Background: Intraluminal pancreatic enzymes have been shown in animal models to be associated with multiple organ failure after hemorrhagic shock, independent of pancreatitis. The translocation of these enzymes into the circulation may serve as a marker of hemorrhagic shock-induced gut ischemia in critically injured trauma patients. We hypothesized that serum amylase and lipase would be significantly elevated in patients presenting in hemorrhagic shock and in those who develop organ failure.
Methods: Review of a prospective database at a level-1 trauma center from 2000 to 2005. Two thousand seven hundred eleven critically injured trauma patients without pancreatic injuries were evaluated for shock (systolic pressure <90 mm Hg in the emergency department), massive transfusion (10 units of packed red blood cells within the first 24 hours), and organ failure (standard criteria for acute pulmonary, cardiovascular, renal, and hepatic system failure were used). Serum levels >2 times the upper limit of normal for amylase (30–130 U/L) and lipase (7–60 U/L) were defined as elevated. Univariate analyses were performed with the Pearson’s χ2, and binary logistic regression was used to determine significant risk factors for organ failure. Results with a p value <0.05 were considered significant and are reported.
Results: Patients with elevated amylase (n = 481, 18%) were more likely to present in shock (16% vs. 8%), require massive transfusion (19% vs. 9%), develop organ failure (34% vs. 16%), and die (23% vs. 13%). Patients with elevated lipase (n = 288, 11%) were more likely to require massive transfusion (18% vs. 10%) and develop organ failure (43% vs. 16%). Independent predictors of organ failure were age (odds ratio [OR] = 1.016), Injury Severity Score (OR = 1.02), massive transfusion (OR = 3.1), elevated amylase (OR = 1.9), and elevated lipase (OR = 3.2). Elevated amylase was also an independent predictor of mortality (OR = 1.3).
Conclusions: Serum levels of pancreatic enzymes are elevated in patients who present in shock or require a massive transfusion and are independent predictors of organ failure. Whether these elevations are caused by ischemic pancreatitis or the translocation of intraluminal enteric pancreatic enzymes is uncertain and future studies are needed. Trauma patients with elevated pancreatic enzymes in the absence of a pancreatic injury have an increased risk of morbidity and mortality.