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Evaluation of the American Academy of Orthopaedic Surgeons Appropriate Use Criteria for the Nonarthroplasty Treatment of Knee Osteoarthritis in Veterans

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While patients without knee instability use more nonarthroplasty treatments over a longer period prior to total knee arthroplasty, patients with less severe knee osteoarthritis are at risk of receiving interventions judged to be rarely appropriate.

Knee osteoarthritis (OA) affects almost 9.3 million adults in the US and accounts for $27 billion in annual health care expenses.1,2 Due to the increasing cost of health care and an aging population, there has been renewed interest in establishing criteria for nonarthroplasty treatment of knee OA.

In 2013, using the RAND/UCLA Appropriateness method, the American Academy of Orthopaedic Surgeons (AAOS) developed an appropriate use criteria (AUC) for nonarthroplasty management of primary OA of the knee, based on orthopaedic literature and expert opinion.3 Interventions such as activity modification, weight loss, prescribed physical therapy, nonsteroidal anti-inflammatory drugs, tramadol, prescribed oral or transcutaneous opioids, acetaminophen, intra-articular corticosteroids, hinged or unloading knee braces, arthroscopic partial menisectomy or loose body removal, and realignment osteotomy were assessed. An algorithm was developed for 576 patients scenarios that incorporated patient-specific, prognostic/predictor variables to assign designations of “appropriate,” “may be appropriate,” or “rarely appropriate,” to treatment interventions.4,5 An online version of the algorithm (orthoguidelines.org) is available for physicians and surgeons to judge appropriateness of nonarthroplasty treatments; however, it is not intended to mandate candidacy for treatment or intervention.

Clinical evaluation of the AAOS AUC is necessary to determine how treatment recommendations correlate with current practice. A recent examination of the AAOS Appropriateness System for Surgical Management of Knee OA found that prognostic/predictor variables, such as patient age, OA severity, and pattern of knee OA involvement were more heavily weighted when determining arthroplasty appropriateness than was pain severity or functional loss.6 Furthermore, non-AAOS AUC prognostic/predictor variables, such as race and gender, have been linked to disparities in utilization of knee OA interventions.7-9 Such disparities can be costly not just from a patient perceptive, but also employer and societal perspectives.10

The Department of Veterans Affairs (VA) health care system represents a model of equal-access-to care system in the US that is ideal for examination of issues about health care utilization and any disparities within the AAOS AUC model and has previously been used to assess utilization of total knee arthroplasty.9 The aim of this study was to characterize utilization of the AAOS AUC for nonarthroplasty treatment of knee OA in a VA patient population. We asked the following questions: (1) What variables are predictive of receiving a greater number of AAOS AUC evaluated nonarthroplasty treatments? (2) What variables are predictive of receiving “rarely appropriate” AAOS AUC evaluated nonarthroplasty treatment? (3) What factors are predictive of duration of nonarthroplasty care until total knee arthroplasty (TKA)?

Methods

The institutional review board at the Louis Stokes Cleveland VA Medical Center in Ohio approved a retrospective chart review of nonarthroplasty treatments utilized by patients presenting to its orthopaedic section who subsequently underwent knee arthroplasty between 2013 and 2016. Eligibility criteria included patients aged ≥ 30 years with a diagnosis of unilateral or bilateral primary knee OA. Patients with posttraumatic OA, inflammatory arthritis, and a history of infectious arthritis or Charcot arthropathy of the knee were excluded. Patients with a body mass index (BMI) > 40 or a hemoglobin A1c > 8.0 at presentation were excluded as nonarthroplasty care was the recommended course of treatment above these thresholds.

 

 

Data collected included race, gender, duration of nonarthroplasty treatment, BMI, and Kellgren-Lawrence classification of knee OA at time of presentation for symptomatic knee OA.11 All AAOS AUC-evaluated nonarthroplasty treatments utilized prior to arthroplasty intervention also were recorded (Table 1). 

Indications and classifications for each subject were entered into the AAOS AUC online algorithm, and every AAOS AUC evaluated treatment utilized was assigned a rating of appropriate, may be appropriate, or rarely appropriate, based on the algorithm results for that clinical scenario (Table 2). 
Information regarding anti-inflammatory, analgesic, and prescribed oral or transcutaneous opioid use for chronic knee pain during the period of nonoperative management of knee OA prior to TKA was obtained by review of medication lists and reconciliation with orthopaedic consultation notes in the electronic health record. Peri-operative anti-inflammatory, analgesic, and prescribed oral or transcutaneous opioid use did not constitute an AUC intervention.

Statistical Analysis

Statistical analysis was completed with GraphPad Software Prism 7.0a (La Jolla, CA) and Mathworks MatLab R2016b software (Natick, MA). Univariate analysis with Student t tests with Welch corrections in the setting of unequal variance, Mann-Whitney nonparametric tests, and Fisher exact test were generated in the appropriate setting. Multivariable analyses also were conducted. For continuous outcomes, stepwise multiple linear regression was used to generate predictive models; for binary outcomes, binomial logistic regression was used.

Factors analyzed in regression modeling for the total number of AAOS AUC evaluated nonarthroplasty treatments utilized and the likelihood of receiving a rarely appropriate treatment included gender, race, function-limiting pain, range of motion (ROM), ligamentous instability, arthritis pattern, limb alignment, mechanical symptoms, BMI, age, and Kellgren-Lawrence grade. Factors analyzed in timing of TKA included the above variables plus the total number of AUC interventions, whether the patient received an inappropriate intervention, and average appropriateness of the interventions received. Residual analysis with Cook’s distance was used to identify outliers in regression. Observations with Cook’s distance > 3 times the mean Cook’s distance were identified as potential outliers, and models were adjusted accordingly. All statistical analyses were 2-tailed. Statistical significance was set to P ≤ .05 for all outputs.

Results

In the study, 97.8% of participants identified as male, and the mean age was 62.8 years (Table 3). 

The study group was predominantly white (70.3%). All participants had a diagnosis of primary OA. The majority of patients were aged 51 to 70 years (68.1%) and presented with pain occurring following short-distance ambulation (79.1%) but without mechanical symptoms (80.2%). On examination, the majority of patients were found to have full knee ROM (53.8%), no ligamentous instability (97.8%), and normal limb alignment (60.4%). Radiographically, patients most often had multicompartmental disease (69.2%) with evidence of severe joint-space narrowing (63.7%), resulting in a plurality of patients having a Kellgren-Lawrence arthritis grade of 3 (46.2%) (Table 4).

Appropriate Use Criteria Interventions

Patients received a mean of 5.2 AAOS AUC evaluated interventions before undergoing arthroplasty management at a mean of 32.3 months (range 2-181 months) from initial presentation. The majority of these interventions were classified as either appropriate or may be appropriate, according to the AUC definitions (95.1%). Self-management and physical therapy programs were widely utilized (100% and 90.1%, respectively), with all use of these interventions classified as appropriate.

 

 

Hinged or unloader knee braces were utilized in about half the study patients; this intervention was classified as rarely appropriate in 4.4% of these patients. Medical therapy was also widely used, with all use of NSAIDs, acetaminophen, and tramadol classified as appropriate or may be appropriate. Oral or transcutaneous opioid medications were prescribed in 14.3% of patients, with 92.3% of this use classified as rarely appropriate. Although the opioid medication prescribing provider was not specifically evaluated, there were no instances in which the orthopaedic service provided an oral or transcutaneous opioid prescriptions. Procedural interventions, with the exception of corticosteroid injections, were uncommon; no patient received realignment osteotomy, and only 12.1% of patients underwent arthroscopy. The use of arthroscopy was deemed rarely appropriate in 72.7% of these cases.

Factors Associated With AAOS AUC Intervention Use

There was no difference in the number of AAOS AUC evaluated interventions received based on BMI (mean [SD] BMI < 35, 5.2 [1.0] vs BMI ≥ 35, 5.3 [1.1], P = .49), age (mean [SD] aged < 60 years, 5.4 [1.0] vs aged ≥ 60 years, 5.1 [1.2], P = .23), or Kellgren-Lawrence arthritic grade (mean [SD] grade ≤ 2, 5.5 [1.0] vs grade > 2, 5.1 [1.1], P = .06). These variables also were not associated with receiving a rarely appropriate intervention (mean [SD] BMI < 35, 0.27 [0.5] vs BMI > 35, 0.2 [0.4], P = .81; aged > 60 years, 0.3 [0.5] vs aged < 60 years, 0.2 [0.4], P = .26; Kellgren-Lawrence grade < 2, 0.4 [0.6] vs grade > 2, 0.2 [0.4], P = .1).

Regression modeling to predict total number of AAOS AUC evaluated interventions received produced a significant model (R2 = 0.111, P = .006). The presence of ligamentous instability (β coefficient, -1.61) and the absence of mechanical symptoms (β coefficient, -0.67) were negative predictors of number of AUC interventions received. Variance inflation factors were 1.014 and 1.012, respectively. Likewise, regression modeling to identify factors predictive of receiving a rarely appropriate intervention also produced a significant model (pseudo R2= 0.06, P = .025), with lower Kellgren-Lawrence grade the only significant predictor of receiving a rarely appropriate intervention (odds ratio [OR] 0.54; 95% CI, 0.42 -0.72, per unit increase).

Timing from presentation to arthroplasty intervention was also evaluated. Age was a negative predictor (β coefficient -1.61), while positive predictors were reduced ROM (β coefficient 15.72) and having more AUC interventions (β coefficient 7.31) (model R2= 0.29, P = < .001). Age was the most significant predictor. Variance inflations factors were 1.02, 1.01, and 1.03, respectively. Receiving a rarely appropriate intervention was not associated with TKA timing.

Discussion

This single-center retrospective study examined the utilization of AAOS AUC-evaluated nonarthroplasty interventions for symptomatic knee OA prior to TKA. The aims of this study were to validate the AAOS AUC in a clinical setting and identify predictors of AAOS AUC utilization. In particular, this study focused on the number of interventions utilized prior to knee arthroplasty, whether interventions receiving a designation of rarely appropriate were used, and the duration of nonarthroplasty treatment.

 

 

Patients with knee instability used fewer total AAOS AUC evaluated interventions prior to TKA. Subjective instability has been reported as high as 27% in patients with OA and has been associated with fear of falling, poor balance confidence, activity limitations, and lower Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) physical function scores.12 However, it has not been found to correlate with knee laxity.13 Nevertheless, significant functional impairment with the risk of falling may reduce the number of nonarthroplasty interventions attempted. On the other hand, the presence of mechanical symptoms resulted in greater utilization of nonarthroplasty interventions. This is likely due to the greater utilization of arthroscopic partial menisectomy or loose body removal in this group of patients. Despite its inclusion as an AAOS AUC evaluated intervention, arthroscopy remains a contentious treatment for symptomatic knee pain in the setting of OA.14,15

For every unit decrease in Kellgren-Lawrence OA grade, patients were 54% more likely to receive a rarely appropriate intervention prior to knee arthroplasty. This is supported by the recent literature examining the AAOS AUC for surgical management of knee OA. Riddle and colleagues developed a classification tree to determine the contributions of various prognostic variables in final classifications of the 864 clinical vignettes used to develop the appropriateness algorithm and found that OA severity was strongly favored, with only 4 of the 432 vignettes with severe knee OA judged as rarely appropriate for surgical intervention.6

Our findings, too, may be explained by an AAOS AUC system that too heavily weighs radiographic severity of knee OA, resulting in more frequent rarely appropriate interventions in patients with less severe arthritis, including nonarthroplasty treatments. It is likely that rarely appropriate interventions were attempted in this subset of our study cohort based on patient’s subjective symptoms and functional status, both of which have been shown to be discordant with radiographic severity of knee OA.16

Oral or transcutaneous prescribed opioid medications were the most frequent intervention that received a rarely appropriate designation. Patients with preoperative opioid use undergoing TKA have been shown to have a greater risk for postoperative complications and longer hospital stay, particularly those patients aged < 75 years. Younger age, use of more interventions, and decreased knee ROM at presentation were predictive of longer duration of nonarthroplasty treatment. The use of more AAOS AUC evaluated interventions in these patients suggests that the AAOS AUC model may effectively be used to manage symptomatic OA, increasing the time from presentation to knee arthroplasty.

Interestingly, the use of rarely appropriate interventions did not affect TKA timing, as would be expected in a clinically effective nonarthroplasty treatment model. The reasons for rarely appropriate nonsurgical interventions are complex and require further investigation. One possible explanation is that decreased ROM was a marker for mechanical symptoms that necessitated additional intervention in the form of knee arthroscopy, delaying time to TKA.

Limitations

There are several limitations of this study. First, the small sample size (N = 90) requires acknowledgment; however, this limitation reflects the difficulty in following patients for years prior to an operative intervention. Second, the study population consists of veterans using the VA system and may not be reflective of the general population, differing with respect to gender, racial, and socioeconomic factors. Nevertheless, studies examining TKA utilization found, aside from racial and ethnic variability, patient gender and age do not affect arthroplasty utilization rate in the VA system.17

 

 

Additional limitations stem from the retrospective nature of this study. While the Computerized Patient Record System and centralized care of the VA system allows for review of all physical therapy consultations, orthotic consultations, and medications within the VA system, any treatments and intervention delivered by non-VA providers were not captured. Furthermore, the ability to assess for confounding variables limiting the prescription of certain medications, such as chronic kidney disease with NSAIDs or liver disease with acetaminophen, was limited by our study design.

Although our study suffers from selection bias with respect to examination of nonarthroplasty treatment in patients who have ultimately undergone TKA, we feel that this subset of patients with symptomatic knee OA represents the majority of patients evaluated for knee OA by orthopaedic surgeons in the clinic setting. It should be noted that although realignment osteotomies were sometimes indicated as appropriate by AAOS AUC model in our study population, this intervention was never performed due to patient and surgeon preference. Additionally, although it is not an AAOS AUC evaluated intervention, viscosupplementation was sporadically used during the study period; however, it is now off formulary at the investigation institution.

Conclusion

Our study suggests that patients without knee instability use more nonarthroplasty treatments over a longer period before TKA, and those patients with less severe knee OA are at risk of receiving an intervention judged to be rarely appropriate by the AAOS AUC. Such interventions do not affect timing of TKA. Nonarthroplasty care should be individualized to patients’ needs, and the decision to proceed with arthroplasty should be considered only after exhausting appropriate conservative measures. We recommend that providers use the AAOS AUC, especially when treating younger patients with less severe knee OA, particularly if considering opiate therapy or knee arthroscopy.

Acknowledgments
The authors would like to acknowledge Patrick Getty, MD, for his surgical care of some of the study patients. This material is the result of work supported with resources and the use of facilities at the Louis Stokes Cleveland VA Medical Center in Ohio.

References

1. Cross M, Smith E, Hoy D, et al. The global burden of hip and knee osteoarthritis: estimates from the Global Burden of Disease 2010 study. Ann Rheum Dis. 2014;73(7):1323-1330.

2. Losina E, Walensky RP, Kessler CL, et al. Cost-effectiveness of total knee arthroplasty in the United States: patient risk and hospital volume. Arch Intern Med. 2009;169(12):1113-1121; discussion 1121-1122.

3. Members of the Writing, Review, and Voting Panels of the AUC on the Non-Arthroplasty Treatment of Osteoarthritis of the Knee, Sanders JO, Heggeness MH, Murray J, Pezold R, Donnelly P. The American Academy of Orthopaedic Surgeons Appropriate Use Criteria on the Non-Arthroplasty Treatment of Osteoarthritis of the Knee. J Bone Joint Surg Am. 2014;96(14):1220-1221.

4. Sanders JO, Murray J, Gross L. Non-arthroplasty treatment of osteoarthritis of the knee. J Am Acad Orthop Surg. 2014;22(4):256-260.

5. Yates AJ Jr, McGrory BJ, Starz TW, Vincent KR, McCardel B, Golightly YM. AAOS appropriate use criteria: optimizing the non-arthroplasty management of osteoarthritis of the knee. J Am Acad Orthop Surg. 2014;22(4):261-267.

6. Riddle DL, Perera RA. Appropriateness and total knee arthroplasty: an examination of the American Academy of Orthopaedic Surgeons appropriateness rating system. Osteoarthritis Cartilage. 2017;25(12):1994-1998.

7. Morgan RC Jr, Slover J. Breakout session: ethnic and racial disparities in joint arthroplasty. Clin Orthop Relat Res. 2011;469(7):1886-1890.

8. O’Connor MI, Hooten EG. Breakout session: gender disparities in knee osteoarthritis and TKA. Clin Orthop Relat Res. 2011;469(7):1883-1885.

9. Ibrahim SA. Racial and ethnic disparities in hip and knee joint replacement: a review of research in the Veterans Affairs Health Care System. J Am Acad Orthop Surg. 2007;15(suppl 1):S87-S94.

10. Karmarkar TD, Maurer A, Parks ML, et al. A fresh perspective on a familiar problem: examining disparities in knee osteoarthritis using a Markov model. Med Care. 2017;55(12):993-1000.

11. Kohn MD, Sassoon AA, Fernando ND. Classifications in brief: Kellgren-Lawrence Classification of Osteoarthritis. Clin Orthop Relat Res. 2016;474(8):1886-1893.

12. Nguyen U, Felson DT, Niu J, et al. The impact of knee instability with and without buckling on balance confidence, fear of falling and physical function: the Multicenter Osteoarthritis Study. Osteoarthritis Cartilage. 2014;22(4):527-534.

13. Schmitt LC, Fitzgerald GK, Reisman AS, Rudolph KS. Instability, laxity, and physical function in patients with medial knee osteoarthritis. Phys Ther. 2008;88(12):1506-1516.

14. Laupattarakasem W, Laopaiboon M, Laupattarakasem P, Sumananont C. Arthroscopic debridement for knee osteoarthritis. Cochrane Database Syst Rev. 2008;(1):CD005118.

15. Lamplot JD, Brophy RH. The role for arthroscopic partial meniscectomy in knees with degenerative changes: a systematic review. Bone Joint J. 2016;98-B(7):934-938.

16. Whittle R, Jordan KP, Thomas E, Peat G. Average symptom trajectories following incident radiographic knee osteoarthritis: data from the Osteoarthritis Initiative. RMD Open. 2016;2(2):e000281.

17. Jones A, Kwoh CK, Kelley ME, Ibrahim SA. Racial disparity in knee arthroplasty utilization in the Veterans Health Administration. Arthritis Rheum. 2005;53(6):979-981.

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Todd Morrison and Christopher Flanagan are Resident Physician Orthopaedic Surgeons in the Department of Orthopaedic Surgery at University Hospitals Cleveland Medical Center at Case Western Reserve University Medical School in Cleveland, Ohio. Susie Ivanov is a Physician Assistant and Glenn Wera is an Attending Orthopaedic Surgeon, both in the Orthopaedic Surgery Section at Louis Stokes Cleveland Veterans Affairs Medical Center in Ohio. Correspondence: Todd Morrison ([email protected])

Author disclosures
Glenn Wera is a board committee member for American Academy of Orthopaedic Surgeons. The other authors report no actual or potential conflicts of interest with regard to this article.

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The opinions expressed herein are those of the authors and do not necessarily reflect those of Federal Practitioner, Frontline Medical Communications Inc., the US Government, or any of its agencies.

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Todd Morrison and Christopher Flanagan are Resident Physician Orthopaedic Surgeons in the Department of Orthopaedic Surgery at University Hospitals Cleveland Medical Center at Case Western Reserve University Medical School in Cleveland, Ohio. Susie Ivanov is a Physician Assistant and Glenn Wera is an Attending Orthopaedic Surgeon, both in the Orthopaedic Surgery Section at Louis Stokes Cleveland Veterans Affairs Medical Center in Ohio. Correspondence: Todd Morrison ([email protected])

Author disclosures
Glenn Wera is a board committee member for American Academy of Orthopaedic Surgeons. The other authors report no actual or potential conflicts of interest with regard to this article.

Disclaimer
The opinions expressed herein are those of the authors and do not necessarily reflect those of Federal Practitioner, Frontline Medical Communications Inc., the US Government, or any of its agencies.

Author and Disclosure Information

Todd Morrison and Christopher Flanagan are Resident Physician Orthopaedic Surgeons in the Department of Orthopaedic Surgery at University Hospitals Cleveland Medical Center at Case Western Reserve University Medical School in Cleveland, Ohio. Susie Ivanov is a Physician Assistant and Glenn Wera is an Attending Orthopaedic Surgeon, both in the Orthopaedic Surgery Section at Louis Stokes Cleveland Veterans Affairs Medical Center in Ohio. Correspondence: Todd Morrison ([email protected])

Author disclosures
Glenn Wera is a board committee member for American Academy of Orthopaedic Surgeons. The other authors report no actual or potential conflicts of interest with regard to this article.

Disclaimer
The opinions expressed herein are those of the authors and do not necessarily reflect those of Federal Practitioner, Frontline Medical Communications Inc., the US Government, or any of its agencies.

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Related Articles
While patients without knee instability use more nonarthroplasty treatments over a longer period prior to total knee arthroplasty, patients with less severe knee osteoarthritis are at risk of receiving interventions judged to be rarely appropriate.
While patients without knee instability use more nonarthroplasty treatments over a longer period prior to total knee arthroplasty, patients with less severe knee osteoarthritis are at risk of receiving interventions judged to be rarely appropriate.

Knee osteoarthritis (OA) affects almost 9.3 million adults in the US and accounts for $27 billion in annual health care expenses.1,2 Due to the increasing cost of health care and an aging population, there has been renewed interest in establishing criteria for nonarthroplasty treatment of knee OA.

In 2013, using the RAND/UCLA Appropriateness method, the American Academy of Orthopaedic Surgeons (AAOS) developed an appropriate use criteria (AUC) for nonarthroplasty management of primary OA of the knee, based on orthopaedic literature and expert opinion.3 Interventions such as activity modification, weight loss, prescribed physical therapy, nonsteroidal anti-inflammatory drugs, tramadol, prescribed oral or transcutaneous opioids, acetaminophen, intra-articular corticosteroids, hinged or unloading knee braces, arthroscopic partial menisectomy or loose body removal, and realignment osteotomy were assessed. An algorithm was developed for 576 patients scenarios that incorporated patient-specific, prognostic/predictor variables to assign designations of “appropriate,” “may be appropriate,” or “rarely appropriate,” to treatment interventions.4,5 An online version of the algorithm (orthoguidelines.org) is available for physicians and surgeons to judge appropriateness of nonarthroplasty treatments; however, it is not intended to mandate candidacy for treatment or intervention.

Clinical evaluation of the AAOS AUC is necessary to determine how treatment recommendations correlate with current practice. A recent examination of the AAOS Appropriateness System for Surgical Management of Knee OA found that prognostic/predictor variables, such as patient age, OA severity, and pattern of knee OA involvement were more heavily weighted when determining arthroplasty appropriateness than was pain severity or functional loss.6 Furthermore, non-AAOS AUC prognostic/predictor variables, such as race and gender, have been linked to disparities in utilization of knee OA interventions.7-9 Such disparities can be costly not just from a patient perceptive, but also employer and societal perspectives.10

The Department of Veterans Affairs (VA) health care system represents a model of equal-access-to care system in the US that is ideal for examination of issues about health care utilization and any disparities within the AAOS AUC model and has previously been used to assess utilization of total knee arthroplasty.9 The aim of this study was to characterize utilization of the AAOS AUC for nonarthroplasty treatment of knee OA in a VA patient population. We asked the following questions: (1) What variables are predictive of receiving a greater number of AAOS AUC evaluated nonarthroplasty treatments? (2) What variables are predictive of receiving “rarely appropriate” AAOS AUC evaluated nonarthroplasty treatment? (3) What factors are predictive of duration of nonarthroplasty care until total knee arthroplasty (TKA)?

Methods

The institutional review board at the Louis Stokes Cleveland VA Medical Center in Ohio approved a retrospective chart review of nonarthroplasty treatments utilized by patients presenting to its orthopaedic section who subsequently underwent knee arthroplasty between 2013 and 2016. Eligibility criteria included patients aged ≥ 30 years with a diagnosis of unilateral or bilateral primary knee OA. Patients with posttraumatic OA, inflammatory arthritis, and a history of infectious arthritis or Charcot arthropathy of the knee were excluded. Patients with a body mass index (BMI) > 40 or a hemoglobin A1c > 8.0 at presentation were excluded as nonarthroplasty care was the recommended course of treatment above these thresholds.

 

 

Data collected included race, gender, duration of nonarthroplasty treatment, BMI, and Kellgren-Lawrence classification of knee OA at time of presentation for symptomatic knee OA.11 All AAOS AUC-evaluated nonarthroplasty treatments utilized prior to arthroplasty intervention also were recorded (Table 1). 

Indications and classifications for each subject were entered into the AAOS AUC online algorithm, and every AAOS AUC evaluated treatment utilized was assigned a rating of appropriate, may be appropriate, or rarely appropriate, based on the algorithm results for that clinical scenario (Table 2). 
Information regarding anti-inflammatory, analgesic, and prescribed oral or transcutaneous opioid use for chronic knee pain during the period of nonoperative management of knee OA prior to TKA was obtained by review of medication lists and reconciliation with orthopaedic consultation notes in the electronic health record. Peri-operative anti-inflammatory, analgesic, and prescribed oral or transcutaneous opioid use did not constitute an AUC intervention.

Statistical Analysis

Statistical analysis was completed with GraphPad Software Prism 7.0a (La Jolla, CA) and Mathworks MatLab R2016b software (Natick, MA). Univariate analysis with Student t tests with Welch corrections in the setting of unequal variance, Mann-Whitney nonparametric tests, and Fisher exact test were generated in the appropriate setting. Multivariable analyses also were conducted. For continuous outcomes, stepwise multiple linear regression was used to generate predictive models; for binary outcomes, binomial logistic regression was used.

Factors analyzed in regression modeling for the total number of AAOS AUC evaluated nonarthroplasty treatments utilized and the likelihood of receiving a rarely appropriate treatment included gender, race, function-limiting pain, range of motion (ROM), ligamentous instability, arthritis pattern, limb alignment, mechanical symptoms, BMI, age, and Kellgren-Lawrence grade. Factors analyzed in timing of TKA included the above variables plus the total number of AUC interventions, whether the patient received an inappropriate intervention, and average appropriateness of the interventions received. Residual analysis with Cook’s distance was used to identify outliers in regression. Observations with Cook’s distance > 3 times the mean Cook’s distance were identified as potential outliers, and models were adjusted accordingly. All statistical analyses were 2-tailed. Statistical significance was set to P ≤ .05 for all outputs.

Results

In the study, 97.8% of participants identified as male, and the mean age was 62.8 years (Table 3). 

The study group was predominantly white (70.3%). All participants had a diagnosis of primary OA. The majority of patients were aged 51 to 70 years (68.1%) and presented with pain occurring following short-distance ambulation (79.1%) but without mechanical symptoms (80.2%). On examination, the majority of patients were found to have full knee ROM (53.8%), no ligamentous instability (97.8%), and normal limb alignment (60.4%). Radiographically, patients most often had multicompartmental disease (69.2%) with evidence of severe joint-space narrowing (63.7%), resulting in a plurality of patients having a Kellgren-Lawrence arthritis grade of 3 (46.2%) (Table 4).

Appropriate Use Criteria Interventions

Patients received a mean of 5.2 AAOS AUC evaluated interventions before undergoing arthroplasty management at a mean of 32.3 months (range 2-181 months) from initial presentation. The majority of these interventions were classified as either appropriate or may be appropriate, according to the AUC definitions (95.1%). Self-management and physical therapy programs were widely utilized (100% and 90.1%, respectively), with all use of these interventions classified as appropriate.

 

 

Hinged or unloader knee braces were utilized in about half the study patients; this intervention was classified as rarely appropriate in 4.4% of these patients. Medical therapy was also widely used, with all use of NSAIDs, acetaminophen, and tramadol classified as appropriate or may be appropriate. Oral or transcutaneous opioid medications were prescribed in 14.3% of patients, with 92.3% of this use classified as rarely appropriate. Although the opioid medication prescribing provider was not specifically evaluated, there were no instances in which the orthopaedic service provided an oral or transcutaneous opioid prescriptions. Procedural interventions, with the exception of corticosteroid injections, were uncommon; no patient received realignment osteotomy, and only 12.1% of patients underwent arthroscopy. The use of arthroscopy was deemed rarely appropriate in 72.7% of these cases.

Factors Associated With AAOS AUC Intervention Use

There was no difference in the number of AAOS AUC evaluated interventions received based on BMI (mean [SD] BMI < 35, 5.2 [1.0] vs BMI ≥ 35, 5.3 [1.1], P = .49), age (mean [SD] aged < 60 years, 5.4 [1.0] vs aged ≥ 60 years, 5.1 [1.2], P = .23), or Kellgren-Lawrence arthritic grade (mean [SD] grade ≤ 2, 5.5 [1.0] vs grade > 2, 5.1 [1.1], P = .06). These variables also were not associated with receiving a rarely appropriate intervention (mean [SD] BMI < 35, 0.27 [0.5] vs BMI > 35, 0.2 [0.4], P = .81; aged > 60 years, 0.3 [0.5] vs aged < 60 years, 0.2 [0.4], P = .26; Kellgren-Lawrence grade < 2, 0.4 [0.6] vs grade > 2, 0.2 [0.4], P = .1).

Regression modeling to predict total number of AAOS AUC evaluated interventions received produced a significant model (R2 = 0.111, P = .006). The presence of ligamentous instability (β coefficient, -1.61) and the absence of mechanical symptoms (β coefficient, -0.67) were negative predictors of number of AUC interventions received. Variance inflation factors were 1.014 and 1.012, respectively. Likewise, regression modeling to identify factors predictive of receiving a rarely appropriate intervention also produced a significant model (pseudo R2= 0.06, P = .025), with lower Kellgren-Lawrence grade the only significant predictor of receiving a rarely appropriate intervention (odds ratio [OR] 0.54; 95% CI, 0.42 -0.72, per unit increase).

Timing from presentation to arthroplasty intervention was also evaluated. Age was a negative predictor (β coefficient -1.61), while positive predictors were reduced ROM (β coefficient 15.72) and having more AUC interventions (β coefficient 7.31) (model R2= 0.29, P = < .001). Age was the most significant predictor. Variance inflations factors were 1.02, 1.01, and 1.03, respectively. Receiving a rarely appropriate intervention was not associated with TKA timing.

Discussion

This single-center retrospective study examined the utilization of AAOS AUC-evaluated nonarthroplasty interventions for symptomatic knee OA prior to TKA. The aims of this study were to validate the AAOS AUC in a clinical setting and identify predictors of AAOS AUC utilization. In particular, this study focused on the number of interventions utilized prior to knee arthroplasty, whether interventions receiving a designation of rarely appropriate were used, and the duration of nonarthroplasty treatment.

 

 

Patients with knee instability used fewer total AAOS AUC evaluated interventions prior to TKA. Subjective instability has been reported as high as 27% in patients with OA and has been associated with fear of falling, poor balance confidence, activity limitations, and lower Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) physical function scores.12 However, it has not been found to correlate with knee laxity.13 Nevertheless, significant functional impairment with the risk of falling may reduce the number of nonarthroplasty interventions attempted. On the other hand, the presence of mechanical symptoms resulted in greater utilization of nonarthroplasty interventions. This is likely due to the greater utilization of arthroscopic partial menisectomy or loose body removal in this group of patients. Despite its inclusion as an AAOS AUC evaluated intervention, arthroscopy remains a contentious treatment for symptomatic knee pain in the setting of OA.14,15

For every unit decrease in Kellgren-Lawrence OA grade, patients were 54% more likely to receive a rarely appropriate intervention prior to knee arthroplasty. This is supported by the recent literature examining the AAOS AUC for surgical management of knee OA. Riddle and colleagues developed a classification tree to determine the contributions of various prognostic variables in final classifications of the 864 clinical vignettes used to develop the appropriateness algorithm and found that OA severity was strongly favored, with only 4 of the 432 vignettes with severe knee OA judged as rarely appropriate for surgical intervention.6

Our findings, too, may be explained by an AAOS AUC system that too heavily weighs radiographic severity of knee OA, resulting in more frequent rarely appropriate interventions in patients with less severe arthritis, including nonarthroplasty treatments. It is likely that rarely appropriate interventions were attempted in this subset of our study cohort based on patient’s subjective symptoms and functional status, both of which have been shown to be discordant with radiographic severity of knee OA.16

Oral or transcutaneous prescribed opioid medications were the most frequent intervention that received a rarely appropriate designation. Patients with preoperative opioid use undergoing TKA have been shown to have a greater risk for postoperative complications and longer hospital stay, particularly those patients aged < 75 years. Younger age, use of more interventions, and decreased knee ROM at presentation were predictive of longer duration of nonarthroplasty treatment. The use of more AAOS AUC evaluated interventions in these patients suggests that the AAOS AUC model may effectively be used to manage symptomatic OA, increasing the time from presentation to knee arthroplasty.

Interestingly, the use of rarely appropriate interventions did not affect TKA timing, as would be expected in a clinically effective nonarthroplasty treatment model. The reasons for rarely appropriate nonsurgical interventions are complex and require further investigation. One possible explanation is that decreased ROM was a marker for mechanical symptoms that necessitated additional intervention in the form of knee arthroscopy, delaying time to TKA.

Limitations

There are several limitations of this study. First, the small sample size (N = 90) requires acknowledgment; however, this limitation reflects the difficulty in following patients for years prior to an operative intervention. Second, the study population consists of veterans using the VA system and may not be reflective of the general population, differing with respect to gender, racial, and socioeconomic factors. Nevertheless, studies examining TKA utilization found, aside from racial and ethnic variability, patient gender and age do not affect arthroplasty utilization rate in the VA system.17

 

 

Additional limitations stem from the retrospective nature of this study. While the Computerized Patient Record System and centralized care of the VA system allows for review of all physical therapy consultations, orthotic consultations, and medications within the VA system, any treatments and intervention delivered by non-VA providers were not captured. Furthermore, the ability to assess for confounding variables limiting the prescription of certain medications, such as chronic kidney disease with NSAIDs or liver disease with acetaminophen, was limited by our study design.

Although our study suffers from selection bias with respect to examination of nonarthroplasty treatment in patients who have ultimately undergone TKA, we feel that this subset of patients with symptomatic knee OA represents the majority of patients evaluated for knee OA by orthopaedic surgeons in the clinic setting. It should be noted that although realignment osteotomies were sometimes indicated as appropriate by AAOS AUC model in our study population, this intervention was never performed due to patient and surgeon preference. Additionally, although it is not an AAOS AUC evaluated intervention, viscosupplementation was sporadically used during the study period; however, it is now off formulary at the investigation institution.

Conclusion

Our study suggests that patients without knee instability use more nonarthroplasty treatments over a longer period before TKA, and those patients with less severe knee OA are at risk of receiving an intervention judged to be rarely appropriate by the AAOS AUC. Such interventions do not affect timing of TKA. Nonarthroplasty care should be individualized to patients’ needs, and the decision to proceed with arthroplasty should be considered only after exhausting appropriate conservative measures. We recommend that providers use the AAOS AUC, especially when treating younger patients with less severe knee OA, particularly if considering opiate therapy or knee arthroscopy.

Acknowledgments
The authors would like to acknowledge Patrick Getty, MD, for his surgical care of some of the study patients. This material is the result of work supported with resources and the use of facilities at the Louis Stokes Cleveland VA Medical Center in Ohio.

Knee osteoarthritis (OA) affects almost 9.3 million adults in the US and accounts for $27 billion in annual health care expenses.1,2 Due to the increasing cost of health care and an aging population, there has been renewed interest in establishing criteria for nonarthroplasty treatment of knee OA.

In 2013, using the RAND/UCLA Appropriateness method, the American Academy of Orthopaedic Surgeons (AAOS) developed an appropriate use criteria (AUC) for nonarthroplasty management of primary OA of the knee, based on orthopaedic literature and expert opinion.3 Interventions such as activity modification, weight loss, prescribed physical therapy, nonsteroidal anti-inflammatory drugs, tramadol, prescribed oral or transcutaneous opioids, acetaminophen, intra-articular corticosteroids, hinged or unloading knee braces, arthroscopic partial menisectomy or loose body removal, and realignment osteotomy were assessed. An algorithm was developed for 576 patients scenarios that incorporated patient-specific, prognostic/predictor variables to assign designations of “appropriate,” “may be appropriate,” or “rarely appropriate,” to treatment interventions.4,5 An online version of the algorithm (orthoguidelines.org) is available for physicians and surgeons to judge appropriateness of nonarthroplasty treatments; however, it is not intended to mandate candidacy for treatment or intervention.

Clinical evaluation of the AAOS AUC is necessary to determine how treatment recommendations correlate with current practice. A recent examination of the AAOS Appropriateness System for Surgical Management of Knee OA found that prognostic/predictor variables, such as patient age, OA severity, and pattern of knee OA involvement were more heavily weighted when determining arthroplasty appropriateness than was pain severity or functional loss.6 Furthermore, non-AAOS AUC prognostic/predictor variables, such as race and gender, have been linked to disparities in utilization of knee OA interventions.7-9 Such disparities can be costly not just from a patient perceptive, but also employer and societal perspectives.10

The Department of Veterans Affairs (VA) health care system represents a model of equal-access-to care system in the US that is ideal for examination of issues about health care utilization and any disparities within the AAOS AUC model and has previously been used to assess utilization of total knee arthroplasty.9 The aim of this study was to characterize utilization of the AAOS AUC for nonarthroplasty treatment of knee OA in a VA patient population. We asked the following questions: (1) What variables are predictive of receiving a greater number of AAOS AUC evaluated nonarthroplasty treatments? (2) What variables are predictive of receiving “rarely appropriate” AAOS AUC evaluated nonarthroplasty treatment? (3) What factors are predictive of duration of nonarthroplasty care until total knee arthroplasty (TKA)?

Methods

The institutional review board at the Louis Stokes Cleveland VA Medical Center in Ohio approved a retrospective chart review of nonarthroplasty treatments utilized by patients presenting to its orthopaedic section who subsequently underwent knee arthroplasty between 2013 and 2016. Eligibility criteria included patients aged ≥ 30 years with a diagnosis of unilateral or bilateral primary knee OA. Patients with posttraumatic OA, inflammatory arthritis, and a history of infectious arthritis or Charcot arthropathy of the knee were excluded. Patients with a body mass index (BMI) > 40 or a hemoglobin A1c > 8.0 at presentation were excluded as nonarthroplasty care was the recommended course of treatment above these thresholds.

 

 

Data collected included race, gender, duration of nonarthroplasty treatment, BMI, and Kellgren-Lawrence classification of knee OA at time of presentation for symptomatic knee OA.11 All AAOS AUC-evaluated nonarthroplasty treatments utilized prior to arthroplasty intervention also were recorded (Table 1). 

Indications and classifications for each subject were entered into the AAOS AUC online algorithm, and every AAOS AUC evaluated treatment utilized was assigned a rating of appropriate, may be appropriate, or rarely appropriate, based on the algorithm results for that clinical scenario (Table 2). 
Information regarding anti-inflammatory, analgesic, and prescribed oral or transcutaneous opioid use for chronic knee pain during the period of nonoperative management of knee OA prior to TKA was obtained by review of medication lists and reconciliation with orthopaedic consultation notes in the electronic health record. Peri-operative anti-inflammatory, analgesic, and prescribed oral or transcutaneous opioid use did not constitute an AUC intervention.

Statistical Analysis

Statistical analysis was completed with GraphPad Software Prism 7.0a (La Jolla, CA) and Mathworks MatLab R2016b software (Natick, MA). Univariate analysis with Student t tests with Welch corrections in the setting of unequal variance, Mann-Whitney nonparametric tests, and Fisher exact test were generated in the appropriate setting. Multivariable analyses also were conducted. For continuous outcomes, stepwise multiple linear regression was used to generate predictive models; for binary outcomes, binomial logistic regression was used.

Factors analyzed in regression modeling for the total number of AAOS AUC evaluated nonarthroplasty treatments utilized and the likelihood of receiving a rarely appropriate treatment included gender, race, function-limiting pain, range of motion (ROM), ligamentous instability, arthritis pattern, limb alignment, mechanical symptoms, BMI, age, and Kellgren-Lawrence grade. Factors analyzed in timing of TKA included the above variables plus the total number of AUC interventions, whether the patient received an inappropriate intervention, and average appropriateness of the interventions received. Residual analysis with Cook’s distance was used to identify outliers in regression. Observations with Cook’s distance > 3 times the mean Cook’s distance were identified as potential outliers, and models were adjusted accordingly. All statistical analyses were 2-tailed. Statistical significance was set to P ≤ .05 for all outputs.

Results

In the study, 97.8% of participants identified as male, and the mean age was 62.8 years (Table 3). 

The study group was predominantly white (70.3%). All participants had a diagnosis of primary OA. The majority of patients were aged 51 to 70 years (68.1%) and presented with pain occurring following short-distance ambulation (79.1%) but without mechanical symptoms (80.2%). On examination, the majority of patients were found to have full knee ROM (53.8%), no ligamentous instability (97.8%), and normal limb alignment (60.4%). Radiographically, patients most often had multicompartmental disease (69.2%) with evidence of severe joint-space narrowing (63.7%), resulting in a plurality of patients having a Kellgren-Lawrence arthritis grade of 3 (46.2%) (Table 4).

Appropriate Use Criteria Interventions

Patients received a mean of 5.2 AAOS AUC evaluated interventions before undergoing arthroplasty management at a mean of 32.3 months (range 2-181 months) from initial presentation. The majority of these interventions were classified as either appropriate or may be appropriate, according to the AUC definitions (95.1%). Self-management and physical therapy programs were widely utilized (100% and 90.1%, respectively), with all use of these interventions classified as appropriate.

 

 

Hinged or unloader knee braces were utilized in about half the study patients; this intervention was classified as rarely appropriate in 4.4% of these patients. Medical therapy was also widely used, with all use of NSAIDs, acetaminophen, and tramadol classified as appropriate or may be appropriate. Oral or transcutaneous opioid medications were prescribed in 14.3% of patients, with 92.3% of this use classified as rarely appropriate. Although the opioid medication prescribing provider was not specifically evaluated, there were no instances in which the orthopaedic service provided an oral or transcutaneous opioid prescriptions. Procedural interventions, with the exception of corticosteroid injections, were uncommon; no patient received realignment osteotomy, and only 12.1% of patients underwent arthroscopy. The use of arthroscopy was deemed rarely appropriate in 72.7% of these cases.

Factors Associated With AAOS AUC Intervention Use

There was no difference in the number of AAOS AUC evaluated interventions received based on BMI (mean [SD] BMI < 35, 5.2 [1.0] vs BMI ≥ 35, 5.3 [1.1], P = .49), age (mean [SD] aged < 60 years, 5.4 [1.0] vs aged ≥ 60 years, 5.1 [1.2], P = .23), or Kellgren-Lawrence arthritic grade (mean [SD] grade ≤ 2, 5.5 [1.0] vs grade > 2, 5.1 [1.1], P = .06). These variables also were not associated with receiving a rarely appropriate intervention (mean [SD] BMI < 35, 0.27 [0.5] vs BMI > 35, 0.2 [0.4], P = .81; aged > 60 years, 0.3 [0.5] vs aged < 60 years, 0.2 [0.4], P = .26; Kellgren-Lawrence grade < 2, 0.4 [0.6] vs grade > 2, 0.2 [0.4], P = .1).

Regression modeling to predict total number of AAOS AUC evaluated interventions received produced a significant model (R2 = 0.111, P = .006). The presence of ligamentous instability (β coefficient, -1.61) and the absence of mechanical symptoms (β coefficient, -0.67) were negative predictors of number of AUC interventions received. Variance inflation factors were 1.014 and 1.012, respectively. Likewise, regression modeling to identify factors predictive of receiving a rarely appropriate intervention also produced a significant model (pseudo R2= 0.06, P = .025), with lower Kellgren-Lawrence grade the only significant predictor of receiving a rarely appropriate intervention (odds ratio [OR] 0.54; 95% CI, 0.42 -0.72, per unit increase).

Timing from presentation to arthroplasty intervention was also evaluated. Age was a negative predictor (β coefficient -1.61), while positive predictors were reduced ROM (β coefficient 15.72) and having more AUC interventions (β coefficient 7.31) (model R2= 0.29, P = < .001). Age was the most significant predictor. Variance inflations factors were 1.02, 1.01, and 1.03, respectively. Receiving a rarely appropriate intervention was not associated with TKA timing.

Discussion

This single-center retrospective study examined the utilization of AAOS AUC-evaluated nonarthroplasty interventions for symptomatic knee OA prior to TKA. The aims of this study were to validate the AAOS AUC in a clinical setting and identify predictors of AAOS AUC utilization. In particular, this study focused on the number of interventions utilized prior to knee arthroplasty, whether interventions receiving a designation of rarely appropriate were used, and the duration of nonarthroplasty treatment.

 

 

Patients with knee instability used fewer total AAOS AUC evaluated interventions prior to TKA. Subjective instability has been reported as high as 27% in patients with OA and has been associated with fear of falling, poor balance confidence, activity limitations, and lower Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) physical function scores.12 However, it has not been found to correlate with knee laxity.13 Nevertheless, significant functional impairment with the risk of falling may reduce the number of nonarthroplasty interventions attempted. On the other hand, the presence of mechanical symptoms resulted in greater utilization of nonarthroplasty interventions. This is likely due to the greater utilization of arthroscopic partial menisectomy or loose body removal in this group of patients. Despite its inclusion as an AAOS AUC evaluated intervention, arthroscopy remains a contentious treatment for symptomatic knee pain in the setting of OA.14,15

For every unit decrease in Kellgren-Lawrence OA grade, patients were 54% more likely to receive a rarely appropriate intervention prior to knee arthroplasty. This is supported by the recent literature examining the AAOS AUC for surgical management of knee OA. Riddle and colleagues developed a classification tree to determine the contributions of various prognostic variables in final classifications of the 864 clinical vignettes used to develop the appropriateness algorithm and found that OA severity was strongly favored, with only 4 of the 432 vignettes with severe knee OA judged as rarely appropriate for surgical intervention.6

Our findings, too, may be explained by an AAOS AUC system that too heavily weighs radiographic severity of knee OA, resulting in more frequent rarely appropriate interventions in patients with less severe arthritis, including nonarthroplasty treatments. It is likely that rarely appropriate interventions were attempted in this subset of our study cohort based on patient’s subjective symptoms and functional status, both of which have been shown to be discordant with radiographic severity of knee OA.16

Oral or transcutaneous prescribed opioid medications were the most frequent intervention that received a rarely appropriate designation. Patients with preoperative opioid use undergoing TKA have been shown to have a greater risk for postoperative complications and longer hospital stay, particularly those patients aged < 75 years. Younger age, use of more interventions, and decreased knee ROM at presentation were predictive of longer duration of nonarthroplasty treatment. The use of more AAOS AUC evaluated interventions in these patients suggests that the AAOS AUC model may effectively be used to manage symptomatic OA, increasing the time from presentation to knee arthroplasty.

Interestingly, the use of rarely appropriate interventions did not affect TKA timing, as would be expected in a clinically effective nonarthroplasty treatment model. The reasons for rarely appropriate nonsurgical interventions are complex and require further investigation. One possible explanation is that decreased ROM was a marker for mechanical symptoms that necessitated additional intervention in the form of knee arthroscopy, delaying time to TKA.

Limitations

There are several limitations of this study. First, the small sample size (N = 90) requires acknowledgment; however, this limitation reflects the difficulty in following patients for years prior to an operative intervention. Second, the study population consists of veterans using the VA system and may not be reflective of the general population, differing with respect to gender, racial, and socioeconomic factors. Nevertheless, studies examining TKA utilization found, aside from racial and ethnic variability, patient gender and age do not affect arthroplasty utilization rate in the VA system.17

 

 

Additional limitations stem from the retrospective nature of this study. While the Computerized Patient Record System and centralized care of the VA system allows for review of all physical therapy consultations, orthotic consultations, and medications within the VA system, any treatments and intervention delivered by non-VA providers were not captured. Furthermore, the ability to assess for confounding variables limiting the prescription of certain medications, such as chronic kidney disease with NSAIDs or liver disease with acetaminophen, was limited by our study design.

Although our study suffers from selection bias with respect to examination of nonarthroplasty treatment in patients who have ultimately undergone TKA, we feel that this subset of patients with symptomatic knee OA represents the majority of patients evaluated for knee OA by orthopaedic surgeons in the clinic setting. It should be noted that although realignment osteotomies were sometimes indicated as appropriate by AAOS AUC model in our study population, this intervention was never performed due to patient and surgeon preference. Additionally, although it is not an AAOS AUC evaluated intervention, viscosupplementation was sporadically used during the study period; however, it is now off formulary at the investigation institution.

Conclusion

Our study suggests that patients without knee instability use more nonarthroplasty treatments over a longer period before TKA, and those patients with less severe knee OA are at risk of receiving an intervention judged to be rarely appropriate by the AAOS AUC. Such interventions do not affect timing of TKA. Nonarthroplasty care should be individualized to patients’ needs, and the decision to proceed with arthroplasty should be considered only after exhausting appropriate conservative measures. We recommend that providers use the AAOS AUC, especially when treating younger patients with less severe knee OA, particularly if considering opiate therapy or knee arthroscopy.

Acknowledgments
The authors would like to acknowledge Patrick Getty, MD, for his surgical care of some of the study patients. This material is the result of work supported with resources and the use of facilities at the Louis Stokes Cleveland VA Medical Center in Ohio.

References

1. Cross M, Smith E, Hoy D, et al. The global burden of hip and knee osteoarthritis: estimates from the Global Burden of Disease 2010 study. Ann Rheum Dis. 2014;73(7):1323-1330.

2. Losina E, Walensky RP, Kessler CL, et al. Cost-effectiveness of total knee arthroplasty in the United States: patient risk and hospital volume. Arch Intern Med. 2009;169(12):1113-1121; discussion 1121-1122.

3. Members of the Writing, Review, and Voting Panels of the AUC on the Non-Arthroplasty Treatment of Osteoarthritis of the Knee, Sanders JO, Heggeness MH, Murray J, Pezold R, Donnelly P. The American Academy of Orthopaedic Surgeons Appropriate Use Criteria on the Non-Arthroplasty Treatment of Osteoarthritis of the Knee. J Bone Joint Surg Am. 2014;96(14):1220-1221.

4. Sanders JO, Murray J, Gross L. Non-arthroplasty treatment of osteoarthritis of the knee. J Am Acad Orthop Surg. 2014;22(4):256-260.

5. Yates AJ Jr, McGrory BJ, Starz TW, Vincent KR, McCardel B, Golightly YM. AAOS appropriate use criteria: optimizing the non-arthroplasty management of osteoarthritis of the knee. J Am Acad Orthop Surg. 2014;22(4):261-267.

6. Riddle DL, Perera RA. Appropriateness and total knee arthroplasty: an examination of the American Academy of Orthopaedic Surgeons appropriateness rating system. Osteoarthritis Cartilage. 2017;25(12):1994-1998.

7. Morgan RC Jr, Slover J. Breakout session: ethnic and racial disparities in joint arthroplasty. Clin Orthop Relat Res. 2011;469(7):1886-1890.

8. O’Connor MI, Hooten EG. Breakout session: gender disparities in knee osteoarthritis and TKA. Clin Orthop Relat Res. 2011;469(7):1883-1885.

9. Ibrahim SA. Racial and ethnic disparities in hip and knee joint replacement: a review of research in the Veterans Affairs Health Care System. J Am Acad Orthop Surg. 2007;15(suppl 1):S87-S94.

10. Karmarkar TD, Maurer A, Parks ML, et al. A fresh perspective on a familiar problem: examining disparities in knee osteoarthritis using a Markov model. Med Care. 2017;55(12):993-1000.

11. Kohn MD, Sassoon AA, Fernando ND. Classifications in brief: Kellgren-Lawrence Classification of Osteoarthritis. Clin Orthop Relat Res. 2016;474(8):1886-1893.

12. Nguyen U, Felson DT, Niu J, et al. The impact of knee instability with and without buckling on balance confidence, fear of falling and physical function: the Multicenter Osteoarthritis Study. Osteoarthritis Cartilage. 2014;22(4):527-534.

13. Schmitt LC, Fitzgerald GK, Reisman AS, Rudolph KS. Instability, laxity, and physical function in patients with medial knee osteoarthritis. Phys Ther. 2008;88(12):1506-1516.

14. Laupattarakasem W, Laopaiboon M, Laupattarakasem P, Sumananont C. Arthroscopic debridement for knee osteoarthritis. Cochrane Database Syst Rev. 2008;(1):CD005118.

15. Lamplot JD, Brophy RH. The role for arthroscopic partial meniscectomy in knees with degenerative changes: a systematic review. Bone Joint J. 2016;98-B(7):934-938.

16. Whittle R, Jordan KP, Thomas E, Peat G. Average symptom trajectories following incident radiographic knee osteoarthritis: data from the Osteoarthritis Initiative. RMD Open. 2016;2(2):e000281.

17. Jones A, Kwoh CK, Kelley ME, Ibrahim SA. Racial disparity in knee arthroplasty utilization in the Veterans Health Administration. Arthritis Rheum. 2005;53(6):979-981.

References

1. Cross M, Smith E, Hoy D, et al. The global burden of hip and knee osteoarthritis: estimates from the Global Burden of Disease 2010 study. Ann Rheum Dis. 2014;73(7):1323-1330.

2. Losina E, Walensky RP, Kessler CL, et al. Cost-effectiveness of total knee arthroplasty in the United States: patient risk and hospital volume. Arch Intern Med. 2009;169(12):1113-1121; discussion 1121-1122.

3. Members of the Writing, Review, and Voting Panels of the AUC on the Non-Arthroplasty Treatment of Osteoarthritis of the Knee, Sanders JO, Heggeness MH, Murray J, Pezold R, Donnelly P. The American Academy of Orthopaedic Surgeons Appropriate Use Criteria on the Non-Arthroplasty Treatment of Osteoarthritis of the Knee. J Bone Joint Surg Am. 2014;96(14):1220-1221.

4. Sanders JO, Murray J, Gross L. Non-arthroplasty treatment of osteoarthritis of the knee. J Am Acad Orthop Surg. 2014;22(4):256-260.

5. Yates AJ Jr, McGrory BJ, Starz TW, Vincent KR, McCardel B, Golightly YM. AAOS appropriate use criteria: optimizing the non-arthroplasty management of osteoarthritis of the knee. J Am Acad Orthop Surg. 2014;22(4):261-267.

6. Riddle DL, Perera RA. Appropriateness and total knee arthroplasty: an examination of the American Academy of Orthopaedic Surgeons appropriateness rating system. Osteoarthritis Cartilage. 2017;25(12):1994-1998.

7. Morgan RC Jr, Slover J. Breakout session: ethnic and racial disparities in joint arthroplasty. Clin Orthop Relat Res. 2011;469(7):1886-1890.

8. O’Connor MI, Hooten EG. Breakout session: gender disparities in knee osteoarthritis and TKA. Clin Orthop Relat Res. 2011;469(7):1883-1885.

9. Ibrahim SA. Racial and ethnic disparities in hip and knee joint replacement: a review of research in the Veterans Affairs Health Care System. J Am Acad Orthop Surg. 2007;15(suppl 1):S87-S94.

10. Karmarkar TD, Maurer A, Parks ML, et al. A fresh perspective on a familiar problem: examining disparities in knee osteoarthritis using a Markov model. Med Care. 2017;55(12):993-1000.

11. Kohn MD, Sassoon AA, Fernando ND. Classifications in brief: Kellgren-Lawrence Classification of Osteoarthritis. Clin Orthop Relat Res. 2016;474(8):1886-1893.

12. Nguyen U, Felson DT, Niu J, et al. The impact of knee instability with and without buckling on balance confidence, fear of falling and physical function: the Multicenter Osteoarthritis Study. Osteoarthritis Cartilage. 2014;22(4):527-534.

13. Schmitt LC, Fitzgerald GK, Reisman AS, Rudolph KS. Instability, laxity, and physical function in patients with medial knee osteoarthritis. Phys Ther. 2008;88(12):1506-1516.

14. Laupattarakasem W, Laopaiboon M, Laupattarakasem P, Sumananont C. Arthroscopic debridement for knee osteoarthritis. Cochrane Database Syst Rev. 2008;(1):CD005118.

15. Lamplot JD, Brophy RH. The role for arthroscopic partial meniscectomy in knees with degenerative changes: a systematic review. Bone Joint J. 2016;98-B(7):934-938.

16. Whittle R, Jordan KP, Thomas E, Peat G. Average symptom trajectories following incident radiographic knee osteoarthritis: data from the Osteoarthritis Initiative. RMD Open. 2016;2(2):e000281.

17. Jones A, Kwoh CK, Kelley ME, Ibrahim SA. Racial disparity in knee arthroplasty utilization in the Veterans Health Administration. Arthritis Rheum. 2005;53(6):979-981.

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Today’s Care Must Extend Beyond the Exam Room

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Today’s Care Must Extend Beyond the Exam Room

In May 2014, a 70-year-old retiree underwent repair of a fracture of her left ankle. The procedure was performed at a local hospital. A splint was applied to the ankle, and a nurse provided crutches.

Following discharge from the hospital, the patient hailed a taxi to take her home. As she was exiting the taxi at her residence, the patient fell and sustained comminuted fractures to the distal radius and distal ulna of her right (dominant) wrist and a trimalleolar fracture to her repaired left ankle.

The plaintiff was transported back to the hospital via ambulance. She underwent closed reduction of her wrist fractures and 11 days later was transferred to another facility for open reduction and internal fixation of her left ankle fracture. Her hospitalizations totaled 13 days and were followed by a course of inpatient rehabilitative therapy; the latter lasted until late August 2014, with a brief interruption in June when she underwent open reduction and internal fixation of her wrist fractures. When she returned home in August, the patient required the assistance of visiting aides and 3 additional months of rehabilitative therapy.

At trial, the plaintiff claimed that her left ankle and her right wrist remained painful, that she sustained a mild residual diminution of each area’s range of motion, and that these residual effects hindered her performance of basic physical activities (eg, cleaning and cooking).

The plaintiff alleged that her fall while exiting the taxi resulted from unsteadiness, which was a lingering effect of morphine that was administered during the repair of her fracture. She sought recovery of damages for past and future pain and suffering from the hospital’s operator. The lawsuit alleged that the nurse had failed to provide instructions on the proper use of crutches, that the nurse had failed to undertake measures that would have diminished the plaintiff’s likelihood of falling, that the nurse’s failures constituted malpractice and negligence, and that the hospital operator was vicariously liable for the nurse’s actions.

The plaintiff claimed that she repeatedly warned that she did not believe that she could safely use the crutches provided by the nurse. She claimed that she was unsteady and lightheaded, and that when she requested a wheelchair, an escort, or an ambulance, the nurse rejected the request. The nursing standards expert for the plaintiff opined that the request should have been satisfied or alternatively, that the nurse should have explained the manner in which a crutch-dependent person could safely enter and exit a vehicle.

Defense counsel claimed that the nurse explained proper use of the crutches, the plaintiff indicated that she understood the explanation, and the plaintiff demonstrated proper use and did not express concern. The defense’s expert contended that the nurse did not have to explain how a crutch-dependent person could safely enter and exit a vehicle and that the plaintiff’s fall resulted from her own failure to exercise appropriate caution. The defense further contended that the plaintiff achieved an excellent recovery.

Continue to: After a 7-day trial...

 

 

After a 7-day trial and 3 hours and 45 minutes’ deliberation, the jury found in favor of the plaintiff. It found that the nurse was negligent in her provision of crutches and that the act was a substantial cause of the plaintiff’s injuries. The jury also found that the nurse did not properly explain the use of crutches but determined that the error was not a substantial cause of the plaintiff’s injuries.

VERDICT

The jury awarded the plaintiff a total of $850,000 in damages. The plaintiff also recovered stipulated medical expenses.

COMMENTARY

Medical malpractice litigation involves recovery for acts or omissions that constitute a departure from the standard of care. We all recognize injurious acts—improper esophageal intubation in the emergency department, transection of a nerve in the operating room, or prescription of a contraindicated medication to an allergic patient—and acknowledge damaging omissions, such as failure to screen for colon cancer or recognize treatable diabetes.

However, some cases are disposition related; they arise from how patients are discharged, what instructions they are given, where they go, and what they do after discharge. These cases involve the patient’s medical issues engrafted on his or her transportation, job, and more generally, living environment.

The lay public expects patients to have a right of self-determination, to control the nature and course of their medical care. Yet, the modern lay public also expects the medical profession to act as an authority figure—exercising a degree of paternalism to safeguard patients from harm. This expectation is commonly articulated in retrospect, after something has gone wrong. Consequently, clinicians must be aware of what will happen to the patient after discharge.

Continue to: With all interventions...

 

 

With all interventions, weigh the post-discharge consequences. If you give an injection of hydromorphone, you cannot discharge the patient to drive home 45 minutes later. If you have diagnosed vertigo in a patient, you cannot prescribe meclizine and return that patient to her job working on scaffolding 50 ft above ground. If a frail patient lives alone and cannot safely walk, and you’ve started him on furosemide, you cannot discharge him without considering how he will get to the bathroom. Other concerns are even more difficult—for example, the homeless patient who does not have the environment or resources to follow your instructions.

It is tempting to view these concerns as not our responsibility or dismiss them as “not medicine.” Clinicians can feel frustrated at being pulled into the realm of social work, where we are ill equipped to deal with and sort out the patient’s “life problems.” For one thing, we don’t often have the resources to deal with these issues. And for another, addressing the patient’s postdischarge living situation takes time—something in short supply and intangible to the other patients in the waiting room, who are expecting your attention and wondering, “What’s the holdup?”

In the case presented, the plaintiff was a 70-year-old retiree. She was discharged from the hospital with crutches. Crutches are age-old and familiar devices. Nevertheless, crutches are for people who are able to use their arms for weight bearing and propulsion and require a fair amount of physical strength, timing, and dexterity. While a potentially debatable point, an assumption that a 70-year-old patient has the arm strength and dexterity to properly propel herself with crutches may be faulty. There was disagreement between the patient, who claimed she could not safely use the crutches, and the nurse, who said the patient accepted the crutches without concern. The safest course of action would be for discharge personnel to demonstrate the use of crutches, observe the patient using the crutches, and document that in the record.

In this case, it is unclear if the nurse demonstrated how to use the crutches or witnessed the plaintiff demonstrating she could safely use them. The jury found the nurse was negligent “in her provision” of crutches—an act they deemed a substantial cause of the plaintiff’s injuries. Interestingly, the jury did not consider the lack of explanation on the crutches’ use to be a substantial cause of injury. But the bottom line is, they faulted the nurse for the act of giving this patient crutches and awarded $850,000 in damages.

Society is changing. Fifty years ago, jurors would expect people to be familiar with crutches, and if you fell while using them, that was your own fault. Modern jurors expect hospitals and providers to get more involved in what happens to a patient after discharge. The news media has heavily publicized cases of alleged “patient dumping.”

Continue to: As a result...

 

 

As a result, we see legislative changes, such as the recently passed California Senate Bill 1152, which requires that homeless patients be fed; provided weather-appropriate clothing, filled prescriptions, and vaccinations; given medical screening, examination, and evaluation that requires the “treating physician” to arrange behavioral health care; and enrolled in “any affordable health insurance coverage for which he or she is eligible.”

Whether it is appropriate to ask hospitals and clinicians to get this involved is beyond the scope of this column. What is clear is that society increasingly expects clinicians and hospitals to take responsibility for patients. This societal change has an impact on the lay public’s perception of what is expected of health care providers. Tomorrow’s juror comes to court with a belief that hospitals and clinicians owe a duty of care that extends beyond the walls of the exam room.

IN SUMMARY

Reality test your post-treatment instructions to be sure they will work for the patient and are not grossly incompatible with his or her known postdischarge environment. To the extent possible, involve discharge planning personnel in your practice. Let your record reflect that you are acting in the patient’s best interest, and evade the temptation to squint narrowly to avoid seeing circumstances in the patient’s life that prevent safe implementation of your plan.

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In May 2014, a 70-year-old retiree underwent repair of a fracture of her left ankle. The procedure was performed at a local hospital. A splint was applied to the ankle, and a nurse provided crutches.

Following discharge from the hospital, the patient hailed a taxi to take her home. As she was exiting the taxi at her residence, the patient fell and sustained comminuted fractures to the distal radius and distal ulna of her right (dominant) wrist and a trimalleolar fracture to her repaired left ankle.

The plaintiff was transported back to the hospital via ambulance. She underwent closed reduction of her wrist fractures and 11 days later was transferred to another facility for open reduction and internal fixation of her left ankle fracture. Her hospitalizations totaled 13 days and were followed by a course of inpatient rehabilitative therapy; the latter lasted until late August 2014, with a brief interruption in June when she underwent open reduction and internal fixation of her wrist fractures. When she returned home in August, the patient required the assistance of visiting aides and 3 additional months of rehabilitative therapy.

At trial, the plaintiff claimed that her left ankle and her right wrist remained painful, that she sustained a mild residual diminution of each area’s range of motion, and that these residual effects hindered her performance of basic physical activities (eg, cleaning and cooking).

The plaintiff alleged that her fall while exiting the taxi resulted from unsteadiness, which was a lingering effect of morphine that was administered during the repair of her fracture. She sought recovery of damages for past and future pain and suffering from the hospital’s operator. The lawsuit alleged that the nurse had failed to provide instructions on the proper use of crutches, that the nurse had failed to undertake measures that would have diminished the plaintiff’s likelihood of falling, that the nurse’s failures constituted malpractice and negligence, and that the hospital operator was vicariously liable for the nurse’s actions.

The plaintiff claimed that she repeatedly warned that she did not believe that she could safely use the crutches provided by the nurse. She claimed that she was unsteady and lightheaded, and that when she requested a wheelchair, an escort, or an ambulance, the nurse rejected the request. The nursing standards expert for the plaintiff opined that the request should have been satisfied or alternatively, that the nurse should have explained the manner in which a crutch-dependent person could safely enter and exit a vehicle.

Defense counsel claimed that the nurse explained proper use of the crutches, the plaintiff indicated that she understood the explanation, and the plaintiff demonstrated proper use and did not express concern. The defense’s expert contended that the nurse did not have to explain how a crutch-dependent person could safely enter and exit a vehicle and that the plaintiff’s fall resulted from her own failure to exercise appropriate caution. The defense further contended that the plaintiff achieved an excellent recovery.

Continue to: After a 7-day trial...

 

 

After a 7-day trial and 3 hours and 45 minutes’ deliberation, the jury found in favor of the plaintiff. It found that the nurse was negligent in her provision of crutches and that the act was a substantial cause of the plaintiff’s injuries. The jury also found that the nurse did not properly explain the use of crutches but determined that the error was not a substantial cause of the plaintiff’s injuries.

VERDICT

The jury awarded the plaintiff a total of $850,000 in damages. The plaintiff also recovered stipulated medical expenses.

COMMENTARY

Medical malpractice litigation involves recovery for acts or omissions that constitute a departure from the standard of care. We all recognize injurious acts—improper esophageal intubation in the emergency department, transection of a nerve in the operating room, or prescription of a contraindicated medication to an allergic patient—and acknowledge damaging omissions, such as failure to screen for colon cancer or recognize treatable diabetes.

However, some cases are disposition related; they arise from how patients are discharged, what instructions they are given, where they go, and what they do after discharge. These cases involve the patient’s medical issues engrafted on his or her transportation, job, and more generally, living environment.

The lay public expects patients to have a right of self-determination, to control the nature and course of their medical care. Yet, the modern lay public also expects the medical profession to act as an authority figure—exercising a degree of paternalism to safeguard patients from harm. This expectation is commonly articulated in retrospect, after something has gone wrong. Consequently, clinicians must be aware of what will happen to the patient after discharge.

Continue to: With all interventions...

 

 

With all interventions, weigh the post-discharge consequences. If you give an injection of hydromorphone, you cannot discharge the patient to drive home 45 minutes later. If you have diagnosed vertigo in a patient, you cannot prescribe meclizine and return that patient to her job working on scaffolding 50 ft above ground. If a frail patient lives alone and cannot safely walk, and you’ve started him on furosemide, you cannot discharge him without considering how he will get to the bathroom. Other concerns are even more difficult—for example, the homeless patient who does not have the environment or resources to follow your instructions.

It is tempting to view these concerns as not our responsibility or dismiss them as “not medicine.” Clinicians can feel frustrated at being pulled into the realm of social work, where we are ill equipped to deal with and sort out the patient’s “life problems.” For one thing, we don’t often have the resources to deal with these issues. And for another, addressing the patient’s postdischarge living situation takes time—something in short supply and intangible to the other patients in the waiting room, who are expecting your attention and wondering, “What’s the holdup?”

In the case presented, the plaintiff was a 70-year-old retiree. She was discharged from the hospital with crutches. Crutches are age-old and familiar devices. Nevertheless, crutches are for people who are able to use their arms for weight bearing and propulsion and require a fair amount of physical strength, timing, and dexterity. While a potentially debatable point, an assumption that a 70-year-old patient has the arm strength and dexterity to properly propel herself with crutches may be faulty. There was disagreement between the patient, who claimed she could not safely use the crutches, and the nurse, who said the patient accepted the crutches without concern. The safest course of action would be for discharge personnel to demonstrate the use of crutches, observe the patient using the crutches, and document that in the record.

In this case, it is unclear if the nurse demonstrated how to use the crutches or witnessed the plaintiff demonstrating she could safely use them. The jury found the nurse was negligent “in her provision” of crutches—an act they deemed a substantial cause of the plaintiff’s injuries. Interestingly, the jury did not consider the lack of explanation on the crutches’ use to be a substantial cause of injury. But the bottom line is, they faulted the nurse for the act of giving this patient crutches and awarded $850,000 in damages.

Society is changing. Fifty years ago, jurors would expect people to be familiar with crutches, and if you fell while using them, that was your own fault. Modern jurors expect hospitals and providers to get more involved in what happens to a patient after discharge. The news media has heavily publicized cases of alleged “patient dumping.”

Continue to: As a result...

 

 

As a result, we see legislative changes, such as the recently passed California Senate Bill 1152, which requires that homeless patients be fed; provided weather-appropriate clothing, filled prescriptions, and vaccinations; given medical screening, examination, and evaluation that requires the “treating physician” to arrange behavioral health care; and enrolled in “any affordable health insurance coverage for which he or she is eligible.”

Whether it is appropriate to ask hospitals and clinicians to get this involved is beyond the scope of this column. What is clear is that society increasingly expects clinicians and hospitals to take responsibility for patients. This societal change has an impact on the lay public’s perception of what is expected of health care providers. Tomorrow’s juror comes to court with a belief that hospitals and clinicians owe a duty of care that extends beyond the walls of the exam room.

IN SUMMARY

Reality test your post-treatment instructions to be sure they will work for the patient and are not grossly incompatible with his or her known postdischarge environment. To the extent possible, involve discharge planning personnel in your practice. Let your record reflect that you are acting in the patient’s best interest, and evade the temptation to squint narrowly to avoid seeing circumstances in the patient’s life that prevent safe implementation of your plan.

In May 2014, a 70-year-old retiree underwent repair of a fracture of her left ankle. The procedure was performed at a local hospital. A splint was applied to the ankle, and a nurse provided crutches.

Following discharge from the hospital, the patient hailed a taxi to take her home. As she was exiting the taxi at her residence, the patient fell and sustained comminuted fractures to the distal radius and distal ulna of her right (dominant) wrist and a trimalleolar fracture to her repaired left ankle.

The plaintiff was transported back to the hospital via ambulance. She underwent closed reduction of her wrist fractures and 11 days later was transferred to another facility for open reduction and internal fixation of her left ankle fracture. Her hospitalizations totaled 13 days and were followed by a course of inpatient rehabilitative therapy; the latter lasted until late August 2014, with a brief interruption in June when she underwent open reduction and internal fixation of her wrist fractures. When she returned home in August, the patient required the assistance of visiting aides and 3 additional months of rehabilitative therapy.

At trial, the plaintiff claimed that her left ankle and her right wrist remained painful, that she sustained a mild residual diminution of each area’s range of motion, and that these residual effects hindered her performance of basic physical activities (eg, cleaning and cooking).

The plaintiff alleged that her fall while exiting the taxi resulted from unsteadiness, which was a lingering effect of morphine that was administered during the repair of her fracture. She sought recovery of damages for past and future pain and suffering from the hospital’s operator. The lawsuit alleged that the nurse had failed to provide instructions on the proper use of crutches, that the nurse had failed to undertake measures that would have diminished the plaintiff’s likelihood of falling, that the nurse’s failures constituted malpractice and negligence, and that the hospital operator was vicariously liable for the nurse’s actions.

The plaintiff claimed that she repeatedly warned that she did not believe that she could safely use the crutches provided by the nurse. She claimed that she was unsteady and lightheaded, and that when she requested a wheelchair, an escort, or an ambulance, the nurse rejected the request. The nursing standards expert for the plaintiff opined that the request should have been satisfied or alternatively, that the nurse should have explained the manner in which a crutch-dependent person could safely enter and exit a vehicle.

Defense counsel claimed that the nurse explained proper use of the crutches, the plaintiff indicated that she understood the explanation, and the plaintiff demonstrated proper use and did not express concern. The defense’s expert contended that the nurse did not have to explain how a crutch-dependent person could safely enter and exit a vehicle and that the plaintiff’s fall resulted from her own failure to exercise appropriate caution. The defense further contended that the plaintiff achieved an excellent recovery.

Continue to: After a 7-day trial...

 

 

After a 7-day trial and 3 hours and 45 minutes’ deliberation, the jury found in favor of the plaintiff. It found that the nurse was negligent in her provision of crutches and that the act was a substantial cause of the plaintiff’s injuries. The jury also found that the nurse did not properly explain the use of crutches but determined that the error was not a substantial cause of the plaintiff’s injuries.

VERDICT

The jury awarded the plaintiff a total of $850,000 in damages. The plaintiff also recovered stipulated medical expenses.

COMMENTARY

Medical malpractice litigation involves recovery for acts or omissions that constitute a departure from the standard of care. We all recognize injurious acts—improper esophageal intubation in the emergency department, transection of a nerve in the operating room, or prescription of a contraindicated medication to an allergic patient—and acknowledge damaging omissions, such as failure to screen for colon cancer or recognize treatable diabetes.

However, some cases are disposition related; they arise from how patients are discharged, what instructions they are given, where they go, and what they do after discharge. These cases involve the patient’s medical issues engrafted on his or her transportation, job, and more generally, living environment.

The lay public expects patients to have a right of self-determination, to control the nature and course of their medical care. Yet, the modern lay public also expects the medical profession to act as an authority figure—exercising a degree of paternalism to safeguard patients from harm. This expectation is commonly articulated in retrospect, after something has gone wrong. Consequently, clinicians must be aware of what will happen to the patient after discharge.

Continue to: With all interventions...

 

 

With all interventions, weigh the post-discharge consequences. If you give an injection of hydromorphone, you cannot discharge the patient to drive home 45 minutes later. If you have diagnosed vertigo in a patient, you cannot prescribe meclizine and return that patient to her job working on scaffolding 50 ft above ground. If a frail patient lives alone and cannot safely walk, and you’ve started him on furosemide, you cannot discharge him without considering how he will get to the bathroom. Other concerns are even more difficult—for example, the homeless patient who does not have the environment or resources to follow your instructions.

It is tempting to view these concerns as not our responsibility or dismiss them as “not medicine.” Clinicians can feel frustrated at being pulled into the realm of social work, where we are ill equipped to deal with and sort out the patient’s “life problems.” For one thing, we don’t often have the resources to deal with these issues. And for another, addressing the patient’s postdischarge living situation takes time—something in short supply and intangible to the other patients in the waiting room, who are expecting your attention and wondering, “What’s the holdup?”

In the case presented, the plaintiff was a 70-year-old retiree. She was discharged from the hospital with crutches. Crutches are age-old and familiar devices. Nevertheless, crutches are for people who are able to use their arms for weight bearing and propulsion and require a fair amount of physical strength, timing, and dexterity. While a potentially debatable point, an assumption that a 70-year-old patient has the arm strength and dexterity to properly propel herself with crutches may be faulty. There was disagreement between the patient, who claimed she could not safely use the crutches, and the nurse, who said the patient accepted the crutches without concern. The safest course of action would be for discharge personnel to demonstrate the use of crutches, observe the patient using the crutches, and document that in the record.

In this case, it is unclear if the nurse demonstrated how to use the crutches or witnessed the plaintiff demonstrating she could safely use them. The jury found the nurse was negligent “in her provision” of crutches—an act they deemed a substantial cause of the plaintiff’s injuries. Interestingly, the jury did not consider the lack of explanation on the crutches’ use to be a substantial cause of injury. But the bottom line is, they faulted the nurse for the act of giving this patient crutches and awarded $850,000 in damages.

Society is changing. Fifty years ago, jurors would expect people to be familiar with crutches, and if you fell while using them, that was your own fault. Modern jurors expect hospitals and providers to get more involved in what happens to a patient after discharge. The news media has heavily publicized cases of alleged “patient dumping.”

Continue to: As a result...

 

 

As a result, we see legislative changes, such as the recently passed California Senate Bill 1152, which requires that homeless patients be fed; provided weather-appropriate clothing, filled prescriptions, and vaccinations; given medical screening, examination, and evaluation that requires the “treating physician” to arrange behavioral health care; and enrolled in “any affordable health insurance coverage for which he or she is eligible.”

Whether it is appropriate to ask hospitals and clinicians to get this involved is beyond the scope of this column. What is clear is that society increasingly expects clinicians and hospitals to take responsibility for patients. This societal change has an impact on the lay public’s perception of what is expected of health care providers. Tomorrow’s juror comes to court with a belief that hospitals and clinicians owe a duty of care that extends beyond the walls of the exam room.

IN SUMMARY

Reality test your post-treatment instructions to be sure they will work for the patient and are not grossly incompatible with his or her known postdischarge environment. To the extent possible, involve discharge planning personnel in your practice. Let your record reflect that you are acting in the patient’s best interest, and evade the temptation to squint narrowly to avoid seeing circumstances in the patient’s life that prevent safe implementation of your plan.

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Emicizumab performs well in surgical setting

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– Emicizumab appears safe and effective for patients with hemophilia A undergoing surgical procedures, based on experience with a subpopulation of HAVEN 3 trial participants.

Dr. Elena Santagostino

Out of 28 minor procedures performed without preventive factor VIII (FVIII), only 2 were associated with postoperative bleeds requiring treatment, reported lead author Elena Santagostino, MD, PhD, of Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico in Milan, and her colleagues.

All events requiring bleeding treatment were associated with dental procedures, highlighting an area where clinicians and dentists may need to exercise caution. Still, overall results supported emicizumab in a surgical setting.

“There were no thrombotic complications or other unexpected events, including inhibitor development,” Dr. Santagostino said at the annual congress of the European Association for Haemophilia and Allied Disorders.

The findings were drawn from 30 patients who underwent 50 surgeries (46 minor, 4 major) during HAVEN 3, a previously reported phase 3 trial investigating the use of emicizumab, a humanized bispecific monoclonal antibody for patients with hemophilia A without inhibitors.

The minor surgeries included dental or orthopedic procedures, esophagogastroduodenoscopy, or colonoscopy. The four major procedures were all orthopedic (knee arthroscopic synovectomy, biceps femoris tear repair, total ankle arthroplasty, and total hip replacement). The investigators analyzed surgery-related bleeds and the nature of FVIII usage.

Preventive FVIII was used in 18 procedures; infusion duration was 24 hours or less in 14 procedures, between 25 hours and 48 hours in 2 procedures, and more than 72 hours in 2 procedures. The median cumulative preventive FVIII dose per procedure was 30 IU/kg.



Of the 46 minor procedures, 28 (61%) were performed without preventive FVIII, and 2 (7.1%) were associated with bleeding requiring treatment, both after dental procedures. Two other participants who received preventive FVIII also needed postoperative bleeding treatment. Of note, these events were also after dental procedures, meaning all four instances of bleeding requiring treatment during the trial were associated with dentistry.

“[I]n this experience, dental procedures were somewhat tricky because the bleeding complications were mainly there,” Dr. Santagostino said.

When asked by an audience member if this trend was unique to mucosal bleeding, Dr. Santagostino said it was too early to draw such a conclusion but offered some insight. “To control and prevent bleeding during a dental procedure is not trivial, because … sometimes if you stop factor VIII treatment quite early, you may have late bleeding, mainly due to local reasons, because … dental procedures are very heterogenous.”

Among three other participants who had postoperative bleeding but did not require treatment, two underwent dental procedures, further supporting this association. Although the study numbers are relatively small, the findings may at least support caution, if not preventive FVIII in the dental setting, Dr. Santagostino said.

The four major procedures – all orthopedic – were knee arthroscopic synovectomy, biceps femoris tear repair, total ankle arthroplasty, and total hip replacement. Along with preoperative preventive FVIII, three of four patients undergoing major surgery received preventive FVIII for 14-18 days postoperatively. Doses ranged from 99-522 IU/kg. No postoperative bleeds occurred in this subgroup.

Study funding was provided by F. Hoffmann–La Roche and Chugai Pharmaceutical. The investigators reported financial relationships with Bayer, Shire, Pfizer, Novo Nordisk, and others.

SOURCE: Santagostino E et al. EAHAD 2019, Abstract OR15.

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– Emicizumab appears safe and effective for patients with hemophilia A undergoing surgical procedures, based on experience with a subpopulation of HAVEN 3 trial participants.

Dr. Elena Santagostino

Out of 28 minor procedures performed without preventive factor VIII (FVIII), only 2 were associated with postoperative bleeds requiring treatment, reported lead author Elena Santagostino, MD, PhD, of Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico in Milan, and her colleagues.

All events requiring bleeding treatment were associated with dental procedures, highlighting an area where clinicians and dentists may need to exercise caution. Still, overall results supported emicizumab in a surgical setting.

“There were no thrombotic complications or other unexpected events, including inhibitor development,” Dr. Santagostino said at the annual congress of the European Association for Haemophilia and Allied Disorders.

The findings were drawn from 30 patients who underwent 50 surgeries (46 minor, 4 major) during HAVEN 3, a previously reported phase 3 trial investigating the use of emicizumab, a humanized bispecific monoclonal antibody for patients with hemophilia A without inhibitors.

The minor surgeries included dental or orthopedic procedures, esophagogastroduodenoscopy, or colonoscopy. The four major procedures were all orthopedic (knee arthroscopic synovectomy, biceps femoris tear repair, total ankle arthroplasty, and total hip replacement). The investigators analyzed surgery-related bleeds and the nature of FVIII usage.

Preventive FVIII was used in 18 procedures; infusion duration was 24 hours or less in 14 procedures, between 25 hours and 48 hours in 2 procedures, and more than 72 hours in 2 procedures. The median cumulative preventive FVIII dose per procedure was 30 IU/kg.



Of the 46 minor procedures, 28 (61%) were performed without preventive FVIII, and 2 (7.1%) were associated with bleeding requiring treatment, both after dental procedures. Two other participants who received preventive FVIII also needed postoperative bleeding treatment. Of note, these events were also after dental procedures, meaning all four instances of bleeding requiring treatment during the trial were associated with dentistry.

“[I]n this experience, dental procedures were somewhat tricky because the bleeding complications were mainly there,” Dr. Santagostino said.

When asked by an audience member if this trend was unique to mucosal bleeding, Dr. Santagostino said it was too early to draw such a conclusion but offered some insight. “To control and prevent bleeding during a dental procedure is not trivial, because … sometimes if you stop factor VIII treatment quite early, you may have late bleeding, mainly due to local reasons, because … dental procedures are very heterogenous.”

Among three other participants who had postoperative bleeding but did not require treatment, two underwent dental procedures, further supporting this association. Although the study numbers are relatively small, the findings may at least support caution, if not preventive FVIII in the dental setting, Dr. Santagostino said.

The four major procedures – all orthopedic – were knee arthroscopic synovectomy, biceps femoris tear repair, total ankle arthroplasty, and total hip replacement. Along with preoperative preventive FVIII, three of four patients undergoing major surgery received preventive FVIII for 14-18 days postoperatively. Doses ranged from 99-522 IU/kg. No postoperative bleeds occurred in this subgroup.

Study funding was provided by F. Hoffmann–La Roche and Chugai Pharmaceutical. The investigators reported financial relationships with Bayer, Shire, Pfizer, Novo Nordisk, and others.

SOURCE: Santagostino E et al. EAHAD 2019, Abstract OR15.

 

– Emicizumab appears safe and effective for patients with hemophilia A undergoing surgical procedures, based on experience with a subpopulation of HAVEN 3 trial participants.

Dr. Elena Santagostino

Out of 28 minor procedures performed without preventive factor VIII (FVIII), only 2 were associated with postoperative bleeds requiring treatment, reported lead author Elena Santagostino, MD, PhD, of Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico in Milan, and her colleagues.

All events requiring bleeding treatment were associated with dental procedures, highlighting an area where clinicians and dentists may need to exercise caution. Still, overall results supported emicizumab in a surgical setting.

“There were no thrombotic complications or other unexpected events, including inhibitor development,” Dr. Santagostino said at the annual congress of the European Association for Haemophilia and Allied Disorders.

The findings were drawn from 30 patients who underwent 50 surgeries (46 minor, 4 major) during HAVEN 3, a previously reported phase 3 trial investigating the use of emicizumab, a humanized bispecific monoclonal antibody for patients with hemophilia A without inhibitors.

The minor surgeries included dental or orthopedic procedures, esophagogastroduodenoscopy, or colonoscopy. The four major procedures were all orthopedic (knee arthroscopic synovectomy, biceps femoris tear repair, total ankle arthroplasty, and total hip replacement). The investigators analyzed surgery-related bleeds and the nature of FVIII usage.

Preventive FVIII was used in 18 procedures; infusion duration was 24 hours or less in 14 procedures, between 25 hours and 48 hours in 2 procedures, and more than 72 hours in 2 procedures. The median cumulative preventive FVIII dose per procedure was 30 IU/kg.



Of the 46 minor procedures, 28 (61%) were performed without preventive FVIII, and 2 (7.1%) were associated with bleeding requiring treatment, both after dental procedures. Two other participants who received preventive FVIII also needed postoperative bleeding treatment. Of note, these events were also after dental procedures, meaning all four instances of bleeding requiring treatment during the trial were associated with dentistry.

“[I]n this experience, dental procedures were somewhat tricky because the bleeding complications were mainly there,” Dr. Santagostino said.

When asked by an audience member if this trend was unique to mucosal bleeding, Dr. Santagostino said it was too early to draw such a conclusion but offered some insight. “To control and prevent bleeding during a dental procedure is not trivial, because … sometimes if you stop factor VIII treatment quite early, you may have late bleeding, mainly due to local reasons, because … dental procedures are very heterogenous.”

Among three other participants who had postoperative bleeding but did not require treatment, two underwent dental procedures, further supporting this association. Although the study numbers are relatively small, the findings may at least support caution, if not preventive FVIII in the dental setting, Dr. Santagostino said.

The four major procedures – all orthopedic – were knee arthroscopic synovectomy, biceps femoris tear repair, total ankle arthroplasty, and total hip replacement. Along with preoperative preventive FVIII, three of four patients undergoing major surgery received preventive FVIII for 14-18 days postoperatively. Doses ranged from 99-522 IU/kg. No postoperative bleeds occurred in this subgroup.

Study funding was provided by F. Hoffmann–La Roche and Chugai Pharmaceutical. The investigators reported financial relationships with Bayer, Shire, Pfizer, Novo Nordisk, and others.

SOURCE: Santagostino E et al. EAHAD 2019, Abstract OR15.

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A Pain He Can’t Walk Off

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A Pain He Can’t Walk Off

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The radiograph shows a right knee prosthesis in place with no evidence of failure or displacement. Of note, there is a hyperdense, somewhat elongated lesion along the distal third of the femur. Radiographically, this is most likely consistent with an enchondroma. Enchondromas are typically benign bone lesions that originate from cartilage. They seldom cause pain and are usually found incidentally. No specific treatment is warranted.

The patient was referred to his orthopedist for follow-up.

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A Pain He Can’t Walk Off

ANSWER

The radiograph shows a right knee prosthesis in place with no evidence of failure or displacement. Of note, there is a hyperdense, somewhat elongated lesion along the distal third of the femur. Radiographically, this is most likely consistent with an enchondroma. Enchondromas are typically benign bone lesions that originate from cartilage. They seldom cause pain and are usually found incidentally. No specific treatment is warranted.

The patient was referred to his orthopedist for follow-up.

A Pain He Can’t Walk Off

ANSWER

The radiograph shows a right knee prosthesis in place with no evidence of failure or displacement. Of note, there is a hyperdense, somewhat elongated lesion along the distal third of the femur. Radiographically, this is most likely consistent with an enchondroma. Enchondromas are typically benign bone lesions that originate from cartilage. They seldom cause pain and are usually found incidentally. No specific treatment is warranted.

The patient was referred to his orthopedist for follow-up.

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A Pain He Can’t Walk Off

A 70-year-old man presents to the urgent care clinic for evaluation of right knee pain. He denies any specific injury or trauma. For the past several months, he says, he has had a “deep aching pain” that is exacerbated by walking and weight bearing.

His medical history is significant for mild hypertension and diabetes. His surgical history is significant for remote right total knee arthroplasty.

On examination, you note an elderly male in no obvious distress. His vital signs are normal. Inspection of the right knee shows a well-healed incision with no obvious effusion or erythema. He demonstrates a fairly good active range of motion. There is no evidence of ligament laxity.

You obtain a radiograph of the knee (shown). What is your impression?

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TNFi use may not affect joint replacement rates for RA patients

Other factors likely explain decreased rate of joint replacement
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Patients with rheumatoid arthritis using tumor necrosis factor inhibitors do not appear to have a lower rate of joint replacement when compared with patients taking conventional synthetic disease-modifying antirheumatic drugs, according to an analysis of data in the British Society for Rheumatology Biologics Register for RA.

Samuel Hawley

Although there was not a general protective effect, patients with rheumatoid arthritis (RA) who were 60 years or older had a 40% reduction in total hip replacement (THR) when using tumor necrosis factor inhibitors (TNFi), according to first author Samuel Hawley from the Nuffield Department of Orthopaedics in the Rheumatology and Musculoskeletal Sciences at the University of Oxford (England) and his colleagues.

“While a reduction in THR amongst older TNFi users offers some support for biologics playing a role in reducing need for joint replacement, it must also be noted that the lack of an overall protective effect is suggestive that other factors apart from TNFi are likely to be involved in the ... downward population trends in joint replacement rates in RA,” Mr. Hawley and his colleagues wrote in their report published in the journal Rheumatology.

The researchers analyzed prospectively collected data on 11,202 RA patients from the British Society for Rheumatology Biologics Register for RA (BSRBR-RA) from 2001-2016 who were using TNFi (n = 9,558) or conventional synthetic disease-modifying antirheumatic drugs (csDMARDs; n = 1,644). Patients had a median disease duration of 11.0 years in the TNFi group and 10.8 years in the csDMARD group. TNFi and csDMARD users were matched based on their propensity to receive treatment, and researchers used a Cox regression analysis to compare the rates of total knee replacement (TKR), THR, and other joint replacement. The researchers utilized each csDMARD user a median of three times (interquartile range, one to six) in the comparisons.


The incidence rate for THR was 5.22/1,000 person-years for TNFi users and 6.30/1,000 person-years for csDMARD users, while the incidence rate for TKR was 8.89/1,000 person-years for TNFi users and 8.09/1,000 person-years for csDMARD users. Mr. Hawley and his colleagues found no association between TNFi use and THR when compared with csDMARD users (adjusted pooled hazard ratio, 0.86; 95% confidence interval, 0.60-1.22; P = .39) based on 589 THRs during follow-up. There was also no association between the incidence of TKR and TNFi use when compared with csDMARD users (adjusted pooled HR, 1.11; 95% CI, 0.84-1.47; P = .46) based on 846 TKRs during follow-up. When the researchers examined 336 other joint replacements performed during follow-up, there was also no significant difference in incidence between TNFi and csDMARD users (HR, 1.15; 95% CI, 0.75-1.77).

For patients 60 years or older, TNFi use was associated with a 40% reduction in THR incidence (HR, 0.60; 95% CI, 0.41-0.87; P = .008), but not in TKR incidence. However, younger patients using TNFi did not have a reduced incidence of THR, and there were no associations between TNFi use and incidence of TKR or other joint replacements.

“It could be that the relatively long disease duration at our baseline meant there was greater potential for prevention of joint destruction at the hip over knee, although details of differential natural history of RA disease at these two joints are not well established,” the researchers wrote. “It is also very difficult to disentangle the impact of TNFi on improved function and overall quality of life and how this may have mediated effects on longer-term progression of joint damage, potentially differentially at the knee and hip.”

The researchers said the study was limited by the potential for residual confounding by indication, and the long disease duration of patients means that the results would not be generalizable to patients with early RA. In addition, underreporting of joint replacement could create bias because the registry information is a combination of physician-reported and self-reported incidences, they added.

This study was funded by an award from the National Institute for Health Research (NIHR) and support from the Oxford NIHR Biomedical Research Unit. Four authors disclosed financial relationships with industry, including many companies marketing biologics for RA. Other authors reported no relevant conflicts of interest.

SOURCE: Hawley S et al. Rheumatology. 2019 Jan 10. doi: 10.1093/rheumatology/key424.

Body

The arrival and widespread use of tumor necrosis factor inhibitors (TNFi) in the late 1990s has “created a perception of causality” that led many to believe that TNFi use was associated with decreased rates of joint replacement. However, the decline in total hip arthroplasties (THAs), total knee arthroplasties (TKAs), and other joint replacements is likely because of a confluence of factors, Susan M. Goodman, MD, and Anne R. Bass, MD, wrote in an editorial accompanying the report by Hawley et al. (Rheumatology. 2019 Jan 10. doi: 10.1093/rheumatology/kez022).

Dr. Susan M. Goodman
“The early and aggressive management of RA, plus expansion of the treatment armamentarium available for refractory patients (including, of course, TNFi), likely had a greater impact on disease outcomes and joint replacement rates over the last 20 years than the introduction of any particular class of drug,” the authors wrote. “While this paper adds some clarity to the debate regarding the impact of TNFi on arthroplasty rates, further work is needed.”

Although Hawley et al. attempted to mitigate confounding in their study by using a propensity score when comparing TNFi and conventional synthetic disease-modifying antirheumatic drug (csDMARD) users, there was a preference for physicians prescribing biologics at a rate of 87% versus 13%, and the biologic preference was associated with disease severity, which is “a strong driver of the need for surgery.” In addition, in patients 60 years or older for whom TNFi reduced indications for joint replacement, “[t]he differential effect of TNFi use on THA utilization in the elderly is especially curious because a previous study by the same authors demonstrated that TKA, but not THA, rates were impacted by introduction of NICE guidance in 2002.”

Dr. Anne R. Bass
“This paradox may not be explained until the reasons for less TNFi use among the elderly are better understood and its confounding effect can be addressed in study design,” Dr. Goodman and Dr. Bass said.

The authors also noted clinicians should exercise caution in extrapolating the results of Hawley et al. because the effects of biologic treatment in patients with a long disease duration, such as in this study, may not be generalizable to most RA patients.

Dr. Goodman and Dr. Bass are rheumatologists and professors of clinical medicine at Cornell University and the Hospital for Special Surgery, both in New York. Dr. Goodman disclosed financial relationships with Novartis and UCB outside the scope of this work.

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The arrival and widespread use of tumor necrosis factor inhibitors (TNFi) in the late 1990s has “created a perception of causality” that led many to believe that TNFi use was associated with decreased rates of joint replacement. However, the decline in total hip arthroplasties (THAs), total knee arthroplasties (TKAs), and other joint replacements is likely because of a confluence of factors, Susan M. Goodman, MD, and Anne R. Bass, MD, wrote in an editorial accompanying the report by Hawley et al. (Rheumatology. 2019 Jan 10. doi: 10.1093/rheumatology/kez022).

Dr. Susan M. Goodman
“The early and aggressive management of RA, plus expansion of the treatment armamentarium available for refractory patients (including, of course, TNFi), likely had a greater impact on disease outcomes and joint replacement rates over the last 20 years than the introduction of any particular class of drug,” the authors wrote. “While this paper adds some clarity to the debate regarding the impact of TNFi on arthroplasty rates, further work is needed.”

Although Hawley et al. attempted to mitigate confounding in their study by using a propensity score when comparing TNFi and conventional synthetic disease-modifying antirheumatic drug (csDMARD) users, there was a preference for physicians prescribing biologics at a rate of 87% versus 13%, and the biologic preference was associated with disease severity, which is “a strong driver of the need for surgery.” In addition, in patients 60 years or older for whom TNFi reduced indications for joint replacement, “[t]he differential effect of TNFi use on THA utilization in the elderly is especially curious because a previous study by the same authors demonstrated that TKA, but not THA, rates were impacted by introduction of NICE guidance in 2002.”

Dr. Anne R. Bass
“This paradox may not be explained until the reasons for less TNFi use among the elderly are better understood and its confounding effect can be addressed in study design,” Dr. Goodman and Dr. Bass said.

The authors also noted clinicians should exercise caution in extrapolating the results of Hawley et al. because the effects of biologic treatment in patients with a long disease duration, such as in this study, may not be generalizable to most RA patients.

Dr. Goodman and Dr. Bass are rheumatologists and professors of clinical medicine at Cornell University and the Hospital for Special Surgery, both in New York. Dr. Goodman disclosed financial relationships with Novartis and UCB outside the scope of this work.

Body

The arrival and widespread use of tumor necrosis factor inhibitors (TNFi) in the late 1990s has “created a perception of causality” that led many to believe that TNFi use was associated with decreased rates of joint replacement. However, the decline in total hip arthroplasties (THAs), total knee arthroplasties (TKAs), and other joint replacements is likely because of a confluence of factors, Susan M. Goodman, MD, and Anne R. Bass, MD, wrote in an editorial accompanying the report by Hawley et al. (Rheumatology. 2019 Jan 10. doi: 10.1093/rheumatology/kez022).

Dr. Susan M. Goodman
“The early and aggressive management of RA, plus expansion of the treatment armamentarium available for refractory patients (including, of course, TNFi), likely had a greater impact on disease outcomes and joint replacement rates over the last 20 years than the introduction of any particular class of drug,” the authors wrote. “While this paper adds some clarity to the debate regarding the impact of TNFi on arthroplasty rates, further work is needed.”

Although Hawley et al. attempted to mitigate confounding in their study by using a propensity score when comparing TNFi and conventional synthetic disease-modifying antirheumatic drug (csDMARD) users, there was a preference for physicians prescribing biologics at a rate of 87% versus 13%, and the biologic preference was associated with disease severity, which is “a strong driver of the need for surgery.” In addition, in patients 60 years or older for whom TNFi reduced indications for joint replacement, “[t]he differential effect of TNFi use on THA utilization in the elderly is especially curious because a previous study by the same authors demonstrated that TKA, but not THA, rates were impacted by introduction of NICE guidance in 2002.”

Dr. Anne R. Bass
“This paradox may not be explained until the reasons for less TNFi use among the elderly are better understood and its confounding effect can be addressed in study design,” Dr. Goodman and Dr. Bass said.

The authors also noted clinicians should exercise caution in extrapolating the results of Hawley et al. because the effects of biologic treatment in patients with a long disease duration, such as in this study, may not be generalizable to most RA patients.

Dr. Goodman and Dr. Bass are rheumatologists and professors of clinical medicine at Cornell University and the Hospital for Special Surgery, both in New York. Dr. Goodman disclosed financial relationships with Novartis and UCB outside the scope of this work.

Title
Other factors likely explain decreased rate of joint replacement
Other factors likely explain decreased rate of joint replacement

Patients with rheumatoid arthritis using tumor necrosis factor inhibitors do not appear to have a lower rate of joint replacement when compared with patients taking conventional synthetic disease-modifying antirheumatic drugs, according to an analysis of data in the British Society for Rheumatology Biologics Register for RA.

Samuel Hawley

Although there was not a general protective effect, patients with rheumatoid arthritis (RA) who were 60 years or older had a 40% reduction in total hip replacement (THR) when using tumor necrosis factor inhibitors (TNFi), according to first author Samuel Hawley from the Nuffield Department of Orthopaedics in the Rheumatology and Musculoskeletal Sciences at the University of Oxford (England) and his colleagues.

“While a reduction in THR amongst older TNFi users offers some support for biologics playing a role in reducing need for joint replacement, it must also be noted that the lack of an overall protective effect is suggestive that other factors apart from TNFi are likely to be involved in the ... downward population trends in joint replacement rates in RA,” Mr. Hawley and his colleagues wrote in their report published in the journal Rheumatology.

The researchers analyzed prospectively collected data on 11,202 RA patients from the British Society for Rheumatology Biologics Register for RA (BSRBR-RA) from 2001-2016 who were using TNFi (n = 9,558) or conventional synthetic disease-modifying antirheumatic drugs (csDMARDs; n = 1,644). Patients had a median disease duration of 11.0 years in the TNFi group and 10.8 years in the csDMARD group. TNFi and csDMARD users were matched based on their propensity to receive treatment, and researchers used a Cox regression analysis to compare the rates of total knee replacement (TKR), THR, and other joint replacement. The researchers utilized each csDMARD user a median of three times (interquartile range, one to six) in the comparisons.


The incidence rate for THR was 5.22/1,000 person-years for TNFi users and 6.30/1,000 person-years for csDMARD users, while the incidence rate for TKR was 8.89/1,000 person-years for TNFi users and 8.09/1,000 person-years for csDMARD users. Mr. Hawley and his colleagues found no association between TNFi use and THR when compared with csDMARD users (adjusted pooled hazard ratio, 0.86; 95% confidence interval, 0.60-1.22; P = .39) based on 589 THRs during follow-up. There was also no association between the incidence of TKR and TNFi use when compared with csDMARD users (adjusted pooled HR, 1.11; 95% CI, 0.84-1.47; P = .46) based on 846 TKRs during follow-up. When the researchers examined 336 other joint replacements performed during follow-up, there was also no significant difference in incidence between TNFi and csDMARD users (HR, 1.15; 95% CI, 0.75-1.77).

For patients 60 years or older, TNFi use was associated with a 40% reduction in THR incidence (HR, 0.60; 95% CI, 0.41-0.87; P = .008), but not in TKR incidence. However, younger patients using TNFi did not have a reduced incidence of THR, and there were no associations between TNFi use and incidence of TKR or other joint replacements.

“It could be that the relatively long disease duration at our baseline meant there was greater potential for prevention of joint destruction at the hip over knee, although details of differential natural history of RA disease at these two joints are not well established,” the researchers wrote. “It is also very difficult to disentangle the impact of TNFi on improved function and overall quality of life and how this may have mediated effects on longer-term progression of joint damage, potentially differentially at the knee and hip.”

The researchers said the study was limited by the potential for residual confounding by indication, and the long disease duration of patients means that the results would not be generalizable to patients with early RA. In addition, underreporting of joint replacement could create bias because the registry information is a combination of physician-reported and self-reported incidences, they added.

This study was funded by an award from the National Institute for Health Research (NIHR) and support from the Oxford NIHR Biomedical Research Unit. Four authors disclosed financial relationships with industry, including many companies marketing biologics for RA. Other authors reported no relevant conflicts of interest.

SOURCE: Hawley S et al. Rheumatology. 2019 Jan 10. doi: 10.1093/rheumatology/key424.

Patients with rheumatoid arthritis using tumor necrosis factor inhibitors do not appear to have a lower rate of joint replacement when compared with patients taking conventional synthetic disease-modifying antirheumatic drugs, according to an analysis of data in the British Society for Rheumatology Biologics Register for RA.

Samuel Hawley

Although there was not a general protective effect, patients with rheumatoid arthritis (RA) who were 60 years or older had a 40% reduction in total hip replacement (THR) when using tumor necrosis factor inhibitors (TNFi), according to first author Samuel Hawley from the Nuffield Department of Orthopaedics in the Rheumatology and Musculoskeletal Sciences at the University of Oxford (England) and his colleagues.

“While a reduction in THR amongst older TNFi users offers some support for biologics playing a role in reducing need for joint replacement, it must also be noted that the lack of an overall protective effect is suggestive that other factors apart from TNFi are likely to be involved in the ... downward population trends in joint replacement rates in RA,” Mr. Hawley and his colleagues wrote in their report published in the journal Rheumatology.

The researchers analyzed prospectively collected data on 11,202 RA patients from the British Society for Rheumatology Biologics Register for RA (BSRBR-RA) from 2001-2016 who were using TNFi (n = 9,558) or conventional synthetic disease-modifying antirheumatic drugs (csDMARDs; n = 1,644). Patients had a median disease duration of 11.0 years in the TNFi group and 10.8 years in the csDMARD group. TNFi and csDMARD users were matched based on their propensity to receive treatment, and researchers used a Cox regression analysis to compare the rates of total knee replacement (TKR), THR, and other joint replacement. The researchers utilized each csDMARD user a median of three times (interquartile range, one to six) in the comparisons.


The incidence rate for THR was 5.22/1,000 person-years for TNFi users and 6.30/1,000 person-years for csDMARD users, while the incidence rate for TKR was 8.89/1,000 person-years for TNFi users and 8.09/1,000 person-years for csDMARD users. Mr. Hawley and his colleagues found no association between TNFi use and THR when compared with csDMARD users (adjusted pooled hazard ratio, 0.86; 95% confidence interval, 0.60-1.22; P = .39) based on 589 THRs during follow-up. There was also no association between the incidence of TKR and TNFi use when compared with csDMARD users (adjusted pooled HR, 1.11; 95% CI, 0.84-1.47; P = .46) based on 846 TKRs during follow-up. When the researchers examined 336 other joint replacements performed during follow-up, there was also no significant difference in incidence between TNFi and csDMARD users (HR, 1.15; 95% CI, 0.75-1.77).

For patients 60 years or older, TNFi use was associated with a 40% reduction in THR incidence (HR, 0.60; 95% CI, 0.41-0.87; P = .008), but not in TKR incidence. However, younger patients using TNFi did not have a reduced incidence of THR, and there were no associations between TNFi use and incidence of TKR or other joint replacements.

“It could be that the relatively long disease duration at our baseline meant there was greater potential for prevention of joint destruction at the hip over knee, although details of differential natural history of RA disease at these two joints are not well established,” the researchers wrote. “It is also very difficult to disentangle the impact of TNFi on improved function and overall quality of life and how this may have mediated effects on longer-term progression of joint damage, potentially differentially at the knee and hip.”

The researchers said the study was limited by the potential for residual confounding by indication, and the long disease duration of patients means that the results would not be generalizable to patients with early RA. In addition, underreporting of joint replacement could create bias because the registry information is a combination of physician-reported and self-reported incidences, they added.

This study was funded by an award from the National Institute for Health Research (NIHR) and support from the Oxford NIHR Biomedical Research Unit. Four authors disclosed financial relationships with industry, including many companies marketing biologics for RA. Other authors reported no relevant conflicts of interest.

SOURCE: Hawley S et al. Rheumatology. 2019 Jan 10. doi: 10.1093/rheumatology/key424.

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Key clinical point: The rate of joint replacement did not differ among patients with RA using conventional synthetic disease-modifying antirheumatic drugs (csDMARDs) or tumor necrosis factor inhibitors (TNFis).

Major finding: There was no association between TNFi use and total hip replacement when compared with csDMARD users based on an adjusted pooled hazard ratio of 0.86 (95% confidence interval, 0.60-1.22), but patients older than 60 years using TNFi had a significantly greater reduction in total hip replacement.

Study details: An observational study of 11,202 prospectively collected RA patients in the British Society for Rheumatology Biologics Register for RA.

Disclosures: This study was funded by an award from the National Institute for Health Research (NIHR) and support from the Oxford NIHR Biomedical Research Unit. Four authors disclosed financial relationships with industry, including many companies marketing biologics for RA. Other authors reported no relevant conflicts of interest.

Source: Hawley S et al. Rheumatology. 2019 Jan 10. doi: 10.1093/rheumatology/key424.

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Heberden’s nodes linked to knee OA progression

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Heberden’s nodes do more than just ride along with knee OA; they predict progression, according to a review of 575 participants in a substudy of the Osteoarthritis Initiative cohort.

After assessing Heberden’s nodes (HNs) – bony enlargements of the last finger joint – and knee MRI findings at baseline and 24 months, the investigators found that HNs were associated with periarticular bone area expansion in the knee. The investigators reported their findings in Arthritis & Rheumatology.

Drahreg01/Wikimedia Commons/CC BY-SA 3.0


Comparing the 395 subjects with HNs with the 180 without, there was more periarticular bone area expansion among HN patients at 2 years in the knee joint (adjusted odds ratio, 1.39; 95% confidence interval, 1.06-1.83), especially in the medial femur (aOR, 1.49; 95% CI, 1.05-2.13), lateral femur (aOR, 2.51; 95% CI, 1.58-3.97), femoral notch (aOR, 1.37; 95% CI, 1.02-1.84), and lateral trochlea (aOR, 1.44; 95% CI, 1.08-1.9). The comparisons were adjusted for age, sex, body mass index, and bone remodeling agent use.

“The presence of Heberden’s nodes in a physical examination is associated with a distinct pattern of worsening of osteoarthritis-related structural damage in the knee joint,” lead investigator Arya Haj-Mirzaian, MD, a radiologist and postdoctoral fellow at Johns Hopkins University, Baltimore, said in a press release.

However, HNs were also associated with less worsening of knee osteophytes, especially at the femoral end of the knee joint (aOR, 0.54; 95% CI, 0.31-0.95); the finding seemed to contradict the overall picture of worsening knee osteoarthritis with HNs.



“Although osteophytes are thought to be a late secondary sequel or compensatory repair mechanism in OA and indicator of advanced knee OA, less worsening in osteophytes’ score ... may propose that less ossification is involved in the pathophysiology of knee OA in the presence of HNs,” the investigators wrote. It’s a subject for future research.

Patients with HNs were older, more often female, and had a lower frequency for other knee OA risk factors, such as excessive body mass index and knee injury. Patients with gout were excluded.

There was no external funding, and the investigators reported no disclosures.

SOURCE: Haj-Mirzaian A et al. Arthritis Rheumatol. 2019 Jan 9. doi: 10.1002/art.40811.

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Heberden’s nodes do more than just ride along with knee OA; they predict progression, according to a review of 575 participants in a substudy of the Osteoarthritis Initiative cohort.

After assessing Heberden’s nodes (HNs) – bony enlargements of the last finger joint – and knee MRI findings at baseline and 24 months, the investigators found that HNs were associated with periarticular bone area expansion in the knee. The investigators reported their findings in Arthritis & Rheumatology.

Drahreg01/Wikimedia Commons/CC BY-SA 3.0


Comparing the 395 subjects with HNs with the 180 without, there was more periarticular bone area expansion among HN patients at 2 years in the knee joint (adjusted odds ratio, 1.39; 95% confidence interval, 1.06-1.83), especially in the medial femur (aOR, 1.49; 95% CI, 1.05-2.13), lateral femur (aOR, 2.51; 95% CI, 1.58-3.97), femoral notch (aOR, 1.37; 95% CI, 1.02-1.84), and lateral trochlea (aOR, 1.44; 95% CI, 1.08-1.9). The comparisons were adjusted for age, sex, body mass index, and bone remodeling agent use.

“The presence of Heberden’s nodes in a physical examination is associated with a distinct pattern of worsening of osteoarthritis-related structural damage in the knee joint,” lead investigator Arya Haj-Mirzaian, MD, a radiologist and postdoctoral fellow at Johns Hopkins University, Baltimore, said in a press release.

However, HNs were also associated with less worsening of knee osteophytes, especially at the femoral end of the knee joint (aOR, 0.54; 95% CI, 0.31-0.95); the finding seemed to contradict the overall picture of worsening knee osteoarthritis with HNs.



“Although osteophytes are thought to be a late secondary sequel or compensatory repair mechanism in OA and indicator of advanced knee OA, less worsening in osteophytes’ score ... may propose that less ossification is involved in the pathophysiology of knee OA in the presence of HNs,” the investigators wrote. It’s a subject for future research.

Patients with HNs were older, more often female, and had a lower frequency for other knee OA risk factors, such as excessive body mass index and knee injury. Patients with gout were excluded.

There was no external funding, and the investigators reported no disclosures.

SOURCE: Haj-Mirzaian A et al. Arthritis Rheumatol. 2019 Jan 9. doi: 10.1002/art.40811.

 

Heberden’s nodes do more than just ride along with knee OA; they predict progression, according to a review of 575 participants in a substudy of the Osteoarthritis Initiative cohort.

After assessing Heberden’s nodes (HNs) – bony enlargements of the last finger joint – and knee MRI findings at baseline and 24 months, the investigators found that HNs were associated with periarticular bone area expansion in the knee. The investigators reported their findings in Arthritis & Rheumatology.

Drahreg01/Wikimedia Commons/CC BY-SA 3.0


Comparing the 395 subjects with HNs with the 180 without, there was more periarticular bone area expansion among HN patients at 2 years in the knee joint (adjusted odds ratio, 1.39; 95% confidence interval, 1.06-1.83), especially in the medial femur (aOR, 1.49; 95% CI, 1.05-2.13), lateral femur (aOR, 2.51; 95% CI, 1.58-3.97), femoral notch (aOR, 1.37; 95% CI, 1.02-1.84), and lateral trochlea (aOR, 1.44; 95% CI, 1.08-1.9). The comparisons were adjusted for age, sex, body mass index, and bone remodeling agent use.

“The presence of Heberden’s nodes in a physical examination is associated with a distinct pattern of worsening of osteoarthritis-related structural damage in the knee joint,” lead investigator Arya Haj-Mirzaian, MD, a radiologist and postdoctoral fellow at Johns Hopkins University, Baltimore, said in a press release.

However, HNs were also associated with less worsening of knee osteophytes, especially at the femoral end of the knee joint (aOR, 0.54; 95% CI, 0.31-0.95); the finding seemed to contradict the overall picture of worsening knee osteoarthritis with HNs.



“Although osteophytes are thought to be a late secondary sequel or compensatory repair mechanism in OA and indicator of advanced knee OA, less worsening in osteophytes’ score ... may propose that less ossification is involved in the pathophysiology of knee OA in the presence of HNs,” the investigators wrote. It’s a subject for future research.

Patients with HNs were older, more often female, and had a lower frequency for other knee OA risk factors, such as excessive body mass index and knee injury. Patients with gout were excluded.

There was no external funding, and the investigators reported no disclosures.

SOURCE: Haj-Mirzaian A et al. Arthritis Rheumatol. 2019 Jan 9. doi: 10.1002/art.40811.

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Key clinical point: Heberden’s nodes may be an indicator of knee OA progression.

Major finding: There was more periarticular bone area expansion among patients with Heberden’s nodes at 2 years in the knee joint (adjusted odds ratio, 1.39; 95% confidence interval, 1.06-1.83).

Study details: A substudy of 575 participants in the Osteoarthritis Initiative cohort

Disclosures: There was no external funding, and the investigators reported no disclosures.

Source: Haj-Mirzaian A et al. Arthritis Rheumatol. 2019 Jan 9. doi: 10.1002/art.40811.

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Knee pathologies, including multiple meniscal tears, predict accelerated OA

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Accelerated knee osteoarthritis is characterized by distinct features that include destabilizing meniscal tears in two or more areas as well as other pathologies, based on data from the Osteoarthritis Initiative.

Courtesy National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS)

The possibility of accelerated knee osteoarthritis (AKOA) as a unique subset of knee osteoarthritis has not been well studied, wrote Jeffrey B. Driban, PhD, of Tufts University, Boston, and his colleagues.

“If specific pathologies differentiate people at risk for AKOA it may help identify adults with early-stage or high-risk for AKOA and inspire novel prevention strategies,” they wrote in their report, published in Arthritis & Rheumatology.

The researchers reviewed data from three groups of adults selected from participants in the Osteoarthritis Initiative, a cohort of 4,796 adults with KOA or at risk for symptomatic KOA who were recruited at four clinical sites in the United States. These groups included 125 with AKOA, 125 with typical knee osteoarthritis (KOA), and 125 without knee OA.



Overall, patients with AKOA were approximately seven times more likely than were patients with KOA to have destabilizing meniscal tears in two or more areas at the time of the index visit (42% vs. 14%); less than 5% of adults with no KOA experienced destabilizing meniscal tears. In addition, patients with AKOA were more than four times as likely to have miscellaneous pathology starting the year before the index visit, compared with those without AKOA.

Approximately 63% of the participants in each group were women, and the majority were overweight. The average age, weight, and global impact of arthritis were greater in the AKOA group when compared against the typical KOA and no-KOA groups.

Participants were assessed via MRI reviewed by radiologists who were blinded to the groups.

At the index visit, 49% of adults with AKOA had either a destabilizing meniscal tear or miscellaneous pathology, compared with 15% of adults with KOA and 6% of adults without KOA.

Adults with AKOA also showed significantly greater cartilage loss prior to the index visit in comparison with typical KOA patients, and AKOA patients had less cartilage in the medial and lateral tibia and medial femur, compared with adults who had typical KOA or no KOA after the index visit.

Adults who developed AKOA showed a significantly higher bone marrow lesion volume when compared against the typical KOA and no-KOA groups at 1 year prior to the index visit, and their bone marrow lesion volume increased on average 13 times more compared with typical KOA patients over the 2 years before the index visit, the researchers noted (2.00 mL vs. 0.15 mL, respectively).

“These findings add to the evidence that AKOA is different [from] the typically perceived archetype of slow-progressing osteoarthritis” with a unique risk profile, the researchers said.



The study findings were limited by several factors, including the relatively small sample size, uncertain timing of disease onset, a potentially limited definition of a destabilizing meniscal tear (defined as a root tear, radial tear, or complex tear, which almost always featured a radial component), a lack of a universal AKOA pathology, and some missing MRI data, the researchers noted. However, the results support previous studies suggesting a link between meniscal pathology and increased risk for AKOA, they said.

“It is important to acknowledge that it remains unclear if AKOA has any relation to type 2 rapidly progressive osteoarthritis, which was characterized by a more dramatic joint space narrowing (2 mm or more within 1 year) and greater abnormal bone loss/destruction,” they noted.

“Future research with a larger sample size of adults at risk for AKOA may help further refine our understanding of AKOA and help develop a clinically useful predictive model,” they added.

The study was supported in part by a grant from the National Institute of Arthritis and Musculoskeletal and Skin Diseases, and private funding included Merck, Novartis, GlaxoSmithKline, and Pfizer. The researchers had no financial conflicts to disclose.

SOURCE: Driban JB et al. Arthritis Rheumatol. 2018 Dec 28. doi: 10.1002/art.40826.

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Accelerated knee osteoarthritis is characterized by distinct features that include destabilizing meniscal tears in two or more areas as well as other pathologies, based on data from the Osteoarthritis Initiative.

Courtesy National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS)

The possibility of accelerated knee osteoarthritis (AKOA) as a unique subset of knee osteoarthritis has not been well studied, wrote Jeffrey B. Driban, PhD, of Tufts University, Boston, and his colleagues.

“If specific pathologies differentiate people at risk for AKOA it may help identify adults with early-stage or high-risk for AKOA and inspire novel prevention strategies,” they wrote in their report, published in Arthritis & Rheumatology.

The researchers reviewed data from three groups of adults selected from participants in the Osteoarthritis Initiative, a cohort of 4,796 adults with KOA or at risk for symptomatic KOA who were recruited at four clinical sites in the United States. These groups included 125 with AKOA, 125 with typical knee osteoarthritis (KOA), and 125 without knee OA.



Overall, patients with AKOA were approximately seven times more likely than were patients with KOA to have destabilizing meniscal tears in two or more areas at the time of the index visit (42% vs. 14%); less than 5% of adults with no KOA experienced destabilizing meniscal tears. In addition, patients with AKOA were more than four times as likely to have miscellaneous pathology starting the year before the index visit, compared with those without AKOA.

Approximately 63% of the participants in each group were women, and the majority were overweight. The average age, weight, and global impact of arthritis were greater in the AKOA group when compared against the typical KOA and no-KOA groups.

Participants were assessed via MRI reviewed by radiologists who were blinded to the groups.

At the index visit, 49% of adults with AKOA had either a destabilizing meniscal tear or miscellaneous pathology, compared with 15% of adults with KOA and 6% of adults without KOA.

Adults with AKOA also showed significantly greater cartilage loss prior to the index visit in comparison with typical KOA patients, and AKOA patients had less cartilage in the medial and lateral tibia and medial femur, compared with adults who had typical KOA or no KOA after the index visit.

Adults who developed AKOA showed a significantly higher bone marrow lesion volume when compared against the typical KOA and no-KOA groups at 1 year prior to the index visit, and their bone marrow lesion volume increased on average 13 times more compared with typical KOA patients over the 2 years before the index visit, the researchers noted (2.00 mL vs. 0.15 mL, respectively).

“These findings add to the evidence that AKOA is different [from] the typically perceived archetype of slow-progressing osteoarthritis” with a unique risk profile, the researchers said.



The study findings were limited by several factors, including the relatively small sample size, uncertain timing of disease onset, a potentially limited definition of a destabilizing meniscal tear (defined as a root tear, radial tear, or complex tear, which almost always featured a radial component), a lack of a universal AKOA pathology, and some missing MRI data, the researchers noted. However, the results support previous studies suggesting a link between meniscal pathology and increased risk for AKOA, they said.

“It is important to acknowledge that it remains unclear if AKOA has any relation to type 2 rapidly progressive osteoarthritis, which was characterized by a more dramatic joint space narrowing (2 mm or more within 1 year) and greater abnormal bone loss/destruction,” they noted.

“Future research with a larger sample size of adults at risk for AKOA may help further refine our understanding of AKOA and help develop a clinically useful predictive model,” they added.

The study was supported in part by a grant from the National Institute of Arthritis and Musculoskeletal and Skin Diseases, and private funding included Merck, Novartis, GlaxoSmithKline, and Pfizer. The researchers had no financial conflicts to disclose.

SOURCE: Driban JB et al. Arthritis Rheumatol. 2018 Dec 28. doi: 10.1002/art.40826.

 

Accelerated knee osteoarthritis is characterized by distinct features that include destabilizing meniscal tears in two or more areas as well as other pathologies, based on data from the Osteoarthritis Initiative.

Courtesy National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS)

The possibility of accelerated knee osteoarthritis (AKOA) as a unique subset of knee osteoarthritis has not been well studied, wrote Jeffrey B. Driban, PhD, of Tufts University, Boston, and his colleagues.

“If specific pathologies differentiate people at risk for AKOA it may help identify adults with early-stage or high-risk for AKOA and inspire novel prevention strategies,” they wrote in their report, published in Arthritis & Rheumatology.

The researchers reviewed data from three groups of adults selected from participants in the Osteoarthritis Initiative, a cohort of 4,796 adults with KOA or at risk for symptomatic KOA who were recruited at four clinical sites in the United States. These groups included 125 with AKOA, 125 with typical knee osteoarthritis (KOA), and 125 without knee OA.



Overall, patients with AKOA were approximately seven times more likely than were patients with KOA to have destabilizing meniscal tears in two or more areas at the time of the index visit (42% vs. 14%); less than 5% of adults with no KOA experienced destabilizing meniscal tears. In addition, patients with AKOA were more than four times as likely to have miscellaneous pathology starting the year before the index visit, compared with those without AKOA.

Approximately 63% of the participants in each group were women, and the majority were overweight. The average age, weight, and global impact of arthritis were greater in the AKOA group when compared against the typical KOA and no-KOA groups.

Participants were assessed via MRI reviewed by radiologists who were blinded to the groups.

At the index visit, 49% of adults with AKOA had either a destabilizing meniscal tear or miscellaneous pathology, compared with 15% of adults with KOA and 6% of adults without KOA.

Adults with AKOA also showed significantly greater cartilage loss prior to the index visit in comparison with typical KOA patients, and AKOA patients had less cartilage in the medial and lateral tibia and medial femur, compared with adults who had typical KOA or no KOA after the index visit.

Adults who developed AKOA showed a significantly higher bone marrow lesion volume when compared against the typical KOA and no-KOA groups at 1 year prior to the index visit, and their bone marrow lesion volume increased on average 13 times more compared with typical KOA patients over the 2 years before the index visit, the researchers noted (2.00 mL vs. 0.15 mL, respectively).

“These findings add to the evidence that AKOA is different [from] the typically perceived archetype of slow-progressing osteoarthritis” with a unique risk profile, the researchers said.



The study findings were limited by several factors, including the relatively small sample size, uncertain timing of disease onset, a potentially limited definition of a destabilizing meniscal tear (defined as a root tear, radial tear, or complex tear, which almost always featured a radial component), a lack of a universal AKOA pathology, and some missing MRI data, the researchers noted. However, the results support previous studies suggesting a link between meniscal pathology and increased risk for AKOA, they said.

“It is important to acknowledge that it remains unclear if AKOA has any relation to type 2 rapidly progressive osteoarthritis, which was characterized by a more dramatic joint space narrowing (2 mm or more within 1 year) and greater abnormal bone loss/destruction,” they noted.

“Future research with a larger sample size of adults at risk for AKOA may help further refine our understanding of AKOA and help develop a clinically useful predictive model,” they added.

The study was supported in part by a grant from the National Institute of Arthritis and Musculoskeletal and Skin Diseases, and private funding included Merck, Novartis, GlaxoSmithKline, and Pfizer. The researchers had no financial conflicts to disclose.

SOURCE: Driban JB et al. Arthritis Rheumatol. 2018 Dec 28. doi: 10.1002/art.40826.

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Key clinical point: Meniscal tears and other pathologies are significantly more likely in adults with accelerated knee OA, compared with typical knee OA or no knee OA.

Major finding: One year before the knee OA index visit, more than 75% of patients with accelerated knee OA had meniscal damage in at least two regions.

Study details: The data come from 375 adults with typical knee OA, accelerated knee OA, or no knee OA in the longitudinal Osteoarthritis Initiative cohort study.

Disclosures: The study was supported in part by a grant from the National Institute of Arthritis and Musculoskeletal and Skin Diseases, and private funding included Merck, Novartis, GlaxoSmithKline, and Pfizer. The researchers had no financial conflicts to disclose.

Source: Driban JB et al. Arthritis Rheumatol. 2018 Dec 28. doi: 10.1002/art.40826.

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Antidepressants tied to greater hip fracture incidence in older adults

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Older patients in a Swedish registry who took antidepressants had a greater incidence of hip fracture the year before beginning antidepressant therapy and the year after starting therapy, compared with individuals in a matched control group.

The use of antidepressants is associated with adverse events such as a higher risk of falls, wrote Jon Brännström, MD, and his colleagues in JAMA Psychiatry. Some evidence also suggests that antidepressants “might affect bone metabolism, thereby increasing the risk of hip fracture.”

To examine the relationship between antidepressants and hip fracture, Dr. Brännström and his colleagues performed a nationwide cohort study of 204,072 individuals in the Prescribed Drug Register of Sweden’s National Board of Health and Welfare. All of the individuals were aged at least 65 years (mean age, 80.1 years; 63.1% women) and filled a prescription for an antidepressant between July 2006 and December 2011. Selective serotonin reuptake inhibitors made up 62.6% of the antidepressants used.

Patients who filled an antidepressant prescription during that time period were matched with a control group of individuals by birth year and gender and were studied the year before and after beginning antidepressant therapy.

In the year before initiating antidepressant therapy, the rate of hip fractures was more than twice (2.8% vs. 1.1%) that of the control group. In the year after initiating antidepressant therapy, there was a 3.5% incidence rate for hip fractures, compared with 1.3% in the control group.

After adjusting the results using a conditional logistic regression model, the highest rate of hip fracture among antidepressant users occurred between 16 days and 30 days prior to filling the prescription (odds ratio, 5.76; 95% confidence interval, 4.73-7.01); this association persisted in further subgroup analyses based on age, reported Dr. Brännström, who is affiliated with the department of community medicine and rehabilitation and geriatric medicine at Umeå University (Sweden), and his colleagues.

They noted that, although the study included all Swedish individuals who filled prescriptions for antidepressants during the study period, there is an absence of primary care comorbidity data and indications for antidepressant use. In addition, the definition of high- and low-medication doses does not always match what is considered high and low therapeutically and the information that can be gleaned from merging data from several different registries was limited.

“These findings raise questions about associations between antidepressant use and hip fracture seen in previous observational studies,” Dr. Brännström and his colleagues wrote. “Further analysis of this association in treatment studies and examination of the incidence of hip fracture before and after the discontinuation of treatment is required and may shed further light on the possible residual risk associated with treatment.”

This study was funded by the Swedish Research Council. The authors reported no relevant conflicts of interest.

SOURCE: Brännström J et al. JAMA Psychiatry. 2019 Jan 2. doi: 10.1001/jamapsychiatry.2018.3679.

Body

In many cases where an adverse event is linked to a medication, such as in the case of gastrointestinal bleeds and blood thinners, the adverse event is not linked to the medication. However, this is not the case with antidepressants and hip fracture, Andrea Iaboni, MD, DPhil, and Donovan T. Maust, MD, wrote in a related editorial (JAMA Psychiatry. 2019 Jan 2. doi: 10.1001/jamapsychiatry.2018.3632).

“Patients are routinely prescribed antidepressants following a fracture,” the authors wrote, noting that depression can occur for patients who do not have a history of depression and can last as long as 1 year after hip fracture. The reasons for depression after hip fracture are possibly caused by the consequences of the event or a comorbid condition, such as cerebrovascular disease burden, cognitive impairment, frailty, and impaired functional status. In addition, new antidepressant prescriptions are 10 times the normal rate for older adults in the months after a hip fracture.

Many older users of antidepressants have a hip fracture event in their past, which could be caused by an untreated case of depression and an elevated risk of elevated fall or fracture, as suggested by Brännström et al., while other reasons could include off-label indications such as insomnia, poor motivation during rehabilitation therapy, pain, or hyperactive delirium.

“If individuals with untreated depression are at risk of falls and fractures, it follows that there would be an elevated rate of fractures before antidepressant use,” the authors wrote. “However, as discussed earlier, it is also important to recognize that, during the postfracture period, rightly or wrongly, antidepressants are prescribed at a high rate.”

Clinicians who treat these patients should not stop all antidepressant prescribing to this population. Instead, “a pragmatic preventive approach is warranted, starting with selecting the antidepressant, a cautious initial dose and dose-escalation schedule, a review of potentially interacting therapies ... and referral to fall prevention programs for patients with other risk factors for falls,” they wrote.

“For most older adults, the toll of untreated depression will likely outweigh the potential risks associated with antidepressant use.”

Dr. Iabroni is with the Toronto Rehabilitation Institute and the University of Toronto. He reported receiving fees from serving as a scientific adviser for Winterlight Labs. Dr. Maust is with the department of psychiatry at the University of Michigan, Ann Arbor. He reported no relevant conflicts of interest.

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In many cases where an adverse event is linked to a medication, such as in the case of gastrointestinal bleeds and blood thinners, the adverse event is not linked to the medication. However, this is not the case with antidepressants and hip fracture, Andrea Iaboni, MD, DPhil, and Donovan T. Maust, MD, wrote in a related editorial (JAMA Psychiatry. 2019 Jan 2. doi: 10.1001/jamapsychiatry.2018.3632).

“Patients are routinely prescribed antidepressants following a fracture,” the authors wrote, noting that depression can occur for patients who do not have a history of depression and can last as long as 1 year after hip fracture. The reasons for depression after hip fracture are possibly caused by the consequences of the event or a comorbid condition, such as cerebrovascular disease burden, cognitive impairment, frailty, and impaired functional status. In addition, new antidepressant prescriptions are 10 times the normal rate for older adults in the months after a hip fracture.

Many older users of antidepressants have a hip fracture event in their past, which could be caused by an untreated case of depression and an elevated risk of elevated fall or fracture, as suggested by Brännström et al., while other reasons could include off-label indications such as insomnia, poor motivation during rehabilitation therapy, pain, or hyperactive delirium.

“If individuals with untreated depression are at risk of falls and fractures, it follows that there would be an elevated rate of fractures before antidepressant use,” the authors wrote. “However, as discussed earlier, it is also important to recognize that, during the postfracture period, rightly or wrongly, antidepressants are prescribed at a high rate.”

Clinicians who treat these patients should not stop all antidepressant prescribing to this population. Instead, “a pragmatic preventive approach is warranted, starting with selecting the antidepressant, a cautious initial dose and dose-escalation schedule, a review of potentially interacting therapies ... and referral to fall prevention programs for patients with other risk factors for falls,” they wrote.

“For most older adults, the toll of untreated depression will likely outweigh the potential risks associated with antidepressant use.”

Dr. Iabroni is with the Toronto Rehabilitation Institute and the University of Toronto. He reported receiving fees from serving as a scientific adviser for Winterlight Labs. Dr. Maust is with the department of psychiatry at the University of Michigan, Ann Arbor. He reported no relevant conflicts of interest.

Body

In many cases where an adverse event is linked to a medication, such as in the case of gastrointestinal bleeds and blood thinners, the adverse event is not linked to the medication. However, this is not the case with antidepressants and hip fracture, Andrea Iaboni, MD, DPhil, and Donovan T. Maust, MD, wrote in a related editorial (JAMA Psychiatry. 2019 Jan 2. doi: 10.1001/jamapsychiatry.2018.3632).

“Patients are routinely prescribed antidepressants following a fracture,” the authors wrote, noting that depression can occur for patients who do not have a history of depression and can last as long as 1 year after hip fracture. The reasons for depression after hip fracture are possibly caused by the consequences of the event or a comorbid condition, such as cerebrovascular disease burden, cognitive impairment, frailty, and impaired functional status. In addition, new antidepressant prescriptions are 10 times the normal rate for older adults in the months after a hip fracture.

Many older users of antidepressants have a hip fracture event in their past, which could be caused by an untreated case of depression and an elevated risk of elevated fall or fracture, as suggested by Brännström et al., while other reasons could include off-label indications such as insomnia, poor motivation during rehabilitation therapy, pain, or hyperactive delirium.

“If individuals with untreated depression are at risk of falls and fractures, it follows that there would be an elevated rate of fractures before antidepressant use,” the authors wrote. “However, as discussed earlier, it is also important to recognize that, during the postfracture period, rightly or wrongly, antidepressants are prescribed at a high rate.”

Clinicians who treat these patients should not stop all antidepressant prescribing to this population. Instead, “a pragmatic preventive approach is warranted, starting with selecting the antidepressant, a cautious initial dose and dose-escalation schedule, a review of potentially interacting therapies ... and referral to fall prevention programs for patients with other risk factors for falls,” they wrote.

“For most older adults, the toll of untreated depression will likely outweigh the potential risks associated with antidepressant use.”

Dr. Iabroni is with the Toronto Rehabilitation Institute and the University of Toronto. He reported receiving fees from serving as a scientific adviser for Winterlight Labs. Dr. Maust is with the department of psychiatry at the University of Michigan, Ann Arbor. He reported no relevant conflicts of interest.

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Use “pragmatic preventive approach”
Use “pragmatic preventive approach”

Older patients in a Swedish registry who took antidepressants had a greater incidence of hip fracture the year before beginning antidepressant therapy and the year after starting therapy, compared with individuals in a matched control group.

The use of antidepressants is associated with adverse events such as a higher risk of falls, wrote Jon Brännström, MD, and his colleagues in JAMA Psychiatry. Some evidence also suggests that antidepressants “might affect bone metabolism, thereby increasing the risk of hip fracture.”

To examine the relationship between antidepressants and hip fracture, Dr. Brännström and his colleagues performed a nationwide cohort study of 204,072 individuals in the Prescribed Drug Register of Sweden’s National Board of Health and Welfare. All of the individuals were aged at least 65 years (mean age, 80.1 years; 63.1% women) and filled a prescription for an antidepressant between July 2006 and December 2011. Selective serotonin reuptake inhibitors made up 62.6% of the antidepressants used.

Patients who filled an antidepressant prescription during that time period were matched with a control group of individuals by birth year and gender and were studied the year before and after beginning antidepressant therapy.

In the year before initiating antidepressant therapy, the rate of hip fractures was more than twice (2.8% vs. 1.1%) that of the control group. In the year after initiating antidepressant therapy, there was a 3.5% incidence rate for hip fractures, compared with 1.3% in the control group.

After adjusting the results using a conditional logistic regression model, the highest rate of hip fracture among antidepressant users occurred between 16 days and 30 days prior to filling the prescription (odds ratio, 5.76; 95% confidence interval, 4.73-7.01); this association persisted in further subgroup analyses based on age, reported Dr. Brännström, who is affiliated with the department of community medicine and rehabilitation and geriatric medicine at Umeå University (Sweden), and his colleagues.

They noted that, although the study included all Swedish individuals who filled prescriptions for antidepressants during the study period, there is an absence of primary care comorbidity data and indications for antidepressant use. In addition, the definition of high- and low-medication doses does not always match what is considered high and low therapeutically and the information that can be gleaned from merging data from several different registries was limited.

“These findings raise questions about associations between antidepressant use and hip fracture seen in previous observational studies,” Dr. Brännström and his colleagues wrote. “Further analysis of this association in treatment studies and examination of the incidence of hip fracture before and after the discontinuation of treatment is required and may shed further light on the possible residual risk associated with treatment.”

This study was funded by the Swedish Research Council. The authors reported no relevant conflicts of interest.

SOURCE: Brännström J et al. JAMA Psychiatry. 2019 Jan 2. doi: 10.1001/jamapsychiatry.2018.3679.

Older patients in a Swedish registry who took antidepressants had a greater incidence of hip fracture the year before beginning antidepressant therapy and the year after starting therapy, compared with individuals in a matched control group.

The use of antidepressants is associated with adverse events such as a higher risk of falls, wrote Jon Brännström, MD, and his colleagues in JAMA Psychiatry. Some evidence also suggests that antidepressants “might affect bone metabolism, thereby increasing the risk of hip fracture.”

To examine the relationship between antidepressants and hip fracture, Dr. Brännström and his colleagues performed a nationwide cohort study of 204,072 individuals in the Prescribed Drug Register of Sweden’s National Board of Health and Welfare. All of the individuals were aged at least 65 years (mean age, 80.1 years; 63.1% women) and filled a prescription for an antidepressant between July 2006 and December 2011. Selective serotonin reuptake inhibitors made up 62.6% of the antidepressants used.

Patients who filled an antidepressant prescription during that time period were matched with a control group of individuals by birth year and gender and were studied the year before and after beginning antidepressant therapy.

In the year before initiating antidepressant therapy, the rate of hip fractures was more than twice (2.8% vs. 1.1%) that of the control group. In the year after initiating antidepressant therapy, there was a 3.5% incidence rate for hip fractures, compared with 1.3% in the control group.

After adjusting the results using a conditional logistic regression model, the highest rate of hip fracture among antidepressant users occurred between 16 days and 30 days prior to filling the prescription (odds ratio, 5.76; 95% confidence interval, 4.73-7.01); this association persisted in further subgroup analyses based on age, reported Dr. Brännström, who is affiliated with the department of community medicine and rehabilitation and geriatric medicine at Umeå University (Sweden), and his colleagues.

They noted that, although the study included all Swedish individuals who filled prescriptions for antidepressants during the study period, there is an absence of primary care comorbidity data and indications for antidepressant use. In addition, the definition of high- and low-medication doses does not always match what is considered high and low therapeutically and the information that can be gleaned from merging data from several different registries was limited.

“These findings raise questions about associations between antidepressant use and hip fracture seen in previous observational studies,” Dr. Brännström and his colleagues wrote. “Further analysis of this association in treatment studies and examination of the incidence of hip fracture before and after the discontinuation of treatment is required and may shed further light on the possible residual risk associated with treatment.”

This study was funded by the Swedish Research Council. The authors reported no relevant conflicts of interest.

SOURCE: Brännström J et al. JAMA Psychiatry. 2019 Jan 2. doi: 10.1001/jamapsychiatry.2018.3679.

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Key clinical point: An association was found between greater hip fracture incidence for older individuals taking antidepressants in the year before beginning therapy and the year after starting therapy.

Major finding: Individuals who took antidepressants had a greater incidence of hip fractures in the year before (2.8% vs. 1.1%) and the year after (3.5% vs. 1.3%) beginning antidepressants, compared with individuals in a matched control group.

Study details: A nationwide cohort study of 408,144 individuals in the Prescribed Drugs Register of Sweden’s National Board of Health and Welfare who were aged 65 years or older.

Disclosures: This study was funded by the Swedish Research Council. The authors reported no relevant conflicts of interest.

Source: Brännström J et al. JAMA Psychiatry. 2019 Jan 2. doi: 10.1001/jamapsychiatry.2018.3679.

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Unicondylar Knee Arthroplasty in the U.S. Patient Population: Prevalence and Epidemiology

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ABSTRACT

Publications on the prevalence of unicompartmental knee arthroplasty in the United States using a single database may have underestimated the “true” number of cases performed, given that several unicondylar knee arthroplasty (UKA) patients are <65 years and have private insurance. The prevalence of UKA in elderly (≥65 years) and younger (<65 years) populations was evaluated using the 2002 to 2011 5% sample of the Medicare data (Part B) and the 2004 to June 2012 MarketScan Commercial and Medicare Supplemental databases, respectively. The prevalence of UKA was stratified by age, gender, census region, Charlson comorbidity index, Medicare buy-in status, and diagnosis. The annual rate of change in the UKA rate was examined using Poisson regression to evaluate temporal changes considering year as a covariate.

A total of 5235 and 23,310 UKA procedures were identified from the 5% Medicare and MarketScan databases, respectively. The rates of UKA generally increased until 2008, after which there was a decline. In both cohorts, gender and year of operation were found to be significantly associated with UKA rate. Analysis of data obtained over the past few years revealed that males 55 to 64 years, 65 to 69 years, and 70 to 74 years were the only age-gender groups whose UKA rates appeared to be trending upward.

From 2002 to 2011, the rate of UKAs performed in the United States has increased, and a significant proportion of the surgeries were performed in younger (<65 years) patients.

Continue to: Unicondylar knee arthroplasty...

 

 

Unicondylar knee arthroplasty (UKA) is an effective surgical treatment for symptomatic degenerative joint disease of a single compartment of the knee, providing improved functional outcomes compared with total knee arthroplasty (TKA).1-3 It has been estimated that the proportion of patients undergoing TKA, who meet the criteria for UKA, varies between 21% and 47%.4,5 However, it has been variably estimated that the usage of UKA ranges from 0% to 50% (mean, 8%) of all primary knee arthroplasties.5-8 It is believed that this discrepancy between the percentage of patients who meet indications for the surgery and those who receive it is associated with various factors, including surgeon training and experiences, diverse indications, economic factors, as well as acknowledgment of the reportedly higher revision rates of UKA than those of TKA in national joint registries.7,9-11

According to their classic article, Kozinn and Scott12 outlined the indications for UKA that, in their experience, led to the most successful outcomes, including age >60 years, weight <82 kg, low physical demand, localized arthritis with no full-thickness chondromalacia elsewhere in the joint, intact anterior cruciate ligament, minimal deformity, and flexion >90°. More recently, indications have been expanded to include younger and more active patients, higher body mass index, and some patterns of patellofemoral chondromalacia, with an increasing number of publications reporting successful clinical outcomes in these cohorts as well.13-17 Taken together, it is clear that the “classic” strict indications for UKA can be safely expanded, which have and will result in an increased number of these procedures being performed above and beyond that which might be predicted based on demographic trends alone.

A growing body of literature has been published on the prevalence and projections of orthopedic procedures in the United States.18-20 Several studies have focused their analysis on 1 of several large administrative databases, including the Nationwide Inpatient Sample, the 5% Medicare Part B database, and the National Hospital Discharge Survey.18,20-23 A concern with limiting an analysis of the prevalence of unicompartmental knee arthroplasty to these particular databases is that it may underestimate the “true” number of cases performed in the United States, given that several UKA patients are <65 years and have private insurance, and therefore, would not be captured statistically by a database that collects data on patients ≥65 years.

The purpose of this study was to quantify the current prevalence and epidemiology of UKA in the U.S. patient population. Our hypothesis was that the number of procedures and the procedural rate of UKA are increasing over time. Furthermore, this increase may be attributed to an increase in select age- or gender-based segments of the population. To test this hypothesis, we analyzed 2 separate large claims databases to capture patients over a spectrum of age and inclusive of both private and public payers, including the 5% Medicare Part B database (2002–2011) for patients ≥65 years and the MarketScan database (2004 to June 2011) for patients <65 years. Understanding the accurate trends in the use of UKA on a national scale is important for legislative bodies, healthcare administrators, and physicians.

MATERIALS AND METHODS

The 2002 to 2011 5% sample of the Medicare data (Part B) and the 2004 to June 2012 MarketScan Commercial and Medicare Supplemental databases were used to evaluate the prevalence of UKA in elderly (≥65 years) and younger (<65 years) populations, respectively. The UKA procedures were identified using the CPT code 27446.

The prevalence of UKA was stratified by age, gender, census region, Charlson Comorbidity Index, Medicare buy-in status, and diagnosis. The buy-in status is a proxy for the socioeconomic status as it reflects the state subsidizing the health insurance premium for the beneficiary. The Charlson Comorbidity Index is a composite score that has been used to assess the comorbidity level of a patient by taking into account the number and the severity of comorbid conditions.24 For the elderly population, the rate of UKA was subsequently evaluated based on the number of beneficiaries for that particular age-gender group and year in both databases. Poisson regression was used to evaluate the annual rate of change in the UKA rate for assessing temporal changes considering year as a covariate. Age and gender, as well as 2-way interaction terms for age, gender, and year, were also considered as covariates. 

Continue to: RESULTS...

 

 

RESULTS

For the time periods analyzed, a total of 5235 and 23,310 UKA procedures were identified from the 5% Medicare and MarketScan databases, respectively. A peak in the prevalence appeared around 2008 for the elderly population and in 2009 for the younger population (Figure 1). When normalized by the size of the population segment, the rate of UKA was found to be approximately 5 times greater in the elderly population, increasing from 369 in 2002 to 639 in 2008, but plateauing to 561 in 2011. Extrapolating to the 100% Medicare population, these numbers increased to 7380, 12,780, and 11,220, respectively. Temporal changes in the UKA rate were significant, increasing from 24.5 UKAs per 100,000 persons in 2002 to 43.1 UKAs in 2008, followed by a decline to 36.5 in 2011 (P < .0001) (Figure 2). The rates of UKA generally increased from 2002 to 2008 for both males and females in the Medicare cohort; however, the rates of UKA in female patients continuously declined from 2008 onward, whereas the UKA rates in male patients decreased in 2009, followed by an increase in 2010 and 2011 (Figure 2). For the younger population, there was a slight increase in the rate of UKA from 2004 to approximately 2009, after which the rates for both males and females remained relatively steady. When put in the context of the prevalence of TKA, the prevalence of UKA fluctuated during the same time period. In the Medicare population, the prevalence of UKA ranged from 4.3% (2005) to 5.9% (2008) of the TKA prevalence between 2002 and 2011. In the younger MarketScan population, the prevalence of UKA ranged from 6.7% (2005) to 8.9% (2008) between 2004 and June 2012.

The UKA rate differed significantly according to gender (P = .0209), with higher rates for males. Although there were no age-related differences (P = .3723), age–gender interactions were found to be significant (P < .0001). For males, the largest rate of UKA in the most recent year of data was observed in the 70- to 74-year-old group, followed by the 75- to 79- and the 65- to 69-year-old groups (Figure 3). For females, those in the 65- to 69- and the 70- to 74-year-old groups had the highest rate of UKA. In the younger cohort, there were increases in the UKA rates since 2004. These rates appeared to be relatively stable from the 2008 or 2009 period onward, except for females 55–64 years, which demonstrated a steady decline since 2008. Analysis of data obtained over the past few years showed that males 55–64, 65–69, and 70–74 years were the only age–gender groups whose UKA rates appeared to be trending upward.

The vast majority of elderly UKA patients were white (95.5%), and when stratified by census region, the highest proportion of UKA procedures was observed in the South and the Midwest (Figure 4). Furthermore, among patients <65 years, 64.2% had a Charlson score of 0 compared to 40.8% in the elderly group (Figure 5). For the Medicare population, based on their receipt of state subsidies for their insurance premiums, 5.1% of patients were of lower socioeconomic status. Osteoarthritis was diagnosed in 99.4% and 97.3% of the MarketScan and Medicare cohorts, respectively.

In the Medicare cohort, gender (P = .0209) and year of operation (P < .0001) were found to be significantly associated with the rate of UKA, along with age-gender (P < .0001) and gender-year (P = .0202) interaction terms. In the MarketScan cohort, age (P = .0173), gender (P = .0017), and year of operation (P = .0002) were found to be significantly associated with UKA rate. Two-way interactions between age-gender (P = .0018), age–year (P = .0207), and gender-year (P = .0017) were also found to be statistically significant factors.

Continue to: DISCUSSION...

 

 

DISCUSSION

The results of our study indicate that between 2002 and 2011, a steadily increasing number of UKA procedures was performed in the United States, and a significant proportion of the surgeries was performed on patients <65 years. Without the MarketScan database data, we would have missed more than 23,000 UKA cases performed during this 10-year time period. This finding validates our research methodology that incorporated data on privately insured younger (<65 years) patients, which is something that has not been done when examining the epidemiology of UKA.

To our knowledge, there are only 2 other publications attempting to quantify the incidence of UKA procedures performed in the United States. Bolognesi and colleagues23 used the Medicare 5% sample to assess trends in the use of knee arthroplasty from 2000 to 2009. The authors reported that a total of 68,603 patients underwent unilateral total knee arthroplasty (n = 65,505) or unicompartmental knee arthroplasty (n = 3098) over this 10-year time period. Given that there is substantial overlap of our time periods, it is not surprising that our Medicare numbers are similar (3098 vs 5235). In their study, the use of TKA increased 1.7-fold, whereas the use of UKA increased 6.2-fold23. In our analysis of the Medicare (2011 vs 2002) and MarketScan (2011 vs 2004) databases, there was a 1.3-fold and a 3.4-fold increase in the number of TKAs performed. Concomitantly, the use of UKA increased 1.5-fold and 2.8-fold, respectively, in these databases over the same time periods. The reason for the slight discrepancy in the numbers may be attributable to the peak occurring in 2008. The other publication on the subject by Riddle and colleagues8 focused on the time period 1998 to 2005 and used implant manufacturer’s sales data cross-referenced to a database of 44 hospitals to derive their national estimates. Using their unique methodology, the authors calculated an incidence of UKA, ranging from 6570 implants in 1998 to 44,990 in 2005. They reported that UKA use during the study period increased by 3 times the rate of TKA in the United States, with an average yearly percentage increase in the number of UKA procedures of 32.5% compared to 9.4% for TKA procedures. It is difficult to account for the discrepancy in the number of UKAs performed reported between our current study and that of Riddle and colleagues;8 however, the fact that the authors used implant manufacturer’s individual sales numbers may indicate that a portion of UKA patients was not captured in either the Medicare 5% or the MarketScan database. Nonetheless, in our analysis, the annual increase in the number of UKA procedures performed during the time periods studied averaged 5.8% in the older population and 25.4% in the younger population compared to the increase in the number of TKA procedures, which averaged 3.6% and 33.9% in the older and younger populations, respectively. In addition, in our study, the percentage of UKAs performed relative to the number of TKAs during the time intervals studied varied from a low of 4.3% to a high of 5.9% in the older population and from a low of 6.7% to a high of 8.9% in the younger population.

During the 10-year period of this study, a general upward trend appeared in the total number of unicompartmental knee arthroplasties performed in both the Medicare and the MarketScan databases. The rate at which the procedure was performed increased in the Medicare population from 24.5 to 36.5 (per 100,000 persons) over a 10-year time period and in the MarketScan cohort from 5.9 to 7.4 (per 100,000 persons) over an 8.5-year time period. This indicates both a larger absolute and a relative rate increase in UKA procedures in the elderly population. Around 2008 and 2009, the data showed a slight dip in the rate of UKA in the Medicare population and a plateau in the rate in the MarketScan database. Although this may be a spurious finding in the data that would be smoothed out with a longer time period investigated, it is interesting that this finding coincided with a national economic downturn. Although it might be expected that macroeconomics may affect the utilization of elective surgery such as total joint replacement, Kurtz and colleagues25 investigated this particular question and found that neither the economic downturns of 2001 or those of 2008 and 2009 had a significant impact on the incidence of total joint replacement surgeries.

Incorporation of the MarketScan database data indicated that a significant proportion of patients undergoing UKA were <65 years and that there was a slight but increasing rate of procedures performed on this age cohort over the past decade. A similar finding has been reported in the Finnish Arthroplasty Registry. Leskinen and colleagues26 reported that the incidence of UKAs among individuals 30 to 59 years increased from 0.2 (per 100,000 persons) to 10 (per 100,000 persons) from 1980 to 2006 and that most of the increase occurred among patients 50 to 59 years. The fact that younger age is no longer observed as a relative contraindication to this procedure is supported by several clinical investigations. Cartier and colleagues27 reported 93% survival at 10 years in patients with a mean age of 65 years, but included patients as young as 28 years, claiming that the results for younger patients were no worse than those for older patients in the series. Pandit and colleagues17 compared the results of 245 young patients (<60 years) to those of 755 older patients (>60 years) and found a survival rate of 97% at 10 years, with no significant difference in mean functional outcomes, failure rate, or survival between the groups at >5 years of follow-up. Given that patients <65 years now account for approximately half of the TKAs performed each year, with the greatest increase in volume among patients between 45 and 54, it is clear that investigations on the epidemiology of UKA must take into account this increasingly relevant younger patient cohort.28

Continue to: Our data indicate...

 

 

Our data indicate that only approximately 5% of UKA patients were non-white and another 5% were from lower socioeconomic status. These findings have been observed in multiple other studies looking at the epidemiology of total joint replacement in the United States.29 Bolognesi and colleagues23 reported that although “non-white race” patients made up 12% of the general Medicare sample they were analyzing, these patients accounted for only 5% and 3% of the total knee arthroplasty and unicompartmental knee arthroplasty populations, respectively. Although it is beyond the scope of this paper to delve into the reasons for this discrepancy, it may be related to differences in access to care, healthcare literacy, and trust of patients in the healthcare system.30,31

Our study, like all those based on administrative claims, has several notable inherent limitations. Coding inaccuracies as well as the potential for systematic bias (eg, underreporting) may affect the accuracy of our results. Although the MarketScan Commercial Research Database (Truven Health Analytics) includes nationally representative information for >180 million patients covered with private insurance, it is possible that we have missed some patients who underwent UKA during the time period investigated. However, we feel that the number missed is probably small and does not affect our conclusions in any meaningful manner.

CONCLUSION

This novel analysis of 2 separate administrative claims databases, which more accurately captures all patients undergoing UKA, indicates that there has been a steady increase in the rate of the procedure over the past decade and that a significant proportion of the surgeries were performed in younger (<65 years) patients. Understanding the accurate trends in the use of UKA on a national scale is important for legislative bodies, healthcare administrators, as well as physicians. Furthermore, given the increasing rates of UKA in patients <65 years old, and the increased burden on implants for withstanding increased activities and repetitive loads, it remains imperative to strive to optimize materials, implant designs, and surgical techniques to enhance implant durability.

References
  1. Hopper GP, Leach WJ. Participation in sporting activities following knee replacement: total versus unicompartmental. Knee Surg Sports Traumatol Arthrosc. 2008;16(10):973-979. doi: 10.1007/s00167-008-0596-9.
  2. Lygre SH, Espehaug B, Havelin LI, Furnes O, Vollset SE. Pain and function in patients after primary unicompartmental and total knee arthroplasty. J Bone Joint Surg, (Am). 2010;92(18):2890-2897. doi: 10.2106/JBJS.I.00917.
  3. Liddle AD, Pandit H, Judge A, Murray DW. Patient-reported outcomes after total and unicompartmental knee arthroplasty: a study of 14,076 matched patients from the National Joint Registry for England and Wales. Bone Joint J. 2015;97-B(6):793-801. doi: 10.1302/0301-620X.97B6.35155.
  4. Arno S, Maffei D, Walker PS, Schwarzkopf R, Desai P, Steiner GC. Retrospective analysis of total knee arthroplasty cases for visual, histological, and clinical eligibility of unicompartmental knee arthroplasties. J Arthroplast. 2011;26(8):1396-1403. doi: 10.1016/j.arth.2010.12.023.
  5. Willis-Owen CA, Brust K, Alsop H, Miraldo M, Cobb JP. Unicondylar knee arthroplasty in the UK National Health Service: an analysis of candidacy, outcome and cost efficacy. Knee. 2009;16(6):473-478. doi: 10.1016/j.knee.2009.04.006.
  6. Murray DW, Liddle AD, Dodd CA, Pandit H. Unicompartmental knee arthroplasty: is the glass half full or half empty? Bone Joint J. 2015;97-B(10 Suppl. A):3-8. doi: 10.1302/0301-620X.97B10.36542.
  7. Liddle AD, Judge A, Pandit H, Murray DW. Adverse outcomes after total and unicompartmental knee replacement in 101,330 matched patients: a study of data from the National Joint Registry for England and Wales. Lancet. 2014;384(9952):1437-1445. doi: 10.1016/S0140-6736(14)60419-0.
  8. Riddle DL, Jiranek WA, McGlynn FJ. Yearly incidence of unicompartmental knee arthroplasty in the United States. J Arthroplast. 2008;23(3):408-412. doi: 10.1016/j.arth.2007.04.012.
  9. Argenson JN, Blanc G, Aubaniac JM, Parratte S. Modern unicompartmental knee arthroplasty with cement: a concise follow-up, at a mean of twenty years, of a previous report. J Bone Joint Surg, (Am). 2013;95(10):905-909. doi: 10.2106/JBJS.L.00963.
  10. Koskinen E, Eskelinen A, Paavolainen P, Pulkkinen P, Remes V. Comparison of survival and cost-effectiveness between unicondylar arthroplasty and total knee arthroplasty in patients with primary osteoarthritis: a follow-up study of 50,493 knee replacements from the Finnish Arthroplasty Register. Acta Orthop. 2008;79(4):499-507. doi: 10.1080/17453670710015490.
  11. Knutson K, Lewold S, Robertsson O, Lidgren L. The Swedish knee arthroplasty register. A nation-wide study of 30,003 knees 1976-1992. Acta Orthop Scand. 1994;65(4):375-386. doi: 10.3109/17453679408995475.
  12. Kozinn SC, Scott R. Unicondylar knee arthroplasty. J Bone Joint Surg, (Am). 1989;71(1):145-150. doi: 10.2106/00004623-198971010-00023.
  13. Pennington DW. Unicompartmental knee arthroplasty in patients sixty years of age or younger. J Bone Joint Surg, (Am). 2003;85-A(10):1968-1973. doi: 10.2106/00004623-200310000-00016.
  14. Biswas D, Van Thiel GS, Wetters NG, Pack BJ, Berger RA, Della Valle CJ. Medial unicompartmental knee arthroplasty in patients less than 55 years old: minimum of two years of follow-up. J Arthroplast. 2014;29(1):101-105. doi: 10.1016/j.arth.2013.04.046.
  15. Murray DW, Pandit H, Weston-Simons JS, et al. Does body mass index affect the outcome of unicompartmental knee replacement? Knee. 2013;20(6):461-465. doi: 10.1016/j.knee.2012.09.017.
  16. Kang SN, Smith TO, Sprenger De Rover WB, Walton NP. Pre-operative patellofemoral degenerative changes do not affect the outcome after medial Oxford unicompartmental knee replacement: a report from an independent centre. J Bone Joint Surg Br. 2011;93(4):476-478. doi: 10.1302/0301-620X.93B4.25562.
  17. Pandit H, Jenkins C, Gill HS, et al. Unnecessary contraindications for mobile-bearing unicompartmental knee replacement. J Bone Joint Surg Br. 2011;93(5):622-628. doi: 10.1302/0301-620X.93B5.26214.
  18. Kurtz S, Mowat F, Ong K, Chan N, Lau E, Halpern M. Prevalence of primary and revision total hip and knee arthroplasty in the United States from 1990 through 2002. J Bone Joint Surg Am. 2005;87(7):1487-1497. doi: 10.2106/JBJS.D.02441.
  19. Kurtz SM, Ong KL, Schmier J, et al. Future clinical and economic impact of revision total hip and knee arthroplasty. J Bone Joint Surg, (Am). 2007;89(Suppl. 3):144-151. doi: 10.2106/JBJS.G.00587.
  20. Day JS, Lau E, Ong KL, Williams GR, Ramsey ML, Kurtz SM. Prevalence and projections of total shoulder and elbow arthroplasty in the United States to 2015. J Shoulder Elbow Surg. 2010;19(8):1115-1120. doi: 10.1016/j.jse.2010.02.009.
  21. Kurtz S, Ong K, Lau E, Mowat F, Halpern M. Projections of primary and revision hip and knee arthroplasty in the United States from 2005 to 2030. J Bone Joint Surg, (Am). 2007;89(4):780-785. doi: 10.2106/JBJS.F.00222.
  22. Kamath AF, Ong KL, Lau E, et al. Quantifying the burden of revision total joint arthroplasty for periprosthetic infection. J Arthroplast. 2015;30(9):1492-1497. doi: 10.1016/j.arth.2015.03.035.
  23. Bolognesi MP, Greiner MA, Attarian DE, et al. Unicompartmental knee arthroplasty and total knee arthroplasty among Medicare beneficiaries, 2000 to 2009. J Bone Joint Surg, (Am). 2013;95(22):e174. doi: 10.2106/JBJS.L.00652.
  24. Charlson ME, Pompei P, Ales KL, MacKenzie CR. A new method of classifying prognostic comorbidity in longitudinal studies: development and validation. J Chronic Dis. 1987;40(5):373-383. doi: 10.1016/0021-9681(87)90171-8.
  25. Kurtz SM, Ong KL, Lau E, Bozic KJ. Impact of the economic downturn on total joint replacement demand in the United States: updated projections to 2021. J Bone Joint Surg, (Am). 2014;96(8):624-630. doi: 10.2106/JBJS.M.00285.
  26. Leskinen J, Eskelinen A, Huhtala H, Paavolainen P, Remes V. The incidence of knee arthroplasty for primary osteoarthritis grows rapidly among baby boomers: a population-based study in Finland. Arthritis Rheum. 2012;64(2):423-428. doi: 10.1002/art.33367.
  27. Cartier P, Sanouiller JL, Grelsamer RP. Unicompartmental knee arthroplasty surgery. 10-year minimum follow-up period. J Arthroplast. 1996;11(7):782-788. doi: 10.1016/S0883-5403(96)80177-X.
  28. Kurtz SM, Lau E, Ong K, Zhao K, Kelly M, Bozic KJ. Future young patient demand for primary and revision joint replacement: national projections from 2010 to 2030. Clin Orthop Relat Res. 2009;467(10):2606-2612. doi: 10.1007/s11999-009-0834-6.
  29. Singh JA, Lu X, Rosenthal GE, Ibrahim S, Cram P. Racial disparities in knee and hip total joint arthroplasty: an 18-year analysis of national Medicare data. Ann Rheum Dis. 2014;73(12):2107-2115. doi: 10.1136/annrheumdis-2013-203494.
  30. Pierce TP, Elmallah RK, Lavernia CJ, et al. Racial disparities in lower extremity arthroplasty outcomes and use. Orthopedics. 2015;38(12): e1139-e1146. doi: 10.3928/01477447-20151123-05.
  31. Irgit K, Nelson CL. Defining racial and ethnic disparities in THA and TKA. Clin Orthop Relat Res. 2011;469(7):1817-1823. doi: 10.1007/s11999-011-1885-z.
Author and Disclosure Information

Dr. Hansen is Associate Professor, Department of Orthopaedic Surgery, University of California, San Francisco, San Francisco, CA. Dr. Ong is Principal Engineer, Biomedical Engineering, Exponent Inc, Philadelphia, PA. Mr. Lau is Senior Managing Scientist, Health Sciences, Exponent Inc, Menlo Park, CA. Dr. Lonner is Professor, Department of Orthopaedic Surgery, Rothman Institute, Sidney Kimmel Medical College at Thomas Jefferson University, Philadelphia, PA. Dr. Kurtz is Corporate Vice President, Principal & Practice Director, Biomedical Engineering, Exponent Inc. Philadelphia, PA.

Authors’ Disclosure Statement: This article was funded in part by a research grant provided by Mako Surgical. Dr. Lonner reports being a consultant for ZimmerBiomet, Smith and Nephew, Force Therapeutics, and Muvr Labs and receiving royalties from ZimmerBiomet and Smith and Nephew. He is a shareholder in Force Therapeutics and Muvs Labs. The other authors report no actual or potential conflict of interest in relation to this article.

Address correspondence to: Jess H Lonner, MD, Rothman Institute, Sidney Kimmel Medical College at Thomas Jefferson University, 825 Old Lancaster Ave, PA 19010 (tel, 610-672-1151; email, [email protected]).

Erik Nathan Hansen, MD Kevin L. Ong PhD Edmund Lau, MS Steven M Kurtz, PhD Jess H. Lonner, MD . Unicondylar Knee Arthroplasty in the U.S. Patient Population: Prevalence and Epidemiology. Am J Orthop.

December 28, 2018

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Author and Disclosure Information

Dr. Hansen is Associate Professor, Department of Orthopaedic Surgery, University of California, San Francisco, San Francisco, CA. Dr. Ong is Principal Engineer, Biomedical Engineering, Exponent Inc, Philadelphia, PA. Mr. Lau is Senior Managing Scientist, Health Sciences, Exponent Inc, Menlo Park, CA. Dr. Lonner is Professor, Department of Orthopaedic Surgery, Rothman Institute, Sidney Kimmel Medical College at Thomas Jefferson University, Philadelphia, PA. Dr. Kurtz is Corporate Vice President, Principal & Practice Director, Biomedical Engineering, Exponent Inc. Philadelphia, PA.

Authors’ Disclosure Statement: This article was funded in part by a research grant provided by Mako Surgical. Dr. Lonner reports being a consultant for ZimmerBiomet, Smith and Nephew, Force Therapeutics, and Muvr Labs and receiving royalties from ZimmerBiomet and Smith and Nephew. He is a shareholder in Force Therapeutics and Muvs Labs. The other authors report no actual or potential conflict of interest in relation to this article.

Address correspondence to: Jess H Lonner, MD, Rothman Institute, Sidney Kimmel Medical College at Thomas Jefferson University, 825 Old Lancaster Ave, PA 19010 (tel, 610-672-1151; email, [email protected]).

Erik Nathan Hansen, MD Kevin L. Ong PhD Edmund Lau, MS Steven M Kurtz, PhD Jess H. Lonner, MD . Unicondylar Knee Arthroplasty in the U.S. Patient Population: Prevalence and Epidemiology. Am J Orthop.

December 28, 2018

Author and Disclosure Information

Dr. Hansen is Associate Professor, Department of Orthopaedic Surgery, University of California, San Francisco, San Francisco, CA. Dr. Ong is Principal Engineer, Biomedical Engineering, Exponent Inc, Philadelphia, PA. Mr. Lau is Senior Managing Scientist, Health Sciences, Exponent Inc, Menlo Park, CA. Dr. Lonner is Professor, Department of Orthopaedic Surgery, Rothman Institute, Sidney Kimmel Medical College at Thomas Jefferson University, Philadelphia, PA. Dr. Kurtz is Corporate Vice President, Principal & Practice Director, Biomedical Engineering, Exponent Inc. Philadelphia, PA.

Authors’ Disclosure Statement: This article was funded in part by a research grant provided by Mako Surgical. Dr. Lonner reports being a consultant for ZimmerBiomet, Smith and Nephew, Force Therapeutics, and Muvr Labs and receiving royalties from ZimmerBiomet and Smith and Nephew. He is a shareholder in Force Therapeutics and Muvs Labs. The other authors report no actual or potential conflict of interest in relation to this article.

Address correspondence to: Jess H Lonner, MD, Rothman Institute, Sidney Kimmel Medical College at Thomas Jefferson University, 825 Old Lancaster Ave, PA 19010 (tel, 610-672-1151; email, [email protected]).

Erik Nathan Hansen, MD Kevin L. Ong PhD Edmund Lau, MS Steven M Kurtz, PhD Jess H. Lonner, MD . Unicondylar Knee Arthroplasty in the U.S. Patient Population: Prevalence and Epidemiology. Am J Orthop.

December 28, 2018

ABSTRACT

Publications on the prevalence of unicompartmental knee arthroplasty in the United States using a single database may have underestimated the “true” number of cases performed, given that several unicondylar knee arthroplasty (UKA) patients are <65 years and have private insurance. The prevalence of UKA in elderly (≥65 years) and younger (<65 years) populations was evaluated using the 2002 to 2011 5% sample of the Medicare data (Part B) and the 2004 to June 2012 MarketScan Commercial and Medicare Supplemental databases, respectively. The prevalence of UKA was stratified by age, gender, census region, Charlson comorbidity index, Medicare buy-in status, and diagnosis. The annual rate of change in the UKA rate was examined using Poisson regression to evaluate temporal changes considering year as a covariate.

A total of 5235 and 23,310 UKA procedures were identified from the 5% Medicare and MarketScan databases, respectively. The rates of UKA generally increased until 2008, after which there was a decline. In both cohorts, gender and year of operation were found to be significantly associated with UKA rate. Analysis of data obtained over the past few years revealed that males 55 to 64 years, 65 to 69 years, and 70 to 74 years were the only age-gender groups whose UKA rates appeared to be trending upward.

From 2002 to 2011, the rate of UKAs performed in the United States has increased, and a significant proportion of the surgeries were performed in younger (<65 years) patients.

Continue to: Unicondylar knee arthroplasty...

 

 

Unicondylar knee arthroplasty (UKA) is an effective surgical treatment for symptomatic degenerative joint disease of a single compartment of the knee, providing improved functional outcomes compared with total knee arthroplasty (TKA).1-3 It has been estimated that the proportion of patients undergoing TKA, who meet the criteria for UKA, varies between 21% and 47%.4,5 However, it has been variably estimated that the usage of UKA ranges from 0% to 50% (mean, 8%) of all primary knee arthroplasties.5-8 It is believed that this discrepancy between the percentage of patients who meet indications for the surgery and those who receive it is associated with various factors, including surgeon training and experiences, diverse indications, economic factors, as well as acknowledgment of the reportedly higher revision rates of UKA than those of TKA in national joint registries.7,9-11

According to their classic article, Kozinn and Scott12 outlined the indications for UKA that, in their experience, led to the most successful outcomes, including age >60 years, weight <82 kg, low physical demand, localized arthritis with no full-thickness chondromalacia elsewhere in the joint, intact anterior cruciate ligament, minimal deformity, and flexion >90°. More recently, indications have been expanded to include younger and more active patients, higher body mass index, and some patterns of patellofemoral chondromalacia, with an increasing number of publications reporting successful clinical outcomes in these cohorts as well.13-17 Taken together, it is clear that the “classic” strict indications for UKA can be safely expanded, which have and will result in an increased number of these procedures being performed above and beyond that which might be predicted based on demographic trends alone.

A growing body of literature has been published on the prevalence and projections of orthopedic procedures in the United States.18-20 Several studies have focused their analysis on 1 of several large administrative databases, including the Nationwide Inpatient Sample, the 5% Medicare Part B database, and the National Hospital Discharge Survey.18,20-23 A concern with limiting an analysis of the prevalence of unicompartmental knee arthroplasty to these particular databases is that it may underestimate the “true” number of cases performed in the United States, given that several UKA patients are <65 years and have private insurance, and therefore, would not be captured statistically by a database that collects data on patients ≥65 years.

The purpose of this study was to quantify the current prevalence and epidemiology of UKA in the U.S. patient population. Our hypothesis was that the number of procedures and the procedural rate of UKA are increasing over time. Furthermore, this increase may be attributed to an increase in select age- or gender-based segments of the population. To test this hypothesis, we analyzed 2 separate large claims databases to capture patients over a spectrum of age and inclusive of both private and public payers, including the 5% Medicare Part B database (2002–2011) for patients ≥65 years and the MarketScan database (2004 to June 2011) for patients <65 years. Understanding the accurate trends in the use of UKA on a national scale is important for legislative bodies, healthcare administrators, and physicians.

MATERIALS AND METHODS

The 2002 to 2011 5% sample of the Medicare data (Part B) and the 2004 to June 2012 MarketScan Commercial and Medicare Supplemental databases were used to evaluate the prevalence of UKA in elderly (≥65 years) and younger (<65 years) populations, respectively. The UKA procedures were identified using the CPT code 27446.

The prevalence of UKA was stratified by age, gender, census region, Charlson Comorbidity Index, Medicare buy-in status, and diagnosis. The buy-in status is a proxy for the socioeconomic status as it reflects the state subsidizing the health insurance premium for the beneficiary. The Charlson Comorbidity Index is a composite score that has been used to assess the comorbidity level of a patient by taking into account the number and the severity of comorbid conditions.24 For the elderly population, the rate of UKA was subsequently evaluated based on the number of beneficiaries for that particular age-gender group and year in both databases. Poisson regression was used to evaluate the annual rate of change in the UKA rate for assessing temporal changes considering year as a covariate. Age and gender, as well as 2-way interaction terms for age, gender, and year, were also considered as covariates. 

Continue to: RESULTS...

 

 

RESULTS

For the time periods analyzed, a total of 5235 and 23,310 UKA procedures were identified from the 5% Medicare and MarketScan databases, respectively. A peak in the prevalence appeared around 2008 for the elderly population and in 2009 for the younger population (Figure 1). When normalized by the size of the population segment, the rate of UKA was found to be approximately 5 times greater in the elderly population, increasing from 369 in 2002 to 639 in 2008, but plateauing to 561 in 2011. Extrapolating to the 100% Medicare population, these numbers increased to 7380, 12,780, and 11,220, respectively. Temporal changes in the UKA rate were significant, increasing from 24.5 UKAs per 100,000 persons in 2002 to 43.1 UKAs in 2008, followed by a decline to 36.5 in 2011 (P < .0001) (Figure 2). The rates of UKA generally increased from 2002 to 2008 for both males and females in the Medicare cohort; however, the rates of UKA in female patients continuously declined from 2008 onward, whereas the UKA rates in male patients decreased in 2009, followed by an increase in 2010 and 2011 (Figure 2). For the younger population, there was a slight increase in the rate of UKA from 2004 to approximately 2009, after which the rates for both males and females remained relatively steady. When put in the context of the prevalence of TKA, the prevalence of UKA fluctuated during the same time period. In the Medicare population, the prevalence of UKA ranged from 4.3% (2005) to 5.9% (2008) of the TKA prevalence between 2002 and 2011. In the younger MarketScan population, the prevalence of UKA ranged from 6.7% (2005) to 8.9% (2008) between 2004 and June 2012.

The UKA rate differed significantly according to gender (P = .0209), with higher rates for males. Although there were no age-related differences (P = .3723), age–gender interactions were found to be significant (P < .0001). For males, the largest rate of UKA in the most recent year of data was observed in the 70- to 74-year-old group, followed by the 75- to 79- and the 65- to 69-year-old groups (Figure 3). For females, those in the 65- to 69- and the 70- to 74-year-old groups had the highest rate of UKA. In the younger cohort, there were increases in the UKA rates since 2004. These rates appeared to be relatively stable from the 2008 or 2009 period onward, except for females 55–64 years, which demonstrated a steady decline since 2008. Analysis of data obtained over the past few years showed that males 55–64, 65–69, and 70–74 years were the only age–gender groups whose UKA rates appeared to be trending upward.

The vast majority of elderly UKA patients were white (95.5%), and when stratified by census region, the highest proportion of UKA procedures was observed in the South and the Midwest (Figure 4). Furthermore, among patients <65 years, 64.2% had a Charlson score of 0 compared to 40.8% in the elderly group (Figure 5). For the Medicare population, based on their receipt of state subsidies for their insurance premiums, 5.1% of patients were of lower socioeconomic status. Osteoarthritis was diagnosed in 99.4% and 97.3% of the MarketScan and Medicare cohorts, respectively.

In the Medicare cohort, gender (P = .0209) and year of operation (P < .0001) were found to be significantly associated with the rate of UKA, along with age-gender (P < .0001) and gender-year (P = .0202) interaction terms. In the MarketScan cohort, age (P = .0173), gender (P = .0017), and year of operation (P = .0002) were found to be significantly associated with UKA rate. Two-way interactions between age-gender (P = .0018), age–year (P = .0207), and gender-year (P = .0017) were also found to be statistically significant factors.

Continue to: DISCUSSION...

 

 

DISCUSSION

The results of our study indicate that between 2002 and 2011, a steadily increasing number of UKA procedures was performed in the United States, and a significant proportion of the surgeries was performed on patients <65 years. Without the MarketScan database data, we would have missed more than 23,000 UKA cases performed during this 10-year time period. This finding validates our research methodology that incorporated data on privately insured younger (<65 years) patients, which is something that has not been done when examining the epidemiology of UKA.

To our knowledge, there are only 2 other publications attempting to quantify the incidence of UKA procedures performed in the United States. Bolognesi and colleagues23 used the Medicare 5% sample to assess trends in the use of knee arthroplasty from 2000 to 2009. The authors reported that a total of 68,603 patients underwent unilateral total knee arthroplasty (n = 65,505) or unicompartmental knee arthroplasty (n = 3098) over this 10-year time period. Given that there is substantial overlap of our time periods, it is not surprising that our Medicare numbers are similar (3098 vs 5235). In their study, the use of TKA increased 1.7-fold, whereas the use of UKA increased 6.2-fold23. In our analysis of the Medicare (2011 vs 2002) and MarketScan (2011 vs 2004) databases, there was a 1.3-fold and a 3.4-fold increase in the number of TKAs performed. Concomitantly, the use of UKA increased 1.5-fold and 2.8-fold, respectively, in these databases over the same time periods. The reason for the slight discrepancy in the numbers may be attributable to the peak occurring in 2008. The other publication on the subject by Riddle and colleagues8 focused on the time period 1998 to 2005 and used implant manufacturer’s sales data cross-referenced to a database of 44 hospitals to derive their national estimates. Using their unique methodology, the authors calculated an incidence of UKA, ranging from 6570 implants in 1998 to 44,990 in 2005. They reported that UKA use during the study period increased by 3 times the rate of TKA in the United States, with an average yearly percentage increase in the number of UKA procedures of 32.5% compared to 9.4% for TKA procedures. It is difficult to account for the discrepancy in the number of UKAs performed reported between our current study and that of Riddle and colleagues;8 however, the fact that the authors used implant manufacturer’s individual sales numbers may indicate that a portion of UKA patients was not captured in either the Medicare 5% or the MarketScan database. Nonetheless, in our analysis, the annual increase in the number of UKA procedures performed during the time periods studied averaged 5.8% in the older population and 25.4% in the younger population compared to the increase in the number of TKA procedures, which averaged 3.6% and 33.9% in the older and younger populations, respectively. In addition, in our study, the percentage of UKAs performed relative to the number of TKAs during the time intervals studied varied from a low of 4.3% to a high of 5.9% in the older population and from a low of 6.7% to a high of 8.9% in the younger population.

During the 10-year period of this study, a general upward trend appeared in the total number of unicompartmental knee arthroplasties performed in both the Medicare and the MarketScan databases. The rate at which the procedure was performed increased in the Medicare population from 24.5 to 36.5 (per 100,000 persons) over a 10-year time period and in the MarketScan cohort from 5.9 to 7.4 (per 100,000 persons) over an 8.5-year time period. This indicates both a larger absolute and a relative rate increase in UKA procedures in the elderly population. Around 2008 and 2009, the data showed a slight dip in the rate of UKA in the Medicare population and a plateau in the rate in the MarketScan database. Although this may be a spurious finding in the data that would be smoothed out with a longer time period investigated, it is interesting that this finding coincided with a national economic downturn. Although it might be expected that macroeconomics may affect the utilization of elective surgery such as total joint replacement, Kurtz and colleagues25 investigated this particular question and found that neither the economic downturns of 2001 or those of 2008 and 2009 had a significant impact on the incidence of total joint replacement surgeries.

Incorporation of the MarketScan database data indicated that a significant proportion of patients undergoing UKA were <65 years and that there was a slight but increasing rate of procedures performed on this age cohort over the past decade. A similar finding has been reported in the Finnish Arthroplasty Registry. Leskinen and colleagues26 reported that the incidence of UKAs among individuals 30 to 59 years increased from 0.2 (per 100,000 persons) to 10 (per 100,000 persons) from 1980 to 2006 and that most of the increase occurred among patients 50 to 59 years. The fact that younger age is no longer observed as a relative contraindication to this procedure is supported by several clinical investigations. Cartier and colleagues27 reported 93% survival at 10 years in patients with a mean age of 65 years, but included patients as young as 28 years, claiming that the results for younger patients were no worse than those for older patients in the series. Pandit and colleagues17 compared the results of 245 young patients (<60 years) to those of 755 older patients (>60 years) and found a survival rate of 97% at 10 years, with no significant difference in mean functional outcomes, failure rate, or survival between the groups at >5 years of follow-up. Given that patients <65 years now account for approximately half of the TKAs performed each year, with the greatest increase in volume among patients between 45 and 54, it is clear that investigations on the epidemiology of UKA must take into account this increasingly relevant younger patient cohort.28

Continue to: Our data indicate...

 

 

Our data indicate that only approximately 5% of UKA patients were non-white and another 5% were from lower socioeconomic status. These findings have been observed in multiple other studies looking at the epidemiology of total joint replacement in the United States.29 Bolognesi and colleagues23 reported that although “non-white race” patients made up 12% of the general Medicare sample they were analyzing, these patients accounted for only 5% and 3% of the total knee arthroplasty and unicompartmental knee arthroplasty populations, respectively. Although it is beyond the scope of this paper to delve into the reasons for this discrepancy, it may be related to differences in access to care, healthcare literacy, and trust of patients in the healthcare system.30,31

Our study, like all those based on administrative claims, has several notable inherent limitations. Coding inaccuracies as well as the potential for systematic bias (eg, underreporting) may affect the accuracy of our results. Although the MarketScan Commercial Research Database (Truven Health Analytics) includes nationally representative information for >180 million patients covered with private insurance, it is possible that we have missed some patients who underwent UKA during the time period investigated. However, we feel that the number missed is probably small and does not affect our conclusions in any meaningful manner.

CONCLUSION

This novel analysis of 2 separate administrative claims databases, which more accurately captures all patients undergoing UKA, indicates that there has been a steady increase in the rate of the procedure over the past decade and that a significant proportion of the surgeries were performed in younger (<65 years) patients. Understanding the accurate trends in the use of UKA on a national scale is important for legislative bodies, healthcare administrators, as well as physicians. Furthermore, given the increasing rates of UKA in patients <65 years old, and the increased burden on implants for withstanding increased activities and repetitive loads, it remains imperative to strive to optimize materials, implant designs, and surgical techniques to enhance implant durability.

ABSTRACT

Publications on the prevalence of unicompartmental knee arthroplasty in the United States using a single database may have underestimated the “true” number of cases performed, given that several unicondylar knee arthroplasty (UKA) patients are <65 years and have private insurance. The prevalence of UKA in elderly (≥65 years) and younger (<65 years) populations was evaluated using the 2002 to 2011 5% sample of the Medicare data (Part B) and the 2004 to June 2012 MarketScan Commercial and Medicare Supplemental databases, respectively. The prevalence of UKA was stratified by age, gender, census region, Charlson comorbidity index, Medicare buy-in status, and diagnosis. The annual rate of change in the UKA rate was examined using Poisson regression to evaluate temporal changes considering year as a covariate.

A total of 5235 and 23,310 UKA procedures were identified from the 5% Medicare and MarketScan databases, respectively. The rates of UKA generally increased until 2008, after which there was a decline. In both cohorts, gender and year of operation were found to be significantly associated with UKA rate. Analysis of data obtained over the past few years revealed that males 55 to 64 years, 65 to 69 years, and 70 to 74 years were the only age-gender groups whose UKA rates appeared to be trending upward.

From 2002 to 2011, the rate of UKAs performed in the United States has increased, and a significant proportion of the surgeries were performed in younger (<65 years) patients.

Continue to: Unicondylar knee arthroplasty...

 

 

Unicondylar knee arthroplasty (UKA) is an effective surgical treatment for symptomatic degenerative joint disease of a single compartment of the knee, providing improved functional outcomes compared with total knee arthroplasty (TKA).1-3 It has been estimated that the proportion of patients undergoing TKA, who meet the criteria for UKA, varies between 21% and 47%.4,5 However, it has been variably estimated that the usage of UKA ranges from 0% to 50% (mean, 8%) of all primary knee arthroplasties.5-8 It is believed that this discrepancy between the percentage of patients who meet indications for the surgery and those who receive it is associated with various factors, including surgeon training and experiences, diverse indications, economic factors, as well as acknowledgment of the reportedly higher revision rates of UKA than those of TKA in national joint registries.7,9-11

According to their classic article, Kozinn and Scott12 outlined the indications for UKA that, in their experience, led to the most successful outcomes, including age >60 years, weight <82 kg, low physical demand, localized arthritis with no full-thickness chondromalacia elsewhere in the joint, intact anterior cruciate ligament, minimal deformity, and flexion >90°. More recently, indications have been expanded to include younger and more active patients, higher body mass index, and some patterns of patellofemoral chondromalacia, with an increasing number of publications reporting successful clinical outcomes in these cohorts as well.13-17 Taken together, it is clear that the “classic” strict indications for UKA can be safely expanded, which have and will result in an increased number of these procedures being performed above and beyond that which might be predicted based on demographic trends alone.

A growing body of literature has been published on the prevalence and projections of orthopedic procedures in the United States.18-20 Several studies have focused their analysis on 1 of several large administrative databases, including the Nationwide Inpatient Sample, the 5% Medicare Part B database, and the National Hospital Discharge Survey.18,20-23 A concern with limiting an analysis of the prevalence of unicompartmental knee arthroplasty to these particular databases is that it may underestimate the “true” number of cases performed in the United States, given that several UKA patients are <65 years and have private insurance, and therefore, would not be captured statistically by a database that collects data on patients ≥65 years.

The purpose of this study was to quantify the current prevalence and epidemiology of UKA in the U.S. patient population. Our hypothesis was that the number of procedures and the procedural rate of UKA are increasing over time. Furthermore, this increase may be attributed to an increase in select age- or gender-based segments of the population. To test this hypothesis, we analyzed 2 separate large claims databases to capture patients over a spectrum of age and inclusive of both private and public payers, including the 5% Medicare Part B database (2002–2011) for patients ≥65 years and the MarketScan database (2004 to June 2011) for patients <65 years. Understanding the accurate trends in the use of UKA on a national scale is important for legislative bodies, healthcare administrators, and physicians.

MATERIALS AND METHODS

The 2002 to 2011 5% sample of the Medicare data (Part B) and the 2004 to June 2012 MarketScan Commercial and Medicare Supplemental databases were used to evaluate the prevalence of UKA in elderly (≥65 years) and younger (<65 years) populations, respectively. The UKA procedures were identified using the CPT code 27446.

The prevalence of UKA was stratified by age, gender, census region, Charlson Comorbidity Index, Medicare buy-in status, and diagnosis. The buy-in status is a proxy for the socioeconomic status as it reflects the state subsidizing the health insurance premium for the beneficiary. The Charlson Comorbidity Index is a composite score that has been used to assess the comorbidity level of a patient by taking into account the number and the severity of comorbid conditions.24 For the elderly population, the rate of UKA was subsequently evaluated based on the number of beneficiaries for that particular age-gender group and year in both databases. Poisson regression was used to evaluate the annual rate of change in the UKA rate for assessing temporal changes considering year as a covariate. Age and gender, as well as 2-way interaction terms for age, gender, and year, were also considered as covariates. 

Continue to: RESULTS...

 

 

RESULTS

For the time periods analyzed, a total of 5235 and 23,310 UKA procedures were identified from the 5% Medicare and MarketScan databases, respectively. A peak in the prevalence appeared around 2008 for the elderly population and in 2009 for the younger population (Figure 1). When normalized by the size of the population segment, the rate of UKA was found to be approximately 5 times greater in the elderly population, increasing from 369 in 2002 to 639 in 2008, but plateauing to 561 in 2011. Extrapolating to the 100% Medicare population, these numbers increased to 7380, 12,780, and 11,220, respectively. Temporal changes in the UKA rate were significant, increasing from 24.5 UKAs per 100,000 persons in 2002 to 43.1 UKAs in 2008, followed by a decline to 36.5 in 2011 (P < .0001) (Figure 2). The rates of UKA generally increased from 2002 to 2008 for both males and females in the Medicare cohort; however, the rates of UKA in female patients continuously declined from 2008 onward, whereas the UKA rates in male patients decreased in 2009, followed by an increase in 2010 and 2011 (Figure 2). For the younger population, there was a slight increase in the rate of UKA from 2004 to approximately 2009, after which the rates for both males and females remained relatively steady. When put in the context of the prevalence of TKA, the prevalence of UKA fluctuated during the same time period. In the Medicare population, the prevalence of UKA ranged from 4.3% (2005) to 5.9% (2008) of the TKA prevalence between 2002 and 2011. In the younger MarketScan population, the prevalence of UKA ranged from 6.7% (2005) to 8.9% (2008) between 2004 and June 2012.

The UKA rate differed significantly according to gender (P = .0209), with higher rates for males. Although there were no age-related differences (P = .3723), age–gender interactions were found to be significant (P < .0001). For males, the largest rate of UKA in the most recent year of data was observed in the 70- to 74-year-old group, followed by the 75- to 79- and the 65- to 69-year-old groups (Figure 3). For females, those in the 65- to 69- and the 70- to 74-year-old groups had the highest rate of UKA. In the younger cohort, there were increases in the UKA rates since 2004. These rates appeared to be relatively stable from the 2008 or 2009 period onward, except for females 55–64 years, which demonstrated a steady decline since 2008. Analysis of data obtained over the past few years showed that males 55–64, 65–69, and 70–74 years were the only age–gender groups whose UKA rates appeared to be trending upward.

The vast majority of elderly UKA patients were white (95.5%), and when stratified by census region, the highest proportion of UKA procedures was observed in the South and the Midwest (Figure 4). Furthermore, among patients <65 years, 64.2% had a Charlson score of 0 compared to 40.8% in the elderly group (Figure 5). For the Medicare population, based on their receipt of state subsidies for their insurance premiums, 5.1% of patients were of lower socioeconomic status. Osteoarthritis was diagnosed in 99.4% and 97.3% of the MarketScan and Medicare cohorts, respectively.

In the Medicare cohort, gender (P = .0209) and year of operation (P < .0001) were found to be significantly associated with the rate of UKA, along with age-gender (P < .0001) and gender-year (P = .0202) interaction terms. In the MarketScan cohort, age (P = .0173), gender (P = .0017), and year of operation (P = .0002) were found to be significantly associated with UKA rate. Two-way interactions between age-gender (P = .0018), age–year (P = .0207), and gender-year (P = .0017) were also found to be statistically significant factors.

Continue to: DISCUSSION...

 

 

DISCUSSION

The results of our study indicate that between 2002 and 2011, a steadily increasing number of UKA procedures was performed in the United States, and a significant proportion of the surgeries was performed on patients <65 years. Without the MarketScan database data, we would have missed more than 23,000 UKA cases performed during this 10-year time period. This finding validates our research methodology that incorporated data on privately insured younger (<65 years) patients, which is something that has not been done when examining the epidemiology of UKA.

To our knowledge, there are only 2 other publications attempting to quantify the incidence of UKA procedures performed in the United States. Bolognesi and colleagues23 used the Medicare 5% sample to assess trends in the use of knee arthroplasty from 2000 to 2009. The authors reported that a total of 68,603 patients underwent unilateral total knee arthroplasty (n = 65,505) or unicompartmental knee arthroplasty (n = 3098) over this 10-year time period. Given that there is substantial overlap of our time periods, it is not surprising that our Medicare numbers are similar (3098 vs 5235). In their study, the use of TKA increased 1.7-fold, whereas the use of UKA increased 6.2-fold23. In our analysis of the Medicare (2011 vs 2002) and MarketScan (2011 vs 2004) databases, there was a 1.3-fold and a 3.4-fold increase in the number of TKAs performed. Concomitantly, the use of UKA increased 1.5-fold and 2.8-fold, respectively, in these databases over the same time periods. The reason for the slight discrepancy in the numbers may be attributable to the peak occurring in 2008. The other publication on the subject by Riddle and colleagues8 focused on the time period 1998 to 2005 and used implant manufacturer’s sales data cross-referenced to a database of 44 hospitals to derive their national estimates. Using their unique methodology, the authors calculated an incidence of UKA, ranging from 6570 implants in 1998 to 44,990 in 2005. They reported that UKA use during the study period increased by 3 times the rate of TKA in the United States, with an average yearly percentage increase in the number of UKA procedures of 32.5% compared to 9.4% for TKA procedures. It is difficult to account for the discrepancy in the number of UKAs performed reported between our current study and that of Riddle and colleagues;8 however, the fact that the authors used implant manufacturer’s individual sales numbers may indicate that a portion of UKA patients was not captured in either the Medicare 5% or the MarketScan database. Nonetheless, in our analysis, the annual increase in the number of UKA procedures performed during the time periods studied averaged 5.8% in the older population and 25.4% in the younger population compared to the increase in the number of TKA procedures, which averaged 3.6% and 33.9% in the older and younger populations, respectively. In addition, in our study, the percentage of UKAs performed relative to the number of TKAs during the time intervals studied varied from a low of 4.3% to a high of 5.9% in the older population and from a low of 6.7% to a high of 8.9% in the younger population.

During the 10-year period of this study, a general upward trend appeared in the total number of unicompartmental knee arthroplasties performed in both the Medicare and the MarketScan databases. The rate at which the procedure was performed increased in the Medicare population from 24.5 to 36.5 (per 100,000 persons) over a 10-year time period and in the MarketScan cohort from 5.9 to 7.4 (per 100,000 persons) over an 8.5-year time period. This indicates both a larger absolute and a relative rate increase in UKA procedures in the elderly population. Around 2008 and 2009, the data showed a slight dip in the rate of UKA in the Medicare population and a plateau in the rate in the MarketScan database. Although this may be a spurious finding in the data that would be smoothed out with a longer time period investigated, it is interesting that this finding coincided with a national economic downturn. Although it might be expected that macroeconomics may affect the utilization of elective surgery such as total joint replacement, Kurtz and colleagues25 investigated this particular question and found that neither the economic downturns of 2001 or those of 2008 and 2009 had a significant impact on the incidence of total joint replacement surgeries.

Incorporation of the MarketScan database data indicated that a significant proportion of patients undergoing UKA were <65 years and that there was a slight but increasing rate of procedures performed on this age cohort over the past decade. A similar finding has been reported in the Finnish Arthroplasty Registry. Leskinen and colleagues26 reported that the incidence of UKAs among individuals 30 to 59 years increased from 0.2 (per 100,000 persons) to 10 (per 100,000 persons) from 1980 to 2006 and that most of the increase occurred among patients 50 to 59 years. The fact that younger age is no longer observed as a relative contraindication to this procedure is supported by several clinical investigations. Cartier and colleagues27 reported 93% survival at 10 years in patients with a mean age of 65 years, but included patients as young as 28 years, claiming that the results for younger patients were no worse than those for older patients in the series. Pandit and colleagues17 compared the results of 245 young patients (<60 years) to those of 755 older patients (>60 years) and found a survival rate of 97% at 10 years, with no significant difference in mean functional outcomes, failure rate, or survival between the groups at >5 years of follow-up. Given that patients <65 years now account for approximately half of the TKAs performed each year, with the greatest increase in volume among patients between 45 and 54, it is clear that investigations on the epidemiology of UKA must take into account this increasingly relevant younger patient cohort.28

Continue to: Our data indicate...

 

 

Our data indicate that only approximately 5% of UKA patients were non-white and another 5% were from lower socioeconomic status. These findings have been observed in multiple other studies looking at the epidemiology of total joint replacement in the United States.29 Bolognesi and colleagues23 reported that although “non-white race” patients made up 12% of the general Medicare sample they were analyzing, these patients accounted for only 5% and 3% of the total knee arthroplasty and unicompartmental knee arthroplasty populations, respectively. Although it is beyond the scope of this paper to delve into the reasons for this discrepancy, it may be related to differences in access to care, healthcare literacy, and trust of patients in the healthcare system.30,31

Our study, like all those based on administrative claims, has several notable inherent limitations. Coding inaccuracies as well as the potential for systematic bias (eg, underreporting) may affect the accuracy of our results. Although the MarketScan Commercial Research Database (Truven Health Analytics) includes nationally representative information for >180 million patients covered with private insurance, it is possible that we have missed some patients who underwent UKA during the time period investigated. However, we feel that the number missed is probably small and does not affect our conclusions in any meaningful manner.

CONCLUSION

This novel analysis of 2 separate administrative claims databases, which more accurately captures all patients undergoing UKA, indicates that there has been a steady increase in the rate of the procedure over the past decade and that a significant proportion of the surgeries were performed in younger (<65 years) patients. Understanding the accurate trends in the use of UKA on a national scale is important for legislative bodies, healthcare administrators, as well as physicians. Furthermore, given the increasing rates of UKA in patients <65 years old, and the increased burden on implants for withstanding increased activities and repetitive loads, it remains imperative to strive to optimize materials, implant designs, and surgical techniques to enhance implant durability.

References
  1. Hopper GP, Leach WJ. Participation in sporting activities following knee replacement: total versus unicompartmental. Knee Surg Sports Traumatol Arthrosc. 2008;16(10):973-979. doi: 10.1007/s00167-008-0596-9.
  2. Lygre SH, Espehaug B, Havelin LI, Furnes O, Vollset SE. Pain and function in patients after primary unicompartmental and total knee arthroplasty. J Bone Joint Surg, (Am). 2010;92(18):2890-2897. doi: 10.2106/JBJS.I.00917.
  3. Liddle AD, Pandit H, Judge A, Murray DW. Patient-reported outcomes after total and unicompartmental knee arthroplasty: a study of 14,076 matched patients from the National Joint Registry for England and Wales. Bone Joint J. 2015;97-B(6):793-801. doi: 10.1302/0301-620X.97B6.35155.
  4. Arno S, Maffei D, Walker PS, Schwarzkopf R, Desai P, Steiner GC. Retrospective analysis of total knee arthroplasty cases for visual, histological, and clinical eligibility of unicompartmental knee arthroplasties. J Arthroplast. 2011;26(8):1396-1403. doi: 10.1016/j.arth.2010.12.023.
  5. Willis-Owen CA, Brust K, Alsop H, Miraldo M, Cobb JP. Unicondylar knee arthroplasty in the UK National Health Service: an analysis of candidacy, outcome and cost efficacy. Knee. 2009;16(6):473-478. doi: 10.1016/j.knee.2009.04.006.
  6. Murray DW, Liddle AD, Dodd CA, Pandit H. Unicompartmental knee arthroplasty: is the glass half full or half empty? Bone Joint J. 2015;97-B(10 Suppl. A):3-8. doi: 10.1302/0301-620X.97B10.36542.
  7. Liddle AD, Judge A, Pandit H, Murray DW. Adverse outcomes after total and unicompartmental knee replacement in 101,330 matched patients: a study of data from the National Joint Registry for England and Wales. Lancet. 2014;384(9952):1437-1445. doi: 10.1016/S0140-6736(14)60419-0.
  8. Riddle DL, Jiranek WA, McGlynn FJ. Yearly incidence of unicompartmental knee arthroplasty in the United States. J Arthroplast. 2008;23(3):408-412. doi: 10.1016/j.arth.2007.04.012.
  9. Argenson JN, Blanc G, Aubaniac JM, Parratte S. Modern unicompartmental knee arthroplasty with cement: a concise follow-up, at a mean of twenty years, of a previous report. J Bone Joint Surg, (Am). 2013;95(10):905-909. doi: 10.2106/JBJS.L.00963.
  10. Koskinen E, Eskelinen A, Paavolainen P, Pulkkinen P, Remes V. Comparison of survival and cost-effectiveness between unicondylar arthroplasty and total knee arthroplasty in patients with primary osteoarthritis: a follow-up study of 50,493 knee replacements from the Finnish Arthroplasty Register. Acta Orthop. 2008;79(4):499-507. doi: 10.1080/17453670710015490.
  11. Knutson K, Lewold S, Robertsson O, Lidgren L. The Swedish knee arthroplasty register. A nation-wide study of 30,003 knees 1976-1992. Acta Orthop Scand. 1994;65(4):375-386. doi: 10.3109/17453679408995475.
  12. Kozinn SC, Scott R. Unicondylar knee arthroplasty. J Bone Joint Surg, (Am). 1989;71(1):145-150. doi: 10.2106/00004623-198971010-00023.
  13. Pennington DW. Unicompartmental knee arthroplasty in patients sixty years of age or younger. J Bone Joint Surg, (Am). 2003;85-A(10):1968-1973. doi: 10.2106/00004623-200310000-00016.
  14. Biswas D, Van Thiel GS, Wetters NG, Pack BJ, Berger RA, Della Valle CJ. Medial unicompartmental knee arthroplasty in patients less than 55 years old: minimum of two years of follow-up. J Arthroplast. 2014;29(1):101-105. doi: 10.1016/j.arth.2013.04.046.
  15. Murray DW, Pandit H, Weston-Simons JS, et al. Does body mass index affect the outcome of unicompartmental knee replacement? Knee. 2013;20(6):461-465. doi: 10.1016/j.knee.2012.09.017.
  16. Kang SN, Smith TO, Sprenger De Rover WB, Walton NP. Pre-operative patellofemoral degenerative changes do not affect the outcome after medial Oxford unicompartmental knee replacement: a report from an independent centre. J Bone Joint Surg Br. 2011;93(4):476-478. doi: 10.1302/0301-620X.93B4.25562.
  17. Pandit H, Jenkins C, Gill HS, et al. Unnecessary contraindications for mobile-bearing unicompartmental knee replacement. J Bone Joint Surg Br. 2011;93(5):622-628. doi: 10.1302/0301-620X.93B5.26214.
  18. Kurtz S, Mowat F, Ong K, Chan N, Lau E, Halpern M. Prevalence of primary and revision total hip and knee arthroplasty in the United States from 1990 through 2002. J Bone Joint Surg Am. 2005;87(7):1487-1497. doi: 10.2106/JBJS.D.02441.
  19. Kurtz SM, Ong KL, Schmier J, et al. Future clinical and economic impact of revision total hip and knee arthroplasty. J Bone Joint Surg, (Am). 2007;89(Suppl. 3):144-151. doi: 10.2106/JBJS.G.00587.
  20. Day JS, Lau E, Ong KL, Williams GR, Ramsey ML, Kurtz SM. Prevalence and projections of total shoulder and elbow arthroplasty in the United States to 2015. J Shoulder Elbow Surg. 2010;19(8):1115-1120. doi: 10.1016/j.jse.2010.02.009.
  21. Kurtz S, Ong K, Lau E, Mowat F, Halpern M. Projections of primary and revision hip and knee arthroplasty in the United States from 2005 to 2030. J Bone Joint Surg, (Am). 2007;89(4):780-785. doi: 10.2106/JBJS.F.00222.
  22. Kamath AF, Ong KL, Lau E, et al. Quantifying the burden of revision total joint arthroplasty for periprosthetic infection. J Arthroplast. 2015;30(9):1492-1497. doi: 10.1016/j.arth.2015.03.035.
  23. Bolognesi MP, Greiner MA, Attarian DE, et al. Unicompartmental knee arthroplasty and total knee arthroplasty among Medicare beneficiaries, 2000 to 2009. J Bone Joint Surg, (Am). 2013;95(22):e174. doi: 10.2106/JBJS.L.00652.
  24. Charlson ME, Pompei P, Ales KL, MacKenzie CR. A new method of classifying prognostic comorbidity in longitudinal studies: development and validation. J Chronic Dis. 1987;40(5):373-383. doi: 10.1016/0021-9681(87)90171-8.
  25. Kurtz SM, Ong KL, Lau E, Bozic KJ. Impact of the economic downturn on total joint replacement demand in the United States: updated projections to 2021. J Bone Joint Surg, (Am). 2014;96(8):624-630. doi: 10.2106/JBJS.M.00285.
  26. Leskinen J, Eskelinen A, Huhtala H, Paavolainen P, Remes V. The incidence of knee arthroplasty for primary osteoarthritis grows rapidly among baby boomers: a population-based study in Finland. Arthritis Rheum. 2012;64(2):423-428. doi: 10.1002/art.33367.
  27. Cartier P, Sanouiller JL, Grelsamer RP. Unicompartmental knee arthroplasty surgery. 10-year minimum follow-up period. J Arthroplast. 1996;11(7):782-788. doi: 10.1016/S0883-5403(96)80177-X.
  28. Kurtz SM, Lau E, Ong K, Zhao K, Kelly M, Bozic KJ. Future young patient demand for primary and revision joint replacement: national projections from 2010 to 2030. Clin Orthop Relat Res. 2009;467(10):2606-2612. doi: 10.1007/s11999-009-0834-6.
  29. Singh JA, Lu X, Rosenthal GE, Ibrahim S, Cram P. Racial disparities in knee and hip total joint arthroplasty: an 18-year analysis of national Medicare data. Ann Rheum Dis. 2014;73(12):2107-2115. doi: 10.1136/annrheumdis-2013-203494.
  30. Pierce TP, Elmallah RK, Lavernia CJ, et al. Racial disparities in lower extremity arthroplasty outcomes and use. Orthopedics. 2015;38(12): e1139-e1146. doi: 10.3928/01477447-20151123-05.
  31. Irgit K, Nelson CL. Defining racial and ethnic disparities in THA and TKA. Clin Orthop Relat Res. 2011;469(7):1817-1823. doi: 10.1007/s11999-011-1885-z.
References
  1. Hopper GP, Leach WJ. Participation in sporting activities following knee replacement: total versus unicompartmental. Knee Surg Sports Traumatol Arthrosc. 2008;16(10):973-979. doi: 10.1007/s00167-008-0596-9.
  2. Lygre SH, Espehaug B, Havelin LI, Furnes O, Vollset SE. Pain and function in patients after primary unicompartmental and total knee arthroplasty. J Bone Joint Surg, (Am). 2010;92(18):2890-2897. doi: 10.2106/JBJS.I.00917.
  3. Liddle AD, Pandit H, Judge A, Murray DW. Patient-reported outcomes after total and unicompartmental knee arthroplasty: a study of 14,076 matched patients from the National Joint Registry for England and Wales. Bone Joint J. 2015;97-B(6):793-801. doi: 10.1302/0301-620X.97B6.35155.
  4. Arno S, Maffei D, Walker PS, Schwarzkopf R, Desai P, Steiner GC. Retrospective analysis of total knee arthroplasty cases for visual, histological, and clinical eligibility of unicompartmental knee arthroplasties. J Arthroplast. 2011;26(8):1396-1403. doi: 10.1016/j.arth.2010.12.023.
  5. Willis-Owen CA, Brust K, Alsop H, Miraldo M, Cobb JP. Unicondylar knee arthroplasty in the UK National Health Service: an analysis of candidacy, outcome and cost efficacy. Knee. 2009;16(6):473-478. doi: 10.1016/j.knee.2009.04.006.
  6. Murray DW, Liddle AD, Dodd CA, Pandit H. Unicompartmental knee arthroplasty: is the glass half full or half empty? Bone Joint J. 2015;97-B(10 Suppl. A):3-8. doi: 10.1302/0301-620X.97B10.36542.
  7. Liddle AD, Judge A, Pandit H, Murray DW. Adverse outcomes after total and unicompartmental knee replacement in 101,330 matched patients: a study of data from the National Joint Registry for England and Wales. Lancet. 2014;384(9952):1437-1445. doi: 10.1016/S0140-6736(14)60419-0.
  8. Riddle DL, Jiranek WA, McGlynn FJ. Yearly incidence of unicompartmental knee arthroplasty in the United States. J Arthroplast. 2008;23(3):408-412. doi: 10.1016/j.arth.2007.04.012.
  9. Argenson JN, Blanc G, Aubaniac JM, Parratte S. Modern unicompartmental knee arthroplasty with cement: a concise follow-up, at a mean of twenty years, of a previous report. J Bone Joint Surg, (Am). 2013;95(10):905-909. doi: 10.2106/JBJS.L.00963.
  10. Koskinen E, Eskelinen A, Paavolainen P, Pulkkinen P, Remes V. Comparison of survival and cost-effectiveness between unicondylar arthroplasty and total knee arthroplasty in patients with primary osteoarthritis: a follow-up study of 50,493 knee replacements from the Finnish Arthroplasty Register. Acta Orthop. 2008;79(4):499-507. doi: 10.1080/17453670710015490.
  11. Knutson K, Lewold S, Robertsson O, Lidgren L. The Swedish knee arthroplasty register. A nation-wide study of 30,003 knees 1976-1992. Acta Orthop Scand. 1994;65(4):375-386. doi: 10.3109/17453679408995475.
  12. Kozinn SC, Scott R. Unicondylar knee arthroplasty. J Bone Joint Surg, (Am). 1989;71(1):145-150. doi: 10.2106/00004623-198971010-00023.
  13. Pennington DW. Unicompartmental knee arthroplasty in patients sixty years of age or younger. J Bone Joint Surg, (Am). 2003;85-A(10):1968-1973. doi: 10.2106/00004623-200310000-00016.
  14. Biswas D, Van Thiel GS, Wetters NG, Pack BJ, Berger RA, Della Valle CJ. Medial unicompartmental knee arthroplasty in patients less than 55 years old: minimum of two years of follow-up. J Arthroplast. 2014;29(1):101-105. doi: 10.1016/j.arth.2013.04.046.
  15. Murray DW, Pandit H, Weston-Simons JS, et al. Does body mass index affect the outcome of unicompartmental knee replacement? Knee. 2013;20(6):461-465. doi: 10.1016/j.knee.2012.09.017.
  16. Kang SN, Smith TO, Sprenger De Rover WB, Walton NP. Pre-operative patellofemoral degenerative changes do not affect the outcome after medial Oxford unicompartmental knee replacement: a report from an independent centre. J Bone Joint Surg Br. 2011;93(4):476-478. doi: 10.1302/0301-620X.93B4.25562.
  17. Pandit H, Jenkins C, Gill HS, et al. Unnecessary contraindications for mobile-bearing unicompartmental knee replacement. J Bone Joint Surg Br. 2011;93(5):622-628. doi: 10.1302/0301-620X.93B5.26214.
  18. Kurtz S, Mowat F, Ong K, Chan N, Lau E, Halpern M. Prevalence of primary and revision total hip and knee arthroplasty in the United States from 1990 through 2002. J Bone Joint Surg Am. 2005;87(7):1487-1497. doi: 10.2106/JBJS.D.02441.
  19. Kurtz SM, Ong KL, Schmier J, et al. Future clinical and economic impact of revision total hip and knee arthroplasty. J Bone Joint Surg, (Am). 2007;89(Suppl. 3):144-151. doi: 10.2106/JBJS.G.00587.
  20. Day JS, Lau E, Ong KL, Williams GR, Ramsey ML, Kurtz SM. Prevalence and projections of total shoulder and elbow arthroplasty in the United States to 2015. J Shoulder Elbow Surg. 2010;19(8):1115-1120. doi: 10.1016/j.jse.2010.02.009.
  21. Kurtz S, Ong K, Lau E, Mowat F, Halpern M. Projections of primary and revision hip and knee arthroplasty in the United States from 2005 to 2030. J Bone Joint Surg, (Am). 2007;89(4):780-785. doi: 10.2106/JBJS.F.00222.
  22. Kamath AF, Ong KL, Lau E, et al. Quantifying the burden of revision total joint arthroplasty for periprosthetic infection. J Arthroplast. 2015;30(9):1492-1497. doi: 10.1016/j.arth.2015.03.035.
  23. Bolognesi MP, Greiner MA, Attarian DE, et al. Unicompartmental knee arthroplasty and total knee arthroplasty among Medicare beneficiaries, 2000 to 2009. J Bone Joint Surg, (Am). 2013;95(22):e174. doi: 10.2106/JBJS.L.00652.
  24. Charlson ME, Pompei P, Ales KL, MacKenzie CR. A new method of classifying prognostic comorbidity in longitudinal studies: development and validation. J Chronic Dis. 1987;40(5):373-383. doi: 10.1016/0021-9681(87)90171-8.
  25. Kurtz SM, Ong KL, Lau E, Bozic KJ. Impact of the economic downturn on total joint replacement demand in the United States: updated projections to 2021. J Bone Joint Surg, (Am). 2014;96(8):624-630. doi: 10.2106/JBJS.M.00285.
  26. Leskinen J, Eskelinen A, Huhtala H, Paavolainen P, Remes V. The incidence of knee arthroplasty for primary osteoarthritis grows rapidly among baby boomers: a population-based study in Finland. Arthritis Rheum. 2012;64(2):423-428. doi: 10.1002/art.33367.
  27. Cartier P, Sanouiller JL, Grelsamer RP. Unicompartmental knee arthroplasty surgery. 10-year minimum follow-up period. J Arthroplast. 1996;11(7):782-788. doi: 10.1016/S0883-5403(96)80177-X.
  28. Kurtz SM, Lau E, Ong K, Zhao K, Kelly M, Bozic KJ. Future young patient demand for primary and revision joint replacement: national projections from 2010 to 2030. Clin Orthop Relat Res. 2009;467(10):2606-2612. doi: 10.1007/s11999-009-0834-6.
  29. Singh JA, Lu X, Rosenthal GE, Ibrahim S, Cram P. Racial disparities in knee and hip total joint arthroplasty: an 18-year analysis of national Medicare data. Ann Rheum Dis. 2014;73(12):2107-2115. doi: 10.1136/annrheumdis-2013-203494.
  30. Pierce TP, Elmallah RK, Lavernia CJ, et al. Racial disparities in lower extremity arthroplasty outcomes and use. Orthopedics. 2015;38(12): e1139-e1146. doi: 10.3928/01477447-20151123-05.
  31. Irgit K, Nelson CL. Defining racial and ethnic disparities in THA and TKA. Clin Orthop Relat Res. 2011;469(7):1817-1823. doi: 10.1007/s11999-011-1885-z.
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  • Prior publications on prevalence of unicondylar knee arthroplasty (UKA) in the United States using a single database may have underestimated the “true” number of cases performed.
  • For the time periods analyzed, a total of 5,235 and 23,310 UKA procedures were identified from the 5% Medicare and MarketScan databases, respectively.
  • Rates of UKA generally increased until 2008, after which there was a decline through 2012.
  • Gender and year of operation were found to be significantly associated with UKA rate.
  • Males ages 55-64, 65-69, and 70-74 were the only age-gender groups whose UKA rates appear to be trending upward.
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Fragility Fractures: Diagnosis and Treatment

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ABSTRACT

Fragility fractures are estimated to affect 3 million people annually in the United States. As they are associated with a significant mortality rate, the prevention of these fractures should be a priority for orthopedists. At-risk patients include the elderly and those with thyroid disease, diabetes, hypertension, and heart disease. Osteoporosis is diagnosed by the presence of a fragility fracture or by dual-energy x-ray absorptiometry (DXA) in the absence of a fragility fracture. In 2011, the United States Preventive Services Task Force (USPSTF) recommended that all women ≥65 years should be screened for osteoporosis by DXA. Women <65 years with a 10-year fracture risk =/> than that of a 65-year-old white woman should also be screened for osteoporosis. Lifestyle changes, such as calcium and vitamin D supplementation, exercise, and smoking cessation, are non-pharmacologic treatment options. The National Osteoporosis Foundation recommends treating osteoporosis with pharmacotherapy in patients with a high risk for fracture (T score <–2.5) or history of fragility fracture. Understanding risk factors and eliminating medications known to cause decreased BMD are vital to prevention and will be necessary to limit these fractures and their associated expenses in the future.

Continue to: Fragility fractures are caused by...

 

 

Fragility fractures are caused by falls from standing height or repetitive physiological loads.1 With the growing aging population in the United States, it is estimated that 3 million people will be affected by fragility fractures yearly.2 In the setting of osseous insufficiency, fractures that are typically associated with high-energy trauma are encountered in patients who simply trip over a parking lot curb or fall off their bike. After surgery, the severe disruption of patients’ lives continues with a prolonged rehabilitation period.

Fragility fractures are not only traumatizing for patients; they are also associated with significantly increased mortality. A study by Gosch and colleagues found that 70.6% of patients died during the normal follow-up period, and 29.4% of patients died within the first year of suffering a fracture.3 Also, the mean life expectancy post-fragility fracture was only 527 days.3 Diagnosis and treatment of osteoporosis is imperative to prevent fragility fractures before they occur.

RISK FACTORS AND CAUSES

The incidence of fragility fractures increases in patients with comorbidities such as thyroid disease, diabetes, hypertension, and heart disease.4 Hyperthyroidism and treated hypothyroidism cause an imbalance between osteoblast and osteoclast activity, resulting in osteoporosis.5 A thyroid-stimulating hormone level < 0.1 increases the risk of vertebral and non-vertebral fractures by a factor of 4.5 and 3.2 mIU/L respectively.4 Patients with diabetes also have an increased risk of fragility fractures, which is due to impaired healing capabilities, especially that of bone healing. Approximately 2 million people are affected by type 1 diabetes in the United States, and 20% of those patients will develop osteoporosis.6

Hypertension and osteoporosis are 2 diseases that occur often in the elderly. Common etiological factors believed to cause both hypertension and osteoporosis are low calcium intake, high consumption of salt, and vitamin D and vitamin K deficiency. Also, hypertension treated with loop diuretics has been found to cause negative effects on bone and increase the risk of osteoporosis.7 The only antihypertensive medications that preserve bone mineral density (BMD) and reduce fracture risk are thiazide diuretics.7 Lastly, an association between coronary artery disease and osteoporosis has been hypothesized. The link is not completely understood, but it is believed that oxidative stress and inflammation are the culprits in both diseases.8 In contrast to previous hypotheses, Sosa and colleagues found an independent association between beta blockers and fragility fractures.9 The idea that beta blockers and fragility fractures are linked is still controversial and needs more study. Unlike beta blockers, statins provide a protective effect on bone. They increase BMD and reduce fracture risk by inhibiting osteoclastogenesis.10

In addition to loop diuretics and beta blockers, inhaled glucocorticoids, oral glucocorticoids, proton pump inhibitors (PPIs), Hreceptor antagonists, and anticonvulsants decrease bone density and increase the incidence of fragility fractures.11 Chronic glucocorticoid therapy is the most common cause of secondary osteoporosis. Osteoblasts and osteocytes undergo apoptosis in the presence of glucocorticoids.12 Patients on glucocorticoid therapy have an increased risk of fracture, even with higher BMD values.13 Bone changes that occur while a patient is taking glucocorticoids may not be detected during BMD testing. Therefore, a high level of suspicion of osteoporosis in patients on long-term glucocorticoids is imperative.

Proton pump inhibitors are among the most prescribed medications in the world; they reduce bone resorption, increasing the risk of fracture.14 Proton pump inhibitors and H2 receptor antagonists are hypothesized to cause malabsorption of calcium and indirectly cause osteoporosis. The risk of osteoporosis increases with the length of PPI treatment.15 However, exposure lasting <7 years does not increase the risk of fracture.16 It is recommended that patients on long-term PPIs be referred for BMD testing.

An association between anticonvulsants and osteoporosis has been found in observational studies. The mechanism of this association is not yet fully understood, but it is believed that exacerbation of vitamin D deficiency leads to increased bone metabolism.17 Gastrointestinal (GI) calcium absorption also decreases with anticonvulsant use. Prolonged antiepileptic therapy and high-dose therapy rapidly decrease BMD. Primidone, carbamazepine, phenobarbital, and phenytoin are the drugs most often associated with decreased BMD. Osteoporosis and fragility fracture in these patients can be prevented with calcium, vitamin D, and the bisphosphonate risedronate. These medications have been shown to improve BMD by 69%.18

Continue to: DIAGNOSIS...

 

 

DIAGNOSIS

Osteoporosis is diagnosed by the presence of a fragility fracture or by dual-energy x-ray absorptiometry (DXA) in the absence of a fragility fracture.19 Measurements of the femoral neck by DXA are used to diagnose osteoporosis, although DXA can also be used to measure the bone density of the spine and peripheral skeleton.20

The World Health Organization developed a set of T score criteria to diagnose osteoporosis in postmenopausal women (Table 1). A T score >-1 is normal, <-1 but >-2.5 signifies osteopenia, <-2.5 is osteoporosis, and <-2.5 with fragility fracture is severe osteoporosis.19 The Z score, not the T score, should be used to assess osteoporosis in premenopausal women, men <50 years, and children (Table 2). The Z score is calculated by comparing the patient’s BMD with the mean BMD of their peers of a similar age, race, and gender.19 Z scores <-2.0 indicate low BMD for chronological age. A Z score > -2.0 is considered within the expected range for age.20 Bone mineral density testing is the rate- limiting step to starting osteoporosis treatment.21 Without testing, treatment of osteoporosis is very unlikely.

Table 1. T Score Criteria

T score

Diagnosis

> -1.0

Normal

-1.0 to -2.5

Osteopenia

< -2.5

Osteoporosis

< -2.5 with fragility fracture

Severe osteoporosis

 

 

 

 

 

 

 

 

 

Table 2. Z Score Criteria

Z score

Diagnosis

> -2.0

Normal BMD for age

< -2.0

Low BMD for age

 

 

 

 

 

The World Health Organization also developed a tool to predict fracture risk. The Fracture Risk Assessment Tool uses fracture history in addition to other risk factors to predict a patient’s 10-year risk of major fracture.22 Risk factors used to assess fracture risk include age, sex, weight, height, previous fracture, parental hip fracture history, current smoker, glucocorticoid use, rheumatoid arthritis, secondary osteoporosis, excessive alcohol use, and femoral neck BMD.

In 2011, the United States Preventive Services Task Force (USPSTF) recommended that all women ≥65 years should be screened for osteoporosis by DXA. Women <65 years with a 10-year fracture risk =/> than that of a 65-year-old white woman should also be screened for osteoporosis. These recommendations are different for men. It was concluded that the evidence was insufficient to support osteoporosis screening in men.23 As of April 2017, Centers for Medicare and Medicaid Services current reimbursement rates for DXA scans are, on average, $123.10 in the hospital setting and $41.63 in the office setting. The axial DXA CPT code is 77080.

Continue to: TREATMENT...

 

 

TREATMENT

NONPHARMACOLOGIC

Patients with mild osteoporosis may be treated first non-pharmacologically. Lifestyle changes such as calcium and vitamin D supplementation, exercise, and smoking cessation are non-pharmacologic treatment options. Calcium carbonate and calcium citrate are common supplements. Calcium carbonate is 40% elemental calcium, whereas calcium citrate supplements are only 21% elemental calcium. Calcium supplements are best absorbed when taken with food.24 The recommended daily total calcium intake is 1200 mg.25 Only 500 to 600 milligrams of calcium can be absorbed by the GI tract at a time. Therefore, calcium supplements should be taken at least 4 to 5 hours apart.24Patients should also be counseled that calcium supplements may cause GI side effects such as bloating and constipation. To reduce side effects, patients can slowly increase the dose of calcium to a therapeutic level.

Vitamin D supplementation works best in conjunction with calcium supplementation. Vitamin D functions to regulate calcium absorption in the intestine and stimulate bone resorption and maintain the serum calcium concentration. The National Osteoporosis Foundation recommends 800 to 1000 international units of vitamin D daily.24 Lifestyle changes may be sufficient to stop the progression of osteoporosis in its early stages. Once osteoporosis becomes severe enough, pharmacotherapy is needed to stop further bone destruction and improve BMD.

PHARMACOLOGIC

After an initial fragility fracture, the risk of additional ones increases significantly, making treatment of osteoporosis essential. The National Osteoporosis Foundation recommends treating osteoporosis with pharmacotherapy in patients with a high risk of fracture (T score <-2.5) or history of fragility fracture.26 Bisphosphonates inhibit bone resorption and are considered the first-line therapy for postmenopausal women with osteoporosis. A common side effect of oral bisphosphonates is GI toxicity. Patients are advised to avoid lying down for at least 30 minutes after medication administration to avoid esophageal irritation. Oral bisphosphonates should also be taken in the morning on an empty stomach with at least 8 ounces of water. Recurrent bisphosphonate use should be avoided in patients with chronic kidney disease. Oral alendronate and risedronate are typically discontinued after 5 years of use.27 Long-term bisphosphonate use may cause an increased risk of fragility fracture due to oversuppression of bone turnover. To avoid this risk, bisphosphonate “drug holidays” are an option. Bisphosphonates accumulate over time, creating reservoirs. Even after therapy is stopped, patients continue to have therapeutic effects for 2 to 5 years.28

Bisphosphonates are available in both oral and intravenous forms. Alendronate is available in doses of 10 mg and 70 mg for daily and weekly administration, respectively. Both are available in tablet form, but the 70 mg weekly dose is also available in a dissolvable formulation. Alendronate is available in a reduced dose for osteoporosis prevention. Alendronate dosing for osteoporosis prevention is 5 mg daily or 35 mg weekly. Risedronate is dosed as 5 mg daily, 35 mg weekly, or 150 mg monthly. Intravenous bisphosphonates are indicated when oral bisphosphonates are not tolerated, only after vitamin D has been assessed and is within the normal range. Zoledronic acid is administered as a 15-minute infusion once a year.

Teriparatide (Forteo; PTH-1-34) is available for glucocorticoid-induced osteoporosis, postmenopausal women, and men with severe osteoporosis. It is indicated for patients in whom bisphosphonate treatment has failed or those who do not tolerate bisphosphonates. Teriparatide is a synthetic parathyroid hormone (PTH) that acts as an anabolic agent, stimulating bone formation, maturation, and remodeling.29 In addition to its application as a bone-building hormone, teriparatide has gained popularity for various off-label uses. These include accelerated osteosynthesis, stress fracture healing, and in the nonoperative treatment of osteoarthritis.29 Parathyroid hormone has been shown to stimulate the maturation, proliferation, and maintenance of osteoblast progenitor cells. More recently, PTH has been shown to regulate chondrocyte signaling, as well as differentiation and maturation. Further study on the chondroregenerative potential of PTH has demonstrated its efficacy as a novel disease-modifying agent in the treatment of osteoarthritis.29 Teriparatide is administered as a daily subcutaneous injection. The United States dosing is 600 mcg/2.4 mL. Adverse effects such as orthostatic hypotension and osteosarcoma may occur. BMD testing should be performed 1 to 2 years after initiation of teriparatide and every 2 years thereafter.26

Abaloparatide (Tymlos), a human parathyroid hormone, is another treatment option for postmenopausal women at risk of osteoporotic fracture. In a study comparing the efficacy of abaloparatide and teriparatide, treatment with abaloparatide was found to induce higher BMD levels in a time frame of 12 months. The BMD differences could be attributed to many factors, such as an enhanced net anabolic effect or a reduced osteoblast expression. Furthermore, the risk of developing new vertebral and nonvertebral fractures decreased in the abaloparatide group compared with the placebo group over a period of 18 months.30

Continue to: The recommended daily dose for abaloparatide...

 

 

The recommended daily dose for abaloparatide is 80 mcg via subcutaneous injection with calcium and vitamin D supplements.31 Adverse reactions were consistent between abaloparatide and teriparatide, and included hypercalcemia, hypercalciuria, and orthostatic hypotension.30 The use of parathyroid analogs for >2 years is not recommended due to the risk of osteosarcoma.

Denosumab (Prolia) is a monoclonal antibody that stops osteoclastogenesis by blocking the binding of RANKL to RANK.31 It is indicated for patients intolerant to bisphosphonates or with impaired kidney function. Prolia is administered subcutaneously in 60 mg doses every 6 months in men and postmenopausal women with osteoporosis. Prolia is contraindicated in patients with hypersensitivity to any component of the medication, pregnancy, and hypocalcemia.

Selective estrogen receptor modulators (SERMs), such as raloxifene and tamoxifen, can treat osteoporosis effectively in postmenopausal women. Raloxifene is considered the SERM of choice due to the availability of more robust safety and efficacy data. Raloxifene increases BMD while decreasing bone resorption and bone turnover.32 It is also used to reduce breast cancer risk; however, it increases the risk of thromboembolic events and hot flashes. Tamoxifen is not typically used to treat osteoporosis, but women treated for breast cancer with tamoxifen receive some bone protection.

Lastly, calcitonin and strontium ranelate are also options to treat osteoporosis. However, both calcitonin and strontium ranelate have weak effects on BMD. Calcitonin only transiently inhibits osteoclast activity.33 Therefore, medications like bisphosphonates, teriparatide, denosumab, and SERMs are preferred.

A summary of medications used to treat osteoporosis can be found in Table 3.

Table 3. Overview of Common Medications Used in the Treatment and Prevention of Osteoporosis

Medication

Indication

Dosing

Calcium supplementation

Mild osteoporosis

1200 mg oral/d

Vitamin D supplementation

Mild osteoporosis

800 to 1000 IU oral/d

Alendronate

Postmenopausal osteoporosis

 

 

Osteoporosis prevention

10 mg oral/d

70 mg oral/wk

 

5 mg/d

35 mg/wk

Risedronate

Postmenopausal osteoporosis

5 mg oral/d

35 mg oral/wk

150 mg oral/mo

Teriparatide (Forteo)

Glucocorticoid-inducted osteoporosis, postmenopausal osteoporosis, men with severe osteoporosis

600 mcg/2.4 mL subcutaneous/d

Abaloparatide (Tymlos)

Postmenopausal osteoporosis

80 mcg subcutaneous/d

Denosumab (Prolia)

Patients intolerant to bisphosphonates; patients with impaired kidney function.

60 mg subcutaneous every 6 mo

Raloxifene

Postmenopausal osteoporosis

60 mg oral/d

Tamoxifen

Postmenopausal osteoporosis

20 mg oral/d

Calcitonin

Postmenopausal osteoporosis

100 units intramuscular or subcutaneous/d

200 units (1 spray) intranasal/d

Strontium ranelate

Postmenopausal osteoporosis Severe osteoporosis in men

2 g/d dissolved in water, prior to bedtime

Not recommended in CrCl <30 mL/min

Abbreviation: CrCl, creatinine clearance.

CONCLUSION

With a growing aging population, the prevalence of osteoporosis is expected to increase. By 2025, experts estimate that there will be 2 million fractures yearly, costing the United States upwards of $25 billion.34,35 This estimate does not include the cost of lost productivity or disability, which will likely cost billions more.34,35 Understanding risk factors and eliminating medications known to cause decreased BMD are vital. Obtaining a BMD measurement is the rate-limiting step for treatment initiation. Without an appropriate diagnosis, treatment is unlikely. As providers, it us our responsibility to maintain a high level of suspicion of osteoporosis in the elderly and promptly diagnose and treat them.

References
  1. Dietz SO, Hofmann A, Rommens PM. Haemorrhage in fragility fractures of the pelvis. Eur J Trauma Emerg Surg. 2015;41:363-367. doi: 10.1007/s00068-014-0452-1
  2. Burge R, Dawson-Hughes B, Solomon DH, Wong JB, King A, Tosteson A. Incidence and economic burden of osteoporosis-related fractures in the United States, 2005-2025. J Bone Miner Res. 2007;22(3):465-475. doi: 10.1359/jbmr.061113.
  3. Gosch M, Hoffmann-Weltin Y, Roth T, Blauth M, Nicholas JA, Kammerlander C. Orthogeriatric co-management improves the outcome of long-term care residents with fragility fractures. Arch Orthop Trauma Surg. 2016; 136(10):1403-1409. doi: 10.1007/s00402-016-2543-4.
  4. Maccagnano G, Notarnicola A, Pesce V, Mudoni S, Tafuri S, Moretti B. The prevalence of fragility fractures in a population of a region of southern Italy affected by thyroid disorders. BioMed Res Int. 2016. doi: 10.1155/2016/6017165.
  5. Mosekilde L, Eriksen EF, Charles P. Effects of thyroid hormones on bone and mineral metabolism. Endocrinol Metab Clin North Am. 1990;19(1):35-63. doi: 10.1016/S0889-8529(18)30338-4.
  6. Liporace FA, Breitbart EA, Yoon RS, Doyle E, Paglia DM, Lin S. The effect of locally delivered recombinant human bone morphogenic protein-2 with hydroxyapatite/tri-calcium phosphate on the biomechanical properties of bone in diabetes-related osteoporosis. J Orthop Traumatol.2015;16(2):151-159. doi: 10.1007/s10195-014-0327-6.
  7. Ilic K, Obradovic N, Vujasinovic-Stupar N. The relationship among hypertension, antihypertensive medications, and osteoporosis: a narrative review. Calcif. Tissue Int. 2013;92(3):217-227. doi: 10.1007/s00223-012-9671-9.
  8. Yesil Y, Ulger, Z, Halil M, et al. Coexistence of osteoporosis (OP) and coronary artery disease (CAD) in the elderly: it is not just a by chance event. Arch Gerontol Geriatr. 2012;54(3):473-476. doi: 10.1016/j.archger.2011.06.007.
  9. Sosa M, Saavedra P, de Tejada MJG, et al, GIUMO Cooperative Group. Beta-blocker use is associated with fragility fractures in postmenopausal women with coronary heart disease. Aging Clin Exp Res.2011;23(3):112-117. doi: 10.3275/7041.
  10. An T, Hao J, Li R, Yang M, Cheng G, Zou M. Efficacy of statins for osteoporosis: a systematic review and met-analysis. Osteoporos Int. 2017;28(1):47-57. doi: 10.1007/s00198-016-3844-8.
  11. Munson JC, Bynum JP, Bell J, et al. Patterns of prescription drug use before and after fragility fracture. JAMA Intern Med. 2016;176(10):1531-1538. doi: 10.1001/jamainternmed.2016.4814.
  12. Saag KG, Agnesdei D, Hans D, et al. Trabecular bone score in patients with chronic glucocorticoid therapy-induced osteoporosis treated with alendronate or teriparatide. Arthritis Rheumatol. 2016;68(9):2122-2128. doi: 10.1002/art.39726.
  13. Chuang MH, Chuang TL, Koo M, Wang YF. Trabecular bone score reflects trabecular microarchitecture deterioration and fragility fracture in female adult patients receiving glucocorticoid therapy: A pre-post controlled study. BioMed Res Int. 2017. doi: 10.1155/2017/4210217.
  14. Andersen BN, Johansen PB, Abrahamsen B. Proton pump inhibitors and osteoporosis. Curr Opin Rheumatol. 2016;28(4):420-425. doi: 10.1097/BOR.0000000000000291.
  15. Jacob L, Hadji P, Kostev K. The use of proton pump inhibitors is positively associated with osteoporosis in postmenopausal women in Germany. Climacteric. 2016; 19(5):478-481. doi: 10.1080/13697137.2016.1200549.
  16. Targownik LE, Lix LM, Metge CJ, Prior HJ, Leung S, Leslie WD. Use of proton pump inhibitors and risk of osteoporosis-related fracture. Can Med Assoc J. 2008;179:319-326. doi: 10.1503/cmaj.071330.
  17. Lee RH, Lyles KH, Colon-Emeric C. A review of the effect of anticonvulsant medications on bone mineral density and fracture risk. Am J Geriatr Pharmacother. 2010;8(1):34-46. doi: 10.1016/j.amjopharm.2010.02.003.
  18. Arora E, Singh H, Gupta YK. Impact of antiepileptic drugs on bone health: Need for monitoring, treatment, and prevention. J Family Med Prim Care. 2016;5(2):248-253. doi: 10.4103/2249-4863.192338.
  19. Maghraoui AE, Roux C. DXA scanning in clinical practice. Q J Med. 2008;101(8):605-617. doi: 10.1093/qjmed/hcn022.
  20. Watts NB, Lewiecki EM, Miller PD, Baim S. National osteoporosis foundation 2008 clinician’s guide to prevention and treatment of osteoporosis and the world health organization fracture risk assessment tool (FRAX): What they mean to the bone densiometrist and bone technologist. J Clin Densitom. 2008;11(4):473-477. doi: 10.1016/j.jocd.2008.04.003.
  21. MacLean C, Newberry S, Maglione M, et al. Systematic review: comparative effectiveness of treatments to prevent fractures in men and women with low bone density or osteoporosis. Ann Intern Med. 2007;148(3):197-213. doi: 10.7326/0003-4819-148-3-200802050-00198.
  22. Beaton DE, Vidmar M, Pitzul KB, et al. Addition of a fracture risk assessment to a coordinator’s role improved treatment rates within 6 months of screening in a fragility fracture screening program. J Am Geriatr Soc. 2017; 28(3):863-869. doi: 10.1007/s00198-016-3794-1.
  23. U.S. Preventative Services Task Force. Screening for osteoporosis. Ann Intern Med. 2011;154(5):356-364. doi: 10.7326/0003-4819-154-5-201103010-00307.
  24. Sunyecz JA. The use of calcium and vitamin D in the management of osteoporosis. Ther Clin Risk Manag. 2008;4(4):827-836.
  25. Eastell, R. (1998). Treatment of postmenopausal osteoporosis. N Engl J Med. 1998;338:736-746. doi: 10.1056/NEJM199803123381107.
  26. Cosman F, de Beur SJ, LeBoff MS, et al, National Osteoporosis Foundation. Clinician’s guide to prevention and treatment of osteoporosis. Osteoporos Int. 2014;25(10):2359-2381. doi: 10.1007/s00198-014-2794-2.
  27. Black DM, Schartz AV, Ensrud KE, et al, doi:10.1001/jama.296.24.2927.
  28. Schmidt GA, Horner KE, McDanel DL, Ross MB, Moores KG. Risks and benefits of long-term bisphosphonate therapy. Am J Health Syst Pharm. 2010;67(12):994-1001. doi: 10.2146/ajhp090506.
  29. Kraenzlin, ME, Meier C. Parathyroid hormone analogues in the treatment of osteoporosis. Nat Rev Endocrinol. 2011;7(11):647-656. doi: 10.1038/nrendo.2011.108.
  30. Miller P, Hattersley G, Riis B, et al. Effect of abaloparatide vs placebo on new vertebral fractures in postmenopausal women with osteoporosis. JAMA. 2016;316(7):722-733. doi: 10.1001/jama.2016.11136.
  31. TYMLOSTM [prescribing information]. Waltham, MA: Radius Health, Inc; 2017.
  32. Tetsunaga T, Tetsunaga T, Nishida K, et al. Denosumab and alendronate treatment in patients with back pain due to fresh osteoporotic vertebral fractures. J Orthop Sci. 2017;22(2):230-236. doi: 10.1016/j.jos.2016.11.017.
  33. Recker, RR, Mitlak BH, Ni X, Krege JH. Long-term raloxifene for postmenopausal osteoporosis. Curr Med Res Opin. 2011;27(9):1755-1761. doi: 10.1185/03007995.2011.606312.
  34. Yildirim K, Gureser G, Karatay S, et al. Comparison of the effects of alendronate, risedronate and calcitonin treatment in postmenopausal osteoporosis. J Back Musculoskelet Rehabil.2005;18(3/4):85-89. doi: 10.3233/BMR-2005-183-405.
  35. Christensen L, Iqbal S, Macarios D, Badamgarav E, Harley C. Cost of fractures commonly associated with osteoporosis in a managed-care population. J Med Econ. 2010;13(2):302-313. doi: 10.3111/13696998.2010.488969.
Author and Disclosure Information

Ms. Bledsoe is a physician assistant, Naples Neprhology, Naples, Florida. Ms. Alessi is a biomedical engineering student, University of Florida, Gainesville. Dr, Toro is Orthopaedic Traumatologist, Orange Regional Medical Center, Middletown New York. Dr. Giordano is Associate Professor, Department of Orthopaedics and Rehabilitation, Division of Sports Medicine, University of Rochester, New York. Dr. Hanypsiak is Orthopedic Surgeon, Department of Orthopedic Surgery, Physician's Regional Medical Center, Naples, Florida, and Course Director, Innovative Techniques: Knee, Hip, and Shoulder Course, Las Vegas, Nevada.

Authors’ Disclosure Statement: The authors report no actual or potential conflict of interest in relation to this article.

Address correspondence to: Bryan T. Hanypsiak, MD, Physicians Regional Hospital, 6101 Pine Ridge Road, Desk 23A, Naples FL 34119 (tel, 239-348-4221; email, [email protected]).

Lauren Bledsoe, RPAC Kaitlyn Alessi Jose B. Toro, MD Brian Giordano, MD Bryan T. Hanypsiak, MD . Fragility Fractures: Diagnosis and Treatment . Am J Orthop.

December 19, 2018

Publications
Topics
Author and Disclosure Information

Ms. Bledsoe is a physician assistant, Naples Neprhology, Naples, Florida. Ms. Alessi is a biomedical engineering student, University of Florida, Gainesville. Dr, Toro is Orthopaedic Traumatologist, Orange Regional Medical Center, Middletown New York. Dr. Giordano is Associate Professor, Department of Orthopaedics and Rehabilitation, Division of Sports Medicine, University of Rochester, New York. Dr. Hanypsiak is Orthopedic Surgeon, Department of Orthopedic Surgery, Physician's Regional Medical Center, Naples, Florida, and Course Director, Innovative Techniques: Knee, Hip, and Shoulder Course, Las Vegas, Nevada.

Authors’ Disclosure Statement: The authors report no actual or potential conflict of interest in relation to this article.

Address correspondence to: Bryan T. Hanypsiak, MD, Physicians Regional Hospital, 6101 Pine Ridge Road, Desk 23A, Naples FL 34119 (tel, 239-348-4221; email, [email protected]).

Lauren Bledsoe, RPAC Kaitlyn Alessi Jose B. Toro, MD Brian Giordano, MD Bryan T. Hanypsiak, MD . Fragility Fractures: Diagnosis and Treatment . Am J Orthop.

December 19, 2018

Author and Disclosure Information

Ms. Bledsoe is a physician assistant, Naples Neprhology, Naples, Florida. Ms. Alessi is a biomedical engineering student, University of Florida, Gainesville. Dr, Toro is Orthopaedic Traumatologist, Orange Regional Medical Center, Middletown New York. Dr. Giordano is Associate Professor, Department of Orthopaedics and Rehabilitation, Division of Sports Medicine, University of Rochester, New York. Dr. Hanypsiak is Orthopedic Surgeon, Department of Orthopedic Surgery, Physician's Regional Medical Center, Naples, Florida, and Course Director, Innovative Techniques: Knee, Hip, and Shoulder Course, Las Vegas, Nevada.

Authors’ Disclosure Statement: The authors report no actual or potential conflict of interest in relation to this article.

Address correspondence to: Bryan T. Hanypsiak, MD, Physicians Regional Hospital, 6101 Pine Ridge Road, Desk 23A, Naples FL 34119 (tel, 239-348-4221; email, [email protected]).

Lauren Bledsoe, RPAC Kaitlyn Alessi Jose B. Toro, MD Brian Giordano, MD Bryan T. Hanypsiak, MD . Fragility Fractures: Diagnosis and Treatment . Am J Orthop.

December 19, 2018

ABSTRACT

Fragility fractures are estimated to affect 3 million people annually in the United States. As they are associated with a significant mortality rate, the prevention of these fractures should be a priority for orthopedists. At-risk patients include the elderly and those with thyroid disease, diabetes, hypertension, and heart disease. Osteoporosis is diagnosed by the presence of a fragility fracture or by dual-energy x-ray absorptiometry (DXA) in the absence of a fragility fracture. In 2011, the United States Preventive Services Task Force (USPSTF) recommended that all women ≥65 years should be screened for osteoporosis by DXA. Women <65 years with a 10-year fracture risk =/> than that of a 65-year-old white woman should also be screened for osteoporosis. Lifestyle changes, such as calcium and vitamin D supplementation, exercise, and smoking cessation, are non-pharmacologic treatment options. The National Osteoporosis Foundation recommends treating osteoporosis with pharmacotherapy in patients with a high risk for fracture (T score <–2.5) or history of fragility fracture. Understanding risk factors and eliminating medications known to cause decreased BMD are vital to prevention and will be necessary to limit these fractures and their associated expenses in the future.

Continue to: Fragility fractures are caused by...

 

 

Fragility fractures are caused by falls from standing height or repetitive physiological loads.1 With the growing aging population in the United States, it is estimated that 3 million people will be affected by fragility fractures yearly.2 In the setting of osseous insufficiency, fractures that are typically associated with high-energy trauma are encountered in patients who simply trip over a parking lot curb or fall off their bike. After surgery, the severe disruption of patients’ lives continues with a prolonged rehabilitation period.

Fragility fractures are not only traumatizing for patients; they are also associated with significantly increased mortality. A study by Gosch and colleagues found that 70.6% of patients died during the normal follow-up period, and 29.4% of patients died within the first year of suffering a fracture.3 Also, the mean life expectancy post-fragility fracture was only 527 days.3 Diagnosis and treatment of osteoporosis is imperative to prevent fragility fractures before they occur.

RISK FACTORS AND CAUSES

The incidence of fragility fractures increases in patients with comorbidities such as thyroid disease, diabetes, hypertension, and heart disease.4 Hyperthyroidism and treated hypothyroidism cause an imbalance between osteoblast and osteoclast activity, resulting in osteoporosis.5 A thyroid-stimulating hormone level < 0.1 increases the risk of vertebral and non-vertebral fractures by a factor of 4.5 and 3.2 mIU/L respectively.4 Patients with diabetes also have an increased risk of fragility fractures, which is due to impaired healing capabilities, especially that of bone healing. Approximately 2 million people are affected by type 1 diabetes in the United States, and 20% of those patients will develop osteoporosis.6

Hypertension and osteoporosis are 2 diseases that occur often in the elderly. Common etiological factors believed to cause both hypertension and osteoporosis are low calcium intake, high consumption of salt, and vitamin D and vitamin K deficiency. Also, hypertension treated with loop diuretics has been found to cause negative effects on bone and increase the risk of osteoporosis.7 The only antihypertensive medications that preserve bone mineral density (BMD) and reduce fracture risk are thiazide diuretics.7 Lastly, an association between coronary artery disease and osteoporosis has been hypothesized. The link is not completely understood, but it is believed that oxidative stress and inflammation are the culprits in both diseases.8 In contrast to previous hypotheses, Sosa and colleagues found an independent association between beta blockers and fragility fractures.9 The idea that beta blockers and fragility fractures are linked is still controversial and needs more study. Unlike beta blockers, statins provide a protective effect on bone. They increase BMD and reduce fracture risk by inhibiting osteoclastogenesis.10

In addition to loop diuretics and beta blockers, inhaled glucocorticoids, oral glucocorticoids, proton pump inhibitors (PPIs), Hreceptor antagonists, and anticonvulsants decrease bone density and increase the incidence of fragility fractures.11 Chronic glucocorticoid therapy is the most common cause of secondary osteoporosis. Osteoblasts and osteocytes undergo apoptosis in the presence of glucocorticoids.12 Patients on glucocorticoid therapy have an increased risk of fracture, even with higher BMD values.13 Bone changes that occur while a patient is taking glucocorticoids may not be detected during BMD testing. Therefore, a high level of suspicion of osteoporosis in patients on long-term glucocorticoids is imperative.

Proton pump inhibitors are among the most prescribed medications in the world; they reduce bone resorption, increasing the risk of fracture.14 Proton pump inhibitors and H2 receptor antagonists are hypothesized to cause malabsorption of calcium and indirectly cause osteoporosis. The risk of osteoporosis increases with the length of PPI treatment.15 However, exposure lasting <7 years does not increase the risk of fracture.16 It is recommended that patients on long-term PPIs be referred for BMD testing.

An association between anticonvulsants and osteoporosis has been found in observational studies. The mechanism of this association is not yet fully understood, but it is believed that exacerbation of vitamin D deficiency leads to increased bone metabolism.17 Gastrointestinal (GI) calcium absorption also decreases with anticonvulsant use. Prolonged antiepileptic therapy and high-dose therapy rapidly decrease BMD. Primidone, carbamazepine, phenobarbital, and phenytoin are the drugs most often associated with decreased BMD. Osteoporosis and fragility fracture in these patients can be prevented with calcium, vitamin D, and the bisphosphonate risedronate. These medications have been shown to improve BMD by 69%.18

Continue to: DIAGNOSIS...

 

 

DIAGNOSIS

Osteoporosis is diagnosed by the presence of a fragility fracture or by dual-energy x-ray absorptiometry (DXA) in the absence of a fragility fracture.19 Measurements of the femoral neck by DXA are used to diagnose osteoporosis, although DXA can also be used to measure the bone density of the spine and peripheral skeleton.20

The World Health Organization developed a set of T score criteria to diagnose osteoporosis in postmenopausal women (Table 1). A T score >-1 is normal, <-1 but >-2.5 signifies osteopenia, <-2.5 is osteoporosis, and <-2.5 with fragility fracture is severe osteoporosis.19 The Z score, not the T score, should be used to assess osteoporosis in premenopausal women, men <50 years, and children (Table 2). The Z score is calculated by comparing the patient’s BMD with the mean BMD of their peers of a similar age, race, and gender.19 Z scores <-2.0 indicate low BMD for chronological age. A Z score > -2.0 is considered within the expected range for age.20 Bone mineral density testing is the rate- limiting step to starting osteoporosis treatment.21 Without testing, treatment of osteoporosis is very unlikely.

Table 1. T Score Criteria

T score

Diagnosis

> -1.0

Normal

-1.0 to -2.5

Osteopenia

< -2.5

Osteoporosis

< -2.5 with fragility fracture

Severe osteoporosis

 

 

 

 

 

 

 

 

 

Table 2. Z Score Criteria

Z score

Diagnosis

> -2.0

Normal BMD for age

< -2.0

Low BMD for age

 

 

 

 

 

The World Health Organization also developed a tool to predict fracture risk. The Fracture Risk Assessment Tool uses fracture history in addition to other risk factors to predict a patient’s 10-year risk of major fracture.22 Risk factors used to assess fracture risk include age, sex, weight, height, previous fracture, parental hip fracture history, current smoker, glucocorticoid use, rheumatoid arthritis, secondary osteoporosis, excessive alcohol use, and femoral neck BMD.

In 2011, the United States Preventive Services Task Force (USPSTF) recommended that all women ≥65 years should be screened for osteoporosis by DXA. Women <65 years with a 10-year fracture risk =/> than that of a 65-year-old white woman should also be screened for osteoporosis. These recommendations are different for men. It was concluded that the evidence was insufficient to support osteoporosis screening in men.23 As of April 2017, Centers for Medicare and Medicaid Services current reimbursement rates for DXA scans are, on average, $123.10 in the hospital setting and $41.63 in the office setting. The axial DXA CPT code is 77080.

Continue to: TREATMENT...

 

 

TREATMENT

NONPHARMACOLOGIC

Patients with mild osteoporosis may be treated first non-pharmacologically. Lifestyle changes such as calcium and vitamin D supplementation, exercise, and smoking cessation are non-pharmacologic treatment options. Calcium carbonate and calcium citrate are common supplements. Calcium carbonate is 40% elemental calcium, whereas calcium citrate supplements are only 21% elemental calcium. Calcium supplements are best absorbed when taken with food.24 The recommended daily total calcium intake is 1200 mg.25 Only 500 to 600 milligrams of calcium can be absorbed by the GI tract at a time. Therefore, calcium supplements should be taken at least 4 to 5 hours apart.24Patients should also be counseled that calcium supplements may cause GI side effects such as bloating and constipation. To reduce side effects, patients can slowly increase the dose of calcium to a therapeutic level.

Vitamin D supplementation works best in conjunction with calcium supplementation. Vitamin D functions to regulate calcium absorption in the intestine and stimulate bone resorption and maintain the serum calcium concentration. The National Osteoporosis Foundation recommends 800 to 1000 international units of vitamin D daily.24 Lifestyle changes may be sufficient to stop the progression of osteoporosis in its early stages. Once osteoporosis becomes severe enough, pharmacotherapy is needed to stop further bone destruction and improve BMD.

PHARMACOLOGIC

After an initial fragility fracture, the risk of additional ones increases significantly, making treatment of osteoporosis essential. The National Osteoporosis Foundation recommends treating osteoporosis with pharmacotherapy in patients with a high risk of fracture (T score <-2.5) or history of fragility fracture.26 Bisphosphonates inhibit bone resorption and are considered the first-line therapy for postmenopausal women with osteoporosis. A common side effect of oral bisphosphonates is GI toxicity. Patients are advised to avoid lying down for at least 30 minutes after medication administration to avoid esophageal irritation. Oral bisphosphonates should also be taken in the morning on an empty stomach with at least 8 ounces of water. Recurrent bisphosphonate use should be avoided in patients with chronic kidney disease. Oral alendronate and risedronate are typically discontinued after 5 years of use.27 Long-term bisphosphonate use may cause an increased risk of fragility fracture due to oversuppression of bone turnover. To avoid this risk, bisphosphonate “drug holidays” are an option. Bisphosphonates accumulate over time, creating reservoirs. Even after therapy is stopped, patients continue to have therapeutic effects for 2 to 5 years.28

Bisphosphonates are available in both oral and intravenous forms. Alendronate is available in doses of 10 mg and 70 mg for daily and weekly administration, respectively. Both are available in tablet form, but the 70 mg weekly dose is also available in a dissolvable formulation. Alendronate is available in a reduced dose for osteoporosis prevention. Alendronate dosing for osteoporosis prevention is 5 mg daily or 35 mg weekly. Risedronate is dosed as 5 mg daily, 35 mg weekly, or 150 mg monthly. Intravenous bisphosphonates are indicated when oral bisphosphonates are not tolerated, only after vitamin D has been assessed and is within the normal range. Zoledronic acid is administered as a 15-minute infusion once a year.

Teriparatide (Forteo; PTH-1-34) is available for glucocorticoid-induced osteoporosis, postmenopausal women, and men with severe osteoporosis. It is indicated for patients in whom bisphosphonate treatment has failed or those who do not tolerate bisphosphonates. Teriparatide is a synthetic parathyroid hormone (PTH) that acts as an anabolic agent, stimulating bone formation, maturation, and remodeling.29 In addition to its application as a bone-building hormone, teriparatide has gained popularity for various off-label uses. These include accelerated osteosynthesis, stress fracture healing, and in the nonoperative treatment of osteoarthritis.29 Parathyroid hormone has been shown to stimulate the maturation, proliferation, and maintenance of osteoblast progenitor cells. More recently, PTH has been shown to regulate chondrocyte signaling, as well as differentiation and maturation. Further study on the chondroregenerative potential of PTH has demonstrated its efficacy as a novel disease-modifying agent in the treatment of osteoarthritis.29 Teriparatide is administered as a daily subcutaneous injection. The United States dosing is 600 mcg/2.4 mL. Adverse effects such as orthostatic hypotension and osteosarcoma may occur. BMD testing should be performed 1 to 2 years after initiation of teriparatide and every 2 years thereafter.26

Abaloparatide (Tymlos), a human parathyroid hormone, is another treatment option for postmenopausal women at risk of osteoporotic fracture. In a study comparing the efficacy of abaloparatide and teriparatide, treatment with abaloparatide was found to induce higher BMD levels in a time frame of 12 months. The BMD differences could be attributed to many factors, such as an enhanced net anabolic effect or a reduced osteoblast expression. Furthermore, the risk of developing new vertebral and nonvertebral fractures decreased in the abaloparatide group compared with the placebo group over a period of 18 months.30

Continue to: The recommended daily dose for abaloparatide...

 

 

The recommended daily dose for abaloparatide is 80 mcg via subcutaneous injection with calcium and vitamin D supplements.31 Adverse reactions were consistent between abaloparatide and teriparatide, and included hypercalcemia, hypercalciuria, and orthostatic hypotension.30 The use of parathyroid analogs for >2 years is not recommended due to the risk of osteosarcoma.

Denosumab (Prolia) is a monoclonal antibody that stops osteoclastogenesis by blocking the binding of RANKL to RANK.31 It is indicated for patients intolerant to bisphosphonates or with impaired kidney function. Prolia is administered subcutaneously in 60 mg doses every 6 months in men and postmenopausal women with osteoporosis. Prolia is contraindicated in patients with hypersensitivity to any component of the medication, pregnancy, and hypocalcemia.

Selective estrogen receptor modulators (SERMs), such as raloxifene and tamoxifen, can treat osteoporosis effectively in postmenopausal women. Raloxifene is considered the SERM of choice due to the availability of more robust safety and efficacy data. Raloxifene increases BMD while decreasing bone resorption and bone turnover.32 It is also used to reduce breast cancer risk; however, it increases the risk of thromboembolic events and hot flashes. Tamoxifen is not typically used to treat osteoporosis, but women treated for breast cancer with tamoxifen receive some bone protection.

Lastly, calcitonin and strontium ranelate are also options to treat osteoporosis. However, both calcitonin and strontium ranelate have weak effects on BMD. Calcitonin only transiently inhibits osteoclast activity.33 Therefore, medications like bisphosphonates, teriparatide, denosumab, and SERMs are preferred.

A summary of medications used to treat osteoporosis can be found in Table 3.

Table 3. Overview of Common Medications Used in the Treatment and Prevention of Osteoporosis

Medication

Indication

Dosing

Calcium supplementation

Mild osteoporosis

1200 mg oral/d

Vitamin D supplementation

Mild osteoporosis

800 to 1000 IU oral/d

Alendronate

Postmenopausal osteoporosis

 

 

Osteoporosis prevention

10 mg oral/d

70 mg oral/wk

 

5 mg/d

35 mg/wk

Risedronate

Postmenopausal osteoporosis

5 mg oral/d

35 mg oral/wk

150 mg oral/mo

Teriparatide (Forteo)

Glucocorticoid-inducted osteoporosis, postmenopausal osteoporosis, men with severe osteoporosis

600 mcg/2.4 mL subcutaneous/d

Abaloparatide (Tymlos)

Postmenopausal osteoporosis

80 mcg subcutaneous/d

Denosumab (Prolia)

Patients intolerant to bisphosphonates; patients with impaired kidney function.

60 mg subcutaneous every 6 mo

Raloxifene

Postmenopausal osteoporosis

60 mg oral/d

Tamoxifen

Postmenopausal osteoporosis

20 mg oral/d

Calcitonin

Postmenopausal osteoporosis

100 units intramuscular or subcutaneous/d

200 units (1 spray) intranasal/d

Strontium ranelate

Postmenopausal osteoporosis Severe osteoporosis in men

2 g/d dissolved in water, prior to bedtime

Not recommended in CrCl <30 mL/min

Abbreviation: CrCl, creatinine clearance.

CONCLUSION

With a growing aging population, the prevalence of osteoporosis is expected to increase. By 2025, experts estimate that there will be 2 million fractures yearly, costing the United States upwards of $25 billion.34,35 This estimate does not include the cost of lost productivity or disability, which will likely cost billions more.34,35 Understanding risk factors and eliminating medications known to cause decreased BMD are vital. Obtaining a BMD measurement is the rate-limiting step for treatment initiation. Without an appropriate diagnosis, treatment is unlikely. As providers, it us our responsibility to maintain a high level of suspicion of osteoporosis in the elderly and promptly diagnose and treat them.

ABSTRACT

Fragility fractures are estimated to affect 3 million people annually in the United States. As they are associated with a significant mortality rate, the prevention of these fractures should be a priority for orthopedists. At-risk patients include the elderly and those with thyroid disease, diabetes, hypertension, and heart disease. Osteoporosis is diagnosed by the presence of a fragility fracture or by dual-energy x-ray absorptiometry (DXA) in the absence of a fragility fracture. In 2011, the United States Preventive Services Task Force (USPSTF) recommended that all women ≥65 years should be screened for osteoporosis by DXA. Women <65 years with a 10-year fracture risk =/> than that of a 65-year-old white woman should also be screened for osteoporosis. Lifestyle changes, such as calcium and vitamin D supplementation, exercise, and smoking cessation, are non-pharmacologic treatment options. The National Osteoporosis Foundation recommends treating osteoporosis with pharmacotherapy in patients with a high risk for fracture (T score <–2.5) or history of fragility fracture. Understanding risk factors and eliminating medications known to cause decreased BMD are vital to prevention and will be necessary to limit these fractures and their associated expenses in the future.

Continue to: Fragility fractures are caused by...

 

 

Fragility fractures are caused by falls from standing height or repetitive physiological loads.1 With the growing aging population in the United States, it is estimated that 3 million people will be affected by fragility fractures yearly.2 In the setting of osseous insufficiency, fractures that are typically associated with high-energy trauma are encountered in patients who simply trip over a parking lot curb or fall off their bike. After surgery, the severe disruption of patients’ lives continues with a prolonged rehabilitation period.

Fragility fractures are not only traumatizing for patients; they are also associated with significantly increased mortality. A study by Gosch and colleagues found that 70.6% of patients died during the normal follow-up period, and 29.4% of patients died within the first year of suffering a fracture.3 Also, the mean life expectancy post-fragility fracture was only 527 days.3 Diagnosis and treatment of osteoporosis is imperative to prevent fragility fractures before they occur.

RISK FACTORS AND CAUSES

The incidence of fragility fractures increases in patients with comorbidities such as thyroid disease, diabetes, hypertension, and heart disease.4 Hyperthyroidism and treated hypothyroidism cause an imbalance between osteoblast and osteoclast activity, resulting in osteoporosis.5 A thyroid-stimulating hormone level < 0.1 increases the risk of vertebral and non-vertebral fractures by a factor of 4.5 and 3.2 mIU/L respectively.4 Patients with diabetes also have an increased risk of fragility fractures, which is due to impaired healing capabilities, especially that of bone healing. Approximately 2 million people are affected by type 1 diabetes in the United States, and 20% of those patients will develop osteoporosis.6

Hypertension and osteoporosis are 2 diseases that occur often in the elderly. Common etiological factors believed to cause both hypertension and osteoporosis are low calcium intake, high consumption of salt, and vitamin D and vitamin K deficiency. Also, hypertension treated with loop diuretics has been found to cause negative effects on bone and increase the risk of osteoporosis.7 The only antihypertensive medications that preserve bone mineral density (BMD) and reduce fracture risk are thiazide diuretics.7 Lastly, an association between coronary artery disease and osteoporosis has been hypothesized. The link is not completely understood, but it is believed that oxidative stress and inflammation are the culprits in both diseases.8 In contrast to previous hypotheses, Sosa and colleagues found an independent association between beta blockers and fragility fractures.9 The idea that beta blockers and fragility fractures are linked is still controversial and needs more study. Unlike beta blockers, statins provide a protective effect on bone. They increase BMD and reduce fracture risk by inhibiting osteoclastogenesis.10

In addition to loop diuretics and beta blockers, inhaled glucocorticoids, oral glucocorticoids, proton pump inhibitors (PPIs), Hreceptor antagonists, and anticonvulsants decrease bone density and increase the incidence of fragility fractures.11 Chronic glucocorticoid therapy is the most common cause of secondary osteoporosis. Osteoblasts and osteocytes undergo apoptosis in the presence of glucocorticoids.12 Patients on glucocorticoid therapy have an increased risk of fracture, even with higher BMD values.13 Bone changes that occur while a patient is taking glucocorticoids may not be detected during BMD testing. Therefore, a high level of suspicion of osteoporosis in patients on long-term glucocorticoids is imperative.

Proton pump inhibitors are among the most prescribed medications in the world; they reduce bone resorption, increasing the risk of fracture.14 Proton pump inhibitors and H2 receptor antagonists are hypothesized to cause malabsorption of calcium and indirectly cause osteoporosis. The risk of osteoporosis increases with the length of PPI treatment.15 However, exposure lasting <7 years does not increase the risk of fracture.16 It is recommended that patients on long-term PPIs be referred for BMD testing.

An association between anticonvulsants and osteoporosis has been found in observational studies. The mechanism of this association is not yet fully understood, but it is believed that exacerbation of vitamin D deficiency leads to increased bone metabolism.17 Gastrointestinal (GI) calcium absorption also decreases with anticonvulsant use. Prolonged antiepileptic therapy and high-dose therapy rapidly decrease BMD. Primidone, carbamazepine, phenobarbital, and phenytoin are the drugs most often associated with decreased BMD. Osteoporosis and fragility fracture in these patients can be prevented with calcium, vitamin D, and the bisphosphonate risedronate. These medications have been shown to improve BMD by 69%.18

Continue to: DIAGNOSIS...

 

 

DIAGNOSIS

Osteoporosis is diagnosed by the presence of a fragility fracture or by dual-energy x-ray absorptiometry (DXA) in the absence of a fragility fracture.19 Measurements of the femoral neck by DXA are used to diagnose osteoporosis, although DXA can also be used to measure the bone density of the spine and peripheral skeleton.20

The World Health Organization developed a set of T score criteria to diagnose osteoporosis in postmenopausal women (Table 1). A T score >-1 is normal, <-1 but >-2.5 signifies osteopenia, <-2.5 is osteoporosis, and <-2.5 with fragility fracture is severe osteoporosis.19 The Z score, not the T score, should be used to assess osteoporosis in premenopausal women, men <50 years, and children (Table 2). The Z score is calculated by comparing the patient’s BMD with the mean BMD of their peers of a similar age, race, and gender.19 Z scores <-2.0 indicate low BMD for chronological age. A Z score > -2.0 is considered within the expected range for age.20 Bone mineral density testing is the rate- limiting step to starting osteoporosis treatment.21 Without testing, treatment of osteoporosis is very unlikely.

Table 1. T Score Criteria

T score

Diagnosis

> -1.0

Normal

-1.0 to -2.5

Osteopenia

< -2.5

Osteoporosis

< -2.5 with fragility fracture

Severe osteoporosis

 

 

 

 

 

 

 

 

 

Table 2. Z Score Criteria

Z score

Diagnosis

> -2.0

Normal BMD for age

< -2.0

Low BMD for age

 

 

 

 

 

The World Health Organization also developed a tool to predict fracture risk. The Fracture Risk Assessment Tool uses fracture history in addition to other risk factors to predict a patient’s 10-year risk of major fracture.22 Risk factors used to assess fracture risk include age, sex, weight, height, previous fracture, parental hip fracture history, current smoker, glucocorticoid use, rheumatoid arthritis, secondary osteoporosis, excessive alcohol use, and femoral neck BMD.

In 2011, the United States Preventive Services Task Force (USPSTF) recommended that all women ≥65 years should be screened for osteoporosis by DXA. Women <65 years with a 10-year fracture risk =/> than that of a 65-year-old white woman should also be screened for osteoporosis. These recommendations are different for men. It was concluded that the evidence was insufficient to support osteoporosis screening in men.23 As of April 2017, Centers for Medicare and Medicaid Services current reimbursement rates for DXA scans are, on average, $123.10 in the hospital setting and $41.63 in the office setting. The axial DXA CPT code is 77080.

Continue to: TREATMENT...

 

 

TREATMENT

NONPHARMACOLOGIC

Patients with mild osteoporosis may be treated first non-pharmacologically. Lifestyle changes such as calcium and vitamin D supplementation, exercise, and smoking cessation are non-pharmacologic treatment options. Calcium carbonate and calcium citrate are common supplements. Calcium carbonate is 40% elemental calcium, whereas calcium citrate supplements are only 21% elemental calcium. Calcium supplements are best absorbed when taken with food.24 The recommended daily total calcium intake is 1200 mg.25 Only 500 to 600 milligrams of calcium can be absorbed by the GI tract at a time. Therefore, calcium supplements should be taken at least 4 to 5 hours apart.24Patients should also be counseled that calcium supplements may cause GI side effects such as bloating and constipation. To reduce side effects, patients can slowly increase the dose of calcium to a therapeutic level.

Vitamin D supplementation works best in conjunction with calcium supplementation. Vitamin D functions to regulate calcium absorption in the intestine and stimulate bone resorption and maintain the serum calcium concentration. The National Osteoporosis Foundation recommends 800 to 1000 international units of vitamin D daily.24 Lifestyle changes may be sufficient to stop the progression of osteoporosis in its early stages. Once osteoporosis becomes severe enough, pharmacotherapy is needed to stop further bone destruction and improve BMD.

PHARMACOLOGIC

After an initial fragility fracture, the risk of additional ones increases significantly, making treatment of osteoporosis essential. The National Osteoporosis Foundation recommends treating osteoporosis with pharmacotherapy in patients with a high risk of fracture (T score <-2.5) or history of fragility fracture.26 Bisphosphonates inhibit bone resorption and are considered the first-line therapy for postmenopausal women with osteoporosis. A common side effect of oral bisphosphonates is GI toxicity. Patients are advised to avoid lying down for at least 30 minutes after medication administration to avoid esophageal irritation. Oral bisphosphonates should also be taken in the morning on an empty stomach with at least 8 ounces of water. Recurrent bisphosphonate use should be avoided in patients with chronic kidney disease. Oral alendronate and risedronate are typically discontinued after 5 years of use.27 Long-term bisphosphonate use may cause an increased risk of fragility fracture due to oversuppression of bone turnover. To avoid this risk, bisphosphonate “drug holidays” are an option. Bisphosphonates accumulate over time, creating reservoirs. Even after therapy is stopped, patients continue to have therapeutic effects for 2 to 5 years.28

Bisphosphonates are available in both oral and intravenous forms. Alendronate is available in doses of 10 mg and 70 mg for daily and weekly administration, respectively. Both are available in tablet form, but the 70 mg weekly dose is also available in a dissolvable formulation. Alendronate is available in a reduced dose for osteoporosis prevention. Alendronate dosing for osteoporosis prevention is 5 mg daily or 35 mg weekly. Risedronate is dosed as 5 mg daily, 35 mg weekly, or 150 mg monthly. Intravenous bisphosphonates are indicated when oral bisphosphonates are not tolerated, only after vitamin D has been assessed and is within the normal range. Zoledronic acid is administered as a 15-minute infusion once a year.

Teriparatide (Forteo; PTH-1-34) is available for glucocorticoid-induced osteoporosis, postmenopausal women, and men with severe osteoporosis. It is indicated for patients in whom bisphosphonate treatment has failed or those who do not tolerate bisphosphonates. Teriparatide is a synthetic parathyroid hormone (PTH) that acts as an anabolic agent, stimulating bone formation, maturation, and remodeling.29 In addition to its application as a bone-building hormone, teriparatide has gained popularity for various off-label uses. These include accelerated osteosynthesis, stress fracture healing, and in the nonoperative treatment of osteoarthritis.29 Parathyroid hormone has been shown to stimulate the maturation, proliferation, and maintenance of osteoblast progenitor cells. More recently, PTH has been shown to regulate chondrocyte signaling, as well as differentiation and maturation. Further study on the chondroregenerative potential of PTH has demonstrated its efficacy as a novel disease-modifying agent in the treatment of osteoarthritis.29 Teriparatide is administered as a daily subcutaneous injection. The United States dosing is 600 mcg/2.4 mL. Adverse effects such as orthostatic hypotension and osteosarcoma may occur. BMD testing should be performed 1 to 2 years after initiation of teriparatide and every 2 years thereafter.26

Abaloparatide (Tymlos), a human parathyroid hormone, is another treatment option for postmenopausal women at risk of osteoporotic fracture. In a study comparing the efficacy of abaloparatide and teriparatide, treatment with abaloparatide was found to induce higher BMD levels in a time frame of 12 months. The BMD differences could be attributed to many factors, such as an enhanced net anabolic effect or a reduced osteoblast expression. Furthermore, the risk of developing new vertebral and nonvertebral fractures decreased in the abaloparatide group compared with the placebo group over a period of 18 months.30

Continue to: The recommended daily dose for abaloparatide...

 

 

The recommended daily dose for abaloparatide is 80 mcg via subcutaneous injection with calcium and vitamin D supplements.31 Adverse reactions were consistent between abaloparatide and teriparatide, and included hypercalcemia, hypercalciuria, and orthostatic hypotension.30 The use of parathyroid analogs for >2 years is not recommended due to the risk of osteosarcoma.

Denosumab (Prolia) is a monoclonal antibody that stops osteoclastogenesis by blocking the binding of RANKL to RANK.31 It is indicated for patients intolerant to bisphosphonates or with impaired kidney function. Prolia is administered subcutaneously in 60 mg doses every 6 months in men and postmenopausal women with osteoporosis. Prolia is contraindicated in patients with hypersensitivity to any component of the medication, pregnancy, and hypocalcemia.

Selective estrogen receptor modulators (SERMs), such as raloxifene and tamoxifen, can treat osteoporosis effectively in postmenopausal women. Raloxifene is considered the SERM of choice due to the availability of more robust safety and efficacy data. Raloxifene increases BMD while decreasing bone resorption and bone turnover.32 It is also used to reduce breast cancer risk; however, it increases the risk of thromboembolic events and hot flashes. Tamoxifen is not typically used to treat osteoporosis, but women treated for breast cancer with tamoxifen receive some bone protection.

Lastly, calcitonin and strontium ranelate are also options to treat osteoporosis. However, both calcitonin and strontium ranelate have weak effects on BMD. Calcitonin only transiently inhibits osteoclast activity.33 Therefore, medications like bisphosphonates, teriparatide, denosumab, and SERMs are preferred.

A summary of medications used to treat osteoporosis can be found in Table 3.

Table 3. Overview of Common Medications Used in the Treatment and Prevention of Osteoporosis

Medication

Indication

Dosing

Calcium supplementation

Mild osteoporosis

1200 mg oral/d

Vitamin D supplementation

Mild osteoporosis

800 to 1000 IU oral/d

Alendronate

Postmenopausal osteoporosis

 

 

Osteoporosis prevention

10 mg oral/d

70 mg oral/wk

 

5 mg/d

35 mg/wk

Risedronate

Postmenopausal osteoporosis

5 mg oral/d

35 mg oral/wk

150 mg oral/mo

Teriparatide (Forteo)

Glucocorticoid-inducted osteoporosis, postmenopausal osteoporosis, men with severe osteoporosis

600 mcg/2.4 mL subcutaneous/d

Abaloparatide (Tymlos)

Postmenopausal osteoporosis

80 mcg subcutaneous/d

Denosumab (Prolia)

Patients intolerant to bisphosphonates; patients with impaired kidney function.

60 mg subcutaneous every 6 mo

Raloxifene

Postmenopausal osteoporosis

60 mg oral/d

Tamoxifen

Postmenopausal osteoporosis

20 mg oral/d

Calcitonin

Postmenopausal osteoporosis

100 units intramuscular or subcutaneous/d

200 units (1 spray) intranasal/d

Strontium ranelate

Postmenopausal osteoporosis Severe osteoporosis in men

2 g/d dissolved in water, prior to bedtime

Not recommended in CrCl <30 mL/min

Abbreviation: CrCl, creatinine clearance.

CONCLUSION

With a growing aging population, the prevalence of osteoporosis is expected to increase. By 2025, experts estimate that there will be 2 million fractures yearly, costing the United States upwards of $25 billion.34,35 This estimate does not include the cost of lost productivity or disability, which will likely cost billions more.34,35 Understanding risk factors and eliminating medications known to cause decreased BMD are vital. Obtaining a BMD measurement is the rate-limiting step for treatment initiation. Without an appropriate diagnosis, treatment is unlikely. As providers, it us our responsibility to maintain a high level of suspicion of osteoporosis in the elderly and promptly diagnose and treat them.

References
  1. Dietz SO, Hofmann A, Rommens PM. Haemorrhage in fragility fractures of the pelvis. Eur J Trauma Emerg Surg. 2015;41:363-367. doi: 10.1007/s00068-014-0452-1
  2. Burge R, Dawson-Hughes B, Solomon DH, Wong JB, King A, Tosteson A. Incidence and economic burden of osteoporosis-related fractures in the United States, 2005-2025. J Bone Miner Res. 2007;22(3):465-475. doi: 10.1359/jbmr.061113.
  3. Gosch M, Hoffmann-Weltin Y, Roth T, Blauth M, Nicholas JA, Kammerlander C. Orthogeriatric co-management improves the outcome of long-term care residents with fragility fractures. Arch Orthop Trauma Surg. 2016; 136(10):1403-1409. doi: 10.1007/s00402-016-2543-4.
  4. Maccagnano G, Notarnicola A, Pesce V, Mudoni S, Tafuri S, Moretti B. The prevalence of fragility fractures in a population of a region of southern Italy affected by thyroid disorders. BioMed Res Int. 2016. doi: 10.1155/2016/6017165.
  5. Mosekilde L, Eriksen EF, Charles P. Effects of thyroid hormones on bone and mineral metabolism. Endocrinol Metab Clin North Am. 1990;19(1):35-63. doi: 10.1016/S0889-8529(18)30338-4.
  6. Liporace FA, Breitbart EA, Yoon RS, Doyle E, Paglia DM, Lin S. The effect of locally delivered recombinant human bone morphogenic protein-2 with hydroxyapatite/tri-calcium phosphate on the biomechanical properties of bone in diabetes-related osteoporosis. J Orthop Traumatol.2015;16(2):151-159. doi: 10.1007/s10195-014-0327-6.
  7. Ilic K, Obradovic N, Vujasinovic-Stupar N. The relationship among hypertension, antihypertensive medications, and osteoporosis: a narrative review. Calcif. Tissue Int. 2013;92(3):217-227. doi: 10.1007/s00223-012-9671-9.
  8. Yesil Y, Ulger, Z, Halil M, et al. Coexistence of osteoporosis (OP) and coronary artery disease (CAD) in the elderly: it is not just a by chance event. Arch Gerontol Geriatr. 2012;54(3):473-476. doi: 10.1016/j.archger.2011.06.007.
  9. Sosa M, Saavedra P, de Tejada MJG, et al, GIUMO Cooperative Group. Beta-blocker use is associated with fragility fractures in postmenopausal women with coronary heart disease. Aging Clin Exp Res.2011;23(3):112-117. doi: 10.3275/7041.
  10. An T, Hao J, Li R, Yang M, Cheng G, Zou M. Efficacy of statins for osteoporosis: a systematic review and met-analysis. Osteoporos Int. 2017;28(1):47-57. doi: 10.1007/s00198-016-3844-8.
  11. Munson JC, Bynum JP, Bell J, et al. Patterns of prescription drug use before and after fragility fracture. JAMA Intern Med. 2016;176(10):1531-1538. doi: 10.1001/jamainternmed.2016.4814.
  12. Saag KG, Agnesdei D, Hans D, et al. Trabecular bone score in patients with chronic glucocorticoid therapy-induced osteoporosis treated with alendronate or teriparatide. Arthritis Rheumatol. 2016;68(9):2122-2128. doi: 10.1002/art.39726.
  13. Chuang MH, Chuang TL, Koo M, Wang YF. Trabecular bone score reflects trabecular microarchitecture deterioration and fragility fracture in female adult patients receiving glucocorticoid therapy: A pre-post controlled study. BioMed Res Int. 2017. doi: 10.1155/2017/4210217.
  14. Andersen BN, Johansen PB, Abrahamsen B. Proton pump inhibitors and osteoporosis. Curr Opin Rheumatol. 2016;28(4):420-425. doi: 10.1097/BOR.0000000000000291.
  15. Jacob L, Hadji P, Kostev K. The use of proton pump inhibitors is positively associated with osteoporosis in postmenopausal women in Germany. Climacteric. 2016; 19(5):478-481. doi: 10.1080/13697137.2016.1200549.
  16. Targownik LE, Lix LM, Metge CJ, Prior HJ, Leung S, Leslie WD. Use of proton pump inhibitors and risk of osteoporosis-related fracture. Can Med Assoc J. 2008;179:319-326. doi: 10.1503/cmaj.071330.
  17. Lee RH, Lyles KH, Colon-Emeric C. A review of the effect of anticonvulsant medications on bone mineral density and fracture risk. Am J Geriatr Pharmacother. 2010;8(1):34-46. doi: 10.1016/j.amjopharm.2010.02.003.
  18. Arora E, Singh H, Gupta YK. Impact of antiepileptic drugs on bone health: Need for monitoring, treatment, and prevention. J Family Med Prim Care. 2016;5(2):248-253. doi: 10.4103/2249-4863.192338.
  19. Maghraoui AE, Roux C. DXA scanning in clinical practice. Q J Med. 2008;101(8):605-617. doi: 10.1093/qjmed/hcn022.
  20. Watts NB, Lewiecki EM, Miller PD, Baim S. National osteoporosis foundation 2008 clinician’s guide to prevention and treatment of osteoporosis and the world health organization fracture risk assessment tool (FRAX): What they mean to the bone densiometrist and bone technologist. J Clin Densitom. 2008;11(4):473-477. doi: 10.1016/j.jocd.2008.04.003.
  21. MacLean C, Newberry S, Maglione M, et al. Systematic review: comparative effectiveness of treatments to prevent fractures in men and women with low bone density or osteoporosis. Ann Intern Med. 2007;148(3):197-213. doi: 10.7326/0003-4819-148-3-200802050-00198.
  22. Beaton DE, Vidmar M, Pitzul KB, et al. Addition of a fracture risk assessment to a coordinator’s role improved treatment rates within 6 months of screening in a fragility fracture screening program. J Am Geriatr Soc. 2017; 28(3):863-869. doi: 10.1007/s00198-016-3794-1.
  23. U.S. Preventative Services Task Force. Screening for osteoporosis. Ann Intern Med. 2011;154(5):356-364. doi: 10.7326/0003-4819-154-5-201103010-00307.
  24. Sunyecz JA. The use of calcium and vitamin D in the management of osteoporosis. Ther Clin Risk Manag. 2008;4(4):827-836.
  25. Eastell, R. (1998). Treatment of postmenopausal osteoporosis. N Engl J Med. 1998;338:736-746. doi: 10.1056/NEJM199803123381107.
  26. Cosman F, de Beur SJ, LeBoff MS, et al, National Osteoporosis Foundation. Clinician’s guide to prevention and treatment of osteoporosis. Osteoporos Int. 2014;25(10):2359-2381. doi: 10.1007/s00198-014-2794-2.
  27. Black DM, Schartz AV, Ensrud KE, et al, doi:10.1001/jama.296.24.2927.
  28. Schmidt GA, Horner KE, McDanel DL, Ross MB, Moores KG. Risks and benefits of long-term bisphosphonate therapy. Am J Health Syst Pharm. 2010;67(12):994-1001. doi: 10.2146/ajhp090506.
  29. Kraenzlin, ME, Meier C. Parathyroid hormone analogues in the treatment of osteoporosis. Nat Rev Endocrinol. 2011;7(11):647-656. doi: 10.1038/nrendo.2011.108.
  30. Miller P, Hattersley G, Riis B, et al. Effect of abaloparatide vs placebo on new vertebral fractures in postmenopausal women with osteoporosis. JAMA. 2016;316(7):722-733. doi: 10.1001/jama.2016.11136.
  31. TYMLOSTM [prescribing information]. Waltham, MA: Radius Health, Inc; 2017.
  32. Tetsunaga T, Tetsunaga T, Nishida K, et al. Denosumab and alendronate treatment in patients with back pain due to fresh osteoporotic vertebral fractures. J Orthop Sci. 2017;22(2):230-236. doi: 10.1016/j.jos.2016.11.017.
  33. Recker, RR, Mitlak BH, Ni X, Krege JH. Long-term raloxifene for postmenopausal osteoporosis. Curr Med Res Opin. 2011;27(9):1755-1761. doi: 10.1185/03007995.2011.606312.
  34. Yildirim K, Gureser G, Karatay S, et al. Comparison of the effects of alendronate, risedronate and calcitonin treatment in postmenopausal osteoporosis. J Back Musculoskelet Rehabil.2005;18(3/4):85-89. doi: 10.3233/BMR-2005-183-405.
  35. Christensen L, Iqbal S, Macarios D, Badamgarav E, Harley C. Cost of fractures commonly associated with osteoporosis in a managed-care population. J Med Econ. 2010;13(2):302-313. doi: 10.3111/13696998.2010.488969.
References
  1. Dietz SO, Hofmann A, Rommens PM. Haemorrhage in fragility fractures of the pelvis. Eur J Trauma Emerg Surg. 2015;41:363-367. doi: 10.1007/s00068-014-0452-1
  2. Burge R, Dawson-Hughes B, Solomon DH, Wong JB, King A, Tosteson A. Incidence and economic burden of osteoporosis-related fractures in the United States, 2005-2025. J Bone Miner Res. 2007;22(3):465-475. doi: 10.1359/jbmr.061113.
  3. Gosch M, Hoffmann-Weltin Y, Roth T, Blauth M, Nicholas JA, Kammerlander C. Orthogeriatric co-management improves the outcome of long-term care residents with fragility fractures. Arch Orthop Trauma Surg. 2016; 136(10):1403-1409. doi: 10.1007/s00402-016-2543-4.
  4. Maccagnano G, Notarnicola A, Pesce V, Mudoni S, Tafuri S, Moretti B. The prevalence of fragility fractures in a population of a region of southern Italy affected by thyroid disorders. BioMed Res Int. 2016. doi: 10.1155/2016/6017165.
  5. Mosekilde L, Eriksen EF, Charles P. Effects of thyroid hormones on bone and mineral metabolism. Endocrinol Metab Clin North Am. 1990;19(1):35-63. doi: 10.1016/S0889-8529(18)30338-4.
  6. Liporace FA, Breitbart EA, Yoon RS, Doyle E, Paglia DM, Lin S. The effect of locally delivered recombinant human bone morphogenic protein-2 with hydroxyapatite/tri-calcium phosphate on the biomechanical properties of bone in diabetes-related osteoporosis. J Orthop Traumatol.2015;16(2):151-159. doi: 10.1007/s10195-014-0327-6.
  7. Ilic K, Obradovic N, Vujasinovic-Stupar N. The relationship among hypertension, antihypertensive medications, and osteoporosis: a narrative review. Calcif. Tissue Int. 2013;92(3):217-227. doi: 10.1007/s00223-012-9671-9.
  8. Yesil Y, Ulger, Z, Halil M, et al. Coexistence of osteoporosis (OP) and coronary artery disease (CAD) in the elderly: it is not just a by chance event. Arch Gerontol Geriatr. 2012;54(3):473-476. doi: 10.1016/j.archger.2011.06.007.
  9. Sosa M, Saavedra P, de Tejada MJG, et al, GIUMO Cooperative Group. Beta-blocker use is associated with fragility fractures in postmenopausal women with coronary heart disease. Aging Clin Exp Res.2011;23(3):112-117. doi: 10.3275/7041.
  10. An T, Hao J, Li R, Yang M, Cheng G, Zou M. Efficacy of statins for osteoporosis: a systematic review and met-analysis. Osteoporos Int. 2017;28(1):47-57. doi: 10.1007/s00198-016-3844-8.
  11. Munson JC, Bynum JP, Bell J, et al. Patterns of prescription drug use before and after fragility fracture. JAMA Intern Med. 2016;176(10):1531-1538. doi: 10.1001/jamainternmed.2016.4814.
  12. Saag KG, Agnesdei D, Hans D, et al. Trabecular bone score in patients with chronic glucocorticoid therapy-induced osteoporosis treated with alendronate or teriparatide. Arthritis Rheumatol. 2016;68(9):2122-2128. doi: 10.1002/art.39726.
  13. Chuang MH, Chuang TL, Koo M, Wang YF. Trabecular bone score reflects trabecular microarchitecture deterioration and fragility fracture in female adult patients receiving glucocorticoid therapy: A pre-post controlled study. BioMed Res Int. 2017. doi: 10.1155/2017/4210217.
  14. Andersen BN, Johansen PB, Abrahamsen B. Proton pump inhibitors and osteoporosis. Curr Opin Rheumatol. 2016;28(4):420-425. doi: 10.1097/BOR.0000000000000291.
  15. Jacob L, Hadji P, Kostev K. The use of proton pump inhibitors is positively associated with osteoporosis in postmenopausal women in Germany. Climacteric. 2016; 19(5):478-481. doi: 10.1080/13697137.2016.1200549.
  16. Targownik LE, Lix LM, Metge CJ, Prior HJ, Leung S, Leslie WD. Use of proton pump inhibitors and risk of osteoporosis-related fracture. Can Med Assoc J. 2008;179:319-326. doi: 10.1503/cmaj.071330.
  17. Lee RH, Lyles KH, Colon-Emeric C. A review of the effect of anticonvulsant medications on bone mineral density and fracture risk. Am J Geriatr Pharmacother. 2010;8(1):34-46. doi: 10.1016/j.amjopharm.2010.02.003.
  18. Arora E, Singh H, Gupta YK. Impact of antiepileptic drugs on bone health: Need for monitoring, treatment, and prevention. J Family Med Prim Care. 2016;5(2):248-253. doi: 10.4103/2249-4863.192338.
  19. Maghraoui AE, Roux C. DXA scanning in clinical practice. Q J Med. 2008;101(8):605-617. doi: 10.1093/qjmed/hcn022.
  20. Watts NB, Lewiecki EM, Miller PD, Baim S. National osteoporosis foundation 2008 clinician’s guide to prevention and treatment of osteoporosis and the world health organization fracture risk assessment tool (FRAX): What they mean to the bone densiometrist and bone technologist. J Clin Densitom. 2008;11(4):473-477. doi: 10.1016/j.jocd.2008.04.003.
  21. MacLean C, Newberry S, Maglione M, et al. Systematic review: comparative effectiveness of treatments to prevent fractures in men and women with low bone density or osteoporosis. Ann Intern Med. 2007;148(3):197-213. doi: 10.7326/0003-4819-148-3-200802050-00198.
  22. Beaton DE, Vidmar M, Pitzul KB, et al. Addition of a fracture risk assessment to a coordinator’s role improved treatment rates within 6 months of screening in a fragility fracture screening program. J Am Geriatr Soc. 2017; 28(3):863-869. doi: 10.1007/s00198-016-3794-1.
  23. U.S. Preventative Services Task Force. Screening for osteoporosis. Ann Intern Med. 2011;154(5):356-364. doi: 10.7326/0003-4819-154-5-201103010-00307.
  24. Sunyecz JA. The use of calcium and vitamin D in the management of osteoporosis. Ther Clin Risk Manag. 2008;4(4):827-836.
  25. Eastell, R. (1998). Treatment of postmenopausal osteoporosis. N Engl J Med. 1998;338:736-746. doi: 10.1056/NEJM199803123381107.
  26. Cosman F, de Beur SJ, LeBoff MS, et al, National Osteoporosis Foundation. Clinician’s guide to prevention and treatment of osteoporosis. Osteoporos Int. 2014;25(10):2359-2381. doi: 10.1007/s00198-014-2794-2.
  27. Black DM, Schartz AV, Ensrud KE, et al, doi:10.1001/jama.296.24.2927.
  28. Schmidt GA, Horner KE, McDanel DL, Ross MB, Moores KG. Risks and benefits of long-term bisphosphonate therapy. Am J Health Syst Pharm. 2010;67(12):994-1001. doi: 10.2146/ajhp090506.
  29. Kraenzlin, ME, Meier C. Parathyroid hormone analogues in the treatment of osteoporosis. Nat Rev Endocrinol. 2011;7(11):647-656. doi: 10.1038/nrendo.2011.108.
  30. Miller P, Hattersley G, Riis B, et al. Effect of abaloparatide vs placebo on new vertebral fractures in postmenopausal women with osteoporosis. JAMA. 2016;316(7):722-733. doi: 10.1001/jama.2016.11136.
  31. TYMLOSTM [prescribing information]. Waltham, MA: Radius Health, Inc; 2017.
  32. Tetsunaga T, Tetsunaga T, Nishida K, et al. Denosumab and alendronate treatment in patients with back pain due to fresh osteoporotic vertebral fractures. J Orthop Sci. 2017;22(2):230-236. doi: 10.1016/j.jos.2016.11.017.
  33. Recker, RR, Mitlak BH, Ni X, Krege JH. Long-term raloxifene for postmenopausal osteoporosis. Curr Med Res Opin. 2011;27(9):1755-1761. doi: 10.1185/03007995.2011.606312.
  34. Yildirim K, Gureser G, Karatay S, et al. Comparison of the effects of alendronate, risedronate and calcitonin treatment in postmenopausal osteoporosis. J Back Musculoskelet Rehabil.2005;18(3/4):85-89. doi: 10.3233/BMR-2005-183-405.
  35. Christensen L, Iqbal S, Macarios D, Badamgarav E, Harley C. Cost of fractures commonly associated with osteoporosis in a managed-care population. J Med Econ. 2010;13(2):302-313. doi: 10.3111/13696998.2010.488969.
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TAKE-HOME POINTS

  • 3 million people sustain fragility fractures annually, and nearly 30% die within a year of the fracture.
  • The incidence of fragility fractures increases in patients with comorbidities such as thyroid disease, diabetes, hypertension, and heart disease.
  • The World Health Organization has developed a set of T-core criteria to diagnose osteoporosis in postmenopausal women: a score >–1 is normal; <–1 but >–2.5 signifies osteopenia; <–2.5 denotes osteoporosis; and <–2.5 with fragility fracture indicates severe osteoporosis.
  • The Z score, not the T score, should be used to assess osteoporosis in premenopausal women, men <50 years, and children. The Z score is calculated by comparing the patient’s BMD with the mean BMD of their peers of a similar age, race, and gender. Z scores <–2.0 indicate low BMD for chronological age. A Z score > –2.0 is considered within the expected range for age.
  • After an initial fragility fracture, the risk for additional ones increases significantly, making treatment of osteoporosis essential. The National Osteoporosis Foundation recommends treating osteoporosis with pharmacotherapy in patients with a high risk for fracture (T score <–2.5) or history of fragility fracture.26
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