Abstract
As the population ages, emergency physicians are confronted with a growing number of trauma patients receiving antithrombotic and antiplatelet medication prior to injury. In cases of traumatic brain injury, pre-injury treatment with anticoagulants has been associated with an increased risk of posttraumatic intracranial haemorrhage. Since high age itself is a well-recognised risk factor in traumatic brain injury, this population is at special risk for increased morbidity and mortality. The effects of antiplatelet medication on coagulation pathways in posttraumatic intracranial haemorrhage are not well understood, but available data suggest that the use of these agents increases the risk of an unfavourable outcome, especially in cases of severe traumatic brain injury. Standard laboratory investigations are insufficient to evaluate platelet activity, but new assays for monitoring platelet activity have been developed. Commonly used interventions to restore platelet activity include platelet transfusion and application of haemostatic drugs. Nevertheless, controlled clinical trials have not been carried out and, therefore, clinical practice guidelines are not available. In addition to the risks of the acute trauma, patients are at risk for cardiac events such as life-threatening stent thrombosis if antiplatelet therapy is withdrawn. In this review article, we summarize the pathophysiologic mechanisms of the most commonly used antiplatelet agents and analyse results of studies on the effects of this treatment on patients with traumatic brain injury. Additionally, we focus on opportunities to counteract antiplatelet effects in those patients as well as on considerations regarding the withdrawal of antiplatelet therapy. In those chronically ill patients, an interdisciplinary approach involving intensivists, neurosurgeons as well as cardiologists is often mandatory.
Highlights
Cardiovascular disease remains the leading cause of death in industrialized countries despite significant improvements in the therapy of acute coronary syndromes [1]
In patients with traumatic brain injury (TBI), occurrence of posttraumatic intracranial haemorrhage (ICH) may increase intracranial pressure and aggravate secondary brain damage. erapeutic mechanisms of antiplatelet agents include inhibition of platelet aggregation, so normal haemostasis is impaired. is impairment may lead to an increased incidence of ICH and enlargement of haematomas in TBI, potentially increasing mortality and morbidity
Outcome was not analysed in this study, the results suggest that pre-injury use of clopidogrel may increase the risk of an unfavourable outcome after TBI
Summary
Cardiovascular disease remains the leading cause of death in industrialized countries despite significant improvements in the therapy of acute coronary syndromes [1]. In contrast to these findings, Fabbri and colleagues [28] showed that pre-injury use of aspirin and indobufen (a NSAID) was associated with an increased risk of posttraumatic intracranial lesions in 14,288 patients with mild TBI The results of those studies are conflicting and do not allow a comprehensive characterisation of antiplatelet agent effects on patients with TBI. 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. In light of available data of studies, routine platelet transfusion cannot be recommended in TBI patients with pre-injury antiplatelet therapy and further trials clarify ing this issue are needed. Decisions should be re-evaluated on a regular basis, depending on the patient’s clinical course
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