12th April 2024

Cerebral Salt Wasting

Cerebral salt wasting is characterised by the following:  

• Hyponatraemia < 135mEq/L with low plasma osmolality 
• Inappropriately elevated urine osmolality > 100mosmol/kg (usually above 300mosmol/kg)
• Urine sodium concentration above 40mEq/l
• Low serum uric acid concentration due to urate wasting in urine

It is believed that the impaired sodium resorption may be due to increased Brain Natriuretic peptide (BNP) typically released in patients with brain injuries or due to diminished central sympathetic activity. Both mechanisms cause inhibition of the renin-angiotensin system. Normally, sympathetic stimulation triggers sodium, urate and water resorption in the proximal tubule. However, diminished sympathetic input results in reduced sodium and urate absorption as well as ADH release due to the volume depletion.  The reduced renin and aldosterone released can explain the absence of hypokalaemia in CSW, as there is a failure of aldosterone to be released in response to volume depletion. 

CSW can be caused by subarachnoid haemorrhage, head trauma, intracranial neoplasm, metastatic neoplasm, infections such as meningitis, encephalitis, CNS surgery. In patients with neurosurgical procedures CSW would typically manifest within the first 10 days. However, CSW only accounts for a small percentage of hyponatraemia in patients with brain injury.

It can be difficult to differentiate between SIADH and CSW, however one key feature is clinical evidence of volume depletion e.g. hypotension, decreased skin turgor, elevated haematocrit and possibly increased BUN/ serum creatinine ratio. Response to isotonic saline could also help distinguish, as restoration of euvolaemia in CSW should remove the stimulus to release ADH resulting in dilute urine and correction of hyponatraemia. Whereas isotonic saline worsens the hyponatraemia in SIADH. However, this is not carried out in practice, as treating hyponatraemia with isotonic saline in patients with cerebral disease can cause fatal levels of hyponatraemia. 

In contrast to SIADH, which is managed with fluid restriction, in patients with subarachnoid haemorrhage fluid restriction could worsen the volume depletion, hypotension and lead to cerebral infarction. So, instead, CSW is managed with 3% hypertonic saline to raise serum sodium levels. Salt tablets can also be given once they can take oral medications, as well as mineralocorticoids.  

Table 2 detailing the differences between DI, SIADH and CSW