Open AccessBivalirudin resistance in a patient on veno-venous extracorporeal membrane oxygenation with a therapeutic response to argatroban
Author(s) -
Beric E Berlioz,
Haya Kaseer,
Devang Sanghavi,
Pramod Guru
Publication year - 2020
Publication title -
bmj case reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.231
H-Index - 26
ISSN - 1757-790X
DOI - 10.1136/bcr-2019-232262
Subject(s) - bivalirudin , argatroban , medicine , extracorporeal membrane oxygenation , heparin induced thrombocytopenia , direct thrombin inhibitor , discovery and development of direct thrombin inhibitors , heparin , thrombin , cardiology , anesthesia , intensive care medicine , pharmacology , platelet , warfarin , dabigatran , atrial fibrillation , percutaneous coronary intervention , myocardial infarction
A 48-year-old male patient requiring extracorporeal membrane oxygenation (ECMO) support for hypoxaemic respiratory failure failed to achieve therapeutic anticoagulation with bivalirudin after continuous dose escalations, and continued to have recurrent fibrin stranding in the circuit over a 6-day course of treatment. Suspecting bivalirudin resistance, the patient was transitioned to argatroban and achieved a therapeutic response in less than 24 hours. The case describes the challenges of anticoagulation in ECMO supported patients. The interplay between bivalirudin metabolism, renal replacement therapy, and immunological effects leading to a heparin-like-effect, inflammatory mediators, and thrombotic burdens may all impact the clinical effect during bivalirudin therapy. The structural biochemistry of thrombin and bivalirudin likely plays a role in the presented patient's successful response to argatroban. Bivalirudin may fail at achieving therapeutic anticoagulation in patients with genetic thrombin mutations or structural defects that alter the binding pockets at the thrombin exosites.