Elevated serum sodium concentration due to sodium retention and/or water loss, or failure to replace water loss. Water loss is most often due to dehydration, gastrointestinal fluid depletion (vomiting, diarrhea), excessive sweating, evaporation, urination, impairment of thirst regulators, osmotic diuresis, untreated central or nephrogenic diabetes insipidus, drug-induced reactions (mannitol, diuretics, laxatives) or due to seizures, burns, or excessive exercise (water loss into cells).

Sodium overload or retention may be due to administration or intake of hypertonic sodium solutions (most commonly IV fluid administration, but also therapeutic abortion or enema use) or salt poisoning. Other causes may be Cushing syndrome, adipsia, hypodipsia, lactic acidosis, azotemia, and primary hyperaldosteronism.

Patients most vulnerable are the elderly, young children, and critically ill or impaired who are unable to monitor and modify their fluid intake, or may inadvertently substitute salt for sugar.

Acute hypernatremia can be asymptomatic, but severe cases are characterized by neurological signs, from lethargy, irritability, and weakness to muscular tics, seizures, and coma. Severe hypernatremia can lead to life-threatening brain volume depletion, cerebral vein rupture, and hemorrhage. Drastic loss of blood volume can lead to complications of hypovolemic shock, characterized by cyanosis, tachycardia, confusion, agitation, cold or clammy hands and feet, and anuria.

Pediatric hypernatremia is often mild and may be due to gastroenteritis (vomiting, diarrhea, anorexia) leading to dehydration. Signs and symptoms include restlessness, irritability, weakness, vomiting, muscle twitching, and fever. Infants may present with tachypnea and a high-pitched cry. Lack of fluid replacement can lead to volume depletion, and more severe hypernatremia may present with lethargy and altered mental status. Seizures and coma can occur, and as fluid exits the brain cells, cerebral contraction progresses with the threat of cerebral and subarachnoid hemorrhage.

Management primarily involves calculation of the free water deficit in the patient and repletion of this over a period of 24-48 hours.