Guidelines on the diagnosis and management of heparin‐induced thrombocytopenia: second edition

Abstract

• Patients who are to receive any heparin should have a baseline platelet count (2C). • Post-operative patients including obstetric cases receiving unfractionated heparin (UFH) should have platelet count monitoring performed every 2–3 d from days 4 to 14 or until heparin is stopped (2C). • Post-cardiopulmonary bypass patients receiving low molecular weight heparin (LMWH) should have platelet count monitoring performed every 2–3 d from days 4 to 14 or until heparin is stopped (2C). • Post-operative patients (other than cardiopulmonary bypass patients) receiving LMWH do not need routine platelet monitoring (2C). • Post-operative patients and cardiopulmonary bypass patients who have been exposed to heparin in the previous 100 d and are receiving any type of heparin should have a platelet count determined 24 h after starting heparin (2C). • Medical patients and obstetric patients receiving heparin do not need routine platelet monitoring (2C). • If the platelet count falls by 30% or more and/or the patient develops new thrombosis or skin allergy or any of the other rarer manifestations of heparin-induced thrombocytopenia (HIT) between days 4 and 14 of heparin administration, HIT should be considered and a clinical assessment made (2C). • HIT can be excluded by a low pre-test probability score without the need for laboratory investigation (2B). • If the pre-test probability of HIT is not low, heparin should be stopped and an alternative anticoagulant started in full dosage whilst laboratory tests are performed (1C). • Platelet aggregation assays using platelet-rich plasma (PRP) lack sensitivity and are not recommended (2C). • Platelet activation assays using washed platelets [heparin-induced platelet activation assay (HIPA) and serotonin release assay (SRA)] have a higher sensitivity than platelet aggregation assays using PRP and are regarded as the reference standard, but are technically demanding and their use should be restricted to experienced laboratories (2C). • Non-expert laboratories should use an antigen assay of high sensitivity. Only the IgG class needs to be measured. Useful information is gained by reporting the actual optical density, degree of inhibition by high dose heparin, and the cut-off point for a positive test rather than simply reporting the test as positive or negative (1B). • In making a diagnosis of HIT, the clinician’s estimate of the pre-test probability of HIT, together with the type of assay used and its quantitative result [enzyme-linked immunosorbent assay (ELISA) only] and information on reversal using higher doses of heparin should be used to determine the post-test probability of HIT (2B). • HIT can be excluded in patients with an intermediate pre-test score who have a negative particle gel immunoassay (2B). • HIT can be excluded in all patients by a negative antigen assay of high sensitivity (1A). • Clinical decisions should be made following consideration of the risks and benefits of treatment with an alternative anticoagulant (1C). • For patients with suspected (non-low pre-test probability) or confirmed HIT, heparin should be stopped and full dose anticoagulation with an alternative anticoagulant commenced (1B). • LMWH should not be used in the treatment of HIT (1A). • Warfarin should not be used until the platelet count has recovered to the normal range. When introduced, an alternative anticoagulant must be continued until the International Normalized Ratio (INR) is therapeutic. Argatroban affects the INR and this needs to be considered when using this drug. A minimum overlap of 5 d between non-heparin anticoagulants and vitamin K antagonist (VKA) therapy is recommended (1B). Correspondence: Dr Henry Watson, British Society for Haematology, 100 White Lion Street, London, N1 9PF, UK. E-mail bcsh@b-s-h.org.uk