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Hyponatremia



Hyponatremia
Classification & external resources
Sodium
ICD-10 E87.1
ICD-9 276.1

The electrolyte disturbance hyponatremia (British hyponatraemia) exists in humans when the sodium (Natrium in Latin) concentration in the plasma falls below 135 mmol/L. At lower levels water intoxication may result, an urgently dangerous condition. Hyponatremia is an abnormality that can occur in isolation or, as most often is the case, as a complication of other medical illnesses. In the case of other mammals, particularly agricultural animals, different indications are relevant. The following refers to humans; an introduction to sodium deficiency in cattle is appended.

Additional recommended knowledge

Contents

Symptoms

Most patients with chronic water intoxication are asymptomatic, but may have symptoms related to the underlying cause.

Severe hyponatremia 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 circle of hyponatremia and its symptoms exists.

Causes

  An abnormally low plasma sodium level is best considered in conjunction with the person's plasma osmolarity and extracellular fluid volume status.

Most cases of hyponatremia are associated with reduced plasma osmolarity. In fact, the vast majority of adult cases are due to increased vasopressin, i.e., anti-diuretic hormone (ADH). Vasopressin is a hormone that causes retention of water, but not salt. Hence, the patient with hyponatremia can be viewed as the patient with increased ADH activity. It is the physician's task to identify the cause of the increased ADH activity in each case.

In patients who are volume depleted, i.e., their blood volume is too low, ADH secretion is increased, since volume depletion is a potent stimulus for ADH secretion. As a result, the kidneys of such patients hold on to water and produce a very concentrated urine. Treatment is simple (if not without risk)  — simply restore the patient's blood volume, thereby turning off the stimulus for ongoing ADH release and water retention.

Some patients with hyponatremia have normal blood volume. In those patients, the increased ADH activity and subsequent water retention may be due to "physiologic" causes of ADH release such as pain or nausea. Alternatively, they may have the Syndrome of Inappropriate ADH (SIADH). SIADH represents the sustained, non-physiologic release of ADH and most often occurs as a side effect of certain medicines, lung problems such as pneumonia or abscess, brain disease, or certain cancers (most often small cell lung carcinoma).

A third group of patients with hyponatremia are often said to be "hypervolemic". They are identified by the presence of peripheral edema. In fact, the term "hypervolemic" is misleading since their blood volume is actually low. The edema underscores the fact that fluid has left the circulation, i.e., the edema represents fluid that has exited the circulation and settled in dependent areas. Since such patients do, in fact, have reduced blood volume, and since reduced blood volume is a potent stimulus for ADH release, it is easy to see why they have retained water and become hyponatremic. Treatment of these patients involves treating the underlying disease that caused the fluid to leak out of the circulation in the first place. In many cases, this is easier said than done when one recognizes that the responsible underlying conditions are diseases such as liver cirrhosis or heart failure — conditions that are notoriously difficult to manage, let alone cure.

Hyponatremia can result from dysfunctions of the mineralocorticoid aldosterone (i.e. hypoaldosteronism) due to adrenal insufficiency, congenital adrenal hyperplasia, and some medications.

It is worth considering separately, the hyponatremia that occurs in the setting of diuretic use. Patients taking diuretic medications such as furosemide (Lasix), hydrochlorothiazide, chlorthalidone, etc., become volume depleted. That is to say that their diuretic medicine, by design, has caused their kidneys to produce more urine than they would otherwise make. This extra urine represents blood volume that is no longer there, that has been lost from the body. As a result, their blood volume is reduced. As mentioned above, lack of adequate blood volume is a potent stimulus for ADH secretion and thence water retention.

A recent surge in death from hyponatremia has been attributed to overintake of water while under the influence of MDMA. This may also be related to inappropriate release of ADH that is stimulated by the drug[1].

Also, Almond et al.[2] found hyponatremia in as many as 13% of runners in a recent Boston Marathon, with life-threatening hyponatremia (serum Na below 120 mmol/L) in 0.6%. The runners at greatest risk of serious water intoxication had moderate weight gain during the race due to excessive water consumption (see reference). Siegel et al. [3] recently found that in addition to over-zealous drinking, the cause of exercise-associated hyponatremia (EAH) is from an inappropriate secretion of the hormone arginine vasopressin, or antidiuretic hormone. This excess hormone secretion prevents the kidneys from excreting the excess water in the urine.

Notable cases

  • Matthew Carrington, a student at California State University in Chico, California, died of hyponatremia in February 2005 during a fraternity hazing ritual [1].
  • 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[2].
  • Leah Betts[4] died on the 16th of 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.
  • 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.[3]. The fact that the contest was called, "Hold your wee for a Wii" has led some to believe that not urinating is related to hyponatremia. This is untrue; this type of water intoxication is caused by excessive and rapid consumption of (sodium-free) water.
  • After completing the 2007 London Marathon, 22-year-old David Rogers collapsed and later died as a result of hyponatremia.[4]

Pseudohyponatremia

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. This is called pseudohyponatremia, and can occur when laboratories use the flame-photometric and indirect (but not direct) ion-selective electrode assays.[5][6] This is distinct from a true dilutional hyponatremia that can be caused by an osmotic shift of water from cells to the bloodstream after large infusions on mannitol or intravenous immunoglobulin.

Hypoosmolar hyponatremia

When the plasma osmolarity is low, the extracellular fluid volume status may be in one of three states:

  • Low volume. Loss of water is accompanied by loss of sodium.
    • Excessive sweating
    • Burns
    • Vomiting
    • Diarrhea
    • Urinary loss
      • Diuretic drugs (especially thiazides)
      • Addison's disease
      • Cerebral salt-wasting syndrome
      • Other salt-wasting kidney diseases

Treat underlying cause and give IV isotonic saline. It is important to note that sudden restoration of blood volume to normal will turn off the stimulus for continued ADH secretion. Hence, a prompt water diuresis will occur. This can cause a sudden and dramatic increase the serum sodium concentration and place the patient at risk for so-called "central pontine myelinolysis" (CPM). That disorder is characterized by major neurologic damage, often of a permanent nature.

Because of the risk of CPM, patients with low volume hyponatremia may eventually require water infusion as well as volume replacement. Doing so lessens the chance of a too rapid increase of the serum sodium level as blood volume rises and ADH levels fall.

  • Normal volume.

The cornerstone of therapy for SIADH is reduction of water intake. If hyponatremia persists, then demeclocycline (an antibiotic with the side effect of inhibiting ADH) can be used. SIADH can also be treated with specific antagonists of the ADH receptors, such as conivaptan or tolvaptan.

  • High volume. There is retention of water.
    • Congestive heart failure
    • Hypothyroidism and hypocortisolism
    • Liver cirrhosis
    • Nephrotic syndrome
    • Psychogenic polydipsia

Placing the patient on water restriction can also help in these cases.

Severe hyponatremia may result from a few hours of heavy exercise in high temperature conditions, such as hiking in desert areas, or from endurance athletic events when electrolytes are not supplied. (Such an incident notably happened to long-distance athlete Craig Barrett in 1998).

Bovines

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 (see sources below).

See also

References

  1. ^ Wolff K et al. (2005) Vasopressin and oxytocin secretion in response to the consumption of ecstasy in a clubbing population. J Psychopharmacology, 20:400-410. PMID 16574714
  2. ^ Almond CS et al. (2005) Hyponatremia among runners in the Boston Marathon. N Engl J Med, 352(15):1550-6. PMID 15829535
  3. ^ Siegel AJ et al. (2007) Am J Med, 120(5):461.e11-7. PMID 17466660
  4. ^ Hyponatremia ("Water Intoxication"). The DEA.org. Retrieved on 2007-05-10.
  5. ^ Weisberg LS. (1989) Pseudohyponatremia: a reappraisal. Am J Med, 86(3):315-8. PMID 2645773
  6. ^ Nguyen MK et al. (2007) A new method for determining plasma water content: application in pseudohyponatremia. Am J Phys - Renal, 292(5):F1652-6. PMID 17299138

Sources

  • Hyponatremia at eMedicine
  • Sports Medicine
  • honoluluclub
  • DDB 6483
  • Lindsay Falvey (1979) 'Factors Limiting Cattle Production in the Northern Thailand Highlands'. Ph.D. Dissertation, University of Queensland, Australia.
 
This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Hyponatremia". A list of authors is available in Wikipedia.
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