Anthony D Holley1, Michael C Reade. 1. aRoyal Australian Navy Reserve bDepartment of Intensive Care Medicine, Royal Brisbane & Women's Hospital, Brisbane cRoyal Australian Army Medical Corps dBurns, Trauma and Critical Care Research Centre, University of Queensland, Herston, Queensland, Australia.
Abstract
PURPOSE OF REVIEW: Although early acute traumatic coagulopathy has received much recent attention, the procoagulopathy that often follows appears less appreciated. Thromboembolic disease following trauma is common and lethal, but very effective prophylactic strategies are available. These strategies are variably implemented because of the difficulty in quantifying the magnitude of procoagulopathy in individual patients. RECENT FINDINGS: The principal mechanisms of the procoagulopathy of trauma include inflammation and disseminated intravascular coagulation, tissue factor and thrombin dysregulation, and circulating microparticles and phospholipids. Quantification of these factors may allow better risk assessment in individual patients, but as yet none of these tests is in routine practice. Viscoelastic measurement of developing clot strength identifies a procoagulant state in many trauma patients, and may be a guide to the best choice of the many options for thromboembolic prophylaxis. SUMMARY: The logical next step following from the improved pathophysiological understanding of the procoagulopathy of trauma should be a simultaneous clinical trial of procoagulopathy diagnosis and thromboembolic prophylaxis.
PURPOSE OF REVIEW: Although early acute traumatic coagulopathy has received much recent attention, the procoagulopathy that often follows appears less appreciated. Thromboembolic disease following trauma is common and lethal, but very effective prophylactic strategies are available. These strategies are variably implemented because of the difficulty in quantifying the magnitude of procoagulopathy in individual patients. RECENT FINDINGS: The principal mechanisms of the procoagulopathy of trauma include inflammation and disseminated intravascular coagulation, tissue factor and thrombin dysregulation, and circulating microparticles and phospholipids. Quantification of these factors may allow better risk assessment in individual patients, but as yet none of these tests is in routine practice. Viscoelastic measurement of developing clot strength identifies a procoagulant state in many traumapatients, and may be a guide to the best choice of the many options for thromboembolic prophylaxis. SUMMARY: The logical next step following from the improved pathophysiological understanding of the procoagulopathy of trauma should be a simultaneous clinical trial of procoagulopathy diagnosis and thromboembolic prophylaxis.
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