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{{DiseaseDisorder infobox |
__NOTOC__
  Name        = Hyponatremia |
{| class="infobox" style="float:right;"
  Image      = Na-TableImage.png  |
  Caption    = [[Sodium]] |
  ICD10      = {{ICD10|E|87|1|e|70}} |
  ICD9        = {{ICD9|276.1}} |
}}
{{SI}}
 
'''For patient information click [[Hyponatremia (patient information)|here]]'''
 
{{CMG}}
 
{{SK}} Hyponatraemia
 
==Overview==
The [[electrolyte disturbance]] '''hyponatremia''' exists in humans when the [[sodium]] (''Natrium'' in [[Latin]]) concentration in the [[blood plasma|plasma]] falls below 130 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.
 
==Classification==
 
The etiology of hyponatremia can be categorized pathophysiologically in three primary ways, based on the patient's plasma osmolality.
 
*'''''Hypertonic hyponatremia''''', caused by resorption of water drawn by osmols such as glucose (hyperglycemia or diabetes) or mannitol (hypertonic infusion).
 
*'''''Isotonic hyponatremia''''', more commonly called "pseudohyponatremia," is caused by lab error due to hypertriglyceridemia (most common) or hyperparaproteinemia.
 
*'''''Hypotonic hyponatremia''''' is by far the most common type, and is often used interchangeably with "hyponatremia."  Hypotonic hyponatremia is categorized in 3 ways based on the patient's blood volume status. Each category represents a different underlying reason for the increase in ADH that led to the water retention and thence hyponatremia:
 
** '''''Hypervolemic hyponatremia''''', wherein there is decreased [[effective circulating volume]] even though total body volume is increased (by the presence of [[edema]]). The decreased effective circulating volume stimulates the release of ADH, which in turn leads to water retention. Hypervolemic hyponatremia is most commonly the result of [[congestive heart failure]], liver failure ([[cirrhosis]]), or kidney disease ([[nephrotic syndrome]]).
 
** '''''Euvolemic hyponatremia''''', wherein the increase in ADH is secondary to either physiologic but excessive ADH release (as occurs with nausea or severe pain) or inappropriate and non-physiologic secretion of ADH, i.e. [[syndrome of inappropriate antidiuretic hormone hypersecretion]] (SIADH).  Often categorized under euvolemic is hyponatremia due to inadequate urine solute as occurs in beer potomania or "tea and toast" hyponatremia, hyponatremia due to [[hypothyroidism]] or [[adrenal insufficiency]], and those rare instances of hyponatremia that are truly secondary to excess water intake (i.e., extreme psychogenic [[polydipsia]])
 
** '''''Hypovolemic hyponatremia''''', wherein ADH secretion is stimulated by volume depletion.
 
The volemic classification fails to include spurious and/or artifactual hyponatremia, which is addressed in the osmolar classification.  This includes hyponatremia that occurs in the presence of massive [[hypertriglyceridemia]], severe [[hyperglycemia]], and extreme elevation of [[immunoglobulin]] levels.
 
In '''''chronic hyponatremia''''', sodium levels drop gradually over several days or weeks and symptoms and complications are typically moderate. Chronic hyponatremia is often called asymptomatic hyponatremia in clinical settings because it is thought to have no symptoms; however, emerging data suggests that "asymptomatic" hyponatremia is not actually asymptomatic.<ref name="autogenerated185"/>
 
In '''''acute hyponatremia''''' sodium levels drop rapidly, resulting in potentially dangerous effects, such as rapid brain swelling, which can result in coma and death.
 
== Causes ==
[[Image:Hyponatraemia Causes.png|left|thumb|400px|Causes of hyponatraemia]]
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) &nbsp;&mdash; 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&nbsp;&mdash; 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]].  Also, Almond ''et al.''<ref>Almond CS et al. (2005) Hyponatremia among runners in the Boston Marathon. N Engl J Med, 352(15):1550-6.  PMID 15829535</ref> 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'' <ref> Siegel AJ et al. (2007) Am J Med, 120(5):461.e11-7.
PMID 17466660</ref> 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.
===Common Causes===
===Causes by Organ System===
 
{|style="width:80%; height:100px" border="1"
|style="height:100px"; style="width:25%" border="1" bgcolor="LightSteelBlue" | '''Cardiovascular'''
|style="height:100px"; style="width:75%" border="1" bgcolor="Beige" | [[Congestive heart failure ]]
|-
|-bgcolor="LightSteelBlue"
| '''Chemical / poisoning'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Dermatologic'''
|bgcolor="Beige"| [[Burns]]
|-
|-bgcolor="LightSteelBlue"
| '''Drug Side Effect'''
|bgcolor="Beige"| [[ACE inhibitors]], [[Ajuga nipponensis makino ]], [[Diuretics]], [[Nonsteriodal anti-inflammatory drugs ]]
|-
|-bgcolor="LightSteelBlue"
| '''Ear Nose Throat'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Endocrine'''
|bgcolor="Beige"| [[Addison's disease]], [[Corticosterone methyloxidase type I deficiency ]], [[Diabetes mellitus]], [[Diabetic coma]], [[Glucocorticoid deficiency]], [[Familial hyperreninemic hypoaldosteronism type 2]], [[Hypothyroidism]], [[Mineralocorticoid deficiency]], [[Myxedema coma ]], [[Syndrome of inappropriate antidiuretic hormone ]], [[Thyrotropin deficiency]], [[18-Hydroxylase deficiency ]], [[Familial  hypoaldosteronism ]]
|-
|-bgcolor="LightSteelBlue"
| '''Environmental'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Gastroenterologic'''
|bgcolor="Beige"| [[Acute liver failure ]], [[Cirrhosis]], [[Congenital chloride diarrhea ]], [[Diarrhea]], [[Gastrointestinal fistula]], [[Ileus]], [[Necrotizing enterocolitis ]], [[Pancreatitis]], [[Peritonitis]], [[Vomiting]], [[Cystic fibrosis]]
|-
|-bgcolor="LightSteelBlue"
| '''Genetic'''
|bgcolor="Beige"| [[18-Hydroxylase deficiency ]], [[Bartter Syndrome type 4 ]], [[Cystic fibrosis]], [[Familial  hypoaldosteronism ]], [[Corticosterone methyloxidase type I deficiency ]], [[Familial hyperreninemic hypoaldosteronism type 2]], [[Congenital chloride diarrhea ]]
|-
|-bgcolor="LightSteelBlue"
| '''Hematologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Iatrogenic'''
|bgcolor="Beige"| [[After pituitary surgery]], [[After surgery]], [[Ascitic tap]], [[Gastric drainage]], [[Hypotonic infusions]], [[Pleuracentesis]]
|-
|-bgcolor="LightSteelBlue"
| '''Infectious Disease'''
|bgcolor="Beige"| [[Malignant boutonneuse fever ]], [[Neonatal bacterial meningitis ]], [[Peritonitis]]
|-
|-bgcolor="LightSteelBlue"
| '''Musculoskeletal / Ortho'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Neurologic'''
|bgcolor="Beige"| [[Intracranial hemorrhage]], [[Subarachnoid hemorrhage]], [[Pituitary cancer]]
|-
|-bgcolor="LightSteelBlue"
| '''Nutritional / Metabolic'''
|bgcolor="Beige"| [[Hyperlipidemia]], [[Hyperproteinemia]], [[Hypoalbuminemia]], [[Low sodium diet]], [[Metabolic acidosis]], [[Diabetic coma]]
|-
|-bgcolor="LightSteelBlue"
| '''Obstetric/Gynecologic'''
|bgcolor="Beige"| [[Pregnancy]]
|-
|-bgcolor="LightSteelBlue"
| '''Oncologic'''
|bgcolor="Beige"| [[Pituitary cancer]]
|-
|-bgcolor="LightSteelBlue"
| '''Opthalmologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Overdose / Toxicity'''
|bgcolor="Beige"| [[Water intoxication]]
|-
|-bgcolor="LightSteelBlue"
| '''Psychiatric'''
|bgcolor="Beige"| [[Psychogenic polydipsia]], [[Psychosis]], [[Renal Failure]], [[Self-induced water intoxication and schizophrenic disorders syndrome ]]
|-
|-bgcolor="LightSteelBlue"
| '''Pulmonary'''
|bgcolor="Beige"| [[Cystic fibrosis]]
|-
|-bgcolor="LightSteelBlue"
| '''Renal / Electrolyte'''
|bgcolor="Beige"| [[Acute  kidney disease]], [[Chronic kidney disease]], [[Diuresis]], [[Glucosuria]], [[Ketonuria]], [[Nephrotic syndrome]], [[Renal Tubular Acidosis]], [[Tubulointerstitial kidney disease]], [[Bartter Syndrome type 4 ]], [[Corticosterone methyloxidase type I deficiency ]]
|-
|-bgcolor="LightSteelBlue"
| '''Rheum / Immune / Allergy'''
|bgcolor="Beige"| [[Addison's disease]], [[Nephrotic syndrome]]
|-
|-bgcolor="LightSteelBlue"
| '''Sexual'''
|bgcolor="Beige"| [[Cystic fibrosis]]
|-
|-bgcolor="LightSteelBlue"
| '''Trauma'''
|bgcolor="Beige"| [[Burns]]
|-
|-bgcolor="LightSteelBlue"
| '''Urologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Dental'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Miscellaneous'''
|bgcolor="Beige"| [[Beer potomania]], [[Ecstasy abuse ]], [[Factitious hyponatremia]], [[Hydration]], [[Massive edema]], [[Pseudohyponatremia]], [[Water Intoxication  ]], [[Hyperlipidemia]], [[Hyperproteinemia]], [[Hypoalbuminemia]], [[Exercise associated hyponatremia]]
|-
|-
| [[File:Siren.gif|30px|link=Hyponatremia resident survival guide]]|| <br> || <br>
| [[Hyponatremia resident survival guide|'''Resident'''<br>'''Survival'''<br>'''Guide''']]
|}
|}
'''For patient information, click [[Hyponatremia (patient information)|here]]'''
{{Hyponatremia}}{{CMG}}{{AE}}{{Saeedeh}}


=== Causes in Alphabetical Order===
{{SK}} Hyponatraemia; Low sodium.
 
{{MultiCol}}
*[[18-Hydroxylase deficiency ]]
*[[ACE inhibitors]]
*[[Acute  kidney disease]]
*[[Acute liver failure ]]
*[[Addison's disease]]
*[[After pituitary surgery]]
*[[After surgery]]
*[[Ajuga nipponensis makino ]]
*[[Ascitic tap]]
*[[Bartter Syndrome type 4 ]]
*[[Beer potomania]]
*[[Burns]]
*[[Chronic kidney disease]]
*[[Cirrhosis]]
*[[Congenital chloride diarrhea ]]
*[[Congestive heart failure ]]
*[[Corticosterone methyloxidase type I deficiency ]]
*[[Cystic fibrosis]]
*[[Diabetes mellitus]]
*[[Diabetic coma]]
*[[Diarrhea]]
*[[Diuresis]]
*[[Diuretics]]
*[[Ecstasy abuse ]]
*[[Exercise associated hyponatremia]]
*[[Factitious hyponatremia]]
*[[Familial  hypoaldosteronism ]]
*[[Familial hyperreninemic hypoaldosteronism type 2]]
*[[Gastric drainage]]
*[[Gastrointestinal fistula]]
*[[Glucocorticoid deficiency]]
*[[Glucosuria]]
*[[Hydration]]
*[[Hyperlipidemia]]
{{ColBreak}}
*[[Hyperproteinemia]]
*[[Hypoalbuminemia]]
*[[Hypothyroidism]]
*[[Hypotonic infusions]]
*[[Ileus]]
*[[Intracranial hemorrhage]]
*[[Ketonuria]]
*[[Low sodium diet]]
*[[Malignant boutonneuse fever ]]
*[[Massive edema]]
*[[Metabolic acidosis]]
*[[Mineralocorticoid deficiency]]
*[[Myxedema coma ]]
*[[Necrotizing enterocolitis ]]
*[[Neonatal bacterial meningitis ]]
*[[Nephrotic syndrome]]
*[[Nonsteriodal anti-inflammatory drugs ]]
*[[Pancreatitis]]
*[[Peritonitis]]
*[[Pituitary cancer]]
*[[Pleuracentesis]]
*[[Pregnancy]]
*[[Pseudohyponatremia]]
*[[Psychogenic polydipsia]]
*[[Psychosis]]
*[[Renal Failure]]
*[[Renal Tubular Acidosis]]
*[[Self-induced water intoxication and schizophrenic disorders syndrome ]]
*[[Subarachnoid hemorrhage]]
*[[Syndrome of inappropriate antidiuretic hormone ]]
*[[Thyrotropin deficiency]]
*[[Tubulointerstitial kidney disease]]
*[[Vomiting]]
*[[Water Intoxication  ]]
{{EndMultiCol}}
 
=== 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.<ref>Weisberg LS. (1989) Pseudohyponatremia: a reappraisal. Am J Med, 86(3):315-8.  PMID 2645773 </ref><ref>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</ref>  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 [[IVIG|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 [[sweat]]ing
**[[Burn (injury)|Burns]]
**[[Vomit]]ing
**[[Diarrhea]]
**[[Urine|Urinary]] loss
***[[Diuretic]] drugs (especially [[thiazide]]s)
***[[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'''.
**[[SIADH]] (syndrome of inappropriate [[antidiuretic hormone]])
**Some cases of psychogenic [[polydipsia]]
 
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 [[antidiuretic hormone|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).
 
==Epidemiology and Demographics==
 
Hyponatremia is the most common electrolyte disorder. Its frequency is higher in females, the elderly, and in patients who are hospitalized. The incidence of hyponatremia depends largely on the patient population. A hospital incidence of 15–20% is common, while only 3–5% of patients who are hospitalized have a serum sodium level of less than 130 mEq/L. Hyponatremia has been reported in up to 30% of elderly patients in nursing homes and is also present in approximately 30% of depressed patients on [[selective serotonin reuptake inhibitor]]s.<ref name="autogenerated185">Schrier, Robert W. "Does 'asymptomatic hyponatremia' exist?" Nature Reviews Nephrology. Vol 6, Apr 2010; p 185.</ref>
 
==Natural History, Complications and Prognosis==
 
Chronic hyponatremia can lead to such complications as neurological impairments. These neurological impairments most often affect gait and attention and can lead to falls, osteoporosis, and increased reaction time.
 
Complications for chronic hyponatremia are most dangerous for geriatric patients. Falls are the leading cause of deaths related to injury among people 65 years or older. In a recent study<ref>Harminder, S. Sandhu et al. "Hyponatremia associated with large-bone fracture in elderly patients." Int Urol Nephrol (2009) 41:733-737.</ref> the incidence of hyponatremia in elderly patients with large-bone fractures was more than double that of non-fracture patients. Recent work by Verbalis ''et al.''<ref>Ayus, Juan Carlos and Michael L. Moritz. "Bone Disease as a New Complication of Hyponatremia: Moving Beyond Brain Injury". CJASN ePress. Jan 14, 2010. 10.2215/CJN.09281209.</ref> suggests that hyponatremia induces osteoporosis and found the adjusted odds ratio for developing osteoporosis to be 2.87 times higher among adults with mild hyponatremia compared to those without.
 
Acute hyponatremia can lead to much more serious complications including brain disease, brain herniation, cardiopulmonary arrest, cerebral edema, seizures, coma, and death.
 
==Diagnosis==
=== Symptoms ===
Most patients with chronic water intoxication are asymptomatic, but may have [[symptom]]s related to the underlying cause.


Severe hyponatremia may cause [[osmosis|osmotic]] shift of water from the plasma into the [[brain]] [[cell (biology)|cells]]. Typical symptoms include [[nausea]], [[vomit]]ing, [[headache]] and [[malaise]]. As the hyponatremia worsens, confusion, diminished [[reflex]]es, [[convulsion]]s, [[stupor]] or [[coma]] may occur. Since nausea is, itself, a stimulus for the release of [[Vasopressin|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.
== [[Hyponatremia overview|Overview]] ==


===Laboratory Findings===
== [[Hyponatremia historical perspective|Historical Perspective]] ==
* [[Serum osmolality]]
* [[Blood urea nitrogen]] ([[BUN]])/[[creatinine]]
* [[Calcium]]
* [[Magnesium]]
* [[Urine sodium]]
* [[Thyroid stimulating hormone]] ([[TSH]])
* [[Serum glucose]]


==Treatment==
== [[Hyponatremia classification|Classification]] ==
*Hyponatremia is due to an excess of free water in the body, not due to a deficiency of sodium.
*The treatment of hyponatremia is therefore free water restriction.
*In patients who are receiving intravenous therapy, you should make sure that D<sub>5</sub>W is not infusing, and that drug infusions are mixed in normal saline, and not D<sub>5</sub>W.
*The patients access to water and juice should be restricted.
*In some refractory cases, the water to the room must be turned off.


The treatment of hyponatremia will depend on the underlying cause and whether the patient's volume status is hypervolemic, euvolemic, or hypovolemic. In the setting of hypovolemia, intravenous administration of normal saline may be effective, but caution must be exercised not to raise the serum sodium level too quickly (see below). Euvolemic hyponatremia is usually managed by fluid restriction and treatment to abolish any stimuli for ADH secretion such as nausea. Likewise, drugs causing SIADH should be discontinued if possible. Patients with euvolemic hyponatremia that persists despite those measures may be candidates for a so-called vaptan drug as discussed below. Hypervolemic hyponatremia should be treated by treating the underlying cause (e.g. heart failure, cirrhosis). In practice, it may not be possible to do so, in which case the treatment of the hyponatremia becomes the same as that for euvolemic hyponatremia (i.e. fluid restriction and/or use of a vaptan drug).
== [[Hyponatremia pathophysiology|Pathophysiology]] ==


Hyponatremia must be corrected slowly in order to lessen the chance of the development of [[central pontine myelinolysis]] (CPM), a severe neurological disease. In fact, overly rapid correction of hyponatremia is the most common cause of that potentially devastating disorder.<ref name="pmid10544728">{{cite journal |author=Bernsen HJ, Prick MJ |title=Improvement of central pontine myelinolysis as demonstrated by repeated magnetic resonance imaging in a patient without evidence of hyponatremia |journal=Acta Neurol Belg |volume=99 |issue=3 |pages=189–93 |year=1999 |month=September |pmid=10544728 |doi= |url=}}</ref> During treatment of hyponatremia, the serum sodium should not be allowed to rise by more than 8&nbsp;mmol/l over 24 hours (i.e. 0.33&nbsp;mmol/l/h rate of rise). In practice, too rapid correction of hyponatremia and thence CPM is most likely to occur during the treatment of hypovolemic hyponatremia. In particular, once the hypovolemic state has been corrected, the signal for ADH release disappears. At that point, there will be an abrupt water diuresis (since there is no longer any ADH acting to retain the water). A rapid and profound rise in serum sodium can then occur. Should the rate of rise of serum sodium exceed 0.33&nbsp;mmol/l/h over several hours, vasopressin may be administered to prevent ongoing rapid water diuresis.<ref>{{cite web|url=http://www.nejm.org/doi/full/10.1056/NEJM200005253422107|title=Hyponatremia|date=2000-05-25|author=Horacio J. Adrogué, M.D. and Nicolaos E. Madias, M.D|work=N Engl J Med 2000; 342:1581-1589|publisher=[[The New England Journal of Medicine]]}}</ref>
== [[Hyponatremia causes|Causes]]==
==[[Hyponatremia differential diagnosis|Differentiating Hyponatremia]]==


Pharmaceutically, [[vasopressin receptor antagonist]]s can be used in the treatment of hyponatremia, especially in patients with SIADH, congestive heart failure or liver cirrhosis. A vasopressin receptor antagonist is an agent that interferes with the action at the vasopressin receptors. A new class of medication, the "vaptan" drugs has been specifically developed to inhibit the action of vasopressin on its receptors (V1A, V1B, and V2). These receptors have a variety of functions, with the V1A and V2 receptors are expressed peripherally and involved in the modulation of blood pressure and kidney function respectively, while the V1A and V1B receptors are expressed in the central nervous system. V1A is expressed in many regions of the brain, and has been linked to a variety of social behaviors in humans and animals.
== [[Hyponatremia epidemiology and demographics|Epidemiology and Demographics]] ==


=== Vaptan drugs ===
== [[Hyponatremia risk factors|Risk Factors]] ==
The “vaptan” class of drugs contains a number of compounds with varying selectivity, several of which are either already in clinical use or in clinical trials as of 2010.


Unselective (mixed V1A, V2)
== [[Hyponatremia screening|Screening]] ==


* [[Conivaptan]]
== [[Hyponatremia natural history, complications and prognosis|Natural History, Complications and Prognosis]] ==


V1A selective
== Diagnosis ==


* Relcovaptan
[[Hyponatremia diagnostic study of choice|Diagnostic Study of choice]] | [[Hyponatremia history and symptoms|History and Symptoms]] | [[Hyponatremia physical examination|Physical Examination]] | [[Hyponatremia laboratory findings|Laboratory Findings]] | [[Hyponatremia electrocardiogram|Electrocardiogram]] | [[Hyponatremia X-ray|X-ray]] | [[Hyponatremia echocardiogram or ultrasound|Echocardiogram or Ultarsound]] | [[Hyponatremia CT|CT scan]] | [[Hyponatremia MRI|MRI]] | [[Hyponatremia other imaging findings|Other Imaging Findings]] | [[Hyponatremia other diagnostic studies|Other Diagnostic Studies]]


V1B selective
== Treatment ==


* Nelivaptan
[[Hyponatremia medical therapy|Medical Therapy]] | [[Hyponatremia surgery|Surgery]] | [[Hyponatremia primary prevention|Primary Prevention]] | [[Hyponatremia secondary prevention|Secondary Prevention]] | [[Hyponatremia cost-effectiveness of therapy|Cost Effectiveness of Therapy]] | [[Hyponatremia future or investigational therapies|Future or Investigational Therapies]]


V2 selective
== Case Studies ==


* [[Lixivaptan]]
[[Hyponatremia case study one|Case #1]]
 
* Mozavaptan
 
* Satavaptan
 
* [[Tolvaptan]]
 
The V2-receptor antagonists tolvaptan and conivaptan allow excretion of electrolyte free water and are effective in increasing serum sodium in euvolemic and hypervolemic hyponatremia.<ref name="Hospital Practice 2010">{{cite journal | author= Robert D. Zenenberg,Do, et. al | title= Hyponatremia: Evaluation and Management | journal=Hospital Practice. | month=February | pages=89–96 | pmid= 20469629 | volume=38 | issue=1 | url=http://hosppract.com/index.php?article=283#none | doi=10.3810/hp.2010.02.283 | date=2010-04-27}}</ref>
 
===Rate of Na Correction===
The rate of correction of [[hyponatremia]] should be 0.5-1.0meq/L/hr, with not more than a 12 meq/l correction in 24 hrs. If the patient has ongoing [[seizures]] (or [Na<sup>+</sup>]<115 meq/li), correction can be attempted at up to 2 meq/L/hr, but only while [[seizure activity]] lasts and the [Na<sup>+</sup>] exceeds 125-130 meq/Li.
 
== Related Chapters ==
*[[Water intoxication]]
*[[Hypernatremia]]
*[[Edible salt]]
*[[Osmotic demyelination syndrome]]
 
==References==
{{Reflist|2}}


{{Endocrine, nutritional and metabolic pathology}}
{{Endocrine, nutritional and metabolic pathology}}
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Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Hyponatremia from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Study of Choice

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

X-ray

Echocardiogram or Ultarsound

CT scan

MRI

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Hyponatremia On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Hyponatremia

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Hyponatremia

CDC on Hyponatremia

Hyponatremia in the news

Blogs on Hyponatremia

Directions to Hospitals Treating hyponatremia

Risk calculators and risk factors for Hyponatremia

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Saeedeh Kowsarnia M.D.[2]

Synonyms and keywords: Hyponatraemia; Low sodium.

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Hyponatremia

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Study of choice | History and Symptoms | Physical Examination | Laboratory Findings | Electrocardiogram | X-ray | Echocardiogram or Ultarsound | CT scan | MRI | Other Imaging Findings | Other Diagnostic Studies

Treatment

Medical Therapy | Surgery | Primary Prevention | Secondary Prevention | Cost Effectiveness of Therapy | Future or Investigational Therapies

Case Studies

Case #1

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cs:Hyponatremie de:Hyponatriämie sv:Hyponatremi


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