Hypernatremia is an elevated serum sodium concentration > 145 mmol/L. Serum sodium is the greatest contributor to plasma osmolality, which is very tightly controlled by the hypothalamus via the thirst mechanism and antidiuretic hormone (ADH) release. Hypernatremia occurs either from a lack of access to water or an excessive intake of sodium. The total volume of water lost (usually via GI or renal routes) is regained through normal oral intake. Therefore, if a patient has access to water and an intact thirst mechanism, many etiologies of hypernatremia may remain hidden. The etiology of hypernatremia is often easily determined by clinical history. Treatment is primarily a replacement of the free water deficit by IV or oral routes.

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Water Regulation

Water regulation is controlled by the interplay between the osmoreceptors in the hypothalamus and the response to antidiuretic hormone (ADH) in the kidneys, resulting in very tight control of serum sodium and plasma osmolality.

Hypothalamic osmoreceptors

  • Detect changes in water balance as a result of changes in plasma osmolality:
    • ↑ Water intake causes ↓ plasma osmolality (↓ serum sodium) → ↓ ADH release and ↓ thirst
    • ↓ Water intake causes ↑ plasma osmolality (↑ serum sodium) → ↑ ADH release and ↑ thirst
  • Maintain the plasma osmolality very tightly: 
    • ADH levels are minimal when plasma osmolality is normal (280–290 mmol/L).
    • ADH increases linearly in response to very small changes in plasma osmolality.

Response to ADH in the kidney

  • Aquaporin channels are the target of ADH:
    • Allows water to move from the tubular fluid into the renal medulla via diffusion
    • The renal medulla is hypertonic (due to the thick ascending limb and distal convoluted tubule).
  • ADH stimulates the production and insertion of aquaporin channels in the collecting duct:
    • High ADH levels → maximal levels of water reabsorption → concentrated urine
    • Low ADH levels → minimal levels of water reabsorption → dilute urine
Plasma Osmolality

Plasma osmolality and antidiuretic hormone (ADH): graph illustrating the relationship between the plasma osmolality of ADH release

Image by Lecturio.


Etiologies of hypernatremia are organized according to volume status.

Hypervolemic hypernatremia

  • Gain of more sodium than water
  • Excessive intake of sodium:
    • Infusion of isotonic saline, hypertonic saline, or sodium bicarbonate solutions
    • Oral ingestion of salt tablets (i.e., for the treatment of hyponatremia)
    • Salt poisoning (i.e., excessive oral ingestion of table salt)
  • Aldosterone mediated:
    • Primary hyperaldosteronism
    • Cushing’s syndrome

Euvolemic hypernatremia

  • Loss of water only
  • Diabetes insipidus (DI) (both central and nephrogenic)
  • Lack of access to water:
    • Infants
    • Elderly
    • Altered mental status
    • Dementia
    • Mechanically ventilated patients
    • Restrained patients
  • Impaired thirst mechanism (elderly)

Hypovolemic hypernatremia

  • Loss of more water than sodium
  • GI losses:
    • Diarrhea
    • Vomiting
    • Nasogastric tube drainage
  • Diuretics 
  • Osmotic diuresis: 
    • Hyperglycemia
    • Mannitol
    • Elevated urea from excessive tube feeding
    • Recovery from AKI
  • Increased insensible water loss (i.e., sweat or burns)

Clinical Presentation

The primary clinical finding in hypernatremia is thirst. If the patient is unable to ingest enough water to keep their serum sodium from rising significantly, dehydration and neurologic findings may also occur. The severity of neurologic findings depends on the acuity and magnitude of the hypernatremia.

Acute hypernatremia

  • Onset < 48 hours
  • More likely to be symptomatic (due to less time for brain adaptation)
  • Less severe increases in serum sodium are needed to induce symptoms.

Chronic hypernatremia

  • Onset > 48 hours
  • Less likely to be symptomatic (due to adequate time for brain adaptation)
  • More severe increases in serum sodium are needed before symptoms will appear.

Mild symptoms

  • Headache
  • Anorexia
  • Nausea
  • Vomiting

Severe symptoms

  • Lethargy
  • Confusion
  • Neuromuscular irritability
  • Seizures
  • Coma


In most cases, the etiology of hypernatremia will be clear and treatment can be initiated without any further testing. If the diagnosis is not clear, the following steps may be helpful:

  1. Quickly identify acute causes and very severe cases.
    • Examples of acute causes: salt poisoning, DI patients without free access to water
    • Example of a very severe case: Na > 160 mmol/L
    • If acute, urgent and aggressive treatment is warranted.
    • If severe but not necessarily acute, prioritize urgent treatment over definitive diagnosis.
  2. Identify reversible factors.
    • Access to water/altered mental status (most likely lower the IV replacement rate once restored)
    • Ongoing losses: Address any other factors to limit further free water replacement needs.
  3. Etiology unknown and only mild hypernatremia?
    • Consider aldosterone-mediated causes. 
    • Cushing’s syndrome diagnosis: Check late-night salivary cortisol, 24-hour urine-free cortisol, and/or an overnight dexamethasone suppression test.
    • Primary hyperaldosteronism diagnosis: Check plasma renin and aldosterone.
  4. Etiology unknown and not aldosterone-mediated?
    • Measure urine osmolality.
    • Urine osmolality < 300 mOsm/kg (< plasma osmolality): DI
      • Give desmopressin (same as ADH).
      • Urine osmolality increases: central DI
      • No change in urine osmolality: nephrogenic DI
    • Urine osmolality indeterminate (300–600 mOsm/kg): DI vs. osmotic diuresis
      • Check the response to desmopressin to diagnose possible DI.
      • Check total solute load to assess for osmotic diuresis.
    • Urine osmolality > 600 mOsm/kg (usually nonrenal water loss (i.e., diarrhea)):
      • Note: high urine osmolality represents the appropriate response by the kidneys to high plasma osmolality in hypernatremia


General considerations

Hypernatremia is treated by replacing the free water deficit by giving a hypotonic solution (i.e., 5% dextrose in water IV). Management is generally empirical with frequent monitoring of the serum sodium and adjustment of the fluid rate.

Volume status considerations:

  • If hypotensive (hypovolemic):
    • Give isotonic fluids to improve blood pressure.
    • After blood pressure rises, switch to hypotonic fluids to address hypernatremia.
  • If DI (euvolemic):
    • Give hypotonic fluids to correct hypernatremia.
    • Resume or start desmopressin to maintain normal serum sodium. 
  • If aldosterone mediated (hypervolemic):
    • May only need free access to oral hypotonic fluids (hypernatremia should be mild)
    • Treat the underlying condition.

Management according to acuity

Acute hypernatremia:

  • Uncommon (only occurs in specific situations):
    • Salt poisoning
    • DI without appropriate compensatory water intake 
    • Severe hyperglycemia without appropriate compensatory water intake 
  • Identify quickly due to the need for prompt and aggressive management.
  • Goal: Replace 100% of the free water deficit within the 1st 24 hours.
  • 5% dextrose in water IV to start
  • Monitor serum sodium closely and adjust the fluid rate as needed:
    • Initially monitor serum sodium and decrease fluid rate once serum sodium < 145 mmol/L.
    • The goal is a decrease in serum sodium by 1–2 mEq/L/hour and a complete correction within 24 hours.

Chronic hypernatremia: 

  • Vast majority of hypernatremia
  • Goal: Decrease serum sodium by 10 mEq/L/day (roughly 0.5 mEq/L/hour) until normal. 
  • 5% dextrose in water IV to start
  • Oral free water is an option if hypernatremia is not severe.
  • Monitor serum sodium and adjust the rate as needed.
  • Overcorrection rarely causes clinical problems in adults but does in infants and children.


An acute rise in tonicity results in abrupt movement of fluid out of the brain. A slow rise in tonicity allows the brain to adapt and minimize the effect of fluid shifts. An overly rapid correction of hypernatremia could result in abrupt movement of fluid into the brain and cause cerebral edema.

Acute hypernatremia

  • Sudden rise in plasma tonicity → rapid shift of water out of the brain
  • The brain essentially shrinks in volume.
  • If severe enough, the shrinking can tear the brain’s blood vessels → intracranial hemorrhage and death

Chronic hypernatremia

  • Slower rise in plasma tonicity → slower shift of water out of the brain
  • The brain responds with adaptive mechanisms to counter the water shift:
    • Takes about 48 hours: the distinction between acute (< 48 hours) and chronic (> 48 hours) hypernatremia
    • Net effect is a much smaller loss of brain volume → no tearing of vessels
    • Does not, however, stop other symptoms from occurring (i.e., lethargy, confusion)

Overcorrection of acute hypernatremia

  • Does not commonly cause clinical problems in adults
  • Does commonly cause clinical problems in children and young adults (i.e., < 40 years old) with severe hyperglycemia (i.e., diabetic ketoacidosis)
  • Severe hyperglycemia results in glucose contributing a significant amount to hypertonicity.
  • Plasma osmolality and serum glucose must be monitored very closely during treatment to prevent cerebral edema:
    • Goal: decrease in plasma osmolality by < 3 mmol/kg/hour
    • Goal: decrease in blood glucose by 50–75 mg/dL/hour

Overcorrection of chronic hypernatremia

  • Water will always shift back into the brain as hypernatremia improves.
  • If the water shift occurs too abruptly, cerebral edema and/or osmotic demyelination syndrome can occur.
  • In practice, complications from hypernatremia overcorrection in adults are extremely rare:
    • Goal for adults: Decrease serum sodium by approximately 10 mEq/L/day.
    • Because overcorrection is not detrimental, therapeutic reraising of serum sodium is not recommended if the target is exceeded.
  • Overcorrection is a common clinical problem with children and young adults:
    • Smaller skull volume → less margin for error if the brain shrinks or swells
    • Much closer monitoring of treatment is needed.
    • Goal for children and young adults: Decrease serum sodium by < 0.5 mEq/L/hour and < 10–12 mEq/L/day.


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