The incidence and magnitude of fibrinolytic activation in trauma patients

Summary. Background:  Trauma is a global disease, with over 2.5 million deaths annually from hemorrhage and coagulopathy. Overt hyperfibrinolysis is rare in trauma, and is associated with massive fatal injuries. Paradoxically, clinical trials suggest a much broader indication for antifibrinolytics. Objective: To determine the incidence and magnitude of fibrinolytic activation in trauma patients and its relationship to clot lysis as measured by thromboelastometry. Methods: A prospective cohort study of 303 consecutive trauma patients admitted between January 2007 and June 2009 was performed. Blood was drawn on arrival for thromboelastometry (TEM) and coagulation assays. Follow‐up was until hospital discharge or death. TEM hyperfibrinolysis was defined as maximum clot lysis of > 15%. Fibrinolytic activation (FA) was deterined according to plasmin–antiplasmin (PAP) complex and D‐dimer levels. Data were collected on demographics, mechanism, severity of injury, and baseline vital signs. The primary outcome measure was 28‐day mortality. The secondary outcome measures were 28‐day ventilator‐free days and 24‐h transfusion requirement. Results: Only 5% of patients had severe fibrinolysis on TEM, but 57% of patients had evidence of ‘moderate’ fibrinolysis, with PAP complex levels elevated to over twice normal (> 1500 μg L^?1) without lysis on TEM. TEM detected clot lysis only when PAP complex levels were increased to 30 times normal (P < 0.001) and antiplasmin levels were < 75% of normal. Patients with FA had increased 28‐day mortality as compared with those with no FA (12% vs. 1%, P < 0.001), fewer ventilator‐free days, and longer hospital stay. Conclusions: FA occurs in the majority of trauma patients, and the magnitude of FA correlates with poor clinical outcome. This was not detected by conventional TEM, which is an insensitive measure of endogenous fibrinolytic activity.     

Hemodynamic consequences of pulmonary embolism: reply to a rebuttal

See also Baglin T. Fifty per cent of patients with pulmonary embolism can be treated as outpatients. J Thromb Haemost 2010; 8: 2404–5; Girard P. Hemodynamic consequences of pulmonary embolism: a rebuttal. This issue, pp 412–3.     

Retinal vein thrombosis: pathogenesis and management: reply to a rebuttal

See also Rehak M, Wiedemann P. Retinal vein thrombosis: pathogenesis and management. J Thromb Haemost 2010; 8: 1886–94; Ageno W, Squizzato A, Lazo‐Langner A. Retinal vein thrombosis: pathogenesis and management: a rebuttal. This issue, pp 418–9.     

Genetic testing in von Willebrand disease: reply to rebuttal

See also Mannucci PM. Genetic testing in von Willebrand disease: a rebuttal. This issue, p 860.     

Cancers in patients with hemophilia: a retrospective study from the Italian Association of Hemophilia Centers: a reply to a rebuttal

See also Shetty S, Ghosh K. Cancers in patients with hemophilia: a retrospective study from the Italian Association of Hemophilia Centers: a rebuttal. This issue, pp 1200–1. Tagliaferri A, Di Perna C, Santoro C, Schinco P, Santoro R, Rossetti G, Coppola A, Morfini M, Franchini M, on behalf of the Italian Association of Hemophilia Centers. Cancers in patients with hemophilia: a retrospective study from the Italian Association of Hemophilia Centers. J Thromb Haemost 2012; 10 : 90–9.     

Effect of platelet turnover on whole blood platelet aggregation in patients with coronary artery disease: reply to a rebuttal

See also Grove EL, Hvas AM, Mortensen SB, Larsen SB, Kristensen SD. Effect of platelet turnover on whole blood platelet aggregation in patients with coronary artery disease. J Thromb Haemost 2011; 9: 185–91; Ege MR, Zorlu A. Effect of platelet turnover on whole blood platelet aggregation in patients with coronary artery disease: a rebuttal. This issue, pp 888.