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2017 Update on obstetrics
In this Update we discuss several exciting new recommendations for preventive treatments in pregnancy and prenatal diagnostic tests. Our A-to-Z coverage includes:
- antenatal steroids in late preterm pregnancy
- expanded list of high-risk conditions warranting low-dose aspirin for preeclampsia prevention
- chromosomal microarray analysis versus karyotype for specific clinical situations
- Zika virus infection evolving information.
Next: New recommendation for timing of late preterm antenatal steroids
New recommendation offered for timing of late preterm antenatal steroids
Gyamfi-Bannerman C, Thom EA, Blackwell SC, et al; for the NICHD Maternal-Fetal Medicine Units Network. Antenatal betamethasone for women at risk for late preterm delivery. N Engl J Med. 2016;374(14):1311-1320.
American College of Obstetricians and Gynecologists. Committee Opinion No. 677. Antenatal corticosteroidtherapy for fetal maturation. Obstet Gynecol. 2016;128(4):e187-e194.
Kamath-Rayne BD, Rozance PJ, Goldenberg RL, Jobe AH. Antenatal corticosteroids beyond 34 weeks gestation: what do we do now? Am J Obstet Gynecol. 2016;215(4):423-430.
A dramatic recommendation for obstetric practice change occurred in 2016: the option of administering antenatal steroids for fetal lung maturity after 34 weeks. In the Antenatal Late Preterm Steroids (ALPS) trial of betamethasone in the late preterm period in patients at "high risk" of imminent delivery, Gyamfi-Bannerman and colleagues demonstrated that the treated group had a significant decrease in the rate of neonatal respiratory complications.
The primary outcome, a composite of respiratory morbidities (including transient tachypnea of the newborn, surfactant use, and need for resuscitation at birth) within the first 72 hours of life, had significant differences between groups, occurring in 165 of 1,427 infants (11.6%) in the betamethasone-treated group and 202 of 1,400 (14.4%) in the placebo group (relative risk in the betamethasone group, 0.80; 95% confidence interval, 0.66-0.97; P = .02). However, there was no statistically significant difference in respiratory distress syndrome, apnea, or pneumonia between groups, and the significant difference noted in bronchopulmonary dysplasia was based on a total number of 11 cases.
In response to these findings, both the American College of Obstetricians and Gynecologists (ACOG) and the Society for Maternal-Fetal Medicine (SMFM) released practice advisories and interim updates, culminating in a final recommendation for a single course of betamethasone in patients at high risk of preterm delivery between 34 and 36 6/7 weeks who have not received a previous course.
Related article:
When could use of antenatal corticosteroids in the late preterm birth period be beneficial?
In a thorough review of the literature on antenatal steroid use, Kamath-Rayne and colleagues highlighted several factors that should be considered before adopting universal use of steroids at >34 weeks. These include:
- The definition of "high risk of imminent delivery" as preterm labor with at least 3-cm dilation or 75% effacement, or spontaneous rupture of membranes. The effect of less stringent inclusion criteria in real-world clinical practice is not known, and many patients who will go on to deliver at term will receive steroids unnecessarily.
- Multiple gestation, patients with pre-existing diabetes, women who had previously received a course of steroids, and fetuses with anomalies were excluded from the ALPS study. Use of antenatal steroids in these groups at >34 weeks should be evaluated before universal adoption.
Related article:
What is the ideal gestational age for twin delivery to minimize perinatal deaths?
- The incidence of neonatal hypoglycemia in the treated group was significantly increased. This affects our colleagues in pediatrics considerably from a systems standpoint (need for changes to newborn protocols and communication between services).
- The long-term outcomes of patients exposed to steroids in the late preterm period are yet to be delineated, specifically, the potential neurodevelopmental effects of a medication known to alter preterm brain development as well as cardiovascular and metabolic consequences.
Next: Low-dose aspirin for reducing preeclampsia risk
Low-dose aspirin clearly is effective for reducing the risk of preeclampsia
American College of Obstetricians and Gynecologists. Hypertension in pregnancy. Report of the American College of Obstetricians and Gynecologists' Task Force on Hypertension in Pregnancy. Obstet Gynecol. 2013;122(5):1122-1131.
Henderson JT, Whitlock EP, O'Connor E, Senger CA, Thompson JH, Rowland MG. Low-dose aspirin for prevention of morbidity and mortality from preeclampsia: a systematic evidence review for the US Preventive Services Task Force. Ann Intern Med. 2014;160(10):695-703.
LeFevre ML; US Preventive Services Task Force. Low-dose aspirin use for the prevention of morbidity and mortality from preeclampsia: US Preventive Services Task Force recommendation statement. Ann Intern Med. 2014;161(11):819-826.
American College of Obstetricians and Gynecologists. Practice advisory on low-dose aspirin and prevention of preeclampsia: updated recommendations. http://www.acog.org/About-ACOG/News-Room/Practice-Advisories/Practice-Advisory-Low-Dose-Aspirin-and-Prevention-of-Preeclampsia-Updated-Recommendations. Published July 11, 2016. Accessed December 6, 2016.
In the 2013 ACOG Task Force on Hypertension in Pregnancy report, low-dose aspirin (60-80 mg) was recommended to be initiated in the late first trimester to reduce preeclampsia risk for women with:
- prior early onset preeclampsia with preterm delivery at <34 weeks' gestation, or
- preeclampsia in more than one prior pregnancy.
This recommendation was based on several meta-analyses that demonstrated a 10% to 17% reduction in risk with no increase in bleeding, placental abruption, or other adverse events.
In 2014, the US Preventive Services Task Force (USPSTF) conducted a systematic evidence review of low-dose aspirin use for prevention of morbidity and mortality from preeclampsia. That report revealed a 24% risk reduction of preeclampsia in high-risk women treated with low-dose aspirin, as well as a 14% reduction in preterm birth and a 20% reduction in fetal growth restriction. A final statement from the USPSTF in 2014 recommended low-dose aspirin (60-150 mg) starting between 12 and 28 weeks' gestation for women at "high" risk who have:
- a history of preeclampsia, especially if accompanied by an adverse outcome
- multifetal gestation
- chronic hypertension
- diabetes (type 1 or type 2)
- renal disease
- autoimmune disease (such as systematic lupus erythematosus, antiphospholipid syndrome).
Related article:
Start offering aspirin to pregnant women at high risk for preeclampsia
As of July 11, 2016, ACOG supports this expanded list of high-risk conditions. Additionally, the USPSTF identified a "moderate" risk group in which low-dose aspirin may be considered if a patient has several risk factors, such as obesity, nulliparity, family history of preeclampsia, age 35 years or older, or another poor pregnancy outcome. ACOG notes, however, that the evidence supporting this practice is uncertain and does not make a recommendation regarding aspirin use in this population. Further study should be conducted to determine the benefit of low-dose aspirin in these patients as well as the long-term effects of treatment on maternal and child outcomes.
Next: CMA for prenatal genetic diagnosis
Chromosomal microarray analysis is preferable to karyotype in certain situations
Pauli JM, Repke JT. Update on obstetrics. OBG Manag. 2013;25(1):28-32.
Society for Maternal-Fetal Medicine (SMFM), Dugoff L, Norton ME, Kuller JA. The use of chromosomal microarray for prenatal diagnosis. Am J Obstet Gynecol. 2016;215(4):B2-B9.
American College of Obstetricians and Gynecologists. Committee Opinion No. 682. Microarrays and next- generation sequencing technology: the use of advanced genetic diagnostic tools in obstetrics and gynecology.Obstet Gynecol. 2016;128(6):e262-e268.
We previously addressed the use of chromosomal microarray analysis (CMA) for prenatal diagnosis in our 2013 "Update on obstetrics," specifically, the question of whether CMA could replace karyotype. The main differences between karyotype and CMA are that 1) only karyotype can detect balanced translocations/inversions and 2) only CMA can detect copy number variants (CNV). There are some differences in the technology and capabilities of the 2 types of CMA currently available as well.
In our 2013 article we concluded that "The total costs of such an approach--test, interpretation, counseling, and long-term follow-up of uncertain results--are unknown at this time and may prove to be unaffordable on a population-wide basis." Today, the cost of CMA is still higher than karyotype, but it is expected to decrease and insurance coverage for this test is expected to increase.
Related article:
Cell-free DNA screening for women at low risk for fetal aneuploidy
Both SMFM and ACOG released recommendations in 2016 regarding the use of CMA in prenatal genetic diagnosis, summarized as follows:
- CMA is recommended over karyotype for fetuses with structural abnormalities on ultrasound
- The detection rate for clinically relevant abnormal CNVs in this population is about 6%
- CMA is recommended for diagnosis for stillbirth specimens
- CMA does not require dividing cells and may be a quicker and more reliable test in this population
- Karotype or fluorescence in situ hybridization (FISH) is recommended for fetuses with ultrasound findings suggestive of aneuploidy
- If it is negative, then CMA is recommended
- Karyotype or CMA is recommended for patients desiring prenatal diagnostic testing with a normal fetal ultrasound
- The detection rate for clinically relevant CNVs in this population (advanced maternal age, abnormal serum screening, prior aneuploidy, parental anxiety) is about 1%
- Pretest and posttest counseling about the limitations of CMA and a 2% risk of detection of variants of unknown significance (VUS) should be performed by a provider who has expertise in CMA and who has access to databases with genotype/phenotype information for VUS
- This counseling should also include the possibility of diagnosis of nonpaternity, consanguinity, and adult-onset disease
- Karyotype is recommended for couples with recurrent pregnancy loss
- The identification of balanced translocations in this population is most relevant in this patient population
- Prenatal diagnosis with routine use of whole-genome or whole-exome sequencing is not recommended.
Next: Zika virus: Check for updates
Zika virus infection: Check often for the latest updates
American College of Obstetricians and Gynecologists, Society for Maternal-Fetal Medicine. Practice advisory on Zika virus. http://www.acog.org/About-ACOG/News-Room/Practice-Advisories/Practice-Advisory-Interim-Guidance-for-Care-of-Obstetric-Patients- During-a-Zika-Virus-Outbreak. Published December 5, 2016. Accessed December 6, 2016.
Centers for Disease Control and Prevention. Zika virus. http://www.cdc.gov/zika/pregnancy/index.html. Updated August 22, 2016. Accessed December 6, 2016.
Petersen EE, Meaney-Delman D, Neblett-Fanfair R, et al. Update: interim guidance for preconception counseling and prevention of sexual transmission of Zika virus for persons with possible Zika virus exposure--United States, September 2016. MMWR Morbid Mortal Wkly Rep. 2016;65(39):1077-1081.
A yearly update on obstetrics would be remiss without mention of the Zika virus and its impact on pregnancy and reproduction. That being said, any recommendations we offer may be out of date by the time this article is published given the rapidly changing picture of Zika virus since it first dominated the headlines in 2016. Here are the basics as summarized from ACOG and the Centers for Disease Control and Prevention (CDC):
Viral spread. Zika virus may be spread in several ways: by an infected Aedes species mosquito, mother to fetus, sexual contact, blood transfusion, or laboratory exposure.
Symptoms of infection include conjunctivitis, fever, rash, and arthralgia, but most patients (4/5) are asymptomatic.
Sequelae. Zika virus infection during pregnancy is believed to cause fetal and neonatal microcephaly, intracranial calcifications, and brain and eye abnormalities. The rate of these findings in infected individuals, as well as the rate of vertical transmission, is not known.
Travel advisory. Pregnant women should not travel to areas with active Zika infection (the CDC website regularly updates these restricted areas).
Preventive measures. If traveling to an area of active Zika infection, pregnant women should take preventative measures day and night against mosquito bites, such as use of insect repellents approved by the Environmental Protection Agency, clothing that covers exposed skin, and staying indoors.
Safe sex. Abstinence or consistent condom use is recommended for pregnant women with partners who travel to or live in areas of active Zika infection.
Delay conception. Conception should be postponed for at least 6 months in men with Zika infection and at least 8 weeks in women with Zika infection.
Testing recommendations. Pregnant women with Zika virus exposure should be tested, regardless of symptoms. Symptomatic exposed nonpregnant women and all men should be tested.
Prenatal surveillance. High-risk consultation and serial ultrasounds for fetal anatomy and growth should be considered in patients with Zika virus infection during pregnancy. Amniocentesis can be considered on a case-by-case basis.
Related article:
Zika virus update: A rapidly moving target
Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.
In this Update we discuss several exciting new recommendations for preventive treatments in pregnancy and prenatal diagnostic tests. Our A-to-Z coverage includes:
- antenatal steroids in late preterm pregnancy
- expanded list of high-risk conditions warranting low-dose aspirin for preeclampsia prevention
- chromosomal microarray analysis versus karyotype for specific clinical situations
- Zika virus infection evolving information.
Next: New recommendation for timing of late preterm antenatal steroids
New recommendation offered for timing of late preterm antenatal steroids
Gyamfi-Bannerman C, Thom EA, Blackwell SC, et al; for the NICHD Maternal-Fetal Medicine Units Network. Antenatal betamethasone for women at risk for late preterm delivery. N Engl J Med. 2016;374(14):1311-1320.
American College of Obstetricians and Gynecologists. Committee Opinion No. 677. Antenatal corticosteroidtherapy for fetal maturation. Obstet Gynecol. 2016;128(4):e187-e194.
Kamath-Rayne BD, Rozance PJ, Goldenberg RL, Jobe AH. Antenatal corticosteroids beyond 34 weeks gestation: what do we do now? Am J Obstet Gynecol. 2016;215(4):423-430.
A dramatic recommendation for obstetric practice change occurred in 2016: the option of administering antenatal steroids for fetal lung maturity after 34 weeks. In the Antenatal Late Preterm Steroids (ALPS) trial of betamethasone in the late preterm period in patients at "high risk" of imminent delivery, Gyamfi-Bannerman and colleagues demonstrated that the treated group had a significant decrease in the rate of neonatal respiratory complications.
The primary outcome, a composite of respiratory morbidities (including transient tachypnea of the newborn, surfactant use, and need for resuscitation at birth) within the first 72 hours of life, had significant differences between groups, occurring in 165 of 1,427 infants (11.6%) in the betamethasone-treated group and 202 of 1,400 (14.4%) in the placebo group (relative risk in the betamethasone group, 0.80; 95% confidence interval, 0.66-0.97; P = .02). However, there was no statistically significant difference in respiratory distress syndrome, apnea, or pneumonia between groups, and the significant difference noted in bronchopulmonary dysplasia was based on a total number of 11 cases.
In response to these findings, both the American College of Obstetricians and Gynecologists (ACOG) and the Society for Maternal-Fetal Medicine (SMFM) released practice advisories and interim updates, culminating in a final recommendation for a single course of betamethasone in patients at high risk of preterm delivery between 34 and 36 6/7 weeks who have not received a previous course.
Related article:
When could use of antenatal corticosteroids in the late preterm birth period be beneficial?
In a thorough review of the literature on antenatal steroid use, Kamath-Rayne and colleagues highlighted several factors that should be considered before adopting universal use of steroids at >34 weeks. These include:
- The definition of "high risk of imminent delivery" as preterm labor with at least 3-cm dilation or 75% effacement, or spontaneous rupture of membranes. The effect of less stringent inclusion criteria in real-world clinical practice is not known, and many patients who will go on to deliver at term will receive steroids unnecessarily.
- Multiple gestation, patients with pre-existing diabetes, women who had previously received a course of steroids, and fetuses with anomalies were excluded from the ALPS study. Use of antenatal steroids in these groups at >34 weeks should be evaluated before universal adoption.
Related article:
What is the ideal gestational age for twin delivery to minimize perinatal deaths?
- The incidence of neonatal hypoglycemia in the treated group was significantly increased. This affects our colleagues in pediatrics considerably from a systems standpoint (need for changes to newborn protocols and communication between services).
- The long-term outcomes of patients exposed to steroids in the late preterm period are yet to be delineated, specifically, the potential neurodevelopmental effects of a medication known to alter preterm brain development as well as cardiovascular and metabolic consequences.
Next: Low-dose aspirin for reducing preeclampsia risk
Low-dose aspirin clearly is effective for reducing the risk of preeclampsia
American College of Obstetricians and Gynecologists. Hypertension in pregnancy. Report of the American College of Obstetricians and Gynecologists' Task Force on Hypertension in Pregnancy. Obstet Gynecol. 2013;122(5):1122-1131.
Henderson JT, Whitlock EP, O'Connor E, Senger CA, Thompson JH, Rowland MG. Low-dose aspirin for prevention of morbidity and mortality from preeclampsia: a systematic evidence review for the US Preventive Services Task Force. Ann Intern Med. 2014;160(10):695-703.
LeFevre ML; US Preventive Services Task Force. Low-dose aspirin use for the prevention of morbidity and mortality from preeclampsia: US Preventive Services Task Force recommendation statement. Ann Intern Med. 2014;161(11):819-826.
American College of Obstetricians and Gynecologists. Practice advisory on low-dose aspirin and prevention of preeclampsia: updated recommendations. http://www.acog.org/About-ACOG/News-Room/Practice-Advisories/Practice-Advisory-Low-Dose-Aspirin-and-Prevention-of-Preeclampsia-Updated-Recommendations. Published July 11, 2016. Accessed December 6, 2016.
In the 2013 ACOG Task Force on Hypertension in Pregnancy report, low-dose aspirin (60-80 mg) was recommended to be initiated in the late first trimester to reduce preeclampsia risk for women with:
- prior early onset preeclampsia with preterm delivery at <34 weeks' gestation, or
- preeclampsia in more than one prior pregnancy.
This recommendation was based on several meta-analyses that demonstrated a 10% to 17% reduction in risk with no increase in bleeding, placental abruption, or other adverse events.
In 2014, the US Preventive Services Task Force (USPSTF) conducted a systematic evidence review of low-dose aspirin use for prevention of morbidity and mortality from preeclampsia. That report revealed a 24% risk reduction of preeclampsia in high-risk women treated with low-dose aspirin, as well as a 14% reduction in preterm birth and a 20% reduction in fetal growth restriction. A final statement from the USPSTF in 2014 recommended low-dose aspirin (60-150 mg) starting between 12 and 28 weeks' gestation for women at "high" risk who have:
- a history of preeclampsia, especially if accompanied by an adverse outcome
- multifetal gestation
- chronic hypertension
- diabetes (type 1 or type 2)
- renal disease
- autoimmune disease (such as systematic lupus erythematosus, antiphospholipid syndrome).
Related article:
Start offering aspirin to pregnant women at high risk for preeclampsia
As of July 11, 2016, ACOG supports this expanded list of high-risk conditions. Additionally, the USPSTF identified a "moderate" risk group in which low-dose aspirin may be considered if a patient has several risk factors, such as obesity, nulliparity, family history of preeclampsia, age 35 years or older, or another poor pregnancy outcome. ACOG notes, however, that the evidence supporting this practice is uncertain and does not make a recommendation regarding aspirin use in this population. Further study should be conducted to determine the benefit of low-dose aspirin in these patients as well as the long-term effects of treatment on maternal and child outcomes.
Next: CMA for prenatal genetic diagnosis
Chromosomal microarray analysis is preferable to karyotype in certain situations
Pauli JM, Repke JT. Update on obstetrics. OBG Manag. 2013;25(1):28-32.
Society for Maternal-Fetal Medicine (SMFM), Dugoff L, Norton ME, Kuller JA. The use of chromosomal microarray for prenatal diagnosis. Am J Obstet Gynecol. 2016;215(4):B2-B9.
American College of Obstetricians and Gynecologists. Committee Opinion No. 682. Microarrays and next- generation sequencing technology: the use of advanced genetic diagnostic tools in obstetrics and gynecology.Obstet Gynecol. 2016;128(6):e262-e268.
We previously addressed the use of chromosomal microarray analysis (CMA) for prenatal diagnosis in our 2013 "Update on obstetrics," specifically, the question of whether CMA could replace karyotype. The main differences between karyotype and CMA are that 1) only karyotype can detect balanced translocations/inversions and 2) only CMA can detect copy number variants (CNV). There are some differences in the technology and capabilities of the 2 types of CMA currently available as well.
In our 2013 article we concluded that "The total costs of such an approach--test, interpretation, counseling, and long-term follow-up of uncertain results--are unknown at this time and may prove to be unaffordable on a population-wide basis." Today, the cost of CMA is still higher than karyotype, but it is expected to decrease and insurance coverage for this test is expected to increase.
Related article:
Cell-free DNA screening for women at low risk for fetal aneuploidy
Both SMFM and ACOG released recommendations in 2016 regarding the use of CMA in prenatal genetic diagnosis, summarized as follows:
- CMA is recommended over karyotype for fetuses with structural abnormalities on ultrasound
- The detection rate for clinically relevant abnormal CNVs in this population is about 6%
- CMA is recommended for diagnosis for stillbirth specimens
- CMA does not require dividing cells and may be a quicker and more reliable test in this population
- Karotype or fluorescence in situ hybridization (FISH) is recommended for fetuses with ultrasound findings suggestive of aneuploidy
- If it is negative, then CMA is recommended
- Karyotype or CMA is recommended for patients desiring prenatal diagnostic testing with a normal fetal ultrasound
- The detection rate for clinically relevant CNVs in this population (advanced maternal age, abnormal serum screening, prior aneuploidy, parental anxiety) is about 1%
- Pretest and posttest counseling about the limitations of CMA and a 2% risk of detection of variants of unknown significance (VUS) should be performed by a provider who has expertise in CMA and who has access to databases with genotype/phenotype information for VUS
- This counseling should also include the possibility of diagnosis of nonpaternity, consanguinity, and adult-onset disease
- Karyotype is recommended for couples with recurrent pregnancy loss
- The identification of balanced translocations in this population is most relevant in this patient population
- Prenatal diagnosis with routine use of whole-genome or whole-exome sequencing is not recommended.
Next: Zika virus: Check for updates
Zika virus infection: Check often for the latest updates
American College of Obstetricians and Gynecologists, Society for Maternal-Fetal Medicine. Practice advisory on Zika virus. http://www.acog.org/About-ACOG/News-Room/Practice-Advisories/Practice-Advisory-Interim-Guidance-for-Care-of-Obstetric-Patients- During-a-Zika-Virus-Outbreak. Published December 5, 2016. Accessed December 6, 2016.
Centers for Disease Control and Prevention. Zika virus. http://www.cdc.gov/zika/pregnancy/index.html. Updated August 22, 2016. Accessed December 6, 2016.
Petersen EE, Meaney-Delman D, Neblett-Fanfair R, et al. Update: interim guidance for preconception counseling and prevention of sexual transmission of Zika virus for persons with possible Zika virus exposure--United States, September 2016. MMWR Morbid Mortal Wkly Rep. 2016;65(39):1077-1081.
A yearly update on obstetrics would be remiss without mention of the Zika virus and its impact on pregnancy and reproduction. That being said, any recommendations we offer may be out of date by the time this article is published given the rapidly changing picture of Zika virus since it first dominated the headlines in 2016. Here are the basics as summarized from ACOG and the Centers for Disease Control and Prevention (CDC):
Viral spread. Zika virus may be spread in several ways: by an infected Aedes species mosquito, mother to fetus, sexual contact, blood transfusion, or laboratory exposure.
Symptoms of infection include conjunctivitis, fever, rash, and arthralgia, but most patients (4/5) are asymptomatic.
Sequelae. Zika virus infection during pregnancy is believed to cause fetal and neonatal microcephaly, intracranial calcifications, and brain and eye abnormalities. The rate of these findings in infected individuals, as well as the rate of vertical transmission, is not known.
Travel advisory. Pregnant women should not travel to areas with active Zika infection (the CDC website regularly updates these restricted areas).
Preventive measures. If traveling to an area of active Zika infection, pregnant women should take preventative measures day and night against mosquito bites, such as use of insect repellents approved by the Environmental Protection Agency, clothing that covers exposed skin, and staying indoors.
Safe sex. Abstinence or consistent condom use is recommended for pregnant women with partners who travel to or live in areas of active Zika infection.
Delay conception. Conception should be postponed for at least 6 months in men with Zika infection and at least 8 weeks in women with Zika infection.
Testing recommendations. Pregnant women with Zika virus exposure should be tested, regardless of symptoms. Symptomatic exposed nonpregnant women and all men should be tested.
Prenatal surveillance. High-risk consultation and serial ultrasounds for fetal anatomy and growth should be considered in patients with Zika virus infection during pregnancy. Amniocentesis can be considered on a case-by-case basis.
Related article:
Zika virus update: A rapidly moving target
Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.
In this Update we discuss several exciting new recommendations for preventive treatments in pregnancy and prenatal diagnostic tests. Our A-to-Z coverage includes:
- antenatal steroids in late preterm pregnancy
- expanded list of high-risk conditions warranting low-dose aspirin for preeclampsia prevention
- chromosomal microarray analysis versus karyotype for specific clinical situations
- Zika virus infection evolving information.
Next: New recommendation for timing of late preterm antenatal steroids
New recommendation offered for timing of late preterm antenatal steroids
Gyamfi-Bannerman C, Thom EA, Blackwell SC, et al; for the NICHD Maternal-Fetal Medicine Units Network. Antenatal betamethasone for women at risk for late preterm delivery. N Engl J Med. 2016;374(14):1311-1320.
American College of Obstetricians and Gynecologists. Committee Opinion No. 677. Antenatal corticosteroidtherapy for fetal maturation. Obstet Gynecol. 2016;128(4):e187-e194.
Kamath-Rayne BD, Rozance PJ, Goldenberg RL, Jobe AH. Antenatal corticosteroids beyond 34 weeks gestation: what do we do now? Am J Obstet Gynecol. 2016;215(4):423-430.
A dramatic recommendation for obstetric practice change occurred in 2016: the option of administering antenatal steroids for fetal lung maturity after 34 weeks. In the Antenatal Late Preterm Steroids (ALPS) trial of betamethasone in the late preterm period in patients at "high risk" of imminent delivery, Gyamfi-Bannerman and colleagues demonstrated that the treated group had a significant decrease in the rate of neonatal respiratory complications.
The primary outcome, a composite of respiratory morbidities (including transient tachypnea of the newborn, surfactant use, and need for resuscitation at birth) within the first 72 hours of life, had significant differences between groups, occurring in 165 of 1,427 infants (11.6%) in the betamethasone-treated group and 202 of 1,400 (14.4%) in the placebo group (relative risk in the betamethasone group, 0.80; 95% confidence interval, 0.66-0.97; P = .02). However, there was no statistically significant difference in respiratory distress syndrome, apnea, or pneumonia between groups, and the significant difference noted in bronchopulmonary dysplasia was based on a total number of 11 cases.
In response to these findings, both the American College of Obstetricians and Gynecologists (ACOG) and the Society for Maternal-Fetal Medicine (SMFM) released practice advisories and interim updates, culminating in a final recommendation for a single course of betamethasone in patients at high risk of preterm delivery between 34 and 36 6/7 weeks who have not received a previous course.
Related article:
When could use of antenatal corticosteroids in the late preterm birth period be beneficial?
In a thorough review of the literature on antenatal steroid use, Kamath-Rayne and colleagues highlighted several factors that should be considered before adopting universal use of steroids at >34 weeks. These include:
- The definition of "high risk of imminent delivery" as preterm labor with at least 3-cm dilation or 75% effacement, or spontaneous rupture of membranes. The effect of less stringent inclusion criteria in real-world clinical practice is not known, and many patients who will go on to deliver at term will receive steroids unnecessarily.
- Multiple gestation, patients with pre-existing diabetes, women who had previously received a course of steroids, and fetuses with anomalies were excluded from the ALPS study. Use of antenatal steroids in these groups at >34 weeks should be evaluated before universal adoption.
Related article:
What is the ideal gestational age for twin delivery to minimize perinatal deaths?
- The incidence of neonatal hypoglycemia in the treated group was significantly increased. This affects our colleagues in pediatrics considerably from a systems standpoint (need for changes to newborn protocols and communication between services).
- The long-term outcomes of patients exposed to steroids in the late preterm period are yet to be delineated, specifically, the potential neurodevelopmental effects of a medication known to alter preterm brain development as well as cardiovascular and metabolic consequences.
Next: Low-dose aspirin for reducing preeclampsia risk
Low-dose aspirin clearly is effective for reducing the risk of preeclampsia
American College of Obstetricians and Gynecologists. Hypertension in pregnancy. Report of the American College of Obstetricians and Gynecologists' Task Force on Hypertension in Pregnancy. Obstet Gynecol. 2013;122(5):1122-1131.
Henderson JT, Whitlock EP, O'Connor E, Senger CA, Thompson JH, Rowland MG. Low-dose aspirin for prevention of morbidity and mortality from preeclampsia: a systematic evidence review for the US Preventive Services Task Force. Ann Intern Med. 2014;160(10):695-703.
LeFevre ML; US Preventive Services Task Force. Low-dose aspirin use for the prevention of morbidity and mortality from preeclampsia: US Preventive Services Task Force recommendation statement. Ann Intern Med. 2014;161(11):819-826.
American College of Obstetricians and Gynecologists. Practice advisory on low-dose aspirin and prevention of preeclampsia: updated recommendations. http://www.acog.org/About-ACOG/News-Room/Practice-Advisories/Practice-Advisory-Low-Dose-Aspirin-and-Prevention-of-Preeclampsia-Updated-Recommendations. Published July 11, 2016. Accessed December 6, 2016.
In the 2013 ACOG Task Force on Hypertension in Pregnancy report, low-dose aspirin (60-80 mg) was recommended to be initiated in the late first trimester to reduce preeclampsia risk for women with:
- prior early onset preeclampsia with preterm delivery at <34 weeks' gestation, or
- preeclampsia in more than one prior pregnancy.
This recommendation was based on several meta-analyses that demonstrated a 10% to 17% reduction in risk with no increase in bleeding, placental abruption, or other adverse events.
In 2014, the US Preventive Services Task Force (USPSTF) conducted a systematic evidence review of low-dose aspirin use for prevention of morbidity and mortality from preeclampsia. That report revealed a 24% risk reduction of preeclampsia in high-risk women treated with low-dose aspirin, as well as a 14% reduction in preterm birth and a 20% reduction in fetal growth restriction. A final statement from the USPSTF in 2014 recommended low-dose aspirin (60-150 mg) starting between 12 and 28 weeks' gestation for women at "high" risk who have:
- a history of preeclampsia, especially if accompanied by an adverse outcome
- multifetal gestation
- chronic hypertension
- diabetes (type 1 or type 2)
- renal disease
- autoimmune disease (such as systematic lupus erythematosus, antiphospholipid syndrome).
Related article:
Start offering aspirin to pregnant women at high risk for preeclampsia
As of July 11, 2016, ACOG supports this expanded list of high-risk conditions. Additionally, the USPSTF identified a "moderate" risk group in which low-dose aspirin may be considered if a patient has several risk factors, such as obesity, nulliparity, family history of preeclampsia, age 35 years or older, or another poor pregnancy outcome. ACOG notes, however, that the evidence supporting this practice is uncertain and does not make a recommendation regarding aspirin use in this population. Further study should be conducted to determine the benefit of low-dose aspirin in these patients as well as the long-term effects of treatment on maternal and child outcomes.
Next: CMA for prenatal genetic diagnosis
Chromosomal microarray analysis is preferable to karyotype in certain situations
Pauli JM, Repke JT. Update on obstetrics. OBG Manag. 2013;25(1):28-32.
Society for Maternal-Fetal Medicine (SMFM), Dugoff L, Norton ME, Kuller JA. The use of chromosomal microarray for prenatal diagnosis. Am J Obstet Gynecol. 2016;215(4):B2-B9.
American College of Obstetricians and Gynecologists. Committee Opinion No. 682. Microarrays and next- generation sequencing technology: the use of advanced genetic diagnostic tools in obstetrics and gynecology.Obstet Gynecol. 2016;128(6):e262-e268.
We previously addressed the use of chromosomal microarray analysis (CMA) for prenatal diagnosis in our 2013 "Update on obstetrics," specifically, the question of whether CMA could replace karyotype. The main differences between karyotype and CMA are that 1) only karyotype can detect balanced translocations/inversions and 2) only CMA can detect copy number variants (CNV). There are some differences in the technology and capabilities of the 2 types of CMA currently available as well.
In our 2013 article we concluded that "The total costs of such an approach--test, interpretation, counseling, and long-term follow-up of uncertain results--are unknown at this time and may prove to be unaffordable on a population-wide basis." Today, the cost of CMA is still higher than karyotype, but it is expected to decrease and insurance coverage for this test is expected to increase.
Related article:
Cell-free DNA screening for women at low risk for fetal aneuploidy
Both SMFM and ACOG released recommendations in 2016 regarding the use of CMA in prenatal genetic diagnosis, summarized as follows:
- CMA is recommended over karyotype for fetuses with structural abnormalities on ultrasound
- The detection rate for clinically relevant abnormal CNVs in this population is about 6%
- CMA is recommended for diagnosis for stillbirth specimens
- CMA does not require dividing cells and may be a quicker and more reliable test in this population
- Karotype or fluorescence in situ hybridization (FISH) is recommended for fetuses with ultrasound findings suggestive of aneuploidy
- If it is negative, then CMA is recommended
- Karyotype or CMA is recommended for patients desiring prenatal diagnostic testing with a normal fetal ultrasound
- The detection rate for clinically relevant CNVs in this population (advanced maternal age, abnormal serum screening, prior aneuploidy, parental anxiety) is about 1%
- Pretest and posttest counseling about the limitations of CMA and a 2% risk of detection of variants of unknown significance (VUS) should be performed by a provider who has expertise in CMA and who has access to databases with genotype/phenotype information for VUS
- This counseling should also include the possibility of diagnosis of nonpaternity, consanguinity, and adult-onset disease
- Karyotype is recommended for couples with recurrent pregnancy loss
- The identification of balanced translocations in this population is most relevant in this patient population
- Prenatal diagnosis with routine use of whole-genome or whole-exome sequencing is not recommended.
Next: Zika virus: Check for updates
Zika virus infection: Check often for the latest updates
American College of Obstetricians and Gynecologists, Society for Maternal-Fetal Medicine. Practice advisory on Zika virus. http://www.acog.org/About-ACOG/News-Room/Practice-Advisories/Practice-Advisory-Interim-Guidance-for-Care-of-Obstetric-Patients- During-a-Zika-Virus-Outbreak. Published December 5, 2016. Accessed December 6, 2016.
Centers for Disease Control and Prevention. Zika virus. http://www.cdc.gov/zika/pregnancy/index.html. Updated August 22, 2016. Accessed December 6, 2016.
Petersen EE, Meaney-Delman D, Neblett-Fanfair R, et al. Update: interim guidance for preconception counseling and prevention of sexual transmission of Zika virus for persons with possible Zika virus exposure--United States, September 2016. MMWR Morbid Mortal Wkly Rep. 2016;65(39):1077-1081.
A yearly update on obstetrics would be remiss without mention of the Zika virus and its impact on pregnancy and reproduction. That being said, any recommendations we offer may be out of date by the time this article is published given the rapidly changing picture of Zika virus since it first dominated the headlines in 2016. Here are the basics as summarized from ACOG and the Centers for Disease Control and Prevention (CDC):
Viral spread. Zika virus may be spread in several ways: by an infected Aedes species mosquito, mother to fetus, sexual contact, blood transfusion, or laboratory exposure.
Symptoms of infection include conjunctivitis, fever, rash, and arthralgia, but most patients (4/5) are asymptomatic.
Sequelae. Zika virus infection during pregnancy is believed to cause fetal and neonatal microcephaly, intracranial calcifications, and brain and eye abnormalities. The rate of these findings in infected individuals, as well as the rate of vertical transmission, is not known.
Travel advisory. Pregnant women should not travel to areas with active Zika infection (the CDC website regularly updates these restricted areas).
Preventive measures. If traveling to an area of active Zika infection, pregnant women should take preventative measures day and night against mosquito bites, such as use of insect repellents approved by the Environmental Protection Agency, clothing that covers exposed skin, and staying indoors.
Safe sex. Abstinence or consistent condom use is recommended for pregnant women with partners who travel to or live in areas of active Zika infection.
Delay conception. Conception should be postponed for at least 6 months in men with Zika infection and at least 8 weeks in women with Zika infection.
Testing recommendations. Pregnant women with Zika virus exposure should be tested, regardless of symptoms. Symptomatic exposed nonpregnant women and all men should be tested.
Prenatal surveillance. High-risk consultation and serial ultrasounds for fetal anatomy and growth should be considered in patients with Zika virus infection during pregnancy. Amniocentesis can be considered on a case-by-case basis.
Related article:
Zika virus update: A rapidly moving target
Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.
Overcoming LARC complications: 7 case challenges
The use of long-acting reversible contraceptive (LARC) methods has shown a steady increase in the United States. The major factors for increasing acceptance include high efficacy, ease of use, and an acceptable adverse effect profile. Since these methods require placement under the skin (implantable device) or into the uterus (intrauterine devices [IUDs]), unique management issues arise during their usage. Recently, the American College of Obstetricians and Gynecologists (ACOG) released a committee opinion addressing several of these clinical challenges—among them: pain with insertion, what to do when the IUD strings are not visualized, and the plan of action for a nonpalpable IUD or contraceptive implant.1 In this article we present 7 cases, and successful management approaches, that reflect ACOG’s recent recommendations and our extensive clinical experience.
Read the first CHALLENGE: Pain with IUD insertion
CHALLENGE 1: Pain with IUD insertion
CASE First-time, nulliparous IUD user apprehensive about insertion pain
A 21-year-old woman (G0) presents for placement of a 52-mg levonorgestrel IUD for contraception and treatment of dysmenorrhea. Her medical and surgical histories are unremarkable. She has heard that IUD insertion “is more painful if you haven’t had a baby yet” and she asks what treatments are available to aid in pain relief.
What can you offer her?
A number of approaches have been used to reduce IUD insertion pain, including:
- placing lidocaine gel into or on the cervix
- lidocaine paracervical block
- preinsertion use of misoprostol or nonsteroidal anti-inflammatory drugs.
Authors of a recent Cochrane review2 indicated that none of these approaches were particularly effective at reducing insertion pain for nulliparous women. Naproxen sodium 550 mg or tramadol 50 mg taken 1 hour prior to IUD insertion have been found to decrease IUD insertion pain in multiparous patients.3 Misoprostol, apart from being ineffective in reducing insertion pain, also requires use for a number of hours before insertion and can cause painful uterine cramping, upset stomach, and diarrhea.2 Some studies do suggest that use of a paracervical block does reduce the pain associated with tenaculum placement but not the IUD insertion itself.
Related article:
Benefit of self-administered vaginal lidocaine gel in IUD placement
A reasonable pain management strategy for nulliparous patients. Given these data, there is not an evidence-based IUD insertion pain management strategy that can be used for the nulliparous case patient. A practical approach for nulliparous patients is to offer naproxen sodium or tramadol, which have been found to be beneficial in multiparous patients, to a nulliparous patient. Additionally, lidocaine gel applied to the cervix or tenaculum-site injection can be considered for tenaculum-associated pain, although it does not appear to help significantly with IUD insertion pain. Misoprostol should be avoided as it does not alleviate the pain of insertion and it can cause bothersome adverse effects.
Read CHALLENGE 2: IUD strings not visualized
CHALLENGE 2: IUD strings not visualized
CASE No strings palpated 6 weeks after postpartum IUD placement
A 26-year-old woman (G2P2) presents to your office for a postpartum visit 6 weeks after an uncomplicated cesarean delivery at term. She had requested that a 52-mg levonorgestrel IUD be placed at the time of delivery, and the delivery report describes an uneventful placement. The patient has not been able to feel the IUD strings using her fingers and you do not find them on examination. She does not remember the IUD falling out.
What are the next steps in her management?
Failure to palpate the IUD strings by the user or failure to visualize the strings is a fairly common occurrence. This is especially true when an IUD is placed immediatelypostpartum, as in this patient’s case.
When the strings cannot be palpated, it is important to exclude pregnancy and recommend a form of backup contraception, such as condoms and emergency contraception if appropriate, until evaluation can be completed.
Steps to locate a device. In the office setting, the strings often can be located by inserting a cytobrush into the endocervical canal to extract them. If that maneuver fails to locate them, an ultrasound should be completed to determine if the device is in the uterus. If the ultrasound does not detect the device in the uterus, obtain an anteroposterior (AP) x-ray encompassing the entire abdomen and pelvis. All IUDs used in the United States are radiopaque and will be observed on x-ray if present. If the IUD is identified, operative removal is indicated.
Related article:
How to identify and localize IUDs on ultrasound
Intraperitoneal location. If an IUD is found in this location, it is usually the result of a perforation that occurred at the time of insertion. In general, the device can be removed via laparoscopy. Occasionally, laparotomy is needed if there is significant pelvic infection, possible bowel perforation, or if there is an inability to locate the device at laparoscopy.4 The copper IUD is more inflammatory than the levonorgestrel IUDs.
Abdominal location. No matter the IUD type, operative removal of intra-abdominal IUDs should take place expeditiously after they are discovered.
In the case of expulsion. If the IUD is not seen on x-ray, expulsion is the likely cause. Expulsion tends to be more common among5:
- parous users
- those younger than age 20
- placements that immediately follow a delivery or second-trimester abortion.
Nulliparity and type of device are not associated with increased risk of expulsion.
Read CHALLENGE 3: Difficult IUD removal
CHALLENGE 3: Difficult IUD removal
CASE Strings not palpated in a patient with history of LEEP
A 37-year-old woman (G3P2) presents to your office for IUD removal. She underwent a loop electrosurgical excision procedure 2 years ago for cervical intraepithelial neoplasia (CIN) 2 and since then has not been able to feel the IUD strings. On pelvic examination, you do not palpate or visualize the IUD strings after speculum placement.
How can you achieve IUD removal for your patient?
When a patient requests that her IUD be removed, but the strings are not visible and the woman is not pregnant, employ ultrasonography to confirm the IUD remains intrauterine and to rule out expulsion or perforation.
Employ alligator forceps or an IUD hook. Once intrauterine position is confirmed, use an alligator forceps of suitable length and with a small diameter to extract the device (FIGURE 1). It is useful to utilize ultrasonography for guidance during the removal procedure. The alligator forceps will grasp both the IUD device itself and IUD strings well, so either can be targeted during removal.
A second useful tool for IUD removal is an IUD hook (FIGURE 2). In a similar way that a curette is used for endometrial sampling, IUD hooks can be used to drag the IUD from the uterus.
Anesthesia is not usually necessary for IUD removal with alligator forceps or an IUD hook, although it may be appropriate in select patients. Data are limited with regard to the utility of paracervical blocks in this situation.
Related article:
Surgical removal of malpositioned IUDs
Hysteroscopy is an option. If removal with an alligator forceps or IUD hook is unsuccessful, or if preferred by the clinician, hysteroscopic-guided removal is a management option. Hysteroscopic removal may be required if the IUD has become embedded in the uterine wall.
Read CHALLENGE 4: Nonfundal IUD location
CHALLENGE 4: Nonfundal IUD location
CASE Copper IUD found in lower uterine segment
A 31-year-old woman (G1P1) calls your office to report that she thinks her copper IUD strings are longer than before. Office examination confirms that the strings are noticeably longer than is typical. Pelvic ultrasonography shows the copper IUD in the lower uterine segment.
What is the appropriate course of action?
Occasionally, IUDs are noted to be located in the lower uterine segment (FIGURE 3) or cervix. With malposition, users may be experiencing cramping or abnormal bleeding.
Cervical malposition calls for removal. ACOG advises that, regardless of a patient’s presenting symptoms, clinicians should remove IUDs located in the cervix (ie, the stem below the internal os) due to an increased risk of pregnancy and address the woman’s contraceptive needs.
Related article:
STOP relying on 2D ultrasound for IUD localization
Lower-uterine-segment malposition man‑agement less clear. If the patient is symptomatic, remove the device and initiate some form of contraception. If the woman is asymptomatic, the woman should be given the option of having the device removed or left in place. The mechanisms of action of both the copper and levonorgestrel-releasing IUDs suggest that this lower location is unlikely to be associated with a significant decrease in efficacy.
Unfortunately, it is difficult to estimate the risk of pregnancy for a patient whose device is located in the lower uterine segment. Braaten and Goldberg discussed case-controlled data in their 2012 article that suggest malposition may be more important to the efficacy of copper IUDs than of levonorgestrel IUDs.6,7 As unintended pregnancy is an important risk to avoid, ultimately, it is the woman’s decision as to whether she wants removal or continued IUD use.
Read CHALLENGE 5: Pregnancy in an IUD user
CHALLENGE 5: Pregnancy in an IUD user
CASE 3-year copper IUD user with positive pregnancy test
A 25-year-old woman (G3P2) presents to your office because of missed menses and a positive home pregnancy test. Her last menstrual period was 6 weeks ago. She has had a copper IUD in place for 3 years and can feel the strings herself. She has experienced light cramping but no bleeding. Office examination is notable for the IUD stem present at the external cervical os. While the pregnancy is unplanned, the patient desires that it continue.
Should you remove the IUD?
The pregnancy rate among IUD users is less than 1%—a rate that is equivalent to that experienced by women undergoing tubal sterilization. Although there is an overall low risk of pregnancy, a higher proportion of pregnancies among IUD users compared with nonusers are ectopic. Therefore, subsequent management of pregnancy in an IUD user needs to be determined by, using ultrasound, both the location of the pregnancy and whether the IUD is in place.
If an ectopic pregnancy is found, it may be managed medically or surgically with the IUD left in place if desired. If you find an intrauterine pregnancy that is undesired, the IUD can be removed at the time of a surgical abortion or before the initiation of a medical abortion.
If you fail to locate the IUD either before or after the abortion procedure, use an AP x-ray of the entire abdomen and pelvis to determine whether the IUD is in the peritoneal cavity or whether it was likely expelled prior to the pregnancy.
Related article:
In which clinical situations can the use of the 52-mg levonorgestrel-releasing IUD (Mirena) and the TCu380A copper-IUD (ParaGard) be extended?
With a desired pregnancy, if the strings are visible, remove the IUD with gentle traction. If the IUD is left in place, the risk of spontaneous abortion is significantly increased. If the strings are not seen, but the device was noted to be in the cervix by ultrasound, remove the device if the stem is below the internal cervical os. For IUDs that are located above the cervix, removal should not be attempted; counsel the patient about the increased risk of spontaneous abortion, infection, and preterm delivery.
Read CHALLENGE 6: Pregnancy in an implant user
CHALLENGE 6: Pregnancy in an implant user
CASE 3-week implant user with positive pregnancy test
Your 21-year-old patient who received a contraceptive implant 3 weeks earlier now pre‑sents with nausea and abdominal cramping. Her last menstrual period was 6 weeks ago. She has regular cycles that are 28 days in length. Results of urine pregnancy testing are positive. Prior to using the implant, the patient inconsistently used condoms.
How should you counsel your patient?
The rate of pregnancy among implant users is very low; it is estimated at 5 pregnancies per 10,000 implant users per year.8 As in this case, apparent “failures” of the contraceptive implant actually may represent placements that occurred before a very early pregnancy was recognized. Similar to IUDs, the proportion of pregnancies that are ectopic among implant users compared to nonusers may be higher.
With a pregnancy that is ectopic or that is intrauterine and undesired, the device may be left in and use continued after the pregnancy has been terminated. Although the effectiveness of medication abortion with pre-existing contraceptive implant in situ is not well known, researchers have demonstrated that medication abortion initiated at the same time as contraceptive implant insertion does not influence success of the medication abortion.9
Related article:
2016 Update on contraception
For women with desired intrauterine pregnancies, remove the device as soon as feasible and counsel the woman that there is no known teratogenic risk associated with the contraceptive implant.
Read CHALLENGE 7: Nonpalpable contraceptive implant
CHALLENGE 7: Nonpalpable contraceptive implant
CASE Patient requests device removal to attempt conception
A 30-year-old woman (G2P2) presents for contraceptive implant removal because she would like to have another child. The device was placed 30 months ago in the patient’s left arm. The insertion note in the patient’s medical record is unremarkable, and standard insertion technique was used. On physical examination, you cannot palpate the device.
What is your next course of action?
Nonpalpable implants, particularly if removal is desired, present a significant clinical challenge. Do not attempt removing a nonpalpable implant before trying to locate the device through past medical records or radiography. Records that describe the original insertion, particularly the location and type of device, are helpful.
Related article:
2015 Update on contraception
Appropriate imaging assistance. Ultrasonography with a high frequency linear array transducer (10 MHz or greater) may allow an experienced radiologist to identify the implant—including earlier versions without barium (Implanon) and later ones with barium (Nexplanon). Magnetic resonance imaging (MRI), computed tomography scan, or plain x-ray also can be used to detect a barium-containing device; MRI can be used to locate a non−barium-containing implant.
Carry out removal using ultrasonographic guidance. If a deep insertion is felt to be close to a neurovascular bundle, device removal should be carried out in an operating room by a surgeon familiar with the anatomy of the upper arm.
When an implant cannot be located despite radiography. This is an infrequent occurrence. Merck, the manufacturer of the etonorgestrel implant, provides advice and support in this circumstance. (Visit https://www.merckconnect.com/nexplanon/over view.html.)
Recently, published case reports detail episodes of implants inserted into the venous system with migration to the heart or lungs.10 While this phenomenon is considered rare, the manufacturer has recommended that insertion of the contraceptive implant avoid the sulcus between the biceps and triceps muscles.
Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.
- American College of Obstetricians and Gynecologists. Committee Opinion No. 672: clinical challenges of long-acting reversible contraceptive methods. Obstet Gynecol. 2016;128(3):e69−e77.
- Lopez LM, Bernholc A, Zeng Y, et al. Interventions for pain with intrauterine device insertion. Cochrane Database Syst Rev. 2015;(7):CD007373.
- Karabayirli S, Ayrim AA, Muslu B. Comparison of the analgesic effects of oral tramadol and naproxen sodium on pain relief during IUD insertion. J Minim Invasive Gynecol. 2012;19(5):581−584.
- Kho KA, Chamsy DJ. Perforated intraperitoneal intrauterine contraceptive devices: diagnosis, management, and clinical outcomes. J Minim Invasive Gynecol. 2014;21(4):596−601.
- Madden T, McNicholas C, Zhao Q, Secura GM, Eisenberg DL, Peipert JF. Association of age and parity with intrauterine device expulsion. Obstet Gynecol. 2014;124(4):718−726.
- Patil E, Bednarek PH. Immediate intrauterine device insertion following surgical abortion. Obstet Gynecol Clin North Am. 2015;42(4):583−546.
- Braaten and Goldberg. OBG Manag. Malpositioned IUDs: When you should intervene (and when you should not). OBG Manag. 2012;24(8):38−46.
- Trussell J. Contraceptive failure in the United States. Contraception. 2011;83(5):397−404.
- Raymond EG, Weaver MA, Tan YL, et al. Effect of immediate compared with delayed insertion of etonogestrel implants on medical abortion efficacy and repeat pregnancy: a randomized controlled trial. Obstet Gynecol. 2017;127(2):306−312.
- Rowlands S, Mansour D, Walling M. Intravascular migration of contraceptive implants: two more cases. Contraception. 2016. In press.
The use of long-acting reversible contraceptive (LARC) methods has shown a steady increase in the United States. The major factors for increasing acceptance include high efficacy, ease of use, and an acceptable adverse effect profile. Since these methods require placement under the skin (implantable device) or into the uterus (intrauterine devices [IUDs]), unique management issues arise during their usage. Recently, the American College of Obstetricians and Gynecologists (ACOG) released a committee opinion addressing several of these clinical challenges—among them: pain with insertion, what to do when the IUD strings are not visualized, and the plan of action for a nonpalpable IUD or contraceptive implant.1 In this article we present 7 cases, and successful management approaches, that reflect ACOG’s recent recommendations and our extensive clinical experience.
Read the first CHALLENGE: Pain with IUD insertion
CHALLENGE 1: Pain with IUD insertion
CASE First-time, nulliparous IUD user apprehensive about insertion pain
A 21-year-old woman (G0) presents for placement of a 52-mg levonorgestrel IUD for contraception and treatment of dysmenorrhea. Her medical and surgical histories are unremarkable. She has heard that IUD insertion “is more painful if you haven’t had a baby yet” and she asks what treatments are available to aid in pain relief.
What can you offer her?
A number of approaches have been used to reduce IUD insertion pain, including:
- placing lidocaine gel into or on the cervix
- lidocaine paracervical block
- preinsertion use of misoprostol or nonsteroidal anti-inflammatory drugs.
Authors of a recent Cochrane review2 indicated that none of these approaches were particularly effective at reducing insertion pain for nulliparous women. Naproxen sodium 550 mg or tramadol 50 mg taken 1 hour prior to IUD insertion have been found to decrease IUD insertion pain in multiparous patients.3 Misoprostol, apart from being ineffective in reducing insertion pain, also requires use for a number of hours before insertion and can cause painful uterine cramping, upset stomach, and diarrhea.2 Some studies do suggest that use of a paracervical block does reduce the pain associated with tenaculum placement but not the IUD insertion itself.
Related article:
Benefit of self-administered vaginal lidocaine gel in IUD placement
A reasonable pain management strategy for nulliparous patients. Given these data, there is not an evidence-based IUD insertion pain management strategy that can be used for the nulliparous case patient. A practical approach for nulliparous patients is to offer naproxen sodium or tramadol, which have been found to be beneficial in multiparous patients, to a nulliparous patient. Additionally, lidocaine gel applied to the cervix or tenaculum-site injection can be considered for tenaculum-associated pain, although it does not appear to help significantly with IUD insertion pain. Misoprostol should be avoided as it does not alleviate the pain of insertion and it can cause bothersome adverse effects.
Read CHALLENGE 2: IUD strings not visualized
CHALLENGE 2: IUD strings not visualized
CASE No strings palpated 6 weeks after postpartum IUD placement
A 26-year-old woman (G2P2) presents to your office for a postpartum visit 6 weeks after an uncomplicated cesarean delivery at term. She had requested that a 52-mg levonorgestrel IUD be placed at the time of delivery, and the delivery report describes an uneventful placement. The patient has not been able to feel the IUD strings using her fingers and you do not find them on examination. She does not remember the IUD falling out.
What are the next steps in her management?
Failure to palpate the IUD strings by the user or failure to visualize the strings is a fairly common occurrence. This is especially true when an IUD is placed immediatelypostpartum, as in this patient’s case.
When the strings cannot be palpated, it is important to exclude pregnancy and recommend a form of backup contraception, such as condoms and emergency contraception if appropriate, until evaluation can be completed.
Steps to locate a device. In the office setting, the strings often can be located by inserting a cytobrush into the endocervical canal to extract them. If that maneuver fails to locate them, an ultrasound should be completed to determine if the device is in the uterus. If the ultrasound does not detect the device in the uterus, obtain an anteroposterior (AP) x-ray encompassing the entire abdomen and pelvis. All IUDs used in the United States are radiopaque and will be observed on x-ray if present. If the IUD is identified, operative removal is indicated.
Related article:
How to identify and localize IUDs on ultrasound
Intraperitoneal location. If an IUD is found in this location, it is usually the result of a perforation that occurred at the time of insertion. In general, the device can be removed via laparoscopy. Occasionally, laparotomy is needed if there is significant pelvic infection, possible bowel perforation, or if there is an inability to locate the device at laparoscopy.4 The copper IUD is more inflammatory than the levonorgestrel IUDs.
Abdominal location. No matter the IUD type, operative removal of intra-abdominal IUDs should take place expeditiously after they are discovered.
In the case of expulsion. If the IUD is not seen on x-ray, expulsion is the likely cause. Expulsion tends to be more common among5:
- parous users
- those younger than age 20
- placements that immediately follow a delivery or second-trimester abortion.
Nulliparity and type of device are not associated with increased risk of expulsion.
Read CHALLENGE 3: Difficult IUD removal
CHALLENGE 3: Difficult IUD removal
CASE Strings not palpated in a patient with history of LEEP
A 37-year-old woman (G3P2) presents to your office for IUD removal. She underwent a loop electrosurgical excision procedure 2 years ago for cervical intraepithelial neoplasia (CIN) 2 and since then has not been able to feel the IUD strings. On pelvic examination, you do not palpate or visualize the IUD strings after speculum placement.
How can you achieve IUD removal for your patient?
When a patient requests that her IUD be removed, but the strings are not visible and the woman is not pregnant, employ ultrasonography to confirm the IUD remains intrauterine and to rule out expulsion or perforation.
Employ alligator forceps or an IUD hook. Once intrauterine position is confirmed, use an alligator forceps of suitable length and with a small diameter to extract the device (FIGURE 1). It is useful to utilize ultrasonography for guidance during the removal procedure. The alligator forceps will grasp both the IUD device itself and IUD strings well, so either can be targeted during removal.
A second useful tool for IUD removal is an IUD hook (FIGURE 2). In a similar way that a curette is used for endometrial sampling, IUD hooks can be used to drag the IUD from the uterus.
Anesthesia is not usually necessary for IUD removal with alligator forceps or an IUD hook, although it may be appropriate in select patients. Data are limited with regard to the utility of paracervical blocks in this situation.
Related article:
Surgical removal of malpositioned IUDs
Hysteroscopy is an option. If removal with an alligator forceps or IUD hook is unsuccessful, or if preferred by the clinician, hysteroscopic-guided removal is a management option. Hysteroscopic removal may be required if the IUD has become embedded in the uterine wall.
Read CHALLENGE 4: Nonfundal IUD location
CHALLENGE 4: Nonfundal IUD location
CASE Copper IUD found in lower uterine segment
A 31-year-old woman (G1P1) calls your office to report that she thinks her copper IUD strings are longer than before. Office examination confirms that the strings are noticeably longer than is typical. Pelvic ultrasonography shows the copper IUD in the lower uterine segment.
What is the appropriate course of action?
Occasionally, IUDs are noted to be located in the lower uterine segment (FIGURE 3) or cervix. With malposition, users may be experiencing cramping or abnormal bleeding.
Cervical malposition calls for removal. ACOG advises that, regardless of a patient’s presenting symptoms, clinicians should remove IUDs located in the cervix (ie, the stem below the internal os) due to an increased risk of pregnancy and address the woman’s contraceptive needs.
Related article:
STOP relying on 2D ultrasound for IUD localization
Lower-uterine-segment malposition man‑agement less clear. If the patient is symptomatic, remove the device and initiate some form of contraception. If the woman is asymptomatic, the woman should be given the option of having the device removed or left in place. The mechanisms of action of both the copper and levonorgestrel-releasing IUDs suggest that this lower location is unlikely to be associated with a significant decrease in efficacy.
Unfortunately, it is difficult to estimate the risk of pregnancy for a patient whose device is located in the lower uterine segment. Braaten and Goldberg discussed case-controlled data in their 2012 article that suggest malposition may be more important to the efficacy of copper IUDs than of levonorgestrel IUDs.6,7 As unintended pregnancy is an important risk to avoid, ultimately, it is the woman’s decision as to whether she wants removal or continued IUD use.
Read CHALLENGE 5: Pregnancy in an IUD user
CHALLENGE 5: Pregnancy in an IUD user
CASE 3-year copper IUD user with positive pregnancy test
A 25-year-old woman (G3P2) presents to your office because of missed menses and a positive home pregnancy test. Her last menstrual period was 6 weeks ago. She has had a copper IUD in place for 3 years and can feel the strings herself. She has experienced light cramping but no bleeding. Office examination is notable for the IUD stem present at the external cervical os. While the pregnancy is unplanned, the patient desires that it continue.
Should you remove the IUD?
The pregnancy rate among IUD users is less than 1%—a rate that is equivalent to that experienced by women undergoing tubal sterilization. Although there is an overall low risk of pregnancy, a higher proportion of pregnancies among IUD users compared with nonusers are ectopic. Therefore, subsequent management of pregnancy in an IUD user needs to be determined by, using ultrasound, both the location of the pregnancy and whether the IUD is in place.
If an ectopic pregnancy is found, it may be managed medically or surgically with the IUD left in place if desired. If you find an intrauterine pregnancy that is undesired, the IUD can be removed at the time of a surgical abortion or before the initiation of a medical abortion.
If you fail to locate the IUD either before or after the abortion procedure, use an AP x-ray of the entire abdomen and pelvis to determine whether the IUD is in the peritoneal cavity or whether it was likely expelled prior to the pregnancy.
Related article:
In which clinical situations can the use of the 52-mg levonorgestrel-releasing IUD (Mirena) and the TCu380A copper-IUD (ParaGard) be extended?
With a desired pregnancy, if the strings are visible, remove the IUD with gentle traction. If the IUD is left in place, the risk of spontaneous abortion is significantly increased. If the strings are not seen, but the device was noted to be in the cervix by ultrasound, remove the device if the stem is below the internal cervical os. For IUDs that are located above the cervix, removal should not be attempted; counsel the patient about the increased risk of spontaneous abortion, infection, and preterm delivery.
Read CHALLENGE 6: Pregnancy in an implant user
CHALLENGE 6: Pregnancy in an implant user
CASE 3-week implant user with positive pregnancy test
Your 21-year-old patient who received a contraceptive implant 3 weeks earlier now pre‑sents with nausea and abdominal cramping. Her last menstrual period was 6 weeks ago. She has regular cycles that are 28 days in length. Results of urine pregnancy testing are positive. Prior to using the implant, the patient inconsistently used condoms.
How should you counsel your patient?
The rate of pregnancy among implant users is very low; it is estimated at 5 pregnancies per 10,000 implant users per year.8 As in this case, apparent “failures” of the contraceptive implant actually may represent placements that occurred before a very early pregnancy was recognized. Similar to IUDs, the proportion of pregnancies that are ectopic among implant users compared to nonusers may be higher.
With a pregnancy that is ectopic or that is intrauterine and undesired, the device may be left in and use continued after the pregnancy has been terminated. Although the effectiveness of medication abortion with pre-existing contraceptive implant in situ is not well known, researchers have demonstrated that medication abortion initiated at the same time as contraceptive implant insertion does not influence success of the medication abortion.9
Related article:
2016 Update on contraception
For women with desired intrauterine pregnancies, remove the device as soon as feasible and counsel the woman that there is no known teratogenic risk associated with the contraceptive implant.
Read CHALLENGE 7: Nonpalpable contraceptive implant
CHALLENGE 7: Nonpalpable contraceptive implant
CASE Patient requests device removal to attempt conception
A 30-year-old woman (G2P2) presents for contraceptive implant removal because she would like to have another child. The device was placed 30 months ago in the patient’s left arm. The insertion note in the patient’s medical record is unremarkable, and standard insertion technique was used. On physical examination, you cannot palpate the device.
What is your next course of action?
Nonpalpable implants, particularly if removal is desired, present a significant clinical challenge. Do not attempt removing a nonpalpable implant before trying to locate the device through past medical records or radiography. Records that describe the original insertion, particularly the location and type of device, are helpful.
Related article:
2015 Update on contraception
Appropriate imaging assistance. Ultrasonography with a high frequency linear array transducer (10 MHz or greater) may allow an experienced radiologist to identify the implant—including earlier versions without barium (Implanon) and later ones with barium (Nexplanon). Magnetic resonance imaging (MRI), computed tomography scan, or plain x-ray also can be used to detect a barium-containing device; MRI can be used to locate a non−barium-containing implant.
Carry out removal using ultrasonographic guidance. If a deep insertion is felt to be close to a neurovascular bundle, device removal should be carried out in an operating room by a surgeon familiar with the anatomy of the upper arm.
When an implant cannot be located despite radiography. This is an infrequent occurrence. Merck, the manufacturer of the etonorgestrel implant, provides advice and support in this circumstance. (Visit https://www.merckconnect.com/nexplanon/over view.html.)
Recently, published case reports detail episodes of implants inserted into the venous system with migration to the heart or lungs.10 While this phenomenon is considered rare, the manufacturer has recommended that insertion of the contraceptive implant avoid the sulcus between the biceps and triceps muscles.
Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.
The use of long-acting reversible contraceptive (LARC) methods has shown a steady increase in the United States. The major factors for increasing acceptance include high efficacy, ease of use, and an acceptable adverse effect profile. Since these methods require placement under the skin (implantable device) or into the uterus (intrauterine devices [IUDs]), unique management issues arise during their usage. Recently, the American College of Obstetricians and Gynecologists (ACOG) released a committee opinion addressing several of these clinical challenges—among them: pain with insertion, what to do when the IUD strings are not visualized, and the plan of action for a nonpalpable IUD or contraceptive implant.1 In this article we present 7 cases, and successful management approaches, that reflect ACOG’s recent recommendations and our extensive clinical experience.
Read the first CHALLENGE: Pain with IUD insertion
CHALLENGE 1: Pain with IUD insertion
CASE First-time, nulliparous IUD user apprehensive about insertion pain
A 21-year-old woman (G0) presents for placement of a 52-mg levonorgestrel IUD for contraception and treatment of dysmenorrhea. Her medical and surgical histories are unremarkable. She has heard that IUD insertion “is more painful if you haven’t had a baby yet” and she asks what treatments are available to aid in pain relief.
What can you offer her?
A number of approaches have been used to reduce IUD insertion pain, including:
- placing lidocaine gel into or on the cervix
- lidocaine paracervical block
- preinsertion use of misoprostol or nonsteroidal anti-inflammatory drugs.
Authors of a recent Cochrane review2 indicated that none of these approaches were particularly effective at reducing insertion pain for nulliparous women. Naproxen sodium 550 mg or tramadol 50 mg taken 1 hour prior to IUD insertion have been found to decrease IUD insertion pain in multiparous patients.3 Misoprostol, apart from being ineffective in reducing insertion pain, also requires use for a number of hours before insertion and can cause painful uterine cramping, upset stomach, and diarrhea.2 Some studies do suggest that use of a paracervical block does reduce the pain associated with tenaculum placement but not the IUD insertion itself.
Related article:
Benefit of self-administered vaginal lidocaine gel in IUD placement
A reasonable pain management strategy for nulliparous patients. Given these data, there is not an evidence-based IUD insertion pain management strategy that can be used for the nulliparous case patient. A practical approach for nulliparous patients is to offer naproxen sodium or tramadol, which have been found to be beneficial in multiparous patients, to a nulliparous patient. Additionally, lidocaine gel applied to the cervix or tenaculum-site injection can be considered for tenaculum-associated pain, although it does not appear to help significantly with IUD insertion pain. Misoprostol should be avoided as it does not alleviate the pain of insertion and it can cause bothersome adverse effects.
Read CHALLENGE 2: IUD strings not visualized
CHALLENGE 2: IUD strings not visualized
CASE No strings palpated 6 weeks after postpartum IUD placement
A 26-year-old woman (G2P2) presents to your office for a postpartum visit 6 weeks after an uncomplicated cesarean delivery at term. She had requested that a 52-mg levonorgestrel IUD be placed at the time of delivery, and the delivery report describes an uneventful placement. The patient has not been able to feel the IUD strings using her fingers and you do not find them on examination. She does not remember the IUD falling out.
What are the next steps in her management?
Failure to palpate the IUD strings by the user or failure to visualize the strings is a fairly common occurrence. This is especially true when an IUD is placed immediatelypostpartum, as in this patient’s case.
When the strings cannot be palpated, it is important to exclude pregnancy and recommend a form of backup contraception, such as condoms and emergency contraception if appropriate, until evaluation can be completed.
Steps to locate a device. In the office setting, the strings often can be located by inserting a cytobrush into the endocervical canal to extract them. If that maneuver fails to locate them, an ultrasound should be completed to determine if the device is in the uterus. If the ultrasound does not detect the device in the uterus, obtain an anteroposterior (AP) x-ray encompassing the entire abdomen and pelvis. All IUDs used in the United States are radiopaque and will be observed on x-ray if present. If the IUD is identified, operative removal is indicated.
Related article:
How to identify and localize IUDs on ultrasound
Intraperitoneal location. If an IUD is found in this location, it is usually the result of a perforation that occurred at the time of insertion. In general, the device can be removed via laparoscopy. Occasionally, laparotomy is needed if there is significant pelvic infection, possible bowel perforation, or if there is an inability to locate the device at laparoscopy.4 The copper IUD is more inflammatory than the levonorgestrel IUDs.
Abdominal location. No matter the IUD type, operative removal of intra-abdominal IUDs should take place expeditiously after they are discovered.
In the case of expulsion. If the IUD is not seen on x-ray, expulsion is the likely cause. Expulsion tends to be more common among5:
- parous users
- those younger than age 20
- placements that immediately follow a delivery or second-trimester abortion.
Nulliparity and type of device are not associated with increased risk of expulsion.
Read CHALLENGE 3: Difficult IUD removal
CHALLENGE 3: Difficult IUD removal
CASE Strings not palpated in a patient with history of LEEP
A 37-year-old woman (G3P2) presents to your office for IUD removal. She underwent a loop electrosurgical excision procedure 2 years ago for cervical intraepithelial neoplasia (CIN) 2 and since then has not been able to feel the IUD strings. On pelvic examination, you do not palpate or visualize the IUD strings after speculum placement.
How can you achieve IUD removal for your patient?
When a patient requests that her IUD be removed, but the strings are not visible and the woman is not pregnant, employ ultrasonography to confirm the IUD remains intrauterine and to rule out expulsion or perforation.
Employ alligator forceps or an IUD hook. Once intrauterine position is confirmed, use an alligator forceps of suitable length and with a small diameter to extract the device (FIGURE 1). It is useful to utilize ultrasonography for guidance during the removal procedure. The alligator forceps will grasp both the IUD device itself and IUD strings well, so either can be targeted during removal.
A second useful tool for IUD removal is an IUD hook (FIGURE 2). In a similar way that a curette is used for endometrial sampling, IUD hooks can be used to drag the IUD from the uterus.
Anesthesia is not usually necessary for IUD removal with alligator forceps or an IUD hook, although it may be appropriate in select patients. Data are limited with regard to the utility of paracervical blocks in this situation.
Related article:
Surgical removal of malpositioned IUDs
Hysteroscopy is an option. If removal with an alligator forceps or IUD hook is unsuccessful, or if preferred by the clinician, hysteroscopic-guided removal is a management option. Hysteroscopic removal may be required if the IUD has become embedded in the uterine wall.
Read CHALLENGE 4: Nonfundal IUD location
CHALLENGE 4: Nonfundal IUD location
CASE Copper IUD found in lower uterine segment
A 31-year-old woman (G1P1) calls your office to report that she thinks her copper IUD strings are longer than before. Office examination confirms that the strings are noticeably longer than is typical. Pelvic ultrasonography shows the copper IUD in the lower uterine segment.
What is the appropriate course of action?
Occasionally, IUDs are noted to be located in the lower uterine segment (FIGURE 3) or cervix. With malposition, users may be experiencing cramping or abnormal bleeding.
Cervical malposition calls for removal. ACOG advises that, regardless of a patient’s presenting symptoms, clinicians should remove IUDs located in the cervix (ie, the stem below the internal os) due to an increased risk of pregnancy and address the woman’s contraceptive needs.
Related article:
STOP relying on 2D ultrasound for IUD localization
Lower-uterine-segment malposition man‑agement less clear. If the patient is symptomatic, remove the device and initiate some form of contraception. If the woman is asymptomatic, the woman should be given the option of having the device removed or left in place. The mechanisms of action of both the copper and levonorgestrel-releasing IUDs suggest that this lower location is unlikely to be associated with a significant decrease in efficacy.
Unfortunately, it is difficult to estimate the risk of pregnancy for a patient whose device is located in the lower uterine segment. Braaten and Goldberg discussed case-controlled data in their 2012 article that suggest malposition may be more important to the efficacy of copper IUDs than of levonorgestrel IUDs.6,7 As unintended pregnancy is an important risk to avoid, ultimately, it is the woman’s decision as to whether she wants removal or continued IUD use.
Read CHALLENGE 5: Pregnancy in an IUD user
CHALLENGE 5: Pregnancy in an IUD user
CASE 3-year copper IUD user with positive pregnancy test
A 25-year-old woman (G3P2) presents to your office because of missed menses and a positive home pregnancy test. Her last menstrual period was 6 weeks ago. She has had a copper IUD in place for 3 years and can feel the strings herself. She has experienced light cramping but no bleeding. Office examination is notable for the IUD stem present at the external cervical os. While the pregnancy is unplanned, the patient desires that it continue.
Should you remove the IUD?
The pregnancy rate among IUD users is less than 1%—a rate that is equivalent to that experienced by women undergoing tubal sterilization. Although there is an overall low risk of pregnancy, a higher proportion of pregnancies among IUD users compared with nonusers are ectopic. Therefore, subsequent management of pregnancy in an IUD user needs to be determined by, using ultrasound, both the location of the pregnancy and whether the IUD is in place.
If an ectopic pregnancy is found, it may be managed medically or surgically with the IUD left in place if desired. If you find an intrauterine pregnancy that is undesired, the IUD can be removed at the time of a surgical abortion or before the initiation of a medical abortion.
If you fail to locate the IUD either before or after the abortion procedure, use an AP x-ray of the entire abdomen and pelvis to determine whether the IUD is in the peritoneal cavity or whether it was likely expelled prior to the pregnancy.
Related article:
In which clinical situations can the use of the 52-mg levonorgestrel-releasing IUD (Mirena) and the TCu380A copper-IUD (ParaGard) be extended?
With a desired pregnancy, if the strings are visible, remove the IUD with gentle traction. If the IUD is left in place, the risk of spontaneous abortion is significantly increased. If the strings are not seen, but the device was noted to be in the cervix by ultrasound, remove the device if the stem is below the internal cervical os. For IUDs that are located above the cervix, removal should not be attempted; counsel the patient about the increased risk of spontaneous abortion, infection, and preterm delivery.
Read CHALLENGE 6: Pregnancy in an implant user
CHALLENGE 6: Pregnancy in an implant user
CASE 3-week implant user with positive pregnancy test
Your 21-year-old patient who received a contraceptive implant 3 weeks earlier now pre‑sents with nausea and abdominal cramping. Her last menstrual period was 6 weeks ago. She has regular cycles that are 28 days in length. Results of urine pregnancy testing are positive. Prior to using the implant, the patient inconsistently used condoms.
How should you counsel your patient?
The rate of pregnancy among implant users is very low; it is estimated at 5 pregnancies per 10,000 implant users per year.8 As in this case, apparent “failures” of the contraceptive implant actually may represent placements that occurred before a very early pregnancy was recognized. Similar to IUDs, the proportion of pregnancies that are ectopic among implant users compared to nonusers may be higher.
With a pregnancy that is ectopic or that is intrauterine and undesired, the device may be left in and use continued after the pregnancy has been terminated. Although the effectiveness of medication abortion with pre-existing contraceptive implant in situ is not well known, researchers have demonstrated that medication abortion initiated at the same time as contraceptive implant insertion does not influence success of the medication abortion.9
Related article:
2016 Update on contraception
For women with desired intrauterine pregnancies, remove the device as soon as feasible and counsel the woman that there is no known teratogenic risk associated with the contraceptive implant.
Read CHALLENGE 7: Nonpalpable contraceptive implant
CHALLENGE 7: Nonpalpable contraceptive implant
CASE Patient requests device removal to attempt conception
A 30-year-old woman (G2P2) presents for contraceptive implant removal because she would like to have another child. The device was placed 30 months ago in the patient’s left arm. The insertion note in the patient’s medical record is unremarkable, and standard insertion technique was used. On physical examination, you cannot palpate the device.
What is your next course of action?
Nonpalpable implants, particularly if removal is desired, present a significant clinical challenge. Do not attempt removing a nonpalpable implant before trying to locate the device through past medical records or radiography. Records that describe the original insertion, particularly the location and type of device, are helpful.
Related article:
2015 Update on contraception
Appropriate imaging assistance. Ultrasonography with a high frequency linear array transducer (10 MHz or greater) may allow an experienced radiologist to identify the implant—including earlier versions without barium (Implanon) and later ones with barium (Nexplanon). Magnetic resonance imaging (MRI), computed tomography scan, or plain x-ray also can be used to detect a barium-containing device; MRI can be used to locate a non−barium-containing implant.
Carry out removal using ultrasonographic guidance. If a deep insertion is felt to be close to a neurovascular bundle, device removal should be carried out in an operating room by a surgeon familiar with the anatomy of the upper arm.
When an implant cannot be located despite radiography. This is an infrequent occurrence. Merck, the manufacturer of the etonorgestrel implant, provides advice and support in this circumstance. (Visit https://www.merckconnect.com/nexplanon/over view.html.)
Recently, published case reports detail episodes of implants inserted into the venous system with migration to the heart or lungs.10 While this phenomenon is considered rare, the manufacturer has recommended that insertion of the contraceptive implant avoid the sulcus between the biceps and triceps muscles.
Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.
- American College of Obstetricians and Gynecologists. Committee Opinion No. 672: clinical challenges of long-acting reversible contraceptive methods. Obstet Gynecol. 2016;128(3):e69−e77.
- Lopez LM, Bernholc A, Zeng Y, et al. Interventions for pain with intrauterine device insertion. Cochrane Database Syst Rev. 2015;(7):CD007373.
- Karabayirli S, Ayrim AA, Muslu B. Comparison of the analgesic effects of oral tramadol and naproxen sodium on pain relief during IUD insertion. J Minim Invasive Gynecol. 2012;19(5):581−584.
- Kho KA, Chamsy DJ. Perforated intraperitoneal intrauterine contraceptive devices: diagnosis, management, and clinical outcomes. J Minim Invasive Gynecol. 2014;21(4):596−601.
- Madden T, McNicholas C, Zhao Q, Secura GM, Eisenberg DL, Peipert JF. Association of age and parity with intrauterine device expulsion. Obstet Gynecol. 2014;124(4):718−726.
- Patil E, Bednarek PH. Immediate intrauterine device insertion following surgical abortion. Obstet Gynecol Clin North Am. 2015;42(4):583−546.
- Braaten and Goldberg. OBG Manag. Malpositioned IUDs: When you should intervene (and when you should not). OBG Manag. 2012;24(8):38−46.
- Trussell J. Contraceptive failure in the United States. Contraception. 2011;83(5):397−404.
- Raymond EG, Weaver MA, Tan YL, et al. Effect of immediate compared with delayed insertion of etonogestrel implants on medical abortion efficacy and repeat pregnancy: a randomized controlled trial. Obstet Gynecol. 2017;127(2):306−312.
- Rowlands S, Mansour D, Walling M. Intravascular migration of contraceptive implants: two more cases. Contraception. 2016. In press.
- American College of Obstetricians and Gynecologists. Committee Opinion No. 672: clinical challenges of long-acting reversible contraceptive methods. Obstet Gynecol. 2016;128(3):e69−e77.
- Lopez LM, Bernholc A, Zeng Y, et al. Interventions for pain with intrauterine device insertion. Cochrane Database Syst Rev. 2015;(7):CD007373.
- Karabayirli S, Ayrim AA, Muslu B. Comparison of the analgesic effects of oral tramadol and naproxen sodium on pain relief during IUD insertion. J Minim Invasive Gynecol. 2012;19(5):581−584.
- Kho KA, Chamsy DJ. Perforated intraperitoneal intrauterine contraceptive devices: diagnosis, management, and clinical outcomes. J Minim Invasive Gynecol. 2014;21(4):596−601.
- Madden T, McNicholas C, Zhao Q, Secura GM, Eisenberg DL, Peipert JF. Association of age and parity with intrauterine device expulsion. Obstet Gynecol. 2014;124(4):718−726.
- Patil E, Bednarek PH. Immediate intrauterine device insertion following surgical abortion. Obstet Gynecol Clin North Am. 2015;42(4):583−546.
- Braaten and Goldberg. OBG Manag. Malpositioned IUDs: When you should intervene (and when you should not). OBG Manag. 2012;24(8):38−46.
- Trussell J. Contraceptive failure in the United States. Contraception. 2011;83(5):397−404.
- Raymond EG, Weaver MA, Tan YL, et al. Effect of immediate compared with delayed insertion of etonogestrel implants on medical abortion efficacy and repeat pregnancy: a randomized controlled trial. Obstet Gynecol. 2017;127(2):306−312.
- Rowlands S, Mansour D, Walling M. Intravascular migration of contraceptive implants: two more cases. Contraception. 2016. In press.
Three good apps for calculating the date of delivery
Technology has changed--and continues to change--the practice of medicine. Health care providers access word processing programs, e-mail, and electronic medical records using desktop and laptop computers. Now, providers are accessing these same tools with handheld devices such as smartphones, tablets, and "phablets" (a class of mobile devices designed to combine the form of a smartphone and a tablet).
Critical to the popularity and functionality of handheld devices are mobile applications, also known as "apps." An app is a self-contained program or piece of software designed to run on handheld devices to perform a specific purpose. App overload and app inaccuracy, however, are major problems. Health care providers do not have the time to search through thousands of medical apps in app stores to find specialty-related apps that might be useful in their practice--or to check the accuracy of those apps.
Vetted apps for ObGyns
My team's research has focused on identifying apps for ObGyns to use in clinical practice.1 In the process, we have developed the APPLICATIONS scoring system, which contains objective and subjective components to help differentiate among the accurate apps.2 This new quarterly "App review" series in OBG Management will showcase recommended apps for the busy ObGyn in the hope of improving work efficiency and the provider-patient relationship.
First up: Apps for calculating the date of delivery. This first app review focuses on pregnancy wheels, or due date calculators. Calculator apps are preferred over other types of apps such as procedure/case documentation apps, as providers use smartphones at point of care to allow rapid decision making.3 Calculating the estimated date of delivery (EDD) and gestational age (GA) is an important, vital task for providers of obstetric care. In fact, new guidelines for calculating EDD were recently developed by the American College of Obstetricians and Gynecologists (ACOG), the American Institute of Ultrasound in Medicine (AIUM), and the Society for Maternal-Fetal Medicine (SMFM).4 Notably, pregnancy wheel apps are more accurate than paper wheels.5 My team checked the accuracy of the pregnancy wheel apps by applying strict criteria to ensure the correct EDD and GA and then scored them in a systematic, nonbiased, conflict-of-interest-free manner.2
Related article:
Elective induction of labor at 39 (vs 41) weeks: Caveats and considerations
The TABLE below lists the top 3 recommended pregnancy wheel or due date calculator apps vetted by our research. The apps are listed alphabetically, and details for each app are provided based on a shortened version of the APPLICATIONS scoring system, APPLI--app comprehensiveness, price, platform, literature use, and important special features.
Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.
- Farag S, Chyjek K, Chen KT. Identification of iPhone and iPad applications for obstetrics and gynecology providers. Obstet Gynecol. 2014;124(5):941-945.
- Chyjek K, Farag S, Chen KT. Rating pregnancy wheel applications using the APPLICATIONS scoring system. Obstet Gynecol. 2015;125(6):1478-1483.
- Payne KB, Wharrad H, Watts K. Smartphone and medical related App use among medical students and junior doctors in the United Kingdom (UK): a regional survey. BMC Inform Decis Mak. 2012;12:121.
- American College of Obstetricians and Gynecologists. Committee Opinion No. 611. Method for estimating due date. Obstet Gynecol. 2014;124(4):863-866.
- Chambliss LR, Clark SL. Paper gestational age wheels are generally inaccurate. Am J Obstet Gynecol. 2014;210(2):145.e1-e4.
Technology has changed--and continues to change--the practice of medicine. Health care providers access word processing programs, e-mail, and electronic medical records using desktop and laptop computers. Now, providers are accessing these same tools with handheld devices such as smartphones, tablets, and "phablets" (a class of mobile devices designed to combine the form of a smartphone and a tablet).
Critical to the popularity and functionality of handheld devices are mobile applications, also known as "apps." An app is a self-contained program or piece of software designed to run on handheld devices to perform a specific purpose. App overload and app inaccuracy, however, are major problems. Health care providers do not have the time to search through thousands of medical apps in app stores to find specialty-related apps that might be useful in their practice--or to check the accuracy of those apps.
Vetted apps for ObGyns
My team's research has focused on identifying apps for ObGyns to use in clinical practice.1 In the process, we have developed the APPLICATIONS scoring system, which contains objective and subjective components to help differentiate among the accurate apps.2 This new quarterly "App review" series in OBG Management will showcase recommended apps for the busy ObGyn in the hope of improving work efficiency and the provider-patient relationship.
First up: Apps for calculating the date of delivery. This first app review focuses on pregnancy wheels, or due date calculators. Calculator apps are preferred over other types of apps such as procedure/case documentation apps, as providers use smartphones at point of care to allow rapid decision making.3 Calculating the estimated date of delivery (EDD) and gestational age (GA) is an important, vital task for providers of obstetric care. In fact, new guidelines for calculating EDD were recently developed by the American College of Obstetricians and Gynecologists (ACOG), the American Institute of Ultrasound in Medicine (AIUM), and the Society for Maternal-Fetal Medicine (SMFM).4 Notably, pregnancy wheel apps are more accurate than paper wheels.5 My team checked the accuracy of the pregnancy wheel apps by applying strict criteria to ensure the correct EDD and GA and then scored them in a systematic, nonbiased, conflict-of-interest-free manner.2
Related article:
Elective induction of labor at 39 (vs 41) weeks: Caveats and considerations
The TABLE below lists the top 3 recommended pregnancy wheel or due date calculator apps vetted by our research. The apps are listed alphabetically, and details for each app are provided based on a shortened version of the APPLICATIONS scoring system, APPLI--app comprehensiveness, price, platform, literature use, and important special features.
Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.
Technology has changed--and continues to change--the practice of medicine. Health care providers access word processing programs, e-mail, and electronic medical records using desktop and laptop computers. Now, providers are accessing these same tools with handheld devices such as smartphones, tablets, and "phablets" (a class of mobile devices designed to combine the form of a smartphone and a tablet).
Critical to the popularity and functionality of handheld devices are mobile applications, also known as "apps." An app is a self-contained program or piece of software designed to run on handheld devices to perform a specific purpose. App overload and app inaccuracy, however, are major problems. Health care providers do not have the time to search through thousands of medical apps in app stores to find specialty-related apps that might be useful in their practice--or to check the accuracy of those apps.
Vetted apps for ObGyns
My team's research has focused on identifying apps for ObGyns to use in clinical practice.1 In the process, we have developed the APPLICATIONS scoring system, which contains objective and subjective components to help differentiate among the accurate apps.2 This new quarterly "App review" series in OBG Management will showcase recommended apps for the busy ObGyn in the hope of improving work efficiency and the provider-patient relationship.
First up: Apps for calculating the date of delivery. This first app review focuses on pregnancy wheels, or due date calculators. Calculator apps are preferred over other types of apps such as procedure/case documentation apps, as providers use smartphones at point of care to allow rapid decision making.3 Calculating the estimated date of delivery (EDD) and gestational age (GA) is an important, vital task for providers of obstetric care. In fact, new guidelines for calculating EDD were recently developed by the American College of Obstetricians and Gynecologists (ACOG), the American Institute of Ultrasound in Medicine (AIUM), and the Society for Maternal-Fetal Medicine (SMFM).4 Notably, pregnancy wheel apps are more accurate than paper wheels.5 My team checked the accuracy of the pregnancy wheel apps by applying strict criteria to ensure the correct EDD and GA and then scored them in a systematic, nonbiased, conflict-of-interest-free manner.2
Related article:
Elective induction of labor at 39 (vs 41) weeks: Caveats and considerations
The TABLE below lists the top 3 recommended pregnancy wheel or due date calculator apps vetted by our research. The apps are listed alphabetically, and details for each app are provided based on a shortened version of the APPLICATIONS scoring system, APPLI--app comprehensiveness, price, platform, literature use, and important special features.
Share your thoughts! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.
- Farag S, Chyjek K, Chen KT. Identification of iPhone and iPad applications for obstetrics and gynecology providers. Obstet Gynecol. 2014;124(5):941-945.
- Chyjek K, Farag S, Chen KT. Rating pregnancy wheel applications using the APPLICATIONS scoring system. Obstet Gynecol. 2015;125(6):1478-1483.
- Payne KB, Wharrad H, Watts K. Smartphone and medical related App use among medical students and junior doctors in the United Kingdom (UK): a regional survey. BMC Inform Decis Mak. 2012;12:121.
- American College of Obstetricians and Gynecologists. Committee Opinion No. 611. Method for estimating due date. Obstet Gynecol. 2014;124(4):863-866.
- Chambliss LR, Clark SL. Paper gestational age wheels are generally inaccurate. Am J Obstet Gynecol. 2014;210(2):145.e1-e4.
- Farag S, Chyjek K, Chen KT. Identification of iPhone and iPad applications for obstetrics and gynecology providers. Obstet Gynecol. 2014;124(5):941-945.
- Chyjek K, Farag S, Chen KT. Rating pregnancy wheel applications using the APPLICATIONS scoring system. Obstet Gynecol. 2015;125(6):1478-1483.
- Payne KB, Wharrad H, Watts K. Smartphone and medical related App use among medical students and junior doctors in the United Kingdom (UK): a regional survey. BMC Inform Decis Mak. 2012;12:121.
- American College of Obstetricians and Gynecologists. Committee Opinion No. 611. Method for estimating due date. Obstet Gynecol. 2014;124(4):863-866.
- Chambliss LR, Clark SL. Paper gestational age wheels are generally inaccurate. Am J Obstet Gynecol. 2014;210(2):145.e1-e4.
Epilepsy Raises Risks for Veterans
Iraq and Afghanistan veterans (IAV) with epilepsy have more than twice the risk of dying than do those without epilepsy, according to VA researchers.
In the study of 320,583 veterans, 2,187 met the epilepsy criteria. About 5 times more veterans with epilepsy had died by the end of follow-up compared with those without epilepsy. Veterans with epilepsy also are more likely to have mental and physical comorbidities, such as posttraumatic stress disorder, depression, traumatic brain injury, substance use disorder, and hypertension.
Related: Providing Quality Epilepsy Care for Veterans
Before their study, which is the first examining mortality in IAV with epilepsy, the researchers say little information existed about comorbidities and mortality. Epilepsy in veterans usually develops during or after service. People with epilepsy usually are excluded from military service (DoD standards require a 5-year period without seizures or treatment for seizures prior to enlistment). The age-adjusted prevalence of seizure disorder in IAV is 6.1 per 1,000 compared with 7.1 to 10 per 1,000 in the general population.
In response to the higher risk of epilepsy in IAV with traumatic brain injury, the VA established the Epilepsy Centers of Excellence, the researchers note, to increase access to comprehensive multidisciplinary epilepsy specialty care. However, the significantly higher prevalence of comorbidities in this population suggests that “closer integration of primary care, epilepsy specialty care, and mental health care might be needed to reduce excess mortality.”
Related: VA to Reexamine 24,000 Veterans for TBI
The researchers suggest that public health agencies, including the VA, implement evidence-based, chronic disease self-management programs and supports that target physical and psychiatric comorbidity, study long-term outcomes, and ensure links to appropriate clinical and community health care facilities and social service providers.
Iraq and Afghanistan veterans (IAV) with epilepsy have more than twice the risk of dying than do those without epilepsy, according to VA researchers.
In the study of 320,583 veterans, 2,187 met the epilepsy criteria. About 5 times more veterans with epilepsy had died by the end of follow-up compared with those without epilepsy. Veterans with epilepsy also are more likely to have mental and physical comorbidities, such as posttraumatic stress disorder, depression, traumatic brain injury, substance use disorder, and hypertension.
Related: Providing Quality Epilepsy Care for Veterans
Before their study, which is the first examining mortality in IAV with epilepsy, the researchers say little information existed about comorbidities and mortality. Epilepsy in veterans usually develops during or after service. People with epilepsy usually are excluded from military service (DoD standards require a 5-year period without seizures or treatment for seizures prior to enlistment). The age-adjusted prevalence of seizure disorder in IAV is 6.1 per 1,000 compared with 7.1 to 10 per 1,000 in the general population.
In response to the higher risk of epilepsy in IAV with traumatic brain injury, the VA established the Epilepsy Centers of Excellence, the researchers note, to increase access to comprehensive multidisciplinary epilepsy specialty care. However, the significantly higher prevalence of comorbidities in this population suggests that “closer integration of primary care, epilepsy specialty care, and mental health care might be needed to reduce excess mortality.”
Related: VA to Reexamine 24,000 Veterans for TBI
The researchers suggest that public health agencies, including the VA, implement evidence-based, chronic disease self-management programs and supports that target physical and psychiatric comorbidity, study long-term outcomes, and ensure links to appropriate clinical and community health care facilities and social service providers.
Iraq and Afghanistan veterans (IAV) with epilepsy have more than twice the risk of dying than do those without epilepsy, according to VA researchers.
In the study of 320,583 veterans, 2,187 met the epilepsy criteria. About 5 times more veterans with epilepsy had died by the end of follow-up compared with those without epilepsy. Veterans with epilepsy also are more likely to have mental and physical comorbidities, such as posttraumatic stress disorder, depression, traumatic brain injury, substance use disorder, and hypertension.
Related: Providing Quality Epilepsy Care for Veterans
Before their study, which is the first examining mortality in IAV with epilepsy, the researchers say little information existed about comorbidities and mortality. Epilepsy in veterans usually develops during or after service. People with epilepsy usually are excluded from military service (DoD standards require a 5-year period without seizures or treatment for seizures prior to enlistment). The age-adjusted prevalence of seizure disorder in IAV is 6.1 per 1,000 compared with 7.1 to 10 per 1,000 in the general population.
In response to the higher risk of epilepsy in IAV with traumatic brain injury, the VA established the Epilepsy Centers of Excellence, the researchers note, to increase access to comprehensive multidisciplinary epilepsy specialty care. However, the significantly higher prevalence of comorbidities in this population suggests that “closer integration of primary care, epilepsy specialty care, and mental health care might be needed to reduce excess mortality.”
Related: VA to Reexamine 24,000 Veterans for TBI
The researchers suggest that public health agencies, including the VA, implement evidence-based, chronic disease self-management programs and supports that target physical and psychiatric comorbidity, study long-term outcomes, and ensure links to appropriate clinical and community health care facilities and social service providers.
Patch Testing for Adverse Drug Reactions
Adverse drug reactions account for 3% to 6% of hospital admissions in the United States and occur in 10% to 15% of hospitalized patients.1,2 The most common culprits are antibiotics and nonsteroidal anti-inflammatory drugs (NSAIDs).3-12 In most cases, diagnoses are made clinically without diagnostic testing. To identify drug allergies associated with diagnostic testing, one center selected patients with suspected cutaneous drug reactions (2006-2010) for further evaluation.13 Of 612 patients who were evaluated, 141 had a high suspicion of drug allergy and were included in the analysis. The excluded patients had pseudoallergic reactions, reactive exanthemas due to infection, histopathologic exclusion of drug allergy, angioedema, or other dermatological conditions such as contact dermatitis and eczema. Of the included patients, 107 were diagnosed with drug reactions, while the remainder had non–drug-related exanthemas or unknown etiology after testing. Identified culprit drugs were predominantly antibiotics (39.8%) and NSAIDs (21.2%); contrast media, anticoagulants, anticonvulsants, antimalarials, antifungals, glucocorticoids, antihypertensives, and proton pump inhibitors also were implicated. They were identified with skin prick, intradermal, and patch tests (62.6%); lymphocyte transformation test (17.7%); oral rechallenge (5.6%); or without skin testing (6.5%). One quarter of patients with a high suspicion for drug allergy did not have a confirmed drug eruption in this study. Another study found that 10% to 20% of patients with reported penicillin allergy had confirmation via skin prick testing.14 These findings suggest that confirmation of suspected drug allergy may require more than one diagnostic test.
Tests for Adverse Drug Reactions
The following tests have been shown to aid in the identification of cutaneous drug eruptions: (1) patch tests15-21; (2) intradermal tests14,15,19,20; (3) drug provocation tests15,20; and (4) lymphocyte transformation tests.20 Intradermal or skin prick tests are most useful in urticarial eruptions but can be considered in nonurticarial eruptions with delayed inspection of test sites up to 1 week after testing. Drug provocation tests are considered the gold standard but involve patient risk. Lymphocyte transformation tests use the principle that T lymphocytes proliferate in the presence of drugs to which the patient is sensitized. Patch tests will be discussed in greater detail below. Immunohistochemistry can determine immunologic mechanisms of eruptions but cannot identify causative agents.16,17,22
A retrospective study of patients referred for evaluation of adverse drug reactions between 1996 and 2006 found the collective negative predictive value (NPV)—the percentage of truly negative skin tests based on provocation or substitution testing—of cutaneous drug tests including patch, prick, and intradermal tests to be 89.6% (95% confidence interval, 85.9%-93.3%).23 The NPVs of each test were not reported. Patients with negative cutaneous tests had subsequent oral rechallenge or substitution testing with medication from the same drug class.23 Another study16 found the NPV of patch testing to be at least 79% after review of data from other studies using patch and provocation testing.16,24 These studies suggest that cutaneous testing can be useful, albeit imperfect, in the evaluation and diagnosis of drug allergy.
Review of the Patch Test
Patch tests can be helpful in diagnosis of delayed hypersensitivities.18 Patch testing is most commonly and effectively used to diagnose allergic contact dermatitis, but its utility in other applications, such as diagnosis of cutaneous drug eruptions, has not been extensively studied.
The development of patch tests to diagnose systemic drug allergies is inhibited by the uncertainty of percutaneous drug penetration, a dearth of studies to determine the best test concentrations of active drug in the patch test, and the potential for nonimmunologic contact urticaria upon skin exposure. Furthermore, cutaneous metabolism of many antigens is well documented, but correlation to systemic metabolism often is unknown, which can confound patch test results and lead to false-negative results when the skin’s metabolic capacity does not match the body’s capacity to generate antigens capable of eliciting immunogenic responses.21 Additionally, the method used to suspend and disperse drugs in patch test vehicles is unfamiliar to most pharmacists, and standardized concentrations and vehicles are available only for some medications.25 Studies sufficient to obtain US Food and Drug Administration approval of patch tests for systemic drug eruptions would be costly and therefore prohibitive to investigators. The majority of the literature consists of case reports and data extrapolated from reviews. Patch test results of many drugs have been reported in the literature, with the highest frequencies of positive results associated with anticonvulsants,26 antibiotics, corticosteroids, calcium channel blockers, and benzodiazepines.21
Patch test placement affects the diagnostic value of the test. Placing patch tests on previously involved sites of fixed drug eruptions improves yield over placement on uninvolved skin.27 Placing patch tests on previously involved sites of other drug eruptions such as toxic epidermal necrolysis also may aid in diagnosis, though the literature is sparse.25,26,28
Patch Testing in Drug Eruptions
Morbilliform eruptions account for 48% to 91% of patients with adverse drug reactions.4-6 Other drug eruptions include urticarial eruptions, acute generalized exanthematous pustulosis (AGEP), drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome, toxic epidermal necrolysis, Stevens-Johnson syndrome, lichenoid drug eruption, symmetric drug-related intertriginous and flexural exanthema (SDRIFE), erythema multiforme (EM), and systemic contact dermatitis. The Table summarizes reports of positive patch tests with various medications for these drug eruptions.
In general, antimicrobials and NSAIDs were the most implicated drugs with positive patch test results in AGEP, DRESS syndrome, EM, fixed drug eruptions, and morbilliform eruptions. In AGEP, positive results also were reported for other drugs, including terbinafine and morphine.29-38 In fixed drug eruptions, patch testing on involved skin showed positive results to NSAIDs, analgesics, platelet inhibitors, and antimicrobials.27,52-55 Patch testing in DRESS syndrome has shown many positive reactions to antiepileptics and antipsychotics.39-43 One study used patch tests in SDRIFE, reporting positive results with antimicrobials, antineoplastics, decongestants, and glucocorticoids.61 Nonsteroidal anti-inflammatory drugs, antimicrobials, calcium channel blockers, and histamine antagonists were implicated in EM.47-51 Positive patch tests were seen in morbilliform eruptions with selective serotonin reuptake inhibitors, antiepileptics/benzodiazepines, NSAIDs, and antimicrobials.28,57-60 In toxic epidermal necrolysis, diagnosis with patch testing was made using patches placed on previously involved skin with sulfamethoxazole.62
Systemic Contact Dermatitis
Drugs historically recognized as causing allergic contact dermatitis (eg, topical gentamycin) can cause systemic contact dermatitis, which can be patch tested. In these situations, systemic contact dermatitis may be due to either the active drug or excipients in the medication formulation. Excipients are inactive ingredients in medications that provide a suitable consistency, appearance, or form. Often overlooked as culprits of drug hypersensitivity because they are theoretically inert, excipients are increasingly implicated in drug allergy. Swerlick and Campbell63 described 11 cases in which chronic unexplained pruritus responded to medication changes to avoid coloring agents. The most common culprits were FD&C Blue No. 1 and FD&C Blue No. 2. Patch testing for allergies to dyes can be clinically useful, though a lack of commercially available patch tests makes diagnosis difficult.64
Other excipients can cause cutaneous reactions. Propylene glycol, commonly implicated in allergic contact dermatitis, also can cause cutaneous eruptions upon systemic exposure.65 Corticosteroid-induced systemic contact dermatitis has been reported, though it is less prevalent than allergic contact dermatitis.66 These reactions usually are due to nonmethylated and nonhalogenated corticosteroids including budesonide, cortisone, hydrocortisone, prednisolone, and methylprednisolone.67,68 Patch testing in these situations is complicated by the possibility of false-negative results due to the anti-inflammatory effects of the corticosteroids. Therefore, patch testing should be performed using standardized and not treatment concentrations.
In our clinic, we have anecdotally observed several patients with chronic dermatitis and suspected NSAID allergies have positive patch test results with propylene glycol and not the suspected drug. Excipients encountered in multiple drugs and foods are more likely to present as chronic dermatitis, while active drug ingredients started in hospital settings more often present as acute dermatitis.
Our Experience
We have patch tested a handful of patients with suspected drug eruptions (University Hospitals Cleveland Medical Center institutional review board #07-12-27). Medications, excipients, and their concentrations (in % weight per weight) and vehicles that were tested include ibuprofen (10% petrolatum), aspirin (10% petrolatum), hydrochlorothiazide (10% petrolatum), captopril (5% petrolatum), and propylene glycol (30% water or 5% petrolatum). Patch tests were read at 48 and 72 hours and scored according to the International Contact Dermatitis Research Group patch test scoring guidelines.69 Two patients tested for ibuprofen reacted positively only to propylene glycol; the 3 other patients did not react to aspirin, hydrochlorothiazide, and captopril. Overall, we observed no positive patch tests to medications and 2 positive tests to propylene glycol in 5 patients tested (unpublished data).
Areas of Uncertainty
Although tests for immediate-type hypersensitivity reactions to drugs exist as skin prick tests, diagnostic testing for the majority of drug reactions does not exist. Drug allergy diagnosis is made with history and temporality, potentially resulting in unnecessary avoidance of helpful medications. Ideal patch test concentrations and vehicles as well as the sensitivity and specificity of these tests are unknown.
Guidelines From Professional Societies
Drug allergy testing guidelines are available from the British Society for Allergy and Clinical Immunology70 and American Academy of Allergy, Asthma and Immunology.71 The guidelines recommend diagnosis by history and temporality, and it is stated that patch testing is potentially useful in maculopapular rashes, AGEP, fixed drug eruptions, and DRESS syndrome.
Conclusion
Case reports in the literature suggest the utility of patch testing in some drug allergies. We suggest testing excipients such as propylene glycol and benzoic acid to rule out systemic contact dermatitis when patch testing with active drugs to confirm cause of suspected adverse cutaneous reactions to medications.
- Arndt KA, Jick H. Rates of cutaneous reactions to drugs. a report from the Boston Collaborative Drug Surveillance Program. JAMA. 1976;235:918-922.
- Bigby M, Jick S, Jick H, et al. Drug-induced cutaneous reactions. a report from the Boston Collaborative Drug Surveillance Program on 15,483 consecutive inpatients, 1975 to 1982. JAMA. 1986;256:3358-3363.
- Fiszenson-Albala F, Auzerie V, Mahe E, et al. A 6-month prospective survey of cutaneous drug reactions in a hospital setting. Br J Dermatol. 2003;149:1018-1022.
- Thong BY, Leong KP, Tang CY, et al. Drug allergy in a general hospital: results of a novel prospective inpatient reporting system. Ann Allergy Asthma Immunol. 2003;90:342-347.
- Hunziker T, Kunzi UP, Braunschweig S, et al. Comprehensive hospital drug monitoring (CHDM): adverse skin reactions, a 20-year survey. Allergy. 1997;52:388-393.
- Swanbeck G, Dahlberg E. Cutaneous drug reactions. an attempt to quantitative estimation. Arch Dermatol Res. 1992;284:215-218.
- Naldi L, Conforti A, Venegoni M, et al. Cutaneous reactions to drugs. an analysis of spontaneous reports in four Italian regions. Br J Clin Pharmacol. 1999;48:839-846.
- French LE, Prins C. Erythema multiforme, Stevens-Johnson syndrome and toxic epidermal necrolysis. In: Bolognia, JL, Jorizzo JL, Schaffer JV, eds. Dermatology. 3rd ed. Philadelphia, PA: Elsevier Saunders; 2012:319-333.
- Vasconcelos C, Magina S, Quirino P, et al. Cutaneous drug reactions to piroxicam. Contact Dermatitis. 1998;39:145.
- Gerber D. Adverse reactions of piroxicam. Drug Intell Clin Pharm. 1987;21:707-710.
- Revuz J, Valeyrie-Allanore L. Drug reactions. In: Bolognia, JL, Jorizzo JL, Schaffer JV, eds. Dermatology. 3rd ed. Philadelphia, PA: Elsevier Saunders; 2012:335-356.
- Husain Z, Reddy BY, Schwartz RA. DRESS syndrome: part II. management and therapeutics. J Am Acad Dermatol. 2013;68:709.e1-709.e9; quiz 718-720.
- Heinzerling LM, Tomsitz D, Anliker MD. Is drug allergy less prevalent than previously assumed? a 5-year analysis. Br J Dermatol. 2012;166:107-114.
- Salkind AR, Cuddy PG. Is this patient allergic to penicillin?: an evidence-based analysis of the likelihood of penicillin allergy. JAMA. 2001;285:2498-2505.
- Torres MJ, Gomez F, Doña I, et al. Diagnostic evaluation of patients with nonimmediate cutaneous hypersensitivity reactions to iodinated contrast media. Allergy. 2012;67:929-935.
- Cham PM, Warshaw EM. Patch testing for evaluating drug reactions due to systemic antibiotics. Dermatitis. 2007;18:63-77.
- Andrade P, Brinca A, Gonçalo M. Patch testing in fixed drug eruptions—a 20-year review. Contact Dermatitis. 2011;65:195-201.
- Romano A, Viola M, Gaeta F, et al. Patch testing in non-immediate drug eruptions. Allergy Asthma Clin Immunol. 2008;4:66-74.
- Rosso R, Mattiacci G, Bernardi ML, et al. Very delayed reactions to beta-lactam antibiotics. Contact Dermatitis. 2000;42:293-295.
- Romano A, Torres MJ, Castells M, et al. Diagnosis and management of drug hypersensitivity reactions. J Allergy Clin Immunol. 2011;127(3 suppl):S67-S73.
- Friedmann PS, Ardern-Jones M. Patch testing in drug allergy. Curr Opin Allergy Clin Immunol. 2010;10:291-296.
- Torres MJ, Mayorga C, Blanca M. Nonimmediate allergic reactions induced by drugs: pathogenesis and diagnostic tests. J Investig Allergol Clin Immunol. 2009;19:80-90.
- Waton J, Tréchot P, Loss-Ayay C, et al. Negative predictive value of drug skin tests in investigating cutaneous adverse drug reactions. Br J Dermatol. 2009;160:786-794.
- Romano A, Viola M, Mondino C, et al. Diagnosing nonimmediate reactions to penicillins by in vivo tests. Int Arch Allergy Immunol. 2002;129:169-174.
- De Groot AC. Patch Testing. Test Concentrations and Vehicles for 4350 Chemicals. 3rd ed. Wapserveen, Netherlands: acdegroot publishing; 2008.
- Elzagallaai AA, Knowles SR, Rieder MJ, et al. Patch testing for the diagnosis of anticonvulsant hypersensitivity syndrome: a systematic review. Drug Saf. 2009;32:391-408.
- Andrade P, Gonçalo M. Fixed drug eruption caused by etoricoxib—2 cases confirmed by patch testing. Contact Dermatitis. 2011;64:118-120.
- Barbaud A, Reichert-Penetrat S, Tréchot P, et al. The use of skin testing in the investigation of cutaneous adverse drug reactions. Br J Dermatol. 1998;139:49-58.
- Wolkenstein P, Chosidow O, Fléchet ML, et al. Patch testing in severe cutaneous adverse drug reactions, including Stevens-Johnson syndrome and toxic epidermal necrolysis. Contact Dermatitis. 1996;35:234-236.
- Harries MJ, McIntyre SJ, Kingston TP. Co-amoxiclav-induced acute generalized exanthematous pustulosis confirmed by patch testing. Contact Dermatitis. 2006;55:372.
- Matsumoto Y, Okubo Y, Yamamoto T, et al. Case of acute generalized exanthematous pustulosis caused by ampicillin/cloxacillin sodium in a pregnant woman. J Dermatol. 2008;35:362-364.
- Chaabane A, Aouam K, Gassab L, et al. Acute generalized exanthematous pustulosis (AGEP) induced by cefotaxime. Fundam Clin Pharmacol. 2010;24:429-432.
- Hausermann P, Scherer K, Weber M, et al. Ciprofloxacin-induced acute generalized exanthematous pustulosis mimicking bullous drug eruption confirmed by a positive patch test. Dermatology. 2005;211:277-280.
- Moreau A, Dompmartin A, Castel B, et al. Drug-induced acute generalized exanthematous pustulosis with positive patch tests. Int J Dermatol. 1995;34:263-266.
- Kempinaire A, De Raevea L, Merckx M, et al. Terbinafine-induced acute generalized exanthematous pustulosis confirmed by a positive patch-test result. J Am Acad Dermatol. 1997;37:653-655.
- Mäkelä L, Lammintausta K. Etoricoxib-induced acute generalized exanthematous pustulosis. Acta Derm Venereol. 2008;88:200-201.
- Yang CC, Lee JY, Chen WC. Acute generalized exanthematous pustulosis caused by celecoxib. J Formos Med Assoc. 2004;103:555-557.
- Kardaun SH, de Monchy JG. Acute generalized exanthematous pustulosis caused by morphine, confirmed by positive patch test and lymphocyte transformation test. J Am Acad Dermatol. 2006;55(2 suppl):S21-S23.
- Inadomi T. Drug rash with eosinophilia and systemic symptoms (DRESS): changing carbamazepine to phenobarbital controlled epilepsy without the recurrence of DRESS. Eur J Dermatol. 2010;20:220-222.
- Buyuktiryaki AB, Bezirganoglu H, Sahiner UM, et al. Patch testing is an effective method for the diagnosis of carbamazepine-induced drug reaction, eosinophilia and systemic symptoms (DRESS) syndrome in an 8-year-old girl. Australas J Dermatol. 2012;53:274-277.
- Aouam K, Ben Romdhane F, Loussaief C, et al. Hypersensitivity syndrome induced by anticonvulsants: possible cross-reactivity between carbamazepine and lamotrigine. J Clin Pharmacol. 2009;49:1488-1491.
- Santiago F, Gonçalo M, Vieira R, et al. Epicutaneous patch testing in drug hypersensitivity syndrome (DRESS). Contact Dermatitis. 2010;62:47-53.
- Prevost P, Bédry R, Lacoste D, et al. Hypersensitivity syndrome with olanzapine confirmed by patch tests. Eur J Dermatol. 2012;22:126-127.
- Hubiche T, Milpied B, Cazeau C, et al. Association of immunologically confirmed delayed drug reaction and human herpesvirus 6 viremia in a pediatric case of drug-induced hypersensitivity syndrome. Dermatology. 2011;222:140-141.
- Song WJ, Shim EJ, Kang MG, et al. Severe drug hypersensitivity induced by erdosteine and doxofylline as confirmed by patch and lymphocyte transformation tests: a case report. J Investig Allergol Clin Immunol. 2012;22:230-232.
- Lee JH, Park HK, Heo J, et al. Drug rash with eosinophilia and systemic symptoms (DRESS) syndrome induced by celecoxib and anti-tuberculosis drugs. J Korean Med Sci. 2008;23:521-525.
- González-Delgado P, Blanes M, Soriano V, et al. Erythema multiforme to amoxicillin with concurrent infection by Epstein-Barr virus. Allergol Immunopathol. 2006;34:76-78.
- Gonzalo Garijo MA, Pérez Calderón R, de Argila Fernández-Durán D, et al. Cutaneous reactions due to diltiazem and cross reactivity with other calcium channel blockers. Allergol Immunopathol (Madr). 2005;33:238-240.
- Peña AL, Henriquezsantana A, Gonzalez-Seco E, et al. Exudative erythema multiforme induced by hydroxyzine. Eur J Dermatol. 2008;18:194-195.
- Arakawa Y, Nakai N, Katoh N. Celecoxib-induced erythema multiforme-type drug eruption with a positive patch test. J Dermatol. 2011;38:1185-1188.
- Prieto A, De barrio M, Pérez C, et al. Piroxicam-induced erythema multiforme. Contact Dermatitis. 2004;50:263.
- Dalmau J, Serra-baldrich E, Roé E, et al. Use of patch test in fixed drug eruption due to metamizole (Nolotil). Contact Dermatitis. 2006;54:127-128.
- Gastaminza G, Anda M, Audicana MT, et al. Fixed-drug eruption due to metronidazole with positive topical provocation. Contact Dermatitis. 2001;44:36.
- Bellini V, Stingeni L, Lisi P. Multifocal fixed drug eruption due to celecoxib. Dermatitis. 2009;20:174-176.
- García CM, Carmena R, García R, et al. Fixed drug eruption from ticlopidine, with positive lesional patch test. Contact Dermatitis. 2001;44:40-41.
- Cruz MJ, Duarte AF, Baudrier T, et al. Lichenoid drug eruption induced by misoprostol. Contact Dermatitis. 2009;61:240-242.
- Alanko K. Patch testing in cutaneous reactions caused by carbamazepine. Contact Dermatitis. 1993;29:254-257.
- Grob M, Scheidegger P, Wüthrich B. Allergic skin reaction to celecoxib. Dermatology. 2000;201:383.
- Alonso JC, Ortega JD, Gonzalo MJ. Cutaneous reaction to oral celecoxib with positive patch test. Contact Dermatitis. 2004;50:48-49.
- Fernandes B, Brites M, Gonçalo M, et al. Maculopapular eruption from sertraline with positive patch tests. Contact Dermatitis. 2000;42:287.
- Häusermann P, Harr T, Bircher AJ. Baboon syndrome resulting from systemic drugs: is there strife between SDRIFE and allergic contact dermatitis syndrome? Contact Dermatitis. 2004;51:297-310.
- Klein CE, Trautmann A, Zillikens D, et al. Patch testing in an unusual case of toxic epidermal necrolysis. Contact Dermatitis. 1996;35:175-176.
- Swerlick RA, Campbell CF. Medication dyes as a source of drug allergy. J Drugs Dermatol. 2013;12:99-102.
- Guin JD. Patch testing to FD&C and D&C dyes. Contact Dermatitis. 2003;49:217-218.
- Lowther A, McCormick T, Nedorost S. Systemic contact dermatitis from propylene glycol. Dermatitis. 2008;19:105-108.
- Baeck M, Goossens A. Systemic contact dermatitis to corticosteroids. Allergy. 2012;67:1580-1585.
- Baeck M, Goossens A. Immediate and delayed allergic hypersensitivity to corticosteroids: practical guidelines. Contact Dermatitis. 2012;66:38-45.
- Basedow S, Eigelshoven S, Homey B. Immediate and delayed hypersensitivity to corticosteroids. J Dtsch Dermatol Ges. 2011;9:885-888.
- Johansen JD, Aalto-korte K, Agner T, et al. European Society of Contact Dermatitis guideline for diagnostic patch testing—recommendations on best practice. Contact Dermatitis. 2015;73:195-221.
- Mirakian R, Ewan PW, Durham SR, et al. BSACI guidelines for the management of drug allergy. Clin Exp Allergy. 2009;39:43-61.
- Joint Task Force on Practice Parameters; American Academy of Allergy, Asthma and Immunology; American College of Allergy, Asthma and Immunology; Joint Council of Allergy, Asthma and Immunology. Drug allergy: an updated practice parameter. Ann Allergy Asthma Immunol. 2010;105:259-273.
Adverse drug reactions account for 3% to 6% of hospital admissions in the United States and occur in 10% to 15% of hospitalized patients.1,2 The most common culprits are antibiotics and nonsteroidal anti-inflammatory drugs (NSAIDs).3-12 In most cases, diagnoses are made clinically without diagnostic testing. To identify drug allergies associated with diagnostic testing, one center selected patients with suspected cutaneous drug reactions (2006-2010) for further evaluation.13 Of 612 patients who were evaluated, 141 had a high suspicion of drug allergy and were included in the analysis. The excluded patients had pseudoallergic reactions, reactive exanthemas due to infection, histopathologic exclusion of drug allergy, angioedema, or other dermatological conditions such as contact dermatitis and eczema. Of the included patients, 107 were diagnosed with drug reactions, while the remainder had non–drug-related exanthemas or unknown etiology after testing. Identified culprit drugs were predominantly antibiotics (39.8%) and NSAIDs (21.2%); contrast media, anticoagulants, anticonvulsants, antimalarials, antifungals, glucocorticoids, antihypertensives, and proton pump inhibitors also were implicated. They were identified with skin prick, intradermal, and patch tests (62.6%); lymphocyte transformation test (17.7%); oral rechallenge (5.6%); or without skin testing (6.5%). One quarter of patients with a high suspicion for drug allergy did not have a confirmed drug eruption in this study. Another study found that 10% to 20% of patients with reported penicillin allergy had confirmation via skin prick testing.14 These findings suggest that confirmation of suspected drug allergy may require more than one diagnostic test.
Tests for Adverse Drug Reactions
The following tests have been shown to aid in the identification of cutaneous drug eruptions: (1) patch tests15-21; (2) intradermal tests14,15,19,20; (3) drug provocation tests15,20; and (4) lymphocyte transformation tests.20 Intradermal or skin prick tests are most useful in urticarial eruptions but can be considered in nonurticarial eruptions with delayed inspection of test sites up to 1 week after testing. Drug provocation tests are considered the gold standard but involve patient risk. Lymphocyte transformation tests use the principle that T lymphocytes proliferate in the presence of drugs to which the patient is sensitized. Patch tests will be discussed in greater detail below. Immunohistochemistry can determine immunologic mechanisms of eruptions but cannot identify causative agents.16,17,22
A retrospective study of patients referred for evaluation of adverse drug reactions between 1996 and 2006 found the collective negative predictive value (NPV)—the percentage of truly negative skin tests based on provocation or substitution testing—of cutaneous drug tests including patch, prick, and intradermal tests to be 89.6% (95% confidence interval, 85.9%-93.3%).23 The NPVs of each test were not reported. Patients with negative cutaneous tests had subsequent oral rechallenge or substitution testing with medication from the same drug class.23 Another study16 found the NPV of patch testing to be at least 79% after review of data from other studies using patch and provocation testing.16,24 These studies suggest that cutaneous testing can be useful, albeit imperfect, in the evaluation and diagnosis of drug allergy.
Review of the Patch Test
Patch tests can be helpful in diagnosis of delayed hypersensitivities.18 Patch testing is most commonly and effectively used to diagnose allergic contact dermatitis, but its utility in other applications, such as diagnosis of cutaneous drug eruptions, has not been extensively studied.
The development of patch tests to diagnose systemic drug allergies is inhibited by the uncertainty of percutaneous drug penetration, a dearth of studies to determine the best test concentrations of active drug in the patch test, and the potential for nonimmunologic contact urticaria upon skin exposure. Furthermore, cutaneous metabolism of many antigens is well documented, but correlation to systemic metabolism often is unknown, which can confound patch test results and lead to false-negative results when the skin’s metabolic capacity does not match the body’s capacity to generate antigens capable of eliciting immunogenic responses.21 Additionally, the method used to suspend and disperse drugs in patch test vehicles is unfamiliar to most pharmacists, and standardized concentrations and vehicles are available only for some medications.25 Studies sufficient to obtain US Food and Drug Administration approval of patch tests for systemic drug eruptions would be costly and therefore prohibitive to investigators. The majority of the literature consists of case reports and data extrapolated from reviews. Patch test results of many drugs have been reported in the literature, with the highest frequencies of positive results associated with anticonvulsants,26 antibiotics, corticosteroids, calcium channel blockers, and benzodiazepines.21
Patch test placement affects the diagnostic value of the test. Placing patch tests on previously involved sites of fixed drug eruptions improves yield over placement on uninvolved skin.27 Placing patch tests on previously involved sites of other drug eruptions such as toxic epidermal necrolysis also may aid in diagnosis, though the literature is sparse.25,26,28
Patch Testing in Drug Eruptions
Morbilliform eruptions account for 48% to 91% of patients with adverse drug reactions.4-6 Other drug eruptions include urticarial eruptions, acute generalized exanthematous pustulosis (AGEP), drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome, toxic epidermal necrolysis, Stevens-Johnson syndrome, lichenoid drug eruption, symmetric drug-related intertriginous and flexural exanthema (SDRIFE), erythema multiforme (EM), and systemic contact dermatitis. The Table summarizes reports of positive patch tests with various medications for these drug eruptions.
In general, antimicrobials and NSAIDs were the most implicated drugs with positive patch test results in AGEP, DRESS syndrome, EM, fixed drug eruptions, and morbilliform eruptions. In AGEP, positive results also were reported for other drugs, including terbinafine and morphine.29-38 In fixed drug eruptions, patch testing on involved skin showed positive results to NSAIDs, analgesics, platelet inhibitors, and antimicrobials.27,52-55 Patch testing in DRESS syndrome has shown many positive reactions to antiepileptics and antipsychotics.39-43 One study used patch tests in SDRIFE, reporting positive results with antimicrobials, antineoplastics, decongestants, and glucocorticoids.61 Nonsteroidal anti-inflammatory drugs, antimicrobials, calcium channel blockers, and histamine antagonists were implicated in EM.47-51 Positive patch tests were seen in morbilliform eruptions with selective serotonin reuptake inhibitors, antiepileptics/benzodiazepines, NSAIDs, and antimicrobials.28,57-60 In toxic epidermal necrolysis, diagnosis with patch testing was made using patches placed on previously involved skin with sulfamethoxazole.62
Systemic Contact Dermatitis
Drugs historically recognized as causing allergic contact dermatitis (eg, topical gentamycin) can cause systemic contact dermatitis, which can be patch tested. In these situations, systemic contact dermatitis may be due to either the active drug or excipients in the medication formulation. Excipients are inactive ingredients in medications that provide a suitable consistency, appearance, or form. Often overlooked as culprits of drug hypersensitivity because they are theoretically inert, excipients are increasingly implicated in drug allergy. Swerlick and Campbell63 described 11 cases in which chronic unexplained pruritus responded to medication changes to avoid coloring agents. The most common culprits were FD&C Blue No. 1 and FD&C Blue No. 2. Patch testing for allergies to dyes can be clinically useful, though a lack of commercially available patch tests makes diagnosis difficult.64
Other excipients can cause cutaneous reactions. Propylene glycol, commonly implicated in allergic contact dermatitis, also can cause cutaneous eruptions upon systemic exposure.65 Corticosteroid-induced systemic contact dermatitis has been reported, though it is less prevalent than allergic contact dermatitis.66 These reactions usually are due to nonmethylated and nonhalogenated corticosteroids including budesonide, cortisone, hydrocortisone, prednisolone, and methylprednisolone.67,68 Patch testing in these situations is complicated by the possibility of false-negative results due to the anti-inflammatory effects of the corticosteroids. Therefore, patch testing should be performed using standardized and not treatment concentrations.
In our clinic, we have anecdotally observed several patients with chronic dermatitis and suspected NSAID allergies have positive patch test results with propylene glycol and not the suspected drug. Excipients encountered in multiple drugs and foods are more likely to present as chronic dermatitis, while active drug ingredients started in hospital settings more often present as acute dermatitis.
Our Experience
We have patch tested a handful of patients with suspected drug eruptions (University Hospitals Cleveland Medical Center institutional review board #07-12-27). Medications, excipients, and their concentrations (in % weight per weight) and vehicles that were tested include ibuprofen (10% petrolatum), aspirin (10% petrolatum), hydrochlorothiazide (10% petrolatum), captopril (5% petrolatum), and propylene glycol (30% water or 5% petrolatum). Patch tests were read at 48 and 72 hours and scored according to the International Contact Dermatitis Research Group patch test scoring guidelines.69 Two patients tested for ibuprofen reacted positively only to propylene glycol; the 3 other patients did not react to aspirin, hydrochlorothiazide, and captopril. Overall, we observed no positive patch tests to medications and 2 positive tests to propylene glycol in 5 patients tested (unpublished data).
Areas of Uncertainty
Although tests for immediate-type hypersensitivity reactions to drugs exist as skin prick tests, diagnostic testing for the majority of drug reactions does not exist. Drug allergy diagnosis is made with history and temporality, potentially resulting in unnecessary avoidance of helpful medications. Ideal patch test concentrations and vehicles as well as the sensitivity and specificity of these tests are unknown.
Guidelines From Professional Societies
Drug allergy testing guidelines are available from the British Society for Allergy and Clinical Immunology70 and American Academy of Allergy, Asthma and Immunology.71 The guidelines recommend diagnosis by history and temporality, and it is stated that patch testing is potentially useful in maculopapular rashes, AGEP, fixed drug eruptions, and DRESS syndrome.
Conclusion
Case reports in the literature suggest the utility of patch testing in some drug allergies. We suggest testing excipients such as propylene glycol and benzoic acid to rule out systemic contact dermatitis when patch testing with active drugs to confirm cause of suspected adverse cutaneous reactions to medications.
Adverse drug reactions account for 3% to 6% of hospital admissions in the United States and occur in 10% to 15% of hospitalized patients.1,2 The most common culprits are antibiotics and nonsteroidal anti-inflammatory drugs (NSAIDs).3-12 In most cases, diagnoses are made clinically without diagnostic testing. To identify drug allergies associated with diagnostic testing, one center selected patients with suspected cutaneous drug reactions (2006-2010) for further evaluation.13 Of 612 patients who were evaluated, 141 had a high suspicion of drug allergy and were included in the analysis. The excluded patients had pseudoallergic reactions, reactive exanthemas due to infection, histopathologic exclusion of drug allergy, angioedema, or other dermatological conditions such as contact dermatitis and eczema. Of the included patients, 107 were diagnosed with drug reactions, while the remainder had non–drug-related exanthemas or unknown etiology after testing. Identified culprit drugs were predominantly antibiotics (39.8%) and NSAIDs (21.2%); contrast media, anticoagulants, anticonvulsants, antimalarials, antifungals, glucocorticoids, antihypertensives, and proton pump inhibitors also were implicated. They were identified with skin prick, intradermal, and patch tests (62.6%); lymphocyte transformation test (17.7%); oral rechallenge (5.6%); or without skin testing (6.5%). One quarter of patients with a high suspicion for drug allergy did not have a confirmed drug eruption in this study. Another study found that 10% to 20% of patients with reported penicillin allergy had confirmation via skin prick testing.14 These findings suggest that confirmation of suspected drug allergy may require more than one diagnostic test.
Tests for Adverse Drug Reactions
The following tests have been shown to aid in the identification of cutaneous drug eruptions: (1) patch tests15-21; (2) intradermal tests14,15,19,20; (3) drug provocation tests15,20; and (4) lymphocyte transformation tests.20 Intradermal or skin prick tests are most useful in urticarial eruptions but can be considered in nonurticarial eruptions with delayed inspection of test sites up to 1 week after testing. Drug provocation tests are considered the gold standard but involve patient risk. Lymphocyte transformation tests use the principle that T lymphocytes proliferate in the presence of drugs to which the patient is sensitized. Patch tests will be discussed in greater detail below. Immunohistochemistry can determine immunologic mechanisms of eruptions but cannot identify causative agents.16,17,22
A retrospective study of patients referred for evaluation of adverse drug reactions between 1996 and 2006 found the collective negative predictive value (NPV)—the percentage of truly negative skin tests based on provocation or substitution testing—of cutaneous drug tests including patch, prick, and intradermal tests to be 89.6% (95% confidence interval, 85.9%-93.3%).23 The NPVs of each test were not reported. Patients with negative cutaneous tests had subsequent oral rechallenge or substitution testing with medication from the same drug class.23 Another study16 found the NPV of patch testing to be at least 79% after review of data from other studies using patch and provocation testing.16,24 These studies suggest that cutaneous testing can be useful, albeit imperfect, in the evaluation and diagnosis of drug allergy.
Review of the Patch Test
Patch tests can be helpful in diagnosis of delayed hypersensitivities.18 Patch testing is most commonly and effectively used to diagnose allergic contact dermatitis, but its utility in other applications, such as diagnosis of cutaneous drug eruptions, has not been extensively studied.
The development of patch tests to diagnose systemic drug allergies is inhibited by the uncertainty of percutaneous drug penetration, a dearth of studies to determine the best test concentrations of active drug in the patch test, and the potential for nonimmunologic contact urticaria upon skin exposure. Furthermore, cutaneous metabolism of many antigens is well documented, but correlation to systemic metabolism often is unknown, which can confound patch test results and lead to false-negative results when the skin’s metabolic capacity does not match the body’s capacity to generate antigens capable of eliciting immunogenic responses.21 Additionally, the method used to suspend and disperse drugs in patch test vehicles is unfamiliar to most pharmacists, and standardized concentrations and vehicles are available only for some medications.25 Studies sufficient to obtain US Food and Drug Administration approval of patch tests for systemic drug eruptions would be costly and therefore prohibitive to investigators. The majority of the literature consists of case reports and data extrapolated from reviews. Patch test results of many drugs have been reported in the literature, with the highest frequencies of positive results associated with anticonvulsants,26 antibiotics, corticosteroids, calcium channel blockers, and benzodiazepines.21
Patch test placement affects the diagnostic value of the test. Placing patch tests on previously involved sites of fixed drug eruptions improves yield over placement on uninvolved skin.27 Placing patch tests on previously involved sites of other drug eruptions such as toxic epidermal necrolysis also may aid in diagnosis, though the literature is sparse.25,26,28
Patch Testing in Drug Eruptions
Morbilliform eruptions account for 48% to 91% of patients with adverse drug reactions.4-6 Other drug eruptions include urticarial eruptions, acute generalized exanthematous pustulosis (AGEP), drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome, toxic epidermal necrolysis, Stevens-Johnson syndrome, lichenoid drug eruption, symmetric drug-related intertriginous and flexural exanthema (SDRIFE), erythema multiforme (EM), and systemic contact dermatitis. The Table summarizes reports of positive patch tests with various medications for these drug eruptions.
In general, antimicrobials and NSAIDs were the most implicated drugs with positive patch test results in AGEP, DRESS syndrome, EM, fixed drug eruptions, and morbilliform eruptions. In AGEP, positive results also were reported for other drugs, including terbinafine and morphine.29-38 In fixed drug eruptions, patch testing on involved skin showed positive results to NSAIDs, analgesics, platelet inhibitors, and antimicrobials.27,52-55 Patch testing in DRESS syndrome has shown many positive reactions to antiepileptics and antipsychotics.39-43 One study used patch tests in SDRIFE, reporting positive results with antimicrobials, antineoplastics, decongestants, and glucocorticoids.61 Nonsteroidal anti-inflammatory drugs, antimicrobials, calcium channel blockers, and histamine antagonists were implicated in EM.47-51 Positive patch tests were seen in morbilliform eruptions with selective serotonin reuptake inhibitors, antiepileptics/benzodiazepines, NSAIDs, and antimicrobials.28,57-60 In toxic epidermal necrolysis, diagnosis with patch testing was made using patches placed on previously involved skin with sulfamethoxazole.62
Systemic Contact Dermatitis
Drugs historically recognized as causing allergic contact dermatitis (eg, topical gentamycin) can cause systemic contact dermatitis, which can be patch tested. In these situations, systemic contact dermatitis may be due to either the active drug or excipients in the medication formulation. Excipients are inactive ingredients in medications that provide a suitable consistency, appearance, or form. Often overlooked as culprits of drug hypersensitivity because they are theoretically inert, excipients are increasingly implicated in drug allergy. Swerlick and Campbell63 described 11 cases in which chronic unexplained pruritus responded to medication changes to avoid coloring agents. The most common culprits were FD&C Blue No. 1 and FD&C Blue No. 2. Patch testing for allergies to dyes can be clinically useful, though a lack of commercially available patch tests makes diagnosis difficult.64
Other excipients can cause cutaneous reactions. Propylene glycol, commonly implicated in allergic contact dermatitis, also can cause cutaneous eruptions upon systemic exposure.65 Corticosteroid-induced systemic contact dermatitis has been reported, though it is less prevalent than allergic contact dermatitis.66 These reactions usually are due to nonmethylated and nonhalogenated corticosteroids including budesonide, cortisone, hydrocortisone, prednisolone, and methylprednisolone.67,68 Patch testing in these situations is complicated by the possibility of false-negative results due to the anti-inflammatory effects of the corticosteroids. Therefore, patch testing should be performed using standardized and not treatment concentrations.
In our clinic, we have anecdotally observed several patients with chronic dermatitis and suspected NSAID allergies have positive patch test results with propylene glycol and not the suspected drug. Excipients encountered in multiple drugs and foods are more likely to present as chronic dermatitis, while active drug ingredients started in hospital settings more often present as acute dermatitis.
Our Experience
We have patch tested a handful of patients with suspected drug eruptions (University Hospitals Cleveland Medical Center institutional review board #07-12-27). Medications, excipients, and their concentrations (in % weight per weight) and vehicles that were tested include ibuprofen (10% petrolatum), aspirin (10% petrolatum), hydrochlorothiazide (10% petrolatum), captopril (5% petrolatum), and propylene glycol (30% water or 5% petrolatum). Patch tests were read at 48 and 72 hours and scored according to the International Contact Dermatitis Research Group patch test scoring guidelines.69 Two patients tested for ibuprofen reacted positively only to propylene glycol; the 3 other patients did not react to aspirin, hydrochlorothiazide, and captopril. Overall, we observed no positive patch tests to medications and 2 positive tests to propylene glycol in 5 patients tested (unpublished data).
Areas of Uncertainty
Although tests for immediate-type hypersensitivity reactions to drugs exist as skin prick tests, diagnostic testing for the majority of drug reactions does not exist. Drug allergy diagnosis is made with history and temporality, potentially resulting in unnecessary avoidance of helpful medications. Ideal patch test concentrations and vehicles as well as the sensitivity and specificity of these tests are unknown.
Guidelines From Professional Societies
Drug allergy testing guidelines are available from the British Society for Allergy and Clinical Immunology70 and American Academy of Allergy, Asthma and Immunology.71 The guidelines recommend diagnosis by history and temporality, and it is stated that patch testing is potentially useful in maculopapular rashes, AGEP, fixed drug eruptions, and DRESS syndrome.
Conclusion
Case reports in the literature suggest the utility of patch testing in some drug allergies. We suggest testing excipients such as propylene glycol and benzoic acid to rule out systemic contact dermatitis when patch testing with active drugs to confirm cause of suspected adverse cutaneous reactions to medications.
- Arndt KA, Jick H. Rates of cutaneous reactions to drugs. a report from the Boston Collaborative Drug Surveillance Program. JAMA. 1976;235:918-922.
- Bigby M, Jick S, Jick H, et al. Drug-induced cutaneous reactions. a report from the Boston Collaborative Drug Surveillance Program on 15,483 consecutive inpatients, 1975 to 1982. JAMA. 1986;256:3358-3363.
- Fiszenson-Albala F, Auzerie V, Mahe E, et al. A 6-month prospective survey of cutaneous drug reactions in a hospital setting. Br J Dermatol. 2003;149:1018-1022.
- Thong BY, Leong KP, Tang CY, et al. Drug allergy in a general hospital: results of a novel prospective inpatient reporting system. Ann Allergy Asthma Immunol. 2003;90:342-347.
- Hunziker T, Kunzi UP, Braunschweig S, et al. Comprehensive hospital drug monitoring (CHDM): adverse skin reactions, a 20-year survey. Allergy. 1997;52:388-393.
- Swanbeck G, Dahlberg E. Cutaneous drug reactions. an attempt to quantitative estimation. Arch Dermatol Res. 1992;284:215-218.
- Naldi L, Conforti A, Venegoni M, et al. Cutaneous reactions to drugs. an analysis of spontaneous reports in four Italian regions. Br J Clin Pharmacol. 1999;48:839-846.
- French LE, Prins C. Erythema multiforme, Stevens-Johnson syndrome and toxic epidermal necrolysis. In: Bolognia, JL, Jorizzo JL, Schaffer JV, eds. Dermatology. 3rd ed. Philadelphia, PA: Elsevier Saunders; 2012:319-333.
- Vasconcelos C, Magina S, Quirino P, et al. Cutaneous drug reactions to piroxicam. Contact Dermatitis. 1998;39:145.
- Gerber D. Adverse reactions of piroxicam. Drug Intell Clin Pharm. 1987;21:707-710.
- Revuz J, Valeyrie-Allanore L. Drug reactions. In: Bolognia, JL, Jorizzo JL, Schaffer JV, eds. Dermatology. 3rd ed. Philadelphia, PA: Elsevier Saunders; 2012:335-356.
- Husain Z, Reddy BY, Schwartz RA. DRESS syndrome: part II. management and therapeutics. J Am Acad Dermatol. 2013;68:709.e1-709.e9; quiz 718-720.
- Heinzerling LM, Tomsitz D, Anliker MD. Is drug allergy less prevalent than previously assumed? a 5-year analysis. Br J Dermatol. 2012;166:107-114.
- Salkind AR, Cuddy PG. Is this patient allergic to penicillin?: an evidence-based analysis of the likelihood of penicillin allergy. JAMA. 2001;285:2498-2505.
- Torres MJ, Gomez F, Doña I, et al. Diagnostic evaluation of patients with nonimmediate cutaneous hypersensitivity reactions to iodinated contrast media. Allergy. 2012;67:929-935.
- Cham PM, Warshaw EM. Patch testing for evaluating drug reactions due to systemic antibiotics. Dermatitis. 2007;18:63-77.
- Andrade P, Brinca A, Gonçalo M. Patch testing in fixed drug eruptions—a 20-year review. Contact Dermatitis. 2011;65:195-201.
- Romano A, Viola M, Gaeta F, et al. Patch testing in non-immediate drug eruptions. Allergy Asthma Clin Immunol. 2008;4:66-74.
- Rosso R, Mattiacci G, Bernardi ML, et al. Very delayed reactions to beta-lactam antibiotics. Contact Dermatitis. 2000;42:293-295.
- Romano A, Torres MJ, Castells M, et al. Diagnosis and management of drug hypersensitivity reactions. J Allergy Clin Immunol. 2011;127(3 suppl):S67-S73.
- Friedmann PS, Ardern-Jones M. Patch testing in drug allergy. Curr Opin Allergy Clin Immunol. 2010;10:291-296.
- Torres MJ, Mayorga C, Blanca M. Nonimmediate allergic reactions induced by drugs: pathogenesis and diagnostic tests. J Investig Allergol Clin Immunol. 2009;19:80-90.
- Waton J, Tréchot P, Loss-Ayay C, et al. Negative predictive value of drug skin tests in investigating cutaneous adverse drug reactions. Br J Dermatol. 2009;160:786-794.
- Romano A, Viola M, Mondino C, et al. Diagnosing nonimmediate reactions to penicillins by in vivo tests. Int Arch Allergy Immunol. 2002;129:169-174.
- De Groot AC. Patch Testing. Test Concentrations and Vehicles for 4350 Chemicals. 3rd ed. Wapserveen, Netherlands: acdegroot publishing; 2008.
- Elzagallaai AA, Knowles SR, Rieder MJ, et al. Patch testing for the diagnosis of anticonvulsant hypersensitivity syndrome: a systematic review. Drug Saf. 2009;32:391-408.
- Andrade P, Gonçalo M. Fixed drug eruption caused by etoricoxib—2 cases confirmed by patch testing. Contact Dermatitis. 2011;64:118-120.
- Barbaud A, Reichert-Penetrat S, Tréchot P, et al. The use of skin testing in the investigation of cutaneous adverse drug reactions. Br J Dermatol. 1998;139:49-58.
- Wolkenstein P, Chosidow O, Fléchet ML, et al. Patch testing in severe cutaneous adverse drug reactions, including Stevens-Johnson syndrome and toxic epidermal necrolysis. Contact Dermatitis. 1996;35:234-236.
- Harries MJ, McIntyre SJ, Kingston TP. Co-amoxiclav-induced acute generalized exanthematous pustulosis confirmed by patch testing. Contact Dermatitis. 2006;55:372.
- Matsumoto Y, Okubo Y, Yamamoto T, et al. Case of acute generalized exanthematous pustulosis caused by ampicillin/cloxacillin sodium in a pregnant woman. J Dermatol. 2008;35:362-364.
- Chaabane A, Aouam K, Gassab L, et al. Acute generalized exanthematous pustulosis (AGEP) induced by cefotaxime. Fundam Clin Pharmacol. 2010;24:429-432.
- Hausermann P, Scherer K, Weber M, et al. Ciprofloxacin-induced acute generalized exanthematous pustulosis mimicking bullous drug eruption confirmed by a positive patch test. Dermatology. 2005;211:277-280.
- Moreau A, Dompmartin A, Castel B, et al. Drug-induced acute generalized exanthematous pustulosis with positive patch tests. Int J Dermatol. 1995;34:263-266.
- Kempinaire A, De Raevea L, Merckx M, et al. Terbinafine-induced acute generalized exanthematous pustulosis confirmed by a positive patch-test result. J Am Acad Dermatol. 1997;37:653-655.
- Mäkelä L, Lammintausta K. Etoricoxib-induced acute generalized exanthematous pustulosis. Acta Derm Venereol. 2008;88:200-201.
- Yang CC, Lee JY, Chen WC. Acute generalized exanthematous pustulosis caused by celecoxib. J Formos Med Assoc. 2004;103:555-557.
- Kardaun SH, de Monchy JG. Acute generalized exanthematous pustulosis caused by morphine, confirmed by positive patch test and lymphocyte transformation test. J Am Acad Dermatol. 2006;55(2 suppl):S21-S23.
- Inadomi T. Drug rash with eosinophilia and systemic symptoms (DRESS): changing carbamazepine to phenobarbital controlled epilepsy without the recurrence of DRESS. Eur J Dermatol. 2010;20:220-222.
- Buyuktiryaki AB, Bezirganoglu H, Sahiner UM, et al. Patch testing is an effective method for the diagnosis of carbamazepine-induced drug reaction, eosinophilia and systemic symptoms (DRESS) syndrome in an 8-year-old girl. Australas J Dermatol. 2012;53:274-277.
- Aouam K, Ben Romdhane F, Loussaief C, et al. Hypersensitivity syndrome induced by anticonvulsants: possible cross-reactivity between carbamazepine and lamotrigine. J Clin Pharmacol. 2009;49:1488-1491.
- Santiago F, Gonçalo M, Vieira R, et al. Epicutaneous patch testing in drug hypersensitivity syndrome (DRESS). Contact Dermatitis. 2010;62:47-53.
- Prevost P, Bédry R, Lacoste D, et al. Hypersensitivity syndrome with olanzapine confirmed by patch tests. Eur J Dermatol. 2012;22:126-127.
- Hubiche T, Milpied B, Cazeau C, et al. Association of immunologically confirmed delayed drug reaction and human herpesvirus 6 viremia in a pediatric case of drug-induced hypersensitivity syndrome. Dermatology. 2011;222:140-141.
- Song WJ, Shim EJ, Kang MG, et al. Severe drug hypersensitivity induced by erdosteine and doxofylline as confirmed by patch and lymphocyte transformation tests: a case report. J Investig Allergol Clin Immunol. 2012;22:230-232.
- Lee JH, Park HK, Heo J, et al. Drug rash with eosinophilia and systemic symptoms (DRESS) syndrome induced by celecoxib and anti-tuberculosis drugs. J Korean Med Sci. 2008;23:521-525.
- González-Delgado P, Blanes M, Soriano V, et al. Erythema multiforme to amoxicillin with concurrent infection by Epstein-Barr virus. Allergol Immunopathol. 2006;34:76-78.
- Gonzalo Garijo MA, Pérez Calderón R, de Argila Fernández-Durán D, et al. Cutaneous reactions due to diltiazem and cross reactivity with other calcium channel blockers. Allergol Immunopathol (Madr). 2005;33:238-240.
- Peña AL, Henriquezsantana A, Gonzalez-Seco E, et al. Exudative erythema multiforme induced by hydroxyzine. Eur J Dermatol. 2008;18:194-195.
- Arakawa Y, Nakai N, Katoh N. Celecoxib-induced erythema multiforme-type drug eruption with a positive patch test. J Dermatol. 2011;38:1185-1188.
- Prieto A, De barrio M, Pérez C, et al. Piroxicam-induced erythema multiforme. Contact Dermatitis. 2004;50:263.
- Dalmau J, Serra-baldrich E, Roé E, et al. Use of patch test in fixed drug eruption due to metamizole (Nolotil). Contact Dermatitis. 2006;54:127-128.
- Gastaminza G, Anda M, Audicana MT, et al. Fixed-drug eruption due to metronidazole with positive topical provocation. Contact Dermatitis. 2001;44:36.
- Bellini V, Stingeni L, Lisi P. Multifocal fixed drug eruption due to celecoxib. Dermatitis. 2009;20:174-176.
- García CM, Carmena R, García R, et al. Fixed drug eruption from ticlopidine, with positive lesional patch test. Contact Dermatitis. 2001;44:40-41.
- Cruz MJ, Duarte AF, Baudrier T, et al. Lichenoid drug eruption induced by misoprostol. Contact Dermatitis. 2009;61:240-242.
- Alanko K. Patch testing in cutaneous reactions caused by carbamazepine. Contact Dermatitis. 1993;29:254-257.
- Grob M, Scheidegger P, Wüthrich B. Allergic skin reaction to celecoxib. Dermatology. 2000;201:383.
- Alonso JC, Ortega JD, Gonzalo MJ. Cutaneous reaction to oral celecoxib with positive patch test. Contact Dermatitis. 2004;50:48-49.
- Fernandes B, Brites M, Gonçalo M, et al. Maculopapular eruption from sertraline with positive patch tests. Contact Dermatitis. 2000;42:287.
- Häusermann P, Harr T, Bircher AJ. Baboon syndrome resulting from systemic drugs: is there strife between SDRIFE and allergic contact dermatitis syndrome? Contact Dermatitis. 2004;51:297-310.
- Klein CE, Trautmann A, Zillikens D, et al. Patch testing in an unusual case of toxic epidermal necrolysis. Contact Dermatitis. 1996;35:175-176.
- Swerlick RA, Campbell CF. Medication dyes as a source of drug allergy. J Drugs Dermatol. 2013;12:99-102.
- Guin JD. Patch testing to FD&C and D&C dyes. Contact Dermatitis. 2003;49:217-218.
- Lowther A, McCormick T, Nedorost S. Systemic contact dermatitis from propylene glycol. Dermatitis. 2008;19:105-108.
- Baeck M, Goossens A. Systemic contact dermatitis to corticosteroids. Allergy. 2012;67:1580-1585.
- Baeck M, Goossens A. Immediate and delayed allergic hypersensitivity to corticosteroids: practical guidelines. Contact Dermatitis. 2012;66:38-45.
- Basedow S, Eigelshoven S, Homey B. Immediate and delayed hypersensitivity to corticosteroids. J Dtsch Dermatol Ges. 2011;9:885-888.
- Johansen JD, Aalto-korte K, Agner T, et al. European Society of Contact Dermatitis guideline for diagnostic patch testing—recommendations on best practice. Contact Dermatitis. 2015;73:195-221.
- Mirakian R, Ewan PW, Durham SR, et al. BSACI guidelines for the management of drug allergy. Clin Exp Allergy. 2009;39:43-61.
- Joint Task Force on Practice Parameters; American Academy of Allergy, Asthma and Immunology; American College of Allergy, Asthma and Immunology; Joint Council of Allergy, Asthma and Immunology. Drug allergy: an updated practice parameter. Ann Allergy Asthma Immunol. 2010;105:259-273.
- Arndt KA, Jick H. Rates of cutaneous reactions to drugs. a report from the Boston Collaborative Drug Surveillance Program. JAMA. 1976;235:918-922.
- Bigby M, Jick S, Jick H, et al. Drug-induced cutaneous reactions. a report from the Boston Collaborative Drug Surveillance Program on 15,483 consecutive inpatients, 1975 to 1982. JAMA. 1986;256:3358-3363.
- Fiszenson-Albala F, Auzerie V, Mahe E, et al. A 6-month prospective survey of cutaneous drug reactions in a hospital setting. Br J Dermatol. 2003;149:1018-1022.
- Thong BY, Leong KP, Tang CY, et al. Drug allergy in a general hospital: results of a novel prospective inpatient reporting system. Ann Allergy Asthma Immunol. 2003;90:342-347.
- Hunziker T, Kunzi UP, Braunschweig S, et al. Comprehensive hospital drug monitoring (CHDM): adverse skin reactions, a 20-year survey. Allergy. 1997;52:388-393.
- Swanbeck G, Dahlberg E. Cutaneous drug reactions. an attempt to quantitative estimation. Arch Dermatol Res. 1992;284:215-218.
- Naldi L, Conforti A, Venegoni M, et al. Cutaneous reactions to drugs. an analysis of spontaneous reports in four Italian regions. Br J Clin Pharmacol. 1999;48:839-846.
- French LE, Prins C. Erythema multiforme, Stevens-Johnson syndrome and toxic epidermal necrolysis. In: Bolognia, JL, Jorizzo JL, Schaffer JV, eds. Dermatology. 3rd ed. Philadelphia, PA: Elsevier Saunders; 2012:319-333.
- Vasconcelos C, Magina S, Quirino P, et al. Cutaneous drug reactions to piroxicam. Contact Dermatitis. 1998;39:145.
- Gerber D. Adverse reactions of piroxicam. Drug Intell Clin Pharm. 1987;21:707-710.
- Revuz J, Valeyrie-Allanore L. Drug reactions. In: Bolognia, JL, Jorizzo JL, Schaffer JV, eds. Dermatology. 3rd ed. Philadelphia, PA: Elsevier Saunders; 2012:335-356.
- Husain Z, Reddy BY, Schwartz RA. DRESS syndrome: part II. management and therapeutics. J Am Acad Dermatol. 2013;68:709.e1-709.e9; quiz 718-720.
- Heinzerling LM, Tomsitz D, Anliker MD. Is drug allergy less prevalent than previously assumed? a 5-year analysis. Br J Dermatol. 2012;166:107-114.
- Salkind AR, Cuddy PG. Is this patient allergic to penicillin?: an evidence-based analysis of the likelihood of penicillin allergy. JAMA. 2001;285:2498-2505.
- Torres MJ, Gomez F, Doña I, et al. Diagnostic evaluation of patients with nonimmediate cutaneous hypersensitivity reactions to iodinated contrast media. Allergy. 2012;67:929-935.
- Cham PM, Warshaw EM. Patch testing for evaluating drug reactions due to systemic antibiotics. Dermatitis. 2007;18:63-77.
- Andrade P, Brinca A, Gonçalo M. Patch testing in fixed drug eruptions—a 20-year review. Contact Dermatitis. 2011;65:195-201.
- Romano A, Viola M, Gaeta F, et al. Patch testing in non-immediate drug eruptions. Allergy Asthma Clin Immunol. 2008;4:66-74.
- Rosso R, Mattiacci G, Bernardi ML, et al. Very delayed reactions to beta-lactam antibiotics. Contact Dermatitis. 2000;42:293-295.
- Romano A, Torres MJ, Castells M, et al. Diagnosis and management of drug hypersensitivity reactions. J Allergy Clin Immunol. 2011;127(3 suppl):S67-S73.
- Friedmann PS, Ardern-Jones M. Patch testing in drug allergy. Curr Opin Allergy Clin Immunol. 2010;10:291-296.
- Torres MJ, Mayorga C, Blanca M. Nonimmediate allergic reactions induced by drugs: pathogenesis and diagnostic tests. J Investig Allergol Clin Immunol. 2009;19:80-90.
- Waton J, Tréchot P, Loss-Ayay C, et al. Negative predictive value of drug skin tests in investigating cutaneous adverse drug reactions. Br J Dermatol. 2009;160:786-794.
- Romano A, Viola M, Mondino C, et al. Diagnosing nonimmediate reactions to penicillins by in vivo tests. Int Arch Allergy Immunol. 2002;129:169-174.
- De Groot AC. Patch Testing. Test Concentrations and Vehicles for 4350 Chemicals. 3rd ed. Wapserveen, Netherlands: acdegroot publishing; 2008.
- Elzagallaai AA, Knowles SR, Rieder MJ, et al. Patch testing for the diagnosis of anticonvulsant hypersensitivity syndrome: a systematic review. Drug Saf. 2009;32:391-408.
- Andrade P, Gonçalo M. Fixed drug eruption caused by etoricoxib—2 cases confirmed by patch testing. Contact Dermatitis. 2011;64:118-120.
- Barbaud A, Reichert-Penetrat S, Tréchot P, et al. The use of skin testing in the investigation of cutaneous adverse drug reactions. Br J Dermatol. 1998;139:49-58.
- Wolkenstein P, Chosidow O, Fléchet ML, et al. Patch testing in severe cutaneous adverse drug reactions, including Stevens-Johnson syndrome and toxic epidermal necrolysis. Contact Dermatitis. 1996;35:234-236.
- Harries MJ, McIntyre SJ, Kingston TP. Co-amoxiclav-induced acute generalized exanthematous pustulosis confirmed by patch testing. Contact Dermatitis. 2006;55:372.
- Matsumoto Y, Okubo Y, Yamamoto T, et al. Case of acute generalized exanthematous pustulosis caused by ampicillin/cloxacillin sodium in a pregnant woman. J Dermatol. 2008;35:362-364.
- Chaabane A, Aouam K, Gassab L, et al. Acute generalized exanthematous pustulosis (AGEP) induced by cefotaxime. Fundam Clin Pharmacol. 2010;24:429-432.
- Hausermann P, Scherer K, Weber M, et al. Ciprofloxacin-induced acute generalized exanthematous pustulosis mimicking bullous drug eruption confirmed by a positive patch test. Dermatology. 2005;211:277-280.
- Moreau A, Dompmartin A, Castel B, et al. Drug-induced acute generalized exanthematous pustulosis with positive patch tests. Int J Dermatol. 1995;34:263-266.
- Kempinaire A, De Raevea L, Merckx M, et al. Terbinafine-induced acute generalized exanthematous pustulosis confirmed by a positive patch-test result. J Am Acad Dermatol. 1997;37:653-655.
- Mäkelä L, Lammintausta K. Etoricoxib-induced acute generalized exanthematous pustulosis. Acta Derm Venereol. 2008;88:200-201.
- Yang CC, Lee JY, Chen WC. Acute generalized exanthematous pustulosis caused by celecoxib. J Formos Med Assoc. 2004;103:555-557.
- Kardaun SH, de Monchy JG. Acute generalized exanthematous pustulosis caused by morphine, confirmed by positive patch test and lymphocyte transformation test. J Am Acad Dermatol. 2006;55(2 suppl):S21-S23.
- Inadomi T. Drug rash with eosinophilia and systemic symptoms (DRESS): changing carbamazepine to phenobarbital controlled epilepsy without the recurrence of DRESS. Eur J Dermatol. 2010;20:220-222.
- Buyuktiryaki AB, Bezirganoglu H, Sahiner UM, et al. Patch testing is an effective method for the diagnosis of carbamazepine-induced drug reaction, eosinophilia and systemic symptoms (DRESS) syndrome in an 8-year-old girl. Australas J Dermatol. 2012;53:274-277.
- Aouam K, Ben Romdhane F, Loussaief C, et al. Hypersensitivity syndrome induced by anticonvulsants: possible cross-reactivity between carbamazepine and lamotrigine. J Clin Pharmacol. 2009;49:1488-1491.
- Santiago F, Gonçalo M, Vieira R, et al. Epicutaneous patch testing in drug hypersensitivity syndrome (DRESS). Contact Dermatitis. 2010;62:47-53.
- Prevost P, Bédry R, Lacoste D, et al. Hypersensitivity syndrome with olanzapine confirmed by patch tests. Eur J Dermatol. 2012;22:126-127.
- Hubiche T, Milpied B, Cazeau C, et al. Association of immunologically confirmed delayed drug reaction and human herpesvirus 6 viremia in a pediatric case of drug-induced hypersensitivity syndrome. Dermatology. 2011;222:140-141.
- Song WJ, Shim EJ, Kang MG, et al. Severe drug hypersensitivity induced by erdosteine and doxofylline as confirmed by patch and lymphocyte transformation tests: a case report. J Investig Allergol Clin Immunol. 2012;22:230-232.
- Lee JH, Park HK, Heo J, et al. Drug rash with eosinophilia and systemic symptoms (DRESS) syndrome induced by celecoxib and anti-tuberculosis drugs. J Korean Med Sci. 2008;23:521-525.
- González-Delgado P, Blanes M, Soriano V, et al. Erythema multiforme to amoxicillin with concurrent infection by Epstein-Barr virus. Allergol Immunopathol. 2006;34:76-78.
- Gonzalo Garijo MA, Pérez Calderón R, de Argila Fernández-Durán D, et al. Cutaneous reactions due to diltiazem and cross reactivity with other calcium channel blockers. Allergol Immunopathol (Madr). 2005;33:238-240.
- Peña AL, Henriquezsantana A, Gonzalez-Seco E, et al. Exudative erythema multiforme induced by hydroxyzine. Eur J Dermatol. 2008;18:194-195.
- Arakawa Y, Nakai N, Katoh N. Celecoxib-induced erythema multiforme-type drug eruption with a positive patch test. J Dermatol. 2011;38:1185-1188.
- Prieto A, De barrio M, Pérez C, et al. Piroxicam-induced erythema multiforme. Contact Dermatitis. 2004;50:263.
- Dalmau J, Serra-baldrich E, Roé E, et al. Use of patch test in fixed drug eruption due to metamizole (Nolotil). Contact Dermatitis. 2006;54:127-128.
- Gastaminza G, Anda M, Audicana MT, et al. Fixed-drug eruption due to metronidazole with positive topical provocation. Contact Dermatitis. 2001;44:36.
- Bellini V, Stingeni L, Lisi P. Multifocal fixed drug eruption due to celecoxib. Dermatitis. 2009;20:174-176.
- García CM, Carmena R, García R, et al. Fixed drug eruption from ticlopidine, with positive lesional patch test. Contact Dermatitis. 2001;44:40-41.
- Cruz MJ, Duarte AF, Baudrier T, et al. Lichenoid drug eruption induced by misoprostol. Contact Dermatitis. 2009;61:240-242.
- Alanko K. Patch testing in cutaneous reactions caused by carbamazepine. Contact Dermatitis. 1993;29:254-257.
- Grob M, Scheidegger P, Wüthrich B. Allergic skin reaction to celecoxib. Dermatology. 2000;201:383.
- Alonso JC, Ortega JD, Gonzalo MJ. Cutaneous reaction to oral celecoxib with positive patch test. Contact Dermatitis. 2004;50:48-49.
- Fernandes B, Brites M, Gonçalo M, et al. Maculopapular eruption from sertraline with positive patch tests. Contact Dermatitis. 2000;42:287.
- Häusermann P, Harr T, Bircher AJ. Baboon syndrome resulting from systemic drugs: is there strife between SDRIFE and allergic contact dermatitis syndrome? Contact Dermatitis. 2004;51:297-310.
- Klein CE, Trautmann A, Zillikens D, et al. Patch testing in an unusual case of toxic epidermal necrolysis. Contact Dermatitis. 1996;35:175-176.
- Swerlick RA, Campbell CF. Medication dyes as a source of drug allergy. J Drugs Dermatol. 2013;12:99-102.
- Guin JD. Patch testing to FD&C and D&C dyes. Contact Dermatitis. 2003;49:217-218.
- Lowther A, McCormick T, Nedorost S. Systemic contact dermatitis from propylene glycol. Dermatitis. 2008;19:105-108.
- Baeck M, Goossens A. Systemic contact dermatitis to corticosteroids. Allergy. 2012;67:1580-1585.
- Baeck M, Goossens A. Immediate and delayed allergic hypersensitivity to corticosteroids: practical guidelines. Contact Dermatitis. 2012;66:38-45.
- Basedow S, Eigelshoven S, Homey B. Immediate and delayed hypersensitivity to corticosteroids. J Dtsch Dermatol Ges. 2011;9:885-888.
- Johansen JD, Aalto-korte K, Agner T, et al. European Society of Contact Dermatitis guideline for diagnostic patch testing—recommendations on best practice. Contact Dermatitis. 2015;73:195-221.
- Mirakian R, Ewan PW, Durham SR, et al. BSACI guidelines for the management of drug allergy. Clin Exp Allergy. 2009;39:43-61.
- Joint Task Force on Practice Parameters; American Academy of Allergy, Asthma and Immunology; American College of Allergy, Asthma and Immunology; Joint Council of Allergy, Asthma and Immunology. Drug allergy: an updated practice parameter. Ann Allergy Asthma Immunol. 2010;105:259-273.
Practice Points
- Consider patch testing in suspected eczematous drug rashes and fixed drug eruption.
- Patch test to inactive excipients as well as active ingredients.
- Caution patients that sensitivity of patch testing for systemic drug reactions is unknown and likely lower than specificity.
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.
Evolution of Femoroacetabular Impingement Treatment: The ANCHOR Experience
Take-Home Points
- Our understanding of FAI has evolved from cam-type and pincer-type impingement to much more complex disease patterns.
- Most surgeons are performing less aggressive acetabular rim trimming.
- Inadequate osseous correction is still the most common cause of the failed hip arthroscopy.
- Labral preservation is important to maintaining suction seal effect.
- Open surgical techniques have a role for more severe and complex FAI deformities.
Femoroacetabular impingement (FAI) was described by Ganz and colleagues1 in 2003 as a refinement of concepts introduced decades earlier. This description advanced our understanding of FAI as a mechanism for prearthritic hip pain and secondary hip osteoarthritis1 (OA) and allowed for treatment of FAI. The concept of proximal femoral and acetabular/pelvic deformity contributing to OA had been previously speculated by Smith-Petersen,2 Murray,3 Solomon,4 and Stulberg.5 Early cases of overcorrection of dysplasia using the periacetabular osteotomy created iatrogenic FAI, which further stimulated early development of the FAI concept.6 Improved anatomical characterization of the proximal femoral blood supply (medial femoral circumflex artery) allowed for development of the open surgical hip dislocation.7 Through open surgical hip dislocation, an improved understanding of hip pathomechanics by direct visualization helped pave the way for a better understanding of FAI. Open surgical hip dislocation allows for global treatment of labrochondral pathology and deformity of the proximal femoral head–neck junction and/or acetabular rim in FAI.
Hip arthroscopy has further developed and improved our understanding of FAI. Early hip arthroscopy was generally limited to débridement of labral and chondral pathology, and management of the soft-tissue structures. Advances in the understanding of FAI through open techniques allowed for application of similar techniques to hip arthroscopy. Improvements in arthroscopic instrumentation and techniques have allowed for treatment of labrochondral and acetabular-sided rim deformity in the central compartment and cam morphologies in the peripheral compartment through arthroscopic surgery. Appropriate bony correction by arthroscopic techniques has always been a concern, but improved techniques, dynamic assessment, and accurate use of intraoperative imaging have made this feasible and more predictable. Treatment of cam deformities extending adjacent and proximal to the retinacular vessels is possible but more technically demanding. Inadequate bony correction of FAI by arthroscopic means remains one of the most common causes of failure.8-10In 2013, the Academic Network of Conservational Hip Outcome Research (ANCHOR) Study Group reported the characteristics of a FAI cohort of 1130 hips (1076 patients) that underwent surgical treatment of FAI across 8 institutions and 12 surgeons.11 At that time, most ANCHOR surgeons (or surgeon groups) performed both open and arthroscopic surgeries and had significant referral volumes of complex cases that may have overrepresented the proportion of complex FAI cases in the cohort. During the 2008 to 2011 study period, FAI was treated with arthroscopy in 56% of these cases, open surgical hip dislocation in 34%, and reverse periacetabular osteotomy in 9%. FAI was characterized as isolated cam-type in 48%, combined cam–pincer type in 45%, and isolated pincer-type in 8%. Fifty-five percent of the patients were female. Patient-reported outcome studies in this cohort of patients are ongoing.
The FAI Concept
In 2003, after treating more than 600 open surgical hip dislocations over the previous decade, Ganz and colleagues1 coined the term femoroacetabular impingement to describe a “mechanism for the development of early osteoarthritis for most nondysplastic hips.” They reported surgical treatment focused on “improving the clearance for hip motion and alleviation of femoral abutment against the acetabular rim” with the goal of improving pain and possibly of halting progression of the degenerative process. FAI was defined as “abnormal contact between the proximal femur and acetabular rim that occurs during terminal motion of the hip” leading to “lesions of the acetabular labrum and/or the adjacent acetabular cartilage.” Subtle, previously overlooked deformities of the proximal femur and acetabulum were recognized as the cause of FAI, “including the presence of a bony prominence usually in the anterolateral head and neck junction that is seen best on the lateral radiographs, reduced offset of the femoral neck and head junction, and changes on the acetabular rim such as os acetabuli or a double line that is seen with rim ossification.” Ganz and colleagues1 recognized that “normal or near normal” hips could also experience FAI in the setting of excessive or supraphysiologic range of motion. Cam-type and pincer-type FAI deformities were introduced as 2 distinct mechanisms of FAI. By 2003, arthroscopic hip surgery was increasingly being used as a treatment for labral tears but not bony abnormalities. These FAI concepts seemed to explain the prevalence of labral tears at the anterosuperior rim, which had been noted during hip arthroscopy, and paved the way for major changes in arthroscopic hip surgery during the next decade. The ANCHOR group reported the descriptive epidemiology of a cohort of more than 1000 patients with FAI.11
Cam-Type FAI
Cam-type impingement results from femoral-sided deformities. The mechanism was described as inclusion-type impingement in which “jamming of an abnormal femoral head with increasing radius into the acetabulum during forceful motion, especially flexion.”1 This results in outside-in abrasion of the acetabular cartilage of the anterosuperior rim with detachment of the “principally uninvolved labrum”1 and potentially delamination of the adjacent cartilage from the subchondral bone. Ganz and colleagues1 recognized in their initial descriptions of FAI that cam-type FAI could involve decreased femoral version, femoral head–neck junction asphericity, and decreased head–neck offset. The complexity and variability in the topography and geography of the cam morphology have been increasingly recognized. Accurate understanding and characterization of the proximal femoral deformity are important in guiding surgical correction of the cam deformity.
Advances in understanding the prevalence of the cam morphology and the association with OA have been important to our understanding of the pathophysiology of FAI. Several studies12 have established that a cam morphology of the proximal femur (defined by a variety of different metrics) is common among asymptomatic individuals. In light of this fact, a description of the femoral anatomy as a “cam morphology” rather than a cam deformity is now favored. Similarly, FAI is better used to refer to symptomatic individuals and is not equivalent to a cam morphology. The cam morphology seems significantly more common among athletes. Siebenrock and colleagues13 demonstrated the correlation of high-level athletics during late stages of skeletal immaturity and development of a cam morphology. A recent systematic review of 9 studies found that elite male athletes in late skeletal immaturity were 2 to 8 times more likely to develop a cam morphology before skeletal maturity.14Several population-based studies15,16 have quantified the apparent association of the cam morphology with hip OA. However, the studies were limited in their ability to adequately define the presence of cam morphology based on anteroposterior (AP) pelvis radiographs.
In a prospective study, Agricola and colleagues15 found the risk of OA was increased 2.4 times in the setting of moderate cam morphology (α angle, >60°) over a 5-year period. Thomas and colleagues16 found increased risk in a female cohort when the α angle was >65°.
Treatment of cam-type FAI is focused on adequate correction of the abnormal bone morphology. Inadequate or inappropriate bony correction of FAI is a common cause of treatment failure and is more common with arthroscopic techniques.9,10,17 Inadequate bony resection may be the result of surgical inexperience, poor visualization, or lack of understanding of the underlying bony deformity. Modern osteoplasty techniques also focus on gradual bony contour correction that restores the normal concavity–convexity transition of the head–neck junction. Overresection of the cam deformity not only may increase the risk of femoral neck fracture but may result in early disruption of the hip fluid seal from loss of contact between the femoral head and the acetabular labrum earlier in the arc of motion. In addition, high range-of-motion impingement can be seen in various athletic populations (dance, gymnastics, martial arts, hockey goalies), and the regions of impingement tend to be farther away from classically described impingement. Impingement in these situations occurs at the distal femoral neck and subspine regions, adding a level of complexity and unpredictability from a surgical standpoint.
FAI can also occur in the setting of more complex deformities than the typical cam morphology. Complex cases of FAI caused by slipped capital femoral epiphysis (SCFE) and residual Legg-Calvé-Perthes disease are relatively common. Complex deformities may also result in extra-articular impingement of the proximal femur (greater/lesser trochanter, distal femoral neck) on the pelvis (ilium, ischium) in addition to typical FAI. Mild to moderate cases of residual SCFE may be adequately treated with osteoplasty by arthroscopic techniques. In the setting of more severe residual SCFE, presence of underlying femoral retroversion and retrotilt of the femoral epiphysis may prevent adequate deformity correction and motion improvement by arthroscopy. Surgical hip dislocation (with or without relative femoral neck lengthening) and/or proximal femoral flexion derotational osteotomy may be the best means of treatment in these more severe deformities but may be dependent on the chronicity of the deformity and associated compensatory changes occurring on the acetabular side. Similarly, in moderate to severe residual Legg-Calvé-Perthes disease, presence of coxa vara, high greater trochanter, short femoral neck, and ovoid femoral head may be better treated in open techniques to allow comprehensive deformity correction, including correction of acetabular dysplasia in some cases.
Pincer-Type FAI
Pincer-type FAI results from acetabular-sided deformities in which acetabular deformity leads to impaction-type impingement with “linear contact between the acetabular rim and the femoral head–neck junction.”1 Pincer FAI causes primarily labral damage with progressive degeneration and, in some cases, ossification of the acetabular labrum that further worsens the acetabular overcoverage and premature rim impaction. Chondral damage in pincer-type FAI is generally less significant and limited to the peripheral acetabular rim.
Pincer-type FAI may be caused by acetabular retroversion, coxa profunda, or protrusio acetabuli. Our understanding of what defines a pincer morphology has evolved significantly. Through efforts to better define structural features of the acetabular rim that represent abnormalities, we have improved our understanding of how these features may influence OA development. One example of improved understanding involves coxa profunda, classically defined as the medial acetabular fossa touching or projecting medial to the ilioischial line on an AP pelvis radiograph. Several studies have found that this classic definition poorly describes the “overcovered” hip, as it is present in 70% of females and commonly present (41%) in the setting of acetabular dysplasia.18,19 Acetabular retroversion was previously associated with hip OA. Although central acetabular retroversion is relatively uncommon, cranial acetabular retroversion is more common. Presence of a crossover sign on AP pelvis radiographs generally has been viewed as indicative of acetabular retroversion. However, alterations in pelvic tilt on supine or standing AP pelvis radiographs can result in apparent retroversion in the setting of normal acetabular anatomy20 and potentially influence the development of impingement.21 Zaltz and colleagues22 found that abnormal morphology of the anterior inferior iliac spine can also lead to the presence of a crossover sign in an otherwise anteverted acetabulum. Larson and colleagues23 recently found that a crossover sign is present in 11% of asymptomatic hips (19% of males) and may be considered a normal variant. A crossover sign can also be present in the setting of posterior acetabular deficiency with normal anterior acetabular coverage. Ultimately, acetabular retroversion might indicate pincer-type FAI or dysplasia or be a normal variant that does not require treatment. Global acetabular overcoverage, including coxa protrusio, may be associated with OA in population-based studies but is not uniformly demonstrated in all studies.16,24,25 A lateral center edge angle of >40° and a Tönnis angle (acetabular inclination) of <0° are commonly viewed as markers of global overcoverage.
FAI Treatment
Improvements in hip arthroscopy techniques and instrumentation have led to hip arthroscopy becoming the primary surgical technique for the treatment of most cases of FAI. Hip arthroscopy allows for precise visualization and treatment of labral and chondral disease in the central compartment by traction. Larson and colleagues26 reported complication rates for hip arthroscopy in a prospective series of >1600 cases. The overall complication rate was 8.3%, with higher rates noted in female patients and in the setting of traction time longer than 60 minutes. Nonetheless, major complications occurred in 1.1%, with only 0.1% having persistent disability. The most common complications were lateral femoral cutaneous nerve dysesthesias (1.6%), pudendal nerve neuropraxia (1.4%), and iatrogenic labral/chondral damage (2.1%).
The importance of preserving the acetabular labrum is now well accepted from clinical and biomechanical evidence.27-29 As in previous studies in surgical hip dislocation,30 arthroscopic labral repair (vs débridement) results in improved clinical outcomes.31,32 Labral repair techniques currently focus on stable fixation of the labrum while maintaining the normal position of the labrum relative to the femoral head and avoiding labral eversion, which may compromise the hip suction seal. With continued technical advancements and biomechanical support, arthroscopic labral reconstruction is possible in the setting of labral deficiency, often resulting from prior resection. However, the optimal indications, surgical techniques, and long-term outcomes continue to be better defined. Open and arthroscopic techniques have shown similar ability to correct the typical mild to moderate cam morphology in FAI.33 Yet, inadequate femoral bony correction of FAI seems to be the most common cause for revision hip preservation surgery.9,10,17Mild to moderate acetabular rim deformities are commonly treated with hip arthroscopy. As our understanding of pincer-type FAI continues to improve, many surgeons are performing less- aggressive bone resection along the anterior rim. On the other hand, subspinous impingement was recently recognized as a form of extra-articular pincer FAI variant.34 Subspine decompression without true acetabular rim resection has become a more common treatment for pincer lesions and may be a consideration even with restricted range of motion after periacetabular osteotomy. Severe acetabular deformities with global overcoverage or acetabular protrusion are particularly challenging by arthroscopy, even for the most experienced surgeons. Although some improvement in deformity is feasible with arthroscopy, even cases reported in the literature have demonstrated incomplete deformity correction. Open surgical hip dislocation may continue to be the ideal treatment technique for severe pincer impingement.
Cam-type FAI is commonly treated with hip arthroscopy (Figures A-F).
Open surgical techniques will continue to have an important role in the treatment of severe and complex FAI deformities in which arthroscopic techniques do not consistently achieve adequate bony correction (Figures A-F). Surgical hip dislocation remains a powerful surgical technique for deformity correction in FAI. Sink and colleagues37 reported rates of complications after open surgical hip dislocation in the ANCHOR study group. In a cohort of 334 hips (302 patients), trochanteric nonunion occurred in 1.8% of cases, and there were no cases of avascular necrosis. Overall major complications were observed in 4.8% of cases, with 0.3% having chronic disability. Excellent outcomes, including high rates of return to sports, have been reported after surgical hip dislocation for FAI.38 Midterm studies from the early phase of surgical treatment of FAI have helped identify factors that may play a major role in optimizing patient outcomes.
Conclusion
Our understanding and treatment of FAI continue to evolve. Both open and arthroscopic techniques have demonstrated excellent outcomes in the treatment of FAI. Most cases of FAI are now amenable to arthroscopic treatment. Inadequate resection and underlying acetabular dysplasia remain common causes of treatment failure. Open surgical hip dislocation continues to play a role in the treatment of severe deformities that are poorly accessible by arthroscopy—including cam lesions with posterior extension, severe global acetabular overcoverage, or extra-articular impingement. The association of FAI with OA is most apparent for cam-type FAI. Future research will define the optimal treatment strategies and determine if they modify disease progression.
Am J Orthop. 2017;46(1):28-34. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
1. 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.
2. Smith-Petersen MN. The classic: treatment of malum coxae senilis, old slipped upper femoral epiphysis, intrapelvic protrusion of the acetabulum, and coxa plana by means of acetabuloplasty. 1936. Clin Orthop Relat Res. 2009;467(3):608-615.
3. Murray RO. The aetiology of primary osteoarthritis of the hip. Br J Radiol. 1965;38(455):810-824.
4. Solomon L. Patterns of osteoarthritis of the hip. J Bone Joint Surg Br. 1976;58(2):176-183.
5. Stulberg SD. Unrecognized childhood hip disease: a major cause of idiopathic osteoarthritis of the hip. In: Cordell LD, Harris WH, Ramsey PL, MacEwen GD, eds. The Hip: Proceedings of the Third Open Scientific Meeting of the Hip Society. St. Louis, MO: Mosby; 1975:212-228.
6. Myers SR, Eijer H, Ganz R. Anterior femoroacetabular impingement after periacetabular osteotomy. Clin Orthop Relat Res. 1999;(363):93-99.
7. Ganz R, Gill TJ, Gautier E, Ganz K, Krügel N, Berlemann U. Surgical dislocation of the adult hip: a technique with full access to the femoral head and acetabulum without the risk of avascular necrosis. J Bone Joint Surg Br. 2001;83(8):1119-1124.
8. Ross JR, Larson CM, Adeoye O, Kelly BT, Bedi A. Residual deformity is the most common reason for revision hip arthroscopy: a three-dimensional CT study. Clin Orthop Relat Res. 2015;473(4):1388-1395.
9. Clohisy JC, Nepple JJ, Larson CM, Zaltz I, Millis M; Academic Network of Conservation Hip Outcome Research (ANCHOR) Members. Persistent structural disease is the most common cause of repeat hip preservation surgery. Clin Orthop Relat Res. 2013;471(12):3788-3794.
10. Heyworth BE, Shindle MK, Voos JE, Rudzki JR, Kelly BT. Radiologic and intraoperative findings in revision hip arthroscopy. Arthroscopy. 2007;23(12):1295-1302.
11. Clohisy JC, Baca G, Beaulé PE, et al; ANCHOR Study Group. Descriptive epidemiology of femoroacetabular impingement: a North American cohort of patients undergoing surgery. Am J Sports Med. 2013;41(6):1348-1356.
12. Frank JM, Harris JD, Erickson BJ, et al. Prevalence of femoroacetabular impingement imaging findings in asymptomatic volunteers: a systematic review. Arthroscopy. 2015;31(6):1199-11204.
13. Siebenrock KA, Ferner F, Noble PC, Santore RF, Werlen S, Mamisch TC. The cam-type deformity of the proximal femur arises in childhood in response to vigorous sporting activity. Clin Orthop Relat Res. 2011;469(11):3229-3240.
14. Nepple JJ, Vigdorchik JM, Clohisy JC. What is the association between sports participation and the development of proximal femoral cam deformity? A systematic review and meta-analysis. Am J Sports Med. 2015;43(11):2833-2840.
15. Agricola R, Waarsing JH, Arden NK, et al. Cam impingement of the hip: a risk factor for hip osteoarthritis. Nat Rev Rheumatol. 2013;9(10):630-634.
16. Thomas GE, Palmer AJ, Batra RN, et al. Subclinical deformities of the hip are significant predictors of radiographic osteoarthritis and joint replacement in women. A 20 year longitudinal cohort study. Osteoarthritis Cartilage. 2014;22(10):1504-1510.
17. Philippon MJ, Schenker ML, Briggs KK, Kuppersmith DA, Maxwell RB, Stubbs AJ. Revision hip arthroscopy. Am J Sports Med. 2007;35(11):1918-1921.
18. 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.
19. Anderson LA, Kapron AL, Aoki SK, Peters CL. Coxa profunda: is the deep acetabulum overcovered? Clin Orthop Relat Res. 2012;470(12):3375-3382.
20. 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.
21. Ross JR, Nepple JJ, Philippon MJ, Kelly BT, Larson CM, Bedi A. Effect of changes in pelvic tilt on range of motion to impingement and radiographic parameters of acetabular morphologic characteristics. Am J Sports Med. 2014;42(10):2402-2409.
22. Zaltz I, Kelly BT, Hetsroni I, Bedi A. The crossover sign overestimates acetabular retroversion. Clin Orthop Relat Res. 2013;471(8):2463-2470.
23. Larson CM, Moreau-Gaudry A, Kelly BT, et al. Are normal hips being labeled as pathologic? A CT-based method for defining normal acetabular coverage. Clin Orthop Relat Res. 2015;473(4):1247-1254.
24. Gosvig KK, Jacobsen S, Sonne-Holm S, Palm H, Troelsen A. Prevalence of malformations of the hip joint and their relationship to sex, groin pain, and risk of osteoarthritis: a population-based survey. J Bone Joint Surg Am. 2010;92(5):1162-1169.
25. Agricola R, Heijboer MP, Roze RH, et al. Pincer deformity does not lead to osteoarthritis of the hip whereas acetabular dysplasia does: acetabular coverage and development of osteoarthritis in a nationwide prospective cohort study (CHECK). Osteoarthritis Cartilage. 2013;21(10):1514-1521.
26. Larson CM, Clohisy JC, Beaulé PE, et al; ANCHOR Study Group. Intraoperative and early postoperative complications after hip arthroscopic surgery: a prospective multicenter trial utilizing a validated grading scheme. Am J Sports Med. 2016;44(9):2292-2298.
27. Ferguson SJ, Bryant JT, Ganz R, Ito K. An in vitro investigation of the acetabular labral seal in hip joint mechanics. J Biomech. 2003;36(2):171-178.
28. Nepple JJ, Philippon MJ, Campbell KJ, et al. The hip fluid seal—part II: the effect of an acetabular labral tear, repair, resection, and reconstruction on hip stability to distraction. Knee Surg Sports Traumatol Arthrosc. 2014;22(4):730-736.
29. 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.
30. Espinosa N, Rothenfluh DA, Beck M, Ganz R, Leunig M. Treatment of femoro-acetabular impingement: preliminary results of labral refixation. J Bone Joint Surg Am. 2006;88(5):925-935.
31. Krych AJ, Thompson M, Knutson Z, Scoon J, Coleman SH. Arthroscopic labral repair versus selective labral debridement in female patients with femoroacetabular impingement: a prospective randomized study. Arthroscopy. 2013;29(1):46-53.
32. Larson CM, Giveans MR. Arthroscopic debridement versus refixation of the acetabular labrum associated with femoroacetabular impingement. Arthroscopy. 2009;25(4):369-376.
33. Bedi A, Zaltz I, De La Torre K, Kelly BT. Radiographic comparison of surgical hip dislocation and hip arthroscopy for treatment of cam deformity in femoroacetabular impingement. Am J Sports Med. 2011;39(suppl):20S–28S.
34. Larson CM, Kelly BT, Stone RM. Making a case for anterior inferior iliac spine/subspine hip impingement: three representative case reports and proposed concept. Arthroscopy. 2011;27(12):1732-1737.
35. Ross JR, Bedi A, Stone RM, et al. Intraoperative fluoroscopic imaging to treat cam deformities: correlation with 3-dimensional computed tomography [published correction appears in Am J Sports Med. 2015;43(8):NP27]. Am J Sports Med. 2014;42(6):1370-1376.
36. Fabricant PD, Fields KG, Taylor SA, Magennis E, Bedi A, Kelly BT. The effect of femoral and acetabular version on clinical outcomes after arthroscopic femoroacetabular impingement surgery. J Bone Joint Surg Am. 2015;97(7):537-543.
37. Sink EL, Beaulé PE, Sucato D, et al. Multicenter study of complications following surgical dislocation of the hip. J Bone Joint Surg Am. 2011;93(12):1132-1136.
38. Naal FD, Miozzari HH, Wyss TF, Nötzli HP. Surgical hip dislocation for the treatment of femoroacetabular impingement in high-level athletes. Am J Sports Med. 2011;39(3):544-550.
Take-Home Points
- Our understanding of FAI has evolved from cam-type and pincer-type impingement to much more complex disease patterns.
- Most surgeons are performing less aggressive acetabular rim trimming.
- Inadequate osseous correction is still the most common cause of the failed hip arthroscopy.
- Labral preservation is important to maintaining suction seal effect.
- Open surgical techniques have a role for more severe and complex FAI deformities.
Femoroacetabular impingement (FAI) was described by Ganz and colleagues1 in 2003 as a refinement of concepts introduced decades earlier. This description advanced our understanding of FAI as a mechanism for prearthritic hip pain and secondary hip osteoarthritis1 (OA) and allowed for treatment of FAI. The concept of proximal femoral and acetabular/pelvic deformity contributing to OA had been previously speculated by Smith-Petersen,2 Murray,3 Solomon,4 and Stulberg.5 Early cases of overcorrection of dysplasia using the periacetabular osteotomy created iatrogenic FAI, which further stimulated early development of the FAI concept.6 Improved anatomical characterization of the proximal femoral blood supply (medial femoral circumflex artery) allowed for development of the open surgical hip dislocation.7 Through open surgical hip dislocation, an improved understanding of hip pathomechanics by direct visualization helped pave the way for a better understanding of FAI. Open surgical hip dislocation allows for global treatment of labrochondral pathology and deformity of the proximal femoral head–neck junction and/or acetabular rim in FAI.
Hip arthroscopy has further developed and improved our understanding of FAI. Early hip arthroscopy was generally limited to débridement of labral and chondral pathology, and management of the soft-tissue structures. Advances in the understanding of FAI through open techniques allowed for application of similar techniques to hip arthroscopy. Improvements in arthroscopic instrumentation and techniques have allowed for treatment of labrochondral and acetabular-sided rim deformity in the central compartment and cam morphologies in the peripheral compartment through arthroscopic surgery. Appropriate bony correction by arthroscopic techniques has always been a concern, but improved techniques, dynamic assessment, and accurate use of intraoperative imaging have made this feasible and more predictable. Treatment of cam deformities extending adjacent and proximal to the retinacular vessels is possible but more technically demanding. Inadequate bony correction of FAI by arthroscopic means remains one of the most common causes of failure.8-10In 2013, the Academic Network of Conservational Hip Outcome Research (ANCHOR) Study Group reported the characteristics of a FAI cohort of 1130 hips (1076 patients) that underwent surgical treatment of FAI across 8 institutions and 12 surgeons.11 At that time, most ANCHOR surgeons (or surgeon groups) performed both open and arthroscopic surgeries and had significant referral volumes of complex cases that may have overrepresented the proportion of complex FAI cases in the cohort. During the 2008 to 2011 study period, FAI was treated with arthroscopy in 56% of these cases, open surgical hip dislocation in 34%, and reverse periacetabular osteotomy in 9%. FAI was characterized as isolated cam-type in 48%, combined cam–pincer type in 45%, and isolated pincer-type in 8%. Fifty-five percent of the patients were female. Patient-reported outcome studies in this cohort of patients are ongoing.
The FAI Concept
In 2003, after treating more than 600 open surgical hip dislocations over the previous decade, Ganz and colleagues1 coined the term femoroacetabular impingement to describe a “mechanism for the development of early osteoarthritis for most nondysplastic hips.” They reported surgical treatment focused on “improving the clearance for hip motion and alleviation of femoral abutment against the acetabular rim” with the goal of improving pain and possibly of halting progression of the degenerative process. FAI was defined as “abnormal contact between the proximal femur and acetabular rim that occurs during terminal motion of the hip” leading to “lesions of the acetabular labrum and/or the adjacent acetabular cartilage.” Subtle, previously overlooked deformities of the proximal femur and acetabulum were recognized as the cause of FAI, “including the presence of a bony prominence usually in the anterolateral head and neck junction that is seen best on the lateral radiographs, reduced offset of the femoral neck and head junction, and changes on the acetabular rim such as os acetabuli or a double line that is seen with rim ossification.” Ganz and colleagues1 recognized that “normal or near normal” hips could also experience FAI in the setting of excessive or supraphysiologic range of motion. Cam-type and pincer-type FAI deformities were introduced as 2 distinct mechanisms of FAI. By 2003, arthroscopic hip surgery was increasingly being used as a treatment for labral tears but not bony abnormalities. These FAI concepts seemed to explain the prevalence of labral tears at the anterosuperior rim, which had been noted during hip arthroscopy, and paved the way for major changes in arthroscopic hip surgery during the next decade. The ANCHOR group reported the descriptive epidemiology of a cohort of more than 1000 patients with FAI.11
Cam-Type FAI
Cam-type impingement results from femoral-sided deformities. The mechanism was described as inclusion-type impingement in which “jamming of an abnormal femoral head with increasing radius into the acetabulum during forceful motion, especially flexion.”1 This results in outside-in abrasion of the acetabular cartilage of the anterosuperior rim with detachment of the “principally uninvolved labrum”1 and potentially delamination of the adjacent cartilage from the subchondral bone. Ganz and colleagues1 recognized in their initial descriptions of FAI that cam-type FAI could involve decreased femoral version, femoral head–neck junction asphericity, and decreased head–neck offset. The complexity and variability in the topography and geography of the cam morphology have been increasingly recognized. Accurate understanding and characterization of the proximal femoral deformity are important in guiding surgical correction of the cam deformity.
Advances in understanding the prevalence of the cam morphology and the association with OA have been important to our understanding of the pathophysiology of FAI. Several studies12 have established that a cam morphology of the proximal femur (defined by a variety of different metrics) is common among asymptomatic individuals. In light of this fact, a description of the femoral anatomy as a “cam morphology” rather than a cam deformity is now favored. Similarly, FAI is better used to refer to symptomatic individuals and is not equivalent to a cam morphology. The cam morphology seems significantly more common among athletes. Siebenrock and colleagues13 demonstrated the correlation of high-level athletics during late stages of skeletal immaturity and development of a cam morphology. A recent systematic review of 9 studies found that elite male athletes in late skeletal immaturity were 2 to 8 times more likely to develop a cam morphology before skeletal maturity.14Several population-based studies15,16 have quantified the apparent association of the cam morphology with hip OA. However, the studies were limited in their ability to adequately define the presence of cam morphology based on anteroposterior (AP) pelvis radiographs.
In a prospective study, Agricola and colleagues15 found the risk of OA was increased 2.4 times in the setting of moderate cam morphology (α angle, >60°) over a 5-year period. Thomas and colleagues16 found increased risk in a female cohort when the α angle was >65°.
Treatment of cam-type FAI is focused on adequate correction of the abnormal bone morphology. Inadequate or inappropriate bony correction of FAI is a common cause of treatment failure and is more common with arthroscopic techniques.9,10,17 Inadequate bony resection may be the result of surgical inexperience, poor visualization, or lack of understanding of the underlying bony deformity. Modern osteoplasty techniques also focus on gradual bony contour correction that restores the normal concavity–convexity transition of the head–neck junction. Overresection of the cam deformity not only may increase the risk of femoral neck fracture but may result in early disruption of the hip fluid seal from loss of contact between the femoral head and the acetabular labrum earlier in the arc of motion. In addition, high range-of-motion impingement can be seen in various athletic populations (dance, gymnastics, martial arts, hockey goalies), and the regions of impingement tend to be farther away from classically described impingement. Impingement in these situations occurs at the distal femoral neck and subspine regions, adding a level of complexity and unpredictability from a surgical standpoint.
FAI can also occur in the setting of more complex deformities than the typical cam morphology. Complex cases of FAI caused by slipped capital femoral epiphysis (SCFE) and residual Legg-Calvé-Perthes disease are relatively common. Complex deformities may also result in extra-articular impingement of the proximal femur (greater/lesser trochanter, distal femoral neck) on the pelvis (ilium, ischium) in addition to typical FAI. Mild to moderate cases of residual SCFE may be adequately treated with osteoplasty by arthroscopic techniques. In the setting of more severe residual SCFE, presence of underlying femoral retroversion and retrotilt of the femoral epiphysis may prevent adequate deformity correction and motion improvement by arthroscopy. Surgical hip dislocation (with or without relative femoral neck lengthening) and/or proximal femoral flexion derotational osteotomy may be the best means of treatment in these more severe deformities but may be dependent on the chronicity of the deformity and associated compensatory changes occurring on the acetabular side. Similarly, in moderate to severe residual Legg-Calvé-Perthes disease, presence of coxa vara, high greater trochanter, short femoral neck, and ovoid femoral head may be better treated in open techniques to allow comprehensive deformity correction, including correction of acetabular dysplasia in some cases.
Pincer-Type FAI
Pincer-type FAI results from acetabular-sided deformities in which acetabular deformity leads to impaction-type impingement with “linear contact between the acetabular rim and the femoral head–neck junction.”1 Pincer FAI causes primarily labral damage with progressive degeneration and, in some cases, ossification of the acetabular labrum that further worsens the acetabular overcoverage and premature rim impaction. Chondral damage in pincer-type FAI is generally less significant and limited to the peripheral acetabular rim.
Pincer-type FAI may be caused by acetabular retroversion, coxa profunda, or protrusio acetabuli. Our understanding of what defines a pincer morphology has evolved significantly. Through efforts to better define structural features of the acetabular rim that represent abnormalities, we have improved our understanding of how these features may influence OA development. One example of improved understanding involves coxa profunda, classically defined as the medial acetabular fossa touching or projecting medial to the ilioischial line on an AP pelvis radiograph. Several studies have found that this classic definition poorly describes the “overcovered” hip, as it is present in 70% of females and commonly present (41%) in the setting of acetabular dysplasia.18,19 Acetabular retroversion was previously associated with hip OA. Although central acetabular retroversion is relatively uncommon, cranial acetabular retroversion is more common. Presence of a crossover sign on AP pelvis radiographs generally has been viewed as indicative of acetabular retroversion. However, alterations in pelvic tilt on supine or standing AP pelvis radiographs can result in apparent retroversion in the setting of normal acetabular anatomy20 and potentially influence the development of impingement.21 Zaltz and colleagues22 found that abnormal morphology of the anterior inferior iliac spine can also lead to the presence of a crossover sign in an otherwise anteverted acetabulum. Larson and colleagues23 recently found that a crossover sign is present in 11% of asymptomatic hips (19% of males) and may be considered a normal variant. A crossover sign can also be present in the setting of posterior acetabular deficiency with normal anterior acetabular coverage. Ultimately, acetabular retroversion might indicate pincer-type FAI or dysplasia or be a normal variant that does not require treatment. Global acetabular overcoverage, including coxa protrusio, may be associated with OA in population-based studies but is not uniformly demonstrated in all studies.16,24,25 A lateral center edge angle of >40° and a Tönnis angle (acetabular inclination) of <0° are commonly viewed as markers of global overcoverage.
FAI Treatment
Improvements in hip arthroscopy techniques and instrumentation have led to hip arthroscopy becoming the primary surgical technique for the treatment of most cases of FAI. Hip arthroscopy allows for precise visualization and treatment of labral and chondral disease in the central compartment by traction. Larson and colleagues26 reported complication rates for hip arthroscopy in a prospective series of >1600 cases. The overall complication rate was 8.3%, with higher rates noted in female patients and in the setting of traction time longer than 60 minutes. Nonetheless, major complications occurred in 1.1%, with only 0.1% having persistent disability. The most common complications were lateral femoral cutaneous nerve dysesthesias (1.6%), pudendal nerve neuropraxia (1.4%), and iatrogenic labral/chondral damage (2.1%).
The importance of preserving the acetabular labrum is now well accepted from clinical and biomechanical evidence.27-29 As in previous studies in surgical hip dislocation,30 arthroscopic labral repair (vs débridement) results in improved clinical outcomes.31,32 Labral repair techniques currently focus on stable fixation of the labrum while maintaining the normal position of the labrum relative to the femoral head and avoiding labral eversion, which may compromise the hip suction seal. With continued technical advancements and biomechanical support, arthroscopic labral reconstruction is possible in the setting of labral deficiency, often resulting from prior resection. However, the optimal indications, surgical techniques, and long-term outcomes continue to be better defined. Open and arthroscopic techniques have shown similar ability to correct the typical mild to moderate cam morphology in FAI.33 Yet, inadequate femoral bony correction of FAI seems to be the most common cause for revision hip preservation surgery.9,10,17Mild to moderate acetabular rim deformities are commonly treated with hip arthroscopy. As our understanding of pincer-type FAI continues to improve, many surgeons are performing less- aggressive bone resection along the anterior rim. On the other hand, subspinous impingement was recently recognized as a form of extra-articular pincer FAI variant.34 Subspine decompression without true acetabular rim resection has become a more common treatment for pincer lesions and may be a consideration even with restricted range of motion after periacetabular osteotomy. Severe acetabular deformities with global overcoverage or acetabular protrusion are particularly challenging by arthroscopy, even for the most experienced surgeons. Although some improvement in deformity is feasible with arthroscopy, even cases reported in the literature have demonstrated incomplete deformity correction. Open surgical hip dislocation may continue to be the ideal treatment technique for severe pincer impingement.
Cam-type FAI is commonly treated with hip arthroscopy (Figures A-F).
Open surgical techniques will continue to have an important role in the treatment of severe and complex FAI deformities in which arthroscopic techniques do not consistently achieve adequate bony correction (Figures A-F). Surgical hip dislocation remains a powerful surgical technique for deformity correction in FAI. Sink and colleagues37 reported rates of complications after open surgical hip dislocation in the ANCHOR study group. In a cohort of 334 hips (302 patients), trochanteric nonunion occurred in 1.8% of cases, and there were no cases of avascular necrosis. Overall major complications were observed in 4.8% of cases, with 0.3% having chronic disability. Excellent outcomes, including high rates of return to sports, have been reported after surgical hip dislocation for FAI.38 Midterm studies from the early phase of surgical treatment of FAI have helped identify factors that may play a major role in optimizing patient outcomes.
Conclusion
Our understanding and treatment of FAI continue to evolve. Both open and arthroscopic techniques have demonstrated excellent outcomes in the treatment of FAI. Most cases of FAI are now amenable to arthroscopic treatment. Inadequate resection and underlying acetabular dysplasia remain common causes of treatment failure. Open surgical hip dislocation continues to play a role in the treatment of severe deformities that are poorly accessible by arthroscopy—including cam lesions with posterior extension, severe global acetabular overcoverage, or extra-articular impingement. The association of FAI with OA is most apparent for cam-type FAI. Future research will define the optimal treatment strategies and determine if they modify disease progression.
Am J Orthop. 2017;46(1):28-34. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
Take-Home Points
- Our understanding of FAI has evolved from cam-type and pincer-type impingement to much more complex disease patterns.
- Most surgeons are performing less aggressive acetabular rim trimming.
- Inadequate osseous correction is still the most common cause of the failed hip arthroscopy.
- Labral preservation is important to maintaining suction seal effect.
- Open surgical techniques have a role for more severe and complex FAI deformities.
Femoroacetabular impingement (FAI) was described by Ganz and colleagues1 in 2003 as a refinement of concepts introduced decades earlier. This description advanced our understanding of FAI as a mechanism for prearthritic hip pain and secondary hip osteoarthritis1 (OA) and allowed for treatment of FAI. The concept of proximal femoral and acetabular/pelvic deformity contributing to OA had been previously speculated by Smith-Petersen,2 Murray,3 Solomon,4 and Stulberg.5 Early cases of overcorrection of dysplasia using the periacetabular osteotomy created iatrogenic FAI, which further stimulated early development of the FAI concept.6 Improved anatomical characterization of the proximal femoral blood supply (medial femoral circumflex artery) allowed for development of the open surgical hip dislocation.7 Through open surgical hip dislocation, an improved understanding of hip pathomechanics by direct visualization helped pave the way for a better understanding of FAI. Open surgical hip dislocation allows for global treatment of labrochondral pathology and deformity of the proximal femoral head–neck junction and/or acetabular rim in FAI.
Hip arthroscopy has further developed and improved our understanding of FAI. Early hip arthroscopy was generally limited to débridement of labral and chondral pathology, and management of the soft-tissue structures. Advances in the understanding of FAI through open techniques allowed for application of similar techniques to hip arthroscopy. Improvements in arthroscopic instrumentation and techniques have allowed for treatment of labrochondral and acetabular-sided rim deformity in the central compartment and cam morphologies in the peripheral compartment through arthroscopic surgery. Appropriate bony correction by arthroscopic techniques has always been a concern, but improved techniques, dynamic assessment, and accurate use of intraoperative imaging have made this feasible and more predictable. Treatment of cam deformities extending adjacent and proximal to the retinacular vessels is possible but more technically demanding. Inadequate bony correction of FAI by arthroscopic means remains one of the most common causes of failure.8-10In 2013, the Academic Network of Conservational Hip Outcome Research (ANCHOR) Study Group reported the characteristics of a FAI cohort of 1130 hips (1076 patients) that underwent surgical treatment of FAI across 8 institutions and 12 surgeons.11 At that time, most ANCHOR surgeons (or surgeon groups) performed both open and arthroscopic surgeries and had significant referral volumes of complex cases that may have overrepresented the proportion of complex FAI cases in the cohort. During the 2008 to 2011 study period, FAI was treated with arthroscopy in 56% of these cases, open surgical hip dislocation in 34%, and reverse periacetabular osteotomy in 9%. FAI was characterized as isolated cam-type in 48%, combined cam–pincer type in 45%, and isolated pincer-type in 8%. Fifty-five percent of the patients were female. Patient-reported outcome studies in this cohort of patients are ongoing.
The FAI Concept
In 2003, after treating more than 600 open surgical hip dislocations over the previous decade, Ganz and colleagues1 coined the term femoroacetabular impingement to describe a “mechanism for the development of early osteoarthritis for most nondysplastic hips.” They reported surgical treatment focused on “improving the clearance for hip motion and alleviation of femoral abutment against the acetabular rim” with the goal of improving pain and possibly of halting progression of the degenerative process. FAI was defined as “abnormal contact between the proximal femur and acetabular rim that occurs during terminal motion of the hip” leading to “lesions of the acetabular labrum and/or the adjacent acetabular cartilage.” Subtle, previously overlooked deformities of the proximal femur and acetabulum were recognized as the cause of FAI, “including the presence of a bony prominence usually in the anterolateral head and neck junction that is seen best on the lateral radiographs, reduced offset of the femoral neck and head junction, and changes on the acetabular rim such as os acetabuli or a double line that is seen with rim ossification.” Ganz and colleagues1 recognized that “normal or near normal” hips could also experience FAI in the setting of excessive or supraphysiologic range of motion. Cam-type and pincer-type FAI deformities were introduced as 2 distinct mechanisms of FAI. By 2003, arthroscopic hip surgery was increasingly being used as a treatment for labral tears but not bony abnormalities. These FAI concepts seemed to explain the prevalence of labral tears at the anterosuperior rim, which had been noted during hip arthroscopy, and paved the way for major changes in arthroscopic hip surgery during the next decade. The ANCHOR group reported the descriptive epidemiology of a cohort of more than 1000 patients with FAI.11
Cam-Type FAI
Cam-type impingement results from femoral-sided deformities. The mechanism was described as inclusion-type impingement in which “jamming of an abnormal femoral head with increasing radius into the acetabulum during forceful motion, especially flexion.”1 This results in outside-in abrasion of the acetabular cartilage of the anterosuperior rim with detachment of the “principally uninvolved labrum”1 and potentially delamination of the adjacent cartilage from the subchondral bone. Ganz and colleagues1 recognized in their initial descriptions of FAI that cam-type FAI could involve decreased femoral version, femoral head–neck junction asphericity, and decreased head–neck offset. The complexity and variability in the topography and geography of the cam morphology have been increasingly recognized. Accurate understanding and characterization of the proximal femoral deformity are important in guiding surgical correction of the cam deformity.
Advances in understanding the prevalence of the cam morphology and the association with OA have been important to our understanding of the pathophysiology of FAI. Several studies12 have established that a cam morphology of the proximal femur (defined by a variety of different metrics) is common among asymptomatic individuals. In light of this fact, a description of the femoral anatomy as a “cam morphology” rather than a cam deformity is now favored. Similarly, FAI is better used to refer to symptomatic individuals and is not equivalent to a cam morphology. The cam morphology seems significantly more common among athletes. Siebenrock and colleagues13 demonstrated the correlation of high-level athletics during late stages of skeletal immaturity and development of a cam morphology. A recent systematic review of 9 studies found that elite male athletes in late skeletal immaturity were 2 to 8 times more likely to develop a cam morphology before skeletal maturity.14Several population-based studies15,16 have quantified the apparent association of the cam morphology with hip OA. However, the studies were limited in their ability to adequately define the presence of cam morphology based on anteroposterior (AP) pelvis radiographs.
In a prospective study, Agricola and colleagues15 found the risk of OA was increased 2.4 times in the setting of moderate cam morphology (α angle, >60°) over a 5-year period. Thomas and colleagues16 found increased risk in a female cohort when the α angle was >65°.
Treatment of cam-type FAI is focused on adequate correction of the abnormal bone morphology. Inadequate or inappropriate bony correction of FAI is a common cause of treatment failure and is more common with arthroscopic techniques.9,10,17 Inadequate bony resection may be the result of surgical inexperience, poor visualization, or lack of understanding of the underlying bony deformity. Modern osteoplasty techniques also focus on gradual bony contour correction that restores the normal concavity–convexity transition of the head–neck junction. Overresection of the cam deformity not only may increase the risk of femoral neck fracture but may result in early disruption of the hip fluid seal from loss of contact between the femoral head and the acetabular labrum earlier in the arc of motion. In addition, high range-of-motion impingement can be seen in various athletic populations (dance, gymnastics, martial arts, hockey goalies), and the regions of impingement tend to be farther away from classically described impingement. Impingement in these situations occurs at the distal femoral neck and subspine regions, adding a level of complexity and unpredictability from a surgical standpoint.
FAI can also occur in the setting of more complex deformities than the typical cam morphology. Complex cases of FAI caused by slipped capital femoral epiphysis (SCFE) and residual Legg-Calvé-Perthes disease are relatively common. Complex deformities may also result in extra-articular impingement of the proximal femur (greater/lesser trochanter, distal femoral neck) on the pelvis (ilium, ischium) in addition to typical FAI. Mild to moderate cases of residual SCFE may be adequately treated with osteoplasty by arthroscopic techniques. In the setting of more severe residual SCFE, presence of underlying femoral retroversion and retrotilt of the femoral epiphysis may prevent adequate deformity correction and motion improvement by arthroscopy. Surgical hip dislocation (with or without relative femoral neck lengthening) and/or proximal femoral flexion derotational osteotomy may be the best means of treatment in these more severe deformities but may be dependent on the chronicity of the deformity and associated compensatory changes occurring on the acetabular side. Similarly, in moderate to severe residual Legg-Calvé-Perthes disease, presence of coxa vara, high greater trochanter, short femoral neck, and ovoid femoral head may be better treated in open techniques to allow comprehensive deformity correction, including correction of acetabular dysplasia in some cases.
Pincer-Type FAI
Pincer-type FAI results from acetabular-sided deformities in which acetabular deformity leads to impaction-type impingement with “linear contact between the acetabular rim and the femoral head–neck junction.”1 Pincer FAI causes primarily labral damage with progressive degeneration and, in some cases, ossification of the acetabular labrum that further worsens the acetabular overcoverage and premature rim impaction. Chondral damage in pincer-type FAI is generally less significant and limited to the peripheral acetabular rim.
Pincer-type FAI may be caused by acetabular retroversion, coxa profunda, or protrusio acetabuli. Our understanding of what defines a pincer morphology has evolved significantly. Through efforts to better define structural features of the acetabular rim that represent abnormalities, we have improved our understanding of how these features may influence OA development. One example of improved understanding involves coxa profunda, classically defined as the medial acetabular fossa touching or projecting medial to the ilioischial line on an AP pelvis radiograph. Several studies have found that this classic definition poorly describes the “overcovered” hip, as it is present in 70% of females and commonly present (41%) in the setting of acetabular dysplasia.18,19 Acetabular retroversion was previously associated with hip OA. Although central acetabular retroversion is relatively uncommon, cranial acetabular retroversion is more common. Presence of a crossover sign on AP pelvis radiographs generally has been viewed as indicative of acetabular retroversion. However, alterations in pelvic tilt on supine or standing AP pelvis radiographs can result in apparent retroversion in the setting of normal acetabular anatomy20 and potentially influence the development of impingement.21 Zaltz and colleagues22 found that abnormal morphology of the anterior inferior iliac spine can also lead to the presence of a crossover sign in an otherwise anteverted acetabulum. Larson and colleagues23 recently found that a crossover sign is present in 11% of asymptomatic hips (19% of males) and may be considered a normal variant. A crossover sign can also be present in the setting of posterior acetabular deficiency with normal anterior acetabular coverage. Ultimately, acetabular retroversion might indicate pincer-type FAI or dysplasia or be a normal variant that does not require treatment. Global acetabular overcoverage, including coxa protrusio, may be associated with OA in population-based studies but is not uniformly demonstrated in all studies.16,24,25 A lateral center edge angle of >40° and a Tönnis angle (acetabular inclination) of <0° are commonly viewed as markers of global overcoverage.
FAI Treatment
Improvements in hip arthroscopy techniques and instrumentation have led to hip arthroscopy becoming the primary surgical technique for the treatment of most cases of FAI. Hip arthroscopy allows for precise visualization and treatment of labral and chondral disease in the central compartment by traction. Larson and colleagues26 reported complication rates for hip arthroscopy in a prospective series of >1600 cases. The overall complication rate was 8.3%, with higher rates noted in female patients and in the setting of traction time longer than 60 minutes. Nonetheless, major complications occurred in 1.1%, with only 0.1% having persistent disability. The most common complications were lateral femoral cutaneous nerve dysesthesias (1.6%), pudendal nerve neuropraxia (1.4%), and iatrogenic labral/chondral damage (2.1%).
The importance of preserving the acetabular labrum is now well accepted from clinical and biomechanical evidence.27-29 As in previous studies in surgical hip dislocation,30 arthroscopic labral repair (vs débridement) results in improved clinical outcomes.31,32 Labral repair techniques currently focus on stable fixation of the labrum while maintaining the normal position of the labrum relative to the femoral head and avoiding labral eversion, which may compromise the hip suction seal. With continued technical advancements and biomechanical support, arthroscopic labral reconstruction is possible in the setting of labral deficiency, often resulting from prior resection. However, the optimal indications, surgical techniques, and long-term outcomes continue to be better defined. Open and arthroscopic techniques have shown similar ability to correct the typical mild to moderate cam morphology in FAI.33 Yet, inadequate femoral bony correction of FAI seems to be the most common cause for revision hip preservation surgery.9,10,17Mild to moderate acetabular rim deformities are commonly treated with hip arthroscopy. As our understanding of pincer-type FAI continues to improve, many surgeons are performing less- aggressive bone resection along the anterior rim. On the other hand, subspinous impingement was recently recognized as a form of extra-articular pincer FAI variant.34 Subspine decompression without true acetabular rim resection has become a more common treatment for pincer lesions and may be a consideration even with restricted range of motion after periacetabular osteotomy. Severe acetabular deformities with global overcoverage or acetabular protrusion are particularly challenging by arthroscopy, even for the most experienced surgeons. Although some improvement in deformity is feasible with arthroscopy, even cases reported in the literature have demonstrated incomplete deformity correction. Open surgical hip dislocation may continue to be the ideal treatment technique for severe pincer impingement.
Cam-type FAI is commonly treated with hip arthroscopy (Figures A-F).
Open surgical techniques will continue to have an important role in the treatment of severe and complex FAI deformities in which arthroscopic techniques do not consistently achieve adequate bony correction (Figures A-F). Surgical hip dislocation remains a powerful surgical technique for deformity correction in FAI. Sink and colleagues37 reported rates of complications after open surgical hip dislocation in the ANCHOR study group. In a cohort of 334 hips (302 patients), trochanteric nonunion occurred in 1.8% of cases, and there were no cases of avascular necrosis. Overall major complications were observed in 4.8% of cases, with 0.3% having chronic disability. Excellent outcomes, including high rates of return to sports, have been reported after surgical hip dislocation for FAI.38 Midterm studies from the early phase of surgical treatment of FAI have helped identify factors that may play a major role in optimizing patient outcomes.
Conclusion
Our understanding and treatment of FAI continue to evolve. Both open and arthroscopic techniques have demonstrated excellent outcomes in the treatment of FAI. Most cases of FAI are now amenable to arthroscopic treatment. Inadequate resection and underlying acetabular dysplasia remain common causes of treatment failure. Open surgical hip dislocation continues to play a role in the treatment of severe deformities that are poorly accessible by arthroscopy—including cam lesions with posterior extension, severe global acetabular overcoverage, or extra-articular impingement. The association of FAI with OA is most apparent for cam-type FAI. Future research will define the optimal treatment strategies and determine if they modify disease progression.
Am J Orthop. 2017;46(1):28-34. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
1. 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.
2. Smith-Petersen MN. The classic: treatment of malum coxae senilis, old slipped upper femoral epiphysis, intrapelvic protrusion of the acetabulum, and coxa plana by means of acetabuloplasty. 1936. Clin Orthop Relat Res. 2009;467(3):608-615.
3. Murray RO. The aetiology of primary osteoarthritis of the hip. Br J Radiol. 1965;38(455):810-824.
4. Solomon L. Patterns of osteoarthritis of the hip. J Bone Joint Surg Br. 1976;58(2):176-183.
5. Stulberg SD. Unrecognized childhood hip disease: a major cause of idiopathic osteoarthritis of the hip. In: Cordell LD, Harris WH, Ramsey PL, MacEwen GD, eds. The Hip: Proceedings of the Third Open Scientific Meeting of the Hip Society. St. Louis, MO: Mosby; 1975:212-228.
6. Myers SR, Eijer H, Ganz R. Anterior femoroacetabular impingement after periacetabular osteotomy. Clin Orthop Relat Res. 1999;(363):93-99.
7. Ganz R, Gill TJ, Gautier E, Ganz K, Krügel N, Berlemann U. Surgical dislocation of the adult hip: a technique with full access to the femoral head and acetabulum without the risk of avascular necrosis. J Bone Joint Surg Br. 2001;83(8):1119-1124.
8. Ross JR, Larson CM, Adeoye O, Kelly BT, Bedi A. Residual deformity is the most common reason for revision hip arthroscopy: a three-dimensional CT study. Clin Orthop Relat Res. 2015;473(4):1388-1395.
9. Clohisy JC, Nepple JJ, Larson CM, Zaltz I, Millis M; Academic Network of Conservation Hip Outcome Research (ANCHOR) Members. Persistent structural disease is the most common cause of repeat hip preservation surgery. Clin Orthop Relat Res. 2013;471(12):3788-3794.
10. Heyworth BE, Shindle MK, Voos JE, Rudzki JR, Kelly BT. Radiologic and intraoperative findings in revision hip arthroscopy. Arthroscopy. 2007;23(12):1295-1302.
11. Clohisy JC, Baca G, Beaulé PE, et al; ANCHOR Study Group. Descriptive epidemiology of femoroacetabular impingement: a North American cohort of patients undergoing surgery. Am J Sports Med. 2013;41(6):1348-1356.
12. Frank JM, Harris JD, Erickson BJ, et al. Prevalence of femoroacetabular impingement imaging findings in asymptomatic volunteers: a systematic review. Arthroscopy. 2015;31(6):1199-11204.
13. Siebenrock KA, Ferner F, Noble PC, Santore RF, Werlen S, Mamisch TC. The cam-type deformity of the proximal femur arises in childhood in response to vigorous sporting activity. Clin Orthop Relat Res. 2011;469(11):3229-3240.
14. Nepple JJ, Vigdorchik JM, Clohisy JC. What is the association between sports participation and the development of proximal femoral cam deformity? A systematic review and meta-analysis. Am J Sports Med. 2015;43(11):2833-2840.
15. Agricola R, Waarsing JH, Arden NK, et al. Cam impingement of the hip: a risk factor for hip osteoarthritis. Nat Rev Rheumatol. 2013;9(10):630-634.
16. Thomas GE, Palmer AJ, Batra RN, et al. Subclinical deformities of the hip are significant predictors of radiographic osteoarthritis and joint replacement in women. A 20 year longitudinal cohort study. Osteoarthritis Cartilage. 2014;22(10):1504-1510.
17. Philippon MJ, Schenker ML, Briggs KK, Kuppersmith DA, Maxwell RB, Stubbs AJ. Revision hip arthroscopy. Am J Sports Med. 2007;35(11):1918-1921.
18. 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.
19. Anderson LA, Kapron AL, Aoki SK, Peters CL. Coxa profunda: is the deep acetabulum overcovered? Clin Orthop Relat Res. 2012;470(12):3375-3382.
20. 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.
21. Ross JR, Nepple JJ, Philippon MJ, Kelly BT, Larson CM, Bedi A. Effect of changes in pelvic tilt on range of motion to impingement and radiographic parameters of acetabular morphologic characteristics. Am J Sports Med. 2014;42(10):2402-2409.
22. Zaltz I, Kelly BT, Hetsroni I, Bedi A. The crossover sign overestimates acetabular retroversion. Clin Orthop Relat Res. 2013;471(8):2463-2470.
23. Larson CM, Moreau-Gaudry A, Kelly BT, et al. Are normal hips being labeled as pathologic? A CT-based method for defining normal acetabular coverage. Clin Orthop Relat Res. 2015;473(4):1247-1254.
24. Gosvig KK, Jacobsen S, Sonne-Holm S, Palm H, Troelsen A. Prevalence of malformations of the hip joint and their relationship to sex, groin pain, and risk of osteoarthritis: a population-based survey. J Bone Joint Surg Am. 2010;92(5):1162-1169.
25. Agricola R, Heijboer MP, Roze RH, et al. Pincer deformity does not lead to osteoarthritis of the hip whereas acetabular dysplasia does: acetabular coverage and development of osteoarthritis in a nationwide prospective cohort study (CHECK). Osteoarthritis Cartilage. 2013;21(10):1514-1521.
26. Larson CM, Clohisy JC, Beaulé PE, et al; ANCHOR Study Group. Intraoperative and early postoperative complications after hip arthroscopic surgery: a prospective multicenter trial utilizing a validated grading scheme. Am J Sports Med. 2016;44(9):2292-2298.
27. Ferguson SJ, Bryant JT, Ganz R, Ito K. An in vitro investigation of the acetabular labral seal in hip joint mechanics. J Biomech. 2003;36(2):171-178.
28. Nepple JJ, Philippon MJ, Campbell KJ, et al. The hip fluid seal—part II: the effect of an acetabular labral tear, repair, resection, and reconstruction on hip stability to distraction. Knee Surg Sports Traumatol Arthrosc. 2014;22(4):730-736.
29. 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.
30. Espinosa N, Rothenfluh DA, Beck M, Ganz R, Leunig M. Treatment of femoro-acetabular impingement: preliminary results of labral refixation. J Bone Joint Surg Am. 2006;88(5):925-935.
31. Krych AJ, Thompson M, Knutson Z, Scoon J, Coleman SH. Arthroscopic labral repair versus selective labral debridement in female patients with femoroacetabular impingement: a prospective randomized study. Arthroscopy. 2013;29(1):46-53.
32. Larson CM, Giveans MR. Arthroscopic debridement versus refixation of the acetabular labrum associated with femoroacetabular impingement. Arthroscopy. 2009;25(4):369-376.
33. Bedi A, Zaltz I, De La Torre K, Kelly BT. Radiographic comparison of surgical hip dislocation and hip arthroscopy for treatment of cam deformity in femoroacetabular impingement. Am J Sports Med. 2011;39(suppl):20S–28S.
34. Larson CM, Kelly BT, Stone RM. Making a case for anterior inferior iliac spine/subspine hip impingement: three representative case reports and proposed concept. Arthroscopy. 2011;27(12):1732-1737.
35. Ross JR, Bedi A, Stone RM, et al. Intraoperative fluoroscopic imaging to treat cam deformities: correlation with 3-dimensional computed tomography [published correction appears in Am J Sports Med. 2015;43(8):NP27]. Am J Sports Med. 2014;42(6):1370-1376.
36. Fabricant PD, Fields KG, Taylor SA, Magennis E, Bedi A, Kelly BT. The effect of femoral and acetabular version on clinical outcomes after arthroscopic femoroacetabular impingement surgery. J Bone Joint Surg Am. 2015;97(7):537-543.
37. Sink EL, Beaulé PE, Sucato D, et al. Multicenter study of complications following surgical dislocation of the hip. J Bone Joint Surg Am. 2011;93(12):1132-1136.
38. Naal FD, Miozzari HH, Wyss TF, Nötzli HP. Surgical hip dislocation for the treatment of femoroacetabular impingement in high-level athletes. Am J Sports Med. 2011;39(3):544-550.
1. 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.
2. Smith-Petersen MN. The classic: treatment of malum coxae senilis, old slipped upper femoral epiphysis, intrapelvic protrusion of the acetabulum, and coxa plana by means of acetabuloplasty. 1936. Clin Orthop Relat Res. 2009;467(3):608-615.
3. Murray RO. The aetiology of primary osteoarthritis of the hip. Br J Radiol. 1965;38(455):810-824.
4. Solomon L. Patterns of osteoarthritis of the hip. J Bone Joint Surg Br. 1976;58(2):176-183.
5. Stulberg SD. Unrecognized childhood hip disease: a major cause of idiopathic osteoarthritis of the hip. In: Cordell LD, Harris WH, Ramsey PL, MacEwen GD, eds. The Hip: Proceedings of the Third Open Scientific Meeting of the Hip Society. St. Louis, MO: Mosby; 1975:212-228.
6. Myers SR, Eijer H, Ganz R. Anterior femoroacetabular impingement after periacetabular osteotomy. Clin Orthop Relat Res. 1999;(363):93-99.
7. Ganz R, Gill TJ, Gautier E, Ganz K, Krügel N, Berlemann U. Surgical dislocation of the adult hip: a technique with full access to the femoral head and acetabulum without the risk of avascular necrosis. J Bone Joint Surg Br. 2001;83(8):1119-1124.
8. Ross JR, Larson CM, Adeoye O, Kelly BT, Bedi A. Residual deformity is the most common reason for revision hip arthroscopy: a three-dimensional CT study. Clin Orthop Relat Res. 2015;473(4):1388-1395.
9. Clohisy JC, Nepple JJ, Larson CM, Zaltz I, Millis M; Academic Network of Conservation Hip Outcome Research (ANCHOR) Members. Persistent structural disease is the most common cause of repeat hip preservation surgery. Clin Orthop Relat Res. 2013;471(12):3788-3794.
10. Heyworth BE, Shindle MK, Voos JE, Rudzki JR, Kelly BT. Radiologic and intraoperative findings in revision hip arthroscopy. Arthroscopy. 2007;23(12):1295-1302.
11. Clohisy JC, Baca G, Beaulé PE, et al; ANCHOR Study Group. Descriptive epidemiology of femoroacetabular impingement: a North American cohort of patients undergoing surgery. Am J Sports Med. 2013;41(6):1348-1356.
12. Frank JM, Harris JD, Erickson BJ, et al. Prevalence of femoroacetabular impingement imaging findings in asymptomatic volunteers: a systematic review. Arthroscopy. 2015;31(6):1199-11204.
13. Siebenrock KA, Ferner F, Noble PC, Santore RF, Werlen S, Mamisch TC. The cam-type deformity of the proximal femur arises in childhood in response to vigorous sporting activity. Clin Orthop Relat Res. 2011;469(11):3229-3240.
14. Nepple JJ, Vigdorchik JM, Clohisy JC. What is the association between sports participation and the development of proximal femoral cam deformity? A systematic review and meta-analysis. Am J Sports Med. 2015;43(11):2833-2840.
15. Agricola R, Waarsing JH, Arden NK, et al. Cam impingement of the hip: a risk factor for hip osteoarthritis. Nat Rev Rheumatol. 2013;9(10):630-634.
16. Thomas GE, Palmer AJ, Batra RN, et al. Subclinical deformities of the hip are significant predictors of radiographic osteoarthritis and joint replacement in women. A 20 year longitudinal cohort study. Osteoarthritis Cartilage. 2014;22(10):1504-1510.
17. Philippon MJ, Schenker ML, Briggs KK, Kuppersmith DA, Maxwell RB, Stubbs AJ. Revision hip arthroscopy. Am J Sports Med. 2007;35(11):1918-1921.
18. 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.
19. Anderson LA, Kapron AL, Aoki SK, Peters CL. Coxa profunda: is the deep acetabulum overcovered? Clin Orthop Relat Res. 2012;470(12):3375-3382.
20. 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.
21. Ross JR, Nepple JJ, Philippon MJ, Kelly BT, Larson CM, Bedi A. Effect of changes in pelvic tilt on range of motion to impingement and radiographic parameters of acetabular morphologic characteristics. Am J Sports Med. 2014;42(10):2402-2409.
22. Zaltz I, Kelly BT, Hetsroni I, Bedi A. The crossover sign overestimates acetabular retroversion. Clin Orthop Relat Res. 2013;471(8):2463-2470.
23. Larson CM, Moreau-Gaudry A, Kelly BT, et al. Are normal hips being labeled as pathologic? A CT-based method for defining normal acetabular coverage. Clin Orthop Relat Res. 2015;473(4):1247-1254.
24. Gosvig KK, Jacobsen S, Sonne-Holm S, Palm H, Troelsen A. Prevalence of malformations of the hip joint and their relationship to sex, groin pain, and risk of osteoarthritis: a population-based survey. J Bone Joint Surg Am. 2010;92(5):1162-1169.
25. Agricola R, Heijboer MP, Roze RH, et al. Pincer deformity does not lead to osteoarthritis of the hip whereas acetabular dysplasia does: acetabular coverage and development of osteoarthritis in a nationwide prospective cohort study (CHECK). Osteoarthritis Cartilage. 2013;21(10):1514-1521.
26. Larson CM, Clohisy JC, Beaulé PE, et al; ANCHOR Study Group. Intraoperative and early postoperative complications after hip arthroscopic surgery: a prospective multicenter trial utilizing a validated grading scheme. Am J Sports Med. 2016;44(9):2292-2298.
27. Ferguson SJ, Bryant JT, Ganz R, Ito K. An in vitro investigation of the acetabular labral seal in hip joint mechanics. J Biomech. 2003;36(2):171-178.
28. Nepple JJ, Philippon MJ, Campbell KJ, et al. The hip fluid seal—part II: the effect of an acetabular labral tear, repair, resection, and reconstruction on hip stability to distraction. Knee Surg Sports Traumatol Arthrosc. 2014;22(4):730-736.
29. 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.
30. Espinosa N, Rothenfluh DA, Beck M, Ganz R, Leunig M. Treatment of femoro-acetabular impingement: preliminary results of labral refixation. J Bone Joint Surg Am. 2006;88(5):925-935.
31. Krych AJ, Thompson M, Knutson Z, Scoon J, Coleman SH. Arthroscopic labral repair versus selective labral debridement in female patients with femoroacetabular impingement: a prospective randomized study. Arthroscopy. 2013;29(1):46-53.
32. Larson CM, Giveans MR. Arthroscopic debridement versus refixation of the acetabular labrum associated with femoroacetabular impingement. Arthroscopy. 2009;25(4):369-376.
33. Bedi A, Zaltz I, De La Torre K, Kelly BT. Radiographic comparison of surgical hip dislocation and hip arthroscopy for treatment of cam deformity in femoroacetabular impingement. Am J Sports Med. 2011;39(suppl):20S–28S.
34. Larson CM, Kelly BT, Stone RM. Making a case for anterior inferior iliac spine/subspine hip impingement: three representative case reports and proposed concept. Arthroscopy. 2011;27(12):1732-1737.
35. Ross JR, Bedi A, Stone RM, et al. Intraoperative fluoroscopic imaging to treat cam deformities: correlation with 3-dimensional computed tomography [published correction appears in Am J Sports Med. 2015;43(8):NP27]. Am J Sports Med. 2014;42(6):1370-1376.
36. Fabricant PD, Fields KG, Taylor SA, Magennis E, Bedi A, Kelly BT. The effect of femoral and acetabular version on clinical outcomes after arthroscopic femoroacetabular impingement surgery. J Bone Joint Surg Am. 2015;97(7):537-543.
37. Sink EL, Beaulé PE, Sucato D, et al. Multicenter study of complications following surgical dislocation of the hip. J Bone Joint Surg Am. 2011;93(12):1132-1136.
38. Naal FD, Miozzari HH, Wyss TF, Nötzli HP. Surgical hip dislocation for the treatment of femoroacetabular impingement in high-level athletes. Am J Sports Med. 2011;39(3):544-550.
Multicenter Outcomes After Hip Arthroscopy: Epidemiology (MASH Study Group). What Are We Seeing in the Office, and Who Are We Choosing to Treat?
Take-Home Points
- MASH is a multicenter arthroscopic study of the hip that features a large prospective database of 10 separate institutions in the United States.
- The mean patient demographic was age 34.6 years, BMI 25.9 kg/m2, 62.8% females, and 97% white.
- Most patients had anterior or groin pain, but 17.6% had lateral hip pain, 13.8% had posterior hip pain, and 2.9% had low back or sacral pain.
- Patients typically had pain for about 1 year that was worsened with athletic activity as well as sitting.
- The most common surgical procedures that were performed included labral surgery in 64.7%, femoroplasty in 49.9%, acetabuloplasty in 33.3%, and chondroplasty in 31.1%
Arthroscopic surgery of the hip has been growing over the past decade, with drastically increasing rates of arthroscopic hip procedures and increased education and interest in orthopedic trainees.1-3 The rise of this minimally invasive surgical technique may be attributed to expanding knowledge of surgical management of morphologic hip disorders as a means of hip preservation. Many arthroscopic techniques have been developed to treat intra-articular hip joint pathologies, including femoroacetabular impingement (FAI), labral tears, and cartilage damage.4-11 These hip pathologies are widely recognized as painful limitations to activities of daily living and sports as well as early indicators of hip osteoarthritis.12,13 Limited evidence suggests that arthroscopic treatment of these intra-articular hip joint pathologies preserves the hip from osteoarthritis and progression to total hip arthroplasty.13-15
FAI is the most common etiology of pathologies related to arthroscopic surgery of the hip, including both labral tears and cartilage damage.4,7,14 FAI is a morphologic bone disorder characterized by impingement of the femur and the acetabulum on flexion or rotation. The etiology of FAI is not completely understood, but evidence suggests that stress to the proximal femoral physis during skeletal growth increases the risk of developing femoral head and neck deformations leading to cam-type FAI.15-17 Understanding the characteristics of the patient population in which FAI occurs may shed light on the processes of intra-articular damage, such as labral tears and cartilage damage.
In the present study, we collected epidemiologic data, including demographics, pathologic entities treated, patient-reported measures of disease, and surgical treatment preferences, on a hip pathology population that elected to undergo arthroscopic surgery. These data are important in gaining a better understanding of the population and environment in which hip arthroscopy is performed across multiple centers throughout the United States and may help guide clinical practice and research to advance hip arthroscopy.
Methods
The Multicenter Arthroscopic Study of the Hip (MASH) Study Group conducts multicenter clinical studies in arthroscopic hip preservation surgery. Patients are enrolled in this large prospective longitudinal study at 10 sites nationwide by 10 fellowship-trained hip arthroscopists. Institutional Review Board approval was obtained from all institutions before patient enrollment. After enrollment, we collected comprehensive patient data, including demographics, common symptoms and their duration, provocative activities, patient-reported outcome measures (modified Harris Hip Score, International Hip Outcome Tool, 12-item Short Form Health Survey, visual analog scale pain rating, Hip Outcome Score), physical examination findings, imaging findings, diagnoses, surgical findings, and surgical procedures.
All study participants were patients undergoing arthroscopic hip surgery by one of the members of the MASH Study Group. Patients with incomplete preoperative information (needed for data analysis) were excluded. Data analysis was performed with SPSS Statistics Version 21.0 (SPSS Inc.) to obtain descriptive statistics of the quantitative data and frequencies of the nominal data.
Results
Between January 2014 and November 2016, we enrolled 1738 patients (647 male, 1091 female) in the study. Table 1 lists the demographics of the population.
Regarding symptom location, 40.9% of patients described pain in the groin region, 24.2% in the anterior hip region, and 11.3% in a C-sign distribution (Table 2).
Table 3 lists the results of the patient-reported outcome measures.
Of the 1738 patients enrolled, 424 (24.4%) had prior surgery related to current symptoms, 252 (14.5%) had 1 previous surgery, 120 (6.9%) had 2 previous surgeries, and 52 (3%) had 3 previous surgeries. Twenty-six patients (1.5%) had a previous revision hip arthroscopy on the ipsilateral side, and 14 (0.8%) had a previous hip arthroscopy on the contralateral side. Before surgery, 80% of patients received an intra-articular injection of corticosteroid and lidocaine. The peritrochanteric region was injected in 11.5% of patients and the psoas bursa in 2.2% (Table 4).
Of the 1011 patients who had magnetic resonance imaging (MRI) performed, 943 (93.3%) had abnormal acetabular labrum findings, and 163 (17.1%) had acetabular articular damage. According to radiographic evaluation, 953 patients had abnormal hip joint morphology consistent with FAI. Figure 3 shows the FAI classification percentages.
On clinical examination, 1079 patients (62.1%) had a positive anterior impingement sign. The subspine impingement sign was positive in 447 patients (25.7%), and the trochanteric pain sign was positive in 400 (23%). Table 5 lists range-of-motion values for flexion and hip rotation from 90° of flexion.
As seen in Table 6, labral pathology was the most common diagnosis (1426/1738 patients, 82%).
As seen in Table 7, the most common procedure was femoroplasty (867/1738, 49.9%).
Discussion
In this study, we collected epidemiologic data (demographics, pathologic entities treated, patient-reported measures of disease, surgical treatment preferences) from a large multicenter population of hip pathology patients who elected to undergo arthroscopic surgery. Our results showed these patients were most commonly younger to middle-aged white females with pain primarily in the groin region. Most had pain for at least 1 year, and it was commonly exacerbated by sitting and athletics. Patients reported clinically significant pain and functional limitation, which showed evidence of affecting general physical and mental health. It was not uncommon for patients to have undergone another, related surgery and nonoperative treatments, including intra-articular injection and/or physical therapy, before surgery. There was a high incidence of abnormal hip morphology suggestive of a cam lesion, but the incidence of arthritic changes on radiographs was relatively low. Labral tear was the most common diagnosis, and most often it was addressed with repair. Many patients underwent femoroplasty, acetabuloplasty, and chondroplasty in addition to labral repair.
According to patient-reported outcome measures administered before surgery, 40% to 65% of patients seeking hip preservation surgery reported functional deficits and pain—which falls within the range of results from other multicenter studies on the epidemiology of FAI.18,19 There was, however, a high amount of variability in individual scores on the functional and pain measures; some patients rated their functional ability very high. These findings were supported by the general health forms measuring global physical and mental health. Mean Physical Health and Mental Health scores on the 12-item Short Form Health Survey indicated that patients seeking hip preservation surgery thought their hip condition affected their general well-being. This finding is consistent with research on FAI,18 hip arthritis,20 and total hip arthroplasty.19Our results further showed that hip arthroscopists commonly prescribed alternative treatment measures ahead of surgery. Before elective surgery, 80% of patients received an intra-articular injection, underwent physical therapy, or both. This could suggest a high failure rate for patients who chose conservative treatment approaches for hip-related pathology. However, our study was limited in that it may have included patients who had improved significantly with conservative measures and decided to forgo arthroscopic hip surgery. Although conservative treatment often is recommended in an effort to potentially avoid surgery, there is a lack of research evaluating the efficacy of nonoperative care.21,22Analysis of diagnostic imaging and clinical examination findings revealed some unique characteristics of patients undergoing elective hip preservation surgery. MRI showed labral pathology in an overwhelming majority of these patients, but few had evidence of articular damage. Previous research has found a 67% rate of arthritic changes on diagnostic imaging, but our rate was much lower (17%).23 Radiograph evaluation confirmed the pattern: More than 90% of our patients had Tönnis grade 0 osteoarthritis. Tönnis grade 1 or 2 osteoarthritis is a predictor of acetabular cartilage degeneration,23 and long-term studies have related these osteoarthritic changes to poorer hip arthroscopy outcomes.24 Thus, the lower incidence of osteoarthritis in our study population may reflect current evidence-based practice and a contemporary approach to patient selection.
Most of our patients had isolated cam-type FAI as opposed to pincer-type FAI or a combination of cam and pincer—contrary to research findings that combination cam–pincer FAI is most prevalent.25,26 Our results are more consistent with more recent research findings of a higher incidence of isolated cam lesion, particularly in female patients, and combination cam–pincer in male patients.18,27,28 Similar distributions of surgical procedures and diagnoses exist between the present study and other multicenter evaluations of the epidemiologic characteristics of patients with hip pathology.18Our study had several limitations. First, the population consisted entirely of patients who sought evaluation by a hip arthroscopy specialist and underwent elective surgery. Therefore, the data cannot be applied to a more general orthopedic population or to patients who consult other medical specialists. Second, the population, which was 97% white and had small percentages of African-American, Latino, and Asian patients, lacked ethnic diversity. This finding is consistent with recent epidemiologic research in which ethnicity was identified as a factor in patterns of hip disease.13,29,30 Access to specialists, however, was likely affected by multiple other factors. Fourth, the validity and the reliability of the imaging modalities used have been questioned.31-33 There is controversy regarding ideal imaging modalities for assessment of articular cartilage damage31,32 and FAI. However, the modalities that we used to determine diagnoses in this study are well supported26 and represent common practice patterns.
Am J Orthop. 2017;46(1):35-41. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
1. Cvetanovich GL, Chalmers PN, Levy DM, et al. Hip arthroscopy surgical volume trends and 30-day postoperative complications. Arthroscopy. 2016;32(7):1286-1292.
2. Peters CL, Aoki SK, Erickson JA, Anderson LA, Anderson AE. Early experience with a comprehensive hip preservation service intended to improve clinical care, education, and academic productivity. Clin Orthop Relat Res. 2012;470(12):3446-3452.
3. Siebenrock KA, Peters CL. ABJS Carl T. Brighton workshop on hip preservation surgery: editorial comment. Clin Orthop Relat Res. 2012;470(12):3281-3283.
4. Parvizi J, Leunig M, Ganz R. Femoroacetabular impingement. J Am Acad Orthop Surg. 2007;15(9):561-570.
5. Poh SY, Hube R, Dienst M. Arthroscopic treatment of femoroacetabular pincer impingement. Oper Orthop Traumatol. 2015;27(6):536-552.
6. Javed A, O’Donnell JM. Arthroscopic femoral osteochondroplasty for cam femoroacetabular impingement in patients over 60 years of age. J Bone Joint Surg Br. 2011;93(3):326-331.
7. Groh MM, Herrera J. A comprehensive review of hip labral tears. Curr Rev Musculoskelet Med. 2009;2(2):105-117.
8. 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.
9. White BJ, Herzog MM. Labral reconstruction: when to perform and how. Front Surg. 2015;2:27.
10. Yen YM, Kocher MS. Chondral lesions of the hip: microfracture and chondroplasty. Sports Med Arthrosc. 2010;18(2):83-89.
11. Jordan MA, Van Thiel GS, Chahal J, Nho SJ. Operative treatment of chondral defects in the hip joint: a systematic review. Curr Rev Musculoskelet Med. 2012;5(3):244-253.
12. Griffin DW, Kinnard MJ, Formby PM, McCabe MP, Anderson TD. Outcomes of hip arthroscopy in the older adult: a systematic review of the literature [published online October 18, 2016]. Am J Sports Med. doi:10.1177/0363546516667915.
13. Ganz R, Leunig M, Leunig-Ganz K, Harris WH. The etiology of osteoarthritis of the hip. Clin Orthop Relat Res. 2008;466(2):264-272.
14. Kaya M, Suzuki T, Emori M, Yamashita T. Hip morphology influences the pattern of articular cartilage damage. Knee Surg Sports Traumatol Arthrosc. 2016;24(6):2016-2023.
15. Beck M, Leunig M, Parvizi J, Boutier V, Wyss D, Ganz R. Anterior femoroacetabular impingement: part II. Midterm results of surgical treatment. Clin Orthop Relat Res. 2004;(418):67-73.
16. Byrd JT. Hip arthroscopy in athletes. Oper Tech Sports Med. 2005;13(1):24-36.
17. Werner BC, Gaudiani MA, Ranawat AS. The etiology and arthroscopic surgical management of cam lesions. Clin Sports Med. 2016;35(3):391-404.
18. Clohisy JC, Baca G, Beaulé PE, et al; ANCHOR Study Group. Descriptive epidemiology of femoroacetabular impingement: a North American cohort of patients undergoing surgery. Am J Sports Med. 2013;41(6):1348-1356.
19. Shia DS, Clohisy JC, Schinsky MF, Martell JM, Maloney WJ. THA with highly cross-linked polyethylene in patients 50 years or younger. Clin Orthop Relat Res. 2009;467(8):2059-2065.
20. Gandhi SK, Salmon JW, Zhao SZ, Lambert BL, Gore PR, Conrad K. Psychometric evaluation of the 12-item Short-Form Health Survey (SF-12) in osteoarthritis and rheumatoid arthritis clinical trials. Clin Ther. 2001;23(7):1080-1098.
21. Loudon JK, Reiman MP. Conservative management of femoroacetabular impingement (FAI) in the long distance runner. Phys Ther Sport. 2014;15(2):82-90.
22. Wall PD, Fernandez M, Griffin DR, Foster NE. Nonoperative treatment for femoroacetabular impingement: a systematic review of the literature. PM R. 2013;5(5):418-426.
23. 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.
24. McCormick F, Nwachukwu BU, Alpaugh K, Martin SD. Predictors of hip arthroscopy outcomes for labral tears at minimum 2-year follow-up: the influence of age and arthritis. Arthroscopy. 2012;28(10):1359-1364.
25. Beck M, Kalhor M, Leunig M, Ganz R. Hip morphology influences the pattern of damage to the acetabular cartilage: femoroacetabular impingement as a cause of early osteoarthritis of the hip. J Bone Joint Surg Br. 2005;87(7):1012-1018.
26. Tannast M, Siebenrock KA, Anderson SE. Femoroacetabular impingement: radiographic diagnosis—what the radiologist should know. AJR Am J Roentgenol. 2007;188(6):1540-1552.
27. Kapron AL, Peters CL, Aoki SK, et al. The prevalence of radiographic findings of structural hip deformities in female collegiate athletes. Am J Sports Med. 2015;43(6):1324-1330.
28. Lee WY, Kang C, Hwang DS, Jeon JH, Zheng L. Descriptive epidemiology of symptomatic femoroacetabular impingement in young athlete: single center study. Hip Pelvis. 2016;28(1):29-34.
29. Dudda M, Kim YJ, Zhang Y, et al. Morphologic differences between the hips of Chinese women and white women: could they account for the ethnic difference in the prevalence of hip osteoarthritis? Arthritis Rheum. 2011;63(10):2992-2999.
30. Solomon L, Beighton P. Osteoarthrosis of the hip and its relationship to pre-existing in an African population. J Bone Joint Surg Br. 1973;55(1):216-217.
31. Keeney JA, Peelle MW, Jackson J, Rubin D, Maloney WJ, Clohisy JC. Magnetic resonance arthrography versus arthroscopy in the evaluation of articular hip pathology. Clin Orthop Relat Res. 2004;(429):163-169.
32. Schmid MR, Nötzli HP, Zanetti M, Wyss TF, Hodler J. Cartilage lesions in the hip: diagnostic effectiveness of MR arthrography. Radiology. 2003;226(2):382-386.
33. Chevillotte CJ, Ali MH, Trousdale RT, Pagnano MW. Variability in hip range of motion on clinical examination. J Arthroplasty. 2009;24(5):693-697.
Take-Home Points
- MASH is a multicenter arthroscopic study of the hip that features a large prospective database of 10 separate institutions in the United States.
- The mean patient demographic was age 34.6 years, BMI 25.9 kg/m2, 62.8% females, and 97% white.
- Most patients had anterior or groin pain, but 17.6% had lateral hip pain, 13.8% had posterior hip pain, and 2.9% had low back or sacral pain.
- Patients typically had pain for about 1 year that was worsened with athletic activity as well as sitting.
- The most common surgical procedures that were performed included labral surgery in 64.7%, femoroplasty in 49.9%, acetabuloplasty in 33.3%, and chondroplasty in 31.1%
Arthroscopic surgery of the hip has been growing over the past decade, with drastically increasing rates of arthroscopic hip procedures and increased education and interest in orthopedic trainees.1-3 The rise of this minimally invasive surgical technique may be attributed to expanding knowledge of surgical management of morphologic hip disorders as a means of hip preservation. Many arthroscopic techniques have been developed to treat intra-articular hip joint pathologies, including femoroacetabular impingement (FAI), labral tears, and cartilage damage.4-11 These hip pathologies are widely recognized as painful limitations to activities of daily living and sports as well as early indicators of hip osteoarthritis.12,13 Limited evidence suggests that arthroscopic treatment of these intra-articular hip joint pathologies preserves the hip from osteoarthritis and progression to total hip arthroplasty.13-15
FAI is the most common etiology of pathologies related to arthroscopic surgery of the hip, including both labral tears and cartilage damage.4,7,14 FAI is a morphologic bone disorder characterized by impingement of the femur and the acetabulum on flexion or rotation. The etiology of FAI is not completely understood, but evidence suggests that stress to the proximal femoral physis during skeletal growth increases the risk of developing femoral head and neck deformations leading to cam-type FAI.15-17 Understanding the characteristics of the patient population in which FAI occurs may shed light on the processes of intra-articular damage, such as labral tears and cartilage damage.
In the present study, we collected epidemiologic data, including demographics, pathologic entities treated, patient-reported measures of disease, and surgical treatment preferences, on a hip pathology population that elected to undergo arthroscopic surgery. These data are important in gaining a better understanding of the population and environment in which hip arthroscopy is performed across multiple centers throughout the United States and may help guide clinical practice and research to advance hip arthroscopy.
Methods
The Multicenter Arthroscopic Study of the Hip (MASH) Study Group conducts multicenter clinical studies in arthroscopic hip preservation surgery. Patients are enrolled in this large prospective longitudinal study at 10 sites nationwide by 10 fellowship-trained hip arthroscopists. Institutional Review Board approval was obtained from all institutions before patient enrollment. After enrollment, we collected comprehensive patient data, including demographics, common symptoms and their duration, provocative activities, patient-reported outcome measures (modified Harris Hip Score, International Hip Outcome Tool, 12-item Short Form Health Survey, visual analog scale pain rating, Hip Outcome Score), physical examination findings, imaging findings, diagnoses, surgical findings, and surgical procedures.
All study participants were patients undergoing arthroscopic hip surgery by one of the members of the MASH Study Group. Patients with incomplete preoperative information (needed for data analysis) were excluded. Data analysis was performed with SPSS Statistics Version 21.0 (SPSS Inc.) to obtain descriptive statistics of the quantitative data and frequencies of the nominal data.
Results
Between January 2014 and November 2016, we enrolled 1738 patients (647 male, 1091 female) in the study. Table 1 lists the demographics of the population.
Regarding symptom location, 40.9% of patients described pain in the groin region, 24.2% in the anterior hip region, and 11.3% in a C-sign distribution (Table 2).
Table 3 lists the results of the patient-reported outcome measures.
Of the 1738 patients enrolled, 424 (24.4%) had prior surgery related to current symptoms, 252 (14.5%) had 1 previous surgery, 120 (6.9%) had 2 previous surgeries, and 52 (3%) had 3 previous surgeries. Twenty-six patients (1.5%) had a previous revision hip arthroscopy on the ipsilateral side, and 14 (0.8%) had a previous hip arthroscopy on the contralateral side. Before surgery, 80% of patients received an intra-articular injection of corticosteroid and lidocaine. The peritrochanteric region was injected in 11.5% of patients and the psoas bursa in 2.2% (Table 4).
Of the 1011 patients who had magnetic resonance imaging (MRI) performed, 943 (93.3%) had abnormal acetabular labrum findings, and 163 (17.1%) had acetabular articular damage. According to radiographic evaluation, 953 patients had abnormal hip joint morphology consistent with FAI. Figure 3 shows the FAI classification percentages.
On clinical examination, 1079 patients (62.1%) had a positive anterior impingement sign. The subspine impingement sign was positive in 447 patients (25.7%), and the trochanteric pain sign was positive in 400 (23%). Table 5 lists range-of-motion values for flexion and hip rotation from 90° of flexion.
As seen in Table 6, labral pathology was the most common diagnosis (1426/1738 patients, 82%).
As seen in Table 7, the most common procedure was femoroplasty (867/1738, 49.9%).
Discussion
In this study, we collected epidemiologic data (demographics, pathologic entities treated, patient-reported measures of disease, surgical treatment preferences) from a large multicenter population of hip pathology patients who elected to undergo arthroscopic surgery. Our results showed these patients were most commonly younger to middle-aged white females with pain primarily in the groin region. Most had pain for at least 1 year, and it was commonly exacerbated by sitting and athletics. Patients reported clinically significant pain and functional limitation, which showed evidence of affecting general physical and mental health. It was not uncommon for patients to have undergone another, related surgery and nonoperative treatments, including intra-articular injection and/or physical therapy, before surgery. There was a high incidence of abnormal hip morphology suggestive of a cam lesion, but the incidence of arthritic changes on radiographs was relatively low. Labral tear was the most common diagnosis, and most often it was addressed with repair. Many patients underwent femoroplasty, acetabuloplasty, and chondroplasty in addition to labral repair.
According to patient-reported outcome measures administered before surgery, 40% to 65% of patients seeking hip preservation surgery reported functional deficits and pain—which falls within the range of results from other multicenter studies on the epidemiology of FAI.18,19 There was, however, a high amount of variability in individual scores on the functional and pain measures; some patients rated their functional ability very high. These findings were supported by the general health forms measuring global physical and mental health. Mean Physical Health and Mental Health scores on the 12-item Short Form Health Survey indicated that patients seeking hip preservation surgery thought their hip condition affected their general well-being. This finding is consistent with research on FAI,18 hip arthritis,20 and total hip arthroplasty.19Our results further showed that hip arthroscopists commonly prescribed alternative treatment measures ahead of surgery. Before elective surgery, 80% of patients received an intra-articular injection, underwent physical therapy, or both. This could suggest a high failure rate for patients who chose conservative treatment approaches for hip-related pathology. However, our study was limited in that it may have included patients who had improved significantly with conservative measures and decided to forgo arthroscopic hip surgery. Although conservative treatment often is recommended in an effort to potentially avoid surgery, there is a lack of research evaluating the efficacy of nonoperative care.21,22Analysis of diagnostic imaging and clinical examination findings revealed some unique characteristics of patients undergoing elective hip preservation surgery. MRI showed labral pathology in an overwhelming majority of these patients, but few had evidence of articular damage. Previous research has found a 67% rate of arthritic changes on diagnostic imaging, but our rate was much lower (17%).23 Radiograph evaluation confirmed the pattern: More than 90% of our patients had Tönnis grade 0 osteoarthritis. Tönnis grade 1 or 2 osteoarthritis is a predictor of acetabular cartilage degeneration,23 and long-term studies have related these osteoarthritic changes to poorer hip arthroscopy outcomes.24 Thus, the lower incidence of osteoarthritis in our study population may reflect current evidence-based practice and a contemporary approach to patient selection.
Most of our patients had isolated cam-type FAI as opposed to pincer-type FAI or a combination of cam and pincer—contrary to research findings that combination cam–pincer FAI is most prevalent.25,26 Our results are more consistent with more recent research findings of a higher incidence of isolated cam lesion, particularly in female patients, and combination cam–pincer in male patients.18,27,28 Similar distributions of surgical procedures and diagnoses exist between the present study and other multicenter evaluations of the epidemiologic characteristics of patients with hip pathology.18Our study had several limitations. First, the population consisted entirely of patients who sought evaluation by a hip arthroscopy specialist and underwent elective surgery. Therefore, the data cannot be applied to a more general orthopedic population or to patients who consult other medical specialists. Second, the population, which was 97% white and had small percentages of African-American, Latino, and Asian patients, lacked ethnic diversity. This finding is consistent with recent epidemiologic research in which ethnicity was identified as a factor in patterns of hip disease.13,29,30 Access to specialists, however, was likely affected by multiple other factors. Fourth, the validity and the reliability of the imaging modalities used have been questioned.31-33 There is controversy regarding ideal imaging modalities for assessment of articular cartilage damage31,32 and FAI. However, the modalities that we used to determine diagnoses in this study are well supported26 and represent common practice patterns.
Am J Orthop. 2017;46(1):35-41. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
Take-Home Points
- MASH is a multicenter arthroscopic study of the hip that features a large prospective database of 10 separate institutions in the United States.
- The mean patient demographic was age 34.6 years, BMI 25.9 kg/m2, 62.8% females, and 97% white.
- Most patients had anterior or groin pain, but 17.6% had lateral hip pain, 13.8% had posterior hip pain, and 2.9% had low back or sacral pain.
- Patients typically had pain for about 1 year that was worsened with athletic activity as well as sitting.
- The most common surgical procedures that were performed included labral surgery in 64.7%, femoroplasty in 49.9%, acetabuloplasty in 33.3%, and chondroplasty in 31.1%
Arthroscopic surgery of the hip has been growing over the past decade, with drastically increasing rates of arthroscopic hip procedures and increased education and interest in orthopedic trainees.1-3 The rise of this minimally invasive surgical technique may be attributed to expanding knowledge of surgical management of morphologic hip disorders as a means of hip preservation. Many arthroscopic techniques have been developed to treat intra-articular hip joint pathologies, including femoroacetabular impingement (FAI), labral tears, and cartilage damage.4-11 These hip pathologies are widely recognized as painful limitations to activities of daily living and sports as well as early indicators of hip osteoarthritis.12,13 Limited evidence suggests that arthroscopic treatment of these intra-articular hip joint pathologies preserves the hip from osteoarthritis and progression to total hip arthroplasty.13-15
FAI is the most common etiology of pathologies related to arthroscopic surgery of the hip, including both labral tears and cartilage damage.4,7,14 FAI is a morphologic bone disorder characterized by impingement of the femur and the acetabulum on flexion or rotation. The etiology of FAI is not completely understood, but evidence suggests that stress to the proximal femoral physis during skeletal growth increases the risk of developing femoral head and neck deformations leading to cam-type FAI.15-17 Understanding the characteristics of the patient population in which FAI occurs may shed light on the processes of intra-articular damage, such as labral tears and cartilage damage.
In the present study, we collected epidemiologic data, including demographics, pathologic entities treated, patient-reported measures of disease, and surgical treatment preferences, on a hip pathology population that elected to undergo arthroscopic surgery. These data are important in gaining a better understanding of the population and environment in which hip arthroscopy is performed across multiple centers throughout the United States and may help guide clinical practice and research to advance hip arthroscopy.
Methods
The Multicenter Arthroscopic Study of the Hip (MASH) Study Group conducts multicenter clinical studies in arthroscopic hip preservation surgery. Patients are enrolled in this large prospective longitudinal study at 10 sites nationwide by 10 fellowship-trained hip arthroscopists. Institutional Review Board approval was obtained from all institutions before patient enrollment. After enrollment, we collected comprehensive patient data, including demographics, common symptoms and their duration, provocative activities, patient-reported outcome measures (modified Harris Hip Score, International Hip Outcome Tool, 12-item Short Form Health Survey, visual analog scale pain rating, Hip Outcome Score), physical examination findings, imaging findings, diagnoses, surgical findings, and surgical procedures.
All study participants were patients undergoing arthroscopic hip surgery by one of the members of the MASH Study Group. Patients with incomplete preoperative information (needed for data analysis) were excluded. Data analysis was performed with SPSS Statistics Version 21.0 (SPSS Inc.) to obtain descriptive statistics of the quantitative data and frequencies of the nominal data.
Results
Between January 2014 and November 2016, we enrolled 1738 patients (647 male, 1091 female) in the study. Table 1 lists the demographics of the population.
Regarding symptom location, 40.9% of patients described pain in the groin region, 24.2% in the anterior hip region, and 11.3% in a C-sign distribution (Table 2).
Table 3 lists the results of the patient-reported outcome measures.
Of the 1738 patients enrolled, 424 (24.4%) had prior surgery related to current symptoms, 252 (14.5%) had 1 previous surgery, 120 (6.9%) had 2 previous surgeries, and 52 (3%) had 3 previous surgeries. Twenty-six patients (1.5%) had a previous revision hip arthroscopy on the ipsilateral side, and 14 (0.8%) had a previous hip arthroscopy on the contralateral side. Before surgery, 80% of patients received an intra-articular injection of corticosteroid and lidocaine. The peritrochanteric region was injected in 11.5% of patients and the psoas bursa in 2.2% (Table 4).
Of the 1011 patients who had magnetic resonance imaging (MRI) performed, 943 (93.3%) had abnormal acetabular labrum findings, and 163 (17.1%) had acetabular articular damage. According to radiographic evaluation, 953 patients had abnormal hip joint morphology consistent with FAI. Figure 3 shows the FAI classification percentages.
On clinical examination, 1079 patients (62.1%) had a positive anterior impingement sign. The subspine impingement sign was positive in 447 patients (25.7%), and the trochanteric pain sign was positive in 400 (23%). Table 5 lists range-of-motion values for flexion and hip rotation from 90° of flexion.
As seen in Table 6, labral pathology was the most common diagnosis (1426/1738 patients, 82%).
As seen in Table 7, the most common procedure was femoroplasty (867/1738, 49.9%).
Discussion
In this study, we collected epidemiologic data (demographics, pathologic entities treated, patient-reported measures of disease, surgical treatment preferences) from a large multicenter population of hip pathology patients who elected to undergo arthroscopic surgery. Our results showed these patients were most commonly younger to middle-aged white females with pain primarily in the groin region. Most had pain for at least 1 year, and it was commonly exacerbated by sitting and athletics. Patients reported clinically significant pain and functional limitation, which showed evidence of affecting general physical and mental health. It was not uncommon for patients to have undergone another, related surgery and nonoperative treatments, including intra-articular injection and/or physical therapy, before surgery. There was a high incidence of abnormal hip morphology suggestive of a cam lesion, but the incidence of arthritic changes on radiographs was relatively low. Labral tear was the most common diagnosis, and most often it was addressed with repair. Many patients underwent femoroplasty, acetabuloplasty, and chondroplasty in addition to labral repair.
According to patient-reported outcome measures administered before surgery, 40% to 65% of patients seeking hip preservation surgery reported functional deficits and pain—which falls within the range of results from other multicenter studies on the epidemiology of FAI.18,19 There was, however, a high amount of variability in individual scores on the functional and pain measures; some patients rated their functional ability very high. These findings were supported by the general health forms measuring global physical and mental health. Mean Physical Health and Mental Health scores on the 12-item Short Form Health Survey indicated that patients seeking hip preservation surgery thought their hip condition affected their general well-being. This finding is consistent with research on FAI,18 hip arthritis,20 and total hip arthroplasty.19Our results further showed that hip arthroscopists commonly prescribed alternative treatment measures ahead of surgery. Before elective surgery, 80% of patients received an intra-articular injection, underwent physical therapy, or both. This could suggest a high failure rate for patients who chose conservative treatment approaches for hip-related pathology. However, our study was limited in that it may have included patients who had improved significantly with conservative measures and decided to forgo arthroscopic hip surgery. Although conservative treatment often is recommended in an effort to potentially avoid surgery, there is a lack of research evaluating the efficacy of nonoperative care.21,22Analysis of diagnostic imaging and clinical examination findings revealed some unique characteristics of patients undergoing elective hip preservation surgery. MRI showed labral pathology in an overwhelming majority of these patients, but few had evidence of articular damage. Previous research has found a 67% rate of arthritic changes on diagnostic imaging, but our rate was much lower (17%).23 Radiograph evaluation confirmed the pattern: More than 90% of our patients had Tönnis grade 0 osteoarthritis. Tönnis grade 1 or 2 osteoarthritis is a predictor of acetabular cartilage degeneration,23 and long-term studies have related these osteoarthritic changes to poorer hip arthroscopy outcomes.24 Thus, the lower incidence of osteoarthritis in our study population may reflect current evidence-based practice and a contemporary approach to patient selection.
Most of our patients had isolated cam-type FAI as opposed to pincer-type FAI or a combination of cam and pincer—contrary to research findings that combination cam–pincer FAI is most prevalent.25,26 Our results are more consistent with more recent research findings of a higher incidence of isolated cam lesion, particularly in female patients, and combination cam–pincer in male patients.18,27,28 Similar distributions of surgical procedures and diagnoses exist between the present study and other multicenter evaluations of the epidemiologic characteristics of patients with hip pathology.18Our study had several limitations. First, the population consisted entirely of patients who sought evaluation by a hip arthroscopy specialist and underwent elective surgery. Therefore, the data cannot be applied to a more general orthopedic population or to patients who consult other medical specialists. Second, the population, which was 97% white and had small percentages of African-American, Latino, and Asian patients, lacked ethnic diversity. This finding is consistent with recent epidemiologic research in which ethnicity was identified as a factor in patterns of hip disease.13,29,30 Access to specialists, however, was likely affected by multiple other factors. Fourth, the validity and the reliability of the imaging modalities used have been questioned.31-33 There is controversy regarding ideal imaging modalities for assessment of articular cartilage damage31,32 and FAI. However, the modalities that we used to determine diagnoses in this study are well supported26 and represent common practice patterns.
Am J Orthop. 2017;46(1):35-41. Copyright Frontline Medical Communications Inc. 2017. All rights reserved.
1. Cvetanovich GL, Chalmers PN, Levy DM, et al. Hip arthroscopy surgical volume trends and 30-day postoperative complications. Arthroscopy. 2016;32(7):1286-1292.
2. Peters CL, Aoki SK, Erickson JA, Anderson LA, Anderson AE. Early experience with a comprehensive hip preservation service intended to improve clinical care, education, and academic productivity. Clin Orthop Relat Res. 2012;470(12):3446-3452.
3. Siebenrock KA, Peters CL. ABJS Carl T. Brighton workshop on hip preservation surgery: editorial comment. Clin Orthop Relat Res. 2012;470(12):3281-3283.
4. Parvizi J, Leunig M, Ganz R. Femoroacetabular impingement. J Am Acad Orthop Surg. 2007;15(9):561-570.
5. Poh SY, Hube R, Dienst M. Arthroscopic treatment of femoroacetabular pincer impingement. Oper Orthop Traumatol. 2015;27(6):536-552.
6. Javed A, O’Donnell JM. Arthroscopic femoral osteochondroplasty for cam femoroacetabular impingement in patients over 60 years of age. J Bone Joint Surg Br. 2011;93(3):326-331.
7. Groh MM, Herrera J. A comprehensive review of hip labral tears. Curr Rev Musculoskelet Med. 2009;2(2):105-117.
8. 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.
9. White BJ, Herzog MM. Labral reconstruction: when to perform and how. Front Surg. 2015;2:27.
10. Yen YM, Kocher MS. Chondral lesions of the hip: microfracture and chondroplasty. Sports Med Arthrosc. 2010;18(2):83-89.
11. Jordan MA, Van Thiel GS, Chahal J, Nho SJ. Operative treatment of chondral defects in the hip joint: a systematic review. Curr Rev Musculoskelet Med. 2012;5(3):244-253.
12. Griffin DW, Kinnard MJ, Formby PM, McCabe MP, Anderson TD. Outcomes of hip arthroscopy in the older adult: a systematic review of the literature [published online October 18, 2016]. Am J Sports Med. doi:10.1177/0363546516667915.
13. Ganz R, Leunig M, Leunig-Ganz K, Harris WH. The etiology of osteoarthritis of the hip. Clin Orthop Relat Res. 2008;466(2):264-272.
14. Kaya M, Suzuki T, Emori M, Yamashita T. Hip morphology influences the pattern of articular cartilage damage. Knee Surg Sports Traumatol Arthrosc. 2016;24(6):2016-2023.
15. Beck M, Leunig M, Parvizi J, Boutier V, Wyss D, Ganz R. Anterior femoroacetabular impingement: part II. Midterm results of surgical treatment. Clin Orthop Relat Res. 2004;(418):67-73.
16. Byrd JT. Hip arthroscopy in athletes. Oper Tech Sports Med. 2005;13(1):24-36.
17. Werner BC, Gaudiani MA, Ranawat AS. The etiology and arthroscopic surgical management of cam lesions. Clin Sports Med. 2016;35(3):391-404.
18. Clohisy JC, Baca G, Beaulé PE, et al; ANCHOR Study Group. Descriptive epidemiology of femoroacetabular impingement: a North American cohort of patients undergoing surgery. Am J Sports Med. 2013;41(6):1348-1356.
19. Shia DS, Clohisy JC, Schinsky MF, Martell JM, Maloney WJ. THA with highly cross-linked polyethylene in patients 50 years or younger. Clin Orthop Relat Res. 2009;467(8):2059-2065.
20. Gandhi SK, Salmon JW, Zhao SZ, Lambert BL, Gore PR, Conrad K. Psychometric evaluation of the 12-item Short-Form Health Survey (SF-12) in osteoarthritis and rheumatoid arthritis clinical trials. Clin Ther. 2001;23(7):1080-1098.
21. Loudon JK, Reiman MP. Conservative management of femoroacetabular impingement (FAI) in the long distance runner. Phys Ther Sport. 2014;15(2):82-90.
22. Wall PD, Fernandez M, Griffin DR, Foster NE. Nonoperative treatment for femoroacetabular impingement: a systematic review of the literature. PM R. 2013;5(5):418-426.
23. 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.
24. McCormick F, Nwachukwu BU, Alpaugh K, Martin SD. Predictors of hip arthroscopy outcomes for labral tears at minimum 2-year follow-up: the influence of age and arthritis. Arthroscopy. 2012;28(10):1359-1364.
25. Beck M, Kalhor M, Leunig M, Ganz R. Hip morphology influences the pattern of damage to the acetabular cartilage: femoroacetabular impingement as a cause of early osteoarthritis of the hip. J Bone Joint Surg Br. 2005;87(7):1012-1018.
26. Tannast M, Siebenrock KA, Anderson SE. Femoroacetabular impingement: radiographic diagnosis—what the radiologist should know. AJR Am J Roentgenol. 2007;188(6):1540-1552.
27. Kapron AL, Peters CL, Aoki SK, et al. The prevalence of radiographic findings of structural hip deformities in female collegiate athletes. Am J Sports Med. 2015;43(6):1324-1330.
28. Lee WY, Kang C, Hwang DS, Jeon JH, Zheng L. Descriptive epidemiology of symptomatic femoroacetabular impingement in young athlete: single center study. Hip Pelvis. 2016;28(1):29-34.
29. Dudda M, Kim YJ, Zhang Y, et al. Morphologic differences between the hips of Chinese women and white women: could they account for the ethnic difference in the prevalence of hip osteoarthritis? Arthritis Rheum. 2011;63(10):2992-2999.
30. Solomon L, Beighton P. Osteoarthrosis of the hip and its relationship to pre-existing in an African population. J Bone Joint Surg Br. 1973;55(1):216-217.
31. Keeney JA, Peelle MW, Jackson J, Rubin D, Maloney WJ, Clohisy JC. Magnetic resonance arthrography versus arthroscopy in the evaluation of articular hip pathology. Clin Orthop Relat Res. 2004;(429):163-169.
32. Schmid MR, Nötzli HP, Zanetti M, Wyss TF, Hodler J. Cartilage lesions in the hip: diagnostic effectiveness of MR arthrography. Radiology. 2003;226(2):382-386.
33. Chevillotte CJ, Ali MH, Trousdale RT, Pagnano MW. Variability in hip range of motion on clinical examination. J Arthroplasty. 2009;24(5):693-697.
1. Cvetanovich GL, Chalmers PN, Levy DM, et al. Hip arthroscopy surgical volume trends and 30-day postoperative complications. Arthroscopy. 2016;32(7):1286-1292.
2. Peters CL, Aoki SK, Erickson JA, Anderson LA, Anderson AE. Early experience with a comprehensive hip preservation service intended to improve clinical care, education, and academic productivity. Clin Orthop Relat Res. 2012;470(12):3446-3452.
3. Siebenrock KA, Peters CL. ABJS Carl T. Brighton workshop on hip preservation surgery: editorial comment. Clin Orthop Relat Res. 2012;470(12):3281-3283.
4. Parvizi J, Leunig M, Ganz R. Femoroacetabular impingement. J Am Acad Orthop Surg. 2007;15(9):561-570.
5. Poh SY, Hube R, Dienst M. Arthroscopic treatment of femoroacetabular pincer impingement. Oper Orthop Traumatol. 2015;27(6):536-552.
6. Javed A, O’Donnell JM. Arthroscopic femoral osteochondroplasty for cam femoroacetabular impingement in patients over 60 years of age. J Bone Joint Surg Br. 2011;93(3):326-331.
7. Groh MM, Herrera J. A comprehensive review of hip labral tears. Curr Rev Musculoskelet Med. 2009;2(2):105-117.
8. 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.
9. White BJ, Herzog MM. Labral reconstruction: when to perform and how. Front Surg. 2015;2:27.
10. Yen YM, Kocher MS. Chondral lesions of the hip: microfracture and chondroplasty. Sports Med Arthrosc. 2010;18(2):83-89.
11. Jordan MA, Van Thiel GS, Chahal J, Nho SJ. Operative treatment of chondral defects in the hip joint: a systematic review. Curr Rev Musculoskelet Med. 2012;5(3):244-253.
12. Griffin DW, Kinnard MJ, Formby PM, McCabe MP, Anderson TD. Outcomes of hip arthroscopy in the older adult: a systematic review of the literature [published online October 18, 2016]. Am J Sports Med. doi:10.1177/0363546516667915.
13. Ganz R, Leunig M, Leunig-Ganz K, Harris WH. The etiology of osteoarthritis of the hip. Clin Orthop Relat Res. 2008;466(2):264-272.
14. Kaya M, Suzuki T, Emori M, Yamashita T. Hip morphology influences the pattern of articular cartilage damage. Knee Surg Sports Traumatol Arthrosc. 2016;24(6):2016-2023.
15. Beck M, Leunig M, Parvizi J, Boutier V, Wyss D, Ganz R. Anterior femoroacetabular impingement: part II. Midterm results of surgical treatment. Clin Orthop Relat Res. 2004;(418):67-73.
16. Byrd JT. Hip arthroscopy in athletes. Oper Tech Sports Med. 2005;13(1):24-36.
17. Werner BC, Gaudiani MA, Ranawat AS. The etiology and arthroscopic surgical management of cam lesions. Clin Sports Med. 2016;35(3):391-404.
18. Clohisy JC, Baca G, Beaulé PE, et al; ANCHOR Study Group. Descriptive epidemiology of femoroacetabular impingement: a North American cohort of patients undergoing surgery. Am J Sports Med. 2013;41(6):1348-1356.
19. Shia DS, Clohisy JC, Schinsky MF, Martell JM, Maloney WJ. THA with highly cross-linked polyethylene in patients 50 years or younger. Clin Orthop Relat Res. 2009;467(8):2059-2065.
20. Gandhi SK, Salmon JW, Zhao SZ, Lambert BL, Gore PR, Conrad K. Psychometric evaluation of the 12-item Short-Form Health Survey (SF-12) in osteoarthritis and rheumatoid arthritis clinical trials. Clin Ther. 2001;23(7):1080-1098.
21. Loudon JK, Reiman MP. Conservative management of femoroacetabular impingement (FAI) in the long distance runner. Phys Ther Sport. 2014;15(2):82-90.
22. Wall PD, Fernandez M, Griffin DR, Foster NE. Nonoperative treatment for femoroacetabular impingement: a systematic review of the literature. PM R. 2013;5(5):418-426.
23. 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.
24. McCormick F, Nwachukwu BU, Alpaugh K, Martin SD. Predictors of hip arthroscopy outcomes for labral tears at minimum 2-year follow-up: the influence of age and arthritis. Arthroscopy. 2012;28(10):1359-1364.
25. Beck M, Kalhor M, Leunig M, Ganz R. Hip morphology influences the pattern of damage to the acetabular cartilage: femoroacetabular impingement as a cause of early osteoarthritis of the hip. J Bone Joint Surg Br. 2005;87(7):1012-1018.
26. Tannast M, Siebenrock KA, Anderson SE. Femoroacetabular impingement: radiographic diagnosis—what the radiologist should know. AJR Am J Roentgenol. 2007;188(6):1540-1552.
27. Kapron AL, Peters CL, Aoki SK, et al. The prevalence of radiographic findings of structural hip deformities in female collegiate athletes. Am J Sports Med. 2015;43(6):1324-1330.
28. Lee WY, Kang C, Hwang DS, Jeon JH, Zheng L. Descriptive epidemiology of symptomatic femoroacetabular impingement in young athlete: single center study. Hip Pelvis. 2016;28(1):29-34.
29. Dudda M, Kim YJ, Zhang Y, et al. Morphologic differences between the hips of Chinese women and white women: could they account for the ethnic difference in the prevalence of hip osteoarthritis? Arthritis Rheum. 2011;63(10):2992-2999.
30. Solomon L, Beighton P. Osteoarthrosis of the hip and its relationship to pre-existing in an African population. J Bone Joint Surg Br. 1973;55(1):216-217.
31. Keeney JA, Peelle MW, Jackson J, Rubin D, Maloney WJ, Clohisy JC. Magnetic resonance arthrography versus arthroscopy in the evaluation of articular hip pathology. Clin Orthop Relat Res. 2004;(429):163-169.
32. Schmid MR, Nötzli HP, Zanetti M, Wyss TF, Hodler J. Cartilage lesions in the hip: diagnostic effectiveness of MR arthrography. Radiology. 2003;226(2):382-386.
33. Chevillotte CJ, Ali MH, Trousdale RT, Pagnano MW. Variability in hip range of motion on clinical examination. J Arthroplasty. 2009;24(5):693-697.