Early coagulopathy after traumatic brain injury: the role of hypoperfusion and the protein C pathway

The Journal of Trauma
Mitchell Jay CohenJean-François Pittet

Abstract

Early coagulopathy after traumatic brain injury (TBI) is thought to be the result of injury-mediated local release of tissue factor, although the precise mechanisms that cause hypoperfusion and early systemic coagulopathy in TBI patients are unknown. We have previously reported that early systemic coagulopathy after trauma is present only when tissue injury is associated with severe hypoperfusion leading to the activation of the protein C pathway. However, the role of hypoperfusion as an important mechanism for the development of coagulopathy early after TBI is unclear. The objective of the present study was to determine the importance of hypoperfusion and protein C activation in causing early coagulopathy in TBI patients. We performed a prospective cohort study including patients with isolated brain injury admitted to a single trauma center. Blood was drawn on average 32 minutes after injury. Plasma samples were assayed for protein C and thrombomodulin by standard laboratory techniques. Routine coagulation measures (prothrombin time, partial thromboplastin time) and arterial blood gas analysis were performed concurrently. Severe hypoperfusion was evidenced by the presence of an arterial base deficit greater than 6. Thirty-nine...Continue Reading

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