Amiodarone

Abstract

Acute liver toxicity: case report A 77-year-old woman developed acute liver toxicity during treatment with IV amiodarone for atrial fibrillation. The woman, who had a history of hyperlipidaemia, atrial fibrillation (AF), chronic obstructive pulmonary disease, non-STelevation myocardial infarction (NSTEMI), coronary artery disease, and heart stent placement, presented to the intensive cardiac care unit (ICCU) after experiencing acute decompensated heart failure and another episode of NSTEMI. Before she entered ICCU, she had received oral amiodarone 400mg every eight hours to control her AF and premature atrial contractions. She exhibited no signs of hepatic impairment. With recurrent bouts of AF and a rapid ventricular rate, she was initiated on non-invasive ventilatory aid in the ICU. Eventually, her oral amiodarone was switched to IV bolus of 150mg of amiodarone and followed by an IV infusion of 360mg at a rate of 1 mg/min for 6 hours. In different doses of drugs, the diluent concentration contains 1.5 mg/mL and 1.8 mg/mL isotonic glucose [dextrose] formulations. Moreover, she received a second intravenous infusion of 360mg at a rate of 0.5 mg/minute. These formularies did not contain polysorbate 80 which was traditionally associated with hepatotoxicity Her sinus rhythm remained normal in this protocol. Eight hours after receiving IV amiodarone, she showed an acute elevation of transaminase. Her aspartate aminotransferase (AST), alanine aminotransferase (ALT), and international normalisation ratio (INR) levels were elevated. Throughout the period of possible toxicity, her platelet count was normal and remained within the standard range. Additionally, her alkaline phosphate, direct bilirubin, and total bilirubin are 92 U/L, 0.7 mg/dL, and 1.3 mg/dL, respectively. There are no other signs of systemic organ failure caused by ischaemia or hypoperfusion, including normal creatinine. A contrast pelvis and CT of the abdomen revealed a normal-sized liver. The backflow of the contrast agent to the liver or renal veins, the stratification of the contrast agent in a dependent manner, or the substantial improvement in the dependent areas of the liver were unrecorded. Due to her history and acute nature of the isolated hepatic injury, no other infectious or serological abnormalities were considered. In addition, she was hospitalised and intubated till then and no toxic intake such as alcohol was considered or tested. Initially, congestive hepatopathy was suspected a pathophysiological cause, but Swan’s findings showed no evidence of sustained cardiogenic shock. The Swan-Ganz monitoring was not consistent with the refractory cardiogenic shock following hepatopathy. In addition, her liver test pattern was not consistent with the pattern usually found in congestive liver disease. The woman’s treatment with IV amiodarone was discontinued after experiencing acute liver impairment and isolated hypertransaminemia. However, she had a history of bleeding and was reluctant to anticoagulated, her treatment was changed to oral amiodarone to preserve NSR and prevent the necessity of unspecified anticoagulant for cardiovascular abnormalities. Within two days, her INR returned to normal. After 4 days, her ALT, AST, and transaminase levels gradually recovered. Oral amiodarone effectively controlled her AF during her stay in ICCU. Based on the finding acute liver toxicity was considered secondary to IV amiodarone. Later, she developed septic shock as a result of toxic megacolon and bacteraemia caused by Clostridium difficile infection. After experiencing multiple organ failures, she died on the day 21 of hospitalisation [immediate cause of death not stated].