Coagulopathy After Traumatic Brain Injury
ABSTRACT 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.
SourceAvailable from: Simone DekkerJournal of Surgical Research 02/2014; 186(2):515. DOI:10.1016/j.jss.2013.11.343 · 2.12 Impact Factor
Journal of Surgical Research 02/2014; 186(2):521. DOI:10.1016/j.jss.2013.11.358 · 2.12 Impact Factor
Article: The coagulopathy of trauma[Show abstract] [Hide abstract]
ABSTRACT: Trauma is a leading cause of death, with uncontrolled hemorrhage and exsanguination being the primary causes of preventable deaths during the first 24 h following trauma. Death usually occurs quickly, typically within the first 6 h after injury. One out of four patients arriving at the Emergency Department after trauma is already in hemodynamic and hemostatic depletion. This early manifestation of hemostatic depletion is referred to as the coagulopathy of trauma, which may distinguished as: (i) acute traumatic coagulopathy (ATC) and (ii) iatrogenic coagulopathy (IC). The principle drivers of ATC have been characterized by tissue trauma, inflammation, hypoperfusion/shock, and the acute activation of the neurohumoral system. Hypoperfusion leads to an activation of protein C with cleavage of activated factors V and VIII and the inhibition of plasminogen activator inhibitor-1 (PAI-1), with subsequent fibrinolysis. Endothelial damage and activation results in Weibel–Palade body degradation and glycocalyx shedding associated with autoheparinization. In contrast, there is an IC which occurs secondary to uncritical volume therapy, leading to acidosis, hypothermia, and hemodilution. This coagulopathy may, then, be an integral part of the “vicious cycle” when combined with acidosis and hypothermia. The awareness of the specific pathophysiology and of the principle drivers underlying the coagulopathy of trauma by the treating physician is paramount. It has been shown that early recognition prompted by appropriate and aggressive management can correct coagulopathy, control bleeding, reduce blood product use, and improve outcome in severely injured patients. This paper summarizes: (i) the current concepts of the pathogenesis of the coagulopathy of trauma, including ATC and IC, (ii) the current strategies available for the early identification of patients at risk for coagulopathy and ongoing life-threatening hemorrhage after trauma, and (iii) the current and updated European guidelines for the management of bleeding and coagulopathy following major trauma.European Journal of Trauma and Emergency Surgery 04/2014; 40(2):113-126. DOI:10.1007/s00068-014-0389-4 · 0.38 Impact Factor