Myxedema coma (decompensated hypothyroidism) is most often recognized through collateral history because patients are usually obtunded rather than able to provide a reliable account. The syndrome classically presents in an older woman, often in winter, with known or undertreated hypothyroidism, tipped into decompensation by an acute stressor. Frank coma is uncommon; the dominant feature is altered mentation of any degree.^[1][2]

Three recurring clinical scenarios should prompt immediate consideration of myxedema coma:^[1]

• An elderly patient who “won’t wake up” or has unexplained decline in consciousness
• Unexplained CO₂ narcosis / hypercapnic encephalopathy
• Clinical deterioration after aggressive diuresis for presumed heart failure

Key historical elements to elicit from the patient (when possible), family, caregivers, EMS, or medical records include:

• Known thyroid disease, Hashimoto/autoimmune thyroiditis, thyroidectomy scar, or prior radioactive iodine therapy
• Levothyroxine nonadherence or recent discontinuation (cost, cognitive decline, hospitalization, gastrointestinal illness)—a leading and reversible trigger
• Acute precipitants: infection (especially pneumonia or urosepsis), cold exposure, myocardial infarction, stroke, trauma, surgery, gastrointestinal bleeding
• Recent use of CNS-depressant or other offending drugs (sedatives, opioids, anesthetics, amiodarone, lithium, diuretics). Hypothyroid patients have reduced clearance of and heightened sensitivity to sedatives, opioids, and anesthetics; a history of recent administration of these agents is both a precipitant and a common route to iatrogenic decline.^[1][2][3][4]

A subacute prodrome of worsening hypothyroid symptoms typically precedes decompensation by weeks to months. The background symptom burden of hypothyroidism (from general clinical-presentation data, not myxedema-coma-specific cohorts) includes fatigue (74%–86%), cold intolerance (35%–65%), weight gain (24%–59%), constipation (33%–41%), and cognitive impairment/memory loss (45%–48%), along with hoarseness, dry skin, and low mood; these worsen insidiously before decompensation. These progress to profound lethargy and thermoregulatory failure that define the emergency presentation. Older patients (≥70 years) — the typical age group for myxedema coma — may present with fewer classic symptoms and are less likely to report cold intolerance or weight gain than younger patients.^[2][5]

^[2][5][1]

• Obtain collateral history early; patients are frequently unable to give a reliable account.
• Actively search for a precipitant in every suspected case—identification and treatment of the trigger is integral to outcome.
• Consider the diagnosis in any afebrile, altered, hypothermic older adult, particularly with a thyroidectomy scar or documented hypothyroidism.
• Absence of fever does not exclude serious infection; hypothyroid patients mount a blunted febrile response.
• Ask specifically about recent levothyroxine interruption.
• Do not require frank coma before considering the diagnosis; most patients present with lesser degrees of obtundation. Myxedema coma may occasionally present de novo without a prior hypothyroidism diagnosis, so absence of a thyroid history does not exclude it.^[1][6][3]