Skip Navigation LinksHome > June 2012 - Volume 70 - Issue 6 > Coagulopathy After Traumatic Brain Injury
doi: 10.1227/NEU.0b013e31824d179b

Coagulopathy After Traumatic Brain Injury

Laroche, Mathieu MD*,‡,‖; Kutcher, Matthew E. MD*,§; Huang, Michael C. MD‡,‖; Cohen, Mitchell Jay MD§; Manley, Geoffrey T. MD, PhD‡,‖

CNS University of Neurosurgery
Collapse Box


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

Copyright © by the Congress of Neurological Surgeons


Article Tools


Article Level Metrics

Search for Similar Articles
You may search for similar articles that contain these same keywords or you may modify the keyword list to augment your search.