Things We Do For No Reason: HIT Testing in Low Probability Patients

Inspired by the ABIM Foundation’s Choosing Wisely^® campaign, the “Things We Do for No Reason” series reviews practices which have become common parts of hospital care but which may provide little value to our patients. Practices reviewed in the TWDFNR series do not represent “black and white” conclusions or clinical practice standards, but are meant as a starting place for research and active discussions among hospitalists and patients. We invite you to be part of that discussion.

A 59-year-old man with cirrhosis secondary to nonalcoholic steatohepatitis was admitted to the intensive care unit (ICU) for management of hepatorenal syndrome and work-up for liver transplantation. On admission, his platelet count was 90 × 109/L (normal 150-400 × 109/L), and he was started on thromboprophylaxis with unfractionated heparin (UFH) 5,000 units subcutaneously twice daily. His platelet count began to fall two days after admission. He did have a history of prior heparin exposure associated with his hemodialysis sessions in the past 30 days. During this period, he also had an episode of fever, and antibiotics were initiated for a presumed line infection. He also required periodic vasopressor support for hypotension. His platelet count reached 14 × 109/L by the end of two weeks. He did not have any symptoms of thrombosis, skin necrosis, or reaction to heparin exposure.

Thrombocytopenia is common, especially during critical illness, occurring in up to 50% of patients.¹ In this population, thrombocytopenia is often due to sepsis, hemorrhage, liver dysfunction, and drug reactions.^1,2 Heparin-induced thrombocytopenia (HIT) is an acquired thrombotic drug reaction resulting from platelet activation secondary to antibodies formed against the heparin-modified platelet factor 4 (PF4) complexes.³ This leads to platelet aggregation and dysregulation of the coagulation cascade, which can result in arterial or venous thromboembolic events in up to 50% of patients.³ Mortality associated with HIT can be as high as 30% in this critically ill population.³ Diagnosis of HIT can be made initially through the enzyme-linked immunosorbent assay (ELISA). Management of HIT involves immediate cessation of heparin and initiation of therapeutic anticoagulation with nonheparin agents in order to prevent or treat the thrombotic events.^4,5

The true incidence of HIT remains low, occurring in 0.2% to 5% of patients exposed to heparin and less than 1% in the ICU population.^2,3,6,7 However, given the high incidence of thrombocytopenia in the ICU, the diagnosis of HIT is often considered, resulting in over-testing in this population. Studies suggest that more than 200 ELISAs are requested per year at many hospitals.^8,9 This can lead to significant clinical and economic consequences.