Heparin-Induced Thrombocytopenia: Diagnostic and Therapeutic Considerations

INTRODUCTION Heparin use is ubiquitous in medicine today. It is used therapeutically in the management of arterial and venous thrombotic processes, such as acute myocardial infarction or deep venous thrombosis, and prophylactically to prevent thrombosis around the time of orthopedic procedures and to prevent prosthetic heart valve thrombosis or stroke in atrial fibrillation. Heparin is bonded to catheters such as pulmonary wedge catheters, and implanted catheters are sometimes flushed with a heparinized solution to prevent clotting. The chance of a significant exposure to heparin exceeds 50% when a patient is admitted to some medical services [1]. The widespread use of heparin exposes patients to the risk of heparin-induced thrombocytopenia (HIT), an antibody-mediated syndrome associated with significant morbidity and mortality. Serologically proven HIT occurs in 1.5% to 3% of patients with heparin exposure [2,3]. Paradoxically, the most feared consequence in these patients with a low platelet count is not bleeding but clotting. Arterial or venous thrombosis resulting in myocardial infarction, stroke, deep venous thrombosis and pulmonary embolism, or limb ischemia and amputation complicate thrombocytopenia in at least 30% to 40% of cases [2,4,5], with a mortality estimated at approximately 30% [3,4,6] and a long length of hospital stay [3]. HIT is an important condition that is unrecognized by many clinicians. When thrombocytopenia is recognized, the diagnosis of HIT can be difficult to confirm, and until recently there was no therapeutic option other than discontinuation of heparin. Improved understanding of this syndrome increases the need for medical personnel to practice prevention, recognize the signs and symptoms of HIT, and know the treatment options available.