Article Author:
Srividya Naganathan
Article Editor:
Mohammed Al-Dhahir
12/6/2017 12:32:49 AM
PubMed Link:


Sodium is the dominant cation in extracellular fluid and necessary for the maintenance of intravascular volume. The human body maintains sodium and water homeostasis by concentrating the urine secondary to the action of antidiuretic hormone (ADH) and increased fluid intake by powerful thirst response. These mechanisms to protect against developing hypernatremia are impaired in certain vulnerable populations and conditions with vasopressin deficiency or unresponsiveness at the renal tubular level. Hypernatremia is defined as a serum sodium concentration of greater than 145 meq/l.


The basic mechanisms of hypernatremia are water deficit and solute excess. Total body water loss relative to solute loss is the most common reason for developing hypernatremia. Hypernatremia usually is associated with hypovolemia, which can occur in conditions that cause combined water and solute loss, where water loss is greater than sodium loss, or free water loss. Combined loss can be seen in extra-renal conditions such as gastroenteritis, vomiting, prolonged suction, burns, and excessive sweating. Renal loss can be seen in chronic kidney disease, diabetes mellitus, post-obstructive diuresis, and with the use of osmotic diuretics. Free water loss is seen in central or nephrogenic diabetes insipidus (DI) and also in conditions with an increased insensible loss. Central DI is due to inadequate production of ADH, structural abnormalities, or acquired by autosomal dominant or recessive pattern. Nephrogenic DI is due to tubular unresponsiveness to the action of ADH and can be inherited in an X-linked pattern or secondary to a number of medications. Rarely, hypernatremia with inadequate fluid intake can be seen in breastfed babies, child or elder abuse, and in patients with an impaired thirst response. Excess sodium usually is iatrogenic and seen in the hospital setting but also can be associated with improper formula mixing, excess sodium bicarbonate ingestion, hyperaldosteronism, and seawater drowning.


Hypernatremia is primarily seen in infants and the elderly population. Infants receiving inadequate water replacement in the setting of gastroenteritis or ineffective breastfeeding are common scenarios. Premature infants are at higher risk due to their relatively small mass to surface area and their dependency on the caretaker to administer fluids. Patients with neurologic impairment also are at risk due to lack of communication of the thirst response to the caregiver. Hypernatremia can occur in the hospital setting due to hypertonic fluid infusions, especially when combined with the patient's inability for water intake.


Sodium is important to maintain ECF volume. Changes in the ECF volume provide feedback to maintain total sodium content by increasing or decreasing sodium excretion in the urine. Sodium excretion also involves regulatory mechanisms such as the renin-angiotensin-aldosterone systems. When serum sodium increases, the plasma osmolality increases and triggers an increase in thirst response and ADH secretion, leading to renal water conservation and concentrated urine.

History and Physical

Most patients present with symptoms suggesting fluid loss and clinical signs of dehydration. Symptoms and signs of hypernatremia are secondary to central nervous system dysfunction and are seen when serum sodium rises rapidly or is greater than 160 meq/L. Children present with irritability and agitation, which can progress to lethargy, somnolence, and coma. Other symptoms include increased thirst response in alert patients and high-pitched cry in infants. The skin can feel doughy or velvety due to intracellular water loss. Other findings include increased tone with brisk reflexes and myoclonus. It is important to remember that the degree of dehydration can be underestimated in children with hypernatremia due to a shift of water from the intracellular space to the extravascular space. The most serious complication of hypernatremia is brain hemorrhage, including subarachnoid or subdural hemorrhage due to rupture of bridging veins and dural sinus thrombosis. Hypernatremia is associated with a mortality rate as high as 15% to 20%.


The etiology of hypernatremia usually is evident based on the history and physical exam. Plasma volume, plasma osmolality, urine volume, concentrating ability, and osmolality can help to further differentiate between renal and extrarenal causes. In DI, the urine is inappropriately diluted with normal urine volume and urine osmolality less than the serum osmolality. When DI is suspected, a water deprivation test may be performed with administration of desmopressin. In central DI, desmopressin administration demonstrates an increase in urine osmolality, while in the nephrogenic variety, there is no response to desmopressin. In extrarenal causes, the body tries to conserve fluids with appropriately low urine volume, high specific gravity, and urine osmolality greater than serum osmolality.

Treatment / Management

Proper management of hypernatremia involves identifying the underlying condition and correcting the hypertonicity. The goal of therapy is to correct both the serum sodium and the intravascular volume. In patients with severe dehydration or shock, the initial step is fluid resuscitation with isotonic fluids before free water correction. Hypernatremia is corrected by calculating the free water deficit using one of the following formulas.

  • 0.6 (1-145/current sodium) x body weight
  • 4ml x body weight x (desired change in serum sodium meq/L)

It is important to remember that rapid correction of hypernatremia can lead to cerebral edema because water moves from the serum into the brain cells. The goal is to decrease the serum sodium by not more than 12 meq in a 24-hour period. Close serial monitoring of serum sodium every 2 to 4 hours is essential during the acute phase of correction. Seizures occurring during correction of hypernatremia is a sign of cerebral edema due to rapid shifts in osmolality, and the administration of hypotonic fluids should be halted. The estimated free water deficit should be corrected over 48 to 72 hours with a decrease in serum sodium not exceeding 0.5 meq per hour. Patients should be carefully monitored for the rate of correction, urine output, and ongoing loss. In cases of sodium intoxication, the free water requirement may be too large and cause volume overload, requiring the use of loop diuretics and, at times, peritoneal dialysis to remove excess sodium. Older children and adults with central DI may need desmopressin, which is available in intranasal and oral forms. Water intoxication and hyponatremia are adverse effects seen with the use of desmopressin.

Pearls and Other Issues

It is important to remember that hypernatremia should be corrected over 48 hours. Rapid correction can lead to cerebral edema and seizures.