23rd May 2025

Myxoedema coma

• Myxoedema describes the clinical syndrome that develops as a result of severe hypothyroidism. This term is also applied to cases with deposition of mucinous substances in the subcutaneous tissue causing skin thickening. 
• Myxoedema coma is a life-threatening condition,  with decreased levels of consciousness, which may result in coma,  and hypothermia. It occurs due to longstanding undiagnosed hypothyroidism. It occurs most commonly in the elderly.  

Causes

• Most commonly occurs as a complication of chronic autoimmune thyroiditis. 
• It also occurs post-thyroidectomy or post-radioactive iodine therapy for hyperthyroidism. 
• Rarely may happen due to medication such as lithium and amiodarone.
• May be triggered by cold exposure,  trauma , infection, cerebrovascular accident, heart failure, or due to CNS depressants administration.
• The long-standing reduced metabolic rate and decreased oxygen consumption due to hypothyroidism affects all body systems resulting in the decreased conscious level and hypothermia.

Clinical picture and prognosis

Features suggestive of a precipitating cause may be present, along with a history of hypothyroidism or thyroidectomy (note that the hypothyroidism may be undiagnosed, but patients will be symptomatic). Precipitating factor features can be present.  Associated with these features are the following:

• depressed conscious level – may be comatose.
• hypothermia (core temperature < 35oc)
• bradycardia or various degrees of heart block.
• hypoventilation with hypoxia and hypercapnia
• other pathologies related to hypothyroidism e.g., heart failure, cyanosis.
• hyporeflexia

This condition has a mortality rate >50%. With immediate recognition of the condition and management, the mortality rate can reach 25%. Death occurs due to respiratory failure, sepsis, and GI bleeding.

Investigations

Assessment of thyroid function is  required alongside investigations for detecting precipitating factors and possible complications. TFTs (taken prior to commencing treatment) usually show increased TSH in primary hypothyroidism and decreased in secondary causes. T3 and T4 are reduced. Investigations for cause and complications may include:

• FBC, urea and electrolytes (U&Es) (deranged due to decreased renal perfusion)
• Hyponatraemia (Na < 130 mmol/l) due to low serum osmolarity.
• Hypoglycaemia is common (due to sepsis, decreased oral intake or adrenal insufficiency).
• ECG: can show sinus bradycardia, stages of heart block, QT interval prolonged or non-specific changes in ST segment or T waves. 
• CXR: might show signs of infection or heart failure (HF).
• Random cortisol level (taken prior to commencing treatment).

Management

This includes treatment of the precipitating factors, hypothyroidism state and treatment of complications. If myxoedema coma is suspected, management should not be delayed pending investigation results.

• Precipitating factors management can be treatment of infection through the acknowledged sepsis 6 management whilst identifying the source of infection.
• Thyroid hormone replacement: There is controversy regarding regimen to follow. An example of a regimen is as follows: 
  • T4 300-500 mcg IV or NG as a starting dose 
  • Followed by 50-100mcg daily until the patient is tolerating oral formulations .
  • If no improvement in 24-48h, T3 10mcg IV 8 hourly or 25mcg IV 8-hourly can be added to the previous replacement. 
  • T3 acts more quickly but may worsen ischemic heart disease.
• Management of complications:
  • Supportive management entails managing hypothermia is managed via passive external rewarming. Aim for slow rise in core temperature of 0.5oC/h. Warm humidified O2 via face mask or mechanical ventilation if needed. IV fluids with caution due to potential risk of left ventricular HF. Cardiac monitoring for possible arrhythmias occurrence. Patient will need ITU admission if comatose.
  • Correction or hypotension, hyponatraemia, and hypoglycaemia.
  • If concurrent hypoadrenalism/adrenal insufficiency, steroid replacement should also be given (this should be given prior to thyroxine replacement, as thyroxine replacement may precipitate ventricular fibrillation in adrenal crisis).