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Cangrelor/heparin Heparin-induced thrombocytopenia, left-arterial thrombosis and rebound effect: case report

A 64-year-old man developed heparin-induced thrombocytopenia (HIT) and left-atrial thrombosis during treatment with heparin. Thereafter, he developed rebound effect following withdrawal of cangrelor for treatment of HIT [not all dosages stated; routes and times to reactions onsets not stated]. The man, who had severely impaired cardiac and renal function, underwent urgent coronary artery bypass grafting and mitral valve replacement with post-operative anticoagulation with heparin [unfractionated heparin]. On postoperative day 8 (POD), his platelet count fell below 100 × 109/L; HIT was suspected with a high-probability 4Ts score, and the diagnosis was confirmed with a strong-positive IgG-specific chemiluminescence immunoassay (CLIA) result of 17.6 U/mL. The man’s anticoagulation was changed from heparin to argatroban. On POD 10, routine echocardiography showed a large, shelllike thrombosis involving the wall and roof of the left atrium (left-atrial thrombosis) secondary to heparin, which required urgent surgical thrombectomy. Repeat CLIA on POD 15 was 10.8 U/mL, which indicated possible persistence of heparin-dependent platelet-activating antibodies. Due to high risk, the chosen strategy was to wait for platelet count recovery and allowing his HIT to transition from acute to subacute HIT and then perform intraoperative anticoagulation with heparin and a new strategy of combined cangrelor and immune globulin [Privigen] for perioperative inhibition of HIT. He was administered immune globulin after anaesthesia induction with unspecified anaesthetic at the time of redo surgery on POD 16. The minutes prior to systemic heparinisation with administration of heparin 400 IU/kg for cardiopulmonary bypass (CPB), a bolus of cangrelor 30 µg/kg was administered, followed by a constant cangrelor infusion of 4 µg/kg/min. Thereafter, the man underwent throbectomy of the large thromboses from the left atrial wall. After 95 minutes of CPB, protamine sulfate [protamine] was administered and cangrelor infusion was discontinued. During the intraoperative period, red cell concentrates, prothrombin complex concentrate and folitixorin [Cofact] were transfused. He was not administered platelet transfusions. Argatroban was restarted in the ICU 6 hours after the surgery. The preoperative platelet count was 375 × 109/L. Immediately after the operation, the platelet count was 206 × 109/L, with a further decline to 129 × 109/L over the next 4 days. No thromboembolic complications were noted, and he was discharged home 3 weeks after redo surgery (HIT and thrombosis recovered). Histopathology of the atrial thrombus showed granulocyte-rich and fibrin-rich haemorrhagic material. His serum and plasma consistently tested negative in the serotonin-release assay (SRA). However, his serum (POD8 sample) induced strong serotonin-release (approximately 88%) in the platelet factor 4 (PF4)-SRA10 as well as in the PF4/heparin-SRA. Immediately prior