• D K Resnick, D W Marion, and J M Darby.
• Department of Neurological Surgery, University of Pittsburgh School of Medicine, Pennsylvania.
• Neurosurgery. 1994 Feb 1;34(2):252-5; discussion 255-6.

AbstractHypothermia has been shown to cause coagulation abnormalities, primarily related to platelet dysfunction. We reviewed coagulation function and the incidence of delayed traumatic intracerebral hemorrhage in a series 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 within 24 hours of randomization. Delayed traumatic intracerebral hemorrhage 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 to 11 of 16 in the normothermic group during the corresponding time period. The partial thromboplastin time was prolonged in 2 of 17 hypothermic patients and 2 of 16 normothermic patients. Three patients in the hypothermic group and one in the normothermic group developed thrombocytopenia (a platelet count of less than 100,000). There were no significant differences between the two groups in the incidence of delayed traumatic intracerebral hemorrhage, in measured coagulopathy, or in the mean values of measured coagulation parameters. Although the possibility of a hypothermia-induced coagulopathy has not yet been excluded, the short-term use of hypothermia does not appear to increase the risk for intracranial hemorrhagic complications in head injuries.

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