Myxedema coma
Myxedema coma is a rare, life-threatening decompensation of severe, longstanding untreated hypothyroidism with hemodynamic compromise and mortality up to 30-40%, typically precipitated by cold exposure, infection, or another acute illness. First-line treatment is empiric intravenous glucocorticoids followed immediately by intravenous levothyroxine (300-500 mcg load, then 1.6 mcg/kg/day), with aggressive supportive care in the ICU.
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What this article covers
- Overview
A rare, life-threatening decompensation of severe, longstanding hypothyroidism with hemodynamic compromise, representing the far end of the hypothyroid spectrum rather than a distinct disease process.
- Epidemiology
Rare, occurring almost exclusively in patients with severe, longstanding, undiagnosed or undertreated hypothyroidism.
- Risk factors
Untreated or undertreated primary hypothyroidism, most often from Hashimoto thyroiditis, prior thyroidectomy, or radioactive iodine therapy without adequate replacement.
- Pathophysiology
Longstanding severe thyroid hormone deficiency impairs the neurovascular adaptations that normally maintain homeostasis, including chronic peripheral vasoconstriction that helps preserve core…
- Clinical features
Mental status changes ranging from lethargy to psychosis to coma, coupled with hypothermia (temperature below 34.4°C/94.0°F), are the defining combination; without hypothermia and depressed free T4…
- Differential diagnosis
Sepsis with metabolic encephalopathy: shares altered mental status and hemodynamic compromise, but distinguished by fever (rather than hypothermia) and a clear infectious source, though sepsis can…
- Diagnosis
The diagnosis is established clinically by altered mental status and hypothermia below 34.4°C (94.0°F) in a patient with an elevated TSH and a low free T4; without an overtly low free T4, myxedema…
- Management
First, secure the airway (intubation if needed for hypoventilation or depressed mental status) and admit to the ICU for continuous monitoring.
- Complications
Cardiovascular collapse and shock from impaired cardiac contractility and vasodilation, especially if levothyroxine is dosed too aggressively in a patient with underlying cardiac disease.
- Prognosis
Mortality remains high, up to 30-40%, even with prompt recognition and treatment, making early empiric therapy the single greatest determinant of survival.
- Prevention
Ensure adherence to levothyroxine therapy in patients with known primary hypothyroidism, since medication nonadherence is a leading preventable precipitant.
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Related articles
- Hypothyroidism
Hypothyroidism is thyroid hormone deficiency, most commonly caused by autoimmune (Hashimoto) thyroid failure in iodine-sufficient countries, diagnosed by an elevated thyroid-stimulating hormone with a low or normal free thyroxine. First-line treatment is levothyroxine dosed at 1.6 mcg/kg lean body weight orally once daily, titrated using thyroid-stimulating hormone rechecked no sooner than 6 weeks after any dose change.
- Hashimoto thyroiditis
Hashimoto thyroiditis is a chronic autoimmune process in which lymphocytic infiltration destroys the thyroid, and is the most common cause of hypothyroidism in iodine-sufficient regions such as the United States. Diagnosis rests on an elevated thyroid-stimulating hormone with a low or normal free thyroxine, and first-line treatment is lifelong levothyroxine replacement dosed to normalize thyroid-stimulating hormone.
- Thyroid storm
Thyroid storm is a rare, life-threatening exaggeration of thyrotoxicosis with multiorgan dysfunction and mortality up to 30%, most often precipitated by discontinuation of antithyroid drugs, infection, surgery, or trauma in a patient with underlying hyperthyroidism. It is a clinical diagnosis treated emergently in the ICU with intravenous beta-blockade, a thionamide (propylthiouracil transitioning to methimazole), potassium iodide given only after the thionamide, and high-dose glucocorticoids.
- Adrenal crisis
Adrenal crisis is life-threatening acute glucocorticoid deficiency, most often precipitated by infection or another physiologic stress in a patient with known or unrecognized adrenal insufficiency, presenting with dehydration, hypotension, or shock out of proportion to the concurrent illness. Treatment is immediate intravenous hydrocortisone 100 mg followed by 50 mg every 6 hours plus isotonic saline with dextrose, without waiting for confirmatory labs.
- Primary adrenal insufficiency
Primary adrenal insufficiency (Addison disease) is destruction or dysfunction of the adrenal cortex, most often autoimmune, causing combined cortisol and aldosterone deficiency with hyperpigmentation, hyponatremia, and hyperkalemia. Lifelong glucocorticoid replacement with hydrocortisone plus mineralocorticoid replacement with fludrocortisone is required, with sick-day dose increases to prevent adrenal crisis.