• Patrick K Davis, Harsha Musunuru, Mark Walsh, Robert Cassady, Robert Yount, Andrew Losiniecki, Ernest E Moore, Max V Wohlauer, Janet Howard, Victoria A Ploplis, Francis J Castellino, and Scott G Thomas.
• W. M. Keck Center for Transgene Research, University of Notre Dame, Notre Dame, IN 46556, USA.
• Neurocrit Care. 2013 Apr 1; 18 (2): 201-8.

BackgroundThe 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.MethodsThis 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.ResultsCompared 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.ConclusionThese 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.

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