%0 Journal Article
%T Acute and delayed mild coagulopathy are related to outcome in patients with isolated traumatic brain injury
%A Sjoerd Greuters
%A Annelies van den Berg
%A Gaby Franschman
%A Victor A Viersen
%A Albertus Beishuizen
%A Saskia M Peerdeman
%A Christa Boer
%A ALARM-BLEEDING investigators
%J Critical Care
%D 2011
%I BioMed Central
%R 10.1186/cc9399
%X The local Human Subjects Committee approved the study. We retrospectively studied the medical records of computed tomography (CT)-confirmed isolated TBI patients with an extracranial abbreviated injury scale (AIS) <3 who were primarily referred to a Level 1 trauma centre in Amsterdam (n = 107). Hemostatic parameters including activated partial thromboplastin time (aPTT), prothrombin time (PT), platelet count, hemoglobin, hematocrit, glucose, pH and lactate levels were recorded throughout a 72-hour period as part of a routine standardized follow-up of TBI. Coagulopathy was defined as a aPPT >40 seconds and/or a PTT in International Normalized Ratio (INR) >1.2 and/or a platelet count <120*109/l.Patients were mostly male, aged 48 ¡À 20 years with a median injury severity score of 25 (range 20 to 25). Early coagulopathy as diagnosed in the emergency department (ED) occurred in 24% of all patients. The occurrence of TBI-related coagulopathy increased to 54% in the first 24 hours post-trauma. In addition to an increased age and disturbed pupillary reflex, both coagulopathy upon ED arrival and during the first 24 hours post-trauma provided an independent prognostic factor for unfavorable outcome (odds ratio (OR) 3.75 (95% CI 1.07 to 12.51; P = 0.04) and OR 11.61 (2.79 to 48.34); P = 0.003).Our study confirms a high prevalence of early and delayed coagulopathy in patients with isolated TBI, which is strongly associated with an unfavorable outcome. These data support close monitoring of hemostasis after TBI and indicate that correction of coagulation disturbances might need to be considered.Acute coagulopathy in the absence of extracranial injuries is a severe complication of traumatic brain injury (TBI) and may contribute to secondary injury and mortality [1,2]. Among others, brain injury is associated with activation of the coagulation cascade through fulminant cerebral tissue factor release, contributing to disseminated intravascular coagulation and cerebral microthrombi.
%U http://ccforum.com/content/15/1/R2