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

Abstract

Heparin-induced platelet activation (HIPA) is a syndrome associated with thrombocytopenia, 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 in 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% 14C-serotonin release after heparin (0.1 to 3 U/ml) was added to a mixture of patient platelet-poor plasma (PPP, two parts) and aspirin-free donor platelet-rich 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).…”

Heparin-induced thrombocytopenia in the pediatric intensive care unit population

“…Venous thrombosis and pulmonary emboli are less frequent and their association with HIT is less clearly defined. Thrombotic complications may occur at multiple anatomic sites and can result in significant morbidity, including loss of limb and mortality rates of up to 30% in adult patients (22)(23)(24). The incidence of morbidity and mortality from HIT is less well defined in pediatric patients.…”

Effects of the prostacyclin analogue iloprost on patency in small arteries and veins: An experimental study in the rabbit

“…In the control group occlusion was often rapid, 15 veins occluding within 30 min of reperfusion. Arterial occlusion was somewhat slower, the cumulative rates being 5 , 8,13, and 13/23 at 30,60,90, and 120 min after reperfusion. The median times-to-occlusion (and interquartile ranges) for vessels in the control group occluded at 2 hrs were 20…”