Sport Hip Injuries PDF

Larson • O’Sullivan
Kelly • Bedi •
Editors
Bryan Kelly | Asheesh Bedi | Chris Larson | Eilish O’Sullivan
Sports Hip Injuries: Diagnosis and Management SLACK

Sports Hip Injuries
Diagnosis and Management
Sports
Hip
In the world of sports, hip injuries among an athletic population can be very difficult to diagnose and
manage. That’s why Sports Hip Injuries: Diagnosis and Management is a comprehensive guide to
diagnosing and managing sports hip injuries and hip preservation.
Drs. Bryan Kelly, Asheesh Bedi, Chris Larson, and Eilish O’Sullivan have been or currently are
team physicians for various professional sports teams and are leaders in the field of hip preservation.
They present Sports Hip Injuries: Diagnosis and Management in a concise manner by focusing
Injuries
on hip and pelvis disorders and cover all of the typical disorders seen in athletes presenting with hip
and pelvic pain. The anatomy, presentation, clinical evaluation, imaging, nonsurgical and surgical
treatment, and post-surgical rehabilitation of hip joint disorders are presented clearly throughout.
Some of the topics include:
• Femoroacetabular impingement
• Hip instability/dysplasia
• Athletic pubalgia/core muscle injury
• Stress fractures and traumatic sports injuries of the hip and pelvis
• Myotendinous injuries and nerve entrapment disorders of the hip and pelvis
Diagnosis and Management
• Rehabilitation guidelines and return-to-sport outcomes
Sports Hip Injuries: Diagnosis and Management is an invaluable resource for sports medicine
providers including orthopedic surgeons and fellows that care for patients presenting with hip pain
for athletes at all levels, as well as physical therapists and athletic trainers.
I N C O R P O R A T E D
SLACK Incorporated
MEDICAL/Orthopedics
®
Editors
Bryan T. Kelly, MD
Chief of Sports Medicine Service
Chief of Hip Preservation Service
Hospital for Special Surgery
New York, New York
Asheesh Bedi, MD
Department of Orthopedic Surgery
University of Michigan Health System
Ann Arbor, Michigan
Christopher M. Larson, MD
Program Director
Minnesota Orthopedic Sports Medicine Institute
Edina, Minnesota
Eilish O’Sullivan, PT, DPT, OCS

Clinical Care Coordinator
Center for Hip Preservation
New York, New York
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fessional standards set for the circumstances that apply in each specific situation. Every effort has been made to confirm
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Library of Congress Cataloging-in-Publication Data
Sports hip injuries : diagnosis and management / editors, Bryan T. Kelly, Asheesh Bedi, Christopher M. Larson, Eilish
O’Sullivan.
p. ; cm.
Includes bibliographical references and index.
ISBN 978-1-61711-046-7 (alk. paper)
I. Kelly, Bryan, editor. II. Bedi, Asheesh, editor. III. Larson, Christopher M., editor. IV. O’Sullivan, Eilish, editor.
[DNLM: 1. Hip Injuries--diagnosis. 2. Hip Injuries--therapy. 3. Athletic Injuries--diagnosis. 4. Athletic Injuries--
therapy. 5. Sports Medicine--methods. WE 855]
RC1211
617.1’027--dc23
2015002468
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DEDICATION
The authors would like to dedicate this book to all of our patients who have allowed us to take
care of them. While we have helped many, we have clearly learned from them as well. Without their
trust in our care, advancement in this field would have been impossible. We would also like to
dedicate this book to our individual mentors who allowed us to move forward in this field, gave
us the tools to be good orthopedic surgeons, and instilled in us the intellectual curiosity to try to
expand upon a field that has often been misunderstood or unrecognized.
CONTENTS
Dedication . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . v
About the Editors. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ix
Contributing Authors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xi
Foreword by Russell F. Warren, MD . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .xiii
Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xv
Section I Basic Injury Patterns . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1

Chapter 1 Anatomical Considerations and Clinical Examination . . . . . . . . . . . . . . . . . . . 3
Alexander E. Weber, MD; Lazaros A. Poultsides, MD, MSc, PhD;
Eilish O’Sullivan, PT, DPT, OCS; Bryan T. Kelly, MD; and Asheesh Bedi, MD
Chapter 2 Femoroacetabular Impingement: I. Pathoanatomy,

Clinical Evaluation, and Arthroscopic Treatment Strategies . . . . . . . . . . . . . 25
Bryan T. Kelly, MD and Christopher M. Larson, MD
Chapter 3 Femoroacetabular Impingement: II. Open Treatment Strategies

and Outcomes in Femoroacetabular Impingement Surgery. . . . . . . . . . . . . . . 49
Lisa M. Tibor, MD and Michael Leunig, MD
Chapter 4 Dysplasia and Instability . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 63

Lazaros A. Poultsides, MD, MSc, PhD; Eilish O’Sullivan, PT, DPT, OCS;
and Michael D. Stover, MD
Chapter 5 Traumatic Hip Subluxation/Dislocation and

Femoroacetabular Impingement-Induced Instability . . . . . . . . . . . . . . . . . . . . 79
Bryan T. Kelly, MD; Eilish O’Sullivan, PT, DPT, OCS;
and Aaron J. Krych, MD
Chapter 6 Anterior Soft Tissue Injuries of the Hip:

Hip Flexor, Iliopsoas, and Subspine Impingement . . . . . . . . . . . . . . . . . . . . . 91
Nikhil Oak, MD; James Voos, MD; and Asheesh Bedi, MD
Chapter 7 Medial Soft Tissue Injuries of the Hip:

Adductor Strains and Athletic Pubalgia/Core Muscle Injury . . . . . . . . . . . . 105
Patrick Birmingham, MD; Eilish O’Sullivan, PT, DPT, OCS;
and Christopher M. Larson, MD
Chapter 8 Posterior Soft Tissue Injuries of the Hip: Hamstring . . . . . . . . . . . . . . . . . . 125

Steven B. Cohen, MD; James P. Bradley, MD; Carlos A. Guanche, MD;
Eddie Y. Lo, MD; and Christopher M. Larson, MD
Chapter 9 Lateral Soft Tissue Injuries of the Hip:

Abductors and Iliotibial Band Syndrome. . . . . . . . . . . . . . . . . . . . . . . . . . . . 141
Eilish O’Sullivan, PT, DPT, OCS; Lazaros A. Poultsides, MD, MSc, PhD;
and Shane Nho, MD
viii Contents
Chapter 10 Nerve Compression Injuries About the Hip

and Deep Gluteal Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 153
Eilish O’Sullivan, PT, DPT, OCS; Stanley Antolak, MD;
and Hal D. Martin, DO
Chapter 11 Stress Fractures of the Hip and Pelvis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 171

Marci Goolsby, MD; Landon Hough, MD; and Marc R. Safran, MD
Section II Sport-Specific Injuries . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .187

Chapter 12 The Contact Athlete: Football and Rugby . . . . . . . . . . . . . . . . . . . . . . . . . . 189
Travis Maak, MD and J. W. Thomas Byrd, MD
Chapter 13 The Pivoting Athlete: Hockey, Soccer, Lacrosse, Basketball,

Wrestling, and Field Hockey . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 209
Christopher M. Larson, MD and Patrick Birmingham, MD
Chapter 14 The Overhead Athlete: Baseball, Volleyball, and Tennis . . . . . . . . . . . . . . . 221

Matthew Thompson, MD; Anil Ranawat, MD;
Struan H. Coleman, MD, PhD; and Marc R. Safran, MD
Chapter 15 The Endurance Athlete: Runners, Cyclists, Rowers, and Triathletes . . . . . . 237
Peter J. Moley, MD; Suzanne Gutierrez-Teissonniere, MD;
and Marc R. Safran, MD
Chapter 16 The Hypermobile Athlete: Dancers, Cheerleaders,

Figure Skaters, and Gymnasts . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 255
Lisa M. Tibor, MD and Ernest L. Sink, MD
Chapter 17 Sport-Specific Rehabilitation Guidelines . . . . . . . . . . . . . . . . . . . . . . . . . . . 273

Pete Draovitch, PT, MS, ATC, CSCS; Toni Dauwalter, PT;
Jaime Edelstein, PT, DScPT, COMT, CSCS;
and Eilish O’Sullivan, PT, DPT, OCS
Chapter 18 Outcomes in Return to Sport. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 291

Asheesh Bedi, MD; Jack G. Skendzel, MD; Karen K. Briggs, MBA, MPH;
Eilish O’Sullivan, PT, DPT, OCS; and Marc J. Philippon, MD
Financial Disclosures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 307

ABOUT THE EDITORS
Bryan T. Kelly, MD, is a specialist in sports medicine injuries and arthroscopic and open surgi-
cal management of nonarthritic disorders around the hip. He has a faculty appointment at Weill
Cornell Medical College and medical staff appointments at Hospital for Special Surgery and
NewYork-Presbyterian Hospital. He cares for several sports teams, serving as the Associate Team
Physician for the New York Giants and the New York Red Bull’s Major League Soccer team, as
well as the Team Consult for hip injuries for the New Jersey Nets and several collegiate teams in
the tri-state region.
Following his residency at Hospital for Special Surgery in 2001, Dr. Kelly completed a two-year
fellowship there, specializing in Sports Medicine and Shoulder Surgery. He then completed a fel-
lowship in Hip Sports Injuries and Arthroscopy at the University of Pittsburgh Medical Center,
Center for Sports Medicine, under the direction of Dr. Marc J. Philippon, MD. Prior to starting
his practice, Dr. Kelly also completed an AO International Traveling Fellowship, where he spent
time with Dr. Herbert Resch at the Landeskliniken Hospital in Salzburg, Austria, as well as with
Professor Reinhold Ganz in Bern, Switzerland, studying advanced techniques in open manage-
ment of hip and shoulder injuries.
Dr. Kelly currently serves as the Chief of the Hip Preservation Service, which is designed to
provide multidisciplinary care for patients at all levels with hip injuries. He has a broad range of
both clinical and basic science research interests, including the development of a clinical outcomes
registry; biomechanical studies evaluating conflict patterns in femoroacetabular impingement and
techniques in labral refixation; the development of synthetic scaffolds for labral reconstruction
and cartilage injuries in the hip; and the development of novel surgical techniques for managing
soft tissue injuries around the hip joint. He has authored over 125 scientific publications, chapters,
review articles, and books.
Asheesh Bedi, MD, is the Harold and Helen W. Gehring Early Career Professor of Orthopaedic
Surgery at the University of Michigan and MedSport Program. He is also an adjunct assistant
professor at Hospital for Special Surgery Center for Hip Preservation. He is a team physician for
the University of Michigan and Eastern Michigan University and a consultant for the National
Football League and National Hockey League Players’ Association, and specializes in both
arthroscopic and open surgery for athletic injuries of the shoulder, elbow, hip, and knee. Dr. Bedi
completed his undergraduate training at Northwestern University, where he graduated summa
cum laude. He graduated from the University of Michigan Medical School with Alpha Omega
Alpha recognition, and remained in Ann Arbor to pursue residency training in Orthopaedic
Surgery at the University of Michigan. Following his training, Dr. Bedi completed an extended fel-
lowship in sports medicine, shoulder surgery, and hip preservation at Hospital for Special Surgery
and Weill Cornell Medical College in New York. He received the Leonard Marmor Outstanding
Orthopaedic Resident Award, and the Hospital for Special Surgery Philip D. Wilson Award for
Excellence in both 2008 and 2009 for his efforts in orthopaedic research and tendon-bone heal-
ing studies with Dr. Scott Rodeo. Dr. Bedi is the winner of the 2010 and 2014 Neer Award of the
American Shoulder and Elbow Surgeons and a recipient of the 2010 Cabaud Award from the
American Orthopaedic Society for Sports Medicine. He has authored over 200 articles, chapters,
and peer-reviewed publications on shoulder, elbow, knee, and hip injuries in athletes.
Christopher M. Larson, MD, is a sports medicine fellowship-trained surgeon who specializes in

hip arthroscopy, treatment of femoroacetabular impingement, anterior cruciate ligament recon-
struction, and proximal hamstring repairs. After completing undergraduate studies (summa cum
laude) and medical school (Alpha Omega Alpha honors) at the University of Minnesota, Dr. Larson
performed his residency at the University of North Carolina, receiving the resident research and
x About the Editors
teaching award, and sports medicine fellowship at the Minneapolis Sports Medicine Center. He
has performed over 3000 hip arthroscopies/femoroacetabular impingement corrective procedures
and regularly lectures nationally and internationally. He is a master instructor for the Arthroscopy
Association of North America, co-chairman for the American Academy of Orthopaedic Surgery
Hip Preservation Course, and has published over 100 peer-reviewed articles and book chap-
ters regarding hip and knee sports medicine. Dr. Larson is currently a Team Physician for the
Minnesota Wild (National Hockey League), and served as Team Physician for the Minnesota
Vikings (National Football League) from 2007 to 2011. He is Program Director for the Minnesota
Orthopedic Sports Medicine Institute/Fairview Orthopaedic Sports Fellowship program and is
certified in orthopedic sports medicine by the American Academy of Orthopaedic Surgeons.
Eilish O’Sullivan, PT, DPT, OCS, is a physical therapist board certified in orthopedics, spe-
cializing in hip and core muscle injuries. She currently serves as Clinical Care Coordinator for
Dr. Bryan Kelly, overseeing the clinical care of his patients and return to play for the athletes.
She also maintains a small clinical practice, treating patients with hip and core muscle injuries.
Dr. O’Sullivan graduated from Princeton University with a bachelor’s degree in psychology. She
went on to Massachusetts General Hospital Institute of Health Professions to obtain her Doctor of
Physical Therapy degree, followed by a year-long internship at Spaulding Rehabilitation Hospital.
She then went on to Hospital for Special Surgery, where she worked at the Sports Rehabilitation
and Performance Center, and lectured at a number of continuing education courses on the top-
ics of hip rehabilitation and core stabilization. Dr. Sullivan is a member of the Sports Section of
the American Physical Therapy Association. Her research interests include hip biomechanics and
return to sport following hip injury, and she has published on both of these topics.
CONTRIBUTING AUTHORS
Stanley Antolak, MD (Chapter 10) Jaime Edelstein, PT, DScPT, COMT, CSCS
Interventional Pain Management (Chapter 17)
Medical Advanced Pain Specialists Hospital for Special Surgery
Edina, Minnesota New York, New York
Patrick Birmingham, MD (Chapter 7, 13) Marci Goolsby, MD (Chapter 11)

Orthopaedic Sports Medicine Primary Care Sports Medicine
NorthShore University HealthSystem Hospital for Special Surgery
Chicago, Illinois New York, New York
James P. Bradley, MD (Chapter 8) Carlos A. Guanche, MD (Chapter 8)

Department of Orthopedic Surgery Southern California Orthopedic Institute
University of Pittsburgh Van Nuys, California
Pittsburgh, Pennsylvania
Suzanne Gutierrez-Teissonniere, MD
Karen K. Briggs, MBA, MPH (Chapter 18) (Chapter 15)
Center for Outcomes-Based NY Sports Med
Orthopaedic Research New York, New York
Steadman Philippon Research Institute
Vail, Colorado Landon Hough, MD (Chapter 11)
Primary Care Sports Medicine
J. W. Thomas Byrd, MD (Chapter 12) Mercy Sports Medicine
Nashville Sports Medicine Foundation Springfield, Missouri
Nashville, Tennessee
Aaron J. Krych, MD (Chapter 5)
Steven B. Cohen, MD (Chapter 8) Department of Orthopedic Surgery
Department of Orthopedic Surgery Mayo Clinic
Sydney Kimmel Medical College at Rochester, Minnesota
Thomas Jefferson University
Rothman Institute Michael Leunig, MD (Chapter 3)
Philadelphia, Pennsylvania Department of Orthopaedic Surgery
Schulthess Clinic
Struan H. Coleman, MD, PhD (Chapter 14) Zurich, Switzerland
Sports Medicine and Shoulder Service
Hospital for Special Surgery Eddie Y. Lo, MD (Chapter 8)
New York, New York Orthopedic Surgery
California Pacific Medical Center
Toni Dauwalter, PT (Chapter 17) San Francisco, California
Accelerated Sports Therapy & Fitness
Plymouth, Minnesota Travis Maak, MD (Chapter 12)
Orthopedic Surgery
Pete Draovitch, PT, MS, ATC, CSCS University Orthopaedic Center
(Chapter 17) Salt Lake City, Utah
Sports Rehabilitation and Performance Center
New York, New York
xii Contributing Authors
Hal D. Martin, DO (Chapter 10) Ernest L. Sink, MD (Chapter 16)

Baylor University Medical Center Center for Hip Preservation
Hip Preservation Center Hospital for Special Surgery
Dallas, Texas New York, New York
Peter J. Moley, MD (Chapter 15) Jack G. Skendzel, MD (Chapter 18)

Department of Physiatry Summit Orthopedics
Hospital for Special Surgery Woodbury, Minnesota
New York, New York
Michael D. Stover, MD (Chapter 4)
Shane Nho, MD (Chapter 9) Department of Orthopaedic Surgery
Hip Preservation Center Feinberg School of Medicine
Department of Orthopaedic Surgery Northwestern University
Rush University Medical Center Chicago, Illinois
Chicago, Illinois
Matthew Thompson, MD (Chapter 14)
Nikhil Oak, MD (Chapter 6) Orthopedic Surgery
Orthopaedic Surgery Drisko, Fee, & Parkins
University of Michigan Health System Independence, Missouri
Ann Arbor, Michigan
Lisa M. Tibor, MD (Chapters 3, 16)
Marc J. Philippon, MD (Chapter 18) Kaiser Permanente Medical Center
Department of Hip Arthroscopy South San Francisco, California
Center for Outcomes-Based
Orthopaedic Research James Voos, MD (Chapter 6)
Steadman Philippon Research Institute Division of Sports Medicine
Vail, Colorado Department of Orthopaedic Surgery
University Hospitals Case Medical Center
Lazaros A. Poultsides, MD, MSc, PhD Cleveland, Ohio
(Chapters 1, 4, 9)
Department of Orthopaedic Surgery Russell F. Warren, MD (Foreword)
Hospital for Special Surgery Sports Medicine and Shoulder Service
New York, New York Hospital for Special Surgery
New York, New York
Anil Ranawat, MD (Chapter 14)
Sports Medicine and Shoulder Service Alexander E. Weber, MD (Chapter 1)
Hospital for Special Surgery Department of Orthopaedic Surgery
New York, New York University of Michigan
Ann Arbor, Michigan
Marc R. Safran, MD (Chapters 11, 14, 15
Department of Orthopaedic Surgery
Stanford University School of Medicine
Redwood City, California
FOREWORD
This book, Sports Hip Injuries: Diagnosis and Management, edited by Dr. Bryan T. Kelly,
Dr. Asheesh Bedi, Dr. Christopher M. Larson, and Dr. Eilish O’Sullivan, brings together a wealth
of knowledge that has developed over the past few years. Formerly, little was known about hip
injuries in athletes as the diagnosis was usually a strain of the hip with little objective informa-
tion noted. This book brings to light the evaluation of hip disease as faced by the sports physi-
cian or therapist. Diagnostic criteria are developed and the sections on imaging highlight these
improvements.
The concepts of cam and pincer disease are clarified and the methods of treatment and their
results noted. The issues of cam impingement and instability are nicely demonstrated. The role of
hip disease and associated injuries, such as sports hernias, adductor strains, and pubic symphysis
symptoms, are well illustrated. The sports physician will find that this book will classify many
formerly puzzling injuries and allow a treatment protocol to be developed. This well-written book,
with an excellent group of contributors, will enable sports physicians to improve their patient care.
Russell F. Warren, MD
Sports Medicine and Shoulder Service
New York, New York
INTRODUCTION
Over the past 5 to 10 years, we have seen a continued improvement in our understanding of
the assessment and management of nonarthritic hip pain. Traditionally, the evaluation of hip pain
and hip injuries has been limited to obvious problems, such as hip arthritis and hip fractures, or
what were previously considered to be insignificant “soft tissue” strains and contusions, such as
“groin pulls,” “hip pointers,” and “bursitis.” Two parallel tracks of progress have provided us with
a vastly improved appreciation for the complexities of this joint in terms of both the capacity for
athletic injury and the underlying biomechanical basis for early hip disease. The first is within the
field of sports medicine, where the role of the hip joint and hip injuries in athletic performance
has evolved because of improved diagnostic skills allowing for better interpretation of debilitating
intra-articular disorders and their effect on core performance. The second is within the field of
hip preservation, where there has been significant evolution in our understanding of the effects
of biomechanical mismatches between the femoral head and the acetabulum on the development
of early hip damage and injury. The integration of these parallel fields has accelerated our under-
standing of the importance of the hip and early hip injury in human performance and function.
The development of symptomatic hip injury is related to the underlying structural anatomy of
the hip joint, combined with the mechanical load to which the joint is subjected. The leaders in the
field of hip preservation have elucidated the complexities of the structural anatomy of the hip joint
and the variety of ways that pathologic hip structure affects the loading characteristics of the joint.
Femoroacetabular impingement (FAI) likely represents the most common mechanism that leads to
the development of early cartilage and labral damage in the nondysplastic hip. Anatomic abnor-
malities of the proximal femur and/or acetabulum result in repetitive collisions occurring during
dynamic hip motion that lead to regional loading of the femoral head-neck junction against the
acetabular rim. The resulting abnormal kinematics can precipitate direct damage to the cartilage,
labrum, and surrounding capsular structures, ultimately resulting in early osteoarthritic changes.
The mechanical load that the hip joint is subjected to during athletic activity can exceed levels of
5 to 7 times body weight. When these loads are combined with the pathologic structural alterations
seen in FAI, the effects of these repetitive collisions occurring during sport-specific dynamic hip
motion are magnified. The exaggerated effects of the mechanical overload during sports allow for
earlier diagnosis and treatment of focal chondral and labral pathology.
The role of arthroscopy in the aforementioned advances lies in its ability to address numerous
intra-articular disorders with a less invasive technique and, consequently, with a more rapid recov-
ery. The importance of decreasing recovery time and reducing associated soft tissue morbidity is
most clearly exemplified in the athletic population, in whom accelerated recovery can determine
the ability for continued sport participation. The technical challenges of hip arthroscopy can be
daunting and require a detailed knowledge of the unique anatomic features of the hip joint. The
hip joint lies deep beneath multiple muscular layers, making soft tissue injury associated with
portal placement and instrument manipulation more problematic than arthroscopy around more
superficial joints like the knee, shoulder, and ankle. Additional anatomic challenges that are
unique to the hip joint include the highly congruent articulation between the ball and the socket,
requiring joint distraction to allow for safe instrument entry, as well as an extremely thick capsule
that allows for limited compliance.
Multiple biomechanical studies have begun to demonstrate the importance of the labrum and
the capsule in the static stability of the hip joint. The labrum forms a circumferential seal around
the femoral head, and appears to create a suction seal effect that is critical to the maintenance of
intra-articular hydrostatic fluid pressurization that decreases cartilage consolidation and com-
pression during joint loading. With the evolution of hip arthroscopy has come improved instru-
mentation and technical ability, allowing for the development of labral repair techniques as well as
techniques for the management of capsular injury and micro-instability of the joint.
xvi Introduction
In the high-level athlete with FAI, the patient’s hip is often brought into excessive and supra-
physiological ranges leading to high impaction loads. Compensatory effects on the soft tissues
surrounding the joint, including the labrum, capsule, and overlying musculature, lead to direct
injury and tearing of the labrum, attenuation of the capsule, and both direct and indirect effects
on the surrounding musculature and local nerves. The rationale for labral repair and hip capsu-
lorrhaphy is to restore labral function through anatomic repair and reduce capsular redundancy
in the patient with an attenuated capsule. The clinical examination of the hip, and the diagnostic
evaluation of labral pathology, FAI, chondral injury, capsular laxity, and extra-articular soft tis-
sue injury, has not been an area of focus for traditional training of orthopedic surgeons. With
our improved understanding of the wide variety of clinical entities that lead to symptomatic hip
pathology, clinical examination skills have become much more sensitive.
Hip arthroscopy has many technical challenges that make advanced surgical procedures more
difficult than typical arthroscopic procedures around other joints. Current thinking on the
importance of labral repair/refixation and the restoration of labral anatomy and function suggests
that appropriate repair techniques, whether performed open or arthroscopically, are important
for normal hip function. The general consensus is that every effort possible for the preservation of
functional labral tissue, whether by limited labral debridement or labral repair, should be made.
However, there is less general agreement on the role of the capsule in stability of the hip joint;
with more advanced techniques utilizing selective capsule cuts for improved exposure of periph-
eral compartment pathology, restoration of normal capsular anatomy is clearly also important in
functional outcomes.
With the continued influence of specialists in the field of hip preservation, it has become evi-
dent that the majority of intra-articular pathology is associated with some identifiable source of
mechanical malalignment. FAI continues to be the most relevant mechanical problem resulting in
labral and chondral pathology that is treatable by arthroscopic intervention. In general, dynamic
mechanical factors that lead to motion-induced injury to the hip joint include cam impingement,
rim impingement, femoral retroversion, and femoral varus. Static overload problems, including
acetabular dysplasia and femoral-sided dysplasia, such as femoral anteversion and femoral varus,
also contribute to intra-articular pathology; however, they are much less likely to be amenable to
arthroscopic techniques because of the inability to influence the underlying mechanical malalign-
ment in these instances. A thorough understanding of the underlying mechanical issues is critical
for the successful diagnosis and treatment of intra-articular hip pathology.
Patients suffering from intra-articular hip injury associated with FAI or instability commonly
present with associated soft tissue compensatory injuries. Soft tissue structures that are frequently
affected by intra-articular hip derangement include the hip flexor complex, psoas tendon, adduc-
tor and rectus abdominis tendons, injuries to the proximal hamstring tendon complex, and failure
of the abductor mechanism. Snapping hip syndromes, including internal snapping hip (psoas
tendon) and external snapping hip (iliotibial band), frequently occur as both audible and palpable
snapping of contracted tendon structures where they cross over bony prominences of the proxi-
mal femur and pelvis. Although these syndromes can occur as isolated problems, they are often
associated with some identifiable structural malalignment and intra-articular injury. Failure of the
abductor mechanism in the form of trochanteric bursitis, abductor tendonitis, and frank tears of
the gluteus medius and minimus tendons can also lead to symptomatic peri-articular soft tissue
dysfunction around the hip.
With the parallel development of our understanding of the assessment and treatment of hip
injuries within the orthopedic subspecialties of sports medicine and hip preservation, a much
more sophisticated understanding of the etiology of symptomatic hip pathology in both the athlet-
ic and the nonathletic patient has emerged. The clear relationship between mechanical malalign-
ment in the hip and the subsequent development of labral and chondral injury can be magnified
in the setting of athletic activity, as the loads that are subjected to the joint through sports will
lead to earlier onset of symptoms and, in many cases, allow for earlier treatment intervention.
Introduction xvii
The use of hip arthroscopy in the management of these intra-articular disorders has evolved over
the last 10 years with the improved understanding of the pathology. Although outcomes continue
to improve with better technique and instrumentation, continued emphasis on proper patient
selection and appropriate treatment of not only the resultant intra-articular pathology, but also the
underlying structural malalignment, is necessary for further advancement in this field.
This textbook is the first of its kind to attempt to integrate the concepts of traditional hip pres-
ervation with the unique issues associated with hip injuries in the high-level athlete. In that sense,
we have tried to divide the textbook into two discreet sections. In Section I, Basic Injury Patterns,
injuries associated with hip pathology in the nonarthritic hip are discussed. This section will
focus on basic pathoanatomic processes; clinical presentation; clinical examination, imaging, and
workup pearls; and different treatment options, including nonoperative, arthroscopic, and open
surgical techniques. General rehabilitation principles will be included in each chapter of this sec-
tion. In Section II, Sport-Specific Injuries, common hip and pelvis injuries will be examined, with
a focus on the sports in which we most frequently see such athletic injuries incurred. The focus in
this section will be geared toward the initial assessment, management, and treatment algorithms
in the acute setting, and it is intended for the athletic trainer and primary care provider who may
be the first to assess these athletes. Issues involving safe return to play, sideline management,
appropriate workup and evaluation, in-season management of injuries, treatment guidelines,
sport-specific rehabilitation, and return to play will be emphasized.
The book is designed to be a valuable reference for orthopedic surgeons who have focused prac-
tices in the treatment and surgical management of these patients, as well as for athletic trainers,
physical therapists, and primary care physicians, who will be able to consult this book for guide-
lines in their initial assessment and evaluation of these athletes.
Bryan T. Kelly, MD
Section I
Basic Injury Patterns
1
Anatomical Considerations
and Clinical Examination
Alexander E. Weber, MD; Lazaros A. Poultsides, MD, MSc, PhD;

Eilish O’Sullivan, PT, DPT, OCS; Bryan T. Kelly, MD;
and Asheesh Bedi, MD
The successful management of sports hip injuries in athletes is predicated on a thorough and
comprehensive diagnostic evaluation. It is paramount that in the evaluation of such a patient a
systematic approach is employed. As such, compartmentalization of the hip normal anatomy
and pathology into layers from deep to superficial allows for a comprehensive and systematic
evaluation of each of the independent and related pain generators in athletes with groin and hip
pain (Table 1-1). In this chapter, we will discuss the aforementioned layered approach in the evalu-
ation of hip pathologic entities, introduce a comprehensive clinical examination, and provide an
overview of the diagnostic imaging necessary to confirm the diagnosis and develop the best
treatment plan.
LAYERED APPROACH TO DIAGNOSTIC EVALUATION

OF THE ATHLETE WITH HIP PAIN
Layer I: Osteochondral Layer

Layer I is the osteochondral layer, which provides joint congruence and normal osteoarticular
kinematics in the hip. The structures comprising this layer are the innominate, acetabulum, and
Kelly BT, Bedi A, Larson CM, O’Sullivan E, eds.

-3- Sports Hip Injuries: Diagnosis and Management (pp 3-23).
© 2015 SLACK Incorporated.
TABLE 1-1
OVERVIEW OF THE LAYERED APPROACH TO THE ANATOMY AND PATHOLOGY OF THE HIP
LAYER NAME STRUCTURE PURPOSE PATHOLOGY
4 Chapter 1
I Osteochondral Femur Joint congruity Static Dynamic

Acetabulum Joint kinematics/biomechanics ● Developmental ● Cam/rim impingement
Innominate dysplasia ● Trochanteric impingement
● Acetabular profunda/ ● Subspine impingement
protrusio ● Delamination
● Femoral/acetabular
version
● Femoral inclination
II Capsulolabral Capsule Static stability ● Capsular instability

Labrum ● Labral tear
Ligamentous complex ● Ligamentum teres tear
Ligamentum teres ● Adhesive capsulitis
III Muscular Peri-articular musculature Dynamic stability Anterior

Lumbosacral musculature ● Pubalgia
Pelvic floor ● Hip flexor strain
● Psoas/rectus femoris impingement
Medial
● Adductor tendinopathy
● Rectus abdominus enthesiopathy
Posterior
● Hamstring strain
● Deep gluteal syndrome
Lateral
● Peritrochanteric disorders
● Gluteus medius tear
IV Neural Neurovasculature of the pelvic Biofeedback Neural Mechanical

girdle and hip Timing and sequencing of ● Nerve entrapment ● Scoliosis
Mechanoreceptors kinematic chain perfusion ● Referred spinal ● Ambulation /foot structure
Thoracolumbar and lower pathology and mechanics
extremity mechanics ● Neuromuscular ● Pelvic posture
dysfunction ● Osteitis pubis
● Regional pain ● Sacroiliac dysfunction
syndromes ● Pubic symphysis dysfunction
Anatomical Considerations and Clinical Examination 5
femur. Abnormalities within this layer can be classified into 3 distinct groups: 1) static overload,
2) dynamic impingement, and 3) dynamic instability.1-8 Anatomical variations resulting in static
overload include lateral or anterior acetabular undercoverage/dysplasia, femoral anteversion, and
femoral valgus. These structural mechanics lead to eccentric load, abnormal and increased stress,
and asymmetric loads between the femoral head and acetabular socket in the axially loaded posi-
tion (ie, standing). During hip motion, dynamic factors may contribute to hip pain as abnormal
stress and contact between the femoral head and acetabular rim occur. Different structural varia-
tions within layer I that may contribute to such dynamic impingement include femoroacetabular
impingement (FAI) (cam and focal or global rim impingement), femoral retroversion, and femoral
varus. When the functional range of motion required to compete in sports or for daily activities
exceeds the physiologic motion allowed by the anatomical structures of the hip, a compensatory
increase in motion must follow. Specifically, increased motion and consequential stresses through
the pubic symphysis, sacroiliac (SI) joint, and lumbar spine may occur. When functional range-of-
motion requirements are greater than normal motion limits, forceful anterior contact occurring
at the end range of internal rotation may lead to dynamic instability in the form of subtle poste-
rior hip subluxation, which occurs as the femoral head levers out of the hip socket.1,9 Anterior
subluxation may occur with premature posterior contact. Various radiographic indices calculated
on plain x-rays, such as Tönnis osteoarthritis grade, lateral center-edge angle, Tönnis angle, and
variables derived from the computed tomography (CT) scan, which better delineates the bone
anatomy, can facilitate the mechanical diagnosis.10-16
Topographic Anatomy
The evaluation of the osteochondral layer of the athlete with hip pain may begin superficially
with an awareness of the bony landmarks about the hip. The principal bony landmarks include
the greater trochanter, ASIS, pubic symphysis, iliac crest, posterior iliac spine, and the ischium
(Figure 1-1). These landmarks are pertinent during the physical examination as reference points
for the deeper soft tissue structures. Likewise, the greater trochanter and the ASIS have been
described as the key landmarks for accurately establishing the lateral and anterior portals, respec-
tively, during hip arthroscopy.
Osteology of the Hip Joint
The hip joint, femur, and pelvis are preformed in cartilage. The iliac, ischial, and pubic ossi-
fication centers are termed the triradiate cartilage. The iliac ossification center appears first, at
approximately 9 weeks of intrauterine development. The ischial and pubic centers appear at 16 and
20 months, respectively. At term, the acetabulum remains a cartilaginous structure and it is not
until 8 to 9 years of life that the acetabulum begins the transition into a bony structure. Fusion of
the cartilage centers becomes complete around 16 to 18 years.17,18
The morphology of the acetabulum also changes during perinatal life, initiating as a deeply set
cavity that almost entirely encompasses the femoral head and progressively remodeling such that
at birth it becomes shallower. In the postnatal period, the process reverses and the acetabulum
deepens.19,20
The two ossification centers of the proximal femur (the femoral epiphysis and the trochanteric
apophysis) do not appear during prenatal life; however, they become evident during the first year
of life. The femoral epiphysis ossification center is offset laterally within the head and undergoes
a similar morphologic change in early development. The anteroposterior (AP) diameter is greater
than the transverse dimension up to the age of 3, at which point the AP and transverse dimen-
sions equalize, followed by the progression of the transverse diameter.21,22 Global bony acetabular
coverage of the femoral head is greater in adults than in children and adolescents. However, with
the addition of the labrum, the total femoral head coverage is greater in children than in adults.23
The articular surface, or lunate fossa, is horseshoe shaped and the central inferior portion of the
acetabulum is devoid of cartilage. This bare area is the location of the acetabular attachment of the
6 Chapter 1
Figure 1-1. Bony landmarks that may

be palpated during the examination
of the hip to provide frame of ref-
erence include anterior superior iliac
spine, pubic symphysis, iliac crest,
posterior superior iliac spine, and
ischial tuberosity.
ligamentum teres, which is surrounded by the pulvinar, a synovial fat pad. The horseshoe-shaped
acetabulum is completed by the transverse acetabular ligament inferiorly (Figure 1-2).17
On the femoral side of the joint, the neck shaft angle averages 125 degrees with approximately
14 degrees of femoral neck anteversion.24 The femoral head articular cartilage is often described
as two-thirds of a sphere. The cartilage is congruous except for a shallow depression in the infero-
medial portion of the head devoid of cartilage known as the fovea capitis, which is the femoral
attachment of the ligamentum teres.17
Deviations from the normal development and morphologic relationships of the bony acetabu-
lum and proximal femur cause mechanical conflict within the hip joint. This conflict may span a
continuum from “undercoverage” (dysplasia) to “overcoverage” (FAI).1,4,5 The specific pathology
resulting in mismatch of femur and acetabulum can further be differentiated by its primary factor,
either a static or dynamic mechanical etiology.1
Static mechanical factors result in abnormal stress and asymmetric load in the standing or
axially loaded position. The bony abnormalities most often associated with static mechanical
Figure 1-2. Illustration of the acetabu-

lum and femoral head, highlighting
the acetabular and femoral head artic-
ular cartilage, ligamentum teres, and
labrum.
stress are lateral acetabular undercoverage, anterior acetabular undercoverage, femoral antever-
sion, and femoral valgus. The mechanical stresses in the aforementioned conditions lead primar-
ily to asymmetric wear of the chondral surfaces of the acetabulum and femur.1,25-27 The primary
bone and cartilage mechanical stress may lead to compensatory muscular injury or overload
(abductors, iliopsoas, and adductors), as the peri-articular musculature attempts to stabilize the
mismatched hip joint and affect the superficial layer III discussed later in this chapter.
In instances of dynamic mechanical problems, the underlying bony deformity leads to abnor-
mal contact between the femoral head and acetabular rim with range of motion of the hip. The
bony abnormalities most often associated with dynamic mechanical stress are a cam-type lesion,
rim lesion (focal, global retroversion, profunda, protrusio), femoral retroversion, or femoral varus.
The mechanical stresses of the above pathologic conditions may primarily lead to hip and antero-
medial groin pain; however, when the athletic demands on the hip are greater than the functional
range of motion, compensatory stress and subsequent pain may develop in the lumbar spine, pubic
symphysis, SI joint, and posterior acetabulum.1 Compensatory stress or demand on the periarticu-
lar musculature may also lead to layer III injuries to the muscle of the adductor longus, proximal
hamstrings, abductors, iliopsoas, and hip flexors.28
Layer II: Capsulolabral Layer

The resultant mechanical stresses of layer I can lead to reactive hip pain related to insufficient
congruency or impingement between the head and socket, leading to asymmetric wear of the
chondral surfaces of the acetabulum and femoral head with or without associated instability of the
hip. Thus, layer I has a direct effect on the inert layer of the hip.
Layer II includes the labrum, joint capsule, ligamentous complex, and ligamentum teres, which
contribute to static stability of the hip joint. When abnormal mechanical stresses are applied to the
hip joint secondary to underlying abnormalities within layer I, pathologies such as labral injury,
ligamentum teres tear, capsular irritation with consequent instability or adhesive capsulitis, and
various ligament tears can result. Magnetic resonance imaging (MRI) can help evaluate the chon-
dral, labral, and capsular damage. Range-of-motion requirements of the joint that are specifically
related to the activities, combined with the underlying structural mechanics of layer I, can predict
the type of injury to layer II structures.
8 Chapter 1
Figure 1-3. Illustration of the

capsular complex: iliofemoral liga-
ment, ischiofemoral ligament, and
pubofemoral ligament.
Capsular Structure and Function

The capsular complex is composed of 4 discrete thickenings that are named ligaments (the ilio-
femoral, the ischiofemoral, and the pubofemoral; Figure 1-3), as well as the zona orbicularis, which
is a distal thickening of the capsule forming a ring around the femoral neck. These ligaments each
originate from 1 of the 3 bones of the pelvis and effectively encapsulate the hip joint from acetabu-
lum to the intertrochanteric crest. From the acetabular origins, the capsule extends laterally to
surround the femoral head and neck and fans out to insert broadly. The femoral insertions run
anteriorly onto the intertrochanteric line, superiorly to the base of the femoral neck, posteriorly
superomedial to the intertrochanteric crest, and inferiorly to the femoral neck.17
The iliofemoral ligament (Y-ligament of Bigelow) makes up the anterior portion of the capsule
and derives its name from its appearance as an inverted “Y.” From a common origin between the
anterior inferior iliac spine (AIIS) and acetabular rim, it divides into a superior arm and an inferior
arm as it crosses the joint.17,29 The superior arm runs horizontally and inserts proximally along the
intertrochanteric line anterior to the joint. The inferior arm has a more vertical course and inserts
caudally along the intertrochanteric line.30 It is the strongest and thickest of the 3 ligaments and
provides restraint to anterior hip subluxation or dislocation, especially when the hip is in exten-
sion and external rotation.17,29 In its contracted position, it causes the hip to shift into a flexed and
internally rotated posture. Given this role, preserving or repairing the iliofemoral ligament during
hip preservation surgery is preferred and may be particularly relevant in patients with hyperlaxity,
anterior instability, or acetabular undercoverage.
The posterior portion of the capsule is predominately the ischiofemoral ligament. It originates
from the ischial rim of the acetabulum and inserts around the posterior aspect of the femoral
neck.29 The ischiofemoral ligament is also divided into 2 bands, with the more superior band
blending with the zona orbicularis fibers and the inferior band inserting more posteriorly on the
intertrochanteric crest.30 The ischiofemoral ligament resists internal rotation and adduction of
the hip. In comparison to the iliofemoral ligament, which is the strongest ligament in the body,
the ischiofemoral ligament has less than half its ultimate strength.29-31
The pubofemoral ligament originates at the pubic portion of the acetabular rim and the obtura-
tor crest of the pubic bone and fans outs distally like a sling to attach to the femoral neck. Fibers
of the pubofemoral ligament blend with the medial band of the iliofemoral ligament, and further
caudally the ligament inserts posteriorly on the femoral neck below the ischiofemoral ligament.
The pubofemoral ligament, in conjunction with the medial and lateral arms of the iliofemoral liga-
ment, serves to control external rotation of the joint.17,30
In contrast to the longitudinally oriented fibers of the outer capsule (iliofemoral, ischiofemoral,
and pubofemoral ligaments), the inner capsule fibers of the zona orbicularis run in a circular,
horizontal fashion. These fibers encircle the femoral neck, forming the narrowest area within the
hip capsule. This leash of capsule fibers acts like a locking ring around the femoral neck, prevent-
ing femoral head distraction from within the acetabulum.32 The importance of these fibers for
hip stability was recently quantitated by Ito et al,32 who substantiated the importance of the zona
orbicularis as the main hip stabilizer against distractive forces by sequentially sectioning the hip
capsule and labrum of cadaveric specimens.
In addition to providing stability to the hip joint, the capsule provides protection to the carti-
lage and blood supply to the acetabulum and femoral head. There are 4 main blood vessels that
penetrate and supply the hip capsule: the superior gluteal artery, the inferior gluteal artery, the
medial femoral circumflex artery, and the lateral femoral circumflex artery (Figure 1-4). The
posterior hip capsule receives its blood supply from the superior and inferior gluteal arteries as
they descend from the pelvis. The anterior capsule is predominately vascularized from the medial
and lateral circumflex arteries as they ascend through the hip capsule.33 In most cases, the medial
femoral circumflex artery travels on to be the primary blood supply to the femoral head; however,
Kalhor et al33 demonstrated that the inferior gluteal artery was the dominant supplier of blood
to the femoral head in a minority of cases. In the majority of cases, the main blood supply to the
femoral head originates distally at the capsular insertion and, thus, overzealous dissection of the
capsule for either exposure or instrumentation during hip arthroscopy can devascularize the
femoral head. Therefore, if the capsule must be opened, by either capsulotomy or capsulectomy,
the incision or split should be made between the lateral and medial synovial folds and in the inter-
muscular plane between the iliocapsularis and gluteus minimus.17,33
Labral Structure and Function
The labrum is a fibrocartilaginous structure that attaches to the bony rim of the acetabulum
and works to effectively deepen the acetabular socket. The labrum is triangular in cross-section
with the apex forming the free edge. Inferiorly, the labrum terminates at the anterior and posterior
edges of the acetabular fossa, at which point it becomes contiguous with the transverse acetabular
ligament (see Figure 1-2).17 The base of the triangular labrum attaches to the acetabular articular
cartilage through a transition zone of calcified cartilage with a distinct tidemark.34 The average
labral thickness is reported to be 5.3 mm (SD = 2.6 mm).35 Labral thickness varies by location, with
the largest diameter in the posterosuperior region and the smallest diameter in the anteroinferior
region. The labrum is a neurovascular structure and its vessels penetrate the labrum from its exte-
rior capsular attachments, leaving the central-most region with the poorest vascular perfusion.
10 Chapter 1
Figure 1-4. Illustration of the major blood vessels to the hip.
In similar fashion to the knee meniscus, it is likely that the peripheral capsulolabral junction has
the highest healing potential.36 Studies suggest that the labrum contains free nerve endings that
contain both proprioceptive and nociceptive fibers. This may substantiate the clinical finding of
decreased proprioception and pain in athletes with torn labral tissues.37
The osseous anatomy of the hip joint provides stability; however, more recent studies suggest
that the soft tissue envelope around the joint, the joint capsule, and labrum may contribute a
large portion of the total hip stability.38-40 Tan et al35 found that acetabular surface area coverage
increases more than 25% and the acetabular volume by approximately 20% in the presence of an
intact labrum as compared with a hip joint devoid of labrum. The efficacy of the labrum in provid-
ing stability likely stems from its ability to act as a “suction-seal,” resisting fluid extravasation from
between the femoral head and acetabulum. This seal effectively divides the central intra-articular
compartment from the peripheral intra-capsular, extra-articular compartment and increases the
intra-articular hydrostatic pressure and uniformity of load distribution. Biomechanical studies
have examined the effect of sequential damage to the labrum and suggest that a correlation does
exist between labral pathology and hip instability.38,40,41
Ligamentum Teres
The ligamentum teres is an intra-articular, but extra-capsular, structure that connects the fem-
oral head to the acetabulum. The ligamentum teres has an average length of 35 mm and runs from
the fovea capitis (area of the femoral head devoid of cartilage) to the acetabular fossa. The remain-
der of the fossa is filled with the pulvinar, a fat pad likely responsible for joint lubrication. The
ligament has 2 bands, anterior and posterior, that diverge as they insert broadly in the acetabular
fossa and blend with the transverse acetabular ligament. Because the ligament becomes taut in
adduction, flexion, and external rotation of the hip, some investigators propose that the ligament
may contribute to hip stability in these positions. This secondary stabilizing effect may be most
applicable in the patient with a deficiency of the labrum or a dysplastic hip.17,42
Layer III: Muscular Layer

Layer III is the contractile layer of the hip and hemipelvis. It consists of all musculature around
the hemipelvis, including the lumbosacral musculature and pelvic floor; it is responsible for the
muscular balance and dynamic stability of the hip, pelvis, and trunk. Abnormal mechanics within
layer I can lead to increased stresses of the SI joint, pubic symphysis, and ischium, and secondary
increases in the strains of the muscles attached to these pelvic structures. Enthesopathies and/or
tendinopathies can result in the peri-articular muscular structures and can be subcategorized
based on their location relative to the hip joint (anterior, medial, posterior, and lateral). Anterior
enthesopathy describes hip flexor strains, psoas impingement, and subspine impingement. Medial
enthesopathy encompasses adductor and rectus tendinopathies that have traditionally been
described as athletic pubalgia or “sports hernia.” Posterior enthesopathies include mainly proxi-
mal hamstring strains, but can also include injuries to the short external rotators including the
piriformis and may involve a constellation of pain patterns described as “deep gluteal syndrome,”
which involves posterior soft tissue injury and irritation or compression of the sciatic nerve.43
Lateral enthesopathies involve the peritrochanteric space and injuries to the gluteus medius
and minimus tendons. Specific patterns of pathology in layer I can be associated with specific
compensatory injury patterns within layer III. The muscles crossing the hip joint are extensive
and total 27 altogether. These muscles can be compartmentalized into groups based on location
and function (Table 1-2). The primary hip flexors are the iliacus, psoas, iliocapsularis, pectineus,
direct and indirect rectus femoris, and sartorius. The hip extensors include the gluteus maximus,
semimembranosus, semitendinosus, short and long head of biceps femoris, and adductor magnus
(ischiocondyle portion). The hip abductors are the gluteus medius, gluteus minimus, tensor fascia
lata, and iliotibial band. The adductors are adductor brevis, adductor longus, adductor magnus
(anterior portion), and gracilis. The external rotators are piriformis, quadratus femoris, superior
and inferior gemellus, obturator externus, and obturator internus.17 Hip internal rotators include
the gluteus minimus and pectineus. A detailed understanding of the muscular attachments, func-
tions, and innervations is critical for the accurate diagnosis of hip pain. Furthermore, this knowl-
edge base is also crucial in order to safely provide open or arthroscopic treatment.
Iliopsoas
Based on the origins and insertions of the iliopsoas, it is the only peri-articular hip muscle
that is able to simultaneously contribute to stability and movement of the trunk, pelvis, and leg.
Because the iliopsoas has 2 portions with separate innervations, the 2 muscles may act in uni-
son or separately. Andersson et al44 investigated the role of the iliacus and psoas separately in
response to different body positions and actions via electromyogram, and their findings suggest
that both muscles are involved in hip flexion and maximal thigh abduction. The iliacus is selec-
tively involved in motions between the hip and pelvis, whereas the psoas is selectively involved
in stabilizing the lumbar spine in the standing position in response to axial load applied to the
contralateral side of the body.44
12 Chapter 1
TABLE 1-2
OVERVIEW OF THE PERI-ARTICULAR HIP MUSCULATURE
MUSCLE GROUP MUSCLES
Hip flexors ● Iliacus
● Psoas
● Direct head of rectus femoris
● Indirect head of rectus femoris
● Sartorius
Hip extensors ● Gluteus maximus
● Semimembranosus
● Semitendinosus
● Long head of biceps femoris
● Short head of biceps femoris
● Adductor magnus: ischiocondylar portion
Hip abductors ● Gluteus medius
● Gluteus minimus
● Tensor fascia lata
Hip adductors ● Adductor brevis
● Adductor longus
● Adductor magnus: anterior portion
● Gracilis
● Pectineus
Hip external rotators ● Piriformis
● Quadratus femoris
● Superior gemellus
● Inferior gemellus
● Obturator externus
● Obturator internus
Hip internal rotators ● Gluteus minimus
● Adductor magnus: posterior portion
Hip stabilizer ● Iliocapsularis
This lesser known muscle lies directly over the anteromedial joint capsule and plays a role in
controlling the hip capsule.45,46 Research suggests that contraction of the iliocapsularis results in
tightening of the hip capsule and subsequent relative stability of the femoral head.45,46 Ward et al46
found that the iliocapsularis was more prominent in the dysplastic hip than in its nondysplastic
counterparts. In addition to its role as a dynamic stabilizer of the hip capsule, the iliocapsularis
functions as an important landmark in hip arthroscopy, in order to make the capsular incision
in the intermuscular plane between the gluteus minimus and the iliocapsularis muscles to avoid
denervation or vascular injury to the capsule and labrum.
Gluteus Minimus
The gluteus minimus muscle originates from both the external ilium and the inside of the pelvis
at the sciatic notch. It inserts at both the greater trochanter and the anterosuperior hip capsule. The
gluteus minimus can act as a flexor, internal rotator, or abductor depending on the position of the
hip. The inserting fibers on the anterosuperior capsule serve as a reproducible landmark during
arthroscopy of the peripheral compartment.
Layer IV: Neural Layer

Layer IV is the neurokinetic layer, including the thoracolumbosacral plexus, lumbopelvic
tissue, and lower extremity structures. This layer serves as the neuromuscular link and thus
functional control of the entire segment as it acts within its environment. Compensatory injuries
within this layer include nerve compression and pain syndromes, neuromuscular dysfunction,
and spine referral patterns. Common peripheral nerve disorders about the hip include lateral
femoral cutaneous neuropathy (meralgia paresthetica), femoral neuropathy, sciatic neuropathy
(piriformis syndrome or deep gluteal syndrome), obturator neuropathy, superior and inferior
gluteal neuropathies, pudendal neuropathy, and ilioinguinal, iliohypogastric, and genitofemo-
ral neuropathies.47-49 The nervous structures around the hip are all linked with their vascular
counterparts except in the case of the superficial lateral femoral cutaneous nerve. The femoral
neurovascular structures (nerve, vein, and artery) exit the pelvis deep to the inguinal ligament
halfway between the anterior superior iliac spine (ASIS) and the pubic tubercle. The nerve is the
most lateral of the 3 structures and superficial in depth, as it is separated from the joint capsule by
the iliopsoas muscle. The femoral nerve provides sensation to the anterior thigh via the anterior
cutaneous branch and motor innervation to the psoas, iliacus, pectineus, sartorius, and quadriceps
muscles. The lateral femoral cutaneous nerve of the thigh originates from the lumbar plexus and
exits the pelvis deep to the inguinal ligament in close proximity to the ASIS. The obturator nerve
originates from the lumbar plexus and exits the pelvis via the obturator canal before splitting into
anterior and posterior division. The obturator nerve provides sensation via its cutaneous branch
to the inferomedial thigh and motor innervation to the gracilis, obturator externus, and adductor
muscle group. The sciatic nerve originates from the lumbosacral plexus, exits the pelvis through
the greater sciatic foramen, and lies deep to the piriformis muscle before coursing superficially
to the remainder of the short external rotators. The sciatic nerve provides motor innervation to
the short external rotators via named branches and distally branches into the tibial nerve and
common peroneal nerve to provide motor innervation to the biceps femoris, semitendinosus, and
semimembranosus. The superior and inferior gluteal nerves exit the greater sciatic foramen with
their arterial counterparts, respectively. The superior gluteal nerve exits the pelvis superior to the
level of the piriformis and innervates the gluteus medius, gluteus minimus, and tensor fascia lata.
The inferior gluteal nerve exits inferior to the piriformis and innervates the gluteus maximus. In
addition to the compressive nerve syndromes and mononeuropathy, it is also possible to have hip
and groin pain secondary to myelopathy or radiculopathy. This should be kept in mind whenever
evaluating the athletic patient with a painful hip.17,47
COMPREHENSIVE CLINICAL EXAMINATION

A thorough, but focused, history and physical examination is critical to help define the specific
mechanical etiologies of patients’ symptoms, and helps to discriminate between primary intra-
articular and extra-articular pathologies. The duration, location, and character of pain should be
noted. Intra-articular pathology and FAI will typically manifest as deep, anterior groin pain.50 In
addition, patients with intra-articular pathology or dysplasia of the hip may also develop second-
ary symptoms of peritrochanteric pain, potentially due to overload of the abductor mechanism.9
14 Chapter 1
Aggravating activities that elicit pain should also be noted, such as getting in and out of a
car, crouching, or twisting maneuvers with sports. Deep hip flexion and/or terminal internal
rotation with these activities can elicit pain from bony impingement and labral pathology.9,50,51
Clearly delineating which positions and activities exacerbate the symptoms can provide insight
into the probable mechanical problem. Bony impingement will typically occur during prolonged
periods of sitting, whereas hip dysplasia or instability will often be aggravated by prolonged weight
bearing.51 Complaints of painful snapping may reflect the presence of intra-articular loose bod-
ies or abnormalities of the psoas tendon, iliotibial band, ligamentum teres, and labrum. All prior
surgeries should be documented, including prior hip arthroscopies, surgical dislocations, or pelvic
osteotomy procedures. Prior treatment for adductor tears or rectus strains in the form of athletic
pubalgia surgery has often been performed in an attempt to treat some of the compensatory mus-
cular injury to layer III across the hemipelvis that may be associated with impingement. Prior
interventions, including nonoperative management with physical therapy and therapeutic intra- or
extra-articular injections, should be documented.
The objective of the physical examination of the hip is to narrow the differential diagnosis
with a focused, reproducible systematic approach. An example of such an examination would
begin with inspection both of the skin for obvious injury, swelling, or ecchymosis and of gait for
abductor weakness, stride symmetry, and foot progression angle. Posture should be assessed for
limb-length discrepancy, pelvic obliquity, scoliosis, and/or muscle contractures. The single-leg
stance phase test is a variation of the traditional Trendelenburg test and assesses the patient’s neu-
ral loop of proprioception of the affected extremity in addition to the ability of the abductors to
hold the pelvis in a balanced position. With the patient in either the seated or supine position, the
hip region should be palpated for localized tenderness or muscle imbalance (either hypertrophy
or atrophy).52 Tenderness to palpation is rarely associated with any intra-articular pathology and
thus can be used to quickly narrow the differential diagnosis. Active and passive range-of-motion
and strength testing should be evaluated in the supine position and compared to the contralateral
side. A complete neurovascular exam of the bilateral lower extremities should also be undertaken.
A comprehensive physical exam has been outlined by Martin et al53 in which the body is exam-
ined in 5 different positions, including standing, sitting, supine, lateral, and prone. The standing
exam focuses on gait disturbances, assessment of the lumbar spine for mechanical malalignment,
Trendelenburg testing for abductor weakness, evaluation for pelvic asymmetry, and general body
habitus and laxity. The seated portion allows for a comprehensive evaluation of nerves and vas-
culature, and abnormalities in the skin and lymphatic systems, and an assessment of internal and
external rotation of the hip with a stabilized pelvis. In the supine position, a complete range-of-
motion evaluation is performed as well as strength and provocative pain testing. The lateral posi-
tion allows for a complete assessment of the peritrochanteric region, and should more completely
assess for associated injuries to the abductors or abnormal snapping of the iliotibial band or gluteus
maximus across the trochanter. Knee flexion diminishes the contribution of the tensor fascia lata
and iliotibial band, and allows for more specific detection of weakness of the medius and/or mini-
mus tendons. Testing in prone should be performed to evaluate posterior hip pain from proximal
hamstring syndrome, sciatic nerve irritation, or an ischial tuberosity avulsion injury. The prone
position is also ideal to assess for SI joint tenderness. Additionally, femoral anteversion is best
examined in this position with the knee flexed to 90 degrees and the foot and lower leg rotated
until the examiner palpates the lateral-most prominence of the greater trochanter. The angle
between this axis and the tibia is approximated as the femoral anteversion, with the normal range
between 8 and 15 degrees. Ely’s test for rectus femoris contracture is also performed in the prone
position by flexing the knee passively. A positive Ely’s test is indicated by the pelvis tilting and the
buttocks lifted from the table with knee flexion in order to compensate for a tight rectus femoris.52
A number of specialized provocative pain tests may be performed to identify the underly-
ing pathology. The first is to log-roll the lower extremity to attempt to discern intra-articular
hip pain.52 The dynamic external rotatory impingement test (DEXRIT) is performed with the
patient in the supine position with the contralateral lower extremity tucked and held against the
chest to eliminate lumbar lordosis. The affected hip is then brought into 90 degrees of flexion and
taken through an arc of abduction and external rotation. A positive test elicits the patient’s pain
and is indicative of impingement or labral tears. The dynamic internal rotatory impingement test is
a recreation of the DEXRIT except that the wide arc of range of motion is through adduction and
internal rotation. Again, recreation of the patient’s pain denotes a positive test for impingement or
labral pathology. The flexion, abduction, external rotation (FABER) test is also performed in the
supine position and can be implemented to distinguish between contralateral SI pathology and/or
ipsilateral psoas pathology. The ankle of the affected lower extremity is placed across the nonaf-
fected thigh, creating the “figure four” position. Once in this position, the patient is asked to local-
ize the pain. The flexion, adduction, internal rotation (FADDIR) test can be performed supine or
in the lateral decubitus position with the affected extremity side up. The examiner passively brings
the affected leg into 90 degrees of flexion, adduction, and internal rotation. A positive test elicits
discomfort that is a recreation of the patient’s subjective complaints. Posterior rim impingement is
tested in the supine position with the patient beginning the exam maneuver with both legs hang-
ing free off the end of the bed to the level of the hip. Both legs are flexed up and the unaffected leg
is held flexed while the affected leg is fully extended, abducted, and externally rotated. A positive
test will recreate pain and is indicative of an impingement of the femoral neck on the posterior
acetabular wall. Several tests are available to assess for piriformis syndrome; however, the most
commonly used test by the senior authors is active external rotation of the lower extremity against
resistance in the seated position.
The senior authors have identified 9 different provocative tests that are associated with different
underlying mechanical alterations in hip anatomy. The precise location of the pain (anterior, pos-
terior, lateral) and the intensity of the pain can help define the mechanical abnormality (Table 1-3).
OVERVIEW OF IMAGING STUDIES

Plain Radiographs
Plain radiographs to evaluate for mechanical causes of hip pain should include an AP pelvis
(both hips), Lequesne’s false profile view, as well as a lateral view of the proximal femur (ie, modi-
fied Dunn and frog lateral views). The AP pelvis is taken with a patient standing with the feet
internally rotated approximately 15 degrees. The beam is directed centrally toward the mid-por-
tion of the pelvis, allowing for clear definition of the iliac bone, sacrum, pubis, ischium, femoral
head and neck, greater or lesser trochanter, anterior and posterior acetabular wall, and sourcil.
The iliopectineal, ilioischial (Kohler’s), and arcuate lines, as well as the acetabular teardrop, sacral
foramina, and SI joints, should be clearly visible. The distance between the sacrococcygeal joint
is on average 47 mm in women and 32 mm in men, denoting a neutrally rotated pelvis. This cor-
responds to approximately 0 to 2 cm of distance between the symphysis and tip of the coccyx and
symmetric obturator foramina on an appropriate AP pelvis radiograph. Joint space narrowing
should be assessed to provide an objective characterization of the degree of degenerative changes
present in the hip, as less than 2 mm of preserved space on weight-bearing images has been
correlated with inferior clinical outcomes after a hip-preservation procedure. Lequesne’s false
profile view provides valuable information regarding the status of the anterior joint space and an
assessment of anterior acetabular undercoverage or overcoverage not possible with the AP pelvis
radiograph. The Dunn lateral view is obtained with the leg in 45 or 90 degrees of flexion, maximal
abduction, and neutral rotation and, together with the frog lateral radiograph, provides a reason-
able assessment of the femoral head-neck junction to appreciate loss of offset and cam deformity,
and estimate of femoral version.10,14,16,54,55
16 Chapter 1
TABLE 1-3
SPECIAL TESTS FOR HIP PATHOLOGY BASED ON LOCATION OF PAIN
PAIN LOCATION SPECIAL TESTS INDICATED
Anterior Impingement test: Groin pain with flexion, adduction, and internal
rotation is the classic test of anteromedial impingement resulting
for typical anterosuperior cam and/or pincer-type morphology.
Psoas impingement test/anterior capsule inflammation test:
Dynamic stressing of an inflamed anteromedial capsulolabral
complex and/or psoas tendon with flexion, abduction, and external
rotation will present with anterior groin pain.
Anterior instability/apprehension test: Stressing of the anterior
capsule with extension and external rotation of the hip can
result in pain and/or apprehension in the setting of instability or
anterior dysplasia.
Subspine impingement: Maximum pain with direct terminal hip
flexion beyond 90 degrees results from rim impingement at a
location just below the AIIS.
Posterior Posterior impingement: Posterior hip and buttock discomfort with
hip extension and external rotation occurs with posterior mechanical
impingement of the hip joint.
Trochanteric pain sign: Flexion of the hip to 45 degrees, abduction,
and external rotation against resistance will elicit pain at the
abductor insertion and posterolateral trochanteric facet and may
reflect abductor tendon pathology.
Ischiofemoral impingement sign: Posterior pain with hip extension
and internal rotation can result from secondary impingement
between the proximal femur/lesser trochanter and ischium.
Lateral Lateral rim impingement: Lateral hip pain with abduction can
reflect impingement of a superolateral femur and acetabular rim at
the 12 o clock position.
Butterfly goalie test: Anterior and lateral hip pain with 40 degrees
of hip flexion, abduction, and internal rotation is suggestive of
superoposterior FAI.
Careful analysis of plain radiographs can provide a remarkable amount of information

regarding morphologic abnormalities both of the femur and acetabulum. On the femoral side, loss
of offset at the head-neck junction and loss of sphericity of the femoral head can be appreciated on
AP and Dunn lateral views. Neck-shaft angle is typically between 125 and 130 degrees, and coxa
vara or valga can be recognized. Trochanteric height can provide a secondary index of varus or
valgus deformity, with the tip of the trochanter superior or inferior to the center of the femoral
head, on the AP view, respectively. The alpha angle can be estimated on AP pelvis and Dunn lat-
eral views and is defined by the angle between the neck axis and a line connecting the center of
the head to the point at which sphericity is lost An absolute value for a pathologic alpha angle is
not agreed upon, but generally values greater than 55-60 degrees may indicate cam impingement
Figure 1-5. Lateral radiograph of the hip demonstrating an

abnormal alpha angle with the corresponding pathologic
cam lesion (white arrow).
morphology (Figure 1-5). Synovial herniation pits may be seen at the femoral head-neck junction
and are consistent with mechanical impingement at this location.12,15,56
On the acetabular side, a number of radiographic findings can help to identify morphological
abnormalities. The teardrop is a radiographic condensation of the innominate bone at the inferior
end of the acetabulum that is continuous with the ilioischial line. On an AP view, a wide teardrop
can signify a shallow acetabulum and/or lateralization of the femur, whereas a narrow teardrop or
teardrop that is medial to the ilioischial line can indicate a deeper than normal acetabulum and
global overcoverage (coxa profunda) when associated with an elevated lateral center-edge angle
(> 35 degrees). Associated medialization of the femoral head in which it touches or crosses the
ilioischial line reflects protrusio deformity.11,13 Acetabular coverage can be difficult to fully assess
on plain radiographs, but certain findings may provide indications of morphological abnormality.
The lateral center-edge angle of Wiberg on the AP view and anterior center-edge angle of Wiberg
on the false profile view are quantitative indices of lateral and anterior coverage, respectively, with
values less than 18 to 25 degrees indicative of dysplasia (Figure 1-6A). The roof, or sourcil, should
cover about 80% of the width of a spherical femoral head. The Tönnis angle, or line connect-
ing the medial and lateral edge of the sourcil, should be horizontal or between 0 and 10 degrees
superiorly angled (Figure 1-6B).11-13,16 Greater upslope may represent dysplasia and/or lateral
subluxation of the head, whereas downsloping may reflect medial translation of the head and/or
medial osteoarthrosis.
Acetabular version is perhaps most difficult to determine on plain radiographs, as it is not
only variable at different locations along the rim but also highly susceptible to subtle changes in
radiographic technique.57 However, certain findings may heighten concern for morphological
abnormality. In the typically anteverted acetabulum, the anterior and posterior walls contact each
other at the lateral edge of the sourcil and should not cross each other (Figure 1-6C). Anterior
overcoverage, or “cranial retroversion,” is suggested by any crossover of the anterior wall over
a normal posterior wall. In addition, the posterior wall should normally pass just medial to the
center of the femoral head. If the posterior wall passes lateral to the head center on an appropri-
ate AP radiograph, posterior overcoverage may be present. Furthermore, prominent appearance
of the ischial spine on an AP view is suggestive of true acetabular retroversion.58 Other findings
suggestive of mechanical abnormalities include subchondral cysts from rim loading in dysplasia
or from impingement related to a pincer lesion. Osteophytes on the rim can develop from labrum/
rim ossification with pincer impingement, and often fractured “pincer rim fragments” can be seen.
Clohisy et al59 recently evaluated the ability of hip specialists to reliably identify important
radiographic features and to make a diagnosis based on plain radiographs. Five hip specialists and
one fellow performed a blinded radiographic review of 25 control hips, 25 hips with developmental
dysplasia, and 27 with FAI. Intraobserver values were highest for acetabular inclination (kappa =
0.72) and determination of femoral head center position (kappa = 0.77). Interobserver reliability
values were highest for acetabular inclination (kappa = 0.61) and Tönnis osteoarthritis grade
18 Chapter 1
Figure 1-6. Anteroposterior radiographs of the pelvis demonstrating (A) center-edge angle of Wiberg, (B) Tönnis
angle measurement, and (C) crossover sign (anterior acetabular rim; solid line) crossing over the posterior acetabular
rim (dashed line) on left hip.
(kappa = 0.59). All other measurements, including diagnosis, had kappa values less than 0.55. It
was concluded that many of the standard radiographic parameters used to diagnose developmental
dysplasia and/or FAI are not reproducible, highlighting the importance of CT imaging to define
morphologic abnormalities.59
Computed Tomography
One of the greatest limitations of plain radiographs is the definition of both femoral torsion and
acetabular version. Acetabular version cannot be summarized in a single value, but rather is
defined by the relative relationship of the anterior and posterior walls and is variable at different
locations along the rim. This relationship cannot be defined on plain radiographs and is highly
vulnerable to error from subtle changes in radiographic technique and tilt or obliquity of the beam
and pelvis. Correspondingly, femoral torsion can be estimated but cannot be reliably measured on
plain radiographs, as the epicondylar axis of the distal femur must be defined (Figure 1-7). The
combined version of the femur and acetabulum, or McKibbin index, has a dramatic influence on
functional hip range of motion and the treatment of symptomatic impingement lesions.60,61 In
addition, focal anterior overcoverage or “cephalad retroversion” can be difficult to distinguish
from true acetabular retroversion on plain radiographs. Distinguishing these lesions is critical,
as an effective surgical treatment for these conditions is dramatically different. In this regard, CT
scans with 3-dimensional reconstruction have proven invaluable not only to define the location of
focal pincer morphology, but to accurately define coverage and version of the acetabulum at each
location along the rim.62 As with plain radiographs, appropriate positioning of the pelvis on the
Figure 1-7. Axial CT images used to calculate femoral version, including (A) alpha angle, (B) femoral anteversion, and
(C) epicondylar axis.
scanner is of paramount importance to accurate interpretation of the CT scan. Since the orientation
of the pelvis with regard to tilt and rotation requires the relationship of one hemipelvis to the con-
tralateral side, the CT scan should include the entire pelvis to make accurate measurements.63-65
Although plain radiographs can demonstrate a loss of offset and cam deformity on the femoral
side, they provide very limited information regarding the 3-dimensional location and topography
of the deformity. An alpha angle indicates loss of sphericity, but is highly variable depending on
where the measurement is taken on axial images of the femoral neck along the circumference
of the head-neck junction, and does not account for further distal femoral offset abnormali-
ties.64 Furthermore, although cam morphology may be evident on the Dunn lateral radiograph,
its extension medially or posterolaterally along the head-neck junction may not be appreciated.
This information with respect to both the size and extent of the cam morphology is critical, as
an effective osteoplasty must restore sphericity and offset at all of these locations to fully address
the mechanical impingement. Furthermore, recognition of impingement that extends superiorly
or even posteriorly behind the lateral retinacular vessels may require a modification of surgical
technique or demand combined open and arthroscopic approaches. In this regard, the CT scan
allows for the critical differentiation of cam morphology that can come close to arthroscopic or
open surgical approaches.64,66
Magnetic Resonance Imaging

MRI continues to be used as a diagnostic instrument for evaluation of the labrum and articular
cartilage.67-70 This may be performed with or without contrast arthrography; however, with the
proper sequencing, noncontrast MRI can fully evaluate the soft tissues of the hip without the inva-
sive nature of MRI arthrography and at a lower cost to the health system.69 All 3 of the standard
planes of imaging (coronal, sagittal, and axial) should be used in the evaluation of the hip by MRI.
The weight-bearing portion of the femoral head and acetabulum are best evaluated in the
sagittal plane. Significant chondral degeneration has been shown to compromise the outcome
of arthroscopic or open surgical interventions for FAI, and recognition of pre-arthritic changes
is critical in patient selection and preoperative counseling.71-73 The type and location of labral
tear provides important information regarding potential pain generators as well as confirma-
tory information regarding the anticipated type and location of bony impingement. The anterior
aspect of the labrum is optimally viewed on sagittal images. The coronal plane is used for the
evaluation of the suprafoveal margin of the femoral head and acetabular dome and to evaluate
the superior segment of the labrum. The trochanteric bursa and the enthesis of gluteus medius
and minimus are also best evaluated in the coronal plane. Tendinopathy and tears of the gluteus
medius and minimus tendons are a common cause of recalcitrant pain along the lateral side of
the hip and can be recognized preoperatively on MRI.74 Pathology within the muscle belly of the
obturator internus, obturator externus, quadratus femoris, and all the adductors is best viewed in
20 Chapter 1
the coronal plane and may indicate ischiofemoral impingement or other extra-articular disorders.
Lastly, the oblique axial plane (oriented along the long axis of the femoral neck) can be used to
quantify the degree of cam impingement by calculating the alpha angle and head-neck offset.15
The oblique axial images are also ideal for assessment of the neurovascular bundles around the
hip. Specifically, the discrete fascicles of the sciatic nerve, obturator nerve, and femoral nerve can
be examined in this plane. The final labral region (posterior) is viewed using the axial plane and
derangements to the posterior labral signal are often indicative of a previous hip subluxation or
dislocation episode.70,75
MRI can also identify precollapse avascular necrosis of the femoral head that is not appreciable
on plain radiographs. In addition, MRI allows for the identification of additional soft tissue pathol-
ogy, such as pigmented villous nodular synovitis, synovial chondromatosis, athletic pubalgia,
myotendinous disorders, and soft tissue masses/tumors that might contribute to the patient’s
symptomatology and overall treatment plan.69,70 Advanced cartilage sensitive sequencing has
increasingly emerged as a standard for assessing the health of articular cartilage. Techniques such
as T2 mapping, T1 rho, and dGEMRIC allow for a more objective measurement of cartilage health
that may provide clinical improvement after surgical intervention.
Diagnostic Injection
Injections have proven to be an extremely valuable diagnostic and therapeutic tool in the
approach to young patients with hip pain. Although the duration and extent of relief is variable,
fluoroscopic-guided, intra-articular injections of corticosteroid and local anesthetic medication
should typically alleviate symptoms attributable to labral tears and FAI. A failed response to a
well-placed injection should prompt evaluation for occult, extra-articular sources of symptoms,
and raise some concern regarding the potential outcome of hip surgery without further evalu-
ation. A fluoroscopically or ultrasound-guided injection into the hip joint may be useful in the
diagnostic workup as an adjunct to clinical examination, radiographs, and MRI. Response to an
intra-articular injection has been shown to be 90% reliable as an indicator of an intra-articular
abnormality.67 It is not uncommon, however, for peritrochanteric or lumbar pain to improve
after an intra-articular injection, providing some evidence to support that these symptoms are
the secondary sequelae of mechanical impingement of the hip that leads to abnormal kinematics
and strain of the lumbar and abductor musculature. Ultrasound-guided injections of the adductor
cleft, pubic symphysis, SI joint, subspine space, psoas tendon, trochanteric bursa, or hamstring
tendon origins can also prove valuable to identify pathological changes in these structures as a
cause of hip pain. Recognition of all potential pain generators is critical in order to thoroughly
address all offending pathology at the time of surgery.
PEARLS AND PITFALLS

● A systematic layered approach to the diagnosis and management of hip pathology aids in elu-
cidating the cause(s) of hip pain and the possible compensatory mechanisms that may result.
● The bony anatomy will inform one about the specific inert, contractile, and neurokinetic
issues that may result. One must first glean whether the pain is intra-articular, extra-articular,
or a combination of both.
● Radiographs are an important component of the patient evaluation and provide further
insight into the patient’s anatomy. These should include an AP pelvis, a false profile, and a
lateral view of the femur (such as a modified Dunn).
● Injections may provide insight into the specific pain generators, and rule in or out
extra-articular pathology in more complex cases.
CONCLUSION
A full understanding of the osseous and soft tissue anatomy of the hip and groin is critical to
perform the complete history, physical examination, and imaging workup of an athlete with a
sports hip injury. A layered approach to the evaluation allows for a systematic and comprehensive
assessment of all potential intra-articular and extra-articular pain generators. Both static and
dynamic mechanical factors may contribute to symptoms and are often interrelated by the abnor-
mal kinematics of the hip joint. Overall, the location and quality of the pain should correspond to
the mechanical diagnosis and primary and secondary injury patterns. If so, then correcting the
mechanical problems and primary and secondary injuries with a hip-preserving procedure should
optimize the outcome.
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40. Greaves LL, Gilbart MK, Yung AC, Kozlowski P, Wilson DR. Effect of acetabular labral tears, repair and resec-
tion on hip cartilage strain: A 7T MR study. J Biomech. 2010;43(5):858-863.
41. Ferguson SJ, Bryant JT, Ganz R, Ito K. An in vitro investigation of the acetabular labral seal in hip joint mechan-
ics. J Biomech. 2003;36(2):171-178.
42. Rao J, Zhou YX, Villar RN. Injury to the ligamentum teres. Mechanism, findings, and results of treatment. Clin
Sports Med. 2001;20(4):791-799, vii.
43. Martin HD, Shears SA, Johnson JC, Smathers AM, Palmer IJ. The endoscopic treatment of sciatic nerve entrap-
ment/deep gluteal syndrome. Arthroscopy. 2011;27(2):172-181.
44. Andersson E, Oddsson L, Grundström H, Thorstensson A. The role of the psoas and iliacus muscles for stability
and movement of the lumbar spine, pelvis and hip. Scand J Med Sci Sports. 1995;5(1):10-16.
45. Babst D, Steppacher SD, Ganz R, Siebenrock KA, Tannast M. The iliocapsularis muscle: an important stabilizer
in the dysplastic hip. Clin Orthop Relat Res. 2011;469(6):1728-1734.
46. Ward WT, Fleisch ID, Ganz R. Anatomy of the iliocapsularis muscle. Relevance to surgery of the hip. Clin
Orthop Relat Res. 2000(374):278-285.
47. Draovitch P, Edelstein J, Kelly BT. The layer concept: utilization in determining the pain generators, pathology
and how structure determines treatment. Curr Rev Musculoskelet Med. 2012;5(1):1-8.
48. Leunig M, Beck M, Stauffer E, Hertel R, Ganz R. Free nerve endings in the ligamentum capitis femoris. Acta
Orthop Scand. 2000;71(5):452-454.
49. Zazulak BT, Hewett TE, Reeves NP, Goldberg B, Cholewicki J. Deficits in neuromuscular control of
the trunk predict knee injury risk: a prospective biomechanical-epidemiologic study. Am J Sports Med.
2007;35(7):1123-1130.
50. Burnett RS, Della Rocca GJ, Prather H, Curry M, Maloney WJ, Clohisy JC. Clinical presentation of patients
with tears of the acetabular labrum. J Bone Joint Surg Am. 2006;88(7):1448-1457.
51. Clohisy JC, Knaus ER, Hunt DM, Lesher JM, Harris-Hayes M, Prather H. Clinical presentation of patients with
symptomatic anterior hip impingement. Clin Orthop Relat Res. 2009;467(3):638-644.
52. Braly BA, Beall DP, Martin HD. Clinical examination of the athletic hip. Clin Sports Med. 2006;25(2):199-210, vii.
53. Martin HD, Kelly BT, Leunig M, et al. The pattern and technique in the clinical evaluation of the adult hip: the
common physical examination tests of hip specialists. Arthroscopy. 2010;26(2):161-172.
54. Jamali AA, Mladenov K, Meyer DC, et al. Anteroposterior pelvic radiographs to assess acetabular retroversion:
high validity of the “cross-over-sign”. J Orthop Res. 2007;25(6):758-765.
55. Mast NH, Impellizzeri F, Keller S, Leunig M. Reliability and agreement of measures used in radiographic evalu-
ation of the adult hip. Clin Orthop Relat Res. 2011;469(1):188-199.
56. Barton C, Salineros MJ, Rakhra KS, Beaule PE. Validity of the alpha angle measurement on plain radiographs
in the evaluation of cam-type femoroacetabular impingement. Clin Orthop Relat Res. 2011;469(2):464-469.
57. Zaltz I, Kelly BT, Hetsroni I, Bedi A. The crossover sign overestimates acetabular retroversion. Clin Orthop
Relat Res. 2013;471(8):2463-2470.
58. Kalberer F, Sierra RJ, Madan SS, Ganz R, Leunig M. Ischial spine projection into the pelvis: a new sign for
acetabular retroversion. Clin Orthop Relat Res. 2008;466(3):677-683.
59. Clohisy JC, Carlisle JC, Trousdale R, et al. Radiographic evaluation of the hip has limited reliability. Clin Orthop
Relat Res. 2009;467(3):666-675.
60. Anda S, Svenningsen S, Dale LG, Benum P. The acetabular sector angle of the adult hip determined by com-
puted tomography. Acta Radiol Diagn (Stockh). 1986;27(4):443-447.
61. Hapa O, Yuksel HY, Muratli HH, et al. Axial plane coverage and torsion measurements in primary osteo-
arthritis of the hip with good frontal plane coverage and spherical femoral head. Arch Orthop Trauma Surg.
2010;130(10):1305-1310.
62. Dandachli W, Islam SU, Liu M, Richards R, Hall-Craggs M, Witt J. Three-dimensional CT analysis to
determine acetabular retroversion and the implications for the management of femoro-acetabular impinge-
ment. J Bone Joint Surg Br. 2009;91(8):1031-1036.
63. Jacobson JA, Bedi A, Sekiya JK, Blankenbaker DG. Evaluation of the painful athletic hip: imaging options and
imaging-guided injections. AJR Am J Roentgenol. 2012;199(3):516-524.
64. Milone MT, Bedi A, Poultsides L, et al. Novel CT-based three-dimensional software improves the characteriza-
tion of cam morphology. Clin Orthop Relat Res. 2013;471(8):2484-2491.
65. Peters CL, Erickson JA, Anderson L, Anderson AA, Weiss J. Hip-preserving surgery: understanding complex
pathomorphology. J Bone Joint Surg Am. 2009;91(Suppl 6):42-58.
66. Nepple JJ, Martel JM, Kim YJ, Zaltz I, Clohisy JC. Do plain radiographs correlate with CT for imaging of cam-
type femoroacetabular impingement? Clin Orthop Relat Res. 2012;470(12):3313-3320.
67. Byrd JW, Jones KS. Diagnostic accuracy of clinical assessment, magnetic resonance imaging, magnetic
resonance arthrography, and intra-articular injection in hip arthroscopy patients. Am J Sports Med.
2004;32(7):1668-1674.
68. Kramer J, Recht MP. MR arthrography of the lower extremity. Radiol Clin North Am. 2002;40(5):1121-1132.
69. Mintz DN, Hooper T, Connell D, Buly R, Padgett DE, Potter HG. Magnetic resonance imaging of the hip:
detection of labral and chondral abnormalities using noncontrast imaging. Arthroscopy. 2005;21(4):385-393.
70. Potter HG, Schachar J. High resolution noncontrast MRI of the hip. J Magn Reson Imaging. 2010;31(2):268-278.
71. Bedi A, Chen N, Robertson W, Kelly BT. The management of labral tears and femoroacetabular impingement
of the hip in the young, active patient. Arthroscopy. 2008;24(10):1135-1145.
72. Clohisy JC, St John LC, Schutz AL. Surgical treatment of femoroacetabular impingement: a systematic review
of the literature. Clin Orthop Relat Res. 2010;468(2):555-564.
73. Ng VY, Arora N, Best TM, Pan X, Ellis TJ. Efficacy of surgery for femoroacetabular impingement: a systematic
review. Am J Sports Med. 2010;38(11):2337-2345.
74. Lequesne M, Djian P, Vuillemin V, Mathieu P. Prospective study of refractory greater trochanter pain syn-
drome. MRI findings of gluteal tendon tears seen at surgery. Clinical and MRI results of tendon repair. Joint
Bone Spine. 2008;75(4):458-464.
75. Gold SL, Burge AJ, Potter HG. MRI of hip cartilage: joint morphology, structure, and composition. Clin Orthop
Relat Res. 2012;470(12):3321-3331.
2
Femoroacetabular
Impingement
I. Pathoanatomy, Clinical Evaluation, and
Arthroscopic Treatment Strategies
Bryan T. Kelly, MD and Christopher M. Larson, MD
Femoroacetabular impingement (FAI) has become increasingly recognized as a disorder

that can lead to progressive labral and chondral injury and early hip degeneration. Dynamic
impingement caused by structural hip pathomorphology can limit hip range of motion (ROM)
and result in repetitive impact of the proximal femoral head and neck against the acetabular rim,
resulting in damage to the labrum and adjacent acetabular articular cartilage. The two primary
structural abnormalities responsible for intra-articular impingement occur on either the femoral
side (cam impingement; Figure 2-1) or the acetabular side (rim impingement; Figure 2-2) of the
hip joint. With internal rotation and flexion or with straight flexion, the labrum and adjacent
soft tissues are compromised, ultimately resulting in irreversible damage to the articular carti-
lage and early-onset joint degeneration.1 Over the past decade, additional patterns and sources
of both intra- and extra-articular impingement have led to a more comprehensive diagnostic and
treatment algorithm. Recognition of these structural abnormalities through appropriate history,
physical examination, and imaging is essential for early diagnosis and surgical correction before
the progression of irreversible articular cartilage damage. Furthermore, recognition of FAI as a
cause of labral pathology and articular cartilage degeneration has led to new treatment strategies
for young adults with hip pain.
The etiology of cam and rim impingement morphology in humans remains controversial and
incompletely defined. An evolutionary explanation has been proposed.2 Hogervorst et al described
2 unique aspects of human evolution that have affected hip and pelvis development: the transition
to an upright gait and the development of a large brain. One type of hip morphology, coxa recta, is

- 25 - Sports Hip Injuries: Diagnosis and Management (pp 25-48).
26 Chapter 2
Figure 2-1. Plain radiograph of a patient

with asphericity of the femoral head
consistent with primary cam impinge-
ment. This pattern of femoroacetabu-
lar impingement (FAI) leads to primary
inclusion pattern of injury, as the cam
morphology enters the acetabulum
and creates abrasive wear to the transi-
tion zone cartilage at the junction of
the labrum and the articular cartilage of
the acetabulum.
Figure 2-2. Plain radiograph of a patient

with primary rim-sided impingement
characterized by proximal overcoverage
of the acetabulum. Traditionally called
“pincer” impingement, this pattern of
femoroacetabular impingement (FAI)
leads to primary impaction injury to the
labrum, with relative sparing of the ace-
tabular transition zone cartilage.
characterized by a straight or aspherical section on the femoral head or head-neck junction, which
is also typical of cam-type morphology. It is a more structurally sound hip that may represent an
evolutionary adaptation for running and hunting, and also explains the increased incidence of
large cam deformities in young, athletic males. The other type of hip, coxa rotunda, is character-
ized by a spherical femoral head with sufficient head-neck offset. It is seen mostly in climbing
and swimming mammals, and also represents a more common hip morphology seen in women.
The coxa rotunda hip allows for increased hip motion and accommodates the positional require-
ments of the hip during the birthing process. The evolutionary conflict between upright gait and
the birth of a large-brained fetus is expressed in the female pelvis and hip, and may provide an
explanation for rim impingement variants such as coxa profunda.2 Subclinical slipped capital
femoral epiphysis or related injury has also been implicated in the etiology of FAI and initially
was thought to be the etiology of the “pistol grip” deformity.3 More recently, other authors have
suggested that the aspherical osteocartilaginous bump at the head-neck junction could be associ-
ated with an epiphyseal extension and/or loss of separation between the femoral epiphysis and
the trochanteric apophysis, resulting from increased loading of the hip during late childhood and
Femoroacetabular Impingement: I 27
early adolescence.4 Lending additional support to this idea, increased athletic loads applied to the
immature hip have been associated with an increased prevalence of cam deformity in young soccer
players.5 The increasing recognition and treatment of symptomatic cam morphology in competi-
tive athletes further supports the theory that high deformational loads to the unfused proximal
femoral physis are an etiologic factor in the development of painful FAI.6-8 Finally, genetic factors
may have a role in the etiology of FAI. Pollard et al9 demonstrated that siblings of patients with FAI
had a relative risk of 2.8 of having cam deformity (66 of 160 sibling hips vs 23 of 154 control hips,
P < .00001) and a relative risk of 2.0 of having rim deformity (43 of 116 sibling hips vs 29 of 154 con-
trol hips, P = .001). The relative risk for bilateral deformity in siblings was 2.6 (42 of 96 siblings vs
13 of 77 control individuals, P = .0002).9 Geographical variation also exists, with a high prevalence
of FAI morphology in the Western world, where it is estimated to be the most common cause of
osteoarthritis in the nondysplastic hip.10 In contrast, the prevalence of FAI is extremely low in the
Eastern world, where dysplasia and osteonecrosis are much more prevalent and that likely reflects
genetic and lifestyle influences.11
PATHOANATOMY OF IMPINGEMENT: OVERVIEW

Understanding the pathophysiology of FAI requires a detailed consideration of the underlying
mechanical factors that predispose hips to asymmetric load and wear across the joint surfaces.
Over the past decade, there has been a substantial increase in evidence that symptomatic injury to
the nonarthritic hip is usually a result of pathologic structural anatomy combined with the applied
mechanical loads subjected to the hip joint. It has been well documented that approximately 90%
of all patients with labral and chondral damage have underlying bony abnormalities of either
femoral and/or acetabular morphology.12,13 In fact, as a result of the work by Ganz and colleagues,
the traditional concept of “idiopathic” osteoarthritis of the hip joint has essentially been elimi-
nated. Instead, it is recognized that definable complex pathologic hip structure predictably leads
to abnormal loading of the chondral, labral, and capsular structures of the joint, with resultant
progressive joint deterioration.14-16
FAI and dysplasia are the 2 most common mechanisms that lead to the development of early
cartilage and labral damage in the hip.10,17,18 With the addition of increased joint-reactive forces
seen in most athletic activities, these structural predispositions to early intra-articular injury can
result in accelerated wear patterns. Although we have historically described alterations in hip joint
mechanics as a continuum between “undercoverage” (dysplasia) and “overcoverage” (FAI), as our
understanding of morphologic alterations in the hip joint has improved, it has become clear that,
often, there are complex combinations of both dynamic and static mechanical factors.
Dynamic Impingement
The most common structural deformities that lead to dynamic mechanical overload are a loss
of femoral head-neck offset (“cam” impingement), focal or global acetabular overcoverage (“rim”
impingement), or a combination of impingement deformities. Alterations in proximal femoral and
acetabular anatomy result in repetitive collisions occurring during dynamic hip motion that lead
to regional loading of the femoral head-neck junction against the acetabular rim. These mechani-
cal stresses precipitate labral injury, chondral delamination, and a degenerative cascade of more
extensive, nonfocal intra-articular injury.1 Ultimately, pain develops secondary to repeated func-
tional movement patterns that exceed the anatomic and physiologic capacity of the hip joint.19
In addition to intra-articular destruction, these altered joint mechanics can change the dynamic
muscular forces and strain other structures around the pelvis. Compensatory muscular dysfunc-
tion secondary to dynamic impingement can affect all of the surrounding peri-articular muscles,
28 Chapter 2
but most commonly involves the adductor longus, proximal hamstrings, abductors, iliopsoas, and
other hip flexor musculature (see Figure 2-1).20-22
Cam Impingement
Cam morphology is defined by loss of femoral head-neck offset and asphericity of the femoral
head. This morphologic variant is the most common mechanical factor that contributes to pre-
arthritic hip pain and is typically encountered in the young, athletic male.23 Insufficient femo-
ral head-neck offset can occur anywhere around the femoral head circumference, but the most
pathologic location is usually in the anterosuperior (1 to 2 o’clock) position using a clock-face
orientation.24 Repetitive entry of the aspherical portion of the femoral head into the hip joint,
typically during flexion and internal rotation, results in a characteristic pattern of shear injury
to the transition zone and adjacent acetabular articular cartilage.25,26 Labral tears secondary to
primary cam impingement typically result in detachment at the transition zone cartilage rather
than intrasubstance injury.12,27
Although these injuries are commonly localized to the anterosuperior region of the acetabular
rim, the location of the labral tear and cartilage delamination injury is predictable on the basis of
the location, size, and topography of the cam morphology. Johnston et al28 studied the relationship
between the size of cam morphology and severity of intra-articular injury and found that a higher
offset alpha angle was associated with the presence of acetabular rim chondral defects (P ≤ .044)
and full-thickness delamination of the acetabular cartilage (P ≤ .034). Patients with detachment of
the base of the labrum had a higher offset alpha angle (P ≤ .016). Another retrospective review of
64 hips with symptomatic FAI reported a 44% prevalence of chondral delamination and demon-
strated a strong association with male sex and the presence of cam morphology (odds ratio, 0.16;
P ≤ .05).29 The severity of the labral and associated cartilaginous injury often depends on the dura-
tion of the untreated injury, indicating the importance of early diagnosis and treatment.27,28,30
These types of labral tears may have more favorable healing rates after refixation compared with
intrasubstance tears because the mechanism of injury and location primarily at the transition zone
preserves tissue quality and the vascular supply from the capsule.31,32
Rim Impingement
Focal acetabular retroversion is a distinct dynamic mechanical cause of FAI and has been
reported to be more common in females.10 Recent data, however, have suggested that a retroverted
acetabulum may be more frequent in males and that females have greater acetabular antever-
sion.33,34 Acetabular retroversion results in repetitive contact stresses of a normal femoral neck
against the region of anterior acetabular overcoverage. On well-aligned anteroposterior (AP)
radiographs, acetabular retroversion is suspected when the anterior acetabular rim is lateral to
the posterior acetabular rim (crossover sign) and is frequently seen in association with a positive
ischial spine and posterior wall sign. These radiographic parameters, however, have limited reli-
ability compared with computed tomography (CT) imaging.19,35,36 Focal acetabular overcoverage
needs to be distinguished from rim impingement caused by global overcoverage seen in the setting
of coxa profunda and protrusio acetabuli. Global overcoverage has been shown to have a female
predominance.18,37,38 Focal and global overcoverage can also result from iatrogenic overcorrection
after periacetabular osteotomy for dysplasia.39
Repetitive abutment of the femoral head-neck junction on the abnormal acetabular rim in flex-
ion and rotation results in degeneration and compressive injury to the anterosuperior labrum, as
well as a characteristic posteroinferior “contrecoup” pattern of cartilage loss of the femoral head
and acetabulum.16,19 Contrecoup chondral injury is believed to result from flexion or rotation of
the hip beyond the physiologic capacity of the joint, resulting in levering of the femoral head and/
or neck on the rim and abnormal shear forces on the posterior chondral surfaces.10,40 In contrast
to cam-induced injury, rim impingement lesions typically induce primary intrasubstance labral
injury and are, therefore, often less reparable lesions. Heterotopic bone apposition often occurs on
the osseous rim adjacent to the base of the labrum and can progress to result in ossification of the
entire damaged anterosuperior labrum. In later stages, the bone formation cannot be distinguished
from the native bone and the labrum may appear to be absent on imaging studies.19 Overall, focal
“impaction” rim injury results in relatively limited chondral damage compared with the deep
chondral injury and delamination associated with the “inclusion” injury pattern associated with
cam impingement.10,15
Mixed-type FAI, with both femoral and acetabular pathomorphologies, is reported to be the
most common FAI injury pattern.10,15 Beck et al15 reported that only 26 of 302 hips had isolated
cam-type morphology and only 16 of 302 hips had isolated pincer-type morphology. Allen et al41
reported on a total of 113 patients with symptomatic cam-type deformity for at least one hip.
Bilateral cam-type deformity was present in 88 patients (77.8%), whereas only 26.1% had bilateral
hip pain. Symptomatic hips had a statistically greater mean alpha angle than asymptomatic hips
(69.9 degrees vs 63.1 degrees, p < .001); among 201 hips with cam-type morphology, 42% also had
focal rim impingement morphology.41
Relative or absolute femoral retrotorsion may exacerbate the cam-type morphology and loss
of motion from FAI, as reduced femoral torsion leads to premature engagement of the proximal
femur against the acetabular rim and pelvis with flexion and internal rotation of the hip. Even
in the absence of femoral or acetabular deformity, retrotorsion of the femur increases functional
external rotation, but correspondingly reduces the range of internal rotation of the hip.19,42 In this
regard, anterior cam-type morphology in a patient with normal or increased femoral antetorsion
may not be symptomatic until terminal hip flexion and internal rotation, without significantly
restricting ROM. This same cam-type morphology in a patient with associated femoral retrotor-
sion may engage the rim with minimal internal rotation, resulting in significant pain and loss of
internal rotation.12,19,42
Extra-Articular Impingement
Dynamic impingement can also result from extra-articular impingement, secondary to
motion-induced conflict between the extra-capsular portion of the proximal femur against the
nonarticulating portion of the acetabulum and/or pelvis. Three specific types of extra-articular
impingement have been described. Trochanteric-pelvic impingement occurs secondary to an
altered relationship between the trochanter and the center of rotation of the femoral head. The
most obvious example of trochanteric-pelvic impingement is the varus deformity associated with
the sequelae of Legg-Calvé-Perthes (LCP) disease, resulting in mechanical reduction in hip flex-
ion and pathologic hinged abduction (Figure 2-3).43,44 Trochanteric-pelvic impingement may also
occur as a result of femoral retrotorsion leading to premature contact of the anterior facet of the
greater trochanter against the anterior inferior iliac spine (AIIS).
Ischio-femoral impingement has recently been described as an abnormal contact between the
ischium and the lesser trochanter in the native hip, leading to the insidious onset of posterior
hip and buttock pain exacerbated by hip extension and external rotation.45,46 Initially described
in 1977 in a patient who had undergone a total hip replacement,47 more recent literature
has documented objective injury to the quadratus femoris due to narrowing of the space
between the ischial tuberosity and the lesser trochanter. This narrowing can occur as a result
of enlargement of the lesser trochanter and/or alterations in ischial anatomy, the most obvi-
ous of which occurs secondary to apophyseal avulsions of the ischial tuberosity in the adoles-
cent population. Ischio-femoral impingement may also occur secondary to increased femoral
antetorsion, resulting in abnormal contact of the posterior facet of the trochanter against the
posterior ilium.
Finally, subspine impingement can occur as a result of abnormal contact between the AIIS
against the inferior neck of the femur during straight flexion.34,48 Although this may be a subtle
30 Chapter 2
Figure 2-3. (A) Trochanteric pelvic

impingement is a variation of dynamic
impingement, which results in the
repetitive conflict between the greater
trochanter and the pelvis. The most
obvious example is an LCP deformity,
but more subtle forms of extra-articular
impingement must be looked for when
evaluating the painful, nonarthritic hip.
(B) These surgeries typically require open
surgical dislocation with capsular repair.
variation of typical rim impingement, characteristic differences in AIIS morphology have been
recognized with increasing frequency. Elongation of the AIIS secondary to adolescent apophy-
seal avulsions or injuries of the direct head of the rectus femoris and secondary heterotopic bone
formation may lead to crushing of the capsule and rectus femoris tendon, rather than direct
intra-articular labral injury as is seen in typical rim impingement. A previous pelvic osteotomy
may also be the source of impingement against the AIIS if the fragment is over-rotated anteriorly.39
Recognition of potential extra-articular forms of dynamic impingement is critical in order to
understand the complete constellation of structural deformity that can be a source of mechanical
hip pain.
Femoroacetabular Impingement-Induced Instability

Dynamic instability occurs in the form of posterior hip subluxation due to early contact of the
femoral head against the acetabulum.49,50 The spectrum of posterior hip instability ranges from
subluxation to frank dislocation. The most common traumatic mechanism of injury in athletic
competition is a fall on a flexed and adducted hip with a posteriorly directed force. Atraumatic and
lower energy mechanisms of hip instability have also been described.49-51 Hip dislocations have
been reported in American football, skiing, rugby, gymnastics, jogging, basketball, biking, and
soccer. It has been proposed that capsular laxity or abnormal bony morphology may predispose
the athlete to hip instability.51
Dynamic Impingement and Static Overload

In contrast to dynamic impingement, static overload pathomorphologies result in abnormal
stress and asymmetric load between the femoral head and acetabular socket in the axially loaded
position (ie, standing). The most common form of static overload is acetabular dysplasia, which
can result in lateral or anterior undercoverage of the femoral head.52,53 Alterations in proximal
femoral anatomy can also lead to relative undercoverage of the femoral head within the acetabu-
lum. Excessive femoral antetorsion can result in static overload of the anterior acetabulum and
capsulolabral complex similar to the mechanical stresses observed in anterior deficiency of the
acetabulum. Femoral valgus can overload the superior acetabulum in a similar fashion to lateral
acetabular undercoverage. All of these static mechanical stresses cause hip pain related to insuf-
ficient congruency between the femoral head and acetabulum, leading to asymmetric wear of the
chondral surfaces of the acetabulum and femoral head with or without associated instability of
the hip. Hip pain related to static overload does not require motion across the hip to manifest.
Similar to the compensatory muscular dysfunction that occurs with dynamic impingement,
patients with static overload of the femoro-acetabular joint frequently suffer from compensatory
dysfunction of the surrounding peri-articular musculature, which must act to dynamically stabilize
the joint in the absence of bony containment.19 Although this chapter focuses on dynamic
impingement patterns, it is important to recognize that complex mixed deformities can coex-
ist. The combination of dysplasia and FAI is reported to be relatively uncommon but the current
authors have recognized this association with increasing frequency. Clohisy et al54 reported on a
series of patients with acetabular dysplasia and coexistent deformity of the proximal part of the
femur resulting in hip dysfunction and degenerative chondral-labral injury. The authors sug-
gested that complex combined injury patterns of FAI and dysplasia may require a periacetabular
osteotomy combined with concurrent impingement surgery in order to achieve a comprehensive
deformity correction and improved hip function.54
CLINICAL EVALUATION PEARLS

FOR FEMOROACETABULAR IMPINGEMENT
History and Physical Examination

As detailed in the previous chapter, a thorough but focused history and physical examination
is critical to help define the specific mechanical etiologies of each patient’s symptoms and allow
for the formulation of a rational treatment plan. A standardized, algorithmic approach, using the
combined information from the history, physical exam, radiographic findings, and special testing
(magnetic resonance imaging [MRI], CT scans, intra-articular injections, dynamic ultrasound
evaluation, and dynamic imaging evaluation), is necessary to achieve this goal.23,27
The history should identify the mechanism of injury, the duration of symptoms, the primary
and secondary pain locations, aggravating activities, the presence of associated mechanical symp-
toms, and the presence of compensatory pain patterns involving areas proximal or distal to the hip
joint. The history alone often provides valuable information regarding the underlying mechanical
etiology of hip pain. Frequently, patients with unrecognized primary hip pathology secondary to
impingement have had symptoms for a prolonged period of time. Clohisy et al23 reported that
the mean time from symptom onset to definitive diagnosis was 3.1 years and that patients were
evaluated by an average of 4.2 health care providers prior to diagnosis. Inaccurate diagnoses were
common, and 13% had unsuccessful surgery at another anatomic site.
The comprehensive physical exam outlined by Martin et al, which has been mentioned, com-
prises 5 different positions.55 Although this comprehensive exam is desirable in all patients,
ultimately the goal is to achieve a specific 4-layer diagnosis for each patient. As detailed in the
previous chapter, the 4 anatomic layers of the hip include the mechanical bone structure, capsulo-
labral complex, peri-articular musculature, and neural layer with associated referred pain patterns
or direct nerve compression syndromes around the hip. The minimal clinical exam necessary to
help make this 4-layer diagnosis includes gait assessment, ROM exam, provocative pain testing,
strength testing, and pain to palpation over the peri-articular hip regions.
For evaluation of impingement, the 2 most critical parts of the clinical assessment include
complete and accurate ROM assessment and thorough documentation of the location and inten-
sity of pain with provocative testing. ROM of both the symptomatic and contralateral hip should
be assessed, including measures of hip flexion, internal rotation at 90 degrees of flexion, external
rotation at 90 degrees of flexion, extension, and abduction in the supine position, as well as inter-
nal and external rotation in the prone and seated positions. Care should be taken to stabilize the
pelvis when assessing ROM in the supine position, as rotation of the whole pelvis or motion of the
hemipelvis at the pubic symphysis and sacroiliac (SI) joint can result in an errant overestimation of
internal and external rotation of the hip joint. Particular attention to hip internal rotation and flex-
ion should be employed. Patients with impingement have a characteristic reduction in hip internal
32 Chapter 2
rotation with the hip flexed between 80 to 90 degrees, as well as a reduction in straight hip flexion.
In extreme cases, obligatory external rotation of the hip may occur during hip flexion. Such altera-
tions in hip motion are important clues in the accurate diagnosis of hip impingement.
The differential diagnosis can be narrowed with specific provocative maneuvers that elicit
pain consistent with FAI. Provocative tests are employed to help define the specific type or
combinations of mechanical pathology that may be responsible for hip pain as each tested posi-
tion represents either compression or tensioning of intra- or extra-articular soft tissue structures.
At least 9 different provocative tests can be associated with different underlying mechanical altera-
tions in hip anatomy. The precise location of the pain (anterior, medial, posterior, lateral) and the
intensity of the pain can help define the mechanical abnormality (refer to Chapter 1). With these
provocative pain tests, a painful arc of motion can be defined by the surgeon to determine the
anticipated locations of the offending pathology. The most common positive provocative pain
positions in anterior and anterosuperior impingement are anteromedial hip pain in flexion, adduc-
tion, and internal rotation (traditional impingement test), and anterior hip pain with straight hip
flexion (subspine impingement test). By using provocative pain testing to provide a preliminary
anatomical diagnosis of layer I (osteochondral) pathomorphology, imaging studies can be used
as confirmatory rather than exploratory tools to further corroborate the mechanical causes of
hip pain.
Compensatory pain and/or dysfunction in peri-articular regions frequently occur in associa-
tion with mechanical hip joint malfunction. Evaluation for such compensatory breakdown can be
done through static and endurance strength testing involving hip flexion, abduction, adduction,
and extension; and pain to palpation over the SI joint, central pubic region, anterior superior iliac
spine, hip flexors, abductors, adductors, proximal hamstrings, and ischium. Core-muscle dysfunc-
tion oftentimes manifests as pain and/or weakness involving the rectus abdominus and adductor
musculature, and the coexistence of athletic pubalgia and FAI is common.21,56
At the completion of the history and physical exam, a preliminary 4-layer diagnosis can be
made. Additional correlation with diagnostic imaging, dynamic imaging assessment, and intra- or
extra-articular diagnostic injections will further support a complete diagnosis. An example of a
4-layer diagnosis follows.
a. Layer I: Osteochondral layer—Primary dynamic impingement with secondary static overload
i. Alpha angle: 74 degrees with maximum at 1:30 and extension in the superior, supero-
lateral, anterior, anterolateral, and inferior segments between 11 (posterosuperior) and
6 (inferior).
ii. Femoral torsion: 5 degrees
iii. Acetabular version at 12, 1, 2, and 3 o’clock: –5 degrees, –8 degrees, 0 degrees, 12 degrees
iv. Lateral center-edge angle: 29 degrees
v. Sourcil angle: 5 degrees
vi. Anterior center-edge angle: 30 degrees
vii. AIIS morphology: Type II
b. Layer II: Capsulolabral layer—Primary injury pattern
i. Labral injury between 12 and 3 o’clock, with elements of impaction and inclusion
mechanical damage.
ii. Reactive synovitis in the subspine region, consistent with subspine impingement.
iii. Grade 3 transition-zone cartilage wear adjacent to the labral pathology (debonding of the
cartilage from the underlying subchondral layer).
iv. No significant chondral wear on the remaining aspects of the acetabulum and
femoral head.
v. Partial injury to the ligamentum teres.
vi. No intra-articular loose bodies.
c. Layer III: Muscular layer—Compensatory patterns

i. Pain without weakness over the adductor longus origin. Pain relieved with intra-
articular injection.
ii. No pain over the central pubic bone or proximal to the pubis at the insertion site of the
rectus abdominus.
iii. Good strength assessment otherwise.
d. Layer IV: Neural layer
i. No evidence of referred pain patterns.
With this detailed 4-layer diagnosis, the steps necessary to address the problem can be carefully
laid out and followed to achieve the desired correction.
IMAGING PEARLS
The minimum diagnostic imaging evaluation for FAI should include an AP pelvis radiograph
and an elongated neck (Dunn) lateral view of the affected hip.57 The AP pelvis has been demon-
strated to be a valid indicator of cranial retroversion in the presence of a positive crossover sign.58
A false profile view should be obtained if suspicion for concomitant dysplasia exists, and also
provides the best radiographic assessment of AIIS morphology. The Dunn view (at either 45 or
90 degrees of hip flexion) provides an improved evaluation of the femoral head-neck geometry.57
This view allows for identification of the cam morphology and calculation of an alpha angle, which
estimates the degree of asphericity of the femoral head. In contrast to a frog lateral, these modified
lateral views allow for a better evaluation of the lateral neck at the 1:30 to 2:00 position without the
greater trochanter obscuring the view. Additional views that can be obtained include cross-table
lateral and frog lateral.
MRI with or without gadolinium contrast of the affected hip will allow accurate delineation
of the intra-articular and peri-articular soft tissue structures, including the femoral and acetabu-
lar chondral surface, labrum, capsule, and surrounding extra-articular tendinous insertions.
Advanced cartilage imaging including T-2 mapping, T1 rho, and delayed gadolinium-enhanced
MRI of cartilage (dGEMRIC) techniques have allowed for improved quantitative assessment of
cartilage integrity.59,60 A CT scan with 3-dimensional reconstruction and femoral version analy-
sis can provide a more detailed analysis of the proximal femoral and acetabular geometry. This
is particularly useful for minimally invasive techniques such as arthroscopic or mini-anterior
approaches to surgical management of impingement. It also helps to delineate complex combined
mechanical pathomorphology.
A fluoroscopically guided intra-articular analgesic and steroid injection into the hip may be
used for both diagnostic as well as therapeutic purposes, and is an important adjunct to the over-
all evaluation. Response to an intra-articular injection has been shown to be 90% reliable as an
indicator of an intra-articular abnormality.61 Occasionally, higher volume injections with gado-
linium can lead to increased discomfort secondary to capsular distention. Lower volume (< 5 cc)
anesthetic injections may subsequently be required in order to better evaluate the hip joint proper
as a source of pain.
Advanced dynamic imaging analysis is currently used in some centers to allow for real-time
assessment of impingement. Dynamic ultrasound can be used to visualize bony abutment and soft
tissue compression during clinical examination of the hip in provocative pain positions. Post-pro-
cessing computer analysis of 3-dimensional CT imaging can allow for analysis of conflict patterns
within the involved hip.48,62 Computer-assisted modeling of surgical corrections can be used for
preoperative planning with improved accuracy of surgical intervention.
34 Chapter 2
MANAGEMENT OPTIONS
Nonoperative Options
A course of nonoperative management may be advisable for the initial treatment of FAI in
some cases. This typically consists of activity modification, anti-inflammatory medication, core
muscular strengthening, balance and coordination training, alterations in pelvic and lumbar
positioning affecting “functional” impingement, and ROM exercises. However, there are no data
demonstrating the efficacy of these interventions on pain relief and functional improvement in
patients with symptomatic FAI. In fact, nonoperative management is frequently ineffective in the
setting of identifiable pathology, since patients with FAI are most frequently young, active, and
have mechanical pathology.
The effect of nonsurgical management on the natural history and progression of degenera-
tive changes with FAI, however, is unknown. Hartofilakidis et al63 retrospectively examined the
long-term outcome of 96 asymptomatic hips in 96 patients with a mean age of 49.3 years who had
radiologic evidence of FAI. Overall, 79 hips (82.3%) remained free of osteoarthritis for a mean of
18.5 years (10 to 40). In contrast, 17 hips (17.7%) developed osteoarthritis at a mean of 12 years
(2 to 28). Regression analysis showed that only the presence of idiopathic osteoarthritis of the con-
tralateral diseased hip was predictive of development of osteoarthritis on the asymptomatic side
(P = .039). The authors concluded that a substantial proportion of hips with FAI may not progress
to develop osteoarthritis in the long term.63 To date, there is no high-level evidence to demonstrate
the efficacy of nonoperative treatment of symptomatic hip impingement. Similarly, there is no
high-level evidence to suggest predictors of progressive chondral degeneration in asymptomatic
hips with impingement morphology.
SURGICAL INDICATIONS
A multitude of studies have demonstrated that both open and arthroscopic surgical approaches
can be effective for correction of mechanical conflicts due to symptomatic FAI.6,17,64-70 Depend-
ing on the pathoanatomy, operative treatment may include acetabuloplasty, femoral head osteo-
plasty, chondroplasty, labral limited debridement with preservation, and labral refixation through
both open and arthroscopic approaches.14 Open surgical approaches include the open surgical hip
dislocation (SHD),14 the Smith-Peterson or Heuter anterior arthrotomy,68 and an anteverting peri-
acetabular osteotomy (PAO) to correct acetabular retroversion.10,71 Arthroscopic treatment of FAI
has become increasingly used because of the minimally invasive approach and excellent visualiza-
tion that is provided by advances in current instrumentation and surgical technique. Nonetheless,
there continues to be an important role for open techniques, particularly for patients with mixed
patterns of dynamic and static overload and patients suspected of having some variation of extra-
articular impingement. Several studies have documented excellent results following both open and
arthroscopic management of FAI.17,72
The indications for surgical treatment of symptomatic FAI include the following:
1. Continued pain despite a trial of conservative measures, including activity modifications,
physical therapy, nonsteroidal anti-inflammatory medications, and functional core training
2. Clear evidence of treatable structural pathoanatomy that correlates with soft tissue injury pat-
terns and pain on clinical exam
3. No evidence of significant cartilage wear within the hip joint
A thorough diagnostic workup provides an accurate 4-layer diagnosis to allow for the creation
of a rational surgical treatment plan. Complete evaluation for both associated compensatory
and/or second primary sources of pain should be completed prior to proceeding with surgical
intervention, especially in the setting of atypical pain. Although special cases may exist, the pres-
ence of > 50% joint space narrowing and/or < 2 mm of joint space anywhere around the weight-
bearing zone on plain radiographs, or the presence of reciprocal full-thickness chondral loss to
exposed subchondral bone on MRI, are associated with poor outcomes.73 The use of diagnostic
injections within or around the hip joint in cases where there is uncertainty as to the location of
the primary pain generator should be considered, recognizing that the use of corticosteroid as
well as some local anesthetic agents may result in regional cartilage damage.74 The presence of a
labral tear on MRI or impingement morphology on advanced 3-dimensional imaging alone are not
indications for surgical treatment, as both labral tears and impingement morphology are common
in asymptomatic volunteers.75 However, evidence continues to mount suggesting that early inter-
vention in symptomatic patients with FAI leads to improved outcomes as the degree of permanent
chondral damage within the hip joint at the time of the index procedure has the greatest long-term
impact on joint function and longevity.62,66,67
The indications for arthroscopic vs open surgical approaches depend on a thorough
understanding of the size and location of the mechanical deformity and the expertise of the
treating surgeon. Independent of surgical approach, it is essential that the intervention primar-
ily address all mechanical factors contributing to the symptomatic impingement and secondarily
address the resultant intra-articular pathology.19 It should be noted that arthroscopic approaches
can readily access the anterior femoral head-neck junction, whereas the superoposterior and
inferoposterior head-neck junction are much more difficult to reach. The posterior head–neck
junction is not accessible arthroscopically, and these posterior cam deformities as well as more
severe angular (coxa vara or coxa valga) deformity, rotational (femoral retrotorsion or antetorsion)
deformity, and greater trochanteric impingement may be more effectively treated through open
surgical hip dislocation with or without proximal femoral osteotomies. Although the majority of
the acetabular rim can be accessed arthroscopically, more severe cases of true acetabular retrover-
sion, and profunda or protrusio acetabular deformity, may require pelvic osteotomy. Ultimately,
the goal of surgery is to relieve pain, improve function and return to activity, and prevent pro-
gressive degeneration of the hip joint.17-19 The treatment of labral pathology without appropriate
identification and management of the underlying bony pathology is the most common cause of
recurrent symptoms.76,77
SURGICAL TECHNIQUE: ARTHROSCOPY

As the understanding of FAI has improved, arthroscopic techniques have evolved to allow for
effective and comprehensive treatment of various impingement patterns. These include correction
of labral injury through limited debridement or refixation, as well as mechanical correction of
both acetabular- and femoral-sided impingement pathomorphology.7,78-81 Techniques for exten-
sile arthroscopic capsulotomies have improved central and peripheral compartment exposure,
resulting in better access for acetabular rim resection, treatment of labral pathology and chon-
dral injury, and femoroplasty for cam resection.6,7,82,83 Recent studies have established that, in
the hands of experienced surgeons, open surgical dislocation and arthroscopy have comparable
efficacy in achieving a surgical correction of impingement deformity. Bedi et al82 reported on
60 active male patients who underwent impingement surgery via surgical dislocation (30 patients)
and arthroscopic decompression (30 patients) for symptomatic FAI and identified no significant
difference in the achieved correction based on preoperative and postoperative alpha-angle mea-
surements on extended neck lateral radiographs between these 2 techniques. However, for patients
with extension of the cam morphology to the superolateral region, as indicated by the presence
of elevated alpha angles on the AP pelvis, correction was better in the open group. This suggests
that, in patients with superolateral extension or posterior extension of the cam morphology, an
open surgical hip dislocation should be considered. Mardones et al84 compared these techniques,
36 Chapter 2
both in cadaveric and clinical studies, and found no statistically significant differences between
the open and arthroscopic procedures in any of the measurements of resection. Positioning of
the osteoplasty, however, was less reliable with the arthroscopic than with the open procedure
because of the tendency to place the osteoplasty more posteriorly and distally than intended. It is
the opinion of these authors that the positioning of the osteoplasty through arthroscopic surgery
is highly dependent on surgeon experience, and that with careful preoperative planning and imag-
ing, these differences can be addressed and corrected.
Hip arthroscopy for the treatment of FAI can be performed with the patient in either the
supine or the lateral position. The procedure can be divided into 8 separate steps: 1. Positioning;
2. Portal access; 3. Interportal capsule cut; 4. Rim preparation/resection; 5. Labral refixation/
selective debridement; 6. Peripheral compartment access/visualization; 7. Femoroplasty; and
8. Capsule closure.
It is critical that the operating surgeon take care to properly and cautiously perform each of
these steps, as technical error at any point can result in poor execution of the procedure, which
ultimately may translate into an inferior patient outcome.
Step 1: Positioning
The positioning of the patient (supine vs lateral) is based on surgeon preference as there are
positives and negatives to each approach. Since the majority of complications associated with hip
arthroscopy are associated with patient positioning and traction, consistent patient setup by the
surgeon and the ancillary staff is essential. Setup for the supine position is similar to that used
for fixation of hip fractures, using a fracture distraction table. The lateral position is frequently
preferred by surgeons trained in arthroplasty, as the position is similar to that required for joint
replacement. For both positions, the feet are well padded and an extra-large perineal cushion is
used to optimize distraction of the hip joint with the least amount of traction. Gentle counterforce
traction is applied to the contralateral limb to help stabilize the patient on the operating table.
Traction is applied under direct fluoroscopic visualization. The initial vector for traction runs
parallel to the femoral neck rather than to the shaft of the femur, and is applied with the hip in
approximately 10 to 30 degrees of abduction, depending on the height of the greater trochanter
and inclination of the acetabular sourcil. When this initial axial distraction is applied with neu-
tral flexion, as the hip is brought into neutral adduction, the lateral distraction force optimizes
displacement of the head from the socket with the least amount of applied axial load. If the hip
is flexed in adduction, this will lead to increased axial load requirements, with an associated
increase in the risk of pudendal nerve injury. Adequate distraction is confirmed with fluoroscopic
visualization and requires approximately 10 mm of joint space widening in the AP plane. If the
seal is not broken with initial traction, excessive traction should be avoided and the seal can be
released in a controlled fashion by careful introduction of a spinal needle at the beginning of the
procedure. Adequate traction typically requires approximately 50 pounds of force. Internal rota-
tion of the hip is the final maneuver that decreases the tension on the anterior capsule and allows
for easier instrument entry. Knowledge of the individual’s hip mechanics can also help fine-tune
patient positioning. For example, patients with increased femoral retrotorsion should be placed in
a reduced position of hip internal rotation. In the presence of femoral retrotorsion, neutral rotation
or even slight external rotation will bring the greater trochanter away from the trajectory of the
anterolateral and distal anterolateral accessory portals. Placing the anterior superior iliac spines
parallel to the floor and/or ceiling with variable degrees of pelvic tilt/Trendelenberg will help to
recreate the preoperative well-centered AP pelvis radiograph on the fluoroscopic images. This
can help to better evaluate the extent of bony resection on the acetabular rim when indicated by
preoperative imaging and intraoperative findings.
Step 2: Portal Access

Accurate portal placement is essential for optimal visualization and safe access to the hip joint.
The portals originally described by Byrd and Jones85 are the anterolateral peritrochanteric portal,
the posterolateral peritrochanteric portal, and the anterior portal. Since this original descrip-
tion, a variety of other portals have been described. These are useful for more advanced technical
procedures with no increased risk to local neurovascular structures. Most current arthroscopic
techniques use some combination of 2 or 3 portals, depending on the surgeon’s preference and
training. The 2 most common “work-horse” portals are the anterolateral (lateral) peritrochanteric,
and either a true anterior or “modified” anterior portal. Additional commonly used portals
include posterolateral peritrochanteric, distal anterolateral accessory, proximal anterolateral
accessory, and a variety of percutaneous distal entry points that allow for more accurate suture
anchor placement.86
The anterolateral peritrochanteric portal is established first approximately 1 to 2 cm superior
and 1 to 2 cm anterior to the anterosuperior “corner” of the greater trochanter. With the hip in
traction, the tight anterior band of the gluteus maximus insertion onto the posterior aspect of the
iliotibial band is a reproducible, palpable soft tissue reference point. Planning for the second por-
tal, however, should be conducted prior to making the primary portal, as a minimum of 6 cm is
required between portals to maximize the working space between instruments. Initially, a spinal
needle is placed in the appropriate position under fluoroscopic guidance. The needle should be
kept as close to the femoral head as possible without hitting the articular cartilage surfaces, as this
position decreases the risk of injury to the labrum. First, a “giving way” of the capsular imped-
ance will occur if the needle is not penetrating the labrum. If a sudden reduction in pressure is not
experienced, then there is concern for placement of the needle through the labrum and it should
be repositioned. Second, an air arthrogram should be visualized on the fluoroscopic image after
the stylet of the spinal needle is removed. Finally, distention of the joint with 15 to 25 mL of saline
solution should produce a fluid flashback. If no flashback occurs, then the needle is either not in
the joint, or is blocked by capsular or labral soft tissue. Once entry into the hip joint is confirmed,
a guidewire is then placed through the spinal needle until it rests in the central fossa region of
the acetabulum. A small-diameter cannula (4.5 or 5.0 mm) and trochar set is passed over the
guidewire. Care should be taken not to bend or break the wire against the acetabulum. A 70-degree
arthroscope is then inserted through the cannula and into the central compartment.
An anterior or modified mid-anterior portal is then established. Of the common portals, the
original anterior portal is at the greatest risk for causing neurovascular injury because of its close
proximity to the lateral femoral cutaneous nerve.86 In order to minimize trauma to the lateral
femoral cutaneous nerve, a modified mid-anterior portal is made slightly more lateral and dis-
tal than the traditional anterior portal. The more distal entry point of this portal also improves
access to the anterior portion of the joint in hips that have cephalad retroversion, and allows for
a better angle for anchor placement and microfracture at the acetabular rim when indicated. A
spinal needle is directed 45 degrees cephalad and 30 degrees medially into the joint. Placement
of the needle into the joint may be confirmed fluoroscopically by visualizing convergence of the
tip of the needle toward the end of the arthroscope. Direct visualization of the anterior triangle
of the hip capsule should allow for careful entry into the hip joint such that the portal is as close
to the labrum as possible without penetrating the tissue. Once the second spinal needle is safely
positioned in the joint, fluid can be turned on to flush the intra-articular fluid and debris, and the
second trochar-cannula set can be placed atraumatically into the joint under direct visualization.
Correction of positioning of the portals should be thought of in 2 planes. In the sagittal plane,
the needle and instruments should move in a medial to lateral direction. Thus, in the supine
position, the needle is dropped parallel to the ground to achieve a more inferomedial location,
and perpendicular to the ground to achieve a more superolateral location. In the axial plane,
the needle and instruments should move in a proximal to distal direction. Thus, the base of the
38 Chapter 2
needle is raised toward the patient’s head if the tip is aimed too proximally (either in the labrum
or against the acetabulum) and the base of the needle is lowered toward the patient’s feet if the tip
is directed toward the femoral head. By making adjustments in needle and instrument position in
these 2 planes throughout the surgical procedure, accurate positioning of all instrumentation can
be expected with minimal soft tissue trauma.
The most commonly used third portals include the posterolateral peritrochanteric portal and
the distal anterolateral accessory portal. The posterolateral peritrochanteric portal is placed just
posterior and proximal to the posterolateral tip of the trochanter. This portal is oftentimes used
when patients are positioned laterally. External rotation of the foot can bring the sciatic nerve in
closer proximity to this portal, so careful attention to patient positioning is critical. The distal
anterolateral accessory portal is placed in line with the lateral portal, approximately 4 to 5 cm
distal. This portal also can be used percutaneously for placement of anchors into the acetabular
rim. A more distal entry point allows for parallel positioning of the anchor along the edge of the
acetabulum and reduces the risk for iatrogenic perforation of the anchor into the hip joint that is
seen with more proximal and anterior-based portal entry. The distal anterolateral accessory portal
can also be used as the working portal for femoroplasty in the peripheral compartment.
Once the portals have been established, a preliminary diagnostic arthroscopy within the cen-
tral compartment is performed to fully evaluate the entire labrum, the cartilaginous surfaces of
the acetabulum and femoral head, the ligamentum teres, and the capsular structures. The diag-
nostic arthroscopy is the final opportunity for the surgeon to confirm the 4-layer diagnosis, as
mechanical structural pathomorphology should lead to a predictable and characteristic pattern of
intra-articular injury based on the combination of joint-loading mechanics related to the specific
3-dimensional anatomy of the joint and the functional loading requirements present in the indi-
vidual athlete’s particular sport.12,87
Step 3: Interportal Capsule Cut

The interportal cut is the portion of the arthroscopic procedure that differs most from arthros-
copy in other joints such as the shoulder and the knee. Ito and colleagues recognized early on that
rim impingement due to focal acetabular retroversion (cephalad retroversion), true acetabular
retroversion (with associated posterior wall deficiency), and global acetabular overcoverage (pro-
funda and protrusion deformities) leads to a characteristic crushing of the labrum against the
femoral neck and is usually associated with a flattened, degenerative, or cystic labrum.40 In the
setting of isolated rim impingement, the acetabular cartilage is typically spared. If the labral tis-
sue is viable, preservation of the labral tissue with labral refixation is optimal.16,67 In these cases,
the rim decompression must be performed with careful protection of the labrum, since resection
of the rim lesion may destabilize or require detachment of the labrum. Exposure of the acetabu-
lar rim along the zone of labral injury is essential for accurate visualization and treatment of the
offending rim impingement. The capsule cut is performed to allow this visualization, and connects
the anterior/mid-anterior portal with the anterolateral/lateral portal. Extension of the interportal
cut further posterior may be required if labral injury or rim pathology is present posterior to the
12 o’clock position. The interportal cut should be carefully planned to cut the capsule only in the
area of the offending rim and labral pathology. Excessive capsular cutting not only is unnecessary,
but can potentially lead to postoperative capsular instability in the absence of routine capsular
repair/closure.33
Step 4: Rim Preparation/Resection

Management of the rim lesion begins with defining the margins of the lesion based on
preoperative imaging as well as direct visualization of capsular-sided labral injury and erythema
(Figure 2-4). Two general techniques have been described. In the first, the capsule is elevated off
of the area of rim overcoverage using a combination of motorized shavers and low-energy radio
Figure 2-4. Characteristic intra-articular findings associ- Figure 2-5. Labral refixation can be performed using a
ated with an impaction pattern of injury to the acetabular variety of different techniques. The general principles
labrum, associated with crushing of the labrum against a should be to preserve as much healthy labral tissue as
prominent acetabular rim (pincer lesion), that requires rim possible, and to restore the labral function back to its
resection and labral refixation for definitive treatment. normal biomechanical role as a suction seal that main-
tains a hydrostatic fluid buffer to reduce cartilage con-
solidation and load transmission during axial loading.
frequency ablation, but the labrum is not primarily detached from the rim. With this technique,
the rim can be decompressed to reestablish the normal relationship between the anterior and pos-
terior acetabular walls. This technique also allows for decompression of any areas of impingement
occurring in the subspine region.34 If this technique is used, then it is critical that decompression
of the acetabular bone extends all the way to the transition zone cartilage so no ridge of bone is
missed. If significant damage to the transition zone cartilage is present, destabilization of the
labrum may occur, which would subsequently require labral refixation/reinforcement. The second
technique is based on the original description of rim decompression outlined by Ganz et al.14,16
Here, primary detachment of the labrum is performed prior to the initiation of rim decompression.
If this technique is chosen, then one must take care to avoid truncation of the labrum leaving the
patient with deficient labral tissue for refixation. In determining the extent and location of the rim
decompression, the AP pelvis and the crossover sign have traditionally been used as diagnostic
parameters on which surgical execution is based. More recent studies have demonstrated that the
crossover sign based on the AP pelvis may inaccurately predict acetabular retroversion secondary
to alterations in AIIS morphology. Subsequent over-resection of the rim based on incomplete or
inaccurate preoperative planning may result in poor outcome.88 Simply relying on the presence
of acetabular anteversion or retroversion when deciding on whether to perform a rim resection
can lead to persistent iatrogenic instability or impingement, respectively. Whichever technique
is used, both fluoroscopy and direct arthroscopic visualization are used to confirm appropriate
rim resection.
Step 5: Labral Refixation/Selective Debridement

Once an adequate rim resection is completed, the areas of destabilized or detached labral tis-
sue are refixed to the rim using standard arthroscopic techniques. A suture anchor is drilled and
placed at the edge of the acetabulum using the most distally oriented portal possible to achieve
parallel entry of the anchor into the acetabular rim without penetration into the joint (Figure 2-5).
Smaller-diameter anchors are optimal, as they allow for more anatomic labral refixation. In
40 Chapter 2
Figure 2-6. Femoroplasty or cam decom-

pression should recreate a normal sphe-
ricity of the femoral head, recreate the
normal offset of the head-neck junction,
and provide adequate clearance of the
femoral head into the acetabulum during
dynamic assessment. Intraoperative fluo-
roscopic guidance and dynamic arthros-
copy should be used to confirm adequate
and complete decompression.
addition, anchor pullout strength requirements are significantly reduced compared with those
needed in the shoulder, where a greater stabilization effect is required. Direct visualization into
the joint should always be used to confirm that the anchor does not penetrate the joint. Once the
anchor is placed, the suture is passed through the labrum in a vertical mattress fashion with use
of either suture penetrators or shuttle sutures. A vertical mattress configuration ensures that the
suture material does not deform the labrum and is not in direct contact with the weight-bearing
acetabular cartilage. In some cases, the labral tissue is friable, and circumferential placement of the
suture may be required to reestablish a stable labral footprint. Attempts to minimize eversion of
the labrum should be made regardless of whether the suture is placed intrasubstance or circumfer-
entially around the labrum. Multiple suture anchors are employed in this fashion until the entire
labrum has been refixed to the acetabulum and the labral seal effect has been reestablished.89-91
Step 6: Peripheral Compartment Access/Visualization

Cam impingement is addressed after the rim resection and labral refixation have been com-
pleted. Since this portion of the procedure is performed in the peripheral compartment, the hip
is taken out of traction and flexed. The maximal deformity of the cam morphology is typically
present anterolaterally or anterosuperiorly (at the 1:30 position) and can be best visualized with
the hip flexed between 30 and 45 degrees.24 Increased flexion and external rotation allow for
visualization of lesions that extend to the inferomedial region. Hip extension and internal rotation
allow for visualization of lesions that extend towards the superolateral neck. If there is superior and
proximal extension of the cam morphology, then this portion of the decompression may be best
achieved while the hip is still in traction. The surgical goal of the femoroplasty is restoration of the
normal offset of the head-neck junction and clearance of the femoral head within the acetabulum
during full flexion and rotation (Figure 2-6).
Although there are numerous approaches to achieve this goal, adequate visualization of the
cam lesion within the peripheral compartment is essential with any technique. Fluoroscopy can be
very helpful for localization and decompression of the cam lesion. Some authors favor the use of a
T-capsulotomy to enhance peripheral compartment visualization, and reduce inadvertent capsular
injury. With the arthroscope in the mid-anterior portal, a switching stick is placed through the
distal anterolateral accessory portal, and the intermuscular interval between the capsular insertion
of the gluteus minimus on the lateral limb of the iliofemoral ligament and the capsular insertion
of the iliocapsularis tendon on the medial limb of the iliofemoral ligament is bluntly dissected.
Once the plane is clearly defined, a radio frequency ablation probe can be used to demarcate this
interval, which separates the medial and lateral limbs of the Y-ligament of Bigelow, with great
caution to avoid any soft tissue damage to the surrounding muscle. A Beaver Blade (Beaver-Visitec
International) is then drawn down the neck of the femur toward the intertrochanteric groove,
leaving sharply divided capsular edges that are easily protected and repaired at the completion of
the femoroplasty. The T-cut should not violate the circumferential thickening of the zona orbi-
cularis, as this does not provide any improvement in visualization and may negatively influence
capsular integrity. This capsulotomy leads to excellent visualization of the femoral neck for the
decompression and allows for complete assessment of the femoral head-neck junction medial to
the inferior vincula, lateral to the superior retinacular vessels, and distal to the intertrochanteric
line. Complete decompression of the head-neck junction can be performed using this technique,
even including the anterior facet of the greater trochanter for certain cases with possible extra-
articular impingement.
Peripheral compartment decompression without a T-capsulotomy can also be performed quite
effectively, but requires rotation of the cam lesion into the area of the capsulotomy throughout
the procedure with greater degrees of hip flexion, extension, internal, and external rotation. The
disadvantage of the T-capsulotomy is that there may be an increased risk for postoperative hetero-
topic bone formation if careful attention to the soft tissue is not adhered to, and it requires suture
closure of the capsulotomy to restore normal capsular anatomy. The disadvantage of performing
the femoroplasty without the T-capsulotomy is the that distal extension of the resection is more
challenging, and that, without careful attention to the capsule, there is the potential for more
extensive capsular damage if performed by inexperienced surgeons. Both techniques, however,
are effective, and adopting the technique that is most reproducible and versatile is likely the most
important consideration.
Step 7: Femoroplasty
Both access techniques to the peripheral compartment allow for dynamic arthroscopy, which
can accurately identify the site of impingement and allow complete visualization of the entire cam
lesion. The boundaries of the cam impingement lesion are marked out, using the more normal
anteromedial head-neck junction as a guide. The position of the camera and working instruments
can and should be changed throughout the case, so that complete visualization and recontouring
of the head-neck junction can be properly accomplished. If the camera is initially placed in the
mid-anterior portal, a 5.5-mm burr can be used for bony resection through either the anterolateral
portal (allowing access to the superior and superolateral cam extension) or the distal anterolateral
accessory portal (allowing direct access to anterior, anterolateral, and inferior cam extension).
If a 3-portal technique is being used, it is helpful to place a switching stick into the third portal
to retract the capsule for improved visibility during the femoroplasty. Sequential removal of the
superior, superolateral, anterior, anterolateral, and inferior portions of the cam morphology is then
performed to recreate a spherical femoral head. Care should be taken to visualize and protect the
lateral retinacular vessels that course along the posterolateral aspect of the femoral neck. Extension
of the decompression posterior to the vessels is possible as long as the resection region is proximal
to the entry of the vessels into the femoral neck. At the completion of the bone resection, all bone
debris is removed from the peripheral compartment, and dynamic arthroscopy is performed to
confirm the absence of any residual impingement. The goal is to restore femoral head-neck sphe-
ricity and offset, with impingement-free ROM achieved during dynamic assessment. A resection
of < 30% of the head-neck junction is recommended because this range has been shown to preserve
the load-bearing capacity of the femoral neck.92 Although postoperative femoral neck fracture or
stress reaction is unusual, there have been reports in the literature describing this complication
even in the absence of excessive bone resection.93
42 Chapter 2
Figure 2-7. Capsular closure is routinely

performed in all cases. Restoring the cap-
sular anatomy back to normal is a critical
component of the procedure in many
cases, especially if there is any concern
for generalized ligamentous laxity, or
micro-instability of the hip joint.
Step 8: Capsule Closure

As previously indicated, careful management of the capsule and a detailed understanding of
capsular anatomy is critical, as postoperative instability has been reported due to overaggressive
rim decompression, excessive capsulectomy, or failure to adequately repair the capsulotomy.33,94
If a T-capsulotomy down the femoral neck has been performed, both the T-cut and the interportal
cut should be repaired. Repair of the interportal cut is only possible if sufficient proximal capsule is
preserved during the rim decompression. First, an arthroscopic suture passer loaded with a suture
loop is passed through the lateral limb of the capsulotomy from the lateral portal. The suture loop
is then deployed from outside-in through the capsule. A penetrating suture retriever is then passed
through the medial limb and is used to retrieve the suture through the distal anterolateral portal.
The suture loop is then used to shuttle a suture through the limbs of the capsulotomy. The suture is
tied down after both suture limbs are brought through a single cannula. The process is repeated for
a total of 4 to 6 stitches depending on the degree of inherent capsular laxity, as well as mechanical
assessment of potential instability based on excessive femoral antetorsion or borderline acetabular
coverage94 (Figure 2-7). In cases in which there is extreme concern for capsular instability, proxi-
mal to distal repair of the capsule can also be performed to provide a complete anatomic closure
of the capsule. The senior authors routinely perform capsular closure of both the T-cut and the
interportal cut at the conclusion of the surgical procedure.
COMPLICATIONS
It is clear that there is a long and steep learning curve due to the technical nuances of the
arthroscopic management of FAI. The steps outlined for arthroscopic impingement surgery can
be modified based on surgeon preference. For example, Dienst et al95 have popularized primary
entry into the peripheral compartment without traction, followed by entry into the central com-
partment under direct visualization. It is clear, however, that given the challenges inherent in this
procedure, each surgeon needs to develop a sequential and reproducible approach to minimize
technical errors and maximize efficiency. Because of improved recognition of treatable pathology
and greater awareness of FAI within the athletic and orthopedic communities, it is estimated that
hip arthroscopy for FAI is proceeding at a rate of 15% per year. Revisions of inadequately or poorly
performed procedures are becoming more frequent.
Although uncommon (reported between < 1% and 10%), complications in hip arthroscopy
can be significant, particularly with inexperience or a lack of familiarity with the peri-articular
anatomy.96 The peri- and postoperative pitfalls that can lead to complications are generally related
to surgeon inexperience involving prolonged traction of the hip and/or inaccurate portal place-
ment.97 Intraoperative complications reported in the literature likely underestimate the rate of
iatrogenic chondral and labral injury due to needle and instrument malpositioning, traumatic
access into the central compartment, and instrument breakage.96 Transient or permanent nerve
palsies (sciatic, femoral, pudendal, or lateral femoral cutaneous) are typically related to improper
positioning, padding, and prolonged traction times during central compartment procedures with
a reported incidence between < 1% and 10%.98,99 Soft tissue injury to the perineal region secondary
to pressure necrosis is also related to excessive traction force and time. As previously described,
capsulotomies improve access and exposure, but also increase the risk of fluid extravasation to
the thigh and abdomen. Several reports of abdominal compartment syndrome have been pub-
lished.100,101 Protection of the lateral retinacular vessels during superolateral extension of the
femoral osteoplasty needs to be exercised to avoid the extremely rare, yet possible, development of
secondary osteonecrosis of the femoral head.102 Although vascular injury is rare, injury to the fem-
oral artery and vein or the medial femoral circumflex artery can occur with malpositioned portals.
Postoperative complications are also extremely rare. Several case reports of postoperative iat-
rogenic hip instability have been published as a result of over-resection of acetabular rim lesions
and/or insufficient capsular repair.33 Heterotopic ossification can occur in as many as 8% of
arthroscopic cases and is likely related to increased attention to bone resection as well as increased
bleeding associated with capsule cuts.103 Routine administration of prophylaxis with postopera-
tive nonsteroidal anti-inflammatories, as well as careful manipulation of surrounding capsular
musculature can reduce this risk to < 1%.103 Although the majority of heterotopic ossification is
asymptomatic, rare cases of symptomatic Brooker III or IV lesions with restricted motion and
pain may require revision surgery. Deep venous thrombosis (DVT) has been reported to occur in
as many as 3.7% of patients,104 although, in our experience and in most of the literature reporting
on postoperative complications, this incidence is much lower (< 0.1%). Routine use of DVT pro-
phylaxis is not indicated with the current evidence available.96 There is one case report on post-
operative minimally displaced femoral neck fracture requiring internal fixation,93 but the overall
incidence of this complication appears to be far less than 1%. Probably the most common, yet
most underreported, reason for continued pain and disability postoperatively is insufficient bone
resection leading to persistent postoperative impingement. With the rapidly increasing volume
of arthroscopic impingement surgery, careful attention to surgical resection is critical to ensure
reproducible and good long-term results.
POSTOPERATIVE CARE AND REHABILITATION

Postoperative rehabilitation is based on the extent of bone resection and the presence of labral
repair. Patients are restricted to 20-pound, foot-flat, weight bearing for 10 days to 4 weeks. Our
protocol includes continuous passive motion for the first 4 weeks for 2 to 4 hours per day to aid in
joint nutrition and to reduce adhesion formation postoperatively. Patients are encouraged to ride a
stationary bicycle with a high seat immediately postoperatively. Over a 3- to 4-month period, a slow
progression to full strength and activity occurs. This gradual progression avoids overactivation
or aggressive loading of the hip flexors, abductors, and adductors, as these muscle groups are
highly susceptible to fatigue and tendinitis postoperatively. A full return-to-sporting activity is
anticipated by 5 to 6 months, but patients may continue to see improvement in symptoms for up to
44 Chapter 2
1 year postoperatively.105,106 Further information regarding nonoperative as well as sport-specific

rehabilitation can be found in Chapter 17.
PEARLS AND PITFALLS

Although proper training and careful adherence to the principles of each of the previously
outlined steps will help to improve patient outcome, there are 3 important keys to the successful
arthroscopic management of FAI.
● Have a detailed knowledge of the patient’s pathoanatomy. Taking the time to develop a
specific 4-layer diagnosis is essential. The more detailed, the better chance for a success-
ful outcome. The ability to arthroscopically visualize and dynamically assess the pre- and
postoperative bony correction is compromised at extreme ROMs, so knowing what the patho-
anatomy is and having a surgical plan is critical.
● Have clear visualization throughout the procedure. Clear visualization throughout the pro-
cedure is crucial, not only to allow for complete correction, but also to avoid iatrogenic injury
to the chondral and labral structures. Visualization can be improved by controlling the pump
pressure and by carefully coagulating areas of hypervascularity that are frequently present
in a synovitic hip. The pump should be kept at the lowest possible setting to avoid iatrogenic
fluid extravasation, and careful monitoring of the pump and the patient should be performed
continuously throughout the case. In the peripheral compartment, retraction of the capsule
will greatly facilitate visualization and allow for complete bony resection.
● Be gentle with the soft tissues. Although arthroscopy is considered a minimally invasive tech-
nique, significant soft tissue damage to the surrounding peri-articular musculature can occur
without careful attention during the insertion and extraction of instruments. It is important
to minimize the number of instrument insertions into the joint, and whenever possible,
instruments should be inserted through cannulas to avoid muscular damage.
CONCLUSION
Arthroscopic management of FAI begins with early diagnosis and appropriately directed treat-
ment. Appreciation of the bone morphology contributing to FAI is essential for achieving the
best outcomes. Although labral tears are commonly identified, they are usually only the sign of
an underlying bony problem. As the role of arthroscopic treatment of FAI continues to evolve,
surgeons must understand the indications for arthroscopic management of FAI, the important
technical aspects of the procedure, and the limitations of arthroscopic management.
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nal extravasation of fluid during arthroscopic removal of a loose body from the hip joint of a patient with an
acetabular fracture. J Orthop Trauma. 1998;12(4):294-299.
101. Sharma A, Sachdev H, Gomillion M. Abdominal compartment syndrome during hip arthroscopy. Anaesthesia.
2009;64:567-569.
102. Scher DL, Belmont PJ Jr, Owens BD. Case report: osteonecrosis of the femoral head after hip arthroscopy. Clin
Orthop Relat Res. 2010;468:3121-3125.
103. Bedi A, Zbeda RM, Bueno VF, Downie B, Dolan M, Kelly BT. The incidence of heterotopic ossification after hip
arthroscopy. Am J Sports Med. 2012;40:854-863.
104. Salvo JP, Troxell CR, Duggan DP. Incidence of venous thromboembolic disease following hip arthroscopy.
Orthopedics. 2010;33(9):664.
105. Edelstein J, Ranawat A, Enseki KR, Yun RJ, Draovitch P. Post-operative guidelines following hip arthroscopy.
Curr Rev Musculoskelet Med. 2012;5:15-23.
106. Enseki KR, Martin RL, Draovitch P, Kelly BT, Philippon MJ, Schenker ML. The hip joint: arthroscopic proce-
dures and postoperative rehabilitation. J Orthop Sports Phys Ther. 2006;36:516-525.
3
Femoroacetabular
Impingement
II. Open Treatment Strategies and Outcomes
in Femoroacetabular Impingement Surgery
Lisa M. Tibor, MD and Michael Leunig, MD
OPEN TREATMENT OF FEMOROACETABULAR IMPINGEMENT

The open surgical hip dislocation (SHD) originally described by Ganz et al1 is the first and most
well-documented approach to the comprehensive treatment of femoroacetabular impingement
(FAI). This approach uses a trochanteric flip osteotomy, which allows for safe anterior dislocation
of the femoral head with preservation and protection of the medial femoral circumflex artery.2
The SHD allows for circumferential inspection of the acetabular rim, including the labrum,
cartilage, and femoral head-neck junction, and simultaneously provides an opportunity to treat
intra-capsular pathology and restore normal joint clearance.3-6 Probably the most important indi-
cation and advantage of the open SHD is for the treatment of patients who have documented or
possible contributory impingement from extra-articular sources that are not visible through the
arthroscopic approach.
The straight anterior technique, sometimes described as the “mini-anterior” approach, uses
either a modified Smith-Peterson7 or the Hueter8 approach, and allows for visualization of the
anterior aspect of the head-neck junction and acetabular rim without performing a trochan-
teric osteotomy. This approach does not allow for any improved visualization provided by the
arthroscopic approach, but may be a useful adjunct for surgeons who are not adequately trained
in arthroscopic techniques. This approach is sometimes employed for treatment of associated

50 Chapter 3
Figure 3-1. Anatomy of the deep branch of the medial femoral

circumflex artery (MFCA). The deep branch of the MFCA emerges
posteriorly from beneath the femoral neck, then runs between
the quadratus femoris and inferior gemellus, posterior to obtu-
rator externus and anterior to superior gemellus (muscular
insertions removed in this figure). It becomes intracapsular just
distal to the piriformis insertion (P) and the terminal branches
then run in the synovial sheath at the posterolateral junction
of the neck. The branches finally enter the head 2 to 4 mm
lateral to the bone-cartilage junction (arrowheads). GT = greater
trochanter; FH = femoral head. (Reprinted with permission from
Katharina Leunig-Ganz, MD.)
impingement in the presence of dysplasia, such that anterior femoral-sided impingement can be
approached concomitantly with periacetabular osteotomy (PAO). Although infrequently used, the
anteverting PAO is performed for correction of anterior acetabular overcoverage with concomitant
posterior undercoverage without any significant contribution to the impingement from asphericity
of the femoral head.9
Indications for open surgical dislocation instead of arthroscopic treatment begin with the
personal limitations of the surgeon. The surgeon must be educated in the pathology and techni-
cally qualified to perform the treatment arthroscopically. A second indication for open surgical
dislocation is a posterior cam lesion causing posterior impingement. This location is not easily
reached arthroscopically. Other contraindications to arthroscopic management include concomi-
tant pathologies such as loose bodies too large to remove arthroscopically, rotational deformities,
and focal chondral lesions on the femoral head being treated with osteochondral transfer from the
knee to the femoral head.
Open management has been integral to the treatment of FAI since the initial discussion of the
concept of FAI.3 Open management of FAI is performed via a SHD with a trochanteric osteotomy.1
The surgical dislocation technique was developed based on studies of the medial femoral circum-
flex artery (MFCA) and its relationship to the posterior hip muscles.1,2 Because the deep branch of
the MFCA is the primary blood supply to the femoral head, understanding its anatomy is critical
to safely performing an SHD and avoiding avascular necrosis (Figure 3-1). After the artery emerges
from under the femoral neck, it runs between the quadratus femoris and the inferior gemellus,
crossing posterior to the obturator externus and anterior to the superior gemellus, obturator inter-
nus, and inferior gemellus.2 It enters the capsule just distal to the insertion of the piriformis. The
terminal branches of the artery then run along the synovial sheath at the posterolateral aspect of
the neck, entering the head 2 to 4 mm lateral to the bone-cartilage junction.2 There is also a large
and consistent anastomosis between the deep branch of the MFCA and the inferior gluteal artery
running just below the piriformis.2 Because this anastomosis may be able to perfuse the femoral
head if the deep branch of the MFCA is injured,2 it should also be protected during the surgery.
Femoroacetabular Impingement: II 51
The important distinction between the SHD described by Ganz et al1 and other posterior
approaches to the hip is the transtrochanteric osteotomy. The osteotomy allows the hip to be dislo-
cated anteriorly, while keeping the piriformis and hip external rotators intact, thus preserving the
blood supply to the femoral head. In the Kocher-Langenbeck approach, the piriformis and external
rotators must be divided to dislocate the hip, which endangers the deep branch of the MFCA and
places the hip at risk for avascular necrosis.
Open management for FAI can be performed for all types of symptomatic FAI; however, it is
specifically indicated where arthroscopy may not be able to completely address the deformities
causing the impingement. This includes pincer impingement due to global acetabular overcover-
age, FAI due to post-Perthes deformity, the need for open reduction and internal fixation of a large
acetabular rim fracture, and far lateral or posterior cam deformities. Open management is also
indicated when additional procedures will be performed in conjunction with the FAI treatment.
These include cartilage restoration procedures for cystic lesions in the acetabulum or femoral
head, labral reconstruction, femoral derotational osteotomies, acetabular osteotomies, and femoral
head reduction osteotomy.
Similar to arthroscopic management of FAI, joint space narrowing or Tönnis grade 1 or higher
arthrosis on x-rays are relative contraindications to open management. For very young patients
in whom arthroplasty is an unfavorable option but who have significant arthrosis (more than
Tönnis grade 1), a surgical dislocation and open management may, however, be the best of the
limited surgical options. In a very select group of patients in whom the degree of cartilage damage
is difficult to assess, a surgical dislocation can be considered, with the potential for either treat-
ment or hip resurfacing depending on the degree of arthrosis found intraoperatively. The caveat
to this approach is that the indications for hip resurfacing have been narrowed in recent years to
young, active adult males with arthrosis, and, given the current controversy over metal-on-metal
implants, may continue to change in the future.
SURGICAL HIP DISLOCATION TECHNIQUE

The patient is positioned in the lateral decubitus position, with supports placed at the sacrum,
thoracic spine, and pubis. A tunneled cushion placed between the legs allows the bottom leg to be
protected and provides a flat surface for the upper leg (Figure 3-2). A sterile bag is placed anteriorly
at the level of the knee to hold the leg when it is dislocated. The incision is centered over the tip of
the greater trochanter and runs lengthwise over the anterior third of the trochanter. The length
of the incision depends somewhat on the size of the patient and the need for other procedures,
although on average is 20 to 25 cm long. If there is excessive soft tissue tension intraoperatively,
the incision can be extended longitudinally in either direction.
The incision is carried down sharply through skin and subcutaneous tissue to the iliotibial (IT)
band and gluteus maximus fascia. Proximally the fascia is split between the gluteus maximus and
medius; distally the fascial incision is extended in line with the femur. The anterior border of the
gluteus can be identified above the fascia by perforating branches of the inferior gluteal artery that
extend through the fascia to the subcutaneous tissue. In athletic patients, the fascia may need to
be released nearly up to the level of the iliac crest, although the skin incision does not need to be
extended this far.
The tissue over the trochanter, including the trochanteric bursa, is then incised and retracted
anteriorly. An attempt is made to preserve this layer for a more anatomic repair at the end of the
case. The vastus lateralis ridge and the trochanteric branch of the MFCA should be visible at this
point. The trochanteric branch of the MFCA can be coagulated prior to performing the trochan-
teric osteotomy for better hemostasis.
The hip is positioned for the trochanteric osteotomy by internally rotating it 20 to 30 degrees
and the posterior border of the gluteus medius and greater trochanter are identified. Some
52 Chapter 3
Figure 3-2. Positioning for the surgical hip dislocation. The patient is placed in the lateral decubitus position with rigid
supports at the sacrum, thoracic spine, pubis, and sternum. A tunneled cushion between the legs protects the bottom
leg and provides a flat surface for the upper leg.
surgeons prefer to identify the piriformis tendon at this point, although it is not necessary. For
greater stability after refixation, a trochanteric step osteotomy is performed10,11 (Figure 3-3). The
level of the osteotomy is identified by placing a finger in the piriformis fossa. The superior cut of
the step is made first with a thin, flexible saw blade, just above the piriformis fossa, and parallel to
the femoral shaft. The cut should stop just before the anterior cortex. A saw blade is then placed
in the osteotomy for visual reference. The inferior portion of the step is made parallel to the first,
but 2 mm distal and 5 to 6 mm more medial. This should result in a fragment that is 1 to 1.5 cm
thick. A thin, straight osteotome is used to cut the bone bridge between the 2 saw cuts. A broad
osteotome is then placed in each of the saw cuts and the trochanteric fragment is hinged forward,
fracturing the anterior cortex. This enables a better reduction of the trochanteric fragment at the
end of the case as well as more rotational stability during fragment healing. A narrow Hohmann
retractor is placed over the anterior edge of the femur to retract the fragment. When the osteotomy
is performed correctly, the gluteus medius and minimus and vastus lateralis insertions are on the
trochanteric fragment, while the insertion of the piriformis and the other external rotators remain
on the femoral side of the trochanter (the stable trochanter). This protects both the deep branch of
the MFCA as well as the anastomosis between the inferior gluteal artery and the MFCA.
There may be some fibers of the gluteus medius, minimus, or vastus lateralis remaining on the
stable trochanter. These should be sharply released to further mobilize the trochanteric fragment.
The piriformis tendon is usually identifiable at this point; any fibers of the piriformis that are
attached to the trochanteric fragment need to be released as well. The leg should then be flexed and
externally rotated, which allows for more anterior retraction of the mobile trochanter.
To fully expose the joint capsule, the vastus lateralis and intermedius are sharply elevated from
the lateral and anterior aspects of the femur. The gluteus medius is retracted anteriorly, which
enables identification of the gluteus minimus and piriformis tendons. It is critical to identify the
interval between the gluteus minimus and the piriformis at this point. The sciatic nerve, inferior
gluteal anastomosis, and deep branch of the MFCA should remain protected if the dissection
remains proximal to the piriformis. The gluteus minimus is carefully elevated off of the capsule
and retracted proximally. The capsule is then entirely exposed and a z-shaped capsulotomy is per-
formed. The initial capsular incision is made in line with the femoral neck. As the capsulotomy
Figure 3-3. Trochanteric step

osteotomy. A step osteotomy is
performed for better stability
after trochanteric refixation. The
superior cut (1) is made first, just
above the piriformis and parallel
to the femoral shaft. The infe-
rior portion of the cut (2) is made
2 mm distally and 5 to 6 mm more
medial to exit the trochanter dis-
tal to the insertion of the vastus
lateralis.
approaches the proximal “corner” near the acetabular rim, the incision is made in an inside-out
manner to avoid damaging the labrum. The proximal limb of the capsulotomy is then continued
parallel to the acetabular rim to the piriformis. The distal limb of the capsulotomy is made in par-
allel with the anterior intertrochanteric line, leaving a small cuff of tissue on the inferior neck for
later reattachment. This should stop anterior to the lesser trochanter to avoid injury to the MFCA
and psoas tendon.
With the capsule open, the joint is inspected for effusion, synovitis, and the location of the
cam deformity. While the femoral head is reduced, the degree of impingement can be evaluated
by flexing and internally rotating the hip. To dislocate the hip, the leg is flexed and externally
rotated. This breaks the labral seal and allows the head to sublux out of the joint. A bone hook is
then placed around the calcar to hold the femur subluxed so the ligamentum teres can be cut with
a curved pair of scissors. Further external rotation of the leg, placing it into the sterile sack, allows
the head to be fully dislocated. The degree of labral and cartilage damage can now be assessed
more completely.
The combination of symptoms, preoperative imaging, and the intraoperative pattern of dam-
age determines which deformities need to be addressed to treat the impingement. Attention is
first directed to the acetabulum. If rim trimming is to be performed and the labrum is intact, the
labrum is sharply released from the acetabular rim, taking care to leave it circumferentially intact.
A curved 15-mm chisel is used to perform the rim trimming. The extent of the rim trimming is
dictated by whether there is focal overcoverage, as in acetabular retroversion, or global overcover-
age, as in patients with acetabular protrusio. This is generally determined from the preoperative
imaging to ensure that the correct area is addressed and that the hip will not be destabilized. Any
unstable acetabular cartilage flaps are debrided back to a stable base, and microfracture is per-
formed, if indicated from the size of the lesion. Finally, the labrum is reattached to the acetabulum
with suture anchors (Figure 3-4) or, if the labrum had been previously resected, a labral recon-
struction is performed.
For best acetabular exposure, the knee should be elevated and pushed towards the surgeon,
while, for the best exposure of the femoral head, the knee should be lowered into the sterile bag.
The leg is now positioned to bring the femoral head out of the wound. With the femoral head
54 Chapter 3
Figure 3-4. Acetabular rim trimming

and labral refixation. The labrum (L)
has been sharply released from the
acetabulum, but left circumferen-
tially intact. Acetabular rim trimming
(arrowheads) was performed with a
chisel and suture anchors have been
placed along the acetabular rim for
labral refixation. Tr = trochanter.
Figure 3-5. Femoral neck osteoplasty. (A) The femoral head and cam deformity prior to osteoplasty. The cartilage
overlying the cam deformity (arrow) is redder than the rest of the femoral head cartilage. (B) The femoral head after
the osteoplasty. Resection of the cam deformity restores the sphericity of the femoral head-neck junction.
exposed, the cartilage should be continuously irrigated. The cartilage on the cam deformity is
usually slightly redder than the cartilage on the round portion of the head (Figure 3-5A). Spherical
templates can also be used to evaluate the nonspherical portion of the head. Most cam deformi-
ties are located on the anterior and superior portions of the femoral head3,12 and resection of cam
deformities anteriorly will not endanger the blood supply to the head.13 Care must be taken with
cam deformities that extend superiorly or posteriorly around the head-neck junction, as resection
here can endanger the blood supply to the head.2,13 The goals of the resection are to eliminate the
impinging bone while protecting the blood supply to the femoral head, re-creating a smooth femo-
ral neck, and avoiding over-resection (> 30% of the neck diameter) that would weaken the femoral
neck.14 A curved chisel is used to resect the cam deformity and restore the head-neck offset. For
cam deformities that extend to the area where the blood vessels perforate the head, small amounts
of bone can be resected from proximal to distal, breaking off the fragment and resecting it with
a knife in an inside-out manner. The extent of the resection can be checked with the spherical
template. Once a satisfactory resection has been achieved (Figure 3-5B), any necessary cartilage
restoration procedures can be performed.
Figure 3-6. (A) Anteroposterior (AP) and (B) lateral x-rays after surgical hip dislocation, acetabular rim trimming, and
femoral head osteoplasty.
Prior to reduction of the femoral head, the remaining stump of the ligamentum teres is sharply
resected and perfusion of the head is assessed either by observing bleeding from the foveal artery
or by a 2-mm drill hole at the fovea. The head is then reduced with longitudinal traction and inter-
nal rotation with the flexed knee, placing the leg back on the table. The range of motion is then
re-evaluated to ensure that the impingement has been adequately treated.
The capsule can be closed with either interrupted or running sutures, although tension on the
capsule should be avoided because it can stretch the retinaculum containing the vessels perfusing
the femoral head. The trochanteric fragment is then reduced and two 3.5- or 4.5-mm parallel lag
screws are used for fragment fixation (Figure 3-6). When possible, the soft tissue layer containing
the trochanteric bursa is repaired over the trochanter for more anatomic movement of the IT band
once the wound has healed. The IT band, subcutaneous layers, and skin are then closed according
to the preference of the surgeon.
MINI-OPEN MANAGEMENT
OF FEMOROACETABULAR IMPINGEMENT
The mini-open technique of treating FAI uses an anterior approach to the hip for resecting the
cam deformity. It has been described both with and without arthroscopy of the central hip joint.
The disadvantage, however, of the mini-open approach of treating FAI without arthroscopy is
that central joint pathology cannot be evaluated or addressed. When used with arthroscopy, the
technique is a compromise between arthroscopic and the surgical hip dislocation for management
of FAI. Specifically, the advantages of the mini-open technique are that the cam deformity can
be addressed under direct visualization if the surgeon is unable to achieve adequate visualization
arthroscopically, and that the capsule can be repaired under direct visualization. In contrast to
a surgical dislocation, the mini-open approach does not require a trochanteric osteotomy and
requires less soft tissue dissection.15,16 The disadvantage of the mini-open technique is that only
the anterior portion of the femoral neck and capsule can be addressed, and both arthroscopic or
a formal surgical hip dislocation allows for better visualization and treatment of the cam mor-
phology. Thus, labral refixation and other intra-articular procedures must still be performed
arthroscopically or with a surgical dislocation.
The mini-open technique is indicated for patients with isolated cam impingement and an ante-
rior or anterosuperior cam deformity. The technique is contraindicated for patients who require
intra-articular procedures including acetabular rim trimming or labral reattachment.
56 Chapter 3
Figure 3-7. Mini-open anterior approach for FAI.

The senior author (ML) performs the anterior
approach via an oblique incision in the anterior
groin skin fold. The deeper muscular interval
between the rectus femoris (R) and gluteus medi-
us is revealed in the floor of the tensor sheath.
FAI = femoroacetabular impingement; Sa = sarto-
rius; T = tensor.
MINI-OPEN SURGICAL TECHNIQUE

The senior author (ML) recommends the use of arthroscopy with the mini-open anterior
approach. Arthroscopy is performed either supine or laterally, according to the preference of
the surgeon. During the arthroscopy, unstable cartilage flaps should be debrided and any labral
pathology should be addressed with either refixation, if technically feasible, or debridement of
unstable portions. Traction is then released and the arthroscopy portals are closed.
If the arthroscopy has been performed in the supine position, there is no additional need to
reprep or drape the leg. If the arthroscopy has been performed in the lateral position, the patient
should be repositioned supine, and the leg reprepped and draped accordingly. The incision and
approach is a standard Hueter approach. Classically, this is performed with a 5- to 8-cm verti-
cal incision 2 cm distal and 2 cm lateral to the anterior superior iliac spine. The senior author
performs this approach, however, with an oblique 5-cm incision in the anterior groin crease,
beginning medially at the inner table of the anterior superior iliac spine and extending laterally.
This is carried down sharply through the skin and subcutaneous tissue to the tensor fascia. Blunt
retractors are used to visualize the tensor fascia (Figure 3-7) and it is incised in line with the inci-
sion. The tensor muscle is then carefully separated from its overlying fascia, using a combination
of sharp and blunt dissection. The deep portion of the tensor sheath allows access to the interval
between the rectus femoris and the gluteus medius. A Cobb elevator is used to define the interval
between the 2 muscles. The rectus is then retracted medially and the medius is retracted laterally.
The pericapsular fat should then be visible, as well as the vastus lateralis in the distal aspect of
the wound. Blunt Hohmann retractors are placed at the level of the greater trochanter and medial
femoral neck for better visualization. The pericapsular fat is sharply debrided so that the capsule
can be visualized. An H-shaped capsulotomy is then made, with the long portion of the incision
in line with the femoral neck, taking care not to damage the labrum with the proximal portion
of the capsulotomy. The Hohmann retractors are then placed around the femoral neck for better
visualization of the cam deformity.
The femur is internally and externally rotated to visualize the full extent of the cam deformity
and a high-speed burr or a curved chisel can be used for the osteoplasty. The same principles
apply for the mini-open osteoplasty apply as for the osteoplasty performed in a surgical disloca-
tion: eliminate the impinging deformity, while protecting the blood supply to the femoral head,
re-creating a smooth femoral neck, and avoiding over-resection. Once the osteoplasty has been sat-
isfactorily completed, the wound is irrigated and the capsule is closed. The tensor fascia is repaired
with a running absorbable suture, and the subcutaneous and skin layers are closed according to
the preference of the surgeon.
COMPLICATIONS
Surgical Dislocation
The most common complication following surgical dislocation is Booker grade I or II
heterotopic ossification,17 seen on postoperative radiographs in about 60% of patients 1 year
postoperatively. This appears to have no effect on the functional outcome, however. Pain over the
greater trochanter is also a frequent occurrence18 and, in one study, was present in just under half
of patients (46%) 1 year postoperatively. In this study, the pain was most often present after activity
and occasionally when lying on the treated side. The trochanteric pain has several potential causes,
and may be related to mechanical irritation from the screws or from residual muscle weakness
as none of these patients had radiographic evidence of trochanteric nonunion. The senior author
removes the trochanteric screws in about half of the patients who undergo surgical dislocation.
Persistent groin pain after surgery may be caused by insufficient correction of the impinge-
ment or by the presence of intra-articular adhesions. Adhesions are frequently found between
the labrum and the capsule or between the area of the osteoplasty and the capsule.19,20 Magnetic
resonance (MR) arthrography can be used to visualize the adhesions and aid in decision making.
Arthroscopy has been found to be helpful for adhesiolysis and improvements in pain and function
after debridement of the adhesions.19,20
The incidence of serious complications following surgical dislocation is very low. No cases of
osteonecrosis or femoral neck fracture were reported in 2 large series of SHD,1,17 although tran-
sient sciatic nerve palsies have been reported.1,17
Mini-Open
The most common complication following treatment of FAI through a mini-open approach
is transient neurapraxia of the lateral femoral cutaneous nerve.16,21 This is undoubtedly related
to the course of the nerve through the surgical field, and is also frequently reported after hip
arthroplasty performed via the anterior approach.22 One series reported a postoperative femoral
neck fracture and 2 deep infections that resolved following debridement and antibiotic therapy.8
This same series reported 13 reoperations for persistent pain following labral repair, with patients
undergoing subsequent labral debridement.8
OUTCOMES
Numerous studies have established that open surgical dislocation, mini-open approaches, and
arthroscopy are all effective and safe methods to treat symptomatic FAI based on available short-
term to mid-term follow-up.23-26 Based on a systematic review of the literature from 1980 to 2008,
Bedi et al27 reported that open surgical dislocation with labral debridement and osteoplasty was
a successful treatment for FAI, with a good correlation between patient satisfaction and favorable
outcomes as defined by the Harris Hip Score (HHS) or Merle d’Aubigné-Postel score.
The studies reviewed support that 65% to 85% of patients will be satisfied with their outcomes
at a mean of 40 months after surgery, although a common finding in all series was an increased
incidence of failure among patients with substantial preexisting osteoarthritis.27
Additional systematic reviews and analysis of the literature have reported similar results.
Clohisy et al 28 performed a systematic review of all studies on FAI between 1950 and 2009. Eleven
studies met the inclusion criteria with a minimum of 2 years of follow-up with clinical outcomes
data. All studies were level-III or level-IV evidence with a mean follow-up of 3.2 years. The Merle
d’Aubigné-Postel score was most commonly used, and improvement ranged from 2.4 to 5 points.
58 Chapter 3
Reduced pain and improvement in hip function were reported in 65% to 96% of patients. Conver-
sion to total hip replacement was reported in 0% to 26% of cases, and major complications were
reported in 0% to 18% of procedures. Poor prognostic factors included advanced preoperative
osteoarthritis, advanced chondral degeneration, and older age.28 Ng et al29 reported on 23 case
studies (970 cases) on the surgical treatment of FAI. Although treatment of FAI consistently
improved mean hip function, patient satisfaction was not universally positive. Mean improvement
in pain ranged from 25% to 100%, and patient dissatisfaction ranged from 0% to 31%. Up to 30%
of patients were converted to hip arthroplasty, with worse outcomes for FAI surgery noted in those
patients with Tönnis grade 2 osteoarthritis on preoperative imaging and/or Outerbridge III or IV
cartilage damage noted intraoperatively.29
Matsuda et al21 recently performed a comparative systemic review of the open surgical dislo-
cation, mini-open, and arthroscopic surgical approaches for FAI. Of 5856 peer-reviewed articles
that were identified by appropriate query, 18 articles (6 open surgical dislocation, 4 mini-open, and
8 arthroscopic studies) with reported clinical outcomes and 1-year follow-up met the inclusion
criteria. In concordance with previous studies, the systematic review analysis concluded that all
approaches were effective in pain relief and improvement in function with short-term to mid-term
follow-up. However, the authors also reported a higher incidence of major complications related to
the trochanteric osteotomy and associated hardware in the open surgical dislocation, and a greater
incidence of lateral femoral cutaneous nerve injury with mini-open approaches. The arthroscopic
approach was reported to have equivalent clinical outcomes with a lower rate of major complica-
tions when performed by experienced surgeons.21
It must be noted that the quality of the literature is universally limited and consists of only
level-III and level-IV evidence studies. In this regard, the results and conclusions of the compara-
tive analysis of the approaches must be interpreted with caution. No prospective or randomized,
controlled trials have been performed to compare the efficacy of nonoperative to operative man-
agement, or to compare the efficacy of open to arthroscopic approaches. The ability to address
these clinical questions via randomized, controlled trials has been limited by the considerable
experience required to achieve technical proficiency with each surgical approach without the
effects of confounding bias or variable skill.
The impact of surgery on the long-term clinical results and natural history of FAI has also not
been established. We are not aware of any long-term follow-up studies to date that demonstrate
prevention of or delay in the onset of osteoarthritis with surgery. However, Beck et al5 did report
no progression of joint space narrowing in 19 hips at 4.7 years after surgical treatment of FAI. In
this regard, the current literature can support surgical intervention for FAI to provide pain relief
and improve function in active patients without significant osteoarthritis. However, existing liter-
ature does not provide support for prophylactic surgical intervention in asymptomatic individuals
to prevent degenerative changes of the hip. While prevention of osteoarthritic change has not been
established, recent studies have reliably demonstrated an improvement, in vivo, in hip kinematics
after surgical correction of FAI.30-32
Bedi et al30 reported on 10 patients with symptomatic, focal cam, and/or pincer impinge-
ment lesions who underwent high-resolution computed tomography scans and computer-assisted
3-dimensional modeling of the involved hip before and after corrective FAI surgery. Mean alpha
angle improved from 59.8 degrees (range, 36 to 76 degrees) preoperatively to 36.4 degrees (range,
22 to 46 degrees) postoperatively. Corrective femoral and rim osteoplasty resulted in significant
improvements in both hip flexion (3.8 degrees; P = .002) and internal rotation (9.3 degrees;
P = .0002), and correlated with significant improvement in the mean HHS from 65.86 ± 6.66
preoperatively to 89.1 ± 13.02 postoperatively at a mean follow-up of 10.9 ± 7.4 months.
POSTOPERATIVE CARE AND REHABILITATION

Surgical Dislocation
The goals of rehabilitation are to protect the trochanteric osteotomy and the intra-articular
repairs during the acute healing phase, to avoid or minimize the formation of adhesions, and
to minimize inflammation by not placing the joint in the impingement position. Thus, patients
use crutches for 4 to 6 weeks with partial weight bearing to protect the trochanteric osteotomy.
Continuous passive motion (CPM) is started while the patients are in the hospital, with flex-
ion limited to 0 to 70 degrees. Patients receive nonsteroidal anti-inflammatories (indometha-
cin) for 10 days postoperatively for heterotopic ossification prophylaxis. Once postoperative
radiographs demonstrate healing of the trochanter, weight bearing is advanced, crutches are
discontinued, and formal physical therapy is initiated for normalization of gait, range of motion,
and strength.
Mini-Open
The postoperative care following a mini-open approach is similar to that for arthroscopy. To
protect any intra-articular repairs, patients use crutches for 2 to 4 weeks, but may be fully weight
bearing. CPM is also used for these patients and formal physical therapy is usually started 5 to
6 weeks postoperatively.
PEARLS AND PITFALLS

● Open procedures allow for the treatment of complex bony abnormalities such as extra-articular
impingement, global overcoverage, and significant deformities.
● Careful preoperative planning is imperative for successfully avoiding over- or under-correction
of the deformity.
● For SHD, the step cut osteotomy significantly decreases the likelihood of trochanteric failure.
● Good understanding of the blood supply to the femoral head and careful dissection decrease
the likelihood of avascular necrosis.
CONCLUSION
Management of FAI begins with early diagnosis and appropriately directed treatment. Appre-
ciation of the bone morphology contributing to FAI is essential for achieving the best outcomes, as
the commonly identified labral tears are often only a sign of the underlying problem.
Both open and arthroscopic hip preservation surgery have become important surgical interven-
tions for the treatment of many patients with early hip disease and have grown in popularity at
an exponential rate over the past 10 years. FAI now likely represents the most common indication
for hip preservation surgery and is the most common mechanism that leads to the development
of early cartilage and labral damage in the nondysplastic hip. The resulting abnormal kinematics
can precipitate not only direct intra-articular damage, but also compensatory injury patterns to
the surrounding musculature around the hip joint. Future research in this field will look to define
the anatomic, mechanical, clinical, and biologic factors that affect the outcomes of hip preserva-
tion surgery for treatment of FAI, and better define the appropriate implementation of open vs
arthroscopic surgeries based on objectively definable, anatomic criteria.
60 Chapter 3
REFERENCES
Br. 2001;83(8):1119-1124.
2. Gautier E, Ganz K, Krügel N, Gill T, Ganz R. Anatomy of the medial femoral circumflex artery and its surgical
implications. J Bone Joint Surg Br. 2000;82(5):679-683.
3. Ganz R, Parvizi J, Beck M, Leunig M, Nötzli H, Siebenrock KA. Femoroacetabular impingement: a cause for
osteoarthritis of the hip. Clin Orthop Relat Res. 2003(417):112-120.
4. Beck M, Leunig M, Clarke E, Ganz R. Femoroacetabular impingement as a factor in the development of non-
union of the femoral neck: a report of three cases. J Orthop Trauma. 2004;18(7):425-430.
5. Beck M, Leunig M, Parvizi J, Boutier V, Wyss D, Ganz R. Anterior femoroacetabular impingement: part II.
Midterm results of surgical treatment. Clin Orthop Relat Res. 2004;418:67-73.
6. Lavigne M, Parvizi J, Beck M, Siebenrock KA, Ganz R, Leunig M. Anterior femoroacetabular impingement:
part I. Techniques of joint preserving surgery. Clin Orthop Relat Res. 2004;418:61-66.
7. Cohen SB, Huang R, Ciccotti MG, Dodson CC, Parvizi J. Treatment of femoroacetabular impingement in ath-
letes using a mini-direct anterior approach. Am J Sports Med. 2012;40(7):1620-1627.
8. Laude F, Sariali E, Nogier A. Femoroacetabular impingement treatment using arthroscopy and anterior
approach. Clin Orthop Relat Res. 2009;467(3):747-752.
9. Siebenrock KA, Schoeniger R, Ganz R. Anterior femoro-acetabular impingement due to acetabular retrover-
sion. Treatment with periacetabular osteotomy. J Bone Joint Surg Am. 2003;85(2):278-286.
10. Bastian JD, Wolf AT, Wyss TF, Nötzli HP. Stepped osteotomy of the trochanter for stable, anatomic refixation.
Clin Orthop Relat Res. 2009;467(3):732-738.
11. Schoeniger R, LaFrance AE, Oxland TR, Ganz R, Leunig M. Does trochanteric step osteotomy provide greater
stability than classic slide osteotomy? A preliminary study. Clin Orthop Relat Res. 2009;467(3):775-782.
12. Rakhra KS, Sheikh AM, Allen D, Beaulé PE. Comparison of MRI alpha angle measurement planes in femoro-
acetabular impingement. Clin Orthop Relat Res. 2009;467(3):660-665.
13. Lavigne M, Kalhor M, Beck M, Ganz R, Leunig M. Distribution of vascular foramina around the femoral head
and neck junction: relevance for conservative intracapsular procedures of the hip. Orthop Clin North Am.
2005;36(2):171-176, viii.
14. Mardones RM, Gonzalez C, Chen Q, Zobitz M, Kaufman KR, Trousdale RT. Surgical treatment of femo-
roacetabular impingement: evaluation of the effect of the size of the resection. J Bone Joint Surg Am.
2005;87(2):273-279.
15. Barton C, Banga K, Beaulé PE. Anterior Hueter approach in the treatment of femoro-acetabular impingement:
rationale and technique. Orthop Clin North Am. 2009;40(3):389-395.
16. Lincoln M, Johnston K, Muldoon M, Santore R. Combined arthroscopic and modified open approach for cam
femoroacetabular impingement: a preliminary experience. Arthroscopy. 2009;25(4):392-399.
17. Sink EL, Beaulé PE, Sucato D, et al. Multicenter study of complications following surgical dislocation of the hip.
18. Beck M, Buchler L. Prevalence and impact of pain at the greater trochanter after open surgery for the treatment
of femoro-acetabular impingement. J Bone Joint Surg Am. 2011;93(Suppl 2):66-69.
19. Beck M. Groin pain after open FAI surgery: the role of intraarticular adhesions. Clin Orthop Relat Res.
2009;467(3):769-774.
20. Krueger A, Leunig M, Siebenrock KA, Beck M. Hip arthroscopy after previous surgical hip dislocation for
femoroacetabular impingement. Arthroscopy. 2007;23(12):1285-1289.e1.
21. Matsuda DK, Carlisle JC, Arthurs SC, Wierks CH, Philippon MJ. Comparative systematic review of the
open dislocation, mini-open, and arthroscopic surgeries for femoroacetabular impingement. Arthroscopy.
2011;27(2):252-269.
22. Matta JM, Shahrdar C, Ferguson T. Single-incision anterior approach for total hip arthroplasty on an orthopae-
dic table. Clin Orthop Relat Res. 2005;441:115-124.
adolescent athletes. Clin Orthop Relat Res. 2012;470(1):261-269.
24. Ilizaliturri VM Jr, Nossa-Barrera JM, Acosta-Rodriguez E, Camacho-Galindo J. Arthroscopic treat-
ment of femoroacetabular impingement secondary to paediatric hip disorders. J Bone Joint Surg Br.
2007;89(8):1025-1030.
25. Ilizaliturri VM Jr, Orozco-Rodriguez L, Acosta-Rodríguez E, Camacho-Galindo J. Arthroscopic treatment of
cam-type femoroacetabular impingement: preliminary report at 2 years minimum follow-up. J Arthroplasty.
2008;23(2):226-234.
26. Larson CM, Giveans MR, Taylor M. Does arthroscopic FAI correction improve function with radiographic
arthritis? Clin Orthop Relat Res. 2011;469(6):1667-1676.
29. Ng VY, Arora N, Best TM, Pan X, Ellis TJ. Efficacy of surgery for femoroacetabular impingement: a systematic
review. Am J Sports Med. 2010;38(11):2337-2345.
30. Bedi A, Dolan M, Hetsroni I, et al. Surgical treatment of femoroacetabular impingement improves hip
kinematics: a computer-assisted model. Am J Sports Med. 2011;39(Suppl):43S-49S.
31. Bedi A, Dolan M, Magennis E, Lipman J, Buly R, Kelly BT. Computer-assisted modeling of osseous impinge-
ment and resection in femoroacetabular impingement. Arthroscopy. 2012;28(2):204-210.
32. Kubiak-Langer M, Tannast M, Murphy SB, Siebenrock KA, Langlotz F. Range of motion in anterior femoroac-
etabular impingement. Clin Orthop Relat Res. 2007;458:117-124.
4
Dysplasia and Instability
Lazaros A. Poultsides, MD, MSc, PhD; Eilish O’Sullivan, PT, DPT, OCS;
and Michael D. Stover, MD
PATHOANATOMY OF DYSPLASIA
Understanding of young adult hip disorders has improved significantly over the last 2 decades,
leading to advancements in surgical treatment of acetabular dysplasia in adults. Acetabular dys-
plasia describes an underdeveloped or shallow, upwardly sloping acetabulum, with variable areas
of deficiency, most commonly in the anterior and lateral coverage of the femoral head. Acetabular
deficiencies can be associated with varying degrees of proximal femoral deformity such as coxa
valga, excessive femoral neck anteversion, or decreased femoral head-neck offset. Developmental
dysplasia of the hip (DDH) may be the result of in utero positioning, with hip flexion and adduc-
tion stretching the posterior hip structures. Breech presentation has been found to increase the
risk of DDH to more than 40%; even after normal ultrasound screening, the risk is 29%.1 These
conditions may result in a spectrum of disorders from neonatal hip instability, joint subluxation,
and frank dislocation, through to adolescent and adult dysplasia. Additional risk factors include
a large neonate, or small uterus, joint hypermobility, female gender, family history, and a prima
para mother.1 It is also important to highlight that not all acetabular dysplasia is due to DDH.
A concave acetabulum cannot develop without a concentric force exerted by a reduced femoral
head. Acetabular growth may be affected by a variety of clinical conditions, including hyperlaxity,
Down’s and Ehlers-Danlos syndromes, cerebral palsy, hereditary motor and sensory neuropathies,
and poliomyelitis. The triradiate cartilage can be injured by trauma or sepsis, which can also lead
to incomplete lateral acetabular growth. Finally, proximal femoral focal deficiency, Legg-Calvé-
Perthes (LCP) disease, and skeletal dysplasias can also affect the acetabular development.1
64 Chapter 4
In contrast to femoroacetabular impingement (FAI), where the movement of the hip joint
results in damage, in the dysplastic hip it is the altered osseous structure that leads to abnormal
joint mechanics with static overload of the cartilage and subsequent degeneration.2 The femoral
and acetabular structural abnormalities seen in the dysplastic hip create decreased contact area
between the femoral head and the acetabulum. The acetabular labrum hypertrophies in response
to the increased load experienced by the lack of anterior and lateral acetabular coverage in order
to improve femoral head coverage and maintain joint lubrication. This labral hypertrophy can
be remarkably successful at maintaining the mechanical equilibrium and preventing symptoms
until adulthood. However, the increases in contact and shear stresses around the anterosuperior
and superolateral aspect of the hip joint may result in labral detachment, and ultimately cartilage
degradation. Analogous to what causes subchondral cysts, the damaged labrum may act as a valve,
leading to the development of ganglion cysts. Dysplasia should be suspected when cysts are seen
on magnetic resonance imaging (MRI). Failure of the bone at the acetabular rim may also occur,
described as acetabular rim syndrome (“os acetabulare”).2
CLINICAL PRESENTATION
In order to make a timely diagnosis of symptomatic acetabular dysplasia, clinicians must have
a familiarity with the clinical presentation, common physical examination, and imaging findings.
Symptoms may be experienced for many years before osteoarthritis (OA) develops. Moreover, the
clinical presentation of symptomatic acetabular dysplasia can be quite variable in adults. Definitive
diagnosis of this condition is commonly delayed, as the specific clinical symptoms and physical
findings may be subtle. Therefore, understanding of early clinical presentation of symptomatic
acetabular dysplasia in skeletally mature patients is paramount, and leads to timely diagnosis and
consequently, appropriate treatment recommendations.
Physical examination, combined with a detailed history, should focus on the patient’s
symptomatology and differentiate whether symptoms originate primarily from dysplasia and
static overload, FAI, or a combination of the two. Importantly, the initial assessment should rule
out pain originating from the spine, pelvis, or periarticular musculature. The onset of hip pain
may be insidious or may be acute following a period of increased physical activity. Symptoms
characteristic of dysplasia include anterolateral or lateral pain independent of motion, and/or
peritrochanteric pain due to abductor fatigue after standing or prolonged periods of walking.3,4
Instability, weakness, or a feeling of a “dead leg” may be additional features of the dysplastic hip.
Symptoms may be exacerbated by rising from a seated position, climbing into or out of a car,
descending stairs, or sudden rotational movements. Pregnancy and weight gain may cause exac-
erbation of symptoms in the dysplastic hip. Symptoms more characteristic of FAI include sharp,
activity-related anteromedial groin pain, exacerbated by activities requiring hip flexion, such as
prolonged sitting. Symptoms in the dysplastic hip arise from the anterior labral injury and adjacent
articular cartilage damage. Because the acetabulum is often deficient anteriorly, these patients
may describe clicking at the front of the hip, or present with psoas irritation and tendonitis (psoas
serves as a secondary anterior stabilizer) or snapping (against the iliopectineal eminence, femoral
head, or medial border of the anterior inferior iliac spine [AIIS]). Patients with dysplasia and an
acetabular rim lesion, however, may present with sharp anterior groin pain.3
A recent prospective study4 examined the early symptoms of symptomatic acetabular dysplasia
in skeletally mature patients; it was found that the initial presentation was insidious in 97% of the
hips, and the majority of the patients reported moderate-to-severe daily pain. Pain was most com-
monly localized to the groin (72%) and/or the lateral aspect of the hip (66%). Activity-related hip
pain was common (88%), and activity restriction frequently diminished hip pain (75%). Patients
saw a mean of 3.3 health care practitioners, and the mean time from the onset of symptoms to the
diagnosis of hip dysplasia was 5 years.
Dysplasia and Instability 65
CLINICAL EXAMINATION PEARLS

Clinical evaluation should include a comprehensive set of questionnaires to detail patients’
history and describe their symptom complex. Demographic data including sex, height, weight,
and age should be recorded for each patient. Patients should be asked to characterize their pain
with regard to its severity, location (medial-groin, anterior, lateral, posterior), character, duration,
mechanical symptoms, and aggravating and alleviating factors. Their activity level (sedentary,
active, recreational athletics, or high-level athletics) should be documented. Questions regarding
limping, use of assistive devices, distance able to ambulate, and ability to ascend/descend stairs,
don/doff shoes and socks, and sit or stand for extended periods of time will elucidate the impact
of the symptoms on daily activities.4
The physical examination should include a gait assessment indicating the presence or absence
of a limp and Trendelenburg sign. Full or increased hip range of motion should be expected for
dyplastic patients with normal acetabular cartilage. Also, when differentiating between FAI and
hip dysplasia, patients with instability have more hip flexion and internal rotation at 90 degrees
of flexion. With extension and external rotation, they may also have a positive apprehension test
(anterior pain due to anterior undercoverage) or posterior pain because of impingement (posterior
facet of the greater trochanter against the ischium), especially in the setting of increased combined
anteversion (McKibbin Index > 45 degrees) and supraphysiologic range of motion.5 In a recently
published study, on physical examination of 57 consecutive skeletally mature patients with a total
of 65 symptomatic hips diagnosed with acetabular dysplasia, 48% exhibited a limp: 38% with a
positive Trendelenburg sign and 97% with a positive impingement sign.4
IMAGING PEARLS
Radiographic analysis may be challenging, especially in patients with borderline or mild ace-
tabular deformity. Preexisting intra-articular damage is a negative prognostic factor, which may
have an impact on surgical decision making and is important to take into account when managing
patient expectations.
Plain X-Rays
Initial radiographs should include a standing anteroposterior (AP) pelvis view, 45- or 90-degree
Dunn lateral view, a false profile view, and a functional view with the affected hip abducted and
internally rotated (von Rosen view). The AP pelvis radiograph is used to assess lateral coverage
(Figure 4-1A), acetabular version, and preoperative degenerative changes, which should be classi-
fied according to the criteria outlined by Tönnis and Heinecke. It is important that the radiograph
be obtained with the pelvis in neutral flexion and rotation. The evaluation of the AP pelvis radio-
graph should include whether there is a break in Shenton’s line (subluxation), acetabular inclination
(Figure 4-1B), the lateral center-edge angle of Wiberg, and the hip-joint-center position. Originally,
Wiberg determined a lateral center-edge angle of less than 20 degrees to be indicative of dysplasia.
The Dunn lateral is used to assess the femoral head-neck offset, as it is important to recognize the
paradoxical coexistence of FAI and dysplasia, and care must be taken in order to decrease the risk
of continued or iatrogenic FAI after acetabular reorientation. The false profile view (Figure 4-1C)
is used to evaluate anterior acetabular coverage by calculating the anterior center-edge angle of
Lequesne and de Seze, whereas the von Rosen view (Figure 4-1D) is used to assess hip congruency
after a potential correction, as well as aid in determining whether subluxation of the femoral head
may contribute to the apparent joint space narrowing observed on the AP radiograph.6,7
66 Chapter 4
A B
C D
Figure 4-1. A preoperative anteroposterior (AP) radiograph of the pelvis allows for the calculation of the
(A) lateral center-edge angle and (B) sourcil angle. A center-edge angle less than 20 degrees suggests
underlying dysplasia. In this example, the center-edge angle of 12.5 degrees demonstrates clear dysplasia.
The sourcil angle measures the inclination of the weight-bearing zone of the acetabulum and is typically
greater than 10 degrees in the setting of dysplasia. (C) The sagittal center-edge angle or false profile view
measures the anterior coverage of the femoral head and should be greater than 20 to 25 degrees in the
nondysplastic hip. (D) The abduction view or von Rosen view can be used to estimate the effect of a reori-
enting acetabular osteotomy on femoral head coverage.

MRI is an invaluable imaging method in assessment of hip pathology, especially in the evalua-
tion of the soft tissue structures around the hip as well as the labrum and cartilage. Intra-articular
pathology is ideally assessed after the administration of intra-articular gadolinium. Underlying
hyaline articular cartilage abnormalities also may be identified but with lower sensitivities compared
with diagnosis of labral detachments.8 The reported sensitivity for detecting cartilage delamination
using magnetic resonance arthrography (MRA) is 22%, while specificity is 100%.2 For patients with
evidence of arthrosis on plain radiographs, cartilage-specific sequences, such as delayed gadolinium-
enhanced MRI of cartilage (dGEMRIC), T1rho, or T2 mapping, may provide better information
regarding the cartilage and may inform surgical decision making.9 MRI may facilitate the character-
ization of abnormal femoral head-neck offset and proximal femoral osseous deformity; radial imag-
ing using the femoral neck as the central axis can display the femoral head-neck junction at other
locations as well to better define the topography of cam deformity.
Paralabral cysts are more commonly seen in the setting of hip dysplasia; they are identified on
MRI in association with labral tears and are seen as fluid-signal, often multilobular cysts that may
fill with intra-articular contrast material (Figure 4-2). OA will appear as joint space narrowing or dye
intrusion in between cartilage layers, osteophytes, variable bone marrow edema, and subchondral
cyst formation. A distended iliopsoas bursa may appear as a well-defined fluid collection anterior to
the femoral head and medial to the iliopsoas tendon, although an iliopsoas bursa may extend deep to
Figure 4-2. Coronal (A) and sagittal (B) MRI views of a labral tear associated with underlying dysplasia. The dysplastic
labrum is frequently hyperplastic and demonstrates intrasubstance degeneration and/or base splits at the attachment
site to the acetabular rim (arrows).
Figure 4-3. Three-dimensional computed tomography (CT)

scans can be helpful to more fully evaluate the femoral head
coverage by the acetabulum. In this example, there is signifi-
cant deficiency of the anterior and lateral femoral head cover-
age due to the underlying dysplasia.
the iliopsoas tendon or wrap superficially to the iliopsoas muscle. Anesthetic agents can be added to
the intra-articular MRA injection, as pain relief may suggest that the intra-articular abnormalities
on MRI are likely a source of pain.10 The iliocapsularis is usually hypertrophied because of its role as
a secondary stabilizer in the dysplastic hip.11
Computed Tomography
Computed tomography (CT) scanning serves as an important addition to plain radiographs for
preoperative planning. Three-dimensional reconstructions improve the assessment of acetabular
version and socket depth (Figure 4-3). Specifically, images are reformatted in the oblique plane as
well as the coronal and sagittal planes; measurements including alpha (α) angle, lateral and anterior
center-edge angles, femoral neck-shaft angle, acetabular version, and femoral version may be calcu-
lated. Three acetabular version measurements obtained from the superior-most image can be used to
better understand the cranial version of the acetabulum.2 Radial imaging along the femoral neck axis
also shows femoral head-neck bony abnormalities not visible on the routine oblique imaging plane.
The morphology of the AIIS can be assessed and classified,12 as a prominent AIIS may contribute to
extra-articular impingement following reorientation. CT-based 3D software may help identify poten-
tial femoral and acetabular morphologies that could create intra- and extra-articular impingement.13
68 Chapter 4
Ultrasound
In dysplastic patients with medial/groin hip pain, ultrasound has an important role in dynamic
assessment of snapping iliopsoas tendon, guiding soft tissue interactions around the hip, and
guiding injections. Normally as the patient straightens the leg from a frog lateral position, the
tendons and muscles that comprise the iliopsoas muscle-tendon complex slowly rotate without
abrupt movement or snapping. In the pathologic situation, medial fibers of the iliacus muscle
are interposed between the psoas major tendon and the ilium. As the leg is further straightened,
the iliopsoas tendon abruptly snaps toward the ilium as the iliacus fibers move and are no longer
interposed. Other causes of internal snapping hip may relate to intra-articular processes, such as
loose bodies.14 Similarly, snapping of the iliotibial band or gluteus maximus relative to the greater
trochanter (external snapping hip) is associated with lateral hip pain when the patient brings the
hip from flexed position to extended and vice versa.10
NONOPERATIVE OPTIONS
The earlier the orthopedic surgeon makes the diagnosis, the greater the number of available
treatment options. An initial trial of nonsurgical treatment may be appropriate for young adults
with either very mild dysplasia or those whose hip dysplasia has resulted in significant cartilage
damage and whose only treatment option would be total hip arthroplasty (THA). The clinician
should closely monitor those with minimal symptoms and dysplasia to detect any progression
that may warrant further treatment. For both groups of patients, anti-inflammatory medication
to reduce inflammation and relieve pain, specific physical therapy to strengthen the core and
abductor musculature, joint injections with steroids and anesthetic, activity modification, weight
loss, and use of a cane may help alleviate symptoms. Lifestyle modification is warranted; choosing
cycling or swimming instead of high-impact sports, like running and basketball, may put less
stress on the hip joint and consequently retard cartilage degeneration.
Important diagnostic information can be obtained with injection of the hip joint and iliopsoas
bursa or peritendinous injections. Injection of short- and long-acting anesthetic agents into the hip
joint can help differentiate between intra- and extra-articular pathology.10 In particular, patients
with combined FAI and mild dysplasia, chondral pathology, or acetabular delamination receive
pain relief after intra-articular anesthetic injection; this type of response to anesthetic injection
would not be seen with extra-articular pathology.15 Inclusion of a diagnostic injection at the time
of the MRA may be used, but because of the volume of dye injected, the results may not be as reli-
able. If anesthetic injections are performed separately, it is always important to include contrast
material to identify where the anesthetic agent is distributed during the procedure. Incidental fill-
ing of the iliopsoas bursa during a hip joint injection indicates a communication between the joint
and bursa and, consequently, the source of pain may include both anatomic structures. Corticoste-
roids may also be added to the anesthetic agents as a therapeutic option. The prescribing physician
must consider risks vs benefits to the patient with regard to any intra-articular injection; cartilage
damage has been reported with several anesthetic agents and corticosteroids.16
The iliopsoas and iliocapsularis muscle—which is directly attached to the anterior
capsule—are generally hypertrophied because of their role as secondary stabilizers in the dys-
plastic hips.11 Uncommonly, tendinosis or tear of the iliopsoas may be encountered. The presence
of iliopsoas tendon pathology can lead to adjacent labral pathology.17 Distention of the iliopsoas
bursa may also occur in isolation and is usually related to a hip joint effusion and underlying hip
joint abnormality. An iliopsoas bursa or peritendinous anesthetic and corticosteroid injection can
be performed accurately using ultrasound guidance. The needle tip is positioned between the ilio-
psoas muscle-tendon complex and the ilium at the level of the iliopectineal eminence. Following
the confirmation that the needle is not within muscle or tendon, the anesthetic and corticosteroids
are injected. A patient with a favorable response after iliopsoas injection may possibly be a candi-
date for an iliopsoas tendon release or lengthening.14
ARTHROSCOPIC TREATMENT
As the diagnosis and surgical treatment of acetabular labral tears have evolved, arthroscopic labral
debridement initially gained popularity and has been associated with overall favorable long-term
results in the absence of arthritis.18 In the setting of borderline or mild dysplasia, early studies have
shown successful clinical outcomes with arthroscopic selective labral debridement and/or refix-
ation.19 However, poor outcomes from arthroscopic labral debridement in the dysplastic hip with
degenerative progression20 have been reported. Because of a compensatory stabilizing function of
the hypertrophic labrum in dysplasia, labral preservation is critical in this setting. In the presence
of acetabular dysplasia, arthroscopic labral debridement may fail to provide long-term symptomatic
relief and functional improvement if the underlying abnormal hip mechanics are not addressed.
The degree of dysplasia as defined by radiographic parameters at which arthroscopic treatment will
reliably fail is becoming better defined. Furthermore, debridement of the labrum may further com-
promise hip stability because of resultant anterolateral migration of the femoral head and increased
shear stress at the acetabular margin.20 Although prior arthroscopic labral treatment may not have
a negative effect on the functional outcome of a subsequent PAO in patients with hip dysplasia, we
believe that the surgeon should proceed with caution when considering the use of arthroscopic treat-
ment of the labrum alone in a dysplastic hip. A thorough physical examination and radiographic
evaluation should be performed before considering arthroscopic treatment, and arthroscopy should
not be the primary treatment modality for symptomatic acetabular dysplasia. If patients with
acetabular dysplasia are experiencing symptoms and do undergo arthroscopic treatment of a labral
tear, careful follow-up is essential. When arthroscopic labral debridement or repair fails to improve
symptoms, PAO may be considered as a joint-preserving procedure that can achieve good functional
results.21 The use of arthroscopy as an adjunct to PAO has become more common. Arthroscopic
visualization of the joint allows for more complete assessment of the degree of chondral injury and
may influence the decision to proceed with a PAO if advanced cartilage damage is present.
OPEN TREATMENT INDICATIONS

The most accepted indication for PAO and reorientation is mild to moderate symptomatic dys-
plasia.3 Initially there was controversy about the degree of dysplasia and concomitant femoral head
deformity that can be adequately addressed with acetabular reorientation.22 However, indications
have been expanded subsequent to satisfactory outcomes that have been published lately for severe
deformities. Dysplasia secondary to flaccid or spastic neuromuscular disorders and LCP disease is
considered an appropriate indication for PAO.23-25 Global acetabular retroversion, particularly if
associated with posterior wall deficiency and/or subsequent posterior instability causing anterior
impingement, is also considered an indication for anteverting PAO.26 PAO may also be performed
in patients with borderline dysplasia (lateral center-edge angle of Wiberg of 20 to 25 degrees) and
clinically symptomatic instability. Mid-term and long-term follow-up outcome studies have shown
that little to no arthritis (Tönnis grade 0 or 1) on plain radiographs, 27 when age is under 35 years
at the time of surgery,28,29 are associated with better results. Preoperative Tönnis grades 2 and
3 are significant predictors of failure following PAO.27,30-32 A cost-efficacy analysis showed that
THA was preferable for Tönnis grade 3 arthrosis, whereas PAO was more appropriate in grade 1 or
2 arthrosis.33 However, some patients with grade 2 or 3 arthrosis demonstrated improved mid-
term follow-up outcome scores and relatively preserved joint space, especially when the hip was
preoperatively concentric.30 Therefore, although arthrosis is a relative contraindication to PAO,
acetabular reorientation may be preferable to THA in certain younger patients.
70 Chapter 4
Figure 4-4. Schematic drawing of the

modified Smith-Petersen approach.
Contraindications
PAO is contraindicated when incongruence on functional radiographs—abduction and internal
rotation images or flexion false profile images—is noted preoperatively. This can occur in non-
spherical femoral heads or when the acetabular radius is smaller than the femoral head radius.3
PAO is also contraindicated in patients younger than 10 or 11 years of age because of the risk of
injury to the triradiate cartilage, through which the PAO bone cuts are made. Series of young
patients with posttraumatic acetabular dysplasia secondary to an acetabular fracture34 revealed
that there seems to be little risk of injury to the triradiate cartilage after the age of 10 or 11. Clohisy
et al22 indicated that those with a false acetabulum, Severin class V, had less predictable outcomes,
which may be attributed to the fibrocartilage articular surface (as opposed to hyaline cartilage).
Authors’ Preferred Technique for Periacetabular Osteotomy

PAO can be performed either with general anesthesia or under combined spinal-epidural
anesthesia and sedation. Continuous electromyographic peripheral nerve monitoring may be used
throughout the procedure in order to minimize the risk of nerve injury. Patients may predonate
1 unit of autologous blood and get reinfused on postoperative day 1. A cell saver is used for blood
collection and potential reinfusion. For the PAO, patients are positioned supine on a standard
radiolucent table. All bony prominences are well padded and the ipsilateral arm is positioned so it
does not impede the placement of the chisel or screw intraoperatively. A foot-rest that can be used
to assist in holding the extremity in a position of hip flexion is secured to the table. The contra-
lateral lower extremity is stabilized to the table. A modified Smith-Petersen approach to the hip is
used for exposure (Figure 4-4). The incision starts proximally lateral to the iliac crest and slightly
curved lateral to the anterior superior iliac spine (ASIS) and extends distally over the tensor fascia
muscle bulge approximately 10 cm inferior to the ASIS. Subcutaneous flaps are raised medially
and laterally, taking care to avoid the lateral femoral cutaneous nerve (LFCN). Proximally, the
interval between the abdominals and abductors is developed at the iliac crest. Distally, the fascia
over the tensor fasciae latae (TFL) is incised in line with the muscle fibers and is opened to expose
the medial aspect of the muscle to its insertion at the pelvis between the ASIS and the AIIS. The
TFL muscle belly is reflected laterally, exposing the rectus medially. The deep lateral rectus fascia
is opened and the rectus is retracted medially, exposing the retinacular fascia over the hip and
the indirect head of the rectus proximally. Often, the transverse vessels of the lateral femoral
circumflex vessels are visualized deep to this fascia, which marks indirectly the distal extent of
Figure 4-5. Intraoperative fluoroscopic

false profile view showing the location of
the ischial cut. The osteotome is first insert-
ed along the medial cortex, aiming at the
ischial spine, and is advanced to the level of
a trajectory bisecting the posterior column.
Care is taken not to overextend the postero-
lateral aspect of the cut due to narrowing
of the posterior column laterally and the
proximity of the sciatic nerve.
the exposure. The interval between the hip capsule and the iliocapsularis is developed and the
iliocapsularis is retracted medially.
The ASIS is then prepared for osteotomy, beginning with the release of the TFL origin and
proximal for 2 cm from the lateral ilium. Next the ASIS is osteotomized 1.5 to 2 cm from its tip,
beginning with a cut perpendicular to the axis of the crest to a depth of 1 to 2 cm. The bone is then
released with an osteotomy beginning at the interspinous area, aiming posteriorly. The bone block
is then reflected medially, preserving the sartorius and the inguinal ligament attachments to the
osteotomized fragment. Care is taken near the ASIS because proximally the LFCN emerges within
5 cm of and medial to the ASIS and can be injured during the approach, but it is uncommonly
visualized.35 Proximally, the external oblique aponeurosis is sharply incised from the top of the
crest and the iliacus origin is elevated subperiosteally from the internal aspect of the crest. At this
point in the procedure, the leg is flexed to 45 degrees, relaxing the hip flexors and allowing them
to be elevated from the internal iliac fossa to the pelvic brim. The conjoint tendon of the rectus
muscle is identified. Although transection facilitates the approach, because of potential prolonged
hip flexor weakness after PAO, the direct and indirect head of the rectus can be left attached (rec-
tus-sparing modification) and retracted laterally during the exposure of the medial capsule. The
iliocapsularis is visualized, and should be carefully elevated off the capsule and reflected medially.
The interval between the anterior hip capsule and the iliopsoas tendon is developed inferomedi-
ally. Next, the iliopsoas bursa is identified and opened by gentle elevation and medial retraction of
the iliacus, iliocapsularis, and rectus. Once the lateral aspect of the superior pubic ramus is visual-
ized, the subperiosteal dissection of the flexors off the ilium can be extended to the quadrilateral
plate. Flexion and adduction of the leg facilitates the exposure. This allows a blunt Hohmann
retractor to be placed on the ischial spine and enables visualization of the inner table of the pelvis.
Electromyographic studies indicate that sciatic nerve irritation does occur intraoperatively, since
the nerve emerges from the greater sciatic notch, which is close to the intrapelvic retractor; thus,
proper retractor placement is crucial.36 The interval between the iliopsoas tendon and the joint
capsule is developed medially. The anterior retinacular tissue over the hip is pierced distal on the
medial aspect of the hip capsule with a curved scissors, allowing access to the subcotyloid groove
of the ischium for the first osteotomy. A small hip skid is inserted into the interval onto the ante-
rior aspect of the ischium. A specially curved or angled chisel is then passed into the interval, fol-
lowing the hip skid path, and used to make the first cut. The location of the osteotome is checked
with anteroposterior and 45-degree oblique fluoroscopy views. The infra-acetabular osteotomy
can be performed using fluoroscopic visualization, and starts just distal to the infracotyloid notch
and aims toward the middle of the ischial spine as visualized on the 45-degree oblique fluoroscopy
view, extending posteriorly for approximately 20 mm. The osteotome is first inserted along the
medial cortex and is advanced to the level of a trajectory bisecting the posterior column (approxi-
mately 1 cm anterior to the posterior cortex of the posterior column; Figure 4-5). The lateral cut
72 Chapter 4
Figure 4-6. Intraoperative fluoroscopic

false profile view demonstrating the
posterior column cut. The osteotome
is directed at a 120-degree angle from
the iliac cut toward the ischial cut. The
posterior cut should be bisecting the
posterior column so as to be located
sufficiently posterior to the hip joint and
anterior to the sciatic notch. The cut
is completed laterally with a 45-degree
angled osteotome.
is only 15 to 20 mm deep because of the narrowing of the posterior column laterally and the
proximity of the sciatic nerve. The lateral cortex cut is made with the involved lower extremity
abducted and extended and the osteotome directing medially to avoid lateral slipping and conse-
quently to minimize the risk of sciatic nerve injury. Moreover, care should be taken to avoid the
damage to the acetabular branch of the obturator artery, which is one of the sources of perfusion
for the fragment.35,37
Attention is then directed to the exposure of the superior pubic ramus. The iliopsoas and the
femoral neurovascular bundle are retracted medially, but excessive force or prolonged traction is
avoided to minimize tension on the femoral neurovascular bundle. Hip flexion and adduction
facilitates exposure of the ramus and, in addition, decreases the tension of the soft tissue sleeve
overlying it. A narrow, pointed Hohmann retractor is hammered into the superior cortex of the
ramus medial for better visualization. The superior pubic ramus is exposed by incising the thick
periosteum along the axis of the ramus, elevating the periosteum anteriorly and posteriorly distal
to the ileopectineal eminence. Narrow, blunt, curved retractors are positioned around the anterior
and posterior aspects of the pubic ramus to protect the obturator nerve, which runs on the inferior
aspect of the ramus. The superior pubic ramus osteotomy is performed with a small oscillating
saw to the deep cortex and is completed with a half-inch angled osteotome. The cut is made just
medial to the pectineal eminence, perpendicular to the bone, which is generally approximately
45 degrees to the plane of the table. It is angled away from the joint and is oriented from antero-
lateral to posterolateral. Fluoroscopy can be used to confirm adequate medial placement of the
ramus osteotomy. Mobility of the pubis is checked. In the setting of younger patients with an
intact periosteum around the osteotomy site, release is performed to ease the mobilization of the
acetabular fragment during reorientation.
Attention is turned to the supra-acetabular iliac osteotomy. The abductors are tunneled only
at the level of the osteotomy, and a blunt, large Hohmann retractor is placed in the greater sciatic
notch. A straight cobra retractor is placed along the inner aspect of the true pelvis toward the ischial
spine. The hip is flexed and adducted to improve visualization. The iliac (first) cut passes through
the iliac wing. It is made from just distal to the osteotomy of the ASIS commonly oriented perpen-
dicular to the longitudinal axis of the body and parallel to the axial plane toward the sciatic notch
using an oscillating saw, first along the medial cortex. A 45-degree oblique fluoroscopy image will
verify optimal orientation and a superior position of the iliac osteotomy. The iliac cut is made with
the oscillating saw with the lower extremity abducted. Before beginning both supra-acetabular
cuts, a target mark or hole (with a high-speed burr) is made approximately 1 cm lateral to the pelvic
brim often in line with the apex of the sciatic notch on false profile views. At this mark the angle
of the osteotomy changes. The retro-acetabular (posterior column) cut angles 120 degrees from the
supra-acetabular cut and is directed toward the first ischial cut (Figure 4-6). It aims at bisecting the
posterior column between the articular surface anteriorly and the posterior border of the innominate
bone. It is performed under direct and fluoroscopic visualization, and the preliminary pass through
the medial cortex can usually be performed with a 15-mm straight osteotome. It is completed with
a calibrated half-inch osteotome and typically extends 5 to 6 cm down the posterior column. A use-
ful fluoroscopic technique to avoid joint of posterior column extension of the osteotomy is to see a
perfect lateral image of the osteotome on false profile view. Once the osteotomy is completed medi-
ally, the fragment will typically be observed to move slightly, but typically remains attached caudally
and laterally. Therefore, 2 additional passes are necessary: one central and one lateral. Placement of a
Schanz pin from the AIIS into the supra-acetabular bone at this point and tension placed on the bone
and maintained with lamina spreaders may facilitate exposure and propagation of the osteotomies
along desired trajectories. Importantly, the lateral cortex is osteotomized as a controlled fracture; it
is extended for only approximately 4 cm because of thinning of the posterior column distally and the
proximity of the sciatic nerve (lies directly inferior).
The osteotomy may be at risk for propagation into adjacent structures, including the sciatic
notch.35 Technical points to help avoid this include beginning the iliac osteotomy in the region just
proximal to the ASIS osteotomy extending posteriorly approximately 1 cm anterior to the greater
sciatic notch and lateral to the pelvic brim. In regards to the retro-acetabular cut, the osteotome
is angled slightly from anterior to posterior to avoid the posterior part of the joint. Fluoroscopy
can be very helpful throughout the procedure, especially for the depth and trajectory of the retro-
acetabular osteotomy, to ensure that it meets the ischial osteotomy.
After completion of all 4 cuts, the Schanz pin is used to gain mobility of the fragment. The
addition of a large reduction clamp placed around the iliac portion of the acetabular fragment and
the Schanz pin can facilitate both fragment mobilization and control of the fragment during cor-
rection. If the acetabulum is not adequately mobile, either the soft tissue or bony hinging impedes
the correction and limits medialization of the joint. For classic dysplasia, lateral and anterior cor-
rection is essential; thus, the fragment should be adducted and flexed. Nevertheless, the correc-
tion should be individualized for each patient and based on the anatomy and planning from the
preoperative radiographs. Once a preliminary correction has been obtained, the fragment is fixed
with 2-mm Kirschner wires and evaluated fluoroscopically. Plain radiographs intraoperatively can
be used to compare with preoperative imaging.
There are some key points to assess and accomplish intraoperatively. The sourcil should be hor-
izontal and balanced over the femoral head.35 The coronal center-edge angle should be between
25 and 35 degrees, with at least 80% of the femoral head being covered. The center of the hip joint
should be slightly medialized to improve joint reactive forces, and commonly can be within 10 mm
from the medial femoral head to the ilioischial line. However, excessive medialization should be
avoided, since it can lead to iatrogenic protrusio.35 Another factor indicating adequate medializa-
tion is position of the teardrop more medial to the ilioischial line than previously. Finally, take care
to maintain anteversion of the acetabular fragment. This is accomplished by maintaining internal
rotation of the acetabulum. Position of the posterior wall relative to the center of the femoral head
will provide information on balance of the rims as well. Overall, the goal of reorientation is to
enhance anterolateral femoral head coverage, to maintain or obtain acetabular anteversion, and
to translate the hip center medially if indicated. Acetabular reduction should be performed with
(1) internal rotation (lateral coverage and anteversion), (2) forward tilt or extension (anterior cover-
age), and (3) medial translation (medialization of joint center).
To ensure accurate assessment of the reduction, a high-quality AP pelvis is viewed with fluorosco-
py. Once a satisfactory correction has been obtained, 3 or 4 size 3.5- or 4.5-mm cortical screws can be
placed for definitive fixation in a divergent fashion on both the AP and oblique views from the ilium
into the acetabulum fragment. The iliac gap is grafted with the resected prominent ASIS. In cer-
tain cases, a front-to-back transverse screw can add extra stabilization. The most common fixation
method consists of 2 posterior to anterior screws and 1 posteriorly directed transverse screw placed at
the AIIS.3 Biomechanical analysis of different 3-screw constructs demonstrated that constructs with
the transverse screw were stiffer and seem to have higher loads to failure.38 The biomechanical effect
of a fourth screw has not been clarified. If there are any concerns about fragment stability, integrity
74 Chapter 4
Figure 4-7. Postoperative standing

anteroposterior (AP) radiograph of the
pelvis of a patient who has undergone
bilateral PAOs. Adequate correction of
the lateral center-edge angle and sourcil
angle is confirmed on this view.
of the posterior column, or bone quality resulting from chronic disuse, supplemental fixation with
small-fragment pelvic reconstruction plates along the pelvic brim down onto the acetabular frag-
ment is recommended. Following reduction, ASIS osteotomy is secured with 2.7- or 3.5-mm cortical
screws and the remainder of the wound is closed in a routine, layered fashion (Figure 4-7).
COMBINED APPROACHES
Hip arthroscopy may be used as an adjuvant therapy with PAO for patients with symptomatic hip
dysplasia. It aims at managing intra-articular pathology and mechanical symptoms due to chondral
flaps and/or labral tears. It has been demonstrated that labral tears are present in 65% to 77% of
patients who have hip dysplasia.39 If adjuvant arthroscopy is performed for labral debridement or
repair and cartilage assessment, the arthroscopy is performed first with the patient on a traction
table using a standardized technique in supine position.40 Although sequential arthroscopy and
PAO under one anesthetic have been previously described,39 outcomes data are not yet available
and the indications for labral repair are unclear. Intact labrum in PAO patients has been found to be
associated with better long-term outcomes scores and a lower risk of arthrosis progression.26 Based
on the published literature on the biomechanical function of the labrum,41,42 in those patients who
present with labral tears, it would be preferable to perform arthroscopic labral repair followed by PAO
under the same anesthetic. However, the arthroscopic portion of the procedure should be performed
efficiently in order to minimize soft tissue fluid extravasation that will increase the difficulty of the
surgical dissection for the PAO. Indications for this combined approach are evolving.
Technique for Open Femoral Osteoplasty

Once the acetabular correction is achieved and fixation is stable, any potential intra- or extra-
articular impingement is addressed. Hip range of motion in flexion and internal and external
rotation or various combinations of positions is evaluated. An anterior capsulotomy along the
femoral neck is performed to inspect the acetabular labrum as well as to assess the anatomy of
the femoral head-neck junction. Any potential sites of intra-articular impingement are evaluated.
Depending on the proximal femoral anatomy, a femoral neck osteoplasty can be performed, par-
ticularly if there are any limits to motion. Commonly, the anterolateral head-neck junction lacks
a normal offset and requires an osteoplasty to optimize impingement-free hip flexion motion
and to reduce the risk of secondary anterior FAI, especially in the cases of forward flexion of the
acetabular fragment aimed at correcting anterior hip undercoverage. In addition, in the scenario
of extra-articular impingement, such as restrictions in motion or impingement from the AIIS, can
be assessed and bone, usually from the anterior and lower part of the AIIS, can be resected if it is
causing extra-articular impingement against the inferomedial part of the neck or the anterior facet
of the greater trochanter. The capsule is then repaired with absorbable suture.
Technique for Central Compartment Assessment

Arthroscopic techniques have evolved to allow for effective treatment of labral injury through
limited debridement or refixation, as well as mechanical correction of acetabular-sided pathomor-
phology. Techniques for extensile arthroscopic capsulotomies have allowed for improved central
compartment exposure and access for acetabular rim evaluation and assessment, and treatment of
labral pathology and chondral injury. The authors’ preferred technique for central compartment
assessment in combined approaches focuses on labral preservation and repair and assessment for
iliopsoas pathology and possible subspine decompression, avoiding acetabular rim resection. Each
step of the process should be carefully executed, as there are errors possible during each. The pro-
cedure is discussed in detail in Chapter 2. The procedure begins with appropriate positioning of
the patient, which is followed by careful portal placement. The interportal capsule cut allows for
adequate exposure, and careful preparation of the acetabular rim is followed by labral refixation.
The paradoxical combination of dysplasia and FAI can also occur.23 Clohisy et al reported on
a series of patients with acetabular dysplasia in association with deformity of the proximal part of
the femur, which resulted in hip dysfunction. The authors concluded that a PAO combined with
concurrent femoral procedures can provide comprehensive deformity correction and improved
hip function for this complex pattern of FAI and dysplasia.23
A recent study43 evaluated retrospectively, after a minimum duration of follow-up of 2 years, a
cohort of patients who underwent PAO with (concurrent) or without open osteochondroplasty of
the femoral head-neck junction. The 2 groups were compared with regard to the modified Harris
Hip Score, radiographic correction, complications, and reoperations. The authors concluded that
this combined procedure for the treatment of symptomatic acetabular dysplasia and associated
femoral head-neck junction deformities is not associated with an increased complication rate; it
provides effective correction of associated femoral head-neck deformities and produces similar
early functional outcomes when compared with isolated PAO.
Furthermore, it has been demonstrated44 in a retrospective series of 147 patients who under-
went PAO with a minimum follow-up of 10 years (range, 10 to 14) that proper acetabular reorienta-
tion and the creation of a spherical femoral head improve long-term survivorship and decelerate
OA progression in patients with DDH; these results underline the necessity of concomitant assess-
ment of proximal femoral deformities.
Kim et al45 prospectively evaluated 43 consecutive hips treated by combined hip arthroscopy
and PAO. Intraoperative arthroscopic examination revealed labral lesions in 38 hips. At a mean
follow-up of 74 months (60 to 97), the mean Harris Hip Score significantly improved from 72.4 to
94.0, as did all the radiological parameters (P< .001). The authors concluded that this combined
surgical treatment might provide good mid-term results in patients with symptomatic hip dysplasia
and that the arthroscopic treatment of intra-articular pathology may alter the progression of OA.
COMPLICATIONS
The complication rate after PAO ranges from 11% to 45%, depending on the series and the learn-
ing curve.31 Injury to the lateral femoral cutaneous nerve is common, with severity of the injury
ranging from transient paresthesias to innocuous numbness to painful neuralgia or neuromas.35
The incidence of other neurologic complications is much less. Intraoperative electromyography
76 Chapter 4
indicates that nerve irritation occurs during surgery, and, accordingly, transient peroneal nerve
palsies are not unusual.31 Injury to the sciatic nerve, secondary to posterior bone fragments, has
also been reported.35 A recent multicenter study has demonstrated that the incidence of major
nerve deficit of the sciatic or femoral nerve during PAO is less than previously reported. The
authors reported an incidence of 2.1%, and that full recovery can be expected in only 50% of the
patients, more commonly with injuries of the femoral nerve (median time to recovery or plateau
was 5.5 months [range, 2 days to 24 months]). They concluded that if direct nerve injury is sus-
pected, exploration may be warranted.46
Vascular complications are less common. Before the widespread adoption of the modified
Smith-Petersen approach, arterial thrombosis was reported with the ilioinguinal approach.35,47
Osteonecrosis of the acetabular fragment is rare but has been reported in cases with severe dysplasia
and intra-articular extension of the ischial osteotomy,35,48 as intra-articular extension of the ischial
osteotomy may injure the acetabular branch of the obturator artery.37 Intra-articular extension of an
osteotomy cut may also result in articular incongruity, nonunion, or loss of correction. Nonunions
or continued instability have been reported in multiple series.31,35 Wound hematoma or infection
and heterotopic ossification have also been reported.31,35,48 Heterotopic ossification decreased dra-
matically once the abductors were routinely preserved. The overall incidence of venous thrombosis is
low, with a rate of 9.4 per 1000 in a multicenter series.49 Finally, iatrogenic impingement from either
overcorrection or undercorrection has also been reported as a complication.35 Recently, a systematic
review of the literature50 has shown that major complications are frequent and occurred in 6% to 37%
of cases. The most common major complications included nerve palsies, intra-articular osteotomies,
symptomatic heterotopic ossification, loss of fixation, mal-reductions, and wound hematomas. The
most common moderate complication was symptomatic hardware requiring removal. Eight of the
13 studies acknowledged the considerable learning curve associated with this surgical procedure,
suggesting the complication rate may diminish with increased experience. Overall, the incidence of
complications has decreased with the evolution of the surgical technique of PAO, the recognition of
FAI, and improvements in preoperative imaging and surgical planning.
POSTOPERATIVE REHABILITATION
Postoperatively, patients remain in the hospital for 3 to 6 days for pain control and mobiliza-
tion. Patients are allowed to be foot-flat weight bearing 20% with crutches for the first 4 to 6 weeks.
Weight bearing is limited because load-to-failure testing of the screw constructs found that ulti-
mate failure can occur with loads as low as 1.27-times body weight,38 and loss of correction has
occurred in patients who began weight bearing too soon after surgery. Gentle continuous passive
motion is used in the hospital to limit adhesion formation and to reassure patients that the hip can
move normally. At 6 weeks, the patient may begin weight bearing and gentle exercises. At 3 months
postoperatively, patients may gradually progress back to normal activity.
PEARLS AND PITFALLS

● Patient selection is a critical component—patients should be relatively young (< 40 years of
age), have good motion (except in the setting of combined FAI and dysplasia), and have well-
preserved joint space.
● There is a steep learning curve for PAO—significant time is required for training, surgical
observation, cadaver training, and cotreating.
● Thorough preoperative planning is imperative in order to ensure adequate correction and
avoid overcorrection.
CONCLUSION
There remains a need for improved awareness of hip dysplasia by clinicians, especially in the set-
ting of radiographically mild disease or subtle clinical symptoms. Skeletally mature patients with
acetabular dysplasia remain at risk for a delayed diagnosis and a lack of timely intervention. In young
patients, complaints of insidious-onset, activity-related groin pain, and/or lateral hip pain should be
carefully investigated so that an accurate diagnosis is obtained and the patients can be counseled
regarding disease prognosis and treatment options. The appropriate management of the patient with
borderline dysplasia, and patients with combined impingement and dysplasia pathomorphologies,
continues to be one of the more challenging areas in the field of hip preservation.
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37. Beck M, Leunig M, Ellis T, Sledge JB, Ganz R. The acetabular blood supply: implications for periacetabular
osteotomies. Surg Radiol Anat. 2003;25(5-6):361-367.
38. Babis GC, Trousdale RT, Jenkyn TR, Kaufman K. Comparison of two methods of screw fixation in periacetabu-
lar osteotomy. Clin Orthop Relat Res. 2002;403:221-227.
39. Ross JR, Zaltz I, Nepple JJ, Schoenecker PL, Clohisy JC. Arthroscopic disease classification and interventions as
an adjunct in the treatment of acetabular dysplasia. Am J Sports Med. 2011;39(Suppl):72S-78S.
40. Tibor LM, Sink EL. Periacetabular osteotomy for hip preservation. Orthop Clin North Am. 2012;43(3):343-357.
41. Crawford MJ, Dy CJ, Alexander JW, et al. The 2007 Frank Stinchfield Award. The biomechanics of the hip
labrum and the stability of the hip. Clin Orthop Relat Res. 2007;465:16-22.
ics. J Biomech. 2003;36(2):171-178.
43. Nassif NA, Schoenecker PL, Thorsness R, Clohisy JC. Periacetabular osteotomy and combined femoral
head-neck junction osteochondroplasty: a minimum two-year follow-up cohort study. J Bone Joint Surg Am.
2012;94(21):1959-1966.
44. Albers CE, Steppacher SD, Ganz R, Tannast M, Siebenrock KA. Impingement adversely affects 10-year survi-
vorship after periacetabular osteotomy for DDH. Clin Orthop Relat Res. 2013;471(5):1602-1614.
45. Kim KI, Cho YJ, Ramteke AA, Yoo MC. Peri-acetabular rotational osteotomy with concomitant hip arthros-
copy for treatment of hip dysplasia. J Bone Joint Surg Br. 2011;93(6):732-737.
46. Sierra RJ, Beaule P, Zaltz I, et al. Prevention of nerve injury after periacetabular osteotomy. Clin Orthop Relat
Res. 2012;470(8):2209-2219.
47. Troelsen A, Elmengaard B, Søballe K. Comparison of the minimally invasive and ilioinguinal approaches
for periacetabular osteotomy: 263 single-surgeon procedures in well-defined study groups. Acta Orthop.
2008;79(6):777-784.
48. Thawrani D, Sucato DJ, Podeszwa DA, DeLaRocha A. Complications associated with the Bernese periacetabu-
lar osteotomy for hip dysplasia in adolescents. J Bone Joint Surg Am. 2010;92(8):1707-1714.
49. Zaltz I, Beaulé P, Clohisy J, et al. Incidence of deep vein thrombosis and pulmonary embolus following periace-
tabular osteotomy. J Bone Joint Surg Am. 2011;93(Suppl 2):62-65.
50. Clohisy JC, Schutz AL, St John L, Schoenecker PL, Wright RW. Periacetabular osteotomy: a systematic literature
review. Clin Orthop Relat Res. 2009;467(8):2041-2052.
Traumatic Hip
5
Subluxation/Dislocation
and Femoroacetabular
Impingement-Induced
Instability
Bryan T. Kelly, MD; Eilish O’Sullivan, PT, DPT, OCS;
and Aaron J. Krych, MD
PATHOANATOMY OF TRAUMATIC SUBLUXATION/

DISLOCATION AND FEMOROACETABULAR IMPINGEMENT-
INDUCED INSTABILITY
Hip instability is now recognized as a fairly common entity because of improved understanding
of the pathomechanics of the hip joint. Hip instability may result from a traumatic insult or atrau-
matic etiology. The spectrum of traumatic posterior hip instability ranges from subluxation to
frank dislocation. While the diagnosis of dislocation is obvious in severe cases, a hip subluxation
instability episode may be misdiagnosed as a hip sprain initially because of its surprisingly subtle
clinical presentation.1 However, even subluxation of the hip can result in avascular necrosis, lead-
ing to severe dysfunction.2 Therefore, clinicians need to have an awareness of the injury patterns
and mechanisms associated with hip instability.
Pathomechanism
In normal anatomical configuration, the hip joint has a deep acetabulum and strong capsulo-
labral complex that can withstand high joint reactive forces sustained during athletic activity.3,4
In the general population, the most common mechanism for hip dislocation is a high-energy
dashboard injury in a motor vehicle accident,5 which overpowers the strong osseous and soft tissue

80 Chapter 5
Figure 5-1. Diagram illustrating

theorized mechanism of injury
for patients with femoroacetabu-
lar impingement (FAI) and poste-
rior hip instability. Top row: With
normal osseous hip anatomy,
internal rotation is not impeded.
Bottom row: In patients with cam-
type FAI, internal rotation is limited
(black arrow). Attempts at achiev-
ing internal rotation cause anterior
impingement and levering, which
drives the femoral head posteriorly
(red arrow).
stabilizers of the hip. In athletic competition, however, lower-energy mechanisms of hip sublux-
ation or dislocation have been reported.1,6 Posterior hip subluxations have been noted to occur in
various sports, including football, skiing, rugby, gymnastics, basketball, jogging, soccer, and bik-
ing, even with noncontact mechanisms of injury.7 Understanding of the underlying mechanism in
these low-energy injuries is currently lacking.
Femoroacetabular impingement (FAI) is a structural disorder causing abnormal contact
stresses in the hip joint that can lead to pain, dysfunction, and early osteoarthritis.8,9 FAI consists
of cam and/or pincer lesions, both of which restrict hip flexion and internal rotation,10 motions
necessary for many athletic maneuvers.8 In certain cases, a posterior hip subluxation or disloca-
tion event may be the first manifestation of occult FAI in competitive athletes.11 The authors
recently described a novel mechanism of hip instability, coined “FAI-induced hip instability.”12
This concept is based on the observation that there is a high incidence of FAI among athletes who
sustain a posterior rim fracture with luxation of the joint. This occurs in the setting of a rela-
tively low-energy mechanism as a result of increased hip flexion and internal rotation for athletic
maneuvers, creating abnormal contact of the cam lesion with the anterior acetabulum and levering
the femoral head posteriorly (Figure 5-1).
Philippon et al reported the intra-articular hip pathology in professional athletes who sustained
hip dislocation during competition and were treated with arthroscopy. In that series of 12 poste-
riorly dislocated hips, FAI existed in 9 hips.13 This may suggest some correlation in that cohort
of professional athletes as well, although no mention of this specific mechanism was made. In
chronic FAI, a contrecoup lesion in the posterior capsularlabral junction develops from a distrac-
tion force due to the femoral head levering out of the socket with continued hip flexion.14 This
micro-levering of the femoral head causes chronic changes to the posterior acetabular cartilage
and labrum.15 In this setting, the additional force on the hip that occurs during athletics could
lever the femoral head even more posteriorly, resulting in a subluxation episode.
Letournel and Judet described a theoretical analysis of the mechanism of hip dislocation in
1981.16 They demonstrated through vector analysis the relationship of the position of the leg and
pelvis to the injury sustained, accounting for the difference in an anterior dislocation, posterior
dislocation, or fracture-dislocation of the hip. Letournel and Judet reported that the degree of
internal or external rotation of the hip dramatically affects the position of the head within the
acetabulum and the resultant injury complex.16 Expanding this concept, ultrasonographic mea-
surements performed by Upadhyay and colleagues on a series of patients who sustained a posterior
hip dislocation demonstrated significantly less anteversion on both the injured and the uninjured
Traumatic Hip Subluxation/Dislocation and FAI-Induced Instability 81
sides compared with controls.17 They proposed that relative femoral retroversion might cause
decreased internal rotation of the hip, creating a predisposition to posterior hip dislocations.
Similarly, a rotational mechanism in a hip with limited internal rotation due to FAI might
mimic these classic vectors.16 Patients with FAI have restricted internal rotation and hip flexion
when compared to normal individuals.10 In a recent 3-dimensional analysis of dynamic motion of
the cam lesion in male patients with symptomatic FAI during motion, Audenaert and colleagues
demonstrated that internal rotation of the hip in 90 degrees of flexion was necessary to cause
intrusion of the cam lesion into the hip joint.18 During competition, attempts to achieve increased
flexion and internal rotation may cause inclusion of the cam lesion into the hip joint, creating
abnormal anterior contact between the cam lesion and the anterior acetabulum, which may lever
the femoral head posteriorly. This can lead to failure of the soft tissue and osseous structures, with
a subsequent posterior acetabular rim fracture and posterior capsulolabral tear. Moorman and
colleagues proposed that one may dislocate in an athletic context with a posteriorly directed force
to an adducted, flexed hip, similar to the posterior dislocation that results from a motor vehicle
accident.1 In contrast to motor vehicle accidents, however, smaller posterior acetabular rim frac-
tures were present in their series, indicating a lower-energy subluxation, rather than dislocation.
In their series of 8 football players, no mention of underlying FAI was noted. We propose that a
hip with normal osseous anatomy may sublux posteriorly with this pathomechanism, concurring
with Letournel and Judet’s original force vector analysis. This mechanism is distinctly different
from the torsion and hyperflexion mechanism of posterior hip subluxation in the setting of FAI.
Associated Injuries
In the authors’ case series12 on 22 hips with FAI-induced hip instability, the most common
pathologic findings included a posterior bony Bankart lesion, anterior labral injury, synovitis,
chondral injury to the femoral head with loose bodies, and ligamentum teres avulsion. The triad of
findings in 8 American football players with posterior hip subluxation has been described as hem-
arthrosis/effusion, iliofemoral ligament (anterior capsular) disruption, and posterior acetabular
rim fracture.1 In the series of 14 athletes treated with arthroscopic surgery, Philippon et al found
labral tears, ligamentum teres avulsion, and chondral defects to be common.13 In their series, 5 of
14 hips (36%) sustained acetabular rim fractures, although none were repaired arthroscopically.13
Laorr and colleagues described magnetic resonance imaging (MRI) findings in 18 consecutive
posterior hip dislocations, with 6 of 18 (33%) having acetabular rim fractures.5 The variation of
pathoanatomy in the different series of patients may be attributed to differing mechanisms of inju-
ry, presence or absence of underlying FAI, and the difference in MRI and arthroscopy findings.
In the shoulder, the Bankart lesion is classically described as an avulsion of the anteroinferior
glenoid labrum at its attachment to the anterior band of the inferior glenohumeral ligament with
capsular disruption.19 A bony Bankart occurs when the avulsion involves a bony fragment of the
glenoid. Similarly, there are case reports that have documented a Bankart-type of injury in the
hip. A case of recurrent posterior hip dislocation was reported in a 21-year-old male after a twist-
ing injury to the hip, characterized by disruption of the posterosuperior acetabular labrum with
formation of a pouch between the posterior acetabular wall and the short rotators.20 A second case
published by Lieberman et al also described a case of recurrent posterior hip dislocation associated
with posterior labrum avulsion.21
It is important to emphasize that while the diagnosis of dislocation is obvious in severe cases,
a low-energy hip subluxation instability episode can be unexpectedly understated in its clinical
presentation. In the authors’ experience, athletes often present months following injury, initially
82 Chapter 5
misdiagnosed.1 In our series of athletes diagnosed with FAI-induced instability, the interval from
injury to presentation in clinic was an average of 83 days (range, 2 to 384). All patients presented
with groin and/or buttock pain. In addition, all patients reported aggravation of hip pain with
stairs and pivoting maneuvers. A history of clicking, locking, catching, giving way, or pain elicited
by positions that reproduce instability should be investigated. The severity of this injury may be
overlooked because athletes are often fairly functional in activities of daily living. Sometimes they
may resume, or at least attempt to play. The clinician should have a high index of suspicion for
intra-articular injury even after a minor trauma. Patients may also have concomitant injuries such
as chondral injuries, labral tears, capsular injuries, or ligamentum teres tears.6 More subtle cases
of instability, especially FAI-induced instability, will have less impressive mechanisms of injury,
sometimes as seemingly benign as a noncontact twisting injury. Although much less frequent,
FAI-induced instability can also occur with premature posterior femoro-pelvic contact and sub-
sequent anterior subluxation or dislocation. This is most likely to be associated with increased
femoral anteversion leading to early contact between the femur and the pelvis during extension
and external rotation.
CLINICAL EXAMINATION
The physical examination for hip instability includes evaluation of gait, range of motion
(ROM), and motor and neurovascular function. Patients with traumatic hip instability caused
by hip dislocations or fracture dislocations present in severe discomfort and are unable to move
their lower extremity. Upon physical examination, patients with a frank posterior dislocation will
present with the hip in a fixed position of flexion, internal rotation, and adduction. A complete
neurovascular examination should be performed, and care should be taken to check for the pres-
ence of sciatic nerve palsy before any closed or open manipulation of the hip.
More subtle cases of instability, especially FAI-induced instability, will be more difficult to
diagnose clinically, and the physical examination becomes a critical tool for the clinician. For
the posterior impingement test, the patient lies supine, and the examiner brings the patient into
hip extension and external rotation (Figure 5-2). Discomfort or apprehension represents a posi-
tive finding. This can also be performed in the side-lying position with the affected hip up. This
implies posterior impingement, either with abnormal motion resulting from soft tissue deficien-
cies, such as anterior capsular laxity, or from normal physiologic motion resulting from abnormal
osseous anatomy, such as coxa profunda.22 Philippon et al have also described the dial test for the
hip, in which the patient lies supine in neutral extension, and the examiner internally rotates the
affected limb, similar to a log roll maneuver.23 The test is positive when the patient’s limb passively
rotates past 45 degrees from vertical in the axial plane and lacks a mechanical endpoint in external
rotation. Philippon has demonstrated a correlation between a positive dial test and atraumatic
anterior capsular laxity.
IMAGING PEARLS
In the setting of a traumatic hip injury, radiologic workup is initiated with plain radiographs
including an anteroposterior (AP) pelvis, cross-table lateral, frog lateral (if able), and Judet views of
the affected hip. In many cases, this will provide a relatively definitive diagnosis such as an acute
traumatic fracture, avulsion fracture, dislocation, or subluxation. However, plain radiographs of
the hip may be interpreted as relatively normal after a low-energy hip subluxation, but should be
carefully scrutinized (Figure 5-3A). The radiographic workup should include Judet radiographs to
evaluate for a small posterior rim fracture of the acetabulum (Figure 5-3B). Once the diagnosis of
Figure 5-2. The instability test can be performed in either

(A) the supine or (B) the side-lying position by placing the
hip into extension and external rotation. A positive test
includes either apprehension or anterior hip pain.
Figure 5-3. (A) Plain pelvic radiograph of a patient having sustained a previous hip injury. (B) Oblique Judet radiograph
of the same hip as in (A) demonstrating a posterior acetabular fracture.
a hip dislocation is made, a careful evaluation of the femoral neck must be performed to rule out
the presence of a fracture before any manipulative procedures are performed.
Computed tomography (CT) is especially helpful in the evaluation of hip instability. Small,
nondisplaced fractures of the acetabulum can be easily identified, and one can also assess for any
intra-articular loose bodies and adequacy of reduction if one was performed. MRI may interpret
the posterior rim fracture as a posterior labral tear, since this bone is cortical and relatively avas-
cular; there is usually not as much associated bony edema as might normally be expected with a
fracture. Laorr et al described findings in 18 consecutive posterior hip dislocations, all of which
had hemarthrosis: 12 had injury to the iliofemoral ligament, 6 had acetabular fractures, 6 had fem-
oral head contusions, 4 had small femoral head fractures, and 4 had intra-articular loose bodies.5
84 Chapter 5
Figure 5-4. Treatment algorithm for the management of traumatic dislocation or subluxation of the hip in athletic
patients. (Reprinted from Clin Sports Med. Vol. 25, M. K. Shindle, A. S. Ranawat, and B. T. Kelly, Diagnosis and manage-
ment of traumatic and atraumatic hip instability in the athletic patient, p. 319 [2006], with permission from Elsevier.)
The treatment algorithm first proposed by the senior author (BTK) in 2006 is still utilized at
our institution (Figure 5-4). Initially, hip dislocations are managed with a rapid reduction of the
dislocation, followed by planning for appropriate secondary interventions.24 Prompt reduction of
the dislocation decreases the likelihood of developing avascular necrosis (AVN). In a retrospec-
tive follow-up of a series of almost 80 cases, closed reduction performed under 6 hours has been
shown to reduce AVN rate.25 Incidence of AVN precipitated by hip dislocation is estimated in the
literature from 1% to 17%.25,26 In order to achieve a safe reduction, it is necessary to have adequate
anesthesia and fluoroscopy available. Following the closed reduction, an AP view of the hip and
a CT scan with fine (3 mm) cuts through the hip joint are usually completed. The CT scan is able
to assess the femoral head and determine whether small intra-articular fragments are present. CT
is also best suited for visualizing acetabular wall fracture size, location, and displacement. In the
acute setting of traumatic hip dislocations, MRI may assist in the diagnosis of labral disruptions,
femoral head contusions and microfractures, sciatic nerve injury, and intra-articular fragments.5
Most athletic hip dislocations are pure dislocations with no associated fractures, or small acetabu-
lar rim fractures due to the low-energy mechanism of injury. In this setting, surgical stabilization
is often not indicated. Active and passive ROM can begin as soon as comfort permits. We do not
permit flexion greater than 90 degrees and internal rotation greater than 10 degrees for 6 weeks to
prevent further instability. The athlete is put on crutches for 6 weeks of protected weight bearing
in order to decrease joint loading.
Figure 5-5. Intraoperative arthroscopy photograph Figure 5-6. Intraoperative arthroscopy photograph
through a lateral viewing portal demonstrating loose through a lateral viewing portal demonstrating femoral
chondral body removal. head chondral injury.
Displaced acetabular fractures involving the weight-bearing zone require surgical management
to restore joint congruence and to permit early ambulation and mobility.27 Fracture-dislocations
in soccer athletes have been reported in the literature involving 20% to 40% of the weight-bearing
area of the posterior acetabular wall, and thus required open reduction and internal fixation
(ORIF).28 Posterior wall injury significance may be elucidated via examination under anesthesia
with stress testing of the hip. Hip arthroscopy may be used to address femoral head pathology,
chondral injuries, loose bodies, and labral pathology. There is concern with arthroscopy in the
setting of a hip dislocation because of the traction required. Hip arthroscopy should be delayed for
at least 6 to 12 weeks to enable performance of a repeat MRI to rule out the presence of early AVN
before placing the patient in traction.
The main indications for arthroscopic treatment include removal of intra-articular loose bodies
(Figures 5-5 and 5-6) and repair of anterior and/or posterior labral tears. Posterior labral tears are
often associated with a small posterior rim fracture, and this can be incorporated into the repair,
analogous to a bony Bankart repair in the dislocated shoulder. Contraindications include presence
of an acute acetabular fracture in which fluid could extravasate, potentially causing abdominal
compartment syndrome.29
Arthroscopic treatment begins with a thorough diagnostic arthroscopy of the central com-
partment. The authors’ preferred technique consists of viewing through a mid-anterior portal,
instrument through a lateral portal, and anchors placed through a distal anterolateral accessory
portal in the case of an anterior labral repair, or through a posterolateral portal for posterior labral
tears.30 Chondral loose bodies will often be present posteriorly in the hip joint, as they fall with
gravity in the supine position (see Figure 5-5). Therefore, a posterolateral portal can facilitate
removal of the loose bodies. Inspection of the femoral head may reveal either a shear injury or an
impaction injury from the posterior instability event (see Figure 5-6). These chondral injuries can
be debrided and chondroplasty performed to prevent further loose body formation or mechanical
symptoms in the hip with catching of the chondral flap. Ligamentum teres tears are common and
may need to be debrided. A wide synovectomy may also be performed.
86 Chapter 5
Figure 5-7. Intra-operative arthroscopy photograph

through a mid-anterior viewing portal demonstrating
cam resection with femoral neck osteochondroplasty
restoring normal offset of the femoral head-neck
junction.
In the authors’ experience, both anterior and posterior labral tears are common. Anterior labral
tears can be repaired with suture anchors in the standard fashion. For posterior labral tears, access
is limited in arthroscopic procedures to approximately the 8 o’ clock position. Viewing through the
mid-anterior portal is preferred, which allows more of a bird’s-eye view, with the correct angle for
anchor placement achieved through the posterolateral portal. Sutures are typically passed using a
sharp tissue-penetrator through the anterolateral portal.
It is important to assess for the presence of a cam lesion as a potential contributing factor if
FAI-induced subluxation is present. After completing arthroscopy of the central compartment,
the cam lesion is addressed from the peripheral compartment. The capsule is exposed by placing a
switching stick through the distal anterolateral accessory portal and finding the interval between
gluteus minimus laterally and the iliocapsularis medially.31 Staying in this interval protects the
surrounding muscles and also facilitates retraction of the capsular limbs. A T-capsulotomy is then
performed in this interval to allow for complete visualization of the cam lesion. The medial and
lateral synovial folds are identified as the arthroscopic landmarks for the retinacular vessels, and
care is taken to preserve these structures to prevent any component of iatrogenic AVN.
Once the bone has been fully exposed, recontouring is performed with a spherical burr. The goal
is to remove the abnormal bone identified on the preoperative CT scan and recreate the normal
offset relationship that should exist where the femoral neck meets the normal cartilage of the fem-
oral head (Figure 5-7). It is important to use fluoroscopy intraoperatively to assess the cam lesion
resection.32 Bony debris is judiciously removed to avoid heterotopic ossification. Postoperatively,
sustained-release indomethacin (75 mg daily for 4 days) and naproxen (500 mg twice a day for
30 days) are used to prevent heterotopic ossification, especially in this posttraumatic setting.
In the setting of previous hip instability, a capsular repair is routinely performed. To accomplish
this, the arthroscope is kept in the mid-anterior portal. Hip flexion is then increased to create
some laxity in the capsule and facilitate repair. A suture passer is first placed through the lateral
limb of the T-capsulotomy via the anterolateral portal, and then retrieved with a sharp tissue-
penetrator placed through the medial limb of the iliofemoral ligament accessed through the distal
anterolateral accessory portal. A suture is then shuttled through both limbs and tied through a
cannula in the anterolateral portal. If pre-existing capsular laxity is present, then a capsular shift
can be performed by suturing back to the horizontal limb of the T-capsulotomy.
OPEN TREATMENT
The indications for open surgical treatment for posterior wall fractures include instability of
the hip joint, intra-articular fragments, marginal impaction, and irreducible fracture-dislocations
of the hip. Fractures of the posterior wall historically have relatively poor results. Failure rates
of 18% to 32% have been reported after ORIF in a large series of patients.33 These fractures fail
even though most series report that 80% to 96% of posterior wall fractures are anatomically
reduced at the time of surgery.27,33 Clinical failure after surgery includes intra-articular hardware,
malreduction, comminution of the posterior fragment, marginal impaction of the articular
surface, extension of the fracture into the weight-bearing portion of the acetabulum, and early
subluxation of the hip joint as a result of failed fixation.
A Kocher-Langenbeck approach in the prone position is preferred. It is important to keep the
knee in a flexed position to lessen tension on the sciatic nerve during the case. In order to pre-
serve the blood supply to the femoral head, it is critical to perform tenotomy of the piriformis and
obturator internus 1.5 cm from their insertion.34 After exposure of the posterior wall, it is vital to
identify all fracture fragments and any marginal impaction that may be present. The anatomical
position of these fragments needs to be restored in order to provide a stable hip. At this point, the
hip can be subluxed with traction in order to visualize and remove any chondral and other intra-
articular loose bodies. After removal of all intra-articular debris, including the torn ligamentum
teres, the fracture fragments can be reduced using the femoral head as a template. The small
fragments can be stabilized with 2.0-mm mini-screws or 1.5-mm bioabsorbable pegs. The large
posterior wall fragment can then be reduced, held in place with a ball spike pusher, the reduction
scrutinized under fluoroscopy in multiple planes, and the entire construct internally fixated with
a 3.5-mm reconstruction buttress plate. It is important for joint stability that this plate be placed as
peripherally as possible.34 The construct can be augmented with a one-third tubular spring plate
in fractures with extensive comminution.
Clinical Results
Between 1998 and 2010, 25 athletes presented to our clinic after sustaining a posterior hip insta-
bility episode during active competition, as defined by an acetabular rim or rim fracture on imag-
ing. Nonoperative treatment included 6 weeks of protected weight bearing with a protective brace.
Posterior hip precautions were instituted to avoid deep flexion and internal rotation. Progressive
weight bearing, ROM, and a hip rehabilitation program were introduced at 6 weeks. Running was
initiated at approximately 3 months. The most common indication for surgery was presence of
symptomatic loose body, or failure of nonoperative management. Only one patient in this series
acutely underwent surgical treatment with ORIF of a large posterior wall fragment. No patients
underwent acute (within 6 weeks) hip arthroscopy. The most common constellation of patho-
anatomy was a posterior labral tear with bony Bankart lesion (N = 22), anterior labral tear (N = 19),
ligamentum teres avulsion (N = 17), and chondral injury of the femoral head (N = 12) with loose
bodies. In this series, there was no difference in return to sports between athletes treated opera-
tively and nonoperatively, with an average of 78% returning to sports in each group. In Moor-
man et al’s study of 8 American football players, all were treated nonoperatively with 6 weeks of
protected weight bearing and a rehabilitation program.1 Six of the 8 returned to full, unrestricted
activity at an average of 13 weeks. Unfortunately, 2 of the hips developed osteonecrosis and sub-
sequently had total hip arthroplasty for the treatment of severe hip arthrosis.1 In Philippon et al’s
study, all 14 patients treated operatively returned to professional sports at their previous level.12
None of the patients in their series developed osteonecrosis. In our series, one athlete developed
focal osteonecrosis, underwent core decompression, and was advised against returning to compe-
tition. At 2 years of follow-up, his radiographs have not demonstrated any secondary arthrosis or
femoral head collapse.
88 Chapter 5
COMPLICATIONS
The most devastating injury associated with a hip instability episode is osteonecrosis. It has also
been the authors’ experience that early signal changes (1 to 3 months following injury) in the femo-
ral head (impaction injuries) are common. In an MRI study of hip dislocation, 6 of the 14 patients
with posterior dislocation had isolated femoral head contusions (trabecular microfractures). It is
important to distinguish these signal changes from avascular necrosis, although the long-term
prognosis of trabecular microfractures is unknown. Overall, athletes seem most likely to return
to sports if osteonecrosis and subsequent chondrolysis are avoided.2 Therefore, if the patient
is evaluated acutely, and hemarthrosis is noted on MRI, we agree with the recommendation of
Moorman et al for fluoroscopic aspiration to decrease intracapsular pressure in an attempt to
avoid osteonecrosis.1
Following an arthroscopic procedure, the athlete maintains partial weight bearing with flat-
foot gait for 3 weeks, whereas it is 6 weeks following an open procedure. It is important that the
athlete ambulates with a foot-flat gait in order to avoid hip flexor irritation. With a significant
capsular shift, it is important to limit external rotation and extension, as this will stretch the
capsular repair. Posterior precautions may be utilized, including avoiding hip flexion greater than
90 degrees and no internal rotation greater than 10 degrees. An abduction brace is worn when
ambulating for the first 2 to 4 weeks following surgery. We also recommend using continuous pas-
sive motion (CPM) 30 to 70 degrees immediately following surgery, progressing to 0 to 90 degrees
for 3 hours per day for 4 weeks, and then advancing past 90 degrees as tolerated. We believe this is
important to prevent any adhesions between the capsule and the labrum. Short-crank stationary
bike can begin almost immediately following surgery. The athlete completes a slow progression to
full strength, and activity ensues over a 4-month period.
PEARLS AND PITFALLS

● Athletes with FAI may be at increased risk for traumatic posterior dislocation or subluxation
due to restricted motion causing the hip to lever out the back of the joint.
● Athletes should be carefully assessed to avoid missing subtle subluxation events with the use
of posterior impingement testing and capsular laxity assessment.
● Following reduction of the athletic traumatic dislocation and in the absence of disruption of
the joint, conservative management is most prudent initially.
● Repeat imaging 6 to 12 weeks following the dislocation may identify resultant avascular necrosis.
CONCLUSION
Hip instability in the athlete is becoming a more recognized pathologic entity. Although frank
dislocations are uncommon, we have observed that there is a high incidence of FAI among ath-
letes who sustain a posterior rim fracture with luxation of the joint. It is likely that athletes with
underlying FAI may be at an increased risk of traumatic posterior dislocation or subluxation.
This presentation may be subtle; therefore, clinicians need to be aware of this injury pattern and
mechanism to optimize outcomes in the athlete.
REFERENCES
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in a professional football player. Am J Sports Med. 1991;19(3):322-324.
3. Blount W. Don’t throw away the cane. J Bone Joint Surg Am. 1956;38(3):695-708.
4. Hewitt J, Glisson R, Guilak F, Vail T. The mechanical properties of the human hip capsule ligaments.
J Arthroplasty. 2002;17(1):82-89.
5. Laorr A, Greenspan A, Anderson M, Moehring H, McKinley T. Traumatic hip dislocation: early MRI find-
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6. Chudik S, Lopez V. Hip dislocations in athletes. Sports Med Arthrosc Rev. 2002;10:123-133.
7. Shindle M, Ranawat A, Kelly B. Diagnosis and management of traumatic and atraumatic hip instability in
the athletic patient. Clin Sports Med. 2006;25(2):309-326.
8. Ganz R, Parvizi J, Beck M, Leunig M, Notzli H, Siebenrock K. Femoroacetabular impingement: a cause of
9. Leunig M, Beaulé P, Ganz R. The concept of femoroacetabular impingement: current status and future per-
spectives. Clin Orthop Relat Res. 2009;616(22):616-622.
10. Clohisy J, Knaus E, Hunt D, Lesher J, Harris-Hayes M, Prather H. Clinical presentation of patients with
11. Shindle M, Voos J, Heyworth B, et al. Hip arthroscopy in the athletic patient: current techniques and spec-
trum of disease. J Bone Joint Surg Am. 2007;89(Suppl 3):29-43.
12. Krych AJ, Thompson M, Larson CM, Byrd JWT, Kelly BT. Is posterior hip instability associated with cam
and pincer deformity? Clin Orthop Relat Res. 2012;470(12):3390-3397.
13. Philippon M, Kuppersmith D, Wolff A, Briggs K. Arthroscopic findings following traumatic hip dislocation
in 14 professional athletes. Arthroscopy. 2009;25(2):169-174.
2005;87(7):1012-1018.
15. Tannast M, Goricki D, Beck M, Murphy S, Siebenrock K. Hip damage occurs at the zone of femoroacetabular
impingement. Clin Orthop Relat Res. 2008;466(2):273-280.
16. Letournel E, Judet R. Fractures of the Acetabulum. New York, NY: Springer-Verlag; 1981.
17. Upadhyay S, Moulton A, Burwell R. Biological factors predisposing to traumatic posterior dislocation of the
hip. A selection process in the mechanism of injury. J Bone Joint Surg Br. 1985;67(2):232-236.
18. Audenaert E, Mahieu P, Pattyn C. Three-dimensional assessment of cam engagement in femoroacetabular
impingement. Arthroscopy. 2011;27(2):167-171.
19. Bankart A. The pathology and treatment of recurrent dislocation of the shoulder-joint. J Bone Joint Surg Br.
1938;26:23-29.
20. Rashleigh-Belcher H, Cannon S. Recurrent dislocation of the hip with a “Bankart-type” lesion. J Bone Joint
Surg Br. 1986;68(3):398-399.
21. Lieberman J, Altchek D, Salvati E. Recurrent dislocation of the hip with a labral lesion: treatment with a
modified Bankart-type repair. J Bone Joint Surg Am. 1993;75(10):1524-1527.
22. Philippon M, Zehms C, Briggs K, Manchester D, Kuppersmith D. Hip instability in the athlete. Oper Tech
Sports Med. 2007;15:189-194.
23. Boykin R, Anz A, Bushnell B, Kocher M, Stubbs A, Philippon M. Hip instability. J Am Acad Orthop Surg.
2011;19(6):340-349.
24. Yang E, Cornwall R. Initial treatment of traumatic hip dislocations in the adult. Clin Orthop. 2000;377:24-31.
25. Paus B. Traumatic dislocations of the hip; late results in 76 cases. Acta Orthop Scand. 1951;21(2):99-112.
26. Rodríguez-Merchán E. Osteonecrosis of the femoral head after traumatic hip dislocation in the adult. Clin
Orthop. 2000;377:68-77.
27. Moed B, WillsonCarr S, Watson J. Results of operative treatment of fractures of the posterior wall of the
acetabulum. J Bone Joint Surg Am. 2002;84(5):752-758.
28. Giza E, Mithofer K, Matthews H, Vrahas M. Hip fracture-dislocation in football: a report of two cases and
review of the literature. Br J Sports Med. 2004;38(4):E17.
29. Bartlett C, DiFelice G, Buly R, Quinn T, Green D, Helfet D. Cardiac arrest as a result of intraabdominal
extravasation of fluid during arthroscopic removal of a loose body from the hip joint of a patient with an
acetabular fracture. J Orthop Trauma. 1998;12(4):294-299.
30. Robertson W, Kelly B. The safe zone for hip arthroscopy: a cadaveric assessment of central, peripheral, and
lateral compartment portal placement. Arthroscopy. 2008;24(9):1019-1026.
31. Ward W, Fleisch I, Ganz R. Anatomy of the iliocapsularis muscle relevance to surgery of the hip. Clin Orthop
Relat Res. 2000;374:278-285.
90 Chapter 5
32. Larson C, Wulf C. Intraoperative fluoroscopy for evaluation of bony resection during arthroscopic manage-
ment of femoroacetabular impingement in the supine position. Arthroscopy. 2009;25(10):1183-1192.
33. Moed B, Carr S, Watson J. Open reduction and internal fixation of posterior wall fractures of the acetabulum.
34. Moed B, McMichael J. Outcomes of posterior wall fractures of the acetabulum. Surgical technique. J Bone
Joint Surg Am. 2008;90(Suppl 2):87-107.
6
Anterior Soft Tissue Injuries
of the Hip
Hip Flexor, Iliopsoas,
and Subspine Impingement
Nikhil Oak, MD; James Voos, MD; and Asheesh Bedi, MD
PATHOANATOMY OF
ANTERIOR SOFT TISSUE INJURIES OF THE HIP
The dynamic layer of the hip, which includes the musculature surrounding the hip joint
and pelvic floor, can be a source of pain and discomfort in the athletic patient. Anterior hip
or groin pain can be caused by several different soft tissue pathologies, the majority of which
can be attributed to hip flexor strains, iliopsoas impingement, and anterior inferior iliac spine
(AIIS) impingement.
Hip Flexor Strains

Pathoanatomy
The most common injuries involving the hip and groin in athletic activity are muscle strains.
Muscles that cross 2 joints, such as the rectus femoris, have a higher tendency for such injury,
which can occur during strong eccentric muscle contractions.1,2 Strains have been shown to be
a result of excessive stretch during muscle activation and are not a result of contraction alone.3
The rectus femoris is frequently injured when actively regulating hip extension and knee flexion,
the mechanism usually being kicking or sprinting.4 The rectus femoris has 2 heads, the direct
originating from the AIIS and the indirect originating from the superior acetabular rim and hip

92 Chapter 6
Figure 6-1. Anatomy of the proximal rectus femoris. Indirect head originates from acetabulum and direct head
originates from AIIS.
capsule (Figure 6-1). Rectus femoris strain injuries typically occur at the myotendinous junction,
but injuries may also occur as an avulsion from the bone in adults, or the apophysis in skeletally
immature patients.5 In cases of acute trauma, the indirect head of the rectus femoris is injured in
most patients, and may sequentially progress to involving the direct head and conjoint tendon with
worsening severity.6
Clinical Presentation and Examination Pearls
Factors that can predispose a patient to injuring the rectus femoris include previous tears, poor
muscle conditioning, muscle fatigue, and insufficient warm-up exercises.3 On physical exam,
patients may present with a mild to moderately antalgic gait. Range of motion, quadriceps
strength, and functional testing should be included as part of the initial clinical exam. Hip flexor
injuries usually result in tenderness in the anterior thigh/groin and can have palpable swelling,
usually 8 to 10 cm below the anterior superior iliac spine (ASIS).1 If there is no muscle retraction,
strains could manifest as diffuse swelling and can even mimic a soft tissue tumor.7 Active hip
flexion and/or knee extension strength may also be diminished and can reproduce pain in the
anterolateral hip when tested.8 Hip rotation and range of motion may also help differentiate the
injury from impingement. Foote et al,9 however, recently reported on 9 patients with rectus avul-
sion injuries and associated labral tears, suggesting that there may be an association between avul-
sion of the reflected head of rectus femoris and labral injuries, and that there may be an underlying
spectrum of traction injuries. Chronic injuries may present as a more indolent pain in the anterior
hip made worse by flexion or kicking. In chronic injuries, a palpable mass is more often present;
however, strength and range of motion can be the same as the contralateral side.10 Wittstein et al11
described a mass-like effect seen in the muscle upon activation, resembling a complete tear, that
can be attributed to retraction at the large musculotendinous junction of the indirect head of the
rectus femoris.
Imaging Pearls
Plain films may be helpful to rule out fractures or bony avulsion injuries but are often negative.
Rectus femoris origin injuries can be missed on radiographs unless heterotopic ossification has
occurred, which would suggest a chronic injury.6 Bianchi et al12 showed that sonography could
demonstrate normal vs posttraumatic changes at the myotendinous junction that correlated well
with magnetic resonance findings. Given the low cost of sonography, it may be a good first-line
Anterior Soft Tissue Injuries of the Hip 93
Figure 6-2. Proximal rectus injury—direct head. (A) Axial T2-weighted fat saturated and (B) sagittal T1-weighted fat
saturated magnetic resonance (MR) arthrograms. (Reprinted with permission from Dr. David Fessell.)
study if there is a high clinical suspicion of rectus femoris injury. The most sensitive and the gold
standard for imaging muscle strains is magnetic resonance imaging (MRI). On MRI, muscle
strains are graded as first-, second-, or third-degree, depending on the involvement of the muscle
fibers. First-degree strains are characterized by microscopic injury, < 5% fiber disruption, and
minimal edema/hemorrhage tracking along muscle fascicles. Second-degree strains involve partial
thickness and show up as high-signal intensity on T2-weighted images within the muscle with
perifascial fluid present. Third-degree strains show complete musculotendinous disruption with
or without retraction.13 The tendon of the direct head is broad and flat and resides anteriorly; the
reflected head tendon continues as a tendon within the muscle mass, so on imaging it appears as a
muscle within a muscle.11 Most commonly, rectus femoris injuries extend along the long portion
of the deep musculotendinous junction. This tear pattern demonstrates a “bull’s-eye” appearance
and can also show a longitudinal scar, retraction, hematoma, and pseudocyst14 (Figure 6-2).
Initial management of hip flexor strains is conservative. Treatment includes controlling
hemorrhage and swelling with rest, compressive wrap and ice, and elevation.1 Nonsteroidal,
anti-inflammatory drugs (NSAIDs) may also be used. In the incipient phase following the resolu-
tion of acute pain, gentle range-of-motion exercises begin. Strengthening and light sport-specific
activities should be initiated once full range of motion has been achieved. Crutches may be used
in the interim if necessary for ambulation. Hsu et al8 used a treatment regimen in National Foot-
ball League (NFL) kickers consisting of a brief period of rest followed by gentle range-of-motion
exercises, isometric followed by isokinetic strengthening, and then moving on to light functional
activities such as light kicking at 10 days’ status postinjury. At 4 to 7 weeks after the index injury,
athletes had returned to their normal kickoff and punting duties. Patients returning to activity
should be followed closely and should return only when they are pain-free because a recurrence
is often more severe, requiring longer rehabilitation than the original injury.1 Gamradt et al15
described a similar course of nonoperative treatment for a group of 11 NFL players who were
able to return to play between 6 and 12 weeks after nonoperative management of rectus femoris
avulsion injuries, with recurrent symptoms noted in only 2 players (Table 6-1).
94 Chapter 6
TABLE 6-1
NONOPERATIVE REHABILITATION GUIDELINES FOR MUSCLE INJURIES
TIME AFTER INJURY TREATMENT
0 to 2 weeks ● Brief period of rest
● Compressive wrap
● Icing/elevation
● Anti-inflammatory medications
● Gentle range-of-motion (ROM) exercises to achieve full ROM
2 to 6 weeks ● Isometric followed by isokinetic and isotonic strengthening
● Light functional activities
6+ weeks ● Return to sports when pain-free
Operative Treatment
As the vast majority of hip flexor strains are effectively managed nonoperatively, rarely would
a patient elect for operative treatment. Bottoni and D’Alleyrand16 described an open anterior
(Smith-Peterson) approach to explore and find the rectus tear in an acute injury. Two sutures
were used to anchor the proximal end and were tied together after being passed through a bony
trough prepared in the AIIS.16 Chronic rectus femoris tears, most commonly of the indirect head,
that continue to be symptomatic despite appropriate rehabilitation may be amenable to surgical
treatment.11,17 Wittstein et al11 described treatment with delayed excision of the indirect head of
the rectus femoris of 5 athletes. They used a straight anterior incision over the muscle deformity,
dissecting the rectus femoris off the quadriceps complex. After using electrical stimulation of the
femoral nerve, the site of the disrupted muscle becomes apparent during contraction. Muscle fibers
were split proximal to the deformity before scarring and fluid around the retracted muscle was
found in all their patients. The soft tissue scar was removed as well as the damaged fibers of the
distal detached muscle. All patients in the study returned to athletics but most still had a degree
of residual pain and weakness.11
Surgical treatment for persistent pain after either an apophyseal avulsion injury of the AIIS or
a rectus femoris tendon with the subsequent development of HO in the injury tract may be neces-
sary. Some athletes, particularly those with deep flexion requirements, will have persistent pain
secondary to impingement of the elongated AIIS against the inferior neck of the femoral head in
straight flexion. Decompression of the AIIS can be performed arthroscopically through an ante-
rior open approach, with or without concomitant repair of the flexor tendon. In the authors’ expe-
rience, decompression of the bony prominence without tendon repair results in good outcomes
without any discernible weakness in hip flexion.
Postoperative Rehabilitation
Postoperative rehabilitation for chronic tears involving resection of the indirect head includes
stretching, massage, gentle range of motion, and progressive exercises.11 In interventions involv-
ing direct repairs, one report described passive range of motion for 4 weeks with weight bearing
in the knee locked in extension before beginning active range of motion at 8 weeks,16 and another
study discussed immobilizing in an extension splint for 6 weeks followed by progressive range of
motion and strengthening.17
Complications
Compartment syndrome has been discussed as an exceptionally uncommon complication
of acute injury but should be caught early to avoid irreversible muscle damage.10 Long-term
complications include residual weakness, recurrence of injury, and the rare possibility of myositis
ossificans or calcific tendinosis.18,19 Postoperative complications include residual pain, weakness,
and recurrence of symptoms.
Iliopsoas Impingement
Pathoanatomy
The iliopsoas is a musculotendinous unit that consists of the psoas major, minor, and iliacus
muscles that acts to flex the thigh and helps maintain an erect position by preventing hyperex-
tension during standing.20 The psoas major originates from the transverse processes of T12-L5,
merges with the iliacus to form the iliopsoas unit, and passes below the inguinal ligament between
the AIIS and iliopectineal eminence before inserting into the lesser trochanter.21,22 When the hip
is in neutral, the iliopsoas tendon lies in the groove between the AIIS and iliopectineal eminence.
When the hip is brought from flexion, abduction, and external rotation into internal rotation and
extension, the tendon subluxes from a lateral to a medial position over the anterior brim of the
pelvis and the anterior aspect of the femoral head and capsule.23 This shift over the anterior hip
capsule or pelvic brim has been attributed to causing painful coxa saltans interna or “internal
snapping hip.”22,23
Alternatively, anterior iliopsoas impingement or tendinitis has been described as a distinct
clinical etiology for persistent anterior hip pain.21,24 Three primary etiologies of iliopsoas tendi-
nitis and impingement have been proposed.24,25 The first is impingement on the anterior labrum,
based on the path and biomechanics of the tendon during hip motion. The iliopsoas makes an
obtuse angle around the iliopectineal eminence and femoral head that increases in hip extension.
Yoshio et al26 measured the pressure and friction exerted on the femoral head and anterior labrum
during hip motion, and found that most pressure was centered over the femoral head between
0 and 30 degrees of flexion and may lead to the 3 o’clock labral injury. A tight or spastic iliopsoas
increases contact pressures beneath the tendon, resulting in impingement.23,24 Second, scarring
or adhesion of the iliopsoas to the anterior capsule and labrum results in a repetitive traction
injury. The normal iliopsoas loses contact with the femoral head at 14 degrees of flexion and the
iliopectineal eminence at 54 degrees.23 A chronically inflamed iliopsoas tendon and/or bursa in
the setting of internal coxa saltans may result in scarring of the tendon to the anterior capsule.
This adherence, in theory, may prevent lift-off from the capsule and lead to a reverse obtuse angle
of the tendon in flexion. The adherent tendon would pull on the anterior capsulolabral complex
with contraction of the iliopsoas muscle, resulting in the characteristic 3 o’clock tear. The third
theory involves the iliocapsularis muscle that originates on the anterior joint capsule and ilio-
pectineal eminence, and inserts slightly distal to the lesser trochanter. Hypertrophy or spastic-
ity of the iliocapsularis may represent an alternative cause of repetitive traction injury on the
anterior capsulolabral complex.24,25 The iliocapsularis and iliopsoas are adjacent to one another,
and it is possible that the tendon overlying a percentage of the labral injuries seen was that of
the iliocapsularis.
Iliopsoas impingement has been observed historically in patient status post-total hip arthro-
plasty when a prominent acetabular component, extruded cement, bony fragments, or screw causes
chronic friction on the iliopsoas, resulting in painful tendinitis.24 Di Lorenzo et al27 described that
arthritic changes to the shape of the anterior acetabular ridge can also cause a psoas impingement
syndrome. At the level of the labrum, the iliopsoas consists of 44.5% tendon and 55.5% muscle
belly.21 A cross-sectional analysis demonstrated the tendon position was directly anterior to the
anterosuperior capsulolabral complex, which is in the 2 to 3 o’clock position.21 A tight iliopsoas
can cause compression over the anterosuperior capsule and can subsequently lead to a labral lesion
from repetitive traction via scarring, adhesions, or direct pressure.21,25
96 Chapter 6
Figure 6-3. Iliopsoas ultrasound-guided injection. All images are transverse (axial). (A) Pre-injection. White
arrow = iliopsoas tendon. (B) Injection with the needle in yellow and fluid around iliopsoas. Asterisk = injected fluid.
(C) Post-injection with fluid around iliopsoas. (Reprinted with permission from Dr. David Fessell.)

Patients with iliopsoas impingement have anterior hip pain for a prolonged period of time, at
a minimum 6 months. There can be a variable injury history from patients reporting a sudden
pop in the anterior hip to symptoms after repetitive overuse during hip flexion activities such as
running. Physical exam findings include a positive impingement test: pain with passive flexion,
adduction, internal rotation (FADIR). Domb et al,25 in a report involving 25 patients, noted that all
patients had a positive impingement sign and had focal tenderness over the iliopsoas at the anterior
joint line. Focal tenderness, however, was noted to be a nonspecific finding. The patient may also
have mechanical symptoms such as groin pain with an audible or palpable snapping sensation.
Iliopsoas impingement may also be associated with increased femoral anteversion as Schutte et al28
noted, describing the psoas as tight despite normal muscle length for individuals with excessive
femoral anteversion.
Imaging Pearls
Plain radiographs such as an anteroposterior (AP) pelvis and elongated neck lateral are needed
in the assessment of hip pain in order to rule out bony pathology. MRI can show secondary find-
ings such as edema, periosteal reaction, and labral pathology (particularly anteromedially) and can
rule out injuries to the articular cartilage. Blankenbaker et al29 stated that MRI shows thickening
and increased intrasubstance signal intensity in iliopsoas tendinosis as well as high T2 intensity
and distension of the iliopsoas bursa. Ultrasonography has the advantage of real-time dynamic
examination, which can detect the site of anterior impingement. A normal tendon would show
a hyperechoic fibrillar texture thought to be secondary to an organized collagenous structure.29
Iliopsoas bursography can be useful in visualizing the tendon flipping back and forth or producing
pain with impingement.23 An image-guided injection of local anesthetic, alone or in combination
with a corticosteroid, into the iliopsoas sheath (not the joint) can serve both a diagnostic and thera-
peutic purpose in differentiating the source of a patient’s symptom24 (Figure 6-3).
All patients typically start with nonoperative therapy for at least 3 to 6 months, including a
period of rest, analgesics, NSAIDs, and physical therapy. Modes of physical therapy include ilio-
psoas stretching, range of motion, and strengthening as well as hydrotherapy. Injection of local
anesthetic with or without corticosteroid into the iliopsoas tendon sheath is helpful in providing
relief; however, the relief is often transient.24 The patient must be pain-free during simple activities
before returning to athletic activities that precipitate discomfort.23
Figure 6-4. Hip arthroscopic views depicting iliopsoas tendon transcapsular release. (A) Arrow depicts iliopsoas
tendon. (B) Radiofrequency ablation and release of tendon.
Operative Options
Surgical treatment is considered for cases refractory to nonoperative management. Treatment
consists of relaxing the iliopsoas by lengthening or releasing the tendon. Options include open
iliopsoas lengthening or release, transcapsular lengthening, and endoscopic release at the lesser
trochanter.
There have been various open techniques described for open iliopsoas lengthening or release by
many authors.23,30-34 An 8- to 10-cm cosmetic transverse incision can be used, bordered medially
by the femoral canal neurovascular bundle and laterally by the lateral femoral cutaneous nerve as
described by Allen and coauthors to perform an anterior (Smith-Peterson) approach.31,33 After
palpating the iliopsoas tendon inserting onto the lesser trochanter, they create 4 partial tenotomies
beginning 1 cm proximal to the lesser trochanter. They describe incising the posterolateral surface
of the tendon, leaving the anterior muscular portion intact, and travelling proximally every 2 cm
with the most proximal tenotomy at the level of the superior portion of the femoral head.33 Gruen
et al30 used an ilioinguinal approach for fractional lengthening of the iliopsoas as they believed the
iliopsoas was most taut over the pelvic brim. They used a 6- to 7-cm incision medial to the ASIS
parallel and slightly cephalad to the inguinal crease.30 Taylor and Clarke34 described a medial
(Ludloff) approach, citing cosmesis and avoidance of sensory deficits (lateral femoral cutaneous
nerve) as its advantages. They released the tendinous portion of the iliopsoas from the lesser tro-
chanter, thus leaving the muscular portion intact.23,34
Endoscopic release of the iliopsoas at the lesser trochanter has been described as an alternative
to traditional open techniques. This technique uses a fluoroscopic-guided approach to the lesser
trochanter. Flanum et al35 and Anderson and Keene36 describe this technique with the patient
supine on a fracture table after arthroscopy was completed to treat any intra-articular lesions. The
patient’s knee is flexed to 30 degrees and maximally externally rotated. A 17-gauge, 6-inch stylet-
enclosed needle, under fluoroscopic guidance, is advanced along the anterior surface of the femur
until it is over the proximal lesser trochanter. A thermal probe is used on a cutting current to clear
off the anterior surface of the femur and lesser trochanter to visualize the iliopsoas tendon. The
tendon is then released from its insertion site on the lesser trochanter, taking care not to transect it
proximally and injure the medial and lateral femoral circumflex arteries (Figure 6-4). Fluoroscopic
views are used intermittently to ensure proper positioning of the cannula/probe and to ensure
the entire tendon has been released. Ilizaliturri et al37 also performed endoscopic releases of the
iliopsoas after arthroscopy of the hip joint was performed. They used a lateral decubitus position
for the arthroscopy, after which traction was removed and the hip externally rotated to bring the
98 Chapter 6
Figure 6-5. Fluoroscopic-guided release of iliopsoas at

lesser trochanter.
lesser trochanter into visualization by fluoroscopy, and the hip was flexed to 30 degrees to relax the
anterior hip capsule and iliopsoas tendon. A hook radiofrequency probe is introduced to release
the iliopsoas tendon at the insertion in a retrograde fashion (Figure 6-5). Sampson22 has described
a similar method but advocates working from the medial side of the tendon and progressing later-
ally to perform a partial or complete release based on clinical judgment. The primary aim is to
lengthen the musculotendinous unit, with a partial release most often accomplishing this goal.
Intra-articular pathology such as labral tears are often associated with iliopsoas impingement.
Domb et al25 describe a transcapsular release of the iliopsoas tendon. After access to the central
compartment and treatment of any concomitant labral pathology, an anterior capsulotomy is
made 1 cm in length directly anterior to the labral injury using a Beaver Blade or radiofrequency
ablation device. The tendinous portion of the iliopsoas can be visualized through the capsular
window and selectively released to lengthen the muscle-tendon unit. Alpert et al21 reported
the circumference of the iliopsoas tendon at the level of the labrum was 28.4 ± 2.8 mm, and the
iliopsoas tendon-muscle belly complex at the level of the labrum was 63.8 ± 7.4 mm. At the level of
the labrum, the iliopsoas is composed of 44.5% tendon and 55.5% muscle belly and helps to guide
the lengthening.
Domb et al 25 reported on 25 patients with complete follow-up (greater than 1 year) who under-
went isolated, primary, unilateral iliopsoas release and either labral debridement or repair. Mean
postoperative outcome scores were 87, 92, and 78 for the modified Harris Hip Score (mHHS),
activities of daily living Hip Outcome Score, and sports-related score, respectively. In patients with
increased femoral anteversion, however, the psoas may have an increased propensity to compress
the anterior labrum as it is functioning as a dynamic stabilizer of the hip joint in external rota-
tion. Fabricant et al38 reported on 67 consecutive patients with symptomatic coxa saltans who
underwent arthroscopic psoas tendon lengthening through a transcapsular approach during a
3-year period. Postoperative mHHS scores were significantly reduced in cases of increased femoral
anteversion (76.9 vs 86.1 for excessive vs low/normal anteversion, P = .031). One should exercise
caution in performing fractional lengthening of the iliopsoas in patients with increased femoral
anteversion, as this may precipitate iatrogenic instability by compromising a dynamic stabilizer
of the joint.
Ilizaliturri et al39 performed a study comparing techniques using an endoscopic iliopsoas
release vs an arthroscopic transcapsular release. They randomized patients into 2 groups and
followed them prospectively with identical postoperative physical therapy as well as hetero-
topic ossification prophylaxis. They did not find any statistical significance in preoperative and
TABLE 6-2
COMPLICATIONS FOLLOWING ILIOPSOAS TENDON RELEASE
● Recurrence of symptoms due to scarring/adhesions
● Flexor weakness
● Sensory deficits along anterolateral thigh (lateral femoral cutaneous nerve)
● Persistent pain
● Unsightly scar
● Infection or hematoma formation
● Heterotopic ossification
postoperative Western Ontario MacMaster (WOMAC) or magnitude of improvement. Open pro-

cedures have had significant morbidity associated with the approach such as flexor weakness and
sensory deficits in the anterolateral aspect of the thigh. Inadequate tendon lengthening or scar-
ring and adhesions are possible explanations if there is a recurrence of symptoms34 (Table 6-2).
Arthroscopic techniques avoid larger open approaches and also permit direct examination of the
hip joint for intra-articular pathology. Persistent pain, bleeding, superficial infection, or hema-
toma formation can occur with any surgical procedure. Heterotopic ossification is a complication
that could be seen with endoscopic procedures, with an incidence of 29 (21 male, 8 female) of
616 (4.7%) consecutive hip procedures for femoroacetabular impingement (FAI) and/or snapping
hip disorders leading to development heterotopic ossification postoperatively by Bedi et al.40
Arthroscopic evaluation of the painful internal snapping hip may demonstrate a focal area of
bony prominence along the inferior border of the AIIS with extension into the iliopectineal emi-
nence. In this setting, decompression of the bony prominence without fractional lengthening of
the tendon is an appealing option. Although most series do not report significant weakness in hip
flexion following partial psoas release, it may be present in some patients. This is most common
in patients with increased femoral anteversion (>25 degrees) and, therefore, one should proceed
with caution in that patient population.
Anterior Inferior Iliac Spine Impingement

Pathoanatomy
Another etiology of anterior hip pain can include a prominent AIIS that can cause impingement
at the level of the acetabular rim. Prominence and extension of the AIIS below the level of the
acetabular rim can decrease the soft tissue space available during hip flexion at the acetabular
rim. This can cause pain with impingement of anterior soft tissues such as the anterior capsule
or iliocapsularis muscle. Cases have been reported in the literature regarding avulsion fractures
of the AIIS causing exostosis and hypertrophy.41-43 Irving42 described exostosis as the cause of
hip pain in a young boy, limiting his hip range of motion and walking, which improved after
surgery. Milankov et al43 wrote of 2 athletes who sustained remote injuries and had limited
range of motion and flexion with hip pain during movement. They described surgical excision
of the exostosis/scar tissue, which in both cases allowed for full range of motion and return to
full functional activity.43 Pan et al44 described impingement occurring between the femoral
head-neck junction and a hypertrophic AIIS without any previous traumatic etiology.
Patients with AIIS subspine impingement will likely have pain insidious in onset and made
worse with deep flexion during range of motion. Pan et al44 described a history of groin pain
100 Chapter 6
TABLE 6-3
VARIATIONS IN ANTERIOR INFERIOR ILIAC SPINE MORPHOLOGY
TYPE DESCRIPTION COMPUTED CLINICAL IMPORTANCE
TOMOGRAPHY
DEFINITIONS
I Upsloping Upsloping on ischium AIIS does not contribute to
view impingement
II Flat Flat or downsloping on AIIS may contribute to
ischium view, but does impingement
not cross the rim
III Downsloping Downsloping and AIIS may contribute to
crosses the rim impingement
induced by running, jumping, or prolonged walking as well as tenderness in the right groin with
restricted hip flexion. Pain will be of a dull, aching character in the anterior groin, most severe
with forced hyperflexion, and absent with abduction. The impingement test (flexion, adduc-
tion, internal rotation) may be positive and crepitus will likely be present with axial loading.
Recent studies have reported the incidence of concomitant FAI to be common.45
Imaging Pearls
Routine plain pelvic radiographs may show abnormalities above the superior rim of the
acetabulum, but may not clearly identify extra-articular impingement.44 A false profile radio-
graph is particularly useful to characterize the shape of the AIIS and relationship relative to the
acetabular rim. Zaltz et al46 recently reported that a crossover sign on an AP pelvis radiograph may
not represent focal acetabular retroversion, but may rather reflect an AIIS extending to or below
the level of the anterior superior acetabular rim in cases of an anteverted acetabulum. Depending
on the history of trauma pathology, differential diagnosis can include prior avulsion injuries to the
AIIS or fracture. MRI may elucidate soft tissue pathology; however, computed tomography (CT)
scan is the imaging modality of choice to define the morphology of the AIIS and relationship to the
acetabular rim. Hetsroni et al45 describe a classification system based on clinical findings and CT
scans with 3-dimensional (3D) reconstruction to demonstrate the morphology of the AIIS. They
described using an ischium view on 3D scan, looking directly posterior at the ischium to draw a
horizontal line at the most distal level of the junction of the AIIS and the ilium wall. The mor-
phology of the AIIS is thus classified based on the relationship to the horizontal line and involves
3 variants: Type I when there is a smooth ilium wall between the AIIS and the acetabular rim,
Type II when the AIIS extends to the level of the rim, and Type III when the AIIS extends distally
to the acetabular rim (Table 6-3 and Figure 6-6). A separate cohort of 78 hips (78 patients) with
impingement was used to compare hip range of motion among the 3 AIIS types. Mean hip flexion
was limited to 120, 107, and 93 degrees in hips with Type I, Type II, and Type III AIIS, respec-
tively. Mean internal rotation was limited to 21, 11, and 8 degrees in hips with Type I, Type II, and
Type III AIIS, respectively.45
Treatment Options
Nonoperative treatment options include rest, cessation of offending activities, NSAIDs, and
physical therapy to work on range of motion and core muscle strengthening. Surgical treatment
may be considered for refractory cases. Arthroscopy can be performed to identify and resolve any
abnormalities in the cartilage or labral lesions as well as cam and pincer-type deformities. Pan
Figure 6-6. 3D reformatted computed tomography (CT) scans of the acetabulum depicting AIIS mor-
phological classification.
et al44 described, after arthroscopy, using an anterior (Smith-Peterson) approach between the
rectus femoris and gluteus medius. They detached part of the fascia lata and gluteus medius from
the crest to display the joint capsule. They flexed the hip to demonstrate impingement occurring
against the hypertrophic AIIS and then resected the spine to a smaller, more normal size before
completing the procedure.44 Larson et al47 recently reported 3 cases of AIIS impingement success-
fully addressed with arthroscopic AIIS decompression. All cases were either development abnor-
malities of the apophysis or the result of a prior AIIS avulsion or pelvic osteotomy. Hetsroni et al48
recently reported on the retrospective results of 10 male patients treated for symptomatic FAI and
extra-articular AIIS impingement. The mean age was 24.9 years, with 8 of 10 patients younger than
30 years. In 9 patients, an anterior cam lesion was identified and decompressed before the AIIS
decompression. The mean follow-up time was 14.7 months (range, 6 to 26). Hip flexion range of
motion improved from 99 ± 7 degrees before surgery to 117 ± 8 degrees after surgery (P< .001). The
mHHS improved from 64 ± 18 before surgery to 98 ± 2 at latest follow-up after surgery (P < .001).48
The potential concern for disruption of the direct head of the rectus femoris tendon after AIIS
decompressions has been raised and has recently been addressed in cadaveric work. Hapa et al49
studied 11 cadaveric hips to define the origin of the direct and indirect heads of the rectus femoris
tendon. All hips were male with a mean age of 54.3 years (range, 33 to 74). The proximal to distal
and medial to lateral rectus femoris origin were on average 2.2 and 1.6 cm, respectively. There was
a characteristic bare area at the anterior and inferomedial AIIS, indicating a reasonable margin of
safety with AIIS decompression given the broad tendon footprint.
PEARLS AND PITFALLS

● High-level athletes have been shown to be able to return from rectus femoris strains with
nonoperative management, but recalcitrant cases may require surgical intervention.
● Dynamic ultrasound is useful in visualizing iliopsoas impingement.
● One must be mindful of an athlete’s femoral version when considering a fractional lengthen-
ing, as the psoas may function as a dynamic stabilizer in those with increased anteversion.
● AIIS impingement may cause pain with hip flexion, and may be incorrectly identified as a
crossover sign on an AP pelvis. The false profile view is useful to visualize morphology of the
AIIS in relation to the acetabular rim.
102 Chapter 6
CONCLUSION
Anterior hip or groin pain can be caused by several different soft tissue pathologies, the major-
ity of which can be attributed to hip flexor strains, iliopsoas impingement, and AIIS impinge-
ment. Failure to recognize and address concomitant compensatory injury patterns associated with
intra-articular hip pathology can result in continued disability in a subset of patients and athletes.
Knowledge of the potential etiology of both intra- and extra-articular hip pain is critical to effec-
tively treating patients who present with dysfunction of the hip joint, hemipelvis, and surrounding
musculature.
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2008;190(3):W182-W186.
15. Gamradt SC, Brophy RH, Barnes R, Warren RF, Byrd JWT, Kelly BT. Nonoperative treatment for proximal
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16. Bottoni CR, D’Alleyrand JG. Operative treatment of a complete rupture of the origination of the rectus femoris.
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19. Yun HH, Park JK, Park JW, Lee JW. Calcific tendinitis of the rectus femoris. Orthopedics. 2009;32(7):490.
20. Blankenbaker DG, Tuite MJ. Iliopsoas musculotendinous unit. Semin Musculoskelet Radiol. 2008;12(1):13-17.
21. Alpert JM, Kozanek M, Li G, Kelly BT, Asnis PD. Cross-sectional analysis of the iliopsoas tendon and its rela-
tionship to the acetabular labrum. Am J Sports Med. 2009;37(8):1594-1598.
22. Sampson TG. Arthroscopic iliopsoas release for coxa saltans interna (snapping hip syndrome). In: Byrd JWT,
ed. Operative Hip Arthroscopy. 2nd ed. New York, NY: Springer; 2005:189-194.
23. Byrd JWT. Snapping hip. Oper Techn Sport Med. 2005;13(1):46-54.
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Orthop Surg. 2009;17(6):337-344.
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fied cause of labral pathology in the hip. HSS J. 2011;7(2):145-150.
26. Yoshio M, Murakami G, Sato T, Sato S, Norisyasu S. The function of the psoas major muscle: passive kinetics
and morphological studies using donated cadavers. J Orthop Sci. 2002;7(2):199-207.
27. Di Lorenzo L, Jennifer Y, Pappagallo M. Psoas impingement syndrome in hip osteoarthritis. Joint Bone Spine.
2009;76(1):98-100.
28. Schutte LM, Hayden SW, Gage JR. Lengths of hamstrings and psoas muscles during crouch gait: effects of
femoral anteversion. J Orthop Res. 1997;15(4):615-621.
29. Blankenbaker DG, De Smet AA, Keene JS. Sonography of the iliopsoas tendon and injection of the iliopsoas
bursa for diagnosis and management of the painful snapping hip. Skeletal Radiol. 2006;35(8):565-571.
30. Gruen GS, Scioscia TN, Lowenstein JE. The surgical treatment of internal snapping hip. Am J Sports Med.
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31. Jacobson T, Allen WC. Surgical correction of the snapping iliopsoas. Am J Sports Med. 1990;18(5):470-474.
32. Dobbs MB, Gordon E, Luhmann SJ, Szymanski DA, Schoenecker PL. Surgical correction of the snapping ilio-
psoas tendon in adolescents. J Bone Joint Surg Am. 2002;84(3):420-424.
33. Hoskins JS, Burd TA, Allen WC. Surgical correction of internal coxa saltans: a 20-year consecutive study. Am
J Sports Med. 2004;32(4):998-1001.
34. Taylor GR, Clarke NMP. Surgical release of the “snapping iliopsoas tendon”. J Bone Joint Surg Br.
1995;77(6):881-883.
35. Flanum ME, Keene JS, Blankenbaker DG, Desmet AA. Arthroscopic treatment of the painful “internal” snap-
ping hip: results of a new endoscopic technique and imaging protocol. Am J Sports Med. 2007;35(5):770-779.
36. Anderson SA, Keene JS. Results of arthroscopic iliopsoas tendon release in competitive and recreational ath-
letes. Am J Sports Med. 2008;36(12):2363-2371.
37. Ilizaliturri VM Jr, Villalobos FE, Chaidez PA, Valero FS Aguilera JM. Internal snapping hip syndrome: treat-
ment by endoscopic release of the iliopsoas tendon. Arthroscopy. 2005;21(11):1375-1380.
38. Fabricant PD, Bedi A, De La Torre K, Kelly BT. Clinical outcomes after arthroscopic psoas lengthening: the
effect of femoral version. Arthroscopy. 2012;28(7):965-971.
39. Ilizaliturri VM Jr, Chaidez C, Villegas P, Briseno A, Camocho-Galindo J. Prospective randomized study of
2 different techniques for endoscopic iliopsoas tendon release in the treatment of internal snapping hip syn-
drome. Arthroscopy. 2009;25(2):159-163.
40. Bedi A, Zbeda RM, Bueno VF, Downie B, Dolan M, Kelly BT. The incidence of heterotopic ossification after hip
arthroscopy. Am J Sports Med. 2012;40(4):845-863.
41. Rajasekhar C, Kumar KS, Bhamra MS. Avulsion fracture of the anterior inferior iliac spine: the case for surgical
intervention. Int Orthop. 2001;24:364-365.
42. Irving MH. Exostosis formation after traumatic avulsion of the anterior inferior iliac spine. J Bone Joint Surg Br.
1964;46:720-722.
43. Milankov M, Miljkovic N, Savic D, Stankovic M. Operative treatment of avulsion fractures of the anterior
inferior iliac spine: a two-case report. J Ortho Traumatol. 2005;6:154-157.
44. Pan HL, Kawanabe K, Akiyama H, Goto K, Onishi E, Nakamura T. Operative treatment of hip impingement
caused by hypertrophy of the anterior inferior iliac spine. J Bone Joint Surg Br. 2008;90(5):677-679.
45. Hetsroni I, Poultisides L, Bedi A, Larson CM, Kelly BT. Anterior inferior iliac spine morphology correlates
with hip range of motion: a classification system and dynamic model. Clin Orthop Relat Res. 2013: http://link.
springer.com/article/10.1007%2Fs11999-013-2847-4. Epub February 15, 2013. Accessed April 7 2013.
46. Zaltz I, Kelly BT, Hetsroni I, Bedi A. The crossover sign overestimates acetabular retroversion. Clin Orthop
Relat Res. 2012: http://link.springer.com/article/10.1007%2Fs11999-012-2689-5. Epub November 8, 2012.
Accessed April 7 2013.
three representative case reports and proposed concept. Arthroscopy. 2011;27(12):1732-1737.
48. Hetsroni I, Larson CM, Dela Torre K, Zbeda RM, Magennis E, Kelly BT. Anterior inferior iliac spine deformity
as an extra-articular source for hip impingement: a series of 10 patients treated with arthroscopic decompres-
sion. Arthroscopy. 2012;28(11):1644-1653.
49. Hapa O, Bedi A, Gursan O, et al. Anatomic footprint of the direct head of the rectus femoris origin: cadav-
eric study and clinical series of hips after arthroscopic anterior inferior iliac spine/subspine decompression.
Arthroscopy. 2013;29(12):1932-1940.
7
Medial Soft Tissue Injuries
of the Hip
Adductor Strains and Athletic Pubalgia/
Core Muscle Injury
Patrick Birmingham, MD; Eilish O’Sullivan, PT, DPT, OCS;

and Christopher M. Larson, MD
PATHOANATOMY OF MEDIAL SOFT TISSUE INJURIES

OF THE HIP
The structures of the hip and pelvis are dynamically codependent and can be categorized based
on a layered anatomic approach as described by Kelly and colleagues.1 Hip pathology and the
resultant compensatory disorders are systematically diagnosed from deep to superficial layers and
an appropriate treatment plan is laid out based on the pathoanatomy.
The pubic symphysis acts as the fulcrum for many of the forces of the anterior pelvis. It is the
common attachment of the confluence of the rectus abdominis fascial sheath with the fascial
sheath of the adductor longus merging anterior to the pubis to form a common sheath (Figure 7-1).2
Injury to both of these structures, or one in isolation as a result of supraphysiologic stresses on
the hemipelvis and pubic symphysis, may lead to an imbalance of forces and instability.3 This may
result in athletic pubalgia and/or an adductor strain with resultant pain and disability.4
One possible cause of symphyseal overload is femoroacetabular impingement (FAI). FAI repre-
sents abnormal femoral and acetabular bony morphology that limits hip motion, and in particular
internal rotation, because of contact between the femoral neck and the acetabular rim early in the
arc of motion.5 The amount of internal rotation at the hip allowed by significant FAI is typically
less than required for functional activities. Therefore, a compensatory increase in motion may
be provided by the lumbar spine, sacroiliac (SI) joints, or pubic symphysis.6 These compensatory

106 Chapter 7
Figure 7-1. Diagram showing the aponeu-

rotic insertion of caudal rectus abdominis
(RA) and adductor longus (AL) muscles on
the anterior pubic symphysis with oppos-
ing vectors of force.
patterns may induce alterations in the muscle forces across the pelvis, and cause supraphysiologic
strain in the other joints (symphysis) and pelvic muscles (adductor).7 The mobility of the pubic
symphysis under physiologic conditions mainly involves vertical shear and anterior-posterior
rotation.8 The motion at the symphysis as a result of cam impingement has recently been studied
in fresh-frozen cadavers. Simulated cam impingement caused a statistically significant increase in
rotational symphysis motion as compared to the non-cam state. The primary rotation was in the
transverse plane and was in the direction of opening the joint anteriorly.9
Increased stress on the anterior pelvis as a result of reduced internal rotation of the hip is not
a novel concept. It was first described by Williams in 1978, who documented a series of patients
with osteitis pubis, all of who had limited internal rotation. He theorized that the reduced internal
rotation put excess stress on the hemipelvis and led to increased motion at the symphysis caus-
ing the osteitis pubis.10 This was confirmed by a study by Verrall et al,11 who found a significant
association between reduced hip range of motion and osteitis pubis.
FAI and athletic pubalgia/core muscle injury have been reported as a combined injury pattern
in multiple studies.5 Meyers et al4 have reported combined athletic pubalgia and hip pathology in
as many as 27% of hockey players referred for chronic groin pain. Rectus abdominis and adduc-
tor strains have been shown to occur in combination with acetabular labral injuries in National
Football League (NFL) players. In this study, all labral tears were associated with FAI, and this
combination of injuries has been coined the “sports hip triad.”7
Females represent only 8% to 15% of patients with athletic pubalgia.12,13 One possible expla-
nation for this is the difference between male and female pelvic anatomy. Females have a wider
subpubic angle, leading to a different distribution of forces and a relatively wider, more stable
pelvis that is more effective at transferring destabilizing forces more distally (Figure 7-2).4 It has
also been suggested that the gender differences in extremity alignment and muscle activation
that predispose women to anterior cruciate ligament injuries may be protective against athletic
pubalgia.14,15 The pubic symphysis also has about 2 to 3 mm more mobility in females than in
males, and can increase to 8 to 10 mm during pregnancy.2
Medial Soft Tissue Injuries of the Hip 107
Figure 7-2. Basic differences in

male vs female anatomy that relate
to the pubic joint and injury. Note
the differences in width between
the pelvis and knees of the 2 gen-
ders. These differences suggest a
different distribution of forces dur-
ing extremes of exertion; for exam-
ple, more lateral forces emanate
from the female pelvis and more
acutely angled forces are transmit-
ted to female knees during landing.
ADDUCTOR STRAINS
Muscle strains have been classically described in muscles that cross 2 joints, and occur dur-
ing eccentric contraction where external load exceeds muscle force.16 Strains that result from
this mechanism typically occur at the myotendonous junction or in the muscle belly.17 However,
adductor strains also occur commonly at the tendonous origin from the pubis, suggesting a differ-
ent mechanism of injury in these cases.
The adductor muscle group, in conjunction with the lower abdominal musculature, works to
stabilize the pelvis during lower-extremity activities.18 This has been confirmed by electromyo-
graphic studies that have demonstrated that the adductor longus has minimal function during
sprinting,19 and functions to stabilize the hip rather than create power for motion during cut-
ting.20 The adductor longus origin at the pubis has a tendon with a small cross-sectional area with
respect to its muscular attachment that may predispose it to strain.18 There has been evidence
that an athlete with a weak adductor to abductor ratio or decreased hip range of motion may be at
increased risk for groin strain.21
ATHLETIC PUBALGIA/CORE MUSCLE INJURY

The anatomy of the abdominal wall can also be described in layers. From superficial to deep, the
layers are skin, fascia, external oblique muscle and fascia, internal oblique muscle and fascia, trans-
versus abdominis muscle and fascia, and transversalis fascia (Figure 7-3).22 The conjoined tendon
consists of the internal oblique and transversus abdominis aponeurosis that fuse medially before
insertion on the pubic tubercle.22 The conjoined tendon inserts anterior to the rectus abdominis
108 Chapter 7
Figure 7-3. The anatomic layers of the groin and the path of the indirect inguinal hernia are illustrated.
Rectus abdominis seen medially.
on the pubis. The fibers of the anterior pubic ligament blend with the rectus abdominis fascia. The
pubic symphysis is a nonsynovial amphiarthrodial joint.2
Athletic pubalgia or core muscle injury is an injury to one of the previously named structures
as it inserts on the pubis, without the presence of a clinically recognizable hernia.23 There have
been many suggested etiologies for the constellation of lower abdominal and groin pain symptoms
associated with athletic pubalgia, sports hernia, or Gilmore’s groin. One popular definition is that
the pain and injury results from a hyperextension injury (microtears) to the rectus abdominis12,13
or internal oblique muscle insertion on the pubic symphysis and/or hyperabduction of the adduc-
tors of the thigh that destabilizes the anterior pelvis.4,12,13 This represents an induced imbalance
between multiple soft tissue structures.4 The so-called Gilmore’s groin has been described as an
injury to the external oblique aponeurosis and conjoined tendon with dehiscence between the
conjoint tendon and the inguinal ligament.23 Taylor24 reported that pubalgia was caused by micro-
scopic tears or avulsions to the internal oblique muscle in the area of the conjoined tendon. Others
have suggested an injury pattern consisting of weakness or tearing of the posterior inguinal wall
(transversalis fascia) without a discrete hernia.22,23 One study of open treatment of sports hernia
in 35 athletes showed tears of the external oblique were most common (56%), followed by a bulge
in the posterior wall (50%), and conjoined tendon disruptions (12%). Thirty-two percent had both
an external oblique tear and deficiency of the posterior wall.25
The strong pull of the adductors against a fixed lower limb in the presence of underconditioned
abdominal muscles can create a shearing force across the hemipelvis, leading to attenuation or
tearing of the structures attached to the pubis.22 Therefore, it stands to reason that any cause of
shearing force across the hemipelvis could lead to the injury patterns associated with sports hernia.
Extremes of hip motion or muscular imbalance between the thigh and abdominal musculature
may lead to shearing forces across the pubic symphysis, which could lead to injury.16,23 One pos-
sible source of pain has been theorized to be the result of entrapment of the genital branches of
the ilioinguinal or genitofemoral nerves.26 The symphysis itself is innervated by branches of the
pudendal and genitofemoral nerves.2 Other reports have suggested the iliohypogastric or obtura-
tor nerves could potentially be involved.27
Osteitis pubis is most likely a stress fracture of the perisymphyseal pubic bone(s) as a result of
increased strain on the anterior pelvis and symphysis.28 It is a chronic overuse injury that initially
causes stress reaction in the pubic bone, and later degenerative changes to the symphysis.29 This
was proven by Verrall et al, who described bone biopsies taken from the pubic rami of athletes
with diagnosed osteitis pubis for histologic examination. The specimens showed formation of new
woven bone, osteoblasts, neovascularization, and stellate fibroblasts with a complete absence of
any inflammatory cells or signs of osteonecrosis.30 In a similar study, biopsies taken of the sym-
physeal cartilage disc at the time of curettage for osteitis pubis showed degenerative cartilage with
complete absence of inflammatory cells.29
Adductor muscle pathology is associated with osteitis pubis as well.31 One obvious question is
why do some patients develop osteitis pubis and why do others develop a sports hernia? Increased
strain on the anterior pelvis is the mechanism of injury for both, and adductor pathology is com-
mon to both. There is scant literature regarding this topic, but the key may be motion of the sym-
physis joint. Like motion or laxity in other joints, motion at the symphysis is patient dependent
and variable. Increased motion at the symphysis secondary to increased anterior pelvic strain leads
to increased strain of the associated musculature (rectus abdominis and adductor) and over time
may lead to injury to the tendinous attachment sites, leading to sports hernia. Along these lines,
increased strain on the anterior pelvis in a patient with a hypermobile symphysis will transmit
force to the adjacent pubic bone and, over time, may lead to a stress reaction or stress fracture of
the bone and osteitis pubis.28 Athletic pubalgia and osteitis pubis may coexist in some patients
as well.
Hip and groin injuries are common among athletes, especially in soccer, hockey, and American
football.32 Injuries to the hip make up about 5% to 9% of injuries in high school athletes.33 Loads of
up to 8 times body weight have been shown in the hip joint during jogging, and up to 6 times body
weight in walking.34 The etiology of the pain can be intra-articular, extra-articular, or combined.
Therefore, it is critical to characterize the location of the pain (medial groin, groin, low abdo-
men, superficial or deep, lateral thigh, etc) and the specific activities or positions that exacerbate
the pain.
Nonorthopedic etiologies of extra-articular pain should also be considered, including gyne-
cologic, urologic, gastrointestinal, and oncologic. Subjective assessment with validated outcome
instruments (modified Harris Hip Score, Hip Outcome Score, nonarthritic hip score, Short Form-
36) should be included as well.
Adductor Strains
Athletes who are involved in repetitive kicking, quick starts, or changes in direction have a
higher incidence of adductor injury.18 One study suggests that baseball pitchers and hockey goalies
have a predisposition for adductor injuries.4
In a study of National Hockey League (NHL) players, preseason hip adduction strength
was 18% lower in players who subsequently sustained an adductor muscle strain compared to
110 Chapter 7
uninjured players.35 In a related study, a preseason hip-strengthening program was found to lower
the incidence of hip strains in elite athletes.36
Athletic Pubalgia/Core Muscle Injury

Eighty-two percent of patients with athletic pubalgia are athletes.24 Sports with rapid change in
direction while running, and repetitive twisting and turning of the trunk on the proximal thigh,
have a higher incidence of athletic pubalgia.12,22,37
Patients typically present with exertional pain without a known injury or event, and limita-
tions during physical activity or sports.12 They have inguinal/lower abdominal pain with activity,
which is alleviated with rest, and pain may radiate to the adductor, perineum, rectus abdominis,
or testicles (4%).12,23 In one series, 88% had adductor pain in addition to their inguinal pain.12
Activities such as kicking, sit-ups, coughing, and Valsalva may exacerbate the pain. Approximately
4.6% of surgical patients had previously undergone unsuccessful traditional hernia repair.3
Osteitis pubis is painful in the anterior and medial groin, increases with weight bearing, and
there is weakness, clicking, and difficulty with uneven surfaces.28,32 Like athletic pubalgia pain,
osteitis pubis is aggravated by running, cutting, kicking, and rapid accelerations and decelera-
tions.28 In one study of 189 athletes with groin pain, osteitis pubis was found to be the primary
cause in 14%. The prevalence is much greater in men than in women, similar to athletic pubalgia.
However, this prevalence may be confounded by a sex disparity in athletic participation.38 Osteitis
pubis and athletic pubalgia can also coexist as a combined pathology in some patients.13

A comprehensive hip exam should be carried out to adequately evaluate for any intra-articular
or extra-articular causes of the pain. In addition to the specific tests for adductor strains and ath-
letic pubalgia below, a hip-specific exam should include palpation of tender areas (psoas, greater
trochanter); a neuromotor exam; range-of-motion testing (flexion, internal rotation, external rota-
tion, extension, abduction); a flexion, adduction, internal rotation (FADIR) impingement test; cir-
cumduction maneuver (psoas impingement); resisted straight leg raise (intra-articular); Ober test
(iliotibial band); a flexion, abduction, external rotation (FABER) test for sacroiliac joint; straight
leg exam (ipsilateral and contralateral for lumbar spine); and heel strike (femoral neck fracture).32
Chronic groin pain, in this setting, often presents with a decrease in internal rotation.21 These
range-of-motion limitations may be seen in the setting both of FAI and osteitis pubis.7,21,39
Adductor Strains
There is tenderness to palpation with focal swelling along the adductors, with decreased
adductor strength and pain with resisted adduction.18 Resisted adduction can cause pain in
athletic pubalgia as well and cannot be used to distinguish the two. A reliable method of testing
resisted adduction is to have patients lie supine then bring their knees up to 90 degrees of flexion
with their feet on the table. The examiner’s forearm is then placed between the knees lengthwise
and the patient is instructed to squeeze the forearm. Patients can also experience pain with passive
abduction, and about 68% will have palpable defects.40

Pain can be precipitated by simulated coughing, with resisted sit-ups (46%), and hip adduction
or Valsalva.12 Upon palpation, there is no detectable hernia; however, there is usually tenderness
around the conjoined tendon, pubic tubercle (22%), adductor longus (36%), superficial inguinal
ring, or posterior inguinal canal.12,23,41 One study found that more patients had pain with resisted
adduction (88%) than had pubic tenderness (22%), but they may also have pain with resisted hip
flexion (9%).12
Osteitis pubis, another cause of chronic groin pain about the pubis, needs to be distinguished
from athletic pubalgia and ruled out. Osteitis pubis is a stress fracture of the pubic bone adjacent
to the symphysis.28 It is associated with decreased hip range of motion, in particular internal rota-
tion.21 Patients present with pain located over the pubic symphysis similar in character to athletic
pubalgia. On being examined, patients have tenderness over the symphysis and pubic rami and
may have pain with resisted adduction. Tenderness over the pubic rami is also common, and
symptoms can be either unilateral or bilateral. Pain may also be elicited by hip flexion or eccentric
loading of the rectus abdominis. As mentioned previously, some patients present with both athletic
pubalgia and osteitis pubis.
IMAGING PEARLS
Plain X-Rays
Plain radiographs obtained for athletes presenting with groin pain should be evaluated for
osteoarthritis, FAI, dysplasia, fracture, apophyseal avulsion, and osteitis pubis. The series should
include an appropriately oriented weight-bearing anteroposterior (AP) pelvis, a Dunn lateral, and
a false profile view.42
The AP pelvis should be used to evaluate for a crossover sign (cephalad acetabular retroversion),
the center-edge angle of Wiberg (dysplasia and lateral overcoverage), acetabular index (dysplasia),
joint space (arthritis), and the pubic symphysis. The Dunn lateral should be used to evaluate the
alpha angle for any decreased head-neck offset (cam), pincer trough, or synovial herniation pits.
The false profile should be used to evaluate for anterior overcoverage or dysplasia, for anterior
center-edge angle (dysplasia), anterior and posterior joint space, and for the morphology of the
anteroinferior iliac spine.
Some authors suggest the use of a “flamingo view,” which is a one-legged AP view of the sym-
physis used to evaluate for pubic instability. Vertical shift of greater than 2 mm or widening greater
than 7 mm indicates instability.43
Osteitis pubis appears normal in acute cases. In chronic cases (> 6 months), radiographs
show cystic changes, sclerosis, and widening or narrowing of the symphysis (Figure 7-4),16 and
one-legged stance films may suggest instability.29

Magnetic resonance imaging (MRI) used for evaluation of groin pain should include sequences
specifically directed to evaluate the intra-articular space in order to identify any possible labral
or chondral pathology, to evaluate the rectus abdominis, adductor longus, psoas, pubis, pubic
symphysis, and femoral neck for stress fracture or avascular necrosis. It is also helpful to include
axial cuts through the knee in order to evaluate femoral neck version. Increased femoral neck
version may be seen in the setting of psoas snapping and subtle anterior hip instability, whereas
relative femoral neck retroversion is associated with dynamic bony impingement.
Whereas intra-articular contrast has been traditionally used with lower resolution 1.5 Tesla
magnets, non-contrast MRI of the hip with a 3 Tesla magnet has been validated using arthroscopy
with a reported 94% to 95% accuracy for identifying labral and chondral pathology, respectively.44
Labral tears most commonly appear in the anterosuperior quadrant and can be seen on the sagittal
sequences, and paralabral cysts are often an indirect sign of a labral tear.45 Acute chondral injuries
usually appear with adjacent bone marrow edema.46 Meyers et al found that 15% of patients with
112 Chapter 7
Figure 7-4. An AP pelvic radiograph of a patient with

osteitis pubis. Note the sclerosis adjacent to the pubic
symphysis.
MRI evidence of athletic pubalgia also had evidence of hip pathology that was confirmed with pain
relief after intra-articular anesthetic injection.3 Feeley et al reported that, in a series of NFL players
presenting with groin or hip flexor strain, 46% had MRI evidence of both adductor strain and ace-
tabular labral lesions, and 15% had a rectus abdominis tear, adductor strain, and a labral lesion.7
Pubalgia refers to a chronic injury to the parasymphyseal location usually involving microtears
of the rectus abdominis or adductor longus, or stress fracture of the pubis (Figure 7-5). Injury can
also involve a deficient posterior inguinal wall (transversalis fascia), and associated tear of the
conjoined tendon (internal oblique and transverse abdominis) or external oblique.46 In one study,
MRI was found to be sensitive and specific both for rectus abdominis and adductor tendon inju-
ries3,37 (Figure 7-6). MRI had a sensitivity and specificity of 68% and 100% for rectus abdominis
pathology and 86% and 89% for adductor tendon pathology.37 A study by Albers et al found that
90% of pubalgia cases show attenuation of the abdominal wall musculofascial layers, which cor-
related well with surgical findings.47 However, in one of their early studies, Meyers et al reported
that only 9% of preoperative MRIs showed a tear of the rectus abdominis. At the time of surgery,
23% of the patients were found to have injury to the rectus abdominis.12 This was prior to the
development of a specific MRI technique, and underlies the importance of getting the correct MRI
sequences in order to accurately identify associated pathology. It is also important to evaluate all of
the potential pain-generating structures, as tears of the rectus abdominis are not present in every
symptomatic sports hernia. Omar et al have put forth a specific technique for MRI evaluation of
sports hernia that correlates well with demonstrable injury.48 This technique uses a surface coil,
a send-receive body coil, as well as oblique planes to maximize the evaluation of the osseous and
musculotendinous pathology of the pelvis.3
Unilateral rectus abdominis injury combined with adductor pathology was the most common
finding on MRIs performed for athletic pubalgia. The second most common finding was isolated
adductor pathology.3
MRI of osteitis pubis may reveal bony edema spanning the symphysis29,37 (Figure 7-7). This is
best seen using short tau inversion recovery (STIR) or T2 fat-suppression sequences in the coronal
plane.3,46 The increased signal may be noted over a broad area of the parasymphyseal bone. It can
also occur as a hyperintense line paralleling the subchondral bone plate of the pubis. In some cases,
on the axial sequences, an abnormal inferior extension of the cleft in the symphyseal fibrocartilage
can be seen and has been called a secondary cleft sign,37 which likely represents a microtear of the
adductor enthesis.
In general, muscle strains that on MRI show greater than 50% cross-sectional area involvement,
fluid collections, and deep muscle tears are associated with longer recovery times.16 In one study
Figure 7-5. An illustration of the close approximation

of the rectus abdominis and the adductor longus at the
pubic symphysis.
Figure 7-6. MRI of the pelvis. Complete tear of the adductor longus tendon from the proximal attachment site
with a 2-cm retraction. (A) Prominent edema and fluid in the muscle as best visualized with the STIR sequence.
(B) The ruptured tendon as visualized on the coronal T1 sequence.
of adductor longus tears, a palpable defect correlated to approximately a 3-cm or greater retraction
on MRI.40
Computed Tomography
Computed tomography (CT) can be used to more accurately evaluate the bony morphology of
the hip joint in the setting of FAI or osteitis pubis. Measurements of the acetabular and femoral
neck version and the alpha angle are taken in addition to 3-dimensional reconstructions to better
characterize pincer and cam morphology.
114 Chapter 7
Figure 7-7. MRI appearance of osteitis pubis. (A) STIR sequence in a coronal plane shows bright bone marrow edema
symmetrically across the pubic symphysis, indicating an inflammatory process. (B) Proton density view shows diffuse
degeneration of the disc.
Ultrasound
Ultrasound may be useful for the evaluation of athletic pubalgia. A high-frequency trans-
ducer (13 MHz) can be used to evaluate the motion of the inguinal canal and its walls during
Valsalva. The size of the defect is typically 2 cm on average, and represents a convex anterior bulge
of the posterior inguinal wall.49 One retrospective blinded, controlled, nonrandomized study of
Australian-rules American football players found that 10 of 14 patients with groin pain had evi-
dence of dynamic posterior abdominal wall insufficiency. However, 11 of 21 asymptomatic players
also showed dynamic wall insufficiency. It is critical to correlate physical examination findings
with imaging results.50 Ultrasound reproducibility is operator-dependent and, therefore, may not
be universally reliable.
Dynamic Imaging Analysis

Herniography can be used to rule out a true hernia or sports hernia. It is performed by
fluoroscopy after intraperitoneal injection of contrast material. The patient performs a Valsalva,
and a positive study will show flow of contrast outside the normal confines of the peritoneum.
In cases that went on to surgery for true hernia repair, it has shown a true positive rate of 96%.51
Two series reported on painful groin without palpable hernias in which herniography dem-
onstrated hernias in 84%.24 This imaging technique is invasive and not universally obtained
by most clinicians.
Nonsteroidal Anti-Inflammatory Drugs
During the initial period of conservative treatment, nonsteroidal anti-inflammatory drugs
(NSAIDs) have been traditionally used, and there is some evidence that recovery time is shortened
by their use.52 However, there is also some evidence that long-term muscle function may be
adversely affected by their use.53
Physical Therapy
Adductor Strains
Activity modification, ice, compression, and gentle range-of-motion physical therapy are the
mainstays of conservative treatment.18
Once the acute pain begins to resolve, physical therapy consisting of soft tissue mobilization,
static stretching, cross-friction massage, and proprioceptive neuromuscular facilitation techniques
should be implemented. Cryotherapy may be helpful for pain relief and swelling reduction, and
electrical stimulation may be used for pain inhibition. Muscle strains with palpable defects take
significantly longer to heal. External wraps may limit the amount of active and passive hip abduc-
tion and have been used in athletes to assist with proprioception and provide comfort.54
Gentle range-of-motion exercises may be initiated with bicycle without resistance and pool
walking, and following the achievement of full range of motion, a strengthening program is intro-
duced.16 This should include core strengthening, light plyometrics, and light treadmill running.
During the first 2 weeks of the strengthening program, patients are gradually progressed to heavier
running and light adductor strengthening. Patients are gradually allowed to participate in sport-
specific practice drills, and advance to return to competition after full strength and pain-free
motion are restored. Mean time for return to play is 6 weeks.16,40
Initial treatment consists of NSAIDs, cryotherapy, and activity modification. Physical therapy
should focus on core strengthening and improving hip and core strength imbalance.23 Therapy
also typically focuses on gluteus maximus recruitment, and avoidance of deep hip flexion heavy
weight squats, cleans, and dead lifts.5 One prospective randomized study of 66 soccer players with
chronic groin pain and failed conservative treatment compared outcomes of surgical sports hernia
repair vs physical therapy with NSAIDs. Only the surgical group showed improvement in symp-
toms and was able to return to sport by 6 to 8 weeks.55
Patients are generally given a 3- to 6-month course of nonoperative treatment. If incremen-
tal improvement is noted by 3 months, therapy is continued for another 3 months. However, if
by 3 months no improvement or a worsening of the symptoms occurs, and there is a continued
inability to participate in desired activities, then nonoperative treatment is considered a failure and
surgical treatment is considered.5
Osteitis Pubis
Conservative treatment of osteitis pubis is carried out in much the same way. There is an ini-
tial period of rest or activity modification after the injury. If this initial period of rest does not
lead to a reduction in symptoms, a symphyseal corticosteroid injection may be considered. The
program then progresses from trunk, pelvic, and hip range of motion, to stability exercises, to a
more complex strength program. Sport-specific exercises are then introduced. Return to activity
is usually based on incremental improvement in pain and the athlete’s willingness to continue
with nonsurgical treatment. If no progress is made by 6 to 12 weeks, then surgical intervention
may be considered.28
Injections
In general, injections are used for 1 of 2 purposes. They can be used to aid in the diagnosis
of the source of pain generation by selective anesthetic injection to the groin, pubis, or hip joint.
Alternatively, they can be used as part of the conservative treatment regimen if therapy and
116 Chapter 7
NSAIDs fail. However, this second use is usually reserved for elite athletes, and not the casual rec-
reational athlete or nonathlete.56 In patients with suspected FAI, intra-articular injection should
be performed to confirm the intra-articular portion of pain.7
Adductor Strains
Simple anesthetic, corticosteroid, and platelet-rich plasma (PRP) have all been described as
options to treat adductor strains.14 Injection at the adductor longus enthesis is indicated in patients
who fail conservative treatment, and has been successful in competitive and recreational athletes.
There have been several reports of intramuscular anesthetic injections for muscle strains to facili-
tate return to play for elite athletes.57 Intramuscular cortisone injection has been described for
NFL players with severe, discrete hamstring strains with palpable defects without any complica-
tions and with a decrease in time to return to play.58 There is one case report of injecting a com-
plete tear of the adductor longus with PRP with return to competitive soccer without surgery.59
Schlegal et al reported that all players with nonsurgically treated adductor ruptures returned to
play in the NFL in half the time as those treated with surgery.40
A diagnosis of osteitis pubis can be confirmed by anesthetic and/or corticosteroid injection
into the symphysis.29,37,60 Corticosteroid injection into the symphysis has also been described for
cases of osteitis pubis that are not progressing.61 Studies have shown that corticosteroid injection
directly into the symphyseal cleft results in a quicker return to sports; however, in most patients,
the symptoms return and require additional treatment or another injection.62
ARTHROSCOPIC/ENDOSCOPIC TREATMENT
General Principles
One series of 35 professional soccer players treated with laparoscopic mesh repair of the pos-
terior wall showed 97% excellent results and return to play at 10 days.63 Genitsaris et al reported
on 131 professional athletes with laparoscopic mesh repair and found that 97% returned to full
sporting activities by 2 to 3 weeks.64
Indications
Surgery may be considered if nonoperative treatment fails after 6 to 12 weeks.16 Athletic pub-
algia can be treated with endoscopic mesh repair.12,37 There has been one report of treatment
of osteitis pubis with arthroscopic decompression of the pubic symphysis in a chronic case that
occurred in association with FAI, which was also treated in the same setting.65 To access the pubic
symphysis, 2 midline portals were used. The first was 2 cm proximal to the superior border of the
symphysis, and the second was directly anterior to the symphysis.
Authors’ Preferred Technique

Laparoscopic treatment of sports hernia can be approached 1 of 2 ways. In the transabdominal
preperitoneal approach, the peritoneal cavity is entered, a flap of peritoneum is raised, and a piece
of polypropylene mesh is placed in the preperitoneal space. In the extraperitoneal approach, the
peritoneal space is not entered and a mesh is placed in the inguinal region.14 Both approaches have
similar outcomes.
OPEN TREATMENT
Adductor Strains
General Principles
The spectrum of adductor injury ranges from mild strains to complete avulsion of the adductor
longus with retraction. In cases of adductor strains, an initial period of nonoperative treatment is
tried for 6 to 12 weeks. If the pain persists and the patient is unable to perform the desired activi-
ties, then release is considered. For acute complete avulsions with retraction greater than 2 cm,
open repair is reported, but a study showed full return to the NFL without surgery in half the time
compared with repair.40
Indications
In cases of chronic groin pain secondary to isolated adductor pathology (pain, weakness, or
a partial tear) that have failed 6 to 12 weeks of conservative treatment, open adductor longus
tenotomy has been described with the majority of athletes being able to return to preinjury activity
quicker than with surgical reattachment.12,40,66
Authors Preferred Technique
For an adductor longus release, a 2- to 3-cm incision 3 to 5 cm distal to the origin at the pubis
is used, so as to create more of a fractional lengthening.41

General Principles
Two series on open repair of posterior wall deficiency showed excellent results in 89% and
93% of patients, respectively, with return to the same level of competition. Hackney showed 87%
of players returned to play 6 weeks after open repair of transversalis deficiency.67 Meyers et al
described a series of 157 athletes treated with open reattachment of the inferolateral edge of the
rectus abdominis to the pubis, with 88% and 96% performing at or above their preinjury level by
3 to 6 months, respectively. The 96% success rate group was made up of patients who underwent
both a rectus repair and an adductor release.12
The use of a polypropylene mesh and an internal oblique flap to reinforce the inguinal floor
and rebalance the rectus abdominis origin from the pubic tubercle has also been described.41 Mesh
repairs are considered to be tension-free repairs as opposed to suture repairs, which are under
tension.14 One other technique described a simple repair of the weakened posterior wall of the
transversalis fascia and ablation of the genital branch of the genitofemoral nerve.49
Overall, the literature does not describe a significant difference in outcome between laparo-
scopic and open treatment of athletic pubalgia or between the use of a mesh or not. However, there
does appear to be a quicker return to sports with laparoscopic procedures.22
Indications
Surgical exploration and repair of the injured structure(s) is indicated after 6 to 8 weeks of failed
directed conservative treatment.12,37 At the time of surgical intervention, the exertional inguinal
pain has typically been present for longer than 3 months.12
Recalcitrant osteitis pubis can be treated with open curettage of the pubis symphysis, with
78% of patients reporting improvement of their symptoms and return to running by 3 months.29
Symphyseal curettage has also been described with arthrodesis and/or adductor release.68
118 Chapter 7

The patient needs to be draped in order to access both the inguinal region and adductor tendon.
A short groin incision along skin crease lines above the external oblique aponeurosis is carried
out. A pelvic floor repair is carried out that consists of broad reattachment of the inferolateral
edge of the rectus abdominis muscle and fascia to the pubis adjacent to the anterior ligaments.
The internal ring is usually left intact. If the posterior wall is weakened, it is reinforced. External
oblique tears are repaired if present. When required, an adductor longus release can be performed
through the same incision or through a separate incision approximately 2 to 3 cm distal to the
pubic origin as described above. Multiple longitudinal incisions can also be made at the tendonous
origin on the pubis to induce bleeding and a healing response there for any degenerative tendon
that may be present.12
If osteitis pubis needs to be addressed surgically, an additional 3-cm transverse incision is
made centered over the pubic symphysis with exposure of the superior parasymphyseal pubic
bones that may be used if needed. An 18-gauge needle is used to isolate the symphysis. Curettage
is then carried out with 0.5- and 1-cm curettes, and the center of the parasymphyseal pubic
bones are then cored with a 2-mm drill. Sixty-nine percent of patients returned to full activity
by 6 months.29
COMBINED APPROACHES
General Principles
If conservative treatment fails, operative management should address all aspects of the injury
pattern, including FAI, labral injury, adductor pathology, and sports hernia.5,7 There is evidence
that patients with both FAI and sports hernia do equally well whether the pathologies are surgi-
cally treated at the same time or with 2 separate procedures.5
Indications
If symptoms of both FAI and athletic pubalgia are present, treatment of only one of the patholo-
gies leads to poor results. Larson et al described a series of patients with both FAI and athletic pub-
algia that was treated either with sports hernia repair, hip arthroscopy for FAI, or both. Return to
sports was 25% for patients treated only with an athletic pubalgia surgery, 50% for patients treated
only with hip arthroscopy, and 85% to 91% for those treated with a combined approach. There was
no statistical difference whether the 2 procedures were performed concurrently or in separate set-
tings. FAI correction led to a 14-degree increase of internal rotation of the hip. It is possible that
the improved range of motion and function could decrease stress on the extra-articular pelvic
structures, allowing the athletic pubalgia pathology to resolve.5

When both hip arthroscopy and sports hernia repair are performed in the same setting, the
hip arthroscopy can be carried out first, but either can be completed without problems. The
dissection for the hernia is a bit easier without the fluid extravasation from the hip scope. This
is performed to avoid excessive stress on the repair from positioning and traction used for hip
arthroscopy. For hip arthroscopy, a 2- or 3-incision technique is used. Under traction, the central
compartment is entered and rim resection, labral repair/debridement, ligamentum teres debride-
ment, and microfracture when needed are carried out. Traction is then taken off. Traction time
is limited to less than 60 to 90 minutes to decrease the risk of pudendal, sciatic, femoral, and
superficial peroneal nerve paresthesias postoperatively. If a significant cam resection needs to be
performed, a third distal anterolateral portal can be made, although this can also be performed
through just 2 portals. Capsular repair may be considered for large capsulotomies, capsular laxity,
and in the setting of borderline structural instability. Sports hernia repair is then carried out as
described previously.69
COMPLICATIONS
Adductor Strains
In proximal adductor procedures, injury to the spermatic cord can occur if dissection or the
repair is carried out medial to the gracilis origin on the pubis.70

The most common postoperative complaint is minor bruising or edema involving the abdomen,
thighs, genitals, and perineum. Postoperative hematoma requiring reoperation occurred in 0.3%
of patients, and the wound infection rate was 0.4%. Dysesthesia of the ilioinguinal, genitofemoral,
and anterior or lateral femoral cutaneous nerve distribution occurred in 0.3% of patients. Penile
vein thrombosis occurred in 0.1% of patients but all resolved.3 It is also possible that surgical dis-
section or postoperative scar tissue could cause dysesthesias in the pudendal nerve since it also
innervates the pubic symphysis.
The most common reason for reoperation was development of similar symptoms on the contra-
lateral side. The second most common was for adductor release not carried out at the first surgery.3
Another common reason for continued disability results from failure to identify associated intra-
articular hip pathology (eg, FAI).
Complications associated with curettage of the symphysis for osteitis pubis include hemosper-
mia, and intermittent scrotal swelling.28
Femoroacetabular Impingement
There is a 5% to 10% incidence of pudendal nerve paresthesia reported in the literature.
Iatrogenic labral and chondral injury can also occur. Other possible complications include hetero-
topic ossification (1% to 5%), meralgia paresthetica, fluid extravasation into the thigh and retro-
peritoneal space, femoral neck fracture, iatrogenic instability, and avascular necrosis.71,72 Overall,
the majority of these are very rare.
Adductor Strains
The postoperative rehabilitation protocol for adductor repair begins with protected weight bear-
ing for 2 to 4 weeks. Strengthening exercises begin at 6 to 8 weeks. Mean return to play is 12 weeks.
In the same study, patients treated nonoperatively returned to play at an average of 6 weeks.40

Most patients return to full activity within 2 to 6 weeks of an endoscopic repair and 1 to
6 months after open repair.12,37 Patients are allowed to bear weight as tolerated immediately
postoperatively. After an initial period of rest of about 10 days, therapy is targeted at abdominal
120 Chapter 7
strengthening, adductor flexibility, and gradual return to flexibility for weeks 2 to 4.24 A pro-
gressive running program is then started, and sport-specific exercises are added at 5 weeks.14,41
Return to play for herniorrhaphy has been reported from 87% to 100%.12,67 Meyers et al reported
that, by 3 months postoperatively, 88% of patients had returned to full activity and, by 6 months,
96% had returned in a series of 157 patients.12 After symphyseal curettage, patients return to play
by 6 months on average.68
Combined Athletic Pubalgia and

Postoperative rehabilitation is begun the day after surgery, and is based on the restrictions for
hip arthroscopy.5 Postoperatively, patients are restricted to 20-pound, flat-foot weight bearing
for 4 weeks. Patients undergo continuous passive motion daily for 4 weeks from 0 to 90 degrees.
Gradual physical therapy and strengthening is started at 4 weeks.7 Plyometric exercises and a run-
ning program are started at 3 months, with return to full activity by 3 to 5 months.
PEARLS AND PITFALLS

● FAI may lead to symphyseal overload and, therefore, osteitis pubis and athletic pubalgia/core
muscle injury.
● The flamingo view, or single-leg stance AP view, of the symphysis, may be used to assess
for pubic instability. Ultrasound may be useful in the identification of posterior abdominal
wall insufficiency.
● Imbalance between hip adductor to abductor strength ratios has been demonstrated to
increase the risk of groin strains. Therefore, muscle-balancing exercises should be used to
defend athletes against these injuries, and also as treatment when they are able to be tolerated.
● Addressing FAI, if present, is a key component to successful outcomes of surgical management
of adductor strains or athletic pubalgia/core muscle injury.
CONCLUSION
Adductor strains are an extremely common athletic hip injury. There may be concomitant FAI,
leading to increased shear forces across the pubic symphysis, which may lead to athletic pubalgia/
core muscle injury and osteitis pubis. Conservative management focusing on re-establishing the
balance of muscle about the pelvis is key. If nonoperative management fails, both open and lapa-
roscopic approaches are available. In the setting of FAI and medial soft tissue pathology, combined
procedures have been used.
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28. Hiti CJ, Stevens KJ, Jamati MK, Garza D, Matheson GO. Athletic osteitis pubis. Sports Med. 2011;41(5):361-376.
29. Radic R, Annear P. Use of pubic symphysis curettage for treatment-resistant osteitis pubis in athletes.
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bone region in athletes with chronic groin injury demonstrates new woven bone formation consistent with a
diagnosis of pubic bone stress injury. Am J Sports Med. 2008;36(12):2425-2431.
31. Tibor LM, Sekiya JK. Differential diagnosis of pain around the hip joint. Arthroscopy. 2008;24(12):1407-1421.
32. Nofsinger C, Kelly BT. Methodical approach to the history and physical exam of athletic groin pain. Oper Tech
Sports Med. 2007;15:152-156.
33. DeLee JC, Farney WC. Incidence of injury in Texas high school football. Am J Sports Med. 1992;20(5):575-580.
34. Crowninshield RD, Johnston RC, Andrews JG, Brand RA. A biomechanical investigation of the human hip.
J Biomech. 1978;11(1-2):75-85.
35. Tyler TF, Nicholas SJ, Campbell RJ, McHugh MP. The association of hip strength and flexibility with the
incidence of adductor muscle strains in professional ice hockey players. Am J Sports Med. 2001;29(2):124-128.
36. Tyler TF, Nicholas SJ, Campbell RJ, Donellan S, McHugh MP. The effectiveness of a preseason exercise program
to prevent adductor muscle strains in professional ice hockey players. Am J Sports Med. 2002;30(5):680-683.
37. Zoga AC, Kavanagh EC, Omar IM, et al. Athletic pubalgia and the “sports hernia”: MR imaging findings.
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38. Lovell G. The diagnosis of chronic groin pain in athletes: a review of 189 cases. Aust J Sci Med Sport.
1995;27(3):76-9.
39. Tönnis D, Heinecke A. Acetabular and femoral anteversion: relationship with osteoarthritis of the hip. J Bone
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tendon ruptures in National Football League athletes. Am J Sports Med. 2009;37(7):1394-1399.
41. Ahumada LA, Ashruf S, Espinosa-de-los-Monteros A, et al. Athletic pubalgia: definition and surgical treat-
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42. Clohisy JC, Carlisle JC, Beaulé PE, et al. A systematic approach to the plain radiographic evaluation of the
young adult hip. J Bone Joint Surg Am. 2008;90(Suppl 4):47-66.
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1991;12(4):266-279.
44. Mintz DN, Hooper T, Connell D, Buly R, Padgett DE, Potter HG. Magnetic resonance imaging of the hip:
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45. Magee T, Hinson G. Association of paralabral cysts with acetabular disorders. AJR Am J Roentgenol.
2000;174(5):1381-1384.
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47. Albers SL, Spritzer CE, Garrett WE Jr, Meyers WC. MR findings in athletes with pubalgia. Skeletal Radiol.
2001;30(5):270-277.
48. Omar IM, Zoga AC, Kavanagh EC, et al. Athletic pubalgia and “sports hernia”: optimal MR imaging technique
and findings. Radiographics. 2008;28(5):1415-1438.
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treat chronic inguinal pain. Hernia. 2010;14(1):27-33.
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53. Mishra DK, Friden J, Schmitz MC, Lieber RL. Anti-inflammatory medication after muscle injury. A
treatment resulting in short-term improvement but subsequent loss of muscle function. J Bone Joint Surg Am.
1995;77(10):1510-1519.
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Scand J Med Sci Sports. 1999;9(2):98-103.
56. Orchard J. Management of muscle and tendon injuries in footballers. Aust Fam Physician. 2003;32(7):489-493.
57. Orchard JW. Benefits and risks of using local anaesthetic for pain relief to allow early return to play in profes-
sional football. Br J Sports Med. 2002;36(3):209-213.
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string injuries. A 13-year experience in the National Football League. Am J Sports Med. 2000;28(3):297-300.
59. Singh J, Roza R, Bartolozzi A. Platelet rich plasma therapy in an athlete with adductor longus tendon tear. UPOJ
2010;20:42-43.
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61. Holt MA, Keene JS, Graf BK, Helwig DC. Treatment of osteitis pubis in athletes. Results of corticosteroid injec-
tions. Am J Sports Med. 1995;23(5):601-606.
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and treatment of osteitis pubis in athletes. AJR Am J Roentgenol. 2002;179(4):955-959.
63. Susmallian S, Ezri T, Elis M, Warters R, Charuzi I, Muggia-Sullam M. Laparoscopic repair of “sportsman’s
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8
Posterior Soft Tissue Injuries
of the Hip
Hamstring
Steven B. Cohen, MD; James P. Bradley, MD; Carlos A. Guanche, MD;

Eddie Y. Lo, MD; and Christopher M. Larson, MD
INTRODUCTION AND EPIDEMIOLOGY

Hamstring injuries are common in athletic populations and can affect all levels of athletes.1-4
From 1989 to 1998, the National Football League surveillance systems identified 1716 hamstring
strains among all players, with a range of 132 to 210 injuries per year.5 This accounts for an overall
injury rate of 0.77 per 1000 athlete-exposures and a reinjury rate of 16.5%. This is consistent with
the rate of muscle strain in high school (12% to 24%) and collegiate (18.9% to 22.2%) football.6-10
Although some studies may suggest relative deconditioning in the offseason, poor flexibility,
strength, core stability, or fatigue may be associated with hamstring injuries, there is little evidence
to support such claims. Mendiguchia et al identified previous hamstring injury as the greatest risk
factor for reinjury (2 to 6 times the risk).11 The study suggested that the injured muscle may have
altered compliance or deformation patterns, predisposing to less tissue motion or higher muscle
strain. Age was found to be an independent risk factor for hamstring injury. Although some
studies suggest that contact activities are a significant cause of hamstring injuries,6,12 Elliott and
colleagues associated 92% and 93.5% of injuries in defensive secondary and wide receivers with
noncontact activities, with the majority of injuries (71%) occurring during sprinting.5
There is a continuum of hamstring injuries that can range from musculotendinous strains to
avulsion injuries.1,2 By definition, a strain is a partial or complete disruption of the musculoten-
dinous unit.1,4 A complete tear or avulsion, in contrast, is a discontinuity of the tendon–bone
unit. In Koulouris and Connell’s study, only 12.3% of 170 cases of hamstring injuries were tendon

126 Chapter 8
Figure 8-1. Cadaveric dissection of the ischium in a left hip,

viewed from posterior. The arrow is pointing to the origin of
the biceps and semitendinosus (B/ST) muscles, which have
been elevated and retracted laterally. SN = sciatic nerve;
SM = origin of semimembranosus.
injuries; the majority of the injuries (90.5%) were muscle belly injuries.13 Most of these hamstring
strains do not require surgical intervention, and resolve with a variety of modalities and relative
rest. The most important point when evaluating these patients is to differentiate the higher-grade
tendon and myotendinous injuries from the lower-grade muscle strain subgroup, as the former
group is associated with more significant disability.
PATHOANATOMY OF HAMSTRING INJURIES

With the exception of the short head of the biceps femoris, the hamstring complex originates
from the ischial tuberosity and inserts distally below the knee on the proximal tibia. The tibial
branch of the sciatic nerve innervates the semitendinosus, the semimembranosus, and the long
head of the biceps femoris, while the short head of the biceps femoris is innervated by the peroneal
branch of the sciatic nerve.3
The proximal hamstring complex has a strong bony attachment on the ischial tuberosity (Fig-
ure 8-1). The footprint on the ischium is composed of the semitendinosus and the long head of
the biceps femoris beginning as a common proximal tendon footprint, with a distinctly separate
semimembranosus footprint.14 The semimembranosus footprint is lateral (and superior) to the
crescent-shaped footprint of the common insertion of the semitendinosus and long head of the
biceps femoris (see Figure 8-1).
Biomechanically, the hamstrings are subjected to high tensile load given their extensive eccen-
tric role in running. During initial swing, the knee and hip are flexing, which requires simulta-
neous eccentric and concentric activity of the hamstrings. During the last portion of swing, the
hamstrings continue to play a dual role of controlling knee extension while extending the hip. The
hamstrings work synergistically with the gluteal musculature to stabilize, decelerate, and propel
the hip. During the propulsion phase, the medial hamstrings assist in decelerating hip external
rotation. This maintains the gluteus maximus at an ideal length to act as an accelerator (along
with the hamstrings) of the femur in the sagittal plane. The hamstrings, along with the rectus
abdominis, are also decelerators of anterior pelvic tilt throughout stance. Given these functional
relationships, it is conceivable that hamstring strain or rupture has its source in the inhibition and
weakness of its closest synergists, the gluteal and abdominal musculature.15
Posterior Soft Tissue Injuries of the Hip 127
There have been a few studies that evaluate hamstring injuries in conjunction with the function
of the gluteal muscles. Sugiura et al recorded the quadriceps, hamstring, and hip extensor strength
of a group of elite sprinters and followed them over 12 months to evaluate the risk of hamstring
injuries.16 The authors found the injured limb associated with a lower hamstring/hip extensors to
quadriceps ratio. The injury also tends to occur in the limb with significantly weaker hip extensor
concentric strength.
If the gluteal muscles work in conjunction with the hamstrings to extend the hip, in the set-
ting of weak agonists (gluteal muscles), an increased relative effort of the hamstrings would be
required to control trunk and hip flexion during the loading phase of running.17 Wagner and
colleagues tested this idea in a triathlete with hamstring cramping pain. The authors measured
the percentage of maximal voluntary isometric contraction (MVIC) of the hamstring muscles
during running, which should average around 19%.18,19 This triathlete used his hamstrings at an
average of 48% MVIC, which predisposed him to an overuse injury. After focused strengthening
and re-educating the gluteus maximus muscle, the MVIC decreased to 36.4% and the cramping
symptoms resolved.
In a prospective evaluation, Sherry and Best rehabilitated 24 athletes in 1 of 2 protocols: either
an isolated hamstring stretching and progressive strengthening protocol or a progressive agility
and trunk stabilization protocol.20 At both short- (2 weeks) and long-term (1 year) follow-up,
the authors found a significantly higher reinjury rate in athletes treated with the isolated ham-
string rehabilitation protocol (54.5% vs 0% and 70% vs 7.7%, respectively). These findings suggest
that strong neuromuscular control of the lumbopelvic region allows the lower extremity muscle
to function at high velocity while maintaining a protected range of motion for the hamstring
musculature.
The history of an acute injury usually involves a traumatic event with forced hip flexion and the
knee in extension, as is classically observed in waterskiing.2,21-23 However, the injury can result
from a wide variety of sporting activities that require rapid acceleration and deceleration.2,24,25
Proximal hamstring injuries can be categorized as complete tendinous avulsions, partial ten-
dinous avulsions, apophyseal avulsions, and degenerative (tendinosis) avulsions.24 Degenerative
tears of the hamstring origin are more insidious in onset and are commonly seen as an overuse
injury in middle- and long-distance runners. The mechanism of injury in these patients is pre-
sumably repetitive irritation of the medial aspect of the hamstring tendon (typically along the
lateral aspect of the tuberosity, where the bursa resides) ultimately causing an attritional tear of
the tendon.
Commonly, athletes with proximal hamstring tendon tears typically describe a popping or
tearing sensation with associated pain and bruising over the posterior hip.26,27 They may also find
themselves having weakness with active knee flexion, sensation of instability, or difficulty control-
ling their legs.25,27-30 Occasionally, patients who present with either acute or chronic tears may
complain of a pins-and-needles sensation in sciatic nerve distribution, much like sciatica.25,27,29,31
This may be due to acute compression from a hematoma in the proximity of the sciatic nerve or
chronic scarring and tethering of the tendon to the nerve. Occasionally, complete proximal ham-
string ruptures are not diagnosed acutely, or are managed nonsurgically and patients may present
late with disability. The frequent complaints associated with chronic proximal hamstring ruptures
include weakness, hamstring spasms, sciatic nerve complaints, and most poor leg control through
the eccentric hamstring phase of gait.26
Symptoms of ischial bursitis include buttock pain or hip pain, and localized tenderness overly-
ing the ischial tuberosity. Additional symptoms of chronic ischial bursitis may include tingling
into the buttock that spreads down the leg. This is presumably from local inflammation and
128 Chapter 8
Figure 8-2. Photograph of typical appearance of the

posterior thigh ecchymosis after complete proximal
hamstring rupture.
swelling in the area of the sciatic nerve. The symptoms usually worsen while sitting. Clinically,
those most affected tend to sit with the painful buttock elevated off their seat.

Physical examination is typically performed with the patient in the prone position. Examina-
tion with the knee slightly flexed will limit muscle spasms and make examination more comfort-
able in acute ruptures. Inspection and palpation of the posterior thigh may reveal muscle spasm.
Ecchymosis may be observed only if the fascial covering is also disrupted (Figure 8-2). Palpation of
the entire posterior thigh is very important to localize the injury. In acute injuries there is typically
focal tenderness and swelling. However, with delayed presentation there is more likely to be diffuse
swelling and tenderness. Low-grade strains typically have limited swelling and tenderness, while
in the more severe strain, a palpable defect may be appreciated.
Sallay et al described an examination technique in which the patient is positioned prone and
asked to actively tension the hamstring tendon.26 This is then compared to the passive tendon
tension while sitting. Decreased tension as compared to the normal side suggests proximal tendon
rupture. In their cohort of 25 patients with complete tears, the exam was able to identify all of
the patients with tendon tears (100% sensitivity); however, no specificity was measured since the
exam was not applied to normal subjects. In the setting of chronic proximal hamstring rupture,
decreased tension (decreased popliteal angle) may be noted with the patient in the supine position
with hip flexion and knee extension compared to the normal contralateral side.
IMAGING PEARLS
After the history and physical examination have been completed, if there is a high level of
suspicion of a proximal hamstring injury, plain radiographic and advanced imaging should be
Figure 8-3. Anteroposterior (AP) view of the pelvis of the right hip
showing bony avulsion of the ischial tuberosity.
Figure 8-4. Magnetic resonance imaging (MRI) views of a partial insertional tear with a “sickle sign”: (A) Coronal view
and (B) axial view.
considered. Plain radiographs of the pelvis and a lateral of the affected hip are performed to rule
out any apophyseal avulsions, particularly to the ischial tuberosity (Figure 8-3). If a fracture is
identified, a computed tomography (CT) scan may assist in the assessment of displacement and
fracture configuration when surgical treatment is contemplated.
More commonly, no fractures are identified and magnetic resonance imaging (MRI) is used to
assess the proximal hamstring origin at the ischial tuberosity. The injury pattern at the hamstring
origin is variable. A complete rupture of all 3 tendons may be evident and most easily identified
on MRI scan. MRI allows for an accurate measurement of the amount of tendon retraction after
proximal tendon rupture.28 A finding commonly associated with an acute complete proximal
hamstring avulsion is a large posterior thigh hematoma. All 3 MRI planes (coronal, sagittal, and
axial) should be used to define the tear pattern.
Partial hamstring origin tears, however, are more difficult to diagnose on imaging. This is par-
ticularly the case in 2-tendon tears, which commonly have an associated musculotendinous junc-
tion injury to the third “intact” tendon. Unfortunately, when the 2 tendons are retracted greater
than 2 cm, this typically renders the intact tendon functionally impaired, which is clinically com-
parable to a complete rupture. Despite this difficulty, MRI is very helpful to distinguish complete
vs partial tears. One or 2 tendon injuries can be identified, and this distinction often determines
a patient’s need for surgical repair. In addition, partial insertional tears without any significant
retraction can be seen on MRI as a “sickle sign” (Figure 8-4). These are typically partial avulsion
of the semimembranosus and are similar to high-grade partial distal biceps tendon tears, which
can be seen only on MRI.
Another imaging modality that can be used for the assessment of proximal hamstring injuries
is ultrasound. While ultrasound can be extremely user-specific, it can also be highly accurate to
130 Chapter 8
evaluate partial tears and insertional tendinosis.32 Its potential for bedside use as a dynamic test
may detect more subtle injuries, particularly in the athletic population. However, currently, ultra-
sound is still less sensitive than MRI and should not be used in its place. In the study by Koulouris
and Connell, 170 cases of hamstring muscle strains were evaluated with MRI and ultrasound.13
In 21 patients with tendon tears, MRI identified 100% of the tears, whereas ultrasound was able to
identify only 58% of the tears. The authors found that, when using ultrasound, large hematomas
can produce mixed echogenic patterns, making visualization of retracted tendons difficult.
TREATMENT
Nonoperative
Nonoperative treatment of proximal hamstring injuries is most commonly recommended
in the setting of low-grade partial tears and insertional tendinosis. Initial treatment consists of
active rest, oral nonsteroidal anti-inflammatory drugs (NSAIDs), and a physical therapy program,
consisting of a gentle hamstring stretching and strengthening program. As the initial symptoms
resolve, core, hip, and quadriceps exercises can be added in association with a more aggressive
hamstring prevention program.33 Full return to sports and activities are allowed when the patient
is asymptomatic.11 If the patient is unable to progress with this program, an ultrasound-guided
corticosteroid injection may be used and has been shown to provide initial relief in up to 50% of
patients at 1 month.32 However, one of the authors (JPB) prefers the use of autologous conditioned
plasma (ACP) injections to corticosteroid injections that are performed using CT guidance; he has
had results similar to Zissen et al, with a greater than 50% success rate of patients not requiring
surgical repair after ACP injections.32 Patients with a failure of nonoperative treatment of partial
tears may benefit from surgical debridement and repair, similar to other commonly seen partial
tendon tears (patella, quadriceps, and biceps).
Nonoperative treatment of complete ruptures of the proximal hamstrings is less frequently
recommended, with reports of continued disability after nonsurgical treatment and successful
results after surgical repair.21,23,26,27,31,34-36 Sallay et al identified 12 waterskiers with hamstring
avulsion injuries that were treated initially without surgery. They found that 83% of the patients
had persistent cramping or pulling sensation with vigorous activity.23 Seven patients returned
to sports activities but at a lower level. Five patients were able to perform only limited activities.
Overall, these patients had a 61% hamstring strength deficit and 23% quadriceps deficit. Two of
these patients had disability that eventually led to delayed surgical repairs.
Surgical Treatment—Endoscopic
To date, there have been few reports of endoscopic management of hamstring injuries. After
developing experience in the open management of these injuries, one of the authors (CAG) has
developed an endoscopic technique that allows a safe approach to the area of damage for most
tears.37 It is expected that the benefits of a more direct approach, without elevating the gluteus
maximus and with the use of endoscopic magnification to protect the sciatic nerve, will improve
the management of these injuries and reduce the potential morbidities associated with the
open approach.
The technique positions the patient in the prone position after induction of anesthesia,
with all prominences and neurovascular structures protected. The posterior aspect of the
hip is then sterilized, ensuring that the leg and thigh are free so that the leg and hip can be
repositioned intraoperatively.
Figure 8-5. Portals for endoscopic approach. Note

the arthroscope is in the medial portal, while the
empty portal is the lateral portal. The shaver is in
the distal portal.
Two portals are then created, 2 cm medial and 2 cm lateral to the palpable ischial tuberosity. The
lateral portal is established first. This is performed using blunt dissection with a switching stick,
as the gluteus maximus muscle is penetrated and the submuscular plane is created. The switching
stick serves to palpate the prominence of the tuberosity and identify the medial and lateral borders
of the ischium. The medial portal is then established, taking care to palpate the medial aspect of
the ischium. A 30-degree arthroscope is then inserted in the lateral portal and an electrocautery
device is placed in the medial portal (Figure 8-5). Any remaining fibrous attachments between the
ischium and the gluteus muscle are then released, taking care to stay along the central and medial
portions of the ischium to avoid any damage to the sciatic nerve. The tip of the ischium and the
medial aspect are delineated, and the lateral aspect is then exposed with the use of a switching stick
as a soft tissue dissector. With the lateral aspect identified, the dissection continues anteriorly and
laterally toward the known area of the sciatic nerve. Very careful and methodical release of any soft
tissue bands is then undertaken in a proximal to distal direction in order to mobilize the nerve and
protect it throughout the exposure and ultimate repair of the hamstring tendon.
With the nerve identified and protected, attention is then directed once again to the area of the
tendinous avulsion. The tip of the ischium is identified through palpation with the instruments.
The tendinous origin is then inspected to identify any obvious tearing. In acute tears, the area
is obvious and the tendon is often retracted distally. In these cases, there is occasionally a large
hematoma that needs to be evacuated. It is especially important to protect the sciatic nerve during
this portion of the procedure, as it is sometimes obscured by the hematoma.
Once the area of pathology is identified (in incomplete tears), an endoscopic knife can be
employed to longitudinally split the tendon along its fibers. Often, this can be identified through
palpation, as there is typically softening over the area of the detachment, making the tissue bal-
lottable against the ischium. The hamstring is then undermined and the partial tearing debrided
with an oscillating shaver. The lateral ischium is debrided of devitalized tissue and a bleeding
corticocancellous bed is prepared in preparation for the tendon repair. The inferior ischium and
the ischial bursa can also be resected and cleared of inflamed tissues as the lateral ischial tissue is
mobilized. By retracting the anterior tissues, the bursa can be entered and debrided.
An inferior portal is then created approximately 4 cm distal to the tip of the ischium and equi-
distant from the medial and lateral portals. This portal is employed for insertion of suture anchors,
as well as suture management. A variety of suture-passing devices can then be used for the repair.
The principles are essentially the same as those employed in arthroscopic rotator cuff repair. Once
all of the sutures are passed through the tissue of the avulsed hamstring, the sutures are tied and
a solid repair of the tendon is completed. In general, one suture anchor is used per centimeter of
detachment (Figure 8-6).
132 Chapter 8
Figure 8-6. Repair of tendinous avulsion: (A) prepared surface with suture passer in place; (B) shuttle suture in place
(arrow; note the proximity of the sciatic nerve to the repair); (C) final mattress sutures in place in the substance of the
tendon; (D) final tendon repair.
Postoperatively, the patient is fitted with a hinged knee brace that is fixed at 90 degrees of flexion
for 4 weeks in order not only to limit weight bearing, but also to restrict excursion of the hamstring
tendons and protect the repair. At 4 weeks, the knee is gradually extended by about 30 degrees per
week in order to allow full weight bearing by 6 to 8 weeks, while maintaining the use of crutches.
Physical therapy is instituted at this point, with the initial phase focused on hip and knee range of
motion. Hamstring strengthening is begun at 10 to 12 weeks, predicated on full range of motion
and a painless gait pattern. Full, unrestricted activity is allowed at approximately 4 months.
Surgical Treatment–Open
The indications for surgical treatment of proximal hamstring ruptures include all acute
complete 3-tendon tears and 2-tendon tears with retraction of 2 cm or more.35 Patients with a
1-tendon tear or those with 2-tendon tears with less than 2 cm of retraction are initially not indi-
cated for acute surgical repair and are treated surgically if nonoperative treatment is unsuccessful.
In addition, less-active patients or patients who are unable to comply with the postoperative
rehabilitation protocol should be managed nonoperatively. For chronic injuries, patients with
complete or partial tears who fail conservative management may be candidates for attempted
chronic repair.
The technique for surgical repair has been previously described.35 The patient is placed prone
with all bony prominences well padded and the trunk in slight flexion. A transverse incision in the
gluteal crease inferior to the ischial tuberosity can be used for the majority of cases. Other authors
have described T-shaped or longitudinal incisions that may be useful for chronic ruptures with
more significant retraction.22,24,36 Loupe magnification and a headlight can be used to ensure pro-
tection of the posterior femoral cutaneous nerve and inferior gluteal nerve, and visualization of the
Figure 8-7. Picture depicting 5-anchor repair of the proximal

hamstring on the ischial tuberosity. (© 2007 American
Academy of Orthopaedic Surgeons. Reprinted from the
Journal of the American Academy of Orthopaedic Surgeons,
Volume 15[6], pp. 350-366 with permission.)
ischial tuberosity for anchor placement. The sciatic nerve is dissected free in cases of chronic injury
with scarring or preoperative sciatic nerve symptoms, but can be palpated lateral to the hamstrings
for acute tears without formal neurolysis. Once the ruptured tendon is visualized, freed up from
scar, and debrided, it is tagged for repair. The ischial tuberosity is then identified and cleared off
with curved and straight curettes or a periosteal elevator as well as a small osteotome, which is
used to fish-scale the tuberosity to allow optimal healing. Of special note, no motorized device
(ie, burr) is used in order to prevent iatrogenic injury to the sciatic nerve. The conjoined hamstring
tendons are then repaired to the bony footprint with suture anchors. A number of techniques and
anchors can be used to repair the hamstring origin. The anchors can be placed in the configura-
tion of an “X” using a total of 5 anchors (Figure 8-7). Sutures are passed through the tendon using
horizontal mattress sutures placed from inferior to superior and are tied down from superior to
inferior with the knee flexed to 30 degrees. This anchor configuration allows for the tendon to
be placed on the lateral aspect of the ischial tuberosity and to lie down in a flat manner to allow
optimal bony healing as well as prevent discomfort with sitting.
Using this technique for both acute42 and chronic repairs,11 2 of the authors (SBC, JPB) in a
study of 52 patients using subjective validated outcome scales at an average of 27 months of follow-
up found a 96% satisfaction rate.38 Lower Extremity Functional Scale (LEFS) results indicated that
acute repairs had statistically significant greater outcomes than chronic repairs (P = .023). Marx
Activity Scale and a specific proximal hamstring questionnaire averages did not have statistically
significant differences when acute and chronic repairs were compared (P = .96 and P = .55, respec-
tively). Thirty-five patients (67%) reported they could participate in strenuous activities at their
latest follow-up. All patients in the study estimated their strength recovery at ≥ 75%.
Brucker and Imhoff treated 8 patients with a similar suture anchor-type of repair.28 In their
series, they did not identify any difference in patients treated with acute or delayed repair. Postop-
erative Cybex testing revealed 88% of peak torque and ratio of hamstring-to-quadriceps strength
134 Chapter 8
of 0.55, which is not significantly different from the other side. Konan and Haddad treated
10 athletes acutely for complete hamstring tendon tears.29 Postoperatively, the average peak torque
was 82% and hamstring-to-quadriceps strength ratio was 0.56. Nine of 10 patients returned to
their previous levels of professional sports activities. It should be noted that 3 patients had an acute
sciatic nerve symptom, which was successfully treated with hematoma evacuation and neurolysis.
Chronic Hamstring Tears

Most studies that have performed late surgical repair were of patients with chronic tears and
who complained of sitting pain, hamstring weakness, poor leg control, and sciatic nerve symp-
toms due to scarring, also known as hamstring syndrome.26,36,39 These chronic repairs yield less
consistent results and the potential exists for scarring of the hamstring stump to the sciatic nerve,
which could require concomitant dissection of the nerve from the avulsed tendons, followed by
sciatic neurolysis.35 As a result, most surgeons experienced with proximal hamstring repair rec-
ommend early reattachment.40 In the study by Sarimo et al, 41 athletes underwent either acute or
chronic surgical repair. The authors found that the odds ratio of having a moderate or poor result
was 29 fold with a delay of greater than 3 months for surgical repair.27 In a few patients with early
surgery, decreased activity, pain, weakness, neuralgia, and difficulty in walking can still occur,
which the authors attributed to immobilization and injuries to the branches of the sciatic nerve.
The surgical outcome may be confounded by one of several issues: retracted tendons can be dif-
ficult to repair anatomically; denervated muscles can have attenuated tissue quality and be prone
to re-rupture; and retracted tendons can be scarred down with the nerves, disposing the nerves to
potential injury with neurolysis.
Chronic proximal hamstring ruptures present a challenging treatment dilemma, and surgical
management is much more difficult than in the acute or subacute setting. Treatment options for
disabling chronic proximal hamstring avulsions include primary repair with or without distal
fractional lengthening, or allograft reconstruction.26,41,42 Larson has described an allograft
reconstruction technique when primary repair is not possible.42 The surgical technique begins
by making a longitudinal incision beginning at the gluteal crease and extending to the point of
the retracted hamstrings. The sciatic nerve must be identified and protected throughout the case
and this can be facilitated with a nerve stimulator. Once the proximal hamstring tendon is mobi-
lized, the ischial tuberosity is identified by retracting the gluteus maximus superiorly and the
lateral aspect of the ischial tuberosity is cleared of soft tissue. The knee is then flexed to between
45 and 90 degrees with an initial attempt for primary repair with suture anchors. If the stump does
not reach the site of origin, an Achilles allograft can be used to reconstruct the hamstring tendon
unit. An Achilles allograft is fashioned with an 8- or 9-mm bone plug and a reamer is used to drill
a 25-mm tunnel at the site of origin on the ischial tuberosity as previously described.41 The bone
plug is secured in the ischial tuberosity with a 7- or 8-mm interference screw or alternatively the
bone plug can be removed and the Achilles tendon can be secured with suture anchors. The knee is
then flexed to between 45 and 70 degrees and the proximal hamstring stump is pulled proximally.
The distal aspect of the Achilles tendon is then sutured to the proximal hamstring stump with
#2 nonabsorbable locking sutures, with the goal of restoring tension and the ability to extend the
knee to 20 to 30 degrees without undue tension.
Apophyseal avulsions in adolescents can also present late with poor leg control, weakness, and
sometimes sitting pain from the mobile apophyseal fragment. If symptoms persist, an approach
similar to that described above is used, and the bony fragment is typically excised prior to repair
or, although less frequently, allograft reconstruction to the ischial tuberosity. One of the authors
(CML) has found that, with greater than 5 cm of retraction, an allograft reconstruction is often
required for both chronic proximal hamstring ruptures and chronic apophyseal avulsions.
For patients with high-grade partial insertional tears who fail nonoperative treatment, surgi-
cal repair is performed. The surgical approach is the same as described for acute repairs. Once
the tendon is exposed, it is incised and released from the tuberosity using an elevator. It is then
repaired using the same technique for complete tears with suture anchors. Treatment of partial
tears has been reported by Lempainen et al with high satisfaction in 47 athletes.41
Chronic proximal hamstring tendinopathy was also included in the generic term hamstring
syndrome. In this specific injury, the tendon is traumatized from repetitive overuse injury. Theo-
retically, the tendon undergoes repetitive stretch and mechanical overload and is unable to fully
heal. The sciatic nerve can undergo similar types of stress, leading to scarring, adhesion, and
impingement from the thickened tendon. In Lempainen et al’s cohort,43 surgical treatment was
performed with tenotomy of the thickened semimembranosus tendon and tenodesis to the biceps
femoris. Eighty-nine percent of the patients had good to excellent results. A few patients with poor
outcomes had persistent adhesions or had regenerated semimembranosus tendons that recreated
impingement.
Complications
It is important, when considering surgical repair of proximal hamstring injuries, to consider the
risks as well as the benefits. There are complications associated with proximal hamstring ruptures
even prior to surgical treatment, related to the mechanism of injury, and these can be early or
delayed. The early complications most commonly involve a neuropraxia injury to the sciatic nerve
as a result of a stretch injury. Depending on the mechanism and force of the injury, the sciatic
nerve can be damaged, leading to burning symptoms radiating down the leg and weakness of the
foot. As mentioned, this is critical to determine during the initial examination to document and
ensure that there is no iatrogenic injury at the time of surgery. Fortunately, however, a neuropraxia
injury most commonly resolves over time, despite being troubling to the patient initially. Delayed
complications of nonoperative treatment of proximal hamstring ruptures have been described by
Puranen and Orava.39 These include knee flexion and hip extension weakness, difficulty sitting,
hamstring deformity, and the potential development of symptoms similar to those of hamstring
syndrome as the tendons scar down to the sciatic nerve. Hamstring syndrome consists of local
posterior buttock pain and discomfort over the ischial tuberosity. In addition, the pain may worsen
with stretching and during exercise (eg, sprinting, hurdling, kicking).
Surgical repair of proximal hamstring ruptures also has its inherent risks. Superficial as well
as deep wound infections can occur similar to other surgeries; however, the location of the inci-
sion can potentially increase this risk because of the proximity of the incision to urination and
bowel movements. Additionally the 3 main nervous structures at risk of iatrogenic injury are the
posterior femoral cutaneous (PFC), inferior gluteal, and sciatic nerves. The PFC nerve comes from
the sacral plexus and enters the pelvis through the greater sciatic foramen below the piriformis
muscle. It then descends beneath the gluteus maximus with the inferior gluteal artery, runs down
the back of the thigh beneath the fascia lata, and runs over the long head of the biceps femoris to
the back of the knee.41,44 It provides sensation to the skin of the posterior surface of the thigh and
leg, as well as to the skin of the perineum. It can be injured during the surgical approach for repair
if it is not protected. The inferior gluteal nerve is the principal extensor of the thigh that leaves
the pelvis through the greater sciatic foramen, below the piriformis, and divides into branches
that enter the deep surface of the gluteus maximus. It can be injured with retraction of the gluteus
during the surgical approach.44
The sciatic nerve is the longest and widest single nerve in the human body. The sciatic provides
innervation of the skin of the leg and the muscles of the posterior compartment of the thigh as well
as divides off into the branches of the tibial and common peroneal nerves that supply the motor
function of the calf and foot. The sciatic nerve is in close proximity to the ischial tuberosity as it
runs along the lateral aspect.44 It may be injured from retraction during exposure of the tuberosity
for repair.27,31
136 Chapter 8
Other potential complications associated with proximal hamstring repair include re-rupture,
weakness, and sitting pain. When evaluating the hamstring repair literature, re-ruptures are
rare. In the cohort of Sarimo et al, 3 of 41 patients were found to have failure of surgical repair.
At reoperation, anatomic repair of the injury was not achievable. The authors believed that the
deteriorated tendon quality can be secondary to delays in surgical treatment, fatty degeneration,
and muscle denervation from nerve injury.27 Although there are no documented re-ruptures in the
literature to our knowledge, one of the authors (CML) had a patient who slipped 6 weeks postop-
eratively with the knee extended and hip flexed and sustained a re-rupture. This was re-repaired
and the patient recovered uneventfully. There have been no documented rates of postoperative
sitting pain. Several studies have tested postoperative hamstring strength after repair. Recently,
Wood et al found that mean postoperative isotonic strength was 84% compared to the contra-
lateral side31; however, other studies have shown a return of strength ranging from 60% to 90%
following repair.24,28,34,36 Unfortunately, unlike other tendon ruptures such as the distal biceps,45
there are few clinical studies26 testing hamstring strength in patients who have had nonoperative
treatment of acute ruptures to have the ability to determine a range of strength deficit if the tendon
is not repaired. As a result, when discussing the options of repair or conservative treatment with
patients after a diagnosis of a complete proximal hamstring rupture, clinicians are unable to pro-
vide patients with a percentage of weakness expected if the repair is not performed. As mentioned
above with distal biceps ruptures, perhaps future studies will accurately document associated
weakness either prior to repair or in patients with chronic ruptures.
A concern that is unique to the endoscopic approach is that of fluid extravasation into the pelvis
as a result of the fluid used in the distension of the potential space around the hamstring tendon.
Every effort should be made to regularly check the abdomen for any evidence of abdominal disten-
sion. Likewise, any unusual blood pressure decreases that may be due to fluid compression from
retroperitoneal extravasation need to be kept in mind. In general, an attempt should be made to
maintain the fluid inflow pressures as low as is feasible for good visualization, and an attempt
should be made to keep track of fluid ingress and egress volumes to ensure that extravasation
is avoided.
REHABILITATION
Following repairs and reconstruction, the affected leg can be placed in a hip orthosis that
restricts hip flexion to a range of 30 to 40 degrees. The patient ambulates on crutches with toe-
touch weight bearing for the first 2 weeks. Weight bearing is advanced to full by 4 weeks with con-
tinued use of crutches until 6 weeks. The brace is removed between 6 and 8 weeks postoperatively.
Alternatively, a hinged knee brace can be used with 60 to 90 degrees of knee flexion based on the
tension of the repair for 4 weeks (acute repairs), 6 weeks for chronic repairs/reconstructions. The
knee brace is brought 30 degrees closer to extension every 2 weeks until the brace is discontinued.
Crutches are used for 5 to 7 weeks with weight bearing as tolerated when the brace is 30 degrees
short of full knee extension. Some authors recommend postoperative aspirin as deep vein throm-
bosis (DVT) prophylaxis for 4 weeks. Secondary to the location of the incision, postoperative
antibiotics are considered by one of the authors (CML). Hamstring strengthening can begin 6 to
10 weeks postoperatively depending on the chronicity of the repair/reconstruction and strength of
repair. Dry land training and sport-specific training are initiated at 12 weeks with return to full
sports participation typically between 5 and 8 months.
PEARLS AND PITFALLS

● Surgical repair for complete proximal hamstring ruptures yields successful outcomes for both
acute and chronic ruptures, although acute ruptures are technically easier to surgically repair
with potentially more predictable outcomes.
● Both the posterior femoral cutaneous nerve and the sciatic nerve must be protected during
surgery, and over-retraction should be avoided.
● Recognition of the mechanism of injury is key—eccentric hamstring contraction with knee
extension and hip flexion. The athlete will also likely demonstrate significant weakness at
15 and 45 degrees of knee flexion.
● Perform a careful surgical approach—a transverse incision in the gluteal crease is usually suf-
ficient, although a longitudinal incision may alternatively be used.
CONCLUSION
One of the most important aspects in the treatment of proximal hamstring ruptures is early
recognition and early treatment. Recognizing the injury early allows for acute repair, which is
substantially easier to perform immediately following injury (< 4 weeks). Later recognition and
delayed surgery provide for a more difficult repair/reconstruction that ultimately may lead to
increased surgical complications and poorer patient outcomes. In general, patients with acute
repairs have had better outcomes in the literature when compared to those with chronic repair.26,27
The surgical approach for hamstring repair may be slightly intimidating for surgeons, as this
is not a common area for surgical treatment that is encountered throughout our orthopedic train-
ing. Although this type of surgery may be unfamiliar, the anatomy should be well known in the
particular areas of concern, including the sciatic nerve. It is recommended that a first-time repair
be performed in the acute setting in a fairly slender patient to allow for an easier approach to the
ischial tuberosity. Loupe magnification and headlight illumination can be helpful for the repair.
A variety of anchor configurations can be used, although we recommend a technique that repro-
duces the anatomic footprint and allows the tendon to lie evenly and flat on the tuberosity, in an
effort to prevent sitting discomfort and maximize bony contact for healing of the repair. The use
of 1-inch curved Deaver Retractors (Sklar) for gluteal retraction as well as a narrow, malleable
retractor for exposure of the ischial tuberosity can be helpful. Preparation of the ischial tuberos-
ity should be performed with curettes, elevators, and an osteotome. In summary, recognition of
proximal hamstring ruptures allows early treatment with surgical repair. Nonsurgical treatment
of complete tears leads to unpredictable results and may result in hamstring weakness with subse-
quent poor leg control and sciatic nerve symptoms. With proper treatment, good functional results
can be achieved.
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9
Lateral Soft Tissue Injuries
of the Hip
Abductors and Iliotibial Band Syndrome
Eilish O’Sullivan, PT, DPT, OCS; Lazaros A. Poultsides, MD, MSc, PhD;
and Shane Nho, MD
The lateral soft tissue structures of the hip are a common source of pain and pathology. Pain in
this area is often misdiagnosed because of multiple pain generators that refer to that area. Based
on specific palpation, examination, and imaging techniques, one may generate a more appropriate
diagnosis and treatment plan.
PATHOANATOMY OF ABDUCTOR FAILURE AND

ILIOTIBIAL BAND SYNDROME
The cornerstone of the lateral hip anatomy is the greater trochanter (Figure 9-1). Its anatomy
has been widely studied in order to determine a better understanding of the structures surround-
ing it and attaching to it. It serves as an attachment site for many strong, stabilizing hip muscles.1
The greater trochanter has 4 facets with 3 different tendon attachment sites.2 The anterior facet
resides anterolaterally and serves as the insertion point for the gluteus minimus tendon. The lateral
facet is most prominent and is at the most caudal portion of the trochanter; it serves as attach-
ment for the gluteus medius tendon. The superoposterior facet is the most superior portion of the
trochanter, and serves as an attachment site for the gluteus medius. The posterior aspect of the
trochanter is aptly the posterior facet; this is the bald facet where no muscular attachments reside
and the trochanteric bursa is located.1

142 Chapter 9
Figure 9-1. The insertion sites of the

gluteus medius and gluteus minimus
have been described in detail by Dwek
et al3 in a magnetic resonance imaging
study. The gluteus medius has 2 distinct
insertion sites on the superoposterior and
the lateral facets of the greater trochan-
ter. The gluteus minimus inserts onto the
anterior facet of the greater trochanter.
The fourth identified facet of the greater
trochanter (the posterior facet) has no
distinct tendon insertion, but rather is
the primary location of the trochanteric
bursae.
Trochanteric Bursae
There are 3 bursae about the greater trochanter. The largest of the 3 is the subgluteus maximus
bursa (also known as the trochanteric bursa), which is on the posterior facet, and beneath the
iliotibial tract and gluteus maximus.3 The subgluteus medius bursa is beneath the lateral gluteus
medius tendon, and is over the superior portion of the lateral facet. The last bursa is the subgluteus
minimus bursa, and it overlies the distal portion of the anterior joint capsule.3
Abductor Muscle Complex

The abductor muscle group includes gluteus medius, gluteus minimus, gluteus maximus, and
tensor fascia lata. The origin of the gluteus medius borders the anterior superior iliac spine (ASIS),
the outer edge of the iliac crest, and the outer edge of the posterior superior iliac crest, encompass-
ing most of the external surface of the ilium.4 The gluteus medius has 3 equal-sized divisions—
anterior, middle, and posterior—and each is innervated by an independent branch of the superior
gluteal nerve through the deep surface of each muscle portion.5 During stance phase of gait, there
is sequential activation from posterior to anterior portions of the gluteus medius. Gottschalk et al5
found that, with isolated abduction, the tensor fascia lata is most active, and there is weak activa-
tion of the gluteus medius. They postulated that the primary function for the gluteus medius and
minimus is to stabilize the pelvis and rotate the pelvis.
The gluteus minimus originates on the external iliac fossa between the anterior and inferior
gluteal lines, running between the anterior inferior and posterior inferior iliac spine.5 Distally, the
fascia of the gluteus minimus capsular head thickens and inserts onto the superior aspect of the
hip capsule, as the rest of the tendon continues toward the greater trochanter. The distal gluteus
minimus tendons have 2 heads, the capsular and long head, that both insert anterior to the gluteus
medius on the inner aspect of the anterior margin of the greater trochanter. The capsular head’s
footprint is directly anterior to the greater trochanter, while the long head’s insertion is both ante-
rior and inferior. The capsular head forms from the gradual thickening of the fascia surrounding
the muscle until it becomes the tendon as it inserts into the femoroacetabular joint capsule, which
at this area of contact is considered to be the iliofemoral ligament at the anterior rim of the greater
trochanter.6 These mechanics are very similar to the rotator cuff of the shoulder, where the supra-
spinatus and infraspinatus initiate and assist the abduction motion that the deltoid completes. Glu-
teus medius and minimus tears are due to increased frequency, and manifestations of symptoms
are analogous to injury of rotator cuff tendons and the insertion on the greater tuberosity of the
humerus. Injury of the gluteus tendons begins with tendinitis, tendinosis, and eventual tear of the
tendon, with the gluteus medius found to tear most frequently.
Lateral Soft Tissue Injuries of the Hip 143
Iliotibial Band
The iliotibial band (ITB) is a fibrous band of tissue that originates largely at the iliac tubercle
and travels down past the hip and knee to insert at the lateral tibial tubercle. The anterior ITB has
superficial and deep layers that envelop the tensor fascia lata. Though the ITB does not directly
attach to the femur, the lesser portion of the gluteus maximus blends into the ITB while the
larger portion inserts onto the gluteal tuberosity, providing indirect attachment of the ITB to the
femur.7 The ITB is most taut at the hip during full extension of the hip and knee, coupled with
full hip adduction.8
External Coxa Saltans

External coxa saltans, also known as “snapping hip syndrome,” is best described as an audible
and potentially painful snapping of the hip during activities that require repetitive flexion, exten-
sion, and abduction. During flexion, the thickened portion of the ITB passes anteriorly over the
greater trochanter; from a flexed position to extension, it passes back over to the posterior greater
trochanter. The sliding back and forth of this taut band causes the snapping. External snapping
hip is usually asymptomatic,9 but it can lead to inflammation of the trochanteric bursa and pain,
significantly reducing the patient’s physical activity.
Iliotibial Band Syndrome

ITB syndrome is the most common cause of pain found in runners, and causes pain on the
lateral aspect of the knee. ITB syndrome manifests from repetitive stretching and flexion of the
ITB over the lateral epicondyle of the femur. Each time the knee bends, the ITB glides over the
lateral femoral epicondyle posteriorly from increased tension. Once the knee straightens, the
ITB glides back over anteriorly. Repetitive bending and straightening of the knee increases the
amount of friction inflicted on the bursa between the ITB and lateral femoral epicondyle, causing
inflammation of the bursa and distal portion of the ITB. The repetitive gliding eventually results
in pain of the lateral aspect of the knee. ITB syndrome has been correlated with abductor weak-
ness, and abductor strengthening has been found to significantly reduce symptoms and increase
function in runners.10
Greater Trochanteric Pain Syndrome

Greater trochanteric pain syndrome (GTPS) is conventionally defined as tenderness to palpation
over the greater trochanter with the patient in the side-lying position, but recent literature has
included several other disorders of the lateral peritrochanteric space under GTPS, such as tro-
chanteric bursitis, tears of the gluteus medius and minimus, and external coxa saltans (snapping
hip). Trochanteric syndrome was described by Leonard in 195811 as lateral hip pain (LHP) that
was frequently thought of as sciatica. He reported that it was LHP that originated in the peritro-
chanteric space and frequently radiated down the posterolateral thigh, similar to bursitis of the
shoulder. He indicated that the abductors were responsible for the pain and that it was caused by
degeneration. Until recently, GTPS has been commonly misdiagnosed because of nonspecific and
misleading symptoms. This, in part, is due to the varying nervous supply of the peritrochanteric
compartment. Inflammation in this area may cause radiating pain and paresthesia, often leading
to many differential diagnoses, including LHP. Recently Fearon et al obtained soft tissue biopsies
from 34 patients with GTPS and 29 controls. Those with GTPS demonstrated more pathology and
a significantly greater presence of substance P in the bursa, but not in the tendon, when compared
with controls.12 This may indicate a physiologic mechanism for this pain syndrome.
144 Chapter 9
Trochanteric Bursitis
Trochanteric bursitis is a commonly diagnosed inflammatory condition that presents with pain
localizing to the region of the greater trochanter, often with radiation down the lateral aspect of
the thigh or into the buttock. Pain manifests from the repetitive friction between the greater tro-
chanter and the ITB with hip flexion and extension. The greater trochanteric bursa resides in an
area innervated by branches of the obturator, femoral, and sciatic nerves; therefore, inflammation
to this area can result in significant pain.
Gluteus Medius/Minimus Tears
Tears of the abductor tendon related to the gluteus medius and minimus are seen in women
more often than men. Symptomatic presentation may be seen with lateral hip pain, tenderness to
palpation at the gluteal insertion on the greater trochanter, and weakness on hip abduction. The
presented symptoms generally are atraumatic, with insidious onset upon development. Patients
with abductor tears often present with buttock pain, LHP, and groin pain. Patients may complain
of difficulty climbing stairs and/or a grinding sensation during movement. Furthermore, though
degeneration is usually concomitantly present, patients may report a fall on that hip. Because of
the stress placed on the greater trochanter, night pain is common in patients who sleep in a lateral
decubitus position.
Trochanteric bursitis is most commonly found in patients with overuse trauma or other
conditions disrupting gait pattern. The conventional presentation of trochanteric bursitis is in
middle-aged patients, but young runners may present with chronic, activity-related pain about the
greater trochanter. Patients will often complain of pain with prolonged standing, pain upon sitting
with the affected leg crossed, and difficulty lying on their affected side secondary to symptoms
from direct compression of the inflamed bursa. Upon examination, the patient most likely will
exhibit secondary signs related to the trochanter, such as osteoarthritis of the ipsilateral hip or
lumbar spine.
Iliotibial Band Syndrome/Snapping Hip

ITB syndrome is found mostly in high-mileage runners who stress large loads on their bod-
ies, as well as cyclists, hikers, and weightlifters. Patients generally present with lateral knee pain.
Runners who consistently utilize the same side of the road may develop ITB syndrome. They may
develop some anterior lateral knee pain due to lateral retinacular tightness. Those with external
snapping hip will report snapping, and sometimes will say that they feel that their hip is “dislocat-
ing” because of the visible snap.

Abductor Tears
Clinical exam of abductor tears of gluteus medius and minimus often shows weakness with
active, resisted abduction in extension and external rotation with the hip flexed to 90 degrees.
Physical exam of the hip begins with observation of the patient’s gait. Patients with significant
abductor weakness exhibit a Trendelenburg gait and may require the use of a walker or cane.
Upon finding this, a Trendelenburg fatigue test should be conducted to observe weakness or loss of
function of the abductor, which would present as a distinct drop of the nonsupported pelvis. Pain
may be reproduced with single-leg stance. Next, the examiner should palpate the peritrochanteric
compartment for tenderness with the patient in a lateral decubitus position, especially the supero-
posterior facet. An abduction strength test should also be performed with the knee flexed and
extended to further observe the strength and function of the gluteus medius and minimus. Spe-
cific tests include the trochanteric pain sign, performed with the patient in a supine position with
the hip flexed to 90 degrees, abducted, and externally rotated, which is positive if pain is elicited.
Resisted external rotation should be performed while the patient is in the supine position with the
hip flexed at 90 degrees.
The trochanteric bursitis physical examination in symptomatic patients reveals tenderness to
palpation on the greater trochanter, predominantly posterolaterally. Diagnostic criteria generally
show LHP, distinct tenderness at the greater trochanter, pain on hip abduction against resistance,
pain radiating down the lateral aspect of the affected lower extremity, and a positive flexion,
abduction, external rotation (FABER) test. These patients frequently demonstrate a positive Ober
test, indicating decreased ITB strength.
Iliotibial Band Syndrome/Snapping Hip

Key signs that present for external coxa saltans include history of activity described typically
as an atraumatic insidious symptom onset. Presentation is regularly diagnosed with the patient
placed on the side of the leg that exhibits pain. When the patient actively flexes the leg, snapping
of the ITB can be palpated by the examiner about the greater trochanter. Diagnosis is confirmed
when pressure is applied over the proximal aspect of the greater trochanter, preventing snapping
with repeated hip flexion. Ober test for length of the ITB will be positive.
On examination of ITB syndrome, the examiner may see local tenderness at the lateral knee
along the inferior epicondyle. Upon presentation there may be no swelling, but the band may be
thickened. There will be a positive Noble’s compression test—pain when the patient’s leg is brought
from a hip flexed/knee flexed position to extension with pressure over the lateral femoral condyle.
IMAGING PEARLS
Plain radiographs and computed tomography (CT) scans may help elucidate underlying hip
bony anatomy, but are not very useful in the diagnosis and treatment of greater trochanteric
pain syndrome.
Plain Radiographs and Computed Tomography

Plain radiographs are not necessarily an effective tool in diagnosing GTPS. In the setting of
trochanteric bursitis, calcifications may be present in the area of the bursa (Figure 9-2). Plain
radiographs are typically not used for abductor tears or external coxa saltans.

Magnetic resonance imaging (MRI) can be used as an exclusionary tool for evaluating trochan-
teric bursitis. The MRI can show inflammation in the region of the greater trochanter, associated
146 Chapter 9
Figure 9-2. Plain x-rays of patients with chronic abductor

tears often will show traction spurs (as indicated by the arrow)
or surface irregularities, but, in partial tears or in the more
acute setting, they may show no discrete abnormalities. It is
important to confirm the absence of any significant joint space
narrowing or secondary signs of joint deterioration, as abduc-
tor dysfunction may coexist with progressive arthritis of the
hip joint.
Figure 9-3. Magnetic resonance imaging is very good at identifying (A) the severity and acuity of tendon injury,
(B) the presence of tendon retraction, and (C) the degree of fatty infiltration that may occur in the chronic setting.
with gluteus medius and minimus tendinitis. In relation to abductor tears of the gluteus medius
and minimus, MRI can differentiate between partial- and full-thickness tears, as well as detect
calcification at the tendon insertion often accompanied by fatty atrophy within muscle substance
(Figure 9-3). MRI may also elucidate changes in soft tissue beneath the ITB, but may not show
changes indicative of external coxa saltans.
Ultrasound/Dynamic Imaging Analysis

Dynamic ultrasound can be an effective diagnostic tool for indicating various forms of GTPS.
Dynamic ultrasound can evaluate the abductor tendon by targeting thickening and fluid consis-
tent with tendinosis or the presence of partial or full tears. Dynamic ultrasound can also be used to
visualize the snapping phenomenon and associated bursitis in external coxa saltans, while ruling
out other sources of pain.
Figure 9-4. (A) Arthroscopic visualization of a high-grade undersurface tear of the gluteus medius tendon from
the lateral facet. The probe is elevating the intact fibers of the gluteus medius to expose the undersurface tear.
(B) Arthroscopic view of a gluteus medius tear after the degenerative fibers of the tendon have been debrided and
the footprint insertion on the lateral facet has been prepared down to a bleeding bony bed.
NONOPERATIVE TREATMENT
Nonoperative options for GTPS may help alleviate pain and improve patients’ quality of life.
Trochanteric bursitis is usually responsive to rest, ice, anti-inflammatory medication, and physi-
cal therapy. The physical therapy should be tailored to the individual, but the overarching themes
include increasing ITB length, increasing abductor strength (within pain-free limits), and improv-
ing functional mobility. If symptoms persist, trochanteric bursa injections with a combination
of anesthetic agent and corticosteroid often serve to reduce pain and therefore increase activity
tolerance.
External coxa saltans and abductor tears related to GTPS generally follow the same treat-
ment as trochanteric bursitis. In the setting of a partial tear, platelet-rich plasma injections have
been used at our institution with good effect. The patients initially have a 2-week period of rela-
tive rest, followed by a progressive core and hip strengthening program that includes eccentric
abductor exercises.
The patient is supine on a fracture table.13 The operative leg is placed in 10 degrees of flexion,
neutral adduction, and abduction, and 15 degrees of internal rotation.14 The mid-anterior portal
provides an advantageous angle for the approach to the peritrochanteric space. The initial mid-
anterior portal should be placed under fluoroscopic guidance to confirm placement over the lateral
prominence of the greater trochanter to avoid entry into the gluteus medius muscle proximally
and vastus lateralis distally. Traction is released, due to the tension that it creates on the ITB. The
space between the ITB and the greater trochanter contains bursal tissue that should be cleared.
A distal anterolateral portal is established to increase access. The arthroscopic examination begins
with the insertion of the gluteus maximus, then toward the gluteus minimus. Once entering the
peritrochanteric space, attention should be directed toward identifying the gluteus maximus ten-
don insertion into the linea aspera; this will allow the surgeon to achieve proper orientation in the
space and, simultaneously, a boundary is provided to protect the sciatic nerve 2 to 4 cm posterior
to its insertion. The gluteus medius may be found posterior to the minimus. The tendon should be
examined to determine the exact pathology—full- or partial-thickness tear (Figure 9-4). The ITB
148 Chapter 9
Figure 9-5. Arthroscopic repair of a gluteus medius tear

is performed using the same principles as for a rotator
cuff tear in the shoulder. (A) After the suture anchors have
been placed into the footprint insertion, (B) the sutures
are sequentially passed through the distal edge of the
tendon using a suture shuttle or standard penetrator.
The configuration of the sutures depends on the anatomy
of the tear. (C) The sutures are then tied down using stan-
dard arthroscopic knot-tying techniques to restore the
footprint at its base.
should then be explored and, in the setting of external coxa saltans, a release may be performed at
the posterolateral part of the greater trochanter. A Z-plasty may be performed in order to lengthen
the portion of the ITB under the greatest tension. The trochanteric bursae may be debrided and
will provide a decompression of the lateral compartment.
The gluteus medius tendon is debrided in preparation for the repair. The greater trochanter is
prepped for repair with a shaver. Suture anchors are placed in order to create an anatomic repair.
Fluoroscopic guidance may aid in anchor placement. The anchors are passed through the edges of
the prepared tendon and tied with an arthroscopic knot pusher (Figure 9-5).
OPEN RECONSTRUCTIVE TREATMENT

Several open reconstruction techniques have been described for the management of massive
abductor tears when arthroscopic direct repair is not feasible. Open repairs allow for improved
proximal tissue mobilization and reduction of tension on the repair. In our experience, direct open
repair of the abductor tendon is preferred if there is a complete tear with retraction, but the muscle
quality is good (Figure 9-6). Chronic tears with retraction and fatty infiltration of the muscle
may require one of several described tendon transfer techniques that are analogous to pectoralis
major transfers for irreparable subscapularis tears, or latissimus dorsi transfers for irreparable
supraspinatus tears.
Figure 9-6. (A) Visualization of a massive gluteus medius

repair with retraction proximally requiring open mobiliza-
tion. (B) After the suture anchors have been placed into the
insertional footprint of the abductor, the sutures are pulled
to confirm that an anatomic reduction can be achieved.
(C) Final fixation of the tear confirms good restoration of
the anatomic footprint. In this example, the muscle qual-
ity of the gluteus medius was good, so transfer of the
gluteus maximus was not necessary to reestablish good
muscle function.
Whiteside et al15 reported the results of a new technique using a posterior gluteus maximus
muscle flap transfer to manage osteolytic destruction of the greater trochanter with abductor
insertion deficiency in the setting of revision total hip arthroplasty (THA). This technique was
used in 5 patients, whereas the trochanter was left unrepaired in 5 other patients; a 6- to 10-cm
posterior flap of gluteus maximus muscle is created, which is transferred into the abductor-greater
trochanteric defect and sutured into the anterior capsule of the hip joint. Rehabilitation protocol
consists of partial weight bearing with bilateral crutches, and abduction exercises are prohibited
for 8 weeks. The authors showed that the patients treated with a gluteus maximus flap had less
pain, reduced limp, and reduced use of assistive devices compared with the patients who were left
untreated. The authors concluded15 that the results of this technique are promising, but confirma-
tion is required by other studies.
AUTHORS’PREFERRED TECHNIQUE
We have used a modification of the aforementioned technique—posterior gluteus maximus
muscle flap transfer—in patients with massive, retracted tendon tears with fatty atrophy of the
muscle. In these cases, the anterior fibers of the fascial bands of the gluteus maximus are mobi-
lized and tenodesed to the lateral facet, providing a lateral buttress and supporting the deficient
abductor tendon.
If there is good muscle quality, a mattress configuration suture anchor repair may be carried
out to restore the function of the gluteus medius muscle. An incision is made over the lateral
aspect of the great trochanter, and taken down to the iliotibial band. The gluteus medius tendon
is exposed with a modified Gibson approach. A bursectomy is frequently required in order to clear
150 Chapter 9
the inflamed, thickened bursal tissue. The edge of the tendon is debrided of nonviable tissue, and
a bleeding bed of bone is prepared. Double-loaded suture anchors are placed into the trochanter,
and the tendon footprint is restored with the sequential passage of sutures. The iliotibial band is
closed, followed by a layered closure of the overlying tissues.
COMPLICATIONS
There are few complications reported inherent to surgical procedures for peritrochanteric space
disorders. Symptomatic heterotopic bone formation in the early postoperative period may occur
as a result of the abductor repair. A postoperative course of anti-inflammatory medications may
decrease this risk. Other potential complications include fluid extravasations into the soft tis-
sues and hematoma. There have been no formal reports in the literature of the incidence of these
complications.
Recurrence of trochanteric bursitis, painful external coxa saltans, and retear of gluteus medius
tendon repairs may all occur. Nevertheless, the incidence of these complications has not been
reported either. Patients may be at a higher risk for deep venous thrombosis (DVT) after surgery
involving the peritrochanteric space because the patient population is generally older, the cases may
be longer, and the postoperative rehabilitation usually requires a period of limited weight bearing.
REHABILITATION FOLLOWING REPAIR

It is imperative to avoid aggravating the lateral hip with aggressive therapy immediately after
surgery. Postoperative rehabilitation following greater trochanteric bursectomy and/or ITB release
should begin with a 2-week protocol of 20-pound, foot-flat weight bearing with crutches, followed
by advancement to full weight bearing as tolerated. Range of motion and hip strengthening with-
out restrictions begins as soon as the patient’s pain allows.
Following gluteus medius repair, all patients are given crutches and a hip abduction brace set
at 10 degrees of abduction, and allowed 20 pounds of foot-flat weight bearing for the first 6 weeks.
Continuous passive motion is started immediately for 2 to 4 hours per day. Passive hip flexion to
90 degrees is allowed, as is passive hip abduction, both of which are important to reduce the risk
of developing scar tissue and adhesions in the lateral space. Patients are instructed to avoid active
abduction and internal or external rotation, or passive adduction past neutral and external rota-
tion past 30 degrees, for a minimum of 6 weeks after the repair. As mentioned previously, given
the older nature of these patients and the sedentary requirements for the first 6 weeks, risk for
DVT should be assessed preoperatively, and appropriate DVT prophylaxis should be considered.
Two weeks postoperatively, patients begin isometric strengthening of the hip extensors, lower
abdominals, and external rotators, as well as the quadriceps. The patient begins to bear weight at
6 weeks, with a gradual progression. It is imperative that these patients demonstrate normal gait
before their assistive device is discontinued. At 10 weeks, lower extremity strengthening and core
strengthening are progressed as tolerated toward a functional weight-bearing exercise program.
A running progression is initiated when the patient demonstrates equal abductor strength, good
control with a step-down test, and good lateral trunk stability.
PEARLS AND PITFALLS

● It is important to distinguish between the inflamed bursa and normal gluteus medius muscle
tissue; this can be accomplished by slight axial traction on the limb, which will help to tension
the gluteus medius fibers.
● Specific pain location about the greater trochanter is helpful in directing the diagnosis of
lateral hip pain. Bursal pain is present about the posterior facet.
● MRI is one of the most useful imaging modalities for lateral hip pain, as it will detect changes
to the abductor tendons, greater trochanteric bursa, and iliotibial band.
CONCLUSION
Management of disorders of the peritrochanteric space should be considered in patients who
have persistent lateral-sided pain and dysfunction after failed nonoperative measures. With greater
surgeon experience in arthroscopic techniques, and improved instrumentation, imaging modali-
ties, and diagnostic understanding, arthroscopic approaches to this region have become important
surgical alternatives in selected patients. Open reconstructive techniques for more complex cases
may be indicated, but there are few studies that have looked at large series of patients to allow for
any generalized recommendations on optimal treatment strategies for patients requiring open
tendon transfer procedures.
REFERENCES
1. Pfirrmann CWA, Chung CB, Theumann NH, Trudell DJ, Resnick D. Greater trochanter of the hip: Attachment
of the abductor mechanism and a complex of three bursae—MR imaging and MR bursography in cadavers and
MR imaging in asymptomatic volunteers. Radiology. 2001;221(2):469-477.
2. Arbuster TG, Guerra J Jr, Resnick D, et al. The adult hip: an anatomic study. Part I: the bony landmarks.
Radiology. 1978;128(1):1-10.
3. Dwek J, Pfirrmann C, Stanley A, Pathria M, Chung C. MR imaging of the hip abductors: normal anatomy and
commonly encountered pathology at the greater trochanter. Magn Reson Imaging Clin N Am. 2005;13:691-704.
4. Lachiewicz PF. Abductor tendon tears of the hip: evaluation and management. J Am Acad Orthop Surg.
2011;19:385-391.
5. Gottschalk F, Kourosh S, Leveau B. The functional anatomy of tensor fasciae latae and gluteus medius and
minimus. J Anat. 1989;166:179.
6. Beck M, Sledge JB, Gautier E, Dora CF, Ganz R. The anatomy and function of the gluteus minimus mus-
cle. J Bone Joint Surg Br. 2000;82:358-363.
7. Birnbaum K, Siebert, Pandorf T, Schopphoff E, Prescer A, Niethard F. Anatomical and biomechanical investi-
gations of the iliotibial tract. Surg Radiol Anat. 2004;26:433-446.
8. Evans P. The postural functional of the iliotibial tract. Ann R Coll Surg Engl. 1979;61:271-280.
9. Ilizaliturri VM Jr, Camacho-Galindo J, Evia Ramirez AN, Gonzalez Ibarra YL, McMillan S, Busconi BD. Soft
tissue pathology around the hip. Clin Sports Med. 2011;30(2):391-415.
10. Fredericson M, Cookingham CL, Chaudhari AM, Dowdell BC, Oestreicher N, Sahrmann SA. Hip abductor
weakness in distance runners with iliotibial band syndrome. Clin J Sport Med. 2000;10:169-175.
11. Leonard MH. Trochanteric syndrome; calcareous and noncalcarueous tendonitis and bursitis about the tro-
chanter major. JAMA. 1958;168(2):175-177.
12. Fearon AM, Twin J, Dahlstrom JE, et al. Increased substance P expression in the trochanteric bursa of patients
with greater trochanteric pain syndrome. Rheumatol Int. 2014. Epub February 23 2014.
13. Byrd JW. Hip arthroscopy utilizing the supine position. Arthroscopy. 1994;10:275-280.
14. Voos JE, Rudzki JR, Shindle MK, Martin H, Kelly BT. Arthroscopic anatomy and surgical techniques for
peritrochanteric space disorders in the hip. Arthroscopy. 2007;23:1295-1302.
15. Whiteside LA, Nayfeh T, Katerberg BJ. Gluteus maximus flap transfer for greater trochanter reconstruction in
revision THA. Clin Orthop Relat Res. 2006;453:203-210.
10
Nerve Compression
Injuries About the Hip and
Deep Gluteal Syndrome
Eilish O’Sullivan, PT, DPT, OCS; Stanley Antolak, MD;

and Hal D. Martin, DO
The neural origins of hip pain may be challenging to ascertain, given that there are a myriad
of pain generators about the hip and pelvis. First and foremost, lumbar pathology must be ruled
out using a comprehensive history and physical, and imaging where appropriate. Discogenic or
radicular pain, especially arising from L1, L2, and L3, may create anterior hip, groin, and thigh
pain. Nerve entrapments about the pelvis may be caused by fascial constriction, direct trauma, or
scarring from surgery. It is sometimes difficult to determine that a nerve entrapment syndrome is
responsible for an athlete’s hip and pelvic pain because there is overlap for many of the nerves’ sen-
sory distributions and some of the nerves lack motor innervation. When no identifiable etiology
exists, the natural history indicates that symptoms will resolve without intervention in a matter
of weeks/months. For persistent cases lasting longer than 3 to 4 weeks, neurological consultation
should be obtained. Therapeutic injections may be administered, and in recalcitrant cases surgical
intervention is possibly required.
SCIATIC NERVE AND DEEP GLUTEAL SYNDROME

The sciatic nerve is the main nerve originating from the lumbosacral plexus roots of L4 through
S3. The nerve exits the pelvis through the sciatic notch beneath the piriformis muscle. There are
normal anatomical variations between the piriformis muscle and sciatic nerve, which are impor-
tant to be aware of. Six categories of piriformis-sciatic nerve variations were first classified by
Beaton and Anson1 (Figure 10-1). The nerve passes between the ischial tuberosity and the greater

154 Chapter 10
Figure 10-1. Schematic of piriformis/sciatic

nerve variants. Six types of arrangement
of the sciatic nerve or of its subdivisions in
relation to the piriformis muscle, arranged
in the order of frequency. Gluteal (exter-
nal) view. The percentage incidence in
240 examples is indicated. Figures E and F
were hypothetical in 1938. (A) Nerve undi-
vided passes out of greater ischiadic fora-
men, below piriformis muscle. (B) Divisions
of nerve pass through and below heads
of muscle. (C) Divisions above and below
undivided muscle. (D) Nerve undivided
between the heads of muscle. (E) Divisions
of nerve between and above heads. (F)
Undivided nerve above undivided muscle.
trochanter (GT) of the femur in close proximity to the posterior hip joint capsule. Neuropathy may
occur from trauma, pelvic fractures, hip fracture or dislocation, hip joint surgery, vascular abnor-
malities,2-4 prolonged surgery in the seated position,5 or space-occupying lesions.
Entrapment of the sciatic nerve is characterized by extrapelvic nerve compression presenting
with symptoms of pain and dysesthesias in the buttock area, hip, or posterior thigh, and/or radicu-
lar pain.2 Yeoman in 1928 first theorized that the piriformis muscle could be the source of sciatic
nerve entrapment.6 In 1934, Freiberg and Vinke described the Lasègue sign and tenderness at the
sciatic notch attributed to sciatica caused by the piriformis muscle.7 The nomenclature “piriformis
muscle syndrome” was introduced in 1947 by Robinson, who described a tender sausage-shaped
mass over the piriformis area.8 In recent years, many etiologies of sciatic nerve entrapment have
been identified, including the piriformis muscle,3,9-18 fibrous bands containing blood vessels,9,15,18
gluteal muscles,19 hamstring muscles, 20,21 the gemelli-obturator internus complex,22-24 ischial
tuberosity,25-27 and acetabular reconstruction surgery.28 Because of these anatomical variations
of entrapment, the term deep gluteal syndrome19 (DGS) has been introduced as a more accurate
description of sciatic nerve entrapment within the subgluteal space.
The subgluteal space is anterior to the gluteus maximus and posterior to the posterior bor-
der of the femoral neck, and is bounded by the linea aspera laterally, the sacrotuberous and
falciform fascia medially, the inferior margin of the sciatic notch superiorly, and the hamstring
origin inferiorly (Figure 10-2). Within this region are the sciatic nerve, piriformis, obturator
internus/externus, gemelli, quadratus femoris, hamstrings, superior and inferior gluteal nerves,
Nerve Compression Injuries About the Hip and Deep Gluteal Syndrome 155
Figure 10-2. The subgluteal space.

HS = hamstring origin; LA = linea aspera; LT =
lesser trochanter; OI = obturator internus; PF =
piriformis; QF = quadratus femoris; SSL = sacro-
spinous ligament; STL = sacrotuberous ligament.
lateral ascending vessels of the medial femoral circumflex artery, ischium, and sacrotuberous and
sacrospinous ligaments. In a case series, 18 out of 35 surgical patients had DGS involving the piri-
formis muscle. This muscle was characterized as split, bulging split with the sciatic nerve passing
through the body, split tendon with an anterior and posterior component, and split in 2 distinct
components with one dorsally and one inferiorly going between a bifurcated sciatic nerve.15
In many cases, a thick tendon can hide under the belly of the piriformis overlying the nerve.3,15
Hypertrophy of the piriformis muscle has also been attributed to sciatic nerve entrapment.3,11,14,28
Atypical fibrovascular scar bands and greater trochanteric bursae hypertrophy have been reported
in many cases of sciatic nerve entrapment.15,18
The insertion of the hamstring tendon can be thickened over the ischium and onto the sciatic
nerve due to trauma or hamstring avulsion.15,29 This may lead to ischial tunnel syndrome involv-
ing the sciatic nerve by scarring around the sciatic nerve or the formation of tight fibrotic bands
in the area of the ischial tuberosity.15,30 Another possible source associated with sciatica-like pain
is the obturator internus/gemelli complex.15,22-24 The sciatic nerve exits the sciatic notch anterior
to the piriformis and anterior to the superior gemelli/obturator internus, which can cause a scissor
effect between the two muscles, resulting in entrapment.15,23,24
Clinical presentation often includes a history of trauma and symptoms of sitting pain (inability
to sit for more than 30 minutes), radicular pain of the lower back or hip, and paresthesias of the
affected leg.11,15 As noted before, several etiologies of posterior extra-articular hip pain exist and
these symptoms should be ruled out by the physical examination.
156 Chapter 10
Figure 10-3. Posterior hip pain seated palpation test. (A) The patient is in the seated position with knee extension.
The examiner passively moves the flexed hip into adduction with internal rotation while palpating 1 cm lateral to the
ischium (middle finger) and proximally at the sciatic notch (index finger). (B) The physician can also palpate in 3 posi-
tions of the gluteal area: the piriformis (lateral/superior), at the level of the external rotators, and lateral to the ischium.
If pain is localized at the ischium, rule out the hamstring bursa or hamstring tears; and if the pain is more medial, one
should evaluate the pudendal nerve more astutely.

To aid in the differential diagnoses, the palpation test for sitting pain is shown in Figure 10-3.
The physician palpates in 3 positions of the gluteal area: the piriformis (lateral/superior), at the
level of the external rotators, and lateral to the ischium. If pain is localized at the ischium, ischial
tunnel syndrome, the hamstring bursa, or hamstring tears must be ruled out; and if the pain is
lateral to the ischium, one should consider ischiofemoral impingement. If pain is more medial,
one should evaluate the pudendal nerve. The seated palpation test can also be performed dur-
ing the seated piriformis stretch test, which is a flexion, adduction, internal rotation test (FAIR)
performed with the patient in the seated position.31 The examiner extends the knee (engaging
the sciatic nerve) and passively moves the flexed hip into adduction with internal rotation while
palpating 1 cm lateral to the ischium (middle finger) and proximally at the sciatic notch (index
finger). A positive test is the recreation of the posterior pain at the level of the piriformis or exter-
nal rotators. An active piriformis test is performed by the patient pushing the heel down into the
table, abducting and externally rotating the leg against resistance, while the examiner monitors
the piriformis. Some patients may present with neurological symptoms of abnormal reflexes or
motor weakness.2
IMAGING PEARLS
Magnetic Resonance Arthrography
Magnetic resonance arthrography (MRA) may be used. Standing anterior-posterior radio-
graphs assist in determining functional alignment and assess joint space, neck-shaft angle. Lat-
eral radiographs also are assessed to determine whether there is concomitant decreased femoral
head-neck offset. MRA may or may not be able to highlight sciatic nerve pathology.
Electromyography/Nerve Conduction Studies

Electromyography (EMG) and nerve conduction studies can also be helpful in diagnosing
DGS, often indicated by H-reflex disturbances of the tibial and/or peroneal nerves.32,33 Patient
positioning is important. With the patient in the lateral position, place the hip in extension,
adduction, and internal rotation (patient in the lateral position) and the knee in flexion. This
position will tighten the piriformis muscle, compressing the sciatic nerve, resulting in a delayed
H-reflex. It is helpful to flex the knee (the H-reflex will result as normal) and compare side to side.
MR neurography in selected patients with sciatica is an aid to diagnosis.
NONOPERATIVE TREATMENT FOR

SCIATIC NERVE ENTRAPMENT/DEEP GLUTEAL SYNDROME
Nonsteroidal Anti-Inflammatory Drugs
A conservative approach to the nonoperative treatment for DGS begins with addressing the
suspected site of impingement. A hypertrophied, contracted, or inflamed muscle (piriformis,
quadratus femoris, obturator internus, superior/inferior gemellus) begins with rest, nonsteroidal
anti-inflammatory drugs (NSAIDs), and/or muscle relaxants.
Physical Therapy
A physical therapy program should be trialed that includes stretching of the external rota-
tors. The piriformis stretch, or FAIR, involves placing the leg in flexion, adduction, and internal
rotation. In a seated position, the patient brings the knee into the chest and across midline, and
pulls the knee to the opposite shoulder. The stretch may be gradually progressed by increas-
ing duration and intensity until a moderate stretch is obtained. Patients with femoroacetabular
impingement or acetabular or femoral retroversion may not be able to adequately stretch in this
position. Therefore, these patients should be evaluated and treated primarily as most cases will
resolve with appropriate surgical intervention.
Injections
Patients who do not respond to physical therapy may find pain relief with 1 to 3 injections of a
muscle anesthetic or corticosteroid, taken on a case-by-case basis.2,14,34 To support the diagnosis
of DGS when the piriformis is involved, guided (computed tomography [CT], fluoroscopy, ultra-
sound, or open magnetic resonance imaging [MRI]) injections are useful. Most cases of DGS/
sciatic nerve entrapment will respond to conservative nonoperative measures.
OPERATIVE TREATMENT
Options for operative treatment include open and endoscopic techniques. The open transglu-
teal approach has been described to effectively perform piriformis muscle resection, and neuro-
plasty of the sciatic and posterior femoral cutaneous nerves.14,18 A number of case studies have
reported success with an open approach, and the largest case series have reported good to excellent
outcomes in 75% to 100% of the procedures.11,14,21 Additionally, release of the hamstrings and
neurolysis of the sciatic nerve at the hamstring origin has been performed, achieving satisfactory
results with significant pain relief and increased hamstring strength.21 Contrasting release is
surgical repair, which is recommended early to avoid involvement of the sciatic nerve.30,35,36 The
surgical technique, indications, and contraindications for surgery have been outlined by Miller
and Webb.29 The concepts of treatment in this area continue to evolve.
158 Chapter 10
TABLE 10-1
ENDOSCOPIC PIRIFORMIS TENDONOTOMY
1. Establish anterolateral, posterolateral, and auxiliary portals.
2. Perform bursectomy, inspect gluteus minimus, medius, and maximus.
3. Internally rotate the extremity, view the quadratus femoris at the entrance of the
deep gluteal space.
4. Free sacrotuberous ligament/hamstring fibers from nerve distally.
5. Turn long scope proximal to inspect, then move the long scope to the posterolat-
eral/auxiliary portal.
6. Internally and externally rotate with hip flexion of 40 to 60 degrees.
7. Identify branch of the inferior gluteal artery and then cauterize (or ligate) and release.
8. Shave distal border of the piriformis muscle.
9. Use arthroscopic scissors for tendon release.
10. Repeat hip motion and probe the sciatic nerve.
Endoscopic Release of the Piriformis

Endoscopy is an effective and minimally invasive approach to the treatment of deep gluteal
syndrome. A case series15 reported on 35 patients with DGS with an average duration of symptoms
of 3.7 years. The average preoperative verbal analog score was 7, which decreased to 2.4 postop-
eratively. Preoperative modified Harris Hip Score was 54.4 and increased to 78 postoperatively.
Twenty-one patients reported preoperative use of narcotics for pain; 2 remained on narcotics post-
operatively (unrelated to initial complaint). Eighty-three percent of patients had no postoperative
sciatic sitting pain (inability to sit for > 30 minutes).15
The supine technique developed by Byrd37 is used. Positioning is modified by placing the
patient in maximal contralateral tilt. During the procedure, nerve conduction and EMG is moni-
tored, and following release can demonstrate immediate improvement. Using a 70-degree long
arthroscope and adjustable/lengthening cannulas, the peri-trochanteric space is entered through
the anterolateral and posterolateral portals. A systematic inspection is performed, then the arthro-
scope is turned proximally and a bursectomy is completed.37 The auxiliary posterolateral portal
is established 3 cm posterior and 3 cm superior to the greater trochanter, which allows for better
visualization of the sciatic nerve up to the sciatic notch. Endoscopic piriformis tendonotomy is
summarized in Table 10-1. An abnormal sciatic nerve will appear white, resembling a shoestring,
will not move with rotation, and will feel taut with probing. Fibrous bands at the level of the qua-
dratus femoris, ischial tunnel, and sacrotuberous ligament should be released. By understanding
the anatomy and biomechanics and applying clinical tests and diagnostic strategies, adequate
treatment of this fourth layer is part of a comprehensive plan of treatment.
REHABILITATION
Following surgery, patients use bilateral axillary crutches for 2 weeks. Wound protection is one
of the early goals, followed by restoration of basic functional mobility, such as gait. The patient
should avoid prolonged sitting for the first 4 to 6 weeks to minimize irritation. Nerve gliding exer-
cises are helpful to maintain mobility of the neural structures. A knee brace is used to avoid knee
extension and maintain a relaxed sciatic nerve when necessary. Activity is gradually progressed
per patient tolerance.
PEARLS
The subgluteal space and asscociated disorders are complex and can be difficult to recognize.
Key tips for the diagnosis and treatment of DGS include a standardized physical examination15,31
with special tests and selective injections. Be aware of extra-articular posterior hip pathologies.
Check the 3-planar osseous anatomy, including femoral and acetabular version, with MRI38 or CT.
A detailed understanding of anatomy, biomechanics, and pathokinematics is required to appreci-
ate disorders of the subgluteal space. Endoscopic decompression of the sciatic nerve is useful in
improving function and diminishing hip pain associated with sciatic nerve entrapment/deep glu-
teal syndrome. During surgery, the hip should be mobilized and the nerve probed to differentiate
underlying causes of the pathology.
PUDENDAL NERVE
Pudendal neuropathy is the most common neuropathic cause of pelvic pain.39 Sacral roots
S2, S3, and S4 form the pudendal nerve, which exits the pelvis through the sciatic notch and runs
deep to the sacrospinous ligament. There are 3 branches: the inferior rectal, the perineal, and the
dorsal nerve of the penis/clitoris. The pudendal nerve is a mixed nerve containing motor and
sensory fibers of both the somatic and autonomic nervous systems. Damage is typically caused
by compression; however, stretch injuries may occur with childbirth and direct trauma from falls,
and surgical trauma or radiation injury may also occur. Chronic pelvic pain is a common phenom-
enon, occurring in 15% to 16% of females and up to 13.8% of males.40 The serpentine course of
the pudendal nerve predisposes it to pathologic events, as it travels in the interligamentary space,
bounded by the sacrotuberous and sacrospinous ligaments. Approximately 90% of neural trauma
to the pudendal nerve occurs here, defining it as a tunnel syndrome.41 The nerve re-enters the pel-
vis at the lesser sciatic notch, where it traverses between the obturator muscle and fascia in Alcock’s
canal. The sacrotuberous and sacrospinous ligaments form the “lobster claw.” The falciform pro-
cess of the sacrotuberous ligament is a potential area of compression that varies significantly in
size and thickness, and can compress the nerve at its medial edge or over the belly of the obturator
internus. Fibers from each of the ligaments may join near the ischial spine, tethering the nerve and
limiting its glide. The chief pathophysiologic cause of pudendal neuropathy is repetitive micro-
trauma. This may occur during athletics or exercise with repeated hip flexion exercises such as
jogging, sit-ups, stair-climbing, and elliptical training. Another common mechanism of injury is
compression with prolonged cycling, which may cause sensory loss or even impotence.42 Asym-
metric broadening or elongation of the ischial spine occurs on the dominant leg used by athletes
such as football players, oarsmen, or cheerleaders (Figure 10-4). The medial growth of the ischium
reduces the functional area of the greater sciatic notch at a time when the piriformis muscle hyper-
trophies because of athleticism. The diameter of the greater sciatic notch is further diminished by
remodeling (elongation) of the inferior lateral angle of the sacrum. Bony remodeling of the ischium
and ischial spines is a frequent finding in patients with pudendal neuropathy. Pudendal neuralgia
is a possible complication from hip arthroscopy due to traction/compression against the perineal
post. A recent retrospective study found the incidence of pudendal neuralgia to be 2%, with resolu-
tion of symptoms occurring between 3 weeks and 6 months.43
160 Chapter 10
Figure 10-4. Computed tomog-

raphy (CT) scan of pelvis (left side
view) 3-dimensional reconstruction.
(1) Elongated ischial spine. (2) Medial
remodeling of ischium. (3) Lateral
growth of inferior lateral angle of
sacrum. These bony changes reduce
the normal round area of the greater
sciatic notch at a time when athletes
are using the piriformis muscle
significantly.
Clinical Presentation
There are 5 essential diagnostic criteria, also known as the Nantes criteria, for pudendal nerve
entrapment.44 The first is pain in the region between the anus to the penis/clitoris. The pain is
primarily experienced while sitting, and is usually lessened by sitting on a toilet seat. Pain should
not wake the patient at night. Objective sensory impairment should raise suspicion of a sacral root
involvement. Pudendal nerve entrapment pain is alleviated by a pudendal nerve block.

Physical examination is an important component in diagnosing pudendal neuropathy. A pin-
prick examination of the genital area may identify sensory changes.45 Each pudendal nerve branch
may be examined: the penis or clitoris for the dorsal nerve of the penis/clitoris, the posterior scro-
tum or labia for the perineal nerve, and the posterior anal skin for the inferior rectal nerve. Skin
changes are frequently found over the coccyx and natal cleft due to sympathetic hyperstimulation,
and there may be trophic changes indicative of chronic regional pain syndrome.
IMAGING PEARLS
Imaging techniques do not provide diagnostic information for pudendal neuropathy, but are
valuable to rule out pathologic conditions or anatomical cause for symptoms. Imaging for preop-
erative planning is appropriate, including MRI of the pelvis and lumbosacral spine. Plain films,
including a Judet view of the pelvis, identify elongation of the ischial and the inferior lateral angle
of the sacrum, and medial remodeling of the ischium will be identified. CT scans of the pelvis may
not aid in diagnosing neural pathology. Magnetic resonance neurogram may demonstrate changes
in the nerve.
Neurophysiological Studies
Neurophysiological tests may be used to provide objective confirmation of neuropathy. A
quantitative sensory test (warmth detection threshold test) measures the first sensation of warmth
at each of the 3 pudendal nerve branches. It is the best test for neuropathic basis of impotence.47
Motor nerve testing using the pudendal nerve terminal motor latency test is abnormal in many
patients. Neurophysiologists may perform somatosensory evoked potentials or pelvic floor eletro-
myograms and/or measure bulbocavernosus reflexes.48 The tests provide quantitative evidence
of neuropathy, but also may provide qualitative evidence of central sensitization of the nervous
system. In this abnormal state, neurons respond excessively and abnormally to normal stimuli.
TREATMENT: NONOPERATIVE OPTIONS

Pudendal neuropathy is a tunnel syndrome and should therefore be treated sequentially using
nonoperative interventions and, when necessary, nerve decompression surgery.46 A patient self-
care program of nerve protection will benefit most patients. The key elements to self-management
are avoiding repeated hip flexion activities including jogging, cycling, elliptical training, sit-ups,
and climbing stairs. Avoidance of sitting is a key component, and when patients must sit they
should use a perineal suspension pad.
Medications
Medical management of pudendal neuropathy is challenging, as compressed or traumatized
nerve fibers do not respond to pain medications. Therefore, narcotics should not be used as they
do not address neuropathic pain. Neurons affected by central sensitization or complex regional
pain syndrome may respond to pharmacologic management. Antidepressants including amitrip-
tyline and nortriptyline are effective in many patients for decreasing neuropathic pain. Selective
serotonin reuptake inhibitors and serotonin-norepinephrine reuptake inhibitors may benefit those
with pain syndromes and have been demonstrated effective in those with pudendal neuropathy.
Antiepileptics including gabapentin and pregabalin are the most commonly used. N-methyl-D-
aspartate receptors have major involvement in mechanisms of neuritic pain; medications such
as baclofen have a blocking effect on these.49 Ketamine may be administered intravenously in
patients with severe central sensitization. In terms of analgesics, tramadol is moderately effective
in treating neuritic pain.
Physical Therapy
Physical therapy is a common mode of treatment for pelvic pain, and should be conducted
within the patient’s tolerance. Patients with proven pudendal neuropathy may require injections
in conjunction with physical therapy in order to make significant gains. Myofascial release may be
effective and is commonly used.50 Lack of response after 8 weeks suggests that alternative treat-
ments should be pursued.
Injections
Pudendal nerve perineural injections using bupivacaine and corticosteroids may cure or control
chronic pelvic pain caused by pudendal neuropathy. A series of 3 blocks at 4-week intervals pro-
vides the best response. The injections are given at the ischial spine and into the pudendal canal.
These may be administered under fluoroscopic guidance or CT guidance (Figure 10-5). Symptom
relief is usually cumulative and may be permanent. A review of responses to perineural injec-
tions of patients originally evaluated in 2005 reported that 56% had continued pain-free status at
162 Chapter 10
Figure 10-5. Computed tomography (CT)-guided

pudendal nerve perineural injection (PNPI) with
needle tip in Alcock’s canal.
Figure 10-6. The left pudendal nerve in the blue

vessel loop is compressed cranially between the
falciform process (arrow) and the sacrospinous liga-
ment. The falciform process has been opened and
is lifted laterally by a Kittner dissecting sponge. The
arrow is at the lateral edge of the falciform process.
24 months.18 Some patients respond to occasional “interval blocks” at irregular intervals dictated
only by recurrent symptoms. Failure of long-term pain control by pudendal nerve perineural injec-
tion (PNPI) is the indication to proceed with decompression surgery.
SURGICAL TREATMENT OF PUDENDAL NEUROPATHY

Transgluteal decompression of the pudendal nerve by transecting the sacrospinous ligament
has been used successfully for more than 20 years.31 Complete resolution of symptoms is possible,
but may require 9 to 24 months. A transgluteal approach provides the best visualization of the
nerve from the subpiriformis region, through the pudendal canal to the trifurcation of the nerve.
Atresia or discoloration of the nerve has grave prognostic implications (Figure 10-6). Robert et al
originated decompression surgery for pudendal neuropathy, transecting both the sacrotuberous
and sacrospinous ligaments.52 However, transecting the sacrotuberous ligament may cause an
unstable pelvis and abnormal gait. Robert et al52 reported on a series of 400 patients treated with
the transgluteal approach. At 1 year, 71.4% of the patients had improved, as opposed to 13.3% of
the nonoperative group. No major complications were reported.
Transgluteal Decompression
An oblique incision is made between the sacral margin and the ischial tuberosity. This is fol-
lowed by an incision through the gluteal fascia to expose the muscle bundles beneath. These are
then separated to expose the sacrotuberous ligament, which is opened along the longitudinal axis
and then retracted (but not transected). The pudendal nerve is then identified and elevated. A dis-
section is carried out in a cranial direction, transecting any fascial restrictions. The sacrospinous
ligament is then transected, which releases the nerve. The coccygeus muscle fibers are separated
from the ischial spine to allow the nerve to be transposed. Alcock’s canal is then opened, releasing
any adhesions along the way. A barrier for adhesions is placed anterior and posterior to the nerve.
A suction drain is inserted. The sacrotuberous ligament and the gluteal fascia are closed. The
patient is usually hospitalized for 2 days.
The patient stands the day of surgery, and ambulates postoperative day 1. Nerve gliding exer-
cises involving hip flexion and rotation are completed on a daily basis. Patients should continue
to use a perineal suspension pad. Return to work may vary from 10 days for those with desk jobs,
to 3 months for those with more active occupations. Some patients with severely damaged nerves
may not have resolution of symptoms. Core strengthening exercises may be beneficial to patients
once initial healing has occurred.
Complications
Urinary retention may occur in 5% of patients, and may require catheterization. Neuropraxia
may take several days or weeks to fully resolve.
OTHER PERIPHERAL NERVES

Many of the peripheral nerves have sensory distributions in the hip area (Figure 10-7). Some of
them lack motor input, and therefore it may be difficult at times to ascertain exactly which nerve
is compressed (Table 10-2). The peripheral nerves of the lower extremity include the iliohypo-
gastric, ilioinguinal, genitofemoral, obturator, lateral femoral cutaneous, femoral, and posterior
femoral cutaneous.
Iliohypogastric Nerve
Variation is common among the sensory nerves of the inguinal region. There is frequently
communication between the genitofemoral, ilioinguinal, and iliohypogastric nerves.53 The ilio-
hypogastric nerve arises from L1 and L2, travels down through the psoas, and then penetrates the
lower abdominal wall. Entrapment of this nerve is rare. Symptoms may include sensory changes,
suprapubic pain, and bulging of the lower abdominal muscles. In athletics, injury may result from
a direct blow to the lateral pelvis.
Ilioinguinal Nerve
Contributions from T12 and L1 form the ilioinguinal nerve.52 The nerve travels from the
lateral border of the psoas major and penetrates the transversus abdominis by the anterior iliac
crest. Entrapment of this nerve creates lower abdominal pain and burning that may radiate to the
164 Chapter 10
Figure 10-7. Cutaneous distribution of the peripheral nerves of the lower extremity.
proximal medial thigh and into the scrotum/labia majora. Lovell54 indicated that ilioinguinal
neuralgia can be a cause of groin pain in athletes. Iliac fossa pain, tenderness to palpation of the
abdominal wall near the anterior superior iliac spine, inguinal pain radiating to the genitals, and
relief of symptoms with an anesthetic block are the hallmark features of ilioinguinal entrapment.19
Kopell et al55 described a correlation between ilioinguinal nerve entrapment and limited internal
rotation range of motion of the hip and asphericity of the femoral head. Lower abdominal pain
syndrome has been described in hockey players.56 The syndrome consists of extensive tearing of
the external oblique aponeurosis in the direction of its fibers, tearing of the superficial inguinal
ring, and entrapment and fibrosis of the ilioinguinal nerve. Following surgical repair, all athletes
returned to play.
The main differential in diagnosing ilioinguinal nerve entrapment is genitofemoral nerve
entrapment. If no conclusive diagnosis can be made, selective nerve blocks may provide more
information.52 If conservative management, including nerve blocks, stretching, soft tissue mobili-
zation, and physical therapy, fails, surgical management may be indicated. Surgical exploration of
the ilioinguinal nerve through an inguinal incision and neurectomy of the entrapped portion of
the nerve has been described.52 Possible complications from surgery include persistent numbness
and loss of cremaster reflex.
Genitofemoral Nerve
The genitofemoral nerve is composed of contributions from L1 and L2, and has a primarily
sensory function. It pierces the psoas and psoas fascia medially and descends along the surface of
the psoas. It provides sensation to a small section of the anterior thigh and the scrotal skin/mons
pubis and labia majora. This nerve is most often entrapped following surgery to the region. Symp-
toms of genitofemoral nerve entrapment include inguinal pain and burning that may radiate to the
genital skin and proximal medial thigh.52 This pain may increase with walking or hyperextension
TABLE 10-2
PERIPHERAL NERVES OF THE LOWER EXTREMITY
NERVE MOTOR SENSORY DISTRIBUTION TESTING
INNERVATION
Iliohypogastric None Upper buttock, suprapubic None
nerve
Ilioinguinal nerve Internal oblique, Superomedial thigh, skin at Nerve conduction
lowest portion the root of the penis and
of transversus anterior scrotum/mons
abdominis pubis and labia majora
(Starling and Harms, 198953)
Genitofemoral Cremaster Anterior thigh, lateral None
nerve scrotum
Obturator nerve Adductor longus Distal medial thigh, knee Needle
and gracilis, joint (sometimes hip joint) electromyography
pectineus,
adductor magnus,
obturnator
externus
Femoral nerve Quadriceps Anterior thigh Nerve conduction
femoris studies
Needle
electromyography
Lateral femoral None Anterolateral thigh Nerve conduction
cutaneous nerve
Sciatic nerve Hamstrings None Nerve conduction
Needle
electromyography
Short latency-
evoked potentials
Pudendal nerve External anal Perineal skin, scrotum/labia, Needle
sphincter, perineal perianal skin electromyography
muscles, external
urethral sphincter
Posterior femoral None Lower buttock, posterior Nerve conduction
cutaneous nerve thigh, perineum
of the hip, and may be alleviated by flexing the thigh or reclining. There is usually tenderness upon
palpation of the inguinal canal and hyperesthesia throughout the cutaneous distribution. Symp-
toms that persist despite conservative treatment may be addressed surgically. A transverse flank
approach is used,52 and the incision is made lateral and proximal to the umbilicus. The internal
and external obliques are divided, followed by exposure of the retroperitoneum. The nerve may be
166 Chapter 10
identified penetrating the psoas muscle. The entrapped site is then excised, which should include
the bifurcation of the nerve.
Obturator Nerve
The obturator nerve is composed of the L2, L3, and L4 nerve roots and descends through the
psoas, passing through a tunnel under the pubic ramus. Groin pain may also be caused by obtura-
tor nerve entrapment.56 Typically there is exercise-induced medial thigh pain that remits with rest.
There may be weakness/denervation of the adductor muscle group on EMG. Paresthesias may be
present along the medial thigh. This is often due to a fascial entrapment that occurs at the obtura-
tor foramen or proximal thigh. Conservatively this may be managed with rest, physical therapy,
soft tissue mobilization, strengthening exercises, NSAIDs, and stretching. If the symptoms are
recalcitrant, a surgical release is warranted. A surgical approach described by Bradshaw et al57 is
through an oblique incision over the lateral aspect of the adductor longus. The tissue is stripped
from the fascia over the adductor longus and pectineus, then the space between the 2 muscles is
bluntly dissected. The anterior branch of the obturator nerve runs over the adductor brevis, and is
covered by thick fascia. This fascia is divided, and the branches of the nerve are following proxi-
mally under the pectineus to the foramen, which is carefully enlarged by the insertion of a digit.
The muscles are then restored to their normal state and subcutaneous tissue and skin are closed.
Patients are instructed to ambulate as tolerated for the first few days. They may then begin to jog
when pain-free. Return to sports typically occurs within 3 to 6 weeks following surgery.
Lateral Femoral Cutaneous Nerve

The lateral femoral cutaneous nerve (LFCN) arises from nerve roots L2 and L3. Iatrogenic
injury to the LFCN may occur during surgery, and with pressure from belts, braces, or trauma
to the ilium. Meralgia paresthetica is characterized by numbness, burning, and pain through the
anterior-lateral thigh. The cause of injury or compression is often difficult to ascertain. There may
be compression as the nerve passes under the inguinal ligament.19 In athletes, injury may occur
from soft tissue trauma to the anterolateral thigh. Gymnasts may have injuries to this nerve from
uneven bar work, where there is repeated trauma. There are a number of anatomical variations that
may occur, and some of these variations may put the nerve at higher risk for injury. In cadaveric
dissections, large pseudoneuromas were found in the variants where the LFCN runs either within
or superficial to the inguinal ligament.58 Most cases resolve without intervention, but in cases
where symptoms persist, surgery may be warranted.
Femoral Nerve
The femoral nerve is formed by L2, L3, and L4 nerve roots. It passes from the lateral border of
the psoas and passes under the iliacus fascia and under the inguinal ligament. Injury to the femoral
nerve may result from psoas bursitis or strain due to the resultant swelling or possible hematoma.19
The other possible mechanics is a hyperextension of the hip that results in a significant stretch of
the nerve. The site of the injury or irritation is often difficult to localize; therefore, conservative
management is preferred.
Posterior Femoral Cutaneous Nerve

The posterior femoral cutaneous nerve originates from S1, S2, and S3, and then travels down
through the sciatic notch beneath the piriformis to the knee. It provides sensory input to the
lower portion of the buttock and posterior thigh, and there may be radiation into the anus and
lateral perineum from the inferior cluneal nerves.19 Injury to the nerve may occur from a fall on
the buttock or sustained pressure from prolonged bicycle riding. Injections may be used both for
diagnostic purposes and to provide symptom relief.
PEARLS AND PITFALLS

● As a first step in differentiating the origins of neural pain in the hip and pelvis, lumbar spine
pathology should be ruled out.
● The palpation test for sitting pain (palpating the gluteal area at the piriformis, the external
rotators, and lateral to the ischium) is useful in the clinical exam and diagnosis of those
with DGS.
● Essential criteria for the diagnosis of pudendal nerve entrapment are pain between the region
of the anus and the penis/clitoris, sitting pain, pain that does not awaken the patient at night,
and pain that is alleviated by a pudendal nerve block.
● Conservative management is the primary treatment in the setting of neuropathic hip pain,
as the natural history indicates that it should resolve. In recalcitrant cases, surgical treatment
may be employed in order to decompress the symptomatic nerve.
CONCLUSION
Peripheral nerves in the pelvis and lower extremity may mimic hip pathology. Careful examina-
tion should be able to direct the clinician to the appropriate interventions, based on the particular
nerve compression syndrome. Activity modification, stretching, and soft tissue mobilization are
usually the first line of treatment. More persistent cases may require selective injections that may
serve to first further delineate the exact cause of the pain, especially in those nerves with similar
distributions. In recalcitrant cases, surgery may be required to alleviate symptoms.
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19. McCrory P, Bell S. Nerve entrapment syndromes as a cause of pain in the hip, groin and buttock. Sports Med.
1999;27(4):261-274.
20. Puranen J, Orava S. The hamstring syndrome. A new diagnosis of gluteal sciatic pain. Am J Sports Med.
1988;16:517-521.
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25. Patti JW, Ouellette H, Bredella MA, Torriani M. Impingement of lesser trochanter on ischium as a potential
cause for hip pain. Skeletal Radiol. 2008;37:939-941.
26. Torriani M, Souto SC, Thomas BJ, Ouellette H, Bredella MA. Ischiofemoral impingement syndrome: an entity
with hip pain and abnormalities of the quadratus femoris muscle. AJR Am J Roentgenol. 2009;193(1):186-190.
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A case report. J Bone Joint Surg Am. 1987;69(1):143-145.
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29. Miller SL, Webb GR. The proximal origin of the hamstrings and surrounding anatomy encountered during
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31. Chakravarthy J, Ramisetty N, Pimpalnerkar A, Mohtadi N. Surgical repair of complete proximal hamstring
tendon ruptures in water skiers and bull riders: a report of four cases and review of the literature. Br J Sports
Med. 2005;39:569-572.
32. Martin H. Clinical examination and imaging of the hip. In: Byrd J, Guanche C, eds. AANA Advanced
Arthroscopy: The Hip. Philadelphia, PA: Saunders; 2010.
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LM, Wilkins AN, eds. Functional Electromyography. New York, NY: Springer US; 2011.
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11
Stress Fractures of the
Hip and Pelvis
Marci Goolsby, MD; Landon Hough, MD; and Marc R. Safran, MD
INTRODUCTION AND EPIDEMIOLOGY OF STRESS FRACTURES

OF THE HIP AND PELVIS
Introduction
Stress fractures are a common cause of missed training and competition among athletes. These
injuries occur most commonly in the lower leg and foot,1,2 but can occur in any bone subjected to
repetitive stress over time. The hip and pelvis are of particular concern, as bone stress injuries of
these structures may be difficult to diagnose, and if not properly treated, may result in significant
morbidity and long-term complications for the athlete.
Pathophysiology of Bone Stress Injuries

The term bone stress injury describes a spectrum of injuries to the bone that encompasses both
stress reactions and stress fractures. Stress-induced remodeling is a normal physiologic aspect of
bone turnover as described by Wolff’s law, but when there is an imbalance between bone resorption
and bone formation, microdamage to the bone can occur.3 A combination of increased mechanical
strain and increased rate of bone loading may stress the bone beyond its normal repair capacity.
Without adequate time to heal, this leads to damage accumulation and fatigue failure of the bone.4,5
Stress fractures are often described as either fatigue fractures or insufficiency fractures.4 Fatigue
fractures occur from repetitive strain over a prolonged time to normal bone structure. Insuffi-
ciency fractures occur as a result of normal stress load to an abnormal bone structure. In athletes
and military recruits, fatigue fractures are the more common type of stress fracture; however,

172 Chapter 11
some athletes may have a combination of the 2 types, such as seen in the female athlete triad when
hormonal and nutritional deficiencies result in suboptimal bone health.3,6,7
The mechanical loading that occurs in the hip and pelvis is affected by gravitational forces as
well as muscle forces.4,7,8 Thus, the muscles in the hip and pelvis may be involved in the devel-
opment of stress injuries. Two theories exist of how this occurs, although each may play a role
depending on the individual and the location of the stress injury.3,7,8 The muscles in the hip and
pelvis are important in balancing torque forces such as those at the femoral neck. If the muscles
are weak and become fatigued with activity, their ability to absorb gravitational forces is lost,
transmitting increased forces to the bone.3,4,7,9 In addition, forces of muscle contraction may con-
centrate at their insertion site, leading to bone stress injury.8
Epidemiology of Stress Injuries

The first stress fracture was described in the Prussian military in 1855,10 with the first femoral
neck stress fracture reported by Blecher in 1905.11 Multiple case series of femoral neck stress frac-
tures have been published since then.12-15 In a 10-year prospective study of track and field athletes,
Bennell et al noted a 21% incidence for all stress fractures, with 8% being in the femoral neck.16
Another study found stress fractures of the femur to be the fourth most common site (7.2%), with
only 1.6% occurring in the pelvis.2 In a study of military recruits, 185 femoral fatigue fractures
(199 per 100,000 person-years) were diagnosed based on symptoms and magnetic resonance imag-
ing (MRI). In this group, 9% were bilateral, 50% were of the femoral neck, and 22% had a fracture
line.17 As described in further detail below, females are at higher risk for pelvic and hip stress inju-
ries. The true incidence of pelvic and hip stress injuries, however, is difficult to determine because
of variation in studies and poor recognition.
TYPES OF STRESS INJURIES

Femoral Neck Stress Injuries
Stress fractures of the femoral neck have been described since the early 1900s,11 with mul-
tiple classification systems proposed since their discovery.3,12-15,18 Devas described tension-sided
(lateral femoral neck) and compression-sided (medial femoral neck) fractures.15 Fullerton and
Snowdy added a separate category for displaced fractures.12 This system was revised by Shin and
Gillingham to include magnetic resonance (MR) descriptions of these 3 categories. The compres-
sion-sided femoral neck stress injuries were subdivided based on the presence of a fatigue line: no
fatigue line, fatigue line greater than 50%, and less than 50% of the femoral neck 3 (Figure 11-1).
Diagnosis of femoral neck stress injuries is often delayed and there is a high incidence of complica-
tions, particularly with displaced fractures.14
Pelvic Stress Injuries

Pelvic stress fractures account for less than 2% of all stress fractures, and occur almost exclu-
sively in females.7,19,20 In the pelvis, stress injuries of the inferior pubic ramus are most common,
frequently at the site of the proximal adductor magnus attachment (Figure 11-2). Shear forces
between the adductor muscles medially and hamstring attachment laterally may introduce the
repetitive forces that lead to stress injuries in this area. Injuries to the pubic symphysis have also
been reported and, similar to the pubic ramus, are likely related to traction stress from the rectus
abdominis, adductors, and/or gracilis.7 Acetabular stress injuries have been reported in the ace-
tabular roof and anterior column. Acetabular stress fractures of the superior lateral roof have been
seen to occur in the setting of femoroacetabular impingement in athletes. Further, the majority
Stress Fractures of the Hip and Pelvis 173
Figure 11-1. Imaging studies of a right compression-sided femoral neck stress fracture in a 26-year-old female runner
with the female athlete triad. (A) Anteroposterior pelvis radiograph does not show any abnormality. (B) Coronal inver-
sion recovery and (C) proton density-weighted MR images show bone marrow edema with a fracture line that involves
approximately 50% of the diameter of the neck. (D) A repeat coronal proton density-weighted MR image performed
6 weeks later shows interval healing with decreased fracture line.
Figure 11-2. Anteroposterior pelvis radiographs of a right inferior pubic ramus stress fracture (A) upon presentation
after 3 weeks of symptoms and (B) at 9 weeks that show interval healing demonstrated by decreased fracture line and
callus formation.
were found to have concomitant stress injuries elsewhere in the hip and pelvis.21 Other sites of
pelvic stress injuries have been reported, but are quite rare.
Sacral Stress Injuries

Sacral stress injuries represent less than 2% of stress injuries reported in athletes, 2 but are being
diagnosed more frequently in recent years, likely because of the sensitivity of MRI, and limited
ability of plain radiographs to make the diagnosis. These injuries are difficult to recognize as they
may present similar to many other causes of low back pain, thus they are likely underdiagnosed.22
They are believed to result from vertical forces transmitted from the spine, through the sacrum,
and into the ilium. Leg length discrepancy has been implicated as a possible risk factor.23,24 Most
sacral stress injuries occur in the sacral ala, near the sacroiliac junction, and are most commonly
unilateral.22 A higher incidence in females has been reported,20,25 particularly in those with the
female athlete triad.23
174 Chapter 11
TABLE 11-1
RISK FACTORS FOR STRESS INJURIES
Extrinsic Intrinsic
Distance running Female gender
Sudden increases in distance, intensity, or duration Low energy availability
Sudden changes in activity Disordered eating habits
Inadequate rest and recovery time Menstrual irregularities
Change in running surface Low bone mineral density
Biomechanical abnormalities
RISK FACTORS
An athlete who presents with a stress injury usually has identifiable risk factors, and therefore
should undergo a comprehensive evaluation. In general, the risk factors for stress injuries can
be thought of in 2 categories: extrinsic and intrinsic (Table 11-1). Extrinsic risk factors are those
that come from outside the athlete such as type of sport, training factors, terrain, and equipment.
Intrinsic factors include aspects of the athlete such as nutritional and metabolic issues, biomechan-
ics, gender, fitness, and musculoskeletal factors.
Extrinsic Risk Factors

Type of Sport
Stress injury incidence has been shown to be highest among endurance athletes.1,2,26 Specifi-
cally, endurance runners are more likely to sustain stress injuries to the pelvis and long bones of
the lower extremities.1,20 Approximately two-thirds of femoral neck stress fractures occur in
runners.1,14 This is thought to be due to the high number of load repetitions in distance running,1
as well as a higher incidence of low energy availability (poor nutrition intake relative to exercise
expenditure) as seen in the female athlete triad.6
Training Factors
Errors in training are often described as common risk factors for development of a stress
injury,8,27 though others have not found these to be significant.1,2,16,28 Increasing intensity (such
as with speed workouts), duration, distance, and/or frequency of the activity can all increase the
load to the bone without adequate time for repair. A change in running terrain may also affect the
strain on bone.29
Footwear/Inserts
The role of shoewear and inserts or orthotics in stress injuries is somewhat unclear. There has
been some evidence that worn shoes may contribute to tibia stress injuries and orthotics may pre-
vent them.5 If malalignment is contributed to by worn shoes or innate biomechanical abnormali-
ties are not corrected, this could affect the biomechanics in the hip and pelvis, but currently there
is no evidence that shoewear or inserts are specific factors in pelvic or hip stress injuries.
Figure 11-3. Female athlete triad composed of 3 interrelated components: energy

availability, menstrual function, and bone health. Patients may present along a
spectrum from healthy to pathologic aspects of the 3 components. BMD = bone min-
eral density. (Reprinted with permission from Nattiv A, Loucks AB, Manore MM, et al.
American College of Sports Medicine position stand. The female athlete triad. Med Sci
Sports Exerc. 2007;39[10]:1867-1882.6)
Intrinsic Risk Factors

Age, Race, and Gender
As an independent factor, it is unclear whether age increases the risk of stress injury, although
osteoporosis does.30 One study did show that femoral and tarsal stress injuries, compared to other
sites, occurred more in older athletes, with the average age being 35.3 years in males and 27.6 years
in females with femoral stress fractures.2 Tension-sided femoral neck stress fractures have been
shown to be more common with older age likely due to osteoporosis, and compression-sided frac-
tures have been shown to be more common with younger age.8 Stress injuries are more common
in Whites than Blacks, which may partly be due to the higher bone mineral density (BMD) seen
in Blacks.30 Female athletes have a higher incidence of stress injuries than men.19 Stress injury
incidence in female athletes is around 10%, compared to 7% in male athletes.19 Compared to other
sites, pelvic and sacral stress injuries occur with a much greater female predominance.17,20,25
A large part of the higher incidence of stress injuries in females may be due to a high prevalence
of the female athlete triad.
Female Athlete Triad
The female athlete triad is a syndrome characterized by low energy availability, functional
hypothalamic amenorrhea, and osteoporosis that exist along a spectrum6 (Figure 11-3). Low
energy availability, which is an imbalance of dietary caloric intake compared to exercise energy
expenditure, may be inadvertent, intentional, or even pathologic as is seen in eating disorders.
Low energy availability can occur from increasing exercise without adjusting diet, decreasing food
intake, practicing abnormal eating habits such as self-induced emesis, or some combination of
these. With high levels of physical activity and training in some sports, it is sometimes difficult to
replenish the amount of calories expended, thus leading to an inadvertent low energy availability.
Many, however, practice disordered eating habits to keep their weight low16 and disordered eat-
ing habits, specifically restrictive eating, have been associated with stress fractures.31 This low
energy availability disrupts the normal hypothalamic-pituitary-gonadal axis function, which
leads to menstrual irregularities and negative effects on bone health.32 This causes the bones to
be more susceptible to stress-induced microdamage. Absence of menses caused by this disruption
of hormonal function is known as functional hypothalamic amenorrhea. Athletes with later age
of menarche and decreased menses per year have lower BMD and more stress fractures.27,31,33,34
Runners with a history of oligomenorrhea were 6 times more likely to sustain a stress fracture in
176 Chapter 11
a retrospective study.31 Menstrual irregularity seems to be of particularly high prevalence in hip

and pelvis stress injuries.23 The female athlete triad is more commonly seen in endurance and
aesthetic sports.6
Low Bone Mineral Density
Lower BMD and bone mineral content (BMC) are considered risk factors as a component of the
female athlete triad but also as independent risk factors that are seen more commonly in athletes
who sustain stress injuries compared to controls.26,31,33 The majority of bone mass is accumulated
in adolescence, when bone is most responsive to the mechanical loading of physical activity. If
optimal bone structure is not obtained during this critical time, an athlete may be at future risk
of fracture.19,26 Specifically, lower BMD has been found in athletes with hip and pelvis stress
fractures.23,35 Pouilles found that athletes with femoral and calcaneal stress fractures had lower
BMD than controls, but those with metatarsal or tibial stress fractures did not.36 Lower levels of
vitamin D and lower calcium intake during bone development may result in decreased BMD and
BMC, and increase the risk of stress fractures in the future.19
Biomechanical/Musculoskeletal Factors
The anatomy and biomechanics of the pelvis and hip can also contribute to the risk of stress
injury. As was described in detail in “Pathophysiology,” asymmetry and weakness in surrounding
musculature can affect the strain in the pelvis and hip, contributing to the risk of stress injury.3,8
In addition, a narrower tibial measurement37 and leg length discrepancy 24 have been associated
with femoral stress injuries.
Prior Injury
A history of prior stress injury is also a risk factor for subsequent stress injuries.7,26,30 More
than 50% of athletes with stress fractures may report having a prior stress fracture.20,31 This
finding indicates the persistence of risk factors in susceptible individuals, thus emphasizing the
importance of evaluation for and correction of these risk factors.
Fitness Level
Lower aerobic fitness levels have also been linked to increased stress injury risk. Athletes and
military recruits who have been active in sports or aerobic training prior to beginning an orga-
nized training program are less likely to suffer from stress fractures after increasing their training
volume.19 Although the reason for this benefit from prior training is not known, it could be related
to the changes in musculoskeletal factors.
The classic description of pain in an athlete with a hip or pelvis stress fracture is that of pain
related to impact activity that is relieved by rest.12,18,29,38 It is often described as a deep ache that
may be sharp at times of quick movements or hard weight-bearing impact. The area of pain may
be vague and difficult to localize. In femoral neck stress fractures, the patients often complain of
anterior hip or groin pain.3,12,18,28,29,38 Pubic ramus stress fractures often present as inguinal,
adductor, or perineal pain.39 Nonspecific low back or buttock pain may be the only complaint in
a patient with a sacral stress fracture. Pain is often related to impact activity but some may also be
worsened with prolonged sitting or standing. Initially, the pain may occur only at the beginning or
end of a run but can progress to pain throughout the run. Often pain with ambulation develops,
sometimes even causing a limp.38 Lifting the leg may be painful, and the patient may complain of
pain at night as well.38,12
It is important to take a comprehensive history, specifically focusing on potential risk factors as
described above.38 A complete training history should be obtained with focus on changes to the
routine. An injury history may identify ongoing risk factors such as a gait abnormality or poor
bone health, particularly when there are recurrent stress injuries. A thorough menstrual history,
including age of menarche and both recent and past history of oligomenorrhea or amenorrhea, are
important clues to the female athlete triad. Use of oral contraceptives and the reason for their use
may be a clue to underlying hormonal abnormalities. With this, a nutrition history should also
be obtained, specifically looking for any eating disorder or disordered eating patterns recently or
in the past. Evaluation of obvious macronutrient or micronutrient deficiencies is important, par-
ticularly calcium and vitamin D. It is also important to note whether the nutrition intake has been
adjusted appropriately for the amount of exercise, as a short-term energy deficiency also increases
the risk of bone stress injury. There may be other factors that negatively affect bone health such
as celiac disease, use of oral steroids, hyperparathyroidism, hypercalciuria, hypothyroidism, prior
radiation, smoking, excessive alcohol intake, or other causes of osteoporosis.
CLINICAL EXAMINATION
The physical examination in patients presenting with possible stress injury should focus on
the identification of the source of pain as well as any potential risk factors. The general appear-
ance or physique of the patient, including a measure of height, weight, and body mass index may
indicate a nutritional issue. The examination should include evaluation of signs of eating disor-
ders such as abnormally thin body habitus, lanugo, calluses on the knuckles, hair loss, and tooth
enamel erosions. A gait analysis may identify an antalgic or Trendelenburg gait. Biomechanical
testing should evaluate for pronation or supination, pes planus or cavus, leg length discrepancy,
abnormal alignment, abnormal joint range of motion, and imbalances of strength and flexibility,
particularly in the hip and pelvis musculature.38 Femoral neck and pubic ramus stress injuries
may have tenderness to palpation in the inguinal area.7,12 The pubic ramus is best palpated with
the leg in a figure-4 position. Sacral stress injuries often have unilateral focal pain overlying the
sacral ala.22,23,25 In some stress fractures of the pelvis and hip, however, a focal area of tender-
ness may not be present. Range of motion of the hip may be limited and cause pain in femoral
neck and pubic ramus stress injuries, particularly with flexion, adduction, and internal rotation
of the hip.3,12,28,38 The pain of sacral stress fractures may be reproduced with low back extension
that localizes to one side with the stork test or with flexion abduction and external rotation of the
hip.25 Log roll and resisted flexion of the affected hip may cause pain in femoral neck stress inju-
ries.3,28 With severe cases of femoral neck injuries, patients may have difficulty actively flexing
the hip with a straight leg because of pain.3,28 Resisted hip adduction may reproduce pain in pubis
ramus stress injuries. Hop test may reproduce pain with any of the hip and pelvic stress injuries.38
Based on a small case series, Noakes and colleagues suggested that, in distance runners with groin
pain, the presence of pain preventing running, pain with standing on the affected leg, and focal
tenderness to palpation over the pubic ramus can diagnose a pubic ramus stress fracture with
confidence even without radiographic findings.39
Differential Diagnosis
There is often a delay in diagnosis of a stress injury in the hip and pelvis14 with initial diagno-
sis of muscle or tendon injury. Other diagnoses to consider are lumbar radiculopathy, myofascial
pain, piriformis syndrome, athletic pubalgia, bursitis, tendinopathy, femoroacetabular impinge-
ment, avascular necrosis, avulsion injury, tumor (ie, osteoid osteoma), infection, synovitis, or
pathologic fracture.3,28,38,40 Because of the challenges with diagnosing a hip or pelvic stress injury
on examination alone, further imaging studies are often needed to differentiate between the above
possible diagnoses.
178 Chapter 11
IMAGING
Since stress fractures were first recognized, multiple imaging techniques have been employed
as diagnostic tools. Plain film radiographs, technetium-99 bone scan, MRI, computed tomography
(CT), and even ultrasound have been used.
Plain Radiographs
Radiographs are often the first imaging modality used when a stress fracture is suspected
because of their widespread availability, relatively low cost, and quality imaging of bony structure.
Notable findings indicative of stress injury include periosteal elevation, endosteal elevation, corti-
cal sclerosis, and subtle blurring of the trabecular margins. With progression to a stress fracture,
a dense linear or curvilinear fracture line is visible41,42 (see Figure 11-2). Unfortunately, most of
the changes visible on plain film radiographs are not apparent in the early stages of stress frac-
tures, and are only apparent if the fracture progresses or the healing process is well underway38
(see Figure 11-1). The sensitivity of radiographs for stress fractures has been shown to be very low,
particularly in the hip and pelvis area,25 where the sensitivity in the posterior pelvis and sacrum
approaches 0%.41
Bone Scan
In radionuclide bone scanning, technetium-99m phosphonate analogs are localized to areas
of osteoblastic activity, and are the reason for its high sensitivity in the diagnosis of stress frac-
tures. A radionuclide bone scan requires an injection of technetium-99 m-labeled phosphorous
complexes. Images are taken immediately after injection, and again a few hours later, to determine
bony activity. Multiple studies have demonstrated the high diagnostic sensitivity especially use-
ful early in stress fracture formation, with positive results as soon as 6 to 72 hours after onset
and even before symptoms develop in some patients.2,41,43 Positive bone scan findings are seen
as uptake on all 3 phases, with more localized uptake in the third phase (Figure 11-4). The stress
injury appears as a sharply marginated or fusiform area of uptake involving at least one cortex.38
However, this increased uptake is not specific for stress fractures and may also be seen in traumatic
fracture, tumors, infections, and avascular necrosis.38 The intensity of uptake on imaging gradu-
ally decreases with healing over the first 3 to 6 months but may persist up to 10 months before
complete resolution.41

Magnetic resonance imaging (MRI) is currently the imaging modality of choice for evalu-
ation of most stress injuries because of its multiple advantages.8 MRI has been shown to have
sensitivity equal to that of radionuclide bone scan, approaching 100%, and a very high specificity
with no exposure to ionizing radiation. MRI also allows detailed evaluation of surrounding soft
tissues, which may be helpful in evaluating for other or concomitant injuries. It can also be used
to grade the severity of a bone stress injury, which may affect the prognosis and treatment plan44
(Table 11-2). MRI is more accurate than bone scan at correlating the degree of bone involvement
with clinical symptoms, and is better at defining the location such as in compression-sided and
tension-sided femoral neck stress injuries. In addition, MRI does not involve any ionizing radia-
tion, is performed in a shorter amount of time than a bone scan, and does not require an injection.
In evaluation of the femoral neck, MRI is more sensitive at diagnosing early stress injuries than
bone scan, and may show evidence of stress injury weeks to months before bone scan or other
imaging techniques28,43 (see Figure 11-1). Shin and colleagues used MRI to evaluate 22 femoral
neck stress fractures diagnosed by bone scan and found that MRI was 100% accurate, whereas
Figure 11-4. Bone scintigraphy of

left sacral stress injury.
TABLE 11-2
MAGNETIC RESONANCE IMAGING GRADING OF BONE STRESS INJURIES
0 Normal in all sequences
1 Positive STIR, normal T1 and T2
2 Positive STIR and T2, normal T1
3 Positive in all sequences, no cortical break
4 Low signal intensity fracture line on all sequences
STIR = short T1 inversion recovery.
bone scan was only 68% accurate.28 Cross-sectional imaging and the ability to diagnose subtle
marrow changes can also help identify bone changes in areas of the sacrum and pelvis that are
difficult to image with other modalities. These advantages have led to consideration of MRI as
the gold standard in stress injury evaluation, especially in the hip and pelvis.23,28,43 Table 11-2
describes the graded findings of stress injuries in MRI, which is based on which sequences show
signal changes. A true fracture line can be seen as a line of low signal intensity continuous from
the cortex to the intramedullary space that is seen on all pulse sequences and surrounded by an
area of bony edema41,43 (see Figure 11-1). Possible drawbacks of MRI include relatively high cost,
and suboptimal imaging of cortical bone. The high level of detail can also provide too much
information that may be difficult to interpret, so clinical correlation is always recommended.
False positive scans can be possible with imaging suggestive of bone edema in an asymptomatic
patient that may not indicate or develop into a true stress fracture, and positive edema patterns can
180 Chapter 11
persist for up to 6 months after initial injury despite healing.42 False negative scans are possible
and are due to reader error, poor choice of imaging planes or sequences, and inhomogeneities in
fat suppression.41,43 Despite these limitations, most experts agree that MRI is the best imaging tool
available for stress injuries of the hip and pelvis.
Computed Tomography
CT can delineate a fracture line well, especially in the long bones, spine, and navicular, and is
sensitive in diagnosing pelvic insufficiency fractures and osteopenia, but overall has poor utility in
the evaluation of stress injuries to the hip and pelvis.41,43 The relatively high cost, higher amount
of ionizing radiation, and poor early sensitivity in diagnosis have limited its utility. The indica-
tion of a stress fracture on CT scanning is similar to that of plain radiographs with periosteal or
endosteal elevation and the development of a fracture line. One particular advantage of CT is in
pediatric patients with marked periosteal proliferation on radiographs or MRI. CT scans can help
demonstrate new endosteal bone formation, which can help distinguish stress fractures from a
malignancy such as an osteoid osteoma.41
Ultrasound
The use of ultrasound for diagnosis of musculoskeletal injuries is increasing in frequency.
Ultrasound is readily available, instantly provides real-time images, and is relatively low cost com-
pared to other imaging techniques. It has been shown to have potential in stress fracture diagnosis
in superficial bones such as the distal tibia and metatarsals.42,43 However, currently no evidence
exists to its role in diagnosing stress fractures of the hip and pelvis.
OTHER DIAGNOSTIC EVALUATION

Metabolic Bone Evaluation
Stress fractures of the hip and pelvis are considered higher risk stress fractures23,35 and may
require further evaluation to rule out an underlying metabolic bone disease and other contribut-
ing factors. As described above, some medical illnesses and medications can affect bone health
and, thus, lower BMD. Consideration of further laboratory evaluation should be individualized
but could include a comprehensive metabolic panel, thyroid-stimulating hormone, calcium, para-
thyroid hormone, vitamin D, magnesium, phosphorus, markers of bone turnover (osteocalcin,
urine N-terminal telopeptide [NTX]), 24-hour urine calcium, celiac panel, complete blood count,
and urinalysis. In addition, a dual-energy x-ray absorptiometry (DXA) scan may be indicated for
evaluation for low BMD. Marx and colleagues showed that stress fractures in cancellous bone were
more likely to be associated with a lower BMD.35 Patients who have disordered eating or amen-
orrhea also have lower BMD than their peers.6,34 In the American College of Sports Medicine
position stand on the female athlete triad in 2007, it was recommended that further evaluation of
BMD by DXA be considered in any athlete with a history of hypoestrogenism, disordered eating
or eating disorders for a cumulative total of 6 months or more, and/or a history of stress fractures
or fractures from minimal trauma.6
Nutrition Evaluation
Athletes with signs of the female athlete triad should be referred to a dietitian for a compre-
hensive evaluation of energy availability based on their total caloric intake and exercise energy
expenditure. Discussion of macronutrient and micronutrient intake and disordered eating habits
should take place with focus on unhealthy behaviors and deficiencies in bone-building nutrients.6
Nutrition and vitamin supplements may be recommended.
Psychiatric Evaluation
A referral to a therapist, psychologist, and/or psychiatrist may be appropriate if the athlete has
an unhealthy relationship with food or exercise, such as an eating disorder or obsession with exer-
cise, or if the athlete has difficulty coping with the psychological aspects of the injury and time
away from sport. Occasionally, the use of antidepressants or other psychiatric medications may be
indicated for concomitant diagnoses such as an eating disorder, depression, or anxiety. The nutri-
tion and psychological issues in patients with stress fractures are important and often overlooked
aspects of evaluation and treatment.
TREATMENT
Nonoperative Treatment Options
The treatment of stress fractures and the athlete’s return to a sports program must be
individualized. There are multiple factors that should be considered when making these deci-
sions, including the bone involved, risk of progression of stress fracture, consequences of pro-
gression, severity of injury, duration of symptoms, underlying risk factors including presence
of low energy availability, response to initial treatment, type and level of sport, and upcoming
training/competition goals.
Modification of Activities/Weight Bearing
The first aspect of treatment is avoidance of impact or symptom-producing activities. For
many, this requires the use of crutches initially because of pain with ambulation. Many factors go
into how long one is kept partial or non-weight bearing. Management of pain, bone healing, and
risk of complications must be considered. Weight bearing may need to be limited for anywhere
from 1 to 6 weeks or more depending on the above factors.8 There are different considerations
for a patient with a stress reaction at a site with low risk of complications, such as the sacrum,
vs one with high risk, such as at the femoral neck. For some patients, no-impact or light-impact
activities may be allowed even early on if the severity is low, the activity causes no pain, there is
no concern for significant low energy availability, and/or the stress injury is not at a high-risk site
of muscle attachment.
Specifically, with regard to femoral neck stress fractures, tension-sided femoral neck stress
fractures are subjected to distraction forces, and thus have a higher propensity to displace and
become complete fractures. As a result, strict limited weight bearing with close observation with
imaging until evidence of healing or surgery is the treatment of choice. On the other hand, com-
pression-sided femoral neck stress fractures are generally inherently stable, thus rarely displace,
and generally are managed with limited weight bearing until asymptomatic, then slow progression
back to activity.
Addressing the Risk Factors
One of the most critical aspects of the treatment plan is the focus on a thorough evaluation and
patient education in order to identify and address risk factors that could affect healing and lead to
injury recurrence.30,38 This should include discussion of pertinent extrinsic and intrinsic factors
from training errors to the female athlete triad. If training errors were present, suggestions for
future training may include a more graduated training program, inclusion of cross-training with
lower impact activities, and incorporating a specific strengthening program. Further evaluation
182 Chapter 11
of intrinsic risk factors may be indicated as described previously. Nutrition and psychological
counseling should be continued as a critical aspect of the healing process. The focus of treatment
for the female athlete triad is to address the low energy availability through education, nutrition
counseling, and exercise changes as indicated. Resumption of menses occurs with correction of
low energy availability.6 General education about bone health and avoidance of risk factors should
be included in the treatment of stress injuries.
If biomechanical factors seem to have contributed to the injury, these should be addressed
with appropriate measures. This often is in the form of physical therapy to correct imbalances in
strengths and weaknesses that may be present. The entire kinetic chain should be evaluated and
addressed by physical therapy. If abnormalities are noted in the foot and ankle, orthotics may
be indicated.
Medications
Medications are not the mainstay of treatment for stress fractures but occasionally play a role.
In addition to limiting weight-bearing status, pain may be managed with acetaminophen, nonste-
roidal anti-inflammatory drugs (NSAIDs), and narcotics if necessary. There are some conflicting
data about NSAIDs having a negative effect on bone healing, so limiting the use of these may be
best. Use of supplements such as calcium and vitamin D may be indicated by nutrition and/or
laboratory evaluation.
Vitamin D and calcium are important components of bone development, and their role in opti-
mizing bone structure is especially essential in adolescence. Lower levels of vitamin D and lower
calcium intake may result in decreased BMD and BMC, and increase the risk of stress fractures
in the future.26,33 Supplementation of calcium and vitamin D in a diet that is deficient has been
shown to reduce the incidence of stress fractures by as much as 20% in some studies.45
For stress fractures in the setting of low BMD, other adjunctive medications have been used
such as nasal calcitonin, bisphosphonates, and recombinant parathyroid hormone (Forteo [teripa-
ratide]), but the evidence of their effectiveness and safety in human clinical trials is lacking. In
addition, bisphosphonates have teratogenic effects and last for many years in the bone, so they
should be avoided in females in their childbearing years. There has been some promising evidence
for recombinant parathyroid hormone improving BMD, BMC, and stress fracture healing in ani-
mal studies, but further research is needed in humans.46
Other Modalities
External bone stimulators have been used for nonhealing stress fractures. There are 3 exter-
nal types of electric and electromagnetic fields used: pulsed electromagnetic fields, capacitively
coupled electric field, and combined magnetic fields.47 There is some promising evidence for the
benefit of electric and electromagnetic fields, as well as low-intensity pulsed ultrasound, in trau-
matic fractures but not in stress fractures.48,49 Currently, there are no data to support the use of
bone stimulators in pelvis and hip stress injuries. In general, further research is needed to evaluate
the effectiveness of adjunctive medications and modalities for stress fracture healing.
RETURN TO ACTIVITIES
The time to full return to activity in hip and pelvis stress injuries is dependent on multiple
factors unique to the individual. The length of symptoms, severity of injury, site of injury, train-
ing goals, type of sport, and underlying risk factors must all be taken into consideration.1,38
Studies have shown it takes 8 to 18 weeks for full, unrestricted return to running.1,8,39 In general,
the criteria for progression of activity are based on pain-free activity, lack of pain on examination,
and, in many cases of true stress fractures, repeat imaging showing signs of healing.7 Pain is used
as a guide throughout the program of graduated impact activities. Initially, the goal is pain-free
ambulation without an assistive device. Once this is accomplished, light-impact activities such
as swimming and stationary bike may be tried. Each step in the process should be taken slowly,
with each new activity introduced with short duration and low frequency initially. If any activity
causes pain during or after, the athlete should adjust to a lower impact one for a week or so before
trying again. Maintenance of fitness is very important for many of these athletes and, when safe
to do so, this can be achieved by light-impact activities such as swimming, biking, aqua jogging,
or use of an anti-gravity treadmill. Activity is then gradually progressed to moderate-impact
activities such as elliptical machine use, then to high-impact activities that include jumping and
running.38,40 It may also be appropriate to include sport-specific activities and physical therapy
when safe to do so.
SURGICAL TREATMENT
Indications
The majority of pelvic and hip stress injuries can be successfully managed nonoperatively.38
Tension-sided femoral neck stress fractures and severe compression-sided femoral neck stress frac-
tures (more than 50% the width of the femoral neck) often require surgical intervention because of
their high risk of progression to complete fracture and displacement, and poor healing potential.2
Some have had success with nonoperative management of tension-sided femoral neck stress frac-
tures3 but the majority of authors advocate surgical fixation.13 Generally, internal fixation with
multiple percutaneously placed cannulated screws is used to reduce the risk of displacement, and
help relieve symptoms. Alternatively, a sliding hip screw may be used, but, because of the more
extensive dissection required, it is not routinely used for femoral neck stress fractures; it is more
frequently used for the less common subtrochanteric or basilar neck fracture. Curettage or ream-
ing to induce biologic reaction may help the fracture site heal, but is rarely necessary. An unfor-
tunate complication of femoral neck stress fracture is displacement, with its inherent increased
risks of nonunion and avascular necrosis. This should be treated like a transcervical fracture and
undergo reduction and internal fixation immediately.3
Contraindications
Surgery may be contraindicated if there are significant surgical risk factors such as a bleeding or
clotting disorder, cardiac or pulmonary disease, or a previous anesthetic or surgical complication.

For the procedure, the patient is supine on a fracture table, allowing the soft tissues of the but-
tock and hip to fall posteriorly. This provides better access to the entire hip and allows easier use
of fluoroscopy during the procedure. Traction on the leg is not required for nondisplaced femoral
neck stress fractures. The leg is usually positioned in neutral flexion-extension, neutral abduction-
adduction, and neutral rotation to slight internal rotation to account for femoral neck anteversion.
In mildly displaced tension-sided fractures, slight abduction may help reduce the fracture. The
surgeons must be sure they can visualize the anterior and lateral femoral head and neck by fluo-
roscopy before prepping the patient for surgery.
The guidewires for cannulated screws are placed in line with the femoral neck axis overly-
ing the skin to determine the appropriate approximate starting point on the skin. The wires are
placed in line with the femoral neck axis through percutaneous poke holes. The first wire is placed
in the femoral neck to end up at the center-center position of the femoral head, 5 mm from the
subchondral bone to ensure good purchase. Generally in young athletes, this can be up to 10 mm
184 Chapter 11
from the subchondral bone with good purchase. A second and third guide wire are placed, often
with a parallel drill guide. Usually these are inferior to the first screw, anterior and posterior.
Once it is confirmed on anterior-posterior and lateral fluoroscopic images that the wires are in the
appropriate positions, small full-depth incisions are made at each guide pin, and the soft tissues are
spread to the bone. After measuring the depth of the guidewires for appropriate screw length, the
lateral cortex is drilled with the cannulated drill. Then self-tapping cannulated screws are placed.
The screws should be long enough that all the screw threads are on the proximal (femoral head)
side of the fracture. Fluoroscopic images are again taken in 2 planes to be sure the screws have
not entered the joint and are of appropriate length. Once this is done, the wounds are closed with
simple sutures and dressings are applied.
Postoperative Rehabilitation/Return to Play
After surgery, the patient continues toe-touch weight bearing with crutches until there is
radiographic evidence of bone healing. A similar protocol is used as outlined for the nonoperative
approach above, with bicycling on an exercise bike and swimming permitted once the wounds are
healed (10 days). When light activities and range of motion are pain-free, usually in 4 to 6 weeks,
aggressive physical therapy is begun to recondition the extremity. A gradual return to sports is
allowed once full strength has returned, which is frequently at 2 to 4 months postoperatively.
Long-term monitoring for complications is necessary, given the high rate of complications as
described below. In a case series of femoral neck stress fractures, none of the elite athletes returned
to their previous level of competition; however, that is not the authors’ experience.14
COMPLICATIONS
The most common complications of pelvis and hip stress injuries are related to risk factors
such as poor bone health, ignored symptoms, missed diagnosis, or a delay in diagnosis. Femoral
neck stress fractures, for example, might be diagnosed as a hip flexor strain and the athlete may
continue to try to run through the pain. This can lead to disastrous complications such as a dis-
placed femoral neck fracture.14 Johansson and colleagues found that in 23 femoral neck fractures,
30% had a complication. Ten of these 23 fractures were displaced, with 50% of these developing a
complication despite surgical fixation.14,50 The complications of a displaced femoral neck fracture
are delayed union, nonunion, and osteonecrosis.14 In a series of 12 displaced femoral neck stress
fractures treated with open reduction and internal fixation, 5 developed osteonecrosis, one had
delayed union, and one went on to not heal (nonunion). In 42 displaced femoral neck fractures
treated surgically, 23.8% of patients developed avascular necrosis at an average of 5.6 years.14,50
Factors that contribute to this risk after a displaced fracture include the degree of displacement,
time between displacement and surgery, type of fixation used, and poor surgical technique (frac-
ture not reduced adequately or with malalignment).51
PEARLS AND PITFALLS

● Identifying all risk factors is key in the successful management of stress fractures in athletes, and
may require a multidisciplinary approach. These athletes may require nutritional assessments
and blood work to identify deficiencies.
● MRI is often the least invasive way to assess early stress fractures to ensure appropriate manage-
ment of the injury.
● Tension-sided femoral neck stress fractures frequently require surgical intervention in the
form of percutaneous screw placement because of the risk of fracture progression and resultant
displacement.
● Athletes should be counseled appropriately to decrease training errors and decrease the likeli-
hood of developing stress injuries.
CONCLUSION
Compared to other sites of injury, stress injuries of the hip and pelvis have a significant risk for
poor outcome without proper treatment and recovery can take longer. The athlete can suffer from
missed competition and training for a prolonged period, but could also require surgical procedures
and have significant long-term negative effects. Multiple risk factors are associated with hip and
pelvis stress injuries, and it is important to be comprehensive in the evaluation, including special
attention to components of the female athlete triad. A high index of suspicion is required to diagnose
these injuries, and MRI has become the diagnostic study of choice in more recent years. Continued
research is needed in order to further identify ways to prevent and treat these injuries.
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Section II
Sport-Specific Injuries
12
The Contact Athlete
Football and Rugby
Travis Maak, MD and J. W. Thomas Byrd, MD
Contact athletes who are involved in collision sports, such as football and rugby, represent a
specific athletic subpopulation that is subjected to increased trauma and subsequent injury risk
compared to other athletes. Hip injuries in this population primarily occur in 3 main groups:
(1) injury secondary to femoroacetabular impingement (FAI), (2) subluxations, dislocations, and
fractures secondary to acute high-energy trauma, and (3) myotendinous injuries including con-
tusions, strains, and ruptures. Contact athletes are particularly prone to FAI-induced hip injury,
including labral and chondral injury, and instability due to the aforementioned increased loads
and impacts that occur at the hip joint in this subpopulation. Subluxations, dislocations, and frac-
tures may also occur and should be considered in the diagnostic algorithm. Lastly, myotendinous
injuries and contusions represent the most common hip injury in the contact athlete and occur
with increased frequency early in the season because of prior inactivity. This chapter will detail
each of these entities with a focus on pathophysiology, on the field and post-game assessment, and
tailored in-season and post-season management, including nonoperative and operative options.

190 Chapter 12
COMMON INJURIES
Clinical Pathophysiology
FAI is a phenomenon that occurs due to asphericity of the femoral head in the setting of cam
impingement, or excessive anterolateral acetabular osseous prominence in the case of rim impinge-
ment. Most commonly, however, these pathologies occur in combination. Cam impingement
principally occurs in young males, who represent the majority of the contact athlete population.
This impingement represents an inclusion mechanism of injury in which the osseous prominence
at the femoral head-neck junction directly impacts the anterolateral intra-articular border of the
labrum and chondrolabral junction during flexion and internal rotation of the hip. Subsequently,
increased shear and compression forces produce selective chondrolabral junction articular delami-
nation followed by secondary intrasubstance labral tears, ossification, and failure. Pincer impinge-
ment, on the other hand, represents an impaction mechanism of injury in which primary labral
failure occurs due to direct impaction of the prominent acetabular rim on the femoral head-neck
junction followed by secondary articular damage.
On-the-Field Evaluation
The game time evaluation of hip and thigh pain includes a focused patient history, physical
examination, and diagnostic assessment including indicated radiographic imaging. The on-field
evaluation including history and physical examination without plain radiographs will often iden-
tify the underlying pathology and enable rapid diagnosis and management during the athletic
activity.
FAI typically presents with complaints of groin pain that is exacerbated with hip hyperflexion,
such as deep squatting. The pain may have previously occurred intermittently and then have
acutely increased at the time of presentation. Mild to severe pain may exist, with up to 86% of
patients reporting moderate to severe pain at the time of presentation.1 Activities that require
increased hip flexion and internal rotation, as well as running and jumping.2-5 Additionally, the
athlete may report mechanical symptoms including popping, clicking, and catching within the hip
joint during motion. This complaint has been associated with the presence of a labral tear in an
athlete with groin pain and normal plain radiographic imaging.1,6,7
A careful sideline physical examination should include an evaluation of the lumbosacral
spine, hips, knees, and ankles. Lower extremity alignment should be assessed at rest and with
ambulation. Range of motion, strength, and stability should be assessed for each joint, and com-
pared to the contralateral side. Complaints of paresthesias warrant a lumbosacral examination,
although neurologic and hip pathology can concomitantly exist. These features of the physical
examination should be conducted for all injuries about the hip, but will not be repeated in the
following sections.
An exam specific for FAI should include a careful assessment of the hip range of motion with
particular focus placed on the internal and external rotation at 90 degrees of hip flexion. Limited
hip internal rotation (< 10 degrees) at 90 degrees of hip flexion has been closely associated with the
presence of FAI.8 The impingement test should also be performed with passive hip flexion, adduc-
tion, and internal rotation recreating the perceived groin pain. The posterior impingement test
with passive hip extension and external rotation should also be performed. Subspine impingement
beneath the anterior inferior iliac spine (AIIS) may be identified by pain elicited with passive hip
hyperflexion.9,10
If on-site radiographic facilities are available, plain anteroposterior (AP), lateral, and oblique
views of the lumbosacral spine and an AP pelvis radiograph and lateral hip view of the affected hip
should be completed. These images will enable evaluation of the acetabular version, or presence of
The Contact Athlete 191
Figure 12-1. (A) Axial oblique magnetic resonance imaging (MRI) and (B) sagittal MRI of a hip with underlying FAI in the
contact athlete. There is a prominent anterior cam morphology (circled) that is causing transition zone delamination
and detachment of the labrum (arrow) from the chondrolabral junction.
a crossover sign, which suggests acetabular retroversion and increased potential for impingement.
The femoral head-neck morphology and presence of a cam lesion can be evaluated through mea-
surement of the alpha angle on the Dunn lateral view. Notably, careful evaluation of these images
should include identification of stress fractures and articular incongruity, as these pathologic enti-
ties may also present with acute groin pain and should not be overlooked.
Post-Game Assessment
The post-game assessment of the athlete with a suspected hip, pelvic, or proximal lower extrem-
ity injury should serve to expand the aforementioned evaluation that was detailed for the injury-
specific on the field evaluation. The post-game assessment section primarily outlines a more exten-
sive, in-depth clinical and diagnostic evaluation that cannot be conducted on the field. Therefore,
this section should not be used in isolation, but rather in concert with the on-the-field evaluation.
The post-game assessment of the patient with suspected FAI should include an elongated
(Dunn) lateral plain radiograph and advanced diagnostic imaging including magnetic resonance
imaging (MRI) of the affected hip. MRI will provide detailed images of the peri-articular soft tis-
sues, including the acetabular and femoral chondral surface, capsule, labrum, and extra-articular
tendinous insertions. The current authors use cartilage-specific MRI sequences to evaluate the
cartilage integrity, although MRI arthrogram has also been used in this regard (Figure 12-1).
Following MRI evaluation, a fluoroscopic or ultrasound-guided hip intra-articular analge-
sic injection may be included in the diagnostic and therapeutic algorithm if there is suspected
intra-articular injury. Corticosteroids may be included in this injection to facilitate a prolonged
anti-inflammatory response, but are not necessary in the diagnostic algorithm. Patient-perceived
post-injection analgesia has been particularly effective in athletes with both intra-articular and
extra-articular pathology such as FAI and athletic pubalgia or lumbosacral pain. The response
to analgesic injection aids in determining which symptoms can be attributed to intra-articular
pathology and to what degree these symptoms will be alleviated by addressing this pathology. This
injection is not necessary in cases in which a clear clinical and radiographic assessment exists.
192 Chapter 12
In-Season Management
The in-season management of the contact athlete depends on multiple factors: specific and
concomitant pathology, injury severity, athletic position performed, response to nonoperative
management, athlete preference, and period within the season. Establishing an effective balance
of these options can be difficult; however, the management decision should primarily optimize the
health of the athlete and secondarily accommodate athletic participation.
Treatment Guidelines: Impingement-Related Injury
Acute operative in-season treatment of FAI is rarely indicated, given the chronic nature of the
pathology. Nevertheless, acute labral injury secondary to FAI can lead to significant debilitation.
In this setting, nonoperative management should include nonsteroidal anti-inflammatory medi-
cations (NSAIDs), intra-articular analgesic/steroid injections, and physical therapy. However, the
current authors rarely suggest more than a single intra-articular injection as chondral viability
may be compromised by repeated use of these medications.11,12 Physical therapy should focus on
hip and trunk muscle strengthening. Training modifications should also be instituted, including
avoiding loaded hip flexion beyond 45 degrees (ie, squats and lunges). A nonoperative management
regimen is particularly effective for athletes with nonspecific hip pain in the absence of mechanical
symptoms and minimal relief with an intra-articular injection. Additionally, this treatment may
allow the athlete to complete the in-season participation, with a plan for operative management to
be performed in the off-season, if indicated. This timing is preferred because of the suggested 4 to
6 months of postoperative rehabilitation that is required prior to return to contact sports.
Although nonoperative management may alleviate the athlete’s symptoms in the short term, it
is frequently ineffective in the setting of the young athlete with a large cam lesion and labral tear
because of the bony mechanical impingement that can only be addressed surgically. This pathol-
ogy frequently presents as isolated groin pain with complaints of mechanical symptoms, such as
locking, popping, and catching; radiographic pincer and/or cam impingement; and significant
pain relief from the intra-articular injection. In this case, consideration should be given to surgical
planning at the beginning of the off-season to maximize postoperative recovery. However, in some
circumstances, nonoperative treatment is ineffective as an in-season treatment, thus requiring
early operative intervention and restriction of athletic participation.
Operative management of FAI includes a combination of femoral head osteoplasty, acetabulo-
plasty, labral repair or debridement, and chondroplasty through an open or arthroscopic approach.
The indication for each of these procedures directly depends on the patient-specific osteology and
labral and chondral integrity. Treatment of FAI through an open surgical dislocation of the hip was
first described by Ganz et al13 and uses a greater trochanteric osteotomy and surgical dissection
to maintain the vastus lateralis insertion, external rotators, hip abductors, and femoral head vas-
culature. This open approach allows complete dislocation of the femoral head from the acetabu-
lum, which allows all of the aforementioned intra-articular pathology to be effectively addressed.
Careful capsular repair; rigid, anatomic fixation of the greater trochanter; and meticulous closure
minimize postoperative morbidity and dislocation risk.
Although open surgical dislocation has been used to effectively treat FAI, the morbidity of
this open procedure may be reduced with an arthroscopic approach. Arthroscopic manage-
ment of FAI has been associated with excellent surgical outcomes.14-16 Current data suggest that
acetabuloplasty, labral repair, and femoral neck osteoplasty may produce superior results, as com-
pared to labral resection.14,15 Preservation of this tissue is particularly critical in the setting of
acetabular dysplasia or excessive femoral anteversion. In these cases, significant iatrogenic injury
to the labrum or excessive acetabular rim osteoplasty may render the hip unstable and prone to
dislocation. The stability of the hip is directly dependent on the complex osseous and soft tissue
stabilizers and thus complete evaluation of the osseous morphology should be performed prior
to operative intervention. Notably, the athlete will require restricted activity for approximately
4 to 6 months postoperatively.
Rehabilitation and Return to Play

Rehabilitation and return to athletic participation is primarily determined by the resolution
of symptoms and return of functional strength and motion. The goal of this regimen is to first
optimize the treatment outcome, and then to minimize the time that is required for return to full
athletic participation.
In-season rehabilitation and return to play must be subdivided into nonoperative treatment
rehabilitation and operative treatment rehabilitation following either open or arthroscopic surgery.
Rehabilitation for nonoperative treatment for FAI should focus on directed trunk, quadriceps, ham-
string, hip extensor, and especially abductor strengthening. Improving the peri-articular muscular
envelope will optimize dynamic hip stability and minimize the risk of FAI-induced instability.
Initial rehabilitation following arthroscopic or open treatment of FAI should occur immedi-
ately in the recovery room. Restricted 50% or 20-pound, foot-flat weight bearing is required with
crutches if a labral refixation or microfracture is performed, respectively. Isolated femoral osteo-
plasty may be allowed to bear weight as tolerated with crutches. These weight-bearing restrictions
are maintained for the first 4 weeks postoperatively. Complete non-weight bearing should not be
used, as this status will increase intra-articular hip joint reaction forces and may cause hip flexor
irritation. Unrestricted weight bearing may be allowed following an isolated acetabuloplasty.
A continued passive motion device or an exercise bike with no resistance may be used postopera-
tively to improve hip range of motion and limit stiffness. Directed active and passive hip range
of motion should also be performed during rehabilitation sessions. A transition to strengthen-
ing exercises typically occurs at the 6-week postoperative time point, when painless hip passive
full range of motion is achieved. This program is similar to the aforementioned regimen used in
nonoperative management of FAI.
Return to full athletic participation is variable and directly correlates with the specific opera-
tive intervention. This period typically ranges between 4 and 6 months following acetabuloplasty,
labral repair, and femoral head-neck osteoplasty. Contact athletes should maintain complete
restriction from impact for at least 3 months to ensure complete osseous remodeling to minimize
the risk of femoral neck fracture at the site of the head-neck osteoplasty.
Subluxations and Dislocations

Hip instability with subluxation or dislocation is relatively rare as compared to dislocations
of the shoulder or knee in the athletic population. Nevertheless, the contact athlete may be at
increased risk for this injury because of the traumatic nature of sports including football, rugby,
and soccer. In fact, posterior hip subluxations or dislocations have largely been described in con-
tact sports, with up to a 28% prevalence among hip injuries in this population.17 These instabil-
ity episodes were also associated with a significantly increased time required prior to return to
play. Permanent sequelae may also occur, including femoral head osteonecrosis. Prior data have
documented severe femoral head osteonecrosis and subsequent total hip arthroplasty in 2 profes-
sional football players.18 The risk of these devastating sequelae is directly proportional to the time
elapsed between hip dislocation and reduction.19 For this reason, rapid diagnosis and treatment of
hip subluxation or dislocation is crucial to optimizing the athlete’s outcome.
Hip subluxations and dislocations in the contact athlete typically occur acutely and in a pos-
terior direction as a result of a fall or direct impact on a flexed, adducted hip. Atraumatic sublux-
ations may also occur but are typically due to underlying hip instability such as in the setting of
joint hypermobility or abnormal osseous anatomy.20,21 The athlete frequently experiences painful
hip motion with a limited range of motion. The pain may occur with standing and ambulation and
194 Chapter 12
Figure 12-2. MRI scans after a posterior hip subluxation. (A)

The sagittal view demonstrates posterior capsular disruption,
large effusion, and a chondral loose fragment (circled) in the
anterior gutter. (B) The axial view demonstrates a posterior
bony labral tear (arrow) with associated bony avulsion frag-
ment, and an anterior labral crush injury. These findings,
along with injury to the ligamentum teres, are typical from
this injury mechanism.
may be exacerbated with hip hyperflexion. The pain is most commonly localized to the groin and
anterior hip and thus may be misdiagnosed as a muscle strain or groin pull.20,21
A focused on-the-field physical examination should include evaluation of the active and passive
range of motion of the hip as well as the attitude of the joint. Athletes who have sustained an unre-
duced posterior hip dislocation maintain a flexed, adducted, and internally rotated hip position
with a perceptible limb length discrepancy due to the proximal migration of the dislocated femoral
head. Also, the passive and active range of motion, specifically hip external rotation, will be signif-
icantly restricted as the femoral head may be positioned posterior to the posterior acetabular wall.
Lower extremity strength and neurologic evaluation should also be assessed, as injury to the sciatic
nerve may occur with a posterior hip dislocation. A single reduction attempt may be attempted on
the field prior to the onset of muscle spasm. Nevertheless, multiple reduction attempts should not
be attempted prior to radiographic evaluation, as exacerbation of more complex injury may occur.
Posterior hip subluxations or spontaneously reduced dislocations are far more difficult to diag-
nose, as a normal range of motion is often maintained and pain may present only at the extremes of
motion. These subluxations and dislocations may also be associated with posterior acetabular rim
fractures, but may not have increased symptoms. As a result, the athlete may attempt to continue
play despite the severity of this injury as seen on postinjury MRI (Figure 12-2).
Plain radiographic evaluation of this suspected injury should include an AP pelvis and cross-
table lateral of the affected hip. Oblique (Judet) views may also be obtained to more carefully evalu-
ate the integrity of the anterior and posterior acetabular wall for potential fracture. Concomitant
posterior acetabular wall fractures have been frequently associated with posterior hip dislocations
and should be identified (Figure 12-3). A high degree of suspicion should be maintained during
this radiographic evaluation as the athlete’s symptoms may be minimal and the on-site radio-
graphic quality may be compromised.
Post-game assessment of subluxations and dislocations about the hip involves more extensive
plain radiographic imaging, computed tomographic (CT) scan, and MRI. A CT scan should also
be obtained, especially in the setting of relocated hip dislocation, to evaluate the congruity of
the reduction and to fully delineate all other associated fractures. In the setting of a congruent
Figure 12-3. (A) Posterior wall fracture seen on the anteroposterior (AP) pelvis view (arrow) should make the clinician
suspicious for a posterior hip subluxation event. (B) Incongruous joint spacing in right hip due to incarcerated labrum
following subluxation event.
reduction, an MRI should be obtained to identify any associated soft tissue injury, including ilio-
femoral ligament or chondrolabral injury, retained intra-articular fragments, or hemarthrosis.20,21
Specific patterns of increased signal have been associated with specific injury types. Signal change
present in the psoas directly adjacent to the anterior hip capsule may indicate an acute anterior
hip subluxation. Similarly, signal change that is present in the posterior hip musculature near the
capsule may indicate an acute posterior hip subluxation. A concomitant posterior acetabular rim
fracture may exist in this setting. The location of this fracture produces a cortical, avascular frac-
ture fragment that may be misinterpreted as a posterior labral tear on MRI. In this case, further
evaluation with a CT scan should be considered (Figure 12-4).
Occult femur and acetabular fractures may also be identified with this modality. The current
authors have anecdotally identified an association between anterior labral tears and posterior hip
subluxation or dislocation episodes. This concomitant injury may occur from an impact between
the cam lesion and anterior acetabular labrum during the dislocation episode.
In-season management of a hip subluxation or dislocation is determined by the specific
concomitant injury, including hemarthrosis, chondrolabral injury, intra-articular loose bod-
ies, and fracture. Hemarthrosis should be managed in the acute setting with an intra-articular
aspiration, restricted hip range of motion, and foot-flat weight bearing for 4 to 6 weeks until
symptoms abate. Chondrolabral injury and intra-articular loose bodies should be addressed with
the aforementioned hip arthroscopic treatment guidelines (Figure 12-5). If hip arthroscopy is
performed less than 6 weeks from the index injury, careful intraoperative abdominal evaluation
should be performed because of the risk of intra-abdominal fluid extravasation secondary to
acetabular or capsular injury. Follow-up diagnostic MRI should be performed 6 weeks following
injury to screen for preliminary signs of femoral head osteonecrosis. Chondrolabral injury may
be addressed in the subacute period if the athlete is able to sufficiently rehabilitate and there are
no intra-articular loose bodies or displaced fractures. However, if intra-articular loose bodies are
identified, acute hip arthroscopic removal should be conducted to minimize the risk of posttrau-
matic hip arthrosis.20,21
196 Chapter 12
Figure 12-4. Computed tomography (CT) scans with

3-dimensional reconstructions can confirm the size and loca-
tion of the posterior rim fracture. With 3 rotational views, very
clear identification of the rim fracture can be made, and an
improved understanding of the mechanical forces that led to
the injury can be predicted.

Directed rehabilitation following a hip subluxation or dislocation in the absence of fracture
should begin with restricted foot-flat weight bearing to minimize the hip joint reaction forces for
a minimum of 6 weeks. A cartilage-sensitive MRI should be obtained at the 6-week time point
to evaluate for intra-articular chondrolabral injury or femoral head osteonecrosis. An additional
6-week period of toe-touch weight bearing is required if femoral head osteonecrosis is identified.
The aforementioned FAI postoperative rehabilitation regimen should be employed if operative
treatment of chondrolabral injury is required. Close observation and careful clinical progression
should be maintained throughout this period because of the high-energy injury mechanism. Gen-
tle active and passive range of motion should begin immediately following injury and may prog-
ress in accordance with the resolution of pain. The aforementioned strengthening should begin
when full range of motion is acquired. Return to full athletic participation requires functional hip
range of motion and strength, and is typically allowed as early as 2 months, but more commonly at
3 to 4 months following injury. Notably, Feeley et al17 documented an average 126.2 days required
to return to play following subluxation or dislocation events, which represented the greatest aver-
age time lost for any hip injury.
Figure 12-5. Arthroscopic findings after acute hip sub-

luxation demonstrate severe intra-articular damage.
(A) Complete avulsion of the ligamentum teres with asso-
ciated chondral loose fragment. (B) Posterior labral injury
with the associated bony attachment of the posterior wall
that is seen on the plain x-rays and the computed tomogra-
phy (CT) scan. (C) Posterior anchor placement.
Fractures of the Femoral Neck and Pelvic Ring

Fractures of the femoral neck and pelvic ring/acetabulum typically present in the athletic
population in the form of a stress fracture due to repetitive activity and overload of physiologi-
cally normal bone (Figure 12-6). This repetitive overload pathophysiology is in direct contrast to
the insufficiency fractures that are commonly seen in the elderly, osteoporotic population. Previ-
ous studies have documented the incidence of stress fractures at approximately 1% in the general
population and up to 20% in the repetitive overload athlete.22 This marked increased prevalence
has been attributed to altering training programs, including increases in duration, intensity, and
frequency that may produce increased osteoclast activation and bone resorption. This imbalance
with increased resorption and insufficient formation due to submaximal, repetitive loading may
produce the clinically documented increased stress fracture risk in the athletic population. Con-
genital osseous femoral neck morphology including coxa vara and weakness of the hip muscula-
ture may also predispose the athlete to stress fractures.
The contact athlete not only is subjected to repetitive loads, and therefore at an increased risk
for stress fractures of the femoral neck and pelvic ring, but also experiences high-energy, acute
impact loading that may increase the risk of an acute, traumatic fracture. These fractures must
be quickly recognized and managed given the high association between femoral neck fractures
and femoral head osteonecrosis.23 Fractures of the acetabulum can produce hip instability, espe-
cially in the setting of a large posterior wall fracture, and can increase the risk of posttraumatic
198 Chapter 12
Figure 12-6. Femoral neck stress fracture on the tension

side of the femoral neck has high risk for fracture and varus
collapse (arrow on MRI). Tension-sided stress fractures
should be treated aggressively with percutaneous, prophy-
lactic pinning to avoid fracture displacement.
hip arthrosis if intra-articular incongruity is not addressed.24,25 These posterior acetabular frac-
tures have been documented to account for 45% of all intra-articular hip injuries in the National
Football League (NFL).17
On-the-field evaluation of femoral neck and pelvic ring fractures is crucial to determine the
ability of the athlete to return to or be removed from play. Athletes who have sustained these
injuries frequently complain of groin and inferior pelvic pain that is increased with weight bear-
ing and further increased with high-impact hip loading such as running and jumping. Pain is
typically relieved with rest and reduced weight bearing such as sitting or lying supine. Femoral
neck and pelvic ring stress fractures frequently present following an acute increase in the intensity,
frequency, or duration of athletic training. For the contact athlete, this increased training typically
occurs during preseason training following the off-season period. Symptoms frequently include an
antalgic gait and groin pain with passive hip rotation. Care should be taken to address hip rotation
at both 0 and 90 degrees of hip flexion as these fractures typically produce pain with rotation in
both positions, as compared to FAI, which typically presents with pain only at 90 degrees of hip
flexion. While sacral insufficiency fractures are rare in the contact athlete, these fractures present
with pain with passive flexion, abduction, and external rotation. Additionally, pelvic brim tender-
ness to palpation may occur, although this tenderness is not a sensitive sign because of the sig-
nificant overlying soft tissue. Finally, a careful lower extremity neurologic examination should be
performed to identify any peripheral nerve injury or injury within the lumbosacral neuroforamen.
Plain radiographic imaging is fundamental for diagnosis and treatment of femoral neck and
pelvic ring fractures, as the location and displacement of the fracture will directly affect the treat-
ment algorithm. Femoral neck stress fractures can be subdivided into tension (superior neck) or
compression (inferior neck) fractures. This fracture is principally identified on the AP pelvis and
lateral hip radiographs, but may vary in presentation depending on chronicity. Fracture sclerosis
or periosteal reaction may be identified in the subacute setting, while acute, nondisplaced stress
fractures may not be evident on plain radiograph at the time of injury. Sclerosis may be identified
at the inferior femoral neck cortex in compression-type femoral neck fractures, and transverse
lucency perpendicular to the superior femoral neck may indicate a tension-type fracture. Oblique
(Judet), inlet, and outlet views of the pelvis should also be obtained when consideration of a pelvic
ring fracture exists. These views allow rapid evaluation of the anterior and posterior walls of the
acetabulum as well as the pelvic ring and sacrum.
The post-game assessment of suspected or confirmed femoral neck and pelvic ring fractures
varies depending on the type of fracture. Identification of a displaced or nondisplaced fracture
on plain radiographic imaging will frequently obviate the need for further diagnostic imaging.
Nevertheless, the current authors frequently obtain MRI of the affected hip to evaluate for con-
comitant soft tissue injury as well as identify potential associated occult fractures, such as those
of the greater trochanter. CT scan may also be obtained in select circumstances to aid in operative
planning, if indicated.
Suspected stress or occult fractures of the femoral neck and pelvic ring, on the other hand,
should be identified using nuclear imaging or MRI. Although nuclear imaging provides a high-
sensitivity examination of the complete skeleton, it requires a significant time commitment,
the spatial resolution is limited, and it is an invasive procedure. Conversely, MRI can be used
effectively to evaluate occult fractures and concomitant soft tissue injury. MRI evidence of stress
fractures includes decreased signal intensity on T1 images and increased intensity on short tau
inversion recovery (STIR) and T2-weighted images. The tomographic location of the fracture is
particularly important for femoral neck and acetabular fractures and serves to guide the manage-
ment decision-making process.
Fractures of the femoral neck and pelvic ring must be subdivided into low-risk and high-risk
fracture patterns in order to guide in-season management. Low-risk fracture patterns include
nondisplaced acetabular fractures of the anterior or posterior acetabular wall compromising less
than 20% of the wall, compression-side nondisplaced stress fractures of the femoral neck, and
pelvic ring and sacral stress fractures. Compression-side stress fractures of the inferior femoral
neck represent a stable fracture pattern that can be appropriately managed nonoperatively. Activity
modification with or without restricted weight bearing (dependent on the athlete’s pain level) will
achieve excellent results in the majority of cases with minimal risk of fracture displacement. Simi-
larly, small, nondisplaced acetabular wall fractures may be managed nonoperatively with initial
restricted weight bearing for 4 to 6 weeks followed by gradual advancement of weight bearing over
a 6-week period. Pelvic ring and sacral stress fractures may be effectively managed with activity
modification in most cases.
High-risk fracture patterns include acetabular fractures of the weight-bearing dome of the
acetabulum, acetabular wall fractures, and tension-side femoral neck stress fractures. Tension-
side femoral neck stress fractures have a higher risk of displacement because of the biomechanical
forces that promote fracture distraction rather than compression. Fracture displacement should
be avoided if possible because of the severe sequelae, including delayed union, nonunion, varus
malunion, and femoral head avascular necrosis (AVN). For this reason, tension-side femoral neck
fractures should be acutely treated with operative internal fixation with cannulated screws. This
operative treatment should also be employed for compression-side fractures that demonstrate
radiographic evidence of displacement. Postoperative management typically includes 12 weeks of
restricted weight bearing that is tailored based on pain resolution and radiographic healing. Large
acetabular wall and column fractures are also typically treated acutely with internal fixation.
The treating medical staff should also evaluate and treat any hormonal or nutritional abnor-
malities that may be present in any athlete with a stress fracture. Although these deficiencies are
infrequent in the contact athlete population as compared to the endurance athlete population, they
should not be overlooked. Connective tissue diseases should also be considered and the evaluation
tailored based on the physical examination and patient history.
Rehabilitation and return to play following femoral neck and pelvic ring fractures is guided by
the resolution of symptoms and radiographic evidence of healing. Low-risk, stable stress fractures
200 Chapter 12
including compression-side femoral neck, pelvic ring, and sacral fractures may be allowed
restricted weight bearing with crutches for comfort to alleviate intra-articular pain. The weight-
bearing status can be progressed as tolerated as pain resolves. Active and passive range-of-motion
exercises should be employed throughout this period to minimize injury-related stiffness. The
athlete may begin low-impact activity as symptoms improve. This activity may be advanced to full
activity if symptoms continue to abate. Return to contact play is closely dependent on the sever-
ity of the lesion; the aforementioned low-risk fractures may be allowed to return to full activity at
3 to 6 weeks and high-risk fractures may require up to 16 weeks before contact sports are allowed.
High-risk fractures including tension-side stress femoral neck, displaced acetabular wall, and
dome fractures should be managed surgically in the aforementioned fashion. Following surgical
stabilization, the rehabilitation may progress as outlined for low-risk fractures. Return to full
athletic activity, including contact sports, is allowed when symptoms are completely resolved,
provocative maneuvers are painless, and the athlete is able to perform sport-specific functional
activities symptom free. Radiographic evaluation including plain radiographs and CT scan may
aid in evaluation of hardware placement and fracture healing. Prior data documented an average
return to play of 100.6 days for all hip fractures.17
Myotendinous Strains and Avulsions

Myotendinous strains and avulsions are extremely prevalent in the athletic population and
are responsible for a significant amount of restricted participation.17 An increased frequency of
these injuries has been identified during pre-season training as compared to in-season play. This
increase has been hypothesized to be associated with the rapid change in training intensity and
duration that occurs between the off-season and pre-season. For this reason, many trainers and
physicians currently emphasize the importance of maintaining a high level of endurance and con-
ditioning during the off-season.
Strains and Avulsions: The Hip
Myotendinous hip strains and avulsions include injury to the rectus femoris, hip adductors, and
rectus abdominis. Strains to the rectus femoris commonly occur with activities that require rapid
muscle contraction such as kicking or sprinting. The risk of injury may be further increased with
eccentric hip extension during active hip and knee flexion. The direct or reflected head may be
injured, and increased disability has been associated with direct head injury 26 (Figure 12-7). Cen-
tral tendon injury may also produce proximal thigh pain and a prominent mass that may require
surgical excision. Proximal strain of the direct and reflected heads of the rectus femoris may also
lead to formation of heterotopic bone at the tendon insertion. This bone can produce subspine
or AIIS impingement with associated groin pain and limited hip flexion. Prior authors have also
documented proximal rectus femoris avulsions in 11 professional football players in the NFL.27 All
of these contact athletes were managed nonoperatively and returned to play within 6 to 12 weeks
following injury.
Hip adductor strains and avulsions commonly present acutely in contact sports that require
rapid pivoting such as ice hockey and soccer. The adductor longus is most commonly involved,
with self-limited pain and rapid return to play within days or 1 to 2 weeks of injury. Chronic
medial hip and groin pain, on the other hand, is more commonly associated with FAI in up to 94%
of athletes.28 Lower abdominal pain that increases with exertion with or without radiation into
the groin may be due to athletic pubalgia or core muscle injury.29,30 Associated proximal adductor
pain may also be present.
Figure 12-7. Avulsion of the direct head of the rectus

femoris with approximately 4 cm of displacement.
Strains and Avulsions: Quadriceps and Hamstrings

Quadriceps strains and distal quadriceps tendon ruptures represent 2 distinct management
entities with a common pathophysiology. Eccentric lengthening of the contracting quadriceps
muscle group is the principal injury mechanism and injury typically occurs at the myotendinous
junction. The distal head of the rectus femoris is most commonly affected. Additionally, quad-
riceps fascial rupture may occur in the mid-anterior region and produce a muscular herniation.
While rare, distal quadriceps tendon ruptures may also occur in the contact athlete because of the
high energy that is sustained during impact.
Acute hamstring strains can require an extended period of restricted activity prior to return
to play ranging from a few days to up to 8 weeks.31 Recurrent injury within 3 weeks of the index
injury has been associated with lateral hamstring injury.31 Contact athletes are particularly sus-
ceptible to proximal hamstring ruptures given the high load and rapid, eccentric lengthening that
may occur during these sports. For this reason, a careful evaluation should be performed and
diagnostic suspicion should be maintained when the athlete presents with complaints of proximal
hamstring, buttock pain. Fortunately, however, these injuries remain relatively rare even in the
contact athlete.
Myotendinous strains and avulsions represent one of the most commonly presenting injuries
surrounding the hip joint. Strains of the rectus femoris, rectus abdominis, and hip adductors
typically present with complaints of anteromedial hip and groin pain that is exacerbated with
increased activity. Pain from proximal rectus femoris strains may localize in a more anterior posi-
tion, as compared to the medial pain experienced with hip adductor and rectus abdominis strains.
Quadriceps strains typically present with anterior mid-thigh pain, although pain may occur along
the length of the muscle from proximal to distal. Hamstring strains present with posterior buttock,
thigh, or knee pain depending on the location of injury. Notably, the myotendinous junction is the
most common site of injury; however, this site is long and variable within the hamstring muscle
group and thus the location of tenderness may be variable along the posterior thigh. The onset of
the pain is acute and frequently coincides with a history of rapid deceleration, acceleration, or cut-
ting event. A history of direct impact may also present with an eccentric elongation during muscle
contraction. The athlete may also report a popping sensation in the buttock region for proximal
avulsions or distal, posterior thigh for distal avulsions.
202 Chapter 12
A careful physical exam may be more effective than the patient history at identifying the
location of injury. Focal tenderness to palpation may aid in pinpointing the location of injury
within each muscle group. Palpation should be conducted along the entire muscle belly, tendon,
and enthesis of each muscle. Avulsions may present with a palpable defect and tender soft tissue
prominence near the region of the defect. Strains, on the other hand, may present with tenderness
within the muscle belly and a palpable fullness at the injury location. Rectus abdominis strains
frequently present with tenderness to palpation at the inguinal ligament, abdominal obliques,
transversus abdominis, and rectus abdominis/conjoined tendon. Focal pain may be elicited with
resisted sit-ups with concomitant hip adduction. Hip adductor injury may present with medial
groin tenderness to palpation along the adductors, gracilis, or pectineus, and pain with resisted
hip adduction. Palpation along the proximal adductor tendons and at the insertion may aid in
differentiating between an enthesis and myotendinous injury. Rectus femoris injury may present
with pain with resisted active hip flexion and knee extension. This pain differs from injury to the
vastus muscle group, in which active hip flexion is typically painless and resisted knee extension is
painful. Hamstring injury produces pain with resisted active knee flexion and hip extension. Care
must be taken during examination of quadriceps and hamstring injuries to palpate the integrity
of the tendon proximally and distally as the management of tendon avulsions significantly differs
from that of intrasubstance muscle strain.
Plain radiographs are frequently normal in the setting of myotendinous strains but may dem-
onstrate small osseous fragments at the site of tendon avulsion. For this reason, plain radiographic
imaging should be obtained for athletes presenting with pain and tenderness proximally at the hip
or distally at the knee. These images can also serve to identify concomitant, confounding pathol-
ogy with a similar presentation such as FAI or osteitis pubis. In the acute setting, pain and tender-
ness in the mid-substance of the quadriceps or hamstring does not require radiographic evaluation
unless the rare suspicion of a diaphyseal femoral fracture exists.
The post-game assessment of myotendinous strains and avulsions should include MRI. The
treating medical staff should identify increased signal on STIR and T2-weighted images to local-
ize the site of injury. The degree of increased signal within or surrounding the injured muscle
may loosely correlate with the severity of injury. Nevertheless, this correlation does not neces-
sarily reflect the time that is required to return to play. Careful evaluation of tendon origins and
insertions should be conducted to ensure that a tendon avulsion or rupture is not overlooked.
Similarly, recurrent or chronic myotendinous injuries about the hip and pelvis should be identi-
fied, as these injuries may suggest a possible association with athletic pubalgia, sports hernia, or
other compensatory soft tissue injury secondary to intra-articular hip pathology. Multiple abnor-
malities identified on MRI have been correlated with athletic pubalgia/sports hernia, including
proximal adductor/gracilis/pectineus abnormalities, perisymphyseal edema, and disruptions of
the rectus abdominis.30 These abnormalities may also occur concomitantly with FAI, in which
case the aforementioned MRI findings may also exist.32 Previous data obtained from a study of
professional football players in the NFL identified a “sports hip triad,” which included an adductor
strain, labral tear, and rectus strain. The etiology for this injury triad was attributed to increased
rotational and axial loads to the hip during high-impact athletics.17
In-season management of myotendinous strains and avulsions, including injuries to the quad-
riceps, hamstrings, adductors, and rectus femoris, commonly includes activity modification,
analgesics, ice, and incremental return to athletic activity as pain abates and functional strength
returns. Acute management of myotendinous strains should include continuous compression of
the injured muscle in a stretched position (hip extension and knee flexion for a quadriceps strain
and hip flexion and knee extension for a hamstring strain) for a minimum of 24 hours. Active,
low-impact range of motion on an exercise bicycle with a seat height that maximizes muscle stretch
(high seat for hamstring and low seat for quadriceps strain) should also be encouraged imme-
diately following injury. This treatment methodology includes treatment of complete proximal
adductor ruptures and minimally retracted complete proximal hamstring ruptures. While both
operative and nonoperative management have previously been used for both injuries, prior data
from the NFL have documented a 6-week return to participation with nonoperative management,
as compared to 3 months with operative management.27 Physical therapy and platelet-rich plasma
(PRP) have also been suggested in the treatment algorithm for these injuries. However, a paucity
of literature exists regarding the efficacy and outcomes of these modalities for treatment of acute
and chronic myotendinous injuries. The use of ultrasound-guided aspiration of local fluid collec-
tions and simultaneous infusion of low-dose corticosteroid medication may reduce the duration of
recovery time and facilitate more rapid return to play in selected cases.
Some exceptions to these cases include (1) chronic, recalcitrant proximal adductor pain,
(2) acute complete proximal hamstring rupture involving 2 or 3 tendons with greater than 2 cm
of retraction, (3) symptomatic chronic proximal hamstring rupture, (4) complete distal quadri-
ceps tendon rupture, and (5) recalcitrant athletic pubalgia/core muscle injury. Surgical tenotomy
has been effectively used for treatment of chronic, recalcitrant proximal adductor pain, and has
resulted in the majority of athletes returning to sports participation. Complete, retracted ham-
string ruptures should be treated acutely with direct repair to minimize long-term strength deficits
and athletic disability.33,34 Chronic, symptomatic hamstring ruptures may be treated with distal
fractional lengthening and repair or proximal hamstring allograft reconstruction, which has been
associated with improved function and strength.33 Athletic pubalgia or sports hernia may be pri-
marily managed with activity modification, rehabilitation with core strengthening, and possible
corticosteroid injection into the pubic symphysis and adductor/pelvic cleft. However, recalcitrant
cases may require surgical intervention, including pelvic floor and modified hernia repairs with
or without complete or partial adductor release.29,30 Previous studies have documented improved
return to athletic participation with these surgical interventions.29,30
Rehabilitation and return to full contact sports following myotendinous strains and avulsions
must be separated into nonoperative rehabilitation and operative rehabilitation. Nonoperative
treatment should occur in the aforementioned fashion as detailed in the in-season management
section. Maintenance of full range of motion of the hip and knee joints should be the initial reha-
bilitation goal, which should be followed by functional strengthening and symptom-free sports-
specific activity. Focused stretching and muscle activation may be employed during this period to
minimize intramuscular edema and optimize muscle contraction. Return to play typically occurs
within days to weeks from the initial injury. Notably, while many NFL treatment regimens cur-
rently exist, all strategies use rest, compression, ice, immobilization with the muscle in a stretched
position, and early range of motion in an attempt to minimize hematoma formation and maximize
injury recovery.10
Operative management of hamstring and quadriceps tendon avulsions requires a carefully
directed postoperative rehabilitation regimen that includes initial joint immobilization with the
knee flexed and extended, respectively. A hinged knee brace is used for joint immobilization
for the first 4 to 6 postoperative weeks to allow tendo-osseous healing. Isometric exercises may
be employed during this period to minimize muscle atrophy. Gradual active and passive range
of motion may be instituted at 4 to 6 weeks and should continue until full motion is achieved.
Strengthening typically begins 3 months postoperatively and requires full range of motion with
minimal pain. Return to full athletic participation is allowed 6 to 9 months postoperatively when
functional motion and strength is established.
204 Chapter 12
Contusions and “Hip Pointers”

Although contusions can occur to any exposed muscle, quadriceps contusions are more com-
mon than any other muscle group contusions. This increased risk is likely due to the location of
the quadriceps at the anterior, mid-body region. These contusions are often due to direct trauma
to the quadriceps that results in acute compression between the offending object and the femur.
Subsequent intramuscular hemorrhage and edema can lead to significant temporary disability.
Contusions represent the second most common injury in the collision athlete.17
Hip pointers occur because of direct compressive trauma to the prominent subcutaneous
iliac crest or prominence over the greater trochanter. This impact produces a painful soft tissue
and bone contusion at the site of impact. This pain mimics that of a focal muscle contusion but
typically does not worsen with increased activity. Subcutaneous, intramuscular, or subperiosteal
hemorrhage may occur. While hip pointers represent up to 32% of hip contusions, the disability
associated with hip pointers significantly varies.17,35
Direct trauma may also occur parallel to the plane of the muscle and skin, which produces
a shearing force and possible degloving injury, as compared to the perpendicular compressive
force seen in muscle contusions. These degloving injuries produce a separation of the skin and
subcutaneous tissue from the underlying fascia.36 When this injury occurs on the lateral aspect
of the thigh, it has been termed a Morel-Lavallée lesion and is frequently associated with high-
energy impact injury. This injury mechanism can also occur in contact and especially collision
sports. The lateral thigh/peritrochanteric region is particularly susceptible to this injury mecha-
nism because of the mobility of the skin and subcutaneous tissue relative to the immobile greater
trochanter. Nevertheless, these lesions can present in any area with a similar anatomic relation-
ship, including the distal medial or lateral aspect of the knee or elbow.
Contusions and hip pointers occur more commonly in the contact athlete than other athletes
because of the high energy and direct impact that occurs in contact athletics. In this vein, the
athlete typically has an acute history of direct impact at the site of the injury with immediate focal
pain. This impact may occur during player-to-player contact, a fall to the ground, or other direct
collision. The athlete typically will describe an ache and swelling that localizes to the region of
injury. The quadriceps represents the most common site of injury because of its anterior exposed
location. The hip pointer is a specific type of direct-impact injury that occurs at the lateral iliac
crest. A direct impact in this location may produce a bone bruise at the site of impact that can
be focally exquisitely painful at rest and exacerbated with trunk motion. The Morel-Lavallée
shearing-type impact injury also represents a unique subset of direct-impact local soft tissue inju-
ries. The athlete will typically present with complaints of a local fluctuant swelling with or without
pain following the aforementioned shearing injury mechanism.
Physical examination of contusions and hip pointers will demonstrate focal tenderness to pal-
pation at the location of injury. Active contraction of the involved muscle group may also elicit
pain due to the local muscle injury. This pain may be less severe than that which is experienced
following a muscle strain; however, the 2 clinical entities may be difficult to differentiate. Swell-
ing and ecchymosis at the site of impact may also exist. Physical examination of the hip pointer
frequently reveals pain at the location of impact with resisted trunk lateral bending toward the site
of injury. This pain is due to abdominal muscular traction at the insertion site on the iliac crest.
The Morel-Lavallée lesion has a very characteristic examination that demonstrates a fluctuant
region localized over a superficial osseous prominence. Ecchymosis and tenderness to palpation
may exist acutely, while the fluctuance may persist for an extended period after the ecchymosis
and tenderness has resolved.
Plain radiographic imaging is rarely required in the setting of muscle contusion or hip pointers.
Typically, imaging is obtained only if there exists a heightened concern for fracture because of pain
out of proportion to the injury or an extremely high-energy injury mechanism.
A post-game assessment of contusions and hip pointers beyond that which was performed
during the on-the-field assessment is rarely required. An MRI may be obtained in the rare cir-
cumstance that a concomitant myotendinous strain, avulsion, or other injury is suspected and the
athlete has persistent pain out of proportion to what is expected for the specific injury. Of note,
however, is the possibility of an associated intramuscular or subfascial hematoma. The presence of
this pathology may be suspected in the setting of significant swelling with or without fluctuance
and increased ecchymosis that is located outside the immediate zone of injury. MRI is particularly
helpful in this setting, both for initial confirmation and to guide potential future aspiration.
In-season management of contusions may be conducted as detailed in the aforementioned dis-
cussion of acute management of myotendinous strains including compression in combination with
muscle stretch for 24 hours followed by immediate motion. In the rare circumstance that an MRI
is required and demonstrates a large hematoma, an ultrasound-guided aspiration of the collection
may be indicated. Hip pointers in higher-level athletes may be acutely managed with an anesthetic
injection over the iliac crest; however, optimum in-season management should focus on carefully
padding the region to minimize future, recurrent injury.
The Morel-Lavellée lesion represents a unique subset injury that can also be initially managed
with ice and compression. This regimen will result in complete resolution of up to 50% of these
injuries. However, refractory cases may be managed with acute aspiration with or without doxy-
cycline sclerodesis and continued compression.36 Reaccumulation of fluid may occur and may be
exacerbated with increased activity. Repeated aspiration may be used as necessary. In rare, refrac-
tory cases, surgical intervention may be necessary to evacuate associated fluid collection and to
close down any dead space that may be causally related to persistent symptoms.
Rehabilitation for muscle contusions of the hip and thigh may be followed in a manner simi-
lar to the aforementioned regimen described for myotendinous strains. Maintenance of range of
motion while optimizing edema control and hematoma formation should be the primary goal.
Prior data have demonstrated a significantly reduced period of restricted activity with the use
of a knee flexion rehabilitation protocol.37,38 In one study, knee flexion to 120 degrees within
10 minutes following injury and maintained for 24 hours reduced the mean disability time to
only 3.5 days.37 In addition, care should be taken to avoid extensive stretching and heating of the
affected area as this may further exacerbate the traumatic hemorrhage. The traumatized region
should also be carefully protected with padding to minimize the potential for repeated injury
and subsequent myositis ossificans. Return to play is allowed when functional range of motion,
strength and symptom-free sport-specific activity has been achieved and generally occurs less than
1 to 2 weeks postinjury. Rehabilitation following a hip pointer is focused on maintenance of trunk
range of motion and reduction of pain. Strength training for trunk musculature should be avoided
until symptoms subside. Return to play is allowed when the contact athlete can acceptably perform
functional activities and typically occurs within days of the injury.
206 Chapter 12
PEARLS AND PITFALLS

● Contact athletes demonstrate an increased risk of FAI-induced injury, including resultant
subluxation/dislocation.
● In this population, subtle instability may be difficult to discern, as the athlete may demon-
strate range of motion within normal limits, with only end-range pain. Athletes may attempt
to play through this; therefore, imaging is extremely important to highlight the extent of intra-
articular injury, and to prevent further injury.
● Off-season conditioning is imperative because of the increase risk of myotendinous injuries
in the preseason or incipient stages of the regular season. One must examine these injuries
very carefully be to able to discriminate avulsions from intrasubstance strains, as there are
disparate treatment paradigms.
● Hip pointers present with varying levels of disability, and padding the injured area to prevent
reinjury is important for those athletes in-season.
● In-season management may require targeted anesthetic or corticosteroid injections to reduce
pain and associated soft tissue inflammation to allow for return to play.
CONCLUSION
Medical treatment of hip, pelvis, and thigh injuries in the contact athlete requires a comprehen-
sive knowledge of the surrounding anatomy, pathophysiology, and injury-specific algorithms that
serve as the foundation for on-the-field assessment, post-game assessment, and in-season manage-
ment and rehabilitation. Regardless of the injury, the primary treatment goal is always to optimize
the medical treatment outcome, with the secondary goal to minimize the time required for safe
return to play. The aforementioned guidelines for both nonoperative and operative management
of FAI, subluxations and dislocations, fractures of the femoral neck and pelvic ring, myotendinous
strains and avulsions, and contusions and hip pointers may be used to achieve these goals.
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13
The Pivoting Athlete
Hockey, Soccer, Lacrosse, Basketball,
Wrestling, and Field Hockey
Christopher M. Larson, MD and Patrick Birmingham, MD
COMMON INJURIES
Some of the commonly associated hip and pelvis disorders seen in cutting and pivoting athletes
include intra-articular disorders, such as femoroacetabular impingement (FAI), and extra-articu-
lar disorders, such as athletic pubalgia/core muscle injury, osteitis pubis, proximal adductor/pec-
tineus/gracilis injuries, and other myotendinous injuries. It is clear that intra-articular hip pathol-
ogy and in particular FAI is a source of significant disability in cutting and pivoting athletes.1-6
In addition, FAI presents with limitations in hip range of motion that might lead to compensatory
problems up and down the kinetic chain. This chapter will present evidence supporting the con-
cept that altered kinematics resulting from FAI in these athletes can lead to the previously men-
tioned disorders as well as potentially predispose them to other injuries down the kinetic chain.
Commonly encountered myotendinous injuries and contusions will also be reviewed. In-season
management, and the role and timing for surgical management of these various injury patterns,
will be discussed in order to allow medical care providers to more efficiently manage these athletic
injuries and minimize time lost from athletic activity.

Athletic pubalgia/core muscle injury is broadly defined as exertional lower abdominal pain
with or without associated proximal adductor-related pain in athletes.7-10 This can be a source of
significant disability and time lost from athletics and is common in cutting and pivoting athletes.

210 Chapter 13
Figure 13-1. Magnetic resonance imaging (MRI) Figure 13-2. Plain radiograph demonstrating erosive changes
of the pelvis demonstrating disruption of the across the pubic symphysis (dashed arrow) consistent with
aponeurosis (arrow) of the adductor origin off of chronic degeneration of the pubic cleft. Historically these
the pubic symphysis, which is confluent with the changes have been described as “osteitis pubis,” but now there
insertion of the rectus abdominis on to the proxi- is a clear association between FAI (solid arrow) and athletic pub-
mal portion of the pubis. algia, suggesting that abnormal hip joint mechanics can lead to
increased stress across the central pubic region.
The typical presentation, physical examination, and imaging findings are outlined in Chapter 7.
Briefly, physical examination reveals tenderness over the internal/external obliques, transversus
abdominus, distal rectus abdominis, proximal adductors, and/or pubic symphysis that reproduces
the athlete’s exertional symptoms. Pain over the distal rectus abdominus and proximal adductors
with resisted sit-ups and resisted adduction, respectively, is also a frequent finding. Imaging find-
ings will often demonstrate disruption of the adductor longus aponeurosis, which is continuous
with the rectus abdominis insertion on magnetic resonance imaging (MRI) (Figure 13-1). Plain
radiographs will frequently demonstrate erosive changes across the pubic symphysis that have
historically been described as osteitis pubis (Figure 13-2).
Once a diagnosis of athletic pubalgia/core muscle injury is made, treatment is dictated by the
ability of the athlete to continue participation safely and productively.
Nonsurgical Treatment
Although reports of the success of nonsurgical treatment of athletic pubalgia/core muscle
injury are lacking, a randomized study of nonsurgical vs surgical treatment in 60 athletes found a
return to sports for 90% of athletes after surgery vs 27% after nonsurgical treatment at 3 months’
follow-up.9 In addition, 23% of athletes in the nonsurgical group ultimately underwent surgery for
persistent, limiting, groin pain.9 Despite these results, however, a well-balanced rehabilitation pro-
gram focusing on core stability as described in Chapter 17 is typically implemented prior to con-
sideration of surgical treatment. The current authors find it helpful to focus on gluteus maximus
strengthening and activation with avoidance of aggressive lower abdominal, adductor, and hip
flexor activation. In addition, avoidance of heavy-weight, low-repetition, deep hip flexion weight
training can be helpful for athletes. Injections can be helpful from a diagnostic standpoint, as the
particular pain generators can be quite elusive. Injections can also be therapeutic in some cases
and help athletes to complete a current season. More specifically, corticosteroid injections into the
pubic symphysis, adductor/pubic cleft, and hip joint may of some benefit to continue competition
for higher-level athletes.
The Pivoting Athlete 211
Surgical Treatment
When symptoms persist despite nonsurgical measures, surgery may be considered. If the
athlete is in season, functional, and able to participate at a high level, surgery is considered at
the completion of the season. If the athlete is unable to perform during the season, then surgery
is considered at that time in order to prepare the athlete for the following season. A number of
surgical approaches for managing sports hernia/athletic pubalgia have been reported to result in a
high return to athletic activity.7-10 These approaches include broad pelvic floor repairs, modified
hernia repairs with or without mesh or fibrin glue, and mini-open repairs, with additional partial
or complete adductor releases varying among authors.7-10 The ideal approach should address the
specific structures involved, which can be quite variable from one athlete to another.
Association of Femoroacetabular Impingement and Athletic Pubalgia/
Core Muscle Injury
There is increasing evidence that a subset of athletes might develop athletic pubalgia/core mus-
cle injury, osteitis pubis, and adductor-related symptoms as a result of hip joint motion limitations
secondary to FAI. Studies have shown an increased incidence of chronic groin pain and osteitis
pubis in athletes with limited hip internal rotation.11,12 One study reported that 94% of athletes
had radiographic evidence for FAI when presenting with long-standing proximal adductor-related
pain.13 A recent biomechanical study found increased symphyseal motion in the presence of cam-
type FAI that the author proposed could lead to athletic pubalgia-type symptoms.14 Finally, in a
series of athletes presenting with both symptomatic hip joint (FAI) and athletic pubalgia-related
findings, surgical management resulted in a return to sports without limitations in 50% of ath-
letes after isolated FAI surgery and 25% of athletes after pubalgia surgery.6 If both were managed
surgically, the rate of return to sports without limitations was 89%.6 It appears that the motion
limitations that result from FAI can lead to extra-articular compensatory patterns resulting in
athletic pubalgia/sports hernia, osteitis pubis, and proximal adductor symptoms in some athletes.
These studies support an association between FAI and athletic pubalgia/sports hernia and the
importance of managing both entities in select cases in order to minimize time lost from athletics
and maximize outcomes (Table 13-1).
Treatment of Femoracetabular Impingement With Associated
Compensatory Hip/Pelvis Pathology
In this situation, treatment is based on the athlete’s primary complaints and pain generators.
We often perform an intra-articular anesthetic hip injection followed by an exercise challenge.
If pain with impingement testing is a significant portion of the overall complaints and is relieved
with the anesthetic injection, then a joint preservation/FAI corrective procedure is considered.
If the lower abdominal/pubalgia pain persists after the injection and this is significantly limiting
for the athlete, then we consider a concomitant athletic pubalgia repair. If there is associated proxi-
mal adductor/pectineus/gracilis pain to palpation and with resisted hip adduction, and this is felt
to be a limiting factor for the athlete, a fractional lengthening/adductor release is considered at the
same setting. It is critical to verify that imaging findings consistent with FAI and intra-articular
pathology are symptomatic and that associated athletic pubalgia/adductor pain is significantly
limiting and recreates a portion of the athlete’s presenting complaints. If any of the above findings
are minimally symptomatic or not consistent with the athlete’s presenting complaints, we do not
address them surgically. Mild pubalgia symptoms in the setting of intra-articular hip pathology
often resolve after surgical management of intra-articular hip pathology in our experience.
Hip-Related Compensatory Patterns Down the Kinetic Chain
There is evidence that range-of-motion restrictions or abnormalities resulting from hip joint
pathology and in particular FAI can create compensatory biomechanics down the kinetic chain
during athletic activity. These biomechanical alterations may predispose these athletes to knee,
212 Chapter 13
TABLE 13-1
HISTORY AND EXAMINATION PEARLS FOR
FEMOROACETABULAR IMPINGEMENT AND ATHLETIC PUBALGIA
FEMOROACETABULAR IMPINGEMENT/ ATHLETIC PUBALGIA/SPORTS HERNIA
INTRA-ARTICULAR HIP PATHOLOGY PHYSICAL EXAM
PHYSICAL EXAM
Deep anterior and/or deep lateral hip pain Exertional lower abdominal/adductor-
related pain
Pain with torsional activities Pain resolves with rest
Pain with prolonged hip flexion Pain to palpation over the abdominal
obliques/transversus abdominis
Pain to palpation over the distal
rectus abdominis
Pain to palpation over the
proximal adductors
Pain with flexion/abduction/internal Pain with resisted sit-ups
rotation Pain with resisted hip adduction
Positive anterior impingement test
(FADIR test)
FADIR = flexion, adduction, and internal rotation.
lower leg, and foot and ankle injuries. Specifically, one study reported that 56% of athletes who had
sustained a noncontact anterior cruciate ligament (ACL) injury had radiographic evidence for hip
impingement (FAI).15 Another study evaluated hip range of motion for 50 athletes who had sus-
tained a noncontact ACL injury compared to a cohort of athletes without history of ACL injury.16
This study found a statistical decrease in hip range of motion and in particular internal rotation
for those athletes who had sustained noncontact ACL injuries compared to the non–ACL-injured
cohort.16 Compensatory biomechanical alterations resulting from range-of-motion restrictions
about the hip and pelvis, however, require further study in order to better define treatment and
injury prevention strategies in this subset of athletes.
Myotendinous Injuries About the Hip and Pelvis in Athletes

Epidemiology
Myotendinous injuries of the hip and pelvis are increasingly recognized in the athletic popula-
tion. A study of the National Collegiate Athletic Association (NCAA) surveillance data revealed
that overall injury rates were higher in games than in practices and higher in pre-season practice
than in regular season, and hip injuries accounted for 4.5% of these injuries.17 A National Hockey
League (NHL) study specifically evaluated groin and abdominal injuries and reported 617 groin/
abdominal injuries over 6 seasons.18 Injuries were 5 times more common in NHL training camp
compared to the regular season and 6 times more common in games compared to practice, and
the majority were reported to be adductor/groin injuries.18 Another study looked at risk factors
for groin injury in 1292 NHL players.19 Risk for groin injury was 3 times higher with less sport-
specific training in the off-season, 2 times higher with a history of prior groin injury, and 5 times
Figure 13-3. Adductor longus avulsion (arrow) off of

the pubic symphysis.
higher in veterans compared to rookies.19 The increased risk of injury pre-season, and with less
off-season training, and history of hip injury, emphasize the importance of optimal physical con-
dition and recovery from injury prior to game situations in order to decrease the risk for recurrent
hip and groin injuries in athletes. Recurrent groin/hip injuries should also alert the clinician to the
possibility of an underlying intra-articular hip joint abnormality (ie, FAI).
Proximal Adductor Injuries

Adductor strains are common in cutting and pivoting sports and ice hockey. An NHL study
reported a 17-fold increase of adductor strain if the adductor strength was less than 80% of abduc-
tor strength.20 In this study, however, there was no correlation with adductor flexibility. These
athletes typically present with the acute onset of groin/proximal medial thigh pain. There is typi-
cally tenderness to palpation over the proximal adductor tendon origin or myotendinous junction,
with the adductor longus being the most frequently injured structure. Anecdotally, partial tears
are conservatively treated with rest, ice, and functional rehabilitation, with a typical return to play
as soon as 1 to 2 weeks, but may cause disability for months in some situations. Chronic athletic-
related proximal adductor pain can be associated with athletic pubalgia or hip impingement/FAI,
and one study looking at athletes with proximal adductor pain reported underlying FAI in 94%
of athletes based on radiographs.13 Chronic, limiting proximal adductor pain can be treated with
platelet-rich plasma (PRP), prolotherapy, or pubic cleft corticosteroid injections, although sup-
porting data regarding these injections are limited.21 Adductor tenotomy resulted in a 63% to 84%
rate of return to play at preinjury levels in 2 studies for recalcitrant, limiting pain.22,23 Complete
proximal adductor ruptures are occasionally seen in athletes (Figure 13-3). Although both surgi-
cal and nonsurgical treatments have been recommended, an NFL study reported a 100% return
to play for both operative and nonoperative treatment of these injuries at 6 weeks and 3 months,
respectively.24 Based on this study, nonsurgical treatment is the treatment of choice for complete
proximal adductor ruptures. It is important to look for associated distal rectus abdominis aponeu-
rotic tears when evaluating patients with partial or complete proximal adductor tears as these may
indicate associated athletic pubalgia.
Rectus Femoris Injuries

Rectus femoris strains are typically the result of sprinting or kicking. They can involve the cen-
tral or peripheral tendon.25,26 One study reported 15 cases and noted a disability time of 27 days
for central disruptions compared to 9 days for peripheral injuries.26 As with any chronic or recur-
rent muscle strain about the hip and pelvis, it is important to rule out any associated intra-articular
hip pathology or pubalgia and, for these injuries in particular, associated myositis ossificans or
anterior inferior iliac spine (AIIS) avulsions. Myositis ossificans, heterotopic bone formation, or
chronic healed AIIS avulsions can lead to subspine/AIIS impingement 27 (Figure 13-4). This can
214 Chapter 13
Figure 13-4. Heterotopic bone formation along the injury

tract of a prior rectus femoris tear with retraction. The bone
forms along the injury tract of the tendon injury (arrow).
result in hip flexion-based pain and hip flexion limitations that may require a decompression of
the AIIS if limiting. One study reported on 10 athletes with proximal rectus femoris strains and
the development of a chronic, proximal, painful mass.25 MRI revealed a mass in the deep/central
tendon of the indirect head of the rectus femoris and surgical excision was curative in all cases.
Complete proximal rectus femoris avulsions do occur, and an NFL study reported on 11 athletes,
all of whom returned to play within 6 to 12 weeks with nonsurgical treatment.28
Proximal Hamstring Injuries

Proximal hamstring strains can lead to prolonged disability times in comparison to middle
and distal injuries, with a median return to sports of 31 weeks in one study.29 Studies have shown
an increased risk of injury with eccentric strength asymmetries, older age, and prior hamstring
injury.30,31 Chronic proximal hamstring tendinopathy is commonly seen in distance runners.
MRI typically shows partial-thickness tearing and degeneration of the proximal hamstring ori-
gin. Although PRP and prolotherapy are reasonable options for treatment, there are no reports
looking at outcomes for this treatment modality. In the rare recalcitrant case, semimembranosus
tenotomy or proximal hamstring debridement and repair can be considered. One study reported
on 90 patients after semimembranosus tenotomy and noted 80 of 90 patients returned to their
prior level of sporting activity.32 Although acute complete proximal hamstring ruptures make up
only 1.5% of all hamstring injuries, early diagnosis is paramount. If an MRI reveals a complete
2- or 3-tendon proximal rupture with greater than 2-cm retraction, early surgical repair should
be considered, to avoid long-term strength deficits and disability 33,34 (Figure 13-5). For patients
presenting with chronic proximal hamstring ruptures, distal fractional lengthening and repair
and more recently proximal hamstring reconstruction with allograft have resulted in improved
strength and function.34,35
OTHER MUSCLE STRAIN INJURIES

Although injuries can involve virtually any muscle about the hip and pelvis, there are a few
injury patterns that may be appreciated on physical exam or MRI that should alert the clinician to
look for a secondary reason for the athlete’s pain. Signal change seen in the psoas adjacent to the
Figure 13-5. Complete 3-tendon avulsion of the hamstring complex (semimembranosus, semitendinosus, and con-
joint tendon) with 2 cm of retraction is best treated with surgical repair of the tendon avulsion.
TABLE 13-2
SURGICAL INDICATIONS FOR HIP/PELVIS MYOTENDINOUS INJURIES
INJURY SURGICAL INDICATION
Proximal adductor Chronic limiting proximal adductor pain
tendinopathy
Rectus femoris avulsion Development of a painful mass in the central tendon
Rectus femoris avulsion Development of hip flexion pain with a healed AIIS
deformity
Proximal hamstring injury Complete disruption with > 2-cm retraction
Proximal hamstring Recalcitrant, limiting proximal hamstring pain
tendinopathy
hip capsule may indicate prior anterior hip subluxation. Signal change seen in the posterior hip
musculature adjacent to the capsule may be indicative of a posterior hip subluxation. As mentioned
previously, recurrent and/or chronic myotendinous injuries about the hip and pelvis should alert
the clinician to the possibility of associated athletic pubalgia/sports hernia or underlying intra-
articular hip disorders (Table 13-2).
216 Chapter 13
CONTUSIONS ABOUT THE HIP AND PELVIS IN ATHLETES

Quadriceps Contusions
Quadriceps contusions are typically the result of a direct blow to the quadriceps, and result in
crushing the deep musculature against the femur.36 Initial management is based on the degree
of disability and ability to perform functional drills prior to considering return to sports the
same day. Often athletes are unable to continue participating, and treatment then begins. Studies
have shown a significant decrease in disability time with a focus on knee flexion protocols.37,38
In a naval study, the knee was flexed to 120 degrees within 10 minutes for 24 hours with a mean
disability time of 3.5 days.37 Aggressive stretching and heat-producing modalities should be avoid-
ed to decrease the risk for further injury and potential for myositis ossificans. Padding the area
for activities of daily living and return to sports helps to minimize the risk for recurrent injury.
Although myositis ossificans is not uncommon after these injuries, this finding does not typically
correlate with disability and generally requires no treatment.36-38
Hip Pointers
Hip pointers are a result of a contusion to the iliac crest, which is protected only by a layer of
subcutaneous fat. Typically these athletes will have significant pain radiating to the associated
abdominal obliques proximally and/or abductors distally. Ecchymosis may eventually develop
over these regions. Initially for higher-level athletes, an anesthetic injection over the iliac crest
can be used to continue sports participation in the same game/event, although a small risk for
anesthetic extravasation to the adjacent femoral nerve with temporary nerve palsy exists. Pad-
ding the area is critical to minimize the risk for recurrent injury until full recovery. The injury is
typically self-limiting.
Morel-Lavallée Lesion
The Morel-Lavallée lesion is an injury that results in degloving of the skin and subcutaneous
tissue from the neighboring fascia. Around the hip and pelvis this most frequently involves the
peritrochanteric region and results in a blood-filled cavity. Although typically the result of high-
energy trauma, this injury has been reported in athletics.39 Initial treatment consists of compres-
sion and cryotherapy, and 50% of these injuries resolve without further treatment.40 If this treat-
ment fails, an early aspiration can be attempted, although there may be a small risk of iatrogenic
infection. If there is continued swelling and discomfort, doxycycline sclerodesis and rarely a surgi-
cal evacuation with vacuum therapy have been reported to be successful treatments.40,41
APOPHYSEAL AVULSIONS OF THE

HIP AND PELVIS IN ADOLESCENTS
Apophyseal avulsions of the hip and pelvis are injuries seen in cutting, pivoting, and kick-
ing by adolescent athletes. The apophyseal growth plate is weaker than tendons, ligaments, and
muscles in these developing athletes and is therefore the site of failure or injury. The locations
for hip and pelvic apophysis and respective muscle groups include the ischial tuberosity (proxi-
mal hamstrings), AIIS (rectus femoris), anterior superior iliac spine (sartorius), lesser trochanter
(psoas), iliac crest (abdominal obliques), inferior pubic ramus (adductors), pubic tubercle (rec-
tus abdominis), and greater trochanter (gluteus medius and minimus). One study reported on
203 apophyseal avulsions in 198 athletic adolescents.42 These injuries were more common in males
Figure 13-6. (A) Apophyseal avulsion of the ischial tuberosity with persistent pain and sciatic nerve radicular symp-
toms should be treated with (B) excision of the bony fragment and advancement and repair of the hamstring complex
to the ischium.
(68.5%) and the mean age at presentation was 13.8 years.42 The most common sites for apophyseal
avulsions were the ischial tuberosity (54%), AIIS (22%), and anterior superior iliac spine (19%),
followed by the pubic tubercle and iliac crest.42 Although the lesser trochanter is also a relatively
common site, the iliac crest, pubic tubercle, inferior pubic ramus, and greater trochanter are less
common sites for apophyseal avulsion.42-44 The most frequent sports involved were soccer and
gymnastics, although other cutting and pivoting sports were reported.42 Anterior superior iliac
spine, AIIS, and lesser trochanteric avulsions are most frequently seen after kicking and sprinting
injuries. Iliac crest avulsions are typically secondary to forceful torsional events. Ischial tuberos-
ity avulsions result from an eccentric contraction of the hamstrings with the hip in flexion and
knee in extension. The vast majority of these injuries are treated nonsurgically. Crutches are used
until the patient is able to ambulate with a nonantalgic gait. A gradual progression of activity is
based on relatively pain-free activity and results in a return to sports in several weeks to several
months. Surgical intervention is rarely considered. The primary consideration for acute surgery
is for ischial tuberosity avulsions with greater than 2 to 3 cm of retraction. Similar to proximal
hamstring avulsions, this can leave these athletes with significant strength deficits and poor leg
control during higher-level athletic activities. For acute ischial tuberosity avulsions with displace-
ment of greater than 2 to 3 cm, open reduction and internal fixation of the fragment is considered.
There are a number of situations for which surgery may be contemplated if problems arise at a
later date. AIIS avulsions can heal, leaving a distal-based bony deformity that can result in painful
hip flexion limitations. In this situation, an open or arthroscopic subspine/AIIS decompression is
considered.27 Pubic tubercle avulsions may rarely result in a presentation consistent with athletic
pubalgia if the rectus abdominis fails to restore its attachment to the pubis. In this situation, a
broad pelvic floor repair is considered if symptoms are limiting. Lesser trochanteric avulsions can
heal with deformity, which may rarely result in psoas/internal snapping or ischiofemoral impinge-
ment between the ischium and lesser trochanter in hip extension. If symptoms are persistent and
limiting, an arthroscopic or open bony decompression and/or psoas tenotomy can be considered.
Ischial tuberosity avulsions can also heal with a prominent deformity that may result in painful
sitting and/or ischiofemoral impingement between the ischial tuberosity deformity and adjacent
lesser trochanter with hip extension. In some cases, local compression of the sciatic nerve can lead
to radicular symptoms due to direct irritation of the nerve by the heterotopic bone. Decompres-
sion of the prominent ischial avulsion with proximal hamstring reattachment may be considered
for recalcitrant symptoms (Figure 13-6). Lastly, chronic, unhealed ischial tuberosity avulsions can
lead to hamstring strength deficits and poor leg control as mentioned previously. In this situation,
open reduction and internal fixation of the fragment vs excision of the fragment and repair or
reconstruction of the proximal hamstring tendon is considered (Table 13-3).
218 Chapter 13
TABLE 13-3
SURGICAL INDICATIONS FOR APOPHYSEAL AVULSIONS
INJURY/SITE INDICATION FOR SURGERY
Acute
Ischial tuberosity Greater than 2 cm to 3 cm retraction
Chronic
Ischial tuberosity nonunion Weakness/poor leg control
Ischial tuberosity deformity Recalcitrant sitting pain
Ischial tuberosity deformity Ischiofemoral Impingement
AIIS deformity Hip flexion pain and limited motion
Pubic tubercle nonunion Athletic pubalgia presentation
Lesser trochanteric deformity Recalcitrant psoas snapping
Lesser trochanteric deformity Ischiofemoral Impingement
PEARLS AND PITFALLS

● In the pivoting athlete, there are often concomitant injury patterns that result, such as athletic
pubalgia and FAI. One must be mindful of the underlying bony structure, and its effect on the
dynamic structures above, in order to successfully treat these athletes.
● In-season management of athletic pubalgia may include gluteus maximus training while
avoiding aggressive adductor and hip flexor activation. Injections may be utilized as well, and
may be directed to the pubic symphysis, adductor/pubic cleft, and hip joint as needed.
● Because of the rotation required from pivoting sports, these athletes will often present with
compensatory pathology down the kinetic chain. This is demonstrated by the increased rate
of noncontact ACL injuries in those with decreased hip internal rotation.
● In the adolescent athlete, apophyseal avulsion injuries should be ruled out in the setting of hip
pain, as the growth plate is often the weakest link.
CONCLUSION
There are specific injuries and injury patterns that are encountered in the cutting and pivoting
athlete. Intra-articular hip pathology, such as labral tears and articular cartilage injuries secondary
to FAI and extra-articular injuries, such as sports hernia/athletic pubalgia, osteitis pubis, proximal
adductor, and other myotendinous injuries about the hip and pelvis, are frequently seen in this
athletic population. Range-of-motion limitations secondary to FAI may lead to compensatory pat-
terns that place these athletes at risk of developing associated extra-articular injury patterns. An
accurate diagnosis and appropriate evidence-based treatment for these specific injuries and injury
patterns will help to minimize time lost from athletic activity and result in a predictable return to
sports for the majority of these athletes.
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14
The Overhead Athlete
Baseball, Volleyball, and Tennis
Matthew Thompson, MD; Anil Ranawat, MD;

Struan H. Coleman, MD, PhD; and Marc R. Safran, MD
One of the unique and challenging aspects of overhead sports is that the athletic movements
require side-specific, integrated motions beginning in the lower extremities and traveling sequen-
tially through the core musculature and spine to the upper extremity, thus putting extreme asym-
metric stresses on the body. Athletes can usually compensate for these stresses with mild adaptive
changes, but, commonly, weakness and/or restricted motion in any part of this kinetic chain
can lead to overcompensation and eventually decompensation and injury. For this reason, there
has recently been increased research interest in the role of hip function and core musculature in
overhead athletic motions such as pitching, serving, spiking, and bat/tennis racket swinging. In
this review, we will discuss the concept of adaptive changes and compensatory overload in the
overhead athlete, the mechanics of each specific sport activity and its associated decompensation,
and the common injuries that are seen in these athletes.
UP THE KINETIC CHAIN

Compensatory Overload to Pelvis, Spine, Shoulder, and Elbow
The throwing, serving, and swinging motions in overhead sports are similar in that they are
initiated in the legs and have a rotational component in the hips and pelvis, where a significant
amount of power is generated that is transferred through the thoracoabdominal core and spine
to the upper extremity. Breakdown in any phase of this kinetic chain, whether in the form of
Kelly BT, Bedi A, Larson CM, O’Sullivan E , eds.

222 Chapter 14
weakness, stiffness, or fatigue, can have downstream effects that may result in poor performance
or injury.
In order to evaluate the overhead athlete, it is first important to understand that asymptomatic
adaptive changes can occur in the body because of years of repetitive overhead motions. These adap-
tive or compensatory changes occur because many athletes begin playing their sport as children,
and by the time they reach adulthood, asymmetric development of the body is often evident in
terms of coordination, musculature, capsular and ligamentous laxity, and even bone structure.
These compensatory adaptive changes are common in the upper extremity but are also found
throughout the kinetic chain as well. Anatomic changes in the throwing arm of baseball players
include changes in glenohumeral range of motion, increased humeral retroversion and phy-
seal widening in the shoulder, and medial epicondylar apophyseal hypertrophy in the elbow.1-5
Asymptomatic pathology is also commonly found in the glenoid labrum, rotator cuff, ulnar
collateral ligament, and posteromedial aspect of the elbow joint.6 Similar shoulder adaptations
have been found in tennis players as well.7 These compensatory changes are likely a result of the
near-maximal torque and tensile stresses placed on the shoulder and elbow during throwing and
serving, as shown in biomechanical studies.6,8,9
Professional pitchers were shown to have decreased range of motion of the nondominant, lead
hip in one study.10 In this study, range of motion of the nondominant hip was correlated with
ball velocity in professional pitchers.10 Other studies with different measurement techniques did
not find the same aggregate differences in hip rotation, though 42% of pitchers had a side-to-side
difference in external rotation of more than 10 degrees in one analysis.11,12 These changes are
likely compensatory because of high loads and repetitive microtrauma to the hip.7,13,14 Like-
wise, tennis players have been shown to have asymmetric muscular development of the rectus
abdominis, changes in hip range of motion, and asymmetric bone density and longitudinal
bone growth.7,15-19
The training and medical staff are placed in a difficult position when evaluating these athletes,
since athletes often have identifiable pathology that is only occasionally symptomatic. For this
reason, it is important to have a thorough understanding of the kinetic chain from lower to upper
extremity in overhead sports, as well as the compensatory mechanisms and pathologic processes
that may be seen throughout this chain.
Understanding the biomechanics of the throwing, serving, spiking, and swinging motions is
necessary in order to properly evaluate and train overhead athletes in baseball, tennis, volleyball,
and similar sports. The biomechanics of pitching, serving, and swinging will be described here
since they are well-studied representative motions in overhead sports. In addition, the proposed
decompensation mechanisms down through the kinetic chain will be explored.
Pitching Mechanics of the Lower Body

Pitching phases can be divided into wind-up/cocking, acceleration, and follow-through.
Wind-Up/Cocking
Pitching begins with the initiation of movement in the lower extremities in order to create
momentum. The pitcher plants the dominant, back leg against the rubber (on the pitcher’s mound)
to begin the wind-up. As the nondominant, leading leg is raised, the dominant leg settles into a
balanced position of slight hip and knee flexion, with its hip abductors firing to keep the pelvis
level.20 At this point the pitcher’s body is facing relatively perpendicular to the batter. As the
nondominant leg undergoes concentric hip flexion (and sometimes adduction and internal rota-
tion depending on pitching style), the dominant leg continues to accept all of the body’s weight,
maintaining balance through continued activation of the paraspinal and gluteal muscles.21
The nondominant, lead leg then moves from a flexed, internally rotated and adducted position
into a relatively extended position with abduction and external rotation in order to plant the foot
The Overhead Athlete 223
directly toward the batter. Range of motion of the nondominant hip has been correlated with ball
velocity in professional pitchers,10 and this may be one phase of pitching in which a deficiency
in lead hip rotation is detrimental. During this process, power is generated in the dominant leg
through contraction of the gluteal muscles as the pitcher pushes off the rubber. Foot separation
increases as both hips abduct, and the pitcher’s push-off strength during this phase is an important
determinant of ball velocity.13,22 As the nondominant foot is planted in the direction of the pitch,
the hips and pelvis rotate toward the batter while the trunk remains relatively perpendicular, stor-
ing elastic energy. Torso and pelvic orientation during this phase have been correlated with ball
velocity and the amount of torque on the shoulder joint.23,24
Acceleration
Once the lead foot contacts the ground, a rapid weight shift occurs. The power generated from
push-off of the dominant leg is combined with rotational power from the hips, pelvis, torso, and
upper extremity to propel the ball forward. During this rapid weight shift and rotation of the pel-
vis, the dominant leg goes into extension as the pelvis rotates toward the batter. The lead leg moves
from a position of external rotation and abduction to internal rotation and adduction as the pelvis
rotates forward. Flexion of the lead hip and flexion and rotation of the trunk occur prior to release
of the ball. Side-specific activation of the rectus abdominis, abdominal oblique, and paraspinal
muscles occurs throughout the acceleration phase, with increased activation of these muscles on
the leading side, contralateral to the throwing arm.21
Follow-Through
After release of the ball, the momentum of the torso results in further flexion and internal
rotation of the lead hip, and the distribution of the majority of the body weight is on the lead
leg. Significant eccentric muscle activity occurs in the follow-through phase in order to reverse
the acceleration that occurs leading up to ball release.21 Deceleration of the arm requires heavy
recruitment of the rotator cuff, latissimus dorsi, and scapular retractors.25
Pitching Decompensation
As stated before, range of motion of the nondominant hip has been correlated with ball veloc-
ity in professional pitchers,10 and this may be one phase of pitching in which a deficit in lead hip
rotation is detrimental. In addition, reduced external rotation and abduction of the lead leg may
result in a closed position of the hip, pelvis, and foot, resulting in the pitcher throwing across the
body, which limits the kinetic energy transfer to the arm while putting undue stress on the upper
extremity.10,24,26,27 An internal rotation deficit of the lead hip may also cause the deceleration
phase to be shortened, requiring increased eccentric forces over a shorter distance to reverse the
momentum of follow-through. This deceleration phase requires recruitment of the core muscles
from the back, abdomen, hips, and pelvis. This may put the hip, core, and shoulder at risk for
injury under this increased eccentric load.
Serving and Spiking Mechanics of the Lower Body

Tennis Serving
The tennis serve has lower extremity mechanics very similar to pitching, except the lead leg
stays in its initial starting position and the overall forces from the ground are more up, away from
the ground and forward, as opposed to the baseball pitch, which is more forward rather than up.
The result is the need for more hip and back extension, to swing the racket up to hit the ball that
is tossed in the air above.28,29 As a result, in addition to pelvis rotation measured at 440 degrees/
sec, high-level servers tilt their trunk at 280 degrees/sec.30 It has been shown, regardless of serve
type, that muscle activation is more pronounced in the rectus abdominis (particularly the rectus
abdominis of the side contralateral to the dominant arm) and external oblique than in internal
oblique and lumbar erector spinae muscles.31
224 Chapter 14
Volleyball Serving/Spiking
The volleyball jump serve and spike have mechanics similar to pitching and serving in baseball
and tennis, though because jumping is required, there is a disconnect in the kinetic chain when
the feet leave the ground. The energy transfer occurs in an open-chain environment since the feet
are not planted; yet, trunk rotation and generation/transference of force is still critical for serving.
Serving/Spiking Decompensation
As in pitching, serving and spiking rely on appropriate positioning of the lower extremities and
core in order to efficiently transfer power to the upper extremity. Lumbar hyperextension is critical
in the tennis serve,28,29 and deficits in lead hip internal rotation and lumbar extension have been
correlated with low back pain in tennis players.7 Though there is little research specifically cor-
relating hip and core functional characteristics to injury in volleyball, extrapolation of data from
other sports suggests a possible link.
Batting/Tennis Stroke Mechanics of the Lower Body

Similar to pitching, batting can be divided into 3 distinct phases. There is first a preparatory
or coiling phase, followed by an acceleration phase, and then follow-through.14 The coiling phase
positions the body for maximal generation of rotational power, the acceleration phase creates
power and translates it into bat speed, and the follow-through phase reverses the momentum of
the swing.
Stance/Coiling
A batter’s stance is highly individual, with significant variance from player to player. However,
there are some common characteristics that most batting stances share. The hips, trunk, and
shoulders are generally perpendicular to the pitcher. The knees and hips may have variable degrees
of flexion with body weight shifted slightly onto the dominant or back leg, and the trunk often
remains erect with a slight forward lean.
Coiling is the first phase of the swing, and begins with shifting of the body weight onto the
back leg. Subtle cocking of the hips and torso also occurs at this time, as they are rotated slightly
toward the dominant side, away from the pitcher. Once all the body weight is on the back leg, the
front foot is lifted off the ground to prepare for the stride.
Acceleration
As the batter strides toward the pitcher, weight is rapidly shifted from the dominant back leg
to the lead leg. At the point the lead foot makes contact with the ground, the swing becomes a
closed-chain energy transfer.14 During this weight shift, the total force of the lead leg reaches 123%
of body weight while the back leg decreases from 102% to 58% body weight. Including shear force
allows total force to exceed body weight in this calculation.14 Following this weight shift, there is
rapid rotation of the pelvis and trunk toward the pitcher, transferring energy up the kinetic chain
in order to generate maximal bat speed. Dominant hip abduction and external rotation coupled
with lead leg knee extension creates a rigid base for pelvic rotation, which occurs at a maximum
angular velocity of 714 degrees/sec.14 During the early phase of acceleration there is maximal
activation of the hamstrings and gluteus maximus in the dominant leg, as well as the dominant
and nondominant erector spinae and internal and external oblique muscles. Maximal abdominal
oblique muscle activation persists through follow-through.32
Follow-Through
After the ball has been struck, the high amount of rotational force that powers the swing must
be dissipated. In addition to eccentric muscle activity in the upper extremities, there is near-
maximal contraction of the core musculature in order to slow the angular velocity of the pelvis
and torso.32 Capsular and bony constraints to internal rotation in the lead hip may help to limit
further pelvic rotation while the lead leg is planted. Shifting of the feet after ball contact can allow
these restraints to relax, and allow more even weight distribution to the lower extremities, helping
to maintain balance at the end of follow-through.
Tennis Stroke
In the tennis ground stroke (forehand and backhand), similar mechanics exist. The forehand
in tennis is very similar to the batting mechanics described above, and from a lower extremity
perspective, the backhand is similar when talking about the lead leg and back leg (though the lead
leg is the leg on the dominant side for the backhand, instead of the power-driving back leg). How-
ever, with current tennis style, in the open stance ground stroke, during the acceleration phase, the
lead leg is not directed toward the net, but abducted and externally rotated. This necessitates the
push-off leg to also be abducted and externally rotated early in the acceleration phase. This allows
a greater arc of motion and force generation from the hips, pelvis, and core. A whipping motion
occurs, with the racket trailing, generating high racket head speed, which affects ball velocity
and/or spin.
Batting/Tennis Stroke Decompensation

During batting, with the lead leg planted, the lead hip must undergo internal rotation, and
an internal rotation deficit in this hip may limit pelvic rotation and power generation.14,23,24
In tennis, the abducted and externally rotated hip position, or open stance, allows a greater arc of
motion and force generation throughout the core and hips, and as in baseball, a deficit in hip range
of motion can lead to injury or decreased power generation. Hip dysfunction may contribute to
injury in any structure up the kinetic chain, from the sacroiliac (SI) joint and pubic symphysis to
the back, abdominal/core muscles, and upper extremities.6,10,33,34
COMMON INJURIES
Hips and Pelvis
As discussed earlier, generation of power for throwing, serving, and swinging is initiated in
the hips and pelvis. Generating maximal rotational power in these side-specific motions relies on
pelvic angular velocity and the range of motion over which this velocity is sustained.10,14,23,24 Thus
the constraints in generating maximal rotational power include hip range of motion and muscle
strength.10,12 Conditions such as femoroacetabular impingement (FAI) and hip abductor weakness
can affect power generation by limiting hip range of motion and muscular strength. This results
either in decreased performance or, more often than not, compensatory behavior by the athlete
in order to overcome these limitations. Compensatory changes can lead to overcompensation,
which can result in increased stress or injury anywhere along the kinetic chain, from the hips to
the elbow.9,24,26,34
FAI is well documented in athletes as a cause of hip pain and disability.34-38 It has been
described as an osseous abnormality of the proximal femur (cam), acetabulum (pincer), or a com-
bination of the two.39 As discussed earlier, throwing, serving, and swinging require high rotational
forces in the pelvis as well as adequate hip range of motion. There are several phases of overhead
activities in which FAI may limit hip range of motion, resulting in labral tears, chondral injury, or
compensatory injury to another part of the body.34,40-43
226 Chapter 14
During the wind-up in pitching, the lead hip goes from a position of flexion, adduction,
and internal rotation to abduction and external rotation, creating the potential for anterior and
superior impingement. Risks for impingement during this phase include an anterosuperior cam
deformity in the femur, acetabular overcoverage, excessive acetabular retroversion, and femoral
retroversion. In the tennis serve, the back hip flexes, adducts, and internally rotates during accel-
eration, also leading to anterosuperior impingement.
In baseball, during the stride, both hips are abducted and externally rotated, creating the poten-
tial for posterosuperior impingement. Risks for impingement during this phase include postero-
superior cam deformity in the femur, acetabular anteversion, and acetabular overcoverage. In the
tennis serve, during late cocking and acceleration, the back hip extends and externally rotates, with
lesser degrees of abduction, which can also result in posterosuperior impingement.
During acceleration and follow-through of the baseball pitch, the lead hip sustains significant
shear forces and undergoes internal rotation, adduction, and flexion, creating the potential for
anterosuperior impingement as the head-neck junction of the femur approaches the acetabular
rim. In the tennis serve, the lead hip also flexes, internally rotates, and adducts during accelera-
tion and follow-through, potentially leading to anterosuperior impingement. In the acceleration
phase of swinging a bat, when the lead foot is planted, the lead hip undergoes internal rotation as
the pelvis rotates forward, also creating the potential for anterosuperior impingement. Risks for
impingement in these phases include anterosuperior cam deformity in the femur, acetabular over-
coverage, excessive acetabular retroversion, and femoral anteversion. The same may occur with the
lead hip in tennis during the ground stroke, but the open-stance style of play reduces the amount
of internal rotation of the lead hip. Alternatively, the extreme external rotation and abduction of
the back hip may result in posterosuperior impingement. Posterior hip instability is also a risk with
forceful flexion, adduction, and internal rotation of the hip, with the proposed mechanism being
a cam lesion that engages the anterior acetabulum, levering the femoral head out posteriorly.44,45
Diagnosis and treatment of FAI has been thoroughly discussed in other chapters, and the same
principles apply for treating FAI in the overhead athlete. If conservative treatment fails, advanced
imaging (Figure 14-1) and guided anesthetic injection into the hip joint can help to distinguish
intra-articular or extra-articular pain generators. Hip arthroscopy with osteochondroplasty and
labral repair as indicated has had a high success rate in returning high-level athletes to their sport,
with 87% to 93% making a full return to their sport.38,46 It is not known if cam lesion decompres-
sion results in increased pitch velocity via increased hip range of motion, though future research
may answer this question.
In the presence of FAI, decreased hip motion can lead to a compensatory increase in motion
through the pubic symphysis, SI joint, and lumbar spine.34 In tennis, limited internal rotation of
the lead hip has been associated with low back pain.7 Although the etiology of limited hip rotation
was not studied, it is likely that FAI may lead to compensatory stresses on the low back in tennis
players, resulting in low back pain. Other sports injuries associated with FAI include osteitis pubis,
SI joint injury, sports hernia/athletic pubalgia, posterior hip subluxation, and muscle injuries.34,43
Some of these injuries are discussed here in more detail.
The term sports hernia is misleading as this injury is not a classic herniation of tissue. The exact
definition of sports hernia has been debated. The term can refer to several different injuries in the
same area of the body, including rectus abdominis and adductor strains, posterior wall weakening
in the inguinal canal and injury to the conjoined tendon, internal and external oblique muscles,
and may be associated with varying degrees of nerve irritation.47-50 For this reason, the term
athletic pubalgia or core muscle injury more accurately describes the full spectrum of myofascial
injuries surrounding the pubic joint. Overlap between hip pathology and athletic pubalgia is com-
mon. In one study, at least 15% of athletes treated for athletic pubalgia were found to have hip
pathology on magnetic resonance imaging (MRI).50 The sports hip triad includes intra-articular
Figure 14-1. (A) Anteroposterior (AP) pelvis radiograph,

(B) hip computed tomography (CT) with 3-dimensional
reconstructions and (C) coronal magnetic resonance imag-
ing (MRI) in a professional tennis player demonstrating
combined cam/pincer (FAI). The radiograph demonstrates
decreased head-neck offset and a crossover sign, the CT
more precisely delineates the cam lesion, and the MRI
shows a labral tear and cyst.
hip pathology (labral tear) and classic findings in athletic pubalgia (rectus abdominis and adduc-
tor strains).47 This constellation of symptoms was based on analysis of hip injuries in the National
Football League.
Athletic pubalgia often is caused by high-energy twisting through the hips and pelvis, causing
shear across the pubic symphysis.48,49 Athletes commonly report a history of lower abdominal or
deep groin pain with an insidious onset that is exacerbated by running, kicking, sit-ups, or sudden
forceful movements through the hips and pelvis.48,49 The majority of these injuries resolve with
nonoperative treatment, which includes nonsteroidal anti-inflammatory drugs (NSAIDs), relative
rest, and physical therapy for the core and hip musculature. When pain persists, hip and pelvic
radiographs and MRI (Figure 14-2) can be ordered to assess for muscular injury, as well as other/
contributing causes of pain such as FAI/intra-articular hip pathology, osteonecrosis, stress frac-
ture, and osteitis pubis. Surgical management in recalcitrant cases has been generally successful,
with return to play 3 months after surgery reported in more than 95% in some series.49,50
Osteitis Pubis
Osteitis pubis is characterized by pain, instability, and bony changes in the pubic symphysis.51
Though it is traditionally associated with sports such as rugby, ice hockey, and soccer in which
228 Chapter 14
Figure 14-2. (A) Axial and (B) coronal magnetic resonance imaging of a professional tennis player with clinical
symptoms consistent with sports hernia/athletic pubalgia. Arrows indicate partial tearing of the rectus abdominis/
adductor aponeurosis.
there are heavy shear forces across the pubic symphysis, it can also be seen in overhead sports due
to repetitive twisting motions involving the pelvis. It should be included in the differential diagno-
sis for groin pain in the overhead athlete since its symptoms may overlap with those seen in FAI,
athletic pubalgia, and muscle strains.34,51 During the throwing, serving, and swinging motions,
restrictions in one portion of the kinetic chain may result in a compensatory increase in motion
through the pubic symphysis.34,43 In a biomechanical study, hip internal rotation in the presence
of cam-type FAI resulted in up to a 35% increase in pubic symphysis motion when compared to a
normal hip.41
Athletes with osteitis pubis complain of pain in and surrounding the pubic symphysis,
with reproduction of the pain with pubic symphysis palpation and resisted hip adduction.34,51
Radiographs may show cystic changes and sclerosis in the pubic symphysis in chronic cases,
while bone marrow edema can be seen on MRI.51 Initial management includes NSAIDs, activity
modification, and physical therapy for core strengthening and flexibility, as well as assessment of
throwing, serving, or swinging mechanics. Second-line therapies include corticosteroid injection
into the pubic symphysis both as a diagnostic and therapeutic tool, and surgical management in
recalcitrant cases.34,51
Sacroiliac Joint Injury
Symptoms arising from the SI joint may manifest as lower back and buttock pain that is wors-
ened with activity. SI joint pain and dysfunction are particularly common in high-level tennis
players, likely due to the significant rotational and extension forces on the low back and pelvis/
hip. Causes of pain in the SI joint include stress fractures, ankylosis, infection, inflammation, and
mechanical imbalances.52 Altered hip joint biomechanics have been shown to result in compensa-
tory motion in the pubic symphysis and SI joint,40,41 which may result in pathologic changes to the
joint and its ligaments. The presence of cam-type FAI has been shown to increase contralateral SI
joint motion by 9% compared to a normal hip in a biomechanical study.40
SI joint pain may be elicited with various provocative tests and by palpation of the posterior
superior iliac spine, though no physical examination tests have been validated that accurately
detect SI joint pathology.52 Initial treatment includes rest, NSAIDs, physical therapy focusing
on flexibility, posture, and core musculature, bracing with pelvic belts, and manual therapy.52
Further workup includes diagnostic and potentially therapeutic SI joint injection. MRI, computed
Figure 14-3. MRI of a female collegiate volleyball

player demonstrating bilateral sacral stress frac-
tures. Plain radiographs were negative.
tomography (CT), and bone scans are more useful for ruling out other causes of pain than they
are for diagnosis SI joint pathology52 (Figure 14-3). Secondary lines of treatment include prolo-
therapy, viscosupplementation, nerve stimulator implantation, radiofrequency neurotomy, and
arthrodesis, though there is limited research into the effectiveness of these techniques.52
Muscle Injury
As discussed previously, overhead and swinging motions require a sufficient amount of hip and
pelvis range of motion and muscular control, and range-of-motion deficits or muscular weakness
may result in compensatory injury.34,43 Evaluating muscle injuries about the hip can be simplified
by grouping them according to muscle function—hip flexors, adductors, and abductors.
Hip flexor injuries often involve the rectus femoris, sartorius, or iliopsoas muscles. Rectus
femoris and sartorius injuries may present as a strain in an adult and an apophyseal avulsion in
an adolescent.53 They are characterized by focal tenderness and pain with resisted hip flexion.
Radiographs are useful to detect an apophyseal avulsion, and MRI (Figure 14-4) may be useful
when the diagnosis is in question.53 Standard rehabilitation protocols result in recovery the major-
ity of the time, though surgical fixation may be considered in large avulsions displaced greater
than 2 cm.53
Iliopsoas muscle injury is unique because it may present as a muscular strain with pain with
resisted hip flexion, or may present as internal snapping hip syndrome. Internal snapping hip is
characterized by bursitis and snapping of the iliopsoas tendon over the iliopectineal eminence
or femoral head as the hip is extended. Treatment initially involves NSAIDs, activity modifica-
tion, and stretching, with ultrasound-guided injection of the iliopsoas bursa and surgical release/
lengthening reserved for persistent cases.54 Other intra-articular hip pathology, such as a labral
tear, can be commonly found during arthroscopic iliopsoas tendon release,54 reiterating the con-
cept that compensatory mechanisms and associated injuries in the hip may be more common than
previously recognized.
Adductor strain is a common cause of groin pain, and as discussed earlier, can be associated
with other hip and athletic pubalgia-type pathology.43,50,51 Physical examination findings include
tenderness at the adductor origin and pain with passive abduction and resisted adduction, and
the diagnosis can be confirmed by MRI, which may show increased signal in the muscle.55 Initial
230 Chapter 14
Figure 14-4. Axial MRI of a professional tennis player with

clinical examination consistent with iliopsoas strain. Arrow
indicates edema in the iliopsoas muscle of the left hip.
treatment involves NSAIDs, activity modification, and standard physical therapy exercises. Failure
of the injury to improve after 6 to 8 weeks should spur a more comprehensive evaluation for associ-
ated hip and pelvic pathology. A single anesthetic and corticosteroid injection into the adductor
origin has been shown to be useful for diagnostic and short-term symptom relief in competitive
athletes who have failed conservative treatment.55 There is also a role for surgical management in
recalcitrant cases.
In regards to hip abductor pathology, research in overhead athletes has focused mainly on glu-
teal muscle strength.12,13,21,32,56 The gluteal muscles are particularly important in the stance leg
during pitching and serving, and relative weakness may manifest gradually over time as decreased
performance or compensatory injury in another part of the body. The dynamic Trendelenburg
test6 and muscle strength testing can assist in diagnosis. Rather than diagnosing and treating
gluteal weakness as an isolated problem, training programs commonly include gluteal muscle
assessment and strengthening in order to prevent weakness and fatigue. Snapping hip syndrome,
in which the iliotibial band snaps over the greater trochanter with hip flexion and extension, may
also be seen in overhead athletes. Treatment for painful snapping hip syndrome involves NSAIDs,
stretching and injection and, for refractory cases, there are multiple surgical procedures that have
been described.53
Lower Back Injuries

Overhead motions can place significant stress on the lumbar spine, especially in the setting
of decreased hip range of motion. In the tennis serve, lumbar hyperextension is a critical part of
the motion.28,29 Decreased hip and lumbar range of motion have been correlated with lower back
pain in tennis players.7 The proposed mechanism is that decreased hip range of motion results in
compensation through the lumbar spine, increasing stress throughout the lower back. Other risk
factors for lower back pain include repetitive loading, improper mechanics, poor conditioning, and
sudden increases in training.57
Initial assessment of back pain in the overhead athlete should include a global evaluation of
mechanics, flexibility, core strength, and range of motion, paying particular attention to lumbar
hyperextension and hip internal rotation.7 Hip range-of-motion deficits and/or pain on exam
may warrant further workup of the hip as a contributing factor to low back pain. FAI that results
in pain and restricted motion with hip internal rotation may be overlooked when evaluating the
athlete. Differentiating hip and back pain on exam can be difficult since symptoms may overlap
in the acute setting. Treatment of specific causes of back pain (strain/sprain, degenerative disc
disease, spondylolysis/spondylolisthesis, disc herniation) is out of the scope of this discussion, but
the important point for medical professionals is to start with a wide differential diagnosis, not just
confined to the lumbar spine, when evaluating the overhead athlete with back pain.
Thoracoabdominal Injuries
A critical component of energy transfer from the hips and pelvis to the upper extremities is
the trunk and abdominal muscles. During batting and pitching, electromyographic analysis has
shown that there is near-maximal activation of the abdominal oblique muscles, with maximal
activation occurring during certain phases of the pitch and swing.21,32 Furthermore, overhead
motions place a dual demand on the abdominal muscles–trunk stabilization and creation of axial
torque.21,32,58 This leaves little to no room for the abdominal muscles to overcompensate for weak-
ness or decreased motion in the hips and pelvis. Abdominal muscle strains are fairly common in
overhead sports, accounting for 5% of all baseball injuries requiring placement on the Disabled List
over the past 20 years, with the majority being internal/external oblique (abdominal muscle) or
intercostal (rib cage muscle) strains.58 They are most commonly seen on the nondominant, or lead,
side and have a 12% reinjury rate.58 Anecdotally, there has been a trend toward increased inci-
dence of abdominal (oblique) muscle strains in professional tennis, associated with the increased
popularity of the open-stance stroke mechanics. This relatively high reinjury rate suggests that
rather than being an isolated event, abdominal muscle strains may indicate dysfunction at another
point along the kinetic chain. Just as hip range of motion has been correlated with groin strains,
pubalgia-type injuries, shoulder problems, and low back pain,7,43 it is plausible that hip pathology
could also correlate with abdominal muscle strain or other trunk injury.
Diagnosing abdominal muscle strains is usually straightforward, characterized by the sudden
onset of side pain with focal tenderness, usually occurring after a serving, throwing, swinging, or
other forceful twisting motion. Occasionally, fascial tearing and muscular herniation can be seen
with these injuries on examination. Other injuries in the differential diagnosis include rib stress
fracture, costochondral rib injury, thoracic disc herniation, and other rare conditions. Abdominal
muscle strains are treated symptomatically with NSAIDs, relative rest, core strengthening, and
flexibility exercises, and return to play occurs when pain-free with maximal exertion. Average
recovery from abdominal muscle strains in Major League Baseball players is reported to be 35 days
for pitchers and 27 days for position players.58 For professional athletes, a treatment algorithm of
MRI to confirm the diagnosis and exact muscle involved (Figure 14-5) followed by ultrasound-
guided corticosteroid injection is sometimes used, though there are no studies comparing this to
more conservative management. An important point in treating abdominal muscle strains, espe-
cially reinjuries, is that it should spur further assessment of the athlete for hip and pelvis dysfunc-
tion and core training habits.
Shoulder and Elbow Injuries

Numerous studies have linked lower extremity and trunk dysfunction with shoulder and elbow
injuries in overhead sports.6,7,10,23,24,26,27,33 Repetitive valgus stress on the elbow can result in
ulnar collateral ligament attenuation and posteromedial elbow impingement. Ulnar nerve symp-
toms and flexor-pronator strain may also be seen at the elbow. Excessive torque and repetitive
stress on the shoulder often results in internal impingement, characterized by posterosuperior
labral injury and articular-sided rotator cuff injury. Posterior capsule contracture is also often
seen, which can result in altered glenohumeral joint motion.6
When training and treating overhead athletes, assessment should begin at the start of the sea-
son and continue periodically throughout, since upper extremity injuries often have prodromal
symptoms, such as loss of velocity, loss of pitch command, and changes in mechanics.6 Standard
lower extremity assessments such as hip range of motion (including flexion and internal rotation
232 Chapter 14
Figure 14-5. Coronal MRI showing

a left internal oblique muscle strain
(arrow) in a professional baseball
pitcher.
to assess for impingement) and the single-leg squat to assess hip abductor strength and core sta-
bilization should be performed in addition to evaluation of mechanics. If lower extremity or core
pathology is discovered in addition to a shoulder or elbow injury, and it is causing pain and affect-
ing mechanics, then the treatment and rehabilitation plan should be designed to address both the
acute injury and underlying causes. Focus should be placed on injury prevention, which includes
avoiding overtraining, monitoring athletes for proper rest and conditioning, and addressing global
functional deficits as soon as they are detected.
PEARLS AND PITFALLS

● A comprehensive assessment is critical in the overhead athlete, examining the entire kinetic
chain to be able to discern where issues are arising from.
● Because of the closed-chain internal rotation required for overhead sports, restrictions in
motion will lead to ramifications through the kinetic chain and may lead to SI joint, pubic
symphysis, lumbar spine, core muscle, and upper extremity injuries.
● Hip abductor weakness may have a significant impact on power generation, and should be
assessed in all overhead athletes.
● The maximal contraction of the obliques during batting and pitching means these muscles
are at risk for injury, especially with the paired demand of trunk stabilization and generation
of rotational torque.
CONCLUSION
In evaluation of the overhead athlete, a global assessment is required. Pitching, serving, spiking,
and bat and tennis racket swinging are integrated movements that require maximal contributions
from the body throughout each part of the kinetic chain, from the lower extremities to the hands.
Athletes can often compensate to a degree, but when weakness or restricted motion in the kinetic
chain becomes significant, athletes often decompensate by placing greater stress downstream in
the kinetic chain and increase the risk of secondary injuries. To properly diagnose and treat the
overhead athlete, in addition to focusing on the body part that is injured, it is important to perform
a global assessment of the hip and core and correct any underlying factors that may contribute
to injury.
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21. Watkins RG, Dennis S, Dillin WH, et al. Dynamic EMG analysis of torque transfer in professional baseball
pitchers. Spine (Phila Pa 1976). 1989;14(4):404-408.
22. Stodden DF, Langendorfer SJ, Fleisig GS, Andrews JR. Kinematic constraints associated with the acquisition of
overarm throwing. Part I: step and trunk actions. Res Q Exerc Sport. 2006;77(4):417-427.
23. Aguinaldo AL, Buttermore J, Chambers H. Effects of upper trunk rotation on shoulder joint torque among
baseball pitchers of various levels. J Appl Biomech. 2007;23(1):42-51.
24. Stodden DF, Fleisig GS, McLean SP, Lyman SL, Andrews JR. Relationship of pelvis and upper torso kinematics
to pitched baseball velocity. J Appl Biomech. 2001;17(2):164-172.
25. Escamilla RF, Andrews JR. Shoulder muscle recruitment patterns and related biomechanics during upper
extremity sports. Sports Med. 2009;39(7):569-590.
26. Davis JT, Limpisvasti O, Fluhme D, et al. The effect of pitching biomechanics on the upper extremity in youth
and adolescent baseball pitchers. Am J Sports Med. 2009;37(8):1484-1491.
27. Wight J, Richards J, Hall S. Influence of pelvis rotation styles on baseball pitching mechanics. Sports Biomech.
2004;3(1):67-84.
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28. Chow JW, Park SA, Tillman MD. Lower trunk kinematics and muscle activity during different types of tennis
serves. Sports Med Arthrosc Rehabil Ther Technol. 2009;1(1):24.
29. Sheets AL, Abrams GD, Corazza S, Safran MR, Andriacchi TP. Kinematics differences between the flat, kick,
and slice serves measured using a markerless motion capture method. Ann Biomed Eng. 2011;39(12):3011-3020.
30. Fleisig G, Nicholls R, Elliott B, Escamilla R. Kinematics used by world class tennis players to produce high‐
velocity serves. Sports Biomech. 2003;2(1):51-64.
31. Chow JW, Shim JH, Lim YT. Lower trunk muscle activity during the tennis serve. J Sci Med Sport.
2003;6(4):512-518.
32. Shaffer BEN, Jobe FW, Pink M, Perry J. Baseball batting: an electromyographic study. Clin Orthop Relat Res.
1993;292:285-293.
33. Aguinaldo AL, Chambers H. Correlation of throwing mechanics with elbow valgus load in adult baseball pitch-
ers. Am J Sports Med. 2009;37(10):2043-2048.
34. Voos JE, Mauro CS, Kelly BT. Femoroacetabular impingement in the athlete: compensatory injury patterns.
Oper Tech Orthop. 2010;20(4):231-236.
2011;39(1 Suppl):7S-13S.
2005;87(7):1012-1018.
40. Birmingham PM. The effect of dynamic femoroacetabular impingement on sacroiliac joint motion. International
Society for Hip Arthroscopy Podium Presentation, October 14-15, 2011, Paris, France.
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ment on pubic symphysis motion: a cadaveric study. Am J Sports Med. 2012;40(5):1113-1118.
42. Shindle MK, Voos JE, Heyworth BE, et al. Hip arthroscopy in the athletic patient: current techniques and
spectrum of disease. J Bone Joint Surg Am. 2007;89(Suppl 3):29-43.
44. Shindle MK, Ranawat AS, Kelly BT. Diagnosis and management of traumatic and atraumatic hip instability in
the athletic patient. Clin Sports Med. 2006;25(2):309-326.
45. Shindle MK, Voos JE, Nho SJ, Heyworth BE, Kelly BT. Arthroscopic management of labral tears in the hip.
46. Byrd JW, Jones KS. Hip arthroscopy in athletes: 10-year follow-up. Am J Sports Med. 2009;37(11):2140-2143.
48. Minnich JM, Hanks JB, Muschaweck U, Brunt LM, Diduch DR. Sports hernia. Am J Sports Med.
2011;39(6):1341-1349.
49. Meyers WC, Foley DP, Garrett WE, Lohnes JH, Mandlebaum BR. Management of severe lower abdominal
or inguinal pain in high-performance athletes. PAIN (Performing Athletes with Abdominal or Inguinal
Neuromuscular Pain Study Group). Am J Sports Med. 2000;28(1):2-8.
51. Paajanen H, Hermunen H, Karonen J. Pubic magnetic resonance imaging findings in surgically and conserva-
tively treated athletes with osteitis pubis compared to asymptomatic athletes during heavy training. Am J Sports
Med. 2008;36(1):117-121.
52. Dreyfuss P, Dreyer SJ, Cole A, Mayo K. Sacroiliac joint pain. J Am Acad Orthop Surg. 2004;12(4):255-265.
54. Anderson SA, Keene JS. Results of arthroscopic iliopsoas tendon release in competitive and recreational ath-
letes. Am J Sports Med. 2008;36(12):2363-2371.
55. Ernest S, Quamar B, Philip R, Philip J, Wayne William G, J Charles T. Adductor-related groin pain in competi-
tive athletes. Role of adductor enthesis, magnetic resonance imaging, and entheseal pubic cleft injections. J Bone
Joint Surg Am. 2007;89(10):2173-2178.
56. Sanchis-Moysi J, Idoate F, Izquierdo M, Calbet JAL, Dorado C. Iliopsoas and gluteal muscles are asymmetric in
tennis players but not in soccer players. PloS One. 2011;6(7):e22858.
57. Lawrence JP, Greene HS, Grauer JN. Back pain in athletes. J Am Acad Orthop Surg. 2006;14(13):726-735.
58. Conte SA, Thompson MM, Marks MA, Dines JS. Abdominal muscle strains in professional baseball: 1991-2010.
Am J Sports Med. 2012;40(3):650-656.
15
The Endurance Athlete
Runners, Cyclists, Rowers, and Triathletes
Peter J. Moley, MD; Suzanne Gutierrez-Teissonniere, MD;

and Marc R. Safran, MD
Sports injuries to the hip and pelvis represent approximately 5% to 6% of athletic injuries in
adults and 10% to 24% of those in children.1 Overuse injuries are more common in endurance
athletes, but acute injuries can occur as well. Endurance athletes alternate periods of intensive
physical training and periods of rest and recovery. Any imbalance between training and recovery
may result in overuse injuries.2-4 A thorough history and physical examination and knowledge of
hip anatomy and function are fundamental to obtaining an accurate diagnosis. Advancements in
imaging studies have facilitated the clinician’s ability to identify soft tissue pathology in the hip.5
The differential diagnosis of hip and groin pain in the athlete is extensive, and may vary based on
the age group.4 A delay in diagnosis may limit or delay return-to-sport activities and may place
athletes at risk for degenerative injury of the hip.6-9
INITIAL EVALUATION
History Evaluation
A careful history evaluation is essential in order to obtain an accurate diagnosis and should
include the patient’s age, presence or absence of trauma, mechanism of injury, timing of events,
location of injury and pain, exacerbating and alleviating factors, previous injury, and prior
treatments.4,10 Limitations of a patient’s function should also be assessed in the initial evaluation.
There should be a low threshold for considering a femoral neck stress fracture, particularly in the

238 Chapter 15
female endurance athlete, given the potentially devastating consequences of misdiagnoses. The
female athlete triad, including amenorrhea, disordered eating, and osteoporosis, should be thor-
oughly worked up.
As mentioned, the differential diagnosis varies according to age group. Younger, skeletally
immature athletes are more likely to develop apophyseal injuries and avulsion fractures.11 Active
young adults are more likely to develop bursitis and muscular strains. This age group is usually
involved in high-intensity training that may lead to a variety of diagnoses secondary to trauma
and/or overuse. Finally, previous acute or chronic injuries to the hip are believed to predispose
athletes to degenerative arthritis, which is more common with advanced age.6,11 In addition to age
group, the type of sport participation may narrow the differential diagnosis of hip pain in the ath-
lete. Certain sports may place the athlete at increased risk of a specific hip pathology based on his
or her individual biomechanics and training methods. Therefore, athletes should also be screened
for alterations in biomechanics and training errors. For example, in runners, it is essential to know
the weekly running mileage, any changes in duration or intensity of training, changes in the type
of running surface, type/age of footwear, or recent changes in gait, shoes, or orthotics.4,12-14 In the
cyclist, the clinician should evaluate for changes in equipment (saddle, shoes, cleats), position on
the bicycle, saddle height, training habits, or terrain.4,15-18 In rowers, training occurs throughout
the entire year. It is important to know the position of the athlete on the boat, if he or she skulls
or sweeps, is starboard or port, ergometer and rowing techniques, and type and quantity of
training.19,20 Some studies have mentioned that 50% of rowing injuries occur in land-based train-
ing, such as ergometer use or running.19
Physical Examination
A careful physical examination of the injured area, including a gait assessment, evaluation for
mechanical malalignment, and biomechanical considerations, should be obtained. Using a consis-
tent and systematic approach for every patient ensures adequate diagnosis, and reduces the chance
of missing significant findings.10,11 Examination of the hip should include inspection, palpation,
range-of-motion testing, strength testing, sensory exam, neurovascular exam, and special tests. In
addition, the patient’s stance, gait, transfers, and leg length symmetry should be evaluated. It is
crucial to compare the affected side to the uninjured leg in order to be able to detect subtle deficits.
Imaging
Imaging studies are an extension of the history and physical evaluation. Thus, requesting
certain studies will depend on the individual athlete’s presentation. Adkins and Figler11 recom-
mended obtaining films of patients after acute injuries presenting with painful gait, inability to
bear weight, point tenderness at a muscular insertion site, or a significant reduced range of motion.
For chronic injuries, obtaining images will depend on the severity of symptoms, diagnosis, or
treatment failure. In our clinic, we perform standard imaging on all new patients to aid in the
evaluation of osteochondral joint space, coronal coverage, neck shaft angle, and alpha angle.
Plain radiographs are usually the first imaging studies obtained in athletic patients with hip
pain. There are several views available: anteroposterior (AP) view of the pelvis, cross-table lateral,
elongated femoral neck, Dunn at 45 or 90 degrees of hip flexion, frog leg lateral, and false profile.
Hip pathology is not always evident on plain radiographs. Computed tomography (CT) scan
of the pelvis and hip has been suggested to be superior to plain film radiography for demonstra-
tion of both bony and structural pathomorphology, especially in trauma evaluation.8 CT scan
with 3-dimensional reconstructed images of the hip allows for recognition of subtle fractures,
assessment of osseous abnormalities in patients with femoroacetabular impingement (FAI), and
assessment of femoral version; it also helps determine the surgical approach, if necessary.21 CT
scan is the preferred modality in the setting of trauma, and for identifying avulsion fractures and
The Endurance Athlete 239
Figure 15-1. Ultrasound-guided hip joint

injection.
myositis ossificans.8,22 Magnetic resonance imaging (MRI) of the hip is the imaging of choice
in athletic patients presenting with hip pain and normal plain radiographs. MRI has been valu-
able in the diagnosis of intra-articular disorders, occult osseous abnormalities, and soft tissue
injuries.7,23-28 Fat-suppressed T2-weighted or short-tau inversion recovery (STIR) sequences are
preferred for detecting edematous changes in the myotendinous unit, identifying cysts, evaluat-
ing stress fractures, and classifying muscle strains and tendon abnormalities.22 Our institution
typically performs screening examination with use of coronal inversion recovery and axial proton
density sequences.21 High-resolution cartilage-sensitive images in 3 planes (coronal, axial, sagit-
tal) are obtained with use of a fast spin-echo pulse sequence and an intermediate echo time.21,23
Diagnostic Hip Injections

Distinguishing between intra-articular and extra-articular pathology in hip pain can often be
difficult. In recent years, physicians have opted to perform a fluoroscopically or ultrasound-guided
intra-articular injection to facilitate the diagnosis. Reduction of symptoms following an intra-
articular injection of anesthetic has been shown to be a 90% reliable indicator of an intra-articular
pathology.29 In our institution, we use the anterosagittal approach for the injection guided by
ultrasound (Figure 15-1). Patients are asked to keep a pain diary for 2 weeks after the injection for
follow-up assessment. Pain relief immediately after the injection would confirm an intra-articular
etiology of pain.30
SPORT-SPECIFIC BIOMECHANICS
Running
Running is a high-impact activity in which significant forces are repeatedly generated across
the hip joint. Running gait is defined by the presence of a float phase in which both limbs are in the
air. Force plate studies demonstrate that there are 2 peaks of ground reaction force: shortly after
impact and right before toe-off. Evidence suggests that impact forces may be mitigated through
usage of an increased cadence with shortened stride length and a midfoot or forefoot strike
pattern.31-33 The majority of the ground reaction force is directed vertically through the femur
onto the acetabulum, and the highest magnitude muscle moments are generated in the sagittal
plane. There are also stabilizing muscle moments in the coronal plane.
240 Chapter 15
The hip and muscles about the joint are important for both force generation and load trans-
mission, and act in flexion and extension at various points in the gait cycle.34 The hip extends to
the greatest degree at toe-off, after which point it flexes, reaching maximum flexion during the
mid-portion of swing phase. The degree of flexion at mid-swing increases with velocity, as does
stride length. The hip extends by stretching the hamstring during the late portion of swing phase
in order to lengthen the stride and buffer the leg against impact forces.
Cycling
When seated, cycling is a relatively non–weight-bearing sport in which the cyclist can only
apply about half of his or her body weight to the pedal. However, when the cyclist stands, a force
up to 3 times body weight can be applied to the pedal.17 The following discussion will be lim-
ited to cycling while seated, with the understanding that standing cycling produces significantly
greater forces.
There are 2 distinct phases in the pedal cycle, defined as the circular motion of one pedal: the
power phase and the recovery phase. The power phase determines the amount the cyclist is able
to push forward, and is defined by 180 degrees of pedal motion from top dead center to bottom
dead center. Although the most power is generated when force is applied tangentially to the axis
of rotation, cyclists generally push down on the pedal throughout the power phase, extending
their hips. The hip extends from a flexed position of approximately 55 degrees during the power
phase, with peak extension occurring at the end of the power phase. The degree of hip flexion at
the beginning of the power phase depends on the degree of forward trunk lean, with greater lean
correlating with higher flexion. However, the thigh is usually 10 to 20 degrees below the horizontal
plane at the beginning of the power phase, regardless of trunk position. Both gluteal and ham-
string muscle groups are responsible for hip extension. The gluteal muscles aid in hip extension
during the first two-thirds of the power phase, while the hamstrings aid in the last three-quarters.
Hence, both muscle groups are involved in the middle and late portions of the power phase, which
happens to be the moment of greatest hip torque.17,35 However, evidence shows that peak cycling
hip loads are lower than peak hip loads during level walking.35 Knee extension follows hip exten-
sion, particularly when the foot is strapped in the pedal. Knee adduction follows knee extension,
causing an increase in the Q-angle, defined as the angle formed between the quadriceps and
patellar tendon.
The recovery phase represents the next 180 degrees of the pedal cycle, in which the pedal moves
up from bottom dead center to top dead center. This applied force in the recovery phase creates a
negative-pedal force, working against the power generated by the other pedal. Advanced cyclists
may try to mitigate this negative force by actively using the iliopsoas and rectus femoris muscles
concentrically to flex the hip and the hamstrings muscles to flex the knee.17 Regardless, the hip
and knee are moved to a flexed position in preparation for the power phase. The knee moves later-
ally as it flexes, decreasing the Q angle.17 This mediolateral movement of the knee relative to the
knee and hip flexion and extension may cause friction at the iliotibial band (ITB).
Several bicycle adjustments can help to minimize injury: seat position (height and forward/
backward orientation), handlebar position (height and distance from cyclist), crank length, and
foot position.17 Seat height determines the degree of maximal knee and hip extension, with a
lower height maintaining the hip and knee in a more flexed position. Individuals with tight ham-
strings and/or short gluteals should have a lowered seat height in order to limit hamstring and
iliotibial tension, respectively, at bottom dead center. The lower limit of seat height should equal
an individual’s inseam length. A seat positioned forward, in addition to reducing power, reduces
hip flexion and increases knee flexion. Slightly shorter crank lengths help with frictional issues
by reducing the amount of knee excursion. Many cyclists lower their handlebars for aerodynamic
reasons. This arrangement bends the cyclist over further, increasing hip flexion and tension on the
gluteal and hamstring muscles.17
Rowing
Rowing is a low-impact endurance sport that involves the pull of a vessel using fixed oars.
There are 2 basic kinds of rowing: sculling and sweeping. During sculling, the athlete uses 2 oars
simultaneously to propel the boat. Individuals who sweep hold one oar in both hands and row
from the same side of the boat throughout the race. Sweeping involves more lateral trunk move-
ment and axial rotation than sculling.36 Ergometers are equipment used for land-based rowing
training. Traditionally, these machines are center-pull; hence, they closely approximate a sculling
motion in which individuals use 2 oars.
The rowing motion involves 4 distinct phases: (1) the catch, (2) the drive, (3) the finish, and
(4) the recovery. During catch phase, when the oar(s) drop down and come in contact with the
water, the arms are extended, hips flexed, knees flexed, and lumbar spine flexed. During the drive
phase, the oar is pulled through the water to the front of the boat. The hips, knees, and spine
extend, while the arms become flexed at the elbow. The finish involves the lifting of the blade out
of the water by a downward push on the oar handle. During recovery, the oar blade moves back-
ward, and the arms are extended and the hips, knees, and lumbar spine flexed as the oar handle
moves forward.
Swimming
Swimming is a non–weight-bearing, low-impact endurance sport. There are 4 major swim-
ming racing strokes: (1) front crawl, (2) backstroke, (3) breaststroke, and (4) butterfly stroke. Each
stroke places different demands on the hip. The mechanics of freestyle include 4 different phases,
including entry/catch, early pull/pull, push, and exit/recovery. The power from the kick is gener-
ated through hip and knee extension, and requires good stabilization through the core. Butterfly
is composed of the catch, the frontsweep, the backsweep, and the recovery. The rapid movement
from flexion of the hips and knees to extension during the backsweep provides the most propulsive
force. The breaststroke is broken into phases including the glide, outsweep, catch, insweep, and
recovery. Breaststroke involves the most amount of hip internal rotation and abduction of all of the
strokes. Breaststrokers have been found to have an increased incidence of hip adductor injuries3
due to the forceful adduction. Additionally, there are 4 distinct phases in competitive swimming:
(1) starting phase, (2) swimming phase, (3) turning phase, and (4) finishing phase. Biomechani-
cal analysis is usually limited to the swimming phase. There is a lack of studies on swimming
kinematics and joint forces, as most studies focus on efficiency and mechanical optimization
for performance.
COMMON INJURIES
Extra-Articular Pathology
Muscle Strains
Hip pain in endurance athletes may be associated with muscle imbalances. Muscle strains tend
to be the most common athletic injuries. They occur more often in muscles that cross 2 joints, in
muscles that contain fast-twitch or type 2 fibers, and during an eccentric contraction.2,8,37 Loca-
tion of the strain or tear is frequently at the myotendinous junction.37 Understanding the mecha-
nism of injury and the location of symptoms is crucial in order to make an accurate diagnosis.
Ultrasound may be useful in assessing thickness of fibers and fluid consistent with tendinosis, or
presence of tears.5 Although not always necessary, MRI has been described as the study of choice
because of its superiority in visualizing soft tissue abnormalities in multiple planes, especially
in the STIR and T2-weighted sequence with fat saturation.2,8 It is superior in the evaluation of a
242 Chapter 15
larger area, though resolution is higher using ultrasound. Some studies have presented a classifica-
tion of muscle strain based on MRI findings: first degree (stretch injury), second degree (partial
tear), and third degree (complete rupture).8 Presence of a hematoma at the myotendinous junction
in MRI is considered pathognomonic of a second-degree strain.8 Common modifiable risk factors
leading to muscle strains include muscle imbalance between agonists and antagonists, fatigue,
lack of flexibility, and poor trunk coordination. Adequate treatment, including addressing these
factors, reduces the likelihood of reinjury in the athletes.
Hamstring Tendinopathy
The most commonly strained muscles in the hip area are the hamstring,2,8,38 the biceps femo-
ris, the semimembranosus, and the semitendinosus. All of them, except for the short head of biceps
femoris, originate from the ischial tuberosity, and insert onto the proximal tibia and fibula. They
are susceptible to injury due to a sudden eccentric contraction, most commonly in the long head of
the biceps femoris.12,38 In high-speed running, the mechanism is usually an eccentric contraction
that occurs during the terminal swing phase of the gait cycle, resulting most often in injury along
an intramuscular tendon and adjacent muscle fibers.2,12,38 The mechanism of injury in other
activities, such as dancing or kicking, is usually due to an extreme stretch during hip flexion with
the knee extended and results in injury to the proximal free tendon, which has been associated
with tears, worse outcomes, and longer recovery. Thus, identification of the mechanism of injury
and localization of pain in the athletes is crucial in order to adequately predict the recovery time.
Athletes, such as runners, will present with sudden onset posterior thigh pain. In addition, weak-
ness in knee flexion and hip extension might be evident on examination in more severe injuries, as
well as limitation in range of motion and tenderness to palpation over the ischial tuberosity. Severe
injuries, especially to the proximal tendon, will result in a partial or complete tear that presents as
an audible tear with associated pain, bruising, and perhaps a palpable defect.
Studies in runners have shown that the more proximal the site of maximum pain, the longer
the time required for complete recovery.12 In cycling, a high seat height position may result in
increased knee extension, leading to excessive tension and injury to the hamstrings, especially
the lateral hamstring.17 Hamstring injuries have a high rate of recurrence. Therefore, athletes
should be screened for modifiable risk factors that could be improved through training in order
to prevent reinjury.
Adductor Tendinopathy
Injuries to the adductor muscles usually occur during movements involving quick accelera-
tion, or change of direction, which occur in running and cycling.3,38 Adductor tendonitis presents
with pain in the groin or medial thigh. Further examination reveals pain near the attachment at
the pubic ramus, reproduction of pain with resisted isometric hip adduction, and tenderness to
palpation of the involved tendon.39-40 However, pain upon resisted adduction is not considered a
hallmark for the diagnosis, since other pathology has been shown to produce similar symptoms,
such as osteitis pubis.39,40 Also, it must be remembered that the adductor magnus originates from
the ischial tuberosity, and if injured, may present with findings similar to a hamstring strain.
Again, understanding the mechanism of injury along with the patient’s symptoms will facilitate
the diagnosis. In breaststroke swimmers, hip adductor overuse injury is common due to repetitive
forceful adduction, with the knees flexed, against the water mass.3
Hip Abductor Injury
Hip abductor injury often occurs due to muscle imbalance and overuse in the athletes, especial-
ly runners. It is more common in women, likely because of the wider female pelvis.5 In addition,
patients with hip dysplasia can have abductor overload.41 Normal strength in the tensor fascia lata
(TFL) with reduced strength in the posterior gluteus medius (abduction with hip extension) may
be present without symptoms, but results in overuse.42,43 Patients will present with hip and but-
tock pain that worsens with prolonged sitting or standing and when lying on the involved side.43
On exam, there is usually tenderness to palpation in the gluteal muscles lateral to the posterior
superior iliac spine (PSIS) and/or over the insertion at the greater trochanter. As mentioned previ-
ously, hip abductor weakness results in Trendelenburg gait. If not treated effectively, this gait may
contribute to low back pain due to lumbar facet irritation,43 as well as greater trochanteric pain
syndrome/bursitis due to abductor muscle tear, or from external snapping from overuse of the
gluteus muscles (see below).
Bursitis
A bursa is a sac lined by a synovial membrane that serves as a cushion between muscle tendons
and bony structures around a joint. Bursitis is used to describe inflammation of a bursa, mainly
due to direct trauma, altered biomechanics, overuse, or excessive rubbing and/or friction.5,8
Patients will present with pain localized to the area. Plain radiographs are mainly used to rule out
intra-articular pathology, but may show calcifications in the region of the bony structures adjacent
to the specific bursa.8 MRI may show increased signal surrounding the bony structure on STIR
sequences.8 Ultrasound may be reliable in identifying the inflamed bursa and its etiology. For the
diagnosis of greater trochanteric pain syndrome, Strauss et al5 reported that ultrasound modali-
ties identify gluteus medius and minimus tears or tendinopathy, evidence of snapping hip, and an
inflamed trochanteric bursa.
Ischial Tuberosity Bursitis
The ischiogluteal bursa lies between the ischial tuberosity and the hamstring tendons. It is most
commonly inflamed in sedentary individuals with prolonged sitting,8 but it may also be affected
in rowers due to a prolonged sitting position on a hard seat,19 as well as runners and cyclists from
overuse injury and irritation of the hamstrings over its origin. In addition, cyclists may experience
this condition due to inadequate fit of the saddle, which causes constant friction on the ischial
bursae.15 Athletes will present with buttock pain that may radiate down the posterior thigh if
the sciatic nerve gets irritated with the bursa inflammation.8 Pain is worst with sitting, climb-
ing stairs, or running. Athletes, especially rowers, should be educated about their sitting position
and biomechanics.
Greater Trochanteric Pain Syndrome
The greater trochanter serves as an attachment for 5 muscles: the fibromuscular sheath com-
posed of the gluteus maximus, TFL, and ITB that lies anterior to the gluteus medius and minimus
tendons.5 Greater trochanteric pain syndrome has been associated with hip abductor injury/over-
use/tear; degenerative arthritis of the lumbosacral spine, knee, and hip; limb length discrepancy;
obesity; and snapping hip syndrome.8 It occurs in 10% to 25% of the general population (most
common in middle-aged females), but incidence has been increasing in younger athletes, especially
in runners.5
Greater Trochanteric Bursistis
The most commonly inflamed bursa is the deep subgluteus maximus bursa, which presents as
lateral hip pain on exam.5 The greater trochanteric bursa lies between the TFL and gluteus medius
and the greater trochanter of the femur. Athletes with trochanteric bursitis present with pinpoint
tenderness at the greater trochanter, exacerbation of pain on hip abduction against resistance, and
a positive flexion, abduction, and external rotation (FABER) test resulting in posterolateral hip
pain. Pain worsens with activity, with prolonged standing, when crossing the legs, or when lying
down on the affected side. Athletes, especially runners and cyclists, should be educated on main-
taining hip abductor muscle strength and good biomechanics. In cyclists, riding with a bike seat
that is too high could lead to tension of the ITB, resulting in trochanteric bursitis.18
244 Chapter 15
Iliopsoas Tendonitis/Bursitis
The iliopsoas bursa lies in the anterior hip between the iliopsoas muscle and pelvic brim. It
is the largest bursa in the body. Young female athletes are most commonly affected.8 Clinical
presentation includes anterior hip pain, and sometimes, a palpable or audible snap. Endurance
athletes are at high risk for this condition from repetitive hip flexion and extension. The rowing
stroke includes full hip flexion during the initial/catch phase, and progression to hip extension for
the rest of the stroke (drive, finish, and recovery phases).20 The excessive hip flexion may result in
inflammation of the tendon over the pelvic brim, excessive rubbing/friction of the bursa, and/or
internal snapping of the hip. In runners, sprinting and hill climbing may cause chronic rubbing
of the iliopsoas tendon on the iliopectineal bursa, leading to bursitis and iliopsoas syndrome.14
Meanwhile, in cyclists, riding with a bike seat that is too high could lead to tension of the iliopsoas,
resulting in iliopsoas tendonitis.18
Coxa Saltans Syndrome (Snapping Hip)
Coxa saltans, or snapping hip, syndrome manifests as an audible snapping or catching sensation
in the hip during certain movements.1,8 It is classified into external (lateral) or internal (medial)
based on symptom location. Most patients with symptomatic snapping of the hip tend to be young
with active lifestyles.5 No imaging modality has been effective in distinguishing between the
etiologies of coxa saltans syndrome, but some believe that performing a static and dynamic ultra-
sound may confirm the diagnosis.1
Internal Coxa Saltans
Internal coxa saltans (ICS) is present when the iliopsoas tendon rubs or snaps against, most
commonly, the iliopectineal eminence of the superior pubic ramus. Some other mechanisms that
have been proposed include accessory iliopsoas tendinous slips, stenosing tenosynovitis of the ilio-
psoas insertion, iliopsoas tendon snapping over a bony ridge at its insertion at the lesser trochanter,
snapping of the iliofemoral ligament over the anterior femoral head, and subluxation of the long
head of the biceps femoris at the ischium (snapping bottom).1 Snapping occurs anteriorly in the
hip when moving from flexion and external rotation into extension and internal rotation,1 which
may be assessed by performing a fan test, which mimics this motion. When the snapping leads to
inflammation and pain, it may be associated with iliopsoas tendonitis/bursitis (see above). Ath-
letes at high risk include those who require hip movements at high flexion angles (associated with
internal and external rotation), and/or those who overtrain or participate in extensive hip flexion
drills, such as rowers and runners.1
External Coxa Saltans
External snapping hip occurs when either the posterior portion of the ITB or the anterior por-
tion of the gluteus maximus rubs or snaps against the greater trochanter.1
External coxa saltans (ECS) is the most common cause of snapping in the hip. If the diagnosis
is ECS, an Ober’s test should be performed to assess for ITB tightness. When the ITB is involved,
it lies posterior to the greater trochanter in hip extension, and glides over it to the anterior position
during hip flexion.8 Snapping occurs on the lateral hip during repetitive flexion and extension
of the joint, which may be assessed by performing the bicycle test. It is usually easier to diagnose
compared to ICS. ECS occurs in endurance athletes, including cyclists and runners, since they
perform repetitive flexion/extension movements of the hip.1
Iliotibial Band Syndrome
The ITB originates from the iliac crest as a connective tissue sheet composed of gluteus maxi-
mus and TFL, runs along the lateral aspect of the thigh, and inserts onto the Gerdy’s tubercle of
the tibia. ITB syndrome is a clinical diagnosis. Imaging studies are not necessary, unless another
pathology needs to be ruled out. It mainly occurs because of repetitive friction against the lateral
femoral condyle of the femur, which may lead to inflammation and pain on the lateral aspect of
Figure 15-2. Ischial apophysitis in a 15-year-old runner.
the knee at 30 degrees of knee flexion.13,43-45 Proximally, it acts as a lateral hip stabilizer. Noehren
et al46 reported that greater hip adduction and knee internal rotation movements tend to result in
greater ITB strain. Although less common, the proximal portion of the ITB could also be strained,
leading to lateral hip pain and ECS.
Some biomechanical factors associated with increased incidence of ITB syndrome include
leg length discrepancy, forefoot varus, rearfoot eversion, hip abductor weakness, and increased
Q angles.13,43,45 ITB syndrome is commonly found in endurance athletes and is due to repetitive
stress to the ITB. Training errors that may be related to ITB syndrome include excessive training,
sudden increase in activity level, sudden increase in distance or frequency of activity, lack of expe-
rience with hill training, and inadequate footwear.
In cycling, the ITB is repetitively irritated due to constant pedaling, especially in a poorly fit
bicycle. It is crucial to evaluate the bicycle fit. Stress to the ITB could arise from a cleat pedal that
is internally rotated or too far forward, a saddle that is too high or too posterior, or misalign-
ment in leg length discrepancy.44 Bicycle adjustments should be directed to reducing stress on the
lateral knee.44 Similarly, misalignment in runners has been addressed with the use of orthotics.
ITB syndrome has been described as the most common cause of lateral knee pain in runners.43
Biomechanical studies show that injury occurs during the deceleration phase or early stance
phase of the gait cycle in runners.45 Symptoms tend to be worse with activity, especially during
downhill running or going down stairs. Faster-paced running has been documented to be less
likely to exacerbate ITB syndrome, since, at foot strike, the knee is flexed beyond 30 degrees.45
Thus, management should emphasize not only biomechanical factors, but also training and activ-
ity modification. Rowers who abruptly switch to running may develop similar problems, likely due
to weakness of hip abductors.19
Apophysitis and Avulsion Fractures
Younger, skeletally immature athletes are prone to apophyseal injuries as well as avulsion
fractures.11 The apophysis is the weakest part in the muscle/tendon/bone unit in the pediatric
population. Injury may occur at any of the ossification centers of the pelvis, such as at the origin
of the hamstrings at the ischial tuberosity (Figure 15-2), rectus femoris at the anterior inferior iliac
spine (AIIS), sartorius at the anterior superior iliac spine, and adductors at the pubic symphysis.39
Injury is due to unbalanced muscle contractions during an extreme event, but if chronic, it is
mainly due to repetitive microtrauma or overuse.8 Mechanism of injury, clinical presentation, and
management are similar to that of muscle strains in adult athletes. The diagnosis is made by clini-
cal exam, and confirmed by imaging.
246 Chapter 15
Athletic Pubalgia (Core Muscle Injury)

The etiology of athletic pubalgia or sports hernia is extremely controversial, but likely multi-
factorial in nature. Litwin et al47 report that it is likely caused by a combination of muscle injuries,
as evident on imaging studies, that lead to weakening of the posterior abdominal wall, with the
resultant formation of an occult direct or indirect hernia. This condition presents with exertional
lower abdominal and groin pain that may radiate to the perineum, scrotum, and inner thigh.47-49
Symptoms tend to resolve with rest, but usually return with resumption of physical activity. It is
more commonly reported in male athletes with high-intensity training, such as in long-distance
runners.47 A true inguinal hernia is not palpable on exam, but tenderness to palpation may be
present at the pubic tubercle/ramus, inguinal canal, and hip adductors origin.47,48 Reproduction of
pain during a supine resisted sit-up, along with palpation of the pubic ramus on the affected side,
is suggestive of sports hernia.
Imaging studies are performed to rule out other conditions. Dynamic ultrasound could be used
to identify the posterior inguinal wall deficiency, but it is operator-dependent.47 MRI is useful to
rule out other conditions in the differential diagnosis. Some studies have shown that MRI has a
high specificity for identifying rectus abdominis and adductor tendon injuries, but also has an
extremely high false-negative rate for rectus abdominis injury.50 Thus, careful attention to the
patient’s symptoms and clinical correlation is recommended. Some cases are self-limiting, but
others become chronic and debilitating.
Osteitis Pubis
Osteitis pubis is a painful inflammatory condition involving the pubic symphysis and its sur-
rounding structures.51 It occurs most commonly in males. The mechanism of action involves
repetitive twisting/cutting movements that result in stretching and tearing of the adductor muscles
and irritation at the pubic symphysis.8,51 There are many predisposing factors that may lead to
this condition. In athletic participation, sprinting, kicking, twisting, and cutting activities may
exacerbate or lead to the condition.51 Running is a common sport that incorporates some of these
activities. Osteitis pubis presents with insidious onset of pain localized to the lower abdomen,
pubic symphysis, and adductor muscles. On examination, patients will have tenderness to palpa-
tion at the pubic symphysis, as well as pain with resisted strength testing of the hip adductors and
lower abdominal muscle groups.51 Imaging studies may include MRI, which would show narrow-
ing of the joint space with diffuse bone marrow edema.8,51 It is a self-limiting condition, but some
cases become chronic and debilitating.
Stress Fractures
Stress fractures account for 20% of all injuries seen in sports medicine clinics,8 and 7% to 10%
involve the hip and pelvis.52-54 Insufficiency fractures occur from normal stresses to abnormal
bone and are commonly seen in the elderly population with underlying osteoporosis, but fatigue
stress fractures that occur from excessive stresses to normal bone are seen in young athletes,8
especially in runners, due to abnormal forces on normal bones (Figure 15-3). In general, female
athletes are more prone to stress fractures,14,53,54 especially those with amenorrhea, low energy
availability, and osteoporosis, which is known as the female athlete triad.14 Please see Chapter 11
for further information.
Intra-Articular Pathology
FAI is due to an abnormal contact between the proximal femur and the acetabular rim during
terminal motion of the hip, most evident during flexion and internal rotation. This abutment leads
to repetitive stress causing pain, damage of soft tissue structures such as the acetabular labrum
and/or adjacent chondral tissue, and progressive degenerative joint disease.6,7,9,28,55,56 It mainly
Figure 15-3. Cortical compression side stress fracture

of the right hip.
results from aberrant morphological features of the femoral head-neck junction (cam), acetabular
rim (pincer), or both.6,9,54,55 A combination of both types of FAI is the most common presenta-
tion, which occurs in the anterior femoral neck and anterosuperior acetabular rim.9,57
Patients typically present with insidious onset of anterolateral hip pain. Sporting activities
requiring hyperflexion, hyperextension, and external rotation of the hip have been associated with
producing high stresses on the acetabular rim, leading to microtrauma and injury of the labro-
chondral complex.27,58 In FAI, patients with repeated flexion and internal rotation will develop a
pinching pain in the hip that may limit their sport participation. Thus, endurance athletes with
structural abnormalities of the hip are predisposed to FAI, since they are continuously exposed to
extremes ranges of motion in the hip.
Other Variant: Subspine Impingement
FAI must be distinguished from a more recently described variation of rim impingement that
is caused by focal impingement against the AIIS. It is an extra-articular impingement that occurs
when the AIIS, which serves as origin of the rectus femoris tendon and muscle, impinges inferiorly
on the femoral neck with straight hip flexion. Patients experience anterior groin pain during hip
flexion. When diagnosis is not clear, an intra-articular diagnostic injection with local anesthetic
would provide symptom relief in patients with FAI, but no relief in those with subspine impinge-
ment due to the extra-articular location of the soft tissue compression and injury.
Acetabular Labral Tears
Acetabular labral tears have been clearly recognized in the literature as a possible cause of hip
pain in athletes.24 A study by Wenger et al59 reported that 87% of 31 patients with labral tears were
found to have at least one structural abnormality, including retroverted acetabulum, abnormal
femoral head-neck offset, and coxa valga. Repetitive microtrauma has been suggested as a possible
mechanism of injury in these patients.
There are several thoughts regarding the higher prevalence of anterior tears, which include poor
vascular supply to that area, weaker tissue, and exposure to higher forces or stresses.26 Sporting
activities that require repetitive twisting motion, hyperextension, hyperflexion, hyperabduction,
and/or frequent external rotation of the hip have been suggested to result in labral tears.24,26
In endurance athletes, runners are most commonly affected because of repetitive high forces
to the joint. Athletes most commonly present with anteromedial groin pain and a clicking audible
sound, or locking sensation. Limitation in the hip range of motion is another common finding.
248 Chapter 15
A previous history of trauma or fall might be recalled, but is not always present. Recent studies have
reported that acetabular labral tears may represent as early stage degenerative hip disease.29,58,60
Other
Other intra-articular pathologies of the hip include loose articular bodies, osteochondral
fractures, synovial chondromatosis, as well as ligamentus teres tear. Although these are found
less commonly in endurance athletes, they should be part of the initial differential diagnosis of
hip pain.
NONOPERATIVE TREATMENT OPTIONS

Regardless of the pathology, an accurate diagnosis will facilitate providing the best manage-
ment available, and allow an estimation of when the athlete can return to play safely. Conserva-
tive therapy is usually the initial treatment in the majority of injuries to the hip in the endurance
athlete.61 However, unique to the endurance running athlete, femoral neck stress fractures are
relatively high on the differential diagnosis for hip and groin pain. Thorough evaluation to rule
out a stress fracture in these patients is mandatory, as certain types have a high risk for displace-
ment and require more aggressive management. Initially, it consists of rest, ice, pain medications,
and physical therapy. In addition, it should be remembered that endurance athletes primarily
sustain overuse injuries due to fatigue, muscle imbalances, training errors, or sudden increase in
frequency or duration of activity. Thus, the treatment must be targeted toward correcting any of
these factors that might have precipitated or contributed to the injury directly or indirectly, such
as with physical therapy and activity modifications.
Moreover, the treatment plan should be individualized based on patients’ specific findings and
diagnosis, as well as tailored to their sport’s biomechanical factors and participation level. It is also
important to remember that athletes may benefit from evaluation and management from a sports
psychologist in order to facilitate their adjustment to the injury and overall recovery. In addition,
the diet and energy expenditure of endurance athletes should be evaluated to ensure that their
energy availability is adequate for sport participation.62 A multidisciplinary team approach is ideal
for effective management, and should include physicians, physical therapists, athletic trainers,
nutritionists, and psychologists.
Rehabilitation/Physical Therapy
When creating a rehabilitation plan for the athlete, the bony structures, supportive muscles,
soft tissue structures, pelvic stability, joint pathology, and neuromuscular control should be taken
into account.63 This will provide a specific plan for the athlete’s individual needs. Treatment
goals should be discussed with the athlete, athletic trainer, and physical therapist. Typically, these
include reducing the pain, restoring the range of motion, improving strength and flexibility, and
progressively returning to sports participation level. Treatment protocol after an acute injury
includes relative rest, ice, compression, and elevation (RICE). If walking exacerbates the pain, the
athlete can be given crutches for a few days with limited weight bearing.63 Gentle massage to the
affected area with ice might alleviate any associated swelling.
Although not many studies exist, literature suggests that strengthening exercise of the hip
and abdominal core is an effective intervention for these athletes.64-67 Ekstrom et al68 found in
their study that specific exercises, such as the bridge, unilateral-bridge, prone-bridge on elbows
and toes, and quadruped arm/lower extremity lift, had increased muscle signal activation during
electromyography (EMG) for endurance training and stabilization of trunk and hips. Many stud-
ies agree that therapy may focus initially in static (isometric) strengthening, but should eventually
progress to dynamic (isokinetic) strengthening.64,65 Overall, there is insufficient evidence about

the most effective intensity, frequency, and duration of exercise.
The program should include modalities with passive exercises initially, followed by an active
training program that should focus on eccentric resistive strengthening of the affected muscles
and correction of any muscle imbalances.2,38,63,66 Once the athlete recovers pain-free range of
motion and strength, sport-specific performance training is started to facilitate a safe return to
play. In general, hip pain associated with extra-articular pathology resolves with an adequate
conservative program, except in refractory conditions and avulsion fractures greater than 2 cm or
displaced more than 1 cm.14 For intra-articular hip pathology, a trial of nonoperative treatment is
usually performed, mainly addressing any muscle imbalances that might be present. If conserva-
tive measures are unsuccessful, surgical procedure options should be discussed with the patient.
Therapeutic Injections
In acute injuries causing limitation in functional activity due to pain related to tendon-
itis or bursitis, an injection with corticosteroids could be performed to alleviate the pain. The
effectiveness of these injections may improve with use of ultrasound or fluoroscopic guidance.
Some studies have found improvement in visual analog pain scale (VAS) with a mean of 2.8 fol-
lowing injection of corticosteroid with local anesthetic in the trochanteric bursa.69,70 Another
study reported that therapeutic injections to the greater trochanteric bursa have been shown to
provide pain relief in 60% to 100% of affected patients.5 These injections could also alleviate pain
from greater trochanteric syndrome associated with ECS.5,8 Injections provide the patient with
pain relief to resume therapy and the use of injections, along with other modalities and physical
therapy, has been found to be most effective in treating the symptoms.71
Training and Activity Modifications

In general, literature has recommended that a warm-up with either jogging or cycling, followed
by dynamic stretching that includes sport-specific movements, should be performed prior to com-
petitions or training.63 Static stretching should be performed at the end of the athletic activity. Our
experience has been that appropriate activity modifications has been one of the most useful means
of decreasing pain and getting athletes back to their sport.
Runners
Runners should be aware that a faster pace is associated with stronger and faster lengthening
of muscles. Thus, a gradual increase in training schedule will allow muscles to adjust to increases
in the eccentric loading.72 Athletes will benefit from nonimpact exercises, such as swimming or
cycling, to enhance conditioning during the recovery period.53 Initially, athletes should alternate
activity with rest days and incorporate cross-training.73 Then, increase in weekly mileage, speed,
and intensity should be guided by the presence or absence of pain. Lowering the impact forces may
reduce the risk of overuse injuries. A study by Crowell and Davis74 found a reduction in the load-
ing forces in runners after completing a gait-retraining program involving the use of a treadmill
with real-time visual feedback of tibial acceleration.74
Cyclists
Activity modifications include ensuring correct seat height and angle and correct cleat posi-
tion, wearing padded shorts, and using a more suitable saddle74 (Figure 15-4). A correct bicycle
fit with regular safety checks is fundamental for the prevention of injuries in the athlete.15,18,74
In addition, training following an injury should increase gradually, as soon as pain-free range of
motion and strength are achieved. Correct cycling technique must be emphasized, such as main-
taining a cadence of more than 80 rpm and using a lower gear in order to reduce pressure on the
250 Chapter 15
Figure 15-4. Bike setup.
limbs.17 Riding too many miles or too many hills at the start of the cycling season would result in
overuse injuries.15
Rowers
Rowers should follow running activity modification and injury prevention indications stated
above to prevent overuse injuries. In addition, ergometer training should be limited after injury
and during recovery time, since it has a greater load to the joints and has been associated with
more injuries, especially during the catch phase.20,76 Intensity of training in the water should
increase gradually in the spring to prevent injuries.20 In rowers who develop an ischial bursitis, a
seat cushion may be utilized.
Medications
Management of an acute injury to the hip usually includes anti-inflammatory medications for
pain relief. The most common medications used are the nonsteroidal anti-inflammatory drugs
(NSAID). In animal studies, NSAIDs have been found to potentially lengthen the healing time
by impairing the mechanical strength return of the injured tissue.77 Although the exact effects
on tissue healing in the clinical setting remain unknown, it has been suggested that the reduced
inflammatory response caused by NSAIDs could potentially result in delayed recovery and/or
reinjury susceptibility.77,78 Thus, we recommend only using a brief course of NSAIDs for pain
relief, if needed.
Orthotics
Orthoses and new shoes should be used to correct for overpronation, excessive calcaneal ever-
sion, pes cavus, and pes planus in order to prevent recurrent injury.79 Some studies have suggested
that the use of either cushioned insoles, cushioned shoes, or custom-made orthoses may reduce
the loading forces in runners.80-82 If a leg length discrepancy of more than 1.5 to 2 cm is identi-
fied, then a shoe lift will assist in correcting the misalignment.10,11 In cyclists, there are specialized
shoes that use toe clips or sole cleats for shoe attachment to the pedals in order to prevent injuries.75
Rigid orthoses have been preferred to help reduce misalignment of overpronated foot in cyclists.17
Surgical Treatment
Surgical indications for the endurance athlete with persistent hip injury should follow similar
recommendations to those previously outlined. Tension-sided stress fractures, or compression-
sided stress fractures that involve greater than 50% of the femoral neck should be treated with
percutaneous pin fixation, as outlined in Chapter 11. Proximal hamstring avulsions involving
2 or more tendons with 2 or more centimeters of retraction should be considered for surgical treat-
ment to avoid loss of power in the extension phase of running and cycling, and the potential for
sciatic nerve irritation. Chronic partial hamstring tears with persistent pain (proximal hamstring
syndrome) that have failed conservative treatment and PRP injections should be considered for
surgical repair. Persistent pain and dysfunction from core muscle injury should be considered for
surgical management. Persistent pain related to underlying FAI morphology and subsequent intra-
articular derangement should be considered for surgical correction of the intra-articular damage
and structural pathomorphology.
PEARLS AND PITFALLS

● A complete evaluation, including a detailed training history and any equipment changes, is
important to be able to glean the pathomechanisms for the injury the athlete presents with.
● When possible, a sport-specific analysis may elucidate technical factors that are predisposing
the athlete to injury in activities where there are a myriad of repetitions of the same motion.
● Activity modification is one of the most effective interventions in the population. Modifica-
tions including an adequate warm-up and dynamic stretching, cool-down, and static stretch-
ing following activity are most effective in decreasing pain.
CONCLUSION
Hip pain is a complicated, multifactorial injury process that affects a great number of athletes.
Though not typically thought of as a common mechanism, endurance sports have a high incidence
of hip injuries. Running is the most common cause among elite and recreational athletes.83 One
must be cognizant of the injuries germane to the endurance athlete that may range from structural
to muscular and neuropathic.
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tions for greater trochanteric pain syndrome: Multicentre randomised controlled trial. BMJ. 2009;338:b1088.
70. Shbeeb MI, O’Duffy JD, Michet CJ Jr, O’Fallon WM, Matteson EL. Evaluation of glucocorticosteroid injection
for the treatment of trochanteric bursitis. J Rheumatol. 1996;23(12):2104-2106.
71. Lustenberger DP, Ng VY, Best TM, Ellis TJ. Efficacy of treatment of trochanteric bursitis: a systematic review.
Clin J Sport Med. 2011;21(5):447-453.
72. Montgomery WH 3rd, Pink M, Perry J. Electromyographic analysis of hip and knee musculature during run-
ning. Am J Sports Med. 1994;22(2):272-278.
73. Fredericson M, Moore W, Guillet M, Beaulieu C. High hamstring tendinopathy in runners: meeting the chal-
lenges of diagnosis, treatment, and rehabilitation. Phys Sports Med. 2005;33(5):32-43.
74. Crowell HP, Davis IS. Gait retraining to reduce lower extremity loading in runners. Clin Biomech (Bristol,
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75. Thompson MJ, Rivara FP. Bicycle-related injuries. Am Fam Physician. 2001;63(10):2007-2014.
76. Wilson F, Gissane C, Gormley J, Simms C. A 12-month prospective cohort study of injury in international row-
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77. Warden SJ. Cyclo-oxygenase-2 inhibitors: beneficial or detrimental for athletes with acute musculoskeletal
injuries? Sports Med. 2005;35(4):271-283.
254 Chapter 15
78. Stanley KL, Weaver JE. Pharmacologic management of pain and inflammation in athletes. Clin Sports Med.
1998;17(2):375-392.
79. Hreljac A. Impact and overuse injuries in runners. Med Sci Sports Exerc. 2004;36(5):845-849.
80. Milani TL, Hennig EM, Lafortune MA. Perceptual and biomechanical variables for running in identical shoe
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81. O’Leary K, Vorpahl KA, Heiderscheit B. Effect of cushioned insoles on impact forces during running. J Am
Podiatr Med Assoc. 2008;98(1):36-41.
82. Mündermann A, Nigg BM, Humble RN, Stefanyshyn DJ. Orthotic comfort is related to kinematics, kinetics,
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2010;468(3):741-746.
16
The Hypermobile Athlete
Dancers, Cheerleaders,
Figure Skaters, and Gymnasts
Lisa M. Tibor, MD and Ernest L. Sink, MD
The athletes who participate in sports that emphasize the extremes of motion, like dance,
cheerleading, figure skating, and gymnastics, are a unique population and often are a challenging
group to treat. In part, this is because these sports require that the participants have a dual mental-
ity—one of an athlete and, simultaneously, one of an artist. Additionally, dancers and gymnasts
generally start at a very young age, sometimes as early as 2 to 4 years old for females and, if they
reach an elite level, are performing or practicing 4 to 8 hours per day.1-4 As such, overuse injuries
are common. At the elite level, these sports are extremely competitive, and as such, athletes often
train or perform through pain.5,6 There is also evidence that dancers, and likely also cheerlead-
ers, gymnasts, and figure skaters, may not be able to distinguish between pain from an injury and
“performance pain”—musculoskeletal soreness that is appropriate for the demands of the sport.6
If the pain is perceived as threatening to one’s career, the dancer tends to use avoidance strategies
or regards the pain as catastrophic to psychologically cope.
Dance, cheerleading, figure skating, and gymnastics have similar demographic and injury pat-
terns. Overuse injuries in the lower extremities are common, with the foot and ankle being most
frequent sites of injury. Nonetheless, hip, groin, thigh, and pelvis injuries are also common in these
sports. In addition, there are more female participants than male in these sports, which may also
influence injury patterns, particularly around the hip.2,3,7-12 Depending on the specific activity
or type of dance, injuries around the hip make up between 4% and 12% of all injuries sustained
in these sports (Table 16-1).2,3,5,7-14 There may also be increased rates of hip osteoarthritis and
arthroplasty in former dancers,15-17 although the reasons for this are not entirely clear.

256 Chapter 16
TABLE 16-1
INJURY PREVALENCE
SPORT/ PREVALENCE OF HIP OR THIGH INJURY REFERENCE, YEAR
ACTIVITY (OUT OF ALL INJURIES REPORTED)
Ballet Hip, thigh, or pelvis: 6.4% to 7.2% Garrick and Requa 19932
Leanderson et al 201110
Musical Hip: 4.6% to 6.2% Evans et al 19967
theater Injured patients were more likely to be Evans et al 19988
female or occur if on a raked stage
Hip-hop or Hip or thigh: 9% to 12% Kauther et al 200913
break dance Ojofeitimi et al 201214
Irish dance Pelvis or lumbar spine: 5.1% Noon et al 20109
(females)
Gymnastics Hip or groin: 6.6% of overuse injury in O Kane et al 201111
club-level gymnasts Sands et al 19935
Hip, groin, thigh, or hamstring: 10.5%
Right-sided injury more common
Cheerleading Upper leg: 1.2% of injuries presenting to the Jacobson et al 201212
emergency department
Figure skating Groin pain: 5.9% Dubravcic-Simunjak et al
Hamstring: 2% 20033
There are some sport-specific patterns to these injuries. In musical theater, injuries were more
likely to occur in females and when performers were on a raked stage. A raked stage is tilted toward
the audience to improve the view of the dancers, which requires accommodation in the dancers’
center of gravity.7,8 In a series of collegiate gymnasts, lower extremity injuries5 occurred more
often on the right, although the authors did not speculate on the underlying reason for this obser-
vation. For cheerleading, injury rates have been reported only by the National Electronic Injury
Surveillance System (NEISS). The NEISS collects data on acute injuries presenting to a network
of hospital emergency departments. In this data set, the upper leg made up 1.2% of acute injuries
in cheerleaders who presented to the emergency department.12 The epidemiology of less acute or
chronic injuries in cheerleaders is unknown. In figure skaters, at least half of all injuries are over-
use injuries that take weeks to months to resolve.3 A disproportionate amount of overuse injury
occurs in singles skaters, whereas pairs and ice dancers are more likely to sustain acute injuries
from falls.3 In adult masters-level skaters, hip injuries were the most common acute or chronic
injuries causing skaters to take time off of the ice.18
BIOMECHANICS
The hip is central to the movements in these sports. Ballet is the most studied, but often other
dancers have some background in ballet.14,19 The turnout is the foundation of many movements in
classical ballet, which involves maximal external rotation of the lower extremity. For the aesthetics
of ballet, 90 degrees of turnout is desirable. The total external rotation is the sum of the rotation
The Hypermobile Athlete 257
Figure 16-1. External rotation is important for hip abduc-

tion because externally rotating the femur moves the
trochanter away from the ilium, where it would otherwise
impinge and limit abduction. (Reprinted with permis-
sion from df028/www.shutterstock.com, 2012. Accessed
September 28, 2012.)
at all of the lower extremity joints, with the hip providing 60% of the external rotation and the
remainder coming from the knee and the ankle. If the necessary external rotation cannot be
obtained at the hip, it may place undue strain on other joints.1,19-21 Achieving maximal external
rotation of the hip is also important for abduction because it rotates the trochanter away from the
ilium, where it would otherwise impinge and limit abduction (Figure 16-1).20
All of these sports also emphasize jumping and landing, yet have a low incidence of anterior
cruciate ligament (ACL) injuries as compared to team sports.22 Male and female elite ballet dancers
were observed to use a hip-dominant strategy for decreasing lower extremity force when landing
a jump.23 There is little frontal plane movement around the hip during the landing. Specifically,
this avoids knee valgus and hip adduction, maintaining overall neutral lower extremity alignment
during the landing and protecting the ACL from injury.23 Figure skaters have even higher jump
speeds and landing forces than dancers. Because the skate boot limits ankle dorsiflexion, skat-
ers must increase hip flexion and/or lumbar hyperextension to absorb the force of landing the
jump.24,25 Using more hip flexion is the preferred landing strategy as it keeps the free leg more
stable and is more aesthetically appealing.24 Relying on muscular control about the hip for jump-
ing and landing, however, necessitates balanced and appropriate patterns of neuromuscular firing.
When the muscular balance around the hip is disrupted, regardless of whether the cause is intra-
or extra-articular, compensatory patterns cause strain on other muscles and place the athlete at
risk of injury lower down on the kinetic chain (ie, at the knee, ankle, or foot).
COMMON INJURIES
Influence of Acquired Range of Motion
The extreme hip range of motion necessary for these sports has been studied in the context of
ballet. There is an emphasis on hip abduction and external rotation, which can lead to adaptive
shortening of the lateral hip capsule, external rotators, gluteus medius, and iliotibial band (ITB).
When compared to nondancers, female ballerinas were found to have increased external rotation
258 Chapter 16
and decreased internal rotation, with a slight increase in the total arc of hip rotation.1,26-28 Girls
who could not maintain this range of motion eventually dropped out of ballet.28 Young female
dancers also had more hip abduction than controls.28 With age, hip abduction decreased, which
is consistent with the normal increase in the depth of the hip as the acetabulum ossifies.29 Male
ballet dancers also had increased external rotation and decreased internal rotation relative to
nondancers, although, in contrast to the women, they displayed a decrease in the overall arc of hip
rotation.1 In general, flexibility decreases with age, with a natural progression over childhood and
adolescence toward less flexibility. Through dance training, dancers are able to maintain more
of this range of motion.28 The relative increase in hip external rotation in dancers is important,
however, because it requires either (or both) relative retroversion of the femoral neck or anterior
soft tissue laxity,30 both of which have biomechanical implications in the context of dysplasia and
femoroacetabular impingement (FAI).
Influence of Gender
Significantly more females than males participate in the dance and flexibility sports. Syllo-
gistically, dance and the flexibility sports are common among females presenting with hip pain.
Although jumping and landing mechanics are similar for male and female dancers,23 there may
be other factors exacerbating hip pain in these women. For example, dysplasia is much more com-
mon in females than males.31-33 Hormonal laxity may also play a role. The prevalence of hyperlax-
ity increases after puberty,34 and high levels of pregnancy-related hormones facilitate loosening
of pelvic ligaments. There is evidence that serum relaxin may be related to a higher rate of ACL
injuries in females,35 although it is unknown if a similar mechanism plays a role in the setting of
hip pathology.
Dysplasia
Because these dance and the other flexibility sports select for athletes with better hip range
of motion, those who reach more elite levels may be predisposed to dysplasia or hyperlaxity.28
Acetabular coverage is one predictor of internal rotation in flexion,36 and, when compared to
impingement patients, patients with dysplasia had significantly more internal rotation and abduc-
tion and showed a trend toward having increased external rotation.36,37 In a series of profes-
sional dancers who underwent hip arthroscopy for labral tears, 55% had radiographic evidence of
dysplasia.38 When a patient with dysplasia also has soft tissue hyperlaxity, hip instability can be
exacerbated. In normal children, the prevalence of hyperlaxity ranges between 1% and 7%,39,40
whereas in children with congenital hip dislocation, hyperlaxity was seen in one-third (females) to
three-fourths (males) of the cohort.39 The extreme examples of this are 2 case reports of dancers
with both hyperlaxity and dysplasia who sustained low-energy (noncontact) anterior hip disloca-
tions while practicing dance.41,42 Furthermore, the combination of hyperlaxity and dysplasia may
also predispose patients to other injuries up and down the kinetic chain.43
Soft Tissue Laxity

The unstable “lax” hip without some element of bony undercoverage is a controversial concept.
It is frequently written about but highly subjective.44-47 Sports medicine surgeons frequently com-
pare the concept and treatment of the painful lax hip to the known association between laxity and
the shoulder with multidirectional instability.44,48 Biomechanically, the iliofemoral ligament is
known to be a primary stabilizer to the hip in external rotation and anterior translation.49 Because
the hip is such a constrained joint, however, the bony morphology and the 3-dimensional relation-
ship between the femur and acetabulum may be significantly more important for hip stability.
Computer models assessing hip stability with variable amounts of anterior and lateral acetabular
coverage50 found that lateral subluxation is eliminated when the center-edge angle is greater than
25 degrees. A cadaveric study of the labral contribution to hip stability that included a full cap-
sulectomy observed no change in the hip stability ratio until a 2-cm partial labrectomy had been
performed.51 When the hip is dysplastic or has excessive acetabular or femoral anteversion, then
the capsule and labrum are likely to play a larger role in hip stability.
The ability to place one’s palms flat on the floor when standing takes some amount of either
routine flexibility training or hyperlaxity and is generally considered an indicator of low back and
hamstring flexibility.28 Dancers are generally able to achieve this; thus the ability to “palm” the
floor is a skill related to their training. However, dancers who are truly hyperlax by other mea-
sures seem to be predisposed to overuse and tendon injuries.1,52 In one series, professional dancers
with joint hypermobility made up one-fifth to one-third of the dance company. The hypermobile
dancers were more likely to have tendon injuries52,53 and to need longer time off from dancing to
recover from injuries.52 There is reasonable evidence that pain in a hyperlax patient may be related
to a strength deficit or an altered pattern of muscular activation because the patient is more reli-
ant on dynamic mechanisms of joint stabilization to compensate for weak static stabilizers. In the
knee and shoulder, laxity is associated with altered neuromuscular firing and reflex patterns.54-56
Furthermore, gait analysis of adults with generalized joint hypermobility revealed a higher abduc-
tor moment around the hip in the midphase of stance as compared to normal controls,57 meaning
that the hypermobile individuals used more abductor force than normal controls. Gait analysis of
people with Ehlers-Danlos syndrome and Down syndrome, representing more extreme examples
of hyperlaxity, showed that the gait pattern was more cautious on the whole to maintain balance.58
The theory behind the gait alterations is that decreased joint stiffness causes a deficit in the correct
transmission of muscular forces.58 As a result, soft tissue pain and, specifically, lateral hip pain
may be prominent complaints. Impaired proprioception has also been implicated as a causative
factor in the soft tissue pain related to hyperlaxity, particularly in the setting of ankle or shoulder
instability.56,59 It is unclear if a similar mechanism occurs around the hip, however. A study of
lumbopelvic control in dancers showed no association between better control and the degree of
soft tissue laxity.53
Strength Imbalances and Proprioceptive Deficiencies

Because dancers spend a disproportionate amount of time in external rotation, they nearly
always have a strength imbalance, with stronger hip abductors and weaker adductors.1 In addi-
tion, side-to-side differences in strength have also been observed.1,27 The muscular imbalance can
be a cause of soft tissue pain or may exacerbate the symptoms from underlying intra-articular
pathology. Subtle proprioceptive impairments can also predispose these athletes to injury, even in
the setting of normal soft tissue laxity. Athletes with impaired postural stability are at increased
risk of injury, or alternatively, can have worsened postural stability as a result of an injury (eg, in
the setting of an ankle sprain).59-61 Dancers with impaired lumbopelvic control had a higher risk
of low back pain and lower extremity injury.53 Another study found that dancers with an injury
lower in the kinetic chain used their hips more when trying to balance than uninjured controls.61
Impingement
FAI or impingement due to supranormal motion in a normal hip may cause a substantial
amount of hip pain and labral tears in dancers. In one series of dancers having arthroscopy for
intra-articular pathology, FAI was thought to be the cause of the pathology in up to half of the
patients.38 A motion analysis study of professional dancers with morphologically normal hips
found that, because of their extensive training and soft tissue laxity, dancers were able to place
their hips at extremes of motion that caused impingement and impingement-induced subluxation
(Figure 16-2).62 The area of impingement was located superiorly and posteriorly, which correlated
with cartilage thinning and labral tears on magnetic resonance imaging (MRI) of the dancers’
hips. Adolescent female dancers made up a large number in a series of adolescents being treated for
260 Chapter 16
Figure 16-2. Posterior and lateral 3-dimensional reconstructions of motion analysis of the dancer’s hip at the extremes
of motion. The green and red area at the posterior-superior acetabular rim indicates contact during hip motion. The
blue area indicates that no collision was detected. For this study, the acetabulum was divided into 8 zones to report
the region of impingement, with 1 being the anterior-most zone, 3 being superior, and 7 being inferior. (Reprinted
with permission from Charbonnier C, Kolo FC, Duthon VB, et al. Assessment of congruence and impingement of the
hip joint in professional ballet dancers: a motion capture study. Am J Sports Med. 2011;39:557-566.)
FAI,63 with pincer FAI being more common than cam FAI in these women. Because of the range
of motion required in dance, patients with retroverted acetabuli may become symptomatic earlier
than they would otherwise. Furthermore, patients with relative acetabular overcoverage (ie, rim or
pincer impingement) can also have impingement-induced instability. Contact between the rim and
femur induces levering of the femoral head and contrecoup cartilage injury.64-66 Extra-articular
impingement may also be a cause of soft tissue pain in these females. Impingement can occur
between the greater trochanter and the lateral acetabulum, the trochanter, and the ischium,67-69
the anterior facet of the trochanter on the acetabular rim, or the area inferior to the anterior
inferior iliac spine and anterior femoral neck.70 Extra-articular impingement is difficult to assess
solely with radiographs, and is most easily observed with range-of-motion testing in a surgical hip
dislocation. We have observed it most commonly in females with a subtle cam deformity, relatively
short femoral neck, prominent ridge at the anterior facet of the trochanter, and/or a high-riding
trochanter (Figure 16-3). On examination, these patients have limited range of motion that does
not correlate with the subtle FAI findings. The post-Perthes hip with the typical high-riding tro-
chanter and impingement of the trochanter on the acetabular rim is an easier-to-visualize example
of extra-articular impingement. It has been successfully treated with relative femoral neck length-
ening during a surgical dislocation (ie, distalization of the mobile fragment of the trochanter).71
Snapping Hip Syndromes

Up to 90% of dancers report snapping around their hip and 80% of snapping is bilateral.4
A majority (58%) report that the snapping is rarely or occasionally painful, 40% reported having
to interrupt or stop dancing temporarily because of the snapping, but only 7% of dancers required
time off for the pain.4 Often the snapping is voluntary and performed to “free” the hip or relieve
pain. In this group of dancers, 20% had a prior diagnosis of “groin pull,” and 32% had been diag-
nosed with hip flexor tendonitis. Hip injuries were also the second most common “worst injury”
in the past year.4
Figure 16-3. (A) Anteroposterior (AP) pelvis image

of a 20-year-old female dancer with left groin pain,
anterior labral tear, and both intra- and extra-articular
impingement. (B) 3-dimensional computed tomogra-
phy (CT) scan reconstruction demonstrating a small
cam lesion and prominent anterior trochanteric facet.
(C) Sagittal MRI showing an anterior labral hypertro-
phy and tearing. The patient underwent a surgical hip
dislocation, labral repair, and osteoplasty. Six months
postoperatively, she was able to begin dance classes
with modifications.
Although specific maneuvers have been advocated for clinically discerning the location of the
snapping, the interrater reliability of these is poor. Ultrasound has been shown to be more accu-
rate for diagnosing the etiology of the snapping hip.4 The psoas tendon is the most common site,
is frequently bilateral, and is present in 60% of dancers reporting a snapping hip.4 ITB or external
snapping is less common; however, patients with varus neck-shaft angles may be more predisposed
to external snapping because the increased offset creates higher tension in the IT band.72 Exter-
nal snapping has a more dramatic visual appearance than other types of snapping; patients may
perceive the snap as a hip “dislocation.”4 Patients with external snapping may also have less hip
adduction due to tightness of the ITB. More unusual causes of snapping around the hip have also
been reported. There are case reports of ischiofemoral snapping68 or hamstring snapping after a
partial hamstring tendon tear,73 both of which were diagnosed with dynamic ultrasound. Thus,
it is important to keep these in mind when patients report a more unusual location or symptom
complex associated with their snapping.
Abductor Failure
Abductor fatigue and generalized weakness is a frequent source of soft tissue pain in dancers.
Because the abductors help create the external rotation necessary for the turnout, some amount
of endurance is necessary. When the abductors are weak, the tensor fascia lata muscle will
262 Chapter 16
Figure 16-4. (A) Axial, (B) coronal, and (C) sagittal proton-
density magnetic resonance (MR) images from a 30-year-
old dancer with dysplasia, a labral tear (arrows), and a
partial gluteus tear (*).
compensate, resulting in overuse and pain.74 In a single-leg stance, abductor weakness also causes
the knee to drop in to valgus, which can exacerbate pre-existing ITB symptoms. For patients with
dysplasia, abductor weakness and fatigue are predominant presenting symptoms (Figure 16-4).
Because of the lateralization of the hip center in dysplasia, there is relative abductor insufficiency
and an increased lever arm of the center of gravity. In addition, low or negative center-edge angles
cause the abductors to have a more vertical force vector. In normal hips, peak contact pressures
do not vary significantly, but in the dysplastic hip the contribution to the vertical force from the
abductors causes the peak contact pressures to change with the position of the hip75 and can
worsen the static stress on the acetabulum.
Hamstring Strain
A specific type of acute proximal hamstring injury has been described in dancers and other
flexibility athletes (Figure 16-5).76 The injury occurs during slow-speed stretching exercises
with the hip in hyperflexion and the knee extended. Athletes describe hearing a “pop” and feel-
ing local warmth at the proximal hamstring tendon insertion. The proximal free tendon of the
Figure 16-5. (A) Fluid-sensitive coronal MR sequence of a

52-year-old recreational dancer with chronic right hamstring
pain. The patient sustained an acute hamstring injury (curved
arrow) during a dance class several years previously, and also has
some evidence of left hamstring tendinosis. (B) Coronal and (C)
axial proton-density sequences show that one tendon remains
intact (arrowhead), but there is evidence of chronic tendinosis at
the insertion (curved arrow). IT = ischial tuberosity.
semimembranosus is the most common site of injury, but the injury can involve 1 to 3 of the ten-
dons as well as the quadratus femoris.76,77 Most important, however, the injury is associated with
a prolonged time to return to sport or dance, with the median time reported as 30 weeks, ranging
from 9 to 104 weeks.76,77
Stress Fractures and Other Causes of Hip Pain

Because of the emphasis placed on aesthetics, this population is at risk for eating disorders.3,19
In females, delayed menarche is common, as is the female athlete triad of amenorrhea, disordered
eating, and osteoporosis. Dancers with amenorrhea have lower bone mineral density than normal
controls, and amenorrhea has been shown to be predictive for stress fractures.78 Stress fractures
are common in dancers, but occur most often in the feet.79 There has, however, been a case report
of an acetabular stress fracture in an elite level dancer,80 and it is important not to miss a femoral
neck stress fracture as this can have catastrophic consequences if it becomes displaced. Another
extreme example of the consequences of the female athlete triad was a case report of femoral head
collapse in a dancer who had severe anorexia for 9 years yet continued to dance.81
It is also important to keep more unusual causes of hip pain in mind. There is a case report of
hip capsule disruption occurring in an 11-year-old gymnast after a maneuver involving hyperab-
duction of the hip.82 The patient reported anteromedial hip pain, the sensation of a deep “pop”
at the time of injury, and an internal snapping sensation. An MR arthrogram revealed a capsular
264 Chapter 16
perforation of the posterior insertion of the left hip. By report, the patient was treated nonopera-
tively, but the ultimate outcome was not stated.82 A pediatrics journal presented a case report of a
dancer with hip and groin pain who was initially treated for muscle strain associated with dance.
However, the pain persisted and the patient reported a 10-kg weight loss, frequent vomiting,
and occasional low-grade fever. Because of the systemic symptoms and an elevated erythrocyte
sedimentation rate (ESR), the patient was admitted to the hospital and was ultimately found to
have Crohn’s disease and a psoas abscess.83
IN-SEASON EVALUATION
In-season is essentially a misnomer for athletes in the flexibility sports as they frequently
train and perform year-round with no defined “season.” Nonetheless, there are findings in the
history and clinical exam that will help to elucidate the cause of hip pain and that are unique to
this population.
The patient’s gait and single-leg stance should be evaluated for abductor weakness or fatigue.
Regardless of which side is symptomatic, both legs should be evaluated. The findings are often
asymmetric because one leg is often the favored stance or landing leg, which takes more load,
while the other leg is the gesturing leg, which requires more range of motion. In ballet, the right
leg is typically the gesturing leg and the left leg is the stance leg84; a similar asymmetry has been
noted in gymnastics, where injuries were more likely to occur to the right lower extremity.5 Stan-
dard range-of-motion and impingement tests should be performed. A positive impingement test
in flexion adduction and internal rotation is frequent in both FAI and dysplasia,37 but is often
an indicator of labral pathology.64,85 Patients with FAI typically have limited internal rotation in
flexion, whereas, in contrast, patients with dysplasia have more internal rotation and more abduc-
tion and, in some cases, also have more external rotation.37 Strength testing should be performed
with special attention directed to the abductors for signs of weakness, fatigue, or pain provoked
with strength testing. Similarly, the psoas tendon should also be carefully evaluated for strength,
pain provoked by resistance, and “clunking.” Athletes who report snapping around the hip should
be asked if they can voluntarily reproduce the snap, which often provides a significant amount of
clinical information. Apprehension and anterior instability can be tested with the hip in exten-
sion and external rotation; patients with instability will report anterior pain and reproduction of
their symptoms in this position. Patients who have posterior impingement will also experience
symptoms in this position, although the symptoms are located posteriorly rather than anteriorly.
Athletes with acute hamstring strain have pain that is most pronounced in the proximal portion of
the rear thigh, usually about 2 cm distal to the ischial tuberosity. As compared to an acute avulsion
of the proximal tendon insertion, however, there is no bruising or bowstringing of the tendons.76,77
Athletes should also be asked about injuries at other sites of the kinetic chain, specifically the
knee, ankle, and low back. These injuries can cause muscular compensation or impaired proprio-
ception, exacerbating or causing a problem at the hip. Low back pain is frequent in dancers,52 fig-
ure skaters,3 and gymnasts.5 At the limits of hip motion, more lumbar hyperextension is necessary
for leg extension, thus athletes with impingement and more limited hip range of motion may have
compensatory or associated back pain.84 In these sports, footwear is highly specific and varies con-
siderably, especially for females. Footwear can include being barefoot or wearing a soft shoe with
no support, the pointe shoe in ballet, character shoes with heels in musical theater, athletic shoes
for cheerleading, or figure skates. The shoes associated with these sports are known to cause and
exacerbate foot and ankle problems, but the contribution to hip and low back pain is unknown.86
Standard imaging studies should be ordered for these athletes. Anteroposterior (AP) pelvis and
lateral x-rays are evaluated for stress fractures, dysplasia, or impingement. MRI is useful for evalu-
ation of early stress fractures, labral tears, status of the cartilage, capsular tears or thinning, and
injury at the proximal hamstring origin.45 If surgery is being considered, a computed tomography
(CT) scan with version analysis and three-dimensional reconstruction views will help to establish
a mechanical diagnosis and facilitate preoperative planning.
Injections have both diagnostic and therapeutic implications. Diagnostically, they are invaluable
for distinguishing intra- vs extra-articular pain.87,88 Selective cortisone or viscosupplementation
for patients with cartilage damage can also help to temporarily relieve pain and facilitate participa-
tion in physical therapy.89,90 Viscosupplementation in the hip appears to be safe,89,90 but may have
a lower placebo effect than in the knee.91 Intra-articular injections should be used sparingly, pos-
sibly with a lifetime limit of 2 in young patients, given the potential risks for chondrotoxicity 92,93
and avascular necrosis94 that have been reported for local anesthetics and cortisone, respectively.
TREATMENT GUIDELINES
Unless there is a clear indication for surgery (eg, intra-articular loose bodies, incarcerated
labrum, hip subluxation with nonconcentric reduction, tendon avulsions with greater than 2 to
4 cm of retraction, tension-sided stress fractures, and long-standing hip pain with progressive
intra-articular joint destruction secondary to mechanical pathomophology, such as severe dyspla-
sia or impingement), nonoperative measures and physical therapy is the preferred initial treatment
for these athletes.
Rehabilitation
Because dancers, gymnasts, and figure skaters are a specialized patient population with unique
physical demands and injuries, they are best served by physical therapists with experience and
interest in working with the flexibility sports. Hip rehabilitation is also a specialized area and
attempts should be made to find a therapist who also has expertise in treating hip patients.
Manual therapy is helpful for relieving acute muscle spasms and muscular tightness, but needs
to be performed judiciously. Because the hip muscles act to dynamically stabilize the hip, particu-
larly for patients with laxity and/or dysplasia, overaggressive release can actually worsen hip pain
because of an increase in hip instability.84 Active release therapy (ART) is one type of manual
therapy that releases adhesions and fibrosis caused by surgery or chronic injury with the goal of
decreasing tissue tension and normalizing tissue function.74 It can be used in the adductors and
lateral hip (tensor fascia lata, gluteus medius and minimus, ITB, and fascia) for ITB snapping.
ART is particularly helpful when used for initial pain relief, allowing the patient to start a lateral
pelvic stability rehabilitation program to address abductor weakness and retrain neuromuscular
firing patterns.74
Pilates exercises are useful for helping to regain strength, and to change or reorganize neuro-
muscular firing patterns. Dancers tend to have weak gluteus medius and minimus and transver-
sus abdominis function.84 Pilates is a particularly helpful means of rehabilitation because there
are specific exercises that target these muscles, and because the rehabilitation can initially be
performed in a non–weight-bearing fashion on the floor or on a machine, and then gradually
transitioned to weight bearing.84 Care should be taken with stretching exercises, however, particu-
larly if the patient has hamstring pain or stretch injury. Patients with acute hamstring stretching
injuries should begin with active voluntary exercises to gradually increase range of motion. Passive
stretching should be used cautiously as it can provoke pain and overstress healing tissue.76 It is also
important to be realistic with these patients about the potential for prolonged return to sports after
these injuries. There is also some evidence that a program of eccentric closed-chain exercises may
be helpful for hamstring pain. Injury rates and reports of hamstring pain substantially decreased
in a series of professional football cheerleaders on a preventive exercise program consisting of
eccentric closed-chain exercises targeting the hamstrings.95
266 Chapter 16
The general progression of therapy should focus initially on neuromuscular re-education and
pain reduction in a non–weight-bearing fashion. Once this has been achieved, the patient may
progress to weight bearing and, for dancers, standing barre exercises. Patients must demonstrate
correct alignment and form before progressing to plyometric exercises, generally somewhere at
weeks 8 to 12 if they have undergone surgery. Nonoperative patients may progress their therapy
as tolerated, but must show mastery of motion and have little to no discomfort. It may also be
important for patients to improve their aerobic fitness as a means of preventing future injuries.96
This may include stationary biking with the seat raised or the elliptical trainer, and can be started
around weeks 5 or 6. Men tend to have less soft tissue laxity than women in these sports and may
be able to progress faster through the phases of therapy. Age may also influence the rate of pro-
gression in therapy. Younger dancers may advance faster, but older dancers have a finer sense of
body awareness.
The time to return to play or performance is variable, and depends on the etiology of the injury.
It may, however, take longer in athletes with lower body fat percentages, who theoretically have
less energy store available for tissue repair.96 In addition, athletes or performers may need more
rest when recovering from a nonoperative injury than is typically allocated for a professional posi-
tion.97 Thus, it is important to discuss this with the athlete early because returning to sport before
the rehabilitation is complete may result in incomplete recovery from the current injury or a future
injury at another site on the kinetic chain.
The Role of Surgery

Surgery is indicated when an athlete or dancer with a discrete mechanical problem—FAI or
dysplasia—has failed nonoperative measures and is unable to perform because of pain, is requiring
pain medication to perform, or has pain with activities of daily living. Hamstring avulsion with
retraction is also an indication for acute surgical repair, as the results are better and the surgery
is more straightforward when it is performed early.98-100 Patients with tension-sided femoral neck
stress fractures should undergo prophylactic pinning to prevent displacement of the fracture,101
and patients who have a hip dislocation event with an intra-articular loose body are also candi-
dates for surgery.102,103 These diagnoses and surgeries are discussed in the other chapters of this
book, and the reader is directed there for further details of the respective surgical techniques.
Complications of Nonsurgical Management

The most frequent complication of nonsurgical management is failure to improve. This can
occur for a number of potential reasons: (1) The therapy may not be appropriate for the diagnosis
and the patient may benefit from switching to a therapist with more experience treating dancers
and/or hip problems. (2) The mechanical diagnosis or perceived cause of hip pain may not be
appropriate. Not infrequently, athletes are diagnosed with muscle strains but have underlying bony
pathoanatomy like dysplasia or impingement. If this is the case, consideration should be given to
referral to advanced imaging and/or a hip preservation specialist for further diagnosis and man-
agement. (3) The patient may have combined muscular dysfunction and bony pathoanatomy. In
this case, even if the muscular dysfunction improves, the bony pathoanatomy is causing continued
impingement or instability and needs to be addressed surgically.
However, the most devastating complication of nonsurgical management is a missed tension-
sided femoral neck stress fracture that goes on to a displaced femoral neck fracture, subsequent
avascular necrosis, and advanced osteoarthrosis, requiring total hip arthroplasty.
Complications of Surgical Management

In addition to the known complications of arthroscopic and open hip preservation surgeries,
there are a few that may be more likely in this patient population. Because the flexibility athlete
may have a labral tear due to a combination of factors including mild dysplasia, increased atten-
tion should be paid to the mechanical diagnosis determined preoperatively66 and intraoperative
management of the capsule to avoid iatrogenic instability.104 There have been at least 3 case
reports of hip dislocation or subluxation due to iatrogenic instability after arthroscopy.105-107 All
3 occurred in patients who had ligamentous laxity, an unrepaired capsulotomy, and mild or iat-
rogenic dysplasia. Furthermore, rapidly progressive hip arthrosis and high rates of labral retears
have been reported after arthroscopic labral repair in the setting of dysplasia.108-110 The salvage
operation for this is a periacetabular osteotomy (PAO) if the cartilage is preserved or, in the case
of rapidly progressive arthrosis, a total hip arthroplasty. Thus, for a painful hip and labral tears
occurring from dysplasia (center-edge angle [CEA] < 20 degrees), PAO should be considered as the
initial procedure, particularly as the success of PAO is directly related to the state of the cartilage
at the time of surgery.111-114 A psoas tenotomy should not be performed in patients with increased
femoral anteversion. These patients may have subtle anterior instability, particularly in the setting
of soft tissue laxity, and the psoas tendon is a dynamic stabilizer. Patients with increased femoral
anteversion who do undergo psoas release tend to have prolonged or incomplete recoveries with
continued anterior hip pain.115
There has been one series describing return to work in a series of professional dancers who
underwent hip arthroscopy.38 In this series, 73% of dancers were able to return to work at their
previous levels after hip arthroscopy. Older patients, those with chondral damage, and professional
ballet dancers (as compared to other types of dance) were all predictors of lower return-to-work
rates.38 In general, this population of patients frequently represents the most challenging athletes
to get back to their preinjury level of function with or without surgery. As such, very detailed
discussions regarding the nature of injury, the complexities of treatment, the limitations of surgi-
cal management, and the clear development of reasonable patient expectations are of paramount
importance.
PEARLS AND PITFALLS

● Careful soft tissue management is of the utmost importance when treating the hypermobile
athlete surgically. One must be mindful of the athlete’s femoral version when considering a
tenotomy, and avoid doing so in the setting of increased anteversion.
● Hypermobile athletes may present with pain in the setting of relatively normal bony anatomy
due to the extremes of motion that they are required to attain, and these must be taken into
consideration when evaluating these athletes.
● Conservative care should be used as a first line of treatment in these athletes, with physical
therapy consisting of manual therapy and specific neuromuscular re-education exercises.
CONCLUSION
When compared to other athletes with hip pain, patients who perform dance, cheerleading,
gymnastics, or figure skating form a unique group. A high emphasis is placed on the aesthetics of
the sports and the extremes of motion. These patients are more likely to be female and have soft tis-
sue laxity, either generalized or acquired, from years of training. Nonetheless, these patients can be
treated both operatively and nonoperatively with reasonable return to performing, provided that
there is appropriate attention to obtaining a correct mechanical diagnosis, careful rehabilitation in
the hands of a skilled therapist, and, when necessary, appropriate surgical treatment.
268 Chapter 16
ACKNOWLEDGMENT
We appreciate the valuable comments from Bob Turner, PT, regarding rehabilitation in dancers.
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113. Cunningham T, Jessel R, Zurakowski D, et al. Delayed gadolinium-enhanced magnetic resonance imaging of
cartilage to predict early failure of Bernese periacetabular osteotomy for hip dysplasia. J Bone Joint Surg Am.
2006;88:1540-1548.
114. Matheney T, Kim YJ, Zurakowski D, et al. Intermediate to long-term results following the Bernese periacetabu-
lar osteotomy and predictors of clinical outcome. J Bone Joint Surg Am. 2009;9:2113-2123.
115. Fabricant PD, Bedi A, De La Torre K, Kelly BT. Clinical outcomes after arthroscopic psoas lengthening: the
effect of femoral version. Arthroscopy. 2012;28(7):965-971.
17
Sport-Specific
Rehabilitation Guidelines
Pete Draovitch, PT, MS, ATC, CSCS; Toni Dauwalter, PT;

Jaime Edelstein, PT, DScPT, COMT, CSCS;
and Eilish O’Sullivan, PT, DPT, OCS
Returning the athlete to the court or the field following a hip injury involves a graduated return
with a progression based on the achievement of functional milestones. The athletes begin by
mastering basic tasks and, as they are able, are subjected to increasingly complex tasks. In sport-
specific rehabilitation, the goal is to integrate activities that simulate the demands of the athlete’s
sport and specific position. The athlete must demonstrate near-symmetrical range of motion
(ROM), flexibility, strength, proprioception, coordination, and power. Prior to engaging in such
activities in a controlled fashion, the athlete must exhibit mastery of fundamental movements
including squatting, running, jumping, cutting, throwing, kicking, hitting, and/or skating. Drills
and exercises should be initiated in a controlled environment and transitioned to a more variable
environment at speeds used in a competitive arena. Simulated competition and return-to-sport
testing consisting of both general and sport-specific components may bridge the gap between drills
and competition. A graded return is carried out, culminating in the athlete competing at a near
maximum physiological capacity of the sport. This chapter will provide one with an understand-
ing of the fundamental movements and sample progressive programs for the athlete’s return to
sport or activity.
Understanding the forces transmitted through the body during sport aids in the design of
both nonoperative and postoperative programs. These programs should be created with the
intent of minimizing joint forces and optimizing kinetic-linking principles. Kibler1 stated that for
kinetic linking to be effective in athletic movements, there must be appropriately placed forces and

274 Chapter 17
Figure 17-1. Modified side

plank with hip abduction.
motions as a result of physiologic muscle activation imparted on functionally intact anatomy. The
mechanisms of injury and the underlying structure involved are important for recognizing and
tailoring specific interventions targeting these areas.
CORE STABILITY AND PROGRESSION OF CONTROL

Core stability is an integral part of hip rehabilitation, as it establishes the stable platform on
which everything else is based. The simplest definition of the core includes the supportive canister
of muscles surrounding the midsection. This is composed of the diaphragm superiorly, the trans-
versus abdominis anteriorly, the multifidi posteriorly, and the pelvic floor inferiorly. The global
core incorporates links to the extremities and prime movers, including the rectus abdominis,
external oblique, internal oblique, psoas, quadratus lumborum, iliocostalis, gluteus maximus,
gluteus medius, hip adductors, hip external rotators, and latissimus dorsi.2 Zazulak et al3 defined
trunk/core stability as the body’s capacity to maintain or resume a position or a trajectory fol-
lowing perturbation. In athletic function, the core serves as the link between the upper and lower
body segments through which force is transmitted. Endurance tests for the trunk musculature
have been deemed reliable and valid in a number of populations.4 Core stability has been related
to performance measures and linked to increased running speed,5 increased throwing velocity,6
and increased vertical takeoff velocity.7 The literature has also linked decreased core stability to
lower extremity injuries8,9 and lower back pain.10
In those with hip pathology, core stability plays an integral part because of its role in modulat-
ing pelvic tilt. The position of the pelvis may be altered by the abdominal musculature, creating
increased anterior acetabular coverage with an anterior pelvic tilt, or decreased anterior acetabular
coverage with a posterior pelvic tilt. This is primarily based on theoretical modeling of muscle
actions and joint mechanics. Murray and colleagues11 found that pelvic rotation contributes to
18.1% of the change in hip flexion, occurring throughout the arc of motion.
The incipient phases of core stabilization should focus on muscle activation and the ability
to isolate specific components of the core. Appropriate sequencing and motor control strategies
should be monitored, as the athlete may have developed compensatory strategies for functioning
with hip pathology and decreased stability. Once one has mastered this, training for endurance
may begin. Exercises such as bridges and side planks elicit very little hip flexor activity and are safe
and effective exercises for those with hip pathology. The side plank may be initiated standing lean-
ing on the wall, and then progress to side-lying with the knees bent, followed by knees extended.
This may culminate with the addition of active hip abduction, first on flexed knee (Figure 17-1),
then extended, to create a more dynamic challenge and markedly increase the gluteus medius
contribution.12 Other exercises that have demonstrated significant levels of core activation are
Sport-Specific Rehabilitation Guidelines 275
front planks/rollups, bird dog,13 and hamstring curls on the physioball. Medicine ball throws
closely mimic the athletic arena, and may be performed in training as well as for testing.14 As the
athlete’s stability improves, the challenge should increase, including multiplanar activities such
as a D2 pattern with a medicine ball. Core stability exercises should become part of the athlete’s
warm-up, priming the stabilizing muscles before practice.
PHYSICAL THERAPY MILESTONES

Monitoring an athlete’s progress throughout his or her physical therapy course is important
in order to tailor appropriate interventions. A systematic approach should be employed, and
functional tasks should be used to determine whether the athlete is ready to progress to the next
phase of rehabilitation. Achievement of milestones is tracked in preparation for return to activ-
ity—whether to weekend recreational sports or professional-level sporting activity.
Restoration of full ROM should be the first goal of rehabilitation. If the contralateral side has
normal bony morphology, one may aim to achieve motion equal to the contralateral side. If there
is contralateral bony pathology that restricts motion, one may aim to achieve 110 degrees of hip
flexion, 30 degrees of hip internal rotation, 50 degrees of hip external rotation, 45 degrees of hip
abduction, and 10 degrees of hip extension. Strength must be built to support the new ROM, and
manual muscle testing may be used with the assistance of a hand-held dynamometer for more
objective measurements.
A step-down progression may be initiated when the athlete demonstrates adequate lumbopel-
vic stability (ie, ability to ambulate without an assistive device). The patient should complete this
motion in a slow, controlled fashion without dropping the knee into valgus while touching the
foot to the floor. Pelvic alignment should be monitored for aberrant movement as well. Compen-
satory mechanics may be present distally at the foot and ankle complex; one may have the athlete
perform this task without shoes in order to fully evaluate the amount of pronation occurring in
the stance leg.
Squatting is a functional task that may elucidate motor control and motion restriction. Athletes
may be instructed to put their hands overhead to examine full kinetic chain effectiveness, or at
their sides to isolate the lower extremity, and squat down. The depth of the squat is noted, as well as
any compensatory movement patterns. Frequently athletes will deviate away from their operative/
injured side, which may be because of pain or decreased ROM. Knee alignment is also noted with
this, as some patients will deviate into genu valgum because of decreased gluteus medius and hip
external rotator strength. This is an important assessment, as athletes must be taught to use their
newly developed motion in the setting of rehabilitation following femoroacetabular impingement
(FAI) surgery. As demonstrated by Moreside and McGill,15 changes in hip ROM do not necessarily
carry over into functional movements, and thus must be relearned.
The 8-inch step down has been used for patients with a variety of lower extremity pathologies
to indicate general lower extremity function. The task is completed in a slow, controlled manner
without deviations through the trunk, hip, or knee. Attention should be paid not only to the move-
ment, but to the quality of the movement as well (ie, whether there is adequate eccentric control
with a controlled landing).
The single-leg squat is another functional movement that is examined (Figure 17-2). This
motion has been correlated with strength and motor control of the gluteus medius, and is one of
the more challenging tasks to execute properly, but it is an important piece of the rehabilitative
process and one indicator for readiness to return-to-sporting activities. In order to be considered
proficient in the single-leg squat, the athlete must be able to perform the squat without upper
extremity support or deviations through the trunk, hip, or knee. With this activity, compensations
can occur on any level of the kinetic chain, so it is important to evaluate thoroughly.
276 Chapter 17
Figure 17-2. Single-leg squat.
In order to be deemed ready to initiate a running/impact progression, athletes complete a

series of qualitative and quantitative assessments to determine adequate core and lower extremity
stability. The first task is 10 repetitions of resisted side-lying hip abduction with a manual muscle
test score of greater than or equal to 4+/5. The second test is 10 repetitions of an 8-inch step
down with good stability throughout the trunk, hip, and knee, and no deviations. The third test
is 10 single-leg squats with good control and no deviations. To demonstrate adequate core stabil-
ity, the athlete should be able to maintain a side plank for at least 60 seconds each side. Once the
patient has successfully completed these tasks, the patient may begin with short runs on a tread-
mill or rubberized track, progressing in a graded fashion. When utilizing the treadmill, one should
be mindful of the potential for the leg to be pulled posteriorly by the belt; similarly, if utilizing a
de-weighting treadmill, there is strong potential for overstriding, which the athlete should be made
aware of. The volume and intensity of running are gradually increased based on the athlete’s toler-
ance. Plyometric activities are increased as well as integrating sport-specific activities.
RETURN-TO-SPORT TESTING
The decision to return the athlete to sport is multifactorial. The goal is to return the injured ath-
lete to practice or competition without putting the individual at undue risk for injury. It behooves
one to remember basic tenets of rehabilitation—soft tissue and bony healing, normalized gait, full
pain-free motion, full strength, muscle length within functional limits, and good joint stability.
There should be no effusion, inflammation, or pain. Most of the current return-to-play literature
is in the anterior cruciate ligament (ACL) reconstruction population, with a dearth of literature in
the hip return-to-sport arena. Drills or warm-ups that are native to the patient’s sport are used to
assess the patient’s readiness to return to formal sport participation. Prior to returning to play, the
athlete should be running and completing plyometric training on a regular basis. There should
be no pain with the increased activity load, full pain-free ROM, adequate trunk stability, normal
motor patterning, normal functional movements, and pain-free sport-specific movement. Athletes
must be exposed to challenges similar to those encountered in competition while they are in a
controlled environment to determine that they are ready to return. The strength program must be
maintained to protect the athlete from further injury.
Assessments for readiness to return to sport have become popularized, with a number of differ-
ent tests available. A battery of tests is ideal in order to assess all possible challenges an athlete will
face upon returning to competition,16 and should include assessments of core strength/endurance,
functional strength, power, and endurance. The athlete must master the basic testing components
before he or she can attempt the sport-specific aspects. Strength assessment should demonstrate
10 repetitions of 5/5 muscle strength of gluteus medius and 10 repetitions of 5/5 gluteus maximus.
In terms of core stability, the athlete should be able to complete at least a 60-second hold of side
plank and front plank. Normative values have been established for the side plank, and those values
should be the ultimate goal.4 The endurance measures may include the Vail Sport Test,17 which
includes both quantitative and qualitative assessments. When the athlete can tolerate single-leg
impact activity, lower extremity power may be assessed. The single-leg hop test has been deemed
reliable and valid18 and may be carried out in conjunction with the vertical jump test. The Limb
Symmetry Index is the main outcome parameter for many functional tests, and most agree that
90% or greater is the goal.19-21 Before returning to play, higher-level skill including the athlete’s
ability to cut, accelerate, reach top speed, and decelerate must be assessed as well.22
JUMPING, LANDING, AND CUTTING

A number of studies have examined the kinematics and neuromuscular control of the lower
extremity during jumping, landing, and cutting in the investigation of noncontact injuries to the
knee and ankle.23-28 It is currently accepted that frontal or coronal plane knee moments including
hip adduction and knee abduction contribute to noncontact ACL injuries.29,30 Neptune et al31 per-
formed an electromyographic study (EMG) examining the side shuffle and V-cut maneuvers and
confirmed that the adductors and abductors of the hip function to stabilize during these move-
ments, as opposed to creating power. Studies examining jumping and landing have demonstrated
and linked a decrease in knee flexion angles and genu valgum during landing to be correlated with
increased ground reaction force and noncontact ACL injuries.26,32 Popovitch and Kulig33 demon-
strated that a decrease in hip muscle strength will be associated with greater lumbopelvic angular
displacement, velocity, and muscle activity during single-leg landing tasks.
Clinically, following hip arthroscopic surgery, lower abdominals, gluteals, abductors, and the
psoas may all be inhibited. Therefore, careful progression is required up through the return-to-
sport phase to ensure muscle imbalances or overuse tendinitis does not occur.
Retraining of the hip flexors is of concern to any physical therapist, coach, or trainer working
with an athlete. Hip flexor tendinitis has been demonstrated as a postoperative complication.34
Prior to retraining running, jumping or cutting, it is imperative to ensure the athlete has full
strength and appropriate timing of muscle firing patterns of the lower abdominals (transverse
abdominis), other core stabilizers (multifidi), gluteals, and hip flexors. Strengthening in isola-
tion is not advocated in this group until the very late phases of rehabilitation, and it must be
closely monitored for deleterious effects. It is important to remember that hip flexor strength is
needed for repetitive athletic movements and is why criterion-based progressions are used in this
population (Table 17-1).
Retraining for plyometric activities including jumping, landing, and cutting requires a combi-
nation of core strength and control, dynamic stability, proprioception, and motor learning for tim-
ing and strength. Athletes require a combination program of strength, dynamic stability, balance,
and plyometrics throughout the return-to-sport progression. With all training programs, form is
the key and should be the focus. Therefore, meticulous attention should be paid to the kinematic
chain through movement patterns, and consistent feedback by the physical therapist, trainer, or
coach is imperative. The movement patterns should not be limited to cardinal plane movements,
but rather progress to multiplanar, mimicking functional and sport-specific movement patterns.
278 Chapter 17
TABLE 17-1
FLEXION PROGRESSION
Prone EMS-facilitated isometric hip flexion with trunk stabilization
Prone isometric bent knee flexion
Eccentric seated hip flexion̶top on bottom
Side-lying table/ground-supported hip flexion
Standing FlexBand-assisted hip flexion
Standing doorway hip flexion
Standing hip flexion
Standing TheraBand hip flexion
Wall-supported running drills
EMS = electrical muscle stimulation
.
AGILITY PROGRESSION
Agility is a foundational element of many sports, and athletes must be trained appropriately in
this to prepare for the competitive environment. Agility can be defined as the ability to rapidly
start, stop, or change direction with control.35 The components of agility include speed, power,
reaction time, balance, and coordination. Prior to initiating plyometric training, athletes must be
able to lift 1.5 times their body weight with their legs and, if they weigh more than 220 pounds,
they should be cautious with depth jumps because of the impact loading.36 In those sports with a
significant upper body component, athletes should be able to lift their body weight as well.
The fundamental patterns that are the building blocks of agility training include side shuffling,
backpedaling, cutting, and drop stepping. It is important that athletes be re-educated in the move-
ment patterns they may already know in order to incorporate the new envelope of motion.
The athlete must meet basic standards within each basic skill. For example, with the side shuf-
fle, the contact is on the balls of the feet and the feet are parallel to the movement and stay close to
the ground. The athletic stance should be maintained, with knees flexed and back flat, with short,
quick arm motions.37 Once the basic skills are mastered, they may be linked together to simulate
sport-specific requirements.37
GENERAL RETURN TO SPORT

As indicated above, adequate strength and stability should be established prior to return. With
the initiation of sport-specific activities, the athlete should be warmed-up well prior to engaging in
activities. It also behooves the athlete to complete a round of core and glute exercises prior to activ-
ity, such as planks, bridges, and squatting, to ensure appropriate muscle activation. Athletes are
to stop any activities that cause pain, and progress as their symptoms allow. A program of main-
tenance exercises should be continued throughout training in order to preserve strength gains.
Return to Running
Gravitational and centrifugal forces during walking combine for less than 5% of total hip joint
contact force, leaving the remaining 95% of the joint contact forces coming from hip and lower
extremity muscles.38 While it is important to treat the injured tissue appropriately, the therapist
must evaluate hip muscle imbalance, strength, and mobility deficits, as well as analyzing these
findings as they relate to running gait.
The running stride requires muscular stabilization at the hip to control forces. Poor muscular
strength and endurance leads to hip adduction and femoral internal rotation, or a position of
“kinetic collapse.”39,40 It also requires repetitive eccentric hamstring loading to decelerate the
trunk over the leg at foot strike.41 All 3 hamstrings perform large amounts of negative work dur-
ing the terminal swing. The biceps femoris has the largest peak strain, the semitendinosus has
the greatest lengthening velocity, and the semimembranosus produces the highest peak force,
absorbing and generating the most power and performing the largest amount of positive and
negative work.42
Studies have concluded that muscular weakness at the hip can increase anteriorly directed
hip forces. The position of hip extension in the running stride combined with this weakness can
contribute to anterior hip pain, instability, and labral tears.43 This information suggests the impor-
tance of designing a rehabilitation program for runners with hip pathology that emphasizes the
restoration of hip mobility and strength. The strengthening program is designed to recruit core
muscles, including oblique abdominals and the muscular slings that link the trunk to the lower
extremity.44 Balance of strength between abductors and adductors and training for neuromus-
cular recruitment of gluteus maximus, gluteus medius, and hamstrings is included with general
strengthening of these proximal groups.
Rehabilitation programs should include form drills that keep the pelvis in line with the head
and shoulders, the chest lifted, and the body mass over the feet.45 Drills for strike position, foot
placement, stride length, cadence or turn over, and arm position can be part of the rehabilitation
program. Some of the classic track drills such as high knees, butt kicks, bounding, and hill bound-
ing can also be included. Neuromuscular integrity may be maintained through the availability of
minimized weight-bearing opportunities through the use of pool running, aqua jogging, and the
de-weighting treadmill. These load-altering options assist the runner psychologically in dealing
with the restricted activity.
A return-to-running program should follow the general guidelines of normalizing ROM,
strength, and function. Clinically, this can be subjectively addressed by testing single-leg squats,
front step downs, and manual muscle test hip abduction for both individual and multiple repeti-
tion sessions. However, it does become more complicated when considering the extrinsic factors
of faulty gait mechanics and training errors. Such errors include excess volume, rapid or sudden
changes in volume, or changes in running surfaces and/or footwear.44 Programs should be indi-
vidualized to address the specific goals of the runner. Goals should be defined based on level of
function both before the injury and at the time of planning, keeping in mind that uninjured run-
ners plan 6 to 12 months out in their goal setting.45
There is an abundance of information available for designing training programs for recre-
ational through elite running, and 5K through marathon training. Following the basic training
concepts of building base with steady, relaxed running and building rest into the program is
important. Base training should be at least 50% of training. Form training is built into base days
twice a week and in 4 to 8 intervals of 100 to 200 yards. Hill training can be 15% of a program and
is designed to build muscular strength. Speed work can comprise up to 35% of training, but is only
necessary if time is a goal.45,46
Training error and history of previous injury serve as the greatest predictors of running-related
pain,44 while some running injuries are potentially preventable. The concept of proximal stabi-
lization for efficient load transfer in running dictates the emphasis on trunk and hip strength
280 Chapter 17
along with recruitment of these hip stabilizers in the form of focused functional drills. Return-
ing to running includes goal setting with adequate time frames for physiological adaptation and
built-in recovery.
Return to Throwing
Hitting and throwing involves rotating around a fixed rear leg followed by linearly moving
toward the target followed by rotating around a fixed front leg.47 It is this motion that allows for
the generation of rotational power. The combination of both open- and closed-chain movements
during these skills exposes the hips to both positions of impingement and instability.48 When the
athlete initiates the return-to-throwing program, it is a good opportunity to examine his or her
technique. Often, athletes will develop compensatory movement patterns and will need to address
these as they venture back into the athletic arena. They should demonstrate good scapular stability
and a strong core, as much of the force in throwing is generated by the lower body.
The athlete begins throwing 3 days a week, and starts with 45-foot throws and gradually
increases first the number of throws (25, 50, 75 repetitions) and then the distance (45, 60, 90,
120, 150, 180 feet). There should never be any discomfort. With the throwing athlete, core stabil-
ity and gluteus medius strength and stability are of supreme importance. Endurance exercises
should be completed for these muscle groups. A windmill exercise (Figure 17-3) is appropriate
to build strength and endurance in the single-limb stance. This position may be used to work on
closed-chain external rotation as well. This is especially beneficial with pitchers, who can transi-
tion from the windmill to a throw in order to work on pelvic stability and endurance. Simulated
innings can be completed with this exercise in order to expose the athlete to repetitions similar to
a game situation.
The intensity of throws is gradually increased as the athlete’s sport-specific strength and
endurance returns. As stated previously, the athlete should be well warmed up prior to throwing
to decrease the likelihood of soft tissue irritation.
Return to Football/Rugby
The demands of football and rugby are different from the other sports because of the extreme
contact situations posed by these sports. There is a fair amount of time spent in a crouched/ready
position that requires hip flexion and soft tissue mobility. Squatting is an integral motion and
should be practiced with and without resistance. Once the appropriate strength and endurance
has been established, the progression to agility activities and plyometric training can begin. Squat
jumps may be used to work on explosive power from the squat position. Running and cutting
activities should be gradually progressed.
Throwing may be initiated once good stability exists throughout the kinetic chain. A gradual
progression of distance thrown may be carried out. Jump training should be incorporated in com-
bination with steps to the front, back, and laterally. Mountain climbing is another activity to build
strength and endurance from the ready stance, but one must be cognizant of the technique and
volume, as there is a potential for hip flexor irritation if one does not proceed prudently.
As mentioned previously, the basic components of agility should be training such as side
shuffles, back peddling, and cutting. These can be linked in sequence to simulate plays with a
teammate. Defensive and offensive plays may be run without contact as the athlete prepares for
return-to-competition scenarios. The final phase of the return-to-sport program includes run-
ning full practices with contact. Athletes should participate in simulated game situations before
returning to the field for actual competitions to ensure that they are able to tolerate the demands
of a game (Table 17-2).
Figure 17-3. Windmill exercise. Pelvis

should be kept level. (A) Starting
position. (B) One arm is lowered
down at a time.
Return to Hockey
The sport of ice hockey requires repetitive mechanical twisting and pivoting motions about the
hip, as well as contributions from other multiple joints.49 Along with repetition, there is significant
load and overload in these positions from the contact nature of the sport. The repetitive nature
of the skating stride from flexion at the hip through extension, abduction, and external rotation
presents with hip injury concerns. Goaltenders, in their position of hip flexion and internal rota-
tion, have the same repetitive and overload concerns.
Rehabilitation for the hockey player after FAI surgery should follow the general postoperative
guidelines.17,50,51 The third and fourth phases of rehabilitation should include considerable sport-
specific training and individualized on-ice programs, where skating mechanics are addressed in
order to accommodate for the muscular adjustments that must take place for the newly found post-
surgical ROM. Unrestricted team training on ice is allowed after flexibility, strength, coordination,
agility, and endurance are restored both on and off the ice.17,51
On-ice training can begin at the end of phase 2 into the beginning of phase 3 in the rehabili-
tation process. First, walking gait has to be pain-free and normalized. When the player has suc-
cessfully worked into functional double- and single-leg weight-bearing exercises without pain,
and with stability and control, a return-to-skate program is initiated. Following hip preservation
surgery, one study has examined the time to return to play for 5 professional ice hockey players
who underwent open surgical procedures for impingement.52 The results indicated that full hip
ROM was achieved in an average of 10.3 weeks and their core and hip strength values reached the
preoperative values at an average of 7.8 months.
282 Chapter 17
TABLE 17-2
QUARTERBACK PROGRAM
The QB progression should consider performing all parts of the dynamic warm-up,
3 to 4 balance exercises, 5 to 6 functional exercises, 3 to 4 core-strengthening exercises,
all sport-specific exercises, and all throwing exercises.
DYNAMIC WARM-UP CORE STRENGTH
1. High knees 1. Bird dog
2. Butt kickers 2. Stir the pot/rollouts
3. Side shuffle 3. Side supports
4. Carioca 4. Kneeling chops
5. In/out heel touches 5. Kneeling lifts
6. Gallops 6. Wall press
7. Power skips 7. Kneeling airplanes
8. Inchworm 8. Kneeling cable crossovers
9. Associated rolling 9. Standing cable pull-throughs
10. Dissociated rolling
BALANCE SPORT-SPECIFIC DRILLS
1. Single-leg eyes-closed running drill 1. Instant replay drop-back resistive
2. Single-leg eyes-closed windmill 2. Instant replay drop-back assistive
3. Single-leg eyes-closed run to windmill 3. TheraBand handoff resistive work
4. Single-leg eyes-closed hip rotations 4. Half kneeling clock drill right (r)/left (l)
5. Bosu ball squats 5. Instant replay resistive rollout r/l
6. Half foam roll pitch drill 6. Instant replay assistive rollout r/l
7. Clockwise/counterclockwise tether drill
FUNCTION THROWING PROGRAM (TOTAL 97 TO
1. TheraBand clock 3/4/5/6 and 9/8/7/6 129 THROWS)
2. Resistive hip hikes 1. Half kneeling 5 to 7 throws right/center/
3. Tubing instant replay clockwise/ left (15 to 21)
counterclockwise 2. Standing stationary 5 to 7 throws right/
4. Heismans center/left (15 to 21)
5. Slide board adductors 3. Stepping 5 to 7 throws right/center/left
6. Lawn mowers (15 to 21)
7. Windmills 4. Tubing single-leg 3 to 5 throws right/
left/front/back (12 to 20)
8. Single-leg bridges
5. Tubing step and throw (feet and knees)
9. Front step downs
5 to 7 throws right/center/left (15 to 21)
10. Prone rowing with external
6. Passing tree 25 throws (25)
rotation
11. Side-lying dumbell external rotation
12. FlexBand push press
13. FlexBand side step snatches
This on-ice program has been adapted from that used at Accelerated Sports Therapy and
Fitness, Plymouth, MN, for hockey athletes following FAI. It is divided into 5 phases (Tables
17-3 and 17-4).
The first phase starts with 3 times per week ice time for 30 minutes at 30% to 50% effort. There
is no stick or puck used in the first week, and the goal of early edge control and form symmetry is
accomplished by drills that include up and down easy strides forward, strides with leg holds and
toe drags, inside edge half circles, and C cuts. Effort and time is gradually progressed so that the
player is ready for phase 2.
Phase 2 increases ice time to 45 minutes and effort to 50% to 70%. The goals are edge agility,
ability to move in tighter forward turns, and forward crossover with symmetry. They are accom-
plished by drilling up and down forward crossovers, crossovers around a circle, and exaggerated
crossovers around the center circle. Crossover side steps are begun, and tight turns in a circle
combined with crossovers out of the circle and back into circle are also drilled. Players should be
already skating with a stick and can begin puck handling and taking easy shots. Before moving
into phase 3, backward skating can be initiated by circling the ice, transitioning to backwards
between the blue lines and then back to forward skating, which helps the player gain confidence
for moving to the next level.
Phase 3 ice time can increase to 4 or 5 days at 45 to 60 minutes and up to 70% to 80% effort.
The goal of this phase is mastery of backward skating drills and tight turns with symmetrical and
pain-free motion. Drills include backward C cuts, bilateral C cuts down and back, C cuts around
a circle, figure 8s with smaller size progression, and forward to backward transitions in a circle.
Players should be passing and moving with the puck and continuing to take shots.
Phase 4 can progress to 5 days per week at 80% to 90% effort for approximately 60 minutes. The
goal of this phase is to demonstrate hip joint tolerance to increases in torque and workload volume.
Drills require starts and stops, quicker transitions from forward to back, and lateral movement.
Modified suicides are designed for edge control in starts and stops. Accelerations are initiated, but
explosive moves are progressive in this phase.
Phase 5 provides a controlled environment for testing return-to-competition tolerance,
somewhere between 80% and 100% effort. The goal is to return to the team environment and
includes drills for accelerations, aggressive and fast starts and stops, movement through resis-
tance and contact of other players, and shooting, to include slap shots and one timers. Drills
include quick transitions, side stepping and step strides, accelerations, and full ice suicides for
cardiovascular conditioning.
Goalie on-ice training starts with the same first 3 phases, but includes specific goalie drills at
this time as well. Goalies generally will spend less time skating out of the crease and can begin
using the stick and blocker in easy shuffles and T pushes in the crease. Butterfly stretching and
general hip stretching in skates and pads is recommended on ice. Taking easy shots in the standing
position and easy shots down is allowed. Standing moves that include shuffles, T pushes, pivots,
and backward pushes can be introduced with progressive intensity. Down moves can include
recovery slides and knee shuffles.
Goalie phase 4 allows for increased torque and efforts should approach 80% to 90% of normal.
Up to down and down to up movements are also allowed. Butterfly, butterfly slides, and recovery
T pushes, which include lateral movement, can be introduced while the goalie can add force to
one-footed stops. As the goalie moves toward 100% effort in phase 5 and is testing for return to
team, shots can be taken at increasing intensity and all movement in the crease can be progres-
sively more explosive.
Adductor muscle strains and tendinopathies occur frequently in ice hockey and are related
to the mechanics of rapid pivot and direction change and the highly repetitive nature of these
maneuvers. The strength ratio between adductors and abductors has been identified as a risk fac-
tor for ice hockey groin injury. Rehabilitation based on adductor strengthening has been shown to
be effective for reducing adductor strains and complaint of groin pain in hockey players.41 Players
284 Chapter 17
TABLE 17-3
SKATING AND SHOOTING PROGRESSION
PHASE 1 Early Edge Control, Form Symmetry
3 days/week ● Up and down, easy forward strides
30 minutes ● Easy strides, circling the rink
50% effort ● Strides with leg holds in the air
No puck, no stick ● Strides with toe drags
week 1 ● Inside edge half circles, C cuts
● Up and down, easy backward strides
PHASE 2 Edge Agility, Tight Turns, Forward Crossover, Transition Forward to Back
3 to 4 days/week ● Up and down forward crossovers
45 minutes ● Crossovers around circle
50% to 70% effort ● Tight turns in a circle
● Crossover side steps
● Crossovers in and out of circle
Transition forward to back, back to forward between blue lines
● Easy passing
● Easy shooting. Slap shots, no wind-up. Slap shots, half wind-up
PHASE 3 Mastery of Backward Skating, Turn Symmetry, Pain-Free Motion
4 to 5 days/week ● Backward C cuts, bilateral C cuts down and back
45 to 60 minutes ● Backward crossovers around circle
70% to 80% effort ● Backward crossovers in and out of circle
● Figure 8s, smaller, tighter progression
● Forward to back crossovers in a circle
● Passing and moving with the puck
● Wrist shot, full wind-up
● Backhand slap shot
PHASE 4 Demonstrate Tolerance for Increases in Torque
5 days/week ● Starts and stops
60 minutes ● Quicker transitions
80% to 90% effort ● Tighter movement, lateral movement
● Modified suicides and accelerations
● Slap shots 50% to 70%
● Quick 1-timers
PHASE 5 Test for Return to Competition
5 to 6 days/week ● Aggressive, fast starts and stops
60 to 90 minutes ● Quick, explosive transitions
90% to 100% effort ● Quick side stepping, step strides
● Movement against players
● Full ice suicides
● Full windup slap shots
TABLE 17-4
HOCKEY GOALIE PROGRESSION
PHASE 1 Early Edge Control, Form Symmetry
3 days/week ● See skating progression for phase 1, no stick,
30 minutes blocker or pads for 1 week
50% effort
PHASE 2 Edge Agility, Standing Crease Agility
3 to 4 days/week ● Skating progression plus
45 minutes ● Moving across net
50% to 70% effort ● Side-to-side push
● Getting set
● Taking easy shots in standing
PHASE 3 Mastery of Standing Moves, Kneeling Moves
4 to 5 days/week ● Standing shuffles
45 to 60 minutes ● T pushes
70% to 80% effort ● Pivots
● Backward pushes
● Butterfly stretches in pads
● Knee shuffles
● Knee slides
● Easy to moderate shots in standing and down
PHASE 4 Demonstrate Tolerance for Increases in Torque
5 days/week ● Up to down, down to up
60 minutes ● Butterfly
80% to 90% effort ● Butterfly slides
● Recovery slides
● T push and recovery
PHASE 5 Test for Return to Competition
5 to 6 days/week ● Increase quickness in movement
60 to 90 minutes ● Increase force in one-footed stops
90% to 100% effort ● Use full flexibility to guard shots
● Take all shooting
identified with adductor to abductor strength ratios of less than 80% were found to be as much at
risk for adductor strains as were players with previous groin injuries.41
In general, rehabilitation of a musculotendinous groin injury is designed to relieve pain, restore
ROM, and finally, restore strength. Six to 12 weeks of active progressive hip and core strengthen-
ing, combined with balance activities and slide board drills for eccentric control, has been proven
effective for treating groin strains. Restoring eccentric strength as well as balance between adduc-
tors and abductors is the goal for return to sport. On-ice drills such as kneeling adductor pull
togethers, skating into lunges with toe drags in all planes, and hip abduction/adduction with skates
286 Chapter 17
on the ice can provide a functional strength base for returning to play. A Pilates reformer for a
standing series of abduction/adduction, lateral lunge, and lunge through has been used to provide
functional resistive eccentric training. There are also modifications to the reformer platform that
can provide functional simulation of goalie recovery slides and knee shuffles. A cable column can
be used for simulating skating strides with resistance.
Progressive on-ice drills as described in FAI rehabilitation can be introduced with increasing
intensity. Groin pain that presents at any level requires a reduction of intensity, torque, and ROM.
Although there is a high incidence of repeated adductor strain injuries, research supports the
effectiveness of an active training program emphasizing eccentrics. Therefore, players are advised
to continue with their strengthening program. They should take on- and off-ice strengthening
beyond the season and continue through the off-season, with a goal of maintaining 80% to 95%
adductor to abductor strength.53
Return to Soccer/Lacrosse
Aerobic power has been indicated as having a significant role in successful soccer and lacrosse
performance. It has been reported that soccer players may cover up to 12,000 meters (13,123 yards)
during a game. With both lacrosse and soccer, often sprints occur while the athlete is already in
motion, but frequent stops and starts occur during the game. Fast speeds must be obtained over
short distances many times throughout the course of the lacrosse game.54 Lacrosse is slightly dif-
ferent in that players are restricted to certain parts of the field based on their position. Therefore,
for lacrosse athletes the ability to stop and start and cut is of the utmost importance. For these
athletes, gluteus medius endurance is critical. Often, if an athlete returns too quickly, he or she
will develop lateral pain due to abductor fatigue. Athletes must maintain a gluteus maximus and
gluteus medius strengthening program to supplement their training. Single-limb balance activities
are key, as is closed-chain external rotation, in order to be able to control the position of the plant
leg during kicking or cutting.
There should be a progression of activities when returning to the field. This should consist of
first building basic fitness and endurance, followed by the introduction of speed, power, and agil-
ity. Phase 1 should include some sport-specific warm-ups and a gradually increased cardiovascular
workout. Phase 2 incorporates increased intensity exercise, and builds on the duration of aerobic
exercise. Drills for soccer-specific or lacrosse-specific skills, including dribbling/cradling, cone
use, and kicking/shooting can be initiated on an individual basis. Phase 3 includes some individual
work and some partner work. This includes increased conditioning, building up to 60 minutes, and
gradual increase in the intensity, as well as incorporating some interval work. There is no contact
involved, but partner passing and kicking/shooting on the goal may be initiated. Phase 4 brings
some team drills, but still precludes contact. Regular conditioning exercises may be resumed at
this point. Team passing and kicking/shooting drills may be initiated. Defensive and offensive
plays may be run without contact. For soccer, heading drills may be initiated—with low intensity
and limited height.
Phase 5 includes full practice and contact. Contact situations should first occur in a practice
environment. Full practices and simulated games should be completed before an actual competi-
tion is attempted.
Some rehabilitation programs have suggested that the athlete cover 9 kilometers, or the average
distance covered in a game, in training prior to returning to a game situation. This may include
a running program that culminates in the completion of 5 minutes of juggling with the ball, jog-
ging with the ball for 3 laps around the field, then 9 laps around the field with increasing speed,
then 10 straight-line run throughs over 100 meters (109 yards) incorporating acceleration, cruis-
ing, deceleration, and jogging back to the starting point. This is followed by running with zigzags,
slalom, horseshoe, and circular patterns (these are completed with walking back in between). This
is completed with 2 laps of jogging, followed by stretching and icing.55
Return to Basketball
The basic motor components of basketball should be mastered prior to return to play. One of
the first exercises that the athlete should be deemed proficient in is the squat. Good alignment
should be maintained without valgus collapse of the knees. This motion is also the foundation for
jumping activities. The plyometric ball pass aids the athlete in ball-handling skills. The abdomi-
nals should be engaged in order to protect the athlete and to generate force. The next fundamental
movement skill is the lunge. With walking lunges, athletes should gradually progress distance cov-
ered with the walking lunge and add resistance (such as a medicine ball) as they are able. A pull-up
may simulate the action of a rebound, especially when performed with palms facing each other.
Athletes should be prompted to engage their abdominals and try to avoid compensation through
the hip flexors in order to drive themselves up. A forceful exhalation will help engage obliques and
transversus abdominis, which facilitate an efficient and effective lift. Aquatic therapy may be used
to initiate plyometric training in order to decrease joint impact loading.
The athlete may begin with easy shooting, every other day, as well as some easy passing with a
teammate in a controlled manner. This is followed by some light dribbling in a controlled man-
ner. The athlete may then initiate shooting easy lay ups, gradually increasing the intensity. Ball-
handling skills are integrated into training with a slow build in the intensity.
Basketball-specific agility training should include crossover dribble, Euro hop, pro hop, power
up, pump fake, stop drive, double clutch, jab step, turnaround jumper, fade away, drop step, and
double pivot. One should prepare the athlete for the specific components with analogous practice
activities. Speed marches may be used to train the jab step, squat jumps to train the power up, pro-
lane agility to train the Euro hop, and the agility ladder to train the crossover dribble. Once the
athlete has a strong cardiovascular and strength base, controlled work with a teammate may begin.
The activities are begun in a noncontact manner with easy passing, shooting, and dribbling. Once
the athlete is cleared, contact activities may begin.
Return to Tennis
Tennis is a repetitive sprint sport with high aerobic demand. It is characterized by quick starts
and stops, repetitive overhead motions, and the involvement of several muscle groups during dif-
ferent strokes that fluctuate randomly from brief periods of maximal/near maximal work to longer
periods of moderate or low-intensity work.56 The average work-to-rest ratio during a match is 5 to
10 seconds:10 to 20 seconds. Return-to-sport training should include intervals of 5 to 15 seconds
on and 10 to 60 seconds off aerobic activity.57 Once adequate stability and has been established, as
well as stability throughout the kinetic chain, hitting may be initiated. Squat press with an elastic
band may be used as a good assessment of stability throughout the kinetic chain. Athletes should
be able to stabilize through their lumbopelvic region with the explosive motion, preparing them
for such strokes as the overhead and the serve.
The athlete should start with 3 days a week. The emphasis should be on stroke technique. The
progression of strokes begins with ground strokes, then volleys, then serves, and then overheads.
This progression is followed by the return to match play. The incipient phase includes low-velocity
strokes and then gradually increases, beginning with ground strokes hit from the baseline. The
balls should be fed directly to the athlete at waist height. There should be a neutral stance, the
knees should be soft, and the body should rotate with the shot. Good mechanics should be empha-
sized. At this time, it is helpful to have a professional involved to analyze technique and correct
errors. A low-compression ball should be used. The second phase replicates the first, but with
use of a standard ball. The next phase incorporates some rallies with ground strokes, with the
athletes resting every 2 to 3 rallies for a total of about 50 to 60 strokes. The next step is to add in
some volleys. Serves are the next component, and should be initiated with a foam ball. The athlete
should start with about 10 easy serves after a good warm-up; he or she may then begin to perform
288 Chapter 17
a combination of strokes and increase the length of rallies and decrease the rest between. The over-
head is added in as well, with easy return to begin, and then gradually adding intensity.
PEARLS AND PITFALLS

● Following impingement surgery, the increase of hip ROM must be accommodated by the soft
tissue envelope. Therefore, neuromuscular patterning and strengthening must be allowed to
occur before high-intensity activity is incorporated.
● It is important to remember the relationships existing between the hip, lumbar spine, thoracic
spine, and shoulder. These compensatory patterns must be highlighted and re-educated dur-
ing the rehabilitative process.
● Functional progression of activities should be carried out, with achievement of specific mile-
stones, in order to prevent soft tissue irritation and prolonged recovery.
● Good core stability provides a stable base on which the hip can perform, as well as improving
efficiency of force transmission throughout the kinetic chain. One should be mindful of the
manipulation of training variables, including volume and intensity, as the athlete progresses
back to sport.
CONCLUSION
Return to sport following a hip injury should follow a functional progression that is milestone-
based, as opposed to time-based. The establishment of core strength and endurance is of critical
importance. Athletes must follow a graduated progression in order to decrease the likelihood of
further injury and increased time to return to play. Once appropriate strength has been restored,
the athlete must complete a maintenance program consistently, even once he or she is back at play.
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18
Outcomes in Return to Sport
Asheesh Bedi, MD; Jack G. Skendzel, MD;

Karen K. Briggs, MBA, MPH; Eilish O’Sullivan, PT, DPT, OCS;
and Marc J. Philippon, MD
Femoroacetabular impingement (FAI) has recently been recognized as an important factor

in the etiology of hip pain, decreased range of motion, and decreased performance in young,
athletic patients; and FAI is also one of the predominant causes of degenerative changes in the
nondysplastic hip.1-3 Ganz and colleagues4 first described the anatomic abnormalities of the
proximal femur and acetabulum responsible for damage to the labrum and articular cartilage. Not
addressing the underlying osseous abnormalities in addition to the chondral and labral pathology
commonly leads to an impaired clinical and functional outcome and failure of surgical treatment
of FAI.5 Athletes who engage in vigorous physical activity place repetitive high stresses across the
hip joint. Those individuals with altered hip joint anatomy, such as loss of femoral offset or focal
acetabular retroversion, may develop cumulative damage to the labrum and articular cartilage as
a result of their sporting activity that leads to pain, altered performance, and premature degenera-
tive changes of the hip joint.
Athletes in many sports may be at risk for developing FAI and groin pain, including athletes
in ice hockey, American football, soccer, baseball, rugby, martial arts, dance, and golf, among
others.6-11 Philippon and Schenker reported that 36% of professional and Olympic-level athletes
who underwent hip arthroscopy required decompression of a FAI lesion between September
2000 and April 2005.12 Byrd and Jones5 reported that labral lesions are the most common intra-
articular hip pathology encountered and presented in the hips of 61% of athletes who underwent

292 Chapter 18
arthroscopy. Unfortunately, however, athletes with persistent groin pain and clinical and radio-
graphic signs of FAI were often treated improperly and diagnosed with a soft tissue injury rather
than an intra-articular lesion.13 In one report, up to 60% of athletes who underwent hip arthros-
copy for hip pain were treated for an average of 7 months postoperatively before the hip joint was
properly identified as the source of pain.5 The implications of a missed injury are substantial,
including permanent damage to the labrum and articular cartilage, missed playing time, financial
loss, and the increased risk of developing osteoarthritis.
FAI and associated groin pain have significant consequences for athletes and their ability to
return to a previous level of sporting activity. Feeley and colleagues13 studied hip injuries in the
National Football League from 1997 to 2006, reporting that intra-articular hip pathology can be
difficult to diagnose and is often found in combination with adductor strains and rectus strains,
the so-called “sports hip triad.” Furthermore, although intra-articular injury accounted for only
5% of all hip injuries in the current study, it was responsible for the largest loss of playing time. It
is therefore paramount that, once the diagnosis of FAI is made, the athlete be treated appropriately.
Several surgical options are available to treat the athlete with FAI. Open surgical dislocation,14,15
as well as arthroscopic procedures,9-11,16-18 have shown improved postoperative outcomes and
have returned athletes to sports. Available techniques to address acetabular impingement include
rim recession with labral debridement or refixation depending on lesion morphology. A femoral
osteochondroplasty is performed to address cam deformity and loss of femoral head-neck offset,
and arthroscopic debridement or microfracture is used to address chondral defects. The purported
benefit of an arthroscopic approach to address FAI includes less postoperative morbidity through
a more limited surgical dissection that may improve a high-level athlete’s ability to return to pro-
fessional sports.9 However, in a recent retrospective review of 22 professional athletes after open
surgical dislocation for FAI by Naal and colleagues,19 96% remained active in professional sports at
a mean of 3.8 years postoperatively. These results suggest that well-executed open and arthroscopic
surgery for FAI can return athletes successfully to their preinjury activity level.
This chapter reviews the currently reported outcomes of athletes after arthroscopic hip surgery
for FAI and ability to return to high-level sporting activity. While recent evidence indicates that
surgical techniques to address FAI in athletes allow for a successful return to high-level sport,
future work is needed to define long-term outcomes and the impact of surgical intervention on
the natural history of FAI. Furthermore, the efficacy of nonoperative management for FAI remains
entirely undefined. The goal is to identify those athletes “at risk” who may benefit from a surgical
procedure to address symptoms that impair performance and prevent progression of the adverse
sequelae of damage to the acetabular labrum and articular cartilage.
OUTCOMES AFTER ARTHROSCOPIC FEMOROACETABULAR

IMPINGEMENT SURGERY
Several authors have reported the results of return to sport for both arthroscopic (Table 18-1)
and open (Table 18-2) management of FAI and labral tears.
Byrd and Jones18 reported on the results of arthroscopic management of FAI in 200 consecu-
tive athletes with a minimum 1-year follow-up. All patients had persistent hip pain that inter-
fered with their ability to participate in their sport; in addition, imaging findings suggested an
intra-articular pain source that did not improve with a period of activity modification. There
was 100% follow-up of all 200 patients, consisting of 23 professional, 56 intercollegiate, 24 high
school, and 97 recreational athletes, at an average of 19 months postoperatively. The most com-
mon activity was recreational running. Among high-level athletes, 18 played football, 10 soccer,
11 baseball, and 8 basketball. Labral tears were present in 89% of the cohort, and damage to the
acetabular articular cartilage was present in 96% of the patients. Of these, 88% demonstrated
TABLE 18-1
SUMMARY OF STUDIES FOR RETURN TO SPORT AFTER ARTHROSCOPIC MANAGEMENT
STUDY NO MEAN MEAN CLINICAL PROCEDURE(S) MEAN RETURN TO NOTES
OF AGE FOLLOW-UP OUTCOMES CHANGE IN PLAY
HIPS SCORE HIP SCORE
Byrd and 200 28.6 years Minimum mHHS Femoroplasty, 20.5 points 95% of 5 transient
Jones5 1 year, avg. acetabuloplasty, professionals; 85% neuropraxias (all
19 months combined of intercollegiate resolved)
procedures athletes
Nho et al10 47 22.8 years 27 months mHHS, HOS Rim trimming/ 20 points 79% to previous 1 revision
labral refixation (mHHS), 12.6 level at avg. 9.4 arthroscopy,
vs debridement/ points (HOS) months; 73% at 5 unable
osteochondroplasty 2-year f/u to return to
competition
Singh and 24 22 years 22 months mHHS, NAHS Rim trimming/ mHHS: 8 points 23 returned to 1 player
O Donnell11 labral repair, femoral at 1 year, 10 top-level football advised to
neck ostectomy, points at 4 years; retire for severe
microfracture, NAHS: 15 points cartilage loss/
excision os at 4 years osteoarthritis
acetabuli
Byrd and 15 31.7 years 10 years mHHS Debridement 45 87% to previous 5 THAs at an
Jones18 level avg. 73 months
postoperatively
(continued)
Outcomes in Return to Sport 293
TABLE 18-1 (continued)
294 Chapter 18
STUDY NO MEAN MEAN CLINICAL PROCEDURES(S) MEAN RETURN TO NOTES

Philippon 16 15 years 1.36 years mHHS, HOS Rim trimming/ 35 points All patients 11 patients
et al9 ADL labral refixation (mHHS), returned to active underwent
vs debridement, 36 points (HOS play in their acetabular
femoral osteoplasty ADL) desired sport chondroplasty;
9 femoral head
chondroplasty
Philippon 45 31 years 1.6 years ‒ Rim trimming/ ‒ 93% returned to 78% remained
et al16 labral refixation professional sport active at
vs debridement/ professional
microfracture/ level at an
osteochondroplasty avg. 1.6 years
postoperatively
Guanche 8 36 years 14 months WOMAC Debridement of ‒ All returned to Avg. postop
and Sikka21 labrum/cartilage/ running at pre- WOMAC: 94
ligamentum teres injury level
McCarthy 13 24 years 18 months ‒ Labral debridement ‒ All 10 patients No
et al8 returned to sport complications
Boykin 21 18.5 years 8 months ‒ Labral debridement, ‒ 56% returned to 2 revision
et al22 combined rowing arthroscopies
procedures
(continued)
STUDY NO MEAN MEAN CLINICAL PROCEDURES(S) MEAN RETURN TO NOTES
Boykin 23 28 years 41.4 months MHHS, HOS, Labral 16.4 points 18/21 returned 2 revisions
et al23 SF-12 reconstruction with (mHHS), to sport, 81% for lysis of
iliotibial autograft, 8.6 points (HOS returned to capsulabral
combined ADL), 20.8 previous level or adhesions (at
procedures points (HOS better 8 months and
Sport), 7 points 25 months) 2
(SF-12 physical), THAs, 1 unable
5 points (SF-12 to return
mental)
McDonald 39 30.1 years 2 years ‒ Microfracture, Performance 77% returned to No
et al24 combined data play complications
procedures
McDonald 17 31 years First full ‒ Microfracture, Performance 82% return to play, No
et al26 season combined data collected 11/17 returned to complications
following procedures previous level of
surgery play; no significant
differences in
performance data
with the matched
controls
FAI = femoroacetabular impingement; mHHS = modified Harris Hip Score; HOS = Hip Outcome Score; WOMAC = Western Ontario and McMaster University Arthritis Index;
SF-12 = Short-Form 12; NAHS = Nonarthritic Hip Score; THA = total hip arthroplasty; ADL = activities of daily living; f/u = follow-up
TABLE 18-2
SUMMARY OF STUDIES FOR RETURN TO SPORT AFTER OPEN MANAGEMENT OF FEMOROACETABULAR IMPINGEMENT
STUDY NO OF MEAN MEAN CLINICAL PROCEDURES (S) MEAN RETURN TO NOTES
HIPS AGE FOLLOW-UP OUTCOMES CHANGE PLAY
296 Chapter 18
SCORE IN HIP
SCORE
Naal et al19 22 19.7 years 45 months SF-12, HOS, Rim trimming with ‒ 21 continued Microfracture did
patients; UCLA, HSAS labral refixation, to compete not significantly
30 hips chondroplasty, professionally; influence
femoral 88% still active postoperative
osteochondroplasty at preoperative outcomes
level at 2-year f/u
Bizzini 5 21.4 years 2.7 years Hip ROM, Open surgical hip ‒ 3 returned No difference
et al14 core/hip dislocation with to Swiss in outcomes
muscle rim trimming/ professional between
strength, labral repair, femoral league; 2 did goaltender and
time to return osteoplasty not reach other field players
to training/ preoperative
game level of sport
Naal et al27 192 hips 30.0 years 59.4 months WOMAC, Labral refixation vs ‒ 84.9% returned Males had
HOS, SF-12, debridement vs to play. 60.3% significantly
PCS, MCS, partial resection. indicated higher HSAS and
UCLA, HSAS Femoral neck sporting ability UCLA scores,
osteochondroplasty subjectively and were more
in all cases. improved with likely to indicate
surgery. deterioration in
sporting ability
following surgery
(continued)
SUMMARY OF STUDIES FOR RETURN TO SPORT AFTER OPEN MANAGEMENT OF FEMOROACETABULAR IMPINGEMENT
STUDY NO OF MEAN MEAN CLINICAL PROCEDURES (S) MEAN RETURN TO NOTES
HIPS AGE FOLLOW-UP OUTCOMES CHANGE PLAY
SCORE IN HIP
SCORE
Novais 29 17 years 1.8 years UCLA, Femoral head-neck 1 point 50% increased 3 patients had
et al31 WOMAC osteochondroplasty (UCLA), their activity significantly
in all cases, as 1.5 points level from decreased
well as combined (WOMAC- preoperatively, activity following
procedures pain) and 30% surgery̶2 had
maintained Beck grade
maximal V acetabular
UCLA scores cartilage injury at
postoperatively time of surgery
FAI = femoroacetabular impingement; ROM = range of motion, UCLA = University of California, Los Angeles Activity Scale; HSAS = Hip Sports Activity Scale; HOS = Hip
Outcome Score; SF-12 = Short-Form 12; WOMAC = Western Ontario and McMaster Universities Arthritis Index; PCS = Physical Component Scale; MCS = Mental Component
Scale; f/u: follow-up
.
298 Chapter 18
Tönnis Grade III or IV changes. The modified Harris Hip Score (mHHS) improved significantly
from a median preoperative score of 72 to a postoperative score of 96 (P< .001) for all patients.
For the 116 athletes who achieved 2-year follow-up, the median mHHS improvement was 21 to
a postoperative score of 96. One hundred eighty-one athletes (90%) were able to return to their
preoperative level of activity, including 95% of those participating in professional sports and 95%
competing at the collegiate level.
Despite some chondral injury in the majority of athletes, the clinical outcomes were excel-
lent and most athletes were able to return to their previous activity level. The authors cautioned,
however, that the mHHS is limited in its ability to evaluate high-functioning athletes and perhaps
lacks some sensitivity to subtle dysfunction in this elite athletic population. The frequency with
which chondral damage was observed is concerning and underscores the importance of early
detection and identification of athletes who are at risk to prevent irreversible secondary damage
to intra-articular structures.
Byrd and Jones20 also published results from a prospective analysis completed on 15 athletes
who underwent hip arthroscopy for pain that occurred during athletic activity. All patients had
120-month (10-year) follow-up. The most common sports included football (3), tennis (3), basket-
ball (2), and golf (2); activity level included 9 recreational, 4 high school, and 2 scholarship inter-
collegiate athletes. The median improvement in the mHHS was 45 points, and 13 patients (87%)
were able to successfully return to their previous level of sport with a median time to return of
3 months. Over the course of the study, 5 patients with arthritis (33%) were eventually converted
to a total hip arthroplasty at an average duration of 6 years postoperatively.
Nho and colleagues10 reported on the clinical outcomes in a mixed population of high-level
athletes who underwent arthroscopic treatment of FAI with a minimum of 1-year follow-up. The
study included 47 athletes who participated at various levels of competition (varsity high school,
college, or professional) with a mean follow-up of 27 months. Thirty-three were available for
follow-up and asked to complete an mHHS and Hip Outcome Score (HOS) at baseline, 6 months,
1 year, and 2 years after surgery. Athletes participated in ice hockey (11), soccer (7), baseball (6),
and several other sports. During arthroscopy, nearly all patients (46/47, 97.9%) demonstrated labral
injury, with all 47 patients showing evidence of cartilage injury with delamination at the chondro-
labral junction. Based on the pathology identified in each patient, surgical treatment included
rim recession in regions of focal acetabular retroversion with labral debridement or refixation,
synovectomy, debridement of the ligamentum teres, and femoral osteochondroplasty. Postop-
eratively, the mean mHHS score improved to 88.5 from a preoperative value of 68.6; in addition,
the HOS improved from 78.8 preoperatively to a mean of 91.4 postoperatively. Twenty-six of the
33 were able to return to play at a mean of 9.4 months. Nearly all (92.3%) returned to the same level
of competition. At 2-year postoperative follow-up, 24 (73%) were still competing at the same level.
There were 5 patients unable to return to competition because of persistent hip pain. Overall, the
authors demonstrated a high rate of return for all levels, including professional athletes (83%), high
school athletes (90%), and collegiate athletes (59%). Despite the limitations of this study, including
a follow-up rate of 70%, the study demonstrated a predictable return to sport after hip arthroscopy
in a population of elite athletes competing in several different sports.
McCarthy and colleagues8 evaluated 13 hips in 10 elite athletes after hip arthroscopy for labral
tears with a mean follow-up of 18 months. There were 7 professional hockey players, 1 football
player, 1 baseball player, and 1 golfer. All patients had anterosuperior labral tears that underwent
debridement, while 2 patients had both anterior and posterior labral tears that were also debrided.
After surgery, 12 of 13 cases (92%) were successful with good or excellent outcomes; only one
patient experienced recurrent symptoms. Of concern, however, is the relatively short follow-up in
this series and the isolated treatment of chondral and labral pathology without treatment of the
underlying bony deformity.
Philippon and colleagues9 reported on 45 professional athletes at an average of 1.6 years fol-
lowing arthroscopic management of symptomatic FAI. The authors evaluated the ability of each
athlete to return to a professional level of play. Eleven of the athletes had previously undergone
hip arthroscopy for isolated treatment of labral and chondral pathology. During arthroscopy,
22 patients had decompression of cam lesions, 3 underwent treatment for focal rim impinge-
ment lesions, and 21 were treated for mixed femoral and acetabular deformity. All patients in the
series had labral tears, 25 underwent labral refixation with suture anchors, while 12 had repair of
intrasubstance tears. Five patients had labral debridement only. Because of previous surgical inter-
vention, 2 patients needed labral grafting with iliotibial band autograft secondary to global labral
deficiency. Twenty-one patients (47%) had focal Tönnis Grade IV changes of the acetabular articu-
lar cartilage, 14 were treated with microfracture, and 5 were treated with thermal chondroplasty.
In total, 42 of the athletes (93%) were able to return to professional sports. Those 3 patients who did
not return all had diffuse osteoarthritic changes at the time of arthroscopy. Five athletes required
reoperation. At an average of 1.6 years postoperatively, 35 (78%) remained active in their profes-
sional career. The authors concluded that professional athletes are able to return to play following
arthroscopic surgery for FAI. In concordance with other studies, the presence of osteoarthritis
was a poor prognostic factor for clinical outcomes and return to play.20 One patient in the series,
a senior Professional Golfers’ Association (PGA) golfer, was able to return to the professional level
despite diffuse osteoarthritis, suggesting that perhaps a low-impact sport may be more forgiving
and allows for a period of return to sport despite the presence of significant chondral injury.
Guanche and Sikka 21 reported on 8 high-level running athletes with complaints of atraumatic
hip pain with running who subsequently underwent hip arthroscopy with debridement of labral
tears in the absence of stress fractures. All patients underwent debridement of anterosuperior
labral tears. Six patients underwent debridement of acetabular chondral lesions. The authors did
not perform an osteochondroplasty for bony deformity. Although the Western Ontario and
McMaster Universities Osteoarthritis Index (WOMAC) was not reported preoperatively, at a mean
follow-up duration of 14 months, the average value was 94 and all patients were able to return
to running at their preinjury level. Once again, however, the limitation of this study is the short
duration of follow-up, which compromises the ability to assess the impact of failure to address the
underlying osseous deformity.
Labral injuries and return to sport following hip arthroscopy in rowers were examined by
Boykin et al.22 Of the rowers identified (18, 21 hips), 85% underwent hip arthroscopy. The mean
age was 18.5 years (range, 14 to 23 years), and they were predominantly female (85%). Of the
18 athletes undergoing hip arthroscopy, 11 underwent isolated labral debridement, 1 underwent
acetabular chondroplasty and labral debridement, 2 underwent labral debridement and femoral
head-neck osteochondroplasty, 1 underwent labral repair and femoral head–neck osteochondro-
plasty, and 3 underwent labral debridement, femoral head-neck osteochondroplasty, and acetabu-
lar rim trimming. Out of these patients, only 56% returned to rowing following surgery at a mean
of 8 months of follow-up (range, 3 to 25 months), 33% did not return, and return data were not
available for 11%. Two patients required revision (1 at 6 months, and the other at 18 months), which
consisted of repeat labral debridement and synovectomy, and were able to return to rowing fol-
lowing revision surgery. The authors postulated that the required repeated hyperflexion (coupled
with internal rotation in some cases) may make it difficult to return to rowing, leading to lower
rate of return than of other sports. A limitation to this study was the narrow window of follow-up.
Outcomes of arthroscopic labral reconstruction of the hip in elite athletes were examined
retrospectively from prospectively collected registry data by Boykin et al.23 The elite athlete
status was designated to those who were Olympic athletes, playing for a professional team,
or considered being an athlete as their primary job and source of revenue. Twenty-three hips
were identified in 21 elite athletes, with an average age of 28. Average length of follow-up was
41.4 months (range, 20 to 74 months). Concomitant procedures included femoral and acetabular
osteoplasty in all hips and microfracture in 9 of 23 hips. Clinical outcomes included mHHS, HOS,
and Short-Form 12, as well as a 10-point patient satisfaction scale. The decision to reconstruct
the labrum was ultimately made intraoperatively in the setting of a diminutive labrum that was
300 Chapter 18
not amenable to repair. An ipsilateral iliotibial graft was used for the labral reconstruction, and
concomitant procedures such as femoral head-neck osteoplasty and/or acetabular rim trimming,
as well as microfracture for Outerbridge IV lesions, were performed as necessary. Time from
injury to surgery averaged 21.9 months. The group was composed of 21 athletes (23 hips) including
7 professional soccer players, 5 professional hockey players, 4 professional football players, 2 Olym-
pic skiers, 1 professional basketball player, and 1 Olympic ice skater. Eleven of the 23 cases had
previous ipsilateral surgery, which was arthroscopic in 10 of the 11 cases. Two patients required
revision surgery for lysis of capsulolabral adhesions, one at 8 months (and also had microfracture
and further femoral head-neck decompression) and one at 25 months. Eighteen of the 21 athletes
returned to professional sports, and 81% of the athletes returned to previous level of play or better.
Of the 3 patients who did not return, 2 went on to arthroplasty and 1 retired from sports. Three
patients of the 18 did not return to their previous level of play. At an average of 41.4 months, high
patient satisfaction and improved clinical outcome scores were demonstrated.
McDonald et al24 examined return to play following hip arthroscopy with microfracture in
elite athletes. Thirty-nine male athletes met the inclusion criteria, and underwent hip arthroscopy
with microfracture for treatment of Outerbridge grade IV chondral defects. These athletes were
compared with a matched group of 94 hips who underwent hip arthroscopy, but without micro-
fracture. The average age was 30.3 years, and the athletes were an average of 10.1 months out from
injury at the time of surgery. The athletes participated in a variety of sports, including football,
hockey, soccer, golf, baseball, and tennis. Athletes who returned to sport were followed for an aver-
age of 3 years (range, 2 to 12). Thirty athletes underwent microfracture of the acetabulum, 5 under-
went microfracture of the femoral head, and 4 athletes underwent microfracture on both sides of
the joint. A total of 77% of the microfracture group returned to play following surgery, whereas
84% in the control group returned. Ninety-three percent of the athletes who returned came back
the season following the arthroscopy (94% in the control group). There was no significant differ-
ence between the microfracture group and the control group in number of seasons played post-
operatively. There also was no increased risk of failing to return to sport because of engaging in a
contact sport, multiple lesions, or lesions on the weight-bearing surface.
Ice Hockey
FAI is recognized as a common source of hip and groin pain in ice hockey players.9,13 Recently,
Stull and colleagues25 described an “at-risk” position during the sprint start for youth ice hockey
players with cam morphology impinging against the femoral neck against the acetabulum; repeti-
tive activity may lead to labral and articular cartilage damage. Several authors have focused spe-
cifically on return to sport in the ice hockey athlete.
Philippon et al16 performed a retrospective review of 28 professional National Hockey League
(NHL) ice hockey players with symptomatic hip pain that precluded their ability to return to
competition. All patients failed nonoperative treatment and underwent arthroscopic treatment of
FAI, including acetabular rim recession, femoral neck osteoplasty, and labral refixation. The mean
time from the onset of symptoms until arthroscopic surgery was 19 months. Players were then
followed to determine their ability to return to sport, which the authors defined as skating as part
of training or the sport of ice hockey. The average time to follow-up was 24 months. Radiographic
analysis showed all patients had evidence of cam deformity, while 85% had evidence of acetabular
retroversion. Ninety-three percent had mixed-type FAI. One patient had isolated cam impinge-
ment and one had an isolated pincer lesion. All players had labral lesions in the superior quadrant
repaired with suture anchors. All players returned to professional hockey (skating/hockey drills)
at a mean of 3.8 months postoperatively. The mHHS improved from a preoperative mean of 70 to
95 (P < .001). The median patient satisfaction was 10, with a range of 5 to 10. The authors showed
that players who underwent surgery within 1 year from the time of hip injury returned to sport
at 3 months, while those who waited for surgery greater than 1 year returned at 4.1 months. Time
from injury until surgery was longer in those players with chondral defects of the acetabulum and
femur when compared to those without degenerative changes (24 months vs 14 months, P < .01).
McDonald et al26 reported on arthroscopic treatment of FAI and chondral lesions with
microfracture in a series of 17 professional hockey players. All athletes had Outerbridge
grade IV chondral lesions and labral and FAI treatment as well. Their performance data were com-
pared with a matched control group, with which there was no statistical difference in age, number
of seasons in the league, games played, time on the ice, points, save percentage, and shots on goal.
Average age was 31 years (range, 23 to 37). Eighty-two percent of the players who underwent an
arthroscopic intervention returned to play. Postoperatively, no statistical difference was found in
the above performance measures; there was, however, a trend toward a decrease in games played
and postoperative points scored. Preoperative performance data were collected for the year prior
to surgery. The average size of the chondral lesion was 119 mm2 (range, 20 to 250). None of the
athletes had isolated rim impingement, 5 had isolated cam impingement, and 12 had combined
impingement. Thirteen were treated with labral repair, 2 with labral reconstruction, and 2 with
labral debridement. Eleven of the 17 athletes returned to their previous level of play. Three athletes
did not return to play. The authors concluded that athletes not only can return following micro-
fracture, but can return to a level of play that they had functioned at previously.
Bizzini and colleagues14 reported on outcomes of 5 professional hockey players after open
surgical dislocation for FAI. All patients underwent hip dislocation with osteochondroplasty and
labral detachment with refixation. The average follow-up was 32 months, and outcome measures
time to return to competitive play, hip range of motion, and core muscle strength were measured.
Hip range of motion was regained by an average of 10 weeks postoperatively, while core strength
reached preoperative levels by a mean of 8 months. Athletes returned to team practice at a mean
of 6.7 months and were cleared to play their first game at a mean of 9.6 months postoperatively.
Sixty percent returned to a previous level of sport, including 3 players to professional competition
while the remaining 2 returned to minor league play.
OPEN FEMOROACETABULAR IMPINGEMENT SURGERY

There is no clear consensus regarding an earlier return to play with the use of arthroscopic
vs open surgical techniques to treat FAI and associated labral injury. It has been suggested that
arthroscopic management causes less operative trauma to the hip joint with a shorter postopera-
tive rehabilitation period than open surgical dislocation, perhaps secondary to the ability to avoid
the need for abductor detachment and refixation.16 Although Philippon et al9 demonstrated a
higher rate of return to professional sport than Bizzini et al14 with the use of arthroscopic tech-
niques, Naal and colleagues19 suggest that both approaches are effective. Their report included
14 professional ice hockey players treated with open surgical dislocation for FAI, 96% of whom
remained professionally active at a mean of 3.8 years after surgery. This suggests that both open
and arthroscopic management of FAI, when well executed with a meticulous surgical technique,
can successfully return high-level athletes to competitive play.
Naal et al27 examined sport and activity levels following open corrections of FAI. A total of
192 hips were included (153 patients), with a mean age of 30 years (range, 14 to 55). The patients
included 59.5% males and 40.5% females. Twenty-six of the 192 hips had previous surgery, the
majority (14) being arthroscopic hip procedures. Mean follow-up was 59.4 months (range, 24 to 90)
after surgery. Outcome tools used were the WOMAC, HOS, Short-Form 12, Physical and Mental
Component Scales, University of California Los Angeles (UCLA) Activity Scale, as well as the Hip
Sports Activity Scale (HSAS). One hundred three hips underwent labral refixation, 53 underwent
debridement, and 14 underwent partial labral resection. Osteochondroplasty of the femoral neck
was performed in all hips. A total of 126 of the 153 patients were active in sports on a regular
basis, and 107 were active in sports following the surgery, resulting in an 84.9% return-to-sports
302 Chapter 18
rate. Subjectively, 75% of the patients were satisfied with their sporting abilities following surgery,
and 60.3% indicated that they had improved following their surgery. Activity levels indicated by
HSAS and UCLA scores were significantly higher in male patients. The authors concluded that the
majority of patients undergoing surgical hip dislocation for the treatment of FAI are able to return
to sports, and that most patients are satisfied with their sporting abilities following surgery.
Australian-Rules Football
Singh and O’Donnell11 retrospectively reviewed 24 consecutive Australian Football League
(AFL) players who underwent hip arthroscopy for probable intra-articular hip pathology with
groin pain aggravated by activity. Hip arthroscopy was performed in the lateral position and
patient outcomes assessed pre- and postoperatively with a mean follow-up of 22 months (range,
6 to 60). There were 4 hips with greater than 2-year follow-up, 5 hips with greater than 3-year
follow-up, 3 hips with greater than 4-year follow-up, and 1 hip with follow-up over 5 years post-
operatively. Nineteen hips (70%) had intra-articular synovitis, and labral pathology was observed
in 9 hips. Articular cartilage lesions at the chondrolabral junction were present in 25 hips. Micro-
fracture was performed in 6 hips with full-thickness cartilage loss up to 3 cm2. Femoral neck
osteoplasty was performed in 22 hips for cam lesions. The mean preoperative mHHS was 86 and
improved to 94 at 1 year, 97 at 2 years, and 96 at 4 years. All players reported high satisfaction and
would have the surgery again if required. Twenty-three players returned to top-level AFL football;
the single player who did not was encouraged to retire from professional football because of the
extensive osteoarthritis noted during arthroscopy. Another who had returned to play retired 1 year
after hip surgery for a knee injury. No patient required a revision surgery at a mean follow-up of
22 months.
Soccer
Saw and Villar28 reported on 6 professional soccer players with intractable hip pain who
underwent hip arthroscopy with debridement for labral tears. All players were able to recall an
acute injury to the hip, and none had radiographic signs of aberrant proximal femoral anatomy
or acetabular dysplasia. At the time of arthroscopy, all players had anterior, traumatic longitu-
dinal labral tears with articular chondral defects. All unstable labral tears were resected back
to a stable margin, and no additional interventions for FAI were performed. All patients were
symptomatically improved postoperatively, and 5 of 6 athletes returned to professional soccer at
a mean of 12 months after surgery. The authors concluded that because of the demands placed
on professional athletes, labral tears and damaged articular cartilage may develop despite normal
bone structure. However, the short duration of follow-up limits the conclusions of this series, and
the report of normal bone structure may more likely have reflected a lack of sensitivity of the
performed imaging studies.
Adolescent Athletes
FAI is a recognized source of hip pain in adolescents. Sink and colleagues29 reported on hip
pain in the adolescent population younger than 18 years who were heavily involved in either sports
or dance. They identified radiographic evidence of focal rim lesions in 43% of the patients, while
cam deformity was present in only 6% of cases. Their results highlight the need for thorough his-
tory, physical examination, and radiographic analysis of adolescent individuals with hip pain to
identify potential lesions that are amenable to surgical treatment to alleviate symptoms, and pre-
vent the deleterious effects of neglected FAI.
Philippon and colleagues30 reported on a series of 16 active adolescent patients younger than
16 years who underwent hip arthroscopy for idiopathic FAI. All patients had hip pain despite a
trial of nonoperative management with clinical and radiographic findings of FAI. Arthroscopic
management of the FAI included femoral head-neck osteoplasty for cam deformity and loss of
offset, with a limited osteoplasty if the proximal femoral physis was still open. Acetabular rim
recession was used to address focal retroversion, and labral pathology was treated with either
debridement or detachment with suture anchor refixation. Outerbridge grades I through III
defects of the articular cartilage were treated with chondroplasty. At a mean follow-up of 1.36 years
(range, 1 to 2), the mean mHHS improved 35 points, and the mean patient satisfaction score was
9 out of 10 (range, 9 to 10). There was a trend toward lower outcome scores in those adolescents
who underwent chondroplasty for articular cartilage lesions, although the study was underpow-
ered to determine any potential significant difference. All patients returned to active play in their
respective sport postoperatively.
Fabricant et al17 conducted a retrospective review of 27 hips (21 patients) in athletic individuals
19 years or younger who underwent hip arthroscopy for FAI. All patients engaged in at least one
organized sport or activity, either at school or in the community. The authors gathered outcome
data from a hip arthroscopy patient registry. All patients had persistent symptoms despite 6 months
of nonoperative treatment, including activity modification, physical therapy, and intra-articular
hip corticosteroid injection. Various labral pathologies were treated based on the pattern of injury,
including fractional psoas tendon lengthening for anteromedial labral contusion-type lesions,
debridement of frayed labral injury, and decompression of the acetabular rim with refixation in
cases of focal rim impingement lesions. If the labrum was unstable, refixation was performed with
sutures to achieve an anatomic repair. A femoral head-neck osteoplasty was performed in all cases
of cam deformity. All patients were evaluated at 6, 12, and 24 months postoperatively with a mini-
mum follow-up of 1 year and mean follow-up of 1.5 years (range, 1 to 2.5). The mHHS improved
by an average of 21 points and 100% of patients reported normal or nearly normal hip function
postoperatively (P < .001). Those patients who underwent labral refixation as compared to labral
debridement had overall high mHHS, although at most recent follow-up the scores were similar for
each group. The study demonstrated encouraging short-term results for arthroscopic management
of FAI in adolescents, but long-term data are needed.
Novais et al31 reported on outcomes of open surgical management of FAI in adolescent athletes.
Twenty-nine patients were identified from a retrospective review of the prospectively collected
registry data. UCLA scores and self-reported activity were used to screen the athletes. Pain was
assessed with the WOMAC pain subscale. There were 20 male and 9 female patients with a mean
age of 17 years (range, 12.7 to 20.7). Mean time for follow-up was 1.8 years (range, 1 to 3.9). Of the
patients, 48.2% had FAI secondary to pediatric hip deformity, and 10 had previous hip surgery—
including 4 screw fixations for slipped capital femoral epiphysis (SCFE); and, out of the 5 patients
with Legg-Calvé-Perthes disease, 3 had intertrochanteric osteotomies, 1 had a shelf procedure, and
1 had an epiphysiodesis of the greater trochanter. One patient with hereditary osteochondroma-
tosis had a prior osteochondroma of the proximal femur resected. Through a surgical hip disloca-
tion, a femoral head–neck junction osteochondroplasty was completed in all cases, acetabular rim
trimming and labral refixation in 10 patients, femoral intertrochanteric osteotomy in 3 patients,
acetabular microfracture in 2 patients, and a relative femoral neck lengthening in 3 patients. There
was a marginally significant improvement in postoperative UCLA scores. Thirty-one percent had
no change in their activity score. There was a significant improvement in WOMAC pain scores,
and a negative correlation was found between UCLA scores and WOMAC pain scores following
surgery. Of the 6 patients with lower levels of activity following surgery, 3 decreased by 1 point
but maintained regular participation in very active events (UCLA ≥ 8), and the other 3 had signifi-
cant decreases in activity (2 of the 3 had Beck Grade V acetabular cartilage damage). The authors
concluded that adolescents undergoing surgical hip dislocation for FAI can resume prior level of
athletic activities.
304 Chapter 18
PEARLS AND PITFALLS

● High-level athletes are able to return to presurgery performance levels (or better).
● Open surgical treatment of FAI does provide results comparable to arthroscopic treatment in
terms of rates of return to play.
● The addition of microfracture to traditional FAI interventions during hip arthroscopy does
not significantly alter outcomes.
CONCLUSION
FAI in athletes can lead to substantial symptoms of groin pain and discomfort that impairs
function and compromises performance. Furthermore, recurrent microtrauma secondary to
FAI results in predictable chondral and labral injury that may accelerate the development of osteo-
arthritic changes. If the mechanical etiologies of hip pain are correctly identified through a careful
history, physical examination, and radiographic studies and appropriately corrected with surgical
intervention, numerous studies demonstrate that the majority of athletes are able to return to
their previous level of sporting activity with good-to-excellent clinical outcomes at moderate-term
follow-up. Significant preoperative chondral damage is a poor prognosis for ability and duration
of return to play independent of surgical approach or deformity. Future investigation is needed
both to fully elucidate the efficacy of surgical correction of FAI and the effect of associated chon-
drolabral pathology on its natural history and the progression of degenerative changes, as well as
to define the long-term outcomes of our current, more comprehensive surgical approaches that
address both osseous and soft tissue pathology.
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Financial Disclosures
Dr. Stanley Antolak has not disclosed any relevant financial relationships.
Dr. Asheesh Bedi is Educational Consultant for Smith & Nephew and is a shareholder in
A3 Surgical.
Dr. Patrick Birmingham has no financial or proprietary interest in the materials presented herein.
Dr. James P. Bradley receives royalties from Arthrex.
Karen K. Briggs has no financial or proprietary interest in the materials presented herein.
Dr. J. W. Thomas Byrd is a consultant for Smith & Nephew and is a consultant and owns stock
in A3 Surgical.
Dr. Steven B. Cohen has no financial or proprietary interest in the materials presented herein.
Dr. Struan H. Coleman is a consultant for Stryker.
Toni Dauwalter has no financial or proprietary interest in the materials presented herein.
Pete Draovitch has not disclosed any relevant financial relationships.
Jaime Edelstein has not disclosed any relevant financial relationships.
Dr. Marci Goolsby has no financial or proprietary interest in the materials presented herein.
Dr. Carlos A. Guanche is a consultant for Smith & Nephew.
- 307 -
308 Financial Disclosures
Dr. Suzanne Gutierrez-Teissonniere has no financial or proprietary interest in the materials

presented herein.
Dr. Landon Hough has no financial or proprietary interest in the materials presented herein.
Dr. Bryan T. Kelly is a consultant for, and has stock options with, A3 Surgical.
Dr. Aaron J. Krych is a consultant for Arthrex.
Dr. Christopher M. Larson is a paid consultant for Smith & Nephew and A3 Surgical. He has
stock options with A3 Surgical. Dr. Larson is on the editorial/governing board of Arthroscopy: The
Journal of Arthroscopic and Related Surgery. He provides educational and research support for
Smith & Nephew.
Dr. Michael Leunig has not disclosed any relevant financial relationships.
Dr. Eddie Y. Lo has no financial or proprietary interest in the materials presented herein.
Dr. Travis Maak has not disclosed any relevant financial relationships.
Dr. Hal D. Martin has not disclosed any relevant financial relationships.
Dr. Peter Moley has no financial or proprietary interest in the materials presented herein.
Dr. Shane Nho is a consultant for Stryker and Össur.
Dr. Nikhil Oak has not disclosed any relevant financial relationships.
Dr. Eilish O’Sullivan has no financial or proprietary interest in the materials presented herein.
Dr. Marc J. Philippon is a consultant for MIS and a paid consultant for Smith & Nephew Endos-
copy. He provides research support to Össur, Arthrex, Siemens, and Smith & Nephew Endoscopy.
Dr. Philippon receives royalties from Arthrosurface, Bledsoe, ConMed Linvatec, DonJoy, SLACK
Incorporated, Elsevier, and Smith & Nephew Endoscopy. He is founding member, board member,
and committee member at International Society for Hip Arthroscopy; board member at Steadman
Philippon Research Institute; committee member at American Orthopaedic Society for Sports
Medicine; and a member of the Arthroscopy Association of North America, Herodicus, the Inter-
national Cartilage Repair Society, the Orthopaedic Research Society, the Canadian Orthopaedic
Association, and American Orthopaedic Society for Sports Medicine. Dr. Philippon is a reviewer
for Journal of Bone and Joint Surgery (American and British), American Journal of Sports Medicine,
Arthroscopy, Journal of Orthopaedic Research, and Clinical Orthopaedics and Related Research. He
is a stockholder in Arthrosurface, HIPCO, and MIS. He has ownership in HIPCO.
Dr. Lazaros A. Poultsides has no financial or proprietary interest in the materials presented herein.
Dr. Anil Ranawat is a consultant for Conformis, ConMed Linvatec, DePuy Mitek, Nova Surgical
Medical Centre, Stryker Corp, and Stryker-MAKO and is on the advisory boards of Conformis,
Nova Surgical Medical Centre, and Stryker-MAKO. Dr. Ranawat receives royalties and is an editor
Financial Disclosures 309
for Elsevier, is a designer for Stryker-MAKO, has stock options with Nova Surgical Medical Centre,
and has ownership interest in Conformis.
Dr. Marc R. Safran has no financial or proprietary interest in the materials presented herein.
Dr. Ernest L. Sink has no financial or proprietary interest in the materials presented herein.
Dr. Jack G. Skendzel has no financial or proprietary interest in the materials presented herein.
Dr. Michael D. Stover has no financial or proprietary interest in the materials presented herein.
Dr. Matthew Thompson has no financial or proprietary interest in the materials presented herein.
Dr. Lisa M. Tibor has no financial or proprietary interest in the materials presented herein.
Dr. James Voos has no financial or proprietary interest in the materials presented herein.
Dr. Russell F. Warren has not disclosed any relevant financial relationships.
Dr. Alexander E. Weber has no financial or proprietary interest in the materials presented herein.

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Larson • O’Sullivan

Sports Hip Injuries: Diagnosis and Management SLACK

Eilish O’Sullivan, PT, DPT, OCS

Copyright © 2015 by SLACK Incorporated

Published by: SLACK Incorporated

Library of Congress Cataloging-in-Publication Data

Section I Basic Injury Patterns . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1

Chapter 2 Femoroacetabular Impingement: I. Pathoanatomy,

Chapter 3 Femoroacetabular Impingement: II. Open Treatment Strategies

Chapter 4 Dysplasia and Instability . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 63

Chapter 5 Traumatic Hip Subluxation/Dislocation and

Chapter 6 Anterior Soft Tissue Injuries of the Hip:

Chapter 7 Medial Soft Tissue Injuries of the Hip:

Chapter 8 Posterior Soft Tissue Injuries of the Hip: Hamstring . . . . . . . . . . . . . . . . . . 125

Chapter 9 Lateral Soft Tissue Injuries of the Hip:

Chapter 10 Nerve Compression Injuries About the Hip

Chapter 11 Stress Fractures of the Hip and Pelvis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 171

Section II Sport-Specific Injuries . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .187

Chapter 13 The Pivoting Athlete: Hockey, Soccer, Lacrosse, Basketball,

Chapter 14 The Overhead Athlete: Baseball, Volleyball, and Tennis . . . . . . . . . . . . . . . 221

Chapter 16 The Hypermobile Athlete: Dancers, Cheerleaders,

Chapter 17 Sport-Specific Rehabilitation Guidelines . . . . . . . . . . . . . . . . . . . . . . . . . . . 273

Chapter 18 Outcomes in Return to Sport. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 291

Financial Disclosures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 307

Christopher M. Larson, MD, is a sports medicine fellowship-trained surgeon who specializes in

Patrick Birmingham, MD (Chapter 7, 13) Marci Goolsby, MD (Chapter 11)

James P. Bradley, MD (Chapter 8) Carlos A. Guanche, MD (Chapter 8)

Hal D. Martin, DO (Chapter 10) Ernest L. Sink, MD (Chapter 16)

Peter J. Moley, MD (Chapter 15) Jack G. Skendzel, MD (Chapter 18)

Alexander E. Weber, MD; Lazaros A. Poultsides, MD, MSc, PhD;

LAYERED APPROACH TO DIAGNOSTIC EVALUATION

Layer I: Osteochondral Layer

Kelly BT, Bedi A, Larson CM, O’Sullivan E, eds.

I Osteochondral Femur Joint congruity Static Dynamic

II Capsulolabral Capsule Static stability ● Capsular instability

III Muscular Peri-articular musculature Dynamic stability Anterior

IV Neural Neurovasculature of the pelvic Biofeedback Neural Mechanical

Figure 1-1. Bony landmarks that may

Figure 1-2. Illustration of the acetabu-

Layer II: Capsulolabral Layer

Figure 1-3. Illustration of the

Capsular Structure and Function

Figure 1-4. Illustration of the major blood vessels to the hip.

Layer III: Muscular Layer

Layer IV: Neural Layer

COMPREHENSIVE CLINICAL EXAMINATION

OVERVIEW OF IMAGING STUDIES

Careful analysis of plain radiographs can provide a remarkable amount of information

Figure 1-5. Lateral radiograph of the hip demonstrating an

Magnetic Resonance Imaging

PEARLS AND PITFALLS

Bryan T. Kelly, MD and Christopher M. Larson, MD

Femoroacetabular impingement (FAI) has become increasingly recognized as a disorder

Kelly BT, Bedi A, Larson CM, O’Sullivan E, eds.

Figure 2-1. Plain radiograph of a patient

Figure 2-2. Plain radiograph of a patient

PATHOANATOMY OF IMPINGEMENT: OVERVIEW

Figure 2-3. (A) Trochanteric pelvic

Femoroacetabular Impingement-Induced Instability

Dynamic Impingement and Static Overload

CLINICAL EVALUATION PEARLS

History and Physical Examination

c. Layer III: Muscular layer—Compensatory patterns

SURGICAL TECHNIQUE: ARTHROSCOPY

Step 2: Portal Access

Step 3: Interportal Capsule Cut