Wikia

Psychology Wiki

Hyponatremia

Talk0
34,135pages on
this wiki

Assessment | Biopsychology | Comparative | Cognitive | Developmental | Language | Individual differences | Personality | Philosophy | Social |
Methods | Statistics | Clinical | Educational | Industrial | Professional items | World psychology |

Biological: Behavioural genetics · Evolutionary psychology · Neuroanatomy · Neurochemistry · Neuroendocrinology · Neuroscience · Psychoneuroimmunology · Physiological Psychology · Psychopharmacology (Index, Outline)


Na-TableImage.png|
Hyponatremia
ICD-10 E871
ICD-9 276.1
OMIM [2]
DiseasesDB 6483
MedlinePlus [3]
eMedicine emerg/275 med/1130 ped/1124
MeSH {{{MeshNumber}}}


Hyponatremia (British: hyponatraemia) is an electrolyte disturbance (disturbance of the salts in the blood) in which the sodium (Natrium in Latin) concentration in the plasma is too low (hypo in Greek; in this case, below 135 mmol/L).

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) 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).

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 central pontine myelinolysis.

Symptoms Edit

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 Edit

File:Hyponatraemia Causes.svg

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; salt is also retained but to a lesser extent. 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 recover water and produce a fairly 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.

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.

Hyponatremia can also result from adrenal insufficiency, congenital adrenal hyperplasia, hypothyroidism, and some medications. However, the vast majority of cases, and perhaps all, of medication-associated hyponatremia is not due to the medication per se. Rather, the medication has caused SIADH or has led to volume depletion (see above)

Recent deaths from hyponatremia have 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].

Detox diets, especially water fasting can lead to hyponatremia if the intake of electrolytes is too low.[2]

Exercise Associated Hyponatremia Edit

Almond et al.[3] 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.

Exercise associated hyponatremia (EAH) is predominantly the occurrence of dilutional hyponatremia during or up to 24 hours after prolonged physical activity, caused by an increase in total body water relative to the amount of total body exchangeable sodium. This means consumption of fluids in excess of total body fluid losses and/or impaired renal water clearance: maximal urinary excretory rate is about 1 L/h in normal adults under resting conditions.

Inappropriate secretion of the hormone arginine vasopressin (AVP), or antidiuretic hormone, is also a contributory factor to the development of EAH. This excess hormone secretion prevents the kidneys from excreting the excess water in the urine. The primary means of avoiding EAH is to avoid excess fluid retention (weight gain during or after exercise). This can be accomplished by drinking only according to thirst and monitoring body weight before and during exercise - it is best to lose around two percent of body weight and never gain weight during exercise.

Ingestion of electrolyte-containing sports drinks cannot prevent the development of EAH in athletes who drink to excess. [4][5]

Pseudohyponatremia Edit

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.[6][7] 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 Edit

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

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.

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.

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

Notable cases Edit

  • 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[8].
  • 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[9].
  • Leah Betts[10] 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.[11] 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.[12]
  • Professional Wrestler, Michelle McCool, was hospitalized for 16 days in 2006 because of hyponatremia.[How to reference and link to summary or text]

Animals Edit

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 Edit

ReferencesEdit

  1. Wolff K, Tsapakis EM, Winstock AR, et al (May 2006). Vasopressin and oxytocin secretion in response to the consumption of ecstasy in a clubbing population. J. Psychopharmacol. (Oxford) 20 (3): 400–10.
  2. Woman left brain damaged by detox, BBC News, 2008-07-23
  3. 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.
  4. Statement of the Second International Exercise-Associated Hyponatremia Consensus Development Conference 2007. (PDF)
  5. Siegel AJ, Verbalis JG, Clement S, et al (May 2007). Hyponatremia in marathon runners due to inappropriate arginine vasopressin secretion. Am. J. Med. 120 (5): 461.e11–7.
  6. Weisberg LS (March 1989). Pseudohyponatremia: a reappraisal. Am. J. Med. 86 (3): 315–8.
  7. Nguyen MK, Ornekian V, Butch AW, Kurtz I (May 2007). A new method for determining plasma water content: application in pseudohyponatremia. Am. J. Physiol. Renal Physiol. 292 (5): F1652–6.
  8. A Fraternity Hazing Gone Wrong : NPR. URL accessed on 2008-05-26.
  9. Fallen Officer's Zeal Will Roll On. URL accessed on 2008-05-26.
  10. Hyponatremia ("Water Intoxication"). The DEA.org. URL accessed on 2007-05-10.
  11. [1]
  12. Father's tribute to marathon son. URL accessed on 2008-11-05.

Sources Edit


External links Edit

Template:Fluid, electrolyte, acid base metabolic pathology

Around Wikia's network

Random Wiki