SAT-339 - Thyroid Storm in the ICU: A Case Report Highlighting Multisystem Involvement

Thyroid storm is a life-threatening endocrine emergency caused by excess thyroid hormone release, most commonly in Graves disease. Although the exact pathophysiology is unclear, precipitating factors such as infection, stress, trauma, iodine exposure, or myocardial infarction may trigger thyroid storm in patients with hyperthyroidism.¹ Mortality rates reach up to 10% due to multisystem involvement, primarily affecting thermoregulatory, cardiovascular, central nervous system, and gastrointestinal systems.¹ Common manifestations include fever, tachycardia, delirium, and vomiting. Diagnosis is clinical, as no specific laboratory findings exist, and scoring systems such as the Burch-Wartofsky scale are used.² Variability in presentation contributes to diagnostic difficulty.

A 68-year-old man with untreated hyperthyroidism, end-stage renal disease on hemodialysis, atrial fibrillation, and severe tricuspid regurgitation presented with tachycardia and diarrhea. He was found to be in atrial fibrillation with rapid ventricular response refractory to diltiazem, digoxin, and amiodarone. Laboratory testing showed undetectable TSH, free T4 of 2.2 ng/dL, and free T3 of 2.7 pg/mL. Thyroid ultrasound demonstrated mild thyromegaly and two TIRADS-4 nodules up to 1.4 cm. Chest imaging revealed pulmonary edema. His Burch-Wartofsky score was 60, consistent with thyroid storm. Treatment was initiated with methimazole 20 mg every 6 hours, hydrocortisone 100 mg every 8 hours, and propranolol 40 mg every 4 hours. Due to worsening respiratory failure, he required BiPAP and was transitioned to continuous renal replacement therapy. Because BiPAP dependency limited oral dosing frequency, methimazole was adjusted to 40 mg twice daily, and Lugol’s iodine was added. Propranolol was discontinued due to hypotension. Despite persistent tachycardia and need for mechanical ventilation, free T4 improved by day 3, allowing down-titration of therapy. Heart rate improved by day 4. A transient rise in free T4 on day 5 was attributed to critical illness, and levels subsequently normalized. Following biochemical improvement, the patient reverted to atrial fibrillation with RVR, requiring amiodarone reinitiation and cardioversion. By day 9, he was hemodynamically stable and discharged on methimazole and amiodarone.

This case illustrates the complexity of managing thyroid storm in patients with significant comorbidities. Prompt diagnosis, aggressive multimodal therapy, and frequent reassessment were essential for stabilization. It highlights the need for individualized, multidisciplinary management and close monitoring of both endocrine and cardiovascular status in severe thyroid storm.

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