What are common etiologies of hypernatremia in hospitalized patients and the primary management principle?

• A. Free water losses (diabetes insipidus, osmotic diuresis) or inadequate water intake; gradual free water replacement to avoid cerebral edema; target correction rates
• B. Excess water intake; rapid correction
• C. Hypertonic saline administration
• D. SIADH with fluid restriction

Answer: (A)

Hypernatremia in hospitalized patients mostly comes from a free water deficit relative to body needs—water losses that aren’t matched by intake. In the hospital, this shows up most commonly with free water losses from diabetes insipidus (where the kidneys are unable to concentrate urine) or from osmotic diuresis (for example, high glucose or other osmoles pulling water into the urine), and it can also occur when patients don’t drink enough water because of illness, impaired access, or fluid restrictions. The elevated sodium reflects increased plasma osmolality, and the brain has to adapt to that change.

The key management principle is to replace free water gradually. Correcting the sodium level too quickly can cause dangerous shifts in brain cells and lead to cerebral edema. So you aim for a slow, controlled decrease in serum sodium, with careful monitoring of sodium levels and the patient’s clinical status. In practice, this means giving hypotonic fluids or encouraging oral water to address the free water deficit while treating the underlying cause (for central DI, desmopressin; for osmotic diuresis, treat the hyperglycemia or stop the offending osmole, and ensure adequate fluids). Monitor frequently and adjust to keep the correction rate within safe limits, typically avoiding rapid drops in sodium.

Why the other ideas don’t fit: excess water intake drives hyponatremia, not hypernatremia; rapid correction of hypernatremia poses a risk of cerebral edema rather than preventing it; hypertonic saline would worsen the hypernatremia; and SIADH with fluid restriction is a cause of hyponatremia, not hypernatremia.