D. Pinto1, T. D. Le1, A. Pusateri2, S. Matthew1, E. J. Kelly1, L. Moffatt1,3,5,6, J. W. Shupp1,3,4,5,6 1Firefighters’ Burn and Surgical Research Laboratory, MedStar Health Research Institute, Washington, DC, USA 2Naval Medical Research Unit San Antonio, JBSA-Fort Sam Houston, San Antonio, TEXAS, USA 3The Burn Center, MedStar Washington Hospital Center, Washington, DC, USA 4Georgetown University School of Medicine, Deaprtment Of Surgery, Washington, DC, USA 5Georgetown University School of Medicine, Department Of Biochemistry, Washington, DC, USA 6Georgetown University School of Medicine, Department Of Plastic And Reconstructive Surgery, Washington, DC, USA
Introduction: Coagulopathy, a dysfunction in hemostasis, plays a major role in morbidity and mortality associated with burn injury. Larger total body surface area (TBSA) burn increases the frequency of burn-induced coagulopathy (BIC), yet the exact mechanism of BIC and the impact of TBSA on it is not fully understood. By analyzing specific coagulation factors after burn injury, a more comprehensive picture of BIC can be obtained and treatment strategies to improve clinical outcomes can be developed.
Methods: This prospective observational study enrolled burn patients admitted to a regional burn center. Patient demographics, injury characteristics, and blood samples for traditional coagulation assays (international normalized ratio (INR), prothrombin time (PT), partial thromboplastin time (PTT)) and activity levels for factor II, V, VII, VIII, IX, X, XI, antithrombin (AT) and free tissue factor pathway inhibitor (TFPI-free) were collected at admission. Factor levels and coagulation assays were compared between groups based on burn size (TBSA <20% and ≥ 20%) using a two-sample t-test or Wilcoxon rank-sum test and chi-square or Fisher exact test. A statistical significance is set at 2-sided p <0.05.
Results: 132 patients were included and most patients were male (70%) with a median age of 40 years and median TBSA of 11.8%. Overall mortality was 12.9% (n=17) and was associated with higher age, higher Baux score, larger burn (≥ 20%), and inhalation injury. When comparing burn size, the median PT level was significantly higher for larger burn size (14.1 vs 13.7). There was no difference in median levels of INR (1.1 vs 1.1) and PTT (29 vs 27.9) between groups. Only 3 out of 46 patients (6.5%) with TBSA ≥ 20% had coagulopathy identified by INR >1.3 and PTT > 35. Except for VIII and IX, all coagulation factors were within normal limits at admission. The mean value of Factor VIII (317%) was double the normal value (70-150%). When comparing burn size, coagulation factor II, IX, X, and XII were all significantly lower for patients with larger burn size (≥ 20% TBSA). Factor V, VII, and XI were also lower, but did not meet statistical significance. At admission, the median level of anti-coagulant factor AT was significantly decreased for patients with larger burn size (80.5 vs 99), and there was no difference for TFPI-free levels between groups.
Conclusion: Despite normal levels for almost all coagulation and anticoagulation factors at admission, there were significant differences in the coagulation profile based on TBSA, suggesting a shift towards coagulopathy. This shift was not fully identified by traditional coagulation assays indicating a need for more accurate and earlier detection methods for BIC. Identifying the rate at which these factors are consumed and regenerated, and the proportions of coagulation to anticoagulation factors over time are topics that need further exploration to improve morbidity and mortality associated with BIC.