SAT-328 - Cardiogenic Shock in Severe Thyrotoxicosis with Recent Cocaine Use: Diagnostic and Therapeutic Challenges

Introduction:
Thyrotoxicosis and cocaine exposure can both produce sympathomimetic physiology and cardiovascular decompensation. In patients with advanced cardiomyopathy, thyroid storm may present atypically, and beta-blockade may worsen cardiogenic shock. We describe a case of severe thyrotoxicosis with cardiogenic shock in the setting of recent cocaine use and highlight management considerations.

Case:
A 50-year-old woman with Graves disease, prior contrast-associated thyroid storm complicated by pulseless electrical activity arrest, heart failure with reduced ejection fraction (baseline LVEF 40%), severe mitral regurgitation, and atrial fibrillation with nonadherence to antithyroid therapy, presented with two days of progressive dyspnea. Initial evaluation revealed severe lactic acidosis (pH 7.26, lactate 9.5 mmol/L), NT-proBNP 1,577 pg/mL, suppressed thyroid-stimulating hormone ( < 0.010 µIU/mL), elevated free thyroxine (2.86 ng/dL), and elevated free triiodothyronine (4.19 pg/ml), with urine drug screen positive for cocaine. Electrocardiogram demonstrated atrial fibrillation. She rapidly developed respiratory failure and cardiogenic shock requiring intubation and vasoactive support, including norepinephrine, vasopressin, and inotropic therapy. Transthoracic echocardiography demonstrated severe biventricular systolic dysfunction with left ventricular ejection fraction of 25-30%.
Given severe decompensated heart failure and concern for impending or atypical thyroid storm, as supported by a Burch-Wartofsky score of 40 driven by severe heart failure, atrial fibrillation, and a clear precipitating factor, she was treated with propylthiouracil followed by Lugol’s iodine 5% solution after thionamide therapy, dexamethasone, and cholestyramine. Beta-blockade was deferred due to cardiogenic shock. Thyroid function improved, with free thyroxine decreasing to 1.14 ng/dL by hospital day 5 with concurrent hemodynamic stabilization and transition to methimazole. At outpatient follow-up, free thyroxine and triiodothyronine remained within reference range on methimazole. Definitive therapy with radioactive iodine ablation is planned following cardiac valve intervention.

Conclusion:
Severe thyrotoxicosis with cardiogenic shock in the setting of recent cocaine use presents diagnostic overlap and therapeutic risk, particularly with respect to beta-blockade. In patients with shock and biventricular failure, prioritizing hemodynamic stabilization and definitive antithyroid therapy while individualizing beta-blocker use may reduce the risk of hemodynamic deterioration.

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