Platelet Dysfunction in Patients with Severe Traumatic Brain Injury

Abstract

Coagulopathy is a common phenomenon in traumatic brain injury (TBI) and a major contributor to a poor outcome. Thrombocytopenia is a strong negative prognostic factor in TBI, but bleeding tendency can be present even with a normal platelet count. We investigated platelet function in patients with TBI by means of modified thromboelastography (i.e., platelet mapping [TEG-PM]). Four groups were studied: (1) patients with severe isolated TBI (n = 20), (2) patients with general trauma without TBI (the ICU group, n = 10), (3) patients with chronic alcohol abuse (n = 7; as alcohol abuse is common in patients with TBI), and (4) healthy volunteers (n = 10). We measured platelet counts in venous blood (Plt), Ivy bleeding time, standard TEG parameters, and platelet responses to arachidonic acid (AA) and adenosindiphosphate (ADP), using TEG-PM. TBI patients had a lower Plt (180 +/- 68 x 10(9) ; mean +/- SD) and a longer bleeding time (674 +/- 230 sec) than healthy controls, (256 +/- 43 x 10(9), p < 0.01) and (320 +/- 95 sec, p < 0.005), respectively. TBI patients had dramatically lower platelet responses to AA (0-86%, mean 22%) compared to healthy controls (57-89%, mean 73%), the ICU group (4-75%, mean 49%), and the alcohol abusers (17-88%, mean 64%; p < 0.001). Responses to ADP did not differ significantly between the groups. Patients with low responsiveness to AA at admittance to the hospital were likely to develop bleeding complications later. Patients with TBI develop platelet dysfunction, which most likely contributes to bleeding complications. The observed platelet dysfunction appears to involve the cyclooxygenase pathway. TEG-PM analysis can be used to identify patients with a high risk of bleeding complications.

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

“…Previous authors have also reported that platelet dysfunction in TBI patients correlates with poor outcomes, [12,37] but to our knowledge, no other publications correlate TBI coagulopathy with mA or alpha-angle TEG values. Kunio et al analyzed 69 polytrauma patients with TBI and found that these patients had an increased R-time on traditional TEG [8].…”

“…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].…”

“…Coagulopathy frequently accompanies severe TBI and compounds the risk of morbidity and mortality [3][4][5][6][7][8][9]. However, the incidence and factors associated with coagulopathy in TBI has not been firmly established [4,7,[10][11][12]. In 2009, Talving et al published the only prospective data to date from a level I urban trauma center, demonstrating a 34-36% incidence of coagulopathy in TBI patients, as measured by International Normalized Ration (INR), activated partial thromboplastin time (aPTT), and platelet count.…”

Coagulation disorder in moderate to severe traumatic brain injuries

“…Brain tissue is rich in thromboplastin, and activation of clotting pathways following traumatic brain injury is thought to occur leading to abnormal coagulation. 1 Many studies have suggested possible adverse effects of disseminated intravascular coagulation and other coagulopathies on outcome of the patients. [2][3][4][5][6][7] Post-traumatic coagulopathy, in particular, appears to be linked to secondary cerebral injury.…”