Treatment of Hypernatremia in Acute Intracranial Hemorrhage
Hypernatremia in acute intracranial hemorrhage should be corrected cautiously and gradually, avoiding rapid correction that could worsen cerebral edema, with a target reduction rate of 10-15 mmol/L per 24 hours using hypotonic fluids such as D5W (5% dextrose in water). 1
Critical Distinction: Therapeutic vs. Pathologic Hypernatremia
The management approach depends fundamentally on whether hypernatremia is iatrogenic/therapeutic (induced for ICP control) or pathologic (unintended metabolic derangement):
If Hypernatremia is Therapeutic (Induced for ICP Control)
Prolonged therapeutic hypernatremia is NOT recommended for ICP control in intracranial hemorrhage patients. 2
- The theoretical benefit requires an intact blood-brain barrier to create an osmotic gradient, but hypertonic saline perfusion can be deleterious with disrupted blood-brain barrier by increasing the size of cerebral contusions 2
- Rapid brain cell volume regulation limits the effectiveness of prolonged hyperosmolarity through synthesis of intracellular osmoles to restore normal cell volume, creating risk of "rebound" ICP during hypernatremia correction 2
- The relationship between serum sodium and ICP is weak 2
- Hypernatremia is associated with hyperchloremia which may be deleterious for renal function 2
If therapeutic hypernatremia was induced, transition away from continuous hypertonic saline infusion and allow gradual normalization while maintaining adequate cerebral perfusion pressure. 2, 3
If Hypernatremia is Pathologic (Unintended)
Correct hypernatremia gradually to prevent osmotic demyelination and worsening cerebral edema:
Correction Rate Guidelines
Maximum correction rate: 10-15 mmol/L per 24 hours 1
- Correction rates faster than 48-72 hours for severe hypernatremia have been associated with increased risk of pontine myelinolysis 1
- In the context of acute brain injury, even mild fluctuations in serum sodium can cause neurological deterioration and evidence of early herniation 4
Fluid Selection and Administration
Primary fluid for correction: D5W (5% dextrose in water) 1
- D5W provides free water replacement without additional sodium load 1
- Avoid isotonic fluids in patients with renal concentrating defects, as these can worsen hypernatremia 5
Monitoring Requirements
Monitor serum sodium every 2-4 hours during active correction 5
- Close monitoring of serum sodium and osmolarity in acute head injured patients is critical, as alterations of these parameters represent substantial risk for cerebral edema 4
- Track neurological examination closely for signs of deterioration
- Monitor for signs of cerebral edema on imaging if neurological status changes 4
Special Considerations for Intracranial Hemorrhage
The strategy of vigilant avoidance of hyponatremia is safer and potentially more efficacious than inducing hypernatremia 3
- In subarachnoid hemorrhage specifically, hyponatremia (not hypernatremia) is the more common concern, occurring in 10-30% of patients 2
- For subarachnoid hemorrhage patients at risk of vasospasm, avoid fluid restriction and maintain euvolemia 2, 5
- Hypertonic saline increases regional cerebral blood flow, brain tissue oxygen, and pH in high-grade subarachnoid hemorrhage, but this benefit applies to bolus dosing for acute ICP crises, not sustained hypernatremia 2
Common Pitfalls to Avoid
Do NOT correct hypernatremia too rapidly (>15 mmol/L per 24 hours), as this increases risk of cerebral edema and osmotic demyelination syndrome 1
Do NOT use continuous hypertonic saline infusion to maintain elevated sodium levels in intracranial hemorrhage patients, as insufficient evidence exists to recommend this practice and it may cause harm 2, 3
Do NOT administer isotonic fluids to patients with hypernatremia and renal concentrating defects, as this can worsen hypernatremia 5
Do NOT ignore even mild sodium fluctuations in acute intracranial hemorrhage, as sudden decreases or increases can cause rapid neurological deterioration 4