Hypothermic Coagulopathy in Trauma

TLDR

Hypothermic trauma patients exhibit coagulopathy that may arise from enzyme inhibition, platelet dysfunction, or fibrinolysis, yet no study has examined all three processes simultaneously. The study aimed to identify specific core temperature thresholds within the clinically common hypothermic range (33.0–36.9 °C) at which each of these coagulation processes becomes altered. Researchers prospectively evaluated 112 adult trauma patients (40 normothermic, 72 hypothermic across 33–36.9 °C subgroups) using temperature‑adjusted thrombelastography and measured PT, aPTT, platelets, CO₂, hemoglobin, hematocrit, and injury severity. Multivariate analysis revealed that at 34 °C enzyme activity and platelet function decline sharply, while fibrinolysis remains unchanged; patients ≥34 °C are hypercoagulable, indicating that enzyme slowing and platelet dysfunction independently drive hypothermic coagulopathy below 34 °C.

Abstract

Background The coagulopathy noted in hypothermic trauma patients has been variously theorized to be caused by either enzyme inhibition, platelet alteration, or fibrinolytic processes, but no study has examined the possibility that all three processes may simultaneously contribute to coagulopathy, but are perhaps triggered at different levels of hypothermia. The purpose of this study was to determine whether, at clinically common levels of hypothermia (33.0-36.9[degree sign]C), there are specific temperature levels at which coagulopathic alterations are seen in each of these processes. Methods Of 232 consecutive adult trauma patients presenting to a Level I trauma center, 112 patients met the inclusion criteria of an Injury Severity Score of 9 or greater and time since injury of less than 2 hours. Of the included patients, 40 were normothermic and 72 were hypothermic (>or=to37[degree sign]C, n = 40; 36.9-36[degree sign]C, n = 29; 35.9-35[degree sign]C, n = 20; 34.9-34[degree sign]C, n = 16; 33.9-33[degree sign]C, n = 7). Included patients were prospectively studied with thrombelastography adjusted to core body temperature. Additionally, PT, aPTT, platelets, CO2, hemoglobin, hematocrit, and Injury Severity Score were measured. Results Analysis by multivariate analysis of variance of the relationship between coagulation and temperature demonstrated that in hypothermic trauma patients, 34[degree sign]C was the critical point at which enzyme activity slowed significantly (p < 0.0001), and at which significant alteration in platelet activity was seen (p < 0.001). Fibrinolysis was not significantly affected at any of the measured temperatures (p > 0.25). Conclusions Patients whose temperature was >or=to34.0[degree sign]C actually demonstrated a significant hypercoagulability. Enzyme activity slowing and decreased platelet function individually contributed to hypothermic coagulopathy in patients with core temperatures below 34.0[degree sign]C. All the coagulation measures affected are part of the polymerization process of platelets and fibrin, and this process may be the mechanism by which the alteration in coagulation occurs.