What is the approach to managing hypernatremia in the Intensive Care Unit (ICU)?

Hypernatremia Workup in the ICU

In critically ill ICU patients with hypernatremia (serum sodium >145 mmol/L), immediately assess volume status and urine electrolytes to determine the mechanism (sodium gain vs. free water loss), then correct with electrolyte-free water at a rate not exceeding 8-10 mmol/L per 24 hours while addressing the underlying cause. 1, 2, 3

Initial Diagnostic Assessment

Volume Status Evaluation:

• Hypovolemic hypernatremia: Look for orthostatic hypotension, dry mucous membranes, decreased skin turgor, tachycardia, and negative fluid balance 3, 4
• Euvolemic hypernatremia: Normal blood pressure, no edema, no signs of dehydration—suggests pure water loss (diabetes insipidus, insensible losses) 3
• Hypervolemic hypernatremia: Peripheral edema, positive fluid balance, elevated jugular venous pressure—indicates sodium gain exceeding water gain 3, 4

Essential Laboratory Tests:

• Serum sodium, potassium, chloride, bicarbonate, BUN, creatinine 4
• Serum osmolality (will be elevated >295 mOsm/kg) 3
• Urine sodium and osmolality 2, 3
• Urine output measurement (polyuria >40 ml/kg suggests osmotic diuresis or diabetes insipidus) 4
• Serum glucose (hyperglycemia causes osmotic diuresis) 3
• Serum albumin (hypoalbuminemia is associated with hypernatremia development) 4

Mechanism Determination

Urine Osmolality Interpretation:

• Urine osmolality >600-800 mOsm/kg: Appropriate renal response to hypertonicity—suggests extrarenal water losses (insensible losses, GI losses, burns) 3
• Urine osmolality <300 mOsm/kg: Inappropriate dilute urine—suggests diabetes insipidus (central or nephrogenic) 3
• Urine osmolality 300-600 mOsm/kg: Partial diabetes insipidus or osmotic diuresis 3

Common ICU-Specific Causes:

• Inadequate free water replacement in sedated/intubated patients unable to express thirst 2, 3
• Osmotic diuresis from mannitol administration (10% of cases), hyperglycemia, or high protein feeds 4
• Excessive sodium administration via sodium bicarbonate (23% of cases), hypertonic saline, or sodium-containing medications 4
• Renal dysfunction impairing water conservation (53% of cases) 4
• Sepsis (9% of cases) causing increased insensible losses 4
• Loop diuretics causing hypotonic urine losses 3

Treatment Strategy

Free Water Deficit Calculation: Use the formula: Free water deficit (L) = 0.5 × body weight (kg) × [(current Na/140) - 1] 3

• This provides an estimate for initial replacement; ongoing losses must be added 3, 5

Correction Rate Guidelines:

• Maximum correction rate: 8-10 mmol/L per 24 hours for chronic hypernatremia 1
• Target rate: 0.5 mmol/L per hour or less 1
• Rapid correction risks: Cerebral edema, seizures, and neurological injury from osmotic water shift into brain cells 1
• Monitor serum sodium every 2-4 hours during active correction 3, 5

Fluid Selection:

• First-line: Electrolyte-free water (D5W IV or free water via NG/OG tube if gut functional) 2, 3, 4
• Alternative: Hypotonic saline (0.45% NaCl) if some sodium replacement needed 3
• Avoid: Isotonic fluids in patients with renal concentrating defects (e.g., nephrogenic diabetes insipidus) as this worsens hypernatremia 6

Volume-Specific Management:

• Hypovolemic: Replace volume deficit first with isotonic saline, then switch to hypotonic fluids once hemodynamically stable 3
• Euvolemic: Pure free water replacement 3
• Hypervolemic: Create negative sodium balance with loop diuretics plus free water replacement 2, 4

Addressing Underlying Causes

Iatrogenic Prevention:

• Calculate daily free water requirements: typically 30-40 ml/kg/day baseline plus replacement of ongoing losses 3
• Review all sodium sources: IV fluids, medications (sodium bicarbonate, antibiotics), enteral nutrition 4
• Reduce sodium intake to <150 mmol/day if hypervolemic 4
• Discontinue mannitol if being used for ICP control (consider alternative agents) 4

Diabetes Insipidus Management:

• Central DI: Desmopressin (DDAVP) 1-2 mcg IV/SC every 12-24 hours 3
• Nephrogenic DI: Discontinue offending agents (lithium, amphotericin), consider thiazide diuretics plus amiloride 3

Osmotic Diuresis:

• Control hyperglycemia with insulin infusion 3
• Reduce protein load in enteral feeds if causing urea-induced osmotic diuresis 3

Monitoring During Correction

Serial Measurements Required:

• Serum sodium every 2-4 hours initially, then every 6-8 hours once stable 3, 5
• Urine output and urine electrolytes every 4-6 hours 5
• Daily weights and strict intake/output records 4
• Neurological examination for signs of cerebral edema (headache, confusion, seizures) 1, 3

Adjust Therapy Based On:

• If sodium correcting too rapidly (>0.5 mmol/L/h): Slow free water administration or add sodium-containing fluids 5
• If sodium not correcting: Increase free water rate, reassess ongoing losses, check for continued sodium administration 5
• If developing cerebral edema: Temporarily stop free water, consider hypertonic saline bolus 1

Critical Pitfalls to Avoid

• Ignoring ongoing losses: ICU patients often have polyuria (40 ml/kg/day average), requiring continuous free water replacement beyond calculated deficit 4, 5
• Overcorrecting with hypertonic fluids: Administering fluids with sodium concentration >133 mmol/L perpetuates hypernatremia despite positive fluid balance 4
• Rapid correction of chronic hypernatremia: Causes cerebral edema, seizures, and permanent neurological damage 1
• Assuming closed system: Formulae estimate initial deficit only; serial electrolyte monitoring essential to adjust for dynamic losses 5
• Prolonged induced hypernatremia in TBI: Not recommended for ICP control due to rebound intracranial hypertension during correction 1

Prognostic Implications

Hypernatremia in the ICU is an independent predictor of mortality (48% vs. 10% in controls), increased length of stay, and post-discharge mortality 4, 7. Both the severity and persistence of hypernatremia correlate with worse outcomes, supporting aggressive correction rather than permissive hypernatremia 7.