Severe Hypernatremia Post-Decompressive Craniectomy: Causes and Management
Most Likely Cause
The rapid rise in sodium from 139 to 160 mEq/L is most likely caused by the combined osmotic diuretic effects of mannitol and furosemide (Lasix), resulting in excessive free water loss that exceeds electrolyte loss. 1, 2
Primary Contributing Factors
Mannitol-induced osmotic diuresis: Mannitol causes obligatory water loss in excess of electrolytes, directly leading to hypernatremia 2. The FDA label explicitly warns that "with continued administration of mannitol, loss of water in excess of electrolytes can cause hypernatremia" 2.
Furosemide potentiation: The addition of furosemide (Lasix) to mannitol therapy intensifies the diuretic effect and free water loss 3, 1. This combination is commonly used but significantly increases hypernatremia risk 1.
Inadequate fluid replacement: Post-craniotomy patients receiving hyperosmolar therapy often have insufficient free water replacement to compensate for obligatory losses 3, 1.
Secondary Considerations
Central diabetes insipidus: Brain injury from the hemorrhagic stroke or surgical manipulation could damage the hypothalamic-pituitary axis, causing DI 4, 5. However, this typically presents earlier and would be evident from massive urine output (>200-300 mL/hour) with low urine osmolality.
Hypodipsia: Stroke lesions affecting the thirst center can impair water intake, though this is less relevant in an intubated ICU patient 5.
Immediate Management Protocol
Step 1: Discontinue or Modify Osmotic Therapy
Stop mannitol immediately if serum osmolality exceeds 320 mOsm/L 1, 6, 7, 2. At sodium of 160 mEq/L, the calculated osmolality is approximately 330 mOsm/L, which exceeds the safety threshold 1.
- Hold furosemide (Lasix) until sodium normalizes 3
- If continued ICP management is needed, consider switching to hypertonic saline (3%), which has less diuretic effect and may be preferable when hypernatremia is already present 1, 6
Step 2: Calculate Free Water Deficit and Correct Gradually
Calculate the free water deficit using the formula:
- Free water deficit (L) = 0.6 × body weight (kg) × [(current Na/140) - 1]
- For a 70 kg patient with Na 160: 0.6 × 70 × [(160/140) - 1] = 6 liters
Correction rate: Lower sodium by no more than 10-12 mEq/L in the first 24 hours to avoid cerebral edema from rapid osmotic shifts 4. In this acute setting with iatrogenic hypernatremia, slightly faster correction (0.5-1 mEq/L per hour initially) is safer than in chronic hypernatremia 4.
Step 3: Fluid Replacement Strategy
Administer hypotonic fluids (0.45% saline or D5W) to replace free water deficit 3, 4:
- Start with 0.45% saline at 150-200 mL/hour initially
- Monitor sodium every 2-4 hours during active correction 1
- Adjust infusion rate based on sodium response
- Avoid pure free water (D5W alone) initially as it may cause too-rapid correction
Maintain isotonic maintenance fluids (0.9% saline) for baseline needs 3. The American Heart Association recommends isotonic or mildly hypertonic maintenance fluids in stroke patients, but this must be modified when severe hypernatremia develops 3.
Step 4: Intensive Monitoring
Check electrolytes every 2-4 hours during active correction 1:
- Serum sodium and potassium
- Serum osmolality
- Urine output and urine osmolality (to assess for DI)
- Neurological examination for signs of worsening cerebral edema
Monitor for complications:
- Cerebral edema from overly rapid correction (watch for declining GCS, new pupillary changes) 4
- Rebound intracranial hypertension if mannitol is stopped abruptly after prolonged use 1
- Acute kidney injury (check creatinine, as mannitol can cause renal failure) 2
Step 5: Address Underlying ICP Management
If ICP remains elevated after stopping mannitol:
- Ensure head of bed elevated 30 degrees 6
- Maintain adequate sedation and analgesia 3
- Consider ventricular drainage if hydrocephalus present 3, 6
- Decompressive craniectomy is the definitive treatment for refractory cerebral edema and should be strongly considered if medical management fails, as it produces reproducible large reductions in mortality 3, 6, 7
Critical Caveats
Dexamethasone (Dexona) is NOT indicated for cytotoxic edema from hemorrhagic stroke 3. The Swiss guidelines explicitly state that corticosteroids are contraindicated (Class III, Level C) 3. Discontinue dexamethasone as it provides no benefit and may worsen hyperglycemia and infection risk.
Rebound phenomenon: After stopping mannitol, ICP may transiently increase by 50-80% above baseline within 6-7 hours due to accumulated mannitol in CSF reversing the osmotic gradient 8, 1. Close neurological monitoring is essential during this period.
Mannitol is only a temporizing measure: Despite intensive medical management, mortality remains 50-70% in patients with massive cerebral edema 6. Early surgical decompression (within 48 hours) is the most effective intervention for large hemispheric strokes with mass effect 3, 6.