Delayed Endovascular Repair With Procedural Anticoagulation: A Safe Strategy for Blunt Aortic Injury.

BACKGROUND: Blunt aortic injury (BAI) and traumatic brain injury (TBI) are the leading causes of death after blunt trauma. The purposes of this study were to identify predictors of mortality for BAI and to examine the impact of procedural heparinization during thoracic endovascular aortic repair (TEVAR) on neurologic outcomes in patients with BAI/TBI. METHODS: Patients with BAI were identified over an 8 year period. Age, gender, severity of injury and shock, time to TEVAR, morbidity, and mortality were recorded and compared. Multivariable logistic regression (MLR) was performed to determine independent predictors of mortality. Youden's index determined optimal time to TEVAR. RESULTS: A total of 129 patients were identified. The majority (74%) were male with a median age and injury severity score (ISS) of 40 years and 29, respectively. Of these, 26 (20%) had a concomitant TBI. Patients with BAI/TBI had higher injury burden at presentation (ISS 37 vs. 29, P = 0.002; Glasgow Coma Scale [GCS] 6 vs. 15, P < 0.0001), underwent fewer TEVAR procedures (31 vs. 53%, P = 0.039), and suffered increased mortality (39 vs. 16%, P = 0.009). All TEVARs had procedural anticoagulation, including patients with TBI, without change in neurologic function. The optimal time to TEVAR was 14.8 hr. Mortality increased in TEVAR patients before 14.8 hr (8.7 vs. 0%, P = 0.210). MLR identified TEVAR as the only modifiable factor that reduced mortality (odds ratio 0.11; 95% confidence interval 0.03-0.45, P = 0.002). CONCLUSIONS: TEVAR use was identified as the only modifiable predictor of reduced mortality in patients with BAI. Delayed TEVAR with the use of procedural heparin provides a safe option regardless of TBI with improved survival and no difference in discharge neurologic function.

Elevated serum cobalamin in patients with decompensated biventricular failure.

BACKGROUND: Serum cobalamin (vitamin B12), bound to transcobalamin II, is taken up by the endothelium of the hepatic vasculature via a receptor-mediated membrane transport process. We hypothesized hepatic congestion is associated with elevated serum B12 without hepatocyte necrosis. METHODS AND RESULTS: Serum B12, aspartate and alanine transaminases, alkaline phosphatase, bilirubin (Bili), and brain natriuretic peptide (BNP) were monitored at the time of admission in 91 hospitalized patients: (a) 38 with decompensated biventricular failure having systemic venous distention, tricuspid regurgitation (TR), and echocardiographic evidence of inferior vena cava dilation and moderate to marked TR; (b) 18 with acute left heart failure having a myocardial infarction, an ischemic cardiomyopathy, or hypertensive heart disease; and (c) 35 without clinical evidence of failure despite myocardial infarction, pericarditis, or atrial arrhythmia. Serum cobalamin (normal 180-600 pg/mL) was elevated with biventricular failure (861.4 +/- 53.0 pg/mL) compared with (P < 0.0001) left heart or no failure, where B12 remained normal. Serum aspartate, alanine, and alkaline phosphatase were normal in each group whereas Bili was increased (1.8 +/- 0.2 mg/dL; P < 0.05) with biventricular failure. Plasma BNP was elevated in each group. CONCLUSIONS: Elevated cobalamin and Bili are respective biomarkers of hepatocellular dysfunction and cholestasis in patients having decompensated biventricular failure with systemic venous distention and TR without hepatocyte necrosis vis-à-vis left heart failure or in the absence of clinical failure. Elevated plasma BNP did not distinguish between the presence or absence of systemic venous congestion.