Hyponatremia and Hypernatremia
| Title: | Hyponatremia and Hypernatremia |
|---|---|
| Authors: | Fried, M.D., Linda F.; Palevsky, M.D., Paul M. |
| Publisher: | Medical Clinics of North America |
| Date Published: | May 01, 1997 |
| Reference Number: | 160 |
Hyponatremia and hypernatremia are common electrolyte disorders resulting from disorders in water homeostasis. Hyponatremia usually results from defects in free water excretion, although increased intake may also contribute. The treatment of hyponatremia has been controversial because of the high associated morbidity and mortality and the observation that rapid correction of hyponatremia is associated with the development of central pontine myelinolysis. Mild hyponatremia should be treated with water restriction alone, whereas severe acute or symptomatic hyponatremia should initially be corrected rapidly until symptoms resolve followed by more gradual correction. In all cases, treatment should be individualized on the basis of severity, cause, and duration of the hyponatremia. Hypernatremia results from impaired water ingestion, although increased water losses are often contributory. Hospital-acquired hypernatremia is usually iatrogenic because of inadequate water prescription and is therefore preventable. Hypernatremia is also associated with high morbidity and mortality, both as a result of the underlying disease and inadequate treatment. The primary treatment of hypernatremia is water replacement-repleting water deficits and replacing ongoing losses. Additional treatment should be directed at eliminating excess water losses.
This translation by the NDI Foundation is to assist the lay reader. To provide a clear, accessible interpretation of the original article, we eliminated or simplified some technical detail and complicated scientific language. We concentrated our translation on those aspects of the article dealing directly with NDI. The NDI Foundation thanks the researchers for their work toward understanding and more effectively treating this disorder.
© Copyright NDI Foundation 2007 (JC)
Osmolality is a measure of the ratio of osmotically active solute content to water content. If the total amount of body water changes without an accompanying change in total body solute, the ratio of solute to water changes, which is to say the body's plasma osmolality changes. If the level of body water decreases in relation to the solutes, then the result is hypernatremia, too high a concentration of salt in the blood plasma. If the body water level increases while the solute level remains the same, then the result is hyponatremia, too low a concentration of sodium in the blood plasma. Again, both these disorders are the result of alterations in body water balance.
Normally, the body keeps its body water in a stable, balanced state: water intake and excretion are matched. Thirst is triggered by the body in response to body fluid osmolality and the volume of fluid outside the cells. Thirst receptors in the brain stimulate thirst as body fluid osmolality rises above a certain threshold.
Water loss occurs through the skin, respiratory and gastrointestinal tracts, and mostly through the kidneys. The kidney regulates the amount of water it excretes in response to changes in serum (the cell-free part of the blood), osmolality, and the effective volume of blood in the arteries. Though normally we may think of the kidney primarily in terms of water loss through urination, the kidney is actually the main defense against water depletion.
Each kidney has about a million tiny units called nephrons, which are a combination of a filter, called a glomerulus, and a little tube called a tubule. The tubule has different segments. The proximal segment is the part closest to the glomerulus. The distal segment is the part furthest from the glomerulus. In-between the proximal and distal segments of the tubule is a long, u-shaped segment called Henle's loop.
Daily, about 150 liters of fluid pass through the glomeruli. The proximal tubule reabsorbs about two-thirds of this fluid. This increases to more than 80% when there is a depletion of the effective arterial volume. In the descending part of Henle's loop more water is absorbed while solute is retained. In the ascending portion of Henle's loop and the distal tubule electrolytes (which are solutes) are reabsorbed.
The tubules drain into the kidney's collecting duct and their water reabsorption is regulated by the antidiuretic hormone, vasopressin (VP). VP is synthesized, stored and secreted from the hypothalamus. When VP secretion is suppressed, the water permeability of the collecting duct is low, so a higher than normal solvent/solute ratio remains in the duct and it is excreted as dilute urine. This means the body is losing more water than it should, causing, among other things, excessive sodium in the blood. When VP secretion is stimulated, the water permeability of the kidney collecting duct is high, permitting water reabsorption and the excretion of concentrated urine (i.e., urine with a relatively high solute to water ratio). VP, then, mediates water reabsorption of the collecting duct and thus regulates urine osmolality. And thus the kidney plays a part in processing body water and maintaining water balance through the osmotic processes that occur in its nephrons and its ability to respond to the antidiuretic hormone, VP.
VP binds to vasopressin-2 receptors (V2Rs) located in specific parts of the collecting duct cells. Binding to the V2R activates adenylate cyclase, which in turn increases the concentration of an important metabolic regulator called cAMP. cAMP initiates a process which results in specific water-transporting proteins called aquaporin-2 (AQP2) inserting themselves in collecting duct cells to make the duct cells more permeable than usual so they can reabsorb the body water.
Normally, the kidney's capacity to excrete water is much greater than water intake. Hyponatremia results when water intake exceeds water excretion. Hyponatremia primarily results from hypotonicity of body fluids, which means body water has a low solute-to-water ratio and as it bathes the body cells it causes a net flow of water across the semipermeable cell membrane into the cell. This produces cell swelling, which, especially in the brain, can be dangerous. Although hypotonicity is always associated with hyponatremia, hyponatremia can also be seen in cases in which the serum osmolarity is normal or high. Careful diagnosis for these types of hyponatremia is important, as they require different types of treatment than normal.
Hypernatremia is generally caused when a person doesn't take in enough water. It is generally accompanied by a hypertonic state where there is a higher solute to solvent ratio that causes a net outflow of water from the cell leading to cell shrinkage. Lack of water causes the serum osmolality to rise and this creates an intense thirst. This thirst provides the ultimate defense against hypernatremia. Sometimes a person's thirst mechanism is defective, or sometimes people are unable to provide themselves with adequate water intake. Diabetes insipidus (DI) is another cause of hypernatremia. DI can result from deficient VP secretion by the hypothalamus. It can also result when there is sufficient VP but the kidneys don't respond to it. Remember, kidney water excretion is under the direct control of VP and when it is undersupplied or ignored the kidney collecting duct cells remain impermeable to water so water can't be reabsorbed and is excreted as dilute urine. People with DI suffer from chronic, excessive passage of large amounts of urine (polyuria) and can excrete up to 20 liters a day.
Both hyponatremia and hypernatremia are tolerated better in their chronic rather than their acute states. The symptoms of acute hyponatremia include nausea, headache, confusion, agitation and incontinence, and in very acute cases, seizures, coma, respiratory arrest and, sometimes, death. Symptoms of chronic hyponatremia are milder: confusion, lethargy and a general feeling of illness or depression.
There is no clear agreement on the best treatment for hyponatremia. Some maintain that the disorder must be treated quickly to avoid neurological damage. And some maintain that rapid correction can cause neurological damage. The most recent information suggests that mild hyponatremia should be treated with water restriction alone, whereas the severe acute form should initially be corrected rapidly until symptoms resolve, followed by a more gradual correction. In any case, the treatment of hyponatremia must be individualized by taking into account its cause, magnitude, duration and symptoms.
The symptoms of hypernatremia are nonspecific and relate to cellular dehydration, especially in the brain. The hypertonicity that accompanies hypernatremia causes a net outflow of water outside the cells, and the cells shrink. There can be restlessness, irritability, lethargy, muscular twitching, spasticity, exaggerated reflexes and intracranial hemorrhage. Treatment for this disorder is to make sure the patient gets enough water.
The treatment approach to hypernatremia caused by DI depends on which form of DI it is. If the DI is caused by insufficient VP secretion, administration of synthetic VP (DDAVP) can provide the needed VP to stimulate the kidney principal collecting duct cells to reabsorb water and restore the body's water balance. In DI caused by the kidney's unresponsiveness to VP, nephrogenic DI, DDAVP replacement doesn't help. A low-salt diet and thiazide diuretics help reduce solute delivery to the diluting segments of the tubules. This can help reduce, but not eliminate, the patient's water loss brought on by polyuria. So the nephrogenic DI patient must be certain to maintain an adequate water intake that balances his water output.