Ann Thorac Surg 2006;82:26-27
© 2006 The Society of Thoracic Surgeons
Original article: Cardiovascular
Invited commentary
John L. Francis, PhD
Center for Hemostasis and Thrombosis, Florida Hospital Center for Hemostasis and Thrombosis, 2501 N Orange Ave, Suite 786, Orlando, FL 32804
(Email: john.francis{at}flhosp.org).
In their article, Wan and colleagues [1] make some important observations on the clinical presentation and temporal relationships of heparin-induced thrombocytopenia (HIT) after cardiotomy. Conventional teaching dictates that HIT occurs within a 5-day to 14-day window after heparin exposure. Importantly, however, this does not allow for pre-sensitization of patients by prior heparin use; an issue that is remarkably common in a cardiovascular surgery population. Thus, the peak occurrence of HIT in Wan and colleagues' study was relatively early, with two thirds of the patients having the complication develop before the fifth postoperative day.
The diagnosis of HIT in the post-cardiotomy patient is complicated by two factors. First, thrombocytopenia immediately after surgery is common and expected. On its own, therefore, thrombocytopenia is not a particularly accurate predictor of HIT in the early postoperative period. Second, more than 50% of such patients may produce antibodies reactive in an anti-heparin-platelet factor 4 (H-PF4) enzyme-linked immunosorbent assay (ELISA) test within 10 days of surgery. Thus, these types of assays have low clinical specificity for HIT in this population, a fact which may lead to over-diagnosis of HIT if used indiscriminately and without regard for other clinical manifestations of the disease. Wan and colleagues [1] wisely considered the pre-test probability of HIT and used this information in their interpretation of the ELISA result. Even so, the use of a functional laboratory test for HIT assay (eg, the serotonin release assay, would have been useful to confirm the diagnosis, especially in those patients with thrombocytopenia alone). Patients 21 and 29, for example, had platelet counts that were unusually low for HIT. It is therefore conceivable that these were due to non-HIT causes, despite the positive ELISA test.
Pouplard and colleagues [2] identified two patterns of post-CPB platelet count behavior that are related to HIT. The first group of patients exhibited the expected early fall-in count, which then fails to recover promptly over the next few days. The second group have a secondary fall-in platelet count, following the initial expected recovery from the immediate postoperative nadir. It is not clear from Wan and colleagues' [1] article if their patients could be similarly categorized.
Wan and colleagues [1] used danaparoid, a heparinoid agent with limited in vivo cross-reactivity with H-PF4 antibodies, to treat their patients with HIT. In the United States, this anticoagulant is no longer available, and most hematologists would instead use one of the Food and Drug Administration-approved direct thrombin inhibitors for this purpose. In addition, because of the high frequency of postoperative H-PF4 antibody formation and consequent risk of HIT, the use of heparin in this period is probably best avoided where possible.
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- Wan C, Warner M, DeVarennes B, Ergina P, Cecere R, Lachapelle K. Clinical presentation, temporal relationship, and outcome in thirty-three patients with type 2 heparin-induced thrombocytopenia after cardiotomy Ann Thorac Surg 2006;82:21-27.[Abstract/Free Full Text]
- Pouplard C, May MA, Regina S, Marchand M, Fusciardi J, Gruel Y. Changes in platelet count after cardiac surgery can effectively predict the development of pathogenic heparin-dependent antibodies Br J Haematol 2005;128:837-841.[Medline]
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