Heparin-Induced Thrombocytopenia in the Intensive Care Unit

Abstract

Heparin-induced thrombocytopenia (HIT) occurs following an immune reaction to the administration of heparin, which results in increased platelet activation and thrombocytopenia, and lead to arterial and venous thrombosis in untreated cases. It may be considered as an idiosyncratic, drug-induced reaction in which heparin injections result in the formation of complexes with platelet factor 4 (PF4), triggering an antibody-mediated reaction in certain individuals. Low platelet count in this instance is secondary to platelet aggregation and can lead to thrombotic complications by vascular occlusion and other mechanisms. Early recognition of this complication is essential to prevent life- and limb-threatening thrombosis. Therefore, it is important that intensive care physicians who administer heparin in different forms are aware of this potential adverse event and follow a regular plan in monitoring the platelet count while the patient is on heparin. In a patient whose platelet count falls while on heparin, when no other diagnostic possibilities can easily explain it, immediate withdrawal of any form of heparin and commencement of an alternative anticoagulant is necessary until the diagnosis of HIT is confirmed or excluded. At the same time, it is important that over-diagnosis of HIT is not made to avoid unwanted bleeding complications from the alternative anticoagulants. This review outlines the pathophysiology, diagnosis and management of HIT with a focus on the intensive care setting.