Heparin-induced platelet activation in sixteen surgical patients: Diagnosis and management

Abstract

Heparin-induced platelet activation (HIPA) is a syndrome associated with thrombocympenia, intravascular thrombosis, and arterial emboli. We have evaluated 16 patients for presumed HIPA because of the occurrence of thrombocytopenia or a new thrombotic complication during heparin therapy. In this group, 16 thrombotic events occurred ha 10 patients with a mortality rate of 18.8%. Diagnosis was confirmed in vitro by the demonstration of at least 20% platelet aggregation and/or 6% ~4C-serotonin release after heparin (0.1 m 3 U/ml) was added to a mixture of patient platelet-poor plasma (PPP, two parts) and aspirin-free donor platelet-rieh plasma (PRP, three parts). After heparin was discontinued, seven patients continued to have HIPA in their own PRP although it could no longer be observed in donor PRP. Iloprost, a potent prostacyclin analog that reversibly inhibits platelet activation, completely prevented HIPA and release in all of nine patients. Aspirin, an irreversible cyclooxygenase inhibitor, failed to prevent HIPA in four of these nine patients. In conclusion, HIPA is associated with an extremely high morbidity and mortality rate. Evaluation of the patients' PRP in response to heparin may improve the diagnostic sensitivity of this assay. Aspirin does not reliably prevent HIPA, which suggests participation of thromboxane-independent pathways. Thus, if further exposure to heparin is unavoidable, a more effective platelet inhibitor such as iloprost is required to reliably prevent in vivo HIPA.

Heparin‐induced thrombocytopenia and thrombosis: a prospective analysis of the incidence in patients with heart and cerebrovascular diseases

“…Although the mean period of heparin treatment was 8·3 d, assumed to be long enough to develop HITT, about 20% of our patients were treated for < 5 d. However, 68% of them had been previously exposed to heparin, which, in itself, predisposes for the development of HITT. We can only speculate on the influence of the high percentage of aspirin usage (> 50%) in our patient group on the occurrence of HITT, particularly in those patients with platelet activating antibodies, since reports about the efficacy of antiplatelet drugs in preventing heparin-dependent antibody-mediated platelet aggregation are scarce and conflicting (Kappa et al, 1987;Laster et al, 1989;Chong et al, 1993).…”

Catastrophic antiphospholipid syndrome: Where do we stand?

“…Heparin‐induced thrombocytopenia may further complicate the clinical picture due to bleeding complications or thrombosis. New thrombotic events have been reported in heparin‐treated patients in association with thrombocytopenia, resulting from irreversible aggregation of platelets induced by heparin, the so‐called “white‐clot syndrome” (13, 14). This occurs due to the presence of antibody that binds to platelet factor IV and heparin (15).…”

Heparin‐induced thrombocytopenia (HIT) due to heparin flushes: a report of three cases

“…We found 29 cases of HIT attributed to heparin flushes of venous or arterial catheters reported between 1986 and 1997 ( Table 2). Nineteen of these were included in reports of larger series of HIT cases that provided no details about the individuals who had received only heparin flushes [4,5,12]. In 25 patients the clinical diagnosis of HIT was confirmed with laboratory tests [3±6, 8, 10±12].…”