hip arthroplasty with direct anterior approach versus posterior approach. Zhongguo Xiu Fu Chong Jian Wai Ke Za Zhi. 2018;32:329–33. 21. Jahng KH, Bas MA, Rodriguez JA, Cooper HJ. Risk factors for wound complications after direct anterior approach hip arthroplasty. J Arthroplast. 2016;31:2583–7. 22. Watts CD, Houdek MT, Wagner ER, Sculco PK, Chalmers BP, Taunton MJ. High risk of wound complications following direct anterior total hip arthroplasty in obese patients. J Arthroplast. 2015;30:2296–8. 23. Barton C, Kim PR. Complications of the direct anterior approach for total hip arthroplasty. Orthop Clin North Am. 2009;40:371–5. 24. Kreuzer S, Leffers K, Kumar S. Direct anterior approach for hip resurfacing: surgical technique and complications. Clin Orthop Relat Res. 2011;469:1574–81. 25. Khemka A, Mograby O, Lord SJ, Doyle Z, Al Muderis M. Total hip arthroplasty by the direct anterior approach using a neck preserving stem: safety, efficacy and learning curve. Indian J Orthop. 2018;52:124–32. 26. Post ZD, Orozco F, Diaz-Ledezma C, Hozack WJ, Ong A. Direct anterior approach for total hip arthroplasty: indications, technique, and results. J Am Acad Orthop Surg. 2014;22:595–603. 27. Wayne N, Stoewe R.  Primary total hip arthroplasty: a comparison of the lateral Hardinge approach to an anterior mini invasive approach. Orthop Rev (Pavia). 2009;1:e27. 28. Faldini C, Mazzotti A, Perna F, et al. Modified minimally invasive direct anterior approach through a bikini incision for total hip arthroplasty: technique and results in young female patients. J Biol Regul Homeost Agents. 2017;31:83–9. 29. Amarasekera H. Surgical approaches to the hip joint and its clinical implications in adult hip arthroplasty. In: Kinov P, editor. Arthroplasty. 1st ed. London: Intech; 2013.

Use of Robotic-Assisted Surgery in Orthopedics

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Jeeshan Rahman, Karam Al-Tawil, and Wasim S. Khan

Introduction The use of robotics in orthopedic surgery is becoming more widespread with developments in the field of surgical technology. Robotic devices are being developed in numerous centers worldwide. There are many acronyms that are used to cover the use of computers and robotics in orthopedic surgery, such as CAOS (computer-­ assisted orthopedic surgery), MRCAS (medical robotics and computer-assisted surgery), MICCAI (medical image computing and computer-assisted intervention), and CARS (computer-aided robotic surgery) [1, 2]. Computer navigation is a passive process which gives the surgeon information about the exact position of a prosthesis relative to bone. In contrast, robotic surgery is semi-autonomous, performed by a robot under direct or indirect control of the surgeon [3]. Over the last two decades, there has been a plethora of evidence of its benefits in joint replacement and spinal surgery. Orthopedic surgery is particularly suited to robotic surgery as bones are rigid structures as compared to mobile viscera, allowing devices to be secured to them. This simplifies control of robotic systems. Robotic surgery is associated with better implant positioning and improved surgical planning. There are several studies demonstrating the short to medium term outcome of robotic surgery. However, strong evidence-based studies showing improvements in outcomes using robotic surgery is not currently reported in literature. The short-term studies that are available do not really show an improvement in the patient’s outcome. They do show that implant positioning is improved but this does not produce better results

J. Rahman (*) · K. Al-Tawil East of England Deanery, Colchester, UK W. S. Khan University of Cambridge, Cambridge, UK Addenbrooke’s Hospital, Cambridge, UK © Springer Nature Switzerland AG 2019 K. M. Iyer, W. S. Khan (eds.), General Principles of Orthopedics and Trauma, https://doi.org/10.1007/978-3-030-15089-1_30

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for the patient, hence the need for long-term studies to show what impact it will have on patient outcomes. The initial cost to the healthcare provider in the provision of robotic surgery is often quite high. This is associated with extra costs in training the surgeon and theater staff in the use of the robotic technology. Robotics has gone through vast improvements over the years with some systems being replaced with newer systems due to safety concerns or better efficacy. However, most systems are still at an experimental stage. Current applications of robotic surgery include total hip replacements, total knee replacements, partial knee replacements, reconstruction of knee ligaments, pedicle screw placement, and trauma surgery. Robotic orthopedic surgery is a rapidly emerging field which is gaining momentum in the orthopedic world [4].

History Orthopedics was one of the earlier specialties in medicine to trial the use of robots [4]. The history of robotic surgery in orthopedics dates back to 1983, with the world’s very first surgical robot called “Arthrobot” developed in Vancouver, BC, which took simple voice commands from the orthopedic surgeon to position the patients limb. The surgeon would still have to perform the operation with assistance from the Arthrobot. In 1988 the Robodoc (Integrated Surgical Systems, Delaware, US) was introduced. This was a system used in total hip arthroplasty to allow precise planning as well as to mill precise femoral fittings. The Robodoc was followed by an automated robot developed in 1992, whereby the patient was rigidly clamped and the surgeon placed the robot and just pressed the start button. The robot then performed the predefined task without the surgeon having to do anything else. This advanced robot could execute the procedure with extreme precision and reliability. Unfortunately surgical times were much longer using this system. There was also increased blood loss associated with the system. The Acrobot system (Acrobot Co Ltd., London, UK) was introduced in 1999. This robot has 6 degrees of freedom and is controlled by the surgeon. It only allows certain predefined trajectories. Its first application was for unicompartmental knee replacements [2]. Mazor was founded in 2001. Its first product was called Spine Assist and was approved for spinal surgery. In 2008 it was replaced by the Renaissance Guidance System, which allowed minimally invasive surgery with reduced fluoroscopy times, with very good results for scoliosis and complex spinal deformity. This consisted of a 12 cm high robot that sits on a T bar and drills pedicle screws with high accuracy [5]. Mako (Mako Surgical Corporation, Florida, USA) developed the RIO orthopedic robot in 2004 for use in unicondylar knee replacements (UKR). It was based on the Barrett Tech seven degrees of freedom WAM arm. This robot was further developed and total hip replacement was added to in 2010. Mako was then sold to Stryker, two months after the acquisition of Acrobot [5]. The Navio system (Smith and Nephew, London, UK), developed by Professor Jaramaz in Pittsburg in 2012, is a handheld open platform sculpting device for use

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in UKR and total knee arthroplasty (TKA). This is a semi-autonomous system which constantly tracks the position of the patient’s leg. The handheld device augments the surgeons movements but with safeguards in place to optimize accuracy in implant positioning and safety.

Types of Robotic Surgery in Orthopedics There are two main types of systems in robotic surgery. In haptic systems, the surgeon drives the robot in performing the operation. The surgeon is constantly in charge and has to drive the robot. The Mako robot (Robotic Arm Interactive Orthopedic System or RIO) requires active surgeon participation to perform unicondylar knee replacements. A prior CT scan of the patient’s knee is used to create a three-dimensional computerized model. This model is used to size the joint and to plan implant positioning. During the operation, the surgeon has to reference the bony surfaces. The computer then uses its algorithm to create a precise cutting zone for the robot. The surgeon controls the burr to resect bone within the confines of a predefined cutting zone. The computer will stop the burr if the surgeon accidentally goes outside the predetermined zone. The robot monitors the operation constantly and provides intraoperative data that ensures that only the required amount of bone is cut. In contrast, autonomous robots require the surgeon to perform the initial approach to the joint and then set up the machine which takes over the operation, allowing the surgeon to take a step back. The Robodoc is an example of an autonomous robot that has now fallen out of favor with the orthopedic community. This was popular in Germany for total hip replacements in the 1990s. A third type of technology adopted recently is the passive surgery system, also known as computer-assisted or computer navigation surgery. These systems monitor the progress of the surgical procedure and also provide surgeons with data during the process. They are used preoperatively to assess joint biomechanics and irregularities. They also monitor accuracy of bone cuts during the operation. These systems usually have several cameras that track instrumentation, bony geometry, and alignment. These are positioned near the patient and communicate with each other with light emitting diodes (LEDs) on the bony landmarks. This system provides detailed information to the surgeon but does not limit the surgeon to predetermined safe zones. The surgeon is free to ignore or override the computer’s suggestions [6]. Cobb et  al. [7] reported that computer navigation could enable component positioning to within 2° of the preoperative plan.

Applications of Robotic Surgery Knee The knee joint has probably seen the most interest with regard to technological advances. One particular area is arthroplasty. In patient-specific cutting block

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technology, the jigs have been designed to improve implant position and fit to the patient, and also in navigation for accurate placement of component and perfect alignment to reduce wear and improve patient outcomes. The ultimate aim is to have a system, whereby the cuts are made to restore perfect alignment and the components placed in the most optimal position. However, despite these two key points, soft tissue balance and release may prove more difficult to address. Another area of interest is soft tissue procedures, mainly in the form of ACL reconstruction; we know that tunnel placement has a significant bearing on outcomes and failure, and this is definitely one area which could be improved with technological advance. As we mentioned earlier, all these advances would carry significant cost, time, and training implications. It also raises the question of whether they would have a clinically statistically significant difference to outcome, rather than just improve the biomechanics with no bearing on the clinical picture. A pilot study from 2009 (total of 31 robotic, 27 conventional) evaluating radiological postoperative markers of UKA found that robotic arm-assisted surgery reduced the error and the variance compared to the conventional system. There were however no clinical results. However, this was based on plain radiographs, rather than CT scans, and also femoral component coronal alignment and overall limb alignment were not studied either [8]. A randomized controlled study of 27 patients undergoing UKA in 2006 concluded that all of the robotic (Acrobot) group had tibio-femoral alignment in the coronal plane within 2° of the planned position, while only 40% of the conventional group achieved this level of accuracy. A longer operative time was recorded but did not result in increased complications [7]. Another study which reported on secondary exploratory analysis of the early clinical outcomes of a randomized clinical trial comparing robotic arm-assisted UKA for medial compartment osteoarthritis of the knee with manual UKA performed using traditional surgical jigs showed that robotic arm-assisted surgery results in improved early pain scores and early function scores in some patient-reported outcomes measures, but no difference was observed at one year postoperatively. Although improved results favored the robotic arm-assisted group in active patients, these do not withstand adjustment for multiple comparisons [9]. In a cadaveric study comparing radiological outcomes in mini-invasive TKR a higher implanted prostheses accuracy and fewer outliers were achieved with robot-­ assisted TKR, thus compensating for the shortcomings of conventional minimally invasive TKR [10]. Although robots improve precision of implant positioning, there are potential complications associated with the learning curve and also the difficulty in establishing how the radiological and technical superiority translates into clinical effectiveness. Interestingly, a prospective randomized study of 100 TKRs from 2012 found that robotic-assisted group had no mechanical axis outliers (>±3° from neutral) compared to 24% in the conventional group. There were also fewer cases where the flexion gap exceeded the extension gap by 2 mm. The robotic cases, however, had longer operating time (an average of 25  min longer) but more importantly there were no differences in postoperative range of movement, and WOMAC and HSS

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knee scores [11]. In a randomized controlled study of 70 patients from 2007, the robotic arm had superior post-op radiological parameters but also increased complications in the early stages of its use [12].

Hip The hip joint is one of the most surgically addressed, mainly in the form of total hip arthroplasty (THA). It is long known that hip arthroplasty significantly improves quality of life for patients and has excellent clinical results; however it is associated with potential complications with burden on the affected patients and cost for the healthcare system. While certain aspects may not be improved with robotics, such as infection, other complications, especially dislocation, and the burden it carries, are certainly an area where robotic use can potentially have an impact. It is reported that the cost of early dislocation, i.e., within 6  weeks of the index procedure, which mostly relates to surgical factors, accounts for 342% of the primary cost. It is, therefore, of great interest to both patient care and healthcare economics to minimize the occurrence of this serious complication. Component position is pivotal, with acetabular component malposition accounting for the single most important factor in instability following THA and 22.5% of all revisions [13]. Lewinneck introduced the idea of safe zone through comparing radiographic markers of dislocated and stable hips. There are various tools which can be used to assist the surgeon in ensuring placement in the safe zone thus reducing dislocation rates. These range from simple measures such as jigs with alignment rods and using transverse acetabular ligament (TAL), to navigation and the use of robotic surgery. There are various robotic options, with the “semi-automated robot.” Stryker’s Mako robotic arm-assisted system being the most commonly applied to acetabular navigation. It requires preoperative CT scanning of the patient’s pelvis in order to predetermine the appropriate reaming and cup implantation. The surgeon is still required to perform the approach and remains in control of the robotic-assisted arm during the acetabular component preparation. However, the Mako robotic arm will restrict the movement of the surgeon to the predefined cup position parameters and not allow significant deviation from the preoperative planning [13]. There is increasing evidence that robotic-assisted acetabular cup positioning performs better than standard methods. In 2014, in a matched control study of 160 THRs, based on radiological analysis for the safe zones [14], those performed with the robot had statistically significant improved radiological cup position on postoperative imaging. There was however no analysis of clinical outcome or rate of dislocation [14]. This is further confirmed by another multi-surgeon study from 2015 which again assessed radiological markers for the safe zone, in addition to leg length discrepancy (LLD) and global offset difference (GOD) across 6 surgical techniques, including robotic assisted. While there was no statistically significant difference in LLD and GOD, however, with safe zone placement, the computer-navigated and

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robotic-­assisted cohorts fared statistically significantly better compared to the other methods, with the robotic-assisted statistically significantly more accurate for Callanan’s safe zones compared to all modalities. While the robotic modality is producing more accurate technical results, the setup and running costs, restriction on implant choice for robotic systems, exposure to radiation for CT scans, along with increased operative time, and the limited clinical outcome data may limit the uptake and rate at which these technologies are rolled out in the future [15]. The femoral component has also been evaluated in a radiological study comparing robotic milling versus traditional rasping with 78 patients in each arm. The robotic milling group showed significantly superior Merle D’Aubigne hip score at 2 years, had no intraoperative fractures, and a radiographically superior implant fit was obtained [16]. However, as with any new technique, a learning curve might lead to increase in complications initially. A study evaluating THA in 97 cases from 2007 found that they had equal results to standard technique but suffered a higher complication rate due to the use of the robot [17]. Another area of interest is hip arthroscopy, mainly dealing with femoral acetabular impingement. This in itself is a less common procedure compared to knee or shoulder arthroscopy, is more difficult to perform, and has a steep learning curve with less exposure to it during training. The main challenges are access and instrumentation due to the depth and anatomical contour of the joint along with a tight capsule, rather than the need for complex technical precision; therefore the role of robotic surgery may be of limited benefit as access and use of the instruments would still present a significant hurdle. An anatomic study in 2014 evaluating the use of the da Vinci system in hip arthroscopy concluded that most areas were reached in comparison to standard arthroscopy, apart from the postero-inferior labrum, which was not observed due to the rigidity of instruments [18].

Spine In spinal surgery, accurate placement of metal work is essential to ensuring no damage is sustained to the spinal cord or nerves with often catastrophic consequences to the patient. One of the most commonly performed procedures involves placement of pedicle screws for instrumentation. There have been numerous advances to improve the accuracy of placement with the use of intraoperative CT scanners to minimize the risk of damaging the neuronal structures along with intraoperatively neuro-­monitoring to warn the surgeon of impending damage. This is one area where robotics may play a significantly increasing role to ensure that the screws are placed optimally with minimal risk of breaching into the spinal canal or neural foramen. An area of particular interest is scoliosis, where there is added deformity in multiple planes, making the task of accurate screw placement more complex. A retrospective study from 2018 evaluated the use of robotic-assisted pedicle screws in 49 patients with idiopathic adolescent scoliosis undergoing corrective surgery. They

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concluded that intraoperative neuro-monitoring (t-EMG) was not needed when using robotic-assisted screw placement [19]. Another retrospective review using postoperative CT scan of 662 pedicle screws in patients undergoing scoliosis corrective surgery from 2016 concluded that the malpositioning rate was lower in robotic-assisted cases compared to other similar studies evaluating non-robotic methods. Only 7.2% of screws had a 2 mm breach reducing to 2.4% with prone preoperative CT scanning. Medial malpositioning was reported at 3% reducing to 0% in combination with prone position preoperative CT scan planning [20]. The increased accuracy of pedicle screw placement using robotic assistance was further demonstrated by a group who examined 487 screws in 112 consecutive patients undergoing minimally invasive spinal surgery. Preoperative and postoperative CT scans were performed. The results showed that 97.7% of the screws were safely positioned and that preoperative planning is accurately executed intraoperatively using the robotic assistance with minimal deviation [21].

Shoulder In shoulder surgery, both arthroscopy and arthroplasty, there is lag behind the hip and knee joints with regard to robotic use. There have been studies evaluating glenoid component placement in arthroplasty with computer navigation, paving the way for a robotic-assisted implantation of the component in the future as is the case with hip and knee arthroplasty. There has also been a cadaveric feasibility study in 2011 evaluating the use of robotic techniques and equipment in shoulder surgery, which concluded that it is possible, safe, and potentially allowing for even more complex procedures to be performed compared to standard arthroscopic technique [22]. Another area of shoulder surgery where robotics has been utilized is shoulder girdle and brachial plexus procedures. It is again still in its very initial stages and requires further evaluation. The advantages of endoscopic/arthroscopic surgery to this area, along with improved precision and vision, magnification, are appealing. One study describes the grafting of a C5 nerve root segment using the robot but still required an open incision in addition [23].

Other Uses The use of robotic techniques has been trialed in other areas of orthopedic surgery, including shoulder, foot and ankle, and trauma surgery but to a lesser extent and there is very limited evidence in the literature relating to its use in these areas. In foot and ankle surgery, the use of robotic device to increase accuracy to perform injections has been described but its clinical implications remain to be understood.

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In trauma surgery, certain applications of robotic surgery such as in intramedullary nailing techniques for the locking screws have been again described.

The Future Although robotic orthopedic surgery is rapidly expanding, we are still in its infancy. Robotic surgery should enable surgeons to make precise preoperative plans that are custom made for the patient and execute surgical procedures according to this plan. It should allow true minimally invasive surgical procedures, reducing blood loss and allowing faster rehabilitation. Surgeons should be able to precisely place implants, increasing reproducibility and reliability. Finally, at the rate at which technology is advancing, a fully automated, fully autonomous robot that performs surgical procedures without the need for any surgeon input is not far from reality.

References 1. Lonner JH. Robotically assisted unicompartmental knee arthroplasty with a handheld image-­ free sculpting tool. Orthop Clin North Am. 2016;47(1):29–40. 2. Bargar WL. Robots in orthopaedic surgery: past, present, and future. Clin Orthop Relat Res. 2007;463:31–6. 3. Specht LM, Koval KJ. Robotics and computer-assisted orthopaedic surgery. Bull Hosp Jt Dis. 2001;60(3-4):168–72. 4. Karthik K, Colegate-Stone T, Dasgupta P, Tavakkolizadeh A, Sinha J.  Robotic surgery in trauma and orthopaedics: a systematic review. Bone Joint J. 2015;97b(3):292–9. 5. Davies PBL. Orthopaedic robotic surgery. J Trauma Orthop. 2017;05(03):2. 6. Lang JE, Mannava S, Floyd AJ, Goddard MS, Smith BP, Mofidi A, et al. Robotic systems in orthopaedic surgery. J Bone Joint Surg Br. 2011;93(10):1296–9. 7. Cobb J, Henckel J, Gomes P, Harris S, Jakopec M, Rodriguez F, et al. Hands-on robotic unicompartmental knee replacement: a prospective, randomised controlled study of the acrobot system. J Bone Joint Surg. 2006;88(2):188–97. 8. Swank ML, Alkire M, Conditt M, Lonner JH.  Technology and cost-effectiveness in knee arthroplasty: computer navigation and robotics. Am J Orthop (Belle Mead NJ). 2009;38(2 Suppl):32–6. 9. Blyth MJG, Anthony I, Rowe P, Banger MS, MacLean A, Jones B. Robotic arm-assisted versus conventional unicompartmental knee arthroplasty: exploratory secondary analysis of a randomised controlled trial. Bone Joint Res. 2017;6(11):631–9. 10. Kim SM, Park YS, Ha CW, Lim SJ, Moon YW. Robot-assisted implantation improves the precision of component position in minimally invasive TKA. Orthopedics. 2012;35(9):e1334–9. 11. Song EK, Seon JK, Yim JH, Netravali NA, Bargar WL. Robotic-assisted TKA reduces postoperative alignment outliers and improves gap balance compared to conventional TKA. Clin Orthop Relat Res. 2013;471(1):118–26. 12. Park SE, Lee CT. Comparison of robotic-assisted and conventional manual implantation of a primary total knee arthroplasty. J Arthroplast. 2007;22(7):1054–9. 13. Davenport D, Kavarthapu V.  Computer navigation of the acetabular component in total hip arthroplasty: a narrative review. EFORT Open Rev. 2016;1(7):279–85. 14. Domb BG, El Bitar YF, Sadik AY, Stake CE, Botser IB. Comparison of robotic-assisted and conventional acetabular cup placement in THA: a matched-pair controlled study. Clin Orthop Relat Res. 2014;472(1):329–36.

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15. Domb BG, Redmond JM, Louis SS, Alden KJ, Daley RJ, LaReau JM, et  al. Accuracy of component positioning in 1980 total hip arthroplasties: a comparative analysis by surgical technique and mode of guidance. J Arthroplast. 2015;30(12):2208–18. 16. Nishihara S, Sugano N, Nishii T, Miki H, Nakamura N, Yoshikawa H. Comparison between hand rasping and robotic milling for stem implantation in cementless total hip arthroplasty. J Arthroplast. 2006;21(7):957–66. 17. Schulz AP, Seide K, Queitsch C, von Haugwitz A, Meiners J, Kienast B, et al. Results of total hip replacement using the Robodoc surgical assistant system: clinical outcome and evaluation of complications for 97 procedures. Int J Med Robot. 2007;3(4):301–6. 18. Isik C, Apaydin N, Acar HI, Cay N, Firat A, Bozkurt M. Robotic hip arthroscopy: a cadaveric feasibility study. Acta Orthop Traumatol Turc. 2014;48(2):207–11. 19. Shaw KA, Murphy JS, Devito DP. Accuracy of robot-assisted pedicle screw insertion in adolescent idiopathic scoliosis: is triggered electromyographic pedicle screw stimulation necessary? J Spine Surg. 2018;4(2):187–94. 20. Macke JJ, Woo R, Varich L. Accuracy of robot-assisted pedicle screw placement for adolescent idiopathic scoliosis in the pediatric population. J Robot Surg. 2016;10(2):145–50. 21. van Dijk JD, van den Ende RP, Stramigioli S, Kochling M, Hoss N. Clinical pedicle screw accuracy and deviation from planning in robot-guided spine surgery: robot-guided pedicle screw accuracy. Spine. 2015;40(17):E986–91. 22. Bozkurt M, Apaydin N, Isik C, Bilgetekin YG, Acar HI, Elhan A. Robotic arthroscopic surgery: a new challenge in arthroscopic surgery Part-I: robotic shoulder arthroscopy; a cadaveric feasibility study. Int J Med Robot. 2011;7(4):496–500. 23. Facca S, Hendriks S, Mantovani G, Selber JC, Liverneaux P.  Robot-assisted surgery of the shoulder girdle and brachial plexus. Semin Plast Surg. 2014;28(1):39–44.

The Interlocking Nailing System and Technique

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Damien F. Gill, Fouzia Khatun, and Wasim S. Khan

Introduction The history of the intramedullary nail dates back to sixteenth-century Mexico where Aztec physicians placed intramedullary wooden sticks into long bone fractures and nonunions [1]. It wasn’t until the late 1800s that Gluck, of Germany, first documented the description of an interlocked intramedullary device consisting of a perforated hollow ivory tube, through which ivory interlocking pins could be inserted [2]. Around the same time, Nicolaysen of Norway described the biomechanical principles of intramedullary devices in the treatment of proximal femur fractures, emphasizing that the length of the implant should be maximized so as to confer an optimal mechanical advantage [3]. During the First World War, Hey Groves of England began inserting metallic rods via the wounds of open fractures of the injured [4]. However, it wasn’t until 1931, when Smith-Petersen successfully treated femoral neck fractures with stainless steel nails, that the use of metallic intramedullary devices began to gain momentum [5]. In 1940 Gerhard Küntscher developed the V-shaped stainless steel nail that was inserted in an antegrade fashion and proposed that the nail would act as an internal splint that created an elastic union with the inner medullary cavity without disturbing the fracture biology [6]. By 1947 Küntscher had adapted the shape of his nail to a cloverleaf and nailing started to gain traction in the United Kingdom and the United States [7], where the Hansen-Street nail was introduced in 1947. This early anterograde system comprised of a solid diamond-shaped nail, designed to resist fracture rotation by achieving a compressive fit within the cancellous bone [8]. D. F. Gill (*) · F. Khatun · W. S. Khan Addenbrooke’s Hospital, Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK ORCA (Orthopaedic Research Collaborative East Anglia), Cambridge, UK © Springer Nature Switzerland AG 2019 K. M. Iyer, W. S. Khan (eds.), General Principles of Orthopedics and Trauma, https://doi.org/10.1007/978-3-030-15089-1_31

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During the 1950s two important breakthroughs occurred. The first was Küntscher’s introduction of flexible intramedullary reamers, on the background of Fischer’s early work, which would enable a larger diameter nail and therefore a greater contact area for a more stable fixation [9]. The second was in 1953 where Modny and Bambara introduced the cruciate-shaped transfixion intramedullary nail with interlocking screws in both coronal and sagittal planes to increase stability of the construct [10, 11]. Advances in plating technology in the 1960s unfortunately stalled the development of intramedullary systems. Despite this lull in creativity the first incarnation of the cephalomedullary nail was introduced in the form of the Zickel nail in 1967. This nail contained a hole in the proximal portion so that a separate nail could be placed through the lateral cortex of the proximal femur into the neck, a precursor to the modern recon screw. Furthermore, a setscrew could be inserted through the proximal portion of the shaft nail to prevent the screw from backing out, creating the first fixed-angle construct [12]. A revival in the 1970s and 1980s saw reaming gain traction and the use of unreamed nails in open fractures. The AO and Grosse-Kempf slotted cloverleaf-­ shaped interlocked nail designs were prominent during this period and had a growing evidence base to support it [13–15]. These rudimentary nailing systems slowly morphed in design, materials, and application of basic science principles to evolve into the current elegant systems we use today. Further advances and application of existing systems, particularly in the management of open femoral and open tibial fractures, continued through the 1990s and to the present day. Designs changed to titanium alloy hollow nails to increase torsional rigidity and the use of Poller screws allowed control of very proximal and very distal tibial metaphyseal fractures [16]. Moreover, surgeons were now encouraging patients to weight bear, which was testament to the strength of their constructs and also to promote micromotion for fracture healing [17].

Biomechanics of Intramedullary Nailing The initial slotted and cloverleaf designs were more flexible and allowed passages down an unreamed intramedullary canal [7]. However, they lacked torsional strength and had higher fatiguability when compared to the cylindrical nails used today. The advent of flexible reamers allowed insertion of larger diameter nails, with more contact area creating three-point fixation [9]. The use of interlocking screws or bolts also provided axial and rotational stability by controlling axial and rotational forces [18–20]. These screw holes do, however, also represent the weakest part of the nail and give rise to potential stress risers and subsequent fractures in the bone, especially if screws are not placed in them [21]. Intramedullary nailing creates a relative stability construct with a mechanical advantage as it utilizes the mechanical axis of the bone. The limb may also be loaded in a controlled fashion allowing micromotion at the fracture site promoting callus formation. The amount of healing depends on three main factors: fracture pattern, diameter of the nail, and working length of the nail [22].

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Fracture Pattern In simple oblique and transverse fracture patterns, the act of passing the nail from proximal to distal fragment aids apposition at the fracture site, correcting length and alignment with rotation being clinically corrected by the surgeon. Applying locking screws in dynamic positions can further encourage interdigitation, compression, and bony union through controlled weight bearing. This is known as load sharing and increases the longevity of the nail in the race between fracture union and inevitable device failure. In multi-fragmentary fracture patterns which are axially less stable, the device is used in a static mode, resulting in the majority of weight transference through the nail, known as load bearing [23].

Nail Diameter Weight for weight, the modern cylindrical shape of nails makes them stronger than their plate counterparts. The ability of a plate to resist a bending force, or stiffness, is governed by the area moment of inertia whereas the stiffness of a nail in torsion (rotational force) and bending is governed by the polar moment of inertia. The area moment of inertia is the ability of a plate (or beam) to resist bending. In simple terms, the thicker the plate, the better it is at resisting bending forces and this is proportional to the third power of its thickness, or mm3. Therefore, increasing the thickness of a plate by just 2 mm increases its stiffness by 23 or 8 times. The polar moment of inertia describes the ability of a cylinder (or nail) to resist a rotational force or bending along its length. The resistance to torsion of a nail is proportional to the fourth power of its radius, or r4. A simple example to illustrate this would be to increase the diameter of solid nail (or even a Kirschner wire) from 1 mm to 2 mm, which would increase its torsional rigidity and stiffness by 24 or 16 times. Similarly choosing an 11 mm nail over a 10 mm nail will increase stiffness by 3–4 times. Therefore, small increases in diameter cause larger increases in stiffness. For any given diameter a solid nail is stronger at resisting bending and rotational forces than a hollow nail. However, you must also appreciate that for any given diameter there is more material in a solid nail than a hollow one. This means that the greater the wall thickness of hollow nail, the stronger it is. This is because for any given mass when more material is distributed away from the center (i.e., the axis of rotation), the greater will be its rigidity and ability to resist bending and rotational forces. Simply put, if a hollow and solid nail is made from the same amount of material, the hollow nail will be stronger as it has a greater diameter (Fig. 31.1). Careful sequential reaming of the intramedullary canal allows the insertion of a larger and therefore much stronger nail (r4). Moreover, the larger the nail, the larger the locking bolts that can be inserted, which again strengthens the overall construct [22, 23]. A larger diameter nail has greater control over fracture reduction, compared to a smaller diameter nail that does not produce an isthmic fit and therefore does not

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Fig. 31.1  Line diagram to demonstrate in the same amount of material the hollow nail diameter is larger

create the three-point bridging construct of relative stability. This is particularly important in the proximal third and distal third metaphyseal fractures where the medullary canal is wider and there is no cortex for the nail to “grip.” Smaller diameter nails on their own (i.e., without Poller or blocking screws) in this region lead to toggling, loss of fracture reduction leading to suboptimal fixation, potential malunion, visible deformity, and reduced functional outcome [24]. Reaming of the intramedullary canal compromises the endosteal blood supply, which would logically seem to adversely affect fracture healing [25]. Paradoxically, this stimulates proliferation in the periosteal blood supply, resulting in a shift in the equilibrium of blood flow from centrifugal to centripetal [26].

Working Length The working length of a nail is defined as the distance between the closest proximal and distal statically locked bolts without an isthmic fit (Fig.  31.2). Conversely by increasing the working length the strain also increases at the fracture site and similarly by decreasing the working length the strain at the fracture site decreases [27, 28]. Locking screw holes may either be static or dynamic. The static option is used where the fracture pattern is axially unstable, such as spiral, multi-fragmentary, and segmental fractures. This option ensures that the length, alignment, and rotation are maintained. Controlled weight bearing may be restricted for a period of time in these cases, until radiographic progression to union is demonstrated on follow-up radiographs. The dynamic option is usually an ovalshaped hole and the screw must be inserted furthest away from the fracture, whether in the proximal or distal section of the nail. This option lends itself to axially stable patterns, such as transverse and short oblique fractures, and allows controlled axial shortening of the interdigitated fracture ends without rotational shear forces. This way the fracture site undergoes compression, which is favorable for fracture healing. Some nailing systems have developed a fracture compression function that can be applied to transverse diaphyseal fractures. The nail is locked through the

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Fig. 31.2  Line diagram to illustrate working length, i.e., the distance between the two closest screws either side of the fracture

dynamic hole after which a grub screw or screw driver is inserted which forces the fracture ends to compress by bending the screw to a controlled distance, usually 7–8 mm [29]. As the actual fracture site is compressed using this method, subsequent follow-up X-rays will show less callous formation due to a proportion of primary bone healing. Some surgeons prefer to distal lock the nail and “backslap” the device in order to reduce or appose the fracture ends, which does not produce fracture-site compression.

Indications for Intramedullary Nailing The indications of the intramedullary nail (IMN) are numerous and widely applicable: 1. Particularly where satisfactory alignment of a long bone is not achievable using closed reduction and plastering techniques. 2. High-energy injuries where the soft tissues are not amenable to incisions associated with plating techniques. 3. Where fracture biology is better left undisturbed such as in comminuted and segmental fractures.

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4. In cases of ipsilateral limb injury, such as the floating knee where a single incision at the knee could serve as entry points for antegrade tibial intramedullary and retrograde femoral intramedullary nails. 5. In the polytraumatized patient, where the principles of early appropriate care (EAC) versus damage control orthopedics (DCO) are being applied [30]: A DCO IMN can be inserted relatively quickly as a temporizing measure, as an alternative to external fixation, stabilizing the fracture to allow for more emergent lifesaving surgery to take place in addition to cardiovascular and physiological resuscitation on the intensive care unit before definitive skeletal stabilization can be planned. 6. Bilateral lower extremity fractures, where speed of surgery is crucial in order to avoid a second physiological hit [31]. 7. In the morbidly obese, where infection risk is significantly higher and percutaneous techniques will benefit the patient. 8. Distal femoral periprosthetic fractures around a total knee replacement (TKR), where an IMN can be inserted through the intercondylar notch—prosthesis permitting [32].

Contraindications for Intramedullary Nailing The contradictions for IMNs are fewer, however no less important: 1. Significant preexisting tibial shaft deformity secondary to malunion that may preclude insertion of an IMN. 2. Distal femoral periprosthetic fractures around a TKR, where the IMN cannot pass through the intercondylar notch, e.g., Genesis II posterior stabilizing design. 3. Tibial plateau fracture (relative contraindication) (Fig. 31.3).

General Principles of IM Nailing The indications for IM nailing extend to many long bones and there are many different ways to undertake them. We will discuss the elements that influence the ability to perform a satisfactory nailing case in femoral and tibial fractures, the two long bones in the body most commonly treated with IM nailing. We would like to emphasize that IM nailing often requires two surgeons, the most senior of whom usually reduces and holds the fracture while the more junior surgeon assembles and inserts the implant.

Positioning Positioning of the patient can play a key factor in achieving adequate reduction and allowing for ease of nailing.

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Fig. 31.3  Advanced nailing. X-rays demonstrate a complex fracture configuration: Tibial plateau fracture with segmental tibial fracture. Tibial plateau fracture fixation was performed followed by intramedullary nailing

Femoral Fractures The greatest deformities in femoral shaft fractures are that of translation and shortening. The most effective way to reduce these fractures is with ligamentotaxis, and midshaft femoral fractures are, therefore, well treated in traction on a fracture table. The contralateral leg is held flexed, abducted, and rotated externally in a hemi-­lithotomy position, to allow access for the image intensifier (II) (Fig. 31.4). Access to the entry point at the greater trochanter is optimized by “banana-ing” the patient around the perineal post, with the injured leg slightly adducted and the

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Fig. 31.4  Line diagram showing the positioning of the patient on traction

10-15˚

Fig. 31.5  Line diagram showing the patient positioned with shoulders across the table

torso moved further across the table towards the contralateral side. This is a particularly pertinent step with higher body mass index (BMI) patients (Fig. 31.5). Subtrochanteric fractures can prove to be exceptionally difficult to reduce with traction; traction may indeed exacerbate the flexion deformity of the proximal fragment caused by the pull of the iliopsoas tendon. These fractures are more easily

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reduced in a lateral position, with the hip slightly flexed. The lateral position also helps with access to the greater trochanter. When deciding on the position to use when embarking on an IM nail, thought must be given to both the fracture characteristics and that of the patient. While lateral positions may aid fracture reduction and access in subtrochanteric femoral fractures, a polytraumatized patient may not be an ideal candidate for such positioning. Retrograde nailing of femoral fractures is performed in the supine position, with a padded bolster under the knee, flexing the joint to 30–40 degrees, to reduce the deforming force of the gastrocnemius muscle on the distal fragment. This supine position lends itself to use in polytraumatized patients with multiple injuries.

Tibial Fractures Traditionally, tibial nails have been inserted using an infrapatellar approach and this remains the most commonly used approach. In order to allow access to the entry point, the knee joint must be flexed/hyperflexed over the end of the table or over a draped, padded triangular bolster (Fig.  31.6). The padding is important to avoid traction injuries of the popliteal vessels. The knee is kept in a flexed position throughout the procedure, and the fracture is often reduced manually. The insertion jig for the nail prevents extension of the knee joint while still in situ and can make intraoperative imaging difficult. A newer position for the insertion of an infrapatellar tibial nail is the figure-four (Fig. 31.7). This allows for the tibia to remain flat on the radiolucent operating table throughout surgery, making intraoperative images easier to obtain. The prerequisite to being able to perform an IM nail in this position is the preservation of external rotation of the ipsilateral hip. In a patient with significant stiffness and reduced external rotation, the figure-four position cannot be used. The patient is positioned supine on a radiolucent table with external rotation of the ipsilateral hip and flexion of the knee. A sandbag under the contralateral buttock Fig. 31.6  Line diagram showing a triangular padded bolster and hyperflexed knee

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Fig. 31.7  Line diagram showing the figure-four position (reproduced from Granville-Chapman et al. 2014) [33]

will help increase hip external rotation relative to the table, and allow the tibia to lie flat. The II remains in an AP position over the table throughout the procedure, allowing for lateral images of the tibia. For AP images, the assistant rotates the leg internally, while maintaining hip and knee flexion. This position allows for easier manual control of the fracture and application of reduction maneuvers. More recently, the suprapatellar nail has been gaining traction. This has been most evident in proximal and distal tibial fractures, where there is an emphasis in reducing the deforming forces of the quadriceps bulk, which cause an apex anterior malalignment. These patients are positioned supine on a radiolucent table with a padded bolster under the knee, which is flexed to 15–20° (Fig. 31.8). This position avoids the need to move the leg and can be useful in polytraumatized patients.

Approach IM nailing is often utilized due to the minimal soft-tissue dissection required for insertion, and much of the approach for any nail is minimally invasive.

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Fig. 31.8 Line diagram showing the semi-extended position (reproduced from Synthes Suprapatellar Instrumentation for Expert Tibial Nail) [34]

In femoral antegrade nailing, the incision for insertion of the nail is made proximal to the greater trochanter, and long enough to allow passage of the nail on its jig. Stab incisions are utilized for proximal and distal locking. In retrograde femoral nailing, a 2 cm vertical incision is made from the inferior pole of the patella. We advocate a transtendinous approach, although parapatellar approaches have been described. This incision is also used for tibial nailing, although extending the incision by 5 mm onto the patellar avoids the risks of skin maceration with the passage of multiple sequential reamers. Again, both transtendinous and paratendinous approaches have been described for tibial nailing. Proponents for paratendinous approaches suggest that there is less tendinopathy and, therefore, less anterior knee pain with a tendon-sparing approach. However, this has not been borne out in any studies [35]. We advocate a transtendinous approach with direct access to the entry point and less risk of deflection from soft tissues.

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Entry Point Using correct entry points when performing IM nails is crucial in determining fracture reduction and preventing iatrogenic malalignment. Poor choice of entry point can increase deformity, malunion, and disability. There are both piriformis and trochanteric entry point nails available for antegrade femoral nailing, the latter of which is most often used in the current climate. When using a trochanteric entry point nail, the insertion point is along the medial face of the tip of greater trochanter (GT). If the entry point is lateral to this, i.e., on the tip of the GT, the curve of the nail will tip the fracture into varus, which increases the stresses over the construct, making it more likely to fail. The medial face of the GT is made of hard, cortical bone and care should be taken to ream this completely; it otherwise will act to deflect instruments and the nail laterally. In the sagittal plane, the entry point lies at the anterior third-posterior two-thirds junction. If the entry point is made more posteriorly, the tip of the nail will end up abutting the anterior cortex of the femur, or possibly perforating the anterior cortex in patients with soft bone (Fig. 31.9).

4˚ Anaiomical axis Guide pin insertion path

Fig. 31.9  Line diagram showing the optimal greater trochanteric entry point

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Blumensaat’s line

Fig. 31.10  Line diagram showing the optimal retrograde entry point

The optimal entry point for retrograde femoral nailing is just medial to the peak of the intercondylar notch on coronal imaging. This point is continuous with the femoral intramedullary canal more proximally. On sagittal imaging, the entry point is just anterior to Blumensaat’s line (Fig. 31.10). The entry point for tibial nailing has been the subject of many cadaveric studies. The Tornetta group [36] described a safe zone with a diameter of 22.9 mm, which allows for safe nail insertion without causing damage to adjacent articular structures. This entry point was initially described as just lateral to the center of the tibial tubercle and at the anterior edge of the anterior articular surface. Subsequent cadaveric assessment by the same group has suggested a slightly more lateral entry point, along the medial aspect of the lateral tibial spine (Fig. 31.11).

Reduction Where able, reduction of the fracture prior to insertion of an IM nail makes the procedure much easier; nailing a reconstructed single hollow tube is easier than nailing several sections of a tube. Furthermore, postoperative gapping has been demonstrated to be a risk factor for nonunion [37, 38], furthering the argument for adequate reduction. Some fractures are amenable to closed manual reduction, and may require the senior surgeon to apply reduction maneuvers while the nail is passed. However, manual maneuvers may not be adequate in achieving reduction, particularly with rotational deformity, and the next step may be to introduce percutaneous instrumentation to help aid reduction. The insertion of Schanz pins in both proximal and distal fragments can help reduce rotational deformity as well as allow correction of angulation.

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Fig. 31.11  Line diagram showing the safe zone for tibial nail entry point

The importance of good reduction cannot be underestimated. When closed and percutaneous reduction techniques fail, poor reduction cannot be accepted. This has led to the use of mini-open reductions and fixation with small plates fixed with unicortical screws, prior to performing an IMN. These incisions and plates are smaller than those that would have been used for definitive open reduction internal fixation (ORIF) and consequently reduce soft-tissue injury. The nail is still required in these circumstances as the small plate construct is not stable enough to withstand the forces of a moving limb all the way to healing. More and more, reduction is being guided with the use of Poller screws [24]. These are inserted percutaneously, thereby preserving the principles of minimal soft-tissue disruption. Metaphyseal fractures, or those patients with a wide canal, lack the natural guide of a narrow diaphysis. Poller screws have been used to create an additional “cortex” to guide the passage of IM nails. They also act to provide an interference fit for the nail in the place of the cortical border, and enable three-point fixation to counter deforming forces. Hannah et  al. have previously described a technique of placing Poller screws in the acute angles of fragments when two lines are drawn, a line along the long axis of the bone bisected by a second drawn along the main fracture line (Fig. 31.12) [39].

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Proximal tibia

Desired direction of reduction

Poller screw

Direction of fracture displacement

Fig. 31.12  Line diagram showing the acute angles for Poller screw placement

Reaming There have been many debates regarding the effect of reaming on fracture healing. While reaming is known to disrupt endosteal blood supply, this has not been shown to have any clinical significance. In fact, The Study to Prospectively Evaluate Reamed Intramedullary Nails in Patients with Tibial Fractures (SPRINT) trial was a randomized control trial of 1319 patients, and found reaming to be beneficial, with lower rates of bone grafting, implant exchange, and debridement for infection [40]. This echoed the findings of an earlier study, which found an earlier time to union with reamed tibial nails [41].

Rotation We would like to take a moment to reiterate that fracture reduction is crucial to a good outcome. The nail itself, along with adjuncts such as Poller screws, helps to correct shortening and translation and angulation in coronal and sagittal planes. However, rotation must be assessed intraoperatively and corrected by the surgeon prior to distal locking.

Distal Locking Distal locking of short femoral nails is performed using a jig. All other nails require freehand distal locking. Good communication with the radiographer is an integral part of being able to perform freehand distal locking. The C-arm beam must be focused to be directly colinear with the holes in the nail for distal locking, creating “perfect circles.” This demarcates the trajectory of the locking screws through the nail, and guides the angle at which to drill and insert the locking

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Fig. 31.13  Line diagram showing the perfect circles for distal locking

screw(s). Before drilling, image intensifier must be used to ensure that the end of the drill bit is in the center of the circle. The drill is then advanced, colinear with the C-arm (Fig. 31.13). Distal locking is undeniably a skill that requires practice and experience to perform efficiently and well. There are a number of targeting devices available commercially, designed to aid with distal locking. These targeting arms use electromagnetic probes in the nail and the targeting device to locate the distal locking holes in the nail without image intensifier. However, they have yet to be proven to reduce operative time or costs, and still require the surgeon to be aware of the “perfect circles” should the software malfunction or if there is interference from metal either in the operating theatre or within the patient with a previous implant.

Tourniquet The use of tourniquet during IM nailing continues to provoke debate. Giannoudis et al. [42] found that use of a tourniquet was not associated with diaphyseal necrosis. However, it has been shown that using a tourniquet for fracture fixation during

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the same sitting as a reamed femoral nail did increase the rates of pulmonary morbidity [43]. We would, therefore, advocate a cautious and considered approach to tourniquet use in patients undergoing nailing, particularly in the context of a polytraumatized patient.

IM Nailing in Metaphyseal Tibial Fractures The aim of surgical fixation of fractures is to restore alignment, length, and rotation. With a narrow isthmus, tibial diaphyseal fractures guide the intramedullary (IM) nail along the only available path, thus indirectly guiding the reduction of the fracture. In fractures of the wide metaphysis, there is a lack of a single channel to guide the path of the nail, thus creating room for error. These proximal and distal tibial fractures, therefore, provide much more of a challenge to the operating surgeon and require a greater amount of planning and experience to treat with a nail. Fractures closer to joints are also under the influence of muscle forces that act to move the adjacent joint. These physiological forces can become deforming forces in the presence of a fracture, and must be identified and countered to ensure adequate reduction of the fracture. These factors help explain why there is a higher rate of malunion in metaphyseal fractures treated with intramedullary nailing as compared to plating [44, 45]. This may lead to questions as to why we would choose to use IM fixation in these fractures. Certainly, Lindvall et al. [46] found that there were no differences in union rates between IM nailing and plating. However, tibial fractures are often associated with high-energy injuries. The paucity of soft-tissue coverage, particularly over the anteromedial aspect of the leg, lends these fractures well to fixation that avoids further soft-tissue injury and stripping. Proximal third tibial fractures can malunite unless the specific challenges posed by these fractures are recognized and addressed. We will describe some of these below. As discussed previously, the entry point of IM nails is crucial to ensuring fracture reduction. This is particularly important in extra-articular fractures of the proximal tibia. In proximal tibial fractures, where there is a propensity for valgus malalignment, utilizing the slightly more lateral entry point described earlier will help reduce the risks of malunion. We must also be mindful of the risk of losing position once the initial entry point has been correctly made. With tibial nailing, the soft tissues at the entry point can deflect the subsequent flexible reamers into a more medial and inferior position on the tibia, causing loss of position and consequent malalignment. It is imperative that the entry point is maintained and reaming must not be undertaken until the reamer is fully seated on the bone and is reamed exactly in line with the trajectory of the guide wire.

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Proximal third fractures are under the deforming influence of both the quadriceps bulk (via the patella tendon), causing an apex anterior deformity, and the insertion of the pes anserinus along the anteromedial aspect of the proximal tibia, causing further deformity with valgus malalignment. Traditionally, tibial nails were inserted through an infrapatellar approach, in a hyperflexed knee. However, this places the quadriceps muscle bulk at maximal stretch, thus aggravating the apex-anterior deformity that can occur. These fractures may, therefore, be better suited to being treated in a semi-extended position. Indeed, Tornetta and Collins [47] found that a semi-extended position with the knee in 15° of flexion led to either no apex anterior angulation or no more than 5° of it. They originally utilized an infrapatellar approach, but the evolution of nailing systems has led to the use of suprapatellar nails, which allows ease of access while exploiting the benefits of a semi-extended approach. While the semi-extended approach has proven to reduce the risk of apex anterior malalignment, it does not tackle the issue of coronal plane malalignment (valgus being most commonly seen with proximal third and distal third fractures). In order to counter the deforming force of the pes anserinus tendons, proximal tibial fractures are likely to require the use of further reduction maneuvers. There have been many different techniques described, including the use of percutaneous clamps and open reduction and fixation with unicortical plates. The disadvantage of plate reduction is that it can undermine the reasons for using a nail, namely that of minimizing soft-tissue stripping. More and more, Poller screws are being used to reduce fractures and guide correct positioning of nails. Poller screws placed in the proximal fragment should lie posteriorly in the sagittal plane and laterally in the coronal plane. Ricci et al. [16] found that blocking screws helped obtain and maintain reduction until union (Fig. 31.14). Similar issues arise with distal tibial fractures, and these can be countered with many of the same techniques used for proximal tibial fractures. The semi-extended position allows for easier reduction and control of the distal fragment, while the use of an AP Poller screw at the level of the tip of the nail, aligned with the middle of

Fig. 31.14  Line diagram showing the correct position of Poller screws to counter deformity

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the tibial plafond, helps to position the nail correctly to just lateral to the middle of the plafond, and avoid valgus malunion. Valgus malalignment has also been shown to be significantly reduced by the use of a semi-extended approach [48]. Moreover, distal tibial fractures have a tendency to propagate further distally, creating a posterior malleolus fracture, and the AP Poller screw could also be used to reduce this fragment prior to insertion of nail, reducing the risk of further propagation or displacement.

Final Word Interlocking nails have revolutionized the treatment of long-bone fractures, beyond the femoral and tibial fractures we have discussed here. They are commonly used in the treatment of humeral fractures, and fibular nails are being employed more frequently in patients with poor soft-tissue envelopes surrounding ankle fractures. Sadly, these additional indications fall outside of the scope of our discussion. Used appropriately, with detail to reduction, the interlocking nail will stand orthopedic surgeons in good stead for many years to come.

References 1. Farill J. Orthopedics in Mexico. J Bone Joint Surg Am. 1952;24:506–12. 2. Gluck T. Autoplastic transplantation. Implantation von Frem-dkörpern. Berl Klin Wochenschr. 1890;19 3. Nicolaysen J.  Lidt on Diagnosen og Behandlungen av. Fr. colli femoris. Nord Med Ark. 1897;8:1. 4. Hey Groves EW. On the application of the principle of extension to comminuted fractures of the long bone, with special reference to gunshot injuries. Br J Surg. 1914;2(7):429–43. 5. Smith-Petersen MN. Intracapsular fractures of the neck of the femur. Treatment by internal fixation. Arch Surg. 1931;23:715–59. 6. Küntscher G.  Die Marknalung von Knochenbruchen. Lan-genbecks. Arch Klin Chir. 1940;200:443–55. 7. Rehnberg SV.  Treatment of fractures and pseudarthroses with marrow nailing. Ann Chir Gynaec Fenn. 1947;36(2) 8. Street DM, Hansen HC, Brewer BJ. The medullary nail. Presentation of a new type and report of 4 cases. Arch Surg. 1947;35:423. 9. Fischer AW, Maatz R. Weitere Erfahrungen mit der Marknage-lung nach Küntscher. Arch Klin Chir. 1942;203:531. 10. Modny MT, Bambara J. The perforated cruciate intramedullary nail: Preliminary report of its use in geriatric patients. J Am Geriatr Soc. 1953;1:579–88. 11. Modny MT, Lewert AH. Transfixion intramedullary nail. Orthop Rev. 1986;15:83–8. 12. Zickel RE.  A new fixation device for subtrochanteric fractures of the femur: a preliminary report. Clin Orthop Relat Res. 1967;54:115–23. 13. Brumback RJ, Reilly JP, Poka A, et al. Intramedullary nailing of femoral shaft fractures. Part I: decision-making errors with interlocking fixation. J Bone Joint Surg Am. 1988;70:1441–52. 14. Brumback RJ, Uwagie-Ero S, Lakatos RP, et  al. Intramedullary nailing of femoral shaft fractures. Part II: fracture-healing with static interlocking fixation. J Bone Joint Surg Am. 1988;70:1453–62.

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15. Brumback RJ, Ellison TS, Poka A, et al. Intramedullary nailing of femoral shaft fractures. Part III: long-term effects of static interlocking fixation. J Bone Joint Surg Am. 1992;74:106–12. 16. Ricci WM, O’Boyle M, Borrelli J, Bellabarba C, Sanders R. Fractures of the proximal third of the tibial shaft treated with intramedullary nails and blocking screws. J Orthop Trauma. 2001;15(4):264–70. 17. Brumback RJ, Toal TR, Murphy-Zane MS, et al. Immediate weight-bearing after treatment of a comminuted fracture of the femoral shaft with a statically locked intramedullary nail. J Bone Joint Surg Am. 1999;81:1538–44. 18. Russell TA, Taylor JC, LaVelle DG, Beals NB, Brumfield DL, Durham AG.  Mechanical characterization of femoral interlocking intramedullary nailing systems. J Orthop Trauma. 1991;5(3):332–40. 19. Beals N, Durham G, Lynch G.  Mechanical characterization of interlocking intramedullary nails. Memphis, Tennessee: Richards Research Report, Smith and Nephew Richards Inc.; 1988. 20. Miles AW, Eveleigh RJ, Wight BJ, Goodwin MI.  An investigation into the load transfer in interlocking intramedullary nails during simulated healing of a femoral fracture. Z Mech E Engineering in Medicine. 1994;208(1):19–26. 21. Erduran M, Karakasli A, Ertem F, Taylan O, Yildiz DV, Celik S, Havitcioglu H. Biomechanical effects of the distance from the fracture zone to the interlocking fixation screw of intramedullary nail. J Biochem. 2001;44:4. https://doi.org/10.1016/j.jbiomech.2011.02.027. 22. Aresti N, Culpan P, Bates P. Biomechanics of fracture fixation. In: Ramachandran M, editor. Basic orthopaedic sciences. 2nd ed. Florida: CRC Press; 2017. p. 451–75. 23. Hak DJ, Mauffrey C.  Trauma. In: Miller MD, Thompson SR, editors. Miller’s review of orthopaedics. 7th ed. Philadelphia: Elsevier; 2016. p. 767–855. 24. Krettek C, Miclau T, Schandelmaier P, Stephan C, Mohlmann U, Tscherne H. The mechanical effect of blocking screws (“Poller screws”) in stabilizing tibia fractures with short proximal or distal fragments after insertion of small-diameter intramedullary nails. J Orthop Trauma. 1999;13:550–3. 25. Haas N, Krettek C, Schandelrnaier P, Frigg R, Tschernc H. A new solid unreamed tibia1 nail for shaft fractures with severe soft tissue injury. Injury. 1993;24(1):49–54. 26. Reichert IL, McCarthy ID, Hughes SP.  The acute vascular response to intramedullary reaming. Microsphere estimation of blood flow in the intact ovine tibia. J Bone Joint Surg Br. 1995;77(3):490–3. 27. Elliott DS, Newman KJ, Forward DP, Hahn DM, Ollivere B, Kojima K, Handley R, Rossiter ND, Wixted JJ, Smith RM, Moran CG. A unified theory of bone healing and nonunion: BHN theory. Bone Joint J. 2016;98-B(7):884–91. 28. Perren SM. Evolution of the internal fixation of long bone fractures. The scientific basis of biological internal fixation: choosing a new balance between stability and biology. J Bone Joint Surg. 2002;84-B:1093–110. 29. Synthes expert TN tibial nail surgical technique: http://synthes.vo.llnwd.net/o16/LLNWMB8/ INT%20Mobile/Synthes%20International/Product%20Support%20Material/legacy_Synthes_ PDF/DSEM-TRM-0814-0173-1_LR.pdf. Accessed 2 Dec 2018. 30. Vallier HA, Wang X, Moore TA, Wilber JH, Como JJ.  Timing of orthopaedic surgery in multiple trauma patients: development of a protocol for early appropriate care. J Orthop Trauma. 2013;27(10):543–51. 31. Lasanianos NG, Kanakaris NK, Dimitriou R, Pape HC, Giannoudis PV.  Second hit phenomenon: existing evidence of clinical implications. Injury. 2011;42(7):617–29. 32. Jones MD, Carpenter C, Mitchell SR, Whitehouse M, Mehendale S.  Retrograde femoral nailing of periprosthetic fractures around total knee replacements. Injury. 2016;47(2):460–4. https://doi.org/10.1016/j.injury.2015.10.030. 33. Granville-Chapman J, Nawaz SZ, Trompeter A, Newman KJ, Elliott DS. Freehand ‘figure 4’ technique for tibial intramedullary nailing: Introduction of technique and review of 87 cases. Eur J Orthop Surg Traumatol. 2014;24(7):1311–5. https://doi.org/10.1007/ s00590-013-1306-y.

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34. Synthes Instrumentation for Suprapatellar nailing: http://synthes.vo.llnwd.net/o16/ LLNWMB8/INT%20Mobile/Synthes%20International/Product%20Support%20Material/ legacy_Synthes_PDF/DSEM-TRM-0115-0289-3_LR.pdf. Accessed 2 Dec 2018. 35. Toivanen JA, Vaisto O, Kannus P, Latvala K, Honkonen SE, Jarvinen MJ. Anterior knee pain after intramedullary nailing of fractures of the tibial shaft, a prospective, randomised study comparing two different nail-insertion techniques. J Bone Joint Surg Am. 2002;84A(4):580–5. 36. McConnell T, Tornetta P 3rd, Tilzey J, Casey D. Tibial portal placement: the radiographic correlate of the anatomic safe zone. J Orthop Trauma. 2001;15(3):207–9. 37. Bhandari M, Tornetta P 3rd, Sprague S, Najibi S, Petrisor B, Griffith L, Guyatt GH. Predictors of reoperation following operative management of fractures of the tibial shaft. J Orthop Trauma. 2003;17(5):353–61. 38. Audigé L, Griffin D, Bhandari M, Kellam J, Rüedi TP. Path analysis of factors for delayed healing and non-union in 416 operatively treated tibial shaft fractures. Clin Orthop Relat Res. 2005;438:221–32. 39. Hannah A, Aboelmegd T, Yip G, Hull P. A novel technique for accurate Poller (blocking) screw placement. Injury. 2014;45(6):1011–4. https://doi.org/10.1016/j.injury.2014.02.029. 40. Bhandari M, Guyatt G, Tornetta P, Schemitsch EH, Swiontkowski M, Sanders D, Walter SD. Randomized trial of reamed and unreamed intramedullary nailing of tibial shaft fractures— the study to prospectively evaluate reamed intramedullary nails in patients with tibial fractures (SPRINT). J Bone Joint Surg Am. 2008;90(12):2567–78. https://doi.org/10.2106/ JBJS.G.01694. 41. Finkemeier CG, Schmidt AH, Kyle RF, Templeman DC, Varecka TF. A prospective, randomized study of intramedullary nails inserted with and without reaming for the treatment of open and closed fractures of the tibial shaft. J Orthop Trauma. 2000;14(3):187–93. 42. Giannoudis PV, Snowden S, Matthews SJ, Smye SW, Smith RM. Friction burns within the tibia during reaming. Are they affected by the use of tourniquet? J Bone Joint Surg Br. 2002;84(4):492–6. 43. Pollak AN, Battistella F, Pettey J, Olson SA, Chapman MW. Reamed femoral nailing in patients with multiple injuries. Adverse effects of tourniquet use. Clin Orthop Relat Res. 1997;339:41–6. 44. Kwok CS, Crossman PT, Loizou CL. Plate versus nail for distal tibial fractures: a systematic review and meta-analysis. J Orthop Trauma. 2014;28(9):542–8. 45. Vallier HA, Cureton BA, Patterson BM. Randomized, prospective comparison of plate versus intramedullary nail fixation for distal tibia shaft fractures. J Orthop Trauma. 2011;25(12):736–41. 46. Lindvall E, Sanders R, Dipasquale T, Herscovici D, Haidukewych G, Sagi C. Intramedullary nailing versus percutaneous locked plating of extra-articular proximal tibial fractures: comparison of 56 cases. J Orthop Trauma. 2009;23(7):485–92. https://doi.org/10.1097/ BOT.0b013e3181b013d2. 47. Tornetta P 3rd, Collins E. Semiextended position of intramedullary nailing of the proximal tibia. Clin Orthop Relat Res. 1996;328:185–9. 48. Avilucea FR, Triantafillou K, Whiting PS, Perez EA, Mir HR. Suprapatellar intramedullary nail technique lowers rate of malalignment of distal tibia fractures. J Orthop Trauma. 2016;30(10):557–60.

Total Knee Replacement

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Nadim Tarazi, Rui Zhou, and Wasim S. Khan

Introduction Total knee replacement is an operation with very reliable results that reconstructs the knee joint. It is now considered the gold standard treatment for patients with symptomatic osteoarthritis in at least two of the three compartments of the knee who have failed nonoperative treatment [1]. The first attempts at total knee arthroplasty date back to 1861, when Dr. Fergusson first performed a resection arthroplasty for knee arthritis. This was followed by Dr. Cambell in 1863 where foreign tissue such as capsule was placed into the joint. However, the technique failed to provide lasting pain relief. In 1950, Walldius Shiers attempted the first bi-compartmental knee arthroplasty where he replaced both the femur and tibial articular surfaces using a hinge with intramedullary stems. This initial design experienced a high rate of loosening and therefore was further developed to form the GUEAR hinge which shifted the axis of rotation posteriorly. This design still failed due to loosening as it failed to account for the complex motion of the native knee [2]. The early 1970s proved to be a major breakthrough for total knee arthroplasty. Earlier designs were replaced with a prosthesis that replicated the shape of the distal femur, preserved the collateral and cruciate ligaments, and consisted of a plastic bearing on the tibia. These first designs—the condylar knee replacement—laid a foundation for current implants, and many of the current concepts and technologies that were developed in the 1970s are used today. The development of the condylar

N. Tarazi (*) · R. Zhou · W. S. Khan University of Cambridge, Cambridge, UK e-mail: [email protected] © Springer Nature Switzerland AG 2019 K. M. Iyer, W. S. Khan (eds.), General Principles of Orthopedics and Trauma, https://doi.org/10.1007/978-3-030-15089-1_32

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knee replacement is widely credited to work by Freeman and Swanson of the London Hospital and Imperial College along with Insall, Burnstein, and Walker of the Hospital for special surgery in New York. Over the next three decades, there had been numerous improvements in design to focus on replicating the anatomy and normal function of the knee joint. Nowadays, total knee replacement has become a reliably effective procedure that reduces pain and improves function. Its successful clinical outcomes continue to rely on the same basic principles of accurate soft-tissue balancing, well-positioned components, and a neutrally aligned mechanical axis [2].

Indications Total knee replacement is a well-documented and reliable treatment option for patients with symptomatic osteoarthritis that fail conservative measures. In addition, the need for correction of a significant or progressive deformity at the knee with evidence of osteoarthritis can also be an indication for a TKA. A complete history and physical examination are essential in localizing pain and disability in the degenerative knee. First-line therapies for arthritis include nonsteroidal anti-inflammatories (NSAIDs) and intra-articular steroid injections and in select cases knee arthroscopy. Other modalities that are often overlooked include an exercise program and weigh loss, both of which have been shown to be of benefit to patients with symptomatic arthritis [3]. It is also essential to recognize the contraindications of total knee replacement surgery as listed below: Absolute contraindications of total knee replacement include: –– –– –– ––

Active or latent (less than 1 year) knee sepsis Presence of active infection elsewhere in the body Extensor mechanism dysfunction Medically unstable patient Relative contraindications of total knee replacement include [1]:

–– –– –– –– –– –– ––

Neuropathic joint Poor overlying skin condition Morbid obesity Noncompliance due to major psychiatric disorder, and alcohol or drug abuse Insufficient one stock for reconstruction Poor patient motivation or unrealistic expectation Severe peripheral vascular disease

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Basic Principles Native Knee Kinematics (Fig. 32.1) The knee motion is controlled by three factors: (1) the articular geometry; (2) the ligamentous balance, and (3) the muscular tension.

 he Articular Geometry (Figs. 32.2a, 32.2b, 32.2c, 32.2d, 32.2e, 32.2f, T 32.2g, and 32.2h) The medial femoral condyle (MFC) has a different size and radius than the lateral femoral condyle (LFC). The MFC is larger and has a more uniform radius, whereas the LFC is smaller and has two condyles, distal and posterior condyles. During knee flexion, the MFC remains mostly stationary while the LFC travels posteriorly on the tibia. This posterior rollback of the LFC is due to the change in radius of curvature. Posterior rollback drives the distal femur to externally rotate and determines the point of terminal flexion. Without rollback, the back of the femoral diaphysis will impinge on the tibia around 90°.

Fig. 32.1  Line diagram showing the vertical axis/mechanical axis/anatomical axis of femur/ anatomical axis of tibia

664 Fig. 32.2a  Line diagram (sagittal view) showing flexion-extension: Instantaneous center of motion

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32  Total Knee Replacement Fig. 32.2b  Line diagram (sagittal view) showing flexion-extension: Instantaneous center pathway

Fig. 32.2c  Line diagram (coronal view) showing sliding/rocking

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Fig. 32.2d  Line diagram (sagittal view) showing flexion—extension: Sliding/rocking of femur

Fig. 32.2e  Line diagram (coronal view) showing gliding/rolling

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Fig. 32.2f  Line diagram (sagittal view) showing gliding/rolling of femur

Fig. 32.2g  Line diagram (sagittal view) showing flexion-extension: Knee glides and slides

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Fig. 32.2h  Line diagram (sagittal view) showing femoral longitudinal axis

The lateral tibial plateau is flat which encourages the LTC rollback during flexion. In contrast, the medial tibial plateau is concave, allowing for less MFC rollback. This creates a pivot motion for the LFC to rotate around the stable MFC.

Ligament Stabilization (Fig. 32.3) Collateral ligaments control coronal plane stability. The superficial medial collateral ligament (MCL) is the major medial stabilizer. It originates from the medial epicondyle, travels deep to the pes anserine muscles, and inserts on the tibia at 4.5 cm distal to the joint line. The deep portion of the MCL is a thickening of the capsule, also known as the medial capsular ligament. In full extension, the posterior-­medial corner contributes 30% of valgus restraint. As the knee flexes, the MCL assumes more responsibility. The lateral collateral ligament provides lateral stability. It originates proximal and posterior to the lateral epicondyle and inserts on the fibular head. Cruciate ligaments control sagittal plane stability. The anterior cruciate ligament (ACL) prevents anterior subluxation of the tibia, particularly in terminal extension. Cartilage wear occurs in the anterior-medial aspect of the knee when the ACL is intact. In ACL-deficient knee, wear occurs in the posterior-medial aspect of the knee. The posterior cruciate ligament (PCL) prevents posterior subluxation of the tibia. If the PCL is deficient, the femur is unable to achieve posterior rollback and terminal flexion.

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669 2a. Anterior cruciate ligament: prevents anterior subluxation of the tibia

2. Cruciate ligaments: resists all translatory movement; 1. Menisci: resists all motion

3. Medial collateral ligament (MCL): resists excessive rotation

2b. Posterior Cruciate ligament: Prevents posterior subluxation of the tibia

Fig. 32.3  Line diagram showing ligaments

Fig. 32.4  Line diagram showing meniscus (1. joint conformity; 2. varus valgus stability; 3. resists translation)

Meniscus increases contact area to reduce joint forces. Menisci transmit 50% of the contact forces in extension and 90% in flexion by transferring axial load into hoop stress. The medial meniscus is more stationary, similar to the MFC. The posterior horn of the medial meniscus acts as an AP stabilizer, particularly in ACL-­ deficient knee (Fig. 32.4).

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Native Knee Alignment The mechanical axis of the leg is a line drawn from the center of the hip to the center of the ankle. The knee is in neutral alignment if this line crosses the center of the knee. The anatomical axis of the femur is 6° from the mechanical axis, whereas the anatomical axis of the tibia is in line with the mechanical axis therefore 0°. The knee angle, also known as the femoral-tibial angle, is 6° of valgus in relation to the mechanical axis. The joint line is on average about 3° of varus relative to the mechanical axis. This means the tibial articular surface is in 3° of varus and the femoral articular surface is in 3° of valgus. In relation to the anatomical axis, the joint line on the femoral side is in 9° of valgus and on the tibial side it is in 3° of varus.

Total Knee Arthroplasty (TKA) Alignment Correct alignment of the TKA implant is essential to restore function and maximize prosthesis survival. There are three classic philosophies: (1) Anatomic axis alignment, (2) mechanical axis alignment, and (3) kinetic alignment

 natomic Axis Alignment A This technique was originally described by Hungeford and Krackow in the 1980s. The purpose of this technique is to position the femoral and tibial component in order to anatomically recreate the joint line with the overall component alignment at 2–3° varus in relation to the mechanical axis of the lower limb. To restore the anatomy, the femur is cut in 9° valgus with the tibia cut in 3° varus. When this is combined, it gives a total alignment of approximately 6° of valgus that approaches the normal tibiofemoral angle [4]. With such a technique, the joint line will be parallel to the ground during normal gait. The rationale supporting this technique is the promotion of a better load distribution on the tibial component and also better patella biomechanics as it reduced the risk of lateral retinacular ligament stretching when flexing the knee [5]. Generally, the technical challenge to precisely achieve bone cuts and prevent excessive varus angles of the tibial implant positioning has limited its widespread use. Nowadays however, this can be overcome with the of precision tools for implant positioning.  echanical Axis Alignment M Described by Insall et al., the mechanical alignment is the commonest method used in TKA. This is done with the use of an intramedullary guide (Fig. 32.5) based on the anatomical axis. It is the angle of the anatomical axis in relation to the mechanical axis that is used to determine the angle of the femoral cut. This is because the goal is to achieve a femoral cut that will be perpendicular to the mechanical axis of the femur. Therefore, the angle of the joint line (around 3°) can be pretty much

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Fig. 32.5  Line diagram showing restoration of the mechanical axis/TKR

ignored. The tibial resection is done perpendicular to the mechanical axis of the tibia (0°). The purpose of this alignment is to create and even load distribution on the new joint line. Insall believed that mechanical alignment was the superior method. His philosophy was that an anatomically aligned knee, because of the increased forces across the medial joint component, leads to medial tibial plateau fixation failure. Insall pointed out that even though the joint loading forces between compartments are even during the stance phase, it will be uneven during the gait phase due to a “laterally” directed ground reaction force [6].

Kinematic Alignment Despite good alignment, a significant part of the patients up to 15% are still disappointed with their artificial knee. For this reason, several studies have questioned if the classical or mechanical alignment may actually be the right technique in order to create a well-balanced and functioning knee. The development of a kinematic alignment aims to realize a well-balanced artificial joint during the whole arc of motion.

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The concept of kinematic alignment is to restore normal knee function by aligning the distal and posterior femoral joint line of the femoral component according to the functional femoral transverse axes and joint line of the tibial component to those of the normal or pre-arthritic status. Such a kinematic approach is still under evaluation and larger studies are needed to establish which alignment method will promote the best clinical outcome after TKA. It is also important to acknowledge that the concept of restoring the normal or prearthritic status when performing a TKA may be valid for a large number of patients but not all [7].

TKA Designs The goal of all TKA designs is to provide stability, longevity, and normal kinematics. Several designs have been developed to improve the durability and function of this procedure. However, the most widely used designs for primary arthroplasty have been, and continue to be today, cruciate-retaining (CR) and posterior-­stabilized (PS). There still remains to be controversy regarding whether the posterior cruciate ligament (PCL) should be retained or removed during the procedure. Some potential advantages of cruciate-retaining prosthetic designs include preservation of bone, more normal knee kinematics, increased proprioception, femoral rollback on the tibia during flexion, and greater stabilization of the prosthesis, with the PCL preventing anterior translation of the femur on the tibia. Posterior-stabilized implants attempt to replace the role of the PCL with a polyethylene post and femoral cam that interact to prevent anterior translation of the femur on the tibia while allowing femoral rollback during flexion. Potential advantages of these designs include a less technically demanding procedure, a more stable component interface, and increased range of motion [8]. Many studies have been performed to compare the outcome of CR versus PS. Most recently In 2018, Serna-Berna et al. performed large case series of 269 patients and compared the clinical outcomes with a minimum follow-up of 10 years between patients who received contemporary CR and PS primary TKA. Their study demonstrated successful survival for both designs with similar clinical outcomes between CR and PS designs at long-term follow-up. Thus, the superiority of one design over the other was not found. This supports the previous literature published. Therefore, the choice of design mainly depends on the status of the PCL and surgeon’s preference [9].

TKA Surgical Technique Patient Positioning and Surgical Approach The patient is positioned supine on a standard surgical table. A cylindrical footstep is placed to support the knee in flexion during the procedure. Generally, it is best

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placed at the level of the widest part of the calf. A thigh tourniquet should be placed as high as possible. However, some surgeons opt to perform the operation without the use of a tourniquet. Hair around the area of the planned skin incision is shaved before sterile preparation. The limb should be then draped in the hospital’s standard sterile fashion. Using a marking pen, the incision is then drawn with the knee in 90-degree flexion to account for the fact that the skin is translated laterally about 1  cm from extension to flexion because the tibia internally rotates. If the patient desires to kneel after surgery with the incision drawn in extension, he or she will likely experience discomfort as they would kneel on incision atop the tibial tubercle [10]. The skin incision is vertical and about 15  cm. It should be centered over the midshaft of distal femur proximally, then descends into the mid-third portion of the patella centrally, and ends just medial to the tibial tuberosity distally. It is essential to recognize that the vascular supply to the skin around the knee relies on an anastomotic ring within the subcutaneous fascia. Therefore, full-thickness flaps above the fascia must be made to avoid de-vascularizing the skin. There are three main approaches to the knee in the setting of a total knee replacement: 1 . Medial parapatellar approach 2. Sub-vastus approach 3. Mid-vastus approach Medial parapatellar is the gold standard for TKA. It was first described by von Langenbeck in 1878. A standard longitudinal midline skin incision starts 5  cm above the superior pole of the patella to 1 cm below tibial tubercle. The incision should be long enough to avoid excessive traction on skin edges. Dissection is through subcutaneous fat down to retinaculum. The muscle fibers of the vastus medialis obliquus (VMO) should be visualized proximally. The medial parapatellar retinaculum is extended proximally along the length of the quadriceps tendon. The incision is continued around the medial side of the patella to the anteromedial surface of the tibia along the medial border of the patellar tendon. Leave a cuff of tendon approximately 5 mm to facilitate closure. Subperiosteally elevating the anteromedial capsule and deep medial collateral ligament off the tibia exposes the medial aspect of the knee. Extending the knee and everting the patella allow an optional release of lateral patellofemoral plicae. The infrapatellar fat pad is excised or retracted. The patella is dislocated and flipped laterally. The knee is then flexed to 90° to gain exposure to the entire knee joint. Overall, the medial parapatellar approach provides an excellent exposure and can be used in virtually every case regardless of the patient characteristics or severity of the deformity. The main goal for the sub-vastus and mid-vastus approaches is to avoid violating the quads tendon. When using the sub-vastus approach, the dissection is maintained below the VMO, therefore avoiding an incision into the quad tendon. It still,

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however, remains debatable whether there are any significant short- or long-term benefits with this approach. Furthermore, this approach compromises the visualization to the knee joint. Therefore, it is not recommended in obese patients or knees with significant deformity. A recent systematic review by Berstock et  al. that compared the medial sub-­ vastus versus the medial parapatellar approach suggested that the early postoperative advantages following the sub-vastus approach (earlier return of active SLR, reduced pain on day 1, reduced blood loss, and lower frequency of lateral release) need to be balanced with longer operative times (10 min) and lack of evidence of medium- or long-term differences between approaches. The incidence of adverse events between the approaches appears similar [11]. The mid-vastus approach is in between the sub-vastus and medial parapatellar approach where it violates less of the quadriceps tendon yet a better visualization than the sub-vastus approach. This would still remain a challenge in cases with significant deformity.

Femoral Preparation and Cuts After a satisfactory exposure is achieved, the anterior cruciate ligament or any remnant is resected. The tibia is then delivered in front of the femur by hyperflexing the knee, pulling the tibia forward, and externally rotating it. Marginal osteophytes around the femoral condyles are excised. Generally, either the femoral or the tibial cuts could be performed first. When the distal femur is cut, three things are affected: (1) mechanical alignment, (2) extension gap, and (3) joint line height. The exact technique for performing the bone cuts in TKA is dependent on the instruments. The following steps are used as a general guidance. Either the femoral or the tibial bone cuts can be made first.

Proximal Tibial Cut Either intra-intramedullary or extramedullary alignment guide can be used. The proximal tibia cut is perpendicular to the long axis of the tibia in coronal plane. The cut jig has either a neutral or a posterior slope depending on the design. Avoid anterior tilt in the proximal tibia cut. Stylus is used to assess the appropriate depth of the tibial resection. Femoral Cuts An intramedullary guide is commonly used. The cut is approximately 5–7° of the anatomical axis. In significant valgus deformity, some surgeons aim for less of a valgus cut. The goal is to restore the neutral mechanical axis. A drill hole is made in intercondylar notch for the insertion of intercondylar guide rod. It is positioned at the notch just

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above the PCL’s femoral insertion. Widen it with a step drill or by rotating the regular drill. This decompresses the intramedullary canal to minimize fat embolism. Size the femur: The common choice is to downsize the prosthesis when the femur is between sizes to avoid overstuffing the joint. It is vitally important to avoid notching when downsizing. Anterior or posterior referencing is used to make the anterior and posterior femoral condylar bone cuts. Protect the medial collateral ligament and pay extra attention to femoral rotation when positioning the instrument. Aim for a rectangular flexion gap with the femoral component placed parallel to the epicondylar axis. This can be achieved with neutral or 3° of external rotation and internal rotation of the component should be avoided. Alignment of these cuts can be accomplished by using either measured resection or gap balancing.

Balancing TKA The two principles in balancing TKA are measured resection and gap balancing. The measured resection is used in cruciate-retaining TKA.  The soft-tissue tension is presumed to be correct and it is used to determine bony cuts. In this approach, the tibial cut is made first. This is used as a guide to plan for distal and posterior femur cuts. Maintaining the joint line position is essential in the measured resection technique to ensure posterior cruciate ligament (PCL) tension. If the PCL is too tight, excessive rollback will lead to posterior wear. If the PCL is too loose, excessive femoral anterior translation occurs, which leads to anterior wear. The gap balancing is used in cruciate-substituting (also known as posterior stabilized) TKA. The goal is to achieve even rectangular space in both flexion and extension. The soft-tissue tension is not trusted and it is redressed once the bony cuts are made. Both the distal femur and the tibia are cut perpendicular to the mechanical axis. This is followed by ligament releases to obtain an even extension gap. The posterior femoral cut is made in flexion based on the balanced ligament tension. A stepwise approach for sequential soft-tissue releases dictated by the type of deformity is essential. The general rule is that anterior ligaments lead to tightness in flexion and posterior ligaments lead to tightness in extension.

Varus Deformity If it is tight in flexion, release the anterior portion of the deep MCL followed by anterior release of the pes anserinus. If it is tight in extension, release the posterior portion of the deep MCL and joint capsule followed by releasing some of the superficial MCL. If it is still tight, then consider releasing the semimembranosus and anterior release of the pes anserinus.

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Valgus Deformity Valgus deformity is assessed by using Ranawat Classification. Normal valgus angle is 6 degrees. Grade 1 is valgus deformity less than 10° and the MCL intact. Grade 2 has a valgus angle between 10 and 20° and the MLC is attenuated but there is a firm endpoint. Grade 3 is a valgus angle more than 20° with absent or severely attenuated MCL. This helps to guide the type of implants needed for TKA. If the MCL is intact, a primary TKA poly insert can be used. If the MCL is elongated, a constrained poly insert may be necessary for coronal stability. If the MCL is completely deficient, a hinged prosthesis should be considered.

Surgical Advancements The vast majority of current total knee arthroplasty implants are versions of the “condylar” knee replacements developed in 1970s. There have been significant advancements in many aspects of the total knee replacement which has resulted in a significant improvement in outcomes and longevity. Changes to the design of the total knee replacement in recent years include modifications to improve flexion and alteration of the implant dimensions based on the patient’s gender.

The High-Flexion Knee Knee range of motion (ROM) and particularly knee flexion have traditionally been among the most important factors used to determine success after TKA as many functional activities are dependent upon it. Following a TKA, patients rarely achieve knee flexion of more than 110°, which may limit their ability to do certain activities like transferring into and out of a bath, kneeling, and squatting as they all require knee flexion of more than 110°. Therefore, multiple innovations in TKA implant designs aimed at improving knee flexion. This was mainly aimed at the younger population. The focus of the design modifications was on increasing the contact area between the femoral component and the polyethylene insert at deeper flexion angles. The “high-flexion-knee” femoral component has an extended sagittal curve and a thicker posterior condyle by 2–4  mm replacing the additional bone cut to maintain contact area at deep flexion, therefore increasing posterior femoral translation and range of flexion [12]. Several authors have initially reported that these high-flexion total knee designs have improved postoperative knee flexion compared with standard total knee designs. But many others have not supported the proposition that high flexion designs provide functional advantages over standard prosthesis. In addition, there has been some concern that high-flexion total knee implants may be more sensitive to loosening than standard total knee implants as the knee joint load increases considerably during flexion [13]. However the results are not consistent. Further long-­ term results regarding flexion and implant survival are needed.

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Gender-Specific Designs Many anatomical studies have shown gender-related differences in the anteroposterior (AP) to mediolateral (ML) ratio of the distal femur. Sizing of the femoral component is typically based on anteroposterior dimensions and therefore an appropriately sized femoral component can be too wide which can alter collateral ligament balancing. A smaller fit may result in laxity in flexion. Therefore, to integrate these male/female differences and achieve optimal anatomical fit, some TKA manufacturers have developed a women-specific product line. However, published studies on the morphological differences between genders provide us with contradictory conclusions. Piriou et al. showed that gender is only a co-variable and that the AP and ML dimensions of the femoral epiphysis solely depend on femur length [14]. Furthermore, recent studies have also shown that gender-specific prostheses do not appear to confer any benefit in terms of clinician- and patient-reported outcomes for the female knee [15].

The Advance Medial Pivot Knee Attempts have also been made to adapt the knee arthroplasty designs as we further our understanding in knee kinematics. Until now, there has been no ideal TKA design which can mimic the normal knee kinematics. This results in a failure to replicate a predictable and physiological knee movement which is considered as one of the main goals in order to improve patient’s function and consequently restore quality of life. The intention of the pivot knee system is to provide increased stability and kinematics that mimic those of a natural knee. The medial-pivot design features an asymmetrical tibial insert that controls the anterior-posterior translation of the femur in the medial compartment while allowing unrestricted movement of the femur in the lateral compartment. This results in the lateral condyle pivoting around the medial condyle to create movement similar to that of the normal knee [16]. The current literature so far has been encouraging. Fitch et al. showed that the medial pivot system was associated with survivorship and KSS similar or better than that reported for other TKR systems with up to 8  years of follow-up [17]. Macheras et al. also demonstrated that based on the clinical and radiographic results, patients with this medial pivot prosthesis experienced excellent long-term results with an average of 15-year follow-up [18].

New Surgical Approaches Minimally Invasive Surgery The medial parapatellar approach (MPPA) remains to be the most commonly used approach in the UK for total knee arthroplasty. However, critics feel that minimally invasive surgery (MIS) represents a natural evolution in the approach to knee

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surgery and that because of the extensive soft-tissue disruption combined with patellar eversion in the traditional approach the rehabilitation after such surgery is often prolonged. Because of the adoption of enhanced recovery techniques resulting in shorter length of stay and faster rehabilitation combined with patients’ demands on smaller scars there has been an increase in the popularity of the minimally invasive procedures [19]. Initial studies showed an improvement in early outcomes for patients undergoing MIS-TKA when compared to MPPA. Detractors of the MIS feel that more limited exposure may result in component malposition and hence increased complication rates. Unwin et al. concluded that in addition to the early benefits regarding hospital stay and complications they have found that at a medium-term follow-up, mean 6 years, there is no statistically significant difference in patient-reported outcome between traditional TKA and MIS-TKA techniques. This supports the majority of the literature surrounding patient follow-up beyond the early stages post-surgery. In addition, they have demonstrated no detrimental effect of MIS surgery on revision for malalignment [20].

Computer-Assisted Navigation Although excellent results have been reported with modern implant designs, malpositioning of implants can contribute significantly to early failure. It is reported that up to 10% may require revision surgery within 10  years of the initial TKA primarily because of prosthesis loosening. The most important determinants of failure secondary to prosthesis loosening are poor positioning of the prosthesis and subsequent malalignment of the postoperative lower limb [21]. A recent metaanalysis found that as little as three degrees of deviation from ideal alignment in the coronal plane significantly increased the risk of TKA failure. Therefore, strategies that increase the accuracy of prosthesis positioning may improve long-term prosthesis survival rates for patients [22]. Computer-assisted surgery or navigation has been introduced in an attempt to improve the accuracy of bone cuts and implant placement. Computer-assisted navigation consists of three elements: computer platform, tracking system, and rigid body marker. Many of these systems are designed to coincide with MIS approaches. Despite improvements some systems are time consuming and in fact multiple studies have assessed the accuracy of computer-assisted procedures over the traditional jig-assisted method in improving component alignment with varying results [23]. Other studies however do support the increased accuracy in bone cuts and alignment. It is still not clear whether the increased accuracy will translate into improved function.

References 1. Hsu H, Siwiec R. Knee arthroplasty. StatPearls Publishing: Michigan State University; 2018. 2. Parcells B, Parcells B.  History of TKA [Internet]. Hip & Knee Book. 2018. https:// hipandkneebook.com/tka-implants/2017/3/15/history-of-tka. Accessed 6 Dec 2018.

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3. Bulstrode C. Oxford textbook of trauma and orthopaedics. 2nd ed. Oxford: Oxford University Press; 2011. 4. Hungerford DS, Krackow KA.  Total joint arthroplasty of the knee. Clin Orthop Relat Res. 1985;192:23. 5. Rivière C, Iranpour F, Auvinet E, Howell S, Vendittoli P, Cobb J, et al. Alignment options for total knee arthroplasty: a systematic review. Orthop Traumatol Surg Res. 2017;103(7):1047–56. 6. Insall JN, Binazzi R, Soudry M, Mestriner LA. Total knee arthroplasty. Clin Orthop Relat Res. 1985;192:13. 7. Schiraldi M, Bonzanini G, Chirillo D, de Tullio V.  Mechanical and kinematic alignment in total knee arthroplasty. Ann Transl Med. 2016;4(7):130. 8. Kolisek F, McGrath M, Marker D, Jessup N.  Posterior-stabilized versus posterior cruciate ligament-retaining total knee arthroplasty. Iowa Orthop J. 2009;29:3–27. 9. Serna-Berna R, Lizaur-Utrilla A, Vizcaya-Moreno M, Miralles Muñoz F, Gonzalez-Navarro B, Lopez-Prats F. Cruciate-retaining vs posterior-stabilized primary total arthroplasty. clinical outcome comparison with a minimum follow-up of 10 years. J Arthroplast. 2018;33(8):2491–5. 10. Yacoubian SV, Scott RD. Skin incision translation in total knee arthroplasty: the difference between flexion and extension. J Arthroplast. 2007;22:353–5. 11. Berstock J, Murray J, Whitehouse M, Blom A, Beswick A. Medial subvastus versus the medial parapatellar approach for total knee replacement. EFORT Open Rev. 2018;3(3):78–84. 12. Kim M, Kim J, Koh I, Jang S, Jeong D, In Y.  Is high-flexion total knee arthroplasty a valid concept? bilateral comparison with standard total knee arthroplasty. J Arthroplast. 2016;31(4):802–8. 13. Zelle J, Janssen D, Eijden JV, Malefijt MDW, Verdonschot N. Does high-flexion total knee arthroplasty promote early loosening of the femoral component? J Orthop Res. 2011;29:976–83. 14. Piriou P, Mabit C, Bonnevialle P, Peronne E, Versier G. Are gender-specific femoral implants for total knee arthroplasty necessary? J Arthroplast. 2014;29(4):742–8. 15. Cheng T, Zhu C, Wang J, Cheng M, Peng X, Wang Q, et al. No clinical benefit of gender-­ specific total knee arthroplasty. Acta Orthop. 2014;85(4):415–21. 16. Miyazaki Y, Nakamura T, Kogame K, et al. Analysis of the kinematics of total knee prostheses with a medial pivot design. J Arthroplast. 2011;26:1038–44. 17. Fitch D, Sedacki K, Yang Y. Mid- to long-term outcomes of a medial-pivot system for primary total knee replacement. Bone Joint Res. 2014;3(10):297–304. 18. Macheras G, Galanakos S, Lepetsos P, Anastasopoulos P, Papadakis S. A long term clinical outcome of the medial pivot knee arthroplasty system. Knee. 2017;24(2):447–53. 19. Alcelik I, Blomfield M, Diana G, Gibbon A, Carrington N, Burr S. A comparison of short-­ term outcomes of minimally invasive computer-assisted vs minimally invasive conventional instrumentation for primary total knee arthroplasty. J Arthroplast. 2016;31(2):410–8. 20. Unwin O, Hassaballa M, Murray J, Harries W, Porteous A. Minimally invasive surgery (MIS) for total knee replacement; medium term results with minimum five year follow-up. Knee. 2017;24(2):454–9. 21. McClelland J, Webster K, Ramteke A, Feller J. Total knee arthroplasty with computer-assisted navigation more closely replicates normal knee biomechanics than conventional surgery. Knee. 2017;24(3):651–6. 22. Bauwens K, Matthes G, Wich M, Gebhard F, Hanson B, Ekkernkamp A, et al. Navigated total knee replacement. A meta-analysis. J Bone Joint Surg Am. 2007;89-A:261–9. 23. Yi-Jan Weng MD, Robert Wen-Wei Hsu MD, Wei-Hsiu Hsu MD. Comparison of computer-­ assisted navigation and conventional instrumentation for bilateral total knee arthroplasty. J Arthroplast. 2009;24(5):668–73. https://doi.org/10.1016/j.arth.2008.03.006.

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Endoscopic surgery developed as a less invasive means to access body cavities. The first documented use of the endoscope was of the bladder in 1806. As technology and light sources progressed the use of endoscopes to investigate and treat joint problems was explored [1]. Globally the earliest arthroscopists include Severin Nordentoft (1866–1922), a surgeon from Denmark who presented his work on endoscopy of the knee using optics and illumination. At a similar time Keji Takagin (1888–1963) in Tokyo reported the use of a knee arthroscope for the diagnosis of TB.  Eugen Bircher of Switzerland (1882–1956) published his work on the arthroendoscope for the diagnosis of conditions of the knee. Phillip Heinrich Kreuscher (1883–1943) was the pioneering arthroscopist of the USA publishing on the diagnosis of cartilage injury in sport by means of the arthroscope. Further development of the arthroscope was carried out by Masaki Watanabe (1911–1994). He continued the work of Takagin. He introduced a supplemental light source and separate portal and in 1970 he introduced the first fiber optic and the concept of triangulation, the use of which is common practise today [1, 2]. The common current setup of the arthroscopy system is an arthroscopic stack (Fig. 33.1) on the opposite side of the patient to the operating surgeon and a back table with the surgical equipment as seen in Fig. 33.2. The arthroscopic system includes the arthroscope, light source, and an irrigation system. The rigid arthroscope is a classic thin lens, a rod-lens system, R. J. Tansey (*) Department of Orthopaedics, Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK Department of Trauma and Orthopaedics, Peterborough City Hospital, Peterborough, UK e-mail: [email protected] M. J. Dunne · W. S. Khan Department of Orthopaedics, Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK e-mail: [email protected]; [email protected] © Springer Nature Switzerland AG 2019 K. M. Iyer, W. S. Khan (eds.), General Principles of Orthopedics and Trauma, https://doi.org/10.1007/978-3-030-15089-1_33

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Monitor

Light source

Infusion pump

Shaver Radiofrequency Ablator

Fig. 33.2  Line diagram to show the layout of operating theatre for shoulder arthroscopy in the beach chair position

or a graded index lens system. The design of the arthroscope and its given field of view vary. This is dependent on the diameter of the arthroscope (these range from 2.7 to 7.5 mm) and the angle of inclination of the distal arthroscopic lens. The angle of inclination is measured between the axis of the arthroscope and a line perpendicular to the surface of the lens (this varies from 10° to 120°) [3]. Most commonly used are 25–30° (70–90° may be used in more specific

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situations for viewing around corners). The field of view is increased by rotating the arthroscope; however a blind spot will be present; its size will depend on the angle of inclination of the arthroscope. For routine procedures the basic arthroscopy set contains the arthroscope with a 30–70° arthroscope, a probe, scissors, grasping forceps, punch forceps, arthroscopic knives, a motorized meniscal cutter and shaver, electrosurgical, laser, and radiofrequency instruments (Fig. 33.3). Procedure-specific instruments have also been developed and variations exist depending on manufacturers and surgeon preferences. Irrigation systems are vital to allow distension of the joint in arthroscopy. These generally flow along the arthroscopic sheath. The solution used is commonly Hartmann’s solution supplied by 2.5 L bags joined by a y connector placed high above the level of the joint allowing a pressure of approximately 66–88 mmHg. Advantages of arthroscopy include the following: • • • • • • • •

Reduced postoperative morbidity Smaller incisions Less intense inflammatory response Improved visualization Reduced length of stay Reduced complication rate Permit easier “second look” surgery Allow access to perform some procedures not possible through arthrotomy Disadvantages of arthroscopy include the following:

• Technically challenging • Learning curve We now look at arthroscopy as relevant to different joints in the body.

Knee The knee was the primary joint in the development of arthroscopy [1, 2]. Arthroscopy of the knee remains a common clinical practise today [4, 5]. The indications for knee arthroscopy include assessment and repair of the meniscus, anterior cruciate ligament, posterior cruciate ligament, synovectomy for rheumatoid arthritis, management of osteochondral injuries, chondroplasty, microfracture, and in some select cases early osteoarthritis. It can also be used as a complementary method in the fixation of tibial plateau fractures and in the management of septic arthritis [1, 5]. There are few contraindications to knee arthroscopy; they include superficial soft-tissue infection due to the risk of introducing infection into the joint. A thorough preoperative assessment including history examination and imaging is necessary to ensure that unnecessary arthroscopies are not undertaken [4].

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1

2

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Fig. 33.3  Arthroscopy instruments: (a) lens, (b) camera, (c) trocar with sheath, (d) arthroscopy probe, (e) punch forceps, (f) shaver, (g) radiofrequency probe (courtesy: permission from Dr. Pradeep and Dr. David V Rajan)

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6

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Fig. 33.3 (continued)

Patient setup for knee arthroscopy is commonly supine on the operating table with a circumferential tourniquet to the upper thigh. A surgical leg holder or side support is placed at the upper thigh (the side support is usually placed approximately 5 cm superior to the upper pole of the patella); this allows an unassisted surgeon to stand between the affected leg and the operating table and apply a valgus strain across the knee during the procedure, thus visualizing the medial compartment. A systematic approach is taken to the assessment of the knee most commonly through two portals (anteromedial and anterolateral). Surface anatomy marking of the patella, tibial tubercle, patella tendon, fibula head, and medial and lateral joint lines can be easily identified. Portals can be made horizontally or vertically (horizontal being more cosmetic, vertical allowing more freedom of movement of the scope). The lateral joint line is slightly higher than the medial. The lateral portal is created first in the soft spot on the anterolateral 1 cm above the joint line next to the patella tendon. The anteromedial portal is identified by

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placing a spinal needle through the soft spot 1 cm above the joint line on the medial side 1 cm medial to the patella tendon; the portal placement is confirmed with the arthroscope entering from the lateral portal [5]. Through movement of the arthroscope within the portals and angling the light source visualization of the suprapatellar pouch, medial gutter, lateral gutter, medial compartment, lateral compartment, intercondylar notch, and posteromedial and posterolateral compartments can be carried out. A standardized and systematic approach to this is essential to ensure that no pathology is missed [6].

Hip The use of the arthroscope in the hip has been less popular than in the knee. Potential reasons for this are the complexity of the procedure, steep learning curve, or requirement of specialist equipment. It requires larger and more flexible instruments than arthroscopy of the knee, use of traction, and fluoroscopy. It does however allow excellent visualization of the articular surfaces of the hip joint as well as the peritrochanteric surfaces and extra-articular space [7, 8]. Its used has been described in the management of septic hip joints, removal of loose bodies, and synovial abnormalities. The most common indication for hip arthroscopy is for lesions of the acetabular labrum for which debridement of repair can be undertaken arthroscopically. It has also been used in the management of the causative factors of femoroacetabular impingement to normalize joint mechanics. Extra-articular indications for hip arthroscopy include refractory cases of snapping hip which have failed conservative management and thermal capsular shrinkage for problematic ligamentous laxity [7]. The patient is placed in the lateral or supine position with traction applied to the operated leg. The joint is distracted under fluoroscopic guidance. The joint is infiltrated with fluid for further distension of the capsule. Superficial landmarks of the greater trochanter, femoral head, and sciatic nerve are marked out [8]. Typically three portals are used: a direct lateral paratrochanteric portal, a second anterolateral paratrochanteric portal, and an anterosuperior portal. The latter can be used to visualize the peripheral compartment, for this traction must be released [7]. Arthroscopy allows visualization of femoral head and acetabular pathology, soft tissue such as the ligamentum teres, acetabular labrum synovial folds, and synovium. Complications of hip arthroscopy are rare and are reported to include bleeding, infection neuropraxia to the sciatic femoral or pudendal nerves secondary to traction and to the lateral femoral cutaneous nerve due to portal placement [9]. Late complications include trochanteric bursitis, osteonecrosis, dislocation of the femoral head and fluid extravasation to the abdomen [7, 10].

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Foot and Ankle Smaller arthroscopes and instrumentation have allowed arthroscopy to be useful in smaller joints. Indications for ankle arthroscopy include impingement syndrome, osteochondral lesions, instability and fracture [11], posttraumatic arthritis, adhesions, locking [12] loose bodies, arthrofibrosis, and synovitis [11]. For ankle arthroscopy the patient is typically positioned supine. The ankle is either dorsiflexed or distracted to allow visualization of the articular surface and ligaments [13]. Distraction can be manual or mechanical, and invasive or noninvasive. Prior to portal placement landmarks of important structures are located; these include both malleoli, the anterior joint line, tibialis anterior tendon, peroneus tertius tendon, and Achilles tendon, great saphenous vein, and superficial peroneal nerve. Numerous portals for ankle arthroscopy have been described due to the anatomic region being covered by an extensive network of neurovascular structures. They include anterior, posterior, transmalleolar, and transtalar. The most frequently used are the anteromedial and anterolateral ones. The anteromedial is medial to the tibialis anterior tendon at the anterior joint line. A visible and palpable soft spot can be found here when the ankle is dorsiflexed. The saphenous nerve and veins are at risk of injury from this portal. The anterolateral portal is identified on the anterior joint line lateral to peroneus tertius tendon, taking care not to injure the superficial peroneal nerve [14]. Posterior portals are more technically challenging and provide increased surgical risk. Complications have been reported to include reflex sympathetic dystrophy, fibular fracture [12], superficial peroneal nerve damage, persistent drainage through portal sites, and infection [15]. Arthroscopy has also been used in other joints of the foot, namely the subtalar and first metatarsophalangeal joints. Arthroscopy of the hallux requires small instruments which are delicate and vulnerable to damage [13].

Shoulder Shoulder arthroscopy remains a commonly performed procedure with an estimated 21,000 subacromial decompressions alone carried out in England in 2009/2010 [16]. Its use for this indication has become more controversial recently with the publication of the results of a pragmatic multicenter randomized controlled trial [17]. However, it is effective for a wide number of conditions ranging from diagnostic surgery, soft-tissue procedures (including cuff repairs, labral/ SLAP repair, glenohumeral joint stabilization, synovectomy, and capsular

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release), bony procedures (AC joint excision and acromioplasty), and even suprascapular nerve release. Patients can be positioned in either the beach chair or the lateral decubitus position depending on surgeon preference. The beach chair position [18] offers the advantages of an anatomical orientation and the use of stand-alone regional anesthesia but may present technical difficulties in terms of mechanical blocks when using the scope via a posterior portal. Via traction applied to the arm, the lateral decubitus position provides excellent joint space visualization albeit in a nonanatomical orientation. The potential for nerve injury is also higher with this approach due to a combination of traction and increased risk when placing the anteroinferior portal to the axillary and musculocutaneous nerves [19]. A number of options for primary and secondary portals exist and combinations are often used depending on the procedure being performed. The posterior portal is the first established for most procedures. It is located 2 cm inferior and 1 cm medial to the posterolateral corner of the acromion with the trochar inserted anteriorly towards the tip of the coracoid, often after the insertion of a spinal needle into the joint with or without infiltration of saline [20, 21]. This portal also allows access to the subacromial space via the same skin incision. The anterior portal is then usually established under direct vision by exploiting the rotator interval ensuring that a skin incision is made lateral to the coracoid process [21]. Secondary portals can be made along a line moving anterior to posterior using the borders of the acromion as a landmark. A superolateral portal placed 1 cm lateral to the anterolateral corner of the acromion allows access to the rotator cuff and anterior glenoid labrum. The lateral subacromial portal, the workhorse of most arthroscopic shoulder procedures, is sited inferior to the midpoint of the acromion. It allows access to the majority of intra- and extra-articular structures of the shoulder. Finally, the posterolateral portal, usually sited 1 cm anteroinferiorly to the posterolateral corner of the acromion, can prove useful when access to the posterior cuff and labrum is required [21]. As with all arthroscopic procedures a systematic approach is required to identify the biceps tendon, supraspinatus, infraspinatus, rotator interval, middle and inferior glenohumeral ligaments, subscapular recess, anterior labrum, and glenohumeral joint [22]. Complications associated with shoulder arthroscopy relate predominantly to the neurological structures around the shoulder. The axillary and suprascapular nerves are at risk with a poorly placed posterior portal while the musculocutaneous nerve is at risk with a misplaced anterior portal [23].

Elbow Elbow joint arthroscopy is a rapidly evolving area of elbow surgery thanks largely to advances in technology and a better understanding of the complex anatomy of the elbow joint [24]. Its use has moved far from merely the purpose of diagnosis and is now indicated for a number of conditions ranging from removal of loose bodies to the treatment of osteo and septic arthritis.

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Patients can be positioned in either a supine, prone, or lateral decubitus position. It is of vital importance to accurately mark out surface anatomy prior to distension of the joint to minimize the risk to the numerous neurovascular structures sited around the joint [25, 26]. The epicondyles of the humerus, olecranon process, and radiocapitellar joint should be identified and marked. When the patient’s body habitus allows, ideally the course of the ulnar nerve should also be determined [25]. Similar to the shoulder a number of potential portals are described about the elbow. Prior to portal creation the elbow joint is usually distended via infiltration of the joint using saline via the lateral “soft spot.” The choice of portal used depends on the procedure being performed. Broadly speaking there are three lateral, three medial, and three posterior portals that may be utilized [24]. Lateral portals include the mid-anterolateral (most commonly used), distal anterolateral, and proximal anterolateral. The radial nerve is at risk with all three of these portals, the highest risk of injury lying with the distal anterolateral portal which has fallen out of favor [24]. The medial portals mirror their lateral counterparts in terms of their positions. The most commonly sited medial portal is the proximal anteromedial portal (often performed under direct vision once a lateral portal has been established) with the anteromedial portal being the second most commonly used. The mid-anteromedial portal is often seen as redundant due to its close proximity to the other two medial portals [24]. The posterior aspect of the elbow joint can be accessed via a direct posterior or “transtricipital” portal which splits the tendinous portion of the triceps allowing visualization of the olecranon fossa as well as the lateral and medial gutters [24] (Camp 23). Direct lateral and distal ulna portals are also described that facilitate access to the radiocapitellar joint. Elbow arthroscopy continues to develop and is technically demanding. The biggest risk is to the nerves surrounding the elbow which can be damaged during portal placement. The most commonly injured is the ulna nerve followed by the radial nerve with the risk increased in patients with underlying contractures or rheumatoid arthritis, or those who have undergone previous ulna nerve transposition [27]. There have been reports also of heterotropic ossification though the reported rates are less than those seen in open surgery [27].

Wrist Like elbow arthroscopy, the indications for wrist arthroscopy have increased over the last few decades. It is now used to treat or assess a wide range of conditions including TFCC injuries, chondral lesions of the carpus, dynamic assessment of carpal instability, soft-tissue pathologies such as ganglions or carpal tunnel syndrome, and even in assisting fracture reductions [28, 29]. Patients undergoing wrist arthroscopy are placed supine with the arm in approximately 7–10 lbs of in-line traction via finger traps. This can be performed either with the elbow flexed at 90° and the forearm vertical or with the arm extended on an arm table [30]. Portals for wrist arthroscopy are named after their relation to

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the extensor compartments of the wrist. Surface landmarks that need to be identified to ensure accurate placement are Lister’s tubercle, scaphoid and lunate, DRUJ, and ECU. Broadly speaking, portals can be divided into radiocarpal portals (primarily used for viewing and TFCC repairs), midcarpal portals (used for visualizing the carpal bones and allowing for evaluation of wrist instability), and portals based around the first extensor compartment that allow for arthroscopic debridement of thumb base osteoarthritis [30, 31]. The 3-4 portal is usually the first established portal in wrist arthroscopy. Complications of wrist arthroscopy (like all other upper limb arthroscopies) are predominantly due to nerve injuries affecting the dorsal sensory branch of the ulnar nerve as well as the superficial branch of the radial nerve. Less commonly the extensor tendons may become damaged or an iatrogenic osteochondral defect may occur, more often than not due to a lack of sufficient space [32].

Sternoclavicular Joint A technique has been described for arthroscopy of the sternoclavicular joint which allows for diagnostic evaluation as well as treatment of degenerative conditions of the medial end of the clavicle [33]. Patients are positioned supine with a sandbag between their scapulae and 2.9 mm instruments are used [34]. The main concerns for most with relation to performing this procedure would be the proximity of important mediastinal structures. The authors describe an inferior portal, made 1 cm directly inferior to the joint line after palpation of the sternum and medial end of clavicle, followed by a more superior portal inserted under direct vision [34]. This relatively new procedure has the potential benefits of better joint visualization, less risk of compromising SCJ stability, and infection but would not be appropriately carried out by an inexperienced surgeon in a low-volume center [34].

References 1. Jackson RW. A history of arthroscopy. Arthroscopy. 2010;26(1):91–103. 2. Treuting R. Minimally invasive orthopedic surgery: arthroscopy. Ochsner J. 2000;2(3):158–63. 3. Ogilvie-Harris DJ.  Operative arthroscopy. 2nd ed. Philadelphia, PA: Lippincott–Raven Publishers; 1996. 4. Onyema C, Oragui E, White J, Khan WS.  Evidence-based practice in arthroscopic knee surgery. J Perioper Pract. 2011;21(4):128–34. 5. Ward BD, Lubowitz JH. Basic knee arthroscopy part 2: surface anatomy and portal placement. Arthrosc Tech. 2013;2(4):e501–2. 6. Ward BD, Lubowitz JH. Basic knee arthroscopy part 3: diagnostic arthroscopy. Arthrosc Tech. 2013;2(4):e503–5. 7. Griffiths EJ, Khanduja V. Hip arthroscopy: evolution, current practice and future developments. Int Orthop. 2012;36(6):1115–21.

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8. Glick JM, Sampson TG, Gordon RB, Behr JT, Schmidt E.  Hip arthroscopy by the lateral approach. Arthroscopy. 1987;3(1):4–12. 9. Griffin DR, Villar RN.  Complications of arthroscopy of the hip. J Bone Joint Surg Br. 1999;81(4):604–6. 10. Matsuda DK. Acute iatrogenic dislocation following hip impingement arthroscopic surgery. Arthroscopy. 2009;25(4):400–4. 11. Cavallo M, Natali S, Ruffilli A, Buda R, Vannini F, Castagnini F, et al. Ankle surgery: focus on arthroscopy. Musculoskelet Surg. 2013;97(3):237–45. 12. Feder KS, Schonholtz GJ.  Ankle arthroscopy: review and long-term results. Foot Ankle. 1992;13(7):382–5. 13. de Leeuw PA, Golanó P, Clavero JA, van Dijk CN. Anterior ankle arthroscopy, distraction or dorsiflexion? Knee Surg Sports Traumatol Arthrosc. 2010;18(5):594–600. 14. Golano P, Vega J, Perez-Carro L, Gotzens V. Ankle anatomy for the arthroscopist. Part I: the portals. Foot Ankle Clin. 2006;11(2):253–73.. v 15. Blazquez Martin T, Iglesias Duran E, San Miguel Campos M. Complications after ankle and hindfoot arthroscopy. Rev Esp Cir Ortop Traumatol. 2016;60(6):387–93. 16. Judge A, Murphy RJ, Maxwell R, Arden NK, Carr AJ.  Temporal trends and geographical variation in the use of subacromial decompression and rotator cuff repair of the shoulder in England. Bone Joint J. 2014;96-B(1):70–4. 17. Beard DJ, Rees JL, Cook JA, Rombach I, Cooper C, Merritt N, et al. Arthroscopic subacromial decompression for subacromial shoulder pain (CSAW): a multicentre, pragmatic, parallel group, placebo-controlled, three-group, randomised surgical trial. Lancet. 2018;391(10118):329–38. 18. Mannava S, Jinnah AH, Plate JF, Stone AV, Tuohy CJ, Freehill MT. Basic shoulder arthroscopy: beach chair patient positioning. Arthrosc Tech. 2016;5(4):e731–e5. 19. Paxton ES, Backus J, Keener J, Brophy RH.  Shoulder arthroscopy: basic principles of positioning, anesthesia, and portal anatomy. J Am Acad Orthop Surg. 2013;21(6):332–42. 20. Farmer KW, Wright TW. Shoulder arthroscopy: the basics. J Hand Surg Am. 2015;40(4):817–21. 21. Boyle S, Haag M, Limb D, Lafosse L. Shoulder arthroscopy, anatomy and variants—part 1. J Orthop Trauma. 2009;23(4):291–6. 22. Snyder SJ. Shoulder arthroscopy. Philadelphia, PA: Lippincott Williams & Wilkins; 2003. 23. Moen TC, Rudolph GH, Caswell K, Espinoza C, Burkhead WZ Jr, Krishnan SG. Complications of shoulder arthroscopy. J Am Acad Orthop Surg. 2014;22(7):410–9. 24. Camp CL, Degen RM, Sanchez-Sotelo J, Altchek DW, Dines JS. Basics of elbow arthroscopy part I: surface anatomy, portals, and structures at risk. Arthrosc Tech. 2016;5(6):e1339–e43. 25. Adams JE, King GJ, Steinmann SP, Cohen MS. Elbow arthroscopy: indications, techniques, outcomes, and complications. J Am Acad Orthop Surg. 2014;22(12):810–8. 26. Stetson WB, Vogeli K, Chung B, Hung NJ, Stevanovic M, Morgan S. Avoiding neurological complications of elbow arthroscopy. Arthrosc Tech. 2018;7(7):e717–e24. 27. King GJ. In: Bain GI, Safran MR, Pederzini LA, editors. Elbow arthroscopy complications. Berlin Heidelberg: Springer-Verlag; 2013. 28. Wagner J, Ipaktchi K, Livermore M, Banegas R. Current indications for and the technique of wrist arthroscopy. Orthopedics. 2014;37(4):251–6. 29. Monaghan BA.  Uses and abuses of wrist arthroscopy. Tech Hand Up Extrem Surg. 2006;10(1):37–42. 30. Parvizi J. Wrist arthroscopy. Philadelphia, PA: WB Saunders; 2010. 31. Michelotti BF, Chung K. Procedure 20—wrist arthroscopy. 3rd ed. Berlin: Elsevier; 2018. 32. Leclercq C, Mathoulin C. Complications of wrist arthroscopy: a multicenter study based on 10,107 arthroscopies. J Wrist Surg. 2016;5(4):320–6. 33. Tytherleigh-Strong G, Rashid A, Lawrence C, Morrissey D.  Arthroscopic sternoclavicular joint diskectomy for acute and chronic tears. Arthroscopy. 2017;33(11):1965–70. 34. Tytherleigh-Strong G, Van Rensburg L.  Arthroscopic excision of the sternoclavicular joint. Arthrosc Tech. 2017;6(5):e1697–e702.

Hip-Preserving Surgery

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Hip-preservation surgery can include a multitude of procedures that essentially prevent or restore damage to articular cartilage, thus slowing the progression of osteoarthritis and the need for arthroplasty. Hip arthroplasty is a successful treatment option to improve pain and function in patients with osteoarthritis but may not be suitable for younger patients with hip pain and chondral damage. Although currently there is no high-level evidence to support it, the detection and treatment of chondral lesions in young patient may prevent the progression to more widespread osteoarthritis. In this chapter I will concentrate on the hip-preservation techniques that may be an option to treat chondral lesions especially in those younger patients. Of note, some of these techniques are rather novel and therefore there is limited good-quality evidence for their use in the hip joint. I will also describe some basic principles of hip arthroscopy, which is an expanding surgical field that is required to carry out the majority of these procedures. There are many causes for chondral damage in the hip.

Femoroacetabular Impingement Femoroacetabular impingement (FAI) is probably the most commonly treated pathology in the hip when considering hip preservation. First proposed by Ganz et  al. it was stated that the FAI initiated a cascade of events that eventually would lead to hip OA [1]. Beck et al. were the first to show that the majority of J. Patel (*) Trauma and Orthopaedics, Addenbrooke’s Hospital, University of Cambridge, Cambridge, UK e-mail: [email protected] W. S. Khan University of Cambridge, Cambridge, UK e-mail: [email protected] © Springer Nature Switzerland AG 2019 K. M. Iyer, W. S. Khan (eds.), General Principles of Orthopedics and Trauma, https://doi.org/10.1007/978-3-030-15089-1_34

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Table 34.1  The causes of chondral damage in the hip:

1 .  2.  3.  4.  5.  6.  7. 

Femoroacetabular impingement (FAI) Trauma Labral tears Arthritis Loose bodies Dysplasia Osteonecrosis

Table 34.2  Advantages and disadvantages of the three main techniques used to restore normal anatomy in the hip (modified from Freeman et al. [2]) Surgical dislocation of the hip

Hip arthroscopy

Periacetabular osteotomy

Advantages Good access Direct visualization of corrections Confirmation of femoral head sphericity using templates Easier treatment of chondral injuries Other corrective procedures can be carried out Minimally invasive Reduced postoperative pain Faster rehabilitation Shorter length of stay Reduced soft-tissue injury

Change acetabulum and femoral orientation Treat pincer FAI without changing coverage Other procedures can be carried out

Disadvantages Metalwork complications Increased blood loss Ligamentum teres disruption Longer recovery

Traction and portal related nerve injury Surgically challenging with a steep learning curve Difficult access and therefore limited visualization Fluid extravasation and abdominal compartment syndrome Invasive Higher complication rate Increased blood loss Slow rehabilitation Long learning curve

patients had a mixed pattern of chondral damage of cam and pincer type. Cam lesions occur due to femoral-based disorders, reduced head-neck ratio, aspherical femoral head, decreased femoral offset, and femoral neck retroversion. Pincer lesions occur due to acetabular disorders, overhanging, retroversion, protrusion, and coxa profunda. The pattern of injury varies between the types of impingement. The goal of surgical treatment of FAI is to restore normal anatomy. The three major techniques used to achieve this are outlined in Table 34.2. Chondral damage is almost always seen in patients with FAI. The principles of treatment are to treat the underlying cause for injury and manage any chondral damage. I will concentrate on arthroscopic techniques that can be used to treat the chondral injuries that are often associated with not only FAI but also those pathologies listed in Table 34.1. The degree of articular damage can be classified using the modified Outerbridge classification system.

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Normal Cartilage with softening and swelling A partial-thickness defect with fissures on the surface that do not reach subchondral bone or exceed 1.5 cm in diameter Fissuring to the level of subchondral bone in an area with a diameter more than 1.5 cm Exposed subchondral bone

The modified Outerbridge classification however does not take into account the different types of chondral damage that can occur in the hip. For example, delamination that is usually as a result of FAI does not necessarily fit into any of the Outerbridge grades. As a result of this, Konan et al. proposed an alternative classification system for chondral damage in the acetabulum associated with FAI [3]. Grade 0 Grade 1 Grade 2 Grade 3 Grade 4

Normal cartilage Loss of fixation to the subchondral bone, positive wave sign Cleavage tear Delamination Exposed bone in the acetabulum

Hip Arthroscopy Hip arthroscopy was initially described by MS Burman in 1931, when he performed an experimental study on cadaveric specimens. He described the difficulties in gaining access to the hip joint and this largely contributed to the slow development of hip arthroscopy when compared to other joints [4]. Open dislocation of he hip to manage conditions such as FAI has shown good and comparable results to arthroscopic surgery. Arthroscopy however offers a lower complication rate and quicker recovery for the patient. Matsuda et al. performed a systematic review that showed complication rates of arthroscopy, open, and mini-open to be 1.7%, 9.2%, and 16%, respectively [5]. As we continue to develop our understanding of the pathophysiology of hip pain and along with development of instrumentations and techniques in hip arthroscopy, the indications and popularity of hip arthroscopy have increased. Patient selection for hip arthroscopy is key. It is likely that patients with a Tonnis grade of 1 or greater or a joint space of less than 2 mm are less likely to benefit from hip arthroscopy and more likely to need total hip arthroscopy (THA) or resurfacing [6].

Hip Arthroscopy Surgical Technique Hip arthroscopy is challenging due to the anatomy of the joint. It is a joint deeply recessed within the pelvis and is covered by a thick fibrous capsule and large musculature. The learning curve for hip arthroscopy is steep and it is thought that complication rates significantly decrease after performing over 500 cases [7]. The surgical technique

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for hip arthroscopy is variable between centers and is both surgeon and equipment dependent. This technique is the standard technique used in our department.

Patient Setup The patient is usually anesthetized using a general or regional anesthetic. Muscle relaxation is required to aid in the distraction of the hip joint. The patient is positioned supine on a trauma table. Hip arthroscopy in the lateral decubitus position is also possible and commonly practiced. A recent systemic review has suggested similar outcomes between the supine and lateral positions [8]. A large perineal post is used in an offset position towards the operative side and the leg positioned in abduction at an angle between 20° and 30°. The position of the leg as described previously allows distraction of the hip joint in a more favorable position that is closer in line of the femoral neck when traction is applied to the operative limb. The laterally offset perineal post helps protect the pudendal and peroneal nerves from traction-related injuries. The legs are placed in specially designed traction boots that allow free movement of the foot and thus rotation of the hip during surgery, which is key in evaluating as much of the joint as possible. The contralateral limb is placed in a flexed position to allow the use of fluoroscopy. To distract the hip, typically 25–50 lbs of traction is required. Confirmation of hip distraction can be confirmed using fluoroscopy. If distraction is not easily achieved immediately, time should be given to allow the capsule to relax. Distraction of the hip causes a negative pressure within the hip joint causing a vacuum phenomenon. Releasing this vacuum can aid in hip distraction and can be easily achieved by using a fluoroscopically guided needle into the joint and also by joint distension with fluid.

Portal Placement and Sequence The placement of portals is important in allowing maximum diagnostic and therapeutic value. Poorly placed portals can restrict the visualization of the hip joint and its surrounding structures as well as impede possible therapeutic procedures. Over 18 possible portal positions have been described over the years but only nine have been shown to be safe and reproducible and therefore of clinical benefit [9]. The three portals we use are summarized in Table 34.3. A detailed understanding of the surrounding tissues and important structures is essential in preventing iatrogenic injuries. With the hip in a neutral position, surface landmarks around the hip are first identified. The borders of the greater trochanter are marked. The first portal usually inserted is the anterolateral portal. The superficial landmark for this portal is 1–2  cm superior and anterior to the tip of the greater trochanter. Under fluoroscopic guidance a needle is inserted into the hip joint. The progression of the needle can be followed using fluoroscopy and the feeling of the needle passing through the capsule is quite distinct. Once the needle has been inserted, fluid is injected into the hip which should cause hip distraction that can be seen on

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Table 34.3  Summary of three main portals used in hip arthroscopy Portal Anterolateral

Anterior

Posterolateral

Structures visualized •  Entire labrum, especially anterior and superior • Recess between superior labrum and capsule •  Iliofemoral ligament •  Femoral head •  Most of the acetabulum •  Fovea capitis •  Psoas tendon and bursa • Visualization of further portal placement •  Anterior femoral head •  Ligamentum teres •  Acetabular fossa •  Superior and posterior labrum •  Anterior femoral neck • Peri-trochanteric region (gluteus medius, minimus, and trochanteric bursa) •  Head–neck junction •  Zona orbicularis •  Posterior recess •  Acetabular fossa •  Posteromedial labrum •  Transverse ligament • Acetabular floor and posterior labral recess (where most loose bodies are found)

Risk •  Intra-articular damage as this port is usually inserted “blind” •  Superior gluteal nerve

•   Lateral femoral cutaneous nerve • Ascending branch of lateral femoral circumflex artery •  Femoral neurovascular bundle

•  Sciatic nerve •  Superior gluteal nerve • Deep branch of medial circumflex artery

fluoroscopy. A guide wire can be safely inserted through the needle and then a cannula over this. The gluteus medius is penetrated to create this portal and the structure most at risk is the superior gluteal nerve. This portal can be adjusted under direct visualization if desired later on. A 70-degree angle camera is commonly used to allow better visualization of the hip joint and its various components. Through direct visualization further portals can then be created. Inserting portals under direct visualization reduces the risk of iatrogenic injuries. The second portal created is the anterior portal. The skin marking for this portal is an intersection between a line drawn from the superior margin of the greater trochanter transversely and a sagittal line from the anterior superior iliac spine. This portal penetrates the rectus femoris and sartorius muscles. Structures at risk during this portal placement include the femoral neurovascular bundle, lateral femoral cutaneous nerve, and lateral circumflex femoral artery. The posterolateral portal is the third portal created. The surface landmark for this portal is approximately 1–2 cm superior and inferior to the tip of the greater trochanter. The gluteus medius and minimus are penetrated by the portal. The most significant structure at risk in this location is the sciatic nerve. Therefore it is important to ensure that the hip is not externally rotated or flexed as this can bring the sciatic nerve closer to the site of portal insertion.

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L4

L2 A4

A3

A5 L5

A1 A6

F3 F2

A2

F4

F5

F1 L1

F6

Fig. 34.1  Line diagram showing Ilizaliturri geographic zone method for describing intra-articular pathology in hip arthroscopy. A1–6 (acetabulum), F1–6 (femoral head), and L1–5 (labrum zones)

Once access to the hip has been gained, a diagnostic arthroscopy is performed to evaluate the hip joint and therapeutic procedures carried out based on these findings. Describing an accurate documentation of chondral lesions in the hip is important. Using a clock face method can be confusing. Ilizaliturri et al. have described and validated an alternative method (Fig. 34.1). His method uses the anatomical landmarks of the acetabular fossa, fovea, and insertion of the ligamentum teres. The acetabulum is divided into six zones using the acetabular fossa as a landmark (A6) and femoral head based on the ligamentum teres insertion (F6). Various techniques can be utilized in the management of chondral lesions in the hip joint. Chondral lesions on both the femoral head and acetabulum can be targeted. Some of these techniques are described below. The techniques can essentially be divided into repair or restoration types. Repairing chondral lesions is challenging due to the anatomic constraints that the hip gives and therefore the literature supporting its use is limited.

Microfracture Including Transchondral Microfracturing Microfracturing is a well-established marrow-stimulating procedure. Subchondral bone releases multipotent cells, platelets, and growth factors that can create a fibrin clot. The fibrin clot created through this process eventually remodels into fibrocartilage. Unfortunately the majority of this new fibrocartilage is made up from type 1 rather than type 2 collagen, which is of poorer quality and does not have the same survival time. The indications for hip microfracture are generally isolated lesions