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Heparin-induced thrombocytopenia in ICU — FFICM MCQ

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HardPharmacologyHeparin-induced thrombocytopenia in ICUFFICM

A 62-year-old man on ICU after vascular surgery has a platelet count fall from 280 to 82 × 10^9/L on day 7 of unfractionated heparin. He develops a new femoral DVT. There is no sepsis deterioration and no major bleeding. The 4Ts score is high. What is the most appropriate management?

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Correct answer: DStop heparin and start a non-heparin anticoagulant while testing

The correct answer is D, stop heparin and start a non-heparin anticoagulant while testing. A high 4Ts score with a falling platelet count around day 5 to 10 of heparin exposure plus a new thrombotic event (femoral DVT) is classic for heparin-induced thrombocytopenia (HIT), an immune-mediated prothrombotic disorder driven by antibodies to platelet factor 4-heparin complexes. Because thrombosis risk remains high despite thrombocytopenia, all heparin (including flushes and heparin-coated lines) must stop immediately and a non-heparin anticoagulant such as argatroban, danaparoid or fondaparinux started empirically at therapeutic dose, without waiting for laboratory confirmation. This reflects current BSH guidance that treatment decisions in intermediate or high-probability HIT should be based on clinical probability scoring, with confirmatory functional and antigen assays run in parallel rather than delaying treatment. Why the other options are wrong: A. Continue heparin until antibody tests return: this perpetuates antibody-mediated platelet activation and thrombin generation, risking extension of the DVT, limb ischaemia or further thromboembolism while awaiting results that may take days. E. Give platelet transfusion as first-line treatment: platelets fuel the prothrombotic process in HIT and transfusion can precipitate further thrombosis; it is reserved for significant bleeding only, not first-line management. C. Start warfarin monotherapy immediately: warfarin alone in acute HIT can cause transient protein C and S depletion, precipitating warfarin-induced skin necrosis or venous limb gangrene; it should only be introduced after platelets recover and while overlapping with a non-heparin anticoagulant. B. Stop anticoagulation because platelets are low: withholding anticoagulation ignores the prothrombotic nature of HIT and leaves the new DVT untreated, risking propagation or pulmonary embolism. Key point: HIT is a prothrombotic state, so all heparin must stop and a non-heparin anticoagulant started empirically at therapeutic dose based on clinical probability, without waiting for antibody test confirmation.

Reference: British Society for Haematology, Diagnosis and management of heparin-induced thrombocytopenia: Third edition, 2024, https://b-s-h.org.uk/guidelines/guidelines/diagnosis-and-management-of-heparin-induced-thrombocytopenia-third-edition