As a result of this increased use of anti-platelet therapy as the population ages, it is vital that trauma clinicians understand the risks involved with their use. Pre-injury anti-platelet use has been increasingly investigated as a risk factor for various poor outcomes in traumatic head injuries. A number of studies have concluded that anti-platelet therapy is a risk factor for both shortterm and Forsythin long-term unfavourable outcomes in subjects with head injury, with increased risk of death, permanent vegetative state and severe disability. A further difficulty currently facing trauma clinicians is that limited research exists that addresses the efficacy or utility of reversing pre-injury anti-platelets therapy in traumatic head injury.. Another difficulty facing emergency physicians in the management of trauma patients using pre-injury anti-platelets is the variation between patients in their response to the medication. Platelet function tests can be carried out on trauma patients in order to assess number and size of platelets and also platelet haemostatic function. The type of tests completed, specifically either global screening tests or specific assays will depend on the testing equipment available at that emergency department. The decision as to whether the blunt poly-trauma patient requires platelet transfusion therefore is dependent on a number of factors. In isolated blunt chest trauma however platelet function may not routinely be considered by the emergency physician even though delayed haemothorax is not an uncommon entity in this patient group. It could 
be suggested that tests for platelet function may be an important consideration for the emergency physician managing the isolated blunt chest trauma patient however further research is required to support this suggestion. To date, no research exists investigating the effect of pre-injury anti-platelet use in blunt chest trauma. Pulmonary contusion occurs in 25�C35% of all blunt chest traumas and is defined as an injury to the alveolar capillaries, in the absence of a lung laceration. This results in accumulation of blood and other fluids within the lung tissue which subsequently interferes with gas exchange leading to hypoxia. If blood and plasma are leaked into the alveoli in rib fractures patients, it Alisol-A-24-acetate possible that this pathophysiological process is exacerbated in patients receiving preinjury anti-platelet therapy. This variable has not been investigated to date as a risk factor for poor outcomes following blunt chest wall trauma. In one previous study, pre-injury anti-platelet therapy was reported to reduce the incidence of acute lung injury in a medical ICU population, of which there were 24 poly-trauma patients in the study cohort and only eight of these were using preinjury anti-platelets. The authors of this study also do not state whether these trauma patients had sustained head injuries and therefore comparison between the studies is not possible. In a recent study by Harr et al, the use of pre-injury antiplatelet therapy was reported to be associated with a decreased risk of lung dysfunction in high risk blunt trauma patients who receive blood transfusions.