Ent of intracranial lesions was not performed in a standardized manner

Ent of intracranial lesions was not performed in a standardized manner, and as several factors have a crucial impact on these findings, such as timing of computed tomography scans, comparison of the results has only limited validity. Finally, the mechanisms of injury and severity of injuries differ substantially between reported studies. While some studies were restricted to `isolated' head injury, others included patients with relevant injuries to other organ systems, such as liver laceration and pulmonary contusions. In the context of polytrauma, attribution of parameters like mortality to TBI or other injuries can be difficult Cyclohept-2-enone and this also may explain differences between the results. In conclusion, despite the deficits of reported studies, the available data suggest that patients on antiplatelet therapy may have a higher risk of mortality and morbidity after TBI, especially in cases of posttraumatic ICH. Although risk factors have not been identified yet, it seems that patients with more severe TBI might be at particular risk of negative effects due to preinjury PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/17184506 antiplatelet therapy. Nevertheless, welldesigned studies are desperately needed to shed light on this important topic. Important factors such as degree of platelet activity inhibition and the impact of antiplatelet medication onneurologic longterm outcome after TBI have to be taken into consideration when conducting the design of prospective studies.Diagnostic evaluation of antiplatelet therapy in TBI patients Standard laboratory coagulation tests in TBI patients include assessment of activated partial thromboplastin time, prothrombin time, fibrinogen, and platelet count. These laboratory values do not allow assessment PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/9871638 of platelet activity. History regarding the use of antiplatelet therapy should be evaluated in all TBI patients, although this may not be possible in all cases. Thrombelastometry is a method allowing for haemostasis testing, including platelet activity, in whole blood [29]. Its use has been suggested for the management of active haemorrhage in trauma victims to guide haemostatic therapy [30] and a recent study showed its results to be predictive of outcome in patients with severe TBI [31]. Further research will show if the use of this 2-Bromo-1,3-difluoro-4-nitrobenzene tool is of benefit in patients with TBI, especially if disorders of the coagu latory system are apparent. Bachelani and colleagues [27] used the specific assay `Aspirin Response Test' (VerifyNow? Accumetrics, San Diego, CA, USA) for identifying effects of aspirin on platelet activity after TBI. Originally, this test was developed for cardiologists to assess the efficacy of aspirininduced platelet inhibitionBeynon et al. Critical Care 2012, 16:228 http://ccforum.com/content/16/4/Page 5 ofand monitor patient compliance. In this study, this test showed that 42 of patients with unknown history of aspirin had signs of platelet inhibition. The authors assessed the efficacy of platelet transfusion through repeating the `Aspirin Response Test' and, interestingly, failure of normalizing platelet function was associated with a trend towards a higher risk of mortality. A specific pointofcare assay for detection of clopidogrelinduced platelet inhibition (VerifyNow 2Y12, Accumetrics) is also available. Bansal and colleagues [32] used this assay in 46 trauma patients and showed that a large percentage of patients had undetectable or low platelet inhibition despite reported use of clopidogrel. Incompliance of patients as well as ineffectivenes.