HYPOTHERMIA HAS BEEN shown to cause coagulation abnormalities, primari
ly related to platelet dysfunction. We reviewed coagulation function a
nd the incidence of delayed traumatic intracerebral hemorrhage in a se
ries of 36 patients with severe head injuries (Glasgow Coma Scale 3-7)
enrolled in a prospective, randomized, clinical trial of therapeutic
moderate hypothermia. Patients were randomized to a normothermic group
(n = 16) or to a group cooled to 32 to 33 degrees C within 6 hours of
injury (n = 20). Prothrombin times, partial thromboplastin times, and
platelet counts were obtained in the emergency room and then again wi
thin 24 hours of randomization. Delayed traumatic intracerebral hemorr
hage occurred in 6 of 20 (30%) hypothermic patients and 5 of 16 (31%)
normothermic patients. In the hypothermic group, 9 of 17 patients had
an increased prothrombin time during hypothermic therapy, as opposed t
o 11 of 16 in the normothermic group during the corresponding time per
iod. The partial thromboplastin time was prolonged in 2 of 17 hypother
mic patients and 2 of 16 normothermic patients. Three patients in the
hypothermic group and one in the normothermic group developed thromboc
ytopenia (a platelet count of less than 100,000). There were no signif
icant differences between the two groups in the incidence of delayed t
raumatic intracerebral hemorrhage, in measured coagulopathy, or in the
mean values of measured coagulation parameters. Although the possibil
ity of a hypothermia-induced coagulopathy has not yet been excluded, t
he short-term use of hypothermia does not appear to increase the risk
for intracranial hemorrhagic complications in head injuries.