How to manage a patient with hyponatremia and suspected tuberculous meningitis?

Management of Hyponatremia in Tuberculous Meningitis

In patients with suspected tuberculous meningitis and hyponatremia, aggressive diagnosis of the cause of hyponatremia and appropriate fluid management are essential, with cerebral salt wasting (CSW) being the most common etiology requiring volume repletion rather than restriction.

Diagnosis of Hyponatremia in Tuberculous Meningitis

• Hyponatremia occurs in 35-65% of children with tuberculous meningitis (TBM) and is associated with increased hospital stay and mortality 1
• The two main causes of hyponatremia in TBM are:
  • Cerebral Salt Wasting Syndrome (CSWS): characterized by excessive natriuresis, polyuria, hypovolemia, and dehydration 1, 2
  • Syndrome of Inappropriate Antidiuretic Hormone (SIADH): characterized by euvolemia or mild hypervolemia with inappropriate water retention 1
• Recent evidence suggests CSWS is more common than SIADH in TBM patients 1, 3

Diagnostic Approach

1. Assess volume status:

   • Hypovolemic: suggests CSWS (weight loss, decreased skin turgor, hypotension, tachycardia) 2
   • Euvolemic: suggests SIADH or medication effect 4
   • Hypervolemic: suggests heart, liver, or kidney disease 5

2. Laboratory evaluation:

   • Serum sodium, osmolality, BUN, creatinine 4
   • Urine sodium and osmolality 2
   • Fractional excretion of uric acid (elevated in CSWS) 6

3. Differentiate CSWS from SIADH:

   • CSWS: hypovolemia, polyuria, high urinary sodium (>60-100 mEq/L), low central venous pressure 2
   • SIADH: euvolemia, normal or low urine output, high urinary sodium 4

Management of Hyponatremia in TBM

General Principles

• Avoid overly rapid correction of chronic hyponatremia to prevent osmotic demyelination syndrome (ODS) 5
• Maximum correction rate should be 4-8 mEq/L per day, not exceeding 10-12 mEq/L in 24 hours 5
• Treatment approach depends on severity of symptoms and underlying cause 4

Management Algorithm

1. For CSWS (most common in TBM):

   • Aggressive salt and volume replacement with 0.9% or 3% sodium chloride based on severity 2, 6
   • Consider fludrocortisone (0.1 mg twice daily) for persistent cases 6
   • Monitor urine output, serum sodium, and fluid balance closely 3

2. For SIADH:

   • Fluid restriction to 1,000 mL/day for moderate hyponatremia (120-125 mEq/L) 5
   • More severe fluid restriction with albumin infusion for severe hyponatremia (<120 mEq/L) 5

3. For medication-induced hyponatremia:

   • Discontinue offending medications (e.g., carbamazepine, sertraline) if possible 5

4. For severely symptomatic hyponatremia (seizures, coma):

   • Administer hypertonic (3%) saline to increase serum sodium by 4-6 mEq/L within 1-2 hours 4
   • Continue careful monitoring to prevent exceeding correction limits 4

Specific Considerations for TBM

• Maintain euvolemia to support normal hemodynamic parameters 5
• Avoid hyperthermia and maintain normoglycemia 5
• Control raised intracranial pressure through appropriate measures 5
• Treat seizures promptly if they occur 5
• Administer dexamethasone along with anti-tuberculous therapy for TBM 5, 7

Monitoring and Follow-up

• Monitor serum sodium levels every 4-6 hours during active correction 4
• Track fluid balance, urine output, and hemodynamic parameters 3
• Assess neurological status regularly for signs of improvement or deterioration 5
• Continue monitoring until serum sodium normalizes and stabilizes 3

Pitfalls and Caveats

• Misdiagnosing CSWS as SIADH can lead to inappropriate fluid restriction and worsening hypovolemia 2
• Mannitol (used for cerebral edema in TBM) can cause or exacerbate hyponatremia and should be discontinued if possible when hyponatremia develops 1
• Overly rapid correction of chronic hyponatremia can lead to osmotic demyelination syndrome, which presents with dysarthria, dysphagia, and quadriparesis 5
• Risk factors for osmotic demyelination include advanced liver disease, alcoholism, malnutrition, and severe metabolic derangements 5