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. 2003 Dec;38(6):1316-22.
doi: 10.1016/s0741-5214(03)00769-9.

Heparin-induced thrombocytopenia: twenty-nine years later

Thomas A Shuster  1 , W Ray Silliman, Richard D Coats, Leila Mureebe, Donald Silver
Affiliations
Free article

Heparin-induced thrombocytopenia: twenty-nine years later

Thomas A Shuster et al. J Vasc Surg. 2003 Dec.
Free article

Abstract

Objective: To determine the current frequency, types of patients, indications for testing, morbidity and mortality, and management of heparin-induced thrombocytopenia (HIT).

Methods: Between December 1998 and July 2001, the charts of 102 inpatients that tested positive for heparin-associated antiplatelet antibodies (HAAb) were reviewed. There were 33,941 inpatients, 10,348 of them having received unfractionated or low molecular weight heparins. HAAb were determined by platelet aggregometry.

Results: There were 58 males and 44 females with a mean age of 56 years. The majority (72%) of patients were admitted to a surgical service (23% were admitted to medicine, and 5% were admitted to obstetrics/pediatrics). Indications for testing included one or more low platelet counts (n = 51), unexplained arterial (n = 33) or venous (n = 6) thromboses, resistance to anticoagulation (n = 1), prior history of HAAb (n = 3), organ transplant (n = 17), or other indication (n = 4). The HAAb "patterns" were variable, with patients having antibodies only to bovine (n = 7) or porcine heparin (n = 5), bovine and porcine heparins (n = 17), enoxaparin (n = 3), fragmin (n = 7), or all 4 heparins (n = 43). The HIT-related mortality was 6.9%, and the morbidity was 30% with 19 arterial and 7 venous thromboses and 5 bleeding events. Management consisted of discontinuation of heparin in 95 patients. Twenty-five patients did not require continued anticoagulation. When needed, anticoagulation was continued with a direct thrombin inhibitor (n = 32), enoxaparin (n = 16), warfarin (n = 15), or aspirin (n = 7). Seven patients continued to receive unfractionated heparin (n = 4) or low molecular weight heparin (n = 3).

Conclusions: HIT occurs in 0.99% of inpatients receiving heparin and remains an important nondiscriminatory contributor to their morbidity and mortality. Patients receiving any form of heparin who develop a decreasing platelet count, unexplained thrombosis, or resistance to heparin anticoagulation should be tested for HAAb. If HAAb are detected, patients must not receive the sensitizing heparin(s).

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