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) nonidiosyncratic heparin-induced platelet activation (see Chap. 5), 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 Chaps. 2 and 12). 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 the other conditions (see Chap. 11). 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, either on clinical or laboratory criteria. Furthermore, these two conditions can coexist (Chong and Castaldi, 1986). Thus, the term "nonimmune heparin-associated thrombocytopenia" (nonimmune HAT) has been recommended to describe patients who develop thrombocytopenia during
Lee and Warkentin
Unfortunately, many early studies of HIT frequency either did not perform laboratory testing or used relatively insensitive or nonspecific assays to diagnose HIT. In contrast, more recent studies have used one, or even two, sensitive and complementary assays. Perhaps for this reason, the understanding of the frequency and clinical import of HIT has shifted over the years. Formerly, the range of views on immune-mediated HIT were divergent: it was considered both nonexistent (Bell, 1988) and common (Kelton, 1986). Nevertheless, both viewpoints acknowledged that thrombosis resulting from HIT was very uncommon. Today's perspective on HIT is very different. The frequency of HIT is now shown to be variable, partly depending on patient population and type of heparin used. For example, the frequency ranges from less than 1% (cardiac medical patients) to 5% (orthopedic surgical patients) receiving unfractionated heparin (UFH); HIT antibody formation following UFH use ranges from 20/0 (cardiac medical patients) to 15% (orthopedic surgical patients) to 50% (cardiac surgical patients). Most importantly, however, it is now becoming clear that the risk for thrombosis in patients who develop HIT is at least 33-50%, a frequency that is far greater than in control patients who do not develop HIT (see Chap. 3).
