• Alisa S Wolberg, Zhi Hong Meng, Dougald M Monroe, and Maureane Hoffman.
• Department of Pathology and Laboratory Medicine, University of North Carolina, Chapel Hill, North Carolina, USA.
• J Trauma. 2004 Jun 1; 56 (6): 1221-8.

BackgroundHypothermia is associated with an increased risk of bleeding and is a significant contributing factor to the morbidity and mortality of trauma and complicated surgical procedures. A core temperature of 33 degrees C is associated with a significantly increased risk of death after trauma compared with 37 degrees C. Hypothermia-associated bleeding has been hypothesized to result from dysregulation of enzymatic function, reduced platelet activity, and/or altered fibrinolysis.MethodsWe systematically evaluated the effects of temperature on isolated pro- and anticoagulant enzyme processes and platelet activation and adhesion. We also evaluated the effects of temperature on complete coagulation systems (activated partial thromboplastin time and an in vitro, cell-based model of coagulation).ResultsEnzyme activities were only slightly reduced at 33 degrees C versus 37 degrees C, and this reduction was not statistically significant (p > 0.05). Platelet activation was also not significantly reduced at 33 degrees C versus 37 degrees C. Conversely, platelet aggregation and adhesion were significantly reduced at 33 degrees C compared with 37 degrees C (p < 0.05). Below 33 degrees C, however, both enzyme activity and platelet function were significantly reduced.ConclusionOur results suggest that bleeding observed at mildly reduced temperatures (33 degrees - 37 degrees C) results primarily from a platelet adhesion defect, and not reduced enzyme activity or platelet activation. However, at temperatures below 33 degrees C, both reduced platelet function and enzyme activity likely contribute to the coagulopathy.

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