Cerebral Salt Wasting

Cerebral salt wasting is a hyponatraemia occurring in the context of intracranial pathology, most classically subarachnoid haemorrhage, but also traumatic brain injury, neurosurgery, meningitis and intracranial tumours ,in which renal sodium loss produces genuine volume depletion alongside the low sodium.

Its clinical importance lies almost entirely in its distinction from SIADH, because the two look superficially similar on biochemistry but require opposite treatment: fluid restriction in SIADH, and salt and water replacement in cerebral salt wasting.

Restricting fluid in a patient who is actually volume deplete after subarachnoid haemorrhage worsens cerebral perfusion and risks precipitating delayed cerebral ischaemia.

• Hyponatraemia in a patient with recent intracranial pathology, usually developing within the first week
• Features of hyponatraemia itself: headache, nausea, confusion, lethargy, and seizures if severe or rapid
• Signs of true volume depletion, which are the discriminating features: postural hypotension, tachycardia, dry mucous membranes, reduced skin turgor, low JVP, reduced urine output relative to intake, and a negative fluid balance on the chart
• High urine output despite clinical hypovolaemia, which is the paradox at the centre of the syndrome

Biochemically, cerebral salt wasting and SIADH both show hyponatraemia with low plasma osmolality, concentrated urine and a high urine sodium. Volume status is the discriminator, and it is a clinical assessment rather than a laboratory one.

• Careful, repeated assessment of volume status: fluid balance charts, daily weights, postural blood pressure, JVP, and response to a fluid challenge
• Urine sodium is high in both conditions and does not distinguish them
• Serum urea and uric acid tend to be higher in cerebral salt wasting (reflecting volume depletion) and lower in SIADH, though there is overlap and neither is definitive
• Central venous pressure or non-invasive haemodynamic assessment may help in the intensive care setting
• Exclude adrenal insufficiency and hypothyroidism as for any hyponatraemia

Differentials: SIADH (the principal one, and the distinction is the entire clinical question), adrenal insufficiency, and iatrogenic hyponatraemia from hypotonic intravenous fluids, which is common and easily overlooked in neurosurgical patients.

• Volume and sodium replacement, which is the opposite of SIADH management: isotonic saline to restore euvolaemia, with hypertonic saline reserved for severe or symptomatic hyponatraemia
• Fludrocortisone is used in some centres to reduce renal sodium loss, particularly after subarachnoid haemorrhage, with monitoring for hypokalaemia and fluid overload
• Salt supplementation, oral or enteral, as an adjunct
• The same correction-rate limits apply as for any hyponatraemia: no more than 8–10 mmol/L in 24 hours, given the risk of osmotic demyelination
• Avoid fluid restriction: in the specific setting of subarachnoid haemorrhage this risks worsening cerebral perfusion and delayed cerebral ischaemia, which is why getting the diagnosis right rather than defaulting to SIADH management matters so much
• Close neurological observation alongside biochemical monitoring

Referral: neurosurgery and intensive care, since these patients are almost always already under specialist care; endocrinology input may help where the distinction from SIADH remains genuinely unclear.