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Conflict of Interest in Sports Medicine: Does It Affect Our Judgment?
As defined by the American Academy of Orthopaedic Surgeons (AAOS) in 1996, conflict of interest (COI) is the “circumstance that exists when, because of personal financial gain, an individual has the potential to be less than objective when called on to reach a judgment or interpret a result.”1 In medical research, COIs often occur in relationships between physician-researchers and pharmaceutical, medical device, and biotechnology companies. These relationships usually take the form of research grants but can also arise when the researcher has a financial interest in the product being tested or in the company that manufactures the product.
Although constructive collaboration between academic medicine and industry has worked to improve health care and ultimately benefit patients, potential drawbacks of such relationships include sequestration and suppression of results that may be disadvantageous to the industry sponsor,2 increased likelihood of reporting positive results (pro-industry),3-7 and biased study designs.8 The nature of such relationships may threaten the integrity of scientific studies, the objectivity of medical education, the quality of patient care, and the public’s trust in medicine.9
Financial relationships and affiliations are increasing as we seek to answer a growing number of clinical questions—with funding often being a limiting factor. At national scientific meetings, the number of presentations reporting COIs reflects this trend. Paper and poster presentations accepted for annual meetings of the Orthopaedic Trauma Association (OTA) and reporting a COI increased from 7.6% in 1993 to 12.6% in 2002 (P = .0129).2
Medical subspecialties outside of orthopedics are experiencing similar trends. Most notable is the American Psychiatric Association (APA). After the APA published a mandatory financial COI disclosure policy in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), the percentage of task force members reporting industry relationships increased by 12%.10 Analysis of the DSM-5 panels demonstrated that the panels with the largest percentage of reported COIs are those for which pharmacological treatment is the first-line intervention, including the panels for mood disorders (67%), psychotic disorders (83%) and sleep/wake disorders (100%).10 Moreover, the industry ties reported are to the pharmaceutical companies that manufacture the medications used to treat these disorders or to companies that service the pharmaceutical industry.10
The degree to which financial COIs affect the interpretation of the orthopedic literature has never been quantified. Although it is clear that COIs can confound the results and reporting of data, how the medical community uses disclosures when interpreting the literature and when formulating opinions that may or may not affect their practice patterns is largely unknown.
We conducted a study to evaluate how a hypothetical financial COI disclosure would influence the interpretation of data by orthopedic clinicians. We also wanted to determine the reliability of the data as perceived in association with different study designs, levels of evidence, research institutional settings, and reporting of positive or negative results.
Methods
We asked members of the Arthroscopy Association of North America (AANA) and the American Orthopaedic Society for Sports Medicine (AOSSM) to complete a multiple-choice situational questionnaire (Table). The questionnaire assesses the degree to which respondents use COI disclosures when interpreting the literature. It further explores the perceived clinical value of a study with a given reported COI, assuming variations in study design, research institutional setting, and significance of results. The fictional research team disclosed the project was funded by a pharmaceutical company and all team members received consulting compensation. The survey and study were reviewed and approved by our institutional review board. The survey consisted of 14 multiple-choice questions that allowed for only 1 answer selection per person and allowed survey takers to skip questions they did not wish to answer. The survey questions and associated response options appear in edited form in the Table. A link to the questionnaire (https://www.surveymonkey.com/s/MPCCLCX) was sent with a message explaining the study. The responses to the questionnaire constituted the data.
Results
We sent a request to participate in the survey to 750 physicians and received 522 responses (overall response rate, 70%). The response rate for each question equaled or exceeded 98%.
The majority of respondents (95.6%) were male. Ninety-nine percent of respondents were orthopedic surgeons. The Northeast (US) was the most common geographical practice location of respondents (32%), followed by the Midwest (19.1%) and the Southeast (16.6%). Most respondents (40%) had been in practice for more than 20 years; 67% had been in practice a minimum of 10 years. The majority (68.8%) were employed by private practice groups, either single specialty (57.8%) or multispecialty (11%).
Eighty percent of respondents strongly agreed that COI disclosure is important when interpreting study results, 62% reported always reading the disclosure slide during academy or other meeting presentations, and 41% reported always using this information when deciding how to interpret scientific data.
Seventy-five percent of respondents thought the study—an academic-center case series with significant results in favor of the pharmaceutical company funding the study—was biased (42% indicated biased with merit, 33% biased without merit). Twenty-three percent thought the study was possibly biased, but likely trustworthy given the academic institutional affiliation. When the study setting was changed to community hospital, 95% thought the study was biased (51% biased with merit, 44% biased without merit). With the same study performed at an academic center, and no statistically significant results (not in favor of the pharmaceutical company funding the study), 88% thought the study had merit (46% biased with merit, 42% unbiased with merit).
When the study design was changed to a randomized controlled trial (level I evidence) conducted at an academic center with negative results, an overwhelming 95% of respondents thought the study had merit (33% biased with merit, 62% unbiased with merit). Given the same study design at an academic center, with positive results, 78% still thought the study had merit (39% biased with merit, 39% unbiased with merit). An additional 18% thought the study was biased, but still likely trustworthy given the academic institutional affiliation. Finally, given a randomized controlled trial and positive results, but with the research setting a small community practice, 90% thought the study had merit (51% biased with merit, 39% unbiased with merit). The percentage of respondents who found the study biased and likely without merit increased from 3.7% to 9.5% when the institutional affiliation changed from academic to community.
Discussion
As governmental funding sources become increasingly limited, the role of industry sponsorship of orthopedic research has grown. Potential drawbacks and biases of such research support have been well described—most notably, increased positive result reporting, suppression of results that may be disadvantageous to the industry sponsor, and biased study designs.2-8 However, the extent to which financial COIs affect the orthopedic medical community’s interpretation of the literature has never been quantified. To our knowledge, the present study is the first to quantify the impact of reported COI on study interpretation.
Our goal was to examine how reported financial COIs influence the interpretation of the literature by the orthopedic medical community. Moreover, we wanted to determine the perceived reliability of the data when variables (study design, institutional affiliation, positive vs negative results) were changed. The results of our survey indicate that, when a financial COI is reported, study reliability is perceived as highest when negative results were found.
Our survey noted a discrepancy between the documented importance of the hypothetical research team’s COI disclosure and the use of such disclosures when interpreting study results. Eighty percent of respondents agreed that COI disclosure is important when interpreting study results, but only 62% reported always reading disclosures, and even fewer (41%) reported always using the information when interpreting results. It is unclear exactly why this trend exists, as one would expect the percentages to be more similar. These particular survey questions were formed around using COI disclosures when interpreting study results during academic presentations at national meetings and not during the review of published literature. It is possible that positioning the COI disclosure at the beginning of a presentation has an effect, but only 3.7% of respondents indicated they seldom remembered the disclosure by the end of the presentation. The results of our survey may have varied if the questions had targeted reading and interpreting the literature.
Interestingly, the results of these survey questions tended to be more consistent with rates of reported financial COI by presenters at national orthopedic meetings. A study published in the New England Journal of Medicine found that less than 80% of orthopedic surgeons reported their disclosures at a large annual meeting (AAOS), even when the disclosure involved payments pertinent to the research they were presenting.5 When the payments were indirectly related to the research, the percentage of surgeons reporting disclosures was 50%, almost the same as the disclosure rate for unrelated payments.5
When the study was changed to a level I randomized controlled trial, more survey respondents found it to be less biased and have more merit. Although it would seem intuitive for a study with a higher level of evidence to carry more clinical value during interpretation, this may not hold true in the setting of industry-sponsored clinical trials. Several studies have documented a significant association between the reporting of positive results and industry-sponsored randomized clinical trials. In 2008, Khan and colleagues3 examined 100 orthopedic randomized clinical trials reported in 5 major orthopedic subspecialty journals over a 2-year period. The association between industry funding and favorable outcome in all original randomized clinical trials was strong and significant (P < .001). This is not surprising, given the amount of time and money required for a well-designed clinical study. Commercial products with preclinical promise are pushed to testing in a clinical trial, whereas resources would not be wasted on products lacking preclinical merit.
The most important variable affecting interpretation of study merit by survey respondents was the reporting of negative results. As more researchers are developing COIs, many studies are discovering a relationship between COIs and outcomes of research studies. Reviewing the adult total joint literature, Ezzet8 found an industry funding rate of 50%. Positive results were reported in 93% of cases in commercially funded studies versus 37% of cases in independently funded studies. Furthermore, no negative results were reported by investigators who were receiving royalties from the respective companies.
Studies across the medical literature have also found this association between industry sponsorship and reporting of positive results. One such study, reported by Valachis and colleagues7 in the Journal of Clinical Oncology, examined more than 80 economic analyses of targeted oncologic therapies and found the studies funded by pharmaceutical companies were more likely to report favorable qualitative cost estimates. In addition, when studies with a COI disclosure were examined, those reporting any financial relationship with a manufacturer (eg, author affiliation, funding) were more likely than those without such a relationship to report favorable results.
Our study had several limitations. First, as most of the survey respondents were orthopedic surgeons, extrapolating their data to the medical community at large may not be appropriate, as each specialty may view industry affiliations differently. In addition, respondents were asked to base their interpretations of a study on conclusions we predetermined—no direct visualization of the data set or statistical testing methods. It is possible that these responses may have been different had the respondents had the opportunity to further evaluate the study in question. In a recent study, Altwairgi and colleagues11 found that 10% of randomized clinical trials involving lung cancer treatment were reported with different conclusions in their full manuscripts relative to their abstracts. We think our survey design perhaps best mimics an annual meeting environment in which participants have very limited ability to interpret studies and may rely more heavily on the factors we investigated—study design, significance of findings, and setting, all similar to information presented in an abstract—when making informed decisions. Although our response rate was only 70%, this is comparable to or better than the rates in similar survey studies that used email-based questionnaires.12,13
Another limitation was that our survey may have forced respondents into answers they did not entirely agree with, given the limited options of the multiple-choice response format and the specific wording of the questions. Our conclusions may have been more dramatic when we were evaluating whether the study was deemed meritorious or not. However, there is no adopted standard for evaluating the extent of bias perceived by a clinician. We thought it was important to include answer options indicating a study had merit despite obvious bias in design and execution. That a study had merit can mean different things. It may change clinical practice, may require further study and reproducibility, or may not be significant enough to matter. Asking follow-up questions to evaluate this perception among the respondents could have provided validity to the term merit. Further studies in this field are needed to determine how studies are interpreted and translated into clinical practice by various clinicians.
Conclusion
Although the present study is not a quantitative analysis of the determination of bias in the orthopedic community, it is the first to evaluate orthopedic surgeons’ perceptions on the basis of key fundamentals of orthopedic research relative to COI. It is clear from our study results that introducing levels of evidence to the orthopedic milieu has had a significant impact both on the quality of research and on the foundational use of deductive reasoning when interpreting the literature. Reporting negative outcomes is perhaps the most important factor in eliminating the perception of bias among orthopedic surgeons. To what extent a perceived COI plays into medical decision-making and the ultimate treatment of patients is still relatively unknown.
1. Lubahn JD, Mankin CJ, Mankin HJ, Kuhn PJ. Orthopaedics, ethics, and industry. Appropriateness of gifts, grants, and awards. Clin Orthop Relat Res. 2000;(371):256-263.
2. Kubiak EN, Park SS, Egol K, Zuckerman JD, Koval KJ. Increasingly conflicted: an analysis of conflicts of interest reported at the annual meetings of the Orthopaedic Trauma Association. Bull Hosp Jt Dis. 2006;63(3-4):83-87.
3. Khan SN, Mermer MJ, Myers E, Sandhu HS. The roles of funding source, clinical trial outcome, and quality of reporting in orthopedic surgery literature. Am J Orthop. 2008;37(12):E205-E212.
4. Okike K, Kocher MS, Mehlman CT, Bhandari M. Conflict of interest in orthopaedic research. An association between findings and funding in scientific presentations. J Bone Joint Surg Am. 2007;89(3):608-613.
5. Okike K, Kocher MS, Wei EX, Mehlman CT, Bhandari M. Accuracy of conflict-of-interest disclosures reported by physicians. N Engl J Med. 2009;361(15):1466-1474.
6. Shah RV, Albert TJ, Bruegel-Sanchez V, Vaccaro AR, Hilibrand AS, Grauer JN. Industry support and correlation to study outcome for papers published in Spine. Spine. 2005;30(9):1099-1104.
7. Valachis A, Polyzos NP, Nearchou A, Lind P, Mauri D. Financial relationships in economic analyses of targeted therapies in oncology. J Clin Oncol. 2012;30(12):1316-1320.
8. Ezzet KA. The prevalence of corporate funding in adult lower extremity research and its correlation with reported results. J Arthroplasty. 2003;18(7 suppl 1):138-145.
9. Lo B, Field MJ, eds; Institute of Medicine, Committee on Conflict of Interest in Medical Research, Education, and Practice, Board on Health Sciences Policy. Conflict of Interest in Medical Research, Education, and Practice. Washington, DC: National Academies Press; 2009. http://www.ncbi.nlm.nih.gov/books/NBK22942. Accessed September 29, 2015.
10. Cosgrove L, Krimsky S. A comparison of DSM-IV and DSM-5 panel members’ financial associations with industry: a pernicious problem persists. PLoS Med. 2012;9(3):e1001190.
11. Altwairgi AK, Booth CM, Hopman WM, Baetz TD. Discordance between conclusions stated in the abstract and conclusions in the article: analysis of published randomized controlled trials of systemic therapy in lung cancer. J Clin Oncol. 2012;30(28):3552-3557.
12. Decoster LC, Vailas JC, Swartz WG. Functional ACL bracing. A survey of current opinion and practice. Am J Orthop. 1995;24(11):838-843.
13. Mann BJ, Grana WA, Indelicato PA, O’Neill DF, George SZ. A survey of sports medicine physicians regarding psychological issues in patient-athletes. Am J Sports Med. 2007;35(12):2140-2147.
As defined by the American Academy of Orthopaedic Surgeons (AAOS) in 1996, conflict of interest (COI) is the “circumstance that exists when, because of personal financial gain, an individual has the potential to be less than objective when called on to reach a judgment or interpret a result.”1 In medical research, COIs often occur in relationships between physician-researchers and pharmaceutical, medical device, and biotechnology companies. These relationships usually take the form of research grants but can also arise when the researcher has a financial interest in the product being tested or in the company that manufactures the product.
Although constructive collaboration between academic medicine and industry has worked to improve health care and ultimately benefit patients, potential drawbacks of such relationships include sequestration and suppression of results that may be disadvantageous to the industry sponsor,2 increased likelihood of reporting positive results (pro-industry),3-7 and biased study designs.8 The nature of such relationships may threaten the integrity of scientific studies, the objectivity of medical education, the quality of patient care, and the public’s trust in medicine.9
Financial relationships and affiliations are increasing as we seek to answer a growing number of clinical questions—with funding often being a limiting factor. At national scientific meetings, the number of presentations reporting COIs reflects this trend. Paper and poster presentations accepted for annual meetings of the Orthopaedic Trauma Association (OTA) and reporting a COI increased from 7.6% in 1993 to 12.6% in 2002 (P = .0129).2
Medical subspecialties outside of orthopedics are experiencing similar trends. Most notable is the American Psychiatric Association (APA). After the APA published a mandatory financial COI disclosure policy in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), the percentage of task force members reporting industry relationships increased by 12%.10 Analysis of the DSM-5 panels demonstrated that the panels with the largest percentage of reported COIs are those for which pharmacological treatment is the first-line intervention, including the panels for mood disorders (67%), psychotic disorders (83%) and sleep/wake disorders (100%).10 Moreover, the industry ties reported are to the pharmaceutical companies that manufacture the medications used to treat these disorders or to companies that service the pharmaceutical industry.10
The degree to which financial COIs affect the interpretation of the orthopedic literature has never been quantified. Although it is clear that COIs can confound the results and reporting of data, how the medical community uses disclosures when interpreting the literature and when formulating opinions that may or may not affect their practice patterns is largely unknown.
We conducted a study to evaluate how a hypothetical financial COI disclosure would influence the interpretation of data by orthopedic clinicians. We also wanted to determine the reliability of the data as perceived in association with different study designs, levels of evidence, research institutional settings, and reporting of positive or negative results.
Methods
We asked members of the Arthroscopy Association of North America (AANA) and the American Orthopaedic Society for Sports Medicine (AOSSM) to complete a multiple-choice situational questionnaire (Table). The questionnaire assesses the degree to which respondents use COI disclosures when interpreting the literature. It further explores the perceived clinical value of a study with a given reported COI, assuming variations in study design, research institutional setting, and significance of results. The fictional research team disclosed the project was funded by a pharmaceutical company and all team members received consulting compensation. The survey and study were reviewed and approved by our institutional review board. The survey consisted of 14 multiple-choice questions that allowed for only 1 answer selection per person and allowed survey takers to skip questions they did not wish to answer. The survey questions and associated response options appear in edited form in the Table. A link to the questionnaire (https://www.surveymonkey.com/s/MPCCLCX) was sent with a message explaining the study. The responses to the questionnaire constituted the data.
Results
We sent a request to participate in the survey to 750 physicians and received 522 responses (overall response rate, 70%). The response rate for each question equaled or exceeded 98%.
The majority of respondents (95.6%) were male. Ninety-nine percent of respondents were orthopedic surgeons. The Northeast (US) was the most common geographical practice location of respondents (32%), followed by the Midwest (19.1%) and the Southeast (16.6%). Most respondents (40%) had been in practice for more than 20 years; 67% had been in practice a minimum of 10 years. The majority (68.8%) were employed by private practice groups, either single specialty (57.8%) or multispecialty (11%).
Eighty percent of respondents strongly agreed that COI disclosure is important when interpreting study results, 62% reported always reading the disclosure slide during academy or other meeting presentations, and 41% reported always using this information when deciding how to interpret scientific data.
Seventy-five percent of respondents thought the study—an academic-center case series with significant results in favor of the pharmaceutical company funding the study—was biased (42% indicated biased with merit, 33% biased without merit). Twenty-three percent thought the study was possibly biased, but likely trustworthy given the academic institutional affiliation. When the study setting was changed to community hospital, 95% thought the study was biased (51% biased with merit, 44% biased without merit). With the same study performed at an academic center, and no statistically significant results (not in favor of the pharmaceutical company funding the study), 88% thought the study had merit (46% biased with merit, 42% unbiased with merit).
When the study design was changed to a randomized controlled trial (level I evidence) conducted at an academic center with negative results, an overwhelming 95% of respondents thought the study had merit (33% biased with merit, 62% unbiased with merit). Given the same study design at an academic center, with positive results, 78% still thought the study had merit (39% biased with merit, 39% unbiased with merit). An additional 18% thought the study was biased, but still likely trustworthy given the academic institutional affiliation. Finally, given a randomized controlled trial and positive results, but with the research setting a small community practice, 90% thought the study had merit (51% biased with merit, 39% unbiased with merit). The percentage of respondents who found the study biased and likely without merit increased from 3.7% to 9.5% when the institutional affiliation changed from academic to community.
Discussion
As governmental funding sources become increasingly limited, the role of industry sponsorship of orthopedic research has grown. Potential drawbacks and biases of such research support have been well described—most notably, increased positive result reporting, suppression of results that may be disadvantageous to the industry sponsor, and biased study designs.2-8 However, the extent to which financial COIs affect the orthopedic medical community’s interpretation of the literature has never been quantified. To our knowledge, the present study is the first to quantify the impact of reported COI on study interpretation.
Our goal was to examine how reported financial COIs influence the interpretation of the literature by the orthopedic medical community. Moreover, we wanted to determine the perceived reliability of the data when variables (study design, institutional affiliation, positive vs negative results) were changed. The results of our survey indicate that, when a financial COI is reported, study reliability is perceived as highest when negative results were found.
Our survey noted a discrepancy between the documented importance of the hypothetical research team’s COI disclosure and the use of such disclosures when interpreting study results. Eighty percent of respondents agreed that COI disclosure is important when interpreting study results, but only 62% reported always reading disclosures, and even fewer (41%) reported always using the information when interpreting results. It is unclear exactly why this trend exists, as one would expect the percentages to be more similar. These particular survey questions were formed around using COI disclosures when interpreting study results during academic presentations at national meetings and not during the review of published literature. It is possible that positioning the COI disclosure at the beginning of a presentation has an effect, but only 3.7% of respondents indicated they seldom remembered the disclosure by the end of the presentation. The results of our survey may have varied if the questions had targeted reading and interpreting the literature.
Interestingly, the results of these survey questions tended to be more consistent with rates of reported financial COI by presenters at national orthopedic meetings. A study published in the New England Journal of Medicine found that less than 80% of orthopedic surgeons reported their disclosures at a large annual meeting (AAOS), even when the disclosure involved payments pertinent to the research they were presenting.5 When the payments were indirectly related to the research, the percentage of surgeons reporting disclosures was 50%, almost the same as the disclosure rate for unrelated payments.5
When the study was changed to a level I randomized controlled trial, more survey respondents found it to be less biased and have more merit. Although it would seem intuitive for a study with a higher level of evidence to carry more clinical value during interpretation, this may not hold true in the setting of industry-sponsored clinical trials. Several studies have documented a significant association between the reporting of positive results and industry-sponsored randomized clinical trials. In 2008, Khan and colleagues3 examined 100 orthopedic randomized clinical trials reported in 5 major orthopedic subspecialty journals over a 2-year period. The association between industry funding and favorable outcome in all original randomized clinical trials was strong and significant (P < .001). This is not surprising, given the amount of time and money required for a well-designed clinical study. Commercial products with preclinical promise are pushed to testing in a clinical trial, whereas resources would not be wasted on products lacking preclinical merit.
The most important variable affecting interpretation of study merit by survey respondents was the reporting of negative results. As more researchers are developing COIs, many studies are discovering a relationship between COIs and outcomes of research studies. Reviewing the adult total joint literature, Ezzet8 found an industry funding rate of 50%. Positive results were reported in 93% of cases in commercially funded studies versus 37% of cases in independently funded studies. Furthermore, no negative results were reported by investigators who were receiving royalties from the respective companies.
Studies across the medical literature have also found this association between industry sponsorship and reporting of positive results. One such study, reported by Valachis and colleagues7 in the Journal of Clinical Oncology, examined more than 80 economic analyses of targeted oncologic therapies and found the studies funded by pharmaceutical companies were more likely to report favorable qualitative cost estimates. In addition, when studies with a COI disclosure were examined, those reporting any financial relationship with a manufacturer (eg, author affiliation, funding) were more likely than those without such a relationship to report favorable results.
Our study had several limitations. First, as most of the survey respondents were orthopedic surgeons, extrapolating their data to the medical community at large may not be appropriate, as each specialty may view industry affiliations differently. In addition, respondents were asked to base their interpretations of a study on conclusions we predetermined—no direct visualization of the data set or statistical testing methods. It is possible that these responses may have been different had the respondents had the opportunity to further evaluate the study in question. In a recent study, Altwairgi and colleagues11 found that 10% of randomized clinical trials involving lung cancer treatment were reported with different conclusions in their full manuscripts relative to their abstracts. We think our survey design perhaps best mimics an annual meeting environment in which participants have very limited ability to interpret studies and may rely more heavily on the factors we investigated—study design, significance of findings, and setting, all similar to information presented in an abstract—when making informed decisions. Although our response rate was only 70%, this is comparable to or better than the rates in similar survey studies that used email-based questionnaires.12,13
Another limitation was that our survey may have forced respondents into answers they did not entirely agree with, given the limited options of the multiple-choice response format and the specific wording of the questions. Our conclusions may have been more dramatic when we were evaluating whether the study was deemed meritorious or not. However, there is no adopted standard for evaluating the extent of bias perceived by a clinician. We thought it was important to include answer options indicating a study had merit despite obvious bias in design and execution. That a study had merit can mean different things. It may change clinical practice, may require further study and reproducibility, or may not be significant enough to matter. Asking follow-up questions to evaluate this perception among the respondents could have provided validity to the term merit. Further studies in this field are needed to determine how studies are interpreted and translated into clinical practice by various clinicians.
Conclusion
Although the present study is not a quantitative analysis of the determination of bias in the orthopedic community, it is the first to evaluate orthopedic surgeons’ perceptions on the basis of key fundamentals of orthopedic research relative to COI. It is clear from our study results that introducing levels of evidence to the orthopedic milieu has had a significant impact both on the quality of research and on the foundational use of deductive reasoning when interpreting the literature. Reporting negative outcomes is perhaps the most important factor in eliminating the perception of bias among orthopedic surgeons. To what extent a perceived COI plays into medical decision-making and the ultimate treatment of patients is still relatively unknown.
As defined by the American Academy of Orthopaedic Surgeons (AAOS) in 1996, conflict of interest (COI) is the “circumstance that exists when, because of personal financial gain, an individual has the potential to be less than objective when called on to reach a judgment or interpret a result.”1 In medical research, COIs often occur in relationships between physician-researchers and pharmaceutical, medical device, and biotechnology companies. These relationships usually take the form of research grants but can also arise when the researcher has a financial interest in the product being tested or in the company that manufactures the product.
Although constructive collaboration between academic medicine and industry has worked to improve health care and ultimately benefit patients, potential drawbacks of such relationships include sequestration and suppression of results that may be disadvantageous to the industry sponsor,2 increased likelihood of reporting positive results (pro-industry),3-7 and biased study designs.8 The nature of such relationships may threaten the integrity of scientific studies, the objectivity of medical education, the quality of patient care, and the public’s trust in medicine.9
Financial relationships and affiliations are increasing as we seek to answer a growing number of clinical questions—with funding often being a limiting factor. At national scientific meetings, the number of presentations reporting COIs reflects this trend. Paper and poster presentations accepted for annual meetings of the Orthopaedic Trauma Association (OTA) and reporting a COI increased from 7.6% in 1993 to 12.6% in 2002 (P = .0129).2
Medical subspecialties outside of orthopedics are experiencing similar trends. Most notable is the American Psychiatric Association (APA). After the APA published a mandatory financial COI disclosure policy in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), the percentage of task force members reporting industry relationships increased by 12%.10 Analysis of the DSM-5 panels demonstrated that the panels with the largest percentage of reported COIs are those for which pharmacological treatment is the first-line intervention, including the panels for mood disorders (67%), psychotic disorders (83%) and sleep/wake disorders (100%).10 Moreover, the industry ties reported are to the pharmaceutical companies that manufacture the medications used to treat these disorders or to companies that service the pharmaceutical industry.10
The degree to which financial COIs affect the interpretation of the orthopedic literature has never been quantified. Although it is clear that COIs can confound the results and reporting of data, how the medical community uses disclosures when interpreting the literature and when formulating opinions that may or may not affect their practice patterns is largely unknown.
We conducted a study to evaluate how a hypothetical financial COI disclosure would influence the interpretation of data by orthopedic clinicians. We also wanted to determine the reliability of the data as perceived in association with different study designs, levels of evidence, research institutional settings, and reporting of positive or negative results.
Methods
We asked members of the Arthroscopy Association of North America (AANA) and the American Orthopaedic Society for Sports Medicine (AOSSM) to complete a multiple-choice situational questionnaire (Table). The questionnaire assesses the degree to which respondents use COI disclosures when interpreting the literature. It further explores the perceived clinical value of a study with a given reported COI, assuming variations in study design, research institutional setting, and significance of results. The fictional research team disclosed the project was funded by a pharmaceutical company and all team members received consulting compensation. The survey and study were reviewed and approved by our institutional review board. The survey consisted of 14 multiple-choice questions that allowed for only 1 answer selection per person and allowed survey takers to skip questions they did not wish to answer. The survey questions and associated response options appear in edited form in the Table. A link to the questionnaire (https://www.surveymonkey.com/s/MPCCLCX) was sent with a message explaining the study. The responses to the questionnaire constituted the data.
Results
We sent a request to participate in the survey to 750 physicians and received 522 responses (overall response rate, 70%). The response rate for each question equaled or exceeded 98%.
The majority of respondents (95.6%) were male. Ninety-nine percent of respondents were orthopedic surgeons. The Northeast (US) was the most common geographical practice location of respondents (32%), followed by the Midwest (19.1%) and the Southeast (16.6%). Most respondents (40%) had been in practice for more than 20 years; 67% had been in practice a minimum of 10 years. The majority (68.8%) were employed by private practice groups, either single specialty (57.8%) or multispecialty (11%).
Eighty percent of respondents strongly agreed that COI disclosure is important when interpreting study results, 62% reported always reading the disclosure slide during academy or other meeting presentations, and 41% reported always using this information when deciding how to interpret scientific data.
Seventy-five percent of respondents thought the study—an academic-center case series with significant results in favor of the pharmaceutical company funding the study—was biased (42% indicated biased with merit, 33% biased without merit). Twenty-three percent thought the study was possibly biased, but likely trustworthy given the academic institutional affiliation. When the study setting was changed to community hospital, 95% thought the study was biased (51% biased with merit, 44% biased without merit). With the same study performed at an academic center, and no statistically significant results (not in favor of the pharmaceutical company funding the study), 88% thought the study had merit (46% biased with merit, 42% unbiased with merit).
When the study design was changed to a randomized controlled trial (level I evidence) conducted at an academic center with negative results, an overwhelming 95% of respondents thought the study had merit (33% biased with merit, 62% unbiased with merit). Given the same study design at an academic center, with positive results, 78% still thought the study had merit (39% biased with merit, 39% unbiased with merit). An additional 18% thought the study was biased, but still likely trustworthy given the academic institutional affiliation. Finally, given a randomized controlled trial and positive results, but with the research setting a small community practice, 90% thought the study had merit (51% biased with merit, 39% unbiased with merit). The percentage of respondents who found the study biased and likely without merit increased from 3.7% to 9.5% when the institutional affiliation changed from academic to community.
Discussion
As governmental funding sources become increasingly limited, the role of industry sponsorship of orthopedic research has grown. Potential drawbacks and biases of such research support have been well described—most notably, increased positive result reporting, suppression of results that may be disadvantageous to the industry sponsor, and biased study designs.2-8 However, the extent to which financial COIs affect the orthopedic medical community’s interpretation of the literature has never been quantified. To our knowledge, the present study is the first to quantify the impact of reported COI on study interpretation.
Our goal was to examine how reported financial COIs influence the interpretation of the literature by the orthopedic medical community. Moreover, we wanted to determine the perceived reliability of the data when variables (study design, institutional affiliation, positive vs negative results) were changed. The results of our survey indicate that, when a financial COI is reported, study reliability is perceived as highest when negative results were found.
Our survey noted a discrepancy between the documented importance of the hypothetical research team’s COI disclosure and the use of such disclosures when interpreting study results. Eighty percent of respondents agreed that COI disclosure is important when interpreting study results, but only 62% reported always reading disclosures, and even fewer (41%) reported always using the information when interpreting results. It is unclear exactly why this trend exists, as one would expect the percentages to be more similar. These particular survey questions were formed around using COI disclosures when interpreting study results during academic presentations at national meetings and not during the review of published literature. It is possible that positioning the COI disclosure at the beginning of a presentation has an effect, but only 3.7% of respondents indicated they seldom remembered the disclosure by the end of the presentation. The results of our survey may have varied if the questions had targeted reading and interpreting the literature.
Interestingly, the results of these survey questions tended to be more consistent with rates of reported financial COI by presenters at national orthopedic meetings. A study published in the New England Journal of Medicine found that less than 80% of orthopedic surgeons reported their disclosures at a large annual meeting (AAOS), even when the disclosure involved payments pertinent to the research they were presenting.5 When the payments were indirectly related to the research, the percentage of surgeons reporting disclosures was 50%, almost the same as the disclosure rate for unrelated payments.5
When the study was changed to a level I randomized controlled trial, more survey respondents found it to be less biased and have more merit. Although it would seem intuitive for a study with a higher level of evidence to carry more clinical value during interpretation, this may not hold true in the setting of industry-sponsored clinical trials. Several studies have documented a significant association between the reporting of positive results and industry-sponsored randomized clinical trials. In 2008, Khan and colleagues3 examined 100 orthopedic randomized clinical trials reported in 5 major orthopedic subspecialty journals over a 2-year period. The association between industry funding and favorable outcome in all original randomized clinical trials was strong and significant (P < .001). This is not surprising, given the amount of time and money required for a well-designed clinical study. Commercial products with preclinical promise are pushed to testing in a clinical trial, whereas resources would not be wasted on products lacking preclinical merit.
The most important variable affecting interpretation of study merit by survey respondents was the reporting of negative results. As more researchers are developing COIs, many studies are discovering a relationship between COIs and outcomes of research studies. Reviewing the adult total joint literature, Ezzet8 found an industry funding rate of 50%. Positive results were reported in 93% of cases in commercially funded studies versus 37% of cases in independently funded studies. Furthermore, no negative results were reported by investigators who were receiving royalties from the respective companies.
Studies across the medical literature have also found this association between industry sponsorship and reporting of positive results. One such study, reported by Valachis and colleagues7 in the Journal of Clinical Oncology, examined more than 80 economic analyses of targeted oncologic therapies and found the studies funded by pharmaceutical companies were more likely to report favorable qualitative cost estimates. In addition, when studies with a COI disclosure were examined, those reporting any financial relationship with a manufacturer (eg, author affiliation, funding) were more likely than those without such a relationship to report favorable results.
Our study had several limitations. First, as most of the survey respondents were orthopedic surgeons, extrapolating their data to the medical community at large may not be appropriate, as each specialty may view industry affiliations differently. In addition, respondents were asked to base their interpretations of a study on conclusions we predetermined—no direct visualization of the data set or statistical testing methods. It is possible that these responses may have been different had the respondents had the opportunity to further evaluate the study in question. In a recent study, Altwairgi and colleagues11 found that 10% of randomized clinical trials involving lung cancer treatment were reported with different conclusions in their full manuscripts relative to their abstracts. We think our survey design perhaps best mimics an annual meeting environment in which participants have very limited ability to interpret studies and may rely more heavily on the factors we investigated—study design, significance of findings, and setting, all similar to information presented in an abstract—when making informed decisions. Although our response rate was only 70%, this is comparable to or better than the rates in similar survey studies that used email-based questionnaires.12,13
Another limitation was that our survey may have forced respondents into answers they did not entirely agree with, given the limited options of the multiple-choice response format and the specific wording of the questions. Our conclusions may have been more dramatic when we were evaluating whether the study was deemed meritorious or not. However, there is no adopted standard for evaluating the extent of bias perceived by a clinician. We thought it was important to include answer options indicating a study had merit despite obvious bias in design and execution. That a study had merit can mean different things. It may change clinical practice, may require further study and reproducibility, or may not be significant enough to matter. Asking follow-up questions to evaluate this perception among the respondents could have provided validity to the term merit. Further studies in this field are needed to determine how studies are interpreted and translated into clinical practice by various clinicians.
Conclusion
Although the present study is not a quantitative analysis of the determination of bias in the orthopedic community, it is the first to evaluate orthopedic surgeons’ perceptions on the basis of key fundamentals of orthopedic research relative to COI. It is clear from our study results that introducing levels of evidence to the orthopedic milieu has had a significant impact both on the quality of research and on the foundational use of deductive reasoning when interpreting the literature. Reporting negative outcomes is perhaps the most important factor in eliminating the perception of bias among orthopedic surgeons. To what extent a perceived COI plays into medical decision-making and the ultimate treatment of patients is still relatively unknown.
1. Lubahn JD, Mankin CJ, Mankin HJ, Kuhn PJ. Orthopaedics, ethics, and industry. Appropriateness of gifts, grants, and awards. Clin Orthop Relat Res. 2000;(371):256-263.
2. Kubiak EN, Park SS, Egol K, Zuckerman JD, Koval KJ. Increasingly conflicted: an analysis of conflicts of interest reported at the annual meetings of the Orthopaedic Trauma Association. Bull Hosp Jt Dis. 2006;63(3-4):83-87.
3. Khan SN, Mermer MJ, Myers E, Sandhu HS. The roles of funding source, clinical trial outcome, and quality of reporting in orthopedic surgery literature. Am J Orthop. 2008;37(12):E205-E212.
4. Okike K, Kocher MS, Mehlman CT, Bhandari M. Conflict of interest in orthopaedic research. An association between findings and funding in scientific presentations. J Bone Joint Surg Am. 2007;89(3):608-613.
5. Okike K, Kocher MS, Wei EX, Mehlman CT, Bhandari M. Accuracy of conflict-of-interest disclosures reported by physicians. N Engl J Med. 2009;361(15):1466-1474.
6. Shah RV, Albert TJ, Bruegel-Sanchez V, Vaccaro AR, Hilibrand AS, Grauer JN. Industry support and correlation to study outcome for papers published in Spine. Spine. 2005;30(9):1099-1104.
7. Valachis A, Polyzos NP, Nearchou A, Lind P, Mauri D. Financial relationships in economic analyses of targeted therapies in oncology. J Clin Oncol. 2012;30(12):1316-1320.
8. Ezzet KA. The prevalence of corporate funding in adult lower extremity research and its correlation with reported results. J Arthroplasty. 2003;18(7 suppl 1):138-145.
9. Lo B, Field MJ, eds; Institute of Medicine, Committee on Conflict of Interest in Medical Research, Education, and Practice, Board on Health Sciences Policy. Conflict of Interest in Medical Research, Education, and Practice. Washington, DC: National Academies Press; 2009. http://www.ncbi.nlm.nih.gov/books/NBK22942. Accessed September 29, 2015.
10. Cosgrove L, Krimsky S. A comparison of DSM-IV and DSM-5 panel members’ financial associations with industry: a pernicious problem persists. PLoS Med. 2012;9(3):e1001190.
11. Altwairgi AK, Booth CM, Hopman WM, Baetz TD. Discordance between conclusions stated in the abstract and conclusions in the article: analysis of published randomized controlled trials of systemic therapy in lung cancer. J Clin Oncol. 2012;30(28):3552-3557.
12. Decoster LC, Vailas JC, Swartz WG. Functional ACL bracing. A survey of current opinion and practice. Am J Orthop. 1995;24(11):838-843.
13. Mann BJ, Grana WA, Indelicato PA, O’Neill DF, George SZ. A survey of sports medicine physicians regarding psychological issues in patient-athletes. Am J Sports Med. 2007;35(12):2140-2147.
1. Lubahn JD, Mankin CJ, Mankin HJ, Kuhn PJ. Orthopaedics, ethics, and industry. Appropriateness of gifts, grants, and awards. Clin Orthop Relat Res. 2000;(371):256-263.
2. Kubiak EN, Park SS, Egol K, Zuckerman JD, Koval KJ. Increasingly conflicted: an analysis of conflicts of interest reported at the annual meetings of the Orthopaedic Trauma Association. Bull Hosp Jt Dis. 2006;63(3-4):83-87.
3. Khan SN, Mermer MJ, Myers E, Sandhu HS. The roles of funding source, clinical trial outcome, and quality of reporting in orthopedic surgery literature. Am J Orthop. 2008;37(12):E205-E212.
4. Okike K, Kocher MS, Mehlman CT, Bhandari M. Conflict of interest in orthopaedic research. An association between findings and funding in scientific presentations. J Bone Joint Surg Am. 2007;89(3):608-613.
5. Okike K, Kocher MS, Wei EX, Mehlman CT, Bhandari M. Accuracy of conflict-of-interest disclosures reported by physicians. N Engl J Med. 2009;361(15):1466-1474.
6. Shah RV, Albert TJ, Bruegel-Sanchez V, Vaccaro AR, Hilibrand AS, Grauer JN. Industry support and correlation to study outcome for papers published in Spine. Spine. 2005;30(9):1099-1104.
7. Valachis A, Polyzos NP, Nearchou A, Lind P, Mauri D. Financial relationships in economic analyses of targeted therapies in oncology. J Clin Oncol. 2012;30(12):1316-1320.
8. Ezzet KA. The prevalence of corporate funding in adult lower extremity research and its correlation with reported results. J Arthroplasty. 2003;18(7 suppl 1):138-145.
9. Lo B, Field MJ, eds; Institute of Medicine, Committee on Conflict of Interest in Medical Research, Education, and Practice, Board on Health Sciences Policy. Conflict of Interest in Medical Research, Education, and Practice. Washington, DC: National Academies Press; 2009. http://www.ncbi.nlm.nih.gov/books/NBK22942. Accessed September 29, 2015.
10. Cosgrove L, Krimsky S. A comparison of DSM-IV and DSM-5 panel members’ financial associations with industry: a pernicious problem persists. PLoS Med. 2012;9(3):e1001190.
11. Altwairgi AK, Booth CM, Hopman WM, Baetz TD. Discordance between conclusions stated in the abstract and conclusions in the article: analysis of published randomized controlled trials of systemic therapy in lung cancer. J Clin Oncol. 2012;30(28):3552-3557.
12. Decoster LC, Vailas JC, Swartz WG. Functional ACL bracing. A survey of current opinion and practice. Am J Orthop. 1995;24(11):838-843.
13. Mann BJ, Grana WA, Indelicato PA, O’Neill DF, George SZ. A survey of sports medicine physicians regarding psychological issues in patient-athletes. Am J Sports Med. 2007;35(12):2140-2147.
Medial Patellar Subluxation: Diagnosis and Treatment
Medial patellar subluxation (MPS) is a disabling condition caused by an imbalance in the medial and lateral forces in the normal knee, allowing the patella to displace medially. Normally, the patella glides appropriately in the femoral trochlea, but alteration in this medial–lateral equilibrium can lead to pain and instability.1 MPS was first described in 1987 by Betz and colleagues2 as a complication of lateral retinacular release. Since then, multiple cases of iatrogenic, traumatic, and isolated medial subluxation have been reported.3–15 However, MPS after lateral release is the most common cause, accounting for the majority of published cases, whereas only 8 cases of isolated MPS have been reported to date.
Optimal treatment for MPS is not well understood. To better comprehend and manage MPS, we must fully appreciate the pathoanatomy, biomechanics, and current research. In this review, we focus on the anatomy of the lateral retinaculum, diagnosis and treatment of MPS, and outcomes of current treatment techniques.
Anatomy
In 1980, Fulkerson and Gossling16 delineated the anatomy of the knee joint lateral retinaculum. They described a 2-layered system with separate distinct anatomical structures. The lateral retinaculum is oriented longitudinally with the knee extended but exerts a posterolateral force on the lateral aspect of the patella as the knee is flexed. The superficial layer is composed of oblique fibers of the lateral retinaculum originating from the iliotibial band and the vastus lateralis fascia and inserting into the lateral margin of the patella and the patella tendon. The deep layer of the retinaculum consists of several structures, including the deep transverse retinaculum, lateral patellofemoral ligament (LPFL), and the patellotibial band.
Over the years, several studies have described the importance of the lateral retinaculum and, in particular, the LPFL. Examining the functional anatomy of the knee in 1962, Kaplan17 first described the lateral epicondylopatellar ligament as a palpable thickening of the joint capsule. Reider and colleagues18 later named this structure the lateral patellofemoral ligament in their anatomical study of 21 fresh cadaver knees. They described its width as ranging from 3 to 10 mm. In a comprehensive cadaveric study of the LPFL, Navarro and colleagues19,20 found it to be a distinct structure present in all 20 of their dissected specimens. They found its femoral insertion at the lateral epicondyle with a fanlike expansion of the fibers predominantly in the posterior region proximal to the lateral epicondyle. The patellar insertion was found in the posterior half and upper lateral aspect, also with expanded fibers. Mean length of the LPFL is 42.1 mm, and mean width is 16.1 mm.
Medial and lateral forces are balanced in a normal knee, and the patella glides appropriately in the femoral trochlea. Alteration in this medial–lateral equilibrium can lead to pain and instability.1 Normally, the patella lies laterally with the knee extended, but in early flexion the patella moves medially as it engages in the trochlea. As the knee continues to flex, the patella flexes and translates distally.21 By 45°, the patella is fully engaged in the trochlear groove throughout the remainder of the knee’s range of motion (ROM).
Lateral release procedures, as described in the literature, result in sectioning of both layers of the lateral retinaculum. In a biomechanical study, Merican and colleagues22 found that staged release of the lateral retinaculum reduced the medial stability of the patellofemoral joint progressively, making it easier to push the patella medially. At 30° of flexion, the transverse fibers of the midsection of the lateral retinaculum were found to be the main contributor to the lateral restraint of the patella. When the release extends too far proximally, the transverse fibers that anchor the lateral patella and the vastus lateralis oblique tendon to the iliotibial band are disrupted. Subsequent loss of a dynamic muscular pull in the orientation of the lateral stabilizing structures results in medial subluxation in a range from full knee extension to about 30° of flexion.
Furthermore, the attachments of the LPFL and the orientation of its fibers suggest that the LPFL may have a significant role in limiting medial excursion of the patella. Vieira and colleagues23 resected the LPFL in 10 fresh cadaver knees. They noticed that, after resection, the patella spontaneously traveled medially, demonstrating the importance of this ligament in patellar stability. In cases of isolated MPS, there have been no reports of associated pathology, such as muscular imbalance or coronal/rotational malalignment of the lower extremity. With an intact lateral retinaculum, medial subluxation is likely caused by pathology in the normal histologic structure of the LPFL and lateral retinaculum. However, the histologic structure of the LPFL and its contribution to the understanding of the pathoetiology of MPS have not been documented.
Diagnosis
MPS diagnosis can be challenging. Often, clinical examination findings are subtle, and radiographs may not show significant pathology. The most accurate diagnosis is obtained by combining patient history, physical examination findings, imaging studies, and diagnostic arthroscopy.
Patient History
Patients with MPS report chronic pain localized to the inferior medial patella and anterior-medial joint line. Occasionally, they complain of crepitus and intermittent swelling. Other symptoms include pain with knee flexion activity, such as squatting and climbing or descending stairs. Some patients describe episodes of giving way and feelings of instability. Often, they are aware the direction of instability is medial. The pain typically is not relieved by medication, physical therapy, or bracing.
Physical Examination
MPS must be identified by clinical examination. Peripatellar tenderness is typically noted. There is often no effusion or crepitus, but the patella is unstable in early flexion. Active and passive ROM is painful through the first 30° of knee flexion. The patient may have a positive medial apprehension test7 in which he or she experiences apprehension of the patella being subluxated with a medially directed force on the lateral border of the patella.
The gravity subluxation test described by Nonweiler and DeLee6 is useful in detecting MPS after lateral release and indicates that the vastus lateralis muscle has been detached from the patella and that the lateral retinaculum is lax. In this test, the patient is positioned in the lateral decubitus position with the involved knee farthest from the table. In this position, gravity causes the patella to subluxate out of the trochlea. The test is positive for MPS when a voluntary contraction of the quadriceps does not center the patella into the trochlear groove. Patients with MPS without previous lateral release can have the patella subluxate medially in the lateral decubitus position, but it is pulled back into the trochlea with active quadriceps contraction (Figure 1).
Patients with MPS often have lateral patellar laxity (LPL), which allows the patella to rotate upward on the lateral side and skid across the medial facet of the femoral trochlea. A physical examination sign combining lateral patellar glide and tilt was described by Shneider24 to identify LPL. This “lateral patellar float” sign is present when the patella translates laterally and rotates or tilts upward with medial pressure on the patella (Figure 2). Another maneuver to test for subtle MPS involves manually centering the patella in the trochlea during active knee flexion and extension. The involved knee is examined in the seated position. The examiner attempts to center the patella in the trochlea with a laterally directed force from the examiner’s thumb on the medial border of the patella. This will usually provide immediate relief as the patient actively ranges the knee.
Imaging Studies
Diagnostic imaging is a crucial component of the evaluation and treatment decision process. Plain radiographs often are not helpful in diagnosing MPS but may provide additional information.5 A variety of radiographic measurements have been described as indicators of structural disease, but there is a lack of comprehensive information recommending radiographic evaluation and interpretation of patients with patellofemoral dysfunction. It is crucial that orthopedic surgeons have common and consistent radiographic views for plain radiographic assessment that can serve as a basis for accurate diagnosis and surgical decision-making.
Standard knee radiographs should include a standing anteroposterior view of bilateral knees, a standing lateral view of the symptomatic knee in 30° of flexion, a patellar axial view, and a tunnel view. These views, occasionally combined with magnetic resonance imaging (MRI), can yield information vital to surgical decision-making. Image quality is highly technique-dependent, and variability in patient positioning can substantially affect the ability to properly diagnose structural abnormalities. For improved diagnostic accuracy and disease classification, radiographs must be obtained with use of the same standardized imaging protocol.
Kinetic MRI was shown by Shellock and colleagues25 to provide diagnostic information related to patellar malalignment. As kinetic MRI can image the patellofemoral joint within the initial 20° to 30° of flexion, it is useful in detecting some of the more subtle patellar tracking problems. In their study of 43 knees (40 patients) with symptoms after lateral release, Shellock and colleagues25 found that 27 knees (63%) had medial subluxation of the patella as the knee moved from extension to flexion. Furthermore, MPS was noted on the contralateral, unoperated knee in 17 (43%) of the 40 patients.
Diagnostic Arthroscopy
Once MPS is suspected after a thorough history and physical examination, examination under anesthesia accompanied by diagnostic arthroscopy confirms the diagnosis. Lateral forces are applied to the patella in full knee extension and 30° of flexion (Figure 3). During arthroscopy, the patellofemoral compartment is viewed from the anterolateral portal. With the knee at full extension, the lateral laxity and medial tilt of the patella can be identified (Figure 4). As the knee is flexed to 30°, the patella moves medially and can subluxate over the edge of the medial facet of the trochlea (Figure 5).
Treatment
Nonsurgical Management
Treatment of MPS depends entirely on making an accurate diagnosis and determining the degree of impairment. Patients with symptomatic MPS should initially undergo supervised rehabilitation focusing on balancing the medial and lateral forces that influence patellar tracking. Patients should be evaluated for specific muscle tightness, weakness, and biomechanical abnormalities. Each problem should be addressed with an individualized rehabilitation prescription. Emphasis is placed on balance, proprioception, and strengthening of the quadriceps, hip abductors/external rotators, and abdominal core muscle groups.
In some patients, symptomatic MPS may be reduced with a patella-stabilizing brace with a medial buttress.3,5,26 Although bracing should be regarded as an adjuvant to a structured physical therapy program, it can also be helpful in confirming the diagnosis of MPS. Shannon and Keene3 reported that all patients in their study experienced significant pain relief and decreased medial patellar subluxations when they wore a medial patella–stabilizing brace. Shellock and colleagues25 used kinematic MRI to investigate the effect of a patella-realignment brace and found that bracing counteracted patellar subluxation in the majority of knees studied.
Surgical Management
When conservative management fails and patients continue to experience pain and instability, surgical intervention is often required. Although various surgical techniques have been used (Table),3–6,8–10,14,15,27,28 the optimal surgical treatment for MPS has not been identified.
Lateral Retinaculum Imbrication. Lateral retinaculum imbrication has been used to centralize patella tracking and stabilize the patella. Richman and Scheller5 reported on a 17-year-old patient who had isolated medial subluxation of the patella without having undergone a previous lateral release. At 3-month follow-up, there was no recurrent instability; there was only intermittent medial knee soreness with weight-bearing activity.
Lateral Retinaculum Repair/Reconstruction. Hughston and colleagues8 treated 65 knees for MPS. Most had undergone lateral release. Of the 65 knees, 39 were treated with direct repair of the lateral retinaculum, and 26 with reconstruction of the lateral patellotibial ligament using locally available tissue, such as strips of iliotibial band or patellar tendon. Results were good to excellent in 80% of patients at a mean follow-up of 53.7 months. Nonweiler and DeLee6 reconstructed the lateral retinaculum in 5 patients with MPS that developed after isolated lateral retinacular release. Four (80%) of the 5 patients had no symptoms or physical signs of instability at a mean follow-up of 3.3 years. Results were excellent (3 knees) and good (2 knees) according to the Merchant and Mercer rating scale. Akşahin and colleagues28 reported on a single case of spontaneous medial patellar instability. At surgery, imbrication of the lateral structures failed to prevent the medial subluxation. Lateral patellotibial ligament augmentation was performed using an iliotibial band flap that effectively corrected the instability. At 1 year, the patient was characterized as engaging in vigorous recreational activity, according to the clinical score defined by Hughston and colleagues.8 He had mild pain with competitive sports but no pain with daily activity. Abhaykumar and Craig9 reported on 4 surgically treated knees with medial instability. They reconstructed the lateral retinaculum using a strip of fascia lata. By follow-up (5-7 years), each knee had its instability resolved and full ROM restored. Johnson and Wakeley26 reported on a case of iatrogenic MPS after lateral release. Treatment consisted of mobilization and direct repair of the lateral retinaculum. At 12-month follow-up, there was no instability. Although symptom-free with light activity, the patient had patellofemoral pain with strenuous activity. Sanchis-Alfonso and colleagues14 reported the results of isolated lateral retinacular reconstruction for iatrogenic MPS in 17 patients. At mean follow-up of 56 months, results were good or excellent in 65% of patients, and the Lysholm score improved from 36.4 preoperatively to 86.1 postoperatively.
Medial Retinaculum Release. Medial retinaculum release has been used as an alternative to open reconstruction. Shannon and Keene3 reported the results of medial retinacular release procedures on 9 knees. Four (44%) of the 9 patients had either spontaneous or traumatic onset of instability. All cases were treated with arthroscopic medial retinacular release, extending 2 cm medial to the superior pole of the patella down to the anteromedial portal. This avoided releasing the attachment of the vastus medialis oblique muscle to the patella and removing its dynamic medial stabilizing force. At a mean follow-up of 2.7 years, both medial subluxation and knee pain were relieved in all 9 knees without complications or further realignment surgery. Results were excellent in 6 knees (66.7%) and good in 3 knees (33.3%). Shannon and Keene3 emphasized that the procedure should not be used in patients with hypermobile patellae or in cases of failed lateral retinacular releases in which MPS is not clearly and carefully documented.
LPFL Reconstruction. Before coming to our practice, most patients have tried several months of formal physical rehabilitation, medications, and bracing. Many have already had surgical procedures, including arthroscopy, lateral release, and tibial tubercle transfer. When the diagnosis of MPS is suspected after a thorough history and physical examination, LPFL reconstruction is offered. Management of MPS with LPFL reconstruction has yielded excellent and reliable clinical results. Teitge and Torga Spak10 described an LPFL reconstruction technique that is used as a salvage procedure in managing medial iatrogenic patellar instability (the patient’s own quadriceps tendon is used). In their experience, direct repair or imbrication of the lateral retinaculum failed to provide long-term stability because medial excursion usually appeared after 1 year. The 60 patients’ outcomes were excellent with respect to patellar stability, and there were no cases of recurrent subluxation. Borbas and colleagues15 reported a case of LPFL reconstruction in a symptomatic medial subluxated patella resulting from TKA and extended lateral release. Using a free gracilis autograft through patellar bone tunnels to reconstruct the LPFL, the patient was free of pain and very satisfied with the result at 1 year postoperatively. Our current strategy is anatomical reconstruction of the LPFL using a quadriceps tendon graft and no bone tunnels, screws, or anchors in the patella.27 We previously reported a single case of isolated medial instability.4 At 2-year follow-up, there was no recurrent instability, and the functional outcome was excellent. This LPFL reconstruction method has been used in 10 patients with isolated MPS. There has been no residual medial subluxation on follow-up ranging from 3 months to 2 years. Outcome studies are in progress.
Rehabilitation. The initial goal of rehabilitation after surgical reconstruction of the lateral retinaculum or LPFL is to protect the healing soft tissues, restore normal knee ROM, and normalize gait. The knee is immobilized in a brace for weight-bearing activity for 4 to 6 weeks, until limb control is sufficient to prevent rotational stress on the knee. Gradual increase to full weight-bearing without bracing is permitted as quadriceps strength is restored. As motion is regained, strength, balance, and proprioception are emphasized for the entire lower extremity and core.
Functional limb training, including rotational activity, begins at 12 weeks. As strength and neuromuscular control progress, single-leg activity may be started with particular attention to proper alignment of the pelvis and the entire lower extremity. For competitive or recreational athletes, the final stages of rehabilitation focus on dynamic lower extremity control during sport-specific movements. Patients return to unrestricted activity by 6 months to 1 year after surgery.
Summary
MPS is a disabling condition that can limit daily functional activity because of apprehension and pain. Initially described as a complication of lateral retinacular release, isolated MPS can occur in the absence of a previous lateral release. Thorough physical examination and identification during arthroscopy are crucial for proper MPS diagnosis and management. When nonsurgical measures fail, LPFL reconstruction can provide patellofemoral stability and excellent functional outcomes.
1. Marumoto JM, Jordan C, Akins R. A biomechanical comparison of lateral retinacular releases. Am J Sports Med. 1995;23(2):151-155.
2. Betz RR, Magill JT, Lonergan RP. The percutaneous lateral retinacular release. Am J Sports Med. 1987;15(5):477-482.
3. Shannon BD, Keene JS. Results of arthroscopic medial retinacular release for treatment of medial subluxation of the patella. Am J Sports Med. 2007;35(7):1180-1187.
4. Saper MG, Shneider DA. Medial patellar subluxation without previous lateral release: a case report. J Pediatr Orthop B. 2014;23(4):350-353.
5. Richman NM, Scheller AD Jr. Medial subluxation of the patella without previous lateral retinacular release. Orthopedics. 1998;21(7):810-813.
6. Nonweiler DE, DeLee JC. The diagnosis and treatment of medial subluxation of the patella after lateral retinacular release. Am J Sports Med. 1994;22(5):680-686.
7. Hughston JC, Deese M. Medial subluxation of the patella as a complication of lateral retinacular release. Am J Sports Med. 1988;16(4):383-388.
8. Hughston JC, Flandry F, Brinker MR, Terry GC, Mills JC 3rd. Surgical correction of medial subluxation of the patella. Am J Sports Med. 1996;24(4):486-491.
9. Abhaykumar S, Craig DM. Fascia lata sling reconstruction for recurrent medial dislocation of the patella. The Knee. 1999;6(1):55-57.
10. Teitge RA, Torga Spak R. Lateral patellofemoral ligament reconstruction. Arthroscopy. 2004;20(9):998-1002.
11. Kusano M, Horibe S, Tanaka Y, et al. Simultaneous MPFL and LPFL reconstruction for recurrent lateral patellar dislocation with medial patellofemoral instability. Asia-Pac J Sports Med Arthrosc Rehabil Technol. 2014;1:42-46.
12. Saper MG, Shneider DA. Simultaneous medial and lateral patellofemoral ligament reconstruction for combined medial and lateral patellar subluxation. Arthrosc Tech. 2014,3(2):e227-e231.
13. Udagawa K, Niki Y, Matsumoto H, et al. Lateral patellar retinaculum reconstruction for medial patellar instability following lateral retinacular release: a case report. Knee. 2014;21(1):336-339.
14. Sanchis-Alfonso V, Montesinos-Berry E, Monllau JC, Merchant AC. Results of isolated lateral retinacular reconstruction for iatrogenic medial patellar instability. Arthroscopy. 2015;31(3):422-427.
15. Borbas P, Koch PP, Fucentese SF. Lateral patellofemoral ligament reconstruction using a free gracilis autograft. Orthopedics. 2014;37(7):e665-e668.
16. Fulkerson JP, Gossling H. Anatomy of the knee joint lateral retinaculum. Clin Orthop Relat Res. 1980;153:183-188.
17. Kaplan E. Some aspects of functional anatomy of the human knee joint. Clin Orthop Relat Res. 1962;23:18-29.
18. Reider B, Marshall J, Koslin B, Ring B, Girgis F. The anterior aspect of the knee joint. J Bone Joint Surg Am. 1981;63(3):351-356.
19. Navarro MS, Navarro RD, Akita Junior J, Cohen M. Anatomical study of the lateral patellofemoral ligament in cadaver knees. Rev Bras Ortop. 2008;43(7):300-307.
20. Navarro MS, Beltrani Filho CA, Akita Junior J, Navarro RD, Cohen M. Relationship between the lateral patellofemoral ligament and the width of the lateral patellar facet. Acta Ortop Bras. 2010;18(1):19-22.
21. Salsich GB, Ward SR, Terk MR, Powers CM. In vivo assessment of patellofemoral joint contact area in individuals who are pain free. Clin Orthop Relat Res. 2003;417:277-284.
22. Merican AM, Kondo E, Amis AA. The effect on patellofemoral joint stability of selective cutting of lateral retinacular and capsular structures. J Biomech. 2009;42(3):291-296.
23. Vieira EL, Vieira EÁ, da Silva RT, Berlfein PA, Abdalla RJ, Cohen M. An anatomic study of the iliotibial tract. Arthroscopy. 2007;23(3):269-274.
24. Shneider DA. Lateral patellar laxity—identification, significance, treatment. Poster session presented at: Annual Meeting of the American Academy of Orthopaedic Surgeons; February 25-28, 2009; Las Vegas, NV.
25. Shellock FG, Mink JH, Deutsch A, Fox JM, Ferkel RD. Evaluation of patients with persistent symptoms after lateral retinacular release by kinematic magnetic resonance imaging of the patellofemoral joint. Arthroscopy. 1990;6(3):226-234.
26. Johnson DP, Wakeley C. Reconstruction of the lateral patellar retinaculum following lateral release: a case report. Knee Surg Sports Traumatol Arthrosc. 2002;10(6):361-363.
27. Saper MG, Shneider DA. Lateral patellofemoral ligament reconstruction using a quadriceps tendon graft. Arthrosc Tech. 2014;3(4):e445-e448.
28. Akşahin E, Yumrukçal F, Yüksel HY, Doğruyol D, Celebi L. Role of pathophysiology of patellofemoral instability in the treatment of spontaneous medial patellofemoral subluxation: a case report. J Med Case Rep. 2010;4:148.
Medial patellar subluxation (MPS) is a disabling condition caused by an imbalance in the medial and lateral forces in the normal knee, allowing the patella to displace medially. Normally, the patella glides appropriately in the femoral trochlea, but alteration in this medial–lateral equilibrium can lead to pain and instability.1 MPS was first described in 1987 by Betz and colleagues2 as a complication of lateral retinacular release. Since then, multiple cases of iatrogenic, traumatic, and isolated medial subluxation have been reported.3–15 However, MPS after lateral release is the most common cause, accounting for the majority of published cases, whereas only 8 cases of isolated MPS have been reported to date.
Optimal treatment for MPS is not well understood. To better comprehend and manage MPS, we must fully appreciate the pathoanatomy, biomechanics, and current research. In this review, we focus on the anatomy of the lateral retinaculum, diagnosis and treatment of MPS, and outcomes of current treatment techniques.
Anatomy
In 1980, Fulkerson and Gossling16 delineated the anatomy of the knee joint lateral retinaculum. They described a 2-layered system with separate distinct anatomical structures. The lateral retinaculum is oriented longitudinally with the knee extended but exerts a posterolateral force on the lateral aspect of the patella as the knee is flexed. The superficial layer is composed of oblique fibers of the lateral retinaculum originating from the iliotibial band and the vastus lateralis fascia and inserting into the lateral margin of the patella and the patella tendon. The deep layer of the retinaculum consists of several structures, including the deep transverse retinaculum, lateral patellofemoral ligament (LPFL), and the patellotibial band.
Over the years, several studies have described the importance of the lateral retinaculum and, in particular, the LPFL. Examining the functional anatomy of the knee in 1962, Kaplan17 first described the lateral epicondylopatellar ligament as a palpable thickening of the joint capsule. Reider and colleagues18 later named this structure the lateral patellofemoral ligament in their anatomical study of 21 fresh cadaver knees. They described its width as ranging from 3 to 10 mm. In a comprehensive cadaveric study of the LPFL, Navarro and colleagues19,20 found it to be a distinct structure present in all 20 of their dissected specimens. They found its femoral insertion at the lateral epicondyle with a fanlike expansion of the fibers predominantly in the posterior region proximal to the lateral epicondyle. The patellar insertion was found in the posterior half and upper lateral aspect, also with expanded fibers. Mean length of the LPFL is 42.1 mm, and mean width is 16.1 mm.
Medial and lateral forces are balanced in a normal knee, and the patella glides appropriately in the femoral trochlea. Alteration in this medial–lateral equilibrium can lead to pain and instability.1 Normally, the patella lies laterally with the knee extended, but in early flexion the patella moves medially as it engages in the trochlea. As the knee continues to flex, the patella flexes and translates distally.21 By 45°, the patella is fully engaged in the trochlear groove throughout the remainder of the knee’s range of motion (ROM).
Lateral release procedures, as described in the literature, result in sectioning of both layers of the lateral retinaculum. In a biomechanical study, Merican and colleagues22 found that staged release of the lateral retinaculum reduced the medial stability of the patellofemoral joint progressively, making it easier to push the patella medially. At 30° of flexion, the transverse fibers of the midsection of the lateral retinaculum were found to be the main contributor to the lateral restraint of the patella. When the release extends too far proximally, the transverse fibers that anchor the lateral patella and the vastus lateralis oblique tendon to the iliotibial band are disrupted. Subsequent loss of a dynamic muscular pull in the orientation of the lateral stabilizing structures results in medial subluxation in a range from full knee extension to about 30° of flexion.
Furthermore, the attachments of the LPFL and the orientation of its fibers suggest that the LPFL may have a significant role in limiting medial excursion of the patella. Vieira and colleagues23 resected the LPFL in 10 fresh cadaver knees. They noticed that, after resection, the patella spontaneously traveled medially, demonstrating the importance of this ligament in patellar stability. In cases of isolated MPS, there have been no reports of associated pathology, such as muscular imbalance or coronal/rotational malalignment of the lower extremity. With an intact lateral retinaculum, medial subluxation is likely caused by pathology in the normal histologic structure of the LPFL and lateral retinaculum. However, the histologic structure of the LPFL and its contribution to the understanding of the pathoetiology of MPS have not been documented.
Diagnosis
MPS diagnosis can be challenging. Often, clinical examination findings are subtle, and radiographs may not show significant pathology. The most accurate diagnosis is obtained by combining patient history, physical examination findings, imaging studies, and diagnostic arthroscopy.
Patient History
Patients with MPS report chronic pain localized to the inferior medial patella and anterior-medial joint line. Occasionally, they complain of crepitus and intermittent swelling. Other symptoms include pain with knee flexion activity, such as squatting and climbing or descending stairs. Some patients describe episodes of giving way and feelings of instability. Often, they are aware the direction of instability is medial. The pain typically is not relieved by medication, physical therapy, or bracing.
Physical Examination
MPS must be identified by clinical examination. Peripatellar tenderness is typically noted. There is often no effusion or crepitus, but the patella is unstable in early flexion. Active and passive ROM is painful through the first 30° of knee flexion. The patient may have a positive medial apprehension test7 in which he or she experiences apprehension of the patella being subluxated with a medially directed force on the lateral border of the patella.
The gravity subluxation test described by Nonweiler and DeLee6 is useful in detecting MPS after lateral release and indicates that the vastus lateralis muscle has been detached from the patella and that the lateral retinaculum is lax. In this test, the patient is positioned in the lateral decubitus position with the involved knee farthest from the table. In this position, gravity causes the patella to subluxate out of the trochlea. The test is positive for MPS when a voluntary contraction of the quadriceps does not center the patella into the trochlear groove. Patients with MPS without previous lateral release can have the patella subluxate medially in the lateral decubitus position, but it is pulled back into the trochlea with active quadriceps contraction (Figure 1).
Patients with MPS often have lateral patellar laxity (LPL), which allows the patella to rotate upward on the lateral side and skid across the medial facet of the femoral trochlea. A physical examination sign combining lateral patellar glide and tilt was described by Shneider24 to identify LPL. This “lateral patellar float” sign is present when the patella translates laterally and rotates or tilts upward with medial pressure on the patella (Figure 2). Another maneuver to test for subtle MPS involves manually centering the patella in the trochlea during active knee flexion and extension. The involved knee is examined in the seated position. The examiner attempts to center the patella in the trochlea with a laterally directed force from the examiner’s thumb on the medial border of the patella. This will usually provide immediate relief as the patient actively ranges the knee.
Imaging Studies
Diagnostic imaging is a crucial component of the evaluation and treatment decision process. Plain radiographs often are not helpful in diagnosing MPS but may provide additional information.5 A variety of radiographic measurements have been described as indicators of structural disease, but there is a lack of comprehensive information recommending radiographic evaluation and interpretation of patients with patellofemoral dysfunction. It is crucial that orthopedic surgeons have common and consistent radiographic views for plain radiographic assessment that can serve as a basis for accurate diagnosis and surgical decision-making.
Standard knee radiographs should include a standing anteroposterior view of bilateral knees, a standing lateral view of the symptomatic knee in 30° of flexion, a patellar axial view, and a tunnel view. These views, occasionally combined with magnetic resonance imaging (MRI), can yield information vital to surgical decision-making. Image quality is highly technique-dependent, and variability in patient positioning can substantially affect the ability to properly diagnose structural abnormalities. For improved diagnostic accuracy and disease classification, radiographs must be obtained with use of the same standardized imaging protocol.
Kinetic MRI was shown by Shellock and colleagues25 to provide diagnostic information related to patellar malalignment. As kinetic MRI can image the patellofemoral joint within the initial 20° to 30° of flexion, it is useful in detecting some of the more subtle patellar tracking problems. In their study of 43 knees (40 patients) with symptoms after lateral release, Shellock and colleagues25 found that 27 knees (63%) had medial subluxation of the patella as the knee moved from extension to flexion. Furthermore, MPS was noted on the contralateral, unoperated knee in 17 (43%) of the 40 patients.
Diagnostic Arthroscopy
Once MPS is suspected after a thorough history and physical examination, examination under anesthesia accompanied by diagnostic arthroscopy confirms the diagnosis. Lateral forces are applied to the patella in full knee extension and 30° of flexion (Figure 3). During arthroscopy, the patellofemoral compartment is viewed from the anterolateral portal. With the knee at full extension, the lateral laxity and medial tilt of the patella can be identified (Figure 4). As the knee is flexed to 30°, the patella moves medially and can subluxate over the edge of the medial facet of the trochlea (Figure 5).
Treatment
Nonsurgical Management
Treatment of MPS depends entirely on making an accurate diagnosis and determining the degree of impairment. Patients with symptomatic MPS should initially undergo supervised rehabilitation focusing on balancing the medial and lateral forces that influence patellar tracking. Patients should be evaluated for specific muscle tightness, weakness, and biomechanical abnormalities. Each problem should be addressed with an individualized rehabilitation prescription. Emphasis is placed on balance, proprioception, and strengthening of the quadriceps, hip abductors/external rotators, and abdominal core muscle groups.
In some patients, symptomatic MPS may be reduced with a patella-stabilizing brace with a medial buttress.3,5,26 Although bracing should be regarded as an adjuvant to a structured physical therapy program, it can also be helpful in confirming the diagnosis of MPS. Shannon and Keene3 reported that all patients in their study experienced significant pain relief and decreased medial patellar subluxations when they wore a medial patella–stabilizing brace. Shellock and colleagues25 used kinematic MRI to investigate the effect of a patella-realignment brace and found that bracing counteracted patellar subluxation in the majority of knees studied.
Surgical Management
When conservative management fails and patients continue to experience pain and instability, surgical intervention is often required. Although various surgical techniques have been used (Table),3–6,8–10,14,15,27,28 the optimal surgical treatment for MPS has not been identified.
Lateral Retinaculum Imbrication. Lateral retinaculum imbrication has been used to centralize patella tracking and stabilize the patella. Richman and Scheller5 reported on a 17-year-old patient who had isolated medial subluxation of the patella without having undergone a previous lateral release. At 3-month follow-up, there was no recurrent instability; there was only intermittent medial knee soreness with weight-bearing activity.
Lateral Retinaculum Repair/Reconstruction. Hughston and colleagues8 treated 65 knees for MPS. Most had undergone lateral release. Of the 65 knees, 39 were treated with direct repair of the lateral retinaculum, and 26 with reconstruction of the lateral patellotibial ligament using locally available tissue, such as strips of iliotibial band or patellar tendon. Results were good to excellent in 80% of patients at a mean follow-up of 53.7 months. Nonweiler and DeLee6 reconstructed the lateral retinaculum in 5 patients with MPS that developed after isolated lateral retinacular release. Four (80%) of the 5 patients had no symptoms or physical signs of instability at a mean follow-up of 3.3 years. Results were excellent (3 knees) and good (2 knees) according to the Merchant and Mercer rating scale. Akşahin and colleagues28 reported on a single case of spontaneous medial patellar instability. At surgery, imbrication of the lateral structures failed to prevent the medial subluxation. Lateral patellotibial ligament augmentation was performed using an iliotibial band flap that effectively corrected the instability. At 1 year, the patient was characterized as engaging in vigorous recreational activity, according to the clinical score defined by Hughston and colleagues.8 He had mild pain with competitive sports but no pain with daily activity. Abhaykumar and Craig9 reported on 4 surgically treated knees with medial instability. They reconstructed the lateral retinaculum using a strip of fascia lata. By follow-up (5-7 years), each knee had its instability resolved and full ROM restored. Johnson and Wakeley26 reported on a case of iatrogenic MPS after lateral release. Treatment consisted of mobilization and direct repair of the lateral retinaculum. At 12-month follow-up, there was no instability. Although symptom-free with light activity, the patient had patellofemoral pain with strenuous activity. Sanchis-Alfonso and colleagues14 reported the results of isolated lateral retinacular reconstruction for iatrogenic MPS in 17 patients. At mean follow-up of 56 months, results were good or excellent in 65% of patients, and the Lysholm score improved from 36.4 preoperatively to 86.1 postoperatively.
Medial Retinaculum Release. Medial retinaculum release has been used as an alternative to open reconstruction. Shannon and Keene3 reported the results of medial retinacular release procedures on 9 knees. Four (44%) of the 9 patients had either spontaneous or traumatic onset of instability. All cases were treated with arthroscopic medial retinacular release, extending 2 cm medial to the superior pole of the patella down to the anteromedial portal. This avoided releasing the attachment of the vastus medialis oblique muscle to the patella and removing its dynamic medial stabilizing force. At a mean follow-up of 2.7 years, both medial subluxation and knee pain were relieved in all 9 knees without complications or further realignment surgery. Results were excellent in 6 knees (66.7%) and good in 3 knees (33.3%). Shannon and Keene3 emphasized that the procedure should not be used in patients with hypermobile patellae or in cases of failed lateral retinacular releases in which MPS is not clearly and carefully documented.
LPFL Reconstruction. Before coming to our practice, most patients have tried several months of formal physical rehabilitation, medications, and bracing. Many have already had surgical procedures, including arthroscopy, lateral release, and tibial tubercle transfer. When the diagnosis of MPS is suspected after a thorough history and physical examination, LPFL reconstruction is offered. Management of MPS with LPFL reconstruction has yielded excellent and reliable clinical results. Teitge and Torga Spak10 described an LPFL reconstruction technique that is used as a salvage procedure in managing medial iatrogenic patellar instability (the patient’s own quadriceps tendon is used). In their experience, direct repair or imbrication of the lateral retinaculum failed to provide long-term stability because medial excursion usually appeared after 1 year. The 60 patients’ outcomes were excellent with respect to patellar stability, and there were no cases of recurrent subluxation. Borbas and colleagues15 reported a case of LPFL reconstruction in a symptomatic medial subluxated patella resulting from TKA and extended lateral release. Using a free gracilis autograft through patellar bone tunnels to reconstruct the LPFL, the patient was free of pain and very satisfied with the result at 1 year postoperatively. Our current strategy is anatomical reconstruction of the LPFL using a quadriceps tendon graft and no bone tunnels, screws, or anchors in the patella.27 We previously reported a single case of isolated medial instability.4 At 2-year follow-up, there was no recurrent instability, and the functional outcome was excellent. This LPFL reconstruction method has been used in 10 patients with isolated MPS. There has been no residual medial subluxation on follow-up ranging from 3 months to 2 years. Outcome studies are in progress.
Rehabilitation. The initial goal of rehabilitation after surgical reconstruction of the lateral retinaculum or LPFL is to protect the healing soft tissues, restore normal knee ROM, and normalize gait. The knee is immobilized in a brace for weight-bearing activity for 4 to 6 weeks, until limb control is sufficient to prevent rotational stress on the knee. Gradual increase to full weight-bearing without bracing is permitted as quadriceps strength is restored. As motion is regained, strength, balance, and proprioception are emphasized for the entire lower extremity and core.
Functional limb training, including rotational activity, begins at 12 weeks. As strength and neuromuscular control progress, single-leg activity may be started with particular attention to proper alignment of the pelvis and the entire lower extremity. For competitive or recreational athletes, the final stages of rehabilitation focus on dynamic lower extremity control during sport-specific movements. Patients return to unrestricted activity by 6 months to 1 year after surgery.
Summary
MPS is a disabling condition that can limit daily functional activity because of apprehension and pain. Initially described as a complication of lateral retinacular release, isolated MPS can occur in the absence of a previous lateral release. Thorough physical examination and identification during arthroscopy are crucial for proper MPS diagnosis and management. When nonsurgical measures fail, LPFL reconstruction can provide patellofemoral stability and excellent functional outcomes.
Medial patellar subluxation (MPS) is a disabling condition caused by an imbalance in the medial and lateral forces in the normal knee, allowing the patella to displace medially. Normally, the patella glides appropriately in the femoral trochlea, but alteration in this medial–lateral equilibrium can lead to pain and instability.1 MPS was first described in 1987 by Betz and colleagues2 as a complication of lateral retinacular release. Since then, multiple cases of iatrogenic, traumatic, and isolated medial subluxation have been reported.3–15 However, MPS after lateral release is the most common cause, accounting for the majority of published cases, whereas only 8 cases of isolated MPS have been reported to date.
Optimal treatment for MPS is not well understood. To better comprehend and manage MPS, we must fully appreciate the pathoanatomy, biomechanics, and current research. In this review, we focus on the anatomy of the lateral retinaculum, diagnosis and treatment of MPS, and outcomes of current treatment techniques.
Anatomy
In 1980, Fulkerson and Gossling16 delineated the anatomy of the knee joint lateral retinaculum. They described a 2-layered system with separate distinct anatomical structures. The lateral retinaculum is oriented longitudinally with the knee extended but exerts a posterolateral force on the lateral aspect of the patella as the knee is flexed. The superficial layer is composed of oblique fibers of the lateral retinaculum originating from the iliotibial band and the vastus lateralis fascia and inserting into the lateral margin of the patella and the patella tendon. The deep layer of the retinaculum consists of several structures, including the deep transverse retinaculum, lateral patellofemoral ligament (LPFL), and the patellotibial band.
Over the years, several studies have described the importance of the lateral retinaculum and, in particular, the LPFL. Examining the functional anatomy of the knee in 1962, Kaplan17 first described the lateral epicondylopatellar ligament as a palpable thickening of the joint capsule. Reider and colleagues18 later named this structure the lateral patellofemoral ligament in their anatomical study of 21 fresh cadaver knees. They described its width as ranging from 3 to 10 mm. In a comprehensive cadaveric study of the LPFL, Navarro and colleagues19,20 found it to be a distinct structure present in all 20 of their dissected specimens. They found its femoral insertion at the lateral epicondyle with a fanlike expansion of the fibers predominantly in the posterior region proximal to the lateral epicondyle. The patellar insertion was found in the posterior half and upper lateral aspect, also with expanded fibers. Mean length of the LPFL is 42.1 mm, and mean width is 16.1 mm.
Medial and lateral forces are balanced in a normal knee, and the patella glides appropriately in the femoral trochlea. Alteration in this medial–lateral equilibrium can lead to pain and instability.1 Normally, the patella lies laterally with the knee extended, but in early flexion the patella moves medially as it engages in the trochlea. As the knee continues to flex, the patella flexes and translates distally.21 By 45°, the patella is fully engaged in the trochlear groove throughout the remainder of the knee’s range of motion (ROM).
Lateral release procedures, as described in the literature, result in sectioning of both layers of the lateral retinaculum. In a biomechanical study, Merican and colleagues22 found that staged release of the lateral retinaculum reduced the medial stability of the patellofemoral joint progressively, making it easier to push the patella medially. At 30° of flexion, the transverse fibers of the midsection of the lateral retinaculum were found to be the main contributor to the lateral restraint of the patella. When the release extends too far proximally, the transverse fibers that anchor the lateral patella and the vastus lateralis oblique tendon to the iliotibial band are disrupted. Subsequent loss of a dynamic muscular pull in the orientation of the lateral stabilizing structures results in medial subluxation in a range from full knee extension to about 30° of flexion.
Furthermore, the attachments of the LPFL and the orientation of its fibers suggest that the LPFL may have a significant role in limiting medial excursion of the patella. Vieira and colleagues23 resected the LPFL in 10 fresh cadaver knees. They noticed that, after resection, the patella spontaneously traveled medially, demonstrating the importance of this ligament in patellar stability. In cases of isolated MPS, there have been no reports of associated pathology, such as muscular imbalance or coronal/rotational malalignment of the lower extremity. With an intact lateral retinaculum, medial subluxation is likely caused by pathology in the normal histologic structure of the LPFL and lateral retinaculum. However, the histologic structure of the LPFL and its contribution to the understanding of the pathoetiology of MPS have not been documented.
Diagnosis
MPS diagnosis can be challenging. Often, clinical examination findings are subtle, and radiographs may not show significant pathology. The most accurate diagnosis is obtained by combining patient history, physical examination findings, imaging studies, and diagnostic arthroscopy.
Patient History
Patients with MPS report chronic pain localized to the inferior medial patella and anterior-medial joint line. Occasionally, they complain of crepitus and intermittent swelling. Other symptoms include pain with knee flexion activity, such as squatting and climbing or descending stairs. Some patients describe episodes of giving way and feelings of instability. Often, they are aware the direction of instability is medial. The pain typically is not relieved by medication, physical therapy, or bracing.
Physical Examination
MPS must be identified by clinical examination. Peripatellar tenderness is typically noted. There is often no effusion or crepitus, but the patella is unstable in early flexion. Active and passive ROM is painful through the first 30° of knee flexion. The patient may have a positive medial apprehension test7 in which he or she experiences apprehension of the patella being subluxated with a medially directed force on the lateral border of the patella.
The gravity subluxation test described by Nonweiler and DeLee6 is useful in detecting MPS after lateral release and indicates that the vastus lateralis muscle has been detached from the patella and that the lateral retinaculum is lax. In this test, the patient is positioned in the lateral decubitus position with the involved knee farthest from the table. In this position, gravity causes the patella to subluxate out of the trochlea. The test is positive for MPS when a voluntary contraction of the quadriceps does not center the patella into the trochlear groove. Patients with MPS without previous lateral release can have the patella subluxate medially in the lateral decubitus position, but it is pulled back into the trochlea with active quadriceps contraction (Figure 1).
Patients with MPS often have lateral patellar laxity (LPL), which allows the patella to rotate upward on the lateral side and skid across the medial facet of the femoral trochlea. A physical examination sign combining lateral patellar glide and tilt was described by Shneider24 to identify LPL. This “lateral patellar float” sign is present when the patella translates laterally and rotates or tilts upward with medial pressure on the patella (Figure 2). Another maneuver to test for subtle MPS involves manually centering the patella in the trochlea during active knee flexion and extension. The involved knee is examined in the seated position. The examiner attempts to center the patella in the trochlea with a laterally directed force from the examiner’s thumb on the medial border of the patella. This will usually provide immediate relief as the patient actively ranges the knee.
Imaging Studies
Diagnostic imaging is a crucial component of the evaluation and treatment decision process. Plain radiographs often are not helpful in diagnosing MPS but may provide additional information.5 A variety of radiographic measurements have been described as indicators of structural disease, but there is a lack of comprehensive information recommending radiographic evaluation and interpretation of patients with patellofemoral dysfunction. It is crucial that orthopedic surgeons have common and consistent radiographic views for plain radiographic assessment that can serve as a basis for accurate diagnosis and surgical decision-making.
Standard knee radiographs should include a standing anteroposterior view of bilateral knees, a standing lateral view of the symptomatic knee in 30° of flexion, a patellar axial view, and a tunnel view. These views, occasionally combined with magnetic resonance imaging (MRI), can yield information vital to surgical decision-making. Image quality is highly technique-dependent, and variability in patient positioning can substantially affect the ability to properly diagnose structural abnormalities. For improved diagnostic accuracy and disease classification, radiographs must be obtained with use of the same standardized imaging protocol.
Kinetic MRI was shown by Shellock and colleagues25 to provide diagnostic information related to patellar malalignment. As kinetic MRI can image the patellofemoral joint within the initial 20° to 30° of flexion, it is useful in detecting some of the more subtle patellar tracking problems. In their study of 43 knees (40 patients) with symptoms after lateral release, Shellock and colleagues25 found that 27 knees (63%) had medial subluxation of the patella as the knee moved from extension to flexion. Furthermore, MPS was noted on the contralateral, unoperated knee in 17 (43%) of the 40 patients.
Diagnostic Arthroscopy
Once MPS is suspected after a thorough history and physical examination, examination under anesthesia accompanied by diagnostic arthroscopy confirms the diagnosis. Lateral forces are applied to the patella in full knee extension and 30° of flexion (Figure 3). During arthroscopy, the patellofemoral compartment is viewed from the anterolateral portal. With the knee at full extension, the lateral laxity and medial tilt of the patella can be identified (Figure 4). As the knee is flexed to 30°, the patella moves medially and can subluxate over the edge of the medial facet of the trochlea (Figure 5).
Treatment
Nonsurgical Management
Treatment of MPS depends entirely on making an accurate diagnosis and determining the degree of impairment. Patients with symptomatic MPS should initially undergo supervised rehabilitation focusing on balancing the medial and lateral forces that influence patellar tracking. Patients should be evaluated for specific muscle tightness, weakness, and biomechanical abnormalities. Each problem should be addressed with an individualized rehabilitation prescription. Emphasis is placed on balance, proprioception, and strengthening of the quadriceps, hip abductors/external rotators, and abdominal core muscle groups.
In some patients, symptomatic MPS may be reduced with a patella-stabilizing brace with a medial buttress.3,5,26 Although bracing should be regarded as an adjuvant to a structured physical therapy program, it can also be helpful in confirming the diagnosis of MPS. Shannon and Keene3 reported that all patients in their study experienced significant pain relief and decreased medial patellar subluxations when they wore a medial patella–stabilizing brace. Shellock and colleagues25 used kinematic MRI to investigate the effect of a patella-realignment brace and found that bracing counteracted patellar subluxation in the majority of knees studied.
Surgical Management
When conservative management fails and patients continue to experience pain and instability, surgical intervention is often required. Although various surgical techniques have been used (Table),3–6,8–10,14,15,27,28 the optimal surgical treatment for MPS has not been identified.
Lateral Retinaculum Imbrication. Lateral retinaculum imbrication has been used to centralize patella tracking and stabilize the patella. Richman and Scheller5 reported on a 17-year-old patient who had isolated medial subluxation of the patella without having undergone a previous lateral release. At 3-month follow-up, there was no recurrent instability; there was only intermittent medial knee soreness with weight-bearing activity.
Lateral Retinaculum Repair/Reconstruction. Hughston and colleagues8 treated 65 knees for MPS. Most had undergone lateral release. Of the 65 knees, 39 were treated with direct repair of the lateral retinaculum, and 26 with reconstruction of the lateral patellotibial ligament using locally available tissue, such as strips of iliotibial band or patellar tendon. Results were good to excellent in 80% of patients at a mean follow-up of 53.7 months. Nonweiler and DeLee6 reconstructed the lateral retinaculum in 5 patients with MPS that developed after isolated lateral retinacular release. Four (80%) of the 5 patients had no symptoms or physical signs of instability at a mean follow-up of 3.3 years. Results were excellent (3 knees) and good (2 knees) according to the Merchant and Mercer rating scale. Akşahin and colleagues28 reported on a single case of spontaneous medial patellar instability. At surgery, imbrication of the lateral structures failed to prevent the medial subluxation. Lateral patellotibial ligament augmentation was performed using an iliotibial band flap that effectively corrected the instability. At 1 year, the patient was characterized as engaging in vigorous recreational activity, according to the clinical score defined by Hughston and colleagues.8 He had mild pain with competitive sports but no pain with daily activity. Abhaykumar and Craig9 reported on 4 surgically treated knees with medial instability. They reconstructed the lateral retinaculum using a strip of fascia lata. By follow-up (5-7 years), each knee had its instability resolved and full ROM restored. Johnson and Wakeley26 reported on a case of iatrogenic MPS after lateral release. Treatment consisted of mobilization and direct repair of the lateral retinaculum. At 12-month follow-up, there was no instability. Although symptom-free with light activity, the patient had patellofemoral pain with strenuous activity. Sanchis-Alfonso and colleagues14 reported the results of isolated lateral retinacular reconstruction for iatrogenic MPS in 17 patients. At mean follow-up of 56 months, results were good or excellent in 65% of patients, and the Lysholm score improved from 36.4 preoperatively to 86.1 postoperatively.
Medial Retinaculum Release. Medial retinaculum release has been used as an alternative to open reconstruction. Shannon and Keene3 reported the results of medial retinacular release procedures on 9 knees. Four (44%) of the 9 patients had either spontaneous or traumatic onset of instability. All cases were treated with arthroscopic medial retinacular release, extending 2 cm medial to the superior pole of the patella down to the anteromedial portal. This avoided releasing the attachment of the vastus medialis oblique muscle to the patella and removing its dynamic medial stabilizing force. At a mean follow-up of 2.7 years, both medial subluxation and knee pain were relieved in all 9 knees without complications or further realignment surgery. Results were excellent in 6 knees (66.7%) and good in 3 knees (33.3%). Shannon and Keene3 emphasized that the procedure should not be used in patients with hypermobile patellae or in cases of failed lateral retinacular releases in which MPS is not clearly and carefully documented.
LPFL Reconstruction. Before coming to our practice, most patients have tried several months of formal physical rehabilitation, medications, and bracing. Many have already had surgical procedures, including arthroscopy, lateral release, and tibial tubercle transfer. When the diagnosis of MPS is suspected after a thorough history and physical examination, LPFL reconstruction is offered. Management of MPS with LPFL reconstruction has yielded excellent and reliable clinical results. Teitge and Torga Spak10 described an LPFL reconstruction technique that is used as a salvage procedure in managing medial iatrogenic patellar instability (the patient’s own quadriceps tendon is used). In their experience, direct repair or imbrication of the lateral retinaculum failed to provide long-term stability because medial excursion usually appeared after 1 year. The 60 patients’ outcomes were excellent with respect to patellar stability, and there were no cases of recurrent subluxation. Borbas and colleagues15 reported a case of LPFL reconstruction in a symptomatic medial subluxated patella resulting from TKA and extended lateral release. Using a free gracilis autograft through patellar bone tunnels to reconstruct the LPFL, the patient was free of pain and very satisfied with the result at 1 year postoperatively. Our current strategy is anatomical reconstruction of the LPFL using a quadriceps tendon graft and no bone tunnels, screws, or anchors in the patella.27 We previously reported a single case of isolated medial instability.4 At 2-year follow-up, there was no recurrent instability, and the functional outcome was excellent. This LPFL reconstruction method has been used in 10 patients with isolated MPS. There has been no residual medial subluxation on follow-up ranging from 3 months to 2 years. Outcome studies are in progress.
Rehabilitation. The initial goal of rehabilitation after surgical reconstruction of the lateral retinaculum or LPFL is to protect the healing soft tissues, restore normal knee ROM, and normalize gait. The knee is immobilized in a brace for weight-bearing activity for 4 to 6 weeks, until limb control is sufficient to prevent rotational stress on the knee. Gradual increase to full weight-bearing without bracing is permitted as quadriceps strength is restored. As motion is regained, strength, balance, and proprioception are emphasized for the entire lower extremity and core.
Functional limb training, including rotational activity, begins at 12 weeks. As strength and neuromuscular control progress, single-leg activity may be started with particular attention to proper alignment of the pelvis and the entire lower extremity. For competitive or recreational athletes, the final stages of rehabilitation focus on dynamic lower extremity control during sport-specific movements. Patients return to unrestricted activity by 6 months to 1 year after surgery.
Summary
MPS is a disabling condition that can limit daily functional activity because of apprehension and pain. Initially described as a complication of lateral retinacular release, isolated MPS can occur in the absence of a previous lateral release. Thorough physical examination and identification during arthroscopy are crucial for proper MPS diagnosis and management. When nonsurgical measures fail, LPFL reconstruction can provide patellofemoral stability and excellent functional outcomes.
1. Marumoto JM, Jordan C, Akins R. A biomechanical comparison of lateral retinacular releases. Am J Sports Med. 1995;23(2):151-155.
2. Betz RR, Magill JT, Lonergan RP. The percutaneous lateral retinacular release. Am J Sports Med. 1987;15(5):477-482.
3. Shannon BD, Keene JS. Results of arthroscopic medial retinacular release for treatment of medial subluxation of the patella. Am J Sports Med. 2007;35(7):1180-1187.
4. Saper MG, Shneider DA. Medial patellar subluxation without previous lateral release: a case report. J Pediatr Orthop B. 2014;23(4):350-353.
5. Richman NM, Scheller AD Jr. Medial subluxation of the patella without previous lateral retinacular release. Orthopedics. 1998;21(7):810-813.
6. Nonweiler DE, DeLee JC. The diagnosis and treatment of medial subluxation of the patella after lateral retinacular release. Am J Sports Med. 1994;22(5):680-686.
7. Hughston JC, Deese M. Medial subluxation of the patella as a complication of lateral retinacular release. Am J Sports Med. 1988;16(4):383-388.
8. Hughston JC, Flandry F, Brinker MR, Terry GC, Mills JC 3rd. Surgical correction of medial subluxation of the patella. Am J Sports Med. 1996;24(4):486-491.
9. Abhaykumar S, Craig DM. Fascia lata sling reconstruction for recurrent medial dislocation of the patella. The Knee. 1999;6(1):55-57.
10. Teitge RA, Torga Spak R. Lateral patellofemoral ligament reconstruction. Arthroscopy. 2004;20(9):998-1002.
11. Kusano M, Horibe S, Tanaka Y, et al. Simultaneous MPFL and LPFL reconstruction for recurrent lateral patellar dislocation with medial patellofemoral instability. Asia-Pac J Sports Med Arthrosc Rehabil Technol. 2014;1:42-46.
12. Saper MG, Shneider DA. Simultaneous medial and lateral patellofemoral ligament reconstruction for combined medial and lateral patellar subluxation. Arthrosc Tech. 2014,3(2):e227-e231.
13. Udagawa K, Niki Y, Matsumoto H, et al. Lateral patellar retinaculum reconstruction for medial patellar instability following lateral retinacular release: a case report. Knee. 2014;21(1):336-339.
14. Sanchis-Alfonso V, Montesinos-Berry E, Monllau JC, Merchant AC. Results of isolated lateral retinacular reconstruction for iatrogenic medial patellar instability. Arthroscopy. 2015;31(3):422-427.
15. Borbas P, Koch PP, Fucentese SF. Lateral patellofemoral ligament reconstruction using a free gracilis autograft. Orthopedics. 2014;37(7):e665-e668.
16. Fulkerson JP, Gossling H. Anatomy of the knee joint lateral retinaculum. Clin Orthop Relat Res. 1980;153:183-188.
17. Kaplan E. Some aspects of functional anatomy of the human knee joint. Clin Orthop Relat Res. 1962;23:18-29.
18. Reider B, Marshall J, Koslin B, Ring B, Girgis F. The anterior aspect of the knee joint. J Bone Joint Surg Am. 1981;63(3):351-356.
19. Navarro MS, Navarro RD, Akita Junior J, Cohen M. Anatomical study of the lateral patellofemoral ligament in cadaver knees. Rev Bras Ortop. 2008;43(7):300-307.
20. Navarro MS, Beltrani Filho CA, Akita Junior J, Navarro RD, Cohen M. Relationship between the lateral patellofemoral ligament and the width of the lateral patellar facet. Acta Ortop Bras. 2010;18(1):19-22.
21. Salsich GB, Ward SR, Terk MR, Powers CM. In vivo assessment of patellofemoral joint contact area in individuals who are pain free. Clin Orthop Relat Res. 2003;417:277-284.
22. Merican AM, Kondo E, Amis AA. The effect on patellofemoral joint stability of selective cutting of lateral retinacular and capsular structures. J Biomech. 2009;42(3):291-296.
23. Vieira EL, Vieira EÁ, da Silva RT, Berlfein PA, Abdalla RJ, Cohen M. An anatomic study of the iliotibial tract. Arthroscopy. 2007;23(3):269-274.
24. Shneider DA. Lateral patellar laxity—identification, significance, treatment. Poster session presented at: Annual Meeting of the American Academy of Orthopaedic Surgeons; February 25-28, 2009; Las Vegas, NV.
25. Shellock FG, Mink JH, Deutsch A, Fox JM, Ferkel RD. Evaluation of patients with persistent symptoms after lateral retinacular release by kinematic magnetic resonance imaging of the patellofemoral joint. Arthroscopy. 1990;6(3):226-234.
26. Johnson DP, Wakeley C. Reconstruction of the lateral patellar retinaculum following lateral release: a case report. Knee Surg Sports Traumatol Arthrosc. 2002;10(6):361-363.
27. Saper MG, Shneider DA. Lateral patellofemoral ligament reconstruction using a quadriceps tendon graft. Arthrosc Tech. 2014;3(4):e445-e448.
28. Akşahin E, Yumrukçal F, Yüksel HY, Doğruyol D, Celebi L. Role of pathophysiology of patellofemoral instability in the treatment of spontaneous medial patellofemoral subluxation: a case report. J Med Case Rep. 2010;4:148.
1. Marumoto JM, Jordan C, Akins R. A biomechanical comparison of lateral retinacular releases. Am J Sports Med. 1995;23(2):151-155.
2. Betz RR, Magill JT, Lonergan RP. The percutaneous lateral retinacular release. Am J Sports Med. 1987;15(5):477-482.
3. Shannon BD, Keene JS. Results of arthroscopic medial retinacular release for treatment of medial subluxation of the patella. Am J Sports Med. 2007;35(7):1180-1187.
4. Saper MG, Shneider DA. Medial patellar subluxation without previous lateral release: a case report. J Pediatr Orthop B. 2014;23(4):350-353.
5. Richman NM, Scheller AD Jr. Medial subluxation of the patella without previous lateral retinacular release. Orthopedics. 1998;21(7):810-813.
6. Nonweiler DE, DeLee JC. The diagnosis and treatment of medial subluxation of the patella after lateral retinacular release. Am J Sports Med. 1994;22(5):680-686.
7. Hughston JC, Deese M. Medial subluxation of the patella as a complication of lateral retinacular release. Am J Sports Med. 1988;16(4):383-388.
8. Hughston JC, Flandry F, Brinker MR, Terry GC, Mills JC 3rd. Surgical correction of medial subluxation of the patella. Am J Sports Med. 1996;24(4):486-491.
9. Abhaykumar S, Craig DM. Fascia lata sling reconstruction for recurrent medial dislocation of the patella. The Knee. 1999;6(1):55-57.
10. Teitge RA, Torga Spak R. Lateral patellofemoral ligament reconstruction. Arthroscopy. 2004;20(9):998-1002.
11. Kusano M, Horibe S, Tanaka Y, et al. Simultaneous MPFL and LPFL reconstruction for recurrent lateral patellar dislocation with medial patellofemoral instability. Asia-Pac J Sports Med Arthrosc Rehabil Technol. 2014;1:42-46.
12. Saper MG, Shneider DA. Simultaneous medial and lateral patellofemoral ligament reconstruction for combined medial and lateral patellar subluxation. Arthrosc Tech. 2014,3(2):e227-e231.
13. Udagawa K, Niki Y, Matsumoto H, et al. Lateral patellar retinaculum reconstruction for medial patellar instability following lateral retinacular release: a case report. Knee. 2014;21(1):336-339.
14. Sanchis-Alfonso V, Montesinos-Berry E, Monllau JC, Merchant AC. Results of isolated lateral retinacular reconstruction for iatrogenic medial patellar instability. Arthroscopy. 2015;31(3):422-427.
15. Borbas P, Koch PP, Fucentese SF. Lateral patellofemoral ligament reconstruction using a free gracilis autograft. Orthopedics. 2014;37(7):e665-e668.
16. Fulkerson JP, Gossling H. Anatomy of the knee joint lateral retinaculum. Clin Orthop Relat Res. 1980;153:183-188.
17. Kaplan E. Some aspects of functional anatomy of the human knee joint. Clin Orthop Relat Res. 1962;23:18-29.
18. Reider B, Marshall J, Koslin B, Ring B, Girgis F. The anterior aspect of the knee joint. J Bone Joint Surg Am. 1981;63(3):351-356.
19. Navarro MS, Navarro RD, Akita Junior J, Cohen M. Anatomical study of the lateral patellofemoral ligament in cadaver knees. Rev Bras Ortop. 2008;43(7):300-307.
20. Navarro MS, Beltrani Filho CA, Akita Junior J, Navarro RD, Cohen M. Relationship between the lateral patellofemoral ligament and the width of the lateral patellar facet. Acta Ortop Bras. 2010;18(1):19-22.
21. Salsich GB, Ward SR, Terk MR, Powers CM. In vivo assessment of patellofemoral joint contact area in individuals who are pain free. Clin Orthop Relat Res. 2003;417:277-284.
22. Merican AM, Kondo E, Amis AA. The effect on patellofemoral joint stability of selective cutting of lateral retinacular and capsular structures. J Biomech. 2009;42(3):291-296.
23. Vieira EL, Vieira EÁ, da Silva RT, Berlfein PA, Abdalla RJ, Cohen M. An anatomic study of the iliotibial tract. Arthroscopy. 2007;23(3):269-274.
24. Shneider DA. Lateral patellar laxity—identification, significance, treatment. Poster session presented at: Annual Meeting of the American Academy of Orthopaedic Surgeons; February 25-28, 2009; Las Vegas, NV.
25. Shellock FG, Mink JH, Deutsch A, Fox JM, Ferkel RD. Evaluation of patients with persistent symptoms after lateral retinacular release by kinematic magnetic resonance imaging of the patellofemoral joint. Arthroscopy. 1990;6(3):226-234.
26. Johnson DP, Wakeley C. Reconstruction of the lateral patellar retinaculum following lateral release: a case report. Knee Surg Sports Traumatol Arthrosc. 2002;10(6):361-363.
27. Saper MG, Shneider DA. Lateral patellofemoral ligament reconstruction using a quadriceps tendon graft. Arthrosc Tech. 2014;3(4):e445-e448.
28. Akşahin E, Yumrukçal F, Yüksel HY, Doğruyol D, Celebi L. Role of pathophysiology of patellofemoral instability in the treatment of spontaneous medial patellofemoral subluxation: a case report. J Med Case Rep. 2010;4:148.
Study eyes liability associated with implantable devices for chronic pain
SAN DIEGO – The maintenance of implantable drug delivery systems for the management of chronic pain was associated with death, permanent brain damage, or permanent neurological injury from granuloma, and was largely associated with substandard care.
Those are key findings from an analysis of data from the Anesthesia Closed Claims Project that were presented by Dr. Dermot R. Fitzgibbon at the annual meeting of the American Society of Anesthesiologists.
“Implantable devices are relatively new in chronic pain management, and have only been available since the early 1990s,” said Dr. Fitzgibbon, professor of anesthesiology and pain medicine at the University of Washington, Seattle. Such devices are considered advanced techniques for refractory chronic pain and include implantable drug delivery systems, spinal cord stimulators, and peripheral nerve stimulators. Previous studies have demonstrated that morbidity and mortality from implantable drug delivery systems (IDDS) and spinal cord stimulators typically occur during implantation or removal of devices or during device maintenance (Neuromodulation. 2012;15[5]:467-82 and Clin J Pain. 2007;23[2]:180-95). The purpose of the current study was to investigate liability associated with implantable devices used to manage chronic pain.
Dr. Fitzgibbon and his associates used the Anesthesia Closed Claims Project Database to identify 970 claims related to chronic pain that have occurred since 1990. A total of 148 of these claims were related to implantable devices, and the majority of them were for surgical procedures (107 [72%] vs. 41 [28%] for IDDS maintenance).
Of the 107 surgical device procedures, 50% were for an IDDS system, followed by spinal cord stimulator (40%), tunneled epidural (7%), and peripheral nerve stimulator (3%). Temporary minor injury occurred in 74% of the surgical device procedures, followed by permanent cord injury (16%), death/permanent brain damage (8%), and other permanent injury (2%). The most common reasons for permanent spinal cord injury were needle or catheter trauma to the cord (7 cases), epidural hematoma (3 cases), and incorrect placement of the stimulator (2 cases). Infections occurred in 25 of the surgical device procedures. Among these 25 claims, 3 resulted in death or severe permanent injury, 7 involved retained parts and sponges, and 5 were cases of epidural abscess – 4 of which were associated with a tunneled epidural catheter.
Of the 41 damaging events that occurred during IDDS maintenance, 44% were temporary minor injuries, while 32% involved death or permanent brain damage from medication administration errors and 24% involved permanent spinal cord injury, primarily from a delay in recognition of granuloma formation at the catheter tip.
The researchers found that maintenance of IDDS, compared with claims related to other surgical devices, were more commonly associated with a risk of death or permanent damage, less commonly resulted in temporary minor injury, were more likely to have care deemed as substandard, and were more commonly associated with payments (P = .001 for all comparisons). The median payment for all claims was $274,000.
The Anesthesia Closed Claims Project is funded by the Anesthesia Quality Institute. Dr. Fitzgibbon reported having no financial disclosures.
SAN DIEGO – The maintenance of implantable drug delivery systems for the management of chronic pain was associated with death, permanent brain damage, or permanent neurological injury from granuloma, and was largely associated with substandard care.
Those are key findings from an analysis of data from the Anesthesia Closed Claims Project that were presented by Dr. Dermot R. Fitzgibbon at the annual meeting of the American Society of Anesthesiologists.
“Implantable devices are relatively new in chronic pain management, and have only been available since the early 1990s,” said Dr. Fitzgibbon, professor of anesthesiology and pain medicine at the University of Washington, Seattle. Such devices are considered advanced techniques for refractory chronic pain and include implantable drug delivery systems, spinal cord stimulators, and peripheral nerve stimulators. Previous studies have demonstrated that morbidity and mortality from implantable drug delivery systems (IDDS) and spinal cord stimulators typically occur during implantation or removal of devices or during device maintenance (Neuromodulation. 2012;15[5]:467-82 and Clin J Pain. 2007;23[2]:180-95). The purpose of the current study was to investigate liability associated with implantable devices used to manage chronic pain.
Dr. Fitzgibbon and his associates used the Anesthesia Closed Claims Project Database to identify 970 claims related to chronic pain that have occurred since 1990. A total of 148 of these claims were related to implantable devices, and the majority of them were for surgical procedures (107 [72%] vs. 41 [28%] for IDDS maintenance).
Of the 107 surgical device procedures, 50% were for an IDDS system, followed by spinal cord stimulator (40%), tunneled epidural (7%), and peripheral nerve stimulator (3%). Temporary minor injury occurred in 74% of the surgical device procedures, followed by permanent cord injury (16%), death/permanent brain damage (8%), and other permanent injury (2%). The most common reasons for permanent spinal cord injury were needle or catheter trauma to the cord (7 cases), epidural hematoma (3 cases), and incorrect placement of the stimulator (2 cases). Infections occurred in 25 of the surgical device procedures. Among these 25 claims, 3 resulted in death or severe permanent injury, 7 involved retained parts and sponges, and 5 were cases of epidural abscess – 4 of which were associated with a tunneled epidural catheter.
Of the 41 damaging events that occurred during IDDS maintenance, 44% were temporary minor injuries, while 32% involved death or permanent brain damage from medication administration errors and 24% involved permanent spinal cord injury, primarily from a delay in recognition of granuloma formation at the catheter tip.
The researchers found that maintenance of IDDS, compared with claims related to other surgical devices, were more commonly associated with a risk of death or permanent damage, less commonly resulted in temporary minor injury, were more likely to have care deemed as substandard, and were more commonly associated with payments (P = .001 for all comparisons). The median payment for all claims was $274,000.
The Anesthesia Closed Claims Project is funded by the Anesthesia Quality Institute. Dr. Fitzgibbon reported having no financial disclosures.
SAN DIEGO – The maintenance of implantable drug delivery systems for the management of chronic pain was associated with death, permanent brain damage, or permanent neurological injury from granuloma, and was largely associated with substandard care.
Those are key findings from an analysis of data from the Anesthesia Closed Claims Project that were presented by Dr. Dermot R. Fitzgibbon at the annual meeting of the American Society of Anesthesiologists.
“Implantable devices are relatively new in chronic pain management, and have only been available since the early 1990s,” said Dr. Fitzgibbon, professor of anesthesiology and pain medicine at the University of Washington, Seattle. Such devices are considered advanced techniques for refractory chronic pain and include implantable drug delivery systems, spinal cord stimulators, and peripheral nerve stimulators. Previous studies have demonstrated that morbidity and mortality from implantable drug delivery systems (IDDS) and spinal cord stimulators typically occur during implantation or removal of devices or during device maintenance (Neuromodulation. 2012;15[5]:467-82 and Clin J Pain. 2007;23[2]:180-95). The purpose of the current study was to investigate liability associated with implantable devices used to manage chronic pain.
Dr. Fitzgibbon and his associates used the Anesthesia Closed Claims Project Database to identify 970 claims related to chronic pain that have occurred since 1990. A total of 148 of these claims were related to implantable devices, and the majority of them were for surgical procedures (107 [72%] vs. 41 [28%] for IDDS maintenance).
Of the 107 surgical device procedures, 50% were for an IDDS system, followed by spinal cord stimulator (40%), tunneled epidural (7%), and peripheral nerve stimulator (3%). Temporary minor injury occurred in 74% of the surgical device procedures, followed by permanent cord injury (16%), death/permanent brain damage (8%), and other permanent injury (2%). The most common reasons for permanent spinal cord injury were needle or catheter trauma to the cord (7 cases), epidural hematoma (3 cases), and incorrect placement of the stimulator (2 cases). Infections occurred in 25 of the surgical device procedures. Among these 25 claims, 3 resulted in death or severe permanent injury, 7 involved retained parts and sponges, and 5 were cases of epidural abscess – 4 of which were associated with a tunneled epidural catheter.
Of the 41 damaging events that occurred during IDDS maintenance, 44% were temporary minor injuries, while 32% involved death or permanent brain damage from medication administration errors and 24% involved permanent spinal cord injury, primarily from a delay in recognition of granuloma formation at the catheter tip.
The researchers found that maintenance of IDDS, compared with claims related to other surgical devices, were more commonly associated with a risk of death or permanent damage, less commonly resulted in temporary minor injury, were more likely to have care deemed as substandard, and were more commonly associated with payments (P = .001 for all comparisons). The median payment for all claims was $274,000.
The Anesthesia Closed Claims Project is funded by the Anesthesia Quality Institute. Dr. Fitzgibbon reported having no financial disclosures.
AT THE ASA ANNUAL MEETING
Key clinical point: Malpractice claims for implantable devices for chronic pain are most often associated with maintenance of implantable drug delivery systems (IDDS) rather than the surgical placement of the devices.
Major finding: Maintenance of IDDS, compared with claims related to other surgical devices, was more commonly associated with a risk of death or permanent damage, less commonly resulted in temporary minor injury, was more likely to have care deemed as substandard, and was more commonly associated with payments (P = .001 for all comparisons).
Data source: An analysis of 970 claims related to chronic pain that have occurred since 1990.
Disclosures: The Anesthesia Closed Claims Project is funded by the Anesthesia Quality Institute. The researchers reported having no financial disclosures.
Biceps Tenodesis and Superior Labrum Anterior to Posterior (SLAP) Tears
Injuries of the superior labrum–biceps complex (SLBC) have been recognized as a cause of shoulder pain since they were first described by Andrews and colleagues1 in 1985. Superior labrum anterior to posterior (SLAP) tears are relatively uncommon injuries of the shoulder, and their true incidence is difficult to establish. However, recently there has been a significant increase in the reported incidence and operative treatment of SLAP tears.2 SLAP tears can occur in isolation, but they are commonly seen in association with other shoulder lesions, including rotator cuff tear, Bankart lesion, glenohumeral arthritis, acromioclavicular joint pathology, and subacromial impingement.
Although SLAP tears are well described and classified,3-6 our understanding of symptomatic SLAP tears and of their contribution to glenohumeral instability is limited. Diagnosing a SLAP tear on the basis of history and physical examination is a clinical challenge. Pain is the most common presentation of SLAP tears, though localization and characterization of pain are variable and nonspecific.7 The mechanism of injury is helpful in acute presentation (traction injury; fall on outstretched, abducted arm), but an overhead athlete may present with no distinct mechanism other than chronic, repetitive use of the shoulder.8-11 Numerous provocative physical examination tests have been used to assist in the diagnosis of SLAP tear, yet there is no consensus regarding the ideal physical examination test, with high sensitivity, specificity, and accuracy.12-14 Magnetic resonance arthrography, the gold standard imaging modality, is highly sensitive and specific (>95%) for diagnosing SLAP tears.
SLAP tear management is based on lesion type and severity, age, functional demands, and presence of coexisting intra-articular lesions. Management options include nonoperative treatment, débridement or repair of SLBC, biceps tenotomy, and biceps tenodesis.15-19
In this 5-point review, we present an evidence-based analysis of the role of the SLBC in glenohumeral stability and the role of biceps tenodesis in the management of SLAP tears.
1. Role of SLBC in stability of glenohumeral joint
The anatomy of the SLBC has been well described,20,21 and there is consensus that SLBC pathology can be a source of shoulder pain. The superior labrum is relatively more mobile than the rest of the glenoid labrum, and it provides attachment to the long head of the biceps tendon (LHBT) and the superior glenohumeral and middle glenohumeral ligaments.
The functional role of the SLBC in glenohumeral stability and its contribution to the pathogenesis of shoulder instability are not clearly defined. Our understanding of SLBC function is largely derived from simulated cadaveric experiments of SLAP tears. Controlled laboratory studies with simulated type II SLAP tears in cadavers have shown significantly increased glenohumeral translation in the anterior-posterior and superior-inferior directions, suggesting a role of the superior labrum in maintaining glenohumeral stability.22-26 Interestingly, there is conflicting evidence regarding restoration of normal glenohumeral translation in cadaveric shoulders after repair of simulated SLAP lesions in the presence or absence of simulated anterior capsular laxity.22,25-27 However, it is important to understand the limitations of cadaveric experiments in order to appreciate and truly comprehend the results of these experiments. There are inconsistencies in the size of simulated type II SLAP lesions in different studies, which can affect the degree of glenohumeral translation and the results of repair.23-25,28 The amount of glenohumeral translation noticed after simulated SLAP tears in cadavers, though statistically significant, is small in amplitude, and its relevance may not translate to a clinically significant level. The impact of dynamic components of stability (eg, rotator cuff muscles), capsular stretch, and other in vivo variables that affect glenohumeral stability are unaccounted for during cadaveric experiments.
LHBT is a recognized cause of shoulder pain, but its contribution to shoulder stability is a point of continued debate. According to one school of thought, LHBT is a vestigial structure that can be sacrificed without any loss of stability. Another school of thought holds that LHBT is an important active stabilizer of the glenohumeral joint. Cadaveric studies have demonstrated that loading the LHBT decreases glenohumeral translation and rotational range of motion, especially in lower and mid ranges of abduction.23,29,30 Furthermore, LHBT contributes to anterior glenohumeral stability by resisting torsional forces in the abducted and externally rotated shoulder and reducing stress on the inferior glenohumeral ligaments.31-33 Strauss and colleagues22 recently found that simulated anterior and posterior type II SLAP lesions in cadaveric shoulders increased glenohumeral translation in all planes, and biceps tenodesis did not further worsen this abnormal glenohumeral translation. Furthermore, repair of posterior SLAP lesions along with biceps tenodesis restored abnormal glenohumeral translation with no significant difference from the baseline in any plane of motion. Again, the limitations of cadaveric studies should be considered when interpreting these results and applying them clinically.
2. Biceps tenodesis as primary treatment for SLAP tears
A growing body of evidence suggests that primary tenodesis of LHBT may be an effective alternative treatment to SLAP repairs in select patients.34-36 However, the evidence is weak, and high-quality studies comparing SLAP repair and primary biceps tenodesis are required in order to make a strong recommendation for one technique over another. Gupta and colleagues35 retrospectively analyzed 28 cases of concomitant SLAP tear and biceps tendonitis treated with primary open subpectoral biceps tenodesis. There was significant improvement in patients’ functional outcome scores postoperatively [SANE (Single Assessment Numeric Evaluation), ASES (American Shoulder and Elbow Surgeons shoulder index), SST (Simple Shoulder Test), VAS (visual analog scale), and SF-12 (Short Form-12)]. In addition, 80% of patients were satisfied with their outcome. Mean age was 43.7 years. Forty-two percent of patients had a worker’s compensation claim. Interestingly, 15 patients in this cohort had a type I SLAP tear. Boileau and colleagues34 prospectively followed 25 cases of type II SLAP tear treated with either SLAP repair (10 patients; mean age, 37 years) or primary arthroscopic biceps tenodesis (15 patients; mean age, 52 years). Compared with the SLAP repair group, the biceps tenodesis group had significantly higher rates of satisfaction and return to previous level of sports participation. However, group assignments were nonrandomized, and the decision to treat a patient with SLAP repair versus biceps tenodesis was made by the senior surgeon purely on the basis of age (SLAP repair for patients under 30 years). Ek and colleagues36 retrospectively compared the cases of 10 patients who underwent SLAP repair (mean age, 32 years) and 15 who underwent biceps tenodesis (mean age, 47 years) for type II SLAP tear. There was no significant difference between the groups with respect to outcome scores, return to play or preinjury activity level, or complications.
There continues to be significant debate as to which patient will benefit from primary SLAP repair versus biceps tenodesis. Multiple factors are involved: age, presence of associated shoulder pathology, occupation, preinjury activity level, and worker’s compensation status. Age has convincingly been shown to affect the outcomes of treatment of type II SLAP tears.34,35,37-40 There is consensus that patients over age 40 years will benefit from primary biceps tenodesis for SLAP tears. However, the evidence for this recommendation is weak.
3. Biceps tenodesis and failed SLAP repair
The definition of a failed SLAP repair is not well documented in the literature, but dissatisfaction after SLAP repair can result from continued shoulder pain, poor shoulder function, or inability to return to preinjury functional level.15,41 The etiologic determination and treatment of a failed SLAP repair are challenging, and outcomes of revision SLAP repair are not very promising.42,43 Biceps tenodesis has been proposed as an alternative treatment to revision SLAP repair for failed SLAP repair. McCormick and colleagues41 prospectively evaluated 42 patients (mean age, 39.2 years; minimum follow-up, 2 years) with failed type II SLAP repairs that were treated with open subpectoral biceps tenodesis. There was significant improvement in ASES, SANE, and Western Ontario Shoulder Instability Index (WOSI) outcome scores and in postoperative shoulder range of motion at a mean follow-up of 3.6 years. One patient had transient musculocutaneous neurapraxia after surgery. In a retrospective cohort study, Gupta and colleagues44 found significant improvement in ASES, SANE, SST, SF-12, and VAS outcome scores in 11 patients who underwent open subpectoral biceps tenodesis for failed arthroscopic SLAP repair (mean age at surgery, 40 years; mean follow-up, 26 months). Three of the 11 patients had worker’s compensation claims, and there were no complications and no revision surgeries required after biceps tenodesis. Werner and colleagues16 retrospectively evaluated 17 patients who underwent biceps tenodesis for failed SLAP repair (mean age, 39 years; minimum follow-up, 2 years). Twenty-nine percent of patients had worker’s compensation claims. Compared with the contralateral shoulder, the treated shoulder had better postoperative ASES, SANE, SST, and Veteran RAND 36-item health survey outcome scores; range of motion was near normal.
There are no high-quality studies comparing revision SLAP repair and biceps tenodesis in the management of failed SLAP repair.16,41-44 Case series studies have found improved outcomes and pain relief after biceps tenodesis for failed SLAP repair, but the quality of evidence has been poor (level IV evidence).16,41-44 The senior author recommends treating failed SLAP repairs with biceps tenodesis.
4. Biceps tenodesis as treatment option for SLAP tear in overhead throwing athletes
Biceps tenodesis is a potential alternative treatment to SLAP repair in overhead throwing athletes. Although outcome scores and satisfaction rates after SLAP repair are high in overhead athletes, the rates of return to sport are relatively low, especially in baseball players.38,45-47 In a level III cohort study, Boileau and colleagues34 found that 13 (87%) of 15 patients with type II SLAP tears, including 8 overhead athletes, had returned to their previous level of activity by a mean of 30 months after biceps tenodesis. In contrast, only 2 of 10 patients returned to their previous level of activity after SLAP repair. Interestingly, 3 patients who underwent biceps tenodesis for failed SLAP repair returned to overhead sports. Schöffl and colleagues48 reported on the outcomes of biceps tenodesis for SLAP lesions in 6 high-level rock climbers. By a mean follow-up of 6 months, all 6 patients had returned to their previous level of climbing. Their satisfaction rate was 96.8%. Gupta and colleagues35 reported on a cohort of 28 patients who underwent biceps tenodesis for SLAP tears and concomitant biceps tendonitis. Of the 8 athletes in the group, 5 were able to return to their previous level of play, and 1 was able to return to a lower level of sporting activity. There was significant improvement from preoperative to postoperative scores on ASES, SST, SANE, VAS, SF-12 overall, and SF-12 components.
Chalmers and colleagues49 recently described motion analyses with simultaneous surface electromyographic measurements in 18 baseball pitchers. Of these 18 players, 7 were uninjured (controls), 6 were pitching after SLAP repair, and 5 were pitching after subpectoral biceps tenodesis. There were no significant differences between controls and postoperative patients with respect to pitching kinematics. Interestingly, compared with the controls and the patients who underwent open biceps tenodesis, the patients who underwent SLAP repair had altered patterns of thoracic rotation during pitching. However, the clinical significance of this finding and the impact of this finding on pitching efficacy are not currently known.
Biceps tenodesis as a primary procedure for type II SLAP lesion in an overhead athlete is a concept in evolution. Increasing evidence suggests a role for primary biceps tenodesis in an overhead athlete with type II SLAP lesion and concomitant biceps pathology. However, this evidence is of poor quality, and the strength of the recommendation is weak. Still to be determined is whether return to preinjury performance level is better with primary biceps tenodesis or with SLAP repair in overhead athletes with type II SLAP lesion. As per the senior author’s treatment algorithm, we prefer SLAP repair for overhead athletes with type II SLAP tears and reserve biceps tenodesis for cases involving significant biceps pathology and/or clinical symptoms involving the bicipital groove consistent with extra-articular biceps pain.
5. Biceps tenodesis for type II SLAP tear in contact athletes and occupations demanding heavy labor (blue-collar jobs)
SLAP tears are less common in contact athletes, and there is general agreement that SLAP repair outcomes are better in contact athletes than in overhead athletes. In a retrospective review of 18 rugby players with SLAP tears, Funk and Snow50 reported excellent results and quicker return to sport after SLAP repair. Patients with isolated SLAP tears had the earliest return to play. Enad and colleagues51 reported SLAP repair outcomes in an active military population. SLAP tears are more common in the military versus the general population because of the unique physical demands placed on military personnel. The authors retrospectively reviewed 27 cases of type II SLAP tears treated with SLAP repair and suture anchors. Outcomes were measured at a mean of 30.5 months after surgery. Twenty-four (89%) of the 27 patients had good to excellent results, and 94% had returned to active duty by a mean of 4.4 months after SLAP repair.
Given the poor-quality evidence in the literature, we believe that biceps tenodesis should be reserved for revision surgery in contact athletes. There is insufficient evidence to recommend biceps tenodesis as primary treatment for type II SLAP tears in contact athletes. SLAP repair should be performed for primary SLAP lesions in contact athletes and for patients in physically demanding professions (eg, military, laborer, weightlifter).
Conclusion
SLAP tears can result in persistent shoulder pain and dysfunction. SLAP tear management depends on lesion type and severity, age, and functional demands. SLAP repair is the treatment of choice for type II SLAP lesions in young, active patients. Biceps tenodesis is a preferred alternative to SLAP repair in failed SLAP repair and in type II SLAP patients who are older than 40 years and who are less active and have a worker’s compensation claim. These recommendations are based on poor-quality evidence. There is an unmet need for randomized clinical studies comparing SLAP repair with biceps tenodesis for type II SLAP tears in different patient populations so as to optimize the current decision-making algorithm for SLAP tears.
1. Andrews JR, Carson WG Jr, McLeod WD. Glenoid labrum tears related to the long head of the biceps. Am J Sports Med. 1985;13(5):337-341.
2. Weber SC, Martin DF, Seiler JG 3rd, Harrast JJ. Superior labrum anterior and posterior lesions of the shoulder: incidence rates, complications, and outcomes as reported by American Board of Orthopaedic Surgery. Part II candidates. Am J Sports Med. 2012;40(7):1538-1543.
3. Snyder SJ, Karzel RP, Del Pizzo W, Ferkel RD, Friedman MJ. SLAP lesions of the shoulder. Arthroscopy. 1990;6(4):274-279.
4. Morgan CD, Burkhart SS, Palmeri M, Gillespie M. Type II SLAP lesions: three subtypes and their relationships to superior instability and rotator cuff tears. Arthroscopy. 1998;14(6):553-565.
5. Powell SE, Nord KD, Ryu RKN. The diagnosis, classification, and treatment of SLAP lesions. Oper Tech Sports Med. 2012;20(1):46-56.
6. Maffet MW, Gartsman GM, Moseley B. Superior labrum-biceps tendon complex lesions of the shoulder. Am J Sports Med. 1995;23(1):93-98.
7. Kim TK, Queale WS, Cosgarea AJ, McFarland EG. Clinical features of the different types of SLAP lesions: an analysis of one hundred and thirty-nine cases. J Bone Joint Surg Am. 2003;85(1):66-71.
8. Abrams GD, Safran MR. Diagnosis and management of superior labrum anterior posterior lesions in overhead athletes. Br J Sports Med. 2010;44(5):311-318.
9. Keener JD, Brophy RH. Superior labral tears of the shoulder: pathogenesis, evaluation, and treatment. J Am Acad Orthop Surg. 2009;17(10):627-637.
10. Abrams GD, Hussey KE, Harris JD, Cole BJ. Clinical results of combined meniscus and femoral osteochondral allograft transplantation: minimum 2-year follow-up. Arthroscopy. 2014;30(8):964-970.e1.
11. Burkhart SS, Morgan CD, Kibler WB. The disabled throwing shoulder: spectrum of pathology part I: pathoanatomy and biomechanics. Arthroscopy. 2003;19(4):404-420.
12. Virk MS, Arciero RA. Superior labrum anterior to posterior tears and glenohumeral instability. Instr Course Lect. 2013;62:501-514.
13. Calvert E, Chambers GK, Regan W, Hawkins RH, Leith JM. Special physical examination tests for superior labrum anterior posterior shoulder tears are clinically limited and invalid: a diagnostic systematic review. J Clin Epidemiol. 2009;62(5):558-563.
14. Jones GL, Galluch DB. Clinical assessment of superior glenoid labral lesions: a systematic review. Clin Orthop Relat Res. 2007;455:45-51.
15. Werner BC, Brockmeier SF, Miller MD. Etiology, diagnosis, and management of failed SLAP repair. J Am Acad Orthop Surg. 2014;22(9):554-565.
16. Werner BC, Pehlivan HC, Hart JM, et al. Biceps tenodesis is a viable option for salvage of failed SLAP repair. J Shoulder Elbow Surg. 2014;23(8):e179-e184.
17. Erickson J, Lavery K, Monica J, Gatt C, Dhawan A. Surgical treatment of symptomatic superior labrum anterior-posterior tears in patients older than 40 years: a systematic review. Am J Sports Med. 2015;43(5):1274-1282.
18. Huri G, Hyun YS, Garbis NG, McFarland EG. Treatment of superior labrum anterior posterior lesions: a literature review. Acta Orthop Traumatol Turc. 2014;48(3):290-297.
19. Li X, Lin TJ, Jager M, et al. Management of type II superior labrum anterior posterior lesions: a review of the literature. Orthop Rev. 2010;2(1):e6.
20. Cooper DE, Arnoczky SP, O’Brien SJ, Warren RF, DiCarlo E, Allen AA. Anatomy, histology, and vascularity of the glenoid labrum. An anatomical study. J Bone Joint Surg Am. 1992;74(1):46-52.
21. Vangsness CT, Jorgenson SS, Watson T, Johnson DL. The origin of the long head of the biceps from the scapula and glenoid labrum. An anatomical study of 100 shoulders. J Bone Joint Surg Br. 1994;76(6):951-954.
22. Strauss EJ, Salata MJ, Sershon RA, et al. Role of the superior labrum after biceps tenodesis in glenohumeral stability. J Shoulder Elbow Surg. 2014;23(4):485-491.
23. Pagnani MJ, Deng XH, Warren RF, Torzilli PA, Altchek DW. Effect of lesions of the superior portion of the glenoid labrum on glenohumeral translation. J Bone Joint Surg Am. 1995;77(7):1003-1010.
24. McMahon PJ, Burkart A, Musahl V, Debski RE. Glenohumeral translations are increased after a type II superior labrum anterior-posterior lesion: a cadaveric study of severity of passive stabilizer injury. J Shoulder Elbow Surg. 2004;13(1):39-44.
25. Burkart A, Debski R, Musahl V, McMahon P, Woo SL. Biomechanical tests for type II SLAP lesions of the shoulder joint before and after arthroscopic repair [in German]. Orthopade. 2003;32(7):600-607.
26. Panossian VR, Mihata T, Tibone JE, Fitzpatrick MJ, McGarry MH, Lee TQ. Biomechanical analysis of isolated type II SLAP lesions and repair. J Shoulder Elbow Surg. 2005;14(5):529-534.
27. Mihata T, McGarry MH, Tibone JE, Fitzpatrick MJ, Kinoshita M, Lee TQ. Biomechanical assessment of type II superior labral anterior-posterior (SLAP) lesions associated with anterior shoulder capsular laxity as seen in throwers: a cadaveric study. Am J Sports Med. 2008;36(8):1604-1610.
28. Youm T, Tibone JE, ElAttrache NS, McGarry MH, Lee TQ. Simulated type II superior labral anterior posterior lesions do not alter the path of glenohumeral articulation: a cadaveric biomechanical study. Am J Sports Med. 2008;36(4):767-774.
29. Youm T, ElAttrache NS, Tibone JE, McGarry MH, Lee TQ. The effect of the long head of the biceps on glenohumeral kinematics. J Shoulder Elbow Surg. 2009;18(1):122-129.
30. McGarry MH, Nguyen ML, Quigley RJ, Hanypsiak B, Gupta R, Lee TQ. The effect of long and short head biceps loading on glenohumeral joint rotational range of motion and humeral head position [published online ahead of print September 26, 2014]. Knee Surg Sports Traumatol Arthrosc.
31. Glousman R, Jobe F, Tibone J, Moynes D, Antonelli D, Perry J. Dynamic electromyographic analysis of the throwing shoulder with glenohumeral instability. J Bone Joint Surg Am. 1988;70(2):220-226.
32. Gowan ID, Jobe FW, Tibone JE, Perry J, Moynes DR. A comparative electromyographic analysis of the shoulder during pitching. Professional versus amateur pitchers. Am J Sports Med. 1987;15(6):586-590.
33. Rodosky MW, Harner CD, Fu FH. The role of the long head of the biceps muscle and superior glenoid labrum in anterior stability of the shoulder. Am J Sports Med. 1994;22(1):121-130.
34. Boileau P, Parratte S, Chuinard C, Roussanne Y, Shia D, Bicknell R. Arthroscopic treatment of isolated type II SLAP lesions: biceps tenodesis as an alternative to reinsertion. Am J Sports Med. 2009;37(5):929-936.
35. Gupta AK, Chalmers PN, Klosterman EL, et al. Subpectoral biceps tenodesis for bicipital tendonitis with SLAP tear. Orthopedics. 2015;38(1):e48-e53.
36. Ek ET, Shi LL, Tompson JD, Freehill MT, Warner JJ. Surgical treatment of isolated type II superior labrum anterior-posterior (SLAP) lesions: repair versus biceps tenodesis. J Shoulder Elbow Surg. 2014;23(7):1059-1065.
37. Alpert JM, Wuerz TH, O’Donnell TF, Carroll KM, Brucker NN, Gill TJ. The effect of age on the outcomes of arthroscopic repair of type II superior labral anterior and posterior lesions. Am J Sports Med. 2010;38(11):2299-2303.
38. Provencher MT, McCormick F, Dewing C, McIntire S, Solomon D. A prospective analysis of 179 type 2 superior labrum anterior and posterior repairs: outcomes and factors associated with success and failure. Am J Sports Med. 2013;41(4):880-886.
39. Denard PJ, Lädermann A, Burkhart SS. Long-term outcome after arthroscopic repair of type II SLAP lesions: results according to age and workers’ compensation status. Arthroscopy. 2012;28(4):451-457.
40. Burns JP, Bahk M, Snyder SJ. Superior labral tears: repair versus biceps tenodesis. J Shoulder Elbow Surg. 2011;20(2 suppl):S2-S8.
41. McCormick F, Nwachukwu BU, Solomon D, et al. The efficacy of biceps tenodesis in the treatment of failed superior labral anterior posterior repairs. Am J Sports Med. 2014;42(4):820-825.
42. Katz LM, Hsu S, Miller SL, et al. Poor outcomes after SLAP repair: descriptive analysis and prognosis. Arthroscopy. 2009;25(8):849-855.
43. Park S, Glousman RE. Outcomes of revision arthroscopic type II superior labral anterior posterior repairs. Am J Sports Med. 2011;39(6):1290-1294.
44. Gupta AK, Bruce B, Klosterman EL, McCormick F, Harris J, Romeo AA. Subpectoral biceps tenodesis for failed type II SLAP repair. Orthopedics. 2013;36(6):e723-e728.
45. Neuman BJ, Boisvert CB, Reiter B, Lawson K, Ciccotti MG, Cohen SB. Results of arthroscopic repair of type II superior labral anterior posterior lesions in overhead athletes: assessment of return to preinjury playing level and satisfaction. Am J Sports Med. 2011;39(9):1883-1888.
46. Fedoriw WW, Ramkumar P, McCulloch PC, Lintner DM. Return to play after treatment of superior labral tears in professional baseball players. Am J Sports Med. 2014;42(5):1155-1160.
47. Park JY, Chung SW, Jeon SH, Lee JG, Oh KS. Clinical and radiological outcomes of type 2 superior labral anterior posterior repairs in elite overhead athletes. Am J Sports Med. 2013;41(6):1372-1379.
48. Schöffl V, Popp D, Dickschass J, Küpper T. Superior labral anterior-posterior lesions in rock climbers—primary double tenodesis? Clin J Sport Med. 2011;21(3):261-263.
49. Chalmers PN, Trombley R, Cip J, et al. Postoperative restoration of upper extremity motion and neuromuscular control during the overhand pitch: evaluation of tenodesis and repair for superior labral anterior-posterior tears. Am J Sports Med. 2014;42(12):2825-2836.
50. Funk L, Snow M. SLAP tears of the glenoid labrum in contact athletes. Clin J Sport Med. 2007;17(1):1-4.
51. Enad JG, Gaines RJ, White SM, Kurtz CA. Arthroscopic superior labrum anterior-posterior repair in military patients. J Shoulder Elbow Surg. 2007;16(3):300-305.
Injuries of the superior labrum–biceps complex (SLBC) have been recognized as a cause of shoulder pain since they were first described by Andrews and colleagues1 in 1985. Superior labrum anterior to posterior (SLAP) tears are relatively uncommon injuries of the shoulder, and their true incidence is difficult to establish. However, recently there has been a significant increase in the reported incidence and operative treatment of SLAP tears.2 SLAP tears can occur in isolation, but they are commonly seen in association with other shoulder lesions, including rotator cuff tear, Bankart lesion, glenohumeral arthritis, acromioclavicular joint pathology, and subacromial impingement.
Although SLAP tears are well described and classified,3-6 our understanding of symptomatic SLAP tears and of their contribution to glenohumeral instability is limited. Diagnosing a SLAP tear on the basis of history and physical examination is a clinical challenge. Pain is the most common presentation of SLAP tears, though localization and characterization of pain are variable and nonspecific.7 The mechanism of injury is helpful in acute presentation (traction injury; fall on outstretched, abducted arm), but an overhead athlete may present with no distinct mechanism other than chronic, repetitive use of the shoulder.8-11 Numerous provocative physical examination tests have been used to assist in the diagnosis of SLAP tear, yet there is no consensus regarding the ideal physical examination test, with high sensitivity, specificity, and accuracy.12-14 Magnetic resonance arthrography, the gold standard imaging modality, is highly sensitive and specific (>95%) for diagnosing SLAP tears.
SLAP tear management is based on lesion type and severity, age, functional demands, and presence of coexisting intra-articular lesions. Management options include nonoperative treatment, débridement or repair of SLBC, biceps tenotomy, and biceps tenodesis.15-19
In this 5-point review, we present an evidence-based analysis of the role of the SLBC in glenohumeral stability and the role of biceps tenodesis in the management of SLAP tears.
1. Role of SLBC in stability of glenohumeral joint
The anatomy of the SLBC has been well described,20,21 and there is consensus that SLBC pathology can be a source of shoulder pain. The superior labrum is relatively more mobile than the rest of the glenoid labrum, and it provides attachment to the long head of the biceps tendon (LHBT) and the superior glenohumeral and middle glenohumeral ligaments.
The functional role of the SLBC in glenohumeral stability and its contribution to the pathogenesis of shoulder instability are not clearly defined. Our understanding of SLBC function is largely derived from simulated cadaveric experiments of SLAP tears. Controlled laboratory studies with simulated type II SLAP tears in cadavers have shown significantly increased glenohumeral translation in the anterior-posterior and superior-inferior directions, suggesting a role of the superior labrum in maintaining glenohumeral stability.22-26 Interestingly, there is conflicting evidence regarding restoration of normal glenohumeral translation in cadaveric shoulders after repair of simulated SLAP lesions in the presence or absence of simulated anterior capsular laxity.22,25-27 However, it is important to understand the limitations of cadaveric experiments in order to appreciate and truly comprehend the results of these experiments. There are inconsistencies in the size of simulated type II SLAP lesions in different studies, which can affect the degree of glenohumeral translation and the results of repair.23-25,28 The amount of glenohumeral translation noticed after simulated SLAP tears in cadavers, though statistically significant, is small in amplitude, and its relevance may not translate to a clinically significant level. The impact of dynamic components of stability (eg, rotator cuff muscles), capsular stretch, and other in vivo variables that affect glenohumeral stability are unaccounted for during cadaveric experiments.
LHBT is a recognized cause of shoulder pain, but its contribution to shoulder stability is a point of continued debate. According to one school of thought, LHBT is a vestigial structure that can be sacrificed without any loss of stability. Another school of thought holds that LHBT is an important active stabilizer of the glenohumeral joint. Cadaveric studies have demonstrated that loading the LHBT decreases glenohumeral translation and rotational range of motion, especially in lower and mid ranges of abduction.23,29,30 Furthermore, LHBT contributes to anterior glenohumeral stability by resisting torsional forces in the abducted and externally rotated shoulder and reducing stress on the inferior glenohumeral ligaments.31-33 Strauss and colleagues22 recently found that simulated anterior and posterior type II SLAP lesions in cadaveric shoulders increased glenohumeral translation in all planes, and biceps tenodesis did not further worsen this abnormal glenohumeral translation. Furthermore, repair of posterior SLAP lesions along with biceps tenodesis restored abnormal glenohumeral translation with no significant difference from the baseline in any plane of motion. Again, the limitations of cadaveric studies should be considered when interpreting these results and applying them clinically.
2. Biceps tenodesis as primary treatment for SLAP tears
A growing body of evidence suggests that primary tenodesis of LHBT may be an effective alternative treatment to SLAP repairs in select patients.34-36 However, the evidence is weak, and high-quality studies comparing SLAP repair and primary biceps tenodesis are required in order to make a strong recommendation for one technique over another. Gupta and colleagues35 retrospectively analyzed 28 cases of concomitant SLAP tear and biceps tendonitis treated with primary open subpectoral biceps tenodesis. There was significant improvement in patients’ functional outcome scores postoperatively [SANE (Single Assessment Numeric Evaluation), ASES (American Shoulder and Elbow Surgeons shoulder index), SST (Simple Shoulder Test), VAS (visual analog scale), and SF-12 (Short Form-12)]. In addition, 80% of patients were satisfied with their outcome. Mean age was 43.7 years. Forty-two percent of patients had a worker’s compensation claim. Interestingly, 15 patients in this cohort had a type I SLAP tear. Boileau and colleagues34 prospectively followed 25 cases of type II SLAP tear treated with either SLAP repair (10 patients; mean age, 37 years) or primary arthroscopic biceps tenodesis (15 patients; mean age, 52 years). Compared with the SLAP repair group, the biceps tenodesis group had significantly higher rates of satisfaction and return to previous level of sports participation. However, group assignments were nonrandomized, and the decision to treat a patient with SLAP repair versus biceps tenodesis was made by the senior surgeon purely on the basis of age (SLAP repair for patients under 30 years). Ek and colleagues36 retrospectively compared the cases of 10 patients who underwent SLAP repair (mean age, 32 years) and 15 who underwent biceps tenodesis (mean age, 47 years) for type II SLAP tear. There was no significant difference between the groups with respect to outcome scores, return to play or preinjury activity level, or complications.
There continues to be significant debate as to which patient will benefit from primary SLAP repair versus biceps tenodesis. Multiple factors are involved: age, presence of associated shoulder pathology, occupation, preinjury activity level, and worker’s compensation status. Age has convincingly been shown to affect the outcomes of treatment of type II SLAP tears.34,35,37-40 There is consensus that patients over age 40 years will benefit from primary biceps tenodesis for SLAP tears. However, the evidence for this recommendation is weak.
3. Biceps tenodesis and failed SLAP repair
The definition of a failed SLAP repair is not well documented in the literature, but dissatisfaction after SLAP repair can result from continued shoulder pain, poor shoulder function, or inability to return to preinjury functional level.15,41 The etiologic determination and treatment of a failed SLAP repair are challenging, and outcomes of revision SLAP repair are not very promising.42,43 Biceps tenodesis has been proposed as an alternative treatment to revision SLAP repair for failed SLAP repair. McCormick and colleagues41 prospectively evaluated 42 patients (mean age, 39.2 years; minimum follow-up, 2 years) with failed type II SLAP repairs that were treated with open subpectoral biceps tenodesis. There was significant improvement in ASES, SANE, and Western Ontario Shoulder Instability Index (WOSI) outcome scores and in postoperative shoulder range of motion at a mean follow-up of 3.6 years. One patient had transient musculocutaneous neurapraxia after surgery. In a retrospective cohort study, Gupta and colleagues44 found significant improvement in ASES, SANE, SST, SF-12, and VAS outcome scores in 11 patients who underwent open subpectoral biceps tenodesis for failed arthroscopic SLAP repair (mean age at surgery, 40 years; mean follow-up, 26 months). Three of the 11 patients had worker’s compensation claims, and there were no complications and no revision surgeries required after biceps tenodesis. Werner and colleagues16 retrospectively evaluated 17 patients who underwent biceps tenodesis for failed SLAP repair (mean age, 39 years; minimum follow-up, 2 years). Twenty-nine percent of patients had worker’s compensation claims. Compared with the contralateral shoulder, the treated shoulder had better postoperative ASES, SANE, SST, and Veteran RAND 36-item health survey outcome scores; range of motion was near normal.
There are no high-quality studies comparing revision SLAP repair and biceps tenodesis in the management of failed SLAP repair.16,41-44 Case series studies have found improved outcomes and pain relief after biceps tenodesis for failed SLAP repair, but the quality of evidence has been poor (level IV evidence).16,41-44 The senior author recommends treating failed SLAP repairs with biceps tenodesis.
4. Biceps tenodesis as treatment option for SLAP tear in overhead throwing athletes
Biceps tenodesis is a potential alternative treatment to SLAP repair in overhead throwing athletes. Although outcome scores and satisfaction rates after SLAP repair are high in overhead athletes, the rates of return to sport are relatively low, especially in baseball players.38,45-47 In a level III cohort study, Boileau and colleagues34 found that 13 (87%) of 15 patients with type II SLAP tears, including 8 overhead athletes, had returned to their previous level of activity by a mean of 30 months after biceps tenodesis. In contrast, only 2 of 10 patients returned to their previous level of activity after SLAP repair. Interestingly, 3 patients who underwent biceps tenodesis for failed SLAP repair returned to overhead sports. Schöffl and colleagues48 reported on the outcomes of biceps tenodesis for SLAP lesions in 6 high-level rock climbers. By a mean follow-up of 6 months, all 6 patients had returned to their previous level of climbing. Their satisfaction rate was 96.8%. Gupta and colleagues35 reported on a cohort of 28 patients who underwent biceps tenodesis for SLAP tears and concomitant biceps tendonitis. Of the 8 athletes in the group, 5 were able to return to their previous level of play, and 1 was able to return to a lower level of sporting activity. There was significant improvement from preoperative to postoperative scores on ASES, SST, SANE, VAS, SF-12 overall, and SF-12 components.
Chalmers and colleagues49 recently described motion analyses with simultaneous surface electromyographic measurements in 18 baseball pitchers. Of these 18 players, 7 were uninjured (controls), 6 were pitching after SLAP repair, and 5 were pitching after subpectoral biceps tenodesis. There were no significant differences between controls and postoperative patients with respect to pitching kinematics. Interestingly, compared with the controls and the patients who underwent open biceps tenodesis, the patients who underwent SLAP repair had altered patterns of thoracic rotation during pitching. However, the clinical significance of this finding and the impact of this finding on pitching efficacy are not currently known.
Biceps tenodesis as a primary procedure for type II SLAP lesion in an overhead athlete is a concept in evolution. Increasing evidence suggests a role for primary biceps tenodesis in an overhead athlete with type II SLAP lesion and concomitant biceps pathology. However, this evidence is of poor quality, and the strength of the recommendation is weak. Still to be determined is whether return to preinjury performance level is better with primary biceps tenodesis or with SLAP repair in overhead athletes with type II SLAP lesion. As per the senior author’s treatment algorithm, we prefer SLAP repair for overhead athletes with type II SLAP tears and reserve biceps tenodesis for cases involving significant biceps pathology and/or clinical symptoms involving the bicipital groove consistent with extra-articular biceps pain.
5. Biceps tenodesis for type II SLAP tear in contact athletes and occupations demanding heavy labor (blue-collar jobs)
SLAP tears are less common in contact athletes, and there is general agreement that SLAP repair outcomes are better in contact athletes than in overhead athletes. In a retrospective review of 18 rugby players with SLAP tears, Funk and Snow50 reported excellent results and quicker return to sport after SLAP repair. Patients with isolated SLAP tears had the earliest return to play. Enad and colleagues51 reported SLAP repair outcomes in an active military population. SLAP tears are more common in the military versus the general population because of the unique physical demands placed on military personnel. The authors retrospectively reviewed 27 cases of type II SLAP tears treated with SLAP repair and suture anchors. Outcomes were measured at a mean of 30.5 months after surgery. Twenty-four (89%) of the 27 patients had good to excellent results, and 94% had returned to active duty by a mean of 4.4 months after SLAP repair.
Given the poor-quality evidence in the literature, we believe that biceps tenodesis should be reserved for revision surgery in contact athletes. There is insufficient evidence to recommend biceps tenodesis as primary treatment for type II SLAP tears in contact athletes. SLAP repair should be performed for primary SLAP lesions in contact athletes and for patients in physically demanding professions (eg, military, laborer, weightlifter).
Conclusion
SLAP tears can result in persistent shoulder pain and dysfunction. SLAP tear management depends on lesion type and severity, age, and functional demands. SLAP repair is the treatment of choice for type II SLAP lesions in young, active patients. Biceps tenodesis is a preferred alternative to SLAP repair in failed SLAP repair and in type II SLAP patients who are older than 40 years and who are less active and have a worker’s compensation claim. These recommendations are based on poor-quality evidence. There is an unmet need for randomized clinical studies comparing SLAP repair with biceps tenodesis for type II SLAP tears in different patient populations so as to optimize the current decision-making algorithm for SLAP tears.
Injuries of the superior labrum–biceps complex (SLBC) have been recognized as a cause of shoulder pain since they were first described by Andrews and colleagues1 in 1985. Superior labrum anterior to posterior (SLAP) tears are relatively uncommon injuries of the shoulder, and their true incidence is difficult to establish. However, recently there has been a significant increase in the reported incidence and operative treatment of SLAP tears.2 SLAP tears can occur in isolation, but they are commonly seen in association with other shoulder lesions, including rotator cuff tear, Bankart lesion, glenohumeral arthritis, acromioclavicular joint pathology, and subacromial impingement.
Although SLAP tears are well described and classified,3-6 our understanding of symptomatic SLAP tears and of their contribution to glenohumeral instability is limited. Diagnosing a SLAP tear on the basis of history and physical examination is a clinical challenge. Pain is the most common presentation of SLAP tears, though localization and characterization of pain are variable and nonspecific.7 The mechanism of injury is helpful in acute presentation (traction injury; fall on outstretched, abducted arm), but an overhead athlete may present with no distinct mechanism other than chronic, repetitive use of the shoulder.8-11 Numerous provocative physical examination tests have been used to assist in the diagnosis of SLAP tear, yet there is no consensus regarding the ideal physical examination test, with high sensitivity, specificity, and accuracy.12-14 Magnetic resonance arthrography, the gold standard imaging modality, is highly sensitive and specific (>95%) for diagnosing SLAP tears.
SLAP tear management is based on lesion type and severity, age, functional demands, and presence of coexisting intra-articular lesions. Management options include nonoperative treatment, débridement or repair of SLBC, biceps tenotomy, and biceps tenodesis.15-19
In this 5-point review, we present an evidence-based analysis of the role of the SLBC in glenohumeral stability and the role of biceps tenodesis in the management of SLAP tears.
1. Role of SLBC in stability of glenohumeral joint
The anatomy of the SLBC has been well described,20,21 and there is consensus that SLBC pathology can be a source of shoulder pain. The superior labrum is relatively more mobile than the rest of the glenoid labrum, and it provides attachment to the long head of the biceps tendon (LHBT) and the superior glenohumeral and middle glenohumeral ligaments.
The functional role of the SLBC in glenohumeral stability and its contribution to the pathogenesis of shoulder instability are not clearly defined. Our understanding of SLBC function is largely derived from simulated cadaveric experiments of SLAP tears. Controlled laboratory studies with simulated type II SLAP tears in cadavers have shown significantly increased glenohumeral translation in the anterior-posterior and superior-inferior directions, suggesting a role of the superior labrum in maintaining glenohumeral stability.22-26 Interestingly, there is conflicting evidence regarding restoration of normal glenohumeral translation in cadaveric shoulders after repair of simulated SLAP lesions in the presence or absence of simulated anterior capsular laxity.22,25-27 However, it is important to understand the limitations of cadaveric experiments in order to appreciate and truly comprehend the results of these experiments. There are inconsistencies in the size of simulated type II SLAP lesions in different studies, which can affect the degree of glenohumeral translation and the results of repair.23-25,28 The amount of glenohumeral translation noticed after simulated SLAP tears in cadavers, though statistically significant, is small in amplitude, and its relevance may not translate to a clinically significant level. The impact of dynamic components of stability (eg, rotator cuff muscles), capsular stretch, and other in vivo variables that affect glenohumeral stability are unaccounted for during cadaveric experiments.
LHBT is a recognized cause of shoulder pain, but its contribution to shoulder stability is a point of continued debate. According to one school of thought, LHBT is a vestigial structure that can be sacrificed without any loss of stability. Another school of thought holds that LHBT is an important active stabilizer of the glenohumeral joint. Cadaveric studies have demonstrated that loading the LHBT decreases glenohumeral translation and rotational range of motion, especially in lower and mid ranges of abduction.23,29,30 Furthermore, LHBT contributes to anterior glenohumeral stability by resisting torsional forces in the abducted and externally rotated shoulder and reducing stress on the inferior glenohumeral ligaments.31-33 Strauss and colleagues22 recently found that simulated anterior and posterior type II SLAP lesions in cadaveric shoulders increased glenohumeral translation in all planes, and biceps tenodesis did not further worsen this abnormal glenohumeral translation. Furthermore, repair of posterior SLAP lesions along with biceps tenodesis restored abnormal glenohumeral translation with no significant difference from the baseline in any plane of motion. Again, the limitations of cadaveric studies should be considered when interpreting these results and applying them clinically.
2. Biceps tenodesis as primary treatment for SLAP tears
A growing body of evidence suggests that primary tenodesis of LHBT may be an effective alternative treatment to SLAP repairs in select patients.34-36 However, the evidence is weak, and high-quality studies comparing SLAP repair and primary biceps tenodesis are required in order to make a strong recommendation for one technique over another. Gupta and colleagues35 retrospectively analyzed 28 cases of concomitant SLAP tear and biceps tendonitis treated with primary open subpectoral biceps tenodesis. There was significant improvement in patients’ functional outcome scores postoperatively [SANE (Single Assessment Numeric Evaluation), ASES (American Shoulder and Elbow Surgeons shoulder index), SST (Simple Shoulder Test), VAS (visual analog scale), and SF-12 (Short Form-12)]. In addition, 80% of patients were satisfied with their outcome. Mean age was 43.7 years. Forty-two percent of patients had a worker’s compensation claim. Interestingly, 15 patients in this cohort had a type I SLAP tear. Boileau and colleagues34 prospectively followed 25 cases of type II SLAP tear treated with either SLAP repair (10 patients; mean age, 37 years) or primary arthroscopic biceps tenodesis (15 patients; mean age, 52 years). Compared with the SLAP repair group, the biceps tenodesis group had significantly higher rates of satisfaction and return to previous level of sports participation. However, group assignments were nonrandomized, and the decision to treat a patient with SLAP repair versus biceps tenodesis was made by the senior surgeon purely on the basis of age (SLAP repair for patients under 30 years). Ek and colleagues36 retrospectively compared the cases of 10 patients who underwent SLAP repair (mean age, 32 years) and 15 who underwent biceps tenodesis (mean age, 47 years) for type II SLAP tear. There was no significant difference between the groups with respect to outcome scores, return to play or preinjury activity level, or complications.
There continues to be significant debate as to which patient will benefit from primary SLAP repair versus biceps tenodesis. Multiple factors are involved: age, presence of associated shoulder pathology, occupation, preinjury activity level, and worker’s compensation status. Age has convincingly been shown to affect the outcomes of treatment of type II SLAP tears.34,35,37-40 There is consensus that patients over age 40 years will benefit from primary biceps tenodesis for SLAP tears. However, the evidence for this recommendation is weak.
3. Biceps tenodesis and failed SLAP repair
The definition of a failed SLAP repair is not well documented in the literature, but dissatisfaction after SLAP repair can result from continued shoulder pain, poor shoulder function, or inability to return to preinjury functional level.15,41 The etiologic determination and treatment of a failed SLAP repair are challenging, and outcomes of revision SLAP repair are not very promising.42,43 Biceps tenodesis has been proposed as an alternative treatment to revision SLAP repair for failed SLAP repair. McCormick and colleagues41 prospectively evaluated 42 patients (mean age, 39.2 years; minimum follow-up, 2 years) with failed type II SLAP repairs that were treated with open subpectoral biceps tenodesis. There was significant improvement in ASES, SANE, and Western Ontario Shoulder Instability Index (WOSI) outcome scores and in postoperative shoulder range of motion at a mean follow-up of 3.6 years. One patient had transient musculocutaneous neurapraxia after surgery. In a retrospective cohort study, Gupta and colleagues44 found significant improvement in ASES, SANE, SST, SF-12, and VAS outcome scores in 11 patients who underwent open subpectoral biceps tenodesis for failed arthroscopic SLAP repair (mean age at surgery, 40 years; mean follow-up, 26 months). Three of the 11 patients had worker’s compensation claims, and there were no complications and no revision surgeries required after biceps tenodesis. Werner and colleagues16 retrospectively evaluated 17 patients who underwent biceps tenodesis for failed SLAP repair (mean age, 39 years; minimum follow-up, 2 years). Twenty-nine percent of patients had worker’s compensation claims. Compared with the contralateral shoulder, the treated shoulder had better postoperative ASES, SANE, SST, and Veteran RAND 36-item health survey outcome scores; range of motion was near normal.
There are no high-quality studies comparing revision SLAP repair and biceps tenodesis in the management of failed SLAP repair.16,41-44 Case series studies have found improved outcomes and pain relief after biceps tenodesis for failed SLAP repair, but the quality of evidence has been poor (level IV evidence).16,41-44 The senior author recommends treating failed SLAP repairs with biceps tenodesis.
4. Biceps tenodesis as treatment option for SLAP tear in overhead throwing athletes
Biceps tenodesis is a potential alternative treatment to SLAP repair in overhead throwing athletes. Although outcome scores and satisfaction rates after SLAP repair are high in overhead athletes, the rates of return to sport are relatively low, especially in baseball players.38,45-47 In a level III cohort study, Boileau and colleagues34 found that 13 (87%) of 15 patients with type II SLAP tears, including 8 overhead athletes, had returned to their previous level of activity by a mean of 30 months after biceps tenodesis. In contrast, only 2 of 10 patients returned to their previous level of activity after SLAP repair. Interestingly, 3 patients who underwent biceps tenodesis for failed SLAP repair returned to overhead sports. Schöffl and colleagues48 reported on the outcomes of biceps tenodesis for SLAP lesions in 6 high-level rock climbers. By a mean follow-up of 6 months, all 6 patients had returned to their previous level of climbing. Their satisfaction rate was 96.8%. Gupta and colleagues35 reported on a cohort of 28 patients who underwent biceps tenodesis for SLAP tears and concomitant biceps tendonitis. Of the 8 athletes in the group, 5 were able to return to their previous level of play, and 1 was able to return to a lower level of sporting activity. There was significant improvement from preoperative to postoperative scores on ASES, SST, SANE, VAS, SF-12 overall, and SF-12 components.
Chalmers and colleagues49 recently described motion analyses with simultaneous surface electromyographic measurements in 18 baseball pitchers. Of these 18 players, 7 were uninjured (controls), 6 were pitching after SLAP repair, and 5 were pitching after subpectoral biceps tenodesis. There were no significant differences between controls and postoperative patients with respect to pitching kinematics. Interestingly, compared with the controls and the patients who underwent open biceps tenodesis, the patients who underwent SLAP repair had altered patterns of thoracic rotation during pitching. However, the clinical significance of this finding and the impact of this finding on pitching efficacy are not currently known.
Biceps tenodesis as a primary procedure for type II SLAP lesion in an overhead athlete is a concept in evolution. Increasing evidence suggests a role for primary biceps tenodesis in an overhead athlete with type II SLAP lesion and concomitant biceps pathology. However, this evidence is of poor quality, and the strength of the recommendation is weak. Still to be determined is whether return to preinjury performance level is better with primary biceps tenodesis or with SLAP repair in overhead athletes with type II SLAP lesion. As per the senior author’s treatment algorithm, we prefer SLAP repair for overhead athletes with type II SLAP tears and reserve biceps tenodesis for cases involving significant biceps pathology and/or clinical symptoms involving the bicipital groove consistent with extra-articular biceps pain.
5. Biceps tenodesis for type II SLAP tear in contact athletes and occupations demanding heavy labor (blue-collar jobs)
SLAP tears are less common in contact athletes, and there is general agreement that SLAP repair outcomes are better in contact athletes than in overhead athletes. In a retrospective review of 18 rugby players with SLAP tears, Funk and Snow50 reported excellent results and quicker return to sport after SLAP repair. Patients with isolated SLAP tears had the earliest return to play. Enad and colleagues51 reported SLAP repair outcomes in an active military population. SLAP tears are more common in the military versus the general population because of the unique physical demands placed on military personnel. The authors retrospectively reviewed 27 cases of type II SLAP tears treated with SLAP repair and suture anchors. Outcomes were measured at a mean of 30.5 months after surgery. Twenty-four (89%) of the 27 patients had good to excellent results, and 94% had returned to active duty by a mean of 4.4 months after SLAP repair.
Given the poor-quality evidence in the literature, we believe that biceps tenodesis should be reserved for revision surgery in contact athletes. There is insufficient evidence to recommend biceps tenodesis as primary treatment for type II SLAP tears in contact athletes. SLAP repair should be performed for primary SLAP lesions in contact athletes and for patients in physically demanding professions (eg, military, laborer, weightlifter).
Conclusion
SLAP tears can result in persistent shoulder pain and dysfunction. SLAP tear management depends on lesion type and severity, age, and functional demands. SLAP repair is the treatment of choice for type II SLAP lesions in young, active patients. Biceps tenodesis is a preferred alternative to SLAP repair in failed SLAP repair and in type II SLAP patients who are older than 40 years and who are less active and have a worker’s compensation claim. These recommendations are based on poor-quality evidence. There is an unmet need for randomized clinical studies comparing SLAP repair with biceps tenodesis for type II SLAP tears in different patient populations so as to optimize the current decision-making algorithm for SLAP tears.
1. Andrews JR, Carson WG Jr, McLeod WD. Glenoid labrum tears related to the long head of the biceps. Am J Sports Med. 1985;13(5):337-341.
2. Weber SC, Martin DF, Seiler JG 3rd, Harrast JJ. Superior labrum anterior and posterior lesions of the shoulder: incidence rates, complications, and outcomes as reported by American Board of Orthopaedic Surgery. Part II candidates. Am J Sports Med. 2012;40(7):1538-1543.
3. Snyder SJ, Karzel RP, Del Pizzo W, Ferkel RD, Friedman MJ. SLAP lesions of the shoulder. Arthroscopy. 1990;6(4):274-279.
4. Morgan CD, Burkhart SS, Palmeri M, Gillespie M. Type II SLAP lesions: three subtypes and their relationships to superior instability and rotator cuff tears. Arthroscopy. 1998;14(6):553-565.
5. Powell SE, Nord KD, Ryu RKN. The diagnosis, classification, and treatment of SLAP lesions. Oper Tech Sports Med. 2012;20(1):46-56.
6. Maffet MW, Gartsman GM, Moseley B. Superior labrum-biceps tendon complex lesions of the shoulder. Am J Sports Med. 1995;23(1):93-98.
7. Kim TK, Queale WS, Cosgarea AJ, McFarland EG. Clinical features of the different types of SLAP lesions: an analysis of one hundred and thirty-nine cases. J Bone Joint Surg Am. 2003;85(1):66-71.
8. Abrams GD, Safran MR. Diagnosis and management of superior labrum anterior posterior lesions in overhead athletes. Br J Sports Med. 2010;44(5):311-318.
9. Keener JD, Brophy RH. Superior labral tears of the shoulder: pathogenesis, evaluation, and treatment. J Am Acad Orthop Surg. 2009;17(10):627-637.
10. Abrams GD, Hussey KE, Harris JD, Cole BJ. Clinical results of combined meniscus and femoral osteochondral allograft transplantation: minimum 2-year follow-up. Arthroscopy. 2014;30(8):964-970.e1.
11. Burkhart SS, Morgan CD, Kibler WB. The disabled throwing shoulder: spectrum of pathology part I: pathoanatomy and biomechanics. Arthroscopy. 2003;19(4):404-420.
12. Virk MS, Arciero RA. Superior labrum anterior to posterior tears and glenohumeral instability. Instr Course Lect. 2013;62:501-514.
13. Calvert E, Chambers GK, Regan W, Hawkins RH, Leith JM. Special physical examination tests for superior labrum anterior posterior shoulder tears are clinically limited and invalid: a diagnostic systematic review. J Clin Epidemiol. 2009;62(5):558-563.
14. Jones GL, Galluch DB. Clinical assessment of superior glenoid labral lesions: a systematic review. Clin Orthop Relat Res. 2007;455:45-51.
15. Werner BC, Brockmeier SF, Miller MD. Etiology, diagnosis, and management of failed SLAP repair. J Am Acad Orthop Surg. 2014;22(9):554-565.
16. Werner BC, Pehlivan HC, Hart JM, et al. Biceps tenodesis is a viable option for salvage of failed SLAP repair. J Shoulder Elbow Surg. 2014;23(8):e179-e184.
17. Erickson J, Lavery K, Monica J, Gatt C, Dhawan A. Surgical treatment of symptomatic superior labrum anterior-posterior tears in patients older than 40 years: a systematic review. Am J Sports Med. 2015;43(5):1274-1282.
18. Huri G, Hyun YS, Garbis NG, McFarland EG. Treatment of superior labrum anterior posterior lesions: a literature review. Acta Orthop Traumatol Turc. 2014;48(3):290-297.
19. Li X, Lin TJ, Jager M, et al. Management of type II superior labrum anterior posterior lesions: a review of the literature. Orthop Rev. 2010;2(1):e6.
20. Cooper DE, Arnoczky SP, O’Brien SJ, Warren RF, DiCarlo E, Allen AA. Anatomy, histology, and vascularity of the glenoid labrum. An anatomical study. J Bone Joint Surg Am. 1992;74(1):46-52.
21. Vangsness CT, Jorgenson SS, Watson T, Johnson DL. The origin of the long head of the biceps from the scapula and glenoid labrum. An anatomical study of 100 shoulders. J Bone Joint Surg Br. 1994;76(6):951-954.
22. Strauss EJ, Salata MJ, Sershon RA, et al. Role of the superior labrum after biceps tenodesis in glenohumeral stability. J Shoulder Elbow Surg. 2014;23(4):485-491.
23. Pagnani MJ, Deng XH, Warren RF, Torzilli PA, Altchek DW. Effect of lesions of the superior portion of the glenoid labrum on glenohumeral translation. J Bone Joint Surg Am. 1995;77(7):1003-1010.
24. McMahon PJ, Burkart A, Musahl V, Debski RE. Glenohumeral translations are increased after a type II superior labrum anterior-posterior lesion: a cadaveric study of severity of passive stabilizer injury. J Shoulder Elbow Surg. 2004;13(1):39-44.
25. Burkart A, Debski R, Musahl V, McMahon P, Woo SL. Biomechanical tests for type II SLAP lesions of the shoulder joint before and after arthroscopic repair [in German]. Orthopade. 2003;32(7):600-607.
26. Panossian VR, Mihata T, Tibone JE, Fitzpatrick MJ, McGarry MH, Lee TQ. Biomechanical analysis of isolated type II SLAP lesions and repair. J Shoulder Elbow Surg. 2005;14(5):529-534.
27. Mihata T, McGarry MH, Tibone JE, Fitzpatrick MJ, Kinoshita M, Lee TQ. Biomechanical assessment of type II superior labral anterior-posterior (SLAP) lesions associated with anterior shoulder capsular laxity as seen in throwers: a cadaveric study. Am J Sports Med. 2008;36(8):1604-1610.
28. Youm T, Tibone JE, ElAttrache NS, McGarry MH, Lee TQ. Simulated type II superior labral anterior posterior lesions do not alter the path of glenohumeral articulation: a cadaveric biomechanical study. Am J Sports Med. 2008;36(4):767-774.
29. Youm T, ElAttrache NS, Tibone JE, McGarry MH, Lee TQ. The effect of the long head of the biceps on glenohumeral kinematics. J Shoulder Elbow Surg. 2009;18(1):122-129.
30. McGarry MH, Nguyen ML, Quigley RJ, Hanypsiak B, Gupta R, Lee TQ. The effect of long and short head biceps loading on glenohumeral joint rotational range of motion and humeral head position [published online ahead of print September 26, 2014]. Knee Surg Sports Traumatol Arthrosc.
31. Glousman R, Jobe F, Tibone J, Moynes D, Antonelli D, Perry J. Dynamic electromyographic analysis of the throwing shoulder with glenohumeral instability. J Bone Joint Surg Am. 1988;70(2):220-226.
32. Gowan ID, Jobe FW, Tibone JE, Perry J, Moynes DR. A comparative electromyographic analysis of the shoulder during pitching. Professional versus amateur pitchers. Am J Sports Med. 1987;15(6):586-590.
33. Rodosky MW, Harner CD, Fu FH. The role of the long head of the biceps muscle and superior glenoid labrum in anterior stability of the shoulder. Am J Sports Med. 1994;22(1):121-130.
34. Boileau P, Parratte S, Chuinard C, Roussanne Y, Shia D, Bicknell R. Arthroscopic treatment of isolated type II SLAP lesions: biceps tenodesis as an alternative to reinsertion. Am J Sports Med. 2009;37(5):929-936.
35. Gupta AK, Chalmers PN, Klosterman EL, et al. Subpectoral biceps tenodesis for bicipital tendonitis with SLAP tear. Orthopedics. 2015;38(1):e48-e53.
36. Ek ET, Shi LL, Tompson JD, Freehill MT, Warner JJ. Surgical treatment of isolated type II superior labrum anterior-posterior (SLAP) lesions: repair versus biceps tenodesis. J Shoulder Elbow Surg. 2014;23(7):1059-1065.
37. Alpert JM, Wuerz TH, O’Donnell TF, Carroll KM, Brucker NN, Gill TJ. The effect of age on the outcomes of arthroscopic repair of type II superior labral anterior and posterior lesions. Am J Sports Med. 2010;38(11):2299-2303.
38. Provencher MT, McCormick F, Dewing C, McIntire S, Solomon D. A prospective analysis of 179 type 2 superior labrum anterior and posterior repairs: outcomes and factors associated with success and failure. Am J Sports Med. 2013;41(4):880-886.
39. Denard PJ, Lädermann A, Burkhart SS. Long-term outcome after arthroscopic repair of type II SLAP lesions: results according to age and workers’ compensation status. Arthroscopy. 2012;28(4):451-457.
40. Burns JP, Bahk M, Snyder SJ. Superior labral tears: repair versus biceps tenodesis. J Shoulder Elbow Surg. 2011;20(2 suppl):S2-S8.
41. McCormick F, Nwachukwu BU, Solomon D, et al. The efficacy of biceps tenodesis in the treatment of failed superior labral anterior posterior repairs. Am J Sports Med. 2014;42(4):820-825.
42. Katz LM, Hsu S, Miller SL, et al. Poor outcomes after SLAP repair: descriptive analysis and prognosis. Arthroscopy. 2009;25(8):849-855.
43. Park S, Glousman RE. Outcomes of revision arthroscopic type II superior labral anterior posterior repairs. Am J Sports Med. 2011;39(6):1290-1294.
44. Gupta AK, Bruce B, Klosterman EL, McCormick F, Harris J, Romeo AA. Subpectoral biceps tenodesis for failed type II SLAP repair. Orthopedics. 2013;36(6):e723-e728.
45. Neuman BJ, Boisvert CB, Reiter B, Lawson K, Ciccotti MG, Cohen SB. Results of arthroscopic repair of type II superior labral anterior posterior lesions in overhead athletes: assessment of return to preinjury playing level and satisfaction. Am J Sports Med. 2011;39(9):1883-1888.
46. Fedoriw WW, Ramkumar P, McCulloch PC, Lintner DM. Return to play after treatment of superior labral tears in professional baseball players. Am J Sports Med. 2014;42(5):1155-1160.
47. Park JY, Chung SW, Jeon SH, Lee JG, Oh KS. Clinical and radiological outcomes of type 2 superior labral anterior posterior repairs in elite overhead athletes. Am J Sports Med. 2013;41(6):1372-1379.
48. Schöffl V, Popp D, Dickschass J, Küpper T. Superior labral anterior-posterior lesions in rock climbers—primary double tenodesis? Clin J Sport Med. 2011;21(3):261-263.
49. Chalmers PN, Trombley R, Cip J, et al. Postoperative restoration of upper extremity motion and neuromuscular control during the overhand pitch: evaluation of tenodesis and repair for superior labral anterior-posterior tears. Am J Sports Med. 2014;42(12):2825-2836.
50. Funk L, Snow M. SLAP tears of the glenoid labrum in contact athletes. Clin J Sport Med. 2007;17(1):1-4.
51. Enad JG, Gaines RJ, White SM, Kurtz CA. Arthroscopic superior labrum anterior-posterior repair in military patients. J Shoulder Elbow Surg. 2007;16(3):300-305.
1. Andrews JR, Carson WG Jr, McLeod WD. Glenoid labrum tears related to the long head of the biceps. Am J Sports Med. 1985;13(5):337-341.
2. Weber SC, Martin DF, Seiler JG 3rd, Harrast JJ. Superior labrum anterior and posterior lesions of the shoulder: incidence rates, complications, and outcomes as reported by American Board of Orthopaedic Surgery. Part II candidates. Am J Sports Med. 2012;40(7):1538-1543.
3. Snyder SJ, Karzel RP, Del Pizzo W, Ferkel RD, Friedman MJ. SLAP lesions of the shoulder. Arthroscopy. 1990;6(4):274-279.
4. Morgan CD, Burkhart SS, Palmeri M, Gillespie M. Type II SLAP lesions: three subtypes and their relationships to superior instability and rotator cuff tears. Arthroscopy. 1998;14(6):553-565.
5. Powell SE, Nord KD, Ryu RKN. The diagnosis, classification, and treatment of SLAP lesions. Oper Tech Sports Med. 2012;20(1):46-56.
6. Maffet MW, Gartsman GM, Moseley B. Superior labrum-biceps tendon complex lesions of the shoulder. Am J Sports Med. 1995;23(1):93-98.
7. Kim TK, Queale WS, Cosgarea AJ, McFarland EG. Clinical features of the different types of SLAP lesions: an analysis of one hundred and thirty-nine cases. J Bone Joint Surg Am. 2003;85(1):66-71.
8. Abrams GD, Safran MR. Diagnosis and management of superior labrum anterior posterior lesions in overhead athletes. Br J Sports Med. 2010;44(5):311-318.
9. Keener JD, Brophy RH. Superior labral tears of the shoulder: pathogenesis, evaluation, and treatment. J Am Acad Orthop Surg. 2009;17(10):627-637.
10. Abrams GD, Hussey KE, Harris JD, Cole BJ. Clinical results of combined meniscus and femoral osteochondral allograft transplantation: minimum 2-year follow-up. Arthroscopy. 2014;30(8):964-970.e1.
11. Burkhart SS, Morgan CD, Kibler WB. The disabled throwing shoulder: spectrum of pathology part I: pathoanatomy and biomechanics. Arthroscopy. 2003;19(4):404-420.
12. Virk MS, Arciero RA. Superior labrum anterior to posterior tears and glenohumeral instability. Instr Course Lect. 2013;62:501-514.
13. Calvert E, Chambers GK, Regan W, Hawkins RH, Leith JM. Special physical examination tests for superior labrum anterior posterior shoulder tears are clinically limited and invalid: a diagnostic systematic review. J Clin Epidemiol. 2009;62(5):558-563.
14. Jones GL, Galluch DB. Clinical assessment of superior glenoid labral lesions: a systematic review. Clin Orthop Relat Res. 2007;455:45-51.
15. Werner BC, Brockmeier SF, Miller MD. Etiology, diagnosis, and management of failed SLAP repair. J Am Acad Orthop Surg. 2014;22(9):554-565.
16. Werner BC, Pehlivan HC, Hart JM, et al. Biceps tenodesis is a viable option for salvage of failed SLAP repair. J Shoulder Elbow Surg. 2014;23(8):e179-e184.
17. Erickson J, Lavery K, Monica J, Gatt C, Dhawan A. Surgical treatment of symptomatic superior labrum anterior-posterior tears in patients older than 40 years: a systematic review. Am J Sports Med. 2015;43(5):1274-1282.
18. Huri G, Hyun YS, Garbis NG, McFarland EG. Treatment of superior labrum anterior posterior lesions: a literature review. Acta Orthop Traumatol Turc. 2014;48(3):290-297.
19. Li X, Lin TJ, Jager M, et al. Management of type II superior labrum anterior posterior lesions: a review of the literature. Orthop Rev. 2010;2(1):e6.
20. Cooper DE, Arnoczky SP, O’Brien SJ, Warren RF, DiCarlo E, Allen AA. Anatomy, histology, and vascularity of the glenoid labrum. An anatomical study. J Bone Joint Surg Am. 1992;74(1):46-52.
21. Vangsness CT, Jorgenson SS, Watson T, Johnson DL. The origin of the long head of the biceps from the scapula and glenoid labrum. An anatomical study of 100 shoulders. J Bone Joint Surg Br. 1994;76(6):951-954.
22. Strauss EJ, Salata MJ, Sershon RA, et al. Role of the superior labrum after biceps tenodesis in glenohumeral stability. J Shoulder Elbow Surg. 2014;23(4):485-491.
23. Pagnani MJ, Deng XH, Warren RF, Torzilli PA, Altchek DW. Effect of lesions of the superior portion of the glenoid labrum on glenohumeral translation. J Bone Joint Surg Am. 1995;77(7):1003-1010.
24. McMahon PJ, Burkart A, Musahl V, Debski RE. Glenohumeral translations are increased after a type II superior labrum anterior-posterior lesion: a cadaveric study of severity of passive stabilizer injury. J Shoulder Elbow Surg. 2004;13(1):39-44.
25. Burkart A, Debski R, Musahl V, McMahon P, Woo SL. Biomechanical tests for type II SLAP lesions of the shoulder joint before and after arthroscopic repair [in German]. Orthopade. 2003;32(7):600-607.
26. Panossian VR, Mihata T, Tibone JE, Fitzpatrick MJ, McGarry MH, Lee TQ. Biomechanical analysis of isolated type II SLAP lesions and repair. J Shoulder Elbow Surg. 2005;14(5):529-534.
27. Mihata T, McGarry MH, Tibone JE, Fitzpatrick MJ, Kinoshita M, Lee TQ. Biomechanical assessment of type II superior labral anterior-posterior (SLAP) lesions associated with anterior shoulder capsular laxity as seen in throwers: a cadaveric study. Am J Sports Med. 2008;36(8):1604-1610.
28. Youm T, Tibone JE, ElAttrache NS, McGarry MH, Lee TQ. Simulated type II superior labral anterior posterior lesions do not alter the path of glenohumeral articulation: a cadaveric biomechanical study. Am J Sports Med. 2008;36(4):767-774.
29. Youm T, ElAttrache NS, Tibone JE, McGarry MH, Lee TQ. The effect of the long head of the biceps on glenohumeral kinematics. J Shoulder Elbow Surg. 2009;18(1):122-129.
30. McGarry MH, Nguyen ML, Quigley RJ, Hanypsiak B, Gupta R, Lee TQ. The effect of long and short head biceps loading on glenohumeral joint rotational range of motion and humeral head position [published online ahead of print September 26, 2014]. Knee Surg Sports Traumatol Arthrosc.
31. Glousman R, Jobe F, Tibone J, Moynes D, Antonelli D, Perry J. Dynamic electromyographic analysis of the throwing shoulder with glenohumeral instability. J Bone Joint Surg Am. 1988;70(2):220-226.
32. Gowan ID, Jobe FW, Tibone JE, Perry J, Moynes DR. A comparative electromyographic analysis of the shoulder during pitching. Professional versus amateur pitchers. Am J Sports Med. 1987;15(6):586-590.
33. Rodosky MW, Harner CD, Fu FH. The role of the long head of the biceps muscle and superior glenoid labrum in anterior stability of the shoulder. Am J Sports Med. 1994;22(1):121-130.
34. Boileau P, Parratte S, Chuinard C, Roussanne Y, Shia D, Bicknell R. Arthroscopic treatment of isolated type II SLAP lesions: biceps tenodesis as an alternative to reinsertion. Am J Sports Med. 2009;37(5):929-936.
35. Gupta AK, Chalmers PN, Klosterman EL, et al. Subpectoral biceps tenodesis for bicipital tendonitis with SLAP tear. Orthopedics. 2015;38(1):e48-e53.
36. Ek ET, Shi LL, Tompson JD, Freehill MT, Warner JJ. Surgical treatment of isolated type II superior labrum anterior-posterior (SLAP) lesions: repair versus biceps tenodesis. J Shoulder Elbow Surg. 2014;23(7):1059-1065.
37. Alpert JM, Wuerz TH, O’Donnell TF, Carroll KM, Brucker NN, Gill TJ. The effect of age on the outcomes of arthroscopic repair of type II superior labral anterior and posterior lesions. Am J Sports Med. 2010;38(11):2299-2303.
38. Provencher MT, McCormick F, Dewing C, McIntire S, Solomon D. A prospective analysis of 179 type 2 superior labrum anterior and posterior repairs: outcomes and factors associated with success and failure. Am J Sports Med. 2013;41(4):880-886.
39. Denard PJ, Lädermann A, Burkhart SS. Long-term outcome after arthroscopic repair of type II SLAP lesions: results according to age and workers’ compensation status. Arthroscopy. 2012;28(4):451-457.
40. Burns JP, Bahk M, Snyder SJ. Superior labral tears: repair versus biceps tenodesis. J Shoulder Elbow Surg. 2011;20(2 suppl):S2-S8.
41. McCormick F, Nwachukwu BU, Solomon D, et al. The efficacy of biceps tenodesis in the treatment of failed superior labral anterior posterior repairs. Am J Sports Med. 2014;42(4):820-825.
42. Katz LM, Hsu S, Miller SL, et al. Poor outcomes after SLAP repair: descriptive analysis and prognosis. Arthroscopy. 2009;25(8):849-855.
43. Park S, Glousman RE. Outcomes of revision arthroscopic type II superior labral anterior posterior repairs. Am J Sports Med. 2011;39(6):1290-1294.
44. Gupta AK, Bruce B, Klosterman EL, McCormick F, Harris J, Romeo AA. Subpectoral biceps tenodesis for failed type II SLAP repair. Orthopedics. 2013;36(6):e723-e728.
45. Neuman BJ, Boisvert CB, Reiter B, Lawson K, Ciccotti MG, Cohen SB. Results of arthroscopic repair of type II superior labral anterior posterior lesions in overhead athletes: assessment of return to preinjury playing level and satisfaction. Am J Sports Med. 2011;39(9):1883-1888.
46. Fedoriw WW, Ramkumar P, McCulloch PC, Lintner DM. Return to play after treatment of superior labral tears in professional baseball players. Am J Sports Med. 2014;42(5):1155-1160.
47. Park JY, Chung SW, Jeon SH, Lee JG, Oh KS. Clinical and radiological outcomes of type 2 superior labral anterior posterior repairs in elite overhead athletes. Am J Sports Med. 2013;41(6):1372-1379.
48. Schöffl V, Popp D, Dickschass J, Küpper T. Superior labral anterior-posterior lesions in rock climbers—primary double tenodesis? Clin J Sport Med. 2011;21(3):261-263.
49. Chalmers PN, Trombley R, Cip J, et al. Postoperative restoration of upper extremity motion and neuromuscular control during the overhand pitch: evaluation of tenodesis and repair for superior labral anterior-posterior tears. Am J Sports Med. 2014;42(12):2825-2836.
50. Funk L, Snow M. SLAP tears of the glenoid labrum in contact athletes. Clin J Sport Med. 2007;17(1):1-4.
51. Enad JG, Gaines RJ, White SM, Kurtz CA. Arthroscopic superior labrum anterior-posterior repair in military patients. J Shoulder Elbow Surg. 2007;16(3):300-305.
Caring for gender-nonconforming youth
As a member of a multidisciplinary clinic that cares for gender-nonconforming (GN) youth, I frequently field questions from providers about how to handle gender identity concerns in the primary care setting. The specific health care needs of these youth matter as GN youth are at increased risk of self-harm, suicide attempts, mood disorders, eating disorders, substance use, and low school performance.1, 2 These increased risks appear to be related to the rejection and stigma associated with gender nonconformity that can extend to the health care setting.
More than 50% of transgender adults report experiences of discrimination in health care.3 The literature suggests that creating a supportive and affirming environment for GN youth may decrease these risks. If we can do just that during their health care visits, we can make a positive impact on our patients.
Terminology
A review of terminology and clarification of the difference between biologic sex, gender identity, gender expression, and sexual orientation are necessary before discussing the care of GN youth. Biologic sex is typically assigned at birth and is determined by a person’s chromosomes, hormones, and anatomy. Sex most commonly is female or male. For a minority of the population, there may be disorders or differences of sex development in which the development of chromosomal, gonadal, or anatomic sex is atypical. Examples of these conditions are congenital adrenal hyperplasia and androgen insensitivity syndrome. Gender includes the behavioral, cultural, and psychological characteristics associated with femaleness or maleness.2 Gender identity is a person’s innate sense of feeling male, female, or somewhere in between. Individuals who have a gender identity that is congruent with their assigned sex are referred to as cisgender; those who have a gender identity that does not align with their birth sex are often referred to as transgender. Gender expression is how people choose to present themselves to the world. A person’s gender may or may not be consistent with his/her internal gender identity. For example, an individual may be female biologically (XX chromosomes, with a uterus, ovaries, and vagina) and self-identify as female, but express herself in a masculine way by having her hair cut short and wearing more masculine clothing.
Gender dysphoria occurs when an individual experiences psychological distress caused by the incongruence between his/her biologic sex and his/her internal gender identity, and this mismatch leads to clinically significant distress or impairment in daily functioning. Gender dysphoria is a diagnosis in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5). It has replaced the earlier diagnosis of gender identity disorder in the DSM-IV. The new diagnosis focuses on the distress related to an incongruence between gender identity and biologic sex and does not label it as pathologic. Gender-nonconforming individuals do not follow other people’s ideas or stereotypes about how they should look or act based on the sex they were assigned at birth. It is important to note that an individual’s gender identity is separate from sexual orientation. Sexual orientation describes an individual’s pattern of sexual and physical attraction. An individual may be attracted to members of the same sex (homosexual, lesbian, gay), opposite sex (heterosexual), or both sexes (bisexual). Increasingly youth are using a variety of terms to describe their gender (for example, genderqueer, asexual, gender fluid) and sexual orientation (for example, pansexual, asexual). These terms may have different meanings for different youth, and it is important to respectfully ask and clarify what these terms mean to each individual patient.
Trajectory of gender identity
Experimenting with gender expression and gender roles is a normal part of childhood. The majority of young children with nonconforming gender identification will not persist with this identification through adolescence. Some of these children will go on to have a nonheterosexual sexual orientation when they are older. While it can be difficult to predict the trajectory of cross-gender identification in early childhood, those with a persistent, insistent, and consistent cross-gender identification in childhood are more likely to experience gender dysphoria and continue with a transgender identity into adulthood. Adolescence is a particularly difficult time for GN youth. The development of secondary sex characteristics that are not consistent with an individual’s identified gender, in addition to the psychosocial challenges of adolescent development, can lead to increased suicidal thoughts, self-harm behaviors, anxiety, isolation, and risk-taking behaviors. Gender dysphoria that increases with the onset of puberty rarely subsides with time.
Approach to GN patients in practice
Research is ongoing related to best practices for the care of GN youth. Clinical guidelines and standards of care have been published and endorsed by organizations including the Endocrine Society, Pediatric Endocrine Society, World Professional Association for Transgender Health, and the American Academy of Pediatrics. My recommendations for the care of GN youth are based on these guidelines.
Primary care providers are often the first place families turn when a child experiences gender identity concerns. Primary care providers can play an important role in providing a safe nonjudgmental environment for patients and families to discuss their concerns, and connecting patients and families to appropriate resources. Providers should first work to educate themselves and their staff about issues affecting GN youth and learn to provide culturally competent care to these youth. Asking youth their preferred names and preferred pronouns (for example, “he/him/his,” “she/her/hers,” “they/them/their,” or something else), documenting this in the medical record, and training clinic staff to use preferred names and pronouns creates an environment that validates, supports, and respects these youth.
It is important to ask all adolescents if they have questions or concerns about their gender identity, in addition to asking questions about sexual identity. It is important when asking these questions to avoid assumptions about an individual’s gender identity based on his or her gender expression. Providers also should familiarize themselves with local referral resources for these youth. As mentioned earlier, GN youth are at high risk for mental health complications including suicide, self-harm, and mood disorders. When referring patients for mental health services, you should be familiar with providers who have expertise in issues of gender identity. A recent report by the Substance Abuse and Mental Health Services Administration states that variations in gender identity are normal, and conversion therapies or other efforts to change gender identity are not effective, are harmful, and are not appropriate therapeutic practices.4
As increasing numbers of youth are identifying as transgender or gender nonconforming, the number of clinics that can coordinate with local providers to provide multidisciplinary care for GN patients is growing.
Resources for health care professionals
• National LGBT Health Education Center, the Fenway Institute. At its website, learning modules, webinars, and other educational resources are available for health care organizations.
• World Professional Association of Transgender Health. This website provides standards of care for transgender patients and a provider directory.
• The Genderbread Person. This website has a helpful infographic illustrating differences between biologic sex, gender identity, gender expression, and sexual orientation, which can be useful for education with patients, families, and trainees.
• Center of Excellence for Transgender Health. This organization works to increase access to comprehensive, effective, and affirming health care services for trans communities.
Resources for patients and families
• The Trevor Project. This website provides crisis intervention and suicide prevention services.
• National Center for Transgender Equality. This advocacy organization works to promote policy change to advance transgender equality.
• Family Acceptance Project. This research, intervention, education, and policy initiative works to prevent health and mental health risks for lesbian, gay, bisexual, and transgender children and youth, including suicide, homelessness, and HIV – in the context of their families, cultures, and faith communities.
References
1. Pediatrics. 2012 Mar;129(3):418-25.
2. Pediatrics. 2014 Dec;134(6):1184-92.
3. When Health Care Isn’t Caring: Lambda Legal’s Survey of Discrimination Against LGBT People and People with HIV, Lambda Legal, 2010. Available at www.lambdalegal.org/health-care-report.
4. Substance Abuse and Mental Health Services Administration. Ending Conversion Therapy: Supporting and Affirming LGBTQ Youth. HHS Publication No. (SMA) 15-4928. October 2015. Available at http://store.samhsa.gov/shin/content//SMA15-4928/SMA15-4928.pdf.
Dr. Chelvakumar is an attending physician in the division of adolescent medicine at Nationwide Children’s Hospital and an assistant professor of clinical pediatrics at the Ohio State University, both in Columbus.
As a member of a multidisciplinary clinic that cares for gender-nonconforming (GN) youth, I frequently field questions from providers about how to handle gender identity concerns in the primary care setting. The specific health care needs of these youth matter as GN youth are at increased risk of self-harm, suicide attempts, mood disorders, eating disorders, substance use, and low school performance.1, 2 These increased risks appear to be related to the rejection and stigma associated with gender nonconformity that can extend to the health care setting.
More than 50% of transgender adults report experiences of discrimination in health care.3 The literature suggests that creating a supportive and affirming environment for GN youth may decrease these risks. If we can do just that during their health care visits, we can make a positive impact on our patients.
Terminology
A review of terminology and clarification of the difference between biologic sex, gender identity, gender expression, and sexual orientation are necessary before discussing the care of GN youth. Biologic sex is typically assigned at birth and is determined by a person’s chromosomes, hormones, and anatomy. Sex most commonly is female or male. For a minority of the population, there may be disorders or differences of sex development in which the development of chromosomal, gonadal, or anatomic sex is atypical. Examples of these conditions are congenital adrenal hyperplasia and androgen insensitivity syndrome. Gender includes the behavioral, cultural, and psychological characteristics associated with femaleness or maleness.2 Gender identity is a person’s innate sense of feeling male, female, or somewhere in between. Individuals who have a gender identity that is congruent with their assigned sex are referred to as cisgender; those who have a gender identity that does not align with their birth sex are often referred to as transgender. Gender expression is how people choose to present themselves to the world. A person’s gender may or may not be consistent with his/her internal gender identity. For example, an individual may be female biologically (XX chromosomes, with a uterus, ovaries, and vagina) and self-identify as female, but express herself in a masculine way by having her hair cut short and wearing more masculine clothing.
Gender dysphoria occurs when an individual experiences psychological distress caused by the incongruence between his/her biologic sex and his/her internal gender identity, and this mismatch leads to clinically significant distress or impairment in daily functioning. Gender dysphoria is a diagnosis in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5). It has replaced the earlier diagnosis of gender identity disorder in the DSM-IV. The new diagnosis focuses on the distress related to an incongruence between gender identity and biologic sex and does not label it as pathologic. Gender-nonconforming individuals do not follow other people’s ideas or stereotypes about how they should look or act based on the sex they were assigned at birth. It is important to note that an individual’s gender identity is separate from sexual orientation. Sexual orientation describes an individual’s pattern of sexual and physical attraction. An individual may be attracted to members of the same sex (homosexual, lesbian, gay), opposite sex (heterosexual), or both sexes (bisexual). Increasingly youth are using a variety of terms to describe their gender (for example, genderqueer, asexual, gender fluid) and sexual orientation (for example, pansexual, asexual). These terms may have different meanings for different youth, and it is important to respectfully ask and clarify what these terms mean to each individual patient.
Trajectory of gender identity
Experimenting with gender expression and gender roles is a normal part of childhood. The majority of young children with nonconforming gender identification will not persist with this identification through adolescence. Some of these children will go on to have a nonheterosexual sexual orientation when they are older. While it can be difficult to predict the trajectory of cross-gender identification in early childhood, those with a persistent, insistent, and consistent cross-gender identification in childhood are more likely to experience gender dysphoria and continue with a transgender identity into adulthood. Adolescence is a particularly difficult time for GN youth. The development of secondary sex characteristics that are not consistent with an individual’s identified gender, in addition to the psychosocial challenges of adolescent development, can lead to increased suicidal thoughts, self-harm behaviors, anxiety, isolation, and risk-taking behaviors. Gender dysphoria that increases with the onset of puberty rarely subsides with time.
Approach to GN patients in practice
Research is ongoing related to best practices for the care of GN youth. Clinical guidelines and standards of care have been published and endorsed by organizations including the Endocrine Society, Pediatric Endocrine Society, World Professional Association for Transgender Health, and the American Academy of Pediatrics. My recommendations for the care of GN youth are based on these guidelines.
Primary care providers are often the first place families turn when a child experiences gender identity concerns. Primary care providers can play an important role in providing a safe nonjudgmental environment for patients and families to discuss their concerns, and connecting patients and families to appropriate resources. Providers should first work to educate themselves and their staff about issues affecting GN youth and learn to provide culturally competent care to these youth. Asking youth their preferred names and preferred pronouns (for example, “he/him/his,” “she/her/hers,” “they/them/their,” or something else), documenting this in the medical record, and training clinic staff to use preferred names and pronouns creates an environment that validates, supports, and respects these youth.
It is important to ask all adolescents if they have questions or concerns about their gender identity, in addition to asking questions about sexual identity. It is important when asking these questions to avoid assumptions about an individual’s gender identity based on his or her gender expression. Providers also should familiarize themselves with local referral resources for these youth. As mentioned earlier, GN youth are at high risk for mental health complications including suicide, self-harm, and mood disorders. When referring patients for mental health services, you should be familiar with providers who have expertise in issues of gender identity. A recent report by the Substance Abuse and Mental Health Services Administration states that variations in gender identity are normal, and conversion therapies or other efforts to change gender identity are not effective, are harmful, and are not appropriate therapeutic practices.4
As increasing numbers of youth are identifying as transgender or gender nonconforming, the number of clinics that can coordinate with local providers to provide multidisciplinary care for GN patients is growing.
Resources for health care professionals
• National LGBT Health Education Center, the Fenway Institute. At its website, learning modules, webinars, and other educational resources are available for health care organizations.
• World Professional Association of Transgender Health. This website provides standards of care for transgender patients and a provider directory.
• The Genderbread Person. This website has a helpful infographic illustrating differences between biologic sex, gender identity, gender expression, and sexual orientation, which can be useful for education with patients, families, and trainees.
• Center of Excellence for Transgender Health. This organization works to increase access to comprehensive, effective, and affirming health care services for trans communities.
Resources for patients and families
• The Trevor Project. This website provides crisis intervention and suicide prevention services.
• National Center for Transgender Equality. This advocacy organization works to promote policy change to advance transgender equality.
• Family Acceptance Project. This research, intervention, education, and policy initiative works to prevent health and mental health risks for lesbian, gay, bisexual, and transgender children and youth, including suicide, homelessness, and HIV – in the context of their families, cultures, and faith communities.
References
1. Pediatrics. 2012 Mar;129(3):418-25.
2. Pediatrics. 2014 Dec;134(6):1184-92.
3. When Health Care Isn’t Caring: Lambda Legal’s Survey of Discrimination Against LGBT People and People with HIV, Lambda Legal, 2010. Available at www.lambdalegal.org/health-care-report.
4. Substance Abuse and Mental Health Services Administration. Ending Conversion Therapy: Supporting and Affirming LGBTQ Youth. HHS Publication No. (SMA) 15-4928. October 2015. Available at http://store.samhsa.gov/shin/content//SMA15-4928/SMA15-4928.pdf.
Dr. Chelvakumar is an attending physician in the division of adolescent medicine at Nationwide Children’s Hospital and an assistant professor of clinical pediatrics at the Ohio State University, both in Columbus.
As a member of a multidisciplinary clinic that cares for gender-nonconforming (GN) youth, I frequently field questions from providers about how to handle gender identity concerns in the primary care setting. The specific health care needs of these youth matter as GN youth are at increased risk of self-harm, suicide attempts, mood disorders, eating disorders, substance use, and low school performance.1, 2 These increased risks appear to be related to the rejection and stigma associated with gender nonconformity that can extend to the health care setting.
More than 50% of transgender adults report experiences of discrimination in health care.3 The literature suggests that creating a supportive and affirming environment for GN youth may decrease these risks. If we can do just that during their health care visits, we can make a positive impact on our patients.
Terminology
A review of terminology and clarification of the difference between biologic sex, gender identity, gender expression, and sexual orientation are necessary before discussing the care of GN youth. Biologic sex is typically assigned at birth and is determined by a person’s chromosomes, hormones, and anatomy. Sex most commonly is female or male. For a minority of the population, there may be disorders or differences of sex development in which the development of chromosomal, gonadal, or anatomic sex is atypical. Examples of these conditions are congenital adrenal hyperplasia and androgen insensitivity syndrome. Gender includes the behavioral, cultural, and psychological characteristics associated with femaleness or maleness.2 Gender identity is a person’s innate sense of feeling male, female, or somewhere in between. Individuals who have a gender identity that is congruent with their assigned sex are referred to as cisgender; those who have a gender identity that does not align with their birth sex are often referred to as transgender. Gender expression is how people choose to present themselves to the world. A person’s gender may or may not be consistent with his/her internal gender identity. For example, an individual may be female biologically (XX chromosomes, with a uterus, ovaries, and vagina) and self-identify as female, but express herself in a masculine way by having her hair cut short and wearing more masculine clothing.
Gender dysphoria occurs when an individual experiences psychological distress caused by the incongruence between his/her biologic sex and his/her internal gender identity, and this mismatch leads to clinically significant distress or impairment in daily functioning. Gender dysphoria is a diagnosis in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5). It has replaced the earlier diagnosis of gender identity disorder in the DSM-IV. The new diagnosis focuses on the distress related to an incongruence between gender identity and biologic sex and does not label it as pathologic. Gender-nonconforming individuals do not follow other people’s ideas or stereotypes about how they should look or act based on the sex they were assigned at birth. It is important to note that an individual’s gender identity is separate from sexual orientation. Sexual orientation describes an individual’s pattern of sexual and physical attraction. An individual may be attracted to members of the same sex (homosexual, lesbian, gay), opposite sex (heterosexual), or both sexes (bisexual). Increasingly youth are using a variety of terms to describe their gender (for example, genderqueer, asexual, gender fluid) and sexual orientation (for example, pansexual, asexual). These terms may have different meanings for different youth, and it is important to respectfully ask and clarify what these terms mean to each individual patient.
Trajectory of gender identity
Experimenting with gender expression and gender roles is a normal part of childhood. The majority of young children with nonconforming gender identification will not persist with this identification through adolescence. Some of these children will go on to have a nonheterosexual sexual orientation when they are older. While it can be difficult to predict the trajectory of cross-gender identification in early childhood, those with a persistent, insistent, and consistent cross-gender identification in childhood are more likely to experience gender dysphoria and continue with a transgender identity into adulthood. Adolescence is a particularly difficult time for GN youth. The development of secondary sex characteristics that are not consistent with an individual’s identified gender, in addition to the psychosocial challenges of adolescent development, can lead to increased suicidal thoughts, self-harm behaviors, anxiety, isolation, and risk-taking behaviors. Gender dysphoria that increases with the onset of puberty rarely subsides with time.
Approach to GN patients in practice
Research is ongoing related to best practices for the care of GN youth. Clinical guidelines and standards of care have been published and endorsed by organizations including the Endocrine Society, Pediatric Endocrine Society, World Professional Association for Transgender Health, and the American Academy of Pediatrics. My recommendations for the care of GN youth are based on these guidelines.
Primary care providers are often the first place families turn when a child experiences gender identity concerns. Primary care providers can play an important role in providing a safe nonjudgmental environment for patients and families to discuss their concerns, and connecting patients and families to appropriate resources. Providers should first work to educate themselves and their staff about issues affecting GN youth and learn to provide culturally competent care to these youth. Asking youth their preferred names and preferred pronouns (for example, “he/him/his,” “she/her/hers,” “they/them/their,” or something else), documenting this in the medical record, and training clinic staff to use preferred names and pronouns creates an environment that validates, supports, and respects these youth.
It is important to ask all adolescents if they have questions or concerns about their gender identity, in addition to asking questions about sexual identity. It is important when asking these questions to avoid assumptions about an individual’s gender identity based on his or her gender expression. Providers also should familiarize themselves with local referral resources for these youth. As mentioned earlier, GN youth are at high risk for mental health complications including suicide, self-harm, and mood disorders. When referring patients for mental health services, you should be familiar with providers who have expertise in issues of gender identity. A recent report by the Substance Abuse and Mental Health Services Administration states that variations in gender identity are normal, and conversion therapies or other efforts to change gender identity are not effective, are harmful, and are not appropriate therapeutic practices.4
As increasing numbers of youth are identifying as transgender or gender nonconforming, the number of clinics that can coordinate with local providers to provide multidisciplinary care for GN patients is growing.
Resources for health care professionals
• National LGBT Health Education Center, the Fenway Institute. At its website, learning modules, webinars, and other educational resources are available for health care organizations.
• World Professional Association of Transgender Health. This website provides standards of care for transgender patients and a provider directory.
• The Genderbread Person. This website has a helpful infographic illustrating differences between biologic sex, gender identity, gender expression, and sexual orientation, which can be useful for education with patients, families, and trainees.
• Center of Excellence for Transgender Health. This organization works to increase access to comprehensive, effective, and affirming health care services for trans communities.
Resources for patients and families
• The Trevor Project. This website provides crisis intervention and suicide prevention services.
• National Center for Transgender Equality. This advocacy organization works to promote policy change to advance transgender equality.
• Family Acceptance Project. This research, intervention, education, and policy initiative works to prevent health and mental health risks for lesbian, gay, bisexual, and transgender children and youth, including suicide, homelessness, and HIV – in the context of their families, cultures, and faith communities.
References
1. Pediatrics. 2012 Mar;129(3):418-25.
2. Pediatrics. 2014 Dec;134(6):1184-92.
3. When Health Care Isn’t Caring: Lambda Legal’s Survey of Discrimination Against LGBT People and People with HIV, Lambda Legal, 2010. Available at www.lambdalegal.org/health-care-report.
4. Substance Abuse and Mental Health Services Administration. Ending Conversion Therapy: Supporting and Affirming LGBTQ Youth. HHS Publication No. (SMA) 15-4928. October 2015. Available at http://store.samhsa.gov/shin/content//SMA15-4928/SMA15-4928.pdf.
Dr. Chelvakumar is an attending physician in the division of adolescent medicine at Nationwide Children’s Hospital and an assistant professor of clinical pediatrics at the Ohio State University, both in Columbus.
High Self-Contamination among Healthcare Workers
Florescent lotion and black light revealed that health care workers often contaminate their skin and clothing while removing their protective gear, researchers say.
"It was surprising for the participants in the study to see that they frequently contaminated themselves during [personal protective equipment] removal," said senior author Dr. Curtis J. Donskey of the Cleveland Veterans Affairs Medical Center.
"Most of the participants appeared to be unaware of the high risk for contamination and many reported receiving minimal or no training in putting on and taking off [personal protective equipment]," he said by email.
The researchers recruited doctors, nurses and ancillary personnel such as phlebotomists and physical therapists at four Cleveland-area hospitals to participate in the simulations. More than half of the 435 simulations were performed by nurses.
As reported online October 12 in JAMA Internal Medicine, the participants put on protective gowns and gloves in their usual manner and then had a small amount of fluorescent lotion placed in the palm of their hands, which they then rubbed between their hands for 15 seconds to simulate dirtied gloves, then smeared the gloves over the chest and abdomen area of the gown. Then the gloves were exchanged for clean ones.
After they removed their gloves and gowns in their usual manners, researchers used a black light to check for lotion contamination of the hands, forearms, neck, face, hair or clothing.
Skin or clothing contamination happened 46% of the time, more frequently during glove removal.
Researchers also noted whether participants had used proper protective equipment technique, e.g., wearing gloves extended over the wrists of the gown, gown removed first by pulling away from the neck and body, and gloves removed second. Contamination happened 70% of the time when proper technique was not followed, compared to 30% of the time when it was followed.
"When dealing with pathogens that are potentially fatal, the goal has to be zero contamination," Dr. Donskey said. "In routine care settings, we would like personnel to be well trained and confident that they can minimize contamination, but would not insist on zero contamination."
It is important for personnel to perform hand hygiene after removing gloves and gowns, he said.
The researchers also conducted these tests with a group of personnel who had attended special infection control sessions, with a 10-minute video presentation and 20 minutes of demonstrations and practice in using and removing protective gear.
Before the training sessions, these individuals contaminated themselves 60% of the time, compared to roughly 19% after the sessions. The improvements were still seen at re-tests done one and three months later.
"This suggests that training using fluorescent lotion can be useful to identify minor deficiencies in technique that lead to contamination," Donskey said.
Recent experience with the Ebola virus in the U.S. showed that self-contamination during removal of protective equipment does occur, but this study exposes a more widespread issue that may be happening during routine patient care, said Dr. Michelle Doll of Virginia Commonwealth University in Richmond who coauthored a commentary on the new study.
"Use of gowns and gloves for contact precautions on a busy inpatient unit is costly on multiple levels," Doll said by email. "In situations when we do decide to use these tools for infection prevention, we need to optimize techniques to achieve the best efficacy possible. Otherwise it is wasteful of healthcare worker efforts and hospital resources."
The sight of fluorescent dye on one's face and hands would be a powerful and lasting lesson, she said.
"Being able to see where contamination occurs allows personnel to make adjustments in their technique," Dr. Donskey said. "Because training alone did not result in zero contamination, there is a need for other approaches such as improving [equipment] design or disinfection of [equipment] prior to removal."
Florescent lotion and black light revealed that health care workers often contaminate their skin and clothing while removing their protective gear, researchers say.
"It was surprising for the participants in the study to see that they frequently contaminated themselves during [personal protective equipment] removal," said senior author Dr. Curtis J. Donskey of the Cleveland Veterans Affairs Medical Center.
"Most of the participants appeared to be unaware of the high risk for contamination and many reported receiving minimal or no training in putting on and taking off [personal protective equipment]," he said by email.
The researchers recruited doctors, nurses and ancillary personnel such as phlebotomists and physical therapists at four Cleveland-area hospitals to participate in the simulations. More than half of the 435 simulations were performed by nurses.
As reported online October 12 in JAMA Internal Medicine, the participants put on protective gowns and gloves in their usual manner and then had a small amount of fluorescent lotion placed in the palm of their hands, which they then rubbed between their hands for 15 seconds to simulate dirtied gloves, then smeared the gloves over the chest and abdomen area of the gown. Then the gloves were exchanged for clean ones.
After they removed their gloves and gowns in their usual manners, researchers used a black light to check for lotion contamination of the hands, forearms, neck, face, hair or clothing.
Skin or clothing contamination happened 46% of the time, more frequently during glove removal.
Researchers also noted whether participants had used proper protective equipment technique, e.g., wearing gloves extended over the wrists of the gown, gown removed first by pulling away from the neck and body, and gloves removed second. Contamination happened 70% of the time when proper technique was not followed, compared to 30% of the time when it was followed.
"When dealing with pathogens that are potentially fatal, the goal has to be zero contamination," Dr. Donskey said. "In routine care settings, we would like personnel to be well trained and confident that they can minimize contamination, but would not insist on zero contamination."
It is important for personnel to perform hand hygiene after removing gloves and gowns, he said.
The researchers also conducted these tests with a group of personnel who had attended special infection control sessions, with a 10-minute video presentation and 20 minutes of demonstrations and practice in using and removing protective gear.
Before the training sessions, these individuals contaminated themselves 60% of the time, compared to roughly 19% after the sessions. The improvements were still seen at re-tests done one and three months later.
"This suggests that training using fluorescent lotion can be useful to identify minor deficiencies in technique that lead to contamination," Donskey said.
Recent experience with the Ebola virus in the U.S. showed that self-contamination during removal of protective equipment does occur, but this study exposes a more widespread issue that may be happening during routine patient care, said Dr. Michelle Doll of Virginia Commonwealth University in Richmond who coauthored a commentary on the new study.
"Use of gowns and gloves for contact precautions on a busy inpatient unit is costly on multiple levels," Doll said by email. "In situations when we do decide to use these tools for infection prevention, we need to optimize techniques to achieve the best efficacy possible. Otherwise it is wasteful of healthcare worker efforts and hospital resources."
The sight of fluorescent dye on one's face and hands would be a powerful and lasting lesson, she said.
"Being able to see where contamination occurs allows personnel to make adjustments in their technique," Dr. Donskey said. "Because training alone did not result in zero contamination, there is a need for other approaches such as improving [equipment] design or disinfection of [equipment] prior to removal."
Florescent lotion and black light revealed that health care workers often contaminate their skin and clothing while removing their protective gear, researchers say.
"It was surprising for the participants in the study to see that they frequently contaminated themselves during [personal protective equipment] removal," said senior author Dr. Curtis J. Donskey of the Cleveland Veterans Affairs Medical Center.
"Most of the participants appeared to be unaware of the high risk for contamination and many reported receiving minimal or no training in putting on and taking off [personal protective equipment]," he said by email.
The researchers recruited doctors, nurses and ancillary personnel such as phlebotomists and physical therapists at four Cleveland-area hospitals to participate in the simulations. More than half of the 435 simulations were performed by nurses.
As reported online October 12 in JAMA Internal Medicine, the participants put on protective gowns and gloves in their usual manner and then had a small amount of fluorescent lotion placed in the palm of their hands, which they then rubbed between their hands for 15 seconds to simulate dirtied gloves, then smeared the gloves over the chest and abdomen area of the gown. Then the gloves were exchanged for clean ones.
After they removed their gloves and gowns in their usual manners, researchers used a black light to check for lotion contamination of the hands, forearms, neck, face, hair or clothing.
Skin or clothing contamination happened 46% of the time, more frequently during glove removal.
Researchers also noted whether participants had used proper protective equipment technique, e.g., wearing gloves extended over the wrists of the gown, gown removed first by pulling away from the neck and body, and gloves removed second. Contamination happened 70% of the time when proper technique was not followed, compared to 30% of the time when it was followed.
"When dealing with pathogens that are potentially fatal, the goal has to be zero contamination," Dr. Donskey said. "In routine care settings, we would like personnel to be well trained and confident that they can minimize contamination, but would not insist on zero contamination."
It is important for personnel to perform hand hygiene after removing gloves and gowns, he said.
The researchers also conducted these tests with a group of personnel who had attended special infection control sessions, with a 10-minute video presentation and 20 minutes of demonstrations and practice in using and removing protective gear.
Before the training sessions, these individuals contaminated themselves 60% of the time, compared to roughly 19% after the sessions. The improvements were still seen at re-tests done one and three months later.
"This suggests that training using fluorescent lotion can be useful to identify minor deficiencies in technique that lead to contamination," Donskey said.
Recent experience with the Ebola virus in the U.S. showed that self-contamination during removal of protective equipment does occur, but this study exposes a more widespread issue that may be happening during routine patient care, said Dr. Michelle Doll of Virginia Commonwealth University in Richmond who coauthored a commentary on the new study.
"Use of gowns and gloves for contact precautions on a busy inpatient unit is costly on multiple levels," Doll said by email. "In situations when we do decide to use these tools for infection prevention, we need to optimize techniques to achieve the best efficacy possible. Otherwise it is wasteful of healthcare worker efforts and hospital resources."
The sight of fluorescent dye on one's face and hands would be a powerful and lasting lesson, she said.
"Being able to see where contamination occurs allows personnel to make adjustments in their technique," Dr. Donskey said. "Because training alone did not result in zero contamination, there is a need for other approaches such as improving [equipment] design or disinfection of [equipment] prior to removal."
Find Answers, Share Stories at SHM's New Patient Experience Community
Have you had successes with improving the patient experience at your hospital? Or have you had a challenge or question? SHM’s new Patient Experience community on HMX is a great way to find answers and share your stories. In just the first few days of the community, participants are talking about the impact of computers and smartphones on the patient experience. To join the conversation, SHM members can find the Patient Experience community in HMX.
Have you had successes with improving the patient experience at your hospital? Or have you had a challenge or question? SHM’s new Patient Experience community on HMX is a great way to find answers and share your stories. In just the first few days of the community, participants are talking about the impact of computers and smartphones on the patient experience. To join the conversation, SHM members can find the Patient Experience community in HMX.
Have you had successes with improving the patient experience at your hospital? Or have you had a challenge or question? SHM’s new Patient Experience community on HMX is a great way to find answers and share your stories. In just the first few days of the community, participants are talking about the impact of computers and smartphones on the patient experience. To join the conversation, SHM members can find the Patient Experience community in HMX.
Post-Operative Transfusions after Noncardiac Surgery Associated with Increased Adverse Outcomes
Clinical question: Do transfusions affect post-operative outcomes after noncardiac surgery?
Background: Studies have demonstrated that a restrictive transfusion strategy is probably superior to a liberal transfusion strategy in many clinical settings. Despite this data, there continues to be wide variation in the use of blood transfusions in the peri-operative setting.
Study design: Retrospective cohort study.
Setting: Fifty-two community and academic hospitals in Michigan.
Synopsis: Demographic, operative, and outcomes data were extracted from the Michigan Surgical Quality Collaborative and reviewed for 48,720 patients who underwent noncardiac surgery between 2012-2014. A total of 4.6% of patients received a blood transfusion within 72 hours after surgery. The patients who received blood products were at increased risk for death at 30 days (3.6% excess absolute risk), for infectious complications (1% excess absolute risk), and for having at least one post-operative noninfectious complication (4.4% increased absolute risk).
Bottom line: Although observational in nature, this study adds to the increasing body of evidence supporting an increase in surgical morbidity and mortality associated with blood transfusions.
Citation: Abdelsattar ZM, Hendren S, Wong SL, Campbell DA Jr, Henke P. Variation in transfusion practices and the effect on outcomes after noncardiac surgery. Ann Surg. 2015;262(1):1-6.
Clinical question: Do transfusions affect post-operative outcomes after noncardiac surgery?
Background: Studies have demonstrated that a restrictive transfusion strategy is probably superior to a liberal transfusion strategy in many clinical settings. Despite this data, there continues to be wide variation in the use of blood transfusions in the peri-operative setting.
Study design: Retrospective cohort study.
Setting: Fifty-two community and academic hospitals in Michigan.
Synopsis: Demographic, operative, and outcomes data were extracted from the Michigan Surgical Quality Collaborative and reviewed for 48,720 patients who underwent noncardiac surgery between 2012-2014. A total of 4.6% of patients received a blood transfusion within 72 hours after surgery. The patients who received blood products were at increased risk for death at 30 days (3.6% excess absolute risk), for infectious complications (1% excess absolute risk), and for having at least one post-operative noninfectious complication (4.4% increased absolute risk).
Bottom line: Although observational in nature, this study adds to the increasing body of evidence supporting an increase in surgical morbidity and mortality associated with blood transfusions.
Citation: Abdelsattar ZM, Hendren S, Wong SL, Campbell DA Jr, Henke P. Variation in transfusion practices and the effect on outcomes after noncardiac surgery. Ann Surg. 2015;262(1):1-6.
Clinical question: Do transfusions affect post-operative outcomes after noncardiac surgery?
Background: Studies have demonstrated that a restrictive transfusion strategy is probably superior to a liberal transfusion strategy in many clinical settings. Despite this data, there continues to be wide variation in the use of blood transfusions in the peri-operative setting.
Study design: Retrospective cohort study.
Setting: Fifty-two community and academic hospitals in Michigan.
Synopsis: Demographic, operative, and outcomes data were extracted from the Michigan Surgical Quality Collaborative and reviewed for 48,720 patients who underwent noncardiac surgery between 2012-2014. A total of 4.6% of patients received a blood transfusion within 72 hours after surgery. The patients who received blood products were at increased risk for death at 30 days (3.6% excess absolute risk), for infectious complications (1% excess absolute risk), and for having at least one post-operative noninfectious complication (4.4% increased absolute risk).
Bottom line: Although observational in nature, this study adds to the increasing body of evidence supporting an increase in surgical morbidity and mortality associated with blood transfusions.
Citation: Abdelsattar ZM, Hendren S, Wong SL, Campbell DA Jr, Henke P. Variation in transfusion practices and the effect on outcomes after noncardiac surgery. Ann Surg. 2015;262(1):1-6.
Left Atrial Appendage Closure Favorable Over Warfarin for Atrial Fibrillation
Clinical question: Is there a favorable risk-benefit ratio for left atrial appendage closure (LAAC) compared to warfarin for prevention of stroke, systemic embolism, and cardiovascular death in nonvalvular atrial fibrillation?
Background: LAAC with the WATCHMAN device was shown to be noninferior to warfarin for the prevention of stroke, systemic embolism, and cardiovascular death in nonvalvular atrial fibrillation in two trials: PROTECT AF and PREVAIL. Further efficacy concerns were raised following routine regulatory filings, leading to the need for continued evaluation.
Study design: Meta-analysis.
Setting: Patient-level data were combined and analyzed from the PROTECT AF and PREVAIL trails and two nonrandomized registries of LAAC with the WATCHMAN device: the Continued Access PROTECT AF registry (CAP) and the Continued Access to PREVAIL registry (CAP2).
Synopsis: A total of 2,406 patients were enrolled from all four data sets from 2005-2014. Of those, 1,877 were treated with the WATCHMAN device and 382 were treated with warfarin. Annualized risk of stroke if untreated with anticoagulation for all patients was 5.7% to 7.6%, indicating that all were eligible to be treated with warfarin. Ninety percent of patients had moderate to high risk of bleeding. Analysis showed that LAAC was noninferior to warfarin for stroke, systemic embolism, and cardiovascular death.
A slight increase in ischemic stroke in the LAAC group was counterbalanced by the significant reduction in hemorrhagic stroke in the LAAC group versus the warfarin group. Cardiovascular deaths were significantly fewer in the LAAC cohort; all-cause mortality favored LAAC but did not reach statistical significance. There was also a significant reduction in nonprocedure-related major bleeding in the LAAC group. Limitations of this study include the limited number of patients treated with warfarin and lack of comparison to new oral anticoagulants (NOACs).
Bottom line: Patients with increased stroke risk from nonvalvular atrial fibrillation treated with the WATCHMAN device for LAAC have significant reductions in hemorrhagic stroke, cardiovascular death, and nonprocedure-related major bleeding, but slightly increased risk of ischemic stroke compared to those treated with warfarin.
Citaiton: Holmes DR Jr, Doshi SK, Kar S, et al. Left atrial appendage closure as an alternative to warfarin for stroke prevention in atrial fibrillation: a patient-level meta-analysis. J Am Coll Cardiol. 2015;65(24):2614-2623.
Clinical question: Is there a favorable risk-benefit ratio for left atrial appendage closure (LAAC) compared to warfarin for prevention of stroke, systemic embolism, and cardiovascular death in nonvalvular atrial fibrillation?
Background: LAAC with the WATCHMAN device was shown to be noninferior to warfarin for the prevention of stroke, systemic embolism, and cardiovascular death in nonvalvular atrial fibrillation in two trials: PROTECT AF and PREVAIL. Further efficacy concerns were raised following routine regulatory filings, leading to the need for continued evaluation.
Study design: Meta-analysis.
Setting: Patient-level data were combined and analyzed from the PROTECT AF and PREVAIL trails and two nonrandomized registries of LAAC with the WATCHMAN device: the Continued Access PROTECT AF registry (CAP) and the Continued Access to PREVAIL registry (CAP2).
Synopsis: A total of 2,406 patients were enrolled from all four data sets from 2005-2014. Of those, 1,877 were treated with the WATCHMAN device and 382 were treated with warfarin. Annualized risk of stroke if untreated with anticoagulation for all patients was 5.7% to 7.6%, indicating that all were eligible to be treated with warfarin. Ninety percent of patients had moderate to high risk of bleeding. Analysis showed that LAAC was noninferior to warfarin for stroke, systemic embolism, and cardiovascular death.
A slight increase in ischemic stroke in the LAAC group was counterbalanced by the significant reduction in hemorrhagic stroke in the LAAC group versus the warfarin group. Cardiovascular deaths were significantly fewer in the LAAC cohort; all-cause mortality favored LAAC but did not reach statistical significance. There was also a significant reduction in nonprocedure-related major bleeding in the LAAC group. Limitations of this study include the limited number of patients treated with warfarin and lack of comparison to new oral anticoagulants (NOACs).
Bottom line: Patients with increased stroke risk from nonvalvular atrial fibrillation treated with the WATCHMAN device for LAAC have significant reductions in hemorrhagic stroke, cardiovascular death, and nonprocedure-related major bleeding, but slightly increased risk of ischemic stroke compared to those treated with warfarin.
Citaiton: Holmes DR Jr, Doshi SK, Kar S, et al. Left atrial appendage closure as an alternative to warfarin for stroke prevention in atrial fibrillation: a patient-level meta-analysis. J Am Coll Cardiol. 2015;65(24):2614-2623.
Clinical question: Is there a favorable risk-benefit ratio for left atrial appendage closure (LAAC) compared to warfarin for prevention of stroke, systemic embolism, and cardiovascular death in nonvalvular atrial fibrillation?
Background: LAAC with the WATCHMAN device was shown to be noninferior to warfarin for the prevention of stroke, systemic embolism, and cardiovascular death in nonvalvular atrial fibrillation in two trials: PROTECT AF and PREVAIL. Further efficacy concerns were raised following routine regulatory filings, leading to the need for continued evaluation.
Study design: Meta-analysis.
Setting: Patient-level data were combined and analyzed from the PROTECT AF and PREVAIL trails and two nonrandomized registries of LAAC with the WATCHMAN device: the Continued Access PROTECT AF registry (CAP) and the Continued Access to PREVAIL registry (CAP2).
Synopsis: A total of 2,406 patients were enrolled from all four data sets from 2005-2014. Of those, 1,877 were treated with the WATCHMAN device and 382 were treated with warfarin. Annualized risk of stroke if untreated with anticoagulation for all patients was 5.7% to 7.6%, indicating that all were eligible to be treated with warfarin. Ninety percent of patients had moderate to high risk of bleeding. Analysis showed that LAAC was noninferior to warfarin for stroke, systemic embolism, and cardiovascular death.
A slight increase in ischemic stroke in the LAAC group was counterbalanced by the significant reduction in hemorrhagic stroke in the LAAC group versus the warfarin group. Cardiovascular deaths were significantly fewer in the LAAC cohort; all-cause mortality favored LAAC but did not reach statistical significance. There was also a significant reduction in nonprocedure-related major bleeding in the LAAC group. Limitations of this study include the limited number of patients treated with warfarin and lack of comparison to new oral anticoagulants (NOACs).
Bottom line: Patients with increased stroke risk from nonvalvular atrial fibrillation treated with the WATCHMAN device for LAAC have significant reductions in hemorrhagic stroke, cardiovascular death, and nonprocedure-related major bleeding, but slightly increased risk of ischemic stroke compared to those treated with warfarin.
Citaiton: Holmes DR Jr, Doshi SK, Kar S, et al. Left atrial appendage closure as an alternative to warfarin for stroke prevention in atrial fibrillation: a patient-level meta-analysis. J Am Coll Cardiol. 2015;65(24):2614-2623.
Pediatric Trigger Tool Helps Identify Inpatient Pediatric Harm
Clinical question: Can a trigger tool identify harms for hospitalized children?
Background: An estimated 400,000 people die annually in the United States as a result of hospital-associated harm. The Centers for Medicare and Medicaid Services define harm as “unintended physical injury … by medical care that required additional monitoring, treatment, or hospitalization or that resulted in death.” Although harm is common, voluntary reporting of events has been shown to capture only 2%-8% of harm. Global Trigger Tools (GTT) are an alternative to voluntary reports. These tools use “triggers,” or clues, to help reviewers identify potential harms when reviewing the electronic heath record. The Institute for Healthcare Improvement (IHI) has created an adult-focused GTT; however, no pediatric-focused GTT exists.
Study design: Cross-sectional, retrospective chart review.
Setting: Children <22 years old discharged from six freestanding U.S. children’s hospitals in February 2012.
Synopsis: In a prior paper, the authors described how they used a modified Delphi technique to develop a pediatric GTT based upon the IHI GTT. Here they piloted this new pediatric-focused GTT through a retrospective chart review. One clinical nonphysician reviewer and one physician reviewer were selected from each site and received training on use of the pediatric GTT and the identification of harms. One hundred charts from each site were randomly selected for application of the GTT. The reviewers examined the charts for harms and then applied the GTT. When reviewers found a harm, they determined the likelihood that the harm was preventable.
Of the 600 records reviewed, 240 harms were found. The GTT identified 1,093 potential harms, leading to identification of 204 harms. The remaining 36 harms did not cause a trigger and were found by chart review. The positive predictive value of the aggregate GTT was 22%. There were 40 harms per 100 patients, and 24.3% of patients had one or more harm. Sixty-eight percent of harms were of the least severe type, and only one led to a patient death. The most common harms were intravenous catheter infiltration, respiratory distress, constipation, pain, and surgical complications.
Bottom line: The pediatric GTT appears to be a moderately sensitive indicator for inpatient pediatric harm. Inpatient pediatric harm occurs frequently, with about one in four pediatric inpatients suffering from harm. Serious harm appears uncommon.
Citation: Stockwell DC, Bisarya H, Classen DC, et al. A trigger tool to detect harm in pediatric inpatient settings. Pediatrics. 2015;135(6):1036-1042.
Clinical question: Can a trigger tool identify harms for hospitalized children?
Background: An estimated 400,000 people die annually in the United States as a result of hospital-associated harm. The Centers for Medicare and Medicaid Services define harm as “unintended physical injury … by medical care that required additional monitoring, treatment, or hospitalization or that resulted in death.” Although harm is common, voluntary reporting of events has been shown to capture only 2%-8% of harm. Global Trigger Tools (GTT) are an alternative to voluntary reports. These tools use “triggers,” or clues, to help reviewers identify potential harms when reviewing the electronic heath record. The Institute for Healthcare Improvement (IHI) has created an adult-focused GTT; however, no pediatric-focused GTT exists.
Study design: Cross-sectional, retrospective chart review.
Setting: Children <22 years old discharged from six freestanding U.S. children’s hospitals in February 2012.
Synopsis: In a prior paper, the authors described how they used a modified Delphi technique to develop a pediatric GTT based upon the IHI GTT. Here they piloted this new pediatric-focused GTT through a retrospective chart review. One clinical nonphysician reviewer and one physician reviewer were selected from each site and received training on use of the pediatric GTT and the identification of harms. One hundred charts from each site were randomly selected for application of the GTT. The reviewers examined the charts for harms and then applied the GTT. When reviewers found a harm, they determined the likelihood that the harm was preventable.
Of the 600 records reviewed, 240 harms were found. The GTT identified 1,093 potential harms, leading to identification of 204 harms. The remaining 36 harms did not cause a trigger and were found by chart review. The positive predictive value of the aggregate GTT was 22%. There were 40 harms per 100 patients, and 24.3% of patients had one or more harm. Sixty-eight percent of harms were of the least severe type, and only one led to a patient death. The most common harms were intravenous catheter infiltration, respiratory distress, constipation, pain, and surgical complications.
Bottom line: The pediatric GTT appears to be a moderately sensitive indicator for inpatient pediatric harm. Inpatient pediatric harm occurs frequently, with about one in four pediatric inpatients suffering from harm. Serious harm appears uncommon.
Citation: Stockwell DC, Bisarya H, Classen DC, et al. A trigger tool to detect harm in pediatric inpatient settings. Pediatrics. 2015;135(6):1036-1042.
Clinical question: Can a trigger tool identify harms for hospitalized children?
Background: An estimated 400,000 people die annually in the United States as a result of hospital-associated harm. The Centers for Medicare and Medicaid Services define harm as “unintended physical injury … by medical care that required additional monitoring, treatment, or hospitalization or that resulted in death.” Although harm is common, voluntary reporting of events has been shown to capture only 2%-8% of harm. Global Trigger Tools (GTT) are an alternative to voluntary reports. These tools use “triggers,” or clues, to help reviewers identify potential harms when reviewing the electronic heath record. The Institute for Healthcare Improvement (IHI) has created an adult-focused GTT; however, no pediatric-focused GTT exists.
Study design: Cross-sectional, retrospective chart review.
Setting: Children <22 years old discharged from six freestanding U.S. children’s hospitals in February 2012.
Synopsis: In a prior paper, the authors described how they used a modified Delphi technique to develop a pediatric GTT based upon the IHI GTT. Here they piloted this new pediatric-focused GTT through a retrospective chart review. One clinical nonphysician reviewer and one physician reviewer were selected from each site and received training on use of the pediatric GTT and the identification of harms. One hundred charts from each site were randomly selected for application of the GTT. The reviewers examined the charts for harms and then applied the GTT. When reviewers found a harm, they determined the likelihood that the harm was preventable.
Of the 600 records reviewed, 240 harms were found. The GTT identified 1,093 potential harms, leading to identification of 204 harms. The remaining 36 harms did not cause a trigger and were found by chart review. The positive predictive value of the aggregate GTT was 22%. There were 40 harms per 100 patients, and 24.3% of patients had one or more harm. Sixty-eight percent of harms were of the least severe type, and only one led to a patient death. The most common harms were intravenous catheter infiltration, respiratory distress, constipation, pain, and surgical complications.
Bottom line: The pediatric GTT appears to be a moderately sensitive indicator for inpatient pediatric harm. Inpatient pediatric harm occurs frequently, with about one in four pediatric inpatients suffering from harm. Serious harm appears uncommon.
Citation: Stockwell DC, Bisarya H, Classen DC, et al. A trigger tool to detect harm in pediatric inpatient settings. Pediatrics. 2015;135(6):1036-1042.