Hypernatremia Management in the ICU
Immediate Assessment and Initial Treatment
Assess volume status and urine electrolytes immediately, then correct with electrolyte-free water at a rate not exceeding 8-10 mmol/L per 24 hours (maximum 0.5 mmol/L per hour) while addressing the underlying cause. 1
Volume Status Determination
- Hypovolemic hypernatremia: Look for orthostatic hypotension, dry mucous membranes, decreased skin turgor, and flat neck veins—indicates water loss exceeding sodium loss 1, 2
- Euvolemic hypernatremia: Normal volume status with pure water deficit, often from diabetes insipidus or inadequate water intake 1, 3
- Hypervolemic hypernatremia: Presence of edema, ascites, or jugular venous distention—indicates sodium gain exceeding water gain 2, 3
Urine Studies for Mechanism Identification
- Urine osmolality <300 mOsm/kg: Suggests diabetes insipidus (central or nephrogenic) 3
- Urine osmolality >600 mOsm/kg: Indicates appropriate renal response to hypernatremia with extrarenal water losses 3
- Urine sodium >20 mmol/L with polyuria: Points toward osmotic diuresis or renal sodium wasting 2
Fluid Replacement Strategy
Primary Treatment: Electrolyte-Free Water
Electrolyte-free water is first-line treatment for hypernatremia. 1 Use 5% dextrose in water (D5W) as the primary replacement fluid, as it delivers no renal osmotic load and allows controlled decrease in plasma osmolality 1
- Calculate free water deficit: Free water deficit (L) = 0.5 × body weight (kg) × [(current Na/140) - 1] 1
- Add ongoing losses: Must account for continued insensible losses (typically 500-1000 mL/day) and any ongoing pathologic losses 1, 3
Alternative: Hypotonic Saline
Use 0.45% NaCl (half-normal saline) if some sodium replacement is needed, particularly in hypovolemic hypernatremia where both water and sodium deficits exist 1
Critical Contraindication
Never use isotonic fluids (0.9% NaCl) in patients with renal concentrating defects such as nephrogenic diabetes insipidus—this will worsen hypernatremia. 1 These patients require hypotonic fluid replacement to match their excessive free water losses 1
Correction Rate Guidelines
Standard Correction Rate
Maximum correction rate: 8-10 mmol/L per 24 hours, with target rate of 0.5 mmol/L per hour or less. 1 This prevents cerebral edema, seizures, and neurological injury from osmotic water shift into brain cells 1
Evidence on Rapid Correction
Recent research challenges traditional conservative approaches: A 2019 study of 449 critically ill patients found no increased mortality or neurologic complications with rapid correction (>0.5 mmol/L per hour) compared to slower rates 4. However, guideline recommendations remain conservative at ≤0.5 mmol/L per hour until further evidence emerges 1, prioritizing safety in the absence of definitive data showing benefit from faster correction.
Acute vs. Chronic Hypernatremia
- Acute hypernatremia (<48 hours): Can tolerate slightly faster correction as brain adaptation has not occurred 3
- Chronic hypernatremia (>48 hours): Requires strict adherence to maximum 8-10 mmol/L per 24 hours due to brain cell adaptation 1, 3
Monitoring Protocol
Intensive Monitoring Phase
- Serum sodium every 2-4 hours initially during active correction 1
- Every 6-8 hours once stable and correction rate established 1
- Urine output and urine electrolytes to assess ongoing losses and renal response 1, 3
Treatment Adjustments
If sodium correcting too rapidly (>0.5 mmol/L per hour): Slow free water administration or add sodium-containing fluids to prevent overcorrection 1
If sodium correcting too slowly: Increase free water administration rate while ensuring total correction stays within 8-10 mmol/L per 24 hours 1
Special ICU Considerations
Iatrogenic Hypernatremia
ICU-acquired hypernatremia is largely preventable and increasingly common, with incidence nearly doubling over two decades (13% to 24%) 5. This shift is attributed to:
- Increased use of sodium-containing infusions (sodium bicarbonate, hypertonic saline) 2, 5
- Aggressive diuretic therapy 2, 5
- Hydrocortisone administration 5
- Inadequate free water provision in patients with impaired consciousness 6
Mechanism in ICU Patients
Hypernatremia develops from "too little water and too much salt": 2
- Negative fluid balance (80% of cases): Average -31 mL/kg/day with polyuria (40 mL/kg) 2
- Positive fluid balance (20% of cases): Receiving relatively hypertonic fluids (148 mmol/L sodium+potassium vs. 133 mmol/L) 2
Risk Factors in Critical Illness
- Sepsis: 9-fold higher incidence in hypernatremic patients 2
- Renal dysfunction: Present in 53% of hypernatremic ICU patients 2
- Mannitol use: 10% vs. 1% in controls 2
- Sodium bicarbonate: 23% vs. 0.4% in controls 2
Traumatic Brain Injury Considerations
Avoid prolonged induced hypernatremia for intracranial pressure control due to risk of "rebound" ICP during correction 1. Additionally, hypernatremia with hyperchloremia may impair renal function in these patients 1
Mortality and Outcomes
Hypernatremia is an independent risk factor for mortality in critically ill patients. 6 The association between severity and mortality is dose-dependent, with more severe hypernatremia correlating with higher death rates 5. However, this may reflect underlying illness severity rather than direct causation 4, 6
Common Pitfalls to Avoid
- Using isotonic saline in diabetes insipidus: Worsens hypernatremia by providing osmotic load without adequate free water 1
- Inadequate monitoring: Failure to check sodium every 2-4 hours during initial correction risks overcorrection 1
- Ignoring ongoing losses: Not accounting for continued insensible and pathologic water losses leads to undercorrection 1, 3
- Correcting too rapidly: Exceeding 0.5 mmol/L per hour or 8-10 mmol/L per 24 hours risks cerebral edema 1
- Treating hypernatremia without addressing underlying cause: Sepsis, renal dysfunction, and medication effects must be managed concurrently 6, 2