Insights into Avascular Necrosis of the Femoral Head: Learning for the Trainees and Professionals [1st ed. 2023] 9819913454, 9789819913459

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Insights into Avascular Necrosis of the Femoral Head Learning for the Trainees and Professionals

Prasoon Kumar Sameer Aggarwal Vishal Kumar Editors

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Insights into Avascular Necrosis of the Femoral Head

Prasoon Kumar  •  Sameer Aggarwal Vishal Kumar Editors

Insights into Avascular Necrosis of the Femoral Head Learning for the Trainees and Professionals

Editors Prasoon Kumar Department of Orthopaedics PGIMER Chandigarh, India

Sameer Aggarwal Department of Orthopaedics PGIMER Chandigarh, India

Vishal Kumar Department of Orthopaedics PGIMER Chandigarh, India

ISBN 978-981-99-1345-9    ISBN 978-981-99-1346-6 (eBook) https://doi.org/10.1007/978-981-99-1346-6 © The Editor(s) (if applicable) and The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2023 This work is subject to copyright. All rights are solely and exclusively licensed 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, expressed 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 Singapore Pte Ltd. The registered company address is: 152 Beach Road, #21-01/04 Gateway East, Singapore 189721, Singapore

For my son Kiyaan, my wife Tanu, and my parents. —Dr Prasoon Kumar

Foreword

Despite advances in modern surgical methods and techniques, avascular necrosis (AVN) of the femoral head still debilitates many young individuals worldwide; this was highlighted in the press too, during and after the recent COVID pandemic as many new cases emerged due to excessive steroid use. As orthopedic surgeons, we are all too familiar with the challenges presented by AVN and the significant impact it has on young patients’ lives. It is with great pleasure that I introduce this outstanding book, Insights into Avascular Necrosis of the Femoral Head: Learning for the Trainees and Professionals, edited by Dr. Prasoon Kumar, Prof. Sameer Aggarwal, and Dr. Vishal Kumar, who have worked with and have evolved into authorities on the subject from the Postgraduate Institute of Medical Education and Research (PGIMER), Chandigarh. The editors have harnessed the talents of a diverse group of authors, and it seems to have been a remarkable journey to compile this comprehensive resource. Their collective expertise, dedication, and commitment are noted in every chapter, making this book an invaluable asset for both trainees and professionals in the field of orthopedics. The volume provides a wealth of knowledge and practical insights that will enhance the understanding and management of this challenging condition. With 17 meticulously crafted chapters, this book covers a wide array of topics related to AVN of the femoral head. The authors, all young and accomplished orthopedic surgeons from various institutions, have contributed their unique perspectives and experiences, enriching the content with a broad range of clinical insights. Insights into Avascular Necrosis of the Femoral Head addresses various aspects of the condition, including its etiology, pathogenesis, diagnostic modalities, and treatment strategies. Each chapter is a meticulous exploration of a subject, backed by evidence-based research and clinical expertise. The editors have ensured that the content is both easy reading and informative, making it a valuable resource for professionals at all stages of their careers. This multidimensional perspective not only enriches the content but also reflects the dynamic and evolving nature of the field.

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Foreword

This book is not only an invaluable resource for trainees and professionals but also a testament to the power of collaboration and the potential of collective knowledge. It serves as a guiding light for individuals seeking to expand their understanding of avascular necrosis of the femoral head and refine their clinical skills. The editors and authors have set a high standard for future generations to aspire to, as they work towards further advancements in the field of orthopedics. I commend Dr. Prasoon Kumar, Dr. Sameer Aggarwal, Dr. Vishal Kumar, and their team of talented authors for this remarkable effort in compiling this comprehensive resource. Their commitment to advancing knowledge and improving patient care is evident in every page of this exceptional book. I have no doubt that Insights into Avascular Necrosis of the Femoral Head: Learning for the Trainees and Professionals will have a lasting impact on the medical community. Mandeep S. Dhillon Department of Orthopaedics and PMR PGIMER Chandigarh, India

Preface

Avascular necrosis of the femoral head is a challenging and multifaceted condition that affects individuals across all age groups. As orthopedic surgeons, we are constantly driven to enhance our understanding and management of this complex disorder to provide the best possible care for our patients. It is with great pleasure that we present this comprehensive book, Insights into Avascular Necrosis of the Femoral Head: Learning for the Trainees and Professionals, expertly edited by the three of us esteemed colleagues from the Postgraduate Institute of Medical Education and Research (PGIMER), Chandigarh. This book is the culmination of our collective efforts to compile the latest advancements, practical insights, and evidence-based knowledge related to avascular necrosis of the femoral head. Our aim is to provide a comprehensive resource that caters to both trainees seeking to deepen their understanding and professionals looking to stay updated with the evolving landscape of this condition. Each of the 17 chapters offer a meticulous exploration of the subject matter, supported by current research and the extensive clinical experiences of our esteemed contributors. The young orthopedic surgeons, who have authored the 17 chapters, have been instrumental in enriching the content with their unique perspectives, innovative approaches, and diverse experiences, making this book a well-rounded resource. We have strived to strike a balance between academic rigor and clinical applicability. Our intent is to equip readers with practical insights that can be readily translated into their daily clinical practice. We have emphasized the importance of evidence-based medicine, providing a strong foundation for decision-making, while acknowledging the need for individualized treatment approaches based on patient characteristics and preferences. Furthermore, we have incorporated numerous case illustrations, and clinical scenarios throughout the book to facilitate a deeper understanding of avascular necrosis. These real-life examples aim to bridge the gap between theory and practice, enabling readers to navigate the intricacies of this condition with confidence. We are indebted to all the authors who have contributed their expertise and time to bring out the chapters. Their dedication, passion, and commitment to advancing the field of orthopedics are truly commendable. It is their collective efforts that have made this book a valuable resource for trainees, professionals, and researchers alike.

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Preface

We extend our gratitude to the team at Springer Nature, whose unwavering support and guidance have been instrumental in bringing this project to fruition. Their expertise and commitment to excellence have ensured that this book meets the highest standards of quality and serves as a reliable reference for the medical community. As editors, we hope that Insights into Avascular Necrosis of the Femoral Head: Learning for the Trainees and Professionals proves to be an invaluable resource for all those seeking to enhance their knowledge and skills in managing avascular necrosis. It is our sincere desire that this book empowers readers to provide the best possible care to patients affected by this challenging condition. We would like to express our deepest gratitude to our families, friends, and mentors who have supported us throughout this journey. Their unwavering encouragement and understanding have been crucial in accomplishing this endeavor. Finally, we dedicate this book to all the patients who have battled avascular necrosis of the femoral head. Their resilience, strength, and trust in our abilities continue to inspire us to strive for excellence in our pursuit of better treatment options and improved outcomes. Chandigarh, India Chandigarh, India Chandigarh, India

Prasoon Kumar Sameer Aggarwal Vishal Kumar

Contents

1

 emoral Head: Anatomical Considerations��������������������������������������������   1 F Chiman Kumari and Komal Parmar

2

 vascular Necrosis of the Hip: Historical Perspective����������������������������  13 A Mehar Dhillon, Vishal Kumar, and Prasoon Kumar

3

 pidemiology and Risk Factors����������������������������������������������������������������  23 E Pratik M. Rathod, Ankit Dadra, and Prasoon Kumar

4

 tiology and Pathophysiology of AVN������������������������������������������������������  33 E Tarkik Thami and Ankit Dadra

5

 linical Features and Staging of AVN Hip����������������������������������������������  45 C Rajesh Kumar Rajnish and Kuldeep Rathor

6

 vascular Necrosis Hip: How to Examine a Suspected Case����������������  57 A Shahnawaz Khan and Siddhartha Sharma

7

 VN Hip: Radiology��������������������������������������������������������������������������������   75 A Sarthak Sharma and Siddhartha Sharma

8

 reatment Principles: An Overview ��������������������������������������������������������  87 T Mehar Dhillon and Prasoon Kumar

9

Core Decompression����������������������������������������������������������������������������������  99 Sandeep Patel and Akshat Srivastava

10 O  steotomies for Osteonecrosis Hip���������������������������������������������������������� 109 Mohak Kataria and Sameer Aggarwal 11 H  ead Preservation: Recent Advances������������������������������������������������������ 119 Lav Mehta and Ankit Dadra 12 H  ip Arthrodesis: Current Concepts �������������������������������������������������������� 127 Naveen Mittal and Sudhir Kumar Garg 13 Hip Arthroplasty���������������������������������������������������������������������������������������� 135 Ramesh Kalappagol Basappa and Prasoon Kumar

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Contents

14 A  vascular Necrosis of the Hip: Replace or Resurface?�������������������������� 151 Karan Jindal, Vivek Ksheerasagar, and Sameer Aggarwal 15 A  VN Hip: Bedside Case Presentation������������������������������������������������������ 159 Parth Bansal and Vishal Kumar 16 F  requently Asked Viva Questions (AVN Hip)������������������������������������������ 169 Ankit Gaurav and Vishal Kumar 17 Multiple-Choice Questions������������������������������������������������������������������������ 183 Ankit Dadra and Pratik M. Rathod

Editors and Contributors

About the Editors Prasoon  Kumar  is an Assistant Professor of Orthopaedics at PGIMER, Chandigarh. He is a versatile trauma surgeon specializing in the hip, elbow, and wrist. Dr. Kumar has multiple research papers and presentations on avascular necrosis of the hip, along with some ongoing projects on the subject. He is an academician with more than 80 publications and several book chapters.

Sameer  Aggarwal  is a Professor of Orthopaedics at PGIMER, Chandigarh, and is an authority in the field of hip disorders and trauma surgeries. He has been trained for several years through fellowships at centers of repute. He is the nodal officer of the Advanced Trauma Center—a center of excellence for teaching, training, and patient care. He has about 200 publications in peer-reviewed journals of repute and has authored more than twenty chapters in different textbooks on orthopedics, which are well read throughout the globe. He has several authoritative publications on the topic of this book. Vishal  Kumar  is an Associate Professor of Orthopaedics at PGIMER, Chandigarh. He is an academician of international accolades with more than 130 publications; he has editored two books, has written 15 book chapters, and has filed three patents. He has developed, described, and published three indigenous surgical approaches. He has won more than 25 international and national awards based on his exceptional curriculum vitae.

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Editors and Contributors

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Contributors Sameer Aggarwal  Department of Orthopaedics, PGIMER, Chandigarh, India Parth Bansal  Department of Orthopaedics, PGIMER, Chandigarh, India Ankit Dadra  Department of Orthopaedics, PGIMER, Chandigarh, India Mehar Dhillon  Department of Orthopaedics, PGIMER, Chandigarh, India Sudhir Kumar Garg  Orthopaedics, GMCH, Sector-32, Chandigarh, India Ankit Gaurav  Department of Orthopaedics, PGIMER, Chandigarh, India Karan Jindal  Orthopaedics, AIMS, Mohali, India Ramesh  Kalappagol  Basappa  Department Chandigarh, India

of

Orthopaedics,

PGIMER,

Mohak Kataria  Department of Orthopaedics, PGIMER, Chandigarh, India Shahnawaz Khan  Orthopaedics, AIIMS, Bhuvaneshwar, India Vivek Ksheerasagar  Department of Orthopaedics, PGIMER, Chandigarh, India Prasoon Kumar  Department of Orthopaedics, PGIMER, Chandigarh, India Vishal Kumar  Department of Orthopaedics, PGIMER, Chandigarh, India Chiman Kumari  Anatomy, PGIMER, Chandigarh, India Lav Mehta  Department of Orthopaedics, PGIMER, Chandigarh, India Naveen Mittal  Orthopaedics, GMCH, Sector-32, Chandigarh, India Komal Parmar  Anatomy, PGIMER, Chandigarh, India Sandeep Patel  Department of Orthopaedics, PGIMER, Chandigarh, India Rajesh  Kumar  Rajnish  Department of Orthopaedics, All India Institute of Medical Sciences, Jodhpur, India Pratik M. Rathod  Department of Orthopaedics, PGIMER, Chandigarh, India Kuldeep  Rathor  Department of Orthopaedics, All India Institute of Medical Sciences, Jodhpur, India Sarthak Sharma  Jammu Healthcare & Diagnostics Pvt. Ltd., Jammu, Jammu and Kashmir, India Siddhartha Sharma  Department of Orthopaedics, PGIMER, Chandigarh, India Akshat Srivastava  Department of Orthopaedics, PGIMER, Chandigarh, India Tarkik Thami  Department of Orthopaedics, PGIMER, Chandigarh, India

1

Femoral Head: Anatomical Considerations Chiman Kumari and Komal Parmar

1.1 Introduction For dealing with any orthopedic disease, understanding of the normal anatomy and physiology is of paramount importance. In order to gauge the severity of a pathology like avascular necrosis of the hip, we must be aware of the normal structure, vascularity, surface landmarks, and anatomical relations of the femoral head. The present chapter details the relevant anatomy and development of the head of the femur. The femoral head is a component of the proximal end of the femur which forms the hip joint by articulating with the acetabulum (Fig. 1.1a–c). The other components of the proximal end of the femur include the neck and the trochanters. The head represents two-third of a sphere and faces antero-superomedially. It is connected to the shaft through the femoral neck at an inclination (anteversion) that is essential for the free movement of the hip joint. The subcapital sulcus demarcates the head and neck of the femur, which may disappear due to some underlying cause, resulting in a cam deformity, because of its resemblance to a camshaft [1]. The articular margin of the head is sharp all around except in the anterior part where it extends slightly onto the neck. It articulates with the reciprocally concave acetabular cavity of the hip bone to form a multiaxial spheroidal joint, which allows relatively unhindered motion in three degrees of freedom, i.e., flexion/extension, abduction/adduction, and medial/lateral rotation. The acetabular labrum encircles the head distal to the equator and remains within the capsule of the hip joint. The capsule remains attached to the acetabular boundary and the neck in such a way that the head is positioned within a natural suction within the hip joint cavity. A tear in

C. Kumari (*) · K. Parmar Anatomy, PGIMER, Chandigarh, India © The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2023 P. Kumar et al. (eds.), Insights into Avascular Necrosis of the Femoral Head, https://doi.org/10.1007/978-981-99-1346-6_1

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C. Kumari and K. Parmar Neck

a Head

Greater trochanter Intertrochanteric line Lesser trochanter

Shaft

b

Neck

Trochanteric fossa Greater trochanter

Head Fovea capitis femoris Sub-capital sulcus Groove for insertion of obturator externus

Quadrate tubercle

Intertrochanteric crest Lesser trochanter

Gluteal tuberosity

Pectineal line

Shaft

c Trochanteric fossa

Greater trochanter

Nutrient foramina in the neck

Head

Fovea capitis femoris

Fig. 1.1 (a) Proximal end of the left femur, anterior view. (b) Proximal end of the left femur, posterior view. (c) Proximal end of the left femur, superior view

1  Femoral Head: Anatomical Considerations

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the acetabular labrum may lead to the loss of this natural suction seal, and the position of the head may be displaced. The displaced head may cause impingement at the adjacent cartilages. Congenital anomaly in the acetabulum may also dislocate the head of the femur. Proper positioning of the head within the acetabular cavity is an important factor in maintaining the stability of the hip joint [1]. Due to bipedalism, a significant portion of the femoral head lies outside of the acetabular cavity in the neutral position, whereas all the posterior portion and a part of head-neck junction lie within the acetabular cavity [2].

1.2 Articular Surface (Fig. 1.2) The articular surface is smooth and covered by hyaline cartilage. However, the posteroinferior part is interrupted by a rough fovea (fovea capitis) which gives attachment to the ligamentum teres [3]. The articular surface along with the cartilage extends slightly toward the neck anteriorly [4]. This articular hyaline cartilage is thicker in the center and thinner towards the periphery. The thickness of the articular cartilage decreases with age. The articular cartilage is not lined by synovial membrane [5].

Articular surface of acetabulum Ligamentum teres Transverse acetabular ligament Acetabular branch of obturator artery

Artery of ligamentum teres

Femoral head covered with articular cartilage Greater trochanter

Lesser trochanter

Fig. 1.2  Hip joint cavity opened to show ligament of the head of the femur

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1.3 Structure of the Head of the Femur (Fig. 1.3) The head of the femur is walled by thin compact bone, with trabecular bone within the cavity. The marrow cavity within the head consists of red bone marrow. The dimensions of the femoral head vary with gender, stature, and ethnicity [6–8]. The pressure lamellae represented by the trabecular bone within the neck of the femur radiate toward the head and indicate the transmission of pressure along the lines of weight-bearing. These trabeculae are initially fine bony rods with high anisotropy, but as the child starts walking, these become thicker and more separated and gradually the trabeculae become flattened in adult life [9, 10]. These bony plates run perpendicular to the articular surface of the head. The lamellae are arranged in such a manner that they resist both tension and compression forces. These laminae are not straight but are spirally arranged, the direction of which is often taken up by fracture in that region. The vertically arranged primary trabecular compressive group extends from the superior aspect of the capitulum to the inferior border of the neck. The curved trabecular plate extending from the inferior part of the head to the cortical bone just below the greater trochanter constitutes the primary tensile trabecular group. The radiolucent area inferior to the intersection of these two groups of trabeculae constitutes Babcock’s triangle [11, 12] (Fig. 1.3). Primary compressive group

Fovea capitis

Neck

Greater trochanter

Primary tensile group Area for Babcock’s triangle (Appreciated in an X-ray)

Compact bone Medullary cavity within the shaft

Fig. 1.3  Coronal section of proximal end of the right femur (posterior view) showing the trabecular architecture

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Fig. 1.4  Femoral offset (red double arrowhead) is the distance from the center of the femoral head to a line that bisects the long axis of the shaft Centre of the head of femur

Long axis of femur

1.4 Femoral Offset (Fig. 1.4) The geometric center of the femoral head constitutes the center through which the axis of rotation of the hip joint passes. The distance from this point to a line that bisects the long axis of the femur is considered the femoral offset. In normal conditions, the length of the femoral offset varies with age, sex, gender, and ethnicity [13].

1.5 Ligament of the Head of the Femur (Ligamentum Capitis Femoris) (Fig. 1.2) The ligament of the head of the femur is a band of connective tissue which extends from the transverse acetabular ligament and margins of the acetabular notch to the fovea in the head of the femur. This flat triangular ligament has its apex toward the femoral head. The ligament is covered by the synovial sheath. In rare cases, the ligament may be absent with the presence of only the synovial sheath, or both the ligament and the sheath may be absent. The ligament acts as a route for the neurovascular structures to the head of the femur. In a fetus, it may also act as a support to the developing hip joint, while in adults, it acts as secondary functional support to the joint. It is tensed during adduction of the hip joint [1].

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1.6 Femoral Neck The femoral neck (Fig. 1.1a, b) is a constricted region joining the femoral head with the shaft and the trochanters. It provides the attachment site to the distal end of hip joint capsule. The anterior surface of the femoral neck is completely intracapsular as the hip joint capsule attaches to the intertrochanteric line. Posteriorly, the capsule extends little distal to the midpoint of the neck. Beyond the capsular attachment site, the surface of the neck is grooved by the tendon of the obturator externus. The anterior surface may rarely present with facets and fossae covered with the extension of articular cartilage [14]. The femoral neck is surrounded by vascular anastomoses and is dotted by several nutrient foramina (Fig. 1.1c), highlighting its role in the vascularity of the femoral head. The fracture of the femoral neck is one of the most common traumatic causes that leads to the avascular necrosis of the femoral head. The superior surface presents with maximum number of nutrient foramina (3–8 in number) followed by anterior and posterior surfaces (1–3 in number). The nutrient foramina are usually absent from the lower surface [15, 16]. The femoral neck is 4–5 cm long. Under the influence of factors like heredity, mechanical forces, and intrauterine position, the femoral neck and hence the head of the femur lie in a different three-dimensional (D) orientation, when compared to the femoral shaft and condyles. Many parameters have been defined to describe the relationship of the femoral head with the remaining femur. Femoral neck-shaft angle is measured in the coronal plane 2D images, as the angle between the axis of the femoral neck and femoral shaft. It decreases with increase in BMI and shows positive association with height. The femoral neck anteversion angle (FNA) represents the angle between the plane of the femoral neck axis and the coronal plane of distal condylar axis, indicating the degree of twist of the femoral neck with respect to the shaft [17, 18]. In early gestation, the femoral neck axis is parallel to the distal condylar axis. The femoral neck is anteverted by approximately 40° at birth, and the angle decreases gradually as a result of upright posture and walking (10–20°) [18, 19]. Another angle called femoral neck torsion angle (FNTA) has been described as the twist in the femoral neck along its central axis [17]. The current studies describe its value to be around 20–30° [17, 20, 21]. The neck torsion angle is important in determining screw space configuration for internal fixation of femoral neck fractures, screw hole design of the proximal femoral neck plate, and the proximal femoral medullary opening point in the femoral prosthesis placement during hip joint replacement [21].

1.7 Surface Landmark The head of the femur can be marked in the body 2–4 cm superior to the midpoint of a line between the superior margin of the greater trochanter and the pubic tubercle [the greater trochanter of the femur sits on the upper lateral thigh, inferior to the midpoint of the iliac crest and approximately level with a horizontal plane passing through the pubic tubercle] [1].

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1.8 Relations (Fig. 1.5a–c) The anterior surface of the head is separated inferomedially from the femoral artery by the tendon of the psoas major, the iliopectineal bursa, and the articular capsule. A finger on the femoral pulse lies directly over the head of the femur. Superiorly, the head is related to the reflected head of the rectus femoris, while the gluteus medius and minimus cross posteriorly under the cover of the gluteus maximus. Posterior to the femoral head, the piriformis muscle and tendons of the obturator internus with superior and inferior gamelli cross in a mediolateral direction and separate the a Psoas major

Iliacus Inguinal ligament

b Gluteus medius Gluteus munimus Gemellus superior Obturator internus Gemellus inferior

Piriformi Gluteus medius Quadratus femoris

Fig. 1.5 (a) Psoas major and iliacus are anterior to the head of the femur, anterior view. (b) Posterior relation of the head of the femur. (c) Femoral vessels are related anteriorly and sciatic nerve is posterior to the head of the femur

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c

Sciatic nerve Femoral vessels

Fig. 1.5 (continued) Retinacular arteries

Femoral head covered with articular cartilage Fovea capitis Greater trochanter

Ascending branch of lateral circumflex femoral artery

Femoral shaft

Joint Capsule (cut) Medial circumflex femoral artery

Profunda femoris artery Lateral circumflex femoral artery

Fig. 1.6  Blood supply of the head of the femur

sciatic nerve from the capsule of the hip joint. Inferiorly, the femoral head is related to the medial circumflex femoral artery and pectineus, obturator externus, and adductor longus muscles, as they curve toward their insertion onto the femur [1, 22].

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1.9 Vascular Supply (Fig. 1.6) The trochanteric anastomosis is the main source of blood supply to the head of the femur [4]. The vascular supply is contributed by medial and lateral femoral circumflex vessels along with superior and inferior gluteal vessels. These vessels form an arterial ring around the neck of the femur outside the capsular attachment. From this ring, ascending cervical branches pierce the capsule (under zona orbicularis) to lie beneath the reflected synovial membrane. These vessels become the retinacular arteries and form a subsynovial intracapsular anastomosis. This anastomosis may be compromised in fractures of the neck of the femur which in turn may bring ischemic changes in the head of the femur leading to avascular necrosis (AVN). Extracapsular fractures of the neck may spare the ischemic changes in the head as the anastomotic ring remains intact, which in turn gives unhampered blood to the retinacular arteries. In a growing femur, the main source of blood supply to the femoral head is through the retinacular branches of the medial circumflex femoral artery which enter the joint capsule at the level of the trochanteric fossa and ascend the femoral neck posterosuperiorly. Since the growth plate is avascular, these arteries pass around its edge. Any injury may easily lead to a fracture along the growth plate, which represents a line of weakness. Metaphyseal arteries shoot off from the ascending cervical branches, while the medial and lateral epiphyseal arteries arise from the intracapsular arterial ring. In a developing femur, the epiphysial plate separates the territories of the metaphysial and epiphysial vessels. Following the epiphyseal fusion, these vessels anastomose freely with each other. Initially, both the medial and lateral circumflex femoral arteries equally contribute to the arterial ring, but later in the developmental process, the lateral femoral artery diminishes in size, and the major contribution comes from the medial circumflex artery. In children, small epiphyseal arteries from the acetabular branches of the obturator and medial circumflex femoral artery may pass through the ligament of the head of the femur and supply the epiphysis from the medial side [1]. The venous drainage corresponds to that of the arteries. However, posteroinferiorly a single cervical artery may be present [1].

1.10 Nerve Supply The head of the femur has both autonomic and sensory innervations. The periosteum of the head of the femur is supplied by the nerve fibers contributed by the nerves supplying the hip joint and includes the femoral, obturator, accessory obturator (if present), superior gluteal, inferior gluteal, sciatic, nerve to the quadratus femoris, and direct supply from sacral plexus [1]. Hip pain can get referred to the knee owing to the common nerve supply to both the joints.

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Secondary centre for head (around 6 months of age)

Secondary centres appear for the trochanters

Fusion with the shaft

Growth plate

First Year of life

12-14

18-20

Fig. 1.7  Ossification of the head of the femur

1.11 Development (Fig. 1.7) The lower limb bud develops from the somatopleuric mesoderm where endochondral ossification takes place for the formation of the bones. The head of the femur appears during the first 6 months after birth, from the secondary center of ossification. The head of the developing femur is a part of compound epiphysis (the other components being that of the lesser and greater trochanters), which fuses with the rest of the bone by the 14th year in females and the 17th year in males. The epiphysial line follows the articular margin except where it is separated superiorly from the articular surface by a nonarticular area where blood vessels enter the head [1, 22, 23].

1.12 Conclusion An intact normal anatomy of the head of the femur is crucial for proper functioning of the hip joint. Any deviation from this will lead to abnormal gait and will affect the adjacent structures related to the head of the femur. Any hindrance in the vascular supply to the head of the femur will lead to the death of the osteocytes and further necrosis. This will further aggravate the condition.

References 1. Standring S, editor. Gray’s anatomy e-book: the anatomical basis of clinical practice. Elsevier Health Sciences; 2021. 2. Hogervorst T, Vereecke EE.  Evolution of the human hip. Part 1: the osseous framework. J Hip Preserv Surg. 2014;1(2):39–45. https://doi.org/10.1093/jhps/hnu013. PMID: 27011802; PMCID: PMC4765288.

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3. Rosse C, Gaddum-Rosse P.  Hollinshed’s textbook of anatomy. Philadelphia: Lippincott-­ Raven; 1997. p. 314–6. 4. Sinnatamby CS. Last’s anatomy e-book: regional and applied. Elsevier Health Sciences; 2011. 5. Armstrong CG, Gardner DL.  Thickness and distribution of human femoral head articular cartilage. Changes with age. Ann Rheum Dis. 1977;36(5):407–12. https://doi.org/10.1136/ ard.36.5.407. PMID: 921339; PMCID: PMC1000131. 6. Dixon AF. The architecture of the cancellous tissue forming the upper end of the femur. J Anat Physiol. 1910;44(Pt 3):223. 7. Rawal B, Ribeiro R, Malhotra R, Bhatnagar N. Anthropometric measurements to design best-­ fit femoral stem for the Indian population. Indian J Orthop. 2012;46(1):46–53. https://doi. org/10.4103/0019-­5413.91634. PMID: 22345806; PMCID: PMC3270605. 8. Young EY, Gebhart J, Cooperman D, Ahn NU. Are the left and right proximal femurs symmetric? Clin Orthop Relat Res. 2013;471(5):1593–601. https://doi.org/10.1007/s11999-­012-­2704-­x. 9. Ryan TM, Krovitz GE. Trabecular bone ontogeny in the human proximal femur. J Hum Evol. 2006;51(6):591–602. https://doi.org/10.1016/j.jhevol.2006.06.004. Epub 2006 Aug 5. PMID: 16963108. 10. Milovanovic P, Djonic D, Hahn M, Amling M, Busse B, Djuric M. Region-dependent patterns of trabecular bone growth in the human proximal femur: a study of 3D bone microarchitecture from early postnatal to late childhood period. Am J Phys Anthropol. 2017;164(2):281–91. 11. Singh M, Nagrath AR, Maini PS. Changes in trabecular pattern of the upper end of the femur as an index of osteoporosis. J Bone Joint Surg Am. 1970;52(3):457–67. 12. Macchiarelli R, Bondioli L.  Linear densitometry and digital image processing of proximal femur radiographs: implications for archaeological and forensic anthropology. Am J Phys Anthropol. 1994;93(1):109–22. 13. Lecerf G, Fessy MH, Philippot R, Massin P, Giraud F, Flecher X, Girard J, Mertl P, Marchetti E, Stindel E. Femoral offset: anatomical concept, definition, assessment, implications for preoperative templating and hip arthroplasty. Orthop Traumatol Surg Res. 2009;95(3):210–9. 14. Finnegan M, Faust MA. Variants of the femur. In: Research report 14: bibliography of human and non-human, non-metric variation. Anthropology Department Research Reports Series. Amherst, MA: University of Massachusetts Department of Anthropology Research Reports Series; 1974. 15. Mei J, Ni M, Wang G, Jia G, Liu S, Cui X, Jiang C, Wang H, Dai Y, Quan K, Chen R. Number and distribution of nutrient foramina within the femoral neck and their relationship to the retinacula of Weitbrecht: an anatomical study. Anat Sci Int. 2017;92(1):91–7. 16. Kamath V, Gupta C. Morphological study on distribution of nutrient foramina in femoral neck in relation to retinacula of Weitbrecht with its surgical implications. J Orthop. 2022;31:57–60. 17. Kate BR. Anteversion versus torsion of the femoral neck. Acta Anat (Basel). 1976;94(3):457–63. 18. Scorcelletti M, Reeves ND, Rittweger J, Ireland A. Femoral anteversion: significance and measurement. J Anat. 2020;237(5):811–26. 19. Souza AD, Ankolekar VH, Padmashali S, Das A, Souza A, Hosapatna M. Femoral neck anteversion and neck shaft angles: determination and their clinical implications in fetuses of different gestational ages. Malays Orthop J. 2015;9(2):33–6. 20. Zhu Q, Shi B, Xu B, Yuan J. Obtuse triangle screw configuration for optimal internal fixation of femoral neck fracture—an anatomical analysis. Hip Int. 2018;29(1):72–6. 21. Zhang RY, Su XY, Zhao JX, Li JT, Zhang LC, Tang PF.  Three-dimensional morphological analysis of the femoral neck torsion angle—an anatomical study. J Orthop Surg Res. 2020;15(1):192. https://doi.org/10.1186/s13018-­020-­01712-­8. PMID: 32460899; PMCID: PMC7251911. 22. Ellis H.  Clinical anatomy: a revision and applied anatomy for clinical students. Blackwell Publishing Ltd; 2006. p. 12. 23. Schoenwolf GC, Bleyl SB, Brauer PR, Francis-West PH.  Larsen’s human embryology. Elsevier Health Sciences; 2014.

2

Avascular Necrosis of the Hip: Historical Perspective Mehar Dhillon, Vishal Kumar, and Prasoon Kumar

2.1 Introduction Alexander Munro in the year 1738 was the first to describe avascular necrosis (AVN) [1]. In the year 1794, James Russel, a Professor of Clinical Surgery at the University of Edinburgh, published regarding a certain condition of the bone termed as “necrosis,” which was the first description regarding bone necrosis and at that time was solely considered septic in origin [2]. Jean Cruveilhier, a French anatomist between the years 1829 and 1842, recorded the deformation of the femoral head due to vascular damage after traumatic injury and further described the morphogenic changes occurring due to interruption of blood supply [3]. Kragelund in 1886 and Konig in 1888 further published regarding necrosis of the bone as a disease entity [1]. However, it was not until the year 1928 that Axhausen proposed aseptic origin of bone necrosis in the absence of infection [4]. The first case was published by Haemisch in 1925 with an anatomical description given by Freund in 1926 [5]. Chandler emphasized in 1936 the seriousness and common bilateral nature of idiopathic necrosis of the hip terming it as coronary artery disease of the hip [6]. Mankin and Brower in 1962 reported more cases and further emphasized on the bilateral nature of idiopathic AVN hip [7]. The twentieth century witnessed an increased reporting of aseptic necrosis of the bone in deep sea divers primarily, tunnel workers, and patients undergoing corticosteroid therapy, especially in organ transplantation patients. Eventually, by the end of the twentieth century, aseptic necrosis of the hip became one of the leading

M. Dhillon (*) · P. Kumar · V. Kumar Department of Orthopaedics, PGIMER, Chandigarh, India © The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2023 P. Kumar et al. (eds.), Insights into Avascular Necrosis of the Femoral Head, https://doi.org/10.1007/978-981-99-1346-6_2

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1738 Munro first described the condition

M. Dhillon et al.

1794 James Russel described "necrosis" of the bone

1829-1842 Cruveilhier French anatomist published deformation of femoral head

1928 Axhauxen described aseptic origin of necrosis of the bone

1930 Phemister coined the term "aseptic necrosis"

1936 Chandler described "Coronary artery disease of the hip"

Fig. 2.1  Timeline depicting the evolution of the term “avascular necrosis of the hip”

causes of hip pain among osteoarthritis, inflammatory arthritis, and trauma (Fig. 2.1) [8]. In this chapter we aim to further elaborate the historical evolution of various aspects of AVN hip.

2.2 Pathogenesis The term aseptic necrosis of the hip was first coined by Phemister in 1930 as a result of thrombosis or embolism, and contrary to present scenario, it was found to be a rare condition in those days [9]. Ernst Freund was the first to report a case of posttraumatic AVN in 1936 [5]. In 1948 Chandler described coronary artery disease of the hip as idiopathic AVN hip, where most patients had history of prolonged alcohol consumption or treatment history with steroids. He further elaborated it as a type of infarction in the femoral head dominated by bony collapse, due to prolonged anoxemia and depletion of arterial nutrition of the femoral head, leading to degenerative changes and necrosis of the bone. He compared the femoral head with the heart as both contain cells that require continuous oxygenation despite having a different histological origin. The femoral head protrudes into the capsule of the hip joint that is lined by the synovium, just like the heart which is enclosed by the pericardial cavity. The nutrient vessels of each have limited anastomoses and in a sense are end arteries. Coronary disease of the hip depicts inadequate nutrition and disruption of circulation of the cancellous bone of the femoral head and neck. Previously in 1936, he even suggested that effusion of the joint leads to increased joint pressure causing deficiency in the circulation among the synovial folds. The head of the femur loses its inherent ability to resist stresses caused by load bearing, and thus musculature action collapses to a large extent leading to loss of function and increased pain. In cases where the insult to the vasculature is beyond repair, there is progression of degeneration and necrosis [6]. Boettcher et al. in 1970 described a discrepancy between the metabolic requirements of the osteocytes and the ability of the circulatory system to meet those requirements leading to bone death and ultimately aseptic necrosis, which further elaborated on the pathogenesis [10]. The causes leading to AVN were described early on, yet mechanism was found to be uncertain and was not easily explained. The histopathology of the core

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biopsies taken by Ficat and Arlet depicted vascular insult due to increased intraosseous pressure, which was further elaborated and published by Hungerford [11, 12]. Mankin and Brower in 1962 reported five cases of aseptic necrosis of the hip, with bilateral occurrence. They further reported an incidence of 42–60% cases [7]. In 1966 Mccallum and Walder reported incidence of 30.4% among 900 divers, who covered more than 200 m and suffered from decompression sickness at the time of ascending, leading to the occurrence of bony lesions and dysbaric osteonecrosis, indicating disruption of oxygenation as the primary mechanism of action. It was also proposed in fliers who covered high altitudes ascending from atmospheric pressure to hypobaric conditions. Even the oxygen and carbon dioxide can be transported to the lungs, however the nitrogen bubbles are not easily removed and tend to aggregate within the tissue cells, and being five times more fat soluble, they build up an adequate pressure leading to disruption of the flow of the vessels and lead to the formation of intra-arterial gas emboli [13]. First such case was reported by Twynam in 1888. It was not seen on radiology and was not reported until irreversible changes had occurred. Alder in 1978 described dysbaric osteonecrosis of two types—juxta-articular and that occurring in neck or shaft which is asymptomatic [14]. Medical research council in 1971 reported an incidence of 18% for bone lesions with 12% occurring in the femoral head [15]. In 1968 Cruess et al. reported cases of AVN in renal transplantation patients with history of steroid therapy [16]. Glimcher and Kenzora in 1979 elaborated on steroid-­induced AVN due to the hyperlipidimic effects of steroids along with hyperviscosity leading to sludging, which further decreases microvascular blood flow [8].

2.3 Evolution of Classification Systems Ficat and Arlet proposed the first classification of AVN hip in the 1960s based on the changes in the femoral head, before the development of MRI; however it still remains the most widely used classification and not only gives a better understanding about the stages of progression but also helps determine the management and prognosis [17]. In 1985 they also proposed early diagnosis of AVN in patients with hip pain without radiographic changes by measurement of bone marrow pressure. The pressure was recorded by the placement of a cannula in the intertrochanteric region under image guidance, with the normal pressure ranging between 20 and 30 mmHg [18]. Steinberg et al. proposed a seven-stage classification, where authors used radiographs, bone scans, and MR images. They further elaborated on the various changes in the femoral head, based on various imaging techniques, and gave a better understanding of the mechanism and evolution of the condition [19]. The ARCO system (Association Research Circulation Osseous) further improvised on the Ficat and Steinberg staging models; however widespread use was limited due to lack of consensus [20].

16 Fig. 2.2 Classification systems for AVN

M. Dhillon et al.

Ficat & Arlet (femoral head changes before development of MRI)

Steinberg (7 stage based on radiographs,scans and MRI)

ARCO (improvisation of Ficat & Arlet)

Japanese Investigation Committee (MRI changes to classify necrosis based on its location)

The Japanese Investigation Committee classification utilized the MR images to classify the necrosis based on its location, which was ultimately used to quantify the prognosis and progression (Fig. 2.2) [21].

2.4 Treatment Avascular necrosis has remained a problem historically not just in the diagnosis but also in the appropriate management at various stages with the primary goal of preserving the congruity of the joint. However, various treatment modalities in the past have shown subjective results, and hence the treatment has been unpredictable and previously lacked universal consensus. AVN hip depicts a natural history of relentless progression, and thus the main aim of treatment modalities is to halt the progression to maintain joint congruity [22].

2.5 Preservation of the Femoral Head 2.5.1 Core Decompression The history of core decompression as a technique dates back to the times of the Second World War, when Klienberg in 1939 and Bozsan in 1941 described drilling procedure as a method for the replacement of the necrotic bone by creating appropriate paths through which revascularization could take place [23]. Further improvisations of core decompression have occurred over the years. The French surgeons Paul Ficat and Jacques Arlet were among first to identify core decompression as a treatment modality for early stages of AVN hip. They reported relief of symptoms in patients who underwent core biopsy sampling, which further led to their proposed etiology of increased intraosseous pressure in the femoral head, which was incidentally relieved by the core needle biopsy [18].

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David Hungerford was one of the premier surgeons in the United States to use core decompression as a treatment technique for osteonecrosis of the femoral head. He developed the foundation of Centre for Osteonecrosis Education and Research at Johns Hopkins University. This center was devoted to promote the understanding of the etiopathogenesis, diagnosis, and treatment of osteonecrosis by Michael Mont and Dr. Lynne Jones. In 1978 Hungerford and Zizic claimed that by drilling, the high intraosseous pressure was decompressed and pain was relieved. This procedure not only promoted neovascularization but also facilitated the occurrence of creeping substitution in the necrotic degenerative area by drilling channels. Thus, this technique not only provided symptomatic relief but also halted progression. Their combined work reported a 65% success rate in patients undergoing core decompression procedure compared with nonoperative treatment, as well as its evident effectiveness with respect to patients in pre- and post-collapse stages of the femoral head, which made a major difference in the management protocol of the disease stagewise [24]. The original core decompression procedure consisted of the use of a 6- or 8-mm hollow trephine. The technique has evolved over the years and subsequently modernized to include single or multiple channels created by drills and trephines of various diameters [25]. Hernigou and Beaujean published a new improvement of the core decompression technique that advocated the utilization of the bone marrow aspirate from the patient’s iliac crest during the surgery. The aspirate obtained was concentrated after processing and reinserted into the head of the femur that was decompressed. This not only relieved intraosseous pressure but further improved the revascularization of the femoral head. Their study showed that patients with pre-collapse disease who underwent BMAC along with core decompression had a comparatively delayed disease progression and were less likely to undergo conversion to total hip arthroplasty (THA) than the patients who did not undergo BMAC therapy. Those patients with higher Harris Hip Scores (HHS) before operative therapy also had better outcomes emphasizing the importance of intervening at an earlier stage [26, 27]. Gangii et al. further advocated the possible advantages of BMAC in a 5-year prospective controlled double-blind trial (Fig. 2.3) [26–28].

1939-1941 Klienberg & Bozsan first decribed the technique in second world war

1964 Ficat & Arlet advised use in early stages of AVN

1978 Hungerford further improvised the technique

2002 Hernigou described the use of CD+BMAC in AVN

Fig. 2.3  Evolution of development of core decompression to delay the development of AVN of the femoral head

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2.5.2 Grafting In 1915 Albee et al. introduced peg bone into a drill channel, which was earlier used to obtain union of the bone in the femoral neck fractures and was later elaborated by Scheurmann and Phemister for the management of posttraumatic avascular necrosis of the hip in 1949. According to them, the bony pegs not only provided revascularization and union but also acted as structural support to the weakened degenerated head, preventing collapse [29, 30]. Phemister first popularized the use of grafting and developed the concept of creeping substitution of the bone, which was later modified by Bonfiglio (1968) and Boettcher (1970) by the use of cortico-cancellous strut placement in the necrotic segment of the bone after drilling just lower to the level of the greater trochanter through the de-vascularized necrotic segment [31]. Taylor et al. first described the use of free fibular grafts in AVN femoral head, with the use of anastomosis of its nutrient vessel to anterior circumflex vessel in 1975. This technique not only provided structural support but the anastomosis promoted revascularization [32]. Furthermore, the use of muscle pedicle grafts to boost the revascularization came into vogue which were earlier developed in 1962 by Judet and further promoted by Meyers et al. in 1978, where they shared their experience of the use of muscular pedicle bone graft that was reintroduced into a posterior window at the head-neck junction after curetting of the necrotic avascular area and packing it with cancellous bone [8].

2.6 Joint Reconstruction Cup arthroplasty was a previously used treatment modality for hip reconstruction in end-stage disease; however results were not satisfactory due to the collapse of the degenerated avascular head beneath the cup. In 1974 Kerboul et al. elaborated on the “adjusted cup,” which consisted of reaming the femoral head and impacting the cup firmly, rather than allowing the cup to move adequately on the head of the femur. However, they concluded that total hip replacement is the treatment of choice in advanced cases [33]. Sir John Charnley reported a major breakthrough in the 1960s, by introducing the use of polymethyl methacrylate ( PMMA) in total hip arthroplasty, where bone cement functioned as a grout and was used to fix the acetabular and femoral component [34]. Bone cement is a chemical polymer comprising of PMMA, which was first introduced by the chemical industry in 1843 [35]. Themustocles Gluck in 1891 was a German surgeon who first advocated the use of bone cement in replacement sugery [36]. Scales and Herschell in 1945 along with Judet and Judet in 1950 employed PMMA prostheses of the femoral head for arthritis of the hip initially [37]. Although Charnley reported a minute incidence of structural failure at the cement bone interface of just 2.2% in 8 years, other surgeons were unable to replicate such results; this further emphasized the need to maintain the longevity of the

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implants, as total hip replacements in cases of AVN hip were mostly performed in a comparatively younger age group as compared to the conventional arthritic hip. McKee and Watson-Farrar first proposed a model of an uncemented artificial hip with mixed results [38, 39]. The first uncemented implant was approved in 1983 [40]. Bone cement is a viscoelastic polymer which is subjected to long-term stress, fatigue, and subsidence during periods of loading and unloading, however the bone-­ cement interface provides long-term stability in replacement, and thus, there still is continuous debate between superiority of cemented and uncemented total hip replacement over each other, even in today’s era [41].

2.7 Conclusion Necrosis of the bone has been a well-known clinical concept for centuries yet it has taken a long time to correctly define the condition and understand the mechanism of action of the disease stage by stage, by the collaborative efforts of various authors who were ahead of their time. It is only in the last three decades that we have been able to broadly understand the condition. The staging of the disease proposed by Ficat and Arlet was a monumental revelation not fully appreciated in its time but still holds extreme importance. It not only leads to an accepted algorithm to manage the condition but acted as a prognostic indicator to follow the degenerative process. Phemister’s revascularization techniques also still hold true and have further been modernized in today’s era to maintain integrity of the head of the femur in the early stages of the disease. Joint replacement is still the treatment of choice for late stages of AVN hip.

References 1. Jones JP Jr, Engleman EP. Osseous avascular necrosis associated with systemic abnormalities. Arthritis Rheum. 1966;9(5):728–36. 2. Russell J. A practical essay on a certain disease of the bones termed necrosis. Edinburgh: Neil & Co; 1794. 3. Hines JT, Jo WL, Cui Q, Mont MA, Koo KH, Cheng EY, et al. Osteonecrosis of the femoral head: an updated review of ARCO on pathogenesis, staging and treatment. J Korean Med Sci. 2021;36(24):e177. 4. Axhausen G. Über anämische Infarkte am Knochensystem und ihre Bedeutung für die Lehre von den primären Epiphyseonekrosen. Arch Klin Chir. 1928;151:72–98. 5. Freund E. Bilateral aseptic necrosis of the femoral head: problems arising in a compensation case. Ann Surg. 1936;104(1):100. 6. Chandler FA. Coronary disease of the hip. J Int Coll Surg. 1948;11(1):34–6. 7. Mankin HJ, Brower TD. Bilateral idiopathic aseptic necrosis of the femur in adults: “Chandler’s disease”. Bull Hosp Joint Dis. 1962;23:42–57. 8. Nixon JE. Avascular necrosis of bone: a review. J R Soc Med. 1983;76(8):681–92. 9. Phemister DB.  Changes in bones and joints resulting from interruption of circulation: I. General considerations and changes resulting from injuries. Arch Surg. 1940;41(2):436–72. 10. Boettcher WG, Bonfiglio M, Smith K.  Non-traumatic necrosis of the femoral head. II. Experiences in treatment. J Bone Joint Surg Am. 1970;52:322–9.

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11. Arlet J, Ficat C. Ischemic necrosis of the femoral head. Treatment by core decompression. J Bone Joint Surg Am. 1990;72(1):151–2. PMID: 2295665. 12. Hungerford DS. Core decompression of the femoral head for osteonecrosis. J Bone Joint Surg Am. 1988;70(3):474–5. PubMed PMID: 3346279. 13. McCallum RI, Walder DN, Barnes R, Catto ME, Davidson JK, Fryer DI, Golding FC, Paton WD. Bone lesions in compressed air workers: with special reference to men who worked on the Clyde tunnels 1958 to 1963. J Bone Joint Surg Br. 1966;48(2):207–35. 14. Aseptic bone necrosis in commercial divers. A report from the Decompression Sickness Central Registry and Radiological Panel. Lancet. 1981;2(8243):384–8. 15. Medical Research Council. Decompression Sickness Panel. Br J Ind Med. 1971;28:1–21. 16. Cruess RL, Blennerhassett J, MacDonald FR, MacLean LD, Dossetor J. Aseptic necrosis following renal transplantation. JBJS. 1968;50(8):1577–90. 17. Ficat RP. Idiopathic bone necrosis of the femoral head: early diagnosis and treatment. J Bone Joint Surg Br. 1985;67:3–9. 18. Ficat RP, Arlet J. Forage-biopsie de la tete femorale dans I’osteonecrose primative. Observations histo-pathologiques portant sur huit forages. Rev Rhum. 1964;31:257–64. 19. Steinberg ME, Hayken GD, Steinberg DR. A quantitative system for staging avascular necrosis. J Bone Joint Surg Br. 1995;77(1):34–41. PMID: 7822393. 20. Gardeniers JW. A new international classification of osteonecrosis of the ARCO Committee on terminology and classification. J Jpn Orthop Assoc. 1992;66:18–20. 21. Kuroda Y, Tanaka T, Miyagawa T, Kawai T, Goto K, Tanaka S, Matsuda S, Akiyama H. Classification of osteonecrosis of the femoral head: who should have surgery? Bone Joint Res. 2019;8(10):451–8. 22. Lee CK, Hansen HT, Weiss AB. The “silent hip” of idiopathic ischemic necrosis of the femoral head in adults. J Bone Joint Surg Am. 1980;62(5):795–800. 23. Kleinberg S. Aseptic necrosis of the femoral head following traumatic dislocation: report of two cases. Arch Surg. 1939;39(4):637–46. 24. Hungerford DS, Zizic TM. Alcoholism associated ischemic necrosis of the femoral head: early diagnosis and treatment. Clin Orthop. 1978;130:144. 25. Hougaard K, Kuur E. Femoral head avascular necrosis: MR imaging with clinical-pathologic and 99mTc-SN-pyrophosphate scanning. Injury. 1988;19:389–92. 26. Hernigou P, Beaujean F. Treatment of osteonecrosis with autologous bone marrow grafting. Clin Orthop Relat Res. 2002;405:14–23. 27. Sen RK, Tripathy SK, Aggarwal S, Marwaha N, Sharma RR, Khandelwal N. Early results of core decompression and autologous bone marrow mononuclear cells instillation in femoral head osteonecrosis: a randomized control study. J Arthroplast. 2012;27(5):679–86. 28. Gangji V, De Maertelaer V, Hauzeur JP. Autologous bone marrow cell implantation in the treatment of non-traumatic osteonecrosis of the femoral head: five year follow-up of a prospective controlled study. Bone. 2011;49(5):1005–9. 29. Albee FH. The bone graft peg in the treatment of fractures of neck of femur: author’s technic. Ann Surg. 1915;62(1):85. 30. Phemister DB. Treatment of the necrotic head of the femur in adults. JBJS. 1949;31(1):55–66. 31. Boettcher WG, Bonfiglio M, Hamilton HH, Sheets RF, Smith K. Non-traumatic necrosis of the femoral head: Part I. Relation of altered hemostasis to etiology. JBJS. 1970;52(2):312–21. 32. Taylor GI, Miller GD, Ham FJ. The free vascularized bone graft. A clinical extension of microvascular techniques. Plast Reconstr Surg. 1975;55(5):533–44. 33. Kerboul M, Thomine J, Postel M, d’Aubigné RM. The conservative surgical treatment of idiopathic aseptic necrosis of the femoral head. J Bone Joint Surg Br. 1974;56(2):291–6. 34. Charnley J. Anchorage of the femoral head prosthesis to the shaft of the femur. J Bone Joint Surg Br. 1960;42(1):28–30. 35. Soleymani Eil Bakhtiari S, Bakhsheshi-Rad HR, Karbasi S, Tavakoli M, Hassanzadeh Tabrizi SA, Ismail AF, Seifalian A, RamaKrishna S, Berto F. Poly (methyl methacrylate) bone cement, its rise, growth, downfall and future. Polym Int. 2021;70(9):1182–201.

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36. Hernigou P. Earliest times before hip arthroplasty: from John Rhea Barton to Themistocles Glück. Int Orthop. 2013;37(11):2313–8. 37. Webb JC, Spencer RF. The role of polymethylmethacrylate bone cement in modern orthopaedic surgery. J Bone Joint Surg Br. 2007;89(7):851–7. 38. Charnley J. Low friction arthroplasty of the hip: theory and practice. Springer; 2012. 39. McKee GK, Watson-Farrar J. Replacement of arthritic hips by the McKee-Farrar prosthesis. J Bone Joint Surg Br. 1966;48(2):245–59. 40. McLaughlin JR, Lee KR. Uncemented total hip arthroplasty with a tapered femoral component: a 22-to 26-year follow-up study. Orthopedics. 2010;33(9):639. 41. Lee C. The mechanical properties of PMMA bone cement. In: The well-cemented total hip arthroplasty. Berlin: Springer; 2005. p. 60–6.

3

Epidemiology and Risk Factors Pratik M. Rathod, Ankit Dadra, and Prasoon Kumar

3.1 Introduction Avascular necrosis of the hip (AVN) is one of the most common hip pathologies majorly affecting the working age population [1]. It is one of the leading indications for total hip arthroplasties all over the world [1–4]. It is important to know the epidemiology and risk factors of this disease so as to identify and diagnose it early, when native joint salvage is possible. The present chapter describes these aspects of AVN.

3.2 Epidemiology Incidence of AVN is anywhere between 20,000 and 30,000 cases every year. This high incidence is the cause of the vast numbers of arthroplasties in the developed countries like the United States [1]. In the United States of America, around 250,000 total hip arthroplasties are done due to AVN hip [2] (Fig. 3.1). Men are more commonly affected when compared to women. Overall, the average age of the patients is between 35 and 50 years, and the most common reasons for AVN are trauma, chronic alcohol consumption, and steroid administration [3, 4]. Looking at the Indian scenario, Harsh Vardhan et al., in their study on 382 AVN hips from the northern part of the country, revealed that men formed most cases with five times more incidence than their female counterparts. Moreover, the average age of the patients suffering from AVN hip was 34  years in their series, which is

P. M. Rathod (*) · A. Dadra · P. Kumar Department of Orthopaedics, PGIMER, Chandigarh, India © The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2023 P. Kumar et al. (eds.), Insights into Avascular Necrosis of the Femoral Head, https://doi.org/10.1007/978-981-99-1346-6_3

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Normal hip with its blood supply. The black lines of femur head show congruent joint.

AVN hip with collapsing head. Dotted lines represent the previously congruent joint. The head is collapsing due to AVN

Fig. 3.1  Diagrammatic representation of normal (left) vs AVN hip (right)

comparable to the average mean in the studies done in other parts of the world. The most common cause of atraumatic AVN in the Indian population is steroid administration, followed by idiopathic causes and chronic alcoholism [5]. In India, AVN has also been shown as the leading indication for performing a total hip arthroplasty, among all hip pathologies [6] (Fig. 3.1). In Japan, every year, nearly 2200 new patients are diagnosed with AVN hip; the most common cause is steroid intake, followed by chronic alcoholism [7]. The number of females affected is more than the Indian scenario, with reported sex ratio being 5:4; the mean age of 40 years is also slightly more [7]. Similarly, in epidemiological studies in China, the preponderance of AVN was higher significantly in males than females (2.4 times). The common attributable causes were alcohol and steroids. The mean age of the patients has been reported to be 50 years in the Chinese [8].

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Overall nontraumatic AVN hip is a disease of the young to middle-aged population mostly affecting males, with steroids and alcohol as the prominent causes along with the idiopathic variety.

3.3 Risk Factors for AVN Hip 3.3.1 Non-modifiable Risk Factors 3.3.1.1 Age AVN is a disease of the relatively young. When avascular necrosis occurs in the pediatric age group, it is termed “Legg-Calve disease/Perthes disease.” From the available epidemiological data (Table 3.1), the mean/median age group of the adult patients suffering from AVN ranges from 35 to 50 years [9]. This vital age group is the working population of any civilization; therefore, it has a direct detrimental economic impact on the country’s growth. Looking at the vast prevalence, osteonecrosis of femoral head (ONFH) is one of the leading causes of disability among the active working population. Sometimes, age can also help in knowing the associated cause/risk factor of AVN in a particular patient; Steinberg et al. in their epidemiological studies highlighted that younger patient suffered more from steroid and alcohol-induced AVN, whereas the older patients mostly have AVN due to idiopathic causes [1]. 3.3.1.2 Genetic Predisposition Multiple studies have shown a predominant link between genetic polymorphism and AVN of the hip [10, 11]. It is a well-known fact that all people consuming alcohol or steroids don’t end up having AVN hip. That’s why there have been numerous research on the single nucleotide polymorphisms (SNPs), which may be the critical factor having impact on actual incidence of AVN hip in patients with these risk factors. Some of the common genes that have been shown to undergo SNP and cause AVN are: • PPARγ, RUNX2, COL2A1, IGFBP3 • NFATC1, SOX-9 Table 3.1  Regional differences and similarities Geographical region Western world India China Japan

Incidence/prevalence 10,000–20,000 per year – 8.2 million cases above the age of 15 2200 per year

Mean age 30–60 years 34 50

Male-tofemale ratio – 5:1 2.4:1

Common cause Alcohol, steroids Steroids, alcohol Alcohol, steroids

40

5:4

Steroids, alcohol

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• MMP2, MMP10 • NOS3, ABCB1, and IL23R • PAI-1 SNPs of the gene vary according to the demographic profile and race; some of the SNPs have been found to be protective against AVN, while some SNPs have role in causing AVN hip [11].

3.3.1.3 Race Races of African descent who commonly have sickle cell anemia are predisposed to suffer from AVN hip due to disturbance in the microcirculation of the femoral head. Few parts of India, like Sindh and regions around Madhya Pradesh, have a greater number of patients suffering from sickle cell anemia (also known as sickle cell belt of India) and commonly report higher numbers of AVN hip cases [12].

3.3.2 Modifiable Risk Factors 3.3.2.1 Substance Abuse • Alcohol • Although alcohol has been widely associated with causing ONFH, the exact amount of dose causing AVN hip is unknown. An epidemiological study conducted in Japan showed that occasional alcohol consumption had 3.2 odds of developing AVN hip and regular alcohol consumption had 13.2-time odds of causing AVN hip [13]. Matsuo et al. showed that consumption of more than 400 mL/320 g per week had a ten times greater risk of developing AVN hip [14] (Fig. 3.2). Fig. 3.2 Common substance abuse causing AVN hip

Increased lipogenesis

Decreased Osteogenesis

AVN

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• Smoking • Smoking is a controversial risk factor which is inconclusively described as contributor to the occurrence of AVN hip. A recent meta-analysis by Wen et  al., which included seven case-control studies, showed that active smokers were at a higher risk for developing AVN. They also showed that even the former smokers who might have quit the addiction were at a heightened risk for developing AVN hip. Heavy smokers (>20 pack-years) were shown to be at a higher risk of developing AVN with odds of 2.26 times to nonsmokers [15] (Fig. 3.2). • Unapproved Supplements for Weight Gain • A recent observational study from Iran has shown that unapproved weight-­ gaining supplements that youngsters usually take to boost their weight or body mass have led to an increase in AVN cases among individuals with no other risk factors for AVN.  They also reiterated that educational programs must be run to make the youth aware of such side effects due to these supplements [16] (Fig. 3.2).

3.3.2.2 Drug Intake • Steroids • Harvey Cushing was one of the first to recognize the adverse effects of steroids on bone health as early as the 1930s. With time, the evidence supporting the same has increased manifolds [17]. Steroids have been proven to be one of the leading causes of AVN hip across the world, being administered as a treatment modality for a wide spectrum of diseases. Chronic use of steroids leads to decreased osteogenesis and increased lipogenesis. Thus, it disturbs the normal bony homeostasis (Fig. 3.2). • Steroids, though, have been attributed to causing osteonecrosis; it is yet to be ascertained whether the disease is cumulative dose-dependent, duration-­ dependent, or maximum dose-dependent. Steroids are approved for infections and allergies in the form of creams and sprays. Thus, it is vital to identify those at risk for developing AVN.  The incidence of steroid-induced AVN is nearly 20,000 per year in the United States alone. Seventy-five percent of these patients are aged between 30 and 60 [18]. Regarding the dose of steroids causing AVN, Massardo et  al. in 1992 found that more than 40  mg of prednisone per day increases chances of AVN hip [19]. • Patients exposed to a high dose of steroids with a more extended treatment period in immunosuppression therapy are at the highest risk. At the same time, there have been reports of AVN in patients who have had a short treatment period as well; pulse therapy for SLE has shown to make patients more prone for AVN hip. • Overall although steroids are detrimental for femoral head vascularity, exact dose, duration, and quantity are still unclear, and the pathology may vary on individual susceptibility where in other non-modifiable factors may play some role, as discussed in the previous section. • Protease Inhibitors (Antiretroviral Drugs)

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• Hyperlipidemia and peripheral lipodystrophy are known complications of protease inhibitors. These, when given as therapy for HIV, have been linked to causing AVN of the hip and shoulders [20].

3.3.2.3 Autoimmune Disease In autoimmune diseases like SLE and RA, steroids are the mainstay treatment to avoid flares of the disease which affect multiple joints and systems. But this cumulative dose may again lead to AVN in the hip and other body parts [19]. 3.3.2.4 Trauma The most common cause of AVN hip is trauma. Fractures of the femoral neck or head cause disruption of the blood supply of the femoral head by damaging deep branches of MCFA (medial circumflex femoral artery) and other contributory branches, leading to sequential death of bone cells in the subchondral part of the femoral head, ultimately leading to AVN hip [21] (Fig. 3.3). 3.3.2.5 Metabolic Disorders • Gauchers: It’s a lipid storage disorder and, consequently, can cause lipids to accumulate in various parts of the body, including the bone marrow, and cause disturbance in bone homeostasis, causing AVN hip [22]. • Hypercholesterolemia: Hyperlipidemia causes occlusion of the microvasculature and can cause AVN. • Pregnancy: Transient osteoporosis of the hip is an uncommon condition seen in pregnant females in the third trimester. It is a self-limiting disease but can progress to fractures or full-blown AVN. AVN primarily in pregnancy is rare but may be seen, and it is essential to differentiate it from transient hip osteoporosis, as many signs and symptoms overlap between the two. The cause for AVN is not entirely known and may be due to the hypercoagulable state and may need early surgical intervention [23]. Fig. 3.3 Diagrammatic representation of the blood supply of femoral head which gets affected in traumatic cases (MCFA)

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• Cushing’s: Secondary increase in the level of sterols in the body can cause an imbalance in the microcirculation of the femoral head and cause AVN hip.

3.3.2.6 Irradiation Irradiation can have a stochastic and non-stochastic relationship with the causation of the AVN hip. But the theory existing behind AVN secondary to irradiation is that it obliterates the nutrition to the bone, causes direct destruction of osteoblasts, and impairs the repair/regenerative process needed to maintain the bone homeostasis. But it’s unclear why only a few exposed people develop the disease while others don’t, and again the role of non-modifiable and genetic factors may play an additional role [24]. 3.3.2.7 Dysbaric Diseases This results from long-term subclinical decompression sickness; as a deep sea diver resurfaces, arterial gas emboli form, which may subsequently occlude the vasculature of the femoral head, leading to venous thrombosis and increased venous congestion. This increases intraosseous pressure and can thereby impede the arterial flow and cause bone necrosis [25]. 3.3.2.8 Hematological Some hematological diseases like sickle cell anemia, thalassemia, polycythemia, and hemophilia may cause AVN. It is due to increased venous congestion due to its sluggish flow (increased viscosity of blood due to abnormal cells). This causes injury to the existing vascular supply of the femoral head leading to the cell death and subsequent collapse of the femoral head. Myeloproliferative disorders, too, are proven risk factors to cause AVN hip [26].

3.4 Conclusion Understanding epidemiology and associated risk factors of AVN help in the identification and diagnosis of AVN in the early stages or prevent the complications arising out of advanced disease. Identification in the early stages can lead to hip joint salvage and give an active life to the patient which would otherwise not be possible with a total hip replacement. Additionally, this aspect can aid in lifestyle modifications and developing screening strategies for the high-risk populations.

References 1. Steinberg ME, Steinberg DR. Osteonecrosis: historical perspective. In: Koo KH, Mont MA, Jones LC, editors. Osteonecrosis. Heidelberg: Springer; 2014. p. 3–15. 2. Moya-Angeler J, Gianakos AL, Villa JC, Ni A, Lane JM. Current concepts on osteonecrosis of the femoral head. World J Orthop. 2015;6(8):590–601. 3. Sakaguchi M, Tanaka T, Fukushima W, Kubo T, Hirota Y, et al. Idiopathic ONF Multicenter Case-Control Study Group. Impact of oral corticosteroid use for idiopathic osteonecrosis

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of the femoral head: a nationwide multicenter case-control study in Japan. J Orthop Sci. 2010;15:185–91. 4. Mont MA, Jones LC, Hungerford DS. Nontraumatic osteonecrosis of the femoral head: ten years later. J Bone Joint Surg Am. 2006;88:1117–32. 5. Vardhan H, Tripathy SK, Sen RK, Aggarwal S, Goyal T. Epidemiological profile of femoral head osteonecrosis in the North Indian population. Indian J Orthop. 2018;52(2):140–6. https:// doi.org/10.4103/ortho.IJOrtho_292_16. 6. Kumar P, Sen RK, Aggarwal S, Jindal K. Common hip conditions requiring primary total hip arthroplasty and comparison of their post-operative functional outcomes. J Clin Orthop Trauma. 2020;11(Suppl 2):S192–5. https://doi.org/10.1016/j.jcot.2019.02.009. Epub 2019 Feb 10. 7. Kubo T, Ueshima K, Saito M, Ishida M, Arai Y, Fujiwara H. Clinical and basic research on steroid-induced osteonecrosis of the femoral head in Japan. J Orthop Sci. 2016;21(4):407–13. https://doi.org/10.1016/j.jos.2016.03.008. Epub 2016 Apr 6. 8. Zhao DW, Yu M, Hu K, Wang W, Yang L, Wang BJ, Gao XH, Guo YM, Xu YQ, Wei YS, Tian SM, Yang F, Wang N, Huang SB, Xie H, Wei XW, Jiang HS, Zang YQ, Ai J, Chen YL, Lei GH, Li YJ, Tian G, Li ZS, Cao Y, Ma L. Prevalence of nontraumatic osteonecrosis of the femoral head and its associated risk factors in the Chinese population: results from a nationally representative survey. Chin Med J (Engl). 2015;128(21):2843–50. 9. Petek D, Hannouche D, Suva D.  Osteonecrosis of the femoral head: pathophysiology and current concepts of treatment. EFORT Open Rev. 2019;4(3):85–97. https://doi. org/10.1302/2058-­5241.4.180036. 10. Song Y, Du ZW, Yang QW, Ren M, Wang QY, Wang A, et al. Association of genes variants in RANKL/RANK/OPG signaling pathway with the development of osteonecrosis of the femoral head in Chinese population. Int J Med Sci. 2017;14(7):690–7. 11. Kumar P, Rathod PM, Aggarwal S, Patel S, Kumar V, Jindal K. Association of specific genetic polymorphisms with atraumatic osteonecrosis of the femoral head: a narrative review. Indian J Orthop. 2022;56(5):771–84. https://doi.org/10.1007/s43465-­021-­00583-­3. 12. Serjeant GR, Ghosh K, Patel J. Sickle cell disease in India: a perspective. Indian J Med Res. 2016;143(1):21–4. https://doi.org/10.4103/0971-­5916.178582. 13. Hirota Y, Hirohata T, Fukuda K, Mori M, Yanagawa H, Ohno Y, Sugioka Y. Association of alcohol intake, cigarette smoking, and occupational status with the risk of idiopathic osteonecrosis of the femoral head. Am J Epidemiol. 1993;137(5):530–8. https://doi.org/10.1093/ oxfordjournals.aje.a116706. 14. Matsuo K, Hirohata T, Sugioka Y, et  al. Influence of alcohol intake, cigarette smoking, and occupational status on idiopathic osteonecrosis of the femoral head. Clin Orthop. 1988;234:115–23. 15. Wen Z, Lin Z, Yan W, Zhang J. Influence of cigarette smoking on osteonecrosis of the femoral head (ONFH): a systematic review and metaanalysis. Hip Int. 2017;27(5):425–35. https://doi. org/10.5301/hipint.5000516. Epub 2017 May 29. PMID: 28574127. 16. Mortazavi SMJ, Moharrami A, Shafiei H, Ebrahimzadeh MH, Karimi M. Unapproved weight gain supplement as a cause of avascular necrosis: a cautionary report. Arch Bone Jt Surg. 2019;7(6):561–5. PMID: 31970262; PMCID: PMC6935523. 17. Assouline-Dayan Y, Chang C, Greenspan A, Shoenfeld Y, Gershwin ME.  Pathogenesis and natural history of osteonecrosis. Semin Arthritis Rheum. 2002;32:94–124. 18. D’Aubigne RM, Frain PG. Theory of osteotomies. Rev Chir Orthop Reparatrice Appar Mot. 1972;58:159–67. 19. Massardo L, Jacobelli S, Leissner M, Gonzalez M, Rivero L, Villarroel S. High-dose intravenous methylprednisolone therapy associated with osteonecrosis in patients with systemic lupus erythematosus. Lupus. 1992;1:401–5. 20. Reddy R, Daftary MN, Delapenha R, Dutta A, Oliver J, Frederick W. Avascular necrosis and protease inhibitors. J Natl Med Assoc. 2005;97(11):1543–6. 21. Trueta I, Harrison MHM. The normal vascular anatomy of the femoral head in adult man. J Bone Joint Surg. 1953;35B:442–61.

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22. Linari S, Castaman G. Clinical manifestations and management of Gaucher disease. Clin Cases Miner Bone Metab. 2015;12(2):157–64. https://doi.org/10.11138/ccmbm/2015.12.2.157. Epub 2015 Oct 26. 23. Mouchantaf ME, Freiha KF, Moussa MK, Asfour AH, Yahchouchi C, Moussallem CD. Hip avascular necrosis in a healthy pregnant woman: a case report and review of literature. Int J Surg Case Rep. 2021;85:106197. https://doi.org/10.1016/j.ijscr.2021.106197. Epub 2021 Jul 15. 24. Daoud AM, Hudson M, Magnus KG, Huang F, Danielson BL, Venner P, Saluja R, LeGuerrier B, Daly H, Emmenegger U, Fairchild A. Avascular necrosis of the femoral head after palliative radiotherapy in metastatic prostate cancer: absence of a dose threshold? Cureus. 2016;8(3):e521. https://doi.org/10.7759/cureus.521. PMID: 27081582; PMCID: PMC4829398. 25. White TC, Davis DD, Cooper JS. Dysbaric osteonecrosis. In: StatPearls. Treasure Island (FL): StatPearls Publishing; 2022. PMID: 29493935. 26. Rezus E, Tamba BI, Badescu MC, Popescu D, Bratoiu I, Rezus C. Osteonecrosis of the femoral head in patients with hypercoagulability-from pathophysiology to therapeutic implications. Int J Mol Sci. 2021;22(13):6801. https://doi.org/10.3390/ijms22136801. PMID: 34202897; PMCID: PMC8268880.

4

Etiology and Pathophysiology of AVN Tarkik Thami and Ankit Dadra

4.1 Introduction Avascular necrosis of the femoral head (aka Chandler’s disease) is a disorder characterized by disruption of the blood supply of the head due to any cause which can broadly be divided into traumatic and nontraumatic etiologies. It had been described as coronary artery disease of the hip joint by FA Chandler in 1948. AVN of the femoral head has been reported as early as in the eighteenth century by Alexander Munro. In the year 1936, Ernst Freund [1] described post-traumatic avascular necrosis of the femoral head in a case report. Phemister coined the term “aseptic necrosis” which could result from vascular insult to bone or direct trauma to the femoral neck. Most of the cases reported are idiopathic in nature, and more often than not, they are bilateral and affect young adults predominantly. The incidence of avascular necrosis (due to any cause) has steadily increased over time which can be attributed to recent advances in imaging techniques which allows for early detection even before it is evident on plain radiographic films. There has also been an increase in the frequency of usage of corticosteroids for treatment of conditions like COVID-19 infection, systemic lupus erythematosus (SLE), idiopathic pulmonary fibrosis, and optic neuritis, which explains the increased incidence of AVN of the femoral head seen in patients suffering from these disorders [2]. A definitive cause remains elusive in a vast majority of cases; hence they are reported as idiopathic in nature. Avascular necrosis can contribute significantly to morbidity of the patient and affect their activities of daily living. A comprehensive understanding of the natural history of this disease is crucial in guiding our treatment modalities and planning when to intervene, so as to halt or to delay its progression.

T. Thami (*) · A. Dadra Department of Orthopaedics, PGIMER, Chandigarh, India © The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2023 P. Kumar et al. (eds.), Insights into Avascular Necrosis of the Femoral Head, https://doi.org/10.1007/978-981-99-1346-6_4

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Table 4.1  Etiology of avascular necrosis of hip joint CAUSES OF AVN

TRAUMATIC ETIOLOGIES  Femoral neck fractures  Posterior walI acetabulum fractures  Posterior Hip dislocations  Femoral head fractures

NON TRAUMATIC ETIOLOGIES  Idiopathic  Alcohol overuse  Corticosteroid overuse  Caisson’s Disease (Dysbaric osteonecrosis)

 Slipped capital femoral epiphysis

 AIDS  Sickle cell Anemia

 latrogenic injuries (Posterior approach to hip)

 Hypofibrinolytic disorders • Factor V leiden mutation • Protein C & S deficiency • Myeloproliferative disorders  Gaucher’s Disease  Perthes’ Disease  Smoking  Hyperlipidemia  Radiation Therapy

4.2 Etiology of Avascular Necrosis AVN of the femoral head is caused by any lesion compromising the circulation inside the femoral head, whether it is a traumatic cause or a nontraumatic one. Among the nontraumatic causes, steroid overuse and excessive alcohol consumption contribute to the maximum incidence of AVN [3]. Femoral neck fractures and posterior hip dislocations contribute to majority of incidence among traumatic causes [4]. Genetic predisposition also plays a major role which explains why every individual with high steroid/alcohol intake doesn’t develop AVN of the femoral head [5]. A complex interplay of risk factors at the molecular biological levels can be expected in genetically predisposed patients. The major causes of AVN are summarized below in Table 4.1.

4.3 Blood Supply of the Femoral Head It is crucial to understand the unique blood supply of the femoral head (Fig. 4.1) to establish a basis for the pathophysiology of its avascular necrosis. Uniqueness of the blood supply lies in its retrograde nature. Majority of the blood supply of the femoral head is received from the medial and lateral circumflex femoral arteries which are branches of the profunda femoris artery; another source of blood supply is the foveal artery which runs through the ligamentum teres. The medial and lateral

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Fig. 4.1 Key: MCFA medial circumflex femoral artery, LCFA lateral circumflex femoral artery, PFA profunda femoris artery, FA femoral artery, GT greater trochanter, LT lesser trochanter

circumflex vessels anastomose with each other and form an extracapsular arterial ring at the base of the femoral neck [6]. A subsynovial intracapsular arterial ring also exists mainly between the lateral epiphyseal artery (terminal branch of the medial circumflex femoral artery (MCFA)) and the medial epiphyseal artery (branch of the foveal artery) [7]. The cruciate anastomosis has also been described between the inferior gluteal artery and the deep branch of the medial circumflex femoral artery which can serve as an alternate source of blood supply in case of blockade in the internal or the external iliac arteries. Recent cadaveric studies [6] have shown this anastomosis to be located in an extracapsular location adjacent to the tendon of the obturator externus muscle in most of the specimens.

4.4 Pathoanatomy of Traumatic AVN Anatomical knowledge of its blood supply is crucial in understanding the traumatic causes of avascular necrosis of the femoral head. Posterior hip dislocations and posterior wall acetabulum fractures with hip capsular disruption can injure the deep branch of the MCFA or the cruciate anastomosis; displaced femoral neck fractures can injure the medial or lateral circumflex femoral vessels, hence causing a

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break the retrograde flow of blood to the femoral head (Fig.  4.1); femoral head fractures can injure the epiphyseal vessels perfusing the subchondral bone. Garden et al. reported in 1971 that malreduction of femoral neck fractures caused osteonecrosis of the head in as high as 65.6% cases and anatomic reduction reduced the incidence of AVN to 6.6% (reduction was assessed on the basis of Garden’s index) [8]. Iatrogenic injuries can also occur during posterior approach to the hip while exposing the short external rotators since the deep branch of the MCFA lies in close proximity at this level [6]. This is the basis of practicing safe surgical dislocation (anteriorly) after performing a trochanteric flip osteotomy, popularized by Ganz et al. [9] in 2001.

4.5 Pathoanatomy of Nontraumatic AVN Theories and most evidence from histopathological studies [10] point toward alteration in the microvascular circulation of the cancellous bone of the femoral head. Pathoanatomy involves intravascular and extravascular changes which eventually compromise blood supply of trabecular bone of the femoral head.

4.5.1 Intravascular Changes Small-caliber blood vessels of trabecular bone are occluded by fat microemboli and lipid accumulation (Fig. 4.2) due to higher cholesterol content seen in alcoholics and patients taking steroids for any reason [3]. A hypercoagulable state (Fig. 4.3) also adds to the insult by narrowing lumen of these blood vessels which ultimately cuts off blood supply to a segment of the head of the femur which is now on the verge of becoming avascular. Sickle cell anemia also contributes to avascular necrosis as crenated RBCs can block microvessels in cancellous bone during sickle cell crisis through a similar pathway (Fig. 4.2).

4.5.2 Extravascular Changes Trabecular bone in the femoral head acts a compartment with a fixed volume so extravascular contents like marrow can get edematous due to fat deposition seen in hypercholesterolemia secondary to alcohol overconsumption or chronic steroid intake. This creates external pressure on the sinusoids in cancellous bone which causes venous stasis (Fig. 4.2) and cuts off microvascular circulation of subchondral bone [11] (Fig. 4.3). Eventually over time osteoclasts get activated and eat off this subchondral bone which is usually seen on the imaging as a subchondral fracture. Lack of blood supply makes it look sclerotic on a radiograph which is evident as subchondral sclerosis.

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Fig. 4.2  Schematic diagram illustrating the intravascular and extravascular changes

Alcohol Overuse

Corticosteroids Drugs

Adipocyte Hypertrophy Venous Stasis Arteriole Occlusion

Micro-vascular Thrombosis

Hypercoagulable Disorders

Threshold lschemia

ONSET OF AVN

TRAUMA 

Hip

Direct Vascular Disruption

Dislocation

to Femoral Head



Femoral Neck



Femoral Head

Fig. 4.3  Flowchart depicting the sequential events contributing to pathoanatomy of avascular necrosis

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4.6 Genetic Associations of AVN Single nucleotide polymorphisms (SNPs) in genetic coding of key sources of coagulation cascade such as protein C, protein S, and PAI-1 can predispose to avascular necrosis by creating a prothrombotic environment inside the head of the femur [12]. SNPs have also been reported in gene coding for transferrin (TF), vascular endothelial growth factor (VEGF), and angiotensin I-converting enzyme (ACE) genes [12].

4.7 Pathophysiology of AVN The three main structures involved in the pathophysiology are bone, articular cartilage, and synovium.

4.7.1 Pathological Changes in Bone 1. Stage of Necrosis Necrosis affects both trabecular bone and bone marrow spaces. Bone marrow changes are evident as early as 24 h after the onset of disease process [13]. Histological changes are seen as loss of adipocyte cellular outlines, nuclear pyknosis, and disruption of the cell membranes. Further ischemic insults are evident as empty lacunae which ultimately coalesce and collapse leading to shrinkage of marrow volume. Bone marrow stromal changes are seen at a later stage, earliest ones consisting of endothelial injury to microvessels. Bone cells are more resistant to vascular insult as compared to bone marrow and stroma. Osteoblasts undergo necrosis, loss of basophilic cytoplasm, and nuclear shrinkage as early as 48 h from the onset. Among the bone cells, osteocytes are the last ones to get affected by ongoing ischemic insult. At approximately 2 weeks from the insult, almost all the cells and stroma are affected by necroptosis except osteocytes [13]. Ischemic changes are known to affect only the osteoid component of the bone, and the mineral component is usually unaffected and hence has a protective role in trabecular bone [13]. Although necrosis has set in, the trabecular bone architecture remains intact until 3–4 weeks after onset of ischemic event [11]. No radiological or gross morphological changes are seen in the femoral head at this stage since the early necrotic bone appears similar to healthy bone on radiology. 2. Stage of Revascularization The process of revascularization proceeds from the uninjured blood vessels toward the necrotic segments of the femoral head. Newly formed blood vessels act as a conduit for the ingress of pluripotent cells which shall proliferate and differentiate into osteoblast and osteoclast lineages. Vascular ingrowth depends

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on the degree of necrosis inside the head. Two major sources of neovascularization are metaphyseal vessels and the synovial membrane around the femoral neck. New vessels run along the folds of the synovium and enter the head at its osteochondral junction between the head and neck of the femur. The process of revascularization is slower in humans and takes longer time due to large area of central necrosis. Advanced stages of the disease cause fissuring of the articular cartilage, and the new vessels running along the synovial membrane can penetrate the head through these fissures on the cartilage, representing another way of revascularization [13]. Mesenchymal cells coming from the new vessels also lay down connective tissue and fibroid tissue through proliferation of fibroblasts. 3. Stage of Resorption Revascularization lays down blood vessels through which macrophages and osteoclasts are attracted by chemokines. Early phases of resorption don’t allow complete removal of necrotic bone, and a more robust resorption only takes place at a later stage when the trabecular meshwork is laid down again after new bone formation. The process of resorption follows the same path as revascularization, and subchondral bone is resorbed due to macrophages eating up necrotic bone (due to ingrowth of new vessels through synovial folds). The process of revascularization is faster than resorption [13], so the resorbed areas can become cystic due to fibrous connective tissue filling up these necrotic segments post resorption. 4. Stage of Osteogenesis Osteogenesis mainly occurs via two pathways, i.e., direct ossification through newly formed connective tissue which only occurs in segments of bone with robust growth of new blood vessels and the other pathway involving appositional growth of bone around the necrotic tissue. Pluripotent cells derived from the process of revascularization line themselves along the dead bone and differentiate into osteoblasts. This leads to formation of immature woven bone through appositional growth. These changes can be demonstrated histologically by tetracycline staining of tissue sections as newly formed woven bone takes up tetracycline but the necrotic one doesn’t. This newly formed bone has a disorganized arrangement of connective tissue unlike normal bone; gradually the dead trabeculae are replaced by newly formed trabeculae which give strength to the bone. Gradually woven bone is replaced by lamellar bone, and collagen fibers arrange themselves along the weight-bearing axis of the trabeculae. A peculiar feature of this pathway of osteogenesis is the lack of a remodeling phase. Due to this reason, the newly formed bone lacks the strength and structure of native bone of the femoral head. End of osteogenic phase is marked when new bone gains sufficient tensile and compressive strength. This is followed by periosteocytic osteolysis of necrotic bone [13]. Osteocytes gradually surround themselves at the boundaries of the necrotic bone with widening of their lacunae. These osteocytes ultimately assume the role of an “osteo-

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clast-like cell” causing resorption of necrotic bone. Vascular ingrowth into the necrotic bone brings undifferentiated mesenchymal cells into the picture. These undifferentiated cells can assume the roles of osteoclasts in removing the necrotic bone or the role of osteoblasts in replacing the resorbed necrotic bone segments. This bone is peculiar in the sense that it is always deposited as lamellar bone directly by concentric bone apposition around a vascular core axis. This process is known as corticalization due to deposition of cortical bone in the area of cancellous (trabecular) bone [13]. Eventually this leads to complex appearance of bone which consists of parts of trabecular, cortical, and necrotic bone interspersed in the osteoid. Necrotic segments of bone now stand out on plain roentgenographic films and are clearly delineated from newly formed bone. An overall increase in bone density is seen which is called osteosclerosis; this is seen almost 6 months from the onset of ischemia. 5. Fate of the Necrotic Segment A thin fracture develops in the necrotic zone which is usually seen in the subchondral bone. This is seen as a result of resorption of subchondral necrotic bone through the inflow of macrophages and osteoclast-like cells from the new blood vessels growing along the folds of synovium. These fractures usually involve the weight-bearing bone of the femoral head; hence they don’t unite naturally, and persistent loading impedes fracture healing and produces fibrous connective tissue instead of bone. This thin fracture line gives the appearance of the classical crescent sign seen in avascular necrosis of the femoral head (Fig. 4.4). Subsequent events after subchondral fracture are collapse of epiphyseal bone and articular cartilage followed by fragmentation of the epiphysis (Fig. 4.5).

Fig. 4.4  “Crescent sign” seen as thin subchondral lucency

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Fig. 4.5  Bilateral AVN of femoral heads (left side, advanced collapse with arthritis of hip joint; right side shows early articular collapse and subchondral sclerosis)

4.7.2 Pathological Changes in Articular Cartilage Subchondral collapse causes fissuring of the articular cartilage. Vessels penetrating the head around the osteochondral line lead to revascularization and resorption of subchondral bone. Revascularization also reaches up to the deeper layers of the articular cartilage [10]. Since we know that cartilage is an avascular structure, so vascularization of an avascular zone leads to chondrolysis and decrease in the number of chondrocytes and the matrix.

4.7.3 Pathological Changes in Synovium Synovium plays a key role during the phases of revascularization and resorption. Synovial membrane acts as a conduit for ingrowth of new blood vessels entering the head around the osteochondral junction. Synoviocytes also play a crucial role in the resorption process as they assume the role of phagocytosis of necrotic bone.

4.8 Quantification of the Necrotic Segment Kerboul et al. [14] in 1974 devised a formula to calculate the extent of involvement of subchondral bone in the femoral head. Kerboul’s angle is a radiographic tool of assessment and quantification of osteonecrosis of the femoral head in AVN. Kerboul angle requires an anteroposterior and lateral view of the involved hip with the area of interest being necrotic segment of subchondral bone in the femoral head (Fig. 4.6). Addition of the angle subtended by the sector of osteonecrosis on AP view and on the lateral view gives us the Kerboul angle. If the value of this angle is more than 200 degrees, this signifies a worse prognosis of head salvage. Yong-Chan et al. [15] in 2006 devised a modified Kerboul angle which used midsagittal and mid-coronal sections of MRI to quantify the extent of involvement of subchondral bone of the head. Affected hips can be graded according to the sum of angles on coronal and

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Fig. 4.6  Calculation of Kerboul angle

sagittal sections: Grade 1 (2/3rd of the weight-­ bearing area in subtype C. Stage 2 is characterized by the presence of femoral head flattening and stage 3 by the presence of a cystic lesion in the femoral head. In stage C1 necrotic lesion spread laterally, while in stage C2 extends laterally to the acetabular margin. JIC classification system is summarized below in Table 5.5.

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5  Clinical Features and Staging of AVN Hip Table 5.5  Summary of JIC classification system Type Description 1 The fate of nontraumatic avascular necrosis of the femoral head

2

3

Early flattening of the weight-bearing surface, but does not reveal a demarcation line A cystic lesion in the head

Subtypes Based on the outer end of the demarcation line (sclerosis) 1A. Located in medial 1B. Located in the central part 1C. Located in the outer part of the femoral head Nil

3A. Cystic lesion is located anteriorly or medially, far from the weight-bearing surface 3B. Lesion situated under the lateral weight-bearing surface

Table 5.6  Comparison and correlation between various classification systems of AVN femoral head

Preclinical and pre-radiographic Evident changes on MRI Evident changes on X-ray Subchondral fracture Head collapse 2 mm Joint space narrowing or acetabular changes Advanced osteoarthritis

Modified Ficat-Arlet stage 0 1 2 3

Steinburg stage 0 1 2 3

Revised ARCO-2019

4

4 5

3B 4

1 2 3A

6

5.8 Conclusion Pain is the most consistent and prominent symptom in AVN of hip joints. A limited range of motion at hip joint is the earliest sign elicited. Many classification systems exist but none of the classification system is perfect for this disease; each has their shortcomings. However the most accepted and used classification system at present is Ficat and Arlet classification. We presented a comparison of commonly used classification systems in Table 5.6.

References 1. Sen RK. Management of avascular necrosis of femoral head at pre-collapse stage. Indian J Orthop. 2009;43(1):6–16. 2. Arlet J, Ficat RP. Forage-biopsie de la tête fémorale dans l’ostéonécrose primative. Observations histo-pathologiques portant sur huit forages. Rev Rhumat. 1964;31:257–64. 3. Gardeniers JWM. A new international classification of osteonecrosis of the ARCO committee on terminology and classification. ARCO Newsl. 1992;4:41–6.

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4. Steinberg ME, Hayken GD, Steinberg DR. A new method for evaluation and staging of avascular necrosis of the femoral head. In: Arlet J, Ficat RP, Hungerford DS, editors. Bone circulation. Baltimore: Williams and Wilkins; 1984. p. 398–403. 5. Takashima K, Sakai T, Hamada H, et al. Which classification system is most useful for classifying osteonecrosis of the femoral head? Clin Orthop Relat Res. 2018;476(6):1240. 6. Kerboul M, Thomine J, Postel M, Merle d’Aubigne R. The conservative surgical treatment of idiopathic aseptic necrosis of the femoral head. J Bone Joint Surg Br. 1974;56:291–6. 7. Choi HR, Steinberg ME, Cheng EY. Osteonecrosis of the femoral head: diagnosis and classification systems. Curr Rev Musculoskelet Med. 2015;8:210–20. 8. Mankin HJ.  Nontraumatic necrosis of bone (osteonecrosis). N Engl J Med. 1992;326(22): 1473–9. 9. Moya-Angeler J, Gianakos AL, Villa JC, Ni A, Lane JM. Current concepts on osteonecrosis of the femoral head. World J Orthop. 2015;6:590–601. 10. Ficat RP, Arlet J.  In: Hungerford DS, editor. Ischemia and necrosis of bone. Baltimore: Williams and Wilkins; 1980. 11. Ficat RP. Idiopathic bone necrosis of the femoral head: early diagnosis and treatment. J Bone Joint Surg Br. 1985;67:3–9. 12. Hungerford DS, Zizic TM.  Pathogenesis of ischemic necrosis of the femoral head. In: Hungerford DS, editor. The hip: proceedings of the eleventh open scientific meeting of The Hip Society. St Louis, Toronto: CV Mosby; 1983. p. 249–62. 13. Yoon BH, Mont MA, Koo KH, et  al. The 2019 revised version of Association Research Circulation Osseous staging system of osteonecrosis of the femoral head. J Arthroplasty. 2020;35(4):933–40. 14. Steinberg ME, Hayken GD, Steinberg DR. A quantitative system for staging avascular necrosis. J Bone Joint Surg Br. 1995;77:34–41. 15. Sugano N, Kubo T, Takaoka K, et al. Diagnostic criteria for non-traumatic osteonecrosis of the femoral head. A multicentre study. J Bone Joint Surg Br. 1999;81:590–5. 16. Ono K. Diagnostic criteria, staging system, and roentgenographic classification of avascular necrosis of the femoral head (steroid induced, alcohol associated, or idiopathic nature). In: Ono K, editor. Annual report of Japanese investigation committee for intractable diseases, avascular necrosis of the femoral head, under the auspices of Ministry of Health and Welfare; 1987. p. 331. 17. Sugano N, Atsumi T, Ohzono K, et al. The 2001 revised criteria for diagnosis, classification, and staging of idiopathic osteonecrosis of the femoral head. J Orthop Sci. 2002;7(5):601–5.

6

Avascular Necrosis Hip: How to Examine a Suspected Case Shahnawaz Khan and Siddhartha Sharma

Osteonecrosis of the femur head, also known as avascular necrosis (AVN) hip, is a favorite examination long case. Hence, trainees should be well versed with the salient clinical examination findings, as well as the differential diagnoses. In this chapter, we discuss key points in history and examination that should be borne in mind when a trainee is presented with a suspected case of AVN hip.

6.1 History The most common symptoms of a case of AVN hip are pain, limp, and restriction of hip movements. In most cases, it is the pain that brings the patient to the clinician. We discuss these symptoms in more detail below. 1. Pain • Site: The pain of any hip pathology, AVN included, is generally localized to the groin region. In many cases, the pathology is bilateral, and the patient may not be aware of early-stage disease in the other hip. • Onset: Many patients may be asymptomatic for a long time. Most patients present with pain that is gradual in onset. Acute onset of pain in AVN hip signifies a subchondral insufficiency fracture. • Character: The pain is dull aching type. Sharp pain is noted in cases of a subchondral insufficiency fracture. • Radiation: The pain may radiate to ipsilateral knee, especially on the medial side. S. Khan Orthopaedics, AIIMS, Bhuvaneshwar, India S. Sharma (*) Department of Orthopaedics, PGIMER, Chandigarh, India © The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2023 P. Kumar et al. (eds.), Insights into Avascular Necrosis of the Femoral Head, https://doi.org/10.1007/978-981-99-1346-6_6

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• Exacerbating and relieving factors: The pain in AVN is mechanical in nature, which increases on walking, activity, squatting, etc. and is relieved on taking rest and analgesics. 2. Limp • Patients with early AVN hip may not complain of limp. • When it does occur, the limp in the AVN hip is a painful one. Limp is generally noted by the patient or his caregivers after the onset of pain. • As the disease process worsens, so does the limp. This may be attributable to restriction of hip range of motion, shortening, and eventual arthritis. 3. Restriction of hip range of motion • Restriction of hip range of motion is a late symptom of AVN hip. • It occurs due to a change in the shape of the femoral head or hip arthrosis. • These restrictions manifest by difficulty in squatting (flexion), difficulty in getting on to a motorbike or bicycle (abduction in extension of the hip), or difficulty in cross-legged sitting (abduction in hip flexion). 4. Limb shortening • Shortening in AVN hip occurs due to progressive collapse of the femoral head and due to reduction in joint space. • Shortening is a late finding and seldom exceeds 2 cm. Any shortening more than 4 cm should alert the clinician to hip pathologies other than AVN.

6.2 Past Medical, Family, and Personal History • AVN of the hip can be secondary to several well-known disorders, such a hypothyroidism, hypercoagulable states, sickle cell anemia, hemoglobinopathies, chronic kidney disease, etc. The clinician must determine whether there are any predisposing medical conditions. • A thorough enquiry should be made regarding any history of trauma to the hip, especially femoral neck fractures and hip dislocations. • One should also enquire for history of hip disorders in childhood (Perthes disease, septic arthritis, and DDH). • Several drugs are known to result in AVN and include corticosteroids, HAART, cancer chemotherapy, cyclosporine, NSAIDs, etc. These should be ascertained in detail. • Surgical history: Any history of prior surgery to the hip must be noted, including surgery for reduction and fixation of the femoral neck and head fractures or open reduction for hip dislocations. • One must also enquire for history of sickle cell anemia, hemoglobinopathies, and coagulopathies which are familial in nature. • Personal history: In many cases, AVN can be attributed to chronic smoking or alcohol intake. In case the patient is a smoker, the clinician must quantify this in terms of pack-years, i.e., the number of cigarette packs smoked every day multiplied by the total number of years that the patient has been a smoker. Similarly,

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the clinician must also determine the magnitude of alcohol consumption. Any history of deep-sea diving should also be ascertained if relevant, as this can point to dysbarism and consequent AVN.

6.3 General Examination As should be the norm in every case, the patient’s consent is a must before commencing examination. The patient must be made comfortable, and a thorough head to toe examination should be performed in a suspected case of AVN hip, as it can point to the etiology. Some of the important findings that should be ascertained include: • Pallor: This may point toward sickle cell anemia, hemoglobinopathy, or chronic disease. • Cyanosis and clubbing: May be seen in smokers. • Edema: Non-pitting edema may indicate hypothyroidism, whereas pitting edema may be a sign of chronic liver failure secondary to alcohol abuse. • Signs of chronic alcohol intake should be ascertained. These include icterus, palmar erythema, spider angiomas, hepatic fetor, hepatomegaly, and dilated veins. • Signs of steroid intake: These include cataracts, acne, central obesity, buffalo hump, moon facies, gynecomastia, purple striae, etc. • Signs of chronic smoking: Staining of nails and teeth, bluish-black discoloration of lips and teeth, clubbing, and nail dystrophy may indicate that the patient is a chronic smoker.

6.4 Gait Patients with early AVN may have minimal pain and no gait abnormality. Most patients who are symptomatic present with an antalgic gait [1]. In advanced cases with collapse of the femoral head and arthrosis, patients may present with varying degrees of stiff hip or short limb gait. The examiner must also ascertain whether the patient uses any walking aids.

6.5 Local Examination The hip should be carefully examined; examination is guided by the history. A look-­ feel-­move (inspection, palpation, movement) scheme is followed so that no important findings are missed. It is of utmost importance to expose the hip completely while taking care to cover the genitalia, or else important clinical findings may be missed. In case of female patients, it is imperative that a female chaperone (nurse or a colleague) be present at all times during the examination.

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• Inspection • Inspection is performed with the patient standing, sitting, and lying down position, from the front, side, and back. –– With patient standing Front: Look for the level of both shoulders, anterior superior iliac spine (ASIS), and superior poles of patellae and malleoli. In case of shortening, these landmarks are at a lower level than the normal side. One should look for muscle wasting in the thigh (Fig. 6.1). Side: Look for exaggeration of lumbar lordosis, knee flexion, and position of the ankle. Any flexion deformity at the hip is compensated by lumbar lordosis, knee flexion, and ankle equinus. Make a note of any surgical scars around the hip (Fig. 6.2). Back: Look for level of shoulders, dimple of Venus (posterior superior iliac spines), and gluteal folds. A scar on posterior aspect of hip region may point toward previous surgery for an acetabulum or femoral head fracture. Fig. 6.1 Examination from the front. Check for symmetry of the shoulder tips, anterior superior iliac spines, superior pole of patellae, and tips of medial malleolus. The ASIS tips have been marked in this picture (black dots); the right ASIS is seen to lie at lower level

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Fig. 6.2 Examination from the side. Note the exaggeration of lumbar lordosis

Also look for any scoliosis, which may point toward a coronal plane deformity (abduction deformity) of the hip (Fig. 6.3). –– With the patient sitting Note whether the position of the anterior superior iliac spine (ASIS) on the affected side changes when the patient is made to sit. If the ASIS remains lower than that of the normal side in the standing as well as sitting position, it indicates an abduction deformity of the hip. If the ASIS becomes level with the opposite side on sitting, it indicates pelvis tilt due to limb shortening. –– With patient in the supine position The patient is asked to lie straight on a firm couch, with his or her arms crossed over the chest, and asked to keep both limbs in full extension at the hip and knee, with both patellae facing upward. The examiner may instruct the patient to assume this position, and only then should the attitude of the limb be commented upon.

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Fig. 6.3 Examination from the back. The posterior superior iliac spines have been marked (black dots). Note flattening of the left gluteal fold (solid arrow)

Similar to examination in the standing position, one must look for scars, muscle wasting, sinuses, pulsation, and pigmentation. Look for the level of bony landmarks. The ASIS, patella, and the medial malleolus may be at a higher level than the unaffected side if the limb is short. If the ASIS is lower than the contralateral side, it indicates abduction deformity at the hip. • Palpation –– Tenderness: A case of AVN usually presents with tenderness over anterior and posterior joint lines. The pain is deep in nature and not a superficial one. The anterior joint line is located 2 cm below and lateral to mid-inguinal point. The posterior joint line is at the junction of medial 2/3 and lateral 1/3 of a line joining greater trochanter and posterior superior iliac spine. –– Morris bitrochanteric compression test: In this test, the examiner compresses both greater trochanters simultaneously. A positive test is indicated by pain in the hip.

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–– The hip is carefully and systematically palpated from the front, side, and back to identify any tender areas or swellings. • Assessment of Hip Deformity • Before checking for movements, it is imperative to ascertain whether the patient has any hip deformity in the coronal, sagittal, or axial plane. –– Frontal Plane Deformities: This includes adduction and abduction deformity. An adduction deformity is indicated by a higher position of the ipsilateral ASIS and vice versa. The magnitude of a frontal plane deformity can be assessed by Perkin’s or Kothari’s method (Figs. 6.4 and 6.5). In the Perkin’s method (Fig. 6.5), the examiner moves the limb in the direction of the deformity (e.g., abduct the leg for abduction deformity) until the ASIS are at the same level. The magnitude of movement needed to level (or square) the pelvis is equivalent to the deformity at the hip. Kothari’s method can be used when squaring of the pelvis is not possible (Fig. 6.4). In this method both the lower limbs are placed parallel and aligned with the long axis of the trunk. A horizontal line is drawn joining both the ASIS, and another vertical line is drawn joining the suprasternal notch and the symphysis pubis. Perpendicular lines are dropped from the vertical line to the right and the left ASIS. The angle between the perpendicular and the horizontal lines indicates the magnitude of the adduction or abduction deformity.

Fig. 6.4  Kothari’s method of determining the frontal plane deformity of the pelvis. The pelvis is not squared. The anterior superior iliac spines are marked (points A and B). A horizontal line (AB) is drawn joining both anterior superior iliac spines. Another vertical line (CD) is drawn from the tip of xiphisternum to the pubic symphysis. Perpendiculars (AA′ and BB′) are dropped from points A and B to the vertical line (CD). The angle between lines AA′ (or BB′) and AB denotes the amount of frontal plane deformity

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Fig. 6.5  Perkin’s method of estimation of frontal plane deformity. The pelvis is “squared” by moving the affected limb in the direction of the deformity (e.g., abduct the hip for abduction deformity). This maneuver is continued until both anterior superior iliac spines are at the same level. The angle between the midline (line AB) and the long axis of the lower limb (line CD) denotes the magnitude of frontal plane deformity

–– Sagittal Plane Deformity: A flexion deformity of the pelvis is usually present in AVN hip. This is assessed by the Thomas test [2, 3] (Fig. 6.6a, b). To begin with, the examiner makes a note of exaggerated lumbar lordosis and places his or her hand under the patient’s lumbar spine. The contralateral hip is then flexed until the lumbar lordosis is obliterated. At this stage, the examiner makes a note of the angle subtended between the long axis of the affected thigh and the bed, which denotes the magnitude of the flexion deformity. –– Axial Plane deformity: These include internal or external rotation deformities and should be assessed with the hip in extension as well as flexion. This visualization is best performed from the foot end of the table. If an external rota-

6  Avascular Necrosis Hip: How to Examine a Suspected Case Fig. 6.6 (a) Thomas test—the patient is made to lie on a firm couch. Exaggeration of lumbar lordosis is noted (blue arrows). (b) Thomas Test—the contralateral hip is flexed until lumbar lordosis disappears. The angle subtended by the long axis of the thigh (line AB) and the couch (line CD) denotes the magnitude of sagittal plane deformity

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a

b

tion deformity is present, the affected limb will be seen to lie in more external rotation as compared to the opposite side and vice versa. To confirm that this truly is a deformity and not related to postural positioning, the examiner should attempt to internally rotate the hip. Absence of internal rotation indicates an external rotation deformity and vice versa. • Movements –– The movements of the hip joints should be checked with knees extended and then with knees flexed. –– One must make a note of both the active and passive range of motion and compare it with the opposite side. Limitations of abduction and internal rotations are common findings in AVN hip [4]. –– Rotations of the hip (internal and external) should be measured with the hip in 90° of flexion, as well as in full extension (Fig. 6.7). In AVN, internal rotation in 90° of hip flexion is less as compared to that in full extension of the hip. This is because of the deformation of the superolateral weight bearing part of the femoral head, which engages the acetabulum, when the hip is flexed to 90°. This finding can be considered as a corollary to the sectoral sign, which is described below. –– Sectoral Sign: This sign is elicited with the patient in the supine position. The examiner flexes the knee to 90° and flexes the hip. In normal hips, the examiner can flex the knee with the patella pointing to the opposite shoulder. In cases of AVN hip, the patella points to the ipsilateral shoulder as the hip is flexed. This is because of the obligatory external rotation of the femoral head as the hip is brought into flexion (Fig. 6.8). • Measurements –– Circumferential measurements: Since AVN hip is a chronic pathology, one must look for wasting of thigh muscles. This can be done by measuring the

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Fig. 6.7  Assessment of hip internal rotation with the hip in 90° of flexion. Line AB denotes the long axis of the leg, and line CD denotes the long axis of the trunk. The angle between these two lines denotes the amount of hip internal rotation

thigh girth at a fixed point above the knee joint line, taking care to avoid the suprapatellar bursa, and it is compared with the opposite side. –– Linear measurements of the lower limb Apparent length of the lower limb (AL): This is measured from xiphisternum to the tip of medial malleolus. The difference between the two sides, if any, is noted (Fig. 6.9). Apparent length takes into account the true length discrepancy as well as the apparent discrepancy due to any deformities. It is pertinent to mention here that an abduction deformity will lead to

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Fig. 6.8  Sectoral sign. The examiner performs hip flexion with the knee flexed. If the hip is normal, it rotates internally with progressive hip flexion beyond 90°, and the flexed knee points to the contralateral shoulder. In a hip with flattening of the femoral head, there is obligatory external rotation with hip flexion, and the flexed knee points toward the ipsilateral shoulder (arrow). This is the “sectoral sign”

a­ pparent lengthening of the limb, whereas an adduction deformity will lead to apparent shortening of the limb. True length (TL): With the pelvis squared, the distance between the tip of the ASIS and the tip of medial malleolus denotes the true length of the limb (Fig. 6.10). The pelvis is squared by moving the limb in the direction of the frontal plane deformity until both ASIS are at the same level. Following this, the opposite limb is placed in the same amount of adduction or abduction which was necessary to square the pelvis (mirror position). The tip of ASIS can be found with the metallic end of a measuring tape. The examiner starts palpation with the metallic end of the tape below the ASIS. The point of first resistance denotes the ASIS tip and is marked on both sides. The tip of the medial malleolus can be marked in a similar fashion.

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Fig. 6.9  The apparent limb length is measured from the tip of xiphisternum to the tip of medial malleolus. The pelvis is not squared

Comparison of true and apparent length gives the examiner an idea of limb shortening and presence of coronal plane deformities, if any. If the true length discrepancy equals apparent length discrepancy, it denotes limb shortening without any coronal plane deformity. If there is discrepancy on true measurements but no discrepancy on apparent measurements, it indicates that an abduction deformity has compensated for the limb shortening. As a rule of thumb, there is 1 cm of apparent lengthening for every 10° of abduction deformity. A case of AVN may present with either of the two scenarios described above. If the apparent shortening exceeds the true shortening, it indicates an adduction deformity in addition to the limb length discrepancy. This scenario is very rare in AVN hip. Segmental length measurements: The thigh and leg segments should be measured separately (Figs. 6.11 and 6.12), as this gives the examiner an idea about the anatomical location of limb length discrepancy. The leg length can be measured from the medial knee joint line to the tip of medial

6  Avascular Necrosis Hip: How to Examine a Suspected Case Fig. 6.10  Measurement of true length. The pelvis is squared and the opposite limb kept in an identical (mirror) position. The length is measured from the tip of anterior superior iliac spine to the tip of medial malleolus

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70 Fig. 6.11  The segmental length of the thigh is measured from the tip of the anterior superior iliac spine to the medial knee joint line (marked as red dots)

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6  Avascular Necrosis Hip: How to Examine a Suspected Case Fig. 6.12  The segmental length of the leg is measured from the medial knee joint line to tip of the medial malleolus (marked as red dots)

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malleolus (Fig. 6.12). The thigh length can be measured from the ASIS to the medial knee joint line (Fig. 6.11). Allis test and Galeazzi test: The Allis and Galeazzi tests are quick methods to determine the anatomical location of limb length discrepancy. In later stages of AVN, there is true femoral shortening [5]. The Allis test (Fig. 6.13) is performed by flexing both hips to 90°, resting the legs on the examiner’s forearms, and comparing the levels of the patellae. In cases with thigh shortening, the affected patella is seen to lie at a lower level. The Galeazzi test (Fig. 6.14) is performed by flexing both hips to 45°, knees to 90°, and placing the foot flat on the couch. In case of femoral shortening, the patella Fig. 6.13  Allis test. Note that the knee on the affected side (black arrow) lies at a lower and proximal level than the normal, contralateral side (blue arrow)

Fig. 6.14  Galeazzi test. Note that the knee on the affected side (dotted line) lies at a lower level than the normal, contralateral side

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Fig. 6.15  Bryant triangle. Point A denotes the anterior superior iliac spine, and B, the tip of the greater trochanter. A perpendicular line is dropped from point A. A line is extended proximally from point B, parallel to the couch. The intersection of points A and B, i.e., point C, forms the third point for the Bryant triangle. Line BC denotes the amount of supratrochanteric shortening

on the affected side is seen to lie at a proximal and lower level than the other side. In cases of tibial shortening, the patella on the affected side lies at a distal and lower level [6]. If thigh shortening is discovered, which is invariably the case in AVN hip, one must also determine whether this originates from the hip joint (supratrochanteric shortening) or the femoral shaft (infratrochanteric ­shortening). Supratrochanteric shortening can be determined by several ways, i.e., by Bryant triangle method, Shoemaker’s line, Nelaton’s line, etc. Bryant triangle: The landmarks of this triangle are the ASIS, tip of the greater trochanter, and a perpendicular line drawn from the ASIS (Fig.  6.15). Supratrochanteric shortening is indicated by decrease in the distance between the greater trochanter and the perpendicular from anterosuperior iliac spine in Bryant triangle. Shoemaker’s line: The lines joining the ASIS and the tips of the greater trochanter cross each other above the umbilicus in the midline in a normal hip. In cases with supratrochanteric shortening, there is upward migration of the greater trochanter, and these lines cross on the unaffected side, below the umbilicus. Nelaton’s line: When the hip is flexed to 90°, the line joining the ASIS to ischial tuberosity touches the tip of the greater trochanter. In case of an up-­riding greater trochanter, the tip of the trochanter lies above this line. • Examination of other joints: In many cases, the disease process is bilateral. Hence, the opposite hip must be examined, even though the patient may be asymptomatic. A quick examination of the spine and sacroiliac joints is also warranted, to rule out spondyloarthropathies such as ankylosing spondylitis [7].

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6.6 Summary A suspected case of AVN hip warrants meticulous history taking and a systematic clinical examination. Insidious onset of pain and limp is the most common clinical presentation. Salient clinical findings include hip joint line tenderness, restriction of abduction and internal rotation, a positive sectoral sign, and a supratrochanteric shortening of not more than 2 cm. Finally, the examiner must remember that the disease may be bilateral in many cases, and examination of the contralateral hip is mandatory.

References 1. Byrd JWT. Evaluation of the hip: history and physical examination. N Am J Sports Phys Ther. 2007;2(4):231–40. 2. Thomas HO.  The classic. Diseases of the hip, knee and ankle joint with their deformities treated by a new and efficient method. Clin Orthop Relat Res. 1974;(102):4–9. 3. Thurston A.  Assessment of fixed flexion deformity of the hip. Clin Orthop Relat Res. 1982;(169):186–9. 4. Polkowski GG, Clohisy JC. Hip biomechanics. Sports Med Arthrosc Rev. 2010;18(2):56–62. 5. Alassaf N. Predictors of femoral shortening for pediatric developmental hip dysplasia surgery: an observational study in 435 patients. Patient Saf Surg. 2018;12(1):29. 6. Martin HD, Shears SA, Palmer IJ.  Evaluation of the hip. Sports Med Arthrosc Rev. 2010;18(2):63–75. 7. Han Q, Zheng Z, Zhang K, Ding J, Baraliakos X, Zhu P. A comprehensive assessment of hip damage in ankylosing spondylitis, especially early features. Front Immunol. 2021;12:668969.

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AVN Hip: Radiology Sarthak Sharma and Siddhartha Sharma

7.1 Introduction Avascular necrosis (AVN) or osteonecrosis of the femoral head is a term broadly applied to ischaemic marrow lesions resulting from a wide range of conditions ranging from systemic causes and post-traumatic sequelae to a significant proportion of idiopathic cases. The imaging features reflect underlying pathophysiology of reduced femoral head perfusion and resultant infarction. The purpose of this chapter is to provide an insight into the radiological features of femoral head AVN, how various radiological findings correlate with underlying histopathological marrow changes and which findings are pertinent to prognostication and clinical management.

7.2 Pathophysiology A brief review of relevant pathophysiology is essential to understand the progression of radiological features of femoral head AVN through various phases of its natural course. At the centre of the histopathological changes is an area of subchondral ischaemic necrosis, often referred to as an infarct, regardless of the underlying aetiology. As the femoral head has a preponderance of relatively poorly vascularised fatty marrow, developing infarcts tend to be mostly non-haemorrhagic with preservation of a core of non-viable fatty marrow. Surrounding this core, there is a reparative interface of fibrovascular tissue interposed between the infarct and normal marrow, often referred to as the zone of creeping substitution. In the earlier stages of disease S. Sharma Jammu Healthcare & Diagnostics Pvt. Ltd., Jammu, Jammu and Kashmir, India S. Sharma (*) Department of Orthopaedics, PGIMER, Chandigarh, India © The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2023 P. Kumar et al. (eds.), Insights into Avascular Necrosis of the Femoral Head, https://doi.org/10.1007/978-981-99-1346-6_7

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which precede subchondral collapse, the typical radiological appearances are ascribed to the infarct core with surrounding reparative interface [1, 2]. Progression of the disease is characterised by fracture of the subchondral bone plate and subchondral bone collapse, owing to altered weight-bearing dynamics during the reparative phase. This is followed by development of secondary degenerative joint changes. However, smaller infarcts, especially those located in non-­ weight-­ bearing locations may remain stable over time without progression to collapse and degenerative joint disease [1, 2].

7.3 Radiological Features A brief modality-wise review of typical features is presented with special emphasis on conventional radiographs (X-rays) and MRI.

7.3.1 Radiographs The majority of early-stage AVN is occult on radiographs. This is because infarcted fatty marrow as well as the surrounding reactive interface is radiographically indistinguishable from adjacent normal marrow. The earliest detectable radiographic findings are areas of subchondral lucency secondary to trabecular resorption, which may be ill-defined or may have well-defined circumscribed geographic margins, as well as patchy sclerosis secondary to calcification of the reactive fibrovascular interface, although these findings per se develop relatively later on in the disease course (Fig. 7.1). Both anteroposterior and lateral radiographic projections are needed to minimise the chances of missing small lesions. The frog leg lateral view is especially useful in this regard [2]. The characteristic finding of subchondral fracture is crescent sign (a subchondral lucent line oriented parallel to articular surface of the femoral head) (Fig. 7.2). Subchondral collapse manifests as loss of femoral head sphericity/flattening of the femoral head in the weight-bearing region. Findings on advanced stages include joint space reduction and other features of degenerative joint disease (osteophytes/subchondral cysts, sclerosis and gross deformation of femoral head contour) (Fig. 7.3).

7.3.2 CT CT is not widely used for diagnosis, due to its insensitivity in detecting early-stage AVN, a limitation shared with radiographs. However, it provides better definition and assessment of subchondral fracture/collapse as compared to radiographs. Its most significant utility is in the peri-collapse stage occurring between late pre-­collapse stage and early post-collapse stages, where it can detect subtle subchondral fractures and early femoral head collapse (defined as femoral head subsidence 2  gm of prednisolone or its equivalent within a time frame of 3 months What are the clinical differential diagnoses of AVN hip? [3, 4] (a) Primary osteoarthritis: Complaints of joint stiffness and constant deep aching pain that gets worse with weight bearing. On examination, marked limitation of ROM will be there and more common in the elderly. (b) Femoroacetabular impingement: History of deep pain, especially pain on standing after prolonged sitting and getting in and out of a car. FADIR test elicits pain and apprehension. (c) Hip labral tear: History of dull or sharp pain with weight bearing. Mechanical symptoms such as catching or painful clicking along with antecedent history of trauma can be present. (d) Internal snapping hip: History of deep pain along with intermittent catching and audible click or snap arising from the groin. ROM will be normal. (e) Occult/stress fractures: History of deep pain on weight bearing, more common in athletes. On examination, there will be painful ROM and trochanteric tenderness. (f) Transient synovitis: History of acute-onset atraumatic pain. Mostly in children, self-limiting condition, along with history of concurrent fever and antecedent trauma at times. Patient refuses to bear weight. (g) Septic arthritis: History of acute-onset atraumatic pain. Mostly in children and immunocompromised individuals. There will be fever, local redness, tenderness, and swelling along with pain on passive ROM.  Patient refuses to bear weight. (h) Transient osteoporosis of the hip: Acute pain which improves on protected weight bearing and preserved hip ROM except at extremes. (i) Lumbar radiculopathy: History of pain and paresthesia in the distribution area of nerve root along with predominant symptom of back pain. (j) Spinal stenosis: Predominant symptom of back pain which aggravates on back extension and gets relieved on back flexion. Pain will also radiate down to the distal extremity along with symptoms of paresthesia, numbness, and muscle weakness. What is sectoral sign? [5] (a) Due to the sectoral involvement of anterolateral femoral head in AVN hip (Fig. 16.1), there is differential rotation of the hip in the flexion and extension planes. There is a resultant more internal rotation of the hip with the hip in extension as compared to flexion. What is the best radiological test to diagnose AVN hip? [4] (a) MRI: 98% sensitivity and specificity (Fig. 16.2)

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Fig. 16.1  Figures showing areas of sectoral involvement

Fig. 16.2  MRI sections showing areas of osteonecrosis

What is the pathognomonic sign of AVN hip on MRI? [6] ( a) Double-line sign (Fig. 16.3) What is double-line sign? [7] (a) It is seen on T2-weighted MRI sequences. Double-line sign is formed due to lower-intensity outer ring representing sclerotic bone and higher-intensity inner ring representing reparative granulation tissue.

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Fig. 16.3  T2 MRI sections representing the double line sign

What are the various medical management options for AVN hip? [1, 4, 8] (a) Bisphosphonates: Inhibits osteoclast activity and bone turnover, thus thought to prevent collapse (b) Statins: Decreases adipogenesis and stimulates osteoblastic differentiation (c) Anticoagulants: Slows and reverses the osteonecrosis by breakdown of venous thrombosis and thus decreases the intraosseous hypertension and ischemia (d) Prostacyclin analogues: Inhibits platelet aggregation and bone resorption, causes vasodilation, and mediates bone modeling (e) Hyperbaric oxygen: Increases extracellular oxygen concentration, reduces intraosseous hypertension and bone edema (f) Pulsed electromagnetic therapy: Strong anti-inflammatory effect on the joint environment and facilitates the synthesis of extracellular proteins and tissue repair (g) Extracorporeal shockwave therapy: Stimulates osteoblasts, which results in increased density of bone How do you classify AVN hip? [9] (a) Ficat-Arlet classification system (Table 16.1) (b) Modified Ficat-Arlet classification system (Table 16.2) (c) Steinberg classification system (d) Association Research Circulation Osseous (ARCO) classification system (Table 16.3) (e) The Japanese Investigation Committee (JIC) classification system What is the classification based only on MRI for AVN hip? [10] (a) Shimizu classification (Table 16.4) What are the various surgical options in the management of AVN hip? [11] (a) Core decompression + bone grafting (b) Osteotomy (c) Resurfacing arthroplasty

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16  Frequently Asked Viva Questions (AVN Hip) Table 16.1  Ficat-Arlet classification Stage Symptoms 0 None

Radiographs Normal

1

None/mild

Normal

2

Mild

3

Mild to moderate

4

Moderate to severe

Density changes in head, cystic and sclerotic changes, normal head contour and joint line Flattening of the head (crescent sign), loss of head contour and collapse Joint space narrowing, acetabular changes

Bone scan Decreased uptake? Cold spot on femoral head

Pathological findings – Infarction of the weight-bearing portion of the head

Biopsy – Abundant dead marrow cells, osteoblasts, osteogenic cells New bone deposition between dead trabeculae

Increased uptake

Spontaneous repair of infarction

Increased uptake

Subchondral fracture, collapse, and fragmentation of the necrotic part

Dead bone

Increased uptake

Osteoarthritic changes

Acetabular cartilage degenerative changes

Table 16.2  Modified Ficat-Arlet classification Bone scan Decreased uptake? Cold spot on femoral head

Pathological findings –

Stage Symptoms 0 None

Radiographs Normal

1

None/mild

Normal

2

Mild

Increased uptake

Spontaneous repair of infarction

3

Mild to moderate

Density changes in femoral head 2A: cystic and sclerotic changes, normal head contour and joint line 2B: Crescent sign (subchondral fracture) Loss of head contour and collapse

Increased uptake

4

Moderate to severe

Joint space narrowing, acetabular changes

Increased uptake

Subchondral fracture, collapse, and fragmentation of the necrotic part Osteoarthritic changes

Infarction of the weight-bearing portion of the head

Biopsy – Abundant dead marrow cells, osteoblasts, osteogenic cells New bone deposition between dead trabeculae

Dead bone

Acetabular cartilage degenerative changes

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Table 16.3  Revised ARCO staging The 2019 revised ARCO staging for osteonecrosis of the femoral head ARCO stage Image findings I X-ray: normal MRI: low-signal band on T1-weighted MRI II X-ray: abnormal MRI: abnormal III Subchondral fracture on X-ray or CT  IIIA (early)  Femoral head depression ≤2 mm  IIIB (late)  Femoral head depression >2 mm IV X-ray: osteoarthritis ARCO Association Research Circulation Osseous, MRI magnetic resonance imaging, CT computed tomography Table 16.4  Shimizu classification Grade Extent A Lesion less than 1/4th the diameter of the circle B Lesion 1/4th to less than 1/2 the diameter of the circle C Lesion equal to or greater than 1/2 the diameter of the circle

Location Lesion involving less than 1/3rd of the weight-bearing part Lesion involving 1/3rd to less than 2/3rd of the weight-bearing part Lesion involving 2/3rd or greater of the weight-bearing part

Intensity of lesion High Mixed Low

( d) Total hip replacement (e) Arthrodesis What osteotomies can you do in AVN hip? [11] (a) Transtrochanteric rotational osteotomy (Fig. 16.4) (b) Intertrochanteric varus/valgus osteotomy in combination with flexion/extension (Fig. 16.5) What is core decompression? [11] (a) It is a method (Fig.  16.6) used to treat early stages of AVN hip whereby the femoral head is decompressed using various techniques to restore the blood supply by relieving intraosseous hypertension. What are the various methods of core decompression and bone grafting? [1] (a) Phemister technique (b) Trapdoor technique (Fig. 16.7a) (c) Light-bulb technique (Fig. 16.7b) What is modified Kerboul combined necrotic angle (CNA)? [2] (a) It is the necrotic angle measured on midsagittal and mid-coronal MRI sections (Fig. 16.8) and grades the lesions into three categories. What is positive axis deviation sign? [5] (a) Due to the sectoral involvement of the femoral head, the knee and patella point to the ipsilateral shoulder/axilla on flexing the hip >90° with the flexed knee. This is positive axis deviation sign (Fig. 16.9).

16  Frequently Asked Viva Questions (AVN Hip)

Fig. 16.4  Transtrochanteric rotational osteotomy illustration

Fig. 16.5  Valgus intertrochanteric osteotomy illustration

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Fig. 16.6 Core decompression illustration

Fig. 16.7  Figures illustrating (a) “trapdoor technique” and (b) “light-bulb technique”

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Fig. 16.8 (a) Necrotic angle in mid-coronal MR image. (b) Necrotic angle in midsagittal MR image. Combined necrotic angle: A + B. Three categories: small lesion (combined necrotic angle ≤190°), medium-sized lesion (combined necrotic angle between 190° and 240°), and large lesion (combined necrotic angle ≥240°) Fig. 16.9  Axis deviation sign illustration

What are the other radiological investigations that can be done for AVN hip? [6] (a) Plain radiograph (b) Radionuclide bone scanning (c) NCCT (d) SPECT What is the common end pathway resulting in AVN in non-trauma cases? [11] (a) Intravascular coagulation and intraosseous hypertension. Steroids and alcohol along with being toxic to the bone cells also lead to increased intracellular lipid accumulation and intraosseous hypertension. As a result of intraosseous hypertension, endothelial cells get damaged leading to local microcirculatory thrombosis and resultant ischemia.

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What are the adjuvants used along with core decompression in hip preservation surgery in AVN hip? [12, 13] (a) Bone marrow aspirate concentrate (BMAC) (b) Platelet-rich plasma (PRP) (c) Bone morphogenetic proteins (BMPs) (d) Autologous bone grafts (e) Synthetic bone substitutes (f) Autologous chondrocyte implantation (ACI) (g) Mosaicplasty and osteochondral transplantation What are the diagnostic criteria for nontraumatic osteonecrosis? [5] (a) The Japanese Investigation Committee criteria Major criteria Radiological—femoral head depression/demarcating sclerosis/crescent sign Bone scan—cold or hot MRI—low-intensity band on T1-weighted scan Histology—trabecular and marrow necrosis Minor criteria Radiological—femoral head depression with joint-space narrowing/cystic radiolucency or mottled appearance/flattening of superior portion of the femoral head Bone scan—cold or hot MRI—homogeneous or inhomogeneous low intensity on T1-weighted scans without band pattern Symptoms—pain on bearing weight History—alcohol or corticosteroid use history present What is crescent sign? [1] (a) Subchondral fractures of the femoral head seen as radiolucent changes in stage 2 of Ficat and Arlet classification of AVN hip (Fig. 16.10). What is the chief complaint in a patient with AVN hip? [4] (a) Groin pain of insidious onset with occasional referred pain in the thigh and buttock is the most common symptom. Initially, pain is present on weight bearing, while in the later stages, rest pain and night pain are also common along with decreased ROM. What is the common clinical examination finding in a patient with AVN hip? [14] (a) A painful hip and limitation of motion, especially loss of internal rotation of the hip, is the earliest clinical finding. In later stages deformities and limb-­length discrepancies are commonly seen as well. What investigations will you suggest for the management of a AVN hip case? [4] (a) Clinical evaluation followed by radiological studies. Radiological studies include plain radiographs AP and frog-leg lateral views, followed by MRI. (b) Blood investigations to rule out infectious or rheumatic etiology

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Fig. 16.10 X-ray depicting “crescent sign”

How are the various clinical differentials of AVN hip different from each other in presentation? [15, 16] (a) Osteoarthritis: Osteophytes and subchondral cysts are present on both sides of the joint along with simultaneous presence of joint-space narrowing. On clinical examination, there will be a global restriction of movements of the hip joint. However these findings may also be seen in late stages of AVN. (b) Idiopathic transient osteoporosis of the hip: Commonly affects the pregnant females and middle-aged adults. On MRI, there will be bone edema extending up to the intertrochanteric region. (c) Subchondral insufficiency fractures: On MRI, fracture appears irregular, convex, and discontinuous as opposed to AVN which appears smooth and concave. (d) Neoplasm: It appears as a radiolucent area and lacks the serpiginous pattern and bone edema as seen in AVN. What is the mechanism of action of various medical management options for AVN hip? [17] (a) Bisphosphonates: It inhibits the activation of osteoclast, thereby decreasing the rate of remodeling and preventing collapse. (b) Iloprost: It is a potent vasodilator and reduces edema and platelet aggregation. (c) Enoxaparin: It is an anticoagulant which reduces the venous thrombosis and improves the blood flow. (d) Statins: It decreases the adipocytes in the marrow and relieves the intraosseous hypertension along with pro-osteoblastic effects. (e) Hyperbaric oxygen therapy: It increases the effective oxygen concentration and also decreases edema due to vasoconstriction effect. (f) Extracorporeal shockwave therapy: It stimulates angiogenesis and osteogenesis. (g) Pulsed electromagnetic field therapy: It also stimulates angiogenesis and osteogenesis.

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What are the different principles underlying the classification systems for AVN hip? [9] (a) Ficat and Arlet classification system: It relies on the findings present on plain radiographs to determine the disease stage. (b) Steinberg’s classification system: It combines the findings of plain radiographs and MRI to quantify the lesion size and disease severity. (c) ARCO classification system: It incorporates the findings of plain radiographs, CT, MRI, and scintigraphy to determine the lesion size and location. (d) The Japanese Investigation Committee (JIC) classification system: It uses the T1-weighted MRI sequences to stage the disease based on the location of osteonecrosis. What are the factors to be considered while planning for the surgical management in cases of AVN hip? [18] (a) Age. (b) Stage and classification of osteonecrosis. (c) Etiology: Nontraumatic etiology leads to bilateral involvement frequently and has a poor prognosis, so joint-preserving procedures may not be effective in these cases. (d) Necrosis volume. (e) Joint function. (f) Occupation. (g) Compliance with joint preservation treatment strategies. (h) Activity level. What are the principles of osteotomy performed in cases of AVN hip? [18] (a) The principle of performing osteotomy is to move the necrotic area of the femoral head outside the weight-bearing zone to prevent further damage. The type of osteotomy to be performed is guided by the location of the lesion in the femoral head. What is the principle of core decompression and till what stage it is useful? [12] (a) It involves bone drilling which is thought to relieve the intraosseous hypertension and help restoring the vascular supply. It is helpful up to Ficat stage 2. For further stages one or more adjuvants have been advocated along with CD. What are the principles behind different bone grafting techniques? [19] (a) It is to remove the nonviable bone and supporting the remaining subchondral bone and articular cartilage with cortical and cancellous autograft. This graft is helpful in preventing further collapse and may induce osteogenesis. Is positive axis deviation different from sectoral sign? [5] (a) Yes, sectoral sign is differential rotation of the hip in flexion and extension, that is, more internal rotation with the hip in extended position as compared to the flexed position. What are the rationale and reasons behind other radiological investigations for AVN hip? [18, 20] (a) Other radiological investigations which can be used for AVN hip are: • NCCT: CT scan displays the extent of involvement accurately. It displays area of sclerosis around the necrotic bone and subchondral fractures. It is also helpful in planning the surgical procedure.

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• Bone scan: It is helpful in detecting multifocal osteonecrosis in the body. • SPECT: It can be used when MRI is not possible or when results of MRI are not determinate. • DSA: It can be used to plan the hip preservation surgical procedure in patients with AVN hip. What is the principle and mechanism of action of various adjuvants used along with core decompression surgery for AVN hip? [21, 22] (a) PRP: Growth factors contained in the platelets help in osteogenesis, angiogenesis, and a reduction in inflammation. (b) BMAC: They contain stem cells that are osteogenic and help in building the bony architecture. (c) BMPs: These are osteoinductive agents which can enhance bony repair and healing via recruitment of surrounding mesenchymal cells. How does a crescent sign appear and what is the rationale for it? [23] (a) Crescent sign appears due to bony trabecular failure leading to subchondral fractures in the femoral head, and it appears as an area of subchondral radiolucency.

References 1. Lespasio MJ, Sodhi N, Mont MA. Osteonecrosis of the hip: a primer. Perm J. 2019;23:18–100. https://doi.org/10.7812/TPP/18-­100. PMID: 30939270; PMCID: PMC6380478. 2. Hines JT, Jo WL, Cui Q, Mont MA, Koo KH, Cheng EY, Goodman SB, Ha YC, Hernigou P, Jones LC, Kim SY, Sakai T, Sugano N, Yamamoto T, Lee MS, Zhao D, Drescher W, Kim TY, Lee YK, Yoon BH, Baek SH, Ando W, Kim HS, Park JW. Osteonecrosis of the femoral head: an updated review of ARCO on pathogenesis, staging and treatment. J Korean Med Sci. 2021;36(24):e177. https://doi.org/10.3346/jkms.2021.36.e177. PMID: 34155839; PMCID: PMC8216992. 3. Wilson JJ, Furukawa M.  Evaluation of the patient with hip pain. Am Fam Physician. 2014;89(1):27–34. PMID: 24444505. 4. Hsu H, Nallamothu SV.  Hip osteonecrosis. In: StatPearls. Treasure Island (FL): StatPearls Publishing; 2021. PMID: 29763129. 5. Epomedicine. Sectoral Sign: AVN hip [Internet]. Epomedicine; 2020 [cited 15 Jun 2022]. https://epomedicine.com/clinical-­medicine/sectoral-­sign-­avn-­hip/. 6. Steinberg ME. Diagnostic imaging and the role of stage and lesion size in determining outcome in osteonecrosis of the femoral head. Tech Orthop. 2001;16(1):6–15. 7. Gaillard, F., Feger, J.  Double line sign. Reference article, Radiopaedia.org. https://doi. org/10.53347/rID-­1236. Accessed 10 Jul 2022. 8. Tripathy SK, Goyal T, Sen RK. Management of femoral head osteonecrosis: current concepts. IJOO. 2015;49:28–45. https://doi.org/10.4103/0019-­5413.143911. 9. Sultan AA, Mohamed N, Samuel LT, Chughtai M, Sodhi N, Krebs VE, Stearns KL, Molloy RM, Mont MA. Classification systems of hip osteonecrosis: an updated review. Int Orthop. 2019;43(5):1089–95. https://doi.org/10.1007/s00264-­018-­4018-­4. Epub 2018 Jun 18. PMID: 29916002. 10. Sakamoto M, Shimizu K, Iida S, Akita T, Moriya H, Nawata YA. Osteonecrosis of the femoral head: a prospective study with MRI. J Bone Joint Surg Br Vol. 1997;79(2):213–9. 11. Lieberman JR, Berry DJ, Montv MA, Aaron RK, Callaghan JJ, Rayadhyaksha A, Urbaniak JR.  Osteonecrosis of the hip: management in the twenty-first century. J Bone Joint Surg. 2002;84(5):834–53.

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12. Kumar P, Shetty VD, Dhillon MS. Efficacy of orthobiologic adjuvants to core decompression for hip preservation in avascular necrosis hip. J Hip Preserv Surg. 2020;7(3):423–38. https:// doi.org/10.1093/jhps/hnaa051. 13. Alshameeri Z, McCaskie A.  The role of orthobiologics in hip preservation surgery. J Hip Preserv Surg. 2015;2(4):339–54. https://doi.org/10.1093/jhps/hnv042. 14. Zalavras CG, Lieberman JR.  Osteonecrosis of the femoral head. J Am Acad Orthop Surg. 2014;22(7):455–64. https://doi.org/10.5435/jaaos-­22-­07-­455. 15. George G, Lane JM. Osteonecrosis of the femoral head. J Am Acad Orthop Surg Glob Res Rev. 2022;6(5):e21.00176. https://doi.org/10.5435/JAAOSGlobal-­D-­21-­00176. PMID: 35511598; PMCID: PMC9076447. 16. Jackson SM, Major NM. Pathologic conditions mimicking osteonecrosis. Orthop Clin North Am. 2004;35(3):315–20. https://doi.org/10.1016/j.ocl.2004.02.006. 17. Rajpura A, Wright AC, Board TN. Medical management of osteonecrosis of the hip: a review. HIP Int. 2011;21(4):385–92. https://doi.org/10.5301/hip.2011.8538. 18. Zhao D, Zhang F, Wang B, Liu B, Li L, Kim SY, Goodman SB, Hernigou P, Cui Q, Lineaweaver WC, Xu J. Guidelines for clinical diagnosis and treatment of osteonecrosis of the femoral head in adults (2019 version). J Orthop Transl. 2020;21:100–10. 19. Seyler TM, Marker DR, Ulrich SD, Fatscher T, Mont MA.  Nonvascularized bone grafting defers joint arthroplasty in hip osteonecrosis. Clin Orthop Relat Res. 2008;466(5):1125–32. https://doi.org/10.1007/s11999-­008-­0211-­x. 20. Stoica Z, Dumitrescu D, Popescu M, Gheonea I, Gabor M, Bogdan N.  Imaging of avascular necrosis of femoral head: familiar methods and newer trends. Curr Health Sci J. 2009;35(1):23–8. Epub 2009 Mar 21. PMID: 24778812; PMCID: PMC3945237. 21. Liu N, Zheng C, Wang Q, Huang Z. Treatment of non-traumatic avascular necrosis of the femoral head (Review). Exp Ther Med. 2022;23(5):321. https://doi.org/10.3892/etm.2022.11250. Epub 2022 Mar 10. PMID: 35386618; PMCID: PMC8972838. 22. Stiehl JB, Ulrich SD, Seyler TM, Bonutti PM, Marker DR, Mont MA. Bone morphogenetic proteins in total hip arthroplasty, osteonecrosis and trauma surgery. Expert Rev Med Devices. 2008;5(2):231–8. https://doi.org/10.1586/17434440.5.2.231. 23. Cohen-Rosenblum A, Cui Q.  Osteonecrosis of the femoral head. Orthop Clin North Am. 2019;50(2):139–49. https://doi.org/10.1016/j.ocl.2018.10.001.

Multiple-Choice Questions

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1. The trabeculae of the femoral head are formed on the basis of which law? (a) Wolf’s law (b) Hilton’s law (c) Davis’ law (d) Perren’s law Answer: (a). Wolf’s law states that bone in a healthy animal will adapt to the loads under which it is placed. Hilton’s law refers to the nerve supply of a joint and dermatomes. Perren’s law is based on strain theory, which defines the type of tissue that is generated under different amounts of strain. Davis’ law is used in anatomy and physiology to describe how soft tissue models along imposed demands. 2. The secondary compressive and tensile groups are oriented as follows: (a) Along the lateral wall of the proximal femur (b) Along the medial wall of the proximal femur (c) Along the medial and lateral walls of the proximal femur, respectively (d) Along the lateral and medial walls of the proximal femur, respectively Answer: (c). (Fig. 17.1) 3. Ward’s triangle is bound by all of the following lines except (a) Primary compressive trabeculae (b) Secondary compressive trabeculae (c) Principle tensile group of trabeculae (d) Trochanteric tensile group of trabeculae Answer: (d). As seen in the diagrammatic representation above, Ward’s triangle is bounded by all of the given options except the trochanteric group of trabeculae.

A. Dadra · P. M. Rathod (*) Department of Orthopaedics, PGIMER, Chandigarh, India © The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2023 P. Kumar et al. (eds.), Insights into Avascular Necrosis of the Femoral Head, https://doi.org/10.1007/978-981-99-1346-6_17

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Fig. 17.1 Representation of arrangement of proximal femur trabeculae

Fig. 17.2 Representation of blood supply of proximal femur (GT greater trochanter, LT lesser trochanter, FA femoral artery, MCFA/ LCFA medial/lateral circumflex femoral artery, OA obturator artery)

4. The blood supply to the femoral head is contributed by all except (a) Lateral epiphyseal branch of medial femoral circumflex (b) Ascending branch of lateral femoral circumflex (c) The ligamentum teres artery (d) Inferior gluteal artery Answer: (d). Though in a minor subset of the population inferior gluteal artery is a dominant blood vessel in the majority of the population, the femur head is mainly supplied by lateral and medial circumflex femoral arteries (LCFA, MCFA) and artery of the ligamentum teres [1] (Fig. 17.2). 5. Which blood vessel is preserved during “safe surgical dislocation,” thereby preventing avascular necrosis? (a) The deep branch of MFCA (medial femoral circumflex artery) (b) The superficial branch of MFCA (c) Ascending branch of MFCA (d) Acetabular branch of MFCA Answer: (a). This surgical approach prevents injury to posterior capsular vessels which contain the deep branch of MCFA. It prevents capsular stretch and injury to the ascending retinacular vessels running posterior to the neck of the femur [2].

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6. The deep branch of MFCA can be found between (a) Quadratus femoris and obturator externus (b) Pyriformis and superior gemellus (c) Superior gemellus and obturator internus (d) Obturator internus and inferior gemelli Answer: (a). The deep branch runs obliquely upward upon the tendon of the obturator externus and in front of the quadratus femoris, and it anastomoses with twigs from the superior and inferior gluteal arteries [1]. 7. Who coined the term “coronary disease of the hip” for AVN hip? (a) Freund (b) Chandler (c) Fairbank (d) Mankin and Brower Answer: (b). Fremont A.  Chandler (1893–1954) has done extensive work on aseptic necrosis of the head of the femur which led to this eponym for AVN hip [3]. 8. AVN hip is known as all of the following except (a) Osteochondritis dissecans (b) Chandler’s disease (c) Albers-Schonberg disease (d) Bilateral idiopathic necrosis Answer: (c). Albers-Schonberg disease is a type of osteopetrosis characterized by an increased skeletal mass due to defective cartilage and bone resorption. All other given options were named synonymous with AVN hip. 9. All of the following are known risk factors for atraumatic AVN hip except (a) Steroids (b) Sickle cell disease (c) Gaucher’s disease (d) Alcohol intake (e) Smoking (f) Caisson’s disease Answer: (e). Although few reports suggest smoking to be a risk factor, among given options, it’s the least likely cause for atraumatic AVN [4]. 10. All of the following are proven genetic polymorphisms contributing to AVN except (a) SOX-9 (b) RETN (c) COL2A1 (d) PPAR gamma (e) RUNX2 Answer: (b). In the review by Kumar et al. (2022), RETN gene polymorphism is protective against the atraumatic steroid-induced AVN [5].

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1 1. All of the following are true about AVN hip except (a) Typical age ranges from 35 to 50 years old. (b) Prevalence is higher in females than in males. (c) There is a high prevalence of bilateral disease. (d) Core decompression in the early stage is the treatment of choice. Answer: (b). There is a higher preponderance of AVN in males as compared to females [6]. 12. All of the following are clinical signs in the early stage of AVN hip except (a) Joint tenderness (b) Antalgic gait (c) Limitation of external rotation in flexion and extension of the hip (d) Cystic formation on plain radiographs Answers: (c). In the early stage, internal rotation is affected more as compared to external rotation in the AVN hip [7]. 13. All of the following are first-line investigations for AVN hip except (a) Standing AP X-rays of the bilateral hip with the pelvis (b) Frog leg lateral view of both hips (c) MRI of bilateral hips with the pelvis (d) Bone scan Answers: (d). Bone scan is useful in assessing the status of multiple joints. The uptake of technetium-99m is usually variable or increased at a stage when symptoms occur. However, when the patient is symptomatic, there is no relationship between the scintigraphic appearance of the femoral head and the pain and function of the hip [8]. 14. All of the statements are true regarding AVN hip except (a) MRI has a sensitivity and specificity of 98% in diagnosing AVN hip. (b) The crescent sign precedes collapse. (c) The presence of a bright signal on the T1 sequence of MRI indicates edema and is predictive of worsening pain and progression of the disease. (d) Double density appearance is seen in T1 as well as T2 sequences. Answer: (c). The bright signal is seen on the T2 sequence rather than T1. It is due to areas of necrosis when viable, fatty marrow is still present. Chronic ischemia leads to a signal intensity pattern resembling that of fluid, with low signal intensity on T1-weighted images and high signal intensity on T2-weighted images [9]. 15. All of the following are treatment modality options for the early stages of AVN hip except (a) Bisphosphonates (b) Core decompression with bone marrow aspirate concentrate (c) Vascularized free fibula graft (d) Muscle pedicle flap

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(e) Rotational osteotomies (f) Total hip arthroplasty Answer: (f). Total hip arthroplasty is reserved for advanced diseases with debilitating secondary osteoarthritis where hip-preserving modalities are not effective in providing relief to the patients [10]. 16. All of the following are modalities of treatment of bilateral hip AVN except (a) Core decompression (b) Bisphosphonates (c) Arthrodesis (d) Total hip arthroplasty (e) Hip resurfacing Answer: (c). Bilateral arthrodesis is not indicated as it becomes difficult for the patient to mobilize. Hip arthrodesis is indicated for young symptomatic patients who have a unilateral affection of the hip and have failed preservation surgeries [11]. 17. All of the following are indications for a hip resurfacing except (a) Stage III Ficat-Arlet AVN (b) 200° 2. Medium: 161–199° 3. Large: >200°

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Stress fracture of the tibia is a known complication after the vascularized free fibular graft. Ivy et al. and Emery et al., in their papers, have mentioned this uncommon adverse effect. It occurs due to increased stress going through the tibia after a part of the fibula has been harvested [16]. 23. A 26-year-old man comes with complaints of pain in the right knee more than the left and the inability to do squats and lunges. He gives a history of going to the gym and consuming supplements in the form of pills and powder. On ­examination, his knee is normal. His hip joint line is tender on both sides. On examination, his rotations are limited on both sides with the right side being severe. X-rays of the hip and knee are normal. Next step in management (a) Repeat X-ray of the knee and hip in AP and lateral views (b) MRI of both hips with the pelvis (c) Bone scan (d) Surgery Answer: (b). The classical case history with the signs and symptoms suggests the diagnosis of AVN hip. The next step in management is to get an MRI to confirm and quantify the disease as X-rays are normal [10]. 24. A 35-year-old man native of the Deccan plateau region of central India comes to your OPD with a history of limp and groin pain for the past 1 year, which subsides with NSAIDs. He gives a history of frequent admissions for repeated infections and blood transfusions. He hasn’t been on any other medication, especially steroids. His X-rays show the collapse of both femoral heads secondary to AVN covering almost 60–70% area. Best management is (a) Rotational arthroplasty (b) Core decompression (c) Bisphosphonates (d) Hip resurfacing (e) Total hip arthroplasty Answer: (e). Total hip arthroplasty. The above patient probably has sickle cell anemia from the endemic region he comes from. Necrotic area more than 60–70% excludes hip resurfacing and rotational plasty. Collapse excludes core decompression and bisphosphonates therapy [17]. 25. A 30-year-old male presents to your OPD with the diagnosis of grade IV AVN affecting both his hips. His activities of daily living are severely hampered. He is given the option of total hip arthroplasty. He requests for getting a ceramic-­ on-­ ceramic total hip arthroplasty. What should he be informed regarding CoC THA? (a) Increased risk of dislocation (b) Increased risk of infection compared to poly-on-ceramic THA (c) Risk of squeaking sounds when mobilizing and fracture of ceramic components (d) Increased risk of wear (e) Reduced range of motion compared to poly-on-ceramic THA

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Answer: (c). Ceramic on ceramic has the lowest friction and lowest wear and lasts longer than poly. But they have increased fracture risk and may end up having squeaking sounds [18]. 26. All of the following are classification systems used for AVN hip except (a) ARCO classification (b) Steinberg classification (c) Ficat and Arlet classification (d) Moore classification Answer: (d). Moore classification. All the other three classification systems are used for AVN hip. Hohl and Moore’s classification is used for proximal tibia fractures. 27. Which bisphosphonates have been proven to prevent femoral head collapse in AVN hip? (a) Ibandronate (b) Alendronate (c) Zolendrenate (d) Pamidronate Answer: (b). Chen et  al. in their prospective randomized double-blind study concluded that alendronate is effective in the treatment of early-stage adult nontraumatic AVN of the femoral head [19]. 28. All of the following pathways are contributory to AVN femur except (a) Lipid metabolism disorders (b) Decreased viscosity of blood (c) Angiogenesis pathway/disrupted blood supply/venous congestion (d) Coagulation disorders Answer: (b). Increase in the viscosity of blood leads to AVN rather than a decrease [20]. 29. All of the following are true regarding latest ARCO classification except (a) Combination of FICAT, JOA, and Steinberg classification. (b) Stage 0 is eliminated. (c) Stage III is subdivided into A and B (less than 2 versus more than 2 mm depression). (d) Acetabular involvement was incorporated into stage V. Answer: (d). There is no stage V in ARCO.  This was recently modified by ARCO in 2019 [21]. 30. The most common cause of total hip arthroplasty in India is (a) AVN (b) Osteoarthritis primary (c) Rheumatoid hip (d) Ankylosing spondylitis Answer: (a). Kumar P et al. in their study have shown that the commonest indication of THA is AVN hip in India [17].

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31. The following drugs have been shown to be beneficial in the early stages of AVN hip except (a) Core decompression with intravenous prostacyclin (b) Core decompression with intralesional ibandronate (c) Ginsenoside Rb1 (d) Electrocorporeal shock wave therapy Answer: (b). Core decompression with intralesional ibandronate. There is not enough evidence yet that this modality is beneficial when compared to core decompression alone or core decompression combined with intralesional BMAC.  The other drugs have in reviews shown to be beneficial [10]. 32. Pulsed electromagnetic field stimulation works by the following mecha nism except (a) Local control of inflammation (b) Angiogenesis (c) Increases repair activity (d) Blunts the nerve endings of the hip joint, thereby decreasing pain Answer: (b). Angiogenesis. It is postulated that it uses hyperstimulation analgesia by increasing the threshold of pain and promoting bone healing as a result of microfractures [22]. 33. All of the following are recent methods to treat early AVN hip except (a) Hyperbaric oxygen therapy (b) Pulsed electromagnetic field therapy (c) Intravenous prostacyclin (d) Core decompression Answer: (d). Core decompression. The other three modalities are comparatively recent advances as compared to core decompression. 34. All are true regarding mesenchymal stem cells in the treatment of AVN hip except (a) They are multipotent cells that differentiate into fibroblastic, osteogenic, myogenic, adipogenic, and reticular cells. (b) Stem cell instillation should be done only if the concentration is 1 × 106. (c) The bone marrow aspirate contains BMP-2 which is introduced into the femoral head. (d) Bone marrow stromal cells when supplemented with FGF-2 increase the lifespan of bone marrow stromal cells. Answer: (b). Stem cell instillation should be done only if the minimum concentration of cells is 2 × 106, not 1 × 106 [23]. 35. Which among the following has been most beneficial in treating the early stages of AVN hip? (a) Core decompression with BMAC (bone marrow aspirate concentrate) (b) Core decompression alone (c) Core decompression with tantalum implant (d) Core decompression with fibular strut graft

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Answer: (a). Core decompression with BMAC. Sen et al. in their systematic review concluded that the proven and reproducible method of treatment of non-collapsed early AVN hip is “core decompression and BMAC instillation.” However, collapsed heads do better with THA [10]. 36. All are true about Ficat-Arlet classification except (a) Have four stages. (b) Based on X-rays. (c) Stage I is normal-looking X-rays. (d) Stage II consists of flattening of the head. Answer: (d). Flattening of the head occurs in stage III [10]. 37. Corticosteroids and excessive alcohol intake act by all of the following mechanisms to cause AVN except (a) Vascular endothelial damage (b) Microvascular thrombosis (c) Induce intramedullary adipogenesis (d) Decrease osteoclast lifespan Answer: (d). Steroid and excessive alcohol can increase osteoclast lifespan [24]. 38. All of the following are true about the modified Kerboul angle except (a) It is done in MR images. (b) Mid-coronal and midsagittal images of the hips are used. (c) Grade II was between 150° and 250° combined necrotic angle. (d) Grade IV was more than 300° combined necrotic angle. Answer: (c). Grade I is less than 200°. Grade II is 200–249°. Grade III is 250–299°. Grade IV is more than 300°. Modified Kerboul angle is measured in MRI rather than X-rays. This has been shown to predict collapse [25]. 39. The least common concomitant intraarticular finding which can be seen in patients with early-stage AVN planned for core decompression through hip arthroscopy is (a) Labral injury (b) CAM lesion (c) Chondral defects (d) Foveal ligament anomaly Answer: (d). Foveal ligament anomaly. Serong et al. in their study found that the most common concomitant intraarticular findings through a hip arthroscopy in patients with ARCO stage II and stage III are CAM lesions, labral lesions, and chondral defects [26]. 40. Standard hip portals that are used in hip arthroscopy for arthroscopy-assisted core decompression and labral repair are all except (a) Anterolateral (b) Anterior portal

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(c) Direct anterolateral (d) Mid-anterior portal (e) Medial portal Answer: (e). The first four options are the most commonly used portals, with added posterolateral for posterior joint access [27]. 41. The lateral femoral nerve is at risk during the creation of which hip arthroscopy portal? (a) Anterior portal (b) Anterolateral portal (c) Direct anterolateral portal (d) Mid-anterior portal Answer: (c). Direct anterolateral portal as it is close to the anatomy of the nerve [27]. 42. Which of the following is the primary viewing portal in hip arthroscopy? (a) Anterolateral (b) Direct anterolateral (c) Mid-anterior portal (d) Posterolateral portal Answer: (a). (Fig. 17.4). Anterolateral is the primary portal used for visualizing the hip joint during arthroscopy [27]. 43. A 35-year-old male patient comes to your OPD wishing to get operated on with THA on the right side due to stage IV AVN. He had undergone uncemented total hip arthroplasty on the left side for the same diagnosis 4 years ago. On examination, you find out that the patient has slight discomfort after walking about 100 m. On serial examination of the previous X-rays, you find out that there is a clear space between the acetabular cup and the acetabulum of the left side. The first step in management is to investigate with (a) ESR and CRP (b) Bone scan Fig. 17.4 Representation of hip scope portals (ASIS anterior superior iliac spine, MAP mid-anterior portal, ALP anterolateral portal, PL posterolateral)

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(c) MRI (d) NCCT left hip Answer: (a). The above history is suggestive of the loosening of the acetabular cup. It is imperative to evaluate the cause of component loosening. First thing is to rule out any underlying infection. ESR and CRP are established markers to rule out septic loosening [28]. 44. A 40-year-old male comes to your OPD after 1 year of total hip replacement on the right side for AVN hip, complaining of a new onset of pain in the hip. You suspect implant loosening after seeing the serial X-rays and perform hematological tests including ESR and CRP. X-rays and hematological tests are within normal limits. The next best step in management is (a) Bone scan along with synovial fluid aspiration (b) NCCT hip (c) MRI hip (d) Immediate revision surgery Answer: (a). The three-phase bone scan is the initial test for differentiating an aseptic loosening of hip vs periprosthetic joint infection, along with the aspiration of synovial fluid for examination [28]. 45. A 23-year-old college-going student presents with bilateral groin pain. Radiological investigations reveal that he has grade IV AVN of both hips. You advise him to undergo staged bilateral total hip replacement. The patient asks for your expert opinion on which type of implant he must choose among the options that he surfed on the Internet. (a) Cemented total hip arthroplasty (b) Hybrid total hip arthroplasty (c) Dual-mobility uncemented arthroplasty (d) Uncemented total hip arthroplasty Answer: (d). Uncemented total hip arthroplasty is the preferred choice in a young-aged patient requiring total hip arthroplasty [29].

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5. Kumar P, Rathod PM, Aggarwal S, Patel S, Kumar V, Jindal K. Association of specific genetic polymorphisms with atraumatic osteonecrosis of the femoral head: a narrative review. Indian J Orthop. 2022;56(5):771–84. 6. Hsu H, Nallamothu SV. Hip osteonecrosis. In: StatPearls. 2022. PMID: 29763129. 7. Barney J, Piuzzi NS, Akhondi H. Femoral head avascular necrosis. In: StatPearls. [Updated 4 Jul 2022]. 8. Azar FM, Canale ST, Beaty JH. Campbell’s operative orthopaedics. 13th ed. Philadelphia, PA: Elsevier/Mosby; 2013. p. 359–60. 9. Stoica Z, Dumitrescu D, Popescu M, Gheonea I, Gabor M, Bogdan N.  Imaging of avascular necrosis of femoral head: familiar methods and newer trends. Curr Health Sci J. 2009;35(1):23–8. 10. Sen RK. Management of avascular necrosis of femoral head at pre-collapse stage. Indian J Orthop. 2009;43(1):6–16. 11. Clohisy JC, Beaulé PE, O’Malley A, et al. Hip disease in the young adult: current concepts of etiology and surgical treatment. J Bone Joint Surg A. 2008;90:2267–81. 12. Waewsawangwong W, Ruchiwit P, Huddleston JI, Goodman SB. Hip arthroplasty for treatment of advanced osteonecrosis: a comprehensive review of implant options, outcomes and complications. Orthop Res Rev. 2016;8:13–29. 13. Azar FM, Canale ST, Beaty JH. Campbell’s operative orthopaedics. 13th ed. Philadelphia, PA: Elsevier/Mosby; 2013. p. 381. 14. Kerboul M, Thomine J, Postel M, Merle d’Aubigné R. The conservative surgical treatment of idiopathic aseptic necrosis of the femoral head. J Bone Joint Surg Br. 1974;56:291–6. 15. Azar FM, Canale ST, Beaty JH. Campbell’s operative orthopaedics. 13th ed. Philadelphia, PA: Elsevier/Mosby; 2013. p. 385. 16. Ivey M, Hicks CA, Hook JD. Stress fracture of the tibia after harvest of a vascularized fibular graft for repair of nonunion of the humerus. Orthopaedics. 1995;18:57–60. 17. Kumar P, Sen RK, Aggarwal S, Jindal K.  Common hip conditions requiring primary total hip arthroplasty and comparison of their post-operative functional outcomes. J Clin Orthop Trauma. 2020;1:S192–5. 18. Castagnini F, Cosentino M, Bracci G, Masetti C, Faldini C, Traina F.  Ceramic-on-ceramic total hip arthroplasty with large diameter heads: a systematic review. Med Princ Pract. 2021;30:29–36. 19. Chen CH, Chang JK, Lai KA, Hou SM, Chang CH, Wang GJ.  Alendronate in the prevention of collapse of the femoral head in nontraumatic osteonecrosis: a two-year multicenter, prospective, randomized, double-blind, placebo-controlled study. Arthritis Rheum. 2012;64(5):1572–8. 20. Kleinman RG, Bleck EE. Increased blood viscosity in patients with Legg-Perthes disease: a preliminary report. J Pediatr Orthop. 1981;1(2):131–6. 21. Hines JT, Jo WL, Cui Q, Mont MA, Koo KH, Cheng EY, et al. Osteonecrosis of the femoral head: an updated review of ARCO on pathogenesis, staging and treatment. J Korean Med Sci. 2021;36(24):e177. 22. Wang CJ, Wang FS, Huang CC, Yang KD, Weng LH, Huang HY. Treatment for osteonecrosis of the femoral head: comparison of extracorporeal shock waves with core decompression and bone-grafting. J Bone Joint Surg Am. 2005;87(11):2380–7. 23. Hernigou P, Poignard A, Manicom O, Mathieu G, Rouard H. The use of percutaneous autologous bone marrow transplantation in nonunion and avascular necrosis of bone. J Bone Joint Surg Br. 2005;87:896–902. 24. Weinstein RS.  Clinical practice. Glucocorticoid-induced bone disease. N Engl J Med. 2011;365(1):62–70. 25. Koo KH, Ha YC, Kim HJ, Yoo JJ, Kim YM. Quantifying the extent of femoral head osteonecrosis: a modified Kerboul method using magnetic resonance imaging. Orthop Proc. 2004;86:146.

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26. Serong S, Haubold J, Theysohn J, Landgraeber S. Arthroscopic assessment of concomitant intraarticular pathologies in patients with osteonecrosis of the femoral head. J Hip Preserv Surg. 2020;7(3):458–65. 27. Aprato A, Giachino M, Masse A.  Arthroscopic approach and anatomy of the hip. Muscles Ligaments Tendons J. 2016;6(3):309–16. 28. Pinski JM, Chen AF, Estok DM, Kavolus JJ. Nuclear medicine scans in total joint replacement. J Bone Joint Surg Am. 2021;103(4):359–72. 29. Azar FM, Canale ST, Beaty JH. Campbell’s operative orthopaedics. 13th ed. Philadelphia, PA: Elsevier/Mosby; 2013. p. 180.