What is cerebral salt wasting?

Cerebral Salt Wasting Syndrome

Cerebral salt wasting (CSW) is a syndrome characterized by inappropriate natriuresis and volume contraction in patients with neurological disorders, leading to hyponatremia due to excessive renal sodium loss and subsequent hypovolemia. 1, 2

Pathophysiology

• CSW is produced by excessive secretion of natriuretic peptides, causing hyponatremia through excessive natriuresis, which may also provoke volume contraction 1
• The exact mechanisms are not fully delineated, but evidence strongly implicates abnormal elevations in circulating natriuretic peptides 3
• Unlike SIADH (which is euvolemic), CSW is characterized by hypovolemia due to renal salt wasting 2, 3

Clinical Presentation

• More common in patients with poor clinical grade, ruptured anterior communicating artery aneurysms, and hydrocephalus 1
• May be an independent risk factor for poor outcome in patients with neurological disorders 1
• Presents with hyponatremia, reduced volume status, and inappropriately high renal sodium loss 4
• Commonly occurs following subarachnoid hemorrhage, traumatic brain injury, brain surgery, or other cerebral pathologies 5, 6

Diagnosis

Key Diagnostic Features

• Hyponatremia (serum Na < 135 mmol/L) 2
• Evidence of extracellular volume depletion (hypotension, tachycardia, dry mucous membranes) 1, 3
• Inappropriately high urinary sodium concentration (typically > 20 mmol/L) 1, 2
• High urine osmolality relative to serum osmolality 1, 2
• Low serum uric acid level (< 4 mg/dL) 2, 5

Differentiating from SIADH

• Volume status assessment is the critical factor in distinguishing CSW from SIADH 1, 2
• CSW: Hypovolemic hyponatremia with evidence of volume depletion 2, 3
• SIADH: Euvolemic hyponatremia without clinical signs of volume depletion 2, 7
• Central venous pressure (CVP) can help differentiate: CSW (CVP < 6 cm H₂O) vs. SIADH (CVP 6-10 cm H₂O) 2

Treatment

Acute Management

• For severe symptoms (mental status changes, seizures):
  • Transfer to ICU for close monitoring 2
  • Administer 3% hypertonic saline with goal to correct 6 mmol/L over 6 hours or until severe symptoms resolve 1, 2
  • Monitor serum sodium every 2 hours during initial correction 2
  • Total correction should not exceed 8 mmol/L in 24 hours to prevent osmotic demyelination syndrome 1, 2

Ongoing Management

• Treatment focuses on volume and sodium replacement, not fluid restriction 1, 2
• Isotonic or hypertonic saline administration based on severity 1, 2
• Aggressive volume resuscitation with crystalloid or colloid agents can ameliorate the effect of CSW on the risk of cerebral ischemia 1
• One retrospective study suggested that 3% saline solution is effective in correcting hyponatremia in this setting 1

Pharmacological Therapy

• Fludrocortisone (a mineralocorticoid) has shown benefit in managing CSW 1, 2, 8
  • Two randomized controlled trials found that fludrocortisone helped correct negative sodium balance and reduced the need for fluids 1
  • Typically reduces the doses of hypertonic saline required and can maintain serum sodium levels 4
  • May be considered in subarachnoid hemorrhage patients at risk of vasospasm 1, 2
• Hydrocortisone has also shown benefit in reducing natriuresis and hyponatremia rates in subarachnoid hemorrhage patients 1, 2

Special Considerations

• Fluid restriction should NOT be used in CSW as it can worsen outcomes 1, 2
• Particularly important in subarachnoid hemorrhage patients at risk of vasospasm 1, 2
• Duration of therapy may range from days to months depending on the resolution of the underlying neurological condition 8
• Hypertonic saline increases regional cerebral blood flow, brain tissue oxygen, and pH in patients with high-grade subarachnoid hemorrhage 1
• Potential complications of fludrocortisone therapy include hypokalemia and hypertension, which may require dose adjustment 8

Common Pitfalls

• Misdiagnosing CSW as SIADH, leading to inappropriate fluid restriction 2, 6
• Inadequate monitoring during active correction of sodium levels 2
• Failing to recognize the underlying neurological cause 2
• Correcting sodium too rapidly (>8 mmol/L in 24 hours), risking osmotic demyelination syndrome 1, 2
• Underestimating the volume of fluid and sodium replacement needed 4