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Familial antithrombin-III deficiency during cardiopulmonary bypass: a case report

Department of Extracorporeal Circulation, University Medical Centre St. Radboud, Nijmegen, A.Brinks{at}thchir.azn.nl

P W Weerwind

Department of Extracorporeal Circulation, University Medical Centre St. Radboud, Nijmegen

M WA Verkroost

Department of Cardiothoracic Surgery, University Medical Centre St. Radboud, Nijmegen

I. Nováková

Department of Haematology, University Medical Centre St. Radboud, Nijmegen

M HJ Brouwer

Department Cardiothoracic Surgery, University Medical Centre St. Radboud, Nijmegen

The serine protease inhibitor antithrombin-III (AT-III) is the principal in vivo inhibitor of blood coagulation, inactivating mainly thrombin, but also other serine proteases. Binding of AT-III to heparin dramatically increases its inhibitory effect. AT-III deficiency during cardiopulmonary bypass (CPB) can lead to insufficient anticoagulation which cannot be treated by higher doses of heparin.

A 60-year-old male with familial AT-III deficiency was admitted to our hospital for coronary artery bypass surgery and aortic valve replacement. Four days before the operation, acenocoumarol was stopped and anti-X_anadroparincalcium (Fraxiparine) was started. AT-III activity at that time was 56%. Two hours before the operation, a single dose of 4500 IU AT-III concentrate was administered. Heparinization was performed with 400 IU/kg of porcine mucosal heparin, increasing the activated coagulation time (ACT) from a baseline of 115 to 549 s. AT-III activity at that time was above 100% and the plasma D-dimer concentration was 230 ng/l. ACTs during CPB remained above 999 s, whereas the AT-III activity dropped to 54% and the D-dimer increased up to 500 ng/l at the end of CPB. CPB was terminated uneventfully. Heparin was reversed with 3 mg/kg protamine chloride, decreasing the ACT to 155 s. In the intensive care unit (ICU), the patient received prophylactic Fraxiparine and 1500 IU AT-III, increasing the AT-III activity to 84%. Postoperatively, there was continued blood loss, which necessitated the administration of whole blood and eventually re-exploration.

The case presented illustrates an uneventful treatment of a patient with a hereditary AT-III deficiency undergoing CPB. In spite of an uneventful treatment with AT-III pre-CPB, administration of prophylactic AT-III concentrate after surgery should be considered with caution, as this might increase the postoperative morbidity.

Perfusion, Vol. 15, No. 6, 553-556 (2000)
DOI: 10.1177/026765910001500613


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