Immune-mediated HIT type 2, on the other hand, occurs in up to 5% of heparin patients and has potentially catastrophic sequelae.¹ (HIT type 2 will be referred to as HIT throughout this website.) HIT is most common in patients receiving intravenous unfractionated heparin, but also occurs in patients receiving low-molecular weight heparin (LMWH), heparin flushes, hemodialysis, and heparin-coated catheters.^1, 2 It is characterized by thrombocytopenia, thromboses, and thromboembolic complications (TECs), and can occur with any type of heparin and any dose or route of administration.¹ HIT places patients at risk for life- and limb-threatening consequences, including peripheral arterial occlusion, ischemic stroke, limb gangrene, acute myocardial infarction, and pulmonary embolism.¹ Although the condition typically appears 4 to 14 days after initiation of heparin therapy, it can also occur as early as 10 hours after administration if the patient has been exposed to heparin within the previous 100 days (re-exposure), or can occur several days after withdrawal of all forms of heparin.^1-3

Potential heparin exposures1: Type of heparin used: low molecular weight or unfractionated heparin Duration of heparin use: short-term, long-term, re-exposure Dose or route of heparin administration: catheters, flushes, heparin-coated devices, intravenous, subcutaneous Patient types: may include cardiac, medical, orthopedic, surgical

Heparin-Induced Thrombocytopenia (HIT) Heparin Use Clinical Consequences of HIT Thromboembolic Complications (TECs) Iceberg Model of HIT Economic Consequences of HIT-Associated TECs When to Suspect HIT Type 2 Vigilant Monitoring is Critical General Diagnosis and Treatment Algorithm for HIT Laboratory confirmation of diagnosis