ABSTRACT
Thrombocytopenia is a common problem encountered in hospitalized patients. For patients receiving heparin, there are three general explanations for thrombocytopenia: (1) heparin-induced thrombocytopenia (HIT), (2) non-idiosyncratic heparininduced platelet activation (see Chapter 4), and-perhaps most often-(3) an unrelated clinical problem, either common (e.g., hemodilution, septicemia) or rare (e.g., posttransfusion purpura, drug-induced immune thrombocytopenic purpura) (see Chapter 11). The availability of sensitive and specific laboratory assays (e.g., enzyme immunoassay [EIA] and serotonin release assay [SRA]) for pathogenic HIT antibodies means that patients with HIT can usually be readily distinguished from those with the other conditions (see Chapter 10). However, the role of heparin in causing thrombocytopenia because of nonimmune platelet activation cannot readily be separated from other common medical problems encountered in hospitalized patients, on either clinical or laboratory criteria. Furthermore, these two conditions can coexist (Chong and Castaldi, 1986). Thus, the term “nonimmune heparinassociated thrombocytopenia” (nonimmune HAT) has been recommended to describe patients who develop thrombocytopenia during heparin treatment in which a role for HIT antibodies cannot be implicated (Warkentin et al., 1998a).
