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Delays in Diagnosis and Treatment of Infantile Spasms Are Common
HOUSTON—Children with infantile spasms commonly endure substantial delays in diagnosis and treatment, according to research presented at the 70th Annual Meeting of the American Epilepsy Society. “A simple lack of awareness of infantile spasms among healthcare providers may be responsible for potentially catastrophic delays in diagnosis and treatment,” said Shaun Hussain, MD, Director of the University of California, Los Angeles Infantile Spasms Program, and colleagues. “There is a desperate need for effective interventions to increase basic familiarity with infantile spasms among healthcare providers.”
Dr. Hussain and his colleagues performed a study to measure delays in diagnosis and treatment of infantile spasms and identify barriers to optimal care. The researchers retrospectively identified children with video-EEG-confirmed infantile spasms in a clinical database.
When the children’s parents presented for follow-up, they were surveyed about their experiences with diagnosis and treatment. The investigators asked about medical and sociodemographic factors that could affect the care of infantile spasms. Specifically, the researchers determined the dates of infantile spasms onset, first visit with any healthcare provider, first visit with any neurologist, and first visit with an effective provider. Dr. Hussain and colleagues defined an effective provider as a healthcare provider who identified infantile spasms and prescribed a first-line treatment (ie, ACTH, corticosteroids, vigabatrin, or surgical resection). The investigators reviewed medical records to corroborate parents’ survey responses. They calculated the time to first effective provider using Cox proportional hazards regression.
The parents of 100 children with previous or ongoing infantile spasms were included in the study. Approximately 29% of patients were seen by an effective provider within one week of spasms onset. The median time from spasms onset to the first visit with an effective provider was 24.5 days. In sequential univariate analyses, parental sociodemographic attributes (eg, race, ethnicity, religion, household income, education level, type of healthcare insurance, and distance from patients’ home to the tertiary center) did not predict time to first effective provider. In open-ended discussions, numerous parents reported that their suspicions that “something was wrong” often had been discounted by pediatricians, emergency room physicians, and neurologists. In a qualitative analysis, many parents reported self-diagnosis using Internet resources and self-referral after various diagnostic difficulties and false reassurance by health care providers.
HOUSTON—Children with infantile spasms commonly endure substantial delays in diagnosis and treatment, according to research presented at the 70th Annual Meeting of the American Epilepsy Society. “A simple lack of awareness of infantile spasms among healthcare providers may be responsible for potentially catastrophic delays in diagnosis and treatment,” said Shaun Hussain, MD, Director of the University of California, Los Angeles Infantile Spasms Program, and colleagues. “There is a desperate need for effective interventions to increase basic familiarity with infantile spasms among healthcare providers.”
Dr. Hussain and his colleagues performed a study to measure delays in diagnosis and treatment of infantile spasms and identify barriers to optimal care. The researchers retrospectively identified children with video-EEG-confirmed infantile spasms in a clinical database.
When the children’s parents presented for follow-up, they were surveyed about their experiences with diagnosis and treatment. The investigators asked about medical and sociodemographic factors that could affect the care of infantile spasms. Specifically, the researchers determined the dates of infantile spasms onset, first visit with any healthcare provider, first visit with any neurologist, and first visit with an effective provider. Dr. Hussain and colleagues defined an effective provider as a healthcare provider who identified infantile spasms and prescribed a first-line treatment (ie, ACTH, corticosteroids, vigabatrin, or surgical resection). The investigators reviewed medical records to corroborate parents’ survey responses. They calculated the time to first effective provider using Cox proportional hazards regression.
The parents of 100 children with previous or ongoing infantile spasms were included in the study. Approximately 29% of patients were seen by an effective provider within one week of spasms onset. The median time from spasms onset to the first visit with an effective provider was 24.5 days. In sequential univariate analyses, parental sociodemographic attributes (eg, race, ethnicity, religion, household income, education level, type of healthcare insurance, and distance from patients’ home to the tertiary center) did not predict time to first effective provider. In open-ended discussions, numerous parents reported that their suspicions that “something was wrong” often had been discounted by pediatricians, emergency room physicians, and neurologists. In a qualitative analysis, many parents reported self-diagnosis using Internet resources and self-referral after various diagnostic difficulties and false reassurance by health care providers.
HOUSTON—Children with infantile spasms commonly endure substantial delays in diagnosis and treatment, according to research presented at the 70th Annual Meeting of the American Epilepsy Society. “A simple lack of awareness of infantile spasms among healthcare providers may be responsible for potentially catastrophic delays in diagnosis and treatment,” said Shaun Hussain, MD, Director of the University of California, Los Angeles Infantile Spasms Program, and colleagues. “There is a desperate need for effective interventions to increase basic familiarity with infantile spasms among healthcare providers.”
Dr. Hussain and his colleagues performed a study to measure delays in diagnosis and treatment of infantile spasms and identify barriers to optimal care. The researchers retrospectively identified children with video-EEG-confirmed infantile spasms in a clinical database.
When the children’s parents presented for follow-up, they were surveyed about their experiences with diagnosis and treatment. The investigators asked about medical and sociodemographic factors that could affect the care of infantile spasms. Specifically, the researchers determined the dates of infantile spasms onset, first visit with any healthcare provider, first visit with any neurologist, and first visit with an effective provider. Dr. Hussain and colleagues defined an effective provider as a healthcare provider who identified infantile spasms and prescribed a first-line treatment (ie, ACTH, corticosteroids, vigabatrin, or surgical resection). The investigators reviewed medical records to corroborate parents’ survey responses. They calculated the time to first effective provider using Cox proportional hazards regression.
The parents of 100 children with previous or ongoing infantile spasms were included in the study. Approximately 29% of patients were seen by an effective provider within one week of spasms onset. The median time from spasms onset to the first visit with an effective provider was 24.5 days. In sequential univariate analyses, parental sociodemographic attributes (eg, race, ethnicity, religion, household income, education level, type of healthcare insurance, and distance from patients’ home to the tertiary center) did not predict time to first effective provider. In open-ended discussions, numerous parents reported that their suspicions that “something was wrong” often had been discounted by pediatricians, emergency room physicians, and neurologists. In a qualitative analysis, many parents reported self-diagnosis using Internet resources and self-referral after various diagnostic difficulties and false reassurance by health care providers.
January 2017 Quiz 2
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.
Q2: A 23-year-old woman with a history of Crohn’s disease presents to a GI clinic stating that she took a pregnancy test, and it is positive. She is concerned because she takes azathioprine and is worried about the risk of birth defects. She asks about alternative medications she could take. She also asks if she could have an endoscopy while pregnant, and if it is normal, she wants to consider stopping the azathioprine. She is doing well and has no complaints. Her Crohn’s disease appears to be in clinical remission.
January 2017 Quiz 1
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.
Q1: A 60-year-old woman complains of progressive weakness and fatigue and has a stumbling gait. She has three soft, loose stools each day, which has been a stable pattern since her gastric bypass (standard bariatric gastrojejunostomy) 10 years ago. Her physical exam is notable only for some pallor of the mucosal membranes, diminished touch sensation of the extremities, and an abnormal gait with impaired tandem walking and balance. There was no glossitis or rash. Stool testing was negative for occult blood. Initial lab tests revealed a moderate microcytic anemia, normal electrolytes, renal function, and liver tests. Iron supplementation was provided for 3 months, after which the microcytic anemia was noted to have worsened despite normal iron values on follow-up testing.
Nonalcoholic Fatty Liver Disease Accelerates Brain Aging
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
Study identifies predictors of poor outcome in status epilepticus
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.
Neither age nor gender predicted poor outcome, and there was no difference in outcome between structural and nonstructural causes of status epilepticus. However, prior history of epilepsy was a strong negative predictor of poor outcome. In fact, only 14 of 70 patients (20%) with a prior history of epilepsy had a poor outcome (P less than .01). “The theory is that [these patients] were already on treatment for epilepsy in the past and that affected their outcome in a positive way,” Dr. Mahulikar explained.
When outcome was analyzed based on status semiology on initial presentation, poor outcome was seen in 16 of the 37 patients (43%) with CPSE (P = .04); 9 of 48 patients (19%) with generalized convulsive status epilepticus, all patients with myoclonic status epilepticus (n = 2), and 3 of 9 (33%) who had NCSE (P less than .01). The type of status epilepticus was unknown for four patients, one of whom had an unknown outcome. NCSE at any time during the hospital course (including at presentation) was seen in 31 patients. Of these, 14 (45%) had a poor outcome (P = .02).
The mean number of ventilator days was higher in patients with NCSE than in those without NCSE (9.2 vs. 1.6 days; P = .0001) and also higher in those with new-onset seizures than in those without (7.8 vs. 2.9 days; P = .001). Analysis of methods of treatments revealed that only 7 of 31 (22.5%) patients who received adequate benzodiazepine dosing had poor outcomes (P = .2247). “The take-home message is to diagnose NCSE as early as possible because I think some patients who come in initially we may attribute to metabolic or autoimmune causes, and we tend to miss NCSE sometimes due to delay in diagnosis of NCSE,” Dr. Mahulikar said. “Treat aggressively at the beginning.”
He reported having no financial disclosures.
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.
Neither age nor gender predicted poor outcome, and there was no difference in outcome between structural and nonstructural causes of status epilepticus. However, prior history of epilepsy was a strong negative predictor of poor outcome. In fact, only 14 of 70 patients (20%) with a prior history of epilepsy had a poor outcome (P less than .01). “The theory is that [these patients] were already on treatment for epilepsy in the past and that affected their outcome in a positive way,” Dr. Mahulikar explained.
When outcome was analyzed based on status semiology on initial presentation, poor outcome was seen in 16 of the 37 patients (43%) with CPSE (P = .04); 9 of 48 patients (19%) with generalized convulsive status epilepticus, all patients with myoclonic status epilepticus (n = 2), and 3 of 9 (33%) who had NCSE (P less than .01). The type of status epilepticus was unknown for four patients, one of whom had an unknown outcome. NCSE at any time during the hospital course (including at presentation) was seen in 31 patients. Of these, 14 (45%) had a poor outcome (P = .02).
The mean number of ventilator days was higher in patients with NCSE than in those without NCSE (9.2 vs. 1.6 days; P = .0001) and also higher in those with new-onset seizures than in those without (7.8 vs. 2.9 days; P = .001). Analysis of methods of treatments revealed that only 7 of 31 (22.5%) patients who received adequate benzodiazepine dosing had poor outcomes (P = .2247). “The take-home message is to diagnose NCSE as early as possible because I think some patients who come in initially we may attribute to metabolic or autoimmune causes, and we tend to miss NCSE sometimes due to delay in diagnosis of NCSE,” Dr. Mahulikar said. “Treat aggressively at the beginning.”
He reported having no financial disclosures.
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.
Neither age nor gender predicted poor outcome, and there was no difference in outcome between structural and nonstructural causes of status epilepticus. However, prior history of epilepsy was a strong negative predictor of poor outcome. In fact, only 14 of 70 patients (20%) with a prior history of epilepsy had a poor outcome (P less than .01). “The theory is that [these patients] were already on treatment for epilepsy in the past and that affected their outcome in a positive way,” Dr. Mahulikar explained.
When outcome was analyzed based on status semiology on initial presentation, poor outcome was seen in 16 of the 37 patients (43%) with CPSE (P = .04); 9 of 48 patients (19%) with generalized convulsive status epilepticus, all patients with myoclonic status epilepticus (n = 2), and 3 of 9 (33%) who had NCSE (P less than .01). The type of status epilepticus was unknown for four patients, one of whom had an unknown outcome. NCSE at any time during the hospital course (including at presentation) was seen in 31 patients. Of these, 14 (45%) had a poor outcome (P = .02).
The mean number of ventilator days was higher in patients with NCSE than in those without NCSE (9.2 vs. 1.6 days; P = .0001) and also higher in those with new-onset seizures than in those without (7.8 vs. 2.9 days; P = .001). Analysis of methods of treatments revealed that only 7 of 31 (22.5%) patients who received adequate benzodiazepine dosing had poor outcomes (P = .2247). “The take-home message is to diagnose NCSE as early as possible because I think some patients who come in initially we may attribute to metabolic or autoimmune causes, and we tend to miss NCSE sometimes due to delay in diagnosis of NCSE,” Dr. Mahulikar said. “Treat aggressively at the beginning.”
He reported having no financial disclosures.
AT AES 2016
Key clinical point:
Major finding: Poor outcome was seen in 43% of patients with CPSE, 19% with generalized convulsive status epilepticus, all patients with myoclonic status epilepticus, and in 33% of those who had NCSE.
Data source: A retrospective review of 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.
Disclosures: Dr. Mahulikar reported having no financial disclosures.
Scientific skepticism
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.
Medicine has a long history of being biased by the belief that its therapies work. Even faith healers who consider themselves scientists will cite repeated examples of personal success as evidence that their approach works. However, they were looking for confirmation. To truly be a scientist, one cannot seek to affirm one’s beliefs. One must to the best of one’s ability seek to disprove them.
In 2016, postmodern voices have challenged the very existence of truth. The falsehoods rampant in politics have spilled over into a distrust of science. This distrust is manifest in vaccine deniers and the debate about climate change. There are a few charlatans and mercenaries in every field who sell their soul and skills to the highest bidder. Science is no exception. These disreputable scientists seek to obfuscate rather than clarify. They have been employed by the tobacco industry, the oil industry, and various groups with agendas other than seeking truth. They, with the help of weak journalism, have tainted the perception of science in the public arena. The uproar has prominent scientists defending the scientific method and arguing for science as the determiner of facts. Sen. Daniel Patrick Moynihan once said, “Everyone is entitled to his own opinion, but not to his own facts.”
In the 19th century, hawking snake oil was big business. In the early 20th century, the ethical drug industry was created in the United States. The Pure Food and Drug Act of 1906 and the Federal Food, Drug, and Cosmetic Act of 1938 empowered the Food and Drug Administration to regulate what has become 25% of U.S. industry. Those regulations demand honest labeling, good manufacturing processes, proof of efficacy, and an assessment of safety. The FDA deals with many stakeholders in the process for approving new drugs. The system is an imperfect balance between getting lifesaving new discoveries to market quickly while avoiding disasters. The most recent news has been the head of the FDA defending the need for proof of effectiveness in addition to proof of safety.
Even after a year in which truth seemed elusive and science hit a low point in prestige, it is still bizarre to me that the government would consider turning the drug industry into one in which proof of effectiveness is not a minimum requirement. That is postmodern thinking run amok. But the root of the problem lies deeper. When scientists stop being skeptics and instead focus on finding something publishable, the temptation is already leading them along the road illuminated by Dante Alighieri.
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.
Medicine has a long history of being biased by the belief that its therapies work. Even faith healers who consider themselves scientists will cite repeated examples of personal success as evidence that their approach works. However, they were looking for confirmation. To truly be a scientist, one cannot seek to affirm one’s beliefs. One must to the best of one’s ability seek to disprove them.
In 2016, postmodern voices have challenged the very existence of truth. The falsehoods rampant in politics have spilled over into a distrust of science. This distrust is manifest in vaccine deniers and the debate about climate change. There are a few charlatans and mercenaries in every field who sell their soul and skills to the highest bidder. Science is no exception. These disreputable scientists seek to obfuscate rather than clarify. They have been employed by the tobacco industry, the oil industry, and various groups with agendas other than seeking truth. They, with the help of weak journalism, have tainted the perception of science in the public arena. The uproar has prominent scientists defending the scientific method and arguing for science as the determiner of facts. Sen. Daniel Patrick Moynihan once said, “Everyone is entitled to his own opinion, but not to his own facts.”
In the 19th century, hawking snake oil was big business. In the early 20th century, the ethical drug industry was created in the United States. The Pure Food and Drug Act of 1906 and the Federal Food, Drug, and Cosmetic Act of 1938 empowered the Food and Drug Administration to regulate what has become 25% of U.S. industry. Those regulations demand honest labeling, good manufacturing processes, proof of efficacy, and an assessment of safety. The FDA deals with many stakeholders in the process for approving new drugs. The system is an imperfect balance between getting lifesaving new discoveries to market quickly while avoiding disasters. The most recent news has been the head of the FDA defending the need for proof of effectiveness in addition to proof of safety.
Even after a year in which truth seemed elusive and science hit a low point in prestige, it is still bizarre to me that the government would consider turning the drug industry into one in which proof of effectiveness is not a minimum requirement. That is postmodern thinking run amok. But the root of the problem lies deeper. When scientists stop being skeptics and instead focus on finding something publishable, the temptation is already leading them along the road illuminated by Dante Alighieri.
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.
Medicine has a long history of being biased by the belief that its therapies work. Even faith healers who consider themselves scientists will cite repeated examples of personal success as evidence that their approach works. However, they were looking for confirmation. To truly be a scientist, one cannot seek to affirm one’s beliefs. One must to the best of one’s ability seek to disprove them.
In 2016, postmodern voices have challenged the very existence of truth. The falsehoods rampant in politics have spilled over into a distrust of science. This distrust is manifest in vaccine deniers and the debate about climate change. There are a few charlatans and mercenaries in every field who sell their soul and skills to the highest bidder. Science is no exception. These disreputable scientists seek to obfuscate rather than clarify. They have been employed by the tobacco industry, the oil industry, and various groups with agendas other than seeking truth. They, with the help of weak journalism, have tainted the perception of science in the public arena. The uproar has prominent scientists defending the scientific method and arguing for science as the determiner of facts. Sen. Daniel Patrick Moynihan once said, “Everyone is entitled to his own opinion, but not to his own facts.”
In the 19th century, hawking snake oil was big business. In the early 20th century, the ethical drug industry was created in the United States. The Pure Food and Drug Act of 1906 and the Federal Food, Drug, and Cosmetic Act of 1938 empowered the Food and Drug Administration to regulate what has become 25% of U.S. industry. Those regulations demand honest labeling, good manufacturing processes, proof of efficacy, and an assessment of safety. The FDA deals with many stakeholders in the process for approving new drugs. The system is an imperfect balance between getting lifesaving new discoveries to market quickly while avoiding disasters. The most recent news has been the head of the FDA defending the need for proof of effectiveness in addition to proof of safety.
Even after a year in which truth seemed elusive and science hit a low point in prestige, it is still bizarre to me that the government would consider turning the drug industry into one in which proof of effectiveness is not a minimum requirement. That is postmodern thinking run amok. But the root of the problem lies deeper. When scientists stop being skeptics and instead focus on finding something publishable, the temptation is already leading them along the road illuminated by Dante Alighieri.
Dr. Powell is a pediatric hospitalist and clinical ethics consultant living in St. Louis.
Hip Arthroscopy
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.
Mastering the Physical Examination of the Athlete’s Hip
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.
Am J Orthop. 2017;46(1):10-16. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
1. Boyd KT, Peirce NS, Batt ME. Common hip injuries in sport. Sports Med. 1997;24(4):273-288.
2. Duthon VB, Charbonnier C, Kolo FC, et al. Correlation of clinical and magnetic resonance imaging findings in hips of elite female ballet dancers. Arthroscopy. 2013;29(3):411-419.
3. Prather H, Cheng A. Diagnosis and treatment of hip girdle pain in the athlete. PM R. 2016;8(3 suppl):S45-S60.
4. Larson CM. Sports hernia/athletic pubalgia: evaluation and management. Sports Health. 2014;6(2):139-144.
5. Bizzini M, Notzli HP, Maffiuletti NA. Femoroacetabular impingement in professional ice hockey players: a case series of 5 athletes after open surgical decompression of the hip. Am J Sports Med. 2007;35(11):1955-1959.
6. Lynch TS, Terry MA, Bedi A, Kelly BT. Hip arthroscopic surgery: patient evaluation, current indications, and outcomes. Am J Sports Med. 2013;41(5):1174-1189.
7. Anderson K, Strickland SM, Warren R. Hip and groin injuries in athletes. Am J Sports Med. 2001;29(4):521-533.
8. Fon LJ, Spence RA. Sportsman’s hernia. Br J Surg. 2000;87(5):545-552.
9. Kluin J, den Hoed PT, van Linschoten R, IJzerman JC, van Steensel CJ. Endoscopic evaluation and treatment of groin pain in the athlete. Am J Sports Med. 2004;32(4):944-949.
10. Ward D, Parvizi J. Management of hip pain in young adults. Orthop Clin North Am. 2016;47(3):485-496.
11. Byrd JW. Hip arthroscopy. J Am Acad Orthop Surg. 2006;14(7):433-444.
12. Martin HD, Palmer IJ. History and physical examination of the hip: the basics. Curr Rev Musculoskelet Med. 2013;6(3):219-225.
13. Shindle MK, Voos JE, Nho SJ, Heyworth BE, Kelly BT. Arthroscopic management of labral tears in the hip. J Bone Joint Surg Am. 2008;90(suppl 4):2-19.
14. Morelli V, Smith V. Groin injuries in athletes. Am Fam Physician. 2001;64(8):1405-1414.
15. Ekstrand J, Hagglund M, Walden M. Epidemiology of muscle injuries in professional football (soccer). Am J Sports Med. 2011;39(6):1226-1232.
16. Ekstrand J, Gillquist J. The avoidability of soccer injuries. Int J Sports Med. 1983;4(2):124-128.
17. Tyler TF, Nicholas SJ, Campbell RJ, McHugh MP. The association of hip strength and flexibility with the incidence of adductor muscle strains in professional ice hockey players. Am J Sports Med. 2001;29(2):124-128.
18. Farber AJ, Wilckens JH. Sports hernia: diagnosis and therapeutic approach. J Am Acad Orthop Surg. 2007;15(8):507-514.
19. De Paulis F, Cacchio A, Michelini O, Damiani A, Saggini R. Sports injuries in the pelvis and hip: diagnostic imaging. Eur J Radiol. 1998;27(suppl 1):S49-S59.
20. Lovell G. The diagnosis of chronic groin pain in athletes: a review of 189 cases. Aust J Sci Med Sport. 1995;27(suppl 1):76-79.
21. Strosberg DS, Ellis TJ, Renton DB. The role of femoroacetabular impingement in core muscle injury/athletic pubalgia: diagnosis and management. Front Surg. 2016;3:6.
22. Meyers WC, Foley DP, Garrett WE, Lohnes JH, Mandlebaum BR. Management of severe lower abdominal or inguinal pain in high-performance athletes. PAIN (Performing Athletes with Abdominal or Inguinal Neuromuscular Pain Study Group). Am J Sports Med. 2000;28(1):2-8.
23. Ahumada LA, Ashruf S, Espinosa-de-los-Monteros A, et al. Athletic pubalgia: definition and surgical treatment. Ann Plast Surg. 2005;55(4):393-396.
24. Angoules AG. Osteitis pubis in elite athletes: diagnostic and therapeutic approach. World J Orthop. 2015;6(9):672-679.
25. Hiti CJ, Stevens KJ, Jamati MK, Garza D, Matheson GO. Athletic osteitis pubis. Sports Med. 2011;41(5):361-376.
26. Mehin R, Meek R, O’Brien P, Blachut P. Surgery for osteitis pubis. Can J Surg. 2006;49(3):170-176.
27. Grace JN, Sim FH, Shives TC, Coventry MB. Wedge resection of the symphysis pubis for the treatment of osteitis pubis. J Bone Joint Surg Am. 1989;71(3):358-364.
28. Amanatullah DF, Antkowiak T, Pillay K, et al. Femoroacetabular impingement: current concepts in diagnosis and treatment. Orthopedics. 2015;38(3):185-199.
29. Ganz R, Parvizi J, Beck M, Leunig M, Nötzli H, Siebenrock KA. Femoroacetabular impingement: a cause for osteoarthritis of the hip. Clin Orthop Relat Res. 2003;(417):112-120.
30. Redmond JM, Gupta A, Hammarstedt JE, Stake CE, Dunne KF, Domb BG. Labral injury: radiographic predictors at the time of hip arthroscopy. Arthroscopy. 2015;31(1):51-56.
31. Clohisy JC, Knaus ER, Hunt DM, Lesher JM, Harris-Hayes M, Prather H. Clinical presentation of patients with symptomatic anterior hip impingement. Clin Orthop Relat Res. 2009;467(3):638-644.
32. Klaue K, Durnin CW, Ganz R. The acetabular rim syndrome. A clinical presentation of dysplasia of the hip. J Bone Joint Surg Br. 1991;73(3):423-429.
33. Philippon MJ, Schenker ML. Arthroscopy for the treatment of femoroacetabular impingement in the athlete. Clin Sports Med. 2006;25(2):299-308.
34. McCarthy JC, Lee JA. Hip arthroscopy: indications, outcomes, and complications. Instr Course Lect. 2006;55:301-308.
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.
Am J Orthop. 2017;46(1):10-16. 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.
Am J Orthop. 2017;46(1):10-16. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
1. Boyd KT, Peirce NS, Batt ME. Common hip injuries in sport. Sports Med. 1997;24(4):273-288.
2. Duthon VB, Charbonnier C, Kolo FC, et al. Correlation of clinical and magnetic resonance imaging findings in hips of elite female ballet dancers. Arthroscopy. 2013;29(3):411-419.
3. Prather H, Cheng A. Diagnosis and treatment of hip girdle pain in the athlete. PM R. 2016;8(3 suppl):S45-S60.
4. Larson CM. Sports hernia/athletic pubalgia: evaluation and management. Sports Health. 2014;6(2):139-144.
5. Bizzini M, Notzli HP, Maffiuletti NA. Femoroacetabular impingement in professional ice hockey players: a case series of 5 athletes after open surgical decompression of the hip. Am J Sports Med. 2007;35(11):1955-1959.
6. Lynch TS, Terry MA, Bedi A, Kelly BT. Hip arthroscopic surgery: patient evaluation, current indications, and outcomes. Am J Sports Med. 2013;41(5):1174-1189.
7. Anderson K, Strickland SM, Warren R. Hip and groin injuries in athletes. Am J Sports Med. 2001;29(4):521-533.
8. Fon LJ, Spence RA. Sportsman’s hernia. Br J Surg. 2000;87(5):545-552.
9. Kluin J, den Hoed PT, van Linschoten R, IJzerman JC, van Steensel CJ. Endoscopic evaluation and treatment of groin pain in the athlete. Am J Sports Med. 2004;32(4):944-949.
10. Ward D, Parvizi J. Management of hip pain in young adults. Orthop Clin North Am. 2016;47(3):485-496.
11. Byrd JW. Hip arthroscopy. J Am Acad Orthop Surg. 2006;14(7):433-444.
12. Martin HD, Palmer IJ. History and physical examination of the hip: the basics. Curr Rev Musculoskelet Med. 2013;6(3):219-225.
13. Shindle MK, Voos JE, Nho SJ, Heyworth BE, Kelly BT. Arthroscopic management of labral tears in the hip. J Bone Joint Surg Am. 2008;90(suppl 4):2-19.
14. Morelli V, Smith V. Groin injuries in athletes. Am Fam Physician. 2001;64(8):1405-1414.
15. Ekstrand J, Hagglund M, Walden M. Epidemiology of muscle injuries in professional football (soccer). Am J Sports Med. 2011;39(6):1226-1232.
16. Ekstrand J, Gillquist J. The avoidability of soccer injuries. Int J Sports Med. 1983;4(2):124-128.
17. Tyler TF, Nicholas SJ, Campbell RJ, McHugh MP. The association of hip strength and flexibility with the incidence of adductor muscle strains in professional ice hockey players. Am J Sports Med. 2001;29(2):124-128.
18. Farber AJ, Wilckens JH. Sports hernia: diagnosis and therapeutic approach. J Am Acad Orthop Surg. 2007;15(8):507-514.
19. De Paulis F, Cacchio A, Michelini O, Damiani A, Saggini R. Sports injuries in the pelvis and hip: diagnostic imaging. Eur J Radiol. 1998;27(suppl 1):S49-S59.
20. Lovell G. The diagnosis of chronic groin pain in athletes: a review of 189 cases. Aust J Sci Med Sport. 1995;27(suppl 1):76-79.
21. Strosberg DS, Ellis TJ, Renton DB. The role of femoroacetabular impingement in core muscle injury/athletic pubalgia: diagnosis and management. Front Surg. 2016;3:6.
22. Meyers WC, Foley DP, Garrett WE, Lohnes JH, Mandlebaum BR. Management of severe lower abdominal or inguinal pain in high-performance athletes. PAIN (Performing Athletes with Abdominal or Inguinal Neuromuscular Pain Study Group). Am J Sports Med. 2000;28(1):2-8.
23. Ahumada LA, Ashruf S, Espinosa-de-los-Monteros A, et al. Athletic pubalgia: definition and surgical treatment. Ann Plast Surg. 2005;55(4):393-396.
24. Angoules AG. Osteitis pubis in elite athletes: diagnostic and therapeutic approach. World J Orthop. 2015;6(9):672-679.
25. Hiti CJ, Stevens KJ, Jamati MK, Garza D, Matheson GO. Athletic osteitis pubis. Sports Med. 2011;41(5):361-376.
26. Mehin R, Meek R, O’Brien P, Blachut P. Surgery for osteitis pubis. Can J Surg. 2006;49(3):170-176.
27. Grace JN, Sim FH, Shives TC, Coventry MB. Wedge resection of the symphysis pubis for the treatment of osteitis pubis. J Bone Joint Surg Am. 1989;71(3):358-364.
28. Amanatullah DF, Antkowiak T, Pillay K, et al. Femoroacetabular impingement: current concepts in diagnosis and treatment. Orthopedics. 2015;38(3):185-199.
29. Ganz R, Parvizi J, Beck M, Leunig M, Nötzli H, Siebenrock KA. Femoroacetabular impingement: a cause for osteoarthritis of the hip. Clin Orthop Relat Res. 2003;(417):112-120.
30. Redmond JM, Gupta A, Hammarstedt JE, Stake CE, Dunne KF, Domb BG. Labral injury: radiographic predictors at the time of hip arthroscopy. Arthroscopy. 2015;31(1):51-56.
31. Clohisy JC, Knaus ER, Hunt DM, Lesher JM, Harris-Hayes M, Prather H. Clinical presentation of patients with symptomatic anterior hip impingement. Clin Orthop Relat Res. 2009;467(3):638-644.
32. Klaue K, Durnin CW, Ganz R. The acetabular rim syndrome. A clinical presentation of dysplasia of the hip. J Bone Joint Surg Br. 1991;73(3):423-429.
33. Philippon MJ, Schenker ML. Arthroscopy for the treatment of femoroacetabular impingement in the athlete. Clin Sports Med. 2006;25(2):299-308.
34. McCarthy JC, Lee JA. Hip arthroscopy: indications, outcomes, and complications. Instr Course Lect. 2006;55:301-308.
1. Boyd KT, Peirce NS, Batt ME. Common hip injuries in sport. Sports Med. 1997;24(4):273-288.
2. Duthon VB, Charbonnier C, Kolo FC, et al. Correlation of clinical and magnetic resonance imaging findings in hips of elite female ballet dancers. Arthroscopy. 2013;29(3):411-419.
3. Prather H, Cheng A. Diagnosis and treatment of hip girdle pain in the athlete. PM R. 2016;8(3 suppl):S45-S60.
4. Larson CM. Sports hernia/athletic pubalgia: evaluation and management. Sports Health. 2014;6(2):139-144.
5. Bizzini M, Notzli HP, Maffiuletti NA. Femoroacetabular impingement in professional ice hockey players: a case series of 5 athletes after open surgical decompression of the hip. Am J Sports Med. 2007;35(11):1955-1959.
6. Lynch TS, Terry MA, Bedi A, Kelly BT. Hip arthroscopic surgery: patient evaluation, current indications, and outcomes. Am J Sports Med. 2013;41(5):1174-1189.
7. Anderson K, Strickland SM, Warren R. Hip and groin injuries in athletes. Am J Sports Med. 2001;29(4):521-533.
8. Fon LJ, Spence RA. Sportsman’s hernia. Br J Surg. 2000;87(5):545-552.
9. Kluin J, den Hoed PT, van Linschoten R, IJzerman JC, van Steensel CJ. Endoscopic evaluation and treatment of groin pain in the athlete. Am J Sports Med. 2004;32(4):944-949.
10. Ward D, Parvizi J. Management of hip pain in young adults. Orthop Clin North Am. 2016;47(3):485-496.
11. Byrd JW. Hip arthroscopy. J Am Acad Orthop Surg. 2006;14(7):433-444.
12. Martin HD, Palmer IJ. History and physical examination of the hip: the basics. Curr Rev Musculoskelet Med. 2013;6(3):219-225.
13. Shindle MK, Voos JE, Nho SJ, Heyworth BE, Kelly BT. Arthroscopic management of labral tears in the hip. J Bone Joint Surg Am. 2008;90(suppl 4):2-19.
14. Morelli V, Smith V. Groin injuries in athletes. Am Fam Physician. 2001;64(8):1405-1414.
15. Ekstrand J, Hagglund M, Walden M. Epidemiology of muscle injuries in professional football (soccer). Am J Sports Med. 2011;39(6):1226-1232.
16. Ekstrand J, Gillquist J. The avoidability of soccer injuries. Int J Sports Med. 1983;4(2):124-128.
17. Tyler TF, Nicholas SJ, Campbell RJ, McHugh MP. The association of hip strength and flexibility with the incidence of adductor muscle strains in professional ice hockey players. Am J Sports Med. 2001;29(2):124-128.
18. Farber AJ, Wilckens JH. Sports hernia: diagnosis and therapeutic approach. J Am Acad Orthop Surg. 2007;15(8):507-514.
19. De Paulis F, Cacchio A, Michelini O, Damiani A, Saggini R. Sports injuries in the pelvis and hip: diagnostic imaging. Eur J Radiol. 1998;27(suppl 1):S49-S59.
20. Lovell G. The diagnosis of chronic groin pain in athletes: a review of 189 cases. Aust J Sci Med Sport. 1995;27(suppl 1):76-79.
21. Strosberg DS, Ellis TJ, Renton DB. The role of femoroacetabular impingement in core muscle injury/athletic pubalgia: diagnosis and management. Front Surg. 2016;3:6.
22. Meyers WC, Foley DP, Garrett WE, Lohnes JH, Mandlebaum BR. Management of severe lower abdominal or inguinal pain in high-performance athletes. PAIN (Performing Athletes with Abdominal or Inguinal Neuromuscular Pain Study Group). Am J Sports Med. 2000;28(1):2-8.
23. Ahumada LA, Ashruf S, Espinosa-de-los-Monteros A, et al. Athletic pubalgia: definition and surgical treatment. Ann Plast Surg. 2005;55(4):393-396.
24. Angoules AG. Osteitis pubis in elite athletes: diagnostic and therapeutic approach. World J Orthop. 2015;6(9):672-679.
25. Hiti CJ, Stevens KJ, Jamati MK, Garza D, Matheson GO. Athletic osteitis pubis. Sports Med. 2011;41(5):361-376.
26. Mehin R, Meek R, O’Brien P, Blachut P. Surgery for osteitis pubis. Can J Surg. 2006;49(3):170-176.
27. Grace JN, Sim FH, Shives TC, Coventry MB. Wedge resection of the symphysis pubis for the treatment of osteitis pubis. J Bone Joint Surg Am. 1989;71(3):358-364.
28. Amanatullah DF, Antkowiak T, Pillay K, et al. Femoroacetabular impingement: current concepts in diagnosis and treatment. Orthopedics. 2015;38(3):185-199.
29. Ganz R, Parvizi J, Beck M, Leunig M, Nötzli H, Siebenrock KA. Femoroacetabular impingement: a cause for osteoarthritis of the hip. Clin Orthop Relat Res. 2003;(417):112-120.
30. Redmond JM, Gupta A, Hammarstedt JE, Stake CE, Dunne KF, Domb BG. Labral injury: radiographic predictors at the time of hip arthroscopy. Arthroscopy. 2015;31(1):51-56.
31. Clohisy JC, Knaus ER, Hunt DM, Lesher JM, Harris-Hayes M, Prather H. Clinical presentation of patients with symptomatic anterior hip impingement. Clin Orthop Relat Res. 2009;467(3):638-644.
32. Klaue K, Durnin CW, Ganz R. The acetabular rim syndrome. A clinical presentation of dysplasia of the hip. J Bone Joint Surg Br. 1991;73(3):423-429.
33. Philippon MJ, Schenker ML. Arthroscopy for the treatment of femoroacetabular impingement in the athlete. Clin Sports Med. 2006;25(2):299-308.
34. McCarthy JC, Lee JA. Hip arthroscopy: indications, outcomes, and complications. Instr Course Lect. 2006;55:301-308.
Imaging for Nonarthritic Hip Pathology
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.
AP radiographs allow for evaluation of fractures, intraosseous sclerosis, acetabular depth, inclination and version, acetabular overcoverage, joint-space narrowing, femoroacetabular congruency, femoral head sphericity, and femoral head–neck offset.7,8,10 Inspection for labral calcification is important, as it can indicate repetitive damage at the extremes of range of motion.
On AP pelvis radiographs, it is important to distinguish coxa profunda from acetabular protrusion. These entities are on the same pathomorphologic spectrum and are similar but distinctively different. Coxa profunda refers to the depth of the acetabulum relative to the ilioischial line, and acetabular protrusion refers to the depth (or medial position) of the femoral head relative to the ilioischial line. Each condition suggests—but is not diagnostic for—pincer-type femoroacetabular impingement (FAI).11Acetabular rotation is another important entity that can be evaluated on well-centered, nontilted AP pelvic radiographs. Acetabular rotation refers to the opening direction of the acetabulum. It may be anterior (anteverted), neutral, or posterior (retroverted). Anteversion is present when the anterior acetabular rim does not traverse the posterior rim shadow4; in other words, the ring formed by the acetabulum is not twisted. When the walls overlap but do not intersect, the cup has neutral version. Retroversion is qualitatively determined by the crossover (figure-of-8) and posterior wall signs12 and is associated with pincer-type FAI and the development of hip osteoarthritis.12Dunn lateral radiographs (Figure 2A), taken with 90° hip flexion, were originally used to measure femoral neck anteversion.13
False-profile radiographs (Figure 6), valuable in evaluating anterior acetabular coverage and femoral head–neck junction morphology,14,15 allow characterization of both cam-type and pincer-type FAI.
Quantitative measures warrant specific consideration (Table). Femoroacetabular morphology is quantitatively measured by α angle, Tönnis angle (acetabular inclination angle), and lateral center-edge angle (LCEA).7,8,10 The α angle (Figure 4) detects the loss of normal anterosuperior femoral head–neck junction concavity caused by a convex osseous prominence. An α angle >50° represents a cam deformity.16 In a cohort study of 338 patients, Nepple and colleagues17 qualitatively associated increased α angle with severe intra-articular hip disease. Murphy and colleagues18 found a Tönnis angle >15° to be a poor prognostic factor in untreated hip dysplasia. LCEA quantifies superolateral femoral head coverage,19 and its normal range is 20° to 40°.20 LCEA <20° indicates dysplasia of the femoroacetabular joint, and LCEA >40° indicates overcoverage and pincer-type FAI. As with any quantitative radiographic measurement, results should be interpreted within the presenting clinical context.
Radiographic findings, even findings based on these special radiographs, may underestimate the pathologic process.
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
Chondral damage is identified much as labral tears are. With chondral injury, the normal intermediate signal is interrupted by a fluid-intense signal extending to the subchondral bone. A fat-saturated T2or short-tau inversion recovery (STIR) sequence is useful in emphasizing this finding.27
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.
1. McCall DA, Safran MR. MRI and arthroscopy correlations of the hip: a case-based approach. Instr Course Lect . 2012;61:327-344.
2. Register B, Pennock AT, Ho CP, Strickland CD, Lawand A, Philippon MJ. Prevalence of abnormal hip findings in asymptomatic participants: a prospective, blinded study. Am J Sports Med . 2012;40(12):2720-2724.
3. Campbell SE. Radiography of the hip: lines, signs, and patterns of disease. Semin Roentgenol . 2005;40(3):290-319.
4. Clohisy JC, Carlisle JC, Beaulé PE, et al. A systematic approach to the plain radiographic evaluation of the young adult hip. J Bone Joint Surg Am . 2008;90(suppl 4):47-66.
5. Malviya A, Raza A, Witt JD. Reliability in the diagnosis of femoroacetabular impingement and dysplasia among hip surgeons: role of surgeon volume and experience. Hip Int . 2016;26(3):284-289.
6. Nepple JJ, Martel JM, Kim YJ, Zaltz I, Clohisy JC, Group AS. Do plain radiographs correlate with CT for imaging of cam-type femoroacetabular impingement? Clin Orthop Relat Res . 2012;470(12):3313-3320.
7. Kosuge D, Cordier T, Solomon LB, Howie DW. Dilemmas in imaging for peri-acetabular osteotomy: the influence of patient position and imaging technique on the radiological features of hip dysplasia. Bone Joint J . 2014;96(9):1155-1160.
8. Tannast M, Fritsch S, Zheng G, Siebenrock KA, Steppacher SD. Which radiographic hip parameters do not have to be corrected for pelvic rotation and tilt? Clin Orthop Relat Res . 2015;473(4):1255-1266.
9. Siebenrock KA, Kalbermatten DF, Ganz R. Effect of pelvic tilt on acetabular retroversion: a study of pelves from cadavers. Clin Orthop Relat Res . 2003;(407):241-248.
10. Griffin JW, Weber AE, Kuhns B, Lewis P, Nho SJ. Imaging in hip arthroscopy for femoroacetabular impingement: a comprehensive approach. Clin Sports Med . 2016;35(3):331-344.
11. Nepple JJ, Lehmann CL, Ross JR, Schoenecker PL, Clohisy JC. Coxa profunda is not a useful radiographic parameter for diagnosing pincer-type femoroacetabular impingement. J Bone Joint Surg Am . 2013;95(5):417-423.
12. Reynolds D, Lucas J, Klaue K. Retroversion of the acetabulum. A cause of hip pain. J Bone Joint Surg Br . 1999;81(2):281-288.
13. Dunn DM. Anteversion of the neck of the femur; a method of measurement. J Bone Joint Surg Br . 1952;34(2):181-186.
14. Meyer DC, Beck M, Ellis T, Ganz R, Leunig M. Comparison of six radiographic projections to assess femoral head/neck asphericity. Clin Orthop Relat Res . 2006;(445):181-185.
15. Hellman MD, Mascarenhas R, Gupta A, et al. The false-profile view may be used to identify cam morphology. Arthroscopy . 2015;31(9):1728-1732.
16. Barton C, Salineros MJ, Rakhra KS, Beaulé PE. Validity of the alpha angle measurement on plain radiographs in the evaluation of cam-type femoroacetabular impingement. Clin Orthop Relat Res . 2011;469(2):464-469.
17. Nepple JJ, Carlisle JC, Nunley RM, Clohisy JC. Clinical and radiographic predictors of intra-articular hip disease in arthroscopy. Am J Sports Med . 2011;39(2):296-303.
18. Murphy SB, Ganz R, Muller ME. The prognosis in untreated dysplasia of the hip. A study of radiographic factors that predict the outcome. J Bone Joint Surg Am . 1995;77(7):985-989.
19. Mast NH, Impellizzeri F, Keller S, Leunig M. Reliability and agreement of measures used in radiographic evaluation of the adult hip. Clin Orthop Relat Res . 2011;469(1):188-199.
20. Monazzam S, Bomar JD, Cidambi K, Kruk P, Hosalkar H. Lateral center-edge angle on conventional radiography and computed tomography. Clin Orthop Relat Res . 2013;471(7):2233-2237.
21. Weber AE, Jacobson JA, Bedi A. A review of imaging modalities for the hip. Curr Rev Musculoskelet Med . 2013;6(3):226-234.
22. Bencardino JT, Palmer WE. Imaging of hip disorders in athletes. Radiol Clin North Am . 2002;40(2):267-287, vi-vii.
23. Byrd JW, Jones KS. Diagnostic accuracy of clinical assessment, magnetic resonance imaging, magnetic resonance arthrography, and intra-articular injection in hip arthroscopy patients. Am J Sports Med . 2004;32(7):1668-1674.
24. Mintz DN, Hooper T, Connell D, Buly R, Padgett DE, Potter HG. Magnetic resonance imaging of the hip: detection of labral and chondral abnormalities using noncontrast imaging. Arthroscopy . 2005;21(4):385-393.
25. Blankenbaker DG, De Smet AA, Keene JS, Fine JP. Classification and localization of acetabular labral tears. Skeletal Radiol . 2007;36(5):391-397.
26. Aydingöz U, Oztürk MH. MR imaging of the acetabular labrum: a comparative study of both hips in 180 asymptomatic volunteers. Eur Radiol . 2001;11(4):567-574.
27. Gold GE, Chen CA, Koo S, Hargreaves BA, Bangerter NK. Recent advances in MRI of articular cartilage. AJR Am J Roentgenol . 2009;193(3):628-638.
28. Liong SY, Whitehouse RW. Lower extremity and pelvic stress fractures in athletes. Br J Radiol . 2012;85(1016):1148-1156.
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.
AP radiographs allow for evaluation of fractures, intraosseous sclerosis, acetabular depth, inclination and version, acetabular overcoverage, joint-space narrowing, femoroacetabular congruency, femoral head sphericity, and femoral head–neck offset.7,8,10 Inspection for labral calcification is important, as it can indicate repetitive damage at the extremes of range of motion.
On AP pelvis radiographs, it is important to distinguish coxa profunda from acetabular protrusion. These entities are on the same pathomorphologic spectrum and are similar but distinctively different. Coxa profunda refers to the depth of the acetabulum relative to the ilioischial line, and acetabular protrusion refers to the depth (or medial position) of the femoral head relative to the ilioischial line. Each condition suggests—but is not diagnostic for—pincer-type femoroacetabular impingement (FAI).11Acetabular rotation is another important entity that can be evaluated on well-centered, nontilted AP pelvic radiographs. Acetabular rotation refers to the opening direction of the acetabulum. It may be anterior (anteverted), neutral, or posterior (retroverted). Anteversion is present when the anterior acetabular rim does not traverse the posterior rim shadow4; in other words, the ring formed by the acetabulum is not twisted. When the walls overlap but do not intersect, the cup has neutral version. Retroversion is qualitatively determined by the crossover (figure-of-8) and posterior wall signs12 and is associated with pincer-type FAI and the development of hip osteoarthritis.12Dunn lateral radiographs (Figure 2A), taken with 90° hip flexion, were originally used to measure femoral neck anteversion.13
False-profile radiographs (Figure 6), valuable in evaluating anterior acetabular coverage and femoral head–neck junction morphology,14,15 allow characterization of both cam-type and pincer-type FAI.
Quantitative measures warrant specific consideration (Table). Femoroacetabular morphology is quantitatively measured by α angle, Tönnis angle (acetabular inclination angle), and lateral center-edge angle (LCEA).7,8,10 The α angle (Figure 4) detects the loss of normal anterosuperior femoral head–neck junction concavity caused by a convex osseous prominence. An α angle >50° represents a cam deformity.16 In a cohort study of 338 patients, Nepple and colleagues17 qualitatively associated increased α angle with severe intra-articular hip disease. Murphy and colleagues18 found a Tönnis angle >15° to be a poor prognostic factor in untreated hip dysplasia. LCEA quantifies superolateral femoral head coverage,19 and its normal range is 20° to 40°.20 LCEA <20° indicates dysplasia of the femoroacetabular joint, and LCEA >40° indicates overcoverage and pincer-type FAI. As with any quantitative radiographic measurement, results should be interpreted within the presenting clinical context.
Radiographic findings, even findings based on these special radiographs, may underestimate the pathologic process.
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
Chondral damage is identified much as labral tears are. With chondral injury, the normal intermediate signal is interrupted by a fluid-intense signal extending to the subchondral bone. A fat-saturated T2or short-tau inversion recovery (STIR) sequence is useful in emphasizing this finding.27
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.
AP radiographs allow for evaluation of fractures, intraosseous sclerosis, acetabular depth, inclination and version, acetabular overcoverage, joint-space narrowing, femoroacetabular congruency, femoral head sphericity, and femoral head–neck offset.7,8,10 Inspection for labral calcification is important, as it can indicate repetitive damage at the extremes of range of motion.
On AP pelvis radiographs, it is important to distinguish coxa profunda from acetabular protrusion. These entities are on the same pathomorphologic spectrum and are similar but distinctively different. Coxa profunda refers to the depth of the acetabulum relative to the ilioischial line, and acetabular protrusion refers to the depth (or medial position) of the femoral head relative to the ilioischial line. Each condition suggests—but is not diagnostic for—pincer-type femoroacetabular impingement (FAI).11Acetabular rotation is another important entity that can be evaluated on well-centered, nontilted AP pelvic radiographs. Acetabular rotation refers to the opening direction of the acetabulum. It may be anterior (anteverted), neutral, or posterior (retroverted). Anteversion is present when the anterior acetabular rim does not traverse the posterior rim shadow4; in other words, the ring formed by the acetabulum is not twisted. When the walls overlap but do not intersect, the cup has neutral version. Retroversion is qualitatively determined by the crossover (figure-of-8) and posterior wall signs12 and is associated with pincer-type FAI and the development of hip osteoarthritis.12Dunn lateral radiographs (Figure 2A), taken with 90° hip flexion, were originally used to measure femoral neck anteversion.13
False-profile radiographs (Figure 6), valuable in evaluating anterior acetabular coverage and femoral head–neck junction morphology,14,15 allow characterization of both cam-type and pincer-type FAI.
Quantitative measures warrant specific consideration (Table). Femoroacetabular morphology is quantitatively measured by α angle, Tönnis angle (acetabular inclination angle), and lateral center-edge angle (LCEA).7,8,10 The α angle (Figure 4) detects the loss of normal anterosuperior femoral head–neck junction concavity caused by a convex osseous prominence. An α angle >50° represents a cam deformity.16 In a cohort study of 338 patients, Nepple and colleagues17 qualitatively associated increased α angle with severe intra-articular hip disease. Murphy and colleagues18 found a Tönnis angle >15° to be a poor prognostic factor in untreated hip dysplasia. LCEA quantifies superolateral femoral head coverage,19 and its normal range is 20° to 40°.20 LCEA <20° indicates dysplasia of the femoroacetabular joint, and LCEA >40° indicates overcoverage and pincer-type FAI. As with any quantitative radiographic measurement, results should be interpreted within the presenting clinical context.
Radiographic findings, even findings based on these special radiographs, may underestimate the pathologic process.
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
Chondral damage is identified much as labral tears are. With chondral injury, the normal intermediate signal is interrupted by a fluid-intense signal extending to the subchondral bone. A fat-saturated T2or short-tau inversion recovery (STIR) sequence is useful in emphasizing this finding.27
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.
1. McCall DA, Safran MR. MRI and arthroscopy correlations of the hip: a case-based approach. Instr Course Lect . 2012;61:327-344.
2. Register B, Pennock AT, Ho CP, Strickland CD, Lawand A, Philippon MJ. Prevalence of abnormal hip findings in asymptomatic participants: a prospective, blinded study. Am J Sports Med . 2012;40(12):2720-2724.
3. Campbell SE. Radiography of the hip: lines, signs, and patterns of disease. Semin Roentgenol . 2005;40(3):290-319.
4. Clohisy JC, Carlisle JC, Beaulé PE, et al. A systematic approach to the plain radiographic evaluation of the young adult hip. J Bone Joint Surg Am . 2008;90(suppl 4):47-66.
5. Malviya A, Raza A, Witt JD. Reliability in the diagnosis of femoroacetabular impingement and dysplasia among hip surgeons: role of surgeon volume and experience. Hip Int . 2016;26(3):284-289.
6. Nepple JJ, Martel JM, Kim YJ, Zaltz I, Clohisy JC, Group AS. Do plain radiographs correlate with CT for imaging of cam-type femoroacetabular impingement? Clin Orthop Relat Res . 2012;470(12):3313-3320.
7. Kosuge D, Cordier T, Solomon LB, Howie DW. Dilemmas in imaging for peri-acetabular osteotomy: the influence of patient position and imaging technique on the radiological features of hip dysplasia. Bone Joint J . 2014;96(9):1155-1160.
8. Tannast M, Fritsch S, Zheng G, Siebenrock KA, Steppacher SD. Which radiographic hip parameters do not have to be corrected for pelvic rotation and tilt? Clin Orthop Relat Res . 2015;473(4):1255-1266.
9. Siebenrock KA, Kalbermatten DF, Ganz R. Effect of pelvic tilt on acetabular retroversion: a study of pelves from cadavers. Clin Orthop Relat Res . 2003;(407):241-248.
10. Griffin JW, Weber AE, Kuhns B, Lewis P, Nho SJ. Imaging in hip arthroscopy for femoroacetabular impingement: a comprehensive approach. Clin Sports Med . 2016;35(3):331-344.
11. Nepple JJ, Lehmann CL, Ross JR, Schoenecker PL, Clohisy JC. Coxa profunda is not a useful radiographic parameter for diagnosing pincer-type femoroacetabular impingement. J Bone Joint Surg Am . 2013;95(5):417-423.
12. Reynolds D, Lucas J, Klaue K. Retroversion of the acetabulum. A cause of hip pain. J Bone Joint Surg Br . 1999;81(2):281-288.
13. Dunn DM. Anteversion of the neck of the femur; a method of measurement. J Bone Joint Surg Br . 1952;34(2):181-186.
14. Meyer DC, Beck M, Ellis T, Ganz R, Leunig M. Comparison of six radiographic projections to assess femoral head/neck asphericity. Clin Orthop Relat Res . 2006;(445):181-185.
15. Hellman MD, Mascarenhas R, Gupta A, et al. The false-profile view may be used to identify cam morphology. Arthroscopy . 2015;31(9):1728-1732.
16. Barton C, Salineros MJ, Rakhra KS, Beaulé PE. Validity of the alpha angle measurement on plain radiographs in the evaluation of cam-type femoroacetabular impingement. Clin Orthop Relat Res . 2011;469(2):464-469.
17. Nepple JJ, Carlisle JC, Nunley RM, Clohisy JC. Clinical and radiographic predictors of intra-articular hip disease in arthroscopy. Am J Sports Med . 2011;39(2):296-303.
18. Murphy SB, Ganz R, Muller ME. The prognosis in untreated dysplasia of the hip. A study of radiographic factors that predict the outcome. J Bone Joint Surg Am . 1995;77(7):985-989.
19. Mast NH, Impellizzeri F, Keller S, Leunig M. Reliability and agreement of measures used in radiographic evaluation of the adult hip. Clin Orthop Relat Res . 2011;469(1):188-199.
20. Monazzam S, Bomar JD, Cidambi K, Kruk P, Hosalkar H. Lateral center-edge angle on conventional radiography and computed tomography. Clin Orthop Relat Res . 2013;471(7):2233-2237.
21. Weber AE, Jacobson JA, Bedi A. A review of imaging modalities for the hip. Curr Rev Musculoskelet Med . 2013;6(3):226-234.
22. Bencardino JT, Palmer WE. Imaging of hip disorders in athletes. Radiol Clin North Am . 2002;40(2):267-287, vi-vii.
23. Byrd JW, Jones KS. Diagnostic accuracy of clinical assessment, magnetic resonance imaging, magnetic resonance arthrography, and intra-articular injection in hip arthroscopy patients. Am J Sports Med . 2004;32(7):1668-1674.
24. Mintz DN, Hooper T, Connell D, Buly R, Padgett DE, Potter HG. Magnetic resonance imaging of the hip: detection of labral and chondral abnormalities using noncontrast imaging. Arthroscopy . 2005;21(4):385-393.
25. Blankenbaker DG, De Smet AA, Keene JS, Fine JP. Classification and localization of acetabular labral tears. Skeletal Radiol . 2007;36(5):391-397.
26. Aydingöz U, Oztürk MH. MR imaging of the acetabular labrum: a comparative study of both hips in 180 asymptomatic volunteers. Eur Radiol . 2001;11(4):567-574.
27. Gold GE, Chen CA, Koo S, Hargreaves BA, Bangerter NK. Recent advances in MRI of articular cartilage. AJR Am J Roentgenol . 2009;193(3):628-638.
28. Liong SY, Whitehouse RW. Lower extremity and pelvic stress fractures in athletes. Br J Radiol . 2012;85(1016):1148-1156.
1. McCall DA, Safran MR. MRI and arthroscopy correlations of the hip: a case-based approach. Instr Course Lect . 2012;61:327-344.
2. Register B, Pennock AT, Ho CP, Strickland CD, Lawand A, Philippon MJ. Prevalence of abnormal hip findings in asymptomatic participants: a prospective, blinded study. Am J Sports Med . 2012;40(12):2720-2724.
3. Campbell SE. Radiography of the hip: lines, signs, and patterns of disease. Semin Roentgenol . 2005;40(3):290-319.
4. Clohisy JC, Carlisle JC, Beaulé PE, et al. A systematic approach to the plain radiographic evaluation of the young adult hip. J Bone Joint Surg Am . 2008;90(suppl 4):47-66.
5. Malviya A, Raza A, Witt JD. Reliability in the diagnosis of femoroacetabular impingement and dysplasia among hip surgeons: role of surgeon volume and experience. Hip Int . 2016;26(3):284-289.
6. Nepple JJ, Martel JM, Kim YJ, Zaltz I, Clohisy JC, Group AS. Do plain radiographs correlate with CT for imaging of cam-type femoroacetabular impingement? Clin Orthop Relat Res . 2012;470(12):3313-3320.
7. Kosuge D, Cordier T, Solomon LB, Howie DW. Dilemmas in imaging for peri-acetabular osteotomy: the influence of patient position and imaging technique on the radiological features of hip dysplasia. Bone Joint J . 2014;96(9):1155-1160.
8. Tannast M, Fritsch S, Zheng G, Siebenrock KA, Steppacher SD. Which radiographic hip parameters do not have to be corrected for pelvic rotation and tilt? Clin Orthop Relat Res . 2015;473(4):1255-1266.
9. Siebenrock KA, Kalbermatten DF, Ganz R. Effect of pelvic tilt on acetabular retroversion: a study of pelves from cadavers. Clin Orthop Relat Res . 2003;(407):241-248.
10. Griffin JW, Weber AE, Kuhns B, Lewis P, Nho SJ. Imaging in hip arthroscopy for femoroacetabular impingement: a comprehensive approach. Clin Sports Med . 2016;35(3):331-344.
11. Nepple JJ, Lehmann CL, Ross JR, Schoenecker PL, Clohisy JC. Coxa profunda is not a useful radiographic parameter for diagnosing pincer-type femoroacetabular impingement. J Bone Joint Surg Am . 2013;95(5):417-423.
12. Reynolds D, Lucas J, Klaue K. Retroversion of the acetabulum. A cause of hip pain. J Bone Joint Surg Br . 1999;81(2):281-288.
13. Dunn DM. Anteversion of the neck of the femur; a method of measurement. J Bone Joint Surg Br . 1952;34(2):181-186.
14. Meyer DC, Beck M, Ellis T, Ganz R, Leunig M. Comparison of six radiographic projections to assess femoral head/neck asphericity. Clin Orthop Relat Res . 2006;(445):181-185.
15. Hellman MD, Mascarenhas R, Gupta A, et al. The false-profile view may be used to identify cam morphology. Arthroscopy . 2015;31(9):1728-1732.
16. Barton C, Salineros MJ, Rakhra KS, Beaulé PE. Validity of the alpha angle measurement on plain radiographs in the evaluation of cam-type femoroacetabular impingement. Clin Orthop Relat Res . 2011;469(2):464-469.
17. Nepple JJ, Carlisle JC, Nunley RM, Clohisy JC. Clinical and radiographic predictors of intra-articular hip disease in arthroscopy. Am J Sports Med . 2011;39(2):296-303.
18. Murphy SB, Ganz R, Muller ME. The prognosis in untreated dysplasia of the hip. A study of radiographic factors that predict the outcome. J Bone Joint Surg Am . 1995;77(7):985-989.
19. Mast NH, Impellizzeri F, Keller S, Leunig M. Reliability and agreement of measures used in radiographic evaluation of the adult hip. Clin Orthop Relat Res . 2011;469(1):188-199.
20. Monazzam S, Bomar JD, Cidambi K, Kruk P, Hosalkar H. Lateral center-edge angle on conventional radiography and computed tomography. Clin Orthop Relat Res . 2013;471(7):2233-2237.
21. Weber AE, Jacobson JA, Bedi A. A review of imaging modalities for the hip. Curr Rev Musculoskelet Med . 2013;6(3):226-234.
22. Bencardino JT, Palmer WE. Imaging of hip disorders in athletes. Radiol Clin North Am . 2002;40(2):267-287, vi-vii.
23. Byrd JW, Jones KS. Diagnostic accuracy of clinical assessment, magnetic resonance imaging, magnetic resonance arthrography, and intra-articular injection in hip arthroscopy patients. Am J Sports Med . 2004;32(7):1668-1674.
24. Mintz DN, Hooper T, Connell D, Buly R, Padgett DE, Potter HG. Magnetic resonance imaging of the hip: detection of labral and chondral abnormalities using noncontrast imaging. Arthroscopy . 2005;21(4):385-393.
25. Blankenbaker DG, De Smet AA, Keene JS, Fine JP. Classification and localization of acetabular labral tears. Skeletal Radiol . 2007;36(5):391-397.
26. Aydingöz U, Oztürk MH. MR imaging of the acetabular labrum: a comparative study of both hips in 180 asymptomatic volunteers. Eur Radiol . 2001;11(4):567-574.
27. Gold GE, Chen CA, Koo S, Hargreaves BA, Bangerter NK. Recent advances in MRI of articular cartilage. AJR Am J Roentgenol . 2009;193(3):628-638.
28. Liong SY, Whitehouse RW. Lower extremity and pelvic stress fractures in athletes. Br J Radiol . 2012;85(1016):1148-1156.
Treatment of Femoroacetabular Impingement: Labrum, Cartilage, Osseous Deformity, and Capsule
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.
With proper patient selection, these techniques have excellent clinical outcomes.4,7 Severe osteoarthritis (joint space <2 mm) is a contraindication for these procedures.8
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).
A hypertrophic AIIS can impinge the femur (extra-articular subspinal impingement). Patients present with limited range of motion (especially hip flexion), pain in the AIIS area, and, in some cases, a history of avulsion injury.11 Seeing a bruised labrum (Figure 3) during surgery is common with this pathology.
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).
A ring curette is used to prepare the defect, and perpendicular borders are created to hold the clot in place. Deep débridement removes the calcified layer while maintaining the integrity of the subchondral plate.15 As a recent study found microfracture performed with small-diameter awls improved cartilage repair more effectively than microfracture with large-diameter awls,16 we prefer making small-diameter holes when establishing the maximum number of holes possible. As it is important to make a perpendicular hole, not a scratch, we use an XL Microfracture Pick (Smith & Nephew) 90° curve, which is suitable for creating a vertical entry point. The 60° curved awl is then used to further deepen the hole. Creation and stability of the marrow clot are ensured by shutting down the infusion pump device and verifying that blood and marrow elements are released from the microfractures.
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.
1. Philippon MJ, Nepple JJ, Campbell KJ, et al. The hip fluid seal—part I: the effect of an acetabular labral tear, repair, resection, and reconstruction on hip fluid pressurization. Knee Surg Sports Traumatol Arthrosc. 2014;22(4):722-729.
2. Philippon MJ, Faucet SC, Briggs KK. Arthroscopic hip labral repair. Arthrosc Tech. 2013;2(2):e73-e76.
3. Lertwanich P, Ejnisman L, Torry MR, Giphart JE, Philippon MJ. Defining a safety margin for labral suture anchor insertion using the acetabular rim angle. Am J Sports Med. 2011;39(suppl):111S-116S.
4. Sawyer GA, Briggs KK, Dornan GJ, Ommen ND, Philippon MJ. Clinical outcomes after arthroscopic hip labral repair using looped versus pierced suture techniques. Am J Sports Med. 2015;43(7):1683-1688.
5. Ferro FP, Philippon MJ, Rasmussen MT, Smith SD, LaPrade RF, Wijdicks CA. Tensile properties of the human acetabular labrum and hip labral reconstruction grafts. Am J Sports Med. 2015;43(5):1222-1227.
6. Philippon MJ, Briggs KK, Boykin RE. Results of arthroscopic labral reconstruction of the hip in elite athletes: response. Am J Sports Med. 2014;42(10):NP48.
7. Geyer MR, Philippon MJ, Fagrelius TS, Briggs KK. Acetabular labral reconstruction with an iliotibial band autograft: outcome and survivorship analysis at minimum 3-year follow-up. Am J Sports Med. 2013;41(8):1750-1756.
8. Skendzel JG, Philippon MJ, Briggs KK, Goljan P. The effect of joint space on midterm outcomes after arthroscopic hip surgery for femoroacetabular impingement. Am J Sports Med. 2014;42(5):1127-1133.
9. Yeung M, Kowalczuk M, Simunovic N, Ayeni OR. Hip arthroscopy in the setting of hip dysplasia: a systematic review. Bone Joint Res. 2016;5(6):225-231.
10. Locks R, Chahla J, Mitchell JJ, Soares E, Philippon MJ. Dynamic hip examination for assesment of impingement during hip arthroscopy. Arthroscopy Tech. 2016 Nov 28. http://dx.doi.org/10.1016/j.eats.2016.08.011
11. Nabhan DC, Moreau WJ, McNamara SC, Briggs KK, Philippon MJ. Subspine hip impingement: an unusual cause of hip pain in an elite weightlifter. Curr Sports Med Rep. 2016;15(5):315-319.
12. Philippon MJ, Michalski MP, Campbell KJ, et al. An anatomical study of the acetabulum with clinical applications to hip arthroscopy. J Bone Joint Surg Am. 2014;96(20):1673-1682.
13. Ho CP, Ommen ND, Bhatia S, et al. Predictive value of 3-T magnetic resonance imaging in diagnosing grade 3 and 4 chondral lesions in the hip. Arthroscopy. 2016;32(9):1808-1813.
14. Bhatia S, Nowak DD, Briggs KK, Patterson DC, Philippon MJ. Outerbridge grade IV cartilage lesions in the hip identified at arthroscopy. Arthroscopy. 2016;32(5):814-819.
15. Frisbie DD, Morisset S, Ho CP, Rodkey WG, Steadman JR, McIlwraith CW. Effects of calcified cartilage on healing of chondral defects treated with microfracture in horses. Am J Sports Med. 2006;34(11):1824-1831.
16. Orth P, Duffner J, Zurakowski D, Cucchiarini M, Madry H. Small-diameter awls improve articular cartilage repair after microfracture treatment in a translational animal model. Am J Sports Med. 2016;44(1):209-219.
17. Domb BG, Philippon MJ, Giordano BD. Arthroscopic capsulotomy, capsular repair, and capsular plication of the hip: relation to atraumatic instability. Arthroscopy. 2013;29(1):162-173.
18. Asopa V, Singh PJ. The intracapsular atraumatic arthroscopic technique for closure of the hip capsule. Arthrosc Tech. 2014;3(2):e245-e247.
19. Frank RM, Lee S, Bush-Joseph CA, Kelly BT, Salata MJ, Nho SJ. Improved outcomes after hip arthroscopic surgery in patients undergoing T-capsulotomy with complete repair versus partial repair for femoroacetabular impingement: a comparative matched-pair analysis. Am J Sports Med. 2014;42(11):2634-2642.
20. Menge TJ, Chahla J, Soares E, Mitchell JJ, Philippon MJ. The Quebec City slider: a technique for capsular closure and plication in hip arthroscopy. Arthrosc Tech. 2016;5(5):e971-e974.
21. Chahla J, Mikula JD, Schon JM, et al. Hip capsular closure: a biomechanical analysis of failure torque. Am J Sports Med. doi:10.1177/0363546516666353.
22. Philippon MJ, Schenker ML, Briggs KK, Kuppersmith DA, Maxwell RB, Stubbs AJ. Revision hip arthroscopy. Am J Sports Med. 2007;35(11):1918-1921.
23. Trindade CA, Sawyer GA, Fukui K, Briggs KK, Philippon MJ. Arthroscopic capsule reconstruction in the hip using iliotibial band allograft. Arthrosc Tech. 2015;4(1):e71-e74.
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.
With proper patient selection, these techniques have excellent clinical outcomes.4,7 Severe osteoarthritis (joint space <2 mm) is a contraindication for these procedures.8
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).
A hypertrophic AIIS can impinge the femur (extra-articular subspinal impingement). Patients present with limited range of motion (especially hip flexion), pain in the AIIS area, and, in some cases, a history of avulsion injury.11 Seeing a bruised labrum (Figure 3) during surgery is common with this pathology.
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).
A ring curette is used to prepare the defect, and perpendicular borders are created to hold the clot in place. Deep débridement removes the calcified layer while maintaining the integrity of the subchondral plate.15 As a recent study found microfracture performed with small-diameter awls improved cartilage repair more effectively than microfracture with large-diameter awls,16 we prefer making small-diameter holes when establishing the maximum number of holes possible. As it is important to make a perpendicular hole, not a scratch, we use an XL Microfracture Pick (Smith & Nephew) 90° curve, which is suitable for creating a vertical entry point. The 60° curved awl is then used to further deepen the hole. Creation and stability of the marrow clot are ensured by shutting down the infusion pump device and verifying that blood and marrow elements are released from the microfractures.
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.
With proper patient selection, these techniques have excellent clinical outcomes.4,7 Severe osteoarthritis (joint space <2 mm) is a contraindication for these procedures.8
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).
A hypertrophic AIIS can impinge the femur (extra-articular subspinal impingement). Patients present with limited range of motion (especially hip flexion), pain in the AIIS area, and, in some cases, a history of avulsion injury.11 Seeing a bruised labrum (Figure 3) during surgery is common with this pathology.
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).
A ring curette is used to prepare the defect, and perpendicular borders are created to hold the clot in place. Deep débridement removes the calcified layer while maintaining the integrity of the subchondral plate.15 As a recent study found microfracture performed with small-diameter awls improved cartilage repair more effectively than microfracture with large-diameter awls,16 we prefer making small-diameter holes when establishing the maximum number of holes possible. As it is important to make a perpendicular hole, not a scratch, we use an XL Microfracture Pick (Smith & Nephew) 90° curve, which is suitable for creating a vertical entry point. The 60° curved awl is then used to further deepen the hole. Creation and stability of the marrow clot are ensured by shutting down the infusion pump device and verifying that blood and marrow elements are released from the microfractures.
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.
1. Philippon MJ, Nepple JJ, Campbell KJ, et al. The hip fluid seal—part I: the effect of an acetabular labral tear, repair, resection, and reconstruction on hip fluid pressurization. Knee Surg Sports Traumatol Arthrosc. 2014;22(4):722-729.
2. Philippon MJ, Faucet SC, Briggs KK. Arthroscopic hip labral repair. Arthrosc Tech. 2013;2(2):e73-e76.
3. Lertwanich P, Ejnisman L, Torry MR, Giphart JE, Philippon MJ. Defining a safety margin for labral suture anchor insertion using the acetabular rim angle. Am J Sports Med. 2011;39(suppl):111S-116S.
4. Sawyer GA, Briggs KK, Dornan GJ, Ommen ND, Philippon MJ. Clinical outcomes after arthroscopic hip labral repair using looped versus pierced suture techniques. Am J Sports Med. 2015;43(7):1683-1688.
5. Ferro FP, Philippon MJ, Rasmussen MT, Smith SD, LaPrade RF, Wijdicks CA. Tensile properties of the human acetabular labrum and hip labral reconstruction grafts. Am J Sports Med. 2015;43(5):1222-1227.
6. Philippon MJ, Briggs KK, Boykin RE. Results of arthroscopic labral reconstruction of the hip in elite athletes: response. Am J Sports Med. 2014;42(10):NP48.
7. Geyer MR, Philippon MJ, Fagrelius TS, Briggs KK. Acetabular labral reconstruction with an iliotibial band autograft: outcome and survivorship analysis at minimum 3-year follow-up. Am J Sports Med. 2013;41(8):1750-1756.
8. Skendzel JG, Philippon MJ, Briggs KK, Goljan P. The effect of joint space on midterm outcomes after arthroscopic hip surgery for femoroacetabular impingement. Am J Sports Med. 2014;42(5):1127-1133.
9. Yeung M, Kowalczuk M, Simunovic N, Ayeni OR. Hip arthroscopy in the setting of hip dysplasia: a systematic review. Bone Joint Res. 2016;5(6):225-231.
10. Locks R, Chahla J, Mitchell JJ, Soares E, Philippon MJ. Dynamic hip examination for assesment of impingement during hip arthroscopy. Arthroscopy Tech. 2016 Nov 28. http://dx.doi.org/10.1016/j.eats.2016.08.011
11. Nabhan DC, Moreau WJ, McNamara SC, Briggs KK, Philippon MJ. Subspine hip impingement: an unusual cause of hip pain in an elite weightlifter. Curr Sports Med Rep. 2016;15(5):315-319.
12. Philippon MJ, Michalski MP, Campbell KJ, et al. An anatomical study of the acetabulum with clinical applications to hip arthroscopy. J Bone Joint Surg Am. 2014;96(20):1673-1682.
13. Ho CP, Ommen ND, Bhatia S, et al. Predictive value of 3-T magnetic resonance imaging in diagnosing grade 3 and 4 chondral lesions in the hip. Arthroscopy. 2016;32(9):1808-1813.
14. Bhatia S, Nowak DD, Briggs KK, Patterson DC, Philippon MJ. Outerbridge grade IV cartilage lesions in the hip identified at arthroscopy. Arthroscopy. 2016;32(5):814-819.
15. Frisbie DD, Morisset S, Ho CP, Rodkey WG, Steadman JR, McIlwraith CW. Effects of calcified cartilage on healing of chondral defects treated with microfracture in horses. Am J Sports Med. 2006;34(11):1824-1831.
16. Orth P, Duffner J, Zurakowski D, Cucchiarini M, Madry H. Small-diameter awls improve articular cartilage repair after microfracture treatment in a translational animal model. Am J Sports Med. 2016;44(1):209-219.
17. Domb BG, Philippon MJ, Giordano BD. Arthroscopic capsulotomy, capsular repair, and capsular plication of the hip: relation to atraumatic instability. Arthroscopy. 2013;29(1):162-173.
18. Asopa V, Singh PJ. The intracapsular atraumatic arthroscopic technique for closure of the hip capsule. Arthrosc Tech. 2014;3(2):e245-e247.
19. Frank RM, Lee S, Bush-Joseph CA, Kelly BT, Salata MJ, Nho SJ. Improved outcomes after hip arthroscopic surgery in patients undergoing T-capsulotomy with complete repair versus partial repair for femoroacetabular impingement: a comparative matched-pair analysis. Am J Sports Med. 2014;42(11):2634-2642.
20. Menge TJ, Chahla J, Soares E, Mitchell JJ, Philippon MJ. The Quebec City slider: a technique for capsular closure and plication in hip arthroscopy. Arthrosc Tech. 2016;5(5):e971-e974.
21. Chahla J, Mikula JD, Schon JM, et al. Hip capsular closure: a biomechanical analysis of failure torque. Am J Sports Med. doi:10.1177/0363546516666353.
22. Philippon MJ, Schenker ML, Briggs KK, Kuppersmith DA, Maxwell RB, Stubbs AJ. Revision hip arthroscopy. Am J Sports Med. 2007;35(11):1918-1921.
23. Trindade CA, Sawyer GA, Fukui K, Briggs KK, Philippon MJ. Arthroscopic capsule reconstruction in the hip using iliotibial band allograft. Arthrosc Tech. 2015;4(1):e71-e74.
1. Philippon MJ, Nepple JJ, Campbell KJ, et al. The hip fluid seal—part I: the effect of an acetabular labral tear, repair, resection, and reconstruction on hip fluid pressurization. Knee Surg Sports Traumatol Arthrosc. 2014;22(4):722-729.
2. Philippon MJ, Faucet SC, Briggs KK. Arthroscopic hip labral repair. Arthrosc Tech. 2013;2(2):e73-e76.
3. Lertwanich P, Ejnisman L, Torry MR, Giphart JE, Philippon MJ. Defining a safety margin for labral suture anchor insertion using the acetabular rim angle. Am J Sports Med. 2011;39(suppl):111S-116S.
4. Sawyer GA, Briggs KK, Dornan GJ, Ommen ND, Philippon MJ. Clinical outcomes after arthroscopic hip labral repair using looped versus pierced suture techniques. Am J Sports Med. 2015;43(7):1683-1688.
5. Ferro FP, Philippon MJ, Rasmussen MT, Smith SD, LaPrade RF, Wijdicks CA. Tensile properties of the human acetabular labrum and hip labral reconstruction grafts. Am J Sports Med. 2015;43(5):1222-1227.
6. Philippon MJ, Briggs KK, Boykin RE. Results of arthroscopic labral reconstruction of the hip in elite athletes: response. Am J Sports Med. 2014;42(10):NP48.
7. Geyer MR, Philippon MJ, Fagrelius TS, Briggs KK. Acetabular labral reconstruction with an iliotibial band autograft: outcome and survivorship analysis at minimum 3-year follow-up. Am J Sports Med. 2013;41(8):1750-1756.
8. Skendzel JG, Philippon MJ, Briggs KK, Goljan P. The effect of joint space on midterm outcomes after arthroscopic hip surgery for femoroacetabular impingement. Am J Sports Med. 2014;42(5):1127-1133.
9. Yeung M, Kowalczuk M, Simunovic N, Ayeni OR. Hip arthroscopy in the setting of hip dysplasia: a systematic review. Bone Joint Res. 2016;5(6):225-231.
10. Locks R, Chahla J, Mitchell JJ, Soares E, Philippon MJ. Dynamic hip examination for assesment of impingement during hip arthroscopy. Arthroscopy Tech. 2016 Nov 28. http://dx.doi.org/10.1016/j.eats.2016.08.011
11. Nabhan DC, Moreau WJ, McNamara SC, Briggs KK, Philippon MJ. Subspine hip impingement: an unusual cause of hip pain in an elite weightlifter. Curr Sports Med Rep. 2016;15(5):315-319.
12. Philippon MJ, Michalski MP, Campbell KJ, et al. An anatomical study of the acetabulum with clinical applications to hip arthroscopy. J Bone Joint Surg Am. 2014;96(20):1673-1682.
13. Ho CP, Ommen ND, Bhatia S, et al. Predictive value of 3-T magnetic resonance imaging in diagnosing grade 3 and 4 chondral lesions in the hip. Arthroscopy. 2016;32(9):1808-1813.
14. Bhatia S, Nowak DD, Briggs KK, Patterson DC, Philippon MJ. Outerbridge grade IV cartilage lesions in the hip identified at arthroscopy. Arthroscopy. 2016;32(5):814-819.
15. Frisbie DD, Morisset S, Ho CP, Rodkey WG, Steadman JR, McIlwraith CW. Effects of calcified cartilage on healing of chondral defects treated with microfracture in horses. Am J Sports Med. 2006;34(11):1824-1831.
16. Orth P, Duffner J, Zurakowski D, Cucchiarini M, Madry H. Small-diameter awls improve articular cartilage repair after microfracture treatment in a translational animal model. Am J Sports Med. 2016;44(1):209-219.
17. Domb BG, Philippon MJ, Giordano BD. Arthroscopic capsulotomy, capsular repair, and capsular plication of the hip: relation to atraumatic instability. Arthroscopy. 2013;29(1):162-173.
18. Asopa V, Singh PJ. The intracapsular atraumatic arthroscopic technique for closure of the hip capsule. Arthrosc Tech. 2014;3(2):e245-e247.
19. Frank RM, Lee S, Bush-Joseph CA, Kelly BT, Salata MJ, Nho SJ. Improved outcomes after hip arthroscopic surgery in patients undergoing T-capsulotomy with complete repair versus partial repair for femoroacetabular impingement: a comparative matched-pair analysis. Am J Sports Med. 2014;42(11):2634-2642.
20. Menge TJ, Chahla J, Soares E, Mitchell JJ, Philippon MJ. The Quebec City slider: a technique for capsular closure and plication in hip arthroscopy. Arthrosc Tech. 2016;5(5):e971-e974.
21. Chahla J, Mikula JD, Schon JM, et al. Hip capsular closure: a biomechanical analysis of failure torque. Am J Sports Med. doi:10.1177/0363546516666353.
22. Philippon MJ, Schenker ML, Briggs KK, Kuppersmith DA, Maxwell RB, Stubbs AJ. Revision hip arthroscopy. Am J Sports Med. 2007;35(11):1918-1921.
23. Trindade CA, Sawyer GA, Fukui K, Briggs KK, Philippon MJ. Arthroscopic capsule reconstruction in the hip using iliotibial band allograft. Arthrosc Tech. 2015;4(1):e71-e74.