Abstract #1408136: The Calm Before the Storm: Cardiogenic Shock in Graves’ Disease

Abstract

This case highlights the endocrine and cardiopulmonary physiology of thyroid storm in a patient with comorbid rapid atrial fibrillation, severe heart failure with reduced ejection fraction and resultant cardiogenic shock in order to raise awareness regarding the risk of circulatory collapse, as well as the value of bedside ultrasound in management. A 42-year-old man presented to our hospital with 2 months of worsening dyspnea and lower extremity edema, 2 years of diarrhea and 50-pound weight loss followed by weight gain. He was hypertensive and in rapid atrial fibrillation (HR 180/min). A diltiazem drip was initiated, but he continued to be tachycardic (HR 120/min). Bedside point-of-care ultrasound (POCUS) was concerning for a severe cardiomyopathy. Chest x-ray demonstrated pulmonary edema. Labs demonstrated TSH < 0.01 mcIUnit/mL, free T4 2.9 mcg/dL (0.7-1.5 mcg/dL), and free T3 12.1 pg/mL (1.6-3.9 pg/mL). He met criteria highly suggestive of thyroid storm by the Burch-Wartofsky Point Scale, scoring 70 points, so management became focused on this. The diltiazem drip was discontinued in favor of an intravenous metoprolol challenge. Soon thereafter, his heart rate decreased to 80 bpm with low-normal mean arterial pressures. He developed acute hypoxemic respiratory failure with cool, cyanotic extremities. He was placed on non-invasive positive pressure ventilation with norepinephrine and dobutamine for treatment of cardiogenic shock secondary to thyroid storm. Hydrocortisone and propylthiouracil were administered. Echocardiogram showed severe left ventricular global hypokinesis with ejection fraction of 15%. As vasopressors were weaned, he underwent cautious diuresis. A short course of propranolol was started, which was subsequently switched to metoprolol tartrate. Thyrotropin receptor and thyroperoxidase antibodies were elevated. Thyroid ultrasound suggested autoimmune thyroiditis. He was transitioned to methimazole and discharged home. Thyroid storm patients are at risk of circulatory collapse after treatment with rate-control agents, especially in the presence of systolic dysfunction. In one study, underlying hyperthyroidism was unknown in 32% of patients admitted to the ICU for thyroid storm, and ICU mortality rates were 17%. Thyroid hormone sensitizes the myocardium to adrenergic input by upregulating adrenergic receptors, resulting in baseline tachycardia to maintain cardiac output and subsequent high-output heart failure.