Sodium is the primary determinant of total serum osmolality.
Defined as a plasma sodium concentration greater than 145 mEq per liter and represents an increase in the quantity of sodium relative to the volume of water in the extracellular fluid.
Refers to an elevated sodium level in the blood.
Hypernatremia is generally not caused by an excess of sodium, but rather by a relative deficit of free water in the body.
It is most commonly caused by a loss of hypotonic fluids and results in the hypovolemic or euvolemic state, depending upon the amount of sodium intake.
Extra kidney loss of hypotonic fluid through sweating, hyperventilation, vomiting, osmotic diarrhea causes excretion of low volume of concentrated urine.
A common electrolyte disorder encountered in the hospital.
Hypernatremia often coincides with dehydration.
Water is lost from the body by perspiration, imperceptible losses from breathing, and in the feces and urine.
All forms of hypernatremia are associated with in-hospital mortality.
Independently associated with in hospital mortality, prolongation of length of stay, and discharge to a short/long term care facility.
In unselected hospitalized patients mortality associated with serum sodium of >142 mEquivalents per liter(Tsipotis E).
In the above study hypernatremia of greater than 142 mEquivalents per liter occurred in 21% of patients on admission, and in 11.7% of those it worsened during the hospitalization.
If the amount of water ingested consistently falls below the amount of water lost, the plasma sodium level will lead to hypernatremia.
Rarely, hypernatremia can result from massive salt ingestion from drinking seawater or excessive amounts of a salty liquid.
A small rise in the plasma sodium concentration above normal results in a sensation of thirst to increase in free water intake, and correction of the abnormality.
An increase in plasma sodium level is sensed by osmoreceptors in the hypothhalomus, which causes a release of arginine vasopressin from the posterior pituitary and stimulates thirst.
Arginine vasopressin binds to the vasopressin 2 receptors in the kidney collecting ducts, leading water to flow from the tubular lumen to the surrounding interstitium, producing a small volume of concentrated urine.
Hypernatremia subsequently resolves with ingestion of water but can process if there is a defect in sensing thirst or in ability to obtain water, or both.
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.
Clinical manifestations of hypernatremia include: lethargy, weakness, irritability, neuromuscular excitability, and edema.
With severe elevations of the sodium level, seizures and coma may occur.
Severe symptoms are usually due to acute elevation of the plasma sodium concentration to above 157 mEq/L
Values above 180 mEq/L are associated with a high mortality rate.
Common causes of hypernatremia include:
Hypovolemia with inadequate intake of free water associated with total body sodium depletion.
Typically patients who are unable to take in water as their thirst dictates and also are sodium depleted.
Hypovolemia is the most common cause of hypernatremia.
Excessive losses of water from the urinary tract, which may be caused by glycosuria, or other osmotic diuretics.
Excessive losses of water leads to a combination of sodium and free water losses.
Water losses associated with extreme sweating.
Severe watery diarrhea
Euvolemic hypernatremia:
Excessive excretion of water from the kidneys caused by diabetes insipidus, which involves either inadequate production of the hormone vasopressin, from the pituitary gland or impaired responsiveness of the kidneys to vasopressin.
Intake of a hypertonic fluid with restricted free water intake can occur after a vigorous resuscitation where a patient receives a large volume of a concentrated sodium bicarbonate solution.
Ingesting seawater causes hypernatremia because seawater is hypertonic and free water is not available.
Mineralcorticoid excess due to a disease state such as Conn’s syndrome usually does not lead to hypernatremia unless free water intake is restricted.
Treatment is administration of free water to correct the relative water deficit, and it can be replaced orally or intravenously.
Water can be given with addition to dextrose or saline infusion solutions.
Rapid correction of hypernatremia is potentially very dangerous as the brain adapts to the higher sodium concentration.
The rapidly lowering of sodium concentration with free water causes water to flow into brain cells and causes them to swell.
Cerebral edema, mat precipitate seizures, permanent brain damage, or death.
Defined as a rise in serum sodium concentration to a value exceeding 145 mmol/L.
Strictly defined as a hyperosmolar condition caused by a decrease in total body water relative to electrolyte content.
In both community-acquired and hospital-acquired hypernatremia even mild hypernatremia is associated with adverse outcomes.
Hypernatremia is a water problem, not one of sodium homeostasis.
Patients that develop hypernatremia outside of the hospital are generally elderly with mentally and physically impaired, often with an acute infection.
Hospitalized patients who develop hypernatremia during have an age distribution similar to that of the general hospital population.
Caused by impaired thirst and/or restricted access to water, often exacerbated by pathologic conditions with increased fluid loss.
The development of hyperosmolality from the water loss can lead to neuronal cell shrinkage and resultant brain injury.
Loss of volume can lead to circulatory problems such as tachycardia, and hypotension.
The best initial evaluation test in hypernatremia is urinary osmolality.
At a serum sodium level above 150 mmol/l, urinary osmolality would be expected to be greater than 800 mOsm/kg per kilogram and often greater than 1000 mOsm/Kg with coexisting hypovolemia.
Dilute urine in the setting of hypernatremia suggest the presence of diabetes insipidus.
Serum arginine vasopressin is helpful to distinguish between central diabetes insipidus and peripheral diabetes insipidus.
Acute hypernatremia of less than 48 hours can be rapidly corrected by decreasing sodium by 1-2 mmol per liter per hour until normalized.
Chronic hypernatremia or hypernatremia of unknown duration must be corrected more slowly, with a maximum correction goal of a decrease in serum sodium of no greater than 10 mmol per liter in 24 hours.
Intravenous correction with normal saline is inadequate to correct hypernatremia, particularly if there is ongoing free water losses.
1% of nursing home residents.
Of nursing home patients requiring hospitalization more than 30% have hypernatremia.