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Indicators of fibrinolysis during cardiopulmonary bypass after exogenous antithrombin-III administration for acquired antithrombin III deficiency

1997; Elsevier BV; Volume: 11; Issue: 6 Linguagem: Inglês

10.1016/s1053-0770(97)90172-5

1532-8422

Gail A. Van Norman, Terry Gernsheimer, Wayne L. Chandler, Richard P. Cochran, Bruce D. Spiess,

Venous Thromboembolism Diagnosis and Management

elapsed time for the heparin boluses and ACT testing was 30 minutes. A presumptive diagnosis of AT-III deficiency was made, and 2,500 U of pooled AT III was administered. The dose was based on the assumption that the patient's circulating AT-III activity was decreased by approximately 50%, and that adding 2,500 U of AT llI to his circulating volume would bring AT-III activity back to 100%. The ACT rose to 635 seconds, and cardiopulmonary bypass (CPB) was immediately initiated. CPB lasted 59 minutes, and no further heparin was required. After CPB, protamine sulfate, 200 rag, was administered IV, and the resulting ACT was 119 seconds. Postoperatively, the thromboelastogram was normal. The patient received 450 mL of autologous blood that had been withdrawn at the start of the case for the purpose of euvolemic hemodilution, and he received no other blood products. His postoperative course was uneventful, and he was discharged on the 5th postoperative day. When it was determined during the case that the patient was heparin resistant, blood samples were withdrawn from his autologous blood unit for baseline studies. This unit had been stored at 34°C for 30 minutes before sampling. Additional samples were drawn from the patient after the second and third boluses of heparin, after AT-Ill administration just before initiation of CPB, 30 minutes after initiation of CPB, and after administration of protamine at the end of CPB. The patient's temperature, as recorded by simultaneous esophageal/urinary temperature probes, was 35.5°/35.9°C, 35.1/35.7°C, 36.2/ 35.6°C, 36.1/37°C, and 36.1/36.8°C, respectively. Blood samples, including the sample withdrawn from the autologous unit, were placed on ice for transport to the clinical laboratory. Blood was anticoagulated by addition of 4.5 mL of whole blood to 0.5 mL of 130 mmol/L sodium citrate. All samples were centrifuged for 10 minutes at 2,500g at room temperature. Citrated plasma was frozen at -80°C. The patient's permission was obtained to run the blood samples for determination of F1 + 2, plasminogen activator inhibitor 1 (PAI-1), tissue plasminogen activator antigen (TPA Ag), and AT III activity levels. RESULTS