In a 70‑kg adult with hemorrhagic stroke and severe hypernatremia (serum sodium ≈160 mmol/L), how should the hypernatremia be corrected orally?

Oral Correction of Severe Hypernatremia in Hemorrhagic Stroke

In a 70-kg adult with hemorrhagic stroke and severe hypernatremia (serum sodium ≈160 mmol/L), oral correction should be achieved through scheduled free water administration via nasogastric tube or oral intake (if safe swallow), targeting a reduction of 10–15 mmol/L per 24 hours, with close monitoring every 4–6 hours to prevent cerebral edema from overly rapid correction. 1, 2, 3

Immediate Assessment and Safety Considerations

Before initiating oral correction, you must evaluate:

• Swallow safety and aspiration risk – If the patient cannot safely swallow due to stroke-related dysphagia, a nasogastric tube is mandatory for water administration 4
• Volume status – Assess for signs of hypovolemia (orthostatic hypotension, dry mucous membranes, reduced skin turgor) versus hypervolemia (edema, jugular venous distension) to guide fluid type 1, 3
• Neurological symptoms – Document baseline mental status, as severe hypernatremia causes somnolence (42%), disorientation (30%), and recent falls (17%) 5
• Underlying cause – In hemorrhagic stroke, hypernatremia typically results from impaired thirst mechanism (hypodipsia) due to hypothalamic injury, not from deliberate therapeutic hypernatremia 4, 2

Critical pitfall: Do not attempt oral hydration in patients with altered mental status or unsafe swallow without first securing a nasogastric tube, as aspiration risk is prohibitively high 5.

Calculating Free Water Deficit

Use the Adrogue-Madias formula to estimate total free water deficit:

Free water deficit (L) = 0.5 × body weight (kg) × [(current Na ÷ 140) – 1]

For a 70-kg patient with Na 160 mmol/L:

• Free water deficit = 0.5 × 70 × [(160 ÷ 140) – 1] = 5 liters 1

However, this calculation assumes stable fluid balance and does not account for ongoing losses (insensible losses, urine output), so you must add maintenance water requirements 1.

Oral Fluid Selection and Administration Protocol

Preferred Oral Fluids

• Pure water (free water) is the optimal choice for oral/NG administration in hypernatremia, as it provides maximum free water without additional osmotic load 1, 4
• Hypotonic oral solutions (diluted juice, weak tea) can be used if pure water is not tolerated, but avoid high-osmolality beverages 1
• Avoid isotonic or hypertonic fluids (sports drinks, high-sodium broths) as these worsen hypernatremia 1

Dosing Schedule

For severe hypernatremia (Na 160 mmol/L), implement scheduled water administration:

1. Initial 24 hours: Target reduction of 10–15 mmol/L (bringing Na from 160 to 145–150 mmol/L) 1, 2, 3

   • Divide total daily water requirement into hourly or 2-hourly boluses (e.g., 200–300 mL every 2 hours via NG tube)
   • This typically requires 4–6 liters of free water over 24 hours (deficit replacement plus maintenance) 1, 3

2. Subsequent days: Continue correction at 10–15 mmol/L per 24 hours until Na reaches 145 mmol/L 1, 2, 3

Critical safety limit: Never exceed a correction rate of 12 mmol/L per 24 hours, as faster correction risks cerebral edema, seizures, and permanent neurological injury 2, 3. In hemorrhagic stroke patients with disrupted blood-brain barrier, this risk is amplified 2.

Monitoring Protocol

Serum Sodium Monitoring

• First 24 hours: Check serum sodium every 4–6 hours to ensure correction rate stays within 10–15 mmol/L/day 1, 3
• After initial correction: Check every 12–24 hours until Na stabilizes at 145 mmol/L 1, 3
• If correction is too slow (<2 mmol/L in first 24 hours): Increase water administration rate 5
• If correction is too rapid (>15 mmol/L in 24 hours): Temporarily reduce water intake and recheck Na in 2–4 hours 2, 3

Clinical Monitoring

• Neurological status: Monitor for signs of cerebral edema (worsening mental status, seizures, focal deficits) during correction 2, 3
• Fluid balance: Track intake/output, daily weights, and urine specific gravity 1, 3
• Renal function: Monitor BUN/creatinine, as hypernatremia-associated hyperchloremia may impair renal function 2

Special Considerations in Hemorrhagic Stroke

Post-Stroke Hypodipsia Management

• Hemorrhagic stroke frequently damages the hypothalamic thirst center, causing chronic hypodipsia and recurrent hypernatremia 4
• Long-term management requires scheduled water intake (e.g., 200 mL every 2 hours while awake) rather than relying on patient-initiated drinking 4
• Educate caregivers to provide scheduled fluids even when the patient denies thirst 4

Avoid Deliberate Hypernatremia for ICP Control

• Do not maintain therapeutic hypernatremia (Na 150–155 mmol/L) for intracranial pressure control in hemorrhagic stroke, as the blood-brain barrier is disrupted, limiting efficacy and increasing risk of rebound ICP elevation during correction 2
• The weak correlation between serum sodium and ICP, combined with renal toxicity from hyperchloremia, makes this strategy inadvisable 2

Common Pitfalls and How to Avoid Them

1. Under-recognition and delayed treatment: Hypernatremia in stroke patients often presents with non-specific symptoms (somnolence, disorientation) that may be attributed to the stroke itself. Check serum sodium on admission and daily thereafter 5, 6

2. Inadequate correction rate: 35% of hypernatremic patients receive inadequate correction (<2 mmol/L in first 24 hours), which is associated with increased mortality 5. Calculate fluid requirements accurately and monitor closely 3, 5

3. Overly rapid correction: Although less common than under-correction, rapid reduction (>15 mmol/L/24h) risks cerebral edema. Use scheduled boluses rather than continuous infusion to maintain control 2, 3

4. Failure to address underlying cause: In post-stroke hypodipsia, hypernatremia will recur unless scheduled water intake is maintained long-term 4

5. Ignoring concurrent hyponatremia risk: If the patient develops hyponatremia during stroke hospitalization (45% incidence), distinguish SIADH from cerebral salt wasting, as treatments are opposite 7, 6

Prognosis and Outcome

• Mortality in hypernatremic stroke patients is 25%, with significantly higher mortality in those who experience inadequate correction (0 mmol/L correction vs. -6 mmol/L in survivors) 5
• Prolonged hypernatremia increases hospital stay and mortality, making prompt correction essential 3
• Hyponatremia (if it develops) is an independent predictor of short-term mortality in hemorrhagic stroke (36.5% mortality in SIADH, 50% in CSWS vs. 13.1% in normonatremic patients), so vigilant sodium monitoring throughout hospitalization is critical 7, 6