OBJECTIVE: To investigate how often a prolongation of the activated partial thromboplastin time in critically ill patients is caused by lupus anticoagulants and to identify possible triggering events. DESIGN: Prospective study. SETTING: Internal medicine intensive care unit (University Hospital of Vienna, Vienna, Austria). PATIENTS: Fifty-one critically ill patients without severe coagulopathy, hepatopathy, or anticoagulant treatment (35 male, 16 female, median age 60 yrs, range: 22-85 yrs). INTERVENTIONS: All patients were screened daily for lupus anticoagulants with the activated partial thromboplastin time STA assay. MEASUREMENTS AND MAIN RESULTS: Diluted Russell's viper venom time, plasma mixing studies, and confirmation assays were used to identify lupus anticoagulants at the time of an unexplained prolongation of the activated partial thromboplastin time. The influence of heparin was excluded by determination of thrombin clotting time and anti-Xa activity. In 27 of 51 patients (52.9 %) lupus anticoagulants were found after a median stay of 13 days. None of the patients had concomitant immune thrombocytopenia, hypoprothrombinemia, bleeding, or thromboembolic complications. Sepsis (p =.006) and/or catecholamine treatment (p =.002) were significantly associated with the development of lupus anticoagulants. Extracorporeal circulation, transfusion of blood products, or surgery did not increase this risk. Lupus anticoagulants resolved spontaneously in 63% of the patients after a median stay of 17 days. CONCLUSIONS: Lupus anticoagulants are frequent in critically ill patients and associated with sepsis syndrome and/or catecholamine treatment. The prolonged activated partial thromboplastin time does not warrant the administration of coagulation factors or the cessation of anticoagulant therapy or prophylaxis, inasmuch as this phenomenon is not associated with bleeding or thromboembolic complications.
OBJECTIVE: To investigate how often a prolongation of the activated partial thromboplastin time in critically illpatients is caused by lupus anticoagulants and to identify possible triggering events. DESIGN: Prospective study. SETTING: Internal medicine intensive care unit (University Hospital of Vienna, Vienna, Austria). PATIENTS: Fifty-one critically illpatients without severe coagulopathy, hepatopathy, or anticoagulant treatment (35 male, 16 female, median age 60 yrs, range: 22-85 yrs). INTERVENTIONS: All patients were screened daily for lupus anticoagulants with the activated partial thromboplastin time STA assay. MEASUREMENTS AND MAIN RESULTS: Diluted Russell's viper venom time, plasma mixing studies, and confirmation assays were used to identify lupus anticoagulants at the time of an unexplained prolongation of the activated partial thromboplastin time. The influence of heparin was excluded by determination of thrombin clotting time and anti-Xa activity. In 27 of 51 patients (52.9 %) lupus anticoagulants were found after a median stay of 13 days. None of the patients had concomitant immune thrombocytopenia, hypoprothrombinemia, bleeding, or thromboembolic complications. Sepsis (p =.006) and/or catecholamine treatment (p =.002) were significantly associated with the development of lupus anticoagulants. Extracorporeal circulation, transfusion of blood products, or surgery did not increase this risk. Lupus anticoagulants resolved spontaneously in 63% of the patients after a median stay of 17 days. CONCLUSIONS: Lupus anticoagulants are frequent in critically illpatients and associated with sepsis syndrome and/or catecholamine treatment. The prolonged activated partial thromboplastin time does not warrant the administration of coagulation factors or the cessation of anticoagulant therapy or prophylaxis, inasmuch as this phenomenon is not associated with bleeding or thromboembolic complications.