MON-350 - When Standard Therapy Fails: Refractory Thyroid Storm with AF-RVR and Cardiomyopathy Requiring Prolonged Plasma Exchange

Background:
Thyroid storm can precipitate atrial fibrillation with rapid ventricular response and acute cardiomyopathy. While standard medical therapy is effective in most cases, therapeutic plasma exchange (TPE) is infrequently utilized and typically reserved for patients with refractory disease. In severe thyrotoxicosis, concurrent physiologic stressors such as infection or stimulant exposure may exacerbate the hyperadrenergic state and limit responsiveness to conventional therapy.

Case Presentation:
A 47-year-old man with recently diagnosed atrial fibrillation presented to the emergency department with dyspnea and anasarca. He was febrile to 104.5°F, tachycardic to 190 beats/min, and required high-flow nasal cannula. Thyroid testing showed TSH < 0.008 mcIU/mL (0.35–5.00), free T4 5.0 ng/dL (0.8–1.5), and free T3 14.0 pg/mL (2.2–4.0), with elevated thyroid-stimulating immunoglobulin and thyrotropin receptor antibody, consistent with Graves disease. Urine toxicology was positive for methamphetamines and cannabinoids, and respiratory pathogen testing detected influenza A (H3). The Burch-Wartofsky score was 80–85, consistent with thyroid storm.

Transthoracic echocardiography revealed new biventricular systolic dysfunction with left ventricular ejection fraction (LVEF) of 30–35%. Endocrinology initiated methimazole at 10 mg twice daily due to mild baseline transaminitis ( < 2 × upper limit of normal) and cautiously dosed propranolol given reduced LVEF, along with Lugol’s iodine, intravenous stress-dose hydrocortisone, and cholestyramine. Despite these constraints, antithyroid and beta-blocker therapy were systematically escalated as hepatic function and hemodynamics permitted, reaching methimazole 30 mg twice daily and propranolol 40 mg three times daily by hospital day 3.

Despite stepwise escalation of methimazole, propranolol, and cholestyramine to 4 g four times daily, thyroid indices worsened, with free T3 rising from 4.9 to 10.8 pg/mL and free T4 from 4.0 to 4.6 ng/dL. Given progressive biochemical thyrotoxicosis despite maximally tolerated medical therapy, TPE was initiated on hospital day three. After seven exchange sessions achieved sustained thyroid hormone control, the patient was stabilized and underwent thyroidectomy. He was transitioned to levothyroxine and cardiac function recovered with improvement of LVEF to 56% during hospitalization.

Clinical Lessons:
Thyroid storm may remain refractory despite guideline-directed medical therapy, particularly during concurrent infection and stimulant exposure that can amplify adrenergic stress. In cases of objective thyrotoxicosis progression despite appropriate escalation of antithyroid therapy, timely consideration of therapeutic plasma exchange may facilitate stabilization and enable definitive treatment.

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