Research Productivity and Impact in Foot and Ankle Surgery: Insights From Relative Citation Ratio Analysis of Recent Fellowship Graduates.

INTRODUCTION: The relative citation ratio (RCR), a novel bibliometric tool supported by the National Institute of Health, provides a standardized approach to evaluate research productivity and impact across different fields. This study aims to evaluate RCR of fellowship-trained foot and ankle orthopaedic surgeons to analyze the influence of various surgeon demographics. METHODS: Fellow names listed on the American Orthopaedic Foot and Ankle Society website were extracted from the year 2008 to 2009 to the year 2022 to 2023. Demographic information for each fellow was collected including sex, degree type, and academic title. The iCite database developed by the National Institute of Health was used to obtain total publications, mean RCR, weighted RCR, and change in RCR after fellowship graduation for each fellow. Univariate and multivariate analysis was conducted to predict these four parameters based on sex, degree type, academic position, and career longevity. RESULTS: Of the 820 fellows, 674 (82%) were male. Most fellows (n = 587, 71%) did not go on to hold academic positions. Multivariate analysis revealed that male sex (ß = 2.32, P < 0.001), holding an academic position (ß = 6.44, P < 0.001), holding a PhD (ß = 22.96, P < 0.001), and a shorter length time since graduation (ß = -0.50, P < 0.001) were independent predictors of number of total publications. Holding a DO degree was an independent predictor of decreased mean RCR (ß = 0.39, P = 0.039). Finally, multivariate analysis revealed that male sex (ß = 4.05, P = 0.003), a career in academics (ß = 4.61, P < 0.001), and a shorter time since graduation (ß = -0.45, P = 0.001) were associated with a larger weighted RCR. DISCUSSION: The findings highlight the importance of addressing gender disparities and promoting research opportunities across different programs. Moreover, academic institutions should provide adequate support and mentorship to early-career foot and ankle-trained orthopaedic surgeons to foster sustained research productivity.

Surgical Setting in Achilles Tendon Repair: How Does It Relate to Costs and Complications?

Background: Primary Achilles tendon repair (ATR) can be performed in ambulatory surgery centers (ASCs) or hospitals. We compared costs and complication rates of ATR performed in these settings. Methods: We retrospectively queried the electronic medical record of our academic health system and identified 97 adults who underwent primary ATR from 2015 to 2021. Variables were compared between patients treated at ASCs vs those treated in hospitals. We compared continuous variables with Wilcoxon rank-sum tests and categorical variables with χ2 tests. We used an α of 0.05. Multivariable logistic regression was performed to determine associations between surgical setting and costs. Linear regression was performed between each charge subtype and total cost to identify which charge subtypes were most associated with total cost. Results: Patients who underwent ATR in hospitals had a higher rate of unanticipated postoperative hospital admission (13%) than those treated in ASCs (0%) (P = .01). We found no differences with regard to postoperative complications, emergency department visits, readmission, rerupture, reoperation/revision, or death. Patients treated in hospitals had a higher mean (±SD) implant cost ($664 ± $810) than those treated in ASCs ($175 ± $585) (P < .01). We found no differences between settings with regard to total cost, supply costs, operating room charges, or anesthesia charges. Higher implant cost was associated with hospital setting (odds ratio = 16 [95% CI: 1.7-157]) and body mass index > 25 (odds ratio = 1.2 [95% CI: 1.0-1.5]). Operating room costs were strongly correlated with total costs (R2 = .94). Conclusion: The overall cost and complication rate of ATRs were not significantly different between ASCs and hospitals. ATRs performed in hospitals had higher implant costs and higher rates of postoperative admission than those performed in ASCs. Level of Evidence: Level III, retrospective comparative study.

Anemia and Its Severity Is Associated With Worse Postoperative Outcomes Following Open Reduction Internal Fixation of Ankle Fractures.

BACKGROUND: Ankle fractures are often treated in a nonemergent fashion and therefore offer the chance for treatment of preoperative anemia. Although preoperative anemia has been associated with postoperative morbidity following certain types of orthopaedic procedures, its effect on postoperative outcomes following open reduction internal fixation (ORIF) of ankle fractures has not been evaluated. The purpose of this study was to determine the influence of preoperative anemia on 30-day postoperative outcomes following ankle fracture ORIF. METHODS: The American College of Surgeons National Surgical Quality Improvement Program (ASC-NSQIP) registry was queried from 2005 to 2019 for patients undergoing ankle fracture ORIF. Patients were stratified into nonanemic, mildly anemic, and moderately to severely anemic. Univariate analyses were used to assess differences in patient characteristics between cohorts. Multivariate logistic regressions adjusting for these differences were performed to assess the effect of preoperative anemia on 30-day postoperative outcomes. RESULTS: We obtained data for 21 211 patients, of whom 14 931 (70.39%) were not anemic, 3982 (18.77%) were mildly anemic, and 2298 (10.83%) were moderately to severely anemic. After adjustment, mild preoperative anemia was associated with higher odds of any adverse event (P < .001), deep surgical site infections (SSIs; P = .013), sepsis (P = .001), 30-day readmission (P < .001), and extended length of stay (LOS) (P < .001). Similarly, moderate to severe anemia in these patients was also associated with increased odds of any adverse event (P < .001), deep SSIs (P = .003), sepsis (P = .001), readmission (P < .001), and extended LOS (P < .001). Both mild (P = .004) and moderate to severe (P < .001) anemia groups had higher odds of requiring a blood transfusion. CONCLUSION: Preoperative anemia is associated with an increased risk of adverse postoperative outcomes in patients undergoing ORIF for ankle fractures. Future studies should evaluate whether optimization of hematocrit in these patients results in improved outcomes. LEVEL OF EVIDENCE: Level III, comparative study.

Reimbursement for Orthopaedic Surgeries in Commercial and Public Payors: A Race to the Bottom.

INTRODUCTION: The purpose of this study was to compare surgeon professional fee reimbursement and trends from Medicare versus commercial payors for inpatient orthopaedic surgeries: total knee arthroplasty (TKA), total hip arthroplasty (THA), total shoulder arthroplasty (TSA), anterior cervical diskectomy and fusion (ACDF), and posterior lumbar fusion (PLF). METHODS: Patients undergoing TKA, THA, TSA, single-level ACDF, and single-level PLF from 2010 to 2018 were queried in a commercially insured claims database. Medicare reimbursements and the work relative value unit (wRVU) of each procedure were obtained from the Medicare Physician Fee Schedule. All costs were adjusted for inflation and reported in 2018 real dollars. Compound annual growth rates were calculated to assess the mean growth rate for each procedure. Linear regression was done to assess trends. RESULTS: On average, payments from Medicare were 57% less than payments from commercial payors. From 2010 to 2018, both Medicare and commercial payments decreased significantly for each surgery (P < 0.05 for all). Compared with inflation-adjusted commercial payments, Medicare payments decreased 2.1 times faster for TKA (-2.1% versus -1.0%), 2.8 times faster for THA (-1.4% versus -0.5%), 1.3 times faster for TSA (-1.0% versus -0.8%), and 1.9 times faster for ACDF (-1.1% versus -0.6%). PLF was the only procedure for which Medicare payments declined slower than commercial payments (-0.6% versus -1.21%). Medicare payments per wRVU markedly declined for TKA (-0.83%), THA (-0.80%), TSA (-0.75%), and ACDF (-1.10%), whereas commercial payments per wRVU for those surgeries showed no notable change. For PLF, there was a notable decrease in both Medicare (-0.63%) and commercial (-1.21%) payments per wRVU. CONCLUSION: Over the past decade, both commercial and Medicare surgeon payments for commonly performed inpatient orthopaedic surgeries decreased markedly, with Medicare payments decreasing an average of 1.5 times faster than commercial payments. The impact of declining reimbursements on access and quality of care merits additional investigation.

Posterolateral Diskectomies for Treatment of Pediatric Spinal Deformities.

STUDY DESIGN: Retrospective. OBJECTIVE: To investigate the indications, radiographic outcomes, and complications in children with spinal deformities treated with posterolateral diskectomy with posterior fusion (PLDF), and to compare them against those of patients treated with anteroposterior spinal fusion (APSF). SUMMARY OF BACKGROUND DATA: A novel technique for treating large, rigid spinal deformities in children has been proposed, consisting of PLDF at the apex of the deformity using an all-posterior approach. METHODS: We evaluated records of all patients 21 years or younger who underwent treatment for spinal deformity between 2010 and 2015 by one surgeon using PLDF (n = 56) or APSF (n = 21). RESULTS: The indications for PLDF were large, rigid curves (37 patients); focal curves with severe rotation (10 patients); or large curves with open triradiate cartilage (nine patients). PLDF patients had a mean (± standard deviation) of 3 ±â€Š1 diskectomies and 14 ±â€Š3 posterior spinal levels fused. Compared with the APSF group, the PLDF group had significantly greater major curve correction (86% vs. 57%, P = 0.006), less blood transfused (mean, 2.5 ±â€Š2.6 vs. 4.0 ±â€Š3.3 units, P = 0.038), and a lower rate of staged surgery (1.8% vs. 86%, P < 0.001). There were no significant differences between the PLDF and APSF groups in T1-S1 length gained (mean, 6.2 ±â€Š3.4 vs. 6.6 ±â€Š8.8 cm, respectively; P = 0.77) or in the rate of major complications (P = 0.557). CONCLUSION: PLDF is an effective alternative to APSF for treating children with severe spinal deformities. It is effective for treating large, rigid curves with severe rotation and may be useful for treating large curves in children with open triradiate cartilage. LEVEL OF EVIDENCE: 4.

Knee Extensor Mechanism Reconstruction With Complete Extensor Allograft After Failure of Patellar Tendon Repair.

Disruptions of the extensor mechanism of the knee may be bony or tendinous in nature. The consequences of such disruptions are not favorable because they prevent normal function of the knee, which is critical for independent ambulation. We report on a 30-year-old man who underwent a successful knee extensor mechanism reconstruction with allograft after his initial tendon repair failed.

Does obesity affect fracture healing in children?

BACKGROUND: Obesity is a risk factor for various orthopaedic diseases, including fractures. Obesity's influence on circulating hormones and cytokines and bone mineralization ultimately influences the body's osteogenic response and bone mineralization, potentially increasing the risk of fracture and impacting fracture healing. QUESTIONS/PURPOSES: Does obesity delay fracture recovery in overweight or obese children as measured by the time to release to normal activity? Is this average time for return to activity influenced by the mechanism of the injury? Does obesity's effect on mineralization and loading in overweight or obese children lead to a greater proportion of upper extremity fracture versus lower extremity fracture? METHODS: We prospectively followed 273 patients with nonpathologic long bone fractures treated from January 2010 to October 2011. Patients were stratified into obese/overweight, normal weight, and underweight groups. All patients were followed until release to regular activities (mean, 41 days; range, 13-100 days). RESULTS: Release to regular activities occurred sooner in obese/overweight than in normal weight patients: 39 and 42 days, respectively. A greater proportion of obese/overweight patients had low to moderate energy mechanisms of injury than did normal weight patients, but we found no difference between the groups in terms of return to activity when stratified by mechanism. There was also no difference in the proportion of upper extremity injuries between the two groups. CONCLUSIONS: Obese/overweight children did not have a delay in release to activities compared with children of normal weight. LEVEL OF EVIDENCE: Level II, prognostic study. See Guidelines for Authors for a complete description of levels of evidence.

MIP-1δ activates NFATc1 and enhances osteoclastogenesis: involvement of both PLCγ2 and NFκB signaling.

Pathological bone resorption is a source of significant morbidity in diseases affecting the skeleton such as rheumatoid arthritis, periodontitis, and cancer metastasis to bone. Evidence indicates that elevated levels of inflammatory mediators such as IL-1, IL-6, and TNF-α play a role in this process by promoting the formation of bone-resorbing osteoclasts. Additionally, current studies have identified inflammatory chemokines of the macrophage inflammatory protein (MIP) family as potential mediators of pathological bone resorption, where both MIP-1α and -3α have been shown to enhance osteoclast (OCL) development. In this study we provide evidence that MIP-1δ, whose expression is associated with renal cell carcinoma bone metastasis and rheumatoid arthritis, enhances OCL formation in vitro via a direct effect on OCL precursors. Consistent with this ability, exposure of OCL precursors to MIP-1δ resulted in the activation of PLCγ2 and NF-κB, two signaling pathways known to regulate OCL differentiation. Moreover, MIP-1δ induced expression and nuclear translocation of NFATc1, a master regulator of osteoclastogenesis, which was dependent on activation of both the PLCγ2 and NFκB signaling pathways. Lastly, consistent with in vitro studies, in vivo administration of MIP-1δ significantly increased OCL number and resorption area as determined using a murine calvarial bone resorption model. Taken together, these data highlight the potential of MIP-1δ as a mediator of pathological bone resorption and provide insight into the molecular mechanism through which MIP-1δ enhances osteoclastogenesis.

Myogenic Akt signaling attenuates muscular degeneration, promotes myofiber regeneration and improves muscle function in dystrophin-deficient mdx mice.

Duchenne muscular dystrophy, the most common form of childhood muscular dystrophy, is caused by X-linked inherited mutations in the dystrophin gene. Dystrophin deficiencies result in the loss of the dystrophin-glycoprotein complex at the plasma membrane, which leads to structural instability and muscle degeneration. Previously, we induced muscle-specific overexpression of Akt, a regulator of cellular metabolism and survival, in mdx mice at pre-necrotic (<3.5 weeks) ages and demonstrated upregulation of the utrophin-glycoprotein complex and protection against contractile-induced stress. Here, we found that delaying exogenous Akt treatment of mdx mice after the onset of peak pathology (>6 weeks) similarly increased the abundance of compensatory adhesion complexes at the extrasynaptic sarcolemma. Akt introduction after onset of pathology reverses the mdx histopathological measures, including decreases in blood serum albumin infiltration. Akt also improves muscle function in mdx mice as demonstrated through in vivo grip strength tests and in vitro contraction measurements of the extensor digitorum longus muscle. To further explore the significance of Akt in myofiber regeneration, we injured wild-type muscle with cardiotoxin and found that Akt induced a faster regenerative response relative to controls at equivalent time points. We demonstrate that Akt signaling pathways counteract mdx pathogenesis by enhancing endogenous compensatory mechanisms. These findings provide a rationale for investigating the therapeutic activation of the Akt pathway to counteract muscle wasting.

Myogenic Akt signaling upregulates the utrophin-glycoprotein complex and promotes sarcolemma stability in muscular dystrophy.

Duchenne muscular dystrophy is caused by dystrophin mutations that lead to structural instability of the sarcolemma membrane, myofiber degeneration/regeneration and progressive muscle wasting. Here we show that myogenic Akt signaling in mouse models of dystrophy promotes increased expression of utrophin, which replaces the function of dystrophin thereby preventing sarcolemma damage and muscle wasting. In contrast to previous suggestions that increased Akt in dystrophy was a secondary consequence of pathology, our findings demonstrate a pivotal role for this signaling pathway such that modulation of Akt can significantly affect disease outcome by amplification of existing, physiological compensatory mechanisms.