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Thyroid Biology and Disease

SUN-349 - Myxedema Coma Masquerading as Shock and Opioid Toxicity

Sunday, June 14, 2026
9:00 AM - 4:00 PM CT
Location: ENDOExpo; Poster Floor
Introduction

Myxedema coma is a rare, life-threatening manifestation of severe hypothyroidism associated with high mortality. Diagnosis is challenging due to nonspecific presentations and frequent confounding comorbidities, leading to delays in appropriate therapy.

Case

A 46-year-old woman with past medical history of Crohn’s disease status post colectomy and ileostomy and no history of thyroid disease presented with generalized weakness. She was initially admitted for small bowel obstruction after initial CTAP revealed small bowel dilation with associate obstruction. She was taking opioids at home from pain management, which complicated her diagnosis. Initially, her course was uncomplicated; however, she developed progressive somnolence, hypotension, bradycardia, and hypoxic respiratory failure. Her mental status changes were initially attributed to opioid exposure and possible sepsis due to leukocytosis and lactatemia seen on initial labs. Sedating medications were held. The patient received naloxone, IV fluids, and was started on empiric antibiotics, but her clinical status failed to improve with the patient remaining hypotensive, bradycardic, and encephalopathic. On physical examination, she was somnolent, but arousable. She had 2+ pitting edema on bilateral lower extremities. Bowel sounds were present and abdomen was soft and non-tender. Despite naloxone administration, she remained hypotensive and bradycardic with persistent encephalopathy, requiring upgrade to ICU level care. Patient was placed on noninvasive ventilation and started on vasopressors as well as stress dose steroids. Imaging demonstrated a pericardial effusion without tamponade. The decision was made to check ammonia and TSH given persistent bradycardia and hypotension despite pressors. These labs were not initially checked, and they revealed decompensated hypothyroidism with TSH greater than 50 uIU/mL and Free T4 less than 0.3 ng/dL. Given concern for myxedema coma, intravenous levothyroxine was initiated, resulting in marked clinical improvement, including improved mental status, hemodynamics, and respiratory function. She was successfully weaned off vasopressors and respiratory support and transitioned to oral thyroid hormone therapy with endocrinology follow-up.

Conclusion

This case highlights the diagnostic challenge of myxedema coma in patients with complex medical comorbidities and overlapping causes of shock and encephalopathy. Persistent bradycardia, hypotension, and altered mental status refractory to standard interventions should prompt evaluation for severe hypothyroidism. Early recognition and prompt initiation of intravenous thyroid hormone are critical for improved outcomes.

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