Case Presentation: A 77-year-old male with a history of bladder cancer who had not seen a primary care physician in 11 years presented to the emergency department (ED) for progressive decline in his mental status over 4-6 weeks, with significant worsening starting one week before his ED assessment. Associated symptoms included fatigue, constipation, and decreased oral intake and urine output.Initial vital signs revealed profound hypothermia (T = 27°C), bradycardia (HR = 31-40 bpm), and labile blood pressure (BP = 86-129/56-71 mmHg). His altered mental status raised concern about the need for airway protection, and this prompted endotracheal intubation and the initiation of mechanical ventilation. A Bair Hugger was applied to treat his hypothermia, and he also required pressor support due to his hypotension. Laboratory evaluation demonstrated evidence of severe hypothyroidism with a markedly elevated TSH level = 51.22 mIU/mL (normal range 0.45-5.33 mcIU/mL). Levels of free T4 < 0.30 ng/dL (normal range 0.58-1.64 ng/dL) and free T3 = 18 pg/dL (normal range 87-178 ng/dL) were suppressed. Random cortisol level = 29 mcg/dL (normal AM value 6.7 - 22.6 mcg/dL, normal PM value < 10 mcg/dL). The patient's myxedema coma was managed with a loading dose of levothyroxine 300 mcg IV, followed by a maintenance dose of 100 mcg IV daily. Concomitant therapy with liothyronine 2.5 mg IV every 8 hours was initiated to accelerate thyroid hormone repletion. After approximately 2 weeks, levothyroxine was switched to the oral route. Stress-dose hydrocortisone therapy was initiated at a dose of 50 mg IV every 6 hours, and it was tapered and discontinued upon resolution of hemodynamic instability. The patient's mental status improved significantly during his hospitalization; however, persistent confusion necessitated placement in a subacute rehabilitation facility on the day of discharge.
Discussion: Myxedema coma, a life-threatening complication of untreated hypothyroidism, is associated with a high mortality rate of 26-52% (1,2). Prompt diagnosis and initiation of treatment are crucial to improve patient outcomes. Common clinical manifestations include altered mental status, hypothermia, bradycardia, hypotension, hyponatremia, hypoglycemia, and hypoventilation; however, a complete spectrum of these findings may not be present in every patient (3). Treatment involves aggressive supportive measures, immediate administration of parenteral thyroid hormone, glucocorticoid therapy to address potential adrenal insufficiency, and management of any underlying conditions that may have precipitated the development of myxedema coma (4).
Conclusions: Myxedema coma is a life-threatening complication of untreated hypothyroidism with a high mortality rate. Early recognition and immediate treatment are essential to improve patient outcomes. Timely intervention, even before definitive laboratory confirmation, can significantly increase survival rates.