A 50‑year‑old man with a history of hypertension was brought to the emergency department for evaluation of altered mental status. History was limited due to significant lethargy, and there was no reliable collateral information available at the time of presentation. Given the acute change in mentation, an expedited neurologic evaluation was performed.
Laboratory studies revealed severe hypothyroidism, with a thyroid‑stimulating hormone level of 145 μIU/mL and a free thyroxine level of 0.11 ng/dL. Thyroid peroxidase antibodies were elevated at 205 IU/mL, consistent with Hashimoto thyroiditis. Serum cortisol levels were within normal limits. Additional findings included marked hyperlipidemia, with an LDL cholesterol of 180 mg/dL and a total cholesterol level of 273 mg/dL.
In light of the patient’s profound biochemical hypothyroidism, altered mental status, bradycardia, and characteristic physical findings, myxedema coma was strongly suspected. Empiric treatment was initiated with intravenous hydrocortisone 100 mg every eight hours, along with intravenous levothyroxine at a loading dose of 200 mcg, then 100 mcg daily and adjunctive liothyronine 5 mcg every eight hours. Hydrocortisone continued until adrenal insufficiency was excluded. MRI Brain was remarkable for a subacute infarct involving the posterior limb of the internal capsule and patient was started on dual antiplatelet therapy.
Over the subsequent hospital course, the patient demonstrated gradual but consistent improvement in mental status. Thyroid hormone levels improved steadily, with free T4 normalizing to 0.9 ng/dL and TSH 18.9I uIU/ml over approximately 10 days. This biochemical recovery was accompanied by parallel clinical improvement. The patient was transitioned to oral levothyroxine 150 mcg and liothyronine 5 mcg daily.
Myxedema coma represents the most severe end of the hypothyroid disease spectrum and carries a high mortality rate of 6.8% to 30% even with prompt treatment. Neurologic manifestations are common and are typically the result of global metabolic and neurophysiologic dysfunction rather than focal structural abnormalities. Management consists of intensive care unit level care, treatment of precipitating causes, empiric glucocorticoid therapy until adrenal insufficiency is ruled out, and thyroid hormone replacement [5]. The American Thyroid Association recommends IV levothyroxine as first line therapy, with loading dose of 200 -400mcg followed by daily dosing of 1.6 mcg/kg, reduced to 75% for intravenous administration Concomitant liothyronine in critically ill patients. In our patient, combination therapy with IV levothyroxine with oral liothyronine achieved clinical stabilization and eventual recovery.
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