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Heparin-induced thrombocytopenia and lack of efficacy: case report A 73-year-old woman developed heparin-induced thrombocytopenia (HIT) during treatment with tinzaparin sodium as an anticoagulation therapy. Additionally, she exhibited lack of efficacy during treatment with rivaroxaban and fondaparinux sodium [dosages and durations of treatments to reactions onsets not stated; not all routes stated]. The woman was diagnosed with chronic thromboembolic pulmonary hypertension (CTEPH) 9 months following acute bilateral pulmonary emboli after right knee replacement. Soon following the diagnosis of CTEPH, recurrent pulmonary emboli developed in spite of her being on oral anticoagulation therapy with rivaroxaban [Xarelto]. Her therapy was then changed to a low molecular weight heparin, tinzaparin sodium [tinzaparin; Innohep]. A month afterwards, she was readmitted because of a syncopal episode. Her platelet count had reduced by more than 50%, and she was diagnosed with HIT by immunoassay, confirmed by platelet serotonin-release assay. Therefore, the woman’s anticoagulation therapy was changed to warfarin and then to SC fondaparinux sodium [fondaparinux] 7.5mg daily. It was decided to delay her pulmonary endarterectomy (PEA) to allow the HIT antibodies to clear and to achieve a period of clinical stability with no thromboembolic events. However, 2 months afterwards, she presented with clinical deterioration, necessitating hospital admission for decompensated right heart failure. No new thromboemboli were observed on repeat imaging. She was initiated on a regimen of unspecified diuretic drugs and epoprostenol to facilitate transfer to the institution (current presentation). On arrival, she developed two syncopal episodes and needed admission to the ICU. She was stabilised with norepinephrine [noradrenaline] and milrinone, but her clinical condition was still precarious. The HIT Immunoassay also remained strongly positive. Her condition continued to deteriorate, and she urgently required stabilisation with venoarterial extracorporeal membrane oxygenation (VA-ECMO). Given the period of instability, it was decided to delay the PEA by a few days to optimise her clinical condition and allow the fondaparinux sodium to fully wear off before the surgery to curb the risk of perioperative bleeding. During this period, her anticoagulation therapy was managed by argatroban with a target activated partial thromboplastin time of 65 to 85 seconds. Following 4 days on VA-ECMO, she was transferred to the operating room, and underwent a 2.0 plasma exchange, replacement with full fresh frozen plasma using central vascular access. This was performed with no complication and was followed by PEA on cardiopulmonary bypass (CPB) and deep hypothermic circulatory arrest at 20°C. She underwent a second exchange before the administration of heparin. For the surgery, standard heparin [unfractionated heparin] was used, and at the end of the surgery, it was partially reversed for haemostasis using protamine. After termination of CPB, she was convert