Hypothermic coagulopathy in trauma: effect of varying levels of hypothermia on enzyme speed, platelet function, and fibrinolytic activity.
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 degrees 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 =37 degrees C, n = 40; 36.9-36 degrees C, n = 29; 35.9-35 degrees C, n = 20; 34.9-34 degrees C, n = 16; 33.9-33 degrees 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 degrees 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 =34.0 degrees 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 degrees 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.
Watts
D D
DD
Department of Trauma Services, Inova Regional Trauma Center, Falls Church, Virgina 22042-3300, USA.
Trask
A
A
Soeken
K
K
Perdue
P
P
Dols
S
S
Kaufmann
C
C
D000293:Adolescent; D000328:Adult; D001777:Blood Coagulation / Q000502:physiology; D001778:Blood Coagulation Disorders / Q000097:blood / Q000209:etiology*; D001792:Blood Platelets / Q000502:physiology; D001831:Body Temperature; D005260:Female; D005342:Fibrinolysis; D005440:Fluid Therapy; D006400:Hematocrit; D006801:Humans; D007035:Hypothermia / Q000097:blood / Q000150:complications*; D015601:Injury Severity Score; D008297:Male; D015999:Multivariate Analysis; D010314:Partial Thromboplastin Time; D011446:Prospective Studies; D013916:Thrombelastography; D014947:Wounds and Injuries / Q000097:blood / Q000145:classification / Q000150:complications*