Context

Distal femoral osteotomy (DFO) is a joint preservation procedure that corrects genu valgum deformities and patellofemoral maltracking, thereby restoring kinematics and unloading contact pressures in the lateral tibiofemoral and patellofemoral compartments.

Objective

To evaluate the rates of return to work (RTW) and return to sport (RTS) after DFO for valgus malalignment and lateral compartment osteoarthritis through a systematic review of the literature.

Data sources

A systematic review using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines was conducted on the PubMed, Cochrane, and Embase databases.

Study selection

The search terms femoral osteotomy AND (sports OR work) were used. Studies in which patients underwent concomitant total knee arthroplasty were excluded.

Study design

Systematic review.

Level of evidence

Level 4 (systematic review of level 4 studies).

Data extraction

Data included the number of patients, age, gender, laterality of operation, time to follow-up, rate of RTW and RTS, time to RTS, activity level on return, and activity level scores (Tegner, Marx, Lysholm, and the International Knee Documentation Committee). Risk of bias was assessed using the Methodological Index for Non-Randomized Studies (MINORS) criteria.

Results

Seven articles with 194 patients were included. The average age ranged from 19 to 49 years with a mean postoperative follow-up range of 36 to 90 months. RTW data were available for 125 patients, of whom 42.1% to 91.3% returned by final follow-up. Data on RTS were available for 149 patients, of whom 70% to 100% returned at a range of 8.3 to 16.9 months postoperatively, and 41.6% to 100% returned to the same or greater level of sports activity. The Tegner and Marx activity level scores ranged from 3 to 4 and from 5 to 11, respectively, at final follow-up.

Conclusion

Patients treated with DFO reported high rates of RTW and RTS, with most patients being able to return to recreational sport after surgery.

BACKGROUND: Numerous studies have been published on the use of platelet-rich plasma (PRP) for knee osteoarthritis (OA), with conflicting results. PURPOSE: To determine the fragility index (FI) and fragility quotient (FQ) of randomized controlled trials (RCTs) that evaluated the use of PRP to treat knee OA. STUDY DESIGN: Systematic review. METHODS: RCTs evaluating the efficacy of PRP injections for knee OA from 2000 to 2020 were included for analysis according to PRISMA guidelines. The FI was determined by calculating the number of outcome event reversals required to change the statistical significance. The associated FQ was determined by dividing the FI by the sample size. RESULTS: Our initial search resulted in 41,149 studies, of which 8 RCTs (678 patients, 72 outcome events) were included in the analysis. One study failed to report PRP formulation details, whereas 87.5% of studies reported using either leukocyte-rich or leukocyte-poor PRP. The platelet concentration was reported in 25% of the included trials. The overall FI of the 72 outcome events was 8.5. Accounting for sample size, the associated FQ was determined to be 0.14, suggesting that the reversal of 14% of outcome events was required to change outcome significance. There were 51 statistically significant outcomes, of which the FI and FQ were 12 and 0.164, respectively. CONCLUSION: Comprehensive fragility analysis suggested that the published literature evaluating the efficacy of PRP use for knee OA may lack statistical stability. We recommend the reporting of both an FI and FQ in addition to P value analysis to provide a clear and thorough understanding of the statistical integrity of studies reporting on PRP use for knee OA.

BACKGROUND CONTEXT: COVID-19 has been shown to adversely affect multiple organ systems, yet little is known about its effect on perioperative complications after spine surgery or the optimal timing of surgery after an infection. We used the NIH National COVID Cohort Collaborative (N3C) database to characterize the risk profile in patients undergoing spine surgery during multiple time windows following COVID-19 infection. METHODS: We queried the National COVID Cohort Collaborative, a database of 17.4 million persons with 6.9 million COVID-19 cases, for patients undergoing lumbar spinal fusion surgery. Patients were stratified into those with an initial documented COVID-19 infection within 3 time periods: 0 to 2 weeks, 2 to 6 weeks, or 6 to 12 weeks before surgery. RESULTS: A total of 60,541 patients who underwent lumbar spinal fusion procedures were included. Patients who underwent surgery within 2 weeks of their COVID-19 diagnosis had a significantly increased risk for venous thromboembolic events (OR 2.29, 95% CI 1.58-3.32), sepsis (OR 1.56, 95% CI 1.03-2.36), 30-day mortality (OR 5.55, 95% CI 3.53-8.71), and 1-year mortality (OR 2.70, 95% CI 1.91-3.82) compared with patients who were COVID negative during the same period. There was no significant difference in the rates of acute kidney injury or surgical site infection. Patients undergoing surgery between 2 and 6 weeks or between 6 and 12 weeks from the date of COVID-19 infection did not show significantly elevated rates of any complication analyzed. CONCLUSIONS: Patients undergoing lumbar spinal fusion within 2 weeks from initial COVID-19 diagnosis are at increased risk for perioperative venous thromboembolic events and sepsis. This effect does not persist beyond 2 weeks, however, so it may be warranted to postpone non-urgent spine surgeries for at least 2 weeks following a COVID-19 infection or to consider a more aggressive VTE chemoprophylaxis regimen for urgent surgery in COVID-19 patients.

Upper extremity amputations represent a prime opportunity to restore function through replantation. There are a variety of options that treating surgeons use to protect neurovascular repairs and restore function including Kirschner wire fixation, external fixation, wrist arthrodesis, and proximal row carpectomy. Additionally, the dorsal spanning plate may be a valuable tool for protecting neurovascular repairs. Compared to temporary immobilization with Kirschner wire fixation, which has previously been described in conjunction with upper extremity replantation, dorsal spanning plates can be left in place for longer durations with a lower risk of loosening and loss of fixation and for preventing postoperative sabotage or repeat amputation of the replant by the patient. In this article, we describe a unique case of a patient with acute psychiatric illness that presented with a self-inflicted amputation through the radiocarpal joint and was initially treated with emergent replantation and application of a dorsal spanning plate to protect the neurovascular repair from patient sabotage and allow for early rehabilitation. We found the dorsal spanning plate to be an effective option in this complex clinical scenario. This case illustrates the utility of the dorsal spanning plate in protecting complex neurovascular repairs in the setting of severe skeletal and psychiatric instability.

Central nervous system (CNS) lymphoma is an extranodal non-Hodgkin B-cell lymphoma characterized by malignant lymph tissue arising in the brain or spinal cord, associated with inflammation and blood-brain barrier (BBB) disruption. Although BBB disruption is known to occur in patients with CNS lymphoma, a direct link between these two has not been shown. Herein, abundant deposition of the blood coagulation protein fibrinogen around B-cell lymphoma was detected in CNS lymphoma patients and in the CNS parenchyma in an orthotopic mouse model. Functional enrichment analysis of unbiased cerebrospinal fluid proteomics of CNS B-cell lymphoma patients showed that coagulation protein networks were highly connected with tumor-associated biological signaling pathways. In vivo two-photon imaging demonstrated that lymphoma growth was associated with BBB disruption, and in vitro experiments identified a role for fibrinogen in promoting lymphoma cell adhesion. Overall, these results identify perivascular lymphoma clustering at sites of fibrinogen deposition, and suggest that fibrinogen may be a target for pharmacologic intervention in metastatic B-cell lymphoma associated with BBB disruption.

Background

We analyzed the role of hypoalbuminemia, dialysis, and other risk factors that increase morbidity/ mortality following surgery for primary pyogenic spinal infections (PSIs). The American College of Surgeons' National Surgical Quality Improvement Program (ACS-NSQIP) that included 627 patients was utilized as our database.

Methods

Primary spinal surgery for spondylodiscitis was evaluated in a ACS-NSQIP database involving 627 patients between 2010 and 2019. Outcome assessment included evaluation of 30-day postoperative morbidity, and mortality rates.

Results

Within 30 postoperative days, complications occurred in 14.6% (92/627) of patients; 59 (9.4%) required readmission, and 39 (6.2%) required additional surgery. The most common complications were: wound infections, pneumonia, septic shock, and death (1.8%). Hypoalbuminemia (i.e., significantly associated with unplanned readmission and reoperation), and dialysis were the two major risk factors contributing to increased perioperative morbidity and mortality.

Conclusion

Among 627 ACS-NSQIP patients undergoing primary surgery for PSIs, hypoalbuminemia and dialysis were associated with higher risks of major perioperative morbidity (i.e., within 30 postoperative days - mostly readmissions and reoperations) and mortality.

Enterohemorrhagic Escherichia coli and related food and waterborne pathogens pose significant threats to human health. These attaching/effacing microbes infect the apical surface of intestinal epithelial cells (IEC), causing severe diarrheal disease. Colonizing the intestinal luminal surface helps segregate these microbes from most host inflammatory responses. Based on studies using Citrobacter rodentium, a related mouse pathogen, we speculate that hosts rely on immune-mediated changes in IEC, including goblet cells to defend against these pathogens. These changes include a CD4+ T cell-dependent increase in IEC proliferation to replace infected IEC, as well as altered production of the goblet cell-derived mucin Muc2. Another goblet cell mediator, REsistin-Like Molecule (RELM)-β is strongly induced within goblet cells during C. rodentium infection, and was detected in the stool as well as serum. Despite its dramatic induction, RELM-β's role in host defense is unclear. Thus, wildtype and RELM-β gene deficient mice (Retnlb-/-) were orally infected with C. rodentium. While their C. rodentium burdens were only modestly elevated, infected Retnlb-/- mice suffered increased mortality and mucosal ulceration due to deep pathogen penetration of colonic crypts. Immunostaining for Ki67 and BrDU revealed Retnlb-/- mice were significantly impaired in infection-induced IEC hyper-proliferation. Interestingly, exposure to RELM-β did not directly increase IEC proliferation, rather RELM-β acted as a CD4+ T cell chemoattractant. Correspondingly, Retnlb-/- mice showed impaired CD4+ T cell recruitment to their infected colons, along with reduced production of interleukin (IL)-22, a multifunctional cytokine that directly increased IEC proliferation. Enema delivery of RELM-β to Retnlb-/- mice restored CD4+ T cell recruitment, concurrently increasing IL-22 levels and IEC proliferation, while reducing mucosal pathology. These findings demonstrate that RELM-β and goblet cells play an unexpected, yet critical role in recruiting CD4+ T cells to the colon to protect against an enteric pathogen, in part via the induction of increased IEC proliferation.

Autoimmunity and macrophage recruitment into the central nervous system (CNS) are critical determinants of neuroinflammatory diseases. However, the mechanisms that drive immunological responses targeted to the CNS remain largely unknown. Here we show that fibrinogen, a central blood coagulation protein deposited in the CNS after blood-brain barrier disruption, induces encephalitogenic adaptive immune responses and peripheral macrophage recruitment into the CNS leading to demyelination. Fibrinogen stimulates a unique transcriptional signature in CD11b(+) antigen-presenting cells inducing the recruitment and local CNS activation of myelin antigen-specific Th1 cells. Fibrinogen depletion reduces Th1 cells in the multiple sclerosis model, experimental autoimmune encephalomyelitis. Major histocompatibility complex (MHC) II-dependent antigen presentation, CXCL10- and CCL2-mediated recruitment of T cells and macrophages, respectively, are required for fibrinogen-induced encephalomyelitis. Inhibition of the fibrinogen receptor CD11b/CD18 protects from all immune and neuropathologic effects. Our results show that the final product of the coagulation cascade is a key determinant of CNS autoimmunity.

Obesity and metabolic syndrome reflect the dysregulation of molecular pathways that control energy homeostasis. Here, we show that the p75 neurotrophin receptor (p75(NTR)) controls energy expenditure in obese mice on a high-fat diet (HFD). Despite no changes in food intake, p75(NTR)-null mice were protected from HFD-induced obesity and remained lean as a result of increased energy expenditure without developing insulin resistance or liver steatosis. p75(NTR) directly interacts with the catalytic subunit of protein kinase A (PKA) and regulates cAMP signaling in adipocytes, leading to decreased lipolysis and thermogenesis. Adipocyte-specific depletion of p75(NTR) or transplantation of p75(NTR)-null white adipose tissue (WAT) into wild-type mice fed a HFD protected against weight gain and insulin resistance. Our results reveal that signaling from p75(NTR) to cAMP/PKA regulates energy balance and suggest that non-CNS neurotrophin receptor signaling could be a target for treating obesity and the metabolic syndrome.

Astrocytes modulate neuronal activity and inhibit regeneration. We show that cleaved p75 neurotrophin receptor (p75(NTR)) is a component of the nuclear pore complex (NPC) required for glial scar formation and reduced gamma oscillations in mice via regulation of transforming growth factor (TGF)-β signaling. Cleaved p75(NTR) interacts with nucleoporins to promote Smad2 nucleocytoplasmic shuttling. Thus, NPC remodeling by regulated intramembrane cleavage of p75(NTR) controls astrocyte-neuronal communication in response to profibrotic factors.