Hypernatremia pathophysiology

; Associate Editor-In-Chief: ; Assistant Editor(s)-In-Chief: Jack Khouri

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 is overwhelmed or defective.

Pathophysiology
Water is lost from the body in a variety of ways, including 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 hypenatremia 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.

As discussed before, thirst is an essential process 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.