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of thrombocytopenia (<150 X 109/L) may be inadequate for many patients with HIT. Particularly in postoperative patients, a major fall in the platelet count can occur without the nadir falling to less than 150 X 109/L (Figs. 1b and 3). Indeed, studies indicate that a 50% or greater fall in the platelet count from the postoperative peak is strongly associated with HIT antibodies, even when the platelet count nadir remains higher than 150 X 109/L (Ganzer et al., 1997; Warkentin et al., 2003). Moreover, this patient subgroup is at increased risk for thrombosis.

Rule 3

A platelet count fall of more than 50% from the postoperative peak between days 5 and 14 after surgery associated with heparin treatment can indicate HIT even if the platelet count remains higher than 150 x 109/L.

It is possible that a greater than 50% platelet count fall definition is also appropriate for medical patients (Girolami et al., 2003). Regardless of the patient population, a clinician should have a high index of suspicion when unexpected large-percentage declines in the platelet count occur during heparin treatment, irrespective of whether an arbitrary absolute threshold for "thrombocytopenia" is crossed. Indeed, some investigators have used other thresholds to define thrombo-cytopenia, such as platelet count declines of 40% (Pouplard et al., 2005) or even 30% (Greinacher et al., 2005a).

Platelet Count Monitoring in Patients Receiving Heparin

In postoperative patients, the onset of HIT coincides with rising platelet counts (postoperative thrombocytosis); thus, the platelet count profile of HIT resembles an "inverted V" (A Fig. 1a,b). The postoperative peak platelet count preceding HIT is often higher than the preoperative platelet count. Therefore, the postoperative peak platelet count is the appropriate baseline for calculating the magnitude of a subsequent platelet count fall (Warkentin et al., 2003; Pouplard et al., 2005) (Table 2).

HIT-Associated Thrombosis Without Thrombocytopenia

Anecdotal reports indicate that HIT-associated thrombosis can occur in the absence of thrombocytopenia, as conventionally defined (Phelan, 1983; Hach-Wunderle et al., 1994; Warkentin, 1996a, 1997; Houston, 2000). However, most of these patients do have an associated fall in the platelet count, although the nadir remains higher than 150 X 109/L. Perhaps the most dramatic example of this phenomenon was a patient with essential thrombocythemia who developed serologically confirmed HIT: the platelet count fell by 49% from 1235 to 633, i.e., concomitant "thrombocytopenia" and thrombocytosis (Risch et al., 2000).

A study suggested that HIT antibody formation without thrombocytopenia is not associated with a thrombosis rate greater than control patients (Warkentin et al., 1995, 2003). However, the subset of patients who formed HIT antibodies and whose platelet count fell by 50% or more—but remained above 150 X 109/L—did have an increased risk for thrombosis (odds ratio, 6.0). Figure 7 illustrates this concept of the central importance of thrombocytopenia (defined broadly as a large relative fall in the platelet count) in determining risk for thrombosis. These observations provide indirect evidence suggesting that in vivo platelet activation by HIT antibodies probably contributes to the pathogenesis of HIT-associated thrombosis.

As shown by Figure 6, thrombosis commonly complicates HIT irrespective of the severity of the thrombocytopenia. Nevertheless, there is evidence that both

TABLE 2 Determining the Day of Onset of Thrombocytopenia: A 35-Year-Old Woman Who Developed HIT After Heart Surgery

Postoperative day

TABLE 2 Determining the Day of Onset of Thrombocytopenia: A 35-Year-Old Woman Who Developed HIT After Heart Surgery

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