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Traumatic brain injury associated coagulopathy is a widely recognized risk factor for secondary brain damage and a powerful predictor related to outcome and prognosis. It is estimated that two thirds of patients with severe TBI will develop a coagulopathy. Pathophysiological pathway of TBI associated coagulopathy remains poorly defined. It includes combination of hypercoagulable and hypofibrinolytic states that result in persistent and delayed intracranial haemorrhage and systemic bleeding. The proposed mechanisms include release of tissue factor, hyperfibrinolysis, disseminated intravascular coagulopathy, platelet disfunction and protein C activation. The goal of this review is to summarize the current knowledge regarding the mechanisms of traumatic brain injury associated coagulopathy and treatment options.67, Koagulopatije kod traumatske ozljede mozga bitan su faktor u razvoju sekundarnih ozljeda mozga i snažan su prediktor za ishod i prognozu liječenja. Procijenjuje se da dvije trećine pacijenata sa teškom traumom mozga razvije koagulopatiju. Patofiziološki mehanizam koagulopatije kod traumatske ozljede mozga je slabo razjašnjen. Uključuje otpuštanje tkivnog faktora, hiperfibrinolizu, diseminiranu intravaskularnu koagulopatiju, poremećaj funkcije trombocita i aktivaciju proteina C. Cilj ovoga rada je osvrnuti se na aktualna saznanja o patofiziologiji koagulopatije kod traumatske ozljede mozga i metode liječenja.