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Myxoedema

Up Cortisol deficiency Diabetes insipidus Diabetes Myxoedema Thyroid crisis


Myxoedematous coma

- terminal state of decompensated hypothyroidism
- typically presents in winter in elderly females

Precipitating factors

- hypothermia, sometimes due to CNS depressants (eg phenothiazines, narcotics, anaesthetics)
- surgery
- drugs with antithyroid action (eg amiodarone)
- infections

Pathogenesis

- obscure, but hypothermia, respiratory acidosis and hyponatraemia with inappropriate ADH may all play a part.

Clinical features

General

- hypothermia with absence of shivering. May be profound

CVS

- hypotension: commonly accompanied by bradycardia. Baroreceptor dysfunction, and reduction in plasma volume contribute. Small heart suggests adrenal insufficiency
- bradycardia

RS

- hypoventilation: very frequent. Contributing factors include: decreased responsiveness to hypoxia and hypercarbia, respiratory muscle fatigue, obesity, thickening of vocal cords, drugs

Metabolic

- slow metabolism
- lactic acidosis frequent and may be severe
- hypoglycaemia often present
- hyponatraemia
- uraemia
- hypophosphataemia

GI & GU

- paralytic ileus, megacolon and urinary retention frequent

CNS

- coma: due to combination of hypothermia, hypercarbia, hypoxia, cerebral oedema and other metabolic derangements.
- may present with coma; more common is insidious progression from somnolence and torpor to coma.
- preceded by fits in 25% of patients

Differential diagnosis

- drugs (eg phenytoin, frusemide, NSAIDs, steroids, dopamine) can affect thyroid hormone concentrations and thus mimic biochemical hypothyroidism
- diagnosis of hypothyroidism in critically ill should be made with caution
- coma in association with sick euthyroid syndrome may be difficult to distinguish from myxoedema coma

Treatment

- monitor in ICU
- thyroid hormone

  • optimum regime unknown
  • intestinal absorption of thyroid hormones (esp T4) very variable in severe hypothyroidism and peripheral conversion of T4 to T3 decreased
  • some advocate larger doses. Suggest that loading doses necessary to saturate binding protein and restore levels to low-normal range
  • If T4 used give IV. 400-500 mcg then 50 mcg IV od. Change to PO when GI function resumes. Response slow. Improvements in temperature, HR and mental state barely begin within 24 h.
  • T3 IV/NG 25-50 mcg bolus then 10-20 mcg tds. Clinical response more rapid

- 200-300 mg hydrocortisone per day. Patients with myxoedema coma may have impaired glucocorticoid response to stress or even frank co-existent adrenal insufficiency (Schmidt's syndrome; may be masked by hypothyroidism). (Synacthen test not valid in hypothyroid patients).
- IV fluids (usually dextrose)
- oxygen
- supportive. Intubation and ventilation often required. Beware difficult airway especially in view of impaired GI function in these patients
- treat precipitants

Prognosis

  • 50% mortality

© Charles Gomersall December 1999

 

©Charles Gomersall, April, 2014 unless otherwise stated. The author, editor and The Chinese University of Hong Kong take no responsibility for any adverse event resulting from the use of this webpage.
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