Hypernatremia is a medical condition characterized by high sodium level measuring above 145mmol/L in the blood. This is the most common type of electrolyte imbalance in the United States. The most common cause of hypernatremia is deficiency of free water. Thus the term dehydration is often loosely used interchangeably with hypernatremia. Dehydration occurs because of excessive water loss following severe diarrhea, vomiting, heavy perspiration or inadequate water intake usually seen in infants and elderly person. Hypernatremia can rarely occur due to excessive ingestion of sodium like with drinking large amounts of sea water. Replacement of deficient free water usually intravenously and management of underlying causes are the mainstay of treatment.
In many cases the presenting symptoms are not easily identifiable, even in cases of severe high level of serum sodium. The common symptoms are :
- Altered mental status characterized by :
– Altered consciousness
– Ultimately coma
- Epileptic fits
- Muscle cramps
- Nausea and vomiting
Dehydration is the main cause for hypernatremia therefore symptoms of dehydration often co-exist. These include :
- Low urine volume
- Dryness of oral mucosa and tongue
- Drying of eyes because of less tear production
- Loss of skin elasticity
- Increased heart rate
- Low blood pressure
Sodium is the predominant extracellular electrolyte. During hypernatremia osmolality of plasma is increased leading to a hyperosmolar state. Maintenance of both normal sodium level and plasma osmolality is regulated by adequate water intake and water excretion, achieved through thirst and urine concentrating ability of the kidney under influence of anti diuretic hormone (ADH).
Adequate secretion and action of ADH is responsible for production of adequately concentrated urine. ADH is synthesized in the supraoptic and paraventricular nuclei of the hypothalamus and transported to the posterior pituitary gland which secretes the hormone. Rise in plasma osmolality leads to increased secretion of ADH, which inserts water channels in the renal collecting duct and enabling the otherwise water impermeable renal collecting ducts freely permeable to water. Therefore there is production of concentrated urine, maintenance of plasma osmolality and correction of hypernatremia.
To correct hypernatremia and associated plasma hyperosmolality body shifts water from inside of the cell to outside. This particularly leads to shrinkage of brain cells. Brain cells compensate this loss of volume by increasing other intracellular electrolyte, amino acids and methylamines. Therefore rapid correction of hypernatremia by rapid intravenous fluid replacement may lead to brain cell damage due to swelling of the cells.
Hypernatremia can be associated with :
- Low water level (hypovolemic) : inadequate water intake, excessive loss as in diarrhea, vomiting or profuse sweating
- Normal water level (euvolemic): diabetes insipidus
- Excessive water level (hypervolemic): intake of large amount of sea water
- Infants, elderly and mentally challenged persons
- Severe burns
Thirst is one of effective defensive mechanisms of the body to avoid hypernatremia. Thirst centers (osmoreceptors) are located in the anteroventral hypothalamus. Plasma osmolality change even by 2% to 3% stimulates the osmoreceptors which increases water intake by the person and corrects the free water deficit and hypernatremia. Therefore drinking sufficient water, but in controlled amounts, can both prevent and treat hypernatremia.
The aims of treatment are :
- Correction of water deficit by oral or intravenous saline or dextrose infusion. Slow replacement is to done to avoid brain damage.
- Management of underlying diseases like ACE inhibitors in heart failure and corticosteroids in nephropathy (kidney disease).