Prolongation of at least one phospholipid-dependent tests
Lack of correction of mixing studies
Correction of the abnormal result with the addition of excess phospholipids
Lack of any other specific inhibitor
apy. About 36% to 50% of patients with HIT develop life-threatening thrombosis. The thrombotic tendency can last for at least 30 days.1 Venous thrombosis (extremity venous thrombosis) is more common than arterial thrombosis. Other complications of HIT include thrombocytopenia, heparin-induced skin lesions (10% to 20% of patients), and heparin resistance.1 The pathogenesis of HIT is that antibodies are produced against heparin-platelet factor 4 complex. This immune complex binds to platelet FC receptors, causing platelet activation, formation of platelet microparticles, thrombocytopenia, and hypercoagula-ble state (Fig. 19.5).
HIT is independent of dosage or route of administration of heparin. This condition should be suspected in any patient whose platelet count falls below 50% of the baseline value after 5 days of heparin treatment1 and in patients who develop thrombosis with or without thrombocytopenia during heparin therapy.1
Laboratory diagnosis of HIT includes functional assays or immunoassays. Functional assays measure platelet activation or aggregation in the presence of HIT serum and heparin. Functional assays include heparin-induced platelet aggregation, heparin-induced platelet adenosine triphosphate (ATP) release by lumiaggre-gometry, 14C-serotonin release assay (14C-SRA) release by ELISA, and platelet microparticle formation by flow cytometry. Heparin-platelet factor 4 antibodies are detected by ELISA. When HIT is suspected, heparin should be stopped immediately and be replaced by alternative anticoagulant drugs (danaparoid, arga-troban). Warfarin should be avoided in the acute phase of thrombosis because it may cause venous limb gangrene.1 Patients receiving heparin should have a base line platelet count and platelet monitoring every third day between 5 and 14 days.1
Was this article helpful?