Heparin‐induced thrombocytopenia

Thrombocytopenia is a common adverse effect of heparin therapy. Two types of heparin l induced thrombocytopenia (HIT) are observed clinically ‐ an early onset mild thrombocytopenia (Type I) in which the patients remain asymptomatic and a delayed onset severe thrombocytopenia (Type II). Patients with Type II HIT have an increased risk of thrombotic complications which frequently cause crippling disability e.g. limb amputation or even death. Type I HIT, the commoner of the two types, is believed to be due to the platelet proaggregating effect of heparin itself but Type II HIT is generally agreed to be caused by an immune mechanism, in which heparin‐antibody complexes bind to platelets resulting in platelet activation, reduced platelet survival, thrombocytopenia and, in some cases, thrombosis. The diagnosis of HIT is made mainly on a clinical basis but in patients with suspected Type II HIT, laboratory test for the heparin‐dependent antibody using platelet aggregometry or the two‐point 14 C‐serotonin release method, allows confirmation of the diagnosis. In most Type I and all Type II patients, heparin should be stopped and warfarin commenced if there is a recent or new thrombosis requiring continuing anticoagulation. An alternative antithrombotic drug such as low molecular weight heparinoid (Org 10172) or dextran should be given at the same time until warfarin becomes therapeutic. The use of low molecular weight heparins (e.g. Fragmin) should be avoided unless it can be demonstrated that the HIT antibody does not cross‐react with these drugs. (Aust NZ J Med 1992; 22: 145–152.)