What is the diagnosis and treatment approach for cerebral salt wasting (CSW) in patients with hyponatremia and signs of volume depletion?

Cerebral Salt Wasting Diagnosis

Cerebral salt wasting (CSW) is diagnosed by the combination of hyponatremia, clinical evidence of volume depletion, and inappropriately elevated urinary sodium (>20 mEq/L) in the context of central nervous system disease. 1

Key Diagnostic Features

The hallmark triad of CSW includes: 1, 2

• Hyponatremia (serum sodium <135 mEq/L) 1
• Extracellular volume depletion with clinical signs of hypovolemia (hypotension, tachycardia, dry mucous membranes, decreased skin turgor, orthostatic changes) 3, 1
• Inappropriately high urinary sodium concentration (typically >20 mEq/L, often much higher) despite hypovolemia 1, 2

Additional supportive laboratory findings include: 1, 4

• Elevated urine osmolality (inappropriately concentrated relative to serum osmolality, often >300-500 mOsm/kg) 1, 4
• Low serum uric acid (<4 mg/dL), though this overlaps with SIADH 4
• Markedly elevated fractional excretion of sodium (often >2%, can be >6%) 1

Critical Distinction from SIADH

The single most important distinguishing feature between CSW and SIADH is volume status: CSW presents with hypovolemia while SIADH presents with euvolemia. 1, 2 Both conditions share identical laboratory findings (hyponatremia, elevated urine sodium >20 mEq/L, concentrated urine), making volume assessment critical. 1, 5

However, physical examination alone has poor accuracy for determining volume status (sensitivity 41.1%, specificity 80%). 1, 4 When clinical assessment is unclear, invasive monitoring may be necessary: 1

• Central venous pressure (CVP) <6 cm H₂O suggests CSW (hypovolemia) 1
• CVP 6-10 cm H₂O suggests SIADH (euvolemia) 1

Clinical Context

CSW typically occurs in patients with: 1, 5

• Subarachnoid hemorrhage (most common) 3
• Traumatic brain injury 6, 7
• Brain tumors or neurosurgery 1
• Other intracranial pathology (meningitis, encephalitis) 5

CSW is more common than SIADH in neurosurgical patients, making it an essential diagnosis to consider in this population. 1, 8

Diagnostic Workup

Initial laboratory evaluation should include: 8, 4

• Serum sodium, osmolality, and uric acid 4
• Urine sodium and osmolality (spot urine is sufficient) 4
• Assessment of volume status (clinical examination, CVP if needed) 1
• Thyroid and adrenal function to exclude other causes 4

A urinary sodium >20 mEq/L with hyponatremia indicates renal sodium losses, characteristic of CSW, diuretic use, or adrenal insufficiency. 1 The fractional excretion of sodium can be calculated to quantify renal sodium wasting. 1

Common Pitfalls

• Misdiagnosing CSW as SIADH leads to inappropriate fluid restriction, which worsens hypovolemia and outcomes 8, 1
• Relying solely on physical examination to determine volume status without considering invasive monitoring when uncertain 4
• Obtaining ADH or natriuretic peptide levels is not supported by evidence and delays treatment 8, 4
• Ignoring the clinical context of CNS disease, which should raise suspicion for CSW over SIADH 1, 5

Treatment Implications

Treatment for CSW requires volume and sodium replacement—NOT fluid restriction—which is the opposite of SIADH management. 8, 1 This fundamental difference makes accurate diagnosis critical. 2, 5

Treatment approach includes: 8, 1

• Isotonic (0.9%) or hypertonic (3%) saline depending on severity 8, 1
• Fludrocortisone (mineralocorticoid) to enhance sodium reabsorption, particularly in refractory cases 3, 8, 6
• Oral salt supplementation (sodium chloride 100 mEq three times daily) for maintenance 8, 1
• Correction rate must not exceed 8 mmol/L in 24 hours to prevent osmotic demyelination syndrome 8, 4