Fluid Management for Hypernatremia in Adults

1. Estimating the Free‑Water Deficit

In an adult patient weighing ≈ 60 kg, the free‑water deficit can be estimated with the formula : Free‑water deficit = 0.5 × body weight (kg) × [(current Na ÷ 140) − 1] [2].
Using a serum sodium of 160 mmol/L, the calculated deficit is ≈ 4.3 L, representing the total volume required to normalize sodium; this volume should be administered over 24–48 h depending on the chronicity of the hypernatremia [1].

When the corrected serum sodium is normal or elevated, a hypotonic solution such as 0.45 % NaCl is recommended [1, 2].
If the corrected serum sodium is low, isotonic saline (0.9 % NaCl) should be used [1, 2].
For a pure free‑water deficit without significant volume depletion, 5 % dextrose in water (D5W) is appropriate [1, 2].
The corrected sodium for hyperglycemia is obtained by adding 1.6 mEq/L for each 100 mg/dL glucose above 100 mg/dL [1, 2].

In hypovolemic or severely dehydrated patients, begin with 0.9 % NaCl at 15–20 mL/kg/h for the first hour to restore intravascular volume and renal perfusion; for a 60‑kg adult this equals ≈ 900–1200 mL in the first hour [1, 2].

After initial volume restoration, switch to a hypotonic fluid (0.45 % NaCl or D5W) [1, 2].
Infusion rates of 4–14 mL/kg/h (≈ 240–840 mL/h for a 60‑kg adult) are recommended, titrated to the evolving serum sodium [1].
Serum sodium should be checked every 2–4 h initially to verify that the correction rate remains within safe limits [1, 2].

The correction speed must not exceed 0.5 mmol/L per hour (≈ 12 mmol/L per 24 h) to minimize the risk of cerebral edema [1, 2].
The induced change in serum osmolality should be ≤ 3 mOsm/kg H₂O per hour [1].

Serum sodium: measure at least every 2 h during active correction [1].
Neurologic status: watch for headache, confusion, or seizures as early signs of cerebral edema [1].
Fluid balance and hemodynamics: continuous assessment of input/output, blood pressure, and cardiac status, especially in patients with renal or cardiac compromise [1, 2].

Over‑rapid correction is the most serious error and can cause cerebral edema, seizures, and permanent neurologic injury [1, 2].
Continuing isotonic saline alone after the initial resuscitation will not adequately lower serum sodium because its sodium concentration (≈ 154 mmol/L) exceeds the target [1, 2].
Neglecting ongoing free‑water losses (e.g., diabetes insipidus, osmotic diuresis) leads to under‑correction; these losses must be replaced in addition to the calculated deficit [1, 2].
Infrequent monitoring allows unpredictable sodium shifts, increasing the risk of over‑ or under‑correction [1, 2].