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Classification and external resources

ICD-10 E87.1
ICD-9 276.1
DiseasesDB 6483
eMedicine emerg/275 med/1130 ped/1124
MeSH D007010

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), specifically below 135 mEq/L.[1]. The large majority of cases of hyponatremia occurring in adults result from an excess amount or effect of the water retaining hormone known as Antidiuretic Hormone commonly abbreviated as ADH.

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 (rarely) or syndrome of inappropriate antidiuretic hormone, SIADH). Regarding sodium loss as a cause of hyponatremia, it is important to note that such losses promote hyponatremia only in an indirect manner. In particular, hyponatremia occurring in association with sodium loss does not reflect inadequate sodium availability as a result of the losses. Rather, the sodium loss leads to a state of volume depletion, with volume depletion serving as a signal for the release of ADH. As a result of ADH-stimulated water retention, blood sodium becomes diluted and hyponatremia results.

There may also be spurious hyponatremia (pseudohyponatremia or factitious hyponatremia) if other substances expand the serum and dilute the sodium (for example, high blood sugar (hyperglycemia) or if a blood constituent leads to the creation of a sodium-free phase in the blood thereby causing the blood plasma volume to be overestimated (e.g. extreme hypertriglyceridemia).

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.



Patients 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.


One approach to determining causes of hyponatremia

An abnormally low plasma sodium level is best considered in conjunction with the person's plasma osmolality and extracellular fluid volume status. Indeed, correct ascertainment of volume status, as well as determination of the presence or absence of edema, are both critical in establishing the cause of hyponatremia. As described above, a state of volume depletion leads to increased blood levels of ADH and thus water retention. The greater the amount of water that is retained, the more the blood sodium will become diluted to cause worsening degrees of hyponatremia. The presence of edema indicates that blood volume has been lost insofar as fluid from the blood has shifted out into the peripheral tissues to cause the edema. In other words, edema is usually reflecting a state of blood volume depletion. As a result, edematous states are also associated with increased blood levels of ADH, water retention, and hyponatremia. In all cases of volume depletion-associated hyponatremia, it is important to note that retention of water per se, such as that promoted by ADH, does not correct the volume depleted state.

In addition to volume depletion, there are other causes of increased ADH levels (and ultimately, therefore, of hyponatremia). These include nausea, pain, and opiate drugs such as codeine and morphine. Such factors often play a role in the hyponatremia that is frequently seen in hospitalized patients.

Type Serum osmolality (mOsm/kg) Description
Hypotonic hyponatremia < 280 When the plasma osmolality is low, the extracellular fluid volume status may be in one of three states: low volume, normal volume, or high volume.
Isotonic hyponatremia between 280 and 295 Certain conditions that interfere with laboratory tests of serum sodium concentration (such as extraordinarily high blood levels of lipid or protein) may lead to an erroneously low measurement of sodium.[4] This is called pseudohyponatremia.
Hypertonic hyponatremia > 295 Hypertonic hyponatremia can be associated with shifts of fluid due to osmotic pressure.[4]

Although accounting for only a small minority of cases, hyponatremia due to excessive water intake does occur. This form of hyponatremia is not due to ADH action. Rather, in such instances, the amount of water ingested has exceeded the kidney's ability to excrete it. This typically occurs when the kidney lacks sufficient solute to accompany the water. In other words, the kidney cannot excrete pure water. Water must be accompanied by a solute such as urea in order to become urine. Hyponatremia arising due to a lack of solute in the kidney can occur if there has been grossly inadequate intake of nutrition (and thus inadequate urea production) at the same time as there has been excessive water intake (e.g. "beer potomania"). It can also occur even in normally nourished individuals when huge quantities (> 12 liters/day) of water have been ingested. Such high volumes of water require a solute accompaniment which exceeds the availability of solute even to the kidneys of a well-nourished individual.


The 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]

Notable cases

  • Craig Barrett, a New Zealand athlete, collapsed during a 50 km walk, probably due to water intoxication.
  • Matthew Carrington, a student at California State University in Chico, California, died of hyponatremia in February 2005 during a fraternity hazing ritual.[6]
  • James McBride, a police officer with the Metropolitan Police Department of the District of Columbia, died of hyponatremia on August 10, 2005. Officer McBride had been participating in a strenuous bicycle patrol training course. During a 12-mile (19 km) training ride on the second day of the course, Officer McBride drank as much as three gallons (11 liters) of water.[7]
  • Leah Betts[8] died on 16 November 1995 after taking an ecstasy tablet at her 18th birthday party and subsequently drinking too much water; the case received mass media coverage throughout the United Kingdom, which focused on the dangers of ecstasy.
  • Cynthia Lucero, who collapsed between miles 19 and 20 (31 and 32 km) of the Boston Marathon in 2002 was the second person ever to die in the history of the race.
  • In January 2007, Jennifer Strange, a woman in Sacramento, California, died following a water-drinking contest sponsored by a local radio station, Sacramento-based KDND-FM.[9] The contest was called "Hold Your Wee for a Wii".
  • After completing the 2007 London Marathon, 22-year-old David Rogers collapsed and later died as a result of hyponatremia.[10]
  • Anna Wood (schoolgirl), a Sydney schoolgirl who died after taking ecstasy in 1995 and then consuming too much water.[11]


Sodium 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.[12]

See also


  1. ^ Almond CS, Shin AY, Fortescue EB, et al. (April 2005). "Hyponatremia among runners in the Boston Marathon". N. Engl. J. Med. 352 (15): 1550–6. doi:10.1056/NEJMoa043901. PMID 15829535. 
  2. ^ Hyponatremia and athletes
  3. ^ Pestaña, C. (2000). Fluids and electrolytes in the surgical patient. Philadelphia, PA: Lippincott Williams and Wilkins. 75.
  4. ^ a b "emedicine.medschttp:". http://emedicine.medsc Retrieved 2009-08-02. 
  5. ^
  6. ^ "A Fraternity Hazing Gone Wrong : NPR". Retrieved 2008-05-26. 
  7. ^ "Fallen Officer's Zeal Will Roll On". Retrieved 2008-05-26. 
  8. ^ "Hyponatremia ("Water Intoxication")". The Retrieved 2007-05-10. 
  9. ^ Local report
  10. ^ "Father's tribute to marathon son". BBC News. 2007-04-24. Retrieved 2008-11-05. 
  11. ^
  12. ^ Lindsay Falvey (1979) 'Factors Limiting Cattle Production in the Northern Thailand Highlands'. Ph.D. Dissertation, University of Queensland, Australia.

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