Introduction

Heparin-induced thrombocytopenia (HIT) is a potentially catastrophic side effect of heparin therapy. Paradoxically, HIT is associated with a high risk of thrombosis despite heparin treatment and a low platelet count.

Pathophysiology

Heparin administration may often trigger an immunogenic reaction, and up to 50% of patients develop heparin-dependent antibodies after cardiac surgery and cardiopulmonary bypass (CPB), usually within 5 to 10 days of exposure.

An immune disorder, HIT is characterized by the binding of immunoglobulin G antibodies to the heparin molecule, building a complex of hep-arin and platelet factor 4. In a proportion of these patients, this immune complex will bind to the platelet FC receptor, activate platelets and trigger thrombin generation.

In contrast with many immunological disorders, there is convincing evidence that in HIT the antibodies are transient and typically disappear 40 to 100 days after cessation of heparin therapy. Reintroduction of heparin within that time period reinitiates the reaction instantly, but it is accepted that heparin can be used again after 100 days (if a patient require heparinization for CPB, for example).

Incidence

The true incidence of HIT in cardiothoracic critical care patients is unknown. It is estimated that it affects about 1% of cardiac surgical patients treated postoperatively with unfractionated bovine hep-arin. The incidence is lower when low molecular weight heparins are used (0.1%). About 50% of patients have suffered a thrombotic event by the time of diagnosis, and 50% of the those remaining progress to a clinically significant thrombotic event.