Myxedema Coma

This is not a case you start - Myxedema coma carries mortality reported as high as 60% and belongs in an ICU. If it declares itself preoperatively, cancel the elective case and treat.

Recognize it at the bedside - Altered mental status plus hypothermia below 35.5 C in a patient with a thyroidectomy scar, no palpable thyroid tissue, goiter, sparse hair, dry skin or non-pitting edema. Loss of the mild diastolic hypertension that normally compensates in severe hypothyroidism is a warning sign of impending decompensation. Send TSH, free T4, free T3 and a random cortisol; high TSH with low free T4 is primary disease, while a normal or low TSH with low free T4 points to central hypothyroidism.

Hydrocortisone first, thyroid hormone second - Give hydrocortisone 100 mg IV to start (200 to 400 mg per day) before levothyroxine, because levothyroxine increases cortisol metabolism and hypothyroidism can mask underlying adrenal insufficiency. Then levothyroxine 200 to 400 mcg IV once — the lower end for the elderly and for underlying cardiac disease or arrhythmia — followed by 1.6 mcg/kg/day reduced to 75% when given IV. Draw the cortisol and thyroid studies first, but do not wait for results to treat.

Secure the airway and ventilate - Most patients need mechanical ventilation. Altered mental status brings aspiration risk and laryngeal myxedema can obstruct outright. Follow serial arterial blood gases and do not wean until both hypercapnia and hypoxemia have resolved and the patient has regained consciousness.

Rewarm slowly - Warming blankets and a warmer room. Rapid rewarming vasodilates a patient who is already vasoconstricted to maintain pressure, and drops them into shock.

Hypotension has four causes at once - Reduced contractility and cardiac output, compounded by hyponatremia, hypoglycemia and hypothermia. Resuscitate with fluid while watching sodium; if pressure stays refractory, start a vasopressor and hold it until levothyroxine has had time to work.

Avoid hypotonic fluids - Hyponatremia comes from impaired free water delivery to the distal nephron and increased ADH, and it is a major contributor to the altered mental status. For sodium below 120 mmol/L, careful 3% saline with IV furosemide; a 4 to 6 mmol/L rise resolves most neurologic symptoms and correction should not exceed 6 to 8 mmol/L in 24 hours to avoid osmotic demyelination.

Hypoglycemia - Treat with 5 to 10% dextrose in half normal saline, given carefully when hyponatremia coexists.

Read the ECG for the whole picture - Bradycardia, low voltage, flattened T waves, bundle branch block and complete heart block are all described. Low voltage should prompt an echo for pericardial effusion from mucopolysaccharide-rich fluid. QT prolongation with torsades has been reported and resolves with treatment. Rule out myocardial infarction, since aggressive T4 replacement may raise MI risk.

Expect surgical bleeding - Myxedema coma carries an acquired type 1 von Willebrand syndrome plus reduced factors V, VII, VIII, IX and X, and it is reversible with T4 therapy. Check a coagulation panel and von Willebrand studies before an invasive procedure, and note that GI bleeding is a described complication.

Sedatives and opioids are precipitants, not just risks - Sedative medications and opioids are among the recognized triggers of myxedema coma. Titrate in small increments and expect exaggerated respiratory depression.

Treat the gut as obstructed - Abdominal pain, nausea, vomiting, ileus that can progress to megacolon, anorexia and ascites are common, and impaired motility and bowel wall edema make oral absorption unreliable — which is why levothyroxine goes IV. Plan for a full stomach.

Find and treat the precipitant - Infection is the classic trigger and the patient will be hypothermic rather than febrile, so a normal temperature does not rule it out. Blood and urine cultures, chest imaging, lumbar puncture where indicated, and empiric antibiotics.

Myxedema coma is decompensated end-stage hypothyroidism. Long-standing hypothyroidism from any cause — autoimmune disease, iodine deficiency, congenital abnormality, or drugs such as lithium and amiodarone — strips away the adaptive mechanisms that hold homeostasis, and a stressor such as infection, myocardial infarction, or a sedative or opioid dose tips the patient over. Thyroid hormone drives whole-body metabolism, which falls 40 to 50% in its complete absence.

The result is multisystem failure: reduced myocardial contractility and cardiac output with bradycardia, hypotension and shock; hypoventilation from blunted hypoxic and hypercapnic ventilatory responses plus diaphragmatic weakness; mucin deposition in skin, tongue and vocal cords that narrows the airway; hyponatremia, hypoglycemia, hypothermia, ileus, and a bleeding diathesis. Mortality runs 20 to 60%. The name misleads — the salient finding is deteriorating mentation, not coma.