Subsequent Development of Thrombocytopenia and Coagulopathy in Moderate and Severe Head Injury: Support for Serial Laboratory Examination

Abstract

Patients with moderate and severe TBI are at risk for thrombocytopenia and coagulopathy, not only at admission but also on subsequent laboratory examination. Repeat laboratory evaluation is warranted even if initial results are normal in this population.

Multicenter Evaluation of the Course of Coagulopathy in Patients with Isolated Traumatic Brain Injury: Relation to CT Characteristics and Outcome

“…Although we and others show that the occurrence of coagulopathy in the first 48 h after trauma is independently and strongly associated with unfavorable outcome in TBI (Carrick et al, 2005;Greuters et al, 2011;Harhangi et al, 2008;Wafaisade et al, 2010;Zehtabchi et al, 2008;), it is not identified as an independent risk factor for survival (Chesnut et al, 2000;Perel et al, 2008;Steyerberg et al, 2008). Our study further provides additional information with respect to the course of coagulopathy and its relation to initial CT findings in these patients.…”

“…Our finding that not only the mere presence but also the time course of coagulopathy holds predictive value for patient outcome, underlines the importance of systematic hemostatic monitoring over time and the need for development of treatment strategies for coagulation abnormalities in TBI patients (Carrick et al, 2005;Lustenberger et al, 2010). However, this requires closer evaluation of diagnostic tools and treatment modalities for hemostatic disturbances other than those that are currently available.…”

Hypocoagulability in Traumatic Brain Injury as Measured by Traditional Means and Thrombelastography

“…Abnormalities in admission PT, aPTT, INR, and fibrinogen degradation products have all been linked to increased morbidity and mortality in TBI patients [3,4,7,12,27,28,[32][33][34][35][36][37]. However, when we analyzed admission CCT values on 1924 of our highest-level trauma activations over 18 months, no statistically significant difference in the prevalence of coagulopathy based on these values was detected in TBI patients compared to non-TBI patients (Table 2).…”

“…A variety of mechanisms have been hypothesized including alterations in the release of tissue factor, platelet dysfunction, consumptive coagulopathy, and the activation of protein C pathways secondary to hypoperfusion [12,[23][24][25][26][27][28][29][30][31].…”

Viral hemorrhagic fevers due to endotheliopathy-associated disseminated intravascular microthrombosis and hepatic coagulopathy: pathogenesis based on “two activation theory of the endothelium”

“…This term has been applied to etiologyundetermined thrombocytopenia after exclusion of known causes of acute thrombocytopenia (e.g., heparin-induced, drug or transfusionassociated, DIC-associated, hypersplenism-related, etc.). An interesting finding is TCIP not only occurs in sepsis/septic shock, but also occurs in other critical illnesses (e.g., severe trauma, complications of surgery, pregnancy and transplant, and immunologic and collagen vascular diseases) [10][11][12][13]. Recently, significant correlation was noted between the degree of thrombocytopenia and severity of the disease, and TCIP influenced the prognosis and likelihood of recovery [14,15].…”