What is the recommended acute management for myxedema coma in an older woman with long‑standing untreated hypothyroidism?

Myxedema Coma: Acute Management

Immediately initiate intravenous liothyronine (T3) 5–20 mcg bolus followed by 2.5–10 mcg every 8 hours, combined with intravenous hydrocortisone 100 mg every 8 hours, while providing aggressive supportive care including passive rewarming, mechanical ventilation if needed, and hemodynamic support—treatment must begin on clinical suspicion alone without waiting for laboratory confirmation, as mortality approaches 25–60% even with optimal therapy. 1

Immediate Hormone Replacement (First Priority)

Thyroid Hormone Administration

• Administer intravenous liothyronine sodium (T3) as the preferred initial agent because myxedema coma represents a true endocrine emergency requiring rapid restoration of thyroid hormone levels 1, 2, 3
• Start with an IV loading dose of 5–20 mcg of liothyronine, followed by maintenance dosing of 2.5–10 mcg every 8 hours until the patient can tolerate oral therapy 1
• The intravenous preparation (Triostat®) is specifically marketed for myxedema coma/precoma because oral absorption is unreliable in critically ill patients with decreased gastrointestinal motility 1
• Do not delay treatment waiting for thyroid function test results—the diagnosis is clinical, and treatment should begin immediately in any patient with altered mental status, hypothermia, and suspected long-standing hypothyroidism 2, 3, 4

Mandatory Glucocorticoid Coverage

• Simultaneously administer intravenous hydrocortisone 100 mg every 8 hours (or equivalent stress-dose glucocorticoid) before or concurrent with thyroid hormone replacement 1
• This is non-negotiable: thyroid hormone therapy in patients with concomitant adrenal cortical insufficiency aggravates symptoms and can precipitate adrenal crisis 1
• The therapy of myxedema coma requires simultaneous administration of glucocorticoids because hypothyroidism may mask coexisting adrenal insufficiency, and thyroid hormone replacement increases cortisol metabolism 1
• Continue stress-dose steroids until adrenal function is confirmed adequate, typically 48–72 hours after clinical stabilization 1

Critical Supportive Care (Concurrent with Hormones)

Airway and Ventilation

• Assess for hypoventilation and hypercapnia immediately—myxedema coma causes decreased respiratory drive and CO2 retention 2, 3, 4
• Intubate and mechanically ventilate if: respiratory rate <8–10 breaths/minute, PaCO2 >50 mmHg with altered mental status, or inability to protect airway 2, 3
• Avoid sedatives and anesthetics if possible, as these are precipitating factors that worsen respiratory depression 1

Temperature Management

• Passive rewarming only—use blankets and increase ambient temperature, but avoid active external rewarming (heating blankets, forced air warmers) 2, 3
• Active rewarming causes peripheral vasodilation that can precipitate cardiovascular collapse in patients with already compromised cardiac output 5
• Target core temperature rise of 0.5–1°C per hour to avoid hemodynamic instability 2, 3

Hemodynamic Support

• Expect bradycardia, hypotension, and decreased cardiac output due to delayed myocardial relaxation, reduced contractility, and increased systemic vascular resistance 5
• Decreased ventricular filling combined with increased afterload further compromises hemodynamic stability 5
• Use cautious fluid resuscitation—these patients often have impaired free water clearance and are at risk for hyponatremia and fluid overload 2, 3
• Avoid aggressive vasopressor use initially—thyroid hormone replacement will improve cardiac function over 24–48 hours 5
• If vasopressors are required, use the minimum dose necessary while thyroid hormone takes effect 2, 3

Metabolic Corrections

• Check and correct hypoglycemia immediately—this is a critical precipitating factor that must be identified and treated urgently 6
• Monitor and correct hyponatremia cautiously—rapid correction risks osmotic demyelination syndrome 2, 3
• Hyponatremia in myxedema coma results from impaired free water excretion and should improve with thyroid hormone replacement 2, 3

Identification of Precipitating Factors

Common Triggers to Address

• Surgery and trauma are major physiologic stressors that precipitate myxedema coma by overwhelming compensatory mechanisms 5, 6
• Infection/sepsis—obtain cultures and initiate broad-spectrum antibiotics if infection is suspected 2, 3
• Cold exposure—inquire about environmental temperature and recent cold exposure 2, 3
• Medications—review for sedatives, anesthetics, amiodarone, lithium, or other drugs that suppress thyroid function 2, 3
• Cerebrovascular accidents, gastrointestinal bleeding, or other acute medical events can trigger decompensation 2, 3
• History of neck radiation for any malignancy may have contributed to underlying hypothyroidism 6

Monitoring and Transition to Oral Therapy

Laboratory Monitoring

• Obtain baseline TSH, free T4, free T3, cortisol, and ACTH before treatment if possible, but do not delay therapy 2, 3, 4
• Expect undetectable or very low free T4 and free T3 with variable TSH (may be low in central hypothyroidism or elevated in primary hypothyroidism) 7
• Monitor cardiac rhythm continuously—bradycardia should improve within 24–48 hours of treatment 5, 2
• Recheck thyroid function tests after 24–48 hours to guide ongoing dosing 1

Transition Strategy

• Once the patient is alert, hemodynamically stable, and able to tolerate oral intake, transition from IV liothyronine to oral levothyroxine 1
• Discontinue IV liothyronine and initiate oral levothyroxine at 50–100 mcg daily (or 1.6 mcg/kg ideal body weight), recognizing that residual effects of IV T3 will persist for several days 1
• Taper glucocorticoids to physiologic replacement doses (hydrocortisone 15–20 mg/day in divided doses) once adrenal function is confirmed adequate 1
• Continue to monitor TSH and free T4 every 6–8 weeks during dose titration, targeting TSH 0.5–4.5 mIU/L 8

Critical Pitfalls to Avoid

• Never delay treatment waiting for laboratory confirmation—myxedema coma is a clinical diagnosis with 25–60% mortality even with treatment 2, 3
• Never give thyroid hormone without glucocorticoid coverage—this can precipitate fatal adrenal crisis 1
• Never use active external rewarming—this causes peripheral vasodilation and cardiovascular collapse 2, 3
• Never assume the patient is "just" hypothermic from environmental exposure—consider myxedema coma in any patient with hypothermia plus altered mental status, especially with a history of thyroidectomy or long-standing hypothyroidism 2, 3, 4
• Never overlook pericardial effusion—echocardiography may reveal significant effusion without tamponade, which improves with thyroid hormone replacement 2

Special Considerations for This Patient Population

Elderly Women with Long-Standing Untreated Hypothyroidism

• This demographic represents the majority of myxedema coma cases 7
• The brain's metabolic demands cannot be met with critically low thyroid hormone levels, leading to altered mental status and coma—this is the defining feature 5
• Long-standing hypothyroidism means compensatory mechanisms have been exhausted, making these patients extremely vulnerable to acute stressors 5, 3
• Start with lower initial doses in very elderly patients (liothyronine 5 mcg bolus, then 2.5 mcg every 8 hours) to avoid unmasking cardiac ischemia, but do not withhold treatment 1

Cardiac Considerations

• Cardiac dysfunction in myxedema coma includes delayed myocardial relaxation, reduced contractility, bradycardia, and abnormal cardiac output 5
• Decreased ventricular filling and increased systemic vascular resistance further compromise hemodynamics 5
• Expect gradual improvement in cardiac function over 24–72 hours as thyroid hormone levels rise—do not expect immediate resolution 5