+++
TEXTBOOK PRESENTATION
++
Patients with hypernatremia due to inadequate water ingestion usually have an altered neurologic status or physical disability. A superimposed illness may worsen cognitive function, decrease oral intake, and promote hypernatremia. Mental status is almost always impaired and may vary from confusion to frank coma.
+++
EVIDENCE-BASED DIAGNOSIS
++
The diagnosis is easily confirmed by the presence of hypernatremia, increased urine osmolality, and absence of hyperglycemia.
++
The brain adapts to hypernatremia by increasing intracellular osmolality to minimize cellular dehydration.
Rapid correction of hypernatremia makes the serum hypotonic relative to the brain. This promotes osmotic movement of water into the brain and cerebral edema. Seizures and death can occur if correction is too rapid, although this occurs almost exclusively in children.
Hypernatremia should be corrected slowly ≅ 0.4 mEq/L/h (≤ 10 mEq/L/day).
A recommended approach includes the following:
Normal saline to correct the patient’s concomitant volume deficit
Hypernatremic patients are usually markedly hypovolemic. If hypotensive, they may be 10% dehydrated (7L in a 70-kg man).
Often patients will take several 1-liter boluses to improve BP, resolve orthostasis, and improve urinary output.
Normal saline boluses commonly administered as 500–1000 mL over 1 hour
Patients should be reevaluated after each bolus. Vital signs and orthostasis should be rechecked, and patients should have a careful heart and lung exam to ensure they are not receiving excessive fluid. Urinary output should be monitored.
Once BP and urinary output are restored, boluses can be stopped and the remaining fluid deficit divided over the next 48 hours.
D5W @ 1.35 mL/hour/kg should be administered to restore the free water deficit and correct hyponatremia by < 10 mEq/L/day.
Add ongoing free water losses, if any.
Remeasure serum sodium frequently (every 4–6 hours) to ensure rate is neither too excessive nor too slow.