- Douglas S Ross, MD
Douglas S Ross, MD
- Section Editor — Thyroid Disease
- Professor of Medicine
- Harvard Medical School
Myxedema coma is defined as severe hypothyroidism leading to decreased mental status, hypothermia, and other symptoms related to slowing of function in multiple organs. It is a medical emergency with a high mortality rate. Fortunately, it is now a rare presentation of hypothyroidism, likely due to earlier diagnosis as a result of the widespread availability of thyroid-stimulating hormone (TSH) assays.
Early recognition and therapy of myxedema coma are essential. Treatment should be begun on the basis of clinical suspicion without waiting for laboratory results. Important clues to the possible presence of myxedema coma in a poorly responsive patient are the presence of a thyroidectomy scar or a history of radioiodine therapy or hypothyroidism. A history obtained from family members often reveals antecedent symptoms of thyroid dysfunction followed by progressive lethargy, stupor, and coma.
The clinical presentation, diagnosis, and treatment of myxedema coma will be reviewed here. The diagnosis and treatment of hypothyroidism are reviewed separately. (See "Disorders that cause hypothyroidism" and "Clinical manifestations of hypothyroidism" and "Treatment of primary hypothyroidism in adults".)
Myxedema coma can occur as the culmination of severe, long-standing hypothyroidism or be precipitated by an acute event such as infection, myocardial infarction, cold exposure, or the administration of sedative drugs, especially opioids.
The demographics of patients who develop myxedema coma are those of hypothyroidism in general, with older women being most often affected. Myxedema coma can result from any of the usual causes of hypothyroidism, particularly chronic autoimmune thyroiditis, because of its often insidious course compared with post-surgical or post-ablative hypothyroidism (see "Disorders that cause hypothyroidism"). It can occur in patients with secondary hypothyroidism, and there are case reports of its occurrence in patients with lithium- or amiodarone-induced hypothyroidism [1-3].
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