by Adam George


  • Hypernatremia refers to a high blood sodium concentration. Hypernatremia can be classified as follows:
    • Acute (<48 hours) or Chronic (>48 hours)
    • Mild (146-149 mmol/L)
    • Moderate (150-169 mmol/L)
    • Severe (>170 mmol/L)
  • Sodium concentration is dependent not only on sodium levels but also on water levels in vivo. Water in the body exists either intracellularly or extracellularly, with approximately 13 of the body’s water being intracellular and 23 being extracellular.
    • Intracellular fluid is simply fluid within the cell, whereas extracellular fluid comprises fluid in blood vessels, lymphatic vessels, and the interstitial space.
  • Ordinarily both the intracellular and extracellular compartments have equivalent solute concentrations (osmolarity) enabling free movement of water between both spaces. However, they exhibit contrasting solute compositions. Intracellularly, the prevailing anions are phosphate and negatively charged proteins, and the most common cations are potassium and magnesium. Extracellularly, the prevalent anion is chloride, and the most common cation is sodium. It is sodium though that determines the balance of osmolarity. Sodium is continually in flux between both compartments and minute fluctuations in sodium concentration shift the balance of osmolarity, precipitating the movement of water. Fundamentally, water follows the migration of sodium.
  • In hypernatremia, a high extracellular sodium concentration (thus a high blood sodium concentration) can materialise either via the loss of more water than sodium, or the acquisition of more sodium than water. In both instances the result is the same – the extracellular sodium concentration is increased, and water is drawn out of the cell.
  • In protracted instances of sodium imbalance, the body can adapt via the intracellular production of sodium, preventing water loss due to osmosis. However, in acute scenarios adaptation is not possible and water flows out of the cell faster than it able to be replaced. This leads to crenation (shrivelling) of the cell and potential cell death.


  • For hypernatremia to occur there are then three possibilities.
    • Decreased intake of water
    • Increased excretion of water
    • Increased intake of sodium

Decreased Water Intake

  • Insufficient water intake: The most common cause of hypernatremia is inadequate intake of water. This is usually due to either water being unavailable (eg: lack of communication in paediatric or dementia patients), or impairment of the urge to drink (hypothalamic dysfunction).

Increased Water Loss

  • The hypothalamus: – via the kidneys – can be responsible for causing hypernatremia in several ways. After the nephrons produce urine, a portion of the water contained in the filtrate is reabsorbed in the distal convoluted tubule and the collecting duct. The amount of water reabsorbed is dictated by the hypothalamus. When dehydrated, the hypothalamus stimulates the release of ADH (also known as arginine vasopressin/AVP) from the posterior pituitary gland. ADH, in turn, acts on the receptors at the nephrons and triggers increased water uptake.
  • Central diabetes insipidus: Incapacitation of the hypothalamus’ functioning subverts the body’s ability to reabsorb water. This results in greater amounts of water lost through more dilute urine, and a consequently higher blood sodium concentration. En masse, this phenomenon is known simply as central diabetes insipidus.
  • Nephrogenic diabetes insipidus: Similarly, if hypothalamic function is normal, but the receptors at the nephrons are impaired the result is the same. Namely, higher urine osmolality and blood sodium concentration. Due to the issue originating renally this pathology is referred to as nephrogenic diabetes insipidus.
  • Diuretic use: (eg: thiazides) can precipitate hypernatremia through excessive water loss.
  • Burns: can cause systemic changes which promote a hypercatabolic state and carry an increased risk of water balance disorders.

Decreased Water Intake and Increased Water Loss Combined

  • Absence of the urge to drink: Moreover, if the lamina terminalis of the hypothalamus is damaged then the urge to drink can be destroyed. This damage in isolation begets hypernatremia due to lack water consumption. If there is widespread hypothalamic damage however, loss of the urge to drink can be combined with impairment of ADH secretion, precipitating both a lack of water intake and excessive water loss – a particularly precarious constellation.

Increased Sodium Intake

  • Excess sodium: Conversely, hypernatremia can be caused by accrual of excessive amounts of sodium. This most frequently occurs due to intravenous overcorrection of hyponatremia in the hospital setting, although a diet exceptionally high in salt could also eventually result in hypernatremia. In either instance, concurrent renal dysfunction is generally required to overwhelm the body’s ability to regulate sodium.


  • CNS dysfunction: The signs and symptoms of hypernatremia are usually associated with central nervous system (CNS) dysfunction. These include weakness, lethargy, confusion, irritability, altered speech, hyperreflexia, myoclonic jerks, spasticity, seizures, and coma.
  • Dehydration and hypovolemia: Hypernatremia related to reduced water intake/water loss can present with dry mucous membranes, reduced skin turgor, oliguria, tachycardia, and/or orthostatic hypotension.
  • Diabetes insipidus: When either form of diabetes insipidus (DI) is the cause of hypernatremia, classic symptoms and signs of DI are likely to be present including nocturia, polyuria, and polydipsia.



    • Serum osmolality (also urine osmolality if suspected DI)
    • Serum electrolytes (Na+, K+, Ca2+)
    • Urea
    • Creatinine
    • Glucose
    • Lithium levels (if appropriate – hypernatremia reduces excretion and increases toxicity risk)


    • Urine electrolytes (Na+, K+)
    • Urinary Na
    • Urine osmolality
  • Assessment of urine osmolality should focus upon determining whether intravascular volume is hypovolemic or euvolemic. In cases of hypovolemia, the body will attempt to retain water and sodium. Concentrated urine will be produced with urine osmolality usually >600 mOsm/kg and urinary sodium <20mmol/L. Kidney dysfunction or diuretic (eg: osmotic/loop) use can be indicated by urinary sodium >20mmol/L. Euvolemia generally illustrates the body endeavouring to jettison water, such as in DI, with expected urine osmolality <300mOsm/kg and urinary sodium <20mmol/L.


  • Treatment should always begin by correcting the underlying cause and redressing any fluid deficiency.
  • The safest method of fluid correction is oral, however, IV glucose 5% (no added Na+) may be necessary. Mild hypernatremia with an intact urge to drink may potentially be corrected via free access to water only.
  • Rapid correction of chronic hypernatremia must not be undertaken due to the risk of cerebral oedema.
  • Serum sodium concentration should be reduced by:
    • Not more than 0.5 mmol/L per hour
    • Not more than 10 mmol/L per 24 hours
  • Serum sodium should be monitored every 4 hours in the first 12-24 hours. The goal should be gradual reduction to a serum sodium concentration of approximately 145 mmol/L.

Additional considerations

  • DI with an impaired urge to drink is rare but can precipitate severe hypernatremia that is challenging to manage. The suggested treatment is full dosage of ADH combined with fastidious regulation of water intake to maintain normal serum sodium concentration.


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