Q2: Answer: E

Objective: Recall that the major risk to pregnant patients with inflammatory bowel disease (IBD) is a flare of IBD.

Rationale: The most important factor in a successful pregnancy is the maintenance of IBD in a quiescent state. Most of the medications typically used to treat IBD are considered relatively safe in pregnancy. In fact, the risk of a flare of disease during pregnancy usually outweighs the risk of these medications.

Endoscopic procedures are generally well tolerated when proper precautions are taken, but should be deferred until the second trimester if possible, and performed only when there is a strong indication. The decision to proceed with endoscopy should be made in consultation with an obstetrician, regardless of gestational age.

References

1. Schulze H., Esters P., Dignass A. Review article: The management of Crohn’s disease and ulcerative colitis during pregnancy and lactation. Aliment Pharmacol Ther. 2014;40:991-1008.

2. ASGE Standard of Practice Committee. Shergill A.K., Ben-Menachem T., Chandrasekhara V., et al. Guidelines for endoscopy in pregnant and lactating women. Gastrointest Endosc. 2012:76:18-24.

Q2: Answer: E

Objective: Recall that the major risk to pregnant patients with inflammatory bowel disease (IBD) is a flare of IBD.

Rationale: The most important factor in a successful pregnancy is the maintenance of IBD in a quiescent state. Most of the medications typically used to treat IBD are considered relatively safe in pregnancy. In fact, the risk of a flare of disease during pregnancy usually outweighs the risk of these medications.

Endoscopic procedures are generally well tolerated when proper precautions are taken, but should be deferred until the second trimester if possible, and performed only when there is a strong indication. The decision to proceed with endoscopy should be made in consultation with an obstetrician, regardless of gestational age.

References

1. Schulze H., Esters P., Dignass A. Review article: The management of Crohn’s disease and ulcerative colitis during pregnancy and lactation. Aliment Pharmacol Ther. 2014;40:991-1008.

2. ASGE Standard of Practice Committee. Shergill A.K., Ben-Menachem T., Chandrasekhara V., et al. Guidelines for endoscopy in pregnant and lactating women. Gastrointest Endosc. 2012:76:18-24.

Q2: Answer: E

Objective: Recall that the major risk to pregnant patients with inflammatory bowel disease (IBD) is a flare of IBD.

Rationale: The most important factor in a successful pregnancy is the maintenance of IBD in a quiescent state. Most of the medications typically used to treat IBD are considered relatively safe in pregnancy. In fact, the risk of a flare of disease during pregnancy usually outweighs the risk of these medications.

Endoscopic procedures are generally well tolerated when proper precautions are taken, but should be deferred until the second trimester if possible, and performed only when there is a strong indication. The decision to proceed with endoscopy should be made in consultation with an obstetrician, regardless of gestational age.

References

1. Schulze H., Esters P., Dignass A. Review article: The management of Crohn’s disease and ulcerative colitis during pregnancy and lactation. Aliment Pharmacol Ther. 2014;40:991-1008.

2. ASGE Standard of Practice Committee. Shergill A.K., Ben-Menachem T., Chandrasekhara V., et al. Guidelines for endoscopy in pregnant and lactating women. Gastrointest Endosc. 2012:76:18-24.

Q1: Answer: B

Rationale: Although copper deficiency could be a complication of extensive enteropathy from conditions such as Crohn’s disease, celiac disease, short gut syndrome, or HIV enteropathy, it is more commonly recognized as a complication of gastric bypass surgeries. Copper absorption is thought to be primarily in the stomach and proximal small intestine. Copper is partially excreted in the bile, and patients with chronic external biliary drains may also develop copper deficiency. Deficiency in copper has also been recognized as a complication of zinc toxicity from deliberate chronic ingestion of zinc or unintentional industrial overexposure to zinc, and can also be a complication of chronic total parenteral nutrition in the absence of routine micronutrient supplementation. Complaints of muscle weakness and gait disturbance with copper deficiency are secondary to a myeloneuropathy similar to vitamin B12 deficiency. Copper deficiency may present as a microcytic anemia and neutropenia and, in advanced cases, may mimic a myelodysplastic syndrome. The microcytic anemia of copper deficiency is worsened by iron supplementation, which can reduce copper absorption.

Riboflavin deficiency may manifest with photophobia, burning mouth sensation, and glossitis. Zinc deficiency may manifest as diarrhea, altered taste sensation (dysgeusia), night blindness, and a characteristic acrodermatitis. Iron deficiency principally manifests as a microcytic anemia. Vitamin B12 deficiency is associated with gastric bypass surgery, as well as resection of the ileum, and may result in myeloneuropathy, but characteristically is associated with a megaloblastic, macrocytic anemia.

Q1: Answer: B

Rationale: Although copper deficiency could be a complication of extensive enteropathy from conditions such as Crohn’s disease, celiac disease, short gut syndrome, or HIV enteropathy, it is more commonly recognized as a complication of gastric bypass surgeries. Copper absorption is thought to be primarily in the stomach and proximal small intestine. Copper is partially excreted in the bile, and patients with chronic external biliary drains may also develop copper deficiency. Deficiency in copper has also been recognized as a complication of zinc toxicity from deliberate chronic ingestion of zinc or unintentional industrial overexposure to zinc, and can also be a complication of chronic total parenteral nutrition in the absence of routine micronutrient supplementation. Complaints of muscle weakness and gait disturbance with copper deficiency are secondary to a myeloneuropathy similar to vitamin B12 deficiency. Copper deficiency may present as a microcytic anemia and neutropenia and, in advanced cases, may mimic a myelodysplastic syndrome. The microcytic anemia of copper deficiency is worsened by iron supplementation, which can reduce copper absorption.

Riboflavin deficiency may manifest with photophobia, burning mouth sensation, and glossitis. Zinc deficiency may manifest as diarrhea, altered taste sensation (dysgeusia), night blindness, and a characteristic acrodermatitis. Iron deficiency principally manifests as a microcytic anemia. Vitamin B12 deficiency is associated with gastric bypass surgery, as well as resection of the ileum, and may result in myeloneuropathy, but characteristically is associated with a megaloblastic, macrocytic anemia.

Q1: Answer: B

Rationale: Although copper deficiency could be a complication of extensive enteropathy from conditions such as Crohn’s disease, celiac disease, short gut syndrome, or HIV enteropathy, it is more commonly recognized as a complication of gastric bypass surgeries. Copper absorption is thought to be primarily in the stomach and proximal small intestine. Copper is partially excreted in the bile, and patients with chronic external biliary drains may also develop copper deficiency. Deficiency in copper has also been recognized as a complication of zinc toxicity from deliberate chronic ingestion of zinc or unintentional industrial overexposure to zinc, and can also be a complication of chronic total parenteral nutrition in the absence of routine micronutrient supplementation. Complaints of muscle weakness and gait disturbance with copper deficiency are secondary to a myeloneuropathy similar to vitamin B12 deficiency. Copper deficiency may present as a microcytic anemia and neutropenia and, in advanced cases, may mimic a myelodysplastic syndrome. The microcytic anemia of copper deficiency is worsened by iron supplementation, which can reduce copper absorption.

Riboflavin deficiency may manifest with photophobia, burning mouth sensation, and glossitis. Zinc deficiency may manifest as diarrhea, altered taste sensation (dysgeusia), night blindness, and a characteristic acrodermatitis. Iron deficiency principally manifests as a microcytic anemia. Vitamin B12 deficiency is associated with gastric bypass surgery, as well as resection of the ileum, and may result in myeloneuropathy, but characteristically is associated with a megaloblastic, macrocytic anemia.

TORONTO—Nonalcoholic fatty liver disease seems to accelerate physical brain aging by as much as seven years, according to a new subanalysis of the ongoing Framingham Heart Study. However, while the finding suggests that the liver disorder directly endangers brains, the study also offers hope, said Galit Weinstein, MSc, PhD, at the 2016 Alzheimer’s Association International Conference. “If indeed nonalcoholic fatty liver disease is a risk factor for brain aging and subsequent dementia, then it is a modifiable one,” said Dr. Weinstein, an Adjunct Assistant Professor of Neurology at Boston University. “We have reason to hope that nonalcoholic fatty liver disease remission could possibly improve cognitive outcomes.”

She and her colleagues examined the relationship of nonalcoholic fatty liver disease and total brain volume in 906 subjects enrolled in the Framingham Offspring Cohort. This substudy was initiated in 1971 and includes 5,124 children of the original Framingham cohort.

For their study, the researchers assessed the presence of nonalcoholic fatty liver disease by abdominal CT scans and white-matter hyperintensities and brain volume (total, frontal, and hippocampal) by MRI. The resulting associations were then adjusted for age, sex, alcohol consumption, visceral adipose tissue, BMI, menopausal status, systolic blood pressure, current smoking, diabetes, history of cardiovascular disease, physical activity, insulin resistance, and C-reactive protein.

There were no significant associations with white-matter hyperintensities or with hippocampal volume, but the researches did find a significant association with total brain volume. Even after adjustment for all of the covariates, patients with nonalcoholic fatty liver disease had smaller-than-normal brains for their age. This result can be seen as a pathologic acceleration of the brain aging process, Dr. Weinstein said.

The finding was most striking among the youngest subjects, she said, accounting for about a seven-year advance in brain aging for those younger than 60. Older patients with nonalcoholic fatty liver disease showed about a two-year advance in brain aging.

The effect is probably mediated by the liver’s complex interplay in metabolism and vascular functions, Dr. Weinstein said.

—Michele G. Sullivan

TORONTO—Nonalcoholic fatty liver disease seems to accelerate physical brain aging by as much as seven years, according to a new subanalysis of the ongoing Framingham Heart Study. However, while the finding suggests that the liver disorder directly endangers brains, the study also offers hope, said Galit Weinstein, MSc, PhD, at the 2016 Alzheimer’s Association International Conference. “If indeed nonalcoholic fatty liver disease is a risk factor for brain aging and subsequent dementia, then it is a modifiable one,” said Dr. Weinstein, an Adjunct Assistant Professor of Neurology at Boston University. “We have reason to hope that nonalcoholic fatty liver disease remission could possibly improve cognitive outcomes.”

She and her colleagues examined the relationship of nonalcoholic fatty liver disease and total brain volume in 906 subjects enrolled in the Framingham Offspring Cohort. This substudy was initiated in 1971 and includes 5,124 children of the original Framingham cohort.

For their study, the researchers assessed the presence of nonalcoholic fatty liver disease by abdominal CT scans and white-matter hyperintensities and brain volume (total, frontal, and hippocampal) by MRI. The resulting associations were then adjusted for age, sex, alcohol consumption, visceral adipose tissue, BMI, menopausal status, systolic blood pressure, current smoking, diabetes, history of cardiovascular disease, physical activity, insulin resistance, and C-reactive protein.

There were no significant associations with white-matter hyperintensities or with hippocampal volume, but the researches did find a significant association with total brain volume. Even after adjustment for all of the covariates, patients with nonalcoholic fatty liver disease had smaller-than-normal brains for their age. This result can be seen as a pathologic acceleration of the brain aging process, Dr. Weinstein said.

The finding was most striking among the youngest subjects, she said, accounting for about a seven-year advance in brain aging for those younger than 60. Older patients with nonalcoholic fatty liver disease showed about a two-year advance in brain aging.

The effect is probably mediated by the liver’s complex interplay in metabolism and vascular functions, Dr. Weinstein said.

—Michele G. Sullivan

TORONTO—Nonalcoholic fatty liver disease seems to accelerate physical brain aging by as much as seven years, according to a new subanalysis of the ongoing Framingham Heart Study. However, while the finding suggests that the liver disorder directly endangers brains, the study also offers hope, said Galit Weinstein, MSc, PhD, at the 2016 Alzheimer’s Association International Conference. “If indeed nonalcoholic fatty liver disease is a risk factor for brain aging and subsequent dementia, then it is a modifiable one,” said Dr. Weinstein, an Adjunct Assistant Professor of Neurology at Boston University. “We have reason to hope that nonalcoholic fatty liver disease remission could possibly improve cognitive outcomes.”

She and her colleagues examined the relationship of nonalcoholic fatty liver disease and total brain volume in 906 subjects enrolled in the Framingham Offspring Cohort. This substudy was initiated in 1971 and includes 5,124 children of the original Framingham cohort.

For their study, the researchers assessed the presence of nonalcoholic fatty liver disease by abdominal CT scans and white-matter hyperintensities and brain volume (total, frontal, and hippocampal) by MRI. The resulting associations were then adjusted for age, sex, alcohol consumption, visceral adipose tissue, BMI, menopausal status, systolic blood pressure, current smoking, diabetes, history of cardiovascular disease, physical activity, insulin resistance, and C-reactive protein.

There were no significant associations with white-matter hyperintensities or with hippocampal volume, but the researches did find a significant association with total brain volume. Even after adjustment for all of the covariates, patients with nonalcoholic fatty liver disease had smaller-than-normal brains for their age. This result can be seen as a pathologic acceleration of the brain aging process, Dr. Weinstein said.

The finding was most striking among the youngest subjects, she said, accounting for about a seven-year advance in brain aging for those younger than 60. Older patients with nonalcoholic fatty liver disease showed about a two-year advance in brain aging.

The effect is probably mediated by the liver’s complex interplay in metabolism and vascular functions, Dr. Weinstein said.

—Michele G. Sullivan

HOUSTON – Predictors of poor outcomes in patients with status epilepticus admitted to the neurointensive care unit include complex partial status epilepticus (CPSE), refractory status epilepticus, or the development of nonconvulsive status epilepticus (NCSE) at any time during the hospital course, according to results from a single-center study.

“Not a lot of data exist as to what predicts the poor outcomes and what’s known about the outcome in patients with status epilepticus,” lead study author Advait Mahulikar, MD, said in an interview at the annual meeting of the American Epilepsy Society. To find out, he and his associates retrospectively reviewed data from 100 patients with status epilepticus who were admitted to the neurointensive care unit at Detroit Medical Center from November 2013 to January 2016. Variables of interest included patient demographics, initial presentation, refractoriness to treatment, presence or absence of underlying etiology, past history of epilepsy, and use of benzodiazepines on admission. Another variable of interest was NCSE, either from initial presentation or developed during the course of convulsive status epilepticus. A good outcome was defined as a Glasgow Outcome Scale (GOS) score of 4 or 5, and a poor outcome was defined as a GOS score of 1-3.

Doug Brunk/Frontline Medical News

[email protected]

HOUSTON – Predictors of poor outcomes in patients with status epilepticus admitted to the neurointensive care unit include complex partial status epilepticus (CPSE), refractory status epilepticus, or the development of nonconvulsive status epilepticus (NCSE) at any time during the hospital course, according to results from a single-center study.

“Not a lot of data exist as to what predicts the poor outcomes and what’s known about the outcome in patients with status epilepticus,” lead study author Advait Mahulikar, MD, said in an interview at the annual meeting of the American Epilepsy Society. To find out, he and his associates retrospectively reviewed data from 100 patients with status epilepticus who were admitted to the neurointensive care unit at Detroit Medical Center from November 2013 to January 2016. Variables of interest included patient demographics, initial presentation, refractoriness to treatment, presence or absence of underlying etiology, past history of epilepsy, and use of benzodiazepines on admission. Another variable of interest was NCSE, either from initial presentation or developed during the course of convulsive status epilepticus. A good outcome was defined as a Glasgow Outcome Scale (GOS) score of 4 or 5, and a poor outcome was defined as a GOS score of 1-3.

Doug Brunk/Frontline Medical News

[email protected]

HOUSTON – Predictors of poor outcomes in patients with status epilepticus admitted to the neurointensive care unit include complex partial status epilepticus (CPSE), refractory status epilepticus, or the development of nonconvulsive status epilepticus (NCSE) at any time during the hospital course, according to results from a single-center study.

“Not a lot of data exist as to what predicts the poor outcomes and what’s known about the outcome in patients with status epilepticus,” lead study author Advait Mahulikar, MD, said in an interview at the annual meeting of the American Epilepsy Society. To find out, he and his associates retrospectively reviewed data from 100 patients with status epilepticus who were admitted to the neurointensive care unit at Detroit Medical Center from November 2013 to January 2016. Variables of interest included patient demographics, initial presentation, refractoriness to treatment, presence or absence of underlying etiology, past history of epilepsy, and use of benzodiazepines on admission. Another variable of interest was NCSE, either from initial presentation or developed during the course of convulsive status epilepticus. A good outcome was defined as a Glasgow Outcome Scale (GOS) score of 4 or 5, and a poor outcome was defined as a GOS score of 1-3.

Doug Brunk/Frontline Medical News

[email protected]

Contrary to popular belief, great scientists do not spend their days proving that their new ideas are correct. That is just the romantic portrait of the field that is taught to schoolchildren. The reality is that great scientists do everything they can think of to disprove their theories. They exhaustively consider all other plausible explanations, challenge any potential bias in their methodology, rule out random flukes in the data collection, and refine any error in the data measurement. Only after doing all that, when no other conclusion is possible, do true scientists publish their new theories as truth. Then they await confirmation from their peers.

That is the philosophy behind the modern scientific method. In the hard sciences like chemistry and physics, this paradigm is reinforced because a scientist stakes his or her reputation on every publication. Funding from various government agencies often is controlled by peers in the field. If published work is inaccurate, the likelihood of receiving funding is markedly diminished.

Dr. Powell is a pediatric hospitalist and clinical ethics consultant living in St. Louis.

Contrary to popular belief, great scientists do not spend their days proving that their new ideas are correct. That is just the romantic portrait of the field that is taught to schoolchildren. The reality is that great scientists do everything they can think of to disprove their theories. They exhaustively consider all other plausible explanations, challenge any potential bias in their methodology, rule out random flukes in the data collection, and refine any error in the data measurement. Only after doing all that, when no other conclusion is possible, do true scientists publish their new theories as truth. Then they await confirmation from their peers.

That is the philosophy behind the modern scientific method. In the hard sciences like chemistry and physics, this paradigm is reinforced because a scientist stakes his or her reputation on every publication. Funding from various government agencies often is controlled by peers in the field. If published work is inaccurate, the likelihood of receiving funding is markedly diminished.

Dr. Powell is a pediatric hospitalist and clinical ethics consultant living in St. Louis.

Contrary to popular belief, great scientists do not spend their days proving that their new ideas are correct. That is just the romantic portrait of the field that is taught to schoolchildren. The reality is that great scientists do everything they can think of to disprove their theories. They exhaustively consider all other plausible explanations, challenge any potential bias in their methodology, rule out random flukes in the data collection, and refine any error in the data measurement. Only after doing all that, when no other conclusion is possible, do true scientists publish their new theories as truth. Then they await confirmation from their peers.

That is the philosophy behind the modern scientific method. In the hard sciences like chemistry and physics, this paradigm is reinforced because a scientist stakes his or her reputation on every publication. Funding from various government agencies often is controlled by peers in the field. If published work is inaccurate, the likelihood of receiving funding is markedly diminished.

Dr. Powell is a pediatric hospitalist and clinical ethics consultant living in St. Louis.

Editor’s Note: AJO is fortunate to have Shane Nho, one of the nation’s leading hip arthroscopists, as our Deputy Editor-in-Chief. He has compiled an outstanding update for all orthopedic surgeons who see hip patients. It’s my pleasure to turn this issue over to him. On a side note, we’ve added a new feature for our speed readers. From now on, all articles published in AJO will feature a “Take-Home Points” text box. These points represent the most important items that the authors wish to convey from their article. Please enjoy this month’s issue and keep the feedback coming. We are striving to continuously improve AJO and make it your go-to journal for practical information that you can apply directly to your practice.

—Bryan T. Hanypsiak, MD

Hip arthroscopy has been evolving over the past 2 decades as our techniques have been refined and our clinical outcomes have been reported. We have reached a point in our field to look back at the progress that has been made while also providing our readers with the most up-to-date information on diagnosis, imaging studies, and decision making for appropriate treatment.

Trofa and colleagues provide an excellent overview on intra- and extra-articular pathology of the hip and pelvis in their article, “Mastering the Physical Examination of the Athlete’s Hip”. The authors review common injuries in the athlete and provide physical examination tests to differentiate between adductor strain, athletic pubalgia, osteitis pubis, and femoroacetabular impingement (FAI). Also in this issue, Lewis and colleagues provide a comprehensive review of imaging studies in the “Imaging for Nonarthritic Hip Pathology”. The authors review the most common radiographic measurements to detect FAI as well as describe the role of computed tomography and magnetic resonance imaging.

The mastery of hip arthroscopy for the treatment of FAI has a steep learning curve and the techniques have evolved along with our understanding of the importance of the labrum and capsule. We are fortunate to have an article provided by one of the pioneers in the field, Dr. Marc J. Philippon, describing his role in advancing the field in the article “Treatment of FAI: Labrum, Cartilage, Osseous Deformity, and Capsule”. Kollmorgen and Mather provide the most up-to-date techniques for labrum repair and reconstruction. Friel and colleagues report on capsular repair and plication using the T-capsulotomy and the extensile interportal capsulotomy.

We also have the opportunity to read about a number of clinical studies describing the experiences of multi-center studies and epidemiologic studies on large volumes of data. The ANCHOR group provides a summary of the experiences of some of the most renowned hip surgeons in North America as the treatment of FAI evolved from an open approach to an all-arthroscopic approach. The MASH group is a large multi-center group of hip arthroscopists in the United States who describe their current indications for surgical treatment of FAI.

On AmJOrthopedics.com, Matsuda and colleagues describe the outcomes of borderline dysplasia patients compared to normal controls across multiple centers. Anthony and colleagues report on the complication rates using the National Surgical Quality Improvement Program database.

I believe that our Hip Arthroscopy issue will not disappoint you. It is a comprehensive review of the state-of-the-art in hip arthroscopy from physical examination to current surgical techniques to clinical outcomes from large databases for the treatment of FAI. After reviewing this issue, you will be equipped with the most up-to-date information on the treatment of nonarthritic hip disease.

Am J Orthop. 2017;46(1):8. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Editor’s Note: AJO is fortunate to have Shane Nho, one of the nation’s leading hip arthroscopists, as our Deputy Editor-in-Chief. He has compiled an outstanding update for all orthopedic surgeons who see hip patients. It’s my pleasure to turn this issue over to him. On a side note, we’ve added a new feature for our speed readers. From now on, all articles published in AJO will feature a “Take-Home Points” text box. These points represent the most important items that the authors wish to convey from their article. Please enjoy this month’s issue and keep the feedback coming. We are striving to continuously improve AJO and make it your go-to journal for practical information that you can apply directly to your practice.

—Bryan T. Hanypsiak, MD

Hip arthroscopy has been evolving over the past 2 decades as our techniques have been refined and our clinical outcomes have been reported. We have reached a point in our field to look back at the progress that has been made while also providing our readers with the most up-to-date information on diagnosis, imaging studies, and decision making for appropriate treatment.

Trofa and colleagues provide an excellent overview on intra- and extra-articular pathology of the hip and pelvis in their article, “Mastering the Physical Examination of the Athlete’s Hip”. The authors review common injuries in the athlete and provide physical examination tests to differentiate between adductor strain, athletic pubalgia, osteitis pubis, and femoroacetabular impingement (FAI). Also in this issue, Lewis and colleagues provide a comprehensive review of imaging studies in the “Imaging for Nonarthritic Hip Pathology”. The authors review the most common radiographic measurements to detect FAI as well as describe the role of computed tomography and magnetic resonance imaging.

The mastery of hip arthroscopy for the treatment of FAI has a steep learning curve and the techniques have evolved along with our understanding of the importance of the labrum and capsule. We are fortunate to have an article provided by one of the pioneers in the field, Dr. Marc J. Philippon, describing his role in advancing the field in the article “Treatment of FAI: Labrum, Cartilage, Osseous Deformity, and Capsule”. Kollmorgen and Mather provide the most up-to-date techniques for labrum repair and reconstruction. Friel and colleagues report on capsular repair and plication using the T-capsulotomy and the extensile interportal capsulotomy.

We also have the opportunity to read about a number of clinical studies describing the experiences of multi-center studies and epidemiologic studies on large volumes of data. The ANCHOR group provides a summary of the experiences of some of the most renowned hip surgeons in North America as the treatment of FAI evolved from an open approach to an all-arthroscopic approach. The MASH group is a large multi-center group of hip arthroscopists in the United States who describe their current indications for surgical treatment of FAI.

On AmJOrthopedics.com, Matsuda and colleagues describe the outcomes of borderline dysplasia patients compared to normal controls across multiple centers. Anthony and colleagues report on the complication rates using the National Surgical Quality Improvement Program database.

I believe that our Hip Arthroscopy issue will not disappoint you. It is a comprehensive review of the state-of-the-art in hip arthroscopy from physical examination to current surgical techniques to clinical outcomes from large databases for the treatment of FAI. After reviewing this issue, you will be equipped with the most up-to-date information on the treatment of nonarthritic hip disease.

Am J Orthop. 2017;46(1):8. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Editor’s Note: AJO is fortunate to have Shane Nho, one of the nation’s leading hip arthroscopists, as our Deputy Editor-in-Chief. He has compiled an outstanding update for all orthopedic surgeons who see hip patients. It’s my pleasure to turn this issue over to him. On a side note, we’ve added a new feature for our speed readers. From now on, all articles published in AJO will feature a “Take-Home Points” text box. These points represent the most important items that the authors wish to convey from their article. Please enjoy this month’s issue and keep the feedback coming. We are striving to continuously improve AJO and make it your go-to journal for practical information that you can apply directly to your practice.

—Bryan T. Hanypsiak, MD

Hip arthroscopy has been evolving over the past 2 decades as our techniques have been refined and our clinical outcomes have been reported. We have reached a point in our field to look back at the progress that has been made while also providing our readers with the most up-to-date information on diagnosis, imaging studies, and decision making for appropriate treatment.

Trofa and colleagues provide an excellent overview on intra- and extra-articular pathology of the hip and pelvis in their article, “Mastering the Physical Examination of the Athlete’s Hip”. The authors review common injuries in the athlete and provide physical examination tests to differentiate between adductor strain, athletic pubalgia, osteitis pubis, and femoroacetabular impingement (FAI). Also in this issue, Lewis and colleagues provide a comprehensive review of imaging studies in the “Imaging for Nonarthritic Hip Pathology”. The authors review the most common radiographic measurements to detect FAI as well as describe the role of computed tomography and magnetic resonance imaging.

The mastery of hip arthroscopy for the treatment of FAI has a steep learning curve and the techniques have evolved along with our understanding of the importance of the labrum and capsule. We are fortunate to have an article provided by one of the pioneers in the field, Dr. Marc J. Philippon, describing his role in advancing the field in the article “Treatment of FAI: Labrum, Cartilage, Osseous Deformity, and Capsule”. Kollmorgen and Mather provide the most up-to-date techniques for labrum repair and reconstruction. Friel and colleagues report on capsular repair and plication using the T-capsulotomy and the extensile interportal capsulotomy.

We also have the opportunity to read about a number of clinical studies describing the experiences of multi-center studies and epidemiologic studies on large volumes of data. The ANCHOR group provides a summary of the experiences of some of the most renowned hip surgeons in North America as the treatment of FAI evolved from an open approach to an all-arthroscopic approach. The MASH group is a large multi-center group of hip arthroscopists in the United States who describe their current indications for surgical treatment of FAI.

On AmJOrthopedics.com, Matsuda and colleagues describe the outcomes of borderline dysplasia patients compared to normal controls across multiple centers. Anthony and colleagues report on the complication rates using the National Surgical Quality Improvement Program database.

I believe that our Hip Arthroscopy issue will not disappoint you. It is a comprehensive review of the state-of-the-art in hip arthroscopy from physical examination to current surgical techniques to clinical outcomes from large databases for the treatment of FAI. After reviewing this issue, you will be equipped with the most up-to-date information on the treatment of nonarthritic hip disease.

Am J Orthop. 2017;46(1):8. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

• Perform a comprehensive examination to determine intra-articular pathology as well as potential extra-articular sources of hip and pelvic pain.
• Adductor strains can be prevented with adequate rehabilitation focused on correcting predisposing factors (ie, adductor weakness or tightness, limited range of motion, and core imbalance).
• Athletic pubalgia is diagnosed when tenderness can be elicited over the pubic tubercle.
• Osteitis pubis is diagnosed with pain over the pubic symphysis.
• FAI and labral injury classically present with a C-sign but can also present with lateral hip pain, buttock pain, low back pain, anterior thigh pain, and knee pain.

Hip and groin pain is a common finding among athletes of all ages and activity levels. Such pain most often occurs among athletes in sports such as football, hockey, rugby, soccer, and ballet, which demand frequent cutting, pivoting, and acceleration.^1-4 Previously, pain about the hip and groin was attributed to muscular strains and soft-tissue contusions, but improvements in physical examination skills, imaging modalities, and disease-specific treatment options have led to increased recognition of hip injuries as a significant source of disability in the athletic population.^5,6 These injuries make up 6% or more of all sports injuries, and the rate is increasing.^7-9

In this review, we describe precise methods for evaluating the athlete’s hip or groin with an emphasis on recognizing the most common extra-articular and intra-articular pathologies, including adductor strains, athletic pubalgia, osteitis pubis, and femoroacetabular impingement (FAI) with labral tears.

Hip Pathoanatomy

The first step in determining the etiology of pain is to establish if there is true pathology of the hip joint and surrounding structures, or if the pain is referred from another source.

Patient History

The physical examination is guided by the patient’s history. Important patient-specific factors to be ascertained include age, sport(s) played, competition level, seasonal timing, and effect of the injury on performance. Regarding presenting symptoms, attention should be given to pain location, timing (acute vs chronic), onset, nature (clicking, catching, instability), and precipitating factors. Acute-onset pain with muscle contraction or stretching, possibly accompanied by an audible pop, is likely musculotendinous in origin. Insidious-onset dull aching pain that worsens with activity more commonly involves intra-articular processes. Most classically, this pain occurs deep in the groin and is demonstrated by the C sign: The patient cups a hand with its fingers pointing toward the anterior groin at the level of the greater trochanter (Figure 1).¹¹

A comprehensive hip evaluation can be performed with the patient in the standing, seated, supine, lateral, and prone positions, as previously described (Table 2).^6,12,13

Extra-Articular Hip Pathologies

Adductor Strains

The adductor muscle group includes the adductor magnus, adductor brevis, gracilis, obturator externus, pectineus, and adductor longus, which is the most commonly strained. Adductor strains are the most common cause of groin pain in athletes, and usually occur in sports that require forceful eccentric contraction of the adductors.¹⁴ Among professional soccer players, adductor strains represent almost one fourth of all muscle injuries and result in lost playing time averaging 2 weeks and an 18% reinjury rate.¹⁵ These injuries are particularly detrimental to performance because the adductor muscles help stabilize the pelvis during closed-chain activities.³ Diagnosis and adequate rehabilitation focused on correcting predisposing factors (eg, adductor weakness or tightness, loss of hip range of motion, core imbalance) are paramount in reinjury prevention.^16,17

On presentation, athletes complain of aching groin or medial thigh pain. The examiner should assess for swelling or ecchymosis. There typically is tenderness to palpation at or near the origin on the pubic bones, with pain exacerbated with resisted adduction and passive stretch into abduction during examination. Palpation of adductors requires proper exposure and is most easily performed with the patient supine and the lower extremity in a figure-of-4 position (Figure 2A).

Athletic Pubalgia

Athletic pubalgia, also known as sports hernia or core muscle injury, is an injury to the soft tissues of the lower abdominal or posterior inguinal wall. Although not fully understood, the condition is considered the result of repetitive trunk hyperextension and thigh hyperabduction resulting in shearing at the pubic symphysis where there is a muscle imbalance between the strong proximal thigh muscles and weaker abdominals. This condition is more common in men and typically is insidious in onset with a prolonged course recalcitrant to nonoperative treatment.¹⁸ In studies of chronic groin pain in athletes, the rate of athletic pubalgia as the primary etiology ranges from 39% to 85%.^9,19,20

Patients typically complain of increasing pain in the lower abdominal and proximal adductors during activity. Symptoms include unilateral or bilateral lower abdominal pain, which can radiate toward the perineum, rectus muscle, and proximal adductors during sport but usually abates with rest.¹⁸ Athletes endorse they are not capable of playing at their full athletic potential. Symptoms are initiated with sudden forceful movements, as in sit-ups, sprints, and valsalva maneuvers like coughs and sneezes. Valsalva maneuvers worsen pain in about 10% of patients.^21-23On physical examination with the patient supine, tenderness can be elicited over the pubic tubercle, abdominal obliques, and/or rectus abdominis insertion (Figure 3A). Athletes may also have tenderness at the adductor longus tendon origin at or near the pubic symphysis, which may make the diagnosis difficult to distinguish from an adductor strain.

Osteitis Pubis

Osteitis pubis is a painful overuse injury that results in noninfectious inflammation of the pubic symphysis from increased motion at this normally stable immobile joint.³ As with athletic pubalgia, the exact mechanism is unclear, but likely it is similar to the repetitive stress placed on the pubic symphysis by unequal forces of the abdominal and adductor muscles.²⁴ The disease can result in bony erosions and cartilage breakdown with irregularity of the pubic symphysis.

Athletes may complain of anterior and medial groin pain that can radiate to the lower abdominal muscles, perineum, inguinal region, and medial thigh. Walking, pelvic motion, adductor stretching, abdominal muscle exercises, and standing up can exacerbate pain.²⁴ Some cases involve impaired internal or external rotation of the hip, sacroiliac joint dysfunction, or adductor and abductor muscle weakness.²⁵The distinguishing feature of osteitis pubis is pain over the pubic symphysis with direct palpation (Figure 4A). Examination maneuvers that place stress on the pubic symphysis can aid in diagnosis.²⁶

Intra-Articular Hip Pathology: Femoroacetabular Impingement

In athletes, FAI is a leading cause of intra-articular pathology, which can lead to labral tears.^28,29 FAI lesions include cam-type impingement from an aspherical femoral head and pincer impingement from acetabular overcoverage, both of which limit internal rotation and cause acetabular rim abutment, which damages the labrum.

Athletes present with activity-related groin or hip pain that is exacerbated by hip flexion and internal rotation, with possible mechanical symptoms from labral tearing.³⁰ However, the pain distribution varies. In a study by Clohisy and colleagues,³¹ of patients with symptomatic FAI that required surgical intervention, 88% had groin pain, 67% had lateral hip pain, 35% had anterior thigh pain, 29% had buttock pain, 27% had knee pain, and 23% had low back pain.

Careful attention should be given to range of motion in FAI patients, as they can usually flex their hip to 90° to 110°, and in this position there is limited internal rotation and asymmetric external rotation relative to the contralateral leg.³² The anterior impingement test is one of the most reliable tests for FAI (Figure 5A).³² With the patient supine, the hip is dynamically flexed to 90°, adducted, and internally rotated. A positive test elicits deep anterior groin pain that generally replicates the patient’s symptoms.²⁹

Conclusion

Careful, directed history taking and physical examination are essential in narrowing the diagnostic possibilities before initiating a workup for the common intra-articular and extra-articular causes of hip and groin pain in athletes.

Take-Home Points

• Perform a comprehensive examination to determine intra-articular pathology as well as potential extra-articular sources of hip and pelvic pain.
• Adductor strains can be prevented with adequate rehabilitation focused on correcting predisposing factors (ie, adductor weakness or tightness, limited range of motion, and core imbalance).
• Athletic pubalgia is diagnosed when tenderness can be elicited over the pubic tubercle.
• Osteitis pubis is diagnosed with pain over the pubic symphysis.
• FAI and labral injury classically present with a C-sign but can also present with lateral hip pain, buttock pain, low back pain, anterior thigh pain, and knee pain.

Hip and groin pain is a common finding among athletes of all ages and activity levels. Such pain most often occurs among athletes in sports such as football, hockey, rugby, soccer, and ballet, which demand frequent cutting, pivoting, and acceleration.^1-4 Previously, pain about the hip and groin was attributed to muscular strains and soft-tissue contusions, but improvements in physical examination skills, imaging modalities, and disease-specific treatment options have led to increased recognition of hip injuries as a significant source of disability in the athletic population.^5,6 These injuries make up 6% or more of all sports injuries, and the rate is increasing.^7-9

In this review, we describe precise methods for evaluating the athlete’s hip or groin with an emphasis on recognizing the most common extra-articular and intra-articular pathologies, including adductor strains, athletic pubalgia, osteitis pubis, and femoroacetabular impingement (FAI) with labral tears.

Hip Pathoanatomy

The first step in determining the etiology of pain is to establish if there is true pathology of the hip joint and surrounding structures, or if the pain is referred from another source.

Patient History

The physical examination is guided by the patient’s history. Important patient-specific factors to be ascertained include age, sport(s) played, competition level, seasonal timing, and effect of the injury on performance. Regarding presenting symptoms, attention should be given to pain location, timing (acute vs chronic), onset, nature (clicking, catching, instability), and precipitating factors. Acute-onset pain with muscle contraction or stretching, possibly accompanied by an audible pop, is likely musculotendinous in origin. Insidious-onset dull aching pain that worsens with activity more commonly involves intra-articular processes. Most classically, this pain occurs deep in the groin and is demonstrated by the C sign: The patient cups a hand with its fingers pointing toward the anterior groin at the level of the greater trochanter (Figure 1).¹¹

A comprehensive hip evaluation can be performed with the patient in the standing, seated, supine, lateral, and prone positions, as previously described (Table 2).^6,12,13

Extra-Articular Hip Pathologies

Adductor Strains

The adductor muscle group includes the adductor magnus, adductor brevis, gracilis, obturator externus, pectineus, and adductor longus, which is the most commonly strained. Adductor strains are the most common cause of groin pain in athletes, and usually occur in sports that require forceful eccentric contraction of the adductors.¹⁴ Among professional soccer players, adductor strains represent almost one fourth of all muscle injuries and result in lost playing time averaging 2 weeks and an 18% reinjury rate.¹⁵ These injuries are particularly detrimental to performance because the adductor muscles help stabilize the pelvis during closed-chain activities.³ Diagnosis and adequate rehabilitation focused on correcting predisposing factors (eg, adductor weakness or tightness, loss of hip range of motion, core imbalance) are paramount in reinjury prevention.^16,17

On presentation, athletes complain of aching groin or medial thigh pain. The examiner should assess for swelling or ecchymosis. There typically is tenderness to palpation at or near the origin on the pubic bones, with pain exacerbated with resisted adduction and passive stretch into abduction during examination. Palpation of adductors requires proper exposure and is most easily performed with the patient supine and the lower extremity in a figure-of-4 position (Figure 2A).

Athletic Pubalgia

Athletic pubalgia, also known as sports hernia or core muscle injury, is an injury to the soft tissues of the lower abdominal or posterior inguinal wall. Although not fully understood, the condition is considered the result of repetitive trunk hyperextension and thigh hyperabduction resulting in shearing at the pubic symphysis where there is a muscle imbalance between the strong proximal thigh muscles and weaker abdominals. This condition is more common in men and typically is insidious in onset with a prolonged course recalcitrant to nonoperative treatment.¹⁸ In studies of chronic groin pain in athletes, the rate of athletic pubalgia as the primary etiology ranges from 39% to 85%.^9,19,20

Patients typically complain of increasing pain in the lower abdominal and proximal adductors during activity. Symptoms include unilateral or bilateral lower abdominal pain, which can radiate toward the perineum, rectus muscle, and proximal adductors during sport but usually abates with rest.¹⁸ Athletes endorse they are not capable of playing at their full athletic potential. Symptoms are initiated with sudden forceful movements, as in sit-ups, sprints, and valsalva maneuvers like coughs and sneezes. Valsalva maneuvers worsen pain in about 10% of patients.^21-23On physical examination with the patient supine, tenderness can be elicited over the pubic tubercle, abdominal obliques, and/or rectus abdominis insertion (Figure 3A). Athletes may also have tenderness at the adductor longus tendon origin at or near the pubic symphysis, which may make the diagnosis difficult to distinguish from an adductor strain.

Osteitis Pubis

Osteitis pubis is a painful overuse injury that results in noninfectious inflammation of the pubic symphysis from increased motion at this normally stable immobile joint.³ As with athletic pubalgia, the exact mechanism is unclear, but likely it is similar to the repetitive stress placed on the pubic symphysis by unequal forces of the abdominal and adductor muscles.²⁴ The disease can result in bony erosions and cartilage breakdown with irregularity of the pubic symphysis.

Athletes may complain of anterior and medial groin pain that can radiate to the lower abdominal muscles, perineum, inguinal region, and medial thigh. Walking, pelvic motion, adductor stretching, abdominal muscle exercises, and standing up can exacerbate pain.²⁴ Some cases involve impaired internal or external rotation of the hip, sacroiliac joint dysfunction, or adductor and abductor muscle weakness.²⁵The distinguishing feature of osteitis pubis is pain over the pubic symphysis with direct palpation (Figure 4A). Examination maneuvers that place stress on the pubic symphysis can aid in diagnosis.²⁶

Intra-Articular Hip Pathology: Femoroacetabular Impingement

In athletes, FAI is a leading cause of intra-articular pathology, which can lead to labral tears.^28,29 FAI lesions include cam-type impingement from an aspherical femoral head and pincer impingement from acetabular overcoverage, both of which limit internal rotation and cause acetabular rim abutment, which damages the labrum.

Athletes present with activity-related groin or hip pain that is exacerbated by hip flexion and internal rotation, with possible mechanical symptoms from labral tearing.³⁰ However, the pain distribution varies. In a study by Clohisy and colleagues,³¹ of patients with symptomatic FAI that required surgical intervention, 88% had groin pain, 67% had lateral hip pain, 35% had anterior thigh pain, 29% had buttock pain, 27% had knee pain, and 23% had low back pain.

Careful attention should be given to range of motion in FAI patients, as they can usually flex their hip to 90° to 110°, and in this position there is limited internal rotation and asymmetric external rotation relative to the contralateral leg.³² The anterior impingement test is one of the most reliable tests for FAI (Figure 5A).³² With the patient supine, the hip is dynamically flexed to 90°, adducted, and internally rotated. A positive test elicits deep anterior groin pain that generally replicates the patient’s symptoms.²⁹

Conclusion

Careful, directed history taking and physical examination are essential in narrowing the diagnostic possibilities before initiating a workup for the common intra-articular and extra-articular causes of hip and groin pain in athletes.

Take-Home Points

• Perform a comprehensive examination to determine intra-articular pathology as well as potential extra-articular sources of hip and pelvic pain.
• Adductor strains can be prevented with adequate rehabilitation focused on correcting predisposing factors (ie, adductor weakness or tightness, limited range of motion, and core imbalance).
• Athletic pubalgia is diagnosed when tenderness can be elicited over the pubic tubercle.
• Osteitis pubis is diagnosed with pain over the pubic symphysis.
• FAI and labral injury classically present with a C-sign but can also present with lateral hip pain, buttock pain, low back pain, anterior thigh pain, and knee pain.

Hip and groin pain is a common finding among athletes of all ages and activity levels. Such pain most often occurs among athletes in sports such as football, hockey, rugby, soccer, and ballet, which demand frequent cutting, pivoting, and acceleration.^1-4 Previously, pain about the hip and groin was attributed to muscular strains and soft-tissue contusions, but improvements in physical examination skills, imaging modalities, and disease-specific treatment options have led to increased recognition of hip injuries as a significant source of disability in the athletic population.^5,6 These injuries make up 6% or more of all sports injuries, and the rate is increasing.^7-9

In this review, we describe precise methods for evaluating the athlete’s hip or groin with an emphasis on recognizing the most common extra-articular and intra-articular pathologies, including adductor strains, athletic pubalgia, osteitis pubis, and femoroacetabular impingement (FAI) with labral tears.

Hip Pathoanatomy

The first step in determining the etiology of pain is to establish if there is true pathology of the hip joint and surrounding structures, or if the pain is referred from another source.

Patient History

The physical examination is guided by the patient’s history. Important patient-specific factors to be ascertained include age, sport(s) played, competition level, seasonal timing, and effect of the injury on performance. Regarding presenting symptoms, attention should be given to pain location, timing (acute vs chronic), onset, nature (clicking, catching, instability), and precipitating factors. Acute-onset pain with muscle contraction or stretching, possibly accompanied by an audible pop, is likely musculotendinous in origin. Insidious-onset dull aching pain that worsens with activity more commonly involves intra-articular processes. Most classically, this pain occurs deep in the groin and is demonstrated by the C sign: The patient cups a hand with its fingers pointing toward the anterior groin at the level of the greater trochanter (Figure 1).¹¹

A comprehensive hip evaluation can be performed with the patient in the standing, seated, supine, lateral, and prone positions, as previously described (Table 2).^6,12,13

Extra-Articular Hip Pathologies

Adductor Strains

The adductor muscle group includes the adductor magnus, adductor brevis, gracilis, obturator externus, pectineus, and adductor longus, which is the most commonly strained. Adductor strains are the most common cause of groin pain in athletes, and usually occur in sports that require forceful eccentric contraction of the adductors.¹⁴ Among professional soccer players, adductor strains represent almost one fourth of all muscle injuries and result in lost playing time averaging 2 weeks and an 18% reinjury rate.¹⁵ These injuries are particularly detrimental to performance because the adductor muscles help stabilize the pelvis during closed-chain activities.³ Diagnosis and adequate rehabilitation focused on correcting predisposing factors (eg, adductor weakness or tightness, loss of hip range of motion, core imbalance) are paramount in reinjury prevention.^16,17

On presentation, athletes complain of aching groin or medial thigh pain. The examiner should assess for swelling or ecchymosis. There typically is tenderness to palpation at or near the origin on the pubic bones, with pain exacerbated with resisted adduction and passive stretch into abduction during examination. Palpation of adductors requires proper exposure and is most easily performed with the patient supine and the lower extremity in a figure-of-4 position (Figure 2A).

Athletic Pubalgia

Athletic pubalgia, also known as sports hernia or core muscle injury, is an injury to the soft tissues of the lower abdominal or posterior inguinal wall. Although not fully understood, the condition is considered the result of repetitive trunk hyperextension and thigh hyperabduction resulting in shearing at the pubic symphysis where there is a muscle imbalance between the strong proximal thigh muscles and weaker abdominals. This condition is more common in men and typically is insidious in onset with a prolonged course recalcitrant to nonoperative treatment.¹⁸ In studies of chronic groin pain in athletes, the rate of athletic pubalgia as the primary etiology ranges from 39% to 85%.^9,19,20

Patients typically complain of increasing pain in the lower abdominal and proximal adductors during activity. Symptoms include unilateral or bilateral lower abdominal pain, which can radiate toward the perineum, rectus muscle, and proximal adductors during sport but usually abates with rest.¹⁸ Athletes endorse they are not capable of playing at their full athletic potential. Symptoms are initiated with sudden forceful movements, as in sit-ups, sprints, and valsalva maneuvers like coughs and sneezes. Valsalva maneuvers worsen pain in about 10% of patients.^21-23On physical examination with the patient supine, tenderness can be elicited over the pubic tubercle, abdominal obliques, and/or rectus abdominis insertion (Figure 3A). Athletes may also have tenderness at the adductor longus tendon origin at or near the pubic symphysis, which may make the diagnosis difficult to distinguish from an adductor strain.

Osteitis Pubis

Osteitis pubis is a painful overuse injury that results in noninfectious inflammation of the pubic symphysis from increased motion at this normally stable immobile joint.³ As with athletic pubalgia, the exact mechanism is unclear, but likely it is similar to the repetitive stress placed on the pubic symphysis by unequal forces of the abdominal and adductor muscles.²⁴ The disease can result in bony erosions and cartilage breakdown with irregularity of the pubic symphysis.

Athletes may complain of anterior and medial groin pain that can radiate to the lower abdominal muscles, perineum, inguinal region, and medial thigh. Walking, pelvic motion, adductor stretching, abdominal muscle exercises, and standing up can exacerbate pain.²⁴ Some cases involve impaired internal or external rotation of the hip, sacroiliac joint dysfunction, or adductor and abductor muscle weakness.²⁵The distinguishing feature of osteitis pubis is pain over the pubic symphysis with direct palpation (Figure 4A). Examination maneuvers that place stress on the pubic symphysis can aid in diagnosis.²⁶

Intra-Articular Hip Pathology: Femoroacetabular Impingement

In athletes, FAI is a leading cause of intra-articular pathology, which can lead to labral tears.^28,29 FAI lesions include cam-type impingement from an aspherical femoral head and pincer impingement from acetabular overcoverage, both of which limit internal rotation and cause acetabular rim abutment, which damages the labrum.

Athletes present with activity-related groin or hip pain that is exacerbated by hip flexion and internal rotation, with possible mechanical symptoms from labral tearing.³⁰ However, the pain distribution varies. In a study by Clohisy and colleagues,³¹ of patients with symptomatic FAI that required surgical intervention, 88% had groin pain, 67% had lateral hip pain, 35% had anterior thigh pain, 29% had buttock pain, 27% had knee pain, and 23% had low back pain.

Careful attention should be given to range of motion in FAI patients, as they can usually flex their hip to 90° to 110°, and in this position there is limited internal rotation and asymmetric external rotation relative to the contralateral leg.³² The anterior impingement test is one of the most reliable tests for FAI (Figure 5A).³² With the patient supine, the hip is dynamically flexed to 90°, adducted, and internally rotated. A positive test elicits deep anterior groin pain that generally replicates the patient’s symptoms.²⁹

Conclusion

Careful, directed history taking and physical examination are essential in narrowing the diagnostic possibilities before initiating a workup for the common intra-articular and extra-articular causes of hip and groin pain in athletes.

Take-Home Points

• Be sure to have a well centered AP pelvis without rotation.
• Get at least 3 plain radiographs—AP pelvis, false profile, and lateral hip view.
• Ensure that there is sufficient acetabular coverage, LCEA >20° on AP pelvis and ACEA >20° on false profile view.
• CT scans are helpful for precise hip pathomor­phology but must be weighed against risk of radiation exposure.
• MRI or MRA can be helpful to diagnose intra-articular as well as extra-articular hip and pelvis abnormalities.

In the work-up for nonarthritic hip pain, the value of diagnostic imaging is in objective findings, which can support or weaken the leading diagnoses based on subjective complaints, recalled history, and, in some cases, elusive physical examination findings. Morphologic changes alone, however, do not always indicate pathology.^1,2 At presentation and at each step in the work-up, it is imperative to evaluate the entire clinical picture. The prudent clinician uses both clinical and radiographic findings to make the diagnosis and direct treatment.

Radiography

The first step in diagnostic imaging is radiography. Although use of plain radiographs is routine, their value cannot be understated. Standard hip radiographs—an anteroposterior (AP) radiograph of the pelvis and AP and frog-leg (cross-table lateral) radiographs of the hip—provide a wealth of information.^3-6

Evaluated first is the radiograph itself. For example, the ideal AP radiograph of the pelvis (Figure 1) is centered on the lower sacrum, and the patient is not rotated.

13

Computed Tomography

The benefits of computed tomography (CT) outweigh the risk of radiation exposure. CT is most useful in characterizing osseous morphology.²¹ In FAI cases, CT can distinguish acetabular version abnormalities from femoral torsion (Figures 7A-7C), entities with very different treatment approaches.²¹

Magnetic Resonance Imaging

MRI is becoming essential in the work-up for nonarthritic hip pain.^11,22 It is used for assessment of osseous, chondral, and musculotendinous soft tissues. Further, it affords appreciation of outside-the-hip-joint pathology that may mimic joint-centered pathology.

MRI techniques range from noncontrast to indirect and direct magnetic resonance arthrography (MRA).²² Indirect MRA is performed with contrast medium administered through an intravenous line. Direct MRA has contrast administered intra-articularly and is more sensitive and specific for labral tears and ligamentous injury.²³ Excellent detection of intra-articular pathology on noncontrast studies questions the need for MRA.²⁴ Nevertheless, direct MRA can also be used as a therapeutic procedure when lidocaine is included in the injected gadolinium.

Labral tears, focal chondral defects, and stress or insufficiency fractures are important differentials in the work-up for nonarthritic hip pain. Over the dysplasia-to-FAI spectrum, MRI distinguishes symptomatic pathoanatomy from asymptomatic anatomical variants by revealing underlying bone edema. Capsule findings should also be considered.²¹The most practical classification of labral tears, proposed by Blankenbaker and colleagues,²⁵ is based on tear type (frayed, unstable, flap), location, and extent. More than half of labral tears occur in the anterosuperior quadrant of the labrum.²⁵

26

MRI detects osseous pathology from surrounding soft-tissue edema and bone remodeling to stress and fragility fractures. In athletes, the most common fractures are pubic rami, sacral, and apophyseal avulsion fractures.²⁸ In all patients, attention should be given to the lower spine and the proximal femurs. Aside from MRI, nuclear medicine bone scan might also identify active osseous reaction representative of a fracture.

Conclusion

The work-up for nonarthritic hip pain substantiates differential diagnoses. A case’s complexity determines the course of diagnostic imaging. At presentation and at each step in the work-up, it is imperative to evaluate the entire clinical picture. The prudent clinician uses both clinical and radiographic findings to make the diagnosis and direct treatment.

Am J Orthop . 2017;46(1):17-22. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

• Be sure to have a well centered AP pelvis without rotation.
• Get at least 3 plain radiographs—AP pelvis, false profile, and lateral hip view.
• Ensure that there is sufficient acetabular coverage, LCEA >20° on AP pelvis and ACEA >20° on false profile view.
• CT scans are helpful for precise hip pathomor­phology but must be weighed against risk of radiation exposure.
• MRI or MRA can be helpful to diagnose intra-articular as well as extra-articular hip and pelvis abnormalities.

In the work-up for nonarthritic hip pain, the value of diagnostic imaging is in objective findings, which can support or weaken the leading diagnoses based on subjective complaints, recalled history, and, in some cases, elusive physical examination findings. Morphologic changes alone, however, do not always indicate pathology.^1,2 At presentation and at each step in the work-up, it is imperative to evaluate the entire clinical picture. The prudent clinician uses both clinical and radiographic findings to make the diagnosis and direct treatment.

Radiography

The first step in diagnostic imaging is radiography. Although use of plain radiographs is routine, their value cannot be understated. Standard hip radiographs—an anteroposterior (AP) radiograph of the pelvis and AP and frog-leg (cross-table lateral) radiographs of the hip—provide a wealth of information.^3-6

Evaluated first is the radiograph itself. For example, the ideal AP radiograph of the pelvis (Figure 1) is centered on the lower sacrum, and the patient is not rotated.

13

Computed Tomography

The benefits of computed tomography (CT) outweigh the risk of radiation exposure. CT is most useful in characterizing osseous morphology.²¹ In FAI cases, CT can distinguish acetabular version abnormalities from femoral torsion (Figures 7A-7C), entities with very different treatment approaches.²¹

Magnetic Resonance Imaging

MRI is becoming essential in the work-up for nonarthritic hip pain.^11,22 It is used for assessment of osseous, chondral, and musculotendinous soft tissues. Further, it affords appreciation of outside-the-hip-joint pathology that may mimic joint-centered pathology.

MRI techniques range from noncontrast to indirect and direct magnetic resonance arthrography (MRA).²² Indirect MRA is performed with contrast medium administered through an intravenous line. Direct MRA has contrast administered intra-articularly and is more sensitive and specific for labral tears and ligamentous injury.²³ Excellent detection of intra-articular pathology on noncontrast studies questions the need for MRA.²⁴ Nevertheless, direct MRA can also be used as a therapeutic procedure when lidocaine is included in the injected gadolinium.

Labral tears, focal chondral defects, and stress or insufficiency fractures are important differentials in the work-up for nonarthritic hip pain. Over the dysplasia-to-FAI spectrum, MRI distinguishes symptomatic pathoanatomy from asymptomatic anatomical variants by revealing underlying bone edema. Capsule findings should also be considered.²¹The most practical classification of labral tears, proposed by Blankenbaker and colleagues,²⁵ is based on tear type (frayed, unstable, flap), location, and extent. More than half of labral tears occur in the anterosuperior quadrant of the labrum.²⁵

26

MRI detects osseous pathology from surrounding soft-tissue edema and bone remodeling to stress and fragility fractures. In athletes, the most common fractures are pubic rami, sacral, and apophyseal avulsion fractures.²⁸ In all patients, attention should be given to the lower spine and the proximal femurs. Aside from MRI, nuclear medicine bone scan might also identify active osseous reaction representative of a fracture.

Conclusion

The work-up for nonarthritic hip pain substantiates differential diagnoses. A case’s complexity determines the course of diagnostic imaging. At presentation and at each step in the work-up, it is imperative to evaluate the entire clinical picture. The prudent clinician uses both clinical and radiographic findings to make the diagnosis and direct treatment.

Am J Orthop . 2017;46(1):17-22. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

• Be sure to have a well centered AP pelvis without rotation.
• Get at least 3 plain radiographs—AP pelvis, false profile, and lateral hip view.
• Ensure that there is sufficient acetabular coverage, LCEA >20° on AP pelvis and ACEA >20° on false profile view.
• CT scans are helpful for precise hip pathomor­phology but must be weighed against risk of radiation exposure.
• MRI or MRA can be helpful to diagnose intra-articular as well as extra-articular hip and pelvis abnormalities.

In the work-up for nonarthritic hip pain, the value of diagnostic imaging is in objective findings, which can support or weaken the leading diagnoses based on subjective complaints, recalled history, and, in some cases, elusive physical examination findings. Morphologic changes alone, however, do not always indicate pathology.^1,2 At presentation and at each step in the work-up, it is imperative to evaluate the entire clinical picture. The prudent clinician uses both clinical and radiographic findings to make the diagnosis and direct treatment.

Radiography

The first step in diagnostic imaging is radiography. Although use of plain radiographs is routine, their value cannot be understated. Standard hip radiographs—an anteroposterior (AP) radiograph of the pelvis and AP and frog-leg (cross-table lateral) radiographs of the hip—provide a wealth of information.^3-6

Evaluated first is the radiograph itself. For example, the ideal AP radiograph of the pelvis (Figure 1) is centered on the lower sacrum, and the patient is not rotated.

13

Computed Tomography

The benefits of computed tomography (CT) outweigh the risk of radiation exposure. CT is most useful in characterizing osseous morphology.²¹ In FAI cases, CT can distinguish acetabular version abnormalities from femoral torsion (Figures 7A-7C), entities with very different treatment approaches.²¹

Magnetic Resonance Imaging

MRI is becoming essential in the work-up for nonarthritic hip pain.^11,22 It is used for assessment of osseous, chondral, and musculotendinous soft tissues. Further, it affords appreciation of outside-the-hip-joint pathology that may mimic joint-centered pathology.

MRI techniques range from noncontrast to indirect and direct magnetic resonance arthrography (MRA).²² Indirect MRA is performed with contrast medium administered through an intravenous line. Direct MRA has contrast administered intra-articularly and is more sensitive and specific for labral tears and ligamentous injury.²³ Excellent detection of intra-articular pathology on noncontrast studies questions the need for MRA.²⁴ Nevertheless, direct MRA can also be used as a therapeutic procedure when lidocaine is included in the injected gadolinium.

Labral tears, focal chondral defects, and stress or insufficiency fractures are important differentials in the work-up for nonarthritic hip pain. Over the dysplasia-to-FAI spectrum, MRI distinguishes symptomatic pathoanatomy from asymptomatic anatomical variants by revealing underlying bone edema. Capsule findings should also be considered.²¹The most practical classification of labral tears, proposed by Blankenbaker and colleagues,²⁵ is based on tear type (frayed, unstable, flap), location, and extent. More than half of labral tears occur in the anterosuperior quadrant of the labrum.²⁵

26

MRI detects osseous pathology from surrounding soft-tissue edema and bone remodeling to stress and fragility fractures. In athletes, the most common fractures are pubic rami, sacral, and apophyseal avulsion fractures.²⁸ In all patients, attention should be given to the lower spine and the proximal femurs. Aside from MRI, nuclear medicine bone scan might also identify active osseous reaction representative of a fracture.

Conclusion

The work-up for nonarthritic hip pain substantiates differential diagnoses. A case’s complexity determines the course of diagnostic imaging. At presentation and at each step in the work-up, it is imperative to evaluate the entire clinical picture. The prudent clinician uses both clinical and radiographic findings to make the diagnosis and direct treatment.

Am J Orthop . 2017;46(1):17-22. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

• Repair the labrum when tissue quality is good.
• Avoid overcorrection of acetabulum by measuring center edge angle.
• Cam resection should be comprehensive and restore a smooth head-neck offset to restore the suction seal.
• Chondral débridement for Outerbridge grade 0-3 and microfracture for grade 4.
• Routine capsular closure to prevent postoperative instability.

The surgical approach of femoroacetabular impingement (FAI) pathology should cover the entire hip joint. Both bony and cartilaginous tissue pathology should be adequately addressed. However, treating soft-tissue abnormalities (acetabular labrum and joint capsule) is also crucial. Overall, any surgical intervention should focus on restoring the hip labrum seal mechanism to ensure successful clinical outcomes. This restoration, combined with the use of biological therapies and rehabilitation, will produce the maximum benefit for the patient.

Management of Acetabular Labrum

The final decision regarding how to surgically approach the acetabular labrum is made during the operation. We focus restoring the labrum seal mechanism, which is crucial for proper function and health of the hip joint.¹ The intra-articular hydrostatic pressure loss caused by labral deficiency results in abnormal load distribution and joint microinstability, which have detrimental effects on cartilage and periarticular tissues. A biomechanical study highlighted the role of the hip labrum in maintaining intra-articular fluid pressurization and showed that labral reconstruction restores intra-articular fluid pressure to levels similar to those of the intact state.¹

In cases in which the remaining labral tissue is adequate and of good quality (reparable), the labral repair technique is preferred.² After diagnostic arthroscopy, the labral tear is identified, and a 4.5-mm burr is used to correct (rim-trim) any osseous deformity of the acetabulum to create a “new rim” for labrum reattachment. Suture anchors are placed on the rim about 2 mm to 3 mm below the cartilage surface. Considering the rim angle³ is helpful in avoiding acetabular cartilage damage. Labral sutures can be looped around or pierced through the labrum to secure it to the acetabulum. No difference in clinical outcomes was found between the 2 suture types,⁴ though biomechanically piercing sutures help restore the labrum seal better.¹ When the labrum is deficient and longitudinal fibers remain but are insufficient for seal restoration, the repair can be augmented with adjacent iliotibial band (ITB) tissue. This technique is similar to labral reconstruction but involves placing a graft on top of the remaining labral tissue, and suture around both the native tissue and the graft. The additional tissue gives the labrum the volume it needs to recreate the seal.

The labral reconstruction technique is indicated when the remaining labrum is irreparable, absent, or severely hypotrophic or deficient, or when an irreparable complex tear or poor-quality tissue is present. Different types of grafts can be used to reconstruct the labrum. ITB, semitendinosus, gracilis, and anterior tibialis grafts and the human acetabular labrum exhibit similar cyclic elongation behavior in response to simulated physiologic forces, though there is variability in both elongation and geometry for all graft types.⁵ We prefer the ITB autograft technique.⁶ The graft should be about 30% to 40% longer than the labral defect as measured with arthroscopic probe. With the leg in traction, the graft is inserted through the mid-anterior portal, and a suture anchor is used to secure it against the acetabulum medially.

Osseous Deformity

On approaching the bony structures of the hip joint, the surgeon should examine the acetabular rim (pincer lesion), the femoral head and neck shape (cam lesion), and the anterior inferior iliac spine (AIIS). Preoperative imaging and physical examination are important for identifying severe bone deformities that can complicate the procedure.⁹

The acetabular rim can be directly viewed after labrum detachment, but usually complete detachment is not necessary. Pincer deformity causes focal or global overcoverage of the femoral head. Rim trimming is performed with a 4.5-mm round curved burr. Resection is usually performed to the end of rim chondrosis (about 3-5 mm). Using a simple formula, you can calculate how the lateral center edge will be reduced by the amount of rim resected, maintaining a safe margin.² A new acetabular “bed” is created where the to-be-attached labral tissue will contribute to the suction seal mechanism of the joint.²Cam lesion correction is challenging, and the amount of bone that should be resected is a matter of disagreement. We perform cam osteochondroplasty² with a 5.5-mm round burr inserted through the anterolateral portal while the hip is positioned in 45° of flexion, neutral rotation, and adduction/abduction. This position allows an osteoplasty from 6 to 10 o’clock on the head–neck junction. Osteoplasty performed between 10 and 12 o’clock requires hip extension and slight traction. The proximal limit of osteochondroplasty is about 15 mm from the labral edge, while distally the resection stops beneath the zona orbicularis. The lateral epiphyseal vessels and the Weitbrecht ligament constitute the lateral and medial borders, respectively.

The surgeon should create a smooth head–neck offset that prevents elevation of the labrum during flexion and achieves a nearly perfect anatomical relationship between the femoral head and the acetabular labrum, restoring the hip joint seal (Figure 2).

Treatment of Cartilage Lesions

The indications and contraindications for hip arthroscopy in patients with cartilage lesions are important. Our study’s 5-year outcomes of treating FAI with hip arthroscopy in patients with preserved joint space (>2 mm) were promising, though 86% of patients with limited joint space (≤2 mm) converted to total hip arthroplasty.⁸ We regard patients with severe osteoarthritis as not being candidates for hip arthroscopy.

As 3 Tesla magnetic resonance imaging has low positive predictive value in identifying severe cartilage damage,¹³ the cartilage should be examined during surgery to further define the diagnosis. Nearly half of the hip arthroscopy patients in our study had at least 1 Outerbridge grade 3 or 4 cartilage lesion.¹⁴ Compared with the femoral head, acetabular cartilage was damaged 3 times more often. More than 90% of acetabular cartilage lesions were in the anterosuperior region.

Grades 0 and 1 cartilage lesions are usually left untreated; no intervention is necessary. Grades 2 and 3 cartilage lesions are reduced by partial débridement and/or thermal shrinkage. With the improved joint microenvironment arising from simple correction of the underlying hip bony abnormalities, these lesions should not produce further symptoms.

Grade 4 hip cartilage defects are challenging. We prefer microfracture for grade 4 lesions (Figure 4).

Capsule Management

The increase in hip arthroscopies performed worldwide has generated interest in proper capsular management and development of iatrogenic microinstability.¹⁷ Hip capsulotomy is routinely performed for adequate visualization of the intra-articular compartment. Standard anterosuperior interportal capsulotomy for hip arthroscopic surgery (12 to 3 o’clock) sacrifices the integrity of the iliofemoral ligament (ligament of Bigelow),¹⁸ which provides rotational stability. Failure to restore the anatomical and biomechanical properties of the iliofemoral ligament after arthroscopic surgery increases the likelihood of postoperative microinstability or gross instability,¹⁹ which can lead to persistent pain and/or sense of an unstable joint, in addition to accelerated cartilage wear.

Capsulotomies are useful in obtaining adequate intraoperative exposure of the central and peripheral compartments. In the past, little attention was given to capsular closure on completion of the procedure. However, concern about postoperative instability from capsular laxity or deficiency made the introduction of capsular repair techniques necessary. Although deciding between capsular closure and plication remains debatable, we routinely perform capsular closure with a Quebec City slider knot.²⁰ Mindful management of the capsule throughout the procedure is important in avoiding irreversible capsular damage, which would complicate capsular closure. Mindful management involves leaving a proximal leaflet of at least 1 cm during the capsulotomy, avoiding capsular thinning during shaver use, and using a cannula to prevent soft-tissue bridging.

Recent evidence suggests that capsule repair restores near native hip joint stability.¹⁷ In addition to capsular shift or capsulorrhaphy, 2 to 6 sutures have been used for capsular closure or plication after an interportal or T capsulotomy. Chahla and colleagues²¹ reported that 2- and 3-suture constructs produced comparable biomechanical failure torques when external rotation forces were applied to conventional hip capsulotomy on cadavers. Three-suture constructs were significantly stronger than 1-suture constructs, but there was no significant difference between 2- and 3-suture constructs. All constructs failed at about 36° of external rotation. Therefore, restricted external rotation is recommended for 3 weeks after surgery.

In one study, 35% of revision hip arthroscopy patients had undiagnosed hip instability from iatrogenic injury,²² which can lead to labral and chondral injury.¹⁷ Capsular reconstruction is recommended in cases of symptomatic capsular deficiency; capsular deficiency caused by adhesion removal; and pain and range-of-motion limitation caused by capsular adhesions. However, indications need to be further established. We have performed capsular reconstruction with ITB allograft²³ (Figure 5).

Biologics

At the end of the procedure, we use platelet-rich plasma and/or bone marrow aspirate injections (individualized to the patient) to potentiate the biological healing of the tissues. Further research is planned to determine how to prepare these biological products to provide the best mix of biological factors for improved healing. Antifibrotic factors are useful in preventing adhesions, and angiotensin II receptor blockers are effective, but clinical studies are needed to establish their use.

Rehabilitation

Immediately after surgery, a postoperative hip brace and antirotational boots are applied to the patient to protect the operative site and reduce pain. The actual postoperative protocol is based on the procedure and individualized to the patient. During microfractures, the patient is kept 20 pounds touch-toe weight-bearing for 4 to 8 weeks. The capsular closure is brace-protected by limiting abduction to 0° to 45° and hip flexion to 0° to 90° while external rotation and extension are prohibited (first 3 weeks). Immediate mobilization with passive rotational movement is crucial in preventing adhesions. Stationary bike exercise and use of a continuous passive motion machine are helpful. Progressive functional and sport-specific rehabilitation help the patient return to full activity, though the decision to return to full activity is based on several factors, both objective (functional tests) and subjective (physician–patient co-decisions).

Conclusion

Although hip arthroscopic techniques have expanded significantly in recent years, our treatment approach is based on restoring the normal anatomy of the hip joint—combining the procedures with biological therapies and a postoperative rehabilitation program that is individualized to the patient’s special needs.

Am J Orthop. 2017;46(1):23-27. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

• Repair the labrum when tissue quality is good.
• Avoid overcorrection of acetabulum by measuring center edge angle.
• Cam resection should be comprehensive and restore a smooth head-neck offset to restore the suction seal.
• Chondral débridement for Outerbridge grade 0-3 and microfracture for grade 4.
• Routine capsular closure to prevent postoperative instability.

The surgical approach of femoroacetabular impingement (FAI) pathology should cover the entire hip joint. Both bony and cartilaginous tissue pathology should be adequately addressed. However, treating soft-tissue abnormalities (acetabular labrum and joint capsule) is also crucial. Overall, any surgical intervention should focus on restoring the hip labrum seal mechanism to ensure successful clinical outcomes. This restoration, combined with the use of biological therapies and rehabilitation, will produce the maximum benefit for the patient.

Management of Acetabular Labrum

The final decision regarding how to surgically approach the acetabular labrum is made during the operation. We focus restoring the labrum seal mechanism, which is crucial for proper function and health of the hip joint.¹ The intra-articular hydrostatic pressure loss caused by labral deficiency results in abnormal load distribution and joint microinstability, which have detrimental effects on cartilage and periarticular tissues. A biomechanical study highlighted the role of the hip labrum in maintaining intra-articular fluid pressurization and showed that labral reconstruction restores intra-articular fluid pressure to levels similar to those of the intact state.¹

In cases in which the remaining labral tissue is adequate and of good quality (reparable), the labral repair technique is preferred.² After diagnostic arthroscopy, the labral tear is identified, and a 4.5-mm burr is used to correct (rim-trim) any osseous deformity of the acetabulum to create a “new rim” for labrum reattachment. Suture anchors are placed on the rim about 2 mm to 3 mm below the cartilage surface. Considering the rim angle³ is helpful in avoiding acetabular cartilage damage. Labral sutures can be looped around or pierced through the labrum to secure it to the acetabulum. No difference in clinical outcomes was found between the 2 suture types,⁴ though biomechanically piercing sutures help restore the labrum seal better.¹ When the labrum is deficient and longitudinal fibers remain but are insufficient for seal restoration, the repair can be augmented with adjacent iliotibial band (ITB) tissue. This technique is similar to labral reconstruction but involves placing a graft on top of the remaining labral tissue, and suture around both the native tissue and the graft. The additional tissue gives the labrum the volume it needs to recreate the seal.

The labral reconstruction technique is indicated when the remaining labrum is irreparable, absent, or severely hypotrophic or deficient, or when an irreparable complex tear or poor-quality tissue is present. Different types of grafts can be used to reconstruct the labrum. ITB, semitendinosus, gracilis, and anterior tibialis grafts and the human acetabular labrum exhibit similar cyclic elongation behavior in response to simulated physiologic forces, though there is variability in both elongation and geometry for all graft types.⁵ We prefer the ITB autograft technique.⁶ The graft should be about 30% to 40% longer than the labral defect as measured with arthroscopic probe. With the leg in traction, the graft is inserted through the mid-anterior portal, and a suture anchor is used to secure it against the acetabulum medially.

Osseous Deformity

On approaching the bony structures of the hip joint, the surgeon should examine the acetabular rim (pincer lesion), the femoral head and neck shape (cam lesion), and the anterior inferior iliac spine (AIIS). Preoperative imaging and physical examination are important for identifying severe bone deformities that can complicate the procedure.⁹

The acetabular rim can be directly viewed after labrum detachment, but usually complete detachment is not necessary. Pincer deformity causes focal or global overcoverage of the femoral head. Rim trimming is performed with a 4.5-mm round curved burr. Resection is usually performed to the end of rim chondrosis (about 3-5 mm). Using a simple formula, you can calculate how the lateral center edge will be reduced by the amount of rim resected, maintaining a safe margin.² A new acetabular “bed” is created where the to-be-attached labral tissue will contribute to the suction seal mechanism of the joint.²Cam lesion correction is challenging, and the amount of bone that should be resected is a matter of disagreement. We perform cam osteochondroplasty² with a 5.5-mm round burr inserted through the anterolateral portal while the hip is positioned in 45° of flexion, neutral rotation, and adduction/abduction. This position allows an osteoplasty from 6 to 10 o’clock on the head–neck junction. Osteoplasty performed between 10 and 12 o’clock requires hip extension and slight traction. The proximal limit of osteochondroplasty is about 15 mm from the labral edge, while distally the resection stops beneath the zona orbicularis. The lateral epiphyseal vessels and the Weitbrecht ligament constitute the lateral and medial borders, respectively.

The surgeon should create a smooth head–neck offset that prevents elevation of the labrum during flexion and achieves a nearly perfect anatomical relationship between the femoral head and the acetabular labrum, restoring the hip joint seal (Figure 2).

Treatment of Cartilage Lesions

The indications and contraindications for hip arthroscopy in patients with cartilage lesions are important. Our study’s 5-year outcomes of treating FAI with hip arthroscopy in patients with preserved joint space (>2 mm) were promising, though 86% of patients with limited joint space (≤2 mm) converted to total hip arthroplasty.⁸ We regard patients with severe osteoarthritis as not being candidates for hip arthroscopy.

As 3 Tesla magnetic resonance imaging has low positive predictive value in identifying severe cartilage damage,¹³ the cartilage should be examined during surgery to further define the diagnosis. Nearly half of the hip arthroscopy patients in our study had at least 1 Outerbridge grade 3 or 4 cartilage lesion.¹⁴ Compared with the femoral head, acetabular cartilage was damaged 3 times more often. More than 90% of acetabular cartilage lesions were in the anterosuperior region.

Grades 0 and 1 cartilage lesions are usually left untreated; no intervention is necessary. Grades 2 and 3 cartilage lesions are reduced by partial débridement and/or thermal shrinkage. With the improved joint microenvironment arising from simple correction of the underlying hip bony abnormalities, these lesions should not produce further symptoms.

Grade 4 hip cartilage defects are challenging. We prefer microfracture for grade 4 lesions (Figure 4).

Capsule Management

The increase in hip arthroscopies performed worldwide has generated interest in proper capsular management and development of iatrogenic microinstability.¹⁷ Hip capsulotomy is routinely performed for adequate visualization of the intra-articular compartment. Standard anterosuperior interportal capsulotomy for hip arthroscopic surgery (12 to 3 o’clock) sacrifices the integrity of the iliofemoral ligament (ligament of Bigelow),¹⁸ which provides rotational stability. Failure to restore the anatomical and biomechanical properties of the iliofemoral ligament after arthroscopic surgery increases the likelihood of postoperative microinstability or gross instability,¹⁹ which can lead to persistent pain and/or sense of an unstable joint, in addition to accelerated cartilage wear.

Capsulotomies are useful in obtaining adequate intraoperative exposure of the central and peripheral compartments. In the past, little attention was given to capsular closure on completion of the procedure. However, concern about postoperative instability from capsular laxity or deficiency made the introduction of capsular repair techniques necessary. Although deciding between capsular closure and plication remains debatable, we routinely perform capsular closure with a Quebec City slider knot.²⁰ Mindful management of the capsule throughout the procedure is important in avoiding irreversible capsular damage, which would complicate capsular closure. Mindful management involves leaving a proximal leaflet of at least 1 cm during the capsulotomy, avoiding capsular thinning during shaver use, and using a cannula to prevent soft-tissue bridging.

Recent evidence suggests that capsule repair restores near native hip joint stability.¹⁷ In addition to capsular shift or capsulorrhaphy, 2 to 6 sutures have been used for capsular closure or plication after an interportal or T capsulotomy. Chahla and colleagues²¹ reported that 2- and 3-suture constructs produced comparable biomechanical failure torques when external rotation forces were applied to conventional hip capsulotomy on cadavers. Three-suture constructs were significantly stronger than 1-suture constructs, but there was no significant difference between 2- and 3-suture constructs. All constructs failed at about 36° of external rotation. Therefore, restricted external rotation is recommended for 3 weeks after surgery.

In one study, 35% of revision hip arthroscopy patients had undiagnosed hip instability from iatrogenic injury,²² which can lead to labral and chondral injury.¹⁷ Capsular reconstruction is recommended in cases of symptomatic capsular deficiency; capsular deficiency caused by adhesion removal; and pain and range-of-motion limitation caused by capsular adhesions. However, indications need to be further established. We have performed capsular reconstruction with ITB allograft²³ (Figure 5).

Biologics

At the end of the procedure, we use platelet-rich plasma and/or bone marrow aspirate injections (individualized to the patient) to potentiate the biological healing of the tissues. Further research is planned to determine how to prepare these biological products to provide the best mix of biological factors for improved healing. Antifibrotic factors are useful in preventing adhesions, and angiotensin II receptor blockers are effective, but clinical studies are needed to establish their use.

Rehabilitation

Immediately after surgery, a postoperative hip brace and antirotational boots are applied to the patient to protect the operative site and reduce pain. The actual postoperative protocol is based on the procedure and individualized to the patient. During microfractures, the patient is kept 20 pounds touch-toe weight-bearing for 4 to 8 weeks. The capsular closure is brace-protected by limiting abduction to 0° to 45° and hip flexion to 0° to 90° while external rotation and extension are prohibited (first 3 weeks). Immediate mobilization with passive rotational movement is crucial in preventing adhesions. Stationary bike exercise and use of a continuous passive motion machine are helpful. Progressive functional and sport-specific rehabilitation help the patient return to full activity, though the decision to return to full activity is based on several factors, both objective (functional tests) and subjective (physician–patient co-decisions).

Conclusion

Although hip arthroscopic techniques have expanded significantly in recent years, our treatment approach is based on restoring the normal anatomy of the hip joint—combining the procedures with biological therapies and a postoperative rehabilitation program that is individualized to the patient’s special needs.

Am J Orthop. 2017;46(1):23-27. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

• Repair the labrum when tissue quality is good.
• Avoid overcorrection of acetabulum by measuring center edge angle.
• Cam resection should be comprehensive and restore a smooth head-neck offset to restore the suction seal.
• Chondral débridement for Outerbridge grade 0-3 and microfracture for grade 4.
• Routine capsular closure to prevent postoperative instability.

The surgical approach of femoroacetabular impingement (FAI) pathology should cover the entire hip joint. Both bony and cartilaginous tissue pathology should be adequately addressed. However, treating soft-tissue abnormalities (acetabular labrum and joint capsule) is also crucial. Overall, any surgical intervention should focus on restoring the hip labrum seal mechanism to ensure successful clinical outcomes. This restoration, combined with the use of biological therapies and rehabilitation, will produce the maximum benefit for the patient.

Management of Acetabular Labrum

The final decision regarding how to surgically approach the acetabular labrum is made during the operation. We focus restoring the labrum seal mechanism, which is crucial for proper function and health of the hip joint.¹ The intra-articular hydrostatic pressure loss caused by labral deficiency results in abnormal load distribution and joint microinstability, which have detrimental effects on cartilage and periarticular tissues. A biomechanical study highlighted the role of the hip labrum in maintaining intra-articular fluid pressurization and showed that labral reconstruction restores intra-articular fluid pressure to levels similar to those of the intact state.¹

In cases in which the remaining labral tissue is adequate and of good quality (reparable), the labral repair technique is preferred.² After diagnostic arthroscopy, the labral tear is identified, and a 4.5-mm burr is used to correct (rim-trim) any osseous deformity of the acetabulum to create a “new rim” for labrum reattachment. Suture anchors are placed on the rim about 2 mm to 3 mm below the cartilage surface. Considering the rim angle³ is helpful in avoiding acetabular cartilage damage. Labral sutures can be looped around or pierced through the labrum to secure it to the acetabulum. No difference in clinical outcomes was found between the 2 suture types,⁴ though biomechanically piercing sutures help restore the labrum seal better.¹ When the labrum is deficient and longitudinal fibers remain but are insufficient for seal restoration, the repair can be augmented with adjacent iliotibial band (ITB) tissue. This technique is similar to labral reconstruction but involves placing a graft on top of the remaining labral tissue, and suture around both the native tissue and the graft. The additional tissue gives the labrum the volume it needs to recreate the seal.

The labral reconstruction technique is indicated when the remaining labrum is irreparable, absent, or severely hypotrophic or deficient, or when an irreparable complex tear or poor-quality tissue is present. Different types of grafts can be used to reconstruct the labrum. ITB, semitendinosus, gracilis, and anterior tibialis grafts and the human acetabular labrum exhibit similar cyclic elongation behavior in response to simulated physiologic forces, though there is variability in both elongation and geometry for all graft types.⁵ We prefer the ITB autograft technique.⁶ The graft should be about 30% to 40% longer than the labral defect as measured with arthroscopic probe. With the leg in traction, the graft is inserted through the mid-anterior portal, and a suture anchor is used to secure it against the acetabulum medially.

Osseous Deformity

On approaching the bony structures of the hip joint, the surgeon should examine the acetabular rim (pincer lesion), the femoral head and neck shape (cam lesion), and the anterior inferior iliac spine (AIIS). Preoperative imaging and physical examination are important for identifying severe bone deformities that can complicate the procedure.⁹

The acetabular rim can be directly viewed after labrum detachment, but usually complete detachment is not necessary. Pincer deformity causes focal or global overcoverage of the femoral head. Rim trimming is performed with a 4.5-mm round curved burr. Resection is usually performed to the end of rim chondrosis (about 3-5 mm). Using a simple formula, you can calculate how the lateral center edge will be reduced by the amount of rim resected, maintaining a safe margin.² A new acetabular “bed” is created where the to-be-attached labral tissue will contribute to the suction seal mechanism of the joint.²Cam lesion correction is challenging, and the amount of bone that should be resected is a matter of disagreement. We perform cam osteochondroplasty² with a 5.5-mm round burr inserted through the anterolateral portal while the hip is positioned in 45° of flexion, neutral rotation, and adduction/abduction. This position allows an osteoplasty from 6 to 10 o’clock on the head–neck junction. Osteoplasty performed between 10 and 12 o’clock requires hip extension and slight traction. The proximal limit of osteochondroplasty is about 15 mm from the labral edge, while distally the resection stops beneath the zona orbicularis. The lateral epiphyseal vessels and the Weitbrecht ligament constitute the lateral and medial borders, respectively.

The surgeon should create a smooth head–neck offset that prevents elevation of the labrum during flexion and achieves a nearly perfect anatomical relationship between the femoral head and the acetabular labrum, restoring the hip joint seal (Figure 2).

Treatment of Cartilage Lesions

The indications and contraindications for hip arthroscopy in patients with cartilage lesions are important. Our study’s 5-year outcomes of treating FAI with hip arthroscopy in patients with preserved joint space (>2 mm) were promising, though 86% of patients with limited joint space (≤2 mm) converted to total hip arthroplasty.⁸ We regard patients with severe osteoarthritis as not being candidates for hip arthroscopy.

As 3 Tesla magnetic resonance imaging has low positive predictive value in identifying severe cartilage damage,¹³ the cartilage should be examined during surgery to further define the diagnosis. Nearly half of the hip arthroscopy patients in our study had at least 1 Outerbridge grade 3 or 4 cartilage lesion.¹⁴ Compared with the femoral head, acetabular cartilage was damaged 3 times more often. More than 90% of acetabular cartilage lesions were in the anterosuperior region.

Grades 0 and 1 cartilage lesions are usually left untreated; no intervention is necessary. Grades 2 and 3 cartilage lesions are reduced by partial débridement and/or thermal shrinkage. With the improved joint microenvironment arising from simple correction of the underlying hip bony abnormalities, these lesions should not produce further symptoms.

Grade 4 hip cartilage defects are challenging. We prefer microfracture for grade 4 lesions (Figure 4).

Capsule Management

The increase in hip arthroscopies performed worldwide has generated interest in proper capsular management and development of iatrogenic microinstability.¹⁷ Hip capsulotomy is routinely performed for adequate visualization of the intra-articular compartment. Standard anterosuperior interportal capsulotomy for hip arthroscopic surgery (12 to 3 o’clock) sacrifices the integrity of the iliofemoral ligament (ligament of Bigelow),¹⁸ which provides rotational stability. Failure to restore the anatomical and biomechanical properties of the iliofemoral ligament after arthroscopic surgery increases the likelihood of postoperative microinstability or gross instability,¹⁹ which can lead to persistent pain and/or sense of an unstable joint, in addition to accelerated cartilage wear.

Capsulotomies are useful in obtaining adequate intraoperative exposure of the central and peripheral compartments. In the past, little attention was given to capsular closure on completion of the procedure. However, concern about postoperative instability from capsular laxity or deficiency made the introduction of capsular repair techniques necessary. Although deciding between capsular closure and plication remains debatable, we routinely perform capsular closure with a Quebec City slider knot.²⁰ Mindful management of the capsule throughout the procedure is important in avoiding irreversible capsular damage, which would complicate capsular closure. Mindful management involves leaving a proximal leaflet of at least 1 cm during the capsulotomy, avoiding capsular thinning during shaver use, and using a cannula to prevent soft-tissue bridging.

Recent evidence suggests that capsule repair restores near native hip joint stability.¹⁷ In addition to capsular shift or capsulorrhaphy, 2 to 6 sutures have been used for capsular closure or plication after an interportal or T capsulotomy. Chahla and colleagues²¹ reported that 2- and 3-suture constructs produced comparable biomechanical failure torques when external rotation forces were applied to conventional hip capsulotomy on cadavers. Three-suture constructs were significantly stronger than 1-suture constructs, but there was no significant difference between 2- and 3-suture constructs. All constructs failed at about 36° of external rotation. Therefore, restricted external rotation is recommended for 3 weeks after surgery.

In one study, 35% of revision hip arthroscopy patients had undiagnosed hip instability from iatrogenic injury,²² which can lead to labral and chondral injury.¹⁷ Capsular reconstruction is recommended in cases of symptomatic capsular deficiency; capsular deficiency caused by adhesion removal; and pain and range-of-motion limitation caused by capsular adhesions. However, indications need to be further established. We have performed capsular reconstruction with ITB allograft²³ (Figure 5).

Biologics

At the end of the procedure, we use platelet-rich plasma and/or bone marrow aspirate injections (individualized to the patient) to potentiate the biological healing of the tissues. Further research is planned to determine how to prepare these biological products to provide the best mix of biological factors for improved healing. Antifibrotic factors are useful in preventing adhesions, and angiotensin II receptor blockers are effective, but clinical studies are needed to establish their use.

Rehabilitation

Immediately after surgery, a postoperative hip brace and antirotational boots are applied to the patient to protect the operative site and reduce pain. The actual postoperative protocol is based on the procedure and individualized to the patient. During microfractures, the patient is kept 20 pounds touch-toe weight-bearing for 4 to 8 weeks. The capsular closure is brace-protected by limiting abduction to 0° to 45° and hip flexion to 0° to 90° while external rotation and extension are prohibited (first 3 weeks). Immediate mobilization with passive rotational movement is crucial in preventing adhesions. Stationary bike exercise and use of a continuous passive motion machine are helpful. Progressive functional and sport-specific rehabilitation help the patient return to full activity, though the decision to return to full activity is based on several factors, both objective (functional tests) and subjective (physician–patient co-decisions).

Conclusion

Although hip arthroscopic techniques have expanded significantly in recent years, our treatment approach is based on restoring the normal anatomy of the hip joint—combining the procedures with biological therapies and a postoperative rehabilitation program that is individualized to the patient’s special needs.

Am J Orthop. 2017;46(1):23-27. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

• Our understanding of FAI has evolved from cam-type and pincer-type impingement to much more complex disease patterns.
• Most surgeons are performing less aggressive acetabular rim trimming.
• Inadequate osseous correction is still the most common cause of the failed hip arthroscopy.
• Labral preservation is important to maintaining suction seal effect.
• Open surgical techniques have a role for more severe and complex FAI deformities.

Femoroacetabular impingement (FAI) was described by Ganz and colleagues¹ in 2003 as a refinement of concepts introduced decades earlier. This description advanced our understanding of FAI as a mechanism for prearthritic hip pain and secondary hip osteoarthritis¹ (OA) and allowed for treatment of FAI. The concept of proximal femoral and acetabular/pelvic deformity contributing to OA had been previously speculated by Smith-Petersen,² Murray,³ Solomon,⁴ and Stulberg.⁵ Early cases of overcorrection of dysplasia using the periacetabular osteotomy created iatrogenic FAI, which further stimulated early development of the FAI concept.⁶ Improved anatomical characterization of the proximal femoral blood supply (medial femoral circumflex artery) allowed for development of the open surgical hip dislocation.⁷ Through open surgical hip dislocation, an improved understanding of hip pathomechanics by direct visualization helped pave the way for a better understanding of FAI. Open surgical hip dislocation allows for global treatment of labrochondral pathology and deformity of the proximal femoral head–neck junction and/or acetabular rim in FAI.

Hip arthroscopy has further developed and improved our understanding of FAI. Early hip arthroscopy was generally limited to débridement of labral and chondral pathology, and management of the soft-tissue structures. Advances in the understanding of FAI through open techniques allowed for application of similar techniques to hip arthroscopy. Improvements in arthroscopic instrumentation and techniques have allowed for treatment of labrochondral and acetabular-sided rim deformity in the central compartment and cam morphologies in the peripheral compartment through arthroscopic surgery. Appropriate bony correction by arthroscopic techniques has always been a concern, but improved techniques, dynamic assessment, and accurate use of intraoperative imaging have made this feasible and more predictable. Treatment of cam deformities extending adjacent and proximal to the retinacular vessels is possible but more technically demanding. Inadequate bony correction of FAI by arthroscopic means remains one of the most common causes of failure.^8-10In 2013, the Academic Network of Conservational Hip Outcome Research (ANCHOR) Study Group reported the characteristics of a FAI cohort of 1130 hips (1076 patients) that underwent surgical treatment of FAI across 8 institutions and 12 surgeons.¹¹ At that time, most ANCHOR surgeons (or surgeon groups) performed both open and arthroscopic surgeries and had significant referral volumes of complex cases that may have overrepresented the proportion of complex FAI cases in the cohort. During the 2008 to 2011 study period, FAI was treated with arthroscopy in 56% of these cases, open surgical hip dislocation in 34%, and reverse periacetabular osteotomy in 9%. FAI was characterized as isolated cam-type in 48%, combined cam–pincer type in 45%, and isolated pincer-type in 8%. Fifty-five percent of the patients were female. Patient-reported outcome studies in this cohort of patients are ongoing.

The FAI Concept

In 2003, after treating more than 600 open surgical hip dislocations over the previous decade, Ganz and colleagues¹ coined the term femoroacetabular impingement to describe a “mechanism for the development of early osteoarthritis for most nondysplastic hips.” They reported surgical treatment focused on “improving the clearance for hip motion and alleviation of femoral abutment against the acetabular rim” with the goal of improving pain and possibly of halting progression of the degenerative process. FAI was defined as “abnormal contact between the proximal femur and acetabular rim that occurs during terminal motion of the hip” leading to “lesions of the acetabular labrum and/or the adjacent acetabular cartilage.” Subtle, previously overlooked deformities of the proximal femur and acetabulum were recognized as the cause of FAI, “including the presence of a bony prominence usually in the anterolateral head and neck junction that is seen best on the lateral radiographs, reduced offset of the femoral neck and head junction, and changes on the acetabular rim such as os acetabuli or a double line that is seen with rim ossification.” Ganz and colleagues¹ recognized that “normal or near normal” hips could also experience FAI in the setting of excessive or supraphysiologic range of motion. Cam-type and pincer-type FAI deformities were introduced as 2 distinct mechanisms of FAI. By 2003, arthroscopic hip surgery was increasingly being used as a treatment for labral tears but not bony abnormalities. These FAI concepts seemed to explain the prevalence of labral tears at the anterosuperior rim, which had been noted during hip arthroscopy, and paved the way for major changes in arthroscopic hip surgery during the next decade. The ANCHOR group reported the descriptive epidemiology of a cohort of more than 1000 patients with FAI.¹¹

Cam-Type FAI

Cam-type impingement results from femoral-sided deformities. The mechanism was described as inclusion-type impingement in which “jamming of an abnormal femoral head with increasing radius into the acetabulum during forceful motion, especially flexion.”¹ This results in outside-in abrasion of the acetabular cartilage of the anterosuperior rim with detachment of the “principally uninvolved labrum”¹ and potentially delamination of the adjacent cartilage from the subchondral bone. Ganz and colleagues¹ recognized in their initial descriptions of FAI that cam-type FAI could involve decreased femoral version, femoral head–neck junction asphericity, and decreased head–neck offset. The complexity and variability in the topography and geography of the cam morphology have been increasingly recognized. Accurate understanding and characterization of the proximal femoral deformity are important in guiding surgical correction of the cam deformity.

Advances in understanding the prevalence of the cam morphology and the association with OA have been important to our understanding of the pathophysiology of FAI. Several studies¹² have established that a cam morphology of the proximal femur (defined by a variety of different metrics) is common among asymptomatic individuals. In light of this fact, a description of the femoral anatomy as a “cam morphology” rather than a cam deformity is now favored. Similarly, FAI is better used to refer to symptomatic individuals and is not equivalent to a cam morphology. The cam morphology seems significantly more common among athletes. Siebenrock and colleagues¹³ demonstrated the correlation of high-level athletics during late stages of skeletal immaturity and development of a cam morphology. A recent systematic review of 9 studies found that elite male athletes in late skeletal immaturity were 2 to 8 times more likely to develop a cam morphology before skeletal maturity.¹⁴Several population-based studies^15,16 have quantified the apparent association of the cam morphology with hip OA. However, the studies were limited in their ability to adequately define the presence of cam morphology based on anteroposterior (AP) pelvis radiographs.

In a prospective study, Agricola and colleagues¹⁵ found the risk of OA was increased 2.4 times in the setting of moderate cam morphology (α angle, >60°) over a 5-year period. Thomas and colleagues¹⁶ found increased risk in a female cohort when the α angle was >65°.

Treatment of cam-type FAI is focused on adequate correction of the abnormal bone morphology. Inadequate or inappropriate bony correction of FAI is a common cause of treatment failure and is more common with arthroscopic techniques.^9,10,17 Inadequate bony resection may be the result of surgical inexperience, poor visualization, or lack of understanding of the underlying bony deformity. Modern osteoplasty techniques also focus on gradual bony contour correction that restores the normal concavity–convexity transition of the head–neck junction. Overresection of the cam deformity not only may increase the risk of femoral neck fracture but may result in early disruption of the hip fluid seal from loss of contact between the femoral head and the acetabular labrum earlier in the arc of motion. In addition, high range-of-motion impingement can be seen in various athletic populations (dance, gymnastics, martial arts, hockey goalies), and the regions of impingement tend to be farther away from classically described impingement. Impingement in these situations occurs at the distal femoral neck and subspine regions, adding a level of complexity and unpredictability from a surgical standpoint.

FAI can also occur in the setting of more complex deformities than the typical cam morphology. Complex cases of FAI caused by slipped capital femoral epiphysis (SCFE) and residual Legg-Calvé-Perthes disease are relatively common. Complex deformities may also result in extra-articular impingement of the proximal femur (greater/lesser trochanter, distal femoral neck) on the pelvis (ilium, ischium) in addition to typical FAI. Mild to moderate cases of residual SCFE may be adequately treated with osteoplasty by arthroscopic techniques. In the setting of more severe residual SCFE, presence of underlying femoral retroversion and retrotilt of the femoral epiphysis may prevent adequate deformity correction and motion improvement by arthroscopy. Surgical hip dislocation (with or without relative femoral neck lengthening) and/or proximal femoral flexion derotational osteotomy may be the best means of treatment in these more severe deformities but may be dependent on the chronicity of the deformity and associated compensatory changes occurring on the acetabular side. Similarly, in moderate to severe residual Legg-Calvé-Perthes disease, presence of coxa vara, high greater trochanter, short femoral neck, and ovoid femoral head may be better treated in open techniques to allow comprehensive deformity correction, including correction of acetabular dysplasia in some cases.

Pincer-Type FAI

Pincer-type FAI results from acetabular-sided deformities in which acetabular deformity leads to impaction-type impingement with “linear contact between the acetabular rim and the femoral head–neck junction.”¹ Pincer FAI causes primarily labral damage with progressive degeneration and, in some cases, ossification of the acetabular labrum that further worsens the acetabular overcoverage and premature rim impaction. Chondral damage in pincer-type FAI is generally less significant and limited to the peripheral acetabular rim.

Pincer-type FAI may be caused by acetabular retroversion, coxa profunda, or protrusio acetabuli. Our understanding of what defines a pincer morphology has evolved significantly. Through efforts to better define structural features of the acetabular rim that represent abnormalities, we have improved our understanding of how these features may influence OA development. One example of improved understanding involves coxa profunda, classically defined as the medial acetabular fossa touching or projecting medial to the ilioischial line on an AP pelvis radiograph. Several studies have found that this classic definition poorly describes the “overcovered” hip, as it is present in 70% of females and commonly present (41%) in the setting of acetabular dysplasia.^18,19 Acetabular retroversion was previously associated with hip OA. Although central acetabular retroversion is relatively uncommon, cranial acetabular retroversion is more common. Presence of a crossover sign on AP pelvis radiographs generally has been viewed as indicative of acetabular retroversion. However, alterations in pelvic tilt on supine or standing AP pelvis radiographs can result in apparent retroversion in the setting of normal acetabular anatomy²⁰ and potentially influence the development of impingement.²¹ Zaltz and colleagues²² found that abnormal morphology of the anterior inferior iliac spine can also lead to the presence of a crossover sign in an otherwise anteverted acetabulum. Larson and colleagues²³ recently found that a crossover sign is present in 11% of asymptomatic hips (19% of males) and may be considered a normal variant. A crossover sign can also be present in the setting of posterior acetabular deficiency with normal anterior acetabular coverage. Ultimately, acetabular retroversion might indicate pincer-type FAI or dysplasia or be a normal variant that does not require treatment. Global acetabular overcoverage, including coxa protrusio, may be associated with OA in population-based studies but is not uniformly demonstrated in all studies.^16,24,25 A lateral center edge angle of >40° and a Tönnis angle (acetabular inclination) of <0° are commonly viewed as markers of global overcoverage.

FAI Treatment

Improvements in hip arthroscopy techniques and instrumentation have led to hip arthroscopy becoming the primary surgical technique for the treatment of most cases of FAI. Hip arthroscopy allows for precise visualization and treatment of labral and chondral disease in the central compartment by traction. Larson and colleagues²⁶ reported complication rates for hip arthroscopy in a prospective series of >1600 cases. The overall complication rate was 8.3%, with higher rates noted in female patients and in the setting of traction time longer than 60 minutes. Nonetheless, major complications occurred in 1.1%, with only 0.1% having persistent disability. The most common complications were lateral femoral cutaneous nerve dysesthesias (1.6%), pudendal nerve neuropraxia (1.4%), and iatrogenic labral/chondral damage (2.1%).

The importance of preserving the acetabular labrum is now well accepted from clinical and biomechanical evidence.^27-29 As in previous studies in surgical hip dislocation,³⁰ arthroscopic labral repair (vs débridement) results in improved clinical outcomes.^31,32 Labral repair techniques currently focus on stable fixation of the labrum while maintaining the normal position of the labrum relative to the femoral head and avoiding labral eversion, which may compromise the hip suction seal. With continued technical advancements and biomechanical support, arthroscopic labral reconstruction is possible in the setting of labral deficiency, often resulting from prior resection. However, the optimal indications, surgical techniques, and long-term outcomes continue to be better defined. Open and arthroscopic techniques have shown similar ability to correct the typical mild to moderate cam morphology in FAI.³³ Yet, inadequate femoral bony correction of FAI seems to be the most common cause for revision hip preservation surgery.^9,10,17Mild to moderate acetabular rim deformities are commonly treated with hip arthroscopy. As our understanding of pincer-type FAI continues to improve, many surgeons are performing less- aggressive bone resection along the anterior rim. On the other hand, subspinous impingement was recently recognized as a form of extra-articular pincer FAI variant.³⁴ Subspine decompression without true acetabular rim resection has become a more common treatment for pincer lesions and may be a consideration even with restricted range of motion after periacetabular osteotomy. Severe acetabular deformities with global overcoverage or acetabular protrusion are particularly challenging by arthroscopy, even for the most experienced surgeons. Although some improvement in deformity is feasible with arthroscopy, even cases reported in the literature have demonstrated incomplete deformity correction. Open surgical hip dislocation may continue to be the ideal treatment technique for severe pincer impingement.

Cam-type FAI is commonly treated with hip arthroscopy (Figures A-F).

Conclusion

Our understanding and treatment of FAI continue to evolve. Both open and arthroscopic techniques have demonstrated excellent outcomes in the treatment of FAI. Most cases of FAI are now amenable to arthroscopic treatment. Inadequate resection and underlying acetabular dysplasia remain common causes of treatment failure. Open surgical hip dislocation continues to play a role in the treatment of severe deformities that are poorly accessible by arthroscopy—including cam lesions with posterior extension, severe global acetabular overcoverage, or extra-articular impingement. The association of FAI with OA is most apparent for cam-type FAI. Future research will define the optimal treatment strategies and determine if they modify disease progression.

Am J Orthop. 2017;46(1):28-34. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

• Our understanding of FAI has evolved from cam-type and pincer-type impingement to much more complex disease patterns.
• Most surgeons are performing less aggressive acetabular rim trimming.
• Inadequate osseous correction is still the most common cause of the failed hip arthroscopy.
• Labral preservation is important to maintaining suction seal effect.
• Open surgical techniques have a role for more severe and complex FAI deformities.

Femoroacetabular impingement (FAI) was described by Ganz and colleagues¹ in 2003 as a refinement of concepts introduced decades earlier. This description advanced our understanding of FAI as a mechanism for prearthritic hip pain and secondary hip osteoarthritis¹ (OA) and allowed for treatment of FAI. The concept of proximal femoral and acetabular/pelvic deformity contributing to OA had been previously speculated by Smith-Petersen,² Murray,³ Solomon,⁴ and Stulberg.⁵ Early cases of overcorrection of dysplasia using the periacetabular osteotomy created iatrogenic FAI, which further stimulated early development of the FAI concept.⁶ Improved anatomical characterization of the proximal femoral blood supply (medial femoral circumflex artery) allowed for development of the open surgical hip dislocation.⁷ Through open surgical hip dislocation, an improved understanding of hip pathomechanics by direct visualization helped pave the way for a better understanding of FAI. Open surgical hip dislocation allows for global treatment of labrochondral pathology and deformity of the proximal femoral head–neck junction and/or acetabular rim in FAI.

Hip arthroscopy has further developed and improved our understanding of FAI. Early hip arthroscopy was generally limited to débridement of labral and chondral pathology, and management of the soft-tissue structures. Advances in the understanding of FAI through open techniques allowed for application of similar techniques to hip arthroscopy. Improvements in arthroscopic instrumentation and techniques have allowed for treatment of labrochondral and acetabular-sided rim deformity in the central compartment and cam morphologies in the peripheral compartment through arthroscopic surgery. Appropriate bony correction by arthroscopic techniques has always been a concern, but improved techniques, dynamic assessment, and accurate use of intraoperative imaging have made this feasible and more predictable. Treatment of cam deformities extending adjacent and proximal to the retinacular vessels is possible but more technically demanding. Inadequate bony correction of FAI by arthroscopic means remains one of the most common causes of failure.^8-10In 2013, the Academic Network of Conservational Hip Outcome Research (ANCHOR) Study Group reported the characteristics of a FAI cohort of 1130 hips (1076 patients) that underwent surgical treatment of FAI across 8 institutions and 12 surgeons.¹¹ At that time, most ANCHOR surgeons (or surgeon groups) performed both open and arthroscopic surgeries and had significant referral volumes of complex cases that may have overrepresented the proportion of complex FAI cases in the cohort. During the 2008 to 2011 study period, FAI was treated with arthroscopy in 56% of these cases, open surgical hip dislocation in 34%, and reverse periacetabular osteotomy in 9%. FAI was characterized as isolated cam-type in 48%, combined cam–pincer type in 45%, and isolated pincer-type in 8%. Fifty-five percent of the patients were female. Patient-reported outcome studies in this cohort of patients are ongoing.

The FAI Concept

In 2003, after treating more than 600 open surgical hip dislocations over the previous decade, Ganz and colleagues¹ coined the term femoroacetabular impingement to describe a “mechanism for the development of early osteoarthritis for most nondysplastic hips.” They reported surgical treatment focused on “improving the clearance for hip motion and alleviation of femoral abutment against the acetabular rim” with the goal of improving pain and possibly of halting progression of the degenerative process. FAI was defined as “abnormal contact between the proximal femur and acetabular rim that occurs during terminal motion of the hip” leading to “lesions of the acetabular labrum and/or the adjacent acetabular cartilage.” Subtle, previously overlooked deformities of the proximal femur and acetabulum were recognized as the cause of FAI, “including the presence of a bony prominence usually in the anterolateral head and neck junction that is seen best on the lateral radiographs, reduced offset of the femoral neck and head junction, and changes on the acetabular rim such as os acetabuli or a double line that is seen with rim ossification.” Ganz and colleagues¹ recognized that “normal or near normal” hips could also experience FAI in the setting of excessive or supraphysiologic range of motion. Cam-type and pincer-type FAI deformities were introduced as 2 distinct mechanisms of FAI. By 2003, arthroscopic hip surgery was increasingly being used as a treatment for labral tears but not bony abnormalities. These FAI concepts seemed to explain the prevalence of labral tears at the anterosuperior rim, which had been noted during hip arthroscopy, and paved the way for major changes in arthroscopic hip surgery during the next decade. The ANCHOR group reported the descriptive epidemiology of a cohort of more than 1000 patients with FAI.¹¹

Cam-Type FAI

Cam-type impingement results from femoral-sided deformities. The mechanism was described as inclusion-type impingement in which “jamming of an abnormal femoral head with increasing radius into the acetabulum during forceful motion, especially flexion.”¹ This results in outside-in abrasion of the acetabular cartilage of the anterosuperior rim with detachment of the “principally uninvolved labrum”¹ and potentially delamination of the adjacent cartilage from the subchondral bone. Ganz and colleagues¹ recognized in their initial descriptions of FAI that cam-type FAI could involve decreased femoral version, femoral head–neck junction asphericity, and decreased head–neck offset. The complexity and variability in the topography and geography of the cam morphology have been increasingly recognized. Accurate understanding and characterization of the proximal femoral deformity are important in guiding surgical correction of the cam deformity.

Advances in understanding the prevalence of the cam morphology and the association with OA have been important to our understanding of the pathophysiology of FAI. Several studies¹² have established that a cam morphology of the proximal femur (defined by a variety of different metrics) is common among asymptomatic individuals. In light of this fact, a description of the femoral anatomy as a “cam morphology” rather than a cam deformity is now favored. Similarly, FAI is better used to refer to symptomatic individuals and is not equivalent to a cam morphology. The cam morphology seems significantly more common among athletes. Siebenrock and colleagues¹³ demonstrated the correlation of high-level athletics during late stages of skeletal immaturity and development of a cam morphology. A recent systematic review of 9 studies found that elite male athletes in late skeletal immaturity were 2 to 8 times more likely to develop a cam morphology before skeletal maturity.¹⁴Several population-based studies^15,16 have quantified the apparent association of the cam morphology with hip OA. However, the studies were limited in their ability to adequately define the presence of cam morphology based on anteroposterior (AP) pelvis radiographs.

In a prospective study, Agricola and colleagues¹⁵ found the risk of OA was increased 2.4 times in the setting of moderate cam morphology (α angle, >60°) over a 5-year period. Thomas and colleagues¹⁶ found increased risk in a female cohort when the α angle was >65°.

Treatment of cam-type FAI is focused on adequate correction of the abnormal bone morphology. Inadequate or inappropriate bony correction of FAI is a common cause of treatment failure and is more common with arthroscopic techniques.^9,10,17 Inadequate bony resection may be the result of surgical inexperience, poor visualization, or lack of understanding of the underlying bony deformity. Modern osteoplasty techniques also focus on gradual bony contour correction that restores the normal concavity–convexity transition of the head–neck junction. Overresection of the cam deformity not only may increase the risk of femoral neck fracture but may result in early disruption of the hip fluid seal from loss of contact between the femoral head and the acetabular labrum earlier in the arc of motion. In addition, high range-of-motion impingement can be seen in various athletic populations (dance, gymnastics, martial arts, hockey goalies), and the regions of impingement tend to be farther away from classically described impingement. Impingement in these situations occurs at the distal femoral neck and subspine regions, adding a level of complexity and unpredictability from a surgical standpoint.

FAI can also occur in the setting of more complex deformities than the typical cam morphology. Complex cases of FAI caused by slipped capital femoral epiphysis (SCFE) and residual Legg-Calvé-Perthes disease are relatively common. Complex deformities may also result in extra-articular impingement of the proximal femur (greater/lesser trochanter, distal femoral neck) on the pelvis (ilium, ischium) in addition to typical FAI. Mild to moderate cases of residual SCFE may be adequately treated with osteoplasty by arthroscopic techniques. In the setting of more severe residual SCFE, presence of underlying femoral retroversion and retrotilt of the femoral epiphysis may prevent adequate deformity correction and motion improvement by arthroscopy. Surgical hip dislocation (with or without relative femoral neck lengthening) and/or proximal femoral flexion derotational osteotomy may be the best means of treatment in these more severe deformities but may be dependent on the chronicity of the deformity and associated compensatory changes occurring on the acetabular side. Similarly, in moderate to severe residual Legg-Calvé-Perthes disease, presence of coxa vara, high greater trochanter, short femoral neck, and ovoid femoral head may be better treated in open techniques to allow comprehensive deformity correction, including correction of acetabular dysplasia in some cases.

Pincer-Type FAI

Pincer-type FAI results from acetabular-sided deformities in which acetabular deformity leads to impaction-type impingement with “linear contact between the acetabular rim and the femoral head–neck junction.”¹ Pincer FAI causes primarily labral damage with progressive degeneration and, in some cases, ossification of the acetabular labrum that further worsens the acetabular overcoverage and premature rim impaction. Chondral damage in pincer-type FAI is generally less significant and limited to the peripheral acetabular rim.

Pincer-type FAI may be caused by acetabular retroversion, coxa profunda, or protrusio acetabuli. Our understanding of what defines a pincer morphology has evolved significantly. Through efforts to better define structural features of the acetabular rim that represent abnormalities, we have improved our understanding of how these features may influence OA development. One example of improved understanding involves coxa profunda, classically defined as the medial acetabular fossa touching or projecting medial to the ilioischial line on an AP pelvis radiograph. Several studies have found that this classic definition poorly describes the “overcovered” hip, as it is present in 70% of females and commonly present (41%) in the setting of acetabular dysplasia.^18,19 Acetabular retroversion was previously associated with hip OA. Although central acetabular retroversion is relatively uncommon, cranial acetabular retroversion is more common. Presence of a crossover sign on AP pelvis radiographs generally has been viewed as indicative of acetabular retroversion. However, alterations in pelvic tilt on supine or standing AP pelvis radiographs can result in apparent retroversion in the setting of normal acetabular anatomy²⁰ and potentially influence the development of impingement.²¹ Zaltz and colleagues²² found that abnormal morphology of the anterior inferior iliac spine can also lead to the presence of a crossover sign in an otherwise anteverted acetabulum. Larson and colleagues²³ recently found that a crossover sign is present in 11% of asymptomatic hips (19% of males) and may be considered a normal variant. A crossover sign can also be present in the setting of posterior acetabular deficiency with normal anterior acetabular coverage. Ultimately, acetabular retroversion might indicate pincer-type FAI or dysplasia or be a normal variant that does not require treatment. Global acetabular overcoverage, including coxa protrusio, may be associated with OA in population-based studies but is not uniformly demonstrated in all studies.^16,24,25 A lateral center edge angle of >40° and a Tönnis angle (acetabular inclination) of <0° are commonly viewed as markers of global overcoverage.

FAI Treatment

Improvements in hip arthroscopy techniques and instrumentation have led to hip arthroscopy becoming the primary surgical technique for the treatment of most cases of FAI. Hip arthroscopy allows for precise visualization and treatment of labral and chondral disease in the central compartment by traction. Larson and colleagues²⁶ reported complication rates for hip arthroscopy in a prospective series of >1600 cases. The overall complication rate was 8.3%, with higher rates noted in female patients and in the setting of traction time longer than 60 minutes. Nonetheless, major complications occurred in 1.1%, with only 0.1% having persistent disability. The most common complications were lateral femoral cutaneous nerve dysesthesias (1.6%), pudendal nerve neuropraxia (1.4%), and iatrogenic labral/chondral damage (2.1%).

The importance of preserving the acetabular labrum is now well accepted from clinical and biomechanical evidence.^27-29 As in previous studies in surgical hip dislocation,³⁰ arthroscopic labral repair (vs débridement) results in improved clinical outcomes.^31,32 Labral repair techniques currently focus on stable fixation of the labrum while maintaining the normal position of the labrum relative to the femoral head and avoiding labral eversion, which may compromise the hip suction seal. With continued technical advancements and biomechanical support, arthroscopic labral reconstruction is possible in the setting of labral deficiency, often resulting from prior resection. However, the optimal indications, surgical techniques, and long-term outcomes continue to be better defined. Open and arthroscopic techniques have shown similar ability to correct the typical mild to moderate cam morphology in FAI.³³ Yet, inadequate femoral bony correction of FAI seems to be the most common cause for revision hip preservation surgery.^9,10,17Mild to moderate acetabular rim deformities are commonly treated with hip arthroscopy. As our understanding of pincer-type FAI continues to improve, many surgeons are performing less- aggressive bone resection along the anterior rim. On the other hand, subspinous impingement was recently recognized as a form of extra-articular pincer FAI variant.³⁴ Subspine decompression without true acetabular rim resection has become a more common treatment for pincer lesions and may be a consideration even with restricted range of motion after periacetabular osteotomy. Severe acetabular deformities with global overcoverage or acetabular protrusion are particularly challenging by arthroscopy, even for the most experienced surgeons. Although some improvement in deformity is feasible with arthroscopy, even cases reported in the literature have demonstrated incomplete deformity correction. Open surgical hip dislocation may continue to be the ideal treatment technique for severe pincer impingement.

Cam-type FAI is commonly treated with hip arthroscopy (Figures A-F).

Conclusion

Our understanding and treatment of FAI continue to evolve. Both open and arthroscopic techniques have demonstrated excellent outcomes in the treatment of FAI. Most cases of FAI are now amenable to arthroscopic treatment. Inadequate resection and underlying acetabular dysplasia remain common causes of treatment failure. Open surgical hip dislocation continues to play a role in the treatment of severe deformities that are poorly accessible by arthroscopy—including cam lesions with posterior extension, severe global acetabular overcoverage, or extra-articular impingement. The association of FAI with OA is most apparent for cam-type FAI. Future research will define the optimal treatment strategies and determine if they modify disease progression.

Am J Orthop. 2017;46(1):28-34. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.

Take-Home Points

• Our understanding of FAI has evolved from cam-type and pincer-type impingement to much more complex disease patterns.
• Most surgeons are performing less aggressive acetabular rim trimming.
• Inadequate osseous correction is still the most common cause of the failed hip arthroscopy.
• Labral preservation is important to maintaining suction seal effect.
• Open surgical techniques have a role for more severe and complex FAI deformities.

Femoroacetabular impingement (FAI) was described by Ganz and colleagues¹ in 2003 as a refinement of concepts introduced decades earlier. This description advanced our understanding of FAI as a mechanism for prearthritic hip pain and secondary hip osteoarthritis¹ (OA) and allowed for treatment of FAI. The concept of proximal femoral and acetabular/pelvic deformity contributing to OA had been previously speculated by Smith-Petersen,² Murray,³ Solomon,⁴ and Stulberg.⁵ Early cases of overcorrection of dysplasia using the periacetabular osteotomy created iatrogenic FAI, which further stimulated early development of the FAI concept.⁶ Improved anatomical characterization of the proximal femoral blood supply (medial femoral circumflex artery) allowed for development of the open surgical hip dislocation.⁷ Through open surgical hip dislocation, an improved understanding of hip pathomechanics by direct visualization helped pave the way for a better understanding of FAI. Open surgical hip dislocation allows for global treatment of labrochondral pathology and deformity of the proximal femoral head–neck junction and/or acetabular rim in FAI.

Hip arthroscopy has further developed and improved our understanding of FAI. Early hip arthroscopy was generally limited to débridement of labral and chondral pathology, and management of the soft-tissue structures. Advances in the understanding of FAI through open techniques allowed for application of similar techniques to hip arthroscopy. Improvements in arthroscopic instrumentation and techniques have allowed for treatment of labrochondral and acetabular-sided rim deformity in the central compartment and cam morphologies in the peripheral compartment through arthroscopic surgery. Appropriate bony correction by arthroscopic techniques has always been a concern, but improved techniques, dynamic assessment, and accurate use of intraoperative imaging have made this feasible and more predictable. Treatment of cam deformities extending adjacent and proximal to the retinacular vessels is possible but more technically demanding. Inadequate bony correction of FAI by arthroscopic means remains one of the most common causes of failure.^8-10In 2013, the Academic Network of Conservational Hip Outcome Research (ANCHOR) Study Group reported the characteristics of a FAI cohort of 1130 hips (1076 patients) that underwent surgical treatment of FAI across 8 institutions and 12 surgeons.¹¹ At that time, most ANCHOR surgeons (or surgeon groups) performed both open and arthroscopic surgeries and had significant referral volumes of complex cases that may have overrepresented the proportion of complex FAI cases in the cohort. During the 2008 to 2011 study period, FAI was treated with arthroscopy in 56% of these cases, open surgical hip dislocation in 34%, and reverse periacetabular osteotomy in 9%. FAI was characterized as isolated cam-type in 48%, combined cam–pincer type in 45%, and isolated pincer-type in 8%. Fifty-five percent of the patients were female. Patient-reported outcome studies in this cohort of patients are ongoing.

The FAI Concept

In 2003, after treating more than 600 open surgical hip dislocations over the previous decade, Ganz and colleagues¹ coined the term femoroacetabular impingement to describe a “mechanism for the development of early osteoarthritis for most nondysplastic hips.” They reported surgical treatment focused on “improving the clearance for hip motion and alleviation of femoral abutment against the acetabular rim” with the goal of improving pain and possibly of halting progression of the degenerative process. FAI was defined as “abnormal contact between the proximal femur and acetabular rim that occurs during terminal motion of the hip” leading to “lesions of the acetabular labrum and/or the adjacent acetabular cartilage.” Subtle, previously overlooked deformities of the proximal femur and acetabulum were recognized as the cause of FAI, “including the presence of a bony prominence usually in the anterolateral head and neck junction that is seen best on the lateral radiographs, reduced offset of the femoral neck and head junction, and changes on the acetabular rim such as os acetabuli or a double line that is seen with rim ossification.” Ganz and colleagues¹ recognized that “normal or near normal” hips could also experience FAI in the setting of excessive or supraphysiologic range of motion. Cam-type and pincer-type FAI deformities were introduced as 2 distinct mechanisms of FAI. By 2003, arthroscopic hip surgery was increasingly being used as a treatment for labral tears but not bony abnormalities. These FAI concepts seemed to explain the prevalence of labral tears at the anterosuperior rim, which had been noted during hip arthroscopy, and paved the way for major changes in arthroscopic hip surgery during the next decade. The ANCHOR group reported the descriptive epidemiology of a cohort of more than 1000 patients with FAI.¹¹

Cam-Type FAI

Cam-type impingement results from femoral-sided deformities. The mechanism was described as inclusion-type impingement in which “jamming of an abnormal femoral head with increasing radius into the acetabulum during forceful motion, especially flexion.”¹ This results in outside-in abrasion of the acetabular cartilage of the anterosuperior rim with detachment of the “principally uninvolved labrum”¹ and potentially delamination of the adjacent cartilage from the subchondral bone. Ganz and colleagues¹ recognized in their initial descriptions of FAI that cam-type FAI could involve decreased femoral version, femoral head–neck junction asphericity, and decreased head–neck offset. The complexity and variability in the topography and geography of the cam morphology have been increasingly recognized. Accurate understanding and characterization of the proximal femoral deformity are important in guiding surgical correction of the cam deformity.

Advances in understanding the prevalence of the cam morphology and the association with OA have been important to our understanding of the pathophysiology of FAI. Several studies¹² have established that a cam morphology of the proximal femur (defined by a variety of different metrics) is common among asymptomatic individuals. In light of this fact, a description of the femoral anatomy as a “cam morphology” rather than a cam deformity is now favored. Similarly, FAI is better used to refer to symptomatic individuals and is not equivalent to a cam morphology. The cam morphology seems significantly more common among athletes. Siebenrock and colleagues¹³ demonstrated the correlation of high-level athletics during late stages of skeletal immaturity and development of a cam morphology. A recent systematic review of 9 studies found that elite male athletes in late skeletal immaturity were 2 to 8 times more likely to develop a cam morphology before skeletal maturity.¹⁴Several population-based studies^15,16 have quantified the apparent association of the cam morphology with hip OA. However, the studies were limited in their ability to adequately define the presence of cam morphology based on anteroposterior (AP) pelvis radiographs.

In a prospective study, Agricola and colleagues¹⁵ found the risk of OA was increased 2.4 times in the setting of moderate cam morphology (α angle, >60°) over a 5-year period. Thomas and colleagues¹⁶ found increased risk in a female cohort when the α angle was >65°.

Treatment of cam-type FAI is focused on adequate correction of the abnormal bone morphology. Inadequate or inappropriate bony correction of FAI is a common cause of treatment failure and is more common with arthroscopic techniques.^9,10,17 Inadequate bony resection may be the result of surgical inexperience, poor visualization, or lack of understanding of the underlying bony deformity. Modern osteoplasty techniques also focus on gradual bony contour correction that restores the normal concavity–convexity transition of the head–neck junction. Overresection of the cam deformity not only may increase the risk of femoral neck fracture but may result in early disruption of the hip fluid seal from loss of contact between the femoral head and the acetabular labrum earlier in the arc of motion. In addition, high range-of-motion impingement can be seen in various athletic populations (dance, gymnastics, martial arts, hockey goalies), and the regions of impingement tend to be farther away from classically described impingement. Impingement in these situations occurs at the distal femoral neck and subspine regions, adding a level of complexity and unpredictability from a surgical standpoint.

FAI can also occur in the setting of more complex deformities than the typical cam morphology. Complex cases of FAI caused by slipped capital femoral epiphysis (SCFE) and residual Legg-Calvé-Perthes disease are relatively common. Complex deformities may also result in extra-articular impingement of the proximal femur (greater/lesser trochanter, distal femoral neck) on the pelvis (ilium, ischium) in addition to typical FAI. Mild to moderate cases of residual SCFE may be adequately treated with osteoplasty by arthroscopic techniques. In the setting of more severe residual SCFE, presence of underlying femoral retroversion and retrotilt of the femoral epiphysis may prevent adequate deformity correction and motion improvement by arthroscopy. Surgical hip dislocation (with or without relative femoral neck lengthening) and/or proximal femoral flexion derotational osteotomy may be the best means of treatment in these more severe deformities but may be dependent on the chronicity of the deformity and associated compensatory changes occurring on the acetabular side. Similarly, in moderate to severe residual Legg-Calvé-Perthes disease, presence of coxa vara, high greater trochanter, short femoral neck, and ovoid femoral head may be better treated in open techniques to allow comprehensive deformity correction, including correction of acetabular dysplasia in some cases.

Pincer-Type FAI

Pincer-type FAI results from acetabular-sided deformities in which acetabular deformity leads to impaction-type impingement with “linear contact between the acetabular rim and the femoral head–neck junction.”¹ Pincer FAI causes primarily labral damage with progressive degeneration and, in some cases, ossification of the acetabular labrum that further worsens the acetabular overcoverage and premature rim impaction. Chondral damage in pincer-type FAI is generally less significant and limited to the peripheral acetabular rim.

Pincer-type FAI may be caused by acetabular retroversion, coxa profunda, or protrusio acetabuli. Our understanding of what defines a pincer morphology has evolved significantly. Through efforts to better define structural features of the acetabular rim that represent abnormalities, we have improved our understanding of how these features may influence OA development. One example of improved understanding involves coxa profunda, classically defined as the medial acetabular fossa touching or projecting medial to the ilioischial line on an AP pelvis radiograph. Several studies have found that this classic definition poorly describes the “overcovered” hip, as it is present in 70% of females and commonly present (41%) in the setting of acetabular dysplasia.^18,19 Acetabular retroversion was previously associated with hip OA. Although central acetabular retroversion is relatively uncommon, cranial acetabular retroversion is more common. Presence of a crossover sign on AP pelvis radiographs generally has been viewed as indicative of acetabular retroversion. However, alterations in pelvic tilt on supine or standing AP pelvis radiographs can result in apparent retroversion in the setting of normal acetabular anatomy²⁰ and potentially influence the development of impingement.²¹ Zaltz and colleagues²² found that abnormal morphology of the anterior inferior iliac spine can also lead to the presence of a crossover sign in an otherwise anteverted acetabulum. Larson and colleagues²³ recently found that a crossover sign is present in 11% of asymptomatic hips (19% of males) and may be considered a normal variant. A crossover sign can also be present in the setting of posterior acetabular deficiency with normal anterior acetabular coverage. Ultimately, acetabular retroversion might indicate pincer-type FAI or dysplasia or be a normal variant that does not require treatment. Global acetabular overcoverage, including coxa protrusio, may be associated with OA in population-based studies but is not uniformly demonstrated in all studies.^16,24,25 A lateral center edge angle of >40° and a Tönnis angle (acetabular inclination) of <0° are commonly viewed as markers of global overcoverage.

FAI Treatment

Improvements in hip arthroscopy techniques and instrumentation have led to hip arthroscopy becoming the primary surgical technique for the treatment of most cases of FAI. Hip arthroscopy allows for precise visualization and treatment of labral and chondral disease in the central compartment by traction. Larson and colleagues²⁶ reported complication rates for hip arthroscopy in a prospective series of >1600 cases. The overall complication rate was 8.3%, with higher rates noted in female patients and in the setting of traction time longer than 60 minutes. Nonetheless, major complications occurred in 1.1%, with only 0.1% having persistent disability. The most common complications were lateral femoral cutaneous nerve dysesthesias (1.6%), pudendal nerve neuropraxia (1.4%), and iatrogenic labral/chondral damage (2.1%).

The importance of preserving the acetabular labrum is now well accepted from clinical and biomechanical evidence.^27-29 As in previous studies in surgical hip dislocation,³⁰ arthroscopic labral repair (vs débridement) results in improved clinical outcomes.^31,32 Labral repair techniques currently focus on stable fixation of the labrum while maintaining the normal position of the labrum relative to the femoral head and avoiding labral eversion, which may compromise the hip suction seal. With continued technical advancements and biomechanical support, arthroscopic labral reconstruction is possible in the setting of labral deficiency, often resulting from prior resection. However, the optimal indications, surgical techniques, and long-term outcomes continue to be better defined. Open and arthroscopic techniques have shown similar ability to correct the typical mild to moderate cam morphology in FAI.³³ Yet, inadequate femoral bony correction of FAI seems to be the most common cause for revision hip preservation surgery.^9,10,17Mild to moderate acetabular rim deformities are commonly treated with hip arthroscopy. As our understanding of pincer-type FAI continues to improve, many surgeons are performing less- aggressive bone resection along the anterior rim. On the other hand, subspinous impingement was recently recognized as a form of extra-articular pincer FAI variant.³⁴ Subspine decompression without true acetabular rim resection has become a more common treatment for pincer lesions and may be a consideration even with restricted range of motion after periacetabular osteotomy. Severe acetabular deformities with global overcoverage or acetabular protrusion are particularly challenging by arthroscopy, even for the most experienced surgeons. Although some improvement in deformity is feasible with arthroscopy, even cases reported in the literature have demonstrated incomplete deformity correction. Open surgical hip dislocation may continue to be the ideal treatment technique for severe pincer impingement.

Cam-type FAI is commonly treated with hip arthroscopy (Figures A-F).

Conclusion

Our understanding and treatment of FAI continue to evolve. Both open and arthroscopic techniques have demonstrated excellent outcomes in the treatment of FAI. Most cases of FAI are now amenable to arthroscopic treatment. Inadequate resection and underlying acetabular dysplasia remain common causes of treatment failure. Open surgical hip dislocation continues to play a role in the treatment of severe deformities that are poorly accessible by arthroscopy—including cam lesions with posterior extension, severe global acetabular overcoverage, or extra-articular impingement. The association of FAI with OA is most apparent for cam-type FAI. Future research will define the optimal treatment strategies and determine if they modify disease progression.

Am J Orthop. 2017;46(1):28-34. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.