Hypernatremia

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Feham Tariq, MD [2]

In 1858, Claude Bernard, French physiologist first proposed a direct relationship between the central nervous system and renal excretion of osmotically active solutes. In 1913, Jungmann and Meyer in Germany induced polyuria and increased urinary salt excretion in animals through medullary lesion. In 1950, Peters, Welt, and co-workers described few patients with encephalitis, hypertensive intracranial hemorrhage, and bulbar poliomyelitis who presented with severe dehydration and hypernatremia.

The historical perspective of hypernatremia is as follows:^[1][2][3][4]

• In 1858, Claude Bernard, French physiologist first proposed a direct relationship between the central nervous system and renal excretion of osmotically active solutes.
• In 1913, Jungmann and Meyer in Germany induced polyuria and increased urinary salt excretion in animals through medullary lesion.
• in 1950, Peters, Welt, and co-workers described few patients with encephalitis, hypertensive intracranial hemorrhage, and bulbar poliomyelitis who presented with severe dehydration and hypernatremia.

• In 1952, Welt and colleagues presented patients with cerebral lesions (including trauma, tumor, and infection) and severe hypernatremia with clinical dehydration but no potassium retention.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Feham Tariq, MD [2]

Sodium regulation is key to maintain normal cellular function. The kidney is a major organ involved in sodium and water balance. Once water loss is excessive or sodium intake is high, sodium levels go up. However, osmoreceptors in our hypothalamus detect alterations in plasma osmolarity and stimulate the thirst response and the secretion of vasopressin (the antidiuretic hormone (ADH) in order to restore the body’s fluid balance. As a result, hypernatremia is seen when our body’s defense against hyperosmolarity becomes overwhelmed or defective.

The pathophysiology of hypernatremia is as follows:^{[1][2][3][4][5][6]}

• Hypernatremia can develop in the body via three main mechanisms:
  • Water losses from the body are not replaced
  • Urge to drink is impaired
  • Intake of salt without water
  • Administration of hypertonic sodium solutions

The regulation of sodium in the body is as follows:

• The osmolality of the plasma is determined mailny by the sodium concentration in the extracellular fluid.
• The term “effective osmolality” also known as “tonicity” essentially means the activity of solutes that cannot cross the cell membrane, manage the transcellular distribution of water and and therefore determine the tonicity of the plasma.
• Water is lost from the body in a variety of ways such as perspiration, insensible losses from breathing and in the feces and urine.

• If the amount of water ingested consistently falls below the amount of water lost, the serum sodium level will begin to rise, leading to hypernatremia.
• Rarely, hypernatremia can result from massive salt ingestion, such as may occur from drinking seawater.
• The kidney has concentrating mechanisms that prevent hypernatremia. Once the kidney’s function is impaired due to any cause, thirst becomes the main defense mechanism that prevents hypernatremia unless it is dysfunctional or access to water is limited (most often occurs in people such as infants, those with impaired mental status, or the elderly, who may have an intact thirst mechanism but are unable to ask for or obtain water).
• The hyperosmolarity caused by the high serum sodium concentrations drives water out of the cells.
• The most sensitive organ to this water shift is the brain where the neurons and other cells become dehydrated and are responsible for the neurologic symptoms associated with hypernatremia.
• Thirst is the main regulatory force that impedes hypernatremia.
• Consequently, hypernatremia above 150 mEq/l is very rare in alert patients and those who have access to free water who increase their water intake to match water loss.

• As water moves freely across most cell membranes, solute concentrations in the extracellular and intracellular fluids must be equal.
• Due to the presence of Na-K-ATPase, which pumps sodium out of cells in exchange for potassium, sodium is largely extracellular, and potassium is intracellular.
• The relationship between the plasma sodium concentration, body electrolyte and water contents is described by the following simple equation, where Na is sodium, K is potassium and TBW is total body water:

Plasma Na concentration = Total body (Na + K)/TBW

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Feham Tariq, MD [2]

Hypernatremia can be caused by many disease processes and drugs. Free water loss is the most important mechanism leading to sodium excess. Diarrhea, diabetes insipidus, diuretics, osmotic agents, insensible losses or impaired thirst response due to any disease process affecting the hypothalamus are common causes. Primary sodium excess is a rare cause of hypernatremia and ca be due to sodium salt ingestion or minaralocorticoid excess.

Hypernatremia can result from water loss (most common) or sodium retention (rare).

• Inadequate intake of water: typically in elderly or otherwise disabled patients who are unable to take in water as their thirst dictates. This is the most common cause of hypernatremia. Hypothalamic disorders can lead to impairement of the thirst mechanism (primary hypodipsia, essential hypernatremia caused by the loss of the hypothalamic osmoreceptor function (the plasma osmolarity sensor that stimulates thirst once the plasma is hyperosmolar))
• Renal loss: Inappropriate excretion of water, often in the urine, which can be due to medications like diuretics or lithium or can be due to a medical condition called diabetes insipidus. Osmotic diuresis can occur when osmotically active substances are present in large amounts in the plasma (glucose, [[urea, mannitol, etc)
• GI loss: osmotic diarrhea (infectious, malabsorptive, lactulose intake)
• Insensible losses: excessive sweating in the context of exercise or warm climate
• Water loss into cells: seizure, severe exercise, rhabdomyolysis

• Intake of a hypertonic fluid (a fluid with a higher concentration of solutes than the remainder of the body). This is relatively uncommon, though it can occur after a vigorous resuscitation where a patient receives a large volume of a concentrated sodium bicarbonate solution. Ingesting seawater also causes hypernatremia because seawater is hypertonic.
• Mineralcorticoid excess due to a disease state such as Conn’s syndrome or Cushing’s Syndrome.

• Diarrhea
• Vomiting
• Inappropriate IV fluids
• Renal failure
• Diuretics

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aida Javanbakht, M.D.

Hypernatremia must be differentiated among diseases that cause hypernatremia.

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The incidence of hypernatremia in hospitalized patients is approximately 3-5 per 100,000 individuals worldwide. The prevalence of hypernatremia in critically ill patients is approximately 9-26 per 100,000 individuals. Hypernatremia commonly affects older age.

• The incidence of hypernatremia in hospitalized patients is approximately 3-5 per 100,000 individuals worldwide.

• The prevalence of hypernatremia in critically ill patients is approximately 9-26 per 100,000 individuals.

• Hypernatremia commonly affects older age.

• There is no racial predilection to hypernatremia.

• Hyperntremia affects men and women equally.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Feham Tariq, MD [2]

The patients at risk of developing hypernatremia are more likely to be hospitalized, elderly patients with neurological deficits and having higher rate of free water insensible losses such as burn victims and patients with diarrhea.

The patients at risk of developing hypernatremia are more likely to be hospitalized, elderly patients with neurological deficits and having higher rate of free water insensible losses such as burn victims and patients with diarrhea.

The more common risk factors of hypernatremia are as follows:^[1][2]

• Elderly patient
• Impairment of thirst
• Restricted access to water
• Mental impairment
• Physcial impairment
• Uncontrolled diabetes (solute diuresis)

The less common risk factors of hypernatremia are as follows:

• Tube feedings
• Hypertonic infusions
• Mechanical ventilation
• Osmotic diuresis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Feham Tariq, MD [2]

If left untreated, [#]% of patients with [disease name] may progress to develop [manifestation 1], [manifestation 2], and [manifestation 3].

OR

Common complications of [disease name] include [complication 1], [complication 2], and [complication 3].

OR

Prognosis is generally excellent/good/poor, and the 1/5/10-year mortality/survival rate of patients with [disease name] is approximately [#]%.

• Common complications of hypernatremia include:^[1]
  • Subarachnoid hemorrhage
  • Cerebral bleeding
  • Brain cells shrinkage leasding to permanent loss of brain function
  • Convulsions

• The prognosis of hypernatremia is good as long as the underlying cause is identified early before the onset of complications and treated early.

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