Key result
Extensive thrombus formation during extracorporeal circulation despite standard heparin doses was linked to antithrombin III deficiency in a 15-year-old boy.
Case Report (n=1)
Antithrombin III deficiency should be considered when heparin resistance is encountered during extracorporeal circulation, even without a history of thromboses.
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ATIII deficiency may explain heparin resistance in extracorporeal circulation; this case leaves screening implications open.
Extensive thrombus formation during extracorporeal circulation despite the administration of heparin sodium prompted investigation of a 15-year-old boy with a calcified right ventricular thrombus and a history of subacute bacterial endocarditis. In vitro studies confirmed the failure of heparin in standard doses to have an anticoagulant effect. Antithrombin III concentrations were low. The patient's mother, who had no history of thromboembolic disease, was also antithrombin III deficient. Resistance to heparin is a theoretical, but inconsistently documented, feature of antithrombin III deficiency. This deficiency state should be considered whenever heparin resistance is encountered, even in the absence of a personal and family history of thromboses.
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Lois E. Nielsen (1987) conducted a case report in Heparin resistance / Antithrombin III deficiency (n=1). Heparin sodium was evaluated on Anticoagulant effect / thrombus formation. Extensive thrombus formation during extracorporeal circulation despite standard heparin doses was linked to antithrombin III deficiency in a 15-year-old boy.
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