Hypernatremia pathophysiology

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

Overview

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.

Pathophysiology

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

Physiology of sodium regulation in the body:

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.

Determinants of plasma sodium concentration:

  • 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

References

  1. Agrawal V, Agarwal M, Joshi SR, Ghosh AK (December 2008). "Hyponatremia and hypernatremia: disorders of water balance". J Assoc Physicians India. 56: 956–64. PMID 19322975.
  2. Guillaumin J, DiBartola SP (March 2017). "A Quick Reference on Hypernatremia". Vet. Clin. North Am. Small Anim. Pract. 47 (2): 209–212. doi:10.1016/j.cvsm.2016.10.002. PMID 28164834.
  3. Hardy RM (March 1989). "Hypernatremia". Vet. Clin. North Am. Small Anim. Pract. 19 (2): 231–40. PMID 2648664.
  4. Kasai CM, King R (April 2009). "Hypernatremia". Compend Contin Educ Vet. 31 (4): E1–6, quiz E7. PMID 19517406.
  5. Marks SL, Taboada J (May 1998). "Hypernatremia and hypertonic syndromes". Vet. Clin. North Am. Small Anim. Pract. 28 (3): 533–43. PMID 9597713.
  6. Manning AM (November 2001). "Electrolyte disorders". Vet. Clin. North Am. Small Anim. Pract. 31 (6): 1289–321, vii–viii. PMID 11727338.



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