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Hyponatremia (British: hyponatraemia) is an electrolyte disturbance (a disturbance of the salts in the blood) in which the sodium (Natrium in Latin) concentration in the plasma is lower than normal (hypo in Greek; in this case, below 135 mmol/L).[1] Severe or rapidly progressing hyponatremia can result in swelling of the brain (cerebral edema), and the symptoms of hyponatremia are mainly neurological. Hyponatremia is most often a complication of other medical illnesses in which either fluids rich in sodium are lost (for example because of diarrhea or vomiting), or excess water accumulates in the body at a higher rate than it can be excreted (for example in polydipsia or syndrome of inappropriate antidiuretic hormone, SIADH). There may also be spurious hyponatremia (pseudohyponatremia or factitious hyponatremia) if other substances expand the serum and dilute the sodium (for example, high blood levels of fats in hypertriglyceridemia or high blood sugar in hyperglycemia). Hyponatremia can also affect athletes who consume too much fluid during endurance events,[2] people who fast on juice or water for extended periods and people whose dietary sodium intake is chronically insufficient. The diagnosis of hyponatremia relies mainly on the medical history, clinical examination and blood and urine tests. Treatment can be directed at the cause (for example, corticosteroids in Addison's disease) or involve restriction of water intake, intravenous saline or drugs like diuretics, demeclocycline, urea or vaptans (antidiuretic hormone receptor antagonists). Correcting the salt and fluid balance needs to occur in a controlled fashion, as too rapid correction can lead to severe complications such as heart failure or a sometimes irreversible brain lesion known as central pontine myelinolysis.
[edit] SymptomsPatients with low-level, chronic water intoxication are often asymptomatic, but may have symptoms related to the underlying cause. Severe hyponatremia in acute or chronic form may cause osmotic shift of water from the plasma into the brain cells. Typical symptoms include nausea, vomiting, headache and malaise. As the hyponatremia worsens, confusion, diminished reflexes, convulsions, stupor or coma may occur. Since nausea is, itself, a stimulus for the release of ADH, which promotes the retention of water, a positive feedback loop may be created and the potential for a vicious cycle of hyponatremia and its symptoms exists. A feedback loop can also be created by severe thirst, which is a symptom of some hyponatremic individuals.[3] When these people consume large quantities of water without an adequate increase in sodium, the hyponatremic condition worsens. [edit] CausesAn abnormally low plasma sodium level is best considered in conjunction with the person's plasma osmolality and extracellular fluid volume status.
[edit] TreatmentThe treatment of hyponatremia usually depends on the underlying cause. If a person has few symptoms, little treatment other than water restriction may be required. In the setting of volume depletion, intravenous administration of normal saline may be effective. Over aggressive correction of hyponatremia may lead to a syndrome of central pontine myelinolysis. Thus, correction of serum sodium should not exceed 12 mEq/L per 24 hours nor 18 mEq/L per 48h. Seizures associated with hyponatremia are typically treated with a 100 mL bolus of 3 % hypertonic saline.[5] [edit] Notable cases
[edit] AnimalsSodium deficiency exists in grazing animals where soil sodium levels have been depleted by leaching. This is more common in mountainous regions. Agricultural science research conducted in the northern Thai highlands in the 1970s found that an endemic sodium deficiency masked all other nutrient deficiencies across all seasons and reduced productivity. Sodium supplementation increased liveweight gain by around 30% and also reproductive rates by around 30%. Simple salt supplementation is now recommended in this region and neighbouring mountains, as both a herd management tool and for increased productivity (see sources below). [edit] See also[edit] References
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