The patient’s Burch-Wartofsky score was calculated to be 60. Thyroid function tests prior to initiation of amiodarone were reviewed and previously were within normal limits ( Table 1). In the intensive care unit, workup yielded undetectable thyroid-stimulating hormone (TSH) and an elevated free thyroxine of 5.46 ng/dL. He was treated with intravenous (IV) amiodarone, lidocaine, and ultimately intubated and sedated for unremitting ventricular tachycardia storm. During the interview period he continued to receive tachytherapies from his implanted device including three defibrillations. Initial electrocardiogram (EKG) demonstrated monomorphic ventricular tachycardia and ICD interrogation reveled that he had been defibrillated eight times during his syncopal episode. His home medications included amiodarone and digoxin for underlying chronic atrial fibrillation started 4 months prior, metoprolol, dabigatran, and rosuvastatin. Neck exam revealed a non-tender 6-cm thyroid nodule and cardiac auscultation revealed I/VI holosystolic murmur. On physical exam he appeared anxious and tachypneic. He was afebrile and normotensive but tachycardic with heart rate (HR) 140 - 160 beats per minute (bpm). On presentation he had anterograde amnesia following the event but was alert and not altered. Case ReportĪ 75-year-old man with a history of ischemic cardiomyopathy status post coronary artery bypass graft (CABG), chronic atrial fibrillation on amiodarone, heart failure with reduced ejection fraction (EF) of 25-30%, primary prevention implantable cardiac defibrillator (ICD), and non-toxic large left-sided colloid thyroid nodule presented to the emergency department after an episode of syncope after a prodrome of feeling faint while walking. We report a case and management of AIT resulting in severe thyroid storm and monomorphic ventricular tachycardia. In a retrospective analysis, incidence of AIT was found to be associated with a 2.7-fold increased risk of major adverse cardiovascular events including myocardial infarction, stroke, heart failure, or ventricular arrhythmias compared to euthyroid patients on amiodarone. Amiodarone-induced thyrotoxicosis (AIT) results either from increased synthesis of T4 and T3 (AIT type I), or from the destructive thyroiditis resulting in excess hormone release (AIT type II). Side effects are many, including thyroid dysfunction, both hyper- and hypothyroidism. Īmiodarone, a type III antiarrhythmic approved for the use of ventricular and supraventricular arrhythmias, is 37% iodine by molecular weight. Current treatment modalities revolve around decreasing hormone synthesis, inhibiting the release of thyroid hormone, and blocking peripheral effects of existing systemic thyroid hormone. Proposed in 1993, the Burch-Wartofsky score is a scoring metric based on clinical findings used for the identification of thyroid storm. Currently, there are no universally accepted clinical criteria for the diagnosis of thyroid storm. Thyroid storm traditionally has been identified as a clinical syndrome involving thyrotoxicosis, altered mentation, hyperthermia, and a precipitating event. Thyrotoxicosis associated with thyroid storm carries with it a 12-fold higher mortality rate than thyrotoxicosis alone. Based on the National Inpatient Sample database, a retrospective longitudinal analysis found one in six patients with a discharge diagnosis of thyrotoxicosis was also diagnosed with thyroid storm. Thyroid storm is a rare endocrine emergency that presents with exaggerated clinical manifestations of thyrotoxicosis. Keywords: Amiodarone Thyrotoxicosis Ventricular tachycardia Plasmapheresis Thyroid storm Introduction Under the circumstances of limited medical therapies, plasmapheresis can be an effective treatment option. Amiodarone-induced thyroid storm can lead to monomorphic ventricular tachycardia. We describe a case of amiodarone-induced thyrotoxicosis and thyroid storm leading to refractory ventricular tachycardias treated with plasmapheresis when anti-arrhythmic therapy became contraindicated. The mainstay of treatment includes supportive intensive care and initiation of thionamides, beta blockers, corticosteroids, and if necessary anti-arrhythmics in the presence of refractory ventricular arrhythmias. It manifests with the exaggerated symptoms of hyperthyroidism including hyperpyrexia, hypotension, cardiac arrhythmias, and death. Thyroid storm is a rare endocrine emergency with a high mortality rate approaching 20%.
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