Abstract

PATIENTS WITH heparin-induced thrombocytopenia (HIT) present a challenge when managing anticoagulation during cardiopulmonary bypass (CPB). HIT is usually associated with the administration of unfractionated heparin. Nonimmune (type I) and immune (type II) mechanisms have been implicated. HIT type I typically occurs within minutes after heparin administration, produces only a mild decrease in platelet count, and is not associated with platelet activation and aggregation. HIT type II is generally manifested 5 to 14 days after initiation of heparin therapy. A heparin-dependent IgG antibody is responsible for platelet activation and aggregation, which can lead to arterial and venous thrombosis.1 The overall incidence of HIT type II is approximately 3%.2 In cardiac surgery, HIT type II is present in approximately 1.3% of patients undergoing CPB.3 Thromboembolic complications have been reported in 51% of patients with a lethality of 37%3; alternatives to unfractionated heparin must be employed. One strategy is the use of danaparoid (Orgaran), a lowmolecular-weight heparinoid derived from porcine gut mucosa. Danaparoid is a mixture of 84% heparan sulfate, 12% dermatan sulfate, and 4% chondroitin sulfate and has a low cross-reactivity with heparin-dependent IgG antibodies. Although the use of danaparoid for anticoagulation during cardiac surgery was first described in 1990, there are only a few reports of its use in the literature.4-9 The authors describe their experience with danaparoid in 5 patients with HIT type II, undergoing cardiac surgery with full CPB and moderate hypothermia (Table 1). HIT was confirmed in all cases by positive antiheparin antibody as well as thrombocytopenia or thrombotic events after heparin therapy. Danaparoid was administered in all cases according to the dosing protocol10* currently recommended for CPB patients with HIT.

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