Total body sodium is believed to be normal to increased, but it is the impaired excretion of water that causes hyponatraemia. Low serum sodium may cause a semicomatose state or seizures even in euthyroid patients, and the very severe hyponatraemia (105– 120 mmol/ L) in profound myxoedema is likely to contribute substantially to the coma in these patients. With such severe hyponatraemia, it may be appropriate to administer a small amount of hypertonic saline (50– 100 ml 3% sodium chloride), enough to increase sodium concentration by about 2 mmol/ L early in the course of treatment, and this can be followed by an intravenous bolus dose of 40– 120 mg furosemide to promote a water diuresis. A small quick increase in the serum sodium concentration (2– 4 mmol/ L) is effective in acute hyponatraemia because even a slight reduction in brain swelling results in a substantial decrease in intracerebral pressure. On the other hand, too rapid correction of hyponatraemia can cause a very dangerous complication, the osmotic demyelination syndrome. In patients with chronic hyponatraemia this complication is avoided by limiting the sodium correction to less than 10– 12 mmol/ L in 24 h and to less than 18 mmol/ L in 48 h.

After achieving a sodium level of more than 120 mmol/ L, no further hypertonic saline infusion should be required, and restriction of fluids may be all that is necessary to correct hyponatraemia, especially if it is mild (120– 130 mmol/ L). Because of the likelihood of decreased cardiac reserve, therapy with saline or other intravenous fluids must be approached cautiously. If hypoglycaemia is present, dextrose in 0.5 N sodium chloride may be used to correct the low blood glucose. With regard to fluid or saline therapy, careful monitoring of volume status based on clinical parameters and central venous pressure measurements is essential in patients with significant cardiovascular decompensation.

New vasopressin antagonists named vaptans (conivaptan and tolvaptan), have been approved by the Food and Drug Administration (FDA) in the United States for the treatment of patients with euvolaemic and hypervolaemic hyponatraemia. These treatments could be attempted in this clinical setting in view of the high vasopressin levels observed in myxoedema coma. Conivaptan current dosing recommendations are a 20- mg loading dose to be infused over 30 min followed by a 20 mg/ day continuous infusion for up to 4 days. Tolvaptan is administered orally in a starting dose of 15 mg the first day followed by titration up to 30 mg and 60 mg at 24 hours if necessary. During the active phase of correction with tolvaptan, fluid restriction is not recommended in order to reduce the risk of overcorrection. With both therapies, serum [Na+] concentration should be measured frequently during the active phase of correction of the hyponatraemia at a minimum of every 6– 8 hours. No data are available on the use of vaptans in severe hyponatraemia (<115 mmol/ L) in hypothyroid patients, or whether sole therapy with vaptans without hypertonic saline would be effective.

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مواضيع ذات صلة

Myxoedema Coma: Thyroid Hormone Therapy

Diagnosis of Myxoedema Coma

Pathophysiology of Unstable Hemoglobin Disorders

Central Hypothyroidism

Severe Iodine Deficiency and natural Goitrogens

Iatrogenic Hypothyroidism

Pathobiology of Sickle Cell Disease: The Basis of Phenotypic Diversity

The Unique Systems Biology of Sickle Cell Anemia

Abnormalities of Sickle Red Blood Cells

Abnormal Molecular Behaviors of Sickle Hemoglobin

Clinical Assessment and Systemic Manifestations of Hypothyroidism: Diagnostic Accuracy

Clinical Aspects of Hypothyroidism due to Different Aetiologies