The Affordable Care Act currently requires hospitals to report 30-day readmission rates for certain medical conditions. It has been suggested that surveillance will expand to include hip and knee surgery-related readmissions in the future. To ensure quality of care and avoid penalties, readmissions related to hip fractures require further investigation. The goal of this study was to evaluate factors associated with 30-day hospital readmission after hip fracture at a level I trauma center. This retrospective cohort study included 1486 patients who were 65 years or older and had a surgical procedure performed to treat a femoral neck, intertrochanteric, and/or subtrochanteric hip fracture during an 8-year period. Analysis of these patients showed a 30-day readmission rate of 9.35% (n=139). Patients in the readmission group had a significantly higher rate of pre-existing diabetes and pulmonary disease and a longer initial hospital length of stay. Readmissions were primarily the result of medical complications, with only one-fourth occurring secondary to orthopedic surgical failure. Pre-existing pulmonary disease (odds ratio [OR], 1.885; 95% confidence interval [CI], 1.305–2.724), initial hospitalization of 8 days or longer (OR, 1.853; 95% CI, 1.223–2.807), and discharge to a skilled nursing facility (OR, 1.586; 95% CI, 1.043–2.413) were determined to be predictors of readmission. Accordingly, patient management should be consistently geared toward optimizing chronic disease states while concomitantly working to minimize the duration of initial hospitalization and decrease readmission rates.

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Objective The objective of this study was to assess the predictive value of lactate and base deficit in determining outcomes in trauma patients who are positive for ethanol. Methods Retrospective cohort study of patients admitted to a level 1 trauma center between 2005 and 2014. Adult patients who had a serum ethanol, lactate, base deficit, and negative urine drug screen obtained upon presentation were included. Results Data for 2482 patients were analyzed with 1127 having an elevated lactate and 1092 an elevated base deficit. In these subgroups, patients with a positive serum ethanol had significantly lower 72-hour mortality, overall mortality, and hospital length of stay compared with the negative ethanol group. Abnormal lactate (odds ratio [OR], 2.607; 95% confidence interval [CI], 1.629–4.173; P = .000) and base deficit (OR, 1.917; 95% CI, 1.183–3.105; P = .008) were determined to be the strongest predictors of mortality in the ethanol-negative patients. Injury Severity Score was found to be the lone predictor of mortality in patients positive for ethanol (OR, 1.104; 95% CI, 1.070–1.138; P=.000). Area under the curve and Youden index analyses supported a relationship between abnormal lactate, base deficit, and mortality in ethanol-positive patients when the serum lactate was greater than 4.45 mmol/L and base deficit was greater than −6.95 mmol/L. Conclusions Previously established relationships between elevated lactate, base deficit, and outcome do not remain consistent in patients presenting with positive serum ethanol concentrations. Ethanol skews the relationship between lactate, base deficit, and mortality thus resetting the threshold in which lactate and base deficit are associated with increased mortality.

Enoxaparin regimens commonly used for prophylaxis fail to achieve optimal anti-factor Xa levels in up to 70 per cent of trauma patients. Accordingly, trauma services at the study institution endeavored to develop a standardized approach to optimize pharmacologic prevention with enoxaparin. An enoxaparin venous thromboembolism (VTE) prophylaxis protocol implemented in October 2015 provided weight-adjusted initial dosing parameters with subsequent dose titration to achieve targeted anti-factor Xa levels. Symptomatic VTE rate was evaluated 12 months pre- and post-implementation. Data were obtained from the trauma registry and charts were reviewed from electronic medical records. The rate of symptomatic VTE significantly declined post-implementation (2.0% vs 0.9%, P = 0.009). Enoxaparin use was comparable in these two phases validating that the decline in symptomatic VTEs was not due to an increase in enoxaparin use. Symptomatic VTE rate for patients who received enoxaparin in the post-implementation cohort decreased from 3.2 to 1.0 per cent (P = 0.023, 95% confidence interval = 0.124–0.856). There was also a significant decrease in the rate of symptomatic deep vein thrombosis (2.8% vs 0.9%, P = 0.040, 95% confidence interval = 0.117–0.950). This approach to VTE prophylaxis with enoxaparin resulted in a significant reduction in symptomatic VTE rates. Implementation of similar practices may be equally impactful in other institutions that use enoxaparin.

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