Management of Hypernatremia
Correct chronic hypernatremia slowly at a rate not exceeding 8-10 mmol/L per 24 hours to prevent cerebral edema and neurological complications, while acute symptomatic hypernatremia can be corrected more rapidly up to 0.5-1 mmol/L per hour. 1, 2
Correction Rate Based on Chronicity
Chronic Hypernatremia (>48 hours):
- Maximum correction rate: 8-10 mmol/L per 24 hours 1, 3
- Alternative recommendation: ≤0.5 mmol/L per hour 1
- Slower correction is critical because brain cells synthesize intracellular osmolytes over 48 hours to adapt to hyperosmolar conditions 4
- Rapid correction causes water to shift into brain cells faster than osmolytes can be extruded, resulting in cerebral edema, seizures, and permanent neurological injury 1, 2, 5
Acute Hypernatremia (<24-48 hours):
- Can be corrected more rapidly: up to 1 mmol/L per hour if severely symptomatic 2
- Brain adaptation has not yet occurred, so risk of cerebral edema with rapid correction is lower 6
- For severe acute cases, hemodialysis is an effective option to rapidly normalize sodium levels 3
Treatment Strategy by Volume Status
Hypovolemic Hypernatremia:
- Administer hypotonic fluids to replace free water deficit 2, 5
- Avoid isotonic saline as initial therapy, especially in nephrogenic diabetes insipidus 2
- In unstable patients, start with isotonic IV fluid for hemodynamic stabilization, then switch to hypotonic solutions 5
Euvolemic Hypernatremia:
- Evaluate for diabetes insipidus (central vs. nephrogenic) 6
- For central diabetes insipidus: administer desmopressin (dDAVP) 3
- For nephrogenic diabetes insipidus: hypotonic fluid replacement and address underlying cause (medications like lithium, hypokalemia) 6
- Consider low salt diet (<6 g/day) and protein restriction (<1 g/kg/day) 2
Hypervolemic Hypernatremia:
- Focus on negative water balance rather than aggressive fluid administration 2
- In heart failure: implement sodium and fluid restriction (1.5-2 L/day) 2
- In cirrhosis: discontinue IV fluids and implement free water restriction 2
- For persistent severe hypernatremia with cognitive symptoms in heart failure: consider short-term vasopressin antagonists (tolvaptan, conivaptan) 2, 7
Specific Clinical Scenarios
Severe Symptomatic Hypernatremia:
- Combine IV hypotonic fluids with free water via nasogastric tube 2
- Target correction rate: 10-15 mmol/L per 24 hours 2
- Monitor for neurological deterioration during correction 1
Traumatic Brain Injury:
- Do not use prolonged induced hypernatremia to control intracranial pressure 4, 1
- Rationale: requires intact blood-brain barrier to be effective; with disrupted BBB, hypertonic saline may worsen cerebral contusions 4
- Risk of "rebound" ICP elevation during correction as brain cells synthesize intracellular osmolytes 4
- Weak relationship between serum sodium and ICP 4
Monitoring Requirements
Essential Laboratory Monitoring:
- Serum sodium, potassium, chloride, and bicarbonate levels regularly during treatment 2
- Renal function and urine osmolality 2
- Clinical status and neurological examination for signs of deterioration 1
- Body weight and fluid balance 2
Monitoring Frequency:
- Close laboratory controls initially, especially when correcting chronic hypernatremia 3
- Continuous vigilance for signs of cerebral edema (confusion, seizures, altered consciousness) during correction 1, 8
Critical Pitfalls to Avoid
Overly Rapid Correction:
- Correcting chronic hypernatremia too rapidly leads to cerebral edema, seizures, and permanent neurological injury 1, 2
- This is the most dangerous complication and can be fatal 5, 8
Hyperchloremia:
- Hypernatremia is associated with hyperchloremia, which may impair renal function 4, 1
- Monitor renal function during treatment 2
Renal Replacement Therapy:
- When initiating dialysis in patients with chronic hypernatremia, avoid rapid sodium drops 3
- Adjust dialysate composition to prevent overly rapid correction 3
Drug-Induced Hypernatremia: