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.
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ABSTRACT: Prehospital management affects long-term outcome of patients with severe traumatic brain injury (TBI). This article reviews the current concepts and ongoing controversies of prehospital treatment of severe TBI. Prehospital management focuses on the prevention of secondary brain injury and rapid transport to a neurotrauma center for definitive diagnosis and life- as well as brain-saving emergency treatment such as decompressive craniotomy. There is a broad consensus that adequate airway management, prevention of hypoxia, hypocapnia or hypercapnia, prevention of hypotension and control of hemorrhage represent preclinical therapeutic modalities that may contribute to improved survival in severe TBI. The precise role of prehospital endotracheal intubation, osmotic agents and early therapeutic hypothermia needs to be clarified in the context of time required for transportation, local infrastructure, geographical factors and availability of experienced emergency teams. Prehospital management of TBI remains challenging. There are no universal objectives suitable to all patients. Randomized, controlled clinical trials are necessary for developing optimal protocols for paramedic and physician emergency medical teams.Current opinion in anaesthesiology 07/2012; 25(5):556-62. DOI:10.1097/ACO.0b013e328357225c · 2.53 Impact Factor
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ABSTRACT: BACKGROUND: The goal of this study is to determine the presence of platelet dysfunction in patients with traumatic brain injury (TBI). The mechanisms underlying the coagulopathy associated with TBI remain elusive. The question of platelet dysfunction in TBI is unclear. METHODS: This was a prospective observational study conducted at Memorial Hospital of South Bend, IN, and Denver Health Medical Center, CO. A total of 50 patients sustaining TBI, and not under treatment with anticoagulants or platelet inhibitors, were analyzed utilizing modified thromboelastography (TEG) with platelet mapping (TEG/PM), along with standard coagulation tests. RESULTS: Compared to normal controls, patients with severe TBI had a significantly increased percentage of platelet ADP and arachidonic acid (AA) receptor inhibition. Furthermore, the percentage of ADP inhibition distinguished between survivors and non-survivors in patients with TBI (Mann-Whitney test, P = 0.035). ADP inhibition correlates strongly with severity of TBI (Mann-Whitney test, P = 0.014), while AA inhibition did not. CONCLUSION: These data indicate that early platelet dysfunction is prevalent after severe TBI, can be measured in a point-of-care setting using TEG/PM, and correlates with mortality. The mechanism responsible for this platelet dysfunction and associated implications for TBI management remains to be defined.Neurocritical Care 07/2012; 18(2). DOI:10.1007/s12028-012-9745-6 · 2.60 Impact Factor
- Journal of the American College of Surgeons 09/2012; 215(3):S60. DOI:10.1016/j.jamcollsurg.2012.06.169 · 4.45 Impact Factor