Traumatic brain injury has long been associated with abnormal coagulation parameters, but the exact mechanisms underlying this phenomenon are poorly understood. Coagulopathy after traumatic brain injury includes hypercoagulable and hypocoagulable states that can lead to secondary injury by either the induction of microthrombosis or the progression of hemorrhagic brain lesions. Multiple hypotheses have been proposed to explain this phenomenon, including the release of tissue factor, disseminated intravascular coagulation, hyperfibrinolysis, hypoperfusion with protein C activation, and platelet dysfunction. The diagnosis and management of these complex patients are difficult given the lack of understanding of the underlying mechanisms. The goal of this review is to summarize the current knowledge regarding the mechanisms of coagulopathy after blunt traumatic brain injury. The current and emerging diagnostic tools, radiological findings, treatment options, and prognosis are discussed.
ABBREVIATIONS: aPC, activated protein C
FFP, fresh-frozen plasma
INR, international normalized ratio
PT, thromboplastin time
PTT, partial thromboplastin time
TBI, traumatic brain injury
TF, tissue factor
tPA, tissue-type plasminogen activator
Departments of ‡Neurological Surgery; and
‖Brain and Spinal Injury Center, University of California, San Francisco, California
Correspondence: Geoffrey T. Manley, MD, PhD, Professor and Vice Chairman of Neurological Surgery University of California, San Francisco, Chief of Neurosurgery, San Francisco General Hospital, Codirector, Brain and Spinal Injury Center (BASIC), 1001 Potrero Ave, Bldg 1, Room 101, San Francisco, CA 94110. E-mail: firstname.lastname@example.org
* These authors have contributed equally to this article.
Received May 20, 2011
Accepted December 14, 2011