Hyponatremia is a serum sodium concentration of less than 135 mmol/L (135 mEql/L).
Sodium is the most plentiful electrolyte in the ECF compartment with a concentration ranging from 135 to 145 mEq/L (135 to145 mmol/L). Of this, only a small amount (10 to 14 mEq/L is found in the intracellular compartment.
What are the functions of sodium?
Sodium functions mainly in regulating the extracellular volume. It is a major cation in the ECF compartment.
- Regulation of serum osmolarity- A change in serum sodium concentration changes the Serum osmolality ou or into its normal range of 275 to 295 mOsm/kg
- Regulation of acid-base balance- This is because sodium is part of the sodium bicarbonate molecule.
- Nervous system function as a current-carrying ion,and in other excitable tissues.
Sodium gets into the body through the GI tract and is eliminated by the kidneys or lost from the GI tract or skin. Majority of the sodium intake normally is derived from dietary sources.
Body needs for sodium can be met by as little as 500 mg/day
Other sources of sodium are intravenous saline infusions and medications which contain sodium.
The kidneys are extremely efficient in the regulation of sodium output. The kidneys have the ability to reabsorb all the filtered sodium when sodium intake is limited resulting in essentially sodium-free urine. Conversely, urinary losses of sodium increase as intake increases.
Sodium losses increase with conditions such as vomiting, diarrhea, fistula drainage, and gastrointestinal suction that remove sodium from the stomach or small intestine.
Sodium leaves the skin by way of the sweat glands.
Sweat is a hypotonic solution containing both sodium and chloride. Although sodium losses due to sweating are usually negligible, they can increase greatly during exercise and periods of exposure to a hot environment.
What is hyponatremia?
Hyponatremia is a serum sodium concentration of less than 135 mmol/L (135 mEql/L).
It is one of the most common electrolyte disorders seen in hospitalized patients and is also common in the outpatient population, particularly in the elderly.
Elderly people at a higher risk of developing hypionatremia due to a number of age-related events such as a decrease in renal function accompanied by limitations in sodium conservation.
Types of hyponatremia
Non-Isotonic hyponatremia can present as a hypotonic or hypertonic states due to the effects of osmotically active particles like glucose. Therefore there are a number of types of hyponatremia
- Hypertonic (translocational) hyponatraemia occurs due to an osmoticshift in water from the intracellular compartment to the extracellular compartment.
It develops when there is a significant increase in the concentration of extracellular solutes, as occurs in hyperglycaemia, drawing water out of cells into the ECF.
In this situation, the sodium in the ECF becomes diluted as water moves out of body cells in response to the osmotic effects of hyperglycemia.
- Hypotonic (dilutional) hyponatraemia is the most common type. This form is usually associated with a dilution of sodium levels in the extracellular fluid relative to that of water.
It is caused by water retention (an excessive gain in water), an excessive loss of sodium ion or a combination of both.
This type can be classified as hypovolemic, euvolemic, or hypervolemic based on accompanying ECF fluid volumes.
Diuretic therapy, which affects both sodium and water elimination, can cause either hypovolemic or euvolemic hyponatremia.
In dilutional hyponatraemia, the relatively low sodium levels and elevated water content will inhibit the release of aldosterone, further contributing to sodium loss.
- Hypovolemic hypotonic hyponatremia. This typeoccurs when water and sodium is lost, but in this cace the loss of water far exceeds the loss of sodium and then only the water is replaced.
Causes: Excessive sweating in hot weather or during heavy exercise causing loss of salt and water.
Hyponatremia develops when water, rather than electrolyte-containing liquids, is used to replace fluids lost in sweating.
Loss of sodium from the gastrointestinal tract as a result of frequent GI irrigations with distilled water.
Iso-osmotic fluid loss, such as occurs in vomiting or diarrhea, does not usually lower serum sodium levels unless these losses are replaced with disproportionate amounts of orally ingested or parenterally administered water.
Gastrointestinal fluid loss and ingestion of excessive water are common causes of acute hyponatremia in infants and children.
Complication of adrenal insufficiency and is due to a decrease in aldosterone levels.
A lack of aldosterone increases renal losses of sodium and a cortisol deficiency leads to increased release of ADH with water retention.
- Euvolemic or normovolemic hypotonic hyponatremiais the retention of water with dilution of sodium while maintaining the extracelular volume within a normal range.
It is caused by SIADH. The risk of its development is increased during the post operative period due to hugh ADH levels that produce an increase in water reabsorption by the kidneys.
It can also result due to IV fluid replacement with electrolyte-free fluids such as 5% glucose in water.
- Hypervolemic hypotonic hyponatremia.This type is seen when hyponatremia is accompanied by edema-associated disorders such as decompensated heart failure, advanced liver disease, and renal disease.
Although the total body sodium is increased in heart failure, the extracellular volume is sensed as inadequate by the baroreceptors due to relative arterial underfifilling. This results in increased ADH levels known as nonosmotic ADH secretion.
An example of an excessive water gain involves the oversecretion of antidiuretic hormone (ADH). More water is reabsorbed from the forming urine in the distal convoluting tubules and collecting ducts into the blood, diluting the sodium concentration in the ECF.
In another situation, a person with a psychological disorder can compulsively drink water to a point where they induce a hyponatraemic state. This is known as water intoxication.
Signs and symptoms of hyponatremia.
The signs and symptoms of hyponatremia depend on the severity and the rate of onset of the sodium dilution.
These features may be acute or more insidious in onset and less severe.
Because of water movement, this state causes an increase in intracellular water that is responsible for its clinical features.
Fingerprint edema demonstrated by pressing the finger firmly over the bony surface of the sternum for 15 to 30 seconds is a sign of excess intracellular water. A fingerprint similar to that observed when pressing on a piece of modeling clay is seen
Muscle cramps, weakness, and fatigue are early signs due to the effect of low sodium on skeletal muscle functionthat mostly occur during heavy exercise in hot weather.
Nausea and vomiting, abdominal cramps, and diarrhea may also develop.
Central nervous system manifestations such as lethargy, apathy, and headache can progress to disorientation, confusion, gross motor weakness, and depression of deep tendon reflexes.
People with extremely low sodium levels present with seizures and coma due to cerebral edema.
If the condition develops slowly, signs and symptoms do not usually develop until serum sodium levels approach 120 mmol/L in severe hyponatremia.
Water intoxication is a neurologic effects of acute hypotonic hyponatremia.
The severity of symptoms changes with the degree of hyponatraemia and the rate at which it develops. A severe case of hyponatraemia can be fatal.
The diagnosis can be based on physical examination of the patient that shows the presence of conditions which predispose an individual to sodium loss or water retention.
Diagnosis of hyponatremia is also based on laboratory reports of a
- Decreased serum sodium concentration,
- Serum osmolarity and
- Urine osmolality, and urine sodium concentration;
Treatment of hyponatremia
The treatment of hyponatremia is determined by the underlying cause, severity, and rapidity of onset.
When hyponatremia is caused by water intoxication, limiting water intake or discontinuing medications that contribute to SIADH may be sufficient.
The administration of a saline solution orally or intravenously may be needed when hyponatremia is caused by sodium deficiency.
Symptomatic hyponatremia is often treated with hypertonic saline solution and a loop diuretic, such as furosemide, to increase water elimination. This combination allows for correction of serum sodium levels while ridding the body of excess water.
The ADH V2 receptor antagonists may be used in the treatment of euvolemic hyponatremia.
The treatment of severe hyponatremia varies dependent on the timing of the onset of the disorder. In acute severe hyponatremia, rapid treatment with a hypertonic saline (3% normal saline) solution is emergent.
When the onset of hyponatremia occurs after 48 hours, there is concern about the rapidity with which serum sodium levels are corrected.
Cells, particularly those in the brain, tend to defend against changes in cell volume caused by changes in ECF osmolality by increasing or decreasing their concentration of organic osmolytes.
In the case of prolonged water intoxication, brain cells reduce their concentration of osmolytes as a means of preventing an increase in cell volume.
It takes several days for brain cells to restore the osmolytes lost during hyponatremia.
Thus, treatment measures that produce rapid changes in serum osmolality may cause a dramatic change in brain cell volume. One of the reported effects of rapid treatment of hyponatremia, called the osmotic demyelination syndrome, is characterized by destruction of the myelin sheath of the axons passing through the brain stem.This syndrome can cause serious neurologic injury and sometimes death.
As the consequences of hyponatraemia can result in an altered level of consciousness, initial interventions to assess and protect the airway are critical.
However, these neurological signs are quite late in the clinical progression, so frequent and comprehensive neurological assessment is indicated in individuals with suspected sodium imbalances to prevent life-threatening deterioration.
Generally speaking, sodium deficiency should be corrected. In an individual with an intact gag and swallow reflex, oral supplementation is most beneficial.
The cause of the sodium deficit should be identified and managed as appropriate.
Reducing sodium loss through ceasing any natriuretic drugs is also important.
It is critical that hyponatraemia is corrected slowly so as to prevent osmotic demyelination syndrome.
Fluid restrictions may be necessary if the hyponatraemia is related to haemodilution.
Hypertonic solutions may be used to increase the speed of hyponatraemia correction if severe neurological signs occur; however, this must be closely monitored and still not corrected too quickly.