How to manage hyponatremia (low sodium levels) after a stroke?

Management of Hyponatremia After Stroke

Hyponatremia after stroke should be managed with isotonic fluids for volume contraction and fludrocortisone acetate or hypertonic saline for correction of sodium levels, while avoiding hypotonic fluids and fluid restriction. 1

Pathophysiology and Incidence

Hyponatremia is common after stroke, occurring in 10-35% of patients 1, 2. It is more frequent in:

• Patients with poor clinical grade
• Anterior communicating artery aneurysms
• Hydrocephalus
• Hemorrhagic stroke (particularly right putamen hemorrhage) 2, 3

Two main mechanisms cause hyponatremia after stroke:

1. Syndrome of Inappropriate Antidiuretic Hormone (SIADH) - accounts for 67-71% of cases 2, 3
2. Cerebral Salt Wasting Syndrome (CSWS) - accounts for 33% of cases 2

CSWS is characterized by excessive natriuresis and volume contraction, while SIADH typically presents with euvolemia or mild hypervolemia.

Assessment Algorithm

1. Measure serum sodium levels in all stroke patients (hyponatremia defined as <135 mEq/L)
2. Determine volume status using:
   • Central venous pressure
   • Pulmonary artery wedge pressure
   • Fluid balance
   • Body weight
   • Clinical signs of volume depletion 1
3. Differentiate between SIADH and CSWS by assessing:
   • Volume status (hypovolemic in CSWS, euvolemic/hypervolemic in SIADH)
   • Urine sodium (elevated in both)
   • Serum osmolality (low in both)
   • Clinical response to volume replacement

Treatment Recommendations

For All Patients with Hyponatremia After Stroke:

1. Avoid large volumes of hypotonic fluids as they can worsen hyponatremia and brain edema 1
2. Maintain euvolemia as the primary goal 1

For Hypovolemic Hyponatremia (CSWS):

1. Administer isotonic fluids (0.9% saline) for volume replacement 1

   • Rapid replacement of depleted intravascular volume followed by maintenance fluids
   • Daily fluid maintenance: 30 mL/kg body weight 1

2. Consider fludrocortisone acetate (Class IIa, Level of Evidence B) 1

   • Helps correct negative sodium balance
   • Reduces need for fluid administration
   • Improves sodium levels

3. Use 3% hypertonic saline for correction of severe hyponatremia (Class IIa, Level of Evidence B) 1

   • Particularly effective in correcting hyponatremia
   • Increases regional cerebral blood flow and tissue oxygenation

4. Consider 5% albumin as volume expander 1

For Euvolemic/Hypervolemic Hyponatremia (SIADH):

1. Consider fludrocortisone acetate (Class IIa, Level of Evidence B) 1
2. Use 3% hypertonic saline for correction of severe hyponatremia 1
3. Consider tolvaptan (vasopressin receptor antagonist) for resistant cases 4
   • Effective for euvolemic or hypervolemic hyponatremia
   • Increases serum sodium levels significantly
   • Monitor for rapid correction and hypernatremia

Monitoring and Precautions

1. Monitor serum sodium levels regularly to avoid:

   • Too rapid correction (risk of osmotic demyelination syndrome)
   • Hypernatremia (reported in 1.7% of patients on tolvaptan) 4

2. Monitor volume status using central venous pressure, fluid balance, and body weight 1

3. Avoid fluid restriction if possible, especially in the first 24 hours after subarachnoid hemorrhage 1

   • Fluid restriction has been associated with increased delayed ischemic deficits
   • Volume contraction linked to symptomatic vasospasm

Clinical Significance

Hyponatremia significantly affects stroke outcomes, particularly when caused by CSWS rather than SIADH 2. Proper management can potentially reduce mortality and improve outcomes, though more research is needed to definitively establish this connection 5.

Common Pitfalls to Avoid

1. Misdiagnosing SIADH vs. CSWS - treatment approaches differ significantly
2. Fluid restriction in CSWS - can worsen volume depletion and increase risk of vasospasm
3. Too rapid correction of hyponatremia - can lead to osmotic demyelination syndrome
4. Overlooking hyponatremia - can mimic stroke symptoms or worsen existing deficits 6
5. Using hypotonic solutions - can exacerbate ischemic brain edema 1