Have You Been HIT?

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initiated until the platelet count has been recovered and there should be an overlap of at least 5 days between starting warfarin and stopping the alternative ...
Hemostasis Angiology 62(8) 641-644 ª The Author(s) 2011 Reprints and permission: sagepub.com/journalsPermissions.nav DOI: 10.1177/0003319711405509 http://ang.sagepub.com

Have You Been HIT? Jane Cross, FRCS1, Mary Weisters, MRCS1, Robina Aslam, MRCS2, David Keeling, FRCP3, and Ashok Handa, FRCS1

Abstract This review is specifically designed to aid the vascular surgeon in the management of heparin-induced thrombocytopenia (HIT). Heparin-induced thrombocytopenia is a rare complication of heparin administration, which poses significant morbidity and mortality. Its onset is usually 5 to 10 days after the heparin administration and should be suspected if platelet counts drop by at least 50%. Confirmation is given by the presence of HIT antibodies on an enzyme-linked immunosorbent assay (ELISA) or in functional platelet activation assays. The major complication is thrombosis and surprisingly bleeding is rare. Heparin must be stopped immediately if there is a clinical suspicion of HIT and alternative anticoagulation must be started. Anticoagulation is required for at least 2 to 3 months to prevent recurrence of thrombosis. Oral anticoagulation with warfarin should not be initiated until the platelet count has been recovered and there should be an overlap of at least 5 days between starting warfarin and stopping the alternative anticoagulant. Keywords heparin-induced thrombocytopenia, lepirudin, danaparoid, thrombosis

Introduction The vascular surgeon regularly runs the anticoagulation gauntlet. An intraoperative heparin bolus may aid a successful bypass procedure however the risk of bleeding is always a threat. Heparin-induced thrombocytopenia (HIT) adds an extra complication into the equation. This article is designed to help the vascular surgeon manage patients with HIT. Heparin-induced thrombocytopenia is a complication of heparin administration occurring with both fractionated low-molecular-weight heparin (LMWH) and unfractionated heparin (UFH). It is the most important and most frequent drug-induced, immune-mediated type of thrombocytopenia. Unrecognized HIT poses significant morbidity and mortality. It presents as a decrease in platelet count following exposure to heparin.1 Although rare, as many as 8% of heparinized patients will develop the antibody associated with HIT2 and approximately 1% to 5% of patients on heparin will progress to develop HIT.3,4 Heparin-induced thrombocytopenia paradoxically increases the risk of thrombosis and one third of cases may develop arterial or venous thrombosis.5,6

receptor and this triggers activation and aggregation of the platelets, releasing further PF-4 and thus perpetuating the cycle. In addition, there is further activation of the coagulation cascade, thrombin generation, and the production of a prothrombotic phenotype.7 Activation of endothelium and monocytes occurs perhaps directly by HIT antibodies but more likely through activated platelet (or microparticle)–endothelial– leukocyte interactions.

Clinical Features The onset of thrombocytopenia is usually 5 to 10 days after heparin administration in patients receiving heparin for the first time. However, in patients with preexisting heparin PF-4 antibodies, thrombocytopenia may occur within hours to days after reexposure to heparin.8 All patients should routinely have platelet levels checked during heparin administration. Heparin-induced thrombocytopenia should be suspected when platelet levels drop by at least 50% post heparin administration.7 Confirmation of HIT is provided by the presence of HIT 1

Pathology

Department of Vascular Surgery, John Radcliffe Hospital, Oxford, UK Department of General Surgery, John Radcliffe Hospital, Oxford, UK 3 Department of Haematology, Churchill Hospital, Oxford, UK 2

Platelet activation leads to the release of platelet factor 4 (PF-4). Heparin binds to the PF-4 molecules exposing neo-epitopes; these can act as immunogens leading to immunoglobulin G (IgG) antibody production. In patients who develop HIT the antibody-antigen complex binds to the platelet Fcg

Corresponding Author: Jane Cross, Department of Vascular Surgery, John Radcliffe Hospital, Oxford, UK Email: [email protected]

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Angiology 62(8)

Table 1. The 4Ts Clinical Scoring System9,a Score

0

1

2

Platelet fall >50% and platelet Platelet fall