Clinical features and diagnosis of heparin-induced thrombocytopenia
Heparin-induced thrombocytopenia (HIT) is an uncommon but dangerous complication of heparin therapy. It is an immune-mediated condition caused by autoantibodies directed against heparin complexed with endogenous platelet factor 4. In surgical patients, HIT was found to have an incidence of 2.6% after unfractionated heparin (UFH) exposure and 0.2% after low molecular weight heparin (LMWH) exposureMartel, 2005. If HIT is not recognised and managed early, thrombosis can occur in up to 50% of patients, with thrombosis-related deaths ranging from 5 to 10%Kang, 2015.
Clinical features of HIT include:
- new-onset thrombocytopenia or a fall in platelet count of at least 50% from baseline within 5 to 14 days of exposure to heparin or low molecular weight heparin (or earlier if the patient has preformed antibodies from previous heparin exposure)
- development of arterial or venous thrombosis
- necrotic skin lesions at heparin injection sites
- acute systemic response to intravenous heparin (fever, tachycardia, hypertension, dyspnoea, cardiopulmonary arrest).
The diagnosis of HIT is made by a combination of the clinical features listed above, and by laboratory demonstration of specific antibodies. It can take several days to obtain definitive laboratory antibody test results, so a clinical risk calculator (such as the 4Ts score) can make a presumptive diagnosis for the urgent management of HIT; see the 4Ts score via the MSD Manuals website for more information.
For more detailed information on the diagnosis and management of HIT, see the Thrombosis and Haemostasis Society of Australia and New Zealand consensus statement.
Vaccine-induced immune thrombotic thrombocytopenia (VITT) (also known as thrombosis with thrombocytopenia syndrome [TTS]) refers to an immunothrombotic syndrome that occurs rarely after exposure to adenoviral vector COVID-19 vaccinations, predominantly, but not limited to, the ChAdOx1-nCov-19 AstraZeneca vaccination. Postvaccination antibodies to platelet antigens (PF4) have been detected; these antibodies have some similarities to HIT but they are heparin independent. Management includes anticoagulation with non-heparin drugs. For more detailed information on VITT, see the Thrombosis and Haemostasis Society of Australia and New Zealand advisory statement.