Background

Bilateral total knee arthroplasties (BTKA) performed during the same hospitalization carry increased risk for morbidity and mortality as compared to the unilateral approach. However, no evidence-based stratifications to identify patients at risk for major morbidity and mortality are available. Our objective was to determine the incidence and patient-related risk factors for major morbidity and mortality among patients undergoing BTKA.

Methods

Nationwide Inpatient Survey data collected for the years 1998–2007 were analyzed and cases of elective BTKA procedures were included. Patient demographics, including comorbidities, were analyzed and frequencies of mortality and major complications were computed. Subsequently, a multivariate analysis was conducted to determine independent risk factors for major morbidity and mortality.

Results

Included were 42,003 database entries, representing an estimated 206,573 elective BTKA. The incidence of major in-hospital complications and mortality was 9.5%. Risk factors for adverse outcome included advanced age [odds ratios (OR) for age groups 65–74 and >75 years were 1.88 (Confidence Interval (CI) 1.72; 2.05) and 2.66 (CI 2.42; 2.92), respectively, compared to the 45–65 year group], male gender [OR 1.54 (CI 1.44; 1.66)], and a number of comorbidities. The presence of congestive heart failure (OR 5.55 (CI 4.81; 6.39)) and pulmonary hypertension [OR 4.10 (CI2.72; 6.10)] were the most significant risk factors associated with increased odds for adverse outcome.

Conclusions

We identified patient-related risk factors for major morbidity and mortality in patients undergoing BTKA. Our data can be used to aid in the selection of patients for this procedure.

Background

Recent studies have implied that osteoarthritis (OA) is a metabolic disease linked to deregulation of genes involved in lipid metabolism and cholesterol efflux. Sterol Regulatory Element Binding Proteins (SREBPs) are transcription factors regulating lipid metabolism with so far no association with OA. Our aim was to test the hypothesis that SREBP-2, a gene that plays a key role in cholesterol homeostasis, is crucially involved in OA pathogenesis and to identify possible mechanisms of action.

Methodology/Principal Findings

We performed a genetic association analysis using a cohort of 1,410 Greek OA patients and healthy controls and found significant association between single nucleotide polymorphism (SNP) 1784G>C in SREBP-2 gene and OA development. Moreover, the above SNP was functionally active, as normal chondrocytes’ transfection with SREBP-2-G/C plasmid resulted in interleukin-1β and metalloproteinase-13 (MMP-13) upregulation. We also evaluated SREBP-2, its target gene 3-hydroxy-3-methylglutaryl-coenzymeA reductase (HMGCR), phospho-phosphoinositide3-kinase (PI3K), phospho-Akt, integrin-alphaV (ITGAV) and transforming growth factor-β (TGF-β) mRNA and protein expression levels in osteoarthritic and normal chondrocytes and found that they were all significantly elevated in OA chondrocytes. To test whether TGF-β alone can induce SREBP-2, we treated normal chondrocytes with TGF-β and found significant upregulation of SREBP-2, HMGCR, phospho-PI3K and MMP-13. We also showed that TGF-β activated aggrecan (ACAN) in chondrocytes only through Smad3, which interacts with SREBP-2. Finally, we examined the effect of an integrin inhibitor, cyclo-RGDFV peptide, on osteoarthritic chondrocytes, and found that it resulted in significant upregulation of ACAN and downregulation of SREBP-2, HMGCR, phospho-PI3K and MMP-13 expression levels.

Conclusions/Significance

We demonstrated, for the first time, the association of SREBP-2 with OA pathogenesis and provided evidence on the molecular mechanism involved. We suggest that TGF-β induces SREBP-2 pathway activation through ITGAV and PI3K playing a key role in OA and that integrin blockage may be a potential molecular target for OA treatment.

The association between cytokine gene polymorphisms and chronic osteomyelitis was investigated in order to determine whether genetic variability in cytokine genes predisposes to osteomyelitis susceptibility. Significant genotypic and allelic associations were observed between interleukin 1α (IL-1α) −889-C/T, IL-4 −1098-G/T and −590-C/T, and IL-6 −174-G/C polymorphisms and osteomyelitis in the Greek population, pointing towards their potential involvement in osteomyelitis pathogenesis.

Introduction

Epidural bleeding as a complication of catheterization or epidural catheter removal is often associated with perioperative thromboprophylaxis especially in adult reconstructive surgery.

Case presentation

We report on a case of a 19 years old male athlete that underwent anterior cruciate ligament reconstruction, receiving low molecular weight heparin for thromboprophylaxis and developed an epidural hematoma and subsequent cauda equina syndrome two days after removal of the epidural catheter. An urgent magnetic resonance imaging scan revealed an epidural hematoma from the level of L3 to L4. Emergent decompression and hematoma evacuation resulted in patient's significant neurological improvement immediately postoperatively.

Conclusion

A high index of clinical suspicion and surgical intervention are necessary to prevent such potentially disabling complications especially after procedures on a day-case basis and early patient's discharge.