Comparing clinical predictors of deep venous thrombosis versus pulmonary embolus after severe injury: A new paradigm for posttraumatic venous thromboembolism?

BackgroundThe traditional paradigm is that deep venous thrombosis (DVT) and pulmonary embolus (PE) are different temporal phases of a single disease process, most often labeled as the composite end point venous thromboembolism (VTE). However, we theorize that after severe blunt injury, DVT and PE may represent independent thrombotic entities rather than different stages of a single pathophysiologic process and therefore exhibit different clinical risk factor profiles.MethodsWe examined a large, multicenter prospective cohort of severely injured blunt trauma patients to compare clinical risk factors for DVT and PE, including indicators of injury severity, shock, resuscitation parameters, comorbidities, and VTE prophylaxis. Independent risk factors for each outcome were determined by cross-validated logistic regression modeling using advanced exhaustive model search procedures.ResultsThe study cohort consisted of 1,822 severely injured blunt trauma patients (median Injury Severity Score [ISS], 33; median base deficit, -9.5). Incidence of DVT and PE were 5.1% and 3.9%, respectively. Only 9 (5.7%) of 73 patients with a PE were also diagnosed with DVT. Independent risk factors associated with DVT include prophylaxis initiation within 48 hours (odds ratio [OR], 0.57; 95% confidence interval [CI], 0.36-0.90) and thoracic Abbreviated Injury Scale (AIS) score of 3 or greater (OR, 1.82; 95% CI, 1.12-2.95), while independent risk factors for PE were serum lactate of greater than 5 (OR, 2.33; 95% CI, 1.43-3.79) and male sex (OR, 2.12; 95% CI, 1.17-3.84). Both DVT and PE exhibited differing risk factor profiles from the classic composite end point of VTE.ConclusionDVT and PE exhibit differing risk factor profiles following severe injury. Clinical risk factors for diagnosis of DVT after severe blunt trauma include the inability to initiate prompt pharmacologic prophylaxis and severe thoracic injury, which may represent overall injury burden. In contrast, risk factors for PE are male sex and physiologic evidence of severe shock. We hypothesize that postinjury DVT and PE may represent a broad spectrum of pathologic thrombotic processes as opposed to the current conventional wisdom of peripheral thrombosis and subsequent embolus

Pathophysiology and treatment of coagulopathy in massive hemorrhage and hemodilution

Fluid resuscitation after massive hemorrhage in major surgery and trauma may result in extensive hemodilution and coagulopathy, which is of a multifactorial nature. Although coagulopathy is often perceived as hemorrhagic, extensive hemodilution affects procoagulants as well as anticoagulant, profibrinolytic, and antifibrinolytic elements, leading to a complex coagulation disorder. Reduced thrombin activation is partially compensated by lower inhibitory activities of antithrombin and other protease inhibitors, whereas plasma fibrinogen is rapidly decreased proportional to the extent of hemodilution. Adequate fibrinogen levels are essential in managing dilutional coagulopathy. After extensive hemodilution, fibrin clots are more prone to fibrinolysis because major antifibrinolytic proteins are decreased.Fresh frozen plasma, platelet concentrate, and cryoprecipitate are considered the mainstay hemostatic therapies. Purified factor concentrates of plasma origin and from recombinant synthesis are increasingly used for a rapid restoration of targeted factors. Future clinical studies are necessary to establish the specific indication, dosing, and safety of novel hemostatic interventions