SUN-867 - Concurrent Thyroid Storm and Diabetic Ketoacidosis with Persistent Tachycardia and Reversible Cardiomyopathy

Background:
Diabetic ketoacidosis (DKA) and thyroid storm are independent endocrine emergencies with high morbidity and mortality. Severe thyrotoxicosis may precipitate DKA through increased insulin resistance and counter‑regulatory hormone excess. Concurrent presentation is rare and may be obscured by overlapping metabolic and cardiovascular features.

Case Presentation:
A 37‑year‑old woman with no known medical history presented with one week of weakness, nausea, and vomiting, and several months of polyuria, polydipsia, and unintentional weight loss. Laboratory evaluation confirmed DKA, and treatment was initiated per protocol. Initial electrocardiogram demonstrated atrial fibrillation with rapid ventricular response up to 215 bpm, which converted to sinus tachycardia at approximately 140 bpm following amiodarone.

Despite metabolic improvement, she remained tachycardic and altered. Thyroid studies resulted the following morning, revealing suppressed TSH < 0.10 µIU/mL, free T4 3.67 ng/dL, and free T3 10.6 pg/mL. Her Burch‑Wartofsky score was 75, consistent with thyroid storm. Amiodarone was discontinued, and an esmolol infusion was initiated for rapid, titratable rate control. Once heart rate improved, esmolol was discontinued and low‑dose oral propranolol was initiated along with propylthiouracil and hydrocortisone.

The patient’s mentation and metabolic parameters initially improved; however, she subsequently developed acute bradycardia, hypotension, and pulseless electrical activity requiring brief cardiopulmonary resuscitation with return of spontaneous circulation. All beta‑blockers were held. Transthoracic echocardiography demonstrated new systolic dysfunction with an ejection fraction of 25–30%. She required vasopressor support with continued DKA and thyroid storm management. Over 48 hours, she demonstrated marked clinical recovery. Propranolol was cautiously reintroduced at a low dose once hemodynamically stable. Thyroid‑stimulating hormone receptor antibodies confirmed Graves disease. Repeat echocardiography showed recovery of left ventricular systolic function.

Conclusion:
This case highlights diagnostic masking between DKA and thyroid storm. Persistent or disproportionate tachycardia despite appropriate DKA management should prompt evaluation for thyrotoxicosis. Although thyroid storm–associated cardiomyopathy is often reversible, heightened sensitivity to beta‑blockade may lead to abrupt hemodynamic collapse, underscoring the need for cautious titration and close monitoring.

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