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A Systematic Evaluation of the Effect of Temperature on Coagulation Enzyme Activity and Platelet Function

Wolberg, Alisa S. PhD; Meng, Zhi Hong MPH; Monroe, Dougald M. III PhD; Hoffman, Maureane MD, PhD

The Journal of Trauma: Injury, Infection, and Critical Care: June 2004 - Volume 56 - Issue 6 - p 1221-1228
doi: 10.1097/01.TA.0000064328.97941.FC

Background: Hypothermia 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°C is associated with a significantly increased risk of death after trauma compared with 37°C. Hypothermia-associated bleeding has been hypothesized to result from dysregulation of enzymatic function, reduced platelet activity, and/or altered fibrinolysis.

Methods: We 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).

Results: Enzyme activities were only slightly reduced at 33°C versus 37°C, and this reduction was not statistically significant (p > 0.05). Platelet activation was also not significantly reduced at 33°C versus 37°C. Conversely, platelet aggregation and adhesion were significantly reduced at 33°C compared with 37°C (p < 0.05). Below 33°C, however, both enzyme activity and platelet function were significantly reduced.

Conclusion: Our results suggest that bleeding observed at mildly reduced temperatures (33°–37°C) results primarily from a platelet adhesion defect, and not reduced enzyme activity or platelet activation. However, at temperatures below 33°C, both reduced platelet function and enzyme activity likely contribute to the coagulopathy.

From the Department of Pathology, Duke University Medical Center (Z.H.M., M.H.), Pathology and Laboratory Medicine Service, Durham VA Medical Center (M.H.), Durham, and Departments of Pathology and Laboratory Medicine (A.S.W.) and Medicine (D.M.M.), University of North Carolina, Chapel Hill, North Carolina.

Submitted for publication November 5, 2002.

Accepted for publication February 6, 2003.

Supported by National Institutes of Health grant RO1 HL48320, American Heart Association grant 0160418U, and the United States Department of Veteran’s Affairs.

Address for reprints: Maureane Hoffman, MD, PhD, Pathology and Laboratory Medicine Service (113), Durham VA Medical Center, 508 Fulton Street, Durham, NC 27705; email:

© 2004 Lippincott Williams & Wilkins, Inc.