• Sherry L Sixta, Quinton M Hatch, Nena Matijevic, Charles E Wade, John B Holcomb, and Bryan A Cotton.
• The Department of Surgery and The Center for Translational Injury Research, The University of Texas Health Science Center Houston, TX.
• Int J Burns Trauma. 2012 Jan 1; 2 (3): 158-66.

IntroductionThe development of acute coagulopathy of trauma (ACoT) is associated with a significant increase in mortality. However, the contributory mechanisms behind ACoT have yet to be clearly defined. The purpose of this study was to evaluate the influence of multiple variables, including base deficit and injury severity, on development of ACoT within a subset of critically ill trauma patients.MethodsA retrospective review of all trauma laparotomies between 01/2004-12/2009 was performed. ACoT (+) was defined as an arrival INR ≥1.5, ACoT (-) defined as INR<1.5. Univariate and multivariate analyses were performed.ResultsOf 1218 patients, 337 (27%) were ACoT (+) and 881 (73%) were ACoT (-) upon presentation. Groups were similar in demographics, ED fluid administration, GCS scores, and admission temperatures. Admission base deficit (8.5 vs. 4, p<0.001) and ISS (median 25 vs. 16, p<0.001) were higher in the ACoT (+) group, as were intra-operative RBC (median 4 vs. 0 U) and plasma (3 vs. 0 U) transfusions; both p<0.001. Multiple-linear regression revealed INR values were independently associated with arrival base deficit and pre-hospital fluid volumes (both p<0.001). On logistic regression, the development of ACoT (+) was associated with base deficit (OR 0.92, p=0.013) as well as ISS (OR 1.05, p<0.001). However, blunt mechanism alone was not an independent predictor of ACoT.ConclusionThe current study revealed that ACoT is independently associated with both shock (base deficit) and tissue injury. Additionally, tissue injury is a significant contributor to the development of early ACoT regardless of blunt or penetrating mechanism.

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