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BACKGROUND Utilization of intracranial pressure monitors (ICPMs) has not been consistently shown to improve mortality in patients with severe traumatic brain injury (TBI). A single-center analysis concluded that venous thromboembolism (VTE) chemoprophylaxis (CP) posed no significant bleeding risk in patients following ICPM implementation; however, there is still debate about the optimal use and timing of CP in patients with ICPMs for fear of worsening intracranial hemorrhage. We hypothesized that ICPM use is associated with increased time to VTE CP and thus increased VTE in patients with severe TBI. METHODS A retrospective analysis of the Trauma Quality Improvement Program (2010-2016) was performed to compare severe TBI patients with and without ICPMs. A multivariable logistic regression analysis was completed. RESULTS From 35,673 patients with severe TBI, 12,487 (35%) had an ICPM. Those with ICPMs had a higher rate of VTE CP (64.3% vs. 49.4%, p  less then  0.001) but a longer median time to CP initiation (5 vs. 4 days, p  less then  0.001) as well as a longer hospital length of stay (LOS) (18 vs. 9 days, p  less then  0.001) compared to those without ICPMs. After adjusting for covariates, ICPM use was found to be associated with a higher risk of VTE (9.2% vs 4.3%, OR = 1.75, CI = 1.42-2.15, p  less then  0.001). CONCLUSIONS Compared to patients without ICPMs, those with ICPMs had a longer delay to initiation of CP leading to an increase in VTE. In addition, there was a nearly two-fold higher associated risk for VTE in patients with ICPMs even when controlling for known VTE risk factors. Improved adherence to initiation of CP in the setting of ICPMs may help decrease the associated risk of VTE with ICPMs.INTRODUCTION High alcohol consumption has been associated with decreased fibrinolysis and enhanced thrombosis risk in cardiovascular disease. In trauma, alcohol has been associated with poor clot formation; however, its effect on fibrinolysis has not been fully investigated. We assessed the association of blood alcohol levels and fibrinolysis in trauma activation patients. METHODS We queried our prospective registry of trauma activations from 2014 to 2016. Associations between viscoelastic measurements [rapid thrombelastography (rTEG)] and blood alcohol level (BAL) were determined and adjusted for confounders by a multinomial logistic regression. Lysis phenotypes were defined by the % lysis in 30 min (LY30) as follows hyperfibrinolysis ≥ 3%, physiologic 0.9-2.9%, and fibrinolysis shutdown  150 mg/dL were independently associated with a threefold increase in the odds of shutdown compared to undetectable BAL (OR 3.37, 95% CI 1.04-8.05, p = 0.006). High BAL was also significantly associated with higher odds of shutdown compared to low BAL (OR 2.63, 95% CI 1.15-6.06). Compared to physiologic fibrinolysis, fibrinolysis shutdown was associated with increased mortality (OR 2.87, 95% CI 1.41-5.83) and VFD  less then  28 (OR 2.54, 95% CI 1.47-4.39). BMS-986397 nmr CONCLUSION In the injured patient, high blood alcohol levels are associated with increased incidence of fibrinolysis shutdown. This finding has implications for postinjury hemostatic resuscitation as these patients may be harmed by anti-fibrinolytics. Further research is needed to assess whether the association with fibrinolysis is modified by the chronicity and type of alcohol consumed and whether anti-fibrinolytic therapy in intoxicated patients produces adverse effects.OBJECTIVE The modified advanced core decompression (mACD) combines the advantages of a low invasive core decompression with maximal removal of osteonecrotic bone and a biologic reconstruction of the resulting bone defect. INDICATIONS Avascular (atraumatic) osteonecrosis of the femoral head (ARCO stage II). CONTRAINDICATIONS Subchondral fractures (ARCO stage III); advanced osteoarthritis (e.g., ACRO stage IV); persisting risk factors such as high-dose corticoid therapy, chemotherapy, alcohol abuse; open growth plates; history of side effects or intolerance to components of the applied bone substitute; lack of patient compliance; osteomyelitis or other septic conditions. SURGICAL TECHNIQUE Supine positioning on the operation table, skin disinfection, and sterile draping. Skin incision and core decompression using a 3.2 mm guide wire. Removal of a bone cylinder from a nonaffected area of the femoral neck using a hollow trephine. Drilling of the osteonecrotic area over the applied wire up to 5 mm to the subchondral bone under fluoroscopy, insertion of an expandable bone knife and removal of the osteonecrotic bone supported by a curette. Bone grafting of the autologous bone into the subchondral defect zone and filling of the drill canal by resorbable bone substitute. POSTOPERATIVE MANAGEMENT Bed rest for 24 h, then partial weight bearing (20 kg) on crutches for 2-6 weeks depending on the bone quality in the defect zone and the applied bone substitute. RESULTS Midterm superiority (2 years) in hip survival of the mACD over advanced core depression and core depression, especially in ARCO stage II.OBJECTIVE All arthroscopic treatment of deep cartilage defects in the knee for reconstruction of the articular surface. INDICATIONS Focal cartilage defects of the knee (ICRS ≥ grade 3) from a size of 2.5 cm2 and more. CONTRAINDICATIONS Osteoarthritis (Kellgren-Lawrence > grade 2), osseus defect situation, cartilage lesion of the opposing articular surfaces (ICRS > grade 2), instability, malalignment (>3-4°), inflammatory joint diseases. SURGICAL TECHNIQUE First procedure (cell harvesting) Treatment of additional pathologies, preparation of the cartilage defect, harvesting of osteochondral cylinders for cell culture. Second procedure (cell implantation) Dry arthroscopy, cleaning and drying of the already prepared defect, implantation of the in situ crosslinking cartilage cell suspension. POSTOPERATIVE MANAGEMENT First procedure (cell harvesting) Early functional treatment with weight bearing as tolerated. Second procedure (cell implantation) No drains, extension brace for 4 days, then free range of motion, partial weight bearing for 4 weeks in patellofemoral implantation and for 8 weeks in tibiofemoral implantation, continuous passive motion beginning in postoperative week 2, cycling from postoperative week 9.