This is the first article in the series, “Heparin-Induced Thrombocytopenia.” The remaining articles are Presentation and History; Diagnosis; Treatment/Management; and References.
Heparin-induced thrombocytopenia (HIT) is an immune-mediated drug reaction that requires prompt detection and treatment in order to minimize patient morbidity and mortality.1 HIT is caused by the development of antibodies to platelet factor 4 (PF4), although it is important to note that not all patients who develop PF4 antibodies will experience the clinical syndrome of HIT.2-4 In fact, about 50% of patients who undergo cardiovascular surgery develop PF4 antibodies, but only 1% to 2% of patients with antibodies actually experience HIT.5-7 There is currently no explanation for the phenomenon of HIT.8
In 2012, with an intent to limit HIT-associated morbidity and mortality, the American College of Chest Physicians (ACCP) unveiled the ninth edition of its evidence-based practice guidelines for the detection of HIT and appropriate treatment.5 Much of the information provided in this article emerged from these guidelines.
Epidemiology
Of the 12 million patients treated each year with either unfractionated heparin (UFH) or low-molecular-weight heparin (LMWH), 600,000 (0.5%) will develop HIT. Among these patients, 300,000 will develop thrombosis, and 90,000 will die. In 2009 alone, the HIT-associated cost to the US health care system was estimated at $100 million.1
As growing numbers of patients require anticoagulation therapy, it becomes increasingly important for clinicians to understand the importance of screening for deep vein thrombosis (DVT), one of the two most common thromboses; the other is pulmonary embolism.9,10 Continuing to administer heparin or warfarin to patients with undetected HIT predisposes them to severe complications, including venous and arterial thromboses and gangrenous skin lesions—which can result in loss of life and/or limb.1,11,12
Risk Factors for HIT
Several factors influence a patient’s risk for HIT, including the type and dosing regimen of the heparin being administered. Generally, the risk for HIT is about 10-fold in patients treated with UFH (3% to 5%), compared with those receiving LMWH (0.5%).5,13 The risk for HIT is also greater in patients receiving UFH of bovine origin, compared with those taking porcine-derived UFH.8,14,15
In a recent meta-analysis of postsurgical patients who underwent heparin thromboprophylaxis, those given LMWH had a 76% relative risk reduction for HIT, compared with patients taking UFH.16 The incidence of HIT increases among patients receiving LMWH if they have been treated with UFH within the previous 100 days.9 HIT onset may be delayed for several days in patients given heparin for the first time (or for the first time in several months), whereas previously exposed patients who have already developed antiheparin PF4 antibodies can experience severe HIT within hours.9
Patient-Specific Risk Factors
Certain patient characteristics also have an impact on HIT risk. For example, the risk for HIT is approximately doubled in women, compared with men,1,5,15 and the incidence of HIT is greater in surgical patients than in medical patients.7,17 Among surgical patients, 5% of orthopedic patients have been reported to develop HIT, compared with 3% of cardiac patients and 1% of patients undergoing surgery for vascular illnesses.1 The reasons for these differences are poorly understood, but current theory focuses on the inflammatory response of individual patients and the degree of associated platelet activation.2,12
This is the first article in the series, “Heparin-Induced Thrombocytopenia.” The remaining articles are Presentation and History; Diagnosis; Treatment/Management; and References.