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Development of resistance and lack of efficacy: case report A 48-year-old man developed resistance to bivalirudin as an anticoagulation therapy. Additionally, the patient exhibited lack of efficacy during treatment with oseltamivir for influenza A pneumonia. The man, who had a medical history of smoking and alcohol abuse, bipolar disorder, anxiety and chronic obstructive pulmonary disorder, was admitted to the ICU as a hospital transfer for escalation in management of acute hypoxic respiratory failure secondary to influenza A pneumonia acute respiratory distress syndrome. He had progressively deteriorating respiratory failure despite being on maximal lung protective ventilatory support including neuromuscular blockade and prone positioning, a fluid restrictive strategy and antiviral therapy with oseltamivir. He underwent veno-venous extracorporeal membrane oxygenation (ECMO) placement with the return cannulas and drainage to the right internal jugular vein and right femoral vein, respectively. On 25 April (year not specified), he was started on bivalirudin 0.15 mg/kg/hour as part of the ECMO anticoagulation protocol at the institution (current presentation). In this patient, when a suspicion of resistance to anticoagulation therapy was made and increased in-circuit fibrin stranding was noted in the setting of suboptimal anticoagulation, the activated partial thromboplastin time (aPTT) therapeutic range was increased from 50–70 to 60–90 after 4 days. The course of therapy, he needed continuous bivalirudin dose escalation up to 0.54 mg/kg/hour with only a mild elevation of his aPTT ranging between 44.2 and 62.8s with a required goal of 60–90s. After day 4 of therapy (on 29 April), the route of administration was changed, and bivalirudin was infused directly into the ECMO circuit preoxygenator. On day 6 of bivalirudin therapy, despite increasing the dose of bivalirudin from 0.34 mg/kg/ hour to 0.54 mg/kg/hour within a 24-hour window, the ECMO circuit developed fibrin strands. Owing to the concern of bivalirudin resistance, the man’s anticoagulation therapy was changed to argatroban on 1 May. The argatroban dose was increased with an aPTT range of 72–85.1s and no fibrin stranding in the ECMO circuit. On day 12 of ECMO, he underwent the placement of a tracheostomy, and following 35 days of ECMO support, he was successfully decannulated. He developed thromboses in the right femoral vein and right internal jugular at the cannulation sites diagnosed one day following decannulation. One week later, he was weaned from mechanical ventilation and was switched to apixaban at the time of discharge. Berlioz B, et al. Bivalirudin resistance in a patient on veno-venous extracorporeal membrane oxygenation with a therapeutic response to argatroban. BMJ Case Reports 13: 803501799 No. 1, 7 Jan 2020. Available from: URL: http://doi.org/10.1136/bcr-2019-232262

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Reactions 19 Sep 2020 No. 1822