Cerebral Salt Wasting Syndrome

Cerebral salt wasting syndrome is renal sodium loss with extracellular volume depletion and hyponatraemia in a patient with intracranial disease and no other cause. Its existence as a distinct entity is debated.

Hyponatraemia occurs in up to one third of patients after subarachnoid haemorrhage, and most are due to the syndrome of inappropriate antidiuresis rather than salt wasting. True cerebral salt wasting is uncommon.

Causes are subarachnoid haemorrhage, traumatic brain injury, neurosurgery (especially pituitary and skull base), brain tumour and meningitis. It usually resolves within 2 to 4 weeks.

Pathophysiology.

Proposed mechanisms are reduced sympathetic renal input and release of natriuretic peptides (brain natriuretic peptide, atrial natriuretic peptide, C-type natriuretic peptide), causing natriuresis and diuresis.

Volume depletion then stimulates antidiuretic hormone appropriately, which worsens hyponatraemia.

• Hypovolaemia: postural hypotension, tachycardia, dry mucous membranes, weight loss, low central venous pressure and high urine output with negative fluid balance.
• Hyponatraemia symptoms: confusion, headache, nausea, seizures and coma.

Red flags.

• Sodium under 120 mmol/L, seizures or reduced consciousness.
• Fall in sodium of more than 10 mmol/L in 24 hours.
• Subarachnoid haemorrhage (volume loss raises the risk of delayed cerebral ischaemia).

• Serum sodium under 135 mmol/L, serum osmolality under 275 mOsm/kg, urine osmolality over 100 mOsm/kg (often over 300), urine sodium over 40 mmol/L, with clinical hypovolaemia.
• Volume assessment is the key discriminator: daily weights, fluid balance, urine volume and central venous pressure. Urate and fractional urate excretion do not reliably separate it from antidiuresis while hyponatraemic.
• Exclude adrenal insufficiency (cortisol), hypothyroidism, diuretic use, osmotic diuresis (glucose, mannitol) and primary polydipsia.

Differential diagnosis.

• Syndrome of inappropriate antidiuresis (euvolaemic; improves with fluid restriction).
• Adrenal insufficiency and hypothyroidism.
• Diuretic effect, osmotic diuresis and diabetes insipidus.
• Excess hypotonic fluid and heart failure.

• Restore volume and sodium: intravenous 0.9% sodium chloride to replace losses, and oral sodium chloride 2 g three times daily when able to take oral intake.
• Severe symptoms (seizure, coma, vomiting): 3% sodium chloride 150 mL intravenously over 20 minutes, repeated up to twice, checking sodium 20 minutes after each dose, aiming for a rise of 5 mmol/L and stopping when symptoms improve.
• Limit correction to 8 to 10 mmol/L in 24 hours (8 mmol/L in patients with chronic hyponatraemia, hypokalaemia, alcohol use, malnutrition or liver disease) to avoid osmotic demyelination. If over correction occurs, give desmopressin and hypotonic fluid under specialist advice.
• Fludrocortisone 0.1 mg once or twice daily (up to 0.2 mg twice daily) if natriuresis persists, with potassium and blood pressure checks.
• Avoid fluid restriction, particularly after subarachnoid haemorrhage.

Special groups. Children: use weight based hypertonic saline under paediatric critical care supervision.

Monitoring. Sodium every 6 hours at first, then daily, with daily weights, fluid balance, urine volume and sodium, potassium and blood pressure.

Referral and escalation. Neurosurgical or neurocritical care team and endocrinology; critical care for seizures, sodium under 120 mmol/L or falling consciousness.